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DIAGNOSTIC AND STATISTICAL
MANUAL OF
MENTAL DISORDERS
FIFTH EDITION
DSM-5"
American Psychiatric Association
Officers 2012-2013
PRESIDENT DILIP V. JESTE, M.D.
PRESIDENT-ELECT JEFFREY A. LIEBERMAN, M.D.
TREASURER DAVID FASSLER, M.D.
SECRETARY ROGER PEELE, M.D.
Assembly
SPEAKER R. SCOTT BENSON, M.D.
SPEAKER-ELECT MELINDA L. YOUNG, M.D.
Board of Trustees
JEFFREY AKAKA, M.D.
CAROL A. BERNSTEIN, M.D.
BRIAN CROWLEY, M.D.
ANITA 8. EVERETT, M.D.
JEFFREY GELLER, M.D., M.P.H.
Marc DAVID GRAFF, M.D.
sJAMES:A. GREENEY M.D.
JUDITH F. KASHTAN, M.D.
MOLLY K. McVoy, M.D.
JAMES E. NININGER, M.D.
JOHN M. OLDHAM, M.D.
ALAN F. SCHATZBERG, M.D.
ALIK S. WIDGE, M.D., PH.D.
ERIK R. VANDERLIP, M.D.,
MEMBER-IN-TRAINING TRUSTEE-ELECT
DIAGNOSTIC AND STATISTICAL
MANUAL OF
MENTAL DISORDERS,
FIFTH EDITION
DSM-S"
Copyright © 2013 American Psychiatric Association
DSM and DSM-5 are trademarks of the American Psychiatric Association. Use of these terms
is prohibited without permission of the American Psychiatric Association.
ALL RIGHTS RESERVED. Unless authorized in writing by the APA, no part of this book may
be reproduced or used in a manner inconsistent with the APA’s copyright. This prohibition
applies to unauthorized uses or reproductions in any form, including electronic applications.
Correspondence regarding copyright permissions should be directed to DSM Permissions,
American Psychiatric Publishing, 1000 Wilson Boulevard, Suite 1825, Arlington, VA 22209-
3901.
Manufactured in the United States of America on acid-free paper.
ISBN 978-0-89042-554-1 (Hardcover)
ISBN 978-0-89042-555-8 (Paperback)
American Psychiatric Association
1000 Wilson Boulevard
Arlington, VA 22209-3901
www. psych.org
The correct citation for this book is American Psychiatric Association: Diagnostic and Statisti-
cal Manual of Mental Disorders, Fifth Edition. Arlington, VA, American Psychiatric Associa-
tion, 2013.
Library of Congress Cataloging-in-Publication Data
Diagnostic and statistical manual of mental disorders : DSM-5. — 5th ed.
p.;cm.
DSM-5
DSM-V
Includes index.
ISBN 978-0-89042-554-1 (hardcover : alk. paper) — ISBN 978-0-89042-555-8 (pbk. : alk. paper)
I. American Psychiatric Association. I]. American Psychiatric Association. DSM-5 Task Force.
III. Title: DSM-5. IV. Title: DSM-V.
[DNLM: 1. Diagnostic and statistical manual of mental disorders, 5th ed. 2. Mental Disorders—
classification. 3. Mental Disorders—diagnosis. WM 15]
RC455.2.C4
616.89'075—dc23
2013011061
British Library Cataloguing in Publication Data me a
A CIP record is available from the British Library.
Text Design—Tammy J. Cordova bE
Manufacturing—Edwards Brothers Malloy 2
cu
Contents
DSN-5 Classification. .........0 000 0c ee ee eee eee eee xiii
PRETACE icc cee eases eins ea ee Paes a ei eee TS xli
Section |
DSM-5 Basics
INIPORUCHON is 5555.5 ores Ro-oe wed owe oh we beeen e eer 5
Use of the: Manual sé 2a5 56s wksetawe dis cs cee eee 19
Cautionary Statement for Forensic Use of DSM-5............ 25
Section ll
Diagnostic Criteria and Codes
Neurodevelopmental Disorders ........... ccs ener een enene 31
Schizophrenia Spectrum and Other Psychotic Disorders...... 87
Bipolar and Related Disorders...........200cnesencencnes 123
Depressive Disorders ........0: cece eee neneenee 155
Anxiety DISOIGelrs, «ice cise ice ds He eines ete enw s 189
Obsessive-Compulsive and Related Disorders ............. 235
Trauma- and Stressor-Related Disorders. .........ecse0e0: 265
Dissociative Disorders ....... 0.00: ccc e newt ne ten eee enene 291
Somatic Symptom and Related Disorders ............-.+.+. 309
Feeding and Eating Disorders ............02 00 eeeeeeeenes 329
Elimination Disorders ..........0 000 e eee eee eee eee 355
Sleep-Wake Disorders. ........... 0020 c cece cence eens 361
Sexual DysfunctionS ......... ccc ener ncceetenencocncner 423
Gender Dysphoria ............00 cece eee eee eens 451
Disruptive, Impulse-Control, and Conduct Disorders........
Substance-Related and Addictive Disorders ...............
Neurocognitive Disorders. ......-. 0.0.00 0 cece eee eee eee
Personality Disorders ........ 0c cece cece eens
Paraphilic Disorders ......... 000s cuennenneneeenenennas
Other Mental Disorders .......-.00.. cece eee nen e rte enene
Medication-Induced Movement Disorders
and Other Adverse Effects of Medication ................
Other Conditions That May Be a Focus of Clinical Attention. .
Section Ill
Emerging Measures and Models
Assessment MeasSureS ..........0 cece eee e terete nese nae
Cultural Formulation. ........ 000. c cece cere teeter enone
Alternative DSM-5 Model for Personality Disorders .........
Conditions for Further Study .............2.0 200 c eee eeee
Appendix
Highlights of Changes From DSM-IV to DSM-5.............
Glossary of Technical TermS ...........000ceneneuenenees
Glossary of Cultural Concepts of Distress ..............055
Alphabetical Listing of DSM-5 Diagnoses and Codes
(ICD-9-CM and ICD-10-CM)........ 00.0 e cece eee eee
Numerical Listing of DSM-5 Diagnoses and Codes
(OSIM) oss 'a. so wh aera ao ana we ace nee ree a A
Numerical Listing of DSM-5 Diagnoses and Codes
(CD=10-CM) 5s od Sh ce wien d eae Se Ga alewet ee ve SON
DSN-5 Advisors and Other Contributors ...............00.-
DSM-5 Task Force
DAVID J. KUPFER, M.D.
Task Force Chair
DARREL A. REGIER, M.D., M.P.H.
Task Force Vice-Chair
William E. Narrow, M.D., M.P.H.,
Research Director
Dan G. Blazer, M.D., Ph.D., M.P.H.
Jack D. Burke Jr., M.D., M.P.H.
William T. Carpenter Jr., M.D.
F. Xavier Castellanos, M.D.
Wilson M. Compton, M.D., M.P.E.
Joel E. Dimsdale, M.D.
Javier I. Escobar, M.D., M.Sc.
Jan A. Fawcett, M.D.
Bridget F. Grant, Ph.D., Ph.D. (2009-)
Steven E. Hyman, M.D. (2007-2012)
Dilip V. Jeste, M.D. (2007-2011)
Helena C. Kraemer, Ph.D.
Daniel T. Mamah, M.D., M.P.E.
James P. McNulty, A.B., Sc.B.
Howard B. Moss, M.D. (2007-2009)
Susan K. Schultz, M.D., Text Editor
Emily A. Kuhl, Ph.D., APA Text Editor
Charles P. O’Brien, M.D., Ph.D.
Roger Peele, M.D.
Katharine A. Phillips, M.D.
Daniel S. Pine, M.D.
Charles F. Reynolds II], M.D.
Maritza Rubio-Stipec, Sc.D.
David Shaffer, M.D.
Andrew E. Skodol II, M.D.
Susan E. Swedo, M.D.
B. Timothy Walsh, M.D.
Philip Wang, M.D., Dr.P.H. (2007-2012)
William M. Womack, M.D.
Kimberly A. Yonkers, M.D.
Kenneth J. Zucker, Ph.D.
Norman Sartorius, M.D., Ph.D., Consultant
APA Division of Research Staff on DSM-5
Darrel A. Regier, M.D., M.P.H.,
Director, Division of Research
William E. Narrow, M.D., M.P.H.,
Associate Director
Emily A. Kuhl, Ph.D., Senior Science
Writer; Staff Text Editor
Diana E. Clarke, Ph.D., M.Sc., Research
Statistician
Lisa H. Greiner, M.S.S.A., DSM-5 Field
Trials Project Manager
Eve K. Moscicki, Sc.D., M.P.H.,
Director, Practice Research Network
S. Janet Kuramoto, Ph.D. M.HLS.,
Senior Scientific Research Associate,
Practice Research Network
Amy Porfiri, M.B.A.
Director of Finance and Administration
Jennifer J. Shupinka, Assistant Director,
DSM Operations
Seung-Hee Hong, DSM Senior Research
Associate
Anne R. Hiller, DSM Research Associate
Alison S. Beale, DSM Research Associate
Spencer R. Case, DSM Research Associate
Joyce C. West, Ph.D., M.P.P.,
Health Policy Research Director, Practice
Research Network
Farifteh F. Duffy, Ph.D.,
Quality Care Research Director, Practice
Research Network
Lisa M. Countis, Field Operations
Manager, Practice Research Network
Christopher M. Reynolds,
Executive Assistant
APA Office of the Medical Director
JAMES H. SCULLY JR., M.D.
Medical Director and CEO
Editorial and Coding Consultants
Michael B. First, M.D.
Maria N. Ward, M.Ed., RHIT, CCS-P
DSM-5 Work Groups
ADHD and Disruptive Behavior Disorders
DAVID SHAFFER, M.D.
Chair
F. XAVIER CASTELLANOS, M.D.
Paul J. Frick, Ph.D., Text Coordinator
Glorisa Canino, Ph.D.
Terrie E. Moffitt, Ph.D.
Joel T. Nigg, Ph.D.
Co-Chair
Luis Augusto Rohde, M.D., Sc.D.
Rosemary Tannock, Ph.D.
Eric A. Taylor, M.B.
Richard Todd, Ph.D., M.D. (d. 2008)
Anxiety, Obsessive-Compulsive Spectrum, Posttraumatic,
and Dissociative Disorders
KATHARINE A. PHILLIPS, M.D.
Michelle G. Craske, Ph.D., Text
Coordinator
J. Gavin Andrews, M.D.
Susan M. Bégels, Ph.D.
Matthew J. Friedman, M.D., Ph.D.
Eric Hollander, M.D. (2007-2009)
Roberto Lewis-Fernandez, M.D., M.T.S.
Robert S. Pynoos, M.D., M.P.H.
Chair
Scott L. Rauch, M.D.
H. Blair Simpson, M.D., Ph.D.
David Spiegel, M.D.
Dan J. Stein, M.D., Ph.D.
Murray B. Stein, M.D.
Robert J. Ursano, M.D.
Hans-Ulrich Wittchen, Ph.D.
Childhood and Adolescent Disorders
DANIEL S. PINE, M.D.
Ronald E. Dahl, M.D.
E. Jane Costello, Ph.D. (2007-2009)
Regina Smith James, M.D.
Rachel G. Klein, Ph.D.
Chair
James F. Leckman, M.D.
Ellen Leibenluft, M.D.
Judith H. L. Rapoport, M.D.
Charles H. Zeanah, M.D.
Eating Disorders
B. TIMOTHY WALSH, M.D.
Stephen A. Wonderlich, Ph.D.,
Text Coordinator
Evelyn Attia, M.D.
Anne E. Becker, M.D., Ph.D., Sc.M.
Rachel Bryant-Waugh, M.D.
Hans W. Hoek, M.D., Ph.D.
Chair
Richard E. Kreipe, M.D.
Marsha D. Marcus, Ph.D.
James E. Mitchell, M.D.
Ruth H. Striegel-Moore, Ph.D.
G. Terence Wilson, Ph.D.
Barbara E. Wolfe, Ph.D. A.P.R.N.
Mood Disorders
‘ JAN A. FAWCETT, M.D.
Chair
Ellen Frank, Ph.D., Text Coordinator Kenneth S. Kendler, M.D., Ph.D.
Jules Angst, M.D. (2007-2008) (2007-2010)
William H. Coryell, M.D. Mario Maj, M.D., Ph.D.
Lori L. Davis, M.D. Husseini K. Manji, M.D. (2007-2008)
Raymond J. DePaulo, M.D. Michael R. Phillips, M.D.
Sir David Goldberg, M.D. Trisha Suppes, M.D., Ph.D.
James S. Jackson, Ph.D. Carlos A. Zarate, M.D.
Neurocognitive Disorders
DILIP V. JESTE, M.D. (2007-2011)
Chair Emeritus
DAN G. BLAZER, M.D., PH.D., M.P.H.
Chair
RONALD C. PETERSEN, M.D., PH.D.
Co-Chair
Mary Ganguli, M.D., M.P.H., Igor Grant, M.D.
Text Coordinator Eric J. Lenze, M.D.
Deborah Blacker, M.D., Sc.D. Jane S. Paulsen, Ph.D.
Warachal Faison, M.D. (2007-2008) Perminder S. Sachdev, M.D., Ph.D.
Neurodevelopmental Disorders
SUSAN E. SWEDO, M.D.
Chair
Gillian Baird, M.A., M.B., B.Chir., Catherine E. Lord, Ph.D.
Text Coordinator Joseph Piven, M.D.
Edwin H. Cook Jr., M.D. Sally J. Rogers, Ph.D.
Francesca G. Happé, Ph.D. Sarah J. Spence, M.D., Ph.D.
James C. Harris, M.D. Fred Volkmar, M.D. (2007-2009)
Walter E. Kaufmann, M.D. Amy M. Wetherby, Ph.D.
Bryan H. King, M.D. Harry H. Wright, M.D.
Personality and Personality Disorders!
ANDREW E. SKODOL, M.D.
ir
JOHN M. OLDHAM, M.D.
Co-Chair
Robert F. Krueger, Ph.D., Text Lee Anna Clark, Ph.D.
Coordinator W. John Livesley, M.D., Ph.D. (2007-2012)
Renato D. Alarcon, M.D., M.P.H. Leslie C. Morey, Ph.D.
Carl C. Bell, M.D. Larry J. Siever, M.D.
Donna §. Bender, Ph.D. Roel Verheul, Ph.D. (2008-2012)
1 The members of the Personality and Personality Disorders Work Group are responsible for the
alternative DSM-5 model for personality disorders that is included in Section III. The Section II
personality disorders criteria and text (with updating of the text) are retained from DSM-IV-TR.
Psychotic Disorders
WILLIAM T. CARPENTER JR., M.D.
Chair
Deanna M. Barch, Ph.D., Text Dolores Malaspina, M.D., M.S.P.H.
Coordinator Michael J. Owen, M.D., Ph.D.
Juan R. Bustillo, M.D. Susan K. Schultz, M.D.
Wolfgang Gaebel, M.D. Rajiv Tandon, M.D.
Raquel E. Gur, M.D., Ph.D. Ming T. Tsuang, M.D., Ph.D.
Stephan H. Heckers, M.D. Jim van Os, M.D.
Sexual and Gender Identity Disorders
KENNETH J. ZUCKER, PH.D.
Chair
Lori Brotto, Ph.D., Text Coordinator Martin P. Kafka, M.D.
Irving M. Binik, Ph.D. Richard B. Krueger, M.D.
Ray M. Blanchard, Ph.D. Niklas Langstrém, M.D., Ph.D.
Peggy T. Cohen-Kettenis, Ph.D. Heino F.L. Meyer-Bahlburg, Dr. rer. nat.
Jack Drescher, M.D. Friedemann Pfafflin, M.D.
Cynthia A. Graham, Ph.D. Robert Taylor Segraves, M.D., Ph.D.
Sleep-Wake Disorders
CHARLES F. REYNOLDS III, M.D.
Chair
Ruth M. O’Hara, Ph.D., Text Coordinator Kathy P. Parker, Ph.D., R.N.
Charles M. Morin, Ph.D. Susan Redline, M.D., M.P.H.
Allan I. Pack, Ph.D. Dieter Riemann, Ph.D.
Somatic Symptom Disorders
JOEL E. DIMSDALE, M.D.
Chair
James L. Levenson, M.D., Text Michael R. Irwin, M.D.
Coordinator Francis J. Keefe, Ph.D. (2007-2011)
Arthur J. Barsky HI, M.D. Sing Lee, M.D.
Francis Creed, M.D. Michael Sharpe, M.D.
Nancy Frasure-Smith, Ph.D. (2007-2011) Lawson R. Wulsin, M.D.
Substance-Related Disorders
CHARLES P. O’BRIEN, M.D., PH.D.
Chair
THOMAS J. CROWLEY, M.D.
Co-Chair
Wilson M. Compton, M.D., M.P.E., Thomas R. Kosten, M.D. (2007-2008)
Text Coordinator Walter Ling, M.D.
Marc Auriacombe, M.D. Spero M. Manson, Ph.D. (2007-2008)
Guilherme L. G. Borges, M.D., Dr.Sc. A. Thomas McLellan, Ph.D. (2007-2008)
Kathleen K. Bucholz, Ph.D. Nancy M. Petry, Ph.D.
Alan J. Budney, Ph.D. Marc A. Schuckit, M.D.
Bridget F. Grant, Ph.D., Ph.D. Wim van den Brink, M.D., Ph.D.
Deborah S. Hasin, Ph.D. (2007-2008)
DSM-5 Study Groups
Diagnostic Spectra and DSM/ICD Harmonization
STEVEN E. HYMAN, M.D.
Chair (2007-2012)
x
William T. Carpenter Jr., M.D. William E. Narrow, M.D., M.P.H.
Wilson M. Compton, M.D., M.P.E. Charles P. O’Brien, M.D., Ph.D.
Jan A. Fawcett, M.D. John M. Oldham, M.D.
Helena C. Kraemer, Ph.D. Katharine A. Phillips, M.D.
David J. Kupfer, M.D. Darrel A. Regier, M.D., M.P.H.
Lifespan Developmental Approaches
Eric J. LENZE, M.D.
Chair
SUSAN K. SCHULTZ, M.D.
Chair Emeritus
DANIEL S. PINE, M.D.
Chair Emeritus
Dan G. Blazer, M.D., Ph.D., M.P.H. Daniel T. Mamah, M.D., M.P.E.
F. Xavier Castellanos, M.D. Andrew E. Skodol II, M.D.
Wilson M. Compton, M.D., M.P.E. Susan E. Swedo, M.D.
Gender and Cross-Cultural Issues
KIMBERLY A. YONKERS, M.D.
Chair
ROBERTO LEWIS-FERNANDEZ, M.D., M.T.S.
Co-Chair, Cross-Cultural Issues
Renato D. Alarcon, M.D., M.P.H. Leslie C. Morey, Ph.D.
Diana E. Clarke, Ph.D., M.Sc. William E. Narrow, M.D., M.P.H.
Javier I. Escobar, M.D., M.Sc. Roger Peele, M.D.
Ellen Frank, Ph.D. Philip Wang, M.D., Dr.P.H. (2007-2012)
James S. Jackson, Ph.D. William M. Womack, M.D.
Spiro M. Manson, Ph.D. (2007-2008) Kenneth J. Zucker, Ph.D.
James P. McNulty, A.B., Sc.B.
Psychiatric/General Medical Interface
LAWSON R. WULSIN, M.D.
Chair
Ronald E. Dahl, M.D. Richard E. Kreipe, M.D.
Joel E. Dimsdale, M.D. Ronald C. Petersen, Ph.D., M.D.
Javier I. Escobar, M.D., M.Sc. Charles F. Reynolds III, M.D.
Dilip V. Jeste, M.D. (2007-2011) Robert Taylor Segraves, M.D., Ph.D.
Walter E. Kaufmann, M.D. B. Timothy Walsh, M.D.
Impairment and Disability
JANE S. PAULSEN, PH.D.
Chair
J. Gavin Andrews, M.D. Hans W. Hoek, M.D., Ph.D.
Glorisa Canino, Ph.D. Helena C. Kraemer, Ph.D.
Lee Anna Clark, Ph.D. William E. Narrow, M.D., M.P.H.
Diana E. Clarke, Ph.D., M.Sc. David Shaffer, M.D.
Michelle G. Craske, Ph.D.
Diagnostic Assessment Instruments
JACK D. BURKE JR., M.D., M.P.H.
Chair
Lee Anna Clark, Ph.D. Helena C. Kraemer, Ph.D.
Diana E. Clarke, Ph.D., M.Sc. William E. Narrow, M.D., M.P.H.
Bridget F. Grant, Ph.D., Ph.D. David Shaffer, M.D.
DSM-5 Research Group
WILLIAM E. NARROW, M.D., M.P.H.
Chair
Jack D. Burke Jr., M.D., M.P.H. David J. Kupfer, M.D.
Diana E. Clarke, Ph.D., M.Sc. Darrel A. Regier, M.D., M.P.H.
Helena C. Kraemer, Ph.D. David Shaffer, M.D.
Course Specifiers and Glossary
WOLFGANG GAEBEL, M.D.
Chair
Ellen Frank, Ph.D. Dan J. Stein, M.D., Ph.D.
Charles P. O’Brien, M.D., Ph.D. Eric A. Taylor, M.B.
Norman Sartorius, M.D., Ph.D., David J. Kupfer, M.D.
Consultant Darrel A. Regier, M.D., M.P.H.
Susan K. Schultz, M.D.
&i
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Before each disorder name, ICD-9-CM codes are provided, followed by ICD-10-CM codes
in parentheses. Blank lines indicate that either the ICD-9-CM or the ICD-10-CM code is not
applicable. For some disorders, the code can be indicated only according to the subtype or
specifier.
ICD-9-CM codes are to be used for coding purposes in the United States through Sep-
tember 30, 2014. ICD-10-CM codes are to be used starting October 1, 2014.
Following chapter titles and disorder names, page numbers for the corresponding text
or criteria are included in parentheses.
Note for all mental disorders due to another medical condition: Indicate the name of
the other medical condition in the name of the mental disorder due to [the medical condi-
tion]. The code and name for the other medical condition should be listed first immedi-
ately before the mental disorder due to the medical condition.
Neurodevelopmental Disorders (31)
Intellectual Disabilities (33)
319 (. )} Intellectual Disability (Intellectual Developmental Disorder) (33)
Specify current severity:
(F70) Mild
(F71) Moderate
(F72) Severe
(F73) Profound
315.8 (F88) Global Developmental Delay (41)
319 {(F79) Unspecified Intellectual Disability (Intellectual Developmental
Disorder) (41)
Communication Disorders (41)
315.39 (F80.9) Language Disorder (42)
315.39 (F80.0) Speech Sound Disorder (44)
315.35 (F80.81) = Childhood-Onset Fluency Disorder (Stuttering) (45)
Note: Later-onset cases are diagnosed as 307.0 (F98.5) adult-onset fluency
disorder.
315.39 (F80.89) Social (Pragmatic) Communication Disorder (47)
307.9 (F80.9) Unspecified Communication Disorder (49)
xiii
xiv DSM-5 Classification
Autism Spectrum Disorder (50)
299.00 (F84.0) Autism Spectrum Disorder (50)
Specify if: Associated with a known medical or genetic condition or envi-
ronmental factor; Associated with another neurodevelopmental, men-
tal, or behavioral disorder
Specify current severity for Criterion A and Criterion B: Requiring very
substantial support, Requiring substantial support, Requiring support
Specify if: With or without accompanying intellectual impairment, With
or without accompanying language impairment, With catatonia (use
additional code 293.89 [F06.1])
Attention-Deficit/Hyperactivity Disorder (59)
Attention-Deficit/ Hyperactivity Disorder (59)
a= Vi
Specify whether:
314.01 (F90.2) Combined presentation
314.00 (F90.0) Predominantly inattentive presentation
314.01 (F90.1) Predominantly hyperactive/impulsive presentation
Specify if: In partial remission
Specify current severity: Mild, Moderate, Severe
314.01 (F90.8) | Other Specified Attention-Deficit/Hyperactivity Disorder (65)
314.01 (F90.9) Unspecified Attention-Deficit/Hyperactivity Disorder (66)
Specific Learning Disorder (66)
ea) Specific Learning Disorder (66)
Specify if:
315.00 (F81.0) With impairment in reading (specify if with word reading
accuracy, reading rate or fluency, reading comprehension)
315.2 (F81.81) With impairment in written expression (specify if with spelling
accuracy, grammar and punctuation accuracy, clarity or
organization of written expression)
315.1 (F81.2) With impairment in mathematics (specify if with number sense,
memorization of arithmetic facts, accurate or fluent
calculation, accurate math reasoning)
Specify current severity: Mild, Moderate, Severe
Motor Disorders (74)
315.4 (F82) Developmental Coordination Disorder (74)
307.3 (F98.4) Stereotypic Movement Disorder (77)
Specify if: With self-injurious behavior, Without self-injurious behavior
Specify if: Associated with a known medical or genetic condition, neuro-
developmental disorder, or environmental factor
Specify current severity: Mild, Moderate, Severe
Tic Disorders
307.23 (F95.2) Tourette's Disorder (81)
307.22 (F95.1) Persistent (Chronic) Motor or Vocal Tic Disorder (81)
Specify if: With motor tics only, With vocal tics only
DSN-5 Classification xv
307.21 (F95.0) Provisional Tic Disorder (81)
307.20 (F95.8), Other Specified Tic Disorder (85)
307.20 (F95.9) Unspecified Tic Disorder (85)
Other Neurodevelopmental Disorders (86)
315.8 (F88) Other Specified Neurodevelopmental Disorder (86)
315.9 (F89) Unspecified Neurodevelopmental Disorder (86)
Schizophrenia Spectrum
and Other Psychotic Disorders (87)
The following specifiers apply to Schizophrenia Spectrum and Other Psychotic Disorders
where indicated:
“Specify if: The following course specifiers are only to be used after a 1-year duration of the dis-
order: First episode, currently in acute episode; First episode, currently in partial remission;
First episode, currently in full remission; Multiple episodes, currently in acute episode; Mul-
tiple episodes, currently in partial remission; Multiple episodes, currently in full remission;
Continuous; Unspecified
>Snecify if: With catatonia (use additional code 293.89 [F06.1])
“specify current severity of delusions, hallucinations, disorganized speech, abnormal psycho-
motor behavior, negative symptoms, impaired cognition, depression, and mania symptoms
301.22 (F21) Schizotypal (Personality) Disorder (90)
297.1 (F22) Delusional Disorder*’ © (90)
Specify whether: Erotomanic type, Grandiose type, Jealous type, Persecu-
tory type, Somatic type, Mixed type, Unspecified type
Specify if: With bizarre content
298.8 (F23) Brief Psychotic Disorder” ¢ (94)
Specify if: With marked stressor(s), Without marked stressor(s), With
postpartum onset
295.40 (F20.81) Schizophreniform Disorder” © (96)
Specify if: With good prognostic features, Without good prognostic fea-
tures
295.90 (F20.9) Schizophrenia® 5, ¢ (99)
tet ie)
Schizoaffective Disorder” ’¢ (105)
Specify whether:
295.70 (F25.0) Bipolar type
295.70 (F25.1) Depressive type
ee Cree | Substance /Medication-Induced Psychotic Disorder‘ (110)
Note: See the criteria set and corresponding recording procedures for
substance-specific codes and ICD-9-CM and ICD-10-CM coding.
Specify if: With onset during intoxication, With onset during withdrawal
__._ (__...} Psychotic Disorder Due to Another Medical Condition‘ (115)
Specify whether:
293.81 (FO6.2) With delusions
293.82 (FO6.0) With hallucinations
xvi
293.89 (F06.1)
293.89 (F06.1)
293.89 (F06.1)
298.8 (F28)
298.9 (F29)
DSN-5 Classification
Catatonia Associated With Another Mental Disorder (Catatonia
Specifier) (119)
Catatonic Disorder Due to Another Medical Condition (120)
Unspecified Catatonia (121)
Note: Code first 781.99 (R29.818) other symptoms involving nervous and
musculoskeletal systems.
Other Specified Schizophrenia Spectrum and Other Psychotic
Disorder (122)
Unspecified Schizophrenia Spectrum and Other Psychotic
Disorder (122)
Bipolar and Related Disorders (123)
The following specifiers apply to Bipolar and Related Disorders where indicated:
Specify: With anxious distress (specify current severity: mild, moderate, moderate-severe, severe);
With mixed features; With rapid cycling; With melancholic features; With atypical features;
With mood-congruent psychotic features; With mood-incongruent psychotic features; With
catatonia (use additional code 293.89 [F06.1]); With peripartum onset; With seasonal pattern
ee)
a ae |
296.41 (F31.11)
296.42 (F31.12)
296.43 (F31.13)
296.44 (F31.2)
296.45 (F31.73)
296.46 (F31.74)
296.40 (F31.9)
296.40 (F31.0)
296.45 (F31.73)
296.46 (F31.74)
296.40 (F31.9)
a een, ae a
296.51 (F31.31)
296.52 (F31.32)
296.53 (F31.4)
296.54 (F31.5)
296.55 (F31.75)
296.56 (F31.76)
296.50 (F31.9)
296.7 (F31.9)
296.89 (F31.81)
Bipolar I Disorder* (123)
Current or most recent episode manic
Mild
Moderate
Severe
With psychotic features
In partial remission
In full remission
Unspecified
Current or most recent episode hypomanic
In partial remission
In full remission
Unspecified
Current or most recent episode depressed
Mild
Moderate
Severe
With psychotic features
In partial remission
In full remission
Unspecified
Current or most recent episode unspecified
Bipolar II Disorder® (132)
Specify current or most recent episode: Hypomanic, Depressed
Specify course if full criteria for a mood episode are not currently met: In
partial remission, In full remission
Specify severity if full criteria for a mood episode are not currently met:
Mild, Moderate, Severe
DSN-5 Classification
301.13 (F34.0)
\
a oe) Saree
293.83 (__._)
(F06.33)
(F06.33)
(F06.34)
296.89 (F31.89)
296.80 (F31.9)
xvii
Cyclothymic Disorder (139)
Specify if: With anxious distress
Substance /Medication-Induced Bipolar and Related Disorder (142)
Note: See the criteria set and corresponding recording procedures for
substance-specific codes and ICD-9-CM and ICD-10-CM coding.
Specify if: With onset during intoxication, With onset during withdrawal
Bipolar and Related Disorder Due to Another Medical Condition
(145)
Specify if:
With manic features
With manic- or hypomanic-like episode
With mixed features
Other Specified Bipolar and Related Disorder (148)
Unspecified Bipolar and Related Disorder (149)
Depressive Disorders (155)
The following specifiers apply to Depressive Disorders where indicated:
Specify: With anxious distress (specify current severity: mild, moderate, moderate-severe,
severe); With mixed features; With melancholic features; With atypical features; With mood-
congruent psychotic features; With mood-incongruent psychotic features; With catatonia
(use additional code 293.89 [F06.1]); With peripartum onset; With seasonal pattern
296.99 (F34.8)
Ss (ae)
pats, Wie)
296.21 (F32.0)
296.22 (F32.1)
296.23 (F32.2)
296.24 (F32.3)
296.25 (F32.4)
296.26 (F32.5)
296.20 (F32.9)
was ee}
296.31 (F33.0)
296.32 (F33.1)
296.33 (F33.2)
296.34 (F33.3)
296.35 (F33.41)
296.36 (F33.42)
296.30 (F33.9)
300.4 (F34.1)
Disruptive Mood Dysregulation Disorder (156)
Major Depressive Disorder* (160)
Single episode
Mild
Moderate
Severe
With psychotic features
In partial remission
In full remission
Unspecified
Recurrent episode
Mild
Moderate
Severe
With psychotic features
In partial remission
In full remission
Unspecified
Persistent Depressive Disorder (Dysthymia)* (168)
Specify if: In partial remission, In full remission
Specify if: Early onset, Late onset
Specify if: With pure dysthymic syndrome; With persistent major depres-
sive episode; With intermittent major depressive episodes, with current
xviii
625.4 (N94.3)
ae eet Ca eee
DSMN-5 Classification
episode; With intermittent major depressive episodes, without current
episode
Specify current severity: Mild, Moderate, Severe
Premenstrual Dysphoric Disorder (171)
Substance /Medication-Induced Depressive Disorder (175)
Note: See the criteria set and corresponding recording procedures for
substance-specific codes and ICD-9-CM and ICD-10-CM coding.
Specify if: With onset during intoxication, With onset during withdrawal
293.83 (__._) Depressive Disorder Due to Another Medical Condition (180)
Specify if:
(F06.31) With depressive features
(FO6.32) With major depressive-like episode
(F06.34) With mixed features
311 (F32.8) Other Specified Depressive Disorder (183)
311 (F32.9) Unspecified Depressive Disorder (184)
Anxiety Disorders (189)
309.21 (F93.0) Separation Anxiety Disorder (190)
312.23 (F94.0) Selective Mutism (195)
300.29 (__._) Specific Phobia (197)
Specify if:
(F40.218) Animal
(F40.228) Natural environment
{_.) Blood-injection-injury
(F40.230) Fear of blood
(F40.231) Fear of injections and transfusions
(F40.232) Fear of other medical care
(F40.233) Fear of injury
{F40.248) Situational
(F40.298) Other
300.23 (F40.10)
300.01 (F41.0)
—_- Ct .)}
300.22 (F40.00)
300.02 (F41.1)
fae tae) Seamed
Social Anxiety Disorder (Social Phobia) (202)
Specify if: Performance only
Panic Disorder (208)
Panic Attack Specifier (214)
Agoraphobia (217)
Generalized Anxiety Disorder (222)
Substance /Medication-Induced Anxiety Disorder (226)
Note: See the criteria set and corresponding recording procedures for
substance-specific codes and ICD-9-CM and ICD-10-CM coding.
Specify if: With onset during intoxication, With onset during withdrawal,
With onset after medication use
DSN-5 Classification xix
293.84 (FO6.4) Anxiety Disorder Due to Another Medical Condition (230)
300.09 (F41.8), Other Specified Anxiety Disorder (233)
300.00 (F41.9) Unspecified Anxiety Disorder (233)
Obsessive-Compulsive and Related Disorders (235)
The following specifier applies to Obsessive-Compulsive and Related Disorders where indicated:
Specify if: With good or fair insight, With poor insight, With absent insight/delusional beliefs
300.3 {(F42) Obsessive-Compulsive Disorder* (237)
Specify if: Tic-related
300.7 (F45.22) Body Dysmorphic Disorder* (242)
Specify if: With muscle dysmorphia
300.3 (F42) Hoarding Disorder* (247)
Specify if: With excessive acquisition
312.39 (F63.2) Trichotillomania (Hair-Pulling Disorder) (251)
698.4 (L98.1) Excoriation (Skin-Picking) Disorder (254)
$= ea) Substance /Medication-Induced Obsessive-Compulsive and
Related Disorder (257)
Note: See the criteria set and corresponding recording procedures for
substance-specific codes and ICD-9-CM and ICD-10-CM coding.
Specify if: With onset during intoxication, With onset during withdrawal,
With onset after medication use
294.8 (FO6.8) Obsessive-Compulsive and Related Disorder Due to Another
Medical Condition (260)
Specify if: With obsessive-compulsive disorder-like symptoms, With
appearance preoccupations, With hoarding symptoms, With hair-
pulling symptoms, With skin-picking symptoms
300.3 (F42) Other Specified Obsessive-Compulsive and Related Disorder
(263)
300.3 (F42) Unspecified Obsessive-Compulsive and Related Disorder (264)
Trauma- and Stressor-Related Disorders (265)
313.89 (F94.1) Reactive Attachment Disorder (265)
Specify if: Persistent
Specify current severity: Severe
313.89 (F94.2) Disinhibited Social Engagement Disorder (268)
Specify if: Persistent
Specify current severity: Severe
309.81 (F43.10) Posttraumatic Stress Disorder (includes Posttraumatic Stress
Disorder for Children 6 Years and Younger) (271)
Specify whether: With dissociative symptoms
Specify if: With delayed expression
308.3 (F43.0) Acute Stress Disorder (280)
xx
ee ee, ee
309.0 (F43.21)
309.24 (F43.22)
309.28 (F43.23)
309.3 (F43.24)
309.4 (F43.25)
309.9 (F43.20)
309.89 (F43.8)
309.9 (F43.9)
300.14 (F44.81)
300.12 (F44.0)
300.13 (F44.1)
300.6 (F48.1)
300.15 (F44.89)
300.15 (F44.9)
DSM-5 Classification
Adjustment Disorders (286)
Specify whether:
With depressed mood
With anxiety
With mixed anxiety and depressed mood
With disturbance of conduct
With mixed disturbance of emotions and conduct
Unspecified
Other Specified Trauma- and Stressor-Related Disorder (289)
Unspecified Trauma- and Stressor-Related Disorder (290)
Dissociative Disorders (291)
Dissociative Identity Disorder (292)
Dissociative Amnesia (298)
Specify if:
With dissociative fugue
Depersonalization/Derealization Disorder (302)
Other Specified Dissociative Disorder (306)
Unspecified Dissociative Disorder (307)
Somatic Symptom and Related Disorders (309)
300.82 (F45.1)
300.7 (F45.21)
300.11 {(__.__)
(F44.4)
(F44.4)
(F44.4)
(F44.4)
(F44.5)
(F44.6)
(F44.6)
(F44.7)
Somatic Symptom Disorder (311)
Specify if: With predominant pain
Specify if: Persistent
Specify current severity: Mild, Moderate, Severe
Illness Anxiety Disorder (315)
Specify whether: Care seeking type, Care avoidant type
Conversion Disorder (Functional Neurological Symptom
Disorder) (318)
Specify symptom type:
With weakness or paralysis
With abnormal movement
With swallowing symptoms
With speech symptom
With attacks or seizures
With anesthesia or sensory loss
With special sensory symptom
With mixed symptoms
Specify if: Acute episode, Persistent
Specify if: With psychological stressor (specify stressor), Without psycho-
logical stressor
DSN-5 Classification
316 (F54)
300.19 (F68.10)
300.89 (F45.8)
300.82 (F45.9)}
xxi
Psychological Factors Affecting Other Medical Conditions (322)
Specify current severity: Mild, Moderate, Severe, Extreme
Factitious Disorder (includes Factitious Disorder Imposed on Self,
Factitious Disorder Imposed on Another) (324)
Specify Single episode, Recurrent episodes
Other Specified Somatic Symptom and Related Disorder (327)
Unspecified Somatic Symptom and Related Disorder (327)
Feeding and Eating Disorders (329)
The following specifiers apply to Feeding and Eating Disorders where indicated:
Specify if: In remission
bSpecify if: In partial remission, In full remission
“Specify current severity: Mild, Moderate, Severe, Extreme
307.52(__._)
(F98.3)
(F50.8)
307.53 (F98.21)
307.59 (F50.8)
307.14 (_._)
(F50.01)
(F50.02)
307.51 (F50.2)
307.51 (F50.8)
307.59 (F50.8)
307.50 (F50.9)
307.6 (F98.0)
307.7 (F98.1)
—» (_.)
788.39 (N39.498)
787.60 (R15.9)
— (_._)
788.30 (R32)
787.60 (R15.9)
Pica* (329)
In children
In adults
Rumination Disorder? (332)
Avoidant/Restrictive Food Intake Disorder* (334)
Anorexia Nervosa” © (338)
Specify whether:
Restricting type
Binge-eating / purging type
Bulimia Nervosa?’ (345)
Binge-Eating Disorder”: ¢ (350)
Other Specified Feeding or Eating Disorder (353)
Unspecified Feeding or Eating Disorder (354)
Elimination Disorders (355)
Enuresis (355)
Specify whether: Nocturnal only, Diurnal only, Nocturnal and diurnal
Encopresis (357)
Specify whether: With constipation and overflow incontinence, Without
constipation and overflow incontinence
Other Specified Elimination Disorder (359)
With urinary symptoms
With fecal symptoms
Unspecified Elimination Disorder (360)
With urinary symptoms
With fecal symptoms
xxii
DSN-5 Classification
Sleep-Wake Disorders (361)
The following specifiers apply to Sleep-Wake Disorders where indicated:
Specify if: Episodic, Persistent, Recurrent
bSpecify if: Acute, Subacute, Persistent
“Specify current severity: Mild, Moderate, Severe
780.52 (G47.00)
780.54 (G47.10)
ae as)
347.00 (G47.419)
347.01 (G47.411)
347.00 (G47.419)
347.00 (G47.419)
347.10 (G47.429)
Insomnia Disorder* (362)
Specify if: With non-sleep disorder mental comorbidity, With other
medical comorbidity, With other sleep disorder
Hypersomnolence Disorder”: ¢ (368)
Specify if: With mental disorder, With medical condition, With another
sleep disorder
Narcolepsy‘ (372)
Specify whether:
Narcolepsy without cataplexy but with hypocretin deficiency
Narcolepsy with cataplexy but without hypocretin deficiency
Autosomal dominant cerebellar ataxia, deafness, and
narcolepsy
Autosomal dominant narcolepsy, obesity, and type 2 diabetes
Narcolepsy secondary to another medical condition
Breathing-Related Sleep Disorders (378)
327.23 (G47.33)
ie Ai)
327.21 (G47.31)
786.04 (R06.3)
780.57 (G47.37)
eee em ee an
327.24 (G47.34)
327.25 (G47.35)
327.26 (G47.36)
eee aes (|
307.45 (G47.21)
307.45 (G47.22)
307.45 (G47.23)
307.45 (G47.24)
Obstructive Sleep Apnea Hypopnea‘ (378)
Central Sleep Apnea (383)
Specify whether:
Idiopathic central sleep apnea
Cheyne-Stokes breathing
Central sleep apnea comorbid with opioid use
Note: First code opioid use disorder, if present.
Specify current severity
Sleep-Related Hypoventilation (387)
Specify whether:
Idiopathic hypoventilation
Congenital central alveolar hypoventilation
Comorbid sleep-related hypoventilation
Specify current severity
Circadian Rhythm Sleep-Wake Disorders? (390)
Specify whether:
Delayed sleep phase type (391)
Specify if: Familial, Overlapping with non-24-hour sleep-wake type
Advanced sleep phase type (393)
Specify if: Familial
Irregular sleep-wake type (394)
Non-24-hour sleep-wake type (396)
DSM-5 Classification
307.45 (G47.26)
307.45 (G47.20)
xxiii
Shift work type (397)
Unspecified type
Parasomnias (399)
ees Te)
307.46 (F51.3)
307.46 (F51.4)
307.47 (F51.5)
327.42 (G47.52)
333.94 (G25.81)
eee See
780.52 (G47.09)
780.52 (G47.00)
780.54 (G47.19)
780.54 (G47.10)
780.59 (G47.8)
780.59 (G47.9)
Non-Rapid Eye Movement Sleep Arousal Disorders (399)
Specify whether:
Sleepwalking type
Specify if: With sleep-related eating, With sleep-related sexual
behavior (sexsomnia)
Sleep terror type
Nightmare Disorder?’ ¢ (404)
Specify if: During sleep onset
Specify if: With associated non-sleep disorder, With associated other
medical condition, With associated other sleep disorder
Rapid Eye Movement Sleep Behavior Disorder (407)
Restless Legs Syndrome (410)
Substance /Medication-Induced Sleep Disorder (413)
Note: See the criteria set and corresponding recording procedures for
substance-specific codes and ICD-9-CM and ICD-10-CM coding.
Specify whether: Insomnia type, Daytime sleepiness type, Parasomnia
type, Mixed type
Specify if: With onset during intoxication, With onset during discontinua-
tion/ withdrawal
Other Specified Insomnia Disorder (420)
Unspecified Insomnia Disorder (420)
Other Specified Hypersomnolence Disorder (421)
Unspecified Hypersomnolence Disorder (421)
Other Specified Sleep-Wake Disorder (421)
Unspecified Sleep-Wake Disorder (422)
Sexual Dysfunctions (423)
The following specifiers apply to Sexual Dysfunctions where indicated:
Specify whether: Lifelong, Acquired
Specify whether: Generalized, Situational
“Specify current severity: Mild, Moderate, Severe
302.74 (F52.32)
302.72 (F52.21)
302.73 (F52.31)
302.72 (F52.22)
302.76 (F52.6)
Delayed Ejaculation® > ¢ (424)
Erectile Disorder* > ¢ (426)
Female Orgasmic Disorder” » ¢ (429)
Specify if: Never experienced an orgasm under any situation
Female Sexual Interest / Arousal Disorder® >: ¢ (433)
Genito-Pelvic Pain/ Penetration Disorder* ° (437)
xxiv
302.71 (F52.0)
302.75 (F52.4)
pte Ne
302.79 (F52.8)
302.70 (F52.9)
DSN-5 Classification
Male Hypoactive Sexual Desire Disorder® >, € (440)
Premature (Early) Ejaculation® >: (443)
Substance /Medication-Induced Sexual Dysfunction‘ (446)
Note: See the criteria set and corresponding recording procedures for
substance-specific codes and ICD-9-CM and ICD-10-CM coding.
Specify if: With onset during intoxication, With onset during withdrawal,
With onset after medication use
Other Specified Sexual Dysfunction (450)
Unspecified Sexual Dysfunction (450)
Gender Dysphoria (451)
ao. (a)
302.6 (F64.2)
302.85 (F64.1)
302.6 (F64.8)
302.6 (F64.9)
Gender Dysphoria (452)
Gender Dysphoria in Children
Specify if: With a disorder of sex development
Gender Dysphoria in Adolescents and Adults
Specify if: With a disorder of sex development
Specify if: Posttransition
Note: Code the disorder of sex development if present, in addition to
gender dysphoria.
Other Specified Gender Dysphoria (459)
Unspecified Gender Dysphoria (459)
Disruptive, Impulse-Control, and Conduct Disorders (461)
313.81 (F91.3)
312.34 (F63.81)
aoe ig
312.81 (F91.1)
312.32 (F91.2)
312.89 (F91.9)
301.7 (F60.2)
312.33 (F63.1)
312.32 (F63.3)
312.89 (F91.8)
312.9 (F91.9)
Oppositional Defiant Disorder (462)
Specify current severity: Mild, Moderate, Severe
Intermittent Explosive Disorder (466)
Conduct Disorder (469)
Specify whether:
Childhood-onset type
Adolescent-onset type
Unspecified onset
Specify if: With limited prosocial emotions
Specify current severity: Mild, Moderate, Severe
Antisocial Personality Disorder (476)
Pyromania (476)
Kleptomania (478)
Other Specified Disruptive, Impulse-Control, and Conduct
Disorder (479)
Unspecified Disruptive, Impulse-Control, and Conduct Disorder
(480)
DSM-5 Classification XXV
Substance-Related and Addictive Disorders (481)
The following specifiers and note apply to Substance-Related and Addictive Disorders where
indicated:
Specify if: In early remission, In sustained remission
>Specify if: In a controlled environment
“Specify if: With perceptual disturbances
The ICD-10-CM code indicates the comorbid presence of a moderate or severe substance use
disorder, which must be present in order to apply the code for substance withdrawal.
Substance-Related Disorders (483)
Alcohol-Related Disorders (490)
_._ (_._) — Alcohol Use Disorder® » (490)
Specify current severity:
305.00 (F10.10) Mild
303.90 (F10.20) Moderate
303.90 (F10.20) Severe
303.00 {. ) Alcohol Intoxication (497)
(F10.129) With use disorder, mild
(F10.229) With use disorder, moderate or severe
(F10.929) Without use disorder
291.81 {__._) | Alcohol Withdrawal® 4 (499)
(F10.239) Without perceptual disturbances
(F10.232) With perceptual disturbances
—_. (__._) = Other Alcohol-Induced Disorders (502)
291.9 (F10.99) Unspecified Alcohol-Related Disorder (503)
Caffeine-Related Disorders (503)
305.90 (F15.929) Caffeine Intoxication (503)
292.0 (F15.93) Caffeine Withdrawal (506)
te BO FL) Other Caffeine-Induced Disorders (508)
292.9 (F15.99) Unspecified Caffeine-Related Disorder (509)
Cannabis-Related Disorders (509)
2%. (e252) Cannabis Use Disorder® © (509)
Specify current severity:
305.20 (F12.10) Mild
304.30 (F12.20) Moderate
304.30 (F12.20) Severe
XXVI
292.89 (__._)
(F12.129)
(F12.229)
(F12.929)
(F12.122)
(F12.222)
(F12.922)
292.0 (F12.288)
oat ES a}
292.9 (F12.99)
DSM-5 Classification
Cannabis Intoxication‘ (516)
Without perceptual disturbances
With use disorder, mild
With use disorder, moderate or severe
Without use disorder
With perceptual disturbances
With use disorder, mild
With use disorder, moderate or severe
Without use disorder
Cannabis Withdrawal (517)
Other Cannabis-Induced Disorders (519)
Unspecified Cannabis-Related Disorder (519)
Hallucinogen-Related Disorders (520)
a Lo)
305.90 (F16.10)
304.60 (F16.20)
304.60 (F16.20)
Een (ees Hx)
305.30 (F16.10)
304.50 (F16.20)
304.50 (F16.20)
292.89 (_._)
(F16.129)
(F16.229)
(F16.929)
292.89 (__._)
(F16.129)
(F16.229)
(F16.929)
292.89 (F16.983)
ee eae ee P|
ae ee |
292.9 (F16.99)
292.9 (F16.99)
Phencyclidine Use Disorder* > (520)
Specify current severity:
Mild
Moderate
Severe
Other Hallucinogen Use Disorder™ b (523)
Specify the particular hallucinogen
Specify current severity:
Mild
Moderate
Severe
Phencyclidine Intoxication (527)
With use disorder, mild
With use disorder, moderate or severe
Without use disorder
Other Hallucinogen Intoxication (529)
With use disorder, mild
With use disorder, moderate or severe
Without use disorder
Hallucinogen Persisting Perception Disorder (531)
Other Phencyclidine-Induced Disorders (532)
Other Hallucinogen-Induced Disorders (532)
Unspecified Phencyclidine-Related Disorder (533)
Unspecified Hallucinogen-Related Disorder (533)
Inhalant-Related Disorders (533)
pata Uy)
305.90 (F18.10)
Inhalant Use Disorder® > (533)
Specify the particular inhalant
Specify current severity:
Mild
DSM-5 Classification
304.60 (F18.20) Moderate
304.60 (F18.20) Severe
292.89 (__._) —_Inhalant Intoxication (538)
(F18.129) With use disorder, mild
(F18.229) With use disorder, moderate or severe
(F18.929) Without use disorder
eee (eee | Other Inhalant-Induced Disorders (540)
292.9 (F18.99) Unspecified Inhalant-Related Disorder (540)
Opioid-Related Disorders (540)
_) Opioid Use Disorder* (541)
Specify if: On maintenance therapy, In a controjled environment
Specify current severity:
305.50 (F11.10) Mild
304.00 (F11.20) Moderate
304.00 (F11.20) Severe
cer ae ee
292.89 (__._} Opioid Intoxication‘ (546)
Without perceptual disturbances
(F11.129) With use disorder, mild
(F 11.229) With use disorder, moderate or severe
(F11.929) Without use disorder
With perceptual disturbances
(F11.122) With use disorder, mild
(F11.222) With use disorder, moderate or severe
(F11.922) Without use disorder
292.0 (F11.23) Opioid Withdrawal® (547)
wot (45) Other Opioid-Induced Disorders (549)
292.9 (F11.99) Unspecified Opioid-Related Disorder (550)
Sedative-, Hypnotic-, or Anxiolytic-Related Disorders (550)
_. (__._) Sedative, Hypnotic, or Anxiolytic Use Disorder® » (550)
Specify current severity:
305.40 (F13.10) Mild
304.10 (F13.20) Moderate
304.10 (F13.20) Severe
292.89 (_._) Sedative, Hypnotic, or Anxiolytic Intoxication (556)
(F13.129) With use disorder, mild
(F13.229) With use disorder, moderate or severe
(F13.929) Without use disorder
292.0 (_. } Sedative, Hypnotic, or Anxiolytic Withdrawal” d (557)
(F13.239) Without perceptual disturbances
(F13.232) With perceptual disturbances
xxviii DSM-5 Classification
.__) | Other Sedative-, Hypnotic-, or Anxiolytic-Induced Disorders
(560)
292.9 (F13.99} Unspecified Sedative-, Hypnotic-, or Anxiolytic-Related Disorder
(560)
eae ee ee
Stimulant-Related Disorders (561)
__.— {._) — Stimulant Use Disorder® ° (561)
Specify current severity:
re eee ee Mild
305.70 (F15.10) Amphetamine-type substance
305.60 (F14.10) Cocaine
305.70 (F15.10) Other or unspecified stimulant
fades oes) Moderate
304.40 (F15.20) Amphetamine-type substance
304.20 (F14.20) Cocaine
304.40 (F15.20) Other or unspecified stimulant
2 ee) Severe
304.40 (F15.20) Amphetamine-type substance
304.20 (F14.20) Cocaine
304.40 (F15.20) Other or unspecified stimulant
292.89 (__._) | Stimulant Intoxication‘ (567)
Specify the specific intoxicant
292.89 (_._) Amphetamine or other stimulant, Without perceptual
disturbances
(F15.129) With use disorder, mild
(F15.229} With use disorder, moderate or severe
(F15.929) Without use disorder
292.89 (__._) Cocaine, Without perceptual disturbances
(F14.129) With use disorder, mild
(F14.229) With use disorder, moderate or severe
(F14.929) Without use disorder
292.89 (_ . ) Amphetamine or other stimulant, With perceptual
disturbances
(F15.122) With use disorder, mild
(F15.222) With use disorder, moderate or severe
(F15.922) Without use disorder
292.89 (__._) Cocaine, With perceptual disturbances
(F14.122) With use disorder, mild
(F14.222) With use disorder, moderate or severe
(F14.922) Without use disorder
292.0 (_._) Stimulant Withdrawal? (569)
Specify the specific substance causing the withdrawal syndrome
(F15.23) Amphetamine or other stimulant
(F14.23) Cocaine
~ 8s Other Stimulant-Induced Disorders (570)
DSN-5 Classification xxix
2929 (_. )
(F15.99)
(F14.99)
Unspecified Stimulant-Related Disorder (570)
Amphetamine or other stimulant
Cocaine
Tobacco-Related Disorders (571)
aa oe)
305.1 (Z72.0)
305.1 (F17.200)
305.1 (F17.200)
292.0 (F17.203)
sa (Ae)
292.9 (F17.209)
Tobacco Use Disorder* (571)
Specify if: On maintenance therapy, In a controlled environment
Specify current severity:
Mild
Moderate
Severe
Tobacco Withdrawal (575)
Other Tobacco-Induced Disorders (576)
Unspecified Tobacco-Related Disorder (577)
Other (or Unknown) Substance-Related Disorders (577)
ae) Ea
305.90 (F19.10)
304.90 (F19.20)
304.90 (F19.20)
292.89 (__._)
(F19.129)
(F19.229)
(F19.929)
292.0 (F19.239)
ae eae Soe ee
292.9 (F19.99)
Other (or Unknown) Substance Use Disorder® > (577)
Specify current severity:
Mild
Moderate
Severe
Other (or Unknown) Substance Intoxication (581)
With use disorder, mild
With use disorder, moderate or severe
Without use disorder
Other (or Unknown) Substance Withdrawal® (583)
Other (or Unknown) Substance—Induced Disorders (584)
Unspecified Other (or Unknown) Substance-Related Disorder (585)
Non-Substance-Related Disorders (585)
312.31 (F63.0)
—— L_)
= fa)
— (-_)
292.81 (__._)
293.0 (FO5)
Gambling Disorder* (585)
Specify if: Episodic, Persistent
Specify current severity: Mild, Moderate, Severe
Neurocognitive Disorders (591)
Delirium (596)
“Note: See the criteria set and corresponding recording procedures for
substance-specific codes and ICD-9-CM and ICD-10-CM coding.
Specify whether:
Substance intoxication delirium?
Substance withdrawal delirium?
Medication-induced delirium?
Delirium due to another medical condition
Xxx DSN-5 Classification
293.0 (FO5) Delirium due to multiple etiologies
Specify if: Acute, Persistent
Specify if: Hyperactive, Hypoactive, Mixed level of activity
780.09 (R41.0) Other Specified Delirium (602)
780.09 (R41.0) Unspecified Delirium (602)
Major and Mild Neurocognitive Disorders (602)
Specify whether due to: Alzheimer’s disease, Frontotemporal lobar degeneration, Lewy body
disease, Vascular disease, Traumatic brain injury, Substance/ medication use, HIV infection,
Prion disease, Parkinson's disease, Huntington’s disease, Another medical condition, Multi-
ple etiologies, Unspecified
Specify Without behavioral disturbance, With behavioral disturbance. For possible major neuro-
cognitive disorder and for mild neurocognitive disorder, behavioral disturbance cannot be coded but
should still be indicated in writing.
>Specify current severity: Mild, Moderate, Severe. This specifier applies only to major neurocogni-
tive disorders (including probable and possible).
Note: As indicated for each subtype, an additional medical code is needed for probable major
neurocognitive disorder or major neurocognitive disorder. An additional medical code should
not be used for possible major neurocognitive disorder or mild neurocognitive disorder.
Major or Mild Neurocognitive Disorder Due to Alzheimer’s Disease (611)
__»_ (__._} Probable Major Neurocognitive Disorder Due to Alzheimer’s
Disease?
Note: Code first 331.0 (G30.9) Alzheimer’s disease.
294.11 (F02.81) With behavioral disturbance
294.10 (F02.80) Without behavioral disturbance
331.9 (G31.9) Possible Major Neurocognitive Disorder Due to Alzheimer’s
Disease” P
331.83 (G31.84) Mild Neurocognitive Disorder Due to Alzheimer’s Disease*
Major or Mild Frontotemporal Neurocognitive Disorder (614)
__.»_ (__._} Probable Major Neurocognitive Disorder Due to Frontotemporal
Lobar Degeneration?
Note: Code first 331.19 (G31.09) frontotemporal disease.
294.11 (F02.81) With behavioral disturbance
294.10 (F02.80) Without behavioral disturbance
331.9 (G31.9) | Possible Major Neurocognitive Disorder Due to Frontotemporal
Lobar Degeneration® >
331.83 (G31.84) Mild Neurocognitive Disorder Due to Frontotemporal Lobar
Degeneration*
Major or Mild Neurocognitive Disorder With Lewy Bodies (618)
__._ (__._) Probable Major Neurocognitive Disorder With Lewy Bodies”
Note: Code first 331.82 (G31.83) Lewy body disease.
294.11 (F02.81) With behavioral disturbance
294.10 (F02.80) Without behavioral disturbance
DSM-5 Classification XXxi
331.9 (G31.9) Possible Major Neurocognitive Disorder With Lewy Bodies” b
331.83 (G31.84) Mild Neurocognitive Disorder With Lewy Bodies*
Major or Mild Vascular Neurocognitive Disorder (621)
serine he Ge) Probable Major Vascular Neurocognitive Disorder?
Note: No additional medical code for vascular disease.
290.40 (F01.51) With behavioral disturbance
290.40 (FO1.50) Without behavioral disturbance
331.9 (G31.9) Possible Major Vascular Neurocognitive Disorder*
331.83 (G31.84) | Mild Vascular Neurocognitive Disorder®
Major or Mild Neurocognitive Disorder Due to Traumatic Brain Injury (624)
._) Major Neurocognitive Disorder Due to Traumatic Brain Injury”
Note: For ICD-9-CM, code first 907.0 late effect of intracranial injury without
skull fracture. For ICD-10-CM, code first $06.2X9S diffuse traumatic brain
injury with loss of consciousness of unspecified duration, sequela.
294.11 (FO02.81) With behavioral disturbance
294.10 (F02.80) Without behavioral disturbance
331.83 (G31.84) Mild Neurocognitive Disorder Due to Traumatic Brain Injury*
—— L-
Substance/Medication-Induced Major or Mild Neurocognitive Disorder* (627)
Note: No additional medical code. See the criteria set and corresponding recording procedures
for substance-specific codes and ICD-9-CM and ICD-10-CM coding.
Specify if: Persistent
Major or Mild Neurocognitive Disorder Due to HIV Infection (632)
-_) | Major Neurocognitive Disorder Due to HIV Infection
Note: Code first 042 (B20) HIV infection.
294.11 (F02.81) With behavioral disturbance
294.10 (F02.80) Without behavioral disturbance
331.83 (G31.84) | Mild Neurocognitive Disorder Due to HIV Infection®
seers.
Major or Mild Neurocognitive Disorder Due to Prion Disease (634}
owe ¢( Major Neurocognitive Disorder Due to Prion Disease?
Note: Code first 046.79 (A81.9) prion disease.
294.11 (F02.81} With behavioral disturbance
294.10 (F02.80) Without behavioral disturbance
331.83 (G31.84) Mild Neurocognitive Disorder Due to Prion Disease*
Major or Mild Neurocognitive Disorder Due to Parkinson’s Disease (636)
5. (ee) Major Neurocognitive Disorder Probably Due to Parkinson’s
Disease?
Note: Code first 332.0 (G20) Parkinson’s disease.
294.11 (F02.81) With behavioral disturbance
294.10 (F02.80) Without behavioral disturbance
Xxxii DSN-5 Classification
331.9 (G31.9) | Major Neurocognitive Disorder Possibly Due to Parkinson’s
Disease” >
331.83 (G31.84) | Mild Neurocognitive Disorder Due to Parkinson’s Disease*
Major or Mild Neurocognitive Disorder Due to Huntington’s Disease (638)
-_) | Major Neurocognitive Disorder Due to Huntington’s Disease”
Note: Code first 333.4 (G10) Huntington’s disease.
294.11 (F02.81) With behavioral disturbance
294.10 (F02.80) Without behavioral disturbance
331.83 (G31.84) Mild Neurocognitive Disorder Due to Huntington’s Disease*
ee
Major or Mild Neurocognitive Disorder Due to Another Medical Condition (641)
Ce fe) Major Neurocognitive Disorder Due to Another Medical
Condition?
Note: Code first the other medical condition.
294.11 (F02.81) With behavioral disturbance
294.10 (F02.80) Without behavioral disturbance
331.83 (G31.84) Mild Neurocognitive Disorder Due to Another Medical
Condition
Major or Mild Neurocognitive Disorder Due to Multiple Etiologies (642)
-_) Major Neurocognitive Disorder Due to Multiple Etiologies?
Note: Code first all the etiological medical conditions (with the exception
of vascular disease).
294.11 (F02.81) With behavioral disturbance
294.10 (FO2.80) Without behavioral disturbance
331.83 (G31.84) Mild Neurocognitive Disorder Due to Multiple Etiologies*
oe ay eae
Unspecified Neurocognitive Disorder (643)
799.59 (R41.9) Unspecified Neurocognitive Disorder*
Personality Disorders (645)
Cluster A Personality Disorders
301.0 (F60.0) Paranoid Personality Disorder (649)
301.20 (F60.1) Schizoid Personality Disorder (652)
301.22 (F21) Schizotypal Personality Disorder (655)
Cluster B Personality Disorders
301.7 (F60.2) Antisocial Personality Disorder (659)
301.83 (F60.3) Borderline Personality Disorder (663)
301.50 (F60.4) Histrionic Personality Disorder (667)
301.81 (F60.81) Narcissistic Personality Disorder (669)
DSM-5 Classification xxxiii
Cluster C Personality Disorders
301.82 (F60.6), Avoidant Personality Disorder (672)
301.6 (F60.7) Dependent Personality Disorder (675)
301.4 (F60.5) Obsessive-Compulsive Personality Disorder (678)
Other Personality Disorders
310.1 (FO7.0) Personality Change Due to Another Medical Condition (682)
Specify whether: Labile type, Disinhibited type, Aggressive type, Apathetic
type, Paranoid type, Other type, Combined type, Unspecified type
301.89 (F60.89) Other Specified Personality Disorder (684)
301.9 (F60.9) Unspecified Personality Disorder (684)
Paraphilic Disorders (685)
The following specifier applies to Paraphilic Disorders where indicated:
Specify if: In a controlled environment, In full remission
302.82 (F65.3) Voyeuristic Disorder* (686)
302.4 (F65.2) Exhibitionistic Disorder* (689)
Specify whether: Sexually aroused by exposing genitals to prepubertal
children, Sexually aroused by exposing genitals to physically mature
individuals, Sexually aroused by exposing genitals to prepubertal chil-
dren and to physically mature individuals
302.89 (F65.81) Frotteuristic Disorder* (691)
302.83 (F65.51) Sexual Masochism Disorder? (694)
Specify if: With asphyxiophilia
302.84 (F65.52) Sexual Sadism Disorder® (695)
302.2 (F65.4) Pedophilic Disorder (697)
Specify whether: Exclusive type, Nonexclusive type
Specify if: Sexually attracted to males, Sexually attracted to females, Sexu-
ally attracted to both
Specify if: Limited to incest
302.81 (F65.0) Fetishistic Disorder* (700)
Specify: Body part(s), Nonliving object(s), Other
302.3 (F65.1) Transvestic Disorder® (702)
Specify if: With fetishism, With autogynephilia
302.89 (F65.89) Other Specified Paraphilic Disorder (705)
302.9 (F65.9) Unspecified Paraphilic Disorder (705)
Other Mental Disorders (707)
294.8 (F06.8) Other Specified Mental Disorder Due to Another Medical
Condition (707)
294.9 (FO9) Unspecified Mental Disorder Due to Another Medical Condition
(708)
300.9 (F99) Other Specified Mental Disorder (708)
300.9 (F99) Unspecified Mental Disorder (708)
Xxxiv DSN-5 Classification
Medication-Induced Movement Disorders and
Other Adverse Effects of Medication (709)
332.1 (G21.11} Neuroleptic-Induced Parkinsonism (709)
332.1 (G21.19) Other Medication-Induced Parkinsonism (709)
333.92 (G21.0) Neuroleptic Malignant Syndrome (709)
333.72 (G24.02) Medication-Induced Acute Dystonia (711)
333.99 (G25.71) Medication-Induced Acute Akathisia (711)
333.85 (G24.01) Tardive Dyskinesia (712)
333.72 (G24.09) Tardive Dystonia (712)
333.99 (G25.71) Tardive Akathisia (712)
333.1 (G25.1) Medication-Induced Postural Tremor (712)
333.99 (G25.79)
a ee)
995.29 (T43.205A)
995.29 (T43.205D)
995.29 (T43.205S)
— {_._)
995.20 (T50.905A)
995.20 (T50.905D)
995.20 (150.9058)
Other Medication-Induced Movement Disorder (712)
Antidepressant Discontinuation Syndrome (712)
Initial encounter
Subsequent encounter
Sequelae
Other Adverse Effect of Medication (714)
Initial encounter
Subsequent encounter
Sequelae
Other Conditions That May Be a Focus
of Ciinicai Attention (715)
Relational Problems (715)
Problems Related to Family Upbringing (715)
V61.20 (262.820)
V61.8 (Z62.891)
V61.8 (Z62.29)
V61.29 (262.898)
Parent-Child Relational Problem (715)
Sibling Relational Problem (716)
Upbringing Away From Parents (716)
Child Affected by Parental Relationship Distress (716)
Other Problems Related to Primary Support Group (716)
V61.10 (263.0)
V61.03 (Z63.5)
V61.8 (Z63.8)
V62.82 (263.4)
Relationship Distress With Spouse or Intimate Partner (716)
Disruption of Family by Separation or Divorce (716)
High Expressed Emotion Level Within Family (716)
Uncomplicated Bereavement (716)
DSM-5 Classification XXXV
Abuse and Neglect (717)
Child Maltreatment and Neglect Problems (717)
Child Physical Abuse (717)
Child Physical Abuse, Confirmed (717)
995.54 (T74.12XA) Initial encounter
995.54 (T74.12XD) Subsequent encounter
Child Physical Abuse, Suspected (717)
995.54 (T76.12XA) Initial encounter
995.54 (T76.12XD} Subsequent encounter
Other Circumstances Related to Child Physical Abuse (718)
V61.21 (Z69.010) Encounter for mental health services for victim of child abuse
by parent
V61.21 (Z69.020) Encounter for mental health services for victim of nonparental
child abuse
V15.41 (262.810) Personal history (past history) of physical abuse in childhood
V61.22 (269.011) Encounter for mental health services for perpetrator of parental
child abuse
V62.83 (269.021) Encounter for mental health services for perpetrator of
nonparental child abuse
Child Sexual Abuse (718)
Child Sexual Abuse, Confirmed (718)
995.53 (T74.22XA) _ Initial encounter
995.53 (T74.22XD) Subsequent encounter
Child Sexual Abuse, Suspected (718)
995.53 (T76.22XA) Initial encounter
995.53 (T76.22XD) Subsequent encounter
Other Circumstances Related to Child Sexual Abuse (718)
V61.21 (269.010) Encounter for mental health services for victim of child sexual
abuse by parent
V61.21 (269.020) Encounter for mental health services for victim of nonparental
child sexual abuse
V15.41 (262.810) Personal history (past history) of sexual abuse in childhood
V61.22 (Z69.011) Encounter for mental health services for perpetrator of parental
child sexual abuse
V62.83 (Z69.021)} Encounter for mental health services for perpetrator of
nonparental child sexual abuse
Child Neglect (718)
Child Neglect, Confirmed (718)
995.52 (T74.02XA) Initial encounter
995.52 (T74.02XD) Subsequent encounter
XXXVI DSN-5 Classification
Child Neglect, Suspected (719)
995.52 (T76.02XA) Initial encounter
995.52 (T76.02XD) Subsequent encounter
Other Circumstances Related to Child Neglect (719)
V61.21 (Z69.010) Encounter for mental health services for victim of child neglect
by parent
V61.21 (Z69.020) Encounter for mental health services for victim of nonparental
child neglect
V15.42 (Z62.812) Personal history (past history) of neglect in childhood
V61.22 (269.011) Encounter for mental health services for perpetrator of parental
child neglect
V62.83 (Z69.021) Encounter for mental health services for perpetrator of
nonparental child neglect
Child Psychological Abuse (719)
Child Psychological Abuse, Confirmed (719)
995.51 (T74.32XA} Initial encounter
995.51 (T74.32XD) Subsequent encounter
Child Psychological Abuse, Suspected (719)
995.51 (T76.32XA) Initial encounter
995.51 (T76.32XD) Subsequent encounter
Other Circumstances Related to Child Psychological Abuse (719)
V61.21 (Z69.010) Encounter for mental health services for victim of child
psychological abuse by parent
V61.21 (Z69.020) Encounter for mental health services for victim of nonparental
child psychological abuse
V15.42 (262.811) Personal history (past history) of psychological abuse in
childhood
V61.22 (269.011) Encounter for mental health services for perpetrator of parental
child psychological abuse
V62.83 (269.021) Encounter for mental health services for perpetrator of
nonparental child psychological abuse
Adult Maltreatment and Neglect Problems (720)
Spouse or Partner Violence, Physical (720)
Spouse or Partner Violence, Physical, Confirmed (720)
995.81 (T74.11XA) Initial encounter
995.81 (T74.11XD) Subsequent encounter
Spouse or Partner Violence, Physical, Suspected (720)
995.81 (T76.11XA) Initial encounter
995.81 (T76.11XD) Subsequent encounter
Other Circumstances Related to Spouse or Partner Violence, Physical (720)
V61.11 (269.11) Encounter for mental health services for victim of spouse or
partner violence, physical
DSN-5 Classification Xxxvii
V15.41 (Z91.410) Personal history (past history) of spouse or partner violence,
, physical
V61.12 (Z69.12) Encounter for mental health services for perpetrator of spouse
or partner violence, physical
Spouse or Partner Violence, Sexual (720)
Spouse or Partner Violence, Sexual, Confirmed (720)
995.83 (T74.21XA) Initial encounter
995.83 (T74.21XD) Subsequent encounter
Spouse or Partner Violence, Sexual, Suspected (720)
995.83 (T76.21XA) Initial encounter
995.83 (T76.21XD) Subsequent encounter
Other Circumstances Related to Spouse or Partner Violence, Sexual (720)
V61.11 (Z69.81) Encounter for mental health services for victim of spouse or
partner violence, sexual
V15.41 (Z91.410) Personal history (past history) of spouse or partner violence,
sexual
V61.12 (Z69.12) Encounter for mental health services for perpetrator of spouse
or partner violence, sexual
Spouse or Partner, Neglect (721)
Spouse or Partner Neglect, Confirmed (721)
995.85 (T74.01XA) Initial encounter
995.85 (T74.01XD) Subsequent encounter
Spouse or Partner Neglect, Suspected (721)
995.85 (T76.01XA) Initial encounter
995.85 (T76.01XD) Subsequent encounter
Other Circumstances Related to Spouse or Partner Neglect (721)
V61.11 (Z69.11) Encounter for mental health services for victim of spouse or
partner neglect
V15.42 (291.412) Personal history (past history) of spouse or partner neglect
V61.12 (269.12) Encounter for mental health services for perpetrator of spouse
or partner neglect
Spouse or Partner Abuse, Psychological (721)
Spouse or Partner Abuse, Psychological, Confirmed (721)
995,82 (T74.31XA) Initial encounter
995.82 (T74.31XD) Subsequent encounter
Spouse or Partner Abuse, Psychological, Suspected (721)
995.82 (T76.31XA) Initial encounter
995.82 (T76.31XD) Subsequent encounter
Other Circumstances Related to Spouse or Partner Abuse, Psychological (721)
V61.11 (Z69.11) Encounter for mental health services for victim of spouse or
partner psychological abuse
Xxxviii DSN-5 Classification
V15.42 (291.411) Personal history (past history) of spouse or partner
psychological abuse
V61.12 (269.12) Encounter for mental health services for perpetrator of spouse
or partner psychological abuse
Adult Abuse by Nonspouse or Nonpartner (722)
Adult Physical Abuse by Nonspouse or Nonpartner, Confirmed (722)
995.81 (T74.11XA) Initial encounter
995.81 (T74.11XD) Subsequent encounter
Adult Physical Abuse by Nonspouse or Nonpartner, Suspected (722)
995.81 (T76.11XA) Initial encounter
995.81 (T76.11XD) Subsequent encounter
Adult Sexual Abuse by Nonspouse or Nonpartner, Confirmed (722)
995.83 (T74.21XA) Initial encounter
995.83 (T74.21XD) Subsequent encounter
Adult Sexual Abuse by Nonspouse or Nonpartner, Suspected (722)
995.83 (T76.21XA) Initial encounter
995.83 (T76.21XD) Subsequent encounter
Adult Psychological Abuse by Nonspouse or Nonpartner, Confirmed (722)
995.82 (T74.31XA) Initial encounter
995.82 (T74.31XD) Subsequent encounter
Adult Psychological Abuse by Nonspouse or Nonpartner, Suspected (722)
995.82 (T76.31XA) Initial encounter
995.82 (T76.31XD) Subsequent encounter
Other Circumstances Related to Adult Abuse by Nonspouse or Nonpartner (722)
V65.49 (Z69.81) Encounter for mental health services for victim of nonspousal
adult abuse
V62.83 (269.82) Encounter for mental health services for perpetrator of
nonspousal adult abuse
Educational and Occupational Problems (723)
Educational Problems (723)
V62.3 (Z55.9) Academic or Educational Problem (723)
Occupational Problems (723)
V62.21 (256.82) Problem Related to Current Military Deployment Status (723)
V62.29 (Z56.9) Other Problem Related to Employment (723)
Housing and Economic Problems (723)
Housing Problems (723)
V60.0 (Z59.0) Homelessness (723)
V60.1 (259.1) Inadequate Housing (723)
DSM-5 Classification
V60.89 (Z59.2)
V60.6 (Z59.3},
Xxxix
Discord With Neighbor, Lodger, or Landlord (723)
Problem Related to Living in a Residential Institution (724)
Economic Problems (724)
V60.2 (Z59.4)
V60.2 (Z59.5)
V60.2 (Z59.6)
V60.2 (Z59.7)
V60.9 (Z59.9)
Lack of Adequate Food or Safe Drinking Water (724)
Extreme Poverty (724)
Low Income (724)
Insufficient Social Insurance or Welfare Support (724)
Unspecified Housing or Economic Problem (724)
Other Problems Related to the Social Environment (724)
V62.89 (Z60.0)
V60.3 (Z60.2)
V62.4 (Z60.3)
V62.4 (Z60.4)
V62.4 (Z60.5)
V62.9 (Z60.9)
Phase of Life Problem (724)
Problem Related to Living Alone (724)
Acculturation Difficulty (724)
Social Exclusion or Rejection (724)
Target of (Perceived) Adverse Discrimination or Persecution (724)
Unspecified Problem Related to Social Environment (725)
Problems Related to Crime or Interaction With the Legal System (725)
V62.89 (Z65.4)
V62.5 (Z65.0)
V62.5 (Z65.1)
V62.5 (Z65.2)
V62.5 (Z65.3)
Victim of Crime (725)
Conviction in Civil or Criminal Proceedings Without
Imprisonment (725)
Imprisonment or Other Incarceration (725)
Problems Related to Release From Prison (725)
Problems Related to Other Legal Circumstances (725)
Other Health Service Encounters for Counseling and Medical Advice (725)
V65.49 (270.9)
V65.40 (Z71.9)
Sex Counseling (725)
Other Counseling or Consultation (725)
Problems Related to Other Psychosocial, Personal, and Environmental
Circumstances (725)
V62.89 (Z65.8)
V61.7 (264.0)
V61.5 (264.1)
V62.89 (Z64.4)
V62.89 (265.4)
V62.22 (265.5)
V62.89 (Z65.8)
V62.9 (Z65.9)
Religious or Spiritual Problem (725)
Problems Related to Unwanted Pregnancy (725)
Problems Related to Multiparity (725)
Discord With Social Service Provider, Including Probation
Officer, Case Manager, or Social Services Worker (725)
Victim of Terrorism or Torture (725)
Exposure to Disaster, War, or Other Hostilities (725)
Other Problem Related to Psychosocial Circumstances (725)
Unspecified Problem Related to Unspecified Psychosocial
Circumstances (725)
xl
DSN-5 Classification
Other Circumstances of Personal History (726)
V15.49 (291.49)
V15.59 (Z91.5)
V62.22 (291.82)
V15.89 (Z91.89)
V69.9 (Z72.9)
V71.01 (272.811)
V71.02 (272.810)
Other Personal History of Psychological Trauma (726)
Personal History of Self-Harm (726)
Personal History of Military Deployment (726)
Other Personal Risk Factors (726)
Problem Related to Lifestyle (726)
Adult Antisocial Behavior (726)
Child or Adolescent Antisocial Behavior (726)
Problems Related to Access to Medical and Other Health Care (726)
V63.9 (Z75.3)
V63.8 (275.4)
Unavailability or Inaccessibility of Health Care Facilities (726)
Unavailability or Inaccessibility of Other Helping Agencies (726)
Nonadherence to Medical Treatment (726)
V15.81 (Z91.19)
278.00 (E66.9)
V65.2 (276.5)
V40.31 (Z91.83)
V62.89 (R41.83)
Nonadherence to Medical Treatment (726)
Overweight or Obesity (726)
Malingering (726)
Wandering Associated With a Mental Disorder (727)
Borderline Intellectual Functioning (727)
Preface
The American Psychiatric Association’s Diagnostic and Statistical Manual of
Mental Disorders (DSM) is a classification of mental disorders with associated criteria de-
signed to facilitate more reliable diagnoses of these disorders. With successive editions
over the past 60 years, it has become a standard reference for clinical practice in the mental
health field. Since a complete description of the underlying pathological processes is not
possible for most mental disorders, it is important to emphasize that the current diagnos-
tic criteria are the best available description of how mental disorders are expressed and
can be recognized by trained clinicians. DSM is intended to serve as a practical, functional,
and flexible guide for organizing information that can aid in the accurate diagnosis and
treatment of mental disorders. It is a tool for clinicians, an essential educational resource
for students and practitioners, and a reference for researchers in the field.
Although this edition of DSM was designed first and foremost to be a useful guide to
clinical practice, as an official nomenclature it must be applicable in a wide diversity of
contexts. DSM has been used by clinicians and researchers from different orientations (bi-
ological, psychodynamic, cognitive, behavioral, interpersonal, family /systems), all of
whom strive for a common language to communicate the essential characteristics of men-
tal disorders presented by their patients. The information is of value to all professionals
associated with various aspects of mental health care, including psychiatrists, other
physicians, psychologists, social workers, nurses, counselors, forensic and legal special-
ists, occupational and rehabilitation therapists, and other health professionals. The criteria
are concise and explicit and intended to facilitate an objective assessment of symptom pre-
sentations in a variety of clinical settings—inpatient, outpatient, partial hospital, consul-
tation-liaison, clinical, private practice, and primary care—as well in general community
epidemiological studies of mental disorders. DSM-5 is also a tool for collecting and com-
municating accurate public health statistics on mental disorder morbidity and mortality
rates. Finally, the criteria and corresponding text serve as a textbook for students early in
their profession who need a structured way to understand and diagnose mental disorders
as well as for seasoned professionals encountering rare disorders for the first time. Fortu-
nately, all of these uses are mutually compatible.
These diverse needs and interests were taken into consideration in planning DSM-5.
The classification of disorders is harmonized with the World Health Organization’s Inter-
national Classification of Diseases (ICD), the official coding system used in the United States,
so that the DSM criteria define disorders identified by ICD diagnostic names and code
numbers. In DSM-5, both ICD-9-CM and ICD-10-CM codes (the latter scheduled for adop-
tion in October 2014) are attached to the relevant disorders in the classification.
Although DSM-5 remains a categorical classification of separate disorders, we recog-
nize that mental disorders do not always fit completely within the boundaries of a single
disorder. Some symptom domains, such as depression and anxiety, involve multiple di-
agnostic categories and may reflect common underlying vulnerabilities for a larger group
of disorders. In recognition of this reality, the disorders included in DSM-5 were reordered
into a revised organizational structure meant to stimulate new clinical perspectives. This
new structure corresponds with the organizational arrangement of disorders planned for
ICD-11 scheduled for release in 2015. Other enhancements have been introduced to pro-
mote ease of use across all settings:
xli
xiii Preface
¢ Representation of developmental issues related to diagnosis. The change in chapter
organization better reflects a lifespan approach, with disorders more frequently diag-
nosed in childhood (e.g., neurodevelopmental disorders) at the beginning of the man-
ual and disorders more applicable to older adulthood (e.g., neurocognitive disorders)
at the end of the manual. Also, within the text, subheadings on development and course
provide descriptions of how disorder presentations may change across the lifespan.
Age-related factors specific to diagnosis (e.g., symptom presentation and prevalence
differences in certain age groups) are also included in the text. For added emphasis,
these age-related factors have been added to the criteria themselves where applicable
(e.g., in the criteria sets for insomnia disorder and posttraumatic stress disorder, spe-
cific criteria describe how symptoms might be expressed in children). Likewise, gender
and cultural issues have been integrated into the disorders where applicable.
¢ Integration of scientific findings from the latest research in genetics and neuroimag-
ing. The revised chapter structure was informed by recent research in neuroscience and
by emerging genetic linkages between diagnostic groups. Genetic and physiological
risk factors, prognostic indicators, and some putative diagnostic markers are high-
lighted in the text. This new structure should improve clinicians’ ability to identify di-
agnoses in a disorder spectrum based on common neurocircuitry, genetic vulnerability,
and environmental exposures.
¢ Consolidation of autistic disorder, Asperger's disorder, and pervasive developmen-
tal disorder into autism spectrum disorder. Symptoms of these disorders represent a
single continuum of mild to severe impairments in the two domains of social commu-
nication and restrictive repetitive behaviors/interests rather than being distinct disor-
ders. This change is designed to improve the sensitivity and specificity of the criteria for
the diagnosis of autism spectrum disorder and to identify more focused treatment tar-
gets for the specific impairments identified.
¢ Streamlined classification of bipolar and depressive disorders. Bipolar and depres-
sive disorders are the most commonly diagnosed conditions in psychiatry. It was there-
fore important to streamline the presentation of these disorders to enhance both clinical
and educational use. Rather than separating the definition of manic, hypomanic, and
major depressive episodes from the definition of bipolar I disorder, bipolar II disorder,
and major depressive disorder as in the previous edition, we included all of the com-
ponent criteria within the respective criteria for each disorder. This approach will facil-
itate bedside diagnosis and treatment of these important disorders. Likewise, the
explanatory notes for differentiating bereavement and major depressive disorders will
provide far greater clinical guidance than was previously provided in the simple be-
reavement exclusion criterion. The new specifiers of anxious distress and mixed fea-
tures are now fully described in the narrative on specifier variations that accompanies
the criteria for these disorders.
* Restructuring of substance use disorders for consistency and clarity. The categories
of substance abuse and substance dependence have been eliminated and replaced with
an overarching new category of substance use disorders—with the specific substance
used defining the specific disorders. “Dependence” has been easily confused with the
term “addiction” when, in fact, the tolerance and withdrawal that previously defined
dependence are actually very normal responses to prescribed medications that affect
the central nervous system and do not necessarily indicate the presence of an addiction.
By revising and clarifying these criteria in DSM-5, we hope to alleviate some of the
widespread misunderstanding about these issues.
¢ Enhanced specificity for major and mild neurocognitive disorders. Given the explo-
sion in neuroscience, neuropsychology, and brain imaging over the past 20 years, it was
critical to convey the current state-of-the-art in the diagnosis of specific types of disor-
ders that were previously referred to as the “dementias” or organic brain diseases. Bi-
ological markers identified by imaging for vascular and traumatic brain disorders and
Preface xliii
specific molecular genetic findings for rare variants of Alzheimer’s disease and Hun-
tington’s disease have greatly advanced clinical diagnoses, and these disorders and
others have now been separated into specific subtypes.
e Transition in conceptualizing personality disorders. Although the benefits of a more
dimensional approach to personality disorders have been identified in previous edi-
tions, the transition from a categorical diagnostic system of individual disorders to one
based on the relative distribution of personality traits has not been widely accepted. In
DSM-5, the categorical personality disorders are virtually unchanged from the previous
edition. However, an alternative “hybrid” model has been proposed in Section II] to
guide future research that separates interpersonal functioning assessments and the ex-
pression of pathological personality traits for six specific disorders. A more dimensional
profile of personality trait expression is also proposed for a trait-specified approach.
¢ Section ITI: new disorders and features. A new section (Section III) has been added to
highlight disorders that require further study but are not sufficiently well established to
be a part of the official classification of mental disorders for routine clinical use. Dimen-
sional measures of symptom severity in 13 symptom domains have also been incorpo-
rated to allow for the measurement of symptom levels of varying severity across all
diagnostic groups. Likewise, the WHO Disability Assessment Schedule (WHODAS), a
standard method for assessing global disability levels for mental disorders that is based
on the International Classification of Functioning, Disability and Health (ICF) and is ap-
plicable in all of medicine, has been provided to replace the more limited Global As-
sessment of Functioning scale. It is our hope that as these measures are implemented
over time, they will provide greater accuracy and flexibility in the clinical description of
individual symptomatic presentations and associated disability during diagnostic as-
sessments.
e Online enhancements. DSM-5 features online supplemental information.
Additional cross-cutting and diagnostic severity measures are available online
(www.psychiatry.org/dsm5), linked to the relevant disorders. In addition, the Cul-
tural Formulation Interview, Cultural Formulation Interview—Informant Version, and
supplementary modules to the core Cultural Formulation Interview are also included
online at www.psychiatry.org/dsm5.
These innovations were designed by the leading authorities on mental disorders in the
world and were implemented on the basis of their expert review, public commentary, and
independent peer review. The 13 work groups, under the direction of the DSM-5 Task
Force, in conjunction with other review bodies and, eventually, the APA Board of Trust-
ees, collectively represent the global expertise of the specialty. This effort was supported
by an extensive base of advisors and by the professional staff of the APA Division of Re-
search; the names of everyone involved are too numerous to mention here but are listed in
the Appendix. We owe tremendous thanks to those who devoted countless hours and in-
valuable expertise to this effort to improve the diagnosis of mental disorders.
We would especially like to acknowledge the chairs, text coordinators, and members of
the 13 work groups, listed in the front of the manual, who spent many hours in this vol-
unteer effort to improve the scientific basis of clinical practice over a sustained 6-year pe-
riod. Susan K. Schultz, M.D., who served as text editor, worked tirelessly with Emily A.
Kuhl, Ph.D., senior science writer and DSM-5 staff text editor, to coordinate the efforts of
the work groups into a cohesive whole. William E. Narrow, M.D., M.P.H., led the research
group that developed the overall research strategy for DSM-5, including the field trials,
that greatly enhanced the evidence base for this revision. In addition, we are grateful to
those who contributed so much time to the independent review of the revision proposals,
including Kenneth S. Kendler, M.D., and Robert Freedman, M.D., co-chairs of the Scien-
tific Review Committee; John S. McIntyre, M.D., and Joel Yager, M.D., co-chairs of the
Clinical and Public Health Committee; and Glenn Martin, M.D., chair of the APA Assem-
xliv Preface
bly review process. Special thanks go to Helena C. Kraemer, Ph.D., for her expert statistical
consultation; Michael B. First, M.D., for his valuable input on the coding and review of cri-
teria; and Paul S. Appelbaum, M.D., for feedback on forensic issues. Maria N. Ward,
M.Ed., RHIT, CCS-P, also helped in verifying all ICD coding. The Summit Group, which
included these consultants, the chairs of all review groups, the task force chairs, and the
APA executive officers, chaired by Dilip V. Jeste, M.D., provided leadership and vision in
helping to achieve compromise and consensus. This level of commitment has contributed
to the balance and objectivity that we feel are hallmarks of DSM-5.
We especially wish to recognize the outstanding APA Division of Research staff—
identified in the Task Force and Work Group listing at the front of this manual—who
worked tirelessly to interact with the task force, work groups, advisors, and reviewers to
resolve issues, serve as liaisons between the groups, direct and manage the academic and
routine clinical practice field trials, and record decisions in this important process. In par-
ticular, we appreciate the support and guidance provided by James H. Scully Jr., M.D.,
Medical Director and CEO of the APA, through the years and travails of the development
process. Finally, we thank the editorial and production staff of American Psychiatric Pub-
lishing—specifically, Rebecca Rinehart, Publisher; John McDuffie, Editorial Director; Ann
Eng, Senior Editor; Greg Kuny, Managing Editor; and Tammy Cordova, Graphics Design
Manager—for their guidance in bringing this all together and creating the final product. It
is the culmination of efforts of many talented individuals who dedicated their time, exper-
tise, and passion that made DSM-5 possible.
David }. Kupfer, M.D.
DSM-5 Task Force Chair
Darrel A. Regier, M.D., M.P.H.
DSM-5 Task Force Vice-Chair
December 19, 2012
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Cautionary Statement for Forensic Use of DSM-5..................25
ThiS Section is a basic orientation to the purpose, structure, content, and
use of DSN-5. It is not intended to provide an exhaustive account of the evo-
lution of DSM-5, but rather to give readers a succinct overview of its key ele-
ments. The introductory section describes the public, professional, and expert
review process that was used to extensively evaluate the diagnostic criteria
presented in Section il. Asummary of the DSM-5 structure, harmonization with
ICD-11, and the transition to a non-axial system with a new approach to as-
sessing disability is also presented. “Use of the Manual” includes “Definition of
a Mentat Disorder,” forensic considerations, and a brief overview of the diag-
nostic process and use of coding and recording procedures.
Introduction
The creation of the fifth edition of Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) was a massive undertaking that involved hundreds of people working toward a
common goal over a 12-year process. Much thought and deliberation were involved in
evaluating the diagnostic criteria, considering the organization of every aspect of the man-
ual, and creating new features believed to be most useful to clinicians. All of these efforts
were directed toward the goal of enhancing the clinical usefulness of DSM-5 as a guide in
the diagnosis of mental disorders.
Reliable diagnoses are essential for guiding treatment recommendations, identifying
prevalence rates for mental health service planning, identifying patient groups for clinical
and basic research, and documenting important public health information such as mor-
bidity and mortality rates. As the understanding of mental disorders and their treatments
has evolved, medical, scientific, and clinical professionals have focused on the character-
istics of specific disorders and their implications for treatment and research.
While DSM has been the cornerstone of substantial progress in reliability, it has been well
recognized by both the American Psychiatric Association (APA) and the broad scientific com-
munity working on mental disorders that past science was not mature enough to yield fully
validated diagnoses—that is, to provide consistent, strong, and objective scientific validators
of individual DSM disorders. The science of mental disorders continues to evolve. However,
the last two decades since DSM-IV was released have seen real and durable progress in such
areas as cognitive neuroscience, brain imaging, epidemiology, and genetics. The DSM-5 Task
Force overseeing the new edition recognized that research advances will require careful, iter-
ative changes if DSM is to maintain its place as the touchstone classification of mental disor-
ders. Finding the right balance is critical. Speculative results do not belong in an official
nosology, but at the same time, DSM must evolve in the context of other clinical research ini-
tiatives in the field. One important aspect of this transition derives from the broad recognition
that a too-rigid categorical system does not capture clinical experience or important scientific
observations. The results of numerous studies of comorbidity and disease transmission in fam-
ilies, including twin studies and molecular genetic studies, make strong arguments for what
many astute clinicians have long observed: the boundaries between many disorder “catego-
ries” are more fluid over the life course than DSM-IV recognized, and many symptoms as-
signed to a single disorder may occur, at varying levels of severity, in many other disorders.
These findings mean that DSM, like other medical disease classifications, should accommo-
date ways to introduce dimensional approaches to mental disorders, including dimensions
that cut across current categories. Such an approach should permit a more accurate description
of patient presentations and increase the validity of a diagnosis (i.e., the degree to which diag-
nostic criteria reflect the comprehensive manifestation of an underlying psychopathological
disorder). DSM-5 is designed to better fill the need of clinicians, patients, families, and re-
searchers for a clear and concise description of each mental disorder organized by explicit di-
agnostic criteria, supplemented, when appropriate, by dimensional measures that cross
diagnostic boundaries, and a brief digest of information about the diagnosis, risk factors, as-
sociated features, research advances, and various expressions of the disorder.
Clinical training and experience are needed to use DSM for determining a diagnosis. The
diagnostic criteria identify symptoms, behaviors, cognitive functions, personality traits, phys-
ical signs, syndrome combinations, and durations that require clinical expertise to differenti-
ate from normal life variation and transient responses to stress. To facilitate a thorough
6 Introduction
examination of the range of symptoms present, DSM can serve clinicians as a guide to identify
the most prominent symptoms that should be assessed when diagnosing a disorder. Although
some mental disorders may have well-defined boundaries around symptom clusters, scien-
tific evidence now places many, if not most, disorders on a spectrum with closely related dis-
orders that have shared symptoms, shared genetic and environmental risk factors, and
possibly shared neural substrates (perhaps most strongly established for a subset of anxiety
disorders by neuroimaging and animal models). In short, we have come to recognize that the
boundaries between disorders are more porous than originally perceived.
Many health profession and educational groups have been involved in the development
and testing of DSM-5, including physicians, psychologists, social workers, nurses, counselors,
epidemiologists, statisticians, neuroscientists, and neuropsychologists. Finally, patients, fam-
ilies, lawyers, consumer organizations, and advocacy groups have all participated in revising
DSMG5 by providing feedback on the mental disorders described in this volume. Their moni-
toring of the descriptions and explanatory text is essential to improve understanding, reduce
stigma, and advance the treatment and eventual cures for these conditions.
A Brief History
The APA first published a predecessor of DSM in 1844, as a statistical classification of in-
stitutionalized mental patients. It was designed to improve communication about the
types of patients cared for in these hospitals. This forerunner to DSM also was used as a
component of the full U.S. census. After World War II, DSM evolved through four major
editions into a diagnostic classification system for psychiatrists, other physicians, and
other mental health professionals that described the essential features of the full range of
mental disorders. The current edition, DSM-5, builds on the goal of its predecessors (most
recently, DSM-IV-TR, or Text Revision, published in 2000) of providing guidelines for di-
agnoses that can inform treatment and management decisions.
DSM-5 Revision Process
In 1999, the APA launched an evaluation of the strengths and weaknesses of DSM based on
emerging research that did not support the boundaries established for some mental disor-
ders. This effort was coordinated with the World Health Organization (WHO) Division of
Mental Health, the World Psychiatric Association, and the National Institute of Mental
Health (NIMH) in the form of several conferences, the proceedings of which were published
in 2002 in a monograph entitled A Research Agenda for DSM-V. Thereafter, from 2003 to 2008,
a cooperative agreement with the APA and the WHO was supported by the NIMH, the Na-
tional Institute on Drug Abuse (NIDA), and the National Institute on Alcoholism and Alco-
hol Abuse (NIAAA) to convene 13 international DSM-5 research planning conferences,
involving 400 participants from 39 countries, to review the world literature in specific diag-
nostic areas to prepare for revisions in developing both DSM-5 and the International Classi-
fication of Diseases, 11th Revision (ICD-11). Reports from these conferences formed the basis
for future DSM-5 Task Force reviews and set the stage for the new edition of DSM.
In 2006, the APA named David J. Kupfer, M.D., as Chair and Darrel A. Regier, M.D.,
M.P.H., as Vice-Chair of the DSM-5 Task Force. They were charged with recommending
chairs for the 13 diagnostic work groups and additional task force members with a multi-
disciplinary range of expertise who would oversee the development of DSM-5. An addi-
tional vetting process was initiated by the APA Board of Trustees to disclose sources of
income and thus avoid conflicts of interest by task force and work group members. The full
disclosure of all income and research grants from commercial sources, including the phar-
maceutical industry, in the previous 3 years, the imposition of an income cap from all com-
mercial sources, and the publication of disclosures on a Web site set a new standard for the
Introduction 7
field. Thereafter, the task force of 28 members was approved in 2007, and appointments of
more than 130 work group members were approved in 2008. More than 400 additional
work group advisors with no voting authority were also approved to participate in the pro-
cess. A clear concept of the next evolutionary stage for the classification of mental disorders
was central to the efforts of the task force and the work groups. This vision emerged as the
task force and work groups recounted the history of DSM-IV’s classification, its current
strengths and limitations, and strategic directions for its revision. An intensive 6-year pro-
cess involved conducting literature reviews and secondary analyses, publishing research
reports in scientific journals, developing draft diagnostic criteria, posting preliminary
drafts on the DSM-5 Web site for public comment, presenting preliminary findings at pro-
fessional meetings, performing field trials, and revising criteria and text.
Proposals for Revisions
Proposals for the revision of DSM-5 diagnostic criteria were developed by members of the
work groups on the basis of rationale, scope of change, expected impact on clinical man-
agement and public health, strength of the supporting research evidence, overall clarity,
and clinical utility. Proposals encompassed changes to diagnostic criteria; the addition of
new disorders, subtypes, and specifiers; and the deletion of existing disorders.
In the proposals for revisions, strengths and weaknesses in the current criteria and no-
sology were first identified. Novel scientific findings over the previous two decades were
considered, leading to the creation of a research plan to assess potential changes through
literature reviews and secondary data analyses. Four principles guided the draft revisions:
1) DSM-5 is primarily intended to be a manual to be used by clinicians, and revisions must
be feasible for routine clinical practice; 2) recommendations for revisions should be guided
by research evidence; 3) where possible, continuity should be maintained with previous
editions of DSM; and 4) no a priori constraints should be placed on the degree of change
between DSM-IV and DSM-5.
Building on the initial literature reviews, work groups identified key issues within
their diagnostic areas. Work groups also examined broader methodological concerns,
such as the presence of contradictory findings within the literature; development of a re-
fined definition of mental disorder; cross-cutting issues relevant to all disorders; and the
revision of disorders categorized in DSM-IV as “not otherwise specified.” Inclusion of a
proposal for revision in Section II was informed by consideration of its advantages and
disadvantages for public health and clinical utility, the strength of the evidence, and the
magnitude of the change. New diagnoses and disorder subtypes and specifiers were sub-
ject to additional stipulations, such as demonstration of reliability (i.e., the degree to which
two clinicians could independently arrive at the same diagnosis for a given patient). Dis-
orders with low clinical utility and weak validity were considered for deletion. Placement
of conditions in “Conditions for Further Study” in Section III was contingent on the
amount of empirical evidence generated on the diagnosis, diagnostic reliability or valid-
ity, presence of clear clinical need, and potential benefit in advancing research.
DSM-5 Field Trials
The use of field trials to empirically demonstrate reliability was a noteworthy improvement in-
troduced in DSM-III. The design and implementation strategy of the DSM-5 Field Trials rep-
resent several changes over approaches used for DSM-III and DSM-IV, particularly in
obtaining data on the precision of kappa reliability estimates (a statistical measure that assesses
level of agreement between raters that corrects for chance agreement due to prevalence rates)
in the context of clinical settings with high levels of diagnostic comorbidity. For DSM-5, field
trials were extended by using two distinctive designs: one in large, diverse medical-academic
settings, and the other in routine clinical practices. The former capitalized on the need for large
sample sizes to test hypotheses on reliability and clinical utility of a range of diagnoses in a
8 Introduction
variety of patient populations; the latter supplied valuable information about how proposed
revisions performed in everyday clinical settings among a diverse sample of DSM users. It is
anticipated that future clinical and basic research studies will focus on the validity of the re-
vised categorical diagnostic criteria and the underlying dimensional features of these disor-
ders (including those now being explored by the NIMH Research Domain Criteria initiative).
The medical-academic field trials were conducted at 11 North American medical-academic
sites and assessed the reliability, feasibility, and clinical utility of select revisions, with priority
given to those that represented the greatest degree of change from DSM-IV or those potentially
having the greatest public health impact. The full clinical patient populations coming to each
site were screened for DSM-IV diagnoses or qualifying symptoms likely to predict several spe-
cific DSM-5 disorders of interest. Stratified samples of four to seven specific disorders, plus a
stratum containing a representative sample of all other diagnoses, were identified for each site.
Patients consented to the study and were randomly assigned for a clinical interview by a cli-
nician blind to the diagnosis, followed by a second interview with a clinician blind to previous
diagnoses. Patients first filled out a computer-assisted inventory of cross-cutting symptoms in
more than a dozen psychological domains. These inventories were scored by a central server,
and results were provided to clinicians before they conducted a typical clinical interview (with
no structured protocol). Clinicians were required to score the presence of qualifying criteria on
a computer-assisted DSM-5 diagnostic checklist, determine diagnoses, score the severity of the
diagnosis, and submit all data to the central Web-based server. This study design allowed the
calculation of the degree to which two independent clinicians could agree on a diagnosis (us-
ing the intraclass kappa statistic) and the agreement of a single patient or two different clini-
cians on two separate ratings of cross-cutting symptoms, personality traits, disability, and
diagnostic severity measures (using intraclass correlation coefficients) along with information
on the precision of these estimates of reliability. It was also possible to assess the prevalence
rates of both DSM-IV and DSM-5 conditions in the respective clinical populations.
The routine clinical practice field trials involved recruitment of individual psychiatrists
and other mental health clinicians. A volunteer sample was recruited that included gener-
alist and specialty psychiatrists, psychologists, licensed clinical social workers, counselors,
marriage and family therapists, and advanced practice psychiatric mental health nurses.
The field trials provided exposure of the proposed DSM-5 diagnoses and dimensional mea-
sures to a wide range of clinicians to assess their feasibility and clinical utility.
Public and Professional Review
In 2010, the APA launched a unique Web site to facilitate public and professional input into
DSM 5. All draft diagnostic criteria and proposed changes in organization were posted on
www.dsm5.org for a 2-month comment period. Feedback totaled more than 8,000 submis-
sions, which were systematically reviewed by each of the 13 work groups, whose members,
where appropriate, integrated questions and comments into discussions of draft revisions
and plans for field trial testing. After revisions to the initial draft criteria and proposed
chapter organization, a second posting occurred in 2011. Work groups considered feedback
from both Web postings and the results of the DSM-5 Field Trials when drafting proposed
final criteria, which were posted on the Web site for a third and final time in 2012. These
three iterations of external review produced more than 13,000 individually signed com-
ments on the Web site that were received and reviewed by the work groups, plus thousands
of organized petition signers for and against some proposed revisions, all of which allowed
the task force to actively address concerns of DSM users, as well as patients and advocacy
groups, and ensure that clinical utility remained a high priority.
Expert Review
The members of the 13 work groups, representing expertise in their respective areas, col-
laborated with advisors and reviewers under the overall direction of the DSM-5 Task
Introduction 9
Force to draft the diagnostic criteria and accompanying text. This effort was supported by
a team of APA Division of Research staff and developed through a network of text coor-
dinators from each work group. The preparation of the text was coordinated by the text
editor, working in close collaboration with the work groups and under the direction of the
task force chairs. The Scientific Review Committee (SRC) was established to provide a sci-
entific peer review process that was external to that of the work groups. The SRC chair,
vice-chair, and six committee members were charged with reviewing the degree to which
the proposed changes from DSM-IV could be supported with scientific evidence. Each
proposal for diagnostic revision required a memorandum of evidence for change pre-
pared by the work group and accompanied by a summary of supportive data organized
around validators for the proposed diagnostic criteria (i.e., antecedent validators such as
familial aggregation, concurrent validators such as biological markers, and prospective
validators such as response to treatment or course of illness). The submissions were re-
viewed by the SRC and scored according to the strength of the supportive scientific data.
Other justifications for change, such as those arising from clinical experience or need or
from a conceptual reframing of diagnostic categories, were generally seen as outside the
purview of the SRC. The reviewers’ scores, which varied substantially across the different
proposals, and an accompanying brief commentary were then returned to the APA Board
of Trustees and the work groups for consideration and response.
The Clinical and Public Health Committee (CPHC), composed of a chair, vice-chair, and
six members, was appointed to consider additional clinical utility, public health, and log-
ical clarification issues for criteria that had not yet accumulated the type or level of evi-
dence deemed sufficient for change by the SRC. This review process was particularly
important for DSM-IV disorders with known deficiencies for which proposed remedies
had neither been previously considered in the DSM revision process nor been subjected to
replicated research studies. These selected disorders were evaluated by four to five exter-
nal reviewers, and the blinded results were reviewed by CPHC members, who in turn
made recommendations to the APA Board of Trustees and the work groups.
Forensic reviews by the members of the APA Council on Psychiatry and Law were con-
ducted for disorders frequently appearing in forensic environments and ones with high
potential for influencing civil and criminal judgments in courtroom settings. Work groups
also added forensic experts as advisors in pertinent areas to complement expertise pro-
vided by the Council on Psychiatry and Law.
The work groups themselves were charged with the responsibility to review the entire re-
search literature surrounding a diagnostic area, including old, revised, and new diagnostic cri-
teria, in an intensive 6-year review process to assess the pros and cons of making either small
iterative changes or major conceptual changes to address the inevitable reification that occurs
with diagnostic conceptual approaches that persist over several decades. Such changes in-
cluded the merger of previously separate diagnostic areas into more dimensional spectra, such
as that which occurred with autism spectrum disorder, substance use disorders, sexual dys-
functions, and somatic symptom and related disorders. Other changes included correcting
flaws that had become apparent over time in the choice of operational criteria for some disor-
ders. These types of changes posed particular challenges to the SRC and CPHC review pro-
cesses, which were not constructed to evaluate the validity of DSM-IV diagnostic criteria.
However, the DSM-5 Task Force, which had reviewed proposed changes and had responsi-
bility for reviewing the text describing each disorder contemporaneously with the work
groups during this period, was ina unique position to render an informed judgment on the sci-
entific merits of such revisions. Furthermore, many of these major changes were subject to field
trial testing, although comprehensive testing of all proposed changes could not be accommo-
dated by such testing because of time limitations and availability of resources.
A final recommendation from the task force was then provided to the APA Board of
Trustees and the APA Assembly’s Committee on DSM-5 to consider some of the clinical
utility and feasibility features of the proposed revisions. The assembly is a deliberative
10 Introduction
body of the APA representing the district branches and wider membership that is com-
posed of psychiatrists from throughout the United States who provide geographic, prac-
tice size, and interest-based diversity. The Committee on DSM-5 is a committee made up
of a diverse group of assembly leaders.
Following all of the preceding review steps, an executive “summit committee” session
was held to consolidate input from review and assembly committee chairs, task force
chairs, a forensic advisor, and a statistical advisor, for a preliminary review of each disor-
der by the assembly and APA Board of Trustees executive committees. This preceded a
preliminary review by the full APA Board of Trustees. The assembly voted, in November
2012, to recommend that the board approve the publication of DSM-5, and the APA Board
of Trustees approved its publication in December 2012. The many experts, reviewers, and
advisors who contributed to this process are listed in the Appendix.
Organizational Structure
The individual disorder definitions that constitute the operationalized sets of diagnostic
criteria provide the core of DSM-5 for clinical and research purposes. These criteria have
been subjected to scientific review, albeit to varying degrees, and many disorders have un-
dergone field testing for interrater reliability. In contrast, the classification of disorders (the
way in which disorders are grouped, which provides a high-level organization for the man-
ual) has not generally been thought of as scientifically significant, despite the fact that judg-
ments had to be made when disorders were initially divided into chapters for DSM-III.
DSM is a medical classification of disorders and as such serves as a historically deter-
mined cognitive schema imposed on clinical and scientific information to increase its com-
prehensibility and utility. Not surprisingly, as the foundational science that ultimately led
to DSM-IiI has approached a half-century in age, challenges have begun to emerge for cli-
nicians and scientists alike that are inherent in the DSM structure rather than in the de-
scription of any single disorder. These challenges include high rates of comorbidity within
and across DSM chapters, an excessive use of and need to rely on “not otherwise specified”
(NOS) criteria, and a growing inability to integrate DSM disorders with the results of ge-
netic studies and other scientific findings.
As the APA and the WHO began to plan their respective revisions of the DSM and the
International Classification of Disorders (ICD), both considered the possibility of improving
clinical utility (e.g., by helping to explain apparent comorbidity) and facilitating scientific
investigation by rethinking the organizational structures of both publications in a linear
system designated by alphanumeric codes that sequence chapters according to some ra-
tional and relational structure. It was critical to both the DSM-5 Task Force and the WHO
International Advisory Group on the revision of the ICD-10 Section on Mental and Behav-
ioral Disorders that the revisions to the organization enhance clinical utility and remain
within the bounds of well-replicated scientific information. Although the need for reform
seemed apparent, it was important to respect the state of the science as well as the chal-
lenge that overly rapid change would pose for the clinical and research communities. In
that spirit, revision of the organization was approached as a conservative, evolutionary di-
agnostic reform that would be guided by emerging scientific evidence on the relationships
between disorder groups. By reordering and regrouping the existing disorders, the re-
vised structure is meant to stimulate new clinical perspectives and to encourage research-
ers to identify the psychological and physiological cross-cutting factors that are not bound
by strict categorical designations.
The use of DSM criteria has the clear virtue of creating a common language for com-
munication between clinicians about the diagnosis of disorders. The official criteria and
disorders that were determined to have accepted clinical applicability are located in Sec-
tion II of the manual. However, it should be noted that these diagnostic criteria and their
Introduction 11
relationships within the classification are based on current research and may need to be
modified as new evidence is gathered by future research both within and across the do-
mains of proposed disorders. “Conditions for Further Study,” described in Section III, are
those for which we determined that the scientific evidence is not yet available to support
widespread clinical use. These diagnostic criteria are included to highlight the evolution
and direction of scientific advances in these areas to stimulate further research.
With any ongoing review process, especially one of this complexity, different viewpoints
emerge, and an effort was made to consider various viewpoints and, when warranted, ac-
commodate them. For example, personality disorders are included in both Sections II and
III. Section IT represents an update of the text associated with the same criteria found in
DSM-IV-TR, whereas Section II] includes the proposed research model for personality dis-
order diagnosis and conceptualization developed by the DSM-5 Personality and Personality
Disorders Work Group. As this field evolves, it is hoped that both versions will serve clin-
ical practice and research initiatives.
Harmonization With ICD-11
The groups tasked with revising the DSM and ICD systems shared the overarching goal of
harmonizing the two classifications as much as possible, for the following reasons:
¢ The existence of two major classifications of mental disorders hinders the collection and
use of national health statistics, the design of clinical trials aimed at developing new
treatments, and the consideration of global applicability of the results by international
regulatory agencies.
¢ More broadly, the existence of two classifications complicates attempts to replicate sci-
entific results across national boundaries.
¢ Even when the intention was to identify identical patient populations, DSM-IV and
ICD-10 diagnoses did not always agree.
Early in the course of the revisions, it became apparent that a shared organizational
structure would help harmonize the classifications. In fact, the use of a shared framework
helped to integrate the work of DSM and ICD work groups and to focus on scientific is-
sues. The DSM-5 organization and the proposed linear structure of the ICD-11 have been
endorsed by the leadership of the NIMH Research Domain Criteria (RDoC) project as con-
sistent with the initial overall structure of that project.
Of course, principled disagreements on the classification of psychopathology and on
specific criteria for certain disorders were expected given the current state of scientific
knowledge. However, most of the salient differences between the DSM and the ICD classi-
fications do not reflect real scientific differences, but rather represent historical by-products
of independent committee processes.
To the surprise of participants in both revision processes, large sections of the content
fell relatively easily into place, reflecting real strengths in some areas of the scientific lit-
erature, such as epidemiology, analyses of comorbidity, twin studies, and certain other ge-
netically informed designs. When disparities emerged, they almost always reflected the
need to make a judgment about where to place a disorder in the face of incomplete—or,
more often, conflicting—data. Thus, for example, on the basis of patterns of symptoms, co-
morbidity, and shared risk factors, attention-deficit/hyperactivity disorder (ADHD) was
placed with neurodevelopmental disorders, but the same data also supported strong ar-
guments to place ADHD within disruptive, impulse-control, and conduct disorders.
These issues were settled with the preponderance of evidence (most notably validators ap-
proved by the DSM-5 Task Force). The work groups recognize, however, that future dis-
coveries might change the placement as well as the contours of individual disorders and,
furthermore, that the simple and linear organization that best supports clinical practice
12 Introduction
may not fully capture the complexity and heterogeneity of mental disorders. The revised
organization is coordinated with the mental and behavioral disorders chapter (Chapter V)
of ICD-11, which will utilize an expanded numeric-alphanumeric coding system. How-
ever, the official coding system in use in the United States at the time of publication of this
manual is that of the International Classification of Diseases, Ninth Revision, Clinical Modifica-
tion (ICD-9-CM)—the U.S. adaptation of ICD-9. International Classification of Diseases, Tenth
Revision, Clinical Modification (ICD-10-CM), adapted from ICD-10, is scheduled for imple-
mentation in the United States in October 2014. Given the impending release of ICD-11, it
was decided that this iteration, and not ICD-10, would be the most relevant on which to focus
harmonization. However, given that adoption of the ICD-9-CM coding system will remain
at the time of the DSM-5 release, it will be necessary to use the ICD-9-CM codes. Further-
more, given that DSM-5’s organizational structure reflects the anticipated structure of
ICD-11, the eventual ICD-11 codes will follow the sequential order of diagnoses in the
DSM-5 chapter structure more closely. At present, both the ICD-9-CM and the ICD-10-CM
codes have been indicated for each disorder. These codes will not be in sequential order
throughout the manual because they were assigned to complement earlier organizational
structures.
Dimensional Approach to Diagnosis
Structural problems rooted in the basic design of the previous DSM classification, con-
structed of a large number of narrow diagnostic categories, have emerged in both clinical
practice and research. Relevant evidence comes from diverse sources, including studies of
comorbidity and the substantial need for not otherwise specified diagnoses, which repre-
sent the majority of diagnoses in areas such as eating disorders, personality disorders, and
autism spectrum disorder. Studies of both genetic and environmental risk factors, whether
based on twin designs, familial transmission, or molecular analyses, also raise concerns
about the categorical structure of the DSM system. Because the previous DSM approach
considered each diagnosis as categorically separate from health and from other diagnoses,
it did not capture the widespread sharing of symptoms and risk factors across many dis-
orders that is apparent in studies of comorbidity. Earlier editions of DSM focused on ex-
cluding false-positive results from diagnoses; thus, its categories were overly narrow, as is
apparent from the widespread need to use NOS diagnoses. Indeed, the once plausible goal
of identifying homogeneous populations for treatment and research resulted in narrow di-
agnostic categories that did not capture clinical reality, symptom heterogeneity within dis-
orders, and significant sharing of symptoms across multiple disorders. The historical
aspiration of achieving diagnostic homogeneity by progressive subtyping within disorder
categories no longer is sensible; like most common human ills, mental disorders are het-
erogeneous at many levels, ranging from genetic risk factors to symptoms.
Related to recommendations about alterations in the chapter structure of DSM-5, mem-
bers of the diagnostic spectra study group examined whether scientific validators could
inform possible new groupings of related disorders within the existing categorical frame-
work. Eleven such indicators were recommended for this purpose: shared neural sub-
strates, family traits, genetic risk factors, specific environmental risk factors, biomarkers,
temperamental antecedents, abnormalities of emotional or cognitive processing, symptom
similarity, course of illness, high comorbidity, and shared treatment response. These indi-
cators served as empirical guidelines to inform decision making by the work groups and
the task force about how to cluster disorders to maximize their validity and clinical utility.
A series of papers was developed and published in a prominent international journal
(Psychological Medicine, Vol. 39, 2009) as part of both the DSM-5 and the ICD-11 develop-
mental processes to document that such validators were most useful for suggesting large
groupings of disorders rather than for “validating” individual disorder diagnostic criteria.
The regrouping of mental disorders in DSM-5 is intended to enable future research to en-
Introduction 13
hance understanding of disease origins and pathophysiological commonalities between
disorders and provide a base for future replication wherein data can be reanalyzed over
time to continually assess validity. Ongoing revisions of DSM-5 will make it a “living doc-
ument,” adaptable to future discoveries in neurobiology, genetics, and epidemiology.
On the basis of the published findings of this common DSM-5 and ICD-11 analysis, it
was demonstrated that clustering of disorders according to what has been termed internal-
izing and externalizing factors represents an empirically supported framework. Within both
the internalizing group (representing disorders with prominent anxiety, depressive, and
somatic symptoms) and the externalizing group (representing disorders with prominent
impulsive, disruptive conduct, and substance use symptoms), the sharing of genetic and
environmental risk factors, as shown by twin studies, likely explains much of the system-
atic comorbidities seen in both clinical and community samples. The adjacent placement of
“internalizing disorders,” characterized by depressed mood, anxiety, and related physio-
logical and cognitive symptoms, should aid in developing new diagnostic approaches, in-
cluding dimensional approaches, while facilitating the identification of biological markers.
Similarly, adjacencies of the “externalizing group,” including disorders exhibiting antiso-
cial behaviors, conduct disturbances, addictions, and impulse-control disorders, should en-
courage advances in identifying diagnoses, markers, and underlying mechanisms.
Despite the problem posed by categorical diagnoses, the DSM-5 Task Force recognized
that it is premature scientifically to propose alternative definitions for most disorders. The
organizational structure is meant to serve as a bridge to new diagnostic approaches with-
out disrupting current clinical practice or research. With support from DSM-associated
training materials, the National Institutes of Health other funding agencies, and scientific
publications, the more dimensional DSM-5 approach and organizational structure can fa-
cilitate research across current diagnostic categories by encouraging broad investigations
within the proposed chapters and across adjacent chapters. Such a reformulation of re-
search goals should also keep DSM-5 central to the development of dimensional approaches
to diagnosis that will likely supplement or supersede current categorical approaches in
coming years.
Developmental and Lifespan Considerations
To improve clinical utility, DSM-5 is organized on developmental! and lifespan consider-
ations. It begins with diagnoses thought to reflect developmental processes that manifest
early in life (e.g., neurodevelopmental and schizophrenia spectrum and other psychotic
disorders), followed by diagnoses that more commonly manifest in adolescence and
young adulthood (e.g., bipolar, depressive, and anxiety disorders), and ends with diagno-
ses relevant to adulthood and later life (e.g., neurocognitive disorders). A similar approach
has been taken, where possible, within each chapter. This organizational structure facili-
tates the comprehensive use of lifespan information as a way to assist in diagnostic deci-
sion making.
The proposed organization of chapters of DSM-5, after the neurodevelopmental disor-
ders, is based on groups of internalizing (emotional and somatic) disorders, externalizing
disorders, neurocognitive disorders, and other disorders. It is hoped that this organization
will encourage further study of underlying pathophysiological processes that give rise to
diagnostic comorbidity and symptom heterogeneity. Furthermore, by arranging disorder
clusters to mirror clinical reality, DSM-5 should facilitate identification of potential diag-
noses by non—mental health specialists, such as primary care physicians.
The organizational structure of DSM-5, along with ICD harmonization, is designed to
provide better and more flexible diagnostic concepts for the next epoch of research and to
serve as a useful guide to clinicians in explaining to patients why they might have received
multiple diagnoses or why they might have received additional or altered diagnoses over
their lifespan.
14 Introduction
Cultural Issues
Mental disorders are defined in relation to cultural, social, and familial norms and values.
Culture provides interpretive frameworks that shape the experience and expression of the
symptoms, signs, and behaviors that are criteria for diagnosis. Culture is transmitted, re-
vised, and recreated within the family and other social systems and institutions. Diagnostic
assessment must therefore consider whether an individual’s experiences, symptoms, and
behaviors differ from sociocultural norms and lead to difficulties in adaptation in the cul-
tures of origin and in specific social or familial contexts. Key aspects of culture relevant to di-
agnostic classification and assessment have been considered in the development of DSM-5.
In Section II, the “Cultural Formulation” contains a detailed discussion of culture and
diagnosis in DSM-5, including tools for in-depth cultural assessment. In the Appendix, the
“Glossary of Cultural Concepts of Distress” provides a description of some common cul-
tural syndromes, idioms of distress, and causal explanations relevant to clinical practice.
The boundaries between normality and pathology vary across cultures for specific types
of behaviors. Thresholds of tolerance for specific symptoms or behaviors differ across cul-
tures, social settings, and families. Hence, the level at which an experience becomes prob-
lematic or pathological will differ. The judgment that a given behavior is abnormal and
requires clinical attention depends on cultural norms that are internalized by the individual
and applied by others around them, including family members and clinicians. Awareness of
the significance of culture may correct mistaken interpretations of psychopathology, but cul-
ture may also contribute to vulnerability and suffering (e.g., by amplifying fears that main-
tain panic disorder or health anxiety). Cultural meanings, habits, and traditions can also
contribute to either stigma or support in the social and familial response to mental illness.
Culture may provide coping strategies that enhance resilience in response to illness, or sug-
gest help seeking and options for accessing health care of various types, including alterna-
tive and complementary health systems. Culture may influence acceptance or rejection of a
diagnosis and adherence to treatments, affecting the course of illness and recovery. Culture
also affects the conduct of the clinical encounter; as a result, cultural differences between the
clinician and the patient have implications for the accuracy and acceptance of diagnosis as
well as for treatment decisions, prognostic considerations, and clinical outcomes.
Historically, the construct of the culture-bound syndrome has been a key interest of
cultural psychiatry. In DSM-5, this construct has been replaced by three concepts that offer
greater clinical utility:
1. Cultural syndrome is a cluster or group of co-occurring, relatively invariant symptoms
found in a specific cultural group, community, or context (e.g., ataque de nervios). The
syndrome may or may not be recognized as an illness within the culture (e.g., it might
be labeled in various ways), but such cultural patterns of distress and features of illness
may nevertheless be recognizable by an outside observer.
2. Cultural idiom of distress is a linguistic term, phrase, or way of talking about suffering
among individuals of a cultural group (e.g., similar ethnicity and religion) referring to
shared concepts of pathology and ways of expressing, communicating, or naming es-
sential features of distress (e.g., kufungisisa). An idiom of distress need not be associated
with specific symptoms, syndromes, or perceived causes. It may be used to convey a
wide range of discomfort, including everyday experiences, subclinical conditions, or
suffering due to social circumstances rather than mental disorders. For example, most
cultures have common bodily idioms of distress used to express a wide range of suf-
fering and concerns.
3. Cultural explanation or perceived cause is a label, attribution, or feature of an explanatory
model that provides a culturally conceived etiology or cause for symptoms, illness, or
distress (e.g., maladi moun). Causal explanations may be salient features of folk classi-
fications of disease used by laypersons or healers.
Introduction 15
These three concepts (for which discussion and examples are provided in Section III
and the Appendix) suggest cultural ways of understanding and describing illness experi-
ences that can be elicited in the clinical encounter. They influence symptomatology, help
seeking, clinical presentations, expectations of treatment, illness adaptation, and treat-
ment response. The same cultural term often serves more than one of these functions.
Gender Differences
Sex and gender differences as they relate to the causes and expression of medical conditions
are established for a number of diseases, including selected mental disorders. Revisions to
DSM-5 included review of potential differences between men and women in the expression
of mental illness. In terms of nomenclature, sex differences are variations attributable to an
individual’s reproductive organs and XX or XY chromosomal complement. Gender differ-
ences are variations that result from biological sex as well as an individual's self-represen-
tation that includes the psychological, behavioral, and social consequences of one’s
perceived gender. The term gender differences is used in DSM-5 because, more commonly,
the differences between men and women are a result of both biological sex and individual
self-representation. However, some of the differences are based on only biological sex.
Gender can influence illness in a variety of ways. First, it may exclusively determine
whether an individual is at risk for a disorder (e.g., as in premenstrual dysphoric disor-
der). Second, gender may moderate the overall risk for development of a disorder as
shown by marked gender differences in the prevalence and incidence rates for selected
mental disorders. Third, gender may influence the likelihood that particular symptoms of
a disorder are experienced by an individual. Attention-deficit/hyperactivity disorder is
an example of a disorder with differences in presentation that are most commonly expe-
rienced by boys or girls. Gender likely has other effects on the experience of a disorder that
are indirectly relevant to psychiatric diagnosis. It may be that certain symptoms are more
readily endorsed by men or women, and that this contributes to differences in service pro-
vision (e.g., women may be more likely to recognize a depressive, bipolar, or anxiety dis-
order and endorse a more comprehensive list of symptoms than men).
Reproductive life cycle events, including estrogen variations, also contribute to gender
differences in risk and expression of illness. Thus, a specifier for postpartum onset of mania
or major depressive episode denotes a time frame wherein women may be at increased risk
for the onset of an illness episode. In the case of sleep and energy, alterations are often nor-
mative postpartum and thus may have lower diagnostic reliability in postpartum women.
The manual is configured to include information on gender at multiple levels. If there
are gender-specific symptoms, they have been added to the diagnostic criteria. A gender-
related specifier, such as perinatal onset of a mood episode, provides additional informa-
tion on gender and diagnosis. Finally, other issues that are pertinent to diagnosis and gen-
der considerations can be found in the section “Gender-Related Diagnostic Issues.”
Use of Other Specified and Unspecified Disorders
To enhance diagnostic specificity, DSM-5 replaces the previous NOS designation with two
options for clinical use: other specified disorder and unspecified disorder. The other specified
disorder category is provided to allow the clinician to communicate the specific reason
that the presentation does not meet the criteria for any specific category within a diagnos-
tic class. This is done by recording the name of the category, followed by the specific rea-
son. For example, for an individual with clinically significant depressive symptoms
lasting 4 weeks but whose symptomatology falls short of the diagnostic threshold for a
major depressive episode, the clinician would record “other specified depressive disorder,
depressive episode with insufficient symptoms.” If the clinician chooses not to specify the
16 Introduction
reason that the criteria are not met for a specific disorder, then “unspecified depressive
disorder” would be diagnosed. Note that the differentiation between other specified and
unspecified disorders is based on the clinician’s decision, providing maximum flexibility
for diagnosis. Clinicians do not have to differentiate between other specified and unspec-
ified disorders based on some feature of the presentation itself. When the clinician deter-
mines that there is evidence to specify the nature of the clinical presentation, the other
specified diagnosis can be given. When the clinician is not able to further specify and de-
scribe the clinical presentation, the unspecified diagnosis can be given. This is left entirely
up to clinical judgment.
For a more detailed discussion of how to use other specified and unspecified designa-
tions, see “Use of the Manual” in Section I.
The Multiaxial System
Despite widespread use and its adoption by certain insurance and governmental agencies,
the multiaxial system in DSM-IV was not required to make a mental disorder diagnosis. A
nonaxial assessment system was also included that simply listed the appropriate Axis I, IL,
and III disorders and conditions without axial designations. DSM-5 has moved to a nonax-
ia] documentation of diagnosis (formerly Axes J, II, and III), with separate notations for
important psychosocial and contextual factors {formerly Axis IV) and disability (formerly
Axis V). This revision is consistent with the DSM-IV text that states, “The multiaxial dis-
tinction among Axis I, Axis II, and Axis III disorders does not imply that there are funda-
mental differences in their conceptualization, that mental disorders are unrelated to
physical or biological factors or processes, or that general medical conditions are unrelated
to behavioral or psychosocial factors or processes.” The approach of separately noting di-
agnosis from psychosocial and contextual factors is also consistent with established WHO
and ICD guidance to consider the individual’s functional status separately from his or her
diagnoses or symptom status. In DSM-5, Axis III has been combined with Axes IJ and II.
Clinicians should continue to list medical conditions that are important to the understand-
ing or management of an individual’s mental disorder(s).
DSM-IV Axis IV covered psychosocial and environmental problems that may affect the
diagnosis, treatment, and prognosis of mental disorders. Although this axis provided
helpful information, even if it was not used as frequently as intended, the DSM-5 Task
Force recommended that DSM-5 should not develop its own classification of psychosocial
and environmental problems, but rather use a selected set of the ICD-9-CM V codes and
the new Z codes contained in ICD-10-CM. The ICD-10 Z codes were examined to deter-
mine which are most relevant to mental disorders and also to identify gaps.
DSM-IV Axis V consisted of the Global Assessment of Functioning (GAF) scale, repre-
senting the clinician's judgment of the individual’s overall level of “functioning on a hy-
pothetical continuum of mental health-illness.” It was recommended that the GAF be
dropped from DSM-5 for several reasons, including its conceptual lack of clarity (i.e., in-
cluding symptoms, suicide risk, and disabilities in its descriptors) and questionable psy-
chometrics in routine practice. In order to provide a global measure of disability, the WHO
Disability Assessment Schedule (WHODAS) is included, for further study, in Section III of
DSM-5 (see the chapter “Assessment Measures”). The WHODAS is based on the Interna-
tional Classification of Functioning, Disability and Health (ICF) for use across all of medicine
and health care. The WHODAS (version 2.0), and a modification developed for children/
adolescents and their parents by the Impairment and Disability Study Group were in-
cluded in the DSM-S field trial.
Introduction 17
Online Enhancements
It was challenging to determine what to include in the print version of DSM-5 to be most
clinically relevant and useful and at the same time maintain a manageable size. For this
reason, the inclusion of clinical rating scales and measures in the print edition is limited to
those considered most relevant. Additional assessment measures used in the field trials
are available online (www.psychiatry.org/dsm5), linked to the relevant disorders. The
Cultural Formulation Interview, Cultural Formulation Interview—Informant Version, and
supplementary modules to the core Cultural Formulation Interview are also available on-
line at www.psychiatry.org/dsm5.
DSM- 5 is available as an online subscription at PsychiatryOnline.org as well as an e-
book. The online component contains modules and assessment tools to enhance the diag-
nostic criteria and text. Also available online is a complete set of supportive references as
well as additional helpful information. The organizational structure of DSM-5, its use of
dimensional measures, and compatibility with ICD codes will allow it to be readily adapt-
able to future scientific discoveries and refinements in its clinical utility. DSM-5 will be an-
alyzed over time to continually assess its validity and enhance its value to clinicians.
Use of the Manual
The introduction contains much of the history and developmental process of the
DSM 5 revision. This section is designed to provide a practical guide to using DSM-5, par-
ticularly in clinical practice. The primary purpose of DSM-5 is to assist trained clinicians
in the diagnosis of their patients’ mental disorders as part of a case formulation assess-
ment that leads to a fully informed treatment plan for each individual. The symptoms con-
tained in the respective diagnostic criteria sets do not constitute comprehensive
definitions of underlying disorders, which encompass cognitive, emotional, behavioral,
and physiological processes that are far more complex than can be described in these brief
summaries. Rather, they are intended to summarize characteristic syndromes of signs and
symptoms that point to an underlying disorder with a characteristic developmental his-
tory, biological and environmental risk factors, neuropsychological and physiological cor-
relates, and typical clinical course.
Approach to Clinical Case Formulation
The case formulation for any given patient must involve a careful clinical history and con-
cise summary of the social, psychological, and biological factors that may have contrib-
uted to developing a given mental disorder. Hence, it is not sufficient to simply check off
the symptoms in the diagnostic criteria to make a mental disorder diagnosis. Although a
systematic check for the presence of these criteria as they apply to each patient will assure
a more reliable assessment, the relative severity and valence of individual criteria and
their contribution to a diagnosis require clinical judgment. The symptoms in our diagnos-
tic criteria are part of the relatively limited repertoire of human emotional responses to in-
ternal and external stresses that are generally maintained in a homeostatic balance without
a disruption in normal functioning. It requires clinica] training to recognize when the com-
bination of predisposing, precipitating, perpetuating, and protective factors has resulted
in a psychopathological condition in which physical signs and symptoms exceed normal
ranges. The ultimate goal of a clinical case formulation is to use the available contextual
and diagnostic information in developing a comprehensive treatment plan that is in-
formed by the individual's cultural and social context. However, recommendations for the
selection and use of the most appropriate evidence-based treatment options for each dis-
order are beyond the scope of this manual.
Although decades of scientific effort have gone into developing the diagnostic criteria
sets for the disorders included in Section IL, it is well recognized that this set of categorical
diagnoses does not fully describe the full range of mental disorders that individuals ex-
perience and present to clinicians on a daily basis throughout the world. As noted previ-
ously in the introduction, the range of genetic/environmental interactions over the course
of human development affecting cognitive, emotional and behavioral function is virtually
limitless. As a result, it is impossible to capture the full range of psychopathology in the
categorical diagnostic categories that we are now using. Hence, it is also necessary to in-
clude “other specified/ unspecified” disorder options for presentations that do not fit
exactly into the diagnostic boundaries of disorders in each chapter. In an emergency de-
partment setting, it may be possible to identify only the most prominent symptom ex-
pressions associated with a particular chapter—for example, delusions, hallucinations,
19
20 Use of the Manual
mania, depression, anxiety, substance intoxication, or neurocognitive symptoms—so that
an “unspecified” disorder in that category is identified until a fuller differential diagnosis
is possible.
Definition of a Mental Disorder
Each disorder identified in Section II of the manual (excluding those in the chapters enti-
tled “Medication-Induced Movement Disorders and Other Adverse Effects of Medica-
tion” and “Other Conditions That May Be a Focus of Clinical Attention”) must meet the
definition of a mental disorder. Although no definition can capture all aspects of all dis-
orders in the range contained in DSM-5, the following elements are required:
A mental disorder is a syndrome characterized by clinically significant distur-
bance in an individual’s cognition, emotion regulation, or behavior that reflects
a dysfunction in the psychological, biological, or developmental processes un-
derlying mental functioning. Mental disorders are usually associated with signif-
icant distress or disability in social, occupational, or other important activities.
An expectable or culturally approved response to a common stressor or loss,
such as the death of a loved one, is not a mental disorder. Socially deviant be-
havior (e.g., political, religious, or sexual) and conflicts that are primarily be-
tween the individual and society are not mental disorders unless the deviance
or conflict results from a dysfunction in the individual, as described above.
The diagnosis of a mental disorder should have clinical utility: it should help clinicians
to determine prognosis, treatment plans, and potential treatment outcomes for their pa-
tients. However, the diagnosis of a mental disorder is not equivalent to a need for treat-
ment. Need for treatment is a complex clinical decision that takes into consideration
symptom severity, symptom salience (e.g., the presence of suicidal ideation), the patient's
distress (mental pain) associated with the symptom(s), disability related to the patient’s
symptoms, risks and benefits of available treatments, and other factors (e.g., psychiatric
symptoms complicating other illness). Clinicians may thus encounter individuals whose
symptoms do not meet full criteria for a mental disorder but who demonstrate a clear need
for treatment or care. The fact that some individuals do not show all symptoms indicative
of a diagnosis should not be used to justify limiting their access to appropriate care.
Approaches to validating diagnostic criteria for discrete categorical mental disorders
have included the following types of evidence: antecedent validators (similar genetic mark-
ers, family traits, temperament, and environmental exposure), concurrent validators (simi-
lar neural substrates, biomarkers, emotional and cognitive processing, and symptom
similarity), and predictive validators (similar clinical course and treatment response). In
DSM-5, we recognize that the current diagnostic criteria for any single disorder will not nec-
essarily identify a homogeneous group of patients who can be characterized reliably with all
of these validators. Available evidence shows that these validators cross existing diagnostic
boundaries but tend to congregate more frequently within and across adjacent DSM-5 chap-
ter groups. Until incontrovertible etiological or pathophysiological mechanisms are identi-
fied to fully validate specific disorders or disorder spectra, the most important standard for
the DSM-5 disorder criteria will be their clinical utility for the assessment of clinical course
and treatment response of individuals grouped by a given set of diagnostic criteria.
This definition of mental disorder was developed for clinical, public health, and re-
search purposes. Additional information is usually required beyond that contained in the
DSM-5 diagnostic criteria in order to make legal judgments on such issues as criminal re-
sponsibility, eligibility for disability compensation, and competency (see “Cautionary
Statement for Forensic Use of DSM-5” elsewhere in this manual).
Use of the Manual 21
Criterion for Ciinical Significance
There have beeh substantial efforts by the DSM-5 Task Force and the World Health Orga-
nization (WHO) to separate the concepts of mental disorder and disability (impairment in
social, occupational, or other important areas of functioning). In the WHO system, the In-
ternational Classification of Diseases (ICD) covers all diseases and disorders, while the In-
ternational Classification of Functioning, Disability and Health (ICF) provides a separate
classification of global disability. The WHO Disability Assessment Schedule (WHODAS)
is based on the ICF and has proven useful as a standardized measure of disability for men-
tal disorders. However, in the absence of clear biological markers or clinically useful mea-
surements of severity for many mental disorders, it has not been possible to completely
separate normal and pathological symptom expressions contained in diagnostic criteria.
This gap in information is particularly problematic in clinical situations in which the pa-
tient’s symptom presentation by itself (particularly in mild forms) is not inherently path-
ological and may be encountered in individuals for whom a diagnosis of “mental
disorder” would be inappropriate. Therefore, a generic diagnostic criterion requiring dis-
tress or disability has been used to establish disorder thresholds, usually worded “the dis-
turbance causes clinically significant distress or impairment in social, occupational, or
other important areas of functioning.” The text following the revised definition of a mental
disorder acknowledges that this criterion may be especially helpful in determining a pa-
tient’s need for treatment. Use of information from family members and other third parties
(in addition to the individual) regarding the individual's performance is recommended
when necessary.
Elements of a Diagnosis
Diagnostic Criteria and Descriptors
Diagnostic criteria are offered as guidelines for making diagnoses, and their use should be
informed by clinical judgment. Text descriptions, including introductory sections of each
diagnostic chapter, can help support diagnosis (e.g., providing differential diagnoses; de-
scribing the criteria more fully under “Diagnostic Features”).
Following the assessment of diagnostic criteria, clinicians should consider the applica-
tion of disorder subtypes and/or specifiers as appropriate. Severity and course specifiers
should be applied to denote the individual’s current presentation, but only when the full
criteria are met. When full criteria are not met, clinicians should consider whether the
symptom presentation meets criteria for an “other specified” or “unspecified” designa-
tion. Where applicable, specific criteria for defining disorder severity (e.g., mild, moder-
ate, severe, extreme), descriptive features (e.g., with good to fair insight; in a controlled
environment), and course (e.g., in partial remission, in full remission, recurrent) are pro-
vided with each diagnosis. On the basis of the clinical interview, text descriptions, criteria,
and clinician judgment, a final diagnosis is made.
The general convention in DSM-5 is to allow multiple diagnoses to be assigned for
those presentations that meet criteria for more than one DSM-5 disorder.
Subtypes and Specifiers
Subtypes and specifiers (some of which are coded in the fourth, fifth, or sixth digit) are
provided for increased specificity. Subtypes define mutually exclusive and jointly exhaus-
tive phenomenological subgroupings within a diagnosis and are indicated by the instruc-
tion “Specify whether” in the criteria set. In contrast, specifiers are not intended to be
mutually exclusive or jointly exhaustive, and as a consequence, more than one specifier
may be given. Specifiers are indicated by the instruction “Specify” or “Specify if” in the cri-
teria set. Specifiers provide an opportunity to define a more homogeneous subgrouping of
22 Use of the Manual
individuals with the disorder who share certain features (e.g., major depressive disorder,
with mixed features) and to convey information that is relevant to the management of the
individual’s disorder, such as the “with other medical comorbidity” specifier in sleep-
wake disorders. Although a fifth digit is sometimes assigned to code a subtype or specifier
(e.g., 294.11 [F02.81] major neurocognitive disorder due to Alzheimer’s disease, with be-
havioral disturbance) or severity (296.21 [F32.0] major depressive disorder, single episode,
mild), the majority of subtypes and specifiers included in DSM-5 cannot be coded within
the ICD-9-CM and ICD-10-CM systems and are indicated only by including the subtype or
specifier after the name of the disorder (e.g., social anxiety disorder [social phobia], per-
formance type). Note that in some cases, a specifier or subtype is codable in ICD-10-CM
but not in ICD-9-CM. Accordingly, in some cases the 4th or 5th character codes for the sub-
types or specifiers are provided only for the ICD-10-CM coding designations.
A DSM -5 diagnosis is usually applied to the individual's current presentation; previ-
ous diagnoses from which the individual has recovered should be clearly noted as such.
Specifiers indicating course (e.g., in partial remission, in full remission) may be listed after
the diagnosis and are indicated in a number of criteria sets. Where available, severity spec-
ifiers are provided to guide clinicians in rating the intensity, frequency, duration, symptom
count, or other severity indicator of a disorder. Severity specifiers are indicated by the in-
struction “Specify current severity” in the criteria set and include disorder-specific defini-
tions. Descriptive features specifiers have also been provided in the criteria set and convey
additional information that can inform treatment planning (e.g., obsessive-compulsive
disorder, with poor insight). Not all disorders include course, severity, and/or descriptive
features specifiers.
Medication-Induced Movement Disorders and Other
Conditions That May Be a Focus of Ciinicai Attention
In addition to important psychosocial and environmental factors (see “The Multiaxial Sys-
tem” in the “Introduction” elsewhere in this manual), these chapters in Section II also con-
tain other conditions that are not mental disorders but may be encountered by mental
health clinicians. These conditions may be listed as a reason for clinical visit in addition to,
or in place of, the mental disorders listed in Section II. A separate chapter is devoted to
medication-induced disorders and other adverse effects of medication that may be as-
sessed and treated by clinicians in mental health practice such as akathisia, tardive dyski-
nesia, and dystonia. The description of neuroleptic malignant syndrome is expanded from
that provided in DSM-IV-TR to highlight the emergent and potentially life-threatening na-
ture of this condition, and a new entry on antidepressant discontinuation syndrome is pro-
vided. An additional chapter discusses other conditions that may be a focus of clinical
attention. These include relational problems, problems related to abuse and neglect, prob-
lems with adherence to treatment regimens, obesity, antisocial behavior, and malingering.
Principal Diagnosis
When more than one diagnosis for an individual is given in an inpatient setting, the prin-
cipal diagnosis is the condition established after study to be chiefly responsible for occa-
sioning the admission of the individual. When more than one diagnosis is given for an
individual in an outpatient setting, the reason for visit is the condition that is chiefly re-
sponsible for the ambulatory care medical services received during the visit. In most cases,
the principal diagnosis or the reason for visit is also the main focus of attention or treat-
ment. It is often difficult (and somewhat arbitrary) to determine which diagnosis is the
principal diagnosis or the reason for visit, especially when, for example, a substance-
related diagnosis such as alcohol use disorder is accompanied by a non-substance-related
diagnosis such as schizophrenia. For example, it may be unclear which diagnosis should
Use of the Manual 23
be considered “principal” for an individual hospitalized with both schizophrenia and al-
cohol use disorder, because each condition may have contributed equally to the need for
admission and treatment. The principal diagnosis is indicated by listing it first, and the re-
maining disorders are listed in order of focus of attention and treatment. When the prin-
cipal diagnosis or reason for visit is a mental disorder due to another medical condition
(e.g., major neurocognitive disorder due to Alzheimer’s disease, psychotic disorder due to
malignant lung neoplasm), ICD coding rules require that the etiological medical condition
be listed first. In that case, the principal diagnosis or reason for visit would be the mental
disorder due to the medical condition, the second listed diagnosis. In most cases, the dis-
order listed as the principal diagnosis or the reason for visit is followed by the qualifying
phrase “(principal diagnosis)” or “(reason for visit).”
Provisional Diagnosis
The specifier “provisional” can be used when there is a strong presumption that the full
criteria will ultimately be met for a disorder but not enough information is available to
make a firm diagnosis. The clinician can indicate the diagnostic uncertainty by recording
“(provisional)” following the diagnosis. For example, this diagnosis might be used when
an individual who appears to have a major depressive disorder is unable to give an ade-
quate history, and thus it cannot be established that the full criteria are met. Another use of
the term provisional is for those situations in which differential diagnosis depends exclu-
sively on the duration of illness. For example, a diagnosis of schizophreniform disorder re-
quires a duration of less than 6 months but of at least 1 month and can only be given
provisionally if assigned before remission has occurred.
Coding and Reporting Procedures
Each disorder is accompanied by an identifying diagnostic and statistical code, which is
typically used by institutions and agencies for data collection and billing purposes. There
are specific recording protocols for these diagnostic codes (identified as coding notes in
the text) that were established by WHO, the U.S. Centers for Medicare and Medicaid Ser-
vices (CMS), and the Centers for Disease Control and Prevention’s National Center for
Health Statistics to ensure consistent international recording of prevalence and mortality
rates for identified health conditions. For most clinicians, the codes are used to identify the
diagnosis or reason for visit for CMS and private insurance service claims. The official
coding system in use in the United States as of publication of this manual is ICD-9-CM. Of-
ficial adoption of ICD-10-CM is scheduled to take place on October 1, 2014, and these
codes, which are shown parenthetically in this manual, should not be used until the offi-
cial implementation occurs. Both ICD-9-CM and ICD-10-CM codes have been listed 1) pre-
ceding the name of the disorder in the classification and 2) accompanying the criteria set
for each disorder. For some diagnoses (e.g., neurocognitive and substance /medication-
induced disorders), the appropriate code depends on further specification and is listed
within the criteria set for the disorder, as coding notes, and, in some cases, further clarified
in a section on recording procedures. The names of some disorders are followed by alter-
native terms enclosed in parentheses, which, in most cases, were the DSM-IV names for
the disorders.
Looking to the Future:
Assessment and Monitoring Tools
The various components of DSM-5 are provided to facilitate patient assessment and to aid
in developing a comprehensive case formulation. Whereas the diagnostic criteria in Sec-
tion II are well-established measures that have undergone extensive review, the assess-
24 Use of the Manual
ment tools, a cultural formulation interview, and conditions for further study included in
Section III are those for which we determined that the scientific evidence is not yet avail-
able to support widespread clinical use. These diagnostic aids and criteria are included to
highlight the evolution and direction of scientific advances in these areas and to stimulate
further research.
Each of the measures in Section III is provided to aid in a comprehensive assessment of
individuals that will contribute to a diagnosis and treatment plan tailored to the individ-
ual presentation and clinical context. Where cultural dynamics are particularly important
for diagnostic assessment, the cultural formulation interview should be considered as a
useful aid to communication with the individual. Cross-cutting symptom and diagnosis-
specific severity measures provide quantitative ratings of important clinical areas that are
designed to be used at the initial evaluation to establish a baseline for comparison with rat-
ings on subsequent encounters to monitor changes and inform treatment planning.
The use of such measures will undoubtedly be facilitated by digital applications, and
the measures are included in Section II] to provide for further evaluation and develop-
ment. As with each DSM edition, the diagnostic criteria and the DSM-5 classification of
mental disorders reflect the current consensus on the evolving knowledge in our field.
‘Cautionary Statement for
Forensic Use of DSM-5
Although the DSM-5 diagnostic criteria and text are primarily designed to assist
clinicians in conducting clinical assessment, case formulation, and treatment planning,
DSM- 5 is also used as a reference for the courts and attorneys in assessing the forensic con-
sequences of mental disorders. As a result, it is important to note that the definition of
mental disorder included in DSM-5 was developed to meet the needs of clinicians, public
health professionals, and research investigators rather than all of the technical needs of the
courts and legal professionals. It is also important to note that DSM-5 does not provide
treatment guidelines for any given disorder.
When used appropriately, diagnoses and diagnostic information can assist legal deci-
sion makers in their determinations. For example, when the presence of a mental disorder
is the predicate for a subsequent legal determination (e.g., involuntary civil commitment),
the use of an established system of diagnosis enhances the value and reliability of the de-
termination. By providing a compendium based on a review of the pertinent clinical and
research literature, DSM-5 may facilitate legal decision makers’ understanding of the rel-
evant characteristics of mental disorders. The literature related to diagnoses also serves as
a check on ungrounded speculation about mental] disorders and about the functioning of a
particular individual. Finally, diagnostic information about longitudinal course may im-
prove decision making when the legal issue concerns an individual’s mental functioning
at a past or future point in time.
However, the use of DSM-5 should be informed by an awareness of the risks and lim-
itations of its use in forensic settings. When DSM-5 categories, criteria, and textual descrip-
tions are employed for forensic purposes, there is a risk that diagnostic information will be
misused or misunderstood. These dangers arise because of the imperfect fit between the
questions of ultimate concern to the law and the information contained in a clinical diagno-
sis. In most situations, the clinical diagnosis of a DSM-5 mental disorder such as intellec-
tual disability (intellectual developmental disorder), schizophrenia, major neurocognitive
disorder, gambling disorder, or pedophilic disorder does not imply that an individual
with such a condition meets legal criteria for the presence of a mental disorder or a speci-
fied legal standard (e.g., for competence, criminal responsibility, or disability). For the latter,
additional information is usually required beyond that contained in the DSM-5 diagnosis,
which might include information about the individual’s functional impairments and how
these impairments affect the particular abilities in question. It is precisely because impair-
ments, abilities, and disabilities vary widely within each diagnostic category that assign-
ment of a particular diagnosis does not imply a specific level of impairment or disability.
Use of DSM-S5 to assess for the presence of a mental disorder by nonclinical, nonmed-
ical, or otherwise insufficiently trained individuals is not advised. Nonclinical decision
makers should also be cautioned that a diagnosis does not carry any necessary implica-
tions regarding the etiology or causes of the individual’s mental disorder or the individ-
ual’s degree of control over behaviors that may be associated with the disorder. Even
when diminished control over one’s behavior is a feature of the disorder, having the diag-
nosis in itself does not demonstrate that a particular individual is (or was) unable to con-
trol his or her behavior at a particular time.
25
Neurodevelopmental Disorders ..........0 cece eee ec eee eee eeee 31
Schizophrenia Spectrum and Other Psychotic Disorders ............ 87
Bipolar and Related Disorders. ....... 0.0.00 cece eee cere eeeaee 123
Depressive Disorders ............ 0.0 cee eee eee eee 155
Anxisty DiSONMIerS «2202. Swot eed Sees DER S bet eens ehaiee 189
Obsessive-Compulsive and Related Disorders. .............0-0.55 235
Trauma- and Stressor-Related Disorders ......... 00.00 ee eeeeenes 265
Dissociative Disorders ........-- ccc cee eee ee eee renee eerees 291
Somatic Symptom and Related Disorders ...........0.0020eee eee 309
Feeding and Eating Disorders ............ cece eee e erent eens 329
Elimination DiSOrd6rs:..oci hee eb iC ES eS ee oa eee sees sae bee 355
Sleep-Wake Disorders ........---. 0-2 cece cee eee eee e et eene 361
Sexual Dysfunctions. «ccc ecw Weed dee eae eee ewe eat 423
Gender Dysphoria. soca i cccc nce pat eeciueeeeer ens aanneeee eae 451
Disruptive, lmpulse-Control, and Conduct Disorders............... 461
Substance-Related and Addictive Disorders ..........0.2-seen eee 481
Neurocognitive Disorders... .. 0... 0.000 cee eee eee 591
Personality Disorders ......... ccc eee cece eee nee eee eeeee 645
Paraphili¢: Disorders soc ocd daa ees chen et isdaceewieiwi cee 685
Other Mental. Disorders «x 23.4.5 svie oie ete cee ied Daee a tees 707
Medication-Induced Movement Disorders and
Other Adverse Effects of Medication........-.... 0000+ eeeeeees 709
Other Conditions That May Be a Focus of Clinical Attention......... 715
| hiS SECTION contains the diagnostic criteria approved for routine clinical
use along with the ICD-9-CM codes {ICD-10 codes are shown parenthetically).
For each mental disorder, the diagnostic criteria are followed by descriptive
text to assist in diagnostic decision making. Where needed, specific recording
procedures are presented with the diagnostic criteria to provide guidance in
selecting the most appropriate code. In some cases, separate recording pro-
cedures for ICD-9-CM and ICD-10-CM are provided. Although not considered
as official DSM-5 disorders, medication-induced movement disorders and other
adverse effects of medication, as well as other conditions that may be a focus
of clinical attention (including additional ICD-9-CM V codes and forthcoming
ICD-10-CM Z codes), are provided to indicate other reasons for a clinical visit
such as environmental factors and relational problems. These codes are adapted
from ICD-9-CM and ICD-10-CM and were neither reviewed nor approved as
official DSM-5 diagnoses, but can provide additional context for a clinical for-
mulation and treatment plan. These three components—the criteria and their
descriptive text, the medication-induced movement disorders and other ad-
verse effects of medication, and the descriptions of other conditions that may
be a focus of clinical attention—represent the key elements of the clinical di-
agnostic process and thus are presented together.
eurodevelopmenta
Disorders
The neu rodevelopmental disorders are a group of conditions with onset in the
developmental period. The disorders typically manifest early in development, often be-
fore the child enters grade school, and are characterized by developmental deficits that
produce impairments of personal, social, academic, or occupational functioning. The
range of developmental deficits varies from very specific limitations of learning or control
of executive functions to global impairments of social skills or intelligence. The neurode-
velopmental disorders frequently co-occur; for example, individuals with autism spec-
trum disorder often have intellectual disability (intellectual developmental disorder), and
many children with attention-deficit/hyperactivity disorder (ADHD) also have a specific
learning disorder. For some disorders, the clinical presentation includes symptoms of ex-
cess as well as deficits and delays in achieving expected milestones. For example, autism
spectrum disorder is diagnosed only when the characteristic deficits of social communi-
cation are accompanied by excessively repetitive behaviors, restricted interests, and insis-
tence on sameness.
Intellectual disability (intellectual developmental disorder) is characterized by deficits
in general mental abilities, such as reasoning, problem solving, planning, abstract thinking,
judgment, academic learning, and learning from experience. The deficits result in impair-
ments of adaptive functioning, such that the individual fails to meet standards of personal
independence and social responsibility in one or more aspects of daily life, including com-
munication, social participation, academic or occupational functioning, and personal inde-
pendence at home or in community settings. Global developmental delay, as its name
implies, is diagnosed when an individual fails to meet expected developmental milestones
in several areas of intellectual functioning. The diagnosis is used for individuals who are
unable to undergo systematic assessments of intellectual functioning, including children
who are too young to participate in standardized testing. Intellectual disability may result
from an acquired insult during the developmental period from, for example, a severe head
injury, in which case a neurocognitive disorder also may be diagnosed.
The communication disorders include language disorder, speech sound disorder, so-
cial (pragmatic) communication disorder, and childhood-onset fluency disorder (stutter-
ing). The first three disorders are characterized by deficits in the development and use of
language, speech, and social communication, respectively. Childhood-onset fluency dis-
order is characterized by disturbances of the normal fluency and motor production of
speech, including repetitive sounds or syllables, prolongation of consonants or vowel
sounds, broken words, blocking, or words produced with an excess of physical tension.
Like other neurodevelopmental disorders, communication disorders begin early in life
and may produce lifelong functional impairments.
Autism spectrum disorder is characterized by persistent deficits in social communica-
tion and social interaction across multiple contexts, including deficits in social reciprocity,
nonverbal communicative behaviors used for social interaction, and skills in developing,
maintaining, and understanding relationships. In addition to the social communication
deficits, the diagnosis of autism spectrum disorder requires the presence of restricted, re-
petitive patterns of behavior, interests, or activities. Because symptoms change with de-
velopment and may be masked by compensatory mechanisms, the diagnostic criteria may
31
32 Neurodevelopmental Disorders
be met based on historical information, although the current presentation must cause sig-
nificant impairment.
Within the diagnosis of autism spectrum disorder, individual clinical characteristics
are noted through the use of specifiers (with or without accompanying intellectual impair-
ment; with or without accompanying structural language impairment; associated with a
known medical/genetic or environmental/acquired condition; associated with another
neurodevelopmental, mental, or behavioral disorder), as well as specifiers that describe
the autistic symptoms (age at first concern; with or without loss of established skills; sever-
ity). These specifiers provide clinicians with an opportunity to individualize the diagnosis
and communicate a richer clinical description of the affected individuals. For example, many
individuals previously diagnosed with Asperger’s disorder would now receive a diagnosis
of autism spectrum disorder without language or intellectual impairment.
ADHD is a neurodevelopmental disorder defined by impairing levels of inattention, dis-
organization, and/or hyperactivity-impulsivity. Inattention and disorganization entail inabil-
ity to stay on task, seeming not to listen, and losing materials, at levels that are inconsistent
with age or developmental level. Hyperactivity-impulsivity entails overactivity, fidgeting, in-
ability to stay seated, intruding into other people’s activities, and inability to wait—symptoms
that are excessive for age or developmental level. In childhood, ADHD frequently overlaps
with disorders that are often considered to be “externalizing disorders,” such as oppositional
defiant disorder and conduct disorder. ADHD often persists into adulthood, with resultant
impairments of social, academic and occupational functioning.
The neurodevelopmental motor disorders include developmental coordination disor-
der, stereotypic movement disorder, and tic disorders. Developmental coordination dis-
order is characterized by deficits in the acquisition and execution of coordinated motor
skills and is manifested by clumsiness and slowness or inaccuracy of performance of mo-
tor skills that cause interference with activities of daily living. Stereotypic movement dis-
order is diagnosed when an individual has repetitive, seemingly driven, and apparently
purposeless motor behaviors, such as hand flapping, body rocking, head banging, self-
biting, or hitting. The movements interfere with social, academic, or other activities. If the
behaviors cause self-injury, this should be specified as part of the diagnostic description.
Tic disorders are characterized by the presence of motor or vocal tics, which are sudden,
rapid, recurrent, nonrhythmic, sterotyped motor movements or vocalizations. The dura-
tion, presumed etiology, and clinical presentation define the specific tic disorder that is di-
agnosed: Tourette’s disorder, persistent (chronic) motor or vocal tic disorder, provisional
tic disorder, other specified tic disorder, and unspecified tic disorder. Tourette’s disorder
is diagnosed when the individual has multiple motor and vocal tics that have been present
for at least 1 year and that have a waxing-waning symptom course.
Specific learning disorder, as the name implies, is diagnosed when there are specific defi-
cits in an individual’s ability to perceive or process information efficiently and accurately. This
neurodevelopmental disorder first manifests during the years of formal schooling and is
characterized by persistent and impairing difficulties with learning foundational academic
skills in reading, writing, and/or math. The individual’s performance of the affected academic
skills is well below average for age, or acceptable performance levels are achieved only with
extraordinary effort. Specific learning disorder may occur in individuals identified as intellec-
tually gifted and manifest only when the learning demands or assessment procedures (e.g.,
timed tests) pose barriers that cannot be overcome by their innate intelligence and compensa-
tory strategies. For all individuals, specific learning disorder can produce lifelong impairments
in activities dependent on the skills, including occupational performance.
The use of specifiers for the neurodevelopmental disorder diagnoses enriches the clin-
ical description of the individual's clinical course and current symptomatology. In addi-
tion to specifiers that describe the clinical presentation, such as age at onset or severity
ratings, the neurodevelopmental disorders may include the specifier “associated with a
known medical or genetic condition or environmental factor.” This specifier gives clini-
Intellectual Disability (Intellectual Developmental Disorder) 33
cians an opportunity to document factors that may have played a role in the etiology of the
disorder, as well as those that might affect the clinical course. Examples include genetic
disorders, such as fragile X syndrome, tuberous sclerosis, and Rett syndrome; medical con-
ditions such as epilepsy; and environmental factors, including very low birth weight and
fetal alcohol exposure (even in the absence of stigmata of fetal alcohol syndrome).
Intellectual Disabilities
Intellectual Disability
(Intellectual Developmental Disorder)
Diagnostic Criteria
Intellectual disability (intellectual developmental disorder) is a disorder with onset during
the developmental period that includes both intellectual and adaptive functioning deficits
in conceptual, social, and practical domains. The following three criteria must be met:
A. Deficits in intellectual functions, such as reasoning, problem solving, planning, abstract
thinking, judgment, academic learning, and learning from experience, confirmed by
both clinical assessment and individualized, standardized intelligence testing.
B. Deficits in adaptive functioning that result in failure to meet developmental and socio-
cultural standards for personal independence and social responsibility. Without ongo-
ing support, the adaptive deficits limit functioning in one or more activities of daily life,
such as communication, social participation, and independent living, across multiple
environments, such as home, school, work, and community.
C. Onset of intellectual and adaptive deficits during the developmental period.
Note: The diagnostic term intellectual disability is the equivalent term for the ICD-11 diag-
nosis of intellectual developmental disorders. Although the term intellectua/ disability is
used throughout this manual, both terms are used in the title to clarify relationships with
other classification systems. Moreover, a federal statute in the United States (Public Law
111-256, Rosa’s Law) replaces the term mental retardation with intellectual disability, and
research journals use the term intefllectua/ disability. Thus, intellectual disability is the
term in common use by medical, educational, and other professions and by the lay public
and advocacy groups.
Coding note: The ICD-9-CM code for intellectual disability (intellectual developmental
disorder) is 319, which is assigned regardless of the severity specifier. The ICD-10-CM code
depends on the severity specifier (see below).
Specify current severity (see Table 1):
(F70) Mild
(F71) Moderate
(F72) Severe
(F73) Profound
Specifiers
The various levels of severity are defined on the basis of adaptive functioning, and not IQ
scores, because it is adaptive functioning that determines the level of supports required.
Moreover, IQ measures are less valid in the lower end of the IQ range.
Neurodevelopmental Disorders
34
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35
Intellectual Disability (Intellectual Developmental Disorder)
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Neurodevelopmental Disorders
36
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Intellectual Disability (Intellectual Developmental Disorder) 37
Diagnostic Features
The essential features of intellectual disability (intellectual developmental disorder) are
deficits in general mental abilities (Criterion A) and impairment in everyday adaptive
functioning, in comparison to an individual's age-, gender-, and socioculturally matched
peers (Criterion B). Onset is during the developmental period (Criterion C). The diagnosis
of intellectual disability is based on both clinical assessment and standardized testing of
intellectual and adaptive functions.
Criterion A refers to intellectual functions that involve reasoning, problem solving,
planning, abstract thinking, judgment, learning from instruction and experience, and
practical understanding. Critical components include verbal comprehension, working
memory, perceptual reasoning, quantitative reasoning, abstract thought, and cognitive ef-
ficacy. Intellectual functioning is typically measured with individually administered and
psychometrically valid, comprehensive, culturally appropriate, psychometrically sound
tests of intelligence. Individuals with intellectual disability have scores of approximately
two standard deviations or more below the population mean, including a margin for mea-
surement error (generally +5 points). On tests with a standard deviation of 15 and a mean
of 100, this involves a score of 65-75 (70 + 5). Clinical training and judgment are required
to interpret test results and assess intellectual performance.
Factors that may affect test scores include practice effects and the “Flynn effect’ (ie.,
overly high scores due to out-of-date test norms). Invalid scores may result from the use of
brief intelligence screening tests or group tests; highly discrepant individual subtest scores
may make an overall IQ score invalid. Instruments must be normed for the individual's so-
ciocultural background and native language. Co-occurring disorders that affect communi-
cation, language, and/or motor or sensory function may affect test scores. Individual
cognitive profiles based on neuropsychological testing are more useful for understanding
intellectual abilities than a single IQ score. Such testing may identify areas of relative
strengths and weaknesses, an assessment important for academic and vocational planning.
IQ test scores are approximations of conceptual functioning but may be insufficient to
assess reasoning in real-life situations and mastery of practical tasks. For example, a per-
son with an IQ score above 70 may have such severe adaptive behavior problems in social
judgment, social understanding, and other areas of adaptive functioning that the person’s
actual functioning is comparable to that of individuals with a lower IQ score. Thus, clinical
judgment is needed in interpreting the results of IQ tests.
Deficits in adaptive functioning (Criterion B) refer to how well a person meets community
standards of personal independence and social responsibility, in comparison to others of sim-
ilar age and sociocultural background. Adaptive functioning involves adaptive reasoning in
three domains: conceptual, social, and practical. The conceptual (academic) domain involves
competence in memory, language, reading, writing, math reasoning, acquisition of practical
knowledge, problem solving, and judgment in novel situations, among others. The social do-
main involves awareness of others’ thoughts, feelings, and experiences; empathy; interper-
sonal communication skills; friendship abilities; and social judgment, among others. The
practical domain involves learning and self-management across life settings, including personal
care, job responsibilities, money management, recreation, self-management of behavior, and
school and work task organization, among others. Intellectual capacity, education, motivation,
socialization, personality features, vocational opportunity, cultural experience, and coexisting
general medical conditions or mental disorders influence adaptive functioning.
Adaptive functioning is assessed using both clinical evaluation and individualized,
culturally appropriate, psychometrically sound measures. Standardized measures are
used with knowledgeable informants (e.g., parent or other family member; teacher; coun-
selor; care provider) and the individual to the extent possible. Additional sources of infor-
mation include educational, developmental, medical, and mental health evaluations.
Scores from standardized measures and interview sources must be interpreted using clin-
ical judgment. When standardized testing is difficult or impossible, because of a variety of
38 Neurodevelopmental Disorders
factors (e.g., sensory impairment, severe problem behavior), the individual may be diag-
nosed with unspecified intellectual disability. Adaptive functioning may be difficult to
assess in a controlled setting (e.g., prisons, detention centers); if possible, corroborative in-
formation reflecting functioning outside those settings should be obtained.
Criterion B is met when at least one domain of adaptive functioning—conceptual, so-
cial, or practical—is sufficiently impaired that ongoing support is needed in order for the
person to perform adequately in one or more life settings at school, at work, at home, or in
the community. To meet diagnostic criteria for intellectual disability, the deficits in adap-
tive functioning must be directly related to the intellectual impairments described in Cri-
terion A. Criterion C, onset during the developmental period, refers to recognition that
intellectual and adaptive deficits are present during childhood or adolescence.
Associated Features Supporting Diagnosis
Intellectual disability is a heterogeneous condition with multiple causes. There may be
associated difficulties with social judgment; assessment of risk; self-management of behav-
ior, emotions, or interpersonal relationships; or motivation in school or work environments.
Lack of communication skills may predispose to disruptive and aggressive behaviors. Gull-
ibility is often a feature, involving naiveté in social situations and a tendency for being easily
led by others. Gullibility and lack of awareness of risk may result in exploitation by others
and possible victimization, fraud, unintentional criminal involvement, false confessions,
and risk for physical and sexual abuse. These associated features can be important in crim-
inal cases, including Atkins-type hearings involving the death penalty.
Individuals with a diagnosis of intellectual disability with co-occurring mental disor-
ders are at risk for suicide. They think about suicide, make suicide attempts, and may die
from them. Thus, screening for suicidal thoughts is essential in the assessment process. Be-
cause of a lack of awareness of risk and danger, accidental injury rates may be increased.
Prevalence
Intellectual disability has an overall general population prevalence of approximately 1%,
and prevalence rates vary by age. Prevalence for severe intellectual disability is approxi-
mately 6 per 1,000.
Development and Course
Onset of intellectual disability is in the developmental period. The age and characteristic
features at onset depend on the etiology and severity of brain dysfunction. Delayed motor,
language, and social milestones may be identifiable within the first 2 years of life among
those with more severe intellectual disability, while mild levels may not be identifiable un-
til school age when difficulty with academic learning becomes apparent. All criteria (in-
cluding Criterion C) must be fulfilled by history or current presentation. Some children
under age 5 years whose presentation will eventually meet criteria for intellectual disabil-
ity have deficits that meet criteria for global developmental delay.
When intellectual disability is associated with a genetic syndrome, there may be a char-
acteristic physical appearance (as in, e.g., Down syndrome). Some syndromes have a
behavioral phenotype, which refers to specific behaviors that are characteristic of particular
genetic disorder (e.g., Lesch-Nyhan syndrome). In acquired forms, the onset may be
abrupt following an illness such as meningitis or encephalitis or head trauma occurring
during the developmental period. When intellectual disability results from a loss of pre-
viously acquired cognitive skills, as in severe traumatic brain injury, the diagnoses of in-
tellectual disability and of a neurocognitive disorder may both be assigned.
Although intellectual disability is generally nonprogressive, in certain genetic disor-
ders (e.g., Rett syndrome) there are periods of worsening, followed by stabilization, and in
Intellectual Disability (Intellectual Developmental Disorder) 39
others (e.g., San Phillippo syndrome) progressive worsening of intellectual function. After
early childhood, the disorder is generally lifelong, although severity levels may change
over time. The course may be influenced by underlying medical or genetic conditions and
co-occurring conditions (e.g., hearing or visual impairments, epilepsy). Early and ongoing in-
terventions may improve adaptive functioning throughout childhood and adulthood. In
some cases, these result in significant improvement of intellectual functioning, such that
the diagnosis of intellectual disability is no longer appropriate. Thus, it is common practice
when assessing infants and young children to delay diagnosis of intellectual disability un-
til after an appropriate course of intervention is provided. For older children and adults,
the extent of support provided may allow for full participation in all activities of daily liv-
ing and improved adaptive function. Diagnostic assessments must determine whether im-
proved adaptive skills are the result of a stable, generalized new skill acquisition (in which
case the diagnosis of intellectual disability may no longer be appropriate) or whether the
improvement is contingent on the presence of supports and ongoing interventions (in
which case the diagnosis of intellectual disability may still be appropriate).
Risk and Prognostic Factors
Genetic and physiological. Prenatal etiologies include genetic syndromes (e.g., se-
quence variations or copy number variants involving one or more genes; chromosomal
disorders), inborn errors of metabolism, brain malformations, maternal disease (including
placental disease), and environmental influences (e.g., alcohol, other drugs, toxins, terato-
gens). Perinatal causes include a variety of labor and delivery-related events leading to
neonatal encephalopathy. Postnatal causes include hypoxic ischemic injury, traumatic
brain injury, infections, demyelinating disorders, seizure disorders (e.g., infantile spasms),
severe and chronic social deprivation, and toxic metabolic syndromes and intoxications
(e.g., lead, mercury).
Culture-Reiated Diagnostic Issues
Intellectual disability occurs in ail races and cultures. Cultural sensitivity and knowledge
are needed during assessment, and the individual’s ethnic, cultural, and linguistic back-
ground, available experiences, and adaptive functioning within his or her community and
cultural setting must be taken into account.
Gender-Reiated Diagnostic Issues
Overall, males are more likely than females to be diagnosed with both mild (average
male:female ratio 1.6:1) and severe (average male-female ratio 1.2:1) forms of intellectual
disability. However, gender ratios vary widely in reported studies. Sex-linked genetic fac-
tors and male vulnerability to brain insult may account for some of the gender differences.
Diagnostic Markers
A comprehensive evaluation includes an assessment of intellectual capacity and adaptive
functioning; identification of genetic and nongenetic etiologies; evaluation for associated
medical conditions (e.g., cerebral palsy, seizure disorder); and evaluation for co-occurring
mental, emotional, and behavioral disorders. Components of the evaluation may include
basic pre- and perinatal medical history, three-generational family pedigree, physical exam-
ination, genetic evaluation (e.g., karyotype or chromosomal microarray analysis and testing
for specific genetic syndromes), and metabolic screening and neuroimaging assessment.
Differential Diagnosis
The diagnosis of intellectual disability should be made whenever Criteria A, B, and C are
met. A diagnosis of intellectual disability should not be assumed because of a particular
40 Neurodevelopmental Disorders
genetic or medical condition. A genetic syndrome linked to intellectual disability should
be noted as a concurrent diagnosis with the intellectual disability.
Major and mild neurocognitive disorders. Intellectual disability is categorized as a neu-
rodevelopmental disorder and is distinct from the neurocognitive disorders, which are
characterized by a loss of cognitive functioning. Major neurocognitive disorder may co-
occur with intellectual disability (e.g., an individual with Down syndrome who develops
Alzheimer’s disease, or an individual with intellectual disability who loses further cogni-
tive capacity following a head injury). In such cases, the diagnoses of intellectual disability
and neurocognitive disorder may both be given.
Communication disorders and specific learning disorder. These neurodevelopmental
disorders are specific to the communication and learning domains and do not show defi-
cits in intellectual and adaptive behavior. They may co-occur with intellectual disability.
Both diagnoses are made if full criteria are met for intellectual disability and a communi-
cation disorder or specific learning disorder.
Autism spectrum disorder. Intellectual disability is common among individuals with
autism spectrum disorder. Assessment of intellectual] ability may be complicated by so-
cial-communication and behavior deficits inherent to autism spectrum disorder, which
may interfere with understanding and complying with test procedures. Appropriate as-
sessment of intellectual functioning in autism spectrum disorder is essential, with reas-
sessment across the developmental period, because IQ scores in autism spectrum disorder
may be unstable, particularly in early childhood.
Comorbidity
Co-occurring mental, neurodevelopmental, medical, and physical conditions are frequent
in intellectual disability, with rates of some conditions (e.g., mental disorders, cerebral
palsy, and epilepsy) three to four times higher than in the general population. The prognosis
and outcome of co-occurring diagnoses may be influenced by the presence of intellectual
disability. Assessment procedures may require modifications because of associated disor-
ders, including communication disorders, autism spectrum disorder, and motor, sensory,
or other disorders. Knowledgeable informants are essential for identifying symptoms
such as irritability, mood dysregulation, aggression, eating problems, and sleep problems,
and for assessing adaptive functioning in various community settings.
The most common co-occurring mental and neurodevelopmental disorders are atten-
tion-deficit/hyperactivity disorder; depressive and bipolar disorders; anxiety disorders;
autism spectrum disorder; stereotypic movement disorder (with or without self-injurious
behavior); impulse-control disorders; and major neurocognitive disorder. Major depres-
sive disorder may occur throughout the range of severity of intellectual disability. Self-
injurious behavior requires prompt diagnostic attention and may warrant a separate di-
agnosis of stereotypic movement disorder. Individuals with intellectual disability, partic-
ularly those with more severe intellectual disability, may also exhibit aggression and
disruptive behaviors, including harm of others or property destruction.
Relationship to Other Classifications
ICD-11 (in development at the time of this publication) uses the term intellectual develop-
mental disorders to indicate that these are disorders that involve impaired brain functioning
early in life. These disorders are described in ICD-11 as a metasyndrome occurring in the
developmental period analogous to dementia or neurocognitive disorder in later life.
There are four subtypes in ICD-11: mild, moderate, severe, and profound.
The American Association on Intellectual and Developmental Disabilities (AAIDD)
also uses the term intellectual disability with a similar meaning to the term as used in this
Global Developmental Delay 41
manual. The AAIDD’s classification is multidimensional rather than categorical and is
based on the disability construct. Rather than listing specifiers as is done in DSM-5, the
AAIDD emphasizes a profile of supports based on severity.
Global Developmental Delay
315.8 (F88)
This diagnosis is reserved for individuals under the age of 5 years when the clinical severity
level cannot be reliably assessed during early childhood. This category is diagnosed when
an individual fails to meet expected developmental milestones in several areas of intellec-
tual functioning, and applies to individuals who are unable to undergo systematic assess-
ments of intellectual functioning, including children who are too young to participate in
standardized testing. This category requires reassessment after a period of time.
Unspecified Intellectual Disability
(Intellectual Developmental Disorder)
319 (F79)
This category is reserved for individuals over the age of 5 years when assessment of the
degree of intellectual disability (intellectual developmental disorder) by means of locally
available procedures is rendered difficult or impossible because of associated sensory or
physical impairments, as in blindness or prelingual deafness; locomotor disability; or pres-
ence of severe problem behaviors or co-occurring mental disorder. This category should
only be used in exceptional circumstances and requires reassessment after a period of time.
Communication Disorders
Disorders of communication include deficits in language, speech, and communication.
Speech is the expressive production of sounds and includes an individual's articulation,
fluency, voice, and resonance quality. Language includes the form, function, and use of a
conventional system of symbols (i.e., spoken words, sign language, written words, pic-
tures) in a rule-governed manner for communication. Communication includes any verbal
or nonverbal behavior (whether intentional or unintentional) that influences the behavior,
ideas, or attitudes of another individual. Assessments of speech, language and communi-
cation abilities must take into account the individual's cultural and language context,
particularly for individuals growing up in bilingual environments. The standardized mea-
sures of language development and of nonverbal intellectual capacity must be relevant for
the cultural and linguistic group (i.e., tests developed and standardized for one group may
not provide appropriate norms for a different group). The diagnostic category of commu-
nication disorders includes the following: language disorder, speech sound disorder,
childhood-onset fluency disorder (stuttering), social (pragmatic) communication disor-
der, and other specified and unspecified communication disorders.
42 Neurodevelopmental Disorders
Language Disorder
Diagnostic Criteria 315.39 (F80.9)
A. Persistent difficulties in the acquisition and use of language across modalities (i.e.,
spoken, written, sign language, or other) due to deficits in comprehension or produc-
tion that include the following:
1. Reduced vocabulary (word knowledge and use).
2. Limited sentence structure (ability to put words and word endings together to form
sentences based on the rules of grammar and morphology).
3. Impairments in discourse (ability to use vocabulary and connect sentences to ex-
plain or describe a topic or series of events or have a conversation).
B. Language abilities are substantially and quantifiably below those expected for age, re-
sulting in functional limitations in effective communication, social participation, aca-
demic achievement, or occupational performance, individually or in any combination.
C. Onset of symptoms is in the early developmental period.
D. The difficulties are not attributable to hearing or other sensory impairment, motor dys-
function, or another medical or neurological condition and are not better explained by in-
tellectual disability (intellectual developmental disorder) or global developmental delay.
Diagnostic Features
The core diagnostic features of language disorder are difficulties in the acquisition and use
of language due to deficits in the comprehension or production of vocabulary, sentence
structure, and discourse. The language deficits are evident in spoken communication,
written communication, or sign language. Language learning and use is dependent on
both receptive and expressive skills. Expressive ability refers to the production of vocal, ges-
tural, or verbal signals, while receptive ability refers to the process of receiving and com-
prehending language messages. Language skills need to be assessed in both expressive
and receptive modalities as these may differ in severity. For example, an individual's ex-
pressive language may be severely impaired, while his receptive language is hardly im-
paired at all.
Language disorder usually affects vocabulary and grammar, and these effects then
limit the capacity for discourse. The child’s first words and phrases are likely to be delayed
in onset; vocabulary size is smaller and less varied than expected; and sentences are
shorter and less complex with grammatical errors, especially in past tense. Deficits in com-
prehension of language are frequently underestimated, as children may be good at using
context to infer meaning. There may be word-finding problems, impoverished verbal def-
initions, or poor understanding of synonyms, multiple meanings, or word play appro-
priate for age and culture. Problems with remembering new words and sentences are
manifested by difficulties following instructions of increasing length, difficulties rehears-
ing strings of verbal information (e.g., remembering a phone number or a shopping list),
and difficulties remembering novel sound sequences, a skill that may be important for
learning new words. Difficulties with discourse are shown by a reduced ability to provide
adequate information about the key events and to narrate a coherent story.
The language difficulty is manifest by abilities substantially and quantifiably below
that expected for age and significantly interfering with academic achievement, occupa-
tional performance, effective communication, or socialization (Criterion B), A diagnosis of
language disorder is made based on the synthesis of the individual's history, direct clinical
observation in different contexts (i.e., home, school, or work), and scores from standard-
ized tests of language ability that can be used to guide estimates of severity.
Language Disorder 43
Associated Features Supporting Diagnosis
A positive family history of language disorders is often present. Individuals, even chil-
dren, can be adept at accommodating to their limited language. They may appear to be shy
or reticent to talk. Affected individuals may prefer to communicate only with family mem-
bers or other familiar individuals. Although these social indicators are not diagnostic of a
language disorder, if they are notable and persistent, they warrant referral for a full lan-
guage assessment. Language disorder, particularly expressive deficits, may co-occur with
speech sound disorder.
Deveiopment and Course
Language acquisition is marked by changes from onset in toddlerhood to the adult level of
competency that appears during adolescence. Changes appear across the dimensions of
language (sounds, words, grammar, narratives/expository texts, and conversational
skills) in age-graded increments and synchronies. Language disorder emerges during the
early developmental period; however, there is considerable variation in early vocabulary
acquisition and early word combinations, and individual differences are not, as single
indicators, highly predictive of later outcomes. By age 4 years, individual differences in
language ability are more stable, with better measurement accuracy, and are highly pre-
dictive of later outcomes. Language disorder diagnosed from 4 years of age is likely to be
stable over time and typically persists into adulthood, although the particular profile of
language strengths and deficits is likely to change over the course of development.
Risk and Prognostic Factors
Children with receptive language impairments have a poorer prognosis than those with
predominantly expressive impairments. They are more resistant to treatment, and diffi-
culties with reading comprehension are frequently seen.
Genetic and physiological. Language disorders are highly heritable, and family mem-
bers are more likely to have a history of language impairment.
Differential Diagnosis
Normal variations in language. Language disorder needs to be distinguished from nor-
mal developmental variations, and this distinction may be difficult to make before 4 years
of age. Regional, social, or cultural/ethnic variations of language (e.g., dialects) must be
considered when an individual is being assessed for language impairment.
Hearing or other sensory impairment. Hearing impairment needs to be excluded as the
primary cause of language difficulties. Language deficits may be associated with a hearing
impairment, other sensory deficit, or a speech-motor deficit. When language deficits are in
excess of those usually associated with these problems, a diagnosis of language disorder
may be made.
Intellectual disability (intellectual developmental disorder). Language delay is often the
presenting feature of intellectual disability, and the definitive diagnosis may not be made
until the child is able to complete standardized assessments. A separate diagnosis is not
given unless the language deficits are clearly in excess of the intellectual limitations.
Neurological disorders. Language disorder can be acquired in association with neuro-
logical disorders, including epilepsy (e.g., acquired aphasia or Landau-Kleffner syndrome).
Language regression. Loss of speech and language in a child younger than 3 years may
be a sign of autism spectrum disorder (with developmental regression) or a specific neuro-
logical condition, such as Landau-Kleffner syndrome. Among children older than 3 years,
language loss may be a symptom of seizures, and a diagnostic assessment is necessary to
exclude the presence of epilepsy (e.g., routine and sleep electroencephalogram).
44 Neurodevelopmental Disorders
Comorbidity
Language disorder is strongly associated with other neurodevelopmental disorders in
terms of specific learning disorder (literacy and numeracy), attention-deficit/hyperactiv-
ity disorder, autism spectrum disorder, and developmental coordination disorder. It is
also associated with social (pragmatic) communication disorder. A positive family history
of speech or language disorders is often present.
Speech Sound Disorder
Diagnostic Criteria 315.39 (F80.0)
A. Persistent difficulty with speech sound production that interferes with speech intelligi-
bility or prevents verbal communication of messages.
B. The disturbance causes limitations in effective communication that interfere with social
participation, academic achievement, or occupational performance, individually or in
any combination.
C. Onset of symptoms is in the early developmental period.
D. The difficulties are not attributable to congenital or acquired conditions, such as cere-
bral palsy, cleft palate, deafness or hearing loss, traumatic brain injury, or other medi-
cal or neurological conditions.
Diagnostic Features
Speech sound production describes the clear articulation of the phonemes (i.e., individual
sounds) that in combination make up spoken words. Speech sound production requires both
the phonological knowledge of speech sounds and the ability to coordinate the movements of
the articulators (i.e., the jaw, tongue, and lips,) with breathing and vocalizing for speech. Chil-
dren with speech production difficulties may experience difficulty with phonological knowl-
edge of speech sounds or the ability to coordinate movements for speech in varying degrees.
Speech sound disorder is thus heterogeneous in its underlying mechanisms and includes pho-
nological disorder and articulation disorder. A speech sound disorder is diagnosed when
speech sound production is not what would be expected based on the child’s age and devel-
opmental stage and when the deficits are not the result of a physical, structural, neurological,
or hearing impairment. Among typically developing children at age 4 years, overall speech
should be intelligible, whereas at age 2 years, only 50% may be understandable.
Associated Features Supporting Diagnosis
Language disorder, particularly expressive deficits, may be found to co-occur with speech
sound disorder. A positive family history of speech or language disorders is often present.
If the ability to rapidly coordinate the articulators is a particular aspect of difficulty,
there may be a history of delay or incoordination in acquiring skills that also utilize the
articulators and related facial musculature; among others, these skills include chewing,
maintaining mouth closure, and blowing the nose. Other areas of motor coordination may
be impaired as in developmental coordination disorder. Verbal dyspraxia is a term also
used for speech production problems.
Speech may be differentially impaired in certain genetic conditions (e.g., Down syn-
drome, 22q deletion, FoxP2 gene mutation). If present, these should also be coded.
Development and Course
Learning to produce speech sounds clearly and accurately and learning to produce con-
nected speech fluently are developmental skills. Articulation of speech sounds follows a
Childhood-Onset Fluency Disorder (Stuttering) 45
developmental pattern, which is reflected in the age norms of standardized tests. It is not
unusual for typically developing children to use developmental processes for shortening
words and syllables as they are learning to talk, but their progression in mastering speech
sound production should result in mostly intelligible speech by age 3 years. Children with
speech sound disorder continue to use immature phonological simplification processes
past the age when most children can produce words clearly.
Most speech sounds should be produced clearly and most words should be pronounced
accurately according to age and community norms by age 7 years. The most frequently mis-
articulated sounds also tend to be learned later, leading them to be called the “late eight” (1, 7,
s, z, th, ch, dzh, and zh). Misarticulation of any of these sounds by itself could be considered
within normal limits up to age 8 years. When multiple sounds are involved, it may be appro-
priate to target some of those sounds as part of a plan to improve intelligibility prior to the age
at which almost all children can produce them accurately. Lisping (i.e., misarticulating sibi-
lants) is particularly common and may involve frontal or lateral patterns of airstream direc-
tion. It may be associated with an abnormal tongue-thrust swallowing pattern.
Most children with speech sound disorder respond well to treatment, and speech dif-
ficulties improve over time, and thus the disorder may not be lifelong. However, when a
language disorder is also present, the speech disorder has a poorer prognosis and may be
associated with specific learning disorders.
Differential Diagnosis
Normai variations in speech. Regional, social, or cultural/ethnic variations of speech
should be considered before making the diagnosis.
Hearing or other sensory impairment. Hearing impairment or deafness may result in
abnormalities of speech. Deficits of speech sound production may be associated with a
hearing impairment, other sensory deficit, or a speech-motor deficit. When speech deficits
are in excess of those usually associated with these problems, a diagnosis of speech sound
disorder may be made.
Structural deficits. Speechimpairment may be due to structural deficits (e.g., cleft palate).
Dysarthria. Speech impairment may be attributable to a motor disorder, such as cerebral
palsy. Neurological signs, as well as distinctive features of voice, differentiate dysarthria
from speech sound disorder, although in young children (under 3 years) differentiation
may be difficult, particularly when there is no or minimal general body motor involve-
ment (as in, e.g., Worster-Drought syndrome).
Selective mutism. Limited use of speech may be a sign of selective mutism, an anxiety
disorder that is characterized by a lack of speech in one or more contexts or settings. Se-
lective mutism may develop in children with a speech disorder because of embarassment
about their impairments, but many children with selective mutism exhibit normal speech
in “safe” settings, such as at home or with close friends.
Childhood-Onset Fluency Disorder (Stuttering)
Diagnostic Criteria 315.35 (F80.81)
A. Disturbances in the normal fluency and time patterning of speech that are inappropri-
ate for the individual’s age and language skills, persist over time, and are characterized
by frequent and marked occurrences of one (or more) of the following:
1. Sound and syllable repetitions.
2. Sound prolongations of consonants as well as vowels.
46 Neurodevelopmental Disorders
Broken words (e.g., pauses within a word).
Audible or silent blocking (filled or unfilled pauses in speech).
Circumlocutions (word substitutions to avoid problematic words).
Words produced with an excess of physical tension.
Monosyllabic whole-word repetitions (e.g., “I-I-l-l see him”).
NO S &
B. The disturbance causes anxiety about speaking or limitations in effective communica-
tion, social participation, or academic or occupational performance, individually or in
any combination.
C. The onset of symptoms is in the early developmental period. (Note: Later-onset cases
are diagnosed as 307.0 [F98.5] adult-onset fluency disorder.)
D. The disturbance is not attributable to a speech-motor or sensory deficit, dysfluency as-
sociated with neurological insult (e.g., stroke, tumor, trauma), or another medical con-
dition and is not better explained by another mental disorder.
Diagnostic Features
The essential feature of childhood-onset fluency disorder (stuttering) is a disturbance in
the normal fluency and time patterning of speech that is inappropriate for the individual's
age. This disturbance is characterized by frequent repetitions or prolongations of sounds
or syllables and by other types of speech dysfluencies, including broken words (e.g.,
pauses within a word), audible or silent blocking (i.e., filled or unfilled pauses in speech),
circumlocutions (i.e., word substitutions to avoid problematic words), words produced
with an excess of physical tension, and monosyllabic whole-word repetitions (e.g., “I-I-I-I
see him”). The disturbance in fluency interferes with academic or occupational achieve-
ment or with social communication. The extent of the disturbance varies from situation to
situation and often is more severe when there is special pressure to communicate (e.g., giv-
ing a report at school, interviewing for a job). Dysfluency is often absent during oral read-
ing, singing, or talking to inanimate objects or to pets.
Associated Features Supporting Diagnosis
Fearful anticipation of the problem may develop. The speaker may attempt to avoid dys-
fluencies by linguistic mechanisms (e.g., altering the rate of speech, avoiding certain
words or sounds) or by avoiding certain speech situations, such as telephoning or public
speaking. In addition to being features of the condition, stress and anxiety have been
shown to exacerbate dysfluency.
Childhood-onset fluency disorder may also be accompanied by motor movements
(e.g., eye blinks, tics, tremors of the lips or face, jerking of the head, breathing movements,
fist clenching). Children with fluency disorder show a range of language abilities, and the
relationship between fluency disorder and language abilities is unclear.
Deveiopment and Course
Childhood-onset fluency disorder, or developmental stuttering, occurs by age 6 for 80%-—
90% of affected individuals, with age at onset ranging from 2 to 7 years. The onset can be
insidious or more sudden. Typically, dysfluencies start gradually, with repetition of initial
consonants, first words of a phrase, or long words. The child may not be aware of dysflu-
encies. As the disorder progresses, the dysfluencies become more frequent and interfering,
occurring on the most meaningful words or phrases in the utterance. As the child becomes
aware of the speech difficulty, he or she may develop mechanisms for avoiding the dys-
fluencies and emotional responses, including avoidance of public speaking and use of
short and simple utterances. Longitudinal research shows that 65%-85% of children re-
Social (Pragmatic) Communication Disorder 47
cover from the dysfluency, with severity of fluency disorder at age 8 years predicting re-
covery or persistence into adolescence and beyond.
Risk and Prognostic Factors
Genetic and physiological. The risk of stuttering among first-degree biological rela-
tives of individuals with childhood-onset fluency disorder is more than three times the
risk in the general population.
Functional Consequences of
Childhood-Onset Fluency Disorder (Stuttering)
In addition to being features of the condition, stress and anxiety can exacerbate dysflu-
ency. Impairment of social functioning may result from this anxiety.
Differential Diagnosis
Sensory deficits. Dysfluencies of speech may be associated with a hearing impairment
or other sensory deficit or a speech-motor deficit. When the speech dysfluencies are in ex-
cess of those usually associated with these problems, a diagnosis of childhood-onset flu-
ency disorder may be made.
Normal speech dysfluencies. The disorder must be distinguished from normal dysflu-
encies that occur frequently in young children, which include whole-word or phrase rep-
etitions (e.g., “I want, I want ice cream”), incomplete phrases, interjections, unfilled
pauses, and parenthetical remarks. If these difficulties increase in frequency or complexity
as the child grows older, a diagnosis of childhood-onset fluency disorder is appropriate.
Medication side effects. Stuttering may occur as a side effect of medication and may be
detected by a temporal relationship with exposure to the medication.
Adult-onset dysfluencies. If onset of dysfluencies is during or after adolescence, it is an
“adult-onset dysfluency” rather than a neurodevelopmental disorder. Adult-onset dysflu-
encies are associated with specific neurological insults and a variety of medical conditions
and mental disorders and may be specified with them, but they are not a DSM-5 diagnosis.
Tourette’s disorder. Vocal tics and repetitive vocalizations of Tourette’s disorder
should be distinguishable from the repetitive sounds of childhood-onset fluency disorder
by their nature and timing.
Social (Pragmatic) Communication Disorder
Diagnostic Criteria 315.39 (F80.89)
A. Persistent difficulties in the social use of verbal and nonverbal communication as man-
ifested by all of the following:
1. Deficits in using communication for social purposes, such as greeting and sharing
information, in a manner that is appropriate for the social context.
2. Impairment of the ability to change communication to match context or the needs of
the listener, such as speaking differently in a classroom than on a playground, talk-
ing differently to a child than to an adult, and avoiding use of overly formal language.
3. Difficulties following rules for conversation and storytelling, such as taking turns in
conversation, rephrasing when misunderstood, and knowing how to use verbal and
nonverbal signals to regulate interaction.
48 Neurodevelopmental Disorders
4. Difficulties understanding what is not explicitly stated (e.g., making inferences) and
nonliteral or ambiguous meanings of language (e.g., idioms, humor, metaphors,
multiple meanings that depend on the context for interpretation).
B. The deficits result in functional limitations in effective communication, social participa-
tion, social relationships, academic achievement, or occupational performance, indi-
vidually or in combination.
C. The onset of the symptoms is in the early developmental period (but deficits may not
become fully manifest until social communication demands exceed limited capacities).
D. The symptoms are not attributable to another medical or neurological condition or to low
abilities in the domains of word structure and grammar, and are not better explained by
autism spectrum disorder, intellectual disability (intellectual developmental disorder),
global developmental detay, or another mental disorder.
Diagnostic Features
Social (pragmatic) communication disorder is characterized by a primary difficulty with
pragmatics, or the social use of language and communication, as manifested by deficits in
understanding and following social rules of verbal and nonverbal communication in nat-
uralistic contexts, changing language according to the needs of the listener or situation,
and following rules for conversations and storytelling. The deficits in social communica-
tion result in functional limitations in effective communication, social participation, devel-
opment of social relationships, academic achievement, or occupational performance. The
deficits are not better explained by low abilities in the domains of structural language or
cognitive ability.
Associated Features Supporting Diagnosis
The most common associated feature of social (pragmatic) communication disorder is lan-
guage impairment, which is characterized by a history of delay in reaching language mile-
stones, and historical, if not current, structural language problems (see “Language Disorder”
earlier in this chapter). Individuals with social communication deficits may avoid social inter-
actions. Attention-deficit/hyperactivity disorder (ADHD), behavioral problems, and specific
learning disorders are also more common among affected individuals.
Development and Course
Because social (pragmatic) communication depends on adequate developmental progress
in speech and language, diagnosis of social (pragmatic) communication disorder is rare
among children younger than 4 years. By age 4 or 5 years, most children should possess
adequate speech and language abilities to permit identification of specific deficits in social
communication. Milder forms of the disorder may not become apparent until early ado-
lescence, when language and social interactions become more complex.
The outcome of social (pragmatic) communication disorder is variable, with some chil-
dren improving substantially over time and others continuing to have difficulties persist-
ing into adulthood. Even among those who have significant improvements, the early
deficits in pragmatics may cause lasting impairments in social relationships and behavior
and also in acquisition of other related skills, such as written expression.
Risk and Prognostic Factors
Genetic and physiological. A family history of autism spectrum disorder, communica-
tion disorders, or specific learning disorder appears to increase the risk for social (prag-
matic) communication disorder.
Unspecified Communication Disorder 49
Differential Diagnosis
Autism spectrum disorder. Autism spectrum disorder is the primary diagnostic con-
sideration for individuals presenting with social communication deficits. The two disor-
ders can be differentiated by the presence in autism spectrum disorder of restricted /
repetitive patterns of behavior, interests, or activities and their absence in social (prag-
matic) communication disorder. Individuals with autism spectrum disorder may only dis-
play the restricted /repetitive patterns of behavior, interests, and activities during the early
developmental period, so a comprehensive history should be obtained. Current absence of
symptoms would not preclude a diagnosis of autism spectrum disorder, if the restricted
interests and repetitive behaviors were present in the past. A diagnosis of social (prag-
matic) communication disorder should be considered only if the developmental history
fails to reveal any evidence of restricted/repetitive patterns of behavior, interests, or ac-
tivities.
Attention-deficit/hyperactivity disorder. Primary deficits of ADHD may cause impair-
ments in social communication and functional limitations of effective communication, so-
cial participation, or academic achievement.
Social anxiety disorder (social phobia). The symptoms of social communication disor-
der overlap with those of social anxiety disorder. The differentiating feature is the timing
of the onset of symptoms. In social (pragmatic) communication disorder, the individual
has never had effective social communication; in social anxiety disorder, the social com-
munication skills developed appropriately but are not utilized because of anxiety, fear, or
distress about social interactions.
Intellectual disability (intellectual developmental disorder) and global developmental
delay. Social communication skills may be deficient among individuals with global de-
velopmental delay or intellectual disability, but a separate diagnosis is not given unless
the social communication deficits are clearly in excess of the intellectual limitations.
Unspecified Communication Disorder
307.9 (F80.9)
This category applies to presentations in which symptoms characteristic of communication
disorder that cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning predominate but do not meet the full criteria for com-
munication disorder or for any of the disorders in the neurodevelopmental disorders diag-
nostic class. The unspecified communication disorder category is used in situations in
which the clinician chooses not to specify the reason that the criteria are not met for com-
munication disorder or for a specific neurodevelopmental disorder, and includes presen-
tations in which there is insufficient information to make a more specific diagnosis.
Neurodevelopmental Disorders
Autism Spectrum Disorder
Autism Spectrum Disorder
Diagnostic Criteria 299.00 (F84.0)
A. Persistent deficits in social communication and social interaction across multiple con-
texts, as manifested by the following, currently or by history (examples are illustrative,
not exhaustive; see text):
1. Deficits in social-emotional reciprocity, ranging, for example, from abnormal social
approach and failure of normal back-and-forth conversation; to reduced sharing of
interests, emotions, or affect; to failure to initiate or respond to social interactions.
2. Deficits in nonverbal communicative behaviors used for social interaction, ranging,
for example, from poorly integrated verbal and nonverbal communication; to abnor-
malities in eye contact and body language or deficits in understanding and use of
gestures; to a total lack of facial expressions and nonverbal communication.
3. Deficits in developing, maintaining, and understanding relationships, ranging, for ex-
ample, from difficulties adjusting behavior to suit various social contexts; to difficulties
in sharing imaginative play or in making friends; to absence of interest in peers.
Specify current severity:
Severity is based on social communication impairments and restricted, re-
petitive patterns of behavior (seeTable 2).
. Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at
least two of the following, currently or by history (examples are illustrative, not exhaus-
tive; see text):
1. Stereotyped or repetitive motor movements, use of objects, or speech (e.g., simple
motor stereotypies, lining up toys or flipping objects, echolalia, idiosyncratic
phrases).
2. Insistence on sameness, inflexible adherence to routines, or ritualized patterns of
verbal or nonverbal behavior (e.g., extreme distress at small changes, difficulties
with transitions, rigid thinking patterns, greeting rituals, need to take same route or
eat same food every day).
3. Highly restricted, fixated interests that are abnormal in intensity or focus (e.g.,
strong attachment to or preoccupation with unusual objects, excessively circum-
scribed or perseverative interests).
4. Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of
the environment (e.g., apparent indifference to pain/temperature, adverse re-
sponse to specific sounds or textures, excessive smelling or touching of objects,
visual fascination with lights or movement).
Specify current severity:
Severity is based on social communication impairments and restricted, re-
petitive patterns of behavior (see Table 2).
. Symptoms must be present in the early developmental period (but may not become
fully manifest until social demands exceed limited capacities, or may be masked by
learned strategies in later life).
. Symptoms cause clinically significant impairment in social, occupational, or other im-
portant areas of current functioning.
Autism Spectrum Disorder 51
E. These disturbances are not better explained by intellectual disability (intellectual devel-
opmental disorder) or global developmental delay. Intellectual disability and autism
spectrum disorder frequently co-occur; to make comorbid diagnoses of autism spec-
trum disorder and intellectual disability, social communication should be below that ex-
pected for general developmental level.
Note: Individuals with a well-established DSM-IV diagnosis of autistic disorder, Asperger's
disorder, or pervasive developmental disorder not otherwise specified should be given the
diagnosis of autism spectrum disorder. Individuals who have marked deficits in social
communication, but whose symptoms do not otherwise meet criteria for autism spectrum
disorder, should be evaluated for social (pragmatic) communication disorder.
Specify if:
With or without accompanying inteliectual impairment
With or without accompanying language impairment
Associated with a known medicai or genetic condition or environmental factor
(Coding note: Use additional code to identify the associated medical or genetic condition.)
Associated with another neurodevelopmental, mental, or behavioral disorder
(Coding note: Use additional code[s] to identify the associated neurodevelopmental,
mental, or behavioral disorder{s].)
With catatonia (refer to the criteria for catatonia associated with another mental dis-
order, pp. 119-120, for definition) (Coding note: Use additional code 293.89 [FO06. 1]
catatonia associated with autism spectrum disorder to indicate the presence of the co-
morbid catatonia.)
Recording Procedures
For autism spectrum disorder that is associated with a known medical or genetic condition
or environmental factor, or with another neurodevelopmental, mental, or behavioral dis-
order, record autism spectrum disorder associated with (name of condition, disorder, or
factor) (e.g., autism spectrum disorder associated with Rett syndrome). Severity should be
recorded as level of support needed for each of the two psychopathological domains in
Table 2 (e.g., “requiring very substantial support for deficits in social communication and
requiring substantial support for restricted, repetitive behaviors”). Specification of “with
accompanying intellectual impairment” or “without accompanying intellectual impair-
ment” should be recorded next. Language impairment specification should be recorded
thereafter. If there is accompanying language impairment, the current level of verbal func-
tioning should be recorded (e.g., “with accompanying language impairment—no intelligi-
ble speech” or “with accompanying language impairment—phrase speech”). If catatonia is
present, record separately “catatonia associated with autism spectrum disorder.”
Specifiers
The severity specifiers (see Table 2) may be used to describe succinctly the current symp-
tomatology (which might fall below level 1), with the recognition that severity may vary by
context and fluctuate over time. Severity of social communication difficulties and re-
stricted, repetitive behaviors should be separately rated. The descriptive severity categories
should not be used to determine eligibility for and provision of services; these can only be
developed at an individual level and through discussion of personal priorities and targets.
Regarding the specifier “with or without accompanying intellectual impairment,” un-
derstanding the (often uneven) intellectual profile of a child or adult with autism spectrum
disorder is necessary for interpreting diagnostic features. Separate estimates of verbal and
nonverbal skill are necessary (e.g., using untimed nonverbal tests to assess potential
strengths in individuals with limited language).
Neurodevelopmental Disorders
52
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Autism Spectrum Disorder 53
To use the specifier “with or without accompanying language impairment,” the cur-
rent level of verbal functioning should be assessed and described. Examples of the specific
descriptions for “with accompanying language impairment” might include no intelligible
speech (nonverbal), single words only, or phrase speech. Language level in individuals
“without accompanying language impairment” might be further described by speaks in
full sentences or has fluent speech. Since receptive language may lag behind expressive
language development in autism spectrum disorder, receptive and expressive language
skills should be considered separately.
The specifier “associated with a known medical or genetic condition or environmental fac-
tor” should be used when the individual has a known genetic disorder (e.g., Rett syndrome,
Fragile X syndrome, Down syndrome), a medical disorder (e.g. epilepsy), or a history of envi-
ronmental exposure (e.g., valproate, fetal alcohol syndrome, very low birth weight).
Additional neurodevelopmental, mental or behavioral conditions should also be noted
(e.g., attention-deficit/hyperactivity disorder; developmental coordination disorder; dis-
ruptive behavior, impulse-control, or conduct disorders; anxiety, depressive, or bipolar
disorders; tics or Tourette’s disorder; self-injury; feeding, elimination, or sleep disorders).
Diagnostic Features
The essential features of autism spectrum disorder are persistent impairment in reciprocal
social communication and social interaction (Criterion A), and restricted, repetitive pat-
terns of behavior, interests, or activities (Criterion B). These symptoms are present from
early childhood and limit or impair everyday functioning (Criteria C and D). The stage at
which functional impairment becomes obvious will vary according to characteristics of
the individual and his or her environment. Core diagnostic features are evident in the
developmental period, but intervention, compensation, and current supports may mask
difficulties in at least some contexts. Manifestations of the disorder also vary greatly de-
pending on the severity of the autistic condition, developmental level, and chronological age;
hence, the term spectrum. Autism spectrum disorder encompasses disorders previously re-
ferred to as early infantile autism, childhood autism, Kanner’s autism, high-functioning
autism, atypical autism, pervasive developmental disorder not otherwise specified, child-
hood disintegrative disorder, and Asperger’s disorder.
The impairments in communication and social interaction specified in Criterion A are
pervasive and sustained. Diagnoses are most valid and reliable when based on multiple
sources of information, including clinician’s observations, caregiver history, and, when
possible, self-report. Verbal and nonverbal deficits in social communication have varying
manifestations, depending on the individual's age, intellectual level, and language ability,
as well as other factors such as treatment history and current support. Many individuals
have language deficits, ranging from complete lack of speech through language delays,
poor comprehension of speech, echoed speech, or stilted and overly literal language. Even
when formal language skills (e.g., vocabulary, grammar) are intact, the use of language for
reciprocal social communication is impaired in autism spectrum disorder.
Deficits in social-emotional reciprocity (i.e., the ability to engage with others and share
thoughts and feelings) are clearly evident in young children with the disorder, who may
show little or no initiation of social interaction and no sharing of emotions, along with re-
duced or absent imitation of others’ behavior. What language exists is often one-sided,
lacking in social reciprocity, and used to request or label rather than to comment, share
feelings, or converse. In adults without intellectual disabilities or language delays, deficits
in social-emotional reciprocity may be most apparent in difficulties processing and re-
sponding to complex social cues (e.g., when and how to join a conversation, what not to
say). Adults who have developed compensation strategies for some social challenges still
struggle in novel or unsupported situations and suffer from the effort and anxiety of con-
sciously calculating what is socially intuitive for most individuals.
54 Neurodevelopmental Disorders
Deficits in nonverbal communicative behaviors used for social interaction are mani-
fested by absent, reduced, or atypical use of eye contact (relative to cultural norms), ges-
tures, facia] expressions, body orientation, or speech intonation. An early feature of autism
spectrum disorder is impaired joint attention as manifested by a lack of pointing, showing,
or bringing objects to share interest with others, or failure to follow someone’s pointing or
eye gaze. Individuals may learn a few functional gestures, but their repertoire is smaller
than that of others, and they often fail to use expressive gestures spontaneously in com-
munication. Among adults with fluent language, the difficulty in coordinating nonverbal
communication with speech may give the impression of odd, wooden, or exaggerated
“body language” during interactions. Impairment may be relatively subtle within indi-
vidual modes (e.g., someone may have relatively good eye contact when speaking) but
noticeable in poor integration of eye contact, gesture, body posture, prosody, and facial ex-
pression for social communication.
Deficits in developing, maintaining, and understanding relationships should be
judged against norms for age, gender, and culture. There may be absent, reduced, or atyp-
ical social interest, manifested by rejection of others, passivity, or inappropriate ap-
proaches that seem aggressive or disruptive. These difficulties are particularly evident in
young children, in whom there is often a lack of shared social play and imagination (e.g.,
age-appropriate flexible pretend play) and, later, insistence on playing by very fixed rules.
Older individuals may struggle to understand what behavior is considered appropriate in
one situation but not another (e.g., casual behavior during a job interview), or the different
ways that language may be used to communicate (e.g., irony, white lies). There may be an
apparent preference for solitary activities or for interacting with much younger or older
people. Frequently, there is a desire to establish friendships without a complete or realistic
idea of what friendship entails (e.g., one-sided friendships or friendships based solely on
shared special interests). Relationships with siblings, co-workers, and caregivers are also
important to consider (in terms of reciprocity).
Autism spectrum disorder is also defined by restricted, repetitive patterns of behavior,
interests, or activities (as specified in Criterion B), which show a range of manifestations
according to age and ability, intervention, and current supports. Stereotyped or repetitive
behaviors include simple motor stereotypies (e.g., hand flapping, finger flicking), repeti-
tive use of objects (e.g., spinning coins, lining up toys), and repetitive speech (e.g., echola-
lia, the delayed or immediate parroting of heard words; use of “you” when referring to
self; stereotyped use of words, phrases, or prosodic patterns). Excessive adherence to rou-
tines and restricted patterns of behavior may be manifest in resistance to change (e.g., dis-
tress at apparently small changes, such as in packaging of a favorite food; insistence on
adherence to rules; rigidity of thinking) or ritualized patterns of verbal or nonverbal be-
havior (e.g., repetitive questioning, pacing a perimeter). Highly restricted, fixated interests
in autism spectrum disorder tend to be abnormal in intensity or focus (e.g., a toddler
strongly attached to a pan; a child preoccupied with vacuum cleaners; an adult spending
hours writing out timetables). Some fascinations and routines may relate to apparent hy-
per- or hyporeactivity to sensory input, manifested through extreme responses to specific
sounds or textures, excessive smelling or touching of objects, fascination with lights or
spinning objects, and sometimes apparent indifference to pain, heat, or cold. Extreme re-
action to or rituals involving taste, smell, texture, or appearance of food or excessive food
restrictions are common and may be a presenting feature of autism spectrum disorder.
Many adults with autism spectrum disorder without intellectual or language disabili-
ties learn to suppress repetitive behavior in public. Special interests may be a source of
pleasure and motivation and provide avenues for education and employment later in life.
Diagnostic criteria may be met when restricted, repetitive patterns of behavior, interests,
or activities were clearly present during childhood or at some time in the past, even if
symptoms are no longer present.
Autism Spectrum Disorder 55
Criterion D requires that the features must cause clinically significant impairment in so-
cial, occupational, or other important areas of current functioning. Criterion E specifies that
the social communication deficits, although sometimes accompanied by intellectual disabil-
ity (intellectual developmental disorder), are not in line with the individual’s developmental
level; impairments exceed difficulties expected on the basis of developmental level.
Standardized behavioral diagnostic instruments with good psychometric properties,
including caregiver interviews, questionnaires and clinician observation measures, are
available and can improve reliability of diagnosis over time and across clinicians.
Associated Features Supporting Diagnosis
Many individuals with autism spectrum disorder also have intellectual impairment and/or
language impairment (e.g., slow to talk, language comprehension behind production). Even
those with average or high intelligence have an uneven profile of abilities. The gap between
intellectual and adaptive functional] skills is often large. Motor deficits are often present, in-
cluding odd gait, clumsiness, and other abnormal motor signs (e.g., walking on tiptoes). Self-
injury (e.g., head banging, biting the wrist) may occur, and disruptive/challenging behav-
iors are more common in children and adolescents with autism spectrum disorder than
other disorders, including intellectual disability. Adolescents and adults with autism spec-
trum disorder are prone to anxiety and depression. Some individuals develop catatonic-like
motor behavior (slowing and “freezing” mid-action), but these are typically not of the mag-
nitude of a catatonic episode. However, it is possible for individuals with autism spectrum
disorder to experience a marked deterioration in motor symptoms and display a full cata-
tonic episode with symptoms such as mutism, posturing, grimacing and waxy flexibility.
The risk period for comorbid catatonia appears to be greatest in the adolescent years.
Prevalence
In recent years, reported frequencies for autism spectrum disorder across U.S. and non-
U.S. countries have approached 1% of the population, with similar estimates in child and
adult samples. It remains unclear whether higher rates reflect an expansion of the diag-
nostic criteria of DSM-IV to include subthreshold cases, increased awareness, differences
in study methodology, or a true increase in the frequency of autism spectrum disorder.
Development and Course
The age and pattern of onset also should be noted for autism spectrum disorder. Symptoms
are typically recognized during the second year of life (12-24 months of age) but may be seen
earlier than 12 months if developmental delays are severe, or noted later than 24 months if
symptoms are more subtle. The pattern of onset description might include information
about early developmental delays or any losses of social or language skills. In cases where
skills have been lost, parents or caregivers may give a history of a gradual or relatively
rapid deterioration in social behaviors or language skills. Typically, this would occur be-
tween 12 and 24 months of age and is distinguished from the rare instances of developmen-
tal regression occurring after at least 2 years of normal development (previously described
as childhood disintegrative disorder).
The behavioral features of autism spectrum disorder first become evident in early
childhood, with some cases presenting a lack of interest in social interaction in the first
year of life. Some children with autism spectrum disorder experience developmental pla-
teaus or regression, with a gradual or relatively rapid deterioration in social behaviors or
use of language, often during the first 2 years of life. Such losses are rare in other disor-
ders and may be a useful “red flag” for autism spectrum disorder. Much more unusual
and warranting more extensive medical investigation are losses of skills beyond social
communication (e.g., loss of self-care, toileting, motor skills) or those occurring after the
56 Neurodevelopmental Disorders
second birthday (see also Rett syndrome in the section “Differential Diagnosis” for this
disorder).
First symptoms of autism spectrum disorder frequently involve delayed language de-
velopment, often accompanied by lack of social interest or unusual social interactions (e.g.,
pulling individuals by the hand without any attempt to look at them), odd play patterns
(e.g., carrying toys around but never playing with them), and unusual communication
patterns (e.g., knowing the alphabet but not responding to own name). Deafness may be
suspected but is typically ruled out. During the second year, odd and repetitive behaviors
and the absence of typical play become more apparent. Since many typically developing
young children have strong preferences and enjoy repetition (e.g., eating the same foods,
watching the same video multiple times), distinguishing restricted and repetitive behav-
iors that are diagnostic of autism spectrum disorder can be difficult in preschoolers. The
clinical distinction is based on the type, frequency, and intensity of the behavior (e.g., a
child who daily lines up objects for hours and is very distressed if any item is moved).
Autism spectrum disorder is not a degenerative disorder, and it is typical for learning
and compensation to continue throughout life. Symptoms are often most marked in early
childhood and early school years, with developmental gains typical in later childhood in
at least some areas (e.g., increased interest in social interaction). A small proportion of in-
dividuals deteriorate behaviorally during adolescence, whereas most others improve.
Only a minority of individuals with autism spectrum disorder live and work indepen-
dently in adulthood; those who do tend to have superior language and intellectual abilities
and are able to find a niche that matches their special interests and skills. In general, indi-
viduals with lower levels of impairment may be better able to function independently.
However, even these individuals may remain socially naive and vulnerable, have difficul-
ties organizing practical demands without aid, and are prone to anxiety and depression.
Many adults report using compensation strategies and coping mechanisms to mask their
difficulties in public but suffer from the stress and effort of maintaining a socially accept-
able facade. Scarcely anything is known about old age in autism spectrum disorder.
Some individuals come for first diagnosis in adulthood, perhaps prompted by the diagno-
sis of autism ina child in the family or a breakdown of relations at work or home. Obtaining de-
tailed developmental history in such cases may be difficult, and it is important to consider self-
reported difficulties. Where clinical observation suggests criteria are currently met, autism
spectrum disorder may be diagnosed, provided there is no evidence of good social and com-
munication skills in childhood. For example, the report (by parents or another relative) that the
individual had ordinary and sustained reciprocal friendships and good nonverbal communi-
cation skills throughout childhood would rule out a diagnosis of autism spectrum disorder;
however, the absence of developmental information in itself should not do so.
Manifestations of the social and communication impairments and restricted /repeti-
tive behaviors that define autism spectrum disorder are clear in the developmental period.
In later life, intervention or compensation, as well as current supports, may mask these dif-
ficulties in at least some contexts. However, symptoms remain sufficient to cause current
impairment in social, occupational, or other important areas of functioning.
Risk and Prognostic Factors
The best established prognostic factors for individual outcome within autism spectrum
disorder are presence or absence of associated intellectual disability and language impair-
ment (e.g., functional language by age 5 years is a good prognostic sign) and additional
mental health problems. Epilepsy, as a comorbid diagnosis, is associated with greater in-
tellectual disability and lower verbal ability.
Environmental. A variety of nonspecific risk factors, such as advanced parental age, low
birth weight, or fetal exposure to valproate, may contribute to risk of autism spectrum dis-
order.
Autism Spectrum Disorder 57
Genetic and physiological. Heritability estimates for autism spectrum disorder have
ranged from 37% to higher than 90%, based on twin concordance rates. Currently, as many
as 15% of cases of autism spectrum disorder appear to be associated with a known genetic
mutation, with different de novo copy number variants or de novo mutations in specific
genes associated with the disorder in different families. However, even when an autism
spectrum disorder is associated with a known genetic mutation, it does not appear to be
fully penetrant. Risk for the remainder of cases appears to be polygenic, with perhaps hun-
dreds of genetic loci making relatively small contributions.
Culture-Related Diagnostic Issues
Cultural differences will exist in norms for social interaction, nonverbal communication,
and relationships, but individuals with autism spectrum disorder are markedly impaired
against the norms for their cultural context. Cultural and socioeconomic factors may affect
age at recognition or diagnosis; for example, in the United States, late or underdiagnosis of
autism spectrum disorder among African American children may occur.
Gender-Related Diagnostic Issues
Autism spectrum disorder is diagnosed four times more often in males than in females. In
clinic samples, females tend to be more likely to show accompanying intellectual disabil-
ity, suggesting that girls without accompanying intellectual impairments or language
delays may go unrecognized, perhaps because of subtler manifestation of social and com-
munication difficulties.
Functional Consequences of Autism Spectrum Disorder
In young children with autism spectrum disorder, lack of social and communication abil-
ities may hamper learning, especially learning through social interaction or in settings
with peers. In the home, insistence on routines and aversion to change, as well as sensory
sensitivities, may interfere with eating and sleeping and make routine care (e.g., haircuts,
dental work) extremely difficult. Adaptive skills are typically below measured IQ. Ex-
treme difficulties in planning, organization, and coping with change negatively impact
academic achievement, even for students with above-average intelligence. During adult-
hood, these individuals may have difficulties establishing independence because of con-
tinued rigidity and difficulty with novelty.
Many individuals with autism spectrum disorder, even without intellectual disability,
have poor adult psychosocial functioning as indexed by measures such as independent
living and gainful employment. Functional consequences in old age are unknown, but so-
cial isolation and communication problems (e.g., reduced help-seeking) are likely to have
consequences for health in older adulthood.
Differential Diagnosis
Rett syndrome. Disruption of social interaction may be observed during the regressive
phase of Rett syndrome (typically between 1~4 years of age); thus, a substantial proportion
of affected young girls may have a presentation that meets diagnostic criteria for autism
spectrum disorder. However, after this period, most individuals with Rett syndrome im-
prove their social communication skills, and autistic features are no longer a major area of
concern. Consequently, autism spectrum disorder should be considered only when all di-
agnostic criteria are met.
Selective mutism. In selective mutism, early development is not typically disturbed.
The affected child usually exhibits appropriate communication skills in certain contexts
and settings. Even in settings where the child is mute, social reciprocity is not impaired,
nor are restricted or repetitive patterns of behavior present.
58 Neurodevelopmental Disorders
Language disorders and social (pragmatic) communication disorder. In some forms
of language disorder, there may be problems of communication and some secondary so-
cial difficulties. However, specific language disorder is not usually associated with abnor-
mal nonverbal communication, nor with the presence of restricted, repetitive patterns of
behavior, interests, or activities.
When an individual shows impairment in social communication and social interactions
but does not show restricted and repetitive behavior or interests, criteria for social (prag-
matic) communication disorder, instead of autism spectrum disorder, may be met. The di-
agnosis of autism spectrum disorder supersedes that of social (pragmatic) communication
disorder whenever the criteria for autism spectrum disorder are met, and care should be
taken to enquire carefully regarding past or current restricted /repetitive behavior.
Intellectual disability (intellectual developmental disorder) without autism spectrum
disorder. Intellectual disability without autism spectrum disorder may be difficult to
differentiate from autism spectrum disorder in very young children. Individuals with in-
tellectual disability who have not developed language or symbolic skills also present a
challenge for differential diagnosis, since repetitive behavior often occurs in such individ-
uals as well. A diagnosis of autism spectrum disorder in an individual with intellectual
disability is appropriate when social communication and interaction are significantly im-
paired relative to the developmental level of the individual’s nonverbal skills (e.g., fine
motor skills, nonverbal problem solving). In contrast, intellectual disability is the appropri-
ate diagnosis when there is no apparent discrepancy between the level of social-commu-
nicative skills and other intellectual skills.
Stereotypic movement disorder. Motor stereotypies are among the diagnostic charac-
teristics of autism spectrum disorder, so an additional diagnosis of stereotypic movement
disorder is not given when such repetitive behaviors are better explained by the presence
of autism spectrum disorder. However, when stereotypies cause self-injury and become a
focus of treatment, both diagnoses may be appropriate.
Attention-deficit/hyperactivity disorder. Abnormalities of attention (overly focused or
easily distracted) are common in individuals with autism spectrum disorder, as is hy-
peractivity. A diagnosis of attention-deficit/hyperactivity disorder (ADHD) should be
considered when attentional difficulties or hyperactivity exceeds that typically seen in in-
dividuals of comparable mental age.
Schizophrenia. Schizophrenia with childhood onset usually develops after a period of
normal, or near normal, development. A prodromal state has been described in which so-
cial impairment and atypical interests and beliefs occur, which could be confused with the
social deficits seen in autism spectrum disorder. Hallucinations and delusions, which are
defining features of schizophrenia, are not features of autism spectrum disorder. How-
ever, clinicians must take into account the potential for individuals with autism spectrum
disorder to be concrete in their interpretation of questions regarding the key features of
schizophrenia (e.g., “Do you hear voices when no one is there?” ”Yes [on the radio]”).
Comorbidity
Autism spectrum disorder is frequently associated with intellectual impairment and struc-
tural language disorder (i.e., an inability to comprehend and construct sentences with proper
grammar), which should be noted under the relevant specifiers when applicable. Many in-
dividuals with autism spectrum disorder have psychiatric symptoms that do not form part of
the diagnostic criteria for the disorder (about 70% of individuals with autism spectrum dis-
order may have one comorbid mental disorder, and 40% may have two or more comorbid
mental disorders). When criteria for both ADHD and autism spectrum disorder are met, both
diagnoses should be given. This same principle applies to concurrent diagnoses of autism
spectrum disorder and developmental coordination disorder, anxiety disorders, depressive
Attention-Deficit/Hyperactivity Disorder 59
disorders, and other comorbid diagnoses. Among individuals who are nonverbal or have
language deficits, observable signs such as changes in sleep or eating and increases in chal-
lenging behavior should trigger an evaluation for anxiety or depression. Specific learning dif-
ficulties (literacy and numeracy) are common, as is developmental coordination disorder.
Medical conditions commonly associated with autism spectrum disorder should be noted
under the “associated with a known medical /genetic or environmental /acquired condition”
specifier. Such medical conditions include epilepsy, sleep problems, and constipation.
Avoidant-restrictive food intake disorder is a fairly frequent presenting feature of autism
spectrum disorder, and extreme and narrow food preferences may persist.
Attention-Deficit/Hyperactivity
Disorder
Attention-Deficit/Hyperactivity Disorder
Diagnostic Criteria
A. A persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with
functioning or development, as characterized by (1) and/or (2):
1. Inattention: Six (or more) of the following symptoms have persisted for at least
6 months to a degree that is inconsistent with developmental level and that nega-
tively impacts directly on social and academic/occupational activities:
Note: The symptoms are not solely a manifestation of oppositional behavior, defi-
ance, hostility, or failure to understand tasks or instructions. For older adolescents
and adults (age 17 and older), at least five symptoms are required.
a. Often fails to give close attention to details or makes careless mistakes in
schoolwork, at work, or during other activities (e.g., overlooks or misses details,
work is inaccurate).
b. Often has difficulty sustaining attention in tasks or play activities (e.g., has diffi-
culty remaining focused during lectures, conversations, or lengthy reading).
c. Often does not seem to listen when spoken to directly (e.g., mind seems else-
where, even in the absence of any obvious distraction).
d. Often does not follow through on instructions and fails to finish schoolwork,
chores, or duties in the workplace (e.g., starts tasks but quickly loses focus and
is easily sidetracked).
e. Often has difficulty organizing tasks and activities (e.g., difficulty managing se-
quential tasks; difficulty keeping materials and belongings in order; messy, dis-
organized work; has poor time management; fails to meet deadlines).
f. Often avoids, dislikes, or is reluctant to engage in tasks that require sustained
mental effort (e.g., schoolwork or homework; for older adolescents and adults,
preparing reports, completing forms, reviewing lengthy papers).
g. Often loses things necessary for tasks or activities (e.g., school materials, pen-
cils, books, tools, wallets, keys, paperwork, eyeglasses, mobile telephones).
h. Is often easily distracted by extraneous stimuli (for older adolescents and
adults, may include unrelated thoughts).
i. Is often forgetful in daily activities (e.g., doing chores, running errands; for older
adolescents and adults, returning calls, paying bills, keeping appointments).
60
Neurodevelopmental Disorders
2. Hyperactivity and impulsivity: Six (or more) of the following symptoms have per-
sisted for at least 6 months to a degree that is inconsistent with developmental level
and that negatively impacts directly on social and academic/occupational activities:
Note: The symptoms are not solely a manifestation of oppositional behavior, defi-
ance, hostility, or a failure to understand tasks or instructions. For older adolescents
and adults (age 17 and older), at least five symptoms are required.
a. Often fidgets with or taps hands or feet or squirms in seat.
b. Often leaves seat in situations when remaining seated is expected (e.g., leaves
his or her place in the classroom, in the office or other workplace, or in other
situations that require remaining in place).
c. Often runs about or climbs in situations where it is inappropriate. (Note: In ad-
olescents or adults, may be limited to feeling restless.)
d. Often unable to play or engage in leisure activities quietly.
e. Is often “on the go,” acting as if “driven by a motor’ (e.g., is unable to be or un-
comfortable being still for extended time, as in restaurants, meetings; may be
experienced by others as being restless or difficult to keep up with).
f. Often talks excessively.
g. Often blurts out an answer before a question has been completed (e.g., com-
pletes people’s sentences; cannot wait for turn in conversation).
h. Often has difficulty waiting his or her turn (e.g., while waiting in line).
i. Often interrupts or intrudes on others (e.g., butts into conversations, games, or
activities; may start using other people’s things without asking or receiving per-
mission; for adolescents and adults, may intrude into or take over what others
are doing).
. Several inattentive or hyperactive-impulsive symptoms were present prior to age
12 years.
. Several inattentive or hyperactive-impulsive symptoms are present in two or more set-
tings {e.g., at home, school, or work; with friends or relatives; in other activities).
. There is clear evidence that the symptoms interfere with, or reduce the quality of, so-
cial, academic, or occupational functioning.
. The symptoms do not occur exclusively during the course of schizophrenia or another
psychotic disorder and are not better explained by another mental disorder (e.g., mood
disorder, anxiety disorder, dissociative disorder, personality disorder, substance intox-
ication or withdrawal).
Specify whether:
314.01 (F90.2) Combined presentation: If both Criterion A1 (inattention) and Crite-
rion A2 (hyperactivity-impulsivity) are met for the past 6 months.
314.00 (F90.0) Predominantly inattentive presentation: If Criterion A1 (inattention)
is met but Criterion A2 (hyperactivity-impulsivity) is not met for the past 6 months.
314.01 (F90.1) Predominantly hyperactive/impulsive presentation: If Criterion A2 (hy-
peractivity-impulsivity) is met and Criterion A1 (inattention) is not met for the past 6 months.
Specify if:
in partial remission: When full criteria were previously met, fewer than the full criteria
have been met for the past 6 months, and the symptoms still result in impairment in
social, academic, or occupational functioning.
Specify current severity:
Mild: Few, if any, symptoms in excess of those required to make the diagnosis are
present, and symptoms result in no more than minor impairments in social or occupa-
tional functioning.
Moderate: Symptoms or functional impairment between “mild” and “severe” are present.
Attention-Deficit/Hyperactivity Disorder 61
Severe: Many symptoms in excess of those required to make the diagnosis, or several
symptoms that are particularly severe, are present, or the symptoms result in marked
impairment ih social or occupational functioning.
Diagnostic Features
The essential feature of attention-deficit/hyperactivity disorder (ADHD) is a persistent
pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or
development. Inattention manifests behaviorally in ADHD as wandering off task, lacking
persistence, having difficulty sustaining focus, and being disorganized and is not due to
defiance or lack of comprehension. Hyperactivity refers to excessive motor activity (such as
a child running about) when it is not appropriate, or excessive fidgeting, tapping, or talk-
ativeness. In adults, hyperactivity may manifest as extreme restlessness or wearing others
out with their activity. Impulsivity refers to hasty actions that occur in the moment without
forethought and that have high potential for harm to the individual (e.g., darting into the
street without looking). Impulsivity may reflect a desire for immediate rewards or an in-
ability to delay gratification. Impulsive behaviors may manifest as social intrusiveness
(e.g., interrupting others excessively) and/or as making important decisions without con-
sideration of long-term consequences (e.g., taking a job without adequate information).
ADHD begins in childhood. The requirement that several symptoms be present before
age 12 years conveys the importance of a substantial clinical presentation during child-
hood. At the same time, an earlier age at onset is not specified because of difficulties in es-
tablishing precise childhood onset retrospectively. Adult recall of childhood symptoms
tends to be unreliable, and it is beneficial to obtain ancillary information.
Manifestations of the disorder must be present in more than one setting (e.g., home and
school, work). Confirmation of substantial symptoms across settings typically cannot be
done accurately without consulting informants who have seen the individual in those set-
tings. Typically, symptoms vary depending on context within a given setting. Signs of the
disorder may be minimal or absent when the individual is receiving frequent rewards for
appropriate behavior, is under close supervision, is in a novel setting, is engaged in espe-
cially interesting activities, has consistent external stimulation (e.g., via electronic screens),
or is interacting in one-on-one situations (e.g., the clinician's office).
Associated Features Supporting Diagnosis
Mild delays in language, motor, or social development are not specific to ADHD but often co-
occur. Associated features may include low frustration tolerance, irritability, or mood lability.
Even in the absence of a specific learning disorder, academic or work performance is often im-
paired. Inattentive behavior is associated with various underlying cognitive processes, and in-
dividuals with ADHD may exhibit cognitive problems on tests of attention, executive
function, or memory, although these tests are not sufficiently sensitive or specific to serve as di-
agnostic indices. By early adulthood, ADHD is associated with an increased risk of suicide at-
tempt, primarily when comorbid with mood, conduct, or substance use disorders.
No biological marker is diagnostic for ADHD. As a group, compared with peers, chil-
dren with ADHD display increased slow wave electroencephalograms, reduced total
brain volume on magnetic resonance imaging, and possibly a delay in posterior to anterior
cortical maturation, but these findings are not diagnostic. In the uncommon cases where
there is a known genetic cause (e.g., Fragile X syndrome, 22q11 deletion syndrome), the
ADHD presentation should still be diagnosed.
Prevalence
Population surveys suggest that ADHD occurs in most cultures in about 5% of children
and about 2.5% of adults.
