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3GFFIRS 06/26/2014 11:18:24 Page i
Adult Psychopathology
and Diagnosis

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3GFFIRS 06/26/2014 11:18:24 Page iii
Adult Psychopathology
and Diagnosis
Seventh Edition
Edited by
Deborah C. Beidel, B. Christopher Frueh,
and Michel Hersen

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This book is printed on acid-free paper.
∞
Copyright 2014 by John Wiley & Sons, Inc. All rights reserved.
Published by John Wiley & Sons, Inc., Hoboken, New Jersey.Published simultaneously in Canada.No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or byany means, electronic, mechanical, photocopying, recording, scanning, or otherwise, except as permittedunder Section 107 or 108 of the 1976 United States Copyright Act, without either the prior written permissionof the Publisher, or authorization through payment of the appropriate per-copy fee to the CopyrightClearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, (978) 750-8400, fax (978) 646-8600, or onthe web at www.copyright.com. Requests to the Publisher for permission should be addressed to the
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ISBN 978-1-118-65708-9Printed in the United States of America1 0987654321

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Contents
Preface vii
Contributors ix
PARTI OVERVIEW 1
1 Mental Disorders as Discrete Clinical Conditions: Dimensional Versus
Categorical Classi ﬁcation 3
Thomas A. Widiger and Whitney L. Gore
2 The Problem of Dual Diagnosis 35
Melanie E. Bennett, Jason Peer, and Selvija Gjonbalaj-Marovic
3 Structured and Semistructured Interviews for Differential Diagnosis:
Fundamental Issues, Applications, and Features 103
Daniel L. Segal and Kadija N. Williams
4 Impact of Race, Ethnicity, and Culture on the Expression and
Assessment of Psychopathology 131
L. Kevin Chapman, Ryan C. T. DeLapp, Monnica T. Williams
PARTII SPECIFIC DISORDERS 163
5 Schizophrenia 165
Dennis R. Combs, Kim T. Mueser, and Emily Drake
6 Bipolar and Related Disorders 217
David J. Miklowitz and Sheri L. Johnson
7 Mood Disorders: Depressive Disorders 253
Leilani Feliciano and Brenna N. Renn
8 Anxiety Disorders 299
David P. Valentiner, Thomas A. Fergus, Evelyn Behar, andDaniel J. Conybeare
9 Obsessive-Compulsive and Related Disorders 355
Sandra M. Neer and Katie A. Ragsdale
10 Trauma and Stressor-Related Disorders 387
Anouk L. Grubaugh
11 Dissociative Disorders 407
Steven Jay Lynn, Joanna M. Berg, Scott O. Lilienfeld,Harald Merckelbach, Timo Giesbrecht, Michelle Accardi , and Colleen Cleere
12 Somatic Symptom and Related Disorders 451
Gordon J. G. Asmundson, Michel A. Thibodeau, and Daniel L. Peluso
v

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13 Feeding and Eating Disorders 473
Cynthia M. Bulik, Sara E. Trace, Susan C. Kleiman, and Suzanne E. Mazzeo
14 Sleep-Wake Disorders 523
Candice A. Alfano and Simon Lau
15 Sexual Dysfunctions and Paraphilic Disorders 547
Lori A. Brotto, Carolin Klein, and Kenneth J. Zucker
16 Gender Dysphoria 603
Anne A. Lawrence and Kenneth J. Zucker
17 Substance-Related Disorders: Alcohol 641
Eric F. Wagner, Michelle M. Hospital, Mark B. Sobell, and Linda C. Sobell
18 Psychoactive Substance Use Disorders: Drugs 673
Stacey B. Daughters and Matthew Cohen
19 Neurocognitive Disorders 705
Gerald Goldstein
20 Personality Disorders 739
Christopher J. Hopwood and Katherine M. Thomas
Author Index 775
Subject Index 815vi C ONTENTS

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Preface
This is the seventh edition of Adult Psychopathology and Diagnosis and the second that
does not bear Samuel M. Turner ’s name due to his untimely passing. His spirit is here,
however, and we again dedicate this volume to him.
Since publication of the previous edition, the DSM-5 has been released and new
data continue to emerge that force us to continuously reconsider how we approachand conceptualize psychological disorders. Psychopathology is a vibrant ﬁeld and
continuing discoveries regarding the roles of genetics, neurobiology, and behaviorrequire that we continue to update this volume for students and professionals alike.We believe that our eminent authors have captured both major changes and morenuanced ﬁndings in their respective chapters.
The seventh edition contains 20 chapters divided into two parts (Part I: Overview;
Part II: Speci ﬁc Disorders). Part I has four chapters by experts in the ﬁeld: Chapter 1:
Mental Disorders as Discrete Clinical Conditions: Dimensional Versus CategoricalClassi ﬁcation; Chapter 2: The Problem of Dual Diagnosis; Chapter 3: Structured and
Semistructured Interviews for Differential Diagnosis: Fundamentals, Applications,and Features; and Chapter 4: Impact of Race, Ethnicity, and Culture on the Expressionand Assessment of Psychopathology.
Part II on Speciﬁ c Disorders includes 16 chap ters that cover many of the
diagnostic entities and problems seen in daily clinical work by our colleagues inhospitals, clinics, and private practice . Approximately 30% of the chapters have new
authors for this edition. Additionally, as a testament to the vibrancy of the ﬁeld of
psychopathology, the original anxiety disorders chapter has now been split into
three chapters (Chapter 8: Panic Disord er, Agoraphobia, Generalized Anxiety
Disorder, Social Anxiety Disorder, and Speciﬁ c Phobias; Chapter 9: Obsessive-
Compulsive and Related Disorders; and C hapter 10: Trauma and Stress-Related
Disorders: Posttraumatic Stress Disorder, Acute Stress Disorder, and AdjustmentDisorders) in order to adequately address the extensive work in these areas andchanges in DSM-5 .
To the extent possible, we have asked our gracious contributors to follow a
standard format. Exceptions, of course, were granted as dictated by the data inherentin each chapter. Generally, however, each chapter has a description of the disorder, acase study, and material documenting epidemiology, clinical picture, course andprognosis, diagnostic considerations, psychological and biological assessment, andetiological considerations. Each chapter also contains a summary.
Many individuals have contributed to th e seventh edition of this book. First, we
thank our experts, who agreed to share their vast knowledge about their areas of
vii

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study. And as always, we thank Patricia Rossi and her exceptionally professionalstaff at John Wiley & Sons, for underst a n d i n gt h ei m p o r t a n c eo ft h i sa r e ai n
clinical psychology.
Deborah C. Beidel, Orlando, Florida
B. Christopher Frueh, Hilo, Hawaii
Michel Hersen, Hillsboro, Oregonviii P
REFACE

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Contributors
Michelle AccardiDepartment of PsychologyBinghamton University (SUNY)Binghamton, NYCandice A. Alfano, PhDDepartment of PsychologyUniversity of HoustonHouston, TXGordon J. G. Asmundson, PhDDepartment of PsychologyUniversity of ReginaRegina, Saskatchewan, CanadaEvelyn Behar, PhDDepartment of PsychologyUniversity of Illinois
at Chicago
Chicago, ILMelanie E. Bennett, PhDDepartment of PsychiatryUniversity of Maryland,
School of Medicine
Baltimore, MDJoanna BergDepartment of PsychologyEmory UniversityAtlanta, GALori A. Brotto, PhDDepartment of Obstetrics and
Gynecology
University of British ColumbiaVancouver, BC, CanadaCynthia M. Bulik, PhDDepartment of Psychiatry and
Department of Nutrition
University of North Carolina at Chapel HillChapel Hill, NCL. Kevin ChapmanCenter for Mental Health DisparitiesDepartment of PsychologyUniversity of LouisvilleLouisville, KYColleen CleereDepartment of PsychologyBinghamton University (SUNY)Binghamton, NYMatthew CohenDepartment of PsychologyUniversity of North Carolina at Chapel HillChapel Hill, NCDennis R. Combs, PhDDepartment of PsychologyUniversity of Texas at TylerTyler, TXDaniel J. ConybeareDepartment of PsychologyUniversity of Illinois at ChicagoChicago, ILStacey B. Daughters, PhDDepartment of PsychologyUniversity of North Carolina
at Chapel Hill
Chapel Hill, NC
ix

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Ryan C. T. DeLappCenter for Mental Health DisparitiesDepartment of PsychologyUniversity of LouisvilleLouisville, KYEmily DrakeDepartment of PsychologyUniversity of Texas at TylerTyler, TXLeilani Feliciano, PhDDepartment of PsychologyUniversity of Colorado at
Colorado Springs
Colorado Springs, COThomas A. FergusDepartment of PsychologyNorthern Illinois UniversityDekalb, ILTimo Giesbrecht, PhDDepartment of Experimental PsychologyUniversity of MaastrichtMaastricht, The NetherlandsSelvija Gjonbalaj-Marovic, PhDDepartment of PsychiatryUniversity of Maryland, School of
Medicine
College Park, MDGerald Goldstein, PhDPsychological ServiceVeterans Affairs Medical CenterPittsburgh, PAWhitney L. GoreDepartment of PsychologyUniversity of KentuckyLexington, KYAnouk L. Grubaugh, PhDDepartment of PsychiatryMedical University of South CarolinaCharleston, SCChristopher J. Hopwood, PhDDepartment of PsychologyMichigan State UniversityEast Lansing, MIMichelle M. Hospital, PhDDepartment of PsychologyFlorida International UniversityMiami, FLSheri L. Johnson, PhDDepartment of PsychologyUniversity of California, BerkeleyBerkeley, CASusan C. KleimanDepartment of Psychiatry and
Department of Nutrition
University of North Carolina
at Chapel Hill
Chapel Hill, NCCarolin Klein, PhDDepartment of Obstetrics and
Gynecology
University of British ColumbiaVancouver, BC, CanadaSimon LauDepartment of PsychologyUniversity of HoustonHouston, TXAnne A. Lawrence, MD, PhDDepartment of PsychologyUniversity of LethbridgeLethbridge, Alberta, CanadaScott Lilienfeld, PhDDepartment of PsychologyEmory UniversityAtlanta, GASteven Jay Lynn, PhDDepartment of PsychologyBinghamton University (SUNY)Binghamton, NYxC
ONTRIBUTORS