62 Neurodevelopmental Disorders
Development and Course
Many parents first observe excessive motor activity when the child is a toddler, but symp-
toms are difficult to distinguish from highly variable normative behaviors before age 4
years. ADHD is most often identified during elementary school years, and inattention be-
comes more prominent and impairing. The disorder is relatively stable through early ad-
olescence, but some individuals have a worsened course with development of antisocial
behaviors. In most individuals with ADHD, symptoms of motoric hyperactivity become
less obvious in adolescence and adulthood, but difficulties with restlessness, inattention,
poor planning, and impulsivity persist. A substantial proportion of children with ADHD
remain relatively impaired into adulthood.
In preschool, the main manifestation is hyperactivity. Inattention becomes more prom-
inent during elementary school. During adolescence, signs of hyperactivity (e.g., running
and climbing) are less common and may be confined to fidgetiness or an inner feeling of
jitteriness, restlessness, or impatience. In adulthood, along with inattention and restless-
ness, impulsivity may remain problematic even when hyperactivity has diminished.
Risk and Prognostic Factors
Temperamental. ADHD is associated with reduced behavioral inhibition, effortful con-
trol, or constraint; negative emotionality; and/or elevated novelty seeking. These traits
may predispose some children to ADHD but are not specific to the disorder.
Environmental. Very low birth weight (less than 1,500 grams) conveys a two- to three-
fold risk for ADHD, but most children with low birth weight do not develop ADHD. Al-
though ADHD is correlated with smoking during pregnancy, some of this association
reflects common genetic risk. A minority of cases may be related to reactions to aspects of
diet. There may be a history of child abuse, neglect, multiple foster placements, neurotoxin
exposure (e.g., lead), infections (e.g., encephalitis), or alcohol exposure in utero. Exposure
to environmental] toxicants has been correlated with subsequent ADHD, but it is not
known whether these associations are causal.
Genetic and physiological. ADHD is elevated in the first-degree biological] relatives of
individuals with ADHD. The heritability of ADHD is substantial. While specific genes
have been correlated with ADHD, they are neither necessary nor sufficient causal factors.
Visual and hearing impairments, metabolic abnormalities, sleep disorders, nutritional de-
ficiencies, and epilepsy should be considered as possible influences on ADHD symptoms.
ADHD is not associated with specific physical features, although rates of minor phys-
ical anomalies (e.g., hypertelorism, highly arched palate, low-set ears) may be relatively
elevated. Subtle motor delays and other neurological soft signs may occur. (Note that
marked co-occurring clumsiness and motor delays should be coded separately [e.g., de-
velopmental coordination disorder].)
Course modifiers. Family interaction patterns in early childhood are unlikely to cause
ADHD but may influence its course or contribute to secondary development of conduct
problems.
Culture-Related Diagnostic Issues
Differences in ADHD prevalence rates across regions appear attributable mainly to differ-
ent diagnostic and methodological practices. However, there also may be cultural varia-
tion in attitudes toward or interpretations of children’s behaviors. Clinical identification
rates in the United States for African American and Latino populations tend to be lower
than for Caucasian populations. Informant symptom ratings may be influenced by cul-
tural group of the child and the informant, suggesting that culturally appropriate practices
are relevant in assessing ADHD.
Attention-Deficit/Hyperactivity Disorder 63
Gender-Related Diagnostic Issues
ADHD is more frequent in males than in females in the general population, with a ratio of
approximately 2:1 in children and 1.6:1 in adults. Females are more likely than males to
present primarily with inattentive features.
Functional Consequences of
Attention-Deficit/Hyperactivity Disorder
ADHD is associated with reduced school performance and academic attainment, social re-
jection, and, in adults, poorer occupational performance, attainment, attendance, and
higher probability of unemployment as well as elevated interpersonal conflict. Children
with ADHD are significantly more likely than their peers without ADHD to develop con-
duct disorder in adolescence and antisocial personality disorder in adulthood, conse-
quently increasing the likelihood for substance use disorders and incarceration. The risk of
subsequent substance use disorders is elevated, especially when conduct disorder or an-
tisocial personality disorder develops. Individuals with ADHD are more likely than peers
to be injured. Traffic accidents and violations are more frequent in drivers with ADHD.
There may be an elevated likelihood of obesity among individuals with ADHD.
Inadequate or variable self-application to tasks that require sustained effort is often in-
terpreted by others as laziness, irresponsibility, or failure to cooperate. Family relation-
ships may be characterized by discord and negative interactions. Peer relationships are
often disrupted by peer rejection, neglect, or teasing of the individual with ADHD. On av-
erage, individuals with ADHD obtain less schooling, have poorer vocational achievement,
and have reduced intellectual scores than their peers, although there is great variability. In
its severe form, the disorder is markedly impairing, affecting social, familial, and scholas-
tic/occupational adjustment.
Academic deficits, school-related problems, and peer neglect tend to be most associ-
ated with elevated symptoms of inattention, whereas peer rejection and, to a lesser extent,
accidental injury are most salient with marked symptoms of hyperactivity or impulsivity.
Differential Diagnosis
Oppositional defiant disorder. Individuals with oppositional defiant disorder may re-
sist work or school tasks that require self-application because they resist conforming to
others’ demands. Their behavior is characterized by negativity, hostility, and defiance.
These symptoms must be differentiated from aversion to school or mentally demanding
tasks due to difficulty in sustaining mental effort, forgetting instructions, and impulsivity
in individuals with ADHD. Complicating the differential diagnosis is the fact that some
individuals with ADHD may develop secondary oppositional attitudes toward such tasks
and devalue their importance.
Intermittent explosive disorder. ADHD and intermittent explosive disorder share high
levels of impulsive behavior. However, individuals with intermittent explosive disorder
show serious aggression toward others, which is not characteristic of ADHD, and they do
not experience problems with sustaining attention as seen in ADHD. In addition, intermit-
tent explosive disorder is rare in childhood. Intermittent explosive disorder may be diag-
nosed in the presence of ADHD.
Other neurodevelopmental disorders. The increased motoric activity that may occur in
ADHD must be distinguished from the repetitive motor behavior that characterizes stereo-
typic movement disorder and some cases of autism spectrum disorder. In stereotypic
movement disorder, the motoric behavior is generally fixed and repetitive (e.g., body rock-
ing, self-biting), whereas the fidgetiness and restlessness in ADHD are typically general-
ized and not characterized by repetitive stereotypic movements. In Tourette’s disorder,
64 Neurodevelopmental Disorders
frequent multiple tics can be mistaken for the generalized fidgetiness of ADHD. Prolonged
observation may be needed to differentiate fidgetiness from bouts of multiple tics.
Specific learning disorder. Children with specific learning disorder may appear inat-
tentive because of frustration, lack of interest, or limited ability. However, inattention in
individuals with a specific learning disorder who do not have ADHD is not impairing out-
side of academic work.
Intellectual disability (intellectual developmental disorder). Symptoms of ADHD are
common among children placed in academic settings that are inappropriate to their intel-
lectual ability. In such cases, the symptoms are not evident during non-academic tasks. A
diagnosis of ADHD in intellectual disability requires that inattention or hyperactivity be
excessive for mental age.
Autism spectrum disorder. Individuals with ADHD and those with autism spectrum
disorder exhibit inattention, social dysfunction, and difficult-to-manage behavior. The so-
cial dysfunction and peer rejection seen in individuals with ADHD must be distinguished
from the social disengagement, isolation, and indifference to facial and tonal communica-
tion cues seen in individuals with autism spectrum disorder. Children with autism spec-
trum disorder may display tantrums because of an inability to tolerate a change from their
expected course of events. In contrast, children with ADHD may misbehave or have a tan-
trum during a major transition because of impulsivity or poor self-control.
Reactive attachment disorder. Children with reactive attachment disorder may show
social disinhibition, but not the full ADHD symptom cluster, and display other features
such as a lack of enduring relationships that are not characteristic of ADHD.
Anxiety disorders. ADHD shares symptoms of inattention with anxiety disorders. Indi-
viduals with ADHD are inattentive because of their attraction to external stimuli, new
activities, or preoccupation with enjoyable activities. This is distinguished from the inat-
tention due to worry and rumination seen in anxiety disorders. Restlessness might be seen
in anxiety disorders. However, in ADHD, the symptom is not associated with worry and
rumination.
Depressive disorders. Individuals with depressive disorders may present with inabil-
ity to concentrate. However, poor concentration in mood disorders becomes prominent
only during a depressive episode.
Bipolar disorder. Individuals with bipolar disorder may have increased activity, poor
concentration, and increased impulsivity, but these features are episodic, occurring sev-
eral days at a time. In bipolar disorder, increased impulsivity or inattention is accompa-
nied by elevated mood, grandiosity, and other specific bipolar features. Children with
ADHD may show significant changes in mood within the same day; such lability is dis-
tinct from a manic episode, which must last 4 or more days to be a clinical indicator of bi-
polar disorder, even in children. Bipolar disorder is rare in preadolescents, even when
severe irritability and anger are prominent, whereas ADHD is common among children
and adolescents who display excessive anger and irritability.
Disruptive mood dysregulation disorder. Disruptive mood dysregulation disorder is
characterized by pervasive irritability, and intolerance of frustration, but impulsiveness
and disorganized attention are not essential features. However, most children and adoles-
cents with the disorder have symptoms that also meet criteria for ADHD, which is diag-
nosed separately.
Substance use disorders. Differentiating ADHD from substance use disorders may be
problematic if the first presentation of ADHD symptoms follows the onset of abuse or fre-
quent use. Clear evidence of ADHD before substance misuse from informants or previous
records may be essential for differential diagnosis.
Other Specified Attention-Deficit/Hyperactivity Disorder 65
Personality disorders. In adolescents and adults, it may be difficult to distinguish ADHD
from borderline, narcissistic, and other personality disorders. All these disorders tend to
share the features of disorganization, social intrusiveness, emotional dysregulation, and
cognitive dysregulation. However, ADHD is not characterized by fear of abandonment,
self-injury, extreme ambivalence, or other features of personality disorder. It may take
extended clinical observation, informant interview, or detailed history to distinguish im-
pulsive, socially intrusive, or inappropriate behavior from narcissistic, aggressive, or dom-
ineering behavior to make this differential diagnosis.
Psychotic disorders. ADHD is not diagnosed if the symptoms of inattention and hyperac-
tivity occur exclusively during the course of a psychotic disorder.
Medication-induced symptoms of ADHD. Symptoms of inattention, hyperactivity, or
impulsivity attributable to the use of medication (e.g., bronchodilators, isoniazid, neuro-
leptics [resulting in akathisia], thyroid replacement medication) are diagnosed as other
specified or unspecified other (or unknown) substance-related disorders.
Neurocognitive disorders. Early major neurocognitive disorder (dementia) and/or
mild neurocognitive disorder are not known to be associated with ADHD but may present
with similar clinical features. These conditions are distinguished from ADHD by their late
onset.
Comorbidity
In clinical settings, comorbid disorders are frequent in individuals whose symptoms meet
criteria for ADHD. In the general population, oppositional defiant disorder co-occurs with
ADHD in approximately half of children with the combined presentation and about a
quarter with the predominantly inattentive presentation. Conduct disorder co-occurs in
about a quarter of children or adolescents with the combined presentation, depending on
age and setting. Most children and adolescents with disruptive mood dysregulation dis-
order have symptoms that also meet criteria for ADHD; a lesser percentage of children
with ADHD have symptoms that meet criteria for disruptive mood dysregulation disor-
der. Specific learning disorder commonly co-occurs with ADHD. Anxiety disorders and
major depressive disorder occur in a minority of individuals with ADHD but more often
than in the general population. Intermittent explosive disorder occurs in a minority of
adults with ADHD, but at rates above population levels. Although substance use disor-
ders are relatively more frequent among adults with ADHD in the general population, the
disorders are present in only a minority of adults with ADHD. In adults, antisocial and
other personality disorders may co-occur with ADHD. Other disorders that may co-occur
with ADHD include obsessive-compulsive disorder, tic disorders, and autism spectrum
disorder.
Other Specified Attention-Deficit/
Hyperactivity Disorder
314.01 (F90.8)
This category applies to presentations in which symptoms characteristic of attention-
deficit/hyperactivity disorder that cause clinically significant distress or impairment in so-
cial, occupational or other important areas of functioning predominate but do not meet the
full criteria for attention-deficit/hyperactivity disorder or any of the disorders in the neuro-
developmental disorders diagnostic class. The other specified attention-deficit/nyperactiv-
ity disorder category is used in situations in which the clinician chooses to communicate
66 Neurodevelopmental Disorders
the specific reason that the presentation does not meet the criteria for attention-deficit/
hyperactivity disorder or any specific neurodevelopmental disorder. This is done by re-
cording “other specified attention-deficit/hyperactivity disorder” followed by the specific
reason (e.g., “with insufficient inattention symptoms’).
Unspecified Attention-Deficit/
Hyperactivity Disorder
314.01 (F90.9)
This category applies to presentations in which symptoms characteristic of attention-
deficit/hyperactivity disorder that cause clinically significant distress or impairment in so-
cial, occupational, or other important areas of functioning predominate but do not meet the
full criteria for attention-deficit/hyperactivity disorder or any of the disorders in the neuro-
developmental disorders diagnostic class. The unspecified attention-deficit/hyperactivity
disorder category is used in situations in which the clinician chooses not to specify the rea-
son that the criteria are not met for attention-deficit/hyperactivity disorder or for a specific
neurodevelopmental disorder, and includes presentations in which there is insufficient in-
formation to make a more specific diagnosis.
Specific Learning Disorder
Specific Learning Disorder
Diagnostic Criteria
A. Difficulties learning and using academic skills, as indicated by the presence of at least
one of the following symptoms that have persisted for at least 6 months, despite the
provision of interventions that target those difficulties:
1. Inaccurate or slow and effortful word reading (e.g., reads single words aloud incor-
rectly or slowly and hesitantly, frequently guesses words, has difficulty sounding
out words).
2. Difficulty understanding the meaning of what is read (e.g., may read text accurately
but not understand the sequence, relationships, inferences, or deeper meanings of
what is read).
3. Difficulties with spelling (e.g., may add, omit, or substitute vowels or consonants).
4. Difficulties with written expression (e.g., makes multiple grammatical or punctua-
tion errors within sentences; employs poor paragraph organization; written expres-
sion of ideas lacks clarity).
5. Difficulties mastering number sense, number facts, or calculation (e.g., has poor
understanding of numbers, their magnitude, and relationships; counts on fingers to
add single-digit numbers instead of recalling the math fact as peers do; gets lost in
the midst of arithmetic computation and may switch procedures).
6. Difficulties with mathematical reasoning (e.g., has severe difficulty applying math-
ematical concepts, facts, or procedures to solve quantitative problems).
Specific Learning Disorder 67
B. The affected academic skills are substantially and quantifiably below those expected
for the individual’s chronological age, and cause significant interference with academic
or occupational performance, or with activities of daily living, as confirmed by individu-
ally administered standardized achievement measures and comprehensive clinical
assessment. For individuals age 17 years and older, a documented history of impairing
learning difficulties may be substituted for the standardized assessment.
C. The learning difficulties begin during school-age years but may not become fully man-
ifest until the demands for those affected academic skills exceed the individual's lim-
ited capacities (e.g., as in timed tests, reading or writing lengthy complex reports for a
tight deadline, excessively heavy academic loads).
D. The learning difficulties are not better accounted for by intellectual disabilities, uncor-
rected visual or auditory acuity, other mental or neurological disorders, psychosocial
adversity, lack of proficiency in the language of academic instruction, or inadequate
educational instruction.
Note: The four diagnostic criteria are to be met based on a clinical synthesis of the indi-
vidual’s history (developmental, medical, family, educational), school reports, and psycho-
educational assessment.
Coding note: Specify all academic domains and subskills that are impaired. When more
than one domain is impaired, each one should be coded individually according to the fol-
lowing specifiers.
Specify if:
315.00 (F81.0) With impairment in reading:
Word reading accuracy
Reading rate or fluency
Reading comprehension
Note: Dysi/exia is an alternative term used to refer to a pattern of learning difficulties
characterized by problems with accurate or fluent word recognition, poor decoding,
and poor spelling abilities. If dyslexia is used to specify this particutar pattern of dif-
ficulties, it is important also to specify any additional difficulties that are present,
such as difficulties with reading comprehension or math reasoning.
315.2 (F81.81) With impairment in written expression:
Spelling accuracy
Grammar and punctuation accuracy
Clarity or organization of written expression
315.1 (F81.2) With impairment in mathematics:
Number sense
Memorization of arithmetic facts
Accurate or fluent calculation
Accurate math reasoning
Note: Dyscaiculia is an alternative term used to refer to a pattern of difficulties char-
acterized by problems processing numerical information, learning arithmetic facts,
and performing accurate or fluent calculations. If dyscalculia is used to specify this
particular pattern of mathematic difficulties, it is important also to specify any addi-
tional difficulties that are present, such as difficulties with math reasoning or word rea-
soning accuracy.
Specify current severity:
Miid: Some difficulties learning skills in one or two academic domains, but of mild enough
severity that the individual may be able to compensate or function well when provided with
appropriate accommodations or support services, especially during the school years.
68 Neurodevelopmental Disorders
Moderate: Marked difficulties learning skills in one or more academic domains, so that
the individual is unlikely to become proficient without some intervals of intensive and
specialized teaching during the school years. Some accommodations or supportive
services at least part of the day at school, in the workplace, or at home may be needed
to complete activities accurately and efficiently.
Severe: Severe difficulties learning skills, affecting several academic domains, so that
the individual is unlikely to learn those skills without ongoing intensive individualized
and specialized teaching for most of the school years. Even with an array of appropri-
ate accommodations or services at home, at school, or in the workplace, the individual
may not be able to complete all activities efficiently.
Recording Procedures
Each impaired academic domain and subskill of specific learning disorder should be re-
corded. Because of ICD coding requirements, impairments in reading, impairments in writ-
ten expression, and impairments in mathematics, with their corresponding impairments in
subskills, must be coded separately. For example, impairments in reading and mathematics
and impairments in the subskills of reading rate or fluency, reading comprehension, accu-
rate or fluent calculation, and accurate math reasoning would be coded and recorded as
315.00 (F81.0) specific learning disorder with impairment in reading, with impairment in
reading rate or fluency and impairment in reading comprehension; 315.1 (F81.2) specific
learning disorder with impairment in mathematics, with impairment in accurate or fluent
calculation and impairment in accurate math reasoning.
Diagnostic Features
Specific learning disorder is a neurodevelopmental disorder with a biological origin that is
the basis for abnormalities at a cognitive level that are associated with the behavioral signs
of the disorder. The biological origin includes an interaction of genetic, epigenetic, and en-
vironmental factors, which affect the brain’s ability to perceive or process verbal or non-
verbal information efficiently and accurately.
One essential feature of specific learning disorder is persistent difficulties learning key-
stone academic skills (Criterion A), with onset during the years of formal schooling (i.e., the de-
velopmental period). Key academic skills include reading of single words accurately and
fluently, reading comprehension, written expression and spelling, arithmetic calculation, and
mathematical reasoning (solving mathematical problems). In contrast to talking or walking,
which are acquired developmental milestones that emerge with brain maturation, academic
skills (e.g., reading, spelling, writing, mathematics) have to be taught and learned explicitly.
Specific learning disorder disrupts the normal pattern of learning academic skills; it is not sim-
ply a consequence of lack of opportunity of learning or inadequate instruction. Difficulties
mastering these key academic skills may also impede learning in other academic subjects (e.g.,
history, science, social studies), but those problems are attributable to difficulties learning the
underlying academic skills. Difficulties learning to map letters with the sounds of one’s lan-
guage—to read printed words (often called dyslexia)—is one of the most common manifesta-
tions of specific learning disorder. The learning difficulties manifest as a range of observable,
descriptive behaviors or symptoms (as listed in Criteria A1-A6). These clinical symptoms may
be observed, probed by means of the clinical interview, or ascertained from school reports, rat-
ing scales, or descriptions in previous educational or psychological assessments. The learning
difficulties are persistent, not transitory. In children and adolescents, persistence is defined as
restricted progress in learning (i.e., no evidence that the individual is catching up with class-
mates) for at least 6 months despite the provision of extra help at home or school. For example,
difficulties learning to read single words that do not fully or rapidly remit with the provision of
instruction in phonological skills or word identification strategies may indicate a specific
Specific Learning Disorder 69
learning disorder. Evidence of persistent learning difficulties may be derived from cumulative
school reports, portfolios of the child’s evaluated work, curriculum-based measures, or clinical
interview. In adults, persistent difficulty refers to ongoing difficulties in literacy or numeracy
skills that manifest during childhood or adolescence, as indicated by cumulative evidence
from school reports, evaluated portfolios of work, or previous assessments.
A second key feature is that the individual’s performance of the affected academic skills is
well below average for age (Criterion B). One robust clinical indicator of difficulties learning
academic skills is low academic achievement for age or average achievement that is sustain-
able only by extraordinarily high levels of effort or support. In children, the low academic skills
cause significant interference in school performance (as indicated by school reports and
teacher's grades or ratings). Another clinical indicator, particularly in adults, is avoidance of
activities that require the academic skills. Also in adulthood, low academic skills interfere with
occupational performance or everyday activities requiring those skills (as indicated by self-re-
port or report by others). However, this criterion also requires psychometric evidence from an
individually administered, psychometrically sound and culturally appropriate test of aca-
demic achievement that is norm-referenced or criterion-referenced. Academic skills are dis-
tributed along a continuum, so there is no natural cutpoint that can be used to differentiate
individuals with and without specific learning disorder. Thus, any threshold used to specify
what constitutes significantly low academic achievement (e.g., academic skills well below age
expectation) is to a large extent arbitrary. Low achievement scores on one or more standard-
ized tests or subtests within an academic domain (i.e., at least 1.5 standard deviations [SD] be-
low the population mean for age, which translates to a standard score of 78 or less, which is
below the 7th percentile) are needed for the greatest diagnostic certainty. However, precise
scores will vary according to the particular standardized tests that are used. On the basis of
clinical judgment, a more lenient threshold may be used (e.g., 1.0-2.5 SD below the pop-
ulation mean for age), when learning difficulties are supported by converging evidence
from clinical assessment, academic history, school reports, or test scores. Moreover, since
standardized tests are not available in all languages, the diagnosis may then be based in
part on clinical judgment of scores on available test measures.
A third core feature is that the learning difficulties are readily apparent in the early
school years in most individuals (Criterion C). However, in others, the learning difficulties
may not manifest fully until later school years, by which time learning demands have in-
creased and exceed the individual's limited capacities.
Another key diagnostic feature is that the learning difficulties are considered “spe-
cific,” for four reasons. First, they are not attributable to intellectual disabilities (intellec-
tual disability [intellectual developmental disorder]); global developmental delay;
hearing or vision disorders, or neurological or motor disorders) (Criterion D). Specific
learning disorder affects learning in individuals who otherwise demonstrate normal lev-
els of intellectual functioning (generally estimated by an IQ score of greater than about 70
[+5 points allowing for measurement error]). The phrase “unexpected academic under-
achievement” is often cited as the defining characteristic of specific learning disorder in
that the specific learning disabilities are not part of a more general learning difficulty as
manifested in intellectual disability or global developmental delay. Specific learning dis-
order may also occur in individuals identified as intellectually “gifted.” These individuals
may be able to sustain apparently adequate academic functioning by using compensatory
strategies, extraordinarily high effort, or support, until the learning demands or assess-
ment procedures (e.g., timed tests) pose barriers to their demonstrating their learning or
accomplishing required tasks. Second, the learning difficulty cannot be attributed to more
general external factors, such as economic or environmental disadvantage, chronic absen-
teeism, or lack of education as typically provided in the individual’s community context.
Third, the learning difficulty cannot be attributed to a neurological (e.g., pediatric stroke)
or motor disorders or to vision or hearing disorders, which are often associated with prob-
lems learning academic skills but are distinguishable by presence of neurological signs.
70 Neurodevelopmental Disorders
Finally, the learning difficulty may be restricted to one academic skill or domain (e.g., read-
ing single words, retrieving or calculating number facts).
Comprehensive assessment is required. Specific learning disorder can only be diagnosed
after formal] education starts but can be diagnosed at any point afterward in children, adoles-
cents, or adults, providing there is evidence of onset during the years of formal schooling (ie.,
the developmental period). No single data source is sufficient for a diagnosis of specific learn-
ing disorder. Rather, specific learning disorder is a clinical diagnosis based on a synthesis of
the individual's medical, developmental, educational, and family history; the history of the
learning difficulty, including its previous and current manifestation; the impact of the diffi-
culty on academic, occupational, or social functioning; previous or current school reports;
portfolios of work requiring academic skills; curriculum-based assessments; and previous or
current scores from individual standardized tests of academic achievement. If an intellectual,
sensory, neurological, or motor disorder is suspected, then the clinical assessment for specific
learning disorder should also include methods appropriate for these disorders. Thus, compre-
hensive assessment will involve professionals with expertise in specific learning disorder and
psychological /cognitive assessment. Since specific learning disorder typically persists into
adulthood, reassessment is rarely necessary, unless indicated by marked changes in the learn-
ing difficulties (amelioration or worsening) or requested for specific purposes.
Associated Features Supporting Diagnosis
Specific learning disorder is frequently but not invariably preceded, in preschool years, by
delays in attention, language, or motor skills that may persist and co-occur with specific
learning disorder. An uneven profile of abilities is common, such as above-average abili-
ties in drawing, design, and other visuospatial abilities, but slow, effortful, and inaccurate
reading and poor reading comprehension and written expression. Individuals with spe-
cific learning disorder typically (but not invariably) exhibit poor performance on psycho-
logical tests of cognitive processing. However, it remains unclear whether these cognitive
abnormalities are the cause, correlate, or consequence of the learning difficulties. Also, al-
though cognitive deficits associated with difficulties learning to read words are well doc-
umented, those associated with other manifestations of specific learning disorder (e.g.,
reading comprehension, arithmetic computation, written expression) are underspecified
or unknown. Moreover, individuals with similar behavioral symptoms or test scores are
found to have a variety of cognitive deficits, and many of these processing deficits are also
found in other neurodevelopmental disorders (e.g., attention-deficit/hyperactivity disor-
der [ADHD], autistic spectrum disorder, communication disorders, developmental coor-
dination disorder). Thus, assessment of cognitive processing deficits is not required for
diagnostic assessment. Specific learning disorder is associated with increased risk for sui-
cidal ideation and suicide attempts in children, adolescents, and adults.
There are no known biological markers of specific learning disorder. As a group, indi-
viduals with the disorder show circumscribed alterations in cognitive processing and
brain structure and function. Genetic differences are also evident at the group level. But
cognitive testing, neuroimaging, or genetic testing are not useful for diagnosis at this time.
Prevalence
The prevalence of specific learning disorder across the academic domains of reading, writ-
ing, and mathematics is 5%-15% among school-age children across different languages
and cultures. Prevalence in adults is unknown but appears to be approximately 4%.
Development and Course
Onset, recognition, and diagnosis of specific learning disorder usually occurs during the
elementary school years when children are required to learn to read, spell, write, and learn
Specific Learning Disorder 71
mathematics. However, precursors such as language delays or deficits, difficulties in
rhyming or counting, or difficulties with fine motor skills required for writing commonly
occur in early childhood before the start of formal schooling. Manifestations may be be-
havioral (e.g., a reluctance to engage in learning; oppositional behavior). Specific learning
disorder is lifelong, but the course and clinical expression are variable, in part depending
on the interactions among the task demands of the environment, the range and severity of
the individual’s learning difficulties, the individual's learning abilities, comorbidity, and
the available support systems and intervention. Nonetheless, problems with reading flu-
ency and comprehension, spelling, written expression, and numeracy skills in everyday life
typically persist into adulthood.
Changes in manifestation of symptoms occur with age, so that an individual may have
a persistent or shifting array of learning difficulties across the lifespan.
Examples of symptoms that may be observed among preschool-age children include a lack
of interest in playing games with language sounds (e.g., repetition, rhyming), and they may
have trouble learning nursery rhymes. Preschool children with specific learning disorder may
frequently use baby talk, mispronounce words, and have trouble remembering names of let-
ters, numbers, or days of the week. They may fail to recognize letters in their own names and.
have trouble learning to count. Kindergarten-age children with specific learning disorder may
be unable to recognize and write letters, may be unable to write their own names, or may use
invented spelling. They may have trouble breaking down spoken words into syllables (e.g.,
“cowboy” into “cow” and “boy”) and trouble recognizing words that rhyme (e.g., cat, bat, hat).
Kindergarten-age children also may have trouble connecting letters with their sounds (e.g, let-
ter b makes the sound /b/) and may be unable to recognize phonemes (e.g., do not know
which in a set of words [e.g., dog, man, car] starts with the same sound as “cat”).
Specific learning disorder in elementary school-age children typically manifests as
marked difficulty learning letter-sound correspondence (particularly in English-speaking
children), fluent word decoding, spelling, or math facts; reading aloud is slow, inaccurate,
and effortful, and some children struggle to understand the magnitude that a spoken or
written number represents. Children in primary grades (grades 1-3) may continue to have
problems recognizing and manipulating phonemes, be unable to read common one-sylla-
ble words (such as mat or top), and be unable recognize common irregularly spelled
words (e.g., said, two). They may commit reading errors that indicate problems in con-
necting sounds and letters (e.g., “big” for “got”) and have difficulty sequencing numbers
and letters. Children in grades 1-3 also may have difficulty remembering number facts or
arithmetic procedures for adding, subtracting, and so forth, and may complain that read-
ing or arithmetic is hard and avoid doing it. Children with specific learning disorder in the
middle grades (grades 4-6) may mispronounce or skip parts of long, multisyllable words
{e.g., say “conible” for “convertible,” “aminal” for “animal”) and confuse words that
sound alike (e.g., “tornado” for “volcano”). They may have trouble remembering dates,
names, and telephone numbers and may have trouble completing homework or tests on
time. Children in the middle grades also may have poor comprehension with or without
slow, effortful, and inaccurate reading, and they may have trouble reading small function
words (e.g., that, the, an, in). They may have very poor spelling and poor written work.
They may get the first part of a word correctly, then guess wildly (e.g., read “clover” as
“clock”), and may express fear of reading aloud or refuse to read aloud.
By contrast, adolescents may have mastered word decoding, but reading remains slow
and effortful, and they are likely to show marked problems in reading comprehension and
written expression (including poor spelling) and poor mastery of math facts or mathemat-
ical problem solving. During adolescence and into adulthood, individuals with specific
learning disorder may continue to make numerous spelling mistakes and read single
words and connected text slowly and with much effort, with trouble pronouncing multi-
syllable words. They may frequently need to reread material to understand or get the main
point and have trouble making inferences from written text. Adolescents and adults may
72 Neurodevelopmental Disorders
avoid activities that demand reading or arithmetic (reading for pleasure, reading instruc-
tions). Adults with specific learning disorder have ongoing spelling problems, slow and
effortful reading, or problems making important inferences from numerical information
in work-related written documents. They may avoid both leisure and work-related activ-
ities that demand reading or writing or use alternative approaches to access print (e.g.,
text-to-speech/speech-to-text software, audiobooks, audiovisual media).
An alternative clinical expression is that of circumscribed learning difficulties that per-
sist across the lifespan, such as an inability to master the basic sense of number (e.g., to
know which of a pair of numbers or dots represents the larger magnitude), or lack of pro-
ficiency in word identification or spelling. Avoidance of or reluctance to engage in activi-
ties requiring academic skills is common in children, adolescents, and adults. Episodes of
severe anxiety or anxiety disorders, including somatic complaints or panic attacks, are
common across the lifespan and accompany both the circumscribed and the broader ex-
pression of learning difficulties.
Risk and Prognostic Factors
Environmental. Prematurity or very low birth weight increases the risk for specific
learning disorder, as does prenatal exposure to nicotine.
Genetic and physiological. Specific learning disorder appears to aggregate in families,
particularly when affecting reading, mathematics, and spelling. The relative risk of spe-
cific learning disorder in reading or mathematics is substantially higher (e.g., 4-8 times
and 5-10 times higher, respectively) in first-degree relatives of individuals with these
learning difficulties compared with those without them. Family history of reading diffi-
culties (dyslexia) and parental literacy skills predict literacy problems or specific learning
disorder in offspring, indicating the combined role of genetic and environmental factors.
There is high heritability for both reading ability and reading disability in alphabetic and
nonalphabetic languages, including high heritability for most manifestations of learning abil-
ities and disabilities (e.g., heritability estimate values greater than 0.6). Covariation between
various manifestations of learning difficulties is high, suggesting that genes related to one
presentation are highly correlated with genes related to another manifestation.
Course modifiers. Marked problems with inattentive behavior in preschool years is pre-
dictive of later difficulties in reading and mathematics (but not necessarily specific learn-
ing disorder) and nonresponse to effective academic interventions. Delay or disorders in
speech or language, or impaired cognitive processing (e.g., phonological awareness,
working memory, rapid serial naming) in preschool years, predicts later specific learning
disorder in reading and written expression. Comorbidity with ADHD is predictive of
worse mental health outcome than that associated with specific learning disorder without
ADHD. Systematic, intensive, individualized instruction, using evidence-based interven-
tions, may improve or ameliorate the learning difficulties in some individuals or promote
the use of compensatory strategies in others, thereby mitigating the otherwise poor out-
comes.
Culture-Related Diagnostic Issues
Specific learning disorder occurs across languages, cultures, races, and socioeconomic
conditions but may vary in its manifestation according to the nature of the spoken and
written symbol systems and cultural and educational practices. For example, the cognitive
processing requirements of reading and of working with numbers vary greatly across or-
thographies. In the English language, the observable hallmark clinical symptom of diffi-
culties learning to read is inaccurate and slow reading of single words; in other alphabetic
languages that have more direct mapping between sounds and letters (e.g., Spanish, Ger-
man) and in non-alphabetic languages (e.g., Chinese, Japanese), the hallmark feature is
Specific Learning Disorder 73
slow but accurate reading. In English-language learners, assessment should include con-
sideration of whether the source of reading difficulties is a limited proficiency with Eng-
lish or a specific learning disorder. Risk factors for specific learning disorder in English-
language learners include a family history of specific learning disorder or language delay
in the native language, as well as learning difficulties in English and failure to catch up
with peers. If there is suspicion of cultural or language differences (e.g., as in an English-
language learner), the assessment needs to take into account the individual's language
proficiency in his or her first or native language as well as in the second language (in this
example, English). Also, assessment should consider the linguistic and cultural context in
which the individual is living, as well as his or her educational and learning history in the
original culture and language.
Gender-Related Diagnostic Issues
Specific learning disorder is more common in males than in females (ratios range from
about 2:1 to 3:1) and cannot be attributed to factors such as ascertainment bias, definitional
or measurement variation, language, race, or socioeconomic status.
Functionai Consequences of
Specific Learning Disorder
Specific learning disorder can have negative functional consequences across the lifespan,
including lower academic attainment, higher rates of high school dropout, lower rates of
postsecondary education, high levels of psychological distress and poorer overall mental
health, higher rates of unemployment and under-employment, and lower incomes. School
dropout and co-occurring depressive symptoms increase the risk for poor mental health
outcomes, including suicidality, whereas high levels of social or emotional support predict
better mental health outcomes.
Differential Diagnosis
Normal variations in academic attainment. Specific learning disorder is distinguished
from normal variations in academic attainment due to external factors (e.g., lack of edu-
cational opportunity, consistently poor instruction, learning in a second language), be-
cause the learning difficulties persist in the presence of adequate educational opportunity
and exposure to the same instruction as the peer group, and competency in the language of
instruction, even when it is different from one’s primary spoken language.
Intellectual disability (intellectual developmental disorder). Specific learning disorder
differs from general learning difficulties associated with intellectual disability, because the
learning difficulties occur in the presence of normal levels of intellectual functioning (ie.,
IQ score of at least 70 + 5). If intellectual disability is present, specific learning disorder can
be diagnosed only when the learning difficulties are in excess of those usually associated
with the intellectual disability.
Learning difficulties due to neurological or sensory disorders. Specific learning dis-
order is distinguished from learning difficulties due to neurological or sensory disorders
(e.g., pediatric stroke, traumatic brain injury, hearing impairment, vision impairment), be-
cause in these cases there are abnormal findings on neurological examination.
Neurocognitive disorders. Specific learning disorder is distinguished from learning
problems associated with neurodegenerative cognitive disorders, because in specific
learning disorder the clinical expression of specific learning difficulties occurs during the
developmental period, and the difficulties do not manifest as a marked decline from a for-
mer state.
74 Neurodevelopmental Disorders
Attention-deficit/hyperactivity disorder. Specific learning disorder is distinguished from
the poor academic performance associated with ADHD, because in the latter condition the
problems may not necessarily reflect specific difficulties in learning academic skills but
rather may reflect difficulties in performing those skills. However, the co-occurrence of
specific learning disorder and ADHD is more frequent than expected by chance. If criteria
for both disorders are met, both diagnoses can be given.
Psychotic disorders. Specific learning disorder is distinguished from the academic and
cognitive-processing difficulties associated with schizophrenia or psychosis, because with
these disorders there is a decline (often rapid) in these functional domains.
Comorbidity
Specific learning disorder commonly co-occurs with neurodevelopmental (e.g., ADHD,
communication disorders, developmental coordination disorder, autistic spectrum disor-
der) or other mental! disorders (e.g., anxiety disorders, depressive and bipolar disorders).
These comorbidities do not necessarily exclude the diagnosis specific learning disorder
but may make testing and differential diagnosis more difficult, because each of the co-
occurring disorders independently interferes with the execution of activities of daily liv-
ing, including learning. Thus, clinical judgment is required to attribute such impairment to
learning difficulties. If there is an indication that another diagnosis could account for the
difficulties learning keystone academic skills described in Criterion A, specific learning
disorder should not be diagnosed.
Motor Disorders
Developmental Coordination Disorder
Diagnostic Criteria 315.4 (F82)
A. The acquisition and execution of coordinated motor skills is substantially below that ex-
pected given the individual’s chronological age and opportunity for skill learning and
use. Difficulties are manifested as clumsiness (e.g., dropping or bumping into objects)
as well as slowness and inaccuracy of performance of motor skills {e.g., catching an
object, using scissors or cutlery, handwriting, riding a bike, or participating in sports).
B. The motor skills deficit in Criterion A significantly and persistently interferes with activ-
ities of daily living appropriate to chronological age (e.g., self-care and self-mainte-
nance) and impacts academic/school productivity, prevocational and vocational
activities, leisure, and play.
C. Onset of symptoms is in the early developmental period.
D. The motor skills deficits are not better explained by intellectual disability (intellectual devel-
opmental disorder) or visual impairment and are not attributable to a neurological condi-
tion affecting movement (e.g., cerebral palsy, muscular dystrophy, degenerative disorder).
Diagnostic Features
The diagnosis of developmental coordination disorder is made by a clinical synthesis of the
history (developmental and medical), physical examination, school or workplace report, and
individual assessment using psychometrically sound and culturally appropriate standardized
tests. The manifestation of impaired skills requiring motor coordination (Criterion A) varies
Developmental Coordination Disorder 75
with age. Young children may be delayed in achieving motor milestones (i.e., sitting, crawling,
walking), although many achieve typical motor milestones. They also may be delayed in de-
veloping skills such as negotiating stairs, pedaling, buttoning shirts, completing puzzles, and
using zippers. Even when the skill is achieved, movement execution may appear awkward,
slow, or less precise than that of peers. Older children and adults may display slow speed or in-
accuracy with motor aspects of activities such as assembling puzzles, building models, playing
ball games (especially in teams), handwriting, typing, driving, or carrying out self-care skills.
Developmental coordination disorder is diagnosed only if the impairment in motor
skills significantly interferes with the performance of, or participation in, daily activities in
family, social, school, or community life (Criterion B). Examples of such activities include
getting dressed, eating meals with age-appropriate utensils and without mess, engaging
in physical games with others, using specific tools in class such as rulers and scissors, and
participating in team exercise activities at school. Not only is ability to perform these ac-
tions impaired, but also marked slowness in execution is common. Handwriting compe-
tence is frequently affected, consequently affecting legibility and/or speed of written output
and affecting academic achievement (the impact is distinguished from specific learning
difficulty by the emphasis on the motoric component of written output skills). In adults,
everyday skills in education and work, especially those in which speed and accuracy are
required, are affected by coordination problems.
Criterion C states that the onset of symptoms of developmental coordination disorder
must be in the early developmental period. However, developmental coordination disorder is
typically not diagnosed before age 5 years because there is considerable variation in the age at
acquisition of many motor skills or a lack of stability of measurement in early childhood (e.g.,
some children catch up) or because other causes of motor delay may not have fully manifested.
Criterion D specifies that the diagnosis of developmental coordination disorder is
made if the coordination difficulties are not better explained by visual impairment or at-
tributable to a neurological condition. Thus, visual function examination and neurological
examination must be included in the diagnostic evaluation. If intellectual disability (intel-
lectual developmental disorder) is present, the motor difficulties are in excess of those ex-
pected for the mental age; however, no IQ cut-off or discrepancy criterion is specified.
Developmental coordination disorder does not have discrete subtypes; however, indi-
viduals may be impaired predominantly in gross motor skills or in fine motor skills, in-
cluding handwriting skills.
Other terms used to describe developmental coordination disorder include childhood
dyspraxia, specific developmental disorder of motor function, and clumsy child syndrome.
Associated Features Supporting Diagnosis
Some children with developmental coordination disorder show additional] (usually sup-
pressed) motor activity, such as choreiform movements of unsupported limbs or mirror
movements. These “overflow” movements are referred to as neurodevelopmental immaturities or
neurological soft signs rather than neurological abnormalities. In both current literature and
clinical practice, their role in diagnosis is still unclear, requiring further evaluation.
Prevaience
The prevalence of developmental coordination disorder in children ages 5-11 years is 5%—
6% (in children age 7 years, 1.8% are diagnosed with severe developmental coordination
disorder and 3% with probable developmental coordination disorder). Males are more of-
ten affected than females, with a male:female ratio between 2:1 and 7:1.
Development and Course
The course of developmental coordination disorder is variable but stable at least to 1 year
follow-up. Although there may be improvement in the longer term, problems with coor-
76 Neurodevelopmental Disorders
dinated movements continue through adolescence in an estimated 50%-70% of children.
Onset is in early childhood. Delayed motor milestones may be the first signs, or the disor-
der is first recognized when the child attempts tasks such as holding a knife and fork, but-
toning clothes, or playing ball games. In middle childhood, there are difficulties with
motor aspects of assembling puzzles, building models, playing ball, and handwriting, as
well as with organizing belongings, when motor sequencing and coordination are re-
quired. In early adulthood, there is continuing difficulty in learning new tasks involving
complex/automatic motor skills, including driving and using tools. Inability to take notes
and handwrite quickly may affect performance in the workplace. Co-occurrence with
other disorders (see the section “Comorbidity” for this disorder) has an additional impact
on presentation, course, and outcome.
Risk and Prognostic Factors
Environmental. Developmental coordination disorder is more common following pre-
natal exposure to alcohol and in preterm and low-birth-weight children.
Genetic and physiological. Impairments in underlying neurodevelopmental processes—
particularly in visual-motor skills, both in visual-motor perception and spatial mentalizing—
have been found and affect the ability to make rapid motoric adjustments as the complexity of
the required movements increases. Cerebellar dysfunction has been proposed, but the neural
basis of developmental coordination disorder remains unclear. Because of the co-occurrence of
developmental coordination disorder with attention-deficit /hyperactivity disorder (ADHD),
specific learning disabilities, and autism spectrum disorder, shared genetic effect has been pro-
posed. However, consistent co-occurrence in twins appears only in severe cases.
Course modifiers. Individuals with ADHD and with developmental coordination dis-
order demonstrate more impairment than individuals with ADHD without developmen-
tal coordination disorder.
Culture-Related Diagnostic Issues
Developmental coordination disorder occurs across cultures, races, and socioeconomic
conditions. By definition, “activities of daily living” implies cultural differences necessi-
tating consideration of the context in which the individual child is living as well as
whether he or she has had appropriate opportunities to learn and practice such activities.
Functional Consequences of
Developmental Coordination Disorder
Developmental coordination disorder leads to impaired functional performance in activ-
ities of daily living (Criterion B), and the impairment is increased with co-occurring con-
ditions. Consequences of developmental coordination disorder include reduced
participation in team play and sports; poor self-esteem and sense of self-worth; emotional
or behavior problems; impaired academic achievement; poor physical fitness; and re-
duced physical activity and obesity.
Differential Diagnosis
Motor impairments due to another medical condition. Problems in coordination may
be associated with visual function impairment and specific neurological disorders (e.g.,
cerebral palsy, progressive lesions of the cerebellum, neuromuscular disorders). In such
cases, there are additional findings on neurological examination.
Intellectual disability (intellectual developmental disorder). If intellectual disability is
present, motor competences may be impaired in accordance with the intellectual disabil-
Stereotypic Movement Disorder 77
ity. However, if the motor difficulties are in excess of what could be accounted for by the
intellectual disability, and criteria for developmental coordination disorder are met, de-
velopmental coordination disorder can be diagnosed as well.
Attention-deficit/hyperactivity disorder. Individuals with ADHD may fall, bump into
objects, or knock things over. Careful observation across different contexts is required to
ascertain if lack of motor competence is attributable to distractibility and impulsiveness
rather than to developmental coordination disorder. If criteria for both ADHD and devel-
opmental coordination disorder are met, both diagnoses can be given.
Autism spectrum disorder. Individuals with autism spectrum disorder may be uninter-
ested in participating in tasks requiring complex coordination skills, such as ball sports,
which will affect test performance and function but not reflect core motor competence. Co-
occurrence of developmental coordination disorder and autism spectrum disorder is com-
mon. If criteria for both disorders are met, both diagnoses can be given.
Joint hypermobility syndrome. Individuals with syndromes causing hyperextensible
joints (found on physical examination; often with a complaint of pain) may present with
symptoms similar to those of developmental coordination disorder.
Comorbidity
Disorders that commonly co-occur with developmental coordination disorder include
speech and language disorder; specific learning disorder (especially reading and writing);
problems of inattention, including ADHD (the most frequent coexisting condition, with
about 50% co-occurrence); autism spectrum disorder; disruptive and emotional behavior
problems; and joint hypermobility syndrome. Different clusters of co-occurrence may be
present (e.g., a cluster with severe reading disorders, fine motor problems, and handwriting
problems; another cluster with impaired movement control and motor planning). Presence
of other disorders does not exclude developmental coordination disorder but may make
testing more difficult and may independently interfere with the execution of activities of
daily living, thus requiring examiner judgment in ascribing impairment to motor skills.
Stereotypic Movement Disorder
Diagnostic Criteria 307.3 (F98.4)
A. Repetitive, seemingly driven, and apparently purposeless motor behavior (e.g., hand
shaking or waving, body rocking, head banging, self-biting, hitting own body).
B. The repetitive motor behavior interferes with social, academic, or other activities and
may result in self-injury.
C. Onset is in the early developmental period.
D. The repetitive motor behavior is not attributable to the physiological effects of a sub-
stance or neurological condition and is not better explained by another neurodevel-
opmental or mental disorder (e.g., trichotillomania [hair-pulling disorder), obsessive-
compulsive disorder).
Specify if:
With self-injurious behavior (or behavior that would result in an injury if preventive
measures were not used)
Without self-injurious behavior
Specify if:
Associated with a known medical or genetic condition, neurodevelopmental dis-
order, or environmental factor (e.g., Lesch-Nyhan syndrome, intellectual disability
[intellectual developmental disorder], intrauterine alcohol exposure)
78 Neurodevelopmental Disorders
Coding note: Use additional code to identify the associated medical or genetic
condition, or neurodevelopmental disorder.
Specify current severity:
Mild: Symptoms are easily suppressed by sensory stimulus or distraction.
Moderate: Symptoms require explicit protective measures and behavioral modification.
Severe: Continuous monitoring and protective measures are required to prevent seri-
ous injury.
Recording Procedures
For stereotypic movement disorder that is associated with a known medical or genetic
condition, neurodevelopmental disorder, or environmental factor, record stereotypic
movement disorder associated with (name of condition, disorder, or factor) (e.g., stereo-
typic movement disorder associated with Lesch-Nyhan syndrome).
Specifiers
The severity of non-self-injurious stereotypic movements ranges from mild presentations
that are easily suppressed by a sensory stimulus or distraction to continuous movements
that markedly interfere with all activities of daily living. Self-injurious behaviors range in se-
verity along various dimensions, including the frequency, impact on adaptive functioning,
and severity of bodily injury (from mild bruising or erythema from hitting hand against
body, to lacerations or amputation of digits, to retinal detachment from head banging).
Diagnostic Features
The essential feature of stereotypic movement disorder is repetitive, seemingly driven,
and apparently purposeless motor behavior (Criterion A). These behaviors are often
rhythmical movements of the head, hands, or body without obvious adaptive function.
The movements may or may not respond to efforts to stop them. Among typically devel-
oping children, the repetitive movements may be stopped when attention is directed to
them or when the child is distracted from performing them. Among children with neuro-
developmental disorders, the behaviors are typically less responsive to such efforts. In
other cases, the individual demonstrates self-restraining behaviors (e.g., sitting on hands,
wrapping arms in clothing, finding a protective device).
The repertoire of behaviors is variable; each individual presents with his or her own in-
dividually patterned, “signature” behavior. Examples of non-self-injurious stereotypic
movements include, but are not limited to, body rocking, bilateral flapping or rotating
hand movements, flicking or fluttering fingers in front of the face, arm waving or flapping,
and head nodding. Stereotyped self-injurious behaviors include, but are not limited to, re-
petitive head banging, face slapping, eye poking, and biting of hands, lips, or other body
parts. Eye poking is particularly concerning; it occurs more frequently among children
with visual impairment. Multiple movements may be combined (e.g., cocking the head,
rocking the torso, waving a small string repetitively in front of the face).
Stereotypic movements may occur many times during a day, lasting a few seconds to
several minutes or longer. Frequency can vary from many occurrences in a single day to
several weeks elapsing between episodes. The behaviors vary in context, occurring when
the individual is engrossed in other activities, when excited, stressed, fatigued, or bored.
Criterion A requires that the movements be “apparently” purposeless. However, some
functions may be served by the movements. For example, stereotypic movements might
reduce anxiety in response to external stressors.
Criterion B states that the stereotypic movements interfere with social, academic, or
other activities and, in some children, may result in self-injury (or would if protective mea-
sures were not used). If self-injury is present, it should be coded using the specifier. Onset
Stereotypic Movement Disorder 79
of stereotypic movements is in the early developmental period (Criterion C). Criterion D
states that the repetitive, stereotyped behavior in stereotypic movement disorder is not at-
tributable to the physiological effects of a substance or neurological condition and is not
better explained by another neurodevelopmental or mental disorder. The presence of
stereotypic movements may indicate an undetected neurodevelopmental problem, espe-
cially in children ages 1-3 years.
Prevalence
Simple stereotypic movements (e.g., rocking) are common in young typically developing chil-
dren. Complex stereotypic movements are much less common (occurring in approximately
3% 4%). Between 4% and 16% of individuals with intellectual disability (intellectual develop-
mental disorder) engage in stereotypy and self-injury. The risk is greater in individuals with
severe intellectual disability. Among individuals with intellectual disability living in res-
idential facilities, 10%-15% may have stereotypic movement disorder with self-injury.
Development and Course
Stereotypic movements typically begin within the first 3 years of life. Simple stereotypic move-
ments are common in infancy and may be involved in acquisition of motor mastery. In chil-
dren who develop complex motor stereotypies, approximately 80% exhibit symptoms before
24 months of age, 12% between 24 and 35 months, and 8% at 36 months or older. In mast typ-
ically developing children, these movements resolve over time or can be suppressed. Onset of
complex motor stereotypies may be in infancy or later in the developmental period. Among
individuals with intellectual disability, the stereotyped, self-injurious behaviors may persist
for years, even though the typography or pattern of self-injury may change.
Risk and Prognostic Factors
Environmental. Social isolation is a risk factor for self-stimulation that may progress to
stereotypic movements with repetitive self-injury. Environmental stress may also trigger
stereotypic behavior. Fear may alter physiological state, resulting in increased frequency
of stereotypic behaviors.
Genetic and physiological. Lower cognitive functioning is linked to greater risk for stereo-
typic behaviors and poorer response to interventions. Stereotypic movements are more fre-
quent among individuals with moderate-to-severe/ profound intellectual disability, who by
virtue of a particular syndrome (e.g., Rett syndrome) or environmental factor (e.g., an environ-
ment with relatively insufficient stimulation) seem to be at higher risk for stereotypies. Repet-
itive self-injurious behavior may be a behavioral phenotype in neurogenetic syndromes. For
example, in Lesch-Nyhan syndrome, there are both stereotypic dystonic movements and self-
mutilation of fingers, lip biting, and other forms of self-injury unless the individual is re-
strained, and in Rett syndrome and Cornelia de Lange syndrome, self-injury may result from
the hand-to-mouth stereotypies. Stereotypic behaviors may result from a painful medical con-
dition (e.g., middle ear infection, dental problems, gastroesophageal reflux).
Culture-Related Diagnostic Issues
Stereotypic movement disorder, with or without self-injury, occurs in all races and cultures.
Cultural attitudes toward unusual behaviors may result in delayed diagnosis. Overall cultural
tolerance and attitudes toward stereotypic movement vary and must be considered.
Differential Diagnosis
Normal development. Simple stereotypic movements are common in infancy and early
childhood. Rocking may occur in the transition from sleep to awake, a behavior that usu-
80 Neurodevelopmental Disorders
ally resolves with age. Complex stereotypies are less common in typically developing
children and can usually be suppressed by distraction or sensory stimulation. The indi-
vidual’s daily routine is rarely affected, and the movements generally do not cause the
child distress. The diagnosis would not be appropriate in these circumstances.
Autism spectrum disorder. Stereotypic movements may be a presenting symptom of
autism spectrum disorder and should be considered when repetitive movements and be-
haviors are being evaluated. Deficits of social communication and reciprocity manifesting
in autism spectrum disorder are generally absent in stereotypic movement disorder, and
thus social interaction, social communication, and rigid repetitive behaviors and interests
are distinguishing features. When autism spectrum disorder is present, stereotypic move-
ment disorder is diagnosed only when there is self-injury or when the stereotypic behav-
iors are sufficiently severe to become a focus of treatment.
Tic disorders. Typically, stereotypies have an earlier age at onset (before 3 years) than
do tics, which have a mean age at onset of 5-7 years. They are consistent and fixed in their
pattern or topography compared with tics, which are variable in their presentation. Ste-
reotypies may involve arms, hands, or the entire body, while tics commonly involve eyes,
face, head, and shoulders. Stereotypies are more fixed, rhythmic, and prolonged in dura-
tion than tics, which, generally, are brief, rapid, random, and fluctuating. Tics and stereo-
typic movements are both reduced by distraction.
Obsessive-compulsive and related disorders. Stereotypic movement disorder is dis-
tinguished from obsessive-compulsive disorder (OCD) by the absence of obsessions, as
well as by the nature of the repetitive behaviors. In OCD the individual feels driven to per-
form repetitive behaviors in response to an obsession or according to rules that must be ap-
plied rigidly, whereas in stereotypic movement disorder the behaviors are seemingly
driven but apparently purposeless. Trichotillomania (hair-pulling disorder) and excoria-
tion (skin-picking) disorder are characterized by body-focused repetitive behaviors (i.e.,
hair pulling and skin picking) that may be seemingly driven but that are not apparently
purposeless, and that may not be patterned or rhythmical. Furthermore, onset in tricho-
tillomania and excoriation disorder is not typically in the early developmental period, but
rather around puberty or later.
Other neurological and medical conditions. The diagnosis of stereotypic movements
requires the exclusion of habits, mannerisms, paroxysmal dyskinesias, and benign he-
reditary chorea. A neurological history and examination are required to assess features
suggestive of other disorders, such as myoclonus, dystonia, tics, and chorea. Involuntary
movements associated with a neurological condition may be distinguished by their signs
and symptoms. For example, repetitive, stereotypic movements in tardive dyskinesia can
be distinguished by a history of chronic neuroleptic use and characteristic oral or facial
dyskinesia or irregular trunk or limb movements. These types of movements do not result
in self-injury. A diagnosis of stereotypic movement disorder is not appropriate for repet-
itive skin picking or scratching associated with amphetamine intoxication or abuse (e.g.,
patients are diagnosed with substance /medication-induced obsessive-compulsive and re-
lated disorder) and repetitive choreoathetoid movements associated with other neurolog-
ical disorders.
Comorbidity
Stereotypic movement disorder may occur as a primary diagnosis or secondary to another
disorder. For example, stereotypies are a common manifestation of a variety of neuro-
genetic disorders, such as Lesch-Nyhan syndrome, Rett syndrome, fragile X syndrome,
Cornelia de Lange syndrome, and Smith-Magenis syndrome. When stereotypic move-
ment disorder co-occurs with another medical condition, both should be coded.
Tic Disorders 81
Tic Disorders
Diagnostic Criteria
Note: A tic is a sudden, rapid, recurrent, nonrhythmic motor movement or vocalization.
Tourette’s Disorder 307.23 (F95.2)
A. Both multiple motor and one or more vocal tics have been present at some time during
the illness, although not necessarily concurrently.
B. The tics may wax and wane in frequency but have persisted for more than 1 year since
first tic onset.
C. Onset is before age 18 years.
D. The disturbance is not attributable to the physiological effects of a substance (e.g., co-
caine) or another medical condition (e.g., Huntington’s disease, postviral encephalitis).
Persistent (Chronic) Motor or Vocal Tic Disorder 307.22 (F95.1)
A. Single or multiple motor or vocal tics have been present during the illness, but not both
motor and vocal.
B. The tics may wax and wane in frequency but have persisted for more than 1 year since
first tic onset.
C. Onset is before age 18 years.
D. The disturbance is not attributable to the physiological effects of a substance (e.g., co-
caine) or another medical condition (e.g., Huntington’s disease, postviral encephalitis).
E. Criteria have never been met for Tourette’s disorder.
Specify if:
With motor tics only
With vocal tics only
Provisional Tic Disorder 307.21 (F95.0)
A. Single or multiple motor and/or vocal tics.
B. The tics have been present for less than 1 year since first tic onset.
C. Onset is before age 18 years.
D. The disturbance is not attributable to the physiological effects of a substance (e.g., co-
caine} or another medical condition (e.g., Huntington’s disease, postviral encephalitis).
E. Criteria have never been met for Tourette’s disorder or persistent (chronic) motor or
vocal tic disorder.
Specifiers
The “motor tics only” or “vocal tics only” specifier is only required for persistent (chronic)
motor or vocal tic disorder.
Diagnostic Features
Tic disorders comprise four diagnostic categories: Tourette’s disorder, persistent (chronic)
motor or vocal tic disorder, provisional tic disorder, and the other specified and unspecified
tic disorders, Diagnosis for any tic disorder is based on the presence of motor and/or vocal
tics (Criterion A), duration of tic symptoms (Criterion B), age at onset (Criterion C), and ab-
sence of any known cause such as another medical condition or substance use (Criterion D).
The tic disorders are hierarchical in order (i-e., Tourette’s disorder, followed by persistent
[chronic] motor or vocal tic disorder, followed by provisional tic disorder, followed by the
82 Neurodevelopmental Disorders
other specified and unspecified tic disorders), such that once a tic disorder at one level of the
hierarchy is diagnosed, a lower hierarchy diagnosis cannot be made (Criterion E).
Tics are sudden, rapid, recurrent, nonrhythmic motor movements or vocalizations. An
individual may have various tic symptoms over time, but at any point in time, the tic rep-
ertoire recurs in a characteristic fashion. Although tics can include almost any muscle group
or vocalization, certain tic symptoms, such as eye blinking or throat clearing, are common
across patient populations. Tics are generally experienced as involuntary but can be vol-
untarily suppressed for varying lengths of time.
Tics can be either simple or complex. Simple motor tics are of short duration (i.e., milli-
seconds) and can include eye blinking, shoulder shrugging, and extension of the extrem-
ities. Simple vocal tics include throat clearing, sniffing, and grunting often caused by
contraction of the diaphragm or muscles of the oropharynx. Complex motor tics are of lon-
ger duration (i.e., seconds) and often include a combination of simple tics such as simul-
taneous head turning and shoulder shrugging. Complex tics can appear purposeful, such
as a tic-like sexual or obscene gesture (copropraxia) or a tic-like imitation of someone else’s
movements (echopraxia). Similarly, complex vocal tics include repeating one’s own sounds
or words (palilalia), repeating the last-heard word or phrase (echolalia), or uttering socially
unacceptable words, including obscenities, or ethnic, racial, or religious slurs (coprolalia).
Importantly, coprolalia is an abrupt, sharp bark or grunt utterance and lacks the prosody
of similar inappropriate speech observed in human interactions.
The presence of motor and/or vocal tics varies across the four tic disorders (Criterion
A). For Tourette’s disorder, both motor and vocal tics must be present, whereas for per-
sistent (chronic) motor or vocal tic disorder, only motor or only vocal tics are present. For
provisional tic disorder, motor and/or vocal tics may be present. For other specified or un-
specified tic disorders, the movement disorder symptoms are best characterized as tics but
are atypical in presentation or age at onset, or have a known etiology.
The 1-year minimum duration criterion (Criterion B) assures that individuals diag-
nosed with either Tourette’s disorder or persistent (chronic) motor or vocal tic disorder
have had persistent symptoms. Tics wax and wane in severity, and some individuals may
have tic-free periods of weeks to months; however, an individual who has had tic symp-
toms of greater than 1 year’s duration since first tic onset would be considered to have per-
sistent symptoms regardless of duration of tic-free periods. For an individual with motor
and/or vocal tics of less than 1 year since first tic onset, a provisional tic disorder diagnosis
can be considered. There is no duration specification for other specified and unspecified tic
disorders. The onset of tics must occur prior to age 18 years (Criterion C). Tic disorders
typically begin in the prepubertal period, with an average age at onset between 4 and 6
years, and with the incidence of new-onset tic disorders decreasing in the teen years. New
onset of tic symptoms in adulthood is exceedingly rare and is often associated with expo-
sures to drugs (e.g., excessive cocaine use) or is a result of a central nervous system insult
(e.g., postviral encephalitis). Although tic onset is uncommon in teenagers and adults, it is
not uncommon for adolescents and adults to present for an initial diagnostic assessment
and, when carefully evaluated, provide a history of milder symptoms dating back to child-
hood. New-onset abnormal movements suggestive of tics outside of the usual age range
should result in evaluation for other movement disorders or for specific etiologies.
Tic symptoms cannot be attributable to the physiological effects of a substance or an-
other medical condition (Criterion D). When there is strong evidence from the history,
physical examination, and/or laboratory results to suggest a plausible, proximal, and
probable cause fora tic disorder, a diagnosis of other specified tic disorder should be used.
Having previously met diagnostic criteria for Tourette’s disorder negates a possible di-
agnosis of persistent (chronic) motor or vocal tic disorder (Criterion E). Similarly, a previ-
ous diagnosis of persistent (chronic) motor or vocal tic disorder negates a diagnosis of
provisional tic disorder or other specified or unspecified tic disorder (Criterion E).
Tic Disorders 83
Prevalence
Tics are common in childhood but transient in most cases. The estimated prevalence of
Tourette’s disorder ranges from 3 to 8 per 1,000 in school-age children. Males are more
commonly affected than females, with the ratio varying from 2:1 to 4:1. A national survey
in the United States estimated 3 per 1,000 for the prevalence of clinically identified cases.
The frequency of identified cases was lower among African Americans and Hispanic
Americans, which may be related to differences in access to care.
Development and Course
Onset of tics is typically between ages 4 and 6 years. Peak severity occurs between ages 10
and 12 years, with a decline in severity during adolescence. Many adults with tic disorders
experience diminished symptoms. A small percentage of individuals will have persis-
tently severe or worsening symptoms in adulthood.
Tic symptoms manifest similarly in all age groups and across the lifespan. Tics wax and
wane in severity and change in affected muscle groups and vocalizations over time. As
children get older, they begin to report their tics being associated with a premonitory
urge—a somatic sensation that precedes the tic—and a feeling of tension reduction follow-
ing the expression of the tic. Tics associated with a premonitory urge may be experienced
as not completely “involuntary” in that the urge and the tic can be resisted. An individual
may also feel the need to perform a tic in a specific way or repeat it until he or she achieves
the feeling that the tic has been done “just right.”
The vulnerability toward developing co-occurring conditions changes as individuals
pass through the age of risk for various co-occurring conditions. For example, prepubertal
children with tic disorders are more likely to experience attention-deficit/hyperactivity
disorder (ADHD), obsessive-compulsive disorder (OCD), and separation anxiety disorder
than are teenagers and adults, who are more likely to experience the new onset of major
depressive disorder, substance use disorder, or bipolar disorder.
Risk and Prognostic Factors
Temperamental. Tics are worsened by anxiety, excitement, and exhaustion and are better
during calm, focused activities. Individuals may have fewer tics when engaged in schoolwork
or tasks at work than when relaxing at home after school or in the evening. Stressful /exciting
events (e.g., taking a test, participating in exciting activities) often make tics worse.
Environmental. Observing a gesture or sound in another person may result in an indi-
vidual with a tic disorder making a similar gesture or sound, which may be incorrectly
perceived by others as purposeful. This can be a particular problem when the individual is
interacting with authority figures (e.g., teachers, supervisors, police).
Genetic and physiological. Genetic and environmental factors influence tic symptom
expression and severity. Important risk alleles for Tourette’s disorder and rare genetic
variants in families with tic disorders have been identified. Obstetrical complications,
older paternal age, lower birth weight, and maternal smoking during pregnancy are as-
sociated with worse tic severity.
Culture-Related Diagnostic Issues
Tic disorders do not appear to vary in clinical characteristics, course, or etiology by race,
ethnicity, and culture. However, race, ethnicity, and culture may impact how tic disorders
are perceived and managed in the family and community, as well as influencing patterns
of help seeking, and choices of treatment.
84 Neurodevelopmental Disorders
Gender-Related Diagnostic Issues
Males are more commonly affected than females, but there are no gender differences in the
kinds of tics, age at onset, or course. Women with persistent tic disorders may be more
likely to experience anxiety and depression.
Functional Consequences of Tic Disorders
Many individuals with mild to moderate tic severity experience no distress or impairment
in functioning and may even be unaware of their tics. Individuals with more severe symp-
toms generally have more impairment in daily living, but even individuals with moderate
or even severe tic disorders may function well. The presence of a co-occurring condition,
such as ADHD or OCD, can have greater impact on functioning. Less commonly, tics dis-
rupt functioning in daily activities and result in social isolation, interpersonal conflict,
peer victimization, inability to work or to go to school, and lower quality of life. The indi-
vidual also may experience substantial psychological distress. Rare complications of Tou-
rette’s disorder include physical injury, such as eye injury (from hitting oneself in the face),
and orthopedic and neurological injury (e.g., disc disease related to forceful head and neck
movements).
Differential Diagnosis
Abnormal movements that may accompany other medical conditions and stereotypic
movement disorder. Motor stereotypies are defined as involuntary rhythmic, repetitive,
predictable movements that appear purposeful but serve no obvious adaptive function or
purpose and stop with distraction. Examples include repetitive hand waving/ rotating,
arm flapping, and finger wiggling. Motor stereotypies can be differentiated from tics based
on the former's earlier age at onset (younger than 3 years), prolonged duration (seconds to
minutes), constant repetitive fixed form and location, exacerbation when engrossed in ac-
tivities, lack of a premonitory urge, and cessation with distraction (e.g., name called or
touched). Chorea represents rapid, random, continual, abrupt, irregular, unpredictable,
nonstereotyped actions that are usually bilateral and affect all parts of the body (i.e., face,
trunk, and limbs). The timing, direction, and distribution of movements vary from mo-
ment to moment, and movements usually worsen during attempted voluntary action. Dys-
tonia is the simultaneous sustained contracture of both agonist and antagonist muscles,
resulting ina distorted posture or movement of parts of the body. Dystonic postures are of-
ten triggered by attempts at voluntary movements and are not seen during sleep.
Substance-induced and paroxysmal dyskinesias. Paroxysmal dyskinesias usually oc-
cur as dystonic or choreoathetoid movements that are precipitated by voluntary move-
ment or exertion and less commonly arise from normal background activity.
Myoclonus. Myoclonus is characterized by a sudden unidirectional movement that is
often nonrhythmic. It may be worsened by movement and occur during sleep. Myoclonus
is differentiated from tics by its rapidity, lack of suppressibility, and absence of a premon-
itory urge.
Obsessive-compulsive and related disorders. Differentiating obsessive-compulsive
behaviors from tics may be difficult. Clues favoring an obsessive-compulsive behavior in-
clude a cognitive-based drive (e.g., fear of contamination) and the need to perform the ac-
tion in a particular fashion a certain number of times, equally on both sides of the body, or
until a “just right” feeling is achieved. Impulse-contro] problems and other repetitive be-
haviors, including persistent hair pulling, skin picking, and nail biting, appear more goal
directed and complex than tics.
Other Specified Tic Disorder 85
Comorbidity
Many medical and psychiatric conditions have been described as co-occurring with tic disor-
ders, with ADHD and obsessive-compulsive and related disorders being particularly com-
mon. The obsessive-compulsive symptoms observed in tic disorder tend to be characterized
by more aggressive symmetry and order symptoms and poorer response to pharmacotherapy
with selective serotonin reuptake inhibitors. Children with ADHD may demonstrate disrup-
tive behavior, social immaturity, and learning difficulties that may interfere with academic
progress and interpersonal relationships and lead to greater impairment than that caused by a
tic disorder. Individuals with tic disorders can also have other movement disorders and other
mental disorders, such as depressive, bipolar, or substance use disorders.
Other Specified Tic Disorder
307.20 (F95.8)
This category applies to presentations in which symptoms characteristic of a tic disorder
that cause clinically significant distress or impairment in social, occupational, or other im-
portant areas of functioning predominate but do not meet the full criteria for a tic disorder
or any of the disorders in the neurodevelopmental disorders diagnostic class. The other
specified tic disorder category is used in situations in which the clinician chooses to com-
municate the specific reason that the presentation does not meet the criteria for a tic disor-
der or any specific neurodevelopmental disorder. This is done by recording “other specified
tic disorder’ followed by the specific reason (e.g., “with onset after age 18 years”).
Unspecified Tic Disorder
307.20 (F95.9)
This category applies to presentations in which symptoms characteristic of a tic disorder
that cause Clinically significant distress or impairment in social, occupational, or other im-
portant areas of functioning predominate but do not meet the full criteria for a tic disorder
or for any of the disorders in the neurodevelopmental disorders diagnostic class. The un-
specified tic disorder category is used in situations in which the clinician chooses not to
specify the reason that the criteria are not met for a tic disorder or for a specific neurode-
velopmental disorder, and includes presentations in which there is insufficient information
to make a more specific diagnosis.
86 Neurodevelopmental Disorders
Other Neurodevelopmental Disorders
Other Specified Neurodevelopmental Disorder
315.8 (F88)
This category applies to presentations in which symptoms characteristic of a neurodevel-
opmental disorder that cause impairment in social, occupational, or other important areas
of functioning predominate but do not meet the full criteria for any of the disorders in the
neurodevelopmental disorders diagnostic class. The other specified neurodevelopmental
disorder category is used in situations in which the clinician chooses to communicate the
specific reason that the presentation does not meet the criteria for any specific neurode-
velopmental disorder. This is done by recording “other specified neurodevelopmental dis-
order’ followed by the specific reason (e.g., “neurodevelopmental disorder associated with
prenatal alcohol exposure”).
An example of a presentation that can be specified using the “other specified” desig-
nation is the following:
Neurodevelopmental disorder associated with prenatal alcohol exposure: Neu-
rodevelopmental disorder associated with prenatal alcohol exposure is characterized
by a range of developmental disabilities following exposure to alcohol in utero.
Unspecified Neurodevelopmental Disorder
315.9 (F89)
This category applies to presentations in which symptoms characteristic of a neurodevel-
opmental disorder that cause impairment in social, occupational, or other important areas
of functioning predominate but do not meet the full criteria for any of the disorders in the
neurodevelopmental disorders diagnostic class. The unspecified neurodevelopmental dis-
order category is used in situations in which the clinician chooses not to specify the reason
that the criteria are not met for a specific neurodevelopmental disorder, and includes pre-
sentations in which there is insufficient information to make a more specific diagnosis
(e.g., in emergency room settings).
Sch izophrenia SpectrumM and other psychotic disorders include schizophrenia,
other psychotic disorders, and schizotypal (personality) disorder. They are defined by ab-
normalities in one or more of the following five domains: delusions, hallucinations, disor-
ganized thinking (speech), grossly disorganized or abnormal motor behavior (including
catatonia), and negative symptoms.
Key Features That Define the Psychotic Disorders
Delusions
Delusions are fixed beliefs that are not amenable to change in light of conflicting evidence.
Their content may include a variety of themes (e.g., persecutory, referential, somatic, reli-
gious, grandiose). Persecutory delusions (i.e., belief that one is going to be harmed, harassed,
and so forth by an individual, organization, or other group) are most common. Referential
delusions (i.e., belief that certain gestures, comments, environmental cues, and so forth are
directed at oneself} are also common. Grandiose delusions (i.e., when an individual believes
that he or she has exceptional abilities, wealth, or fame) and erotomanic delusions (i-e., when
an individual believes falsely that another person is in love with him or her) are also seen.
Nihilistic delusions involve the conviction that a major catastrophe will occur, and somatic
delusions focus on preoccupations regarding health and organ function.
Delusions are deemed bizarre if they are clearly implausible and not understandable to
same-culture peers and do not derive from ordinary life experiences. An example of a bi-
zarre delusion is the belief that an outside force has removed his or her internal organs and
replaced them with someone else’s organs without leaving any wounds or scars. An ex-
ample of a nonbizarre delusion is the belief that one is under surveillance by the police, de-
spite a lack of convincing evidence. Delusions that express a loss of control over mind or
body are generally considered to be bizarre; these include the belief that one’s thoughts
have been “removed” by some outside force (thought withdrawal), that alien thoughts have
been put into one’s mind (thought insertion), or that one’s body or actions are being acted on
or manipulated by some outside force (delusions of control). The distinction between a de-
lusion and a strongly held idea is sometimes difficult to make and depends in part on the
degree of conviction with which the belief is held despite clear or reasonable contradictory
evidence regarding its veracity.
Hallucinations
Hallucinations are perception-like experiences that occur without an external stimulus.
They are vivid and clear, with the full force and impact of normal perceptions, and not
under voluntary control. They may occur in any sensory modality, but auditory halluci-
nations are the most common in schizophrenia and related disorders. Auditory hallucina-
tions are usually experienced as voices, whether familiar or unfamiliar, that are perceived
as distinct from the individual’s own thoughts. The hallucinations must occur in the con-
text of a clear sensorium; those that occur while falling asleep (hypnagogic) or waking up
87
88 Schizophrenia Spectrum and Other Psychotic Disorders
(hypnopompic) are considered to be within the range of normal experience. Hallucinations
may be a normal part of religious experience in certain cultural contexts.
Disorganized Thinking (Speech)
Disorganized thinking (formal thought disorder) is typically inferred from the individual's
speech. The individual may switch from one topic to another (derailment or loose associa-
tions). Answers to questions may be obliquely related or completely unrelated (tangential-
ity). Rarely, speech may be so severely disorganized that it is nearly incomprehensible and
resembles receptive aphasia in its linguistic disorganization (incoherence or “word salad”).
Because mildly disorganized speech is common and nonspecific, the symptom must be se-
vere enough to substantially impair effective communication. The severity of the impair-
ment may be difficult to evaluate if the person making the diagnosis comes from a
different linguistic background than that of the person being examined. Less severe dis-
organized thinking or speech may occur during the prodromal and residual periods of
schizophrenia.
Grossly Disorganized or Abnormai Motor Behavior
(Inciuding Catatonia)
Grossly disorganized or abnormal motor behavior may manifest itself in a variety of ways,
ranging from childlike “silliness” to unpredictable agitation. Problems may be noted in
any form of goal-directed behavior, leading to difficulties in performing activities of daily
living.
Catatonic behavior is a marked decrease in reactivity to the environment. This ranges
from resistance to instructions (negativism); to maintaining a rigid, inappropriate or bi-
zarre posture; to a complete lack of verbal and motor responses (mutism and stupor). It can
also include purposeless and excessive motor activity without obvious cause (catatonic
excitement). Other features are repeated stereotyped movements, staring, grimacing,
mutism, and the echoing of speech. Although catatonia has historically been associated
with schizophrenia, catatonic symptoms are nonspecific and may occur in other mental
disorders (e.g., bipolar or depressive disorders with catatonia) and in medical conditions
(catatonic disorder due to another medical condition).
Negative Symptoms
Negative symptoms account for a substantial portion of the morbidity associated with
schizophrenia but are less prominent in other psychotic disorders. Two negative symp-
toms are particularly prominent in schizophrenia: diminished emotional expression and
avolition. Diminished emotional expression includes reductions in the expression of emo-
tions in the face, eye contact, intonation of speech (prosody), and movements of the hand,
head, and face that normally give an emotional emphasis to speech. Avolition is a decrease
in motivated self-initiated purposeful activities. The individual may sit for long periods of
time and show little interest in participating in work or social activities. Other negative
symptoms include alogia, anhedonia, and asociality. Alogia is manifested by diminished
speech output. Anhedonia is the decreased ability to experience pleasure from positive
stimuli or a degradation in the recollection of pleasure previously experienced. Asociality
refers to the apparent lack of interest in social interactions and may be associated with avo-
lition, but it can also be a manifestation of limited opportunities for social interactions.
Disorders in This Chapter
This chapter is organized along a gradient of psychopathology. Clinicians should first con-
sider conditions that do not reach full criteria for a psychotic disorder or are limited to one
Schizophrenia Spectrum and Other Psychotic Disorders 89
domain of psychopathology. Then they should consider time-limited conditions. Finally,
the diagnosis of a schizophrenia spectrum disorder requires the exclusion of another con-
dition that may give rise to psychosis.
Schizotypal personality disorder is noted within this chapter as it is considered within
the schizophrenia spectrum, although its full description is found in the chapter “Person-
ality Disorders.” The diagnosis schizotypal personality disorder captures a pervasive pat-
tern of social and interpersonal deficits, including reduced capacity for close relationships;
cognitive or perceptual distortions; and eccentricities of behavior, usually beginning by
early adulthood but in some cases first becoming apparent in childhood and adolescence.
Abnormalities of beliefs, thinking, and perception are below the threshold for the diagno-
sis of a psychotic disorder.
Two conditions are defined by abnormalities limited to one domain of psychosis: delu-
sions or catatonia. Delusional disorder is characterized by at least 1 month of delusions but
no other psychotic symptoms. Catatonia is described later in the chapter and further in this
discussion.
Brief psychotic disorder lasts more than 1 day and remits by 1 month. Schizophreni-
form disorder is characterized by a symptomatic presentation equivalent to that of schizo-
phrenia except for its duration (less than 6 months) and the absence of a requirement for a
decline in functioning.
Schizophrenia lasts for at least 6 months and includes at least 1 month of active-phase
symptoms. In schizoaffective disorder, a mood episode and the active-phase symptoms of
schizophrenia occur together and were preceded or are followed by at least 2 weeks of de-
lusions or hallucinations without prominent mood symptoms.
Psychotic disorders may be induced by another condition. In substance/medication-
induced psychotic disorder, the psychotic symptoms are judged to be a physiological con-
sequence of a drug of abuse, a medication, or toxin exposure and cease after removal of the
agent. In psychotic disorder due to another medical condition, the psychotic symptoms
are judged to be a direct physiological consequence of another medical condition.
Catatonia can occur in several disorders, including neurodevelopmental, psychotic, bi-
polar, depressive, and other mental disorders. This chapter also includes the diagnoses
catatonia associated with another mental disorder (catatonia specifier), catatonic disorder
due to another medical condition, and unspecified catatonia, and the diagnostic criteria for
all three conditions are described together.
Other specified and unspecified schizophrenia spectrum and other psychotic disor-
ders are included for classifying psychotic presentations that do not meet the criteria for
any of the specific psychotic disorders, or psychotic symptomatology about which there is
inadequate or contradictory information.
Clinician-Rated Assessment of Symptoms and
Related Clinical Phenomena in Psychosis
Psychotic disorders are heterogeneous, and the severity of symptoms can predict impor-
tant aspects of the illness, such as the degree of cognitive or neurobiological deficits. To
move the field forward, a detailed framework for the assessment of severity is included in
Section {IJ “Assessment Measures,” which may help with treatment planning, prognostic
decision making, and research on pathophysiological mechanisms. Section III “Assess-
ment Measures” also contains dimensional assessments of the primary symptoms of psy-
chosis, including hallucinations, delusions, disorganized speech (except for substance/
medication-induced psychotic disorder and psychotic disorder due to another medical
condition), abnormal psychomotor behavior, and negative symptoms, as well as dimen-
sional assessments of depression and mania. The severity of mood symptoms in psychosis
has prognostic value and guides treatment. There is growing evidence that schizoaffective
90 Schizophrenia Spectrum and Other Psychotic Disorders
disorder is not a distinct nosological category. Thus, dimensional assessments of depres-
sion and mania for all psychotic disorders alert clinicians to mood pathology and the need
to treat where appropriate. The Section III scale also includes a dimensional assessment of
cognitive impairment. Many individuals with psychotic disorders have impairments in a
range of cognitive domains that predict functional status. Clinical neuropsychological as-
sessment can help guide diagnosis and treatment, but brief assessments without formal
neuropsychological assessment can provide useful information that can be sufficient for
diagnostic purposes. Formal neuropsychological testing, when conducted, should be ad-
ministered and scored by personnel trained in the use of testing instruments. If a formal
neuropsychological assessment is not conducted, the clinician should use the best avail-
able information to make a judgment. Further research on these assessments is necessary
in order to determine their clinical utility; thus, the assessments available in Section III
should serve as a prototype to stimulate such research.
Schizotypal (Personality) Disorder
Criteria and text for schizotypal personality disorder can be found in the chapter “Person-
ality Disorders.” Because this disorder is considered part of the schizophrenia spectrum of
disorders, and is labeled in this section of ICD-9 and ICD-10 as schizotypal disorder, it is
listed in this chapter and discussed in detail in the DSM-5 chapter “Personality Disorders.”
Delusional Disorder
Diagnostic Criteria 297.1 (F22)
A. The presence of one (or more) delusions with a duration of 1 month or longer.
B. Criterion A for schizophrenia has never been met.
Note: Hallucinations, if present, are not prominent and are related to the delusional
theme (e.g., the sensation of being infested with insects associated with delusions of
infestation).
C. Apart from the impact of the delusion(s) or its ramifications, functioning is not markedly
impaired, and behavior is not obviously bizarre or odd.
D. If manic or major depressive episodes have occurred, these have been brief relative
to the duration of the delusional periods.
E. The disturbance is not attributable to the physiological effects of a substance or an-
other medical condition and is not better explained by another mental disorder, such
as body dysmorphic disorder or obsessive-compulsive disorder.
Specify whether:
Erotomanic type: This subtype applies when the central theme of the delusion is that
another person is in love with the individual.
Grandiose type: This subtype applies when the central theme of the delusion is the
conviction of having some great (but unrecognized) talent or insight or having made
some important discovery.
Jealous type: This subtype applies when the central theme of the individual's delusion
is that his or her spouse or lover is unfaithful.
Persecutory type: This subtype applies when the central theme of the delusion in-
volves the individual’s belief that he or she is being conspired against, cheated, spied
on, followed, poisoned or drugged, maticiously maligned, harassed, or obstructed in
the pursuit of long-term goals.
Somatic type: This subtype applies when the central theme of the delusion involves
bodily functions or sensations.
Delusional Disorder 91
Mixed type: This subtype applies when no one delusional theme predominates.
Unspecified type: This subtype applies when the dominant delusional belief cannot
be clearly determined or is not described in the specitic types (e.g., referential delu-
sions without a prominent persecutory or grandiose component).
Specify if:
With bizarre content: Delusions are deemed bizarre if they are clearly implausible, not
understandable, and not derived from ordinary life experiences (e.g., an individual’s be-
lief that a stranger has removed his or her internal organs and replaced them with some-
one else’s organs without leaving any wounds or scars).
Specify if:
The following course specifiers are only to be used after a 1-year duration of the disorder:
First episode, currently in acute episode: First manifestation of the disorder meet-
ing the defining diagnostic symptom and time criteria. An acute episode is a time pe-
riod in which the symptom criteria are fulfilled.
First episode, currently in partial remission: Partial remission is a time period dur-
ing which an improvement after a previous episode is maintained and in which the de-
fining criteria of the disorder are only partially fulfilled.
First episode, currently in full remission: Ful! remission is a period of time after a
previous episode during which no disorder-specific symptoms are present.
Multiple episodes, currently in acute episode
Multiple episodes, currently in partial remission
Multiple episodes, currently in full remission
Continuous: Symptoms fulfilling the diagnostic symptom criteria of the disorder are
remaining for the majority of the illness course, with subthreshold symptom periods be-
ing very brief relative to the overall course.
Unspecified
Specify current severity:
Severity is rated by a quantitative assessment of the primary symptoms of psychosis,
including delusions, hallucinations, disorganized speech, abnormal psychomotor be-
havior, and negative symptoms. Each of these symptoms may be rated for its current
severity (most severe in the last 7 days) on a 5-point scale ranging from 0 (not present)
to 4 (present and severe). (See Clinician-Rated Dimensions of Psychosis Symptom
Severity in the chapter “Assessment Measures.”)
Note: Diagnosis of delusional disorder can be made without using this severity specifier.
Subtypes
In erotomanic type, the central theme of the delusion is that another person is in love with
the individual. The person about whom this conviction is held is usually of higher status
(e.g., a famous individual or a superior at work) but can be a complete stranger. Efforts to
contact the object of the delusion are common. In grandiose type, the central theme of the de-
lusion is the conviction of having some great talent or insight or of having made some im-
portant discovery. Less commonly, the individual may have the delusion of having a
special relationship with a prominent individual or of being a prominent person (in which
case the actual individual may be regarded as an impostor). Grandiose delusions may
have a religious content. In jealous type, the central theme of the delusion is that of an un-
faithful partner. This belief is arrived at without due cause and is based on incorrect infer-
ences supported by small bits of “evidence” (e.g., disarrayed clothing). The individual
with the delusion usually confronts the spouse or lover and attempts to intervene in the
imagined infidelity. In persecutory type, the central theme of the delusion involves the in-
92 Schizophrenia Spectrum and Other Psychotic Disorders
dividual’s belief of being conspired against, cheated, spied on, followed, poisoned, mali-
ciously maligned, harassed, or obstructed in the pursuit of long-term goals. Small slights
may be exaggerated and become the focus of a delusional system. The affected individual
may engage in repeated attempts to obtain satisfaction by legal or legislative action. Indi-
viduals with persecutory delusions are often resentful and angry and may resort to vio-
lence against those they believe are hurting them. In somatic type, the central theme of the
delusion involves bodily functions or sensations. Somatic delusions can occur in several
forms. Most common is the belief that the individual emits a foul odor; that there is an in-
festation of insects on or in the skin; that there is an internal parasite; that certain parts of
the body are misshapen or ugly; or that parts of the body are not functioning.
Diagnostic Features
The essential feature of delusional disorder is the presence of one or more delusions that
persist for at least 1 month (Criterion A). A diagnosis of delusional disorder is not given if
the individual has ever had a symptom presentation that met Criterion A for schizophre-
nia (Criterion B). Apart from the direct impact of the delusions, impairments in psychoso-
cial functioning may be more circumscribed than those seen in other psychotic disorders
such as schizophrenia, and behavior is not obviously bizarre or odd (Criterion C). If mood
episodes occur concurrently with the delusions, the total duration of these mood episodes
is brief relative to the total duration of the delusional periods (Criterion D). The delusions
are not attributable to the physiological effects of a substance (e.g., cocaine) or another
medical condition (e.g., Alzheimer’s disease) and are not better explained by another men-
tal disorder, such as body dysmorphic disorder or obsessive-compulsive disorder (Crite-
rion E).
In addition to the five symptom domain areas identified in the diagnostic criteria, the
assessment of cognition, depression, and mania symptom domains is vital for making crit-
ically important distinctions between the various schizophrenia spectrum and other psy-
chotic disorders.
Associated Features Supporting Diagnosis
Social, marital, or work problems can result from the delusional beliefs of delusional dis-
order. Individuals with delusional disorder may be able to factually describe that others
view their beliefs as irrational but are unable to accept this themselves (i.e., there may be
“factual insight” but no true insight). Many individuals develop irritable or dysphoric
mood, which can usually be understood as a reaction to their delusional beliefs. Anger and
violent behavior can occur with persecutory, jealous, and erotomanic types. The individ-
ual may engage in litigious or antagonistic behavior (e.g., sending hundreds of letters of
protest to the government). Legal difficulties can occur, particularly in jealous and eroto-
manic types.
Prevalence
The lifetime prevalence of delusional disorder has been estimated at around 0.2%, and the
most frequent subtype is persecutory. Delusional disorder, jealous type, is probably more
common in males than in females, but there are no major gender differences in the overall
frequency of delusional disorder.
Deveiopment and Course
On average, global function is generally better than that observed in schizophrenia. Al-
though the diagnosis is generally stable, a proportion of individuals go on to develop
Delusional Disorder 93
schizophrenia. Delusional disorder has a significant familial relationship with both
schizophrenia and schizotypal personality disorder. Although it can occur in younger age
groups, the condition may be more prevalent in older individuals.
Culture-Related Diagnostic Issues
An individual's cultural and religious background must be taken into account in evaluat-
ing the possible presence of delusional disorder. The content of delusions also varies
across cultural contexts.
Functional Consequences of Delusional Disorder
The functional impairment is usually more circumscribed than that seen with other psy-
chotic disorders, although in some cases, the impairment may be substantial and include
poor occupational functioning and social isolation. When poor psychosocial functioning is
present, delusional beliefs themselves often play a significant role. A common character-
istic of individuals with delusional disorder is the apparent normality of their behavior
and appearance when their delusional ideas are not being discussed or acted on.
Differential Diagnosis
Obsessive-compulsive and related disorders. If an individual with obsessive-compul-
sive disorder is completely convinced that his or her obsessive-compulsive disorder beliefs
are true, then the diagnosis of obsessive-compulsive disorder, with absent insight/delu-
sional beliefs specifier, should be given rather than a diagnosis of delusional disorder.
Similarly, if an individual with body dysmorphic disorder is completely convinced that
his or her body dysmorphic disorder beliefs are true, then the diagnosis of body dysmor-
phic disorder, with absent insight / delusional beliefs specifier, should be given rather than
a diagnosis of delusional] disorder.
Delirium, major neurocognitive disorder, psychotic disorder due to another medical con-
dition, and substance/medication-induced psychotic disorder. Individuals with these
disorders may present with symptoms that suggest delusional disorder. For example, sim-
ple persecutory delusions in the context of major neurocognitive disorder would be di-
agnosed as major neurocognitive disorder, with behavioral disturbance. A substance/
medication-induced psychotic disorder cross-sectionally may be identical in symptom-
atology to delusional disorder but can be distinguished by the chronological relationship
of substance use to the onset and remission of the delusional beliefs.
Schizophrenia and schizophreniform disorder. Delusional disorder can be distinguished
from schizophrenia and schizophreniform disorder by the absence of the other character-
istic symptoms of the active phase of schizophrenia.
Depressive and bipolar disorders and schizoaffective disorder. These disorders may
be distinguished from delusional disorder by the temporal relationship between the mood
disturbance and the delusions and by the severity of the mood symptoms. If delusions oc-
cur exclusively during mood episodes, the diagnosis is depressive or bipolar disorder with
psychotic features. Mood symptoms that meet full criteria for a mood episode can be su-
perimposed on delusional disorder. Delusional disorder can be diagnosed only if the total
duration of all mood episodes remains brief relative to the total duration of the delusional
disturbance. If not, then a diagnosis of other specified or unspecified schizophrenia spec-
trum and other psychotic disorder accompanied by other specified depressive disorder,
unspecified depressive disorder, other specified bipolar and related disorder, or unspeci-
fied bipolar and related disorder is appropriate.
94 Schizophrenia Spectrum and Other Psychotic Disorders
Brief Psychotic Disorder
Diagnostic Criteria 298.8 (F23)
A. Presence of one (or more) of the following symptoms. At least one of these must be
(1), (2), or (3):
1. Delusions.
2. Hallucinations.
3. Disorganized speech (e.g., frequent derailment or incoherence).
4. Grossly disorganized or catatonic behavior.
Note: Do not include a symptom if it is a culturally sanctioned response.
B. Duration of an episode of the disturbance is at least 1 day but less than 1 month, with
eventual full return to premorbid level of functioning.
C. The disturbance is not better explained by major depressive or bipolar disorder with
psychotic features or another psychotic disorder such as schizophrenia or catatonia,
and is not attributable to the physiological effects of a substance (e.g., a drug of abuse,
a medication) or another medical condition.
Specity if:
With marked stressor(s) (brief reactive psychosis): If symptoms occur in response to
events that, singly or together, would be markedly stressful to almost anyone in similar
circumstances in the individual’s culture.
Without marked stressor(s): If symptoms do not occur in response to events that,
singly or together, would be markedly stressful to almost anyone in similar circum-
stances in the individual’s culture.
With postpartum onset: If onset is during pregnancy or within 4 weeks postpartum.
Specify if:
With catatonia (refer to the criteria for catatonia associated with another mental dis-
order, pp. 119-120, for definition)
Coding note: Use additional code 293.89 (F06.1) catatonia associated with brief
psychotic disorder to indicate the presence of the comorbid catatonia.
Specify current severity:
Severity is rated by a quantitative assessment of the primary symptoms of psychosis,
including delusions, hallucinations, disorganized speech, abnormal psychomotor be-
havior, and negative symptoms. Each of these symptoms may be rated for its current
severity (most severe in the last 7 days) on a 5-point scale ranging from 0 (not present)
to 4 (present and severe). (See Clinician-Rated Dimensions of Psychosis Symptom
Severity in the chapter “Assessment Measures.”)
Note: Diagnosis of brief psychotic disorder can be made without using this severity
specifier.
Diagnostic Features
The essential feature of brief psychotic disorder is a disturbance that involves the sudden
onset of at least one of the following positive psychotic symptoms: delusions, hallucina-
tions, disorganized speech (e.g., frequent derailment or incoherence), or grossly abnormal
psychomotor behavior, including catatonia (Criterion A). Sudden onset is defined as
change from a nonpsychotic state to a clearly psychotic state within 2 weeks, usually with-
out a prodrome. An episode of the disturbance lasts at least 1 day but less than 1 month,
and the individual eventually has a full return to the premorbid level of functioning (Cri-
Brief Psychotic Disorder 95
terion B). The disturbance is not better explained by a depressive or bipolar disorder with
psychotic features, by schizoaffective disorder, or by schizophrenia and is not attributable
to the physiological effects of a substance (e.g., a hallucinogen) or another medical condi-
tion (e.g., subdural hematoma) (Criterion C).
In addition to the five symptom domain areas identified in the diagnostic criteria, the
assessment of cognition, depression, and mania symptom domains is vital for making crit-
ically important distinctions between the various schizophrenia spectrum and other psy-
chotic disorders.
Associated Features Supporting Diagnosis
Individuals with brief psychotic disorder typically experience emotional turmoil or over-
whelming confusion. They may have rapid shifts from one intense affect to another.
Although the disturbance is brief, the level of impairment may be severe, and supervision
may be required to ensure that nutritional and hygienic needs are met and that the indi-
vidual is protected from the consequences of poor judgment, cognitive impairment, or act-
ing on the basis of delusions. There appears to be an increased risk of suicidal behavior,
particularly during the acute episode.
Prevaience
In the United States, brief psychotic disorder may account for 9% of cases of first-onset
psychosis. Psychotic disturbances that meet Criteria A and C, but not Criterion B, for brief
psychotic disorder (i-e., duration of active symptoms is 1-6 months as opposed to remis-
sion within 1 month) are more common in developing countries than in developed coun-
tries. Brief psychotic disorder is twofold more common in females than in males.
Deveiopment and Course
Brief psychotic disorder may appear in adolescence or early adulthood, and onset can oc-
cur across the lifespan, with the average age at onset being the mid 30s. By definition, a
diagnosis of brief psychotic disorder requires a full remission of all symptoms and an
eventual full return to the premorbid level of functioning within 1 month of the onset of the
disturbance. In some individuals, the duration of psychotic symptoms may be quite brief
(e.g., a few days).
Risk and Prognostic Factors
Temperamental. Preexisting personality disorders and traits (e.g., schizotypal person-
ality disorder; borderline personality disorder; or traits in the psychoticism domain, such
as perceptual dysregulation, and the negative affectivity domain, such as suspiciousness)
may predispose the individual to the development of the disorder.
Culture-Reiated Diagnostic Issues
It is important to distinguish symptoms of brief psychotic disorder from culturally sanc-
tioned response patterns. For example, in some religious ceremonies, an individual may
report hearing voices, but these do not generally persist and are not perceived as abnormal
by most members of the individual’s community. In addition, cultural and religious back-
ground must be taken into account when considering whether beliefs are delusional.
Functionai Consequences of Brief Psychotic Disorder
Despite high rates of relapse, for most individuals, outcome is excellent in terms of social
functioning and symptomatology.
96 Schizophrenia Spectrum and Other Psychotic Disorders
Differential Diagnosis
Other medical conditions. A variety of medical disorders can manifest with psychotic
symptoms of short duration. Psychotic disorder due to another medical condition or a de-
lirium is diagnosed when there is evidence from the history, physical examination, or lab-
oratory tests that the delusions or hallucinations are the direct physiological consequence
of a specific medical condition (e.g., Cushing’s syndrome, brain tumor) (see “Psychotic
Disorder Due to Another Medical Condition” later in this chapter).
Substance-related disorders. Substance/medication-induced psychotic disorder, sub-
stance-induced delirium, and substance intoxication are distinguished from brief psychotic
disorder by the fact that a substance (e.g., a drug of abuse, a medication, exposure to a toxin)
is judged to be etiologically related to the psychotic symptoms (see “Substance /Medication-
Induced Psychotic Disorder” later in this chapter). Laboratory tests, such as a urine drug
screen or a blood alcohol level, may be helpful in making this determination, as may a care-
ful history of substance use with attention to temporal relationships between substance in-
take and onset of the symptoms and to the nature of the substance being used.
Depressive and bipolar disorders. The diagnosis of brief psychotic disorder cannot be
made if the psychotic symptoms are better explained by a mood episode (i.e., the psychotic
symptoms occur exclusively during a full major depressive, manic, or mixed episode).
Other psychotic disorders. If the psychotic symptoms persist for 1 month or longer, the
diagnosis is either schizophreniform disorder, delusional disorder, depressive disorder
with psychotic features, bipolar disorder with psychotic features, or other specified or un-
specified schizophrenia spectrum and other psychotic disorder, depending on the other
symptoms in the presentation. The differential diagnosis between brief psychotic disorder
and schizophreniform disorder is difficult when the psychotic symptoms have remitted be-
fore 1 month in response to successful treatment with medication. Careful attention should
be given to the possibility that a recurrent disorder (e.g., bipolar disorder, recurrent acute ex-
acerbations of schizophrenia) may be responsible for any recurring psychotic episodes.
Malingering and factitious disorders. An episode of factitious disorder, with predomi-
nantly psychological signs and symptoms, may have the appearance of brief psychotic
disorder, but in such cases there is evidence that the symptoms are intentionally produced.
When malingering involves apparently psychotic symptoms, there is usually evidence
that the illness is being feigned for an understandable goal.
Personality disorders. In certain individuals with personality disorders, psychosocial
stressors may precipitate brief periods of psychotic symptoms. These symptoms are usu-
ally transient and do not warrant a separate diagnosis. If psychotic symptoms persist for at
least 1 day, an additional diagnosis of brief psychotic disorder may be appropriate.
Schizophreniform Disorder
Diagnostic Criteria 295.40 (F20.81)
A. Two (or more) of the following, each present for a significant portion of time during a
1-month period (or less if successfully treated). At least one of these must be (1), (2),
or (3):
1. Delusions.
2. Hallucinations.
3. Disorganized speech (e.g., frequent derailment or incoherence).
4. Grossly disorganized or catatonic behavior.
5. Negative symptoms (i.e., diminished emotional expression or avolition).
Schizophreniform Disorder 97
B. An episode of the disorder lasts at least 1 month but less than 6 months. When the
diagnosis must be made without waiting for recovery, it should be qualified as “provi-
sional.”
C. Schizoaffective disorder and depressive or bipolar disorder with psychotic features have
been ruled out because either 1) no major depressive or manic episodes have occurred
concurrently with the active-phase symptoms, or 2) if mood episodes have occurred dur-
ing active-phase symptoms, they have been present for a minority of the total duration
of the active and residual periods of the illness.
D. The disturbance is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication) or another medical condition.
Specify if:
With good prognostic features: This specifier requires the presence of at least two
of the following features: onset of prominent psychotic symptoms within 4 weeks of the
first noticeable change in usual behavior or functioning; confusion or perplexity; good
premorbid social and occupational functioning; and absence of blunted or flat affect.
Without good prognostic features: This specifier is applied if two or more of the
above features have not been present.
Specify if:
With catatonia (refer to the criteria for catatonia associated with another mental disor-
der, pp. 119-120, for definition).
Coding note: Use additional code 293.89 (F06.1) catatonia associated with schizo-
phreniform disorder to indicate the presence of the comorbid catatonia.
Specify current severity:
Severity is rated by a quantitative assessment of the primary symptoms of psychosis,
including delusions, hallucinations, disorganized speech, abnormal psychomotor be-
havior, and negative symptoms. Each of these symptoms may be rated for its current
severity (most severe in the last 7 days) on a 5-point scale ranging from 0 (not present)
to 4 (present and severe). (See Clinician-Rated Dimensions of Psychosis Symptom
Severity in the chapter “Assessment Measures.”)
Note: Diagnosis of schizophreniform disorder can be made without using this severity
specifier.
Note: For additional information on Associated Features Supporting Diagnosis, Develop-
ment and Course (age-related factors), Culture-Related Diagnostic Issues, Gender-Related
Diagnostic Issues, Differential Diagnosis, and Comorbidity, see the corresponding sec-
tions in schizophrenia.
Diagnostic Features
The characteristic symptoms of schizophreniform disorder are identical to those of schizo-
phrenia (Criterion A). Schizophreniform disorder is distinguished by its difference in du-
ration: the total duration of the illness, including prodromal, active, and residual phases, is
at least 1 month but less than 6 months (Criterion B). The duration requirement for schizo-
phreniform disorder is intermediate between that for brief psychotic disorder, which lasts
more than 1 day and remits by 1 month, and schizophrenia, which lasts for at least 6 months.
The diagnosis of schizophreniform disorder is made under two conditions. 1) when an ep-
isode of illness lasts between 1 and 6 months and the individual has already recovered,
and 2) when an individual is symptomatic for less than the 6 months’ duration required for
the diagnosis of schizophrenia but has not yet recovered. In this case, the diagnosis should
be noted as “schizophreniform disorder (provisional)” because it is uncertain if the indi-
vidual will recover from the disturbance within the 6-month period. If the disturbance per-
sists beyond 6 months, the diagnosis should be changed to schizophrenia.
98 Schizophrenia Spectrum and Other Psychotic Disorders
Another distinguishing feature of schizophreniform disorder is the lack of a criterion
requiring impaired social and occupational functioning. While such impairments may po-
tentially be present, they are not necessary for a diagnosis of schizophreniform disorder.
In addition to the five symptom domain areas identified in the diagnostic criteria, the
assessment of cognition, depression, and mania symptom domains is vital for making crit-
ically important distinctions between the various schizophrenia spectrum and other psy-
chotic disorders.
Associated Features Supporting Diagnosis
As with schizophrenia, currently there are no laboratory or psychometric tests for schizo-
phreniform disorder. There are multiple brain regions where neuroimaging, neuropa-
thological, and neurophysiological research has indicated abnormalities, but none are
diagnostic.
Prevaience
Incidence of schizophreniform disorder across sociocultural settings is likely similar to
that observed in schizophrenia. In the United States and other developed countries, the in-
cidence is low, possibly fivefold less than that of schizophrenia. In developing countries,
the incidence may be higher, especially for the specifier “with good prognostic features”;
in some of these settings schizophreniform disorder may be as common as schizophrenia.
Development and Course
The development of schizophreniform disorder is similar to that of schizophrenia. About
one-third of individuals with an initial diagnosis of schizophreniform disorder (provi-
sional) recover within the 6-month period and schizophreniform disorder is their final di-
agnosis. The majority of the remaining two-thirds of individuals will eventually receive a
diagnosis of schizophrenia or schizoaffective disorder.
Risk and Prognostic Factors
Genetic and physiological. Relatives of individuals with schizophreniform disorder
have an increased risk for schizophrenia.
Functional Consequences of
Schizophreniform Disorder
For the majority of individuals with schizophreniform disorder who eventually receive a
diagnosis of schizophrenia or schizoaffective disorder, the functional consequences are
similar to the consequences of those disorders. Most individuals experience dysfunction in
several areas of daily functioning, such as school or work, interpersonal relationships, and
self-care. Individuals who recover from schizophreniform disorder have better functional
outcomes.
Differential Diagnosis
Other mental disorders and medical conditions. A wide variety of mental and medical
conditions can manifest with psychotic symptoms that must be considered in the differ-
ential diagnosis of schizophreniform disorder. These include psychotic disorder due to
another medical condition or its treatment; delirium or major neurocognitive disorder;
substance/medication-induced psychotic disorder or delirium; depressive or bipolar
disorder with psychotic features; schizoaffective disorder; other specified or unspecified bi-
polar and related disorder; depressive or bipolar disorder with catatonic features; schizophre-
Schizophrenia 99
nia; brief psychotic disorder; delusional disorder; other specified or unspecified schizo-
phrenia spectrum and other psychotic disorder; schizotypal, schizoid, or paranoid
personality disorders; autism spectrum disorder; disorders presenting in childhood with
disorganized speech; attention-deficit/hyperactivity disorder; obsessive-compulsive dis-
order; posttraumatic stress disorder; and traumatic brain injury.
Since the diagnostic criteria for schizophreniform disorder and schizophrenia differ
primarily in duration of illness, the discussion of the differential diagnosis of schizophre-
nia also applies to schizophreniform disorder.
Brief psychotic disorder. Schizophreniform disorder differs in duration from brief psy-
chotic disorder, which has a duration of less than 1 month.
Schizophrenia
Diagnostic Criteria 295.90 (F20.9)
A. Two (or more) of the following, each present for a significant portion of time during a
1-month period (or less if successfully treated). At least one of these must be (1), (2), or (3):
1. Delusions.
Hailucinations.
Disorganized speech (e.g., frequent derailment or incoherence).
Grossly disorganized or catatonic behavior.
Negative symptoms (i.e., diminished emotional expression or avolition).
B. For a significant portion of the time since the onset of the disturbance, level of function-
ing in one or more major areas, such as work, interpersonal relations, or self-care, is
markedly below the level achieved prior to the onset (or when the onset is in childhood
or adolescence, there is failure to achieve expected level of interpersonal, academic,
or occupational functioning).
C. Continuous signs of the disturbance persist for at least 6 months. This 6-month period
must include at least 1 month of symptoms (or less if successfully treated) that meet Cri-
terion A (i.e., active-phase symptoms) and may include periods of prodromal or residual
symptoms. During these prodromal or residual periods, the signs of the disturbance may
be manifested by only negative symptoms or by two or more symptoms listed in Criterion
A present in an attenuated form (e.g., odd beliefs, unusual perceptual experiences).
D. Schizoaffective disorder and depressive or bipolar disorder with psychotic features
have been ruled out because either 1) no major depressive or manic episodes have
occurred concurrently with the active-phase symptoms, or 2) if mood episodes have
occurred during active-phase symptoms, they have been present for a minority of the
total duration of the active and residual periods of the illness.
E. The disturbance is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication) or another medical condition.
F. If there is a history of autism spectrum disorder or a communication disorder of child-
hood onset, the additional diagnosis of schizophrenia is made only if prominent delu-
sions or hallucinations, in addition to the other required symptoms of schizophrenia,
are also present for at least 1 month (or less if successfully treated).
aronh
Specify if:
The following course specifiers are only to be used after a 1-year duration of the disorder
and if they are not in contradiction to the diagnostic course criteria.
First episode, currently in acute episode: First manifestation of the disorder meet-
ing the defining diagnostic symptom and time criteria. An acute episode is a time pe-
riod in which the symptom criteria are fulfilled.
100 Schizophrenia Spectrum and Other Psychotic Disorders
First episode, currently in partial remission: Partia/ remission is a period of time
during which an improvement after a previous episode is maintained and in which the
defining criteria of the disorder are only partially fulfilled.
First episode, currently in full remission: Full remission is a period of time after a
previous episode during which no disorder-specific symptoms are present.
Multiple episodes, currently in acute episode: Multiple episodes may be deter-
mined after a minimum of two episodes {i.e., after a first episode, a remission and a
minimum of one relapse).
Multiple episodes, currently in partial remission
Multiple episodes, currently in full remission
Continuous: Symptoms fulfilling the diagnostic symptom criteria of the disorder are
remaining for the majority of the illness course, with subthreshold symptom periods be-
ing very brief relative to the overall course.
Unspecified
Specify if:
With catatonia (refer to the criteria for catatonia associated with another mental disorder,
pp. 119-120, for definition).
Coding note: Use additional code 293.89 (F06.1) catatonia associated with
schizophrenia to indicate the presence of the comorbid catatonia.
Specify current severity:
Severity is rated by a quantitative assessment of the primary symptoms of psychosis,
including delusions, hallucinations, disorganized speech, abnormal psychomotor be-
havior, and negative symptoms. Each of these symptoms may be rated for its current
severity (most severe in the last 7 days) on a 5-point scale ranging from 0 (not present)
to 4 (present and severe). (See Clinician-Rated Dimensions of Psychosis Symptom
Severity in the chapter “Assessment Measures.”)
Note: Diagnosis of schizophrenia can be made without using this severity specifier.
Diagnostic Features
The characteristic symptoms of schizophrenia involve a range of cognitive, behavioral, and
emotional dysfunctions, but no single symptom is pathognomonic of the disorder. The di-
agnosis involves the recognition of a constellation of signs and symptoms associated with
impaired occupational or social functioning. Individuals with the disorder will vary sub-
stantially on most features, as schizophrenia is a heterogeneous clinical syndrome.
At least two Criterion A symptoms must be present for a significant portion of time
during a 1-month period or longer. At least one of these symptoms must be the clear pres-
ence of delusions (Criterion A1), hallucinations (Criterion A2), or disorganized speech
(Criterion A3). Grossly disorganized or catatonic behavior (Criterion A4) and negative
symptoms (Criterion A5) may also be present. In those situations in which the active-
phase symptoms remit within a month in response to treatment, Criterion A is still met if the
clinician estimates that they would have persisted in the absence of treatment.
Schizophrenia involves impairment in one or more major areas of functioning (Crite-
rion B). If the disturbance begins in childhood or adolescence, the expected level of func-
tion is not attained. Comparing the individual with unaffected siblings may be helpful. The
dysfunction persists for a substantial period during the course of the disorder and does not
appear to be a direct result of any single feature. Avolition (i.e., reduced drive to pursue
goal-directed behavior; Criterion A5) is linked to the social dysfunction described under
Criterion B. There is also strong evidence for a relationship between cognitive impairment
(see the section “Associated Features Supporting Diagnosis” for this disorder) and func-
tional impairment in individuals with schizophrenia.
Schizophrenia 101
Some signs of the disturbance must persist for a continuous period of at least 6 months
(Criterion C). Prodromal symptoms often precede the active phase, and residual symp-
toms may follow it, characterized by mild or subthreshold forms of hallucinations or
delusions. Individuals may express a variety of unusual or odd beliefs that are not of de-
lusional proportions (e.g., ideas of reference or magical thinking); they may have unusual
perceptual experiences (e.g., sensing the presence of an unseen person); their speech may
be generally understandable but vague; and their behavior may be unusual but not grossly
disorganized (e.g., mumbling in public). Negative symptoms are common in the pro-
dromal and residual phases and can be severe. Individuals who had been socially active
may become withdrawn from previous routines. Such behaviors are often the first sign of
a disorder.
Mood symptoms and full mood episodes are common in schizophrenia and may be con-
current with active-phase symptomatology. However, as distinct from a psychotic mood dis-
order, a schizophrenia diagnosis requires the presence of delusions or hallucinations in the
absence of mood episodes. In addition, mood episodes, taken in total, should be present for
only a minority of the total duration of the active and residual periods of the illness.
In addition to the five symptom domain areas identified in the diagnostic criteria, the
assessment of cognition, depression, and mania symptom domains is vital for making crit-
ically important distinctions between the various schizophrenia spectrum and other psy-
chotic disorders.
Associated Features Supporting Diagnosis
Individuals with schizophrenia may display inappropriate affect (e.g., laughing in the ab-
sence of an appropriate stimulus); a dysphoric mood that can take the form of depression,
anxiety, or anger; a disturbed sleep pattern (e.g., daytime sleeping and nighttime activity);
and a lack of interest in eating or food refusal. Depersonalization, derealization, and so-
matic concerns may occur and sometimes reach delusional proportions. Anxiety and pho-
bias are common. Cognitive deficits in schizophrenia are common and are strongly linked
to vocational and functional impairments. These deficits can include decrements in declar-
ative memory, working memory, language function, and other executive functions, as well
as slower processing speed. Abnormalities in sensory processing and inhibitory capacity,
as well as reductions in attention, are also found. Some individuals with schizophrenia
show social cognition deficits, including deficits in the ability to infer the intentions of
other people (theory of mind), and may attend to and then interpret irrelevant events or
stimuli as meaningful, perhaps leading to the generation of explanatory delusions. These
impairments frequently persist during symptomatic remission.
Some individuals with psychosis may lack insight or awareness of their disorder (i.e.,
anosognosia). This lack of “insight” includes unawareness of symptoms of schizophrenia
and may be present throughout the entire course of the illness. Unawareness of illness is
typically a symptom of schizophrenia itself rather than a coping strategy. It is comparable
to the lack of awareness of neurological deficits following brain damage, termed anoso-
gnosia. This symptom is the most common predictor of non-adherence to treatment, and it
predicts higher relapse rates, increased number of involuntary treatments, poorer psycho-
social functioning, aggression, and a poorer course of illness.
Hostility and aggression can be associated with schizophrenia, although spontaneous
or random assault is uncommon. Aggression is more frequent for younger males and for
individuals with a past history of violence, non-adherence with treatment, substance
abuse, and impulsivity. It should be noted that the vast majority of persons with schizo-
phrenia are not aggressive and are more frequently victimized than are individuals in the
general population.
Currently, there are no radiological, laboratory, or psychometric tests for the disorder.
Differences are evident in multiple brain regions between groups of healthy individuals
102 Schizophrenia Spectrum and Other Psychotic Disorders
and persons with schizophrenia, including evidence from neuroimaging, neuropatholog-
ical, and neurophysiological studies. Differences are also evident in cellular architecture,
white matter connectivity, and gray matter volume in a variety of regions such as the pre-
frontal and temporal cortices. Reduced overall brain volume has been observed, as well as
increased brain volume reduction with age. Brain volume reductions with age are more
pronounced in individuals with schizophrenia than in healthy individuals. Finally, indi-
viduals with schizophrenia appear to differ from individuals without the disorder in eye-
tracking and electrophysiological indices.
Neurological soft signs common in individuals with schizophrenia include impairments
in motor coordination, sensory integration, and motor sequencing of complex movements;
left-right confusion; and disinhibition of associated movements. In addition, minor phys-
ical anomalies of the face and limbs may occur.
Prevalence
The lifetime prevalence of schizophrenia appears to be approximately 0.3%—0.7%, al-
though there is reported variation by race/ethnicity, across countries, and by geographic
origin for immigrants and children of immigrants. The sex ratio differs across samples and
populations: for example, an emphasis on negative symptoms and longer duration of dis-
order (associated with poorer outcome) shows higher incidence rates for males, whereas
definitions allowing for the inclusion of more mood symptoms and brief presentations
{associated with better outcome) show equivalent risks for both sexes.
Development and Course
The psychotic features of schizophrenia typically emerge between the late teens and the
mid-30s; onset prior to adolescence is rare. The peak age at onset for the first psychotic ep-
isode is in the early- to mid-20s for males and in the late-20s for females. The onset may be
abrupt or insidious, but the majority of individuals manifest a slow and gradual develop-
ment of a variety of clinically significant signs and symptoms. Half of these individuals
complain of depressive symptoms. Earlier age at onset has traditionally been seen as a pre-
dictor of worse prognosis. However, the effect of age at onset is likely related to gender,
with males having worse premorbid adjustment, lower educational achievement, more
prominent negative symptoms and cognitive impairment, and in general a worse out-
come. Impaired cognition is common, and alterations in cognition are present during de-
velopment and precede the emergence of psychosis, taking the form of stable cognitive
impairments during adulthood. Cognitive impairments may persist when other symptoms
are in remission and contribute to the disability of the disease.
The predictors of course and outcome are largely unexplained, and course and outcome
may not be reliably predicted. The course appears to be favorable in about 20% of those
with schizophrenia, and a small number of individuals are reported to recover completely.
However, most individuals with schizophrenia still require formal or informal daily living
supports, and many remain chronically ill, with exacerbations and remissions of active
symptoms, while others have a course of progressive deterioration.
Psychotic symptoms tend to diminish over the life course, perhaps in association with
normal age-related declines in dopamine activity. Negative symptoms are more closely re-
lated to prognosis than are positive symptoms and tend to be the most persistent. Further-
more, cognitive deficits associated with the illness may not improve over the course of the
illness.
The essential features of schizophrenia are the same in childhood, but it is more diffi-
cult to make the diagnosis. In children, delusions and hallucinations may be less elaborate
than in adults, and visual hallucinations are more common and should be distinguished
from normal fantasy play. Disorganized speech occurs in many disorders with childhood
onset (e.g., autism spectrum disorder), as does disorganized behavior (e.g., attention-deficit/
Schizophrenia 103
hyperactivity disorder). These symptoms should not be attributed to schizophrenia with-
out due consideration of the more common disorders of childhood. Childhood-onset cases
tend to resemble poor-outcome adult cases, with gradual onset and prominent negative
symptoms. Children who later receive the diagnosis of schizophrenia are more likely to
have experienced nonspecific emotional-behavioral disturbances and psychopathology,
intellectual and language alterations, and subtle motor delays.
Late-onset cases (i.e., onset after age 40 years) are overrepresented by females, who
may have married. Often, the course is characterized by a predominance of psychotic
symptoms with preservation of affect and social functioning. Such late-onset cases can still
meet the diagnostic criteria for schizophrenia, but it is not yet clear whether this is the
same condition as schizophrenia diagnosed prior to mid-life (e.g., prior to age 55 years).
Risk and Prognostic Factors
Environmental. Season of birth has been linked to the incidence of schizophrenia, in-
cluding late winter/early spring in some locations and summer for the deficit form of the
disease. The incidence of schizophrenia and related disorders is higher for children grow-
ing up in an urban environment and for some minority ethnic groups.
Genetic and physiological. There is a strong contribution for genetic factors in deter-
mining risk for schizophrenia, although most individuals who have been diagnosed with
schizophrenia have no family history of psychosis. Liability is conferred by a spectrum of
risk alleles, common and rare, with each allele contributing only a small fraction to the to-
tal population variance. The risk alleles identified to date are also associated with other
mental disorders, including bipolar disorder, depression, and autism spectrum disorder.
Pregnancy and birth complications with hypoxia and greater paternal age are associated
with a higher risk of schizophrenia for the developing fetus. In addition, other prenatal
and perinatal adversities, including stress, infection, malnutrition, maternal diabetes, and
other medical conditions, have been linked with schizophrenia. However, the vast major-
ity of offspring with these risk factors do not develop schizophrenia.
Culture-Related Diagnostic Issues
Cultural and socioeconomic factors must be considered, particularly when the individual
and the clinician do not share the same cultural and socioeconomic background. Ideas that
appear to be delusional in one culture (e.g., witchcraft) may be commonly held in another.
In some cultures, visual or auditory hallucinations with a religious content (e.g., hearing
God’s voice) are a normal part of religious experience. In addition, the assessment of dis-
organized speech may be made difficult by linguistic variation in narrative styles across
cultures. The assessment of affect requires sensitivity to differences in styles of emotional
expression, eye contact, and body language, which vary across cultures. If the assessment
is conducted in a language that is different from the individual’s primary language, care
must be taken to ensure that alogia is not related to linguistic barriers. In certain cultures,
distress may take the form of hallucinations or pseudo-hallucinations and overvalued
ideas that may present clinically similar to true psychosis but are normative to the pa-
tient’s subgroup.
Gender-Related Diagnostic Issues
A number of features distinguish the clinical expression of schizophrenia in females and
males. The general incidence of schizophrenia tends to be slightly lower in females, par-
ticularly among treated cases. The age at onset is later in females, with a second mid-life
peak as described earlier (see the section “Development and Course” for this disorder).
Symptoms tend to be more affect-laden among females, and there are more psychotic
symptoms, as well as a greater propensity for psychotic symptoms to worsen in later life.
104 Schizophrenia Spectrum and Other Psychotic Disorders
Other symptom differences include less frequent negative symptoms and disorganization.
Finally, social functioning tends to remain better preserved in females. There are, how-
ever, frequent exceptions to these general caveats.
Suicide Risk
Approximately 5%-6% of individuals with schizophrenia die by suicide, about 20% attempt
suicide on one or more occasions, and many more have significant suicidal ideation. Suicidal
behavior is sometimes in response to command hallucinations to harm oneself or others.
Suicide risk remains high over the whole lifespan for males and females, although it may be
especially high for younger males with comorbid substance use. Other risk factors include
having depressive symptoms or feelings of hopelessness and being unemployed, and the
risk is higher, also, in the period after a psychotic episode or hospital discharge.
Functional Consequences of Schizophrenia
Schizophrenia is associated with significant social and occupational dysfunction. Making
educational progress and maintaining employment are frequently impaired by avolition
or other disorder manifestations, even when the cognitive skills are sufficient for the tasks
at hand. Most individuals are employed at a lower level than their parents, and most, par-
ticularly men, do not marry or have limited social contacts outside of their family.
Differential Diagnosis
Major depressive or bipolar disorder with psychotic or catatonic features. The distinc-
tion between schizophrenia and major depressive or bipolar disorder with psychotic
features or with catatonia depends on the temporal relationship between the mood distur-
bance and the psychosis, and on the severity of the depressive or manic symptoms. If de-
lusions or hallucinations occur exclusively during a major depressive or manic episode,
the diagnosis is depressive or bipolar disorder with psychotic features.
Schizoaffective disorder. A diagnosis of schizoaffective disorder requires that a major
depressive or manic episode occur concurrently with the active-phase symptoms and that
the mood symptoms be present for a majority of the total duration of the active periods.
Schizophreniform disorder and brief psychotic disorder. These disorders are of shorter
duration than schizophrenia as specified in Criterion C, which requires 6 months of symp-
toms. In schizophreniform disorder, the disturbance is present less than 6 months, and in
brief psychotic disorder, symptoms are present at least 1 day but less than 1 month.
Delusional disorder. Delusional disorder can be distinguished from schizophrenia by
the absence of the other symptoms characteristic of schizophrenia (e.g., delusions, prom-
inent auditory or visual hallucinations, disorganized speech, grossly disorganized or cata-
tonic behavior, negative symptoms).
Schizotypal personality disorder. Schizotypal personality disorder may be distinguished
from schizophrenia by subthreshold symptoms that are associated with persistent person-
ality features.
Obsessive-compulsive disorder and body dysmorphic disorder. Individuals with
obsessive-compulsive disorder and body dysmorphic disorder may present with poor or
absent insight, and the preoccupations may reach delusional proportions. But these
disorders are distinguished from schizophrenia by their prominent obsessions, compul-
sions, preoccupations with appearance or body odor, hoarding, or body-focused repeti-
tive behaviors.
Posttraumatic stress disorder. Posttraumatic stress disorder may include flashbacks that
have a hallucinatory quality, and hypervigilance may reach paranoid proportions. Buta trau-
Schizoaffective Disorder 105
matic event and characteristic symptom features relating to reliving or reacting to the event
are required to make the diagnosis.
Autism spectrum disorder or communication disorders. These disorders may also have
symptoms resembling a psychotic episode but are distinguished by their respective defi-
cits in social interaction with repetitive and restricted behaviors and other cognitive and
communication deficits. An individual with autism spectrum disorder or communication
disorder must have symptoms that meet full criteria for schizophrenia, with prominent
hallucinations or delusions for at least 1 month, in order to be diagnosed with schizophre-
nia as a comorbid condition.
Other mental disorders associated with a psychotic episode. The diagnosis of schizo-
phrenia is made only when the psychotic episode is persistent and not attributable to the
physiological effects of a substance or another medical condition. Individuals with a de-
lirium or major or minor neurocognitive disorder may present with psychotic symptoms,
but these would have a temporal relationship to the onset of cognitive changes consistent
with those disorders. Individuals with substance /medication-induced psychotic disorder
may present with symptoms characteristic of Criterion A for schizophrenia, but the sub-
stance/medication-induced psychotic disorder can usually be distinguished by the chron-
ological relationship of substance use to the onset and remission of the psychosis in the
absence of substance use.
Comorbidity
Rates of comorbidity with substance-related disorders are high in schizophrenia. Over
half of individuals with schizophrenia have tobacco use disorder and smoke cigarettes
regularly. Comorbidity with anxiety disorders is increasingly recognized in schizophre-
nia. Rates of obsessive-compulsive disorder and panic disorder are elevated in individuals
with schizophrenia compared with the general population. Schizotypal or paranoid per-
sonality disorder may sometimes precede the onset of schizophrenia.
Life expectancy is reduced in individuals with schizophrenia because of associated
medical conditions. Weight gain, diabetes, metabolic syndrome, and cardiovascular and
pulmonary disease are more common in schizophrenia than in the general population.
Poor engagement in health maintenance behaviors (e.g., cancer screening, exercise) in-
creases the risk of chronic disease, but other disorder factors, including medications, life-
style, cigarette smoking, and diet, may also play a role. A shared vulnerability for
psychosis and medical disorders may explain some of the medical comorbidity of schizo-
phrenia.
Schizoaffective Disorder
Diagnostic Criteria
A. An uninterrupted period of illness during which there is a major mood episode (major
depressive or manic) concurrent with Criterion A of schizophrenia.
Note: The major depressive episode must include Criterion A1: Depressed mood.
B. Delusions or hallucinations for 2 or more weeks in the absence of a major mood epi-
sode (depressive or manic) during the lifetime duration of the illness.
C. Symptoms that meet criteria for a major mood episode are present for the majority of
the total duration of the active and residual portions of the illness.
D. The disturbance is not attributable to the effects of a substance (e.g., a drug of abuse,
a medication) or another medical condition.
106 Schizophrenia Spectrum and Other Psychotic Disorders
Specify whether:
295.70 (F25.0) Bipolar type: This subtype applies if a manic episode is part of the pre-
sentation. Major depressive episodes may also occur.
295.70 (F25.1) Depressive type: This subtype applies if only major depressive epi-
sodes are part of the presentation.
Specify if:
With catatonia (refer to the criteria for catatonia associated with another mental disorder,
pp. 119-120, for definition).
Coding note: Use additional code 293.89 (F06.1} catatonia associated with
schizoaffective disorder to indicate the presence of the comorbid catatonia.
Specify if:
The following course specifiers are only to be used after a 1-year duration of the disorder
and if they are not in contradiction to the diagnostic course criteria.
First episode, currently in acute episode: First manifestation of the disorder meet-
ing the defining diagnostic symptom and time criteria. An acute episode is a time pe-
riod in which the symptom criteria are fulfilled.
First episode, currently in partial remission: Partia/ remission is a time period dur-
ing which an improvement after a previous episode is maintained and in which the de-
fining criteria of the disorder are only partially fulfilled.
First episode, currently in full remission: Fui/ remission is a period of time after a
previous episode during which no disorder-specific symptoms are present.
Multiple episodes, currently in acute episode: Multiple episodes may be deter-
mined after a minimum of two episodes (i.e., after a first episode, a remission and a
minimum of one relapse).
Multiple episodes, currently in partial remission
Multiple episodes, currently in full remission
Continuous: Symptoms fulfilling the diagnostic symptom criteria of the disorder are
remaining for the majority of the illness course, with subthreshold symptom periods be-
ing very brief relative to the overall course.
Unspecified
Specify current severity:
Severity is rated by a quantitative assessment of the primary symptoms of psychosis,
including delusions, hallucinations, disorganized speech, abnormal psychomotor be-
havior, and negative symptoms. Each of these symptoms may be rated for its current
severity (most severe in the last 7 days) on a 5-point scale ranging from 0 (not present)
to 4 (present and severe). (See Clinician-Rated Dimensions of Psychosis Symptom
Severity in the chapter “Assessment Measures.”)
Note: Diagnosis of schizoaffective disorder can be made without using this severity
specifier.
Note: For additional information on Development and Course (age-related factors), Risk
and Prognostic Factors (environmental risk factors), Culture-Related Diagnostic Issues,
and Gender-Related Diagnostic Issues, see the corresponding sections in schizophrenia,
bipolar I and II disorders, and major depressive disorder in their respective chapters.
Diagnostic Features
The diagnosis of schizoaffective disorder is based on the assessment of an uninterrupted
period of illness during which the individual continues to display active or residual symp-
toms of psychotic illness. The diagnosis is usually, but not necessarily, made during the
period of psychotic illness. At some time during the period, Criterion A for schizophrenia
Schizoaffective Disorder 107
has to be met. Criteria B (social dysfunction) and F (exclusion of autism spectrum disorder
or other communication disorder of childhood onset) for schizophrenia do not have to be
met. In addition to meeting Criterion A for schizophrenia, there is a major mood episode
{major depressive or manic) (Criterion A for schizoaffective disorder). Because loss of in-
terest or pleasure is common in schizophrenia, to meet Criterion A for schizoaffective dis-
order, the major depressive episode must include pervasive depressed mood (i.e., the
presence of markedly diminished interest or pleasure is not sufficient). Episodes of de-
pression or mania are present for the majority of the total duration of the illness (i.e., after
Criterion A has been met) (Criterion C for schizoaffective disorder). To separate schizoaf-
fective disorder from a depressive or bipolar disorder with psychotic features, delusions
or hallucinations must be present for at least 2 weeks in the absence of a major mood epi-
sode (depressive or manic) at some point during the lifetime duration of the illness (Cri-
terion B for schizoaffective disorder). The symptoms must not be attributable to the effects
of a substance or another medical condition (Criterion D for schizoaffective disorder).
Criterion C for schizoaffective disorder specifies that mood symptoms meeting criteria
for a major mood episode must be present for the majority of the total duration of the ac-
tive and residual portion of the illness. Criterion C requires the assessment of mood symp-
toms for the entire course of a psychotic illness, which differs from the criterion in DSM-IV,
which required only an assessment of the current period of illness. If the mood symptoms
are present for only a relatively brief period, the diagnosis is schizophrenia, not schizoaf-
fective disorder. When deciding whether an individual's presentation meets Criterion C,
the clinician should review the total duration of psychotic illness {i-e., both active and re-
sidual symptoms) and determine when significant mood symptoms (untreated or in need
of treatment with antidepressant and/or mood-stabilizing medication) accompanied the
psychotic symptoms. This determination requires sufficient historical information and
clinical judgment. For example, an individual with a 4-year history of active and residual
symptoms of schizophrenia develops depressive and manic episodes that, taken together,
do not occupy more than 1 year during the 4-year history of psychotic illness. This presen-
tation would not meet Criterion C.
In addition to the five symptom domain areas identified in the diagnostic criteria, the
assessment of cognition, depression, and mania symptom domains is vital for making crit-
ically important distinctions between the various schizophrenia spectrum and other psy-
chotic disorders.
Associated Features Supporting Diagnosis
Occupational functioning is frequently impaired, but this is not a defining criterion (in
contrast to schizophrenia). Restricted social contact and difficulties with self-care are as-
sociated with schizoaffective disorder, but negative symptoms may be less severe and less
persistent than those seen in schizophrenia. Anosognosia (i.e., poor insight) is also com-
mon in schizoaffective disorder, but the deficits in insight may be less severe and perva-
sive than those in schizophrenia. Individuals with schizoaffective disorder may be at
increased risk for later developing episodes of major depressive disorder or bipolar disor-
der if mood symptoms continue following the remission of symptoms meeting Criterion A
for schizophrenia. There may be associated alcohol and other substance-related disorders.
There are no tests or biological measures that can assist in making the diagnosis of
schizoaffective disorder. Whether schizoaffective disorder differs from schizophrenia
with regard to associated features such as structural or functional brain abnormalities,
cognitive deficits, or genetic risk factors is not clear.
Prevalence
Schizoaffective disorder appears to be about one-third as common as schizophrenia. Life-
time prevalence of schizoaffective disorder is estimated to be 0.3%. The incidence of
108 Schizophrenia Spectrum and Other Psychotic Disorders
schizoaffective disorder is higher in females than in males, mainly due to an increased in-
cidence of the depressive type among females.
Development and Course
The typical age at onset of schizoaffective disorder is early adulthood, although onset can
occur anywhere from adolescence to late in life. A significant number of individuals diag-
nosed with another psychotic illness initially will receive the diagnosis schizoaffective dis-
order later when the pattern of mood episodes has become more apparent. With the
current diagnostic Criterion C, it is expected that the diagnosis for some individuals will
convert from schizoaffective disorder to another disorder as mood symptoms become less
prominent. The prognosis for schizoaffective disorder is somewhat better than the prog-
nosis for schizophrenia but worse than the prognosis for mood disorders.
Schizoaffective disorder may occur in a variety of temporal patterns. The following is
a typical pattern: An individual may have pronounced auditory hallucinations and per-
secutory delusions for 2 months before the onset of a prominent major depressive episode.
The psychotic symptoms and the full major depressive episode are then present for 3 months.
Then, the individual recovers completely from the major depressive episode, but the psy-
chotic symptoms persist for another month before they too disappear. During this period
of illness, the individual’s symptoms concurrently met criteria for a major depressive ep-
isode and Criterion A for schizophrenia, and during this same period of illness, auditory
hallucinations and delusions were present both before and after the depressive phase. The
total period of illness lasted for about 6 months, with psychotic symptoms alone present
during the initial 2 months, both depressive and psychotic symptoms present during the
next 3 months, and psychotic symptoms alone present during the last month. In this in-
stance, the duration of the depressive episode was not brief relative to the total duration of
the psychotic disturbance, and thus the presentation qualifies for a diagnosis of schizoaf-
fective disorder.
The expression of psychotic symptoms across the lifespan is variable. Depressive or
manic symptoms can occur before the onset of psychosis, during acute psychotic episodes,
during residual! periods, and after cessation of psychosis. For example, an individual
might present with prominent mood symptoms during the prodromal stage of schizo-
phrenia. This pattern is not necessarily indicative of schizoaffective disorder, since it is the
co-occurrence of psychotic and mood symptoms that is diagnostic. For an individual with
symptoms that clearly meet the criteria for schizoaffective disorder but who on further fol-
low-up only presents with residual psychotic symptoms (such as subthreshold psychosis
and/or prominent negative symptoms), the diagnosis may be changed to schizophrenia,
as the total proportion of psychotic illness compared with mood symptoms becomes more
prominent. Schizoaffective disorder, bipolar type, may be more common in young adults,
whereas schizoaffective disorder, depressive type, may be more common in older adults.
Risk and Prognostic Factors
Genetic and physiological. Among individuals with schizophrenia, there may be an in-
creased risk for schizoaffective disorder in first-degree relatives. The risk for schizoaffec-
tive disorder may be increased among individuals who have a first-degree relative with
schizophrenia, bipolar disorder, or schizoaffective disorder.
Culture-Related Diagnostic Issues
Cultural and socioeconomic factors must be considered, particularly when the individual
and the clinician do not share the same cultural and economic background. Ideas that ap-
pear to be delusional in one culture (e.g., witchcraft) may be commonly held in another.
There is also some evidence in the literature for the overdiagnosis of schizophrenia com-
Schizoaffective Disorder 109
pared with schizoaffective disorder in African American and Hispanic populations, so
care must be taken to ensure a culturally appropriate evaluation that includes both psy-
chotic and affective symptoms.
Suicide Risk
The lifetime risk of suicide for schizophrenia and schizoaffective disorder is 5%, and the
presence of depressive symptoms is correlated with a higher risk for suicide. There is ev-
idence that suicide rates are higher in North American populations than in European,
Eastern European, South American, and Indian populations of individuals with schizo-
phrenia or schizoaffective disorder.
Functional Consequences of Schizoaffective Disorder
Schizoaffective disorder is associated with social and occupational dysfunction, but dys-
function is not a diagnostic criterion (as it is for schizophrenia), and there is substantial
variability between individuals diagnosed with schizoaffective disorder.
Differential Diagnosis
Other mental disorders and medical conditions. A wide variety of psychiatric and med-
ical conditions can manifest with psychotic and mood symptoms that must be considered
in the differential diagnosis of schizoaffective disorder. These include psychotic disorder
due to another medical condition; delirium; major neurocognitive disorder; substance /
medication-induced psychotic disorder or neurocognitive disorder; bipolar disorders
with psychotic features; major depressive disorder with psychotic features; depressive or
bipolar disorders with catatonic features; schizotypal, schizoid, or paranoid personality
disorder; brief psychotic disorder; schizophreniform disorder; schizophrenia; delusional
disorder; and other specified and unspecified schizophrenia spectrum and other psychotic
disorders. Medical conditions and substance use can present with a combination of psy-
chotic and mood symptoms, and thus psychotic disorder due to another medical condition
needs to be excluded. Distinguishing schizoaffective disorder from schizophrenia and
from depressive and bipolar disorders with psychotic features is often difficult. Criterion
C is designed to separate schizoaffective disorder from schizophrenia, and Criterion B is
designed to distinguish schizoaffective disorder from a depressive or bipolar disorder
with psychotic features. More specifically, schizoaffective disorder can be distinguished
from a depressive or bipolar disorder with psychotic features due to the presence of prom-
inent delusions and/or hallucinations for at least 2 weeks in the absence of a major mood
episode. In contrast, in depressive or bipolar disorders with psychotic features, the psy-
chotic features primarily occur during the mood episode(s). Because the relative propor-
tion of mood to psychotic symptoms may change over time, the appropriate diagnosis
may change from and to schizoaffective disorder (e.g., a diagnosis of schizoaffective dis-
order for a severe and prominent major depressive episode lasting 3 months during the
first 6 months of a persistent psychotic illness would be changed to schizophrenia if active
psychotic or prominent residual symptoms persist over several years without a recurrence
of another mood episode).
Psychotic disorder due to another medical condition. Other medical conditions and
substance use can manifest with a combination of psychotic and mood symptoms, and
thus psychotic disorder due to another medical condition needs to be excluded.
Schizophrenia, bipolar, and depressive disorders. Distinguishing schizoaffective dis-
order from schizophrenia and from depressive and bipolar disorders with psychotic fea-
tures is often difficult. Criterion C is designed to separate schizoaffective disorder from
schizophrenia, and Criterion B is designed to distinguish schizoaffective disorder from a
110 Schizophrenia Spectrum and Other Psychotic Disorders
depressive or bipolar disorder with psychotic features. More specifically, schizoaffective
disorder can be distinguished from a depressive or bipolar disorder with psychotic features
based on the presence of prominent delusions and/or hallucinations for at least 2 weeks in
the absence of a major mood episode. In contrast, in depressive or bipolar disorder with
psychotic features, the psychotic features primarily occur during the mood episode(s). Be-
cause the relative proportion of mood to psychotic symptoms may change over time, the
appropriate diagnosis may change from and to schizoaffective disorder. (For example, a
diagnosis of schizoaffective disorder for a severe and prominent major depressive episode
lasting 3 months during the first 6 months of a chronic psychotic illness would be changed
to schizophrenia if active psychotic or prominent residual symptoms persist over several
years without a recurrence of another mood episode.)
Comorbidity
Many individuals diagnosed with schizoaffective disorder are also diagnosed with other
mental disorders, especially substance use disorders and anxiety disorders. Similarly, the
incidence of medical conditions is increased above base rate for the general population
and leads to decreased life expectancy.
Substance/Medication-Induced
Psychotic Disorder
Diagnostic Criteria
A. Presence of one or both of the following symptoms:
1. Delusions.
2. Hallucinations.
B. There is evidence from the history, physical examination, or laboratory findings of both
(1) and (2):
1. The symptoms in Criterion A developed during or soon after substance intoxication
or withdrawal or after exposure to a medication.
2. The involved substance/medication is capable of producing the symptoms in Crite-
rion A.
C. The disturbance is not better explained by a psychotic disorder that is not substance/
medication-induced. Such evidence of an independent psychotic disorder could in-
clude the following:
The symptoms preceded the onset of the substance/medication use; the symptoms
persist for a substantial period of time (e.g., about 1 month) after the cessation of
acute withdrawal or severe intoxication; or there is other evidence of an indepen-
dent non-substance/medication-induced psychotic disorder (e.g., a history of recur-
rent non-substance/medication-related episodes).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
Note: This diagnosis should be made instead of a diagnosis of substance intoxication or
substance withdrawal only when the symptoms in Criterion A predominate in the clinical
picture and when they are sufficiently severe to warrant clinical attention.
Substance/Medication-Induced Psychotic Disorder 111
Coding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance/medica-
tion]-induced psychotic disorders are indicated in the table below. Note that the ICD-10-
CM code depends on whether or not there is a comorbid substance use disorder present
for the same class of substance. If a mild substance use disorder is comorbid with the sub-
stance-induced psychotic disorder, the 4th position character is “1,” and the clinician should
record “mild [substance] use disorder” before the substance-induced psychotic disorder
(e.g., “mild cocaine use disorder with cocaine-induced psychotic disorder’). If a moderate or
severe substance use disorder is comorbid with the substance-induced psychotic disor-
der, the 4th position character is “2,” and the clinician should record “moderate [substance]
use disorder’ or “severe [substance] use disorder,” depending on the severity of the co-
morbid substance use disorder. If there is no comorbid substance use disorder (e.g., after
a one-time heavy use of the substance), then the 4th position character is “9,” and the cli-
nician should record only the substance-induced psychotic disorder.
ICD-10-CM
With use
With use disorder, Without
disorder, moderate use
ICD-9-CM mild or severe disorder
Alcohol 291.9 F10.159 F10.259 F10.959
Cannabis 292.9 F12.159 F12.259 F12.959
Phencyclidine 292.9 F16.159 F16.259 F16.959
Other hallucinogen 292.9 F16.159 F16.259 F16.959
Inhalant 292.9 F18.159 F18.259 F18.959
Sedative, hypnotic, or 292.9 F13.159 F13.259 F13.959
anxiolytic
Amphetamine (or other 292.9 F15.159 F15.259 F15.959
stimulant)
Cocaine 292.9 F14.159 F14.259 F14.959
Other (or unknown) substance 292.9 F19.159 F19.259 F19.959
Specify if (see Table 1 in the chapter “Substance-Related and Addictive Disorders” for diag-
noses associated with substance class):
With onset during intoxication: If the criteria are met for intoxication with the sub-
stance and the symptoms develop during intoxication.
With onset during withdrawal: If the criteria are met for withdrawal from the sub-
stance and the symptoms develop during, or shortly after, withdrawal.
Specify current severity:
Severity is rated by a quantitative assessment of the primary symptoms of psychosis,
including delusions, hallucinations, abnorma! psychomotor behavior, and negative
symptoms. Each of these symptoms may be rated for its current severity (most severe
in the last 7 days) on a 5-point scale ranging from 0 (not present) to 4 (present and
severe). (See Clinician-Rated Dimensions of Psychosis Symptom Severity in the chap-
ter “Assessment Measures.”)
Note: Diagnosis of substance/medication-induced psychotic disorder can be made
without using this severity specifier.
112 Schizophrenia Spectrum and Other Psychotic Disorders
Recording Procedures
ICD-9-CM. The name of the substance/medication-induced psychotic disorder begins
with the specific substance (e.g., cocaine, dexamethasone) that is presumed to be causing
the delusions or hallucinations. The diagnostic code is selected from the table included in
the criteria set, which is based on the drug class. For substances that do not fit into any of
the classes (e.g., dexamethasone), the code for “other substance” should be used; and in
cases in which a substance is judged to be an etiological factor but the specific class of sub-
stance is unknown, the category “unknown substance” should be used.
The name of the disorder is followed by the specification of onset (i.e., onset during in-
toxication, onset during withdrawal). Unlike the recording procedures for ICD-10-CM,
which combine the substance-induced disorder and substance use disorder into a single
code, for ICD-9-CM a separate diagnostic code is given for the substance use disorder. For
example, in the case of delusions occurring during intoxication in a man with a severe co-
caine use disorder, the diagnosis is 292.9 cocaine-induced psychotic disorder, with onset
during intoxication. An additional diagnosis of 304.20 severe cocaine use disorder is also
given. When more than one substance is judged to play a significant role in the development
of psychotic symptoms, each should be listed separately (e.g., 292.9 cannabis-induced psy-
chotic disorder with onset during intoxication, with severe cannabis use disorder; 292.9
phencyclidine-induced psychotic disorder, with onset during intoxication, with mild
phencyclidine use disorder).
ICD-10-CM. The name of the substance/medication-induced psychotic disorder begins
with the specific substance (e.g., cocaine, dexamethasone) that is presumed to be causing
the delusions or hallucinations. The diagnostic code is selected from the table included in
the criteria set, which is based on the drug class and presence or absence of a comorbid
substance use disorder. For substances that do not fit into any of the classes (e.g., dexa-
methasone), the code for “other substance” with no comorbid substance use should be
used; and in cases in which a substance is judged to be an etiological factor but the specific
class of substance is unknown, the category “unknown substance” with no comorbid sub-
stance use should be used.
When recording the name of the disorder, the comorbid substance use disorder (if any)
is listed first, followed by the word “with,” followed by the name of the substance-induced
psychotic disorder, followed by the specification of onset (i.e., onset during intoxication,
onset during withdrawal). For example, in the case of delusions occurring during intoxi-
cation in a man with a severe cocaine use disorder, the diagnosis is F14.259 severe cocaine
use disorder with cocaine-induced psychotic disorder, with onset during intoxication. A
separate diagnosis of the comorbid severe cocaine use disorder is not given. If the sub-
stance-induced psychotic disorder occurs without a comorbid substance use disorder
(e.g., after a one-time heavy use of the substance), no accompanying substance use disor-
der is noted (e.g., F16.959 phencyclidine-induced psychotic disorder, with onset during in-
toxication). When more than one substance is judged to play a significant role in the
development of psychotic symptoms, each should be listed separately (e.g., F12.259 severe
cannabis use disorder with cannabis-induced psychotic disorder, with onset during intox-
ication; F16.159 mild phencyclidine use disorder with phencyclidine-induced psychotic
disorder, with onset during intoxication).
Diagnostic Features
The essential features of substance /medication-induced psychotic disorder are prominent
delusions and/or hallucinations (Criterion A) that are judged to be due to the physiolog-
ical effects of a substance / medication (i.e., a drug of abuse, a medication, or a toxin expo-
sure) (Criterion B). Hallucinations that the individual realizes are substance/medication-
induced are not included here and instead would be diagnosed as substance intoxication
Substance/Medication-Induced Psychotic Disorder 113
or substance withdrawal with the accompanying specifier “with perceptual disturbances”
(applies to alcohol withdrawal; cannabis intoxication; sedative, hypnotic, or anxiolytic
withdrawal; and stimulant intoxication).
A substance /medication-induced psychotic disorder is distinguished from a primary
psychotic disorder by considering the onset, course, and other factors. For drugs of abuse,
there must be evidence from the history, physical examination, or laboratory findings of
substance use, intoxication, or withdrawal. Substance /medication-induced psychotic
disorders arise during or soon after exposure to a medication or after substance intoxica-
tion or withdrawal but can persist for weeks, whereas primary psychotic disorders may
precede the onset of substance/medication use or may occur during times of sustained ab-
stinence. Once initiated, the psychotic symptoms may continue as long as the substance/
medication use continues. Another consideration is the presence of features that are atyp-
ical of a primary psychotic disorder (e.g., atypical age at onset or course). For example, the
appearance of delusions de novo in a person older than 35 years without a known history
of a primary psychotic disorder should suggest the possibility of a substance/medication-
induced psychotic disorder. Even a prior history of a primary psychotic disorder does not
rule out the possibility of a substance/medication-induced psychotic disorder. In contrast,
factors that suggest that the psychotic symptoms are better accounted for by a primary
psychotic disorder include persistence of psychotic symptoms for a substantial period of
time (i.e., amonth or more) after the end of substance intoxication or acute substance with-
drawal or after cessation of medication use; or a history of prior recurrent primary psy-
chotic disorders. Other causes of psychotic symptoms must be considered even in an
individual with substance intoxication or withdrawal, because substance use problems are
not uncommon among individuals with non-substance/medication-induced psychotic
disorders.
In addition to the four symptom domain areas identified in the diagnostic criteria, the
assessment of cognition, depression, and mania symptom domains is vital for making crit-
ically important distinctions between the various schizophrenia spectrum and other psy-
chotic disorders.
Associated Features Supporting Diagnosis
Psychotic disorders can occur in association with intoxication with the following classes of
substances: alcohol; cannabis; hallucinogens, including phencyclidine and related sub-
stances; inhalants; sedatives, hypnotics, and anxiolytics; stimulants (including cocaine);
and other (or unknown) substances. Psychotic disorders can occur in association with with-
drawal from the following classes of substances: alcohol; sedatives, hypnotics, and anxio-
lytics; and other (or unknown) substances.
Some of the medications reported to evoke psychotic symptoms include anesthetics
and analgesics, anticholinergic agents, anticonvulsants, antihistamines, antihypertensive
and cardiovascular medications, antimicrobial medications, antiparkinsonian medica-
tions, chemotherapeutic agents (e.g., cyclosporine, procarbazine), corticosteroids, gastro-
intestinal medications, muscle relaxants, nonsteroidal anti-inflammatory medications,
other over-the-counter medications (e.g., phenylephrine, pseudoephedrine), antidepres-
sant medication, and disulfiram. Toxins reported to induce psychotic symptoms include
anticholinesterase, organophosphate insecticides, sarin and other nerve gases, carbon
monoxide, carbon dioxide, and volatile substances such as fuel or paint.
Prevaience
Prevalence of substance/medication-induced psychotic disorder in the general popula-
tion is unknown. Between 7% and 25% of individuals presenting with a first episode of
psychosis in different settings are reported to have substance/medication-induced psy-
chotic disorder.
114 Schizophrenia Spectrum and Other Psychotic Disorders
Development and Course
The initiation of the disorder may vary considerably with the substance. For example,
smoking a high dose of cocaine may produce psychosis within minutes, whereas days or
weeks of high-dose alcohol or sedative use may be required to produce psychosis. Alco-
hol-induced psychotic disorder, with hallucinations, usually occurs only after prolonged,
heavy ingestion of alcohol in individuals who have moderate to severe alcohol use disorder,
and the hallucinations are generally auditory in nature.
Psychotic disorders induced by amphetamine and cocaine share similar clinical fea-
tures. Persecutory delusions may rapidly develop shortly after use of amphetamine or a
similarly acting sympathomimetic. The hallucination of bugs or vermin crawling in or un-
der the skin (formication) can lead to scratching and extensive skin excoriations. Cannabis-
induced psychotic disorder may develop shortly after high-dose cannabis use and usually
involves persecutory delusions, marked anxiety, emotional lability, and depersonalization.
The disorder usually remits within a day but in some cases may persist for a few days.
Substance/medication-induced psychotic disorder may at times persist when the offend-
ing agent is removed, such that it may be difficult initially to distinguish it from an indepen-
dent psychotic disorder. Agents such as amphetamines, phencyclidine, and cocaine have been
reported to evoke temporary psychotic states that can sometimes persist for weeks or longer
despite removal of the agent and treatment with neuroleptic medication. In later life, poly-
pharmacy for medical conditions and exposure to medications for parkinsonism, cardiovas-
cular disease, and other medical disorders may be associated with a greater likelihood of
psychosis induced by prescription medications as opposed to substances of abuse.
Diagnostic Markers
With substances for which relevant blood levels are available (e.g., blood alcohol level,
other quantifiable blood levels such as digoxin), the presence of a level consistent with tox-
icity may increase diagnostic certainty.
Functionai Consequences of
Substance/Medication-Induced Psychotic Disorder
Substance/medication-induced psychotic disorder is typically severely disabling and
consequently is observed most frequently in emergency rooms, as individuals are often
brought to the acute-care setting when it occurs. However, the disability is typically self-
limited and resolves upon removal of the offending agent.
Differential Diagnosis
Substance intoxication or substance withdrawal. Individuals intoxicated with stimu-
lants, cannabis, the opioid meperidine, or phencyclidine, or those withdrawing from alco-
hol or sedatives, may experience altered perceptions that they recognize as drug effects. If
reality testing for these experiences remains intact {i.e., the individual recognizes that the
perception is substance induced and neither believes in nor acts on it), the diagnosis is not
substance/medication-induced psychotic disorder. Instead, substance intoxication or
substance withdrawal, with perceptual disturbances, is diagnosed (e.g., cocaine intoxica-
tion, with perceptual disturbances). “Flashback” hallucinations that can occur long after
the use of hallucinogens has stopped are diagnosed as hallucinogen persisting perception
disorder. If substance /medication-induced psychotic symptoms occur exclusively during
the course of a delirium, as in severe forms of alcohol withdrawal, the psychotic symptoms
are considered to be an associated feature of the delirium and are not diagnosed sepa-
rately. Delusions in the context of a major or mild neurocognitive disorder would be di-
agnosed as major or mild neurocognitive disorder, with behavioral disturbance.
Psychotic Disorder Due to Another Medical Condition 115
Primary psychotic disorder. A substance/medication-induced psychotic disorder is
distinguished from a primary psychotic disorder, such as schizophrenia, schizoaffective
disorder, delusional disorder, brief psychotic disorder, other specified schizophrenia
spectrum and other psychotic disorder, or unspecified schizophrenia spectrum and other
psychotic disorder, by the fact that a substance is judged to be etiologically related to the
symptoms.
Psychotic disorder due to another medical condition. A substance/medication-induced
psychotic disorder due to a prescribed treatment for a mental or medical condition must
have its onset while the individual is receiving the medication (or during withdrawal, if
there is a withdrawal syndrome associated with the medication). Because individuals with
medical conditions often take medications for those conditions, the clinician must con-
sider the possibility that the psychotic symptoms are caused by the physiological conse-
quences of the medical condition rather than the medication, in which case psychotic
disorder due to another medical condition is diagnosed. The history often provides the
primary basis for such a judgment. At times, a change in the treatment for the medical con-
dition (e.g., medication substitution or discontinuation) may be needed to determine em-
pirically for that individual whether the medication is the causative agent. If the clinician
has ascertained that the disturbance is attributable to both a medical condition and sub-
stance/ medication use, both diagnoses (i.e., psychotic disorder due to another medical
condition and substance/medication-induced psychotic disorder) may be given.
Psychotic Disorder
Due to Another Medical Condition
Diagnostic Criteria
A. Prominent hallucinations or delusions.
B. There is evidence from the history, physical examination, or laboratory findings that the
disturbance is the direct pathophysiological consequence of another medical condi-
tion.
C. The disturbance is not better explained by another mental disorder.
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
Specify whether:
Code based on predominant symptom:
293.81 (F06.2) With delusions: If delusions are the predominant symptom.
293.82 (F06.0) With hallucinations: If hallucinations are the predominant symptom.
Coding note: Include the name of the other medical condition in the name of the mental
disorder (e.g., 293.81 [F06.2] psychotic disorder due to malignant lung neoplasm, with de-
lusions). The other medical condition should be coded and listed separately immediately
before the psychotic disorder due to the medical condition (e.g., 162.9 [C34.90] malignant
lung neoplasm; 293.81 [F06.2] psychotic disorder due to malignant lung neoplasm, with
delusions).
Specify current severity:
Severity is rated by a quantitative assessment of the primary symptoms of psychosis,
including delusions, hallucinations, abnormal psychomotor behavior, and negative
symptoms. Each of these symptoms may be rated for its current severity (most severe
in the last 7 days) on a 5-point scale ranging from 0 (not present) to 4 (present and
116 Schizophrenia Spectrum and Other Psychotic Disorders
severe). (See Clinician-Rated Dimensions of Psychosis Symptom Severity in the chap-
ter “Assessment Measures.”)
Note: Diagnosis of psychotic disorder due to another medical condition can be made
without using this severity specifier.
Specifiers
In addition to the symptom domain areas identified in the diagnostic criteria, the assess-
ment of cognition, depression, and mania symptom domains is vital for making critically
important distinctions between the various schizophrenia spectrum and other psychotic
disorders.
Diagnostic Features
The essential features of psychotic disorder due to another medical condition are promi-
nent delusions or hallucinations that are judged to be attributable to the physiological ef-
fects of another medical condition and are not better explained by another mental disorder
(e.g., the symptoms are not a psychologically mediated response to a severe medical con-
dition, in which case a diagnosis of brief psychotic disorder, with marked stressor, would
be appropriate).
Hallucinations can occur in any sensory modality (i.e., visual, olfactory, gustatory, tac-
tile, or auditory), but certain etiological factors are likely to evoke specific hallucinatory
phenomena. Olfactory hallucinations are suggestive of temporal lobe epilepsy. Hallucina-
tions may vary from simple and unformed to highly complex and organized, depending
on etiological and environmental factors. Psychotic disorder due to another medical con-
dition is generally not diagnosed if the individual maintains reality testing for the hallu-
cinations and appreciates that they result from the medical condition. Delusions may have
a variety of themes, including somatic, grandiose, religious, and, most commonly, perse-
cutory. On the whole, however, associations between delusions and particular medical
conditions appear to be less specific than is the case for hallucinations.
In determining whether the psychotic disturbance is attributable to another medical
condition, the presence of a medical condition must be identified and considered to be the
etiology of the psychosis through a physiological mechanism. Although there are no
infallible guidelines for determining whether the relationship between the psychotic distur-
bance and the medical condition is etiological, several considerations provide some guidance.
One consideration is the presence of a temporal association between the onset, exacerba-
tion, or remission of the medical condition and that of the psychotic disturbance. A second
consideration is the presence of features that are atypical for a psychotic disorder (e.g.,
atypical age at onset or presence of visual or olfactory hallucinations). The disturbance must
also be distinguished from a substance/medication-induced psychotic disorder or an-
other mental disorder (e.g., an adjustment disorder).
Associated Features Supporting Diagnosis
The temporal association of the onset or exacerbation of the medical condition offers the
greatest diagnostic certainty that the delusions or hallucinations are attributable to a med-
ical condition. Additional factors may include concomitant treatments for the underlying
medical condition that confer a risk for psychosis independently, such as steroid treatment
for autoimmune disorders.
Prevalence
Prevalence rates for psychotic disorder due to another medical condition are difficult to es-
timate given the wide variety of underlying medical etiologies. Lifetime prevalence has
Psychotic Disorder Due to Another Medical Condition 117
been estimated to range from 0.21% to 0.54%. When the prevalence findings are stratified
by age group, individuals older than 65 years have a significantly greater prevalence of
0.74% compared with those in younger age groups. Rates of psychosis also vary according
to the underlying medical condition; conditions most commonly associated with psy-
chosis include untreated endocrine and metabolic disorders, autoimmune disorders (e.g.,
systemic lupus erythematosus, N-methyl-D-aspartate (NMDA) receptor autoimmune en-
cephalitis), or temporal lobe epilepsy. Psychosis due to epilepsy has been further differ-
entiated into ictal, postictal, and interictal psychosis. The most common of these is postictal
psychosis, observed in 2%-7.8% of epilepsy patients. Among older individuals, there may
be a higher prevalence of the disorder in females, although additional gender-related fea-
tures are not clear and vary considerably with the gender distributions of the underlying
medical conditions.
Development and Course
Psychotic disorder due to another medical condition may be a single transient state or it
may be recurrent, cycling with exacerbations and remissions of the underlying medical
condition. Although treatment of the underlying medical condition often results in a res-
olution of the psychosis, this is not always the case, and psychotic symptoms may persist
long after the medical event (e.g., psychotic disorder due to focal brain injury). In the con-
text of chronic conditions such as multiple sclerosis or chronic interictal psychosis of epi-
lepsy, the psychosis may assume a long-term course.
The expression of psychotic disorder due to another medical condition does not differ
substantially in phenomenology depending on age at occurrence. However, older age
groups have a higher prevalence of the disorder, which is most likely due to the increasing
medical burden associated with advanced age and the cumulative effects of deleterious
exposures and age-related processes (e.g., atherosclerosis). The nature of the underlying
medical conditions is likely to change across the lifespan, with younger age groups more
affected by epilepsy, head trauma, autoimmune, and neoplastic diseases of early to mid-
life, and older age groups more affected by stroke disease, anoxic events, and multiple sys-
tem comorbidities. Underlying factors with increasing age, such as preexisting cognitive
impairment as well as vision and hearing impairments, may incur a greater risk for psy-
chosis, possibly by serving to lower the threshold for experiencing psychosis.
Risk and Prognostic Factors
Course modifiers. Identification and treatment of the underlying medical condition has
the greatest impact on course, although preexisting central nervous system injury may
confer a worse course outcome (e.g., head trauma, cerebrovascular disease).
Diagnostic Markers
The diagnosis of psychotic disorder due to another medical condition depends on the clin-
ical condition of each individual, and the diagnostic tests will vary according to that con-
dition. A variety of medical conditions may cause psychotic symptoms. These include
neurological conditions (e.g., neoplasms, cerebrovascular disease, Huntington's disease,
multiple sclerosis, epilepsy, auditory or visual nerve injury or impairment, deafness,
migraine, central nervous system infections), endocrine conditions (e.g., hyper- and hypo-
thyroidism, hyper- and hypoparathyroidism, hyper- and hypoadrenocorticism), metabolic
conditions (e.g., hypoxia, hypercarbia, hypoglycemia), fluid or electrolyte imbalances,
hepatic or renal diseases, and autoimmune disorders with central nervous system involve-
ment (e.g., systemic lupus erythematosus). The associated physical examination findings,
laboratory findings, and patterns of prevalence or onset reflect the etiological medical
condition.
118 Schizophrenia Spectrum and Other Psychotic Disorders
Suicide Risk
Suicide risk in the context of psychotic disorder due to another medical condition is not
clearly delineated, although certain conditions such as epilepsy and multiple sclerosis are
associated with increased rates of suicide, which may be further increased in the presence
of psychosis.
Functional Consequences of Psychotic Disorder
Due to Another Medical Condition
Functional disability is typically severe in the context of psychotic disorder due to another
medical condition but will vary considerably by the type of condition and likely improve
with successful resolution of the condition.
Differential Diagnosis
Delirium. Hallucinations and delusions commonly occur in the context of a delirium;
however, a separate diagnosis of psychotic disorder due to another medical condition is
not given if the disturbance occurs exclusively during the course of a delirium. Delusions
in the context of a major or mild neurocognitive disorder would be diagnosed as major or
mild neurocognitive disorder, with behavioral disturbance.
Substance/medication-induced psychotic disorder. If there is evidence of recent or
prolonged substance use (including medications with psychoactive effects), withdrawal
from a substance, or exposure to a toxin (e.g., LSD [lysergic acid diethylamide] intoxica-
tion, alcohol withdrawal), a substance /medication-induced psychotic disorder should be
considered. Symptoms that occur during or shortly after (i.e., within 4 weeks) of substance
intoxication or withdrawal or after medication use may be especially indicative of a sub-
stance-induced psychotic disorder, depending on the character, duration, or amount of
the substance used. If the clinician has ascertained that the disturbance is due to both a
medical condition and substance use, both diagnoses (i.e., psychotic disorder due to an-
other medical condition and substance /medication-induced psychotic disorder) can be
given.
Psychotic disorder. Psychotic disorder due to another medical condition must be distin-
guished from a psychotic disorder (e.g., schizophrenia, delusional disorder, schizoaffective
disorder) or a depressive or bipolar disorder, with psychotic features. In psychotic disor-
ders and in depressive or bipolar disorders, with psychotic features, no specific and direct
causative physiological mechanisms associated with a medical condition can be demon-
strated. Late age at onset and the absence of a personal or family history of schizophrenia
or delusional disorder suggest the need for a thorough assessment to rule out the diagno-
sis of psychotic disorder due to another medical condition. Auditory hallucinations that
involve voices speaking complex sentences are more characteristic of schizophrenia than
of psychotic disorder due to a medical condition. Other types of hallucinations (e.g., vi-
sual, olfactory) commonly signal a psychotic disorder due to another medical condition or
a substance/medication-induced psychotic disorder.
Comorbidity
Psychotic disorder due to another medical condition in individuals older than 80 years is
associated with concurrent major neurocognitive disorder (dementia).
Catatonia Associated With Another Mentai Disorder (Catatonia Specifier) 119
Catatonia
Catatonia can occur in the context of several disorders, including neurodevelopmental,
psychotic, bipolar, depressive disorders, and other medical conditions (e.g., cerebral folate
deficiency, rare autoimmune and paraneoplastic disorders. The manual does not treat
catatonia as an independent class but recognizes a) catatonia associated with another men-
tal disorder (i.e., a neurodevelopmental, psychotic disorder, a bipolar disorder, a depres-
sive disorder, or other mental disorder), b) catatonic disorder due to another medical
condition, and c) unspecified catatonia.
Catatonia is defined by the presence of three or more of 12 psychomotor features in the
diagnostic criteria for catatonia associated with another mental disorder and catatonic dis-
order due to another medical condition. The essential feature of catatonia is a marked psy-
chomotor disturbance that may involve decreased motor activity, decreased engagement
during interview or physical examination, or excessive and peculiar motor activity. The
clinical presentation of catatonia can be puzzling, as the psychomotor disturbance may
range from marked unresponsiveness to marked agitation. Motoric immobility may be se-
vere (stupor) or moderate (catalepsy and waxy flexibility). Similarly, decreased engage-
ment may be severe (mutism) or moderate (negativism). Excessive and peculiar motor
behaviors can be complex (e.g., stereotypy) or simple (agitation) and may include echola-
lia and echopraxia. In extreme cases, the same individual may wax and wane between de-
creased and excessive motor activity. The seemingly opposing clinical features and
variable manifestations of the diagnosis contribute to a lack of awareness and decreased
recognition of catatonia. During severe stages of catatonia, the individual may need care-
ful supervision to avoid self-harm or harming others. There are potential risks from mal-
nutrition, exhaustion, hyperpyrexia and self-inflicted injury.
Catatonia Associated With Another
Mental Disorder (Catatonia Specifier)
293.89 (FO6G.1)
A. The clinical picture is dominated by three (or more) of the following symptoms:
Stupor (i.e., no psychomotor activity; not actively relating to environment).
Catalepsy (i.e., passive induction of a posture held against gravity).
Waxy flexibility {i.e., slight, even resistance to positioning by examiner).
Mutism (i.e., no, or very little, verbal response [exclude if known aphasia]).
Negativism (i.e., opposition or no response to instructions or external stimuli).
Posturing (i.e., spontaneous and active maintenance of a posture against gravity).
Mannerism (i.e., odd, circumstantial caricature of normal actions).
Stereotypy (i.e., repetitive, abnormally frequent, non-goal-directed movements).
Agitation, not influenced by external stimuli.
10. Grimacing.
11. Echolalia (i-e., mimicking another's speech).
12. Echopraxia {i-e., mimicking another's movements).
Coding note: Indicate the name of the associated mental disorder when recording the
name of the condition (i.e., 293.89 [F06.1] catatonia associated with major depressive dis-
order). Code first the associated mental disorder (e.g., neurodevelopmental disorder, brief
ONOAPON =
©
120 Schizophrenia Spectrum and Other Psychotic Disorders
psychotic disorder, schizophreniform disorder, schizophrenia, schizoaffective disorder,
bipolar disorder, major depressive disorder, or other mental disorder) (e.g., 295.70 [F25.1]
schizoaffective disorder, depressive type; 293.89 [FO6.1] catatonia associated with
schizoaffective disorder).
Diagnostic Features
Catatonia associated with another mental disorder (catatonia specifier) may be used when
criteria are met for catatonia during the course of a neurodevelopmental, psychotic, bipo-
lar, depressive, or other mental disorder. The catatonia specifier is appropriate when the
clinical picture is characterized by marked psychomotor disturbance and involves at least
three of the 12 diagnostic features listed in Criterion A. Catatonia is typically diagnosed in
an inpatient setting and occurs in up to 35% of individuals with schizophrenia, but the ma-
jority of catatonia cases involve individuals with depressive or bipolar disorders. Before
the catatonia specifier is used in neurodevelopmental, psychotic, bipolar, depressive, or
other mental disorders, a wide variety of other medical conditions need to be ruled out;
these conditions include, but are not limited to, medical conditions due to infectious, met-
abolic, or neurological conditions (see “Catatonic Disorder Due to Another Medical Con-
dition”). Catatonia can also be a side effect of a medication (see the chapter “Medication-
Induced Movement Disorders and Other Adverse Effects of Medication”). Because of the
seriousness of the complications, particular attention should be paid to the possibility that
the catatonia is attributable to 333.92 (G21.0) neuroleptic malignant syndrome.
Catatonic Disorder Due to
Another Medical Condition
Diagnostic Criteria 293.89 (FO6.1)
A. The clinicai picture is dominated by three (or more) of the following symptoms:
1. Stupor (i.e., no psychomotor activity; not actively relating to environment).
Catalepsy (i.e., passive induction of a posture held against gravity).
Waxy flexibility (i.e., slight, even resistance to positioning by examiner).
Mutism (i.e., no, or very little, verbal response [Note: not applicable if there is an
established aphasia]).
Negativism (i.e., opposition or no response to instructions or external stimuli).
Posturing (i.e., spontaneous and active maintenance of a posture against gravity).
Mannerism (i.e., odd, circumstantial caricature of normal actions).
Stereotypy (i.e., repetitive, abnormaily frequent, non-goal-directed movements).
9. Agitation, not influenced by external stimuli.
10. Grimacing.
11. Echolalia (i.e., mimicking another's speech).
12. Echopraxia (i.e., mimicking another's movements).
B. There is evidence from the history, physical examination, or laboratory findings that the
disturbance is the direct pathophysiological consequence of another medical condition.
C. The disturbance is not better explained by another mental disorder (e.g., a manic episode).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
oN
DNA
Unspecified Catatonia 121
Coding note: Include the name of the medical condition in the name of the mental disor-
der (e.g., 293.89 [F06.1]) catatonic disorder due to hepatic encephalopathy). The other
medical condition should be coded and listed separately immediately before the cata-
tonic disorder due to the medical condition (e.g., 572.2 [K71.90] hepatic encephalopathy;
293.89 [F06.1] catatonic disorder due to hepatic encephalopathy).
Diagnostic Features
The essential feature of catatonic disorder due to another medical condition is the presence
of catatonia that is judged to be attributed to the physiological effects of another medical
condition. Catatonia can be diagnosed by the presence of at least three of the 12 clinical fea-
tures in Criterion A. There must be evidence from the history, physical examination, or
laboratory findings that the catatonia is attributable to another medical condition (Crite-
rion B). The diagnosis is not given if the catatonia is better explained by another mental
disorder (e.g., manic episode) (Criterion C) or if it occurs exclusively during the course of
a delirium (Criterion D).
Associated Features Supporting Diagnosis
A variety of medical conditions may cause catatonia, especially neurological conditions
(e.g., neoplasms, head trauma, cerebrovascular disease, encephalitis) and metabolic con-
ditions (e.g., hypercalcemia, hepatic encephalopathy, homocystinuria, diabetic ketoacido-
sis). The associated physical examination findings, laboratory findings, and patterns of
prevalence and onset reflect those of the etiological medical condition.
Differential Diagnosis
A separate diagnosis of catatonic disorder due to another medical condition is not given if
the catatonia occurs exclusively during the course of a delirium or neuroleptic malignant
syndrome. If the individual is currently taking neuroleptic medication, consideration
should be given to medication-induced movement disorders (e.g., abnormal positioning
may be due to neuroleptic-induced acute dystonia) or neuroleptic malignant syndrome
(e.g., catatonic-like features may be present, along with associated vital sign and/or labo-
ratory abnormalities). Catatonic symptoms may be present in any of the following five
psychotic disorders: brief psychotic disorder, schizophreniform disorder, schizophrenia,
schizoaffective disorder, and substance/medication-induced psychotic disorder. It may
also be present in some of the neurodevelopmental disorders, in all of the bipolar and de-
pressive disorders, and in other mental disorders.
Unspecified Catatonia
This category applies to presentations in which symptoms characteristic of catatonia
cause Clinically significant distress or impairment in social, occupational, or other impor-
tant areas of functioning but either the nature of the underlying mental disorder or other
medical condition is unclear, full criteria for catatonia are not met, or there is insufficient
information to make a more specific diagnosis (e.g., in emergency room settings).
Coding note: Code first 781.99 (R29.818) other symptoms involving nervous and muscu-
loskeletal systems, followed by 293.89 (F06.1) unspecified catatonia.
122 Schizophrenia Spectrum and Other Psychotic Disorders
Other Specified Schizophrenia Spectrum and
Other Psychotic Disorder
298.8 (F28)
This category applies to presentations in which symptoms characteristic of a schizophre-
nia spectrum and other psychotic disorder that cause clinically significant distress or im-
pairment in social, occupational, or other important areas of functioning predominate but
do not meet the full criteria for any of the disorders in the schizophrenia spectrum and other
psychotic disorders diagnostic class. The other specified schizophrenia spectrum and oth-
er psychotic disorder category is used in situations in which the clinician chooses to com-
municate the specific reason that the presentation does not meet the criteria for any
specific schizophrenia spectrum and other psychotic disorder. This is done by recording “oth-
er specified schizophrenia spectrum and other psychotic disorder” followed by the specific
reason (e.g., “persistent auditory hallucinations”).
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Persistent auditory hallucinations occurring in the absence of any other features.
2. Delusions with significant overlapping mood episodes: This includes persistent
delusions with periods of overlapping mood episodes that are present for a substantial
portion of the delusional disturbance (such that the criterion stipulating only brief mood
disturbance in delusional disorder is not met).
3. Attenuated psychosis syndrome: This syndrome is characterized by psychotic-like
symptoms that are below a threshold for full psychosis (e.g., the symptoms are less
severe and more transient, and insight is relatively maintained).
4. Deiusionai symptoms in partner of individuai with deiusionai disorder: In the
context of a relationship, the delusional material from the dominant partner provides
content for delusional belief by the individual who may not otherwise entirely meet cri-
teria for delusional disorder.
Unspecified Schizophrenia Spectrum and
Other Psychotic Disorder
298.9 (F29)
This category applies to presentations in which symptoms characteristic of a schizophre-
nia spectrum and other psychotic disorder that cause clinically significant distress or im-
pairment in social, occupational, or other important areas of functioning predominate but
do not meet the full criteria for any of the disorders in the schizophrenia spectrum and oth-
er psychotic disorders diagnostic class. The unspecified schizophrenia spectrum and oth-
er psychotic disorder category is used in situations in which the clinician chooses not to
specify the reason that the criteria are not met for a specific schizophrenia spectrum and
other psychotic disorder, and includes presentations in which there is insufficient informa-
tion to make a more specific diagnosis (e.g., in emergency room settings).
Bipolar and
Related Disorders
Bipolar and related disorders are separated from the depressive disorders in
DSM-5 and placed between the chapters on schizophrenia spectrum and other psychotic
disorders and depressive disorders in recognition of their place as a bridge between the
two diagnostic classes in terms of symptomatology, family history, and genetics. The di-
agnoses included in this chapter are bipolar I disorder, bipolar II disorder, cyclothymic
disorder, substance/medication-induced bipolar and related disorder, bipolar and relat-
ed disorder due to another medical condition, other specified bipolar and related disor-
der, and unspecified bipolar and related disorder.
The bipolar I disorder criteria represent the modern understanding of the classic
manic-depressive disorder or affective psychosis described in the nineteenth century, dif-
fering from that classic description only to the extent that neither psychosis nor the lifetime
experience of a major depressive episode is a requirement. However, the vast majority of
individuals whose symptoms meet the criteria for a fully syndromal manic episode also
experience major depressive episodes during the course of their lives.
Bipolar II disorder, requiring the lifetime experience of at least one episode of major de-
pression and at least one hypomanic episode, is no longer thought to be a “milder” condition
than bipolar I disorder, largely because of the amount of time individuals with this con-
dition spend in depression and because the instability of mood experienced by individuals
with bipolar II disorder is typically accompanied by serious impairment in work and social
functioning.
The diagnosis of cyclothymic disorder is given to adults who experience at least 2 years
(for children, a full year) of both hypomanic and depressive periods without ever fulfilling
the criteria for an episode of mania, hypomania, or major depression.
A large number of substances of abuse, some prescribed medications, and several
medical conditions can be associated with manic-like phenomena. This fact is recognized
in the diagnoses of substance /medication-induced bipolar and related disorder and bipo-
lar and related disorder due to another medical condition.
The recognition that many individuals, particularly children and, to a lesser extent, ad-
olescents, experience bipolar-like phenomena that do not meet the criteria for bipolar I, bi-
polar II, or cyclothymic disorder is reflected in the availability of the other specified
bipolar and related disorder category. Indeed, specific criteria for a disorder involving
short-duration hypomania are provided in Section III in the hope of encouraging further
study of this disorder.
Bipolar | Disorder
Diagnostic Criteria
For a diagnosis of bipolar | disorder, it is necessary to meet the following criteria for a manic
episode. The manic episode may have been preceded by and may be followed by hypo-
manic or major depressive episodes.
123
124 Bipolar and Related Disorders
Manic Episode
A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood
and abnormally and persistently increased goal-directed activity or energy, lasting at
least 1 week and present most of the day, nearly every day (or any duration if hospi-
talization is necessary).
B. During the period of mood disturbance and increased energy or activity, three (or
more) of the following symptoms (four if the mood is only irritable) are present to a sig-
nificant degree and represent a noticeable change from usual behavior:
Inflated self-esteem or grandiosity.
Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
More talkative than usual or pressure to keep talking.
Flight of ideas or subjective experience that thoughts are racing.
Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external
stimuli), as reported or observed.
6. Increase in goal-directed activity (either socially, at work or school, or sexually) or
psychomotor agitation {i.e., purposeless non-goal-directed activity).
7. Excessive involvement in activities that have a high potential for painful conse-
quences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or
foolish business investments).
Aaron >
C. The mood disturbance is sufficiently severe to cause marked impairment in social or
occupational functioning or to necessitate hospitalization to prevent harm to self or oth-
ers, or there are psychotic features.
D. The episode is not attributable to the physiological effects of a substance (e.g., a drug
of abuse, a medication, other treatment) or to another medical condition.
Note: A full manic episode that emerges during antidepressant treatment (e.g., medi-
cation, electroconvulsive therapy) but persists at a fully syndromal level beyond the
physiological effect of that treatment is sufficient evidence for a manic episode and,
therefore, a bipolar | diagnosis.
Note: Criteria A-D constitute a manic episode. At least one lifetime manic episode is re-
quired for the diagnosis of bipolar ! disorder.
Hypomanic Episode
A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood
and abnormally and persistently increased activity or energy, lasting at least 4 consec-
utive days and present most of the day, nearly every day.
B. During the period of mood disturbance and increased energy and activity, three (or
more) of the following symptoms (four if the mood is only irritable) have persisted, rep-
resent a noticeable change from usual behavior, and have been present to a significant
degree:
Inflated self-esteem or grandiosity.
Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
More talkative than usual or pressure to keep talking.
Flight of ideas or subjective experience that thoughts are racing.
Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external
stimuli), as reported or observed.
6. Increase in goal-directed activity (either socially, at work or school, or sexually) or
psychomotor agitation.
7. Excessive involvement in activities that have a high potential for painful conse-
quences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or
foolish business investments).
aPfFoON>
Bipolar | Disorder 125
. The episode is associated with an unequivocal change in functioning that is uncharac-
teristic of the individual when not symptomatic.
. The disturbance in mood and the change in functioning are observable by others.
. The episode is not severe enough to cause marked impairment in social or occupa-
tional functioning or to necessitate hospitalization. If there are psychotic features, the
episode is, by definition, manic.
. The episode is not attributable to the physiological effects of a substance (e.g., a drug
of abuse, a medication, other treatment).
Note: A full hypomanic episode that emerges during antidepressant treatment (e.g.,
medication, electroconvulsive therapy) but persists at a fully syndromal level beyond
the physiological effect of that treatment is sufficient evidence for a hypomanic episode
diagnosis. However, caution is indicated so that one or two symptoms (particularly in-
creased irritability, edginess, or agitation following antidepressant use) are not taken
as sufficient for diagnosis of a hypomanic episode, nor necessarily indicative of a bi-
polar diathesis.
Note: Criteria A-F constitute a hypomanic episode. Hypomanic episodes are common in
bipolar | disorder but are not required for the diagnosis of bipotar | disorder.
Major Depressive Episode
A.
B.
C.
Five (or more) of the following symptoms have been present during the same 2-week
period and represent a change from previous functioning; at least one of the symptoms
is either (1) depressed mood or (2) loss of interest or pleasure.
Note: Do not include symptoms that are clearly attributable to another medical condi-
tion.
1. Depressed mood most of the day, nearly every day, as indicated by either subjec-
tive report (e.g., feels sad, empty, or hopeless) or observation made by others (e.g.,
appears tearful). (Note: In children and adolescents, can be irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost all, activities most of the
day, nearly every day (as indicated by either subjective account or observation).
3. Significant weight loss when not dieting or weight gain (e.g., a change of more than
5% of body weight in a month), or decrease or increase in appetite nearly every
day. (Note: In children, consider failure to make expected weight gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others; not
merely subjective feelings of restlessness or being siowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delu-
sional) nearly every day (not merely self-reproach or guilt about being sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (ei-
ther by subjective account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation with-
out a specific plan, or a suicide attempt or a specific pian for committing suicide.
The symptoms cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
The episode is not attributable to the physiological effects of a substance or another
medical condition.
Note: Criteria A-C constitute a major depressive episode. Major depressive episodes are
common in bipolar | disorder but are not required for the diagnosis of bipolar | disorder.
Note: Responses to a significant loss (e.g., bereavement, financial ruin, losses from a
natural disaster, a serious medical illness or disability) may include the feelings of intense
126 Bipolar and Related Disorders
sadness, rumination about the loss, insomnia, poor appetite, and weight loss noted in Cri-
terion A, which may resemble a depressive episode. Although such symptoms may be un-
derstandable or considered appropriate to the loss, the presence of a major depressive
episode in addition to the normal response to a significant loss should also be carefully
considered. This decision inevitably requires the exercise of clinical judgment based on
the inaiviouals history and the cultural norms for the expression of distress in the context
of loss.
Bipolar | Disorder
A. Criteria have been met for at least one manic episode (Criteria A-D under “Manic Ep-
isode” above).
B. The occurrence of the manic and major depressive episode(s) is not better explained
by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional dis-
order, or other specified or unspecified schizophrenia spectrum and other psychotic
disorder.
Coding and Recording Procedures
The diagnostic code for bipolar | disorder is based on type of current or most recent epi-
sode and its status with respect to current severity, presence of psychotic features, and
remission status. Current severity and psychotic features are only indicated if full criteria
are currently met for a manic or major depressive episode. Remission specifiers are only
indicated if the full criteria are not currently met for a manic, hypomanic, or major depres-
sive episode. Codes are as follows:
Current or Current or Current or Current or
most recent most recent most recent most recent
episode episode episode episode
Bipolar | disorder manic hypomanic* depressed unspecified**
Mild (p. 154) 296.41 NA 296.51 NA
(F31.11) (F31.31)
Moderate (p. 154) 296.42 NA 296.52 NA
(F31.12) (F31.32)
Severe (p. 154) 296.43 NA 296.53 NA
(F31.13) (F31.4)
lin distinguishing grief from a major depressive episode (MDE), it is useful to consider that in
grief the predominant affect is feelings of emptiness and loss, while in MDE it is persistent
depressed mood and the inability to anticipate happiness or pleasure. The dysphoria in grief is
likely to decrease in intensity over days to weeks and occurs in waves, the so-called pangs of
grief. These waves tend to be associated with thoughts or reminders of the deceased. The
depressed mood of a MDE is more persistent and not tied to specific thoughts or preoccupations.
The pain of grief may be accompanied by positive emotions and humor that are uncharacteristic
of the pervasive unhappiness and misery characteristic of a major depressive episode. The
thought content associated with grief generally features a preoccupation with thoughts and
memories of the deceased, rather than the self-critical or pessimistic ruminations seen in a MDE.
In grief, self-esteem is generally preserved, whereas in a MDE, feelings of worthlessness and self-
loathing are common. If self-derogatory ideation is present in grief, it typically involves per-
ceived failings vis-a-vis the deceased (e.g., not visiting frequently enough, not telling the
deceased how much he or she was loved). If a bereaved individual thinks about death and dying,
such thoughts are generally focused on the deceased and possibly about “joining” the deceased,
whereas in a major depressive episode such thoughts are focused on ending one’s own life
because of feeling worthless, undeserving of life, or unable to cope with the pain of depression.
Bipolar | Disorder
127
Current or Current or Current or Current or
most recent most recent most recent most recent
episode episode episode episode
Bipolar | disorder manic hypomanic” depressed unspecified**
With psychotic 296.44 NA 296.54 NA
features*** (F31.2) (F31.5)
(p. 152)
In partial 296.45 296.45 296.55 NA
remission (p. 154) (F31.73) (F31.73) (F31.75)
In full remission 296.46 296.46 296.56 NA
(p. 154) (F31.74) (F31.74) (F31.76)
Unspecified 296.40 296.40 296.50 NA
(F31.9) (F31.9} (F31.9}
“Severity and psychotic specifiers do not apply; code 296.40 (F31.0) for cases not in remission.
“Severity, psychotic, and remission specifiers do not apply. Code 296.7 (F31.9).
“If psychotic features are present, code the "with psychotic features” specifier irrespective of epi-
sode severity.
In recording the name of a diagnosis, terms should be listed in the following order: bipolar
| disorder, type of current or most recent episode, severity/psychotic/remission specifiers,
followed by as many specifiers without codes as apply to the current or most recent epi-
sode.
Specify:
With anxious distress (p. 149)
With mixed features (pp. 149-150)
With rapid cycling (pp. 150-151}
With meianchoiic features (p. 151)
With atypicai features (pp. 151-152)
With mood-congruent psychotic features (p. 152)
With mood-incongruent psychotic features (p. 152)
With catatonia (p. 152). Coding note: Use additional code 293.89 (F06.1).
With peripartum onset (pp. 152-153)
With seasonal pattern (pp. 153-154)
Diagnostic Features
The essential feature of a manic episode is a distinct period during which there is an ab-
normally, persistently elevated, expansive, or irritable mood and persistently increased
activity or energy that is present for most of the day, nearly every day, for a period of at
least 1 week (or any duration if hospitalization is necessary), accompanied by at least three
additional symptoms from Criterion B. If the mood is irritable rather than elevated or ex-
pansive, at least four Criterion B symptoms must be present.
Mood in a manic episode is often described as euphoric, excessively cheerful, high, or
“feeling on top of the world.” In some cases, the mood is of sucha highly infectious quality
that it is easily recognized as excessive and may be characterized by unlimited and hap-
hazard enthusiasm for interpersonal, sexual, or occupational interactions. For example,
the individual may spontaneously start extensive conversations with strangers in public.
Often the predominant mood is irritable rather than elevated, particularly when the indi-
vidual’s wishes are denied or if the individual has been using substances. Rapid shifts in
mood over brief periods of time may occur and are referred to as lability {i.e., the alterna-
128 Bipolar and Related Disorders
tion among euphoria, dysphoria, and irritability). In children, happiness, silliness and
7 goofiness” are normal in the context of special occasions; however, if these symptoms are
recurrent, inappropriate to the context, and beyond what is expected for the developmen-
tal level of the child, they may meet Criterion A. If the happiness is unusual for a child (i-e.,
distinct from baseline}, and the mood change occurs at the same time as symptoms that
meet Criterion B for mania, diagnostic certainty is increased; however, the mood change
must be accompanied by persistently increased activity or energy levels that are obvious
to those who know the child well.
During the manic episode, the individual may engage in multiple overlapping new
projects. The projects are often initiated with little knowledge of the topic, and nothing seems
out of the individual's reach. The increased activity levels may manifest at unusual hours of
the day.
Inflated self-esteem is typically present, ranging from uncritical self-confidence to marked
grandiosity, and may reach delusional proportions (Criterion B1). Despite lack of any partic-
ular experience or talent, the individual may embark on complex tasks such as writing a novel
or seeking publicity for some impractical invention. Grandiose delusions (e.g., of having a
special relationship to a famous person) are common. In children, overestimation of abilities
and belief that, for example, they are the best at a sport or the smartest in the class is normal;
however, when such beliefs are present despite clear evidence to the contrary or the child at-
tempts feats that are clearly dangerous and, most important, represent a change from the
child’s normal behavior, the grandiosity criterion should be considered satisfied.
One of the most common features is a decreased need for sleep (Criterion B2) and is
distinct from insomnia in which the individual wants to sleep or feels the need to sleep but
is unable. The individual may sleep little, if at all, or may awaken several hours earlier than
usual, feeling rested and full of energy. When the sleep disturbance is severe, the individ-
ual may go for days without sleep, yet not feel tired. Often a decreased need for sleep her-
alds the onset of a manic episode.
Speech can be rapid, pressured, loud, and difficult to interrupt (Criterion B3). Individ-
uals may talk continuously and without regard for others’ wishes to communicate, often
in an intrusive manner or without concern for the relevance of what is said. Speech is
sometimes characterized by jokes, puns, amusing irrelevancies, and theatricality, with
dramatic mannerisms, singing, and excessive gesturing. Loudness and forcefulness of
speech often become more important than what is conveyed. If the individual’s mood is
more irritable than expansive, speech may be marked by complaints, hostile comments, or
angry tirades, particularly if attempts are made to interrupt the individual. Both Criterion
A and Criterion B symptoms may be accompanied by symptoms of the opposite (i.e., de-
pressive) pole (see “with mixed features” specifier, pp. 149-150).
Often the individual’s thoughts race at a rate faster than they can be expressed through
speech (Criterion B4). Frequently there is flight of ideas evidenced by a nearly continuous flow
of accelerated speech, with abrupt shifts from one topic to another. When flight of ideas is se-
vere, speech may become disorganized, incoherent, and particularly distressful to the individ-
ual. Sometimes thoughts are experienced as so crowded that it is very difficult to speak.
Distractibility (Criterion B5) is evidenced by an inability to censor immaterial external
stimuli (e.g., the interviewer's attire, background noises or conversations, furnishings in
the room) and often prevents individuals experiencing mania from holding a rational con-
versation or attending to instructions.
The increase in goal-directed activity often consists of excessive planning and partici-
pation in multiple activities, including sexual, occupational, political, or religious activi-
ties. Increased sexual drive, fantasies, and behavior are often present. Individuals in a manic
episode usually show increased sociability (e.g., renewing old acquaintances or calling or
contacting friends or even strangers), without regard to the intrusive, domineering, and
demanding nature of these interactions. They often display psychomotor agitation or rest-
lessness (i.e., purposeless activity) by pacing or by holding multiple conversations simulta-
Bipolar | Disorder 129
neously. Some individuals write excessive letters, e-mails, text messages, and so forth, on
many different topics to friends, public figures, or the media.
The increased activity criterion can be difficult to ascertain in children; however, when
the child takes on many tasks simultaneously, starts devising elaborate and unrealistic
plans for projects, develops previously absent and developmentally inappropriate sexual
preoccupations (not accounted for by sexual abuse or exposure to sexually explicit mate-
rial), then Criterion B might be met based on clinical judgment. It is essential] to determine
whether the behavior represents a change from the child’s baseline behavior; occurs most
of the day, nearly every day for the requisite time period; and occurs in temporal associa-
tion with other symptoms of mania.
The expansive mood, excessive optimism, grandiosity, and poor judgment often lead
to reckless involvement in activities such as spending sprees, giving away possessions,
reckless driving, foolish business investments, and sexual promiscuity that is unusual for
the individual, even though these activities are likely to have catastrophic consequences
(Criterion B7). The individual may purchase many unneeded items without the money to
pay for them and, in some cases, give them away. Sexual] behavior may include infidelity
or indiscriminate sexual encounters with strangers, often disregarding the risk of sexually
transmitted diseases or interpersonal consequences.
The manic episode must result in marked impairment in social or occupational func-
tioning or require hospitalization to prevent harm to self or others (e.g., financial losses, il-
legal activities, loss of employment, self-injurious behavior). By definition, the presence of
psychotic features during a manic episode also satisfies Criterion C.
Manic symptoms or syndromes that are attributable to the physiological effects of a
drug of abuse (e.g., in the context of cocaine or amphetamine intoxication), the side effects
of medications or treatments (e.g., steroids, L-dopa, antidepressants, stimulants), or an-
other medical condition do not count toward the diagnosis of bipolar I disorder. However,
a fully syndromal manic episode that arises during treatment (e.g., with medications, elec-
troconvulsive therapy, light therapy) or drug use and persists beyond the physiological ef-
fect of the inducing agent (i.e., after a medication is fully out of the individual’s system or
the effects of electroconvulsive therapy would be expected to have dissipated completely)
is sufficient evidence for a manic episode diagnosis (Criterion D). Caution is indicated so
that one or two symptoms (particularly increased irritability, edginess, or agitation follow-
ing antidepressant use) are not taken as sufficient for diagnosis of a manic or hypomanic
episode, nor necessarily an indication of a bipolar disorder diathesis. It is necessary to
meet criteria for a manic episode to make a diagnosis of bipolar I disorder, but it is not re-
quired to have hypomanic or major depressive episodes. However, they may precede or
foilow a manic episode. Full descriptions of the diagnostic features of a hypomanic epi-
sode may be found within the text for bipolar II disorder, and the features of a major de-
pressive episode are described within the text for major depressive disorder.
Associated Features Supporting Diagnosis
During a manic episode, individuals often do not perceive that they are ill or in need of treat-
ment and vehemently resist efforts to be treated. Individuals may change their dress, makeup,
or personal appearance to a more sexually suggestive or flamboyant style. Some perceive a
sharper sense of smell, hearing, or vision. Gambling and antisocial behaviors may accompany
the manic episode. Some individuals may become hostile and physically threatening to others
and, when delusional, may become physically assaultive or suicidal. Catastrophic conse-
quences of a manic episode (e.g., involuntary hospitalization, difficulties with the law, serious
financial difficulties) often result from poor judgment, loss of insight, and hyperactivity.
Mood may shift very rapidly to anger or depression. Depressive symptoms may occur’
during a manic episode and, if present, may last moments, hours, or, more rarely, days (see
“with mixed features” specifier, pp. 149-150).
130 Bipolar and Related Disorders
Prevalence
The 12-month prevalence estimate in the continental United States was 0.6% for bipolar I
disorder as defined in DSM-IV. Twelve-month prevalence of bipolar I disorder across 11
countries ranged from 0.0% to 0.6%. The lifetime male-to-female prevalence ratio is ap-
proximately 1.1:1.
Development and Course
Mean age at onset of the first manic, hypomanic, or major depressive episode is approxi-
mately 18 years for bipolar I disorder. Special considerations are necessary to detect the di-
agnosis in children. Since children of the same chronological age may be at different
developmental stages, it is difficult to define with precision what is “normal” or “ex-
pected” at any given point. Therefore, each child should be judged according to his or her
own baseline. Onset occurs throughout the life cycle, including first onsets in the 60s or
70s. Onset of manic symptoms (e.g., sexual or social disinhibition) in late mid-life or late-
life should prompt consideration of medical conditions (e.g., frontotemporal neurocogni-
tive disorder) and of substance ingestion or withdrawal.
More than 90% of individuals who have a single manic episode go on to have recurrent
mood episodes. Approximately 60% of manic episodes occur immediately before a major
depressive episode. Individuals with bipolar I disorder who have multiple (four or more)
mood episodes (major depressive, manic, or hypomanic) within 1 year receive the speci-
fier “with rapid cycling.”
Risk and Prognostic Factors
Environmental. Bipolar disorder is more common in high-income than in low-income
countries (1.4 vs. 0.7%). Separated, divorced, or widowed individuals have higher rates of
bipolar I disorder than do individuals who are married or have never been married, but
the direction of the association is unclear.
Genetic and physiological. A family history of bipolar disorder is one of the strongest and
most consistent risk factors for bipolar disorders. There is an average 10-fold increased risk
among adult relatives of individuals with bipolar I and bipolar II disorders. Magnitude of
risk increases with degree of kinship. Schizophrenia and bipolar disorder likely share a ge-
netic origin, reflected in familial co-aggregation of schizophrenia and bipolar disorder.
Course modifiers. After an individual! has a manic episode with psychotic features, subse-
quent manic episodes are more likely to include psychotic features. Incomplete inter-
episode recovery is more common when the current episode is accompanied by mood-
incongruent psychotic features.
Culture-Related Diagnostic Issues
Little information exists on specific cultural differences in the expression of bipolar I dis-
order. One possible explanation for this may be that diagnostic instruments are often
translated and applied in different cultures with no transcultural validation. In one U.S.
study, 12-month prevalence of bipolar I disorder was significantly lower for Afro-Carib-
beans than for African Americans or whites.
Gender-Related Diagnostic Issues
Females are more likely to experience rapid cycling and mixed states, and to have patterns of
comorbidity that differ from those of males, including higher rates of lifetime eating disor-
ders. Females with bipolar I or II disorder are more likely to experience depressive symptoms
than males. They also have a higher lifetime risk of alcohol use disorder than are males and a
much greater likelihood of alcohol use disorder than do females in the general population.
Bipolar | Disorder 131
Suicide Risk
The lifetime risk of suicide in individuals with bipolar disorder is estimated to be at least
15 times that of the general population. In fact, bipolar disorder may account for one-quar-
ter of all completed suicides. A past history of suicide attempt and percent days spent de-
pressed in the past year are associated with greater risk of suicide attempts or completions.
Functional Consequences of Bipoiar | Disorder
Although many individuals with bipolar disorder return to a fully functional level be-
tween episodes, approximately 30% show severe impairment in work role function. Func-
tional recovery lags substantially behind recovery from symptoms, especially with respect
to occupational recovery, resulting in lower socioeconomic status despite equivalent lev-
els of education when compared with the general population. Individuals with bipolar I
disorder perform more poorly than healthy individuals on cognitive tests. Cognitive im-
pairments may contribute to vocational and interpersonal difficulties and persist through
the lifespan, even during euthymic periods.
Differential Diagnosis
Major depressive disorder. Major depressive disorder may also be accompanied by hy-
pomanic or manic symptoms (i.e., fewer symptoms or for a shorter duration than required
for mania or hypomania). When the individual presents in an episode of major depression,
one must depend on corroborating history regarding past episodes of mania or hypoma-
nia. Symptoms of irritability may be associated with either major depressive disorder or
bipolar disorder, adding to diagnostic complexity.
Other bipolar disorders. Diagnosis of bipolar I disorder is differentiated from bipolar II
disorder by determining whether there have been any past episodes of mania. Other spec-
ified and unspecified bipolar and related disorders should be differentiated from bipolar I
and II disorders by considering whether either the episodes involving manic or hypo-
manic symptoms or the episodes of depressive symptoms fail to meet the full criteria for
those conditions.
Bipolar disorder due to another medical condition may be distinguished from bipolar
Iand II disorders by identifying, based on best clinical evidence, a causally related medical
condition.
Generalized anxiety disorder, panic disorder, posttraumatic stress disorder, or other
anxiety disorders. These disorders need to be considered in the differential diagnosis as
either the primary disorder or, in some cases, a comorbid disorder. A careful history of
symptoms is needed to differentiate generalized anxiety disorder from bipolar disorder,
as anxious ruminations may be mistaken for racing thoughts, and efforts to minimize anx-
ious feelings may be taken as impulsive behavior. Similarly, symptoms of posttraumatic
stress disorder need to be differentiated from bipolar disorder. It is helpful to assess the ep-
isodic nature of the symptoms described, as well as to consider symptom triggers, in mak-
ing this differential diagnosis.
Substance/medication-induced bipolar disorder. Substance use disorders may mani-
fest with substance.medication-induced manic symptoms that must be distinguished
from bipolar I disorder; response to mood stabilizers during a substance /medication-
induced mania may not necessarily be diagnostic for bipolar disorder. There may be sub-
stantial overlap in view of the tendency for individuals with bipolar I disorder to overuse
substances during an episode. A primary diagnosis of bipolar disorder must be estab-
lished based on symptoms that remain once substances are no longer being used.
Attention-deficit/hyperactivity disorder. This disorder may be misdiagnosed as bipolar
disorder, especially in adolescents and children. Many symptoms overlap with the symp-
132 Bipolar and Related Disorders
toms of mania, such as rapid speech, racing thoughts, distractibility, and less need for
sleep. The “double counting” of symptoms toward both ADHD and bipolar disorder can
be avoided if the clinician clarifies whether the symptom(s) represents a distinct episode.
Personality disorders. Personality disorders such as borderline personality disorder
may have substantial symptomatic overlap with bipolar disorders, since mood lability
and impulsivity are common in both conditions. Symptoms must represent a distinct ep-
isode, and the noticeable increase over baseline required for the diagnosis of bipolar dis-
order must be present. A diagnosis of a personality disorder should not be made during an
untreated mood episode.
Disorders with prominent irritability. In individuals with severe irritability, particularly
children and adolescents, care must be taken to apply the diagnosis of bipolar disorder
only to those who have had a clear episode of mania or hypomania—that is, a distinct time
period, of the required duration, during which the irritability was clearly different from
the individual’s baseline and was accompanied by the onset of Criterion B symptoms.
When a child’s irritability is persistent and particularly severe, the diagnosis of disruptive
mood dysregulation disorder would be more appropriate. Indeed, when any child is being
assessed for mania, it is essential that the symptoms represent a clear change from the
child’s typical behavior.
Comorbidity
Co-occurring mental disorders are common, with the most frequent disorders being any
anxiety disorder (e.g., panic attacks, social anxiety disorder [social phobia], specific plio-
bia), occurring in approximately three-fourths of individuals; ADHD, any disruptive, im-
pulse-control, or conduct disorder (e.g., intermittent explosive disorder, oppositional
defiant disorder, conduct disorder), and any substance use disorder (e.g., alcohol use dis-
order) occur in over half of individuals with bipolar I disorder. Adults with bipolar I dis-
order have high rates of serious and/or untreated co-occurring medical conditions.
Metabolic syndrome and migraine are more common among individuals with bipolar dis-
order than in the general population. More than half of individuals whose symptoms meet
criteria for bipolar disorder have an alcohol use disorder, and those with both disorders
are at greater risk for suicide attempt.
Bipolar Il Disorder
Diagnostic Criteria 296.89 (F31.81)
For a diagnosis of bipolar II disorder, it is necessary to meet the following criteria for a cur-
rent or past hypomanic episode and the following criteria for a current or past major de-
pressive episode:
Hypomanic Episode
A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood
and abnormally and persistently increased activity or energy, lasting at least 4 consec-
utive days and present most of the day, nearly every day.
B. During the period of mood disturbance and increased energy and activity, three (or more)
of the following symptoms have persisted (four if the mood is only irritable), represent a no-
ticeable change from usual behavior, and have been present to a significant degree:
1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
3. More talkative than usual or pressure to keep talking.
Bipolar II Disorder 133
>
. Flight of ideas or subjective experience that thoughts are racing.
5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external
stimuli), as reported or observed.
6. Increase in goal-directed activity (either socially, at work or school, or sexually) or
psychomotor agitation.
7. Excessive involvement in activities that have a high potential for painful conse-
quences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or
foolish business investments).
C. The episode is associated with an unequivocal change in functioning that is uncharac-
teristic of the individual when not symptomatic.
D. The disturbance in mood and the change in functioning are observable by others.
E. The episode is not severe enough to cause marked impairment in social or occupa-
tional functioning or to necessitate hospitalization. If there are psychotic features, the
episode is, by definition, manic.
F. The episode is not attributable to the physiological effects of a substance (e.g., a drug
of abuse, a medication or other treatment).
Note: A full hypomanic episode that emerges during antidepressant treatment (e.g.,
medication, electroconvulsive therapy) but persists at a fully syndromal level beyond
the physiological effect of that treatment is sufficient evidence for a hypomanic episode
diagnosis. However, caution is indicated so that one or two symptoms (particularly in-
creased irritability, edginess, or agitation following antidepressant use) are not taken
as sufficient for diagnosis of a hypomanic episode, nor necessarily indicative of a bi-
polar diathesis.
Major Depressive Episode
A. Five (or more) of the following symptoms have been present during the same 2-week
period and represent a change from previous functioning; at least one of the symptoms
is either (1) depressed mood or (2) toss of interest or pleasure.
Note: Do not include symptoms that are clearly attributable to a medical condition.
1. Depressed mood most of the day, nearly every day, as indicated by either subjec-
tive report (e.g., feels sad, empty, or hopeless) or observation made by others (e.g.,
appears tearful). (Note: In children and adolescents, can be irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost all, activities most of the
day, nearly every day (as indicated by either subjective account or observation).
3. Significant weight loss when not dieting or weight gain (e.g., a change of more than
5% of body weight in a month), or decrease or increase in appetite nearly every
day. (Note: In children, consider failure to make expected weight gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others; not
merely subjective feelings of restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delu-
sional) nearly every day (not merely self-reproach or guilt about being sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (ei-
ther by subjective account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation with-
out a specific plan, a suicide attempt, or a specific plan for committing suicide.
B. The symptoms cause Clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
C. The episode is not attributable to the physiological effects of a substance or another
medical condition.
134 Bipolar and Related Disorders
Note: Criteria A-C above constitute a major depressive episode.
Note: Responses to a significant loss (e.g9., bereavement, financial ruin, losses from a nat-
ural disaster, a serious medical illness or disability) may include the feelings of intense sad-
ness, rumination about the loss, insomnia, poor appetite, and weight loss noted in Criterion
A, which may resemble a depressive episode. Although such symptoms may be under-
standable or considered appropriate to the loss, the presence of a major depressive episode
in addition to the normal response to a significant loss should be carefully considered. This
decision inevitably requires the exercise of clinical judgment based on the individual's history
and the cultural norms for the expression of distress in the context of loss. !
Bipolar Il Disorder
A. Criteria have been met for at least one hypomanic episode (Criteria A-F under “Hypo-
manic Episode” above) and at least one major depressive episode (Criteria A-C under
“Major Depressive Episode” above).
B. There has never been a manic episode.
C. The occurrence of the hypomanic episode(s) and major depressive episode(s) is not
better explained by schizoaffective disorder, schizophrenia, schizophreniform disor-
der, delusional disorder, or other specified or unspecified schizophrenia spectrum and
other psychotic disorder.
D. The symptoms of depression or the unpredictability caused by frequent alternation be-
tween periods of depression and hypomania causes clinically significant distress or im-
pairment in social, occupational, or other important areas of functioning.
Coding and Recording Procedures
Bipolar II disorder has one diagnostic code: 296.89 (F31.81). Its status with respect to cur-
rent severity, presence of psychotic features, course, and other specifiers cannot be
coded but should be indicated in writing (e.g., 296.89 [F31.81] bipotar II disorder, current
episode depressed, moderate severity, with mixed features; 296.89 [F31.81] bipolar Il dis-
order, most recent episode depressed, in partial remission).
Specify current or most recent episode:
Hypomanic
Depressed
Specify if:
With anxious distress (p. 149)
With mixed features (pp. 149-150)
lin distinguishing grief from a major depressive episode (MDE), it is useful to consider that in grief
the predominant affect is feelings of emptiness and loss, while in a MDE it is persistent depressed
mood and the inability to anticipate happiness or pleasure. The dysphoria in grief is likely to
decrease in intensity over days to weeks and occurs in waves, the so-called pangs of grief. These
waves tend to be associated with thoughts or reminders of the deceased. The depressed mood of a
MDE is more persistent and not tied to specific thoughts or preoccupations. The pain of grief may
be accompanied by positive emotions and humor that are uncharacteristic of the pervasive unhap-
piness and misery characteristic of a MDE. The thought content associated with grief generally fea-
tures a preoccupation with thoughts and memories of the deceased, rather than the self-critical or
pessimistic ruminations seen in a MDE. In grief, self-esteem is generally preserved, whereas in a
MDE feelings of worthlessness and self-loathing are common. If self-derogatory ideation is present
in grief, it typically involves perceived failings vis-a-vis the deceased (e.g., not visiting frequently
enough, not telling the deceased how much he or she was loved). If a bereaved individual thinks
about death and dying, such thoughts are generally focused on the deceased and possibly about
“Joining” the deceased, whereas in a MDE such thoughts are focused on ending one’s own life
because of feeling worthless, undeserving of life, or unable to cope with the pain of depression.
Bipolar II Disorder 135
With rapid cycling (pp. 150-151)
With mood-congruent psychotic features (p. 152)
With mood-incongruent psychotic features (p. 152)
With catatonia (p. 152). Coding note: Use additional code 293.89 (F06.1).
With peripartum onset (pp. 152-153)
With seasonal pattern (pp. 153-154): Applies only to the pattern of major depressive
episodes.
Specify course if full criteria for a mood episode are not currently met:
In partial remission (p. 154)
In full remission (p. 154)
Specify severity if full criteria for a mood episode are currently met:
Mild (p. 154)
Moderate (p. 154)
Severe (p. 154)
Diagnostic Features
Bipolar II disorder is characterized by a clinical course of recurring mood episodes con-
sisting of one or more major depressive episodes (Criteria A-C under “Major Depressive
Episode”) and at least one hypomanic episode (Criteria A-F under “Hypomanic Epi-
sode”). The major depressive episode must last at least 2 weeks, and the hypomanic epi-
sode must last at least 4 days, to meet the diagnostic criteria. During the mood episode(s),
the requisite number of symptoms must be present most of the day, nearly every day, and
represent a noticeable change from usual behavior and functioning. The presence of a
manic episode during the course of illness precludes the diagnosis of bipolar II disorder
(Criterion B under “Bipolar II Disorder”). Episodes of substance /medication-induced de-
pressive disorder or substance /medication-induced bipolar and related disorder (repre-
senting the physiological effects of a medication, other somatic treatments for depression,
drugs of abuse, or toxin exposure) or of depressive and related disorder due to another
medical condition or bipolar and related disorder due to another medical condition do not
count toward a diagnosis of bipolar II disorder unless they persist beyond the physiolog-
ical effects of the treatment or substance and then meet duration criteria for an episode. In
addition, the episodes must not be better accounted for by schizoaffective disorder and are
not superimposed on schizophrenia, schizophreniform disorder, delusional disorder, or
other specified or unspecified schizophrenia spectrum or other psychotic disorders (Cri-
terion C under “Bipolar II Disorder”). The depressive episodes or hypomanic fluctuations
must cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning (Criterion D under “Bipolar II Disorder”); however, for hy-
pomanic episodes, this requirement does not have to be met. A hypomanic episode that
causes significant impairment would likely qualify for the diagnosis of manic episode and,
therefore, for a lifetime diagnosis of bipolar I disorder. The recurrent major depressive ep-
isodes are often more frequent and lengthier than those occurring in bipolar I disorder.
Individuals with bipolar II disorder typically present to a clinician during a major de-
pressive episode and are unlikely to complain initially of hypomania. Typically, the hy-
pomanic episodes themselves do not cause impairment. Instead, the impairment results
from the major depressive episodes or from a persistent pattern of unpredictable mood
changes and fluctuating, unreliable interpersonal or occupational functioning. Individu-
als with bipolar II disorder may not view the hypomanic episodes as pathological or dis-
advantageous, although others may be troubled by the individual's erratic behavior.
Clinical information from other informants, such as close friends or relatives, is often use-
ful in establishing the diagnosis of bipolar II disorder.
136 Bipolar and Related Disorders
A hypomanic episode should not be confused with the several days of euthymia and re-
stored energy or activity that may follow remission of a major depressive episode. Despite the
substantial differences in duration and severity between a manic and hypomanic episode, bi-
polar II disorder is not a “milder form” of bipolar I disorder. Compared with individuals with
bipolar I disorder, individuals with bipolar II disorder have greater chronicity of illness and
spend, on average, more time in the depressive phase of their illness, which can be severe and /
or disabling. Depressive symptoms co-occurring with a hypomanic episode or hypomanic
symptoms co-occurring with a depressive episode are common in individuals with bipolar II
disorder and are overrepresented in females, particularly hypomania with mixed features. In-
dividuals experiencing hypomania with mixed features may not label their symptoms as hy-
pomania, but instead experience them as depression with increased energy or irritability.
Associated Features Supporting Diagnosis
A common feature of bipolar II disorder is impulsivity, which can contribute to suicide at-
tempts and substance use disorders. Impulsivity may also stem from a concurrent person-
ality disorder, substance use disorder, anxiety disorder, another mental disorder, or a
medical condition. There may be heightened levels of creativity in some individuals with
a bipolar disorder. However, that relationship may be nonlinear; that is, greater lifetime
creative accomplishments have been associated with milder forms of bipolar disorder, and
higher creativity has been found in unaffected family members. The individual's attach-
ment to heightened creativity during hypomanic episodes may contribute to ambivalence
about seeking treatment or undermine adherence to treatment.
Prevaience
The 12-month prevalence of bipolar II disorder, internationally, is 0.3%. In the United
States, 12-month prevalence is 0.8%. The prevalence rate of pediatric bipolar II disorder is
difficult to establish. DSM-IV bipolar I, bipolar II, and bipolar disorder not otherwise spec-
ified yield a combined prevalence rate of 1.8% in U.S. and non-U.S. community samples,
with higher rates (2.7% inclusive) in youths age 12 years or older.
Deveiopment and Course
Although bipolar II disorder can begin in late adolescence and throughout adulthood, av-
erage age at onset is the mid-20s, which is slightly later than for bipolar I disorder but ear-
lier than for major depressive disorder. The illness most often begins with a depressive
episode and is not recognized as bipolar II disorder until a hypomanic episode occurs; this
happens in about 12% of individuals with the initial diagnosis of major depressive disor-
der. Anxiety, substance use, or eating disorders may also precede the diagnosis, compli-
cating its detection. Many individuals experience several episodes of major depression
prior to the first recognized hypomanic episode.
The number of lifetime episodes (both hypomanic and major depressive episodes)
tends to be higher for bipolar II disorder than for major depressive disorder or bipolar I
disorder. However, individuals with bipolar I disorder are actually more likely to experi-
ence hypomanic symptoms than are individuals with bipolar II disorder.The interval
between mood episodes in the course of bipolar II disorder tends to decrease as the indi-
vidual ages. While the hypomanic episode is the feature that defines bipolar II disorder,
depressive episodes are more enduring and disabling over time. Despite the predomi-
nance of depression, once a hypomanic episode has occurred, the diagnosis becomes bi-
polar II disorder and never reverts to major depressive disorder.
Approximately 5%-15% of individuals with bipolar II disorder have multiple (four or
more) mood episodes (hypomanic or major depressive) within the previous 12 months. If
Bipolar Il Disorder 137
this pattern is present, it is noted by the specifier “with rapid cycling.” By definition, psy-
chotic symptoms do not occur in hypomanic episodes, and they appear to be less frequent
in the major depressive episodes in bipolar II disorder than in those of bipolar I disorder.
Switching from a depressive episode to a manic or hypomanic episode (with or with-
out mixed features) may occur, both spontaneously and during treatment for depression.
About 5%-15% of individuals with bipolar II disorder will ultimately develop a manic ep-
isode, which changes the diagnosis to bipolar I disorder, regardless of subsequent course.
Making the diagnosis in children is often a challenge, especially in those with irritabil-
ity and hyperarousal that is nonepisodic (i.e., lacks the well-demarcated periods of altered
mood). Nonepisodic irritability in youth is associated with an elevated risk for anxiety dis-
orders and major depressive disorder, but not bipolar disorder, in adulthood. Persistently
irritable youths have lower familial rates of bipolar disorder than do youths who have bi-
polar disorder. For a hypomanic episode to be diagnosed, the child’s symptoms must ex-
ceed what is expected in a given environment and culture for the child’s developmental
stage. Compared with adult onset of bipolar II disorder, childhood or adolescent onset of
the disorder may be associated with a more severe lifetime course. The 3-year incidence
rate of first-onset bipolar II disorder in adults older than 60 years is 0.34%. However, dis-
tinguishing individuals older than 60 years with bipolar II disorder by late versus early
age at onset does not appear to have any clinical utility.
Risk and Prognostic Factors
Genetic and physiological. The risk of bipolar II disorder tends to be highest among rel-
atives of individuals with bipolar II disorder, as opposed to individuals with bipolar I dis-
order or major depressive disorder. There may be genetic factors influencing the age at
onset for bipolar disorders.
Course modifiers. A rapid-cycling pattern is associated with a poorer prognosis. Return
to previous level of social function for individuals with bipolar II disorder is more likely
for individuals of younger age and with less severe depression, suggesting adverse effects
of prolonged illness on recovery. More education, fewer years of illness, and being mar-
tied are independently associated with functional recovery in individuals with bipolar
disorder, even after diagnostic type (I vs. II), current depressive symptoms, and presence
of psychiatric comorbidity are taken into account.
Gender-Related Diagnostic Issues
Whereas the gender ratio for bipolar I disorder is equal, findings on gender differences in
bipolar II disorder are mixed, differing by type of sample (i.e., registry, community, or
clinical) and country of origin. There is little to no evidence of bipolar gender differences,
whereas some, but not all, clinical samples suggest that bipolar II disorder is more com-
mon in females than in males, which may reflect gender differences in treatment seeking
or other factors.
Patterns of illness and comorbidity, however, seem to differ by gender, with females
being more likely than males to report hypomania with mixed depressive features and a
rapid-cycling course. Childbirth may be a specific trigger for a hypomanic episode, which
can occur in 10%-20% of females in nonclinical populations and most typically in the early
postpartum period. Distinguishing hypomania from the elated mood and reduced sleep
that normally accompany the birth of a child may be challenging. Postpartum hypomania
may foreshadow the onset of a depression that occurs in about half of females who expe-
rience postpartum “highs.” Accurate detection of bipolar If disorder may help in estab-
lishing appropriate treatment of the depression, which may reduce the risk of suicide and
infanticide.
138 Bipolar and Related Disorders
Suicide Risk
Suicide risk is high in bipolar II disorder. Approximately one-third of individuals with bi-
polar II disorder report a lifetime history of suicide attempt. The prevalence rates of life-
time attempted suicide in bipolar II and bipolar I disorder appear to be similar (32.4% and
36.3%, respectively). However, the lethality of attempts, as defined by a lower ratio of at-
tempts to completed suicides, may be higher in individuals with bipolar II disorder com-
pared with individuals with bipolar I disorder. There may be an association between
genetic markers and increased risk for suicidal behavior in individuals with bipolar dis-
order, including a 6.5-fold higher risk of suicide among first-degree relatives of bipolar II
probands compared with those with bipolar I disorder.
Functional Consequences of Bipolar II Disorder
Although many individuals with bipolar II disorder return to a fully functional level be-
tween mood episodes, at least 15% continue to have some inter-episode dysfunction, and
20% transition directly into another mood episode without inter-episode recovery. Func-
tional recovery lags substantially behind recovery from symptoms of bipolar II disorder,
especially in regard to occupational recovery, resulting in lower socioeconomic status de-
spite equivalent levels of education with the general population. Individuals with bipolar
II disorder perform more poorly than healthy individuals on cognitive tests and, with the
exception of memory and semantic fluency, have similar cognitive impairment as do in-
dividuals with bipolar I disorder. Cognitive impairments associated with bipolar II disor-
der may contribute to vocational difficulties. Prolonged unemployment in individuals
with bipolar disorder is associated with more episodes of depression, older age, increased
rates of current panic disorder, and lifetime history of alcohol use disorder.
Differential Diagnosis
Major depressive disorder. Perhaps the most challenging differential diagnosis to con-
sider is major depressive disorder, which may be accompanied by hypomanic or manic
symptoms that do not meet full criteria (i-e., either fewer symptoms or a shorter duration
than required for a hypomanic episode). This is especially true in evaluating individuals
with symptoms of irritability, which may be associated with either major depressive dis-
order or bipolar II disorder.
Cyclothymic disorder. In cyclothymic disorder, there are numerous periods of hypo-
manic symptoms and numerous periods of depressive symptoms that do not meet symp-
tom or duration criteria for a major depressive episode. Bipolar II disorder is distinguished
from cyclothymic disorder by the presence of one or more major depressive episodes. If a
major depressive episode occurs after the first 2 years of cyclothymic disorder, the addi-
tional diagnosis of bipolar II disorder is given.
Schizophrenia spectrum and other related psychotic disorders. Bipolar II disorder must
be distinguished from psychotic disorders (e.g., schizoaffective disorder, schizophrenia,
and delusional disorder). Schizophrenia, schizoaffective disorder, and delusional disor-
der are all characterized by periods of psychotic symptoms that occur in the absence of
prominent mood symptoms. Other helpful considerations include the accompanying
symptoms, previous course, and family history.
Panic disorder or other anxiety disorders. Anxiety disorders need to be considered in
the differential diagnosis and may frequently be present as co-occurring disorders.
Substance use disorders. Substance use disorders are included in the differential diag-
nosis.
Attention-deficit/hyperactivity disorder. Attention-deficit/hyperactivity disorder (ADHD)
may be misdiagnosed as bipolar II disorder, especially in adolescents and children. Many
Cyclothymic Disorder 139
symptoms of ADHD, such as rapid speech, racing thoughts, distractibility, and less need
for sleep, overlap with the symptoms of hypomania. The double counting of symptoms to-
ward both ADHD and bipolar II disorder can be avoided if the clinician clarifies whether
the symptoms represent a distinct episode and if the noticeable increase over baseline re-
quired for the diagnosis of bipolar II disorder is present.
Personality disorders. The same convention as applies for ADHD also applies when
evaluating an individual for a personality disorder such as borderline personality disor-
der, since mood lability and impulsivity are common in both personality disorders and bi-
polar II disorder. Symptoms must represent a distinct episode, and the noticeable increase
over baseline required for the diagnosis of bipolar II disorder must be present. A diagnosis
of a personality disorder should not be made during an untreated mood episode unless
the lifetime history supports the presence of a personality disorder.
Other bipolar disorders. Diagnosis of bipolar II disorder should be differentiated from
bipolar I disorder by carefully considering whether there have been any past episodes of
mania and from other specified and unspecified bipolar and related disorders by confirm-
ing the presence of fully syndromal hypomania and depression.
Comorbidity
Bipolar II disorder is more often than not associated with one or more co-occurring mental
disorders, with anxiety disorders being the most common. Approximately 60% of individ-
uals with bipolar IT disorder have three or more co-occurring mental disorders; 75% have
an anxiety disorder; and 37% have a substance use disorder. Children and adolescents
with bipolar II disorder have a higher rate of co-occurring anxiety disorders compared
with those with bipolar I disorder, and the anxiety disorder most often predates the bi-
polar disorder. Anxiety and substance use disorders occur in individuals with bipolar II
disorder ata higher rate than in the general population. Approximately 14% of individuals
with bipolar II disorder have at least one lifetime eating disorder, with binge-eating dis-
order being more common than bulimia nervosa and anorexia nervosa.
These commonly co-occurring disorders do not seem to follow a course of illness that
is truly independent from that of the bipolar disorder, but rather have strong associations
with mood states. For example, anxiety and eating disorders tend to associate most with
depressive symptoms, and substance use disorders are moderately associated with manic
symptoms.
Cyclothymic Disorder
Diagnostic Criteria 301.13 (F34.0)
A. For at least 2 years (at least 1 year in children and adolescents) there have been nu-
merous periods with hypomanic symptoms that do not meet criteria for a hypomanic
episode and numerous periods with depressive symptoms that do not meet criteria for
a major depressive episode.
B. During the above 2-year period (1 year in children and adolescents), the hypomanic
and depressive periods have been present for at least half the time and the individual
has not been without the symptoms for more than 2 months at a time.
C. Criteria for a major depressive, manic, or hypomanic episode have never been met.
D. The symptoms in Criterion A are not better explained by schizoaffective disorder,
schizophrenia, schizophreniform disorder, delusional disorder, or other specified or un-
specified schizophrenia spectrum and other psychotic disorder.
E. The symptoms are not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication) or another medical condition (e.g., hyperthyroidism).
140 Bipolar and Related Disorders
F. The symptoms cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
Specify if:
With anxious distress (see p. 149)
Diagnostic Features
The essential feature of cyclothymic disorder is a chronic, fluctuating mood disturbance
involving numerous periods of hypomanic symptoms and periods of depressive symp-
toms that are distinct from each other (Criterion A). The hypomanic symptoms are of
insufficient number, severity, pervasiveness, or duration to meet full criteria for a hypo-
manic episode, and the depressive symptoms are of insufficient number, severity, perva-
siveness, or duration to meet full criteria for a major depressive episode. During the initial
2-year period (1 year for children or adolescents), the symptoms must be persistent (pres-
ent more days than not), and any symptom-free intervals last no longer than 2 months
(Criterion B). The diagnosis of cyclothymic disorder is made only if the criteria for a major
depressive, manic, or hypomanic episode have never been met (Criterion C).
If an individual with cyclothymic disorder subsequently (i.e., after the initial 2 years in
adults or 1 year in children or adolescents) experiences a major depressive, manic, or hy-
pomanic episode, the diagnosis changes to major depressive disorder, bipolar I disorder,
or other specified or unspecified bipolar and related disorder (subclassified as hypomanic
episode without prior major depressive episode), respectively, and the cyclothymic disor-
der diagnosis is dropped.
The cyclothymic disorder diagnosis is not made if the pattern of mood swings is better
explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delu-
sional disorder, or other specified and unspecified schizophrenia spectrum and other
psychotic disorders (Criterion D), in which case the mood symptoms are considered asso-
ciated features of the psychotic disorder. The mood disturbance must also not be attribut-
able to the physiological effects of a substance (e.g., a drug of abuse, a medication) or
another medical condition (e.g., hyperthyroidism) (Criterion E). Although some individ-
uals may function particularly well during some of the periods of hypomania, over the
prolonged course of the disorder, there must be clinically significant distress or impair-
ment in social, occupational, or other important areas of functioning as a result of the
mood disturbance (Criterion F). The impairment may develop as a result of prolonged pe-
riods of cyclical, often unpredictable mood changes (e.g., the individual may be regarded
as temperamental, moody, unpredictable, inconsistent, or unreliable).
Prevaience
The lifetime prevalence of cyclothymic disorder is approximately 0.4%~—1%. Prevalence in
mood disorders clinics may range from 3% to 5%. In the general population, cyclothymic
disorder is apparently equally common in males and females. In clinical settings, females
with cyclothymic disorder may be more likely to present for treatment than males.
Development and Course
Cyclothymic disorder usually begins in adolescence or early adult life and is sometimes
considered to reflect a temperamental predisposition to other disorders in this chapter.
Cyclothymic disorder usually has an insidious onset and a persistent course. There is a
15%-50% risk that an individual with cyclothymic disorder will subsequently develop bi-
polar I disorder or bipolar IT disorder. Onset of persistent, fluctuating hypomanic and de-
pressive symptoms late in adult life needs to be clearly differentiated from bipolar and
Cyclothymic Disorder 141
related disorder due to another medical condition and depressive disorder due to another
medical condition (e.g., multiple sclerosis) before the cyclothymic disorder diagnosis is as-
signed. Among children with cyclothymic disorder, the mean age at onset of symptoms is
6.5 years of age.
Risk and Prognostic Factors
Genetic and physiological. Major depressive disorder, bipolar I disorder, and bipolar II
disorder are more common among first-degree biological relatives of individuals with cyclo-
thymic disorder than in the general population. There may also be an increased familial risk of
substance-related disorders. Cyclothymic disorder may be more common in the first-degree
biological relatives of individuals with bipolar I disorder than in the general population.
Differentiai Diagnosis
Bipolar and related disorder due to another medical condition and depressive disorder
due to another medical condition. The diagnosis of bipolar and related disorder due to
another medical condition or depressive disorder due to another medical condition is
made when the mood disturbance is judged to be attributable to the physiological effect of
a specific, usually chronic medical condition (e.g., hyperthyroidism). This determination
is based on the history, physical examination, or laboratory findings. If it is judged that the
hypomanic and depressive symptoms are not the physiological consequence of the med-
ical condition, then the primary mental disorder (i.e., cyclothymic disorder) and the med-
ical condition are coded. For example, this would be the case if the mood symptoms are
considered to be the psychological (not the physiological) consequence of having a chronic
medical condition, or if there is no etiological relationship between the hypomanic and de-
pressive symptoms and the medical condition.
Substance/medication-induced bipolar and related disorder and substance/medica-
tion-induced depressive disorder. Substance /medication-induced bipolar and related
disorder and substance/medication-induced depressive disorder are distinguished from
cyclothymic disorder by the judgment that a substance/ medication (especially stimu-
lants) is etiologically related to the mood disturbance. The frequent mood swings in these
disorders that are suggestive of cyclothymic disorder usually resolve following cessation
of substance/ medication use.
Bipolar | disorder, with rapid cycling, and bipolar || disorder, with rapid cycling.
Both disorders may resemble cyclothymic disorder by virtue of the frequent marked shifts
in mood. By definition, in cyclothymic disorder the criteria for a major depressive, manic,
or hypomanic episode has never been met, whereas the bipolar I disorder and bipolar II
disorder specifier “with rapid cycling” requires that full mood episodes be present.
Borderline personality disorder. Borderline personality disorder is associated with
marked shifts in mood that may suggest cyclothymic disorder. If the criteria are met for
both disorders, both borderline personality disorder and cyclothymic disorder may be di-
agnosed.
Comorbidity
Substance-related disorders and sleep disorders (i.e., difficulties in initiating and main-
taining sleep) may be present in individuals with cyclothymic disorder. Most children
with cyclothymic disorder treated in outpatient psychiatric settings have comorbid mental
conditions; they are more likely than other pediatric patients with mental disorders to
have comorbid attention-deficit/hyperactivity disorder.
142 Bipolar and Related Disorders
Substance/Medication-Induced
Bipolar and Related Disorder
Diagnostic Criteria
A. A prominent and persistent disturbance in mood that predominates in the clinical picture
and is characterized by elevated, expansive, or irritable mood, with or without depressed
mood, or markedly diminished interest or pleasure in all, or almost all, activities.
B. There is evidence from the history, physical examination, or laboratory findings of both
(1) and (2):
1. The symptoms in Criterion A developed during or soon after substance intoxication
or withdrawal or after exposure to a medication.
2. The involved substance/medication is capable of producing the symptoms in Crite-
rion A.
C. The disturbance is not better explained by a bipolar or related disorder that is not sub-
stance/medication-induced. Such evidence of an independent bipolar or related disor-
der could include the following:
The symptoms precede the onset of the substance/medication use; the symptoms per-
sist for a substantial period of time (e.g., about 1 month) after the cessation of acute
withdrawal or severe intoxication; or there is other evidence suggesting the existence
of an independent non-substance/medication-induced bipolar and related disorder
(e.g., a history of recurrent non-substance/medication-related episodes).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
Coding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance/medication]-
induced bipolar and related disorders are indicated in the table below. Note that the ICD-10-
CM code depends on whether or not there is a comorbid substance use disorder present for
the same class of substance. If a mild substance use disorder is comorbid with the substance-
induced bipolar and related disorder, the 4th position character is “1,” and the clinician should
record “mild [substance] use disorder’ before the substance-induced bipolar and related dis-
order (e.g., “mild cocaine use disorder with cocaine-induced bipolar and related disorder’). If a
moderate or severe substance use disorder is comorbid with the substance-induced bipolar
and related disorder, the 4th position character is “2,” and the clinician should record “moder-
ate [substance] use disorder’ or “severe [substance] use disorder,” depending on the severity
of the comorbid substance use disorder. If there is no comorbid substance use disorder (e.g.,
after a one-time heavy use of the substance), then the 4th position character is “9,” and the
clinician should record only the substance-induced bipolar and related disorder.