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Suzanne E. Mazzeo, PhDDepartment of PsychologyVirginia Commonwealth UniversityRichmond, VAHarald Merckelbach, PhDDepartment of Experimental Clinical
Psychology
University of MaastrichtMaastricht, The NetherlandsDavid J. Miklowitz, PhDDepartment of Psychiatry –Semel Institute
University of California, Los AngelesLos Angeles, CAKim T. Mueser, PhDDepartment of Psychiatry and
Community and Family Medicine
Dartmouth College Medical SchoolHanover, NHSandra M. Neer, PhDDepartment of PsychologyUniversity of Central FloridaOrlando, FLDaniel L. PelusoDepartment of PsychologyUniversity of ReginaRegina, Saskatchewan, CanadaJason Peer, PhDDepartment of PsychiatryUniversity of Maryland School of MedicineBaltimore, MDKatie RagsdaleDepartment of PsychologyUniversity of Central FloridaOrlando, FLBrenna N. RennDepartment of PsychologyUniversity of Colorado at Colorado
Springs
Colorado Springs, CODaniel L. Segal, PhDDepartment of PsychologyUniversity of Colorado at Colorado
Springs
Colorado Springs, COMark B. Sobell, PhDCenter for Psychological StudiesNova Southeastern UniversityFort Lauderdale, FLLinda C. Sobell, PhDCenter for Psychological StudiesNova Southeastern UniversityFort Lauderdale, FLMichel A. ThibodeauDepartment of PsychologyUniversity of ReginaRegina, Saskatchewan, CanadaKatherine M. ThomasDepartment of PsychologyMichigan State UniversityEast Lansing, MISara E. Trace, PhDDepartment of PsychiatryUniversity of North Carolina
at Chapel Hill
Chapel Hill, NCDavid P. Valentiner, PhDDepartment of PsychologyNorthern Illinois UniversityDekalb, ILEric F. Wagner, PhDCollege of Public Health and
Social Work
Florida International UniversityMiami, FLThomas A. Widiger, PhDDepartment of PsychologyUniversity of KentuckyLexington, KYContributors xi

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Kadija N. WilliamsDepartment of PsychologyUniversity of Colorado at Colorado
Springs
Colorado Springs, COMonnica T. WilliamsCenter for Mental Health DisparitiesDepartment of PsychologyUniversity of LouisvilleLouisville, KYKenneth J. Zucker, PhDDepartment of Psychiatry and
Psychology
University of TorontoToronto, Ontario, Canadaxii C
ONTRIBUTORS

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PART I
OVERVIEW

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CHAPTER 1
Mental Disorders as Discrete Clinical
Conditions: Dimensional Versus
Categorical Classi ﬁcation
THOMAS A. WIDIGER and WHITNEY L. GORE
INDSM-IV , there [was] no assumption that each category of mental disorder is
a completely discrete entity with absolute boundaries dividing it from othermental disorders or from no mental disorder” (American Psychiatric Association
[APA], 2000, p. xxxi). This carefully worded disclaimer, however, was somewhathollow, as it was the case that “DSM-IV [was] a categorical classi ﬁcation that divides
mental disorders into types based on criterion sets with de ﬁning features ”(APA, 2000,
p. xxxi). The categorical model of classi ﬁcation is consistent with a medical tradition
in which it is believed (and often con ﬁrmed in other areas of medicine) that disorders
have speci ﬁc etiologies, pathologies, and treatments (Guze, 1978; Guze & Helzer, 1987;
Zachar & Kendler, 2007).
Clinicians, following this lead, diagnosed and conceptualized the conditions
presented in DSM-IV-TR as disorders that are qualitatively distinct from normal
functioning and from one another. DSM-IV-TR provided diagnostic criterion sets to
help guide clinicians toward a purportedly correct diagnosis and an additionalsupplementary section devoted to differential diagnosis that indicated “how to
differentiate [the] disorder from other disorders that have similar presenting charac-teristics” (APA, 2000, p. 10). The intention of the manual was to help the clinician
determine which particular mental disorder provides the best explanation for thesymptoms and problems facing the patient. Clinicians devote initial time with a newpatient to identify, through differential diagnosis, which speci ﬁc disorder best
explains a patient ’s presenting complaints. The assumption is that the person is
suffering from a single, distinct clinical condition, caused by a speci ﬁc pathology
for which there will be a speci ﬁc treatment (Frances, First, & Pincus, 1995).
Authors of the diagnostic manual devote a considerable amount of time writing,
revising, and researching diagnostic criteria to improve differential diagnosis. Theybuttress each disorder ’s criterion set, trying to shore up discriminant validity and
distinctiveness, following the rubric of Robins and Guze (1970) that the validity of adiagnosis rests in large part on its “delimitation from other disorders” (p. 108). “These“
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criteria should . . . permit exclusion of borderline cases and doubtful cases (anundiagnosed group) so that the index group may be as homogeneous as possible ”
(Robins & Guze, 1970, p. 108).
Scientists may devote their careers to attempting to identify the speci ﬁc etiology,
pathology, or treatment for a respective diagnostic category. Under the assumptionthat the diagnoses do in fact refer to qualitatively distinct conditions, it follows thatthere should be a speci ﬁc etiology, pathology, and perhaps even a speci ﬁc treatment
for each respective disorder. The theories, hypotheses, ﬁndings, and disputes regard-
ing the speci ﬁc etiology, pathology, and/or treatment of a respective mental disorder
largely inform the respective chapters of professional, graduate, and undergraduatetexts on psychopathology, such as this current edition of Adult Psychopathology and
Diagnosis .
However, the question of whether mental disorders are, in fact, discrete clinical
conditions or arbitrary distinctions along continuous dimensions of functioning hasbeen a long-standing issue (Kendell, 1975) and its signi ﬁcance is escalating with the
growing recognition of the limitations of the categorical model (Hyman, 2010;Widiger & Clark, 2000; Widiger & Samuel, 2005). The principal model for thevalidation of mental disorder diagnostic categories was provided by Robins andGuze (1970), who articulated ﬁve fundamental phases: clinical description, laboratory
study, delimitation from other disorders, follow-up, and family studies. However, theresearch that has accumulated to date has not supported the validity of the delimita-tion of the disorders from one another. “Indeed, in the last 20 years, the categorical
approach has been increasingly questioned as evidence has accumulated that the so-called categorical disorders like major depressive disorder and anxiety disorders,and schizophrenia and bipolar disorder seem to merge imperceptibly both intoone another and into normality . . . with no demonstrable natural boundaries ”(First,
2003, p. 661). As expressed by the vice chair of DSM-5 ,“the failure of DSM-III criteria
to speci ﬁcally de ﬁne individuals with only one disorder served as an alert that the
strict neo-Kraepelinian categorical approach to mental disorder diagnoses advocatedby Robins and Guze (1970), Spitzer, Endicott, & Robins (1978), and others could havesome serious problems ”(Regier, 2008, p. xxi). As acknowledged by Kendell and
Jablensky (2003), “it is likely that, sooner or later, our existing typology will be
abandoned and replaced by a dimensional classi ﬁcation ”(p. 8).
In 1999, a DSM-5 Research Planning Conference was held under joint sponsorship
of the APA and the National Institute of Mental Health (NIMH), the purpose of whichwas to set research priorities that would optimally inform future classi ﬁcations. One
impetus for this effort was the frustration with the existing nomenclature.
In the more than 30 years since the introduction of the Feighner criteria by Robins
and Guze, which eventually led to DSM-III, the goal of validating these syndromes
and discovering common etiologies has remained elusive. Despite many proposedcandidates, not one laboratory marker has been found to be speci ﬁc in identifying any
of the DSM -deﬁned syndromes. Epidemiologic and clinical studies have shown
extremely high rates of comorbidities among the disorders, undermining the hypoth-esis that the syndromes represent distinct etiologies. Furthermore, epidemiologicstudies have shown a high degree of short-term diagnostic instability for manydisorders. With regard to treatment, lack of treatment speciﬁ city is the rule rather
than the exception (Kupfer, First, & Regier, 2002, p. xviii).4OVERVIEW

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DSM-5 Research Planning Work Groups were formed to develop white papers that
would set an effective research agenda for the next edition of the diagnostic manual.The Nomenclature Work Group, charged with addressing fundamental assumptionsof the diagnostic system, concluded that it will be “important that consideration be
given to advantages and disadvantages of basing part or all of DSM-V on dimensionsrather than categories ”(Rounsaville et al., 2002, p. 12).
The white papers developed by the DSM-5 Research Planning Work Groups were
followed by a series of international conferences whose purpose was to further enrichthe empirical data base in preparation for the eventual development of DSM-5 (a
description of this conference series can be found at www.dsm5.org). The ﬁrst
conference was devoted to shifting personality disorders to a dimensional modelof classi ﬁcation (Widiger, Simonsen, Krueger, Livesley, & Verheul, 2005). The ﬁnal
conference was devoted to dimensional approaches across the diagnostic manual,including substance use disorders, major depressive disorder, psychoses, anxietydisorders, and developmental psychopathology, as well as the personality disorders(Helzer, Kraemer, et al., 2008).
In the introduction to DSM-5 (APA, 2013), the apparent failure of the categorical
model of classi ﬁcation is duly noted. “The historical aspiration of achieving diagnostic
homogeneity by progressively subtyping within disorder categories no longer issensible; like most common human ills, mental disorders are heterogeneous atmany levels, ranging from genetic risk factors to symptoms ”(APA, 2013, p. 12). It
was a major purpose of the authors of DSM-5 to have this new edition of the diagnostic
manual be “central to the development of dimensional approaches to diagnosis that
will likely supplement or supersede current categorical approaches in the comingyears ”(APA, 2013, 13). However, as will be discussed herein, the diagnoses of DSM-5
remain largely categorical.
The purpose of this chapter is to review the DSM-IV-TR and DSM-5 categorical
diagnostic approach. The chapter begins with a discussion of the problematic bound-aries among the DSM-IV-TR and DSM-5 categorical diagnoses. We then focus in
particular on depression, alcohol abuse and dependence, personality disorders, andintellectual disability. We conclude with a discussion of the shifts within DSM-5
toward a dimensional classi ﬁcation.
DIAGNOSTIC BOUNDARIES
In an effort to force differential diagnosis, a majority of diagnoses in DSM-III (APA,
1980) contained exclusionary criteria specifying that a respective disorder could not bediagnosed if it occurred in the presence of another disorder. These exclusions by ﬁat
did not prove to be effective (Boyd et al., 1984) and many were deleted in DSM-III-R
(APA, 1987). As expressed at the time by Maser and Cloninger (1990), “it is clear that
the classic Kraepelinian model in which all psychopathology is comprised of discreteand mutually exclusive diseases must be modi ﬁed or rejected ”(p. 12).
Many DSM-5 diagnostic criterion sets, however, continue to include exclusionary
criteria that attempt to force clinicians to make largely arbitrary choices amongalternative diagnoses (APA, 2013), and it is also evident that there will likely continueto be a highly problematic rate of diagnostic co-occurrence (Kessler, Chiu, Demler, &Walters, 2005; Krueger & Markon, 2006; Maser & Patterson, 2002; Widiger & Clark,Mental Disorders as Discrete Clinical Conditions 5

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2000). The term comorbidity refers to the co-occurrence of distinct disorders, apparently
interacting with one another, each presumably with its own etiology, pathology, andtreatment implications (Feinstein, 1970). If one considers the entire diagnostic manual(which has not yet been done by any epidemiological study), it would likely beexceedingly rare for any patient to meet the criteria for just one disorder, and thecomorbidity rises even further if one considers lifetime co-occurrence. Brown, Camp-bell, Lehman, Grisham, and Mancill (2001) reported that 95% of individuals in aclinical setting who meet criteria for lifetime major depression or dysthymia also meetcriteria for a current or past anxiety disorder. In the case of psychopathology,comorbidity may be saying more about the invalidity of existing diagnostic distinc-tions than the presence of multiple coexisting conditions (Krueger, 2002; Widiger &Edmundson, 2011).
Diagnostic comorbidity has become so prevalent that some researchers have
argued for an abandonment of the term comorbidity in favor of a term (e.g., co-
occurrence) that is more simply descriptive and does not imply the presence of distinctclinical entities (Lilienfeld, Waldman, & Israel, 1994). There are instances in which thepresence of multiple diagnoses suggests the presence of distinct yet comorbidpsychopathologies, but in most instances the presence of co-occurring diagnosesdoes appear to suggest the presence of a common, shared pathology and, therefore, apossible failing of the current diagnostic system (Krueger & Markon, 2006; Widiger &Clark, 2000). “Comorbidity may be trying to show us that many current treatments are
not so much treatments for transient ‘state ’mental disorders of affect and anxiety as
they are treatments for core processes, such as negative affectivity, that span normaland abnormal variation as well as undergird multiple mental disorders ”(Krueger,
2002, p. 44).
Diagnostic criteria have traditionally been developed and modi ﬁed in order to
construct a disorder that is as homogeneous as possible, thereby facilitating thelikelihood of identifying a speci ﬁc etiology, pathology, and treatment (Robins &
Guze, 1970). However, the typical result of this effort is to leave many casesunaccounted for. In addition, despite the best effort to construct homogeneous anddistinct syndromes, DSM-IV-TR was still replete with heterogeneous conditions with
overlapping boundaries (Smith & Combs, 2010). New diagnostic categories are addedto the nomenclature in large part to decrease clinicians ’reliance on the nonspeci ﬁc,
wastebasket label of “not otherwise speci ﬁed”(NOS). NOS was among the most
frequent disorders within clinical populations (Widiger & Edmundson, 2011). Thefunction of many of the new disorders that have been added to recent editions of themanual have not involved the identi ﬁcation of uniquely new forms of psycho-
pathology. Their purpose was generally instead to ﬁll problematic gaps. Notable
examples for DSM-IV included bipolar II ( ﬁlling a gap between DSM-III-R bipolar and
cyclothymic mood disorders), mixed anxiety-depressive disorder (a gap betweenanxiety and mood disorders), depressive personality disorder (personality and mooddisorders), postpsychotic depressive disorder of schizophrenia (schizophrenia andmajor depression) (Frances et al., 1995).
When new diagnoses are added to ﬁll gaps, they have the ironic effect of creating
additional boundary problems, thereby making differential diagnosis even moreproblematic (Phillips, Price, Greenburg, & Rasmussen, 2003; Pincus, Frances, Davis,First, & Widiger, 1992; Pincus, McQueen, & Elinson, 2003). One must ask, for instance,6OVERVIEW

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whether it is really meaningful or useful to determine whether mixed anxiety-depressive disorder is a mood or an anxiety disorder, whether schizoaffective disorderis a mood disorder or a form of schizophrenia (Craddock & Owen, 2010, whetherpostpsychotic depressive disorder of schizophrenia is a form of depression orschizophrenia, whether early onset dysthymia is a mood or a personality disorder(Widiger, 2003), whether acute stress disorder is an anxiety or a dissociative disorder(Cardena, Butler, & Spiegel, 2003), whether hypochondriasis is an anxiety disorder ora somatoform disorder, whether body dysmorphic disorder is an anxiety, eating, orsomatoform disorder, and whether generalized social phobia is an anxiety or apersonality disorder (Widiger, 2001a). In all these cases the most accurate answeris likely to be that each respective disorder includes features of different sections of thediagnostic manual. Yet the arbitrary and procrustean decision of which single sectionof the manual in which to place each diagnosis must be made by the authors of acategorical diagnostic manual, and a considerable amount of effort and research isconducted to guide this decision, followed by further discussion and research to refuteand debate whatever particular categorical decision was made.
There are comparable examples of what migh t be arbitrary splitting of categories
inDSM-5 (APA, 2013). DSM-5 split out from reactive attachment disorder a new
diagnosis of disinhibited social engagement disorders. Binge eating disorder (whichwas originally included within the diagn osis of bulimia nervosa) obtained of ﬁcial
recognition. However, for the most part, changes that occurred in DSM-5 were
consistent with the intention to shift t he manual more closely to a dimensional
model. For example, there are cases in which previously “distinct ”diagnoses were
lumped together rather than split apart. For example, DSM-5 autism spectrum
disorder subsumes within one diagnosis DSM-IV-TR autistic disorder, Asperger ’s
disorder, childhood disintegrative disorder, and pervasive developmental disordernot otherwise speci ﬁed. The archaic subtypes of schizophrenia were deleted.
“Instead a dimensional approach to rating severity of core symptoms of schizo-
phrenia is included in DSM-5 Section III ”(APA, 2013, p. 810). The DSM-IV-TR
diagnoses of somatization disorder, hypo chondriasis, and pain disorder were all
subsumed within one diagnosis of somatic symptom disorder. Pathological gam-bling was lumped with substance use diso rders within a new section concerning
addictive disorders, and substance abuse and dependence are no longer concep-tualized as categorically distinct conditions. Included in Section III of DSM-5 is a
proposed dimensional trait model that would subsume all of the existing personal-ity disorder categories.D
EPRESSION
Mood disorders is a section of the APA diagnostic manual for which the presence ofqualitatively distinct conditions is particularly difﬁ cult to defend, especially for the
primary diagnoses of dysthymia and major depressive disorder. Discussed here willbe early onset dysthymia, the continuum of depression, and subthreshold majordepression, along with more general points concerning the boundary between moodand personality disorder.
There is no meaningful distinction between early-onset dysthymia, an of ﬁcially
recognized mood disorder diagnosis, and depressive personality disorder, a diagnosisMental Disorders as Discrete Clinical Conditions 7