ICD-10-CM
With use
With use disorder, Without
disorder, moderate use
ICD-9-CM mild or severe disorder
Alcohol 291.89 F10.14 F10.24 F10.94
Phencyclidine 292.84 F16.14 F16.24 F16.94
Other hallucinogen 292.84 F16.14 F16.24 F16.94
Substance/Medication-Induced Bipolar and Related Disorder 143
ICD-10-CM
With use
With use disorder, Without
disorder, moderate use
ICD-9-CM mild or severe disorder
Sedative, hypnotic, or anxiolytic 292.84 F13,.14 F13,24 F13.94
Amphetamine (or other 292.84 F15.14 F15.24 F15.94
stimulant)
Cocaine 292.84 F14.14 F14.24 F14.94
Other (or unknown) substance 292.84 F19.14 F19.24 F19.94
Specify if (see Table 1 in the chapter “Substance-Related and Addictive Disorders” for di-
agnoses associated with substance class):
With onset during intoxication: If the criteria are met for intoxication with the sub-
stance and the symptoms develop during intoxication.
With onset during withdrawal: If criteria are met for withdrawal from the substance
and the symptoms develop during, or shortly after, withdrawal.
Recording Procedures
ICD-9-CM. The name of the substance/medication-induced bipolar and related disor-
der begins with the specific substance (e.g., cocaine, dexamethasone) that is presumed to
be causing the bipolar mood symptoms. The diagnostic code is selected from the table in-
cluded in the criteria set, which is based on the drug class. For substances that do not fit
into any of the classes (e.g., dexamethasone), the code for “other substance” should be
used; and in cases in which a substance is judged to be an etiological factor but the specific
class of substance is unknown, the category “unknown substance” should be used.
The name of the disorder is followed by the specification of onset (i.e., onset during in-
toxication, onset during withdrawal). Unlike the recording procedures for ICD-10-CM,
which combine the substance-induced disorder and substance use disorder into a single
code, for ICD-9-CM a separate diagnostic code is given for the substance use disorder. For
example, in the case of irritable symptoms occurring during intoxication in a man with a
severe cocaine use disorder, the diagnosis is 292.84 cocaine-induced bipolar and related
disorder, with onset during intoxication. An additional diagnosis of 304.20 severe cocaine
use disorder is also given. When more than one substance is judged to play a significant
role in the development of bipolar mood symptoms, each should be listed separately (e.g.,
292.84 methylphenidate-induced bipolar and related disorder, with onset during intoxi-
cation; 292.84 dexamethasone-induced bipolar and related disorder, with onset during in-
toxication).
ICD-10-CM. The name of the substance/medication-induced bipolar and related disor-
der begins with the specific substance (e.g., cocaine, dexamethasone) that is presumed to
be causing the bipolar mood symptoms. The diagnostic code is selected from the table in-
cluded in the criteria set, which is based on the drug class and presence or absence of a co-
morbid substance use disorder. For substances that do not fit into any of the classes (e.g.,
dexamethasone), the code for “other substance” should be used; and in cases in which a
substance is judged to be an etiological factor but the specific class of substance is un-
known, the category “unknown substance” should be used.
When recording the name of the disorder, the comorbid substance use disorder (if any)
is listed first, followed by the word “with,” followed by the name of the substance-induced
144 Bipolar and Related Disorders
bipolar and related disorder, followed by the specification of onset (i.e., onset during in-
toxication, onset during withdrawal). For example, in the case of irritable symptoms oc-
curring during intoxication in a man with a severe cocaine use disorder, the diagnosis is
F14.24 severe cocaine use disorder with cocaine-induced bipolar and related disorder,
with onset during intoxication. A separate diagnosis of the comorbid severe cocaine use
disorder is not given. If the substance-induced bipolar and related disorder occurs without
a comorbid substance use disorder (e.g., after a one-time heavy use of the substance), no
accompanying substance use disorder is noted (e.g., F15.94 amphetamine-induced bipolar
and related disorder, with onset during intoxication). When more than one substance is
judged to play a significant role in the development of bipolar mood symptoms, each
should be listed separately (e.g., F15.24 severe methylphenidate use disorder with meth-
ylphenidate-induced bipolar and related disorder, with onset during intoxication; F19.94
dexamethasone-induced bipolar and related disorder, with onset during intoxication).
Diagnostic Features
The diagnostic features of substance /medication-induced bipolar and related disorder are es-
sentially the same as those for mania, hypomania, or depression. A key exception to the diag-
nosis of substance/medication-induced bipolar and related disorder is the case of hypomania
or mania that occurs after antidepressant medication use or other treatments and persists be-
yond the physiological effects of the medication. This condition is considered an indicator of
true bipolar disorder, not substance /medication-induced bipolar and related disorder. Simi-
larly, individuals with apparent electroconvulsive therapy—induced manic or hypomanic ep-
isodes that persist beyond the physiological effects of the treatment are diagnosed with
bipolar disorder, not substance/medication-induced bipolar and related disorder.
Side effects of some antidepressants and other psychotropic drugs (e.g., edginess, ag-
itation) may resemble the primary symptoms of a manic syndrome, but they are funda-
mentally distinct from bipolar symptoms and are insufficient for the diagnosis. That is, the
criterion symptoms of mania/hypomania have specificity (simple agitation is not the same
as excess involvement in purposeful activities), and a sufficient number of symptoms
must be present (not just one or two symptoms) to make these diagnoses. In particular, the
appearance of one or two nonspecific symptoms—irritability, edginess, or agitation during
antidepressant treatment—in the absence of a full manic or hypomanic syndrome should
not be taken to support a diagnosis of a bipolar disorder.
Associated Features Supporting Diagnosis
Etiology (causally related to the use of psychotropic medications or substances of abuse
based on best clinical evidence) is the key variable in this etiologically specified form of bi-
polar disorder. Substances / medications that are typically considered to be associated
with substance /medication-induced bipolar and related disorder include the stimulant
class of drugs, as well as phencyclidine and steroids; however, a number of potential sub-
stances continue to emerge as new compounds are synthesized (e.g., so-called bath salts).
A history of such substance use may help increase diagnostic certainty.
Prevalence
There are no epidemiological studies of substance /medication-induced mania or bipolar
disorder. Each etiological substance may have its own individual risk of inducing a bipo-
lar (manic/hypomanic) disorder.
Deveiopment and Course
In phencyclidine-induced mania, the initial presentation may be one of a delirium with af-
fective features, which then becomes an atypically appearing manic or mixed manic state.
Bipolar and Related Disorder Due to Another Medical Condition 145
This condition follows the ingestion or inhalation quickly, usually within hours or, at the
most, a few days. In stimulant-induced manic or hypomanic states, the response is in min-
utes to 1 hour after one or several ingestions or injections. The episode is very brief and
typically resolves over 1-2 days. With corticosteroids and some immunosuppressant
medications, the mania (or mixed or depressed state) usually follows several days of in-
gestion, and the higher doses appear to have a much greater likelihood of producing bi-
polar symptoms.
Diagnostic Markers
Determination of the substance of use can be made through markers in the blood or urine
to corroborate diagnosis.
Differentiai Diagnosis
Substance/medication-induced bipolar and related disorder should be differentiated
from other bipolar disorders, substance intoxication or substance-induced delirium, and
medication side effects (as noted earlier). A full manic episode that emerges during anti-
depressant treatment (e.g., medication, electroconvulsive therapy) but persists at a fully
syndromal level beyond the physiological effect of that treatment is sufficient evidence for
a bipolar I diagnosis. A full hypomanic episode that emerges during antidepressant treat-
ment (e.g., medication, electroconvulsive therapy) but persists at a fully syndromal level
beyond the physiological effect of that treatment is sufficient evidence for a bipolar II di-
agnosis only if preceded by a major depressive episode.
Comorbidity
Comorbidities are those associated with the use of illicit substances (in the case of illegal
stimulants or phencyclidine) or diversion of prescribed stimulants. Comorbidities related
to steroid or immunosuppressant medications are those medical indications for these
preparations. Delirium can occur before or along with manic symptoms in individuals in-
gesting phencyclidine or those who are prescribed steroid medications or other immuno-
suppressant medications.
Bipolar and Related Disorder
Due to Another Medical Condition
Diagnostic Criteria
A. Aprominent and persistent period of abnormally elevated, expansive, or irritable mood
and abnormally increased activity or energy that predominates in the clinical picture.
B. There is evidence from the history, physical examination, or laboratory findings that the dis-
turbance is the direct pathophysiological consequence of another medical condition.
. The disturbance is not better explained by another mental disorder.
. The disturbance does not occur exclusively during the course of a delirium.
. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning, or necessitates hospitalization to pre-
vent harm to self or others, or there are psychotic features.
Coding note: The ICD-9-CM code for bipolar and related disorder due to another medical
condition is 293.83, which is assigned regardiess of the specifier. The ICD-10-CM code
depends on the specifier (see below).
moOQ0
146 Bipolar and Related Disorders
Specify if:
(F06.33) With manic features: Full criteria are not met for a manic or hypomanic ep-
isode.
(F06.33) With manic- or hypomanic-like episode: Full criteria are met except Crite-
rion D for a manic episode or except Criterion F for a hypomanic episode.
(F06.34) With mixed features: Symptoms of depression are also present but do not
predominate in the clinical picture.
Coding note: Include the name of the other medical condition in the name of the mental
disorder (e.g., 293.83 [F06.33] bipolar disorder due to hyperthyroidism, with manic fea-
tures). The other medical condition should also be coded and listed separately immedi-
ately before the bipolar and related disorder due to the medical condition (e.g., 242.90
[E05.90] hyperthyroidism; 293.83 [F06.33] bipolar disorder due to hyperthyroidism, with
manic features).
Diagnostic Features
The essential features of bipolar and related disorder due to another medical condition are
presence of a prominent and persistent period of abnormally elevated, expansive, or irri-
table mood and abnormally increased activity or energy predominating in the clinical pic-
ture that is attributable to another medical condition (Criterion B). In most cases the manic
or hypomanic picture may appear during the initial presentation of the medical condition
(ie., within 1 month); however, there are exceptions, especially in chronic medical condi-
tions that might worsen or relapse and herald the appearance of the manic or hypomanic
picture. Bipolar and related disorder due to another medical condition would not be diag-
nosed when the manic or hypomanic episodes definitely preceded the medical condition,
since the proper diagnosis would be bipolar disorder (except in the unusual circumstance
in which all preceding manic or hypomanic episodes—or, when only one such episode has
occurred, the preceding manic or hypomanic episode—were associated with ingestion of
a substance/medication). The diagnosis of bipolar and related disorder due to another
medical condition should not be made during the course of a delirium (Criterion D). The
manic or hypomanic episode in bipolar and related disorder due to another medical con-
dition must cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning to qualify for this diagnosis (Criterion E).
Associated Features Supporting Diagnosis
Etiology (i.e., a causal relationship to another medical condition based on best clinical ev-
idence) is the key variable in this etiologically specified form of bipolar disorder. The list-
ing of medical conditions that are said to be able to induce mania is never complete, and
the clinician’s best judgment is the essence of this diagnosis. Among the best known of the
medical conditions that can cause a bipolar manic or hypomanic condition are Cushing’s
disease and multiple sclerosis, as well as stroke and traumatic brain injuries.
Development and Course
Bipolar and related disorder due to another medical condition usually has its onset acutely
or subacutely within the first weeks or month of the onset of the associated medical con-
dition. However, this is not always the case, as a worsening or later relapse of the associ-
ated medical condition may precede the onset of the manic or hypomanic syndrome. The
clinician must make a clinical judgment in these situations about whether the medical con-
dition is causative, based on temporal sequence as well as plausibility of a causal relation-
Bipolar and Related Disorder Due to Another Medical Condition 147
ship. Finally, the condition may remit before or just after the medical condition remits,
particularly when treatment of the manic/hypomanic symptoms is effective.
Culture-Related Diagnostic Issues
Culture-related differences, to the extent that there is any evidence, pertain to those asso-
ciated with the medical condition (e.g., rates of multiple sclerosis and stroke vary around
the world based on dietary, genetic factors, and other environmental factors).
Gender-Related Diagnostic Issues
Gender differences pertain to those associated with the medical condition (e.g., systemic
lupus erythematosus is more common in females; stroke is somewhat more common in
middle-age males compared with females).
Diagnostic Markers
Diagnostic markers pertain to those associated with the medical condition (e.g., steroid
levels in blood or urine to help corroborate the diagnosis of Cushing’s disease, which can
be associated with manic or depressive syndromes; laboratory tests confirming the diag-
nosis of multiple sclerosis).
Functional Consequences of Bipolar and Related
Disorder Due to Another Medical Condition
Functional consequences of the bipolar symptoms may exacerbate impairments associ-
ated with the medical condition and may incur worse outcomes due to interference with
medical treatment. In general, it is believed, but not established, that the illness, when in-
duced by Cushing’s disease, will not recur if the Cushing's disease is cured or arrested.
However, it is also suggested, but not established, that mood syndromes, including de-
pressive and manic/hypomanic ones, may be episodic (i.e., recurring) with static brain in-
juries and other central nervous system diseases.
Differential Diagnosis
Symptoms of delirium, catatonia, and acute anxiety. It is important to differentiate
symptoms of mania from excited or hypervigilant delirious symptoms; from excited cata-
tonic symptoms; and from agitation related to acute anxiety states.
Medication-induced depressive or manic symptoms. An important differential diag-
nostic observation is that the other medical condition may be treated with medications
(e.g., steroids or alpha-interferon) that can induce depressive or manic symptoms. In these
cases, clinical judgment using all of the evidence in hand is the best way to try to separate
the most likely and/or the most important of two etiological factors (i.e., association with
the medical condition vs. a substance/medication-induced syndrome). The differential di-
agnosis of the associated medical conditions is relevant but largely beyond the scope of the
present manual.
Comorbidity
Conditions comorbid with bipolar and related disorder due to another medical condition
are those associated with the medical conditions of etiological relevance. Delirium can oc-
cur before or along with manic symptoms in individuals with Cushing’s disease.
148 Bipolar and Related Disorders
Other Specified Bipolar and Related Disorder
296.89 (F31.89)
This category applies to presentations in which symptoms characteristic of a bipolar and
related disorder that cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning predominate but do not meet the full criteria
for any of the disorders in the bipolar and related disorders diagnostic class. The other
specified bipolar and related disorder category is used in situations in which the clinician
chooses to communicate the specific reason that the presentation does not meet the cri-
teria for any specific bipolar and related disorder. This is done by recording “other speci-
fied bipolar and related disorder” followed by the specific reason (e.g., “short-duration
cyclothymia”).
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Short-duration hypomanic episodes (2-3 days) and major depressive episodes: A
lifetime history of one or more major depressive episodes in individuals whose presenta-
tion has never met full criteria for a manic or hypomanic episode but who have experienced
two or more episodes of short-duration hypomania that meet the full symptomatic criteria
for a hypomanic episode but that only last for 2~3 days. The episodes of hypomanic symp-
toms do not overlap in time with the major depressive episodes, so the disturbance does
not meet criteria for major depressive episode, with mixed features.
2. Hypomanic episodes with insufficient symptoms and major depressive epi-
sodes: A lifetime history of one or more major depressive episodes in individuals
whose presentation has never met full criteria for a manic or hypomanic episode but
who have experienced one or more episodes of hypomania that do not meet full symp-
tomatic criteria {i.e., at least 4 consecutive days of elevated mood and one or two of
the other symptoms of a hypomanic episode, or irritable mood and two or three of the
other symptoms of a hypomanic episode). The episodes of hypomanic symptoms do
not overlap in time with the major depressive episodes, so the disturbance does not
meet criteria for major depressive episode, with mixed features.
3. Hypomanic episode without prior major depressive episode: One or more hypo-
manic episodes in an individual whose presentation has never met full criteria for a ma-
jor depressive episode or a manic episode. If this occurs in an individual with an
established diagnosis of persistent depressive disorder (dysthymia), both diagnoses
can be concurrently applied during the periods when the full criteria for a hypomanic
episode are met.
4. Short-duration cyclothymia (less than 24 months): Multiple episodes of hypomanic
symptoms that do not meet criteria for a hypomanic episode and multiple episodes of de-
pressive symptoms that do not meet criteria for a major depressive episode that persist
over a period of less than 24 months (less than 12 months for children or adolescents)
in an individual whose presentation has never met full criteria for a major depressive,
manic, or hypomanic episode and does not meet criteria for any psychotic disorder. Dur-
ing the course of the disorder, the hypomanic or depressive symptoms are present for
more days than not, the individual has not been without symptoms for more than 2 months
ata time, and the symptoms cause clinically significant distress or impairment.
Unspecified Bipolar and Related Disorder 149
Unspecified Bipolar and Related Disorder
296.80 (F31.9)
This category applies to presentations in which symptoms characteristic of a bipolar and
related disorder that cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning predominate but do not meet the full criteria
for any of the disorders in the bipolar and related disorders diagnostic class. The unspec-
ified bipolar and related disorder category is used in situations in which the clinician choos-
es not to specify the reason that the criteria are not met for a specific bipolar and related
disorder, and includes presentations in which there is insufficient information to make a
more specific diagnosis (e.g., in emergency room settings).
Specifiers for Bipolar and Related Disorders
Specify if:
With anxious distress: The presence of at least two of the following symptoms during
the majority of days of the current or most recent episode of mania, hypomania, or de-
pression:
. Feeling keyed up or tense.
. Feeling unusually restless.
. Difficulty concentrating because of worry.
. Fear that something awful may happen.
. Feeling that the individual might lose control of himself or herself.
Specify current severity:
Mild: Two symptoms.
Moderate: Three symptoms.
Moderate-severe: Four or five symptoms.
Severe: Four or five symptoms with motor agitation.
Note: Anxious distress has been noted as a prominent feature of both bipolar and
major depressive disorder in both primary care and specialty mental health set-
tings. High levels of anxiety have been associated with higher suicide risk, longer
duration of illness, and greater likelihood of treatment nonresponse. As a result, it
is clinically useful to specify accurately the presence and severity levels of anxious
distress for treatment planning and monitoring of response to treatment.
With mixed features: The mixed features specifier can apply to the current manic, hy-
pomanic, or depressive episode in bipolar | or bipolar Il disorder:
Manic or hypomanic episode, with mixed features:
A. Full criteria are met for a manic episode or hypomanic episode, and at least
three of the following symptoms are present during the majority of days of the
current or most recent episode of mania or hypomania:
at wWNM
1. Prominent dysphoria or depressed mood as indicated by either subjective
report (e.g., feels sad or empty) or observation made by others (e.g., ap-
pears tearful).
2. Diminished interest or pleasure in all, or almost all, activities (as indicated by
either subjective account or observation made by others).
3. Psychomotor retardation nearly every day (observable by others; not merely
subjective feelings of being slowed down).
150
Bipolar and Related Disorders
4. Fatigue or loss of energy.
5. Feelings of worthlessness or excessive or inappropriate guilt (not merely
self-reproach or guilt about being sick).
6. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ide-
ation without a specific plan, or a suicide attempt or a specific plan for com-
mitting suicide.
B. Mixed symptoms are observable by others and represent a change from the
person’s usual behavior.
C. For individuals whose symptoms meet full episode criteria for both mania and
depression simultaneously, the diagnosis should be manic episode, with mixed
features, due to the marked impairment and clinical severity of full mania.
D. The mixed symptoms are not attributable to the physiological effects of a sub-
stance (e.g., a drug of abuse, a medication, other treatment).
Depressive episode, with mixed features:
A. Full criteria are met for a major depressive episode, and at least three of the fol-
lowing manic/hypomanic symptoms are present during the majority of days of
the current or most recent episode of depression:
1. Elevated, expansive mood.
2. Inflated self-esteem or grandiosity.
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are racing.
5. Increase in energy or goal-directed activity (either socially, at work or school,
or sexually).
. Increased or excessive involvement in activities that have a high potential
for painful consequences (e.g., engaging in unrestrained buying sprees,
sexual indiscretions, or foolish business investments).
7. Decreased need for sleep (feeling rested despite sleeping less than usual;
to be contrasted with insomnia).
B. Mixed symptoms are observable by others and represent a change from the
person’s usual behavior.
C. For individuals whose symptoms meet full episode criteria for both mania and
depression simultaneously, the diagnosis should be manic episode, with mixed
features.
D. The mixed symptoms are not attributable to the physiological effects of a sub-
stance (e.g., a drug of abuse, a medication, or other treatment).
Note: Mixed features associated with a major depressive episode have been found
to be a significant risk factor for the development of bipolar | or bipolar II disorder.
As a result, it is clinically useful to note the presence of this specifier for treatment
planning and monitoring of response to treatment.
fo»)
With rapid cycling (can be applied to bipolar | or bipolar || disorder): Presence of at
least four mood episodes in the previous 12 months that meet the criteria for manic,
hypomanic, or major depressive episode.
Note: Episodes are demarcated by either partial or full remissions of at least 2 months
or a switch to an episode of the opposite polarity (e.g., major depressive episode to
manic episode).
Note: The essential feature of a rapid-cycling bipolar disorder is the occurrence of
at least four mood episodes during the previous 12 months. These episodes can
occur in any combination and order. The episodes must meet both the duration and
Specifiers for Bipolar and Related Disorders 151
symptom number criteria for a major depressive, manic, or hypomanic episode and
must be demarcated by either a period of full remission or a switch to an episode
of the opposite polarity. Manic and hypomanic episodes are counted as being on
the same pole. Except for the fact that they occur more frequently, the episodes that
occur in a rapid-cycling pattern are no different from those that occur in a non-rapid-
cycling pattern. Mood episodes that count toward defining a rapid-cycling pattern
exclude those episodes directly caused by a substance (e.g., cocaine, corticoste-
roids) or another medical condition.
With melancholic features:
A.
B.
One of the following is present during the most severe period of the current episode:
1. Loss of pleasure in all, or almost all, activities.
2. Lack of reactivity to usually pleasurable stimuli (does not feel much better, even
temporarily, when something good happens).
Three (or more) of the following:
1. Adistinct quality of depressed mood characterized by profound despondency,
despair, and/or moroseness or by so-called empty mood.
Depression that is regularly worse in the morning.
Early-morning awakening (i.e., at least 2 hours before usual awakening).
Marked psychomotor agitation or retardation.
Significant anorexia or weight loss.
Excessive or inappropriate guilt.
QOaPran
Note: The specifier “with melancholic features” is applied if these features are pres-
ent at the most severe stage of the episode. There is a near-complete absence of
the capacity for pleasure, not merely a diminution. A guideline for evaluating the
lack of reactivity of mood is that even highly desired events are not associated with
marked brightening of mood. Either mood does not brighten at all, or it brightens
only partially (e.g., up to 20%—40% of normal for only minutes at a time). The “dis-
tinct quality” of mood that is characteristic of the “with melancholic features” speci-
fier is experienced as qualitatively different from that during a nonmelancholic
depressive episode. A depressed mood that is described as merely more severe,
longer lasting, or present without a reason is not considered distinct in quality. Psy-
chomotor changes are nearly always present and are observable by others.
Melancholic features exhibit only a modest tendency to repeat across episodes
in the same individual. They are more frequent in inpatients, as opposed to outpa-
tients; are less likely to occur in milder than in more severe major depressive epi-
sodes; and are more likely to occur in those with psychotic features.
With atypical features: This specifier can be applied when these features predomi-
nate during the majority of days of the current or most recent major depressive epi-
sode.
A.
B.
Mood reactivity (i.e., mood brightens in response to actual or potential positive
events).
Two (or more) of the following features:
1. Significant weight gain or increase in appetite.
2. Hypersomnia.
3. Leaden paralysis (i.e., heavy, leaden feelings in arms or legs).
4. A long-standing pattern of interpersonal rejection sensitivity (not limited to epi-
sodes of mood disturbance) that results in significant social or occupational
impairment.
152
Bipolar and Related Disorders
C. Criteria are not met for “with melancholic features” or “with catatonia” during the
same episode.
Note: “Atypical depression” has historical significance (i.e., atypical in contradis-
tinction to the more classical agitated, “endogenous” presentations of depression
that were the norm when depression was rarely diagnosed in outpatients and al-
most never in adolescents or younger adults) and today does not connote an un-
common or unusual clinical presentation as the term might imply.
Mood reactivity is the capacity to be cheered up when presented with positive
events (€.g., a visit from children, compliments from others). Mood may become
euthymic (not sad) even for extended periods of time if the external circumstances
remain favorable. Increased appetite may be manifested by an obvious increase in
food intake or by weight gain. Hypersomnia may include either an extended period
of nighttime sleep or daytime napping that totals at least 10 hours of sleep per day
(or at least 2 hours more than when not depressed). Leaden paralysis is defined as
feeling heavy, leaden, or weighted down, usually in the arms or legs. This sensation
is generally present for at least an hour a day but often lasts for many hours at a
time. Unlike the other atypical features, pathological sensitivity to perceived inter-
personal rejection is a trait that has an early onset and persists throughout most of
adult life. Rejection sensitivity occurs both when the person is and is not depressed,
though it may be exacerbated during depressive periods.
With psychotic features: Delusions or hallucinations are present at any time in the
episode. If psychotic features are present, specify if mood-congruent or mood-incon-
gruent:
With mood-congruent psychotic features: During manic episodes, the con-
tent of all delusions and hallucinations is consistent with the typical manic
themes of grandiosity, invulnerability, etc., but may also include themes of sus-
piciousness or paranoia, especially with respect to others’ doubts about the in-
dividual’s capacities, accomplishments, and so forth.
With mood-incongruent psychotic features: The content of delusions and
hallucinations is inconsistent with the episode polarity themes as described
above, or the content is a mixture of mood-incongruent and mood-congruent
themes.
With catatonia: This specifier can apply to an episode of mania or depression if cata-
tonic features are present during most of the episode. See criteria for catatonia asso-
ciated with a mental disorder in the chapter “Schizophrenia Spectrum and Other
Psychotic Disorders.”
With peripartum onset: This specifier can be applied to the current or, if the full crite-
ria are not currently met for a mood episode, most recent episode of mania, hypoma-
nia, or major depression in bipolar | or bipolar I! disorder if onset of mood symptoms
occurs during pregnancy or in the 4 weeks following delivery.
Note: Mood episodes can have their onset either during pregnancy or postpartum.
Aithough the estimates differ according to the period of follow-up after delivery, be-
tween 3% and 6% of women will experience the onset of a major depressive epi-
sode during pregnancy or in the weeks or months following delivery. Fifty percent
of “postpartum” major depressive episodes actually begin prior to delivery. Thus,
these episodes are referred to collectively as peripartum episodes. Women with
peripartum major depressive episodes often have severe anxiety and even panic
attacks. Prospective studies have demonstrated that mood and anxiety symptoms
during pregnancy, as well as the “baby blues,” increase the risk for a postpartum
major depressive episode.
Specifiers for Bipolar and Related Disorders 153
Peripartum-onset mood episodes can present either with or without psychotic
features: Infanticide is most often associated with postpartum psychotic episodes
that are characterized by command hallucinations to kill the infant or delusions that
the infant is possessed, but psychotic symptoms can also occur in severe postpar-
tum mood episodes without such specific delusions or hallucinations.
Postpartum mood (major depressive or manic) episodes with psychotic features
appear to occur in from 1 in 500 to 1 in 1,000 deliveries and may be more common
in primiparous women. The risk of postpartum episodes with psychotic features is
particularly increased for women with prior postpartum mood episodes but is also
elevated for those with a prior history of a depressive or bipolar disorder (especially
bipolar | disorder) and those with a family history of bipolar disorders.
Once a woman has had a postpartum episode with psychotic features, the risk
of recurrence with each subsequent delivery is between 30% and 50%. Postpartum
episodes must be differentiated from delirium occurring in the postpartum period,
which is distinguished by a fluctuating level of awareness or attention. The postpar-
tum period is unique with respect to the degree of neuroendocrine alterations and
psychosocial adjustments, the potential impact of breast-feeding on treatment plan-
ning, and the long-term implications of a history of postpartum mood disorder on sub-
sequent family planning.
With seasonal pattern: This specifier applies to the lifetime pattern of mood episodes.
The essential feature is a regular seasonal pattern of at least one type of episode (i.e.,
mania, hypomania, or depression). The other types of episodes may not follow this pat-
tern. For example, an individual may have seasonal manias, but his or her depressions
do not regularly occur at a specific time of year.
A. There has been a regular temporal relationship between the onset of manic, hypo-
manic, or major depressive episodes and a particular time of the year (e.g., in the
fall or winter) in bipolar | or bipolar II disorder.
Note: Do not include cases in which there is an obvious effect of seasonally related
psychosocial stressors (e.g., regularly being unemployed every winter).
B. Full remissions (or a change from major depression to mania or hypomania or vice
versa) also occur at a characteristic time of the year (e.g., depression disappears
in the spring).
C. Inthe last 2 years, the individual’s manic, hypomanic, or major depressive episodes
have demonstrated a temporal seasonal relationship, as defined above, and no
non-seasonal episodes of that polarity have occurred during that 2-year period.
D. Seasonal manias, hypomanias, or depressions (as described above) substantially
outnumber any nonseasonal manias, hypomanias, or depressions that may have
occurred over the individual's lifetime.
Note: This specifier can be applied to the pattern of major depressive episodes in
bipolar | disorder, bipolar II disorder, or major depressive disorder, recurrent. The
essential feature is the onset and remission of major depressive episodes at char-
acteristic times of the year. In most cases, the episodes begin in fall or winter and
remit in spring. Less commonly, there may be recurrent summer depressive epi-
sodes. This pattern of onset and remission of episodes must have occurred during
at least a 2-year period, without any nonseasonal episodes occurring during this
period. In addition, the seasonal depressive episodes must substantially outnum-
ber any nonseasonal depressive episodes over the individual's lifetime.
This specifier does not apply to those situations in which the pattern is better ex-
plained by seasonally linked psychosocial stressors (e.g., seasonal unemployment
or school schedule). Major depressive episodes that occur in a seasonal pattern
154 Bipolar and Related Disorders
are often characterized by prominent energy, hypersomnia, overeating, weight
gain, and a craving for carbohydrates. It is unclear whether a seasonal pattern is
more likely in recurrent major depressive disorder or in bipolar disorders. However,
within the bipolar disorders group, a seasonal pattern appears to be more likely in
bipolar Il disorder than in bipolar | disorder. In some individuals, the onset of manic
or hypomanic episodes may also be linked to a particular season.
The prevalence of winter-type seasonal pattern appears to vary with latitude,
age, and sex. Prevalence increases with higher latitudes. Age is also a strong pre-
dictor of seasonality, with younger persons at higher risk for winter depressive epi-
sodes.
Specify if:
In partial remission: Symptoms of the immediately previous manic, hypomanic, or
depressive episode are present, but full criteria are not met, or there is a period lasting
less than 2 months without any significant symptoms of a manic, hypomanic, or major
depressive episode following the end of such an episode.
In full remission: During the past 2 months, no significant signs or symptoms of the
disturbance were present.
Specify current severity:
Severity is based on the number of criterion symptoms, the severity of those symptoms,
and the degree of functional disability.
Mild: Few, if any, symptoms in excess of those required to meet the diagnostic criteria
are present, the intensity of the symptoms is distressing but manageable, and the
symptoms result in minor impairment in social or occupational functioning.
Moderate: The number of symptoms, intensity of symptoms, and/or functional impair-
ment are between those specified for “mild” and “severe.”
Severe: The number of symptoms is substantially in excess of those required to make
the diagnosis, the intensity of the symptoms is seriously distressing and unmanage-
able, and the symptoms markedly interfere with social and occupational functioning.
Disorde ‘Ss
Depressive diSorders include disruptive mood dysregulation disorder, major
depressive disorder (including major depressive episode), persistent depressive disorder
(dysthymia), premenstrual dysphoric disorder, substance/medication-induced depres-
sive disorder, depressive disorder due to another medical condition, other specified de-
pressive disorder, and unspecified depressive disorder. Unlike in DSM-IV, this chapter
“Depressive Disorders” has been separated from the previous chapter “Bipolar and Re-
lated Disorders.” The common feature of all of these disorders is the presence of sad,
empty, or irritable mood, accompanied by somatic and cognitive changes that signifi-
cantly affect the individual's capacity to function. What differs among them are issues of
duration, timing, or presumed etiology.
In order to address concerns about the potential for the overdiagnosis of and treatment
for bipolar disorder in children, anew diagnosis, disruptive mood dysregulation disorder,
referring to the presentation of children with persistent irritability and frequent episodes
of extreme behavioral dyscontrol, is added to the depressive disorders for children up to
12 years of age. Its placement in this chapter reflects the finding that children with this
symptom pattern typically develop unipolar depressive disorders or anxiety disorders,
rather than bipolar disorders, as they mature into adolescence and adulthood.
Major depressive disorder represents the classic condition in this group of disorders. It
is characterized by discrete episodes of at least 2 weeks’ duration (although most episodes
last considerably longer) involving clear-cut changes in affect, cognition, and neurovege-
tative functions and inter-episode remissions. A diagnosis based on a single episode is
possible, although the disorder is a recurrent one in the majority of cases. Careful consid-
eration is given to the delineation of normal sadness and grief from a major depressive ep-
isode. Bereavement may induce great suffering, but it does not typically induce an episode
of major depressive disorder. When they do occur together, the depressive symptoms and
functional impairment tend to be more severe and the prognosis is worse compared with
bereavement that is not accompanied by major depressive disorder. Bereavement-related
depression tends to occur in persons with other vulnerabilities to depressive disorders,
and recovery may be facilitated by antidepressant treatment.
A more chronic form of depression, persistent depressive disorder (dysthymia), can be
diagnosed when the mood disturbance continues for at least 2 years in adults or 1 year in
children. This diagnosis, new in DSM-5, includes both the DSM-IV diagnostic categories of
chronic major depression and dysthymia.
After careful scientific review of the evidence, premenstrual dysphoric disorder has
been moved from an appendix of DSM-IV (“Criteria Sets and Axes Provided for Further
Study”) to Section II of DSM-5. Almost 20 years of additional of research on this condition
has confirmed a specific and treatment-responsive form of depressive disorder that begins
sometime following ovulation and remits within a few days of menses and has a marked
impact on functioning.
A large number of substances of abuse, some prescribed medications, and several
medical conditions can be associated with depression-like phenomena. This fact is recog-
nized in the diagnoses of substance /medication-induced depressive disorder and depres-
sive disorder due to another medical condition.
155
156 Depressive Disorders
Disruptive Mood Dysregulation Disorder
Diagnostic Criteria 296.99 (F34.8)
A. Severe recurrent temper outbursts manifested verbally (e.g., verbal rages) and/or be-
haviorally (e.g., physical aggression toward people or property) that are grossly out of
proportion in intensity or duration to the situation or provocation.
. The temper outbursts are inconsistent with developmental level.
. The temper outbursts occur, on average, three or more times per week.
. The mood between temper outbursts is persistently irritable or angry most of the day,
nearly every day, and is observable by others (e.g., parents, teachers, peers).
E. Criteria A-D have been present for 12 or more months. Throughout that time, the indi-
vidual has not had a period lasting 3 or more consecutive months without all of the
symptoms in Criteria A—-D.
F. Criteria A and D are present in at least two of three settings (i.e., at home, at school,
with peers) and are severe in at least one of these.
G. The diagnosis should not be made for the first time before age 6 years or after age 18
years.
H. By history or observation, the age at onset of Criteria A-E is before 10 years.
|. There has never been a distinct period lasting more than 1 day during which the full
symptom criteria, except duration, for a manic or hypomanic episode have been met.
Note: Developmentally appropriate mood elevation, such as occurs in the context of a
highly positive event or its anticipation, should not be considered as a symptom of ma-
nia or hypomania.
J. The behaviors do not occur exclusively during an episode of major depressive disorder
and are not better explained by another mental disorder (e.g., autism spectrum disor-
der, posttraumatic stress disorder, separation anxiety disorder, persistent depressive
disorder [dysthymia]).
Note: This diagnosis cannot coexist with oppositional defiant disorder, intermittent ex-
plosive disorder, or bipolar disorder, though it can coexist with others, including major
depressive disorder, attention-deficit/hyperactivity disorder, conduct disorder, and
substance use disorders. Individuals whose symptoms meet criteria for both disruptive
mood dysregulation disorder and oppositional defiant disorder should only be given the
diagnosis of disruptive mood dysregulation disorder. If an individua! has ever experi-
enced a manic or hypomanic episode, the diagnosis of disruptive mood dysregulation
disorder should not be assigned.
K. The symptoms are not attributable to the physiological effects of a substance or to an-
other medical or neurological condition.
008
Diagnostic Features
The core feature of disruptive mood dysregulation disorder is chronic, severe persistent ir-
ritability. This severe irritability has two prominent clinical manifestations, the first of
which is frequent temper outbursts. These outbursts typically occur in response to frus-
tration and can be verbal or behavioral (the latter in the form of aggression against prop-
erty, self, or others). They must occur frequently (i.e., on average, three or more times per
week) (Criterion C) over at least 1 year in at least two settings (Criteria E and F), such as in
the home and at school, and they must be developmentally inappropriate (Criterion B).
The second manifestation of severe irritability consists of chronic, persistently irritable or
angry mood that is present between the severe temper outbursts. This irritable or angry
mood must be characteristic of the child, being present most of the day, nearly every day,
and noticeable by others in the child’s environment (Criterion D).
Disruptive Mood Dysregulation Disorder 157
The clinical presentation of disruptive mood dysregulation disorder must be carefully
distinguished from presentations of other, related conditions, particularly pediatric bi-
polar disorder. In fact, disruptive mood dysregulation disorder was added to DSM-5 to
address the considerable concern about the appropriate classification and treatment of
children who present with chronic, persistent irritability relative to children who present
with classic (i.e., episodic) bipolar disorder.
Some researchers view severe, non-episodic irritability as characteristic of bipolar dis-
order in children, although both DSM-IV and DSM-5 require that both children and adults
have distinct episodes of mania or hypomania to qualify for the diagnosis of bipolar I dis-
order. During the latter decades of the 20th century, this contention by researchers that
severe, nonepisodic irritability is a manifestation of pediatric mania coincided with an up-
surge in the rates at which clinicians assigned the diagnosis of bipolar disorder to their
pediatric patients. This sharp increase in rates appears to be attributable to clinicians com-
bining at least two clinical presentations into a single category. That is, both classic, epi-
sodic presentations of mania and non-episodic presentations of severe irritability have
been labeled as bipolar disorder in children. In DSM-5, the term bipolar disorder is explicitly
reserved for episodic presentations of bipolar symptoms. DSM-IV did not include a diagno-
sis designed to capture youths whose hallmark symptoms consisted of very severe, non-
episodic irritability, whereas DSM-5, with the inclusion of disruptive mood dysregulation
disorder, provides a distinct category for such presentations.
Prevalence
Disruptive mood dysregulation disorder is common among children presenting to pedi-
atric mental health clinics. Prevalence estimates of the disorder in the community are un-
clear. Based on rates of chronic and severe persistent irritability, which is the core feature
of the disorder, the overall 6-month to 1-year period-prevalence of disruptive mood dys-
regulation disorder among children and adolescents probably falls in the 2%-5% range.
However, rates are expected to be higher in males and school-age children than in females
and adolescents.
Development and Course
The onset of disruptive mood dysregulation disorder must be before age 10 years, and the
diagnosis should not be applied to children with a developmental age of less than 6 years.
It is unknown whether the condition presents only in this age-delimited fashion. Because
the symptoms of disruptive mood dysregulation disorder are likely to change as children
mature, use of the diagnosis should be restricted to age groups similar to those in which
validity has been established (7-18 years). Approximately half of children with severe,
chronic irritability will have a presentation that continues to meet criteria for the condition
1 year later. Rates of conversion from severe, nonepisodic irritability to bipolar disorder
are very low. Instead, children with chronic irritability are at risk to develop unipolar de-
pressive and/or anxiety disorders in adulthood.
Age-related variations also differentiate classic bipolar disorder and disruptive mood
dysregulation disorder. Rates of bipolar disorder generally are very low prior to adoles-
cence (<1%), with a steady increase into early adulthood (1%-2% prevalence). Disruptive
mood dysregulation disorder is more common than bipolar disorder prior to adolescence,
and symptoms of the condition generally become less common as children transition into
adulthood.
Risk and Prognostic Factors
Temperamental. Children with chronic irritability typically exhibit complicated psy-
chiatric histories. In such children, a relatively extensive history of chronic irritability is
158 Depressive Disorders
common, typically manifesting before full criteria for the syndrome are met. Such predi-
agnostic presentations may have qualified for a diagnosis of oppositional defiant disorder.
Many children with disruptive mood dysregulation disorder have symptoms that also
meet criteria for attention-deficit /hyperactivity disorder (ADHD) and for an anxiety dis-
order, with such diagnoses often being present from a relatively early age. For some chil-
dren, the criteria for major depressive disorder may also be met.
Genetic and physiological. In terms of familial aggregation and genetics, it has been
suggested that children presenting with chronic, non-episodic irritability can be differen-
tiated from children with bipolar disorder in their family-based risk. However, these two
groups do not differ in familial rates of anxiety disorders, unipolar depressive disorders,
or substance abuse. Compared with children with pediatric bipolar disorder or other men-
tal illnesses, those with disruptive mood dysregulation disorder exhibit both commonal-
ities and differences in information-processing deficits. For example, face-emotion
labeling deficits, as well as perturbed decision making and cognitive control, are present in
children with bipolar disorder and chronically irritable children, as well as in children
with some other psychiatric conditions. There is also evidence for disorder-specific dys-
function, such as during tasks assessing attention deployment in response to emotional
stimuli, which has demonstrated unique signs of dysfunction in children with chronic ir-
ritability.
Gender-Related Diagnostic Issues
Children presenting to clinics with features of disruptive mood dysregulation disorder are
predominantly male. Among community samples, a male preponderance appears to be
supported. This difference in prevalence between males and females differentiates disrup-
tive mood dysregulation disorder from bipolar disorder, in which there is an equal gender
prevalence.
Suicide Risk
In general, evidence documenting suicidal behavior and aggression, as well as other se-
vere functional consequences, in disruptive mood dysregulation disorder should be noted
when evaluating children with chronic irritability.
Functionai Consequences of
Disruptive Mood Dysregulation Disorder
Chronic, severe irritability, such as is seen in disruptive mood dysregulation disorder, is
associated with marked disruption in a child’s family and peer relationships, as well as in
school performance. Because of their extremely low frustration tolerance, such children
generally have difficulty succeeding in school; they are often unable to participate in the
activities typically enjoyed by healthy children; their family life is severely disrupted by
their outbursts and irritability; and they have trouble initiating or sustaining friendships.
Levels of dysfunction in children with bipolar disorder and disruptive mood dysregulation
disorder are generally comparable. Both conditions cause severe disruption in the lives of
the affected individual and their families. In both disruptive mood dysregulation disorder
and pediatric bipolar disorder, dangerous behavior, suicidal ideation or suicide attempts,
severe aggression, and psychiatric hospitalization are common.
Differential Diagnosis
Because chronically irritable children and adolescents typically present with complex histo-
ries, the diagnosis of disruptive mood dysregulation disorder must be made while consid-
ering the presence or absence of multiple other conditions. Despite the need to consider
Disruptive Mood Dysregulation Disorder 159
many other syndromes, differentiation of disruptive mood dysregulation disorder from bi-
polar disorder and oppositional defiant disorder requires particularly careful assessment.
Bipolar disorders. The central feature differentiating disruptive mood dysregulation disor-
der and bipolar disorders in children involves the longitudinal course of the core symptoms. In
children, as in adults, bipolar I disorder and bipolar H disorder manifest as an episodic illness
with discrete episodes of mood perturbation that can be differentiated from the child’s typical
presentation. The mood perturbation that occurs during a manic episode is distinctly different
from the child’s usual mood. In addition, during a manic episode, the change in mood must be
accompanied by the onset, or worsening, of associated cognitive, behavioral, and physical
symptoms (e.g., distractibility, increased goal-directed activity), which are also present to a de-
gree that is distinctly different from the child’s usual baseline. Thus, in the case of a manic ep-
isode, parents (and, depending on developmental level, children) should be able to identify a
distinct time period during which the child’s mood and behavior were markedly different
from usual. In contrast, the irritability of disruptive mood dysregulation disorder is persistent
and is present over many months; while it may wax and wane to a certain degree, severe irri-
tability is characteristic of the child with disruptive mood dysregulation disorder. Thus, while
bipolar disorders are episodic conditions, disruptive mood dysregulation disorder is not. In
fact, the diagnosis of disruptive mood dysregulation disorder cannot be assigned to a child
who has ever experienced a full-duration hypomanic or manic episode (irritable or euphoric)
or who has ever had a manic or hypomanic episode lasting more than 1 day. Another central
differentiating feature between bipolar disorders and disruptive mood dysregulation disorder
is the presence of elevated or expansive mood and grandiosity. These symptoms are common
features of mania but are not characteristic of disruptive mood dysregulation disorder.
Oppositional defiant disorder. While symptoms of oppositional defiant disorder typi-
cally do occur in children with disruptive mood dysregulation disorder, mood symptoms
of disruptive mood dysregulation disorder are relatively rare in children with opposi-
tional defiant disorder. The key features that warrant the diagnosis of disruptive mood
dysregulation disorder in children whose symptoms also meet criteria for oppositional de-
fiant disorder are the presence of severe and frequently recurrent outbursts and a persis-
tent disruption in mood between outbursts. In addition, the diagnosis of disruptive mood
dysregulation disorder requires severe impairment in at least one setting (i.e., home,
school, or among peers) and mild to moderate impairment in a second setting. For this rea-
son, while most children whose symptoms meet criteria for disruptive mood dysregula-
tion disorder will also have a presentation that meets criteria for oppositional defiant
disorder, the reverse is not the case. That is, in only approximately 15% of individuals with
oppositional defiant disorder would criteria for disruptive mood dysregulation disorder
be met. Moreover, even for children in whom criteria for both disorders are met, only the
diagnosis of disruptive mood dysregulation disorder should be made. Finally, both the
prominent mood symptoms in disruptive mood dysregulation disorder and the high risk
for depressive and anxiety disorders in follow-up studies justify placement of disruptive
mood dysregulation disorder among the depressive disorders in DSM-5. (Oppositional
defiant disorder is included in the chapter “Disruptive, Impulse-Control, and Conduct
Disorders.”) This reflects the more prominent mood component among individuals with
disruptive mood dysregulation disorder, as compared with individuals with oppositional
defiant disorder. Nevertheless, it also should be noted that disruptive mood dysregulation
disorder appears to carry a high risk for behavioral problems as well as mood problems.
Attention-deficit/hyperactivity disorder, major depressive disorder, anxiety disorders,
and autism spectrum disorder. Unlike children diagnosed with bipolar disorder or op-
positional defiant disorder, a child whose symptoms meet criteria for disruptive mood
dysregulation disorder also can receive a comorbid diagnosis of ADHD, major depressive
disorder, and/or anxiety disorder. However, children whose irritability is present only in
the context of a major depressive episode or persistent depressive disorder (dysthymia)
160 Depressive Disorders
should receive one of those diagnoses rather than disruptive mood dysregulation disor-
der. Children with disruptive mood dysregulation disorder may have symptoms that also
meet criteria for an anxiety disorder and can receive both diagnoses, but children whose ir-
ritability is manifest only in the context of exacerbation of an anxiety disorder should re-
ceive the relevant anxiety disorder diagnosis rather than disruptive mood dysregulation
disorder. In addition, children with autism spectrum disorders frequently present with
temper outbursts when, for example, their routines are disturbed. In that instance, the
temper outbursts would be considered secondary to the autism spectrum disorder, and
the child should not receive the diagnosis of disruptive mood dysregulation disorder.
Intermittent explosive disorder. Children with symptoms suggestive of intermittent
explosive disorder present with instances of severe temper outbursts, much like children
with disruptive mood dysregulation disorder. However, unlike disruptive mood dysreg-
ulation disorder, intermittent explosive disorder does not require persistent disruption in
mood between outbursts. In addition, intermittent explosive disorder requires only 3 months
of active symptoms, in contrast to the 12-month requirement for disruptive mood dys-
regulation disorder. Thus, these two diagnoses should not be made in the same child. For
children with outbursts and intercurrent, persistent irritability, only the diagnosis of dis-
ruptive mood dysregulation disorder should be made.
Comorbidity
Rates of comorbidity in disruptive mood dysregulation disorder are extremely high. It is
rare to find individuals whose symptoms meet criteria for disruptive mood dysregulation
disorder alone. Comorbidity between disruptive mood dysregulation disorder and other
DSM-defined syndromes appears higher than for many other pediatric mental illnesses;
the strongest overlap is with oppositional defiant disorder. Not only is the overall rate of
comorbidity high in disruptive mood dysregulation disorder, but also the range of comor-
bid illnesses appears particularly diverse. These children typically present to the clinic
with a wide range of disruptive behavior, mood, anxiety, and even autism spectrum
symptoms and diagnoses. However, children with disruptive mood dysregulation disor-
der should not have symptoms that meet criteria for bipolar disorder, as in that context,
only the bipolar disorder diagnosis should be made. If children have symptoms that meet
criteria for oppositional defiant disorder or intermittent explosive disorder and disruptive
mood dysregulation disorder, only the diagnosis of disruptive mood dysregulation disor-
der should be assigned. Also, as noted earlier, the diagnosis of disruptive mood dysregu-
lation disorder should not be assigned if the symptoms occur only in an anxiety-
provoking context, when the routines of a child with autism spectrum disorder or obses-
sive-compulsive disorder are disturbed, or in the context of a major depressive episode.
Major Depressive Disorder
Diagnostic Criteria
A. Five (or more) of the following symptoms have been present during the same 2-week
period and represent a change from previous functioning; at least one of the symptoms
is either (1) depressed mood or (2) loss of interest or pleasure.
Note: Do not include symptoms that are clearly attributable to another medical condition.
1. Depressed mood most of the day, nearly every day, as indicated by either subjec-
tive report (e.g., feels sad, empty, hopeless) or observation made by others (e.g.,
appears tearful). (Note: In children and adolescents, can be irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost ali, activities most of the
day, nearly every day (as indicated by either subjective account or observation).
Major Depressive Disorder 161
3. Significant weight loss when not dieting or weight gain (e.g., a change of more than
5% of body weight in a month), or decrease or increase in appetite nearly every day.
(Note: In children, consider failure to make expected weight gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others, not
merely subjective feelings of restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delu-
sional) nearly every day {not merely self-reproach or guilt about being sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (ei-
ther by subjective account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation with-
out a specific plan, or a suicide attempt or a specific plan for committing suicide.
B. The symptoms cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
C. The episode is not attributable to the physiological effects of a substance or to another
medical condition.
Note: Criteria A-C represent a major depressive episode.
Note: Responses to a significant loss (e.g., bereavement, financial ruin, losses from a nat-
ural disaster, a serious medical illness or disability) may include the feelings of intense sad-
ness, rumination about the loss, insomnia, poor appetite, and weight loss noted in Criterion A,
which may resemble a depressive episode. Although such symptoms may be understand-
able or considered appropriate to the loss, the presence of a major depressive episode in
addition to the normal response to a significant loss should also be carefully considered. This
decision inevitably requires the exercise of clinical judgment based on the individual's history
and the cultural norms for the expression of distress in the context of loss.!
D. The occurrence of the major depressive episode is not better explained by schizoaf-
fective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or
other specified and unspecified schizophrenia spectrum and other psychotic disorders.
E. There has never been a manic episode or a hypomanic episode.
Note: This exclusion does not apply if all of the manic-like or hypomanic-like episodes
are substance-induced or are attributable to the physiological effects of another med-
ical condition.
'In distinguishing grief from a major depressive episode (MDE), it is useful to consider that in
grief the predominant affect is feelings of emptiness and loss, while in MDE it is persistent
depressed mood and the inability to anticipate happiness or pleasure. The dysphoria in grief is
likely to decrease in intensity over days to weeks and occurs in waves, the so-called pangs of
grief. These waves tend to be associated with thoughts or reminders of the deceased. The
depressed mood of MDE is more persistent and not tied to specific thoughts or preoccupations.
The pain of grief may be accompanied by positive emotions and humor that are uncharacteristic
of the pervasive unhappiness and misery characteristic of MDE. The thought content associated
with grief generally features a preoccupation with thoughts and memories of the deceased,
rather than the self-critical or pessimistic ruminations seen in MDE. In grief, self-esteem is gener-
ally preserved, whereas in MDE feelings of worthlessness and self-loathing are common. If self-
derogatory ideation is present in grief, it typically involves perceived failings vis-a-vis the
deceased (e.g., not visiting frequently enough, not telling the deceased how much he or she was
loved). If a bereaved individual thinks about death and dying, such thoughts are generally
focused on the deceased and possibly about “joining” the deceased, whereas in MDE such
thoughts are focused on ending one’s own life because of feeling worthless, undeserving of life,
or unable to cope with the pain of depression.
162 Depressive Disorders
Coding and Recording Procedures
The diagnostic code for major depressive disorder is based on whether this is a single or
recurrent episode, current severity, presence of psychotic features, and remission status.
Current severity and psychotic features are only indicated if full criteria are currently met
for a major depressive episode. Remission specifiers are only indicated if the full criteria
are not currently met for a major depressive episode. Codes are as follows:
Severity/course specifier Single episode Recurrent episode”
Mild {p. 188) 296.21 (F32.0) 296.31 (F33.0)
Moderate (p. 188) 296.22 (F32.1) 296.32 (F33.1)
Severe (p. 188) 296.23 (F32.2) 296.33 (F33.2)
With psychotic features** (p. 186) 296.24 (F32.3) 296.34 (F33.3)
In partial remission (p. 188) 296.25 (F32.4) 296.35 (F33.41)
In full remission (p. 188) 296.26 (F32.5) 296.36 (F33.42)
Unspecified 296.20 (F32.9) 296.30 (F33.9)
*For an episode to be considered recurrent, there must be an interval of at least 2 consecutive months
between separate episodes in which criteria are not met for a major depressive episode. The defini-
tions of specifiers are found on the indicated pages.
“If psychotic features are present, code the “with psychotic features” specifier irrespective of epi-
sode severity.
In recording the name of a diagnosis, terms should be listed in the following order: major
depressive disorder, single or recurrent episode, severity/psychotic/remission specifiers,
followed by as many of the following specifiers without codes that apply to the current
episode.
Specify:
With anxious distress (p. 184)
With mixed features (pp. 184-185)
With melancholic features (p. 185)
With atypical features (pp. 185-186)
With mood-congruent psychotic features (p. 186)
With mood-incongruent psychotic features (p. 186)
With catatonia (p. 186). Coding note: Use additional code 293.89 (F06.1).
With peripartum onset (pp. 186-187)
With seasonal pattern (recurrent episode only) (pp. 187-188)
Diagnostic Features
The criterion symptoms for major depressive disorder must be present nearly every day to
be considered present, with the exception of weight change and suicidal ideation. De-
pressed mood must be present for most of the day, in addition to being present nearly ev-
ery day. Often insomnia or fatigue is the presenting complaint, and failure to probe for
accompanying depressive symptoms will result in underdiagnosis. Sadness may be de-
nied at first but may be elicited through interview or inferred from facial expression and
demeanor. With individuals who focus on a somatic complaint, clinicians should de-
termine whether the distress from that complaint is associated with specific depressive
symptoms. Fatigue and sleep disturbance are present in a high proportion of cases; psy-
chomotor disturbances are much less common but are indicative of greater overall sever-
ity, as is the presence of delusional or near-delusional guilt.
Major Depressive Disorder 163
The essential feature of a major depressive episode is a period of at least 2 weeks during
which there is either depressed mood or the loss of interest or pleasure in nearly all activi-
ties (Criterion A). In children and adolescents, the mood may be irritable rather than sad.
The individual must also experience at least four additional symptoms drawn from a list
that includes changes in appetite or weight, sleep, and psychomotor activity; decreased en-
ergy; feelings of worthlessness or guilt; difficulty thinking, concentrating, or making deci-
sions; or recurrent thoughts of death or suicidal ideation or suicide plans or attempts. To
count toward a major depressive episode, a symptom must either be newly present or must
have clearly worsened compared with the person’s pre-episode status. The symptoms
must persist for most of the day, nearly every day, for at least 2 consecutive weeks. The ep-
isode must be accompanied by clinically significant distress or impairment in social, occu-
pational, or other important areas of functioning. For some individuals with milder
episodes, functioning may appear to be normal but requires markedly increased effort.
The mood in a major depressive episode is often described by the person as depressed,
sad, hopeless, discouraged, or “down in the dumps” (Criterion A1). In some cases, sadness
may be denied at first but may subsequently be elicited by interview (e.g., by pointing out
that the individual looks as if he or she is about to cry). In some individuals who complain
of feeling “blah,” having no feelings, or feeling anxious, the presence of a depressed mood
can be inferred from the person’s facial expression and demeanor. Some individuals em-
phasize somatic complaints (e.g., bodily aches and pains) rather than reporting feelings of
sadness. Many individuals report or exhibit increased irritability (e.g., persistent anger, a
tendency to respond to events with angry outbursts or blaming others, an exaggerated
sense of frustration over minor matters). In children and adolescents, an irritable or cranky
mood may develop rather than a sad or dejected mood. This presentation should be dif-
ferentiated from a pattern of irritability when frustrated.
Loss of interest or pleasure is nearly always present, at least to some degree. Individ-
uals may report feeling less interested in hobbies, “not caring anymore,” or not feeling any
enjoyment in activities that were previously considered pleasurable (Criterion A2). Family
members often notice social withdrawal or neglect of pleasurable avocations (e.g., a for-
merly avid golfer no longer plays, a child who used to enjoy soccer finds excuses not to
practice). In some individuals, there is a significant reduction from previous levels of sex-
ual interest or desire.
Appetite change may involve either a reduction or increase. Some depressed individ-
uals report that they have to force themselves to eat. Others may eat more and may crave
specific foods (e.g., sweets or other carbohydrates). When appetite changes are severe (in
either direction), there may be a significant loss or gain in weight, or, in children, a failure
to make expected weight gains may be noted (Criterion A3).
Sleep disturbance may take the form of either difficulty sleeping or sleeping exces-
sively (Criterion A4). When insomnia is present, it typically takes the form of middle in-
somuia (i.e., waking up during the night and then having difficulty returning to sleep) or
terminal insomnia (i.e., waking too early and being unable to return to sleep). Initial in-
somnia (i.e., difficulty falling asleep) may also occur. Individuals who present with over-
sleeping (hypersomnia) may experience prolonged sleep episodes at night or increased
daytime sleep. Sometimes the reason that the individual seeks treatment is for the dis-
turbed sleep.
Psychomotor changes include agitation (e.g., the inability to sit still, pacing, hand-
wringing; or pulling or rubbing of the skin, clothing, or other objects) or retardation (e.g.,
slowed speech, thinking, and body movements; increased pauses before answering;
speech that is decreased in volume, inflection, amount, or variety of content, or muteness)
(Criterion A5), The psychomotor agitation or retardation must be severe enough to be ob-
servable by others and not represent merely subjective feelings.
Decreased energy, tiredness, and fatigue are common (Criterion A6). A person may re-
port sustained fatigue without physical exertion. Even the smallest tasks seem to require
164 Depressive Disorders
substantial effort. The efficiency with which tasks are accomplished may be reduced. For
example, an individual may complain that washing and dressing in the morning are ex-
hausting and take twice as long as usual.
The sense of worthlessness or guilt associated with a major depressive episode may in-
clude unrealistic negative evaluations of one’s worth or guilty preoccupations or rumina-
tions over minor past failings (Criterion A7). Such individuals often misinterpret neutral
or trivial day-to-day events as evidence of personal defects and have an exaggerated sense
of responsibility for untoward events. The sense of worthlessness or guilt may be of delu-
sional proportions (e.g., an individual who is convinced that he or she is personally re-
sponsible for world poverty). Blaming oneself for being sick and for failing to meet
occupational or interpersonal responsibilities as a result of the depression is very common
and, unless delusional, is not considered sufficient to meet this criterion.
Many individuals report impaired ability to think, concentrate, or make even minor
decisions (Criterion A8). They may appear easily distracted or complain of memory diffi-
culties. Those engaged in cognitively demanding pursuits are often unable to function. In
children, a precipitous drop in grades may reflect poor concentration. In elderly individ-
uals, memory difficulties may be the chief complaint and may be mistaken for early signs
of a dementia (“pseudodementia”). When the major depressive episode is successfully
treated, the memory problems often fully abate. However, in some individuals, particu-
larly elderly persons, a major depressive episode may sometimes be the initial presenta-
tion of an irreversible dementia.
Thoughts of death, suicidal ideation, or suicide attempts (Criterion A9) are common.
They may range from a passive wish not to awaken in the morning or a belief that others
would be better off if the individual were dead, to transient but recurrent thoughts of com-
mitting suicide, to a specific suicide plan. More severely suicidal individuals may have put
their affairs in order (e.g., updated wills, settled debts), acquired needed materials (e.g., a
rope or a gun), and chosen a location and time to accomplish the suicide. Motivations for
suicide may include a desire to give up in the face of perceived insurmountable obstacles,
an intense wish to end what is perceived as an unending and excruciatingly painful emo-
tional state, an inability to foresee any enjoyment in life, or the wish to not be a burden to
others. The resolution of such thinking may be a more meaningful measure of diminished
suicide risk than denial of further plans for suicide.
The evaluation of the symptoms of a major depressive episode is especially difficult
when they occur in an individual who also has a general medical condition (e.g., cancer,
stroke, myocardial infarction, diabetes, pregnancy). Some of the criterion signs and symp-
toms of a major depressive episode are identical to those of general medical conditions
(e.g., weight loss with untreated diabetes; fatigue with cancer; hypersomnia early in preg-
nancy; insomnia later in pregnancy or the postpartum). Such symptoms count toward a
major depressive diagnosis except when they are clearly and fully attributable to a general
medical condition. Nonvegetative symptoms of dysphoria, anhedonia, guilt or worthless-
ness, impaired concentration or indecision, and suicidal thoughts should be assessed with
particular care in such cases. Definitions of major depressive episodes that have been mod-
ified to include only these nonvegetative symptoms appear to identify nearly the same in-
dividuals as do the full criteria.
Associated Features Supporting Diagnosis
Major depressive disorder is associated with high mortality, much of which is accounted
for by suicide; however, it is not the only cause. For example, depressed individuals ad-
mitted to nursing homes have a markedly increased likelihood of death in the first year. In-
dividuals frequently present with tearfulness, irritability, brooding, obsessive rumination,
anxiety, phobias, excessive worry over physical health, and complaints of pain (e.g., head-
aches; joint, abdominal, or other pains). In children, separation anxiety may occur.
Major Depressive Disorder 165
Although an extensive literature exists describing neuroanatomical, neuroendocrino-
logical, and neurophysiological correlates of major depressive disorder, no laboratory test
has yielded results of sufficient sensitivity and specificity to be used as a diagnostic tool for
this disorder. Until recently, hypothalamic-pituitary-adrenal axis hyperactivity had been
the most extensively investigated abnormality associated with major depressive episodes,
and it appears to be associated with melancholia, psychotic features, and risks for eventual
suicide. Molecular studies have also implicated peripheral factors, including genetic vari-
ants in neurotrophic factors and pro-inflammatory cytokines. Additionally, functional
magnetic resonance imaging studies provide evidence for functional abnormalities in spe-
cific neural systems supporting emotion processing, reward seeking, and emotion regula-
tion in adults with major depression.
Prevalence
Twelve-month prevalence of major depressive disorder in the United States is approximately
7%, with marked differences by age group such that the prevalence in 18- to 29-year-old indi-
viduals is threefold higher than the prevalence in individuals age 60 years or older. Females ex-
perience 1.5- to 3-fold higher rates than males beginning in early adolescence.
Development and Course
Major depressive disorder may first appear at any age, but the likelihood of onset in-
creases markedly with puberty. In the United States, incidence appears to peak in the 20s;
however, first onset in late life is not uncommon.
The course of major depressive disorder is quite variable, such that some individuals
rarely, if ever, experience remission (a period of 2 or more months with no symptoms, or
only one or two symptoms to no more than a mild degree), while others experience many
years with few or no symptoms between discrete episodes. It is important to distinguish
individuals who present for treatment during an exacerbation of a chronic depressive ill-
ness from those whose symptoms developed recently. Chronicity of depressive symptoms
substantially increases the likelihood of underlying personality, anxiety, and substance
use disorders and decreases the likelihood that treatment will be followed by full symp-
tom resolution. It is therefore useful to ask individuals presenting with depressive symp-
toms to identify the last period of at least 2 months during which they were entirely free of
depressive symptoms.
Recovery typically begins within 3 months of onset for two in five individuals with ma-
jor depression and within 1 year for four in five individuals. Recency of onset is a strong
determinant of the likelihood of near-term recovery, and many individuals who have been
depressed only for several months can be expected to recover spontaneously. Features as-
sociated with lower recovery rates, other than current episode duration, include psychotic
features, prominent anxiety, personality disorders, and symptom severity.
The risk of recurrence becomes progessively lower over time as the duration of re-
mission increases. The risk is higher in individuals whose preceding episode was severe,
in younger individuals, and in individuals who have already experienced multiple epi-
sodes. The persistence of even mild depressive symptoms during remission is a powerful
predictor of recurrence.
Many bipolar illnesses begin with one or more depressive episodes, and a substantial
proportion of individuals who initially appear to have major depressive disorder will
prove, in time, to instead have a bipolar disorder. This is more likely in individuals with
onset of the illness in adolescence, those with psychotic features, and those with a family
history of bipolar illness. The presence of a “with mixed features” specifier also increases
the risk for future manic or hypomanic diagnosis. Major depressive disorder, particularly
with psychotic features, may also transition into schizophrenia, a change that is much
more frequent than the reverse.
166 Depressive Disorders
Despite consistent differences between genders in prevalence rates for depressive disor-
ders, there appear to be no clear differences by gender in phenomenology, course, or treat-
ment response. Similarly, there are no clear effects of current age on the course or treatment
response of major depressive disorder. Some symptom differences exist, though, such that
hypersomnia and hyperphagia are more likely in younger individuals, and melancholic
symptoms, particularly psychomotor disturbances, are more common in older individuals.
The likelihood of suicide attempts lessens in middle and late life, although the risk of com-
pleted suicide does not. Depressions with earlier ages at onset are more familial and more
likely to involve personality disturbances. The course of major depressive disorder within
individuals does not generally change with aging. Mean times to recovery appear to be sta-
ble over long periods, and the likelihood of being in an episode does not generally increase
or decrease with time.
Risk and Prognostic Factors
Temperamental. Neuroticism (negative affectivity) is a well-established risk factor for the
onset of major depressive disorder, and high levels appear to render individuals more likely
to develop depressive episodes in response to stressful life events.
Environmental. Adverse childhood experiences, particularly when there are multiple
experiences of diverse types, constitute a set of potent risk factors for major depressive dis-
order. Stressful life events are well recognized as precipitants of major depressive epi-
sodes, but the presence or absence of adverse life events near the onset of episodes does
not appear to provide a useful guide to prognosis or treatment selection.
Genetic and physiological. First-degree family members of individuals with major de-
pressive disorder have a risk for major depressive disorder two- to fourfold higher than
that of the general population. Relative risks appear to be higher for early-onset and re-
current forms. Heritability is approximately 40%, and the personality trait neuroticism ac-
counts for a substantial portion of this genetic liability.
Course modifiers. Essentially all major nonmood disorders increase the risk of an indi-
vidual developing depression. Major depressive episodes that develop against the back-
ground of another disorder often follow a more refractory course. Substance use, anxiety,
and borderline personality disorders are among the most common of these, and the pre-
senting depressive symptoms may obscure and delay their recognition. However, sus-
tained clinical improvement in depressive symptoms may depend on the appropriate
treatment of underlying illnesses. Chronic or disabling medical conditions also increase
risks for major depressive episodes. Such prevalent illnesses as diabetes, morbid obesity,
and cardiovascular disease are often complicated by depressive episodes, and these epi-
sodes are more likely to become chronic than are depressive episodes in medically healthy
individuals.
Cuiture-Related Diagnostic Issues
Surveys of major depressive disorder across diverse cultures have shown sevenfold dif-
ferences in 12-month prevalence rates but much more consistency in female-to-male ratio,
mean ages at onset, and the degree to which presence of the disorder raises the likelihood
of comorbid substance abuse. While these findings suggest substantial cultural differences
in the expression of major depressive disorder, they do not permit simple linkages be-
tween particular cultures and the likelihood of specific symptoms. Rather, clinicians
should be aware that in most countries the majority of cases of depression go unrecog-
nized in primary care settings and that in many cultures, somatic symptoms are very likely
to constitute the presenting complaint. Among the Criterion A symptoms, insomnia and
loss of energy are the most uniformly reported.
Major Depressive Disorder 167
Gender-Related Diagnostic Issues
Although the mést reproducible finding in the epidemiology of major depressive disorder
has been a higher prevalence in females, there are no clear differences between genders in
symptoms, course, treatment response, or functional consequences. In women, the risk for
suicide attempts is higher, and the risk for suicide completion is lower. The disparity in
suicide rate by gender is not as great among those with depressive disorders as it is in the
population as a whole.
Suicide Risk
The possibility of suicidal behavior exists at all times during major depressive episodes.
The most consistently described risk factor is a past history of suicide attempts or threats,
but it should be remembered that most completed suicides are not preceded by unsuccess-
ful attempts. Other features associated with an increased risk for completed suicide
include male sex, being single or living alone, and having prominent feelings of hopeless-
ness. The presence of borderline personality disorder markedly increases risk for future
suicide attempts.
Functional Consequences of
Major Depressive Disorder
Many of the functional consequences of major depressive disorder derive from individual
symptoms. Impairment can be very mild, such that many of those who interact with the af-
fected individual are unaware of depressive symptoms. Impairment may, however, range
to complete incapacity such that the depressed individual is unable to attend to basic self-
care needs or is mute or catatonic. Among individuals seen in general medical settings,
those with major depressive disorder have more pain and physical illness and greater de-
creases in physical, social, and role functioning.
Differential Diagnosis
Manic episodes with irritable mood or mixed episodes. Major depressive episodes
with prominent irritable mood may be difficult to distinguish from manic episodes with
irritable mood or from mixed episodes. This distinction requires a careful clinical evalua-
tion of the presence of manic symptoms.
Mood disorder due to another medical condition. A major depressive episode is the
appropriate diagnosis if the mood disturbance is not judged, based on individual history,
physical examination, and laboratory findings, to be the direct pathophysiological conse-
quence of a specific medical condition (e.g., multiple sclerosis, stroke, hypothyroidism).
Substance/medication-induced depressive or bipolar disorder. This disorder is distin-
guished from major depressive disorder by the fact that a substance (e.g., a drug of abuse,
a medication, a toxin) appears to be etiologically related to the mood disturbance. For ex-
ample, depressed mood that occurs only in the context of withdrawal from cocaine would
be diagnosed as cocaine-induced depressive disorder.
Attention-deficit/hyperactivity disorder. Distractibility and low frustration tolerance
can occur in both attention-deficit/ hyperactivity disorder and a major depressive epi-
sode; if the criteria are met for both, attention-deficit/hyperactivity disorder may be diag-
nosed in addition to the mood disorder. However, the clinician must be cautious not to
overdiagnose a major depressive episode in children with attention-deficit/hyperactivity
disorder whose disturbance in mood is characterized by irritability rather than by sadness
or loss of interest.
168 Depressive Disorders
Adjustment disorder with depressed mood. A major depressive episode that occurs in
response to a psychosocial stressor is distinguished from adjustment disorder with de-
pressed mood by the fact that the full criteria for a major depressive episode are not met in
adjustment disorder.
Sadness. Finally, periods of sadness are inherent aspects of the human experience.
These periods should not be diagnosed as a major depressive episode unless criteria are
met for severity (i.e., five out of nine symptoms), duration (i.e., most of the day, nearly ev-
ery day for at least 2 weeks), and clinically significant distress or impairment. The diagno-
sis other specified depressive disorder may be appropriate for presentations of depressed
mood with clinically significant impairment that do not meet criteria for duration or se-
verity.
Comorbidity
Other disorders with which major depressive disorder frequently co-occurs are substance-
related disorders, panic disorder, obsessive-compulsive disorder, anorexia nervosa, buli-
mia nervosa, and borderline personality disorder.
Persistent Depressive Disorder (Dysthymia)
Diagnostic Criteria 300.4 (F34.1)
This disorder represents a consolidation of DSM-IV-defined chronic major depressive dis-
order and dysthymic disorder.
A. Depressed mood for most of the day, for more days than not, as indicated by either
subjective account or observation by others, for at least 2 years.
Note: [n children and adolescents, mood can be irritable and duration must be at least
1 year.
B. Presence, while depressed, of two (or more) of the following:
Poor appetite or overeating.
Insomnia or hypersomnia.
Low energy or fatigue.
Low self-esteem.
Poor concentration or difficulty making decisions.
Feelings of hopelessness.
C. During the 2-year period (1 year for children or adolescents) of the disturbance, the individ-
ual has never been without the symptoms in Criteria A and B for more than 2 months at a
time.
. Criteria for a major depressive disorder may be continuously present for 2 years.
. There has never been a manic episode or a hypomanic episode, and criteria have
never been met for cyclothymic disorder.
F. The disturbance is not better explained by a persistent schizoaffective disorder,
schizophrenia, delusional disorder, or other specified or unspecified schizophrenia
spectrum and other psychotic disorder.
G. The symptoms are not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication) or another medical condition (e.g. hypothyroidism).
H. The symptoms cause clinically significant distress or impairment in social, occupational,
or other important areas of functioning.
Oapron>
moO
Note: Because the criteria for a major depressive episode include four symptoms that are
absent from the symptom list for persistent depressive disorder (dysthymia), a very limited
Persistent Depressive Disorder (Dysthymia) 169
number of individuals will have depressive symptoms that have persisted longer than 2 years
but will not meet criteria for persistent depressive disorder. If full criteria for a major de-
pressive episode have been met at some point during the current episode of illness, they
should be given a diagnosis of major depressive disorder. Otherwise, a diagnosis of other
specified depressive disorder or unspecified depressive disorder is warranted.
Specify if:
With anxious distress (p. 184)
With mixed features (pp. 184-185)
With melancholic features (p. 185)
With atypical features (pp. 185-186)
With mood-congruent psychotic features (p. 186)
With mood-incongruent psychotic features (p. 186)
With peripartum onset (pp. 186-187)
Specify if:
In partial remission (p. 188)
In full remission (p. 188)
Specify if:
Early onset: If onset is before age 21 years.
Late onset: If onset is at age 21 years or older.
Specify if {for most recent 2 years of persistent depressive disorder):
With pure dysthymic syndrome: Full criteria for a major depressive episode have not
been met in at least the preceding 2 years.
With persistent major depressive episode: Full criteria for a major depressive epi-
sode have been met throughout the preceding 2-year period.
With intermittent major depressive episodes, with current episode: Full criteria for
a major depressive episode are currently met, but there have been periods of at least
8 weeks in at least the preceding 2 years with symptoms below the threshold for a full
major depressive episode.
With intermittent major depressive episodes, without current episode: Full crite-
ria for a major depressive episode are not currently met, but there has been one or
more major depressive episodes in at least the preceding 2 years.
Specify current severity:
Mild (p. 188)
Moderate (p. 188)
Severe (p. 188)
Diagnostic Features
The essential feature of persistent depressive disorder (dysthymia) is a depressed mood
that occurs for most of the day, for more days than not, for at least 2 years, or at least 1 year
for children and adolescents (Criterion A). This disorder represents a consolidation of
DSM-IV-defined chronic major depressive disorder and dysthymic disorder. Major de-
pression may precede persistent depressive disorder, and major depressive episodes may
occur during persistent depressive disorder. Individuals whose symptoms meet major de-
pressive disorder criteria for 2 years should be given a diagnosis of persistent depressive
disorder as well as major depressive disorder.
Individuals with persistent depressive disorder describe their mood as sad or “down
in the dumps.” During periods of depressed mood, at least two of the six symptoms from
Criterion B are present. Because these symptoms have become a part of the individual’s
day-to-day experience, particularly in the case of early onset (e.g., “I’ve always been this
170 Depressive Disorders
way”), they may not be reported unless the individual is directly prompted. During the 2-year
period (1 year for children or adolescents), any symptom-free intervals last no longer than
2 months (Criterion C).
Prevalence
Persistent depressive disorder is effectively an amalgam of DSM-IV dysthymic disorder and
chronic major depressive episode. The 12-month prevalence in the United States is approxi-
mately 0.5% for persistent depressive disorder and 1.5% for chronic major depressive disorder.
Development and Course
Persistent depressive disorder often has an early and insidious onset {i.e., in childhood,
adolescence, or early adult life) and, by definition, a chronic course. Among individuals
with both persistent depressive disorder and borderline personality disorder, the covari-
ance of the corresponding features over time suggests the operation of a common mecha-
nism. Early onset (i.e., before age 21 years) is associated with a higher likelihood of
comorbid personality disorders and substance use disorders.
When symptoms rise to the level of a major depressive episode, they are likely to sub-
sequently revert to a lower level. However, depressive symptoms are much less likely to
resolve in a given period of time in the context of persistent depressive disorder than they
are in a major depressive episode.
Risk and Prognostic Factors
Temperamental. Factors predictive of poorer long-term outcome include higher levels
of neuroticism (negative affectivity), greater symptom severity, poorer global functioning,
and presence of anxiety disorders or conduct disorder.
Environmental. Childhood risk factors include parental loss or separation.
Genetic and physiological. There are no clear differences in illness development, course,
or family history between DSM-IV dysthymic disorder and chronic major depressive dis-
order. Earlier findings pertaining to either disorder are therefore likely to apply to per-
sistent depressive disorder. It is thus likely that individuals with persistent depressive
disorder will have a higher proportion of first-degree relatives with persistent depressive
disorder than do individuals with major depressive disorder, and more depressive disor-
ders in general.
A number of brain regions (e.g., prefrontal cortex, anterior cingulate, amygdala, hip-
pocampus) have been implicated in persistent depressive disorder. Possible polysomno-
graphic abnormalities exist as well.
Functional Consequences of
Persistent Depressive Disorder
The degree to which persistent depressive disorder impacts social and occupational func-
tioning is likely to vary widely, but effects can be as great as or greater than those of major
depressive disorder.
Differential Diagnosis
Major depressive disorder. If there is a depressed mood plus two or more symptoms
meeting criteria for a persistent depressive episode for 2 years or more, then the diagnosis of
persistent depressive disorder is made. The diagnosis depends on the 2-year duration,
which distinguishes it from episodes of depression that do not last 2 years. If the symptom
Premenstrual Dysphoric Disorder 171
criteria are sufficient for a diagnosis of a major depressive episode at any time during this pe-
riod, then the diagnosis of major depression should be noted, but it is coded not as a separate
diagnosis but rather as a specifier with the diagnosis of persistent depressive disorder. If the
individual's symptoms currently meet full criteria for a major depressive episode, then the
specifier of “with intermittent major depressive episodes, with current episode” would be
made. If the major depressive episode has persisted for at least a 2-year duration and re-
mains present, then the specifier “with persistent major depressive episode” is used. When
full major depressive episode criteria are not currently met but there has been at least one
previous episode of major depression in the context of at least 2 years of persistent depres-
sive symptoms, then the specifier of “with intermittent major depressive episodes, without
current episode” is used. If the individual has not experienced an episode of major depres-
sion in the last 2 years, then the specifier “with pure dysthymic syndrome” is used.
Psychotic disorders. Depressive symptoms are a common associated feature of chronic
psychotic disorders (e.g., schizoaffective disorder, schizophrenia, delusional disorder). A
separate diagnosis of persistent depressive disorder is not made if the symptoms occur
only during the course of the psychotic disorder (including residual phases).
Depressive or bipolar and related disorder due to another medical condition. Persistent
depressive disorder must be distinguished from a depressive or bipolar and related dis-
order due to another medical condition. The diagnosis is depressive or bipolar and related
disorder due to another medical condition if the mood disturbance is judged, based on his-
tory, physical examination, or laboratory findings, to be attributable to the direct patho-
physiological effects of a specific, usually chronic, medical condition (e.g., multiple
sclerosis). If it is judged that the depressive symptoms are not attributable to the physiolog-
ical effects of another medical condition, then the primary mental disorder (e.g., persistent
depressive disorder) is recorded, and the medical condition is noted as a concomitant med-
ical condition (e.g., diabetes mellitus).
Substance/medication-induced depressive or bipolar disorder. A substance/medi-
cation-induced depressive or bipolar and related disorder is distinguished from persis-
tent depressive disorder when a substance (e.g., a drug of abuse, a medication, a toxin) is
judged to be etiologically related to the mood disturbance.
Personality disorders. Often, there is evidence of a coexisting personality disturbance.
When an individual’s presentation meets the criteria for both persistent depressive disor-
der and a personality disorder, both diagnoses are given.
Comorbidity
In comparison to individuals with major depressive disorder, those with persistent de-
pressive disorder are at higher risk for psychiatric comorbidity in general, and for anxiety
disorders and substance use disorders in particular. Early-onset persistent depressive dis-
order is strongly associated with DSM-IV Cluster B and C personality disorders.
Premenstrual Dysphoric Disorder
Diagnostic Criteria 625.4 (N94.3)
A. In the majority of menstrual cycles, at least five symptoms must be present in the final
week before the onset of menses, start to improve within a few days after the onset of
menses, and become minima! or absent in the week postmenses.
B. One (or more) of the following symptoms must be present:
1. Marked affective lability (e.g., mood swings; feeling suddenly sad or tearful, or in-
creased sensitivity to rejection).
172 Depressive Disorders
2. Marked irritability or anger or increased interpersonal conflicts.
3. Marked depressed mood, feelings of hopelessness, or self-deprecating thoughts.
4. Marked anxiety, tension, and/or feelings of being keyed up or on edge.
C. One (or more) of the following symptoms must additionally be present, to reach a total
of five symptoms when combined with symptoms from Criterion B above.
. Decreased interest in usual activities (e.g., work, school, friends, hobbies).
. Subjective difficulty in concentration.
. Lethargy, easy fatigability, or marked lack of energy.
. Marked change in appetite; overeating; or specific food cravings.
. Hypersomnia or insomnia.
. Asense of being overwhelmed or out of control.
. Physical symptoms such as breast tenderness or swelling, joint or muscle pain, a
sensation of “bloating,” or weight gain.
Note: The symptoms in Criteria A-C must have been met for most menstrual cycles that
occurred in the preceding year.
D. The symptoms are associated with clinically significant distress or interference with
work, school, usual social activities, or relationships with others (e.g., avoidance of so-
cial activities; decreased productivity and efficiency at work, school, or home).
E. The disturbance is not merely an exacerbation of the symptoms of another disorder,
such as major depressive disorder, panic disorder, persistent depressive disorder
(dysthymia), or a personality disorder (although it may co-occur with any of these dis-
orders).
F. Criterion A should be confirmed by prospective daily ratings during at least two symptom-
atic cycles. (Note: The diagnosis may be made provisionally prior to this confirmation.)
G. The symptoms are not attributable to the physiological effects of a substance {e.g., a
drug of abuse, a medication, other treatment) or another medical condition (e.g., hy-
perthyroidism).
NOoh ON +
Recording Procedures
If symptoms have not been confirmed by prospective daily ratings of at least two symp-
tomatic cycles, “provisional” should be noted after the name of the diagnosis (i.e., “pre-
menstrual dysphoric disorder, provisional“).
Diagnostic Features
The essential features of premenstrual dysphoric disorder are the expression of mood la-
bility, irritability, dysphoria, and anxiety symptoms that occur repeatedly during the pre-
menstrual phase of the cycle and remit around the onset of menses or shortly thereafter.
These symptoms may be accompanied by behavioral and physical symptoms. Symptoms
must have occurred in most of the menstrual cycles during the past year and must have an
adverse effect on work or social functioning. The intensity and/or expressivity of the ac-
companying symptoms may be closely related to social and cultural background charac-
teristics of the affected female, family perspectives, and more specific factors such as
religious beliefs, social tolerance, and female gender role issues.
Typically, symptoms peak around the time of the onset of menses. Although it is not
uncommon for symptoms to linger into the first few days of menses, the individual must
have a symptom-free period in the follicular phase after the menstrual period begins.
While the core symptoms include mood and anxiety symptoms, behavioral and somatic
symptoms commonly also occur. However, the presence of physical and/or behavioral
symptoms in the absence of mood and/or anxious symptoms is not sufficient for a diag-
Premenstrual Dysphoric Disorder 173
nosis. Symptoms are of comparable severity (but not duration) to those of another mental
disorder, such as a major depressive episode or generalized anxiety disorder. In order to
confirm a provisional diagnosis, daily prospective symptom ratings are required for at
least two symptomatic cycles.
Associated Features Supporting Diagnosis
Delusions and hallucinations have been described in the late luteal phase of the menstrual
cycle but are rare. The premenstrual phase has been considered by some to be a risk period
for suicide.
Prevalence
Twelve-month prevalence of premenstrual dysphoric disorder is between 1.8% and 5.8%
of menstruating women. Estimates are substantially inflated if they are based on retro-
spective reports rather than prospective daily ratings. However, estimated prevalence
based on a daily record of symptoms for 1-2 months may be less representative, as indi-
viduals with the most severe symptoms may be unable to sustain the rating process. The
most rigorous estimate of premenstrual dysphoric disorder is 1.8% for women whose
symptoms meet the full criteria without functional impairment and 1.3% for women
whose symptoms meet the current criteria with functional impairment and without co-oc-
curring symptoms from another mental disorder.
Development and Course
Onset of premenstrual dysphoric disorder can occur at any point after menarche. Inci-
dence of new cases over a 40-month follow-up period is 2.5% (95% confidence interval =
1.7-3.7). Anecdotally, many individuals, as they approach menopause, report that symp-
toms worsen. Symptoms cease after menopause, although cyclical hormone replacement
can trigger the re-expression of symptoms.
Risk and Prognostic Factors
Environmental. Environmental factors associated with the expression of premenstrual
dysphoric disorder include stress, history of interpersonal trauma, seasonal changes, and
sociocultural aspects of female sexual behavior in general, and female gender role in par-
ticular.
Genetic and physiological. Heritability of premenstrual dysphoric disorder is unknown.
However, for premenstrual symptoms, estimates for heritability range between 30% and
80%, with the most stable component of premenstrual symptoms estimated to be about
50% heritable.
Course modifiers. Women who use ora! contraceptives may have fewer premenstrual
complaints than do women who do not use oral contraceptives.
Culture-Related Diagnostic Issues
Premenstrual dysphoric disorder is not a culture-bound syndrome and has been observed
in individuals in the United States, Europe, India, and Asia. It is unclear as to whether rates
differ by race. Nevertheless, frequency, intensity, and expressivity of symptoms and help-
seeking patterns may be significantly influenced by cultural factors.
Diagnostic Markers
As indicated earlier, the diagnosis of premenstrual dysphoric disorder is appropriately
confirmed by 2 months of prospective symptom ratings. A number of scales, including the
174 Depressive Disorders
Daily Rating of Severity of Problems and the Visual Analogue Scales for Premenstrual
Mood Symptoms, have undergone validation and are commonly used in clinical trials for
premenstrual dysphoric disorder. The Premenstrual Tension Syndrome Rating Scale has a
self-report and an observer version, both of which have been validated and used widely to
measure illness severity in women who have premenstrual dysphoric disorder.
Functional Consequences of
Premenstrual Dysphoric Disorder
Symptoms must be associated with clinically meaningful distress and/or an obvious and
marked impairment in the ability to function socially or occupationally in the week prior
to menses. Impairment in social functioning may be manifested by marital discord and
problems with children, other family members, or friends. Chronic marital or job prob-
lems should not be confused with dysfunction that occurs only in association with pre-
menstrual dysphoric disorder.
Differential Diagnosis
Premenstrual syndrome. Premenstrual syndrome differs from premenstrual dysphoric
disorder in that a minimum of five symptoms is not required, and there is no stipulation of
affective symptoms for individuals who have premenstrual syndrome. This condition
may be more common than premenstrual dysphoric disorder, although the estimated
prevalence of premenstrual syndrome varies. While premenstrual syndrome shares the
feature of symptom expression during the premenstrual phase of the menstrual cycle, itis
generally considered to be less severe than premenstrual dysphoric disorder. The pres-
ence of physical or behavioral symptoms in the premenstruum, without the required
affective symptoms, likely meets criteria for premenstrual syndrome and not for premen-
strual dysphoric disorder.
Dysmenorrhea. Dysmenorrhea is a syndrome of painful menses, but this is distinct from a
syndrome characterized by affective changes. Moreover, symptoms of dysmenorrhea begin
with the onset of menses, whereas symptoms of premenstrual dysphoric disorder, by defini-
tion, begin before the onset of menses, even if they linger into the first few days of menses.
Bipolar disorder, major depressive disorder, and persistent depressive disorder
(dysthymia). Many women with (either naturally occurring or substance/medication-
induced) bipolar or major depressive disorder or persistent depressive disorder believe
that they have premenstrual dysphoric disorder. However, when they chart symptoms,
they realize that the symptoms do not follow a premenstrual pattern. Women with an-
other mental disorder may experience chronic symptoms or intermittent symptoms that
are unrelated to menstrual cycle phase. However, because the onset of menses constitutes
a memorable event, they may report that symptoms occur only during the premenstruum
or that symptoms worsen premenstrually. This is one of the rationales for the requirement
that symptoms be confirmed by daily prospective ratings. The process of differential di-
agnosis, particularly if the clinician relies on retrospective symptoms only, is made more
difficult because of the overlap between symptoms of premenstrual dysphoric disorder
and some other diagnoses. The overlap of symptoms is particularly salient for differenti-
ating premenstrual dysphoric disorder from major depressive episodes, persistent de-
pressive disorder, bipolar disorders, and borderline personality disorder. However, the
rate of personality disorders is no higher in individuals with premenstrual dysphoric dis-
order than in those without the disorder.
Use of hormonal treatments. Some women who present with moderate to severe pre-
menstrual symptoms may be using hormonal treatments, including hormonal contracep-
tives. If such symptoms occur after initiation of exogenous hormone use, the symptoms
Substance/Medication-Induced Depressive Disorder 175
may be due to the use of hormones rather than to the underlying condition of premen-
strual dysphoric disorder. If the woman stops hormones and the symptoms disappear,
this is consistent with substance /medication-induced depressive disorder.
Comorbidity
A major depressive episode is the most frequently reported previous disorder in individuals
presenting with premenstrual dysphoric disorder. A wide range of medical (e.g., migraine,
asthma, allergies, seizure disorders) or other mental disorders (e.g., depressive and bipolar
disorders, anxiety disorders, bulimia nervosa, substance use disorders) may worsen in the
premenstrual phase; however, the absence of a symptom-free period during the postmen-
strual interval obviates a diagnosis of premenstrual dysphoric disorder. These conditions
are better considered premenstrual exacerbation of a current mental or medical disorder. Al-
though the diagnosis of premenstrual dysphoric disorder should not be assigned in situa-
tions in which an individual only experiences a premenstrual exacerbation of another
mental or physical disorder, it can be considered in addition to the diagnosis of another men-
tal or physical disorder if the individual experiences symptoms and changes in level of func-
tioning that are characteristic of premenstrual dysphoric disorder and markedly different
from the symptoms experienced as part of the ongoing disorder.
Substance/Medication-Induced
Depressive Disorder
Diagnostic Criteria
A. A prominent and persistent disturbance in mood that predominates in the clinical pic-
ture and is characterized by depressed mood or markedly diminished interest or plea-
sure in ail, or almost all, activities.
B. There is evidence from the history, physical examination, or laboratory findings of both
(1) and (2):
1. The symptoms in Criterion A developed during or soon after substance intoxication
or withdrawal or after exposure to a medication.
2. The involved substance/medication is capable of producing the symptoms in Crite-
rion A.
C. The disturbance is not better explained by a depressive disorder that is not substance/
medication-induced. Such evidence of an independent depressive disorder could in-
clude the following:
The symptoms preceded the onset of the substance/medication use; the symptoms
persist for a substantial period of time (e.g., about 1 month) after the cessation of acute
withdrawal or severe intoxication; or there is other evidence suggesting the existence
of an independent non-substance/medication-induced depressive disorder (e.g., a his-
tory of recurrent non-substance/medication-related episodes).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
Note: This diagnosis should be made instead of a diagnosis of substance intoxication or
substance withdrawal only when the symptoms in Criterion A predominate in the clinical
picture and when they are sufficiently severe to warrant clinical attention.
Coding note: The ICD-9-CM and !CD-10-CM codes for the {specific substance/medica-
tion}-induced depressive disorders are indicated in the table below. Note that the !CD-10-
176 Depressive Disorders
CM code depends on whether or not there is a comorbid substance use disorder present for
the same class of substance. If a mild substance use disorder is comorbid with the substance-
induced depressive disorder, the 4th position character is “1,” and the clinician should record
“mild [substance] use disorder’ before the substance-induced depressive disorder (e.g.,
“mild cocaine use disorder with cocaine-induced depressive disorder’). If a moderate or se-
vere substance use disorder is comorbid with the substance-induced depressive disorder,
the 4th position character is “2,” and the clinician should record “moderate [substance] use
disorder” or “severe [substance] use disorder,” depending on the severity of the comorbid
substance use disorder. If there is no comorbid substance use disorder (e.g., after a one-
time heavy use of the substance), then the 4th position character is “9,” and the clinician should
record only the substance-induced depressive disorder.
ICD-10-CM
With use
With use disorder, Without
disorder, moderate use
ICD-9-CM mild or severe disorder
Alcohol 291.89 F10.14 F10.24 F10.94
Phencyclidine 292.84 F16.14 F16.24 F16.94
Other hallucinogen 292.84 F16.14 F16.24 F16.94
Inhalant 292.84 F18.14 F18.24 F18.94
Opioid 292.84 F11.14 F11.24 F11.94
Sedative, hypnotic, or anxiolytic 292.84 F13.14 F13.24 F13.94
Amphetamine (or other 292.84 F15.14 F15.24 F15.94
stimulant)
Cocaine 292.84 F14.14 F14.24 F14.94
Other (or unknown) substance 292.84 F19.14 F19.24 F19.94
Specify if (see Table 1 in the chapter “Substance-Related and Addictive Disorders” for di-
agnoses associated with substance class):
With onset during intoxication: If criteria are met for intoxication with the substance
and the symptoms develop during intoxication.
With onset during withdrawal: If criteria are met for withdrawal from the substance
and the symptoms develop during, or shortly after, withdrawal.
Recording Procedures
ICD-9-CM. The name of the substance/medication-induced depressive disorder begins
with the specific substance (e.g., cocaine, dexamethasone) that is presumed to be causing
the depressive symptoms. The diagnostic code is selected from the table included in the
criteria set, which is based on the drug class. For substances that do not fit into any of the
classes (e.g., dexamethasone), the code for “other substance” should be used; and in cases
in which a substance is judged to be an etiological factor but the specific class of substance
is unknown, the category “unknown substance” should be used.
The name of the disorder is followed by the specification of onset (i.e., onset during in-
toxication, onset during withdrawal). Unlike the recording procedures for ICD-10-CM,
which combine the substance-induced disorder and substance use disorder into a single
Substance/Medication-Induced Depressive Disorder 177
code, for ICD-9-CM a separate diagnostic code is given for the substance use disorder. For
example, in the case of depressive symptoms occurring during withdrawal in a man with
a severe cocaine use disorder, the diagnosis is 292.84 cocaine-induced depressive disorder,
with onset during withdrawal. An additional diagnosis of 304.20 severe cocaine use dis-
order is also given. When more than one substance is judged to play a significant role in
the development of depressive mood symptoms, each should be listed separately (e.g.,
292.84 methylphenidate-induced depressive disorder, with onset during withdrawal;
292.84 dexamethasone-induced depressive disorder, with onset during intoxication).
ICD-10-CM. The name of the substance/medication-induced depressive disorder begins
with the specific substance (e.g., cocaine, dexamethasone) that is presumed to be causing
the depressive symptoms. The diagnostic code is selected from the table included in the
criteria set, which is based on the drug class and presence or absence of a comorbid sub-
stance use disorder. For substances that do not fit into any of the classes (e.g., dexameth-
asone), the code for “other substance” should be used; and in cases in which a substance is
judged to be an etiological factor but the specific class of substance is unknown, the category
“unknown substance” should be used.
When recording the name of the disorder, the comorbid substance use disorder (if any) is
listed first, followed by the word “with,” followed by the name of the substance-induced de-
pressive disorder, followed by the specification of onset (i.e., onset during intoxication, onset
during withdrawal). For example, in the case of depressive symptoms occurring during with-
drawal in a man with a severe cocaine use disorder, the diagnosis is F14.24 severe cocaine use
disorder with cocaine-induced depressive disorder, with onset during withdrawal. A separate
diagnosis of the comorbid severe cocaine use disorder is not given. If the substance-induced
depressive disorder occurs without a comorbid substance use disorder (e.g., after a one-time
heavy use of the substance), no accompanying substance use disorder is noted (e.g., F16.94
phencyclidine-induced depressive disorder, with onset during intoxication). When more than
one substance is judged to play a significant role in the development of depressive mood
symptoms, each should be listed separately (e.g., F15.24 severe methylphenidate use disorder
with methylphenidate-induced depressive disorder, with onset during withdrawal; F19.94
dexamethasone-induced depressive disorder, with onset during intoxication).
Diagnostic Features
The diagnostic features of substance /medication-induced depressive disorder include the
symptoms of a depressive disorder, such as major depressive disorder; however, the de-
pressive symptoms are associated with the ingestion, injection, or inhalation of a sub-
stance (e.g., drug of abuse, toxin, psychotropic medication, other medication), and the
depressive symptoms persist beyond the expected length of physiological effects, intoxi-
cation, or withdrawal period. As evidenced by clinical history, physical examination, or
laboratory findings, the relevant depressive disorder should have developed during or
within 1 month after use of a substance that is capable of producing the depressive disor-
der (Criterion B1). In addition, the diagnosis is not better explained by an independent
depressive disorder. Evidence of an independent depressive disorder includes the de-
pressive disorder preceded the onset of ingestion or withdrawal from the substance; the
depressive disorder persists beyond a substantial period of time after the cessation of sub-
stance use; or other evidence suggests the existence of an independent non-substance/
medication-induced depressive disorder (Criterion C). This diagnosis should not be made
when symptoms occur exclusively during the course of a delirium (Criterion D). The de-
pressive disorder associated with the substance use, intoxication, or withdrawal must
cause clinically significant distress or impairment in social, occupational, or other impor-
tant areas of functioning to qualify for this diagnosis (Criterion E).
Some medications (e.g., stimulants, steroids, L-dopa, antibiotics, central nervous
system drugs, dermatological agents, chemotherapeutic drugs, immunological agents)
178 Depressive Disorders
can induce depressive mood disturbances. Clinical judgment is essential to determine
whether the medication is truly associated with inducing the depressive disorder or
whether a primary depressive disorder happened to have its onset while the person was
receiving the treatment. For example, a depressive episode that developed within the first
several weeks of beginning alpha-methyldopa (an antihypertensive agent) in an individ-
ual with no history of major depressive disorder would qualify for the diagnosis of med-
ication-induced depressive disorder. In some cases, a previously established condition
(e.g., major depressive disorder, recurrent) can recur while the individual is coincidentally
taking a medication that has the capacity to cause depressive symptoms (e.g., L-dopa, oral
contraceptives). In such cases, the clinician must make a judgment as to whether the med-
ication is causative in this particular situation.
A substance/medication-induced depressive disorder is distinguished from a primary
depressive disorder by considering the onset, course, and other factors associated with the
substance use. There must be evidence from the history, physical examination, or labora-
tory findings of substance use, abuse, intoxication, or withdrawal prior to the onset of the
depressive disorder. The withdrawal state for some substances can be relatively pro-
tracted, and thus intense depressive symptoms can last for a long period after the cessation
of substance use.
Prevalence
In a nationally representative U.S. adult population, the lifetime prevalence of substance /
medication-induced depressive disorder is 0.26%.
Development and Course
A depressive disorder associated with the use of substance (i.e., alcohol, illicit drugs, or a
prescribed treatment for a mental disorder or another medical condition) must have its on-
set while the individual is using the substance or during withdrawal, if there is a with-
drawal syndrome associated with the substance. Most often, the depressive disorder has
its onset within the first few weeks or 1 month of use of the substance. Once the substance
is discontinued, the depressive symptoms usually remit within days to several weeks, de-
pending on the half-life of the substance /medication and the presence of a withdrawal
syndrome. If symptoms persist 4 weeks beyond the expected time course of withdrawal of
a particular substance/ medication, other causes for the depressive mood symptoms
should be considered.
Although there are a few prospective controlled trials examining the association of de-
pressive symptoms with use of a medication, most reports are from postmarketing sur-
veillance studies, retrospective observational studies, or case reports, making evidence of
causality difficult to determine. Substances implicated in medication-induced depressive
disorder, with varying degrees of evidence, include antiviral agents (efavirenz), cardio-
vascular agents (clonidine, guanethidine, methyldopa, reserpine), retinoic acid deriva-
tives (isotretinoin), antidepressants, anticonvulsants, anti-migraine agents (triptans),
antipsychotics, hormonal agents (corticosteroids, oral contraceptives, gonadotropin-
releasing hormone agonists, tamoxifen), smoking cessation agents (varenicline), and im-
munological agents (interferon). However, other potential substances continue to emerge
as new compounds are synthesized. A history of such substance use may help increase di-
agnostic certainty.
Risk and Prognostic Factors
Temperamental. Factors that appear to increase the risk of substance /medication-
induced depressive disorder can be conceptualized as pertaining to the specific type of
drug or to a group of individuals with underlying alcohol or drug use disorders. Risk fac-
Substance/Medication-Induced Depressive Disorder 179
tors common to all drugs include history of major depressive disorder, history of drug-
induced depression, and psychosocial stressors.
Environmental. There are also risks factors pertaining to a specific type of medication
(e.g., increased immune activation prior to treatment for hepatitis C associated with inter-
feron-alfa-induced depression); high doses (greater than 80 mg/day prednisone-equiva-
lents) of corticosteroids or high plasma concentrations of efavirenz; and high estrogen/
progesterone content in oral contraceptives.
Course modifiers. Inarepresentative U.S. adult population, compared with individuals
with major depressive disorder who did not have a substance use disorder, individuals
with substance-induced depressive disorder were more likely to be male, to be black, to
have at most a high school diploma, to lack insurance, and to have lower family income.
They were also more likely to report higher family history of substance use disorders and
antisocial behavior, higher 12-month history of stressful life events, and a greater number
of DSM-IV major depressive disorder criteria. They were more likely to report feelings of
worthlessness, insomnia/hypersomnia, and thoughts of death and suicide attempts, but
less likely to report depressed mood and parental loss by death before age 18 years.
Diagnostic Markers
Determination of the substance of use can sometimes be made through laboratory assays
of the suspected substance in the blood or urine to corroborate the diagnosis.
Suicide Risk
Drug-induced or treatment-emergent suicidality represents a marked change in thoughts
and behavior from the person’s baseline, is usually temporally associated with initiation of
a substance, and must be distinguished from the underlying primary mental disorders.
In regard to the treatment-emergent suicidality associated with antidepressants, a U.S.
Food and Drug Administration (FDA) advisory committee considered meta-analyses of
99,839 participants enrolled in 372 randomized clinical trials of antidepressants in trials for
mental disorders. The analyses showed that when the data were pooled across all adult
age groups, there was no perceptible increased risk of suicidal behavior or ideation. How-
ever, in age-stratified analyses, the risk for patients ages 18-24 years was elevated, albeit
not significantly (odds ratio [OR] = 1.55; 95% confidence interval [CI] = 0.91-2.70). The
FDA meta-analyses reveal an absolute risk of suicide in patients taking investigational an-
tidepressants of 0.01%. In conclusion, suicide is clearly an extremely rare treatment-emer-
gent phenomenon, but the outcome of suicide was serious enough to prompt the FDA to
issue an expanded black-box warning in 2007 regarding the importance of careful moni-
toring of treatment-emergent suicidal ideation in patients receiving antidepressants.
Differential Diagnosis
Substance intoxication and withdrawal. Depressive symptoms occur commonly in sub-
stance intoxication and substance withdrawal, and the diagnosis of the substance-specific
intoxication or withdrawal will usually suffice to categorize the symptom presentation. A
diagnosis of substance-induced depressive disorder should be made instead of a diag-
nosis of substance intoxication or substance withdrawal when the mood symptoms are
sufficiently severe to warrant independent clinical attention. For example, dysphoric
mood is a characteristic feature of cocaine withdrawal. Substance /medication-induced
depressive disorder should be diagnosed instead of cocaine withdrawal only if the mood
disturbance is substantially more intense or longer lasting than what is usually encountered
with cocaine withdrawal and is sufficiently severe to be a separate focus of attention and
treatment.
180 Depressive Disorders
Primary depressive disorder. A substance/medication-induced depressive disorder is
distinguished from a primary depressive disorder by the fact that a substance is judged to
be etiologically related to the symptoms, as described earlier (see section “Development
and Course” for this disorder).
Depressive disorder due to another medical condition. Because individuals with other
medical conditions often take medications for those conditions, the clinician must consider the
possibility that the mood symptoms are caused by the physiological consequences of the med-
ical condition rather than the medication, in which case depressive disorder due to another
medical condition is diagnosed. The history often provides the primary basis for such a judg-
ment. At times, a change in the treatment for the other medical condition (e.g., medication sub-
stitution or discontinuation) may be needed to determine empirically whether the medication
is the causative agent. If the clinician has ascertained that the disturbance is a function of both
another medical condition and substance use or withdrawal, both diagnoses (i.e., depressive
disorder due to another medical condition and substance/medication-induced depressive
disorder) may be given. When there is insufficient evidence to determine whether the depres-
sive symptoms are associated with substance (including a medication) ingestion or with-
drawal or with another medical condition or are primary (i.e., not a function of either a
substance or another medical condition), a diagnosis of other specified depressive disorder or
unspecified depressive disorder would be indicated.
Comorbidity
Compared with individuals with major depressive disorder and no comorbid substance
use disorder, those with substance /medication-induced depressive disorder have higher
rates of comorbidity with any DSM-IV mental disorder; are more likely to have specific
DSM-IV disorders of pathological gambling and paranoid, histrionic, and antisocial per-
sonality disorders; and are less likely to have persistent depressive disorder (dysthymia).
Compared with individuals with major depressive disorder and a comorbid substance use
disorder, individuals with substance /medication-induced depressive disorder are more
likely to have alcohol use disorder, any other substance use disorder, and histrionic per-
sonality disorder; however, they are less likely to have persistent depressive disorder.
Depressive Disorder
Due to Another Medical Condition
Diagnostic Criteria
A. A prominent and persistent period of depressed mood or markedly diminished interest
or pleasure in all, or almost all, activities that predominates in the clinical picture.
B. There is evidence from the history, physical examination, or laboratory findings that the
disturbance is the direct pathophysiological consequence of another medical condi-
tion.
C. The disturbance is not better explained by another mental disorder (e.g., adjustment
disorder, with depressed mood, in which the stressor is a serious medical condition).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
Coding note: The ICD-9-CM code for depressive disorder due to another medical condi-
tion is 293.83, which is assigned regardless of the specifier. The ICD-10-CM code de-
pends on the specifier (see below).
Depressive Disorder Due to Another Medical Condition 181
Specify if:
(F06.31}) With depressive features: Full criteria are not met for a major depressive
episode.
(F06.32) With major depressive—Ilke episode: Full criteria are met (except Criterion
C) for a major depressive episode.
(F06.34) With mixed features: Symptoms of mania or hypomania are also present but
do not predominate in the clinical picture.
Coding note: Include the name of the other medical condition in the name of the mental dis-
order (€.g., 293.83 [F06.31] depressive disorder due to hypothyroidism, with depressive fea-
tures). The other medical condition should also be coded and listed separately immediately
before the depressive disorder due to the medical condition (e.g., 244.9 [E03.9] hypothyroid-
ism; 293.83 [F06.31] depressive disorder due to hypothyroidism, with depressive features).
Diagnostic Features
The essential feature of depressive disorder due to another medical condition is a promi-
nent and persistent period of depressed mood or markedly diminished interest or plea-
sure in all, or almost all, activities that predominates in the clinical picture (Criterion A)
and that is thought to be related to the direct physiological effects of another medical con-
dition (Criterion B), In determining whether the mood disturbance is due to a general
medical condition, the clinician must first establish the presence of a general medical con-
dition. Further, the clinician must establish that the mood disturbance is etiologically re-
lated to the general medical condition through a physiological mechanism. A careful and
comprehensive assessment of multiple factors is necessary to make this judgment. Al-
though there are no infallible guidelines for determining whether the relationship
between the mood disturbance and the general medical condition is etiological, several
considerations provide some guidance in this area. One consideration is the presence of a
temporal association between the onset, exacerbation, or remission of the general medical
condition and that of the mood disturbance. A second consideration is the presence of fea-
tures that are atypical of primary Mood Disorders (e.g., atypical age at onset or course or
absence of family history). Evidence from the literature that suggests that there can be a di-
rect association between the general medical condition in question and the development
of mood symptoms can provide a useful context in the assessment of a particular situation.
Associated Features Supporting Diagnosis
Etiology (i.e., a causal relationship to another medical condition based on best clinical ev-
idence) is the key variable in depressive disorder due to another medical condition. The
listing of the medical conditions that are said to be able to induce major depression is never
complete, and the clinician’s best judgment is the essence of this diagnosis.
There are clear associations, as well as some neuroanatomical correlates, of depression
with stroke, Huntington’s disease, Parkinson’s disease, and traumatic brain injury. Among
the neuroendocrine conditions most closely associated with depression are Cushing’s dis-
ease and hypothyroidism. There are numerous other conditions thought to be associated
with depression, such as multiple sclerosis. However, the literature’s support for a causal
association is greater with some conditions, such as Parkinson’s disease and Huntington’s
disease, than with others, for which the differential diagnosis may be adjustment disorder,
with depressed mood.
Development and Course
Following stroke, the onset of depression appears to be very acute, occurring within 1 day
or a few days of the cerebrovascular accident (CVA) in the largest case series. However, in
182 Depressive Disorders
some cases, onset of the depression is weeks to months following the CVA. In the largest
series, the duration of the major depressive episode following stroke was 9-11 months on
average. Similarly, in Huntington’s disease the depressive state comes quite early in the
course of the illness. With Parkinson’s disease and Huntington’s disease, it often precedes
the major motor impairments and cognitive impairments associated with each condition.
This is more prominently the case for Huntington’s disease, in which depression is con-
sidered to be the first neuropsychiatric symptom. There is some observational evidence
that depression is less common as the dementia of Huntington’s disease progresses.
Risk and Prognostic Factors
The risk of acute onset of a major depressive disorder following a CVA (within 1 day toa
week of the event) appears to be strongly correlated with lesion location, with greatest risk
associated with left frontal strokes and least risk apparently associated with right frontal
lesions in those individuals who present within days of the stroke. The association with
frontal regions and laterality is not observed in depressive states that occur in the 2-6 months
following stroke.
Gender-Related Diagnostic Issues
Gender differences pertain to those associated with the medical condition (e.g., systemic
lupus erythematosus is more common in females; stroke is somewhat more common in
middle-age males compared with females).
Diagnostic Markers
Diagnostic markers pertain to those associated with the medical condition (e.g., steroid
levels in blood or urine to help corroborate the diagnosis of Cushing’s disease, which can
be associated with manic or depressive syndromes).
Suicide Risk
There are no epidemiological studies that provide evidence to differentiate the risk of sui-
cide from a major depressive episode due to another medical condition compared with the
risk from a major depressive episode in general. There are case reports of suicides in
association with major depressive episodes associated with another medical condition.
There is a clear association between serious medical illnesses and suicide, particularly
shortly after onset or diagnosis of the illness. Thus, it would be prudent to assume that the
risk of suicide for major depressive episodes associated with medical conditions is not less
than that for other forms of major depressive episode, and might even be greater.
Functional Consequences of Depressive Disorder
Due to Another Medical Condition
Functional consequences pertain to those associated with the medical condition. In gen-
eral, it is believed, but not established, that a major depressive episode induced by Cush-
ing’s disease will not recur if the Cushing’s disease is cured or arrested. However, it is also
suggested, but not established, that mood syndromes, including depressive and manic/
hypomanic ones, may be episodic (i.e., recurring) in some individuals with static brain in-
juries and other central nervous system diseases.
Differential Diagnosis
Depressive disorders not due to another medical condition. Determination of whether
a medical condition accompanying a depressive disorder is causing the disorder depends
on a) the absence of an episode(s) of depressive episodes prior to the onset of the medical
Other Specified Depressive Disorder 183
condition, b) the probability that the associated medical condition has a potential to pro-
mote or cause a depressive disorder, and c) a course of the depressive symptoms shortly
after the onset or worsening of the medical condition, especially if the depressive symp-
toms remit near the time that the medical disorder is effectively treated or remits.
Medication-induced depressive disorder. An important caveat is that some medical con-
ditions are treated with medications (e.g., steroids or alpha-interferon) that can induce depres-
sive or manic symptoms. In these cases, clinical judgment, based on all the evidence in hand, is
the best way to try to separate the most likely and/or the most important of two etiological fac-
tors (i.e., association with the medical condition vs. a substance-induced syndrome).
Adjustment disorders. It is important to differentiate a depressive episode from an ad-
justment disorder, as the onset of the medical condition is in itself a life stressor that could
bring on either an adjustment disorder or an episode of major depression. The major dif-
ferentiating elements are the pervasiveness the depressive picture and the number and
quality of the depressive symptoms that the patient reports or demonstrates on the mental
status examination. The differential diagnosis of the associated medical conditions is rel-
evant but largely beyond the scope of the present manual.
Comorbidity
Conditions comorbid with depressive disorder due to another medical condition are those
associated with the medical conditions of etiological relevance. It has been noted that de-
lirium can occur before or along with depressive symptoms in individuals with a variety
of medical conditions, such as Cushing’s disease. The association of anxiety symptoms,
usually generalized symptoms, is common in depressive disorders, regardless of cause.
Other Specified Depressive Disorder
311 (F32.8)
This category applies to presentations in which symptoms characteristic of a depressive
disorder that cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning predominate but do not meet the full criteria for any of
the disorders in the depressive disorders diagnostic class. The other specified depressive
disorder category is used in situations in which the clinician chooses to communicate the
specific reason that the presentation does not meet the criteria for any specific depressive
disorder. This is done by recording “other specified depressive disorder’ followed by the
specific reason (e.g., “short-duration depressive episode’).
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Recurrent brief depression: Concurrent presence of depressed mood and at least
four other symptoms of depression for 2-13 days at least once per month (not associ-
ated with the menstrual cycle) for at least 12 consecutive months in an individual
whose presentation has never met criteria for any other depressive or bipolar disorder
and does not currently meet active or residual criteria for any psychotic disorder.
2. Short-duration depressive episode (4—13 days): Depressed affect and at least four
of the other eight symptoms of a major depressive episode associated with clinically
significant distress or impairment that persists for more than 4 days, but less than 14 days,
in an individual whose presentation has never met criteria for any other depressive or
bipolar disorder, does not currently meet active or residual criteria for any psychotic dis-
order, and does not meet criteria for recurrent brief depression.
3. Depressive episode with insufficient symptoms: Depressed affect and at least one
of the other eight symptoms of a major depressive episode associated with clinically
184 Depressive Disorders
significant distress or impairment that persist for at least 2 weeks in an individual
whose presentation has never met criteria for any other depressive or bipolar disorder,
does not currently meet active or residual criteria for any psychotic disorder, and does
not meet criteria for mixed anxiety and depressive disorder symptoms.
Unspecified Depressive Disorder
311 (F32.9)
This category applies to presentations in which symptoms characteristic of a depressive dis-
order that cause clinically significant distress or impairment in social, occupational, or other im-
portant areas of functioning predominate but do not meet the full criteria for any of the disorders
in the depressive disorders diagnostic class. The unspecified depressive disorder category is
used in situations in which the clinician chooses nof to specify the reason that the criteria are
not met for a specific depressive disorder, and includes presentations for which there is insuf-
ficient information to make a more specific diagnosis (e.g., in emergency room settings).
Specifiers for Depressive Disorders
Specify if:
With anxious distress: Anxious distress is defined as the presence of at least two of
the following symptoms during the majority of days of a major depressive episode or
persistent depressive disorder (dysthymia):
1. Feeling keyed up or tense.
2. Feeling unusually restless.
3. Difficulty concentrating because of worry.
4. Fear that something awful may happen.
5. Feeling that the individual might lose control of himself or herself.
Specify current severity:
Mild: Two symptoms.
Moderate: Three symptoms.
Moderate-severe: Four or five symptoms.
Severe: Four or five symptoms and with motor agitation.
Note: Anxious distress has been noted as a prominent feature of both bipolar and ma-
jor depressive disorder in both primary care and specialty mental health settings. High
levels of anxiety have been associated with higher suicide risk, longer duration of ill-
ness, and greater likelihood of treatment nonresponse. As a result, it is clinically useful
to specify accurately the presence and severity levels of anxious distress for treatment
planning and monitoring of response to treatment.
With mixed features:
A. Atleast three of the following manic/hypomanic symptoms are present nearly every
day during the majority of days of a major depressive episode:
1. Elevated, expansive mood.
Inflated self-esteem or grandiosity.
More talkative than usual or pressure to keep talking.
Flight of ideas or subjective experience that thoughts are racing.
Increase in energy or goal-directed activity (either socially, at work or school, or
sexually).
ap woh
Specifiers for Depressive Disorders 185
6. Increased or excessive involvement in activities that have a high potential for
painful consequences (e.g., engaging in unrestrained buying sprees, sexual in-
discrettons, foolish business investments).
7. Decreased need for sleep (feeling rested despite sleeping less than usual; to be
contrasted with insomnia).
B. Mixed symptoms are observable by others and represent a change from the per-
son’s usual behavior.
C. For individuals whose symptoms meet full criteria for either mania or hypomania,
the diagnosis should be bipolar | or bipolar II disorder.
D. The mixed symptoms are not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication or other treatment).
Note: Mixed features associated with a major depressive episode have been found
to be a significant risk factor for the development of bipolar | or bipolar II disorder.
As a result, it is clinically useful to note the presence of this specifier for treatment
planning and monitoring of response to treatment.
With melancholic features:
A. One of the following is present during the most severe period of the current epi-
sode:
1. Loss of pleasure in all, or almost all, activities.
2. Lack of reactivity to usually pleasurable stimuli (does not feel much better, even
temporarily, when something good happens).
B. Three (or more) of the following:
1. Adistinct quality of depressed mood characterized by profound despondency,
despair, and/or moroseness or by so-called empty mood.
Depression that is regularly worse in the morning.
Early-morning awakening (i.e., at least 2 hours before usual awakening).
Marked psychomotor agitation or retardation.
Significant anorexia or weight loss.
6. Excessive or inappropriate guilt.
Note: The specifier “with melancholic features” is applied if these features are present
at the most severe stage of the episode. There is a near-complete absence of the ca-
pacity for pleasure, not merely a diminution. A guideline for evaluating the lack of reac-
tivity of mood is that even highly desired events are not associated with marked
brightening of mood. Either mood does not brighten at all, or it brightens only partially
(e.g., up to 20%~40% of normal for only minutes at a time). The “distinct quality” of mood
that is characteristic of the “with melancholic features” specifier is experienced as qual-
itatively different from that during a nonmelancholic depressive episode. A depressed
mood that is described as merely more severe, longer lasting, or present without a rea-
son is not considered distinct in quality. Psychomotor changes are nearly always pres-
ent and are observable by others.
Melancholic features exhibit only a modest tendency to repeat across episodes in the
same individual. They are more frequent in inpatients, as opposed to outpatients; are
less likely to occur in milder than in more severe major depressive episodes; and are
more likely to occur in those with psychotic features.
With atypical features: This specifier can be applied when these features predomi-
nate during the majority of days of the current or most recent major depressive episode
or persistent depressive disorder.
aPwn
A. Mood reactivity (i.e., mood brightens in response to actual or potential positive
events).
186 Depressive Disorders
B. Two (or more) of the following:
1. Significant weight gain or increase in appetite.
2. Hypersomnia.
3. Leaden paralysis (i.e., heavy, leaden feelings in arms or legs).
4. A long-standing pattern of interpersonal rejection sensitivity (not limited to epi-
sodes of mood disturbance) that results in significant social or occupational im-
pairment.
C. Criteria are not met for “with melancholic features” or “with catatonia” during the
same episode.
Note: “Atypical depression” has historical significance (i.e., atypical in contradistinction
to the more classical agitated, “endogenous” presentations of depression that were the
norm when depression was rarely diagnosed in outpatients and almost never in ado-
lescents or younger adults) and today does not connote an uncommon or unusual clin-
ical presentation as the term might imply.
Mood reactivity is the capacity to be cheered up when presented with positive events
{e.g., a visit from children, compliments from others). Mood may become euthymic (not
sad) even for extended periods of time if the external circumstances remain favorable.
Increased appetite may be manifested by an obvious increase in food intake or by
weight gain. Hypersomnia may include either an extended period of nighttime sleep or
daytime napping that totals at least 10 hours of sleep per day (or at least 2 hours more
than when not depressed). Leaden paralysis is defined as feeling heavy, leaden, or
weighted down, usually in the arms or legs. This sensation is generally present for at
least an hour a day but often lasts for many hours at a time. Unlike the other atypical
features, pathological sensitivity to perceived interpersonal rejection is a trait that has
an early onset and persists throughout most of adult life. Rejection sensitivity occurs
both when the person is and is not depressed, though it may be exacerbated during
depressive periods.
With psychotic features: Delusions and/or hallucinations are present.
With mood-congruent psychotic features: The content of all delusions and hal-
lucinations is consistent with the typical depressive themes of personal inade-
quacy, guilt, disease, death, nihilism, or deserved punishment.
With mood-incongruent psychotic features: The content of the delusions or hal-
lucinations does not involve typical depressive themes of personal inadequacy,
guilt, disease, death, nihilism, or deserved punishment, or the content is a mixture
of mood-incongruent and mood-congruent themes.
With catatonia: The catatonia specifier can apply to an episode of depression if cata-
tonic features are present during most of the episode. See criteria for catatonia asso-
ciated with a mental disorder {for a description of catatonia, see the chapter
“Schizophrenia Spectrum and Other Psychotic Disorders”).
With peripartum onset: This specifier can be applied to the current or, if full criteria
are not currently met for a major depressive episode, most recent episode of major de-
pression if onset of mood symptoms occurs during pregnancy or in the 4 weeks follow-
ing delivery.
Note: Mood episodes can have their onset either during pregnancy or postpartum.
Although the estimates differ according to the period of follow-up after delivery, be-
tween 3% and 6% of women will experience the onset of a major depressive epi-
sode during pregnancy or in the weeks or months following delivery. Fifty percent
of “postpartum” major depressive episodes actually begin prior to delivery. Thus,
these episodes are referred to collectively as peripartum episodes. Women with
peripartum major depressive episodes often have severe anxiety and even panic
Specifiers for Depressive Disorders 187
attacks. Prospective studies have demonstrated that mood and anxiety symptoms
during pregnancy, as well as the “baby blues,” increase the risk for a postpartum
major depressive episode.
Peripartum-onset mood episodes can present either with or without psychotic
features. Infanticide is most often associated with postpartum psychotic episodes
that are characterized by command hallucinations to kill the infant or delusions that
the infant is possessed, but psychotic symptoms can also occur in severe postpar-
tum mood episodes without such specific delusions or hallucinations.
Postpartum mood (major depressive or manic) episodes with psychotic features
appear to occur in from 1 in 500 to 1 in 1,000 deliveries and may be more common
in primiparous women. The risk of postpartum episodes with psychotic features is
particularly increased for women with prior postpartum mood episodes but is also
elevated for those with a prior history of a depressive or bipolar disorder (especially
bipolar ! disorder) and those with a family history of bipolar disorders.
Once a woman has had a postpartum episode with psychotic features, the risk
of recurrence with each subsequent delivery is between 30% and 50%. Postpartum
episodes must be differentiated from delirium occurring in the postpartum period,
which is distinguished by a fluctuating level of awareness or attention. The postpar-
tum period is unique with respect to the degree of neuroendocrine alterations and
psychosocial adjustments, the potential impact of breast-feeding on treatment
planning, and the long-term implications of a history of postpartum mood disorder
on subsequent family planning.
With seasonal pattern: This specifier applies to recurrent major depressive disorder.
A. There has been a regular temporal relationship between the onset of major depres-
sive episodes in major depressive disorder and a particular time of the year (e.g.,
in the fall or winter).
Note: Do not include cases in which there is an obvious effect of seasonally related
psychosocial stressors (e.g., regularly being unemployed every winter).
B. Full remissions (or a change from major depression to mania or hypomania) also
occur at a characteristic time of the year (e.g., depression disappears in the spring).
C. In the last 2 years, two major depressive episodes have occurred that demonstrate
the temporal seasonal relationships defined above and no nonseasonal major de-
pressive episodes have occurred during that same period.
D. Seasonal major depressive episodes (as described above) substantially outnum-
ber the nonseasonal major depressive episodes that may have occurred over the
individual's lifetime.
Note: The specifier “with seasonal pattern” can be applied to the pattern of major de-
pressive episodes in major depressive disorder, recurrent. The essential feature is the
onset and remission of major depressive episodes at characteristic times of the year.
In most cases, the episodes begin in fall or winter and remit in spring. Less commonly,
there may be recurrent summer depressive episodes. This pattern of onset and remis-
sion of episodes must have occurred during at least a 2-year period, without any non-
seasonal episodes occurring during this period. In addition, the seasonai depressive
episodes must substantially outnumber any nonseasonal depressive episodes over
the individual's lifetime.
This specifier does not apply to those situations in which the pattern is better ex-
plained by seasonally linked psychosocial stressors (e.g., seasonal unemployment or
school schedule). Major depressive episodes that occur in a seasonal pattern are often
characterized by prominent energy, hypersomnia, overeating, weight gain, and a crav-
ing for carbohydrates. It is unclear whether a seasonal pattern is more likely in recur-
rent major depressive disorder or in bipolar disorders. However, within the bipolar
disorders group, a seasonal pattern appears to be more likely in bipolar I! disorder than
188 Depressive Disorders
in bipolar | disorder. In some individuals, the onset of manic or hypomanic episodes
may also be linked to a particular season.
The prevalence of winter-type seasonal pattern appears to vary with latitude, age,
and sex. Prevalence increases with higher latitudes. Age is also a strong predictor of
seasonality, with younger persons at higher risk for winter depressive episodes.
Specify if:
In partial remission: Symptoms of the immediately previous major depressive episode
are present, but full criteria are not met, or there is a period lasting less than 2 months
without any significant symptoms of a major depressive episode following the end of
such an episode.
In full remission: During the past 2 months, no significant signs or symptoms of the
disturbance were present.
Specify current severity:
Severity is based on the number of criterion symptoms, the severity of those symptoms,
and the degree of functional disability.
Mild: Few, if any, symptoms in excess of those required to make the diagnosis are
present, the intensity of the symptoms is distressing but manageable, and the symp-
toms result in minor impairment in social or occupational functioning.
Moderate: The number of symptoms, intensity of symptoms, and/or functional impair-
ment are between those specified for “mild” and “severe.”
Severe: The number of symptoms is substantially in excess of that required to make
the diagnosis, the intensity of the symptoms is seriously distressing and unmanage-
able, and the symptoms markedly interfere with social and occupational functioning.
Anxiety disorders include disorders that share features of excessive fear and anxi-
ety and related behavioral disturbances. Fear is the emotional response to real or per-
ceived imminent threat, whereas anxiety is anticipation of future threat. Obviously, these
two states overlap, but they also differ, with fear more often associated with surges of au-
tonomic arousal necessary for fight or flight, thoughts of immediate danger, and escape
behaviors, and anxiety more often associated with muscle tension and vigilance in prep-
aration for future danger and cautious or avoidant behaviors. Sometimes the level of fear
or anxiety is reduced by pervasive avoidance behaviors. Panic attacks feature prominently
within the anxiety disorders as a particular type of fear response. Panic attacks are not lim-
ited to anxiety disorders but rather can be seen in other mental disorders as well.
The anxiety disorders differ from one another in the types of objects or situations that
induce fear, anxiety, or avoidance behavior, and the associated cognitive ideation. Thus,
while the anxiety disorders tend to be highly comorbid with each other, they can be dif-
ferentiated by close examination of the types of situations that are feared or avoided and
the content of the associated thoughts or beliefs.
Anxiety disorders differ from developmentally normative fear or anxiety by being ex-
cessive or persisting beyond developmentally appropriate periods. They differ from tran-
sient fear or anxiety, often stress-induced, by being persistent (e.g., typically lasting 6 months
or more), although the criterion for duration is intended as a general guide with allowance
for some degree of flexibility and is sometimes of shorter duration in children (as in sepa-
ration anxiety disorder and selective mutism). Since individuals with anxiety disorders
typically overestimate the danger in situations they fear or avoid, the primary determina-
tion of whether the fear or anxiety is excessive or out of proportion is made by the clinician,
taking cultural contextual factors into account. Many of the anxiety disorders develop in
childhood and tend to persist if not treated. Most occur more frequently in females than in
males (approximately 2:1 ratio). Each anxiety disorder is diagnosed only when the symp-
toms are not attributable to the physiological effects of a substance/medication or to another
medical condition or are not better explained by another mental disorder.
The chapter is arranged developmentally, with disorders sequenced according to the
typical age at onset. The individual with separation anxiety disorder is fearful or anxious
about separation from attachment figures to a degree that is developmentally inappro-
priate. There is persistent fear or anxiety about harm coming to attachment figures and
events that could lead to loss of or separation from attachment figures and reluctance to go
away from attachment figures, as well as nightmares and physical symptoms of distress. Al-
though the symptoms often develop in childhood, they can be expressed throughout adult-
hood as well.
Selective mutism is characterized by a consistent failure to speak in social situations in
which there is an expectation to speak (e.g., school) even though the individual speaks in
other situations. The failure to speak has significant consequences on achievement in aca-
demic or occupational settings or otherwise interferes with normal social communication.
Individuals with specific phobia are fearful or anxious about or avoidant of circum-
scribed objects or situations. A specific cognitive ideation is not featured in this disorder,
as it is in other anxiety disorders. The fear, anxiety, or avoidance is almost always imme-
189
190 Anxiety Disorders
diately induced by the phobic situation, to a degree that is persistent and out of proportion
to the actual risk posed. There are various types of specific phobias: animal; natural envi-
ronment; blood-injection-injury; situational; and other situations.
In social anxiety disorder (social phobia), the individual is fearful or anxious about or
avoidant of social interactions and situations that involve the possibility of being scruti-
nized. These include social interactions such as meeting unfamiliar people, situations in
which the individual may be observed eating or drinking, and situations in which the in-
dividual performs in front of others. The cognitive ideation is of being negatively evalu-
ated by others, by being embarrassed, humiliated, or rejected, or offending others.
In panic disorder, the individual experiences recurrent unexpected panic attacks and is
persistently concerned or worried about having more panic attacks or changes his or her
behavior in maladaptive ways because of the panic attacks (e.g., avoidance of exercise or of
unfamiliar locations). Panic attacks are abrupt surges of intense fear or intense discomfort
that reach a peak within minutes, accompanied by physical and/or cognitive symptoms.
Limited-symptom panic attacks include fewer than four symptoms. Panic attacks may be
expected, such as in response to a typically feared object or situation, or unexpected, meaning
that the panic attack occurs for no apparent reason. Panic attacks function as a marker and
prognostic factor for severity of diagnosis, course, and comorbidity across an array of dis-
orders, including, but not limited to, the anxiety disorders (e.g., substance use, depressive
and psychotic disorders). Panic attack may therefore be used as a descriptive specifier for
any anxiety disorder as well as other mental disorders.
Individuals with agoraphobia are fearful and anxious about two or more of the follow-
ing situations: using public transportation; being in open spaces; being in enclosed places;
standing in line or being in a crowd; or being outside of the home alone in other situations.
The individual fears these situations because of thoughts that escape might be difficult or
help might not be available in the event of developing panic-like symptoms or other inca-
pacitating or embarrassing symptoms. These situations almost always induce fear or anx-
iety and are often avoided and require the presence of a companion.
The key features of generalized anxiety disorder are persistent and excessive anxiety
and worry about various domains, including work and school performance, that the indi-
vidual finds difficult to control. In addition, the individual experiences physical symptoms,
including restlessness or feeling keyed up or on edge; being easily fatigued; difficulty con-
centrating or mind going blank; irritability; muscle tension; and sleep disturbance.
Substance /medication-induced anxiety disorder involves anxiety due to substance in-
toxication or withdrawal or to a medication treatment. In anxiety disorder due to another
medical condition, anxiety symptoms are the physiological consequence of another med-
ical condition.
Disorder-specific scales are available to better characterize the severity of each anxiety
disorder and to capture change in severity over time. For ease of use, particularly for in-
dividuals with more than one anxiety disorder, these scales have been developed to have
the same format (but different focus) across the anxiety disorders, with ratings of behav-
ioral symptoms, cognitive ideation symptoms, and physical symptoms relevant to each
disorder.
Separation Anxiety Disorder
Diagnostic Criteria 309.21 (F93.0)
A. Developmentally inappropriate and excessive fear or anxiety concerning separation from
those to whom the individual is attached, as evidenced by at least three of the following:
1. Recurrent excessive distress when anticipating or experiencing separation from
home or from major attachment figures.
Separation Anxiety Disorder 191
2. Persistent and excessive worry about losing major attachment figures or about pos-
sible harm to them, such as illness, injury, disasters, or death.
3. Persistent and excessive worry about experiencing an untoward event (e.g., getting
lost, being kidnapped, having an accident, becoming ill} that causes separation
from a major attachment figure.
4. Persistent reluctance or refusal to go out, away from home, to school, to work, or
elsewhere because of fear of separation.
5. Persistent and excessive fear of or reluctance about being alone or without major
attachment figures at home or in other settings.
6. Persistent reluctance or refusal to sleep away from home or to go to sleep without
being near a major attachment figure.
7. Repeated nightmares involving the theme of separation.
8. Repeated complaints of physical symptoms (e.g., headaches, stomachaches, nau-
sea, vomiting) when separation from major attachment figures occurs or is antici-
pated.
B. The fear, anxiety, or avoidance is persistent, lasting at least 4 weeks in children and
adolescents and typically 6 months or more in adults.
C. The disturbance causes clinically significant distress or impairment in social, aca-
demic, occupational, or other important areas of functioning.
D. The disturbance is not better explained by another mental disorder, such as refusing
to leave home because of excessive resistance to change in autism spectrum disorder;
delusions or hallucinations concerning separation in psychotic disorders; refusal to go
outside without a trusted companion in agoraphobia; worries about ill health or other
harm befalling significant others in generalized anxiety disorder; or concerns about
having an illness in illness anxiety disorder.
Diagnostic Features
The essential feature of separation anxiety disorder is excessive fear or anxiety concerning
separation from home or attachment figures. The anxiety exceeds what may be expected
given the person’s developmental level (Criterion A). Individuals with separation anxiety
disorder have symptoms that meet at least three of the following criteria: They experience
recurrent excessive distress when separation from home or major attachment figures is an-
ticipated or occurs (Criterion A1). They worry about the well-being or death of attachment
figures, particularly when separated from them, and they need to know the whereabouts
of their attachment figures and want to stay in touch with them (Criterion A2). They also
worry about untoward events to themselves, such as getting lost, being kidnapped, or
having an accident, that would keep them from ever being reunited with their major at-
tachment figure (Criterion A3). Individuals with separation anxiety disorder are reluctant
or refuse to go out by themselves because of separation fears (Criterion A4). They have
persistent and excessive fear or reluctance about being alone or without major attachment
figures at home or in other settings. Children with separation anxiety disorder may be un-
able to stay or go in a room by themselves and may display “clinging” behavior, staying
close to or “shadowing” the parent around the house, or requiring someone to be with
them when going to another room in the house (Criterion A5). They have persistent reluc-
tance or refusal to go to sleep without being near a major attachment figure or to sleep
away from home (Criterion A6). Children with this disorder often have difficulty at bed-
time and may insist that someone stay with them until they fall asleep. During the night,
they may make their way to their parents’ bed (or that of a significant other, such as a sib-
ling). Children may be reluctant or refuse to attend camp, to sleep at friends’ homes, or to
go on errands. Adults may be uncomfortable when traveling independently (e.g., sleeping
in a hotel room). There may be repeated nightmares in which the content expresses the in-
192 Anxiety Disorders
dividual’s separation anxiety (e.g., destruction of the family through fire, murder, or other
catastrophe) (Criterion A7). Physical symptoms (e.g., headaches, abdominal complaints,
nausea, vomiting) are common in children when separation from major attachment fig-
ures occurs or is anticipated (Criterion A8). Cardiovascular symptoms such as palpitations,
dizziness, and feeling faint are rare in younger children but may occur in adolescents and
adults.
The disturbance must last for a period of at least 4 weeks in children and adolescents
younger than 18 years and is typically 6 months or longer in adults (Criterion B). However,
the duration criterion for adults should be used as a general guide, with allowance for
some degree of flexibility. The disturbance must cause clinically significant distress or im-
pairment in social, academic, occupational, or other important areas of functioning (Cri-
terion C).
Associated Features Supporting Diagnosis
When separated from major attachment figures, children with separation anxiety disorder
may exhibit social withdrawal, apathy, sadness, or difficulty concentrating on work or
play. Depending on their age, individuals may have fears of animals, monsters, the dark,
muggers, burglars, kidnappers, car accidents, plane travel, and other situations that are
perceived as presenting danger to the family or themselves. Some individuals become
homesick and uncomfortable to the point of misery when away from home. Separation
anxiety disorder in children may lead to school refusal, which in turn may lead to academic
difficulties and social isolation. When extremely upset at the prospect of separation, chil-
dren may show anger or occasionally aggression toward someone who is forcing separa-
tion. When alone, especially in the evening or the dark, young children may report unusual
perceptual experiences (e.g., seeing people peering into their room, frightening creatures
reaching for them, feeling eyes staring at them). Children with this disorder may be de-
scribed as demanding, intrusive, and in need of constant attention, and, as adults, may ap-
pear dependent and overprotective. The individual's excessive demands often become a
source of frustration for family members, leading to resentment and conflict in the family.
Prevalence
The 12-month prevalence of separation anxiety disorder among adults in the United States
is 0.9%~1.9%. In children, 6- to 12-month prevalence is estimated to be approximately 4%.
In adolescents in the United States, the 12-month prevalence is 1.6%. Separation anxiety
disorder decreases in prevalence from childhood through adolescence and adulthood and
is the most prevalent anxiety disorder in children younger than 12 years. In clinical sam-
ples of children, the disorder is equally common in males and females. In the community,
the disorder is more frequent in females.
Development and Course
Periods of heightened separation anxiety from attachment figures are part of normal early
development and may indicate the development of secure attachment relationships (e.g.,
around 1 year of age, when infants may suffer from stranger anxiety). Onset of separation
anxiety disorder may be as early as preschool age and may occur at any time during child-
hood and more rarely in adolescence. Typically there are periods of exacerbation and re-
mission. In some cases, both the anxiety about possible separation and the avoidance of
situations involving separation from the home or nuclear family (e.g., going away to col-
lege, moving away from attachment figures) may persist through adulthood. However,
the majority of children with separation anxiety disorder are free of impairing anxiety dis-
orders over their lifetimes. Many adults with separation anxiety disorder do not recall a
childhood onset of separation anxiety disorder, although they may recall symptoms.
Separation Anxiety Disorder 193
The manifestations of separation anxiety disorder vary with age. Younger children are
more reluctant to go to school or may avoid school altogether. Younger children may not
express worries or specific fears of definite threats to parents, home, or themselves, and the
anxiety is manifested only when separation is experienced. As children age, worries
emerge; these are often worries about specific dangers (e.g., accidents, kidnapping, mug-
ging, death) or vague concerns about not being reunited with attachment figures. In adults,
separation anxiety disorder may limit their ability to cope with changes in circumstances
{e.g., moving, getting married). Adults with the disorder are typically overconcerned about
their offspring and spouses and experience marked discomfort when separated from them.
They may also experience significant disruption in work or social experiences because of
needing to continuously check on the whereabouts of a significant other.
Risk and Prognostic Factors
Environmental. Separation anxiety disorder often develops after life stress, especially a
loss (e.g., the death of a relative or pet; an illness of the individual or a relative; a change of
schools; parental divorce; a move to a new neighborhood; immigration; a disaster that in-
volved periods of separation from attachment figures). In young adults, other examples of
life stress include leaving the parental home, entering into a romantic relationship, and be-
coming a parent. Parental overprotection and intrusiveness may be associated with sepa-
ration anxiety disorder.
Genetic and physiological. Separation anxiety disorder in children may be heritable.
Heritability was estimated at 73% in a community sample of 6-year-old twins, with higher
rates in girls. Children with separation anxiety disorder display particularly enhanced
sensitivity to respiratory stimulation using CO,-enriched air.
Culture-Related Diagnostic Issues
There are cultural variations in the degree to which it is considered desirable to tolerate
separation, so that demands and opportunities for separation between parents and chil-
dren are avoided in some cultures. For example, there is wide variation across countries
and cultures with respect to the age at which it is expected that offspring should leave the
parental home. It is important to differentiate separation anxiety disorder from the high
value some cultures place on strong interdependence among family members.
Gender-Reiated Diagnostic Issues
Girls manifest greater reluctance to attend or avoidance of school than boys. Indirect ex-
pression of fear of separation may be more common in males than in females, for example,
by limited independent activity, reluctance to be away from home alone, or distress when
spouse or offspring do things independently or when contact with spouse or offspring is
not possible.
Suicide Risk
Separation anxiety disorder in children may be associated with an increased risk for sui-
cide. In a community sample, the presence of mood disorders, anxiety disorders, or sub-
stance use has been associated with suicidal ideation and attempts. However, this
association is not specific to separation anxiety disorder and is found in several anxiety
disorders.
Functional Consequences of Separation Anxiety Disorder
Individuals with separation anxiety disorder often limit independent activities away from
home or attachment figures (e.g., in children, avoiding school, not going to camp, having
194 Anxiety Disorders
difficulty sleeping alone; in adolescents, not going away to college; in adults, not leaving the
parental home, not traveling, not working outside the home).
Differential Diagnosis
Generalized anxiety disorder. Separation anxiety disorder is distinguished from gener-
alized anxiety disorder in that the anxiety predominantly concerns separation from attach-
ment figures, and if other worries occur, they do not predominate the clinical picture.
Panic disorder. Threats of separation may lead to extreme anxiety and even a panic at-
tack. In separation anxiety disorder, in contrast to panic disorder, the anxiety concerns the
possibility of being away from attachment figures and worry about untoward events be-
falling them, rather than being incapacitated by an unexpected panic attack.
Agoraphobia. Unlike individuals with agoraphobia, those with separation anxiety dis-
order are not anxious about being trapped or incapacitated in situations from which es-
cape is perceived as difficult in the event of panic-like symptoms or other incapacitating
symptoms.
Conduct disorder. School avoidance (truancy) is common in conduct disorder, but anx-
iety about separation is not responsible for school absences, and the child or adolescent
usually stays away from, rather than returns to, the home.
Social anxiety disorder. School refusal may be due to social anxiety disorder (social pho-
bia). In such instances, the school avoidance is due to fear of being judged negatively by oth-
ers rather than to worries about being separated from the attachment figures.
Posttraumatic stress disorder. Fear of separation from loved ones is common after trau-
matic events such as a disasters, particularly when periods of separation from loved ones
were experienced during the traumatic event. In posttraumatic stress disorder (PTSD), the
central symptoms concern intrusions about, and avoidance of, memories associated with
the traumatic event itself, whereas in separation anxiety disorder, the worries and avoid-
ance concern the well-being of attachment figures and separation from them.
llIness anxiety disorder. Individuals with illness anxiety disorder worry about specific
illnesses they may have, but the main concern is about the medical diagnosis itself, not
about being separated from attachment figures.
Bereavement. Intense yearning or longing for the deceased, intense sorrow and emo-
tional pain, and preoccupation with the deceased or the circumstances of the death are ex-
pected responses occurring in bereavement, whereas fear of separation from other
attachment figures is central in separation anxiety disorder.
Depressive and bipolar disorders. These disorders may be associated with reluctance
to leave home, but the main concern is not worry or fear of untoward events befalling at-
tachment figures, but rather low motivation for engaging with the outside world. How-
ever, individuals with separation anxiety disorder may become depressed while being
separated or in anticipation of separation.
Oppositional defiant disorder. Children and adolescents with separation anxiety disor-
der may be oppositional in the context of being forced to separate from attachment figures.
Oppositional defiant disorder should be considered only when there is persistent opposi-
tional behavior unrelated to the anticipation or occurrence of separation from attachment
figures.
Psychotic disorders. Unlike the hallucinations in psychotic disorders, the unusual per-
ceptual experiences that may occur in separation anxiety disorder are usually based on a
misperception of an actual stimulus, occur only in certain situations (e.g., nighttime), and
are reversed by the presence of an attachment figure.
Selective Mutism 195
Personality disorders. Dependent personality disorder is characterized by an indis-
criminate tendency to rely on others, whereas separation anxiety disorder involves con-
cern about the proximity and safety of main attachment figures. Borderline personality
disorder is characterized by fear of abandonment by loved ones, but problems in identity,
self-direction, interpersonal functioning, and impulsivity are additionally central to that
disorder, whereas they are not central to separation anxiety disorder.
Comorbidity
In children, separation anxiety disorder is highly comorbid with generalized anxiety dis-
order and specific phobia. In adults, common comorbidities include specific phobia,
PTSD, panic disorder, generalized anxiety disorder, social anxiety disorder, agoraphobia,
obsessive-compulsive disorder, and personality disorders. Depressive and bipolar disor-
ders are also comorbid with separation anxiety disorder in adults.
Selective Mutism
Diagnostic Criteria 312.23 (F94.0)
A. Consistent failure to speak in specific social situations in which there is an expectation
for speaking (e.g., at school) despite speaking in other situations.
B. The disturbance interferes with educational or occupational achievement or with social
communication.
C. The duration of the disturbance is at least 1 month (not limited to the first month of
school).
D. The failure to speak is not attributable to a lack of knowledge of, or comfort with, the
spoken language required in the social situation.
E. The disturbance is not better explained by a communication disorder (e.g., childhood-
onset fluency disorder) and does not occur exclusively during the course of autism
spectrum disorder, schizophrenia, or another psychotic disorder.
Diagnostic Features
When encountering other individuals in social interactions, children with selective mut-
ism do not initiate speech or reciprocally respond when spoken to by others. Lack of
speech occurs in social interactions with children or adults. Children with selective mut-
ism will speak in their home in the presence of immediate family members but often not
even in front of close friends or second-degree relatives, such as grandparents or cousins.
The disturbance is often marked by high social anxiety. Children with selective mutism of-
ten refuse to speak at school, leading to academic or educational impairment, as teachers
often find it difficult to assess skills such as reading. The lack of speech may interfere with
social communication, although children with this disorder sometimes use nonspoken or
nonverbal means (e.g., grunting, pointing, writing) to communicate and may be willing or
eager to perform or engage in social encounters when speech is not required (e.g., nonver-
bal parts in school plays).
Associated Features Supporting Diagnosis
Associated features of selective mutism may include excessive shyness, fear of social em-
barrassment, social isolation and withdrawal, clinging, compulsive traits, negativism,
temper tantrums, or mild oppositional behavior. Although children with this disorder
generally have normal language skills, there may occasionally be an associated commu-
196 Anxiety Disorders
nication disorder, although no particular association with a specific communication dis-
order has been identified. Even when these disorders are present, anxiety is present as
well. In clinical settings, children with selective mutism are almost always given an addi-
tional diagnosis of another anxiety disorder—most commonly, social anxiety disorder (so-
cial phobia).
Prevalence
Selective mutism is a relatively rare disorder and has not been included as a diagnostic cat-
egory in epidemiological studies of prevalence of childhood disorders. Point prevalence
using various clinic or school samples ranges between 0.03% and 1% depending on the set-
ting (e.g., clinic vs. school vs. general population) and ages of the individuals in the sample.
The prevalence of the disorder does not seem to vary by sex or race/ethnicity. The disor-
der is more likely to manifest in young children than in adolescents and adults.
Development and Course
The onset of selective mutism is usually before age 5 years, but the disturbance may not
come to clinical attention until entry into school, where there is an increase in social inter-
action and performance tasks, such as reading aloud. The persistence of the disorder is
variable. Although clinical reports suggest that many individuals “outgrow” selective
mutism, the longitudinal course of the disorder is unknown. In some cases, particularly in
individuals with social anxiety disorder, selective mutism may disappear, but symptoms
of social anxiety disorder remain.
Risk and Prognostic Factors
Temperamental. Temperamental risk factors for selective mutism are not well identi-
fied. Negative affectivity (neuroticism) or behavioral inhibition may play a role, as may
parental history of shyness, social isolation, and social anxiety. Children with selective
mutism may have subtle receptive language difficulties compared with their peers, al-
though receptive language is still within the normal range.
Environmental. Social inhibition on the part of parents may serve as a model for social
reticence and selective mutism in children. Furthermore, parents of children with selective
mutism have been described as overprotective or more controlling than parents of chil-
dren with other anxiety disorders or no disorder.
Genetic and physiological factors. Because of the significant overlap between selective
mutism and social anxiety disorder, there may be shared genetic factors between these
conditions.
Culture-Related Diagnostic Issues
Children in families who have immigrated to a country where a different language is spo-
ken may refuse to speak the new language because of lack of knowledge of the language.
If comprehension of the new language is adequate but refusal to speak persists, a diagno-
sis of selective mutism may be warranted.
Functional Consequences of Selective Mutism
Selective mutism may result in social impairment, as children may be too anxious to en-
gage in reciprocal social interaction with other children. As children with selective mutism
mature, they may face increasing social isolation. In school settings, these children may
suffer academic impairment, because often they do not communicate with teachers re-
garding their academic or personal needs (e.g., not understanding a class assignment, not
Specific Phobia 197
asking to use the restroom). Severe impairment in school and social functioning, including
that resulting from teasing by peers, is common. In certain instances, selective mutism
may serve as a compensatory strategy to decrease anxious arousal in social encounters.
Differential Diagnosis
Communication disorders. Selective mutism should be distinguished from speech dis-
turbances that are better explained by a communication disorder, such as language
disorder, speech sound disorder (previously phonological disorder), childhood-onset
fluency disorder (stuttering), or pragmatic (social) communication disorder. Unlike selec-
tive mutism, the speech disturbance in these conditions is not restricted to a specific social
situation.
Neurodevelopmental disorders and schizophrenia and other psychotic disorders.
Individuals with an autism spectrum disorder, schizophrenia or another psychotic disor-
der, or severe intellectual disability may have problems in social communication and be
unable to speak appropriately in social situations. In contrast, selective mutism should be
diagnosed only when a child has an established capacity to speak in some social situations
(e.g., typically at home).
Social anxiety disorder (social phobia). The social anxiety and social avoidance in so-
cial anxiety disorder may be associated with selective mutism. In such cases, both diagno-
ses may be given.
Comorbidity
The most common comorbid conditions are other anxiety disorders, most commonly so-
cial anxiety disorder, followed by separation anxiety disorder and specific phobia. Oppo-
sitional behaviors have been noted to occur in children with selective mutism, although
oppositional behavior may be limited to situations requiring speech. Communication de-
lays or disorders also may appear in some children with selective mutism.
Specific Phobia
Diagnostic Criteria
A. Marked fear or anxiety about a specific object or situation (e.g., flying, heights, animals,
receiving an injection, seeing blood).
Note: In children, the fear or anxiety may be expressed by crying, tantrums, freezing,
or clinging.
. The phobic object or situation almost always provokes immediate fear or anxiety.
. The phobic object or situation is actively avoided or endured with intense fear or anxiety.
. The fear or anxiety is out of proportion to the actual danger posed by the specific object
or situation and to the sociocultural context.
E. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
F. The fear, anxiety, or avoidance causes clinically significant distress or impairment in
social, occupationa!, or other important areas of functioning.
G. The disturbance is not better explained by the symptoms of another mental disorder,
including fear, anxiety, and avoidance of situations associated with panic-like symptoms
or other incapacitating symptoms (as in agoraphobia); objects or situations related to
obsessions (as in obsessive-compulsive disorder); reminders of traumatic events (as in
posttraumatic stress disorder); separation from home or attachment figures (as in sep-
aration anxiety disorder); or social situations (as in social anxiety disorder).
00M
198 Anxiety Disorders
Specify if:
Code based on the phobic stimulus:
300.29 (F40.218) Animal (e.g., spiders, insects, dogs).
300.29 (F40.228) Natural environment (e.g., heights, storms, water).
300.29 (F40.23x) Blood-injection-injury (e.g., needles, invasive medical procedures).
Coding note: Select specific (CD-10-CM code as follows: F40.230 fear of blood;
F40.231 fear of injections and transfusions; F40.232 fear of other medical care; or
F40.233 fear of injury.
300.29 (F40.248) Situational (e.g., airplanes, elevators, enclosed places).
300.29 (F40.298) Other (e.g., situations that may lead to choking or vomiting; in chil-
dren, e.g., loud sounds or costumed characters).
Coding note: When more than one phobic stimulus is present, code all |ICD-10-CM codes
that apply (e.g., for fear of snakes and flying, F40.218 specific phobia, animal, and
F40.248 specific phobia, situational).
Specifiers
It is common for individuals to have multiple specific phobias. The average individual with
specific phobia fears three objects or situations, and approximately 75% of individuals with
specific phobia fear more than one situation or object. In such cases, multiple specific phobia
diagnoses, each with its own diagnostic code reflecting the phobic stimulus, would need to be
given. For example, if an individual fears thunderstorms and flying, then two diagnoses
would be given: specific phobia, natural environment, and specific phobia, situational.
Diagnostic Features
A key feature of this disorder is that the fear or anxiety is circumscribed to the presence of a
particular situation or object (Criterion A), which may be termed the phobic stimulus. The cat-
egories of feared situations or objects are provided as specifiers. Many individuals fear objects
or situations from more than one category, or phobic stimulus. For the diagnosis of specific
phobia, the response must differ from normal, transient fears that commonly occur in the pop-
ulation. To meet the criteria for a diagnosis, the fear or anxiety must be intense or severe (i.e.,
“marked”) (Criterion A). The amount of fear experienced may vary with proximity to the
feared object or situation and may occur in anticipation of or in the actual presence of the object
or situation. Also, the fear or anxiety may take the form of a full or limited symptom panic at-
tack (i.e., expected panic attack). Another characteristic of specific phobias is that fear or anxi-
ety is evoked nearly every time the individual comes into contact with the phobic stimulus
(Criterion B). Thus, an individual who becomes anxious only occasionally upon being con-
fronted with the situation or object (e.g., becomes anxious when flying only on one out of every
five airplane flights) would not be diagnosed with specific phobia. However, the degree of fear
or anxiety expressed may vary (from anticipatory anxiety to a full panic attack) across different
occasions of encountering the phobic object or situation because of various contextual factors
such as the presence of others, duration of exposure, and other threatening elements such as
turbulence on a flight for individuals who fear flying. Fear and anxiety are often expressed dif-
ferently between children and adults. Also, the fear or anxiety occurs as soon as the phobic ob-
ject or situation is encountered (i.e., immediately rather than being delayed).
The individual actively avoids the situation, or if he or she either is unable or decides
not to avoid it, the situation or object evokes intense fear or anxiety (Criterion C). Active
avoidance means the individual intentionally behaves in ways that are designed to prevent
or minimize contact with phobic objects or situations (e.g., takes tunnels instead of bridges
on daily commute to work for fear of heights; avoids entering a dark room for fear of spi-
ders; avoids accepting a job in a locale where a phobic stimulus is more common). Avoid-
Specific Phobia 199
ance behaviors are often obvious (e.g., an individual who fears blood refusing to go to the
doctor) but are sometimes less obvious (e.g., an individual who fears snakes refusing to
look at pictures that resemble the form or shape of snakes). Many individuals with specific
phobias have suffered over many years and have changed their living circumstances in
ways designed to avoid the phobic object or situation as much as possible (e.g., an indi-
vidual diagnosed with specific phobia, animal, who moves to reside in an area devoid of
the particular feared animal). Therefore, they no longer experience fear or anxiety in their
daily life. In such instances, avoidance behaviors or ongoing refusal to engage in activities
that would involve exposure to the phobic object or situation (e.g., repeated refusal to ac-
cept offers for work-related travel because of fear of flying) may be helpful in confirming
the diagnosis in the absence of overt anxiety or panic.
The fear or anxiety is out of proportion to the actual danger that the object or situation
poses, or more intense than is deemed necessary (Criterion D). Although individuals with
specific phobia often recognize their reactions as disproportionate, they tend to overesti-
mate the danger in their feared situations, and thus the judgment of being out of propor-
tion is made by the clinician. The individual’s sociocultural context should also be taken
into account. For example, fears of the dark may be reasonable in a context of ongoing
violence, and fear of insects may be more disproportionate in settings where insects are
consumed in the diet. The fear, anxiety, or avoidance is persistent, typically lasting for
6 months or more (Criterion E), which helps distinguish the disorder from transient fears
that are common in the population, particularly among children. However, the duration
criterion should be used as a general guide, with allowance for some degree of flexibility.
The specific phobia must cause clinically significant distress or impairment in social, oc-
cupational, or other important areas of functioning in order for the disorder to be diag-
nosed (Criterion F).
Associated Features Supporting Diagnosis
Individuals with specific phobia typically experience an increase in physiological arousal
in anticipation of or during exposure to a phobic object or situation. However, the physi-
ological response to the feared situation or object varies. Whereas individuals with situa-
tional, natural environment, and animal specific phobias are likely to show sympathetic
nervous system arousal, individuals with blood-injection-injury specific phobia often
demonstrate a vasovagal fainting or near-fainting response that is marked by initial brief
acceleration of heart rate and elevation of blood pressure followed by a deceleration of
heart rate and a drop in blood pressure. Current neural systems models for specific phobia
emphasize the amygdala and related structures, much as in other anxiety disorders.
Prevalence
In the United States, the 12-month community prevalence estimate for specific phobia is
approximately 7%~-9%. Prevalence rates in European countries are largely similar to those
in the United States (e.g., about 6%), but rates are generally lower in Asian, African, and
Latin American countries (2%—4%). Prevalence rates are approximately 5% in children and
are approximately 16% in 13- to 17-year-olds. Prevalence rates are lower in older individ-
uals (about 3%-5%), possibly reflecting diminishing severity to subclinical levels. Females
are more frequently affected than males, at a rate of approximately 2:1, although rates vary
across different phobic stimuli. That is, animal, natural environment, and situational spe-
cific phobias are predominantly experienced by females, whereas blood-injection-injury
phobia is experienced nearly equally by both genders.
Development and Course
Specific phobia sometimes develops following a traumatic event (e.g., being attacked by
an animal or stuck in an elevator), observation of others going through a traumatic event (e.g.,
200 Anxiety Disorders
watching someone drown), an unexpected panic attack in the to be feared situation (e.g.,
an unexpected panic attack while on the subway), or informational transmission (e.g., ex-
tensive media coverage of a plane crash). However, many individuals with specific phobia
are unable to recall the specific reason for the onset of their phobias. Specific phobia usu-
ally develops in early childhood, with the majority of cases developing prior to age 10
years. The median age at onset is between 7 and 11 years, with the mean at about 10 years.
Situational specific phobias tend to have a later age at onset than natural environment, an-
imal, or blood-injection-injury specific phobias. Specific phobias that develop in child-
hood and adolescence are likely to wax and wane during that period. However, phobias
that do persist into adulthood are unlikely to remit for the majority of individuals.
When specific phobia is being diagnosed in children, two issues should be considered.
First, young children may express their fear and anxiety by crying, tantrums, freezing,
or clinging. Second, young children typically are not able to understand the concept of
avoidance. Therefore, the clinician should assemble additional information from parents,
teachers, or others who know the child well. Excessive fears are quite common in young
children but are usually transitory and only mildly impairing and thus considered devel-
opmentally appropriate. In such cases a diagnosis of specific phobia would not be made.
When the diagnosis of specific phobia is being considered in a child, it is important to
assess the degree of impairment and the duration of the fear, anxiety, or avoidance, and
whether it is typical for the child’s particular developmental stage.
Although the prevalence of specific phobia is lower in older populations, it remains
one of the more commonly experienced disorders in late life. Several issues should be con-
sidered when diagnosing specific phobia in older populations. First, older individuals
may be more likely to endorse natural environment specific phobias, as well as phobias of
falling. Second, specific phobia (like all anxiety disorders) tends to co-occur with medical
concerns in older individuals, including coronary heart disease and chronic obstructive
pulmonary disease. Third, older individuals may be more likely to attribute the symptoms
of anxiety to medical conditions. Fourth, older individuals may be more likely to manifest
anxiety in an atypical manner (e.g., involving symptoms of both anxiety and depression)
and thus be more likely to warrant a diagnosis of unspecified anxiety disorder. Addition-
ally, the presence of specific phobia in older adults is associated with decreased quality of
life and may serve as a risk factor for major neurocognitive disorder.
Although most specific phobias develop in childhood and adolescence, it is possible for a
specific phobia to develop at any age, often as the result of experiences that are traumatic. For
example, phobias of choking almost always follow a near-choking event at any age.
Risk and Prognostic Factors
Temperamental. Temperamental risk factors for specific phobia, such as negative affec-
tivity (neuroticism) or behavioral inhibition, are risk factors for other anxiety disorders as
well.
Environmental. Environmental risk factors for specific phobias, such as parental over-
protectiveness, parental loss and separation, and physical and sexual abuse, tend to pre-
dict other anxiety disorders as well. As noted earlier, negative or traumatic encounters
with the feared object or situation sometimes (but not always) precede the development of
specific phobia.
Genetic and physiological. There may bea genetic susceptibility to a certain category of
specific phobia (e.g., an individual with a first-degree relative with a specific phobia of an-
imals is significantly more likely to have the same specific phobia than any other category
of phobia). Individuals with blood-injection-injury phobia show a unique propensity to
vasovagal syncope (fainting) in the presence of the phobic stimulus.
Specific Phobia 201
Culture-Related Diagnostic Issues
In the United States, Asians and Latinos report significantly lower rates of specific phobia
than non-Latino whites, African Americans, and Native Americans. In addition to having
lower prevalence rates of specific phobia, some countries outside of the United States, par-
ticularly Asian and African countries, show differing phobia content, age at onset, and
gender ratios.
Suicide Risk
Individuals with specific phobia are up to 60% more likely to make a suicide attempt than
are individuals without the diagnosis. However, it is likely that these elevated rates are
primarily due to comorbidity with personality disorders and other anxiety disorders.
Functional Consequences of Specific Phobia
Individuals with specific phobia show similar patterns of impairment in psychosocial
functioning and decreased quality of life as individuals with other anxiety disorders and
alcohol and substance use disorders, including impairments in occupational and inter-
personal functioning. In older adults, impairment may be seen in caregiving duties and
volunteer activities. Also, fear of falling in older adults can lead to reduced mobility and
reduced physical and social functioning, and may lead to receiving formal or informal
home support. The distress and impairment caused by specific phobias tend to increase
with the number of feared objects and situations. Thus, an individual who fears four ob-
jects or situations is likely to have more impairment in his or her occupational and social
roles and a lower quality of life than an individual who fears only one object or situation.
Individuals with blood-injection-injury specific phobia are often reluctant to obtain med-
ical care even when a medical concern is present. Additionally, fear of vomiting and chok-
ing may substantially reduce dietary intake.
Differential Diagnosis
Agoraphobia. Situational specific phobia may resemble agoraphobia in its clinical pre-
sentation, given the overlap in feared situations (e.g., flying, enclosed places, elevators), If
an individual fears only one of the agoraphobia situations, then specific phobia, situa-
tional, may be diagnosed. If two or more agoraphobic situations are feared, a diagnosis of
agoraphobia is likely warranted. For example, an individual who fears airplanes and ele-
vators (which overlap with the “public transportation” agoraphobic situation) but does
not fear other agoraphobic situations would be diagnosed with specific phobia, situa-
tional, whereas an individual who fears airplanes, elevators, and crowds (which overlap
with two agoraphobic situations, “using public transportation” and “standing in line and
or being in a crowd”) would be diagnosed with agoraphobia. Criterion B of agoraphobia
(the situations are feared or avoided “because of thoughts that escape might be difficult or
help might not be available in the event of developing panic-like symptoms or other inca-
pacitating or embarrassing symptoms”) can also be useful in differentiating agoraphobia
from specific phobia. If the situations are feared for other reasons, such as fear of being
harmed directly by the object or situations (e.g., fear of the plane crashing, fear of the an-
imal biting), a specific phobia diagnosis may be more appropriate.
Social anxiety disorder. If the situations are feared because of negative evaluation, so-
cial anxiety disorder should be diagnosed instead of specific phobia.
Separation anxiety disorder. If the situations are feared because of separation from a
primary caregiver or attachment figure, separation anxiety disorder should be diagnosed
instead of specific phobia.
202 Anxiety Disorders
Panic disorder. Individuals with specific phobia may experience panic attacks when con-
fronted with their feared situation or object. A diagnosis of specific phobia would be given if
the panic attacks only occurred in response to the specific object or situation, whereas a di-
agnosis of panic disorder would be given if the individual also experienced panic attacks
that were unexpected (i.e., not in response to the specific phobia object or situation).
Obsessive-compulsive disorder. If an individual's primary fear or anxiety is of an ob-
ject or situation as a result of obsessions (e.g., fear of blood due to obsessive thoughts about
contamination from blood-borne pathogens [i.e., HIV]; fear of driving due to obsessive im-
ages of harming others), and if other diagnostic criteria for obsessive-compulsive disorder
are met, then obsessive-compulsive disorder should be diagnosed.
Trauma- and stressor-related disorders. If the phobia develops following a traumatic
event, posttraumatic stress disorder (PTSD) should be considered as a diagnosis. How-
ever, traumatic events can precede the onset of PTSD and specific phobia. In this case, a di-
agnosis of specific phobia would be assigned only if all of the criteria for PTSD are not met.
Eating disorders. A diagnosis of specific phobia is not given if the avoidance behavior is
exclusively limited to avoidance of food and food-related cues, in which case a diagnosis
of anorexia nervosa or bulimia nervosa should be considered.
Schizophrenia spectrum and other psychotic disorders. When the fear and avoidance
are due to delusional thinking (as in schizophrenia or other schizophrenia spectrum and
other psychotic disorders), a diagnosis of specific phobia is not warranted.
Comorbidity
Specific phobia is rarely seen in medical-clinical settings in the absence of other psycho-
pathology and is more frequently seen in nonmedical mental health settings. Specific pho-
bia is frequently associated with a range of other disorders, especially depression in older
adults. Because of early onset, specific phobia is typically the temporally primary disorder.
Individuals with specific phobia are at increased risk for the development of other dis-
orders, including other anxiety disorders, depressive and bipolar disorders, substance-
related disorders, somatic symptom and related disorders, and personality disorders (par-
ticularly dependent personality disorder).
Social Anxiety Disorder (Social Phobia)
Diagnostic Criteria 300.23 (F40.10)
A. Marked fear or anxiety about one or more social situations in which the individual is
exposed to possible scrutiny by others. Examples include social interactions (e.g., hav-
ing a conversation, meeting unfamiliar people), being observed (e.g., eating or drink-
ing), and performing in front of others (e.g., giving a speech).
Note: In children, the anxiety must occur in peer settings and not just during interac-
tions with adults.
B. The individual fears that he or she will act in a way or show anxiety symptoms that will
be negatively evaluated (i.e., will be humiliating or embarrassing; will lead to rejection
or offend others).
C. The social situations almost always provoke fear or anxiety.
Note: In children, the fear or anxiety may be expressed by crying, tantrums, freezing,
clinging, shrinking, or failing to speak in social situations.
D. The social situations are avoided or endured with intense fear or anxiety.
Social Anxiety Disorder (Social Phobia) 203
E. The fear or anxiety is out of proportion to the actual threat posed by the social situation
and to the sociocultural context.
F, The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
G. The fear, anxiety, or avoidance causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
H. The fear, anxiety, or avoidance is not attributable to the physiological effects of a sub-
stance (e.g., a drug of abuse, a medication) or another medical condition.
|. The fear, anxiety, or avoidance is not better explained by the symptoms of another
mental disorder, such as panic disorder, body dysmorphic disorder, or autism spectrum
disorder.
J. If another medical condition (e.g., Parkinson’s disease, obesity, disfigurement from burns
or injury) is present, the fear, anxiety, or avoidance is clearly unrelated or is excessive.
Specify if:
Performance only: !f the fear is restricted to speaking or performing in public.
Specifiers
Individuals with the performance only type of social anxiety disorder have performance
fears that are typically most impairing in their professional lives (e.g., musicians, dancers,
performers, athletes) or in roles that require regular public speaking. Performance fears
may also manifest in work, school, or academic settings in which regular public presenta-
tions are required. Individuals with performance only social anxiety disorder do not fear
or avoid nonperformance social situations.
Diagnostic Features
The essential feature of social anxiety disorder is a marked, or intense, fear or anxiety of so-
cial situations in which the individual may be scrutinized by others. In children the fear or
anxiety must occur in peer settings and not just during interactions with adults (Criterion
A). When exposed to such social situations, the individual fears that he or she will be neg-
atively evaluated. The individual is concerned that he or she will be judged as anxious,
weak, crazy, stupid, boring, intimidating, dirty, or unlikable. The individual fears that
he or she will act or appear in a certain way or show anxiety symptoms, such as blushing,
trembling, sweating, stumbling over one’s words, or staring, that will be negatively eval-
uated by others (Criterion B). Some individuals fear offending others or being rejected as
a result. Fear of offending others—for example, by a gaze or by showing anxiety symp-
toms—may be the predominant fear in individuals from cultures with strong collectivistic
orientations. An individual with fear of trembling of the hands may avoid drinking, eat-
ing, writing, or pointing in public; an individual with fear of sweating may avoid shaking
hands or eating spicy foods; and an individual with fear of blushing may avoid public per-
formance, bright lights, or discussion about intimate topics. Some individuals fear and
avoid urinating in public restrooms when other individuals are present (i.e., paruresis, or
“shy bladder syndrome”).
The social situations almost always provoke fear or anxiety (Criterion C). Thus, an in-
dividual who becomes anxious only occasionally in the social situation(s) would not be di-
agnosed with social anxiety disorder. However, the degree and type of fear and anxiety
may vary (e.g., anticipatory anxiety, a panic attack) across different occasions. The antici-
patory anxiety may occur sometimes far in advance of upcoming situations (e.g., worrying
every day for weeks before attending a social event, repeating a speech for days in advance).
In children, the fear or anxiety may be expressed by crying, tantrums, freezing, clinging, or
shrinking in social] situations. The individual will often avoid the feared social situations.
Alternatively, the situations are endured with intense fear or anxiety (Criterion D). Avoid-
204 Anxiety Disorders
ance can be extensive (e.g., not going to parties, refusing school) or subtle (e.g., overpre-
paring the text of a speech, diverting attention to others, limiting eye contact).
The fear or anxiety is judged to be out of proportion to the actual risk of being nega-
tively evaluated or to the consequences of such negative evaluation (Criterion E). Some-
times, the anxiety may not be judged to be excessive, because it is related to an actual
danger (e.g., being bullied or tormented by others). However, individuals with social anx-
iety disorder often overestimate the negative consequences of social situations, and thus
the judgment of being out of proportion is made by the clinician. The individual's socio-
cultural context needs to be taken into account when this judgment is being made. For ex-
ample, in certain cultures, behavior that might otherwise appear socially anxious may be
considered appropriate in social situations (e.g., might be seen as a sign of respect).
The duration of the disturbance is typically at least 6 months (Criterion F). This dura-
tion threshold helps distinguish the disorder from transient social fears that are com-
mon, particularly among children and in the community. However, the duration criterion
should be used as a general guide, with allowance for some degree of flexibility. The fear,
anxiety, and avoidance must interfere significantly with the individual's normal routine,
occupational or academic functioning, or social activities or relationships, or must cause
clinically significant distress or impairment in social, occupational, or other important ar-
eas of functioning (Criterion G). For example, an individual who is afraid to speak in pub-
lic would not receive a diagnosis of social anxiety disorder if this activity is not routinely
encountered on the job or in classroom work, and if the individual is not significantly dis-
tressed about it. However, if the individual avoids, or is passed over for, the job or educa-
tion he or she really wants because of social anxiety symptoms, Criterion G is met.
Associated Features Supporting Diagnosis
Individuals with social anxiety disorder may be inadequately assertive or excessively sub-
missive or, less commonly, highly controlling of the conversation. They may show overly
rigid body posture or inadequate eye contact, or speak with an overly soft voice. These in-
dividuals may be shy or withdrawn, and they may be less open in conversations and dis-
close little about themselves. They may seek employment in jobs that do not require social
contact, although this is not the case for individuals with social anxiety disorder, perfor-
mance only. They may live at home longer. Men may be delayed in marrying and having
a family, whereas women who would want to work outside the home may live a life as
homemaker and mother. Self-medication with substances is common (e.g., drinking be-
fore going to a party). Social anxiety among older adults may also include exacerbation of
symptoms of medical illnesses, such as increased tremor or tachycardia. Blushing is a hall-
mark physical response of social anxiety disorder.
Prevalence
The 12-month prevalence estimate of social anxiety disorder for the United States is ap-
proximately 7%. Lower 12-month prevalence estimates are seen in much of the world us-
ing the same diagnostic instrument, clustering around 0.5%-2.0%; median prevalence in
Europe is 2.3%. The 12-month prevalence rates in children and adolescents are comparable
to those in adults. Prevalence rates decrease with age. The 12-month prevalence for older
adults ranges from 2% to 5%. In general, higher rates of social anxiety disorder are found
in females than in males in the general population (with odds ratios ranging from 1.5 to
2.2), and the gender difference in prevalence is more pronounced in adolescents and
young adults. Gender rates are equivalent or slightly higher for males in clinical samples,
and it is assumed that gender roles and social expectations play a significant role in ex-
plaining the heightened help-seeking behavior in male patients. Prevalence in the United
States is higher in American Indians and lower in persons of Asian, Latino, African Amer-
ican, and Afro-Caribbean descent compared with non-Hispanic whites.
Social Anxiety Disorder {Social Phobia) 205
Development and Course
Median age at onset of social anxiety disorder in the United States is 13 years, and 75% of
individuals have an age at onset between 8 and 15 years. The disorder sometimes emerges
out of a childhood history of social inhibition or shyness in U.S. and European studies. On-
set can also occur in early childhood. Onset of social anxiety disorder may follow a stress-
ful or humiliating experience (e.g., being bullied, vomiting during a public speech), or it
may be insidious, developing slowly. First onset in adulthood is relatively rare and is more
likely to occur after a stressful or humiliating event or after life changes that require new
social roles (e.g., marrying someone from a different social class, receiving a job promo-
tion). Social anxiety disorder may diminish after an individual with fear of dating marries
and may reemerge after divorce. Among individuals presenting to clinical care, the disor-
der tends to be particularly persistent.
Adolescents endorse a broader pattern of fear and avoidance, including of dating,
compared with younger children. Older adults express social anxiety at lower levels but
across a broader range of situations, whereas younger adults express higher levels of so-
cial anxiety for specific situations. In older adults, social anxiety may concern disability
due to declining sensory functioning (hearing, vision) or embarrassment about one’s ap-
pearance (e.g., tremor as a symptom of Parkinson’s disease) or functioning due to medical
conditions, incontinence, or cognitive impairment (e.g., forgetting people’s names). In the
community approximately 30% of individuals with social anxiety disorder experience re-
mission of symptoms within 1 year, and about 50% experience remission within a few
years. For approximately 60% of individuals without a specific treatment for social anxiety
disorder, the course takes several years or longer.
Detection of social anxiety disorder in older adults may be challenging because of sev-
eral factors, including a focus on somatic symptoms, comorbid medical illness, limited
insight, changes to social environment or roles that may obscure impairment in social
functioning, or reticence about describing psychological distress.
Risk and Prognostic Factors
Temperamental. Underlying traits that predispose individuals to social anxiety disor-
der include behavioral inhibition and fear of negative evaluation.
Environmental. There is no causative role of increased rates of childhood maltreatment or
other early-onset psychosocial adversity in the development of social anxiety disorder. How-
ever, childhood maltreatment and adversity are risk factors for social anxiety disorder.
Genetic and physiological. Traits predisposing individuals to social anxiety disorder,
such as behavioral inhibition, are strongly genetically influenced. The genetic influence is
subject to gene-environment interaction; that is, children with high behavioral inhibition
are more susceptible to environmental influences, such as socially anxious modeling by
parents. Also, social anxiety disorder is heritable (but performance-only anxiety less so).
First-degree relatives have a two to six times greater chance of having social anxiety dis-
order, and liability to the disorder involves the interplay of disorder-specific (e.g., fear of
negative evaluation) and nonspecific (e.g., neuroticism) genetic factors.
Culture-Related Diagnostic Issues
The syndrome of taijin kyofusho (e.g., in Japan and Korea) is often characterized by social-
evaluative concerns, fulfilling criteria for social anxiety disorder, that are associated with
the fear that the individual makes other people uncomfortable (e.g., “My gaze upsets peo-
ple so they look away and avoid me”), a fear that is at times experienced with delusional
intensity. This symptom may also be found in non-Asian settings. Other presentations
of taijin kyofusho may fulfill criteria for body dysmorphic disorder or delusional disorder.
206 Anxiety Disorders
Immigrant status is associated with significantly lower rates of social anxiety disorder in
both Latino and non-Latino white groups. Prevalence rates of social anxiety disorder may
not be in line with self-reported social anxiety levels in the same culture—that is, societies
with strong collectivistic orientations may report high levels of social anxiety but low prev-
alence of social anxiety disorder.
Gender-Related Diagnostic Issues
Females with social anxiety disorder report a greater number of social fears and comorbid
depressive, bipolar, and anxiety disorders, whereas males are more likely to fear dating,
have oppositional defiant disorder or conduct disorder, and use alcohol and illicit drugs to
relieve symptoms of the disorder. Paruresis is more common in males.
Functional Consequences of Social Anxiety Disorder
Social anxiety disorder is associated with elevated rates of school dropout and with de-
creased well-being, employment, workplace productivity, socioeconomic status, and quality
of life. Social anxiety disorder is also associated with being single, unmarried, or divorced
and with not having children, particularly among men. In older adults, there may be impair-
ment in caregiving duties and volunteer activities. Social anxiety disorder also impedes lei-
sure activities. Despite the extent of distress and social impairment associated with social
anxiety disorder, only about half of individuals with the disorder in Western societies ever
seek treatment, and they tend to do so only after 15-20 years of experiencing symptoms. Not
being employed is a strong predictor for the persistence of social anxiety disorder.
Differential Diagnosis
Normative shyness. Shyness (i.e., social reticence) is a common personality trait and is
not by itself pathological. In some societies, shyness is even evaluated positively. How-
ever, when there is a significant adverse impact on social, occupational, and other impor-
tant areas of functioning, a diagnosis of social anxiety disorder should be considered, and
when full diagnostic criteria for social anxiety disorder are met, the disorder should be di-
agnosed. Only a minority (12%) of self-identified shy individuals in the United States have
symptoms that meet diagnostic criteria for social anxiety disorder.
Agoraphobia. Individuals with agoraphobia may fear and avoid social situations (e.g., go-
ing to a movie) because escape might be difficult or help might not be available in the event of
incapacitation or panic-like symptoms, whereas individuals with social anxiety disorder are
most fearful of scrutiny by others. Moreover, individuals with social anxiety disorder are likely
to be calm when left entirely alone, which is often not the case in agoraphobia.
Panic disorder. Individuals with social anxiety disorder may have panic attacks, but the
concern is about fear of negative evaluation, whereas in panic disorder the concern is
about the panic attacks themselves.
Generalized anxiety disorder. Social worries are common in generalized anxiety disorder,
but the focus is more on the nature of ongoing relationships rather than on fear of negative
evaluation. Individuals with generalized anxiety disorder, particularly children, may have ex-
cessive worries about the quality of their social performance, but these worries also pertain to
nonsocial performance and when the individual is not being evaluated by others. In social anx-
iety disorder, the worries focus on social performance and others’ evaluation.
Separation anxiety disorder. Individuals with separation anxiety disorder may avoid
social settings (including school refusal) because of concerns about being separated from
attachment figures or, in children, about requiring the presence of a parent when it is not
developmentally appropriate. Individuals with separation anxiety disorder are usually
comfortable in social settings when their attachment figure is present or when they are at
Social Anxiety Disorder (Social Phobia) 207
home, whereas those with social anxiety disorder may be uncomfortable when social sit-
uations occur at home or in the presence of attachment figures.
Specific phobias. Individuals with specific phobias may fear embarrassment or humil-
iation (e.g., embarrassment about fainting when they have their blood drawn), but they do
not generally fear negative evaluation in other social situations.
Selective mutism. Individuals with selective mutism may fail to speak because of fear of
negative evaluation, but they do not fear negative evaluation in social situations where no
speaking is required (e.g., nonverbal play).
Major depressive disorder. Individuals with major depressive disorder may be con-
cerned about being negatively evaluated by others because they feel they are bad or not
worthy of being liked. In contrast, individuals with social anxiety disorder are worried
about being negatively evaluated because of certain social behaviors or physical symptoms.
Body dysmorphic disorder. Individuals with body dysmorphic disorder are preoccu-
pied with one or more perceived defects or flaws in their physical appearance that are not
observable or appear slight to others; this preoccupation often causes social anxiety and
avoidance. If their social fears and avoidance are caused only by their beliefs about their
appearance, a separate diagnosis of social anxiety disorder is not warranted.
Delusional disorder. Individuals with delusional disorder may have nonbizarre delu-
sions and/or hallucinations related to the delusional theme that focus on being rejected by
or offending others. Although extent of insight into beliefs about social situations may
vary, many individuals with social anxiety disorder have good insight that their beliefs are
out of proportion to the actual threat posed by the social situation.
Autism spectrum disorder. Social anxiety and social communication deficits are hall-
marks of autism spectrum disorder. Individuals with social anxiety disorder typically
have adequate age-appropriate social relationships and social communication capacity,
although they may appear to have impairment in these areas when first interacting with
unfamiliar peers or adults.
Personality disorders. Given its frequent onset in childhood and its persistence into and
through adulthood, social anxiety disorder may resemble a personality disorder. The most
apparent overlap is with avoidant personality disorder. Individuals with avoidant person-
ality disorder have a broader avoidance pattern than those with social anxiety disorder.
Nonetheless, social anxiety disorder is typically more comorbid with avoidant personality
disorder than with other personality disorders, and avoidant personality disorder is more
comorbid with social anxiety disorder than with other anxiety disorders.
Other mental disorders. Social fears and discomfort can occur as part of schizophrenia,
but other evidence for psychotic symptoms is usually present. In individuals with an eat-
ing disorder, it is important to determine that fear of negative evaluation about eating
disorder symptoms or behaviors (e.g., purging and vomiting) is not the sole source of so-
cial anxiety before applying a diagnosis of social anxiety disorder. Similarly, obsessive-
compulsive disorder may be associated with social anxiety, but the additional diagnosis of
social anxiety disorder is used only when social fears and avoidance are independent of
the foci of the obsessions and compulsions.
Other medical conditions. Medical conditions may produce symptoms that may be em-
barrassing (e.g. trembling in Parkinson’s disease). When the fear of negative evaluation
due to other medical conditions is excessive, a diagnosis of social anxiety disorder should
be considered.
Oppositional defiant disorder. Refusal to speak due to opposition to authority figures
should be differentiated from failure to speak due to fear of negative evaluation.
208 Anxiety Disorders
Comorbidity
Social anxiety disorder is often comorbid with other anxiety disorders, major depressive
disorder, and substance use disorders, and the onset of social anxiety disorder generally
precedes that of the other disorders, except for specific phobia and separation anxiety dis-
order. Chronic social isolation in the course of a social anxiety disorder may result in major
depressive disorder. Comorbidity with depression is high also in older adults. Substances
may be used as self-medication for social fears, but the symptoms of substance intoxica-
tion or withdrawal, such as trembling, may also be a source of (further) social fear. Social
anxiety disorder is frequently comorbid with bipolar disorder or body dysmorphic disor-
der; for example, an individual has body dysmorphic disorder concerning a preoccupa-
tion with a slight irregularity of her nose, as well as social anxiety disorder because of a
severe fear of sounding unintelligent. The more generalized form of social anxiety disor-
der, but not social anxiety disorder, performance only, is often comorbid with avoidant
personality disorder. In children, comorbidities with high-functioning autism and selec-
tive mutism are common.
Panic Disorder
Diagnostic Criteria 300.01 (F41.0)
A. Recurrent unexpected panic attacks. A panic attack is an abrupt surge of intense fear
or intense discomfort that reaches a peak within minutes, and during which time four
(or more) of the following symptoms occur:
Note: The abrupt surge can occur from a calm state or an anxious state.
Palpitations, pounding heart, or accelerated heart rate.
Sweating.
Trembling or shaking.
Sensations of shortness of breath or smothering.
Feelings of choking.
Chest pain or discomfort.
Nausea or abdominal distress.
Feeling dizzy, unsteady, light-headed, or faint.
Chills or heat sensations.
Paresthesias (numbness or tingling sensations).
_ Derealization (feelings of unreality) or depersonalization (being detached from one-
self).
Fear of losing control or “going crazy.”
13. Fear of dying.
POO MNOARWONS
—_ —
—
Note: Culture-specific symptoms (e.g., tinnitus, neck soreness, headache, uncontrol-
lable screaming or crying) may be seen. Such symptoms should not count as one of
the four required symptoms.
B. At least one of the attacks has been followed by 1 month (or more) of one or both of
the following:
1. Persistent concern or worry about additional panic attacks or their consequences
(e.g., losing control, having a heart attack, “going crazy”).
2. A significant maladaptive change in behavior related to the attacks (e.g., behaviors
designed to avoid having panic attacks, such as avoidance of exercise or unfamiliar
situations).
Panic Disorder 209
C. The disturbance is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication) or another medical condition (e.g., hyperthyroidism, car-
diopulmonary disorders).
D. The disturbance is not better explained by another mental disorder (e.g., the panic at-
tacks do not occur only in response to feared social situations, as in social anxiety dis-
order; in response to circumscribed phobic objects or situations, as in specific phobia;
in response to obsessions, as in obsessive-compulsive disorder; in response to re-
minders of traumatic events, as in posttraumatic stress disorder; or in response to sep-
aration from attachment figures, as in separation anxiety disorder).
Diagnostic Features
Panic disorder refers to recurrent unexpected panic attacks (Criterion A). A panic attack is
an abrupt surge of intense fear or intense discomfort that reaches a peak within minutes,
and during which time four or more of a list of 13 physical and cognitive symptoms occur.
The term recurrent literally means more than one unexpected panic attack. The term unex-
pected refers to a panic attack for which there is no obvious cue or trigger at the time of oc-
currence—that is, the attack appears to occur from out of the blue, such as when the
individual is relaxing or emerging from sleep (nocturnal panic attack). In contrast, expected
panic attacks are attacks for which there is an obvious cue or trigger, such as a situation in
which panic attacks typically occur. The determination of whether panic attacks are ex-
pected or unexpected is made by the clinician, who makes this judgment based on a com-
bination of careful questioning as to the sequence of events preceding or leading up to the
attack and the individual's own judgment of whether or not the attack seemed to occur for
no apparent reason, Cultural interpretations may influence the assignment of panic at-
tacks as expected or unexpected (see section “Culture-Related Diagnostic Issues” for this
disorder). In the United States and Europe, approximately one-half of individuals with
panic disorder have expected panic attacks as well as unexpected panic attacks. Thus, the
presence of expected panic attacks does not rule out the diagnosis of panic disorder. For
more details regarding expected versus unexpected panic attacks, see the text accompa-
nying panic attacks (pp. 214-217).
The frequency and severity of panic attacks vary widely. In terms of frequency, there
may be moderately frequent attacks (e.g., one per week) for months at a time, or short
bursts of more frequent attacks (e.g., daily) separated by weeks or months without any at-
tacks or with less frequent attacks (e.g., two per month) over many years. Persons who
have infrequent panic attacks resemble persons with more frequent panic attacks in terms
of panic attack symptoms, demographic characteristics, comorbidity with other disorders,
family history, and biological data. In terms of severity, individuals with panic disorder
may have both full-symptom (four or more symptoms) and limited-symptom (fewer than
four symptoms) attacks, and the number and type of panic attack symptoms frequently
differ from one panic attack to the next. However, more than one unexpected full-symp-
tom panic attack is required for the diagnosis of panic disorder.
The worries about panic attacks or their consequences usually pertain to physical con-
cerns, such as worry that panic attacks reflect the presence of life-threatening illnesses
(e.g., cardiac disease, seizure disorder); social concerns, such as embarrassment or fear of
being judged negatively by others because of visible panic symptoms; and concerns about
mental functioning, such as “going crazy” or losing control (Criterion B). The maladaptive
changes in behavior represent attempts to minimize or avoid panic attacks or their conse-
quences. Examples include avoiding physical exertion, reorganizing daily life to ensure
that help is available in the event of a panic attack, restricting usual daily activities, and
avoiding agoraphobia-type situations, such as leaving home, using public transportation,
or shopping. If agoraphobia is present, a separate diagnosis of agoraphobia is given.
210 Anxiety Disorders
Associated Features Supporting Diagnosis
One type of unexpected panic attack is a nocturnal panic attack (i.e., waking from sleep in
a state of panic, which differs from panicking after fully waking from sleep). In the United
States, this type of panic attack has been estimated to occur at least one time in roughly
one-quarter to one-third of individuals with panic disorder, of whom the majority also
have daytime panic attacks. In addition to worry about panic attacks and their conse-
quences, many individuals with panic disorder report constant or intermittent feelings of
anxiety that are more broadly related to health and mental health concerns. For example,
individuals with panic disorder often anticipate a catastrophic outcome from a mild phys-
ical symptom or medication side effect (e.g., thinking that they may have heart disease or
that a headache means presence of a brain tumor). Such individuals often are relatively in-
tolerant of medication side effects. In addition, there may be pervasive concerns about
abilities to complete daily tasks or withstand daily stressors, excessive use of drugs (e.g.,
alcohol, prescribed medications or illicit drugs) to control panic attacks, or extreme behav-
iors aimed at controlling panic attacks (e.g., severe restrictions on food intake or avoidance
of specific foods or medications because of concerns about physical symptoms that pro-
voke panic attacks).
Prevalence
In the general population, the 12-month prevalence estimate for panic disorder across the
United States and several European countries is about 2%-3% in adults and adolescents. In
the United States, significantly lower rates of panic disorder are reported among Latinos,
African Americans, Caribbean blacks, and Asian Americans, compared with non-Latino
whites; American Indians, by contrast, have significantly higher rates. Lower estimates
have been reported for Asian, African, and Latin American countries, ranging from 0.1%
to 0.8%. Females are more frequently affected than males, at a rate of approximately 2:1. The
gender differentiation occurs in adolescence and is already observable before age 14 years.
Although panic attacks occur in children, the overall prevalence of panic disorder is low
before age 14 years (<0.4%). The rates of panic disorder show a gradual increase during ad-
olescence, particularly in females, and possibly following the onset of puberty, and peak dur-
ing adulthood. The prevalence rates decline in older individuals (i.e., 0.7% in adults over
the age of 64), possibly reflecting diminishing severity to subclinical levels.
Development and Course
The median age at onset for panic disorder in the United States is 20-24 years. A small
number of cases begin in childhood, and onset after age 45 years is unusual but can occur.
The usual course, if the disorder is untreated, is chronic but waxing and waning. Some in-
dividuals may have episodic outbreaks with years of remission in between, and others
may have continuous severe symptomatology. Only a minority of individuals have full
remission without subsequent relapse within a few years. The course of panic disorder
typically is complicated by a range of other disorders, in particular other anxiety disor-
ders, depressive disorders, and substance use disorders (see section “Comorbidity” for
this disorder).
Although panic disorder is very rare in childhood, first occurrence of “fearful spells” is
often dated retrospectively back to childhood. As in adults, panic disorder in adolescents
tends to have a chronic course and is frequently comorbid with other anxiety, depressive,
and bipolar disorders. To date, no differences in the clinical presentation between adoles-
cents and adults have been found. However, adolescents may be less worried about addi-
tional panic attacks than are young adults. Lower prevalence of panic disorder in older
adults appears to be attributable to age-related “dampening” of the autonomic nervous
system response. Many older individuals with “panicky feelings” are observed to have a
“hybrid” of limited-symptom panic attacks and generalized anxiety. Also, older adults
Panic Disorder 211
tend to attribute their panic attacks to certain stressful situations, such as a medical pro-
cedure or social setting. Older individuals may retrospectively endorse explanations for
the panic attack (which would preclude the diagnosis of panic disorder), even if an attack
might actually have been unexpected in the moment (and thus qualify as the basis for a
panic disorder diagnosis). This may result in under-endorsement of unexpected panic at-
tacks in older individuals. Thus, careful questioning of older adults is required to assess
whether panic attacks were expected before entering the situation, so that unexpected
panic attacks and the diagnosis of panic disorder are not overlooked.
While the low rate of panic disorder in children could relate to difficulties in symptom
reporting, this seems unlikely given that children are capable of reporting intense fear or
panic in relation to separation and to phobic objects or phobic situations. Adolescents
might be less willing than adults to openly discuss panic attacks. Therefore, clinicians
should be aware that unexpected panic attacks do occur in adolescents, much as they do in
adults, and be attuned to this possibility when encountering adolescents presenting with
episodes of intense fear or distress.
Risk and Prognostic Factors
Temperamental. Negative affectivity (neuroticism) (i.e., proneness to experiencing neg-
ative emotions) and anxiety sensitivity (i.e., the disposition to believe that symptoms of
anxiety are harmful) are risk factors for the onset of panic attacks and, separately, for
worry about panic, although their risk status for the diagnosis of panic disorder is un-
known. History of “fearful spells” (i.e., limited-symptom attacks that do not meet full cri-
teria for a panic attack) may be a risk factor for later panic attacks and panic disorder.
Although separation anxiety in childhood, especially when severe, may precede the later
development of panic disorder, it is not a consistent risk factor.
Environmental. Reports of childhood experiences of sexual and physical abuse are more
common in panic disorder than in certain other anxiety disorders. Smoking is a risk factor
for panic attacks and panic disorder. Most individuals report identifiable stressors in the
months before their first panic attack (e.g., interpersonal stressors and stressors related to
physical well-being, such as negative experiences with illicit or prescription drugs, dis-
ease, or death in the family).
Genetic and physiological. It is believed that multiple genes confer vulnerability to panic
disorder. However, the exact genes, gene products, or functions related to the genetic re-
gions implicated remain unknown. Current neural systems models for panic disorder em-
phasize the amygdala and related structures, much as in other anxiety disorders. There is
an increased risk for panic disorder among offspring of parents with anxiety, depressive,
and bipolar disorders. Respiratory disturbance, such as asthma, is associated with panic
disorder, in terms of past history, comorbidity, and family history.
Culture-Related Diagnostic Issues
The rate of fears about mental and somatic symptoms of anxiety appears to vary across
cultures and may influence the rate of panic attacks and panic disorder. Also, cultural ex-
pectations may influence the classification of panic attacks as expected or unexpected. For
example, a Vietnamese individual who has a panic attack after walking out into a windy
environment (fring gid; “hit by the wind”) may attribute the panic attack to exposure to
wind as a result of the cultural syndrome that links these two experiences, resulting in clas-
sification of the panic attack as expected. Various other cultural syndromes are associated
with panic disorder, including ataque de nervios (“attack of nerves”) among Latin Ameri-
cans and khyél attacks and “soul loss” among Cambodians. Ataque de nervios may involve
trembling, uncontrollable screaming or crying, aggressive or suicidal behavior, and deper-
sonalization or derealization, which may be experienced longer than the few minutes typical
212 Anxiety Disorders
of panic attacks. Some clinical presentations of ataque de nervios fulfill criteria for condi-
tions other than panic attack (e.g., other specified dissociative disorder). These syndromes
impact the symptoms and frequency of panic disorder, including the individual's attribu-
tion of unexpectedness, as cultural syndromes may create fear of certain situations, rang-
ing from interpersonal arguments (associated with ataque de nervios), to types of exertion
(associated with khyél attacks), to atmospheric wind (associated with tring gié attacks).
Clarification of the details of cultural attributions may aid in distinguishing expected and
unexpected panic attacks. For more information regarding cultural syndromes, refer to the
“Glossary of Cultural Concepts of Distress” in the Appendix.
The specific worries about panic attacks or their consequences are likely to vary from
one culture to another (and across different age groups and gender). For panic disorder,
U.S. community samples of non-Latino whites have significantly less functional impair-
ment than African Americans. There are also higher rates of objectively defined severity in
non-Latino Caribbean blacks with panic disorder, and lower rates of panic disorder over-
all in both African American and Afro-Caribbean groups, suggesting that among individ-
uals of African descent, the criteria for panic disorder may be met only when there is
substantial severity and impairment.
Gender-Related Diagnostic Issues
The clinica! features of panic disorder do not appear to differ between males and females.
There is some evidence for sexual dimorphism, with an association between panic disor-
der and the catechol-O-methyltransferase (COMT) gene in females only.
Diagnostic Markers
Agents with disparate mechanisms of action, such as sodium lactate, caffeine, isoprotere-
nol, yohimbine, carbon dioxide, and cholecystokinin, provoke panic attacks in individuals
with panic disorder to a much greater extent than in healthy control subjects (and in some
cases, than in individuals with other anxiety, depressive, or bipolar disorders without
panic attacks). Also, for a proportion of individuals with panic disorder, panic attacks are
related to hypersensitive medullary carbon dioxide detectors, resulting in hypocapnia and
other respiratory irregularities. However, none of these laboratory findings are consid-
ered diagnostic of panic disorder.
Suicide Risk
Panic attacks and a diagnosis of panic disorder in the past 12 months are related toa higher
rate of suicide attempts and suicidal ideation in the past 12 months even when comorbid-
ity and a history of childhood abuse and other suicide risk factors are taken into account.
Functional Consequences of Panic Disorder
Panic disorder is associated with high levels of social, occupational, and physical disabil-
ity; considerable economic costs; and the highest number of medical visits among the anx-
iety disorders, although the effects are strongest with the presence of agoraphobia.
Individuals with panic disorder may be frequently absent from work or school for doctor
and emergency room visits, which can lead to unemployment or dropping out of school.
In older adults, impairment may be seen in caregiving duties or volunteer activities. Full-
symptom panic attacks typically are associated with greater morbidity (e.g., greater health
care utilization, more disability, poorer quality of life) than limited-symptom attacks.
Differential Diagnosis
Other specified anxiety disorder or unspecified anxiety disorder. Panic disorder should
not be diagnosed if full-symptom (unexpected) panic attacks have never been experienced. In
Panic Disorder 213
the case of only limited-symptom unexpected panic attacks, an other specified anxiety dis-
order or unspecified anxiety disorder diagnosis should be considered.
Anxiety disorder due to another medical condition. Panic disorder is not diagnosed if
the panic attacks are judged to be a direct physiological consequence of another medical
condition. Examples of medical conditions that can cause panic attacks include hyperthy-
roidism, hyperparathyroidism, pheochromocytoma, vestibular dysfunctions, seizure dis-
orders, and cardiopulmonary conditions (e.g., arrhythmias, supraventricular tachycardia,
asthma, chronic obstructive pulmonary disease [COPD]). Appropriate laboratory tests
{e.g., serum calcium levels for hyperparathyroidism; Holter monitor for arrhythmias) or
physical examinations (e.g., for cardiac conditions) may be helpful in determining the eti-
ological role of another medical condition.
Substance/medication-induced anxiety disorder. Panic disorder is not diagnosed if
the panic attacks are judged to be a direct physiological consequence of a substance. In-
toxication with central nervous system stimulants (e.g., cocaine, amphetamines, caffeine)
or cannabis and withdrawal from central nervous system depressants (e.g., alcohol, bar-
biturates) can precipitate a panic attack. However, if panic attacks continue to occur out-
side of the context of substance use (e.g., long after the effects of intoxication or withdrawal
have ended), a diagnosis of panic disorder should be considered. In addition, because
panic disorder may precede substance use in some individuals and may be associated
with increased substance use, especially for purposes of self-medication, a detailed history
should be taken to determine if the individual had panic attacks prior to excessive sub-
stance use. If this is the case, a diagnosis of panic disorder should be considered in addition
to a diagnosis of substance use disorder. Features such as onset after age 45 years or the
presence of atypical symptoms during a panic attack (e.g., vertigo, loss of consciousness,
loss of bladder or bowel control, slurred speech, amnesia) suggest the possibility that an-
other medical condition or a substance may be causing the panic attack symptoms.
Other mental disorders with panic attacks as an associated feature (e.g., other anxiety
disorders and psychotic disorders). Panic attacks that occur as a symptom of other anx-
iety disorders are expected (e.g., triggered by social situations in social anxiety disorder, by
phobic objects or situations in specific phobia or agoraphobia, by worry in generalized anx-
iety disorder, by separation from home or attachment figures in separation anxiety disorder)
and thus would not meet criteria for panic disorder. (Note: Sometimes an unexpected panic
attack is associated with the onset of another anxiety disorder, but then the attacks become
expected, whereas panic disorder is characterized by recurrent unexpected panic attacks.) If
the panic attacks occur only in response to specific triggers, then only the relevant anxiety
disorder is assigned. However, if the individual experiences unexpected panic attacks as
well and shows persistent concern and worry or behavioral change because of the attacks,
then an additional diagnosis of panic disorder should be considered.
Comorbidity
Panic disorder infrequently occurs in clinical settings in the absence of other psychopa-
thology. The prevalence of panic disorder is elevated in individuals with other disorders,
particularly other anxiety disorders (and especially agoraphobia), major depression, bipo-
lar disorder, and possibly mild alcohol use disorder. While panic disorder often has an ear-
lier age at onset than the comorbid disorder(s), onset sometimes occurs after the comorbid
disorder and may be seen as a severity marker of the comorbid illness.
Reported lifetime rates of comorbidity between major depressive disorder and panic
disorder vary widely, ranging from 10% to 65% in individuals with panic disorder. In ap-
proximately one-third of individuals with both disorders, the depression precedes the on-
set of panic disorder. In the remaining two-thirds, depression occurs coincident with or
following the onset of panic disorder. A subset of individuals with panic disorder develop
a substance-related disorder, which for some represents an attempt to treat their anxiety
214 Anxiety Disorders
with alcohol or medications. Comorbidity with other anxiety disorders and illness anxiety
disorder is also common.
Panic disorder is significantly comorbid with numerous general medical symptoms
and conditions, including, but not limited to, dizziness, cardiac arrhythmias, hyperthy-
roidism, asthma, COPD, and irritable bowel syndrome. However, the nature of the asso-
ciation (e.g., cause and effect) between panic disorder and these conditions remains
unclear. Although mitral valve prolapse and thyroid disease are more common among in-
dividuals with panic disorder than in the general population, the differences in prevalence
are not consistent.
Panic Attack Specifier
Note: Symptoms are presented for the purpose of identifying a panic attack; however,
panic attack is not a mental disorder and cannot be coded. Panic attacks can occur in the
context of any anxiety disorder as well as other mental disorders (e.g., depressive disor-
ders, posttraumatic stress disorder, substance use disorders) and some medical condi-
tions (e.g., cardiac, respiratory, vestibular, gastrointestinal). When the presence of a panic
attack is identified, it should be noted as a specifier (e.g., “posttraumatic stress disorder
with panic attacks”). For panic disorder, the presence of panic attack is contained within
the criteria for the disorder and panic attack is not used as a specifier.
An abrupt surge of intense fear or intense discomfort that reaches a peak within minutes,
and during which time four (or more) of the following symptoms occur:
Note: The abrupt surge can occur from a calm state or an anxious state.
1. Palpitations, pounding heart, or accelerated heart rate.
2. Sweating.
3. Trembling or shaking.
4. Sensations of shortness of breath or smothering.
5. Feelings of choking.
6. Chest pain or discomfort.
7. Nausea or abdominal distress.
8. Feeling dizzy, unsteady, light-headed, or faint.
9. Chilis or heat sensations.
10. Paresthesias (numbness or tingling sensations).
11. Derealization (feelings of unreality) or depersonalization (being detached from oneself).
12. Fear of losing control or “going crazy.”
13. Fear of dying.
Note: Culture-specific symptoms (e.g., tinnitus, neck soreness, headache, uncontrollable
screaming or crying) may be seen. Such symptoms should not count as one of the four
required symptoms.
Features
The essential feature of a panic attack is an abrupt surge of intense fear or intense discomfort
that reaches a peak within minutes and during which time four or more of 13 physical and cog-
nitive symptoms occur. Eleven of these 13 symptoms are physical (e.g., palpitations, sweat-
ing), while two are cognitive (i.e., fear of losing control or going crazy, fear of dying). “Fear of
going crazy” is a colloquialism often used by individuals with panic attacks and is not in-
tended as a pejorative or diagnostic term. The term within minutes means that the time to peak
Panic Attack Specifier 215
intensity is literally only a few minutes. A panic attack can arise from either a calm state or an
anxious state, and time to peak intensity should be assessed independently of any preceding
anxiety. That is, the start of the panic attack is the point at which there is an abrupt increase in
discomfort rather than the point at which anxiety first developed. Likewise, a panic attack can
return to either an anxious state or a calm state and possibly peak again. A panic attack is dis-
tinguished from ongoing anxiety by its time to peak intensity, which occurs within minutes; its
discrete nature; and its typically greater severity. Attacks that meet all other criteria but have
fewer than four physical and/or cognitive symptoms are referred to as limited-symptom attacks.
There are two characteristic types of panic attacks: expected and unexpected. Expected
panic attacks are attacks for which there is an obvious cue or trigger, such as situations in
which panic attacks have typically occurred. Unexpected panic attacks are those for which
there is no obvious cue or trigger at the time of occurrence (e.g., when relaxing or out of
sleep [nocturnal panic attack]). The determination of whether panic attacks are expected
or unexpected is made by the clinician, who makes this judgment based on a combination
of careful questioning as to the sequence of events preceding or leading up to the attack
and the individual’s own judgment of whether or not the attack seemed to occur for no ap-
parent reason. Cultural interpretations may influence their determination as expected or
unexpected. Culture-specific symptoms (e.g., tinnitus, neck soreness, headache, uncon-
trollable screaming or crying) may be seen; however, such symptoms should not count as
one of the four required symptoms. Panic attacks can occur in the context of any mental
disorder (e.g., anxiety disorders, depressive disorders, bipolar disorders, eating disorders,
obsessive-compulsive and related disorders, personality disorders, psychotic disorders,
substance use disorders) and some medical conditions (e.g., cardiac, respiratory, vestibu-
lar, gastrointestinal), with the majority never meeting criteria for panic disorder. Recur-
rent unexpected panic attacks are required for a diagnosis of panic disorder.
Associated Features
One type of unexpected panic attack is a nocturnal panic attack (i.e., waking from sleep ina
state of panic), which differs from panicking after fully waking from sleep. Panic attacks
are related to a higher rate of suicide attempts and suicidal ideation even when comorbid-
ity and other suicide risk factors are taken into account.
Prevalence
In the general population, 12-month prevalence estimates for panic attacks in the United
States is 11.2% in adults. Twelve-month prevalence estimates do not appear to differ sig-
nificantly among African Americans, Asian Americans, and Latinos. Lower 12-month
prevalence estimates for European countries appear to range from 2.7% to 3.3%. Females
are more frequently affected than males, although this gender difference is more pro-
nounced for panic disorder. Panic attacks can occur in children but are relatively rare until
the age of puberty, when the prevalence rates increase. The prevalence rates decline in
older individuals, possibly reflecting diminishing severity to subclinical levels.
Development and Course
The mean age at onset for panic attacks in the United States is approximately 22-23 years
among adults. However, the course of panic attacks is likely influenced by the course of
any co-occurring mental disorder(s) and stressful life events. Panic attacks are uncommon,
and unexpected panic attacks are rare, in preadolescent children. Adolescents might be
less willing than adults to openly discuss panic attacks, even though they present with ep-
isodes of intense fear or discomfort. Lower prevalence of panic attacks in older individuals
may be related to a weaker autonomic response to emotional states relative to younger in-
dividuals. Older individuals may be less inclined to use the word “fear” and more inclined
216 Anxiety Disorders
to use the word “discomfort” to describe panic attacks. Older individuals with “panicky
feelings” may have a hybrid of limited-symptom attacks and generalized anxiety. In
addition, older individuals tend to attribute panic attacks to certain situations that are
stressful (e.g., medical procedures, social settings) and may retrospectively endorse expla-
nations for the panic attack even if it was unexpected in the moment. This may result in un-
der-endorsement of unexpected panic attacks in older individuals.
Risk and Prognostic Factors
Temperamental. Negative affectivity (neuroticism) (i.e., proneness to experiencing neg-
ative emotions) and anxiety sensitivity (i.e., the disposition to believe that symptoms of
anxiety are harmful) are risk factors for the onset of panic attacks. History of “fearful
spells” (i.e., limited-symptom attacks that do not meet full criteria for a panic attack) may
be a risk factor for later panic attacks.
Environmental. Smoking is a risk factor for panic attacks. Most individuals report iden-
tifiable stressors in the months before their first panic attack (e.g., interpersonal stressors
and stressors related to physical well-being, such as negative experiences with illicit or
prescription drugs, disease, or death in the family).
Culture-Related Diagnostic issues
Cultural interpretations may influence the determination of panic attacks as expected or
unexpected. Culture-specific symptoms (e.g., tinnitus, neck soreness, headache, and un-
controllable screaming or crying) may be seen; however, such symptoms should not count
as one of the four required symptoms. Frequency of each of the 13 symptoms varies cross-
culturally (e.g., higher rates of paresthesias in African Americans and of dizziness in sev-
eral Asian groups). Cultural syndromes also influence the cross-cultural presentation of
panic attacks, resulting in different symptom profiles across different cultural groups. Ex-
amples include khyél (wind) attacks, a Cambodian cultural syndrome involving dizziness,
tinnitus, and neck soreness; and trting gid (wind-related) attacks, a Vietnamese cultural
syndrome associated with headaches. Ataque de nervios (attack of nerves) is a cultural syn-
drome among Latin Americans that may involve trembling, uncontrollable screaming or
crying, aggressive or suicidal behavior, and depersonalization or derealization, and which
may be experienced for longer than only a few minutes. Some clinical presentations of
ataque de nervios fulfill criteria for conditions other than panic attack (e.g., other specified
dissociative disorder). Also, cultural expectations may influence the classification of panic
attacks as expected or unexpected, as cultural syndromes may create fear of certain situa-
tions, ranging from interpersonal arguments (associated with ataque de nervios), to types of
exertion (associated with khyél attacks), to atmospheric wind (associated with triing gid at-
tacks). Clarification of the details of cultural attributions may aid in distinguishing ex-
pected and unexpected panic attacks. For more information about cultural syndromes, see
“Glossary of Cultural Concepts of Distress” in the Appendix to this manual.
Gender-Related Diagnostic Issues
Panic attacks are more common in females than in males, but clinical features or symp-
toms of panic attacks do not differ between males and females.
Diagnostic Markers
Physiological recordings of naturally occurring panic attacks in individuals with panic
disorder indicate abrupt surges of arousal, usually of heart rate, that reach a peak within
minutes and subside within minutes, and for a proportion of these individuals the panic
attack may be preceded by cardiorespiratory instabilities.
Agoraphobia 217
Functional Consequences of Panic Attacks
In the context of,co-occurring mental disorders, including anxiety disorders, depressive
disorders, bipolar disorder, substance use disorders, psychotic disorders, and personality
disorders, panic attacks are associated with increased symptom severity, higher rates of
comorbidity and suicidality, and poorer treatment response. Also, full-symptom panic at-
tacks typically are associated with greater morbidity (e.g., greater health care utilization,
more disability, poorer quality of life) than limited-symptom attacks.
Differential Diagnosis
Other paroxysmal episodes (e.g., “anger attacks”). Panic attacks should not be diag-
nosed if the episodes do not involve the essential feature of an abrupt surge of intense fear
or intense discomfort, but rather other emotional states (e.g., anger, grief).
Anxiety disorder due to another medical condition. Medical conditions that can cause
or be misdiagnosed as panic attacks include hyperthyroidism, hyperparathyroidism, pheo-
chromocytoma, vestibular dysfunctions, seizure disorders, and cardiopulmonary con-
ditions (e.g., arrhythmias, supraventricular tachycardia, asthma, chronic obstructive
pulmonary disease). Appropriate laboratory tests (e.g., serum calcium levels for hyperpara-
thyroidism; Holter monitor for arrhythmias) or physical examinations (e.g., for cardiac con-
ditions) may be helpful in determining the etiological role of another medical condition.
Substance/medication-induced anxiety disorder. Intoxication with central nervous
system stimulants (e.g., cocaine, amphetamines, caffeine) or cannabis and withdrawal
from central nervous system depressants (e.g., alcohol, barbiturates) can precipitate a
panic attack. A detailed history should be taken to determine if the individual had panic
attacks prior to excessive substance use. Features such as onset after age 45 years or the
presence of atypical symptoms during a panic attack (e.g., vertigo, loss of consciousness,
loss of bladder or bowel control, slurred speech, or amnesia) suggest the possibility that a
medical condition or a substance may be causing the panic attack symptoms.
Panic disorder. Repeated unexpected panic attacks are required but are not sufficient for
the diagnosis of panic disorder (i.e., full diagnostic criteria for panic disorder must be met).
Comorbidity
Panic attacks are associated with increased likelihood of various comorbid mental dis-
orders, including anxiety disorders, depressive disorders, bipolar disorders, impulse-
control disorders, and substance use disorders. Panic attacks are associated with increased
likelihood of later developing anxiety disorders, depressive disorders, bipolar disorders,
and possibly other disorders.
Agoraphobia
Diagnostic Criteria 300.22 (F40.00)
A. Marked fear or anxiety about two (or more) of the following five situations:
1. Using public transportation (e.g., automobiles, buses, trains, ships, planes).
Being in open spaces (e.g., parking lots, marketplaces, bridges).
Being in enclosed places (e.g., shops, theaters, cinemas).
Standing in line or being in a crowd.
5. Being outside of the home alone.
B. The individual fears or avoids these situations because of thoughts that escape might
be difficult or help might not be available in the event of developing panic-like symp-
oN
218 Anxiety Disorders
toms or other incapacitating or embarrassing symptoms (e.g., fear of falling in the el-
derly; fear of incontinence).
C. The agoraphobic situations almost always provoke fear or anxiety.
D. The agoraphobic situations are actively avoided, require the presence of a companion,
or are endured with intense fear or anxiety.
E. The fear or anxiety is out of proportion to the actual danger posed by the agoraphobic
situations and to the sociocultural context.
F. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
G. The fear, anxiety, or avoidance causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
H. If another medical condition (e.g., inflammatory bowel disease, Parkinson’s disease)
is present, the fear, anxiety, or avoidance is clearly excessive.
|. The fear, anxiety, or avoidance is not better explained by the symptoms of another men-
tal disorder—for example, the symptoms are not confined to specific phobia, situational
type; do not involve only social situations (as in social anxiety disorder); and are not re-
lated exclusively to obsessions (as in obsessive-compulsive disorder), perceived defects
or flaws in physical appearance (as in body dysmorphic disorder), reminders of traumatic
events (as in posttraumatic stress disorder), or fear of separation (as in separation anx-
iety disorder).
Note: Agoraphobia is diagnosed irrespective of the presence of panic disorder. If an indi-
vidual’s presentation meets criteria for panic disorder and agoraphobia, both diagnoses
should be assigned.
Diagnostic Features
The essential feature of agoraphobia is marked, or intense, fear or anxiety triggered by the
real or anticipated exposure to a wide range of situations (Criterion A). The diagnosis re-
quires endorsement of symptoms occurring in at least two of the following five situations:
1) using public transporation, such as automobiles, buses, trains, ships, or planes; 2) being
in open spaces, such as parking lots, marketplaces, or bridges; 3) being in enclosed spaces,
such as shops, theaters, or cinemas; 4) standing in line or being in a crowd; or 5) being out-
side of the home alone. The examples for each situation are not exhaustive; other situations
may be feared. When experiencing fear and anxiety cued by such situations, individuals
typically experience thoughts that something terrible might happen (Criterion B). Individ-
uals frequently believe that escape from such situations might be difficult (e.g., “can’t get
out of here”) or that help might be unavailable (e.g., “there is nobody to help me”) when
panic-like symptoms or other incapacitating or embarrassing symptoms occur. “Panic-like
symptoms” refer to any of the 13 symptoms included in the criteria for panic attack, such as
dizziness, faintness, and fear of dying. “Other incapacitating or embarrassing symptoms”
include symptoms such as vomiting and inflammatory bowel symptoms, as well as, in
older adults, a fear of falling or, in children, a sense of disorientation and getting lost.
The amount of fear experienced may vary with proximity to the feared situation and
may occur in anticipation of or in the actual presence of the agoraphobic situation. Also,
the fear or anxiety may take the form of a full- or limited-symptom panic attack (i.e., an ex-
pected panic attack). Fear or anxiety is evoked nearly every time the individual comes into
contact with the feared situation (Criterion C). Thus, an individual who becomes anxious
only occasionally in an agoraphobic situation (e.g., becomes anxious when standing in line
on only one out of every five occasions) would not be diagnosed with agoraphobia. The in-
dividual actively avoids the situation or, if he or she either is unable or decides not to avoid
it, the situation evokes intense fear or anxiety (Criterion D). Active avoidance means the in-
dividual is currently behaving in ways that are intentionally designed to prevent or min-
imize contact with agoraphobic situations. Avoidance can be behavioral (e.g., changing
Agoraphobia 219
daily routines, choosing a job nearby to avoid using public transportation, arranging for
food delivery to avoid entering shops and supermarkets) as well as cognitive (e.g., using
distraction to getthrough agoraphobic situations) in nature. The avoidance can become so
severe that the person is completely homebound. Often, an individual is better able to con-
front a feared situation when accompanied by a companion, such as a partner, friend, or
health professional.
The fear, anxiety, or avoidance must be out of proportion to the actual danger posed by
the agoraphobic situations and to the sociocultural context (Criterion E). Differentiating
clinically significant agoraphobic fears from reasonable fears (e.g., leaving the house dur-
ing a bad storm) or from situations that are deemed dangerous (e.g., walking in a parking
lot or using public transportation in a high-crime area) is important for a number of reasons.
First, what constitutes avoidance may be difficult to judge across cultures and sociocultural
contexts (e.g., it is socioculturally appropriate for orthodox Muslim women in certain parts
of the world to avoid leaving the house alone, and thus such avoidance would not be con-
sidered indicative of agoraphobia). Second, older adults are likely to overattribute their
fears to age-related constraints and are less likely to judge their fears as being out of pro-
portion to the actual risk. Third, individuals with agoraphobia are likely to overestimate
danger in relation to panic-like or other bodily symptoms. Agoraphobia should be diag-
nosed only if the fear, anxiety, or avoidance persists (Criterion F) and if it causes clinically
significant distress or impairment in social, occupational, or other important areas of func-
tioning (Criterion G). The duration of “typically lasting for 6 months or more” is meant to
exclude individuals with short-lived, transient problems. However, the duration criterion
should be used as a general guide, with allowance for some degree of flexibility.
Assoclated Features Supporting Diagnosis
In its most severe forms, agoraphobia can cause individuals to become completely home-
bound, unable to leave their home and dependent on others for services or assistance to pro-
vide even for basic needs. Demoralization and depressive symptoms, as well as abuse of
alcohol and sedative medication as inappropriate self-medication strategies, are common.
Prevalence
Every year approximately 1.7% of adolescents and adults have a diagnosis of agoraphobia.
Females are twice as likely as males to experience agoraphobia. Agoraphobia may occur in
childhood, but incidence peaks in late adolescence and early adulthood. Twelve-month
prevalence in individuals older than 65 years is 0.4%. Prevalence rates do not appear to
vary systematically across cultural/racial groups.
Development and Course
The percentage of individuals with agoraphobia reporting panic attacks or panic disorder
preceding the onset of agoraphobia ranges from 30% in community samples to more than
50% in clinic samples. The majority of individuals with panic disorder show signs of anx-
iety and agoraphobia before the onset of panic disorder.
In two-thirds of all cases of agoraphobia, initial onset is before age 35 years. There is a
substantial incidence risk in late adolescence and early adulthood, with indications for
a second high incidence risk phase after age 40 years. First onset in childhood is rare. The
overall mean age at onset for agoraphobia is 17 years, although the age at onset without
preceding panic attacks or panic disorder is 25-29 years.
The course of agoraphobia is typically persistent and chronic. Complete remission is
rare (10%), unless the agoraphobia is treated. With more severe agoraphobia, rates of full
remission decrease, whereas rates of relapse and chronicity increase. A range of other dis-
orders, in particular other anxiety disorders, depressive disorders, substance use disor-
ders, and personality disorders, may complicate the course of agoraphobia. The long-term
220 Anxiety Disorders
course and outcome of agoraphobia are associated with substantially elevated risk of sec-
ondary major depressive disorder, persistent depressive disorder (dysthymia), and sub-
stance use disorders.
The clinical features of agoraphobia are relatively consistent across the lifespan, although
the type of agoraphobic situations triggering fear, anxiety, or avoidance, as well as the type of
cognitions, may vary. For example, in children, being outside of the home alone is the most fre-
quent situation feared, whereas in older adults, being in shops, standing in line, and being in
open spaces are most often feared. Also, cognitions often pertain to becoming lost (in children),
to experiencing panic-like symptoms (in adults), to falling (in older adults).
The low prevalence of agoraphobia in children could reflect difficulties in symptom re-
porting, and thus assessments in young children may require solicitation of information
from multiple sources, including parents or teachers. Adolescents, particularly males,
may be less willing than adults to openly discuss agoraphobic fears and avoidance; how-
ever, agoraphobia can occur prior to adulthood and should be assessed in children and
adolescents. In older adults, comorbid somatic symptom disorders, as well as motor dis-
turbances (e.g., sense of falling or having medical complications), are frequently men-
tioned by individuals as the reason for their fear and avoidance. In these instances, care is
to be taken in evaluating whether the fear and avoidance are out of proportion to the real
danger involved.
Risk and Prognostic Factors
Temperamental. Behavioral inhibition and neurotic disposition (i.e., negative affectivity
[neuroticism] and anxiety sensitivity) are closely associated with agoraphobia but are rel-
evant to most anxiety disorders (phobic disorders, panic disorder, generalized anxiety dis-
order). Anxiety sensitivity (the disposition to believe that symptoms of anxiety are
harmful) is also characteristic of individuals with agoraphobia.
Environmental. Negative events in childhood (e.g., separation, death of parent) and other
stressful events, such as being attacked or mugged, are associated with the onset of agorapho-
bia. Furthermore, individuals with agoraphobia describe the family climate and child-rearing
behavior as being characterized by reduced warmth and increased overprotection.
Genetic and physiological. Heritability for agoraphobia is 61%. Of the various phobias,
agoraphobia has the strongest and most specific association with the genetic factor that
represents proneness to phobias.
Gender-Reiated Diagnostic Issues
Females have different patterns of comorbid disorders than males. Consistent with gender
differences in the prevalence of mental disorders, males have higher rates of comorbid
substance use disorders.
Functional Consequences of Agoraphobia
Agoraphobia is associated with considerable impairment and disability in terms of role
functioning, work productivity, and disability days. Agoraphobia severity is a strong de-
terminant of the degree of disability, irrespective of the presence of comorbid panic disor-
der, panic attacks, and other comorbid conditions. More than one-third of individuals
with agoraphobia are completely homebound and unable to work.
Differential Diagnosis
When diagnostic criteria for agoraphobia and another disorder are fully met, both diagnoses
should be assigned, unless the fear, anxiety, or avoidance of agoraphobia is attributable to the
other disorder. Weighting of criteria and clinical judgment may be helpful in some cases.
Agoraphobia 221
Specific phobia, situational type. Differentiating agoraphobia from situational specific
phobia can be challenging in some cases, because these conditions share several symptom
characteristics and criteria. Specific phobia, situational type, should be diagnosed versus ago-
raphobia if the fear, anxiety, or avoidance is limited to one of the agoraphobic situations.
Requiring fears from two or more of the agoraphobic situations is a robust means for differen-
tiating agoraphobia from specific phobias, particularly the situational subtype. Additional dif-
ferentiating features include the cognitive ideation. Thus, if the situation is feared for reasons
other than panic-like symptoms or other incapacitating or embarrassing symptoms (e.g., fears
of being directly harmed by the situation itself, such as fear of the plane crashing for individ-
uals who fear flying), then a diagnosis of specific phobia may be more appropriate.
Separation anxiety disorder. Separation anxiety disorder can be best differentiated
from agoraphobia by examining cognitive ideation. In separation anxiety disorder, the
thoughts are about detachment from significant others and the home environment (i.e.,
parents or other attachment figures), whereas in agoraphobia the focus is on panic-like
symptoms or other incapacitating or embarrassing symptoms in the feared situations.
Social anxiety disorder (social phobia). Agoraphobia should be differentiated from so-
cial anxiety disorder based primarily on the situational clusters that trigger fear, anxiety,
or avoidance and the cognitive ideation. In social anxiety disorder, the focus is on fear of
being negatively evaluated.
Panic disorder. When criteria for panic disorder are met, agoraphobia should not be di-
agnosed if the avoidance behaviors associated with the panic attacks do not extend to avoid-
ance of two or more agoraphobic situations.
Acute stress disorder and posttraumatic stress disorder. Acute stress disorder and
posttraumatic stress disorder (PTSD) can be differentiated from agoraphobia by examin-
ing whether the fear, anxiety, or avoidance is related only to situations that remind the
individual of a traumatic event. If the fear, anxiety, or avoidance is restricted to trauma re-
minders, and if the avoidance behavior does not extend to two or more agoraphobic situ-
ations, then a diagnosis of agoraphobia is not warranted.
Major depressive disorder. In major depressive disorder, the individual may avoid leav-
ing home because of apathy, loss of energy, low self-esteem, and anhedonia. If the avoid-
ance is unrelated to fears of panic-like or other incapacitating or embarrassing symptoms,
then agoraphobia should not be diagnosed.
Other medical conditions. Agoraphobia is not diagnosed if the avoidance of situations
is judged to be a physiological consequence of a medical condition. This determination is
based on history, laboratory findings, and a physical examination. Other relevant medical
conditions may include neurodegenerative disorders with associated motor disturbances
(e.g., Parkinson's disease, multiple sclerosis), as well as cardiovascular disorders. Individ-
uals with certain medical conditions may avoid situations because of realistic concerns
about being incapacitated (e.g., fainting in an individual with transient ischemic attacks)
or being embarrassed (e.g., diarrhea in an individual with Crohn’s disease). The diagnosis
of agoraphobia should be given only when the fear or avoidance is clearly in excess of that
usually associated with these medical conditions.
Comorbidity
The majority of individuals with agoraphobia also have other mental disorders. The most
frequent additional diagnoses are other anxiety disorders (e.g., specific phobias, panic dis-
order, social anxiety disorder), depressive disorders (major depressive disorder), PTSD,
and alcohol use disorder. Whereas other anxiety disorders (e.g., separation anxiety disor-
der, specific phobias, panic disorder) frequently precede onset of agoraphobia, depressive
disorders and substance use disorders typically occur secondary to agoraphobia.
222 Anxiety Disorders
Generalized Anxiety Disorder
Diagnostic Criteria 300.02 (F41.1)
A. Excessive anxiety and worry (apprehensive expectation), occurring more days than
not for at least 6 months, about a number of events or activities (such as work or school
performance).
B. The individual finds it difficult to control the worry.
C. The anxiety and worry are associated with three (or more) of the following six symp-
toms (with at least some symptoms having been present for more days than not for the
past 6 months):
Note: Only one item is required in children.
Restlessness or feeling keyed up or on edge.
Being easily fatigued.
Difficulty concentrating or mind going blank.
Irritability.
Muscle tension.
Sleep disturbance (difficulty falling or staying asleep, or restless, unsatisfying
sleep).
Oahaonn>=
D. The anxiety, worry, or physical symptoms cause clinically significant distress or impair-
ment in social, occupational, or other important areas of functioning.
E. The disturbance is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication) or another medical condition (e.g., hyperthyroidism).
F. The disturbance is not better explained by another mental disorder (e.g., anxiety or
worry about having panic attacks in panic disorder, negative evaluation in social anxi-
ety disorder {social phobia], contamination or other obsessions in obsessive-compul-
sive disorder, separation from attachment figures in separation anxiety disorder,
reminders of traumatic events in posttraumatic stress disorder, gaining weight in an-
orexia nervosa, physical complaints in somatic symptom disorder, perceived appear-
ance flaws in body dysmorphic disorder, having a serious illness in illness anxiety
disorder, or the content of delusional beliefs in schizophrenia or delusional disorder).
Diagnostic Features
The essential feature of generalized anxiety disorder is excessive anxiety and worry (ap-
prehensive expectation) about a number of events or activities. The intensity, duration, or
frequency of the anxiety and worry is out of proportion to the actual likelihood or impact
of the anticipated event. The individual finds it difficult to control the worry and to keep
worrisome thoughts from interfering with attention to tasks at hand. Adults with gener-
alized anxiety disorder often worry about everyday, routine life circumstances, such as
possible job responsibilities, health and finances, the health of family members, misfor-
tune to their children, or minor matters (e.g., doing household chores or being late for ap-
pointments). Children with generalized anxiety disorder tend to worry excessively about
their competence or the quality of their performance. During the course of the disorder,
the focus of worry may shift from one concern to another.
Several features distinguish generalized anxiety disorder from nonpathological anxiety.
First, the worries associated with generalized anxiety disorder are excessive and typically in-
terfere significantly with psychosocial functioning, whereas the worries of everyday life
are not excessive and are perceived as more manageable and may be put off when more
pressing matters arise. Second, the worries associated with generalized anxiety disorder are
Generalized Anxiety Disorder 223
more pervasive, pronounced, and distressing; have longer duration; and frequently occur
without precipitants. The greater the range of life circumstances about which a person
worries (e.g., finances, children’s safety, job performance), the more likely his or her symp-
toms are to meet criteria for generalized anxiety disorder. Third, everyday worries are much
less likely to be accompanied by physical symptoms (e.g., restlessness or feeling keyed up
or on edge). Individuals with generalized anxiety disorder report subjective distress due
to constant worry and related impairment in social, occupational, or other important areas
of functioning.
The anxiety and worry are accompanied by at least three of the following additional
symptoms: restlessness or feeling keyed up or on edge, being easily fatigued, difficulty
concentrating or mind going blank, irritability, muscle tension, and disturbed sleep, al-
though only one additional symptom is required in children.
Associated Features Supporting Diagnosls
Associated with muscle tension, there may be trembling, twitching, feeling shaky, and
muscle aches or soreness. Many individuals with generalized anxiety disorder also expe-
rience somatic symptoms (e.g., sweating, nausea, diarrhea) and an exaggerated startle re-
sponse. Symptoms of autonomic hyperarousal (e.g., accelerated heart rate, shortness of
breath, dizziness) are less prominent in generalized anxiety disorder than in other anxiety
disorders, such as panic disorder. Other conditions that may be associated with stress (e.g.,
irritable bowel syndrome, headaches) frequently accompany generalized anxiety disorder.