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proposed for DSM-IV but included within its appendix (APA, 2000). In fact, much of
the empirical and conceptual basis for adding dysthymia to the DSM-III (APA, 1980)
came from research and clinical literature concerning depressive personality (i.e.,Keller, 1989). As acknowledged by the principal architects of DSM-III, dysthymia is
“roughly equivalent to the concept of depressive personality” (Spitzer, Williams, &
Skodol, 1980, p. 159). Depressive personality disorder was included within the mooddisorders section of DSM-III despite the recommendations to recognize its existence as
a disorder of personality (Klerman, Endicott, Spitzer, & Hirschfeld, 1979) because itresembled the symptomatology of other mood disorders (i.e., depressed mood) morethan it resembled the symptoms of other personality disorders (e.g., schizoid).However, whereas mood disorders are de ﬁned largely by similarity in content
(i.e., mood being the predominant feature; APA, 2013), the personality disordersare de ﬁned largely by form (i.e., early onset, pervasive, and chronic) often with quite
different content (e.g., schizoid also shares little resemblance to histrionic personalitydisorder).
After DSM-III was published, it became evident that many of the persons who were
consistently and characteristically pessimistic, gloomy, cheerless, glum, and sullen(i.e., dysthymic) had been that way since childhood and that in many cases no apparentor distinct age of onset could be established. In other words, its conceptualization as apersonality disorder became apparent. DSM-III-R, therefore, added an early-onset
subtype (APA, 1987) and acknowledged that “this disorder usually begins in childhood,
adolescence, or early adult life, and for this reason has often been referred to as aDepressive Personality ”(APA, 1987, p. 231).
Personality disorder resea rchers proposed again for DSM-IV to include a depres-
sive personality disorder diagnosis. They were told that in order for it to beincluded, it needed to be distinguished from the already established diagnosis ofearly-onset dysthymia, a task th at might be considered rather dif ﬁcult, if not unfair,
given that the latter construct was based in large part on the former construct.Nevertheless, the DSM-IV Personality Disorders Work Group developed a pro-posed diagnostic criterion set that place d relatively more emphasis on cognitive
features not currently included within th e criterion set for dysthymia (including
early-onset), as well as excluding somatic features (Task Force on DSM-IV, 1991).
This criterion set was provided to the DSM-IV Mood Disorders Work Group toinclude within their DSM-IV ﬁeld trial to determine empirically whether it was
indeed possible to demarcate an area of func tioning not yet covered by early-onset
dysthymia, or at least identify persons not yet meeting diagnostic criteria for early-onset dysthymia.
The proposed criterion set was successful in reaching this goal (Phillips et al.,
1998), which, perhaps, should not be surp rising because no criterion set for a
categorical diagnosis appears to be entirely successful in covering all cases. How-ever, the Mood Disorders Work Group was equally impressed with the potentialutility of the depressive personality diagn ostic criteria for further describing and
expanding the coverage of dysthymia (Kelle r et al., 1995) and, therefore, incorpo-
rated much of the proposed criteria for dep ressive personality into their proposed
revisions for dysthymia, including early -onset (Task Force on DSM-IV, 1993). The
DSM-IV Task Force recognized that it m ight be problematic to now require the
personality disorder researchers to further rede ﬁne depressive personality to8O
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distinguish it from this further revision of dysthymia. Therefore, the DSM-IV Task
Force decided instead to include both criterion sets in the appendix to DSM-IV
(along with the original criterion set f or dysthymia within the mood disorders
section), with the acknowledgment that th e r em a yn o tb ea n ym e a n i n g f u ld i s t i n c t i o n
between them (APA, 1994; Frances et al., 1995). However, depressive personalitydisorder was not even included within the appendix for DSM-5. Dysthymia and
chronic major depressive disorder are now collapsed within persistent depressive
disorder in DSM-5.
The Continuum of Depression The common view is that many instances of sadness (or
even depression) do not constitute a mental disorder. Persons can be very sad withouthaving a mental disorder (Horwitz & Wake ﬁeld, 2007). However, a simple inspection
of the diagnostic criteria for major depressive disorder would not lend con ﬁdence to a
conceptualization of this condition as being qualitatively distinct from “normal ”
depression or sadness (Andrews et al., 2008). Persons who are just very sad willhave most of the same attributes (if not all of them) but just at a lesser degree ofseverity. The diagnostic criteria for major depressive disorder include depressedmood, loss of interest or pleasure, weight loss (or gain), insomnia (or hypersomnia),psychomotor retardation (or agitation), loss of energy, feelings of worthlessness, and/or diminished capacity to make decisions (APA, 2013). Each of these diagnostic criteriais readily placed along a continuum of severity that would shade imperceptibly intowhat would be considered a “normal ”sadness or depression. DSM-5, therefore,
includes speciﬁ c thresholds for each of them, but they are clearly arbitrary thresholds
that simply demarcate a relatively higher level of severity from a lower level ofseverity (e.g., “nearly every day” or“markedly diminished,” and at least a “2-week”
period; APA, 2013, p. 188). The diagnosis requires ﬁve of these nine criteria, with no
apparent rationale for this threshold other than it would appear to be severe enough tobe defensible to be titled as a “major ”depressive episode, as distinguished from a
“minor ”depressive episode, which is then distinguished from “normal ”sadness
(APA, 2013).
Depression does appear to shade imperceptibly into “normal ”sadness (Andrews
et al., 2008). Üstün and Sartorius (1995) conducted a study of 5,000 primary-carepatients in 14 countries and reported a linear relationship between disability andnumber of depressive symptoms. Kessler, Zhao, Blazer, and Swartz (1997) examinedthe distribution of minor and major symptoms of depression using data from theNational Comorbidity Survey. They considered the relationship of these symptomswith parental history of mental disorder, number and duration of depressive episodes,and comorbidity with other forms of psychopathology. Respective relationshipsincreased with increasing number of symptoms, with no clear, distinct break. Saka-shita, Slade, and Andrews (2007) examined the relationship between the number ofsymptoms of depression and four measures of impairment using data from theAustralian National Survey of Mental Health and Well-Being, and found that therelationship was again simply linear, with no clear or natural discontinuity to supportthe selection of any particular cutoff point.
Taxometrics refers to a series of related statistical techniques to detect whether a set
of items is optimally understood as describing (assessing) a dimensional or acategorical construct (Beauchaine, 2007; Ruscio & Ruscio, 2004). Other statisticalMental Disorders as Discrete Clinical Conditions 9