Prevalence
The 12-month prevalence of generalized anxiety disorder is 0.9% among adolescents and
2.9% among adults in the general community of the United States. The 12-month preva-
lence for the disorder in other countries ranges from 0.4% to 3.6%. The lifetime morbid risk
is 9.0%. Females are twice as likely as males to experience generalized anxiety disorder. The
prevalence of the diagnosis peaks in middle age and declines across the later years of life.
Individuals of European descent tend to experience generalized anxiety disorder more
frequently than do individuals of non-European descent (i.e., Asian, African, Native
American and Pacific Islander). Furthermore, individuals from developed countries are
more likely than individuals from nondeveloped countries to report that they have expe-
rienced symptoms that meet criteria for generalized anxiety disorder in their lifetime.
Development and Course
Many individuals with generalized anxiety disorder report that they have felt anxious and
nervous all of their lives. The median age at onset for generalized anxiety disorder is 30
years; however, age at onset is spread over a very broad range. The median age at onset is
later than that for the other anxiety disorders. The symptoms of excessive worry and anx-
iety may occur early in life but are then manifested as an anxious temperament. Onset of
the disorder rarely occurs prior to adolescence. The symptoms of generalized anxiety dis-
order tend to be chronic and wax and wane across the lifespan, fluctuating between syn-
dromal and subsyndromal forms of the disorder. Rates of full remission are very low.
The clinical expression of generalized anxiety disorder is relatively consistent across
the lifespan. The primary difference across age groups is in the content of the individual’s
worry. Children and adolescents tend to worry more about school and sporting perfor-
mance, whereas older adults report greater concern about the well-being of family or their
own physical heath. Thus, the content of an individual’s worry tends to be age appropri-
ate. Younger adults experience greater severity of symptoms than do older adults.
The earlier in life individuals have symptoms that meet criteria for generalized anxiety
disorder, the more comorbidity they tend to have and the more impaired they are likely to
224 Anxiety Disorders
be. The advent of chronic physical disease can be a potent issue for excessive worry in the
elderly. In the frail elderly, worries about safety—and especially about falling—may limit
activities. In those with early cognitive impairment, what appears to be excessive worry
about, for example, the whereabouts of things is probably better regarded as realistic
given the cognitive impairment.
In children and adolescents with generalized anxiety disorder, the anxieties and wor-
ries often concern the quality of their performance or competence at school or in sporting
events, even when their performance is not being evaluated by others. There may be ex-
cessive concerns about punctuality. They may also worry about catastrophic events, such
as earthquakes or nuclear war. Children with the disorder may be overly conforming, per-
fectionist, and unsure of themselves and tend to redo tasks because of excessive dissatis-
faction with less-than-perfect performance. They are typically overzealous in seeking
reassurance and approval and require excessive reassurance about their performance and
other things they are worried about.
Generalized anxiety disorder may be overdiagnosed in children. When this diagnosis
is being considered in children, a thorough evaluation for the presence of other childhood
anxiety disorders and other mental disorders should be done to determine whether the
wotries may be better explained by one of these disorders. Separation anxiety disorder, so-
cial anxiety disorder (social phobia), and obsessive-compulsive disorder are often accom-
panied by worries that may mimic those described in generalized anxiety disorder. For
example, a child with social anxiety disorder may be concerned about school performance
because of fear of humiliation. Worries about illness may also be better explained by sep-
aration anxiety disorder or obsessive-compulsive disorder.
Risk and Prognostic Factors
Temperamental. Behavioral inhibition, negative affectivity (neuroticism), and harm
avoidance have been associated with generalized anxiety disorder.
Environmental. Although childhood adversities and parental overprotection have been
associated with generalized anxiety disorder, no environmental factors have been identi-
fied as specific to generalized anxiety disorder or necessary or sufficient for making the di-
agnosis.
Genetic and physiological. One-third of the risk of experiencing generalized anxiety
disorder is genetic, and these genetic factors overlap with the risk of neuroticism and are
shared with other anxiety and mood disorders, particularly major depressive disorder.
Culture-Related Diagnostic Issues
There is considerable cultural variation in the expression of generalized anxiety disorder.
For example, in some cultures, somatic symptoms predominate in the expression of the
disorder, whereas in other cultures cognitive symptoms tend to predominate. This differ-
ence may be more evident on initial presentation than subsequently, as more symptoms
are reported over time. There is no information as to whether the propensity for excessive
worrying is related to culture, although the topic being worried about can be culture spe-
cific. It is important to consider the social and cultural context when evaluating whether
worries about certain situations are excessive.
Gender-Related Diagnostic Issues
In clinical settings, generalized anxiety disorder is diagnosed somewhat more frequently
in females than in males (about 55%-60% of those presenting with the disorder are
female). In epidemiological studies, approximately two-thirds are female. Females and
males who experience generalized anxiety disorder appear to have similar symptoms but
Generalized Anxiety Disorder 225
demonstrate different patterns of comorbidity consistent with gender differences in the
prevalence of disorders. In females, comorbidity is largely confined to the anxiety disor-
ders and unipolar depression, whereas in males, comorbidity is more likely to extend to
the substance use disorders as well.
Functional Consequences of
Generalized Anxiety Disorder
Excessive worrying impairs the individual's capacity to do things quickly and efficiently,
whether at home or at work. The worrying takes time and energy; the associated symp-
toms of muscle tension and feeling keyed up or on edge, tiredness, difficulty concentrat-
ing, and disturbed sleep contribute to the impairment. Importantly the excessive worrying
may impair the ability of individuals with generalized anxiety disorder to encourage con-
fidence in their children.
Generalized anxiety disorder is associated with significant disability and distress that is
independent of comorbid disorders, and most non-institutionalized adults with the disorder
are moderately to seriously disabled. Generalized anxiety disorder accounts for 110 mil-
lion disability days per annum in the U.S. population.
Differential Diagnosis
Anxiety disorder due to another medical condition. The diagnosis of anxiety disorder
associated with another medical condition should be assigned if the individual’s anxiety
and worry are judged, based on history, laboratory findings, or physica] examination, to
be a physiological effect of another specific medical condition (e.g., pheochromocytoma,
hyperthyroidism).
Substance/medication-induced anxiety disorder. A substance/medication-induced
anxiety disorder is distinguished from generalized anxiety disorder by the fact that a sub-
stance or medication (e.g., a drug of abuse, exposure to a toxin) is judged to be etiologically
related to the anxiety. For example, severe anxiety that occurs only in the context of heavy
coffee consumption would be diagnosed as caffeine-induced anxiety disorder.
Social anxiety disorder. Individuals with social anxiety disorder often have anticipa-
tory anxiety that is focused on upcoming social situations in which they must perform or
be evaluated by others, whereas individuals with generalized anxiety disorder worry,
whether or not they are being evaluated.
Obsessive-compulsive disorder. Several features distinguish the excessive worry of
generalized anxiety disorder from the obsessional thoughts of obsessive-compulsive dis-
order. In generalized anxiety disorder the focus of the worry is about forthcoming prob-
lems, and it is the excessiveness of the worry about future events that is abnormal. In
obsessive-compulsive disorder, the obsessions are inappropriate ideas that take the form of
intrusive and unwanted thoughts, urges, or images.
Posttraumatic stress disorder and adjustment disorders. Anxiety is invariably pres-
ent in posttraumatic stress disorder. Generalized anxiety disorder is not diagnosed if the
anxiety and worry are better explained by symptoms of posttraumatic stress disorder.
Anxiety may also be present in adjustment disorder, but this residual category should be
used only when the criteria are not met for any other disorder (including generalized anx-
iety disorder). Moreover, in adjustment disorders, the anxiety occurs in response to an
identifiable stressor within 3 months of the onset of the stressor and does not persist for
more than 6 months after the termination of the stressor or its consequences.
Depressive, bipolar, and psychotic disorders. Generalized anxiety/worry is a common
associated feature of depressive, bipolar, and psychotic disorders and should not be di-
226 Anxiety Disorders
agnosed separately if the excessive worry has occurred only during the course of these
conditions.
Comorbidity
Individuals whose presentation meets criteria for generalized anxiety disorder are likely
to have met, or currently meet, criteria for other anxiety and unipolar depressive disor-
ders. The neuroticism or emotional liability that underpins this pattern of comorbidity is
associated with temperamental antecedents and genetic and environmental risk factors
shared between these disorders, although independent pathways are also possible. Co-
morbidity with substance use, conduct, psychotic, neurodevelopmental, and neurocogni-
tive disorders is less common.
Substance/Medication-Induced
Anxiety Disorder
Diagnostic Criteria
A. Panic attacks or anxiety is predominant in the clinical picture.
B. There is evidence from the history, physical examination, or laboratory findings of both
(1) and (2):
1. The symptoms in Criterion A developed during or soon after substance intoxication
or withdrawal or after exposure to a medication.
2. The involved substance/medication is capable of producing the symptoms in Crite-
rion A.
C. The disturbance is not better explained by an anxiety disorder that is not substance/
medication-induced. Such evidence of an independent anxiety disorder could include
the following:
The symptoms precede the onset of the substance/medication use; the symptoms
persist for a substantial period of time (e.g., about 1 month) after the cessation of
acute withdrawal or severe intoxication; or there is other evidence suggesting the
existence of an independent non-substance/medication-induced anxiety disorder
(e.g., a history of recurrent non-substance/medication-related episodes).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
Note: This diagnosis should be made instead of a diagnosis of substance intoxication or
substance withdrawal only when the symptoms in Criterion A predominate in the clinical
picture and they are sufficiently severe to warrant clinical attention.
Coding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance/medica-
tion]-induced anxiety disorders are indicated in the table below. Note that the ICD-10-CM
code depends on whether or not there is a comorbid substance use disorder present for
the same class of substance. If a mild substance use disorder is comorbid with the sub-
stance-induced anxiety disorder, the 4th position character is “1,” and the clinician should
record “mild [substance] use disorder” before the substance-induced anxiety disorder
(e.g., “mild cocaine use disorder with cocaine-induced anxiety disorder’). If a moderate or
severe substance use disorder is comorbid with the substance-induced anxiety disorder,
the 4th position character is “2,” and the clinician should record “moderate [substance] use
disorder” or “severe [substance] use disorder,” depending on the severity of the comorbid
substance use disorder. If there is no comorbid substance use disorder (e.g., after a one-
Substance/Medication-Induced Anxiety Disorder 227
time heavy use of the substance), then the 4th position character is “9,” and the clinician
should record only the substance-induced anxiety disorder.
——SS Se re
ICD-10-CM
With use
With use disorder, Without
disorder, moderate use
ICD-9-CM mild or severe disorder
Alcohol 291.89 F10.180 F10.280 F10.980
Caffeine 292.89 F15.180 F15.280 F15.980
Cannabis 292.89 F12.180 F12.280 F12.980
Phencyclidine 292.89 F16.180 F16.280 F16.980
Other hallucinogen 292.89 F16.180 F16.280 F16.980
Inhalant 292.89 F18.180 F18.280 F18.980
Opioid 292.89 F11.188 F11.288 F11.988
Sedative, hypnotic, or anxiolytic 292.89 F13.180 F13.280 F13.980
Amphetamine (or other 292.89 F15.180 F15.280 F15.980
stimulant)
Cocaine 292.89 F14.180 F14.280 F14,980
Other (or unknown) substance 292.89 F19.180 F19.280 F19.980
Specify if (see Table 1 in the chapter “Substance-Related and Addictive Disorders” for di-
agnoses associated with substance class):
With onset during intoxication: This specifier applies if criteria are met for intoxica-
tion with the substance and the symptoms develop during intoxication.
With onset during withdrawai: This specifier applies if criteria are met for withdrawal
from the substance and the symptoms develop during, or shortly after, withdrawal.
With onset after medication use: Symptoms may appear either at initiation of medi-
cation or after a modification or change in use.
Recording Procedures
ICD-9-CM. The name of the substance/medication-induced anxiety disorder begins
with the specific substance (e.g., cocaine, salbutamol) that is presumed to be causing the
anxiety symptoms. The diagnostic code is selected from the table included in the criteria
set, which is based on the drug class. For substances that do not fit into any of the classes
(e.g., salbutamol), the code for “other substance” should be used; and in cases in which
a substance is judged to be an etiological factor but the specific class of substance is un-
known, the category “unknown substance” should be used.
The name of the disorder is followed by the specification of onset (i.e., onset during in-
toxication, onset during withdrawal, with onset during medication use). Unlike the record-
ing procedures for ICD-10-CM, which combine the substance-induced disorder and
substance use disorder into a single code, for ICD-9-CM a separate diagnostic code is given
for the substance use disorder. For example, in the case of anxiety symptoms occurring dur-
ing withdrawal in a man witha severe lorazepam use disorder, the diagnosis is 292.89 loraz-
epam-induced anxiety disorder, with onset during withdrawal. An additional diagnosis of
304.10 severe lorazepam use disorder is also given. When more than one substance is judged
to play a significant role in the development of anxiety symptoms, each should be listed sep-
228 Anxiety Disorders
arately (e.g., 292.89 methylphenidate-induced anxiety disorder, with onset during intoxica-
tion; 292.89 salbutamol-induced anxiety disorder, with onset after medication use).
ICD-10-CM. The name of the substance/medication-induced anxiety disorder begins
with the specific substance (e.g., cocaine, salbutamol) that is presumed to be causing the
anxiety symptoms. The diagnostic code is selected from the table included in the criteria
set, which is based on the drug class and presence or absence of a comorbid substance use
disorder. For substances that do not fit into any of the classes (e.g., salbutamol), the code
for “other substance” should be used; and in cases in which a substance is judged to be an
etiological factor but the specific class of substance is unknown, the category “unknown
substance” should be used.
When recording the name of the disorder, the comorbid substance use disorder (if any)
is listed first, followed by the word “with,” followed by the name of the substance-induced
anxiety disorder, followed by the specification of onset (i.e., onset during intoxication,
onset during withdrawal, with onset during medication use). For example, in the case of
anxiety symptoms occurring during withdrawal in a man witha severe lorazepam use dis-
order, the diagnosis is F13.280 severe lorazepam use disorder with lorazepam-induced
anxiety disorder, with onset during withdrawal. A separate diagnosis of the comorbid se-
vere lorazepam use disorder is not given. If the substance-induced anxiety disorder occurs
without a comorbid substance use disorder (e.g., after a one-time heavy use of the substance),
no accompanying substance use disorder is noted (e.g., F16.980 psilocybin-induced anxi-
ety disorder, with onset during intoxication). When more than one substance is judged to
play a significant role in the development of anxiety symptoms, each should be listed sep-
arately (e.g., F15.280 severe methylphenidate use disorder with methylphenidate-induced
anxiety disorder, with onset during intoxication; F19.980 salbutamol-induced anxiety dis-
order, with onset after medication use).
Diagnostic Features
The essential features of substance/medication-induced anxiety disorder are prominent
symptoms of panic or anxiety (Criterion A) that are judged to be due to the effects of a sub-
stance (e.g.,a drug of abuse, a medication, or a toxin exposure). The panic or anxiety symp-
toms must have developed during or soon after substance intoxication or withdrawal or
after exposure to a medication, and the substances or medications must be capable of pro-
ducing the symptoms (Criterion B2). Substance /medication-induced anxiety disorder
due to a prescribed treatment for a mental disorder or another medical condition must
have its onset while the individual is receiving the medication (or during withdrawal, if a
withdrawal is associated with the medication). Once the treatment is discontinued, the
panic or anxiety symptoms will usually improve or remit within days to several weeks to
a month (depending on the half-life of the substance / medication and the presence of with-
drawal). The diagnosis of substance/medication-induced anxiety disorder should not be
given if the onset of the panic or anxiety symptoms precedes the substance / medication in-
toxication or withdrawal, or if the symptoms persist for a substantial period of time (i.e.,
usually longer than 1 month) from the time of severe intoxication or withdrawal. If the
panic or anxiety symptoms persist for substantial periods of time, other causes for the
symptoms should be considered.
The substance /medication-induced anxiety disorder diagnosis should be made in-
stead of a diagnosis of substance intoxication or substance withdrawal only when the
symptoms in Criterion A are predominant in the clinical picture and are sufficiently severe
to warrant independent clinical attention.
Associated Features Supporting Diagnosis
Panic or anxiety can occur in association with intoxication with the following classes of sub-
stances: alcohol, caffeine, cannabis, phencyclidine, other hallucinogens, inhalants, stimu-
Substance/Medication-Induced Anxiety Disorder 229
lants (including cocaine), and other (or unknown) substances. Panic or anxiety can occur in
association with withdrawal from the following classes of substances: alcohol; opioids; sed-
atives, hypnotics, and anxiolytics; stimulants (including cocaine); and other (or unknown)
substances. Some medications that evoke anxiety symptoms include anesthetics and anal-
gesics, sympathomimetics or other bronchodilators, anticholinergics, insulin, thyroid prep-
arations, oral contraceptives, antihistamines, antiparkinsonian medications, corticosteroids,
antihypertensive and cardiovascular medications, anticonvulsants, lithium carbonate, an-
tipsychotic medications, and antidepressant medications. Heavy metals and toxins (e.g.,
organophosphate insecticide, nerve gases, carbon monoxide, carbon dioxide, volatile sub-
stances such as gasoline and paint) may also cause panic or anxiety symptoms.
Prevalence
The prevalence of substance/medication-induced anxiety disorder is not clear. General
population data suggest that it may be rare, with a 12-month prevalence of approximately
0.002%. However, in clinical populations, the prevalence is likely to be higher.
Diagnostic Markers
Laboratory assessments (e.g., urine toxicology) may be useful to measure substance intox-
ication as part of an assessment for substance /medication-induced anxiety disorder.
Differential Diagnosis
Substance intoxication and substance withdrawal. Anxiety symptoms commonly oc-
cur in substance intoxication and substance withdrawal. The diagnosis of the substance-
specific intoxication or substance-specific withdrawal will usually suffice to categorize the
symptom presentation. A diagnosis of substance/medication-induced anxiety disorder
should be made in addition to substance intoxication or substance withdrawal when the
panic or anxiety symptoms are predominant in the clinical picture and are sufficiently se-
vere to warrant independent clinical attention. For example, panic or anxiety symptoms
are characteristic of alcohol withdrawal.
Anxiety disorder (i.e., not induced by a substance/medication). Substance/medication-
induced anxiety disorder is judged to be etiologically related to the substance / medication.
Substance /medication-induced anxiety disorder is distinguished from a primary anxiety
disorder based on the onset, course, and other factors with respect to substances /medica-
tions. For drugs of abuse, there must be evidence from the history, physical examination, or
laboratory findings for use, intoxication, or withdrawal. Substance /medication-induced
anxiety disorders arise only in association with intoxication or withdrawal states, whereas
primary anxiety disorders may precede the onset of substance/ medication use. The pres-
ence of features that are atypical of a primary anxiety disorder, such as atypical age at onset
(e.g., onset of panic disorder after age 45 years) or symptoms (e.g., atypical panic attack
symptoms such as true vertigo, loss of balance, loss of consciousness, loss of bladder con-
trol, headaches, slurred speech) may suggest a substance/medication-induced etiology. A
primary anxiety disorder diagnosis is warranted if the panic or anxiety symptoms persist
for a substantial period of time (about 1 month or longer) after the end of the substance in-
toxication or acute withdrawal or there is a history of an anxiety disorder.
Delirium. If panic or anxiety symptoms occur exclusively during the course of delirium,
they are considered to be an associated feature of the delirium and are not diagnosed sep-
arately.
Anxiety disorder due to another medical condition. If the panic or anxiety symptoms
are attributed to the physiological consequences of another medical condition {i-e., rather
than to the medication taken for the medical condition), anxiety disorder due to another
230 Anxiety Disorders
medical condition should be diagnosed. The history often provides the basis for such a
judgment. At times, a change in the treatment for the other medical condition (e.g., med-
ication substitution or discontinuation) may be needed to determine whether the medica-
tion is the causative agent (in which case the symptoms may be better explained by
substance/medication-induced anxiety disorder). If the disturbance is attributable to both
another medical condition and substance use, both diagnoses (i.e., anxiety disorder due to
another medical condition and substance/medication-induced anxiety disorder) may be
given. When there is insufficient evidence to determine whether the panic or anxiety symp-
toms are attributable to a substance/ medication or to another medical condition or are pri-
marty (i.e., not attributable to either a substance or another medical condition), a diagnosis
of other specified or unspecified anxiety disorder would be indicated.
Anxiety Disorder Due to
Another Medical Condition
Diagnostic Criteria 293.84 (F06.4)
A. Panic attacks or anxiety is predominant in the clinical picture.
B. There is evidence from the history, physical examination, or laboratory findings that the dis-
turbance is the direct pathophysiological consequence of another medical condition.
. The disturbance is not better explained by another mental disorder.
. The disturbance does not occur exclusively during the course of a delirium.
. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
moo
Coding note: Include the name of the other medical condition within the name of the men-
tal disorder (e.g., 293.84 [F06.4] anxiety disorder due to pheochromocytoma). The other
medical condition should be coded and listed separately immediately before the anxiety
disorder due to the medical condition (e.g., 227.0 [D35.00] pheochromocytoma; 293.84
[F06.4] anxiety disorder due to pheochromocytoma.
Diagnostic Features
The essential feature of anxiety disorder due to another medical condition is clinically signifi-
cant anxiety that is judged to be best explained as a physiological effect of another medical con-
dition. Symptoms can include prominent anxiety symptoms or panic attacks (Criterion A).
The judgment that the symptoms are best explained by the associated physical condition must
be based on evidence from the history, physical examination, or laboratory findings (Criterion
B). Additionally, it must be judged that the symptoms are not better accounted for by another
mental disorder, in particular, adjustment disorder, with anxiety, in which the stressor is the
medical condition (Criterion C). In this case, an individual with adjustment disorder is espe-
cially distressed about the meaning or the consequences of the associated medical condition.
By contrast, there is often a prominent physical component to the anxiety (e.g., shortness of
breath) when the anxiety is due to another medical condition. The diagnosis is not made if the
anxiety symptoms occur only during the course of a delirium (Criterion D). The anxiety symp-
toms must cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning (Criterion E).
In determining whether the anxiety symptoms are attributable to another medical con-
dition, the clinician must first establish the presence of the medical condition. Further-
more, it must be established that anxiety symptoms can be etiologically related to the
medical condition through a physiological mechanism before making a judgment that this
is the best explanation for the symptoms in a specific individual. A careful and compre-
Anxiety Disorder Due to Another Medical Condition 231
hensive assessment of multiple factors is necessary to make this judgment. Several aspects
of the clinical presentation should be considered: 1) the presence of a clear temporal asso-
ciation between the onset, exacerbation, or remission of the medical condition and the anx-
iety symptoms; 2) the presence of features that are atypical of a primary anxiety disorder
(e.g., atypical age at onset or course); and 3) evidence in the literature that a known phys-
iological mechanism (e.g., hyperthyroidism) causes anxiety. In addition, the disturbance
must not be better explained by a primary anxiety disorder, a substance/medication-
induced anxiety disorder, or another primary mental disorder (e.g., adjustment disorder).
Associated Features Supporting Diagnosis
A number of medical conditions are known to include anxiety as a symptomatic manifes-
tation. Examples include endocrine disease (e.g., hyperthyroidism, pheochromocytoma,
hypoglycemia, hyperadrenocortisolism), cardiovascular disorders (e.g., congestive heart
failure, pulmonary embolism, arrhythmia such as atrial fibrillation), respiratory illness
(e.g., chronic obstructive pulmonary disease, asthma, pneumonia), metabolic distur-
bances (e.g., vitamin B,) deficiency, porphyria), and neurological illness (e.g., neoplasms,
vestibular dysfunction, encephalitis, seizure disorders). Anxiety due to another medical
condition is diagnosed when the medical condition is known to induce anxiety and when
the medical condition preceded the onset of the anxiety.
Prevalence
The prevalence of anxiety disorder due to another medical condition is unclear. There ap-
pears to be an elevated prevalence of anxiety disorders among individuals with a variety
of medical conditions, including asthma, hypertension, ulcers, and arthritis. However, this
increased prevalence may be due to reasons other than the anxiety disorder directly caus-
ing the medical condition.
Development and Course
The development and course of anxiety disorder due to another medical condition gen-
erally follows the course of the underlying illness. This diagnosis is not meant to include
primary anxiety disorders that arise in the context of chronic medical illness. This is im-
portant to consider with older adults, who may experience chronic medical illness and
then develop independent anxiety disorders secondary to the chronic medical illness.
Diagnostic Markers
Laboratory assessments and/or medical examinations are necessary to confirm the diag-
nosis of the associated medical condition.
Differential Diagnosis
Delirium. A separate diagnosis of anxiety disorder due to another medical condition is
not given if the anxiety disturbance occurs exclusively during the course of a delirium.
However, a diagnosis of anxiety disorder due to another medical condition may be given
in addition to a diagnosis of major neurocognitive disorder (dementia) if the etiology of
anxiety is judged to be a physiological consequence of the pathological process causing the
neurocognitive disorder and if anxiety is a prominent part of the clinical presentation.
Mixed presentation of symptoms (e.g., mood and anxiety). _ If the presentation includes
a mix of different types of symptoms, the specific mental disorder due to another medical
condition depends on which symptoms predominate in the clinical picture.
Substance/medication-induced anxiety disorder. If there is evidence of recent or pro-
longed substance use (including medications with psychoactive effects), withdrawal from
232 Anxiety Disorders
a substance, or exposure to a toxin, a substance/medication-induced anxiety disorder
should be considered. Certain medications are known to increase anxiety (e.g., corticoste-
roids, estrogens, metoclopramide}, and when this is the case, the medication may be the
most likely etiology, although it may be difficult to distinguish whether the anxiety is at-
tributable to the medications or to the medical illness itself. When a diagnosis of substance-
induced anxiety is being made in relation to recreational or nonprescribed drugs, it may be
useful to obtain a urine or blood drug screen or other appropriate laboratory evaluation.
Symptoms that occur during or shortly after (i.e., within 4 weeks of) substance intoxication
or withdrawal or after medication use may be especially indicative of a substance/medi-
cation-induced anxiety disorder, depending on the type, duration, or amount of the sub-
stance used. If the disturbance is associated with both another medical condition and
substance use, both diagnoses (i.e., anxiety disorder due to another medical condition and
substance/medication-induced anxiety disorder) can be given. Features such as onset af-
ter age 45 years or the presence of atypical symptoms during a panic attack (e.g., vertigo,
loss of consciousness, loss of bladder or bowel control, slurred speech, amnesia) suggest
the possibility that another medical condition or a substance may be causing the panic at-
tack symptoms.
Anxiety disorder (not due to a known medical condition). Anxiety disorder due to an-
other medical condition should be distinguished from other anxiety disorders (especially
panic disorder and generalized anxiety disorder). In other anxiety disorders, no specific
and direct causative physiological mechanisms associated with another medical condition
can be demonstrated. Late age at onset, atypical symptoms, and the absence of a personal
or family history of anxiety disorders suggest the need for a thorough assessment to rule
out the diagnosis of anxiety disorder due to another medical condition. Anxiety disorders
can exacerbate or pose increased risk for medical conditions such as cardiovascular events
and myocardial infarction and should not be diagnosed as anxiety disorder due to another
medical condition in these cases.
lliness anxiety disorder. Anxiety disorder due to another medical condition should be
distinguished from illness anxiety disorder. Illness anxiety disorder is characterized by
worry about illness, concern about pain, and bodily preoccupations. In the case of illness
anxiety disorder, individuals may or may not have diagnosed medical conditions. Al-
though an individual with illness anxiety disorder and a diagnosed medical condition is
likely to experience anxiety about the medica] condition, the medical condition is not
physiologically related to the anxiety symptoms.
Adjustment disorders. Anxiety disorder due to another medical condition should be
distinguished from adjustment disorders, with anxiety, or with anxiety and depressed
mood. Adjustment disorder is warranted when individuals experience a maladaptive re-
sponse to the stress of having another medical condition. The reaction to stress usually
concerns the meaning or consequences of the stress, as compared with the experience of
anxiety or mood symptoms that occur as a physiological consequence of the other medical
condition. In adjustment disorder, the anxiety symptoms are typically related to coping
with the stress of having a general medical condition, whereas in anxiety disorder due to
another medical condition, individuals are more likely to have prominent physical symp-
toms and to be focused on issues other than the stress of the illness itself.
Associated feature of another mental disorder. Anxiety symptoms may be an associ-
ated feature of another mental disorder (e.g., schizophrenia, anorexia nervosa).
Other specified or unspecified anxiety disorder. This diagnosis is given if it cannot be
determined whether the anxiety symptoms are primary, substance-induced, or associated
with another medical condition.
Other Specified Anxiety Disorder 233
Other Specified Anxiety Disorder
300.09 (F41.8)
This category applies to presentations in which symptoms characteristic of an anxiety dis-
order that cause clinically significant distress or impairment in social, occupational, or oth-
er important areas of functioning predominate but do not meet the full criteria for any of the
disorders in the anxiety disorders diagnostic class. The other specified anxiety disorder
category is used in situations in which the clinician chooses to communicate the specific
reason that the presentation does not meet the criteria for any specific anxiety disorder.
This is done by recording “other specified anxiety disorder” followed by the specific reason
(e.g., “generalized anxiety not occurring more days than not’).
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Limited-symptom attacks.
2. Generalized anxiety not occurring more days than not.
3. Khyal cap (wind attacks): See “Glossary of Cultural Concepts of Distress” in the Ap-
pendix.
4. Ataque de nervios (attack of nerves): See “Glossary of Cultural Concepts of Distress”
in the Appendix.
Unspecified Anxiety Disorder
300.00 (F41.9)
This category applies to presentations in which symptoms characteristic of an anxiety dis-
order that cause clinically significant distress or impairment in social, occupational, or oth-
er important areas of functioning predominate but do not meet the full criteria for any of the
disorders in the anxiety disorders diagnostic class. The unspecified anxiety disorder cate-
gory is used in situations in which the clinician chooses not to specify the reason that the
criteria are not met for a specific anxiety disorder, and includes presentations in which
there is insufficient information to make a more specific diagnosis (e.g., in emergency room
settings).
_ Obsessive-Compulsive and
| Related Disorders
O bsessive-compulsive and related disorders include obsessive-compulsive
disorder (OCD), body dysmorphic disorder, hoarding disorder, trichotillomania (hair-
pulling disorder), excoriation (skin-picking) disorder, substance/medication-induced ob-
sessive-compulsive and related disorder, obsessive-compulsive and related disorder due
to another medical condition, and other specified obsessive-compulsive and related dis-
order and unspecified obsessive-compulsive and related disorder (e.g., body-focused re-
petitive behavior disorder, obsessional jealousy).
OCD is characterized by the presence of obsessions and/or compulsions. Obsessions
are recurrent and persistent thoughts, urges, or images that are experienced as intrusive
and unwanted, whereas compulsions are repetitive behaviors or mental acts that an indi-
vidual feels driven to perform in response to an obsession or according to rules that must
be applied rigidly. Some other obsessive-compulsive and related disorders are also char-
acterized by preoccupations and by repetitive behaviors or mental acts in response to the
preoccupations. Other obsessive-compulsive and related disorders are characterized pri-
marily by recurrent body-focused repetitive behaviors (e.g., hair pulling, skin picking) and
repeated attempts to decrease or stop the behaviors.
The inclusion of a chapter on obsessive-compulsive and related disorders in DSM-5 re-
flects the increasing evidence of these disorders’ relatedness to one another in terms of a
range of diagnostic validators as well as the clinical utility of grouping these disorders in
the same chapter. Clinicians are encouraged to screen for these conditions in individuals
who present with one of them and be aware of overlaps between these conditions. At the
same time, there are important differences in diagnostic validators and treatment ap-
proaches across these disorders. Moreover, there are close relationships between the anx-
iety disorders and some of the obsessive-compulsive and related disorders (e.g., OCD),
which is reflected in the sequence of DSM-5 chapters, with obsessive-compulsive and re-
lated disorders following anxiety disorders.
The obsessive-compulsive and related disorders differ from developmentally norma-
tive preoccupations and rituals by being excessive or persisting beyond developmentally
appropriate periods. The distinction between the presence of subclinical symptoms and a
clinical disorder requires assessment of a number of factors, including the individual's
level of distress and impairment in functioning.
The chapter begins with OCD. It then covers body dysmorphic disorder and hoarding
disorder, which are characterized by cognitive symptoms such as perceived defects or
flaws in physical appearance or the perceived need to save possessions, respectively. The
chapter then covers trichotillomania (hair-pulling disorder) and excoriation (skin-picking)
disorder, which are characterized by recurrent body-focused repetitive behaviors. Finally,
it covers substance/medication-induced obsessive-compulsive and related disorder,
obsessive-compulsive and related disorder due to another medical condition, and other
specified obsessive-compulsive and related disorder and unspecified obsessive-compul-
sive and related disorder.
While the specific content of obsessions and compulsions varies among individuals,
certain symptom dimensions are common in OCD, including those of cleaning (contami-
nation obsessions and cleaning compulsions); symmetry (symmetry obsessions and repeat-
235
236 Obsessive-Compulsive and Related Disorders
ing, ordering, and counting compulsions); forbidden or taboo thoughts (e.g., aggressive,
sexual, and religious obsessions and related compulsions); and harm (e.g., fears of harm to
oneself or others and related checking compulsions). The tic-related specifier of OCD is
used when an individual has a current or past history of a tic disorder.
Body dysmorphic disorder is characterized by preoccupation with one or more per-
ceived defects or flaws in physical appearance that are not observable or appear only slight
to others, and by repetitive behaviors (e.g., mirror checking, excessive grooming, skin
picking, or reassurance seeking) or mental acts (e.g., comparing one’s appearance with that
of other people) in response to the appearance concerns. The appearance preoccupations
are not better explained by concerns with body fat or weight in an individual with an eat-
ing disorder. Muscle dysmorphia is a form of body dysmorphic disorder that is character-
ized by the belief that one’s body build is too small or is insufficiently muscular.
Hoarding disorder is characterized by persistent difficulty discarding or parting with
possessions, regardless of their actual value, as a result of a strong perceived need to save
the items and to distress associated with discarding them. Hoarding disorder differs from
normal collecting. For example, symptoms of hoarding disorder result in the accumula-
tion of a large number of possessions that congest and clutter active living areas to the ex-
tent that their intended use is substantially compromised. The excessive acquisition form
of hoarding disorder, which characterizes most but not all individuals with hoarding dis-
order, consists of excessive collecting, buying, or stealing of items that are not needed or
for which there is no available space.
Trichotillomania (hair-pulling disorder) is characterized by recurrent pulling out of
one's hair resulting in hair loss, and repeated attempts to decrease or stop hair pulling.
Excoriation (skin-picking) disorder is characterized by recurrent picking of one’s skin re-
sulting in skin lesions and repeated attempts to decrease or stop skin picking. The body-
focused repetitive behaviors that characterize these two disorders are not triggered by ob-
sessions or preoccupations; however, they may be preceded or accompanied by various
emotional states, such as feelings of anxiety or boredom. They may also be preceded by an
increasing sense of tension or may lead to gratification, pleasure, or a sense of relief when
the hair is pulled out or the skin is picked. Individuals with these disorders may have vary-
ing degrees of conscious awareness of the behavior while engaging in it, with some indi-
viduals displaying more focused attention on the behavior (with preceding tension and
subsequent relief) and other individuals displaying more automatic behavior (with the be-
haviors seeming to occur without full awareness).
Substance/medication-induced obsessive-compulsive and related disorder consists of
symptoms that are due to substance intoxication or withdrawal or to a medication. Obses-
sive-compulsive and related disorder due to another medical condition involves symptoms
characteristic of obsessive-compulsive and related disorders that are the direct pathophysio-
logical consequence of a medical disorder. Other specified obsessive-compulsive and related
disorder and unspecified obsessive-compulsive and related disorder consist of symptoms
that do not meet criteria for a specific obsessive-compulsive and related disorder because of
atypical presentation or uncertain etiology; these categories are also used for other specific
syndromes that are not listed in Section II and when insufficient information is available to di-
agnose the presentation as another obsessive-compulsive and related disorder. Examples of
specific syndromes not listed in Section II, and therefore diagnosed as other specified obses-
sive-compulsive and related disorder or as unspecified obsessive-compulsive and related
disorder include body-focused repetitive behavior disorder and obsessional jealousy.
Obsessive-compulsive and related disorders that have a cognitive component have in-
sight as the basis for specifiers; in each of these disorders, insight ranges from “good or fair
insight” to “poor insight” to “absent insight/ delusional beliefs” with respect to disorder-
related beliefs. For individuals whose obsessive-compulsive and related disorder symp-
toms warrant the “with absent insight/delusional beliefs” specifier, these symptoms
should not be diagnosed as a psychotic disorder.
Obsessive-Compulsive Disorder 237
Obsessive-Compulsive Disorder
Diagnostic Criteria 300.3 (F42)
A. Presence of obsessions, compulsions, or both:
Obsessions are defined by (1) and (2):
1. Recurrent and persistent thoughts, urges, or images that are experienced, at some
time during the disturbance, as intrusive and unwanted, and that in most individuals
cause marked anxiety or distress.
2. The individual attempts to ignore or suppress such thoughts, urges, or images, or to
neutralize them with some other thought or action (i.e., by performing a compulsion).
Compulsions are defined by (1) and (2):
1. Repetitive behaviors (e.g., hand washing, ordering, checking) or mental acts (e.g.,
praying, counting, repeating words silently) that the individual feels driven to per-
form in response to an obsession or according to rules that must be applied rigidly.
2. The behaviors or mental acts are aimed at preventing or reducing anxiety or dis-
tress, or preventing some dreaded event or situation; however, these behaviors or
mental acts are not connected in a realistic way with what they are designed to neu-
tralize or prevent, or are clearly excessive.
Note: Young children may not be able to articulate the aims of these behaviors or
mental acts.
B. The obsessions or compulsions are time-consuming (e.g., take more than 1 hour per
day) or cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning.
C. The obsessive-compulsive symptoms are not attributable to the physiological effects
of a substance (e.g., a drug of abuse, a medication) or another medical condition.
D. The disturbance is not better explained by the symptoms of another mental disorder
(e.g., excessive worries, as in generalized anxiety disorder; preoccupation with ap-
pearance, as in body dysmorphic disorder; difficulty discarding or parting with posses-
sions, as in hoarding disorder; hair pulling, as in trichotillomania [hair-pulling disorder];
skin picking, as in excoriation [skin-picking] disorder; stereotypies, as in stereotypic
movement disorder; ritualized eating behavior, as in eating disorders; preoccupation
with substances or gambling, as in substance-related and addictive disorders; preoc-
cupation with having an illness, as in illness anxiety disorder; sexual urges or fantasies,
as in paraphilic disorders; impulses, as in disruptive, impulse-control, and conduct dis-
orders; guilty ruminations, as in major depressive disorder; thought insertion or delu-
sional preoccupations, as in schizophrenia spectrum and other psychotic disorders; or
repetitive patterns of behavior, as in autism spectrum disorder).
Specify if:
With good or fair insight: The individuai recognizes that obsessive-compulsive dis-
order beliefs are definitely or probably not true or that they may or may not be true.
With poor insight: The individual thinks obsessive-compuisive disorder beliefs are
probably true.
With absent insight/deiuslonai beiiefs: The individual is comptetely convinced that
obsessive-compulsive disorder beliefs are true.
Specify if:
Tic-related: The individual has a current or past history of a tic disorder.
238 Obsessive-Compulsive and Related Disorders
Specifiers
Many individuals with obsessive-compulsive disorder (OCD) have dysfunctional beliefs.
These beliefs can include an inflated sense of responsibility and the tendency to overesti-
mate threat; perfectionism and intolerance of uncertainty; and over-importance of thoughts
(e.g., believing that having a forbidden thought is as bad as acting on it) and the need to
control thoughts.
Individuals with OCD vary in the degree of insight they have about the accuracy of the
beliefs that underlie their obsessive-compulsive symptoms. Many individuals have good or
fair insight (e.g., the individual believes that the house definitely will not, probably will not,
or may or may not burn down if the stove is not checked 30 times). Some have poor insight
(e.g., the individual believes that the house will probably burn down if the stove is not
checked 30 times), and a few (4% or less) have absent insight/delusional beliefs (e.g., the in-
dividual is convinced that the house will burn down if the stove is not checked 30 times).
Insight can vary within an individual over the course of the illness. Poorer insight has been
linked to worse long-term outcome.
Up to 30% of individuals with OCD have a lifetime tic disorder. This is most common
in males with onset of OCD in childhood. These individuals tend to differ from those with-
out a history of tic disorders in the themes of their OCD symptoms, comorbidity, course,
and pattern of familial transmission.
Diagnostic Features
The characteristic symptoms of OCD are the presence of obsessions and compulsions (Cri-
terion A). Obsessions are repetitive and persistent thoughts (e.g., of contamination), images
(e.g., of violent or horrific scenes), or urges (e.g., to stab someone). Importantly, obsessions
are not pleasurable or experienced as voluntary: they are intrusive and unwanted and
cause marked distress or anxiety in most individuals. The individual attempts to ignore or
suppress these obsessions (e.g., avoiding triggers or using thought suppression) or to neu-
tralize them with another thought or action (e.g., performing a compulsion). Compulsions
(or rituals) are repetitive behaviors (e.g., washing, checking) or mental acts (e.g., counting,
repeating words silently) that the individual feels driven to perform in response to an
obsession or according to rules that must be applied rigidly. Most individuals with OCD
have both obsessions and compulsions. Compulsions are typically performed in response
to an obsession (e.g., thoughts of contamination leading to washing rituals or that some-
thing is incorrect leading to repeating rituals until it feels “just right”). The aim is to reduce
the distress triggered by obsessions or to prevent a feared event (e.g., becoming ill). How-
ever, these compulsions either are not connected in a realistic way to the feared event (e.g.,
arranging items symmetrically to prevent harm to a loved one) or are clearly excessive
(e.g., showering for hours each day). Compulsions are not done for pleasure, although some
individuals experience relief from anxiety or distress.
Criterion B emphasizes that obsessions and compulsions must be time-consuming (e.g.,
more than 1 hour per day) or cause clinically significant distress or impairment to warrant
a diagnosis of OCD. This criterion helps to distinguish the disorder from the occasional in-
trusive thoughts or repetitive behaviors that are common in the general population (e.g.,
double-checking that a door is locked). The frequency and severity of obsessions and com-
pulsions vary across individuals with OCD (e.g., some have mild to moderate symptoms,
spending 1-3 hours per day obsessing or doing compulsions, whereas others have nearly
constant intrusive thoughts or compulsions that can be incapacitating).
Associated Features Supporting Diagnosis
The specific content of obsessions and compulsions varies between individuals. However,
certain themes, or dimensions, are common, including those of cleaning (contamination
obsessions and cleaning compulsions); symmetry (symmetry obsessions and repeating,
Obsessive-Compulsive Disorder 239
ordering, and counting compulsions); forbidden or taboo thoughts (e.g., aggressive, sexual,
or religious obsessions and related compulsions); and harm (e.g., fears of harm to oneself
or others and checking compulsions). Some individuals also have difficulties discarding
and accumulate (hoard) objects as a consequence of typical obsessions and compulsions,
such as fears of harming others. These themes occur across different cultures, are rela-
tively consistent over time in adults with the disorder, and may be associated with differ-
ent neural substrates. Importantly, individuals often have symptoms in more than one
dimension.
Individuals with OCD experience a range of affective responses when confronted with
situations that trigger obsessions and compulsions. For example, many individuals expe-
rience marked anxiety that can include recurrent panic attacks. Others report strong feel-
ings of disgust. While performing compulsions, some individuals report a distressing
sense of “incompleteness” or uneasiness until] things look, feel, or sound “just right.”
It is common for individuals with the disorder to avoid people, places, and things that
trigger obsessions and compulsions. For example, individuals with contamination con-
cerns might avoid public situations (e.g., restaurants, public restrooms) to reduce ex-
posure to feared contaminants; individuals with intrusive thoughts about causing harm
might avoid social interactions.
Prevalence
The 12-month prevalence of OCD in the United States is 1.2%, with a similar prevalence in-
ternationally (1.1%-1.8%). Females are affected at a slightly higher rate than males in
adulthood, although males are more commonly affected in childhood.
Development and Course
In the United States, the mean age at onset of OCD is 19.5 years, and 25% of cases start by
age 14 years. Onset after age 35 years is unusual but does occur. Males have an earlier age
at onset than females: nearly 25% of males have onset before age 10 years. The onset of
symptoms is typically gradual; however, acute onset has also been reported.
If OCD is untreated, the course is usually chronic, often with waxing and waning symp-
toms. Some individuals have an episodic course, and a minority have a deteriorating
course. Without treatment, remission rates in adults are low (e.g., 20% for those reevalu-
ated 40 years later). Onset in childhood or adolescence can lead to a lifetime of OCD. How-
ever, 40% of individuals with onset of OCD in childhood or adolescence may experience
remission by early adulthood. The course of OCD is often complicated by the co-occurrence
of other disorders (see section “Comorbidity” for this disorder).
Compulsions are more easily diagnosed in children than obsessions are because com-
pulsions are observable. However, most children have both obsessions and compulsions
(as do most adults). The pattern of symptoms in adults can be stable over time, but it is
more variable in children. Some differences in the content of obsessions and compulsions
have been reported when children and adolescent samples have been compared with
adult samples. These differences likely reflect content appropriate to different develop-
mental stages (e.g., higher rates of sexual and religious obsessions in adolescents than in
children; higher rates of harm obsessions [e.g., fears of catastrophic events, such as death
or illness to self or loved ones] in children and adolescents than in adults).
Risk and Prognostic Factors
Temperamental. Greater internalizing symptoms, higher negative emotionality, and
behavioral inhibition in childhood are possible temperamental risk factors.
Environmental. Physical and sexual abuse in childhood and other stressful or traumatic
events have been associated with an increased risk for developing OCD. Some children
240 Obsessive-Compulsive and Related Disorders
may develop the sudden onset of obsessive-compulsive symptoms, which has been asso-
ciated with different environmental factors, including various infectious agents and a
post-infectious autoimmune syndrome.
Genetic and physiological. The rate of OCD among first-degree relatives of adults with
OCD is approximately two times that among first-degree relatives of those without the
disorder; however, among first-degree relatives of individuals with onset of OCD in child-
hood or adolescence, the rate is increased 10-fold. Familial transmission is due in part to
genetic factors (e.g., a concordance rate of 0.57 for monozygotic vs. 0.22 for dizygotic twins).
Dysfunction in the orbitofrontal cortex, anterior cingulate cortex, and striatum have been
most strongly implicated.
Culture-Related Diagnostic Issues
OCD occurs across the world. There is substantial similarity across cultures in the gender
distribution, age at onset, and comorbidity of OCD. Moreover, around the globe, there is a
similar symptom structure involving cleaning, symmetry, hoarding, taboo thoughts, or
fear of harm. However, regional variation in symptom expression exists, and cultural
factors may shape the content of obsessions and compulsions.
Gender-Related Diagnostic Issues
Males have an earlier age at onset of OCD than females and are more likely to have co-
morbid tic disorders. Gender differences in the pattern of symptom dimensions have been
reported, with, for example, females more likely to have symptoms in the cleaning dimen-
sion and males more likely to have symptoms in the forbidden thoughts and symmetry di-
mensions. Onset or exacerbation of OCD, as well as symptoms that can interfere with the
mother-infant relationship (e.g., aggressive obsessions leading to avoidance of the infant),
have been reported in the peripartum period.
Suicide Risk
Suicidal thoughts occur at some point in as many as about half of individuals with OCD.
Suicide attempts are also reported in up to one-quarter of individuals with OCD; the pres-
ence of comorbid major depressive disorder increases the risk.
Functional Consequences of
Obsessive-Compulsive Disorder
OCD is associated with reduced quality of life as well as high levels of social and occupa-
tional impairment. Impairment occurs across many different domains of life and is asso-
ciated with symptom severity. Impairment can be caused by the time spent obsessing and
doing compulsions. Avoidance of situations that can trigger obsessions or compulsions
can also severely restrict functioning. In addition, specific symptoms can create specific
obstacles. For example, obsessions about harm can make relationships with family and
friends feel hazardous; the result can be avoidance of these relationships. Obsessions
about symmetry can derail the timely completion of school or work projects because the
project never feels “just right,” potentially resulting in school failure or job loss. Health
consequences can also occur. For example, individuals with contamination concerns may
avoid doctors’ offices and hospitals (e.g., because of fears of exposure to germs) or develop
dermatological problems (e.g., skin lesions due to excessive washing). Sometimes the
symptoms of the disorder interfere with its own treatment (e.g., when medications are con-
sidered contaminated). When the disorder starts in childhood or adolescence, individuals
may experience developmental difficulties. For example, adolescents may avoid socializ-
ing with peers; young adults may struggle when they leave home to live independently.
Obsessive-Compulsive Disorder 241
The result can be few significant relationships outside the family and a lack of autonomy
and financial independence from their family of origin. In addition, some individuals with
OCD try to impose rules and prohibitions on family members because of their disorder
(e.g.,no one in the family can have visitors to the house for fear of contamination), and this
can lead to family dysfunction.
Differential Diagnosis
Anxiety disorders. Recurrent thoughts, avoidant behaviors, and repetitive requests for
reassurance can also occur in anxiety disorders. However, the recurrent thoughts that are
present in generalized anxiety disorder (i-e., worries) are usually about real-life concerns,
whereas the obsessions of OCD usually do not involve real-life concerns and can include
content that is odd, irrational, or of a seemingly magical nature; moreover, compulsions
are often present and usually linked to the obsessions. Like individuals with OCD, indi-
viduals with specific phobia can have a fear reaction to specific objects or situations; how-
ever, in specific phobia the feared object is usually much more circumscribed, and rituals
are not present. In social anxiety disorder (social phobia), the feared objects or situations
are limited to social interactions, and avoidance or reassurance seeking is focused on re-
ducing this social fear.
Major depressive disorder. OCD can be distinguished from the rumination of major
depressive disorder, in which thoughts are usually mood-congruent and not necessarily
experienced as intrusive or distressing; moreover, ruminations are not linked to compul-
sions, as is typical in OCD.
Other obsessive-compulsive and related disorders. In body dysmorphic disorder, the
obsessions and compulsions are limited to concerns about physical appearance; and in
trichotillomania (hair-pulling disorder), the compulsive behavior is limited to hair pulling
in the absence of obsessions. Hoarding disorder symptoms focus exclusively on the per-
sistent difficulty discarding or parting with possessions, marked distress associated with
discarding items, and excessive accumulation of objects. However, if an individual has ob-
sessions that are typical of OCD (e.g., concerns about incompleteness or harm), and these
obsessions lead to compulsive hoarding behaviors (e.g., acquiring all objects in a set to at-
tain a sense of completeness or not discarding old newspapers because they may contain
information that could prevent harm), a diagnosis of OCD should be given instead.
Eating disorders. OCD can be distinguished from anorexia nervosa in that in OCD the
obsessions and compulsions are not limited to concerns about weight and food.
Tics (in tic disorder) and stereotyped movements. A tic is a sudden, rapid, recurrent,
nonrhythmic motor movement or vocalization (e.g., eye blinking, throat clearing). A ste-
reotyped movement is a repetitive, seemingly driven, nonfunctional motor behavior (e.g.,
head banging, body rocking, self-biting). Tics and stereotyped movements are typically
less complex than compulsions and are not aimed at neutralizing obsessions. However,
distinguishing between complex tics and compulsions can be difficult. Whereas compul-
sions are usually preceded by obsessions, tics are often preceded by premonitory sensory
urges. Some individuals have symptoms of both OCD and a tic disorder, in which case
both diagnoses may be warranted.
Psychotic disorders. Some individuals with OCD have poor insight or even delusional
OCD beliefs. However, they have obsessions and compulsions (distinguishing their
condition from delusional disorder) and do not have other features of schizophrenia or
schizoaffective disorder (e.g., hallucinations or formal thought disorder).
Other compulsive-like behaviors. Certain behaviors are sometimes described as “com-
pulsive,” including sexual behavior (in the case of paraphilias), gambling (i.e., gambling
242 Obsessive-Compulsive and Related Disorders
disorder), and substance use (e.g., alcohol use disorder). However, these behaviors differ
from the compulsions of OCD in that the person usually derives pleasure from the activity
and may wish to resist it only because of its deleterious consequences.
Obsessive-compulsive personality disorder. Although obsessive-compulsive person-
ality disorder and OCD have similar names, the clinical manifestations of these disorders
are quite different. Obsessive-compulsive personality disorder is not characterized by in-
trusive thoughts, images, or urges or by repetitive behaviors that are performed in re-
sponse to these intrusions; instead, it involves an enduring and pervasive maladaptive
pattern of excessive perfectionism and rigid control. If an individual manifests symptoms
of both OCD and obsessive-compulsive personality disorder, both diagnoses can be given.
Comorbidity
Individuals with OCD often have other psychopathology. Many adults with the disorder
have a lifetime diagnosis of an anxiety disorder (76%; e.g., panic disorder, social anxiety
disorder, generalized anxiety disorder, specific phobia) or a depressive or bipolar disorder
(63% for any depressive or bipolar disorder, with the most common being major depres-
sive disorder [41%]). Onset of OCD is usually later than for most comorbid anxiety disor-
ders (with the exception of separation anxiety disorder) and PTSD but often precedes that
of depressive disorders. Comorbid obsessive-compulsive personality disorder is also
common in individuals with OCD (e.g., ranging from 23% to 32%).
Up to 30% of individuals with OCD also have a lifetime tic disorder. A comorbid tic
disorder is most common in males with onset of OCD in childhood. These individuals
tend to differ from those without a history of tic disorders in the themes of their OCD
symptoms, comorbidity, course, and pattern of familial transmission. A triad of OCD, tic
disorder, and attention-deficit/hyperactivity disorder can also be seen in children.
Disorders that occur more frequently in individuals with OCD than in those without
the disorder include several obsessive-compulsive and related disorders such as body
dysmorphic disorder, trichotillomania (hair-pulling disorder), and excoriation (skin-pick-
ing) disorder. Finally, an association between OCD and some disorders characterized by
impulsivity, such as oppositional defiant disorder, has been reported.
OCD is also much more common in individuals with certain other disorders than
would be expected based on its prevalence in the general population; when one of those
other disorders is diagnosed, the individual should be assessed for OCD as well. For ex-
ample, in individuals with schizophrenia or schizoaffective disorder, the prevalence of
OCD is approximately 12%. Rates of OCD are also elevated in bipolar disorder; eating dis-
orders, such as anorexia nervosa and bulimia nervosa; and Tourette’s disorder.
Body Dysmorphic Disorder
Diagnostic Criteria 300.7 (F45.22)
A. Preoccupation with one or more perceived defects or flaws in physical appearance that
are not observable or appear slight to others.
B. Atsome point during the course of the disorder, the individual has performed repetitive
behaviors (e.g., mirror checking, excessive grooming, skin picking, reassurance seek-
ing) or mental acts (e.g., comparing his or her appearance with that of others) in re-
sponse to the appearance concerns.
C. The preoccupation causes clinically significant distress or impairment in social, occu-
pational, or other important areas of functioning.
D. The appearance preoccupation is not better explained by concerns with body fat or
weight in an individual whose symptoms meet diagnostic criteria for an eating disorder.
Body Dysmorphic Disorder 243
Specify if:
With muscle dysmorphia: The individual is preoccupied with the idea that his or her
body build is too small or insufficiently muscular. This specifier is used even if the indi-
vidual is preoccupied with other body areas, which is often the case.
Specify if:
Indicate degree of insight regarding body dysmorphic disorder beliefs (e.g., “I look ugly” or
“| look deformed”).
With good or fair insight: The individual recognizes that the body dysmorphic disor-
der beliefs are definitely or probably not true or that they may or may not be true.
With poor insight: The individual thinks that the body dysmorphic disorder beliefs are
probably true.
With absent insight/delusionai beliefs: The individual is completely convinced that
the body dysmorphic disorder beliefs are true.
Diagnostic Features
Individuals with body dysmorphic disorder (formerly known as dysmorphophobia) are pre-
occupied with one or more perceived defects or flaws in their physical appearance, which
they believe look ugly, unattractive, abnormal, or deformed (Criterion A). The perceived
flaws are not observable or appear only slight to other individuals. Concerns range from
looking “unattractive” or “not right” to looking “hideous” or “like a monster.” Preoccu-
pations can focus on one or many body areas, most commonly the skin (e.g., perceived
acne, scars, lines, wrinkles, paleness), hair (e.g., “thinning” hair or “excessive” body or fa-
cial hair), or nose (e.g., size or shape). However, any body area can be the focus of concern
(e.g., eyes, teeth, weight, stomach, breasts, legs, face size or shape, lips, chin, eyebrows,
genitals). Some individuals are concerned about perceived asymmetry of body areas. The
preoccupations are intrusive, unwanted, time-consuming (occurring, on average, 3-8
hours per day), and usually difficult to resist or control.
Excessive repetitive behaviors or mental acts (e.g., comparing) are performed in re-
sponse to the preoccupation (Criterion B). The individual feels driven to perform these be-
haviors, which are not pleasurable and may increase anxiety and dysphoria. They are
typically time-consuming and difficult to resist or control. Common behaviors are com-
paring one’s appearance with that of other individuals; repeatedly checking perceived
defects in mirrors or other reflecting surfaces or examining them directly; excessively
grooming (e.g., combing, styling, shaving, plucking, or pulling hair); camouflaging (e.g.,
repeatedly applying makeup or covering disliked areas with such things as a hat, clothing,
makeup, or hair); seeking reassurance about how the perceived flaws look; touching dis-
liked areas to check them; excessively exercising or weight lifting; and seeking cosmetic
procedures. Some individuals excessively tan (e.g., to darken “pale” skin or diminish per-
ceived acne), repeatedly change their clothes (e.g., to camouflage perceived defects), or
compulsively shop (e.g., for beauty products). Compulsive skin picking intended to
improve perceived skin defects is common and can cause skin damage, infections, or
ruptured blood vessels. The preoccupation must cause clinically significant distress or im-
pairment in social, occupational, or other important areas of functioning (Criterion C);
usually both are present. Body dysmorphic disorder must be differentiated from an eating
disorder.
Muscle dysmorphia, a form of body dysmorphic disorder occurring almost exclusively
in males, consists of preoccupation with the idea that one’s body is too small or insuffi-
ciently lean or muscular. Individuals with this form of the disorder actually have a nor-
mal-looking body or are even very muscular. They may also be preoccupied with other
body areas, such as skin or hair. A majority (but not all) diet, exercise, and/or lift weights
excessively, sometimes causing bodily damage. Some use potentially dangerous anabolic-
244 Obsessive-Compulsive and Related Disorders
androgenic steroids and other substances to try to make their body bigger and more mus-
cular. Body dysmorphic disorder by proxy is a form of body dysmorphic disorder in
which individuals are preoccupied with defects they perceive in another person’s appear-
ance.
Insight regarding body dysmorphic disorder beliefs can range from good to absent/
delusional (i.e., delusional beliefs consisting of complete conviction that the individual’s
view of their appearance is accurate and undistorted). On average, insight is poor; one-
third or more of individuals currently have delusional body dysmorphic disorder beliefs.
Individuals with delusional body dysmorphic disorder tend to have greater morbidity in
some areas (e.g., suicidality), but this appears accounted for by their tendency to have
more severe body dysmorphic disorder symptoms.
Associated Features Supporting Diagnosis
Many individuals with body dysmorphic disorder have ideas or delusions of reference,
believing that other people take special notice of them or mock them because of how they
look. Body dysmorphic disorder is associated with high levels of anxiety, social anxiety,
social avoidance, depressed mood, neuroticism, and perfectionism as well as low extro-
version and low self-esteem. Many individuals are ashamed of their appearance and their
excessive focus on how they look, and are reluctant to reveal their concerns to others. A
majority of individuals receive cosmetic treatment to try to improve their perceived de-
fects. Dermatological treatment and surgery are most common, but any type (e.g., dental,
electrolysis) may be received. Occasionally, individuals may perform surgery on them-
selves. Body dysmorphic disorder appears to respond poorly to such treatments and
sometimes becomes worse. Some individuals take legal action or are violent toward the
clinician because they are dissatisfied with the cosmetic outcome.
Body dysmorphic disorder has been associated with executive dysfunction and visual
processing abnormalities, with a bias for analyzing and encoding details rather than ho-
listic or configura] aspects of visual stimuli. Individuals with this disorder tend to have a
bias for negative and threatening interpretations of facial expressions and ambiguous sce-
narios.
Prevalence
The point prevalence among U.S. adults is 2.4% (2.5% in females and 2.2% in males). Out-
side the United States (i.e., Germany), current prevalence is approximately 1.7%-1.8%,
with a gender distribution similar to that in the United States. The current prevalence is
9%-15% among dermatology patients, 7%-8% among U.S. cosmetic surgery patients, 3%-—
16% among international cosmetic surgery patients (most studies), 8% among adult orth-
odontia patients, and 10% among patients presenting for oral or maxillofacial surgery.
Deveiopment and Course
The mean age at disorder onset is 16-17 years, the median age at onset is 15 years, and the
most common age at onset is 12-13 years. Two-thirds of individuals have disorder onset
before age 18. Subclinical body dysmorphic disorder symptoms begin, on average, at age
12 or 13 years. Subclinical concerns usually evolve gradually to the full disorder, although
some individuals experience abrupt onset of body dysmorphic disorder. The disorder
appears to usually be chronic, although improvement is likely when evidence-based
treatment is received. The disorder’s clinical features appear largely similar in children/
adolescents and adults. Body dysmorphic disorder occurs in the elderly, but little is known
about the disorder in this age group. Individuals with disorder onset before age 18 years
are more likely to attempt suicide, have more comorbidity, and have gradual (rather than
acute) disorder onset than those with adult-onset body dysmorphic disorder.
Body Dysmorphic Disorder 245
Risk and Prognostic Factors
Environmental. ' Body dysmorphic disorder has been associated with high rates of child-
hood neglect and abuse.
Genetic and physiological. The prevalence of body dysmorphic disorder is elevated in
first-degree relatives of individuals with obsessive-compulsive disorder (OCD).
Culture-Related Diagnostic Issues
Body dysmorphic disorder has been reported internationally. It appears that the disorder
may have more similarities than differences across races and cultures but that cultural
values and preferences may influence symptom content to some degree. Taijin kyofusho,
included in the traditional Japanese diagnostic system, has a subtype similar to body dys-
morphic disorder: shubo-kyofu (“the phobia of a deformed body”).
Gender-Reiated Diagnostic Issues
Females and males appear to have more similarities than differences in terms of most clin-
ical features— for example, disliked body areas, types of repetitive behaviors, symptom
severity, suicidality, comorbidity, illness course, and receipt of cosmetic procedures for
body dysmorphic disorder. However, males are more likely to have genital preoccupa-
tions, and females are more likely to have a comorbid eating disorder. Muscle dysmorphia
occurs almost exclusively in males.
Suicide Risk
Rates of suicidal ideation and suicide attempts are high in both adults and children/ado-
lescents with body dysmorphic disorder. Furthermore, risk for suicide appears high in ad-
olescents. A substantial proportion of individuals attribute suicidal ideation or suicide
attempts primarily to their appearance concerns. Individuals with body dysmorphic dis-
order have many risk factors for completed suicide, such as high rates of suicidal ideation
and suicide attempts, demographic characteristics associated with suicide, and high rates
of comorbid major depressive disorder.
Functional Consequences of
Body Dysmorphic Disorder
Nearly all individuals with body dysmorphic disorder experience impaired psychosocial
functioning because of their appearance concerns. Impairment can range from moderate
(e.g., avoidance of some social situations) to extreme and incapacitating (e.g., being com-
pletely housebound). On average, psychosocial functioning and quality of life are mark-
edly poor. More severe body dysmorphic disorder symptoms are associated with poorer
functioning and quality of life. Most individuals experience impairment in their job, aca-
demic, or role functioning (e.g., as a parent or caregiver), which is often severe (e.g., per-
forming poorly, missing school or work, not working). About 20% of youths with body
dysmorphic disorder report dropping out of school primarily because of their body dys-
morphic disorder symptoms. Impairment in social functioning (e.g., social activities, rela-
tionships, intimacy), including avoidance, is common. Individuals may be housebound
because of their body dysmorphic disorder symptoms, sometimes for years. A high pro-
portion of adults and adolescents have been psychiatrically hospitalized.
Differential Diagnosis
Normal appearance concerns and clearly noticeable physical defects. Body dysmor-
phic disorder differs from normal appearance concerns in being characterized by exces-
246 Obsessive-Compulsive and Related Disorders
sive appearance-related preoccupations and repetitive behaviors that are time-consuming,
are usually difficult to resist or control, and cause clinically significant distress or impair-
ment in functioning. Physical defects that are clearly noticeable (i.e., not slight) are not
diagnosed as body dysmorphic disorder. However, skin picking as a symptom of body
dysmorphic disorder can cause noticeable skin lesions and scarring; in such cases, body dys-
morphic disorder should be diagnosed.
Eating disorders. In an individual with an eating disorder, concerns about being fat are
considered a symptom of the eating disorder rather than body dysmorphic disorder.
However, weight concerns may occur in body dysmorphic disorder. Eating disorders and
body dysmorphic disorder can be comorbid, in which case both should be diagnosed.
Other obsessive-compulsive and related disorders. The preoccupations and repetitive
behaviors of body dysmorphic disorder differ from obsessions and compulsions in OCD
in that the former focus only on appearance. These disorders have other differences, such
as poorer insight in body dysmorphic disorder. When skin picking is intended to improve
the appearance of perceived skin defects, body dysmorphic disorder, rather than excoria-
tion (skin-picking) disorder, is diagnosed. When hair removal (plucking, pulling, or other
types of removal) is intended to improve perceived defects in the appearance of facial
or body hair, body dysmorphic disorder is diagnosed rather than trichotillomania (hair-
pulling disorder).
\IIness anxiety disorder. Individuals with body dysmorphic disorder are not preoccu-
pied with having or acquiring a serious illness and do not have particularly elevated levels
of somatization.
Major depressive disorder. The prominent preoccupation with appearance and exces-
sive repetitive behaviors in body dysmorphic disorder differentiate it from major de-
pressive disorder. However, major depressive disorder and depressive symptoms are
common in individuals with body dysmorphic disorder, often appearing to be secondary
to the distress and impairment that body dysmorphic disorder causes. Body dysmorphic
disorder should be diagnosed in depressed individuals if diagnostic criteria for body dys-
morphic disorder are met.
Anxiety disorders. Social anxiety and avoidance are common in body dysmorphic dis-
order. However, unlike social anxiety disorder (social phobia), agoraphobia, and avoidant
personality disorder, body dysmorphic disorder includes prominent appearance-related
preoccupation, which may be delusional, and repetitive behaviors, and the social anxiety
and avoidance are due to concerns about perceived appearance defects and the belief or
fear that other people will consider these individuals ugly, ridicule them, or reject them be-
cause of their physical features. Unlike generalized anxiety disorder, anxiety and worry in
body dysmorphic disorder focus on perceived appearance flaws.
Psychotic disorders. Many individuals with body dysmorphic disorder have delu-
sional appearance beliefs (i.e., complete conviction that their view of their perceived de-
fects is accurate), which is diagnosed as body dysmorphic disorder, with absent insight /
delusional beliefs, not as delusional disorder. Appearance-related ideas or delusions of
reference are common in body dysmorphic disorder; however, unlike schizophrenia or
schizoaffective disorder, body dysmorphic disorder involves prominent appearance pre-
occupations and related repetitive behaviors, and disorganized behavior and other psy-
chotic symptoms are absent (except for appearance beliefs, which may be delusional).
Other disorders and symptoms. Body dysmorphic disorder should not be diagnosed if
the preoccupation is limited to discomfort with or a desire to be rid of one’s primary and /
or secondary sex characteristics in an individual with gender dysphoria or if the preoccu-
pation focuses on the belief that one emits a foul or offensive body odor as in olfactory
reference syndrome (which is not a DSM-5 disorder). Body identity integrity disorder
Hoarding Disorder 247
(apotemnophilia) (which is not a DSM-5 disorder) involves a desire to have a limb ampu-
tated to correct an experience of mismatch between a person’s sense of body identity and
his or her actual anatomy. However, the concern does not focus on the limb’s appearance,
as it would in body dysmorphic disorder. Koro, a culturally related disorder that usually
occurs in epidemics in Southeastern Asia, consists of a fear that the penis (labia, nipples, or
breasts in females) is shrinking or retracting and will disappear into the abdomen, often
accompanied by a belief that death will result. Koro differs from body dysmorphic disor-
der in several ways, including a focus on death rather than preoccupation with perceived
ugliness. Dysmorphic concern (which is not a DSM-5 disorder) is a much broader construct
than, and is not equivalent to, body dysmorphic disorder. It involves symptoms reflecting
an overconcern with slight or imagined flaws in appearance.
Comorbidity
Major depressive disorder is the most common comorbid disorder, with onset usually af-
ter that of body dysmorphic disorder. Comorbid social anxiety disorder (social phobia),
OCD, and substance-related disorders are also common.
Hoarding Disorder
Diagnostic Criteria 300.3 (F42)
A. Persistent difficulty discarding or parting with possessions, regardless of their actual value.
B. This difficulty is due to a perceived need to save the items and to distress associated
with discarding them.
C. The difficulty discarding possessions results in the accumulation of possessions that
congest and clutter active living areas and substantially compromises their intended
use. If living areas are uncluttered, it is only because of the interventions of third parties
(e.g., family members, cleaners, authorities).
D. The hoarding causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning (including maintaining a safe environ-
ment for self and others).
E. The hoarding is not attributable to another medical condition (e.g., brain injury, cere-
brovascular disease, Prader-Willi syndrome).
F. The hoarding is not better explained by the symptoms of another mental disorder (e.g.,
obsessions in obsessive-compulsive disorder, decreased energy in major depressive
disorder, delusions in schizophrenia or another psychotic disorder, cognitive deficits in
major neurocognitive disorder, restricted interests in autism spectrum disorder).
Specify if:
With excessive acqulsition: If difficulty discarding possessions is accompanied by ex-
cessive acquisition of items that are not needed or for which there is no available space.
Specify if:
With good or fair insight: The individual recognizes that hoarding-related beliefs and
behaviors (pertaining to difficulty discarding items, clutter, or excessive acquisition) are
problematic.
With poor insight: The individual is mostly convinced that hoarding-related beliefs
and behaviors (pertaining to difficulty discarding items, clutter, or excessive acquisi-
tion) are not problematic despite evidence to the contrary.
With absent insight/delusional beliefs: The individual is completely convinced that
hoarding-related beliefs and behaviors (pertaining to difficulty discarding items, clutter,
or excessive acquisition) are not problematic despite evidence to the contrary.
248 Obsessive-Compulsive and Related Disorders
Specifiers
With excessive acquisition. Approximately 80%-90% of individuals with hoarding
disorder display excessive acquisition. The most frequent form of acquisition is excessive
buying, followed by acquisition of free items (e.g., leaflets, items discarded by others).
Stealing is less common. Some individuals may deny excessive acquisition when first as-
sessed, yet it may appear later during the course of treatment. Individuals with hoarding
disorder typically experience distress if they are unable to or are prevented from acquiring
items.
Diagnostic Features
The essential feature of hoarding disorder is persistent difficulties discarding or parting
with possessions, regardless of their actual value (Criterion A). The term persistent indi-
cates a long-standing difficulty rather than more transient life circumstances that may lead
to excessive clutter, such as inheriting property. The difficulty in discarding possessions
noted in Criterion A refers to any form of discarding, including throwing away, selling,
giving away, or recycling. The main reasons given for these difficulties are the perceived
utility or aesthetic value of the items or strong sentimental attachment to the possessions.
Some individuals feel responsible for the fate of their possessions and often go to great
lengths to avoid being wasteful. Fears of losing important information are also common.
The most commonly saved items are newspapers, magazines, old clothing, bags, books,
mail, and paperwork, but virtually any item can be saved. The nature of items is not lim-
ited to possessions that most other people would define as useless or of limited value.
Many individuals collect and save large numbers of valuable things as well, which are of-
ten found in piles mixed with other less valuable items.
Individuals with hoarding disorder purposefully save possessions and experience dis-
tress when facing the prospect of discarding them (Criterion B). This criterion emphasizes
that the saving of possessions is intentional, which discriminates hoarding disorder from
other forms of psychopathology that are characterized by the passive accumulation of
items or the absence of distress when possessions are removed.
Individuals accumulate large numbers of items that fill up and clutter active living ar-
eas to the extent that their intended use is no longer possible (Criterion C). For example,
the individual may not be able to cook in the kitchen, sleep in his or her bed, or sit in a
chair. If the space can be used, it is only with great difficulty. Clutter is defined as a large
group of usually unrelated or marginally related objects piled together in a disorganized
fashion in spaces designed for other purposes (e.g., tabletops, floor, hallway). Criterion C
emphasizes the “active” living areas of the home, rather than more peripheral areas, such
as garages, attics, or basements, that are sometimes cluttered in homes of individuals with-
out hoarding disorder. However, individuals with hoarding disorder often have posses-
sions that spill beyond the active living areas and can occupy and impair the use of other
spaces, such as vehicles, yards, the workplace, and friends’ and relatives’ houses. In some
cases, living areas may be uncluttered because of the intervention of third parties (e.g.,
family members, cleaners, local authorities). Individuals who have been forced to clear
their homes still have a symptom picture that meets criteria for hoarding disorder because
the lack of clutter is due to a third-party intervention. Hoarding disorder contrasts with
normative collecting behavior, which is organized and systematic, even if in some cases
the actual amount of possessions may be similar to the amount accumulated by an indi-
vidual with hoarding disorder. Normative collecting does not produce the clutter, dis-
tress, or impairment typical of hoarding disorder.
Symptoms (i.e., difficulties discarding and/or clutter) must cause clinically significant
distress or impairment in social, occupational, or other important areas of functioning, in-
cluding maintaining a safe environment for self and others (Criterion D). In some cases,
Hoarding Disorder 249
particularly when there is poor insight, the individual may not report distress, and the im-
pairment may be apparent only to those around the individual. However, any attempts to
discard or clear the possessions by third parties result in high levels of distress.
Associated Features Supporting Diagnosis
Other common features of hoarding disorder include indecisiveness, perfectionism,
avoidance, procrastination, difficulty planning and organizing tasks, and distractibility.
Some individuals with hoarding disorder live in unsanitary conditions that may be a log-
ical consequence of severely cluttered spaces and/or that are related to planning and or-
ganizing difficulties. Animal hoarding can be defined as the accumulation of a large number
of animals and a failure to provide minimal standards of nutrition, sanitation, and veter-
inary care and to act on the deteriorating condition of the animals (including disease, star-
vation, or death) and the environment (e.g., severe overcrowding, extremely unsanitary
conditions). Animal hoarding may be a special manifestation of hoarding disorder. Most
individuals who hoard animals also hoard inanimate objects. The most prominent differ-
ences between animal and object hoarding are the extent of unsanitary conditions and the
poorer insight in animal hoarding.
Prevalence
Nationally representative prevalence studies of hoarding disorder are not available. Com-
munity surveys estimate the point prevalence of clinically significant hoarding in the
United States and Europe to be approximately 2%-6%. Hoarding disorder affects both
males and females, but some epidemiological studies have reported a significantly greater
prevalence among males. This contrasts with clinical samples, which are predominantly
female. Hoarding symptoms appear to be almost three times more prevalent in older
adults (ages 55-94 years) compared with younger adults (ages 3444 years).
Development and Course
Hoarding appears to begin early in life and spans well into the late stages. Hoarding symp-
toms may first emerge around ages 11-15 years, start interfering with the individual’s ev-
eryday functioning by the mid-20s, and cause clinically significant impairment by the
mid-30s. Participants in clinical research studies are usually in their 50s. Thus, the severity
of hoarding increases with each decade of life. Once symptoms begin, the course of hoard-
ing is often chronic, with few individuals reporting a waxing and waning course.
Pathological hoarding in children appears to be easily distinguished from develop-
mentally adaptive saving and collecting behaviors. Because children and adolescents
typically do not control their living environment and discarding behaviors, the possible
intervention of third parties (e.g., parents keeping the spaces usable and thus reducing in-
terference) should be considered when making the diagnosis.
Risk and Prognostic Factors
Temperamental. Indecisiveness is a prominent feature of individuals with hoarding dis-
order and their first-degree relatives.
Environmental. Individuals with hoarding disorder often retrospectively report stressful
and traumatic life events preceding the onset of the disorder or causing an exacerbation.
Genetic and physiological. Hoarding behavior is familial, with about 50% of individu-
als who hoard reporting having a relative who also hoards. Twin studies indicate that ap-
proximately 50% of the variability in hoarding behavior is attributable to additive genetic
factors.
250 Obsessive-Compulsive and Related Disorders
Culture-Related Diagnostic Issues
While most of the research has been done in Western, industrialized countries and urban
communities, the available data from non-Western and developing countries suggest that
hoarding is a universal phenomenon with consistent clinical features.
Gender-Related Diagnostic Issues
The key features of hoarding disorder (i.e., difficulties discarding, excessive amount of
clutter) are generally comparable in males and females, but females tend to display more
excessive acquisition, particularly excessive buying, than do males.
Functional Consequences of Hoarding Disorder
Clutter impairs basic activities, such as moving through the house, cooking, cleaning, per-
sonal hygiene, and even sleeping. Appliances may be broken, and utilities such as water
and electricity may be disconnected, as access for repair work may be difficult. Quality of
life is often considerably impaired. In severe cases, hoarding can put individuals at risk for
fire, falling (especially elderly individuals), poor sanitation, and other health risks. Hoard-
ing disorder is associated with occupational impairment, poor physical health, and high
social service utilization. Family relationships are frequently under great strain. Conflict
with neighbors and local authorities is common, and a substantial proportion of individ-
uals with severe hoarding disorder have been involved in legal eviction proceedings, and
some have a history of eviction.
Differential Diagnosis
Other medical conditions. Hoarding disorder is not diagnosed if the symptoms are
judged to be a direct consequence of another medical condition (Criterion E), such as trau-
matic brain injury, surgical resection for treatment of a tumor or seizure control, cerebro-
vascular disease, infections of the central nervous system (e.g., herpes simplex encephalitis),
or neurogenetic conditions such as Prader-Willi syndrome. Damage to the anterior ven-
tromedial prefrontal and cingulate cortices has been particularly associated with the ex-
cessive accumulation of objects. In these individuals, the hoarding behavior is not present
prior to the onset of the brain damage and appears shortly after the brain damage occurs.
Some of these individuals appear to have little interest in the accumulated items and are
able to discard them easily or do not care if others discard them, whereas others appear to
be very reluctant to discard anything.
Neurodevelopmental disorders. Hoarding disorder is not diagnosed if the accumula-
tion of objects is judged to be a direct consequence of a neurodevelopmental disorder, such
as autism spectrum disorder or intellectual disability (intellectual developmental disorder).
Schizophrenia spectrum and other psychotic disorders. Hoarding disorder is not di-
agnosed if the accumulation of objects is judged to be a direct consequence of delusions or
negative symptoms in schizophrenia spectrum and other psychotic disorders.
Major depressive episode. Hoarding disorder is not diagnosed if the accumulation of
objects is judged to be a direct consequence of psychomotor retardation, fatigue, or loss of
energy during a major depressive episode.
Obsessive-compulsive disorder. Hoarding disorder is not diagnosed if the symptoms
are judged to be a direct consequence of typical obsessions or compulsions, such as fears
of contamination, harm, or feelings of incompleteness in obsessive-compulsive disorder
(OCD). Feelings of incompleteness (e.g., losing one’s identity, or having to document and
preserve all life experiences) are the most frequent OCD symptoms associated with this
form of hoarding. The accumulation of objects can also be the result of persistently avoid-
Trichotillomania (Hair-Pulling Disorder) 251
ing onerous rituals (e.g., not discarding objects in order to avoid endless washing or check-
ing rituals).
In OCD, the behavior is generally unwanted and highly distressing, and the individual ex-
periences no pleasure or reward from it. Excessive acquisition is usually not present; if exces-
sive acquisition is present, items are acquired because of a specific obsession (e.g., the need to
buy items that have been accidentally touched in order to avoid contaminating other people),
not because of a genuine desire to possess the items. Individuals who hoard in the context of
OCD are also more likely to accumulate bizarre items, such as trash, feces, urine, nails, hair,
used diapers, or rotten food. Accumulation of such items is very unusual in hoarding disorder.
When severe hoarding appears concurrently with other typical symptoms of OCD but
is judged to be independent from these symptoms, both hoarding disorder and OCD may
be diagnosed.
Neurocognitive disorders. Hoarding disorder is not diagnosed if the accumulation of
objects is judged to be a direct consequence of a degenerative disorder, such as neurocog-
nitive disorder associated with frontotemporal lobar degeneration or Alzheimer’s disease.
Typically, onset of the accumulating behavior is gradual and follows onset of the neuro-
cognitive disorder. The accumulating behavior may be accompanied by self-neglect and
severe domestic squalor, alongside other neuropsychiatric symptoms, such as disinhibi-
tion, gambling, rituals/stereotypies, tics, and self-injurious behaviors.
Comorbidity
Approximately 75% of individuals with hoarding disorder have a comorbid mood or anx-
iety disorder. The most common comorbid conditions are major depressive disorder (up
to 50% of cases), social anxiety disorder (social phobia), and generalized anxiety disorder.
Approximately 20% of individuals with hoarding disorder also have symptoms that meet
diagnostic criteria for OCD. These comorbidities may often be the main reason for consul-
tation, because individuals are unlikely to spontaneously report hoarding symptoms, and
these symptoms are often not asked about in routine clinical interviews.
Trichotillomania (Hair-Pulling Disorder)
Diagnostic Criteria 312.39 (F63.2)
A. Recurrent pulling out of one’s hair, resulting in hair loss.
B. Repeated attempts to decrease or stop hair pulling.
C. The hair pulling causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
D. The hair pulling or hair loss is not attributable to another medical condition (e.g., a der-
matological condition).
E. The hair pulling is not better explained by the symptoms of another mental disorder
(e.g., attempts to improve a perceived defect or flaw in appearance in body dysmorphic
disorder).
Diagnostic Features
The essential feature of trichotillomania (hair-pulling disorder) is the recurrent pulling out
of one’s own hair (Criterion A). Hair pulling may occur from any region of the body in
which hair grows; the most common sites are the scalp, eyebrows, and eyelids, while less
common sites are axillary, facial, pubic, and peri-rectal regions. Hair-pulling sites may
vary over time. Hair pulling may occur in brief episodes scattered throughout the day or
during less frequent but more sustained periods that can continue for hours, and such hair
252 Obsessive-Compulsive and Related Disorders
pulling may endure for months or years. Criterion A requires that hair pulling lead to hair
loss, although individuals with this disorder may pull hair in a widely distributed pattern
(i.e., pulling single hairs from all over a site) such that hair loss may not be clearly visible.
Alternatively, individuals may attempt to conceal or camouflage hair loss (e.g., by using
makeup, scarves, or wigs). Individuals with trichotillomania have made repeated at-
tempts to decrease or stop hair pulling (Criterion B), Criterion C indicates that hair pulling
causes clinically significant distress or impairment in social, occupational, or other impor-
tant areas of functioning. The term distress includes negative affects that may be experi-
enced by individuals with hair pulling, such as feeling a loss of control, embarrassment,
and shame. Significant impairment may occur in several different areas of functioning
(e.g., social, occupational, academic, and leisure), in part because of avoidance of work,
school, or other public situations.
Associated Features Supporting Diagnosis
Hair pulling may be accompanied by a range of behaviors or rituals involving hair. Thus,
individuals may search for a particular kind of hair to pull (e.g., hairs with a specific tex-
ture or color), may try to pull out hair in a specific way (e.g., so that the root comes out in-
tact), or may visually examine or tactilely or orally manipulate the hair after it has been
pulled (e.g., rolling the hair between the fingers, pulling the strand between the teeth, bit-
ing the hair into pieces, or swallowing the hair).
Hair pulling may also be preceded or accompanied by various emotional states; it may
be triggered by feelings of anxiety or boredom, may be preceded by an increasing sense of
tension (either immediately before pulling out the hair or when attempting to resist the
urge to pull), or may lead to gratification, pleasure, or a sense of relief when the hair is
pulled out. Hair-pulling behavior may involve varying degrees of conscious awareness,
with some individuals displaying more focused attention on the hair pulling (with pre-
ceding tension and subsequent relief), and other individuals displaying more automatic
behavior (in which the hair pulling seems to occur without full awareness). Many individ-
uals report a mix of both behavioral styles. Some individuals experience an “itch-like” or
tingling sensation in the scalp that is alleviated by the act of pulling hair. Pain does not
usually accompany hair pulling.
Patterns of hair loss are highly variable. Areas of complete alopecia, as well as areas of
thinned hair density, are common. When the scalp is involved, there may be a predilection
for pulling out hair in the crown or parietal regions. There may be a pattern of nearly com-
plete baldness except for a narrow perimeter around the outer margins of the scalp, par-
ticularly at the nape of the neck (“tonsure trichotillomania”). Eyebrows and eyelashes may
be completely absent.
Hair pulling does not usually occur in the presence of other individuals, except imme-
diate family members. Some individuals have urges to pull hair from other individuals
and may sometimes try to find opportunities to do so surreptitiously. Some individuals
may pull hairs from pets, dolls, and other fibrous materials (e.g., sweaters or carpets).
Some individuals may deny their hair pulling to others. The majority of individuals with
trichotillomania also have one or more other body-focused repetitive behaviors, including
skin picking, nail biting, and lip chewing.
Prevalence
In the general population, the 12-month prevalence estimate for trichotillomania in adults
and adolescents is 1%—2%. Females are more frequently affected than males, at a ratio of
approximately 10:1. This estimate likely reflects the true gender ratio of the condition, al-
though it may also reflect differential treatment seeking based on gender or cultural at-
titudes regarding appearance (e.g., acceptance of normative hair loss among males).
Among children with trichotillomania, males and females are more equally represented.
Trichotillomania (Hair-Pulling Disorder) 253
Development and Course
Hair pulling may be seen in infants, and this behavior typically resolves during early devel-
opment. Onset of hair pulling in trichotillomania most commonly coincides with, or follows
the onset of, puberty. Sites of hair pulling may vary over time. The usual course of trichotillo-
mania is chronic, with some waxing and waning if the disorder is untreated. Symptoms may
possibly worsen in females accompanying hormonal changes (e.g., menstruation, perimeno-
pause). For some individuals, the disorder may come and go for weeks, months, or years at a
time. A minority of individuals remit without subsequent relapse within a few years of onset.
Risk and Prognostic Factors
Genetic and physiological. There is evidence for a genetic vulnerability to trichotillo-
mania. The disorder is more common in individuals with obsessive-compulsive disorder
(OCD) and their first-degree relatives than in the general population.
Cuiture-Related Diagnostic Issues
Trichotillomania appears to manifest similarly across cultures, although there is a paucity
of data from non-Western regions.
Diagnostic Markers
Most individuals with trichotillomania admit to hair pulling; thus, dermatopathological
diagnosis is rarely required. Skin biopsy and dermoscopy (or trichoscopy) of trichotillo-
mania are able to differentiate the disorder from other causes of alopecia. In trichotil-
lomania, dermoscopy shows a range of characteristic features, including decreased hair
density, short vellus hair, and broken hairs with different shaft lengths.
Functional Consequences of
Trichotiiiomania (Hair-Puliing Disorder)
Trichotillomania is associated with distress as well as with social and occupational impair-
ment. There may be irreversible damage to hair growth and hair quality. Infrequent med-
ical consequences of trichotillomania include digit purpura, musculoskeletal injury (e.g.,
carpal tunnel syndrome; back, shoulder and neck pain), blepharitis, and dental damage
(e.g., worn or broken teeth due to hair biting). Swallowing of hair (trichophagia) may lead
to trichobezoars, with subsequent anemia, abdominal pain, hematemesis, nausea and
vomiting, bowel obstruction, and even perforation.
Differential Diagnosis
Normative hair removal/manipulation. Trichotillomania should not be diagnosed when
hair removal is performed solely for cosmetic reasons (i.e., to improve one’s physical ap-
pearance). Many individuals twist and play with their hair, but this behavior does not usu-
ally qualify for a diagnosis of trichotillomania. Some individuals may bite rather than pull
hair; again, this does not qualify for a diagnosis of trichotillomania.
Other obsessive-compulsive and related disorders. Individuals with OCD and sym-
metry concerns may pull out hairs as part of their symmetry rituals, and individuals with
body dysmorphic disorder may remove body hair that they perceive as ugly, asymmetri-
cal, or abnormal; in such cases a diagnosis of trichotillomania is not given. The description
of body-focused repetitive behavior disorder in other specified obsessive-compulsive and
related disorder excludes individuals who meet diagnostic criteria for trichotillomania.
254 Obsessive-Compulsive and Related Disorders
Neurodevelopmental disorders. In neurodevelopmental disorders, hair pulling may
meet the definition of stereotypies (e.g., in stereotypic movement disorder). Tics (in tic dis-
orders) rarely lead to hair pulling.
Psychotic disorder. Individuals with a psychotic disorder may remove hair in response
to a delusion or hallucination. Trichotillomania is not diagnosed in such cases.
Another medical condition. Trichotillomania is not diagnosed if the hair pulling or hair
loss is attributable to another medical condition (e.g., inflammation of the skin or other der-
matological conditions). Other causes of scarring alopecia (e.g., alopecia areata, androgenic
alopecia, telogen effluvium) or nonscarring alopecia (e.g., chronic discoid lupus erythema-
tosus, lichen planopilaris, central centrifugal cicatricial alopecia, pseudopelade, folliculitis
decalvans, dissecting folliculitis, acne keloidalis nuchae) should be considered in individu-
als with hair loss who deny hair pulling. Skin biopsy or dermoscopy can be used to differ-
entiate individuals with trichotillomania from those with dermatological disorders.
Substance-related disorders. Hair-pulling symptoms may be exacerbated by certain
substances—for example, stimulants—but it is less likely that substances are the primary
cause of persistent hair pulling.
Comorbidity
Trichotillomania is often accompanied by other mental disorders, most commonly major
depressive disorder and excoriation (skin-picking) disorder. Repetitive body-focused
symptoms other than hair pulling or skin picking (e.g. nail biting) occur in the majority of
individuals with trichotillomania and may deserve an additional diagnosis of other spec-
ified obsessive-compulsive and related disorder (i.e., body-focused repetitive behavior
disorder).
Excoriation (Skin-Picking) Disorder
Diagnostic Criteria 698.4 (L98.1)
A. Recurrent skin picking resulting in skin lesions.
B. Repeated attempts to decrease or stop skin picking.
C. The skin picking causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
D. The skin picking is not attributable to the physiological effects of a substance (e.g., co-
caine) or another medical condition (e.g., scabies).
E. The skin picking is not better explained by symptoms of another mental disorder (e.g.,
delusions or tactile hallucinations in a psychotic disorder, attermpts to improve a per-
ceived defect or flaw in appearance in body dysmorphic disorder, stereotypies in ste-
reotypic movement disorder, or intention to harm oneself in nonsuicidal self-injury).
Diagnostic Features
The essential feature of excoriation (skin-picking) disorder is recurrent picking at one’s
own skin (Criterion A). The most commonly picked sites are the face, arms, and hands, but
many individuals pick from multiple body sites. Individuals may pick at healthy skin, at
minor skin irregularities, at lesions such as pimples or calluses, or at scabs from previous
picking. Most individuals pick with their fingernails, although many use tweezers, pins,
or other objects. In addition to skin picking, there may be skin rubbing, squeezing, lancing,
and biting. Individuals with excoriation disorder often spend significant amounts of time
on their picking behavior, sometimes several hours per day, and such skin picking may
Excoriation (Skin-Picking) Disorder 255
endure for months or years. Criterion A requires that skin picking lead to skin lesions, al-
though individuals with this disorder often attempt to conceal or camouflage such lesions
(e.g., with makeup or clothing). Individuals with excoriation disorder have made repeated
attempts to decrease or stop skin picking (Criterion B).
Criterion C indicates that skin picking causes clinically significant distress or impair-
ment in social, occupational, or other important areas of functioning. The term distress in-
cludes negative affects that may be experienced by individuals with skin picking, such as
feeling a loss of control, embarrassment, and shame. Significant impairment may occur in
several different areas of functioning (e.g., social, occupational, academic, and leisure), in
part because of avoidance of social situations.
Associated Features Supporting Diagnosis
Skin picking may be accompanied by a range of behaviors or rituals involving skin or scabs.
Thus, individuals may search for a particular kind of scab to pull, and they may examine,
play with, or mouth or swallow the skin after it has been pulled. Skin picking may also be pre-
ceded or accompanied by various emotional states. Skin picking may be triggered by feelings
of anxiety or boredom, may be preceded by an increasing sense of tension (either immedi-
ately before picking the skin or when attempting to resist the urge to pick), and may lead to
gratification, pleasure, or a sense of relief when the skin or scab has been picked. Some indi-
viduals report picking in response toa minor skin irregularity or to relieve an uncomfortable
bodily sensation. Pain is not routinely reported to accompany skin picking. Some individuals
engage in skin picking that is more focused (i.e., with preceding tension and subsequent re-
lief), whereas others engage in more automatic picking (i.e., when skin picking occurs with-
out preceding tension and without full awareness), and many have a mix of both behavioral
styles. Skin picking does not usually occur in the presence of other individuals, except im-
mediate family members. Some individuals report picking the skin of others.
Prevaience
In the general population, the lifetime prevalence for excoriation disorder in adults is 1.4%
or somewhat higher. Three-quarters or more of individuals with the disorder are female.
This likely reflects the true gender ratio of the condition, although it may also reflect dif-
ferential treatment seeking based on gender or cultural attitudes regarding appearance.
Development and Course
Although individuals with excoriation disorder may present at various ages, the skin pick-
ing most often has onset during adolescence, commonly coinciding with or following the
onset of puberty. The disorder frequently begins with a dermatological condition, such
as acne. Sites of skin picking may vary over time. The usual course is chronic, with some
waxing and waning if untreated. For some individuals, the disorder may come and go for
weeks, months, or years at a time.
Risk and Prognostic Factors
Genetic and physiological. Excoriation disorder is more common in individuals with
obsessive-compulsive disorder (OCD) and their first-degree family members than in the
general population.
Diagnostic Markers
Most individuals with excoriation disorder admit to skin picking; therefore, dermato-
pathological diagnosis is rarely required. However, the disorder may have characteristic
features on histopathology.
256 Obsessive-Compulsive and Related Disorders
Functional Consequences of
Excoriation (Skin-Picking) Disorder
Excoriation disorder is associated with distress as well as with social and occupational im-
pairment. The majority of individuals with this condition spend at least 1 hour per day
picking, thinking about picking, and resisting urges to pick. Many individuals report
avoiding social or entertainment events as well as going out in public. A majority of indi-
viduals with the disorder also report experiencing work interference from skin picking on
at least a daily or weekly basis. A significant proportion of students with excoriation disor-
der report having missed school, having experienced difficulties managing responsibilities
at school, or having had difficulties studying because of skin picking. Medical complica-
tions of skin picking include tissue damage, scarring, and infection and can be life-threaten-
ing. Rarely, synovitis of the wrists due to chronic picking has been reported. Skin picking
often results in significant tissue damage and scarring. It frequently requires antibiotic treat-
ment for infection, and on occasion it may require surgery.
Differential Diagnosis
Psychotic disorder. Skin picking may occur in response to a delusion (i.e., parasitosis)
or tactile hallucination (i.e., formication) in a psychotic disorder. In such cases, excoriation
disorder should not be diagnosed.
Other obsessive-compulsive and related disorders. Excessive washing compulsions
in response to contamination obsessions in individuals with OCD may lead to skin lesions,
and skin picking may occur in individuals with body dysmorphic disorder who pick their
skin solely because of appearance concerns; in such cases, excoriation disorder should not
be diagnosed. The description of body-focused repetitive behavior disorder in other spec-
ified obsessive-compulsive and related disorder excludes individuals whose symptoms
meet diagnostic criteria for excoriation disorder.
Neurodevelopmenta! disorders. While stereotypic movement disorder may be charac-
terized by repetitive self-injurious behavior, onset is in the early developmental period.
For example, individuals with the neurogenetic condition Prader-Willi syndrome may
have early onset of skin picking, and their symptoms may meet criteria for stereotypic
movement disorder. While tics in individuals with Tourette’s disorder may lead to self-
injury, the behavior is not tic-like in excoriation disorder.
Somatic symptom and related disorders. Excoriation disorder is not diagnosed if the
skin lesion is primarily attributable to deceptive behaviors in factitious disorder.
Other disorders. Excoriation disorder is not diagnosed if the skin picking is primarily
attributable to the intention to harm oneself that is characteristic of nonsuicidal self-injury.
Other medical conditions. Excoriation disorder is not diagnosed if the skin picking is
primarily attributable to another medical condition. For example, scabies is a dermatolog-
ical condition invariably associated with severe itching and scratching. However, excori-
ation disorder may be precipitated or exacerbated by an underlying dermatological
condition. For example, acne may lead to some scratching and picking, which may also be
associated with comorbid excoriation disorder. The differentiation between these two
clinical situations (acne with some scratching and picking vs. acne with comorbid excori-
ation disorder) requires an assessment of the extent to which the individual’s skin picking
has become independent of the underlying dermatological condition.
Substance/medication-induced disorders. Skin-picking symptoms may also be induced
by certain substances (e.g., cocaine), in which case excoriation disorder should not be di-
agnosed. If such skin picking is clinically significant, then a diagnosis of substance /med-
ication-induced obsessive-compulsive and related disorder should be considered.
Substance/Medication-Induced Obsessive-Compulsive and Related Disorder 257
Comorbidity
Excoriation disorder is often accompanied by other mental disorders. Such disorders in-
clude OCD and trichotillomania (hair-puilling disorder), as well as major depressive dis-
order. Repetitive body-focused symptoms other than skin picking and hair pulling (e.g.,
nail biting) occur in many individuals with excoriation disorder and may deserve an ad-
ditional diagnosis of other specified obsessive-compulsive and related disorder (i.e.,
body-focused repetitive behavior disorder).
Substance/Medication-Induced
Obsessive-Compulsive and Related Disorder
Diagnostic Criteria
A. Obsessions, compulsions, skin picking, hair pulling, other body-focused repetitive be-
haviors, or other symptoms characteristic of the obsessive-compulsive and related dis-
orders predominate in the clinical picture.
B. There is evidence from the history, physical examination, or laboratory findings of both
(1) and (2):
1. The symptoms in Criterion A developed during or soon after substance intoxication
or withdrawal or after exposure to a medication.
2. The involved substance/medication is capable of producing the symptoms in Crite-
rion A.
C. The disturbance is not better explained by an obsessive-compulsive and related disor-
der that is not substance/medication-induced. Such evidence of an independent ob-
sessive-compulsive and related disorder could include the following:
The symptoms precede the onset of the substance/medication use; the symptoms
persist for a substantial period of time (e.g., about 1 month) after the cessation of acute
withdrawal or severe intoxication; or there is other evidence suggesting the exis-
tence of an independent non-substance/medication-induced obsessive-compul-
sive and related disorder (e.g., a history of recurrent non-substance/medication-
related episodes).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
Note: This diagnosis should be made in addition to a diagnosis of substance intoxication
or substance withdrawal only when the symptoms in Criterion A predominate in the clinical
picture and are sufficiently severe to warrant clinical attention.
Coding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance/medica-
tion]-induced obsessive-compulsive and related disorders are indicated in the table below.
Note that the ICD-10-CM code depends on whether or not there is a comorbid substance
use disorder present for the same class of substance. If a mild substance use disorder is
comorbid with the substance-induced obsessive-compulsive and related disorder, the 4th
position character is “1,” and the clinician should record “mild [substance] use disorder”
before the substance-induced obsessive-compulsive and related disorder (e.g., “mild co-
caine use disorder with cocaine-induced obsessive-compulsive and related disorder’). If
a moderate or severe substance use disorder is comorbid with the substance-induced ob-
sessive-compulsive and related disorder, the 4th position character is “2,” and the clinician
should record “moderate [substance] use disorder’ or “severe [substance] use disorder,”
depending on the severity of the comorbid substance use disorder. If there is no comorbid
258 Obsessive-Compulsive and Related Disorders
substance use disorder (e.g., after a one-time heavy use of the substance), then the 4th
position character is “9,” and the clinician should record only the substance-induced ob-
sessive-compulsive and related disorder.
ICD-10-CM
With use
With use disorder, Without
disorder, moderate use
ICD-9-CM mild or severe disorder
Amphetamine (or other 292.89 F15.188 F15.288 F15.988
stimulant)
Cocaine 292.89 F14.188 F14.288 F14.988
Other (or unknown) substance 292.89 F19.188 F19.288 F19.988
Specify if (see Table 1 in the chapter “Substance-Related and Addictive Disorders” for di-
agnoses associated with substance class):
With onset during intoxication: If the criteria are met for intoxication with the sub-
stance and the symptoms develop during intoxication.
With onset during withdrawai: If criteria are met for withdrawal from the substance
and the symptoms develop during, or shortly after, withdrawal.
With onset after medication use: Symptoms may appear either at initiation of medi-
cation or after a modification or change in use.
Recording Procedures
ICD-9-CM. The name of the substance/medication-induced obsessive-compulsive and
related disorder begins with the specific substance (e.g., cocaine) that is presumed to be
causing the obsessive-compulsive and related symptoms. The diagnostic code is selected
from the table included in the criteria set, which is based on the drug class. For substances
that do not fit into any of the classes, the code for “other substance” should be used; and in
cases in which a substance is judged to be an etiological factor but the specific class of sub-
stance is unknown, the category “unknown substance” should be used.
The name of the disorder is followed by the specification of onset (i.e., onset during in-
toxication, onset during withdrawal, with onset after medication use). Unlike the record-
ing procedures for ICD-10-CM, which combine the substance-induced disorder and
substance use disorder into a single code, for ICD-9-CM a separate diagnostic code is
given for the substance use disorder. For example, in the case of repetitive behaviors oc-
curring during intoxication in a man with a severe cocaine use disorder, the diagnosis is
292.89 cocaine-induced obsessive-compulsive and related disorder, with onset during in-
toxication. An additional diagnosis of 304.20 severe cocaine use disorder is also given.
When more than one substance is judged to play a significant role in the development of
the obsessive-compulsive and related disorder, each should be listed separately.
ICD-10-CM. Thename of the substance /medication-induced obsessive-compulsive and re-
lated disorder begins with the specific substance (e.g., cocaine) that is presumed to be causing
the obsessive-compulsive and related symptoms. The diagnostic code is selected from the ta-
ble included in the criteria set, which is based on the drug class and presence or absence of a
comorbid substance use disorder. For substances that do not fit into any of the classes,
the code for “other substance” with no comorbid substance use should be used; and in cases in
which a substance is judged to be an etiological factor but the specific class of substance is un-
known, the category “unknown substance” with no comorbid substance use should be used.
Substance/Medication-Induced Obsessive-Compulsive and Related Disorder 259
When recording the name of the disorder, the comorbid substance use disorder (if any) is
listed first, followed by the word “with,” followed by the name of the substance-induced ob-
sessive-compulsive and related disorder, followed by the specification of onset (i-e., onset dur-
ing intoxication, onset during withdrawal, with onset after medication use). For example, in
the case of repetitive behaviors occurring during intoxication in a man with a severe cocaine
use disorder, the diagnosis is F14.288 severe cocaine use disorder with cocaine-induced obses-
sive-compulsive and related disorder, with onset during intoxication. A separate diagnosis of
the comorbid severe cocaine use disorder is not given. If the substance-induced obsessive-
compulsive and related disorder occurs without a comorbid substance use disorder (e.g., after
a one-time heavy use of the substance), no accompanying substance use disorder is noted (e.g.,
F15.988 amphetamine-induced obsessive-compulsive and related disorder, with onset during
intoxication). When more than one substance is judged to play a significant role in the devel-
opment of the obsessive-compulsive and related disorder, each should be listed separately.
Diagnostic Features
The essential features of substance /medication-induced obsessive-compulsive and related
disorder are prominent symptoms of an obsessive-compulsive and related disorder (Criterion
A) that are judged to be attributable to the effects of a substance (e.g., drug of abuse, medica-
tion). The obsessive-compulsive and related disorder symptoms must have developed during
or soon after substance intoxication or withdrawal or after exposure to a medication or toxin,
and the substance/ medication must be capable of producing the symptoms (Criterion B). Sub-
stance/medication-induced obsessive-compulsive and related disorder due to a prescribed
treatment for a mental disorder or general medical condition must have its onset while the in-
dividual is receiving the medication. Once the treatment is discontinued, the obsessive-com-
pulsive and related disorder symptoms will usually improve or remit within days to several
weeks to 1 month (depending on the half-life of the substance/ medication). The diagnosis of
substance /medication-induced obsessive-compulsive and related disorder should not be
given if onset of the obsessive-compulsive and related disorder symptoms precedes the sub-
stance intoxication or medication use, or if the symptoms persist for a substantial period of
time, usually longer than 1 month, from the time of severe intoxication or withdrawal. If the
obsessive-compulsive and related disorder symptoms persist for a substantial period of time,
other causes for the symptoms should be considered. The substance/medication-induced ob-
sessive-compulsive and related disorder diagnosis should be made in addition to a diagnosis
of substance intoxication only when the symptoms in Criterion A predominate in the clinical
picture and are sufficiently severe to warrant independent clinical attention
Associated Features Supporting Diagnosis
Obsessions, compulsions, hair pulling, skin picking, or other body-focused repetitive be-
haviors can occur in association with intoxication with the following classes of substances:
stimulants (including cocaine) and other (or unknown) substances. Heavy metals and tox-
ins may also cause obsessive-compulsive and related disorder symptoms. Laboratory as-
sessments (e.g., urine toxicology) may be useful to measure substance intoxication as part
of an assessment for obsessive-compulsive and related disorders.
Prevalence
In the general population, the very limited data that are available indicate that substance-
induced obsessive-compulsive and related disorder is very rare.
Differentiai Diagnosis
Substance intoxication. Obsessive-compulsive and related disorder symptoms may oc-
cur in substance intoxication. The diagnosis of the substance-specific intoxication will usu-
260 Obsessive-Compulsive and Related Disorders
ally suffice to categorize the symptom presentation. A diagnosis of an obsessive-compulsive
and related disorder should be made in addition to substance intoxication when the symp-
toms are judged to be in excess of those usually associated with intoxication and are suf-
ficiently severe to warrant independent clinical attention.
Obsessive-compulsive and related disorder (i.e., not induced by a substance). Sub-
stance /medication-induced obsessive-compulsive and related disorder is judged to be
etiologically related to the substance/ medication. Substance /medication-induced obses-
sive-compulsive and related disorder is distinguished from a primary obsessive-compul-
sive and related disorder by considering the onset, course, and other factors with respect
to substances / medications. For drugs of abuse, there must be evidence from the history,
physical examination, or laboratory findings for use or intoxication. Substance /medica-
tion-induced obsessive-compulsive and related disorder arises only in association with in-
toxication, whereas a primary obsessive-compulsive and related disorder may precede the
onset of substance /medication use. The presence of features that are atypical of a primary
obsessive-compulsive and related disorder, such as atypical age at onset of symptoms,
may suggest a substance-induced etiology. A primary obsessive-compulsive and related
disorder diagnosis is warranted if the symptoms persist for a substantial period of time
(about 1 month or longer) after the end of the substance intoxication or the individual has
a history of an obsessive-compulsive and related disorder.
Obsessive-compulsive and related disorder due to another medical condition. If the
obsessive-compulsive and related disorder symptoms are attributable to another medical
condition (i.e., rather than to the medication taken for the other medical condition), obses-
sive-compulsive and related disorder due to another medical condition should be diag-
nosed. The history often provides the basis for judgment. At times, a change in the
treatment for the other medical condition (e.g., medication substitution or discontinua-
tion) may be needed to determine whether or not the medication is the causative agent (in
which case the symptoms may be better explained by substance/medication-induced ob-
sessive-compulsive and related disorder). If the disturbance is attributable to both another
medical condition and substance use, both diagnoses (i.e., obsessive-compulsive and related
disorder due to another medical condition and substance /medication-induced obsessive-
compulsive and related disorder) may be given. When there is insufficient evidence to de-
termine whether the symptoms are attributable to either a substance /medication or an-
other medical condition or are primary (i.e., attributable to neither a substance/ medication
nor another medical condition), a diagnosis of other specified or unspecified obsessive-
compulsive and related disorder would be indicated.
Delirium. If obsessive-compulsive and related disorder symptoms occur exclusively
during the course of delirium, they are considered to be an associated feature of the delir-
ium and are not diagnosed separately.
Obsessive-Compulsive and Related Disorder
Due to Another Medical Condition
Diagnostic Criteria 294.8 (FO6.8)
A. Obsessions, compulsions, preoccupations with appearance, hoarding, skin picking,
hair pulling, other body-focused repetitive behaviors, or other symptoms characteristic
of obsessive-compulsive and related disorder predominate in the clinical picture.
B. There is evidence from the history, physical examination, or laboratory findings that the
disturbance is the direct pathophysiological consequence of another medical condition.
C. The disturbance is not better explained by another mental disorder.
Obsessive-Compulsive and Related Disorder Due to Another Medical Condition 261
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
Specify if:
With obsessive-compulsive disorder—like symptoms: If obsessive-compulsive dis-
order—like symptoms predominate in the clinica! presentation.
With appearance preoccupations: If preoccupation with perceived appearance de-
fects or flaws predominates in the clinical presentation.
With hoarding symptoms: If hoarding predominates in the clinical presentation.
With hair-pulling symptoms: If hair pulling predominates in the clinical presentation.
With skin-picking symptoms: If skin picking predominates in the clinical presenta-
tion.
Coding note: Include the name of the other medical condition in the name of the mental
disorder ({e.g., 294.8 [F06.8] obsessive-compulsive and related disorder due to cerebral
infarction}. The other medical condition should be coded and listed separately immediately
before the obsessive-compulsive and related disorder due to the medical condition (e.g.,
438.89 [169.398] cerebral infarction; 294.8 [F06.8] obsessive-compulsive and related dis-
order due to cerebral infarction).
Diagnostic Features
The essential feature of obsessive-compulsive and related disorder due to another medical
condition is clinically significant obsessive-compulsive and related symptoms that are
judged to be best explained as the direct pathophysiological consequence of another med-
ical condition. Symptoms can include prominent obsessions, compulsions, preoccu-
pations with appearance, hoarding, hair pulling, skin picking, or other body-focused
repetitive behaviors (Criterion A). The judgment that the symptoms are best explained by
the associated medical condition must be based on evidence from the history, physical ex-
amination, or laboratory findings (Criterion B). Additionally, it must be judged that the
symptoms are not better explained by another mental disorder (Criterion C). The diagno-
sis is not made if the obsessive-compulsive and related symptoms occur only during the
course of a delirium (Criterion D). The obsessive-compulsive and related symptoms must
cause clinically significant distress or impairment in social, occupational, or other impor-
tant areas of functioning (Criterion E).
In determining whether the obsessive-compulsive and related symptoms are attribut-
able to another medical condition, a relevant medical condition must be present. Further-
more, it must be established that obsessive-compulsive and related symptoms can be
etiologically related to the medical condition through a pathophysiological mechanism
and that this best explains the symptoms in the individual. Although there are no infallible
guidelines for determining whether the relationship between the obsessive-compulsive
and related symptoms and the medical condition is etiological, considerations that may
provide some guidance in making this diagnosis include the presence of a clear temporal
association between the onset, exacerbation, or remission of the medical condition and the
obsessive-compulsive and related symptoms; the presence of features that are atypical of
a primary obsessive-compulsive and related disorder (e.g., atypical age at onset or course);
and evidence in the literature that a known physiological mechanism (e.g., striatal dam-
age) causes obsessive-compulsive and related symptoms. In addition, the disturbance
cannot be better explained by a primary obsessive-compulsive and related disorder, a sub-
stance/medication-induced obsessive-compulsive and related disorder, or another men-
tal disorder.
There is some controversy about whether obsessive-compulsive and related disorders
can be attributed to Group A streptococcal infection. Sydenham’s chorea is the neurolog-
262 Obsessive-Compulsive and Related Disorders
ical manifestation of rheumatic fever, which is in turn due to Group A streptococcal in-
fection. Sydenham’s chorea is characterized by a combination of motor and nonmotor
features. Nonmotor features include obsessions, compulsions, attention deficit, and emo-
tional lability. Although individuals with Sydenham’s chorea may present with non-
neuropsychiatric features of acute rheumatic fever, such as carditis and arthritis, they may
present with obsessive-compulsive disorder-like symptoms; such individuals should
be diagnosed with obsessive-compulsive and related disorder due to another medical
condition.
Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infec-
tions (PANDAS) has been identified as another post-infectious autoimmune disorder
characterized by the sudden onset of obsessions, compulsions, and/or tics accompanied
by a variety of acute neuropsychiatric symptoms in the absence of chorea, carditis, or ar-
thritis, after Group A streptococcal infection. Although there is a body of evidence that
supports the existence of PANDAS, it remains a controversial diagnosis. Given this ongo-
ing controversy, the description of PANDAS has been modified to eliminate etiological
factors and to designate an expanded clinical entity: pediatric acute-onset neuropsychiat-
ric syndrome (PANS) or idiopathic childhood acute neuropsychiatric symptoms (CANS),
which deserves further study.
Associated Features Supporting Diagnosis
A number of other medical disorders are known to include obsessive-compulsive and re-
lated symptoms as a manifestation. Examples include disorders leading to striatal dam-
age, such as cerebral infarction.
Development and Course
The development and course of obsessive-compulsive and related disorder due to another
medical condition generally follows the course of the underlying illness.
Diagnostic Markers
Laboratory assessments and/or medical examinations are necessary to confirm the diag-
nosis of another medical condition.
Differential Diagnosis
Delirium. A separate diagnosis of obsessive-compulsive and related disorder due to an-
other medical condition is not given if the disturbance occurs exclusively during the
course of a delirium. However, a diagnosis of obsessive-compulsive and related disorder
due to another medical condition may be given in addition to a diagnosis of major neuro-
cognitive disorder (dementia) if the etiology of the obsessive-compulsive symptoms is
judged to bea physiological consequence of the pathological process causing the dementia
and if obsessive-compulsive symptoms are a prominent part of the clinical presentation.
Mixed presentation of symptoms (e.g., mood and obsessive-compulsive and related
disorder symptoms). If the presentation includes a mix of different types of symptoms,
the specific mental disorder due to another medical condition depends on which symp-
toms predominate in the clinical picture.
Substance/medication-induced obsessive-compulsive and related disorders. If there
is evidence of recent or prolonged substance use (including medications with psychoac-
tive effects), withdrawal froma substance, or exposure to a toxin, a substance /medication-
induced obsessive-compulsive and related disorder should be considered. When a sub-
stance/medication-induced obsessive-compulsive and related disorder is being diag-
nosed in relation to drugs of abuse, it may be useful to obtain a urine or blood drug screen
Other Specified Obsessive-Compulsive and Related Disorder 263
or other appropriate laboratory evaluation. Symptoms that occur during or shortly after
(i.e., within 4 weeks of) substance intoxication or withdrawal or after medication use may
be especially indicative of a substance /medication-induced obsessive-compulsive and re-
lated disorder, depending on the type, duration, or amount of the substance used.
Obsessive-compulsive and related disorders (primary). Obsessive-compulsive and re-
lated disorder due to another medical condition should be distinguished from a primary
obsessive-compulsive and related disorder. In primary mental disorders, no specific and
direct causative physiological mechanisms associated with a medical condition can be
demonstrated. Late age at onset or atypical symptoms suggest the need for a thorough as-
sessment to rule out the diagnosis of obsessive-compulsive and related disorder due to an-
other medical condition.
IlIness anxiety disorder. Illness anxiety disorder is characterized by a preoccupation with
having or acquiring a serious illness. In the case of illness anxiety disorder, individuals
may or may not have diagnosed medical conditions.
Associated feature of another mental disorder. Obsessive-compulsive and related symp-
toms may be an associated feature of another mental disorder (e.g., schizophrenia, an-
orexia nervosa).
Other specified obsessive-compulsive and related disorder or unspecified obsessive-
compulsive and related disorder. These diagnoses are given if it is unclear whether the
obsessive-compulsive and related symptoms are primary, substance-induced, or due to
another medical condition.
Other Specified Obsessive-Compulsive
and Related Disorder
300.3 (F42)
This category applies to presentations in which symptoms characteristic of an obsessive-
compulsive and related disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the obsessive-compulsive and related disorders
diagnostic class. The other specified obsessive-compulsive and related disorder category
is used in situations in which the clinician chooses to communicate the specific reason that
the presentation does not meet the criteria for any specific obsessive-compulsive and re-
lated disorder. This is done by recording “other specified obsessive-compulsive and retat-
ed disorder” followed by the specific reason {e.g., “body-focused repetitive behavior
disorder’).
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Body dysmorphic-like disorder with actual flaws: This is similar to body dysmor-
phic disorder except that the defects or flaws in physical appearance are clearly ob-
servable by others (i.e., they are more noticeable than “slight’). In such cases, the
preoccupation with these flaws is clearly excessive and causes significant impairment
or distress.
2. Body dysmorphic-like disorder without repetitive behaviors: Presentations that
meet body dysmorphic disorder except that the individual has not performed repetitive
behaviors or mental acts in response to the appearance concerns.
3. Body-focused repetitive behavior disorder: This is characterized by recurrent body-
focused repetitive behaviors (e.g., nail biting, lip biting, cheek chewing) and repeated
attempts to decrease or stop the behaviors. These symptoms cause clinically significant
264 Obsessive-Compulsive and Related Disorders
distress or impairment in social, occupational, or other important areas of functioning
and are not better explained by trichotillomania (hair-pulling disorder), excoriation (skin-
picking) disorder, stereotypic movement disorder, or nonsuicidal self-injury.
4. Obsessional jealousy: This is characterized by nondelusional preoccupation with a
partner's perceived infidelity. The preoccupations may lead to repetitive behaviors or
mental acts in response to the infidelity concerns; they cause clinically significant dis-
tress or impairment in social, occupational, or other important areas of functioning; and
they are not better explained by another mental disorder such as delusional disorder,
jealous type, or paranoid personality disorder.
5. Shubo-kyofu: A variant of taijin kyofusho (see “Glossary of Cultural Concepts of Dis-
tress” in the Appendix) that is similar to body dysmorphic disorder and is characterized
by excessive fear of having a bodily deformity.
6. Koro: Related to dhat syndrome (see “Glossary of Cultural Concepts of Distress” in
the Appendix), an episode of sudden and intense anxiety that the penis (or the vulva
and nipples in femaies) will recede into the body, possibly leading to death.
7. Jikoshu-kyofu: A variant of taijin kyofusho (see “Glossary of Cultural Concepts of Dis-
tress” in the Appendix) characterized by fear of having an offensive body odor (also
termed olfactory reference syndrome).
Unspecified Obsessive-Compulsive
and Related Disorder
300.3 (F42)
This category applies to presentations in which symptoms characteristic of an obsessive-
compulsive and related disorder that cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning predominate but do not meet
the full criteria for any of the disorders in the obsessive-compulsive and related disorders
diagnostic class. The unspecified obsessive-compulsive and related disorder category is
used in situations in which the clinician chooses not to specify the reason that the criteria
are not met for a specific obsessive-compulsive and related disorder, and includes presen-
tations in which there is insufficient information to make a more specific diagnosis (¢.g., in
emergency room settings).
Trauma- and stressor-related disorders include disorders in which exposure to
a traumatic or stressful event is listed explicitly as a diagnostic criterion. These include reactive
attachment disorder, disinhibited social engagement disorder, posttraumatic stress disor-
der (PTSD), acute stress disorder, and adjustment disorders. Placement of this chapter reflects
the close relationship between these diagnoses and disorders in the surrounding chapters on
anxiety disorders, obsessive-compulsive and related disorders, and dissociative disorders.
Psychological distress following exposure to a traumatic or stressful event is quite vari-
able. In some cases, symptoms can be well understood within an anxiety- or fear-based
context. It is clear, however, that many individuals who have been exposed to a traumatic
or stressful event exhibit a phenotype in which, rather than anxiety- or fear-based symp-
toms, the most prominent clinical characteristics are anhedonic and dysphoric symptoms,
externalizing angry and aggressive symptoms, or dissociative symptoms. Because of these
variable expressions of clinical distress following exposure to catastrophic or aversive
events, the aforementioned disorders have been grouped under a separate category:
trauma- and stressor-related disorders. Furthermore, it is not uncommon for the clinical pic-
ture to include some combination of the above symptoms (with or without anxiety- or
fear-based symptoms). Such a heterogeneous picture has long been recognized in adjust-
ment disorders, as well. Social neglect—that is, the absence of adequate caregiving during
childhood—is a diagnostic requirement of both reactive attachment disorder and disin-
hibited social engagement disorder. Although the two disorders share a common etiology,
the former is expressed as an internalizing disorder with depressive symptoms and with-
drawn behavior, while the latter is marked by disinhibition and externalizing behavior.
Reactive Attachment Disorder
Diagnostic Criteria 313.89 (F94.1)
A. Aconsistent pattern of inhibited, emotionally withdrawn behavior toward adult caregiv-
ers, manifested by both of the following:
1. The child rarely or minimally seeks comfort when distressed.
2. The child rarely or minimally responds to comfort when distressed.
B. Apersistent social and emotional disturbance characterized by at least two of the following:
1. Minimal social and emotional responsiveness to others.
2. Limited positive affect.
3. Episodes of unexplained irritability, sadness, or fearfulness that are evident even
during nonthreatening interactions with adult caregivers.
C. The child has experienced a pattern of extremes of insufficient care as evidenced by
at least one of the following:
1. Social neglect or deprivation in the form of persistent lack of having basic emotional
needs for comfort, stimulation, and affection met by caregiving adults.
265
266 Trauma- and Stressor-Related Disorders
2. Repeated changes of primary caregivers that limit opportunities to form stable at-
tachments (e.g., frequent changes in foster care).
3. Rearing in unusual settings that severely limit opportunities to form selective at-
tachments (e.g., institutions with high child-to-caregiver ratios).
D. The care in Criterion C is presumed to be responsible for the disturbed behavior in Cri-
terion A (e.g., the disturbances in Criterion A began following the lack of adequate care
in Criterion C).
E. The criteria are not met for autism spectrum disorder.
F. The disturbance is evident before age 5 years.
G. The child has a developmental age of at least 9 months.
Specity if:
Persistent: The disorder has been present for more than 12 months.
Specify current severity:
Reactive attachment disorder is specified as severe when a child exhibits all symp-
toms of the disorder, with each symptom manifesting at relatively high levels.
Diagnostic Features
Reactive attachment disorder of infancy or early childhood is characterized by a pattern of
markedly disturbed and developmentally inappropriate attachment behaviors, in which a
child rarely or minimally turns preferentially to an attachment figure for comfort, support,
protection, and nurturance. The essential feature is absent or grossly underdeveloped at-
tachment between the child and putative caregiving adults. Children with reactive attach-
ment disorder are believed to have the capacity to form selective attachments. However,
because of limited opportunities during early development, they fail to show the behavioral
manifestations of selective attachments. That is, when distressed, they show no consistent
effort to obtain comfort, support, nurturance, or protection from caregivers. Furthermore,
when distressed, children with this disorder do not respond more than minimally to com-
forting efforts of caregivers. Thus, the disorder is associated with the absence of expected
comfort seeking and response to comforting behaviors. As such, children with reactive
attachment disorder show diminished or absent expression of positive emotions during
routine interactions with caregivers. In addition, their emotion regulation capacity is com-
promised, and they display episodes of negative emotions of fear, sadness, or irritability
that are not readily explained. A diagnosis of reactive attachment disorder should not be
made in children who are developmentally unable to form selective attachments. For this
reason, the child must have a developmental age of at least 9 months.
Associated Features Supporting Diagnosis
Because of the shared etiological association with social neglect, reactive attachment dis-
order often co-occurs with developmental delays, especially in delays in cognition and
language. Other associated features include stereotypies and other signs of severe neglect
(e.g., malnutrition or signs of poor care).
Prevaience
The prevalence of reactive attachment disorder is unknown, but the disorder is seen rela-
tively rarely in clinical settings. The disorder has been found in young children exposed to
severe neglect before being placed in foster care or raised in institutions. However, even in
populations of severely neglected children, the disorder is uncommon, occurring in less
than 10% of such children.
Reactive Attachment Disorder 267
Development and Course
Conditions of social neglect are often present in the first months of life in children diag-
nosed with reactive attachment disorder, even before the disorder is diagnosed. The clin-
ical features of the disorder manifest in a similar fashion between the ages of 9 months and
5 years. That is, signs of absent-to-minimal attachment behaviors and associated emotion-
ally aberrant behaviors are evident in children throughout this age range, although differ-
ing cognitive and motor abilities may affect how these behaviors are expressed. Without
remediation and recovery through normative caregiving environments, it appears that signs
of the disorder may persist, at least for several years.
It is unclear whether reactive attachment disorder occurs in older children and, if so, how
it differs from its presentation in young children. Because of this, the diagnosis should be
made with caution in children older than 5 years.
Risk and Prognostic Factors
Environmental. Serious social neglect is a diagnostic requirement for reactive attach-
ment disorder and is also the only known risk factor for the disorder. However, the ma-
jority of severely neglected children do not develop the disorder. Prognosis appears to
depend on the quality of the caregiving environment following serious neglect.
Cuiture-Related Diagnostic Issues
Similar attachment behaviors have been described in young children in many different
cultures around the world. However, caution should be exercised in making the diagnosis
of reactive attachment disorder in cultures in which attachment has not been studied.
Functional Consequences of
Reactive Attachment Disorder
Reactive attachment disorder significantly impairs young children’s abilities to relate in-
terpersonally to adults or peers and is associated with functional impairment across many
domains of early childhood.
Differential Diagnosis
Autism spectrum disorder. Aberrant social behaviors manifest in young children with
reactive attachment disorder, but they also are key features of autism spectrum disorder.
Specifically, young children with either condition can manifest dampened expression of
positive emotions, cognitive and language delays, and impairments in social reciprocity.
As aresult, reactive attachment disorder must be differentiated from autism spectrum dis-
order. These two disorders can be distinguished based on differential histories of neglect
and on the presence of restricted interests or ritualized behaviors, specific deficit in social
communication, and selective attachment behaviors. Children with reactive attachment
disorder have experienced a history of severe social neglect, although it is not always pos-
sible to obtain detailed histories about the precise nature of their experiences, especially in
initial evaluations. Children with autistic spectrum disorder will only rarely have a history
of social neglect. The restricted interests and repetitive behaviors characteristic of autism
spectrum disorder are not a feature of reactive attachment disorder. These clinical features
manifest as excessive adherence to rituals and routines; restricted, fixated interests; and
unusual sensory reactions. However, it is important to note that children with either con-
dition can exhibit stereotypic behaviors such as rocking or flapping. Children with either
disorder also may exhibit a range of intellectual functioning, but only children with autis-
268 Trauma- and Stressor-Related Disorders
tic spectrum disorder exhibit selective impairments in social communicative behaviors,
such as intentional communication (i.e., impairment in communication that is deliberate,
goal-directed, and aimed at influencing the behavior of the recipient). Children with reac-
tive attachment disorder show social communicative functioning comparable to their
overall level of intellectual functioning. Finally, children with autistic spectrum disorder
regularly show attachment behavior typical for their developmental level. In contrast,
children with reactive attachment disorder do so only rarely or inconsistently, if at all.
Intellectual disability (intellectual developmental disorder). Developmental delays of-
ten accompany reactive attachment disorder, but they should not be confused with the
disorder. Children with intellectual disability should exhibit social and emotional skills
comparable to their cognitive skills and do not demonstrate the profound reduction in
positive affect and emotion regulation difficulties evident in children with reactive attach-
ment disorder. In addition, developmentally delayed children who have reached a cogni-
tive age of 7-9 months should demonstrate selective attachments regardless of their
chronological age. In contrast, children with reactive attachment disorder show lack of
preferred attachment despite having attained a developmental age of at least 9 months.
Depressive disorders. Depression in young children is also associated with reductions
in positive affect. There is limited evidence, however, to suggest that children with depres-
sive disorders have impairments in attachment. That is, young children who have been di-
agnosed with depressive disorders still should seek and respond to comforting efforts by
caregivers.
Comorbidity
Conditions associated with neglect, including cognitive delays, language delays, and ste-
reotypies, often co-occur with reactive attachment disorder. Medical conditions, such as
severe malnutrition, may accompany signs of the disorder. Depressive symptoms also
may co-occur with reactive attachment disorder.
Disinhibited Social Engagement Disorder
Diagnostic Criteria 313.89 (F94.2)
A. Apattern of behavior in which a child actively approaches and interacts with unfamiliar
adults and exhibits at least two of the following:
1. Reduced or absent reticence in approaching and interacting with unfamiliar adults.
2. Overly familiar verba! or physical behavior (that is not consistent with culturally
sanctioned and with age-appropriate social boundaries).
3. Diminished or absent checking back with adult caregiver after venturing away, even
in unfamiliar settings.
4, Willingness to go off with an unfamiliar adult with minimal or no hesitation.
B. The behaviors in Criterion A are not limited to impulsivity (as in attention-deficit/hyper-
activity disorder) but include socially disinhiblted behavior.
C. The child has experienced a pattern of extremes of insufficient care as evidenced by
at least one of the following:
1. Social neglect or deprivation in the form of persistent lack of having basic emotional
needs for comfort, stimulation, and affection met by caregiving adults.
2. Repeated changes of primary caregivers that limit opportunities to form stable at-
tachments (e.g., frequent changes in foster care).
3. Rearing in unusual settings that severely limit opportunities to form selective at-
tachments (e.g., institutions with high child-to-caregiver ratios).
Disinhibited Social Engagement Disorder 269
D. The care in Criterion C is presumed to be responsible for the disturbed behavior in Cri-
terion A (e.g:, the disturbances in Criterion A began following the pathogenic care in
Criterion C)}.
E. The child has a developmental age of at least 9 months.
Specify if:
Persistent: The disorder has been present for more than 12 months.
Specify current severity:
Disinhibited social engagement disorder is specified as severe when the child exhibits
all symptoms of the disorder, with each symptom manifesting at relatively high leveis.
Diagnostic Features
The essential feature of disinhibited social engagement disorder is a pattern of behavior
that involves culturally inappropriate, overly familiar behavior with relative strangers
(Criterion A). This overly familiar behavior violates the social boundaries of the culture. A
diagnosis of disinhibited social engagement disorder should not be made before children
are developmentally able to form selective attachments. For this reason, the child must
have a developmental age of at least 9 months.
Associated Features Supporting Diagnosis
Because of the shared etiological association with social neglect, disinhibited social en-
gagement disorder may co-occur with developmental delays, especially cognitive and lan-
guage delays, stereotypies, and other signs of severe neglect, such as malnutrition or poor
care. However, signs of the disorder often persist even after these other signs of neglect are
no longer present. Therefore, it is not uncommon for children with the disorder to present
with no current signs of neglect. Moreover, the condition can present in children who
show no signs of disordered attachment. Thus, disinhibited social engagement disorder
may be seen in children with a history of neglect who lack attachments or whose attach-
ments to their caregivers range from disturbed to secure.
Prevalence
The prevalence of disinhibited social attachment disorder is unknown. Nevertheless, the
disorder appears to be rare, occurring in a minority of children, even those who have been
severely neglected and subsequently placed in foster care or raised in institutions. In such
high-risk populations, the condition occurs in only about 20% of children. The condition is
seen rarely in other clinical settings.
Development and Course
Conditions of social neglect are often present in the first months of life in children diag-
nosed with disinhibited social engagement disorder, even before the disorder is diag-
nosed. However, there is no evidence that neglect beginning after age 2 years is associated
with manifestations of the disorder. If neglect occurs early and signs of the disorder
appear, clinical features of the disorder are moderately stable over time, particularly if
conditions of neglect persist. Indiscriminate social behavior and lack of reticence with un-
familiar adults in toddlerhood are accompanied by attention-seeking behaviors in pre-
schoolers. When the disorder persists into middle childhood, clinical features manifest as
verbal and physical overfamiliarity as well as inauthentic expression of emotions. These
signs appear particularly apparent when the child interacts with adults. Peer relationships
are most affected in adolescence, with both indiscriminate behavior and conflicts appar-
ent. The disorder has not been described in adults.
270 Trauma- and Stressor-Related Disorders
Disinhibited social engagement disorder has been described from the second year of
life through adolescence. There are some differences in manifestations of the disorder
from early childhood through adolescence. At the youngest ages, across many cultures,
children show reticence when interacting with strangers. Young children with the disorder
fail to show reticence to approach, engage with, and even accompany adults. In preschool
children, verbal and social intrusiveness appear most prominent, often accompanied by
attention-seeking behavior. Verbal and physical overfamiliarity continue through middle
childhood, accompanied by inauthentic expressions of emotion. In adolescence, indis-
criminate behavior extends to peers. Relative to healthy adolescents, adolescents with the
disorder have more “superficial” peer relationships and more peer conflicts. Adult man-
ifestations of the disorder are unknown.
Risk and Prognostic Factors
Environmental. Serious social neglect is a diagnostic requirement for disinhibited social
engagement disorder and is also the only known risk factor for the disorder. However, the
majority of severely neglected children do not develop the disorder. Neurobiological vul-
nerability may differentiate neglected children who do and do not develop the disorder.
However, no clear link with any specific neurobiological factors has been established. The
disorder has not been identified in children who experience social neglect only after age
2 years. Prognosis is only modestly associated with quality of the caregiving environment
following serious neglect. In many cases, the disorder persists, even in children whose
caregiving environment becomes markedly improved.
Course modifiers. Caregiving quality seems to moderate the course of disinhibited so-
cial engagement disorder. Nevertheless, even after placement in normative caregiving
environments, some children show persistent signs of the disorder, at least through ado-
lescence.
Functional Consequences of
Disinhibited Sociai Engagement Disorder
Disinhibited social engagement disorder significantly impairs young children’s abilities to
relate interpersonally to adults and peers.
Differential Diagnosis
Attention-deficit/hyperactivity disorder. Because of social impulsivity that sometimes
accompanies attention-deficit/hyperactivity disorder (ADHD), it is necessary to differ-
entiate the two disorders. Children with disinhibited social engagement disorder may be
distinguished from those with ADHD because the former do not show difficulties with at-
tention or hyperactivity.
Comorbidity
Limited research has examined the issue of disorders comorbid with disinhibited social
engagement disorder. Conditions associated with neglect, including cognitive delays,
language delays, and stereotypies, may co-occur with disinhibited social engagement dis-
order. In addition, children may be diagnosed with ADHD and disinhibited social engage-
ment disorder concurrently.
Posttraumatic Stress Disorder 271
Posttraumatic Stress Disorder
Diagnostic Criteria 309.81 (F43.10)
Posttraumatic Stress Disorder
Note: The following criteria apply to adults, adolescents, and children older than 6 years.
For children 6 years and younger, see corresponding criteria below.
A. Exposure to actual or threatened death, serious injury, or sexual violence in one (or
more) of the following ways:
1.
2.
3.
Directly experiencing the traumatic event(s).
Witnessing, in person, the event(s) as it occurred to others.
Learning that the traumatic event(s) occurred to a close family member or close
friend. In cases of actual or threatened death of a family member or friend, the
event(s) must have been violent or accidental.
Experiencing repeated or extreme exposure to aversive details of the traumatic
event(s) (e.g., first responders collecting human remains; police officers repeatedly
exposed to details of child abuse).
Note: Criterion A4 does not apply to exposure through electronic media, television,
movies, or pictures, unless this exposure is work related.
B. Presence of one (or more) of the following intrusion symptoms associated with the
traumatic event(s), beginning after the traumatic event(s) occurred:
1.
Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s).
Note: In children older than 6 years, repetitive play may occur in which themes or
aspects of the traumatic event(s) are expressed.
. Recurrent distressing dreams in which the content and/or affect of the dream are
related to the traumatic event(s).
Note: In children, there may be frightening dreams without recognizable content.
. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts as if
the traumatic event(s) were recurring. (Such reactions may occur on a continuum,
with the most extreme expression being a complete loss of awareness of present
surroundings.)
Note: In children, trauma-specific reenactment may occur in play.
Intense or prolonged psychological distress at exposure to internal or external cues
that symbolize or resemble an aspect of the traumatic event(s).
Marked physiological reactions to internal or external cues that symbolize or re-
semble an aspect of the traumatic event(s).
C. Persistent avoidance of stimuli associated with the traumatic event(s), beginning after
the traumatic event(s) occurred, as evidenced by one or both of the following:
1.
2.
Avoidance of or efforts to avoid distressing memories, thoughts, or feelings about
or closely associated with the traumatic event(s).
Avoidance of or efforts to avoid external reminders (people, places, conversations,
activities, objects, situations) that arouse distressing memories, thoughts, or feel-
ings about or closely associated with the traumatic event(s).
D. Negative alterations in cognitions and mood associated with the traumatic event(s),
beginning or worsening after the traumatic event(s) occurred, as evidenced by two (or
more) of the following:
1.
Inability to remember an important aspect of the traumatic event(s) (typically due to dis-
sociative amnesia and not to other factors such as head injury, alcohol, or drugs).
272
o
NO os
Trauma- and Stressor-Related Disorders
Persistent and exaggerated negative beliefs or expectations about oneself, others,
or the world (e.g., “l am bad,” “No one can be trusted,” “The world is completely
dangerous,” “My whole nervous system is permanently ruined”).
Persistent, distorted cognitions about the cause or consequences of the traumatic
event(s) that lead the individual to blame himself/herself or others.
Persistent negative emotional state {e.g., fear, horror, anger, guilt, or shame).
Markedly diminished interest or participation in significant activities.
Feelings of detachment or estrangement from others.
. Persistent inability to experience positive emotions {e.g., inability to experience
happiness, satisfaction, or loving feelings).
E. Marked alterations in arousal and reactivity associated with the traumatic event(s), be-
ginning or worsening after the traumatic event(s) occurred, as evidenced by two (or
more) of the following:
1.
aR oN
6.
Irritable behavior and angry outbursts (with little or no provocation) typically ex-
pressed as verbal or physical aggression toward people or objects.
. Reckless or self-destructive behavior.
Hypervigilance.
Exaggerated startle response.
Problems with concentration.
Sleep disturbance (e.g., difficulty falling or staying asleep or restless sleep).
F. Duration of the disturbance (Criteria B, C, D, and E) is more than 1 month.
G. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
H. The disturbance is not attributable to the physiological effects of a substance (e.g.,
medication, alcohol) or another medical condition.
Specify whether:
With dissociative symptoms: The individual’s symptoms meet the criteria for post-
traumatic stress disorder, and in addition, in response to the stressor, the individual ex-
periences persistent or recurrent symptoms of either of the following:
1.
Depersonalization: Persistent or recurrent experiences of feeling detached from,
and as if one were an outside observer of, one’s mental processes or body (e.g.,
feeling as though one were in a dream; feeling a sense of unreality of self or body
or of time moving slowly).
Derealization: Persistent or recurrent experiences of unreality of surroundings
(e.g., the world around the individual is experienced as unreal, dreamlike, distant,
or distorted).
Note: To use this subtype, the dissociative symptoms must not be attributable to the
physiological effects of a substance (e.g., blackouts, behavior during alcohol intoxica-
tion) or another medical condition (e.g., complex partial seizures).
Specify if:
With delayed expression: If the full diagnostic criteria are not met until at least 6 months
after the event (although the onset and expression of some symptoms may be immediate).
Posttraumatic Stress Disorder for Children 6 Years and Younger
A. Inchildren 6 years and younger, exposure to actual or threatened death, serious injury,
or sexual violence in one (or more) of the following ways:
1.
2.
Directly experiencing the traumatic event(s).
Witnessing, in person, the event(s) as it occurred to others, especially primary care-
givers.
Posttraumatic Stress Disorder 273
Note: Witnessing does not include events that are witnessed only in electronic me-
dia, television, movies, or pictures.
3. Learning that the traumatic event(s) occurred to a parent or caregiving figure.
B. Presence of one (or more) of the following intrusion symptoms associated with the
traumatic event(s), beginning after the traumatic event(s) occurred:
1. Recurrent, involuntary, and intrusive distressing memories of the traumatic
event(s).
Note: Spontaneous and intrusive memories may not necessarily appear distress-
ing and may be expressed as play reenactment.
2. Recurrent distressing dreams in which the content and/or affect of the dream are
related to the traumatic event(s).
Note: It may not be possible to ascertain that the frightening content is related to
the traumatic event.
3. Dissociative reactions (e.g., flashbacks) in which the child feels or acts as if the
traumatic event(s) were recurring. (Such reactions may occur on a continuum, with
the most extreme expression being a complete loss of awareness of present sur-
roundings.) Such trauma-specific reenactment may occur in play.
4. Intense or prolonged psychological distress at exposure to internal or external cues
that symbolize or resemble an aspect of the traumatic event(s).
5. Marked physiological reactions to reminders of the traumatic event(s).
C. One (or more) of the following symptoms, representing either persistent avoidance of
stimuli associated with the traumatic event(s) or negative alterations in cognitions and
mood associated with the traumatic event(s), must be present, beginning after the
event(s) or worsening after the event(s):
Persistent Avoidance of Stimuli
1. Avoidance of or efforts to avoid activities, places, or physical reminders that arouse
recollections of the traumatic event(s).
2. Avoidance of or efforts to avoid people, conversations, or interpersonal situations
that arouse recollections of the traumatic event(s).
Negative Alterations in Cognitions
3. Substantially increased frequency of negative emotional states ({e.g., fear, guilt,
sadness, shame, confusion).
4. Markedly diminished interest or participation in significant activities, including con-
striction of play.
5. Socially withdrawn behavior.
6. Persistent reduction in expression of positive emotions.
D. Alterations in arousal and reactivity associated with the traumatic event(s), beginning
or worsening after the traumatic event(s) occurred, as evidenced by two (or more) of
the following:
1. Irritable behavior and angry outbursts (with little or no provocation) typically ex-
pressed as verbal or physical aggression toward people or objects (including ex-
treme temper tantrums).
Hypervigilance.
Exaggerated startle response.
Problems with concentration.
5. Sleep disturbance (e.g., difficulty falling or staying asleep or restless sleep).
E. The duration of the disturbance is more than 1 month.
oN
274 Trauma- and Stressor-Related Disorders
F. The disturbance causes clinically significant distress or impairment in relationships
with parents, siblings, peers, or other caregivers or with school behavior.
G. The disturbance is not attributable to the physiological effects of a substance (e.g.,
medication or alcohol) or another medical condition.
Specify whether:
With dissociative symptoms: The individual’s symptoms meet the criteria for post-
traumatic stress disorder, and the individual experiences persistent or recurrent symp-
toms of either of the following:
1. Depersonalization: Persistent or recurrent experiences of feeling detached from,
and as if one were an outside observer of, one’s mental processes or body (e.g.,
feeling as though one were in a dream; feeling a sense of unreality of self or body
or of time moving slowly).
2. Derealization: Persistent or recurrent experiences of unreality of surroundings
{e.g., the world around the individual is experienced as unreal, dreamlike, distant,
or distorted).
Note: To use this subtype, the dissociative symptoms must not be attributable to the
physiological effects of a substance (e.g., blackouts) or another medical condition
(e.g., complex partial seizures).
Specify if:
With delayed expression: If the full diagnostic criteria are not met until at least
6 months after the event (although the onset and expression of some symptoms may
be immediate).
Diagnostic Features
The essential feature of posttraumatic stress disorder (PTSD) is the development of char-
acteristic symptoms following exposure to one or more traumatic events. Emotional re-
actions to the traumatic event (e.g., fear, helplessness, horror) are no longer a part of
Criterion A. The clinical presentation of PTSD varies. In some individuals, fear-based re-
experiencing, emotional, and behavioral symptoms may predominate. In others, anhe-
donic or dysphoric mood states and negative cognitions may be most distressing. In some
other individuals, arousal and reactive-externalizing symptoms are prominent, while in
others, dissociative symptoms predominate. Finally, some individuals exhibit combina-
tions of these symptom patterns.
The directly experienced traumatic events in Criterion A include, but are not limited
to, exposure to war as a combatant or civilian, threatened or actual physical assault (e.g.,
physical attack, robbery, mugging, childhood physical abuse), threatened or actual sexual
violence (e.g., forced sexual penetration, alcohol /drug-facilitated sexual penetration, abu-
sive sexual contact, noncontact sexual abuse, sexual trafficking), being kidnapped, being
taken hostage, terrorist attack, torture, incarceration as a prisoner of war, natural or hu-
man-made disasters, and severe motor vehicle accidents. For children, sexually violent
events may include developmentally inappropriate sexual experiences without physical
violence or injury. A life-threatening illness or debilitating medical condition is not neces-
sarily considered a traumatic event. Medical incidents that qualify as traumatic events in-
volve sudden, catastrophic events (e.g., waking during surgery, anaphylactic shock).
Witnessed events include, but are not limited to, observing threatened or serious injury,
unnatural death, physical or sexual] abuse of another person due to violent assault, domes-
tic violence, accident, war or disaster, or a medical catastrophe in one’s child (e.g., a life-
threatening hemorrhage). Indirect exposure through learning about an event is limited to
experiences affecting close relatives or friends and experiences that are violent or acciden-
tal (e.g., death due to natural causes does not qualify). Such events include violent per-
Posttraumatic Stress Disorder 275
sonal assault, suicide, serious accident, and serious injury. The disorder may be especially
severe or long-lasting when the stressor is interpersonal and intentional (e.g., torture, sex-
ual violence).
The traumatic event can be reexperienced in various ways. Commonly, the individual
has recurrent, involuntary, and intrusive recollections of the event (Criterion B1). Intrusive
recollections in PTSD are distinguished from depressive rumination in that they apply
only to involuntary and intrusive distressing memories. The emphasis is on recurrent
memories of the event that usually include sensory, emotional, or physiological behavioral
components. A common reexperiencing symptom is distressing dreams that replay the
event itself or that are representative or thematically related to the major threats involved
in the traumatic event (Criterion B2). The individual may experience dissociative states
that last from a few seconds to several hours or even days, during which components of
the event are relived and the individual behaves as if the event were occurring at that mo-
ment (Criterion B3). Such events occur on a continuum from brief visual or other sensory
intrusions about part of the traumatic event without loss of reality orientation, to complete
loss of awareness of present surroundings. These episodes, often referred to as “flash-
backs,” are typically brief but can be associated with prolonged distress and heightened
arousal. For young children, reenactment of events related to trauma may appear in play
or in dissociative states. Intense psychological distress (Criterion B4) or physiological re-
activity (Criterion B5) often occurs when the individual is exposed to triggering events that
resemble or symbolize an aspect of the traumatic event (e.g., windy days after a hurricane;
seeing someone who resembles one’s perpetrator). The triggering cue could be a physical
sensation (e.g., dizziness for survivors of head trauma; rapid heartbeat for a previously
traumatized child), particularly for individuals with highly somatic presentations.
Stimuli associated with the trauma are persistently (e.g., always or almost always)
avoided. The individual commonly makes deliberate efforts to avoid thoughts, memories,
feelings, or talking about the traumatic event (e.g., utilizing distraction techniques to avoid
internal reminders) (Criterion C1) and to avoid activities, objects, situations, or people
who arouse recollections of it (Criterion C2).
Negative alterations in cognitions or mood associated with the event begin or worsen
after exposure to the event. These negative alterations can take various forms, including an
inability to remember an important aspect of the traumatic event; such amnesia is typically
due to dissociative amnesia and is not due to head injury, alcohol, or drugs (Criterion D1).
Another form is persistent (i.e., always or almost always) and exaggerated negative ex-
pectations regarding important aspects of life applied to oneself, others, or the future (e.g.,
“Thave always had bad judgment”; “People in authority can’t be trusted”) that may man-
ifest as a negative change in perceived identity since the trauma (e.g., “I can’t trust anyone
ever again”; Criterion D2). Individuals with PTSD may have persistent erroneous cogni-
tions about the causes of the traumatic event that lead them to blame themselves or others
(e.g., “It’s all my fault that my uncle abused me”) (Criterion D3). A persistent negative
mood state (e.g., fear, horror, anger, guilt, shame) either began or worsened after exposure
to the event (Criterion D4). The individual may experience markedly diminished interest
or participation in previously enjoyed activities (Criterion D5), feeling detached or es-
tranged from other people (Criterion D6), or a persistent inability to feel positive emotions
(especially happiness, joy, satisfaction, or emotions associated with intimacy, tenderness,
and sexuality) (Criterion D7).
Individuals with PTSD may be quick tempered and may even engage in aggressive
verbal and/or physical behavior with little or no provocation (e.g., yelling at people, get-
ting into fights, destroying objects) (Criterion E1). They may also engage in reckless or self-
destructive behavior such as dangerous driving, excessive alcohol or drug use, or self-
injurious or suicidal behavior (Criterion E2). PTSD is often characterized by a heightened
sensitivity to potential threats, including those that are related to the traumatic experience
(e.g., following a motor vehicle accident, being especially sensitive to the threat potentially
276 Trauma- and Stressor-Related Disorders
caused by cars or trucks) and those not related to the traumatic event (e.g., being fearful of
suffering a heart attack) (Criterion E3). Individuals with PTSD may be very reactive to un-
expected stimuli, displaying a heightened startle response, or jumpiness, to loud noises or
unexpected movements (e.g., jumping markedly in response to a telephone ringing) (Cri-
terion E4). Concentration difficulties, including difficulty remembering daily events (e.g.,
forgetting one’s telephone number) or attending to focused tasks (e.g., following a conver-
sation for a sustained period of time), are commonly reported (Criterion E5). Problems
with sleep onset and maintenance are common and may be associated with nightmares
and safety concerns or with generalized elevated arousal that interferes with adequate sleep
(Criterion E6). Some individuals also experience persistent dissociative symptoms of de-
tachment from their bodies (depersonalization) or the world around them (derealization);
this is reflected in the “with dissociative symptoms” specifier.
Associated Features Supporting Diagnosis
Developmental regression, such as loss of language in young children, may occur. Audi-
tory pseudo-hallucinations, such as having the sensory experience of hearing one’s
thoughts spoken in one or more different voices, as well as paranoid ideation, can be pres-
ent. Following prolonged, repeated, and severe traumatic events (e.g., childhood abuse,
torture), the individual may additionally experience difficulties in regulating emotions or
maintaining stable interpersonal relationships, or dissociative symptoms. When the trau-
matic event produces violent death, symptoms of both problematic bereavement and PTSD
may be present.
Prevalence
In the United States, projected lifetime risk for PTSD using DSM-IV criteria at age 75 years
is 8.7%. Twelve-month prevalence among U.S. adults is about 3.5%. Lower estimates are
seen in Europe and most Asian, African, and Latin American countries, clustering around
0.5%-1.0%. Although different groups have different levels of exposure to traumatic
events, the conditional probability of developing PTSD following a similar level of expo-
sure may also vary across cultural groups. Rates of PTSD are higher among veterans and
others whose vocation increases the risk of traumatic exposure (e.g., police, firefighters,
emergency medical personnel). Highest rates (ranging from one-third to more than one-
half of those exposed) are found among survivors of rape, military combat and captivity,
and ethnically or politically motivated internment and genocide. The prevalence of PTSD
may vary across development; children and adolescents, including preschool children,
generally have displayed lower prevalence following exposure to serious traumatic
events; however, this may be because previous criteria were insufficiently developmen-
tally informed. The prevalence of full-threshold PTSD also appears to be lower among
older adults compared with the general population; there is evidence that subthreshold
presentations are more common than full PTSD in later life and that these symptoms are
associated with substantial clinical impairment. Compared with U.S. non-Latino whites,
higher rates of PTSD have been reported among U.S. Latinos, African Americans, and
American Indians, and lower rates have been reported among Asian Americans, after ad-
justment for traumatic exposure and demographic variables.
Development and Course
PTSD can occur at any age, beginning after the first year of life. Symptoms usually begin
within the first 3 months after the trauma, although there may be a delay of months, or
even years, before criteria for the diagnosis are met. There is abundant evidence for what
DSM-IV called “delayed onset” but is now called “delayed expression,” with the recogni-
tion that some symptoms typically appear immediately and that the delay is in meeting
full criteria.
Posttraumatic Stress Disorder 277
Frequently, an individual's reaction to a trauma initially meets criteria for acute stress
disorder in the immediate aftermath of the trauma. The symptoms of PTSD and the rela-
tive predominance of different symptoms may vary over time. Duration of the symptoms
also varies, with complete recovery within 3 months occurring in approximately one-half
of adults, while some individuals remain symptomatic for longer than 12 months and
sometimes for more than 50 years. Symptom recurrence and intensification may occur in
response to reminders of the original trauma, ongoing life stressors, or newly experienced
traumatic events. For older individuals, declining health, worsening cognitive function-
ing, and social isolation may exacerbate PTSD symptoms.
The clinical expression of reexperiencing can vary across development. Young children
may report new onset of frightening dreams without content specific to the traumatic event.
Before age 6 years (see criteria for preschool subtype), young children are more likely to ex-
press reexperiencing symptoms through play that refers directly or symbolically to the
trauma. They may not manifest fearful reactions at the time of the exposure or during reex-
periencing. Parents may report a wide range of emotional or behavioral changes in young
children. Children may focus on imagined interventions in their play or storytelling. In ad-
dition to avoidance, children may become preoccupied with reminders. Because of young
children’s limitations in expressing thoughts or labeling emotions, negative alterations in
mood or cognition tend to involve primarily mood changes. Children may experience co-
occurring traumas (e.g., physical abuse, witnessing domestic violence) and in chronic cir-
cumstances may not be able to identify onset of symptomatology. Avoidant behavior may
be associated with restricted play or exploratory behavior in young children; reduced par-
ticipation in new activities in school-age children; or reluctance to pursue developmental op-
portunities in adolescents (e.g., dating, driving). Older children and adolescents may judge
themselves as cowardly. Adolescents may harbor beliefs of being changed in ways that
make them socially undesirable and estrange them from peers (e.g., “Now I'll never fit in”)
and lose aspirations for the future. Irritable or aggressive behavior in children and adoles-
cents can interfere with peer relationships and school behavior. Reckless behavior may lead
to accidental injury to self or others, thrill-seeking, or high-risk behaviors. Individuals who
continue to experience PTSD into older adulthood may express fewer symptoms of hy-
perarousal, avoidance, and negative cognitions and mood compared with younger adults
with PTSD, although adults exposed to traumatic events during later life may display more
avoidance, hyperarousal, sleep problems, and crying spells than do younger adults exposed
to the same traumatic events. In older individuals, the disorder is associated with negative
health perceptions, primary care utilization, and suicidal ideation.
Risk and Prognostic Factors
Risk (and protective) factors are generally divided into pretraumatic, peritraumatic, and
posttraumatic factors.
Pretraumatic factors
Temperamental. These include childhood emotional problems by age 6 years (e.g., prior
traumatic exposure, externalizing or anxiety problems) and prior mental disorders (e.g.,
panic disorder, depressive disorder, PTSD, or obsessive-compulsive disorder [OCD)).
Environmental. These include lower socioeconomic status; lower education; exposure to
prior trauma (especially during childhood); childhood adversity (e.g., economic depriva-
tion, family dysfunction, parental separation or death); cultural characteristics (e.g., fatal-
istic or self-blaming coping strategies); lower intelligence; minority racial/ethnic status;
and a family psychiatric history. Social support prior to event exposure is protective.
Genetic and physiological. These include female gender and younger age at the time of
trauma exposure (for adults). Certain genotypes may either be protective or increase risk
of PTSD after exposure to traumatic events.
278 Trauma- and Stressor-Related Disorders
Peritraumatic factors
Environmental. These include severity (dose) of the trauma (the greater the magnitude
of trauma, the greater the likelihood of PTSD), perceived life threat, personal injury, in-
terpersonal violence (particularly trauma perpetrated by a caregiver or involving a wit-
nessed threat to a caregiver in children), and, for military personnel, being a perpetrator,
witnessing atrocities, or killing the enemy. Finally, dissociation that occurs during the trauma
and persists afterward is a risk factor.
Posttraumatic factors
Temperamental. These include negative appraisals, inappropriate coping strategies,
and development of acute stress disorder.
Environmental. These include subsequent exposure to repeated upsetting reminders, subse-
quent adverse life events, and financial or other trauma-related losses. Social support (includ-
ing family stability, for children) is a protective factor that moderates outcome after trauma.
Culture-Related Diagnostic Issues
The risk of onset and severity of PTSD may differ across cultural groups as a result of vari-
ation in the type of traumatic exposure (e.g., genocide), the impact on disorder severity of
the meaning attributed to the traumatic event (e.g., inability to perform funerary rites after
a mass killing), the ongoing sociocultural context (e.g., residing among unpunished per-
petrators in postconflict settings), and other cultural factors (e.g., acculturative stress in
immigrants). The relative risk for PTSD of particular exposures (e.g., religious persecu-
tion) may vary across cultural groups. The clinical expression of the symptoms or symp-
tom clusters of PTSD may vary culturally, particularly with respect to avoidance and
numbing symptoms, distressing dreams, and somatic symptoms (e.g., dizziness, short-
ness of breath, heat sensations).
Cultural syndromes and idioms of distress influence the expression of PTSD and the
range of comorbid disorders in different cultures by providing behavioral and cognitive
templates that link traumatic exposures to specific symptoms. For example, panic attack
symptoms may be salient in PTSD among Cambodians and Latin Americans because of
the association of traumatic exposure with panic-like khyal attacks and ataque de nervios.
Comprehensive evaluation of local expressions of PTSD should include assessment of cul-
tural concepts of distress (see the chapter “Cultural Formulation” in Section III).
Gender-Related Diagnostic Issues
PTSD is more prevalent among females than among males across the lifespan. Females in
the general population experience PTSD for a longer duration than do males. At least some
of the increased risk for PTSD in females appears to be attributable to a greater likelihood
of exposure to traumatic events, such as rape, and other forms of interpersonal violence.
Within populations exposed specifically to such stressors, gender differences in risk for
PTSD are attenuated or nonsignificant.
Suicide Risk
Traumatic events such as childhood abuse increase a person’s suicide risk. PTSD is associated
with suicidal ideation and suicide attempts, and presence of the disorder may indicate which
individuals with ideation eventually make a suicide plan or actually attempt suicide.
Functional Consequences of
Posttraumatic Stress Disorder
PTSD is associated with high levels of social, occupational, and physical disability, as well
as considerable economic costs and high levels of medical utilization. Impaired function-
Posttraumatic Stress Disorder 279
ing is exhibited across social, interpersonal, developmental, educational, physical health,
and occupational domains. In community and veteran samples, PTSD is associated with
poor social and family relationships, absenteeism from work, lower income, and lower ed-
ucational and occupational success.
Differential Diagnosis
Adjustment disorders. In adjustment disorders, the stressor can be of any severity or
type rather than that required by PTSD Criterion A. The diagnosis of an adjustment dis-
order is used when the response to a stressor that meets PTSD Criterion A does not meet
all other PTSD criteria (or criteria for another mental disorder). An adjustment disorder is
also diagnosed when the symptom pattern of PTSD occurs in response to a stressor that
does not meet PTSD Criterion A (e.g., spouse leaving, being fired).
Other posttraumatic disorders and conditions. Not all psychopathology that occurs in
individuals exposed to an extreme stressor should necessarily be attributed to PTSD. The
diagnosis requires that trauma exposure precede the onset or exacerbation of pertinent
symptoms. Moreover, if the symptom response pattern to the extreme stressor meets cri-
teria for another mental disorder, these diagnoses should be given instead of, or in addi-
tion to, PTSD. Other diagnoses and conditions are excluded if they are better explained by
PTSD (e.g., symptoms of panic disorder that occur only after exposure to traumatic re-
minders). If severe, symptom response patterns to the extreme stressor may warrant a sep-
arate diagnosis (e.g., dissociative amnesia).
Acute stress disorder. Acute stress disorder is distinguished from PTSD because the
symptom pattern in acute stress disorder is restricted to a duration of 3 days to 1 month
following exposure to the traumatic event.
Anxiety disorders and obsessive-compulsive disorder. In OCD, there are recurrent
intrusive thoughts, but these meet the definition of an obsession. In addition, the intrusive
thoughts are not related to an experienced traumatic event, compulsions are usually pres-
ent, and other symptoms of PTSD or acute stress disorder are typically absent. Neither the
arousal and dissociative symptoms of panic disorder nor the avoidance, irritability, and
anxiety of generalized anxiety disorder are associated with a specific traumatic event. The
symptoms of separation anxiety disorder are clearly related to separation from home or
family, rather than to a traumatic event.
Major depressive disorder. Major depression may or may not be preceded by a trau-
matic event and should be diagnosed if other PTSD symptoms are absent. Specifically, ma-
jor depressive disorder does not include any PTSD Criterion B or C symptoms. Nor does it
include a number of symptoms from PTSD Criterion D or E.
Personality disorders. Interpersonal difficulties that had their onset, or were greatly ex-
acerbated, after exposure to a traumatic event may be an indication of PTSD, rather than a
personality disorder, in which such difficulties would be expected independently of any
traumatic exposure.
Dissociative disorders. Dissociative amnesia, dissociative identity disorder, and de-
personalization-derealization disorder may or may not be preceded by exposure to a trau-
matic event or may or may not have co-occurring PTSD symptoms. When full PTSD criteria
are also met, however, the PTSD “with dissociative symptoms” subtype should be considered.
Conversion disorder (functional neurological symptom disorder). New onset of somatic
symptoms within the context of posttraumatic distress might be an indication of PTSD
rather than conversion disorder (functional neurological symptom disorder).
Psychotic disorders. Flashbacks in PTSD must be distinguished from illusions, halluci-
nations, and other perceptual disturbances that may occur in schizophrenia, brief psy-
chotic disorder, and other psychotic disorders; depressive and bipolar disorders with
280 Trauma- and Stressor-Related Disorders
psychotic features; delirium; substance /medication-induced disorders; and psychotic dis-
orders due to another medical condition.
Traumatic brain injury. When a brain injury occurs in the context of a traumatic event (e.g.,
traumatic accident, bomb blast, acceleration / deceleration trauma), symptoms of PTSD may
appear. An event causing head trauma may also constitute a psychological traumatic event,
and tramautic brain injury (TBI)-related neurocognitive symptoms are not mutually exclusive
and may occur concurrently. Symptoms previously termed postconcussive (e.g., headaches,
dizziness, sensitivity to light or sound, irritability, concentration deficits) can occur in brain-
injured and non-brain-injured populations, including individuals with PTSD. Because symp-
toms of PTSD and TBI-related neurocognitive symptoms can overlap, a differential diagnosis
between PTSD and neurocognitive disorder symptoms attributable to TBI may be possible
based on the presence of symptoms that are distinctive to each presentation. Whereas reexpe-
riencing and avoidance are characteristic of PTSD and not the effects of TBI, persistent disori-
entation and confusion are more specific to TBI (neurocognitive effects) than to PTSD.
Comorbidity
Individuals with PTSD are 80% more likely than those without PTSD to have symptoms
that meet diagnostic criteria for at least one other mental disorder (e.g., depressive, bipo-
lar, anxiety, or substance use disorders). Comorbid substance use disorder and conduct
disorder are more common among males than among females. Among U.S, military per-
sonnel and combat veterans who have been deployed to recent wars in Afghanistan and
Iraq, co-occurrence of PTSD and mild TBI is 48%. Although most young children with
PTSD also have at least one other diagnosis, the patterns of comorbidity are different than
in adults, with oppositional defiant disorder and separation anxiety disorder predominat-
ing. Finally, there is considerable comorbidity between PTSD and major neurocognitive
disorder and some overlapping symptoms between these disorders.
Acute Stress Disorder
Diagnostic Criteria 308.3 (F43.0)
A. Exposure to actual or threatened death, serious injury, or sexual violation in one (or
more) of the following ways:
1. Directly experiencing the traumatic event(s).
2. Witnessing, in person, the event(s) as it occurred to others.
3. Learning that the event(s) occurred to a close family member or close friend. Note:
In cases of actual or threatened death of a family member or friend, the event(s)
must have been violent or accidental.
4. Experiencing repeated or extreme exposure to aversive details of the traumatic
event(s) (e.g., first responders collecting human remains, police officers repeatedly
exposed to details of child abuse).
Note: This does not apply to exposure through electronic media, television, mov-
ies, or pictures, unless this exposure is work related.
B. Presence of nine (or more) of the following symptoms from any of the five categories
of intrusion, negative mood, dissociation, avoidance, and arousal, beginning or wors-
ening after the traumatic event(s) occurred:
Intrusion Symptoms
1. Recurrent, involuntary, and intrusive distressing memories of the traumatic
event(s). Note: In children, repetitive play may occur in which themes or aspects of
the traumatic event(s) are expressed.
Acute Stress Disorder 281
2. Recurrent distressing dreams in which the content and/or affect of the dream are
related to the event(s). Note: In children, there may be frightening dreams without
recognizable content.
3. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts as if
the traumatic event(s) were recurring. (Such reactions may occur on a continuum,
with the most extreme expression being a complete loss of awareness of present
surroundings.) Note: In children, trauma-specific reenactment may occur in play.
4. Intense or prolonged psychological distress or marked physiological reactions in re-
sponse to internal or external cues that symbolize or resemble an aspect of the
traumatic event(s).
Negative Mood
5. Persistent inability to experience positive emotions (e.g., inability to experience
happiness, satisfaction, or loving feelings).
Dissociative Symptoms
6. An altered sense of the reality of one’s surroundings or oneself (e.g., seeing oneself
from another’s perspective, being in a daze, time slowing).
7. Inability to remember an important aspect of the traumatic event(s) (typically due to
dissociative amnesia and not to other factors such as head injury, alcohol, or
drugs).
Avoidance Symptoms
8. Efforts to avoid distressing memories, thoughts, or feelings about or closely asso-
ciated with the traumatic event(s).
9. Efforts to avoid external reminders (people, places, conversations, activities, ob-
jects, situations) that arouse distressing memories, thoughts, or feelings about or
closely associated with the traumatic event(s).
Arousal Symptoms
10. Sleep disturbance (e.g., difficulty falling or staying asleep, restless sleep).
11. Irritable behavior and angry outbursts (with little or no provocation), typically ex-
pressed as verbal or physical aggression toward people or objects.
12. Hypervigilance.
13. Problems with concentration.
14. Exaggerated startle response.
C. Duration of the disturbance (symptoms in Criterion B) is 3 days to 1 month after trauma
exposure.
Note: Symptoms typically begin immediately after the trauma, but persistence for at
least 3 days and up to a month is needed to meet disorder criteria.
D. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
E. The disturbance is not attributable to the physiological effects of a substance (e.g.,
medication or alcohol) or another medical condition (e.g., mild traumatic brain injury)
and is not better explained by brief psychotic disorder.
Diagnostic Features
The essential feature of acute stress disorder is the development of characteristic symp-
toms lasting from 3 days to 1 month following exposure to one or more traumatic events.
Traumatic events that are experienced directly include, but are not limited to, exposure
to war as a combatant or civilian, threatened or actual violent personal assault (e.g., sexual
282 Trauma- and Stressor-Related Disorders
violence, physical attack, active combat, mugging, childhood physical and/or sexual vio-
lence, being kidnapped, being taken hostage, terrorist attack, torture), natural or human-
made disasters (e.g., earthquake, hurricane, airplane crash), and severe accident (e.g.,
severe motor vehicle, industrial accident). For children, sexually traumatic events may
include inappropriate sexual experiences without violence or injury. A life-threatening
illness or debilitating medical condition is not necessarily considered a traumatic event.
Medical incidents that qualify as traumatic events involve sudden, catastrophic events (e.g.,
waking during surgery, anaphylactic shock). Stressful events that do not possess the severe
and traumatic components of events encompassed by Criterion A may lead to an adjust-
ment disorder but not to acute stress disorder.
The clinical presentation of acute stress disorder may vary by individual but typically
involves an anxiety response that includes some form of reexperiencing of or reactivity to
the traumatic event. In some individuals, a dissociative or detached presentation can pre-
dominate, although these individuals typically will also display strong emotional or phys-
iological reactivity in response to trauma reminders. In other individuals, there can be a
strong anger response in which reactivity is characterized by irritable or possibly aggres-
sive responses. The full symptom picture must be present for at least 3 days after the trau-
matic event and can be diagnosed only up to 1 month after the event. Symptoms that occur
immediately after the event but resolve in less than 3 days would not meet criteria for
acute stress disorder.
Witnessed events include, but are not limited to, observing threatened or serious in-
jury, unnatural death, physical or sexual violence inflicted on another individual as a re-
sult of violent assault, severe domestic violence, severe accident, war, and disaster; it may
also include witnessing a medical catastrophe (e.g., a life-threatening hemorrhage) involv-
ing one’s child. Events experienced indirectly through learning about the event are limited
to close relatives or close friends. Such events must have been violent or accidental—death
due to natural causes does not qualify—and include violent personal assault, suicide, se-
rious accident, or serious injury. The disorder may be especially severe when the stressor
is interpersonal and intentional (e.g., torture, rape). The likelihood of developing this dis-
order may increase as the intensity of and physical proximity to the stressor increase.
The traumatic event can be reexperienced in various ways. Commonly, the individual
has recurrent and intrusive recollections of the event (Criterion B1). The recollections are
spontaneous or triggered recurrent memories of the event that usually occur in response
to a stimulus that is reminiscent of the traumatic experience (e.g., the sound of a backfiring
car triggering memories of gunshots). These intrusive memories often include sensory
(e.g., sensing the intense heat that was perceived in a house fire), emotional (e.g., experi-
encing the fear of believing that one was about to be stabbed), or physiological (e.g., expe-
riencing the shortness of breath that one suffered during a near-drowning) components.
Distressing dreams may contain themes that are representative of or thematically re-
lated to the major threats involved in the traumatic event. (For example, in the case of a
motor vehicle accident survivor, the distressing dreams may involve crashing cars gener-
ally; in the case of a combat soldier, the distressing dreams may involve being harmed in
ways other than combat.)
Dissociative states may last from a few seconds to several hours, or even days, during
which components of the event are relived and the individual behaves as though experi-
encing the event at that moment. While dissociative responses are common during a trau-
matic event, only dissociative responses that persist beyond 3 days after trauma exposure
are considered for the diagnosis of acute stress disorder. For young children, reenactment
of events related to trauma may appear in play and may include dissociative moments
(e.g., a child who survives a motor vehicle accident may repeatedly crash toy cars during
play in a focused and distressing manner). These episodes, often referred to as flashbacks,
are typically brief but involve a sense that the traumatic event is occurring in the present
rather than being remembered in the past and are associated with significant distress.
Acute Stress Disorder 283
Some individuals with the disorder do not have intrusive memories of the event itself,
but instead experience intense psychological distress or physiological reactivity when
they are exposed to triggering events that resemble or symbolize an aspect of the traumatic
event (e.g., windy days for children after a hurricane, entering an elevator for a male or fe-
male who was raped in an elevator, seeing someone who resembles one’s perpetrator).
The triggering cue could be a physical sensation (e.g., a sense of heat for a burn victim, diz-
ziness for survivors of head trauma), particularly for individuals with highly somatic pre-
sentations. The individual may have a persistent inability to feel positive emotions (e.g.,
happiness, joy, satisfaction, or emotions associated with intimacy, tenderness, or sexual-
ity) but can experience negative emotions such as fear, sadness, anger, guilt, or shame.
Alterations in awareness can include depersonalization, a detached sense of oneself (e.g.,
seeing oneself from the other side of the room), or derealization, having a distorted view of
one’s surroundings (e.g., perceiving that things are moving in slow motion, seeing things
in a daze, not being aware of events that one would normally encode). Some individuals
also report an inability to remember an important aspect of the traumatic event that was
presumably encoded. This symptom is attributable to dissociative amnesia and is not at-
tributable to head injury, alcohol, or drugs.
Stimuli associated with the trauma are persistently avoided. The individual may refuse
to discuss the traumatic experience or may engage in avoidance strategies to minimize
awareness of emotional reactions (e.g., excessive alcohol use when reminded of the ex-
perience). This behavioral avoidance may include avoiding watching news coverage of
the traumatic experience, refusing to return to a workplace where the trauma occurred, or
avoiding interacting with others who shared the same traumatic experience.
It is very common for individuals with acute stress disorder to experience problems
with sleep onset and maintenance, which may be associated with nightmares or with gen-
eralized elevated arousal that prevents adequate sleep. Individuals with acute stress dis-
order may be quick tempered and may even engage in aggressive verbal and/or physical
behavior with little provocation. Acute stress disorder is often characterized by a height-
ened sensitivity to potential threats, including those that are related to the traumatic ex-
perience (e.g., a motor vehicle accident victim may be especially sensitive to the threat
potentially caused by any cars or trucks) or those not related to the traumatic event (e.g.,
fear of having a heart attack). Concentration difficulties, including difficulty remembering
daily events (e.g., forgetting one’s telephone number) or attending to focused tasks (e.g.,
following a conversation for a sustained period of time), are commonly reported. Individ-
uals with acute stress disorder may be very reactive to unexpected stimuli, displaying a
heightened startle response or jumpiness to loud noises or unexpected movements (e.g.,
the individual may jump markedly in the response to a telephone ringing).
Associated Features Supporting Diagnosis
Individuals with acute stress disorder commonly engage in catastrophic or extremely neg-
ative thoughts about their role in the traumatic event, their response to the traumatic ex-
perience, or the likelihood of future harm. For example, an individual with acute stress
disorder may feel excessively guilty about not having prevented the traumatic event or
about not adapting to the experience more successfully. Individuals with acute stress dis-
order may also interpret their symptoms in a catastrophic manner, such that flashback
memories or emotional numbing may be interpreted as a sign of diminished mental ca-
pacity. It is common for individuals with acute stress disorder to experience panic attacks
in the initial month after trauma exposure that may be triggered by trauma reminders or
may apparently occur spontaneously. Additionally, individuals with acute stress disorder
may display chaotic or impulsive behavior. For example, individuals may drive reck-
lessly, make irrational decisions, or gamble excessively. In children, there may be sig-
nificant separation anxiety, possibly manifested by excessive needs for attention from
284 Trauma- and Stressor-Related Disorders
caregivers. In the case of bereavement following a death that occurred in traumatic cir-
cumstances, the symptoms of acute stress disorder can involve acute grief reactions. In
such cases, reexperiencing, dissociative, and arousal symptoms may involve reactions to
the loss, such as intrusive memories of the circumstances of the individual’s death, disbe-
lief that the individual has died, and anger about the death. Postconcussive symptoms
{e.g., headaches, dizziness, sensitivity to light or sound, irritability, concentration deficits),
which occur frequently following mild traumatic brain injury, are also frequently seen in
individuals with acute stress disorder. Postconcussive symptoms are equally common in
brain-injured and non-brain-injured populations, and the frequent occurrence of postcon-
cussive symptoms could be attributable to acute stress disorder symptoms.
Prevalence
The prevalence of acute stress disorder in recently trauma-exposed populations (i.e.,
within 1 month of trauma exposure) varies according to the nature of the event and the
context in which it is assessed. In both U.S. and non-U.S. populations, acute stress disorder
tends to be identified in less than 20% of cases following traumatic events that do not in-
volve interpersonal assault; 13%-21% of motor vehicle accidents, 14% of mild traumatic
brain injury, 19% of assault, 10% of severe burns, and 6%-12% of industrial accidents.
Higher rates (i.e., 20%-50%) are reported following interpersonal traumatic events, in-
cluding assault, rape, and witnessing a mass shooting.
Development and Course
Acute stress disorder cannot be diagnosed until 3 days after a traumatic event. Although
acute stress disorder may progress to posttraumatic stress disorder (PTSD) after 1 month,
it may also be a transient stress response that remits within 1 month of trauma exposure
and does not result in PTSD. Approximately half of individuals who eventually develop
PTSD initially present with acute stress disorder. Symptom worsening during the initial
month can occur, often as a result of ongoing life stressors or further traumatic events.
The forms of reexperiencing can vary across development. Unlike adults or adoles-
cents, young children may report frightening dreams without content that clearly reflects
aspects of the trauma (e.g., waking in fright in the aftermath of the trauma but being unable
to relate the content of the dream to the traumatic event). Children age 6 years and younger
are more likely than older children to express reexperiencing symptoms through play that
refers directly or symbolically to the trauma. For example, a very young child who sur-
vived a fire may draw pictures of flames. Young children also do not necessarily manifest
fearful reactions at the time of the exposure or even during reexperiencing. Parents typi-
cally report a range of emotional expressions, such as anger, shame, or withdrawal, and
even excessively bright positive affect, in young children who are traumatized. Although
children may avoid reminders of the trauma, they sometimes become preoccupied with
reminders (e.g.,a young child bitten by a dog may talk about dogs constantly yet avoid go-
ing outside because of fear of coming into contact with a dog).
Risk and Prognostic Factors
Temperamental. Risk factors include prior mental disorder, high levels of negative af-
fectivity (neuroticism), greater perceived severity of the traumatic event, and an avoidant
coping style. Catastrophic appraisals of the traumatic experience, often characterized by
exaggerated appraisals of future harm, guilt, or hopelessness, are strongly predictive of
acute stress disorder.
Environmental. First and foremost, an individual must be exposed to a traumatic event to
be at risk for acute stress disorder. Risk factors for the disorder include a history of prior
trauma.
Acute Stress Disorder 285
Genetic and physiological. Females are at greater risk for developing acute stress dis-
order. ’
Elevated reactivity, as reflected by acoustic startle response, prior to trauma exposure
increases the risk for developing acute stress disorder.
Culture-Related Diagnostic Issues
The profile of symptoms of acute stress disorder may vary cross-culturally, particularly
with respect to dissociative symptoms, nightmares, avoidance, and somatic symptoms
(e.g., dizziness, shortness of breath, heat sensations). Cultural syndromes and idioms of
distress shape the local symptom profiles of acute stress disorder. Some cultural groups
may display variants of dissociative responses, such as possession or trancelike behaviors
in the initial month after trauma exposure. Panic symptoms may be salient in acute stress
disorder among Cambodians because of the association of traumatic exposure with panic-
like khydl attacks, and ataque de nervios among Latin Americans may also follow a traumatic
exposure.
Gender-Related Diagnostic Issues
Acute stress disorder is more prevalent among females than among males. Sex-linked neu-
robiological differences in stress response may contribute to females’ increased risk for
acute stress disorder. The increased risk for the disorder in females may be attributable in
part to a greater likelihood of exposure to the types of traumatic events with a high con-
ditional risk for acute stress disorder, such as rape and other interpersonal violence.
Functional Consequences of Acute Stress Disorder
Impaired functioning in social, interpersonal, or occupational domains has been shown
across survivors of accidents, assault, and rape who develop acute stress disorder. The ex-
treme levels of anxiety that may be associated with acute stress disorder may interfere
with sleep, energy levels, and capacity to attend to tasks. Avoidance in acute stress dis-
order can result in generalized withdrawal from many situations that are perceived as
potentially threatening, which can lead to nonattendance of medical appointments, avoid-
ance of driving to important appointments, and absenteeism from work.
Differential Diagnosis
Adjustment disorders. In acute stress disorder, the stressor can be of any severity rather
than of the severity and type required by Criterion A of acute stress disorder. The diagnosis of
an adjustment disorder is used when the response to a Criterion A event does not meet the cri-
teria for acute stress disorder (or another specific mental disorder) and when the symptom pat-
tern of acute stress disorder occurs in response to a stressor that does not meet Criterion A for
exposure to actual or threatened death, serious injury, or sexual violence (e.g., spouse leaving,
being fired). For example, severe stress reactions to life-threatening illnesses that may include
some acute stress disorder symptoms may be more appropriately described as an adjustment
disorder. Some forms of acute stress response do not include acute stress disorder symptoms
and may be characterized by anger, depression, or guilt. These responses are more appro-
priately described as primarily an adjustment disorder. Depressive or anger responses in an
adjustment disorder may involve rumination about the traumatic event, as opposed to invol-
untary and intrusive distressing memories in acute stress disorder.
Panic disorder. Spontaneous panic attacks are very common in acute stress disorder.
However, panic disorder is diagnosed only if panic attacks are unexpected and there is
anxiety about future attacks or maladaptive changes in behavior associated with fear of
dire consequences of the attacks.
286 Trauma- and Stressor-Related Disorders
Dissociative disorders. Severe dissociative responses (in the absence of characteristic
acute stress disorder symptoms) may be diagnosed as derealization/depersonalization
disorder. If severe amnesia of the trauma persists in the absence of characteristic acute
stress disorder symptoms, the diagnosis of dissociative amnesia may be indicated.
Posttraumatic stress disorder. Acute stress disorder is distinguished from PTSD because
the symptom pattern in acute stress disorder must occur within 1 month of the traumatic event
and resolve within that 1-month period. If the symptoms persist for more than 1 month and
meet criteria for PTSD, the diagnosis is changed from acute stress disorder to PTSD.
Obsessive-compulsive disorder. In obsessive-compulsive disorder, there are recurrent
intrusive thoughts, but these meet the definition of an obsession. In addition, the intrusive
thoughts are not related to an experienced traumatic event, compulsions are usually pres-
ent, and other symptoms of acute stress disorder are typically absent.
Psychotic disorders. Flashbacks in acute stress disorder must be distinguished from il-
lusions, hallucinations, and other perceptual disturbances that may occur in schizophre-
nia, other psychotic disorders, depressive or bipolar disorder with psychotic features, a
delirium, substance/medication-induced disorders, and psychotic disorders due to an-
other medical condition. Acute stress disorder flashbacks are distinguished from these
other perceptual disturbances by being directly related to the traumatic experience and by
occurring in the absence of other psychotic or substance-induced features.
Traumatic brain injury. When a brain injury occurs in the context of a traumatic event
(e.g., traumatic accident, bomb blast, acceleration/ deceleration trauma), symptoms of
acute stress disorder may appear. An event causing head trauma may also constitute a
psychological traumatic event, and tramautic brain injury (TBI)-related neurocognitive
symptoms are not mutually exclusive and may occur concurrently. Symptoms previously
termed postconcussive (e.g., headaches, dizziness, sensitivity to light or sound, irritability,
concentration deficits) can occur in brain-injured and non-brain injured populations, in-
cluding individuals with acute stress disorder. Because symptoms of acute stress disorder
and TBl-related neurocognitive symptoms can overlap, a differential diagnosis between
acute stress disorder.and neurocognitive disorder symptoms attributable to TBI may be
possible based on the presence of symptoms that are distinctive to each presenta-
tion. Whereas reexperiencing and avoidance are characteristic of acute stress disorder and
not the effects of TBI, persistent disorientation and confusion are more specific to TBI (neu-
rocognitive effects) than to acute stress disorder. Furthermore, differential is aided by the
fact that symptoms of acute stress disorder persist for up to only 1 month following trauma
exposure.
Adjustment Disorders
Diagnostic Criteria
A. The development of emotional or behavioral symptoms in response to an identifiable
stressor(s) occurring within 3 months of the onset of the stressor(s).
B. These symptoms or behaviors are clinically significant, as evidenced by one or both of
the following:
1. Marked distress that is out of proportion to the severity or intensity of the stressor,
taking into account the external context and the cultural factors that might influence
symptom severity and presentation.
2. Significant impairment in social, occupational, or other important areas of functioning.
C. The stress-related disturbance does not meet the criteria for another mental disorder
and is not merely an exacerbation of a preexisting mental disorder.
Adjustment Disorders 287
D. The symptoms do not represent normal bereavement.
E. Once the stressor or its consequences have terminated, the symptoms do not persist
for more than an additional 6 months.
Specify whether:
309.0 (F43.21) With depressed mood: Low mood, tearfulness, or feelings of hope-
lessness are predominant.
309.24 (F43.22) With anxiety: Nervousness, worry, jitteriness, or separation anxiety
is predominant.
309.28 (F43.23) With mixed anxiety and depressed mood: A combination of de-
pression and anxiety is predominant.
309.3 (F 43.24) With disturbance of conduct: Disturbance of conduct is predominant.
309.4 (F43.25) With mixed disturbance of emotions and conduct: Both emotional
symptoms (e.g., depression, anxiety) and a disturbance of conduct are predominant.
309.9 (F43.20) Unspecified: For maladaptive reactions that are not classifiable as one
of the specific subtypes of adjustment disorder.
Diagnostic Features
The presence of emotional or behavioral symptoms in response to an identifiable stressor
is the essential feature of adjustment disorders (Criterion A). The stressor may be a single
event (e.g., a termination of a romantic relationship), or there may be multiple stressors
(e.g., marked business difficulties and marital problems). Stressors may be recurrent (e.g.,
associated with seasonal business crises, unfulfilling sexual relationships) or continuous
(e.g., a persistent painful illness with increasing disability, living in a crime-ridden neigh-
borhood). Stressors may affect a single individual, an entire family, or a larger group or
community (e.g., a natural disaster). Some stressors may accompany specific developmen-
tal events (e.g., going to school, leaving a parental home, reentering a parental home, get-
ting married, becoming a parent, failing to attain occupational goals, retirement).
Adjustment disorders may be diagnosed following the death of a loved one when the
intensity, quality, or persistence of grief reactions exceeds what normally might be ex-
pected, when cultural, religious, or age-appropriate norms are taken into account. A more
specific set of bereavement-related symptoms has been designated persistent complex be-
reavement disorder.
Adjustment disorders are associated with an increased risk of suicide attempts and
completed suicide.
Prevalence
Adjustment disorders are common, although prevalence may vary widely as a function of
the population studied and the assessment methods used. The percentage of individuals
in outpatient mental] health treatment with a principal diagnosis of an adjustment disorder
ranges from approximately 5% to 20%. In a hospital psychiatric consultation setting, it is
often the most common diagnosis, frequently reaching 50%.
Development and Course
By definition, the disturbance in adjustment disorders begins within 3 months of onset of
a stressor and lasts no longer than 6 months after the stressor or its consequences have
ceased. If the stressor is an acute event (e.g., being fired from a job), the onset of the dis-
turbance is usually immediate (i.e., within a few days) and the duration is relatively brief
(ie., no more than a few months). If the stressor or its consequences persist, the adjustment
disorder may also continue to be present and become the persistent form.
288 Trauma- and Stressor-Related Disorders
Risk and Prognostic Factors
Environmental. Individuals from disadvantaged life circumstances experience a high
rate of stressors and may be at increased risk for adjustment disorders.
Culture-Reiated Diagnostic Issues
The context of the individual's cultural setting should be taken into account in making the
clinical judgment of whether the individual’s response to the stressor is maladaptive or
whether the associated distress is in excess of what would be expected. The nature, mean-
ing, and experience of the stressors and the evaluation of the response to the stressors may
vary across cultures.
Functional Consequences of Adjustment Disorders
The subjective distress or impairment in functioning associated with adjustment disorders
is frequently manifested as decreased performance at work or school and temporary
changes in social relationships. An adjustment disorder may complicate the course of ill-
ness in individuals who have a general medical condition (e.g., decreased compliance with
the recommended medical regimen; increased length of hospital stay).
Differential Diagnosis
Major depressive disorder. If an individual has symptoms that meet criteria for a major
depressive disorder in response to a stressor, the diagnosis of an adjustment disorder is
not applicable. The symptom profile of major depressive disorder differentiates it from ad-
justment disorders.
Posttraumatic stress disorder and acute stress disorder. In adjustment disorders, the
stressor can be of any severity rather than of the severity and type required by Criterion A
of acute stress disorder and posttraumatic stress disorder (PTSD). In distinguishing ad-
justment disorders from these two posttraumatic diagnoses, there are both timing and
symptom profile considerations. Adjustment disorders can be diagnosed immediately
and persist up to 6 months after exposure to the traumatic event, whereas acute stress dis-
order can only occur between 3 days and 1 month of exposure to the stressor, and PTSD
cannot be diagnosed until at least 1 month has passed since the occurrence of the traumatic
stressor. The required symptom profile for PTSD and acute stress disorder differentiates
them from the adjustment disorders. With regard to symptom profiles, an adjustment dis-
order may be diagnosed following a traumatic event when an individual exhibits symptoms
of either acute stress disorder or PTSD that do not meet or exceed the diagnostic threshold
for either disorder. An adjustment disorder should also be diagnosed for individuals who
have not been exposed to a traumatic event but who otherwise exhibit the full symptom pro-
file of either acute stress disorder or PTSD.
Personality disorders. With regard to personality disorders, some personality features
may be associated with a vulnerability to situational distress that may resemble an adjust-
ment disorder. The lifetime history of personality functioning will help inform the in-
terpretation of distressed behaviors to aid in distinguishing a long-standing personality
disorder from an adjustment disorder. In addition to some personality disorders incurring
vulnerability to distress, stressors may also exacerbate personality disorder symptoms. In
the presence of a personality disorder, if the symptom criteria for an adjustment disorder
are met, and the stress-related disturbance exceeds what may be attributable to maladap-
tive personality disorder symptoms (i.e., Criterion C is met), then the diagnosis of an ad-
justment disorder should be made.
Other Specified Trauma- and Stressor-Related Disorder 289
Psychological factors affecting other medical conditions. In psychological factors af-
fecting other medical conditions, specific psychological entities (e.g., psychological symp-
toms, behaviors, other factors) exacerbate a medical condition. These psychological
factors can precipitate, exacerbate, or put an individual at risk for medical illness, or they
can worsen an existing condition. In contrast, an adjustment disorder is a reaction to the
stressor (e.g., having a medical illness).
Normative stress reactions. When bad things happen, most people get upset. This is
not an adjustment disorder. The diagnosis should only be made when the magnitude of
the distress (e.g., alterations in mood, anxiety, or conduct) exceeds what would normally
be expected (which may vary in different cultures) or when the adverse event precipitates
functional impairment.
Comorbidity
Adjustment disorders can accompany most mental disorders and any medical disorder.
Adjustment disorders can be diagnosed in addition to another mental disorder only if the
latter does not explain the particular symptoms that occur in reaction to the stressor. For
example, an individual may develop an adjustment disorder, with depressed mood, after
losing a job and at the same time have a diagnosis of obsessive-compulsive disorder. Or,
an individual may have a depressive or bipolar disorder and an adjustment disorder as
long as the criteria for both are met. Adjustment disorders are common accompaniments
of medical illness and may be the major psychological response to a medical disorder.
Other Specified Trauma- and
Stressor-Related Disorder
309.89 (F43.8)
This category applies to presentations in which symptoms characteristic of a trauma- and
stressor-related disorder that cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate but do not meet the full
criteria for any of the disorders in the trauma- and stressor-related disorders diagnostic
class. The other specified trauma- and stressor-related disorder category is used in situa-
tions in which the clinician chooses to communicate the specific reason that the presenta-
tion does not meet the criteria for any specific trauma- and stressor-related disorder. This
is done by recording “other specified trauma- and stressor-related disorder’ followed by
the specific reason (e.g., “persistent complex bereavement disorder’).
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Adjustment-like disorders with delayed onset of symptoms that occur more than
3 months after the stressor.
2. Adjustment-like disorders with prolonged duration of more than 6 months with-
out prolonged duration of stressor.
3. Ataque de nervios: See “Glossary of Cultural Concepts of Distress” in the Appendix.
4. Other cultural syndromes: See “Glossary of Cultural Concepts of Distress” in the Ap-
pendix.
5. Persistent complex bereavement disorder: This disorder is characterized by severe
and persistent grief and mourning reactions (see the chapter “Conditions for Further
Study”).
290 Trauma- and Stressor-Related Disorders
Unspecified Trauma- and
Stressor-Related Disorder
309.9 (F43.9)
This category applies to presentations in which symptoms characteristic of a trauma- and
stressor-related disorder that cause clinically significant distress or impairment in social, oc-
cupational, or other important areas of functioning predominate but do not meet the full cri-
teria for any of the disorders in the trauma- and stressor-related disorders diagnostic class.
The unspecified trauma- or stressor-related disorder category is used in situations in which
the clinician chooses not to specify the reason that the criteria are not met for a specific
trauma- and stressor-related disorder, and includes presentations in which there is insuffi-
cient information to make a more specific diagnosis (e.g., in emergency room settings).
Dissociative disorders are characterized by a disruption of and/or discontinuity
in the normal integration of consciousness, memory, identity, emotion, perception, body
representation, motor control, and behavior. Dissociative symptoms can potentially dis-
rupt every area of psychological functioning. This chapter includes dissociative identity
disorder, dissociative amnesia, depersonalization/derealization disorder, other specified
dissociative disorder, and unspecified dissociative disorder.
Dissociative symptoms are experienced as a) unbidden intrusions into awareness and
behavior, with accompanying losses of continuity in subjective experience (i.e., “positive”
dissociative symptoms such as fragmentation of identity, depersonalization, and dereal-
ization) and/or b) inability to access information or to control mental functions that nor-
mally are readily amenable to access or control (i.e., “negative” dissociative symptoms such
as amnesia).
The dissociative disorders are frequently found in the aftermath of trauma, and many
of the symptoms, including embarrassment and confusion about the symptoms or a desire
to hide them, are influenced by the proximity to trauma. In DSM-5, the dissociative disor-
ders are placed next to, but are not part of, the trauma- and stressor-related disorders, re-
flecting the close relationship between these diagnostic classes. Both acute stress disorder
and posttraumatic stress disorder contain dissociative symptoms, such as amnesia, flash-
backs, numbing, and depersonalization/derealization.
Depersonalization/derealization disorder is characterized by clinically significant persis-
tent or recurrent depersonalization (i.e., experiences of unreality or detachment from one’s
mind, self, or body) and/or derealization (i.e., experiences of unreality or detachment from
one’s surroundings). These alterations of experience are accompanied by intact reality
testing. There is no evidence of any distinction between individuals with predominantly
depersonalization versus derealization symptoms. Therefore, individuals with this disor-
der can have depersonalization, derealization, or both.
Dissociative amnesia is characterized by an inability to recall autobiographical informa-
tion. This amnesia may be localized (i.e., an event or period of time), selective (i.e., a specific
aspect of an event), or generalized (i.e., identity and life history). Dissociative amnesia is fun-
damentally an inability to recall autobiographical information that is inconsistent with nor-
mal forgetting. It may or may not involve purposeful travel or bewildered wandering (i.e.,
fugue). Although some individuals with amnesia promptly notice that they have “lost time”
or that they have a gap in their memory, most individuals with dissociative disorders are ini-
tially unaware of their amnesias. For them, awareness of amnesia occurs only when personal
identity is lost or when circumstances make these individuals aware that autobiographical
information is missing (e.g., when they discover evidence of events they cannot recall or
when others tell them or ask them about events they cannot recall). Until and unless this hap-
pens, these individuals have “amnesia for their amnesia.” Amnesia is experienced as an es-
sential feature of dissociative amnesia; individuals may experience localized or selective
amnesia most commonly, or generalized amnesia rarely. Dissociative fugue is rare in per-
sons with dissociative amnesia but common in dissociative identity disorder.
Dissociative identity disorder is characterized by a) the presence of two or more distinct
personality states or an experience of possession and b) recurrent episodes of amnesia. The
291
292 Dissociative Disorders
fragmentation of identity may vary with culture (e.g., possession-form presentations) and cir-
cumstance. Thus, individuals may experience discontinuities in identity and memory that
may not be immediately evident to others or are obscured by attempts to hide dysfunction. In-
dividuals with dissociative identity disorder experience a) recurrent, inexplicable intrusions
into their conscious functioning and sense of self (e.g., voices; dissociated actions and speech;
intrusive thoughts, emotions, and impulses), b) alterations of sense of self (e.g., attitudes, pref-
erences, and feeling like one’s body or actions are not one’s own), c) odd changes of perception
(e.g., depersonalization or derealization, such as feeling detached from one’s body while cut-
ting), and d) intermittent functional neurological symptoms. Stress often produces transient
exacerbation of dissociative symptoms that makes them more evident.
The residual category of other specified dissociative disorder has seven examples: chronic
or recurrent mixed dissociative symptoms that approach, but fall short of, the diagnostic cri-
teria for dissociative identity disorder; dissociative states secondary to brainwashing or
thought reform; two acute presentations, of less than 1 month’s duration, of mixed dissociative
symptoms, one of which is also marked by the presence of psychotic symptoms; and three sin-
gle-symptom dissociative presentations—dissociative trance, dissociative stupor or coma, and
Ganser’s syndrome (the giving of approximate and vague answers).
Dissociative Identity Disorder
Diagnostic Criteria 300.14 (F44.81)
A. Disruption of identity characterized by two or more distinct personality states, which
may be described in some cultures as an experience of possession. The disruption in
identity involves marked discontinuity in sense of self and sense of agency, accompa-
nied by related alterations in affect, behavior, consciousness, memory, perception,
cognition, and/or sensory-motor functioning. These signs and symptoms may be ob-
served by others or reported by the individual.
B. Recurrent gaps in the recall of everyday events, tmportant personal information, and/
or traumatic events that are inconsistent with ordinary forgetting.
C. The symptoms cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
D. The disturbance is not a normal part of a broadly accepted cultural or religious practice.
Note: In children, the symptoms are not better explained by imaginary playmates or
other fantasy play.
E. The symptoms are not attributable to the physiological effects of a substance (e.g.,
blackouts or chaotic behavior during alcohol intoxication) or another medical condition
(e.g., complex partial seizures).
Diagnostic Features
The defining feature of dissociative identity disorder is the presence of two or more dis-
tinct personality states or an experience of possession (Criterion A). The overtness or
covertness of these personality states, however, varies as a function of psychological
motivation, current level of stress, culture, internal conflicts and dynamics, and emotional
resilience. Sustained periods of identity disruption may occur when psychosocial pres-
sures are severe and/or prolonged. In many possession-form cases of dissociative identity
disorder, and in a small proportion of non-possession-form cases, manifestations of alter-
nate identities are highly overt. Most individuals with non-possession-form dissociative
identity disorder do not overtly display their discontinuity of identity for long periods of
time; only a small minority present to clinical attention with observable alternation of
Dissociative Identity Disorder 293
identities. When alternate personality states are not directly observed, the disorder can be
identified by two clusters of symptoms: 1) sudden alterations or discontinuities in sense of
self and sense of agency (Criterion A), and 2) recurrent dissociative amnesias (Criterion B).
Criterion A symptoms are related to discontinuities of experience that can affect any
aspect of an individual's functioning. Individuals with dissociative identity disorder may
report the feeling that they have suddenly become depersonalized observers of their
“own” speech and actions, which they may feel powerless to stop (sense of self). Such in-
dividuals may also report perceptions of voices (e.g., a child’s voice; crying; the voice of a
spiritual being). In some cases, voices are experienced as multiple, perplexing, indepen-
dent thought streams over which the individual experiences no control. Strong emotions,
impulses, and even speech or other actions may suddenly emerge, without a sense of per-
sonal ownership or control (sense of agency). These emotions and impulses are frequently
reported as ego-dystonic and puzzling. Attitudes, outlooks, and personal preferences
(e.g., about food, activities, dress) may suddenly shift and then shift back. Individuals may
report that their bodies feel different (e.g., like a small child, like the opposite gender, huge
and muscular). Alterations in sense of self and loss of personal agency may be accompa-
nied by a feeling that these attitudes, emotions, and behaviors—even one’s body—are
“not mine” and/or are “not under my control.” Although most Criterion A symptoms are
subjective, many of these sudden discontinuities in speech, affect, and behavior can be wit-
nessed by family, friends, or the clinician. Non-epileptic seizures and other conversion
symptoms are prominent in some presentations of dissociative identity disorder, espe-
cially in some non-Western settings.
The dissociative amnesia of individuals with dissociative identity disorder manifests in
three primary ways: as 1) gaps in remote memory of personal life events (e.g., periods of
childhood or adolescence; some important life events, such as the death of a grandparent,
getting married, giving birth); 2) lapses in dependable memory (e.g., of what happened
today, of well-learned skills such as how to do their job, use a computer, read, drive); and
3) discovery of evidence of their everyday actions and tasks that they do not recollect do-
ing (e.g., finding unexplained objects in their shopping bags or among their possessions;
finding perplexing writings or drawings that they must have created; discovering injuries;
“coming to” in the midst of doing something). Dissociative fugues, wherein the person
discovers dissociated travel, are common. Thus, individuals with dissociative identity dis-
order may report that they have suddenly found themselves at the beach, at work, ina night-
club, or somewhere at home (e.g., in the closet, on a bed or sofa, in the corner) with no
memory of how they came to be there. Amnesia in individuals with dissociative identity dis-
order is not limited to stressful or traumatic events; these individuals often cannot recall
everyday events as well.
Individuals with dissociative identity disorder vary in their awareness and attitude to-
ward their amnesias. It is common for these individuals to minimize their amnestic symp-
toms. Some of their amnestic behaviors may be apparent to others—as when these persons
do not recall something they were witnessed to have done or said, when they cannot
remember their own name, or when they do not recognize their spouse, children, or close
friends.
Possession-form identities in dissociative identity disorder typically manifest as be-
haviors that appear as if a “spirit,” supernatural being, or outside person has taken control,
such that the individual begins speaking or acting ina distinctly different manner. For ex-
ample, an individual’s behavior may give the appearance that her identity has been
replaced by the “ghost” of a girl who committed suicide in the same community years
before, speaking and acting as though she were still alive. Or an individual may be “taken
over” by a demon or deity, resulting in profound impairment, and demanding that the in-
dividual or a relative be punished for a past act, followed by more subtle periods of iden-
tity alteration. However, the majority of possession states around the world are normal,
usually part of spiritual practice, and do not meet criteria for dissociative identity disor-
294 Dissociative Disorders
der. The identities that arise during possession-form dissociative identity disorder present
recurrently, are unwanted and involuntary, cause clinically significant distress or impair-
ment (Criterion C), and are not a normal part of a broadly accepted cultural or religious
practice (Criterion D).
Associated Features Supporting Diagnosis
Individuals with dissociative identity disorder typically present with comorbid depression,
anxiety, substance abuse, self-injury, non-epileptic seizures, or another common symp-
tom. They often conceal, or are not fully aware of, disruptions in consciousness, amnesia,
or other dissociative symptoms. Many individuals with dissociative identity disorder re-
port dissociative flashbacks during which they undergo a sensory reliving of a previous
event as though it were occurring in the present, often with a change of identity, a partial
or complete loss of contact with or disorientation to current reality during the flashback,
and a subsequent amnesia for the content of the flashback. Individuals with the disorder
typically report multiple types of interpersonal maltreatment during childhood and adult-
hood. Nonmaltreatment forms of overwhelming early life events, such as multiple long,
painful, early-life medical procedures, also may be reported. Self-mutilation and suicidal
behavior are frequent. On standardized measures, these individuals report higher levels
of hypnotizability and dissociativity compared with other clinical groups and healthy con-
trol subjects. Some individuals experience transient psychotic phenomena or episodes.
Several brain regions have been implicated in the pathophysiology of dissociative identity
disorder, including the orbitofrontal cortex, hippocampus, parahippocampal gyrus, and
amygdala.
Prevalence
The 12-month prevalence of dissociative identity disorder among adults in a small U.S.
community study was 1.5%. The prevalence across genders in that study was 1.6% for
males and 1.4% for females.
Development and Course
Dissociative identity disorder is associated with overwhelming experiences, traumatic
events, and/or abuse occurring in childhood. The full disorder may first manifest at al-
most any age (from earliest childhood to late life). Dissociation in children may generate
problems with memory, concentration, attachment, and traumatic play. Nevertheless, chil-
dren usually do not present with identity changes; instead they present primarily with over-
lap and interference among mental states (Criterion A phenomena), with symptoms related
to discontinuities of experience. Sudden changes in identity during adolescence may ap-
pear to be just adolescent turmoil or the early stages of another mental disorder. Older
individuals may present to treatment with what appear to be late-life mood disorders, ob-
sessive-compulsive disorder, paranoia, psychotic mood disorders, or even cognitive dis-
orders due to dissociative amnesia. In some cases, disruptive affects and memories may
increasingly intrude into awareness with advancing age.
Psychological decompensation and overt changes in identity may be triggered by 1) re-
moval from the traumatizing situation (e.g., through leaving home); 2) the individual's
children reaching the same age at which the individual was originally abused or trauma-
tized; 3) later traumatic experiences, even seemingly inconsequential ones, like a minor
motor vehicle accident; or 4) the death of, or the onset of a fatal illness in, their abuser(s).
Risk and Prognostic Factors
Environmental. Interpersonal physical and sexual abuse is associated with an increased
risk of dissociative identity disorder. Prevalence of childhood abuse and neglect in the
Dissociative Identity Disorder 295
United States, Canada, and Europe among those with the disorder is about 90%. Other
forms of traumatizing experiences, including childhood medical and surgical procedures,
war, childhood prostitution, and terrorism, have been reported.
Course modifiers. Ongoing abuse, later-life retraumatization, comorbidity with mental
disorders, severe medical illness, and delay in appropriate treatment are associated with
poorer prognosis.
Culture-Related Diagnostic Issues
Many features of dissociative identity disorder can be influenced by the individual's cul-
tural background. Individuals with this disorder may present with prominent medically
unexplained neurological symptoms, such as non-epileptic seizures, paralyses, or sensory
loss, in cultural settings where such symptoms are common. Similarly, in settings where
normative possession is common (e.g., rural areas in the developing world, among certain
religious groups in the United States and Europe), the fragmented identities may take the
form of possessing spirits, deities, demons, animals, or mythical figures. Acculturation or
prolonged intercultural contact may shape the characteristics of the other identities (e.g.,
identities in India may speak English exclusively and wear Western clothes). Possession-
form dissociative identity disorder can be distinguished from culturally accepted posses-
sion states in that the former is involuntary, distressing, uncontrollable, and often recur-
rent or persistent; involves conflict between the individual and his or her surrounding
family, social, or work milieu; and is manifested at times and in places that violate the
norms of the culture or religion.
Gender-Related Diagnostic Issues
Females with dissociative identity disorder predominate in adult clinical settings but not
in child clinical settings. Adult males with dissociative identity disorder may deny their
symptoms and trauma histories, and this can lead to elevated rates of false negative di-
agnosis. Females with dissociative identity disorder present more frequently with acute
dissociative states (e.g., flashbacks, amnesia, fugue, functional neurological [conversion]
symptoms, hallucinations, self-mutilation). Males commonly exhibit more criminal or vi-
olent behavior than females; among males, common triggers of acute dissociative states in-
clude combat, prison conditions, and physical or sexual assaults.
Suicide Risk
Over 70% of outpatients with dissociative identity disorder have attempted suicide; mul-
tiple attempts are common, and other self-injurious behavior is frequent. Assessment of
suicide risk may be complicated when there is amnesia for past suicidal behavior or when
the presenting identity does not feel suicidal and is unaware that other dissociated iden-
tities do.
Functional Consequences of
Dissociative Identity Disorder
Impairment varies widely, from apparently minimal (e.g., in high-functioning profession-
als) to profound. Regardless of level of disability, individuals with dissociative identity
disorder commonly minimize the impact of their dissociative and posttraumatic symp-
toms. The symptoms of higher-functioning individuals may impair their relational, mar-
ital, family, and parenting functions more than their occupational and professional life
(although the latter also may be affected). With appropriate treatment, many impaired in-
dividuals show marked improvement in occupational and personal functioning. How-
ever, some remain highly impaired in most activities of living. These individuals may only
respond to treatment very slowly, with gradual reduction in or improved tolerance of
296 Dissociative Disorders
their dissociative and posttraumatic symptoms. Long-term supportive treatment may
slowly increase these individuals’ ability to manage their symptoms and decrease use of
more restrictive levels of care.
Differential Diagnosis
Other specified dissociative disorder. The core of dissociative identity disorder is the
division of identity, with recurrent disruption of conscious functioning and sense of self.
This central feature is shared with one form of other specified dissociative disorder, which
may be distinguished from dissociative identity disorder by the presence of chronic or re-
current mixed dissociative symptoms that do not meet Criterion A for dissociative identity
disorder or are not accompanied by recurrent amnesia.
Major depressive disorder. Individuals with dissociative identity disorder are often de-
pressed, and their symptoms may appear to meet the criteria for a major depressive episode.
Rigorous assessment indicates that this depression in some cases does not meet full criteria for
major depressive disorder. Other specified depressive disorder in individuals with dissocia-
tive identity disorder often has an important feature: the depressed mood and cognitions fluc-
tuate because they are experienced in some identity states but not others.
Bipolar disorders. Individuals with dissociative identity disorder are often misdiag-
nosed with a bipolar disorder, most often bipolar II disorder. The relatively rapid shifts in
mood in individuals with this disorder—typically within minutes or hours, in contrast to
the slower mood changes typically seen in individuals with bipolar disorders—are due to
the rapid, subjective shifts in mood commonly reported across dissociative states, some-
times accompanied by fluctuation in levels of activation. Furthermore, in dissociative
identity disorder, elevated or depressed mood may be displayed in conjunction with overt
identities, so one or the other mood may predominate for a relatively long period of time
(often for days) or may shift within minutes.
Posttraumatic stress disorder. Some traumatized individuals have both posttraumatic
stress disorder (PTSD) and dissociative identity disorder. Accordingly, it is crucial to dis-
tinguish between individuals with PTSD only and individuals who have both PTSD and
dissociative identity disorder. This differential diagnosis requires that the clinician estab-
lish the presence or absence of dissociative symptoms that are not characteristic of acute
stress disorder or PTSD. Some individuals with PTSD manifest dissociative symptoms that
also occur in dissociative identity disorder: 1) amnesia for some aspects of trauma, 2) dis-
sociative flashbacks (i.e., reliving of the trauma, with reduced awareness of one’s current
orientation), and 3) symptoms of intrusion and avoidance, negative alterations in cogni-
tion and mood, and hyperarousal that are focused around the traumatic event. On the other
hand, individuals with dissociative identity disorder manifest dissociative symptoms that
are not a manifestation of PTSD: 1) amnesias for many everyday (i.e., nontraumatic) events,
2) dissociative flashbacks that may be followed by amnesia for the content of the flashback,
3) disruptive intrusions (unrelated to traumatic material) by dissociated identity states
into the individual’s sense of self and agency, and 4) infrequent, full-blown changes
among different identity states.
Psychotic disorders. Dissociative identity disorder may be confused with schizophre-
nia or other psychotic disorders. The personified, internally communicative inner voices
of dissociative identity disorder, especially of a child (e.g., “I hear a little girl crying in a
closet and an angry man yelling at her”), may be mistaken for psychotic hallucinations.
Dissociative experiences of identity fragmentation or possession, and of perceived loss of
control over thoughts, feelings, impulses, and acts, may be confused with signs of formal
thought disorder, such as thought insertion or withdrawal. Individuals with dissociative
identity disorder may also report visual, tactile, olfactory, gustatory, and somatic halluci-
nations, which are usually related to posttraumatic and dissociative factors, such as partial
Dissociative Identity Disorder 297
flashbacks. Individuals with dissociative identity disorder experience these symptoms as
caused by alternate identities, do not have delusional explanations for the phenomena,
and often describe the symptoms in a personified way (e.g., “I feel like someone else wants
to cry with my eyes”). Persecutory and derogatory internal voices in dissociative identity
disorder associated with depressive symptoms may be misdiagnosed as major depression
with psychotic features. Chaotic identity change and acute intrusions that disrupt thought
processes may be distinguished from brief psychotic disorder by the predominance of dis-
sociative symptoms and amnesia for the episode, and diagnostic evaluation after cessation
of the crisis can help confirm the diagnosis.
Substance/medication-induced disorders. Symptoms associated with the physiological
effects of a substance can be distinguished from dissociative identity disorder if the sub-
stance in question is judged to be etiologically related to the disturbance.
Personality disorders. Individuals with dissociative identity disorder often present identi-
ties that appear to encapsulate a variety of severe personality disorder features, suggesting a
differential diagnosis of personality disorder, especially of the borderline type. Importantly,
however, the individual’s longitudinal variability in personality style (due to inconsistency
among identities) differs from the pervasive and persistent dysfunction in affect management
and interpersonal relationships typical of those with personality disorders.
Conversion disorder (functional neurological symptom disorder). This disorder may be
distinguished from dissociative identity disorder by the absence of an identity disruption
characterized by two or more distinct personality states or an experience of possession.
Dissociative amnesia in conversion disorder is more limited and circumscribed (e.g., am-
nesia for a non-epileptic seizure).
Seizure disorders. Individuals with dissociative identity disorder may present with sei-
zurelike symptoms and behaviors that resemble complex partial seizures with temporal
lobe foci. These include déja vu, jamais vu, depersonalization, derealization, out-of-body
experiences, amnesia, disruptions of consciousness, hallucinations, and other intrusion
phenomena of sensation, affect, and thought. Normal electroencephalographic findings,
including telemetry, differentiate non-epileptic seizures from the seizurelike symptoms of
dissociative identity disorder. Also, individuals with dissociative identity disorder obtain
very high dissociation scores, whereas individuals with complex partial seizures do not.
Factitious disorder and malingering. Individuals who feign dissociative identity disor-
der do not report the subtle symptoms of intrusion characteristic of the disorder; instead
they tend to overreport well-publicized symptoms of the disorder, such as dissociative
amnesia, while underreporting less-publicized comorbid symptoms, such as depression.
Individuals who feign dissociative identity disorder tend to be relatively undisturbed by
or may even seem to enjoy “having” the disorder. In contrast, individuals with genuine
dissociative identity disorder tend to be ashamed of and overwhelmed by their symptoms
and to underreport their symptoms or deny their condition. Sequential observation, cor-
roborating history, and intensive psychometric and psychological assessment may be
helpful in assessment.
Individuals who malinger dissociative identity disorder usually create limited, stereo-
typed alternate identities, with feigned amnesia, related to the events for which gain is
sought. For example, they may present an “all-good” identity and an “all-bad” identity in
hopes of gaining exculpation for a crime.
Comorbidity
Many individuals with dissociative identity disorder present with a comorbid disorder. If
not assessed and treated specifically for the dissociative disorder, these individuals often
receive prolonged treatment for the comorbid diagnosis only, with limited overall treat-
ment response and resultant demoralization, and disability.
298 Dissociative Disorders
Individuals with dissociative identity disorder usually exhibit a large number of co-
morbid disorders. In particular, most develop PTSD. Other disorders that are highly co-
morbid with dissociative identity disorder include depressive disorders, trauma- and
stressor-related disorders, personality disorders (especially avoidant and borderline per-
sonality disorders), conversion disorder (functional neurological symptom disorder),
somatic symptom disorder, eating disorders, substance-related disorders, obsessive-
compulsive disorder, and sleep disorders. Dissociative alterations in identity, memory,
and consciousness may affect the symptom presentation of comorbid disorders.
Dissociative Amnesia
Diagnostic Criteria 300.12 (F44.0)
A. An inability to recall important autobiographical information, usually of a traumatic or
stressful nature, that is inconsistent with ordinary forgetting.
Note: Dissociative amnesia most often consists of localized or selective amnesia for a
specific event or events; or generalized amnesia for identity and life history.
B. The symptoms cause clinicafly significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
C. The disturbance is not attributable to the physiological effects of a substance (e.g., al-
cohol or other drug of abuse, a medication) or a neurological or other medical condition
(e.g., partial complex seizures, transient global amnesia, sequelae of a closed head in-
jury/traumatic brain injury, other neurological condition).
D. The disturbance is not better explained by dissociative identity disorder, posttraumatic
stress disorder, acute stress disorder, somatic symptom disorder, or major or mild neu-
rocognitive disorder.
Coding note: The code for dissociative amnesia without dissociative fugue is 300.12
(F44.0). The code for dissociative amnesia with dissociative fugue is 300.13 (F44.1).
Specify if:
300.13 (F44.1) With dissociative fugue: Apparently purposeful travel or bewildered
wandering that is associated with amnesia for identity or for other important autobio-
graphical information.
Diagnostic Features
The defining characteristic of dissociative amnesia is an inability to recall important auto-
biographical information that 1) should be successfully stored in memory and 2) ordinar-
ily would be readily remembered (Criterion A). Dissociative amnesia differs from the
permanent amnesias due to neurobiological damage or toxicity that prevent memory stor-
age or retrieval in that it is always potentially reversible because the memory has been suc-
cessfully stored.
Localized amnesia, a failure to recall events during a circumscribed period of time, is the
most common form of dissociative amnesia. Localized amnesia may be broader than am-
nesia for a single traumatic event (e.g., months or years associated with child abuse or in-
tense combat). In selective amnesia, the individual can recall some, but not all, of the events
during a circumscribed period of time. Thus, the individual may remember part of a trau-
matic event but not other parts. Some individuals report both localized and selective am-
nesias.
Generalized amnesia, a complete loss of memory for one’s life history, is rare. Individuals
with generalized amnesia may forget personal identity. Some lose previous knowledge
about the world (i.e., semantic knowledge) and can no longer access well-learned skills
Dissociative Amnesia 299
(i-e., procedural knowledge). Generalized amnesia has an acute onset; the perplexity, dis-
orientation, and purposeless wandering of individuals with generalized amnesia usually
bring them to the attention of the police or psychiatric emergency services. Generalized
amnesia may be more common among combat veterans, sexual assault victims, and indi-
viduals experiencing extreme emotional stress or conflict.
Individuals with dissociative amnesia are frequently unaware (or only partially aware)
of their memory problems. Many, especially those with localized amnesia, minimize the
importance of their memory loss and may become uncomfortable when prompted to ad-
dress it. In systematized amnesia, the individual loses memory for a specific category of in-
formation (e.g., all memories relating to one’s family, a particular person, or childhood
sexual abuse). In continuous amnesia, an individual forgets each new event as it occurs.
Associated Features Supporting Diagnosis
Many individuals with dissociative amnesia are chronically impaired in their ability to
form and sustain satisfactory relationships. Histories of trauma, child abuse, and victim-
ization are common. Some individuals with dissociative amnesia report dissociative flash-
backs (i.e., behavioral reexperiencing of traumatic events). Many have a history of self-
mutilation, suicide attempts, and other high-risk behaviors. Depressive and functional
neurological symptoms are common, as are depersonalization, auto-hypnotic symptoms,
and high hypnotizability. Sexual dysfunctions are common. Mild traumatic brain injury
may precede dissociative amnesia.
Prevalence
The 12-month prevalence for dissociative amnesia among adults in a small U.S. commu-
nity study was 1.8% (1.0% for males; 2.6% for females).
Development and Course
Onset of generalized amnesia is usually sudden. Less is known about the onset of localized
and selective amnesias because these amnesias are seldom evident, even to the individual.
Although overwhelming or intolerable events typically precede localized amnesia, its on-
set may be delayed for hours, days, or longer.
Individuals may report multiple episodes of dissociative amnesia. A single episode
may predispose to future episodes. In between episodes of amnesia, the individual may or
may not appear to be acutely symptomatic. The duration of the forgotten events can range
from minutes to decades. Some episodes of dissociative amnesia resolve rapidly (e.g.,
when the person is removed from combat or some other stressful situation), whereas other
episodes persist for long periods of time. Some individuals may gradually recall the dis-
sociated memories years later. Dissociative capacities may decline with age, but not al-
ways. As the amnesia remits, there may be considerable distress, suicidal behavior, and
symptoms of posttraumatic stress disorder (PTSD).
Dissociative amnesia has been observed in young children, adolescents, and adults.
Children may be the most difficult to evaluate because they often have difficulty under-
standing questions about amnesia, and interviewers may find it difficult to formulate child-
friendly questions about memory and amnesia. Observations of apparent dissociative am-
nesia are often difficult to differentiate from inattention, absorption, anxiety, oppositional
behavior, and learning disorders. Reports from several different sources (e.g., teacher,
therapist, case worker) may be needed to diagnose amnesia in children.
Risk and Prognostic Factors
Environmental. Single or repeated traumatic experiences (e.g., war, childhood maitreat-
ment, natural disaster, internment in concentration camps, genocide) are common ante-
300 Dissociative Disorders
cedents. Dissociative amnesia is more likely to occur with 1) a greater number of adverse
childhood experiences, particularly physical and/or sexual abuse, 2) interpersonal vio-
lence; and 3) increased severity, frequency, and violence of the trauma.
Genetic and physiological. There are no genetic studies of dissociative amnesia. Stud-
ies of dissociation report significant genetic and environmental factors in both clinical and
nonclinical samples.
Course modifiers. Removal from the traumatic circumstances underlying the dissociative
amnesia (e.g., combat) may bring about a rapid return of memory. The memory loss of indi-
viduals with dissociative fugue may be particularly refractory. Onset of PTSD symptoms may
decrease localized, selective, or systematized amnesia. The retuwming memory, however, may
be experienced as flashbacks that alternate with amnesia for the content of the flashbacks.
Culture-Related Diagnostic Issues
In Asia, the Middle East, and Latin America, non-epileptic seizures and other functional
neurological symptoms may accompany dissociative amnesia. In cultures with highly re-
strictive social traditions, the precipitants of dissociative amnesia often do not involve
frank trauma. Instead, the amnesia is preceded by severe psychological stresses or con-
flicts (e.g., marital conflict, other family disturbances, attachment problems, conflicts due
to restriction or oppression).
Suicide Risk
Suicidal and other self-destructive behaviors are common in individuals with dissociative
amnesia. Suicidal behavior may be a particular risk when the amnesia remits suddenly
and overwhelms the individual with intolerable memories.
Functional Consequences of Dissociative Amnesia
The impairment of individuals with localized, selective, or systematized dissociative am-
nesia ranges from limited to severe. Individuals with chronic generalized dissociative am-
nesia usually have impairment in all aspects of functioning. Even when these individuals
“re-learn” aspects of their life history, autobiographical memory remains very impaired.
Most become vocationally and interpersonally disabled.
Differential Diagnosis
Dissociative identity disorder. Individuals with dissociative amnesia may report de-
personalization and auto-hypnotic symptoms. Individuals with dissociative identity dis-
order report pervasive discontinuities in sense of self and agency, accompanied by many
other dissociative symptoms. The amnesias of individuals with localized, selective, and/
or systematized dissociative amnesias are relatively stable. Amnesias in dissociative iden-
tity disorder include amnesia for everyday events, finding of unexplained possessions,
sudden fluctuations in skills and knowledge, major gaps in recall of life history, and brief
amnesic gaps in interpersonal interactions.
Posttraumatic stress disorder. Some individuals with PTSD cannot recall part or all of
a specific traumatic event (e.g., a rape victim with depersonalization and/or derealization
symptoms who cannot recall most events for the entire day of the rape). When that amne-
sia extends beyond the immediate time of the trauma, a comorbid diagnosis of dissociative
amnesia is warranted.
Neurocognitive disorders. In neurocognitive disorders, memory loss for personal infor-
mation is usually embedded in cognitive, linguistic, affective, attentional, and behavioral
Dissociative Amnesia 301
disturbances. In dissociative amnesia, memory deficits are primarily for autobiographical
information; intellectual and cognitive abilities are preserved.
Substance-related disorders. In the context of repeated intoxication with alcohol or
other substances / medications, there may be episodes of “black outs” or periods for which the
individual has no memory. To aid in distinguishing these episodes from dissociative am-
nesia, a longitudinal history noting that the amnestic episodes occur only in the context of
intoxication and do not occur in other situations would help identify the source as sub-
stance-induced; however the distinction may be difficult when the individual with dis-
sociative amnesia may also misuse alcohol or other substances in the context of stressful
situations that may also exacerbate dissociative symptoms. Some individuals with comor-
bid dissociative amnesia and substance use disorders will attribute their memory prob-
lems solely to the substance use. Prolonged use of alcohol or other substances may result in
a substance-induced neurocognitive disorder that may be associated with impaired cog-
nitive function, but in this context the protracted history of substance use and the persis-
tent deficits associated with the neurocognitive disorder would serve to distinguish it
from dissociative amnesia, where there is typically no evidence of persistent impairment in
intellectual functioning.
Posttraumatic amnesia due to brain injury. Amnesia may occur in the context of a trau-
matic brain injury (TBI) when there has been an impact to the head or other mechanisms of
rapid movement or displacement of the brain within the skull TBI. Other characteristics of
TBI include loss of consciousness, disorientation and confusion, or, in more severe cases,
neurological signs (e.g., abnormalities on neuroimaging, a new onset of seizures or a marked
worsening of a preexisting seizure disorder, visual field cuts, anosmia). A neurocognitive
disorder attributable to TBI must present either immediately after brain injury occurs or im-
mediately after the individual recovers consciousness after the injury, and persist past the
acute post-injury period. The cognitive presentation of a neurocognitive disorder following
TBI is variable and includes difficulties in the domains of complex attention, executive func-
tion, learning and memory as well as slowed speed of information processing and distur-
bances in social cognition. These additional features help distinguish it from dissociative
amnesia.
Seizure disorders. Individuals with seizure disorders may exhibit complex behavior dur-
ing seizures or post-ictally with subsequent amnesia. Some individuals with a seizure disorder
engage in nonpurposive wandering that is limited to the period of seizure activity. Con-
versely, behavior during a dissociative fugue is usually purposeful, complex, and goal-
directed and may last for days, weeks, or longer. Occasionally, individuals with a seizure dis-
order will report that earlier autobiographical memories have been “wiped out” as the seizure
disorder progresses. Such memory loss is not associated with traumatic circumstances and ap-
pears to occur randomly. Serial electroencephalograms usually show abnormalities. Telemet-
ric electroencephalographic monitoring usually shows an association between the episodes of
amnesia and seizure activity. Dissociative and epileptic amnesias may coexist.
Catatonic stupor. Mutism in catatonic stupor may suggest dissociative amnesia, but fail-
ure of recall is absent. Other catatonic symptoms (e.g., rigidity, posturing, negativism) are
usually present.
Factitious disorder and malingering. There is no test, battery of tests, or set of procedures
that invariably distinguishes dissociative amnesia from feigned amnesia. Individuals with
factitious disorder or malingering have been noted to continue their deception even during
hypnotic or barbiturate-facilitated interviews. Feigned amnesia is more common in individ-
uals with 1) acute, florid dissociative amnesia; 2) financial, sexual, or legal problems; or 3) a
wish to escape stressful circumstances. True amnesia can be associated with those same cir-
cumstances. Many individuals who malinger confess spontaneously or when confronted.
302 Dissociative Disorders
Normal and age-related changes in memory. Memory decrements in major and mild
neurocognitive disorders differ from those of dissociative amnesia, which are usually as-
sociated with stressful events and are more specific, extensive, and/or complex.
Comorbidity
As dissociative amnesia begins to remit, a wide variety of affective phenomena may sur-
face: dysphoria, grief, rage, shame, guilt, psychological conflict and turmoil, and suicidal
and homicidal ideation, impulses, and acts. These individuals may have symptoms that
then meet diagnostic criteria for persistent depressive disorder (dysthymia); major de-
pressive disorder; other specified or unspecified depressive disorder; adjustment disor-
der, with depressed mood; or adjustment disorder, with mixed disturbance of emotions
and conduct. Many individuals with dissociative amnesia develop PTSD at some point
during their life, especially when the traumatic antecedents of their amnesia are brought
into conscious awareness.
Many individuals with dissociative amnesia have symptoms that meet diagnostic cri-
teria for a comorbid somatic symptom or related disorder (and vice versa), including so-
matic symptom disorder and conversion disorder (functional neurological symptom
disorder). Many individuals with dissociative amnesia have symptoms that meet diagnos-
tic criteria for a personality disorder, especially dependent, avoidant, and borderline.
Depersonalization/Derealization Disorder
Diagnostic Criteria 300.6 (F48.1)
A. The presence of persistent or recurrent experiences of depersonalization, derealiza-
tion, or both:
1. Depersonalization: Experiences of unreality, detachment, or being an outside ob-
server with respect to one’s thoughts, feelings, sensations, body, or actions (e.g.,
perceptual alterations, distorted sense of time, unreal or absent self, emotional and/
or physical numbing).
2. Derealization: Experiences of unreality or detachment with respect to surround-
ings (e.g., individuals or objects are experienced as unreal, dreamlike, foggy, life-
less, or visually distorted).
B. During the depersonalization or derealization experiences, reality testing remains intact.
C. The symptoms cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
D. The disturbance is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, medication) or another medical condition (e.g., seizures).
E. The disturbance is not better explained by another mental disorder, such as schizo-
phrenia, panic disorder, major depressive disorder, acute stress disorder, posttrau-
matic stress disorder, or another dissociative disorder.
Diagnostic Features
The essential features of depersonalization /derealization disorder are persistent or recur-
rent episodes of depersonalization, derealization, or both. Episodes of depersonalization
are characterized by a feeling of unreality or detachment from, or unfamiliarity with, one’s
whole self or from aspects of the self (Criterion Al). The individual may feel detached
from his or her entire being (e.g., “I am no one,” “I have no self”). He or she may also feel
subjectively detached from aspects of the self, including feelings (e.g., hypoemotionality:
Depersonalization/Derealization Disorder 303
“I know I have feelings but I don’t feel them”), thoughts (e.g., “My thoughts don’t feel like
my own,” “head filled with cotton”), whole body or body parts, or sensations (e.g., touch,
proprioception, hunger, thirst, libido). There may also be a diminished sense of agency
(e.g., feeling robotic, like an automaton; lacking control of one’s speech or movements).
The depersonalization experience can sometimes be one of a split self, with one part ob-
serving and one participating, known as an “out-of-body experience” in its most extreme
form. The unitary symptom of “depersonalization” consists of several symptom factors:
anomalous body experiences (i.e., unreality of the self and perceptual alterations); emo-
tional or physical numbing; and temporal distortions with anomalous subjective recall.
Episodes of derealization are characterized by a feeling of unreality or detachment
from, or unfamiliarity with, the world, be it individuals, inanimate objects, or all surround-
ings (Criterion A2). The individual may feel as if he or she were in a fog, dream, or bubble, or
as if there were a veil or a glass wall between the individual and world around. Surround-
ings may be experienced as artificial, colorless, or lifeless. Derealization is commonly ac-
companied by subjective visual distortions, such as blurriness, heightened acuity, widened
or narrowed visual field, two-dimensionality or flatness, exaggerated three-dimensional-
ity, or altered distance or size of objects (i.e., macropsia or micropsia). Auditory distortions
can also occur, whereby voices or sounds are muted or heightened. In addition, Criterion
C requires the presence of clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning, and Criteria D and E describe exclusionary
diagnoses.
Associated Features Supporting Diagnosis
Individuals with depersonalization/derealization disorder may have difficulty describ-
ing their symptoms and may think they are “crazy” or “going crazy”. Another common
experience is the fear of irreversible brain damage. A commonly associated symptom is a
subjectively altered sense of time (i-e., too fast or too slow), as well as a subjective difficulty
in vividly recalling past memories and owning them as personal and emotional. Vague so-
matic symptoms, such as head fullness, tingling, or lightheadedness, are not uncommon.
Individuals may suffer extreme rumination or obsessional preoccupation (e.g., constantly
obsessing about whether they really exist, or checking their perceptions to determine
whether they appear real). Varying degrees of anxiety and depression are also common as-
sociated features. Individuals with the disorder have been found to have physiological
hyporeactivity to emotional stimuli. Neural substrates of interest include the hypotha-
lamic-pituitary-adrenocortical axis, inferior parietal lobule, and prefrontal cortical-limbic
circuits.
Prevalence
Transient depersonalization/derealization symptoms lasting hours to days are common
in the general population. The 12-month prevalence of depersonalization/derealization
disorder is thought to be markedly less than for transient symptoms, although precise es-
timates for the disorder are unavailable. In general, approximately one-half of all adults
have experienced at least one lifetime episode of depersonalization/derealization. How-
ever, symptomatology that meets full criteria for depersonalization/derealization disor-
der is markedly less common than transient symptoms. Lifetime prevalence in U.S. and
non-U.S. countries is approximately 2% (range of 0.8% to 2.8%). The gender ratio for the
disorder is 1:1.
Development and Course
The mean age at onset of depersonalization/derealization disorder is 16 years, although the
disorder can start in early or middle childhood; a minority cannot recall ever not having had
304 Dissociative Disorders
the symptoms. Less than 20% of individuals experience onset after age 20 years and only
5% after age 25 years. Onset in the fourth decade of life or later is highly unusual. Onset can
range from extremely sudden to gradual. Duration of depersonalization/derealization
disorder episodes can vary greatly, from brief (hours or days) to prolonged (weeks,
months, or years). Given the rarity of disorder onset after age 40 years, in such cases the in-
dividual should be examined more closely for underlying medical conditions (e.g., brain
lesions, seizure disorders, sleep apnea). The course of the disorder is often persistent.
About one-third of cases involve discrete episodes; another third, continuous symptoms
from the start; and still another third, an initially episodic course that eventually becomes
continuous.
While in some individuals the intensity of symptoms can wax and wane considerably,
others report an unwavering level of intensity that in extreme cases can be constantly pres-
ent for years or decades. Internal and external factors that affect symptom intensity vary
between individuals, yet some typical patterns are reported. Exacerbations can be trig-
gered by stress, worsening mood or anxiety symptoms, novel or overstimulating settings,
and physical factors such as lighting or lack of sleep.
Risk and Prognostic Factors
Temperamental. Individuals with depersonalization /derealization disorder are charac-
terized by harm-avoidant temperament, immature defenses, and both disconnection and
overconnection schemata. Immature defenses such as idealization/ devaluation, projec-
tion and acting out result in denial of reality and poor adaptation. Cognitive disconnection
schemata reflect defectiveness and emotional inhibition and subsume themes of abuse, ne-
glect, and deprivation. Overconnection schemata involve impaired autonomy with themes
of dependency, vulnerability, and incompetence.
Environmental. There is a clear association between the disorder and childhood interper-
sonal traumas in a substantial portion of individuals, although this association is not as prev-
alent or as extreme in the nature of the traumas as in other dissociative disorders, such as
dissociative identity disorder. In particular, emotional abuse and emotional neglect have been
most strongly and consistently associated with the disorder. Other stressors can include phys-
ical abuse; witnessing domestic violence; growing up with a seriously impaired, mentally ill
parent; or unexpected death or suicide of a family member or close friend. Sexual abuse is a
much less common antecedent but can be encountered. The most common proximal precipi-
tants of the disorder are severe stress (interpersonal, financial, occupational), depression, anx-
iety (particularly panic attacks), and illicit drug use. Symptoms may be specifically induced by
substances such as tetrahydrocannabinol, hallucinogens, ketamine, MDMA (3,4-methylene-
dioxymethamphetamine; “ecstasy”) and salvia. Marijuana use may precipitate new-onset
panic attacks and depersonalization/derealization symptoms simultaneously.
Culture-Related Diagnostic Issues
Volitionally induced experiences of depersonalization/derealization can be a part of med-
itative practices that are prevalent in many religions and cultures and should not be diag-
nosed as a disorder. However, there are individuals who initially induce these states
intentionally but over time lose control over them and may develop a fear and aversion for
related practices.
Functionai Consequences of
Depersonaiization/Dereallzation Disorder
Symptoms of depersonalization/derealization disorder are highly distressing and are as-
sociated with major morbidity. The affectively flattened and robotic demeanor that these
Depersonalization/Derealization Disorder 305
individuals often demonstrate may appear incongruent with the extreme emotional pain
reported by those with the disorder. Impairment is often experienced in both interpersonal
and occupational spheres, largely due to the hypoemotionality with others, subjective diffi-
culty in focusing and retaining information, and a general sense of disconnectedness from
life.
Differential Diagnosis
Illness anxiety disorder. Although individuals with depersonalization/derealization dis-
order can present with vague somatic complaints as well as fears of permanent brain dam-
age, the diagnosis of depersonalization/derealization disorder is characterized by the
presence of a constellation of typical depersonalization/derealization symptoms and the ab-
sence of other manifestations of illness anxiety disorder.
Major depressive disorder. Feelings of numbness, deadness, apathy, and being ina
dream are not uncommon in major depressive episodes. However, in depersonalization/
derealization disorder, such symptoms are associated with further symptoms of the dis-
order. If the depersonalization/derealization clearly precedes the onset of a major depres-
sive episode or clearly continues after its resolution, the diagnosis of depersonalization/
derealization disorder applies.
Obsessive-compulsive disorder. Some individuals with depersonalization/dereal-
ization disorder can become obsessively preoccupied with their subjective experience or
develop rituals checking on the status of their symptoms. However, other symptoms of
obsessive-compulsive disorder unrelated to depersonalization/derealization are not
present.
Other dissociative disorders. In order to diagnose depersonalization/derealization
disorder, the symptoms should not occur in the context of another dissociative disorder,
such as dissociative identity disorder. Differentiation from dissociative amnesia and con-
version disorder (functional neurological symptom disorder) is simpler, as the symptoms
of these disorders do not overlap with those of depersonalization/derealization disorder.
Anxiety disorders. Depersonalization/derealization is one of the symptoms of panic at-
tacks, increasingly common as panic attack severity increases. Therefore, depersonal-
ization/derealization disorder should not be diagnosed when the symptoms occur only
during panic attacks that are part of panic disorder, social anxiety disorder, or specific
phobia. In addition, it is not uncommon for depersonalization/derealization symptoms
to first begin in the context of new-onset panic attacks or as panic disorder progresses and
worsens. In such presentations, the diagnosis of depersonalization/derealization disorder
can be made if 1) the depersonalization/derealization component of the presentation is
very prominent from the start, clearly exceeding in duration and intensity the occurrence
of actual panic attacks; or 2) the depersonalization/derealization continues after panic dis-
order has remitted or has been successfully treated.
Psychotic disorders. The presence of intact reality testing specifically regarding the
depersonalization/derealization symptoms is essential to differentiating depersonal-
ization/derealization disorder from psychotic disorders. Rarely, positive-symptom
schizophrenia can pose a diagnostic challenge when nihilistic delusions are present. For
example, an individual may complain that he or she is dead or the world is not real; this
could be either a subjective experience that the individual knows is not true or a delusional
conviction.
Substance/medication-induced disorders. Depersonalization/derealization associated
with the physiological effects of substances during acute intoxication or withdrawal is not
diagnosed as depersonalization/derealization disorder. The most common precipitating
substances are the illicit drugs marijuana, hallucinogens, ketamine, ecstasy, and salvia. In
306 Dissociative Disorders
about 15% of all cases of depersonalization/derealization disorder, the symptoms are pre-
cipitated by ingestion of such substances. If the symptoms persist for some time in the ab-
sence of any further substance or medication use, the diagnosis of depersonalization/
derealization disorder applies. This diagnosis is usually easy to establish since the vast ma-
jority of individuals with this presentation become highly phobic and aversive to the trig-
gering substance and do not use it again.
Mental disorders due to another medical condition. Features such as onset after age
40 years or the presence of atypical symptoms and course in any individual suggest the
possibility of an underlying medical condition. In such cases, it is essential to conduct a
thorough medical and neurological evaluation, which may include standard laboratory
studies, viral titers, an electroencephalogram, vestibular testing, visual testing, sleep stud-
ies, and/or brain imaging. When the suspicion of an underlying seizure disorder proves
difficult to confirm, an ambulatory electroencephalogram may be indicated; although
temporal lobe epilepsy is most commonly implicated, parietal and frontal lobe epilepsy
may also be associated.
Comorbidity
In a convenience sample of adults recruited for a number of depersonalization research
studies, lifetime comorbidities were high for unipolar depressive disorder and for any
anxiety disorder, with a significant proportion of the sample having both disorders. Comor-
bidity with posttraumatic stress disorder was low. The three most commonly co-occurring
personality disorders were avoidant, borderline, and obsessive-compulsive.
Other Specified Dissociative Disorder
300.15 (F44.89)
This category applies to presentations in which symptoms characteristic of a dissociative
disorder that cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning predominate but do not meet the full criteria for any of
the disorders in the dissociative disorders diagnostic class. The other specified dissocia-
tive disorder category is used in situations in which the clinician chooses to communicate
the specific reason that the presentation does not meet the criteria for any specific disso-
ciative disorder. This is done by recording “other specified dissociative disorder’ followed
by the specific reason (e.g., “dissociative trance”).
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Chronic and recurrent syndromes of mixed dissociative symptoms: This cate-
gory includes identity disturbance associated with less-than-marked discontinuities in
sense of self and agency, or alterations of identity or episodes of possession in an in-
dividual who reports no dissociative amnesia.
2. Identity disturbance due to proionged and intense coercive persuasion: Individ-
uals who have been subjected to intense coercive persuasion (e.g., brainwashing,
thought reform, indoctrination while captive, torture, long-term political imprisonment,
recruitment by sects/cults or by terror organizations) may present with prolonged
changes in, or conscious questioning of, their identity.
3. Acute dissociative reactions to stressfui events: This category is for acute, tran-
sient conditions that typically last less than 1 month, and sometimes only a few hours
or days. These conditions are characterized by constriction of consciousness; deper-
sonalization; derealization; perceptual disturbances (e.g., time slowing, macropsia);
Unspecified Dissociative Disorder 307
micro-amnesias; transient stupor; and/or alterations in sensory-motor functioning (e.g.,
analgesia, paralysis).
4. Dissociative trance: This condition is characterized by an acute narrowing or com-
plete loss of awareness of immediate surroundings that manifests as profound unre-
sponsiveness or insensitivity to environmental stimuli. The unresponsiveness may be
accompanied by minor stereotyped behaviors (e.g., finger movements) of which the in-
dividual is unaware and/or that he or she cannot control, as well as transient paralysis
or loss of consciousness. The dissociative trance is not a normal part of a broadly ac-
cepted collective cultural or religious practice.
Unspecified Dissociative Disorder
300.15 (F44.9)
This category applies to presentations in which symptoms characteristic of a dissociative
disorder that cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning predominate but do not meet the full criteria for any of
the disorders in the dissociative disorders diagnostic class. The unspecified dissociative
disorder category is used in situations in which the clinician chooses not to specify the rea-
son that the criteria are not met for a specific dissociative disorder, and includes presen-
tations for which there is insufficient information to make a more specific diagnosis (e.g.,
in emergency room settings).
Somatic symptom disorder and other disorders with prominent somatic symp-
toms constitute a new category in DSM-5 called somatic symptom and related disorders. This
chapter includes the diagnoses of somatic symptom disorder, illness anxiety disorder, con-
version disorder (functional neurological symptom disorder), psychological factors affect-
ing other medical conditions, factitious disorder, other specified somatic symptom and
related disorder, and unspecified somatic symptom and related disorder. All of the disor-
ders in this chapter share a common feature: the prominence of somatic symptoms associ-
ated with significant distress and impairment. Individuals with disorders with prominent
somatic symptoms are commonly encountered in primary care and other medical settings
but are less commonly encountered in psychiatric and other mental health settings. These
reconceptualized diagnoses, based on a reorganization of DSM-IV somatoform disorder di-
agnoses, are more useful for primary care and other medical (nonpsychiatric) clinicians.
The major diagnosis in this diagnostic class, somatic symptom disorder, emphasizes
diagnosis made on the basis of positive symptoms and signs (distressing somatic symp-
toms plus abnormal thoughts, feelings, and behaviors in response to these symptoms)
rather than the absence of a medical explanation for somatic symptoms. A distinctive char-
acteristic of many individuals with somatic symptom disorder is not the somatic symp-
toms per se, but instead the way they present and interpret them. Incorporating affective,
cognitive, and behavioral components into the criteria for somatic symptom disorder pro-
vides a more comprehensive and accurate reflection of the true clinical picture than can be
achieved by assessing the somatic complaints alone.
The principles behind the changes in the somatic symptom and related diagnoses from
DSM-IV are crucial in understanding the DSM-5 diagnoses. The DSM-IV term somatoform
disorders was confusing and is replaced by somatic symptom and related disorders. In DSM-IV
there was a great deal of overlap across the somatoform disorders and a lack of clarity
about the boundaries of diagnoses. Although individuals with these disorders primarily
present in medical rather than mental health settings, nonpsychiatric physicians found the
DSM-IV somatoform diagnoses difficult to understand and use. The current DSM-5 clas-
sification recognizes this overlap by reducing the total number of disorders as well as their
subcategories.
The previous criteria overemphasized the centrality of medically unexplained symptoms.
Such symptoms are present to various degrees, particularly in conversion disorder, but so-
matic symptom disorders can also accompany diagnosed medical disorders. The reli-
ability of determining that a somatic symptom is medically unexplained is limited, and
grounding a diagnosis on the absence of an explanation is problematic and reinforces
mind-body dualism. It is not appropriate to give an individual a mental disorder diagnosis
solely because a medical cause cannot be demonstrated. Furthermore, the presence of a
medical diagnosis does not exclude the possibility of a comorbid mental disorder, includ-
ing a somatic symptom and related disorder. Perhaps because of the predominant focus
on lack of medical explanation, individuals regarded these diagnoses as pejorative and de-
meaning, implying that their physical symptoms were not “real.” The new classification
defines the major diagnosis, somatic symptom disorder, on the basis of positive symptoms
(distressing somatic symptoms plus abnormal thoughts, feelings, and behaviors in response
309
310 Somatic Symptom and Related Disorders
to these symptoms). However, medically unexplained symptoms remain a key feature in
conversion disorder and pseudocyesis (other specified somatic symptom and related dis-
order) because it is possible to demonstrate definitively in such disorders that the symp-
toms are not consistent with medical pathophysiology.
It is important to note that some other mental disorders may initially manifest with pri-
marily somatic symptoms (e.g., major depressive disorder, panic disorder). Such diagno-
ses may account for the somatic symptoms, or they may occur alongside one of the somatic
symptom and related disorders in this chapter. There is also considerable medical comor-
bidity among somatizing individuals. Although somatic symptoms are frequently associ-
ated with psychological distress and psychopathology, some somatic symptom and
related disorders can arise spontaneously, and their causes can remain obscure. Anxiety
disorders and depressive disorders may accompany somatic symptom and related disor-
ders. The somatic component adds severity and complexity to depressive and anxiety dis-
orders and results in higher severity, functional impairment, and even refractoriness to
traditional treatments. In rare instances, the degree of preoccupation may be so severe as
to warrant consideration of a delusional disorder diagnosis.
A number of factors may contribute to somatic symptom and related disorders. These
include genetic and biological vulnerability (e.g., increased sensitivity to pain), early trau-
matic experiences (e.g., violence, abuse, deprivation), and learning (e.g., attention ob-
tained from illness, lack of reinforcement of nonsomatic expressions of distress), as well as
cultural/social norms that devalue and stigmatize psychological suffering as compared
with physical suffering. Differences in medical care across cultures affect the presentation,
recognition, and management of these somatic presentations. Variations in symptom pre-
sentation are likely the result of the interaction of multiple factors within cultural con-
texts that affect how individuals identify and classify bodily sensations, perceive illness,
and seek medical attention for them. Thus, somatic presentations can be viewed as expres-
sions of personal suffering inserted in a cultural and social context.
All of these disorders are characterized by the prominent focus on somatic concerns
and their initial presentation mainly in medical rather than mental health care settings. So-
matic symptom disorder offers a more clinically useful method of characterizing individ-
uals who may have been considered in the past for a diagnosis of somatization disorder.
Furthermore, approximately 75% of individuals previously diagnosed with hypochon-
driasis are subsumed under the diagnosis of somatic symptom disorder. However, about
25% of individuals with hypochondriasis have high health anxiety in the absence of so-
matic symptoms, and many such individuals’ symptoms would not qualify for an anxiety
disorder diagnosis. The DSM-5 diagnosis of illness anxiety disorder is for this latter group
of individuals. Illness anxiety disorder can be considered either in this diagnostic section
or as an anxiety disorder. Because of the strong focus on somatic concerns, and because ill-
ness anxiety disorder is most often encountered in medical settings, for utility it is listed
with the somatic symptom and related disorders. In conversion disorder, the essential fea-
ture is neurological symptoms that are found, after appropriate neurological assessment,
to be incompatible with neurological pathophysiology. Psychological factors affecting
other medical conditions is also included in this chapter. Its essential feature is the pres-
ence of one or more clinically significant psychological or behavioral factors that adversely
affect a medical condition by increasing the risk for suffering, death, or disability. Like the
other somatic symptom and related disorders, factitious disorder embodies persistent
problems related to illness perception and identity. In the great majority of reported cases
of factitious disorder, both imposed on self and imposed on another, individuals present
with somatic symptoms and medical disease conviction. Consequently, DSM-5 factitious
disorder is included among the somatic symptom and related disorders. Other specified
somatic symptom and related disorder and unspecified somatic symptom and related dis-
order include conditions for which some, but not all, of the criteria for somatic symptom
disorder or illness anxiety disorder are met, as well as pseudocyesis.
Somatic Symptom Disorder 311
Somatic Symptom Disorder
Diagnostic Criteria 300.82 (F45.1)
A. One or more somatic symptoms that are distressing or result in significant disruption
of daily life.
B. Excessive thoughts, feelings, or behaviors related to the somatic symptoms or associ-
ated health concerns as manifested by at least one of the following:
1. Disproportionate and persistent thoughts about the seriousness of one’s symptoms.
2. Persistently high level of anxiety about health or symptoms.
3. Excessive time and energy devoted to these symptoms or health concerns.
C. Although any one somatic symptom may not be continuously present, the state of be-
ing symptomatic is persistent (typically more than 6 months).
Specify if:
With predominant pain (previously pain disorder): This specifier is for individuals
whose somatic symptoms predominantly involve pain.
Specify if:
Persistent: A persistent course is characterized by severe symptoms, marked impair-
ment, and long duration (more than 6 months).
Specify current severity:
Mild: Only one of the symptoms specified in Criterion B is fulfilled.
Moderate: Two or more of the symptoms specified in Criterion B are fulfilled.
Severe: Two or more of the symptoms specified in Criterion B are fulfilled, plus there
are multiple somatic complaints (or one very severe somatic symptom).
Diagnostic Features
Individuals with somatic symptom disorder typically have multiple, current, somatic symp-
toms that are distressing or result in significant disruption of daily life (Criterion A), al-
though sometimes only one severe symptom, most commonly pain, is present. Symptoms
may be specific (e.g., localized pain) or relatively nonspecific (e.g., fatigue). The symptoms
sometimes represent normal bodily sensations or discomfort that does not generally sig-
nify serious disease. Somatic symptoms without an evident medical explanation are not
sufficient to make this diagnosis. The individual’s suffering is authentic, whether or not it
is medically explained.
The symptoms may or may not be associated with another medical condition. The di-
agnoses of somatic symptom disorder and a concurrent medical illness are not mutually
exclusive, and these frequently occur together. For example, an individual may become se-
riously disabled by symptoms of somatic symptom disorder after an uncomplicated myo-
cardial infarction even if the myocardial infarction itself did not result in any disability. If
another medical condition or high risk for developing one is present (e.g., strong family
history), the thoughts, feelings, and behaviors associated with this condition are excessive
(Criterion B).
Individuals with somatic symptom disorder tend to have very high levels of worry
about illness (Criterion B). They appraise their bodily symptoms as unduly threatening,
harmful, or troublesome and often think the worst about their health. Even when there is
evidence to the contrary, some patients still fear the medical seriousness of their symp-
toms. In severe somatic symptom disorder, health concerns may assume a central role in
the individual’s life, becoming a feature of his or her identity and dominating interper-
sonal relationships.
312 Somatic Symptom and Related Disorders
Individuals typically experience distress that is principally focused on somatic symp-
toms and their significance. When asked directly about their distress, some individuals de-
scribe it in relation to other aspects of their lives, while others deny any source of distress
other than the somatic symptoms. Health-related quality of life is often impaired, both
physically and mentally. In severe somatic symptom disorder, the impairment is marked,
and when persistent, the disorder can lead to invalidism.
There is often a high level of medical care utilization, which rarely alleviates the individ-
ual’s concerns. Consequently, the patient may seek care from multiple doctors for the same
symptoms. These individuals often seem unresponsive to medical interventions, and new
interventions may only exacerbate the presenting symptoms. Some individuals with the dis-
order seem unusually sensitive to medication side effects. Some feel that their medical as-
sessment and treatment have been inadequate.
Assoclated Features Supporting Diagnosis
Cognitive features include attention focused on somatic symptoms, attribution of normal
bodily sensations to physical illness (possibly with catastrophic interpretations), worry
about illness, and fear that any physical activity may damage the body. The relevant as-
sociated behavioral features may include repeated bodily checking for abnormalities, re-
peated seeking of medical help and reassurance, and avoidance of physical activity. These
behavioral features are most pronounced in severe, persistent somatic symptom disorder.
These features are usually associated with frequent requests for medical help for different
somatic symptoms. This may lead to medical consultations in which individuals are so fo-
cused on their concerns about somatic symptom(s) that they cannot be redirected to other
matters. Any reassurance by the doctor that the symptoms are not indicative of serious
physical illness tends to be short-lived and/or is experienced by the individuals as the
doctor not taking their symptoms with due seriousness. As the focus on somatic symp-
toms is a primary feature of the disorder, individuals with somatic symptom disorder typ-
ically present to general medical health services rather than mental health services. The
suggestion of referral to a mental health specialist may be met with surprise or even frank
refusal by individuals with somatic symptom disorder.
Since somatic symptom disorder is associated with depressive disorders, there is an in-
creased suicide risk. It is not known whether somatic symptom disorder is associated with
suicide risk independent of its association with depressive disorders.
Prevalence
The prevalence of somatic symptom disorder is not known. However, the prevalence of
somatic symptom disorder is expected to be higher than that of the more restrictive DSM-
IV somatization disorder (<1%) but lower than that of undifferentiated somatoform dis-
order (approximately 19%). The prevalence of somatic symptom disorder in the general
adult population may be around 5%-7%. Females tend to report more somatic symptoms
than do males, and the prevalence of somatic symptom disorder is consequently likely to
be higher in females.
Development and Course
In older individuals, somatic symptoms and concurrent medical illnesses are common,
and a focus on Criterion B is crucial for making the diagnosis. Somatic symptom disorder
may be underdiagnosed in older adults either because certain somatic symptoms (e.g.,
pain, fatigue) are considered part of normal aging or because illness worry is considered
“understandable” in older adults who have more general medical illnesses and medica-
tions than do younger people. Concurrent depressive disorder is common in older people
who present with numerous somatic symptoms.
Somatic Symptom Disorder 313
In children, the most common symptoms are recurrent abdominal pain, headache, fa-
tigue, and nausea. A single prominent symptom is more common in children than in
adults. While young children may have somatic complaints, they rarely worry about “ill-
ness” per se prior to adolescence. The parents’ response to the symptom is important, as
this may determine the level of associated distress. It is the parent who may determine the
interpretation of symptoms and the associated time off school and medical help seeking.
Risk and Prognostic Factors
Temperamental. The personality trait of negative affectivity (neuroticism) has been identi-
fied as an independent correlate /risk factor of a high number of somatic symptoms. Comorbid
anxiety or depression is common and may exacerbate symptoms and impairment.
Environmental. Somaticsymptom disorder is more frequent in individuals with few years
of education and low socioeconomic status, and in those who have recently experienced
stressful life events.
Course modifiers. Persistent somatic symptoms are associated with demographic fea-
tures (female sex, older age, fewer years of education, lower socioeconomic status, un-
employment), a reported history of sexual abuse or other childhood adversity, concurrent
chronic physical illness or psychiatric disorder (depression, anxiety, persistent depressive
disorder [dysthymia], panic), social stress, and reinforcing social factors such as illness
benefits. Cognitive factors that affect clinical course include sensitization to pain, height-
ened attention to bodily sensations, and attribution of bodily symptoms to a possible med-
ical illness rather than recognizing them as a normal phenomenon or psychological stress.
Culture-Related Dlagnostic Issues
Somatic symptoms are prominent in various “culture-bound syndromes.” High numbers
of somatic symptoms are found in population-based and primary care studies around the
world, with a similar pattern of the most commonly reported somatic symptoms, impair-
ment, and treatment seeking. The relationship between number of somatic symptoms and
illness worry is similar in different cultures, and marked illness worry is associated with
impairment and greater treatment seeking across cultures. The relationship between nu-
merous somatic symptoms and depression appears to be very similar around the world
and between different cultures within one country.
Despite these similarities, there are differences in somatic symptoms among cultures
and ethnic groups. The description of somatic symptoms varies with linguistic and other
local cultural factors. These somatic presentations have been described as “idioms of dis-
tress” because somatic symptoms may have special meanings and shape patient-clinician
interactions in the particular cultural contexts. “Burnout,” the sensation of heaviness or
the complaints of “gas”; too much heat in the body; or burning in the head are examples of
symptoms that are common in some cultures or ethnic groups but rare in others. Explan-
atory models also vary, and somatic symptoms may be attributed variously to particular
family, work, or environmental stresses; general medical illness; the suppression of feel-
ings of anger and resentment; or certain culture-specific phenomena, such as semen loss.
There may also be differences in medical treatment seeking among cultural groups, in ad-
dition to differences due to variable access to medical care services. Seeking treatment for
multiple somatic symptoms in general medical clinics is a worldwide phenomenon and
occurs at similar rates among ethnic groups in the same country.
Functional Consequences of Somatic Symptom Disorder
The disorder is associated with marked impairment of health status. Many individuals
with severe somatic symptom disorder are likely to have impaired health status scores
more than 2 standard deviations below population norms.
314 Somatic Symptom and Related Disorders
Differential Diagnosis
If the somatic symptoms are consistent with another mental disorder (e.g., panic disorder),
and the diagnostic criteria for that disorder are fulfilled, then that mental disorder should
be considered as an alternative or additional diagnosis. A separate diagnosis of somatic
symptom disorder is not made if the somatic symptoms and related thoughts, feelings, or
behaviors occur only during major depressive episodes. If, as commonly occurs, the crite-
ria for both somatic symptom disorder and another mental disorder diagnosis are ful-
filled, then both should be coded, as both may require treatment.
Other medical conditions. The presence of somatic symptoms of unclear etiology is not
in itself sufficient to make the diagnosis of somatic symptom disorder. The symptoms of
many individuals with disorders like irritable bowel syndrome or fibromyalgia would not
satisfy the criterion necessary to diagnose somatic symptom disorder (Criterion B). Con-
versely, the presence of somatic symptoms of an established medical disorder (e.g., diabe-
tes or heart disease) does not exclude the diagnosis of somatic symptom disorder if the
criteria are otherwise met.
Panic disorder. In panic disorder, somatic symptoms and anxiety about health tend to
occur in acute episodes, whereas in somatic symptom disorder, anxiety and somatic symp-
toms are more persistent.
Generalized anxiety disorder. Individuals with generalized anxiety disorder worry about
multiple events, situations, or activities, only one of which may involve their health. The
main focus is not usually somatic symptoms or fear of illness as it is in somatic symptom
disorder.
Depressive disorders. Depressive disorders are commonly accompanied by somatic
symptoms. However, depressive disorders are differentiated from somatic symptom dis-
order by the core depressive symptoms of low (dysphoric) mood and anhedonia.
Illness anxiety disorder. If the individual has extensive worries about health but no or
minimal somatic symptoms, it may be more appropriate to consider illness anxiety disorder.
Conversion disorder (functional neurological symptom disorder). In conversion disor-
der, the presenting symptom is loss of function (e.g., of a limb), whereas in somatic symp-
tom disorder, the focus is on the distress that particular symptoms cause. The features
listed under Criterion B of somatic symptom disorder may be helpful in differentiating the
two disorders.
Delusional disorder. In somatic symptom disorder, the individual's beliefs that somatic
symptoms might reflect serious underlying physical illness are not held with delusional
intensity. Nonetheless, the individual's beliefs concerning the somatic symptoms can be
firmly held. In contrast, in delusional disorder, somatic subtype, the somatic symptom be-
liefs and behavior are stronger than those found in somatic symptom disorder.
Body dysmorphic disorder. In body dysmorphic disorder, the individual is excessively
concerned about, and preoccupied by, a perceived defect in his or her physical features. In
contrast, in somatic symptom disorder, the concern about somatic symptoms reflects fear
of underlying illness, not of a defect in appearance.
Obsessive-compulsive disorder. In somatic symptom disorder, the recurrent ideas about
somatic symptoms or illness are less intrusive, and individuals with this disorder do not
exhibit the associated repetitive behaviors aimed at reducing anxiety that occur in obses-
sive-compulsive disorder.
Comorbidity
Somatic symptom disorder is associated with high rates of comorbidity with medical dis-
orders as well as anxiety and depressive disorders. When a concurrent medical illness is
Illness Anxiety Disorder 315
present, the degree of impairment is more marked than would be expected from the phys-
ical illness alone. When an individual’s symptoms meet diagnostic criteria for somatic
symptom disorder, the disorder should be diagnosed; however, in view of the frequent co-
morbidity, especially with anxiety and depressive disorders, evidence for these concur-
rent diagnoses should be sought.
liliness Anxiety Disorder
Diagnostic Criteria 300.7 (F45.21)
A. Preoccupation with having or acquiring a serious illness.
B. Somatic symptoms are not present or, if present, are only mild in intensity. If another
medical condition is present or there is a high risk for developing a medical condition
{e.g., strong family history is present), the preoccupation is clearly excessive or dispro-
portionate.
C. There is a high level of anxiety about health, and the individual is easily alarmed about
personal! health status.
D. The individual performs excessive health-related behaviors (e.g., repeatedly checks
his or her body for signs of illness) or exhibits maladaptive avoidance (e.g., avoids doc-
tor appointments and hospitals).
E. Illness preoccupation has been present for at least 6 months, but the specific illness
that is feared may change over that period of time.
F. The illness-related preoccupation is not better explained by another mental disorder, such
as somatic symptom disorder, panic disorder, generalized anxiety disorder, body dysmor-
phic disorder, obsessive-compulsive disorder, or delusional disorder, somatic type.
Specify whether:
Care-seeking type: Medical care, including physician visits or undergoing tests and
procedures, is frequently used.
Care-avoidant type: Medical care is rarely used.
Diagnostic Features
Most individuals with hypochondriasis are now classified as having somatic symptom
disorder; however, in a minority of cases, the diagnosis of illness anxiety disorder applies
instead. Illness anxiety disorder entails a preoccupation with having or acquiring a seri-
ous, undiagnosed medical illness (Criterion A). Somatic symptoms are not present or, if
present, are only mild in intensity (Criterion B). A thorough evaluation fails to identify a
serious medical condition that accounts for the individual's concerns. While the concern
may be derived from a nonpathological physical sign or sensation, the individual's dis-
tress emanates not primarily from the physical complaint itself but rather from his or her
anxiety about the meaning, significance, or cause of the complaint (i.e., the suspected med-
ical diagnosis). If a physical sign or symptom is present, it is often a normal physiological
sensation (e.g., orthostatic dizziness), a benign and self-limited dysfunction (e.g., transient
tinnitus), or a bodily discomfort not generally considered indicative of disease (e.g., belch-
ing). If a diagnosable medical condition is present, the individual’s anxiety and preoccu-
pation are clearly excessive and disproportionate to the severity of the condition (Criterion
B). Empirical evidence and existing literature pertain to previously defined DSM hypo-
chondriasis, and it is unclear to what extent and how precisely they apply to the descrip-
tion of this new diagnosis.
The preoccupation with the idea that one is sick is accompanied by substantial anxiety
about health and disease (Criterion C). Individuals with illness anxiety disorder are easily
316 Somatic Symptom and Related Disorders
alarmed about illness, such as by hearing about someone else falling ill or reading a health-
related news story. Their concerns about undiagnosed disease do not respond to appro-
priate medical reassurance, negative diagnostic tests, or benign course. The physician’s at-
tempts at reassurance and symptom palliation generally do not alleviate the individual’s
concerns and may heighten them. Illness concerns assume a prominent place in the indi-
vidual’s life, affecting daily activities, and may even result in invalidism. [Iness becomes
a central feature of the individual's identity and self-image, a frequent topic of social dis-
course, and a characteristic response to stressful life events. Individuals with the disorder
often examine themselves repeatedly (e.g., examining one’s throat in the mirror) (Crite-
rion D). They research their suspected disease excessively (e.g., on the Internet) and re-
peatedly seek reassurance from family, friends, or physicians. This incessant worrying often
becomes frustrating for others and may result in considerable strain within the family. In
some cases, the anxiety leads to maladaptive avoidance of situations (e.g., visiting sick
family members) or activities (e.g., exercise) that these individuals fear might jeopardize
their health.
Associated Features Supporting Diagnosis
Because they believe they are medically ill, individuals with illness anxiety disorder are
encountered far more frequently in medical than in mental health settings. The majority of
individuals with illness anxiety disorder have extensive yet unsatisfactory medical care,
though some may be too anxious to seek medical] attention. They generally have elevated
rates of medical utilization but do not utilize mental health services more than the general
population. They often consult multiple physicians for the same problem and obtain re-
peatedly negative diagnostic test results. At times, medical attention leads to a paradoxical
exacerbation of anxiety or to iatrogenic complications from diagnostic tests and proce-
dures. Individuals with the disorder are generally dissatisfied with their medical care and
find it unhelpful, often feeling they are not being taken seriously by physicians. At times,
these concerns may be justified, since physicians sometimes are dismissive or respond
with frustration or hostility. This response can occasionally result in a failure to diagnose
a medical condition that is present.
Prevalence
Prevalence estimates of illness anxiety disorder are based on estimates of the DSM-III and
DSM-IV diagnosis hypochondriasis. The 1- to 2-year prevalence of health anxiety and/or
disease conviction in community surveys and population-based samples ranges from 1.3%
to 10%. In ambulatory medical populations, the 6-month/1-year prevalence rates are be-
tween 3% and 8%. The prevalence of the disorder is similar in males and females.
Development and Course
The development and course of illness anxiety disorder are unclear. IIlness anxiety disor-
der is generally thought to be a chronic and relapsing condition with an age at onset in
early and middle adulthood. In population-based samples, health-related anxiety in-
creases with age, but the ages of individuals with high health anxiety in medical settings
do not appear to differ from those of other patients in those settings. In older individuals,
health-related anxiety often focuses on memory loss; the disorder is thought to be rare in
children.
Risk and Prognostic Factors
Environmental. Illness anxiety disorder may sometimes be precipitated by a major life
stress or a serious but ultimately benign threat to the individual's health. A history of child-
Illness Anxiety Disorder 317
hood abuse or of a serious childhood illness may predispose to development of the disor-
der in adulthood,
Course modifiers. Approximately one-third to one-half of individuals with illness anx-
iety disorder have a transient form, which is associated with less psychiatric comorbidity,
more medical comorbidity, and less severe iliness anxiety disorder.
Culture-Related Diagnostic Issues
The diagnosis should be made with caution in individuals whose ideas about disease are
congruent with widely held, culturally sanctioned beliefs. Little is known about the phe-
nomenology of the disorder across cultures, although the prevalence appears to be similar
across different countries with diverse cultures.
Functional Consequences of Illness Anxiety Disorder
Illness anxiety disorder causes substantial role impairment and decrements in physical
function and health-related quality of life. Health concerns often interfere with interper-
sonal relationships, disrupt family life, and damage occupational performance.
Differential Diagnosis
Other medical conditions. The first differential diagnostic consideration is an underly-
ing medical condition, including neurological or endocrine conditions, occult malignan-
cies, and other diseases that affect multiple body systems. The presence of a medical
condition does not rule out the possibility of coexisting illness anxiety disorder. If a med-
ical condition is present, the health-related anxiety and disease concerns are clearly dis-
proportionate to its seriousness. Transient preoccupations related to a medical condition
do not constitute illness anxiety disorder.
Adjustment disorders. Health-related anxiety is a normal response to serious illness
and is not a mental disorder. Such nonpathological health anxiety is clearly related to the
medical condition and is typically time-limited. If the health anxiety is severe enough, an
adjustment disorder may be diagnosed. However, only when the health anxiety is of suf-
ficient duration, severity, and distress can illness anxiety disorder be diagnosed. Thus, the
diagnosis requires the continuous persistence of disproportionate health-related anxiety
for at least 6 months.
Somatic symptom disorder. Somatic symptom disorder is diagnosed when significant
somatic symptoms are present. In contrast, individuals with illness anxiety disorder have
minimal] somatic symptoms and are primarily concerned with the idea they are ill.
Anxiety disorders. In generalized anxiety disorder, individuals worry about multiple
events, situations, or activities, only one of which may involve health. In panic disorder,
the individual may be concerned that the panic attacks reflect the presence of a medical ill-
ness; however, although these individuals may have health anxiety, their anxiety is typi-
cally very acute and episodic. In illness anxiety disorder, the health anxiety and fears are
more persistent and enduring. Individuals with illness anxiety disorder may experience
panic attacks that are triggered by their illness concerns.
Obsessive-compulsive and related disorders. Individuals with illness anxiety disor-
der may have intrusive thoughts about having a disease and also may have associated
compulsive behaviors (e.g., seeking reassurance). However, in illness anxiety disorder, the
preoccupations are usually focused on having a disease, whereas in obsessive-compulsive
disorder (OCD), the thoughts are intrusive and are usually focused on fears of getting a
disease in the future. Most individuals with OCD have obsessions or compulsions involv-
ing other concerns in addition to fears about contracting disease. In body dysmorphic dis-
318 Somatic Symptom and Related Disorders
order, concerns are limited to the individual’s physical appearance, which is viewed as
defective or flawed.
Major depressive disorder. Some individuals with a major depressive episode rumi-
nate about their health and worry excessively about illness. A separate diagnosis of illness
anxiety disorder is not made if these concerns occur only during major depressive epi-
sodes. However, if excessive illness worry persists after remission of an episode of major
depressive disorder, the diagnosis of illness anxiety disorder should be considered.
Psychotic disorders. Individuals with illness anxiety disorder are not delusional and
can acknowledge the possibility that the feared disease is not present. Their ideas do not
attain the rigidity and intensity seen in the somatic delusions occurring in psychotic dis-
orders (e.g., schizophrenia; delusional disorder, somatic type; major depressive disorder,
with psychotic features). True somatic delusions are generally more bizarre (e.g., that an
organ is rotting or dead) than the concerns seen in illness anxiety disorder. The concerns
seen in illness anxiety disorder, though not founded in reality, are plausible.
Comorbidity
Because illness anxiety disorder is a new disorder, exact comorbidities are unknown. Hy-
pochondriasis co-occurs with anxiety disorders (in particular, generalized anxiety disor-
der, panic disorder, and OCD) and depressive disorders. Approximately two-thirds of
individuals with illness anxiety disorder are likely to have at least one other comorbid ma-
jor mental disorder. Individuals with illness anxiety disorder may have an elevated risk
for somatic symptom disorder and personality disorders.
Conversion Disorder
(Functional Neurological Symptom Disorder)
Diagnostic Criteria
A. One or more symptoms of altered voluntary motor or sensory function.
B. Clinical findings provide evidence of incompatibility between the symptom and recog-
nized neurological or medical conditions.
C. The symptom or deficit is not better explained by another medical or mental disorder.
D. The symptom or deficit causes clinically significant distress or impairment in social, oc-
cupational, or other important areas of functioning or warrants medical evaluation.
Coding note: The ICD-9-CM code for conversion disorder is 300.11, which is assigned
regardless of the symptom type. The ICD-10-CM code depends on the symptom type (see
below).
Specify symptom type:
(F44.4) With weakness or paralysis
(F44.4) With abnormal movement (e.g., tremor, dystonic movement, myoclonus, gait
disorder)
(F44.4) With swallowing symptoms
(F44.4) With speech symptom (e.g., dysphonia, slurred speech)
{F44.5) With attacks or seizures
(F44.6) With anesthesia or sensory loss
(F44.6) With special sensory symptom (e.g., visual, olfactory, or hearing distur-
bance)
(F44.7) With mixed symptoms
Conversion Disorder (Functional Neurological Symptom Disorder) 319
Specify if:
Acute episode: Symptoms present for less than 6 months.
Persistent: Symptoms occurring for 6 months or more.
Specify if:
With psychological stressor (specify stressor)
Without psychologicai stressor
Diagnostic Features
Many clinicians use the alternative names of “functional” (referring to abnormal central
nervous system functioning) or “psychogenic” (referring to an assumed etiology) to de-
scribe the symptoms of conversion disorder (functional neurological symptom disor-
der). In conversion disorder, there may be one or more symptoms of various types. Motor
symptoms include weakness or paralysis; abnormal movements, such as tremor or dys-
tonic movements; gait abnormalities; and abnormal limb posturing. Sensory symptoms
include altered, reduced, or absent skin sensation, vision, or hearing. Episodes of abnor-
mal generalized limb shaking with apparent impaired or loss of consciousness may resem-
ble epileptic seizures (also called psychogenic or non-epileptic seizures). There may be
episodes of unresponsiveness resembling syncope or coma. Other symptoms include re-
duced or absent speech volume (dysphonia/aphonia), altered articulation (dysarthria), a
sensation of a lump in the throat (globus), and diplopia.
Although the diagnosis requires that the symptom is not explained by neurological
disease, it should not be made simply because results from investigations are normal or
because the symptom is “bizarre.” There must be clinical findings that show clear evidence
of incompatibility with neurological disease. Internal inconsistency at examination is one
way to demonstrate incompatibility (i.e., demonstrating that physical signs elicited
through one examination method are no longer positive when tested a different way). Ex-
amples of such examination findings include
¢ Hoover's sign, in which weakness of hip extension returns to normal strength with con-
tralateral hip flexion against resistance.
¢ Marked weakness of ankle plantar-flexion when tested on the bed in an individual who
is able to walk on tiptoes;
¢ Positive findings on the tremor entrainment test. On this test, a unilateral tremor may
be identified as functional if the tremor changes when the individual is distracted away
from it. This may be observed if the individual is asked to copy the examiner in making
a rhythmical movement with their unaffected hand and this causes the functional
tremor to change such that it copies or “entrains” to the rhythm of the unaffected hand
or the functional tremor is suppressed, or no longer makes a simple rhythmical move-
ment.
¢ In attacks resembling epilepsy or syncope (“psychogenic” non-epileptic attacks), the
occurrence of closed eyes with resistance to opening or a normal simultaneous electro-
encephalogram (although this alone does not exclude all forms of epilepsy or syncope).
¢ For visual symptoms, a tubular visual field (i.e., tunnel vision).
It is important to note that the diagnosis of conversion disorder should be based on the
overall clinical picture and not on a single clinical finding.
Associated Features Supporting Diagnosis
A number of associated features can support the diagnosis of conversion disorder. There
may be a history of multiple similar somatic symptoms. Onset may be associated with
stress or trauma, either psychological or physical in nature. The potential etiological rele-
320 Somatic Symptom and Related Disorders
vance of this stress or trauma may be suggested by a close temporal relationship. However,
while assessment for stress and trauma is important, the diagnosis should not be withheld
if none is found.
Conversion disorder is often associated with dissociative symptoms, such as deperson-
alization, derealization, and dissociative amnesia, particularly at symptom onset or during
attacks.
The diagnosis of conversion disorder does not require the judgment that the symptoms
are not intentionally produced (i.e., not feigned), as the definite absence of feigning may
not be reliably discerned. The phenomenon of ia belle indifference (i.e., lack of concern about
the nature or implications of the symptom) has been associated with conversion disorder
but it is not specific for conversion disorder and should not be used to make the diagnosis.
Similarly the concept of secondary gain (i.e., when individuals derive external benefits such
as money or release from responsibilities) is also not specific to conversion disorder and
particularly in the context of definite evidence for feigning, the diagnoses that should be
considered instead would include factitious disorder or malingering (see the section “Dif-
ferential Diagnosis” for this disorder).
Prevalence
Transient conversion symptoms are common, but the precise prevalence of the disorder is
unknown. This is partly because the diagnosis usually requires assessment in secondary
care, where it is found in approximately 5% of referrals to neurology clinics. The incidence
of individual persistent conversion symptoms is estimated to be 2-5/100,000 per year.
Development and Course
Onset has been reported throughout the life course. The onset of non-epileptic attacks
peaks in the third decade, and motor symptoms have their peak onset in the fourth decade.
The symptoms can be transient or persistent. The prognosis may be better in younger chil-
dren than in adolescents and adults.
Risk and Prognostic Factors
Temperamental. Maladaptive personality traits are commonly associated with conver-
sion disorder.
Environmental. There may be a history of childhood abuse and neglect. Stressful life
events are often, but not always, present.
Genetic and physiological. The presence of neurological disease that causes similar symp-
toms is a risk factor (e.g., non-epileptic seizures are more common in patients who also
have epilepsy).
Course modifiers. Short duration of symptoms and acceptance of the diagnosis are pos-
itive prognostic factors. Maladaptive personality traits, the presence of comorbid physical
disease, and the receipt of disability benefits may be negative prognostic factors.
Culture-Related Diagnostic Issues
Changes resembling conversion (and dissociative) symptoms are common in certain
culturally sanctioned rituals. If the symptoms are fully explained within the particular
cultural context and do not result in clinically significant distress or disability, then the di-
agnosis of conversion disorder is not made.
Gender-Related Diagnostic Issues
Conversion disorder is two to three times more common in females.
Conversion Disorder (Functional Neurological Symptom Disorder) 321
Functional Consequences of Conversion Disorder
Individuals with conversion symptoms may have substantial disability. The severity of dis-
ability can be similar to that experienced by individuals with comparable medical diseases.
Differential Diagnosis
If another mental disorder better explains the symptoms, that diagnosis should be made.
However the diagnosis of conversion disorder may be made in the presence of another
mental disorder.
Neurological disease. The main differential diagnosis is neurological disease that might
better explain the symptoms. After a thorough neurological assessment, an unexpected
neurological disease cause for the symptoms is rarely found at follow up. However, reas-
sessment may be required if the symptoms appear to be progressive. Conversion disorder
may coexist with neurological disease.
Somatic symptom disorder. Conversion disorder may be diagnosed in addition to so-
matic symptom disorder. Most of the somatic symptoms encountered in somatic symptom
disorder cannot be demonstrated to be clearly incompatible with pathophysiology (e.g.,
pain, fatigue), whereas in conversion disorder, such incompatibility is required for the di-
agnosis. The excessive thoughts, feelings, and behaviors characterizing somatic symptom
disorder are often absent in conversion disorder.
Factitious disorder and malingering. The diagnosis of conversion disorder does not re-
quire the judgment that the symptoms are not intentionally produced (i.e., not feigned),
because assessment of conscious intention is unreliable. However definite evidence of
feigning (e.g., clear evidence that loss of function is present during the examination but not
at home) would suggest a diagnosis of factitious disorder if the individual’s apparent aim
is to assume the sick role or malingering if the aim is to obtain an incentive such as money.
Dissociative disorders. Dissociative symptoms are common in individuals with con-
version disorder. If both conversion disorder and a dissociative disorder are present, both
diagnoses should be made.
Body dysmorphic disorder. Individuals with body dysmorphic disorder are exces-
sively concerned about a perceived defect in their physical features but do not complain of
symptoms of sensory or motor functioning in the affected body part.
Depressive disorders. In depressive disorders, individuals may report general heavi-
ness of their limbs, whereas the weakness of conversion disorder is more focal and prom-
inent. Depressive disorders are also differentiated by the presence of core depressive
symptoms.
Panic disorder. Episodic neurological symptoms (e.g., tremors and paresthesias) can
occur in both conversion disorder and panic attacks. In panic attacks, the neurological
symptoms are typically transient and acutely episodic with characteristic cardiorespira-
tory symptoms. Loss of awareness with amnesia for the attack and violent limb move-
ments occur in non-epileptic attacks, but not in panic attacks.
Comorbidity
Anxiety disorders, especially panic disorder, and depressive disorders commonly co-occur
with conversion disorder. Somatic symptom disorder may co-occur as well. Psychosis, sub-
stance use disorder, and alcohol misuse are uncommon. Personality disorders are more
common in individuals with conversion disorder than in the general population. Neuro-
logical or other medical conditions commonly coexist with conversion disorder as well.
322 Somatic Symptom and Related Disorders
Psychological Factors Affecting
Other Medical Conditions
Diagnostic Criteria 316 (F54)
A. Amedical symptom or condition (other than a mental disorder) is present.
B. Psychological or behavioral factors adversely affect the medical condition in one of the
following ways:
1. The factors have influenced the course of the medical condition as shown by a
close temporal association between the psychological factors and the development
or exacerbation of, or delayed recovery from, the medical condition.
2. The factors interfere with the treatment of the medical condition (e.g., poor adher-
ence).
3. The factors constitute additional well-established health risks for the individual.
4. The factors influence the underlying pathophysiology, precipitating or exacerbating
symptoms or necessitating medical attention.
C. The psychological and behavioral factors in Criterion B are not better explained by an-
other mental disorder (e.g., panic disorder, major depressive disorder, posttraumatic
stress disorder).
Specify current severity:
Mild: Increases medical risk (e.g., inconsistent adherence with antihypertension treat-
ment).
Moderate: Aggravates underlying medical condition (e.g., anxiety aggravating
asthma).
Severe: Results in medical hospitalization or emergency room visit.
Extreme: Results in severe, life-threatening risk (e.g., ignoring heart attack symp-
toms).
Diagnostic Features
The essential feature of psychological factors affecting other medical conditions is the
presence of one or more clinically significant psychological or behavioral factors that ad-
versely affect a medical condition by increasing the risk for suffering, death, or disability
(Criterion B). These factors can adversely affect the medical condition by influencing its
course or treatment, by constituting an additional well-established health risk factor, or by
influencing the underlying pathophysiology to precipitate or exacerbate symptoms or to
necessitate medical attention.
Psychological or behavioral factors include psychological distress, patterns of interper-
sonal interaction, coping styles, and maladaptive health behaviors, such as denial of symp-
toms or poor adherence to medical recommendations. Common clinical examples are
anxiety-exacerbating asthma, denial of need for treatment for acute chest pain, and manip-
ulation of insulin by an individual with diabetes wishing to lose weight. Many different
psychological factors have been demonstrated to adversely influence medical conditions—
for example, symptoms of depression or anxiety, stressful life events, relationship style,
personality traits, and coping styles. The adverse effects can range from acute, with imme-
diate medical consequences (e.g., Takotsubo cardiomyopathy) to chronic, occurring over a
long period of time (e.g., chronic occupational stress increasing risk for hypertension). Af-
fected medical conditions can be those with clear pathophysiology (e.g., diabetes, cancer,
coronary disease), functional syndromes (e.g., migraine, irritable bowel syndrome, fibro-
myalgia), or idiopathic medical symptoms (e.g., pain, fatigue, dizziness).
Psychological Factors Affecting Other Medical Conditions 323
This diagnosis should be reserved for situations in which the effect of the psychological
factor on the medical condition is evident and the psychological factor has clinically sig-
nificant effects on the course or outcome of the medical condition. Abnormal psychologi-
cal or behavioral symptoms that develop in response to a medical condition are more
properly coded as an adjustment disorder (a clinically significant psychological response
to an identifiable stressor). There must be reasonable evidence to suggest an association
between the psychological factors and the medical condition, although it may often not be
possible to demonstrate direct causality or the mechanisms underlying the relationship.
Prevalence
The prevalence of psychological factors affecting other medical conditions is unclear. In
U.S. private insurance billing data, it is a more common diagnosis than somatic symptom
disorders.
Development and Course
Psychological factors affecting other medical conditions can occur across the lifespan. Par-
ticularly with young children, corroborative history from parents or school can assist the di-
agnostic evaluation. Some conditions are characteristic of particular life stages (e.g., in older
individuals, the stress associated with acting as a caregiver for an ill spouse or partner).
Culture-Related Diagnostic Issues
Many differences between cultures may influence psychological factors and their effects
on medical conditions, such as those in language and communication style, explanatory
models of illness, patterns of seeking health care, service availability and organization,
doctor-patient relationships and other healing practices, family and gender roles, and at-
titudes toward pain and death. Psychological factors affecting other medical conditions
must be differentiated from culturally specific behaviors such as using faith or spiritual
healers or other variations in illness management that are acceptable within a culture and
represent an attempt to help the medical condition rather than interfere with it. These local
practices may complement rather than obstruct evidence-based interventions. If they do
not adversely affect outcomes, they should not be pathologized as psychological factors
affecting other medical conditions.
Functional Consequences of Psychological Factors
Affecting Other Medical Conditions
Psychological and behavioral factors have been demonstrated to affect the course of many
medical diseases.
Differential Diagnosis
Mental disorder due to another medical condition. A temporal association between
symptoms of a mental disorder and those of a medical condition is also characteristic of a
mental disorder due to another medical condition, but the presumed causality is in the op-
posite direction. In a mental disorder due to another medical condition, the medical
condition is judged to be causing the mental disorder through a direct physiological mech-
anism. In psychological factors affecting other medical conditions, the psychological or be-
havioral factors are judged to affect the course of the medical condition.
Adjustment disorders. Abnormal psychological or behavioral symptoms that develop in
response to a medical condition are more properly coded as an adjustment disorder (a clin-
ically significant psychological response to an identifiable stressor). For example, an indi-
324 Somatic Symptom and Related Disorders
vidual with angina that is precipitated whenever he becomes enraged would be diagnosed
as having psychological factors affecting other medical conditions, whereas an individual
with angina who developed maladaptive anticipatory anxiety would be diagnosed as hav-
ing an adjustment disorder with anxiety. In clinical practice, however, psychological fac-
tors and a medical condition are often mutually exacerbating (e.g., anxiety as both a
precipitant and a consequence of angina), in which case the distinction is arbitrary. Other
mental disorders frequently result in medical complications, most notably substance use
disorders (e.g., alcohol use disorder, tobacco use disorder). If an individual has a coexisting
major mental disorder that adversely affects or causes another medical condition, diagno-
ses of the mental disorder and the medical condition are usually sufficient. Psychological
factors affecting other medical conditions is diagnosed when the psychological traits or
behaviors do not meet criteria for a mental diagnosis.
Somatic symptom disorder. Somatic symptom disorder is characterized by a combina-
tion of distressing somatic symptoms and excessive or maladaptive thoughts, feelings,
and behavior in response to these symptoms or associated health concerns. The individual
may or may not have a diagnosable medical condition. In contrast, in psychological factors
affecting other medical conditions, the psychological factors adversely affect a medical
condition; the individual’s thoughts, feelings, and behavior are not necessarily excessive.
The difference is one of emphasis, rather than a clear-cut distinction. In psychological fac-
tors affecting other medical conditions, the emphasis is on the exacerbation of the medical
condition (e.g., an individual with angina that is precipitated whenever he becomes anx-
ious). In somatic symptom disorder, the emphasis is on maladaptive thoughts, feelings,
and behavior (e.g., an individual with angina who worries constantly that she will have a
heart attack, takes her blood pressure multiple times per day, and restricts her activities).
lIiness anxiety disorder. {llness anxiety disorder is characterized by high illness anxiety
that is distressing and/or disruptive to daily life with minimal somatic symptoms. The fo-
cus of clinical concern is the individual's worry about having a disease; in most cases, no
serious disease is present. In psychological factors affecting other medical conditions, anx-
iety may be a relevant psychological factor affecting a medical condition, but the clinical
concern is the adverse effects on the medical condition.
Comorbidity
By definition, the diagnosis of psychological factors affecting other medical conditions entails
a relevant psychological or behavioral syndrome or trait and a comorbid medical condition.
Factitious Disorder
Diagnostic Criteria 300.19 (F68.10)
Factitious Disorder Imposed on Self
A. Falsification of physical or psychological signs or symptoms, or induction of injury or
disease, associated with identified deception.
B. The individual presents himself or herself to others as ill, impaired, or injured.
C. The deceptive behavior is evident even in the absence of obvious external rewards.
D. The behavior is not better expiained by another mental disorder, such as delusional
disorder or another psychotic disorder.
Specify:
Single episode
Recurrent episodes (two or more events of falsification of illness and/or induction of
injury)
Factitious Disorder 325
Factitious Disorder Imposed on Another
(Previously Factitious Disorder by Proxy)
A. Falsification of physical or psychological signs or symptoms, or induction of injury or
disease, in another, associated with identified deception.
B. The individual presents another individual (victim) to others as ill, impaired, or injured.
C. The deceptive behavior is evident even in the absence of obvious external rewards.
D. The behavior is not better explained by another mental disorder, such as delusional
disorder or another psychotic disorder.
Note: The perpetrator, not the victim, receives this diagnosis.
Specify:
Single episode
Recurrent episodes (two or more events of falsification of illness and/or induction of
injury)
Recording Procedures
When an individual falsifies illness in another (e.g., children, adults, pets), the diagnosis is
factitious disorder imposed on another. The perpetrator, not the victim, is given the diag-
nosis. The victim may be given an abuse diagnosis (e.g., 995.54 [T74.12X]; see the chapter
“Other Conditions That May Be a Focus of Clinical Attention”).
Diagnostic Features
The essential feature of factitious disorder is the falsification of medical or psychological signs
and symptoms in oneself or others that are associated with the identified deception. Indi-
viduals with factitious disorder can also seek treatment for themselves or another following
induction of injury or disease. The diagnosis requires demonstrating that the individual is
taking surreptitious actions to misrepresent, simulate, or cause signs or symptoms of ill-
ness or injury in the absence of obvious external rewards. Methods of illness falsification
can include exaggeration, fabrication, simulation, and induction. While a preexisting med-
ical condition may be present, the deceptive behavior or induction of injury associated
with deception causes others to view such individuals (or another) as more ill or impaired,
and this can lead to excessive clinical intervention. Individuals with factitious disorder
might, for example, report feelings of depression and suicidality following the death of a
spouse despite the death not being true or the individual’s not having a spouse; decep-
tively report episodes of neurological symptoms (e.g., seizures, dizziness, or blacking out);
manipulate a laboratory test (e.g., by adding blood to urine) to falsely indicate an abnor-
mality; falsify medical records to indicate an illness; ingest a substance (e.g., insulin or
warfarin) to induce an abnormal laboratory result or illness; or physically injure them-
selves or induce illness in themselves or another (e.g., by injecting fecal material to produce
an abscess or to induce sepsis).
Associated Features Supporting Diagnosis
Individuals with factitious disorder imposed on self or factitious disorder imposed on an-
other are at risk for experiencing great psychological distress or functional impairment by
causing harm to themselves and others. Family, friends, and health care professionals are
also often adversely affected by their behavior. Factitious disorders have similarities to
substance use disorders, eating disorders, impulse-control disorders, pedophilic disorder,
and some other established disorders related to both the persistence of the behavior and
the intentional efforts to conceal the disordered behavior through deception. Whereas
some aspects of factitious disorders might represent criminal behavior (e.g., factitious dis-
326 Somatic Symptom and Related Disorders
order imposed on another, in which the parent’s actions represent abuse and maltreat-
ment of a child), such criminal behavior and mental illness are not mutually exclusive. The
diagnosis of factitious disorder emphasizes the objective identification of falsification of
signs and symptoms of illness, rather than an inference about intent or possible underly-
ing motivation. Moreover, such behaviors, including the induction of injury or disease, are
associated with deception.
Prevalence
The prevalence of factitious disorder is unknown, likely because of the role of deception in
this population. Among patients in hospital settings, it is estimated that about 1% of indi-
viduals have presentations that meet the criteria for factitious disorder.
Development and Course
The course of factitious disorder is usually one of intermittent episodes. Single episodes
and episodes that are characterized as persistent and unremitting are both less common.
Onset is usually in early adulthood, often after hospitalization for a medical condition ora
mental disorder. When imposed on another, the disorder may begin after hospitalization
of the individual’s child or other dependent. In individuals with recurrent episodes of fal-
sification of signs and symptoms of illness and/or induction of injury, this pattern of suc-
cessive deceptive contact with medical personnel, including hospitalizations, may become
lifelong.
Differential Diagnosis
Caregivers who lie about abuse injuries in dependents solely to protect themselves from lia-
bility are not diagnosed with factitious disorder imposed on another because protection from
liability is an external reward (Criterion C, the deceptive behavior is evident even in the ab-
sence of obvious external rewards). Such caregivers who, upon observation, analysis of med-
ical records, and/or interviews with others, are found to lie more extensively than needed for
immediate self-protection are diagnosed with factitious disorder imposed on another.
Somatic symptom disorder. In somatic symptom disorder, there may be excessive at-
tention and treatment seeking for perceived medical concerns, but there is no evidence that
the individual is providing false information or behaving deceptively.
Malingering. Malingering is differentiated from factitious disorder by the intentional re-
porting of symptoms for personal gain (e.g., money, time off work). In contrast, the diag-
nosis of factitious disorder requires the absence of obvious rewards.
Conversion disorder (functional neurological symptom disorder). Conversion disorder
is characterized by neurological symptoms that are inconsistent with neurological patho-
physiology. Factitious disorder with neurological symptoms is distinguished from con-
version disorder by evidence of deceptive falsification of symptoms.
Borderline personality disorder. Deliberate physical self-harm in the absence of suicidal
intent can also occur in association with other mental disorders such as borderline person-
ality disorder. Factitious disorder requires that the induction of injury occur in association
with deception.
Medical condition or mental disorder not associated with intentional symptom falsifi-
cation. Presentation of signs and symptoms of illness that do not conform to an identi-
fiable medical condition or mental disorder increases the likelihood of the presence of a
factitious disorder. However, the diagnosis of factitious disorder does not exclude the
presence of true medical condition or mental disorder, as comorbid illness often occurs in
the individual along with factitious disorder. For example, individuals who might manip-
ulate blood sugar levels to produce symptoms may also have diabetes.
Other Specified Somatic Symptom and Related Disorder 327
Other Specified Somatic Symptom and
Related Disorder
300.89 (F45.8)
This category applies to presentations in which symptoms characteristic of a somatic
symptom and related disorder that cause clinically significant distress or impairment in so-
cial, occupational, or other important areas of functioning predominate but do not meet the
full criteria for any of the disorders in the somatic symptom and related disorders diagnos-
tic class.
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Brief somatic symptom disorder: Duration of symptoms is less than 6 months.
2. Brief illness anxiety disorder: Duration of symptoms is less than 6 months.
3. Illness anxiety disorder without excessive health-related behaviors: Criterion D
for illness anxiety disorder is not met.
4. Pseudocyesis: A false belief of being pregnant that is associated with objective signs
and reported symptoms of pregnancy.
Unspecified Somatic Symptom and
Related Disorder
300.82 (F45.9)
This category applies to presentations in which symptoms characteristic of a somatic
symptom and related disorder that cause Clinically significant distress or impairment in so-
cial, occupational, or other important areas of functioning predominate but do not meet the
full criteria for any of the disorders in the somatic symptom and related disorders diagnos-
tic class. The unspecified somatic symptom and related disorder category should not be
used unless there are decidedly unusual situations where there is insufficient information
to make a more specific diagnosis.
Feedin gan d eatin Q disorders are characterized by a persistent disturbance of eat-
ing or eating-related behavior that results in the altered consumption or absorption of
food and that significantly impairs physical health or psychosocial functioning. Diagnos-
tic criteria are provided for pica, rumination disorder, avoidant/restrictive food intake
disorder, anorexia nervosa, bulimia nervosa, and binge-eating disorder.
The diagnostic criteria for rumination disorder, avoidant/ restrictive food intake dis-
order, anorexia nervosa, bulimia nervosa, and binge-eating disorder result in a classifica-
tion scheme that is mutually exclusive, so that during a single episode, only one of these
diagnoses can be assigned. The rationale for this approach is that, despite a number of
common psychological and behavioral features, the disorders differ substantially in clin-
ical course, outcome, and treatment needs. A diagnosis of pica, however, may be assigned
in the presence of any other feeding and eating disorder.
Some individuals with disorders described in this chapter report eating-related symp-
toms resembling those typically endorsed by individuals with substance use disorders,
such as craving and patterns of compulsive use. This resemblance may reflect the involve-
ment of the same neural systems, including those implicated in regulatory self-control and
reward, in both groups of disorders. However, the relative contributions of shared and
distinct factors in the development and perpetuation of eating and substance use disor-
ders remain insufficiently understood.
Finally, obesity is not included in DSM-5 as a mental disorder. Obesity (excess body fat)
results from the long-term excess of energy intake relative to energy expenditure. A range
of genetic, physiological, behavioral, and environmental factors that vary across individ-
uals contributes to the development of obesity; thus, obesity is not considered a mental
disorder. However, there are robust associations between obesity and a number of mental
disorders (e.g., binge-eating disorder, depressive and bipolar disorders, schizophrenia).
The side effects of some psychotropic medications contribute importantly to the develop-
ment of obesity, and obesity may be a risk factor for the development of some mental dis-
orders (e.g., depressive disorders).
Pica
Diagnostic Criteria
A. Persistent eating of nonnutritive, nonfood substances over a period of at least 1 month.
B. The eating of nonnutritive, nonfood substances is inappropriate to the developmental
level of the individual.
C. The eating behavior is not part of a culturally supported or socially normative practice.
D. If the eating behavior occurs in the context of another mental disorder (e.g., intellectual
disability {intellectual developmental disorder], autism spectrum disorder, schizophre-
nia) or medical condition (including pregnancy), it is sufficiently severe to warrant ad-
ditional clinical attention.
329
330 Feeding and Eating Disorders
Coding note: The ICD-9-CM code for pica is 307.52 and is used for children or adults.
The ICD-10-CM codes for pica are (F98.3) in children and (F50.8) in adults.
Specify it:
In remission: After full criteria for pica were previously met, the criteria have not been
met for a sustained period of time.
Diagnostic Features
The essential feature of pica is the eating of one or more nonnutritive, nonfood substances ona
persistent basis over a period of at least 1 month (Criterion A) that is severe enough to warrant
clinical attention. Typical substances ingested tend to vary with age and availability and might
include paper, soap, cloth, hair, string, wool, soil, chalk, talcum powder, paint, gum, metal,
pebbles, charcoal or coal, ash, clay, starch, or ice. The term nonfood is included because the di-
agnosis of pica does not apply to ingestion of diet products that have minimal nutritional con-
tent. There is typically no aversion to food in general. The eating of nonnutritive, nonfood
substances must be developmentally inappropriate (Criterion B) and not part of a culturally
supported or socially normative practice (Criterion C). A minimum age of 2 years is suggested
for a pica diagnosis to exclude developmentally normal mouthing of objects by infants that re-
sults in ingestion. The eating of nonnutritive, nonfood substances can be an associated feature
of other mental disorders (e.g., intellectual disability [intellectual developmental disorder],
autism spectrum disorder, schizophrenia). If the eating behavior occurs exclusively in the con-
text of another mental disorder, a separate diagnosis of pica should be made only if the eating
behavior is sufficiently severe to warrant additional clinical attention (Criterion D).
Associated Features Supporting Diagnosis
Although deficiencies in vitamins or minerals (e.g., zinc, iron) have been reported in some
instances, often no specific biological abnormalities are found. In some cases, pica comes
to clinical attention only following general medical complications (e.g., mechanical bowel
problems; intestinal obstruction, such as that resulting from a bezoar; intestinal perfora-
tion; infections such as toxoplasmosis and toxocariasis as a result of ingesting feces or dirt;
poisoning, such as by ingestion of lead-based paint).
Prevalence
The prevalence of pica is unclear. Among individuals with intellectual disability, the prev-
alence of pica appears to increase with the severity of the condition.
Development and Course
Onset of pica can occur in childhood, adolescence, or adulthood, although childhood onset
is most commonly reported. Pica can occur in otherwise normally developing children,
whereas in adults, it appears more likely to occur in the context of intellectual disability or
other mental disorders. The eating of nonnutritive, nonfood substances may also manifest
in pregnancy, when specific cravings (e.g., chalk or ice) might occur. The diagnosis of pica
during pregnancy is only appropriate if such cravings lead to the ingestion of nonnutri-
tive, nonfood substances to the extent that the eating of these substances poses potential
medical risks. The course of the disorder can be protracted and can result in medical emer-
gencies (e.g., intestinal obstruction, acute weight loss, poisoning). The disorder can poten-
tially be fatal depending on substances ingested.
Risk and Prognostic Factors
Environmental. Neglect, lack of supervision, and developmental delay can increase the
risk for this condition.
Pica 331
Culture-Retated Diagnostic Issues
In some populations, the eating of earth or other seemingly nonnutritive substances is believed
to be of spiritual, medicinal, or other social value, or may be a culturally supported or socially
normative practice. Such behavior does not warrant a diagnosis of pica (Criterion C).
Gender-Related Diagnostic Issues
Pica occurs in both males and females. It can occur in females during pregnancy; however,
little is known about the course of pica in the postpartum period.
Diagnostic Markers
Abdominal flat plate radiography, ultrasound, and other scanning methods may reveal
obstructions related to pica. Blood tests and other laboratory tests can be used to ascertain
levels of poisoning or the nature of infection.
Functional Consequences of Pica
Pica can significantly impair physical functioning, but it is rarely the sole cause of impair-
ment in social functioning. Pica often occurs with other disorders associated with im-
paired social functioning.
Differential Diagnosis
Eating of nonnutritive, nonfood substances may occur during the course of other mental
disorders (e.g., autism spectrum disorder, schizophrenia) and in Kleine-Levin syndrome.
In any such instance, an additional diagnosis of pica should be given only if the eating be-
havior is sufficiently persistent and severe to warrant additional clinical attention.
Anorexia nervosa. Pica can usually be distinguished from the other feeding and eating
disorders by the consumption of nonnutritive, nonfood substances. It is important to note,
however, that some presentations of anorexia nervosa include ingestion of nonnutritive,
nonfood substances, such as paper tissues, as a means of attempting to control appetite. In
such cases, when the eating of nonnutritive, nonfood substances is primarily used as a
means of weight control, anorexia nervosa should be the primary diagnosis.
Factitious disorder. Some individuals with factitious disorder may intentionally ingest
foreign objects as part of the pattern of falsification of physical symptoms. In such in-
stances, there is an element of deception that is consistent with deliberate induction of in-
jury or disease.
Nonsuicidal self-injury and nonsuicidal self-injury behaviors in personality disorders.
Some individuals may swallow potentially harmful items (e.g., pins, needles, knives) in
the context of maladaptive behavior patterns associated with personality disorders or
nonsuicidal self-injury.
Comorbidity
Disorders most commonly comorbid with pica are autism spectrum disorder and intellec-
tual disability (intellectual developmental disorder), and, to a lesser degree, schizophrenia
and obsessive-compulsive disorder. Pica can be associated with trichotillomania (hair-
pulling disorder) and excoriation (skin-picking) disorder. In comorbid presentations, the
hair or skin is typically ingested. Pica can also be associated with avoidant/restrictive food
intake disorder, particularly in individuals with a strong sensory component to their pre-
sentation. When an individual is known to have pica, assessment should include con-
sideration of the possibility of gastrointestinal complications, poisoning, infection, and
nutritional deficiency.
332 Feeding and Eating Disorders
Rumination Disorder
Diagnostic Criteria 307.53 (F98.21)
A. Repeated regurgitation of food over a period of at least 1 month. Regurgitated food
may be re-chewed, re-swallowed, or spit out.
B. The repeated regurgitation is not attributable to an associated gastrointestinal or other
medical condition (e.g., gastroesophageal reflux, pyloric stenosis).
C. The eating disturbance does not occur exclusively during the course of anorexia nervosa,
bulimia nervosa, binge-eating disorder, or avoidant/restrictive food intake disorder.
D. If the symptoms occur in the context of another mental disorder (e.g., intellectual dis-
ability [intellectual developmental disorder] or another neurodevelopmental disorder),
they are sufficiently severe to warrant additional clinical attention.
Specify if:
In remission: After full criteria for rumination disorder were previously met, the criteria
have not been met for a sustained period of time.
Diagnostic Features
The essential feature of rumination disorder is the repeated regurgitation of food occur-
ring after feeding or eating over a period of at least 1 month (Criterion A). Previously swal-
lowed food that may be partially digested is brought up into the mouth without apparent
nausea, involuntary retching, or disgust. The food may be re-chewed and then ejected
from the mouth or re-swallowed. Regurgitation in rumination disorder should be fre-
quent, occurring at least several times per week, typically daily. The behavior is not better
explained by an associated gastrointestinal or other medical condition (e.g., gastroesoph-
ageal reflux, pyloric stenosis) (Criterion B) and does not occur exclusively during the
course of anorexia nervosa, bulimia nervosa, binge-eating disorder, or avoidant/restric-
tive food intake disorder (Criterion C). If the symptoms occur in the context of another
mental disorder (e.g., intellectual disability [intellectual developmental disorder], neuro-
developmental disorder), they must be sufficiently severe to warrant additional clinical
attention (Criterion D) and should represent a primary aspect of the individual’s presen-
tation requiring intervention. The disorder may be diagnosed across the life span, par-
ticularly in individuals who also have intellectual disability. Many individuals with
rumination disorder can be directly observed engaging in the behavior by the clinician. In
other instances diagnosis can be made on the basis of self-report or corroborative informa-
tion from parents or caregivers. Individuals may describe the behavior as habitual or out-
side of their control.
Associated Features Supporting Diagnosis
Infants with rumination disorder display a characteristic position of straining and arching
the back with the head held back, making sucking movements with their tongue. They
may give the impression of gaining satisfaction from the activity. They may be irritable
and hungry between episodes of regurgitation. Weight loss and failure to make expected
weight gains are common features in infants with rumination disorder. Malnutrition may
occur despite the infant's apparent hunger and the ingestion of relatively large amounts of
food, particularly in severe cases, when regurgitation immediately follows each feeding
episode and regurgitated food is expelled. Malnutrition might also occur in older children
and adults, particularly when the regurgitation is accompanied by restriction of intake.
Adolescents and adults may attempt to disguise the regurgitation behavior by placing a
Rumination Disorder 333
hand over the mouth or coughing. Some will avoid eating with others because of the ac-
knowledged social undesirability of the behavior. This may extend to an avoidance of eat-
ing prior to social situations, such as work or school (e.g., avoiding breakfast because it
may be followed by regurgitation).
Prevalence
Prevalence data for rumination disorder are inconclusive, but the disorder is commonly
reported to be higher in certain groups, such as individuals with intellectual disability.
Development and Course
Onset of rumination disorder can occur in infancy, childhood, adolescence, or adulthood.
The age at onset in infants is usually between ages 3 and 12 months. In infants, the disorder
frequently remits spontaneously, but its course can be protracted and can result in medical
emergencies (e.g., severe malnutrition). It can potentially be fatal, particularly in infancy.
Rumination disorder can have an episodic course or occur continuously until treated. In
infants, as well as in older individuals with intellectual disability (intellectual developmen-
tal disorder) or other neurodevelopmental disorders, the regurgitation and rumination be-
havior appears to have a self-soothing or self-stimulating function, similar to that of other
repetitive motor behaviors such as head banging.
Risk and Prognostic Factors
Environmental. Psychosocial problems such as lack of stimulation, neglect, stressful life
situations, and problems in the parent-child relationship may be predisposing factors in
infants and young children.
Functional Consequences of Rumination Disorder
Malnutrition secondary to repeated regurgitation may be associated with growth delay
and have a negative effect on development and learning potential. Some older individuals
with rumination disorder deliberately restrict their food intake because of the social un-
desirability of regurgitation. They may therefore present with weight loss or low weight.
In older children, adolescents, and adults, social functioning is more likely to be adversely
affected.
Differential Diagnosis
Gastrointestinal conditions. It is important to differentiate regurgitation in rumination
disorder from other conditions characterized by gastroesophageal reflux or vomiting. Con-
ditions such as gastroparesis, pyloric stenosis, hiatal hernia, and Sandifer syndrome in in-
fants should be ruled out by appropriate physical examinations and laboratory tests.
Anorexia nervosa and bulimia nervosa. Individuals with anorexia nervosa and bulimia
nervosa may also engage in regurgitation with subsequent spitting out of food as a means
of disposing of ingested calories because of concerns about weight gain.
Comorbidity
Regurgitation with associated rumination can occur in the context of a concurrent medical
condition or another mental disorder (e.g., generalized anxiety disorder). When the regur-
gitation occurs in this context, a diagnosis of rumination disorder is appropriate only when
the severity of the disturbance exceeds that routinely associated with such conditions or
disorders and warrants additional clinical attention.
334 Feeding and Eating Disorders
Avoidant/Restrictive Food Intake Disorder
Diagnostic Criteria 307.59 (F50.8)
A. An eating or feeding disturbance (e.g., apparent lack of interest in eating or food; avoid-
ance based on the sensory characteristics of food; concern about aversive conse-
quences of eating) as manifested by persistent failure to meet appropriate nutritional
and/or energy needs associated with one (or more) of the following:
1. Significant weight loss (or failure to achieve expected weight gain or faltering
growth in children).
2. Significant nutritional deficiency.
3. Dependence on enteral feeding or oral nutritional supplements.
4. Marked interference with psychosocial functioning.
B. The disturbance is not better explained by lack of available food or by an associated
culturally sanctioned practice.
C. The eating disturbance does not occur exclusively during the course of anorexia ner-
vosa or bulimia nervosa, and there is no evidence of a disturbance in the way in which
one’s body weight or shape is experienced.
D. The eating disturbance is not attributable to a concurrent medical condition or not bet-
ter explained by another mental disorder. When the eating disturbance occurs in the
context of another condition or disorder, the severity of the eating disturbance exceeds
that routinely associated with the condition or disorder and warrants additional clinical
attention.
Specify if:
in remission: After full criteria for avoidant/restrictive food intake disorder were previ-
ously met, the criteria have not been met for a sustained period of time.
Diagnostic Features
Avoidant/restrictive food intake disorder replaces and extends the DSM-IV diagnosis of
feeding disorder of infancy or early childhood. The main diagnostic feature of avoidant/
restrictive food intake disorder is avoidance or restriction of food intake (Criterion A)
manifested by clinically significant failure to meet requirements for nutrition or insuffi-
cient energy intake through oral intake of food. One or more of the following key features
must be present: significant weight loss, significant nutritional deficiency (or related
health impact), dependence on enteral feeding or oral nutritional supplements, or marked
interference with psychosocial functioning. The determination of whether weight loss is
significant (Criterion A1) is a clinical judgment; instead of losing weight, children and ad-
olescents who have not completed growth may not maintain weight or height increases
along their developmental trajectory. ;
Determination of significant nutritional deficiency (Criterion A2) is also based on clin-
ical assessment (e.g., assessment of dietary intake, physical examination, and laboratory
testing), and related impact on physical health can be of a similar severity to that seen in
anorexia nervosa (e.g., hypothermia, bradycardia, anemia). In severe cases, particularly in
infants, malnutrition can be life threatening. “Dependence” on enteral feeding or oral nu-
tritional supplements (Criterion A3) means that supplementary feeding is required to sus-
tain adequate intake. Examples of individuals requiring supplementary feeding include
infants with failure to thrive who require nasogastric tube feeding, children with neuro-
developmental disorders who are dependent on nutritionally complete supplements, and
individuals who rely on gastrostomy tube feeding or complete oral nutrition supplements
in the absence of an underlying medical condition. Inability to participate in normal social
Avoidant/Restrictive Food Intake Disorder 335
activities, such as eating with others, or to sustain relationships as a result of the distur-
bance would indicate marked interference with psychosocial functioning (Criterion A4).
Avoidant/restrictive food intake disorder does not include avoidance or restriction of
food intake related to lack of availability of food or to cultural practices (e.g., religious fast-
ing or normal dieting) (Criterion B), nor does it include developmentally normal behaviors
(e.g., picky eating in toddlers, reduced intake in older adults). The disturbance is not better
explained by excessive concern about body weight or shape (Criterion C) or by concurrent
medical factors or mental disorders (Criterion D).
In some individuals, food avoidance or restriction may be based on the sensory char-
acteristics of qualities of food, such as extreme sensitivity to appearance, color, smell,
texture, temperature, or taste. Such behavior has been described as “restrictive eating,”
“selective eating,” “choosy eating,” “perseverant eating,” “chronic food refusal,” and
“food neophobia” and may manifest as refusal to eat particular brands of foods or to tol-
erate the smell of food being eaten by others. Individuals with heightened sensory sensi-
tivities associated with autism may show similar behaviors.
Food avoidance or restriction may also represent a conditioned negative response as-
sociated with food intake following, or in anticipation of, an aversive experience, such as
choking; a traumatic investigation, usually involving the gastrointestinal tract (e.g., esoph-
agoscopy); or repeated vomiting. The terms functional dysphagia and globus hystericus have
also been used for such conditions.
won
Associated Features Supporting Diagnosis
Several features may be associated with food avoidance or reduced food intake, including
a lack of interest in eating or food, leading to weight loss or faltering growth. Very young
infants may present as being too sleepy, distressed, or agitated to feed. Infants and young
children may not engage with the primary caregiver during feeding or communicate hun-
ger in favor of other activities. In older children and adolescents, food avoidance or restric-
tion may be associated with more generalized emotional difficulties that do not meet
diagnostic criteria for an anxiety, depressive, or bipolar disorder, sometimes called “food
avoidance emotional disorder.”
Development and Course
Food avoidance or restriction associated with insufficient intake or lack of interest in eat-
ing most commonly develops in infancy or early childhood and may persist in adulthood.
Likewise, avoidance based on sensory characteristics of food tends to arise in the first de-
cade of life but may persist into adulthood. Avoidance related to aversive consequences
can arise at any age. The scant literature regarding long-term outcomes suggests that food
avoidance or restriction based on sensory aspects is relatively stable and long-standing,
but when persisting into adulthood, such avoidance/ restriction can be associated with rel-
atively normal functioning. There is currently insufficient evidence directly linking avoid-
ant/restrictive food intake disorder and subsequent onset of an eating disorder.
Infants with avoidant/restrictive food intake disorder may be irritable and difficult to
console during feeding, or may appear apathetic and withdrawn. In some instances, par-
ent-child interaction may contribute to the infant's feeding problem (e.g., presenting food
inappropriately, or interpreting the infant’s behavior as an act of aggression or rejection).
Inadequate nutritional intake may exacerbate the associated features (e.g., irritability, de-
velopmental lags) and further contribute to feeding difficulties. Associated factors include
infant temperament or developmental impairments that reduce an infant's responsiveness
to feeding. Coexisting parental psychopathology, or child abuse or neglect, is suggested if
feeding and weight improve in response to changing caregivers. In infants, children, and
prepubertal adolescents, avoidant/restrictive food intake disorder may be associated with
growth delay, and the resulting malnutrition negatively affects development and learning
336 Feeding and Eating Disorders
potential. In older children, adolescents, and adults, social functioning tends to be ad-
versely affected. Regardless of the age, family function may be affected, with heightened
stress at mealtimes and in other feeding or eating contexts involving friends and relatives.
Avoidant/restrictive food intake disorder manifests more commonly in children than
in adults, and there may be a long delay between onset and clinical presentation. Triggers
for presentation vary considerably and include physical, social, and emotional difficulties.
Risk and Prognostic Factors
Temperamental. Anxiety disorders, autism spectrum disorder, obsessive-compulsive
disorder, and attention-deficit/hyperactivity disorder may increase risk for avoidant or
restrictive feeding or eating behavior characteristic of the disorder.
Environmental. Environmental risk factors for avoidant/restrictive food intake disor-
der include familial anxiety. Higher rates of feeding disturbances may occur in children of
mothers with eating disorders.
Genetic and physiological. History of gastrointestinal conditions, gastroesophageal re-
flux disease, vomiting, and a range of other medical problems has been associated with
feeding and eating behaviors characteristic of avoidant/restrictive food intake disorder.
Culture-Reiated Diagnostic Issues
Presentations similar to avoidant/restrictive food intake disorder occur in various popu-
lations, including in the United States, Canada, Australia, and Europe. Avoidant/restrictive
food intake disorder should not be diagnosed when avoidance of food intake is solely re-
lated to specific religious or cultural practices.
Gender-Reiated Diagnostic Issues
Avoidant/restrictive food intake disorder is equally common in males and females in in-
fancy and early childhood, but avoidant/restrictive food intake disorder comorbid with
autism spectrum disorder has a male predominance. Food avoidance or restriction related
to altered sensory sensitivities can occur in some physiological conditions, most notably
pregnancy, but is not usually extreme and does not meet full criteria for the disorder.
Diagnostic Markers
Diagnostic markers include malnutrition, low weight, growth delay, and the need for ar-
tificial nutrition in the absence of any clear medical condition other than poor intake.
Functionai Consequences of Avoidant/Restrictive
Food Intake Disorder
Associated developmental and functional limitations include impairment of physical de-
velopment and social difficulties that can have a significant negative impact on family
function.
Differentiai Diagnosis
Appetite loss preceding restricted intake is a nonspecific symptom that can accompany a
number of mental diagnoses. Avoidant/restrictive food intake disorder can be diagnosed
concurrently with the disorders below if all criteria are met, and the eating disturbance re-
quires specific clinical attention.
Other medical conditions (e.g., gastrointestinal disease, food allergies and intoler-
ances, occult malignancies). Restriction of food intake may occur in other medical condi-
Avoidant/Restrictive Food Intake Disorder 337
tions, especially those with ongoing symptoms such as vomiting, loss of appetite, nausea, ab-
dominal pain, or diarrhea. A diagnosis of avoidant/ restrictive food intake disorder requires
that the disturbance of intake is beyond that directly accounted for by physical symptoms con-
sistent with a medical condition; the eating disturbance may also persist after being triggered
by a medical condition and following resolution of the medical condition.
Underlying medical or comorbid mental conditions may complicate feeding and eating.
Because older individuals, postsurgical patients, and individuals receiving chemotherapy
often lose their appetite, an additional diagnosis of avoidant/ restrictive food intake dis-
order requires that the eating disturbance is a primary focus for intervention.
Specific neurological/neuromuscular, structural, or congenital disorders and condi-
tions associated with feeding difficulties. Feeding difficulties are common in a number
of congenital and neurological conditions often related to problems with oral/esophageal/
pharyngeal structure and function, such as hypotonia of musculature, tongue protrusion,
and unsafe swallowing. Avoidant/restrictive food intake disorder can be diagnosed in in-
dividuals with such presentations as long as all diagnostic criteria are met.
Reactive attachment disorder. Some degree of withdrawal is characteristic of reactive
attachment disorder and can lead to a disturbance in the caregiver-child relationship that
can affect feeding and the child’s intake. Avoidant/ restrictive food intake disorder should
be diagnosed concurrently only if all criteria are met for both disorders and the feeding
disturbance is a primary focus for intervention.
Autism spectrum disorder. Individuals with autism spectrum disorder often present with
rigid eating behaviors and heightened sensory sensitivities. However, these features do
not always result in the level of impairment that would be required for a diagnosis of
avoidant/ restrictive food intake disorder. Avoidant/ restrictive food intake disorder should
be diagnosed concurrently only if all criteria are met for both disorders and when the eat-
ing disturbance requires specific treatment.
Specific phobia, social anxiety disorder (social phobia), and other anxiety disorders.
Specific phobia, other type, specifies “situations that may lead to choking or vomiting” and
can represent the primary trigger for the fear, anxiety, or avoidance required for diagnosis.
Distinguishing specific phobia from avoidant/restrictive food intake disorder can be dif-
ficult when a fear of choking or vomiting has resulted in food avoidance. Although avoid-
ance or restriction of food intake secondary to a pronounced fear of choking or vomiting
can be conceptualized as specific phobia, in situations when the eating problem becomes
the primary focus of clinical attention, avoidant/ restrictive food intake disorder becomes
the appropriate diagnosis. In social anxiety disorder, the individual may present with a
fear of being observed by others while eating, which can also occur in avoidant/ restrictive
food intake disorder.
Anorexia nervosa. Restriction of energy intake relative to requirements leading to sig-
nificantly low body weight is a core feature of anorexia nervosa. However, individuals
with anorexia nervosa also display a fear of gaining weight or of becoming fat, or persis-
tent behavior that interferes with weight gain, as well as specific disturbances in relation to
perception and experience of their own body weight and shape. These features are not
present in avoidant/restrictive food intake disorder, and the two disorders should not be
diagnosed concurrently. Differential diagnosis between avoidant/ restrictive food intake
disorder and anorexia nervosa may be difficult, especially in late childhood and early ad-
olescence, because these disorders may share a number of common symptoms (e.g., food
avoidance, low weight). Differential diagnosis is also potentially difficult in individuals
with anorexia nervosa who deny any fear of fatness but nonetheless engage in persistent
behaviors that prevent weight gain and who do not recognize the medical seriousness of
their low weight—a presentation sometimes termed “non-fat phobic anorexia nervosa.”
Full consideration of symptoms, course, and family history is advised, and diagnosis may
338 Feeding and Eating Disorders
be best made in the context of a clinical relationship over time. In some individuals, avoid-
ant/restrictive food intake disorder might precede the onset of anorexia nervosa.
Obsessive-compulsive disorder. Individuals with obsessive-compulsive disorder may
present with avoidance or restriction of intake in relation to preoccupations with food or
ritualized eating behavior. Avoidant/ restrictive food intake disorder should be diagnosed
concurrently only if all criteria are met for both disorders and when the aberrant eating is
a major aspect of the clinical presentation requiring specific intervention.
Major depressive disorder. In major depressive disorder, appetite might be affected to
such an extent that individuals present with significantly restricted food intake, usually in
relation to overall energy intake and often associated with weight loss. Usually appetite
loss and related reduction of intake abate with resolution of mood problems. Avoidant/
restrictive food intake disorder should only be used concurrently if full criteria are met for
both disorders and when the eating disturbance requires specific treatment.
Schizophrenia spectrum disorders. Individuals with schizophrenia, delusional disor-
der, or other psychotic disorders may exhibit odd eating behaviors, avoidance of specific
foods because of delusional beliefs, or other manifestations of avoidant or restrictive in-
take. In some cases, delusional beliefs may contribute to a concern about negative conse-
quences of ingesting certain foods. Avoidant/restrictive food intake disorder should be
used concurrently only if all criteria are met for both disorders and when the eating dis-
turbance requires specific treatment.
Factitious disorder or factitious disorder imposed on another. Avoidant/restrictive
food intake disorder should be differentiated from factitious disorder or factitious disor-
der imposed on another. In order to assume the sick role, some individuals with factitious
disorder may intentionally describe diets that are much more restrictive than those they
are actually able to consume, as well as complications of such behavior, such as a need for
enteral feedings or nutritional supplements, an inability to tolerate a normal range of
foods, and/or an inability to participate normally in age-appropriate situations involving
food. The presentation may be impressively dramatic and engaging, and the symptoms re-
ported inconsistently. In factitious disorder imposed on another, the caregiver describes
symptoms consistent with avoidant/restrictive food intake disorder and may induce
physical symptoms such as failure to gain weight. As with any diagnosis of factitious dis-
order imposed on another, the caregiver receives the diagnosis rather than the affected in-
dividual, and diagnosis should be made only on the basis of a careful, comprehensive
assessment of the affected individual, the caregiver, and their interaction.
Comorbidity
The most commonly observed disorders comorbid with avoidant/restrictive food intake
disorder are anxiety disorders, obsessive-compulsive disorder, and neurodevelopmental
disorders (specifically autism spectrum disorder, attention-deficit/hyperactivity disor-
der, and intellectual disability [intellectual developmental disorder]}.
Anorexia Nervosa
Diagnostic Criteria
A. Restriction of energy intake relative to requirements, leading to a significantly tow body
weight in the context of age, sex, developmental trajectory, and physical health. Sig-
nificantly low weight is defined as a weight that is less than minimally normal or, for
children and adolescents, less than that minimally expected.
B. Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes
with weight gain, even though at a significantly low weight.
Anorexia Nervosa 339
C. Disturbance in the way in which one’s body weight or shape is experienced, undue in-
fluence of body weight or shape on self-evaluation, or persistent lack of recognition of
the seriousness of the current low body weight.
Coding note: The ICD-9-CM code for anorexia nervosa is 307.1, which is assigned re-
gardless of the subtype. The ICD-10-CM code depends on the subtype (see below).
Specify whether:
(F50.01)} Restricting type: During the last 3 months, the individual has not engaged in re-
current episodes of binge eating or purging behavior (i.e., self-induced vomiting or the mis-
use of laxatives, diuretics, or enemas). This subtype describes presentations in which
weight loss is accomplished primarily through dieting, fasting, and/or excessive exercise.
(F50.02) Binge-eating/purging type: During the last 3 months, the individual has en-
gaged in recurrent episodes of binge eating or purging behavior (i.e., self-induced
vomiting or the misuse of laxatives, diuretics, or enemas).
Specify if:
In partial remission: After full criteria for anorexia nervosa were previously met, Cri-
terion A (low body weight) has not been met for a sustained period, but either Criterion
B (intense fear of gaining weight or becoming fat or behavior that interferes with weight
gain) or Criterion C (disturbances in self-perception of weight and shape) is still met.
In full remission: After full criteria for anorexia nervosa were previously met, none of
the criteria have been met for a sustained period of time.
Specify current severity:
The minimum level of severity is based, for adults, on current body mass index (BMI) (see
below) or, for children and adolescents, on BMI percentile. The ranges below are derived
from World Health Organization categories for thinness in adults; for children and adoles-
cents, corresponding BMI percentiles should be used. The level of severity may be in-
creased to reflect clinical symptoms, the degree of functional disability, and the need for
supervision.
Mild: BMI > 17 kg/m?
Moderate: BMI 16—16.99 kg/m?
Severe: BMI 15—15.99 kg/m?
Extreme: BMI < 15 kg/m?
Subtypes
Most individuals with the binge-eating / purging type of anorexia nervosa who binge eat
also purge through self-induced vomiting or the misuse of laxatives, diuretics, or enemas.
Some individuals with this subtype of anorexia nervosa do not binge eat but do regularly
purge after the consumption of small amounts of food.
Crossover between the subtypes over the course of the disorder is not uncommon;
therefore, subtype description should be used to describe current symptoms rather than
longitudinal course.
Diagnostic Features
There are three essential features of anorexia nervosa: persistent energy intake restriction;
intense fear of gaining weight or of becoming fat, or persistent behavior that interferes
with weight gain; and a disturbance in self-perceived weight or shape. The individual main-
tains a body weight that is below a minimally normal level for age, sex, developmental tra-
jectory, and physical health (Criterion A). Individuals’ body weights frequently meet this
criterion following a significant weight loss, but among children and adolescents, there
may alternatively be failure to make expected weight gain or to maintain a normal devel-
opmental trajectory (i.e., while growing in height) instead of weight loss.
340 Feeding and Eating Disorders
Criterion A requires that the individual’s weight be significantly low (i.e., less than
minimally normal or, for children and adolescents, less than that minimally expected).
Weight assessment can be challenging because normal weight range differs among indi-
viduals, and different thresholds have been published defining thinness or underweight
status. Body mass index (BMI; calculated as weight in kilograms/height in meters’) isa
useful measure to assess body weight for height. For adults, a BMI of 18.5 kg/m? has been
employed by the Centers for Disease Control and Prevention (CDC) and the World Health
Organization (WHO) as the lower limit a normal body weight. Therefore, most adults with
a BMI greater than or equal to 18.5 kg/m? would not be considered 2 have a significantly
low body weight. On the other hand, a BMI of lower than 17.0 kg/ m? has been considered
by the WHO to me moderate or severe thinness; therefore, an individual with a BMI
less than 17.0 kg/m? would likely be considered to have a significant] ly low weight. An
adult with a BMI between 17.0 and 18.5 kg/m7, or even above 18.5 kg/m”, might be consid-
ered to have a significantly low weight if clinical history or other physiological informa-
tion supports this judgment.
For children and adolescents, determining a BMI-for-age percentile is useful (see, e.g.,
the CDC BMI percentile calculator for children and teenagers. As for adults, it is not pos-
sible to provide definitive standards for judging whether a child’s or an adolescent's weight
is significantly low, and variations in developmental trajectories among youth limit the
utility of simple numerical guidelines. The CDC has used a BMI-for-age below the Sth per-
centile as suggesting underweight; however, children and adolescents with a BMI above
this benchmark may be judged to be significantly underweight in light of failure to main-
tain their expected growth trajectory. In summary, in determining whether Criterion A is
met, the clinician should consider available numerical guidelines, as well as the individual's
body build, weight history, and any physiological disturbances.
Individuals with this disorder typically display an intense fear of gaining weight or of
becoming fat (Criterion B). This intense fear of becoming fat is usually not alleviated by
weight loss. In fact, concern about weight gain may increase even as weight falls. Younger
individuals with anorexia nervosa, as well as some adults, may not recognize or acknowl-
edge a fear of weight gain. In the absence of another explanation for the significantly low
weight, clinician inference drawn from collateral history, observational data, physical and
laboratory findings, or longitudinal course either indicating a fear of weight gain or sup-
porting persistent behaviors that prevent it may be used to establish Criterion B.
The experience and significance of body weight and shape are distorted in these indi-
viduals (Criterion C). Some individuals feel globally overweight. Others realize that they
are thin but are still concerned that certain body parts, particularly the abdomen, buttocks,
and thighs, are “too fat.” They may employ a variety of techniques to evaluate their body
size or weight, including frequent weighing, obsessive measuring of body parts, and per-
sistent use of a mirror to check for perceived areas of “fat.” The self-esteem of individuals
with anorexia nervosa is highly dependent on their perceptions of body shape and weight.
Weight loss is often viewed as an impressive achievement and a sign of extraordinary self-
discipline, whereas weight gain is perceived as an unacceptable failure of self-control. Al-
though some individuals with this disorder may acknowledge being thin, they often do
not recognize the serious medical implications of their malnourished state.
Often, the individual is brought to professional attention by family members after marked
weight loss (or failure to make expected weight gains) has occurred. If individuals seek help
on their own, it is usually because of distress over the somatic and psychological sequelae
of starvation. It is rare for an individual with anorexia nervosa to complain of weight loss
per se. In fact, individuals with anorexia nervosa frequently either lack insight into or deny
the problem. It is therefore often important to obtain information from family members or
other sources to evaluate the history of weight loss and other features of the illness.
Anorexia Nervosa 341
Associated Features Supporting Diagnosis
The semi-starvation of anorexia nervosa, and the purging behaviors sometimes associated
with it, can result in significant and potentially life-threatening medical conditions. The
nutritional compromise associated with this disorder affects most major organ systems
and can produce a variety of disturbances. Physiological disturbances, including amenor-
thea and vital sign abnormalities, are common. While most of the physiological distur-
bances associated with malnutrition are reversible with nutritional rehabilitation, some,
including loss of bone mineral density, are often not completely reversible. Behaviors such
as self-induced vomiting and misuse of laxatives, diuretics, and enemas may cause a num-
ber of disturbances that lead to abnormal laboratory findings; however, some individuals
with anorexia nervosa exhibit no laboratory abnormalities.
When seriously underweight, many individuals with anorexia nervosa have depressive
signs and symptoms such as depressed mood, social withdrawal, irritability, insomnia, and
diminished interest in sex. Because these features are also observed in individuals without
anorexia nervosa who are significantly undernourished, many of the depressive features
may be secondary to the physiological sequelae of semi-starvation, although they may also
be sufficiently severe to warrant an additional diagnosis of major depressive disorder.
Obsessive-compulsive features, both related and unrelated to food, are often prominent.
Most individuals with anorexia nervosa are preoccupied with thoughts of food. Some col-
lect recipes or hoard food. Observations of behaviors associated with other forms of star-
vation suggest that obsessions and compulsions related to food may be exacerbated by
undernutrition. When individuals with anorexia nervosa exhibit obsessions and compul-
sions that are not related to food, body shape, or weight, an additional diagnosis of obses-
sive-compulsive disorder (OCD) may be warranted.
Other features sometimes associated with anorexia nervosa include concerns about
eating in public, feelings of ineffectiveness, a strong desire to control one’s environment,
inflexible thinking, limited social spontaneity, and overly restrained emotional ex-
pression. Compared with individuals with anorexia nervosa, restricting type, those with
binge-eating / purging type have higher rates of impulsivity and are more likely to abuse
alcoho] and other drugs.
A subgroup of individuals with anorexia nervosa show excessive levels of physical ac-
tivity. Increases in physical activity often precede onset of the disorder, and over the
course of the disorder increased activity accelerates weight loss. During treatment, exces-
sive activity may be difficult to control, thereby jeopardizing weight recovery.
Individuals with anorexia nervosa may misuse medications, such as by manipulating
dosage, in order to achieve weight loss or avoid weight gain. Individuals with diabetes
mellitus may omit or reduce insulin doses in order to minimize carbohydrate metabolism.
Prevalence
The 12-month prevalence of anorexia nervosa among young females is approximately
0.4%. Less is known about prevalence among males, but anorexia nervosa is far less com-
mon in males than in females, with clinical populations generally reflecting approximately
a 10:1 female-to-male ratio.
Development and Course
Anorexia nervosa commonly begins during adolescence or young adulthood. It rarely be-
gins before puberty or after age 40, but cases of both early and late onset have been de-
scribed. The onset of this disorder is often associated with a stressful life event, such as
leaving home for college. The course and outcome of anorexia nervosa are highly variable.
Younger individuals may manifest atypical features, including denying “fear of fat.” Older
342 Feeding and Eating Disorders
individuals more likely have a longer duration of illness, and their clinical presentation may
include more signs and symptoms of long-standing disorder. Clinicians should not exclude
anorexia nervosa from the differential diagnosis solely on the basis of older age.
Many individuals have a period of changed eating behavior prior to full criteria for the
disorder being met. Some individuals with anorexia nervosa recover fully after a single
episode, with some exhibiting a fluctuating pattern of weight gain followed by relapse,
and others experiencing a chronic course over many years. Hospitalization may be re-
quired to restore weight and to address medical complications. Most individuals with an-
orexia nervosa experience remission within 5 years of presentation. Among individuals
admitted to hospitals, overall remission rates may be lower. The crude mortality rate (CMR)
for anorexia nervosa is approximately 5% per decade. Death most commonly results from
medical complications associated with the disorder itself or from suicide.
Risk and Prognostic Factors
Temperamental. Individuals who develop anxiety disorders or display obsessional
traits in childhood are at increased risk of developing anorexia nervosa.
Environmental. Historical and cross-cultural variability in the prevalence of anorexia
nervosa supports its association with cultures and settings in which thinness is valued. Oc-
cupations and avocations that encourage thinness, such as modeling and elite athletics, are
also associated with increased risk.
Genetic and physiological. There is an increased risk of anorexia nervosa and bulimia
nervosa among first-degree biological] relatives of individuals with the disorder. An in-
creased risk of bipolar and depressive disorders has also been found among first-degree
relatives of individuals with anorexia nervosa, particularly relatives of individuals with
the binge-eating / purging type. Concordance rates for anorexia nervosa in monozygotic
twins are significantly higher than those for dizygotic twins. A range of brain abnormali-
ties has been described in anorexia nervosa using functional imaging technologies (func-
tional magnetic resonance imaging, positron emission tomography). The degree to which
these findings reflect changes associated with malnutrition versus primary abnormalities
associated with the disorder is unclear.
Culture-Related Diagnostic Issues
Anorexia nervosa occurs across culturally and socially diverse populations, although available
evidence suggests cross-cultural variation in its occurrence and presentation. Anorexia ner-
vosa is probably most prevalent in post-industrialized, high-income countries such as in the
United States, many European countries, Australia, New Zealand, and Japan, but its incidence
in most low- and middle-income countries is uncertain. Whereas the prevalence of anorexia
nervosa appears comparatively low among Latinos, African Americans, and Asians in the
United States, clinicians should be aware that mental health service utilization among individ-
uals with an eating disorder is significantly lower in these ethnic groups and that the low rates
may reflect an ascertainment bias. The presentation of weight concerns among individuals
with eating and feeding disorders varies substantially across cultural contexts. The absence of
an expressed intense fear of weight gain, sometimes referred to as “fat phobia,” appears to be
relatively more common in populations in Asia, where the rationale for dietary restriction is
commonly related to a more culturally sanctioned complaint such as gastrointestinal discom-
fort. Within the United States, presentations without a stated intense fear of weight gain may
be comparatively more common among Latino groups.
Diagnostic Markers
The following laboratory abnormalities may be observed in anorexia nervosa; their pres-
ence may serve to increase diagnostic confidence.
Anorexia Nervosa 343
Hematology. Leukopenia is common, with the loss of all cell types but usually with ap-
parent lymphocytosis. Mild anemia can occur, as well as thrombocytopenia and, rarely,
bleeding problems.
Serum chemistry. Dehydration may be reflected by an elevated blood urea nitrogen
level. Hypercholesterolemia is common. Hepatic enzyme levels may be elevated. Hypo-
magnesemia, hypozincemia, hypophosphatemia, and hyperamylasemia are occasionally
observed. Self-induced vomiting may lead to metabolic alkalosis (elevated serum bicarbon-
ate), hypochloremia, and hypokalemia; laxative abuse may cause a mild metabolic acidosis.
Endocrine. Serum thyroxine (T4) levels are usually in the low-normal range; triiodothy-
ronine (T3) levels are decreased, while reverse T3 levels are elevated. Females have low se-
rum estrogen levels, whereas males have low levels of serum testosterone.
Electrocardiography. Sinus bradycardia is common, and, rarely, arrhythmias are noted.
Significant prolongation of the QTc interval is observed in some individuals.
Bone mass. Low bone mineral density, with specific areas of osteopenia or osteoporo-
sis, is often seen. The risk of fracture is significantly elevated.
Electroencephalography. Diffuse abnormalities, reflecting a metabolic encephalopa-
thy, may result from significant fluid and electrolyte disturbances.
Resting energy expenditure. There is often a significant reduction in resting energy ex-
penditure.
Physical signs and symptoms. Many of the physical signs and symptoms of anorexia
nervosa are attributable to starvation. Amenorrhea is commonly present and appears to
be an indicator of physiological dysfunction. If present, amenorrhea is usually a conse-
quence of the weight loss, but in a minority of individuals it may actually precede the
weight loss. In prepubertal females, menarche may be delayed. In addition to amenorrhea,
there may be complaints of constipation, abdominal pain, cold intolerance, lethargy, and
excess energy.
The most remarkable finding on physical examination is emaciation. Commonly, there
is also significant hypotension, hypothermia, and bradycardia. Some individuals develop
lanugo, a fine downy body hair. Some develop peripheral edema, especially during
weight restoration or upon cessation of laxative and diuretic abuse. Rarely, petechiae or
ecchymoses, usually on the extremities, may indicate a bleeding diathesis. Some individ-
uals evidence a yellowing of the skin associated with hypercarotenemia. As may be seen in
individuals with bulimia nervosa, individuals with anorexia nervosa who self-induce
vomiting may have hypertrophy of the salivary glands, particularly the parotid glands, as
well as dental enamel erosion. Some individuals may have scars or calluses on the dorsal
surface of the hand from repeated contact with the teeth while inducing vomiting.
Suicide Risk
Suicide risk is elevated in anorexia nervosa, with rates reported as 12 per 100,000 per year.
Comprehensive evaluation of individuals with anorexia nervosa should include assess-
ment of suicide-related ideation and behaviors as well as other risk factors for suicide, in-
cluding a history of suicide attempt{s).
Functional Consequences of Anorexia Nervosa
Individuals with anorexia nervosa may exhibit a range of functional limitations associated
with the disorder. While some individuals remain active in social and professional func-
tioning, others demonstrate significant social isolation and/or failure to fulfill academic or
career potential.
344 Feeding and Eating Disorders
Differential Diagnosis
Other possible causes of either significantly low body weight or significant weight loss
should be considered in the differential diagnosis of anorexia nervosa, especially when the
presenting features are atypical (e.g., onset after age 40 years).
Medical conditions (e.g., gastrointestinal disease, hyperthyroidism, occult malignan-
cies, and acquired immunodeficiency syndrome [AIDS]). Serious weight loss may oc-
cur in medical conditions, but individuals with these disorders usually do not also mani-
fest a disturbance in the way their body weight or shape is experienced or an intense fear
of weight gain or persist in behaviors that interfere with appropriate weight gain. Acute
weight loss associated with a medical condition can occasionally be followed by the onset
or recurrence of anorexia nervosa, which can initially be masked by the comorbid medical
condition. Rarely, anorexia nervosa develops after bariatric surgery for obesity.
Major depressive disorder. In major depressive disorder, severe weight loss may occur,
but most individuals with major depressive disorder do not have either a desire for exces-
sive weight loss or an intense fear of gaining weight.
Schizophrenia. Individuals with schizophrenia may exhibit odd eating behavior and oc-
casionally experience significant weight loss, but they rarely show the fear of gaining
weight and the body image disturbance required for a diagnosis of anorexia nervosa.
Substance use disorders. Individuals with substance use disorders may experience low
weight due to poor nutritional intake but generally do not fear gaining weight and do not
manifest body image disturbance. Individuals who abuse substances that reduce appetite
(e.g., cocaine, stimulants) and who also endorse fear of weight gain should be carefully
evaluated for the possibility of comorbid anorexia nervosa, given that the substance use
may represent a persistent behavior that interferes with weight gain (Criterion B).
Social anxiety disorder (social phobia), obsessive-compulsive disorder, and body dys-
morphic disorder. Some of the features of anorexia nervosa overlap with the criteria for
social phobia, OCD, and body dysmorphic disorder. Specifically, individuals may feel hu-
miliated or embarrassed to be seen eating in public, as in social phobia; may exhibit obses-
sions and compulsions related to food, as in OCD; or may be preoccupied with an imagined
defect in bodily appearance, as in body dysmorphic disorder. If the individual with anorexia
nervosa has social fears that are limited to eating behavior alone, the diagnosis of social pho-
bia should not be made, but social fears unrelated to eating behavior (e.g., excessive fear of
speaking in public) may warrant an additional diagnosis of social phobia. Similarly, an ad-
ditional diagnosis of OCD should be considered only if the individual exhibits obsessions
and compulsions unrelated to food (e.g., an excessive fear of contamination), and an addi-
tional diagnosis of body dysmorphic disorder should be considered only if the distortion is
unrelated to body shape and size (e.g., preoccupation that one’s nose is too big).
Bulimia nervosa. Individuals with bulimia nervosa exhibit recurrent episodes of binge
eating, engage in inappropriate behavior to avoid weight gain (e.g., self-induced vomit-
ing), and are overly concerned with body shape and weight. However, unlike individuals
with anorexia nervosa, binge-eating / purging type, individuals with bulimia nervosa main-
tain body weight at or above a minimally normal level.
Avoidant/restrictive food intake disorder. Individuals with this disorder may exhibit
significant weight loss or significant nutritional deficiency, but they do not have a fear of
gaining weight or of becoming fat, nor do they have a disturbance in the way they expe-
rience their body shape and weight.
Comorbidity
Bipolar, depressive, and anxiety disorders commonly co-occur with anorexia nervosa.
Many individuals with anorexia nervosa report the presence of either an anxiety disorder
Bulimia Nervosa 345
or symptoms prior to onset of their eating disorder. OCD is described in some individuals
with anorexia nervosa, especially those with the restricting type. Alcohol use disorder and
other substance use disorders may also be comorbid with anorexia nervosa, especially
among those with the binge-eating / purging type.
Bulimia Nervosa
Diagnostic Criteria 307.51 (F50.2)
A. Recurrent episodes of binge eating. An episode of binge eating is characterized by
both of the following:
1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of
food that is definitely larger than what most individuals would eat in a similar period
of time under similar circumstances.
2. A sense of lack of control over eating during the episode (e.g., a feeling that one
cannot stop eating or control what or how much one is eating).
B. Recurrent inappropriate compensatory behaviors in order to prevent weight gain, such
as self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting;
or excessive exercise.
C. The binge eating and inappropriate compensatory behaviors both occur, on average,
at least once a week for 3 months.
D. Self-evaluation is unduly influenced by body shape and weight.
E. The disturbance does not occur exclusively during episodes of anorexia nervosa.
Specify if:
In partial remission: After full criteria for bulimia nervosa were previously met, some,
but not all, of the criteria have been met for a sustained period of time.
In full remission: After full criteria for bulimia nervosa were previously met, none of
the criteria have been met for a sustained period of time.
Specify current severity:
The minimum levet of severity is based on the frequency of inappropriate compensatory
behaviors (see below). The level of severity may be increased to reflect other symptoms
and the degree of functional disability.
Mild: An average of 1—3 episodes of inappropriate compensatory behaviors per week.
Moderate: An average of 4—7 episodes of inappropriate compensatory behaviors per
week.
Severe: An average of 8—13 episodes of inappropriate compensatory behaviors per
week.
Extreme: An average of 14 or more episodes of inappropriate compensatory behav-
iors per week.
Diagnostic Features
There are three essential features of bulimia nervosa: recurrent episodes of binge eating
(Criterion A), recurrent inappropriate compensatory behaviors to prevent weight gain
(Criterion B), and self-evaluation that is unduly influenced by body shape and weight
(Criterion D). To qualify for the diagnosis, the binge eating and inappropriate compensa-
tory behaviors must occur, on average, at least once per week for 3 months (Criterion C).
An “episode of binge eating” is defined as eating, in a discrete period of time, an
amount of food that is definitely larger than most individuals would eat in a similar period
of time under similar circumstances (Criterion A1). The context in which the eating occurs
346 Feeding and Eating Disorders
may affect the clinician’s estimation of whether the intake is excessive. For example, a
quantity of food that might be regarded as excessive for a typical meal might be consid-
ered normal during a celebration or holiday meal. A “discrete period of time” refers to a
limited period, usually less than 2 hours. A single episode of binge eating need not be re-
stricted to one setting. For example, an individual may begin a binge in a restaurant and
then continue to eat on returning home. Continual snacking on small amounts of food
throughout the day would not be considered an eating binge.
An occurrence of excessive food consumption must be accompanied by a sense of lack
of control (Criterion A2) to be considered an episode of binge eating. An indicator of loss
of control is the inability to refrain from eating or to stop eating once started. Some indi-
viduals describe a dissociative quality during, or following, the binge-eating episodes. The
impairment in control associated with binge eating may not be absolute; for example, an
individual may continue binge eating while the telephone is ringing but will cease if a
roommate or spouse unexpectedly enters the room. Some individuals report that their
binge-eating episodes are no longer characterized by an acute feeling of loss of control but
rather by a more generalized pattern of uncontrolled eating. If individuals report that they
have abandoned efforts to control their eating, loss of control should be considered as
present. Binge eating can also be planned in some instances.
The type of food consumed during binges varies both across individuals and for a
given individual. Binge eating appears to be characterized more by an abnormality in the
amount of food consumed than by a craving for a specific nutrient. However, during binges,
individuals tend to eat foods they would otherwise avoid.
Individuals with bulimia nervosa are typically ashamed of their eating problems and
attempt to conceal their symptoms. Binge eating usually occurs in secrecy or as inconspic-
uously as possible. The binge eating often continues until the individual is uncomfortably,
or even painfully, full. The most common antecedent of binge eating is negative affect.
Other triggers include interpersonal stressors; dietary restraint; negative feelings related
to body weight, body shape, and food; and boredom. Binge eating may minimize or mit-
igate factors that precipitated the episode in the short-term, but negative self-evaluation
and dysphoria often are the delayed consequences.
Another essential feature of bulimia nervosa is the recurrent use of inappropriate com-
pensatory behaviors to prevent weight gain, collectively referred to as purge behaviors or
purging (Criterion B). Many individuals with bulimia nervosa employ several methods to
compensate for binge eating. Vomiting is the most common inappropriate compensatory
behavior. The immediate effects of vomiting include relief from physical discomfort and re-
duction of fear of gaining weight. In some cases, vomiting becomes a goal in itself, and the
individual will binge eat in order to vomit or will vomit after eating a small amount of food.
Individuals with bulimia nervosa may use a variety of methods to induce vomiting, includ-
ing the use of fingers or instruments to stimulate the gag reflex. Individuals generally
become adept at inducing vomiting and are eventually able to vomit at will. Rarely, indi-
viduals consume syrup of ipecac to induce vomiting. Other purging behaviors include the
misuse of laxatives and diuretics. A number of other compensatory methods may also be
used in rare cases. Individuals with bulimia nervosa may misuse enemas following epi-
sodes of binge eating, but this is seldom the sole compensatory method employed. Individ-
uals with this disorder may take thyroid hormone in an attempt to avoid weight gain.
Individuals with diabetes mellitus and bulimia nervosa may omit or reduce insulin doses in
order to reduce the metabolism of food consumed during eating binges. Individuals with
bulimia nervosa may fast for a day or more or exercise excessively in an attempt to prevent
weight gain. Exercise may be considered excessive when it significantly interferes with im-
portant activities, when it occurs at inappropriate times or in inappropriate settings, or
when the individual continues to exercise despite injury or other medical complications.
Individuals with bulimia nervosa place an excessive emphasis on body shape or weight
in their self-evaluation, and these factors are typically extremely important in determining
Bulimia Nervosa 347
self-esteem (Criterion D). Individuals with this disorder may closely resemble those with
anorexia nervosa in their fear of gaining weight, in their desire to lose weight, and in the
level of dissatisfaction with their bodies. However, a diagnosis of bulimia nervosa should
not be given when the disturbance occurs only during episodes of anorexia nervosa (Cri-
terion E).
Associated Features Supporting Diagnosis
Individuals with bulimia nervosa typically are within the normal weight or overweight
range (body mass index [BMI] 2 18.5 and < 30 in adults). The disorder occurs but is un-
common among obese individuals. Between eating binges, individuals with bulimia ner-
vosa typically restrict their total caloric consumption and preferentially select low-calorie
(“diet’’) foods while avoiding foods that they perceive to be fattening or likely to trigger a
binge.
Menstrual irregularity or amenorrhea often occurs among females with bulimia ner-
vosa; it is uncertain whether such disturbances are related to weight fluctuations, to nu-
tritional deficiencies, or to emotional distress. The fluid and electrolyte disturbances
resulting from the purging behavior are sometimes sufficiently severe to constitute med-
ically serious problems. Rare but potentially fatal complications include esophageal tears,
gastric rupture, and cardiac arrhythmias. Serious cardiac and skeletal myopathies have
been reported among individuals following repeated use of syrup of ipecac to induce vom-
iting. Individuals who chronically abuse laxatives may become dependent on their use to
stimulate bowel movements. Gastrointestinal symptoms are commonly associated with
bulimia nervosa, and rectal prolapse has also been reported among individuals with this
disorder.
Prevalence
Twelve-month prevalence of bulimia nervosa among young females is 1%-1.5%. Point
prevalence is highest among young adults since the disorder peaks in older adolescence
and young adulthood. Less is known about the point prevalence of bulimia nervosa in
males, but bulimia nervosa is far less common in males than it is in females, with an ap-
proximately 10:1 female-to-male ratio.
Development and Course
Bulimia nervosa commonly begins in adolescence or young adulthood. Onset before pu-
berty or after age 40 is uncommon. The binge eating frequently begins during or after an
episode of dieting to lose weight. Experiencing multiple stressful life events also can pre-
cipitate onset of bulimia nervosa.
Disturbed eating behavior persists for at least several years in a high percentage of
clinic samples. The course may be chronic or intermittent, with periods of remission
alternating with recurrences of binge eating. However, over longer-term follow-up, the
symptoms of many individuals appear to diminish with or without treatment, although
treatment clearly impacts outcome. Periods of remission longer than 1 year are associated
with better long-term outcome.
Significantly elevated risk for mortality (all-cause and suicide) has been reported for
individuals with bulimia nervosa. The CMR (crude mortality rate) for bulimia nervosa is
nearly 2% per decade.
Diagnostic cross-over from initial bulimia nervosa to anorexia nervosa occurs in a mi-
nority of cases (10%-15%). Individuals who do experience cross-over to anorexia nervosa
commonly will revert back to bulimia nervosa or have multiple occurrences of cross-overs
between these disorders. A subset of individuals with bulimia nervosa continue to binge
eat but no longer engage in inappropriate compensatory behaviors, and therefore their
348 Feeding and Eating Disorders
symptoms meet criteria for binge-eating disorder or other specified eating disorder. Diag-
nosis should be based on the current (i.e., past 3 months) clinical presentation.
Risk and Prognostic Factors
Temperamental. Weight concerns, low self-esteem, depressive symptoms, social anxi-
ety disorder, and overanxious disorder of childhood are associated with increased risk for
the development of bulimia nervosa.
Environmental. Internalization of a thin body ideal has been found to increase risk for
developing weight concerns, which in turn increase risk for the development of bulimia
nervosa. Individuals who experienced childhood sexual or physical abuse are at increased
risk for developing bulimia nervosa.
Genetic and physiological. Childhood obesity and early pubertal maturation increase
risk for bulimia nervosa. Familial transmission of bulimia nervosa may be present, as well
as genetic vulnerabilities for the disorder.
Course modifiers. Severity of psychiatric comorbidity predicts worse long-term outcome
of bulimia nervosa.
Culture-Related Diagnostic Issues
Bulimia nervosa has been reported to occur with roughly similar frequencies in most in-
dustrialized countries, including the United States, Canada, many European countries,
Australia, Japan, New Zealand, and South Africa. In clinical studies of bulimia nervosa in
the United States, individuals presenting with this disorder are primarily white. However,
the disorder also occurs in other ethnic groups and with prevalence comparable to esti-
mated prevalences observed in white samples.
Gender-Related Diagnostic Issues
Bulimia nervosa is far more common in females than in males. Males are especially under-
represented in treatment-seeking samples, for reasons that have not yet been systemati-
cally examined.
Diagnostic Markers
No specific diagnostic test for bulimia nervosa currently exists. However, several labora-
tory abnormalities may occur as a consequence of purging and may increase diagnostic
certainty. These include fluid and electrolyte abnormalities, such as hypokalemia (which
can provoke cardiac arrhythmias), hypochloremia, and hyponatremia. The loss of gastric
acid through vomiting may produce a metabolic alkalosis (elevated serum bicarbonate),
and the frequent induction of diarrhea or dehydration through laxative and diuretic abuse
can cause metabolic acidosis. Some individuals with bulimia nervosa exhibit mildly ele-
vated levels of serum amylase, probably reflecting an increase in the salivary isoenzyme.
Physical examination usually yields no physical findings. However, inspection of the
mouth may reveal significant and permanent loss of dental enamel, especially from lin-
gual surfaces of the front teeth due to recurrent vomiting. These teeth may become
chipped and appear ragged and “moth-eaten.” There may also be an increased frequency
of dental caries. In some individuals, the salivary glands, particularly the parotid glands,
may become notably enlarged. Individuals who induce vomiting by manually stimulating
the gag reflex may develop calluses or scars on the dorsal surface of the hand from re-
peated contact with the teeth. Serious cardiac and skeletal myopathies have been reported
among individuals following repeated use of syrup of ipecac to induce vomiting.
Bulimia Nervosa 349
Suicide Risk
Suicide risk is elevated in bulimia nervosa. Comprehensive evaluation of individuals with
this disorder should include assessment of suicide-related ideation and behaviors as well
as other risk factors for suicide, including a history of suicide attempts.
Functional Consequences of Bulimia Nervosa
Individuals with bulimia nervosa may exhibit a range of functional limitations associated
with the disorder. A minority of individuals report severe role impairment, with the so-
cial-life domain most likely to be adversely affected by bulimia nervosa.
Differential Diagnosis
Anorexia nervosa, binge-eating/purging type. Individuals whose binge-eating behav-
ior occurs only during episodes of anorexia nervosa are given the diagnosis anorexia ner-
vosa, binge-eating/ purging type, and should not be given the additional diagnosis of
bulimia nervosa. For individuals with an initial diagnosis of anorexia nervosa who binge
and purge but whose presentation no longer meets the full criteria for anorexia nervosa,
binge-eating / purging type (e.g., when weight is normal), a diagnosis of bulimia ner-
vosa should be given only when all criteria for bulimia nervosa have been met for at least
3 months.
Binge-eating disorder. Some individuals binge eat but do not engage in regular inap-
propriate compensatory behaviors. In these cases, the diagnosis of binge-eating disorder
should be considered.
Kleine-Levin syndrome. In certain neurological or other medical conditions, such as
Kleine-Levin syndrome, there is disturbed eating behavior, but the characteristic psycho-
logical features of bulimia nervosa, such as overconcern with body shape and weight, are
not present.
Major depressive disorder, with atypical features. Overeating is common in major de-
pressive disorder, with atypical features, but individuals with this disorder do not engage
in inappropriate compensatory behaviors and do not exhibit the excessive concern with
body shape and weight characteristic of bulimia nervosa. If criteria for both disorders are
met, both diagnoses should be given.
Borderline personality disorder. Binge-eating behavior is included in the impulsive be-
havior criterion that is part of the definition of borderline personality disorder. If the cri-
teria for both borderline personality disorder and bulimia nervosa are met, both diagnoses
should be given.
Comorbidity
Comorbidity with mental disorders is common in individuals with bulimia nervosa, with
most experiencing at least one other mental disorder and many experiencing multiple co-
morbidities. Comorbidity is not limited to any particular subset but rather occurs across a
wide range of mental disorders. There is an increased frequency of depressive symptoms
(e.g., low self-esteem) and bipolar and depressive disorders (particularly depressive dis-
orders) in individuals with bulimia nervosa. In many individuals, the mood disturbance
begins at the same time as or following the development of bulimia nervosa, and individ-
uals often ascribe their mood disturbances to the bulimia nervosa. However, in some in-
dividuals, the mood disturbance clearly precedes the development of bulimia nervosa.
There may also be an increased frequency of anxiety symptoms (e.g., fear of social situa-
tions) or anxiety disorders. These mood and anxiety disturbances frequently remit follow-
350 Feeding and Eating Disorders
ing effective treatment of the bulimia nervosa. The lifetime prevalence of substance use,
particularly alcohol or stimulant use, is at least 30% among individuals with bulimia ner-
vosa. Stimulant use often begins in an attempt to control appetite and weight. A substan-
tial percentage of individuals with bulimia nervosa also have personality features that
meet criteria for one or more personality disorders, most frequently borderline personality
disorder.
Binge-Eating Disorder
Diagnostic Criteria 307.51 (F50.8)
A. Recurrent episodes of binge eating. An episode of binge eating is characterized
by both of the following:
1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of
food that is definitely larger than what most people would eat in a similar period of
time under similar circumstances.
2. A sense of lack of control over eating during the episode (e.g., a feeling that one
cannot stop eating or control what or how much one is eating).
B. The binge-eating episodes are associated with three (or more) of the following:
Eating much more rapidly than normal.
Eating until feeling uncomfortably full.
Eating large amounts of food when not feeling physically hungry.
Eating alone because of feeling embarrassed by how much one is eating.
5. Feeling disgusted with oneself, depressed, or very guilty afterward.
Phe
. Marked distress regarding binge eating is present.
. The binge eating occurs, on average, at least once a week for 3 months.
. The binge eating is not associated with the recurrent use of inappropriate compensa-
tory behavior as in bulimia nervosa and does not occur exclusively during the course
of bulimia nervosa or anorexia nervosa.
Specify if:
In partial remission: After full criteria for binge-eating disorder were previously met,
binge eating occurs at an average frequency of less than one episode per week for a
sustained period of time.
In full remission: After full criteria for binge-eating disorder were previously met, none
of the criteria have been met for a sustained period of time.
Specify current severity:
The minimum level of severity is based on the frequency of episodes of binge eating (see
below). The level of severity may be increased to reflect other symptoms and the degree
of functional disability.
Mild: 1—3 binge-eating episodes per week.
Moderate: 4—7 binge-eating episodes per week.
Severe: 8-13 binge-eating episodes per week.
Extreme: 14 or more binge-eating episodes per week.
moo
Diagnostic Features
The essential feature of binge-eating disorder is recurrent episodes binge eating that must
occur, on average, at least once per week for 3 months (Criterion D). An “episode of binge
eating” is defined as eating, in a discrete period of time, an amount of food that is defi-
Binge-Eating Disorder 351
nitely larger than most people would eat in a similar period of time under similar circum-
stances (Criterion A1). The context in which the eating occurs may affect the clinician’s
estimation of whether the intake is excessive. For example, a quantity of food that might be
regarded as excessive for a typical meal might be considered normal during a celebration
or holiday meal. A “discrete period of time” refers to a limited period, usually less than
2 hours. A single episode of binge eating need not be restricted to one setting. For example,
an individual may begin a binge in a restaurant and then continue to eat on returning
home. Continual snacking on small amounts of food throughout the day would not be con-
sidered an eating binge.
An occurrence of excessive food consumption must be accompanied by a sense of lack
of control (Criterion A2) to be considered an episode of binge eating. An indicator of loss
of control is the inability to refrain from eating or to stop eating once started. Some indi-
viduals describe a dissociative quality during, or following, the binge-eating episodes. The
impairment in control associated with binge eating may not be absolute; for example, an
individual may continue binge eating while the telephone is ringing but will cease if a
roommate or spouse unexpectedly enters the room. Some individuals report that their
binge-eating episodes are no longer characterized by an acute feeling of loss of control but
rather by a more generalized pattern of uncontrolled eating. If individuals report that they
have abandoned efforts to control their eating, loss of control may still be considered as
present. Binge eating can also be planned in some instances.
The type of food consumed during binges varies both across individuals and for a given
individual. Binge eating appears to be characterized more by an abnormality in the amount
of food consumed than by a craving for a specific nutrient.
Binge eating must be characterized by marked distress (Criterion C) and at least three
of the following features: eating much more rapidly than normal; eating until feeling un-
comfortably full; eating large amounts of food when not feeling physically hungry; eating
alone because of feeling embarrassed by how much one is eating; and feeling disgusted
with oneself, depressed, or very guilty afterward (Criterion B).
Individuals with binge-eating disorder are typically ashamed of their eating problems
and attempt to conceal their symptoms. Binge eating usually occurs in secrecy or as incon-
spicuously as possible. The most common antecedent of binge eating is negative affect.
Other triggers include interpersonal stressors; dietary restraint; negative feelings related
to body weight, body shape, and food; and boredom. Binge eating may minimize or mit-
igate factors that precipitated the episode in the short-term, but negative self-evaluation
and dysphoria often are the delayed consequences.
Associated Features Supporting Dlagnosis
Binge-eating disorder occurs in normal-weight/overweight and obese individuals. It is re-
liably associated with overweight and obesity in treatment-seeking individuals. Never-
theless, binge-eating disorder is distinct from obesity. Most obese individuals do not
engage in recurrent binge eating. In addition, compared with weight-matched obese indi-
viduals without binge-eating disorder, those with the disorder consume more calories in
laboratory studies of eating behavior and have greater functional impairment, lower qual-
ity of life, more subjective distress, and greater psychiatric comorbidity.
Prevalence
Twelve-month prevalence of binge-eating disorder among U.S. adult (age 18 or older) fe-
males and males is 1.6% and 0.8%, respectively. The gender ratio is far less skewed in binge-
eating disorder than in bulimia nervosa. Binge-eating disorder is as prevalent among fe-
males from racial or ethnic minority groups as has been reported for white females. The
disorder is more prevalent among individuals seeking weight-loss treatment than in the
general population.
352 Feeding and Eating Disorders
Development and Course
Little is known about the development of binge-eating disorder. Both binge eating and
loss-of-control eating without objectively excessive consumption occur in children and are
associated with increased body fat, weight gain, and increases in psychological symptoms.
Binge eating is common in adolescent and college-age samples. Loss-of-control eating or
episodic binge eating may represent a prodromal phase of eating disorders for some indi-
viduals.
Dieting follows the development of binge eating in many individuals with binge-
eating disorder. (This is in contrast to bulimia nervosa, in which dysfunctional dieting
usually precedes the onset of binge eating.) Binge-eating disorder typically begins in ad-
olescence or young adulthood but can begin in later adulthood. Individuals with binge-
eating disorder who seek treatment usually are older than individuals with either bulimia
nervosa or anorexia nervosa who seek treatment.
Remission rates in both natural course and treatment outcome studies are higher for
binge-eating disorder than for bulimia nervosa or anorexia nervosa. Binge-eating disorder
appears to be relatively persistent, and the course is comparable to that of bulimia nervosa
in terms of severity and duration. Crossover from binge-eating disorder to other eating
disorders is uncommon.
Risk and Prognostic Factors
Genetic and physiological. Binge-eating disorder appears to run in families, which may
reflect additive genetic influences.
Culture-Reiated Diagnostic Issues
Binge-eating disorder occurs with roughly similar frequencies in most industrialized
countries, including the United States, Canada, many European countries, Australia, and
New Zealand. In the United States, the prevalence of binge-eating disorder appears com-
parable among non-Latino whites, Latinos, Asians, and African Americans.
Functionai Consequences of Binge-Eating Disorder
Binge-eating disorder is associated with a range of functional consequences, including so-
cial role adjustment problems, impaired health-related quality of life and life satisfaction,
increased medical morbidity and mortality, and associated increased health care utiliza-
tion compared with body mass index (BMI)—-matched control subjects. It may also be as-
sociated with an increased risk for weight gain and the development of obesity.
Differential Diagnosis
Bulimia nervosa. Binge-eating disorder has recurrent binge eating in common with bu-
limia nervosa but differs from the latter disorder in some fundamental respects. In terms of
clinical presentation, the recurrent inappropriate compensatory behavior (e.g., purging,
driven exercise) seen in bulimia nervosa is absent in binge-eating disorder. Unlike in-
dividuals with bulimia nervosa, individuals with binge-eating disorder typically do not
show marked or sustained dietary restriction designed to influence body weight and
shape between binge-eating episodes. They may, however, report frequent attempts at
dieting. Binge-eating disorder also differs from bulimia nervosa in terms of response to treat-
ment. Rates of improvement are consistently higher among individuals with binge-eating
disorder than among those with bulimia nervosa.
Obesity. Binge-eating disorder is associated with overweight and obesity but has
several key features that are distinct from obesity. First, levels of overvaluation of body
Other Specified Feeding or Eating Disorder 353
weight and shape are higher in obese individuals with the disorder than in those without
the disorder. Second, rates of psychiatric comorbidity are significantly higher among
obese individuals with the disorder compared with those without the disorder. Third, the
long-term successful outcome of evidence-based psychological treatments for binge-
eating disorder can be contrasted with the absence of effective long-term treatments for
obesity.
Bipolar and depressive disorders. Increases in appetite and weight gain are included
in the criteria for major depressive episode and in the atypical features specifiers for de-
pressive and bipolar disorders. Increased eating in the context of a major depressive epi-
sode may or may not be associated with loss of control. If the full criteria for both disorders
are met, both diagnoses can be given. Binge eating and other symptoms of disordered eat-
ing are seen in association with bipolar disorder. If the full criteria for both disorders are
met, both diagnoses should be given.
Borderline personality disorder. Binge eating is included in the impulsive behavior cri-
terion that is part of the definition of borderline personality disorder. If the full criteria for
both disorders are met, both diagnoses should be given.
Comorbidity
Binge-eating disorder is associated with significant psychiatric comorbidity that is com-
parable to that of bulimia nervosa and anorexia nervosa. The most common comorbid dis-
orders are bipolar disorders, depressive disorders, anxiety disorders, and, to a lesser
degree, substance use disorders. The psychiatric comorbidity is linked to the severity of
binge eating and not to the degree of obesity.
Other Specified Feeding or Eating Disorder
307.59 (F50.8)
This category applies to presentations in which symptoms characteristic of a feeding and
eating disorder that cause clinically significant distress or impairment in social, occupation-
al, or other important areas of functioning predominate but do not meet the full criteria for
any of the disorders in the feeding and eating disorders diagnostic class. The other spec-
ified feeding or eating disorder category is used in situations in which the clinician chooses
to communicate the specific reason that the presentation does not meet the criteria for any
specific feeding and eating disorder. This is done by recording “other specified feeding or
eating disorder’ followed by the specific reason (e.g., “bulimia nervosa of low frequency”).
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Atypical anorexia nervosa: All of the criteria for anorexia nervosa are met, except
that despite significant weight loss, the individual’s weight is within or above the normal
range.
2. Bulimia nervosa (of low frequency and/or limited duration): All of the criteria for
bulimia nervosa are met, except that the binge eating and inappropriate compensatory
behaviors occur, on average, less than once a week and/or for less than 3 months.
3. Binge-eating disorder (of low frequency and/or limited duration): All of the criteria
for binge-eating disorder are met, except that the binge eating occurs, on average, less
than once a week and/or for less than 3 months.
4. Purging disorder: Recurrent purging behavior to influence weight or shape (e.g., self-
induced vomiting; misuse of laxatives, diuretics, or other medications) in the absence
of binge eating.
354 Feeding and Eating Disorders
5. Night eating syndrome: Recurrent episodes of night eating, as manifested by eating
after awakening from sleep or by excessive food consumption after the evening meal.
There is awareness and recall of the eating. The night eating is not better explained by
externai influences such as changes in the individual’s sleep-wake cycle or by local so-
cial norms. The night eating causes significant distress and/or impairment in function-
ing. The disordered pattern of eating is not better explained by binge-eating disorder
or another mental disorder, including substance use, and is not attributable to another
medical disorder or to an effect of medication.
Unspecified Feeding or Eating Disorder
307.50 (F50.9)
This category applies to presentations in which symptoms characteristic of a feeding and
eating disorder that cause clinicalty significant distress or impairment in social, occupation-
al, or other important areas of functioning predominate but do not meet the full criteria for
any of the disorders in the feeding and eating disorders diagnostic class. The unspecified
feeding and eating disorder category is used in situations in which the clinician chooses
not to specify the reason that the criteria are not met for a specific feeding and eating dis-
order, and includes presentations in which there is insufficient information to make a more
specific diagnosis (e.g., in emergency room settings).
Elimination disorders all involve the inappropriate elimination of urine or feces
and are usually first diagnosed in childhood or adolescence. This group of disorders in-
cludes enuresis, the repeated voiding of urine into inappropriate places, and encopresis, the
repeated passage of feces into inappropriate places. Subtypes are provided to differentiate
nocturnal from diurnal (i.e., during waking hours) voiding for enuresis and the presence or
absence of constipation and overflow incontinence for encopresis. Although there are min-
imum age requirements for diagnosis of both disorders, these are based on developmental
age and not solely on chronological age. Both disorders may be voluntary or involuntary.
Although these disorders typically occur separately, co-occurrence may also be observed.
Enuresis
Diagnostic Criteria 307.6 (F98.0)
A. Repeated voiding of urine into bed or clothes, whether involuntary or intentional.
B. The behavior is clinically significant as manifested by either a frequency of at least twice a
week for at least 3 consecutive months or the presence of clinically significant distress or
impairment in social, academic (occupational), or other important areas of functioning.
C. Chronological age is at least 5 years (or equivalent developmental ievel).
D. The behavior is not attributable to the physiological effects of a substance (e.g., a di-
uretic, an antipsychotic medication) or another medical condition (e.g., diabetes, spina
bifida, a seizure disorder).
Specify whether:
Nocturnal only: Passage of urine only during nighttime sleep.
Diurnal only: Passage of urine during waking hours.
Nocturnal and diurnal: A combination of the two subtypes above.
Subtypes
The nocturnal-only subtype of enuresis, sometimes referred to as monosymptomatic enure-
sis, is the most common subtype and involves incontinence only during nighttime sleep,
typically during the first one-third of the night. The diurnal-only subtype occurs in the
absence of nocturnal enuresis and may be referred to simply as urinary incontinence. Indi-
viduals with this subtype can be divided into two groups. Individuals with “urge incon-
tinence” have sudden urge symptoms and detrusor instability, whereas individuals with
“voiding postponement” consciously defer micturition urges until incontinence results.
The nocturnal-and-diurnal subtype is also known as nonmonosymptomatic enuresis.
Diagnostic Features
The essential feature of enuresis is repeated voiding of urine during the day or at night into
bed or clothes (Criterion A). Most often the voiding is involuntary, but occasionally it may
355
356 Elimination Disorders
be intentional. To qualify for a diagnosis of enuresis, the voiding of urine must occur at
least twice a week for at least 3 consecutive months or must cause clinically significant dis-
tress or impairment in social, academic (occupational), or other important areas of func-
tioning (Criterion B). The individual must have reached an age at which continence is
expected (i.e., a chronological age of at least 5 years or, for children with developmental
delays, a mental age of at least 5 years) (Criterion C). The urinary incontinence is not at-
tributable to the physiological effects of a substance (e.g., a diuretic, an antipsychotic med-
ication) or another medical condition (e.g., diabetes, spina bifida, a seizure disorder)
(Criterion D).
Associated Features Supporting Diagnosis
During nocturnal enuresis, occasionally the voiding takes place during rapid eye movement
(REM) sleep, and the child may recall a dream that involved the act of urinating. During day-
time (diurnal) enuresis, the child defers voiding until incontinence occurs, sometimes because
of a reluctance to use the toilet as a result of social anxiety or a preoccupation with school or
play activity. The enuretic event most commonly occurs in the early afternoon on school days
and may be associated with symptoms of disruptive behavior. The enuresis commonly per-
sists after appropriate treatment of an associated infection.
Prevaience
The prevalence of enuresis is 5%-10% among 5-year-olds, 3%-5% among 10-year-olds,
and around 1% among individuals 15 years or older.
Development and Course
Two types of course of enuresis have been described: a “primary” type, in which the indi-
vidual has never established urinary continence, and a “secondary” type, in which the dis-
turbance develops after a period of established urinary continence. There are no differences
in prevalence of comorbid mental disorders between the two types. By definition, primary
enuresis begins at age 5 years. The most common time for the onset of secondary enuresis
is between ages 5 and 8 years, but it may occur at any time. After age 5 years, the rate of spon-
taneous remission is 5%-10% per year. Most children with the disorder become continent
by adolescence, but in approximately 1% of cases the disorder continues into adulthood.
Diurnal enuresis is uncommon after age 9 years. While occasional diurnal incontinence is
not uncommon in middle childhood, it is substantially more common in those who also
have persistent nocturnal enuresis. When enuresis persists into late childhood or adoles-
cence, the frequency of incontinence may increase, whereas continence in early childhood
is usually associated with a declining frequency of wet nights.
Risk and Prognostic Factors
Environmental. A number of predisposing factors for enuresis have been suggested, in-
cluding delayed or lax toilet training and psychosocial stress.
Genetic and physiological. Enuresis has been associated with delays in the develop-
ment of normal circadian rhythms of urine production, with resulting nocturnal polyuria
or abnormalities of central vasopressin receptor sensitivity, and reduced functional blad-
der capacities with bladder hyperreactivity (unstable bladder syndrome). Nocturnal en-
uresis is a genetically heterogeneous disorder. Heritability has been shown in family, twin,
and segregation analyses. Risk for childhood nocturnal enuresis is approximately 3.6 times
higher in offspring of enuretic mothers and 10.1 times higher in the presence of paternal
urinary incontinence. The risk magnitudes for nocturnal enuresis and diurnal incontinence
are similar.
Encopresis 357
Culture-Related Diagnostic Issues
Enuresis has been reported in a variety of European, African, and Asian countries as well
as in the United States. At a national level, prevalence rates are remarkably similar, and
there is great similarity in the developmental trajectories found in different countries.
There are very high rates of enuresis in orphanages and other residential institutions,
likely related to the mode and environment in which toilet training occurs.
Gender-Related Diagnostic Issues
Nocturnal enuresis is more common in males. Diurnal incontinence is more common in fe-
males. The relative risk of having a child who develops enuresis is greater for previously
enuretic fathers than for previously enuretic mothers.
Functional Consequences of Enuresis
The amount of impairment associated with enuresis is a function of the limitation on the
child’s social activities (e.g., ineligibility for sleep-away camp) or its effect on the child’s
self-esteem, the degree of social ostracism by peers, and the anger, punishment, and rejec-
tion on the part of caregivers.
Differential Diagnosis
Neurogenic bladder or another medical condition. The diagnosis of enuresis is not made
in the presence of a neurogenic bladder or another medical condition that causes polyuria or
urgency (e.g., untreated diabetes mellitus or diabetes insipidus) or during an acute urinary
tract infection. However, a diagnosis is compatible with such conditions if urinary inconti-
nence was regularly present prior to the development of another medical condition or if it per-
sists after the institution of appropriate treatment of the medical condition.
Medication side effects. Enuresis may occur during treatment with antipsychotic med-
ications, diuretics, or other medications that may induce incontinence. In this case, the di-
agnosis should not be made in isolation but may be noted as a medication side effect.
However, a diagnosis of enuresis may be made if urinary incontinence was regularly pres-
ent prior to treatment with the medication.
Comorbidity
Although most children with enuresis do not have a comorbid mental disorder, the prevalence
of comorbid behavioral symptoms is higher in children with enuresis than in children without
enuresis. Developmental delays, including speech, language, learning, and motor skills
delays, are also present in a portion of children with enuresis. Encopresis, sleepwalking, and
sleep terror disorder may be present. Urinary tract infections are more common in children
with enuresis, especially the diurnal subtype, than in those who are continent.
Encopresis
Diagnostic Criteria 307.7 (F98.1)
A. Repeated passage of feces into inappropriate places (e.g., clothing, floor), whether in-
voluntary or intentional.
B. Atleast one such event occurs each month for at least 3 months.
C. Chronological age is at least 4 years (or equivalent developmental level).
D. The behavior is not attributable to the physiological effects of a substance (e.g., laxa-
tives) or another medical condition except through a mechanism involving constipation.
358 Elimination Disorders
Specify whether:
With constipation and overflow incontinence: There is evidence of constipation on
physical examination or by history.
Without constipation and overflow incontinence: There is no evidence of constipa-
tion on physical examination or by history.
Subtypes
Feces in the with constipation and overflow incontinence subtype are characteristically
(but not invariably) poorly formed, and leakage can be infrequent to continuous, occur-
ring mostly during the day and rarely during sleep. Only part of the feces is passed during
toileting, and the incontinence resolves after treatment of the constipation.
In the without constipation and overflow incontinence subtype, feces are likely to be of
normal form and consistency, and soiling is intermittent. Feces may be deposited in a
prominent location. This is usually associated with the presence of oppositional defiant
disorder or conduct disorder or may be the consequence of anal masturbation. Soiling
without constipation appears to be less common than soiling with constipation.
Diagnostic Features
The essential feature of encopresis is repeated passage of feces into inappropriate places (e.g.,
clothing or floor) (Criterion A). Most often the passage is involuntary but occasionally may be
intentional. The event must occur at least once a month for at least 3 months (Criterion B), and
the chronological age of the child must be at least 4 years (or for children with developmental
delays, the mental age must be at least 4 years) (Criterion C). The fecal incontinence must not
be exclusively attributable to the physiological effects of a substance (e.g., laxatives) or another
medical condition except through a mechanism involving constipation (Criterion D).
When the passage of feces is involuntary rather than intentional, it is often related to
constipation, impaction, and retention with subsequent overflow. The constipation may
develop for psychological reasons (e.g., anxiety about defecating in a particular place, a
more general pattern of anxious or oppositional behavior), leading to avoidance of defeca-
tion. Physiological predispositions to constipation include ineffectual straining or paradox-
ical defecation dynamics, with contraction rather than relaxation of the external sphincter
or pelvic floor during straining for defecation. Dehydration associated with a febrile ill-
ness, hypothyroidism, or a medication side effect can also induce constipation. Once con-
stipation has developed, it may be complicated by an anal fissure, painful defecation, and
further fecal retention. The consistency of the stool may vary. In some individuals the stool
may be of normal or near-normal consistency. In other individuals—such as those with
overflow incontinence secondary to fecal retention—it may be liquid.
Associated Features Supporting Diagnosis
The child with encopresis often feels ashamed and may wish to avoid situations (e.g.,
camp, school) that might lead to embarrassment. The amount of impairment is a function
of the effect on the child's self-esteem, the degree of social ostracism by peers, and the an-
ger, punishment, and rejection on the part of caregivers. Smearing feces may be deliberate
or accidental, resulting from the child’s attempt to clean or hide feces that were passed in-
voluntarily. When the incontinence is clearly deliberate, features of oppositional defiant
disorder or conduct disorder may also be present. Many children with encopresis and
chronic constipation also have enuresis symptoms and may have associated urinary reflux
in the bladder or ureters that may lead to chronic urinary infections, the symptoms of
which may remit with treatment of the constipation.
Other Specified Elimination Disorder 359
Prevalence
It is estimated that approximately 1% of 5-year-olds have encopresis, and the disorder is
more common in males than in females.
Development and Course
Encopresis is not diagnosed until a child has reached a chronological age of at least 4 years
(or for children with developmental delays, a mental age of at least 4 years). Inadequate,
inconsistent toilet training and psychosocial stress (e.g., entering school, the birth of a sib-
ling) may be predisposing factors. Two types of course have been described: a “primary”
type, in which the individual has never established fecal continence, and a “secondary”
type, in which the disturbance develops after a period of established fecal continence. En-
copresis can persist, with intermittent exacerbations, for years.
Risk and Prognostic Factors
Genetic and physiological. Painful defecation can lead to constipation and a cycle of with-
holding behaviors that make encopresis more likely. Use of some medications (e.g., anti-
convulsants, cough suppressants) may increase constipation and make encopresis more
likely.
Diagnostic Markers
In addition to physical examination, gastrointestinal imaging (e.g., abdominal radiograph)
may be informative to assess retained stool and gas in the colon. Additional tests, such as
barium enema and anorectal manography, may be used to help exclude other medical
conditions, such as Hirschsprung’s disease.
Differential Diagnosis
A diagnosis of encopresis in the presence of another medical condition is appropriate only
if the mechanism involves constipation that cannot be explained by other medical condi-
tions. Fecal incontinence related to other medical conditions (e.g., chronic diarrhea, spina
bifida, anal stenosis) would not warrant a DSM-5 diagnosis of encopresis.
Comorbidity
Urinary tract infections can be comorbid with encopresis and are more common in females.
Other Specified Elimination Disorder
This category applies to presentations in which symptoms characteristic of an elimination
disorder that cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning predominate but do not meet the full criteria for any of
the disorders in the elimination disorders diagnostic class. The other specified elimination
disorder category is used in situations in which the clinician chooses to communicate the
specific reason that the presentation does not meet the criteria for any specific elimination
disorder. This is done by recording “other specified elimination disorder’ followed by the
specific reason (e.g., “low-frequency enuresis’).
Coding note: Code 788.39 (N39.498) for other specified elimination disorder with urinary
symptoms; 787.60 (R15.9) for other specified elimination disorder with fecal symptoms.
360 Elimination Disorders
Unspecified Elimination Disorder
This category applies to presentations in which symptoms characteristic of an elimination
disorder that cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning predominate but do not meet the full criteria for any of
the disorders in the elimination disorders diagnostic class. The unspecified elimination dis-
order category is used in situations in which the clinician chooses not to specify the reason
that the criteria are not met for a specific elimination disorder, and includes presentations
in which there is insufficient information to make a more specific diagnosis (e.g., in emer-
gency room settings).
Coding note: Code 788.30 (R32) for unspecified elimination disorder with urinary symp-
toms; 787.60 (R15.9) for unspecified elimination disorder with fecal symptoms.
The DSM-5 classification of sleep-wake disorders is intended for use by general
mental health and medical clinicians (those caring for adult, geriatric, and pediatric pa-
tients). Sleep-wake disorders encompass 10 disorders or disorder groups: insomnia disor-
der, hypersomnolence disorder, narcolepsy, breathing-related sleep disorders, circadian
rhythm sleep-wake disorders, non-rapid eye movement (NREM) sleep arousal disorders,
nightmare disorder, rapid eye movement (REM) sleep behavior disorder, restless legs syn-
drome, and substance/medication-induced sleep disorder. Individuals with these disor-
ders typically present with sleep-wake complaints of dissatisfaction regarding the quality,
timing, and amount of sleep. Resulting daytime distress and impairment are core features
shared by all of these sleep-wake disorders.
The organization of this chapter is designed to facilitate differential diagnosis of sleep-
wake complaints and to clarify when referral to a sleep specialist is appropriate for further
assessment and treatment planning. The DSM-5 sleep disorders nosology uses a simple,
clinically useful approach, while also reflecting scientific advances in epidemiology, ge-
netics, pathophysiology, assessment, and interventions research since DSM-IV. In some
cases (e.g., insomnia disorder), a “lumping” approach has been adopted, whereas in oth-
ers (e.g., narcolepsy), a “splitting” approach has been taken, reflecting the availability of
validators derived from epidemiological, neurobiological, and interventions research.
Sleep disorders are often accompanied by depression, anxiety, and cognitive changes
that must be addressed in treatment planning and management. Furthermore, persistent
sleep disturbances (both insomnia and excessive sleepiness) are established risk factors for
the subsequent development of mental illnesses and substance use disorders. They may
also represent a prodromal expression of an episode of mental illness, allowing the possi-
bility of early intervention to preempt or to attenuate a full-blown episode.
The differential diagnosis of sleep-wake complaints necessitates a multidimensional
approach, with consideration of possibly coexisting medical and neurological conditions.
Coexisting clinical conditions are the rule, not the exception. Sleep disturbances furnish a
clinically useful indicator of medical and neurological conditions that often coexist with
depression and other common mental disorders. Prominent among these comorbidities
are breathing-related sleep disorders, disorders of the heart and lungs (e.g., congestive
heart failure, chronic obstructive pulmonary disease), neurodegenerative disorders (e.g.,
Alzheimer’s disease), and disorders of the musculoskeletal system (e.g., osteoarthritis).
These disorders not only may disturb sleep but also may themselves be worsened during
sleep (e.g., prolonged apneas or electrocardiographic arrhythmias during REM sleep; con-
fusional arousals in patients with dementing illness; seizures in persons with complex
partial seizures). REM sleep behavior disorder is often an early indicator of neurodegen-
erative disorders (alpha synucleinopathies) like Parkinson’s disease. For all of these rea-
sons—related to differential diagnosis, clinical comorbidity, and facilitation of treatment
planning—sleep disorders are included in DSM-5.
The approach taken to the classification of sleep-wake disorders in DSM-5 can be under-
stood within the context of “lumping versus splitting.” DSM-IV represented an effort to
simplify sleep-wake disorders classification and thus aggregated diagnoses under broader,
less differentiated labels. At the other pole, the International Classification of Sleep Disorders,
361
362 Sleep-Wake Disorders
2nd Edition (ICSD-2) elaborated numerous diagnostic subtypes. DSM-IV was prepared for
use by mental health and general medical clinicians who are not experts in sleep medicine.
ICSD-2 reflected the science and opinions of the sleep specialist community and was pre-
pared for use by specialists.
The weight of available evidence supports the superior performance characteristics
(interrater reliability, as well as convergent, discriminant, and face validity) of simpler, less-
differentiated approaches to diagnosis of sleep-wake disorders. The text accompanying
each set of diagnostic criteria provides linkages to the corresponding disorders included in
ICSD-2. The DSM-5 sleep-wake disorders classification also specifies corresponding non-
psychiatric listings (e.g., neurology codes) from the International Classification of Diseases
(ICD).
The field of sleep disorders medicine has progressed in this direction since the publi-
cation of DSM-IV. The use of biological validators is now embodied in the DSM-5 classi-
fication of sleep-wake disorders, particularly for disorders of excessive sleepiness, such as
narcolepsy; for breathing-related sleep disorders, for which formal sleep studies (i.e.,
polysomnography) are indicated; and for restless legs syndrome, which can often coexist
with periodic limb movements during sleep, detectable via polysomnography.
Insomnia Disorder
Diagnostic Criteria 780.52 (G47.00)
A. A predominant complaint of dissatisfaction with sleep quantity or quality, associated
with one (or more) of the following symptoms:
1. Difficulty initiating sleep. (In children, this may manifest as difficulty initiating sleep
without caregiver intervention.)
2. Difficulty maintaining sleep, characterized by frequent awakenings or problems re-
turning to sleep after awakenings. (In children, this may manifest as difficulty return-
ing to sleep without caregiver intervention.)
3. Early-morning awakening with inability to return to sleep.
ies]
. The sleep disturbance causes clinically significant distress or impairment in social, oc-
cupational, educational, academic, behavioral, or other important areas of functioning.
. The sleep difficulty occurs at least 3 nights per week.
. The sleep difficulty is present for at least 3 months.
. The sleep difficulty occurs despite adequate opportunity for sleep.
. The insomnia is not better explained by and does not occur exclusively during the
course of another sleep-wake disorder (e.g., narcolepsy, a breathing-related sleep dis-
order, a circadian rhythm sleep-wake disorder, a parasomnia).
G. The insomnia is not attributable to the physiological effects of a substance (e.g., a drug
of abuse, a medication).
H. Coexisting mental disorders and medical conditions do not adequately explain the pre-
dominant complaint of insomnia.
Specify if:
With non-sleep disorder mental comorbidity, including substance use disorders
With other medical comorbidity
With other sleep disorder
Coding note: The code 780.52 (G47.00) applies to all three specifiers. Code also the
relevant associated mental disorder, medical condition, or other sleep disorder imme-
diately after the code for insomnia disorder in order to indicate the association.
m™mOQO
Insomnia Disorder 363
Specify if:
Episodic: Symptoms last at least 1 month but less than 3 months.
Persistent: Symptoms last 3 months or longer.
Recurrent: Two (or more) episodes within the space of 1 year.
Note: Acute and short-term insomnia {i.e., symptoms lasting less than 3 months but oth-
erwise meeting all criteria with regard to frequency, intensity, distress, and/or impairment)
should be coded as an other specified insomnia disorder.
Note. The diagnosis of insomnia disorder is given whether it occurs as an independent
condition or is comorbid with another mental disorder (e.g., major depressive disorder),
medical condition (e.g., pain), or another sleep disorder (e.g., a breathing-related sleep dis-
order). For instance, insomnia may develop its own course with some anxiety and depres-
sive features but in the absence of criteria being met for any one mental disorder. Insomnia
may also manifest as a clinical feature of a more predominant mental disorder. Persistent
insomnia may even be a risk factor for depression and is a common residual symptom af-
ter treatment for this condition. With comorbid insomnia and a mental disorder, treatment
may also need to target both conditions. Given these different courses, it is often impossi-
ble to establish the precise nature of the relationship between these clinical entities, and
this relationship may change over time. Therefore, in the presence of insomnia and a co-
morbid disorder, it is not necessary to make a causal attribution between the two condi-
tions. Rather, the diagnosis of insomnia disorder is made with concurrent specification of
the clinically comorbid conditions. A concurrent insomnia diagnosis should only be con-
sidered when the insomnia is sufficiently severe to warrant independent clinical attention;
otherwise, no separate diagnosis is necessary.
Diagnostic Features
The essential feature of insomnia disorder is dissatisfaction with sleep quantity or quality
with complaints of difficulty initiating or maintaining sleep. The sleep complaints are ac-
companied by clinically significant distress or impairment in social, occupational, or other
important areas of functioning. The sleep disturbance may occur during the course of an-
other mental disorder or medical condition, or it may occur independently.
Different manifestations of insomnia can occur at different times of the sleep period. Sleep-
onset insomnia (or initial insomnia) involves difficulty initiating sleep at bedtime. Sleep mainte-
nance insomnia (or middle insomnia) involves frequent or prolonged awakenings throughout
the night. Late insomnia involves early-morning awakening with an inability to return to sleep.
Difficulty maintaining sleep is the most common single symptom of insomnia, followed by
difficulty falling asleep, while a combination of these symptoms is the most common presen-
tation overall. The specific type of sleep complaint often varies over time. Individuals who
complain of difficulty falling asleep at one time may later complain of difficulty maintaining
sleep, and vice versa. Symptoms of difficulty falling asleep and difficulty maintaining sleep
can be quantified by the individual's retrospective self-report, sleep diaries, or other methods,
such as actigraphy or polysomnography, but the diagnosis of insomnia disorder is based on
the individual's subjective perception of sleep or a caretaker’s report.
Nonrestorative sleep, a complaint of poor sleep quality that does not leave the individual
rested upon awakening despite adequate duration, is a common sleep complaint usually
occurring in association with difficulty initiating or maintaining sleep, or less frequently in
isolation. This complaint can also be reported in association with other sleep disorders
(e.g., breathing-related sleep disorder). When a complaint of nonrestorative sleep occurs
in isolation (i.e., in the absence of difficulty initiating and/or maintaining sleep) but all di-
agnostic criteria with regard to frequency, duration, and daytime distress and impairments
are otherwise met, a diagnosis of other specified insomnia disorder or unspecified insom-
nia disorder is made.
364 Sleep-Wake Disorders
Aside from the frequency and duration criteria required to make the diagnosis, addi-
tional criteria are useful to quantify insomnia severity. These quantitative criteria, while
arbitrary, are provided for illustrative purpose only. For instance, difficulty initiating sleep
is defined by a subjective sleep latency greater than 20-30 minutes, and difficulty maintain-
ing sleep is defined by a subjective time awake after sleep onset greater than 20-30 min-
utes. Although there is no standard definition of early-morning awakening, this symptom
involves awakening at least 30 minutes before the scheduled time and before total sleep
time reaches 6% hours. It is essential to take into account not only the final awakening time
but also the bedtime on the previous evening. Awakening at 4:00 A.M. does not have the
same clinical significance in those who go to bed at 9:00 P.M. as in those who go to bed at
11:00 P.M. Such a symptom may also reflect an age-dependent decrease in the ability to sus-
tain sleep or an age-dependent shift in the timing of the main sleep period.
Insomnia disorder involves daytime impairments as well as nighttime sleep difficulties.
These include fatigue or, less commonly, daytime sleepiness; the latter is more common
among older individuals and when insomnia is comorbid with another medical condition
(e.g., chronic pain) or sleep disorder (e.g., sleep apnea). Impairment in cognitive performance
may include difficulties with attention, concentration and memory, and even with performing
simple manual skills. Associated mood disturbances are typically described as irritability or
mood lability and less commonly as depressive or anxiety symptoms. Not all individuals with
nighttime sleep disturbances are distressed or have functional impairment. For example, sleep
continuity is often interrupted in healthy older adults who nevertheless identify themselves
as good sleepers. A diagnosis of insomnia disorder should be reserved for those individuals
with significant daytime distress or impairment related to their nighttime sleep difficulties.
Associated Features Supporting Diagnosis
Insomnia is often associated with physiological and cognitive arousal and conditioning
factors that interfere with sleep. A preoccupation with sleep and distress due to the inabil-
ity to sleep may lead to a vicious cycle: the more the individual strives to sleep, the more
frustration builds and further impairs sleep. Thus, excessive attention and efforts to sleep,
which override normal sleep-onset mechanisms, may contribute to the development of in-
somnia. Individuals with persistent insomnia may also acquire maladaptive sleep habits
(e.g., spending excessive time in bed; following an erratic sleep schedule; napping) and
cognitions (e.g., fear of sleeplessness; apprehensions of daytime impairments; clock mon-
itoring) during the course of the disorder. Engaging in such activities in an environment in
which the individual has frequently spent sleepless nights may further compound the con-
ditioned arousal and perpetuate sleep difficulties. Conversely, the individual may fall asleep
more easily when not trying to do so. Some individuals also report better sleep when away
from their own bedrooms and their usual routines.
Insomnia may be accompanied by a variety of daytime complaints and symptoms, in-
cluding fatigue, decreased energy, and mood disturbances. Symptoms of anxiety or de-
pression that do not meet criteria for a specific mental disorder may be present, as well as
an excessive focus on the perceived effects of sleep loss on daytime functioning.
Individuals with insomnia may have elevated scores on self-report psychological or
personality inventories with profiles indicating mild depression and anxiety, a worrisome
cognitive style, an emotion-focused and internalizing style of conflict resolution, and a so-
matic focus. Patterns of neurocognitive impairment among individuals with insomnia dis-
order are inconsistent, although there may be impairments in performing tasks of higher
complexity and those requiring frequent changes in performance strategy. Individuals
with insomnia often require more effort to maintain cognitive performance.
Prevalence
Population-based estimates indicate that about one-third of adults report insomnia symp-
toms, 10%-15% experience associated daytime impairments, and 6%—10% have symptoms
insomnia Disorder 365
that meet criteria for insomnia disorder. Insomnia disorder is the most prevalent of all
sleep disorders. In primary care settings, approximately 10%~20% of individuals complain
of significant insomnia symptoms. Insomnia is a more prevalent complaint among fe-
males than among males, with a gender ratio of about 1.44:1. Although insomnia can be a
symptom or an independent disorder, it is most frequently observed as a comorbid con-
dition with another medical condition or mental disorder. For instance, 40%—50% of indi-
viduals with insomnia also present with a comorbid mental disorder.
Development and Course
The onset of insomnia symptoms can occur at any time during life, but the first episode is
more common in young adulthood. Less frequently, insomnia begins in childhood or ad-
olescence. In women, new-onset insomnia may occur during menopause and persist even
after other symptoms (e.g., hot flashes) have resolved. Insomnia may have a late-life onset,
which is often associated with the onset of other health-related conditions.
Insomnia can be situational, persistent, or recurrent. Situational or acute insomnia usu-
ally lasts a few days or a few weeks and is often associated with life events or rapid changes
in sleep schedules or environment. It usually resolves once the initial precipitating event
subsides. For some individuals, perhaps those more vulnerable to sleep disturbances, in-
somnia may persist long after the initial triggering event, possibly because of conditioning
factors and heightened arousal. The factors that precipitate insomnia may differ from
those that perpetuate it. For example, an individual who is bedridden with a painful injury
and has difficulty sleeping may then develop negative associations for sleep. Conditioned
arousal may then persist and lead to persistent insomnia. A similar course may develop in
the context of an acute psychological stress or a mental disorder. For instance, insomnia that
occurs during an episode of major depressive disorder can become a focus of attention,
with consequent negative conditioning, and persist even after resolution of the depressive
episode. In some cases, insomnia may also have an insidious onset without any identifi-
able precipitating factor.
The course of insomnia may also be episodic, with recurrent episodes of sleep difficul-
ties associated with the occurrence of stressful events. Chronicity rates range from 45%
to 75% for follow-ups of 1-7 years. Even when the course of the insomnia has become
chronic, there is night-to-night variability in sleep patterns, with an occasional restful night's
sleep interspersed with several nights of poor sleep. The characteristics of insomnia may
also change over time. Many individuals with insomnia have a history of “light” or easily
disturbed sleep prior to onset of more persistent sleep problems.
Insomnia complaints are more prevalent among middle-age and older adults. The type
of insomnia symptom changes as a function of age, with difficulties initiating sleep being
more common among young adults and problems maintaining sleep occurring more fre-
quently among middle-age and older individuals.
Difficulties initiating and maintaining sleep can also occur in children and adolescents,
but there are more limited data on prevalence, risk factors, and comorbidity during these
developmental phases of the lifespan. Sleep difficulties in childhood can result from con-
ditioning factors (e.g., a child who does not learn to fall asleep or return to sleep without
the presence of a parent) or from the absence of consistent sleep schedules and bedtime
routines. Insomnia in adolescence is often triggered or exacerbated by irregular sleep sched-
ules (e.g., phase delay). In both children and adolescents, psychological and medical fac-
tors can contribute to insomnia.
The increased prevalence of insomnia in older adults is partly explained by the higher
incidence of physical health problems with aging. Changes in sleep patterns associated with
the normal developmental process must be differentiated from those exceeding age-related
changes. Although polysomnography is of limited value in the routine evaluation of in-
somnia, it may be more useful in the differential diagnosis among older adults because the
etiologies of insomnia (e.g., sleep apnea) are more often identifiable in older individuals.
366 Sleep-Wake Disorders
Risk and Prognostic Factors
While the risk and prognostic factors discussed in this section increase vulnerability to in-
somnia, sleep disturbances are more likely to occur when predisposed individuals are ex-
posed to precipitating events, such as major life events (e.g., illness, separation) or less
severe but more chronic daily stress. Most individuals resume normal sleep patterns after
the initial triggering event has disappeared, but others—perhaps those more vulnerable to
insomnia—continue experiencing persistent sleep difficulties. Perpetuating factors such as
poor sleep habits, irregular sleep scheduling, and the fear of not sleeping feed into the in-
somnia problem and may contribute to a vicious cycle that may induce persistent insomnia.
Temperamental. Anxiety or worry-prone personality or cognitive styles, increased arousal
predisposition, and tendency to repress emotions can increase vulnerability to insomnia.
Environmental. Noise, light, uncomfortably high or low temperature, and high altitude
may also increase vulnerability to insomnia.
Genetic and physiological. Female gender and advancing age are associated with in-
creased vulnerability to insomnia. Disrupted sleep and insomnia display a familial dispo-
sition. The prevalence of insomnia is higher among monozygotic twins relative to
dizygotic twins; it is also higher in first-degree family members compared with the general
population. The extent to which this link is inherited through a genetic predisposition,
learned by observations of parental models, or established as a by-product of another psy-
chopathology remains undetermined.
Course modifiers. Deleterious course modifiers include poor sleep hygiene practices
(e.g., excessive caffeine use, irregular sleep schedules).
Gender-Related Diagnostic Issues
Insomnia is a more prevalent complaint among females than among males, with first onset
often associated with the birth of a new child or with menopause. Despite higher preva-
lence among older females, polysomnographic studies suggest better preservation of
sleep continuity and slow-wave sleep in older females than in older males.
Diagnostic Markers
Polysomnography usually shows impairments of sleep continuity (e.g., increased sleep la-
tency and time awake after sleep onset and decreased sleep efficiency [percentage of time
in bed asleep] and may show increased stage 1 sleep and decreased stages 3 and 4 sleep.
The severity of these sleep impairments does not always match the individual's clinical
presentation or subjective complaint of poor sleep, as individuals with insomnia often un-
derestimate sleep duration and overestimate wakefulness relative to polysomnography.
Quantitative electroencephalographic analyses may indicate that individuals with insom-
nia have greater high-frequency electroencephalography power relative to good sleepers
both around the sleep onset period and during non-rapid eye movement sleep, a feature
suggestive of increased cortical arousal. Individuals with insomnia disorder may have a
lower sleep propensity and typically do not show increased daytime sleepiness on objec-
tive sleep laboratory measures compared with individuals without sleep disorders.
Other laboratory measures show evidence, although not consistently, of increased
arousal and a generalized activation of the hypothalamic-pituitary-adrenal axis (e.g., in-
creased cortisol levels, heart rate variability, reactivity to stress, metabolic rate). In general,
findings are consistent with the hypothesis that increased physiological and cognitive
arousal plays a significant role in insomnia disorder.
Individuals with insomnia disorder may appear either fatigued or haggard or, con-
versely, overaroused and “wired.” However, there are no consistent or characteristic
abnormalities on physical examination. There may be an increased incidence of stress-
Insomnia Disorder 367
related psychophysiological symptoms (e.g., tension headache, muscle tension or pain,
gastrointestinal symptoms).
Functional Consequences of Insomnia Disorder
Interpersonal, social, and occupational problems may develop as a result of insomnia or
excessive concern with sleep, increased daytime irritability, and poor concentration. De-
creased attention and concentration are common and may be related to higher rates of ac-
cidents observed in insomnia. Persistent insomnia is also associated with long-term
consequences, including increased risks of major depressive disorder, hypertension, and
myocardial infarction; increased absenteeism and reduced productivity at work; reduced
quality of life; and increased economic burden.
Differential Diagnosis
Normal sleep variations. Normal sleep duration varies considerably across individuals.
Some individuals who require little sleep (“short sleepers”) may be concerned about their
sleep duration. Short sleepers differ from individuals with insomnia disorder by the lack of
difficulty falling or staying asleep and by the absence of characteristic daytime symptoms
(e.g., fatigue, concentration problems, irritability). However, some short sleepers may desire
or attempt to sleep for a longer period of time and, by prolonging time in bed, may create an
insomnia-like sleep pattern. Clinical insomnia also should be distinguished from normal,
age-related sleep changes. Insomnia must also be distinguished from sleep deprivation due
to inadequate opportunity or circumstance for sleep resulting, for example, from an emer-
gency or from professional or family obligations forcing the individual to stay awake.
Situational/acute insomnia. Situational/acute insomnia is a condition lasting a few days
to a few weeks, often associated with life events or with changes in sleep schedules. These
acute or short-term insomnia symptoms may also produce significant distress and inter-
fere with social, personal, and occupational functioning. When such symptoms are fre-
quent enough and meet all other criteria except for the 3-month duration, a diagnosis of
other specified insomnia disorder or unspecified insomnia disorder is made.
Delayed sleep phase and shift work types of circadian rhythm sleep-wake disorder.
Individuals with the delayed sleep phase type of circadian rhythm sleep-wake disorder re-
port sleep-onset insomnia only when they try to sleep at socially normal times, but they do
not report difficulty falling asleep or staying asleep when their bed and rising times are
delayed and coincide with their endogenous circadian rhythm. Shift work type differs from
insomnia disorder by the history of recent shift work.
Restless legs syndrome. Restless legs syndrome often produces difficulties initiating
and maintaining sleep. However, an urge to move the legs and any accompanying unpleas-
ant leg sensations are features that differentiate this disorder from insomnia disorder.
Breathing-related sleep disorders. Most individuals with a breathing-related sleep dis-
order have a history of loud snoring, breathing pauses during sleep, and excessive daytime
sleepiness. Nonetheless, as many as 50% of individuals with sleep apnea may also report
insomnia symptoms, a feature that is more common among females and older adults.
Narcolepsy. Narcolepsy may cause insomnia complaints but is distinguished from in-
somnia disorder by the predominance of symptoms of excessive daytime sleepiness, cat-
aplexy, sleep paralysis, and sleep-related hallucinations.
Parasomnias. Parasomnias are characterized by a complaint of unusual behavior or events
during sleep that may lead to intermittent awakenings and difficulty resuming sleep.
However, it is these behavioral events, rather than the insomnia per se, that dominate the
clinical picture.
368 Sleep-Wake Disorders
Substance/medication-induced sleep disorder, insomnia type. Substance/medication-
induced sleep disorder, insomnia type, is distinguished from insomnia disorder by the fact
that a substance (i.e., a drug of abuse, a medication, or exposure to a toxin) is judged to be
etiologically related to the insomnia (see “Substance/Medication-Induced Sleep Disor-
der” later in this chapter). For example, insomnia occurring only in the context of heavy
coffee consumption would be diagnosed as caffeine-induced sleep disorder, insomnia
type, with onset during intoxication.
Comorbidity
Insomnia is a common comorbidity of many medical conditions, including diabetes, cor-
onary heart disease, chronic obstructive pulmonary disease, arthritis, fibromyalgia, and
other chronic pain conditions. The risk relationship appears to be bidirectional: insomnia
increases the risk of medical conditions, and medical problems increase the risk of insom-
nia. The direction of the relationship is not always clear and may change over time; for this
reason, comorbid insomnia is the preferred terminology in the presence of coexisting in-
somnia with another medical condition (or mental disorder).
Individuals with insomnia disorder frequently have a comorbid mental disorder, par-
ticularly bipolar, depressive, and anxiety disorders. Persistent insomnia represents a risk
factor or an early symptom of subsequent bipolar, depressive, anxiety, and substance use
disorders. Individuals with insomnia may misuse medications or alcohol to help with
nighttime sleep, anxiolytics to combat tension or anxiety, and caffeine or other stimulants
to combat excessive fatigue. In addition to worsening the insomnia, this type of substance
use may in some cases progress to a substance use disorder.
Relationship to International Classification of
Sleep Disorders
There are several distinct insomnia phenotypes relating to the perceived source of the in-
somnia that are recognized by the International Classification of Sleep Disorders, 2nd Edition
(ICSD-2). These include psychophysiological insomnia, idiopathic insomnia, sleep-state mispercep-
tion, and inadequate sleep hygiene. Despite their clinical appeal and heuristic value, there is
limited evidence to support these distinct phenotypes.
Hypersomnolence Disorder
Diagnostic Criteria 780.54 (G47.10)
A. Self-reported excessive sleepiness (hypersomnolence) despite a main sleep period
lasting at least 7 hours, with at least one of the following symptoms:
1. Recurrent periods of sleep or lapses into sleep within the same day.
2. Aprolonged main sleep episode of more than 9 hours per day that is nonrestorative
(i-e., unrefreshing).
3. Difficulty being fully awake after abrupt awakening.
B. The hypersomnolence occurs at least three times per week, for at least 3 months.
C. The hypersomnolence is accompanied by significant distress or impairment in cogni-
tive, social, occupational, or other important areas of functioning.
D. The hypersomnolence is not better explained by and does not occur exclusively during
the course of another sleep disorder (e.g., narcolepsy, breathing-related sleep disor-
der, circadian rhythm sleep-wake disorder, or a parasomnia).
E. The hypersomnolence is not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication).
Hypersomnolence Disorder 369
F. Coexisting mental and medical disorders do not adequately explain the predominant
complaint of hypersomnotlence.
Specify if:
With mental disorder, including substance use disorders
With medical condition
With another sleep disorder
Coding note: The code 780.54 (G47.10) applies to all three specifiers. Code also the
relevant associated mental disorder, medical condition, or other sleep disorder im-
mediately after the code for hypersomnolence disorder in order to indicate the associ-
ation.
Specify if:
Acute: Duration of less than 1 month.
Subacute: Duration of 1-3 months.
Persistent: Duration of more than 3 months.
Specify current severity:
Specify severity based on degree of difficulty maintaining daytime alertness as manifested
by the occurrence of multiple attacks of irresistible sleepiness within any given day occur-
ring, for example, while sedentary, driving, visiting with friends, or working.
Mild: Difficulty maintaining daytime alertness 1-2 days/week.
Moderate: Difficulty maintaining daytime alertness 3-4 days/week.
Severe: Difficulty maintaining daytime alertness 5-7 days/week.
Diagnostic Features
Hypersomnolence is a broad diagnostic term and includes symptoms of excessive quantity
of sleep (e.g., extended nocturnal sleep or involuntary daytime sleep), deteriorated quality
of wakefulness (i.e., sleep propensity during wakefulness as shown by difficulty awaken-
ing or inability to remain awake when required), and sleep inertia (i.e., a period of im-
paired performance and reduced vigilance following awakening from the regular sleep
episode or from a nap) (Criterion A). Individuals with this disorder fall asleep quickly and
have a good sleep efficiency (>90%). They may have difficulty waking up in the morning,
sometimes appearing confused, combative, or ataxic. This prolonged impairment of alert-
ness at the sleep-wake transition is often referred to as sleep inertia (i.e., sleep drunkenness).
It can also occur upon awakening from a daytime nap. During that period, the individual
appears awake, but there is a decline in motor dexterity, behavior may be very inappro-
priate, and memory deficits, disorientation in time and space, and feelings of grogginess
may occur. This period may last some minutes to hours.
The persistent need for sleep can lead to automatic behavior (usually of a very routine,
low-complexity type) that the individual carries out with little or no subsequent recall. For
example, individuals may find themselves having driven several miles from where they
thought they were, unaware of the “automatic” driving they did in the preceding minutes.
For some individuals with hypersomnolence disorder, the major sleep episode (for most
individuals, nocturnal sleep) has a duration of 9 hours or more. However, the sleep is often
nonrestorative and is followed by difficulty awakening in the morning. For other individ-
uals with hypersomnolence disorder, the major sleep episode is of normal nocturnal sleep
duration (6-9 hours). In these cases, the excessive sleepiness is characterized by several un-
intentional daytime naps. These daytime naps tend to be relatively long (often lasting 1 hour
or more), are experienced as nonrestorative (i.e., unrefreshing), and do not lead to improved
alertness. Individuals with hypersomnolence have daytime naps nearly everyday regard-
less of the nocturnal sleep duration. Subjective sleep quality may or may not be reported as
good. Individuals typically feel sleepiness developing over a period of time, rather than
370 Sleep-Wake Disorders
experiencing a sudden sleep “attack.” Unintentional sleep episodes typically occur in low-
stimulation and low-activity situations (e.g., while attending lectures, reading, watching
television, or driving long distances), but in more severe cases they can manifest in high-
attention situations such as at work, in meetings, or at social gatherings.
Associated Features Supporting Diagnosis
Nonrestorative sleep, automatic behavior, difficulties awakening in the morning, and
sleep inertia, although common in hypersomnolence disorder, may also be seen in a variety
of conditions, including narcolepsy. Approximately 80% of individuals with hyper-
somnolence report that their sleep is nonrestorative, and as many have difficulties awak-
ening in the morning. Sleep inertia, though less common (i.e., observed in 36%-50% of
individuals with hypersomnolence disorder), is highly specific to hypersomnolence. Short
naps (i.e., duration of less than 30 minutes) are often unrefreshing. Individuals with hy-
persomnolence often appear sleepy and may even fall asleep in the clinician’s waiting
area.
A subset of individuals with hypersomnolence disorder have a family history of hy-
persomnolence and also have symptoms of autonomic nervous system dysfunction, in-
cluding recurrent vascular-type headaches, reactivity of the peripheral vascular system
(Raynaud’s phenomenon), and fainting.
Prevalence
Approximately 5%-10% of individuals who consult in sleep disorders clinics with com-
plaints of daytime sleepiness are diagnosed as having hypersomnolence disorder. It is es-
timated that about 1% of the European and U.S. general population has episodes of sleep
inertia. Hypersomnolence occurs with relatively equal frequency in males and females.
Development and Course
Hypersomnolence disorder has a persistent course, with a progressive evolution in the se-
verity of symptoms. In most extreme cases, sleep episodes can last up to 20 hours. How-
ever, the average nighttime sleep duration is around 9% hours. While many individuals
with hypersomnolence are able to reduce their sleep time during working days, weekend
and holiday sleep is greatly increased (by up to 3 hours). Awakenings are very difficult
and accompanied by sleep inertia episodes in nearly 40% of cases. Hypersomnolence fully
manifests in most cases in late adolescence or early adulthood, with a mean age at onset of
17-24 years. Individuals with hypersomnolence disorder are diagnosed, on average, 10-15
years after the appearance of the first symptoms. Pediatric cases are rare.
Hypersomnolence has a progressive onset, with symptoms beginning between ages 15
and 25 years, with a gradual progression over weeks to months. For most individuals, the
course is then persistent and stable, unless treatment is initiated. The development of other
sleep disorders (e.g., breathing-related sleep disorder) may worsen the degree of sleepi-
ness. Although hyperactivity may be one of the presenting signs of daytime sleepiness in
children, voluntary napping increases with age. This normal phenomenon is distinct from
hypersomnolence.
Risk and Prognostic Factors
Environmental. Hypersomnolence can be increased temporarily by psychological stress
and alcohol use, but they have not been documented as environmental precipitating
factors. Viral infections have been reported to have preceded or accompanied hyper-
somnolence in about 10% of cases. Viral infections, such as HIV pneumonia, infectious
mononucleosis, and Guillain-Barré syndrome, can also evolve into hypersomnolence within
Hypersomnolence Disorder 371
months after the infection. Hypersomnolence can also appear within 6-18 months follow-
ing a head trauma.
Genetic and physiological. Hypersomnolence may be familial, with an autosomal-
dominant mode of inheritance.
Diagnostic Markers
Nocturnal polysomnography demonstrates a normal to prolonged sleep duration, short
sleep latency, and normal to increased sleep continuity. The distribution of rapid eye
movement (REM) sleep is also normal. Sleep efficiency is mostly greater than 90%. Some
individuals with hypersomnolence disorder have increased amounts of slow-wave sleep.
The multiple sleep latency test documents sleep tendency, typically indicated by mean
sleep latency values of less than 8 minutes. In hypersomnolence disorder, the mean sleep
latency is typically less than 10 minutes and frequently 8 minutes or less. Sleep-onset REM
periods (SOREMPs; i.e., the occurrence of REM sleep within 20 minutes of sleep onset)
may be present but occur less than two times in four to five nap opportunities.
Functional Consequences of Hypersomnoience Disorder
The low level of alertness that occurs while an individual fights the need for sleep can lead
to reduced efficiency, diminished concentration, and poor memory during daytime activ-
ities. Hypersomnolence can lead to significant distress and dysfunction in work and social
relationships. Prolonged nocturnal sleep and difficulty awakening can result in difficulty
in meeting morning obligations, such as arriving at work on time. Unintentional daytime
sleep episodes can be embarrassing and even dangerous, if, for instance, the individual is
driving or operating machinery when the episode occurs.
Differential Diagnosis
Normative variation in sleep. “Normal” sleep duration varies considerably in the general
population. “Long sleepers” (i.e., individuals who require a greater than average amount
of sleep) do not have excessive sleepiness, sleep inertia, or automatic behavior when they
obtain their required amount of nocturnal sleep. Sleep is reported to be refreshing. If social
or occupational demands lead to shorter nocturnal sleep, daytime symptoms may appear.
In hypersomnolence disorder, by contrast, symptoms of excessive sleepiness occur regard-
less of nocturnal sleep duration. An inadequate amount of nocturnal sleep, or behaviorally
induced insufficient sleep syndrome, can produce symptoms of daytime sleepiness very similar
to those of hypersomnolence. An average sleep duration of fewer than 7 hours per night
strongly suggests inadequate nocturnal sleep, and an average of more than 9-10 hours of
sleep per 24-hour period suggests hypersomnolence. Individuals with inadequate noctur-
nal sleep typically “catch up” with longer sleep durations on days when they are free from
social or occupational demands or on vacations. Unlike hypersomnolence, insufficient
nocturnal sleep is unlikely to persist unabated for decades. A diagnosis of hypersomno-
lence disorder should not be made if there is a question regarding the adequacy of noctur-
nal sleep duration. A diagnostic and therapeutic trial of sleep extension for 10-14 days can
often clarify the diagnosis.
Poor sleep quality and fatigue. Hypersomnolence disorder should be distinguished
from excessive sleepiness related to insufficient sleep quantity or quality and fatigue (i.e.,
tiredness not necessarily relieved by increased sleep and unrelated to sleep quantity or
quality). Excessive sleepiness and fatigue are difficult to differentiate and may overlap
considerably.
Breathing-related sleep disorders. Individuals with hypersomnolence and breathing-
related sleep disorders may have similar patterns of excessive sleepiness. Breathing-
372 Sleep-Wake Disorders
related sleep disorders are suggested by a history of loud snoring, pauses in breathing
during sleep, brain injury, or cardiovascular disease and by the presence of obesity, oro-
pharyngeal anatomical abnormalities, hypertension, or heart failure on physical examina-
tion. Polysomnographic studies can confirm the presence of apneic events in breathing-
related sleep disorder (and their absence in hypersomnolence disorder).
Circadian rhythm sleep-wake disorders. Circadian rhythm sleep-wake disorders are
often characterized by daytime sleepiness. A history of an abnormal sleep-wake schedule
(with shifted or irregular hours) is present in individuals with a circadian rhythm sleep-
wake disorder.
Parasomnias. Parasomnias rarely produce the prolonged, undisturbed nocturnal sleep
or daytime sleepiness characteristic of hypersomnolence disorder.
Other mental disorders. Hypersomnolence disorder must be distinguished from mental
disorders that include hypersomnolence as an essential or associated feature. In particular,
complaints of daytime sleepiness may occur in a major depressive episode, with atypical fea-
tures, and in the depressed phase of bipolar disorder. Assessment for other mental disorders is
essential before a diagnosis of hypersomnolence disorder is considered. A diagnosis of hyper-
somnolence disorder can be made in the presence of another current or past mental disorder.
Comorbidity
Hypersomnolence can be associated with depressive disorders, bipolar disorders (during a
depressive episode), and major depressive disorder, with seasonal pattern. Many individu-
als with hypersomnolence disorder have symptoms of depression that may meet criteria for
a depressive disorder. This presentation may be related to the psychosocial consequences of
persistent increased sleep need. Individuals with hypersomnolence disorder are also at
risk for substance-related disorders, particularly related to self-medication with stimulants.
This general lack of specificity may contribute to very heterogeneous profiles among indi-
viduals whose symptoms meet the same diagnostic criteria for hypersomnolence disorder.
Neurodegenerative conditions, such as Alzheimer’s disease, Parkinson’s disease, and mul-
tiple system atrophy, may also be associated with hypersomnolence.
Relationship to Internatlonai Classification of
Sleep Disorders
The International Classification of Sleep Disorders, 2nd Edition (ICSD-2), differentiates nine
subtypes of “hypersomnias of central origin,” including recurrent hypersomnia (Kleine-
Levin syndrome).
Narcolepsy
Diagnostic Criteria
A. Recurrent periods of an irrepressible need to sleep, lapsing into sleep, or napping oc-
curring within the same day. These must have been occurring at least three times per
week over the past 3 months.
B. The presence of at least one of the following:
1. Episodes of cataplexy, defined as either (a) or (b}, occurring at least a few times
per month:
a. In individuals with long-standing disease, brief (seconds to minutes) episodes
of sudden bilateral loss of muscle tone with maintained consciousness that are
precipitated by laughter or joking.
Narcolepsy 373
b. in children or in individuals within 6 months of onset, spontaneous grimaces or
jaw-opening episodes with tongue thrusting or a global hypotonia, without any
obvious emotional triggers.
2. Hypocretin deficiency, as measured using cerebrospinal fluid (CSF) hypocretin-1
immunoreactivity values (less than or equal to one-third of values obtained in
healthy subjects tested using the same assay, or less than or equal to 110 pg/mL).
Low CSF levels of hypocretin-1 must not be observed in the context of acute brain
injury, inflammation, or infection.
3. Nocturnal sleep polysomnography showing rapid eye movement (REM) sleep ia-
tency less than or equal to 15 minutes, or a multiple sleep latency test showing a
mean sleep latency less than or equal to 8 minutes and two or more sleep-onset
REM periods.
Specify whether:
347.00 (G47.419) Narcolepsy without cataplexy but with hypocretin deficiency: Cri-
terion B requirements of low CSF hypocretin-1 levels and positive polysomnography/
multiple sleep latency test are met, but no cataplexy is present (Criterion B1 not met).
347.01 (G47.411) Narcolepsy with cataplexy but without hypocretin deficiency:
In this rare subtype {less than 5% of narcolepsy cases), Criterion B requirements of
cataplexy and positive polysomnography/multiple sleep latency test are met, but CSF
hypocretin-1 levels are normal (Criterion B2 not met).
347.00 (G47.419) Autosomal dominant cerebellar ataxia, deafness, and narco-
lepsy: This subtype is caused by exon 21 DNA (cytosine-5)-methyltransferase-1 mu-
tations and is characterized by late-onset (age 30-40 years) narcolepsy (with low or
intermediate CSF hypocretin-1 ievels), deafness, cerebellar ataxia, and eventually de-
mentia.
347.00 (G47.419) Autosomal dominant narcolepsy, obesity, and type 2 diabetes:
Narcolepsy, obesity, and type 2 diabetes and low CSF hypocretin-1 levels have been
described in rare cases and are associated with a mutation in the myelin oligodendro-
cyte glycoprotein gene.
347.10 (G47.429) Narcolepsy secondary to another medical condition: This sub-
type is for narcolepsy that develops secondary to medical conditions that cause infec-
tious (e.g., Whipple’s disease, sarcoidosis), traumatic, or tumoral destruction of
hypocretin neurons.
Coding note (for ICD-9-CM code 347.10 only): Code first the underlying medical con-
dition (e.g., 040.2 Whipple’s disease; 347.10 narcolepsy secondary to Whipple’s dis-
ease).
Specify current severity:
Mild: Infrequent cataplexy (less than once per week), need for naps only once or twice
per day, and less disturbed nocturnal sleep.
Moderate: Cataplexy once daily or every few days, disturbed nocturnal sleep, and
need for multiple naps daily.
Severe: Drug-resistant cataplexy with multiple attacks daily, nearly constant sleepi-
ness, and disturbed nocturnal sleep (i.e., movements, insomnia, and vivid dreaming).
Subtypes
In narcolepsy without cataplexy but with hypocretin deficiency, unclear “cataplexy-like”
symptoms may be reported (e.g., the symptoms are not triggered by emotions and are un-
usually long lasting). In extremely rare cases, cerebrospinal fluid (CSF) levels of hypocre-
tin-1 are low, and polysomnographic/ multiple sleep latency test (MSLT) results are
negative: repeating the test is advised before establishing the subtype diagnosis. In narco-
374 Sleep-Wake Disorders
lepsy with cataplexy but without hypocretin deficiency, test results for human leukocyte
antigen (HLA) DQB1*06:02 may be negative. Seizures, falls of other origin, and conversion
disorder (functional neurological symptom disorder) should be excluded. In narcolepsy
secondary to infectious (e.g., Whipple’s disease, sarcoidosis), traumatic, or tumoral de-
struction of hypocretin neurons, test results for HLA DQB1*06:02 may be positive and may
result from the insult triggering the autoimmune process. In other cases, the destruction of
hypocretin neurons may be secondary to trauma or hypothalamic surgery. Head trauma
or infections of the central nervous system can, however, produce transitory decreases in
CSF hypocretin-1 levels without hypocretin cell loss, complicating the diagnosis.
Diagnostic Features
The essential features of sleepiness in narcolepsy are recurrent daytime naps or lapses into
sleep. Sleepiness typically occurs daily but must occur at a minimum three times a week
for at least 3 months (Criterion A). Narcolepsy generally produces cataplexy, which most
commonly presents as brief episodes (seconds to minutes) of sudden, bilateral loss of mus-
cle tone precipitated by emotions, typically laughing and joking. Muscles affected may
include those of the neck, jaw, arms, legs, or whole body, resulting in head bobbing, jaw
dropping, or complete falls. Individuals are awake and aware during cataplexy. To meet
Criterion B1(a), cataplexy must be triggered by laughter or joking and must occur at least
a few times per month when the condition is untreated or in the past.
Cataplexy should not be confused with “weakness” occurring in the context of athletic
activities (physiological) or exclusively after unusual emotional triggers such as stress or
anxiety (suggesting possible psychopathology). Episodes lasting hours or days, or those not
triggered by emotions, are unlikely to be cataplexy, nor is rolling on the floor while laugh-
ing hysterically.
In children close to onset, genuine cataplexy can be atypical, affecting primarily the
face, causing grimaces or jaw opening with tongue thrusting (“cataplectic faces”). Alter-
natively, cataplexy may present as low-grade continuous hypotonia, yielding a wobbling
walk. In these cases, Criterion B1(b) can be met in children or in individuals within 6 months
of a rapid onset.
Narcolepsy-cataplexy nearly always results from the loss of hypothalamic hypocretin
(orexin)}-producing cells, causing hypocretin deficiency (less than or equal to one-third of
control values, or 110 pg/mL in most laboratories). Cell loss is likely autoimmune, and ap-
proximately 99% of affected individuals carry HLA-DQB1*06:02 (vs. 12%-38% of control
subjects). Thus, checking for the presence of DQB1*06:02 prior to a lumbar puncture for eval-
uation of CSF hypocretin-1 immunoreactivity may be useful. Rarely, low CSF levels of hypo-
cretin-1 occur without cataplexy, notably in youths who may develop cataplexy later. CSF
hypocretin-1 measurement represents the gold standard, excepting associated severe con-
ditions (neurological, inflammatory, infectious, trauma) that can interfere with the assay.
A nocturnal polysomnographic sleep study followed by an MSLT can also be used to
confirm the diagnosis (Criterion B3). These tests must be performed after the individual
has stopped all psychotropic medications, following 2 weeks of adequate sleep time (as
documented with sleep diaries, actigraphy). Short rapid eye movement (REM) latency
(sleep-onset REM period, REM latency less than or equal to 15 minutes) during polysom-
nography is sufficient to confirm the diagnosis and meets Criterion B3. Alternatively, the
MSLT result must be positive, showing a mean sleep latency of less than or equal to 8 min-
utes and two or more sleep-onset REM periods in four to five naps.
Associated Features Supporting Diagnosis
When sleepiness is severe, automatic behaviors may occur, with the individual continuing
his or her activities in a semi-automatic, hazelike fashion without memory or conscious-
ness. Approximately 20%-60% of individuals experience vivid hypnagogic hallucinations
Narcolepsy 375
before or upon falling asleep or hypnopompic hallucinations just after awakening. These
hallucinations are distinct from the less vivid, nonhallucinatory dreamlike mentation at
sleep onset that occurs in normal sleepers. Nightmares and vivid dreaming are also fre-
quent in narcolepsy, as is REM sleep behavior disorder. Approximately 20%-60% of indi-
viduals experience sleep paralysis upon falling asleep or awakening, leaving them awake
but unable to move or speak. However, many normal sleepers also report sleep paralysis,
especially with stress or sleep deprivation. Nocturnal eating may occur. Obesity is com-
mon. Nocturnal sleep disruption with frequent long or short awakenings is common and
can be disabling.
Individuals may appear sleepy or fall asleep in the waiting area or during clinical ex-
amination. During cataplexy, individuals may slump ina chair and have slurred speech or
drooping eyelids. If the clinician has time to check reflexes during cataplexy (most attacks
are less than 10 seconds), reflexes are abolished—an important finding distinguishing gen-
uine cataplexy from conversion disorder.
Prevalence
Narcolepsy-cataplexy affects 0.02%-0.04% of the general population in most countries.
Narcolepsy affects both genders, with possibly a slight male preponderance.
Development and Course
Onset is typically in children and adolescents/young adults but rarely in older adults.
Two peaks of onset are suggested, at ages 15-25 years and ages 30-35 years. Onset can be
abrupt or progressive (over years). Severity is highest when onset is abrupt in children,
and then decreases with age or with treatment, so that symptoms such as cataplexy can oc-
casionally disappear. Abrupt onset in young, prepubescent children can be associated
with obesity and premature puberty, a phenotype more frequently observed since 2009. In
adolescents, onset is more difficult to pinpoint. Onset in adults is often unclear, with some
individuals reporting having had excessive sleepiness since birth. Once the disorder has
manifested, the course is persistent and lifelong.
In 90% of cases, the first symptom to manifest is sleepiness or increased sleep, followed
by cataplexy (within 1 year in 50% of cases, within 3 years in 85%). Sleepiness, hypnagogic
hallucinations, vivid dreaming, and REM sleep behavior disorder (excessive movements
during REM sleep) are early symptoms. Excessive sleep rapidly progresses to an inability
to stay awake during the day, and to maintain good sleep at night, without a clear increase
in total 24-hour sleep needs. In the first months, cataplexy may be atypical, especially in
children. Sleep paralysis usually develops around puberty in children with prepubertal
onset. Exacerbations of symptoms suggest lack of compliance with medications or devel-
opment of a concurrent sleep disorder, notably sleep apnea.
Young children and adolescents with narcolepsy often develop aggression or behav-
ioral problems secondary to sleepiness and/or nighttime sleep disruption. Workload and
social pressure increase through high school and college, reducing available sleep time at
night. Pregnancy does not seem to modify symptoms consistently. After retirement, indi-
viduals typically have more opportunity for napping, reducing the need for stimulants.
Maintaining a regular schedule benefits individuals at all ages.
Risk and Prognostic Factors
Temperamental. Parasomnias, such as sleepwalking, bruxism, REM sleep behavior dis-
order, and enuresis, may be more common in individuals who develop narcolepsy. Indi-
viduals commonly report that they need more sleep than other family members.
Environmental. Group A streptococcal throat infection, influenza (notably pandemic
HiN1 2009), or other winter infections are likely triggers of the autoimmune process, pro-
376 Sleep-Wake Disorders
ducing narcolepsy a few months later. Head trauma and abrupt changes in sleep-wake
patterns (e.g., job changes, stress) may be additional triggers.
Genetic and physiological. Monozygotic twins are 25%-32% concordant for narcolepsy.
The prevalence of narcolepsy is 1%-2% in first-degree relatives (a 10- to 40-fold increase
overall). Narcolepsy is strongly associated with DQB1*06:02 (99% vs. 12%—38% in control
subjects of various ethnic groups; 25% in the general U.S. population). DQB1*03:01 in-
creases, while DQB1*05:01, DQB1*06:01, and DQB1*06:03 reduce risk in the presence of
DQB1*06:02, but the effect is small. Polymorphisms within the T-cell receptor alpha gene
and other immune modulating genes also modulate risk slightly.
Culture-Related Diagnostic Issues
Narcolepsy has been described in all ethnic groups and in many cultures. Among African
Americans, more cases present without cataplexy or with atypical cataplexy, complicating
diagnosis, especially in the presence of obesity and obstructive sleep apnea.
Diagnostic Markers
Functional imaging suggests impaired hypothalamic responses to humorous stimuli.
Nocturnal polysomnography followed by an MSLT is used to confirm the diagnosis of
narcolepsy, especially when the disorder is first being diagnosed and before treatment has
begun, and if hypocretin deficiency has not been documented biochemically. The poly-
somnography/MSLT should be performed after the individual is no longer taking any
psychotropic drugs and after regular sleep-wake patterns, without shift work or sleep de-
privation, have been documented.
A sleep-onset REM period during the polysomnography (REM sleep latency less than
or equal to 15 minutes) is highly specific (approximately 1% positive in control subjects)
but moderately sensitive (approximately 50%). A positive MSLT result displays an aver-
age sleep latency of less than or equal to 8 minutes, and sleep-onset REM periods in two or
more naps on a four- or five-nap test. The MSLT result is positive in 90%-95% of individ-
uals with narcolepsy versus 2%—4% of control subjects or individuals with other sleep dis-
orders. Additional polysomnographic findings often include frequent arousals, decreased
sleep efficiency, and increased stage 1 sleep. Periodic limb movements (found in about
40% of individuals with narcolepsy) and sleep apnea are often noted.
Hypocretin deficiency is demonstrated by measuring CSF hypocretin-1 immunoreac-
tivity. The test is particularly useful in individuals with suspected conversion disorder
and those without typical cataplexy, or in treatment-refractory cases. The diagnostic value
of the test is not affected by medications, sleep deprivation, or circadian time, but the find-
ings are uninterpretable when the individual is severely ill with a concurrent infection or
head trauma or is comatose. CSF cytology, protein, and glucose are within normal range
even when sampled within weeks of rapid onset. CSF hypocretin-1 in these incipient cases
is typically already very diminished or undetectable.
Functional Consequences of Narcolepsy
Driving and working are impaired, and individuals with narcolepsy should avoid jobs
that place themselves (e.g., working with machinery) or others (e.g., bus driver, pilot) in
danger. Once the narcolepsy is controlled with therapy, patients can usually drive, al-
though rarely long distances alone. Untreated individuals are also at risk for social isola-
tion and accidental injury to themselves or others. Social relations may suffer as these
individuals strive to avert cataplexy by exerting control over emotions.
Differential Diagnosis
Other hypersomnias. Hypersomnolence and narcolepsy are similar with respect to the
degree of daytime sleepiness, age at onset, and stable course over time but can be distin-
Narcolepsy 377
guished based on distinctive clinical and laboratory features. Individuals with hypersom-
nolence typically have longer and less disrupted nocturnal sleep, greater difficulty
awakening, more persistent daytime sleepiness (as opposed to more discrete “sleep at-
tacks” in narcolepsy), longer and less refreshing daytime sleep episodes, and little or no
dreaming during daytime naps. By contrast, individuals with narcolepsy have cataplexy
and recurrent intrusions of elements of REM sleep into the transition between sleep and
wakefulness (e.g., sleep-related hallucinations and sleep paralysis). The MSLT typically
demonstrates shorter sleep latencies (i.e., greater physiological sleepiness) as well as the
presence of multiple sleep-onset REM periods in individuals with narcolepsy.
Sleep deprivation and insufficient nocturnal sleep. Sleep deprivation and insufficient
nocturnal sleep are common in adolescents and shift workers. In adolescents, difficulties
falling asleep at night are common, causing sleep deprivation. The MSLT result may be
positive if conducted while the individual is sleep deprived or while his or her sleep is
phase delayed.
Sleep apnea syndromes. Sleep apneas are especially likely in the presence of obesity.
Because obstructive sleep apnea is more frequent than narcolepsy, cataplexy may be over-
looked (or absent), and the individual is assumed to have obstructive sleep apnea unre-
sponsive to usual therapies.
Major depressive disorder. Narcolepsy or hypersomnia may be associated or confused
with depression. Cataplexy is not present in depression. The MSLT results are most often
normal, and there is dissociation between subjective and objective sleepiness, as measured
by the mean sleep latency during the MSLT.
Conversion disorder (functional neurological symptom disorder). Atypical features,
such as long-lasting cataplexy or unusual triggers, may be present in conversion disorder
(functional neurological symptom disorder). Individuals may report sleeping and dream-
ing, yet the MSLT does not show the characteristic sleep-onset REM period. Full-blown,
long-lasting pseudocataplexy may occur during consultation, allowing the examining
physician enough time to verify reflexes, which remain intact.
Attention-deficit/hyperactivity disorder or other behavioral problems. In children and
adolescents, sleepiness can cause behavioral problems, including aggressiveness and in-
attention, leading to a misdiagnosis of attention-deficit/hyperactivity disorder.
Seizures. In young children, cataplexy can be misdiagnosed as seizures. Seizures are not
commonly triggered by emotions, and when they are, the trigger is not usually laughing or
joking. During a seizure, individuals are more likely to hurt themselves when falling. Sei-
zures characterized by isolated atonia are rarely seen in isolation of other seizures, and
they also have signatures on the electroencephalogram.
Chorea and movement disorders. In young children, cataplexy can be misdiagnosed as
chorea or pediatric autoimmune neuropsychiatric disorders associated with streptococcal
infections, especially in the context of a strep throat infection and high antistreptolysin O
antibody levels. Some children may have an overlapping movement disorder close to on-
set of the cataplexy.
Schizophrenia. In the presence of florid and vivid hypnagogic hallucinations, individuals
may think these experiences are real—a feature that suggests schizophrenia. Similarly,
with stimulant treatment, persecutory delusions may develop. If cataplexy is present, the
clinician should first assume that these symptoms are secondary to narcolepsy before con-
sidering a co-occurring diagnosis of schizophrenia.
Comorbidity
Narcolepsy can co-occur with bipolar, depressive, and anxiety disorders, and in rare cases
with schizophrenia. Narcolepsy is also associated with increased body mass index or obe-
378 Sleep-Wake Disorders
sity, especially when the narcolepsy is untreated. Rapid weight gain is common in young
children with a sudden disease onset. Comorbid sleep apnea should be considered if there
is a sudden aggravation of preexisting narcolepsy.
Relationship to International Classification of
Sleep Disorders
The International Classification of Sleep Disorders, 2nd Edition (ICSD-2), differentiates five
subtypes of narcolepsy.
Breathing-Related Sleep Disorders
The breathing-related sleep disorders category encompasses three relatively distinct dis-
orders: obstructive sleep apnea hypopnea, central sleep apnea, and sleep-related hypo-
ventilation.
Obstructive Sleep Apnea Hypopnea
Diagnostic Criteria 327.23 (G47.33)
A. Either (1) or (2):
1. Evidence by polysomnography of at least five obstructive apneas or hypopneas per
hour of sleep and either of the following sleep symptoms:
a. Nocturnal breathing disturbances: snoring, snorting/gasping, or breathing
pauses during sleep.
b. Daytime sleepiness, fatigue, or unrefreshing sleep despite sufficient opportuni-
ties to sleep that is not better explained by another mental disorder (including a
sleep disorder) and is not attributable to another medical condition.
2. Evidence by polysomnography of 15 or more obstructive aoneas and/or hypopneas
per hour of sleep regardless of accompanying symptoms.
Specify current severity:
Mild: Apnea hypopnea index is less than 15.
Moderate: Apnea hypopnea index is 15-30.
Severe: Apnea hypopnea index is greater than 30.
Specifiers
Disease severity is measured by a count of the number of apneas plus hypopneas per hour
of sleep (apnea hypopnea index) using polysomnography or other overnight monitoring.
Overall severity is also informed by levels of nocturnal desaturation and sleep fragmen-
tation (measured by brain cortical arousal frequency and sleep stages) and degree of as-
sociated symptoms and daytime impairment. However, the exact number and thresholds
may vary according to the specific measurement techniques used, and these numbers may
change over time. Regardless of the apnea hypopnea index (count) per se, the disorder is
considered to be more severe when apneas and hypopneas are accompanied by significant
oxygen hemoglobin desaturation (e.g., when more than 10% of the sleep time is spent at
desaturation levels of less than 90%) or when sleep is severely fragmented as shown by an
Obstructive Sleep Apnea Hypopnea 379
elevated arousal index (arousal index greater than 30) or reduced stages in deep sleep (e.g.,
percentage stage N3 [slow-wave sleep] less than 5%).
Diagnostic Features
Obstructive sleep apnea hypopnea is the most common breathing-related sleep disorder.
It is characterized by repeated episodes of upper (pharyngeal) airway obstruction (apneas
and hypopneas) during sleep. Apnea refers to the total absence of airflow, and hypopnea re-
fers to a reduction in airflow. Each apnea or hypopnea represents a reduction in breathing
of at least 10 seconds in duration in adults or two missed breaths in children and is typi-
cally associated with drops in oxygen saturation of 3% or greater and/or an electroenceph-
alographic arousal. Both sleep-related (nocturnal) and wake-time symptoms are common.
The cardinal symptoms of obstructive sleep apnea hypopnea are snoring and daytime
sleepiness.
Obstructive sleep apnea hypopnea in adults is diagnosed on the basis of polysom-
nographic findings and symptoms. The diagnosis is based on symptoms of 1) nocturnal
breathing disturbances (i.e., snoring, snorting / gasping, breathing pauses during sleep), or
2) daytime sleepiness, fatigue, or unrefreshing sleep despite sufficient opportunities to
sleep that are not better explained by another mental disorder and not attributable to an-
other medical condition, along with 3) evidence by polysomnography of five or more ob-
structive apneas or hypopneas per hour of sleep (Criterion A1). Diagnosis can be made in
the absence of these symptoms if there is evidence by polysomnography of 15 or more ob-
structive apneas and/or hypopneas per hour of sleep (Criterion A2),
Specific attention to disturbed sleep occurring in association with snoring or breathing
pauses and physical findings that increase risk of obstructive sleep apnea hypopnea (e.g.,
central obesity, crowded pharyngeal airway, elevated blood pressure) is needed to reduce
the chance of misdiagnosing this treatable condition.
Associated Features Supporting Diagnosis
Because of the frequency of nocturnal awakenings that occur with obstructive sleep apnea
hypopnea, individuals may report symptoms of insomnia. Other common, though non-
specific, symptoms of obstructive sleep apnea hypopnea are heartburn, nocturia, morning
headaches, dry mouth, erectile dysfunction, and reduced libido. Rarely, individuals may
complain of difficulty breathing while lying supine or sleeping. Hypertension may occur
in more than 60% of individuals with obstructive sleep apnea hypopnea.
Prevalence
Obstructive sleep apnea hypopnea is a very common disorder, affecting at least 1%-2% of
children, 2%~-15% of middle-age adults, and more than 20% of older individuals. In the
general community, prevalence rates of undiagnosed obstructive sleep apnea hypopnea
may be very high in elderly individuals. Since the disorder is strongly associated with obe-
sity, increases in obesity rates are likely to be accompanied by an increased prevalence of
this disorder. Prevalence may be particularly high among males, older adults, and certain
racial/ethnic groups. In adults, the male-to-female ratio of obstructive sleep apnea hypop-
nea ranges from 2:1 to 4:1. Gender differences decline in older age, possibly because of an
increased prevalence in females after menopause. There is no gender difference among
prepubertal children.
Deveiopment and Course
The age distribution of obstructive sleep apnea hypopnea likely follows a J-shaped distri-
bution. There is a peak in children ages 3-8 years when the nasopharynx may be compro-
mised by a relatively large mass of tonsillar tissue compared with the size of the upper
380 Sleep-Wake Disorders
airway. With growth of the airway and regression of lymphoid tissue during later child-
hood, there is reduction in prevalence. Then, as obesity prevalence increases in midlife and
females enter menopause, obstructive sleep apnea hypopnea again increases. The course
in older age is unclear; the disorder may level off after age 65 years, but in other individ-
uals, prevalence may increase with aging. Because there is some age dependency of the oc-
currence of apneas and hypopneas, polysomnographic results must be interpreted in light
of other clinical data. In particular, significant clinical symptoms of insomnia or hyper-
somnia should be investigated regardless of the individual’s age.
Obstructive sleep apnea hypopnea usually has an insidious onset, gradual progression,
and persistent course. Typically the loud snoring has been present for many years, often since
childhood, but an increase in its severity may lead the individual to seek evaluation. Weight
gain may precipitate an increase in symptoms. Although obstructive sleep apnea hypopnea
can occur at any age, it most commonly manifests among individuals ages 40-60 years. Over
45 years, the average apnea hypopnea index increases in adults and older individuals by ap-
proximately two apneas/hypopneas per hour. The apnea hypopnea index is increased and in-
cident obstructive sleep apnea hypopnea is greater among individuals who are older, who are
male, or who have a higher baseline body mass index (BMI) or increase their BMI over time.
Spontaneous resolution of obstructive sleep apnea hypopnea has been reported with weight
loss, particularly after bariatric surgery. In children, seasonal variation in obstructive sleep ap-
nea hypopnea has been observed, as has improvement with overall growth.
In young children, the signs and symptoms of obstructive sleep apnea hypopnea may be
more subtle than in adults, making diagnosis more difficult to establish. Polysomnography is
useful in confirming diagnosis. Evidence of fragmentation of sleep on the polysomnogram
may not be as apparent as in studies of older individuals, possibly because of the high homeo-
static drive in young individuals. Symptoms such as snoring are usually parent-reported and
thus have reduced sensitivity. Agitated arousals and unusual sleep postures, such as sleeping
on the hands and knees, may occur. Nocturnal enuresis also may occur and should raise the
suspicion of obstructive sleep apnea hypopnea if it recurs in a child who was previously dry at
night. Children may also manifest excessive daytime sleepiness, although this is not as com-
mon or pronounced as in adults. Daytime mouth breathing, difficulty in swallowing, and poor
speech articulation are also common features in children. Children younger than 5 years more
often present with nighttime symptoms, such as observed apneas or labored breathing, than
with behavioral symptoms (i.e., the nighttime symptoms are more noticeable and more often
bring the child to clinical attention). In children older than 5 years, daytime symptoms such as
sleepiness and behavioral problems (e.g., impulsivity and hyperactivity), attention-deficit/
hyperactivity disorder, learning difficulties, and morning headaches are more often the focus
of concern. Children with obstructive sleep apnea hypopnea also may present with failure to
thrive and developmental delays. In young children, obesity is a less common risk factor,
while delayed growth and “failure to thrive” may be present.
Risk and Prognostic Factors
Genetic and physiological. The major risk factors for obstructive sleep apnea hypopnea
are obesity and male gender. Others include maxillary-mandibular retrognathia or micro-
gnathia, positive family history of sleep apnea, genetic syndromes that reduce upper
airway patency (e.g., Down’s syndrome, Treacher Collin’s syndrome), adenotonsillar hy-
pertrophy (especially in young children), menopause (in females), and various endocrine
syndromes (e.g., acromegaly). Compared with premenopausal females, males are at in-
creased risk for obstructive sleep apnea hypopnea, possibly reflecting the influences of sex
hormones on ventilatory control and body fat distribution, as well as because of gender
differences in airway structure. Medications for mental disorders and medical conditions
that tend to induce somnolence may worsen the course of apnea symptoms if these med-
ications are not managed carefully.
Obstructive Sleep Apnea Hypopnea 381
Obstructive sleep apnea hypopnea has a strong genetic basis, as evidenced by the sig-
nificant familial aggregation of the apnea hypopnea index. The prevalence of obstructive
sleep apnea hypopnea is approximately twice as high among the first-degree relatives of
probands with obstructive sleep apnea hypopnea as compared with members of control
families. One-third of the variance in the apnea hypopnea index is explained by shared fa-
milial factors. Although genetic markers with diagnostic or prognostic value are not yet
available for use, eliciting a family history of obstructive sleep apnea hypopnea should in-
crease the clinical suspicion for the disorder.
Culture-Related Diagnostic Issues
There is a potential for sleepiness and fatigue to be reported differently across cultures. In
some groups, snoring may be considered a sign of health and thus may not trigger con-
cerns. Individuals of Asian ancestry may be at increased risk for obstructive sleep apnea
hypopnea despite relatively low BMI, possibly reflecting the influence of craniofacial risk
factors that narrow the nasopharynx.
Gender-Related Issues
Females may more commonly report fatigue rather than sleepiness and may underreport
snoring.
Diagnostic Markers
Polysomnography provides quantitative data on frequency of sleep-related respiratory
disturbances and associated changes in oxygen saturation and sleep continuity. Polysom-
nographic findings in children differ from those in adults in that children demonstrate
labored breathing, partial obstructive hypoventilation with cyclical desaturations, hyper-
capnia and paradoxical movements. Apnea hypopnea index levels as low as 2 are used to
define thresholds of abnormality in children.
Arterial blood gas measurements while the individual is awake are usually normal, but
some individuals can have waking hypoxemia or hypercapnia. This pattern should alert the
clinician to the possibility of coexisting lung disease or hypoventilation. Imaging procedures
may reveal narrowing of the upper airway. Cardiac testing may show evidence of impaired
ventricular function. Individuals with severe nocturnal oxygen desaturation may also have el-
evated hemoglobin or hematocrit values. Validated sleep measures (e.g., multiple sleep la-
tency test [MSLT], maintenance of wakefulness test) may identify sleepiness.
Functional Consequences of
Obstructive Sleep Apnea Hypopnea
More than 50% of individuals with moderate to severe obstructive sleep apnea hypopnea
report symptoms of daytime sleepiness. A twofold increased risk of occupational accidents
has been reported in association with symptoms of snoring and sleepiness. Motor vehicle
crashes also have been reported to be as much as sevenfold higher among individuals with
elevated apnea hypopnea index values. Clinicians should be cognizant of state govern-
ment requirements for reporting this disorder, especially in relationship to commercial
drivers. Reduced scores on measures of health-related quality of life are common in individ-
uals with obstructive sleep apnea hypopnea, with the largest decrements observed in the
physical and vitality subscales.
Differential Diagnosis
Primary snoring and other sleep disorders. Individuals with obstructive sleep apnea
hypopnea must be differentiated from individuals with primary snoring (i.e., otherwise
382 Sleep-Wake Disorders
asymptomatic individuals who snore and do not have abnormalities on overnight polysom-
nography). Individuals with obstructive sleep apnea hypopnea may additionally report
nocturnal gasping and choking. The presence of sleepiness or other daytime symptoms
not explained by other etiologies suggests the diagnosis of obstructive sleep apnea hypop-
nea, but this differentiation requires polysomnography. Definitive differential diagnosis
between hypersomnia, central sleep apnea, sleep-related hypoventilation, and obstructive
sleep apnea hypopnea also requires polysomnographic studies.
Obstructive sleep apnea hypopnea must be differentiated from other causes of sleepi-
ness, such as narcolepsy, hypersomnia, and circadian rhythm sleep disorders. Obstructive
sleep apnea hypopnea can be differentiated from narcolepsy by the absence of cataplexy,
sleep-related hallucinations, and sleep paralysis and by the presence of loud snoring,
gasping during sleep, or observed apneas in sleep. Daytime sleep episodes in narcolepsy
are characteristically shorter, more refreshing, and more often associated with dreaming.
Obstructive sleep apnea hypopnea shows characteristic apneas and hypopneas and oxy-
gen desaturation during nocturnal polysomnographic studies. Narcolepsy results in mul-
tiple sleep-onset rapid eye movement (REM) periods during the MSLT. Narcolepsy, like
obstructive sleep apnea hypopnea, may be associated with obesity, and some individuals
have concurrent narcolepsy and obstructive sleep apnea hypopnea. A diagnosis of narco-
lepsy does not exclude the diagnosis of obstructive sleep apnea hypopnea, as the two con-
ditions may co-occur.
Insomnia disorder. For individuals complaining of difficulty initiating or maintaining
sleep or early-morning awakenings, insomnia disorder can be differentiated from obstruc-
tive sleep apnea hypopnea by the absence of snoring and the absence of the history, signs,
and symptoms characteristic of the latter disorder. However, insomnia and obstructive
sleep apnea hypopnea may coexist, and if so, both disorders may need to be addressed
concurrently to improve sleep.
Panic attacks. Nocturnal panic attacks may include symptoms of gasping or choking
during sleep that may be difficult to distinguish clinically from obstructive sleep apnea hy-
popnea. However, the lower frequency of episodes, intense autonomic arousal, and lack of
excessive sleepiness differentiate nocturnal panic attacks from obstructive sleep apnea hy-
popnea. Polysomnography in individuals with nocturnal panic attacks does not reveal the
typical pattern of apneas or oxygen desaturation characteristic of obstructive sleep apnea
hypopnea. Individuals with obstructive sleep apnea hypopnea do not provide a history of
daytime panic attacks.
Attention-deficit/hyperactivity disorder. Attention-deficit/hyperactivity disorder in chil-
dren may include symptoms of inattention, academic impairment, hyperactivity, and in-
ternalizing behaviors, all of which may also be symptoms of childhood obstructive sleep
apnea hypopnea. The presence of other symptoms and signs of childhood obstructive
sleep apnea hypopnea (e.g., labored breathing or snoring during sleep and adenotonsillar
hypertrophy) would suggest the presence of obstructive sleep apnea hypopnea. Obstruc-
tive sleep apnea hypopnea and attention-deficit/hyperactivity disorder may commonly
co-occur, and there may be causal links between them; therefore, risk factors such as en-
larged tonsils, obesity, or a family history of sleep apnea may help alert the clinician to
their co-occurrence.
Substance/medication-induced insomnia or hypersomnia. Substance use and substance
withdrawal (including medications) can produce insomnia or hypersomnia. A careful his-
tory is usually sufficient to identify the relevant substance/ medication, and follow-up
shows improvement of the sleep disturbance after discontinuation of the substance /med-
ication. In other cases, the use of a substance /medication (e.g., alcohol, barbiturates, ben-
zodiazepines, tobacco) has been shown to exacerbate obstructive sleep apnea hypopnea.
An individual with symptoms and signs consistent with obstructive sleep apnea hypop-
Central Sleep Apnea 383
nea should receive that diagnosis, even in the presence of concurrent substance use that is
exacerbating the condition.
\
Comorbidity
Systemic hypertension, coronary artery disease, heart failure, stroke, diabetes, and increased
mortality are consistently associated with obstructive sleep apnea hypopnea. Risk esti-
mates vary from 30% to as much as 300% for moderate to severe obstructive sleep apnea
hypopnea. Evidence of pulmonary hypertension and right heart failure (e.g., cor pulmo-
nale, ankle edema, hepatic congestion) are rare in obstructive sleep apnea hypopnea and
when present indicate either very severe disease or associated hypoventilation or cardio-
pulmonary comorbidities. Obstructive sleep apnea hypopnea also may occur with in-
creased frequency in association with a number of medical or neurological conditions (e.g.,
cerebrovascular disease, Parkinson’s disease). Physical findings reflect the co-occurrence of
these conditions.
As many as one-third of individuals referred for evaluation of obstructive sleep apnea
hypopnea report symptoms of depression, with as many of 10% having depression scores
consistent with moderate to severe depression. Severity of obstructive sleep apnea hypop-
nea, as measured by the apnea hypopnea index, has been found to be correlated with se-
verity of symptoms of depression. This association may be stronger in males than in
females.
Reiationship to International Classification of
Sleep Disorders
The International Classification of Sleep Disorders, 2nd Edition (ICSD-2), differentiates 11 sub-
types of “sleep-related breathing disorders,” including primary central sleep apnea, ob-
structive sleep apnea, and sleep-related hypoventilation.
Central Sleep Apnea
Diagnostic Criteria
A. Evidence by polysomnography of five or more central apneas per hour of sleep.
B. The disorder is not better explained by another current sleep disorder.
Specify whether:
327.21 (G47.31) Idiopathic central sleep apnea: Characterized by repeated epi-
sodes of apneas and hypopneas during sleep caused by variability in respiratory effort
but without evidence of airway obstruction.
786.04 (R06.3}) Cheyne-Stokes breathing: A pattern of periodic crescendo-
decrescendo variation in tidal volume that results in central apneas and hypopneas at
a frequency of at least five events per hour, accompanied by frequent arousal.
780.57 (G47.37) Central sleep apnea comorbid with opioid use: The pathogenesis
of this subtype is attributed to the effects of opioids on the respiratory rhythm genera-
tors in the medulla as well as the differential effects on hypoxic versus hypercapnic re-
spiratory drive.
Coding note (for 780.57 [G47.37] code only): When an opioid use disorder is present, first
code the opioid use disorder: 305.50 (F11.10) mild opioid use disorder or 304.00 (F11.20)
moderate or severe opioid use disorder; then code 780.57 (G47.37) central sleep apnea
comorbid with opioid use. When an opioid use disorder is not present (e.g., after a one-
time heavy use of the substance), code only 780.57 (G47.37) central sleep apnea comor-
bid with opioid use.
384 Steep-Wake Disorders
Note: See the section “Diagnostic Features” in text.
Specify current severity:
Severity of central sleep apnea is graded according to the frequency of the breathing
disturbances as well as the extent of associated oxygen desaturation and sleep frag-
mentation that occur as a consequence of repetitive respiratory disturbances.
Subtypes
Idiopathic central sleep apnea and Cheyne-Stokes breathing are characterized by increased
gain of the ventilatory control system, also referred to as high loop gain, which leads to in-
stability in ventilation and PaCO, levels. This instability is termed periodic breathing and
can be recognized by hyperventilation alternating with hypoventilation. Individuals with
these disorders typically have pCO) levels while awake that are slightly hypocapneic or
normocapneic. Central sleep apnea may also manifest during initiation of treatment of ob-
structive sleep apnea hypopnea or may occur in association with obstructive sleep apnea
hypopnea syndrome (termed complex sleep apnea). The occurrence of central sleep apnea in
association with obstructive sleep apnea is also considered to be due to high loop gain. In
contrast, the pathogenesis of central sleep apnea comorbid with opioid use has been at-
tributed to the effects of opioids on the respiratory rhythm generators in the medulla as
well as to its differential effects on hypoxic versus hypercapneic respiratory drive. These
individuals may have elevated pCO, levels while awake. Individuals receiving chronic
methadone maintenance therapy have been noted to have increased somnolence and de-
pression, although the role of breathing disorders associated with opioid medication in caus-
ing these problems has not been studied.
Specifiers
An increase in the central apnea index (i.e., number of central apneas per hour of sleep) re-
flects an increase in severity of central sleep apnea. Sleep continuity and quality may be
markedly impaired with reductions in restorative stages of non—-rapid eye movement (REM)
sleep (i.e., decreased slow-wave sleep [stage N3}). In individuals with severe Cheyne-
Stokes breathing, the pattern can also be observed during resting wakefulness, a finding
that is thought to be a poor prognostic marker for mortality.
Diagnostic Features
Central sleep apnea disorders are characterized by repeated episodes of apneas and hy-
popneas during sleep caused by variability in respiratory effort. These are disorders of
ventilatory control in which respiratory events occur in a periodic or intermittent pattern.
Idiopathic central sleep apnea is characterized by sleepiness, insomnia, and awakenings due
to dyspnea in association with five or more central apneas per hour of sleep. Central sleep
apnea occurring in individuals with heart failure, stroke, or renal failure typically have a
breathing pattern called Cheyne-Stokes breathing, which is characterized by a pattern of
periodic crescendo-decrescendo variation in tidal volume that results in central apneas
and hypopneas occurring at a frequency of at least five events per hour that are accompa-
nied by frequent arousals. Central and obstructive sleep apneas may coexist; the ratio of
central to obstructive apneas/hypopneas may be used to identify which condition is pre-
dominant.
Alterations in neuromuscular control of breathing can occur in association with med-
ications or substances used in individuals with mental health conditions, which can cause
or exacerbate impairments of respiratory rhythm and ventilation. Individuals taking these
medications have a sleep-related breathing disorder that could contribute to sleep distur-
bances and symptoms such as sleepiness, confusion, and depression. Specifically, chronic
Central Sleep Apnea 385
use of long-acting opioid medications is often associated with impairment of respiratory con-
trol leading to central sleep apnea.
\
Associated Features Supporting Diagnosis
Individuals with central sleep apnea hypopneas can manifest with sleepiness or insomnia.
There can be complaints of sleep fragmentation, including awakening with dyspnea.
Some individuals are asymptomatic. Obstructive sleep apnea hypopnea can coexist with
Cheyne-Stokes breathing, and thus snoring and abruptly terminating apneas may be ob-
served during sleep.
Prevaience
The prevalence of idiopathic central sleep apnea is unknown but thought to be rare. The
prevalence of Cheyne-Stokes breathing is high in individuals with depressed cardiac ven-
tricular ejection fraction. In individuals with an ejection fraction of less than 45%, the prev-
alence has been reported to be 20% or higher. The male-to-female ratio for prevalence is
even more highly skewed toward males than for obstructive sleep apnea hypopnea. Prev-
alence increases with age, and most patients are older than 60 years. Cheyne-Stokes breath-
ing occurs in approximately 20% of individuals with acute stroke. Central sleep apnea
comorbid with opioid use occurs in approximately 30% of individuals taking chronic opi-
oids for nonmalignant pain and similarly in individuals receiving methadone mainte-
nance therapy.
Development and Course
The onset of Cheyne-Stokes breathing appears tied to the development of heart failure. The
Cheyne-Stokes breathing pattern is associated with oscillations in heart rate, blood pres-
sure and oxygen desaturation, and elevated sympathetic nervous system activity that can
promote progression of heart failure. The clinical significance of Cheyne-Stokes breathing
in the setting of stroke is not known, but Cheyne-Stokes breathing may be a transient find-
ing that resolves with time after acute stroke. Central sleep apnea comorbid with opioid
use has been documented with chronic use (i.e., several months).
Risk and Prognostic Factors
Genetic and physiological. Cheyne-Stokes breathing is frequently present in individu-
als with heart failure. The coexistence of atrial fibrillation further increases risk, as do older
age and male gender. Cheyne-Stokes breathing is also seen in association with acute stroke
and possibly renal failure. The underlying ventilatory instability in the setting of heart fail-
ure has been attributed to increased ventilatory chemosensitivity and hyperventilation
due to pulmonary vascular congestion and circulatory delay. Central sleep apnea is seen
in individuals taking long-acting opioids.
Diagnostic Markers
Physical findings seen in individuals with a Cheyne-Stokes breathing pattern relate to its
risk factors. Findings consistent with heart failure, such as jugular venous distension, 53
heart sound, lung crackles, and lower extremity edema, may be present. Polysomnogra-
phy is used to characterize the breathing characteristics of each breathing-related sleep
disorder subtype. Central sleep apneas are recorded when periods of breathing cessation
for longer than 10 seconds occur. Cheyne-Stokes breathing is characterized by a pattern of
periodic crescendo-decrescendo variation in tidal volume that results in central apneas
and hypopneas occurring at a frequency of at least five events per hour that are accompa-
nied by frequent arousals. The cycle length of Cheyne-Stokes breathing (or time from end
of one central apnea to the end of the next apnea) is about 60 seconds.
386 Sleep-Wake Disorders
Functional Consequences of Central Sleep Apnea
Idiopathic central sleep apnea has been reported to cause symptoms of disrupted sleep, in-
cluding insomnia and sleepiness. Cheyne-Stokes breathing with comorbid heart failure
has been associated with excessive sleepiness, fatigue, and insomnia, although many in-
dividuals may be asymptomatic. Coexistence of heart failure and Cheyne-Stokes breath-
ing may be associated with increased cardiac arrhythmias and increased mortality or
cardiac transplantation. Individuals with central sleep apnea comorbid with opioid use
may present with symptoms of sleepiness or insomnia.
Differential Diagnosis
Idiopathic central sleep apnea must be distinguished from other breathing-related sleep
disorders, other sleep disorders, and medical conditions and mental disorders that cause
sleep fragmentation, sleepiness, and fatigue. This is achieved using polysomnography.
Other breathing-related sleep disorders and sleep disorders. Central sleep apnea can
be distinguished from obstructive sleep apnea hypopnea by the presence of at least five
central apneas per hour of sleep. These conditions may co-occur, but central sleep apnea is
considered to predominate when the ratio of central to obstructive respiratory events ex-
ceeds 50%.
Cheyne-Stokes breathing can be distinguished from other mental disorders, including
other sleep disorders, and other medical conditions that cause sleep fragmentation, sleep-
iness, and fatigue based on the presence of a predisposing condition (e.g., heart failure or
stroke) and signs and polysomnographic evidence of the characteristic breathing pattern.
Polysomnographic respiratory findings can help distinguish Cheyne-Stokes breathing
from insomnia due to other medical conditions. High-altitude periodic breathing has a
pattern that resembles Cheyne-Stokes breathing but has a shorter cycle time, occurs only
at high altitude, and is not associated with heart failure.