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techniques, such as cluster or factor analyses, presume that the construct is eithercategorical or dimensional (respectively) and then determines how best to characterizethe variables or items in either a categorical or dimensional format (respectively).Taxometric analyses are uniquely intriguing in providing a direct test of whichstructural model is most valid in characterizing the set of items or variables.
A number of taxometric studies have be en conducted on various symptoms and
measures of depression. The ﬁrst was provided by Ruscio and Ruscio (2000) in their
taxometric analyses of items from the Beck Depression Inventory and, indepen-dently, items from the Zung Self-Rating Depression Scale in a sample of 996 maleveterans who had received a diagnosis of post-traumatic stress disorder but alsohad a high prevalence rate of major depressive disorder, as well as a sample of8,045 individuals from the general population (60% female) who completed theitems from the Depression scale of the Minn esota Multiphasic Personality Inven-
tory. They indicated that “results of both studies, drawing on three widely used
measures of depression, corroborate d the dimensionality of depression ”(Ruscio &
Ruscio, 2000, p. 473).
The taxometric ﬁndings of Ruscio and Ruscio (2000) have been subsequently
replicated, including taxometric analyses of (a) structured interview assessments ofDSM-IV-TR major depressive disorder symptoms and, independently, items from the
Beck Depression Inventory in a sample of 960 psychiatric outpatients (Slade, 2007), (b)major depressive disorder diagnostic criteria assessed in the 1,933 persons whoendorsed at least one criterion in the Australian National Survey of Mental Healthand Well-Being (Slade & Andrews, 2005), (c) self- and parent-reported depressivesymptoms in 845 children and adolescents drawn from the population-based GeorgiaHealth and Behavior Study (Hankin, Fraley, Lahey, & Waldman, 2005), (d) responsesto MMPI-2 depression scales completed by 2,000 psychiatric inpatients and out-patients (Franklin, Strong, & Greene, 2002), (e) epidemiologic survey of depressivesymptoms within 392 college students (Baldwin & Shean, 2006), (f) Beck DepressionInventory items reported by 2,260 college students (Ruscio & Ruscio, 2002), and (g)depression items in the Composite International Diagnostic Interview as administeredin the National Comorbidity Survey to 4,577 participants who endorsed the itemconcerning a lifetime occurrence of sad mood or loss of interest (Prisciandoro &Roberts, 2005). However, in contrast to the ﬁndings from these eight taxometric
studies, three taxometric studies have supported a latent class taxon, includingsemistructured interview assessments of DSM-IV-TR major depressive disorder
symptoms in 1,800 psychiatric outpatients (Ruscio, Zimmerman, McGlinchey,Chelminski, & Young, 2007), interview and self-report assessments of depression in1,400 high school students (Solomon, Ruscio, Seeley, & Lewinsohn, 2006), and self-report and interview data on depression in 378 adolescents receiving treatment fordepression (Ambrosini, Bennett, Cleland, & Haslam, 2002). In sum, the bulk of theevidence does appear to support a dimensional understanding of depression, but thereis some ambiguity and inconsistency in the taxometric ﬁndings (Beach & Amir, 2003;
Beauchaine, 2007; Widiger, 2001b).Subthreshold Major Depression Depression is a section of the diagnostic manual that
does have considerable dif ﬁculty identifying or de ﬁning a clear boundary with
“normal ”sadness. Subthreshold cases of depression (i.e., persons with depressive10 O
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symptoms below the threshold for a DSM-5 mental disorder diagnosis) are clearly
responsive to pharmacologic interventions, do seek treatment for their sadness, andare often being treated within primary care settings (Judd, Schettler, & Akiskal, 2002;Pincus et al., 2003). These facts contributed to the proposal to include within anappendix to DSM-IV a diagnosis of “minor depressive disorder,” which it is acknowl-
edged “can be dif ﬁcult to distinguish from periods of sadness that are an inherent part
of everyday life ”(APA, 2000, p. 776).
Wake ﬁeld (2007) has been critical of the criteria for major depressive disorder for
including an inconsistently applied exclusion criterion. The DSM-IV-TR excluded
most instances of depressive reactions to the loss of a loved one (i.e., uncomplicatedbereavement). Depression after the loss of a loved one could be considered a mentaldisorder if “the symptoms persist for longer than 2 months ”(APA, 2000, p. 356).
Allowing persons just 2 months to grieve before one is diagnosed with a mentaldisorder does appear to be rather arbitrary. More importantly, it is also unclear ifdepression in response to other losses should not also then be comparably excluded,such as depression secondary to the loss of a job or physical health (Wake ﬁeld,
Schimtz, First, & Horwitz, 2007). Why the loss of a person is treated so differently fromthe loss of health or a job is not clear.
On the other hand, one could argue alternatively that all exclusion criteria should be
removed. Perhaps the problem is not that depression in response to a loss of a job orphysical disorder should not be a disorder, analogous to bereavement (Wake ﬁeld,
2007); perhaps the problem is that bereavement should be a mental disorder (Bonannoet al., 2007; Forstmeier & Maercker, 2007; Widiger & Miller, 2008). What is currentlyconsidered to be a normal depression in response to the loss of a loved one does often,if not always, include pain and suffering, meaningful impairment to functioning, andis outside of the ability of the bereaved person to fully control, the essential hallmarksof a mental disorder (Widiger & Sankis, 2000). The depression is a reasonable responseto the loss of a loved one, a psychological trauma, but many physical disorders andinjuries are reasonable and understandable responses to a physical trauma. The loss isperhaps best understood as part of the etiology for the disorder, not a reason for whicha disorder is not considered to be present (Widiger, 2012a).
One of the major revisions for DSM-5 was indeed to weaken the distinction between
normal bereavement and a mental disorder of depression. DSM-5 no longer excludes
the diagnosis of a major depressive disorder if the depression is secondary to the lossof a loved one. “Responses to a signi ﬁcant loss (e.g., bereavement, ﬁnancial ruin, losses
from a natural disaster, a serious medical illness or disability) ”(APA, 2013, p. 161) can
now all be diagnosed as a mental disorder.A
LCOHOL ABUSE AND DEPENDENCE
One of the sections of the diagnostic manual for which a categorical model ofclassi ﬁcation and conceptualization has had a ﬁrmly entrenched tradition has
been the substance use disorders. Alcoholism in particular has long been conceptual-ized as a qualitatively distinct disease (Garbutt, 2008; Goodwin & Guze, 1996). Asigniﬁcant change to its diagnosis and conceptualization occurred with DSM-III-R
(APA, 1987) when it shifted from being understood as a purely physiological
dependence to a broader and less speci ﬁc behavioral dependence (Carroll,Mental Disorders as Discrete Clinical Conditions 11

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Rounsaville, & Bryant, 1994; Edwards & Gross, 1976). “Dependence is seen as a
complex process that re ﬂects the central importance of substances in an individual ’s
life, along with a feeling of compulsion to continue taking the substance and
subsequent problems controlling use ”(Schuckit et al., 1999, p. 41). To many, though,
the diagnosis does still refer to a disease , but one that is developed through a normal
social-learning history (Kandel, 1998).
However, the diagnosis has been broadened considerably in DSM-5 wherein it
is referred to as a behavioral addiction, and would, therefore, be listed along withpathological gambling (Martin, 2005; Petry, 2006; Potenza, 2006). Pathological gamblinghas been considered by many substance use and pathological gambling researchers andclinicians to be an addiction, but it could not be included within the substance relateddisorders section because it does not involve the ingestion of a substance (Bradford,Geller, Lesieur, Rosenthal, & Wise, 1996). This requirement has been deleted in DSM-5,
with the section renamed “substance-related and addictive disorders ”(APA, 2013).
This new class of disorders could eventually contain a wide variety of possible
behavioral addictions, including an exce ssive participation in shopping, sex, or
the Internet. As stated at one point on the DSM-5 website, along with patho-
logical gambling, “other addiction-like behavioral disorders such as ‘Internet
addiction ’. . . will be considered as potential additions to this category as research
data accumulate” (APA, 2010, “Substance Related Disorders, ”para. 1). The preface
to this section of the diagnostic manual ex plicitly states that Internet, sex, and
shopping addictions are not includ ed because there is currently insuf ﬁcient evi-
dence to support their validity. However , it is apparent that the broadening of
the concept of substance dependence to include behavioral forms of addictionwill encourage clinicians to diagnose these additional variants. “This ‘slippery
slope ’makes it dif ﬁcult to know where to draw the line demarcating any excessive
behavior as an addiction ”(Petry, 2005a, p. 7). Provided within an appendix to
DSM-5 for conditions needing further study is Internet gaming disorder (i.e.,
behavioral addiction on Internet games), including its diagnostic criteria, riskfactors, prevalence, and differential diagnosis. Proposed for inclusion in the sexdisorders section of DSM-5 was hypersexual disorder, which can indeed be identi-
ﬁed as a sex addiction (Kafka, 2010; Ragan & Martin, 2000; Winters, 2010).
The distinction between harmful substance use and a substance use disorder is
itself unclear and indistinct. Presumably, persons can choose to consume alcoholwithout being compelled to do so by the presence of a mental disorder. The DSM-5
diagnostic criteria for a substance use diso r d e ra r ef a l l i b l ei n d i c a t o r sf o rh a r m f u l
and dyscontrolled usage (e.g., use more than originally intended, continue to usedespite social consequences, and reduction of other activ ities in preference for the
substance; APA, 2013). The more of these indicators of dyscontrol that are present,the more likely that there is in fact dyscon trol, but none can be considered infal-
lible in the identi ﬁcation of dyscontrol and no particular number of them clearly
demarcates a boundary between the presence versus absence of dyscontrolled
usage. It is not even clear how much purportedly volitional or regulatory controlan
ormal, healthy person has over adaptive, healthy behaviors (Bargh & Ferguson,
2000; Howard & Conway, 1986; Kirsch & Lynn, 2000; Wegner & Wheatley, 2000),let alone the boundary between controlled and dyscontrolled harmful behaviors.Both normal and abnormal human function ing is, at best, the result of a complex12 O
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interaction of apparent volitional choic e with an array of biogenetic and environ-
mental determinants.
The distinction between DSM-IV-TR alcohol abuse and dependence was equally
fuzzy. Abuse has generally been considered to be simply a residual category and/or aless severe form of dependence (Saunders, 2006). Some of the diagnostic criteria forabuse were contained with the criterion set for dependence (e.g., interference withsocial, occupational, or recreational activities), which is always a problem for disordersthat would be considered to be qualitatively distinct. It is largely for this reason thatthe formal distinction between abuse and dependence was abandoned in DSM-5
(APA, 2013).
The diagnostic criteria for alcohol depen dence were written largely in an effort to
describe a prototypic case of the disorder, a practice that is still followed for all but afew of the disorders throughout DSM-5 . However, prototypic cases are typically
understood to be the most severe cases an d/or the cases that involve all possible
features or symptoms of th e disorder (First & Westen , 2007). The construction of
diagnostic criterion sets in terms of prototypic cases does work to an extent, but italso fails to adequately describe many of the actual cases, including the subthresholdcases, and perhaps even the typical case s, depending upon the distribution of
features and symptomatolog y within the population. Constructing criterion sets in
terms of prototypic cases can be comparable to con ﬁning the description and
diagnosis of (for instance) intellectual disability to the most severe variant, andthen attempting to apply this description to mild and moderate variants; a methodof diagnosis that would obviously be sorely l imited. The limitations of this approach
are now becoming more closely appreciated in the diagnosis of dyscontrolledsubstance use and, more speci ﬁcally, alcohol use disorders, where the existing
criterion sets are failing to adequately de scribe (for instance) dyscontrolled and
impairing alcohol usage in adolescents (Crowley, 2006) and other “diagnostic
orphans ”(Saunders, 2006).
The limitation is perhaps most clearl y demonstrated in studies using item
response theory (IRT) methodology. IRT allows the researcher to investigate theﬁdelity with which items are measuring a latent trait along the length of its
continuum, contrasting, for instance, the amount of information that differentdiagnostic criteria provide at different levels of the latent trait (Muthen, 2006).
Some diagnostic criteria, for instance, mig ht be most useful in distinguishing among
mild cases of the disorder, whereas other diagnostic criteria are most useful indistinguishing among the more severe cases of the disorder. A number of IRTanalyses have now been conducted for the diagnosis of substance dependence (and
other disorders) and the ﬁndings are remarkably consistent (Reise & Waller, 2009).
The existing diagnostic criterion sets (and/or symptoms currently assessed inexisting instruments) cluster around t he high end of the disorder as opposed to
being spread out across the entire range of the continuum (e.g., Kahler & Strong,2006; Langenbucher et al., 2004; Muthen, 2006; Proudfoot, Baillie, & Teesson, 2006;Saha, Chou, & Grant, 2006). This consistent pattern of results is in stark contrast to
what is traditionally found in cognitive ability testing, where IRT analyses havebeen largely developed and previou sly applied (Reise & Waller, 2009).
It is evident from the IRT analyses that the existing diagnostic criterion sets are
sorely inadequate in characterizing the lower and even middle range of substance useMental Disorders as Discrete Clinical Conditions 13