Central sleep apnea comorbid with opioid use can be differentiated from other types of
breathing-related sleep disorders based on the use of long-acting opioid medications in
conjunction with polysomnographic evidence of central apneas and periodic or ataxic
breathing. It can be distinguished from insomnia due to drug or substance use based on
polysomnographic evidence of central sleep apnea.
Comorbidity
Central sleep apnea disorders are frequently present in users of long-acting opioids, such
as methadone. Individuals taking these medications have a sleep-related breathing disor-
der that could contribute to sleep disturbances and symptoms such as sleepiness, confu-
sion, and depression. While the individual is asleep, breathing patterns such as central
apneas, periodic apneas, and ataxic breathing may be observed. Obstructive sleep apnea
hypopnea may coexist with central sleep apnea, and features consistent with this condi-
tion can also be present (see “Obstructive Sleep Apnea Hypopnea” earlier in this chapter).
Cheyne-Stokes breathing is more commonly observed in association with conditions that
include heart failure, stroke, and renal failure and is seen more frequently in individuals
with atrial fibrillation. Individuals with Cheyne-Stokes breathing are more likely to be
older, to be male, and to have lower weight than individuals with obstructive sleep apnea
hypopnea.
Sleep-Related Hypoventilation 387
Sleep-Related Hypoventilation
Diagnostic Criteria
A. Polysomnograpy demonstrates episodes of decreased respiration associated with el-
evated COz levets. (Note: In the absence of objective measurement of COs, persistent
tow levels of hemoglobin oxygen saturation unassociated with apneic/hypopneic
events may indicate hypoventilation.)
B. The disturbance is not better explained by another current sleep disorder.
Specify whether:
327.24 (G47.34) Idiopathic hypoventilation: This subtype is not attributable to any
readily identified condition.
327.25 (G47.35) Congenital central alveolar hypoventilation: This subtype is a rare
congenital disorder in which the individual typically presents in the perinatal period with
shaliow breathing, or cyanosis and apnea during sleep.
327.26 (G47.36) Comorbid sleep-related hypoventilation: This subtype occurs as a
consequence of a medical condition, such as a pulmonary disorder (e.g., interstitial
lung disease, chronic obstructive pulmonary disease) or a neuromuscular or chest wall
disorder (e.g., muscular dystrophies, postpolio syndrome, cervical spinal cord injury,
kyphoscoliosis), or medications (e.g., benzodiazepines, opiates). {t also occurs with
obesity (obesity hypoventilation disorder), where it reflects a combination of increased
work of breathing due to reduced chest wall compliance and ventilation-perfusion mis-
match and variably reduced ventilatory drive. Such individuals usually are character-
ized by body mass index of greater than 30 and hypercapnia during wakefulness (with
a pCOz of greater than 45), without other evidence of hypoventilation.
Specify current severity:
Severity is graded according to the degree of hypoxemia and hypercarbia present dur-
ing sleep and evidence of end organ impairment due to these abnormalities (e.g., right-
sided heart failure). The presence of blood gas abnormalities during wakefulness is an
indicator of greater severity.
Subtypes
Regarding obesity hypoventilation disorder, the prevalence of obesity hypoventilation in
the general population is not known but is thought to be increasing in association with the
increased prevalence of obesity and extreme obesity.
Diagnostic Features
Sleep-related hypoventilation can occur independently or, more frequently, comorbid
with medical or neurological disorders, medication use, or substance use disorder. Al-
though symptoms are not mandatory to make this diagnosis, individuals often report
excessive daytime sleepiness, frequent arousals and awakenings during sleep, morning
headaches, and insomnia complaints.
Associated Features Supporting Diagnosis
Individuals with sleep-related hypoventilation can present with sleep-related complaints
of insomnia or sleepiness. Episodes of orthopnea can occur in individuals with diaphragm
weakness. Headaches upon awakening may be present. During sleep, episodes of shallow
breathing may be observed, and obstructive sleep apnea hypopnea or central sleep apnea
may coexist. Consequences of ventilatory insufficiency, including pulmonary hyperten-
sion, cor pulmonale (right heart failure), polycythemia, and neurocognitive dysfunction,
388 Sleep-Wake Disorders
can be present. With progression of ventilatory insufficiency, blood gas abnormalities ex-
tend into wakefulness. Features of the medical condition causing sleep-related hypoven-
tilation can also be present. Episodes of hypoventilation may be associated with frequent
arousals or bradytachycardia. Individuals may complain of excessive sleepiness and in-
somnia or morning headaches or may present with findings of neurocognitive dysfunction
or depression. Hypoventilation may not be present during wakefulness.
Prevalence
Idiopathic sleep-related hypoventilation in adults is very uncommon. The prevalence of
congenital central alveolar hypoventilation is unknown, but the disorder is rare. Comor-
bid sleep-related hypoventilation (i.e., hypoventilation comorbid with other conditions,
such as chronic obstructive pulmonary disease [COPD], neuromuscular disorders, or obe-
sity) is more common.
Development and Course
Idiopathic sleep-related hypoventilation is thought to be a slowly progressive disorder of
respiratory impairment. When this disorder occurs comorbidly with other disorders (e.g.,
COPD, neuromuscular disorders, obesity), disease severity reflects the severity of the un-
derlying condition, and the disorder progresses as the condition worsens. Complications
such as pulmonary hypertension, cor pulmonale, cardiac dysrhythmias, polycythemia,
neurocognitive dysfunction, and worsening respiratory failure can develop with increas-
ing severity of blood gas abnormalities.
Congenital central alveolar hypoventilation usually manifests at birth with shallow,
erratic, or absent breathing. This disorder can also manifest during infancy, childhood,
and adulthood because of variable penetrance of the PHOX2B mutation. Children with
congenital central alveolar hypoventilation are more likely to have disorders of the auto-
nomic nervous system, Hirschsprung’s disease, neural crest tumors, and characteristic box-
shaped face (i.e., the face is short relative to its width).
Risk and Prognostic Factors
Environmental. Ventilatory drive can be reduced in individuals using central nervous
system depressants, including benzodiazepines, opiates, and alcohol.
Genetic and physiological. Idiopathic sleep-related hypoventilation is associated with
reduced ventilatory drive due to a blunted chemoresponsiveness to CO, (reduced respi-
ratory drive; i.e., “won't breathe”), reflecting underlying neurological deficits in centers
governing the control of ventilation. More commonly, sleep-related hypoventilation is co-
morbid with another medical condition, such as a pulmonary disorder, a neuromuscular
or chest wall disorder, or hypothyroidism, or with use of medications (e.g., benzodiaze-
pines, opiates). In these conditions, the hypoventilation may be a consequence of in-
creased work of breathing and/or impairment of respiratory muscle function (i-e., “can’t
breathe”) or reduced respiratory drive (i.e., “won't breathe”).
Neuromuscular disorders influence breathing through impairment of respiratory mo-
tor innervation or respiratory muscle function. They include conditions such as amyo-
trophic lateral sclerosis, spinal cord injury, diaphragmatic paralysis, myasthenia gravis,
Lambert-Eaton syndrome, toxic or metabolic myopathies, postpolio syndrome, and Char-
cot-Marie-Tooth syndrome.
Congenital central alveolar hypoventilation is a genetic disorder attributable to muta-
tions of PHOX2B, a gene that is crucial for the development of the embryonic autonomic
nervous system and neural crest derivatives. Children with congenital central alveolar hy-
poventilation show blunted ventilatory responses to hypercapnia, especially in non-rapid
eye movement sleep.
Sleep-Related Hypoventilation 389
Gender-Related Diagnostic Issues
Gender distributions for sleep-related hypoventilation occurring in association with co-
morbid conditions reflect the gender distributions of the comorbid conditions. For exam-
ple, COPD is more frequently present in males and with increasing age.
Diagnostic Markers
Sleep-related hypoventilation is diagnosed using polysomnography showing sleep-related
hypoxemia and hypercapnia that is not better explained by another breathing-related sleep
disorder. The documentation of increased arterial pCO? levels to greater than 55 mmHg
during sleep or a 10 mmHg or greater increase in pCO, levels (to a level that also exceeds
50 mmHg) during sleep in comparison to awake supine values, for 10 minutes or longer, is
the gold standard for diagnosis. However, obtaining arterial blood gas determinations dur-
ing sleep is impractical, and non-invasive measures of pCO, have not been adequately val-
idated during sleep and are not widely used during polysomnography in adults. Prolonged
and sustained decreases in oxygen saturation (oxygen saturation of less than 90% for more
than 5 minutes with a nadir of at least 85%, or oxygen saturation of less than 90% for at least
30% of sleep time) in the absence of evidence of upper airway obstruction are often used as
an indication of sleep-related hypoventilation; however, this finding is not specific, as there
are other potential causes of hypoxemia, such as that due to lung disease.
Functional Consequences of
Sleep-Related Hypoventilation
The consequences of sleep-related hypoventilation are related to the effects of chronic ex-
posure to hypercapnia and hypoxemia. These blood gas derangements cause vasocon-
striction of the pulmonary vasculature leading to pulmonary hypertension, which, if
severe, can result in right-sided heart failure (cor pulmonale). Hypoxemia can lead to dys-
function of organs such as the brain, blood, and heart, leading to outcomes such as cog-
nitive dysfunction, polycythemia, and cardiac arrhythmias. Hypercapnia can depress
ventilatory drive, leading to progressive respiratory failure.
Differential Diagnosis
Other medical conditions affecting ventilation. In adults, the idiopathic variety of sleep-
related hypoventilation is very uncommon and is determined by excluding the presence of
lung diseases, skeletal malformations, neuromuscular disorders, and other medical and
neurological disorders or medications that affect ventilation. Sleep-related hypoventila-
tion must be distinguished from other causes of sleep-related hypoxemia, such as that due
to lung disease.
Other breathing-related sleep disorders. Sleep-related hypoventilation can be distin-
guished from obstructive sleep apnea hypopnea and central sleep apnea based on clinical
features and findings on polysomnography. Sleep-related hypoventilation typically shows
more sustained periods of oxygen desaturation rather that the periodic episodes seen in
obstructive sleep apnea hypopnea and central sleep apnea. Obstructive sleep apnea hy-
popnea and central sleep apnea also show a pattern of discrete episodes of repeated air-
flow decreases that can be absent in sleep-related hypoventilation.
Comorbidity
Sleep-related hypoventilation often occurs in association with a pulmonary disorder (e.g., in-
terstitial lung disease, COPD), with a neuromuscular or chest wall disorder (e.g., muscular
dystrophies, post-polio syndrome, cervical spinal cord injury, obesity, kyphoscoliosis), or,
390 Sleep-Wake Disorders
most relevant to the mental health provider, with medication use (e.g., benzodiazepines, opi-
ates). Congenital central alveolar hypoventilation often occurs in association with autonomic
dysfunction and may occur in association with Hirschsprung’s disease. COPD, a disorder of
lower airway obstruction usually associated with cigarette smoking, can result in sleep-
related hypoventilation and hypoxemia. The presence of coexisting obstructive sleep apnea
hypopnea is thought to exacerbate hypoxemia and hypercapnia during sleep and wakeful-
ness. The relationship between congenital central alveolar hypoventilation and idiopathic
sleep-related hypoventilation is unclear; in some individuals, idiopathic sleep-related hy-
poventilation may represent cases of late-onset congenital central alveolar hypoventilation.
Relationship to Internationai Ciassification of
Sleep Disorders
The International Classification of Sleep Disorders, 2nd Edition (ICSD-2), combines sleep-
related hypoventilation and sleep-related hypoxemia under the category of sleep-related
hypoventilation/hypoxemic syndromes. This approach to classification reflects the fre-
quent co-occurrence of disorders that lead to hypoventilation and hypoxemia. In contrast,
the classification used in DSM-5 reflects evidence that there are distinct sleep-related
pathogenetic processes leading to hypoventilation.
Circadian Rhythm Sleep-Wake Disorders
Diagnostic Criteria
A. Apersistent or recurrent pattern of sleep disruption that is primarily due to an alteration
of the circadian system or to a misalignment between the endogenous circadian
rhythm and the sleep-wake schedule required by an individual's physical environment
or social or professional schedule.
. The sleep disruption leads to excessive sleepiness or insomnia, or both.
. The sleep disturbance causes clinically significant distress or impairment in social, oc-
cupational, and other important areas of functioning.
Coding note: For ICD-9-CM, code 307.45 for all subtypes. For ICD-10-CM, code is based
on subtype.
Specify whether:
307.45 (G47.21) Delayed sleep phase type: A pattern of delayed sleep onset and
awakening times, with an inability to fall asleep and awaken at a desired or convention-
ally acceptable earlier time.
Specify if:
Familial: A family history of delayed sleep phase is present.
Specify if:
Overlapping with non-24-hour sleep-wake type: Delayed sleep phase type
may overlap with another circadian rhythm sleep-wake disorder, non-24-hour
sleep-wake type.
307.45 (G47.22) Advanced sleep phase type: A pattern of advanced sleep onset and
awakening times, with an inability to remain awake or asleep until the desired or con-
ventionally acceptable later sleep or wake times.
Specify if:
Familial: A family history of advanced sleep phase is present.
307.45 (G47.23) Irregular sleep-wake type: A temporally disorganized sleep-wake
pattern, such that the timing of sleep and wake periods is variable throughout the 24-
hour period.
Oo
Circadian Rhythm Sleep-Wake Disorders 391
307.45 (G47.24) Non-24-hour sleep-wake type: A pattern of sleep-wake cycles that
is not synchronized to the 24-hour environment, with a consistent daily drift (usually to
later and later times) of sleep onset and wake times.
307.45 (G47.26) Shift work type: Insomnia during the major sleep period and/or ex-
cessive sleepiness (including inadvertent sleep) during the major awake period asso-
ciated with a shift work schedule (i.e., requiring unconventional work hours).
307.45 (G47.20) Unspecified type
Specify if:
Episodic: Symptoms last at least 1 month but less than 3 months.
Persistent: Symptoms last 3 months or longer.
Recurrent: Two or more episodes occur within the space of 1 year.
Delayed Sleep Phase Type
Diagnostic Features
The delayed sleep phase type is based primarily ona history of a delay in the timing of the
major sleep period (usually more than 2 hours) in relation to the desired sleep and wake-
up time, resulting in symptoms of insomnia and excessive sleepiness. When allowed to set
their own schedule, individuals with delayed sleep phase type exhibit normal sleep qual-
ity and duration for age. Symptoms of sleep-onset insomnia, difficulty waking in the
morning, and excessive early day sleepiness are prominent.
Associated Features Supporting Diagnosis
Common associated features of delayed sleep phase type include a history of mental dis-
orders or a concurrent mental disorder. Extreme and prolonged difficulty awakening with
morning confusion is also common. Psychophysiological insomnia may develop as a re-
sult of maladaptive behaviors that impair sleep and increase arousal because of repeated
attempts to fall asleep at an earlier time.
Prevaience
Prevalence of delayed sleep phase type in the general population is approximately 0.17%
but appears to be greater than 7% in adolescents. Although the prevalence of familial de-
layed sleep phase type has not been established, a family history of delayed sleep phase is
present in individuals with delayed sleep phase type.
Development and Course
Course is persistent, lasting longer than 3 months, with intermittent exacerbations through-
out adulthood. Although age at onset is variable, symptoms begin typically in adolescence
and early adulthood and persist for several months to years before diagnosis is estab-
lished. Severity may decrease with age. Relapse of symptoms is common.
Clinical expression may vary across the lifespan depending on social, school, and work
obligations. Exacerbation is usually triggered by a change in work or school schedule that
requires an early rise time. Individuals who can alter their work schedules to accommo-
date the delayed circadian sleep and wake timing can experience remission of symptoms.
Increased prevalence in adolescence may be a consequence of both physiological and be-
havioral factors. Hormonal changes may be involved specifically, as delayed sleep phase is as-
sociated with the onset of puberty. Thus, delayed sleep phase type in adolescents should be
differentiated from the common delay in the timing of circadian rhythms in this age group. In
the familial form, the course is persistent and may not improve significantly with age.
392 Sleep-Wake Disorders
Risk and Prognostic Factors
Genetic and physiological. Predisposing factors may include a longer than average cir-
cadian period, changes in light sensitivity, and impaired homeostatic sleep drive. Some in-
dividuals with delayed sleep phase type may be hypersensitive to evening light, which
can serve as a delay signal to the circadian clock, or they may be hyposensitive to morning
light such that its phase-advancing effects are reduced. Genetic factors may play a role in
the pathogenesis of familial and sporadic forms of delayed sleep phase type, including
mutations in circadian genes (e.g., PER3, CKle).
Diagnostic Markers
Confirmation of the diagnosis includes a complete history and use of a sleep diary or actigra-
phy (.e.,a wrist-worn motion detector that monitors motor activity for prolonged periods and
can be used as a proxy for sleep-wake patterns for at least 7 days). The period covered should
include weekends, when social and occupational obligations are less strict, to ensure that the
individual exhibits a consistently delayed sleep-wake pattern. Biomarkers such as salivary
dim light melatonin onset should be obtained only when the diagnosis is unclear.
Functional Consequences of Delayed Sleep Phase Type
Excessive early day sleepiness is prominent. Extreme and prolonged difficulty awakening
with morning confusion (i.e., sleep inertia) is also common. The severity of insomnia and
excessive sleepiness symptoms varies substantially among individuals and largely de-
pends on the occupational and social demands on the individual.
Differential Diagnosis
Normative variations in sleep. Delayed sleep phase type must be distinguished from
“normal” sleep patterns in which an individual has a late schedule that does not cause
personal, social, or occupational distress (most commonly seen in adolescents and young
adults).
Other sleep disorders. Insomnia disorder and other circadian rhythm sleep-wake dis-
orders should be included in the differential. Excessive sleepiness may also be caused by
other sleep disturbances, such as breathing-related sleep disorders, insomnias, sleep-
related movement disorders, and medical, neurological, and mental disorders. Overnight
polysomnography may help in evaluating for other comorbid sleep disorders, such as
sleep apnea. The circadian nature of delayed sleep phase type, however, should differen-
tiate it from other disorders with similar complaints.
Comorbidity
Delayed sleep phase type is strongly associated with depression, personality disorder, and
somatic symptom disorder or illness anxiety disorder. In addition, comorbid sleep disor-
ders, such as insomnia disorder, restless legs syndrome, and sleep apnea, as well as depres-
sive and bipolar disorders and anxiety disorders, can exacerbate symptoms of insomnia
and excessive sleepiness. Delayed sleep phase type may overlap with another circadian
rhythm sleep-wake disorder, non-24-hour sleep-wake type. Sighted individuals with non-
24-hour sleep-wake type disorder commonly also have a history of delayed circadian sleep
phase.
Circadian Rhythm Sleep-Wake Disorders 393
Advanced Sleep Phase Type
\
Specifiers
Advanced sleep phase type may be documented with the specified “familial.” Although
the prevalence of familial advanced sleep phase type has not been established, a family
history of advanced sleep phase is present in individuals with advanced sleep phase type.
In this type, specific mutations demonstrate an autosomal dominant mode of inheritance.
In the familial form, onset of symptoms may occur earlier (during childhood and early
adulthood), the course is persistent, and the severity of symptoms may increase with age.
Diagnostic Features
Advanced sleep phase type is characterized by sleep-wake times that are several hours
earlier than desired or conventional times. Diagnosis is based primarily on a history of an
advance in the timing of the major sleep period (usually more than 2 hours) in relation to
the desired sleep and wake-up time, with symptoms of early morning insomnia and ex-
cessive daytime sleepiness. When allowed to set their schedule, individuals with ad-
vanced sleep phase type will exhibit normal sleep quality and duration for age.
Associated Features Supporting Diagnosis
Individuals with advanced sleep phase type are “morning types,” having earlier sleep-
wake times, with the timing of circadian biomarkers such as melatonin and core body tem-
perature rhythms occurring 2-4 hours earlier than normal. When required to keep a con-
ventional schedule requiring a delay of bedtime, these individuals will continue to have an
early rise time, leading to persistent sleep deprivation and daytime sleepiness. Use of hyp-
notics or alcohol to combat sleep-maintenance insomnia and stimulants to reduce daytime
sleepiness may lead to substance abuse in these individuals.
Prevaience
The estimated prevalence of advanced sleep phase type is approximately 1% in middle-
age adults. Sleep-wake times and circadian phase advance in older individuals, probably
accounting for increased prevalence in this population.
Deveiopment and Course
Onset is usually in late adulthood. In the familial form, onset can be earlier. The course is typ-
ically persistent, lasting more than 3 months, but the severity may increase depending on work
and social schedules. The advanced sleep phase type is more common in older adults.
Clinical expression may vary across the lifespan depending on social, school, and work
obligations. Individuals who can alter their work schedules to accommodate the advanced
circadian sleep and wake timing can experience remission of symptoms. Increasing age
tends to advance the sleep phase, however, it is unclear whether the common age-associ-
ated advanced sleep phase type is due solely to a change in circadian timing (as seen in the
familial form) or also to age-related changes in the homeostatic regulation of sleep, result-
ing in earlier awakening. Severity, remission, and relapse of symptoms suggest lack of ad-
herence to behavioral and environmental treatments designed to control sleep and wake
structure and light exposure.
394 Sleep-Wake Disorders
Risk and Prognostic Factors
Environmental. Decreased late afternoon/early evening exposure to light and/or expo-
sure to early morning light due to early morning awakening can increase the risk of ad-
vanced sleep phase type by advancing circadian rhythms. By going to bed early, these
individuals are not exposed to light in the phase delay region of the curve, resulting in per-
petuation of advanced phase. In familial advanced sleep phase type, a shortening of the
endogenous circadian period can result in an advanced sleep phase, although circadian pe-
riod does not appear to systematically decrease with age.
Genetic and physiological. Advanced sleep phase type has demonstrated an autoso-
ma] dominant mode of inheritance, including a PER2 gene mutation causing hypophos-
phorylation of the PER2 protein and a missense mutation in CKI.
Culture-Reiated Diagnostic Issues
African Americans may have a shorter circadian period and larger magnitude phase ad-
vances to light than do Caucasians, possibly increasing the risk for development of ad-
vanced sleep phase type in this population.
Diagnostic Markers
A sleep diary and actigraphy may be used as diagnostic markers, as described earlier for
delayed sleep phase type.
Functional Consequences of Advanced Sieep Phase Type
Excessive sleepiness associated with advanced sleep phase can have a negative effect on
cognitive performance, social interaction, and safety. Use of wake-promoting agents to
combat sleepiness or sedatives for early morning awakening may increase potential for
substance abuse.
Differentiai Diagnosis
Other sleep disorders. Behavioral factors such as irregular sleep schedules, voluntary
early awakening, and exposure to light in the early morning should be considered, partic-
ularly in older adults, Careful attention should be paid to rule out other sleep-wake dis-
orders, such as insomnia disorder, and other mental disorders and medical conditions that
can cause early morning awakening.
Depressive and bipolar disorders. Because early morning awakening, fatigue, and sleep-
iness are prominent features of major depressive disorder, depressive and bipolar disor-
ders must also be considered.
Comorbidity
Medical conditions and mental disorders with the symptom of early morning awakening,
such as insomnia, can co-occur with the advance sleep phase type.
Irregular Sleep-Wake Type
Diagnostic Features
The diagnosis of irregular sleep-wake type is based primarily on a history of symptoms of
insomnia at night (during the usual sleep period) and excessive sleepiness (napping) dur-
ing the day. Irregular sleep-wake type is characterized by a lack of discernable sleep-wake
Circadian Rhythm Sleep-Wake Disorders 395
circadian rhythm. There is no major sleep period, and sleep is fragmented into at least
three periods during the 24-hour day.
Associated Features Supporting Diagnosis
Individuals with irregular sleep-wake type typically present with insomnia or excessive
sleepiness, depending on the time of day. Sleep and wake periods across 24 hours are frag-
mented, although the longest sleep period tends to occur between 2:00 A.M. and 6:00 A.M.
and is usually less than 4 hours. A history of isolation or reclusion may occur in association
with the disorder and contribute to the symptoms via a lack of external stimuli to help en-
train a normal pattern. Individuals or their caregivers report frequent naps throughout the
day. Irregular sleep-wake type is most commonly associated with neurodegenerative dis-
orders, such as major neurocognitive disorder, and many neurodevelopmental disorders
in children.
Prevalence
Prevalence of irregular sleep-wake type in the general population is unknown.
Deveiopment and Course
The course of irregular sleep-wake type is persistent. Age at onset is variable, but the dis-
order is more common in older adults.
Risk and Prognostic Factors
Temperamental. Neurodegenerative disorders, such as Alzheimer’s disease, Parkinson's
disease, and Huntington’s disease, and neurodevelopmental disorders in children in-
crease the risk for irregular sleep-wake type.
Environmental. Decreased exposure to environmental light and structured daytime ac-
tivity can be associated with a low-amplitude circadian rhythm. Hospitalized individuals
are especially prone to such weak external entraining stimuli, and even outside the hospi-
tal setting, individuals with major neurocognitive disorder (i.e., dementia) are exposed to
significantly less bright light.
Diagnostic Markers
A detailed sleep history and a sleep diary (by a caregiver) or actigraphy help confirm the
irregular sleep-wake pattern.
Functional Consequences of
Irregular Sleep-Wake Type
Lack of a clearly discernible major sleep and wake period in irregular sleep-wake type re-
sults in insomnia or excessive sleepiness, depending on the time of day. Disruption of the
caregiver's sleep also often occurs and is an important consideration.
Differential Diagnosis
Normative variations in sleep. Irregular sleep-wake type should be distinguished from
a voluntary irregular sleep-wake schedule and poor sleep hygiene, which can result in in-
somnia and excessive sleepiness.
Other medical conditions and mental disorders. Other causes of insomnia and daytime
sleepiness, including comorbid medical conditions and mental disorders or medication,
should be considered.
396 Sleep-Wake Disorders
Comorbidity
Irregular sleep-wake type is often comorbid with neurodegenerative and neurodevelop-
mental disorders, such as major neurocognitive disorder, intellectual disability (intellec-
tual developmental disorder), and traumatic brain injury. It is also comorbid with other
medical conditions and mental disorders in which there is social isolation and/or lack of
light and structured activities.
Non-24-Hour Sleep-Wake Type
Diagnostic Features
The diagnosis of non-24-hour sleep-wake type is based primarily on a history of symp-
toms of insomnia or excessive sleepiness related to abnormal synchronization between the
24-hour light-dark cycle and the endogenous circadian rhythm. Individuals typically pre-
sent with periods of insomnia, excessive sleepiness, or both, which alternate with short
asymptomatic periods. Starting with the asymptomatic period, when the individual's
sleep phase is aligned to the external environment, sleep latency will gradually increase
and the individual will complain of sleep-onset insomnia. As the sleep phase continues to
drift so that sleep time is now in the daytime, the individual will have trouble staying
awake during the day and will complain of sleepiness. Because the circadian period is not
aligned to the external 24-hour environment, symptoms will depend on when an individ-
ual tries to sleep in relation to the circadian rhythm of sleep propensity.
Associated Features Supporting Diagnosis
Non-24-hour sleep-wake type is most common among blind or visually impaired individ-
uals who have decreased light perception. In sighted individuals, there is often a history of
delayed sleep phase and of decreased exposure to light and structured social and physical
activity. Sighted individuals with non-24-hour sleep-wake type also demonstrate in-
creased sleep duration.
Prevalence
Prevalence of non-24-hour sleep-wake type in the general population is unclear, but the
disorder appears rare in sighted individuals. The prevalence in blind individuals is esti-
mated to be 50%.
Deveiopment and Course
Course of non-24-hour sleep-wake type is persistent, with intermittent remission and ex-
acerbations due to changes in work and social schedules throughout the lifespan. Age at
onset is variable, depending on the onset of visual impairment. In sighted individuals, be-
cause of the overlap with delayed sleep phase type, non-24-hour sleep-wake type may de-
velop in adolescence or early adulthood. Remission and relapse of symptoms in blind and
sighted individuals largely depend on adherence to treatments designed to control sleep
and wake structure and light exposure.
Clinical expression may vary across the lifespan depending on social, school, and work
obligations. In adolescents and adults, irregular sleep-wake schedules and exposure to
light or lack of light at critical times of the day can exacerbate the effects of sleep loss and
disrupt circadian entrainment. Consequently, symptoms of insomnia, daytime sleepiness,
and school, professional, and interpersonal functioning may worsen.
Risk and Prognostic Factors
Environmental. In sighted individuals, decreased exposure or sensitivity to light and so-
cial and physical activity cues may contribute to a free-running circadian rhythm. With the
Circadian Rhythm Sleep-Wake Disorders 397
high frequency of mental disorders involving social isolation and cases of non-24-hour
sleep-wake type developing after a change in sleep habits (e.g., night shift work, job loss),
behavioral factors in combination with physiological tendency may precipitate and per-
petuate this disorder in sighted individuals. Hospitalized individuals with neurological and
psychiatric disorders can become insensitive to social cues, predisposing them to the de-
velopment of non-24-hour sleep-wake type.
Genetic and physiological. Blindness is a risk factor for non-24-hour sleep-wake type.
Non-24-hour sleep-wake type has been associated with traumatic brain injury.
Diagnostic Markers
Diagnosis is confirmed by history and sleep diary or actigraphy for an extended period.
Sequential measurement of phase markers (e.g., melatonin) can help determine circadian
phase in both sighted and blind individuals.
Functionai Consequences of
Non-24-Hour Sieep-Wake Type
Complaints of insomnia (sleep onset and sleep maintenance), excessive sleepiness, or both
are prominent. The unpredictability of sleep and wake times (typically a daily delay drift)
results in an inability to attend school or maintain a steady job and may increase potential
for social isolation,
Differentiai Diagnosis
Circadian rhythm sleep-wake disorders. In sighted individuals, non-24-hour sleep-wake
type should be differentiated from delayed sleep phase type, as individuals with delayed
sleep phase type may display a similar progressive delay in sleep period for several days.
Depressive disorders. Depressive symptoms and depressive disorders may result in
similar circadian dysregulation and symptoms.
Comorbidity
Blindness is often comorbid with non-24-hour sleep-wake type, as are depressive and bi-
polar disorders with social isolation.
Shift Work Type
Diagnostic Features
Diagnosis is primarily based on a history of the individual working outside of the normal
8:00 A.M. to 6:00 P.M. daytime window (particularly at night) on a regularly scheduled (i.e.,
non-overtime) basis. Symptoms of excessive sleepiness at work, and impaired sleep at
home, on a persistent basis are prominent. Presence of both sets of symptoms are usually
required for a diagnosis of shift work type. Typically, when the individual reverts to a day-
work routine, symptoms resolve. Although the etiology is slightly different, individuals
who travel across many time zones ona very frequent basis may experience effects similar
to those experienced by individuals with shift work type who work rotating shifts.
Prevalence
The prevalence of shift work type is unclear, but the disorder is estimated to affect 5%-10%
of the night worker population (16%~20% of the workforce). Prevalence rises with advance-
ment into middle-age and beyond (Drake et al. 2004).
398 Sleep-Wake Disorders
Development and Course
Shift work type can appear in individuals of any age but is more prevalent in individuals
older than 50 years and typically worsens with the passage of time if the disruptive work
hours persist. Although older adults may show similar rates of circadian phase adjust-
ment to a change in routine as do younger adults, they appear to experience significantly
more sleep disruption as a consequence of the circadian phase shift.
Risk and Prognostic Factors
Temperamental. Predisposing factors include a morning-type disposition, a need for
long (i.e., more than 8 hours) sleep durations in order to feel well rested, and strong com-
peting social and domestic needs (e.g., parents of young children). Individuals who are able
to commit to a nocturnal lifestyle, with few competing day-oriented demands, appear at
lower risk for shift work type.
Genetic and physiological. Because shift workers are more likely than day workers to
be obese, obstructive sleep apnea may be present and may exacerbate the symptoms.
Diagnostic Markers
A history and sleep diary or actigraphy may be useful in diagnosis, as discussed earlier for
delayed sleep phase type.
Functional Consequences of Shift Work Type
Individuals with shift work type not only may perform poorly at work but also appear to
be at risk for accidents both at work and on the drive home. They may also be at risk for
poor mental health (e.g., alcohol use disorder, substance use disorder, depression) and
physical health (e.g., gastrointestinal disorders, cardiovascular disease, diabetes, cancer).
Individuals with a history of bipolar disorder are particularly vulnerable to shift work
type-related episodes of mania resulting from missed nights of sleep. Shift work type of-
ten results in interpersonal problems.
Differential Diagnosis
Normative variations in sleep with shift work. The diagnosis of shift work type, as op-
posed to the “normal” difficulties of shift work, must depend to some extent on the sever-
ity of symptoms and/or level of distress experienced by the individual. Presence of shift
work type symptoms even when the individual is able to live on a day-oriented routine for
several weeks at a time may suggest the presence of other sleep disorders, such as sleep ap-
nea, insomnia, and narcolepsy, which should be ruled out.
Comorbidity
Shift work type has been associated with increased alcohol use disorder, other substance
use disorders, and depression. A variety of physical health disorders (e.g., gastrointestinal
disorders, cardiovascular disease, diabetes, cancer) have been found to be associated with
prolonged exposure to shift work.
Relationship to International Classification of
Sleep Disorders
The International Classification of Sleep Disorders, 2nd Edition (ICSD-2), differentiates nine
circadian rhythm sleep disorders, including jet lag type.
Non-Rapid Eye Movement Sleep Arousal Disorders 399
Parasomnias
Parasomnias are disorders characterized by abnormal behavioral, experiential, or physio-
logical events occurring in association with sleep, specific sleep stages, or sleep-wake tran-
sitions. The most common parasomnias—non-rapid eye movement (NREM) sleep
arousal disorders and rapid eye movement (REM) sleep behavior disorder—represent ad-
mixtures of wakefulness and NREM sleep and wakefulness and REM sleep, respectively.
These conditions serve as a reminder that sleep and wakefulness are not mutually exclu-
sive and that sleep is not necessarily a global, whole-brain phenomenon.
Non-Rapid Eye Movement
Sleep Arousal Disorders
Diagnostic Criteria
A. Recurrent episodes of incomplete awakening from sleep, usually occurring during the
first third of the major sleep episode, accompanied by either one of the following:
1. Sleepwalking: Repeated episodes of rising from bed during sleep and walking
about. While sleepwalking, the individual has a blank, staring face; is relatively un-
responsive to the efforts of others to communicate with him or her; and can be
awakened only with great difficulty.
2. Sleep terrors: Recurrent episodes of abrupt terror arousa{s from sleep, usually be-
ginning with a panicky scream. There is intense fear and signs of autonomic
arousal, such as mydriasis, tachycardia, rapid breathing, and sweating, during
each episode. There is relative unresponsiveness to efforts of others to comfort the
individual during the episodes.
. No or little (e.g., only a single visual scene) dream imagery is recalled.
. Amnesia for the episodes is present.
. The episodes cause clinically significant distress or impairment in social, occupational,
or other important areas of functioning.
E. The disturbance is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication).
F. Coexisting mental and medical disorders do not explain the episodes of sleepwalking
or sleep terrors.
Coding note: For ICD-9-CM, code 307.46 for ail subtypes. For ICD-10-CM, code is based
on subtype.
Specify whether:
307.46 (F51.3) Sleepwalking type
Specify it:
With sleep-related eating
With sleep-related sexual behavior (sexsomnia)
307.46 (F51.4) Sleep terror type
00 BD
400 Sleep-Wake Disorders
Diagnostic Features
The essential feature of non-rapid eye movement (NREM) sleep arousal disorders is the
repeated occurrence of incomplete arousals, usually beginning during the first third of the
major sleep episode (Criterion A), that typically are brief, lasting 1~10 minutes, but may be
protracted, lasting up to 1 hour. The maximum duration of an event is unknown. The eyes
are typically open during these events. Many individuals exhibit both subtypes of arousals
on different occasions, which underscores the unitary underlying pathophysiology. The
subtypes reflect varying degrees of simultaneous occurrence of wakefulness and NREM
sleep, resulting in complex behaviors arising from sleep with varying degrees of conscious
awareness, motor activity, and autonomic activation.
The essential feature of sleepwalking is repeated episodes of complex motor behavior
initiated during sleep, including rising from bed and walking about (Criterion A1). Sleep-
walking episodes begin during any stage of NREM sleep, most commonly during slow-
wave sleep and therefore most often occurring during the first third of the night. During
episodes, the individual has reduced alertness and responsiveness, a blank stare, and rel-
ative unresponsiveness to communication with others or efforts by others to awaken the
individual. If awakened during the episode (or on awakening the following morning), the
individual has limited recall for the episode. After the episode, there may initially be a brief
period of confusion or difficulty orienting, followed by full recovery of cognitive function
and appropriate behavior.
The essential feature of sleep terrors is the repeated occurrence of precipitous awaken-
ings from sleep, usually beginning with a panicky scream or cry (Criterion A2). Sleep ter-
rors usually begin during the first third of the major sleep episode and last 1-10 minutes,
but they may last considerably longer, particularly in children. The episodes are accom-
panied by impressive autonomic arousal and behavioral manifestations of intense fear.
During an episode, the individual is difficult to awaken or comfort. If the individual awak-
ens after the sleep terror, little or none of the dream, or only fragmentary, single images,
are recalled. During a typical episode of sleep terrors, the individual abruptly sits up in
bed screaming or crying, with a frightened expression and autonomic signs of intense anx-
iety (e.g., tachycardia, rapid breathing, sweating, dilation of the pupils). The individual
may be inconsolable and is usually unresponsive to the efforts of others to awaken or com-
fort him or her. Sleep terrors are also called “night terrors” or “pavor nocturnus.”
Associated Features Supporting Diagnosis
Sleepwalking episodes can include a wide variety of behaviors. Episodes may begin with
confusion: the individual may simply sit up in bed, look about, or pick at the blanket or
sheet. This behavior then becomes progressively complex. The individual may actually
leave the bed and walk into closets, out of the room, and even out of buildings. Individuals
may use the bathroom, eat, talk, or engage in more complex behaviors. Running and fran-
tic attempts to escape some apparent threat can also occur. Most behaviors during sleep-
walking episodes are routine and of low complexity. However, cases of unlocking doors
and even operating machinery (driving an automobile) have been reported. Sleepwalking
can also include inappropriate behavior (e.g., commonly, urinating in a closet or waste-
basket). Most episodes last for several minutes to a half hour but may be more protracted.
Inasmuch as sleep is a state of relative analgesia, painful injuries sustained during sleep-
walking may not be appreciated until awakening after the fact.
There are two “specialized” forms of sleepwalking: sleep-related eating behavior and
sleep-related sexual behavior (sexsomnia or sleep sex). Individuals with sleep-related eating
experience unwanted recurrent episodes of eating with varying degrees of amnesia, rang-
ing from no awareness to full awareness without the ability to not eat. During these epi-
sodes, inappropriate foods may be ingested. Individuals with sleep-related eating disorder
may find evidence of their eating only the next morning. In sexsomnia, varying degrees of
Non-Rapid Eye Movement Sleep Arousal Disorders 401
sexual activity (e.g., masturbation, fondling, groping, sexual intercourse) occur as complex
behaviors arising from sleep without conscious awareness. This condition is more common
in males and may result in serious interpersonal relationship problems or medicolegal
consequences.
During a typical episode of sleep terrors, there is often a sense of overwhelming dread,
with a compulsion to escape. Although fragmentary vivid dream images may occur, a story-
like dream sequence (as in nightmares) is not reported. Most commonly, the individual does
not awaken fully, but returns to sleep and has amnesia for the episode on awakening the next
morning. Usually only one episode will occur on any one night. Occasionally several episodes
may occur at intervals throughout the night. These events rarely arise during daytime naps.
Prevalence
Isolated or infrequent NREM sleep arousal disorders are very common in the general pop-
ulation. From 10% to 30% of children have had at least one episode of sleepwalking, and
2%-3% sleepwalk often. The prevalence of sleepwalking disorder, marked by repeated ep-
isodes and impairment or distress, is much lower, probably in the range of 1%—5%. The
prevalence of sleepwalking episodes (not sleepwalking disorder) is 1.0%-7.0% among
adults, with weekly to monthly episodes occurring in 0.5%-0.7%. The lifetime prevalence
of sleepwalking in adults is 29.2%, with a past-year prevalence of sleepwalking of 3.6%.
The prevalence of sleep terrors in the general population is unknown. The prevalence
of sleep terror episodes (as opposed to sleep terror disorder, in which there is recurrence
and distress or impairment) is approximately 36.9% at 18 months of age, 19.7% at 30 months
of age, and 2.2% in adults.
Development and Course
NREM sleep arousal disorders occur most commonly in childhood and diminish in fre-
quency with increasing age. The onset of sleepwalking in adults with no prior history of
sleepwalking as children should prompt a search for specific etiologies, such as obstruc-
tive sleep apnea, nocturnal seizures, or effect of medication.
Risk and Prognostic Factors
Environmental. Sedative use, sleep deprivation, sleep-wake schedule disruptions, fa-
tigue, and physical or emotional stress increase the likelihood of episodes. Fever and sleep
deprivation can produce an increased frequency of NREM sleep arousal disorders.
Genetic and physiological. A family history for sleepwalking or sleep terrors may oc-
cur in up to 80% of individuals who sleepwalk. The risk for sleepwalking is further in-
creased (to as much as 60% of offspring) when both parents have a history of the disorder.
Individuals with sleep terrors frequently have a positive family history of either sleep
terrors or sleepwalking, with as high as a 10-fold increase in the prevalence of the disorder
among first-degree biological relatives. Sleep terrors are much more common in monozy-
gotic twins as compared with dizygotic twins. The exact mode of inheritance is unknown.
Gender-Related Diagnostic Issues
Violent or sexual activity during sleepwalking episodes is more likely to occur in adults.
Eating during sleepwalking episodes is more commonly seen in females. Sleepwalking oc-
curs more often in females during childhood but more often in males during adulthood.
Older children and adults provide a more detailed recollection of fearful images asso-
ciated with sleep terrors than do younger children, who are more likely to have complete
amnesia or report only a vague sense of fear. Among children, sleep terrors are more com-
mon in males than in females. Among adults, the sex ratio is even.
402 Sleep-Wake Disorders
Diagnostic Markers
NREM sleep arousal disorders arise from any stage of NREM sleep but most commonly
from deep NREM sleep (slow-wave sleep). They are most likely to appear in the first third
of the night and do not commonly occur during daytime naps. During the episode, the
polysomnogram may be obscured with movement artifact. In the absence of such artifact,
the electroencephalogram typically shows theta or alpha frequency activity during the ep-
isode, indicating partial or incomplete arousal.
Polysomnography in conjunction with audiovisual monitoring can be used to document
episodes of sleepwalking. In the absence of actually capturing an event during a polysomno-
graphic recording, there are no polysomnographic features that can serve as a marker for
sleepwalking. Sleep deprivation may increase the likelihood of capturing an event. Asa group,
individuals who sleepwalk show instability of deep NREM sleep, but the overlap in findings
with individuals who do not sleepwalk is great enough to preclude use of this indicator in es-
tablishing a diagnosis. Unlike arousals from REM sleep associated with nightmares, in which
there is an increase in heart rate and respiration prior to the arousal, the NREM sleep arousals
of sleep terrors begin precipitously from sleep, without anticipatory autonomic changes. The
arousals are associated with impressive autonomic activity, with doubling or tripling of
the heart rate. The pathophysiology is poorly understood, but there appears to be instability in
the deeper stages of NREM sleep. Absent capturing an event during a formal sleep study,
there are no reliable polysomnographic indicators of the tendency to experience sleep terrors.
Functional Consequences of
Non-REM Sleep Arousal Disorders
For the diagnosis of a NREM sleep arousal disorder to be made, the individual or house-
hold members must experience clinically significant distress or impairment, although pa-
rasomnia symptoms may occur occasionally in nonclinical populations and would be
subthreshold for the diagnosis. Embarrassment concerning the episodes can impair social
relationships. Social isolation or occupational difficulties can result. The determination of a
“disorder” depends on a number of factors, which may vary on an individual basis and
will depend on the frequency of events, potential for violence or injurious behaviors, em-
barrassment, or disruption/distress of other household members. Severity determination
is best made based on the nature or consequence of the behaviors rather than simply on fre-
quency. Uncommonly, NREM sleep arousal disorders may result in serious injury to the
individual or to someone trying to console the individual. Injuries to others are confined to
those in close proximity; individuals are not “sought out.” Typically, sleepwalking in both
children and adults is not associated with significant mental disorders. For individuals
with sleep-related eating behaviors, unknowingly preparing or eating food during the
sleep period may create problems such as poor diabetes control, weight gain, injury (cuts
and burns), or consequences of eating dangerous or toxic inedibles. NREM sleep arousal
disorders may rarely result in violent or injurious behaviors with forensic implications.
Differential Diagnosis
Nightmare disorder. In contrast to individuals with NREM sleep arousal disorders, in-
dividuals with nightmare disorder typically awaken easily and completely, report vivid
storylike dreams accompanying the episodes, and tend to have episodes later in the night.
NREM sleep arousal disorders occur during NREM sleep, whereas nightmares usually oc-
cur during REM sleep. Parents of children with NREM sleep arousal disorders may mis-
interpret reports of fragmentary imagery as nightmares.
Breathing-related sleep disorders. Breathing disorders during sleep can also produce
confusional arousals with subsequent amnesia. However, breathing-related sleep disor-
ders are also characterized by characteristic symptoms of snoring, breathing pauses, and
Non-Rapid Eye Movement Sleep Arousal Disorders 403
daytime sleepiness. In some individuals, a breathing-related sleep disorder may precipi-
tate episodes of sleepwalking.
REM sleep behavior disorder. REM sleep behavior disorder may be difficult to distin-
guish from NREM sleep arousal disorders. REM sleep behavior disorder is characterized
by episodes of prominent, complex movements, often involving personal injury arising
from sleep. In contrast to NREM sleep arousal disorders, REM sleep behavior disorder oc-
curs during REM sleep. Individuals with REM sleep behavior disorder awaken easily and
report more detailed and vivid dream content than do individuals with NREM sleep arousal
disorders. They often report that they “act out dreams.”
Parasomnia overlap syndrome. Parasomnia overlap syndrome consists of clinical and
polysomnographic features of both sleepwalking and REM sleep behavior disorder.
Sleep-related seizures. Some types of seizures can produce episodes of very unusual
behaviors that occur predominantly or exclusively during sleep. Nocturnal seizures may
closely mimic NREM sleep arousal disorders but tend to be more stereotypic in nature, oc-
cur multiple times nightly, and be more likely to occur from daytime naps. The presence of
sleep-related seizures does not preclude the presence of NREM sleep arousal disorders.
Sleep-related seizures should be classified as a form of epilepsy.
Alcohol-induced blackouts. Alcohol-induced blackouts may be associated with extremely
complex behaviors in the absence of other suggestions of intoxication. They do not involve
the loss of consciousness but rather reflect an isolated disruption of memory for events
during a drinking episode. By history, these behaviors may be indistinguishable from those
seen in NREM sleep arousal disorders.
Dissociative amnesia, with dissociative fugue. Dissociative fugue may be extremely
difficult to distinguish from sleepwalking. Unlike all other parasomnias, nocturnal disso-
ciative fugue arises from a period of wakefulness during sleep, rather than precipitously
from sleep without intervening wakefulness. A history of recurrent childhood physical or
sexual abuse is usually present (but may be difficult to obtain).
Malingering or other voluntary behavior occurring during wakefulness. As with disso-
ciative fugue, malingering or other voluntary behavior occurring during wakefulness
arises from wakefulness.
Panic disorder. Panic attacks may also cause abrupt awakenings from deep NREM sleep
accompanied by fearfulness, but these episodes produce rapid and complete awakening with-
out the confusion, amnesia, or motor activity typical of NREM sleep arousal disorders.
Medication-induced complex behaviors. Behaviors similar to those in NREM sleep
arousal disorders can be induced by use of, or withdrawal from, substances or medica-
tions (e.g., benzodiazepines, nonbenzodiazepine sedative-hypnotics, opiates, cocaine, nic-
otine, antipsychotics, tricyclic antidepressants, chloral hydrate). Such behaviors may arise
from the sleep period and may be extremely complex. The underlying pathophysiology
appears to be a relatively isolated amnesia. In such cases, substance /medication-induced
sleep disorder, parasomnia type, should be diagnosed (see “Substance /Medication-
Induced Sleep Disorder” later in this chapter).
Night eating syndrome. The sleep-related eating disorder form of sleepwalking is to be
differentiated from night eating syndrome, in which there is a delay in the circadian rhythm
of food ingestion and an association with insomnia and/or depression.
Comorbidity
In adults, there is an association between sleepwalking and major depressive episodes and
obsessive-compulsive disorder. Children or adults with sleep terrors may have elevated
scores for depression and anxiety on personality inventories.
404 Sleep-Wake Disorders
Relationship to International Classification of
Sleep Disorders
The International Classification of Sleep Disorders, 2nd Edition, includes “confusional
arousal” as a NREM sleep arousal disorder.
Nightmare Disorder
Diagnostic Criteria 307.47 (F51.5)
A. Repeated occurrences of extended, extremely dysphoric, and well-remembered
dreams that usually involve efforts to avoid threats to survival, security, or physical in-
tegrity and that generally occur during the second half of the major sleep episode.
B. On awakening from the dysphoric dreams, the individual rapidly becomes oriented and
alert.
C. The sleep disturbance causes clinically significant distress or impairment in social, oc-
cupational, or other important areas of functioning.
D. The nightmare symptoms are not attributable to the physiological effects of a sub-
stance (e.g., a drug of abuse, a medication).
E. Coexisting mental and medical disorders do not adequately explain the predominant
complaint of dysphoric dreams.
Specify if:
During sleep onset
Specify if:
With associated non-sleep disorder, including substance use disorders
With associated other medical condition
With associated other sleep disorder
Coding note: The code 307.47 (F51.5) applies to all three specifiers. Code also the
relevant associated mental disorder, medical condition, or other sleep disorder imme-
diately after the code for nightmare disorder in order to indicate the association.
Specify if:
Acute: Duration of period of nightmares is 1 month or less.
Subacute: Duration of period of nightmares is greater than 1 month but less than
6 months.
Persistent: Duration of period of nightmares is 6 months or greater.
Specify current severity:
Severity can be rated by the frequency with which the nightmares occur:
Mild: Less than one episode per week on average.
Moderate: One or more episodes per week but less than nightly.
Severe: Episodes nightly.
Diagnostic Features
Nightmares are typically lengthy, elaborate, storylike sequences of dream imagery that
seem real and that incite anxiety, fear, or other dysphoric emotions. Nightmare content
typically focuses on attempts to avoid or cope with imminent danger but may involve
themes that evoke other negative emotions. Nightmares occurring after traumatic experi-
ences may replicate the threatening situation (“replicative nightmares”), but most do not.
On awakening, nightmares are well remembered and can be described in detail. They arise
Nightmare Disorder 405
almost exclusively during rapid eye movement (REM) sleep and can thus occur through-
out sleep but are more likely in the second half of the major sleep episode when dreaming
is longer and more intense. Factors that increase early-night REM intensity, such as sleep
fragmentation or deprivation, jet lag, and REM-sensitive medications, might facilitate
nightmares earlier in the night, including at sleep onset.
Nightmares usually terminate with awakening and rapid return of full alertness. How-
ever, the dysphoric emotions may persist into wakefulness and contribute to difficulty re-
turning to sleep and lasting daytime distress. Some nightmares, known as “bad dreams,”
may not induce awakening and are recalled only later. If nightmares occur during sleep-
onset REM periods (hypnagogic), the dysphoric emotion is frequently accompanied by a
sense of being both awake and unable to move voluntarily (isolated sleep paralysis).
Associated Features Supporting Diagnosis
Mild autonomic arousal, including sweating, tachycardia, and tachypnea, may character-
ize nightmares. Body movements and vocalizations are not characteristic because of REM
sleep—related loss of skeletal muscle tone, but such behaviors may occur under situations
of emotional stress or sleep fragmentation and in posttraumatic stress disorder (PTSD).
When talking or emoting occurs, it is typically a brief event terminating the nightmare.
Individuals with frequent nightmares are at substantially greater risk for suicidal ide-
ation and suicide attempts, even when gender and mental illness are taken into account.
Prevalence
Prevalence of nightmares increases through childhood into adolescence. From 1.3% to
3.9% of parents report that their preschool children have nightmares “often” or “always”.
Prevalence increases from ages 10 to 13 for both males and females but continues to in-
crease to ages 20-29 for females (while decreasing for males), when it can be twice as high
for females as for males. Prevalence decreases steadily with age for both sexes, but the gen-
der difference remains. Among adults, prevalence of nightmares at least monthly is 6%,
whereas prevalence for frequent nightmares is 1%-2%. Estimates often combine idio-
pathic and posttraumatic nightmares indiscriminately.
Development and Course
Nightmares often begin between ages 3 and 6 years but reach a peak prevalence and se-
verity in late adolescence or early adulthood. Nightmares most likely appear in children
exposed to acute or chronic psychosocial stressors and thus may not resolve spontane-
ously. In a minority, frequent nightmares persist into adulthood, becoming virtually a life-
long disturbance. Although specific nightmare content may reflect the individual’s age,
the essential features of the disorder are the same across age groups.
Risk and Prognostic Factors
Temperamental. Individuals who experience nightmares report more frequent past ad-
verse events, but not necessarily trauma, and often display personality disturbances or
psychiatric diagnosis.
Environmental. Sleep deprivation or fragmentation, and irregular sleep-wake schedules
that alter the timing, intensity, or quantity of REM sleep, can put individuals at risk for
nightmares.
Genetic and physiological. Twin studies have identified genetic effects on the disposi-
tion to nightmares and their co-occurrence with other parasomnias (e.g., sleeptalking).
Course modifiers. Adaptive parental bedside behaviors, such as soothing the child fol-
lowing nightmares, may protect against developing chronic nightmares.
406 Sleep-Wake Disorders
Culture-Related Diagnostic Issues
The significance attributed to nightmares may vary by culture, and sensitivity to such be-
liefs may facilitate disclosure.
Gender-Related Diagnostic Issues
Adult females report having nightmares more frequently than do adult males. Nightmare
content differs by sex, with adult females tending to report themes of sexual harassment or
of loved ones disappearing /dying, and adult males tending to report themes of physical
aggression or war/ terror.
Diagnostic Markers
Polysomnographic studies demonstrate abrupt awakenings from REM sleep, usually during
the second half of the night, prior to report of a nightmare. Heart, respiratory, and eye move-
ment rates may quicken or increase in variability before awakening. Nightmares following
traumatic events may also arise during non-REM (NREM), particularly stage 2, sleep. The typ-
ical sleep of individuals with nightmares is mildly impaired (e.g., reduced efficiency, less slow-
wave sleep, more awakenings), with more frequent periodic leg movements in sleep and rel-
ative sympathetic nervous system activation after REM sleep deprivation.
Functional Consequences of Nightmare Disorder
Nightmares cause more significant subjective distress than demonstrable social or occu-
pational impairment. However, if awakenings are frequent or result in sleep avoidance,
individuals may experience excessive daytime sleepiness, poor concentration, depression,
anxiety, or irritability. Frequent childhood nightmares (e.g., several per week), may cause
significant distress to parents and child.
Differential Diagnosis
Sleep terror disorder. Both nightmare disorder and sleep terror disorder include awak-
enings or partial awakenings with fearfulness and autonomic activation, but the two dis-
orders are differentiable. Nightmares typically occur later in the night, during REM sleep,
and produce vivid, storylike, and clearly recalled dreams; mild autonomic arousal; and
complete awakenings. Sleep terrors typically arise in the first third of the night during
stage 3 or 4 NREM sleep and produce either no dream recall or images without an elabo-
rate storylike quality. The terrors lead to partial awakenings that leave the individual con-
fused, disoriented, and only partially responsive and with substantial autonomic arousal.
There is usually amnesia for the event in the morning.
REM sleep behavior disorder. The presence of complex motor activity during fright-
ening dreams should prompt further evaluation for REM sleep behavior disorder, which
occurs more typically among late middle-age males and, unlike nightmare disorder, is as-
sociated with often violent dream enactments and a history of nocturnal injuries. The
dream disturbance of REM sleep behavior disorder is described by patients as nightmares
but is controlled by appropriate medication.
Bereavement. Dysphoric dreams may occur during bereavement but typically involve
loss and sadness and are followed by self-reflection and insight, rather than distress, on
awakening.
Narcolepsy. Nightmares are a frequent complaint in narcolepsy, but the presence of ex-
cessive sleepiness and cataplexy differentiates this condition from nightmare disorder.
Nocturnal seizures. Seizures may rarely manifest as nightmares and should be evalu-
ated with polysomnography and continuous video electroencephalography. Nocturnal
seizures usually involve stereotypical motor activity. Associated nightmares, if recalled,
Rapid Eye Movement Sleep Behavior Disorder 407
are often repetitive in nature or reflect epileptogenic features such as the content of diurnal
auras (e.g., unmotivated dread), phosphenes, or ictal imagery. Disorders of arousal, espe-
cially confusional arousals, may also be present.
Breathing-related sleep disorders. Breathing-related sleep disorders can lead to awaken-
ings with autonomic arousal, but these are not usually accompanied by recall of nightmares.
Panic disorder. Attacks arising during sleep can produce abrupt awakenings with au-
tonomic arousal and fearfulness, but nightmares are typically not reported and symptoms
are similar to panic attacks arising during wakefulness.
Sleep-related dissociative disorders. Individuals may recall actual physical or emo-
tional trauma as a “dream” during electroencephalography-documented awakenings.
Medication or substance use. Numerous substances/medications can precipitate night-
mares, including dopaminergics; beta-adrenergic antagonists and other antihypertensives;
amphetamine, cocaine, and other stimulants; antidepressants; smoking cessation aids;
and melatonin. Withdrawal of REM sleep-suppressant medications (e.g., antidepressants)
and alcohol can produce REM sleep rebound accompanied by nightmares. If nightmares
are sufficiently severe to warrant independent clinical attention, a diagnosis of substance /
medication-induced sleep disorder should be considered.
Comorbidity
Nightmares may be comorbid with several medical conditions, including coronary heart
disease, cancer, parkinsonism, and pain, and can accompany medical treatments, such as he-
modialysis, or withdrawal from medications or substances of abuse. Nightmares frequently
are comorbid with other mental disorders, including PTSD; insomnia disorder; schizophrenia;
psychosis; mood, anxiety, adjustment, and personality disorders; and grief during be-
reavement. A concurrent nightmare disorder diagnosis should only be considered when in-
dependent clinical attention is warranted (i.e., Criteria A-C are met). Otherwise, no separate
diagnosis is necessary. These conditions should be listed under the appropriate comorbid
category specifier. However, nightmare disorder may be diagnosed as a separate disorder in
individuals with PTSD if the nightmares are temporally unrelated to PTSD (ie., preceding
other PTSD symptoms or persisting after other PTSD symptoms have resolved).
Nightmares are normally characteristic of REM sleep behavior disorder, PTSD, and acute
stress disorder, but nightmare disorder may be independently coded if nightmares preceded
the condition and their frequency or severity necessitates independent clinical attention. The
latter may be determined by asking whether nightmares were a problem before onset of the
other disorder and whether they continued after other symptoms had remitted.
Relationshlp to International Ciassification of
Sieep Disorders
The International Classification of Sleep Disorders, 2nd Edition (ICSD-2), presents similar di-
agnostic criteria for nightmare disorder.
Rapid Eye Movement Sleep Behavior Disorder
Diagnostic Criteria 327.42 (G47.52)
A. Repeated episodes of arousal during sleep associated with vocalization and/or com-
plex motor behaviors.
B. These behaviors arise during rapid eye movement (REM) sleep and therefore usually
occur more than 90 minutes after sleep onset, are more frequent during the later por-
tions of the sleep period, and uncommonly occur during daytime naps.
408 Sleep-Wake Disorders
C. Upon awakening from these episodes, the individual is completely awake, alert, and
not confused or disoriented.
D. Either of the following:
1. REM sleep without atonia on polysomnographic recording.
2. Ahistory suggestive of REM sleep behavior disorder and an established synuclein-
opathy diagnosis (e.g., Parkinson’s disease, multiple system atrophy).
E. The behaviors cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning (which may include injury to self or the
bed partner).
F. The disturbance is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication) or another medical condition.
G. Coexisting mental and medical disorders do not explain the episodes.
Diagnostic Features
The essential feature of rapid eye movement (REM) sleep behavior disorder is repeated
episodes of arousal, often associated with vocalizations and/or complex motor behaviors
arising from REM sleep (Criterion A). These behaviors often reflect motor responses to the
content of action-filled or violent dreams of being attacked or trying to escape froma
threatening situation, which may be termed dream enacting behaviors. The vocalizations are
often loud, emotion-filled, and profane. These behaviors may be very bothersome to the
individual and the bed partner and may result in significant injury (e.g., falling, jumping,
or flying out of bed; running, punching, thrusting, hitting, or kicking). Upon awakening,
the individual is immediately awake, alert, and oriented (Criterion C) and is often able to
recall dream mentation, which closely correlates with the observed behavior. The eyes
typically remain closed during these events. The diagnosis of REM sleep behavior disor-
der requires clinically significant distress or impairment (Criterion E); this determination
will depend on a number of factors, including the frequency of events, the potential for vi-
olence or injurious behaviors, embarrassment, and distress in other household members.
Associated Features Supporting Diagnosis
Severity determination is best made based on the nature or consequence of the behavior
rather than simply on frequency. Although the behaviors are typically prominent and vi-
olent, lesser behaviors may also occur.
Prevalence
The prevalence of REM sleep behavior disorder is approximately 0.38%-0.5% in the gen-
eral population. Prevalence in patients with psychiatric disorders may be greater, possibly
related to medications prescribed for the psychiatric disorder.
Deveiopment and Course
The onset of REM sleep behavior disorder may be gradual or rapid, and the course is usu-
ally progressive. REM sleep behavior disorder associated with neurodegenerative disor-
ders may improve as the underlying neurodegenerative disorder progresses. Because of
the very high association with the later appearance of an underlying neurodegenerative
disorder, most notably one of the synucleinopathies (Parkinson’s disease, multiple system
atrophy, or major or mild neurocognitive disorder with Lewy bodies), the neurological
status of individuals with REM sleep behavior disorder should be closely monitored.
REM sleep behavior disorder overwhelmingly affects males older than 50 years, but in-
creasingly this disorder is being identified in females and in younger individuals. Symp-
Rapid Eye Movement Sleep Behavior Disorder 409
toms in young individuals, particularly young females, should raise the possibility of
narcolepsy or medication-induced REM sleep behavior disorder.
Risk and Prognostic Factors
Genetic and physiological. Many widely prescribed medications, including tricyclic
antidepressants, selective serotonin reuptake inhibitors, serotonin-norepinephrine reup-
take inhibitors, and beta-blockers, may result in polysomnographic evidence of REM sleep
without atonia and in frank REM sleep behavior disorder. It is not known whether the
medications per se result in REM sleep behavior disorder or they unmask an underlying
predisposition.
Diagnostic Markers
Associated laboratory findings from polysomnography indicate increased tonic and/or
phasic electromyographic activity during REM sleep that is normally associated with mus-
cle atonia. The increased muscle activity variably affects different muscle groups, mandating
more extensive electromyographic monitoring than is employed in conventional sleep stud-
ies. For this reason, it is suggested that electromyographic monitoring include the submen-
talis, bilateral extensor digitorum, and bilateral anterior tibialis muscle groups. Continuous
video monitoring is mandatory. Other polysomnographic findings may include very fre-
quent periodic and aperiodic extremity electromyography activity during non-REM
(NREM) sleep. This polysomnography observation, termed REM sleep without atonia, is pres-
ent in virtually all cases of REM sleep behavior disorder but may also be an asymptomatic
polysomnographic finding. Clinical dream-enacting behaviors coupled with the polysom-
nographic finding of REM without atonia is necessary for the diagnosis of REM sleep behav-
ior disorder. REM sleep without atonia without a clinical history of dream-enacting
behaviors is simply an asymptomatic polysomnographic observation. It is not known
whether isolated REM sleep without atonia is a precursor to REM sleep behavior disorder.
Functional Consequences of
Rapid Eye Movement Sieep Behavior Disorder
REM sleep behavior disorder may occur in isolated occasions in otherwise unaffected in-
dividuals. Embarrassment concerning the episodes can impair social relationships. Indi-
viduals may avoid situations in which others might become aware of the disturbance,
visiting friends overnight, or sleeping with bed partners. Social isolation or occupational
difficulties can result. Uncommonly, REM sleep behavior disorder may result in serious
injury to the victim or to the bed partner.
Differential Diagnosis
Other parasomnias. Confusional arousals, sleepwalking, and sleep terrors can easily be
confused with REM sleep behavior disorder. In general, these disorders occur in younger
individuals. Unlike REM sleep behavior disorder, they arise from deep NREM sleep and
therefore tend to occur in the early portion of the sleep period. Awakening from a confu-
sional arousal is associated with confusion, disorientation, and incomplete recall of dream
mentation accompanying the behavior. Polysomnographic monitoring in the disorders of
arousal reveals normal REM atonia.
Nocturnal seizures. Nocturnal seizures may perfectly mimic REM sleep behavior disor-
der, but the behaviors are generally more stereotyped. Polysomnographic monitoring em-
ploying a full electroencephalographic seizure montage may differentiate the two. REM
sleep without atonia is not present on polysomnographic monitoring.
410 Sleep-Wake Disorders
Obstructive sleep apnea. Obstructive sleep apnea may result in behaviors indistin-
guishable from REM sleep behavior disorder. Polysomnographic monitoring is necessary
to differentiate between the two. In this case, the symptoms resolve following effective
treatment of the obstructive sleep apnea, and REM sleep without atonia is not present on
polysomnography monitoring.
Other specified dissociative disorder (sleep-related psychogenic dissociative disorder).
Unlike virtually all other parasomnias, which arise precipitously from NREM or REM
sleep, psychogenic dissociative behaviors arise from a period of well-defined wakefulness
during the sleep period. Unlike REM sleep behavior disorder, this condition is more prev-
alent in young females.
Malingering. Many cases of malingering in which the individual reports problematic
sleep movements perfectly mimic the clinical features of REM sleep behavior disorder,
and polysomnographic documentation is mandatory.
Comorbidity
REM sleep behavior disorder is present concurrently in approximately 30% of patients
with narcolepsy. When it occurs in narcolepsy, the demographics reflect the younger age
range of narcolepsy, with equal frequency in males and females. Based on findings from
individuals presenting to sleep clinics, most individuals (>50%) with initially “idiopathic”
REM sleep behavior disorder will eventually develop a neurodegenerative disease—most
notably, one of the synucleinopathies (Parkinson's disease, multiple system atrophy, or
major or mild neurocognitive disorder with Lewy bodies). REM sleep behavior disorder
often predates any other sign of these disorders by many years (often more than a decade).
Relationship to International Classification of
Sleep Disorders
REM sleep behavior disorder is virtually identical to REM sleep behavior disorder in the
International Classification of Sleep Disorders, 2nd Edition (ICSD-2),
Restless Legs Syndrome
Diagnostic Criteria 333.94 (G25.81)
A. Anurge to move the legs, usually accompanied by or in response to uncomfortable and
unpleasant sensations in the legs, characterized by all of the following:
1. The urge to move the legs begins or worsens during periods of rest or inactivity.
2. The urge to move the legs is partially or totally relieved by movement.
3. The urge to move the legs is worse in the evening or at night than during the day,
or occurs only in the evening or at night.
B. The symptoms in Criterion A occur at least three times per week and have persisted
for at least 3 months.
C. The symptoms in Criterion A are accompanied by significant distress or impairment in
social, occupational, educational, academic, behavioral, or other important areas of
functioning.
D. The symptoms in Criterion A are not attributable to another mental disorder or medical
condition (e.g., arthritis, leg edema, peripheral ischemia, leg cramps) and are not better
explained by a behavioral condition (e.g., positional discomfort, habitual foot tapping).
E. The symptoms are not attributable to the physiological effects of a drug of abuse or
medication (e.g., akathisia).
Restless Legs Syndrome 411
Diagnostic Features
Restless legs syndrome (RLS) is a sensorimotor, neurological sleep disorder characterized
by a desire to move the legs or arms, usually associated with uncomfortable sensations
typically described as creeping, crawling, tingling, burning, or itching (Criterion A). The
diagnosis of RLS is based primarily on patient self-report and history. Symptoms are
worse when the individual is at rest, and frequent movements of the legs occur in an effort
to relieve the uncomfortable sensations. Symptoms are worse in the evening or night, and
in some individuals they occur only in the evening or night. Evening worsening occurs in-
dependently of any differences in activity. It is important to differentiate RLS from other
conditions such as positional discomfort and leg cramps (Criterion D).
The symptoms of RLS can delay sleep onset and awaken the individual from sleep and
are associated with significant sleep fragmentation. The relief obtained from moving the
legs may no longer be apparent in severe cases. RLS is associated with daytime sleepiness
and is frequently accompanied by significant clinical distress or functional impairment.
Associated Features Supporting Diagnosis
Periodic leg movements in sleep (PLMS) can serve as corroborating evidence for RLS, with
up to 90% of individuals diagnosed with RLS demonstrating PLMS when recordings are
taken over multiple nights. Periodic leg movements during wakefulness are supportive of
an RLS diagnosis. Reports of difficulty initiating and maintaining sleep and of excessive
daytime sleepiness may also support the diagnosis of RLS. Additional supportive features
include a family history of RLS among first-degree relatives and a reduction in symptoms,
at least initially, with dopaminergic treatment.
Prevalence
Prevalence rates of RLS vary widely when broad criteria are utilized but range from 2% to
7.2% when more defined criteria are employed. When frequency of symptoms is at least
three times per week with moderate or severe distress, the prevalence rate is 1.6%; when
frequency of symptoms is a minimum of one time per week, the prevalence rate is 4.5%.
Females are 1.5-2 times more likely than males to have RLS. RLS also increases with age.
The prevalence of RLS may be lower in Asian populations.
Deveiopment and Course
The onset of RLS typically occurs in the second or third decade. Approximately 40% of in-
dividuals diagnosed with RLS during adulthood report having experienced symptoms
before age 20 years, and 20% report having experienced symptoms before age 10 years.
Prevalence rates of RLS increase steadily with age until about age 60 years, with symptoms
remaining stable or decreasing slightly in older age groups. Compared with nonfamilial
cases, familial RLS usually has a younger age at onset and a slower progressive course. The
clinical course of RLS differs by age at onset. When onset occurs before age 45, there is of-
ten a slow progression of symptoms. In late-onset RLS, rapid progression is typical, and
aggravating factors are common. Symptoms of RLS appear similar across the lifespan, re-
maining stable or decreasing slightly in older age groups.
Diagnosis of RLS in children can be difficult because of the self-report component.
While Criterion A for adults assumes that the description of “urge to move” is by the pa-
tient, pediatric diagnosis requires a description in the child’s own words rather than by a
parent or caretaker. Typically children age 6 years or older are able to provide detailed, ad-
equate descriptors of RLS. However, children rarely use or understand the word “urge,”
reporting instead that their legs “have to” or “got to” move. Also, potentially related to
prolonged periods of sitting during class, two-thirds of children and adolescents report
daytime leg sensations. Thus, for diagnostic Criterion A3, it is important to compare equal
412 Sleep-Wake Disorders
duration of sitting or lying down in the day to sitting or lying down in the evening or night.
Nocturnal worsening tends to persist even in the context of pediatric RLS. As with RLS in
adults, there is a significant negative impact on sleep, mood, cognition, and function. Im-
pairment in children and adolescents is manifested more often in behavioral and educa-
tional domains.
Risk and Prognostic Factors
Genetic and physiological. Predisposing factors include female gender, advancing
age, genetic risk variants, and family history of RLS. Precipitating factors are often time-
limited, such as iron deficiency, with most individuals resuming normal sleep patterns
after the initial triggering event has disappeared. Genetic risk variants also play a role in
RLS secondary to such disorders as uremia, suggesting that individuals with a genetic sus-
ceptibility develop RLS in the presence of further risk factors. RLS has a strong familial
component.
There are defined pathophysiological pathways subserving RLS. Genome-wide asso-
ciation studies have found that RLS is significantly associated with common genetic vari-
ants in intronic or intergenic regions in MEIS1, BTBD9, and MAP2K5 on chromosomes 2p,
6p, and 15q, respectively. The association of these three variants with RLS has been inde-
pendently replicated. BTBD9 confers a very large (80%) excessive risk when even a single
allele is present. Because of the high frequency of this variant in individuals of European
descent, the population attributable risk (PAR) approximates 50%. At-risk alleles associ-
ated with MEIS1 and BTBD9 are less common in individuals of African or Asian descent,
perhaps suggesting lower risk for RLS in these populations.
Pathophysiological mechanisms in RLS also include disturbances in the central dopa-
minergic system and disturbances in iron metabolism. The endogenous opiate system
may also be involved. Treatment effects of dopaminergic drugs (primarily D, and D3 non-
ergot agonists) provide further support that RLS is grounded in dysfunctional central
dopaminergic pathways. While the effective treatment of RLS has also been shown to sig-
nificantly reduce depressive symptoms, serotonergic antidepressants can induce or aggra-
vate RLS in some individuals.
Gender-Reiated Diagnostic Issues
Although RLS is more prevalent in females than in males, there are no diagnostic differ-
ences according to gender. However, the prevalence of RLS during pregnancy is two to
three times greater than in the general population. RLS associated with pregnancy peaks
during the third trimester and improves or resolves in most cases soon after delivery. The
gender difference in prevalence of RLS is explained at least in part by parity, with nullipa-
rous females being at the same risk of RLS as age-matched males.
Diagnostic Markers
Polysomnography demonstrates significant abnormalities in RLS, commonly increased
latency to sleep, and higher arousal index. Polysomnography with a preceding immobili-
zation test may provide an indicator of the motor sign of RLS, periodic limb movements,
under standard conditions of sleep and during quiet resting, both of which can provoke RLS
symptoms.
Functionai Consequences of Restless Legs Syndrome
Forms of RLS severe enough to significantly impair functioning or associated with mental dis-
orders, including depression and anxiety, occur in approximately 2%-3% of the population.
Although the impact of milder symptoms is less well characterized, individuals with
RLS complain of disruption in at least one activity of daily living, with up to 50% reporting
Substance/Medication-Induced Sleep Disorder 413
a negative impact on mood, and 47.6% reporting a lack of energy. The most common conse-
quences of RLS are sleep disturbance, including reduced sleep time, sleep fragmentation,
and overall disturbance; depression, generalized anxiety disorder, panic disorder, and post-
traumatic stress disorder; and quality-of-life impairments. RLS can result in daytime sleep-
iness or fatigue and is frequently accompanied by significant distress or impairment in
affective, social, occupational, educational, academic, behavioral, or cognitive functioning.
Differential Diagnosis
The most important conditions in the differential diagnosis of RLS are leg cramps, posi-
tional discomfort, arthralgias/ arthritis, myalgias, positional ischemia (numbness), leg
edema, peripheral neuropathy, radiculopathy, and habitual foot tapping. “Knotting” of
the muscle (cramps), relief with a single postural shift, limitation to joints, soreness to pal-
pation (myalgias), and other abnormalities on physical examination are not characteristic
of RLS. Unlike RLS, nocturnal leg cramps do not typically present with the desire to move
the limbs nor are there frequent limb movements. Less common conditions to be differen-
tiated from RLS include neuroleptic-induced akathisia, myelopathy, symptomatic venous
insufficiency, peripheral artery disease, eczema, other orthopedic problems, and anxiety-
induced restlessness. Worsening at night and periodic limb movements are more common
in RLS than in medication-induced akathisia or peripheral neuropathy.
While is it important that RLS symptoms not be solely accounted for by another medical
or behavioral condition, it should also be appreciated that any of these similar conditions can
occur in an individual with RLS. This necessitates a separate focus on each possible condi-
tion in the diagnostic process and when assessing impact. For cases in which the diagnosis of
RLS is not certain, evaluation for the supportive features of RLS, particularly PLMS or a fam-
ily history of RLS, may be helpful. Clinical features, such as response to a dopaminergic
agent and positive family history for RLS, can help with the differential diagnosis.
Comorbidity
Depressive disorders, anxiety disorders, and attentional disorders are commonly comor-
bid with RLS and are discussed in the section “Functional Consequences of Restless Legs
Syndrome.” The main medical disorder comorbid with RLS is cardiovascular disease.
There may be an association with numerous other medical disorders, including hyperten-
sion, narcolepsy, migraine, Parkinson's disease, multiple sclerosis, peripheral neuropathy,
obstructive sleep apnea, diabetes mellitus, fibromyalgia, osteoporosis, obesity, thyroid
disease, and cancer. Iron deficiency, pregnancy, and chronic renal failure are also comor-
bid with RLS.
Reiationship to Internationai Ciassification of
Sieep Disorders
The International Classification of Sleep Disorders, 2nd Edition (ICSD-2), presents similar diag-
nostic criteria for RLS but does not contain a criterion specifying frequency or duration of
symptoms.
Substance/Medication-Induced Sleep Disorder
Diagnostic Criteria
A. A prominent and severe disturbance in sleep.
B. There is evidence from the history, physical examination, or laboratory findings of both
(1) and (2):
414 Sleep-Wake Disorders
1. The symptoms in Criterion A developed during or soon after substance intoxication
or after withdrawal from or exposure to a medication.
2. The involved substance/medication is capable of producing the symptoms in Crite-
rion A.
C. The disturbance is not better explained by a sleep disorder that is not substance/
medication-induced. Such evidence of an independent sleep disorder could include
the following:
The symptoms precede the onset of the substance/medication use; the symptoms
persist for a substantial period of time (e.g., about 1 month) after the cessation of
acute withdrawal or severe intoxication; or there is other evidence suggesting the
existence of an independent non-substance/medication-induced sleep disorder
(e.g., a history of recurrent non-substance/medication-related episodes).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
Note: This diagnosis should be made instead of a diagnosis of substance intoxication or
substance withdrawal only when the symptoms in Criterion A predominate in the clinical
picture and when they are sufficiently severe to warrant clinical attention.
Coding note: The ICD-9-CM and ICD-10-CM codes for the [specific supstance/medica-
tion]-induced sleep disorders are indicated in the table below. Note that the ICD-10-CM
code depends on whether or not there is a comorbid substance use disorder present for
the same class of substance. If a mild substance use disorder is comorbid with the sub-
stance-induced sleep disorder, the 4th position character is “1,” and the clinician should
record “mild [substance] use disorder” before the substance-induced sleep disorder (e.g.,
“mild cocaine use disorder with cocaine-induced sleep disorder’). If a moderate or severe
substance use disorder is comorbid with the substance-induced sleep disorder, the 4th po-
sition character is “2,” and the clinician should record “moderate [substance] use disorder”
or “severe [substance] use disorder,” depending on the severity of the comorbid substance
use disorder. If there is no comorbid substance use disorder (e.g., after a one-time heavy
use of the substance), then the 4th position character is “9,” and the clinician should record
only the substance-induced sleep disorder. A moderate or severe tobacco use disorder is
required in order to code a tobacco-induced steep disorder; it is not permissible to code a
comorbid mild tobacco use disorder or no tobacco use disorder with a tobacco-induced
sleep disorder.
Specify whether:
Insomnia type: Characterized by difficulty falling asleep or maintaining sleep, frequent
nocturnal awakenings, or nonrestorative sleep.
Daytime sleepiness type: Characterized by predominant complaint of excessive
sleepiness/fatigue during waking hours or, less commonly, a long sleep period.
Parasomnia type: Characterized by abnormal behavioral events during sleep.
Mixed type: Characterized by a substance/medication-induced sleep problem charac-
terized by multiple types of sleep symptoms, but no symptom clearly predominates.
Specify if (see Table 1 in the chapter “Substance-Related and Addictive Disorders” for di-
agnoses associated with substance class):
With onset during intoxication: This specifier should be used if criteria are met for
intoxication with the substance/medication and symptoms developed during the intox-
ication period.
With onset during discontinuation/withdrawal: This specifier should be used if cri-
teria are met for discontinuation/withdrawat from the substance/medication and symp-
toms developed during, or shortly after, discontinuation of the substance/medication.
Substance/Medication-Induced Sleep Disorder 415
ICD-10-CM
With use
With use disorder, Without
disorder, moderate use
ICD-9-CM mild or severe disorder
Alcohol 291.82 F10.182 F10.282 F10.982
Caffeine 292.85 F15.182 F15.282 F15.982
Cannabis 292.85 F12.188 F12.288 F12.988
Opioid 292.85 F11.182 F11.282 F11.982
Sedative, hypnotic, or anxiolytic 292.85 F13.182 F13.282 F13.982
Amphetamine (or other 292.85 F15.182 F15.282 F15.982
stimulant)
Cocaine 292.85 F14.182 F14.282 Ft4.982
Tobacco 292.85 NA F17.208 NA
Other (or unknown) substance 292.85 F19.182 F19.282 F19.982
Recording Procedures
ICD-9-CM. The name of the substance/medication-induced sleep disorder begins with
the specific substance (e.g., cocaine, bupropion) that is presumed to be causing the sleep
disturbance. The diagnostic code is selected from the table included in the criteria set,
which is based on the drug class. For substances that do not fit into any of the classes (e.g.,
bupropion), the code for “other substance” should be used; and in cases in which a sub-
stance is judged to be an etiological factor but the specific class of substance is unknown,
the category “unknown substance” should be used.
The name of the disorder is followed by the specification of onset (i.e., onset during in-
toxication, onset during discontinuation/ withdrawal), followed by the subtype designa-
tion (i.e., insomnia type, daytime sleepiness type, parasomnia type, mixed type). Unlike
the recording procedures for ICD-10-CM, which combine the substance-induced disorder
and substance use disorder into a single code, for ICD-9-CM a separate diagnostic code
is given for the substance use disorder. For example, in the case of insomnia occurring
during withdrawal in a man with a severe lorazepam use disorder, the diagnosis is 292.85
lorazepam-induced sleep disorder, with onset during withdrawal, insomnia type. An ad-
ditional diagnosis of 304.10 severe lorazepam use disorder is also given. When more than
one substance is judged to play a significant role in the development of the sleep distur-
bance, each should be listed separately (e.g., 292.85 alcohol-induced sleep disorder, with
onset during intoxication, insomnia type; 292.85 cocaine-induced sleep disorder, with on-
set during intoxication, insomnia type).
ICD-10-CM. Thename of thesubstance/medication-induced sleep disorder begins with the
specific substance (e.g., cocaine, bupropion) that is presumed to be causing the sleep distur-
bance. The diagnostic code is selected from the table included in the criteria set, which is based
on the drug class and presence or absence of a comorbid substance use disorder. For sub-
stances that do not fit into any of the classes (e.g., bupropion), the code for “other substance”
should be used; and in cases in which a substance is judged to be an etiological factor but the
specific class of substance is unknown, the category “unknown substance” should be used.
When recording the name of the disorder, the comorbid substance use disorder (if any)
is listed first, followed by the word “with,” followed by the name of the substance-induced
sleep disorder, followed by the specification of onset (i.e., onset during intoxication, onset
416 Sleep-Wake Disorders
during discontinuation / withdrawal), followed by the subtype designation (i.e., insomnia
type, daytime sleepiness type, parasomnia type, mixed type). For example, in the case of
insomnia occurring during withdrawal in a man with a severe lorazepam use disorder, the
diagnosis is F13.282 severe lorazepam use disorder with lorazepam-induced sleep disor-
der, with onset during withdrawal, insomnia type. A separate diagnosis of the comorbid
severe lorazepam use disorder is not given. If the substance-induced sleep disorder occurs
without a comorbid substance use disorder (e.g., with medication use), no accompanying
substance use disorder is noted (e.g., F19.982 bupropion-induced sleep disorder, with on-
set during medication use, insomnia type). When more than one substance is judged to
play a significant role in the development of the sleep disturbance, each should be listed
separately (e.g., F10.282 severe alcohol use disorder with alcohol-induced sleep disorder,
with onset during intoxication, insomnia type; F14.282 severe cocaine use disorder with
cocaine-induced sleep disorder, with onset during intoxication, insomnia type).
Diagnostic Features
The essential feature of substance /medication-induced sleep disorder is a prominent sleep
disturbance that is sufficiently severe to warrant independent clinical attention (Criterion A)
and that is judged to be primarily associated with the pharmacological effects of a substance
(i.e., a drug of abuse, a medication, toxin exposure) (Criterion B). Depending on the sub-
stance involved, one of four types of sleep disturbances is reported. Insomnia type and day-
time sleepiness type are most common, while parasomnia type is seen less often. The mixed
type is noted when more than one type of sleep disturbance-related symptom is present and
none predominates. The disturbance must not be better explained by another sleep disorder
(Criterion C). A substance /medication-induced sleep disorder is distinguished from insom-
nia disorder or a disorder associated with excessive daytime sleepiness by considering onset
and course. For drugs of abuse, there must be evidence of intoxication or withdrawal from
the history, physical examination, or laboratory findings. Substance /medication-induced
sleep disorder arises only in association with intoxication or discontinuation/ withdrawal
states, whereas other sleep disorders may precede the onset of substance use or occur during
times of sustained abstinence. As discontinuation/ withdrawal states for some substances
can be protracted, onset of the sleep disturbance can occur 4 weeks after cessation of sub-
stance use, and the disturbance may have features atypical of other sleep disorders (e.g.,
atypical age at onset or course). The diagnosis is not made if the sleep disturbance occurs
only during a delirium (Criterion D). The symptoms must cause clinically significant dis-
tress or impairment in social, occupational, or other important areas of functioning (Crite-
rion E). This diagnosis should be made instead of a diagnosis of substance intoxication or
substance withdrawal only when the symptoms in Criterion A predominate in the clinical
picture and when the symptoms warrant independent clinical attention.
Associated Features Supporting Diagnosis
During periods of substance /medication use, intoxication, or withdrawal, individuals fre-
quently complain of dysphoric mood, including depression and anxiety, irritability, cog-
nitive impairment, inability to concentrate, and fatigue.
Prominent and severe sleep disturbances can occur in association with intoxication
with the following classes of substances: alcohol; caffeine; cannabis; opioids; sedatives,
hypnotics, or anxiolytics; stimulants (including cocaine); and other (or unknown) sub-
stances. Prominent and severe sleep disturbances can occur in association with withdrawal
from the following classes of substances: alcohol; caffeine; cannabis; opioids; sedatives,
hypnotics, or anxiolytics; stimulant (including cocaine); tobacco; and other (or unknown)
substances. Some medications that invoke sleep disturbances include adrenergic agonists
and antagonists, dopamine agonists and antagonists, cholinergic agonists and antagonists,
serotonergic agonists and antagonists, antihistamines, and corticosteroids.
Substance/Medication-induced Sleep Disorder 417
Alcohol. Alcohol-induced sleep disorder typically occurs as insomnia type. During
acute intoxication, alcohol produces an immediate sedative effect depending on dose, ac-
companied by increased stages 3 and 4 non-rapid eye movement (NREM) sleep and re-
duced rapid eye movement (REM) sleep. Following these initial effects, there may be
increased wakefulness, restless sleep, and vivid and anxiety-laden dreams for the remain-
ing sleep period. In parallel, stages 3 and 4 sleep are reduced, and wakefulness and REM
sleep are increased. Alcohol can aggravate breathing-related sleep disorder. With habitual
use, alcohol continues to show a short-lived sedative effect in the first half of the night, fol-
lowed by sleep continuity disruption in the second half. During alcohol withdrawal, there
is extremely disrupted sleep continuity, and an increased amount and intensity of REM
sleep, associated frequently with vivid dreaming, which in extreme form, constitutes part
of alcohol withdrawal delirium. After acute withdrawal, chronic alcohol users may con-
tinue to complain of light, fragmented sleep for weeks to years associated with a persistent
deficit in slow-wave sleep.
Caffeine. Caffeine-induced sleep disorder produces insomnia in a dose-dependent man-
ner, with some individuals presenting with daytime sleepiness related to withdrawal.
Cannabis. Acute administration of cannabis may shorten sleep latency, though arous-
ing effects with increments in sleep latency also occur. Cannabis enhances slow-wave
sleep and suppresses REM sleep after acute administration. In chronic users, tolerance to
the sleep-inducing and slow-wave sleep—enhancing effects develops. Upon withdrawal,
sleep difficulties and unpleasant dreams have been reported lasting for several weeks.
Polysomnography studies demonstrate reduced slow-wave sleep and increased REM sleep
during this phase.
Opioids. Opioids may produce an increase in sleepiness and in subjective depth of sleep,
and reduced REM sleep, during acute short-term use. With continued administration, tol-
erance to the sedative effects of opioids develops and there are complaints of insomnia.
Consistent with their respiratory depressant effects, opioids exacerbate sleep apnea.
Sedative, hypnotic, or anxiolytic substances. Sedatives, hypnotics, and anxiolytics (e.g.,
barbiturates, benzodiazepines receptor agonists, meprobamate, glutethimide, methypry-
lon) have similar effects as opioids on sleep. During acute intoxication, sedative-hypnotic
drugs produce the expected increase in sleepiness and decrease in wakefulness. Chronic
use (particularly of barbiturates and the older nonbarbiturate, nonbenzodiazepine drugs)
may cause tolerance with subsequent return of insomnia. Daytime sleepiness may occur.
Sedative-hypnotic drugs can increase the frequency and severity of obstructive sleep ap-
nea events. Parasomnias are associated with use of benzodiazepine receptor agonists, es-
pecially when these medications are taken at higher doses and when they are combined
with other sedative drugs. Abrupt discontinuation of chronic sedative, hypnotic, or anx-
iolytic use can lead to withdrawal but more commonly rebound insomnia, a condition of
an exacerbation of insomnia upon drug discontinuation for 1-2 days reported to occur
even with short-term use. Sedative, hypnotic, or anxiolytic drugs with short durations of
action are most likely to produce complaints of rebound insomnia, whereas those with
longer durations of action are more often associated with daytime sleepiness. Any sedative,
hypnotic, or anxiolytic drug can potentially cause daytime sedation, withdrawal, or re-
bound insomnia.
Amphetamines and related substances and other stimulants. Sleep disorders induced
by amphetamine and related substances and other stimulants are characterized by insomnia
during intoxication and excessive sleepiness during withdrawal. During acute intoxication,
stimulants reduce the total amount of sleep, increase sleep latency and sleep continuity distur-
bances, and decrease REM sleep. Slow-wave sleep tends to be reduced. During withdrawal
from chronic stimulant use, there is both prolonged nocturnal sleep duration and excessive
daytime sleepiness. Multiple sleep latency tests may show increased daytime sleepiness dur-
418 Sleep-Wake Disorders
ing the withdrawal phase. Drugs like 3,4-methylenedioxymethamphetamine (MDMA; “ec-
stasy”) and related substances lead to restless and disturbed sleep within 48 hours of intake;
frequent use of these compounds is associated with persisting symptoms of anxiety, depres-
sion, and sleep disturbances, even during longer-term abstinence.
Tobacco. Chronic tobacco consumption is associated primarily with symptoms of insom-
nia, decreased slow-wave sleep with a reduction of sleep efficiency, and increased daytime
sleepiness. Withdrawal from tobacco can lead to impaired sleep. Individuals who smoke
heavily may experience regular nocturnal awakenings caused by tobacco craving.
Other or unknown substances/medications. Other substances /medications may pro-
duce sleep disturbances, particularly medications that affect the central or autonomic
nervous systems (e.g., adrenergic agonists and antagonists, dopamine agonists and antag-
onists, cholinergic agonists and antagonists, serotonergic agonists and antagonists, anti-
histamines, corticosteroids).
Development and Course
Insomnia in children can be identified by either a parent or the child. Often the child has a
clear sleep disturbance associated with initiation of a medication but may not report
symptoms, although parents observe the sleep disturbances. The use of some illicit sub-
stances (e.g., cannabis, ecstasy) is prevalent in adolescence and early adulthood. Insomnia
or any other sleep disturbance encountered in this age group should prompt careful con-
sideration of whether the sleep disturbance is due to consumption of these substances.
Help-seeking behavior for the sleep disturbance in these age groups is limited, and thus
corroborative report may be elicited from a parent, caregiver, or teacher. Older individuals
take more medications and are at increased risk for developing a substance/medication-
induced sleep disorder. They may interpret sleep disturbance as part of normal aging and
fail to report symptoms. Individuals with major neurocognitive disorder (e.g., dementia)
are at risk for substance/medication-induced sleep disorders but may not report symp-
toms, making corroborative report from caregiver(s) particularly important.
Risk and Prognostic Factors
Risk and prognostic factors involved in substance abuse / dependence or medication use
are normative for certain age groups. They are relevant for, and likely applicable to, the
type of sleep disturbance encountered (see the chapter “Substance-Related and Addictive
Disorders” for descriptions of respective substance use disorders).
Temperamental. Substance use generally precipitates or accompanies insomnia in vul-
nerable individuals. Thus, presence of insomnia in response to stress or change in sleep en-
vironment or timing can represent a risk for developing substance /medication-induced
sleep disorder. A similar risk may be present for individuals with other sleep disorders
(e.g., individuals with hypersomnia who use stimulants).
Culture-Related Diagnostic Issues
The consumption of substances, including prescribed medications, may depend in part on
cultural background and specific local drug regulations.
Gender-Related Diagnostic Issues
Gender-specific prevalences (i.e., females affected more than males at a ratio of about 2:1) exist
for patterns of consumption of some substances (e.g., alcohol). The same amount and duration
of consumption of a given substance may lead to highly different sleep-related outcomes in
males and females based on, for example, gender-specific differences in hepatic functioning.
Substance/Medication-Induced Sleep Disorder 419
Diagnostic Markers
Each of the substance /medication-induced sleep disorders produces electroencephalo-
graphic sleep patterns that are associated with, but cannot be considered diagnostic of, other
disorders. The electroencephalographic sleep profile for each substance is related to the
stage of use, whether intake /intoxication, chronic use, or withdrawal following discontinu-
ation of the substance. All-night polysomnography can help define the severity of insomnia
complaints, while the multiple sleep latency test provides information about the severity of
daytime sleepiness. Monitoring of nocturnal respiration and periodic limb movements with
polysomnography may verify a substance’s impact on nocturnal breathing and motor be-
havior. Sleep diaries for 2 weeks and actigraphy are considered helpful in confirming the
presence of substance/medication-induced sleep disorder. Drug screening can be of use
when the individual is not aware or unwilling to relate information about substance intake.
Functional Consequences of
Substance/Medication-Induced Sleep Disorder
While there are many functional consequences associated with sleep disorders, the only
unique consequence for substance/medication-induced sleep disorder is increased risk
for relapse. The degree of sleep disturbance during alcohol withdrawal (e.g., REM sleep
rebound predicts risk of relapse of drinking). Monitoring of sleep quality and daytime
sleepiness during and after withdrawal may provide clinically meaningful information on
whether an individual is at increased risk for relapse.
Differential Diagnosis
Substance intoxication or substance withdrawal. Sleep disturbances are commonly en-
countered in the context of substance intoxication or substance discontinuation /with-
drawal. A diagnosis of substance/medication-induced sleep disorder should be made
instead of a diagnosis of substance intoxication or substance withdrawal only when the
sleep disturbance is predominant in the clinical picture and is sufficiently severe to war-
rant independent clinical attention.
Delirium. If the substance /medication-induced sleep disturbance occurs exclusively dur-
ing the course of a delirium, it is not diagnosed separately.
Other sleep disorders. A substance/medication-induced sleep disorder is distinguished
from another sleep disorder if a substance/medication is judged to be etiologically related to
the symptoms. A substance/medication-induced sleep disorder attributed to a prescribed
medication for a mental disorder or medical condition must have its onset while the individual
is receiving the medication or during discontinuation, if there is a discontinuation/with-
drawal syndrome associated with the medication. Once treatment is discontinued, the sleep
disturbance will usually remit within days to several weeks. If symptoms persist beyond
4 weeks, other causes for the sleep disturbance-related symptoms should be considered. Not
infrequently, individuals with another sleep disorder use medications or drugs of abuse to
self-medicate their symptoms (e.g., alcohol for management of insomnia). If the substance/
medication is judged to play a significant role in the exacerbation of the sleep disturbance, an
additional diagnosis of a substance/medication-induced sleep disorder may be warranted.
Sleep disorder due to another medical condition. Substance/medication-induced sleep
disorder and sleep disorder associated with another medical condition may produce sim-
ilar symptoms of insomnia, daytime sleepiness, or a parasomnia. Many individuals with
other medical conditions that cause sleep disturbance are treated with medications that
may also cause sleep disturbances. The chronology of symptoms is the most important fac-
tor in distinguishing between these two sources of sleep symptoms. Difficulties with sleep
that clearly preceded the use of any medication for treatment of a medical condition would
420 Sleep-Wake Disorders
suggest a diagnosis of sleep disorder associated with another medical condition. Con-
versely, sleep symptoms that appear only after the initiation of a particular medication/
substance suggest a substance/medication-induced sleep disorder. If the disturbance is
comorbid with another medical condition and is also exacerbated by substance use, both
diagnoses (i.e., sleep disorder associated with another medical condition and substance/
medication-induced sleep disorder) are given. When there is insufficient evidence to de-
termine whether the sleep disturbance is attributable to a substance/ medication or to an-
other medical condition or is primary (i.e., not due to either a substance/medication or
another medical condition), a diagnosis of other specified sleep-wake disorder or unspec-
ified sleep-wake disorder is indicated.
Comorbidity
See the “Comorbidity” sections for other sleep disorders in this chapter, including insom-
nia, hypersomnolence, central sleep apnea, sleep-related hypoventilation, and circadian
rhythm sleep-wake disorders, shift work type.
Relationship to Internationai Ciassification of
Sieep Disorders
The International Classification of Sleep Disorders, 2nd Edition (ICSD-2), lists sleep disorders
“due to drug or substance” under their respective phenotypes (e.g., insomnia, hypersomnia).
Other Specified Insomnia Disorder
780.52 (G47.09)
This category applies to presentations in which symptoms characteristic of insomnia disorder
that cause clinically significant distress or impairment in social, occupational, or other important
areas of functioning predominate but do not meet the full criteria for insomnia disorder or any
of the disorders in the sleep-wake disorders diagnostic class. The other specified insomnia dis-
order category is used in situations in which the clinician chooses to communicate the specific
reason that the presentation does not meet the criteria for insomnia disorder or any specific
sleep-wake disorder. This is done by recording “other specified insomnia disorder’ followed by
the specific reason (e.g., “brief insomnia disorder’).
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Brief insomnia disorder: Duration is less than 3 months.
2. Restricted to nonrestorative sleep: Predominant complaint is nonrestorative sleep
unaccompanied by other sleep symptoms such as difficulty falling asleep or remaining
asleep.
Unspecified Insomnia Disorder
780.52 (G47.00)
This category applies to presentations in which symptoms characteristic of insomnia disor-
der that cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning predominate but do not meet the full criteria for insomnia dis-
order or any of the disorders in the sleep-wake disorders diagnostic class. The unspecified
Other Specified Hypersomnolence Disorder 421
insomnia disorder category is used in situations in which the clinician chooses not to specify
the reason that the criteria are not met for insomnia disorder or a specific sleep-wake dis-
order, and includes presentations in which there is insufficient information to make a more
specific diagnosis.
Other Specified Hypersomnolence Disorder
780.54 (G47.19)
This category applies to presentations in which symptoms characteristic of hypersomno-
lence disorder that cause clinically significant distress or impairment in social, occupation-
al, or other important areas of functioning predominate but do not meet the full criteria for
hypersomnolence disorder or any of the disorders in the sleep-wake disorders diagnostic
class. The other specified hypersomnolence disorder category is used in situations in
which the clinician chooses to communicate the specific reason that the presentation does
not meet the criteria for hypersomnolence disorder or any specific sleep-wake disorder.
This is done by recording “other specified hypersomnolence disorder’ followed by the spe-
cific reason (e.g., “brief-duration hypersomnolence,” as in Kieine-Levin syndrome).
Unspecified Hypersomnolence Disorder
780.54 (G47.10)
This category applies to presentations in which symptoms characteristic of hypersomno-
lence disorder that cause clinically significant distress or impairment in social, occupation-
al, or other important areas of functioning predominate but do not meet the full criteria for
hypersomnolence disorder or any of the disorders in the sleep-wake disorders diagnostic
class. The unspecified hypersomnolence disorder category is used in situations in which
the clinician chooses not to specify the reason that the criteria are not met for hypersom-
nolence disorder or a specific sleep-wake disorder, and includes presentations in which
there is insufficient information to make a more specific diagnosis.
Other Specified Sleep-Wake Disorder
780.59 (G47.8)
This category applies to presentations in which symptoms characteristic of a sleep-wake
disorder that cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning predominate but do not meet the full criteria for any of
the disorders in the sleep-wake disorders diagnostic class and do not qualify for a diagno-
sis of other specified insomnia disorder or other specified hypersomnolence disorder. The
other specified sleep-wake disorder category is used in situations in which the ctinician
chooses to communicate the specific reason that the presentation does not meet the
criteria for any specific sleep-wake disorder. This is done by recording “other specified
sleep-wake disorder” followed by the specific reason (e.g., “repeated arousals during rapid
eye movement sleep without polysomnography or history of Parkinson’s disease or other
synucleinopathy’).
422 Sleep-Wake Disorders
Unspecified Sleep-Wake Disorder
780.59 (G47.9)
This category applies to presentations in which symptoms characteristic of a sleep-wake
disorder that cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning predominate but do not meet the full criteria for any of
the disorders in the sleep-wake disorders diagnostic class and do not qualify for a diagno-
sis of unspecified insomnia disorder or unspecified hypersomnolence disorder. The un-
specified sleep-wake disorder category is used in situations in which the clinician chooses
not to specify the reason that the criteria are not met for a specific sleep-wake disorder,
and includes presentations in which there is insufficient information to make a more spe-
cific diagnosis.
apron remnant yee a me
Sexual dysfunctions include delayed ejaculation, erectile disorder, female orgasmic
disorder, female sexual interest/arousal disorder, genito-pelvic pain/penetration disorder,
male hypoactive sexual desire disorder, premature (early) ejaculation, substance/medication-
induced sexual dysfunction, other specified sexual dysfunction, and unspecified sexual dys-
function. Sexual dysfunctions are a heterogeneous group of disorders that are typically char-
acterized by a clinically significant disturbance in a person’s ability to respond sexually or to
experience sexual pleasure. An individual may have several sexual dysfunctions at the same
time. In such cases, all of the dysfunctions should be diagnosed.
Clinical judgment should be used to determine if the sexual difficulties are the result of
inadequate sexual stimulation; in these cases, there may still be a need for care, but a di-
agnosis of a sexual dysfunction would not be made. These cases may include, but are not
limited to, conditions in which lack of knowledge about effective stimulation prevents the
experience of arousal or orgasm.
Subtypes are used to designate the onset of the difficulty. In many individuals with
sexual dysfunctions, the time of onset may indicate different etiologies and interventions.
Lifelong refers to a sexual problem that has been present from first sexual experiences, and
acquired applies to sexual disorders that develop after a period of relatively normal sexual
function. Generalized refers to sexual difficulties that are not limited to certain types of
stimulation, situations, or partners, and situational refers to sexual difficulties that only oc-
cur with certain types of stimulation, situations, or partners.
In addition to the lifelong /acquired and generalized /situational subtypes, a number
of factors must be considered during the assessment of sexual dysfunction, given that they
may be relevant to etiology and/or treatment, and that may contribute, to varying degrees,
across individuals: 1) partner factors (e.g., partner’s sexual problems; partner’s health sta-
tus); 2) relationship factors (e.g., poor communication; discrepancies in desire for sexual
activity); 3) individual vulnerability factors (e.g., poor body image; history of sexual or emo-
tional abuse), psychiatric comorbidity (e.g., depression, anxiety), or stressors (e.g., job loss,
bereavement); 4) cultural or religious factors (e.g., inhibitions related to prohibitions against
sexual activity or pleasure; attitudes toward sexuality); and 5) medical factors relevant to
prognosis, course, or treatment.
Clinical judgment about the diagnosis of sexual dysfunction should take into consideration
cultural factors that may influence expectations or engender prohibitions about the experience
of sexual pleasure. Aging may be associated with a normative decrease in sexual response.
Sexual response has a requisite biological underpinning, yet is usually experienced in
an intrapersonal, interpersonal, and cultural context. Thus, sexual function involves a com-
plex interaction among biological, sociocultural, and psychological factors. In many clinical
contexts, a precise understanding of the etiology of a sexual problem is unknown. Nonethe-
less, a sexual dysfunction diagnosis requires ruling out problems that are better explained
by a nonsexual mental disorder, by the effects of a substance (e.g., drug or medication), by
a medical condition (e.g., due to pelvic nerve damage), or by severe relationship distress,
partner violence, or other stressors.
If the sexual dysfunction is mostly explainable by another nonsexual mental disorder (e.g.,
depressive or bipolar disorder, anxiety disorder, posttraumatic stress disorder, psychotic dis-
423
424 Sexual Dysfunctions
order), then only the other mental disorder diagnosis should be made. If the problem is
thought to be better explained by the use/ misuse or discontinuation of a drug or substance, it
should be diagnosed accordingly as a substance/medication-induced sexual dysfunction. If
the sexual dysfunction is attributable to another medical condition (e.g., peripheral neuropa-
thy), the individual would not receive a psychiatric diagnosis. If severe relationship distress,
partner violence, or significant stressors better explain the sexual difficulties, then a sexual dys-
function diagnosis is not made, but an appropriate V or Z code for the relationship problem or
stressor may be listed. In many cases, a precise etiological relationship between another con-
dition (e.g., a medical condition) and a sexual dysfunction cannot be established.
Delayed Ejaculation
Diagnostic Criteria 302.74 (F52.32)
A. Either of the following symptoms must be experienced on almost all or all occasions
(approximately 75%—-100%) of partnered sexual activity (in identified situational con-
texts or, if generalized, in all contexts), and without the individual desiring delay:
1. Marked delay in ejaculation.
2. Marked infrequency or absence of ejaculation.
B. The symptoms in Criterion A have persisted for a minimum duration of approximately
6 months.
C. The symptoms in Criterion A cause clinically significant distress in the individual.
D. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a
consequence of severe relationship distress or other significant stressors and is not at-
tributable to the effects of a substance/medication or another medical condition.
Specify whether:
Lifelong: The disturbance has been present since the individual became sexually active.
Acquired: The disturbance began after a period of relatively normal sexual function.
Specify whether:
Generalized: Not limited to certain types of stimulation, situations, or partners.
Situational: Only occurs with certain types of stimulation, situations, or partners.
Specify current severity:
Mild: Evidence of mild distress over the symptoms in Criterion A.
Moderate: Evidence of moderate distress over the symptoms in Criterion A.
Severe: Evidence of severe or extreme distress over the symptoms in Criterion A.
Diagnostic Features
The distinguishing feature of delayed ejaculation is a marked delay in or inability to
achieve ejaculation (Criterion A). The man reports difficulty or inability to ejaculate de-
spite the presence of adequate sexual stimulation and the desire to ejaculate. The present-
ing complaint usually involves partnered sexual activity. In most cases, the diagnosis will
be made by self-report of the individual. The definition of “delay” does not have precise
boundaries, as there is noconsensus as to what constitutes a reasonable time to reach or-
gasm or what is unacceptably long for most men and their sexual partners.
Associated Features Supporting Diagnosis
The man and his partner may report prolonged thrusting to achieve orgasm to the point of
exhaustion or genital discomfort and then ceasing efforts. Some men may report avoiding
Delayed Ejaculation 425
sexual activity because of a repetitive pattern of difficulty ejaculating. Some sexual partners
may report feeling less sexually attractive because their partner cannot ejaculate easily.
In addition to the subtypes “lifelong /acquired” and “generalized/situational,” the fol-
lowing five factors must be considered during assessment and diagnosis of delayed ejacu-
lation, given that they may be relevant to etiology and/or treatment: 1) partner factors (e.g.,
partner’s sexual problems, partner’s health status); 2) relationship factors (e.g., poor com-
munication, discrepancies in desire for sexual activity); 3) individual vulnerability factors
(e.g., poor body image; history of sexual or emotional abuse), psychiatric comorbidity (e.g.,
depression, anxiety), or stressors (e.g., job loss, bereavement); 4) cultural/religious factors
(e.g., inhibitions related to prohibitions against sexual activity; attitudes toward sexuality);
and 5) medical factors relevant to prognosis, course, or treatment. Each of these factors may
contribute differently to the presenting symptoms of different men with this disorder.
Prevalence
Prevalence is unclear because of the lack of a precise definition of this syndrome. It is the
least common male sexual complaint. Only 75% of men report always ejaculating during
sexual activity, and less than 1% of men will complain of problems with reaching ejacula-
tion that last more than 6 months.
Development and Course
Lifelong delayed ejaculation begins with early sexual experiences and continues through-
out life. By definition, acquired delayed ejaculation begins after a period of normal sexual
function. There is minimal evidence concerning the course of acquired delayed ejacula-
tion. The prevalence of delayed ejaculation appears to remain relatively constant until
around age 50 years, when the incidence begins to increase significantly. Men in their 80s
report twice as much difficulty ejaculating as men younger than 59 years.
Risk and Prognostic Factors
Genetic and physiological. Age-related loss of the fast-conducting peripheral sensory
nerves and age-related decreased sex steroid secretion may be associated with the increase
in delayed ejaculation in men older than 50 years.
Culture-Related Diagnostic Issues
Complaints of ejaculatory delay vary across countries and cultures. Such complaints are
more common among men in Asian populations than in men living in Europe, Australia,
or the United States. This variation may be attributable to cultural or genetic differences
between cultures.
Functional Consequences of Delayed Ejaculation
Difficulty with ejaculation may contribute to difficulties in conception. Delayed ejacula-
tion is often associated with considerable psychological distress in one or both partners.
Differential Diagnosis
Another medical condition. The major differential diagnosis is between delayed ejacu-
lation fully explained by another medical illness or injury and delayed ejaculation with a
psychogenic, idiopathic, or combined psychological and medical etiology. A situational
aspect to the complaint is suggestive of a psychological basis for the problem (e.g., men
who can ejaculate during sexual activity with one sex but not the other; men who can ejac-
ulate with one partner but not another of the same sex; men with paraphilic arousal pat-
426 Sexual Dysfunctions
terns; men who require highly ritualized activity to ejaculate during partnered sexual
activity). Another medical illness or injury may produce delays in ejaculation independent
of psychological issues. For example, inability to ejaculate can be caused by interruption of
the nerve supply to the genitals, such as can occur after traumatic surgical injury to the
lumbar sympathetic ganglia, abdominoperitoneal surgery, or lumbar sympathectomy.
Ejaculation is thought to be under autonomic nervous system control involving the hypo-
gastric (sympathetic) and pudendal (parasympathetic) nerves. A number of neurodegen-
erative diseases, such as multiple sclerosis and diabetic and alcoholic neuropathy, can
cause inability to ejaculate. Delayed ejaculation should also be differentiated from retro-
grade ejaculation (i.e., ejaculation into the bladder), which may follow transurethral pros-
tatic resection.
Substance/medication use. A number of pharmacological agents, such as antidepres-
sants, antipsychotics, alpha sympathetic drugs, and opioid drugs, can cause ejaculatory
problems.
Dysfunction with orgasm. It is important in the history to ascertain whether the com-
plaint concerns delayed ejaculation or the sensation of orgasm, or both. Ejaculation occurs
in the genitals, whereas the experience of orgasm is believed to be primarily subjective.
Ejaculation and orgasm usually occur together but not always. For example, a man witha
normal ejaculatory pattern may complain of decreased pleasure (i.e., anhedonic ejacula-
tion). Such a complaint would not be coded as delayed ejaculation but could be coded as
other specified sexual dysfunction or unspecified sexual dysfunction.
Comorbidity
There is some evidence to suggest that delayed ejaculation may be more common in severe
forms of major depressive disorder.
Erectile Disorder
Diagnostic Criteria 302.72 (F52.21)
A. Atleast one of the three following symptoms must be experienced on almost all or all
(approximately 75%-100%) occasions of sexual activity (in identified situational con-
texts or, if generatized, in all contexts):
1. Marked difficulty in obtaining an erection during sexual activity.
2. Marked difficulty in maintaining an erection until the completion of sexual activity.
3. Marked decrease in erectile rigidity.
B. The symptoms in Criterion A have persisted for a minimum duration of approximately
6 months.
C. The symptoms in Criterion A cause clinically significant distress in the individual.
D. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a
consequence of severe relationship distress or other significant stressors and is not at-
tributabte to the effects of a substance/medication or another medical condition.
Specify whether:
Lifelong: The disturbance has been present since the individual became sexually ac-
tive.
Acquired: The disturbance began after a period of relatively normal sexual function.
Specify whether:
Generalized: Not limited to certain types of stimulation, situations, or partners.
Situational: Only occurs with certain types of stimulation, situations, or partners.
Erectile Disorder 427
Specify current severity:
Mild: Evidence of mild distress over the symptoms in Criterion A.
Moderate: Evidence of moderate distress over the symptoms in Criterion A.
Severe: Evidence of severe or extreme distress over the symptoms in Criterion A.
Diagnostic Features
The essential feature of erectile disorder is the repeated failure to obtain or maintain erec-
tions during partnered sexual activities (Criterion A). A careful sexual history is necessary
to ascertain that the problem has been present for a significant duration of time (i.e., at least
approximately 6 months) and occurs on the majority of sexual occasions (i.e., at least 75%
of the time). Symptoms may occur only in specific situations involving certain types of
stimulation or partners, or they may occur in a generalized manner in all types of situa-
tions, stimulation, or partners.
Associated Features Supporting Diagnosis
Many men with erectile disorder may have low self-esteem, low self-confidence, and a de-
creased sense of masculinity, and may experience depressed affect. Fear and/or avoid-
ance of future sexual encounters may occur. Decreased sexual satisfaction and reduced
sexual desire in the individual’s partner are common.
In addition to the subtypes “lifelong/acquired” and “generalized/situational,” the fol-
lowing five factors must be considered during assessment and diagnosis of erectile disorder
given that they may be relevant to etiology and/or treatment: 1) partner factors (e.g., part-
ner’s sexual problems, partner’s health status); 2) relationship factors (e.g., poor communi-
cation, discrepancies in desire for sexual activity); 3) individual vulnerability factors (e.g.,
poor body image, history of sexual or emotional abuse), psychiatric comorbidity (e.g., de-
pression, anxiety), or stressors (e.g., job loss, bereavement); 4) cultural /religious factors (e.g.,
inhibitions related to prohibitions against sexual activity; attitudes toward sexuality); and
5) medical factors relevant to prognosis, course, or treatment. Each of these factors may con-
tribute differently to the presenting symptoms of different men with this disorder.
Prevalence
The prevalence of lifelong versus acquired erectile disorder is unknown. There is a strong
age-related increase in both prevalence and incidence of problems with erection, particu-
larly after age 50 years. Approximately 13%-21% of men ages 40-80 years complain of oc-
casional problems with erections. Approximately 2% of men younger than age 40-50 years
complain of frequent problems with erections, whereas 40%~50% of men older than 60-70
years may have significant problems with erections. About 20% of men fear erectile prob-
lems on their first sexual experience, whereas approximately 8% experienced erectile prob-
lems that hindered penetration during their first sexual experience.
Development and Course
Erectile failure on first sexual attempt has been found to be related to having sex with a
previously unknown partner, concomitant use of drugs or alcohol, not wanting to have
sex, and peer pressure. There is minimal evi-2t most of these problems spontaneously re-
mit without professional intervention, but some men may continue to have episodic prob-
lems. In contrast, acquired erectile disorder is often associated with biological factors such
as diabetes and cardiovascular disease. Acquired erectile disorder is likely to be persistent
in most men.
The natural history of lifelong erectile disorder is unknown. Clinical observation sup-
ports the association of lifelong erectile disorder with psychological factors that are self-
428 Sexual Dysfunctions
limiting or responsive to psychological interventions, whereas, as noted above, acquired
erectile disorder is more likely to be related to biological factors and to be persistent. The
incidence of erectile disorder increases with age. A minority of men diagnosed as having
moderate erectile failure may experience spontaneous remission of symptoms without
medical intervention. Distress associated with erectile disorder is lower in older men as
compared with younger men.
Risk and Prognostic Factors
Temperamental. Neurotic personality traits may be associated with erectile problems in col-
lege students, and submissive personality traits may be associated with erectile problems in
men age 40 years and older. Alexithymia (ie., deficits in cognitive processing of emotions) is
common in men diagnosed with “psychogenic” erectile dysfunction. Erectile problems are
common in men diagnosed with depression and posttraumatic stress disorder.
Course modifiers. Risk factors for acquired erectile disorder include age, smoking to-
bacco, lack of physical exercise, diabetes, and decreased desire.
Culture-Reiated Diagnostic Issues
Complaints of erectile disorder have been found to vary across countries. Jt is unclear to
what extent these differences represent differences in cultural expectations as opposed to
genuine differences in the frequency of erectile failure.
Diagnostic Markers
Nocturnal penile tumescence testing and measured erectile turgidity during sleep can be
employed to help differentiate organic from psychogenic erectile problems on the as-
sumption that adequate erections during rapid eye movement sleep indicate a psycholog-
ical etiology to the problem. A number of other diagnostic procedures may be employed
depending on the clinician’s assessment of their relevance given the individual's age, co-
morbid medical problems, and clinical presentation. Doppler ultrasonography and intra-
vascular injection of vasoactive drugs, as well as invasive diagnostic procedures such as
dynamic infusion cavernosography, can be used to assess vascular integrity. Pudendal
nerve conduction studies, including somatosensory evoked potentials, can be employed
when a peripheral neuropathy is suspected. In men also complaining of decreased sexual
desire, serum bioavailable or free testosterone is frequently assessed to determine if the
difficulty is secondary to endocrinological factors. Thyroid function may also be assessed.
Determination of fasting serum glucose is useful to screen for the presence of diabetes mel-
litus. The assessment of serum lipids is important, as erectile disorder in men 40 years and
older is predictive of the future risk of coronary artery disease.
Functionai Consequences of Erectiie Disorder
Erectile disorder can interfere with fertility and produce both individual and interpersonal
distress. Fear and/or avoidance of sexual encounters may interfere with the ability to de-
velop intimate relationships.
Differentiai Diagnosis
Nonsexual mental disorders. Major depressive disorder and erectile disorder are closely
associated, and erectile disorder accompanying severe depressive disorder may occur.
Normal erectile function. The differential should include consideration of normal erec-
tile function in men with excessive expectations.
Female Orgasmic Disorder 429
Substance/medication use. Another major differential diagnosis is whether the erectile
problem is secondary to substance/medication use. An onset that coincides with the be-
ginning of substance /medication use and that dissipates with discontinuation of the sub-
stance/medication or dose reduction is suggestive of a substance /medication-induced
sexual dysfunction.
Another medical condition. The most difficult aspect of the differential diagnosis of erec-
tile disorder is ruling out erectile problems that are fully explained by medical factors. Such
cases would not receive a diagnosis of a mental disorder. The distinction between erectile
disorder as a mental disorder and erectile dysfunction as the result of another medical con-
dition is usually unclear, and many cases will have complex, interactive biological and psy-
chiatric etiologies. If the individual is older than 40-50 years and/or has concomitant
medical problems, the differential diagnosis should include medical etiologies, especially
vascular disease. The presence of an organic disease known to cause erectile problems does
not confirm a causal relationship. For example, a man with diabetes mellitus can develop
erectile disorder in response to psychological stress. In general, erectile dysfunction due to
organic factors is generalized and gradual in onset. An exception would be erectile problems
after traumatic injury to the nervous innervation of the genital organs (e.g., spinal cord injury).
Erectile problems that are situational and inconsistent and that have an acute onset after a
stressful life event are most often due to psychological events. An age of less than 40 years is
also suggestive of a psychological etiology to the difficulty.
Other sexual dysfunctions. Erectile disorder may coexist with premature (early) ejacu-
lation and male hypoactive sexual] desire disorder.
Comorbidity
Erectile disorder can be comorbid with other sexual diagnoses, such as premature (early)
ejaculation and male hypoactive sexual desire disorder, as well as with anxiety and de-
pressive disorders. Erectile disorder is common in men with lower urinary tract symptoms
related to prostatic hypertrophy. Erectile disorder may be comorbid with dyslipidemia, car-
diovascular disease, hypogonadism, multiple sclerosis, diabetes mellitus, and other diseases
that interfere with the vascular, neurological, or endocrine function necessary for normal
erectile function.
Relationship to International Classification of Diseases
Erectile response is coded as failure of genital response in ICD-10 (F2.2).
Female Orgasmic Disorder
Diagnostic Criteria 302.73 (F52.31)
A. Presence of either of the following symptoms and experienced on almost all or all (ap-
proximately 75%—-100%) occasions of sexual activity (in identified situational contexts
or, if generalized, in all contexts):
1. Marked delay in, marked infrequency of, or absence of orgasm.
2. Markedly reduced intensity of orgasmic sensations.
B. The symptoms in Criterion A have persisted for a minimum duration of approximately
6 months.
C. The symptoms in Criterion A cause clinically significant distress in the individual.
D. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a
consequence of severe relationship distress (e.g., partner violence) or other significant
430 Sexual Dysfunctions
stressors and is not attributable to the effects of a substance/medication or another
medical condition.
Specify whether:
Lifelong: The disturbance has been present since the individual became sexually active.
Acquired: The disturbance began after a period of relatively normal sexual function.
Specify whether:
Generaiized: Not limited to certain types of stimulation, situations, or partners.
Situational: Only occurs with certain types of stimulation, situations, or partners.
Specify if:
Never experienced an orgasm under any situation.
Specify current severity:
Mild: Evidence of mild distress over the symptoms in Criterion A.
Moderate: Evidence of moderate distress over the symptoms in Criterion A.
Severe: Evidence of severe or extreme distress over the symptoms in Criterion A.
Diagnostic Features
Female orgasmic disorder is characterized by difficulty experiencing orgasm and/or
markedly reduced intensity of orgasmic sensations (Criterion A). Women show wide vari-
ability in the type or intensity of stimulation that elicits orgasm. Similarly, subjective descrip-
tions of orgasm are extremely varied, suggesting that it is experienced in very different
ways, both across women and on different occasions by the same woman. For a diagnosis
of female orgasmic disorder, symptoms must be experienced on almost all or all (approx-
imately 75%-100%) occasions of sexual activity (in identified situational contexts or, if
generalized, in all contexts) and have a minimum duration of approximately 6 months.
The use of the minimum severity and duration criteria is intended to distinguish transient
orgasm difficulties from more persistent orgasmic dysfunction. The inclusion of “approx-
imately” in Criterion B allows for clinician judgment in cases in which symptom duration
does not meet the recommended 6-month threshold.
For a woman to have a diagnosis of female orgasmic disorder, clinically significant dis-
tress must accompany the symptoms (Criterion C). In many cases of orgasm problems, the
causes are multifactorial or cannot be determined. If female orgasmic disorder is deemed
to be better explained by another mental disorder, the effects of a substance/ medication,
or a medical condition, then a diagnosis of female orgasmic disorder would not be made.
Finally, if interpersonal or significant contextual factors, such as severe relationship dis-
tress, intimate partner violence, or other significant stressors, are present, then a diagnosis
of female orgasmic disorder would not be made.
Many women require clitoral stimulation to reach orgasm, and a relatively small pro-
portion of women report that they always experience orgasm during penile-vaginal inter-
course. Thus, a woman’s experiencing orgasm through clitoral stimulation but not during
intercourse does not meet criteria for a clinical diagnosis of female orgasmic disorder. It is
also important to consider whether orgasmic difficulties are the result of inadequate sex-
ual stimulation; in these cases, there may still be a need for care, but a diagnosis of female
orgasmic disorder would not be made.
Associated Features Supporting Diagnosis
Associations between specific patterns of personality traits or psychopathology and orgas-
mic dysfunction have generally not been supported. Compared with women without the
disorder, some women with female orgasmic disorder may have greater difficulty com-
municating about sexual issues. Overall sexual satisfaction, however, is not strongly cor-
related with orgasmic experience. Many women report high levels of sexual satisfaction
Female Orgasmic Disorder 431
despite rarely or never experiencing orgasm. Orgasmic difficulties in women often co-
occur with problems related to sexual interest and arousal.
In addition to the subtypes “lifelong /acquired” and “generalized /situational,” the fol-
lowing five factors must be considered during assessment and diagnosis of female orgas-
mic disorder given that they may be relevant to etiology and/or treatment: 1) partner
factors (e.g., partner’s sexual problems, partner’s health status); 2) relationship factors
(e.g., poor communication, discrepancies in desire for sexual activity); 3) individual vul-
nerability factors (e.g., poor body image, history of sexual or emotional abuse), psychiatric
comorbidity (e.g., depression, anxiety), or stressors (e.g., job loss, bereavement); (4) cul-
tural/religious factors (e.g., inhibitions related to prohibitions against sexual activity;
attitudes toward sexuality); and 5) medical factors relevant to prognosis, course, or treat-
ment. Each of these factors may contribute differently to the presenting symptoms of dif-
ferent women with this disorder.
Prevalence
Reported prevalence rates for female orgasmic problems in women vary widely, from 10%
to 42%, depending on multiple factors (e.g., age, culture, duration, and severity of symp-
toms); however, these estimates do not take into account the presence of distress. Only a
proportion of women experiencing orgasm difficulties also report associated distress.
Variation in how symptoms are assessed (e.g., the duration of symptoms and the recall pe-
riod) also influence prevalence rates. Approximately 10% of women do not experience or-
gasm throughout their lifetime.
Development and Course
By definition, lifelong female orgasmic disorder indicates that the orgasmic difficulties have
always been present, whereas the acquired subtype would be assigned if the woman’s or-
gasmic difficulties developed after a period of normal orgasmic functioning.
A womans first experience of orgasm can occur any time from the prepubertal period
to well into adulthood. Women show a more variable pattern in age at first orgasm than do
men, and women’s reports of having experienced orgasm increase with age. Many women
learn to experience orgasm as they experience a wide variety of stimulation and acquire
more knowledge about their bodies. Women’s rates of orgasm consistency (defined as
“usually or always” experiencing orgasm) are higher during masturbation than during
sexual activity with a partner.
Risk and Prognostic Factors
Temperamental. A wide range of psychological factors, such as anxiety and concerns
about pregnancy, can potentially interfere with a woman’s ability to experience orgasm.
Environmental. There is a strong association between relationship problems, physical
health, and mental health and orgasm difficulties in women. Sociocultural factors (e.g.,
gender role expectations and religious norms) are also important influences on the expe-
rience of orgasmic difficulties.
Genetic and physiological. Many physiological factors may influence a woman’s expe-
rience of orgasm, including medical conditions and medications. Conditions such as mul-
tiple sclerosis, pelvic nerve damage from radical hysterectomy, and spinal cord injury can
all influence orgasmic functioning in women. Selective serotonin reuptake inhibitors are
known to delay or inhibit orgasm in women. Women with vulvovaginal atrophy (charac-
terized by symptoms such as vaginal dryness, itching, and pain) are significantly more
likely to report orgasm difficulties than are women without this condition. Menopausal
status is not consistently associated with the likelihood of orgasm difficulties. There may
be a significant genetic contribution to variation in female orgasmic function. However,
432 Sexual Dysfunctions
psychological, sociocultural, and physiological factors likely interact in complex ways to
influence women’s experience of orgasm and of orgasm difficulties.
Culture-Related Diagnostic Issues
The degree to which lack of orgasm in women is regarded as a problem that requires treat-
ment may vary depending on cultural context. In addition, women differ in how important
orgasm is to their sexual satisfaction. There may be marked sociocultural and generational
differences in women’s orgasmic ability. For example, the prevalence of inability to reach or-
gasm has ranged from 17.7% (in Northern Europe) to 42.2% (in Southeast Asia).
Diagnostic Markers
Although measurable physiological changes occur during female orgasm, including
changes in hormones, pelvic floor musculature, and brain activation, there is significant
variability in these indicators of orgasm across women. In clinical situations, the diagnosis
of female orgasmic disorder is based on a woman’s self-report.
Functional Consequences of Female Orgasmic Disorder
The functional consequences of female orgasmic disorder are unclear. Although there is a
strong association between relationship problems and orgasmic difficulties in women, it is
unclear whether relationship factors are risk factors for orgasmic difficulties or are conse-
quences of those difficulties.
Differential Diagnosis
Nonsexual mental disorders. Nonsexual mental disorders, such as major depressive
disorder, which is characterized by markedly diminished interest or pleasure in all, or al-
most all, activities, may explain female orgasmic disorder. If the orgasmic difficulties are
better explained by another mental disorder, then a diagnosis of female orgasmic disorder
would not be made.
Substance/medication-induced sexual dysfunction. Substance/medication use may
explain the orgasmic difficulties.
Another medical condition. If the disorder is due to another medical condition (e.g.,
multiple sclerosis, spinal cord injury), then a diagnosis of female orgasmic disorder would
not be made.
Interpersonal factors. If interpersonal or significant contextual factors, such as severe
relationship distress, intimate partner violence, or other significant stressors, are associ-
ated with the orgasmic difficulties, then a diagnosis of female orgasmic disorder would
not be made.
Other sexual dysfunctions. Female orgasmic disorder may occur in association with other
sexual dysfunctions (e.g., female sexual interest/arousal disorder). The presence of another
sexual dysfunction does not rule out a diagnosis of female orgasmic disorder. Occasional or-
gasmic difficulties that are short-term or infrequent and are not accompanied by clinically sig-
nificant distress or impairment are not diagnosed as female orgasmic disorder. A diagnosis is
also not appropriate if the problems are the result of inadequate sexual stimulation.
Comorbidity
Women with female orgasmic disorder may have co-occurring sexual interest / arousal
difficulties. Women with diagnoses of other nonsexual mental disorders, such as major de-
pressive disorder, may experience lower sexual interest/arousal, and this may indirectly
increase the likelihood of orgasmic difficulties.
Female Sexual Interest/Arousal Disorder 433
Female Sexual Interest/Arousal Disorder
Diagnostic Criteria 302.72 (F52.22)
A. Lack of, or significantly reduced, sexual interest/arousal, as manifested by at least
three of the following:
1. Absent/reduced interest in sexual activity.
2. Absent/reduced sexual/erotic thoughts or fantasies.
3. No/reduced initiation of sexual activity, and typically unreceptive to a partner’s at-
tempts to initiate.
4. Absent/reduced sexual excitement/pleasure during sexual activity in almost all or
all (approximately 75%—-100%) sexual encounters (in identified situational contexts
or, if generalized, in all contexts).
5. Absent/reduced sexual interest/arousal in response to any internal or external sex-
ual/erotic cues (e.g., written, verbal, visual).
6. Absent/reduced genital or nongenital sensations during sexual activity in almost all
or all (approximately 75%—100%) sexual encounters (in identified situational con-
texts or, if generalized, in all contexts).
B. The symptoms in Criterion A have persisted for a minimum duration of approximately
6 months.
C. The symptoms in Criterion A cause clinically significant distress in the individual.
D. The sexual dysfunction is not better explained by a nonsexuai mental disorder or as a
consequence of severe relationship distress (e.g., partner violence) or other significant
stressors and is not attributable to the effects of a substance/medication or another
medical condition.
Specify whether:
Lifelong: The disturbance has been present since the individual became sexually
active.
Acquired: The disturbance began after a period of relatively normal sexual function.
Specify whether:
Generalized: Not limited to certain types of stimulation, situations, or partners.
Situational: Only occurs with certain types of stimulation, situations, or partners.
Specify current severity:
Mild: Evidence of mild distress over the symptoms in Criterion A.
Moderate: Evidence of moderate distress over the symptoms in Criterion A.
Severe: Evidence of severe or extreme distress over the symptoms in Criterion A.
Diagnostic Features
In assessing female sexual interest/arousal disorder, interpersonal context must be taken
into account. A “desire discrepancy,” in which a woman has lower desire for sexual activ-
ity than her partner, is not sufficient to diagnose female sexual interest /arousai disorder.
In order for the criteria for the disorder to be met, there must be absence or reduced fre-
quency or intensity of at least three of six indicators (Criterion A) for a minimum duration
of approximately 6 months (Criterion B). There may be different symptom profiles across
women, as well as variability in how sexual interest and arousal are expressed. For exam-
ple, in one woman, sexual interest /arousal disorder may be expressed as a lack of interest
in sexual activity, an absence of erotic or sexual thoughts, and reluctance to initiate sexual
activity and respond to a partner’s sexual invitations. In another woman, an inability to be-
come sexually excited, to respond to sexual stimuli with sexual desire, and a correspond-
434 Sexual Dysfunctions
ing lack of signs of physical sexual arousal may be the primary features. Because sexual
desire and arousal frequently coexist and are elicited in response to adequate sexual cues,
the criteria for female sexual interest /arousal disorder take into account that difficulties in
desire and arousal often simultaneously characterize the complaints of women with this
disorder. Short-term changes in sexual interest or arousal are common and may be adaptive
responses to events ina woman’s life and do not represent a sexual dysfunction. Diagnosis
of female sexual interest /arousal disorder requires a minimum duration of symptoms of
approximately 6 months as a reflection that the symptoms must be a persistent problem.
The estimation of persistence may be determined by clinical judgment when a duration of
6 months cannot be ascertained precisely.
There may be absent or reduced frequency or intensity of interest in sexual activity (Crite-
rion Al), which was previously termed hypoactive sexual desire disorder. The frequency or inten-
sity of sexual and erotic thoughts or fantasies may be absent or reduced (Criterion A2). The
expression of fantasies varies widely across women and may include memories of past sexual
experiences. The normative decline in sexual thoughts with age should be taken into account
when this criterion is being assessed. Absence or reduced frequency of initiating sexual activ-
ity and of receptivity to a partner’s sexual invitations (Criterion A3) is a behaviorally focused
criterion. A couple's beliefs and preferences for sexual initiation patterns are highly relevant to
the assessment of this criterion. There may be absent or reduced sexual excitement or pleasure
during sexual activity in almost all or all (approximately 75%-100%) sexual encounters (Cri-
terion A4). Lack of pleasure is a common presenting clinical complaint in women with low de-
sire. Among women who report low sexual desire, there are fewer sexual or erotic cues that
elicit sexual interest or arousal (i.e., there is a lack of “responsive desire”). Assessment of the
adequacy of sexual stimuli will assist in determining if there is a difficulty with responsive sex-
ual desire (Criterion A5). Frequency or intensity of genital or nongenital sensations during sex-
ual activity may be reduced or absent (Criterion A6). This may include reduced vaginal
lubrication /vasocongestion, but because physiological measures of genital sexual response do
not differentiate women who report sexual arousal concerns from those who do not, the self-
report of reduced or absent genital or nongenital sensations is sufficient.
For a diagnosis of female sexual interest/arousal disorder to be made, clinically signif-
icant distress must accompany the symptoms in Criterion A. Distress may be experienced
as a result of the lack of sexual interest/arousal or as a result of significant interference in
a woman’s life and well-being. If a lifelong lack of sexual desire is better explained by one’s
self-identification as “asexual,” then a diagnosis of female sexual interest/arousal disor-
der would not be made.
Associated Features Supporting Diagnosis
Female sexual interest/arousal disorder is frequently associated with problems in experi-
encing orgasm, pain experienced during sexual activity, infrequent sexual activity, and
couple-level discrepancies in desire. Relationship difficulties and mood disorders are also
frequently associated features of female sexual interest/arousal disorder. Unrealistic ex-
pectations and norms regarding the “appropriate” level of sexual interest or arousal, along
with poor sexual techniques and lack of information about sexuality, may also be evident
in women diagnosed with female sexual interest/arousal disorder. The latter, as well as
normative beliefs about gender roles, are important factors to consider.
In addition to the subtypes “lifelong /acquired” and “generalized /situational,” the follow-
ing five factors must be considered during assessment and diagnosis of female sexual interest/
arousal disorder given that they may be relevant to etiology and/or treatment: 1) partner fac-
tors (e.g., partner’s sexual problems, partner's health status); 2) relationship factors (e.g., poor
communication, discrepancies in desire for sexual activity); 3) individual vulnerability factors
(e.g., poor body image, history of sexual or emotional abuse), psychiatric comorbidity (e.g., de-
pression, anxiety), or stressors (e.g., job loss, bereavement); 4) cultural /religious factors (e.g.,
inhibitions related to prohibitions against sexual activity; attitudes toward sexuality); and
Female Sexual interest/Arousal Disorder 435
5) medical factors relevant to prognosis, course, or treatment. Note that each of these factors
may contribute differently to the presenting symptoms of different women with this disorder.
Prevalence
The prevalence of female sexual interest /arousal disorder, as defined in this manual, is
unknown. The prevalence of low sexual desire and of problems with sexual arousal (with
and without associated distress), as defined by DSM-IV or ICD-10, may vary markedly in
relation to age, cultural setting, duration of symptoms, and presence of distress. Regard-
ing duration of symptoms, there are striking differences in prevalence estimates between
short-term and persistent problems related to lack of sexual interest. When distress about
sexual functioning is required, prevalence estimates are markedly lower. Some older
women report less distress about low sexual! desire than younger women, although sexual
desire may decrease with age.
Development and Course
By definition, lifelong female sexual interest/arousal disorder suggests that the lack of
sexual interest or arousal has been present for the woman’s entire sexual life. For Criteria
A3, A4, and A6, which assess functioning during sexual activity, a subtype of lifelong
would mean presence of symptoms since the individual’s first sexual experiences. The ac-
quired subtype would be assigned if the difficulties with sexual interest or arousal de-
veloped after a period of nonproblematic sexual functioning. Adaptive and normative
changes in sexual functioning may result from partner-related, interpersonal, or personal
events and may be transient in nature. However, persistence of symptoms for approxi-
mately 6 months or more would constitute a sexual dysfunction.
There are normative changes in sexual interest and arousal across the life span. Fur-
thermore, women in relationships of longer duration are more likely to report engaging in
sex despite no obvious feelings of sexual desire at the outset of a sexual encounter com-
pared with women in shorter-duration relationships. Vaginal dryness in older women is
related to age and menopausal status.
Risk and Prognostic Factors
Temperamental. Temperamental factors include negative cognitions and attitudes about
sexuality and past history of mental disorders. Differences in propensity for sexual excitation
and sexual inhibition may also predict the likelihood of developing sexual problems.
Environmental. Environmental factors include relationship difficulties, partner sexual
functioning, and developmental history, such as early relationships with caregivers and
childhood stressors.
Genetic and physiological. Some medical conditions (e.g., diabetes mellitus, thyroid
dysfunction) can be risk factors for female sexual interest /arousal disorder. There appears
to be a strong influence of genetic factors on vulnerability to sexual problems in women.
Psychophysiological research using vaginal photoplethysmography has not found differ-
ences between women with and without perceived lack of genital arousal.
Culture-Related Diagnostic Issues
There is marked variability in prevalence rates of low desire across cultures. Lower rates of
sexual desire may be more common among East Asian women compared with Euro-
Canadian women. Although the lower levels of sexual desire and arousal found in men
and women from East Asian countries compared with Euro-American groups may reflect
less interest in sex in those cultures, the possibility remains that such group differences are
an artifact of the measures used to quantify desire. A judgment about whether low sexual
436 Sexual Dysfunctions
desire reported by a woman from a certain ethnocultural group meets criteria for female
sexual interest /arousal disorder must take into account the fact that different cultures may
pathologize some behaviors and not others.
Gender-Related Diagnostic Issues
By definition, the diagnosis of female sexual interest/arousal disorder is only given to
women. Distressing difficulties with sexual desire in men would be considered under
male hypoactive sexual desire disorder.
Functional Consequences of
Female Sexual Interest/Arousal Disorder
Difficulties in sexual interest /arousal are often associated with decreased relationship sat-
isfaction.
Differential Diagnosis
Nonsexual mental disorders. Nonsexual mental disorders, such as major depressive
disorder, in which there is “markedly diminished interest or pleasure in all, or almost all,
activities most of the day, nearly every day,” may explain the lack of sexual interest /
arousal. If the lack of interest or arousal is completely attributable to another mental dis-
order, then a diagnosis of female sexual interest/arousal disorder would not be made.
Substance/medication use. Substance or medication use may explain the lack of inter-
est/arousal.
Another medical condition. If the sexual symptoms are considered to be almost exclu-
sively associated with the effects of another medical condition (e.g., diabetes mellitus, en-
dothelial disease, thyroid dysfunction, central nervous system disease), then a diagnosis
of female sexual interest /arousal disorder would not be made.
Interpersonal factors. If interpersonal or significant contextual factors, such as severe
relationship distress, intimate partner violence, or other significant stressors, explain the
sexual interest/arousal symptoms, then a diagnosis of female sexual interest /arousal dis-
order would not be made.
Other sexual dysfunctions. The presence of another sexual dysfunction does not rule
out a diagnosis of female sexual interest/arousal disorder. It is common for women to ex-
perience more than one sexual dysfunction. For example, the presence of chronic genital
pain may lead to a lack of desire for the (painful) sexual activity. Lack of interest and
arousal during sexual activity may impair orgasmic ability. For some women, all aspects
of the sexual response may be unsatisfying and distressing.
Inadequate or absent sexual stimuli. When differential diagnoses are being considered,
it is important to assess the adequacy of sexual stimuli within the woman’s sexual experi-
ence. In cases where inadequate or absent sexual stimuli are contributing to the clinical pic-
ture, there may be evidence for clinical care, but a sexual dysfunction diagnosis would not
be made. Similarly, transient and adaptive alterations in sexual functioning that are second-
ary to a significant life or personal event must be considered in the differential diagnosis.
Comorbidity
Comorbidity between sexual interest/arousal problems and other sexual difficulties is
extremely common. Sexual distress and dissatisfaction with sex life are also highly cor-
related in women with low sexual desire. Distressing low desire is associated with depres-
sion, thyroid problems, anxiety, urinary incontinence, and other medical factors. Arthritis
and inflammatory or irritable bowel disease are also associated with sexual arousal prob-
Genito-Pelvic Pain/Penetration Disorder 437
lems. Low desire appears to be comorbid with depression, sexual and physical abuse in
adulthood, global mental functioning, and use of alcohol.
Genito-Pelvic Pain/Penetration Disorder
Diagnostic Criteria 302.76 (F52.6)
A. Persistent or recurrent difficulties with one (or more) of the following:
1. Vaginal penetration during intercourse.
2. Marked vulvovaginal or pelvic pain during vaginal intercourse or penetration attempts.
3. Marked fear or anxiety about vulvovaginal or pelvic pain in anticipation of, during,
or as a result of vaginal penetration.
4. Marked tensing or tightening of the pelvic floor muscles during attempted vaginal
penetration.
B. The symptoms in Criterion A have persisted for a minimum duration of approximately
6 months.
C. The symptoms in Criterion A cause clinically significant distress in the individual.
D. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a
consequence of a severe relationship distress (e.g., partner violence) or other signifi-
cant stressors and is not attributable to the effects of a substance/medication or an-
other medical condition.
Specify whether:
Lifetong: The disturbance has been present since the individual became sexually active.
Acquired: The disturbance began after a period of relatively normal sexual function.
Specify current severity:
Mild: Evidence of mild distress over the symptoms in Criterion A.
Moderate: Evidence of moderate distress over the symptoms in Criterion A.
Severe: Evidence of severe or extreme distress over the symptoms in Criterion A.
Diagnostic Features
Genito-pelvic pain/ penetration disorder refers to four commonly comorbid symptom di-
mensions: 1) difficulty having intercourse, 2) genito-pelvic pain, 3) fear of pain or vaginal
penetration, and 4) tension of the pelvic floor muscles (Criterion A). Because major diffi-
culty in any one of these symptom dimensions is often sufficient to cause clinically sig-
nificant distress, a diagnosis can be made on the basis of marked difficulty in only one
symptom dimension. However, all four symptom dimensions should be assessed even if a
diagnosis can be made on the basis of only one symptom dimension.
Marked difficulty having vaginal intercourse/penetration (Criterion Al) can vary from a total in-
ability to experience vaginal penetration in any situation (e.g., intercourse, gynecological ex-
aminations, tampon insertion) to the ability to easily experience penetration in one situation
and but not in another. Although the most common clinical situation is when a woman is un-
able to experience intercourse or penetration with a partner, difficulties in undergoing re-
quired gynecological examinations may also be present. Marked vulvovaginal or pelvic pain
during vaginal intercourse or penetration attempts (Criterion A2) refers to pain occurring in differ-
ent locations in the genito-pelvic area. Location of pain as well as intensity should be assessed.
Typically, pain can be characterized as superficial (vulvovaginal or occurring during penetra-
tion) or deep (pelvic; i.e., not felt until deeper penetration). The intensity of the pain is often not
linearly related to distress or interference with sexual intercourse or other sexual activities.
Some genito-pelvic pain only occurs when provoked (i.e., by intercourse or mechanical stim-
438 Sexual Dysfunctions
ulation); other genito-pelvic pain may be spontaneous as well as provoked. Genito-pelvic pain
can also be usefully characterized qualitatively (e.g., “burning,” “cutting,” “shooting,” “throb-
bing”). The pain may persist for a period after intercourse is completed and may also occur
during urination. Typically, the pain experienced during sexual intercourse can be reproduced
during a gynecological examination.
Marked fear or anxiety about vulvovaginal or pelvic pain either in anticipation of, or during, or
as a result of vaginal penetration (Criterion A3) is commonly reported by women who have
regularly experienced pain during sexual intercourse. This “normal” reaction may lead to
avoidance of sexual/ intimate situations. In other cases, this marked fear does not appear
to be closely related to the experience of pain but nonetheless leads to avoidance of inter-
course and vaginal penetration situations. Some have described this as similar to a phobic
reaction except that the phobic object may be vaginal penetration or the fear of pain.
Marked tensing or tightening of the pelvic floor muscles during attempted vaginal penetration
(Criterion A4) can vary from reflexive-like spasm of the pelvic floor in response to at-
tempted vaginal entry to “normal]/voluntary” muscle guarding in response to the antici-
pated or the repeated experience of pain or to fear or anxiety. In the case of “normal /
guarding” reactions, penetration may be possible under circumstances of relaxation. The
characterization and assessment of pelvic floor dysfunction is often best undertaken by a
specialist gynecologist or by a pelvic floor physical therapist.
Associated Features Supporting Diagnosis
Genito-pelvic pain / penetration disorder is frequently associated with other sexual dysfunc-
tions, particularly reduced sexual desire and interest (female sexual interest/arousal disor-
der). Sometimes desire and interest are preserved in sexual situations that are not painful or
do not require penetration. Even when individuals with genito-pelvic pain/ penetration dis-
order report sexual interest/motivation, there is often behavioral avoidance of sexual situ-
ations and opportunities. Avoidance of gynecological examinations despite medical
recommendations is also frequent. The pattern of avoidance is similar to that seen in phobic
disorders. It is common for women who have not succeeded in having sexual intercourse to
come for treatment only when they wish to conceive. Many women with genito-pelvic pain/
penetration disorder will experience associated relationship / marital problems; they also of-
ten report that the symptoms significantly diminish their feelings of femininity.
In addition to the subtype “lifelong/acquired,” five factors should be considered dur-
ing assessment and diagnosis of genito-pelvic pain/ penetration disorder because they
may be relevant to etiology and/or treatment: 1) partner factors (e.g., partner’s sexual
problems, partner’s health status); 2) relationship factors (e.g., poor communication, dis-
crepancies in desire for sexual activity); 3) individual vulnerability factors (e.g., poor body
image, history of sexual or emotional abuse), psychiatric comorbidity (e.g., depression,
anxiety), or stressors (e.g., job loss, bereavement); 4) cultural/religious factors (e.g., inhi-
bitions related to prohibitions against sexual activity; attitudes toward sexuality); and
5) medical factors relevant to prognosis, course, or treatment. Each of these factors may
contribute differently to the presenting symptoms of different women with this disorder.
There are no valid physiological measures of any of the component symptom dimen-
sions of genito-pelvic pain/penetration disorder. Validated psychometric inventories may
be used to formally assess the pain and anxiety components related to genito-pelvic pain/
penetration disorder.
Prevalence
The prevalence of genito-pelvic pain/ penetration disorder is unknown. However, approx-
imately 15% of women in North America report recurrent pain during intercourse. Diffi-
culties having intercourse appear to be a frequent referral to sexual dysfunction clinics and
to specialist clinicians.
Genito-Pelvic Pain/Penetration Disorder 439
Development and Course
The development and course of genito-pelvic pain/ penetration disorder is unclear. Because
women generally do not seek treatment until they experience problems in sexual functioning,
it can, in general, be difficult to characterize genito-pelvic pain/ penetration disorder as life-
long (primary) or acquired (secondary). Although women typically come to clinical atten-
tion after the initiation of sexual activity, there are often earlier clinical signs. For example,
difficulty with or the avoidance of use of tampons is an important predictor of later problems.
Difficulties with vaginal penetration (inability or fear or pain) may not be obvious until sex-
ual intercourse is attempted. Even once intercourse is attempted, the frequency of attempts
may not be significant or regular. In cases where it is difficult to establish whether symptom-
atology is lifelong or acquired, it is useful to determine the presence of any consistent period
of successful pain-, fear-, and tension-free intercourse. If the experience of such a period can
be established, then genito-pelvic pain/ penetration disorder can be characterized as ac-
quired. Once symptomatology is well established for a period of approximately 6 months,
the probability of spontaneous and significant symptomatic remission appears to diminish.
Complaints related to genito-pelvic pain peak during early adulthood and in the peri-
and postmenopausal period. Women with complaints about difficulty having intercourse
appear to be primarily premenopausal. There may also be an increase in genito-pelvic
pain-related symptoms in the postpartum period.
Risk and Prognostic Factors
Environmental. Sexual and/or physical abuse have often been cited as predictors of the
DSM-IV-defined sexual pain disorders dyspareunia and vaginismus. This is a matter of con-
troversy in the current literature.
Genetic and physiological. Women experiencing superficial pain during sexual inter-
course often report the onset of the pain after a history of vaginal infections. Even after the in-
fections have resolved and there are no known residual physical findings, the pain persists.
Pain during tampon insertion or the inability to insert tampons before any sexual contact has
been attempted is an important risk factor for genito-pelvic pain/ penetration disorder.
Culture-Related Diagnostic Issues
In the past, inadequate sexual education and religious orthodoxy have often been consid-
ered to be culturally related predisposing factors to the DSM-IV diagnosis of vaginismus.
This perception appears to be confirmed by recent reports from Turkey, a primarily Mus-
lim country, indicating a strikingly high prevalence for the disorder. However, most avail-
able research, although limited in scope, does not support this notion (Lahaie et al. 2010).
Gender-Related Diagnostic Issues
By definition, the diagnosis of genito-pelvic pain/penetration disorder is only given to
women. There is relatively new research concerning urological chronic pelvic pain syn-
drome in men, suggesting that men may experience some similar problems. The research
and clinical experience are not sufficiently developed yet to justify the application of this
diagnosis to men. Other specified sexual dysfunction or unspecified sexual dysfunction
may be diagnosed in men appearing to fit this pattern.
Functional Consequences of
Genito-Pelvic Pain/Penetration Disorder
Functional difficulties in genito-pelvic pain/ penetration disorder are often associated
with interference in relationship satisfaction and sometimes with the ability to conceive
via penile/ vaginal intercourse.
440 Sexual Dysfunctions
Differential Diagnosis
Another medical condition. In many instances, women with genito-pelvic pain/pene-
tration disorder will also be diagnosed with another medical condition (e.g., lichen scle-
rosus, endometriosis, pelvic inflammatory disease, vulvovaginal atrophy). In some cases,
treating the medical condition may alleviate the genito-pelvic pain/ penetration disorder.
Much of the time, this is not the case. There are no reliable tools or diagnostic methods to
allow clinicians to know whether the medical condition or genito-pelvic pain/penetration
disorder is primary. Often, the associated medical conditions are difficult to diagnose and
treat. For example, the increased incidence of postmenopausal pain during intercourse
may sometimes be attributable to vaginal dryness or vulvovaginal atrophy associated with
declining estrogen levels. The relationship, however, between vulvovaginal atrophy /dry-
ness, estrogen, and pain is not well understood.
Somatic symptom and related disorders. Some women with genito-pelvic pain /pene-
tration disorder may also be diagnosable with somatic symptom disorder. Since both
genito-pelvic pain/ penetration disorder and the somatic symptom and related disorders
are new diagnoses, it is not yet clear whether they can be reliably differentiated. Some
women diagnosed with genito-pelvic pain/ penetration disorder will also be diagnosed
with a specific phobia.
Inadequate sexual stimuli. It is important that the clinician, in considering differential diag-
noses, assess the adequacy of sexual stimuli within the woman’s sexual experience. Sexual sit-
uations in which there is inadequate foreplay or arousal may lead to difficulties in penetration,
pain, or avoidance. Erectile dysfunction or premature ejaculation in the male partner may
result in difficulties with penetration. These conditions should be carefully assessed. In some
situations, a diagnosis of genito-pelvic pain/ penetration disorder may not be appropriate.
Comorbidity
Comorbidity between genito-pelvic pain/ penetration disorder and other sexual difficul-
ties appears to be common. Comorbidity with relationship distress is also common. This is
not surprising, since in Western cultures the inability to have (pain-free) intercourse with
a desired partner and the avoidance of sexual opportunities may be either a contributing
factor to or the result of other sexual or relationship problems. Because pelvic floor symp-
toms are implicated in the diagnosis of genito-pelvic pain/ penetration disorder, there is
likely to be a higher prevalence of other disorders related to the pelvic floor or reproduc-
tive organs (e.g., interstitial cystitis, constipation, vaginal infection, endometriosis, irrita-
ble bowel syndrome).
Male Hypoactive Sexual Desire Disorder
Diagnostic Criteria 302.71 (F52.0)
A. Persistently or recurrently deficient (or absent) sexual/erotic thoughts or fantasies and
desire for sexual activity. The judgment of deficiency is made by the clinician, taking
into account factors that affect sexual functioning, such as age and general and socio-
cultural contexts of the individuals life.
B. The symptoms in Criterion A have persisted for a minimum duration of approximately
6 months.
C. The symptoms in Criterion A cause clinically significant distress in the individual.
D. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a
consequence of severe relationship distress or other significant stressors and is not at-
tributable to thes effects of a substance/medication or another medical condition.
Male Hypoactive Sexual Desire Disorder 441
Specify whether:
Lifelong: The disturbance has been present since the individual became sexually
active.
Acquired: The disturbance began after a period of relatively normal sexual function.
Specify whether:
Generalized: Not limited to certain types of stimulation, situations, or partners.
Situational: Only occurs with certain types of stimulation, situations, or partners.
Specify current severity:
Mild: Evidence of mild distress over the symptoms in Criterion A.
Moderate: Evidence of moderate distress over the symptoms in Criterion A.
Severe: Evidence of severe or extreme distress over the symptoms in Criterion A.
Diagnostic Features
When an assessment for male hypoactive sexual desire disorder is being made, inter-
personal context must be taken into account. A “desire discrepancy,” in which a man has
lower desire for sexual activity than his partner, is not sufficient to diagnose male hypo-
active sexual desire disorder. Both low/absent desire for sex and deficient/absent sexual
thoughts or fantasies are required for a diagnosis of the disorder. There may be variation
across men in how sexual desire is expressed.
The lack of desire for sex and deficient/absent erotic thoughts or fantasies must be per-
sistent or recurrent and must occur for a minimum duration of approximately 6 months.
The inclusion of this duration criterion is meant to safeguard against making a diagnosis in
cases in which a man’s low sexual desire may represent an adaptive response to adverse
life conditions (e.g., concern about a partner’s pregnancy when the man is considering ter-
minating the relationship). The introduction of “approximately” in Criterion B allows for
clinician judgment in cases in which symptom duration does not meet the recommended
6-month threshold.
Associated Features Supporting Diagnosis
Male hypoactive sexual desire disorder is sometimes associated with erectile and/or ejac-
ulatory concerns. For example, persistent difficulties obtaining an erection may lead a man
to lose interest in sexual activity. Men with hypoactive sexual desire disorder often report
that they no longer initiate sexual activity and that they are minimally receptive to a part-
ner’s attempt to initiate. Sexual activities (e.g., masturbation or partnered sexual activity)
may sometimes occur even in the presence of low sexual desire. Relationship-specific pref-
erences regarding patterns of sexual initiation must be taken into account when making a
diagnosis of male hypoactive sexual desire disorder. Although men are more likely to ini-
tiate sexual activity, and thus low desire may be characterized by a pattern of non-initiation,
many men may prefer to have their partner initiate sexual activity. In such situations, the
man’s lack of receptivity to a partner's initiation should be considered when evaluating low
desire.
In addition to the subtypes “lifelong /acquired” and “generalized /situational,” the fol-
lowing five factors must be considered during assessment and diagnosis of male hypo-
active sexual desire disorder given that they may be relevant to etiology and/or treatment:
1) partner factors (e.g., partner’s sexual problems, partner’s health status); 2) relationship
factors (e.g., poor communication, discrepancies in desire for sexual activity); 3) individ-
ual vulnerability factors (e.g., poor body image, history of sexual or emotional abuse), psy-
chiatric comorbidity (e.g., depression, anxiety), or stressors (e.g., job loss, bereavement);
4) cultural/ religious factors (e.g., inhibitions related to prohibitions against sexual activity;
attitudes toward sexuality); and 5) medical factors relevant to prognosis, course, or treat-
442 Sexual Dysfunctions
ment. Each of these factors may contribute differently to the presenting symptoms of dif-
ferent men with this disorder.
Prevalence
The prevalence of male hypoactive sexual desire disorder varies depending on country of
origin and method of assessment. Approximately 6% of younger men (ages 18-24 years)
and 41% of older men (ages 66-74 years) have problems with sexual desire. However, a
persistent lack of interest in sex, lasting 6 months or more, affects only a small proportion
of men ages 16-44 (1.8%).
Development and Course
By definition, lifelong male hypoactive sexual desire disorder indicates that low or no sex-
ual desire has always been present, whereas the acquired subtype would be assigned if the
man’s low desire developed after a period of normal sexual desire. There is a requirement
that low desire persist for approximately 6 months or more; thus, short-term changes in
sexual desire should not be diagnosed as male hypoactive sexual desire disorder.
There is a normative age-related decline in sexual desire. Like women, men identify a
variety of triggers for their sexual desire, and they describe a wide range of reasons that
they choose to engage in sexual activity. Although erotic visual cues may be more potent
elicitors of desire in younger men, the potency of sexual cues may decrease with age and
must be considered when evaluating men for hypoactive sexual desire disorder.
Risk and Prognostic Factors
Temperamental. Mood and anxiety symptoms appear to be strong predictors of low de-
sire in men. Up to half of men with a past history of psychiatric symptoms may have mod-
erate or severe loss of desire, compared with only 15% of those without such a history. A
man’s feelings about himself, his perception of his partner’s sexual desire toward him,
feelings of being emotionally connected, and contextual variables may all negatively (as
well as positively) affect sexual desire.
Environmental. Alcohol use may increase the occurrence of low desire. Among gay men,
self-directed homophobia, interpersonal problems, attitudes, lack of adequate sex educa-
tion, and trauma resulting from early life experiences must be taken into account in ex-
plaining the low desire. Social and cultural contextual factors should also be considered.
Genetic and physiological. Endocrine disorders such as hyperprolactinemia signifi-
cantly affect sexual desire in men. Age is a significant risk factor for low desire in men. It is
unclear whether or not men with low desire also have abnormally low levels of testoster-
one; however, among hypogonadal men, low desire is common. There also may be a crit-
ical threshold below which testosterone will affect sexual desire in men and above which
there is little effect of testosterone on men’s desire.
Culture-Related Diagnostic Issues
There is marked variability in prevalence rates of low desire across cultures, ranging from
12.5% in Northern European men to 28% in Southeast Asian men ages 40-80 years. Just as
there are higher rates of low desire among East Asian subgroups of women, men of East
Asian ancestry also have higher rates of low desire. Guilt about sex may mediate this as-
sociation between East Asian ethnicity and sexual desire in men.
Gender-Related Diagnostic Issues
In contrast to the classification of sexual disorders in women, desire and arousal disorders
have been retained as separate constructs in men. Despite some similarities in the experi-
Premature (Early) Ejaculation 443
ence of desire across men and women, and the fact that desire fluctuates over time and is
dependent on contextual factors, men do report a significantly higher intensity and fre-
quency of sexual desire compared with women.
Differential Diagnosis
Nonsexual mental disorders. Nonsexual mental disorders, such as major depressive
disorder, which is characterized by “markedly diminished interest or pleasure in all, or al-
most all, activities,” may explain the lack of sexual desire. If the lack of desire is better
explained by another mental disorder, then a diagnosis of male hypoactive sexual desire
disorder would not be made.
Substance/medication use. Substance/medication use may explain the lack of sexual
desire.
Another medical condition. _ If the low/absent desire and deficient/ absent erotic thoughts
or fantasies are better explained by the effects of another medical condition (e.g., hypogo-
nadism, diabetes mellitus, thyroid dysfunction, central nervous system disease), then a di-
agnosis of male hypoactive sexual desire disorder would not be made.
Interpersonal factors. If interpersonal or significant contextual factors, such as severe
relationship distress or other significant stressors, are associated with the loss of desire in
the man, then a diagnosis of male hypoactive sexual desire disorder would not be made.
Other sexual dysfunctions. The presence of another sexual dysfunction does not rule out a
diagnosis of male hypoactive sexual desire disorder; there is some evidence that up to one-half
of men with low sexual desire also have erectile difficulties, and slightly fewer may also have
early ejaculation difficulties. If the man’s low desire is explained by self-identification as an
asexual, then a diagnosis of male hypoactive sexual desire disorder is not made.
Comorbidity
Depression and other mental disorders, as well as endocrinological factors, are often co-
morbid with male hypoactive sexual desire disorder.
Premature (Early) Ejaculation
Diagnostic Criteria 302.75 (F52.4)
A. Apersistent or recurrent pattern of ejacuiation occurring during partnered sexuai activ-
ity within approximately 1 minute foliowing vaginal penetration and before the individ-
ual wishes it.
Note: Although the diagnosis of premature (early) ejaculation may be applied to indi-
viduais engaged in nonvaginal sexual activities, specific duration criteria have not been
established for these activities.
B. The symptom in Criterion A must have been present for at least 6 months and must be
experienced on almost all or all (approximately 75%—-100%) occasions of sexual activ-
ity (in identified situational contexts or, if generalized, in all contexts).
C. The symptom in Criterion A causes Clinically significant distress in the individual.
D. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a
consequence of severe relationship distress or other significant stressors and is not at-
tributable to the effects of a substance/medication or another medical condition.
Specify whether:
Lifelong: The disturbance has been present since the individual became sexually active.
Acquired: The disturbance began after a period of relatively normal sexual function.
444 Sexual Dysfunctions
Specify whether:
Generalized: Not limited to certain types of stimulation, situations, or partners.
Situational: Only occurs with certain types of stimulation, situations, or partners.
Specify current severity:
Mild: Ejaculation occurring within approximately 30 seconds to 1 minute of vaginal
penetration.
Moderate: Ejaculation occurring within approximately 15~30 seconds of vaginal pen-
etration.
Severe: Ejaculation occurring prior to sexual activity, at the start of sexual activity, or
within approximately 15 seconds of vaginal penetration.
Diagnostic Features
Premature (early) ejaculation is manifested by ejaculation that occurs prior to or shortly af-
ter vaginal penetration, operationalized by an individual's estimate of ejaculatory latency
(i.e., elapsed time before ejaculation) after vaginal penetration. Estimated and measured
intravaginal ejaculatory latencies are highly correlated as long as the ejaculatory latency is
of short duration; therefore, self-reported estimates of ejaculatory latency are sufficient for
diagnostic purposes. A 60-second intravaginal ejaculatory latency time is an appropriate
cutoff for the diagnosis of lifelong premature (early) ejaculation in heterosexual men.
There are insufficient data to determine if this duration criterion can be applied to ac-
quired premature (early) ejaculation. The durational definition may apply to males of
varying sexual orientations, since ejaculatory latencies appear to be similar across men of
different sexual orientations and across different sexual activities.
Associated Features Supporting Diagnosis
Many males with premature (early) ejaculation complain of a sense of lack of control over
ejaculation and report apprehension about their anticipated inability to delay ejaculation
on future sexual encounters.
The following factors may be relevant in the evaluation of any sexual dysfunction:
1) partner factors (e.g., partner’s sexual problems, partner's health status); 2) relationship fac-
tors (e.g., poor communication, discrepancies in desire for sexual activity); 3) individual
vulnerability factors (e.g., poor body image, history of sexual or emotional abuse), psychiatric
comorbidity (e.g., depression, anxiety), and stressors (e.g., job loss, bereavement); 4) cultural /
religious factors (e.g., inhibitions related to prohibitions against sexual activity; attitudes
toward sexuality); and 5) medical factors relevant to prognosis, course, or treatment.
Prevaience
Estimates of the prevalence of premature (early) ejaculation vary widely depending on the
definition utilized. Internationally, more than 20%-30% of men ages 18-70 years report
concern about how rapidly they ejaculate. With the new definition of premature (early)
ejaculation (i.e., ejaculation occurring within approximately 1 minute of vaginal penetra-
tion), only 1%-3% of men would be diagnosed with the disorder. Prevalence of premature
(early) ejaculation may increase with age.
Deveiopment and Course
By definition, lifelong premature (early) ejaculation starts during a male’s initial sexual ex-
periences and persists thereafter. Some men may experience premature (early) ejaculation
during their initial sexual encounters but gain ejaculatory control over time. It is the persis-
tence of ejaculatory problems for longer than 6 months that determines the diagnosis of pre-
mature (early) ejaculation. In contrast, some men develop the disorder after a period of
Premature (Early) Ejaculation 445
having a normal ejaculatory latency, known as acquired premature (early) ejaculation. There is
far less known about acquired premature (early) ejaculation than about lifelong premature
(early) ejaculation. The acquired form likely has a later onset, usually appearing during or af-
ter the fourth decade of life. Lifelong is relatively stable throughout life. Little is known about
the course of acquired premature (early) ejaculation. Reversal of medical conditions such as
hyperthyroidism and prostatitis appears to restore ejaculatory latencies to baseline values.
Lifelong premature (early) ejaculation begins with early sexual experiences and persists
throughout an individual’s life. In approximately 20% of men with premature (early) ejacu-
lation, ejaculatory latencies decrease further with age. Age and relationship length have been
found to be negatively associated with prevalence of premature (early) ejaculation.
Risk and Prognostic Factors
Temperamental. Premature (early) ejaculation may be more common in men with anx-
iety disorders, especially social anxiety disorder (social phobia).
Genetic and physiological. There is a moderate genetic contribution to lifelong prema-
ture (early) ejaculation. Premature (early) ejaculation may be associated with dopamine
transporter gene polymorphism or serotonin transporter gene polymorphism. Thyroid
disease, prostatitis, and drug withdrawal are associated with acquired premature (early)
ejaculation. Positron emission tomography measures of regional cerebral blood flow dur-
ing ejaculation have shown primary activation in the mesocephalic transition zone, includ-
ing the ventral tegmental area.
Culture-Related Diagnostic Issues
Perception of what constitutes a normal ejaculatory latency is different in many cultures.
Measured ejaculatory latencies may differ in some countries. Such differences may be ex-
plained by cultural or religious factors as well as genetic differences between populations.
Gender-Reiated Diagnostic Issues
Premature (early) ejaculation is a sexual disorder in males. Males and their sexual partners
may differ in their perception of what constitutes an acceptable ejaculatory latency. There
may be increasing concerns in females about early ejaculation in their sexual partners,
which may be a reflection of changing societal attitudes concerning female sexual activity.
Diagnostic Markers
Ejaculatory latency is usually monitored in research settings by the sexual partner utilizing
a timing device (e.g., stopwatch), though this is not ideal in real-life sexual] situations. For
vaginal intercourse, the time between intravaginal penetration and ejaculation is measured.
Functional Consequences of
Premature (Eariy) Ejaculation
A pattern of premature (early) ejaculation may be associated with decreased self-esteem, a
sense of lack of control, and adverse consequences for partner relationships. It may also
cause personal distress in the sexual partner and decreased sexual satisfaction in the sexual
partner. Ejaculation prior to penetration may be associated with difficulties in conception.
Differential Diagnosis
Substance/medication-induced sexual dysfunction. When problems with premature
ejaculation are due exclusively to substance use, intoxication, or withdrawal, substance /
medication-induced sexual dysfunction should be diagnosed.
446 Sexual Dysfunctions
Ejaculatory concerns that do not meet diagnostic criteria. It is necessary to identify
males with normal ejaculatory latencies who desire longer ejaculatory latencies and males
who have episodic premature (early) ejaculation (e.g., during the first sexual encounter
with anew partner when a short ejaculatory latency may be common or normative). Neither
of these situations would lead to a diagnosis of premature (early) ejaculation, even though
these situations may be distressing to some males.
Comorbidity
Premature (early) ejaculation may be associated with erectile problems. In many cases, it
may be difficult to determine which difficulty preceded the other. Lifelong premature
(early) ejaculation may be associated with certain anxiety disorders. Acquired premature
(early) ejaculation may be associated with prostatitis, thyroid disease, or drug withdrawal
(e.g., during opioid withdrawal).
Substance/Medication-induced
Sexual Dysfunction
Diagnostic Criteria
A. Actlinically significant disturbance in sexual function is predominant in the clinical picture.
B. There is evidence from the history, physical examination, or laboratory findings of both
(1) and (2):
1. The symptoms in Criterion A developed during or soon after substance intoxication
or withdrawal or after exposure to a medication.
2. The involved substance/medication is capable of producing the symptoms in Crite-
rion A.
C. The disturbance is not better explained by a sexual dysfunction that is not substance/
medication-induced. Such evidence of an independent sexual dysfunction could in-
clude the following:
The symptoms precede the onset of the substance/medication use; the symptoms
persist for a substantial period of time (e.g., about 1 month) after the cessation of
acute withdrawal or severe intoxication; or there is other evidence suggesting the
existence of an independent non-substance/medication-induced sexual dysfunc-
tion (e.g., a history of recurrent non-substance/medication-related episodes).
D. The disturbance does not occur exclusively during the course of a delirium.
E. The disturbance causes clinically significant distress in the individual.
Note: This diagnosis should be made instead of a diagnosis of substance intoxication or
substance withdrawal only when the symptoms in Criterion A predominate in the clinical
picture and are sufficiently severe to warrant clinical attention.
Coding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance/medica-
tion]-induced sexual dysfunctions are indicated in the table below. Note that the ICD-10-CM
code depends on whether or not there is a comorbid substance use disorder present for the
same class of substance. If a mild substance use disorder is comorbid with the substance-
induced sexual dysfunction, the 4th position character is “1,” and the clinician should record
“mild [substance] use disorder’ before the substance-induced sexual dysfunction (e.g., “mild
cocaine use disorder with cocaine-induced sexual dysfunction”). If a moderate or severe
substance use disorder is comorbid with the substance-induced sexual dysfunction, the 4th
position character is “2,” and the clinician should record “moderate [substance] use disorder’
or “severe [substance] use disorder,” depending on the severity of the comorbid substance
Substance/Medication-Induced Sexual Dysfunction 447
use disorder. If there is no comorbid substance use disorder (e.g., after a one-time heavy
use of the substance), then the 4th position character is “9,” and the clinician should record
only the substance-induced sexual dysfunction.
ICD-10-CM
With use
With use disorder, Without
disorder, moderate use
ICD-9-CM mild or severe disorder
Alcohol 291.89 F10.181 F10.281 F10.981
Opioid 292.89 F11.181 F11.281 F11.981
Sedative, hypnotic, or 292.89 F13.181 F13.281 F13.981
anxiolytic
Amphetamine (or other 292.89 F15.181 F15.281 F15.981
stimulant)
Cocaine 292.89 F14.181 F14.281 F14.981
Other (or unknown) substance 292.89 F19.181 F19.281 F19.981
Specify if (see Table 1 in the chapter “Substance-Related and Addictive Disorders” for di-
agnoses associated with substance class):
With onset during intoxication: If the criteria are met for intoxication with the sub-
stance and the symptoms develop during intoxication.
With onset during withdrawal: If criteria are met for withdrawal from the substance
and the symptoms develop during, or shortly after, withdrawal.
With onset after medication use: Symptoms may appear either at initiation of medi-
cation or after a modification or change in use.
Specify current severity:
Mild: Occurs on 25%—50% of occasions of sexual activity.
Moderate: Occurs on 50%—-75% of occasions of sexual activity.
Severe: Occurs on 75% or more of occasions of sexual activity.
Recording Procedures
ICD-9-CM. The name of the substance/medication-induced sexual dysfunction begins
with the specific substance (e.g., alcohol, fluoxetine) that is presumed to be causing the
sexual dysfunction. The diagnostic code is selected from the table included in the criteria
set, which is based on the drug class. For substances that do not fit into any of the classes
(e.g., fluoxetine), the code for “other substance” should be used; and in cases in which a
substance is judged to be an etiological factor but the specific class of substance is un-
known, the category “unknown substance” should be used.
The name of the disorder is followed by the specification of onset {i.e., onset during in-
toxication, onset during withdrawal, with onset after medication use), followed by the se-
verity specifier (e.g., mild, moderate, severe). Unlike the recording procedures for ICD-10-
CM, which combine the substance-induced disorder and substance use disorder into a sin-
gle code, for ICD-9-CM a separate diagnostic code is given for the substance use disorder.
For example, in the case of erectile dysfunction occurring during intoxication in a man
with a severe alcohol use disorder, the diagnosis is 291.89 alcohol-induced sexual dysfunc-
tion, with onset during intoxication, moderate. An additional diagnosis of 303.90 severe
alcohol use disorder is also given. When more than one substance is judged to play a sig-
448 Sexual Dysfunctions
nificant role in the development of the sexual dysfunction, each should be listed separately
(e.g., 292.89 cocaine-induced sexual dysfunction with onset during intoxication, moderate;
292.89 fluoxetine-induced sexual dysfunction, with onset after medication use).
ICD-10-CM. The name of the substance/medication-induced sexual dysfunction begins
with the specific substance (e.g., alcohol, fluoxetine) that is presumed to be causing the
sexual dysfunction. The diagnostic code is selected from the table included in the criteria
set, which is based on the drug class and presence or absence of a comorbid substance use
disorder. For substances that do not fit into any of the classes (e.g., fluoxetine), the code for
“other substance” should be used; and in cases in which a substance is judged to be an eti-
ological factor but the specific class of substance is unknown, the category “unknown sub-
stance” should be used.
When recording the name of the disorder, the comorbid substance use disorder (if any)
is listed first, followed by the word “with,” followed by the name of the substance-induced
sexual dysfunction, followed by the specification of onset (i.e., onset during intoxication,
onset during withdrawal, with onset after medication use), followed by the severity spec-
ifier (e.g., mild, moderate, severe). For example, in the case of erectile dysfunction occur-
ring during intoxication in a man with a severe alcohol use disorder, the diagnosis is
F10.281 moderate alcohol use disorder with alcohol-induced sexual dysfunction, with on-
set during intoxication, moderate. A separate diagnosis of the comorbid severe alcohol use
disorder is not given. If the substance-induced sexual dysfunction occurs without a co-
morbid substance use disorder (e.g., after a one-time heavy use of the substance), no ac-
companying substance use disorder is noted (e.g., F15.981 amphetamine-induced sexual
dysfunction, with onset during intoxication). When more than one substance is judged to
play a significant role in the development of the sexual dysfunction, each should be listed
separately (e.g., F14.181 mild cocaine use disorder with cocaine-induced sexual dysfunc-
tion, with onset during intoxication, moderate; F19.981 fluoxetine-induced sexual dys-
function, with onset after medication use, moderate).
Diagnostic Features
The major feature is a disturbance in sexual function that has a temporal relationship with
substance/ medication initiation, dose increase, or substance / medication discontinuation.
Associated Features Supporting Diagnosis
Sexual dysfunctions can occur in association with intoxication with the following classes of
substances: alcohol; opioids; sedatives, hypnotics, or anxiolytics; stimulants (including co-
caine); and other (or unknown) substances. Sexual dysfunctions can occur in association
with withdrawal from the following classes of substances: alcohol; opioids; sedatives, hyp-
notics, or anxiolytics; and other (or unknown) substances. Medications that can induce sex-
ual dysfunctions include antidepressants, antipsychotics, and hormonal contraceptives.
The most commonly reported side effect of antidepressant drugs is difficulty with or-
gasm or ejaculation. Problems with desire and erection are less frequent. Approximately
30% of sexual complaints are clinically significant. Certain agents, such as bupropion and
mirtazapine, appear not to be associated with sexual side effects.
The sexual problems associated with antipsychotic drugs, including problems with
sexual desire, erection, lubrication, ejaculation, or orgasm, have occurred with typical as
well as atypical agents. However, problems are less common with prolactin-sparing anti-
psychotics than with agents that cause significant prolactin elevation.
Although the effects of mood stabilizers on sexual function are unclear, it is possible
that lithium and anticonvulsants, with the possible exception of lamotrigine, have adverse
effects on sexual desire. Problems with orgasm may occur with gabapentin. Similarly, there
may bea higher prevalence of erectile and orgasmic problems associated with benzodiaz-
epines. There have not been such reports with buspirone.
Substance/Medication-Induced Sexual Dysfunction 449
Many nonpsychiatric medications, such as cardiovascular, cytotoxic, gastrointestinal,
and hormonal agents, are associated with disturbances in sexual function. Illicit substance
use is associated with decreased sexual desire, erectile dysfunction, and difficulty reach-
ing orgasm. Sexual dysfunctions are also seen in individuals receiving methadone but are
seldom reported by patients receiving buprenorphine. Chronic alcohol abuse and chronic
nicotine abuse are associated with erectile problems.
Prevalence
The prevalence and the incidence of substance/medication-induced sexual dysfunction
are unclear, likely because of underreporting of treatment-emergent sexual side effects.
Data on substance/medication-induced sexual dysfunction typically concern the effects of
antidepressant drugs. The prevalence of antidepressant-induced sexual dysfunction var-
ies in part depending on the specific agent. Approximately 25%-80% of individuals taking
monoamine oxidase inhibitors, tricyclic antidepressants, serotonergic antidepressants,
and combined serotonergic-adrenergic antidepressants report sexual side effects. There
are differences in the incidence of sexual side effects between some serotonergic and com-
bined adrenergic-serotonergic antidepressants, although it is unclear if these differences
are clinically significant.
Approximately 50% of individuals taking antipsychotic medications will experience
adverse sexual side effects, including problems with sexual desire, erection, lubrication,
ejaculation, or orgasm. The incidence of these side effects among different antipsychotic
agents is unclear.
Exact prevalence and incidence of sexual dysfunctions among users of nonpsychiatric
medications such as cardiovascular, cytotoxic, gastrointestinal, and hormonal agents are
unknown. Elevated rates of sexual dysfunction have been reported with methadone or
high-dose opioid drugs for pain. There are increased rates of decreased sexual desire, erec-
tile dysfunction, and difficulty reaching orgasm associated with illicit substance use. The
prevalence of sexual problems appears related to chronic drug abuse and appears higher
in individuals who abuse heroin (approximately 60%—-70%) than in individuals who abuse
amphetamines or 3,4-methylenedioxymethamphetamine (i.e., MDMA, ecstasy). Elevated
rates of sexual dysfunction are also seen in individuals receiving methadone but are sel-
dom reported by patients receiving buprenorphine. Chronic alcohol abuse and chronic
nicotine abuse are related to higher rates of erectile problems.
Development and Course
The onset of antidepressant-induced sexual dysfunction may be as early as 8 days after the
agent is first taken. Approximately 30% of individuals with mild to moderate orgasm de-
lay will experience spontaneous remission of the dysfunction within 6 months. In some
cases, serotonin reuptake inhibitor—-induced sexual dysfunction may persist after the
agent is discontinued. The time to onset of sexual dysfunction after initiation of antipsy-
chotic drugs or drugs of abuse is unknown. It is probable that the adverse effects of nico-
tine and alcohol may not appear until after years of use. Premature (early) ejaculation can
sometimes occur after cessation of opioid use. There is some evidence that disturbances in
sexual function related to substance/medication use increase with age.
Culture-Related Diagnostic Issues
There may be an interaction among cultural factors, the influence of medications on sexual
functioning, and the response of the individual to those changes.
Gender-Related Diagnostic Issues
Some gender differences in sexual side effects may exist.
450 Sexual Dysfunctions
Functional Consequences of
Substance/Medication-Induced Sexual Dysfunction
Medication-induced sexual dysfunction may result in medication noncompliance.
Differential Diagnosis
Non-substance/medication-induced sexual dysfunctions. Many mental conditions, such
as depressive, bipolar, anxiety, and psychotic disorders, are associated with disturbances
of sexual function. Thus, differentiating a substance /medication-induced sexual dys-
function from a manifestation of the underlying mental disorder can be quite difficult. The
diagnosis is usually established if a close relationship between substance / medication ini-
tiation or discontinuation is observed. A clear diagnosis can be established if the problem
occurs after substance / medication initiation, dissipates with substance/medication dis-
continuation, and recurs with introduction of the same agent. Most substance/medication-in-
duced side effects occur shortly after initiation or discontinuation. Sexual side effects that
only occur after chronic use of a substance/medication may be extremely difficult to di-
agnose with certainty.
Other Specified Sexual Dysfunction
302.79 (F52.8)
This category applies to presentations in which symptoms characteristic of a sexual dys-
function that cause clinically significant distress in the individual predominate but do not
meet the full criteria for any of the disorders in the sexual dysfunctions diagnostic class.
The other specified sexual dysfunction category is used in situations in which the clinician
chooses to communicate the specific reason that the presentation does not meet the cri-
teria for any specific sexual dysfunction. This is done by recording “other specified sexual
dysfunction” followed by the specific reason (e.g., “sexual aversion”).
Unspecified Sexual Dysfunction
302.70 (F52.9)
This category applies to presentations in which symptoms characteristic of a sexual dys-
function that cause clinically significant distress in the individual predominate but do not
meet the full criteria for any of the disorders in the sexual dysfunctions diagnostic class.
The unspecified sexual dysfunction category is used in situations in which the clinician
chooses not to specify the reason that the criteria are not met for a specific sexual dys-
function, and includes presentations for which there is insufficient information to make a
more specific diagnosis.
ec A RN NA ne aH ESN oe Sees heat nm dm AS md as BIE aN,
Gender
In this Chapter, there is one overarching diagnosis of gender dysphoria, with sepa-
rate developmentally appropriate criteria sets for children and for adolescents and adults.
The area of sex and gender is highly controversial and has led to a proliferation of terms
whose meanings vary over time and within and between disciplines. An additional source
of confusion is that in English “sex” connotes both male/female and sexuality. This chapter
employs constructs and terms as they are widely used by clinicians from various disci-
plines with specialization in this area. In this chapter, sex and sexual refer to the biological
indicators of male and female (understood in the context of reproductive capacity), such
as in sex chromosomes, gonads, sex hormones, and nonambiguous internal and external
genitalia. Disorders of sex development denote conditions of inborn somatic deviations of
the reproductive tract from the norm and/or discrepancies among the biological indica-
tors of male and female. Cross-sex hormone treatment denotes the use of feminizing hor-
mones in an individual assigned male at birth based on traditional biological indicators or
the use of masculinizing hormones in an individual assigned female at birth.
The need to introduce the term gender arose with the realization that for individuals
with conflicting or ambiguous biological indicators of sex (i.e., “intersex”), the lived role in
society and/or the identification as male or female could not be uniformly associated with
or predicted from the biological indicators and, later, that some individuals develop an
identity as female or male at variance with their uniform set of classical biological indica-
tors. Thus, gender is used to denote the public (and usually legally recognized) lived role as
boy or girl, man or woman, but, in contrast to certain social constructionist theories, biolog-
ical factors are seen as contributing, in interaction with social and psychological factors, to
gender development. Gender assignment refers to the initial assignment as male or female.
This occurs usually at birth and, thereby, yields the “natal gender.” Gender-atypical refers to
somatic features or behaviors that are not typical (in a statistical sense) of individuals with
the same assigned gender in a given society and historical era; for behavior, gender-noncon-
forming is an alternative descriptive term. Gender reassignment denotes an official (and usu-
ally legal) change of gender. Gender identity is a category of social identity and refers to an
individual’s identification as male, female, or, occasionally, some category other than male
or female. Gender dysphoria as a general descriptive term refers to an individual’s affective/
cognitive discontent with the assigned gender but is more specifically defined when used
as a diagnostic category. Transgender refers to the broad spectrum of individuals who tran-
siently or persistently identify with a gender different from their natal gender. Transsexual
denotes an individual who seeks, or has undergone, a social transition from male to female
or female to male, which in many, but not all, cases also involves a somatic transition by
cross-sex hormone treatment and genital surgery (sex reassignment surgery).
Gender dysphoria refers to the distress that may accompany the incongruence between
one’s experienced or expressed gender and one’s assigned gender. Although not all indi-
viduals will experience distress as a result of such incongruence, many are distressed if the
desired physical interventions by means of hormones and/or surgery are not available.
The current term is more descriptive than the previous DSM-IV term gender identity disor-
der and focuses on dysphoria as the clinical problem, not identity per se.
451
452 Gender Dysphoria
Gender Dysphoria
Diagnostic Criteria
Gender Dysphoria in Children 302.6 (F64.2)
A. A marked incongruence between one’s experienced/expressed gender and assigned
gender, of at least 6 months’ duration, as manifested by at least six of the following
(one of which must be Criterion A1):
1. Astrong desire to be of the other gender or an insistence that one is the other gen-
der (or some alternative gender different from one’s assigned gender).
2. In boys (assigned gender), a strong preference for cross-dressing or simulating fe-
male attire; or in girls (assigned gender), a strong preference for wearing only typ-
ical masculine clothing and a strong resistance to the wearing of typical feminine
clothing.
A strong preference for cross-gender roles in make-believe play or fantasy play.
4. A strong preference for the toys, games, or activities stereotypically used or en-
gaged in by the other gender.
A strong preference for playmates of the other gender.
6. In boys (assigned gender), a strong rejection of typically masculine toys, games,
and activities and a strong avoidance of rough-and-tumble play; or in girls (as-
signed gender), a strong rejection of typically feminine toys, games, and activities.
7. Astrong dislike of one’s sexual anatomy.
8. A strong desire for the primary and/or secondary sex characteristics that match
one’s experienced gender.
B. The condition is associated with clinically significant distress or impairment in social,
school, or other important areas of functioning.
Specify if:
With a disorder of sex development (e.g., a congenital adrenogenital disorder such
as 255.2 [E25.0} congenital adrenal hyperplasia or 259.50 [E34.50] androgen insensi-
tivity syndrome).
Coding note: Code the disorder of sex development as well as gender dysphoria.
Gender Dysphoria in Adolescents and Adults 302.85 (F64.1)
A. A marked incongruence between one’s experienced/expressed gender and assigned
gender, of at least 6 months’ duration, as manifested by at least two of the following:
1. A marked incongruence between one’s experienced/expressed gender and pri-
mary and/or secondary sex characteristics (or in young adolescents, the antici-
pated secondary sex characteristics).
2. A strong desire to be rid of one’s primary and/or secondary sex characteristics be-
cause of a marked incongruence with one’s experienced/expressed gender (or in
young adolescents, a desire to prevent the development of the anticipated second-
ary sex characteristics).
3. A strong desire for the primary and/or secondary sex characteristics of the other
gender.
4. Astrong desire to be of the other gender (or some alternative gender different from
one’s assigned gender).
5. A strong desire to be treated as the other gender (or some alternative gender dif-
ferent from one’s assigned gender).
6. Astrong conviction that one has the typical feelings and reactions of the other gen-
der (or some alternative gender different from one’s assigned gender).
”
gn
Gender Dysphoria 453
B. The condition is associated with clinically significant distress or impairment in sociat,
occupational, or other important areas of functioning.
Specify if:
With a disorder of sex development (e.g., a congenital adrenogenital disorder such
as 255.2 [E25.0] congenital adrenal hyperplasia or 259.50 [E34.50] androgen insensi-
tivity syndrome).
Coding note: Code the disorder of sex development as well as gender dysphoria.
Specify if:
Posttransition: The individual has transitioned to full-time living in the desired gender
(with or without legalization of gender change) and has undergone (or is preparing to
have) at least one cross-sex medical procedure or treatment regimen—namely, regu-
lar cross-sex hormone treatment or gender reassignment surgery confirming the desired
gender (e.g., penectomy, vaginoplasty in a natal male; mastectomy or phatloptasty in
a natal female).
Specifiers
The posttransition specifier may be used in the context of continuing treatment procedures
that serve to support the new gender assignment.
Diagnostic Features
Individuals with gender dysphoria have a marked incongruence between the gender they
have been assigned to (usually at birth, referred to as natal gender) and their experienced /
expressed gender. This discrepancy is the core component of the diagnosis. There must
also be evidence of distress about this incongruence. Experienced gender may include al-
ternative gender identities beyond binary stereotypes. Consequently, the distress is not
limited to a desire to simply be of the other gender, but may include a desire to be of an al-
ternative gender, provided that it differs from the individual's assigned gender.
Gender dysphoria manifests itself differently in different age groups. Prepubertal natal
girls with gender dysphoria may express the wish to be a boy, assert they are a boy, or as-
sert they will grow up to be a man. They prefer boys’ clothing and hairstyles, are often
perceived by strangers as boys, and may ask to be called by a boy’s name. Usually, they dis-
play intense negative reactions to parental attempts to have them wear dresses or other
feminine attire. Some may refuse to attend school or social events where such clothes are
required. These girls may demonstrate marked cross-gender identification in role-playing,
dreams, and fantasies. Contact sports, rough-and-tumble play, traditional boyhood games,
and boys as playmates are most often preferred. They show little interest in stereotypically
feminine toys (e.g., dolls) or activities (e.g., feminine dress-up or role-play). Occasionally,
they refuse to urinate in a sitting position. Some natal girls may express a desire to have a
penis or claim to have a penis or that they will grow one when older. They may also state that
they do not want to develop breasts or menstruate.
Prepubertal natal boys with gender dysphoria may express the wish to be a girl or as-
sert they are a gir] or that they will grow up to be a woman. They have a preference for
dressing in girls’ or women’s clothes or may improvise clothing from available materials
(e.g., using towels, aprons, and scarves for long hair or skirts). These children may role-
play female figures (e.g., playing “mother”) and often are intensely interested in female
fantasy figures. Traditional feminine activities, stereotypical games, and pastimes (e.g.,
“playing house’; drawing feminine pictures; watching television or videos of favorite fe-
male characters) are most often preferred. Stereotypical female-type dolls (e.g., Barbie) are
often favorite toys, and girls are their preferred playmates. They avoid rough-and-tumble
play and competitive sports and have little interest in stereotypically masculine toys (e.g.,
cars, trucks). Some may pretend not to have a penis and insist on sitting to urinate. More
454 Gender Dysphoria
rarely, they may state that they find their penis or testes disgusting, that they wish them re-
moved, or that they have, or wish to have, a vagina.
In young adolescents with gender dysphoria, clinical features may resemble those of
children or adults with the condition, depending on developmental level. As secondary
sex characteristics of young adolescents are not yet fully developed, these individuals may
not state dislike of them, but they are concerned about imminent physical changes.
In adults with gender dysphoria, the discrepancy between experienced gender and
physical sex characteristics is often, but not always, accompanied by a desire to be rid of
primary and/or secondary sex characteristics and/or a strong desire to acquire some pri-
mary and/or secondary sex characteristics of the other gender. To varying degrees, adults
with gender dysphoria may adopt the behavior, clothing, and mannerisms of the experi-
enced gender. They feel uncomfortable being regarded by others, or functioning in soci-
ety, as members of their assigned gender. Some adults may have a strong desire to be of a
different gender and treated as such, and they may have an inner certainty to feel and re-
spond as the experienced gender without seeking medical treatment to alter body char-
acteristics. They may find other ways to resolve the incongruence between experienced /
expressed and assigned gender by partially living in the desired role or by adopting a gen-
der role neither conventionally male nor conventionally female.
Associated Features Supporting Diagnosis
When visible signs of puberty develop, natal boys may shave their legs at the first signs of
hair growth. They sometimes bind their genitals to make erections less visible. Girls may
bind their breasts, walk with a stoop, or use loose sweaters to make breasts less visible. In-
creasingly, adolescents request, or may obtain without medical prescription and supervi-
sion, hormonal suppressors (“blockers”) of gonadal steroids (e.g., gonadotropin-releasing
hormone [GnRH] analog, spironolactone). Clinically referred adolescents often want hor-
mone treatment and many also wish for gender reassignment surgery. Adolescents living in
an accepting environment may openly express the desire to be and be treated as the experi-
enced gender and dress partly or completely as the experienced gender, have a hairstyle typ-
ical of the experienced gender, preferentially seek friendships with peers of the other gender,
and/or adopt a new first name consistent with the experienced gender. Older adolescents,
when sexually active, usually do not show or allow partners to touch their sexual organs. For
adults with an aversion toward their genitals, sexual activity is constrained by the preference
that their genitals not be seen or touched by their partners. Some adults may seek hormone
treatment (sometimes without medical prescription and supervision) and gender reassign-
ment surgery. Others are satisfied with either hormone treatment or surgery alone.
Adolescents and adults with gender dysphoria before gender reassignment are at in-
creased risk for suicidal ideation, suicide attempts, and suicides. After gender reassign-
ment, adjustment may vary, and suicide risk may persist.
Prevaience
For natal adult males, prevalence ranges from 0.005% to 0.014%, and for natal females,
from 0.002% to 0.003%. Since not all adults seeking hormone treatment and surgical reas-
signment attend specialty clinics, these rates are likely modest underestimates. Sex differ-
ences in rate of referrals to specialty clinics vary by age group. In children, sex ratios of
natal boys to girls range from 2:1 to 4.5:1. In adolescents, the sex ratio is close to parity; in
adults, the sex ratio favors natal males, with ratios ranging from 1:1 to 6.1:1. In two coun-
tries, the sex ratio appears to favor natal females (Japan: 2.2:1; Poland: 3.4:1).
Development and Course
Because expression of gender dysphoria varies with age, there are separate criteria sets for
children versus adolescents and adults. Criteria for children are defined in a more con-
Gender Dysphoria 455
crete, behavioral manner than those for adolescents and adults. Many of the core criteria
draw on well-documented behavioral gender differences between typically developing
boys and girls. Young children are less likely than older children, adolescents, and adults
to express extreme and persistent anatomic dysphoria. In adolescents and adults, incon-
gruence between experienced gender and somatic sex is a central feature of the diagnosis.
Factors related to distress and impairment also vary with age. A very young child may
show signs of distress (e.g., intense crying) only when parents tell the child that he or she
is “really” not a member of the other gender but only “desires” to be. Distress may not be
manifest in social environments supportive of the child’s desire to live in the role of the
other gender and may emerge only if the desire is interfered with. In adolescents and
adults, distress may manifest because of strong incongruence between experienced gender
and somatic sex. Such distress may, however, be mitigated by supportive environments and
knowledge that biomedical treatments exist to reduce incongruence. Impairment (e.g.,
school refusal, development of depression, anxiety, and substance abuse) may be a conse-
quence of gender dysphoria.
Gender dysphoria without a disorder of sex development. For clinic-referred children,
onset of cross-gender behaviors is usually between ages 2 and 4 years. This corresponds to
the developmental time period in which most typically developing children begin ex-
pressing gendered behaviors and interests. For some preschool-age children, both perva-
sive cross-gender behaviors and the expressed desire to be the other gender may be
present, or, more rarely, labeling oneself as a member of the other gender may occur. In
some cases, the expressed desire to be the other gender appears later, usually at entry into
elementary school. A small minority of children express discomfort with their sexual anat-
omy or will state the desire to have a sexual anatomy corresponding to the experienced
gender (“anatomic dysphoria”). Expressions of anatomic dysphoria become more com-
mon as children with gender dysphoria approach and anticipate puberty.
Rates of persistence of gender dysphoria from childhood into adolescence or adulthood
vary. In natal males, persistence has ranged from 2.2% to 30%. In natal females, persistence
has ranged from 12% to 50%. Persistence of gender dysphoria is modestly correlated with
dimensional measures of severity ascertained at the time of a childhood baseline assess-
ment. In one sample of natal males, lower socioeconomic background was also modestly
correlated with persistence. It is unclear if particular therapeutic approaches to gender
dysphoria in children are related to rates of long-term persistence. Extant follow-up sam-
ples consisted of children receiving no formal therapeutic intervention or receiving ther-
apeutic interventions of various types, ranging from active efforts to reduce gender
dysphoria to a more neutral, “watchful waiting” approach. It is unclear if children “en-
couraged” or supported to live socially in the desired gender will show higher rates of per-
sistence, since such children have not yet been followed longitudinally in a systematic
manner. For both natal male and female children showing persistence, almost all are
sexually attracted to individuals of their natal sex. For natal male children whose gender
dysphoria does not persist, the majority are androphilic (sexually attracted to males) and of-
ten self-identify as gay or homosexual (ranging from 63% to 100%). In natal female chil-
dren whose gender dysphoria does not persist, the percentage who are gynephilic (sexually
attracted to females) and self-identify as lesbian is lower (ranging from 32% to 50%).
In both adolescent and adult natal males, there are two broad trajectories for develop-
ment of gender dysphoria: early onset and late onset. Early-onset gender dysphoria starts in
childhood and continues into adolescence and adulthood; or, there is an intermittent pe-
riod in which the gender dysphoria desists and these individuals self-identify as gay or ho-
mosexual, followed by recurrence of gender dysphoria. Late-onset gender dysphoria occurs
around puberty or much later in life. Some of these individuals report having had a desire
to be of the other gender in childhood that was not expressed verbally to others. Others do
not recall any signs of childhood gender dysphoria. For adolescent males with late-onset
gender dysphoria, parents often report surprise because they did not see signs of gender
456 Gender Dysphoria
dysphoria during childhood. Expressions of anatomic dysphoria are more common and
salient in adolescents and adults once secondary sex characteristics have developed.
Adolescent and adult natal males with early-onset gender dysphoria are almost al-
ways sexually attracted to men (androphilic). Adolescents and adults with late-onset gen-
der dysphoria frequently engage in transvestic behavior with sexual excitement. The
majority of these individuals are gynephilic or sexually attracted to other posttransition
natal males with late-onset gender dysphoria. A substantial percentage of adult males
with late-onset gender dysphoria cohabit with or are married to natal females. After gen-
der transition, many self-identify as lesbian. Among adult natal males with gender dyspho-
ria, the early-onset group seeks out clinical care for hormone treatment and reassignment
surgery at an earlier age than does the late-onset group. The late-onset group may have more
fluctuations in the degree of gender dysphoria and be more ambivalent about and less
likely satisfied after gender reassignment surgery.
In both adolescent and adult natal females, the most common course is the early-onset
form of gender dysphoria. The late-onset form is much less common in natal females com-
pared with natal males. As in natal males with gender dysphoria, there may have been a
period in which the gender dysphoria desisted and these individuals self-identified as les-
bian; however, with recurrence of gender dysphoria, clinical consultation is sought, often
with the desire for hormone treatment and reassignment surgery. Parents of natal adoles-
cent females with the late-onset form also report surprise, as no signs of childhood gender
dysphoria were evident. Expressions of anatomic dysphoria are much more common and
salient in adolescents and adults than in children.
Adolescent and adult natal females with early-onset gender dysphoria are almost
always gynephilic. Adolescents and adults with the late-onset form of gender dysphoria
are usually androphilic and after gender transition self-identify as gay men. Natal females
with the late-onset form do not have co-occurring transvestic behavior with sexual ex-
citement.
Gender dysphoria in association with a disorder of sex development. Most individuals
with a disorder of sex development who develop gender dysphoria have already come to
medical attention at an early age. For many, starting at birth, issues of gender assignment
were raised by physicians and parents. Moreover, as infertility is quite common for this
group, physicians are more willing to perform cross-sex hormone treatments and genital
surgery before adulthood.
Disorders of sex development in general are frequently associated with gender-atypi-
cal behavior starting in early childhood. However, in the majority of cases, this does not
lead to gender dysphoria. As individuals with a disorder of sex development become
aware of their medical history and condition, many experience uncertainty about their
gender, as opposed to developing a firm conviction that they are another gender. How-
ever, most do not progress to gender transition. Gender dysphoria and gender transition
may vary considerably as a function of a disorder of sex development, its severity, and as-
signed gender.
Risk and Prognostic Factors
Temperamental. For individuals with gender dysphoria without a disorder of sex de-
velopment, atypical gender behavior among individuals with early-onset gender dyspho-
ria develops in early preschool age, and it is possible that a high degree of atypicality
makes the development of gender dysphoria and its persistence into adolescence and
adulthood more likely.
Environmental. Among individuals with gender dysphoria without a disorder of sex de-
velopment, males with gender dysphoria (in both childhood and adolescence) more com-
monly have older brothers than do males without the condition. Additional predisposing
Gender Dysphoria 457
factors under consideration, especially in individuals with late-onset gender dysphoria (ad-
olescence, adulthood), include habitual fetishistic transvestism developing into autogyne-
philia (i.e., sexual arousal associated with the thought or image of oneself as a woman) and
other forms of more general social, psychological, or developmental problems.
Genetic and physiological. For individuals with gender dysphoria without a disorder of
sex development, some genetic contribution is suggested by evidence for (weak) familial-
ity of transsexualism among nontwin siblings, increased concordance for transsexualism
in monozygotic compared with dizygotic same-sex twins, and some degree of heritability
of gender dysphoria. As to endocrine findings, no endogenous systemic abnormalities in
sex-hormone levels have been found in 46,XY individuals, whereas there appear to be in-
creased androgen levels (in the range found in hirsute women but far below normal male
levels) in 46,XX individuals. Overall, current evidence is insufficient to label gender dys-
phoria without a disorder of sex development as a form of intersexuality limited to the cen-
tral nervous system.
In gender dysphoria associated with a disorder of sex development, the likelihood of
later gender dysphoria is increased if prenatal production and utilization (via receptor
sensitivity) of androgens are grossly atypical relative to what is usually seen in individuals
with the same assigned gender. Examples include 46,XY individuals with a history of nor-
mal male prenatal hormone milieu but inborn nonhormonal genital defects (as in cloacal
bladder exstrophy or penile agenesis) and who have been assigned to the female gender.
The likelihood of gender dysphoria is further enhanced by additional, prolonged, highly
gender-atypical postnatal androgen exposure with somatic virilization as may occur in fe-
male-raised and noncastrated 46,XY individuals with 5-alpha reductase-2 deficiency or
17-beta-hydroxysteroid dehydrogenase-3 deficiency or in female-raised 46,XX individuals
with classical congenital adrenal hyperplasia with prolonged periods of non-adherence to
glucocorticoid replacement therapy. However, the prenatal androgen milieu is more
closely related to gendered behavior than to gender identity. Many individuals with dis-
orders of sex development and markedly gender-atypical behavior do not develop gender
dysphoria. Thus, gender-atypical behavior by itself should not be interpreted as an indi-
cator of current or future gender dysphoria. There appears to be a higher rate of gender
dysphoria and patient-initiated gender change from assigned female to male than from as-
signed male to female in 46,XY individuals with a disorder of sex development.
Culture-Related Diagnostic Issues
Individuals with gender dysphoria have been reported across many countries and cul-
tures. The equivalent of gender dysphoria has also been reported in individuals living in
cultures with institutionalized gender categories other than male or female. It is unclear
whether with these individuals the diagnostic criteria for gender dysphoria would be met.
Diagnostic Markers
Individuals with a somatic disorder of sex development show some correlation of final
gender identity outcome with the degree of prenatal androgen production and utilization.
However, the correlation is not robust enough for the biological factor, where ascertain-
able, to replace a detailed and comprehensive diagnostic interview evaluation for gender
dysphoria.
Functional Consequences of Gender Dysphoria
Preoccupation with cross-gender wishes may develop at all ages after the first 2-3 years of
childhood and often interfere with daily activities. In older children, failure to develop
age-typical same-sex peer relationships and skills may lead to isolation from peer groups
and to distress. Some children may refuse to attend school because of teasing and harass-
458 Gender Dysphoria
ment or pressure to dress in attire associated with their assigned sex. Also in adolescents
and adults, preoccupation with cross-gender wishes often interferes with daily activities.
Relationship difficulties, including sexual relationship problems, are common, and func-
tioning at school or at work may be impaired. Gender dysphoria, along with atypical
gender expression, is associated with high levels of stigmatization, discrimination, and
victimization, leading to negative self-concept, increased rates of mental disorder comor-
bidity, school dropout, and economic marginalization, including unemployment, with at-
tendant social and mental health risks, especially in individuals from resource-poor family
backgrounds. In addition, these individuals’ access to health services and mental health
services may be impeded by structural barriers, such as institutional discomfort or inex-
perience in working with this patient population.
Differential Diagnosis
Nonconformity to gender roles. Gender dysphoria should be distinguished from sim-
ple nonconformity to stereotypical gender role behavior by the strong desire to be of an-
other gender than the assigned one and by the extent and pervasiveness of gender-variant
activities and interests. The diagnosis is not meant to merely describe nonconformity to
stereotypical gender role behavior (e.g., “tomboyism” in girls, “girly-boy” behavior in
boys, occasional cross-dressing in adult men). Given the increased openness of atypical
gender expressions by individuals across the entire range of the transgender spectrum, it
is important that the clinical diagnosis be limited to those individuals whose distress and
impairment meet the specified criteria.
Transvestic disorder. Transvestic disorder occurs in heterosexual (or bisexual) adoles-
cent and adult males (rarely in females) for whom cross-dressing behavior generates sex-
ual excitement and causes distress and/or impairment without drawing their primary
gender into question. It is occasionally accompanied by gender dysphoria. An individual
with transvestic disorder who also has clinically significant gender dysphoria can be given
both diagnoses. In many cases of late-onset gender dysphoria in gynephilic natal males,
transvestic behavior with sexual excitement is a precursor.
Body dysmorphic disorder. An individual with body dysmorphic disorder focuses on
the alteration or removal of a specific body part because it is perceived as abnormally formed,
not because it represents a repudiated assigned gender. When an individual’s presenta-
tion meets criteria for both gender dysphoria and body dysmorphic disorder, both diag-
noses can be given. Individuals wishing to have a healthy limb amputated (termed by
some body integrity identity disorder) because it makes them feel more “complete” usually
do not wish to change gender, but rather desire to live as an amputee or a disabled person.
Schizophrenia and other psychotic disorders. In schizophrenia, there may rarely be
delusions of belonging to some other gender. In the absence of psychotic symptoms, in-
sistence by an individual with gender dysphoria that he or she is of some other gender is
not considered a delusion. Schizophrenia (or other psychotic disorders) and gender dys-
phoria may co-occur.
Other clinical presentations. Some individuals with an emasculinization desire who
develop an alternative, nonmale/nonfemale gender identity do have a presentation that
meets criteria for gender dysphoria. However, some males seek castration and/or penec-
tomy for aesthetic reasons or to remove psychological effects of androgens without chang-
ing male identity; in these cases, the criteria for gender dysphoria are not met.
Comorbidity
Clinically referred children with gender dysphoria show elevated levels of emotional and
behavioral problems—most commonly, anxiety, disruptive and impulse-control, and de-
Other Specified Gender Dysphoria 459
pressive disorders. In prepubertal children, increasing age is associated with having more
behavioral or emotional problems; this is related to the increasing non-acceptance of gen-
der-variant behavior by others. In older children, gender-variant behavior often leads to
peer ostracism, which may lead to more behavioral problems. The prevalence of mental
health problems differs among cultures; these differences may also be related to differences
in attitudes toward gender variance in children. However, also in some non-Western cul-
tures, anxiety has been found to be relatively common in individuals with gender dysphoria,
even in cultures with accepting attitudes toward gender-variant behavior. Autism spec-
trum disorder is more prevalent in clinically referred children with gender dysphoria than
in the general population. Clinically referred adolescents with gender dysphoria appear to
have comorbid mental disorders, with anxiety and depressive disorders being the most
common. As in children, autism spectrum disorder is more prevalent in clinically referred
adolescents with gender dysphoria than in the general population. Clinically referred
adults with gender dysphoria may have coexisting mental health problems, most commonly
anxiety and depressive disorders.
Other Specified Gender Dysphoria
302.6 (F64.8)
This category applies to presentations in which symptoms characteristic of gender dys-
phoria that cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning predominate but do not meet the full criteria for gender dys-
phoria. The other specified gender dysphoria category is used in situations in which the
clinician chooses to communicate the specific reason that the presentation does not meet
the criteria for gender dysphoria. This is done by recording “other specified gender dys-
phoria” followed by the specific reason (e.g., “brief gender dysphoria”).
An exampie of a presentation that can be specified using the “other specified” desig-
nation is the following:
The current disturbance meets symptom criteria for gender dysphoria, but the
duration is iess than 6 months.
Unspecified Gender Dysphoria
302.6 (F64.9)
This category applies to presentations in which symptoms characteristic of gender dys-
phoria that cause clinically significant distress or impairment in social, occupational, or oth-
er important areas of functioning predominate but do not meet the full criteria for gender
dysphoria. The unspecified gender dysphoria category is used in situations in which the
clinician chooses not to specify the reason that the criteria are not met for gender dyspho-
ria, and includes presentations in which there is insufficient information to make a more
specific diagnosis.
Disruptive, impulse-control, and conduct disorders include conditions involv-
ing problems in the self-control of emotions and behaviors. While other disorders in DSM-
5 may also involve problems in emotional and/or behavioral regulation, the disorders in
this chapter are unique in that these problems are manifested in behaviors that violate the
rights of others (e.g., aggression, destruction of property) and/or that bring the individual
into significant conflict with societal norms or authority figures. The underlying causes of
the problems in the self-control of emotions and behaviors can vary greatly across the dis-
orders in this chapter and among individuals within a given diagnostic category.
The chapter includes oppositional defiant disorder, intermittent explosive disorder, con-
duct disorder, antisocial personality disorder (which is described in the chapter “Personality
Disorders”), pyromania, kleptomania, and other specified and unspecified disruptive, im-
pulse-control, and conduct disorders. Although all the disorders in the chapter involve
problems in both emotional and behavioral regulation, the source of variation among the
disorders is the relative emphasis on problems in the two types of self-control. For example,
the criteria for conduct disorder focus largely on poorly controlled behaviors that violate the
rights of others or that violate major societal norms. Many of the behavioral symptoms (e.g,,
aggression) can bea result of poorly controlled emotions such as anger. At the other extreme,
the criteria for intermittent explosive disorder focus largely on such poorly controlled emo-
tion, outbursts of anger that are disproportionate to the interpersonal or other provocation
or to other psychosocial stressors. Intermediate in impact to these two disorders is opposi-
tional defiant disorder, in which the criteria are more evenly distributed between emotions
{anger and irritation) and behaviors (argumentativeness and defiance). Pyromania and
kleptomania are less commonly used diagnoses characterized by poor impulse control re-
lated to specific behaviors (fire setting or stealing) that relieve internal tension. Other speci-
fied disruptive, impulse-control, and conduct disorder is a category for conditions in which
there are symptoms of conduct disorder, oppositional defiant disorder, or other disruptive,
impulse-control, and conduct disorders, but the number of symptoms does not meet the di-
agnostic threshold for any of the disorders in this chapter, even though there is evidence of
clinically significant impairment associated with the symptoms.
The disruptive, impulse-control, and conduct disorders all tend to be more common in
males than in females, although the relative degree of male predominance may differ both
across disorders and within a disorder at different ages. The disorders in this chapter tend to
have first onset in childhood or adolescence. In fact, it is very rare for either conduct disorder or
oppositional defiant disorder to first emerge in adulthood. There is a developmental relation-
ship between oppositional defiant disorder and conduct disorder, in that most cases of con-
duct disorder previously would have met criteria for oppositional defiant disorder, at least in
those cases in which conduct disorder emerges prior to adolescence. However, most children
with oppositional defiant disorder do not eventually develop conduct disorder. Furthermore,
children with oppositional defiant disorder are at risk for eventually developing other prob-
lems besides conduct disorder, including anxiety and depressive disorders.
Many of the symptoms that define the disruptive, impulse-control, and conduct disor-
ders are behaviors that can occur to some degree in typically developing individuals.
Thus, it is critical that the frequency, persistence, pervasiveness across situations, and im-
461
462 Disruptive, Impulse-Control, and Conduct Disorders
pairment associated with the behaviors indicative of the diagnosis be considered relative
to what is normative for a person’s age, gender, and culture when determining if they are
symptomatic of a disorder.
The disruptive, impulse-control, and conduct disorders have been linked to a common
externalizing spectrum associated with the personality dimensions labeled as disinhibition
and (inversely) constraint and, to a lesser extent, negative emotionality. These shared per-
sonality dimensions could account for the high level of comorbidity among these disorders
and their frequent comorbidity with substance use disorders and antisocial personality
disorder. However, the specific nature of the shared diathesis that constitutes the exter-
nalizing spectrum remains unknown.
Oppositional Defiant Disorder
Diagnostic Criteria 313,81 (F91.3)
A. Apattern of angry/irritable mood, argumentative/defiant behavior, or vindictiveness lasting
at least 6 months as evidenced by at least four symptoms from any of the following cate-
gories, and exhibited during interaction with at least one individual who is not a sibling.
Angry/lrritable Mood
1. Often loses temper.
2. Is often touchy or easily annoyed.
3. 1s often angry and resentful.
Argumentative/Defiant Behavior
4. Often argues with authority figures or, for children and adolescents, with adults.
5. Often actively defies or refuses to comply with requests from authority figures or
with rules.
6. Often deliberately annoys others.
7. Often blames others for his or her mistakes or misbehavior.
Vindictiveness
8. Has deen spiteful or vindictive at least twice within the past 6 months.
Note: The persistence and frequency of these behaviors should be used to distinguish
a behavior that is within normal limits from a behavior that is symptomatic. For children
younger than 5 years, the behavior should occur on most days for a period of at least
6 months unless otherwise noted (Criterion A8). For individuals 5 years or older, the
behavior should occur at least once per week for at least 6 months, unless otherwise
noted (Criterion A8). While these frequency criteria provide guidance on a minimal lev-
el of frequency to define symptoms, other factors should also be considered, such as
whether the frequency and intensity of the behaviors are outside a range that is nor-
mative for the individual’s developmental level, gender, and culture.
B. The disturbance in behavior is associated with distress in the individual or others in his or
her immediate social context (e.g., family, peer group, work colleagues), or it impacts neg-
atively on social, educational, occupational, or other important areas of functioning.
C. The behaviors do not occur exclusively during the course of a psychotic, substance
use, depressive, or bipolar disorder. Also, the criteria are not met for disruptive mood
dysregulation disorder.
Specify current severity:
Miid: Symptoms are confined to only one setting (e.g., at home, at school, at work, with
peers).
Oppositional Defiant Disorder 463
Moderate: Some symptoms are present in at least two settings.
Severe: Some symptoms are present in three or more settings.
Specifiers
It is not uncommon for individuals with oppositional defiant disorder to show symptoms
only at home and only with family members. However, the pervasiveness of the symp-
toms is an indicator of the severity of the disorder.
Diagnostic Features
The essential feature of oppositional defiant disorder is a frequent and persistent pattern
of angry /irritable mood, argumentative /defiant behavior, or vindictiveness (Criterion
A). It is not unusual for individuals with oppositional defiant disorder to show the behav-
ioral features of the disorder without problems of negative mood. However, individuals
with the disorder who show the angry /irritable mood symptoms typically show the be-
havioral features as well.
The symptoms of oppositional defiant disorder may be confined to only one setting,
and this is most frequently the home. Individuals who show enough symptoms to meet
the diagnostic threshold, even if it is only at home, may be significantly impaired in their
social functioning. However, in more severe cases, the symptoms of the disorder are pres-
ent in multiple settings. Given that the pervasiveness of symptoms is an indicator of the
severity of the disorder, it is critical that the individual’s behavior be assessed across mul-
tiple settings and relationships. Because these behaviors are common among siblings, they
must be observed during interactions with persons other than siblings. Also, because
symptoms of the disorder are typically more evident in interactions with adults or peers
whom the individual knows well, they may not be apparent during a clinical examination.
The symptoms of oppositional defiant disorder can occur to some degree in individu-
als without this disorder. There are several key considerations for determining if the be-
haviors are symptomatic of oppositional defiant disorder. First, the diagnostic threshold
of four or more symptoms within the preceding 6 months must be met. Second, the per-
sistence and frequency of the symptoms should exceed what is normative for an individ-
ual’s age, gender, and culture. For example, it is not unusual for preschool children to
show temper tantrums ona weekly basis. Temper outbursts for a preschool child would be
considered a symptom of oppositional defiant disorder only if they occurred on most days
for the preceding 6 months, if they occurred with at least three other symptoms of the dis-
order, and if the temper outbursts contributed to the significant impairment associated
with the disorder (e.g., led to destruction of property during outbursts, resulted in the
child being asked to leave a preschool).
The symptoms of the disorder often are part of a pattern of problematic interactions
with others. Furthermore, individuals with this disorder typically do not regard themselves
as angry, oppositional, or defiant. Instead, they often justify their behavior as a response to
unreasonable demands or circumstances. Thus, it can be difficult to disentangle the rela-
tive contribution of the individual with the disorder to the problematic interactions he or
she experiences. For example, children with oppositional defiant disorder may have ex-
perienced a history of hostile parenting, and it is often impossible to determine if the
child’s behavior caused the parents to act in a more hostile manner toward the child, if the
parents’ hostility led to the child’s problematic behavior, or if there was some combination
of both. Whether or not the clinician can separate the relative contributions of potential
causal factors should not influence whether or not the diagnosis is made. In the event that
the child may be living in particularly poor conditions where neglect or mistreatment may
occur (e.g., in institutional settings), clinical attention to reducing the contribution of the
environment may be helpful.
464 Disruptive, Impulse-Control, and Conduct Disorders
Associated Features Supporting Diagnosis
In children and adolescents, oppositional defiant disorder is more prevalent in families in
which child care is disrupted by a succession of different caregivers or in families in which
harsh, inconsistent, or neglectful child-rearing practices are common. Two of the most
common co-occurring conditions with oppositional defiant disorder are attention-deficit/
hyperactivity disorder (ADHD) and conduct disorder (see the section “Comorbidity” for
this disorder). Oppositional defiant disorder has been associated with increased risk for
suicide attempts, even after comorbid disorders are controlled for.
Prevaience
The prevalence of oppositional defiant disorder ranges from 1% to 11%, with an average
prevalence estimate of around 3.3%. The rate of oppositional defiant disorder may vary
depending on the age and gender of the child. The disorder appears to be somewhat more
prevalent in males than in females (1.4:1) prior to adolescence. This male predominance is
not consistently found in samples of adolescents or adults.
Development and Course
The first symptoms of oppositional defiant disorder usually appear during the preschool
years and rarely later than early adolescence. Oppositional defiant disorder often precedes
the development of conduct disorder, especially for those with the childhood-onset type
of conduct disorder. However, many children and adolescents with oppositional defiant
disorder do not subsequently develop conduct disorder. Oppositional defiant disorder
also conveys risk for the development of anxiety disorders.and major depressive disorder,
even in the absence of conduct disorder. The defiant, argumentative, and vindictive symp-
toms carry most of the risk for conduct disorder, whereas the angry-irritable mood symp-
toms carry most of the risk for emotional disorders.
Manifestations of the disorder across development appear consistent. Children and
adolescents with oppositional defiant disorder are at increased risk for a number of prob-
lems in adjustment as adults, including antisocial behavior, impulse-control problems,
substance abuse, anxiety, and depression.
Many of the behaviors associated with oppositional defiant disorder increase in fre-
quency during the preschool period and in adolescence. Thus, it is especially critical dur-
ing these development periods that the frequency and intensity of these behaviors be
evaluated against normative levels before it is decided that they are symptoms of opposi-
tional defiant disorder.
Risk and Prognostic Features
Temperamental. Temperamental factors related to problems in emotional regulation
(e.g., high levels of emotional reactivity, poor frustration tolerance) have been predictive
of the disorder.
Environmental. Harsh, inconsistent, or neglectful child-rearing practices are common in
families of children and adolescents with oppositional defiant disorder, and these parent-
ing practices play an important role in many causal theories of the disorder.
Genetic and physiological. A number of neurobiological markers (e.g., lower heart rate
and skin conductance reactivity; reduced basal cortisol reactivity; abnormalities in the pre-
frontal cortex and amygdala) have been associated with oppositional defiant disorder.
However, the vast majority of studies have not separated children with oppositional de-
fiant disorder from those with conduct disorder. Thus, it is unclear whether there are
markers specific to oppositional defiant disorder.
Oppositional Defiant Disorder 465
Culture-Related Diagnostic Issues
The prevalence of the disorder in children and adolescents is relatively consistent across
countries that differ in race and ethnicity.
Functional Consequences of
Oppositional Defiant Disorder
When oppositional defiant disorder is persistent throughout development, individuals
with the disorder experience frequent conflicts with parents, teachers, supervisors, peers,
and romantic partners. Such problems often result in significant impairments in the indi-
vidual’s emotional, social, academic, and occupational adjustment.
Differential Diagnosis
Conduct disorder. Conduct disorder and oppositional defiant disorder are both related
to conduct problems that bring the individual in conflict with adults and other authority
figures (e.g., teachers, work supervisors). The behaviors of oppositional defiant disorder
are typically of a less severe nature than those of conduct disorder and do not include ag-
gression toward people or animals, destruction of property, or a pattern of theft or deceit.
Furthermore, oppositional defiant disorder includes problems of emotional dysregulation
{i.e., angry and irritable mood) that are not included in the definition of conduct disorder.
Attention-deficit/hyperactivity disorder. ADHD is often comorbid with oppositional de-
fiant disorder. To make the additional diagnosis of oppositional defiant disorder, it is impor-
tant to determine that the individual’s failure to conform to requests of others is not solely in
situations that demand sustained effort and attention or demand that the individual sit still.
Depressive and bipolar disorders. Depressive and bipolar disorders often involve neg-
ative affect and irritability. As a result, a diagnosis of oppositional defiant disorder should
not be made if the symptoms occur exclusively during the course of a mood disorder.
Disruptive mood dysregulation disorder. Oppositional defiant disorder shares with dis-
ruptive mood dysregulation disorder the symptoms of chronic negative mood and temper
outbursts. However, the severity, frequency, and chronicity of temper outbursts are more
severe in individuals with disruptive mood dysregulation disorder than in those with
oppositional defiant disorder. Thus, only a minority of children and adolescents whose
symptoms meet criteria for oppositional defiant disorder would also be diagnosed with dis-
ruptive mood dysregulation disorder. When the mood disturbance is severe enough to meet
criteria for disruptive mood dysregulation disorder, a diagnosis of oppositional defiant dis-
order is not given, even if all criteria for oppositional defiant disorder are met.
Intermittent explosive disorder. Intermittent explosive disorder also involves high
rates of anger. However, individuals with this disorder show serious aggression toward
others that is not part of the definition of oppositional defiant disorder.
intellectual disability (intellectual developmental! disorder). In individuals with intel-
lectual disability, a diagnosis of oppositional defiant disorder is given only if the opposi-
tional behavior is markedly greater than is commonly observed among individuals of
comparable mental age and with comparable severity of intellectual disability.
Language disorder. Oppositional defiant disorder must also be distinguished from a
failure to follow directions that is the result of impaired language comprehension (e.g.,
hearing loss).
Social anxiety disorder (social phobia). Oppositional defiant disorder must also be dis-
tinguished from defiance due to fear of negative evaluation associated with social anxiety
disorder.
466 Disruptive, !mpulse-Control, and Conduct Disorders
Comorbidity
Rates of oppositional defiant disorder are much higher in samples of children, adoles-
cents, and adults with ADHD, and this may be the result of shared temperamental risk fac-
tors. Also, oppositional defiant disorder often precedes conduct disorder, although this
appears to be most common in children with the childhood-onset subtype. Individuals
with oppositional] defiant disorder are also at increased risk for anxiety disorders and ma-
jor depressive disorder, and this seems largely attributable to the presence of the angry-
irritable mood symptoms. Adolescents and adults with oppositional defiant disorder also
show a higher rate of substance use disorders, although it is unclear if this association is in-
dependent of the comorbidity with conduct disorder.
Intermittent Explosive Disorder
Diagnostic Criteria 312.34 (F63.81)
A. Recurrent behavioral outbursts representing a failure to control aggressive impulses
as manifested by either of the following:
1. Verbal aggression (e.g., temper tantrums, tirades, verbal arguments or fights) or
physical aggression toward property, animals, or other individuals, occurring twice
weekly, on average, for a period of 3 months. The physical aggression does not re-
sult in damage or destruction of property and does not result in physical injury to
animals or other individuals.
2, Three behavioral outbursts involving damage or destruction of property and/or
physical assault involving physical injury against animals or other individuals occur-
ring within a 12-month period.
B. The magnitude of aggressiveness expressed during the recurrent outbursts is grossly
out of proportion to the provocation or to any precipitating psychosocial stressors.
C. The recurrent aggressive outbursts are not premeditated (i.e., they are impulsive and/
or anger-based) and are not committed to achieve some tangible objective (e.g.,
money, power, intimidation).
D. The recurrent aggressive outbursts cause either marked distress in the individual or
impairment in occupational or interpersonal functioning, or are associated with finan-
cial or legal consequences.
E. Chronological age is at least 6 years (or equivalent developmental level).
F. The recurrent aggressive outbursts are not better explained by another mental disor-
der (e.g., major depressive disorder, bipolar disorder, disruptive mood dysregulation
disorder, a psychotic disorder, antisocial personality disorder, borderline personality
disorder) and are not attributable to another medical condition (e.g., head trauma, Alz-
heimer’s disease) or to the physiological effects of a substance (e.g., a drug of abuse,
a medication). For children ages 6-18 years, aggressive behavior that occurs as part
of an adjustment disorder should not be considered for this diagnosis.
Note: This diagnosis can be made in addition to the diagnosis of attention-deficit/hyper-
activity disorder, conduct disorder, oppositional defiant disorder, or autism spectrum dis-
order when recurrent impulsive aggressive outbursts are in excess of those usually seen
in these disorders and warrant independent clinical attention.
Diagnostic Features
The impulsive (or anger-based) aggressive outbursts in intermittent explosive disorder have
a rapid onset and, typically, little or no prodromal period. Outbursts typically last for less
Intermittent Explosive Disorder 467
than 30 minutes and commonly occur in response to a minor provocation by a close intimate
or associate. Individuals with intermittent explosive disorder often have less severe epi-
sodes of verbal and/or nondamaging, nondestructive, or noninjurious physical assault (Cri-
terion A1) in between more severe destructive /assaultive episodes (Criterion A2). Criterion
A] defines frequent {i.e., twice weekly, on average, for a period of 3 months) aggressive out-
bursts characterized by temper tantrums, tirades, verbal arguments or fights, or assault
without damage to objects or without injury to animals or other individuals. Criterion A2
defines infrequent (i.e., three in a 1-year period) impulsive aggressive outbursts character-
ized by damaging or destroying an object, regardless of its tangible value, or by assaulting /
striking or otherwise causing physical injury to an animal or to another individual. Regard-
less of the natute of the impulsive aggressive outburst, the core feature of intermittent
explosive disorder is failure to control impulsive aggressive behavior in response to subjec-
tively experienced provocation ({i.e., psychosocial stressor) that would not typically result in
an aggressive outburst (Criterion B). The aggressive outbursts are generally impulsive and/
or anger-based, rather than premeditated or instrumental (Criterion C) and are associated
with significant distress or impairment in psychosocial function (Criterion D). A diagnosis
of intermittent explosive disorder should not be given to individuals younger than 6 years,
or the equivalent developmental level (Criterion E), or to individuals whose aggressive out-
bursts are better explained by another mental disorder (Criterion F). A diagnosis of intermit-
tent explosive disorder should not be given to individuals with disruptive mood
dysregulation disorder or to individuals whose impulsive aggressive outbursts are attribut-
able to another medical condition or to the physiological effects of a substance (Criterion F).
In addition, children ages 6-18 years should not receive this diagnosis when impulsive ag-
gressive outbursts occur in the context of an adjustment disorder (Criterion F).
Associated Features Supporting Diagnosis
Mood disorders (unipolar), anxiety disorders, and substance use disorders are associated
with intermittent explosive disorder, although onset of these disorders is typically later
than that of intermittent explosive disorder.
Prevaience
One-year prevalence data for intermittent explosive disorder in the United States is about
2.7% (narrow definition). Intermittent explosive disorder is more prevalent among
younger individuals (e.g., younger than 35-40 years), compared with older individuals
(older than 50 years), and in individuals with a high school education or less.
Development and Course
The onset of recurrent, problematic, impulsive aggressive behavior is most common in late
childhood or adolescence and rarely begins for the first time after age 40 years. The core
features of intermittent explosive disorder, typically, are persistent and continue for many
years.
The course of the disorder may be episodic, with recurrent periods of impulsive ag-
gressive outbursts. Intermittent explosive disorder appears to follow a chronic and persis-
tent course over many years. It also appears to be quite common regardless of the presence
or absence of attention-deficit/hyperactivity disorder (ADHD) or disruptive, impulse-
control, and conduct disorders (e.g., conduct disorder, oppositional defiant disorder).
Risk and Prognostic Factors
Environmental. Individuals with a history of physical and emotional trauma during the
first two decades of life are at increased risk for intermittent explosive disorder.
468 Disruptive, Impulse-Control, and Conduct Disorders
Genetic and physiological. First-degree relatives of individuals with intermittent ex-
plosive disorder are at increased risk for intermittent explosive disorder, and twin studies
have demonstrated a substantial genetic influence for impulsive aggression.
Research provides neurobiological support for the presence of serotonergic abnormal-
ities, globally and in the brain, specifically in areas of the limbic system (anterior cingulate)
and orbitofrontal cortex in individuals with intermittent explosive disorder. Amygdala
responses to anger stimuli, during functional magnetic resonance imaging scanning, are
greater in individuals with intermittent explosive disorder compared with healthy indi-
viduals.
Culture-Related Diagnostic Issues
The lower prevalence of intermittent explosive disorder in some regions (Asia, Middle
East) or countries (Romania, Nigeria), compared with the United States, suggests that in-
formation about recurrent, problematic, impulsive aggressive behaviors either is not elic-
ited on questioning or is less likely to be present, because of cultural factors.
Gender-Related Diagnostic Issues
In some studies the prevalence of intermittent explosive disorder is greater in males than
in females (odds ratio = 1.4-2.3); other studies have found no gender difference.
Functional Consequences of
Intermittent Explosive Disorder
Social (e.g., loss of friends, relatives, marital instability), occupational (e.g., demotion, loss
of employment), financial (e.g., due to value of objects destroyed), and legal (e.g., civil
suits as a result of aggressive behavior against person or property; criminal charges for as-
sault) problems often develop as a result of intermittent explosive disorder.
Differential Diagnosis
A diagnosis of intermittent explosive disorder should not be made when Criteria Al and/
or A2 are only met during an episode of another mental disorder (e.g., major depressive
disorder, bipolar disorder, psychotic disorder), or when impulsive aggressive outbursts
are attributable to another medical condition or to the physiological effects of a substance
or medication. This diagnosis also should not be made, particularly in children and ado-
lescents ages 6-18 years, when the impulsive aggressive outbursts occur in the context of
an adjustment disorder. Other examples in which recurrent, problematic, impulsive ag-
gressive outbursts may, or may not, be diagnosed as intermittent explosive disorder in-
clude the following.
Disruptive mood dysregulation disorder. In contrast to intermittent explosive disorder,
disruptive mood dysregulation disorder is characterized by a persistently negative mood state
(ie., irritability, anger) most of the day, nearly every day, between impulsive aggressive out-
bursts. A diagnosis of disruptive mood dysregulation disorder can only be given when the on-
set of recurrent, problematic, impulsive aggressive outbursts is before age 10 years. Finally, a
diagnosis of disruptive mood dysregulation disorder should not be made for the first time
after age 18 years. Otherwise, these diagnoses are mutually exclusive.
Antisocial personality disorder or borderline personality disorder. Individuals with an-
tisocial personality disorder or borderline personality disorder often display recurrent,
problematic impulsive aggressive outbursts. However, the level of impulsive aggression
in individuals with antisocial personality disorder or borderline personality disorder is
lower than that in individuals with intermittent explosive disorder.
Conduct Disorder 469
Delirium, major neurocognitive disorder, and personality change due to another med-
ical condition, aggressive type. A diagnosis of intermittent explosive disorder should not
be made when aggressive outbursts are judged to result from the physiological effects of an-
other diagnosable medical condition (e.g., brain injury associated with a change in personality
characterized by aggressive outbursts; complex partial epilepsy). Nonspecific abnormalities
on neurological examination (e.g., “soft signs”) and nonspecific electroencephalographic
changes are compatible with a diagnosis of intermittent explosive disorder unless there is a di-
agnosable medical condition that better explains the impulsive aggressive outbursts.
Substance intoxication or substance withdrawal. A diagnosis of intermittent explosive
disorder should not be made when impulsive aggressive outbursts are nearly always as-
sociated with intoxication with or withdrawal from substances (e.g., alcohol, phencyclidine,
cocaine and other stimulants, barbiturates, inhalants). However, when a sufficient number
of impulsive aggressive outbursts also occur in the absence of substance intoxication or
withdrawal, and these warrant independent clinical attention, a diagnosis of intermittent
explosive disorder may be given.
Attention-deficit/hyperactivity disorder, conduct disorder, oppositional defiant disor-
der, or autism spectrum disorder. Individuals with any of these childhood-onset dis-
orders may exhibit impulsive aggressive outbursts. Individuals with ADHD are typically
impulsive and, as a result, may also exhibit impulsive aggressive outbursts. While indi-
viduals with conduct disorder can exhibit impulsive aggressive outbursts, the form of ag-
gression characterized by the diagnostic criteria is proactive and predatory. Aggression in
oppositional defiant disorder is typically characterized by temper tantrums and verbal ar-
guments with authority figures, whereas impulsive aggressive outbursts in intermittent
explosive disorder are in response to a broader array of provocation and include physical
assault. The level of impulsive aggression in individuals with a history of one or more of
these disorders has been reported as lower than that in comparable individuals whose
symptoms also meet intermittent explosive disorder Criteria A through E. Accordingly, if
Criteria A through E are also met, and the impulsive aggressive outbursts warrant inde-
pendent clinical attention, a diagnosis of intermittent explosive disorder may be given.
Comorbidity
Depressive disorders, anxiety disorders, and substance use disorders are most commonly
comorbid with intermittent explosive disorder. In addition, individuals with antisocial
personality disorder or borderline personality disorder, and individuals with a history of
disorders with disruptive behaviors (e.g., ADHD, conduct disorder, oppositional defiant
disorder), are at greater risk for comorbid intermittent explosive disorder.
Conduct Disorder
Diagnostic Criteria
A. Arepetitive and persistent pattern of behavior in which the basic rights of others or ma-
jor age-appropriate societal norms or rules are violated, as manifested by the presence
of at least three of the following 15 criteria in the past 12 months from any of the cate-
gories below, with at least one criterion present in the past 6 months:
Aggression to People and Animals
1. Often bullies, threatens, or intimidates others.
2. Often initiates physical fights.
3. Has used a weapon that can cause serious physical harm to others (e.g., a bat,
brick, broken bottle, knife, gun).
470 Disruptive, Impulse-Control, and Conduct Disorders
4. Has been physically cruel to people.
5. Has been physically cruel to animals.
6. Has stolen while confronting a victim (e.g., mugging, purse snatching, extortion,
armed robbery).
7. Has forced someone into sexual activity.
Destruction of Property
8. Has deliberately engaged in fire setting with the intention of causing serious damage.
9. Has deliberately destroyed others’ property (other than by fire setting).
Deceitfulness or Theft
10. Has broken into someone else’s house, building, or car.
11. Often lies to obtain goods or favors or to avoid obligations ({i.e., “cons” others).
12. Has stolen items of nontrivial value without confronting a victim (e.g., shoplifting,
but without breaking and entering; forgery).
Serious Violations of Rules
13. Often stays out at night despite parental prohibitions, beginning before age 13 years.
14. Has run away from home overnight at least twice while living in the parental or pa-
rental surrogate home, or once without returning for a lengthy period.
15. 4s often truant from school, beginning before age 13 years.
B. The disturbance in behavior causes clinically significant impairment in social, aca-
demic, or occupational functioning.
C. lf the individual is age 18 years or older, criteria are not met for antisocial personality
disorder.
Specify whether:
312.81 (F91.1) Childhood-onset type: Individuals show at least one symptom char-
acteristic of conduct disorder prior to age 10 years.
312.82 (F91.2} Adolescent-onset type: individuals show no symptom characteristic
of conduct disorder prior to age 10 years.
312.89 (F91.9) Unspecified onset: Criteria for a diagnosis of conduct disorder are
met, but there is not enough information available to determine whether the onset of
the first symptom was before or after age 10 years.
Specify if:
With limited prosocial emotions: To qualify for this specifier, an individual must have dis-
played at least two of the following characteristics persistently over at least 12 months and
in multiple relationships and settings. These characteristics reflect the individual’s typical
pattem of interpersonal and emotional functioning over this period and not just occasional
occurrences in some situations. Thus, to assess the criteria for the specifier, multiple infor-
mation sources are necessary. In addition to the individual's self-report, it is necessary to
consider reports by others who have known the individual for extended periods of time
(e.g., parents, teachers, co-workers, extended family members, peers).
Lack of remorse or guilt: Does not feel bad or guilty when he or she does some-
thing wrong (exclude remorse when expressed only when caught and/or facing
punishment). The individual shows a general lack of concern about the negative
consequences of his or her actions. For example, the individual is not remorseful
after hurting someone or does not care about the consequences of breaking rules.
Callous—lack of empathy: Disregards and is unconcerned about the feelings of
others. The individual is described as cold and uncaring. The person appears more
concerned about the effects of his or her actions on himself or herself, rather than
their effects on others, even when they result in substantial harm to others.
Conduct Disorder 471
Unconcerned about performance: Does not show concern about poor/problem-
atic performance at school, at work, or in other important activities. The individual
does not put forth the effort necessary to perform well, even when expectations are
clear, and typically blames others for his or her poor performance.
Shallow or deficient affect: Does not express feelings or show emotions to others,
except in ways that seem shallow, insincere, or superficial (e.g., actions contradict the
emotion displayed; can turn emotions “on” or “off? quickly) or when emotional expres-
sions are used for gain (e.g., emotions displayed to manipulate or intimidate others).
Specify current severity:
Mild: Few if any conduct problems in excess of those required to make the diagnosis
are present, and conduct problems cause relatively minor harm to others (e.g., lying,
truancy, staying out after dark without permission, other rule breaking).
Moderate: The number of conduct problems and the effect on others are intermediate
between those specified in “mild” and those in “severe” (e.g., stealing without confront-
ing a victim, vandalism).
Severe: Many conduct problems in excess of those required to make the diagnosis are
present, or conduct problems cause considerable harm to others (e.g., forced sex, physical
cruelty, use of a weapon, stealing while confronting a victim, breaking and entering).
Subtypes
Three subtypes of conduct disorder are provided based on the age at onset of the disorder.
Onset is most accurately estimated with information from both the youth and the care-
giver; estimates are often 2 years later than actual onset. Both subtypes can occur ina mild,
moderate, or severe form. An unspecified-onset subtype is designated when there is in-
sufficient information to determine age at onset.
In childhood-onset conduct disorder, individuals are usually male, frequently display
physical aggression toward others, have disturbed peer relationships, may have had op-
positional defiant disorder during early childhood, and usually have symptoms that meet
full criteria for conduct disorder prior to puberty. Many children with this subtype also
have concurrent attention-deficit/hyperactivity disorder (ADHD) or other neurodevel-
opmental difficulties. Individuals with childhood-onset type are more likely to have per-
sistent conduct disorder into adulthood than are those with adolescent-onset type. As
compared with individuals with childhood-onset type, individuals with adolescent-onset
conduct disorder are less likely to display aggressive behaviors and tend to have more
normative peer relationships (although they often display conduct problems in the com-
pany of others). These individuals are less likely to have conduct disorder that persists into
adulthood. The ratio of males to females with conduct disorder is more balanced for the
adolescent-onset type than for the childhood-onset type.
Specifiers
A minority of individuals with conduct disorder exhibit characteristics that qualify for the
“with limited prosocial emotions” specifier. The indicators of this specifier are those that
have often been labeled as callous and unemotional traits in research. Other personality
features, such as thrill seeking, fearlessness, and insensitivity to punishment, may also dis-
tinguish those with characteristics described in the specifier. Individuals with character-
istics described in this specifier may be more likely than other individuals with conduct
disorder to engage in aggression that is planned for instrumental gain. Individuals with
conduct disorder of any subtype or any level of severity can have characteristics that qual-
ify for the specifier “with limited prosocial emotions,” although individuals with the spec-
ifier are more likely to have childhood-onset type and a severity specifier rating of severe.
472 Disruptive, Impulse-Control, and Conduct Disorders
Although the validity of self-report to assess the presence of the specifier has been sup-
ported in some research contexts, individuals with conduct disorder with this specifier
may not readily admit to the traits in a clinical interview. Thus, to assess the criteria for the
specifier, multiple information sources are necessary. Also, because the indicators of the
specifier are characteristics that reflect the individual's typical pattern of interpersonal and
emotional functioning, it is important to consider reports by others who have known the
individual for extended periods of time and across relationships and settings (e.g., par-
ents, teachers, co-workers, extended family members, peers).
Diagnostic Features
The essential feature of conduct disorder is a repetitive and persistent pattern of behavior
in which the basic rights of others or major age-appropriate societal norms or rules are vi-
olated (Criterion A). These behaviors fall into four main groupings: aggressive conduct
that causes or threatens physical harm to other people or animals (Criteria Al—-A7); non-
aggressive conduct that causes property loss or damage (Criteria A8—A9); deceitfulness or
theft (Criteria A10—-A12); and serious violations of rules (Criteria A13—A15). Three or more
characteristic behaviors must have been present during the past 12 months, with at least
one behavior present in the past 6 months. The disturbance in behavior causes clinically
significant impairment in social, academic, or occupational functioning (Criterion B). The
behavior pattern is usually present in a variety of settings, such as home, at school, or in
the community. Because individuals with conduct disorder are likely to minimize their
conduct problems, the clinician often must rely on additional informants. However, infor-
mants’ knowledge of the individual’s conduct problems may be limited if they have inad-
equately supervised the individual or the individual has concealed symptom behaviors.
Individuals with conduct disorder often initiate aggressive behavior and react aggres-
sively to others. They may display bullying, threatening, or intimidating behavior (includ-
ing bullying via messaging on Web-based social media) (Criterion A1); initiate frequent
physical fights (Criterion A2); use a weapon that can cause serious physical harm (e.g., a bat,
brick, broken bottle, knife, gun) (Criterion A3); be physically cruel to people (Criterion A4)
or animals (Criterion A5); steal while confronting a victim (e.g., mugging, purse snatching,
extortion, armed robbery) (Criterion A6); or force someone into sexual activity (Criterion A7).
Physical violence may take the form of rape, assault, or, in rare cases, homicide. Deliberate
destruction of others’ property may include deliberate fire setting with the intention of caus-
ing serious damage (Criterion A8) or deliberate destroying of other people’s property in
other ways (e.g., smashing car windows, vandalizing school property) (Criterion A9). Acts of
deceitfulness or theft may include breaking into someone else’s house, building, or car (Crite-
rion A10); frequently lying or breaking promises to obtain goods or favors or to avoid debts
or obligations (e.g., “conning” other individuals) (Criterion A11); or stealing items of non-
trivial value without confronting the victim (e.g., shoplifting, forgery, fraud) (Criterion A12).
Individuals with conduct disorder may also frequently commit serious violations of
rules (e.g., school, parental, workplace). Children with conduct disorder often have a pat-
tern, beginning before age 13 years, of staying out late at night despite parental prohi-
bitions (Criterion A13). Children may also show a pattern of running away from home
overnight (Criterion A14). To be considered a symptom of conduct disorder, the running
away must have occurred at least twice (or only once if the individual did not return for a
lengthy period). Runaway episodes that occur as a direct consequence of physical or sex-
ual abuse do not typically qualify for this criterion. Children with conduct disorder may
often be truant from school, beginning prior to age 13 years (Criterion A15).
Associated Features Supporting Diagnosis
Especially in ambiguous situations, aggressive individuals with conduct disorder fre-
quently misperceive the intentions of others as more hostile and threatening than is the
Conduct Disorder 473
case and respond with aggression that they then feel is reasonable and justified. Person-
ality features of trait negative emotionality and poor self-control, including poor frustra-
tion tolerance, irritability, temper outbursts, suspiciousness, insensitivity to punishment,
thrill seeking, and recklessness, frequently co-occur with conduct disorder. Substance
misuse is often an associated feature, particularly in adolescent females. Suicidal ideation,
suicide attempts, and completed suicide occur at a higher-than-expected rate in individu-
als with conduct disorder.
Prevalence
One-year population prevalence estimates range from 2% to more than 10%, with a median
of 4%. The prevalence of conduct disorder appears to be fairly consistent across various
countries that differ in race and ethnicity. Prevalence rates rise from childhood to adoles-
cence and are higher among males than among females. Few children with impairing con-
duct disorder receive treatment.
Development and Course
The onset of conduct disorder may occur as early as the preschool years, but the first sig-
nificant symptoms usually emerge during the period from middle childhood through
middle adolescence. Oppositional defiant disorder is a common precursor to the child-
hood-onset type of conduct disorder. Conduct disorder may be diagnosed in adults, how-
ever, symptoms of conduct disorder usually emerge in childhood or adolescence, and
onset is rare after age 16 years. The course of conduct disorder after onset is variable. In a
majority of individuals, the disorder remits by adulthood. Many individuals with conduct
disorder—particularly those with adolescent-onset type and those with few and milder
symptoms—achieve adequate social and occupational adjustment as adults. However, the
early-onset type predicts a worse prognosis and an increased risk of criminal behavior,
conduct disorder, and substance-related disorders in adulthood. Individuals with conduct
disorder are at risk for later mood disorders, anxiety disorders, posttraumatic stress dis-
order, impulse-control disorders, psychotic disorders, somatic symptom disorders, and
substance-related disorders as adults.
Symptoms of the disorder vary with age as the individual develops increased physical
strength, cognitive abilities, and sexual maturity. Symptom behaviors that emerge first
tend to be less serious (e.g., lying, shoplifting), whereas conduct problems that emerge last
tend to be more severe (e.g., rape, theft while confronting a victim). However, there are
wide differences among individuals, with some engaging in the more damaging behaviors
at an early age (which is predictive of a worse prognosis). When individuals with conduct
disorder reach adulthood, symptoms of aggression, property destruction, deceitfulness,
and rule violation, including violence against co-workers, partners, and children, may be ex-
hibited in the workplace and the home, such that antisocial personality disorder may be
considered.
Risk and Prognostic Factors
Temperamental. Temperamental risk factors include a difficult undercontrolled infant
temperament and lower-than-average intelligence, particularly with regard to verbal IQ.
Environmental. Family-level risk factors include parental rejection and neglect, inconsis-
tent child-rearing practices, harsh discipline, physical or sexual abuse, lack of supervision,
early institutional living, frequent changes of caregivers, large family size, parental criminal-
ity, and certain kinds of familial psychopathology (e.g., substance-related disorders). Com-
munity-level risk factors include peer rejection, association with a delinquent peer group,
and neighborhood exposure to violence. Both types of risk factors tend to be more common
and severe among individuals with the childhood-onset subtype of conduct disorder.
474 Disruptive, Impulse-Control, and Conduct Disorders
Genetic and physiological. Conduct disorder is influenced by both genetic and envi-
ronmental factors. The risk is increased in children with a biological or adoptive parent or
a sibling with conduct disorder. The disorder also appears to be more common in children
of biological parents with severe alcohol use disorder, depressive and bipolar disorders, or
schizophrenia or biological parents who have a history of ADHD or conduct disorder.
Family history particularly characterizes individuals with the childhood-onset subtype of
conduct disorder. Slower resting heart rate has been reliably noted in individuals with
conduct disorder compared with those without the disorder, and this marker is not char-
acteristic of any other mental disorder. Reduced autonomic fear conditioning, particularly
low skin conductance, is also well documented. However, these psychophysiological find-
ings are not diagnostic of the disorder. Structural and functional differences in brain areas
associated with affect regulation and affect processing, particularly frontotemporal-limbic
connections involving the brain’s ventral prefrontal cortex and amygdala, have been con-
sistently noted in individuals with conduct disorder compared with those without the dis-
order. However, neuroimaging findings are not diagnostic of the disorder.
Course modifiers. Persistence is more likely for individuals with behaviors that meet
criteria for the childhood-onset subtype and qualify for the specifier “with limited pro-
social emotions”. The risk that conduct disorder will persist is also increased by co-occurring
ADHD and by substance abuse.
Culture-Related Diagnostic Issues
Conduct disorder diagnosis may at times be potentially misapplied to individuals in set-
tings where patterns of disruptive behavior are viewed as near-normative (e.g., in very
threatening, high-crime areas or war zones). Therefore, the context in which the undesir-
able behaviors have occurred should be considered.
Gender-Related Diagnostic Issues
Males with a diagnosis of conduct disorder frequently exhibit fighting, stealing, vandalism,
and school discipline problems. Females with a diagnosis of conduct disorder are more likely
to exhibit lying, truancy, running away, substance use, and prostitution. Whereas males tend
to exhibit both physical aggression and relational aggression (behavior that harms social re-
lationships of others), females tend to exhibit relatively more relational aggression.
Functional Consequences of Conduct Disorder
Conduct disorder behaviors may lead to school suspension or expulsion, problems in
work adjustment, legal difficulties, sexually transmitted diseases, unplanned pregnancy,
and physical injury from accidents or fights. These problems may preclude attendance in
ordinary schools or living in a parental or foster home. Conduct disorder is often associ-
ated with an early onset of sexual behavior, alcohol use, tobacco smoking, use of illegal
substances, and reckless and risk-taking acts. Accident rates appear to be higher among in-
dividuals with conduct disorder compared with those without the disorder. These func-
tional consequences of conduct disorder may predict health difficulties when individuals
reach midlife. It is not uncommon for individuals with conduct disorder to come into con-
tact with the criminal justice system for engaging in illegal behavior. Conduct disorder is
a common reason for treatment referral and is frequently diagnosed in mental health fa-
cilities for children, especially in forensic practice. It is associated with impairment that is
more severe and chronic than that experienced by other clinic-referred children.
Differential Diagnosis
Oppositional defiant disorder. Conduct disorder and oppositional defiant disorder are
both related to symptoms that bring the individual in conflict with adults and other au-
Conduct Disorder 475
thority figures (e.g., parents, teachers, work supervisors). The behaviors of oppositional
defiant disorderare typically of a less severe nature than those of individuals with conduct
disorder and do not include aggression toward individuals or animals, destruction of
property, or a pattern of theft or deceit. Furthermore, oppositional defiant disorder in-
cludes problems of emotional dysregulation (i.e., angry and irritable mood) that are not in-
cluded in the definition of conduct disorder. When criteria are met for both oppositional
defiant disorder and conduct disorder, both diagnoses can be given.
Attention-deficit/hyperactivity disorder. Although children with ADHD often exhibit
hyperactive and impulsive behavior that may be disruptive, this behavior does not by it-
self violate societal norms or the rights of others and therefore does not usually meet cri-
teria for conduct disorder. When criteria are met for both ADHD and conduct disorder, both
diagnoses should be given.
Depressive and bipolar disorders. Irritability, aggression, and conduct problems can
occur in children or adolescents with a major depressive disorder, a bipolar disorder, or
disruptive mood dysregulation disorder. The behaviorial problems associated with these
mood disorders can usually be distinguished from the pattern of conduct problems seen in
conduct disorder based on their course. Specifically, persons with conduct disorder will
display substantial levels of aggressive or non-aggressive conduct problems during peri-
ods in which there is no mood disturbance, either historically (i-e., a history of conduct
problems predating the onset of the mood disturbance) or concurrently (i.e., display of
some conduct problems that are premeditated and do not occur during periods of intense
emotional arousal). In those cases in which criteria for conduct disorder and a mood dis-
order are met, both diagnoses can be given.
Intermittent explosive disorder. Both conduct disorder and intermittent explosive dis-
order involve high rates of aggression. However, the aggression in individuals with inter-
mittent explosive disorder is limited to impulsive aggression and is not premeditated, and
it is not committed in order to achieve some tangible objective (e.g., money, power, intim-
idation). Also, the definition of intermittent explosive disorder does not include the non-
aggressive symptoms of conduct disorder. If criteria for both disorders are met, the diag-
nosis of intermittent explosive disorder should be given only when the recurrent impul-
sive aggressive outbursts warrant independent clinical attention.
Adjustment disorders. The diagnosis of an adjustment disorder (with disturbance of con-
duct or with mixed disturbance of emotions and conduct) should be considered if clinically
significant conduct problems that do not meet the criteria for another specific disorder de-
velop in clear association with the onset of a psychosocial stressor and do not resolve within
6 months of the termination of the stressor (or its consequences). Conduct disorder is diag-
nosed only when the conduct problems represent a repetitive and persistent pattern that is
associated with impairment in social, academic, or occupational functioning.
Comorbidity
ADHD and oppositional defiant disorder are both common in individuals with conduct
disorder, and this comorbid presentation predicts worse outcomes. Individuals who show
the personality features associated with antisocial personality disorder often violate the
basic rights of others or violate major age-appropriate societal norms, and as a result their
pattern of behavior often meets criteria for conduct disorder. Conduct disorder may also
co-occur with one or more of the following mental disorders: specific learning disorder,
anxiety disorders, depressive or bipolar disorders, and substance-related disorders. Aca-
demic achievement, particularly in reading and other verbal skills, is often below the level
expected on the basis of age and intelligence and may justify the additional diagnosis of
specific learning disorder or a communication disorder.
476 Disruptive, Impulse-Control, and Conduct Disorders
Antisocial Personality Disorder
Criteria and text for antisocial personality disorder can be found in the chapter “Person-
ality Disorders.” Because this disorder is closely connected to the spectrum of “external-
izing” conduct disorders in this chapter, as well as to the disorders in the adjoining chapter
“Substance-Related and Addictive Disorders,” it is dual coded here as well as in the chap-
ter “Personality Disorders.”
Pyromania
Diagnostic Criteria 312.33 (F63.1)
A. Deliberate and purposeful fire setting on more than one occasion.
B. Tension or affective arousal before the act.
C. Fascination with, interest in, curiosity about, or attraction to fire and its situational con-
texts (e.g., paraphernalia, uses, consequences).
D. Pleasure, gratification, or relief when setting fires or when witnessing or participating
in their aftermath.
E. The fire setting is not done for monetary gain, as an expression of sociopolitical ideol-
ogy, to conceal criminal activity, to express anger or vengeance, to improve one’s living
circumstances, in response to a delusion or hallucination, or as a result of impaired
judgment (e.g., in major neurocognitive disorder, intellectual disability [intellectual de-
velopmental disorder], substance intoxication).
F. The fire setting is not better explained by conduct disorder, a manic episode, or anti-
social personality disorder.
Diagnostic Features
The essential feature of pyromania is the presence of multiple episodes of deliberate and
purposeful fire setting (Criterion A). Individuals with this disorder experience tension or af-
fective arousal before setting a fire (Criterion B). There is a fascination with, interest in, cu-
riosity about, or attraction to fire and its situational contexts (e.g., paraphernalia, uses,
consequences) (Criterion C). Individuals with this disorder are often regular “watchers” at
fires in their neighborhoods, may set off false alarms, and derive pleasure from institutions,
equipment, and personnel associated with fire. They may spend time at the local fire depart-
ment, set fires to be affiliated with the fire department, or even become firefighters. Individ-
uals with this disorder experience pleasure, gratification, or relief when setting the fire,
witnessing its effects, or participating in its aftermath (Criterion D). The fire setting is not
done for monetary gain, as an expression of sociopolitical ideology, to conceal criminal ac-
tivity, to express anger or vengeance, to improve one’s living circumstances, or in response
to a delusion or a hallucination (Criterion E). The fire setting does not result from impaired
judgment (e.g., in major neurocognitive disorder or intellectual disability [intellectual devel-
opmental disorder]). The diagnosis is not made if the fire setting is better explained by con-
duct disorder, a manic episode, or antisocial personality disorder (Criterion F).
Associated Features Supporting Diagnosis
Individuals with pyromania may make considerable advance preparation for starting a
fire. They may be indifferent to the consequences to life or property caused by the fire, or
Pyromania 477
they may derive satisfaction from the resulting property destruction. The behaviors may
lead to property damage, legal consequences, or injury or loss of life to the fire setter or to
others. Individuals who impulsively set fires (who may or may not have pyromania) often
have a current or past history of alcohol use disorder.
Prevalence
The population prevalence of pyromania is not known. The lifetime prevalence of fire set-
ting, which is just one component of pyromania and not sufficient for a diagnosis by itself,
was reported as 1.13% in a population sample, but the most common comorbidities were
antisocial personality disorder, substance use disorder, bipolar disorder, and pathological
gambling (gambling disorder). In contrast, pyromania as a primary diagnosis appears to
be very rare. Among a sample of persons reaching the criminal system with repeated fire
setting, only 3.3% had symptoms that met full criteria for pyromania.
Development and Course
There are insufficient data to establish a typical age at onset of pyromania. The relation-
ship between fire setting in childhood and pyromania in adulthood has not been docu-
mented. In individuals with pyromania, fire-setting incidents are episodic and may wax
and wane in frequency. Longitudinal course is unknown. Although fire setting is a major
problem in children and adolescents (over 40% of those arrested for arson offenses in the
United States are younger than 18 years), pyromania in childhood appears to be rare. Ju-
venile fire setting is usually associated with conduct disorder, attention-deficit/hyperac-
tivity disorder, or an adjustment disorder.
Gender-Related Diagnostic Issues
Pyromania occurs much more often in males, especially those with poorer social skills and
learning difficulties.
Differential Diagnosis
Other causes of intentional fire setting. It is important to rule out other causes of fire
setting before giving the diagnosis of pyromania. Intentional fire setting may occur for
profit, sabotage, or revenge; to conceal a crime; to make a political statement (e.g., an act of
terrorism or protest); or to attract attention or recognition (e.g., setting a fire in order to dis-
cover it and save the day). Fire setting may also occur as part of developmental experi-
mentation in childhood (e.g., playing with matches, lighters, or fire).
Other mental disorders. A separate diagnosis of pyromania is not given when fire set-
ting occurs as part of conduct disorder, a manic episode, or antisocial personality disorder,
or if it occurs in response to a delusion or a hallucination (e.g., in schizophrenia) or is at-
tributable to the physiological effects of another medical condition (e.g., epilepsy). The di-
agnosis of pyromania should also not be given when fire setting results from impaired
judgment associated with major neurocognitive disorder, intellectual disability, or sub-
stance intoxication.
Comorbidity
There appears to be a high co-occurrence of substance use disorders, gambling disorder,
depressive and bipolar disorders, and other disruptive, impulse-control, and conduct dis-
orders with pyromania.
478 Disruptive, Impulse-Control, and Conduct Disorders
Kleptomania
Diagnostic Criteria 312.32 (F63.3)
A. Recurrent failure to resist impulses to steal objects that are not needed for personal
use or for their monetary value.
B. Increasing sense of tension immediately before committing the theft.
C. Pleasure, gratification, or relief at the time of committing the theft.
D. The stealing is not committed to express anger or vengeance and is not in response
to a delusion or a hallucination.
E. The stealing is not better explained by conduct disorder, a manic episode, or antisocial
personality disorder.
Diagnostic Features
The essential feature of kleptomania is the recurrent failure to resist impulses to steal items
even though the items are not needed for personal use or for their monetary value (Criterion
A). The individual experiences a rising subjective sense of tension before the theft (Criterion B)
and feels pleasure, gratification, or relief when committing the theft (Criterion C). The stealing
is not committed to express anger or vengeance, is not done in response to a delusion or hal-
lucination (Criterion D), and is not better explained by conduct disorder, a manic episode, or
antisocial personality disorder (Criterion E). The objects are stolen despite the fact that they are
typically of little value to the individual, who could have afforded to pay for them and often
gives them away or discards them. Occasionally the individual may hoard the stolen objects or
surreptitiously return them. Although individuals with this disorder will generally avoid
stealing when immediate arrest is probable (e.g., in full view of a police officer), they usually
do not preplan the thefts or fully take into account the chances of apprehension. The stealing is
done without assistance from, or collaboration with, others.
Associated Features Supporting Diagnosis
Individuals with kleptomania typically attempt to resist the impulse to steal, and they are
aware that the act is wrong and senseless. The individual frequently fears being appre-
hended and often feels depressed or guilty about the thefts. Neurotransmitter pathways
associated with behavioral addictions, including those associated with the serotonin, do-
pamine, and opioid systems, appear to play a role in kleptomania as well.
Prevalence
Kleptomania occurs in about 4%-24% of individuals arrested for shoplifting. Its preva-
lence in the general population is very rare, at approximately 0.3% 0.6%. Females outnum-
ber males at a ratio of 3:1.
Development and Course
Age at onset of kleptomania is variable, but the disorder often begins in adolescence. How-
ever, the disorder may begin in childhood, adolescence, or adulthood, and in rare cases
in late adulthood. There is little systematic information on the course of kleptomania, but
three typical courses have been described: sporadic with brief episodes and long periods
of remission; episodic with protracted periods of stealing and periods of remission; and
chronic with some degree of fluctuation. The disorder may continue for years, despite
multiple convictions for shoplifting.
Other Specified Disruptive, Impuise-Control, and Conduct Disorder 479
Risk and Prognostic Factors
Genetic and physiological. There are no controlled family history studies of kleptoma-
nia. However, first-degree relatives of individuals with kleptomania may have higher
rates of obsessive-compulsive disorder than the general population. There also appears to
be a higher rate of substance use disorders, including alcohol use disorder, in relatives of
individuals with kleptomania than in the general population.
Functionai Consequences of Kleptomania
The disorder may cause legal, family, career, and personal difficulties.
Differentiai Diagnosis
Ordinary theft. Kleptomania should be distinguished from ordinary acts of theft or
shoplifting. Ordinary theft (whether planned or impulsive) is deliberate and is motivated
by the usefulness of the object or its monetary worth. Some individuals, especially adoles-
cents, may also steal on a dare, as an act of rebellion, or as a rite of passage. The diagnosis
is not made unless other characteristic features of kleptomania are also present. Klepto-
mania is exceedingly rare, whereas shoplifting is relatively common.
Malingering. In malingering, individuals may simulate the symptoms of kleptomania to
avoid criminal prosecution.
Antisocial personality disorder and conduct disorder. Antisocial personality disorder
and conduct disorder are distinguished from kleptomania by a general pattern of antiso-
cial behavior.
Manic episodes, psychotic episodes, and major neurocognitive disorder. Kleptomania
should be distinguished from intentional or inadvertent stealing that may occur during a
manic episode, in response to delusions or hallucinations (as in, e.g., schizophrenia), or as
a result of a major neurocognitive disorder.
Comorbidity
Kleptomania may be associated with compulsive buying as well as with depressive and
bipolar disorders (especially major depressive disorder), anxiety disorders, eating disor-
ders (particularly bulimia nervosa), personality disorders, substance use disorders (espe-
cially alcohol use disorder), and other disruptive, impulse-control, and conduct disorders.
Other Specified Disruptive, Impulse-Control,
and Conduct Disorder
312.89 (F91.8)
This category applies to presentations in which symptoms characteristic of a disruptive,
impulse-control, and conduct disorder that cause clinicaily significant distress or impair-
ment in social, occupational, or other important areas of functioning predominate but do
not meet the full criteria for any of the disorders in the disruptive, impulse-control, and con-
duct disorders diagnostic class. The other specified disruptive, impulse-control, and con-
duct disorder category is used in situations in which the clinician chooses to communicate
the specific reason that the presentation does not meet the criteria for any specific disrup-
tive, impulse-control, and conduct disorder. This is done by recording “other specified dis-
ruptive, impulse-control, and conduct disorder’ followed by the specific reason (e.g.,
“recurrent behavioral outbursts of insufficient frequency”).
480 Disruptive, Impulse-Control, and Conduct Disorders
Unspecified Disruptive, Impulse-Control,
and Conduct Disorder
312.9 (F91.9)
This category applies to presentations in which symptoms characteristic of a disruptive,
impulse-control, and conduct disorder that cause clinically significant distress or impair-
ment in social, occupational, or other important areas of functioning predominate but do
not meet the full criteria for any of the disorders in the disruptive, impulse-control, and con-
duct disorders diagnostic class. The unspecified disruptive, impulse-control, and conduct
disorder category is used in situations in which the clinician chooses not to specify the rea-
son that the criteria are not met for a specific disruptive, impulse-control, and conduct dis-
order, and includes presentations in which there is insufficient information to make a more
specific diagnosis (e.g., in emergency room settings).
ae eer
- Substance-Related and
Addictive Disorders
The substance-related disorders encompass 10 separate classes of drugs: alco-
hol; caffeine; cannabis; hallucinogens (with separate categories for phencyclidine [or sim-
ilarly acting arylcyclohexylamines] and other hallucinogens); inhalants; opioids;
sedatives, hypnotics, and anxiolytics; stimulants (amphetamine-type substances, cocaine,
and other stimulants); tobacco; and other (or unknown) substances. These 10 classes are
not fully distinct. All drugs that are taken in excess have in common direct activation of
the brain reward system, which is involved in the reinforcement of behaviors and the pro-
duction of memories. They produce such an intense activation of the reward system that
normal activities may be neglected. Instead of achieving reward system activation
through adaptive behaviors, drugs of abuse directly activate the reward pathways. The
pharmacological mechanisms by which each class of drugs produces reward are different,
but the drugs typically activate the system and produce feelings of pleasure, often re-
ferred to as a “high.” Furthermore, individuals with lower levels of self-control, which
may reflect impairments of brain inhibitory mechanisms, may be particularly predisposed
to develop substance use disorders, suggesting that the roots of substance use disorders
for some persons can be seen in behaviors long before the onset of actual substance use
itself.
In addition to the substance-related disorders, this chapter also includes gambling dis-
order, reflecting evidence that gambling behaviors activate reward systems similar to
those activated by drugs of abuse and produce some behavioral symptoms that appear
comparable to those produced by the substance use disorders. Other excessive behavioral
patterns, such as Internet gaming, have also been described, but the research on these and
other behavioral syndromes is less clear. Thus, groups of repetitive behaviors, which some
term behavioral addictions, with such subcategories as “sex addiction,” “exercise addiction,”
or “shopping addiction,” are not included because at this time there is insufficient peer-re-
viewed evidence to establish the diagnostic criteria and course descriptions needed to
identify these behaviors as mental disorders.
The substance-related disorders are divided into two groups: substance use disorders
and substance-induced disorders. The following conditions may be classified as sub-
stance-induced: intoxication, withdrawal, and other substance /medication-induced men-
tal disorders (psychotic disorders, bipolar and related disorders, depressive disorders,
anxiety disorders, obsessive-compulsive and related disorders, sleep disorders, sexual dys-
functions, delirium, and neurocognitive disorders).
The current section begins with a general discussion of criteria sets for a substance
use disorder, substance intoxication and withdrawal, and other substance/medication-
induced mental disorders, at least some of which are applicable across classes of sub-
stances. Reflecting some unique aspects of the 10 substance classes relevant to this chapter,
the remainder of the chapter is organized by the class of substance and describes their
unique aspects. To facilitate differential diagnosis, the text and criteria for the remaining
substance/medication-induced mental disorders are included with disorders with which
they share phenomenology (e.g., substance /medication-induced depressive disorder is in
the chapter “Depressive Disorders”). The broad diagnostic categories associated with each
specific group of substances are shown in Table 1.
481
Substance-Related and Addictive Disorders
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Substance Use Disorders 483
Substance-Related Disorders
Substance Use Disorders
Features
The essential feature of a substance use disorder is a cluster of cognitive, behavioral, and
physiological symptoms indicating that the individual continues using the substance de-
spite significant substance-related problems. As seen in Table 1, the diagnosis of a sub-
stance use disorder can be applied to all 10 classes included in this chapter except caffeine.
For certain classes some symptoms are less salient, and in a few instances not all symptoms
apply (e.g., withdrawal symptoms are not specified for phencyclidine use disorder, other
hallucinogen use disorder, or inhalant use disorder).
An important characteristic of substance use disorders is an underlying change in brain cir-
cuits that may persist beyond detoxification, particularly in individuals with severe disorders.
The behavioral effects of these brain changes may be exhibited in the repeated relapses and in-
tense drug craving when the individuals are exposed to drug-related stimuli. These persistent
drug effects may benefit from long-term approaches to treatment.
Overall, the diagnosis of a substance use disorder is based on a pathological pattern of
behaviors related to use of the substance. To assist with organization, Criterion A criteria can
be considered to fit within overall groupings of impaired control, social impairment, risky use,
and pharmacological criteria. Impaired control over substance use is the first criteria grouping
(Criteria 1-4). The individual may take the substance in larger amounts or over a longer pe-
riod than was originally intended (Criterion 1). The individual may express a persistent de-
sire to cut down or regulate substance use and may report multiple unsuccessful efforts to
decrease or discontinue use (Criterion 2). The individual may spend a great deal of time ob-
taining the substance, using the substance, or recovering from its effects (Criterion 3). In
some instances of more severe substance use disorders, virtually all of the individual's daily
activities revolve around the substance. Craving (Criterion 4) is manifested by an intense de-
sire or urge for the drug that may occur at any time but is more likely when in an environ-
ment where the drug previously was obtained or used. Craving has also been shown to
involve classical conditioning and is associated with activation of specific reward structures
in the brain. Craving is queried by asking if there has ever been a time when they had such
strong urges to take the drug that they could not think of anything else. Current craving is of-
ten used as a treatment outcome measure because it may be a signal of impending relapse.
Social impairment is the second grouping of criteria (Criteria 5-7), Recurrent substance
use may result in a failure to fulfill major role obligations at work, school, or home (Crite-
rion 5). The individual may continue substance use despite having persistent or recurrent
social or interpersonal problems caused or exacerbated by the effects of the substance (Cri-
terion 6). Important social, occupational, or recreational activities may be given up or re-
duced because of substance use (Criterion 7). The individual may withdraw from family
activities and hobbies in order to use the substance.
Risky use of the substance is the third grouping of criteria (Criteria 8-9). This may take
the form of recurrent substance use in situations in which it is physically hazardous (Cri-
terion 8). The individual may continue substance use despite knowledge of having a per-
sistent or recurrent physical or psychological] problem that is likely to have been caused or
exacerbated by the substance (Criterion 9). The key issue in evaluating this criterion is not
the existence of the problem, but rather the individual's failure to abstain from using the
substance despite the difficulty it is causing.
484 Substance-Related and Addictive Disorders
Pharmacological criteria are the final grouping (Criteria 10 and 11). Tolerance (Crite-
rion 10) is signaled by requiring a markedly increased dose of the substance to achieve the
desired effect or a markedly reduced effect when the usual dose is consumed. The degree
to which tolerance develops varies greatly across different individuals as well as across
substances and may involve a variety of central nervous system effects. For example, tol-
erance to respiratory depression and tolerance to sedating and motor coordination may
develop at different rates, depending on the substance. Tolerance may be difficult to de-
termine by history alone, and laboratory tests may be helpful (e.g., high blood levels of the
substance coupled with little evidence of intoxication suggest that tolerance is likely). Tol-
erance must also be distinguished from individual variability in the initial sensitivity to
the effects of particular substances. For example, some first-time alcohol drinkers show
very little evidence of intoxication with three or four drinks, whereas others of similar
weight and drinking histories have slurred speech and incoordination.
Withdrawal (Criterion 11) is a syndrome that occurs when blood or tissue concentra-
tions of a substance decline in an individual who had maintained prolonged heavy use of
the substance. After developing withdrawal symptoms, the individual is likely to con-
sume the substance to relieve the symptoms. Withdrawal symptoms vary greatly across
the classes of substances, and separate criteria sets for withdrawal are provided for the
drug classes. Marked and generally easily measured physiological signs of withdrawal are
common with alcohol, opioids, and sedatives, hypnotics, and anxiolytics. Withdrawal
signs and symptoms with stimulants (amphetamines and cocaine), as well as tobacco and
cannabis, are often present but may be less apparent. Significant withdrawal has not been
documented in humans after repeated use of phencyclidine, other hallucinogens, and in-
halants; therefore, this criterion is not included for these substances. Neither tolerance nor
withdrawal is necessary for a diagnosis of a substance use disorder. However, for most
classes of substances, a past history of withdrawal is associated with a more severe clinical
course (i.e., an earlier onset of a substance use disorder, higher levels of substance intake,
and a greater number of substance-related problems).
Symptoms of tolerance and withdrawal occurring during appropriate medical treat-
ment with prescribed medications (e.g., opioid analgesics, sedatives, stimulants) are spe-
cifically not counted when diagnosing a substance use disorder. The appearance of normal,
expected pharmacological tolerance and withdrawal during the course of medical treat-
ment has been known to lead to an erroneous diagnosis of “addiction” even when these
were the only symptoms present. Individuals whose only symptoms are those that occur
as a result of medical treatment (i-e., tolerance and withdrawal as part of medical care
when the medications are taken as prescribed) should not receive a diagnosis solely on the
basis of these symptoms. However, prescription medications can be used inappropriately,
and a substance use disorder can be correctly diagnosed when there are other symptoms
of compulsive, drug-seeking behavior.
Severity and Specifiers
Substance use disorders occur in a broad range of severity, from mild to severe, with se-
verity based on the number of symptom criteria endorsed. As a general estimate of sever-
ity, a mild substance use disorder is suggested by the presence of two to three symptoms,
moderate by four to five symptoms, and severe by six or more symptoms. Changing severity
across time is also reflected by reductions or increases in the frequency and/or dose of
substance use, as assessed by the individual’s own report, report of knowledgeable others,
clinician’s observations, and biological testing. The following course specifiers and descrip-
tive features specifiers are also available for substance use disorders: “in early remission,”
“in sustained remission,” “on maintenance therapy,” and “in a controlled environment.”
Definitions of each are provided within respective criteria sets.
Substance Use Disorders 485
Recording Procedures for Substance Use Disorders
The clinician should use the code that applies to the class of substances but record the
name of the specific substance. For example, the clinician should record 304.10 (F13.20)
moderate alprazolam use disorder (rather than moderate sedative, hypnotic, or anxiolytic
use disorder) or 305.70 (F15.10) mild methamphetamine use disorder (rather than mild
stimulant use disorder). For substances that do not fit into any of the classes (e.g., anabolic
steroids), the appropriate code for “other substance use disorder” should be used and the
specific substance indicated (e.g., 305.90 [F19.10] mild anabolic steroid use disorder). If the
substance taken by the individual is unknown, the code for the class “other (or unknown)”
should be used (e.g., 304.90 [F19.20] severe unknown substance use disorder). If criteria
are met for more than one substance use disorder, all should be diagnosed (e.g., 304.00
{F11.20] severe heroin use disorder; 304.20 [F14.20] moderate cocaine use disorder).
The appropriate ICD-10-CM code for a substance use disorder depends on whether
there is a comorbid substance-induced disorder (including intoxication and withdrawal). In
the above example, the diagnostic code for moderate alprazolam use disorder, F13.20, re-
flects the absence of a comorbid alprazolam-induced mental disorder. Because ICD-10-CM
codes for substance-induced disorders indicate both the presence (or absence) and severity
of the substance use disorder, ICD-10-CM codes for substance use disorders can be used
only in the absence of a substance-induced disorder. See the individual substance-specific
sections for additional coding information.
Note that the word addiction is not applied as a diagnostic term in this classification,
although it is in common usage in many countries to describe severe problems related to
compulsive and habitual use of substances. The more neutral term substance use disorder is
used to describe the wide range of the disorder, from a mild form to a severe state of chron-
ically relapsing, compulsive drug taking. Some clinicians will choose to use the word ad-
diction to describe more extreme presentations, but the word is omitted from the official
DSM-5 substance use disorder diagnostic terminology because of its uncertain definition
and its potentially negative connotation.
Substance-Induced Disorders
The overall category of substance-induced disorders includes intoxication, withdrawal,
and other substance/medication-induced mental disorders (e.g., substance-induced psy-
chotic disorder, substance-induced depressive disorder).
Substance Intoxication and Withdrawal
Criteria for substance intoxication are included within the substance-specific sections of
this chapter. The essential feature is the development of a reversible substance-specific
syndrome due to the recent ingestion of a substance (Criterion A). The clinically significant
problematic behavioral or psychological changes associated with intoxication (e.g., bellig-
erence, mood lability, impaired judgment) are attributable to the physiological effects of
the substance on the central nervous system and develop during or shortly after use of the
substance (Criterion B). The symptoms are not attributable to another medical condition
and are not better explained by another mental disorder (Criterion D). Substance intoxi-
cation is common among those with a substance use disorder but also occurs frequently in
individuals without a substance use disorder. This category does not apply to tobacco.
The most common changes in intoxication involve disturbances of perception, wake-
fulness, attention, thinking, judgment, psychomotor behavior, and interpersonal behav-
ior. Short-term, or “acute,” intoxications may have different signs and symptoms than
486 Substance-Related and Addictive Disorders
sustained, or “chronic,” intoxications. For example, moderate cocaine doses may initially
produce gregariousness, but social withdrawal may develop if such doses are frequently
repeated over days or weeks.
When used in the physiological sense, the term intoxication is broader than substance
intoxication as defined here. Many substances may produce physiological or psychologi-
cal changes that are not necessarily problematic, For example, an individual with tachy-
cardia from substance use has a physiological effect, but if this is the only symptom in the
absence of problematic behavior, the diagnosis of intoxication would not apply. Intoxica-
tion may sometimes persist beyond the time when the substance is detectable in the body.
This may be due to enduring central nervous system effects, the recovery of which takes
longer than the time for elimination of the substance. These longer-term effects of intoxi-
cation must be distinguished from withdrawal (i.e., symptoms initiated by a decline in
blood or tissue concentrations of a substance).
Criteria for substance withdrawal are included within the substance-specific sections of
this chapter. The essential feature is the development of a substance-specific problematic be-
havioral change, with physiological and cognitive concomitants, that is due to the cessation of,
or reduction in, heavy and prolonged substance use (Criterion A). The substance-specific syn-
drome causes clinically significant distress or impairment in social, occupational, or other im-
portant areas of functioning (Criterion C). The symptoms are not due to another medical
condition and are not better explained by another mental disorder (Criterion D). Withdrawal
is usually, but not always, associated with a substance use disorder. Most individuals with
withdrawal have an urge to re-administer the substance to reduce the symptoms.
Route of Administration and Speed of Substance Effects
Routes of administration that produce more rapid and efficient absorption into the blood-
stream (e.g., intravenous, smoking, intranasal “snorting”) tend to result in a more intense
intoxication and an increased likelihood of an escalating pattern of substance use leading
to withdrawal. Similarly, rapidly acting substances are more likely than slower-acting
substances to produce immediate intoxication.
Duration of Effects
Within the same drug category, relatively short-acting substances tend to have a higher
potential for the development of withdrawal than do those with a longer duration of ac-
tion. However, longer-acting substances tend to have longer withdrawal duration. The
half-life of the substance parallels aspects of withdrawal: the longer the duration of action,
the longer the time between cessation and the onset of withdrawal symptoms and the lon-
ger the withdrawal duration. In general, the longer the acute withdrawal period, the less
intense the syndrome tends to be.
Use of Multiple Substances
Substance intoxication and withdrawal often involve several substances used simultane-
ously or sequentially. In these cases, each diagnosis should be recorded separately.
Associated Laboratory Findings
Laboratory analyses of blood and urine samples can help determine recent use and the specific
substances involved. However, a positive laboratory test result does not by itself indicate that
the individual has a pattern of substance use that meets criteria for a substance-induced or sub-
stance use disorder, and a negative test result does not by itself rule out a diagnosis.
Laboratory tests can be useful in identifying withdrawal. If the individual presents
with withdrawal from an unknown substance, laboratory tests may help identify the sub-
stance and may also be helpful in differentiating withdrawal from other mental disorders.
Substance-Induced Disorders 487
In addition, normal functioning in the presence of high blood levels of a substance sug-
gests considerakle tolerance.
Development and Course
Individuals ages 18-24 years have relatively high prevalence rates for the use of virtually
every substance. Intoxication is usually the initial substance-related disorder and often be-
gins in the teens. Withdrawal can occur at any age as long as the relevant drug has been
taken in sufficient doses over an extended period of time.
Recording Procedures for Intoxication and Withdrawal
The clinician should use the code that applies to the class of substances but record the
name of the specific substance. For example, the clinician should record 292.0 (F13.239) seco-
barbital withdrawal (rather than sedative, hypnotic, or anxiolytic withdrawal) or 292.89
(F15.129) methamphetamine intoxication (rather than stimulant intoxication). Note that
the appropriate ICD-10-CM diagnostic code for intoxication depends on whether there is
a comorbid substance use disorder. In this case, the F15.129 code for methamphetamine in-
dicates the presence of a comorbid mild methamphetamine use disorder. If there had been
no comorbid methamphetamine use disorder, the diagnostic code would have been
F15.929. ICD-10-CM coding rules require that all withdrawal codes imply a comorbid
moderate to severe substance use disorder for that substance. In the above case, the code
for secobarbital withdrawal (F13.239) indicates the comorbid presence of a moderate to se-
vere secobarbital use disorder. See the coding note for the substance-specific intoxication
and withdrawal syndromes for the actual coding options.
For substances that do not fit into any of the classes (e.g., anabolic steroids), the appropriate
code for “other substance intoxication” should be used and the specific substance indicated
(e.g., 292.89 [F19.929] anabolic steroid intoxication). If the substance taken by the individual is
unknown, the code for the class “other (or unknown)” should be used (e.g., 292.89 [F19.929]
unknown substance intoxication). If there are symptoms or problems associated with a partic-
ular substance but criteria are not met for any of the substance-specific disorders, the unspec-
ified category can be used (e.g., 292.9 [F12.99] unspecified cannabis-related disorder).
As noted above, the substance-related codes in ICD-10-CM combine the substance use dis-
order aspect of the clinical picture and the substance-induced aspect into a single combined
code. Thus, if both heroin withdrawal and moderate heroin use disorder are present, the single
code F11.23 is given to cover both presentations. In ICD-9-CM, separate diagnostic codes
(292.0 and 304.00) are given to indicate withdrawal and a moderate heroin use disorder, re-
spectively. See the individual substance-specific sections for additional coding information.
Substance/Medication-Induced Mental Disorders
The substance/medication-induced mental disorders are potentially severe, usually tem-
porary, but sometimes persisting central nervous system (CNS) syndromes that develop
in the context of the effects of substances of abuse, medications, or several toxins. They are
distinguished from the substance use disorders, in which a cluster of cognitive, behav-
ioral, and physiological symptoms contribute to the continued use of a substance despite
significant substance-related problems. The substance/medication-induced mental disor-
ders may be induced by the 10 classes of substances that produce substance use disorders,
or by a great variety of other medications used in medical treatment. Each substance-
induced mental disorder is described in the relevant chapter (e.g., “Depressive Disorders,”
“Neurocognitive Disorders”), and therefore, only a brief description is offered here. All
substance /medication-induced disorders share common characteristics. It is important to
recognize these common features to aid in the detection of these disorders. These features
are described as follows:
488 Substance-Related and Addictive Disorders
A. The disorder represents a clinically significant symptomatic presentation of a relevant
mental disorder.
B. There is evidence from the history, physical examination, or laboratory findings of
both of the following:
1. The disorder developed during or within 1 month of a substance intoxication or
withdrawal or taking a medication; and
2. The involved substance/medication is capable of producing the mental disorder.
C. The disorder is not better explained by an independent mental disorder (i.e., one that is
not substance- or medication-induced). Such evidence of an independent mental dis-
order could include the following:
1. The disorder preceded the onset of severe intoxication or withdrawal or exposure
to the medication; or
2. The full mental disorder persisted for a substantial period of time (e.g., at least 1 month)
after the cessation of acute withdrawal or severe intoxication or taking the medica-
tion. This criterion does not apply to substance-induced neurocognitive disorders
or hallucinogen persisting perception disorder, which persist beyond the cessation
of acute intoxication or withdrawal.
. The disorder does not occur exclusively during the course of a delirium.
The disorder causes clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning.
mo
Features
Some generalizations can be made regarding the categories of substances capable of produc-
ing clinically relevant substance-induced mental disorders. In general, the more sedating
drugs (sedative, hypnotics, or anxiolytics, and alcohol) can produce prominent and clini-
cally significant depressive disorders during intoxication, while anxiety conditions are likely
to be observed during withdrawal syndromes from these substances. Also, during intoxica-
tion, the more stimulating substances (e.g., amphetamines and cocaine) are likely to be as-
sociated with substance-induced psychotic disorders and substance-induced anxiety
disorders, with substance-induced major depressive episodes observed during withdrawal.
Both the more sedating and more stimulating drugs are likely to produce significant but
temporary sleep and sexual disturbances. An overview of the relationship between specific
categories of substances and specific psychiatric syndromes is presented in Table 1.
The medication-induced conditions include what are often idiosyncratic CNS reac-
tions or relatively extreme examples of side effects for a wide range of medications taken
for a variety of medical concerns. These include neurocognitive complications of anesthet-
ics, antihistamines, antihypertensives, and a variety of other medications and toxins (e.g.,
organophosphates, insecticides, carbon monoxide), as described in the chapter on neuro-
cognitive disorders. Psychotic syndromes may be temporarily experienced in the context
of anticholinergic, cardiovascular, and steroid drugs, as well as during use of stimulant-
like and depressant-like prescription or over-the-counter drugs. Temporary but severe
mood disturbances can be observed with a wide range of medications, including steroids,
antihypertensives, disulfiram, and any prescription or over-the-counter depressant or
stimulant-like substances. A similar range of medications can be associated with tempo-
rary anxiety syndromes, sexual dysfunctions, and conditions of disturbed sleep.
In general, to be considered a substance/medication-induced mental disorder, there
must be evidence that the disorder being observed is not likely to be better explained by an
independent mental condition. The latter are most likely to be seen if the mental disorder
was present before the severe intoxication or withdrawal or medication administration, or,
with the exception of several substance-induced persisting disorders listed in Table 1, con-
tinued more than 1 month after cessation of acute withdrawal, severe intoxication, or use
Substance-Induced Disorders 489
of the medications. When symptoms are only observed during a delirium (e.g., alcohol
withdrawal deljrium), the mental disorder should be diagnosed as a delirium, and the
psychiatric syndrome occurring during the delirium should not also be diagnosed sepa-
rately, as many symptoms (including disturbances in mood, anxiety, and reality testing)
are commonly seen during agitated, confused states. The features associated with each rel-
evant major mental disorder are similar whether observed with independent or sub-
stance/medication-induced mental disorders. However, individuals with substance/
medication-induced mental disorders are likely to also demonstrate the associated fea-
tures seen with the specific category of substance or medication, as listed in other subsec-
tions of this chapter.
Development and Course
Substance-induced mental disorders develop in the context of intoxication or withdrawal
from substances of abuse, and medication-induced mental disorders are seen with pre-
scribed or over-the-counter medications that are taken at the suggested doses. Both condi-
tions are usually temporary and likely to disappear within 1 month or so of cessation of acute
withdrawal, severe intoxication, or use of the medication. Exceptions to these generaliza-
tions occur for certain long-duration substance-induced disorders: substance-associated
neurocognitive disorders that relate to conditions such as alcohol-induced neurocognitive
disorder, inhalant-induced neurocognitive disorder, and sedative-, hypnotic-, or anxiolytic-
induced neurocognitive disorder; and hallucinogen persisting perception disorder (“flash-
backs”; see the section “Hallucinogen-Related Disorders” later in this chapter). However,
most other substance /medication-induced mental disorders, regardless of the severity of
the symptoms, are likely to improve relatively quickly with abstinence and unlikely to re-
main clinically relevant for more than 1 month after complete cessation of use.
As is true of many consequences of heavy substance use, some individuals are more
and others less prone toward specific substance-induced disorders. Similar types of pre-
dispositions may make some individuals more likely to develop psychiatric side effects of
some types of medications, but not others. However, it is unclear whether individuals
with family histories or personal prior histories with independent psychiatric syndromes
are more likely to develop the induced syndrome once the consideration is made as to
whether the quantity and frequency of the substance was sufficient to lead to the devel-
opment of a substance-induced syndrome.
There are indications that the intake of substances of abuse or some medications with
psychiatric side effects in the context of a preexisting mental disorder is likely to result in
an intensification of the preexisting independent syndrome. The risk for substance/med-
ication-induced mental disorders is likely to increase with both the quantity and the fre-
quency of consumption of the relevant substance.
The symptom profiles for the substance/medication-induced mental disorders resem-
ble independent mental disorders. While the symptoms of substance /medication-in-
duced mental disorders can be identical to those of independent mental disorders (e.g.,
delusions, hallucinations, psychoses, major depressive episodes, anxiety syndromes), and
although they can have the same severe consequences (e.g., suicide), most induced mental
disorders are likely to improve in a matter of days to weeks of abstinence.
The substance /medication-induced mental disorders are an important part of the dif-
ferential diagnoses for the independent psychiatric conditions. The importance of recog-
nizing an induced mental disorder is similar to the relevance of identifying the possible
role of some medical conditions and medication reactions before diagnosing an indepen-
dent mental disorder. Symptoms of substance- and medication-induced mental disorders
may be identical cross-sectionally to those of independent mental disorders but have dif-
ferent treatments and prognoses from the independent condition.
490 Substance-Related and Addictive Disorders
Functional Consequences of Substance/Medication-
Induced Mental Disorders
The same consequences related to the relevant independent mental disorder (e.g., suicide
attempts) are likely to apply to the substance/medication-induced mental disorders, but
these are likely to disappear within 1 month after abstinence. Similarly, the same func-
tional consequences associated with the relevant substance use disorder are likely to be seen
for the substance-induced mental disorders.
Recording Procedures for Substance/Medication-
Induced Mental Disorders
Coding notes and separate recording procedures for ICD-9-CM and ICD-10-CM codes for
other specific substance/medication-induced mental disorders are provided in other
chapters of the manual with disorders with which they share phenomenology (see the sub-
stance/medication-induced mental disorders in these chapters: “Schizophrenia Spectrum
and Other Psychotic Disorders,” “Bipolar and Related Disorders,” “Depressive Disor-
ders,” “Anxiety Disorders,” “Obsessive-Compulsive and Related Disorders,” “Sleep-
Wake Disorders,” “Sexual Dysfunctions,” and “Neurocognitive Disorders”). Generally,
for ICD-9-CM, if a mental disorder is induced by a substance use disorder, a separate di-
agnostic code is given for the specific substance use disorder, in addition to the code for the
substance /medication-induced mental disorder. For ICD-10-CM, a single code combines
the substance-induced mental disorder with the substance use disorder. A separate diag-
nosis of the comorbid substance use disorder is not given, although the name and severity
of the specific substance use disorder (when present) are used when recording the sub-
stance /medication-induced mental disorder. ICD-10-CM codes are also provided for sit-
uations in which the substance/medication-induced mental disorder is not induced by a
substance use disorder (e.g., when a disorder is induced by one-time use of a substance or
medication). Additional information needed to record the diagnostic name of the sub-
stance/medication-induced mental disorder is provided in the section “Recording Proce-
dures” for each substance /medication-induced mental disorder in its respective chapter.
Alcohol-Related Disorders
Alcohol Use Disorder
Alcohol Intoxication
Alcohol Withdrawal
Other Alcohol-Induced Disorders
Unspecified Alcohol-Related Disorder
Alcohol Use Disorder
Diagnostic Criteria
A. A problematic pattern of alcohol use leading to clinically significant impairment or dis-
tress, as manifested by at least two of the following, occurring within a 12-month period:
1. Alcohol is often taken in larger amounts or over a longer period than was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control alcohol use.
Alcohol Use Disorder 491
3. A great deal of time is spent in activities necessary to obtain alcohol, use alcohol,
or recover from its effects.
4. Craving, or a strong desire or urge to use aicohol.
5. Recurrent alcohol use resulting in a failure to fulfitl major roie obligations at work,
school, or home.
6. Continued alcohol use despite having persistent or recurrent social or interpersonal
problems caused or exacerbated by the effects of alcohol.
7. Important social, occupational, or recreational activities are given up or reduced be-
cause of alcohol use.
8. Recurrent alcohol use in situations in which it is physically hazardous.
9. Alcohol use is continued despite knowledge of having a persistent or recurrent
physical or psychological problem that is likely to have been caused or exacerbated
by alcohol.
10. Tolerance, as defined by either of the following:
a. Aneed for markedly increased amounts of alcohoi to achieve intoxication or de-
sired effect.
b. A markedly diminished effect with continued use of the same amount of alcohol.
11. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for aicohoi (refer to Criteria A and B of
the criteria set for alcohol withdrawal, pp. 499-500).
b. Alcohol (or a closely related substance, such as a benzodiazepine) is taken to
relieve or avoid withdrawal symptoms.
Specify if:
In early remission: After full criteria for alcohol use disorder were previously met,
none of the criteria for alcohol use disorder have been met for at least 3 months but for
less than 12 months (with the exception that Criterion A4, “Craving, or a strong desire
or urge to use alcohol,” may be met).
In sustained remission: After full criteria for alcohol use disorder were previously
met, none of the criteria for aicohoi use disorder have been met at any time during a
period of 12 months or longer (with the exception that Criterion A4, “Craving, or a
strong desire or urge to use aicohol,” may be met).
Specify if:
In a controlled environment: This additional specifier is used if the individual is in an
environment where access to alcohol is restricted.
Code based on current severity: Note for ICD-10-CM codes: If an aicohol intoxication,
alcohol withdrawal, or another alcohol-induced mental disorder is also present, do not use
the codes below for alcohol use disorder. Instead, the comorbid alcohol use disorder is
indicated in the 4th character of the alcohol-induced disorder code (see the coding note
for alcohol intoxication, alcohol withdrawal, or a specific alcohol-induced mentai disorder).
For example, if there is comorbid alcohol intoxication and alcohoi use disorder, only the
alcohol intoxication code is given, with the 4th character indicating whether the comorbid
alcohol use disorder is mild, moderate, or severe: F10.129 for mild alcohol use disorder
with alcohol intoxication or F10.229 for a moderate or severe alcohol use disorder with al-
cohol intoxication.
Specify current severity:
305.00 (F10.10) Mild: Presence of 2-3 symptoms.
303.90 (F10.20) Moderate: Presence of 4-5 symptoms.
303.90 (F10.20) Severe: Presence of 6 or more symptoms.
492 Substance-Related and Addictive Disorders
Specifiers
“Ina controlled environment” applies as a further specifier of remission if the individual is
both in remission and in a controlled environment (i.e., in early remission in a controlled
environment or in sustained remission in a controlled environment). Examples of these
environments are closely supervised and substance-free jails, therapeutic communities,
and locked hospital units.
Severity of the disorder is based on the number of diagnostic criteria endorsed. For a
given individual, changes in severity of alcohol use disorder across time are also reflected
by reductions in the frequency (e.g., days of use per month) and/or dose (e.g., number of
standard drinks consumed per day) of alcohol used, as assessed by the individual's self-
report, report of knowledgeable others, clinician observations, and, when practical, bio-
logical testing (e.g., elevations in blood tests as described in the section “Diagnostic Mark-
ers” for this disorder).
Diagnostic Features
Alcohol use disorder is defined by a cluster of behavioral and physical symptoms, which
can include withdrawal, tolerance, and craving. Alcohol withdrawal is characterized by
withdrawal symptoms that develop approximately 4-12 hours after the reduction of in-
take following prolonged, heavy alcohol ingestion. Because withdrawal from alcohol can
be unpleasant and intense, individuals may continue to consume alcohol despite adverse
consequences, often to avoid or to relieve withdrawal symptoms. Some withdrawal symp-
toms (e.g., sleep problems) can persist at lower intensities for months and can contribute to
relapse. Once a pattern of repetitive and intense use develops, individuals with alcohol
use disorder may devote substantial periods of time to obtaining and consuming alcoholic
beverages.
Craving for alcohol is indicated by a strong desire to drink that makes it difficult to
think of anything else and that often results in the onset of drinking. School and job per-
formance may also suffer either from the aftereffects of drinking or from actual intoxica-
tion at school or on the job; child care or household responsibilities may be neglected; and
alcohol-related absences may occur from school or work. The individual may use alcohol
in physically hazardous circumstances (e.g., driving an automobile, swimming, operating
machinery while intoxicated). Finally, individuals with an alcohol use disorder may con-
tinue to consume alcohol despite the knowledge that continued consumption poses sig-
nificant physical (e.g., blackouts, liver disease), psychological (e.g., depression), social, or
interpersonal problems (e.g., violent arguments with spouse while intoxicated, child
abuse).
Associated Features Supporting Diagnosis
Alcohol use disorder is often associated with problems similar to those associated with
other substances (e.g., cannabis; cocaine; heroin; amphetamines; sedatives, hypnotics, or
anxiolytics). Alcohol may be used to alleviate the unwanted effects of these other
substances or to substitute for them when they are not available. Symptoms of conduct
problems, depression, anxiety, and insomnia frequently accompany heavy drinking and
sometimes precede it.
Repeated intake of high doses of alcohol can affect nearly every organ system, espe-
cially the gastrointestinal tract, cardiovascular system, and the central and peripheral ner-
vous systems. Gastrointestinal effects include gastritis, stomach or duodenal ulcers, and,
in about 15% of individuals who use alcohol heavily, liver cirrhosis and/or pancreatitis.
There is also an increased rate of cancer of the esophagus, stomach, and other parts of the
gastrointestinal tract. One of the most commonly associated conditions is low-grade hy-
pertension. Cardiomyopathy and other myopathies are less common but occur at an in-
Alcohol Use Disorder 493
creased rate among those who drink very heavily. These factors, along with marked
increases in levels of triglycerides and low-density lipoprotein cholesterol, contribute to
an elevated risk of heart disease. Peripheral neuropathy may be evidenced by muscular
weakness, paresthesias, and decreased peripheral sensation. More persistent central ner-
vous system effects include cognitive deficits, severe memory impairment, and degener-
ative changes in the cerebellum. These effects are related to the direct effects of alcohol or
of trauma and to vitamin deficiencies (particularly of the B vitamins, including thiamine).
One devastating central nervous system effect is the relatively rare alcohol-induced per-
sisting amnestic disorder, or Wernicke-Korsakoff syndrome, in which the ability to encode
new memory is severely impaired. This condition would now be described within the chap-
ter “Neurocognitive Disorders” and would be termed a substance/medication-induced neuro-
cognitive disorder.
Alcohol use disorder is an important contributor to suicide risk during severe intoxi-
cation and in the context of a temporary alcohol-induced depressive and bipolar disorder.
There is an increased rate of suicidal behavior as well as of completed suicide among in-
dividuals with the disorder.
Prevalence
Alcohol use disorder is a common disorder. In the United States, the 12-month prevalence
of alcohol use disorder is estimated to be 4.6% among 12- to 17-year-olds and 8.5% among
adults age 18 years and older in the United States. Rates of the disorder are greater among
adult men (12.4%) than among adult women (4.9%). Twelve-month prevalence of alcohol
use disorder among adults decreases in middle age, being greatest among individuals 18-
to 29-years-old (16.2%) and lowest among individuals age 65 years and older (1.5%).
Twelve-month prevalence varies markedly across race/ethnic subgroups of the U.S.
population. For 12- to 17-year-olds, rates are greatest among Hispanics (6.0%) and Native
Americans and Alaska Natives (5.7%) relative to whites (5.0%), African Americans (1.8%),
and Asian Americans and Pacific Islanders (1.6%). In contrast, among adults, the 12-month
prevalence of alcohol use disorder is clearly greater among Native Americans and Alaska
Natives (12.1%) than among whites (8.9%), Hispanics (7.9%), African Americans (6.9%),
and Asian Americans and Pacific Islanders (4.5%).
Development and Course
The first episode of alcohol intoxication is likely to occur during the mid-teens. Alcohol-
related problems that do not meet full criteria for a use disorder or isolated problems may
occur prior to age 20 years, but the age at onset of an alcohol use disorder with two or more
of the criteria clustered together peaks in the late teens or early to mid 20s. The large ma-
jority of individuals who develop alcohol-related disorders do so by their late 30s. The first
evidence of withdrawal is not likely to appear until after many other aspects of an alcohol
use disorder have developed. An earlier onset of alcohol use disorder is observed in ado-
lescents with preexisting conduct problems and those with an earlier onset of intoxication.
Alcohol use disorder has a variable course that is characterized by periods of remission
and relapse. A decision to stop drinking, often in response to a crisis, is likely to be followed
by a period of weeks or more of abstinence, which is often followed by limited periods of
controlled or nonproblematic drinking. However, once alcohol intake resumes, it is highly
likely that consumption will rapidly escalate and that severe problems will once again
develop.
Alcohol use disorder is often erroneously perceived as an intractable condition, per-
haps based on the fact that individuals who present for treatment typically have a history
of many years of severe alcohol-related problems. However, these most severe cases rep-
resent only a small proportion of individuals with this disorder, and the typical individual
with the disorder has a much more promising prognosis.
494 Substance-Related and Addictive Disorders
Among adolescents, conduct disorder and repeated antisocial behavior often co-occur
with alcohol- and with other substance-related disorders. While most individuals with al-
cohol use disorder develop the condition before age 40 years, perhaps 10% have later
onset. Age-related physical changes in older individuals result in increased brain suscep-
tibility to the depressant effects of alcohol; decreased rates of liver metabolism of a variety
of substances, including alcohol; and decreased percentages of body water. These changes
can cause older people to develop more severe intoxication and subsequent problems at
lower levels of consumption. Alcohol-related problems in older people are also especially
likely to be associated with other medical complications.
Risk and Prognostic Factors
Environmental. Environmental risk and prognostic factors may include cultural atti-
tudes toward drinking and intoxication, the availability of alcohol (including price),
acquired personal experiences with alcohol, and stress levels. Additional potential medi-
ators of how alcohol problems develop in predisposed individuals include heavier peer
substance use, exaggerated positive expectations of the effects of alcohol, and suboptimal
ways of coping with stress.
Genetic and physiological. Alcohol use disorder runs in families, with 40%-60% of the
variance of risk explained by genetic influences. The rate of this condition is three to four
times higher in close relatives of individuals with alcohol use disorder, with values highest
for individuals with a greater number of affected relatives, closer genetic relationships to
the affected person, and higher severity of the alcohol-related problems in those relatives.
A significantly higher rate of alcohol use disorders exists in the monozygotic twin than in
the dizygotic twin of an individual with the condition. A three- to fourfold increase in risk
has been observed in children of individuals with alcohol use disorder, even when these
children were given up for adoption at birth and raised by adoptive parents who did not
have the disorder.
Recent advances in our understanding of genes that operate through intermediate
characteristics (or phenotypes) to affect the risk of alcohol use disorder can help to identify
individuals who might be at particularly low or high risk for alcohol use disorder. Among
the low-risk phenotypes are the acute alcohol-related skin flush (seen most prominently in
Asians). High vulnerability is associated with preexisting schizophrenia or bipolar disor-
der, as well as impulsivity (producing enhanced rates of all substance use disorders and
gambling disorder), and a high risk specifically for alcohol use disorder is associated with
a low level of response (low sensitivity) to alcohol. A number of gene variations may ac-
count for low response to alcohol or modulate the dopamine reward systems; it is impor-
tant to note, however, that any one gene variation is likely to explain only 1%~-2% of the risk
for these disorders.
Course modifiers. In general, high levels of impulsivity are associated with an earlier
onset and more severe alcohol use disorder.
Culture-Related Diagnostic Issues
In most cultures, alcohol is the most frequently used intoxicating substance and contrib-
utes to considerable morbidity and mortality. An estimated 3.8% of all global deaths and
4.6% of global disability-adjusted life-years are attributable to alcohol. In the United States,
80% of adults (age 18 years and older) have consumed alcohol at some time in their lives,
and 65% are current drinkers (last 12 months). An estimated 3.6% of the world population
(15-64 years old) has a current (12-month) alcohol use disorder, with a lower prevalence
(1.1%) found in the African region, a higher rate (5.2%) found in the American region (North,
South, and Central America and the Caribbean), and the highest rate (10.9%) found in the
Eastern Europe region.
Alcohol Use Disorder 495
Polymorphisms of genes for the alcohol-metabolizing enzymes alcohol dehydroge-
nase and aldehyde dehydrogenase are most often seen in Asians and affect the response to
alcohol. When consuming alcohol, individuals with these gene variations can experience a
flushed face and palpitations, reactions that can be so severe as to limit or preclude future
alcohol consumption and diminish the risk for alcohol use disorder. These gene variations
are seen in as many as 40% of Japanese, Chinese, Korean, and related groups worldwide
and are related to lower risks for the disorder.
Despite small variations regarding individual criterion items, the diagnostic criteria
perform equally well across most race/ethnicity groups.
Gender-Related Diagnostic Issues
Males have higher rates of drinking and related disorders than females. However, because
females generally weigh less than males, have more fat and less water in their bodies, and
metabolize less alcohol in their esophagus and stomach, they are likely to develop higher
blood alcohol levels per drink than males. Females who drink heavily may also be more
vulnerable than males to some of the physical consequences associated with alcohol, in-
cluding liver disease.
Diagnostic Markers
Individuals whose heavier drinking places them at elevated risk for alcohol use disorder
can be identified both through standardized questionnaires and by elevations in blood test
results likely to be seen with regular heavier drinking. These measures do not establish a
diagnosis of an alcohol-related disorder but can be useful in highlighting individuals for
whom more information should be gathered. The most direct test available to measure al-
cohol consumption cross-sectionally is blood alcohol concentration, which can also be used to
judge tolerance to alcohol. For example, an individual with a concentration of 150 mg of
ethanol per deciliter (dL) of blood who does not show signs of intoxication can be pre-
sumed to have acquired at least some degree of tolerance to alcohol. At 200 mg/dL, most
nontolerant individuals demonstrate severe intoxication.
Regarding laboratory tests, one sensitive laboratory indicator of heavy drinking is a
modest elevation or high-normal levels (>35 units) of gamma-glutamyltransferase (GGT).
This may be the only laboratory finding. At least 70% of individuals with a high GGT level
are persistent heavy drinkers (i.e., consuming eight or more drinks daily on a regular basis).
A second test with comparable or even higher levels of sensitivity and specificity is carbo-
hydrate-deficient transferrin (CDT), with levels of 20 units or higher useful in identifying in-
dividuals who regularly consume eight or more drinks daily. Since both GGT and CDT
levels return toward normal within days to weeks of stopping drinking, both state markers
may be useful in monitoring abstinence, especially when the clinician observes increases,
rather than decreases, in these values over time—a finding indicating that the person is
likely to have returned to heavy drinking. The combination of tests for CDT and GGT may
have even higher levels of sensitivity and specificity than either test used alone. Additional
useful tests include the mean corpuscular volume (MCV), which may be elevated to high-
normal values in individuals who drink heavily—a change that is due to the direct toxic ef-
fects of alcohol on erythropoiesis. Although the MCV can be used to help identify those who
drink heavily, it is a poor method of monitoring abstinence because of the long half-life of
red blood cells. Liver function tests (e.g., alanine aminotransferase [ALT] and alkaline phos-
phatase) can reveal liver injury that is a consequence of heavy drinking. Other potential
markers of heavy drinking that are more nonspecific for alcohol but can help the clinician
think of the possible effects of alcohol include elevations in blood levels or lipids (e.g., tri-
glycerides and high-density lipoprotein cholesterol) and high-normal levels of uric acid.
Additional diagnostic markers relate to signs and symptoms that reflect the consequences
often associated with persistent heavy drinking. For example, dyspepsia, nausea, and bloat-
496 Substance-Related and Addictive Disorders
ing can accompany gastritis, and hepatomegaly, esophageal varices, and hemorrhoids may
reflect alcohol-induced changes in the liver. Other physical signs of heavy drinking include
tremor, unsteady gait, insomnia, and erectile dysfunction. Males with chronic alcohol use dis-
order may exhibit decreased testicular size and feminizing effects associated with reduced
testosterone levels. Repeated heavy drinking in females is associated with menstrual irregu-
larities and, during pregnancy, spontaneous abortion and fetal alcohol syndrome. Individu-
als with preexisting histories of epilepsy or severe head trauma are more likely to develop
alcohol-related seizures. Alcohol withdrawal may be associated with nausea, vomiting, gas-
tritis, hematemesis, dry mouth, puffy blotchy complexion, and mild peripheral edema.
Functional Consequences of Alcohol Use Disorder
The diagnostic features of alcohol use disorder highlight major areas of life functioning
likely to be impaired. These include driving and operating machinery, school and work,
interpersonal relationships and communication, and health. Alcohol-related disorders
contribute to absenteeism from work, job-related accidents, and low employee productiv-
ity. Rates are elevated in homeless individuals, perhaps reflecting a downward spiral in
social and occupational functioning, although most individuals with alcohol use disorder
continue to live with their families and function within their jobs.
Alcohol use disorder is associated with a significant increase in the risk of accidents, vi-
olence, and suicide. It is estimated that one in five intensive care unit admissions in some
urban hospitals is related to alcohol and that 40% of individuals in the United States ex-
perience an alcohol-related adverse event at some time in their lives, with alcohol account-
ing for up to 55% of fatal driving events. Severe alcohol use disorder, especially in
individuals with antisocial personality disorder, is associated with the commission of
criminal acts, including homicide. Severe problematic alcohol use also contributes to dis-
inhibition and feelings of sadness and irritability, which contribute to suicide attempts and
completed suicides.
Unanticipated alcohol withdrawal in hospitalized individuals for whom a diagnosis of
alcohol use disorder has been overlooked can add to the risks and costs of hospitalization
and to time spent in the hospital.
Differential Diagnosis
Nonpathological use of alcohol. The key element of alcohol use disorder is the use of
heavy doses of alcohol with resulting repeated and significant distress or impaired func-
tioning. While most drinkers sometimes consume enough alcohol to feel intoxicated, only
a minority (less than 20%) ever develop alcohol use disorder. Therefore, drinking, even
daily, in low doses and occasional intoxication do not by themselves make this diagnosis.
Sedative, hypnotic, or anxiolytic use disorder. The signs and symptoms of alcohol use
disorder are similar to those seen in sedative, hypnotic, or anxiolytic use disorder. The two
must be distinguished, however, because the course may be different, especially in rela-
tion to medical problems.
Conduct disorder in childhood and adult antisocial personality disorder. Alcohol use
disorder, along with other substance use disorders, is seen in the majority of individuals
with antisocial personality and preexisting conduct disorder. Because these diagnoses are
associated with an early onset of alcohol use disorder as well as a worse prognosis, it is im-
portant to establish both conditions.
Comorbidity
Bipolar disorders, schizophrenia, and antisocial personality disorder are associated with a
markedly increased rate of alcohol use disorder, and several anxiety and depressive disorders
Alcohol Intoxication 497
may relate to alcohol use disorder as well. At least a part of the reported association between
depression and moderate to severe alcohol use disorder may be attributable to temporary, al-
cohol-induced comorbid depressive symptoms resulting from the acute effects of intoxication
or withdrawal. Severe, repeated alcohol intoxication may also suppress immune mechanisms
and predispose individuals to infections and increase the risk for cancers.
Alcohol Intoxication
Diagnostic Criteria
A. Recent ingestion of alcohol.
B. Clinically significant problematic behavioral or psychological changes (e.g., inappropri-
ate sexual or aggressive behavior, mood lability, impaired judgment) that developed
during, or shortly after, alcohol ingestion.
C. One (or more) of the following signs or symptoms developing during, or shortly after,
alcohol use:
Slurred speech.
Incoordination.
Unsteady gait.
Nystagmus.
Impairment in attention or memory.
Stupor or coma.
D. The signs or symptoms are not attributable to another medical condition and are not better
explained by another mental disorder, including intoxication with another substance.
Coding note: The ICD-9-CM code is 303.00. The ICD-10-CM code depends on whether
there is a comorbid alcohol use disorder. If a mild alcohol use disorder is comorbid, the
ICD-10-CM code is F10.129, and if a moderate or severe alcohol use disorder is comorbid,
the ICD-10-CM code is F10.229. lf there is no comorbid alcohol use disorder, then the
ICD-10-CM code is F40.929.
Paron >
Diagnostic Features
The essential feature of alcohol intoxication is the presence of clinically significant problematic
behavioral or psychological changes (e.g., inappropriate sexual or aggressive behavior, mood
lability, impaired judgment, impaired social or occupational functioning) that develop during,
or shortly after, alcohol ingestion (Criterion B). These changes are accompanied by evidence of
impaired functioning and judgment and, if intoxication is intense, can result in a life-threaten-
ing coma. The symptoms must not be attributable to another medical condition (e.g., diabetic
ketoacidosis), are not a reflection of conditions such as delirium, and are not related to intoxi-
cation with other depressant drugs (e.g., benzodiazepines) (Criterion D). The levels of incoor-
dination can interfere with driving abilities and performance of usual activities to the point of
causing accidents. Evidence of alcohol use can be obtained by smelling alcohol on the individ-
ual’s breath, eliciting a history from the individual or another observer, and, when needed,
having the individual provide breath, blood, or urine samples for toxicology analyses.
Associated Features Supporting Diagnosis
Alcohol intoxication is sometimes associated with amnesia for the events that occurred
during the course of the intoxication (“blackouts”). This phenomenon may be related to
the presence of a high blood alcohol level and, perhaps, to the rapidity with which this
level is reached. During even mild alcohol intoxication, different symptoms are likely to be
498 Substance-Related and Addictive Disorders
observed at different time points. Evidence of mild intoxication with alcohol can be seen in
most individuals after approximately two drinks (each standard drink is approximately
10-12 grams of ethanol and raises the blood alcohol concentration approximately 20 mg/
dL). Early in the drinking period, when blood alcohol levels are rising, symptoms often
include talkativeness, a sensation of well-being, and a bright, expansive mood. Later, es-
pecially when blood alcohol levels are falling, the individual is likely to become progres-
sively more depressed, withdrawn, and cognitively impaired. At very high blood alcohol
levels (e.g., 200-300 mg/dL), an individual who has not developed tolerance for alcohol is
likely to fall asleep and enter a first stage of anesthesia. Higher blood alcohol levels (e.g., in
excess of 300-400 mg/dL) can cause inhibition of respiration and pulse and even death in
nontolerant individuals. The duration of intoxication depends on how much alcohol was
consumed over what period of time. In general, the body is able to metabolize approxi-
mately one drink per hour, so that the blood alcohol level generally decreases at a rate of
15-20 mg/dL per hour. Signs and symptoms of intoxication are likely to be more intense
when the blood alcohol level is rising than when it is falling.
Alcohol intoxication is an important contributor to suicidal behavior. There appears to
be an increased rate of suicidal behavior, as well as of completed suicide, among persons
intoxicated by alcohol.
Prevalence
The large majority of alcohol consumers are likely to have been intoxicated to some degree at
some point in their lives. For example, in 2010, 44% of 12th-grade students admitted to having
been “drunk in the past year,” with more than 70% of college students reporting the same.
Development and Course
Intoxication usually occurs as an episode usually developing over minutes to hours and typi-
cally lasting several hours. In the United States, the average age at first intoxication is approx-
imately 15 years, with the highest prevalence at approximately 18-25 years. Frequency and
intensity usually decrease with further advancing age. The earlier the onset of regular intoxi-
cation, the greater the likelihood the individual will go on to develop alcohol use disorder.
Risk and Prognostic Factors
Temperamental. Episodes of alcohol intoxication increase with personality characteris-
tics of sensation seeking and impulsivity.
Environmental. Episodes of alcohol intoxication increase with a heavy drinking envi-
ronment.
Culture-Related Diagnostic Issues
The major issues parallel the cultural differences regarding the use of alcohol overall.
Thus, college fraternities and sororities may encourage alcohol intoxication. This condi-
tion is also frequent on certain dates of cultural significance (e.g., New Year’s Eve) and, for
some subgroups, during specific events (e.g., wakes following funerals). Other subgroups
encourage drinking at religious celebrations (e.g., Jewish and Catholic holidays), while
still others strongly discourage all drinking or intoxication (e.g., some religious groups,
such as Mormons, fundamentalist Christians, and Muslims).
Gender-Related Diagnostic Issues
Historically, in many Western societies, acceptance of drinking and drunkenness is more
tolerated for males, but such gender differences may be much less prominent in recent
years, especially during adolescence and young adulthood.
Alcohol Withdrawal 499
Diagnostic Markers
Intoxication is usually established by observing an individual’s behavior and smelling alcohol
on the breath. The degree of intoxication increases with an individual's blood or breath alcohol
level and with the ingestion of other substances, especially those with sedating effects.
Functional Consequences of Alcohol Intoxication
Alcohol intoxication contributes to the more than 30,000 alcohol-related drinking deaths in
the United States each year. In addition, intoxication with this drug contributes to huge
costs associated with drunk driving, lost time from school or work, as well as interpersonal
arguments and physical fights.
Differential Diagnosis
Other medical conditions. Several medical (e.g., diabetic acidosis) and neurological condi-
tions (e.g., cerebellar ataxia, multiple sclerosis) can temporarily resemble alcohol intoxication.
Sedative, hypnotic, or anxiolytic intoxication. Intoxication with sedative, hypnotic, or
anxiolytic drugs or with other sedating substances (e.g., antihistamines, anticholinergic
drugs) can be mistaken for alcohol intoxication. The differential requires observing alco-
hol on the breath, measuring blood or breath alcohol levels, ordering a medical workup,
and gathering a good history. The signs and symptoms of sedative-hypnotic intoxication
are very similar to those observed with alcohol and include similar problematic behavioral
or psychological changes. These changes are accompanied by evidence of impaired func-
tioning and judgment—which, if intense, can result in a life-threatening coma—and levels
of incoordination that can interfere with driving abilities and with performing usual
activities. However, there is no smell as there is with alcohol, but there is likely to be evi-
dence of misuse of the depressant drug in the blood or urine toxicology analyses.
Comorbidity
Alcohol intoxication may occur comorbidly with other substance intoxication, especially
in individuals with conduct disorder or antisocial personality disorder.
Alcohol Withdrawal
Diagnostic Criteria
A. Cessation of (or reduction in} alcohol use that has been heavy and prolonged.
B. Two (or more) of the following, developing within several hours to a few days after the
cessation of (or reduction in) alcohol use described in Criterion A:
Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 bpm).
Increased hand tremor.
Insomnia.
Nausea or vomiting.
Transient visual, tactile, or auditory hallucinations or illusions.
Psychomotor agitation.
Anxiety.
Generalized tonic-clonic seizures.
ONOaAhwWN =
C. The signs or symptoms in Criterion B cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
500 Substance-Related and Addictive Disorders
D. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including intoxication or withdrawal from
another substance.
Specify if:
With perceptual disturbances: This specifier applies in the rare instance when hal-
lucinations (usually visual or tactile) occur with intact reality testing, or auditory, visual,
or tactile illusions occur in the absence of a delirium.
Coding note: The ICD-9-CM code is 291.81. The ICD-10-CM code for alcohol withdrawal
without perceptual disturbances is F10.239, and the ICD-10-CM code for alcohol withdrawal
with perceptual disturbances is F10.232. Note that the ICD-10-CM code indicates the comor-
bid presence of a moderate or severe alcohol use disorder, reflecting the fact that alcohol with-
drawal can only occur in the presence of a moderate or severe alcohol use disorder. It is not
permissible to code a comorbid mild alcohol use disorder with alcohol withdrawal.
Specifiers
When hallucinations occur in the absence of delirium (i.e., in a clear sensorium), a diagno-
sis of substance/medication-induced psychotic disorder should be considered.
Diagnostic Features
The essential feature of alcohol withdrawal is the presence of a characteristic withdrawal
syndrome that develops within several hours to a few days after the cessation of (or re-
duction in) heavy and prolonged alcohol use (Criteria A and B). The withdrawal syn-
drome includes two or more of the symptoms reflecting autonomic hyperactivity and
anxiety listed in Criterion B, along with gastrointestinal symptoms.
Withdrawal symptoms cause clinically significant distress or impairment in social, oc-
cupational, or other important areas of functioning (Criterion C). The symptoms must not
be attributable to another medical condition and are not better explained by another men-
tal disorder (e.g., generalized anxiety disorder), including intoxication or withdrawal
from another substance (e.g., sedative, hypnotic, or anxiolytic withdrawal) (Criterion D).
Symptoms can be relieved by administering alcohol or benzodiazepines (e.g., diazepam).
The withdrawal symptoms typically begin when blood concentrations of alcohol decline
sharply (.e., within 4-12 hours) after alcohol use has been stopped or reduced. Reflecting the
relatively fast metabolism of alcohol, symptoms of alcohol withdrawal usually peak in inten-
sity during the second day of abstinence and are likely to improve markedly by the fourth or
fifth day. Following acute withdrawal, however, symptoms of anxiety, insomnia, and auto-
nomic dysfunction may persist for up to 3-6 months at lower levels of intensity.
Fewer than 10% of individuals who develop alcohol withdrawal will ever develop dra-
matic symptoms (e.g., severe autonomic hyperactivity, tremors, alcohol withdrawal delir-
ium). Tonic-clonic seizures occur in fewer than 3% of individuals.
Associated Features Supporting Diagnosis
Although confusion and changes in consciousness are not core criteria for alcohol with-
drawal, alcohol withdrawal delirium (see “Delirium” in the chapter “Neurocognitive Dis-
orders”) may occur in the context of withdrawal. As is true for any agitated, confused state,
regardless of the cause, in addition to a disturbance of consciousness and cognition, with-
drawal delirium can include visual, tactile, or (rarely) auditory hallucinations (delirium tre-
mens). When alcohol withdrawal delirium develops, it is likely that a clinically relevant
medical condition may be present (e.g., liver failure, pneumonia, gastrointestinal bleeding,
sequelae of head trauma, hypoglycemia, an electrolyte imbalance, postoperative status).
Alcohol Withdrawal 501
Prevalence
It is estimated that approximately 50% of middle-class, highly functional individuals with
alcohol use disorder have ever experienced a full alcohol withdrawal syndrome. Among
individuals with alcohol use disorder who are hospitalized or homeless, the rate of al-
cohol withdrawal may be greater than 80%. Less than 10% of individuals in withdrawal
ever demonstrate alcohol withdrawal delirium or withdrawal seizures.
Development and Course
Acute alcohol withdrawal occurs as an episode usually lasting 4-5 days and only after
extended periods of heavy drinking. Withdrawal is relatively rare in individuals younger
than 30 years, and the risk and severity increase with increasing age.
Risk and Prognostic Factors
Environmental. The probability of developing alcohol withdrawal increases with the
quantity and frequency of alcohol consumption. Most individuals with this condition are
drinking daily, consuming large amounts (approximately more than eight drinks per day)
for multiple days. However, there are large inter-individual differences, with enhanced
risks for individuals with concurrent medical conditions, those with family histories of al-
cohol withdrawal (i.e., a genetic component), those with prior withdrawals, and individ-
uals who consume sedative, hypnotic, or anxiolytic drugs.
Diagnostic Markers
Autonomic hyperactivity in the context of moderately high but falling blood alcohol levels
and a history of prolonged heavy drinking indicate a likelihood of alcohol withdrawal.
Functional Consequences of Alcohol Withdrawal
Symptoms of withdrawal may serve to perpetuate drinking behaviors and contribute to
relapse, resulting in persistently impaired social and occupational functioning. Symptoms
requiring medically supervised detoxification result in hospital utilization and loss of
work productivity. Overall, the presence of withdrawal is associated with greater func-
tional impairment and poor prognosis.
Differential Diagnosis
Other medical conditions. The symptoms of alcohol withdrawal can also be mimicked
by some medical conditions (e.g., hypoglycemia and diabetic ketoacidosis). Essential
tremor, a disorder that frequently runs in families, may erroneously suggest the tremu-
lousness associated with alcohol withdrawal.
Sedative, hypnotic, or anxiolytic withdrawal. Sedative, hypnotic, or anxiolytic with-
drawal produces a syndrome very similar to that of alcohol withdrawal.
Comorbidity
Withdrawal is more likely to occur with heavier alcohol intake, and that might be most of-
ten observed in individuals with conduct disorder and antisocial personality disorder.
Withdrawal states are also more severe in older individuals, individuals who are also de-
pendent on other depressant drugs (sedative-hypnotics), and individuals who have had
more alcohol withdrawal experiences in the past.
502 Substance-Related and Addictive Disorders
Other Alcohol-Induced Disorders
The following alcohol-induced disorders are described in other chapters of the manual with
disorders with which they share phenomenology (see the substance/medication-induced
mental disorders in these chapters): alcohol-induced psychotic disorder (“Schizophrenia Spec-
trum and Other Psychotic Disorders”); alcohol-induced bipolar disorder (“Bipolar and
Related Disorders”); alcohol-induced depressive disorder (“Depressive Disorders”); alcohol-
induced anxiety disorder (“Anxiety Disorders”); alcohol-induced sleep disorder (“Sleep-
Wake Disorders”); alcohol-induced sexual dysfunction (“Sexual Dysfunctions”); and alcohol-
induced major or mild neurocognitive disorder (“Neurocognitive Disorders”). For alcohol
intoxication delirium and alcohol withdrawal delirium, see the criteria and discussion of de-
lirium in the chapter “Neurocognitive Disorders.” These alcohol-induced disorders are diag-
nosed instead of alcohol intoxication or alcohol withdrawal only when the symptoms are
sufficiently severe to warrant independent clinical attention.
Features
The symptom profiles for an alcohol-induced condition resemble independent mental disor-
ders as described elsewhere in DSM-5. However, the alcohol-induced disorder is temporary
and observed after severe intoxication with and/or withdrawal from alcohol. While the symp-
toms can be identical to those of independent mental disorders (e.g., psychoses, major depres-
sive disorder), and while they can have the same severe consequences (e.g., suicide attempts),
alcohol-induced conditions are likely to improve without formal treatment in a matter of days
to weeks after cessation of severe intoxication and/or withdrawal.
Each alcohol-induced mental disorder is listed in the relevant diagnostic section and there-
fore only a brief description is offered here. Alcohol-induced disorders must have developed
in the context of severe intoxication and/or withdrawal from the substance capable of produc-
ing the mental disorder. In addition, there must be evidence that the disorder being observed
is not likely to be better explained by another non-alcohol-induced mental disorder. The latter
is likely to occur if the mental disorder was present before the severe intoxication or with-
drawal, or continued more than 1 month after the cessation of severe intoxication and/or with-
drawal. When symptoms are observed only during a delirium, they should be considered part
of the delirium and not diagnosed separately, as many symptoms (including disturbances in
mood, anxiety, and reality testing) are commonly seen during agitated, confused states. The al-
cohol-induced disorder must be clinically relevant, causing significant levels of distress or sig-
nificant functional impairment. Finally, there are indications that the intake of substances of
abuse in the context of a preexisting mental disorder are likely to result in an intensification of
the preexisting independent syndrome.
The features associated with each relevant major mental disorder (e.g., psychotic epi-
sodes, major depressive disorder) are similar whether observed with an independent or an
alcohol-induced condition. However, individuals with alcohol-induced disorders are
likely to also demonstrate the associated features seen with an alcohol use disorder, as
listed in the subsections of this chapter.
Rates of alcohol-induced disorders vary somewhat by diagnostic category. For exam-
ple, the lifetime risk for major depressive episodes in individuals with alcohol use disorder
is approximately 40%, but only about one-third to one-half of these represent independent
major depressive syndromes observed outside the context of intoxication. Similar rates of
alcohol-induced sleep and anxiety conditions are likely, but alcohol-induced psychotic ep-
isodes are fairly rare.
Develooment and Course
Once present, the symptoms of an alcohol-induced condition are likely to remain clinically
relevant as long as the individual continues to experience severe intoxication and/or with-
Unspecified Alcohol-Related Disorder 503
drawal. While the symptoms are identical to those of independent mental disorders (e.g.,
psychoses, majar depressive disorder), and while they can have the same severe conse-
quences (e.g., suicide attempts), all alcohol-induced syndromes other than alcohol-
induced neurocognitive disorder, amnestic confabulatory type (alcohol-induced persist-
ing amnestic disorder), regardless of the severity of the symptoms, are likely to improve
relatively quickly and unlikely to remain clinically relevant for more than 1 month after
cessation of severe intoxication and/or withdrawal.
The alcohol-induced disorders are an important part of the differential diagnoses for
the independent mental conditions. Independent schizophrenia, major depressive disor-
der, bipolar disorder, and anxiety disorders, such as panic disorder, are likely to be asso-
ciated with much longer-lasting periods of symptoms and often require longer-term
medications to optimize the probability of improvement or recovery. The alcohol-induced
conditions, on the other hand, are likely to be much shorter in duration and disappear
within several days to 1 month after cessation of severe intoxication and/or withdrawal,
even without psychotropic medications.
The importance of recognizing an alcohol-induced disorder is similar to the relevance
of identifying the possible role of some endocrine conditions and medication reactions be-
fore diagnosing an independent mental disorder. In light of the high prevalence of alcohol
use disorders worldwide, it is important that these alcohol-induced diagnoses be consid-
ered before independent mental disorders are diagnosed.
Unspecified Alcohol-Related Disorder
291.9 (F10.99)
This category applies to presentations in which symptoms characteristic of an alcohol-
related disorder that cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning predominate but do not meet the full criteria
for any specific alcohol-related disorder or any of the disorders in the substance-related
and addictive disorders diagnostic class.
Caffeine-Related Disorders
Caffeine Intoxication
Caffeine Withdrawal
Other Caffeine-Induced Disorders
Unspecified Caffeine-Related Disorder
Caffeine Intoxication
Diagnostic Criteria 305.90 (F15.929)
A. Recent consumption of caffeine (typically a high dose well in excess of 250 mg).
B. Five (or more) of the following signs or symptoms developing during, or shortly after,
caffeine use:
1. Restlessness.
2. Nervousness.
504 Substance-Related and Addictive Disorders
3. Excitement.
4. Insomnia.
5. Flushed face.
6. Diuresis.
7. Gastrointestinal disturbance.
8. Muscle twitching.
9. Rambling flow of thought and speech.
10. Tachycardia or cardiac arrhythmia.
11. Periods of inexhaustibility.
12. Psychomotor agitation.
C. The signs or symptoms in Criterion B cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are not bet-
ter explained by another mental disorder, including intoxication with another substance.
Diagnostic Features
Caffeine can be consumed from a number of different sources, including coffee, tea, caf-
feinated soda, “energy” drinks, over-the-counter analgesics and cold remedies, energy
aids (e.g., drinks), weight-loss aids, and chocolate. Caffeine is also increasingly being used
as an additive to vitamins and to food products. More than 85% of children and adults con-
sume caffeine regularly. Some caffeine users display symptoms consistent with problem-
atic use, including tolerance and withdrawal (see “Caffeine Withdrawal” later in this
chapter); the data are not available at this time to determine the clinical significance of a
caffeine use disorder and its prevalence. In contrast, there is evidence that caffeine with-
drawal and caffeine intoxication are clinically significant and sufficiently prevalent.
The essential feature of caffeine intoxication is recent consumption of caffeine and five
or more signs or symptoms that develop during or shortly after caffeine use (Criteria A
and B). Symptoms include restlessness, nervousness, excitement, insomnia, flushed face,
diuresis, and gastrointestinal complaints, which can occur with low doses (e.g., 200 mg) in
vulnerable individuals such as children, the elderly, or individuals who have not been ex-
posed to caffeine previously. Symptoms that generally appear at levels of more than 1 g/
day include muscle twitching, rambling flow of thought and speech, tachycardia or car-
diac arrhythmia, periods of inexhaustibility, and psychomotor agitation. Caffeine intoxi-
cation may not occur despite high caffeine intake because of the development of tolerance.
The signs or symptoms must cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning (Criterion C). The signs or symp-
toms must not be attributable to another medical condition and are not better explained by
another mental disorder (e.g., an anxiety disorder) or intoxication with another substance
(Criterion D).
Associated Features Supporting Diagnosis
Mild sensory disturbances (e.g., ringing in the ears and flashes of light) may occur with high
doses of caffeine. Although large doses of caffeine can increase heart rate, smaller doses can
slow heart rate. Whether excess caffeine intake can cause headaches is unclear. On physical
examination, agitation, restlessness, sweating, tachycardia, flushed face, and increased
bowel motility may be seen. Caffeine blood levels may provide important information for
diagnosis, particularly when the individual is a poor historian, although these levels are not
diagnostic by themselves in view of the individual variation in response to caffeine.
Caffeine Intoxication 505
Prevalence
The prevalence of caffeine intoxication in the general population is unclear. In the United
States, approximately 7% of individuals in the population may experience five or more symp-
toms along with functional impairment consistent with a diagnosis of caffeine intoxication.
Development and Course
Consistent with a half-life of caffeine of approximately 4-6 hours, caffeine intoxication
symptoms usually remit within the first day or so and do not have any known long-lasting
consequences. However, individuals who consume very high doses of caffeine (i.e., 5-10
g) may require immediate medical attention, as such doses can be lethal.
With advancing age, individuals are likely to demonstrate increasingly intense reac-
tions to caffeine, with greater complaints of interference with sleep or feelings of hyper-
arousal. Caffeine intoxication among young individuals after consumption of highly
caffeinated products, including energy drinks, has been observed. Children and adoles-
cents may be at increased risk for caffeine intoxication because of low body weight, lack of
tolerance, and lack of knowledge about the pharmacological effects of caffeine.
Risk and Prognostic Factors
Environmental. Caffeine intoxication is often seen among individuals who use caffeine
less frequently or in those who have recently increased their caffeine intake by a substan-
tial amount. Furthermore, oral contraceptives significantly decrease the elimination of caf-
feine and consequently may increase the risk of intoxication.
Genetic and physiological. Genetic factors may affect risk of caffeine intoxication.
Functional Consequences of Caffeine intoxication
Impairment from caffeine intoxication may have serious consequences, including dys-
function at work or school, social indiscretions, or failure to fulfill role obligations. More-
over, extremely high doses of caffeine can be fatal. In some cases, caffeine intoxication may
precipitate a caffeine-induced disorder.
Differential Diagnosis
Other mental disorders. Caffeine intoxication may be characterized by symptoms (e.g.,
panic attacks) that resemble primary mental disorders. To meet criteria for caffeine intoxica-
tion, the symptoms must not be associated with another medical condition or another mental
disorder, such as an anxiety disorder, that could better explain them. Manic episodes; panic
disorder; generalized anxiety disorder; amphetamine intoxication; sedative, hypnotic, or anx-
iolytic withdrawal or tobacco withdrawal; sleep disorders; and medication-induced side ef-
fects (e.g., akathisia) can cause a clinical picture that is similar to that of caffeine intoxication.
Other caffeine-induced disorders. The temporal relationship of the symptoms to increased
caffeine use or to abstinence from caffeine helps to establish the diagnosis. Caffeine intoxica-
tion is differentiated from caffeine-induced anxiety disorder, with onset during intoxication
(see “Substance /Medication-Induced Anxiety Disorder” in the chapter “Anxiety Disorders”),
and caffeine-induced sleep disorder, with onset during intoxication (see “Substance /Medica-
tion-Induced Sleep Disorder” in the chapter “Sleep-Wake Disorders”), by the fact that the
symptoms in these latter disorders are in excess of those usually associated with caffeine in-
toxication and are severe enough to warrant independent clinical attention.
506 Substance-Related and Addictive Disorders
Comorbidity
Typical dietary doses of caffeine have not been consistently associated with medical prob-
lems. However, heavy use (e.g., >400 mg) can cause or exacerbate anxiety and somatic
symptoms and gastrointestinal distress. With acute, extremely high doses of caffeine,
grand mal seizures and respiratory failure may result in death. Excessive caffeine use is as-
sociated with depressive disorders, bipolar disorders, eating disorders, psychotic disor-
ders, sleep disorders, and substance-related disorders, whereas individuals with anxiety
disorders are more likely to avoid caffeine.
Caffeine Withdrawal
Diagnostic Criteria 292.0 (F 15.93)
A. Prolonged daily use of caffeine.
B. Abrupt cessation of or reduction in caffeine use, followed within 24 hours by three (or
more) of the following signs or symptoms:
1. Headache.
2. Marked fatigue or drowsiness.
3. Dysphoric mood, depressed mood, or irritability.
4. Difficulty concentrating.
5. Flu-like symptoms (nausea, vomiting, or muscle pain/stiffness).
C. The signs or symptoms in Criterion B cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not associated with the physiological effects of another
medical condition (e.g., migraine, viral illness) and are not better explained by another
mental disorder, including intoxication or withdrawal from another substance.
Diagnostic Features
The essential feature of caffeine withdrawal is the presence of a characteristic withdrawal
syndrome that develops after the abrupt cessation of (or substantial reduction in) pro-
longed daily caffeine ingestion (Criterion B). The caffeine withdrawal syndrome is indi-
cated by three or more of the following (Criterion B): headache; marked fatigue or
drowsiness; dysphoric mood, depressed mood, or irritability; difficulty concentrating;
and flu-like symptoms (nausea, vomiting, or muscle pain/stiffness). The withdrawal syn-
drome causes clinical significant distress or impairment in social, occupational, or other
important areas of functioning (Criterion C). The symptoms must not be associated with
the physiological effects of another medical condition and are not better explained by an-
other mental disorder (Criterion D).
Headache is the hallmark feature of caffeine withdrawal and may be diffuse, gradual
in development, throbbing, severe, and sensitive to movement. However, other symptoms
of caffeine withdrawal can occur in the absence of headache. Caffeine is the most widely
used behaviorally active drug in the world and is present in many different types of bev-
erages (e.g., coffee, tea, maté, soft drinks, energy drinks), foods, energy aids, medications,
and dietary supplements. Because caffeine ingestion is often integrated into social customs
and daily rituals (e.g., coffee break, tea time), some caffeine consumers may be unaware of
their physical dependence on caffeine. Thus, caffeine withdrawal symptoms could be un-
expected and misattributed to other causes (e.g., the flu, migraine). Furthermore, caffeine
withdrawal symptoms may occur when individuals are required to abstain from foods
and beverages prior to medical procedures or when a usual caffeine dose is missed be-
cause of a change in routine (e.g., during travel, weekends).
Caffeine Withdrawal 507
The probability and severity of caffeine withdrawal generally increase as a function of
usual daily caffeine dose. However, there is large variability among individuals and
within individuals across different episodes in the incidence, severity, and time course of
withdrawal symptoms. Caffeine withdrawal symptoms may occur after abrupt cessation
of relatively low chronic daily doses of caffeine (i.e., 100 mg).
Associated Features Supporting Diagnosis
Caffeine abstinence has been shown to be associated with impaired behavioral and cogni-
tive performance (e.g., sustained attention). Electroencephalographic studies have shown
that caffeine withdrawal symptoms are significantly associated with increases in theta
power and decreases in beta-2 power. Decreased motivation to work and decreased socia-
bility have also been reported during caffeine withdrawal. Increased analgesic use during
caffeine withdrawal has been documented.
Prevaience
More than 85% of adults and children in the United States regularly consume caffeine,
with adult caffeine consumers ingesting about 280 mg/day on average. The incidence and
prevalence of the caffeine withdrawal syndrome in the general population are unclear. In
the United States, headache may occur in approximately 50% of cases of caffeine absti-
nence. In attempts to permanently stop caffeine use, more than 70% of individuals may ex-
perience at least one caffeine withdrawal symptom (47% may experience headache), and
24% may experience headache plus one or more other symptoms as well as functional
impairment due to withdrawal. Among individuals who abstain from caffeine for at least
24 hours but are not trying to permanently stop caffeine use, 11% may experience head-
ache plus one or more other symptoms as well as functional impairment. Caffeine con-
sumers can decrease the incidence of caffeine withdrawal by using caffeine daily or only
infrequently (e.g., no more than 2 consecutive days). Gradual reduction in caffeine over a
period of days or weeks may decrease the incidence and severity of caffeine withdrawal.
Deveiopment and Course
Symptoms usually begin 12-24 hours after the last caffeine dose and peak after 1-2 days
of abstinence. Caffeine withdrawal symptoms last for 2-9 days, with the possibility of
withdrawal headaches occurring for up to 21 days. Symptoms usually remit rapidly
(within 30-60 minutes) after re-ingestion of caffeine.
Caffeine is unique in that it is a behaviorally active drug that is consumed by individ-
uals of nearly all ages. Rates of caffeine consumption and overall level of caffeine con-
sumption increase with age until the early to mid-30s and then level off. Although caffeine
withdrawal among children and adolescents has been documented, relatively little is
known about risk factors for caffeine withdrawal among this age group. The use of highly
caffeinated energy drinks is increasing with in young individuals, which could increase
the risk for caffeine withdrawal.
Risk and Prognostic Factors
Temperamental. Heavy caffeine use has been observed among individuals with mental
disorders, including eating disorders; smokers; prisoners; and drug and alcohol abusers.
Thus, these individuals could be at higher risk for caffeine withdrawal upon acute caffeine
abstinence.
Environmental. The unavailability of caffeine is an environmental risk factor for incipi-
ent withdrawal symptoms. While caffeine is legal and usually widely available, there are
conditions in which caffeine use may be restricted, such as during medical procedures,
pregnancy, hospitalizations, religious observances, wartime, travel, and research partici-
508 Substance-Related and Addictive Disorders
pation. These external environmental circumstances may precipitate a withdrawal syn-
drome in vulnerable individuals.
Genetic and physiological factors. Genetic factors appear to increase vulnerability to
caffeine withdrawal, but no specific genes have been identified.
Course modifiers. Caffeine withdrawal symptoms usually remit within 30-60 minutes
of reexposure to caffeine. Doses of caffeine significantly less than one’s usual daily dose
may be sufficient to prevent or attenuate caffeine withdrawal symptoms (e.g., consump-
tion of 25 mg by an individual who typically consumes 300 mg).
Culture-Related Diagnostic Issues
Habitual caffeine consumers who fast for religious reasons may be at increased risk for caf-
feine withdrawal.
Functional Consequences of
Caffeine Withdrawal Disorder
Caffeine withdrawal symptoms can vary from mild to extreme, at times causing functional
impairment in normal daily activities. Rates of functional impairment range from 10% to
55% (median 13%), with rates as high as 73% found among individuals who also show
other problematic features of caffeine use. Examples of functional impairment include be-
ing unable to work, exercise, or care for children; staying in bed all day; missing religious
services; ending a vacation early; and cancelling a social gathering. Caffeine withdrawal
headaches may be described by individuals as “the worst headaches” ever experienced.
Decrements in cognitive and motor performance have also been observed.
Differential Diagnosis
Other medical disorders and medical side effects. Several disorders should be consid-
ered in the differential diagnosis of caffeine withdrawal. Caffeine withdrawal can mimic
migraine and other headache disorders, viral illnesses, sinus conditions, tension, other
drug withdrawal states (e.g., from amphetamines, cocaine), and medication side effects.
The final determination of caffeine withdrawal should rest on a determination of the pat-
tern and amount consumed, the time interval between caffeine abstinence and onset of
symptoms, and the particular clinical features presented by the individual. A challenge
dose of caffeine followed by symptom remission may be used to confirm the diagnosis.
Comorbidity
Caffeine withdrawal may be associated with major depressive disorder, generalized anx-
iety disorder, panic disorder, antisocial personality disorder in adults, moderate to severe
alcohol use disorder, and cannabis and cocaine use.
Other Caffeine-Induced Disorders
The following caffeine-induced disorders are described in other chapters of the manual
with disorders with which they share phenomenology (see the substance /medication-
induced mental disorders in these chapters): caffeine-induced anxiety disorder (“Anxiety
Disorders”) and caffeine-induced sleep disorder (“Sleep-Wake Disorders”). These caf-
feine-induced disorders are diagnosed instead of caffeine intoxication or caffeine with-
drawal only when the symptoms are sufficiently severe to warrant independent clinical
attention.
Unspecified Caffeine-Related Disorder 509
Unspecified Caffeine-Related Disorder
292.9 (F15.99)
This category applies to presentations in which symptoms characteristic of a caffeine-
related disorder that cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning predominate but do not meet the full criteria
for any specific caffeine-related disorder or any of the disorders in the substance-related
and addictive disorders diagnostic class.
Cannabis-Related Disorders
Cannabis Use Disorder
Cannabis Intoxication
Cannabis Withdrawal
Other Cannabis-induced Disorders
Unspecified Cannabis-Related Disorder
Cannabis Use Disorder
Diagnostic Criteria
A. A problematic pattern of cannabis use leading to clinically significant impairment or dis-
tress, as manifested by at least two of the following, occurring within a 12-month period:
1. Cannabis is often taken in larger amounts or over a longer period than was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control cannabis use.
3. A great deal of time is spent in activities necessary to obtain cannabis, use canna-
bis, or recover from its effects.
4. Craving, or a strong desire or urge to use cannabis.
5. Recurrent cannabis use resulting in a failure to fulfill major role obligations at work,
school, or home.
6. Continued cannabis use despite having persistent or recurrent social or interper-
sonal problems caused or exacerbated by the effects of cannabis.
7. (Important social, occupational, or recreational activities are given up or reduced be-
cause of cannabis use.
8. Recurrent cannabis use in situations in which it is physically hazardous.
9, Cannabis use is continued despite knowledge of having a persistent or recurrent
physical or psychological problem that is likely to have been caused or exacerbated
by cannabis.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of cannabis to achieve intoxication or
desired effect.
b. Markedly diminished effect with continued use of the same amount of cannabis.
11. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for cannabis (refer to Criteria A and B
of the criteria set for cannabis withdrawal, pp. 517-518).
510 Substance-Related and Addictive Disorders
b. Cannabis (or a closely related substance) is taken to relieve or avoid withdrawal
symptoms.
Specify if:
In early remission: After full criteria for cannabis use disorder were previously met,
none of the criteria for cannabis use disorder have been met for at least 3 months but
for less than 12 months (with the exception that Criterion A4, “Craving, or a strong de-
sire or urge to use cannabis,” may be met).
In sustained remission: After full criteria for cannabis use disorder were previously
met, none of the criteria for cannabis use disorder have been met at any time during a
period of 12 months or longer (with the exception that Criterion A4, “Craving, or a
strong desire or urge to use cannabis,” may be present).
Specify if:
In a controlled environment: This additional specifier is used if the individual is in an
environment where access to cannabis is restricted.
Code based on current severity: Note for ICD-10-CM codes: If a cannabis intoxication,
cannabis withdrawal, or another cannabis-induced mental disorder is also present, do not
use the codes below for cannabis use disorder. Instead, the comorbid cannabis use disorder
is indicated in the 4th character of the cannabis-induced disorder code (see the coding note
for cannabis intoxication, cannabis withdrawal, or a specific cannabis-induced mental disor-
der). For example, if there is comorbid cannabis-induced anxiety disorder and cannabis use
disorder, only the cannabis-induced anxiety disorder code is given, with the 4th character
indicating whether the comorbid cannabis use disorder is mild, moderate, or severe:
F12.180 for mild cannabis use disorder with cannabis-induced anxiety disorder or F12.280
for a moderate or severe cannabis use disorder with cannabis-induced anxiety disorder.
Specify current severity:
305.20 (F12.10) Mild: Presence of 2-3 symptoms.
304.30 (F12.20) Moderate: Presence of 4—5 symptoms.
304.30 (F12.20) Severe: Presence of 6 or more symptoms.
Specifiers
“Ina controlled environment” applies as a further specifier of remission if the individual is
both in remission and in a controlled environment (ie., in early remission in a controlled
environment or in sustained remission in a controlled environment). Examples of these
environments are closely supervised and substance-free jails, therapeutic communities,
and locked hospital units.
Changing severity across time in an individual may also be reflected by changes in the
frequency (e.g., days of use per month or times used per day) and/or dose (e.g., amount
used per episode) of cannabis, as assessed by individual self-report, report of knowledge-
able others, clinician’s observations, and biological testing.
Diagnostic Features
Cannabis use disorder and the other cannabis-related disorders include problems that are
associated with substances derived from the cannabis plant and chemically similar syn-
thetic compounds. Over time, this plant material has accumulated many names (e.g.,
weed, pot, herb, grass, reefer, mary jane, dagga, dope, bhang, skunk, boom, gangster, kif,
and ganja). A concentrated extraction of the cannabis plant that is also commonly used is
hashish. Cannabis is the generic and perhaps the most appropriate scientific term for the
psychoactive substance(s) derived from the plant, and as such it is used in this manual
to refer to all forms of cannabis-like substances, including synthetic cannabinoid com-
pounds.
Cannabis Use Disorder 511
Synthetic oral formulations (pill/capsules) of delta-9-tetrahydrocannabinol (delta-9-
THC) are available by prescription for a number of approved medical indications (e.g., for
nausea and vomiting caused by chemotherapy; for anorexia and weight loss in individuals
with AIDS). Other synthetic cannabinoid compounds have been manufactured and dis-
tributed for nonmedical use in the form of plant material that has been sprayed with a can-
nabinoid formulation (e.g., K2, Spice, JWH-018, JWH-073).
The cannabinoids have diverse effects in the brain, prominent among which are actions
on CB1 and CB2 cannabinoid receptors that are found throughout the central nervous sys-
tem. Endogenous ligands for these receptors behave essentially like neurotransmitters.
The potency of cannabis (delta-9-THC concentration) that is generally available varies
greatly, ranging from 1% to approximately 15% in typical cannabis plant material and
10%-20% in hashish. During the past two decades, a steady increase in the potency of
seized cannabis has been observed.
Cannabis is most commonly smoked via a variety of methods: pipes, water pipes
(bongs or hookahs), cigarettes (joints or reefers), or, most recently, in the paper from hol-
lowed out cigars (blunts). Cannabis is also sometimes ingested orally, typically by mixing
it into food. More recently, devices have been developed in which cannabis is “vapor-
ized.” Vaporization involves heating the plant material to release psychoactive cannabi-
noids for inhalation. As with other psychoactive substances, smoking (and vaporization)
typically produces more rapid onset and more intense experiences of the desired effects.
Individuals who regularly use cannabis can develop all the general diagnostic features
of a substance use disorder. Cannabis use disorder is commonly observed as the only sub-
stance use disorder experienced by the individual; however, it also frequently occurs con-
currently with other types of substance use disorders (i.e., alcohol, cocaine, opioid). In
cases for which multiple types of substances are used, many times the individual may
minimize the symptoms related to cannabis, as the symptoms may be less severe or cause
less harm than those directly related to the use of the other substances. Pharmacological
and behavioral tolerance to most of the effects of cannabis has been reported in individuals
who use cannabis persistently. Generally, tolerance is lost when cannabis use is discontin-
ued for a significant period of time (i-e., for at least several months).
New to DSM-5 is the recognition that abrupt cessation of daily or near-daily cannabis
use often results in the onset of a cannabis withdrawal syndrome. Common symptoms of
withdrawal include irritability, anger or aggression, anxiety, depressed mood, restless-
ness, sleep difficulty, and decreased appetite or weight loss. Although typically not as
severe as alcohol or opiate withdrawal, the cannabis withdrawal syndrome can cause sig-
nificant distress and contribute to difficulty quitting or relapse among those trying to
abstain.
Individuals with cannabis use disorder may use cannabis throughout the day over a
period of months or years, and thus may spend many hours a day under the influence.
Others may use less frequently, but their use causes recurrent problems related to family,
school, work, or other important activities (e.g., repeated absences at work; neglect of fam-
ily obligations). Periodic cannabis use and intoxication can negatively affect behavioral
and cognitive functioning and thus interfere with optimal performance at work or school,
or place the individual at increased physical risk when performing activities that could be
physically hazardous (e.g., driving a car; playing certain sports; performing manual work
activities, including operating machinery). Arguments with spouses or parents over the
use of cannabis in the home, or its use in the presence of children, can adversely impact
family functioning and are common features of those with cannabis use disorder. Last, in-
dividuals with cannabis use disorder may continue using despite knowledge of physical
problems (e.g., chronic cough related to smoking) or psychological problems (e.g., exces-
sive sedation or exacerbation of other mental health problems) associated with its use.
Whether or not cannabis is being used for legitimate medical reasons may also affect
diagnosis. When a substance is taken as indicated for a medical condition, symptoms of
512 Substance-Related and Addictive Disorders
tolerance and withdrawal will naturally occur and should not be used as the primary cri-
teria for determining a diagnosis of a substance use disorder. Although medical uses of
cannabis remain controversial and equivocal, use for medical circumstances should be
considered when a diagnosis is being made.
Associated Features Supporting Diagnosis
Individuals who regularly use cannabis often report that it is being used to cope with
mood, sleep, pain, or other physiological or psychological problems, and those diagnosed
with cannabis use disorder frequently do have concurrent other mental disorders. Careful
assessment typically reveals reports of cannabis use contributing to exacerbation of these
same symptoms, as well as other reasons for frequent use (e.g., to experience euphoria, to
forget about problems, in response to anger, as an enjoyable social activity). Related to this
issue, some individuals who use cannabis multiple times per day for the aforementioned
reasons do not perceive themselves as (and thus do not report) spending an excessive
amount of time under the influence or recovering from the effects of cannabis, despite be-
ing intoxicated on cannabis or coming down from it effects for the majority of most days.
An important marker of a substance use disorder diagnosis, particularly in milder cases, is
continued use despite a clear risk of negative consequences to other valued activities or re-
lationships (e.g., school, work, sport activity, partner or parent relationship).
Because some cannabis users are motivated to minimize their amount or frequency of
use, it is important to be aware of common signs and symptoms of cannabis use and intox-
ication so as to better assess the extent of use. As with other substances, experienced users
of cannabis develop behavioral and pharmacological tolerance such that it can be difficult
to detect when they are under the influence. Signs of acute and chronic use include red eyes
(conjunctival injection), cannabis odor on clothing, yellowing of finger tips (from smoking
joints), chronic cough, burning of incense (to hide the odor), and exaggerated craving and
impulse for specific foods, sometimes at unusual times of the day or night.
Prevalence
Cannabinoids, especially cannabis, are the most widely used illicit psychoactive sub-
stances in the United States. The 12-month prevalence of cannabis use disorder (DSM-IV
abuse and dependence rates combined) is approximately 3.4% among 12- to 17-year-olds
and 1.5% among adults age 18 years and older. Rates of cannabis use disorder are greater
among adult males (2.2%) than among adult females (0.8%) and among 12- to 17-year-old
males (3.8%) than among 12- to 17-year-old females (3.0%). Twelve-month prevalence
rates of cannabis use disorder among adults decrease with age, with rates highest among
18- to 29-year-olds (4.4%) and lowest among individuals age 65 years and older (0.01%).
The high prevalence of cannabis use disorder likely reflects the much more widespread
use of cannabis relative to other illicit drugs rather than greater addictive potential.
Ethnic and racial differences in prevalence are moderate. Twelve-month prevalences
of cannabis use disorder vary markedly across racial-ethnic subgroups in the United
States. For 12- to 17-year-olds, rates are highest among Native American and Alaska Na-
tives (7.1%) compared with Hispanics (4.1%), whites (3.4%), African Americans (2.7%),
and Asian Americans and Pacific Islanders (0.9%). Among adults, the prevalence of can-
nabis use disorder is also highest among Native Americans and Alaska Natives (3.4%) rel-
ative to rates among African Americans (1.8%), whites (1.4%), Hispanics (1.2%), and Asian
and Pacific Islanders (1.2%). During the past decade the prevalence of cannabis use disor-
der has increased among adults and adolescents. Gender differences in cannabis use dis-
order generally are concordant with those in other substance use disorders. Cannabis use
disorder is more commonly observed in males, although the magnitude of this difference
is less among adolescents.
Cannabis Use Disorder 513
Development and Course
The onset of cannabis use disorder can occur at any time during or following adolescence,
but onset is most commonly during adolescence or young adulthood. Although much less
frequent, onset of cannabis use disorder in the preteen years or in the late 20s or older can
occur. Recent acceptance by some of the use and availability of “medical marijuana” may
increase the rate of onset of cannabis use disorder among older adults.
Generally, cannabis use disorder develops over an extended period of time, although
the progression appears to be more rapid in adolescents, particularly those with pervasive
conduct problems. Most people who develop a cannabis use disorder typically establish a
pattern of cannabis use that gradually increases in both frequency and amount. Cannabis,
along with tobacco and alcohol, is traditionally the first substance that adolescents try.
Many perceive cannabis use as less harmful than alcohol or tobacco use, and this percep-
tion likely contributes to increased use. Moreover, cannabis intoxication does not typically
result in as severe behavioral and cognitive dysfunction as does significant alcohol intox-
ication, which may increase the probability of more frequent use in more diverse situa-
tions than with alcohol. These factors likely contribute to the potential rapid transition
from cannabis use to a cannabis use disorder among some adolescents and the common
pattern of using throughout the day that is commonly observed among those with more
severe cannabis use disorder.
Cannabis use disorder among preteens, adolescents, and young adults is typically ex-
pressed as excessive use with peers that is a component of a pattern of other delinquent
behaviors usually associated with conduct problems. Milder cases primarily reflect con-
tinued use despite clear problems related to disapproval of use by other peers, school ad-
ministration, or family, which also places the youth at risk for physical or behavioral
consequences. In more severe cases, there is a progression to using alone or using through-
out the day such that use interferes with daily functioning and takes the place of previ-
ously established, prosocial activities.
With adolescent users, changes in mood stability, energy level, and eating patterns are
commonly observed. These signs and symptoms are likely due to the direct effects of can-
nabis use (intoxication) and the subsequent effects following acute intoxication (coming
down), as well as attempts to conceal use from others. School-related problems are com-
monly associated with cannabis use disorder in adolescents, particularly a dramatic drop
in grades, truancy, and reduced interest in general school activities and outcomes.
Cannabis use disorder among adults typically involves well-established patterns of daily
cannabis use that continue despite clear psychosocial or medical problems. Many adults have
experienced repeated desire to stop or have failed at repeated cessation attempts. Milder adult
cases may resemble the more common adolescent cases in that cannabis use is not as frequent
or heavy but continues despite potential significant consequences of sustained use. The rate of
use among middle-age and older adults appears to be increasing, likely because of a cohort ef-
fect resulting from high prevalence of use in the late 1960s and the 1970s.
Early onset of cannabis use (e.g., prior to age 15 years) is a robust predictor of the de-
velopment of cannabis use disorder and other types of substance use disorders and mental
disorders during young adulthood. Such early onset is likely related to concurrent other
externalizing problems, most notably conduct disorder symptoms. However, early onset
is also a predictor of internalizing problems and as such probably reflects a general risk
factor for the development of mental health disorders.
Risk and Prognostic Factors
Temperamental. A history of conduct disorder in childhood or adolescence and antiso-
cial personality disorder are risk factors for the development of many substance-related
disorders, including cannabis-related disorders. Other risk factors include externalizing
514 Substance-Related and Addictive Disorders
or internalizing disorders during childhood or adolescence. Youths with high behavioral
disinhibition scores show early-onset substance use disorders, including cannabis use dis-
order, multiple substance involvement, and early conduct problems.
Environmental. Risk factors include academic failure, tobacco smoking, unstable or abu-
sive family situation, use of cannabis among immediate family members, a family history
of a substance use disorder, and low socioeconomic status. As with all substances of abuse,
the ease of availability of the substance is a risk factor; cannabis is relatively easy to obtain
in most cultures, which increases the risk of developing a cannabis use disorder.
Genetic and physiological. Genetic influences contribute to the development of canna-
bis use disorders. Heritable factors contribute between 30% and 80% of the total variance
in risk of cannabis use disorders. It should be noted that common genetic and shared en-
vironmental influences between cannabis and other types of substance use disorders sug-
gest a common genetic basis for adolescent substance use and conduct problems.
Culture-Related Diagnostic Issues
Cannabis is probably the world’s most commonly used illicit substance. Occurrence of
cannabis use disorder across countries is unknown, but the prevalence rates are likely sim-
ilar among developed countries. It is frequently among the first drugs of experimentation
(often in the teens) of all cultural groups in the United States.
Acceptance of cannabis for medical purposes varies widely across and within cultures.
Cultural factors (acceptability and legal status) that might impact diagnosis relate to dif-
ferential consequences across cultures for detection of use (i.e., arrest, school suspensions,
or employment suspension). The general change in substance use disorder diagnostic cri-
teria from DSM-IV to DSM-5 (i.e., removal of the recurrent substance-related legal prob-
lems criterion) mitigates this concern to some degree.
Diagnostic Markers
Biological tests for cannabinoid metabolites are useful for determining if an individual has
recently used cannabis. Such testing is helpful in making a diagnosis, particularly in
milder cases if an individual denies using while others (family, work, school) purport con-
cern about a substance use problem. Because cannabinoids are fat soluble, they persist in
bodily fluids for extended periods of time and are excreted slowly. Expertise in urine test-
ing methods is needed to reliably interpret results.
Functional Consequences of Cannabis Use Disorder
Functional consequences of cannabis use disorder are part of the diagnostic criteria. Many
areas of psychosocial, cognitive, and health functioning may be compromised in relation
to cannabis use disorder. Cognitive function, particularly higher executive function, ap-
pears to be compromised in cannabis users, and this relationship appears to be dose de-
pendent (both acutely and chronically). This may contribute to increased difficulty at
school or work. Cannabis use has been related to a reduction in prosocial goal-directed ac-
tivity, which some have labeled an amotivational syndrome, that manifests itself in poor
school performance and employment problems. These problems may be related to perva-
sive intoxication or recovery from the effects of intoxication. Similarly, cannabis-associated
problems with social relationships are commonly reported in those with cannabis use dis-
order. Accidents due to engagement in potentially dangerous behaviors while under the
influence (e.g., driving, sport, recreational or employment activities) are also of concern.
Cannabis smoke contains high levels of carcinogenic compounds that place chronic users
at risk for respiratory illnesses similar to those experienced by tobacco smokers. Chronic
cannabis use may contribute to the onset or exacerbation of many other mental disorders.
In particular, concern has been raised about cannabis use as a causal factor in schizophrenia
and other psychotic disorders. Cannabis use can contribute to the onset of an acute psy-
Cannabis Use Disorder 515
chotic episode, can exacerbate some symptoms, and can adversely affect treatment of a
major psychotic jllness.
Differential Diagnosis
Nonproblematic use of cannabis. The distinction between nonproblematic use of can-
nabis and cannabis use disorder can be difficult to make because social, behavioral, or psy-
chological problems may be difficult to attribute to the substance, especially in the context
of use of other substances. Also, denial of heavy cannabis use and the attribution that can-
nabis is related to or causing substantial problems are common among individuals who
are referred to treatment by others (i.e., school, family, employer, criminal justice system).
Other mental disorders. Cannabis-induced disorder may be characterized by symp-
toms (e.g., anxiety) that resemble primary mental disorders (e.g., generalized anxiety dis-
order vs. cannabis-induced anxiety disorder, with generalized anxiety, with onset during
intoxication). Chronic intake of cannabis can produce a lack of motivation that resembles
persistent depressive disorder (dysthymia). Acute adverse reactions to cannabis should be
differentiated from the symptoms of panic disorder, major depressive disorder, delusional
disorder, bipolar disorder, or schizophrenia, paranoid type. Physical examination will
usually show an increased pulse and conjunctival injection. Urine toxicological testing can
be helpful in making a diagnosis.
Comorbidity
Cannabis has been commonly thought of as a “gateway” drug because individuals who
frequently use cannabis have a much greater lifetime probability than nonusers of using
what are commonly considered more dangerous substances, like opioids or cocaine. Can-
nabis use and cannabis use disorder are highly comorbid with other substance use disor-
ders. Co-occurring mental conditions are common in cannabis use disorder. Cannabis use
has been associated with poorer life satisfaction; increased mental health treatment and
hospitalization; and higher rates of depression, anxiety disorders, suicide attempts, and
conduct disorder. Individuals with past-year or lifetime cannabis use disorder have high
rates of alcohol use disorder (greater than 50%) and tobacco use disorder (53%). Rates of
other substance use disorders are also likely to be high among individuals with cannabis
use disorder. Among those seeking treatment for a cannabis use disorder, 74% report
problematic use of a secondary or tertiary substance: alcohol (40%), cocaine (12%), meth-
amphetamine (6%), and heroin or other opiates (2%). Among those younger than 18 years,
61% reported problematic use of a secondary substance: alcohol (48%), cocaine (4%), meth-
amphetamine (2%), and heroin or other opiates (2%). Cannabis use disorder is also often
observed as a secondary problem among those with a primary diagnosis of other substance
use disorders, with approximately 25%-80% of those in treatment for another substance
use disorder reporting use of cannabis.
Individuals with past-year or lifetime diagnoses of cannabis use disorder also have
high rates of concurrent mental disorders other than substance use disorders. Major de-
pressive disorder (11%), any anxiety disorder (24%), and bipolar I disorder (13%) are quite
common among individuals with a past-year diagnosis of a cannabis use disorder, as are
antisocial (30%), obsessive-compulsive, (19%), and paranoid (18%) personality disorders.
Approximately 33% of adolescents with cannabis use disorder have internalizing disor-
ders (e.g., anxiety, depression, posttraumatic stress disorder), and 60% have externalizing
disorders (e.g., conduct disorder, attention-deficit/hyperactivity disorder).
Although cannabis use can impact multiple aspects of normal human functioning, in-
cluding the cardiovascular, immune, neuromuscular, ocular, reproductive, and respira-
tory systems, as well as appetite and cognition/ perception, there are few clear medical
conditions that commonly co-occur with cannabis use disorder. The most significant health
516 Substance-Related and Addictive Disorders
effects of cannabis involve the respiratory system, and chronic cannabis smokers exhibit
high rates of respiratory symptoms of bronchitis, sputum production, shortness of breath,
and wheezing.
Cannabis Intoxication
Diagnostic Criteria
A. Recent use of cannabis.
B. Clinically significant problematic behavioral or psychological changes (e.g., impaired
motor coordination, euphoria, anxiety, sensation of slowed time, impaired judgment,
social withdrawal) that developed during, or shortly after, cannabis use.
C. Two (or more) of the following signs or symptoms developing within 2 hours of canna-
bis use:
1. Conjunctival injection.
2. Increased appetite.
3. Dry mouth.
4. Tachycardia.
D. The signs or symptoms are not attributable to another medical condition and are not better
explained by another mental disorder, including intoxication with another substance.
Specify if:
With perceptual disturbances: Hallucinations with intact reality testing or auditory, vi-
sual, or tactile illusions occur in the absence of a delirium.
Coding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether
or not there is a comorbid cannabis use disorder and whether or not there are perceptual
disturbances,
For cannabis intoxication, without perceptual disturbances: If a mild cannabis use
disorder is comorbid, the ICD-10-CM code is F12.129, and if a moderate or severe
cannabis use disorder is comorbid, the ICD-10-CM code is F12.229. If there is no co-
morbid cannabis use disorder, then the }CD-10-CM code is F12.929.
For cannabis intoxication, with perceptual disturbances: If a mild cannabis use
disorder is comorbid, the ICD-10-CM code is F12.122, and if a moderate or severe
cannabis use disorder is comorbid, the ICD-10-CM code is F12.222. If there is no co-
morbid cannabis use disorder, then the ICD-10-CM code is F12.922.
Specifiers
When hallucinations occur in the absence of intact reality testing, a diagnosis of substance /
medication-induced psychotic disorder should be considered.
Diagnostic Features
The essential feature of cannabis intoxication is the presence of clinically significant prob-
lematic behavioral or psychological changes that develop during, or shortly after, canna-
bis use (Criterion B). Intoxication typically begins with a “high” feeling followed by
symptoms that include euphoria with inappropriate laughter and grandiosity, sedation,
lethargy, impairment in short-term memory, difficulty carrying out complex mental pro-
cesses, impaired judgment, distorted sensory perceptions, impaired motor performance,
and the sensation that time is passing slowly. Occasionally, anxiety (which can be severe),
Cannabis Withdrawal 517
dysphoria, or social withdrawal occurs. These psychoactive effects are accompanied by
two or more of the following signs, developing within 2 hours of cannabis use: conjuncti-
val injection, increased appetite, dry mouth, and tachycardia (Criterion C).
Intoxication develops within minutes if the cannabis is smoked but may take a few
hours to develop if the cannabis is ingested orally. The effects usually last 3-4 hours, with
the duration being somewhat longer when the substance is ingested orally. The magnitude
of the behavioral and physiological changes depends on the dose, the method of adminis-
tration, and the characteristics of the individual using the substance, such as rate of absorp-
tion, tolerance, and sensitivity to the effects of the substance. Because most cannabinoids,
including delta-9-tetrahydrocannabinol (delta-9-THC), are fat soluble, the effects of canna-
bis or hashish may occasionally persist or reoccur for 12-24 hours because of the slow re-
lease of psychoactive substances from fatty tissue or to enterohepatic circulation.
Prevalence
The prevalence of actual episodes of cannabis intoxication in the general population is un-
known. However, it is probable that most cannabis users would at some time meet criteria
for cannabis intoxication. Given this, the prevalence of cannabis users and the prevalence
of individuals experiencing cannabis intoxication are likely similar.
Functional Consequences of Cannabis Intoxication
Impairment from cannabis intoxication may have serious consequences, including dys-
function at work or school, social indiscretions, failure to fulfill role obligations, traffic ac-
cidents, and having unprotected sex. In rare cases, cannabis intoxication may precipitate a
psychosis that may vary in duration.
Differential Diagnosis
Note that if the clinical presentation includes hallucinations in the absence of intact reality
testing, a diagnosis of substance/medication-induced psychotic disorder should be con-
sidered.
Other substance intoxication. Cannabis intoxication may resemble intoxication with
other types of substances. However, in contrast to cannabis intoxication, alcohol intoxica-
tion and sedative, hypnotic, or anxiolytic intoxication frequently decrease appetite, in-
crease aggressive behavior, and produce nystagmus or ataxia. Hallucinogens in low doses
may cause a clinical picture that resembles cannabis intoxication. Phencyclidine, like can-
nabis, can be smoked and also causes perceptual changes, but phencyclidine intoxication
is much more likely to cause ataxia and aggressive behavior.
Other cannabis-induced disorders. Cannabis intoxication is distinguished from the other
cannabis-induced disorders (e.g., cannabis-induced anxiety disorder, with onset during
intoxication) because the symptoms in these latter disorders predominate the clinical pre-
sentation and are severe enough to warrant independent clinical attention.
Cannabis Withdrawal
Diagnostic Criteria 292.0 (F12.288)
A. Cessation of cannabis use that has been heavy and prolonged (i.e., usually daily or
almost daily use over a period of at least a few months).
B. Three (or more) of the following signs and symptoms develop within approximately 1 week
after Criterion A:
518 Substance-Related and Addictive Disorders
Irritability, anger, or aggression.
Nervousness or anxiety.
Sleep difficulty (e.g., insomnia, disturbing dreams).
Decreased appetite or weight loss.
Restlessness.
Depressed mood.
At least one of the following physical symptoms causing significant discomfort: ab-
dominal pain, shakiness/tremors, sweating, fever, chills, or headache.
C. The signs or symptoms in Criterion B cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including intoxication or withdrawal from
another substance.
Coding note: The iCD-9-CM code is 292.0. The ICD-10-CM code for cannabis withdrawal
is F12.288. Note that the ICD-10-CM code indicates the comorbid presence of a moderate
or severe cannabis use disorder, reflecting the fact that cannabis withdrawal can only oc-
cur in the presence of a moderate or severe cannabis use disorder. It is not permissible to
code a comorbid mild cannabis use disorder with cannabis withdrawal.
NOahanN>
Diagnostic Features
The essential feature of cannabis withdrawal is the presence of a characteristic withdrawal
syndrome that develops after the cessation of or substantial reduction in heavy and pro-
longed cannabis use. In addition to the symptoms in Criterion B, the following may also be
observed postabstinence: fatigue, yawning, difficulty concentrating, and rebound periods
of increased appetite and hypersomnia that follow initial periods of loss of appetite and in-
somnia. For the diagnosis, withdrawal symptoms must cause clinically significant distress
or impairment in social, occupational, or other important areas of functioning (Criterion
C). Many cannabis users report smoking cannabis or taking other substances to help re-
lieve withdrawal symptoms, and many report that withdrawal symptoms make quitting
difficult or have contributed to relapse. The symptoms typically are not of sufficient se-
verity to require medical attention, but medication or behavioral strategies may help alle-
viate symptoms and improve prognosis in those trying to quit using cannabis.
Cannabis withdrawal is commonly observed in individuals seeking treatment for can-
nabis use as well as in heavy cannabis users who are not seeking treatment. Among indi-
viduals who have used cannabis regularly during some period of their lifetime, up to one-
third report having experienced cannabis withdrawal. Among adults and adolescents en-
rolled in treatment or heavy cannabis users, 50%-95% report cannabis withdrawal. These
findings indicate that cannabis withdrawal occurs among a substantial subset of regular
cannabis users who try to quit.
Development and Course
The amount, duration, and frequency of cannabis smoking that is required to produce an
associated withdrawal disorder during a quit attempt are unknown. Most symptoms have
their onset within the first 24-72 hours of cessation, peak within the first week, and last
approximately 1-2 weeks. Sleep difficulties may last more than 30 days. Cannabis with-
drawal has been documented among adolescents and adults. Withdrawal tends to be more
common and severe among adults, most likely related to the more persistent and greater
frequency and quantity of use among adults.
Unspecified Cannabis-Related Disorder 519
Risk and Prognostic Factors
Environmental. “Most likely, the prevalence and severity of cannabis withdrawal are
greater among heavier cannabis users, and particularly among those seeking treatment for
cannabis use disorders. Withdrawal severity also appears to be positively related to the se-
verity of comorbid symptoms of mental disorders.
Functional Consequences of Cannabis Withdrawal
Cannabis users report using cannabis to relieve withdrawal symptoms, suggesting that
withdrawal might contribute to ongoing expression of cannabis use disorder. Worse out-
comes may be associated with greater withdrawal. A substantial proportion of adults and
adolescents in treatment for moderate to severe cannabis use disorder acknowledge mod-
erate to severe withdrawal symptoms, and many complain that these symptoms make ces-
sation more difficult. Cannabis users report having relapsed to cannabis use or initiating
use of other drugs (e.g., tranquilizers) to provide relief from cannabis withdrawal symp-
toms. Last, individuals living with cannabis users observe significant withdrawal effects,
suggesting that such symptoms are disruptive to daily living.
Differential Diagnosis
Because many of the symptoms of cannabis withdrawal are also symptoms of other sub-
stance withdrawal syndromes or of depressive or bipolar disorders, careful evaluation
should focus on ensuring that the symptoms are not better explained by cessation from an-
other substance (e.g., tobacco or alcohol withdrawal), another mental disorder (general-
ized anxiety disorder, major depressive disorder), or another medical condition.
Other Cannabis-Induced Disorders
The following cannabis-induced disorders are described in other chapters of the manual with
disorders with which they share phenomenology (see the substance /medication-induced
mental disorders in these chapters): cannabis-induced psychotic disorder ("Schizophrenia
Spectrum and Other Psychotic Disorders”); cannabis-induced anxiety disorder (“Anxiety
Disorders”); and cannabis-induced sleep disorder (“Sleep-Wake Disorders”). For cannabis
intoxication delirium, see the criteria and discussion of delirium in the chapter “Neurocog-
nitive Disorders.” These cannabis-induced disorders are diagnosed instead of cannabis in-
toxication or cannabis withdrawal when the symptoms are sufficiently severe to warrant
independent clinical attention.
Unspecified Cannabis-Related Disorder
292.9 (F12.99)
This category applies to presentations in which symptoms characteristic of a cannabis-
related disorder that cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning predominate but do not meet the full criteria
for any specific cannabis-related disorder or any of the disorders in the substance-related
and addictive disorders diagnostic class.
520
Substance-Related and Addictive Disorders
Hallucinogen-Related Disorders
Phencyclidine Use Disorder
Other Hallucinogen Use Disorder
Phencyclidine Intoxication
Other Hallucinogen Intoxication
Hallucinogen Persisting Perception Disorder
Other Phencyclidine-Induced Disorders
Other Hallucinogen-Induced Disorders
Unspecified Phencyclidine-Related Disorder
Unspecified Hallucinogen-Related Disorder
Phencyclidine Use Disorder
Diagnostic Criteria
A. A pattern of phencyclidine (or a pharmacologically similar substance) use leading to
Clinically significant impairment or distress, as manifested by at least two of the follow-
ing, occurring within a 12-month period:
1.
2.
10.
Phencyclidine is often taken in larger amounts or over a longer period than was in-
tended.
There is a persistent desire or unsuccessful efforts to cut down or control phency-
clidine use.
A great deal of time is spent in activities necessary to obtain phencyclidine, use the
phencyclidine, or recover from its effects.
Craving, or a strong desire or urge to use phencyclidine.
Recurrent phencyclidine use resulting in a failure to fulfill major role obligations at
work, school, or home (e.g., repeated absences from work or poor work performance
related to phencyclidine use; phencyclidine-related absences, suspensions, or ex-
pulsions from school; neglect of children or household).
Continued phencyclidine use despite having persistent or recurrent social or inter-
personal problems caused or exacerbated by the effects of the phencyclidine (e.g.,
arguments with a spouse about consequences of intoxication; physical fights).
important social, occupational, or recreational activities are given up or reduced be-
cause of phencyclidine use.
Recurrent phencyclidine use in situations in which it is physically hazardous (e.g.,
driving an automobile or operating a machine when impaired by a phencyclidine).
Phencyclidine use is continued despite knowledge of having a persistent or recur-
rent physical or psychological problem that is likely to have been caused or exac-
erbated by the phencyclidine.
Tolerance, as defined by either of the following:
a. Aneed for markedly increased amounts of the phencyclidine to achieve intoxi-
cation or desired effect.
b. A markedly diminished effect with continued use of the same amount of the
phencyclidine.
Phencyclidine Use Disorder 521
Note: Withdrawal symptoms and signs are not established for phencyclidines, and so this
criterion does not apply. (Withdrawal from phencyclidines has been reported in animals
but not documented in human users.)
Specify if:
In early remission: After full criteria for phencyclidine use disorder were previously
met, none of the criteria for phencyclidine use disorder have been met for at least
3 months but for less than 12 months (with the exception that Criterion A4, “Craving,
or a strong desire or urge to use the phencyclidine,” may be met).
In sustained remission: After full criteria for phencyclidine use disorder were previ-
ously met, none of the criteria for phencyclidine use disorder have been met at any time
during a period of 12 months or longer (with the exception that Criterion A4, “Craving,
or a strong desire or urge to use the phencyclidine,” may be met).
Specify if:
in a controlled environment: This additional specifier is used if the individual is in an
environment where access to phencyclidines is restricted.
Coding based on current severity: Note for ICD-10-CM codes: If a phencyclidine intoxica-
tion or another phencyclidine-induced mental disorder is also present, do not use the codes
below for phencyclidine use disorder. Instead, the comorbid phencyclidine use disorder is in-
dicated in the 4th character of the phencyclidine-induced disorder code (see the coding note
for phencyclidine intoxication or a specific phencyclidine-induced mental disorder). For ex-
ample, if there is comorbid phencyclidine-induced psychotic disorder, only the phencyclidine-
induced psychotic disorder code is given, with the 4th character indicating whether the co-
morbid phencyclidine use disorder is mild, moderate, or severe: F16.159 for mild phencycli-
dine use disorder with phencyclidine-induced psychotic disorder or F16.259 for a moderate
or severe phencyclidine use disorder with phencyclidine-induced psychotic disorder.
Specify current severity:
305.90 (F16.10) Mild: Presence of 2-3 symptoms.
304.60 (F16.20) Moderate: Presence of 4-5 symptoms.
304.60 (F16.20) Severe: Presence of 6 or more symptoms.
Specifiers
“Inacontrolled environment” applies as a further specifier of remission if the individual is
both in remission and in a controlled environment (i.e., in early remission in a controlled
environment or in sustained remission in a controlled environment). Examples of these
environments are closely supervised and substance-free jails, therapeutic communities,
and locked hospital units.
Diagnostic Features
The phencyclidines (or phencyclidine-like substances) include phencyclidine (e.g., PCP,
“angel dust”) and less potent but similarly acting compounds such as ketamine, cyclohex-
amine, and dizocilpine. These substances were first developed as dissociative anesthetics
in the 1950s and became street drugs in the 1960s. They produce feelings of separation
from mind and body (hence “dissociative”) in low doses, and at high doses, stupor and
coma can result. These substances are most commonly smoked or taken orally, but they
may also be snorted or injected. Although the primary psychoactive effects of PCP last for
a few hours, the total elimination rate of this drug from the body typically extends 8 days
or longer. The hallucinogenic effects in vulnerable individuals may last for weeks and may
precipitate a persistent psychotic episode resembling schizophrenia. Ketamine has been
observed to have utility in the treatment of major depressive disorder. Withdrawal symp-
522 Substance-Related and Addictive Disorders
toms have not been clearly established in humans, and therefore the withdrawal criterion
is not included in the diagnosis of phencyclidine use disorder.
Associated Features Supporting Diagnosis
Phencyclidine may be detected in urine for up to 8 days or even longer at very high doses. In
addition to laboratory tests to detect its presence, characteristic symptoms resulting from
intoxication with phencyclidine or related substances may aid in its diagnosis. Phencycli-
dine is likely to produce dissociative symptoms, analgesia, nystagmus, and hypertension,
with risk of hypotension and shock. Violent behavior can also occur with phencyclidine
use, as intoxicated persons may believe that they are being attacked. Residual symptoms
following use may resemble schizophrenia.
Prevalence
The prevalence of phencyclidine use disorder is unknown. Approximately 2.5% of the pop-
ulation reports having ever used phencyclidine. The proportion of users increases with
age, from 0.3% of 12- to 17-year-olds, to 1.3% of 18- to 25-year-olds, to 2.9% of those age 26
years and older reporting ever using phencyclidine. There appears to have been an in-
crease among 12th graders in both ever used (to 2.3% from 1.8%) and past-year use (to 1.3%
from 1.0%) of phencyclidine. Past-year use of ketamine appears relatively stable among
12th graders (1.6%-1.7% over the past 3 years).
Risk and Prognostic Factors
There is little information about risk factors for phencyclidine use disorder. Among indi-
viduals admitted to substance abuse treatment, those for whom phencyclidine was the
primary substance were younger than those admitted for other substance use, had lower
educational levels, and were more likely to be located in the West and Northeast regions of
the United States, compared with other admissions.
Cuiture-Reiated Diagnostic Issues
Ketamine use in youths ages 16-23 years has been reported to be more common among
whites (0.5%) than among other ethnic groups (range 0%-0.3%). Among individuals ad-
mitted to substance abuse treatment, those for whom phencyclidine was the primary sub-
stance were predominantly black (49%) or Hispanic (29%).
Gender-Reiated Diagnostic Issues
Males make up about three-quarters of those with phencyclidine-related emergency room
visits.
Diagnostic Markers
Laboratory testing may be useful, as phencyclidine is present in the urine in intoxicated in-
dividuals up to 8 days after ingestion. The individual’s history, along with certain physical
signs, such as nystagmus, analgesia and prominent hypertension, may aid in distinguish-
ing the phencyclidine clinical picture from that of other hallucinogens.
Functional Consequences of Phencyclidine Use Disorder
In individuals with phencyclidine use disorder, there may be physical evidence of injuries
from accidents, fights, and falls. Chronic use of phencyclidine may lead to deficits in mem-
ory, speech, and cognition that may last for months. Cardiovascular and neurological tox-
icities (e.g., seizures, dystonias, dyskinesias, catalepsy, hypothermia or hyperthermia)
may result from intoxication with phencyclidine. Other consequences include intracranial
hemorrhage, rhabdomyolysis, respiratory problems, and (occasionally) cardiac arrest.
Other Hallucinogen Use Disorder 523
Differential Diagnosis
Other substance use disorders. Distinguishing the effects of phencyclidine from those
of other substances is important, since it may be a common additive to other substances
(e.g., cannabis, cocaine).
Schizophrenia and other mental disorders. Some of the effects of phencyclidine and
related substance use may resemble symptoms of other psychiatric disorders, such as psy-
chosis (schizophrenia), low mood (major depressive disorder), violent aggressive be-
haviors (conduct disorder, antisocial personality disorder). Discerning whether these
behaviors occurred before the intake of the drug is important in the differentiation of acute
drug effects from preexisting mental disorder. Phencyclidine-induced psychotic disorder
should be considered when there is impaired reality testing in individuals experiencing
disturbances in perception resulting from ingestion of phencyclidine.
Other Hallucinogen Use Disorder
Diagnostic Criteria
A. A problematic pattern of hallucinogen (other than phencyclidine) use leading to clini-
cally significant impairment or distress, as manifested by at least two of the following,
occurring within a 12-month period:
1. The hallucinogen is often taken in larger amounts or over a longer period than was
intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control halluci-
nogen use.
3. A great deal of time is spent in activities necessary to obtain the hallucinogen, use
the hallucinogen, or recover from its effects.
4. Craving, or a strong desire or urge to use the hallucinogen.
5. Recurrent hatlucinogen use resulting in a failure to fulfill major role obligations at
work, school, or home (e.g., repeated absences from work or poor work perfor-
mance related to hallucinogen use; hallucinogen-related absences, suspensions,
or expulsions from school; neglect of children or household).
6. Continued hallucinogen use despite having persistent or recurrent social or inter-
personal problems caused or exacerbated by the effects of the hallucinogen (e.g.,
arguments with a spouse about consequences of intoxication; physical fights).
7. Important social, occupational, or recreational activities are given up or reduced be-
cause of hallucinogen use.
8. Recurrent hallucinogen use in situations in which it is physically hazardous (e.g.,
driving an automobile or operating a machine when impaired by the hallucinogen).
9. Hallucinogen use is continued despite knowledge of having a persistent or recur-
rent physical or psychological problem that is likely to have been caused or exac-
erbated by the hallucinogen.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of the hallucinogen to achieve intoxi-
cation or desired effect.
b. Amarkedly diminished effect with continued use of the same amount of the hal-
lucinogen.
Note: Withdrawal symptoms and signs are not established for hallucinogens, and so this
criterion does not apply.
524 Substance-Related and Addictive Disorders
Specify the particular hallucinogen.
Specify if:
In early remission: After full criteria for other hallucinogen use disorder were previ-
ously met, none of the criteria for other hallucinogen use disorder have been met for
at least 3 months but for less than 12 months (with the exception that Criterion A4,
“Craving, or a strong desire or urge to use the hallucinogen,” may be met).
In sustained remission: After full criteria for other hallucinogen use disorder were
previously met, none of the criteria for other hallucinogen use disorder have been met
at any time during a period of 12 months or longer (with the exception that Criterion A4,
“Craving, or a strong desire or urge to use the hallucinogen,” may be met).
Specify if:
In a controlled environment: This additional specifier is used if the individual is in an
environment where access to hallucinogens is restricted.
Coding based on current severity: Note for ICD-10-CM codes: If a hallucinogen intoxication
or another hallucinogen-induced mental disorder is also present, do not use the codes below
for hallucinogen use disorder. Instead, the comorbid hallucinogen use disorder is indicated in
the 4th character of the hallucinogen-induced disorder code (see the coding note for halluci-
nogen intoxication or specific hallucinogen-induced mental disorder). For example, if there is
comorbid hallucinogen-induced psychotic disorder and hallucinogen use disorder, only the
hallucinogen-induced psychotic disorder code is given, with the 4th character indicating wheth-
er the comorbid hallucinogen use disorder is mild, moderate, or severe: F16.159 for mild hal-
lucinogen use disorder with hallucinogen-induced psychotic disorder or F16.259 for a
moderate or severe hallucinogen use disorder with hallucinogen-induced psychotic disorder.
Specify current severity:
305.30 (F16.10) Mild: Presence of 2-3 symptoms.
304.50 (F16.20) Moderate: Presence of 4—5 symptoms.
304.50 (F16.20) Severe: Presence of 6 or more symptoms.
Specifiers
“Ina controlled environment” applies as a further specifier of remission if the individual is
both in remission and in a controlled environment (ie., in early remission in a controlled
environment or in sustained remission in a controlled environment). Examples of these
environments are closely supervised and substance-free jails, therapeutic communities,
and locked hospital units.
Diagnostic Features
Hallucinogens comprise a diverse group of substances that, despite having different chem-
ical structures and possibly involving different molecular mechanisms, produce similar
alterations of perception, mood, and cognition in users. Hallucinogens included are phenyl-
alkylamines (e.g., mescaline, DOM [2,5-dimethoxy-4-methylamphetamine], and MDMA
[3,4-methylenedioxymethamphetamine; also called “ecstasy”]); the indoleamines, includ-
ing psilocybin (i.e., psilocin) and dimethyltryptamine (DMT), and the ergolines, such as LSD
(lysergic acid diethylamide) and morning glory seeds. In addition, miscellaneous other
ethnobotanical compounds are classified as “hallucinogens,” of which Salvia divinorum and
jimsonweed are two examples. Excluded from the hallucinogen group are cannabis and its
active compound, delta-9-tetrahydrocannabinol (THC) (see the section “Cannabis-Related
Disorders”). These substances can have hallucinogenic effects but are diagnosed separately
because of significant differences in their psychological and behavioral effects.
Hallucinogens are usually taken orally, although some forms are smoked (e.g., DMT,
salvia) or (rarely) taken intranasally or by injection (e.g., ecstasy). Duration of effects varies
Other Hallucinogen Use Disorder 525
across types of hallucinogens. Some of these substances (i.e., LSD, MDMA) have a long
half-life and extended duration such that users may spend hours to days using and/or re-
covering from the effects of these drugs. However, other hallucinogenic drugs (e.g., DMT,
salvia) are short acting. Tolerance to hallucinogens develops with repeated use and has
been reported to have both autonomic and psychological effects. Cross-tolerance exists be-
tween LSD and other hallucinogens (e.g., psilocybin, mescaline) but does not extend to
other drug categories such as amphetamines and cannabis.
MDMA /ecstasy as a hallucinogen may have distinctive effects attributable to both its hal-
lucinogenic and its stimulant properties. Among heavy ecstasy users, continued use despite
physical or psychological problems, tolerance, hazardous use, and spending a great deal of
time obtaining the substance are the most commonly reported criteria—over 50% in adults
and over 30% in a younger sample, while legal problems related to substance use and persis-
tent desire/inability to quit are rarely reported. As found for other substances, diagnostic cri-
teria for other hallucinogen use disorder are arrayed along a single continuum of severity.
One of the generic criteria for substance use disorders, a clinically significant with-
drawal syndrome, has not been consistently documented in humans, and therefore the di-
agnosis of hallucinogen withdrawal syndrome is not included in DSM-5. However, there
is evidence of withdrawal from MDMA, with endorsement of two or more withdrawal
symptoms observed in 59%—98% in selected samples of ecstasy users. Both psychological
and physical problems have been commonly reported as withdrawal problems.
Associated Features Supporting Diagnosis
The characteristic symptom features of some of the hallucinogens can aid in diagnosis if
urine or blood toxicology results are not available. For example, individuals who use LSD
tend to experience visual hallucinations that can be frightening. Individuals intoxicated
with hallucinogens may exhibit a temporary increase in suicidality.
Prevalence
Of all substance use disorders, other hallucinogen use disorder is one of the rarest. The
12-month prevalence is estimated to be 0.5% among 12- to 17-year-olds and 0.1% among
adults age 18 and older in the United States. Rates are higher in adult males (0.2%) compared
with females (0.1%), but the opposite is observed in adolescent samples ages 12-17, in which
the 12-month rate is slightly higher in females (0.6%) than in males (0.4%). Rates are highest in
individuals younger than 30 years, with the peak occurring in individuals ages 18-29 years
(0.6%) and decreasing to virtually 0.0% among individuals age 45 and older.
There are marked ethnic differences in 12-month prevalence of other hallucinogen use
disorder. Among youths ages 12-17 years, 12-month prevalence is higher among Native
Americans and Alaska Natives (1.2%) than among Hispanics (0.6%), whites (0.6%), Afri-
can Americans (0.2%), and Asian Americans and Pacific Islanders (0.2%). Among adults,
12-month prevalence of other hallucinogen use disorder is similar for Native Americans
and Alaska Natives, whites, and Hispanics (all 0.2%) but somewhat lower for Asian Amer-
icans and Pacific Islanders (0.07%) and African Americans (0.03%). Past-year prevalence is
higher in clinical samples (e.g., 19% in adolescents in treatment). Among individuals cur-
rently using hallucinogens in the general population, 7.8% (adult) to 17% (adolescent) had
a problematic pattern of use that met criteria for past-year other hallucinogen use disorder.
Among select groups of individuals who use hallucinogens (e.g., recent heavy ecstasy
use), 73.5% of adults and 77% of adolescents have a problematic pattern of use that may
meet other hallucinogen use disorder criteria.
Development and Course
Unlike most substances where an early age at onset is associated with elevations in risk for
the corresponding use disorder, it is unclear whether there is an association of an early age
526 Substance-Related and Addictive Disorders
at onset with elevations in risk for other hallucinogen use disorder. However, patterns of
drug consumption have been found to differ by age at onset, with early-onset ecstasy users
more likely to be polydrug users than their later-onset counterparts. There may be a dis-
proportionate influence of use of specific hallucinogens on risk of developing other hallu-
cinogen use disorder, with use of ecstasy /MDMaA increasing the risk of the disorder
relative to use of other hallucinogens.
Little is known regarding the course of other hallucinogen use disorder, but it is generally
thought to have low incidence, low persistence, and high rates of recovery. Adolescents are es-
pecially at risk for using these drugs, and it is estimated that 2.7% of youths ages 12-17 years
have used one or more of these drugs in the past 12 months, with 44% having used ecstasy /
MDMA. Other hallucinogen use disorder is a disorder observed primarily in individuals
younger than 30 years, with rates vanishingly rare among older adults.
Risk and Prognostic Factors
Temperamental. In adolescents but not consistently in adults, MDMA use is associated with
an elevated rate of other hallucinogen use disorder. Other substance use disorders, particu-
larly alcohol, tobacco, and cannabis, and major depressive disorder are associated with ele-
vated rates of other hallucinogen use disorder. Antisocial personality disorder may be
elevated among individuals who use more than two other drugs in addition to hallucinogens,
compared with their counterparts with less extensive use history. The influence of adult anti-
social behaviors—but not conduct disorder or antisocial personality disorder—on other hal-
lucinogen use disorder may be stronger in females than in males. Use of specific hallucinogens
(e.g., salvia) is prominent among individuals ages 18-25 years with other risk-taking behaviors
and illegal activities. Cannabis use has also been implicated asa precursor to initiation of use of
hallucinogens (e.g., ecstasy), along with early use of alcohol and tobacco. Higher drug use by
peers and high sensation seeking have also been associated with elevated rates of ecstasy use.
MDMA /ecstasy use appears to signify a more severe group of hallucinogen users.
Genetic and physiological. Among male twins, total variance due to additive genetics
has been estimated to range from 26% to 79%, with inconsistent evidence for shared envi-
ronmental influences.
Culture-Related Diagnostic Issues
Historically, hallucinogens have been used as part of established religious practices, such
as the use of peyote in the Native American Church and in Mexico. Ritual use by indige-
nous populations of psilocybin obtained from certain types of mushrooms has occurred in
South America, Mexico, and some areas in the United States, or of ayahuasca in the Santo
Daime and Unido de Vegetal sects. Regular use of peyote as part of religious rituals is not
linked to neuropsychological or psychological deficits. For adults, no race or ethnicity dif-
ferences for the full criteria or for any individual criterion are apparent at this time.
Gender-Related Diagnostic Issues
In adolescents, females may be less likely than males to endorse “hazardous use,” and fe-
male gender may be associated with increased odds of other hallucinogen use disorder.
Diagnostic Markers
Laboratory testing can be useful in distinguishing among the different hallucinogens.
However, because some agents (e.g., LSD) are so potent that as little as 75 micrograms can
produce severe reactions, typical toxicological examination will not always reveal which
substance has been used.
Phencyclidine Intoxication 527
Functional Consequences of
Other Hallucinogen Use Disorder
There is evidence for long-term neurotoxic effects of MDMA/ecstasy use, including im-
pairments in memory, psychological function, and neuroendocrine function; serotonin
system dysfunction; and sleep disturbance; as well as adverse effects on brain microvas-
culature, white matter maturation, and damage to axons. Use of MDMA/ecstasy may di-
minish functional connectivity among brain regions.
Differential Diagnosis
Other substance use disorders. The effects of hallucinogens must be distinguished from
those of other substances (e.g., amphetamines), especially because contamination of the
hallucinogens with other drugs is relatively common.
Schizophrenia. Schizophrenia also must be ruled out, as some affected individuals (e.g.,
individuals with schizophrenia who exhibit paranoia) may falsely attribute their symp-
toms to use of hallucinogens.
Other mental disorders or medical conditions. Other potential disorders or conditions
to consider include panic disorder, depressive and bipolar disorders, alcoho] or sedative
withdrawal, hypoglycemia and other metabolic conditions, seizure disorder, stroke, oph-
thalmological disorder, and central nervous system tumors. Careful history of drug tak-
ing, collateral reports from family and friends (if possible), age, clinical history, physical
examination, and toxicology reports should be useful in arriving at the final diagnostic de-
cision.
Comorbidity
Adolescents who use MDMA/ ecstasy and other hallucinogens, as well as adults who have
recently used ecstasy, have a higher prevalence of other substance use disorders compared
with nonhallucinogen substance users. Individuals who use hallucinogens exhibit eleva-
tions of nonsubstance mental disorders (especially anxiety, depressive, and bipolar disor-
ders), particularly with use of ecstasy and salvia. Rates of antisocial personality disorder (but
not conduct disorder) are significantly elevated among individuals with other hallucinogen
use disorder, as are rates of adult antisocial behavior. However, it is unclear whether the
mental illnesses may be precursors to rather than consequences of other hallucinogen use
disorder (see the section “Risk and Prognostic Factors” for this disorder). Both adults and
adolescents who use ecstasy are more likely than other drug users to be polydrug users and
to have other drug use disorders.
Phencyclidine Intoxication
Diagnostic Criteria
A. Recent use of phencyclidine (or a pharmacologically similar substance).
B. Clinically significant problematic behavioral changes (e.g., belligerence, assaultive-
ness, impulsiveness, unpredictability, psychomotor agitation, impaired judgment) that
developed during, or shortly after, phencyclidine use.
C. Within 1 hour, two (or more) of the following signs or symptoms:
Note: When the drug is smoked, “snorted,” or used intravenously, the onset may be
particularly rapid.
1. Vertical or horizontal nystagmus.
2. Hypertension or tachycardia.
528 Substance-Related and Addictive Disorders
Numbness or diminished responsiveness to pain.
Ataxia.
Dysarthria.
Muscle rigidity.
Seizures or coma.
Hyperacusis.
ONOWRY
D. The signs or symptoms are not attributable to another medical concition and are not better
explained by another mental disorder, including intoxication with another substance.
Coding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether
there is a comorbid phencyclidine use disorder. If a mild phencyclidine use disorder is co-
morbid, the ICD-10-CM code is F16.129, and if a moderate or severe phencyclidine use
disorder is comorbid, the ICD-10-CM code is F16.229. If there is no comorbid phencycli-
dine use disorder, then the ICD-10-CM code is F16.929.
Note: In addition to the section “Functional Consequences of Phencyclidine Intoxication,”
see the corresponding section in phencyclidine use disorder.
Diagnostic Features
Phencyclidine intoxication reflects the clinically significant behavioral changes that occur
shortly after ingestion of this substance (or a pharmacologically similar substance). The
most common clinical presentations of phencyclidine intoxication include disorientation,
confusion without hallucinations, hallucinations or delusions, a catatonic-like syndrome,
and coma of varying severity. The intoxication typically lasts for several hours but, de-
pending on the type of clinical presentation and whether other drugs besides phencycli-
dine were consumed, may last for several days or longer.
Prevalence
Use of phencyclidine or related substances may be taken as an estimate of the prevalence
of intoxication. Approximately 2.5% of the population reports having ever used phency-
clidine. Among high schoo] students, 2.3% of 12th graders report ever using phencycli-
dine, with 57% having used in the past 12 months. This represents an increase from prior
to 2011. Past-year use of ketamine, which is assessed separately from other substances, has
remained stable over time, with about 1.7% of 12th graders reporting use.
Diagnostic Markers
Laboratory testing may be useful, as phencyclidine is detectable in urine for up to 8 days
following use, although the levels are only weakly associated with an individual's clinical
presentation and may therefore not be useful for case management. Creatine phosphoki-
nase and aspartate aminotransferase levels may be elevated.
Functional Consequences of Phencyclidine Intoxication
Phencyclidine intoxication produces extensive cardiovascular and neurological (e.g., sei-
zures, dystonias, dyskinesias, catalepsy, hypothermia or hyperthermia) toxicity.
Differential Diagnosis
In particular, in the absence of intact reality testing (i.e., without insight into any percep-
tual abnormalities), an additional diagnosis of phencyclidine-induced psychotic disorder
should be considered.
Other substance intoxication. Phencyclidine intoxication should be differentiated from
intoxication due to other substances, including other hallucinogens; amphetamine, co-
Other Hallucinogen Intoxication 529
caine, or other stimulants; and anticholinergics, as well as withdrawal from benzodiaze-
pines. Nystagmus and bizarre and violent behavior may distinguish intoxication due to
phencyclidine from that due to other substances. Toxicological tests may be useful in mak-
ing this distinction, since phencyclidine is detectable in urine for up to 8 days after use.
However, there is a weak correlation between quantitative toxicology levels of phencycli-
dine and clinical presentation that diminishes the utility of the laboratory findings for pa-
tient management.
Other conditions. Other conditions to be considered include schizophrenia, depression,
withdrawal from other drugs (e.g., sedatives, alcohol), certain metabolic disorders like hy-
poglycemia and hyponatremia, central nervous system tumors, seizure disorders, sepsis,
neuroleptic malignant syndrome, and vascular insults.
Other Hallucinogen Intoxication
Diagnostic Criteria
A. Recent use of a hallucinogen (other than phencyclidine).
B. Clinically significant problematic behavioral or psychological changes (e.g., marked
anxiety or depression, ideas of reference, fear of “losing one’s mind,” paranoid ide-
ation, impaired judgment) that developed during, or shortly after, hallucinogen use.
C. Perceptual changes occurring in a state of full wakefulness and alertness (e.g., sub-
jective intensification of perceptions, depersonalization, derealization, illusions, hallu-
cinations, synesthesias) that developed during, or shortly after, hallucinogen use.
D. Two (or more) of the following signs developing during, or shortly after, hallucinogen
use:
Pupillary dilation.
Tachycardia.
Sweating.
Palpitations.
Blurring of vision.
Tremors.
7. Incoordination.
AaAhWON =
E. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including intoxication with another sub-
stance.
Coding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether
there is a comorbid hallucinogen use disorder. {f a mild hallucinogen use disorder is co-
morbid, the |CD-10-CM code is F16.129, and if a moderate or severe hallucinogen use
disorder is comorbid, the ICD-10-CM code is F16.229. If there is no comorbid hallucinogen
use disorder, then the ICD-10-CM code is F16.929.
Note: For information on Associated Features Supporting Diagnosis and Culture-Related
Diagnostic Issues, see the corresponding sections in other hallucinogen use disorder.
Diagnostic Features
Other hallucinogen intoxication reflects the clinically significant behavioral or psycholog-
ical changes that occur shortly after ingestion of a hallucinogen. Depending on the specific
hallucinogen, the intoxication may last only minutes (e.g., for salvia) or several hours or
longer (e.g., for LSD [lysergic acid diethylamide] or MDMA [3,4-methylenedioxymetham-
phetamine}).
530 Substance-Related and Addictive Disorders
Prevalence
The prevalence of other hallucinogen intoxication may be estimated by use of those sub-
stances. In the United States, 1.8% of individuals age 12 years or older report using hallu-
cinogens in the past year. Use is more prevalent among younger individuals, with 3.1% of
12- to 17-year-olds and 7.1% of 18- to 25-year-olds using hallucinogens in the past year,
compared with only 0.7% of individuals age 26 years or older. Twelve-month prevalence
for hallucinogen use is more common in males (2.4%) than in females (1.2%), and even
more so among 18- to 25-year-olds (9.2% for males vs. 5.0% for females). In contrast,
among individuals ages 12-17 years, there are no gender differences (3.1% for both gen-
ders). These figures may be used as proxy estimates for gender-related differences in the
prevalence of other hallucinogen intoxication.
Suicide Risk
Other hallucinogen intoxication may lead to increased suicidality, although suicide is rare
among users of hallucinogens.
Functional Consequences of
Other Hallucinogen Intoxication
Other hallucinogen intoxication can have serious consequences. The perceptual distur-
bances and impaired judgment associated with other hallucinogen intoxication can result
in injuries or fatalities from automobile crashes, physical fights, or unintentional self-
injury (e.g., attempts to “fly” from high places). Environmental factors and the personality
and expectations of the individual using the hallucinogen may contribute to the nature of
and severity of hallucinogen intoxication. Continued use of hallucinogens, particularly
MDMA, has also been linked with neurotoxic effects.
Differential Diagnosis
Other substance intoxication. Other hallucinogen intoxication should be differentiated
from intoxication with amphetamines, cocaine, or other stimulants; anticholinergics; in-
halants; and phencyclidine. Toxicological tests are useful in making this distinction, and
determining the route of administration may also be useful.
Other conditions. Other disorders and conditions to be considered include schizophre-
nia, depression, withdrawal from other drugs (e.g., sedatives, alcohol), certain metabolic
disorders (e.g., hypoglycemia), seizure disorders, tumors of the central nervous system,
and vascular insults.
Hallucinogen persisting perception disorder. Other hallucinogen intoxication is dis-
tinguished from hallucinogen persisting perception disorder because the symptoms in the
latter continue episodically or continuously for weeks (or longer) after the most recent in-
toxication.
Other hallucinogen-induced disorders, Other hallucinogen intoxication is distinguished
from the other hallucinogen-induced disorders (e.g., hallucinogen-induced anxiety disor-
der, with onset during intoxication) because the symptoms in these latter disorders pre-
dominate the clinical presentation and are severe enough to warrant independent clinical
attention.
Hallucinogen Persisting Perception Disorder 531
Hallucinogen Persisting Perception Disorder
Diagnostic Criteria 292.89 (F 16.983)
A. Following cessation of use of a hallucinogen, the reexperiencing of one or more of the
perceptual symptoms that were experienced while intoxicated with the hallucinogen
(e.g., geometric hallucinations, false perceptions of movement in the peripheral visual
fields, flashes of color, intensified colors, trails of images of moving objects, positive
afterimages, halos around objects, macropsia and micropsia).
B. The symptoms in Criterion A cause clinically significant distress or impairment in so-
cial, occupational, or other important areas of functioning.
C. The symptoms are not attributable to another medical condition (e.g., anatomical le-
sions and infections of the brain, visual epilepsies) and are not better explained by an-
other mental disorder (e.g., delirium, major neurocognitive disorder, schizophrenia) or
hypnopompic hallucinations.
Diagnostic Features
The hallmark of hallucinogen persisting perception disorder is the reexperiencing, when the
individual is sober, of the perceptual disturbances that were experienced while the individ-
ual was intoxicated with the hallucinogen (Criterion A). The symptoms may include any
perceptual perturbations, but visual disturbances tend to be predominant. Typical of the ab-
normal visual perceptions are geometric hallucinations, false perceptions of movement in
the peripheral visual fields, flashes of color, intensified colors, trails of images of moving ob-
jects (i.e., images left suspended in the path of a moving object as seen in stroboscopic pho-
tography), perceptions of entire objects, positive afterimages (i.e., a same-colored or
complementary-colored “shadow” of an object remaining after removal of the object), halos
around objects, or misperception of images as too large (macropsia) or too small (micropsia).
Duration of the visual disturbances may be episodic or nearly continuous and must cause
clinically significant distress or impairment in social, occupational, or other important areas
of functioning (Criterion B). The disturbances may last for weeks, months, or years. Other
explanations for the disturbances (e.g., brain lesions, preexisting psychosis, seizure disor-
ders, migraine aura without headaches) must be ruled out (Criterion C).
Hallucinogen persisting perception disorder occurs primarily after LSD (lysergic acid
diethylamide) use, but not exclusively. There does not appear to be a strong correlation be-
tween hallucinogen persisting perception disorder and number of occasions of hallucino-
gen use, with some instances of hallucinogen persisting perception disorder occurring in
individuals with minimal exposure to hallucinogens. Some instances of hallucinogen per-
sisting perception disorder may be triggered by use of other substances (e.g., cannabis or
alcohol) or in adaptation to dark environments.
Associated Features Supporting Diagnosis
Reality testing remains intact in individuals with hallucinogen persisting perception dis-
order (i.e., the individual is aware that the disturbance is linked to the effect of the drug).
If this is not the case, another disorder might better explain the abnormal perceptions.
Prevalence
Prevalence estimates of hallucinogen persisting perception disorder are unknown. Initial
prevalence estimates of the disorder among individuals who use hallucinogens is approx-
imately 4.2%,
532 Substance-Related and Addictive Disorders
Development and Course
Little is known about the development of hallucinogen persisting perception disorder. Its
course, as suggested by its name, is persistent, lasting for weeks, months, or even years in
certain individuals.
Risk and Prognostic Factors
There is little evidence regarding risk factors for hallucinogen persisting perception dis-
order, although genetic factors have been suggested as a possible explanation underlying
the susceptibility to LSD effects in this condition.
Functional Consequences of
Haliucinogen Persisting Perception Disorder
Although hallucinogen persisting perception disorder remains a chronic condition in
some cases, many individuals with the disorder are able to suppress the disturbances and
continue to function normally.
Differential Diagnosis
Conditions to be ruled out include schizophrenia, other drug effects, neurodegenerative
disorders, stroke, brain tumors, infections, and head trauma. Neuroimaging results in hal-
lucinogen persisting perception disorder cases are typically negative. As noted earlier, re-
ality testing remains intact (i.e., the individual is aware that the disturbance is linked to the
effect of the drug); if this is not the case, another disorder (e.g., psychotic disorder, another
medical condition) might better explain the abnormal perceptions.
Comorbidity
Common comorbid mental disorders accompanying hallucinogen persisting perception
disorder are panic disorder, alcohol use disorder, and major depressive disorder.
Other Phencyclidine-Induced Disorders
Other phencyclidine-induced disorders are described in other chapters of the manual with
disorders with which they share phenomenology (see the substance /medication-induced
mental disorders in these chapters): phencyclidine-induced psychotic disorder (“Schizo-
phrenia Spectrum and Other Psychotic Disorders”); phencyclidine-induced bipolar dis-
order (“Bipolar and Related Disorders”); phencyclidine-induced depressive disorder
(“Depressive Disorders”); and phencyclidine-induced anxiety disorder (“Anxiety Disor-
ders”). For phencyclidine-induced intoxication delirium, see the criteria and discussion of
delirium in the chapter “Neurocognitive Disorders.” These phencyclidine-induced disor-
ders are diagnosed instead of phencyclidine intoxication only when the symptoms are suf-
ficiently severe to warrant independent clinical attention.
Other Hallucinogen-Induced Disorders
The following other hallucinogen-induced disorders are described in other chapters of the
manual with disorders with which they share phenomenology (see the substance/medi-
cation-induced mental disorders in these chapters): other hallucinogen-induced psychotic
disorder (“Schizophrenia Spectrum and Other Psychotic Disorders”); other hallucinogen
induced bipolar disorder (“Bipolar and Related Disorders”); other hallucinogen-induced
Unspecified Phencyclidine-Related Disorder 533
depressive disorder (“Depressive Disorders”); and other hallucinogen—induced anxiety
disorder (“Anxiety Disorders”). For other hallucinogen intoxication delirium, see the cri-
teria and discussion of delirium in the chapter “Neurocognitive Disorders.” These hallu-
cinogen-induced disorders are diagnosed instead of other hallucinogen intoxication only
when the symptoms are sufficiently severe to warrant independent clinical attention.
Unspecified Phencyclidine-Related Disorder
292.9 (F16.99)
This category applies to presentations in which symptoms characteristic of a phencycli-
dine-related disorder that cause clinically significant distress or impairment in social, oc-
cupational, or other important areas of functioning predominate but do not meet the full
criteria for any specific phencyclidine-related disorder or any of the disorders in the sub-
stance-related and addictive disorders diagnostic class.
Unspecified Hallucinogen-Related Disorder
292.9 (F16.99)
This category applies to presentations in which symptoms characteristic of a hallucinogen-
related disorder that cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning predominate but do not meet the full criteria
for any specific hallucinogen-related disorder or any of the disorders in the substance-
related and addictive disorders diagnostic class.
Inhalant-Related Disorders
inhalant Use Disorder
inhalant Intoxication
Other Inhalant-Induced Disorders
Unspecified Inhalant-Related Disorder
Inhalant Use Disorder
Diagnostic Criteria
A. A problematic pattern of use of a hydrocarbon-based inhalant substance leading to
Clinically significant impairment or distress, as manifested by at least two of the follow-
ing, occurring within a 12-month period:
1. The inhalant substance is often taken in larger amounts or over a longer period than
was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control use of the
inhalant substance.
§34 Substance-Related and Addictive Disorders
3. Agreat deal of time is spent in activities necessary to obtain the inhalant substance,
use it, or recover from its effects.
4. Craving, or a strong desire or urge to use the inhalant substance.
5. Recurrent use of the inhalant substance resulting in a failure to fulfill major role ob-
ligations at work, school, or home.
6. Continued use of the inhalant substance despite having persistent or recurrent so-
cial or interpersonal problems caused or exacerbated by the effects of its use.
7. Important social, occupational, or recreational activities are given up or reduced be-
cause of use of the inhalant substance.
8. Recurrent use of the inhalant substance in situations in which it is physically haz-
ardous.
9. Use of the inhalant substance is continued despite knowledge of having a persis-
tent or recurrent physical or psychological problem that is likely to have been
caused or exacerbated by the substance.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of the inhalant substance to achieve
intoxication or desired effect.
b. A markedly diminished effect with continued use of the same amount of the in-
halant substance.
Specify the particular inhalant: When possible, the particular substance involved should
be named (e.g., “solvent use disorder’).
Specify if:
In early remission: After full criteria for inhalant use disorder were previously met,
none of the criteria for innalant use disorder have been met for at least 3 months but
for less than 12 months (with the exception that Criterion A4, “Craving, or a strong de-
sire or urge to use the inhalant substance,” may be met).
In sustained remission: After full criteria for inhalant use disorder were previously
met, none of the criteria for inhalant use disorder have been met at any time during a
period of 12 months or longer (with the exception that Criterion A4, “Craving, or a
strong desire or urge to use the inhalant substance,” may be met).
Specify if:
In acontrolled environment: This additional specifier is used if the individual is in an
environment where access to inhalant substances is restricted.
Coding based on current severity: Note for ICD-10-CM codes: If an inhalant intoxication
or another inhalant-induced mental disorder is also present, do not use the codes below
for inhalant use disorder. Instead, the comorbid inhalant use disorder is indicated in the
4th character of the inhalant-induced disorder code (see the coding note for inhalant intox-
ication or a specific inhalant-induced mental disorder). For example, if there is comorbid
inhalant-induced depressive disorder and inhalant use disorder, only the inhalant-induced
depressive disorder code is given, with the 4th character indicating whether the comorbid
inhalant use disorder is mild, moderate, or severe: F18.14 for mild inhalant use disorder
with inhalant-induced depressive disorder or F18.24 for a moderate or severe inhalant use
disorder with inhalant-induced depressive disorder.
Specify current severity:
305.90 (F18.10) Mild: Presence of 2-3 symptoms.
304.60 (F18.20) Moderate: Presence of 4~5 symptoms.
304.60 (F18.20) Severe: Presence of 6 or more symptoms.
inhalant Use Disorder 535
Specifiers
This manual recognizes volatile hydrocarbon use meeting the above diagnostic criteria as
inhalant use disorder. Volatile hydrocarbons are toxic gases from glues, fuels, paints, and
other volatile compounds. When possible, the particular substance involved should be
named (e.g., “toluene use disorder”). However, most compounds that are inhaled are a
mixture of several substances that can produce psychoactive effects, and it is often difficult
to ascertain the exact substance responsible for the disorder. Unless there is clear evidence
that a single, unmixed substance has been used, the general term inhalant should be used
in recording the diagnosis. Disorders arising from inhalation of nitrous oxide or of amy]l-,
butyl-, or isobutylnitrite are considered as other (or unknown) substance use disorder.
“In a controlled environment” applies as a further specifier of remission if the individ-
ual is both in remission and in a controlled environment (i.e., in early remission in a con-
trolled environment or in sustained remission in a controlled environment). Examples of
these environments are closely supervised and substance-free jails, therapeutic communi-
ties, and locked hospital units.
The severity of individuals’ inhalant use disorder is assessed by the number of diag-
nostic criteria endorsed. Changing severity of individuals’ inhalant use disorder across
time is reflected by reductions in the frequency (e.g., days used per month) and/or dose
(e.g., tubes of glue per day) used, as assessed by the individual's self-report, report of oth-
ers, clinician’s observations, and biological testing (when practical).
Diagnostic Features
Features of inhalant use disorder include repeated use of an inhalant substance despite the
individual’s knowing that the substance is causing serious problems for the individual
(Criterion A9). Those problems are reflected in the diagnostic criteria.
Missing work or school or inability to perform typical responsibilities at work or school
(Criterion A5), and continued use of the inhalant substance even though it causes arguments
with family or friends, fights, and other social or interpersonal problems (Criterion A6), may
be seen in inhalant use disorder. Limiting family contact, work or school obligations, or rec-
reational activities (e.g., sports, games, hobbies) may also occur (Criterion A7). Use of inhal-
ants when driving or operating dangerous equipment (Criterion A8) is also seen.
Tolerance (Criterion A10) and mild withdrawal are each reported by about 10% of in-
dividuals who use inhalants, and a few individuals use inhalants to avoid withdrawal.
However, because the withdrawal symptoms are mild, this manual neither recognizes a
diagnosis of inhalant withdrawal nor counts withdrawal complaints as a diagnostic crite-
rion for inhalant use disorder.
Associated Features Supporting Diagnosis
A diagnosis of inhalant use disorder is supported by recurring episodes of intoxication
with negative results in standard drug screens (which do not detect inhalants); possession,
or lingering odors, of inhalant substances; peri-oral or peri-nasal “glue-sniffer’s rash”; as-
sociation with other individuals known to use inhalants; membership in groups with prev-
alent inhalant use (e.g., some native or aboriginal communities, homeless children in street
gangs); easy access to certain inhalant substances; paraphernalia possession; presence of
the disorder’s characteristic medical complications (e.g., brain white matter pathology,
rhabdomyolysis); and the presence of multiple substance use disorders. Inhalant use and
inhalant use disorder are associated with past suicide attempts, especially among adults
reporting previous episodes of low mood or anhedonia.
Prevaience
About 0.4% of Americans ages 12-17 years have a pattern of use that meets criteria for in-
halant use disorder in the past 12 months. Among those youths, the prevalence is highest
536 Substance-Related and Addictive Disorders
in Native Americans and lowest in African Americans. Prevalence falls to about 0.1% among
Americans ages 18-29 years, and only 0.02% when all Americans 18 years or older are con-
sidered, with almost no females and a preponderance of European Americans. Of course,
in isolated subgroups, prevalence may differ considerably from these overall rates.
Development and Course
About 10% of 13-year-old American children report having used inhalants at least once;
that percentage remains stable through age 17 years. Among those 12- to 17-year-olds who
use inhalants, the more-used substances include glue, shoe polish, or toluene; gasoline or
lighter fluid; or spray paints.
Only 0.4% of 12- to 17-year-olds progress to inhalant use disorder; those youths tend to
exhibit multiple other problems. The declining prevalence of inhalant use disorder after
adolescence indicates that this disorder usually remits in early adulthood.
Volatile hydrocarbon use disorder is rare in prepubertal children, most common in ad-
olescents and young adults, and uncommon in older persons. Calls to poison-control cen-
ters for “intentional abuse” of inhalants peak with calls involving individuals at age 14 years.
Of adolescents who use inhalants, perhaps one-fifth develop inhalant use disorder; a few
die from inhalant-related accidents, or “sudden sniffing death”. But the disorder apparently
remits in many individuals after adolescence. Prevalence declines dramatically among in-
dividuals in their 20s. Those with inhalant use disorder extending into adulthood often
have severe problems: substance use disorders, antisocial personality disorder, and sui-
cidal ideation with attempts.
Risk and Prognostic Factors
Temperamental. Predictors of progression from nonuse of inhalants, to use, to inhalant
use disorder include comorbid non-inhalant substance use disorders and either conduct
disorder or antisocial personality disorder. Other predictors are earlier onset of inhalant
use and prior use of mental health services.
Environmental. Inhalant gases are widely and legally available, increasing the risk of mis-
use. Childhood maltreatment or trauma also is associated with youthful progression from
inhalant non-use to inhalant use disorder.
Genetic and physiological. Behavioral disinhibition is a highly heritable general propensity
to not constrain behavior in socially acceptable ways, to break social norms and rules, and to
take dangerous risks, pursuing rewards excessively despite dangers of adverse consequences.
Youths with strong behavioral disinhibition show risk factors for inhalant use disorder: early-
onset substance use disorder, multiple substance involvement, and early conduct problems.
Because behavioral disinhibition is under strong genetic influence, youths in families with
substance and antisocial problems are at elevated risk for inhalant use disorder.
Culture-Related Diagnostic Issues
Certain native or aboriginal communities have experienced a high prevalence of inhalant
problems. Also, in some countries, groups of homeless children in street gangs have ex-
tensive inhalant use problems.
Gender-Related Diagnostic Issues
Although the prevalence of inhalant use disorder is almost identical in adolescent males
and females, the disorder is very rare among adult females.
Diagnostic Markers
Urine, breath, or saliva tests may be valuable for assessing concurrent use of non-inhalant
substances by individuals with inhalant use disorder. However, technical problems and
Inhalant Use Disorder 537
the considerable expense of analyses make frequent biological testing for inhalants them-
selves impractical.
Functional Consequences of Inhalant Use Disorder
Because of inherent toxicity, use of butane or propane is not infrequently fatal. Moreover,
any inhaled volatile hydrocarbons may produce “sudden sniffing death” from cardiac ar-
rhythmia. Fatalities may occur even on the first inhalant exposure and are not thought to
be dose-related. Volatile hydrocarbon use impairs neurobehavioral function and causes
various neurological, gastrointestinal, cardiovascular, and pulmonary problems.
Long-term inhalant users are at increased risk for tuberculosis, HIV/AIDS, sexually
transmitted diseases, depression, anxiety, bronchitis, asthma, and sinusitis. Deaths may
occur from respiratory depression, arrhythmias, asphyxiation, aspiration of vomitus, or
accident and injury.
Differential Diagnosis
Inhalant exposure (unintentional) from industrial or other accidents. This designation
is used when findings suggest repeated or continuous inhalant exposure but the involved
individual and other informants deny any history of purposeful inhalant use.
Inhalant use (intentional), without meeting criteria for inhalant use disorder. Inhalant use
is common among adolescents, but for most of those individuals, the inhalant use does not
meet the diagnostic standard of two or more Criterion A items for inhalant use disorder in
the past year.
Inhalant intoxication, without meeting criteria for inhalant use disorder. Inhalant intox-
ication occurs frequently during inhalant use disorder but also may occur among individ-
uals whose use does not meet criteria for inhalant use disorder, which requires at least two
of the 10 diagnostic criteria in the past year.
Inhalant-induced disorders (i.e., inhalant-induced psychotic disorder, depressive dis-
order, anxiety disorder, neurocognitive disorder, other inhalant-induced disorders)
without meeting criteria for inhalant use disorder. Criteria are met for a psychotic, de-
pressive, anxiety, or major neurocognitive disorder, and there is evidence from history,
physical examination, or laboratory findings that the deficits are etiologically related to
the effects of inhalant substances. Yet, criteria for inhalant use disorder may not be met
{i.e., fewer than 2 of the 10 criteria were present).
Other substance use disorders, especially those involving sedating substances (e.g.,
alcohol, benzodiazepines, barbiturates). Inhalant use disorder commonly co-occurs
with other substance use disorders, and the symptoms of the disorders may be similar and
overlapping. To disentangle symptom patterns, it is helpful to inquire about which symp-
toms persisted during periods when some of the substances were not being used.
Other toxic, metabolic, traumatic, neoplastic, or infectious disorders impairing central or
peripheral nervous system function. Individuals with inhalant use disorder may pre-
sent with symptoms of pernicious anemia, subacute combined degeneration of the spinal
cord, psychosis, major or minor cognitive disorder, brain atrophy, leukoencephalopathy,
and many other nervous system disorders. Of course, these disorders also may occur in
the absence of inhalant use disorder. A history of little or no inhalant use helps to exclude
inhalant use disorder as the source of these problems.
Disorders of other organ systems. Individuals with inhalant use disorder may present
with symptoms of hepatic or renal damage, rhabdomyolysis, methemoglobinemia, or symp-
toms of other gastrointestinal, cardiovascular, or pulmonary diseases. A history of little or no
inhalant use helps to exclude inhalant use disorder as the source of such medical problems.
538 Substance-Related and Addictive Disorders
Comorbidity
Individuals with inhalant use disorder receiving clinical care often have numerous other
substance use disorders. Inhalant use disorder commonly co-occurs with adolescent con-
duct disorder and adult antisocial personality disorder. Adult inhalant use and inhalant
use disorder also are strongly associated with suicidal ideation and suicide attempts.
Inhalant Intoxication
Diagnostic Criteria
A. Recent intended or unintended short-term, high-dose exposure to inhalant sub-
stances, including volatile hydrocarbons such as toluene or gasoline.
B. Clinically significant problematic behavioral or psychological changes (e.g., belliger-
ence, assaultiveness, apathy, impaired judgment) that developed during, or shortly af-
ter, exposure to inhalants.
C. Two (or more) of the following signs or symptoms developing during, or shortly after,
inhalant use or exposure:
Dizziness.
Nystagmus.
Incoordination.
Slurred speech.
Unsteady gait.
Lethargy.
Depressed reflexes.
Psychomotor retardation.
9. Tremor.
10. Generalized muscle weakness.
41. Blurred vision or diplopia.
12. Stupor or coma.
13. Euphoria.
ONOaAhwWN =
D. The signs or symptoms are not attributable to another medical condition and are not bet-
ter explained by another mental disorder, including intoxication with another substance.
Coding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether
there is a comorbid inhalant use disorder. If a mild inhalant use disorder is comorbid, the
ICD-10-CM code is F18.129, and if a moderate or severe inhalant use disorder is comor-
bid, the ICD-10-CM code is F18.229. If there is no comorbid inhalant use disorder, then
the ICD-10-CM code is F18.929.
Note: For information on Development and Course, Risk and Prognostic Factors, Culture-
Related Diagnostic Issues, and Diagnostic Markers, see the corresponding sections in in-
halant use disorder.
Diagnostic Features
Inhalant intoxication is an inhalant-related, clinically significant mental disorder that de-
velops during, or immediately after, intended or unintended inhalation of a volatile hy-
drocarbon substance. Volatile hydrocarbons are toxic gases from glues, fuels, paints, and
other volatile compounds. When it is possible to do so, the particular substance involved
should be named (e.g., toluene intoxication). Among those who do, the intoxication clears
within a few minutes to a few hours after the exposure ends. Thus, inhalant intoxication
usually occurs in brief episodes that may recur.
Inhalant Intoxication 539
Associated Features Supporting Diagnosis
inhalant intoxication may be indicated by evidence of possession, or lingering odors, of in-
halant substances (e.g., glue, paint thinner, gasoline, butane lighters); apparent intoxica-
tion occurring in the age range with the highest prevalence of inhalant use (12-17 years);
and apparent intoxication with negative results from the standard drug screens that usu-
ally fail to identify inhalants.
Prevaience
The prevalence of actual episodes of inhalant intoxication in the general population is un-
known, but it is probable that most inhalant users would at some time exhibit use that
would meet criteria for inhalant intoxication disorder. Therefore, the prevalence of inhal-
ant use and the prevalence of inhalant intoxication disorder are likely similar. In 2009 and
2010, inhalant use in the past year was reported by 0.8% of all Americans older than 12 years;
the prevalence was highest in younger age groups (3.6% for individuals 12 to 17 years old,
and 1.7% for individuals 18 to 25 years old).
Gender-Reiated Diagnostic issues
Gender differences in the prevalence of inhalant intoxication in the general population are
unknown. However, if it is assumed that most inhalant users eventually experience inhal-
ant intoxication, gender differences in the prevalence of inhalant users likely approximate
those in the proportions of males and females experiencing inhalant intoxication. Regard-
ing gender differences in the prevalence of inhalant users in the United States, 1% of males
older than 12 years and 0.7% of females older than 12 years have used inhalants in the pre-
vious year, but in the younger age groups more females than males have used inhalants
(e.g., among 12- to 17-year-olds, 3.6% of males and 4.2% of females).
Functional Consequences of Inhalant Intoxication
Use of inhaled substances in a closed container, such as a plastic bag over the head, may
lead to unconsciousness, anoxia, and death. Separately, “sudden sniffing death,” likely
from cardiac arrhythmia or arrest, may occur with various volatile inhalants. The en-
hanced toxicity of certain volatile inhalants, such as butane or propane, also causes fatal-
ities. Although inhalant intoxication itself is of short duration, it may produce persisting
medical and neurological problems, especially if the intoxications are frequent.
Differential Diagnosis
Inhalant exposure, without meeting the criteria for inhalant intoxication disorder.
The individual intentionally or unintentionally inhaled substances, but the dose was in-
sufficient for the diagnostic criteria for inhalant use disorder to be met.
Intoxication and other substance/medication-induced disorders from other sub-
stances, especially from sedating substances (e.g., alcohol, benzodiazepines, barbi-
turates). These disorders may have similar signs and symptoms, but the intoxication is
attributable to other intoxicants that may be identified via a toxicology screen. Differenti-
ating the source of the intoxication may involve discerning evidence of inhalant exposure
as described for inhalant use disorder. A diagnosis of inhalant intoxication may be sug-
gested by possession, or lingering odors, of inhalant substances (e.g., glue, paint thinner,
gasoline, butane lighters,); paraphernalia possession (e.g., rags or bags for concentrating
glue fumes); perioral or perinasal “glue-sniffer’s rash”; reports from family or friends that
the intoxicated individual possesses or uses inhalants; apparent intoxication despite neg-
ative results on standard drug screens (which usually fail to identify inhalants); apparent
intoxication occurring in that age range with the highest prevalence of inhalant use (12-17
540 Substance-Related and Addictive Disorders
years); association with others known to use inhalants; membership in certain small com-
munities with prevalent inhalant use (e.g., some native or aboriginal communities, home-
less street children and adolescents); or unusual access to certain inhalant substances.
Other inhalant-related disorders. Episodes of inhalant intoxication do occur during,
but are not identical with, other inhalant-related disorders. Those inhalant-related disorders
are recognized by their respective diagnostic criteria: inhalant use disorder, inhalant-
induced neurocognitive disorder, inhalant-induced psychotic disorder, inhalant-induced
depressive disorder, inhalant-induced anxiety disorder, and other inhalant-induced dis-
orders.
Other toxic, metabolic, traumatic, neoplastic, or infectious disorders that impair brain
function and cognition. Numerous neurological and other medical conditions may pro-
duce the clinically significant behavioral or psychological changes (e.g., belligerence, as-
saultiveness, apathy, impaired judgment) that also characterize inhalant intoxication.
Other Inhalant-Induced Disorders
The following inhalant-induced disorders are described in other chapters of the manual
with disorders with which they share phenomenology (see the substance/medication-
induced mental disorders in these chapters): inhalant-induced psychotic disorder (“Schizo-
phrenia Spectrum and Other Psychotic Disorders”); inhalant-induced depressive disorder
(“Depressive Disorders”); inhalant-induced anxiety disorder (“Anxiety Disorders”); and in-
halant-induced major or mild neurocognitive disorder (“Neurocognitive Disorders”). For
inhalant intoxication delirium, see the criteria and discussion of delirium in the chapter
“Neurocognitive Disorders.” These inhalant-induced disorders are diagnosed instead of in-
halant intoxication only when symptoms are sufficiently severe to warrant independent
clinical attention.
Unspecified Inhalant-Related Disorder
292.9 (F18.99)
This category applies to presentations in which symptoms characteristic of an inhalant-
related disorder that cause Clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning predominate but do not meet the full criteria
for any specific inhalant-related disorder or any of the disorders in the substance-related
and addictive disorders diagnostic class.
Opioid-Related Disorders
Opioid Use Disorder
Opioid Intoxication
Opioid Withdrawai
Other Opioid-induced Disorders
Unspecified Opioid-Reiated Disorder
Opioid Use Disorder 541
Opioid Use Disorder
Diagnostic Criteria
A. Aproblematic pattern of opioid use leading to clinically significant impairment or distress,
as manifested by at least two of the following, occurring within a 12-month period:
1.
2.
3.
10.
11.
Opioids are often taken in larger amounts or over a longer period than was in-
tended.
There is a persistent desire or unsuccessful efforts to cut down or control opioid use.
A great deal of time is spentin activities necessary to obtain the opioid, use the opi-
oid, or recover from its effects.
Craving, or a strong desire or urge to use opioids.
Recurrent opioid use resulting in a failure to fulfill major role obligations at work,
school, or home.
Continued opioid use despite having persistent or recurrent social or interpersonal
problems caused or exacerbated by the effects of opioids.
Important social, occupational, or recreational activities are given up or reduced be-
cause of opioid use.
Recurrent opioid use in situations in which it is physically hazardous.
Continued opioid use despite knowledge of having a persistent or recurrent physi-
cal or psychological problem that is likely to have been caused or exacerbated by
the substance.
Tolerance, as defined by either of the following:
a. Aneed for markedly increased amounts of opioids to achieve intoxication or de-
sired effect.
b. Amarkedly diminished effect with continued use of the same amount of an opioid.
Note: This criterion is not considered to be met for those taking opioids solely under
appropriate medical supervision.
Withdrawal, as manifested by either of the following:
a. The characteristic opioid withdrawal syndrome (refer to Criteria A and B of the
criteria set for opioid withdrawal, pp. 547-548).
b. Opioids (or a closely related substance) are taken to relieve or avoid withdrawal
symptoms.
Note: This criterion is not considered to be met for those individuals taking opioids
solely under appropriate medical supervision.
Specify if:
in early remission: After full criteria for opioid use disorder were previously met, none
of the criteria for opioid use disorder have been met for at least 3 months but for less
than 12 months (with the exception that Criterion A4, “Craving, or a strong desire or
urge to use opioids,” may be met).
In sustained remission: After full criteria for opioid use disorder were previously met,
none of the criteria for opioid use disorder have been met at any time during a period
of 12 months or longer (with the exception that Criterion A4, “Craving, or a strong de-
sire or urge to use opioids,” may be met).
Specify if:
On maintenance therapy: This additional specifier is used if the individual is taking a
prescribed agonist medication such as methadone or buprenorphine and none of the
criteria for opioid use disorder have been met for that class of medication (except tol-
erance to, or withdrawal from, the agonist). This category also applies to those individ-
542 Substance-Related and Addictive Disorders
uals being maintained on a partial agonist, an agonist/antagonist, or a full antagonist
such as oral naltrexone or depot naltrexone.
In a controlled environment: This additional specifier is used if the individual is in an
environment where access to opioids is restricted.
Coding based on current severity: Note for |(CD-10-CM codes: If an opioid intoxication,
opioid withdrawal, or another opioid-induced mental disorder is also present, do not use
the codes below for opioid use disorder. Instead, the comorbid opioid use disorder is indi-
cated in the 4th character of the opioid-induced disorder code (see the coding note for opi-
oid intoxication, opioid withdrawal, or a specific opioid-induced mental disorder). For
example, if there is comorbid opioid-induced depressive disorder and opioid use disorder,
only the opioid-induced depressive disorder code is given, with the 4th character indicating
whether the comorbid opioid use disorder is mild, moderate, or severe: F11.14 for mild opi-
oid use disorder with opioid-induced depressive disorder or F11.24 for a moderate or se-
vere opioid use disorder with opioid-induced depressive disorder.
Specify current severity:
305.50 (F11.10) Mild: Presence of 2-3 symptoms.
304.00 (F11.20) Moderate: Presence of 4-5 symptoms.
304.00 (F 11.20) Severe: Presence of 6 or more symptoms.
Specifiers
The “on maintenance therapy” specifier applies as a further specifier of remission if the in-
dividual is both in remission and receiving maintenance therapy. “In a controlled environ-
ment” applies as a further specifier of remission if the individual is both in remission and in
acontrolled environment (i.e., in early remission in a controlled environment or in sustained
remission in a controlled environment). Examples of these environments are closely super-
vised and substance-free jails, therapeutic communities, and locked hospital units.
Changing severity across time in an individual is also reflected by reductions in the fre-
quency (e.g., days of use per month) and/or dose (e.g., injections or number of pills) of an
opioid, as assessed by the individual's self-report, report of knowledgeable others, clini-
cian’s observations, and biological testing.
Diagnostic Features
Opioid use disorder includes signs and symptoms that reflect compulsive, prolonged self-
administration of opioid substances that are used for no legitimate medical purpose or, if
another medical condition is present that requires opioid treatment, that are used in doses
greatly in excess of the amount needed for that medical condition. (For example, an indi-
vidual prescribed analgesic opioids for pain relief at adequate dosing will use significantly
more than prescribed and not only because of persistent pain.) Individuals with opioid use
disorder tend to develop such regular patterns of compulsive drug use that daily activities
are planned around obtaining and administering opioids. Opioids are usually purchased
on the illegal market but may also be obtained from physicians by falsifying or exagger-
ating general medical problems or by receiving simultaneous prescriptions from several
physicians. Health care professionals with opioid use disorder will often obtain opioids by
writing prescriptions for themselves or by diverting opioids that have been prescribed for
patients or from pharmacy supplies. Most individuals with opioid use disorder have
significant levels of tolerance and will experience withdrawal on abrupt discontinuation
of opioid substances. Individuals with opioid use disorder often develop conditioned
responses to drug-related stimuli (e.g., craving on seeing any heroin powder-like sub-
stance)—a phenomenon that occurs with most drugs that cause intense psychological
changes. These responses probably contribute to relapse, are difficult to extinguish, and typ-
ically persist long after detoxification is completed.
Opioid Use Disorder 543
Associated Features Supporting Diagnosis
Opioid use disorder can be associated with a history of drug-related crimes (e.g., posses-
sion or distribution of drugs, forgery, burglary, robbery, larceny, receiving stolen goods).
Among health care professionals and individuals who have ready access to controlled
substances, there is often a different pattern of illegal activities involving problems with
state licensing boards, professional staffs of hospitals, or other administrative agencies.
Marital difficulties (including divorce), unemployment, and irregular employment are of-
ten associated with opioid use disorder at all socioeconomic levels.
Prevaience
The 12-month prevalence of opioid use disorder is approximately 0.37% among adults age
18 years and older in the community population. This may be an underestimate because of
the large number of incarcerated individuals with opioid use disorders. Rates are higher in
males than in females (0.49% vs. 0.26%), with the male-to-female ratio typically being 1.5:1
for opioids other than heroin (i.e., available by prescription) and 3:1 for heroin. Female ad-
olescents may have a higher likelihood of developing opioid use disorders. The preva-
lence decreases with age, with the prevalence highest (0.82%) among adults age 29 years or
younger, and decreasing to 0.09% among adults age 65 years and older. Among adults, the
prevalence of opioid use disorder is lower among African Americans at 0.18% and over-
represented among Native Americans at 1.25%. It is close to average among whites (0.38%),
Asian or Pacific Islanders (0.35%), and Hispanics (0.39%).
Among individuals in the United States ages 12-17 years, the overall 12-month prev-
alence of opioid use disorder in the community population is approximately 1.0%, but the
prevalence of heroin use disorder is less than 0.1%. By contrast, analgesic use disorder is
prevalent in about 1.0% of those ages 12-17 years, speaking to the importance of opioid an-
algesics as a group of substances with significant health consequences.
The 12-month prevalence of problem opioid use in European countries in the commu-
nity population ages 15-64 years is between 0.1% and 0.8%. The average prevalence of
problem opioid use in the European Union and Norway is between 0.36% and 0.44%.
Development and Course
Opioid use disorder can begin at any age, but problems associated with opioid use are
most commonly first observed in the late teens or early 20s. Once opioid use disorder
develops, it usually continues over a period of many years, even though brief periods of
abstinence are frequent. In treated populations, relapse following abstinence is common.
Even though relapses do occur, and while some long-term mortality rates may be as high
as 2% per year, about 20%—30% of individuals with opioid use disorder achieve long-term
abstinence. An exception concerns that of military service personnel who became depen-
dent on opioids in Vietnam; over 90% of this population who had been dependent on opi-
oids during deployment in Vietnam achieved abstinence after they returned, but they
experienced increased rates of alcohol or amphetamine use disorder as well as increased
suicidality.
Increasing age is associated with a decrease in prevalence as a result of early mortality
and the remission of symptoms after age 40 years (i.e., “maturing out”). However, many
individuals continue have presentations that meet opioid use disorder criteria for decades.
Risk and Prognostic Factors
Genetic and physiological. The risk for opiate use disorder can be related to individual,
family, peer, and social environmental factors, but within these domains, genetic factors
play a particularly important role both directly and indirectly. For instance, impulsivity
and novelty seeking are individual temperaments that relate to the propensity to develop
544 Substance-Related and Addictive Disorders
a substance use disorder but may themselves be genetically determined. Peer factors may
relate to genetic predisposition in terms of how an individual selects his or her environ-
ment.
Culture-Related Diagnostic Issues
Despite small variations regarding individual criterion items, opioid use disorder diag-
nostic criteria perform equally well across most race/ethnicity groups. Individuals from
ethnic minority populations living in economically deprived areas have been overrep-
resented among individuals with opioid use disorder. However, over time, opioid use
disorder is seen more often among white middle-class individuals, especially females,
suggesting that differences in use reflect the availability of opioid drugs and that other so-
cial factors may impact prevalence. Medical personnel who have ready access to opioids
may be at increased risk for opioid use disorder.
Diagnostic Markers
Routine urine toxicology test results are often positive for opioid drugs in individuals with:
opioid use disorder. Urine test results remain positive for most opioids (e.g., heroin, mor-
phine, codeine, oxycodone, propoxyphene) for 12-36 hours after administration. Fentanyl
is not detected by standard urine tests but can be identified by more specialized proce-
dures for several days. Methadone, buprenorphine (or buprenorphine/naloxone combi-
nation), and LAAM (L-alpha-acetylmethadol) have to be specifically tested for and will not
cause a positive result on routine tests for opiates. They can be detected for several days up
to more than 1 week. Laboratory evidence of the presence of other substances (e.g., co-
caine, marijuana, alcohol, amphetamines, benzodiazepines) is common. Screening test re-
sults for hepatitis A, B, and C virus are positive in as many as 80%-90% of injection opioid
users, either for hepatitis antigen (signifying active infection) or for hepatitis antibody (sig-
nifying past infection). HIV is prevalent in injection opioid users as well. Mildly elevated
liver function test results are common, either as a result of resolving hepatitis or from toxic
injury to the liver due to contaminants that have been mixed with the injected opioid. Sub-
tle changes in cortisol secretion patterns and body temperature regulation have been ob-
served for up to 6 months following opioid detoxification.
Suicide Risk
Similar to the risk generally observed for all substance use disorders, opioid use disorder
is associated with a heightened risk for suicide attempts and completed suicides. Particu-
larly notable are both accidental and deliberate opioid overdoses. Some suicide risk factors
overlap with risk factors for an opioid use disorder. In addition, repeated opioid intoxica-
tion or withdrawal may be associated with severe depressions that, although temporary,
can be intense enough to lead to suicide attempts and completed suicides. Available data
suggest that nonfatal accidental opioid overdose (which is common) and attempted sui-
cide are distinct clinically significant problems that should not be mistaken for each other.
Functional Consequences of Opioid Use Disorder
Opioid use is associated with a lack of mucous membrane secretions, causing dry mouth
and nose. Slowing of gastrointestinal activity and a decrease in gut motility can produce
severe constipation. Visual acuity may be impaired as a result of pupillary constriction
with acute administration. In individuals who inject opioids, sclerosed veins (“tracks”)
and puncture marks on the lower portions of the upper extremities are common. Veins
sometimes become so severely sclerosed that peripheral edema develops, and individuals
switch to injecting in veins in the legs, neck, or groin. When these veins become unusable,
individuals often inject directly into their subcutaneous tissue (“skin-popping”), resulting
Opioid Use Disorder 545
in cellulitis, abscesses, and circular-appearing scars from healed skin lesions. Tetanus and
Clostridium botulinum infections are relatively rare but extremely serious consequences of
injecting opioids, especially with contaminated needles. Infections may also occur in other
organs and include bacterial endocarditis, hepatitis, and HIV infection. Hepatitis C infec-
tions, for example, may occur in up to 90% of persons who inject opioids. In addition, the
prevalence of HIV infection can be high among individuals who inject drugs, a large pro-
portion of whom are individuals with opioid use disorder. HIV infection rates have been
reported to be as high as 60% among heroin users with opioid use disorder in some areas
of the United States or the Russian Federation. However, the incidence may also be 10% or
less in other areas, especially those where access to clean injection material and parapher-
nalia is facilitated.
Tuberculosis is a particularly serious problem among individuals who use drugs in-
travenously, especially those who are dependent on heroin; infection is usually asymptom-
atic and evident only by the presence of a positive tuberculin skin test. However, many cases
of active tuberculosis have been found, especially among those who are infected with HIV.
These individuals often have a newly acquired infection but also are likely to experience
reactivation of a prior infection because of impaired immune function.
Individuals who sniff heroin or other opioids into the nose (“snorting”) often develop
irritation of the nasal mucosa, sometimes accompanied by perforation of the nasal septum.
Difficulties in sexual functioning are common. Males often experience erectile dysfunction
during intoxication or chronic use. Females commonly have disturbances of reproductive
function and irregular menses.
In relation to infections such as cellulitis, hepatitis, HTV infection, tuberculosis, and en-
docarditis, opioid use disorder is associated with a mortality rate as high as 1.5%-2% per
year. Death most often results from overdose, accidents, injuries, AIDS, or other general
medical complications. Accidents and injuries due to violence that is associated with buy-
ing or selling drugs are common. In some areas, violence accounts for more opioid-related
deaths than overdose or HIV infection. Physiological dependence on opioids may occur in
about half of the infants born to females with opioid use disorder; this can produce a se-
vere withdrawal syndrome requiring medical treatment. Although low birth weight is
also seen in children of mothers with opioid use disorder, it is usually not marked and is
generally not associated with serious adverse consequences.
Differential Diagnosis
Opioid-induced mental disorders. Opioid-induced disorders occur frequently in individ-
uals with opioid use disorder. Opioid-induced disorders may be characterized by symptoms
(e.g., depressed mood) that resemble primary mental disorders (e.g., persistent depressive dis-
order [dysthymia] vs. opioid-induced depressive disorder, with depressive features, with on-
set during intoxication). Opioids are less likely to produce symptoms of mental disturbance
than are most other drugs of abuse. Opioid intoxication and opioid withdrawal are distin-
guished from the other opioid-induced disorders (e.g., opioid-induced depressive disorder,
with onset during intoxication) because the symptoms in these latter disorders predominate
the clinical presentation and are severe enough to warrant independent clinical attention.
Other substance intoxication. Alcohol intoxication and sedative, hypnotic, or anxiolytic
intoxication can cause a clinical picture that resembles that for opioid intoxication. A diag-
nosis of alcohol or sedative, hypnotic, or anxiolytic intoxication can usually be made based
on the absence of pupillary constriction or the lack of a response to naloxone challenge. In
some cases, intoxication may be due both to opioids and to alcohol or other sedatives. In
these cases, the naloxone challenge will not reverse all of the sedative effects.
Other withdrawal disorders. The anxiety and restlessness associated with opioid with-
drawal resemble symptoms seen in sedative-hypnotic withdrawal. However, opioid
withdrawal is also accompanied by rhinorrhea, lacrimation, and pupillary dilation, which
546 Substance-Related and Addictive Disorders
are not seen in sedative-type withdrawal. Dilated pupils are also seen in hallucinogen
intoxication and stimulant intoxication. However, other signs or symptoms of opioid
withdrawal, such as nausea, vomiting, diarrhea, abdominal cramps, rhinorrhea, or lacri-
mation, are not present.
Comorbidity
The most common medical conditions associated with opioid use disorder are viral (e.g.,
HIV, hepatitis C virus) and bacterial infections, particularly among users of opioids by in-
jection. These infections are less common in opioid use disorder with prescription opioids.
Opioid use disorder is often associated with other substance use disorders, especially those
involving tobacco, alcohol, cannabis, stimulants, and benzodiazepines, which are often
taken to reduce symptoms of opioid withdrawal or craving for opioids, or to enhance the ef-
fects of administered opioids. Individuals with opioid use disorder are at risk for the devel-
opment of mild to moderate depression that meets symptomatic and duration criteria for
persistent depressive disorder (dysthymia) or, in some cases, for major depressive disorder.
These symptoms may represent an opioid-induced depressive disorder or an exacerbation
of a preexisting primary depressive disorder. Periods of depression are especially common
during chronic intoxication or in association with physical or psychosocial stressors that are
related to the opioid use disorder. Insomnia is common, especially during withdrawal. An-
tisocial personality disorder is much more common in individuals with opioid use disorder
than in the general population. Posttraumatic stress disorder is also seen with increased fre-
quency. A history of conduct disorder in childhood or adolescence has been identified as a
significant risk factor for substance-related disorders, especially opioid use disorder.
Opioid Intoxication
Diagnostic Criteria
A. Recent use of an opioid.
B. Clinically significant problematic behavioral or psychological changes (e.g., initial eu-
phoria followed by apathy, dysphoria, psychomotor agitation or retardation, impaired
judgment) that developed during, or shortly after, opioid use.
C. Pupillary constriction (or pupillary dilation due to anoxia from severe overdose) and
one (or more) of the following signs or symptoms developing during, or shortly after,
opioid use:
1. Drowsiness or coma.
2. Sturred speech.
3. Impairment in attention or memory.
D. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including intoxication with another sub-
stance.
Specify it:
With perceptual disturbances: This specifier may be noted in the rare instance in
which hallucinations with intact reality testing or auditory, visual, or tactile illusions oc-
cur in the absence of a delirium.
Coding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether
or not there is a comorbid opioid use disorder and whether or not there are perceptual dis-
turbances.
For opioid intoxication without perceptual disturbances: {f a mild opioid use dis-
order is comorbid, the 1CD-10-CM code is F11.129, and if a moderate or severe opioid
Opioid Withdrawal 547
use disorder is comorbid, the ICD-10-CM code is F11.229. If there is no comorbid opi-
oid use disorder, then the ICD-10-CM code is F11.929,
For opioid intoxication with perceptual disturbances: If a mild opioid use disorder
is comorbid, the ICD-10-CM code is F11.122, and if a moderate or severe opioid use
disorder is comorbid, the ICD-10-CM code is F11.222. If there is no comorbid opioid
use disorder, then the ICD-10-CM code is F11.922.
Diagnostic Features
The essential feature of opioid intoxication is the presence of clinically significant prob-
lematic behavioral or psychological changes (e.g., initial euphoria followed by apathy,
dysphoria, psychomotor agitation or retardation, impaired judgment) that develop dur-
ing, or shortly after, opioid use (Criteria A and B). Intoxication is accompanied by pupil-
lary constriction (unless there has been a severe overdose with consequent anoxia and
pupillary dilation) and one or more of the following signs: drowsiness (described as be-
ing “on the nod”), slurred speech, and impairment in attention or memory (Criterion C);
drowsiness may progress to coma. Individuals with opioid intoxication may demonstrate
inattention to the environment, even to the point of ignoring potentially harmful events.
The signs or symptoms must not be attributable to another medical condition and are not
better explained by another mental disorder (Criterion D).
Differential Diagnosis
Other substance intoxication. Alcohol intoxication and sedative-hypnotic intoxication
can cause a clinical picture that resembles opioid intoxication. A diagnosis of alcohol or
sedative-hypnotic intoxication can usually be made based on the absence of pupillary con-
striction or the lack of a response to a naloxone challenge. In some cases, intoxication may
be due both to opioids and to alcohol or other sedatives. In these cases, the naloxone chal-
lenge will not reverse all of the sedative effects.
Other opioid-related disorders. Opioid intoxication is distinguished from the other
opioid-induced disorders (e.g., opioid-induced depressive disorder, with onset during in-
toxication) because the symptoms in the latter disorders predominate in the clinical pre-
sentation and meet full criteria for the relevant disorder.
Opioid Withdrawal
Diagnostic Criteria 292.0 (F11.23)
A. Presence of either of the following:
1. Cessation of (or reduction in) opioid use that has been heavy and prolonged (i.e.,
several weeks or longer).
2. Administration of an opioid antagonist after a period of opioid use.
B. Three (or more) of the following developing within minutes to several days after Criterion A:
1. Dysphoric mood.
Nausea or vomiting.
Muscle aches.
Lacrimation or rhinorrhea.
Pupillary dilation, piloerection, or sweating.
oPRaAN
548 Substance-Related and Addictive Disorders
Diarrhea.
Yawning.
Fever.
Insomnia.
OOND
C. The signs or symptoms in Criterion B cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including intoxication or withdrawal from
another substance.
Coding note: The ICD-9-CM code is 292.0. The ICD-10-CM code for opioid withdrawal is
F11.23. Note that the ICD-10-CM code indicates the comorbid presence of a moderate or
severe opioid use disorder, reflecting the fact that opioid withdrawal can only occur in the
presence of a moderate or severe opioid use disorder. It is not permissible to code a co-
morbid mild opioid use disorder with opioid withdrawal.
Diagnostic Features
The essential feature of opioid withdrawal is the presence of a characteristic withdrawal
syndrome that develops after the cessation of (or reduction in) opioid use that has been
heavy and prolonged (Criterion A1). The withdrawal syndrome can also be precipitated
by administration of an opioid antagonist (e.g., naloxone or naltrexone) after a period of
opioid use (Criterion A2). This may also occur after administration of an opioid partial ag-
onist such as buprenorphine to a person currently using a full opioid agonist.
Opioid withdrawal is characterized by a pattern of signs and symptoms that are oppo-
site to the acute agonist effects. The first of these are subjective and consist of complaints of
anxiety, restlessness, and an “achy feeling” that is often located in the back and legs, along
with irritability and increased sensitivity to pain. Three or more of the following must be
present to make a diagnosis of opioid withdrawal: dysphoric mood; nausea or vomiting;
muscle aches; lacrimation or rhinorrhea; pupillary dilation, piloerection, or increased
sweating; diarrhea; yawning; fever; and insomnia (Criterion B). Piloerection and fever are
associated with more severe withdrawal and are not often seen in routine clinical practice
because individuals with opioid use disorder usually obtain substances before with-
drawal becomes that far advanced. These symptoms of opioid withdrawal must cause
clinically significant distress or impairment in social, occupational, or other important ar-
eas of functioning (Criterion C). The symptoms must not be attributable to another med-
ical condition and are not better explained by another mental disorder (Criterion D).
Meeting diagnostic criteria for opioid withdrawal alone is not sufficient for a diagnosis of
opioid use disorder, but concurrent symptoms of craving and drug-seeking behavior are
suggestive of comorbid opioid use disorder. ICD-10-CM codes only allow a diagnosis of
opioid withdrawal in the presence of comorbid moderate to severe opioid use disorder.
The speed and severity of withdrawal associated with opioids depend on the half-life of
the opioid used. Most individuals who are physiologically dependent on short-acting drugs
such as heroin begin to have withdrawal symptoms within 6-12 hours after the last dose.
Symptoms may take 2-4 days to emerge in the case of longer-acting drugs such as metha-
done, LAAM (L-alpha-acetylmethadol), or buprenorphine. Acute withdrawal symptoms for
a short-acting opioid such as heroin usually peak within 1-3 days and gradually subside
over a period of 5-7 days. Less acute withdrawal symptoms can last for weeks to months.
These more chronic symptoms include anxiety, dysphoria, anhedonia, and insomnia.
Opioid Withdrawal 549
Associated Features Supporting Diagnosis
Males with opiotd withdrawal may experience piloerection, sweating, and spontaneous
ejaculations while awake. Opioid withdrawal is distinct from opioid use disorder and
does not necessarily occur in the presence of the drug-seeking behavior associated with
opioid use disorder. Opioid withdrawal may occur in any individual after cessation of re-
peated use of an opioid, whether in the setting of medical management of pain, during
opioid agonist therapy for opioid use disorder, in the context of private recreational use, or
following attempts to self-treat symptoms of mental disorders with opioids.
Prevaience
Among individuals from various clinical settings, opioid withdrawal occurred in 60% of
individuals who had used heroin at least once in the prior 12 months.
Deveiopment and Course
Opioid withdrawal is typical in the course of an opioid use disorder. It can be part of an es-
calating pattern in which an opioid is used to reduce withdrawal symptoms, in turn lead-
ing to more withdrawal at a later time. For persons with an established opioid use
disorder, withdrawal and attempts to relieve withdrawal are typical.
Differential Diagnosis
Other withdrawal disorders. The anxiety and restlessness associated with opioid with-
drawal resemble symptoms seen in sedative-hypnotic withdrawal. However, opioid with-
drawal is also accompanied by rhinorrhea, lacrimation, and pupillary dilation, which are
not seen in sedative-type withdrawal.
Other substance intoxication. Dilated pupils are also seen in hallucinogen intoxication
and stimulant intoxication. However, other signs or symptoms of opioid withdrawal, such
as nausea, vomiting, diarrhea, abdominal cramps, rhinorrhea, and lacrimation, are not
present.
Other opioid-induced disorders. Opioid withdrawal is distinguished from the other
opioid-induced disorders (e.g., opioid-induced depressive disorder, with onset during
withdrawal) because the symptoms in these latter disorders are in excess of those usually
associated with opioid withdrawal and meet full criteria for the relevant disorder.
Other Opioid-Induced Disorders
The following opioid-induced disorders are described in other chapters of the manual with
disorders with which they share phenomenology (see the substance /medication-induced
mental disorders in these chapters): opioid-induced depressive disorder (“Depressive Dis-
orders”); opioid-induced anxiety disorder (“Anxiety Disorders”); opioid-induced sleep
disorder (“Sleep-Wake Disorders”); and opioid-induced sexual dysfunction (“Sexual Dys-
functions”). For opioid intoxication delirium and opioid withdrawal delirium, see the crite-
ria and discussion of delirium in the chapter “Neurocognitive Disorders.” These opioid-
induced disorders are diagnosed instead of opioid intoxication or opioid withdrawal only
when the symptoms are sufficiently severe to warrant independent clinical attention.
550 Substance-Related and Addictive Disorders
Unspecified Opioid-Related Disorder
292.9 (F11.99)
This category applies to presentations in which symptoms characteristic of an opioid-
related disorder that cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning predominate but do not meet the full criteria
for any specific opioid-related disorder or any of the disorders in the substance-related and
addictive disorders diagnostic class.
Sedative-, Hypnotic-,
or Anxiolytic-Related Disorders
Sedative, Hypnotic, or Anxiolytic Use Disorder
Sedative, Hypnotic, or Anxiolytic Intoxication
Sedative, Hypnotic, or Anxiolytic Withdrawal
Other Sedative-, Hypnotic-, or Anxiolytic-Induced Disorders
Unspecified Sedative-, Hypnotic-, or Anxiolytic-Related Disorder
Sedative, Hypnotic, or Anxiolytic Use Disorder
Diagnostic Criteria
A. Aproblematic pattern of sedative, hypnotic, or anxiolytic use leading to clinically signif-
icant impairment or distress, as manifested by at least two of the following, occurring
within a 12-month period:
1. Sedatives, hypnotics, or anxiolytics are often taken in larger amounts or over a lon-
ger period than was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control sedative,
hypnotic, or anxiolytic use.
3. Agreat deal of time is spent in activities necessary to obtain the sedative, hypnotic,
or anxiolytic; use the sedative, hypnotic, or anxiolytic; or recover from its effects.
4. Craving, or a strong desire or urge to use the sedative, hypnotic, or anxiolytic.
5. Recurrent sedative, hypnotic, or anxiolytic use resulting in a failure to fulfill major
role obligations at work, school, or home (e.g., repeated absences from work or
poor work performance related to sedative, hypnotic, or anxiolytic use; sedative-,
hypnotic-, or anxiolytic-related absences, suspensions, or expulsions from school;
neglect of children or household).
6. Continued sedative, hypnotic, or anxiolytic use despite having persistent or re-
current social or interpersonal problems caused or exacerbated by the effects of
sedatives, hypnotics, or anxiolytics (e.g., arguments with a spouse about conse-
quences of intoxication; physical fights).
7. Important social, occupational, or recreational activities are given up or reduced be-
cause of sedative, hypnotic, or anxiolytic use.
Sedative, Hypnotic, or Anxiolytic Use Disorder 551
8. Recurrent sedative, hypnotic, or anxiolytic use in situations in which it is physically
hazardous (e.g., driving an automobile or operating a machine when impaired by
sedative, hypnotic, or anxiolytic use).
9. Sedative, hypnotic, or anxiolytic use is continued despite knowledge of having a
persistent or recurrent physical or psychological problem that is likely to have been
caused or exacerbated by the sedative, hypnotic, or anxiolytic.
10. Tolerance, as defined by either of the following:
a. Aneed for markedly increased amounts of the sedative, hypnotic, or anxiolytic
to achieve intoxication or desired effect.
b. Amarkedly diminished effect with continued use of the same amount of the sed-
ative, hypnotic, or anxiolytic.
Note: This criterion is not considered to be met for individuals taking sedatives,
hypnotics, or anxiolytics under medical supervision.
11. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for sedatives, hypnotics, or anxiolytics
(refer to Criteria A and B of the criteria set for sedative, hypnotic, or anxiolytic
withdrawal, pp. 557-558).
b. Sedatives, hypnotics, or anxiolytics (or a closely related substance, such as al-
cohol) are taken to relieve or avoid withdrawal symptoms.
Note: This criterion is not considered to be met for individuals taking sedatives,
hypnotics, or anxiolytics under medical supervision.
Specify if:
In early remission: After full criteria for sedative, hypnotic, or anxiolytic use disorder
were previously met, none of the criteria for sedative, hypnotic, or anxiolytic use disor-
der have been met for at least 3 months but for less than +2 months (with the exception
that Criterion A4, “Craving, or a strong desire or urge to use the sedative, hypnotic, or
anxiolytic,” may be met).
In sustained remission: After full criteria for sedative, hypnotic, or anxiolytic use dis-
order were previously met, none of the criteria for sedative, hypnotic, or anxiolytic use
disorder have been met at any time during a period of 12 months or longer (with the
exception that Criterion A4, “Craving, or a strong desire or urge to use the sedative,
hypnotic, or anxiolytic,” may be met).
Specify if:
In a controled environment: This additional specifier is used if the individual is in an
environment where access to sedatives, hypnotics, or anxiolytics is restricted.