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dysfunction, consistent with the DSM-IV-TR and DSM-5 descriptions being con ﬁned
to a prototypic case (of the presumably qualitatively distinct disorder). If alcohol usagewas conceptualized along a continuum, the job of the authors of the diagnostic manualwould be to construct a description and measurement of the disorder that adequatelyrepresents each of the levels or degrees to which the disorder appears along thiscontinuum rather than attempt to describe the prototypic case. The DSM-IV-TR
criterion set was con ﬁned to the most severe cases and was not describing well a
large proportion of persons with clinically signi ﬁcant alcohol use dysfunction. As a
result, clinicians had to rely on the nondescriptive, wastebasket diagnosis of NOS todescribe the lower range of the continuum (Saunders, 2006).
A step in the direction of recognizing the continuous nature of substance use
disorder was incorporated in DSM-5. Along with the abandonment of the distinction
between abuse and dependence, DSM-5 also includes a rating of severity for a
substance use disorder, depending upon the number of diagnostic criteria that aremet. For example, a “mild ”substance use disorder is suggested by the presence of just
two to three features (APA, 2013). However, the features for the mildest and the mostsevere cases are still the same. What would be more informative would be to have thedifferent levels be de ﬁned by the features that are relatively speciﬁ c to that level,
analogous to how the comparable distinctions are made between the levels of severityfor an intellectual disability.P
ERSONALITY DISORDERS
There are three major problematic boundaries for the personality disorders: theboundaries between personality disorders and other mental disorders, the boundariesbetween personality disorders and normal personality, and the boundaries among thepersonality disorders. Discussed ﬁrst will be the boundaries with other mental
disorders, followed by the other two boundaries.Boundaries With Other Mental Disorders Among the proposals considered for the
personality disorders at the DSM-5 Research Planning Conference (Kupfer et al., 2002)was the suggestion to replace the diagnosis of personality disorder with early onsetand chronic variants of existing Axis I mental disorders (First et al., 2002). This mightappear at ﬁrst blush to be a radical proposal, and perhaps it is. However, it does have
support from a variety of sources.
There is no clear or consistent boundary between the personality disorders and
many other mental disorders, particularly the mood, anxiety, impulse dyscontrol, andpsychotic disorders (Krueger, 2005). In fact, DSM-5 schizotypal personality disorder
has long been classi ﬁed as a form of schizophrenia rather than as a personality
disorder in the World Health Organization ’sInternational Classi ﬁcation of Diseases
(ICD-10 ; WHO, 1992), the parent classi ﬁcation for the APA ’sDSM-5 . Schizotypal
personality disorder is genetically related to schizophrenia, most of its neurobiologicalrisk factors and psychophysiological correlates are shared with schizophrenia (e.g.,eye tracking, orienting, startle blink, and neurodevelopmental abnormalities), and thetreatments that are effective in ameliorating schizotypal symptoms overlap withtreatments used for persons with Axis I schizophrenia (Kwapil & Barrantes-Vidal, 2012).14 OVERVIEW

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On the other hand, there are also compelling reasons for continuing to consider
schizotypal as a personality disorder (Kwapil & Barrantes-Vidal, 2012; Raine, 2006).Simply because a personality disorder shares a genetic foundation with anotherdisorder does not then indicate that it is a form of that other disorder. Contrary toviewing schizotypal personality disorder as a variant of schizophrenia is that thedisorder is far more comorbid with other personality disorders than it is with anyother schizophrenia-related disorder, persons with schizotypal personality disorderrarely go on to develop schizophrenia, and schizotypal symptomatology is seen inquite a number of persons within the general population who lack any geneticassociation with schizophrenia and who would not be appropriately described ashaving some form of schizophrenia (Raine, 2006).
However, a fate similar to that of schizotypal personality disorder in ICD-10 (WHO,
1992) and depressive personality disorder in DSM-IV (APA, 1994) could await the
other personality disorder diagnostic categories in a future edition of the diagnosticmanual (First et al., 2002). For example, social phobia was a new addition to DSM-III
(Spitzer et al., 1980; Turner & Beidel, 1989). It was considered then to be a distinct,circumscribed condition, consistent with the de ﬁnition of a phobia as a “persistent,
irrational fear of a speciﬁcobject, activity, or situation ”(APA, 1994, p. 336, our
emphasis). However, it became apparent to anxiety disorder researchers and cliniciansthat the fears of many of their patients were rarely so discrete and circumscribed(Spitzer & Williams, 1985). Therefore, the authors of DSM-III-R developed a general-
ized subtype for when “the phobic situation includes most social situations ”(APA,
1987, p. 243). DSM-III-R generalized social phobia, however, merged into the DSM-III
diagnosis of avoidant personality disorder. Both were concerned with a pervasive,generalized social insecurity, discomfort, and timidity. Efforts to distinguish themhave indicated only that avoidant personality disorder tends to be, on average,relatively more dysfunctional than generalized social phobia (Sanislow, da Cruz,Gianoli, & Reagan, 2012; Turner, Beidel, & Townsley, 1992).
DSM-IV provided no solution. In fact, it was acknowledged that generalized social
phobia emerged “out of a childhood history of social inhibition or shyness ”(APA,
1994, p. 414), consistent with the concept of a maladaptive personality trait. Anargument raised for classifying this condition as an anxiety disorder rather than as apersonality disorder was that many persons with the disorder bene ﬁt from pharma-
cologic interventions (Liebowitz, 1992). “One may have to rethink what the personal-
ity disorder concept means in an instance where 6 weeks of phenelzine therapy beginsto reverse long-standing interpersonal hypersensitivity as well as discomfort insocializing ”(Liebowitz, 1992, p. 251). Of course, one might also have to rethink
what the anxiety disorder concept means when an antidepressant is an effective formof treating an anxiety disorder. In addition, it is unclear why a maladaptive personal-ity trait should not be responsive to a pharmacologic intervention (Knorr & Kessing,2010; Knutson et al., 1998; Tang et al., 2009). In any case, the authors of DSM-IV-TR
concluded that these two conditions “may be alternative conceptualizations of the
same or similar conditions ”(APA, 2000, p. 720).
There does not currently appear to be a meaningful distinction between avoidant
personality disorder and generalized social phobia (APA, 2000; Sanislow et al., 2012;Tyrer, 2005; Widiger, 2003). Some suggest that the best solution is to simply abandonthe personality disorder diagnosis in favor of the generalized anxiety disorder (FirstMental Disorders as Discrete Clinical Conditions 15

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et al., 2002; Schneider, Blanco, Anita, & Liebowitz, 2002). “We believe that the more
extensive evidence for syndromal validity of social phobia, including pharmacologicaland cognitive-behavioral treatment ef ﬁcacy, make it the more useful designation in
cases of overlap with avoidant personality ”(Liebowitz et al., 1998, p. 1060). The
reference to treatment ef ﬁcacy by Liebowitz et al. (1998) falls on receptive ears for
many clinicians who struggle to obtain insurance coverage for the treatment ofmaladaptive personality functioning. It is often reported that a personality disorderdiagnosis is stigmatizing, due in large part to its placement on a distinct axis thatcarries the implication of being an untreatable, lifetime disorder (Frances et al., 1991;Kendell, 1983). For reasons such as these, the Assembly of the American PsychiatricAssociation (which has authoritative governance over the approval of revisions to thediagnostic manual) has repeatedly passed resolutions to explore proposals to moveone or more personality disorders to Axis I in large part to address the stigma and lackof reimbursement for their treatment. This proposal is now moot, given the abandon-ment of the multiaxial system in DSM-5 (APA, 2013). Future proposals of the
Assembly though might now take the form of shifting individual personality dis-orders into a respective mood, anxiety, or impulse dyscontrol disorder as an earlyonset, chronic variant.
Just as the depressive, schizotypal, and avoidant personality disorders could be
readily subsumed within an existing section of Axis I, borderline personality disordercould be reclassi ﬁed as a mood dysregulation and/or impulse dyscontrol disorder;
obsessive-compulsive personality disorder could be reclassi ﬁed as a generalized and
chronic variant of obsessive-compulsive anxiety disorder (although there is in factonly weak evidence to support a close relationship between the obsessive-compulsiveanxiety and personality disorders; Samuels & Costa, 2012); and antisocial personalitydisorder by an adult variant of conduct (disruptive behavior) disorder. In DSM-5,
schizotypal personality disorder is cross-listed within the schizophrenia spectrumsection, and antisocial is cross-listed within the disruptive behavior disorders section(APA, 2013).
In sum, the future for many of the personality disorder diagnostic categories might
be reformulations as early-onset chronic variants of existing Axis I disorders, asexplicitly proposed at the initial DSM-5 Research Planning Conference (First et al.,2002). A dif ﬁculty with respect to this proposal, beyond the fundamental concern that
the diagnostic manual would no longer recognize the existence of maladaptivepersonality functioning, is that it might just create more problems than it solves(Widiger, 2003). It is well established that persons have constellations of maladaptivepersonality traits that have signi ﬁcant consequential life outcomes (Ozer & Benet-
Martinez, 2006; Roberts & DelVecchio, 2000). These personality traits are not currentlywell described by just one or even multiple personality disorder diagnoses (Clark,2007; Trull & Durrett, 2005; Widiger, 2012b) and will be described even less well bymultiple diagnoses across the broad classes of mood, anxiety, impulse dyscontrol,psychotic, and disruptive behavior disorders.Boundaries With Other Personality Disorders and Normal Personality Rounsaville et al.
(2002) suggested that the ﬁrst section of the diagnostic manual to shift to a dimensional
classi ﬁcation should be the personality disorders. The personality disorders have been
among the most problematic of disorders to be diagnosed categorically (First et al.,16 OVERVIEW