Coding based on current severity: Note for ICD-10-CM codes: If a sedative, hypnotic, or
anxiolytic intoxication; sedative, hypnotic, or anxiolytic withdrawal; or another sedative-,
hypnotic-, or anxiolytic-induced mental disorder is also present, do not use the codes be-
low for sedative, hypnotic, or anxiolytic use disorder. Instead the comorbid sedative, hyp-
notic, or anxiolytic use disorder is indicated in the 4th character of the sedative-, hypnotic-,
or anxiolytic-induced disorder (see the coding note for sedative, hypnotic, or anxiolytic in-
toxication; sedative, hypnotic, or anxiolytic withdrawal; or specific sedative-, hypnotic-, or
anxiolytic-induced mental disorder). For example, if there is comorbid sedative-, hypnotic-,
or anxiolytic-induced depressive disorder and sedative, hypnotic, or anxiolytic use disor-
der, only the sedative-, hypnotic-, or anxiolytic-induced depressive disorder code is given
with the 4th character indicating whether the comorbid sedative, hypnotic, or anxiolytic use
disorder is mild, moderate, or severe: F13.14 for mild sedative, hypnotic, or anxiolytic use
disorder with sedative-, hypnotic-, or anxiolytic-induced depressive disorder or F13.24 for
a moderate or severe sedative, hypnotic, or anxiolytic use disorder with sedative-, hypnotic-,
or anxiolytic-induced depressive disorder.
552 Substance-Related and Addictive Disorders
Specify current severity:
305.40 (F13.10) Mild: Presence of 2-3 symptoms.
304.10 (F13.20) Moderate: Presence of 4-5 symptoms.
304.10 (F13.20) Severe: Presence of 6 or more symptoms.
Specifiers
“Ina controlled environment” applies as a further specifier of remission if the individual is
both in remission and in a controlled environment (i.e., in early remission in a controlled
environment or in sustained remission in a controlled environment). Examples of these
environments are closely supervised and substance-free jails, therapeutic communities,
and locked hospital units.
Diagnostic Features
Sedative, hypnotic, or anxiolytic substances include benzodiazepines, benzodiazepine-
like drugs (e.g., zolpidem, zaleplon), carbamates (e.g., glutethimide, meprobamate),
barbiturates (e.g., secobarbital), and barbiturate-like hypnotics (e.g., glutethimide, meth-
aqualone). This class of substances includes all prescription sleeping medications and
almost all prescription antianxiety medications. Nonbenzodiazepine antianxiety agents
(e.g., buspirone, gepirone) are not included in this class because they do not appear to be
associated with significant misuse.
Like alcohol, these agents are brain depressants and can produce similar substance /
medication-induced and substance use disorders. Sedative, hypnotic, or anxiolytic sub-
stances are available both by prescription and illegally. Some individuals who obtain these
substances by prescription will develop a sedative, hypnotic, or anxiolytic use disorder,
while others who misuse these substances or use them for intoxication will not develop a
use disorder. In particular, sedatives, hypnotics, or anxiolytics with rapid onset and/or
short to intermediate lengths of action may be taken for intoxication purposes, although
longer acting substances in this class may be taken for intoxication as well.
Craving (Criterion A4), either while using or during a period of abstinence, is a typical
feature of sedative, hypnotic, or anxiolytic use disorder. Misuse of substances from this
class may occur on its own or in conjunction with use of other substances. For example, in-
dividuals may use intoxicating doses of sedatives or benzodiazepines to “come down”
from cocaine or amphetamines or use high doses of benzodiazepines in combination with
methadone to “boost” its effects.
Repeated absences or poor work performance, school absences, suspensions or expul-
sions, and neglect of children or household (Criterion A5) may be related to sedative, hyp-
notic, or anxiolytic use disorder, as may the continued use of the substances despite
arguments with a spouse about consequences of intoxication or despite physical fights
(Criterion A6). Limiting contact with family or friends, avoiding work or school, or stop-
ping participation in hobbies, sports, or games (Criterion A7) and recurrent sedative,
hypnotic, or anxiolytic use when driving an automobile or operating a machine when im-
paired by sedative, hypnotic, or anxiolytic use (Criterion A8) are also seen in sedative,
hypnotic, or anxiolytic use disorder.
Very significant levels of tolerance and withdrawal can develop to the sedative, hyp-
notic, or anxiolytic. There may be evidence of tolerance and withdrawal in the absence of
a diagnosis of a sedative, hypnotic, or anxiolytic use disorder in an individual who has
abruptly discontinued use of benzodiazepines that were taken for long periods of time at
prescribed and therapeutic doses. In these cases, an additional diagnosis of sedative, hyp-
notic, or anxiolytic use disorder is made only if other criteria are met. That is, sedative,
hypnotic, or anxiolytic medications may be prescribed for appropriate medical purposes,
and depending on the dose regimen, these drugs may then produce tolerance and with-
Sedative, Hypnotic, or Anxiolytic Use Disorder 553
drawal. If these drugs are prescribed or recommended for appropriate medical purposes,
and if they are used as prescribed, the resulting tolerance or withdrawal does not meet the
criteria for diagnosing a substance use disorder. However, it is necessary to determine
whether the drugs were appropriately prescribed and used (e.g., falsifying medical symp-
toms to obtain the medication; using more medication than prescribed; obtaining the med-
ication from several doctors without informing them of the others’ involvement).
Given the unidimensional nature of the symptoms of sedative, hypnotic, or anxiolytic
use disorder, severity is based on the number of criteria endorsed.
Associated Features Supporting Diagnosis
Sedative, hypnotic, or anxiolytic use disorder is often associated with other substance use dis-
orders (e.g., alcohol, cannabis, opioid, stimulant use disorders). Sedatives are often used to al-
leviate the unwanted effects of these other substances. With repeated use of the substance,
tolerance develops to the sedative effects, and a progressively higher dose is used. However,
tolerance to brain stem depressant effects develops much more slowly, and as the individual
takes more substance to achieve euphoria or other desired effects, there may be a sudden onset
of respiratory depression and hypotension, which may result in death. Intense or repeated
sedative, hypnotic, or anxiolytic intoxication may be associated with severe depression that,
although temporary, can lead to suicide attempt and completed suicide.
Prevalence
The 12-month prevalences of DSM-IV sedative, hypnotic, or anxiolytic use disorder are es-
timated to be 0.3% among 12- to 17-year-olds and 0.2% among adults age 18 years and
older. Rates of DSM-IV sedative, hypnotic, or anxiolytic use disorder are slightly greater
among adult males (0.3%) than among adult females, but for 12- to 17-year-olds, the rate
for females (0.4%) exceeds that for males (0.2%). The 12-month prevalence of DSM-IV
sedative, hypnotic, or anxiolytic use disorder decreases as a function of age and is great-
est among 18- to 29-year-olds (0.5%) and lowest among individuals 65 years and older
(0.04%).
Twelve-month prevalence of sedative, hypnotic, or anxiolytic use disorder varies across
racial/ethnic subgroups of the U.S. population. For 12- to 17-year-olds, rates are greatest
among whites (0.3%) relative to African Americans (0.2%), Hispanics (0.2%), Native Amer-
icans (0.1%), and Asian Americans and Pacific Islanders (0.1%). Among adults, 12-month
prevalence is greatest among Native Americans and Alaska Natives (0.8%), with rates of
approximately 0.2% among African Americans, whites, and Hispanics and 0.1% among
Asian Americans and Pacific Islanders.
Development and Course
The usual course of sedative, hypnotic, or anxiolytic use disorder involves individuals in
their teens or 20s who escalate their occasional use of sedative, hypnotic, or anxiolytic
agents to the point at which they develop problems that meet criteria for a diagnosis. This
pattern may be especially likely among individuals who have other substance use disor-
ders (e.g., alcohol, opioids, stimulants). An initial pattern of intermittent use socially (e.g.,
at parties) can lead to daily use and high levels of tolerance. Once this occurs, an increasing
level of interpersonal difficulties, as well as increasingly severe episodes of cognitive dys-
function and physiological withdrawal, can be expected.
The second and less frequently observed clinical course begins with an individual who
originally obtained the medication by prescription from a physician, usually for the treat-
ment of anxiety, insomnia, or somatic complaints. As either tolerance or a need for higher
doses of the medication develops, there is a gradual increase in the dose and frequency of
self-administration. The individual is likely to continue to justify use on the basis of his or
her original symptoms of anxiety or insomnia, but substance-seeking behavior becomes
554 Substance-Related and Addictive Disorders
more prominent, and the individual may seek out multiple physicians to obtain sufficient
supplies of the medication. Tolerance can reach high levels, and withdrawal (including
seizures and withdrawal delirium) may occur.
As with many substance use disorders, sedative, hypnotic, or anxiolytic use disorder gen-
erally has an onset during adolescence or early adult life. There is an increased risk for misuse
and problems from many psychoactive substances as individuals age. In particular, cognitive
impairment increases as a side effect with age, and the metabolism of sedatives, hypnotics, or
anxiolytics decreases with age among older individuals. Both acute and chronic toxic effects
of these substances, especially effects on cognition, memory, and motor coordination, are
likely to increase with age as a consequence of pharmacodynamic and pharmacokinetic age-
related changes. Individuals with major neurocognitive disorder (dementia) are more likely
to develop intoxication and impaired physiological functioning at lower doses.
Deliberate intoxication to achieve a “high” is most likely to be observed in teenagers
and individuals in their 20s. Problems associated with sedatives, hypnotics, or anxiolytics
are also seen in individuals in their 40s and older who escalate the dose of prescribed med-
ications. In older individuals, intoxication can resemble a progressive dementia.
Risk and Prognostic Factors
Temperamental. Impulsivity and novelty seeking are individual temperaments that re-
late to the propensity to develop a substance use disorder but may themselves be geneti-
cally determined.
Environmental. Since sedatives, hypnotics, or anxiolytics are all pharmaceuticals, a key
risk factor relates to availability of the substances. In the United States, the historical pat-
terns of sedative, hypnotic, or anxiolytic misuse relate to the broad prescribing patterns.
For instance, a marked decrease in prescription of barbiturates was associated with an in-
crease in benzodiazepine prescribing. Peer factors may relate to genetic predisposition in
terms of how individuals select their environment. Other individuals at heightened risk
might include those with alcohol use disorder who may receive repeated prescriptions in
response to their complaints of alcohol-related anxiety or insomnia.
Genetic and physiological. As for other substance use disorders, the risk for sedative,
hypnotic, or anxiolytic use disorder can be related to individual, family, peer, social, and
environmental factors. Within these domains, genetic factors play a particularly important
role both directly and indirectly. Overall, across development, genetic factors seem to play
a larger role in the onset of sedative, hypnotic, or anxiolytic use disorder as individuals age
through puberty into adult life.
Course modifiers. Early onset of use is associated with greater likelihood for develop-
ing a sedative, hypnotic, or anxiolytic use disorder.
Culture-Related Diagnostic Issues
There are marked variations in prescription patterns (and availability) of this class of sub-
stances in different countries, which may lead to variations in prevalence of sedative, hyp-
notic, or anxiolytic use disorders.
Gender-Related Diagnostic Issues
Females may be at higher risk than males for prescription drug misuse of sedative, hyp-
notic, or anxiolytic substances.
Diagnostic Markers
Almost all sedative, hypnotic, or anxiolytic substances can be identified through labora-
tory evaluations of urine or blood (the latter of which can quantify the amounts of these
Sedative, Hypnotic, or Anxiolytic Use Disorder 555
agents in the body). Urine tests are likely to remain positive for up to approximately 1 week
after the use of lang-acting substances, such as diazepam or flurazepam.
Functional Consequences of
Sedative, Hypnotic, or Anxioiytic Use Disorder
The social and interpersonal consequences of sedative, hypnotic, or anxiolytic use disorder
mimic those of alcohol in terms of the potential for disinhibited behavior. Accidents, interper-
sonal difficulties (such as arguments or fights), and interference with work or school perfor-
mance are all common outcomes. Physical examination is likely to reveal evidence of a mild
decrease in most aspects of autonomic nervous system functioning, including a slower pulse,
a slightly decreased respiratory rate, and a slight drop in blood pressure (most likely to occur
with postural changes). At high doses, sedative, hypnotic, or anxiolytic substances can be le-
thal, particularly when mixed with alcohol, although the lethal dosage varies considerably
among the specific substances. Overdoses may be associated with a deterioration in vital signs
that signals an impending medical emergency (e.g., respiratory arrest from barbiturates).
There may be consequences of trauma (e.g., internal bleeding or a subdural hematoma) from
accidents that occur while intoxicated. Intravenous use of these substances can result in med-
ical complications related to the use of contaminated needles (e.g., hepatitis and HIV).
Acute intoxication can result in accidental injuries and automobile accidents. For elderly
individuals, even short-term use of these sedating medications at prescribed doses can be as-
sociated with an increased risk for cognitive problems and falls. The disinhibiting effects of
these agents, like alcohol, may potentially contribute to overly aggressive behavior, with sub-
sequent interpersonal and legal problems. Accidental or deliberate overdoses, similar to those
observed for alcohol use disorder or repeated alcohol intoxication, can occur. In contrast to
their wide margin of safety when used alone, benzodiazepines taken in combination with al-
cohol can be particularly dangerous, and accidental overdoses are reported commonly. Acci-
dental overdoses have also been reported in individuals who deliberately misuse barbiturates
and other nonbenzodiazepine sedatives (e.g., methaqualone), but since these agents are much
less available than the benzodiazepines, the frequency of overdosing is low in most settings.
Differential Diagnosis
Other mental disorders or medical conditions. Individuals with sedative-, hypnotic-,
or anxiolytic-induced disorders may present with symptoms (e.g., anxiety) that resemble
primary mental disorders (e.g., generalized anxiety disorder vs. sedative-, hypnotic-, or
anxiolytic-induced anxiety disorder, with onset during withdrawal). The slurred speech,
incoordination, and other associated features characteristic of sedative, hypnotic, or anx-
iolytic intoxication could be the result of another medical condition (e.g., multiple sclero-
sis) or of a prior head trauma (e.g., a subdural hematoma).
Alcohol use disorder. Sedative, hypnotic, or anxiolytic use disorder must be differenti-
ated from alcohol use disorder.
Clinically appropriate use of sedative, hypnotic, or anxiolytic medications. Individuals
may continue to take benzodiazepine medication according to a physician's direction for a
legitimate medical indication over extended periods of time. Even if physiological signs of
tolerance or withdrawal are manifested, many of these individuals do not develop symp-
toms that meet the criteria for sedative, hypnotic, or anxiolytic use disorder because they
are not preoccupied with obtaining the substance and its use does not interfere with their
performance of usual social or occupational roles.
Comorbidity
Nonmedical use of sedative, hypnotic, or anxiolytic agents is associated with alcohol use
disorder, tobacco use disorder, and, generally, illicit drug use. There may also be an over-
556 Substance-Related and Addictive Disorders
lap between sedative, hypnotic, or anxiolytic use disorder and antisocial personality dis-
order; depressive, bipolar, and anxiety disorders; and other substance use disorders, such
as alcohol use disorder and illicit drug use disorders. Antisocial behavior and antisocial
personality disorder are especially associated with sedative, hypnotic, or anxiolytic use
disorder when the substances are obtained illegally.
Sedative, Hypnotic, or Anxiolytic Intoxication
Diagnostic Criteria
A. Recent use of a sedative, hypnotic, or anxiolytic.
B. Clinically significant maladaptive behavioral or psychological changes (e.g., inappro-
priate sexual or aggressive behavior, mood lability, impaired judgment) that developed
during, or shortly after, sedative, hypnotic, or anxiolytic use.
C. One (or more) of the following signs or symptoms developing during, or shortly after,
sedative, hypnotic, or anxiolytic use:
Slurred speech.
Incoordination.
Unsteady gait.
Nystagmus.
Impairment in cognition (e.g., attention, memory).
6. Stupor or coma.
aoPwonNns
D. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including intoxication with another sub-
stance.
Coding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether
there is a comorbid sedative, hypnotic, or anxiolytic use disorder. If a mild sedative, hyp-
notic, or anxiolytic use disorder is comorbid, the ICD-10-CM code is F13.129, and if a mod-
erate or severe sedative, hypnotic, or anxiolytic use disorder is comorbid, the ICD-10-CM
code is F13.229. if there is no comorbid sedative, hypnotic, or anxiolytic use disorder, then
the ICD-10-CM code is F13.929.
Note: For information on Development and Course; Risk and Prognostic Factors; Culture-
Related Diagnostic Issues; Diagnostic Markers; Functional Consequences of Sedative,
Hypnotic, or Anxiolytic Intoxication; and Comorbidity, see the corresponding sections in
sedative, hypnotic, or anxiolytic use disorder.
Diagnostic Features
The essential feature of sedative, hypnotic, or anxiolytic intoxication is the presence of clini-
cally significant maladaptive behavioral or psychological changes (e.g., inappropriate sexual
or aggressive behavior, mood lability, impaired judgment, impaired social or occupational
functioning) that develop during, or shortly after, use of a sedative, hypnotic, or anxiolytic
(Criteria A and B). As with other brain depressants, such as alcohol, these behaviors may be ac-
companied by slurred speech, incoordination (at levels that can interfere with driving abilities
and with performing usual activities to the point of causing falls or automobile accidents), an
unsteady gait, nystagmus, impairment in cognition (e.g., attentional or memory problems),
and stupor or coma (Criterion C). Memory impairment is a prominent feature of sedative, hyp-
notic, or anxiolytic intoxication and is most often characterized by an anterograde amnesia that
resembles “alcoholic blackouts,” which can be disturbing to the individual. The symptoms
must not be attributable to another medical condition and are not better explained by another
Sedative, Hypnotic, or Anxiolytic Withdrawal 557
mental disorder (Criterion D). Intoxication may occur in individuals who are receiving these
substances by prescription, are borrowing the medication from friends or relatives, or are de-
liberately taking the substance to achieve intoxication.
Associated Features Supporting Diagnosis
Associated features include taking more medication than prescribed, taking multiple dif-
ferent medications, or mixing sedative, hypnotic, or anxiolytic agents with alcohol, which
can markedly increase the effects of these agents.
Prevaience
The prevalence of sedative, hypnotic, or anxiolytic intoxication in the general population
is unclear. However, it is probable that most nonmedical users of sedatives, hypnotics, or
anxiolytics would at some time have signs or symptoms that meet criteria for sedative,
hypnotic, or anxiolytic intoxication; if so, then the prevalence of nonmedical sedative,
hypnotic, or anxiolytic use in the general population may be similar to the prevalence of
sedative, hypnotic, or anxiolytic intoxication. For example, tranquilizers are used non-
medically by 2.2% of Americans older than 12 years.
Differentiai Diagnosis
Alcohol use disorders. Since the clinical presentations may be identical, distinguishing sed-
ative, hypnotic, or anxiolytic intoxication from alcohol use disorders requires evidence for re-
cent ingestion of sedative, hypnotic, or anxiolytic medications by self-report, informant report,
or toxicological testing. Many individuals who misuse sedatives, hypnotics, or anxiolytics may
also misuse alcohol and other substances, and so multiple intoxication diagnoses are possible.
Alcohol intoxication. Alcohol intoxication may be distinguished from sedative, hypnotic,
or anxiolytic intoxication by the smell of alcohol on the breath. Otherwise, the features of
the two disorders may be similar.
Other sedative-, hypnotic-, or anxiolytic-induced disorders. Sedative, hypnotic, or anx-
iolytic intoxication is distinguished from the other sedative-, hypnotic-, or anxiolytic-
induced disorders (e.g., sedative-, hypnotic-, or anxiolytic-induced anxiety disorder, with
onset during withdrawal) because the symptoms in the latter disorders predominate in
the clinical presentation and are severe enough to warrant clinical attention.
Neurocognitive disorders. In situations of cognitive impairment, traumatic brain in-
jury, and delirium from other causes, sedatives, hypnotics, or anxiolytics may be intoxi-
cating at quite low dosages. The differential diagnosis in these complex settings is based
on the predominant syndrome. An additional diagnosis of sedative, hypnotic, or anxio-
lytic intoxication may be appropriate even if the substance has been ingested at a low dos-
age in the setting of these other (or similar) co-occurring conditions.
Sedative, Hypnotic, or Anxiolytic Withdrawal
Diagnostic Criteria
A. Cessation of (or reduction in) sedative, hypnotic, or anxiolytic use that has been pro-
longed.
B. Two (or more) of the following, developing within several hours to a few days after the ces-
sation of (or reduction in) sedative, hypnotic, or anxiolytic use described in Criterion A:
1. Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 bpm).
2. Hand tremor.
558 Substance-Related and Addictive Disorders
. Insomnia.
. Nausea or vomiting.
. Transient visual, tactile, or auditory hallucinations or illusions.
. Psychomotor agitation.
Anxiety.
. Grand mal seizures.
ONAN AW
C. The signs or symptoms in Criterion B cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including intoxication or withdrawal from
another substance.
Specify if:
With perceptual disturbances: This specifier may be noted when hallucinations with in-
tact reality testing or auditory, visual, or tactile illusions occur in the absence of a delirium.
Coding note: The ICD-9-CM code is 292.0. The ICD-10-CM code for sedative, hypnotic,
or anxiolytic withdrawal depends on whether or not there is a comorbid moderate or se-
vere sedative, hypnotic, or anxiolytic use disorder and whether or not there are perceptual
disturbances. For sedative, hypnotic, or anxiolytic withdrawal without perceptual distur-
bances, the ICD-10-CM code is F13.239. For sedative, hypnotic, or anxiolytic withdrawal
with perceptual disturbances, the ICD-10-CM code is F13.232. Note that the ICD-10-CM
codes indicate the comorbid presence of a moderate or severe sedative, hypnotic, or anx-
iolytic use disorder, reflecting the fact that sedative, hypnotic, or anxiolytic withdrawal can
only occur in the presence of a moderate or severe sedative, hypnotic, or anxiolytic use
disorder. It is not permissible to code a comorbid mild sedative, hypnotic, or anxiolytic use
disorder with sedative, hypnotic, or anxiolytic withdrawal.
Note: For information on Development and Course; Risk and Prognostic Factors; Culture-
Related Diagnostic Issues; Functional Consequences of Sedative, Hypnotic, or Anxiolytic
Withdrawal; and Comorbidity, see the corresponding sections in sedative, hypnotic, or
anxiolytic use disorder.
Diagnostic Features
The essential feature of sedative, hypnotic, or anxiolytic withdrawal is the presence of a char-
acteristic syndrome that develops after a marked decrease in or cessation of intake after several
weeks or more of regular use (Criteria A and B). This withdrawal syndrome is characterized by
two or more symptoms (similar to alcohol withdrawal) that include autonomic hyperactivity
(e.g., increases in heart rate, respiratory rate, blood pressure, or body temperature, along with
sweating); a tremor of the hands; insomnia; nausea, sometimes accompanied by vomiting;
anxiety; and psychomotor agitation. A grand mal seizure may occur in perhaps as many as
20%-30% of individuals undergoing untreated withdrawal from these substances. In severe
withdrawal, visual, tactile, or auditory hallucinations or illusions can occur but are usually in
the context of a delirium. If the individual's reality testing is intact (i.e., he or she knows the
substance is causing the hallucinations) and the illusions occur in a clear sensorium, the spec-
ifier “with perceptual disturbances” can be noted. When hallucinations occur in the absence of
intact reality testing, a diagnosis of substance/medication-induced psychotic disorder should
be considered. The symptoms cause clinically significant distress or impairment in social, oc-
cupational, or other important areas of functioning (Criterion C). The symptoms must not be
attributable to another medical condition and are not better explained by another mental dis-
order (e.g., alcohol withdrawal or generalized anxiety disorder) (Criterion D). Relief of with-
drawal symptoms with administration of any sedative-hypnotic agent would support a
diagnosis of sedative, hypnotic, or anxiolytic withdrawal.
Sedative, Hypnotic, or Anxiolytic Withdrawal 559
Associated Features Supporting Diagnosis
The timing and severity of the withdrawal syndrome will differ depending on the specific
substance and its pharmacokinetics and pharmacodynamics. For example, withdrawal
from shorter-acting substances that are rapidly absorbed and that have no active metabo-
lites (e.g., triazolam) can begin within hours after the substance is stopped; withdrawal
from substances with long-acting metabolites (e.g., diazepam) may not begin for 1-2 days
or longer. The withdrawal syndrome produced by substances in this class may be charac-
terized by the development of a delirium that can be life-threatening. There may be evi-
dence of tolerance and withdrawal in the absence of a diagnosis of a substance use
disorder in an individual who has abruptly discontinued benzodiazepines that were taken
for long periods of time at prescribed and therapeutic doses. However, ICD-10-CM codes
only allow a diagnosis of sedative, hypnotic, or anxiolytic withdrawal in the presence of
comorbid moderate to severe sedative, hypnotic, or anxiolytic use disorder.
The time course of the withdrawal syndrome is generally predicted by the half-life of
the substance. Medications whose actions typically last about 10 hours or less (e.g., loraz-
epam, oxazepam, temazepam) produce withdrawal symptoms within 6-8 hours of de-
creasing blood levels that peak in intensity on the second day and improve markedly by
the fourth or fifth day. For substances with longer half-lives (e.g., diazepam), symptoms
may not develop for more than 1 week, peak in intensity during the second week, and de-
crease markedly during the third or fourth week. There may be additional longer-term
symptoms at a much lower level of intensity that persist for several months.
The longer the substance has been taken and the higher the dosages used, the more likely
it is that there will be severe withdrawal. However, withdrawal has been reported with as little
as 15 mg of diazepam (or its equivalent in other benzodiazepines) when taken daily for several
months. Doses of approximately 40 mg of diazepam (or its equivalent) daily are more likely to
produce clinically relevant withdrawal symptoms, and even higher doses (e.g., 100 mg of di-
azepam) are more likely to be followed by withdrawal seizures or delirium. Sedative, hyp-
notic, or anxiolytic withdrawal delirium is characterized by disturbances in consciousness and
cognition, with visual, tactile, or auditory hallucinations. When present, sedative, hypnotic, or
anxiolytic withdrawal delirium should be diagnosed instead of withdrawal.
Prevalence
The prevalence of sedative, hypnotic, or anxiolytic withdrawal is unclear.
Diagnostic Markers
Seizures and autonomic instability in the setting of a history of prolonged exposure to sed-
ative, hypnotic, or anxiolytic medications suggest a high likelihood of sedative, hypnotic,
or anxiolytic withdrawal.
Differential Diagnosis
Other medical disorders. The symptoms of sedative, hypnotic, or anxiolytic with-
drawal may be mimicked by other medical conditions (e.g., hypoglycemia, diabetic keto-
acidosis). If seizures are a feature of the sedative, hypnotic, or anxiolytic withdrawal, the
differential diagnosis includes the various causes of seizures (e.g., infections, head injury,
poisonings).
Essential tremor. Essential tremor, a disorder that frequently runs in families, may
erroneously suggest the tremulousness associated with sedative, hypnotic, or anxiolytic
withdrawal.
Alcohol withdrawal. Alcohol withdrawal produces a syndrome very similar to that of
sedative, hypnotic, or anxiolytic withdrawal.
560 Substance-Related and Addictive Disorders
Other sedative-, hypnotic-, or anxiolytic-induced disorders. Sedative, hypnotic, or anx-
iolytic withdrawal is distinguished from the other sedative-, hypnotic-, or anxiolytic-
induced disorders (e.g., sedative-, hypnotic-, or anxiolytic-induced anxiety disorder, with
onset during withdrawal) because the symptoms in the latter disorders predominate in
the clinical presentation and are severe enough to warrant clinical attention.
Anxiety disorders. Recurrence or worsening of an underlying anxiety disorder pro-
duces a syndrome similar to sedative, hypnotic, or anxiolytic withdrawal. Withdrawal
would be suspected with an abrupt reduction in the dosage of a sedative, hypnotic, or anx-
iolytic medication. When a taper is under way, distinguishing the withdrawal syndrome
from the underlying anxiety disorder can be difficult. As with alcohol, lingering with-
drawal symptoms (e.g., anxiety, moodiness, and trouble sleeping) can be mistaken for
non-substance/medication-induced anxiety or depressive disorders (e.g., generalized
anxiety disorder).
Other Sedative-, Hypnotic-,
or Anxiolytic-Induced Disorders
The following sedative-, hypnotic-, or anxiolytic-induced disorders are described in other
chapters of the manual with disorders with which they share phenomenology (see the sub-
stance/medication-induced mental disorders in these chapters): sedative-, hypnotic-, or
anxiolytic-induced psychotic disorder (“Schizophrenia Spectrum and Other Psychotic
Disorders”); sedative-, hypnotic-, or anxiolytic-induced bipolar disorder (“Bipolar and Re-
lated Disorders”); sedative-, hypnotic-, or anxiolytic-induced depressive disorder (“De-
pressive Disorders”); sedative-, hypnotic-, or anxiolytic-induced anxiety disorder
(“Anxiety Disorders”); sedative-, hypnotic-, or anxiolytic-induced sleep disorder (“Sleep-
Wake Disorders”); sedative-, hypnotic-, or anxiolytic-induced sexual dysfunction (“Sex-
ual Dysfunctions”); and sedative-, hypnotic-, or anxiolytic-induced major or mild neuro-
cognitive disorder (“Neurocognitive Disorders”). For sedative, hypnotic, or anxiolytic
intoxication delirium and sedative, hypnotic, or anxiolytic withdrawal delirium, see the
criteria and discussion of delirium in the chapter “Neurocognitive Disorders.” These sed-
ative-, hypnotic-, or anxiolytic-induced disorders are diagnosed instead of sedative, hyp-
notic, or anxiolytic intoxication or sedative, hypnotic, or anxiolytic withdrawal only when
the symptoms are sufficiently severe to warrant independent clinical attention.
Unspecified Sedative-, Hypnotic-,
or Anxiolytic-Related Disorder
292.9 (F13.99)
This category applies to presentations in which symptoms characteristic of a sedative-,
hypnotic-, or anxiolytic-related disorder that cause clinically significant distress or impair-
ment in social, occupational, or other important areas of functioning predominate but do
not meet the full criteria for any specific sedative-, hypnotic-, or anxiolytic-related disorder
or any of the disorders in the substance-related and addictive disorders diagnostic class.
Stimulant Use Disorder 561
Stimulant-Related Disorders
Stimulant Use Disorder
Stimulant intoxication
Stimulant Withdrawal
Other Stimulant-induced Disorders
Unspecified Stimulant-Related Disorder
Stimulant Use Disorder
Diagnostic Criteria
A. A pattern of amphetamine-type substance, cocaine, or other stimulant use leading to
Clinically significant impairment or distress, as manifested by at least two of the follow-
ing, occurring within a 12-month period:
1.
2.
3.
11.
The stimulant is often taken in larger amounts or over a longer period than was in-
tended.
There is a persistent desire or unsuccessful efforts to cut down or control stimulant use.
A great deal of time is spent in activities necessary to obtain the stimulant, use the
stimulant, or recover from its effects.
Craving, or a strong desire or urge to use the stimulant.
Recurrent stimulant use resulting in a failure to fulfill major role obligations at work,
school, or home.
Continued stimulant use despite having persistent or recurrent social or interper-
sonal problems caused or exacerbated by the effects of the stimulant.
Important social, occupational, or recreational activities are given up or reduced be-
cause of stimulant use.
Recurrent stimulant use in situations in which it is physically hazardous.
Stimulant use is continued despite knowledge of having a persistent or recurrent
physical or psychological problem that is likely to have been caused or exacerbated
by the stimulant.
. Tolerance, as defined by either of the following:
a. Aneed for markedly increased amounts of the stimulant to achieve intoxication
or desired effect.
b. A markedly diminished effect with continued use of the same amount of the
stimulant.
Note: This criterion is not considered to be met for those taking stimulant medica-
tions solely under appropriate medical supervision, such as medications for atten-
tion-deficit/hyperactivity disorder or narcolepsy.
Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for the stimulant (refer to Criteria A and
B of the criteria set for stimulant withdrawal, p. 569).
b. The stimulant (or a closely related substance) is taken to relieve or avoid with-
drawal symptoms.
562 Substance-Related and Addictive Disorders
Note: This criterion is not considered to be met for those taking stimulant medica-
tions solely under appropriate medical supervision, such as medications for atten-
tion-deficit/hyperactivity disorder or narcolepsy.
Specify if:
In early remission: After full criteria for stimulant use disorder were previously met,
none of the criteria for stimulant use disorder have been met for at least 3 months but
for less than 12 months (with the exception that Criterion A4, “Craving, or a strong de-
sire or urge to use the stimulant,” may be met).
In sustained remission: After full criteria for stimulant use disorder were previously
met, none of the criteria for stimulant use disorder have been met at any time during a
period of 12 months or longer (with the exception that Criterion A4, “Craving, or a
strong desire or urge to use the stimulant,” may be met).
Specify if:
In acontrolied environment: This additional specifier is used if the individual is in an
environment where access to stimulants is restricted.
Coding based on current severity: Note for ICD-10-CM codes: If an amphetamine in-
toxication, amphetamine withdrawal, or another amphetamine-induced mental disorder is
also present, do not use the codes below for amphetamine use disorder. Instead, the co-
morbid amphetamine use disorder is indicated in the 4th character of the amphetamine-
induced disorder code (see the coding note for amphetamine intoxication, amphetamine
withdrawal, or a specific amphetamine-induced mental disorder). For example, if there is
comorbid amphetamine-type or other stimulant-induced depressive disorder and amphet-
amine-type or other stimulant use disorder, only the amphetamine-type or other stimulant-
induced depressive disorder code is given, with the 4th character indicating whether the
comorbid amphetamine-type or other stimulant use disorder is mild, moderate, or severe:
F15.14 for mild amphetamine-type or other stimulant use disorder with amphetamine-type
or other stimulant-induced depressive disorder or F15.24 for a moderate or severe am-
phetamine-type or other stimulant use disorder with amphetamine-type or other stimulant-
induced depressive disorder. Similarly, if there is comorbid cocaine-induced depressive
disorder and cocaine use disorder, only the cocaine-induced depressive disorder code is
given, with the 4th character indicating whether the comorbid cocaine use disorder is mild,
moderate, or severe: F14.14 for mild cocaine use disorder with cocaine-induced depressive
disorder or F14.24 for a moderate or severe cocaine use disorder with cocaine-induced
depressive disorder.
Specify current severity:
Mild: Presence of 2-3 symptoms.
305.70 (F15.10} Amphetamine-type substance
305.60 (F14.10) Cocaine
305.70 (F15.10) Other or unspecified stimulant
Moderate: Presence of 4-5 symptoms.
304.40 (F15.20) Amphetamine-type substance
304.20 (F14.20) Cocaine
304.40 (F15.20) Other or unspecified stimulant
Severe: Presence of 6 or more symptoms.
304.40 (F15.20) Amphetamine-type substance
304.20 (F14.20) Cocaine
304.40 (F15.20) Other or unspecified stimulant
Stimulant Use Disorder 563
Specifiers
“Ina controlled environment” applies as a further specifier of remission if the individual is
both in remission and in a controlled environment (i-e., in early remission in a controlled
environment or in sustained remission in a controlled environment). Examples of these
environments are closely supervised and substance-free jails, therapeutic communities,
and locked hospital units.
Diagnostic Features
The amphetamine and amphetamine-type stimulants include substances with a substi-
tuted-phenylethylamine structure, such as amphetamine, dextroamphetamine, and meth-
amphetamine. Also included are those substances that are structurally different but have
similar effects, such as methylphenidate. These substances are usually taken orally or in-
travenously, although methamphetamine is also taken by the nasal route. In addition to
the synthetic amphetamine-type compounds, there are naturally occurring, plant-derived
stimulants such as khat. Amphetamines and other stimulants may be obtained by prescrip-
tion for the treatment of obesity, attention-deficit/hyperactivity disorder, and narcolepsy.
Consequently, prescribed stimulants may be diverted into the illegal market. The effects of
amphetamines and amphetamine-like drugs are similar to those of cocaine, such that the
criteria for stimulant use disorder are presented here as a single disorder with the ability to
specify the particular stimulant used by the individual. Cocaine may be consumed in sev-
eral preparations (e.g., coca leaves, coca paste, cocaine hydrochloride, and cocaine alka-
loids such as freebase and crack) that differ in potency because of varying levels of purity
and speed of onset. However, in all forms of the substance, cocaine is the active ingredient.
Cocaine hydrochloride powder is usually “snorted” through the nostrils or dissolved in
water and injected intravenously.
Individuals exposed to amphetamine-type stimulants or cocaine can develop stimu-
lant use disorder as rapidly as 1 week, although the onset is not always this rapid. Re-
gardless of the route of administration, tolerance occurs with repeated use. Withdrawal
symptoms, particularly hypersomnia, increased appetite, and dysphoria, can occur and
can enhance craving. Most individuals with stimulant use disorder have experienced tol-
erance or withdrawal.
Use patterns and course are similar for disorders involving amphetamine-type stimu-
lants and cocaine, as both substances are potent central nervous system stimulants with
similar psychoactive and sympathomimetic effects. Amphetamine-type stimulants are
longer acting than cocaine and thus are used fewer times per day. Usage may be chronic or
episodic, with binges punctuated by brief non-use periods. Aggressive or violent behavior
is common when high doses are smoked, ingested, or administered intravenously. Intense
temporary anxiety resembling panic disorder or generalized anxiety disorder, as well as
paranoid ideation and psychotic episodes that resemble schizophrenia, is seen with high-
dose use.
Withdrawal states are associated with temporary but intense depressive symptoms that
can resemble a major depressive episode; the depressive symptoms usually resolve within
1 week. Tolerance to amphetamine-type stimulants develops and leads to escalation of the
dose. Conversely, some users of amphetamine-type stimulants develop sensitization,
characterized by enhanced effects.
Associated Features Supporting Diagnosis
When injected or smoked, stimulants typically produce an instant feeling of well-being,
confidence, and euphoria. Dramatic behavioral changes can rapidly develop with stimu-
lant use disorder. Chaotic behavior, social isolation, aggressive behavior, and sexual dys-
function can result from long-term stimulant use disorder.
564 Substance-Related and Addictive Disorders
Individuals with acute intoxication may present with rambling speech, headache, tran-
sient ideas of reference, and tinnitus. There may be paranoid ideation, auditory halluci-
nations in a clear sensorium, and tactile hallucinations, which the individual usually
recognizes as drug effects. Threats or acting out of aggressive behavior may occur. Depres-
sion, suicidal ideation, irritability, anhedonia, emotional lability, or disturbances in atten-
tion and concentration commonly occur during withdrawal. Mental disturbances associated
with cocaine use usually resolve hours to days after cessation of use but can persist for
1 month. Physiological changes during stimulant withdrawal are opposite to those of the
intoxication phase, sometimes including bradycardia. Temporary depressive symptoms
may meet symptomatic and duration criteria for major depressive episode. Histories con-
sistent with repeated panic attacks, social anxiety disorder (social phobia)-like behavior,
and generalized anxiety-like syndromes are common, as are eating disorders. One ex-
treme instance of stimulant toxicity is stimulant-induced psychotic disorder, a disorder
that resembles schizophrenia, with delusions and hallucinations.
Individuals with stimulant use disorder often develop conditioned responses to drug-
related stimuli (e.g., craving on seeing any white powderlike substance). These responses
contribute to relapse, are difficult to extinguish, and persist after detoxification.
Depressive symptoms with suicidal ideation or behavior can occur and are generally
the most serious problems seen during stimulant withdrawal.
Prevalence
Stimulant use disorder: amphetamine-type stimulants. Estimated 12-month prevalence
of amphetamine-type stimulant use disorder in the United States is 0.2% among 12- to 17-
year-olds and 0.2% among individuals 18 years and older. Rates are similar among adult
males and females (0.2%), but among 12- to 17-year-olds, the rate for females (0.3%) is
greater than that for males (0.1%). Intravenous stimulant use has a male-to-female ratio of
3:1 or 4:1, but rates are more balanced among non-injecting users, with males representing
54% of primary treatment admissions. Twelve-month prevalence is greater among 18- to
29-year-olds (0.4%) compared with 45- to 64-year-olds (0.1%). For 12- to 17-year-olds, rates
are highest among whites and African Americans (0.3%) compared with Hispanics (0.1%)
and Asian Americans and Pacific Islanders (0.01%), with amphetamine-type stimulant use
disorder virtually absent among Native Americans. Among adults, rates are highest among
Native Americans and Alaska Natives (0.6%) compared with whites (0.2%) and Hispanics
(0.2%), with amphetamine-type stimulant use disorder virtually absent among African
Americans and Asian Americans and Pacific Islanders. Past-year nonprescribed use of
prescription stimulants occurred among 5%-9% of children through high school, with
5%-35% of college-age persons reporting past-year use.
Stimulant use disorder: cocaine. Estimated 12-month prevalence of cocaine use disorder
in the United States is 0.2% among 12- to 17-year-olds and 0.3% among individuals 18 years
and older. Rates are higher among males (0.4%) than among females (0.1%). Rates are
highest among 18- to 29-year-olds (0.6%) and lowest among 45- to 64-year-olds (0.1%). Among
adults, rates are greater among Native Americans (0.8%) compared with African Ameri-
cans (0.4%), Hispanics (0.3%), whites (0.2%), and Asian Americans and Pacific Islanders
(0.1%). In contrast, for 12- to 17-year-olds, rates are similar among Hispanics (0.2%), whites
(0.2%), and Asian Americans and Pacific Islanders (0.2%); and lower among African Amer-
icans (0.02%); with cocaine use disorder virtually absent among Native Americans and
Alaska Natives.
Development and Course
Stimulant use disorders occur throughout all levels of society and are more common among
individuals ages 12-25 years compared with individuals 26 years and older. First regular use
Stimulant Use Disorder 565
among individuals in treatment occurs, on average, at approximately age 23 years. For pri-
mary methamphetamine—primary treatment admissions, the average age is 31 years.
Some individuals begin stimulant use to control weight or to improve performance in
school, work, or athletics. This includes obtaining medications such as methylphenidate or
amphetamine salts prescribed to others for the treatment of attention-deficit/hyperac-
tivity disorder. Stimulant use disorder can develop rapidly with intravenous or smoked
administration; among primary admissions for amphetamine-type stimulant use, 66% re-
ported smoking, 18% reported injecting, and 10% reported snorting.
Patterns of stimulant administration include episodic or daily (or almost daily) use.
Episodic use tends to be separated by 2 or more days of non-use (e.g., intense use over a
weekend or on one or more weekdays). “Binges” involve continuous high-dose use over
hours or days and are often associated with physical dependence. Binges usually termi-
nate only when stimulant supplies are depleted or exhaustion ensues. Chronic daily use
may involve high or low doses, often with an increase in dose over time.
Stimulant smoking and intravenous use are associated with rapid progression to se-
vere-level stimulant use disorder, often occurring over weeks to months. Intranasal use of
cocaine and oral use of amphetamine-type stimulants result in more gradual progression
occurring over months to years. With continuing use, there is a diminution of pleasurable
effects due to tolerance and an increase in dysphoric effects.
Risk and Prognostic Factors
Temperamental. Comorbid bipolar disorder, schizophrenia, antisocial personality disor-
der, and other substance use disorders are risk factors for developing stimulant use disorder
and for relapse to cocaine use in treatment samples. Also, impulsivity and similar personality
traits may affect treatment outcomes. Childhood conduct disorder and adult antisocial per-
sonality disorder are associated with the later development of stimulant-related disorders.
Environmental. Predictors of cocaine use among teenagers include prenatal cocaine ex-
posure, postnatal cocaine use by parents, and exposure to community violence during
childhood. For youths, especially females, risk factors include living in an unstable home
environment, having a psychiatric condition, and associating with dealers and users.
Culture-Related Diagnostic Issues
Stimulant use-attendant disorders affect all racial/ethnic, socioeconomic, age, and gender
groups. Diagnostic issues may be related to societal consequences (e.g., arrest, school sus-
pensions, employment suspension). Despite small variations, cocaine and other stimulant
use disorder diagnostic criteria perform equally across gender and race/ethnicity groups.
Chronic use of cocaine impairs cardiac left ventricular function in African Americans.
Approximately 66% of individuals admitted for primary methamphetamine /amphet-
amine-related disorders are non-Hispanic white, followed by 21% of Hispanic origin, 3%
Asian and Pacific Islander, and 3% non-Hispanic black.
Diagnostic Markers
Benzoylecgonine, a metabolite of cocaine, typically remains in the urine for 1-3 days after
a single dose and may be present for 7-12 days in individuals using repeated high doses.
Mildly elevated liver function tests can be present in cocaine injectors or users with con-
comitant alcohol use. There are no neurobiological markers of diagnostic utility. Discon-
tinuation of chronic cocaine use may be associated with electroencephalographic changes,
suggesting persistent abnormalities; alterations in secretion patterns of prolactin; and
downregulation of dopamine receptors.
Short-half-life amphetamine-type stimulants (MDMA [3,4-methylenedioxy-N-methyl-
amphetamine], methamphetamine) can be detected for 1-3 days, and possibly up to 4 days
566 Substance-Related and Addictive Disorders
depending on dosage and metabolism. Hair samples can be used to detect presence of am-
phetamine-type stimulants for up to 90 days. Other laboratory findings, as well as physical
findings and other medical conditions (e.g., weight loss, malnutrition; poor hygiene), are
similar for both cocaine and amphetamine-type stimulant use disorder.
Functional Consequences of Stimulant Use Disorder
Various medical conditions may occur depending on the route of administration. Intrana-
sal users often develop sinusitis, irritation, bleeding of the nasal mucosa, and a perforated
nasal septum. Individuals who smoke the drugs are at increased risk for respiratory prob-
lems (e.g., coughing, bronchitis, and pneumonitis). Injectors have puncture marks and
“tracks,” most commonly on their forearms. Risk of HIV infection increases with frequent
intravenous injections and unsafe sexual activity. Other sexually transmitted diseases,
hepatitis, and tuberculosis and other lung infections are also seen. Weight loss and mal-
nutrition are common.
Chest pain may be a common symptom during stimulant intoxication. Myocardial in-
farction, palpitations and arrhythmias, sudden death from respiratory or cardiac arrest,
and stroke have been associated with stimulant use among young and otherwise healthy
individuals. Seizures can occur with stimulant use. Pneumothorax can result from per-
forming Valsalva-like maneuvers done to better absorb inhaled smoke. Traumatic injuries
due to violent behavior are common among individuals trafficking drugs. Cocaine use is
associated with irregularities in placental blood flow, abruptio placentae, premature labor
and delivery, and an increased prevalence of infants with very low birth weights.
Individuals with stimulant use disorder may become involved in theft, prostitution, or
drug dealing in order to acquire drugs or money for drugs.
Neurocognitive impairment is common among methamphetamine users. Oral health
problems include “meth mouth” with gum disease, tooth decay, and mouth sores related
to the toxic effects of smoking the drug and to bruxism while intoxicated. Adverse pulmo-
nary effects appear to be less common for amphetamine-type stimulants because they are
smoked fewer times per day. Emergency department visits are common for stimulant-re-
lated mental disorder symptoms, injury, skin infections, and dental pathology.
Differential Diagnosis
Primary mental disorders. Stimulant-induced disorders may resemble primary mental
disorders (e.g., major depressive disorder) (for discussion of this differential diagnosis, see
“Stimulant Withdrawal”). The mental disturbances resulting from the effects of stimulants
should be distinguished from the symptoms of schizophrenia; depressive and bipolar dis-
orders; generalized anxiety disorder; and panic disorder.
Phencyclidine intoxication. Intoxication with phencyclidine (“PCP” or “angel dust”) or
synthetic “designer drugs” such as mephedrone (known by different names, including
“bath salts”) may cause a similar clinical picture and can only be distinguished from stim-
ulant intoxication by the presence of cocaine or amphetamine-type substance metabolites
in a urine or plasma sample.
Stimulant intoxication and withdrawal. Stimulant intoxication and withdrawal are dis-
tinguished from the other stimulant-induced disorders (e.g., anxiety disorder, with onset
during intoxication) because the symptoms in the latter disorders predominate the clinical
presentation and are severe enough to warrant independent clinical attention.
Comorbidity
Stimulant-related disorders often co-occur with other substance use disorders, especially
those involving substances with sedative properties, which are often taken to reduce in-
Stimulant Intoxication 567
somnia, nervousness, and other unpleasant side effects. Cocaine users often use alcohol,
while amphetamine-type stimulant users often use cannabis. Stimulant use disorder may
be associated with posttraumatic stress disorder, antisocial personality disorder, atten-
tion-deficit /hyperactivity disorder, and gambling disorder. Cardiopulmonary problems
are often present in individuals seeking treatment for cocaine-related problems, with chest
pain being the most common. Medical problems occur in response to adulterants used as
“cutting” agents. Cocaine users who ingest cocaine cut with levamisole, an antimicrobial
and veterinary medication, may experience agranulocytosis and febrile neutropenia.
Stimulant Intoxication
Diagnostic Criteria
A. Recent use of an amphetamine-type substance, cocaine, or other stimulant.
B. Clinically significant problematic behavioral or psychological changes (e.g., euphoria
or affective blunting; changes in sociability; hypervigilance; interpersonal sensitivity;
anxiety, tension, or anger; stereotyped behaviors; impaired judgment) that developed
during, or shortly after, use of a stimulant.
C. Two (or more) of the following signs or symptoms, developing during, or shortly after,
stimulant use:
Tachycardia or bradycardia.
Pupillary dilation.
Elevated or lowered blood pressure.
Perspiration or chills.
Nausea or vomiting.
Evidence of weight loss.
Psychomotor agitation or retardation.
Muscular weakness, respiratory depression, chest pain, or cardiac arrhythmias.
Confusion, seizures, dyskinesias, dystonias, or coma.
ONAAP WN =
co
D. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including intoxication with another sub-
stance.
Specify the specific intoxicant (i.e., amphetamine-type substance, cocaine, or other
stimulant).
Specify if:
With perceptual disturbances: This specifier may be noted when hallucinations with
intact reality testing or auditory, visual, or tactile illusions occur in the absence of a de-
lirium.
Coding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether
the stimulant is an amphetamine, cocaine, or other stimulant; whether there is a comorbid
amphetamine, cocaine, or other stimulant use disorder; and whether or not there are per-
ceptual disturbances.
For amphetamine, cocaine, or other stimulant intoxication, without perceptual dis-
turbances: If a mild amphetamine or other stimulant use disorder is comorbid, the ICD-
10-CM code is F15.129, and if a moderate or severe amphetamine or other stimulant use
disorder is comorbid, the ICD-10-CM code is F15.229. If there is no comorbid amphet-
amine or other stimulant use disorder, then the ICD-10-CM code is F15.929. Similarly, if
a mild cocaine use disorder is comorbid, the |CD-10-CM code is F14.129, and if a mod-
erate or severe cocaine use disorder is comorbid, the ICD-10-CM code is F14.229. If
there is no comorbid cocaine use disorder, then the ICD-10-CM code is F14.929.
568 Substance-Related and Addictive Disorders
For amphetamine, cocaine, or other stimulant intoxication, with perceptual distur-
bances: If a mild amphetamine or other stimulant use disorder is comorbid, the ICD-10-
CM code is F15.122, and if a moderate or severe amphetamine or other stimulant use
disorder is comorbid, the ICD-10-CM code is F15.222. If there is no comorbid amphet-
amine or other stimulant use disorder, then the ICD-10-CM code is F15.922. Similarly, if
a mild cocaine use disorder is comorbid, the ICD-10-CM code is F14.122, and if a mod-
erate or severe cocaine use disorder is comorbid, the }CD-10-CM code is F14.222. If
there is no comorbid cocaine use disorder, then the ICD-10-CM code is F14.922.
Diagnostic Features
The essential feature of stimulant intoxication, related to amphetamine-type stimulants
and cocaine, is the presence of clinically significant behavioral or psychological changes
that develop during, or shortly after, use of stimulants (Criteria A and B). Auditory hallu-
cinations may be prominent, as may paranoid ideation, and these symptoms must be dis-
tinguished from an independent psychotic disorder such as schizophrenia. Stimulant
intoxication usually begins with a “high” feeling and includes one or more of the follow-
ing: euphoria with enhanced vigor, gregariousness, hyperactivity, restlessness, hypervig-
ilance, interpersonal sensitivity, talkativeness, anxiety, tension, alertness, grandiosity,
stereotyped and repetitive behavior, anger, impaired judgment, and, in the case of chronic
intoxication, affective blunting with fatigue or sadness and social withdrawal. These be-
havioral and psychological changes are accompanied by two or more of the following
signs and symptoms that develop during or shortly after stimulant use: tachycardia or bra-
dycardia; pupillary dilation; elevated or lowered blood pressure; perspiration or chills;
nausea or vomiting; evidence of weight loss; psychomotor agitation or retardation; mus-
cular weakness, respiratory depression, chest pain, or cardiac arrhythmias; and confu-
sion, seizures, dyskinesias, dystonias, or coma (Criterion C). Intoxication, either acute or
chronic, is often associated with impaired social or occupational functioning. Severe in-
toxication can lead to convulsions, cardiac arrhythmias, hyperpyrexia, and death. For the
diagnosis of stimulant intoxication to be made, the symptoms must not be attributable
to another medical condition and not better explained by another mental disorder (Crite-
rion D). While stimulant intoxication occurs in individuals with stimulant use disorders, in-
toxication is not a criterion for stimulant use disorder, which is confirmed by the presence
of two of the 11 diagnostic criteria for use disorder.
Associated Features Supporting Diagnosis
The magnitude and direction of the behavioral and physiological changes depend on many
variables, including the dose used and the characteristics of the individual using the sub-
stance or the context (e.g., tolerance, rate of absorption, chronicity of use, context in which
it is taken). Stimulant effects such as euphoria, increased pulse and blood pressure, and
psychomotor activity are most commonly seen. Depressant effects such as sadness, brady-
cardia, decreased blood pressure, and decreased psychomotor activity are less common
and generally emerge only with chronic high-dose use.
Differentiai Diagnosis
Stimulant-induced disorders. Stimulant intoxication is distinguished from the other
stimulant-induced disorders (e.g., stimulant-induced depressive disorder, bipolar disor-
der, psychotic disorder, anxiety disorder) because the severity of the intoxication symp-
toms exceeds that associated with the stimulant-induced disorders, and the symptoms
warrant independent clinical attention. Stimulant intoxication delirium would be distin-
guished by a disturbance in level of awareness and change in cognition.
Stimulant Withdrawal 569
Other mental disorders. Salient mental disturbances associated with stimulant intoxi-
cation should be distinguished from the symptoms of schizophrenia, paranoid type; bi-
polar and depressive disorders; generalized anxiety disorder; and panic disorder as
described in DSM-5.
Stimulant Withdrawal
Diagnostic Criteria
A. Cessation of (or reduction in) prolonged amphetamine-type substance, cocaine, or
other stimulant use.
B. Dysphoric mood and two (or more) of the following physiological changes, developing
within a few hours to several days after Criterion A:
Fatigue.
Vivid, unpleasant dreams.
Insomnia or hypersomnia.
Increased appetite.
Psychomotor retardation or agitation.
gPon >
C. The signs or symptoms in Criterion B cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including intoxication or withdrawai from
another substance.
Specify the specific substance that causes the withdrawal syndrome (i.e., amphet-
amine-type substance, cocaine, or other stimulant).
Coding note: The ICD-9-CM code is 292.0. The ICD-10-CM code depends on whether
the stimulant is an amphetamine, cocaine, or other stimulant. The ICD-10-CM code for
amphetamine or an other stimulant withdrawal is F15.23, and the ICD-10-CM for cocaine
withdrawal is F14.23. Note that the ICD-10-CM code indicates the comorbid presence of
a moderate or severe amphetamine, cocaine, or other stimulant use disorder, reflecting
the fact that amphetamine, cocaine, or other stimulant withdrawal can only occur in the
presence of a moderate or severe amphetamine, cocaine, or other stimulant use disorder.
It is not permissible to code a comorbid mild amphetamine, cocaine, or other stimulant use
disorder with amphetamine, cocaine, or other stimulant withdrawal.
Diagnostic Features
The essential feature of stimulant withdrawal is the presence of a characteristic with-
drawal syndrome that develops within a few hours to several days after the cessation of
(or marked reduction in) stimulant use (generally high dose) that has been prolonged (Cri-
terion A). The withdrawal syndrome is characterized by the development of dysphoric
mood accompanied by two or more of the following physiological changes: fatigue, vivid
and unpleasant dreams, insomnia or hypersomnia, increased appetite, and psychomotor
retardation or agitation (Criterion B). Bradycardia is often present and is a reliable mea-
sure of stimulant withdrawal.
Anhedonia and drug craving can often be present but are not part of the diagnostic cri-
teria. These symptoms cause clinically significant distress or impairment in social, occu-
pational, or other important areas of functioning (Criterion C). The symptoms must not be
attributable to another medical condition and are not better explained by another mental
disorder (Criterion D).
570 Substance-Related and Addictive Disorders
Associated Features Supporting Diagnosis
Acute withdrawal symptoms (“a crash”) are often seen after periods of repetitive high-dose
use (“runs” or “binges”). These periods are characterized by intense and unpleasant feelings of
lassitude and depression and increased appetite, generally requiring several days of rest and
recuperation. Depressive symptoms with suicidal ideation or behavior can occur and are gen-
erally the most serious problems seen during “crashing” or other forms of stimulant with-
drawal. The majority of individuals with stimulant use disorder experience a withdrawal
syndrome at some point, and virtually all individuals with the disorder report tolerance.
Differential Diagnosis
Stimulant use disorder and other stimulant-induced disorders. Stimulant withdrawal
is distinguished from stimulant use disorder and from the other stimulant-induced disor-
ders (e.g., stimulant-induced intoxication delirium, depressive disorder, bipolar disorder,
psychotic disorder, anxiety disorder, sexual dysfunction, sleep disorder) because the
symptoms of withdrawal predominate the clinical presentation and are severe enough to
warrant independent clinical attention.
Other Stimulant-Induced Disorders
The following stimulant-induced disorders (which include amphetamine-, cocaine-, and
other stimulant—induced disorders) are described in other chapters of the manual with dis-
orders with which they share phenomenology (see the substance /medication-induced
mental disorders in these chapters): stimulant-induced psychotic disorder (“Schizophrenia
Spectrum and Other Psychotic Disorders”); stimulant-induced bipolar disorder (“Bipolar
and Related Disorders”); stimulant-induced depressive disorder (“Depressive Disorders”);
stimulant-induced anxiety disorder (“Anxiety Disorders”); stimulant-induced obsessive-
compulsive disorder (“Obsessive-Compulsive and Related Disorders”); stimulant-induced
sleep disorder (“Sleep-Wake Disorders”); and stimulant-induced sexual dysfunction ("Sex-
ual Dysfunctions”). For stimulant intoxication delirium, see the criteria and discussion of
delirium in the chapter “Neurocognitive Disorders.” These stimulant-induced disorders
are diagnosed instead of stimulant intoxication or stimulant withdrawal only when the
symptoms are sufficiently severe to warrant independent clinical attention.
Unspecified Stimulant-Related Disorder
This category applies to presentations in which symptoms characteristic of a stimulant-
related disorder that cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning predominate but do not meet the full criteria
for any specific stimulant-related disorder or any of the disorders in the substance-related
and addictive disorders diagnostic class.
Coding note: The ICD-9-CM code is 292.9. The ICD-10-CM code depends on whether
the stimulant is an amphetamine, cocaine, or another stimulant. The ICD-10-CM code for
an unspecified amphetamine- or other stimulant-related disorder is F15.99. The ICD-10-
CM code for an unspecified cocaine-related disorder is F14.99.
Tobacco Use Disorder 571
Tobacco-Related Disorders
Tobacco Use Disorder
Tobacco Withdrawal
Other Tobacco-!nduced Disorders
Unspecified Tobacco-Related Disorder
Tobacco Use Disorder
Diagnostic Criteria
A. A problematic pattern of tobacco use leading to clinically significant impairment or dis-
tress, as manifested by at least two of the following, occurring within a 12-month period:
1. Tobacco is often taken in larger amounts or over a longer period than was intended.
There is a persistent desire or unsuccessful efforts to cut down or control tobacco use.
A great deal of time is spent in activities necessary to obtain or use tobacco.
Craving, or a strong desire or urge to use tobacco.
Recurrent tobacco use resulting in a failure to fulfill major role obligations at work,
school, or home (e.g., interference with work).
6. Continued tobacco use despite having persistent or recurrent social or interper-
sonal problems caused or exacerbated by the effects of tobacco (e.g., arguments
with others about tobacco use).
7. Important social, occupational, or recreational activities are given up or reduced be-
cause of tobacco use.
8. Recurrent tobacco use in situations in which it is physically hazardous (e.g., smok-
ing in bed).
9. Tobacco use is continued despite knowledge of having a persistent or recurrent
physical or psychological problem that is likely to have been caused or exacerbated
by tobacco.
10. Tolerance, as defined by either of the following:
aPoh
a. Aneed for markedly increased amounts of tobacco to achieve the desired effect.
b. A markedly diminished effect with continued use of the same amount of tobacco.
11. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for tobacco (refer to Criteria A and B of
the criteria set for tobacco withdrawal).
b. Tobacco (or a closely related substance, such as nicotine) is taken to relieve or
avoid withdrawal symptoms.
Specify if:
in early remission: After full criteria for tobacco use disorder were previously met,
none of the criteria for tobacco use disorder have been met for at least 3 months but
for less than 12 months (with the exception that Criterion A4, “Craving, or a strong de-
sire or urge to use tobacco,” may be met).
In sustained remission: After full criteria for tobacco use disorder were previously
met, none of the criteria for tobacco use disorder have been met at any time during a
period of 12 months or longer (with the exception that Criterion A4, “Craving, or a
strong desire or urge to use tobacco,” may be met).
572 Substance-Related and Addictive Disorders
Specify if:
On maintenance therapy: The individual is taking a long-term maintenance medica-
tion, such as nicotine replacement medication, and no criteria for tobacco use disorder
have been met for that class of medication (except tolerance to, or withdrawal from,
the nicotine replacement medication).
In a controlled environment: This additional specifier is used if the individual is in an
environment where access to tobacco is restricted.
Coding based on current severity: Note for |CD-10-CM codes: If a tobacco withdrawal or
tobacco-induced sleep disorder is also present, do not use the codes below for tobacco use
disorder. Instead, the comorbid tobacco use disorder is indicated in the 4th character of the
tobacco-induced disorder code (see the coding note for tobacco withdrawal or tobacco-
induced sleep disorder). For example, if there is comorbid tobacco-induced sleep disorder and
tobacco use disorder, only the tobacco-induced sleep disorder code is given, with the 4th char-
acter indicating whether the comorbid tobacco use disorder is moderate or severe: F17.208
for moderate or severe tobacco use disorder with tobacco-induced sleep disorder. It is not per-
missible to code a comorbid mild tobacco use disorder with a tobacco-induced sleep disorder.
Specify current severity:
305.1 (Z72.0) Mild: Presence of 2~3 symptoms.
305.1 (F 17.200) Moderate: Presence of 4—5 symptoms.
305.1 (F 17.200) Severe: Presence of 6 or more symptoms.
Specifiers
“On maintenance therapy” applies as a further specifier to individuals being maintained on
other tobacco cessation medication (e.g., bupropion, varenicline) and as a further specifier of
remission if the individual is both in remission and on maintenance therapy. “In a controlled
environment” applies as a further specifier of remission if the individual is both in remission
and in a controlled environment (i.e., in early remission in a controlled environment or in sus-
tained remission in a controlled environment). Examples of these environments are closely su-
pervised and substance-free jails, therapeutic communities, and locked hospital units.
Diagnostic Features
Tobacco use disorder is common among individuals who use cigarettes and smokeless to-
bacco daily and is uncommon among individuals who do not use tobacco daily or who use
nicotine medications. Tolerance to tobacco is exemplified by the disappearance of nausea
and dizziness after repeated intake and with a more intense effect of tobacco the first time
it is used during the day. Cessation of tobacco use can produce a well-defined withdrawal
syndrome. Many individuals with tobacco use disorder use tobacco to relieve or to avoid
withdrawal symptoms (e.g., after being in a situation where use is restricted). Many indi-
viduals who use tobacco have tobacco-related physical symptoms or diseases and con-
tinue to smoke. The large majority report craving when they do not smoke for several hours.
Spending excessive time using tobacco can be exemplified by chain-smoking (i.e., smok-
ing one cigarette after another with no time between cigarettes). Because tobacco sources
are readily and legally available, and because nicotine intoxication is very rare, spending a
great deal of time attempting to procure tobacco or recovering from its effects is uncom-
mon. Giving up important social, occupational, or recreational activities can occur when
an individual forgoes an activity because it occurs in tobacco use-restricted areas. Use of
tobacco rarely results in failure to fulfill major role obligations (e.g., interference with
work, interference with home obligations), but persistent social or interpersonal problems
(e.g., having arguments with others about tobacco use, avoiding social situations because
of others’ disapproval of tobacco use) or use that is physically hazardous (e.g., smoking in
Tobacco Use Disorder 573
bed, smoking around flammable chemicals) occur at an intermediate prevalence. Although
these criteria are less often endorsed by tobacco users, if endorsed, they can indicate a
more severe disorder.
Associated Features Supporting Diagnosis
Smoking within 30 minutes of waking, smoking daily, smoking more cigarettes per day,
and waking at night to smoke are associated with tobacco use disorder. Environmental
cues can evoke craving and withdrawal. Serious medical conditions, such as lung and
other cancers, cardiac and pulmonary disease, perinatal problems, cough, shortness of
breath, and accelerated skin aging, often occur.
Prevalence
Cigarettes are the most commonly used tobacco product, representing over 90% of to-
bacco/nicotine use. In the United States, 57% of adults have never been smokers, 22% are
former smokers, and 21% are current smokers. Approximately 20% of current U.S. smok-
ers are nondaily smokers. The prevalence of smokeless tobacco use is less than 5%, and the
prevalence of tobacco use in pipes and cigars is less than 1%.
DSM-IV nicotine dependence criteria can be used to estimate the prevalence of tobacco
use disorder, but since they are a subset of tobacco use disorder criteria, the prevalence of
tobacco use disorder will be somewhat greater. The 12-month prevalence of DSM-IV nic-
otine dependence in the United States is 13% among adults age 18 years and older. Rates
are similar among adult males (14%) and females (12%) and decline in age from 17%
among 18- to 29-year-olds to 4% among individuals age 65 years and older. The prevalence
of current nicotine dependence is greater among Native American and Alaska Natives
(23%) than among whites (14%) but is less among African Americans (10%), Asian Amer-
icans and Pacific Islanders (6%), and Hispanics (6%). The prevalence among current daily
smokers is approximately 50%.
In many developing nations, the prevalence of smoking is much greater in males than
in females, but this is not the case in developed nations. However, there often is a lag in the
demographic transition such that smoking increases in females at a later time.
Development and Course
The majority of U.S. adolescents experiment with tobacco use, and by age 18 years, about
20% smoke at least monthly. Most of these individuals become daily tobacco users. Initi-
ation of smoking after age 21 years is rare. In general, some of the tobacco use disorder cri-
teria symptoms occur soon after beginning tobacco use, and many individuals’ pattern of
use meets current tobacco use disorder criteria by late adolescence. More than 80% of in-
dividuals who use tobacco attempt to quit at some time, but 60% relapse within 1 week
and less than 5% remain abstinent for life. However, most individuals who use tobacco
make multiple attempts such that one-half of tobacco users eventually abstain. Individuals
who use tobacco who do quit usually do not do so until after age 30 years. Although non-
daily smoking in the United States was previously rare, it has become more prevalent in
the last decade, especially among younger individuals who use tobacco.
Risk and Prognostic Factors
Temperamental. Individuals with externalizing personality traits are more likely to
initiate tobacco use. Children with attention-deficit/hyperactivity disorder or conduct
disorder, and adults with depressive, bipolar, anxiety, personality, psychotic, or other
substance use disorders, are at higher risk of starting and continuing tobacco use and of to-
bacco use disorder.
574 Substance-Related and Addictive Disorders
Environmental. Individuals with low incomes and low educational levels are more likely
to initiate tobacco use and are less likely to stop.
Genetic and physiological. Genetic factors contribute to the onset of tobacco use, the
continuation of tobacco use, and the development of tobacco use disorder, with a degree of
heritability equivalent to that observed with other substance use disorders (i.e., about
50%). Some of this risk is specific to tobacco, and some is common with the vulnerability to
developing any substance use disorder.
Culture-Related Diagnostic Issues
Cultures and subcultures vary widely in their acceptance of the use of tobacco. The prev-
alence of tobacco use declined in the United States from the 1960s through the 1990s, but
this decrease has been less evident in African American and Hispanic populations. Also,
smoking in developing countries is more prevalent than in developed nations. The degree
to which these cultural differences are due to income, education, and tobacco control ac-
tivities in a country is unclear. Non-Hispanic white smokers appear to be more likely to
develop tobacco use disorder than are smokers. Some ethnic differences may be biologi-
cally based. African American males tend to have higher nicotine blood levels for a given
number of cigarettes, and this might contribute to greater difficulty in quitting. Also, the
speed of nicotine metabolism is significantly different for whites compared with African
Americans and can vary by genotypes associated with ethnicities.
Diagnostic Markers
Carbon monoxide in the breath, and nicotine and its metabolite cotinine in blood, saliva, or
urine, can be used to measure the extent of current tobacco or nicotine use; however, these
are only weakly related to tobacco use disorder.
Functional Consequences of Tobacco Use Disorder
Medical consequences of tobacco use often begin when tobacco users are in their 40s and
usually become progressively more debilitating over time. One-half of smokers who do
not stop using tobacco will die early from a tobacco-related illness, and smoking-related
morbidity occurs in more than one-half of tobacco users. Most medical conditions result
from exposure to carbon monoxide, tars, and other non-nicotine components of tobacco.
The major predictor of reversibility is duration of smoking. Secondhand smoke increases
the risk of heart disease and cancer by 30%. Long-term use of nicotine medications does
not appear to cause medical harm.
Comorbidity
The most common medical diseases from smoking are cardiovascular illnesses, chronic
obstructive pulmonary disease, and cancers. Smoking also increases perinatal problems,
such as low birth weight and miscarriage. The most common psychiatric comorbidities are
alcohol/substance, depressive, bipolar, anxiety, personality, and attention-deficit/hyper-
activity disorders. In individuals with current tobacco use disorder, the prevalence of cur-
rent alcohol, drug, anxiety, depressive, bipolar, and personality disorders ranges from
22% to 32%. Nicotine-dependent smokers are 2.7-8.1 times more likely to have these dis-
orders than nondependent smokers, never-smokers, or ex-smokers.
Tobacco Withdrawal 575
Tobacco Withdrawal
Diagnostic Criteria 292.0 (F 17.203)
A. Daily use of tobacco for at least several weeks.
B. Abrupt cessation of tobacco use, or reduction in the amount of tobacco used, followed
within 24 hours by four (or more) of the following signs or symptoms:
. Irritability, frustration, or anger.
. Anxiety.
. Difficulty concentrating.
. Increased appetite.
. Restlessness.
. Depressed mood.
. Insomnia.
NOmnh WD —
C. The signs or symptoms in Criterion B cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributed to another medical condition and are not bet-
ter explained by another mental disorder, including intoxication or withdrawal from an-
other substance.
Coding note: The ICD-9-CM code is 292.0. The ICD-10-CM code for tobacco withdrawal
is F17.203. Note that the ICD-10-CM code indicates the comorbid presence of a moderate
or severe tobacco use disorder, reflecting the fact that tobacco withdrawal can only occur
in the presence of a moderate or severe tobacco use disorder. It is not permissible to code
a comorbid mild tobacco use disorder with tobacco withdrawal.
Diagnostic Features
Withdrawal symptoms impair the ability to stop tobacco use. The symptoms after absti-
nence from tobacco are in large part due to nicotine deprivation. Symptoms are much
more intense among individuals who smoke cigarettes or use smokeless tobacco than
among those who use nicotine medications. This difference in symptom intensity is likely
due to the more rapid onset and higher levels of nicotine with cigarette smoking. Tobacco
withdrawal is common among daily tobacco users who stop or reduce but can also occur
among nondaily users. Typically, heart rate decreases by 5-12 beats per minute in the first
few days after stopping smoking, and weight increases an average of 4-7 |b (2-3 kg) over
the first year after stopping smoking. Tobacco withdrawal can produce clinically signifi-
cant mood changes and functional impairment.
Associated Features Supporting Diagnosis
Craving for sweet or sugary foods and impaired performance on tasks requiring vigilance
are associated with tobacco withdrawal. Abstinence can increase constipation, coughing,
dizziness, dreaming /nightmares, nausea, and sore throat. Smoking increases the metab-
olism of many medications used to treat mental disorders; thus, cessation of smoking can
increase the blood levels of these medications, and this can produce clinically significant
outcomes. This effect appears to be due not to nicotine but rather to other compounds in
tobacco.
576 Substance-Related and Addictive Disorders
Prevalence
Approximately 50% of tobacco users who quit for 2 or more days will have symptoms that
meet criteria for tobacco withdrawal. The most commonly endorsed signs and symptoms
are anxiety, irritability, and difficulty concentrating. The least commonly endorsed symp-
toms are depression and insomnia.
Development and Course
Tobacco withdrawal usually begins within 24 hours of stopping or cutting down on to-
bacco use, peaks at 2-3 days after abstinence, and lasts 2-3 weeks. Tobacco withdrawal
symptoms can occur among adolescent tobacco users, even prior to daily tobacco use. Pro-
longed symptoms beyond 1 month are uncommon.
Risk and Prognostic Factors
Temperamental. Smokers with depressive disorders, bipolar disorders, anxiety disor-
ders, attention-deficit/hyperactivity disorder, and other substance use disorders have
more severe withdrawal.
Genetic and physiological. Genotype can influence the probability of withdrawal upon
abstinence.
Diagnostic Markers
Carbon monoxide in the breath, and nicotine and its metabolite cotinine in blood, saliva, or
urine, can be used to measure the extent of tobacco or nicotine use but are only weakly re-
lated to tobacco withdrawal.
Functional Consequences of Tobacco Withdrawal
Abstinence from cigarettes can cause clinically significant distress. Withdrawal impairs
the ability to stop or control tobacco use. Whether tobacco withdrawal can prompt a new
mental disorder or recurrence of a mental disorder is debatable, but if this occurs, it would
be in a small minority of tobacco users.
Differential Diagnosis
The symptoms of tobacco withdrawal overlap with those of other substance withdrawal
syndromes (e.g., alcohol withdrawal; sedative, hypnotic, or anxiolytic withdrawal; stim-
ulant withdrawal; caffeine withdrawal; opioid withdrawal); caffeine intoxication; anxiety,
depressive, bipolar, and sleep disorders; and medication-induced akathisia. Admission to
smoke-free inpatient units or voluntary smoking cessation can induce withdrawal symp-
toms that mimic, intensify, or disguise other disorders or adverse effects of medications
used to treat mental disorders (e.g., irritability thought to be due to alcohol withdrawal
could be due to tobacco withdrawal). Reduction in symptoms with the use of nicotine
medications confirms the diagnosis.
Other Tobacco-Induced Disorders
Tobacco-induced sleep disorder is discussed in the chapter “Sleep-Wake Disorders” (see
“Substance /Medication-Induced Sleep Disorder”).
Unspecified Tobacco-Related Disorder 577
Unspecified Tobacco-Related Disorder
292.9 (F17.209)
This category applies to presentations in which symptoms characteristic of a tobacco-
related disorder that cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning predominate but do not meet the full criteria
for any specific tobacco-related disorder or any of the disorders in the substance-related
and addictive disorders diagnostic class.
Other (or Unknown)
Substance-Related Disorders
Other (or Unknown) Substance Use Disorder
Other (or Unknown) Substance Intoxication
Other (or Unknown) Substance Withdrawal
Other (or Unknown) Substance-induced Disorders
Unspecified Other (or Unknown) Substance—-Related Disorder
Other (or Unknown) Substance Use Disorder
Diagnostic Criteria
A. A problematic pattern of use of an intoxicating substance not able to be classified
within the alcohol; caffeine; cannabis; hallucinogen (phencyclidine and others); inhal-
ant; opioid; sedative, hypnotic, or anxiolytic; stimulant; or tobacco categories and lead-
ing to clinically significant impairment or distress, as manifested by at least two of the
following, occurring within a 12-month period:
1. The substance is often taken in larger amounts or over a longer period than was
intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control use of the
substance.
3. Agreat deal of time is spent in activities necessary to obtain the substance, use the
substance, or recover from its effects.
4. Craving, or a strong desire or urge to use the substance.
5. Recurrent use of the substance resulting in a failure to fulfill major role obligations
at work, school, or home.
6. Continued use of the substance despite having persistent or recurrent social or in-
terpersonal problems caused or exacerbated by the effects of its use.
7. Important social, occupational, or recreational activities are given up or reduced be-
cause of use of the substance.
8. Recurrent use of the substance in situations in which it is physically hazardous.
9. Use of the substance is continued despite knowledge of having a persistent or re-
current physical or psychological problem that is likely to have been caused or ex-
acerbated by the substance.
578 Substance-Related and Addictive Disorders
10. Tolerance, as defined by either of the following:
a. Aneed for markedly increased amounts of the substance to achieve intoxication
or desired effect.
b. Amarkedly diminished effect with continued use of the same amount of the sub-
stance.
11. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for other (or unknown) substance (refer to
Criteria A and B of the criteria sets for other [or unknown] substance withdrawal,
p. 583).
b. The substance (or a closely related substance) is taken to relieve or avoid with-
drawal symptoms.
Specify if:
In early remission: After full criteria for other (or unknown) substance use disorder were
previously met, none of the criteria for other (or unknown) substance use disorder have
been met for at least 3 months but for less than 12 months (with the exception that Cri-
terion A4, “Craving, or a strong desire or urge to use the substance,” may be met).
In sustained remission: After full criteria for other (or unknown) substance use disor-
der were previously met, none of the criteria for other (or unknown) substance use dis-
order have been met at any time during a period of 12 months or longer (with the
exception that Criterion A4, “Craving, or a strong desire or urge to use the substance,”
may be met).
Specify if:
In a controlled environment: This additional specifier is used if the individual is in an
environment where access to the substance is restricted.
Coding based on current severity: Note for ICD-10-CM codes: If an other (or unknown) sub-
stance intoxication, other (or unknown) substance withdrawal, or another other (or unknown)
substance—induced mental disorder is present, do not use the codes below for other (or un-
known) substance use disorder. Instead, the comorbid other {or unknown) substance use dis-
order is indicated in the 4th character of the other (or unknown) substance—induced disorder
code (see the coding note for other (or unknown) substance intoxication, other (or unknown)
substance withdrawal, or specific other (or unknown) substanceinduced mental disorder).
For example, if there is comorbid other (or unknown) substance—-induced depressive disorder
and other (or unknown) substance use disorder, only the other (or unknown) substance—
induced depressive disorder code is given, with the 4th character indicating whether the co-
morbid other (or unknown) substance use disorder is mild, moderate, or severe: F19.14 for
other (or unknown) substance use disorder with other (or unknown) substance—induced de-
pressive disorder or F19.24 for a moderate or severe other (or unknown) substance use dis-
order with other (or unknown) substance—induced depressive disorder.
Specify current severity:
305.90 (F19.10) Mild: Presence of 2-3 symptoms.
304.90 (F19.20) Moderate: Presence of 4-5 symptoms.
304.90 (F19.20) Severe: Presence of 6 or more symptoms.
Specifiers
“In a controlled environment” applies as a further specifier of remission if the individual is
both in remission and in a controlled environment (i.e., in early remission in a controlled
environment or in sustained remission in a controlled environment). Examples of these
environments are closely supervised and substance-free jails, therapeutic communities,
and locked hospital units.
Other {or Unknown) Substance Use Disorder 579
Diagnostic Features
The diagnostic class other (or unknown) substance use and related disorders comprises
substance-related disorders unrelated to alcohol; caffeine; cannabis; hallucinogens (phen-
cyclidine and others); inhalants; opioids; sedative, hypnotics, or anxiolytics; stimulants
(including amphetamine and cocaine); or tobacco. Such substances include anabolic ste-
roids; nonsteroidal anti-inflammatory drugs; cortisol; antiparkinsonian medications; an-
tihistamines; nitrous oxide; amyl-, butyl-, or isobutyl-nitrites; betel nut, which is chewed
in many cultures to produce mild euphoria and a floating sensation; kava (from a South
Pacific pepper plant), which produces sedation, incoordination, weight loss, mild hepati-
tis, and lung abnormalities; or cathinones (including khat plant agents and synthetic chem-
ical derivatives) that produce stimulant effects. Unknown substance-related disorders are
associated with unidentified substances, such as intoxications in which the individual can-
not identify the ingested drug, or substance use disorders involving either new, black mar-
ket drugs not yet identified or familiar drugs illegally sold under false names.
Other (or unknown) substance use disorder is a mental disorder in which repeated use
of an other or unknown substance typically continues, despite the individual’s knowing
that the substance is causing serious problems for the individual. Those problems are re-
flected in the diagnostic criteria. When the substance is known, it should be reflected in the
name of the disorder upon coding (e.g., nitrous oxide use disorder).
Associated Features Supporting Diagnosis
A diagnosis of other (or unknown) substance use disorder is supported by the individual’s
statement that the substance involved is not among the nine classes listed in this chapter; by re-
curring episodes of intoxication with negative results in standard drug screens (which may not
detect new or rarely used substances); or by the presence of symptoms characteristic of an un-
identified substance that has newly appeared in the individual’s community.
Because of increased access to nitrous oxide (“laughing gas”), membership in certain
populations is associated with diagnosis of nitrous oxide use disorder. The role of this gas
as an anesthetic agent leads to misuse by some medical and dental professionals. Its use as
a propellant for commercial products (e.g., whipped cream dispensers) contributes to
misuse by food service workers. With recent widespread availability of the substance in
“whippet” cartridges for use in home whipped cream dispensers, nitrous oxide misuse by
adolescents and young adults is significant, especially among those who also inhale vola-
tile hydrocarbons. Some continuously using individuals, inhaling from as many as 240
whippets per day, may present with serious medical complications and mental conditions,
including myeloneuropathy, spinal cord subacute combined degeneration, peripheral
neuropathy, and psychosis. These conditions are also associated with a diagnosis of ni-
trous oxide use disorder.
Use of amyl-, butyl-, and isobutyl nitrite gases has been observed among homosexual
men and some adolescents, especially those with conduct disorder. Membership in these
populations may be associated with a diagnosis of amyl-, butyl-, or isobuty]-nitrite use dis-
order. However, it has not been determined that these substances produce a substance use
disorder. Despite tolerance, these gases may not alter behavior through central effects, and
they may be used only for their peripheral effects.
Substance use disorders generally are associated with elevated risks of suicide, but there
is no evidence of unique risk factors for suicide with other (or unknown) substance use
disorder.
Prevalence
Based on extremely limited data, the prevalence of other (or unknown) substance use disorder
is likely lower than that of use disorders involving the nine substance classes in this chapter.
580 Substance-Related and Addictive Disorders
Development and Course
No single pattern of development or course characterizes the pharmacologically varied
other (or unknown) substance use disorders. Often unknown substance use disorders will
be reclassified when the unknown substance eventually is identified.
Risk and Prognostic Factors
Risk and prognostic factors for other (or unknown) substance use disorders are thought to
be similar to those for most substance use disorders and include the presence of any other
substance use disorders, conduct disorder, or antisocial personality disorder in the indi-
vidual or the individual's family; early onset of substance problems; easy availability of
the substance in the individual’s environment; childhood maltreatment or trauma; and ev-
idence of limited early self-control and behavioral disinhibition.
Cuiture-Reiated Diagnostic Issues
Certain cultures may be associated with other (or unknown) substance use disorders in-
volving specific indigenous substances within the cultural region, such as betel nut.
Diagnostic Markers
Urine, breath, or saliva tests may correctly identify a commonly used substance falsely
sold as a novel product. However, routine clinical tests usually cannot identify truly un-
usual or new substances, which may require testing in specialized laboratories.
Differential Diagnosis
Use of other or unknown substances without meeting criteria for other (or unknown)
substance use disorder. Use of unknown substances is not rare among adolescents, but
most use does not meet the diagnostic standard of two or more criteria for other (or un-
known) substance use disorder in the past year.
Substance use disorders. Other (or unknown) substance use disorder may co-occur
with various substance use disorders, and the symptoms of the disorders may be similar
and overlapping. To disentangle symptom patterns, it is helpful to inquire about which
symptoms persisted during periods when some of the substances were not being used.
Other (or unknown) substance/medication-induced disorder. This diagnosis should
be differentiated from instances when the individual’s symptoms meet full criteria for one
of the following disorders, and that disorder is caused by an other or unknown substance:
delirium, major or mild neurocognitive disorder, psychotic disorder, depressive disorder,
anxiety disorder, sexual dysfunction, or sleep disorder.
Other medical conditions. Individuals with substance use disorders, including other
(or unknown) substance use disorder, may present with symptoms of many medical dis-
orders. These disorders also may occur in the absence of other (or unknown) substance use
disorder. A history of little or no use of other or unknown substances helps to exclude
other (or unknown) substance use disorder as the source of these problems.
Comorbidity
Substance use disorders, including other (or unknown) substance use disorder, are com-
monly comorbid with one another, with adolescent conduct disorder and adult antisocial
personality disorder, and with suicidal ideation and suicide attempts.
Other (or Unknown) Substance Intoxication 581
Other (or Unknown) Substance Intoxication
Diagnostic Criteria
A. The development of a reversible substance-specific syndrome attributable to recent in-
gestion of (or exposure to) a substance that is not listed elsewhere or is unknown.
B. Clinically significant problematic behavioral or psychological changes that are attribut-
able to the effect of the substance on the central nervous system (e.g., impaired motor
coordination, psychomotor agitation or retardation, euphoria, anxiety, belligerence,
mood lability, cognitive impairment, impaired judgment, social withdrawal) and develop
during, or shortly after, use of the substance.
C. The signs or symptoms are not attributable to another medical condition and are not bet-
ter explained by another mental disorder, including intoxication with another substance.
Coding note: The ICD-9-CM code is 292.89. The !CD-10-CM code depends on whether
there is a comorbid other (or unknown) substance use disorder involving the same sub-
stance. !f a mild other (or unknown) substance use disorder is comorbid, the }CD-10-CM
code is F19.129, and if a moderate or severe other (or unknown) substance use disorder is
comorbid, the ICD-10-CM code is F19.229. If there is no comorbid other (or unknown) sub-
stance use disorder involving the same substance, then the ICD-10-CM code is F19.929.
Note: For information on Risk and Prognostic Factors, Culture-Related Diagnostic Issues,
and Diagnostic Markers, see the corresponding sections in other (or unknown) substance
use disorder.
Diagnostic Features
Other (or unknown) substance intoxication is a clinically significant mental disorder that
develops during, or immediately after, use of either a) a substance not elsewhere ad-
dressed in this chapter (i.e., alcohol; caffeine; cannabis; phencyclidine and other halluci-
nogens; inhalants; opioids; sedatives, hypnotics, or anxiolytics; stimulants; or tobacco) or
b) an unknown substance. If the substance is known, it should be reflected in the name of
the disorder upon coding.
Application of the diagnostic criteria for other (or unknown) substance intoxication is
very challenging. Criterion A requires development of a reversible “substance-specific
syndrome,” but if the substance is unknown, that syndrome usually will be unknown. To
resolve this conflict, clinicians may ask the individual or obtain collateral history as to
whether the individual has experienced a similar episode after using substances with the
same “street” name or from the same source. Similarly, hospital emergency departments
sometimes recognize over a few days numerous presentations of a severe, unfamiliar in-
toxication syndrome from a newly available, previously unknown substance. Because of
the great variety of intoxicating substances, Criterion B can provide only broad examples
of signs and symptoms from some intoxications, with no threshold for the number of
symptoms required for a diagnosis; clinical judgment guides those decisions. Criterion C
requires ruling out other medical conditions, mental disorders, or intoxications,
Prevalence
The prevalence of other (or unknown) substance intoxication is unknown.
Development and Course
Intoxications usually appear and then peak minutes to hours after use of the substance, but
the onset and course vary with the substance and the route of administration. Generally,
582 Substance-Related and Addictive Disorders
substances used by pulmonary inhalation and intravenous injection have the most rapid
onset of action, while those ingested by mouth and requiring metabolism to an active
product are much slower. (For example, after ingestion of certain mushrooms, the first
signs of an eventually fatal intoxication may not appear for a few days.) Intoxication ef-
fects usually resolve within hours to a very few days. However, the body may completely
eliminate an anesthetic gas such as nitrous oxide just minutes after use ends. At the other
extreme, some “hit-and-run” intoxicating substances poison systems, leaving permanent
impairments. For example, MPTP (1-methyl-4-pheny1-1,2,3,6-tetrahydropyridine), a con-
taminating by-product in the synthesis of a certain opioid, kills dopaminergic cells and in-
duces permanent parkinsonism in users who sought opioid intoxication.
Functional Consequences of
Other (or Unknown) Substance Intoxication
Impairment from intoxication with any substance may have serious consequences, includ-
ing dysfunction at work, social indiscretions, problems in interpersonal relationships, fail-
ure to fulfill role obligations, traffic accidents, fighting, high-risk behaviors (i.e., having
unprotected sex), and substance or medication overdose. The pattern of consequences will
vary with the particular substance.
Differential Diagnosis
Use of other or unknown substance, without meeting criteria for other (or unknown)
substance intoxication. The individual used an other or unknown substance(s), but the
dose was insufficient to produce symptoms that meet the diagnostic criteria required for
the diagnosis.
Substance intoxication or other substance/medication-induced disorders. Familiar sub-
stances may be sold in the black market as novel products, and individuals may experience
intoxication from those substances. History, toxicology screens, or chemical testing of the
substance itself may help to identify it.
Different types of other (or unknown) substance-related disorders. Episodes of other
(or unknown) substance intoxication may occur during, but are distinct from, other (or un-
known) substance use disorder, unspecified other (or unknown) substance-related disor-
der, and other (or unknown) substance—induced disorders.
Other toxic, metabolic, traumatic, neoplastic, vascular, or infectious disorders that impair
brain function and cognition. Numerous neurological and other medical conditions may
produce rapid onset of signs and symptoms mimicking those of intoxications, including the
examples in Criterion B. Paradoxically, drug withdrawals also must be ruled out, because, for
example, lethargy may indicate withdrawal from one drug or intoxication with another drug.
Comorbidity
As with all substance-related disorders, adolescent conduct disorder, adult antisocial per-
sonality disorder, and other substance use disorders tend to co-occur with other (or un-
known) substance intoxication.
Other (or Unknown) Substance Withdrawal 583
Other (or Unknown) Substance Withdrawal
Diagnostic Criteria 292.0 (F 19.239)
A. Cessation of (or reduction in) use of a substance that has been heavy and prolonged.
B. The development of a substance-specific syndrome shortly after the cessation of {or
reduction in) substance use.
C. The substance-specific syndrome causes clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
D. The symptoms are not attributable to another medical condition and are not better ex-
plained by another mental disorder, including withdrawal from another substance.
E. The substance involved cannot be classified under any of the other substance catego-
ries (alcohol; caffeine; cannabis; opioids; sedatives, hypnotics, or anxiolytics; stimu-
lants; or tobacco) or is unknown.
Coding note: The ICD-9-CM code is 292.0. The ICD-10-CM code for other (or unknown) sub-
stance withdrawal is F19.239. Note that the ICD-10-CM code indicates the comorbid presence
of a moderate or severe other (or unknown) substance use disorder. It is not permissible to
code a comorbid mild other (or unknown) substance use disorder with other (or unknown) sub-
stance withdrawal.
Note: For information on Risk and Prognostic Factors and Diagnostic Markers, see the cor-
responding sections in other (or unknown) substance use disorder.
Diagnostic Features
Other (or unknown) substance withdrawal is a clinically significant mental disorder that
develops during, or within a few hours to days after, reducing or terminating dosing with
a substance (Criteria A and B). Although recent dose reduction or termination usually is
clear in the history, other diagnostic procedures are very challenging if the drug is un-
known. Criterion B requires development of a “substance-specific syndrome” (i.e., the in-
dividual’s signs and symptoms must correspond with the known withdrawal syndrome
for the recently stopped drug)—a requirement that rarely can be met with an unknown
substance. Consequently, clinical judgment must guide such decisions when information
is this limited. Criterion D requires ruling out other medical conditions, mental disorders,
or withdrawals from familiar substances. When the substance is known, it should be re-
flected in the name of the disorder upon coding (e.g., betel nut withdrawal).
Prevaience
The prevalence of other (or unknown) substance withdrawal is unknown.
Development and Course
Withdrawal signs commonly appear some hours after use of the substance is terminated,
but the onset and course vary greatly, depending on the dose typically used by the person
and the rate of elimination of the specific substance from the body. At peak severity, with-
drawal symptoms from some substances involve only moderate levels of discomfort,
whereas withdrawal from other substances may be fatal. Withdrawal-associated dyspho-
ria often motivates relapse to substance use. Withdrawal symptoms slowly abate over
days, weeks, or months, depending on the particular drug and doses to which the indi-
vidual became tolerant.
Culture-Related Diagnostic Issues
Culture-related issues in diagnosis will vary with the particular substance.
584 Substance-Related and Addictive Disorders
Functional Consequences of
Other (or Unknown) Substance Withdrawal
Withdrawal from any substance may have serious consequences, including physical signs
and symptoms (e.g., malaise, vital sign changes, abdominal distress, headache), intense
drug craving, anxiety, depression, agitation, psychotic symptoms, or cognitive impairments.
These consequences may lead to problems such as dysfunction at work, problems in in-
terpersonal relationships, failure to fulfill role obligations, traffic accidents, fighting, high-
risk behavior (e.g., having unprotected sex), suicide attempts, and substance or medica-
tion overdose. The pattern of consequences will vary with the particular substance.
Differential Diagnosis
Dose reduction after extended dosing, but not meeting the criteria for other (or un-
known) substance withdrawal. The individual used other (or unknown) substances,
but the dose that was used was insufficient to produce symptoms that meet the criteria re-
quired for the diagnosis.
Substance withdrawal or other substance/medication-induced disorders. Familiar
substances may be sold in the black market as novel products, and individuals may expe-
rience withdrawal when discontinuing those substances. History, toxicology screens, or
chemical testing of the substance itself may help to identify it.
Different types of other (or unknown) substance-related disorders. Episodes of other
(or unknown) substance withdrawal may occur during, but are distinct from, other (or un-
known) substance use disorder, unspecified other (or unknown) substance-related disor-
der, and unspecified other (or unknown) substance-induced disorders.
Other toxic, metabolic, traumatic, neoplastic, vascular, or infectious disorders that im-
pair brain function and cognition. Numerous neurological and other medical condi-
tions may produce rapid onset of signs and symptoms mimicking those of withdrawals.
Paradoxically, drug intoxications also must be ruled out, because, for example, lethargy
may indicate withdrawal from one drug or intoxication with another drug.
Comorbidity
As with all substance-related disorders, adolescent conduct disorder, adult antisocial per-
sonality disorder, and other substance use disorders likely co-occur with other (or un-
known) substance withdrawal.
Other (or Unknown)
Substance-Induced Disorders
Because the category of other or unknown substances is inherently ill-defined, the extent
and range of induced disorders are uncertain. Nevertheless, other (or unknown) sub-
stance-induced disorders are possible and are described in other chapters of the manual
with disorders with which they share phenomenology (see the substance /medication-
induced mental disorders in these chapters): other (or unknown) substance—induced psy-
chotic disorder (“Schizophrenia Spectrum and Other Psychotic Disorders”); other (or un-
known substance—-induced bipolar disorder (“Bipolar and Related Disorders”); other (or
unknown) substance-induced depressive disorder (“Depressive Disorders”); other (or
unknown) substance-induced anxiety disorders (“Anxiety Disorders”); other (or un-
known) substance-induced obsessive-compulsive disorder (“Obsessive-Compulsive and
Related Disorders”); other (or unknown) substance—induced sleep disorder (“Sleep-Wake
Unspecified Other (or Unknown) Substance—Related Disorder 585
Disorders”); other (or unknown) substance—induced sexual dysfunction (“Sexual Dys-
functions”); and other (or unknown) substance/medication—induced major or mild neu-
rocognitive disorder (“Neurocognitive Disorders”). For other (or unknown) substance-
induced intoxication delirium and other (or unknown) substance-induced withdrawal
delirium, see the criteria and discussion of delirium in the chapter “Neurocognitive Dis-
orders.” These other (or unknown) substance—induced disorders are diagnosed instead of
other (or unknown) substance intoxication or other (or unknown) substance withdrawal
only when the symptoms are sufficiently severe to warrant independent clinical attention.
Unspecified Other (or Unknown)
Substance-Related Disorder
292.9 (F 19.99)
This category applies to presentations in which symptoms characteristic of an other (or un-
known) substance-related disorder that cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning predominate but do not
meet the full criteria for any specific other (or unknown) substance-related disorder or any
of the disorders in the substance-related disorders diagnostic class.
Non-Substance-Related Disorders
Gambling Disorder
Diagnostic Criteria 312.31 (F63.0)
A. Persistent and recurrent problematic gambling behavior leading to clinically significant
impairment or distress, as indicated by the individual exhibiting four (or more) of the fol-
lowing in a 12-month period:
1, Needs to gamble with increasing amounts of money in order to achieve the desired
excitement.
2. Is restless or irritable when attempting to cut down or stop gambling.
3. Has made repeated unsuccessful efforts to control, cut back, or stop gambling.
4. ls often preoccupied with gambling (e.g., having persistent thoughts of reliving past
gambling experiences, handicapping or planning the next venture, thinking of ways
to get money with which to gamble).
5. Often gambles when feeling distressed (e.g., helpless, guilty, anxious, depressed).
6. After losing money gambling, often returns another day to get even (“chasing” one’s
losses).
7. Lies to conceal the extent of involvement with gambling.
8. Has jeopardized or lost a significant relationship, job, or educational or career op-
portunity because of gambling.
9. Relies on others to provide money to relieve desperate financial situations caused
by gambling.
B. The gambling behavior is not better explained by a manic episode.
586 Substance-Related and Addictive Disorders
Specify if:
Episodic: Meeting diagnostic criteria at more than one time point, with symptoms sub-
siding between periods of gambling disorder for at least several months.
Persistent: Experiencing continuous symptoms, to meet diagnostic criteria for multiple
years.
Specify it:
In early remission: After full criteria for gambling disorder were previously met, none
of the criteria for gambling disorder have been met for at least 3 months but for less
than 12 months.
in sustained remission: After full criteria for gambling disorder were previously met,
none of the criteria for gambling disorder have been met during a period of 12 months
or longer.
Specify current severity:
Mild: 4—5 criteria met.
Moderate: 6-7 criteria met.
Severe: 8-9 criteria met.
Note: Although some behavioral conditions that do not involve ingestion of substances
have similarities to substance-related disorders, only one disorder—gambling disorder—
has sufficient data to be included in this section.
Specifiers
Severity is based on the number of criteria endorsed. Individuals with mild gambling dis-
order may exhibit only 4-5 of the criteria, with the most frequently endorsed criteria usu-
ally related to preoccupation with gambling and “chasing” losses. Individuals with
moderately severe gambling disorder exhibit more of the criteria (i.e., 6-7). Individuals
with the most severe form will exhibit all or most of the nine criteria (i.e., 8-9). Jeopardiz-
ing relationships or career opportunities due to gambling and relying on others to provide
money for gambling losses are typically the least often endorsed criteria and most often oc-
cur among those with more severe gambling disorder. Furthermore, individuals present-
ing for treatment of gambling disorder typically have moderate to severe forms of the
disorder.
Diagnostic Features
Gambling involves risking something of value in the hopes of obtaining something of
greater value. In many cultures, individuals gamble on games and events, and most do so
without experiencing problems. However, some individuals develop substantial impair-
ment related to their gambling behaviors. The essential feature of gambling disorder is
persistent and recurrent maladaptive gambling behavior that disrupts personal, family,
and/or vocational pursuits (Criterion A). Gambling disorder is defined as a cluster of four
or more of the symptoms listed in Criterion A occurring at any time in the same 12-month
period.
A pattern of “chasing one’s losses” may develop, with an urgent need to keep gam-
bling (often with the placing of larger bets or the taking of greater risks) to undo a loss or
series of losses. The individual may abandon his or her gambling strategy and try to win
back losses all at once. Although many gamblers may “chase” for short periods of time, it
is the frequent, and often long-term, “chase” that is characteristic of gambling disorder
(Criterion A6). Individuals may lie to family members, therapists, or others to conceal the
extent of involvement with gambling; these instances of deceit may also include, but
are not limited to, covering up illegal behaviors such as forgery, fraud, theft, or embez-
zlement to obtain money with which to gamble (Criterion A7). Individuals may also en-
Gambling Disorder 587
gage in “bailout” behavior, turning to family or others for help with a desperate financial
situation that was caused by gambling (Criterion A9).
Associated Features Supporting Diagnosis
Distortions in thinking (e.g., denial, superstitions, a sense of power and control over the
outcome of chance events, overconfidence) may be present in individuals with gambling
disorder. Many individuals with gambling disorder believe that money is both the cause
of and the solution to their problems. Some individuals with gambling disorder are im-
pulsive, competitive, energetic, restless, and easily bored; they may be overly concerned
with the approval of others and may be generous to the point of extravagance when win-
ning. Other individuals with gambling disorder are depressed and lonely, and they may
gamble when feeling helpless, guilty, or depressed. Up to half of individuals in treatment
for gambling disorder have suicidal ideation, and about 17% have attempted suicide.
Prevaience
The past-year prevalence rate of gambling disorder is about 0.2%-0.3% in the general pop-
ulation. In the general population, the lifetime prevalence rate is about 0.4%-1.0%. For fe-
males, the lifetime prevalence rate of gambling disorder is about 0.2%, and for males it is
about 0.6%. The lifetime prevalence of pathological gambling among African Americans is
about 0.9%, among whites about 0.4%, and among Hispanics about 0.3%.
Deveiopment and Course
The onset of gambling disorder can occur during adolescence or young adulthood, but in
other individuals it manifests during middle or even older adulthood. Generally, gam-
bling disorder develops over the course of years, although the progression appears to be
more rapid in females than in males. Most individuals who develop a gambling disorder
evidence a pattern of gambling that gradually increases in both frequency and amount of
wagering. Certainly, milder forms can develop into more severe cases. Most individuals
with gambling disorder report that one or two types of gambling are most problematic for
them, although some individuals participate in many forms of gambling. Individuals are
likely to engage in certain types of gambling (e.g., buying scratch tickets daily) more fre-
quently than others (e.g., playing slot machines or blackjack at the casino weekly). Fre-
quency of gambling can be related more to the type of gambling than to the severity of the
overall gambling disorder. For example, purchasing a single scratch ticket each day may
not be problematic, while less frequent casino, sports, or card gambling may be part of a
gambling disorder. Similarly, amounts of money spent wagering are not in themselves in-
dicative of gambling disorder. Some individuals can wager thousands of dollars per
month and not have a problem with gambling, while others may wager much smaller
amounts but experience substantial gambling-related difficulties.
Gambling patterns may be regular or episodic, and gambling disorder can be persis-
tent or in remission. Gambling can increase during periods of stress or depression and
during periods of substance use or abstinence. There may be periods of heavy gambling
and severe problems, times of total abstinence, and periods of nonproblematic gambling.
Gambling disorder is sometimes associated with spontaneous, long-term remissions.
Nevertheless, some individuals underestimate their vulnerability to develop gambling
disorder or to return to gambling disorder following remission. When in a period of re-
mission, they may incorrectly assume that they will have no problem regulating gambling
and that they may gamble on some forms nonproblematically, only to experience a return
to gambling disorder.
Early expression of gambling disorder is more common among males than among fe-
males. Individuals who begin gambling in youth often do so with family members or
588 Substance-Related and Addictive Disorders
friends. Development of early-life gambling disorder appears to be associated with impul-
sivity and substance abuse. Many high school and college students who develop gambling
disorder grow out of the disorder over time, although it remains a lifelong problem for
some. Mid- and later-life onset of gambling disorder is more common among females than
among males.
There are age and gender variations in the type of gambling activities and the preva-
lence rates of gambling disorder. Gambling disorder is more common among younger and
middle-age persons than among older adults. Among adolescents and young adults, the
disorder is more prevalent in males than in females. Younger individuals prefer different
forms of gambling (e.g., sports betting), while older adults are more likely to develop
problems with slot machine and bingo gambling. Although the proportions of individuals
who seek treatment for gambling disorder are low across all age groups, younger individ-
uals are especially unlikely to present for treatment.
Males are more likely to begin gambling earlier in life and to have a younger age at on-
set of gambling disorder than females, who are more likely to begin gambling later in life
and to develop gambling disorder in a shorter time frame. Females with gambling disor-
der are more likely than males with gambling disorder to have depressive, bipolar, and
anxiety disorders. Females also have a later age at onset of the disorder and seek treatment
sooner, although rates of treatment seeking are low (<10%) among individuals with gam-
bling disorder regardless of gender.
Risk and Prognostic Factors
Temperamental. Gambling that begins in childhood or early adolescence is associated
with increased rates of gambling disorder. Gambling disorder also appears to aggregate
with antisocial personality disorder, depressive and bipolar disorders, and other sub-
stance use disorders, particularly with alcohol disorders.
Genetic and physiological. Gambling disorder can aggregate in families, and this effect
appears to relate to both environmental and genetic factors. Gambling problems are more
frequent in monozygotic than in dizygotic twins. Gambling disorder is also more preva-
lent among first-degree relatives of individuals with moderate to severe alcohol use dis-
order than among the general population.
Course modifiers. Many individuals, including adolescents and young adults, are likely to
resolve their problems with gambling disorder over time, although a strong predictor of
future gambling problems is prior gambling problems.
Culture-Related Diagnostic Issues
Individuals from specific cultures and races/ethnicities are more likely to participate in
some types of gambling activities than others (e.g., pai gow, cockfights, blackjack, horse rac-
ing). Prevalence rates of gambling disorder are higher among African Americans than
among European Americans, with rates for Hispanic Americans similar to those of Euro-
pean Americans. Indigenous populations have high prevalence rates of gambling disorder.
Gender-Related Diagnostic Issues
Males develop gambling disorder at higher rates than females, although this gender gap
may be narrowing. Males tend to wager on different forms of gambling than females, with
cards, sports, and horse race gambling more prevalent among males, and slot machine and
bingo gambling more common among females.
Gambling Disorder 589
Functional Consequences of Gambling Disorder
Areas of psychosocial, health, and mental health functioning may be adversely affected by
gambling disorder. Specifically, individuals with gambling disorder may, because of their
involvement with gambling, jeopardize or lose important relationships with family mem-
bers or friends. Such problems may occur from repeatedly lying to others to cover up the
extent of gambling or from requesting money that is used for gambling or to pay off gam-
bling debts. Employment or educational activities may likewise be adversely impacted by
gambling disorder; absenteeism or poor work or school performance can occur with gam-
bling disorder, as individuals may gamble during work or school hours or be preoccupied
with gambling or its adverse consequence when they should be working or studying. In-
dividuals with gambling disorder have poor general health and utilize medical services at
high rates.
Differential Diagnosis
Nondisordered gambling. Gambling disorder must be distinguished from professional
and social gambling. In professional gambling, risks are limited and discipline is central.
Social gambling typically occurs with friends or colleagues and lasts for a limited period of
time, with acceptable losses. Some individuals can experience problems associated with
gambling (e.g., short-term chasing behavior and loss of control) that do not meet the full
criteria for gambling disorder.
Manic episode. Loss of judgment and excessive gambling may occur during a manic ep-
isode. An additional diagnosis of gambling disorder should be given only if the gambling
behavior is not better explained by manic episodes (e.g., a history of maladaptive gam-
bling behavior at times other than during a manic episode). Alternatively, an individual
with gambling disorder may, during a period of gambling, exhibit behavior that resembles
a manic episode, but once the individual is away from the gambling, these manic-like fea-
tures dissipate.
Personality disorders. Problems with gambling may occur in individuals with antisocial
personality disorder and other personality disorders. If the criteria are met for both disor-
ders, both can be diagnosed.
Other medical conditions. Some patients taking dopaminergic medications (e.g., for
Parkinson‘s disease) may experience urges to gamble. If such symptoms dissipate when
dopaminergic medications are reduced in dosage or ceased, then a diagnosis of gambling
disorder would not be indicated.
Comorbidity
Gambling disorder is associated with poor general health. In addition, some specific med-
ical diagnoses, such as tachycardia and angina, are more common among individuals with
gambling disorder than in the general population, even when other substance use disor-
ders, including tobacco use disorder, are controlled for. Individuals with gambling disor-
der have high rates of comorbidity with other mental disorders, such as substance use
disorders, depressive disorders, anxiety disorders, and personality disorders. In some in-
dividuals, other mental disorders may precede gambling disorder and be either absent or
present during the manifestation of gambling disorder. Gambling disorder may also occur
prior to the onset of other mental disorders, especially anxiety disorders and substance use
disorders.
Neurocognitiv
The neurocognitive disorders (NCDs) (referred to in DSM-IV as “Dementia,
Delirium, Amnestic, and Other Cognitive Disorders”) begin with delirium, followed by
the syndromes of major NCD, mild NCD, and their etiological subtypes. The major or
mild NCD subtypes are NCD due to Alzheimer’s disease; vascular NCD; NCD with Lewy
bodies; NCD due to Parkinson's disease; frontotemporal NCD; NCD due to traumatic
brain injury; NCD due to HIV infection; substance/medication-induced NCD; NCD due
to Huntington's disease; NCD due to prion disease; NCD due to another medical condi-
tion; NCD due to multiple etiologies; and unspecified NCD. The NCD category encom-
passes the group of disorders in which the primary clinical deficit is in cognitive function,
and that are acquired rather than developmental. Although cognitive deficits are present
in many if not all mental disorders (e.g., schizophrenia, bipolar disorders), only disorders
whose core features are cognitive are included in the NCD category. The NCDs are those
in which impaired cognition has not been present since birth or very early life, and thus
represents a decline from a previously attained level of functioning.
The NCDs are unique among DSM-5 categories in that these are syndromes for which
the underlying pathology, and frequently the etiology as well, can potentially be deter-
mined. The various underlying disease entities have all been the subject of extensive re-
search, clinical experience, and expert consensus on diagnostic criteria. The DSM-5 criteria
for these disorders have been developed in close consultation with the expert groups for
each of the disease entities and align as closely as possible with the current consensus cri-
teria for each of them. The potential utility of biomarkers is also discussed in relation to
diagnosis. Dementia is subsumed under the newly named entity major neurocognitive dis-
order, although the term dementia is not precluded from use in the etiological subtypes in
which that term is standard. Furthermore, DSM-5 recognizes a less severe level of cogni-
tive impairment, mild neurocognitive disorder, which can also be a focus of care, and which
in DSM-IV was subsumed under “Cognitive Disorder Not Otherwise Specified.” Diagnos-
tic criteria are provided for both these syndromic entities, followed by diagnostic criteria
for the different etiological subtypes. Several of the NCDs frequently coexist with one an-
other, and their relationships may be multiply characterized under different chapter sub-
headings, including “Differential Diagnosis” (e.g., NCD due to Alzheimer’s disease vs.
vascular NCD), “Risk and Prognostic Factors” (e.g., vascular pathology increasing the
clinical expression of Alzheimer’s disease), and/or “Comorbidity” (e.g., mixed Alzhei-
mer’s disease—vascular pathology).
The term dementia is retained in DSM-5 for continuity and may be used in settings
where physicians and patients are accustomed to this term. Although dementia is the cus-
tomary term for disorders like the degenerative dementias that usually affect older adults,
the term neurocognitive disorder is widely used and often preferred for conditions affect-
ing younger individuals, such as impairment secondary to traumatic brain injury or HIV
infection. Furthermore, the major NCD definition is somewhat broader than the term
dementia, in that individuals with substantial decline in a single domain can receive this di-
agnosis, most notably the DSM-IV category of “Amnestic Disorder,” which would now be
diagnosed as major NCD due to another medical condition and for which the term demen-
tia would not be used.
591
592 Neurocognitive Disorders
Neurocognitive Domains
The criteria for the various NCDs are all based on defined cognitive domains. Table 1 pro-
vides for each of the key domains a working definition, examples of symptoms or obser-
vations regarding impairments in everyday activities, and examples of assessments. The
domains thus defined, along with guidelines for clinical thresholds, form the basis on
which the NCDs, their levels, and their subtypes may be diagnosed.
593
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595
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596 Neurocognitive Disorders
Delirium
Diagnostic Criteria
A.
B.
A disturbance in attention (i.e., reduced ability to direct, focus, sustain, and shift atten-
tion) and awareness (reduced orientation to the environment).
The disturbance develops over a short period of time (usually hours to a few days), rep-
resents a change from baseline attention and awareness, and tends to fluctuate in se-
verity during the course of a day.
. An additional disturbance in cognition (e.g., memory deficit, disorientation, language,
visuospatial ability, or perception).
. The disturbances in Criteria A and C are not better explained by another preexisting,
established, or evolving neurocognitive disorder and do not occur in the context of a
severely reduced level of arousal, such as coma.
. There is evidence from the history, physical examination, or laboratory findings that the
disturbance is a direct physiological consequence of another medical condition, sub-
stance intoxication or withdrawal (i.e., due to a drug of abuse or to a medication), or
exposure to a toxin, or is due to multiple etiologies.
Specify whether:
Substance intoxication delirium: This diagnosis should be made instead of sub-
stance intoxication when the symptoms in Criteria A and C predominate in the clinical
picture and when they are sufficiently severe to warrant clinical attention.
Coding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance] in-
toxication delirium are indicated in the table below. Note that the ICD-10-CM code
depends on whether or not there is a comorbid substance use disorder present for
the same class of substance. If a mild substance use disorder is comorbid with the
substance intoxication delirium, the 4th position character is “1,” and the clinician
should record “mild [substance] use disorder” before the substance intoxication de-
lirium (@.g., “mild cocaine use disorder with cocaine intoxication delirium”). If a mod-
erate or Severe substance use disorder is comorbid with the substance intoxication
delirium, the 4th position character is “2,” and the clinician should record “moderate
[substance] use disorder” or “severe [substance] use disorder,” depending on the
severity of the comorbid substance use disorder. If there is no comorbid substance
use disorder (e.g., after a one-time heavy use of the substance), then the 4th posi-
tion character is “9,” and the clinician should record only the substance intoxication
delirium.
ICD-10-CM
With use
With use disorder,
disorder, moderateor Without use
ICD-9-CM mild severe disorder
Alcohol 291.0 F10.121 F10.221 F10.921
Cannabis 292.81 F12.121 F12.224 F12.921
Phencyclidine 292.81 F16.121 F16.221 F16.921
Other hallucinogen 292.81 F16.121 F16.2214 F16.921
inhalant 292.81 F18.1214 F18.221 F18.921
Opioid 292.81 F11.121 F11.221 F11.921
Delirium 597
ICD-10-CM
With use
With use disorder,
disorder, moderateor Without use
!CD-9-CM mild severe disorder
Sedative, hypnotic, or anxiolytic 292.81 F13.121 F13.221 F13.921
Amphetamine (or other 292.81 F15.121 F15.221 F15.921
stimulant)
Cocaine 292.81 F14.121 F14.221 F14.921
Other (or unknown) substance 292.81 F19.121 F19.221 F19.921
Substance withdrawal delirium: This diagnosis should be made instead of sub-
stance withdrawal when the symptoms in Criteria A and C predominate in the clinical
picture and when they are sufficiently severe to warrant clinical attention.
Code [specific substance] withdrawal delirium: 291.0 (F10.231) alcohol; 292.0
(F11.23) opioid; 292.0 (F13.231) sedative, hypnotic, or anxiolytic; 292.0 (F19.231)
other (or unknown) substance/medication.
Medication-induced delirium: This diagnosis applies when the symptoms in Criteria
A and C arise as a side effect of a medication taken as prescribed.
Coding note: The ICD-9-CM code for [specific medication]-induced delirium is
292.81. The ICD-10-CM code depends on the type of medication. If the medication
is an opioid taken as prescribed, the code is F11.921. If the medication is a seda-
tive, hypnotic, or anxiolytic taken as prescribed, the code is F13.921. if the medica-
tion is an amphetamine-type or other stimulant taken as prescribed, the code is
F15.921. For medications that do not fit into any of the classes (e.g., dexametha-
sone) and in cases in which a substance is judged to be an etiological factor but the
specific class of substance is unknown, the code is F19.921.
293.0 (FO5) Delirium due to another medical condition: There is evidence from the
history, physical examination, or laboratory findings that the disturbance is attributable
to the physiological consequences of another medical condition.
Coding note: Include the name of the other medical condition in the name of the
delirium (e.g., 293.0 [F05] delirium due to hepatic encephalopathy). The other med-
ical condition should also be coded and listed separately immediately before the
delirium due to another medical condition (e.g., 572.2 [K72.90] hepatic encepha-
lopathy; 293.0 [FO5] delirium due to hepatic encephalopathy).
293.0 (FO5) Delirium due to multiple etiologies: There is evidence from the history,
physical examination, or laboratory findings that the delirium has more than one etiol-
ogy (€.g., more than one etiological medica! condition; another medica! condition plus
substance intoxication or medication side effect).
Coding note: Use multiple separate codes reflecting specific delirium etiologies
(e.g., 572.2 [K72.90] hepatic encephalopathy, 293.0 [F05] delirium due to hepatic
failure; 291.0 [F 10.231] alcohol withdrawal delirium). Note that the etiological med-
ical condition both appears as a separate code that precedes the delirium code and
is substituted into the delirium due to another medical condition rubric.
Specify if:
Acute: Lasting a few hours or days.
Persistent: Lasting weeks or months.
598 Neurocognitive Disorders
Specify if:
Hyperactive: The individual has a hyperactive level of psychomotor activity that may be
accompanied by mood lability, agitation, and/or refusal to cooperate with medical care.
Hypoactive: The individual has a hypoactive level of psychomotor activity that may be
accompanied by sluggishness and lethargy that approaches stupor.
Mixed level of activity: The individual has a normal level of psychomotor activity even
though attention and awareness are disturbed. Also includes individuals whose activity
level rapidly fluctuates.
Recording Procedures
Substance intoxication detirium
ICD-9-CM. The name of the substance/ medication intoxication delirium begins with
the specific substance (e.g., cocaine, dexamethasone) that is presumed to be causing the
delirium. The diagnostic code is selected from the table included in the criteria set, which
is based on the drug class. For substances that do not fit into any of the classes (e.g., dexa-
methasone), the code for “other substance” should be used; and in cases in which a sub-
stance is judged to be an etiological factor but the specific class of substance is unknown,
the category “unknown substance” should be used.
The name of the disorder is followed by the course (i.e., acute, persistent), followed by
the specifier indicating level of psychomotor activity (i.e., hyperactive, hypoactive, mixed
level of activity). Unlike the recording procedures for ICD-10-CM, which combine the sub-
stance/ medication intoxication delirium and substance use disorder into a single code, for
ICD-9-CM a separate diagnostic code is given for the substance use disorder. For example,
in the case of acute hyperactive intoxication delirium occurring in a man with a severe co-
caine use disorder, the diagnosis is 292.81 cocaine intoxication delirium, acute, hyperac-
tive. An additional diagnosis of 304.20 severe cocaine use disorder is also given. If the
intoxication delirium occurs without a comorbid substance use disorder (e.g., after a one-
time heavy use of the substance), no accompanying substance use disorder is noted (e.g.,
292.81 phencyclidine intoxication delirium, acute, hypoactive).
ICD-10-CM,. The name of the substance/ medication intoxication delirium begins with the
specific substance (e.g., cocaine, dexamethasone) that is presumed to be causing the delirium.
The diagnostic code is selected from the table included in the criteria set, which is based on the
drug class and presence or absence of a comorbid substance use disorder. For substances that
do not fit into any of the classes (e.g., dexamethasone), the code for “other substance” should
be used; and in cases in which a substance is judged to be an etiological factor but the specific
class of substance is unknown, the category “unknown substance” should be used.
When recording the name of the disorder, the comorbid substance use disorder (if any) is
listed first, followed by the word “with,” followed by the name of the substance intoxication
delirium, followed by the course (i.e., acute, persistent), followed by the specifier indicating
level of psychomotor activity (i.e., hyperactive, hypoactive, mixed level of activity). For exam-
ple, in the case of acute hyperactive intoxication delirium occurring in a man with a severe co-
caine use disorder, the diagnosis is F14.221 severe cocaine use disorder with cocaine
intoxication delirium, acute, hyperactive. A separate diagnosis of the comorbid severe cocaine
use disorder is not given. If the intoxication delirium occurs without a comorbid substance use
disorder (e.g., after a one-time heavy use of the substance), no accompanying substance use
disorder is noted (e.g., F16.921 phencyclidine intoxication delirium, acute, hypoactive).
Substance withdrawal delirium
ICD-9-CM. The name of the substance/medication withdrawal delirium begins with the
specific substance (e.g., alcohol) that is presumed to be causing the withdrawal delirium. The
diagnostic code is selected from substance-specific codes included in the coding note included
Delirium 599
in the criteria set. The name of the disorder is followed by the course (e., acute, persistent), fol-
lowed by the specifier indicating level of psychomotor activity (i.e., hyperactive, hypoactive,
mixed level of activity). Unlike the recording procedures for ICD-10-CM, which combine the
substance/medication withdrawal delirium and substance use disorder into a single code, for
ICD-9-CM a separate diagnostic code is given for the substance use disorder. For example, in
the case of acute hyperactive withdrawal delirium occurring in a man witha severe alcohol use
disorder, the diagnosis is 291.0 alcohol withdrawal delirium, acute, hyperactive. An additional
diagnosis of 303.90 severe alcohol use disorder is also given.
ICD-10-CM, The name of the substance/medication withdrawal delirium begins with
the specific substance (e.g., alcohol) that is presumed to be causing the withdrawal delir-
ium. The diagnostic code is selected from substance-specific codes included in the coding
note included in the criteria set. When recording the name of the disorder, the comorbid
moderate or severe substance use disorder (if any) is listed first, followed by the word
“with,” followed by the substance withdrawal delirium, followed by the course (i.e., acute,
persistent), followed by the specifier indicating level of psychomotor activity (i.e., hyper-
active, hypoactive, mixed level of activity). For example, in the case of acute hyperactive
withdrawal delirium occurring in a man with a severe alcohol use disorder, the diagnosis
is F10.231 severe alcohol use disorder with alcohol withdrawal delirium, acute, hyperac-
tive. A separate diagnosis of the comorbid severe alcohol use disorder is not given.
Medication-induced delirium. The name of the medication-induced delirium begins
with the specific substance (e.g., dexamethasone) that is presumed to be causing the de-
lirium. The name of the disorder is followed by the course (i.e., acute, persistent), followed
by the specifier indicating level of psychomotor activity (i.e., hyperactive, hypoactive,
mixed level of activity). For example, in the case of acute hyperactive medication-induced
delirium occurring in a man using dexamethasone as prescribed, the diagnosis is 292.81
(F19.921) dexamethasone-induced delirium, acute, hyperactive.
Specifiers
Regarding course, in hospital settings, delirium usually lasts about 1 week, but some
symptoms often persist even after individuals are discharged from the hospital.
Individuals with delirium may rapidly switch between hyperactive and hypoactive
states. The hyperactive state may be more common or more frequently recognized and
often is associated with medication side effects and drug withdrawal. The hypoactive state
may be more frequent in older adults.
Diagnostic Features
The essential feature of delirium is a disturbance of attention or awareness that is accom-
panied by a change in baseline cognition that cannot be better explained by a preexisting
or evolving neurocognitive disorder (NCD). The disturbance in attention (Criterion A) is
manifested by reduced ability to direct, focus, sustain, and shift attention. Questions must
be repeated because the individual's attention wanders, or the individual may perseverate
with an answer to a previous question rather than appropriately shift attention. The indi-
vidual is easily distracted by irrelevant stimuli. The disturbance in awareness is mani-
fested by a reduced orientation to the environment or at times even to oneself.
The disturbance develops over a short period of time, usually hours to a few days, and
tends to fluctuate during the course of the day, often with worsening in the evening and
night when external orienting stimuli decrease (Criterion B). There is evidence from the
history, physical examination, or laboratory findings that the disturbance is a physiologi-
cal consequence of an underlying medical condition, substance intoxication or with-
drawal, use of a medication, or a toxin exposure, or a combination of these factors
(Criterion E). The etiology should be coded according to the etiologically appropriate sub-
type (i.e., substance or medication intoxication, substance withdrawal, another medical
600 Neurocognitive Disorders
condition, or multiple etiologies). Delirium often occurs in the context of an underlying
NCD. The impaired brain function of individuals with mild and major NCD renders them
more vulnerable to delirium.
There is an accompanying change in at least one other area that may include memory
and learning (particularly recent memory), disorientation (particularly to time and place),
alteration in language, or perceptual distortion or a perceptual-motor disturbance (Crite-
rion C). The perceptual disturbances accompanying delirium include misinterpretations,
illusions, or hallucinations; these disturbances are typically visual, but may occur in other
modalities as well, and range from simple and uniform to highly complex. Normal atten-
tion /arousal, delirium, and coma lie on a continuum, with coma defined as the lack of any
response to verbal stimuli. The ability to evaluate cognition to diagnose delirium depends
on there being a level of arousal sufficient for response to verbal stimulation; hence, delir-
ium should not be diagnosed in the context of coma (Criterion D). Many noncomatose pa-
tients have a reduced level of arousal. Those patients who show only minimal responses to
verbal stimulation are incapable of engaging with attempts at standardized testing or even
interview. This inability to engage should be classified as severe inattention. Low-arousal
states (of acute onset) should be recognized as indicating severe inattention and cognitive
change, and hence delirium. They are clinically indistinguishable from delirium diag-
nosed on the basis of inattention or cognitive change elicited through cognitive testing and
interview.
Associated Features Supporting Diagnosis
Delirium is often associated with a disturbance in the sleep-wake cycle. This disturbance
can include daytime sleepiness, nighttime agitation, difficulty falling asleep, excessive
sleepiness throughout the day, or wakefulness throughout the night. In some cases, com-
plete reversal of the night-day sleep-wake cycle can occur. Sleep-wake cycle disturbances
are very common in delirium and have been proposed as a core criterion for the diagnosis.
The individual with delirium may exhibit emotional disturbances, such as anxiety,
fear, depression, irritability, anger, euphoria, and apathy. There may be rapid and unpre-
dictable shifts from one emotional state to another. The disturbed emotional state may also
be evident in calling out, screaming, cursing, muttering, moaning, or making other
sounds. These behaviors are especially prevalent at night and under conditions in which
stimulation and environmental cues are lacking.
Prevaience
The prevalence of delirium is highest among hospitalized older individuals and varies
depending on the individuals’ characteristics, setting of care, and sensitivity of the detec-
tion method. The prevalence of delirium in the community overall is low (1%-2%) but in-
creases with age, rising to 14% among individuals older than 85 years. The prevalence is
10%-30% in older individuals presenting to emergency departments, where the delirium
often indicates a medical illness.
The prevalence of delirium when individuals are admitted to the hospital ranges from
14% to 24%, and estimates of the incidence of delirium arising during hospitalization
range from 6% to 56% in general hospital populations. Delirium occurs in 15%-53% of
older individuals postoperatively and in 70%-87% of those in intensive care. Delirium oc-
curs in up to 60% of individuals in nursing homes or post-acute care settings and in up to
83% of all individuals at the end of life.
Development and Course
While the majority of individuals with delirium have a full recovery with or without
treatment, early recognition and intervention usually shortens the duration of the delir-
Delirium 601
ium. Delirium may progress to stupor, coma, seizures, or death, particularly if the under-
lying cause remains untreated. Mortality among hospitalized individuals with delirium is
high, and as many as 40% of individuals with delirium, particularly those with malignan-
cies and other significant underlying medical illness, die within a year after diagnosis.
Risk and Prognostic Factors
Environmental. Delirium may be increased in the context of functional impairment, im-
mobility, a history of falls, low levels of activity, and use of drugs and medications with
psychoactive properties (particularly alcohol and anticholinergics).
Genetic and physiological. Both major and mild NCDs can increase the risk for delir-
ium and complicate the course. Older individuals are especially susceptible to delirium
compared with younger adults. Susceptibility to delirium in infancy and through child-
hood may be greater than in early and middle adulthood. In childhood, delirium may be
related to febrile illnesses and certain medications (e.g., anticholinergics).
Diagnostic Markers
In addition to laboratory findings characteristic of underlying medical conditions (or in-
toxication or withdrawal states), there is often generalized slowing on electroencephalog-
raphy, and fast activity is occasionally found (e.g., in some cases of alcohol withdrawal
delirium). However, electroencephalography is insufficiently sensitive and specific for di-
agnostic use.
Functional Consequences of Deiirium
Delirium itself is associated with increased functional decline and risk of institutional
placement. Hospitalized individuals 65 years or older with delirium have three times the
risk of nursing home placement and about three times the functional decline as hospital-
ized patients without delirium at both discharge and 3 months postdischarge.
Differential Diagnosis
Psychotic disorders and bipolar and depressive disorders with psychotic features.
Delirium that is characterized by vivid hallucinations, delusions, language disturbances,
and agitation must be distinguished from brief psychotic disorder, schizophrenia, schizo-
phreniform disorder, and other psychotic disorders, as well as from bipolar and depres-
sive disorders with psychotic features.
Acute stress disorder. Delirium associated with fear, anxiety, and dissociative symptoms,
such as depersonalization, must be distinguished from acute stress disorder, which is pre-
cipitated by exposure to a severely traumatic event.
Malingering and factitious disorder. Delirium can be distinguished from these disor-
ders on the basis of the often atypical presentation in malingering and factitious disorder
and the absence of another medical condition or substance that is etiologically related to
the apparent cognitive disturbance.
Other neurocognitive disorders. The most common differential diagnostic issue when
evaluating confusion in older adults is disentangling symptoms of delirium and dementia.
The clinician must determine whether the individual has delirium; a delirium superim-
posed on a preexisting NCD, such as that due to Alzheimer’s disease; or an NCD without
delirium. The traditional distinction between delirium and dementia according to acute-
ness of onset and temporal course is particularly difficult in those elderly individuals who
had a prior NCD that may not have been recognized, or who develop persistent cognitive
impairment following an episode of delirium.
602 Neurocognitive Disorders
Other Specified Delirium
780.09 (R41.0)
This category applies to presentations in which symptoms characteristic of delirium that
cause Clinically significant distress or impairment in social, occupational, or other impor-
tant areas of functioning predominate but do not meet the full criteria for delirium or any of
the disorders in the neurocognitive disorders diagnostic class. The other specified delirium
category is used in situations in which the clinician chooses to communicate the specific
reason that the presentation does not meet the criteria for delirium or any specific neuro-
cognitive disorder. This is done by recording “other specified delirium” followed by the spe-
cific reason (e.g., “attenuated delirium syndrome”).
An example of a presentation that can be specified using the “other specified” desig-
nation is the following:
Attenuated delirium syndrome: This syndrome applies in cases of delirium in which
the severity of cognitive impairment falls short of that required for the diagnosis, or in
which some, but not all, diagnostic criteria for delirium are met.
Unspecified Delirium
780.09 (R41.0)
This category applies to presentations in which symptoms characteristic of delirium that
cause Clinically significant distress or impairment in social, occupational, or other impor-
tant areas of functioning predominate but do not meet the full criteria for delirium or any of
the disorders in the neurocognitive disorders diagnostic class. The unspecified delirium
category is used in situations in which the clinician chooses not to specify the reason that
the criteria are not met for delirium, and includes presentations for which there is insuffi-
cient information to make a more specific diagnosis {e.g., in emergency room settings).
Major and Mild Neurocognitive Disorders
Major Neurocognitive Disorder
Diagnostic Criteria
A. Evidence of significant cognitive decline from a previous level of performance in one
or more cognitive domains (complex attention, executive function, learning and mem-
ory, language, perceptual-motor, or social cognition) based on:
1. Concern of the individual, a knowledgeable informant, or the clinician that there has
been a significant decline in cognitive function; and
2. Asubstantial impairment in cognitive performance, preferably documented by stan-
dardized neuropsychological testing or, in its absence, another quantified clinical
assessment.
B. The cognitive deficits interfere with independence in everyday activities (i.e., at a min-
imum, requiring assistance with complex instrumental activities of daily living such as
paying bills or managing medications).
C. The cognitive deficits do not occur exclusively in the context of a delirium.
Major and Mild Neurocognitive Disorders
603
D. The cognitive deficits are not better explained by another mental disorder (e.g., major
depressive disorder, schizophrenia).
Specify whether due to:
Alzheimer’s disease (pp. 611-614)
Frontotemporal lobar degeneration (pp. 614-618)
Lewy body disease (pp. 618-621)
Vascular disease (pp. 621-624)
Traumatic brain injury (pp. 624-627)
Substance/medication use (pp. 627-632)
HIV infection (pp. 632-634)
Prion disease (pp. 634-636)
Parkinson’s disease (pp. 636-638)
Huntington’s disease (pp. 638-641)
Another medical condition (pp. 641-642)
Multiple etiologies (pp. 642-643)
Unspecified (p. 643)
Coding note: Code based on medical or substance etiology. In some cases, there is need
for an additional code for the etiological medical condition, which must immediately pre-
cede the diagnostic code for major neurocognitive disorder, as follows:
Etiological subtype
Alzheimer’s
disease
Frontotemporal
lobar degeneration
Lewy body disease
Vascular disease
Traumatic brain
injury
Substance/
medication-
induced
Associated etiological
medical code for major
Major neurocogni-
Mild neurocogni-
neurocognitive disorder® tive disorder code” tive disorder code°
Probable: 331.0 (G30.9)
Possible: no additional
medical code
Probable: 331.19
(G31.09)
Possible: no additional
medical code
Probable: 331.82
(G31.83)
Possible: no additional
medical code
No additional medical
code
907.0 (S06.2X9S)
No additional medical
code
Probable: 294.1x
(F02.8x)
Possible: 331.9
(G31.9)°
Probable: 294.1x
(FO2.8x)
Possible: 331.9
(G31.9)°
Probable: 294.1x
(F02.8x)
Possible: 331.9
(G31.9)°
Probable: 290.40
(FO1.5x)
Possible: 331.9
(G31.9)°
294.1x (F02.8x)
Code based on the
type of substance
causing the major
neurocognitive
disorder® 4
331.83 (G31.84)
(Do not use addi-
tional code for
Alzheimer’s
disease.)
331.83 (G31.84)
{Do not use addi-
tional code for
frontotemporal
disease.)
331.83 (G31.84)
{Do not use addi-
tional code for
Lewy body disease.)
331.83 (G31.84)
(Do not use addi-
tional code for the
vascular disease.)
331.83 (G31.84)
(Do not use additional
code for the trau-
matic brain injury.)
Code based on the
type of substance
causing the mild
neurocognitive
disorde
604
Etiological subtype
HIV infection
Prion disease
Parkinson’s
disease
Huntington's
disease
Due to another
medical condition
Due to multiple
etiologies
Unspecified neuro-
cognitive disorder
Associated etiological
medical code for major
neurocognitive disorder tive disorder code”
042 (B20)
046.79 (A81.9)
Probable: 332.0 (G20)
Possible: No additional
medical code
333.4 (G10)
Code the other medical
condition first
(e.g., 340 [G35]
multiple sclerosis)
Code all of the etiological
medical conditions first
(with the exception of
vascular disease)
No additional medical
code
Neurocognitive Disorders
Major neurocogni-
294.1x (FO2.8x)
294. 1x (F02.8x)
Probable: 294.1x
(F02.8x)
Possible: 331.9
(G31.9)°
294.1x (FO2.8x)
294.1x (F02.8x)
294.1x (FO2.8x)
(Plus the code for
the relevant sub-
stance/medication-
induced major neu-
rocognitive disor-
ders if substances
or medications
play a role in the
etiology.)
799.59 (R41.9)
*Code first, before code for major neurocognitive disorder.
Code fifth character based on symptom specifier: .x0 without behavioral disturbance; .x1 with be-
havioral disturbance (e.g., psychotic symptoms, mood disturbance, agitation, apathy, or other be-
havioral symptoms).
Mild neurocogni-
tive disorder code®
331.83 (G31.84)
(Do not use addi-
tional code for HIV
infection.)
331.83 (G31.84)
(Do not use addi-
tional code for
prion disease.)
331.83 (G31.84)
(Do not use addi-
tional code for
Parkinson’s
disease.)
331.83 (G31.84)
(Do not use addi-
tional code for
Huntington’s
disease.)
331.83 (G31.84)
(Do not use addi-
tional codes for the
presumed etiologi-
cal medical condi-
tions.)
331.83 (G31.84)
(Plus the code for
the relevant sub-
stance/medication-
induced mild neuro-
cognitive disor-
ders if substances
or medications play
a role in the etiol-
ogy. Do not use ad-
ditional codes for
the presumed
etiological medical
conditions.)
799.59 (R41.9)
‘Note: Behavioral disturbance specifier cannot be coded but should still be indicated in writing.
See “Substance /Medication-Induced Major or Mild Neurocognitive Disorder.”
Major and Mild Neurocognitive Disorders 605
Specify:
Without behavioral disturbance: If the cognitive disturbance is not accompanied by
any clinically significant behavioral disturbance.
With behavioral disturbance (specify disturbance): If the cognitive disturbance is ac-
companied by a clinically significant behavioral disturbance (e.g., psychotic symptoms,
mood disturbance, agitation, apathy, or other behavioral symptoms).
Specify current severity:
Mild: Difficulties with instrumental activities of daily living (e.g., housework, managing
money).
Moderate: Difficulties with basic activities of daily living (e.g., feeding, dressing).
Severe: Fully dependent.
Mild Neurocognitive Disorder
Diagnostic Criteria
A. Evidence of modest cognitive decline from a previous level of performance in one or
more cognitive domains (complex attention, executive function, learning and memory,
language, perceptual motor, or social cognition) based on:
1. Concern of the individual, a knowledgeable informant, or the clinician that there has
been a mild decline in cognitive function; and
2. A modest impairment in cognitive performance, preferably documented by stan-
dardized neuropsychological testing or, in its absence, another quantified clinical
assessment.
B. The cognitive deficits do not interfere with capacity for independence in everyday
activities (i.e., complex instrumental activities of daily living such as paying bills or
managing medications are preserved, but greater effort, compensatory strategies, or
accommodation may be required).
C. The cognitive deficits do not occur exclusively in the context of a delirium.
D. The cognitive deficits are not better explained by another mental disorder (e.g., major
depressive disorder, schizophrenia).
Specify whether due to:
Alzheimer’s disease (pp. 611-614)
Frontotemporal lobar degeneration (pp. 614-618)
Lewy body disease (pp. 618-621)
Vascular disease (pp. 621-624)
Traumatic brain injury (pp. 624-627)
Substance/medication use (pp. 627-632)
HIV infection (pp. 632-634)
Prion disease (pp. 634-636)
Parkinson’s disease (pp. 636-638)
Huntington’s disease (pp. 638-641)
Another medical condition (pp. 641-642)
Multiple etiologies (pp. 642-643)
Unspecified (p. 643)
Coding note: For mild neurocognitive disorder due to any of the medical etiologies listed
above, code 331.83 (G31.84). Do not use additional codes for the presumed etiological
medical conditions. For substance/medication-induced mild neurocognitive disorder, code
based on type of substance; see “Substance/Medication-Induced Major or Mild Neurocog-
nitive Disorder.” For unspecified mild neurocognitive disorder, code 799.59 (R41.9).
606 Neurocognitive Disorders
Specify:
Without behavioral disturbance: If the cognitive disturbance is not accompanied by
any clinically significant behavioral disturbance.
With behavioral disturbance (specify disturbance): If the cognitive disturbance is ac-
companied by a clinically significant behavioral disturbance (e.g., psychotic symptoms,
mood disturbance, agitation, apathy, or other behavioral symptoms).
Subtypes
Major and mild neurocognitive disorders (NCDs) are primarily subtyped according to the
known or presumed etiological / pathological entity or entities underlying the cognitive de-
cline. These subtypes are distinguished on the basis of a combination of time course, charac-
teristic domains affected, and associated symptoms. For certain etiological subtypes, the
diagnosis depends substantially on the presence of a potentially causative entity, such as Par-
kinson’s or Huntington’s disease, or a traumatic brain injury or stroke in the appropriate time
period. For other etiological subtypes (generally the neurodegenerative diseases like Aizhei-
mer’s disease, frontotemporal lobar degeneration, and Lewy body disease), the diagnosis is
based primarily on the cognitive, behavioral, and functional symptoms. Typically, the differ-
entiation among these syndromes that lack an independently recognized etiological entity is
clearer at the level of major NCD than at the level of mild NCD, but sometimes characteristic
symptoms and associated features are present at the mild level as well.
NCDs are frequently managed by clinicians in multiple disciplines. For many sub-
types, multidisciplinary international expert groups have developed specialized consen-
sus criteria based on clinicopathological correlation with underlying brain pathology. The
subtype criteria here have been harmonized with those expert criteria.
Specifiers
Evidence for distinct behavioral features in NCDs has been recognized, particularly in the
areas of psychotic symptoms and depression. Psychotic features are common in many
NCDs, particularly at the mild-to-moderate stage of major NCDs due to Alzheimer’s dis-
ease, Lewy body disease, and frontotemporal lobar degeneration. Paranoia and other
delusions are common features, and often a persecutory theme may be a prominent aspect
of delusional ideation. In contrast to psychotic disorders with onset in earlier life (e.g.,
schizophrenia), disorganized speech and disorganized behavior are not characteristic of
psychosis in NCDs. Hallucinations may occur in any modality, although visual hallucina-
tions are more common in NCDs than in depressive, bipolar, or psychotic disorders.
Mood disturbances, including depression, anxiety, and elation, may occur. Depression
is common early in the course (including at the mild NCD level) of NCD due to Alzhei-
mer’s disease and Parkinson’s disease, while elation may occur more commonly in fron-
totemporal lobar degeneration. When a full affective syndrome meeting diagnostic criteria
for a depressive or bipolar disorder is present, that diagnosis should be coded as well.
Mood symptoms are increasingly recognized to be a significant feature in the earliest stages
of mild NCDs such that clinical recognition and intervention may be important.
Agitation is common in a wide variety of NCDs, particularly in major NCD of moder-
ate to severe severity, and often occurs in the setting of confusion or frustration. It may
arise as combative behaviors, particularly in the context of resisting caregiving duties such
as bathing and dressing. Agitation is characterized as disruptive motor or vocal activity
and tends to occur with advanced stages of cognitive impairment across all of the NCDs.
Individuals with NCD can present with a wide variety of behavioral symptoms that
are the focus of treatment. Sleep disturbance is a common symptom that can create a need
for clinical attention and may include symptoms of insomnia, hypersomnia, and circadian
rhythm disturbances.
Major and Mild Neurocognitive Disorders 607
Apathy is common in mild and mild major NCD. It is observed particularly in NCD due
to Alzheimer’s disease and may be a prominent feature of NCD due to frontotemporal
lobar degeneration. Apathy is typically characterized by diminished motivation and re-
duced goal-directed behavior accompanied by decreased emotional responsiveness.
Symptoms of apathy may manifest early in the course of NCDs when a loss of motivation
to pursue daily activities or hobbies may be observed.
Other important behavioral symptoms include wandering, disinhibition, hyperpha-
gia, and hoarding. Some of these symptoms are characteristic of specific disorders, as dis-
cussed in the relevant sections. When more than one behavioral disturbance is observed,
each type should be noted in writing with the specifier “with behavioral symptoms.”
Diagnostic Features
Major and mild NCDs exist on a spectrum of cognitive and functional impairment. Major
NCD corresponds to the condition referred to in DSM-IV as dementia, retained as an alter-
native in this volume. The core feature of NCDs is acquired cognitive decline in one or
more cognitive domains (Criterion A) based on both 1) a concern about cognition on the
part of the individual, a knowledgeable informant, or the clinician, and 2) performance on
an objective assessment that falls below the expected level or that has been observed to de-
cline over time. Both a concern and objective evidence are required because they are com-
plementary. When there is an exclusive focus on objective testing, a disorder may go
undiagnosed in high-functioning individuals whose currently “normal” performance ac-
tually represents a substantial decline in abilities, or an illness may be incorrectly diag-
nosed in individuals whose currently “low” performance does not represent a change
from their own baseline or is a result of extraneous factors like test conditions or a passing
illness. Alternatively, excessive focus on subjective symptoms may fail to diagnose illness
in individuals with poor insight, or whose informants deny or fail to notice their symptoms,
or it may be overly sensitive in the so-called worried well.
A cognitive concern differs from a complaint in that it may or may not be voiced spon-
taneously. Rather, it may need to be elicited by careful questioning about specific symp-
toms that commonly occur in individuals with cognitive deficits (see Table 1 in the
introduction to this chapter). For example, memory concerns include difficulty remember-
ing a short grocery list or keeping track of the plot of a television program; executive con-
cerns include difficulty resuming a task when interrupted, organizing tax records, or
planning a holiday meal. At the mild NCD level, the individual is likely to describe these
tasks as being more difficult or as requiring extra time or effort or compensatory strategies.
At the major NCD level, such tasks may only be completed with assistance or may be
abandoned altogether. At the mild NCD level, individuals and their families may not no-
tice such symptoms or may view them as normal, particularly in the elderly; thus, careful
history taking is of paramount importance. The difficulties must represent changes rather
than lifelong patterns: the individual or informant may clarify this issue, or the clinician
can infer change from prior experience with the patient or from occupational or other
clues. It is also critical to determine that the difficulties are related to cognitive loss rather
than to motor or sensory limitations.
Neuropsychological testing, with performance compared with norms appropriate to
the patient's age, educational attainment, and cultural background, is part of the standard
evaluation of NCDs and is particularly critical in the evaluation of mild NCD. For major
NCD, performance is typically 2 or more standard deviations below appropriate norms
(3rd percentile or below). For mild NCD, performance typically lies in the 1-2 standard de-
viation range (between the 3rd and 16th percentiles). However, neuropsychological test-
ing is not available in all settings, and neuropsychological thresholds are sensitive to the
specific test(s) and norms employed, as well as to test conditions, sensory limitations, and
intercurrent illness. A variety of brief office-based or “bedside” assessments, as described
608 Neurocognitive Disorders
in Table 1, can also supply objective data in settings where such testing is unavailable or
infeasible. In any case, as with cognitive concerns, objective performance must be inter-
preted in light of the individual’s prior performance. Optimally, this information would
be available from a prior administration of the same test, but often it must be inferred
based on appropriate norms, along with the individual's educational history, occupation,
and other factors. Norms are more challenging to interpret in individuals with very high
or very low levels of education and in individuals being tested outside their own language
or cultural background.
Criterion B relates to the individual’s level of independence in everyday functioning.
Individuals with major NCD will have impairment of sufficient severity so as to interfere
with independence, such that others will have to take over tasks that the individuals were
previously able to complete on their own. Individuals with mild NCD will have preserved
independence, although there may be subtle interference with function or a report that
tasks require more effort or take more time than previously.
The distinction between major and mild NCD is inherently arbitrary, and the disorders
exist along a continuum. Precise thresholds are therefore difficult to determine. Careful
history taking, observation, and integration with other findings are required, and the im-
plications of diagnosis should be considered when an individual's clinical manifestations
lie at a boundary.
Associated Features Supporting Diagnosis
Typically the associated features that support a diagnosis of major or mild NCD will be
specific to the etiological subtype (e.g., neuroleptic sensitivity and visual hallucinations in
NCD due to Lewy body disease). Diagnostic features specific to each of the subtypes are
found in the relevant sections.
Prevalence
The prevalence of NCD varies widely by age and by etiological subtype. Overall preva-
lence estimates are generally only available for older populations. Among individuals
older than 60 years, prevalence increases steeply with age, so prevalence estimates are
more accurate for narrow age bands than for broad categories such as “over 65” (where the
mean age can vary greatly with the life expectancy of the given population). For those eti-
ological subtypes occurring across the lifespan, prevalence estimates for NCD are likely to
be available, if at all, only as the fraction of individuals who develop NCD among those
with the relevant condition (e.g., traumatic brain injury, HIV infection).
Overall prevalence estimates for dementia (which is largely congruent with major
NCD) are approximately 1%-2% at age 65 years and as high as 30% by age 85 years. The
prevalence of mild NCD is very sensitive to the definition of the disorder, particularly in
community settings, where evaluations are less detailed. In addition, in contrast with clin-
ical settings, where cognitive concern must be high to seek and locate care, there may be a
less clear decline from baseline functioning. Estimates of the prevalence of mild cognitive
impairment (which is substantially congruent with mild NCD) among older individuals
are fairly variable, ranging from 2% to 10% at age 65 and 5% to 25% by age 85.
Development and Course
The course of NCD varies across etiological subtypes, and this variation can be useful in
differential diagnosis. Some subtypes (e.g., those related to traumatic brain injury or
stroke) typically begin at a specific time and (at least after initial symptoms related to in-
flammation or swelling subside) remain static. Others may fluctuate over time (although
if this occurs, the possibility of delirium superimposed on NCD should be considered).
NCDs due to neurodegenerative diseases like Alzheimer’s disease or frontotemporal
lobar degeneration typically are marked by insidious onset and gradual progression, and
Major and Mild Neurocognitive Disorders 609
the pattern of onset of cognitive deficits and associated features helps to distinguish among
them.
NCDs with onset in childhood and adolescence may have broad repercussions for so-
cial and intellectual development, and in this setting intellectual disability (intellectual
developmental disorder) and/or other neurodevelopmental disorders may also be diag-
nosed to capture the full diagnostic picture and ensure the provision of a broad range of
services. In older individuals, NCDs often occur in the setting of medical illnesses, frailty,
and sensory loss, which complicate the clinical picture for diagnosis and treatment.
When cognitive loss occurs in youth to midlife, individuals and families are likely to
seek care. NCDs are typically easiest to identify at younger ages, although in some settings
malingering or other factitious disorders may be a concern. Very late in life, cognitive
symptoms may not cause concern or may go unnoticed. In late life, mild NCD must also be
distinguished from the more modest deficits associated with “normal aging,” although a
substantial fraction of what has been ascribed to normal aging likely represents prodromal
phases of various NCDs. In addition, it becomes harder to recognize mild NCD with age
because of the increasing prevalence of medical illness and sensory deficits. It becomes
harder to differentiate among subtypes with age because there are multiple potential sources
of neurocognitive decline.
Risk and Prognostic Factors
Risk factors vary not only by etiological subtype but also by age at onset within etiological
subtypes. Some subtypes are distributed throughout the lifespan, whereas others occur
exclusively or primarily in late life. Even within the NCDs of aging, the relative prevalence
varies with age: Alzheimer’s disease is uncommon before age 60 years, and the prevalence
increases steeply thereafter, while the overall less common frontotemporal lobar degener-
ation has earlier onset and represents a progressively smaller fraction of NCDs with age.
Genetic and physiological. The strongest risk factor for major and mild NCDs is age,
primarily because age increases the risk of neurodegenerative and cerebrovascular dis-
ease. Female gender is associated with higher prevalence of dementia overall, and especially
Alzheimer’s disease, but this difference is largely, if not wholly, attributable to greater lon-
gevity in females.
Culture-Related Diagnostic Issues
Individuals’ and families’ level of awareness and concern about neurocognitive symp-
toms may vary across ethnic and occupational groups. Neurocognitive symptoms are
more likely to be noticed, particularly at the mild level, in individuals who engage in com-
plex occupational, domestic, or recreational activities. In addition, norms for neuropsy-
chological testing tend to be available only for broad populations, and thus they may not
be easily applicable to individuals with less than high school education or those being
evaluated outside their primary language or culture.
Gender-Related Diagnostic Issues
Like age, culture, and occupation, gender issues may affect the level of concern and aware-
ness of cognitive symptoms. In addition, for late-life NCDs, females are likely to be older,
to have more medical comorbidity, and to live alone, which can complicate evaluation and
treatment. In addition, there are gender differences in the frequency of some of the etio-
logical subtypes.
Diagnostic Markers
In addition to a careful history, neuropsychological assessments are the key measures for
diagnosis of NCDs, particularly at the mild level, where functional changes are minimal
610 Neurocognitive Disorders
and symptoms more subtle. Ideally, individuals will be referred for formal neuropsycho-
logical testing, which will provide a quantitative assessment of all relevant domains and
thus help with diagnosis; provide guidance to the family on areas where the individual
may require more support; and serve as a benchmark for further decline or response to
therapies. When such testing is unavailable or not feasible, the brief assessments in Table 1
can provide insight into each domain. More global brief mental status tests may be helpful
but may be insensitive, particularly to modest changes in a single domain or in those with
high premorbid abilities, and may be overly sensitive in those with low premorbid abilities.
In distinguishing among etiological subtypes, additional diagnostic markers may
come into play, particularly neuroimaging studies such as magnetic resonance imaging
scans and positron emission tomography scans. In addition, specific markers may be in-
volved in the assessment of specific subtypes and may become more important as addi-
tional research findings accumulate over time, as discussed in the relevant sections.
Functional Consequences of
Major and Mild Neurocognitive Disorders
By definition, major and mild NCDs affect functioning, given the central role of cognition in
human life. Thus, the criteria for the disorders, and the threshold for differentiating mild
from major NCD, are based in part on functional assessment. Within major NCD there is a
broad range of functional impairment, as implemented in the severity specifiers. In addition,
the specific functions that are compromised can help identify the cognitive domains affected,
particularly when neuropsychological testing is not available or is difficult to interpret.
Differential Diagnosis
Normal cognition. The differential diagnosis between normal cognition and mild NCD,
as between mild and major NCD, is challenging because the boundaries are inherently ar-
bitrary. Careful history taking and objective assessment are critical to these distinctions. A
longitudinal evaluation using quantified assessments may be key in detecting mild NCD.
Delirium. Both mild and major NCD may be difficult to distinguish from a persistent de-
lirium, which can co-occur. Careful assessment of attention and arousal will help to make
the distinction.
Major depressive disorder. The distinction between mild NCD and major depressive
disorder, which may co-occur with NCD, can also be challenging. Specific patterns of cog-
nitive deficits may be helpful. For example, consistent memory and executive function
deficits are typical of Alzheimer’s disease, whereas nonspecific or more variable perfor-
mance is seen in major depression. Alternatively, treatment of the depressive disorder
with repeated observation over time may be required to make the diagnosis.
Specific learning disorder and other neurodevelopmental disorders. A careful clari-
fication of the individual's baseline status will help distinguish an NCD from a specific
learning disorder or other neurodevelopmental disorders. Additional issues may enter the
differential for specific etiological subtypes, as described in the relevant sections.
Comorbidity
NCDs are common in older individuals and thus often co-occur with a wide variety of age-
related diseases that may complicate diagnosis or treatment. Most notable of these is
delirium, for which NCD increases the risk. In older individuals, a delirium during hos-
pitalization is, in many cases, the first time that an NCD is noticed, although a careful his-
tory will often reveal evidence of earlier decline. Mixed NCDs are also common in older
individuals, as many etiological entities increase in prevalence with age. In younger indi-
viduals, NCD often co-occurs with neurodevelopmental disorders; for example, a head in-
Major or Mild Neurocognitive Disorder Due to Alzheimer’s Disease 611
jury in a preschool child may also lead to significant developmental and learning issues.
Additional comorbidity of NCD is often related to the etiological subtype, as discussed in
the relevant sections.
Major or Mild Neurocognitive Disorder
Due to Alzheimer’s Disease
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. There is insidious onset and gradual progression of impairment in one or more cognitive
domains (for major neurocognitive disorder, at least two domains must be impaired).
C. Criteria are met for either probable or possible Alzheimer’s disease as follows:
For major neurocognitive disorder:
Probable Alzheimer’s disease is diagnosed if either of the following is present; oth-
erwise, possible Alzheimer’s disease should be diagnosed.
1. Evidence of a causative Alzheimer’s disease genetic mutation from family history
or genetic testing.
2. All three of the following are present:
a. Clear evidence of decline in memory and learning and at least one other cogni-
tive domain (based on detailed history or serial neuropsychological testing).
b. Steadily progressive, gradual decline in cognition, without extended plateaus.
c. No evidence of mixed etiology (i.e., absence of other neurodegenerative or
cerebrovascular disease, or another neurological, mental, or systemic disease
or condition likely contributing to cognitive decline).
For mild neurocognitive disorder:
Probable Alzheimer’s disease is diagnosed if there is evidence of a causative Alz-
heimer’s disease genetic mutation from either genetic testing or family history.
Possible Alzheimer’s disease is diagnosed if there is no evidence of a causative Alz-
heimer’s disease genetic mutation from either genetic testing or family history, and all
three of the following are present:
1. Clear evidence of decline in memory and learning.
2. Steadily progressive, gradual decline in cognition, without extended plateaus.
3. No evidence of mixed etiology (i.e., absence of other neurodegenerative or cere-
brovascular disease, or another neurological or systemic disease or condition likely
contributing to cognitive decline).
D. The disturbance is not better explained by cerebrovascular disease, another neurode-
generative disease, the effects of a substance, or another mental, neurological, or sys-
temic disorder.
Coding note: For probable major neurocognitive disorder due to Alzheimer’s disease,
with behavioral disturbance, code first 331.0 (G30.9) Alzheimer’s disease, followed by
294.11 (F02.81) major neurocognitive disorder due to Alzheimer’s disease. For probable
neurocognitive disorder due to Alzheimer’s disease, without behavioral disturbance, code
first 331.0 (G30.9) Alzheimer’s disease, followed by 294.10 (F02.80) major neurocognitive
disorder due to Alzheimer’s disease, without behavioral disturbance.
For possible major neurocognitive disorder due to Alzheimer’s disease, code 331.9
(G31.9) possible major neurocognitive disorder due to Alzheimer’s disease. (Note: Do not
use the additional code for Alzheimer’s disease. Behavioral disturbance cannot be coded
but should still be indicated in writing.)
612 Neurocognitive Disorders
For mild neurocognitive disorder due to Alzheimer's disease, code 331.83 (G31.84).
(Note: Do not use the additional code for Alzheimer’s disease. Behavioral disturbance
cannot be coded but should still be indicated in writing.)
Diagnostic Features
Beyond the neurocognitive disorder (NCD) syndrome (Criterion A), the core features of ma-
jor or mild NCD due to Alzheimer’s disease include an insidious onset and gradual pro-
gression of cognitive and behavioral symptoms (Criterion B). The typical presentation is
amnestic (i.e., with impairment in memory and learning). Unusual nonamnestic presen-
tations, particularly visuospatial and logopenic aphasic variants, also exist. At the mild
NCD phase, Alzheimer’s disease manifests typically with impairment in memory and learn-
ing, sometimes accompanied by deficits in executive function. At the major NCD phase,
visuoconstructional/ perceptual motor ability and language will also be impaired, partic-
ularly when the NCD is moderate to severe. Social cognition tends to be preserved until
late in the course of the disease.
A level of diagnostic certainty must be specified denoting Alzheimer’s disease as the
“probable” or “possible” etiology (Criterion C). Probable Alzheimer’s disease is diagnosed in
both major and mild NCD if there is evidence of a causative Alzheimer’s disease gene, ei-
ther from genetic testing or from an autosomal dominant family history coupled with au-
topsy confirmation or a genetic test in an affected family member. For major NCD, a
typical clinical picture, without extended plateaus or evidence of mixed etiology, can also
be diagnosed as due to probable Alzheimer’s disease. For mild NCD, given the lesser de-
gree of certainty that the deficits will progress, these features are only sufficient for a
possible Alzheimer’s etiology. If the etiology appears mixed, mild NCD due to multiple eti-
ologies should be diagnosed. In any case, for both mild and major NCD due to Alzhei-
mer’s disease, the clinical features must not suggest another primary etiology for the NCD
(Criterion D).
Associated Features Supporting Diagnosis
In specialty clinical settings, approximately 80% of individuals with major NCD due to
Alzheimer’s disease have behavioral and psychological manifestations; these features are
also frequent at the mild NCD stage of impairment. These symptoms are as or more dis-
tressing than cognitive manifestations and are frequently the reason that health care is
sought. At the mild NCD stage or the mildest level of major NCD, depression and/or ap-
athy are often seen. With moderately severe major NCD, psychotic features, irritability,
agitation, combativeness, and wandering are common. Late in the illness, gait distur-
bance, dysphagia, incontinence, myoclonus, and seizures are observed.
Prevalence
The prevalence of overall dementia (major NCD) rises steeply with age. In high-income
countries, it ranges from 5% to 10% in the seventh decade to at least 25% thereafter. U.S.
census data estimates suggest that approximately 7% of individuals diagnosed with Alz-
heimer’s disease are between ages 65 and 74 years, 53% are between ages 75 and 84 years,
and 40% are 85 years and older. The percentage of dementias attributable to Alzheimer’s
disease ranges from about 60% to over 90%, depending on the setting and diagnostic cri-
teria. Mild NCD due to Alzheimer’s disease is likely to represent a substantial fraction of
mild cognitive impairment (MCI) as well.
Development and Course
Major or mild NCD due to Alzheimer’s disease progresses gradually, sometimes with
brief plateaus, through severe dementia to death. The mean duration of survival after di-
Major or Mild Neurocognitive Disorder Due to Alzheimer’s Disease 613
agnosis is approximately 10 years, reflecting the advanced age of the majority of individ-
uals rather than the course of the disease; some individuals can live with the disease for as
long as 20 years. ‘Late-stage individuals are eventually mute and bedbound. Death most
commonly results from aspiration in those who survive through the full course. In mild
NCD due to Alzheimer’s disease, impairments increase over time, and functional status
gradually declines until symptoms reach the threshold for the diagnosis of major NCD.
The onset of symptoms is usually in the eighth and ninth decades; early-onset forms
seen in the fifth and sixth decades are often related to known causative mutations. Symp-
toms and pathology do not differ markedly at different onset ages. However, younger in-
dividuals are more likely to survive the full course of the disease, while older individuals
are more likely to have numerous medical comorbidities that affect the course and man-
agement of the illness. Diagnostic complexity is higher in older adults because of the in-
creased likelihood of comorbid medical illness and mixed pathology.
Risk and Prognostic Factors
Environmental. Traumatic brain injury increases risk for major or mild NCD due to Alz-
heimer’s disease.
Genetic and physiological. Age is the strongest risk factor for Alzheimer’s disease. The
genetic susceptibility polymorphism apolipoprotein E4 increases risk and decreases age
at onset, particularly in homozygous individuals. There are also extremely rare causative
Alzheimer’s disease genes. Individuals with Down’s syndrome (trisomy 21) develop Alz-
heimer’s disease if they survive to midlife. Multiple vascular risk factors influence risk for
Alzheimer’s disease and may act by increasing cerebrovascular pathology or also through
direct effects on Alzheimer pathology.
Culture-Related Diagnostic Issues
Detection of an NCD may be more difficult in cultural and socioeconomic settings where
memory loss is considered normal in old age, where older adults face fewer cognitive de-
mands in everyday life, or where very low educational levels pose greater challenges to
objective cognitive assessment.
Diagnostic Markers
Cortical atrophy, amyloid-predominant neuritic plaques, and tau-predominant neurofibril-
lary tangles are hallmarks of the pathological diagnosis of Alzheimer’s disease and may be
confirmed via postmortem histopathological examination. For early-onset cases with auto-
somal dominant inheritance, a mutation in one of the known causative Alzheimer’s disease
genes—amyloid precursor protein (APP), presenilin 1 (PSEN1), or presenilin 2 (PSEN2)-—
may be involved, and genetic testing for such mutations is commercially available, at least
for PSEN1. Apolipoprotein E4 cannot serve as a diagnostic marker because it is only a risk
factor and neither necessary nor sufficient for disease occurrence.
Since amyloid beta-42 deposition in the brain occurs early in the pathophysiological
cascade, amyloid-based diagnostic tests such as amyloid imaging on brain positron emis-
sion tomography (PET) scans and reduced levels of amyloid beta-42 in the cerebrospinal
fluid (CSF) may have diagnostic value. Signs of neuronal injury, such as hippocampal and
temporoparietal cortical atrophy on a magnetic resonance image scan, temporoparietal
hypometabolism on a fluorodeoxyglucose PET scan, and evidence for elevated total tau
and phospho-tau levels in CSF, provide evidence of neuronal damage but are less specific
for Alzheimer’s disease. At present, these biomarkers are not fully validated, and many
are available only in tertiary care settings. However, some of them, along with novel bio-
markers, will likely move into wider clinical practice in the coming years.
614 Neurocognitive Disorders
Functional Consequences of Major or Mild
Neurocognitive Disorder Due to Alzheimer’s Disease
The prominence of memory loss can cause significant difficulties relatively early in the
course. Social cognition (and thus social functioning) and procedural memory (e.g., danc-
ing, playing musical instruments) may be relatively preserved for extended periods.
Differential Diagnosis
Other neurocognitive disorders. Major and mild NCDs due to other neurodegenera-
tive processes (e.g., Lewy body disease, frontotemporal lobar degeneration) share the in-
sidious onset and gradual decline caused by Alzheimer’s disease but have distinctive core
features of their own. In major or mild vascular NCD, there is typically history of stroke
temporally related to the onset of cognitive impairment, and infarcts or white matter hy-
perintensities are judged sufficient to account for the clinical picture. However, particu-
larly when there is no clear history of stepwise decline, major or mild vascular NCD can
share many clinical features with Alzheimer’s disease.
Other concurrent, active neurological or systemic illness. Other neurological or sys-
temic illness should be considered if there is an appropriate temporal relationship and
severity to account for the clinical picture. At the mild NCD level, it may be difficult to dis-
tinguish an Alzheimer’s disease etiology from that of another medical condition (e.g., thy-
roid disorders, vitamin B,7 deficiency).
Major depressive disorder. Particularly at the mild NCD level, the differential diagnosis
also includes major depression. The presence of depression may be associated with re-
duced daily functioning and poor concentration that may resemble an NCD, but improve-
ment with treatment of depression may be useful in making the distinction.
Comorbidity
Most individuals with Alzheimer’s disease are elderly and have multiple medical conditions
that can complicate diagnosis and influence the clinical course. Major or mild NCD due to
Alzheimer’s disease commonly co-occurs with cerebrovascular disease, which contributes
to the clinical picture. When a comorbid condition contributes to the NCD in an individual
with Alzheimer’s disease, then NCD due to multiple etiologies should be diagnosed.
Major or Mild Frontotemporal
Neurocognitive Disorder
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. The disturbance has insidious onset and gradual progression.
C. Either {1} or (2):
1. Behavioral variant:
a. Three or more of the following behavioral symptoms:
i. Behavioral disinhibition.
ii. Apathy or inertia.
ii. Loss of sympathy or empathy.
iv. Perseverative, stereotyped or compulsive/ritualistic behavior.
v. Hyperorality and dietary changes.
b. Prominent decline in social cognition and/or executive abilities.
Major or Mild Frontotemporal Neurocognitive Disorder 615
2. Language variant:
a. Prominent decline in language ability, in the form of speech production, word
finding, object naming, grammar, or word comprehension.
D. Relative sparing of learning and memory and perceptual-motor function.
E. The disturbance is not better explained by cerebrovascular disease, another neurode-
generative disease, the effects of a substance, or another mental, neurological, or sys-
temic disorder.
Probable frontotemporal neurocognitive disorder is diagnosed if either of the following
is present; otherwise, possible frontotemporal neurocognitive disorder should be di-
agnosed:
1. Evidence of a causative frontotemporal neurocognitive disorder genetic mutation, from
either family history or genetic testing.
2. Evidence of disproportionate frontal and/or temporal lobe involvement from neuroim-
aging.
Possible frontotemporal neurocognitive disorder is diagnosed if there is no evidence
of a genetic mutation, and neuroimaging has not been performed.
Coding note: For probable major neurocognitive disorder due to frontotemporal lobar de-
generation, with behavioral disturbance, code first 331.19 (G31.09) frontotemporal dis-
ease, followed by 294.11 (F02.81) probable major neurocognitive disorder due to
frontotemporal lobar degeneration, with behavioral disturbance. For probable major neu-
rocognitive disorder due to frontotemporal lobar degeneration, without behavioral distur-
bance, code first 331.19 (G31.09) frontotemporal disease, followed by 294.10 (F02.80)
probable major neurocognitive disorder due to frontotemporal lobar degeneration, without
behavioral disturbance.
For possible major neurocognitive disorder due to frontotemporal lobar degeneration, code
331.9 (G31.9) possible major neurocognitive disorder due to frontotemporal lobar degen-
eration. (Note: Do not use the additional code for frontotemporal disease. Behavioral distur-
bance cannot be coded but should still be indicated in writing.)
For mild neurocognitive disorder due to frontotemporal lobar degeneration, code 331.83
(G31.84). (Note: Do not use the additional code for frontotemporal disease. Behavioral
disturbance cannot be coded but should still be indicated in writing.)
Diagnostic Features
Major or mild frontotemporal neurocognitive disorder (NCD) comprises a number of syn-
dromic variants characterized by the progressive development of behavioral and personality
change and/or language impairment. The behavioral variant and three language variants (se-
mantic, agrammatic/nonfluent, and logopenic) exhibit distinct patterns of brain atrophy and
some distinctive neuropathology. The criteria must be met for either the behavioral or the lan-
guage variant to make the diagnosis, but many individuals present with features of both.
Individuals with behavioral-variant major or mild frontotemporal NCD present with
varying degrees of apathy or disinhibition. They may lose interest in socialization, self-
care, and personal responsibilities, or display socially inappropriate behaviors. Insight is
usually impaired, and this often delays medical consultation. The first referral is often to a
psychiatrist. Individuals may develop changes in social style, and in religious and political
beliefs, with repetitive movements, hoarding, changes in eating behavior, and hyperoral-
ity. In later stages, loss of sphincter control may occur. Cognitive decline is less prominent,
and formal testing may show relatively few deficits in the early stages. Common neuro-
cognitive symptoms are lack of planning and organization, distractibility, and poor judg-
ment. Deficits in executive function, such as poor performance on tests of mental
616 Neurocognitive Disorders
flexibility, abstract reasoning, and response inhibition, are present, but learning and mem-
ory are relatively spared, and perceptual motor abilities are almost always preserved in
the early stages.
Individuals with language-variant major or mild frontotemporal NCD present with pri-
mary progressive aphasia with gradual onset, with three subtypes commonly described:
semantic variant, agrammatic/nonfluent variant, and logopenic variant, and each variant
has distinctive features and corresponding neuropathology.
“Probable” is distinguished from “possible” frontotemporal NCD by the presence of
causative genetic factors (e.g., mutations in the gene coding for microtubule-associated pro-
tein tau) or by the presence of distinctive atrophy or reduced activity in frontotemporal re-
gions on structural or functional imaging.
Associated Features Supporting Diagnosis
Extrapyramidal features may be prominent in some cases, with an overlap with syn-
dromes such as progressive supranuclear palsy and corticobasal degeneration. Features of
motor neuron disease may be present in some cases (e.g., muscle atrophy, weakness). A
subset of individuals develop visual hallucinations.
Prevalence
Major or mild frontotemporal NCD is a common cause of early-onset NCD in individuals
younger than 65 years. Population prevalence estimates are in the range of 2-10 per
100,000. Approximately 20%-25% of cases of frontotemporal NCD occur in individuals
older than 65 years. Frontotemporal NCD accounts for about 5% of all cases of dementia in
unselected autopsy series. Prevalence estimates of behavioral variant and semantic lan-
guage variant are higher among males, and prevalence estimates of nonfluent language
variant are higher among females.
Development and Course
Individuals with major or mild frontotemporal NCD commonly present in the sixth de-
cade of life, although the age at onset varies from the third to the ninth decades. The dis-
ease is gradually progressive, with median survival being 6-11 years after symptom onset
and 34 years after diagnosis. Survival is shorter and decline is faster in major or mild fron-
totemporal NCD than in typical Alzheimer’s disease.
Risk and Prognostic Factors
Genetic and physiological. Approximately 40% of individuals with major or mild fron-
totemporal NCD have a family history of early-onset NCD, and approximately 10% show an
autosomal dominant inheritance pattern. A number of genetic factors have been identified,
such as mutations in the gene encoding the microtubule associated protein tau (MAPT), the
granulin gene (GRN), and the C9ORF72 gene. A number of families with causative muta-
tions have been identified (see the section “Diagnostic Markers” for this disorder), but many
individuals with known familial transmission do not have a known mutation. The presence
of motor neuron disease is associated with a more rapid deterioration.
Diagnostic Markers
Computed tomography (CT) or structural magnetic resonance imaging (MRI) may show
distinct patterns of atrophy. In behavioral-variant major or mild frontotemporal NCD,
both frontal lobes (especially the medial frontal lobes) and the anterior temporal lobes are
atrophic. In semantic language—variant major or mild frontotemporal NCD, the middle,
inferior, and anterior temporal lobes are atrophic bilaterally but asymmetrically, with the
Major or Mild Frontotemporal Neurocognitive Disorder 617
left side usually being more affected. Nonfluent language—variant major or mild fronto-
temporal NCD is associated with predominantly left posterior frontal-insular atrophy.
The logopenic variant of major or mild frontotemporal NCD is associated with predomi-
nantly left posterior perisylvian or parietal atrophy. Functional imaging demonstrates hy-
poperfusion and/or cortical hypometabolism in the corresponding brain regions, which
may be present in the early stages in the absence of structural abnormality. Emerging bio-
markers for Alzheimer’s disease (e.g., cerebrospinal fluid amyloid-beta and tau levels, and
amyloid imaging) may help in the differential diagnosis, but the distinction from Alzhei-
mer’s disease can remain difficult (the logopenic variant is in fact often a manifestation of
Alzheimer’s disease).
In familial cases of frontotemporal NCD, the identification of genetic mutations may
help confirm the diagnosis. Mutations associated with frontotemporal NCD include
the genes encoding microtubule-associated protein tau (MAPT) and granulin (GRN),
C9IORF72, transactive response DNA-binding protein of 43 kDa (TDP-43, or TARDBP),
valosin-containing protein (VCP), chromatin modifying protein 2B (CHMP2B), and fused
in sarcoma protein (FUS).
Functional Consequences of Major or Mild
Frontotemporal Neurocognitive Disorder
Because of the relative early age at onset of the disorder, the disorder oftens affects work-
place and family life. Because of the involvement of language and/or behavior, function is
often more severely impaired relatively early in the course. For individuals with the be-
havioral variant, prior to diagnostic clarification there may be significant family disrup-
tion, legal involvement, and problems in the workplace because of socially inappropriate
behaviors. The functional impairment due to behavioral change and language dysfunc-
tion, which can include hyperorality, impulsive wandering, and other dishinhibited be-
haviors, may far exceed that due to the cognitive disturbance and may lead to nursing
home placement or institutionalization. These behaviors can be severely disruptive, even
in structured care settings, particularly when the individuals are otherwise healthy, non-
frail, and free of other medical comorbidities.
Differential Diagnosis
Other neurocognitive disorders. Other neurodegenerative diseases may be distinguished
from major or mild frontotemporal NCD by their characteristic features. In major or mild
NCD due to Alzheimer’s disease, decline in learning and memory is an early feature.
However, 10%-30% of patients presenting with a syndrome suggestive of major or mild
frontotemporal NCD are found at autopsy to have Alzheimer’s disease pathology. This oc-
curs more frequently in individuals who present with progressive dysexecutive syn-
dromes in the absence of behavioral changes or movement disorder or in those with the
logopenic variant.
In major or mild NCD with Lewy bodies, core and suggestive features of Lewy bodies
must be present. In major or mild NCD due to Parkinson’s disease, spontaneous parkin-
sonism emerges well before the cognitive decline. In major or mild vascular NCD, depend-
ing on affected brain regions, there may also be loss of executive ability and behavioral
changes such as apathy, and this disorder should be considered in the differential diagno-
sis. However, history of a cerebrovascular event is temporally related to the onset of cog-
nitive impairment in major or mild vascular NCD, and neuroimaging reveals infarctions
or white matter lesions sufficient to account for the clinical picture.
Other neurological conditions. Major or mild frontotemporal NCD overlaps with pro-
gressive supranuclear palsy, corticobasal degeneration, and motor neuron disease
clinically as well as pathologically. Progressive supranuclear palsy is characterized by
618 Neurocognitive Disorders
supranuclear gaze palsies and axial-predominant parkinsonism. Pseudobulbar signs may
be present, and retropulsion is often prominent. Neurocognitive assessment shows psy-
chomotor slowing, poor working memory, and executive dysfunction. Corticobasal degen-
eration presents with asymmetric rigidity, limb apraxia, postural instability, myoclonus,
alien limb phenomenon, and cortical sensory loss. Many individuals with behavioral-variant
major or mild frontotemporal NCD show features of motor neuron disease, which tend to
be mixed upper and predominantly lower motor neuron disease.
Other mental disorders and medical conditions. Behavioral-variant major or mild fron-
totemporal NCD may be mistaken for a primary mental disorder, such as major depression,
bipolar disorders, or schizophrenia, and individuals with this variant often present initially
to psychiatry. Over time, the development of progressive neurocognitive difficulties will
help to make the distinction. A careful medical evaluation will help to exclude treatable
causes of NCDs, such as metabolic disturbances, nutritional deficiencies, and infections.
Major or Mild Neurocognitive Disorder
With Lewy Bodies
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. The disorder has an insidious onset and gradual progression.
C. The disorder meets a combination of core diagnostic features and suggestive diagnos-
tic features for either probable or possible neurocognitive disorder with Lewy bodies.
For probable major or mild neurocognitive disorder with Lewy bodies, the indi-
vidual has two core features, or one suggestive feature with one or more core features.
For possible major or mild neurocognitive disorder with Lewy bodies, the individ-
ual has only one core feature, or one or more suggestive features.
1. Core diagnostic features:
a. Fluctuating cognition with pronounced variations in attention and alertness.
b. Recurrent visual hallucinations that are well formed and detailed.
c. Spontaneous features of parkinsonism, with onset subsequent to the develop-
ment of cognitive decline.
2. Suggestive diagnostic features:
a. Meets criteria for rapid eye movement sleep behavior disorder.
b. Severe neuroleptic sensitivity.
D. The disturbance is not better explained by cerebrovascular disease, another neurode-
generative disease, the effects of a substance, or another mental, neurological, or sys-
temic disorder.
Coding note: For probable major neurocognitive disorder with Lewy bodies, with behav-
ioral disturbance, code first 331.82 (G31.83) Lewy body disease, followed by 294.11
(F02.81) probable major neurocognitive disorder with Lewy bodies, with behavioral distur-
bance. For probable major neurocognitive disorder with Lewy bodies, without behavioral
disturbance, code first 331.82 (G31.83) Lewy body disease, followed by 294.10 (F02.80)
probable major neurocognitive disorder with Lewy bodies, without behavioral disturbance.
For possible major neurocognitive disorder with Lewy bodies, code 331.9 (G31.9) possible
major neurocognitive disorder with Lewy bodies. (Note: Do not use the additional code for
Lewy body disease. Behavioral disturbance cannot be coded but should still be indicated
in writing.)
Major or Mild Neurocognitive Disorder With Lewy Bodies 619
For mild neurocognitive disorder with Lewy bodies, code 331.83 (G31.84). (Note: Do not
use the additional code for Lewy body disease. Behavioral disturbance cannot be coded
but should still be indicated in writing.)
Diagnostic Features
Major or mild neurocognitive disorder with Lewy bodies (NCDLB), in the case of major
neurocognitive disorder (NCD), corresponds to the condition known as dementia with
Lewy bodies (DLB). The disorder includes not only progressive cognitive impairment
(with early changes in complex attention and executive function rather than learning and
memory) but also recurrent complex visual hallucinations; and concurrent symptoms of
rapid eye movement (REM) sleep behavior disorder (which can be a very early manifes-
tation); as well as hallucinations in other sensory modalities, depression, and delusions.
The symptoms fluctuate in a pattern that can resemble a delirium, but no adequate under-
lying cause can be found. The variable presentation of NCDLB symptoms reduces the like-
lihood of all symptoms being observed in a brief clinic visit and necessitates a thorough
assessment of caregiver observations. The use of assessment scales specifically designed to
assess fluctuation may aid in diagnosis. Another core feature is spontaneous parkinson-
ism, which must begin after the onset of cognitive decline; by convention, major cognitive
deficits are observed at least 1 year before the motor symptoms. The parkinsonism must
also be distinguished from neuroleptic-induced extrapyramidal signs. Accurate diagnosis
is essential to safe treatment planning, as up to 50% of individuals with NCDLB have se-
vere sensitivity to neuroleptic drugs, and these medications should be used with extreme
caution in managing the psychotic manifestations.
The diagnosis of mild NCDLB is appropriate for individuals who present with the core
or suggestive features at a stage when cognitive or functional impairments are not of suf-
ficient severity to fulfill criteria for major NCD. However, as for all mild NCDs, there will
often be insufficient evidence to justify any single etiology, and use of the unspecified di-
agnosis is most appropriate.
Associated Features Supporting Diagnosis
Individuals with NCDLB frequently experience repeated falls and syncope and transient
episodes of unexplained loss of consciousness. Autonomic dysfunction, such as ortho-
static hypotension and urinary incontinence, may be observed. Auditory and other
nonvisual hallucinations are common, as are systematized delusions, delusional misiden-
tification, and depression.
Prevalence
The few population-based prevalence estimates for NCDLB available range from 0.1% to
5% of the general elderly population, and from 1.7% to 30.5% of all dementia cases. In
brain bank (autopsy) series, the pathological lesions known as Lewy bodies are present in
20%-35% of cases of dementia. The male-to-female ratio is approximately 1.5:1.
Development and Course
NCDLB is a gradually progressive disorder with insidious onset. However, there is often
a prodromal history of confusional episodes (delirium) of acute onset, often precipitated
by illness or surgery. The distinction between NCDLB, in which Lewy bodies are primar-
ily cortical in location, and major or mild NCD due to Parkinson’s disease, in which the pa-
thology is primarily in the basal ganglia, is the order in which the cognitive and motor
symptoms emerge. In NCDLB, the cognitive decline is manifested early in the course of ill-
ness, at least a year before the onset of motor symptoms (see the section “Differential Di-
620 Neurocognitive Disorders
agnosis” for this disorder). Disease course may be characterized by occasional plateaus
but eventually progresses through severe dementia to death. Average duration of survival
is 5-7 years in clinical series. Onset of symptoms is typically observed from the sixth
through the ninth decades of life, with most cases having their onset when affected indi-
viduals are in their mid-70s.
Risk and Prognostic Factors
Genetic and physiological. Familial aggregation may occur, and several risk genes have
been identified, but in most cases of NCDLB, there is no family history.
Diagnostic Markers
The underlying neurodegenerative disease is primarily a synucleinopathy due to alpha-
synuclein misfolding and aggregation. Cognitive testing beyond the use of a brief screen-
ing instrument may be necessary to define deficits clearly. Assessment scales developed to
measure fluctuation can be useful. The associated condition REM sleep behavior disorder
may be diagnosed through a formal sleep study or identified by questioning the patient or
informant about relevant symptoms. Neuroleptic sensitivity (challenge) is not recom-
mended as a diagnostic marker but raises suspicion of NCDLB if it occurs. A diagnosti-
cally suggestive feature is low striatal dopamine transporter uptake on single photon
emission computed tomography (SPECT) or positron emission tomography (PET) scan.
Other clinically useful markers potentially include relative preservation of medial tempo-
ral structures on computed tomography (CT)/magnetic resonance imaging (MRI) brain
scan; reduced striatal dopamine transporter uptake on SPECT /PET scan; generalized low
uptake on SPECT/PET perfusion scan with reduced occipital activity; abnormal (low up-
take) MIBG myocardial scintigraphy suggesting sympathetic denervation; and prominent
slow-wave activity on the electroencephalogram with temporal lobe transient waves.
Functional Consequences of Major or Miid
Neurocognitive Disorder With Lewy Bodies
Individuals with NCDLB are more functionally impaired than would be expected for their
cognitive deficits when contrasted to individuals with other neurodegenerative diseases,
such as Alzheimer’s disease. This is largely a result of motor and autonomic impairments,
which cause problems with toileting, transferring, and eating. Sleep disorders and prom-
inent psychiatric symptoms may also add to functional difficulties. Consequently, the qual-
ity of life of individuals with NCDLB is often significantly worse than that of individuals
with Alzheimer’s disease.
Differential Diagnosis
Major or mild neurocognitive disorder due to Parkinson’s disease. A key differenti-
ating feature in clinical diagnosis is the temporal sequence in which the parkinsonism and
the NCD appear. For NCD due to Parkinson’s disease, the individual must develop cog-
nitive decline in the context of established Parkinson’s disease; by convention, the decline
should not reach the stage of major NCD until at least 1 year after Parkinson’s is diagnosed.
If less than a year has passed since the onset of motor symptoms, the diagnosis is NCDLB.
This distinction is clearer at the major NCD level than at the mild NCD level.
The timing and sequence of parkinsonism and mild NCD may be more difficult to de-
termine because the onset and clinical presentation can be ambiguous, and unspecified
mild NCD should be diagnosed if the other core and suggestive features are absent.
Major or Mild Vascular Neurocognitive Disorder 621
Comorbidity
Lewy body pathology frequently coexists with Alzheimer’s disease and cerebrovascular
disease pathology, particularly among the oldest age groups. In Alzheimer’s disease, there
is concomitant synuclein pathology in 60% of cases (if amygdala-restricted cases are in-
cluded). In general, there is a higher rate of Lewy body pathology in individuals with de-
mentia than in older individuals without dementia.
Major or Mild Vascular Neurocognitive Disorder
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. The clinical features are consistent with a vascular etiology, as suggested by either of
the following:
1. Onset of the cognitive deficits is temporally related to one or more cerebrovascular
events.
2. Evidence for decline is prominent in complex attention (including processing
speed) and frontal-executive function.
C. There is evidence of the presence of cerebrovascular disease from history, physical
examination, and/or neuroimaging considered sufficient to account for the neurocog-
nitive deficits.
D, The symptoms are not better explained by another brain disease or systemic disorder.
Probable vascular neurocognitive disorder is diagnosed if one of the following is pres-
ent; otherwise possible vascular neurocognitive disorder should be diagnosed:
1. Clinical criteria are supported by neuroimaging evidence of significant parenchymal in-
jury attributed to cerebrovascular disease (neuroimaging-supported).
2. The neurocognitive syndrome is temporally related to one or more documented cere-
brovascular events.
3. Both clinical and genetic (e.g., cerebral autosomal dominant arteriopathy with subcortical
infarcts and leukoencephalopathy) evidence of cerebrovascular disease is present.
Possible vascular neurocognitive disorder is diagnosed if the clinical criteria are met
but neuroimaging is not available and the temporal relationship of the neurocognitive syn-
drome with one or more cerebrovascular events is not established.
Coding note: For probable major vascular neurocognitive disorder, with behavioral dis-
turbance, code 290.40 (F01.51). For probable major vascular neurocognitive disorder,
without behavioral disturbance, code 290.40 (F01.50). For possible major vascular neuro-
cognitive disorder, with or without behavioral disturbance, code 331.9 (G31.9). An addi-
tional medical code for the cerebrovascular disease is not needed.
For mild vascular neurocognitive disorder, code 331.83 (G31.84). (Note: Do not use an
additional code for the vascular disease. Behavioral disturbance cannot be coded but
should still be indicated in writing.)
Diagnostic Features
The diagnosis of major or mild vascular neurocognitive disorder (NCD) requires the es-
tablishment of an NCD (Criterion A) and the determination that cerebrovascular disease is
the dominant if not exclusive pathology that accounts for the cognitive deficits (Criteria B
and C). Vascular etiology may range from large vessel stroke to microvascular disease; the
622 Neurocognitive Disorders
presentation is therefore very heterogeneous, stemming from the types of vascular lesions
and their extent and location. The lesions may be focal, multifocal, or diffuse and occur in
various combinations.
Many individuals with major or mild vascular NCD present with multiple infarctions,
with an acute stepwise or fluctuating decline in cognition, and intervening periods of
stability and even some improvement. Others may have gradual onset with slow pro-
gression, a rapid development of deficits followed by relative stability, or another complex
presentation. Major or mild vascular NCD with a gradual onset and slow progression is
generally due to small vessel disease leading to lesions in the white matter, basal ganglia,
and/or thalamus. The gradual progression in these cases is often punctuated by acute
events that leave subtle neurological deficits. The cognitive deficits in these cases can be at-
tributed to disruption of cortical-subcortical circuits, and complex attention, particularly
speed of information processing, and executive ability are likely to be affected.
Assessing for the presence of sufficient cerebrovascular disease relies on history, phys-
ical examination, and neuroimaging (Criterion C). Etiological certainty requires the dem-
onstration of abnormalities on neuroimaging. The lack of neuroimaging can result in
significant diagnostic inaccuracy by overlooking “silent” brain infarction and white mat-
ter lesions. However, if the neurocognitive impairment is temporally associated with one
or more well-documented strokes, a probable diagnosis can be made in the absence of neu-
roimaging. Clinical evidence of cerebrovascular disease includes documented history of
stroke, with cognitive decline temporally associated with the event, or physical signs con-
sistent with stroke (e.g., hemiparesis; pseudobulbar syndrome, visual field defect). Neuro-
imaging (magnetic resonance imaging [MRI] or computed tomography [CT]) evidence of
cerebrovascular disease comprises one or more of the following: one or more large vessel
infarcts or hemorrhages, a strategically placed single infarct or hemorrhage (e.g., in angu-
lar gyrus, thalamus, basal forebrain), two or more lacunar infarcts outside the brain stem,
or extensive and confluent white matter lesions. The latter is often termed small vessel dis-
ease or subcortical ischemic changes on clinical neuroimaging evaluations.
For mild vascular NCD, history of a single stroke or extensive white matter disease is gen-
erally sufficient. For major vascular NCD, two or more strokes, a strategically placed stroke,
or a combination of white matter disease and one or more lacunes is generally necessary.
The disorder must not be better explained by another disorder. For example, promi-
nent memory deficit early in the course might suggest Alzheimer's disease, early and
prominent parkinsonian features would suggest Parkinson's disease, and a close associa-
tion between onset and depression would suggest depression.
Associated Features Supporting Diagnosis
A neurological assessment often reveals history of stroke and/or transient ischemic epi-
sodes, and signs indicative of brain infarctions. Also commonly associated are personality
and mood changes, abulia, depression, and emotional lability. The development of late-
onset depressive symptoms accompanied by psychomotor slowing and executive dys-
function is a common presentation among older adults with progressive small vessel isch-
emic disease (“vascular depression”).
Prevalence
Major or mild vascular NCD is the second most common cause of NCD after Alzheimer’s
disease. In the United States, population prevalence estimates for vascular dementia range
from 0.2% in the 65-70 years age group to 16% in individuals 80 years and older. Within
3 months following stroke, 20%~30% of individuals are diagnosed with dementia. In neu-
ropathology series, the prevalence of vascular dementia increases from 13% at age 70 years
to 44.6% at age 90 years or older, in comparison with Alzheimer’s disease (23.6%-51%) and
combined vascular dementia and Alzheimer’s disease (2% 46.4%). Higher prevalence has
Major or Mild Vascular Neurocognitive Disorder 623
been reported in African Americans compared with Caucasians, and in East Asian countries
(e.g., Japan, China). Prevalence is higher in males than in females.
Development and Course
Major or mild vascular NCD can occur at any age, although the prevalence increases ex-
ponentially after age 65 years. In older individuals, additional pathologies may partly ac-
count for the neurocognitive deficits. The course may vary from acute onset with partial
improvement to stepwise decline to progressive decline, with fluctuations and plateaus of
varying durations. Pure subcortical major or mild vascular NCD can have a slowly pro-
gressive course that simulates major or mild NCD due to Alzheimer’s disease.
Risk and Prognostic Factors
Environmental. The neurocognitive outcomes of vascular brain injury are influenced by
neuroplasticity factors such as education, physical exercise, and mental activity.
Genetic and physiological. The major risk factors for major or mild vascular NCD are the
same as those for cerebrovascular disease, including hypertension, diabetes, smoking, obesity,
high cholesterol levels, high homocysteine levels, other risk factors for atherosclerosis and ar-
teriolosclerosis, atrial fibrillation, and other conditions increasing the risk of cerebral emboli.
Cerebral amyloid angiopathy is an important risk factor in which amyloid deposits occur
within arterial vessels. Another key risk factor is the hereditary condition cerebral autosomal
dominant arteriopathy with subcortical infarcts and leukoencephalopathy, or CADASIL.
Diagnostic Markers
Structural neuroimaging, using MRI or CT, has an important role in the diagnostic pro-
cess. There are no other established biomarkers of major or mild vascular NCD.
Functional Consequences of
Major or Mild Vascular Neurocognitive Disorder
Major or mild vascular NCD is commonly associated with physical deficits that cause ad-
ditional disability.
Differential Diagnosis
Other neurocognitive disorders. Since incidental brain infarctions and white matter le-
sions are common in older individuals, it is important to consider other possible etiologies
when an NCD is present. A history of memory deficit early in the course, and progressive
worsening of memory, language, executive function, and perceptual-motor abilities in the
absence of corresponding focal lesions on brain imaging, are suggestive of Alzheimer’s
disease as the primary diagnosis. Potential biomarkers currently being validated for Alz-
heimer’s disease, such as cerebrospinal fluid levels of beta-amyloid and phosphorylated
tau, and amyloid imaging, may prove to be helpful in the differential diagnosis. NCD with
Lewy bodies is distinguished from major or mild vascular NCD by its core features of fluc-
tuating cognition, visual hallucinations, and spontaneous parkinsonism. While deficits in
executive function and language occur in major or mild vascular NCD, the insidious onset
and gradual progression of behavioral features or language impairment are characteristic
of frontotemporal NCD and are not typical of vascular etiology.
Other medical conditions. A diagnosis of major or mild vascular NCD is not made if
other diseases (e.g., brain tumor, multiple sclerosis, encephalitis, toxic or metabolic disor-
ders) are present and are of sufficient severity to account for the cognitive impairment.
624 Neurocognitive Disorders
Other mental disorders. A diagnosis of major or mild vascular NCD is inappropriate if
the symptoms can be entirely attributed to delirium, although delirium may sometimes be
superimposed on a preexisting major or mild vascular NCD, in which case both diagnoses
can be made. If the criteria for major depressive disorder are met and the cognitive impair-
ment is temporally related to the likely onset of the depression, major or mild vascular
NCD should not be diagnosed. However, if the NCD preceded the development of the de-
pression, or the severity of the cognitive impairment is out of proportion to the severity of
the depression, both should be diagnosed.
Comorbidity
Major or mild NCD due to Alzheimer’s disease commonly co-occurs with major or mild
vascular NCD, in which case both diagnoses should be made. Major or mild vascular NCD
and depression frequently co-occur.
Major or Mild Neurocognitive Disorder
Due to Traumatic Brain Injury
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. There is evidence of a traumatic brain injury—that is, an impact to the head or other
mechanisms of rapid movement or displacement of the brain within the skull, with one
or more of the following:
1. Loss of consciousness.
2. Posttraumatic amnesia.
3. Disorientation and confusion.
4. Neurological signs (e.g., neuroimaging demonstrating injury; a new onset of sei-
zures; a marked worsening of a preexisting seizure disorder; visual field cuts; an-
osmia; hemiparesis).
C. The neurocognitive disorder presents immediately after the occurrence of the trau-
matic brain injury or immediately after recovery of consciousness and persists past the
acute post-injury period.
Coding note: For major neurocognitive disorder due to traumatic brain injury, with behavioral
disturbance: For {\CD-9-CM, first code 907.0 late effect of intracranial injury without skull frac-
ture, followed by 294.11 major neurocognitive disorder due to traumatic brain injury, with be-
havioral disturbance. For ICD-10-CM, first code $06.2X9S diffuse traumatic brain injury with
loss of consciousness of unspecified duration, sequela; followed by F02.81 major neurocog-
nitive disorder due to traumatic brain injury, with behavioral disturbance.
For major neurocognitive disorder due to traumatic brain injury, without behavioral distur-
bance: For |CD-9-CM, first code 907.0 late effect of intracranial injury without skull fracture,
followed by 294.10 major neurocognitive disorder due to traumatic brain injury, without be-
havioral disturbance. For ICD-10-CM, first code S06.2X9S diffuse traumatic brain injury with
loss of consciousness of unspecified duration, sequela; followed by.F02.80 major neurocog-
nitive disorder due to traumatic brain injury, without behavioral disturbance.
For mild neurocognitive disorder due to traumatic brain injury, code 331.83 (G31.84).
(Note: Do not use the additional code for traumatic brain injury. Behavioral disturbance
cannot be coded but should still be indicated in writing.)
Major or Mild Neurocognitive Disorder Due to Traumatic Brain Injury 625
Specifiers
Rate the severity of the neurocognitive disorder (NCD), not the underlying traumatic brain
injury (see the section “Development and Course” for this disorder).
Diagnostic Features
Major or mild NCD due to traumatic brain injury (TBI) is caused by an impact to the head,
or other mechanisms of rapid movement or displacement of the brain within the skull, as
can happen with blast injuries. Traumatic brain injury is defined as brain trauma with spe-
cific characteristics that include at least one of the following: loss of consciousness, post-
traumatic amnesia, disorientation and confusion, or, in more severe cases, neurological
signs (e.g., positive neuroimaging, a new onset of seizures or a marked worsening of a pre-
existing seizure disorder, visual field cuts, anosmia, hemiparesis) (Criterion B). To be at-
tributable to TBI, the NCD must present either immediately after the brain injury occurs or
immediately after the individual recovers consciousness after the injury and persist past
the acute post-injury period (Criterion C).
The cognitive presentation is variable. Difficulties in the domains of complex attention,
executive ability, learning, and memory are common as well as slowing in speed of infor-
mation processing and disturbances in social cognition. In more severe TBI in which there
is brain contusion, intracranial hemorrhage, or penetrating injury, there may be additional
neurocognitive deficits, such as aphasia, neglect, and constructional dyspraxia.
Associated Features Supporting Diagnosis
Major or mild NCD due to TBI may be accompanied by disturbances in emotional function
(e.g., irritability, easy frustration, tension and anxiety, affective lability); personality
changes (e.g., disinhibition, apathy, suspiciousness, aggression); physical disturbances
(e.g., headache, fatigue, sleep disorders, vertigo or dizziness, tinnitus or hyperacusis, pho-
tosensitivity, anosmia, reduced tolerance to psychotropic medications); and, particularly
in more severe TBI, neurological symptoms and signs (e.g., seizures, hemiparesis, visual
disturbances, cranial nerve deficits) and evidence of orthopedic injuries.
Prevaience
In the United States, 1.7 million TBIs occur annually, resulting in 1.4 million emergency de-
partment visits, 275,000 hospitalizations, and 52,000 deaths. About 2% of the population
lives with TBI-associated disability. Males account for 59% of TBIs in the United States.
The most common etiologies of TBI in the United States are falls, vehicular accidents, and
being struck on the head. Collisions and blows to the head that occur in the course of con-
tact sports are increasingly recognized as sources of mild TBI, with a concern that repeated
mild TBI may have cumulatively persisting sequelae.
Deveiopment and Course
The severity of a TBI is rated at the time of injury /initial assessment as mild, moderate, or
severe according to the thresholds in Table 2.
The severity rating of the TBI itself does not necessarily correspond to the severity of
the resulting NCD. The course of recovery from TBI is variable, depending not only on the
specifics of the injury but also on cofactors, such as age, prior history of brain damage, or
substance abuse, that may favor or impede recovery.
626 Neurocognitive Disorders
TABLE 2 Severity ratings for traumatic brain injury
Injury characteristic Mild TBI Moderate TBI Severe TBI
Loss of consciousness <30 min 30 minutes—24 hours >24 hours
Posttraumatic amnesia <24 hours 24 hours—7 days >7 days
Disorientation and confusion 13-15 (notbelow13 9-12 3-8
at initial assessment at 30 minutes)
(Glasgow Coma Scale
Score)
Neurobehavioral symptoms tend to be most severe in the immediate aftermath of the
TBI. Except in the case of severe TBI, the typical course is that of complete or substantial
improvement in associated neurocognitive, neurological, and psychiatric symptoms and
signs. Neurocognitive symptoms associated with mild TBI tend to resolve within days to
weeks after the injury with complete resolution typical by 3 months. Other symptoms that
may potentially co-occur with the neurological symptoms (e.g., depression, irritability,
fatigue, headache, photosensitivity, sleep disturbance) also tend to resolve in the weeks
following mild TBI. Substantial subsequent deterioration in these areas should trigger con-
sideration of additional diagnoses. However, repeated mild TBI may be associated with
persisting neurocognitive disturbance.
With moderate and severe TBI, in addition to persistence of neurocognitive deficits,
there may be associated neurophysiological, emotional, and behavioral complications.
These include seizures (particularly in the first year), photosensitivity, hyperacusis, irritabil-
ity, aggression, depression, sleep disturbance, fatigue, apathy, inability to resume occu-
pational and social functioning at pre-injury level, and deterioration in interpersonal
relationships. Moderate and severe TBI have been associated with increased risk of depres-
sion, aggression, and possibly neurodegenerative diseases such as Alzheimer’s disease.
The features of persisting major or mild NCD due to TBI will vary by age, specifics of
the injury, and cofactors. Persisting TBI-related impairment in an infant or child may be re-
flected in delays in reaching developmental milestones (e.g., language acquisition), worse
academic performance, and possibly impaired social development. Among older teenag-
ers and adults, persisting symptoms may include various neurocognitive deficits, irrita-
bility, hypersensitivity to light and sound, easy fatigability, and mood changes, including
depression, anxiety, hostility, or apathy. In older individuals with depleted cognitive re-
serve, mild TBI is more likely to result in incomplete recoveries.
Risk and Prognostic Factors
Risk factors for traumatic brain injury. Traumatic brain injury rates vary by age, with
the highest prevalence among individuals younger than 4 years, older adolescents, and in-
dividuals older than 65 years. Falls are the most common cause of TBI, with motor vehicle
accidents being second. Sports concussions are frequent causes of TBI in older children,
teenagers, and young adults.
Risk factors for neurocognitive disorder after traumatic brain injury. Repeated con-
cussions can lead to persistent NCD and neuropathological evidence of traumatic enceph-
alopathy. Co-occurring intoxication with a substance may increase the severity of a TBI
from a motor vehicle accident, but whether intoxication at the time of injury worsens neu-
rocognitive outcome is unknown.
Course modifiers. Mild TBI generally resolves within a few weeks to months, although res-
olution may be delayed or incomplete in the context of repeated TBI. Worse outcome from
Substance/Medication-Induced Major or Mild Neurocognitive Disorder 627
moderate to severe TBI is associated with older age (older than 40 years) and initial clinical pa-
rameters, such as low Glasgow Coma Scale score; worse motor function; pupillary nonreac-
tivity; and computed tomography (CT) evidence of brain injury (e.g., petechial hemorrhages,
subarachnoid hemorrhage, midline shift, obliteration of third ventricle).
Diagnostic Markers
Beyond neuropsychological testing, CT scanning may reveal petechial hemorrhages,
subarachnoid hemorrhage, or evidence of contusion. Magnetic resonance image scanning
may also reveal hyperintensities suggestive of microhemorrhages.
Functionai Consequences of Major or Miid
Neurocognitive Disorder Due to Traumatic Brain Injury
With mild NCD due to TBI, individuals may report reduced cognitive efficiency, difficulty
concentrating, and lessened ability to perform usual activities. With major NCD due to TBI, an
individual may have difficulty in independent living and self-care. Prominent neuromotor
features, such as severe incoordination, ataxia, and motor slowing, may be present in major
NCD due to TBI and may add to functional difficulties. Individuals with TBI histories report
more depressive symptoms, and these can amplify cognitive complaints and worsen func-
tional outcome. Additionally, loss of emotional control, including aggressive or inappropriate
affect and apathy, may be present after more severe TBI with greater neurocognitive impair-
ment. These features may compound difficulties with independent living and self-care.
Differentiai Diagnosis
In some instances, severity of neurocognitive symptoms may appear to be inconsistent
with the severity of the TBI. After previously undetected neurological complications (e.g.,
chronic hematoma) are excluded, the possibility of diagnoses such as somatic symptom
disorder or factitious disorder need to be considered. Posttraumatic stress disorder (PTSD)
can co-occur with the NCD and have overlapping symptoms (e.g., difficulty concentrat-
ing, depressed mood, aggressive behavioral disinhibition).
Comorbidity
Among individuals with substance use disorders, the neurocognitive effects of the sub-
stance contribute to or compound the TBI-associated neurocognitive change. Some symp-
toms associated with TBI may overlap with symptoms found in cases of PTSD, and the two
disorders may co-occur, especially in military populations.
Substance/Medication-Induced
Major or Mild Neurocognitive Disorder
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. The neurocognitive impairments do not occur exclusively during the course of a delir-
ium and persist beyond the usual duration of intoxication and acute withdrawal.
C. The involved substance or medication and duration and extent of use are capable of
producing the neurocognitive impairment.
D. The temporal course of the neurocognitive deficits is consistent with the timing of sub-
stance or medication use and abstinence (e.g., the deficits remain stable or improve
after a period of abstinence).
628 Neurocognitive Disorders
E. The neurocognitive disorder is not attributable to another medical condition or is not
better explained by another mental disorder.
Coding note: The {CD-9-CM and ICD-10-CM codes for the [specific substance/medica-
tion]-induced neurocognitive disorders are indicated in the table below. Note that the ICD-
10-CM code depends on whether or not there is a comorbid substance use disorder present
for the same class of substance. If a mild substance use disorder is comorbid with the sub-
stance-induced neurocognitive disorder, the 4th position character is “1,” and the clinician
should record “mild [substance] use disorder” before the substance-induced neurocognitive
disorder (e.g., “mild inhalant use disorder with inhalant-induced major neurocognitive disor-
der’). If a moderate or severe substance use disorder is comorbid with the substance-
induced neurocognitive disorder, the 4th position character is “2,” and the clinician should
record “moderate [substance] use disorder’ or “severe [substance] use disorder,” depending
on the severity of the comorbid substance use disorder. If there is no comorbid substance
use disorder, then the 4th position character is “9,” and the clinician should record only the
substance-induced neurocognitive disorder. For some classes of substances (i.e., alcohol;
sedatives, hypnotics, anxiolytics), it is not permissible to code a comorbid mild substance
use disorder with a substance-induced neurocognitive disorder; only a comorbid moderate
or severe substance use disorder, or no substance use disorder, can be diagnosed. Behav-
ioral disturbance cannot be coded but should still be indicated in writing.
ICD-10-CM
With use
With use disorder,
disorder, moderateor Withoutuse
ICD-9-CM mild severe disorder
Alcohol (major neurocognitive 291.2 NA F10.27 F10.97
disorder), nonamnestic-
confabulatory type
Alcohol (major neurocognitive 291.1 NA F10.26 F10.96
disorder), amnestic-
confabulatory type
Alcohol (mild neurocognitive 291.89 NA F10.288 F10.988
disorder)
Inhalant (major neurocognitive 292.82 F18.17 F18.27 F18.97
disorder)
Inhalant (mild neurocognitive 292.89 F18.188 F18.288 F18.988
disorder)
Sedative, hypnotic, or anxiolytic 292.82 NA F13.27 F13.97
(major neurocognitive disorder)
Sedative, hypnotic, or anxiolytic 292.89 NA F13.288 F13.988
(mild neurocognitive disorder)
Other (or unknown) substance 292.82 F19.17 F19.27 F19.97
(major neurocognitive disorder)
Other (or unknown) substance 292.89 F19.188 F19.288 F19.988
(mild neurocognitive disorder)
Substance/Medication-Induced Major or Mild Neurocognitive Disorder 629
Specify if:
Persistent:,Neurocognitive impairment continues to be significant after an extended
period of abstinence.
Recording Procedures
ICD-9-CM. The name of the substance/medication-induced neurocognitive disorder be-
gins with the specific substance / medication (e.g., alcohol) that is presumed to be causing
the neurocognitive symptoms. The diagnostic code is selected from the table included in
the criteria set, which is based on the drug class. For substances that do not fit into any of
the classes, the code for “other substance” should be used; and in cases in which a substance
is judged to be an etiological factor but the specific class of substance is unknown, the cat-
egory “unknown substance” should be used.
The name of the disorder (i.e., [specific substance]-induced major neurocognitive dis-
order or [specific substance]-induced mild neurocognitive disorder) is followed by the
type in the case of alcohol (i.e., nonamnestic-confabulatory type, amnestic-confabulatory
type), followed by specification of duration (i.e., persistent). Unlike the recording procedures
for ICD-10-CM, which combine the substance/medication-induced disorder and sub-
stance use disorder into a single code, for ICD-9-CM a separate diagnostic code is given for
the substance use disorder. For example, in the case of persistent amnestic-confabulatory
symptoms in a man with a severe alcohol use disorder, the diagnosis is 291.1 alcohol-
induced major neurocognitive disorder, amnestic-confabulatory type, persistent. An addi-
tional diagnosis of 303.90 severe alcohol use disorder is also given. If the substance/medi-
cation-induced neurocognitive disorder occurs without a comorbid substance use disorder
(e.g., after a sporadic heavy use of inhalants), no accompanying substance use disorder is
noted (e.g., 292.82 inhalant-induced mild neurocognitive disorder).
ICD-10-CM. The name of the substance/medication-induced neurocognitive disorder
begins with the specific substance (e.g., alcohol) that is presumed to be causing the neuro-
cognitive symptoms. The diagnostic code is selected from the table included in the criteria
set, which is based on the drug class and presence or absence of a comorbid substance use
disorder. For substances that do not fit into any of the classes, the code for “other sub-
stance” should be used; and in cases in which a substance is judged to be an etiological fac-
tor but the specific class of substance is unknown, the category “unknown substance”
should be used.
When recording the name of the disorder, the comorbid substance use disorder (if any) is
listed first, followed by the word “with,” followed by the name of the disorder (i.e., [specific
substance]-induced major neurocognitive disorder or [specific substance]-induced mild
neurocognitive disorder), followed by the type in the case of alcohol (i.e., nonamnestic-con-
fabulatory type, amnestic-confabulatory type), followed by specification of duration (i.e.,
persistent). For example, in the case of persistent amnestic-confabulatory symptoms in a
man with a severe alcohol use disorder, the diagnosis is F10.26 severe alcohol use disorder
with alcohol-induced major neurocognitive disorder, amnestic-confabulatory type, persis-
tent. A separate diagnosis of the comorbid severe alcohol use disorder is not given. If the
substance-induced neurocognitive disorder occurs without a comorbid substance use dis-
order (e.g., after a sporadic heavy use of inhalants), no accompanying substance use disor-
der is noted (e.g., F18.988 inhalant-induced mild neurocognitive disorder).
Diagnostic Features
Substance/medication-induced major or mild NCD is characterized by neurocognitive
impairments that persist beyond the usual duration of intoxication and acute withdrawal
(Criterion B). Initially, these manifestations can reflect slow recovery of brain functions
from a period of prolonged substance use, and improvements in neurocognitive as well as
630 Neurocognitive Disorders
brain imaging indicators may be seen over many months. If the disorder continues for an
extended period, persistent should be specified. The given substance and its use must be
known to be capable of causing the observed impairments (Criterion C). While nonspecific
decrements in a range of cognitive abilities can occur with nearly any substance of abuse
and a variety of medications, some patterns occur more frequently with selected drug
classes. For example, NCD due to sedative, hypnotic, or anxiolytic drugs (e.g., benzodiaz-
epines, barbiturates) may show greater disturbances in memory than in other cognitive
functions. NCD induced by alcohol frequently manifests with a combination of impair-
ments in executive-function and memory and learning domains. The temporal course of
the substance-induced NCD must be consistent with that of use of the given substance
(Criterion D). In alcohol-induced amnestic confabulatory (Korsakoff’s} NCD, the features
include prominent amnesia (severe difficulty learning new information with rapid forget-
ting) and a tendency to confabulate. These manifestations may co-occur with signs of thi-
amine encephalopathy (Wernicke’s encephalopathy) with associated features such as
nystagmus and ataxia. Ophthalmoplegia of Wernicke’s encephalopathy is typically charac-
terized by a lateral gaze paralysis.
In addition to or independent of the more common neurocognitive symptoms related
to methamphetamine use (e.g., difficulties with learning and memory; executive func-
tion), methamphetamine use can also be associated with evidence of vascular injury (e.g.,
focal weakness, unilateral incoordination, asymmetrical reflexes). The most common neu-
rocognitive profile approximates that seen in vascular NCD.
Associated Features Supporting Diagnosis
Intermediate-duration NCD induced by drugs with central nervous system depressant effects
may manifest with added symptoms of increased irritability, anxiety, sleep disturbance, and
dysphoria. Intermediate-duration NCD induced by stimulant drugs may manifest with re-
bound depression, hypersomnia, and apathy. In severe forms of substance /medication-
induced major NCD (e.g., associated with long-term alcohol use), there may be prominent
neuromotor features, such as incoordination, ataxia, and motor slowing. There may also be
loss of emotional control, including aggressive or inappropriate affect, or apathy.
Prevalence
The prevalence of these conditions is not known. Prevalence figures for substance abuse are
available, and substance /medication-induced major or mild NCDs are more likely in those
who are older, have longer use, and have other risk factors such as nutritional deficits.
For alcohol abuse, the rate of mild NCD of intermediate duration is approximately 30%-
40% in the first 2 months of abstinence. Mild NCD may persist, particularly in those who do
not achieve stable abstinence until after age 50 years. Major NCD is rare and may result from
concomitant nutritional deficits, as in alcohol-induced amnestic confabulatory NCD.
For individuals quitting cocaine, methamphetamine, opioids, phencyclidine, and sed-
ative, hypnotics, or anxiolytics, substance / medication-induced mild NCD of intermediate
duration may occur in one-third or more, and there is some evidence that these substances
may also be associated with persistent mild NCD. Major NCD associated with these sub-
stances is rare, if it occurs at all. In the case of methamphetamine, cerebrovascular disease
can also occur, resulting in diffuse or focal brain injury that can be of mild or major neu-
rocognitive levels. Solvent exposure has been linked to both major and mild NCD of both
intermediate and persistent duration.
The presence of NCD induced by cannabis and various hallucinogens is controversial.
With cannabis, intoxication is accompanied by various neurocognitive disturbances, but
these tend to clear with abstinence.
Substance/Medication-Induced Major or Mild Neurocognitive Disorder 631
Development and Course
Substance use disorders tend to commence during adolescence and peak in the 20s and
30s. Although longer history of severe substance use disorder is associated with greater
likelihood of NCD, the relationships are not straightforward, with substantial and even
complete recovery of neurocognitive functions being common among individuals who
achieve stable abstinence prior to age 50 years. Substance/medication-induced major or
mild NCD is most likely to become persistent in individuals who continue abuse of sub-
stances past age 50 years, presumably because of a combination of lessened neural plas-
ticity and beginnings of other age-related brain changes. Earlier commencement of abuse,
particularly of alcohol, may lead to defects in later neural development (e.g., later stages of
maturation of frontal circuitries), which may have effects on social cognition as well as
other neurocognitive abilities. For alcohol-induced NCD, there may be an additive effect
of aging and alcohol-induced brain injury.
Risk and Prognostic Factors
Risk factors for substance/medication-induced NCDs include older age, longer use, and
persistent use past age 50 years. In addition, for alcohol-induced NCD, long-term nutri-
tional deficiencies, liver disease, vascular risk factors, and cardiovascular and cerebrovas-
cular disease may contribute to risk.
Diagnostic Markers
Magnetic resonance imaging (MRI) of individuals with chronic alcohol abuse frequently
reveals cortical thinning, white matter loss, and enlargement of sulci and ventricles. While
neuroimaging abnormalities are more common in those with NCDs, it is possible to ob-
serve NCDs without neuroimaging abnormalities, and vice versa. Specialized techniques
(e.g., diffusion tensor imaging) may reveal damage to specific white matter tracts. Mag-
netic resonance spectroscopy may reveal reduction in N-acetylaspartate, and increase in
markers of inflammation (e.g., myoinositol) or white matter injury (e.g., choline). Many of
these brain imaging changes and neurocognitive manifestations reverse following suc-
cessful abstinence. In individuals with methamphetamine use disorder, MRI may also re-
veal hyperintensities suggestive of microhemorrhages or larger areas of infarction.
Functional Consequences of Substance/Medication-
Induced Major or Miid Neurocognitive Disorder
The functional consequences of substance/medication-induced mild NCD are sometimes
augmented by reduced cognitive efficiency and difficulty concentrating beyond that seen
in many other NCDs. In addition, at both major and mild levels, substance /medication-
induced NCDs may have associated motor syndromes that increase the level of functional
impairment.
Differential Diagnosis
Individuals with substance use disorders, substance intoxication, and substance withdrawal
are at increased risk for other conditions that may independently, or through a compounding
effect, result in neurocognitive disturbance. These include history of traumatic brain injury
and infections that can accompany substance use disorder (e.g., HIV, hepatitis C virus, syph-
ilis). Therefore, presence of substance/medication-induced major or mild NCD should be
differentiated from NCDs arising outside the context of substance use, intoxication, and with-
drawal, including these accompanying conditions (e.g., traumatic brain injury).
632 Neurocognitive Disorders
Comorbidity
Substance use disorders, substance intoxication, and substance withdrawal are highly co-
morbid with other mental disorders. Comorbid posttraumatic stress disorder, psychotic
disorders, depressive and bipolar disorders, and neurodevelopmental disorders can con-
tribute to neurocognitive impairment in substance users. Traumatic brain injury occurs
more frequently with substance use, complicating efforts to determine the etiology of NCD
in such cases, Severe, long-term alcohol use disorder can be associated with major organ
system disease, including cerebrovascular disease and cirrhosis. Amphetamine-induced
NCD may be accompanied by major or mild vascular NCD, also secondary to amphet-
amine use.
Major or Mild Neurocognitive Disorder
Due to HIV Infection
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. There is documented infection with human immunodeficiency virus (HIV).
C. The neurocognitive disorder is not better explained by non-HIV conditions, including
secondary brain diseases such as progressive multifocal leukoencephalopathy or
cryptococcal meningitis.
D. The neurocognitive disorder is not attributable to another medical condition and is not
better explained by a mental disorder.
Coding note: For major neurocognitive disorder due to HIV infection, with behavioral dis-
turbance, code first 042 (B20) HIV infection, followed by 294.11 (F02.81} major neurocog-
nitive disorder due to HIV infection, with behavioral disturbance. For major neurocognitive
disorder due to HIV infection, without behavioral disturbance, code first 042 (B20) HIV in-
fection, followed by 294.10 (F02.80) major neurocognitive disorder due to HIV infection,
without behavioral disturbance.
For mild neurocognitive disorder due to HIV infection, code 331.83 (G31.84). (Note: Do
not use the additional code for HIV infection. Behavioral disturbance cannot be coded but
should still be indicated in writing.)
Diagnostic Features
HIV disease is caused by infection with human immunodeficiency virus type-1 (HIV-1),
which is acquired through exposure to bodily fluids of an infected person through injection
drug use, unprotected sexual contact, or accidental or iatrogenic exposure (e.g., contami-
nated blood supply, needle puncture injury to medical personnel). HIV infects several types
of cells, most particularly immune cells. Over time, the infection can cause severe depletion
of “T-helper” (CD4) lymphocytes, resulting in severe immunocompromise, often leading to
opportunistic infections and neoplasms. This advanced form of HIV infection is termed
acquired immune deficiency syndrome (AIDS). Diagnosis of HIV is confirmed by established
laboratory methods such as enzyme-linked immunosorbent assay for HIV antibody with
Western blot confirmation and/or polymerase chain reaction—based assays for HIV.
Some individuals with HIV infection develop an NCD, which generally shows a “sub-
cortical pattern” with prominently impaired executive function, slowing of processing
speed, problems with more demanding attentional tasks, and difficulty in learning new
information, but fewer problems with recall of learned information. In major NCD, slow-
ing may be prominent. Language difficulties, such as aphasia, are uncommon, although
reductions in fluency may be observed. HIV pathogenic processes can affect any part of
the brain; therefore, other patterns are possible.
Major or Mild Neurocognitive Disorder Due to HIV Infection 633
Associated Features Supporting Diagnosis
Major or mild NCD due to HIV infection is usually more prevalent in individuals with
prior episodes of severe immunosuppression, high viral loads in the cerebrospinal fluid,
and indicators of advanced HIV disease such as anemia and hypoalbuminemia. Individ-
uals with advanced NCD may experience prominent neuromotor features such as severe
incoordination, ataxia, and motor slowing. There may be loss of emotional control, includ-
ing aggressive or inappropriate affect or apathy.
Prevaience
Depending on stage of HIV disease, approximately one-third to over one-half of HIV-
infected individuals have at least mild neurocognitive disturbance, but some of these dis-
turbances may not meet the full criteria for mild NCD. An estimated 25% of individuals
with HIV will have signs and symptoms that meet criteria for mild NCD, and in fewer than
5% would criteria for major NCD be met.
Development and Course
An NCD due to HIV infection can resolve, improve, slowly worsen, or have a fluctuating
course. Rapid progression to profound neurocognitive impairment is uncommon in the
context of currently available combination antiviral treatment; consequently, an abrupt
change in mental status in an individual with HIV may prompt an evaluation of other
medical sources for the cognitive change, including secondary infections. Because HIV in-
fection preferentially affects subcortical regions over the course of illness, including deep
white matter, the progression of the disorder follows a “subcortical” pattern. Since HIV
can affect a variety of brain regions, and the illness can take on many different trajectories
depending on associated comorbidities and consequences of HIV, the overall course of an
NCD due to HIV infection has considerable heterogeneity. A subcortical neurocognitive
profile may interact with age over the life course, when psychomotor slowing and motor
impairments such as slowed gait may occur as a consequence of other age-related condi-
tions so that the overall progression may appear more pronounced in later life.
In developed countries, HIV disease is primarily a condition of adults, with acquisition
via risky behaviors (e.g., unprotected sex, injection drug use) beginning in late adolescence
and peaking during young and middle adulthood. In developing countries, particularly
sub-Saharan Africa, where HIV testing and antiretroviral treatments for pregnant women
are not readily available, perinatal transmission is common. The NCD in such infants and
children may present primarily as neurodevelopmental delay. As individuals treated for
HIV survive into older age, additive and interactive neurocognitive effects of HIV and
aging, including other NCDs (e.g., due to Alzheimer’s disease, due to Parkinson’s dis-
ease), are possible.
Risk and Prognostic Factors
Risk and prognostic factors for HIV infection. Risk factors for HIV infection include injec-
tion drug use, unprotected sex, and unprotected blood supply and other iatrogenic factors.
Risk and prognostic factors for major or mild neurocognitive disorder due to HIV in-
fection. Paradoxically, NCD due to HIV infection has not declined significantly with the
advent of combined antiretroviral therapy, although the most severe presentations (con-
sistent with the diagnosis of major NCD) have decreased sharply. Contributory factors
may include inadequate control of HIV in the central nervous system (CNS), the evolution
of drug-resistant viral strains, the effects of chronic long-term systemic and brain inflam-
mation, and the effects of comorbid factors such as aging, drug abuse, past history of CNS
trauma, and co-infections, such as with the hepatitis C virus. Chronic exposure to antiret-
roviral drugs also raises the possibility of neurotoxicity, although this has not been defin-
itively established.
634 Neurocognitive Disorders
Diagnostic Markers
Serum HIV testing is required for the diagnosis. In addition, HIV characterization of the cere-
brospinal fluid may be helpful if it reveals a disproportionately high viral load in cerebrospinal
fluid versus in the plasma. Neuroimaging (i.e., magnetic resonance imaging [MRI]) may reveal
reduction in total brain volume, cortical thinning, reduction in white matter volume, and
patchy areas of abnormal white matter (hyperintensities). MRI or lumbar puncture may be
helpful to exclude a specific medical condition such as cryptococcus infection or herpes en-
cephalitis that may contribute to CNS changes in the context of AIDS. Specialized techniques
such as diffusion tensor imaging may reveal damage to specific white matter tracts.
Functional Consequences of Major or Mild
Neurocognitive Disorder Due to HIV Infection
Functional consequences of major or mild NCD due to HIV infection are variable across
individuals. Thus, impaired executive abilities and slowed information processing may
substantially interfere with the complex disease management decisions required for ad-
herence to the combined antiretroviral therapy regimen. The likelihood of comorbid dis-
ease may further create functional challenges.
Differential Dlagnosis
In the presence of comorbidities, such as other infections (e.g., hepatitis C virus, syphilis),
drug abuse (e.g., methamphetamine abuse), or prior head injury or neurodevelopmental
conditions, major or mild NCD due to HIV infection can be diagnosed provided there is ev-
idence that infection with HIV has worsened any NCDs due to such preexisting or comorbid
conditions. Among older adults, onset of neurocognitive decline related to cerebrovascular
disease or neurodegeneration (e.g., major or mild NCD due to Alzheimer’s disease) may
need to be differentiated. In general, stable, fluctuating (without progression) or improving
neurocognitive status would favor an HIV etiology, whereas steady or stepwise deter-
ioration would suggest neurodegenerative or vascular etiology. Because more severe im-
munodeficiency can result in opportunistic infections of the brain (e.g., toxoplasmosis;
cryptococcosis) and neoplasia (e.g., CNS lymphoma), sudden onset of an NCD or sudden
worsening of that disorder demands active investigation of non-HIV etiologies.
Comorbidity
HIV disease is accompanied by chronic systemic and neuro-inflammation that can be as-
sociated with cerebrovascular disease and metabolic syndrome. These complications can
be part of the pathogenesis of major or mild NCD due to HIV infection. HIV frequently co-
occurs with conditions such as substance use disorders when the substance has been in-
jected and other sexually transmitted disorders.
Major or Mild Neurocognitive Disorder
Due to Prion Disease
Diagnostic Criteria
A. The criteria are met for major or mild neurocognitive disorder.
B. There is insidious onset, and rapid progression of impairment is common.
C. There are motor features of prion disease, such as myoclonus or ataxia, or biomarker
evidence.
Major or Mild Neurocognitive Disorder Due to Prion Disease 635
D. The neurocognitive disorder is not attributable to another medical condition and is not
better explained by another mental disorder.
Coding note: For major neurocognitive disorder due to prion disease, with behavioral dis-
turbance, code first 046.79 (A81.9) prion disease, followed by 294.11 (F02.81) major
neurocognitive disorder due to prion disease, with behavioral disturbance. For major neu-
rocognitive disorder due to prion disease, without behavioral disturbance, code first
046.79 (A81.9) prion disease, followed by 294.10 (F02.80) major neurocognitive disorder
due to prion disease, without behavioral disturbance.
For mild neurocognitive disorder due to prion disease, code 331.83 (G31.84). (Note: Do
not use the additional code for prion disease. Behavioral disturbance cannot be coded but
should still be indicated in writing.)
Diagnostic Features
The classification of major or mild neurocognitive disorder (NCD) due to prion disease in-
cludes NCDs due to a group of subacute spongiform encephalopathies (including Creutz-
feldt-Jakob disease, variant Creutzfeldt-Jakob disease, kuru, Gerstmann-Straussler-
Scheinker syndrome, and fatal insomnia) caused by transmissible agents known as prions.
The most common type is sporadic Creutzfeldt-Jakob disease, typically referred to as
Creutzfeldt-Jakob disease (CJD). Variant CJD is much rarer and is associated with trans-
mission of bovine spongiform encephalopathy, also called “mad cow disease.” Typically,
individuals with CJD present with neurocognitive deficits, ataxia, and abnormal move-
ments such as myoclonus, chorea, or dystonia; a startle reflex is also common. Typically,
the history reveals rapid progression to major NCD over as little as 6 months, and thus the
disorder is typically seen only at the major level. However, many individuals with the dis-
order may have atypical presentations, and the disease can be confirmed only by biopsy or
at autopsy. Individuals with variant CJD may present with a greater preponderance of
psychiatric symptoms, characterized a by low mood, withdrawal, and anxiety. Prion dis-
ease is typically not diagnosed without at least one of the characteristic biomarker fea-
tures: recognized lesions on magnetic resonance imaging with DWI (diffusion-weighted
imaging) or FLAIR (fluid-attenuated inversion recovery), tau or 14-3-3 protein in cerebro-
spinal fluid, characteristic triphasic waves on electroencephalogram, or, for rare familial
forms, family history or genetic testing.
Prevalence
The annual incidence of sporadic CJD is approximately one or two cases per million peo-
ple. Prevalence is unknown but very low given the short survival.
Development and Course
Prion disease may develop at any age in adults—the peak age for the sporadic CJD is ap-
proximately 67 years—although it has been reported to occur in individuals spanning the
teenage years to late life. Prodromal symptoms of prion disease may include fatigue, anx-
iety, problems with appetite or sleeping, or difficulties with concentration. After several
weeks, these symptoms may be followed by incoordination, altered vision, or abnormal
gait or other movements that may be myoclonic, choreoathetoid, or ballistic, along with a
rapidly progressive dementia. The disease typically progresses very rapidly to the major
level of impairment over several months. More rarely, it can progress over 2 years and ap-
pear similar in its course to other NCDs.
636 Neurocognitive Disorders
Risk Factors and Prognosis
Environmental. Cross-species transmission of prion infections, with agents that are
closely related to the human form, has been demonstrated (e.g., the outbreak of bovine
spongiform encephalopathy inducing variant CJD in the United Kingdom during the mid-
1990s). Transmission by corneal transplantation and by human growth factor injection has
been documented, and anecdotal cases of transmission to health care workers have been
reported.
Genetic and physiological. There is a genetic component in up to 15% of cases, associ-
ated with an autosomal dominant mutation.
Diagnostic Markers
Prion disease can be definitively confirmed only by biopsy or at autopsy. Although there are
no distinctive findings on cerebrospinal fluid analysis across the prion diseases, reliable bio-
markers are being developed and include 14-3-3 protein (particularly for sporadic CJD) as
well as tau protein. Magnetic resonance brain imaging is currently considered the most sen-
sitive diagnostic test when DWI is performed, with the most common finding being mullti-
focal gray matter hyperintensities in subcortical and cortical regions. In some individuals,
the electroencephalogram reveals periodic sharp, often triphasic and synchronous dis-
charges at a rate of 0.5-2 Hz at some point during the course of the disorder.
Differential Diagnosis
Other major neurocognitive disorders. Major NCD due to prion disease may appear
similar in its course to other NCDs, but prion diseases are typically distinguished by their
rapid progression and prominent cerebellar and motor symptoms.
Major or Mild Neurocognitive Disorder
Due to Parkinson’s Disease
Diagnostic Criteria
. The criteria are met for major or mild neurocognitive disorder.
. The disturbance occurs in the setting of established Parkinson’s disease.
. There is insidious onset and gradual progression of impairment.
. The neurocognitive disorder is not attributable to another medical condition and is not
better explained by another mental disorder.
Major or mild neurocognitive disorder probably due to Parkinson’s disease should
be diagnosed if 1 and 2 are both met. Major or miid neurocognitive disorder possibly
due to Parkinson’s disease should be diagnosed if 1 or 2 is met:
90 0},
1. There is no evidence of mixed etiology (i.e., absence of other neurodegenerative or
cerebrovascular disease or another neurological, mental, or systemic disease or con-
dition likely contributing to cognitive decline).
2. The Parkinson’s disease clearly precedes the onset of the neurocognitive disorder.
Coding note: For major neurocognitive disorder probably due to Parkinson's disease,
with behavioral disturbance, code first 332.0 (G20) Parkinson’s disease, followed by
294.11 (F02.81) major neurocognitive disorder probably due to Parkinson’s disease, with
behavioral disturbance. For major neurocognitive disorder probably due to Parkinson’s
disease, without behavioral disturbance, code first 332.0 (G20) Parkinson’s disease, fol-
Major or Mild Neurocognitive Disorder Due to Parkinson’s Disease 637
lowed by 294.10 (F02.80) major neurocognitive disorder probably due to Parkinson's dis-
ease, without behavioral disturbance.
For major neurocognitive disorder possibly due to Parkinson’s disease, code 331.9
(G31.9) major neurocognitive disorder possibly due to Parkinson's disease. (Note: Do not
use the additional code for Parkinson’s disease. Behavioral disturbance cannot be coded
but should still be indicated in writing.)
For mild neurocognitive disorder due to Parkinson’s disease, code 331.83 (G31.84).
(Note: Do not use the additional code for Parkinson’s disease. Behavioral disturbance
cannot be coded but should still be indicated in writing.)