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2002; Kendell, 1989). It is the norm for patients to meet diagnostic criteria for more thanone personality disorder (Clark, 2007; Lilienfeld et al., 1994; Livesley, 2003; Trull &Durrett, 2005). Excessive diagnostic co-occurrence was in fact the primary reason that5 of the 10 personality disorder diagnoses were proposed for deletion in DSM-5
(Skodol, 2012). The excessive co-occurrence may be the result of the nature of theconstruct of personality. For instance, it is perhaps self-evident that persons are notwell described by just one trait term (e.g., introverted). Each person has instead aconstellation of personality traits, many of which are adaptive, and some of whichmay also be maladaptive. There is little reason to think that it would be different whena person is said to have a personality disorder (Widiger & Trull, 2007).
There also appears to be no clear or distinct boundary between normal and
abnormal personality functioning. The DSM-IV-TR diagnostic thresholds were not
set at a point that has any theoretical or clinical signi ﬁcance. They were arbitrarily set
at half or one more than half of the diagnostic criteria (APA, 2000). In fact, all thepersonality disorders are readily understood as extreme and/or maladaptive variantsof normal personality traits distributed within the general population; more speci ﬁ-
cally, the domains and facets of the ﬁve-factor dimensional model (FFM) of general
personality structure (Widiger, Samuel, Mullins-Sweatt, Gore, & Crego, 2012;Widiger & Trull, 2007).
The FFM consists of ﬁve broad domains of general personality functioning:
neuroticism (or emotional instability), extraversion versus introversion, opennessversus closedness, agreeableness versus antagonism, and conscientiousness versusundependability. The FFM was derived originally through empirical studies of thetrait terms within the English language (L. Goldberg, 1993). Language can beunderstood as a sedimentary deposit of the observations of persons over the thou-sands of years of the language ’s development and transformation. The most important
domains of personality functioning are those with the most number of trait terms todescribe and differentiate the various manifestations and nuances of a respectivedomain, and the structure of personality is suggested by the empirical relationshipsamong these trait terms. The initial lexical studies with the English language con-verged well onto a ﬁve-factor structure (L. Goldberg, 1993). Subsequent lexical studies
have been conducted on many additional languages (e.g., German, Dutch, Czech,Polish, Russian, Italian, Spanish, Hebrew, Hungarian, Turkish, Korean, & Filipino)and these have con ﬁrmed well the existence of the ﬁve broad domains (Church, 2001).
Theﬁve broad domains have been differentiated into more speci ﬁc facets by Costa and
McCrae (1992) on the basis of their development of and research with the NEOPersonality Inventory-Revised (NEO PI-R), by far the most commonly used andheavily researched measure of the FFM.
Studies have now well documented that all of the DSM-IV-TR personality disorder
symptomatology is readily understood as maladaptive variants of the domains andfacets of the FFM (O ’Connor, 2002, 2005; Samuel & Widiger, 2008; Saulsman & Page,
2004; Widiger & Costa, 2002; Widiger et al., 2012). Saulsman and Page (2004)concluded, “each of the personality disorders shows associations with the ﬁve-factor
model that are meaningful and predictable given their diagnostic criteria ”(p. 1075). As
acknowledged by Livesley (2001b), “all categorical diagnoses of DSM can be accom-
modated within the ﬁve-factor framework ”(p. 24). As expressed by Clark (2007), “the
ﬁve-factor model of personality is widely accepted as representing the higher-orderMental Disorders as Discrete Clinical Conditions 17

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structure of both normal and abnormal personality traits ”(p. 246). The problematic
diagnostic co-occurrence among the DSM-IV-TR personality disorders is well
explained by the extent to which each of the personality disorders shares traits ofthe FFM (Lynam & Widiger, 2001; O ’Connor, 2005).
Proposed for DSM-5 was a ﬁve-domain 25-trait dimensional model that repre-
sented “maladaptive variants of the ﬁve domains of the extensively validated and
replicated personality model known as the ‘Big Five, ’or the Five Factor Model of
personality” (APA, 2013, p. 773). These ﬁve domains are negative affectivity (FFM
neuroticism), detachment (FFM introversion), psychoticism (FFM openness), antago-nism (FFM antagonism), and disinhibition (low FFM conscientiousness). The DSM-5
dimensional trait model does differ in important ways from the FFM; more speci ﬁ-
cally, it is con ﬁned to maladaptive personality functioning and it is unipolar in
structure (e.g., it does not recognize any maladaptive variants of extraversion thatis opposite to detachment, or agreeableness that is opposite to antagonism). Never-theless, there is strong conceptual and empirical support for its alignment with the ﬁve
domains of the FFM (APA, 2013; De Fruyt, De Clerq, De Bolle, Markon, & Krueger,2013; Gore & Widiger, 2013; Thomas et al., 2013; Widiger, 2011).
The FFM of personality disorder has a number of advantages over the existing
categorical approach (Widiger et al., 2012). It would help with the stigmatization ofa personality disorder diagnosis because no longer would a personality disorder beconceptualized as something that is qualita tively distinct from general personality
traits. All persons vary in the extent of thei r neuroticism, in the extent to which they
are agreeable versus antagonistic, and in the extent to which they are conscientious,impulsive, and/or undependable (McCrae & Costa, 2003). The FFM of personalitydisorder will provide not only a more p recise description of each person ’s individual
personality structure but will also pro vide a more complete picture through the
inclusion of normal, adaptive traits, rec ognizing thereby that a person is more than
just the personality disorder and that there are aspects to the self that can beadaptive, even commendable, despite the p resence of the maladaptive personality
traits. Some of the personality strengths may also be quite relevant to treatment,such as openness to experience, indicating an interest in exploratory psychotherapy;agreeableness, indicating an engagement in group therapy; and conscientiousness,
indicating a willingness and ability to adh ere to the demands and rigor of dialectical
behavior therapy (Sanderson & Clarkin, 2002). The FFM of personality disorderwould also bring to the psychiatric nomenclature a wealth of knowledge concerningthe origins, childhood antecedents, stabi lity, and universality of the dispositions
that underlie personality disorder (Widiger et al., 2012; Widiger & Trull, 2007).
The Nomenclature Work Group at the initial DSM-5 Research Planning Confer-
ence called for the replacement of the DSM-IV-TR diagnostic categories by a
dimensional model (Rounsaville et al., 2002). “If a dimensional system of personality
performs well and is acceptable to clinicians, it might then be appropriate to exploredimensional approaches in other domains ”(Rounsaville et al., 2002, p. 13). A sub-
sequent APA DSM-5 preparatory conference was devoted to making this shift,
providing its extensive empirical support (Widiger et al., 2005). The proposal ofthe DSM-5 Personality and Personality Disorders Work Group though was moreconservative. The proposal was not to replace the diagnostic categories with adimensional trait model. It was only to provide a dimensional trait model as a18 OVERVIEW

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supplement for the existing diagnostic categories, although the traits would be partof the criterion sets for these categories (Skodol, 2012). Nevertheless, this more
conservative proposal was still rejected, fo r reasons that are not clear. It is true that
the initial dimensional trait proposal had been created de novo by work groupmembers, thereby lacking a strong empiric al foundation. In addition, rather than
closely tying the proposal to the FFM, the au thors explicitly distanced the proposal
from the FFM (Clark & Krueger, 2010). In the last year of the proposal it was moreclosely tied to the FFM (APA, 2012) but by t hen strong opposition to the proposal
had accumulated (Gunderson, 2010; Shedler et al., 2010). In addition, it was alsostructurally embedded within a much more extensive and complex proposal thatincluded additional features of personal ity disorder concerning self pathology
derived from psychodynamic theory and r esearch (Skodol, 2012). Nevertheless, it
is at least included in Section 3 of DSM-5 for emerging measures and models as an
alternative to the DSM-5 diagnostic categories that have been carried over from
DSM-IV-TR categories without any revision.
I
NTELLECTUAL DISABILITY
Rounsaville et al. (2002) and others suggested that the personality disorders section betheﬁrst to shift toward a dimensional classi ﬁcation, apparently not fully appreciating
that one section has long been dimensional: intellectual disability (previously calledmental retardation). Many persons write as if a shift to a dimensional classi ﬁcation
represents a new, fundamental change to the diagnostic manual (e.g., Regier, 2008).For much of the manual such a shift would certainly represent a fundamental changein how mental disorders are conceptualized and classi ﬁed (Guze, 1978; Guze &
Helzer, 1987; Robins & Guze, 1970). Nevertheless, there is a clear precedent for adimensional classi ﬁcation of psychopathology already included within DSM-5: the
diagnosis of intellectual disability (APA, 2013).
Intellectual disability in DSM-5 is diagnosed along a continuum of cognitive and
social functioning; more precisely, de ﬁcits in adaptive functioning and intellectual
functions con ﬁrmed by standardized intelligence testing. This typically translates to
an intelligence quotient score of 70, plus or minus 5 (APA, 2013). An IQ of 70 does notcarve nature at a discrete joint or identify the presence of a qualitatively distinctcondition, disease, or disorder. On the contrary, it is a quantitative cutoff point alongthe dimension of intelligence. An IQ of 70 is simply two standard deviations below themean (American Association of Mental Retardation [AAMR], 2002).
Intelligence involves the ability to reason, plan, solve problems, think abstractly,
comprehend complex ideas, learn quickly, and learn from experience (AAMR, 2002).Intelligence, like personality, is distributed as a hierarchical, multifactorial continuousvariable. Most persons ’levels of intelligence, including most of those with an
intellectual disability, are the result of a complex interaction of multiple genetic, fetal,and infant development, and environmental in ﬂuences (Deary, Spinath, & Bates,
2006). There are no discrete breaks in its distribution that would provide an absolutedistinction between normal and abnormal intelligence. The point of demarcation forthe diagnosis of an intellectual disability is an arbitrary, quantitative distinction alongthe normally distributed levels of hierarchically and multifactorially de ﬁned intelli-
gence. This point of demarcation is arbitrary in the sense that it does not carve natureMental Disorders as Discrete Clinical Conditions 19

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at a discrete joint, but it was not, of course, randomly or mindlessly chosen. It is adefensible selection that was informed by the impairments in adaptive functioningcommonly associated with an IQ of 70 or below (AAMR, 2002). For example, aprevious cutoff point of an IQ of 79 identi ﬁed too many persons who were in fact able
to function independently.
In addition, the disorder of intellectual disability is not diagnosed simply on the
basis of an IQ of 70 or below (an IQ score is not even necessarily required in DSM-5 ;
APA, 2013). It must be accompanied by a documented impairment to functioning.“Mental retardation is a disability characterized by signi ﬁcant limitation in both
intellectual functioning and in adaptive behavior as expressed in conceptual, socialand practical adaptive skills ”(AAMR, 2002, p. 23). Persons with IQ scores lower than
70 who can function effectively would not be diagnosed with the disorder (APA,2013). The diagnosis is understood in the context of the social and practical require-ments of everyday functioning that must be met by the person (Luckasson & Reeve,2001). The purpose of the diagnosis is not to suggest that a speci ﬁc pathology is
present, but to identify persons who, on the basis of their intellectual disability, wouldbe eligible for public health-care services and bene ﬁts to help them overcome or
compensate for their relatively lower levels of intelligence.
Many instances of intellectual disability are due in large part to speciﬁ c etiologies,
such as tuberous sclerosis, microcephaly, von Recklinghausen ’s disease, Trisomy 21,
Mosaicism, Prader-Willi syndrome, and many, many more (Kendell & Jablensky,2003). Nevertheless, the disorders that result from these speci ﬁc etiologies are
generally understood as medical conditions, an associated feature of which isalso the intellectual disability that would be diagnosed concurrently and indepen-dently. The intellectual disability that is diagnosed as a mental disorder withinDSM-5 is itself a multifactorially determined and heterogeneous dimensional
construct falling along the broad cont inuum of intellectual functioning. “The causes
of intellectual disabilities are typically c omplex interactions of biological, behav-
ioral/psychological, and sociocultural factors ”(Naglieri, Salter, & Rojahn, 2008,
p. 409). An important postnatal cause for intellectual disability is “simply ”psycho-
social deprivation, resulting from poverty , chaotic living environment, and/or child
abuse or neglect. No clear etiology will be evident in up to 40% of cases. In sum,intellectual disability may serve as an effective model for the classi ﬁcation of the rest
of the diagnostic manual, including mood, psy c h o t i c ,p e r s o n a l i t y ,a n x i e t y ,a n do t h e r
mental disorders.
DSM-5 AND DIMENSIONAL CLASSIFICATION
The modern effort to demarcate a taxonomy of distinct clinical conditions is oftentraced to Kraepelin (1917). Kraepelin (1917), however, had himself acknowledged,“wherever we try to mark out the frontier between mental health and disease, we ﬁnd
a neutral territory, in which the imperceptible change from the realm of normal life tothat of obvious derangement takes place ”(p. 295). The Robins and Guze (1970)
paradigm for the validation of categorical diagnosis has also been widely in ﬂuential
within psychiatry (Klerman, 1983; Kupfer et al., 2002). In 1989, L. Robins and Barrett(1989) edited a text in honor of this classic paper. Kendell (1989) provided the ﬁnal
word in his closing chapter. His conclusions, however, were curiously negative.20 OVERVIEW

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“Ninety years have now elapsed since Kraepelin ﬁrst provided the framework of a
plausible classi ﬁcation of mental disorders. Why then, with so many potential
validators available, have we made so little progress since that time? ”(Kendell,
1989, p. 313). He answered his rhetorical question in the next paragraph: “One
important possibility is that the discrete clusters of psychiatric symptoms we aretrying to delineate do not actually exist but are as much a mirage as discretepersonality types ”(Kendell, 1989, p. 313).
It is stated in the preface to DSM-5 that “this edition of DSM was designed ﬁrst and
foremost to be a useful guide to clinical practice” (APA, 2013, p. xii). First (2005)
argued in his rejoinder to a proposal to shift the diagnostic manual into a dimensionmodel, that “the most important obstacle standing in the way of its implementation in
DSM-5 (and beyond) is questions about clinical utility” (p. 561). However, one should
question whether the existing diagnostic manual in fact has appreciable clinical utility(Mullins-Sweatt & Widiger, 2009). “Apologists for categorical diagnoses argue that the
system has clinical utility being easy to use and valuable in formulating cases andplanning treatment [but] there is little evidence for these assertions ”(Livesley, 2001a,
p. 278). First (2005) suggested that “the current categorical system of DSM has clinical
utility with regard to the treatment of individuals ”(p. 562), yet elsewhere has stated
that “with regard to treatment, lack of treatment speci ﬁcity is the rule rather than the
exception ”(Kupfer et al., 2002, p. xviii). The heterogeneity of diagnostic membership,
the lack of precision in description, the excessive diagnostic co-occurrence, the failureto lead to a speci ﬁc diagnosis, the reliance on the “not otherwise speciﬁ ed”waste-
basket diagnosis, and the unstable and arbitrary diagnostic boundaries of the DSM-
IV-TR and DSM-5 categories, are matters of clinical utility that is a source of
considerable frustration for clinicians and public health care agencies (Mullins-Sweatt & Widiger, 2009).
The primary goal of the authors of DSM-5 was to shift the manual toward a
dimensional classi ﬁcation (Helzer, Wittchen, Kru eger, & Kraemer, 2008; Regier,
Narrow, Kuhl, & Kupfer, 2010). This intention represented an explicit recognition ofthe failure of the categorical system (D .G o l d b e r g ,2 0 1 0 ) .A n d ,D S M – 5d o e si n d e e d
include a number of clear and potentially signi ﬁcant shifts toward a dimensional
classi ﬁcation. The introduction to the manual explicitly acknowledges the failure
of the categorical model: “The once plausible goal of identifying homogeneous
populations for treatment and research re sulted in narrow diagnostic categories
that did not capture clinical reality, symp tom heterogeneity within disorders, and
signiﬁcant sharing of symptoms across multiple disorders ”(APA,
2013, p. 12). It is
further asserted that dime nsional approaches will “supersede current categorical
approaches in coming years ”( p .1 3 ) .I na d d i t i o n ,m a n yo ft h ec h a n g e st h a tw e r e
made to the nomenclature re ﬂected a preference for a more dimensional concep-
tualization (e.g., the autism spectrum diso rder, the conceptualization of a schizo-
phrenia spectrum, the level of severity for s ubstance use disorder, and the reference
within the introduction of the manual to th e broad dimensions of internalizing and
externalizing dysfunction that cut across e xisting categories). Included in Section 3
ofDSM-5 for emerging models and measures is a ﬁve-domain 25-trait dimensional
model of maladaptive personality functioning (Krueger et al., 2011) that is alignedconceptually and empirically with the FFM dimensional model of general person-ality structure (APA, 2013; De Fruyt et al., 2013; Gore & Widiger, 2013; Thomas et al.,Mental Disorders as Discrete Clinical Conditions 21

3GC01 06/26/2014 8:10:5 Page 22
2013). This model is presented as an alternative to the traditional diagnosticcategories “to address numerous shortcomings of the current approach ”(APA,
2013, p. 761) and its presence within the d iagnostic manual will help stimulate
further research as well as increase the familiarity and interest of clinicians withrespect to this alternative approach (Widiger, 2013).
Nevertheless, it is also acknowledged that “DSM-5 remains a categorical classi ﬁ-
cation of separate disorders ”(APA, 2013, p. xii). The shifts that did occur were frankly
tentative, if not timid. “What is being proposed for DSM-V is not to substitute
dimensional scales for categorical diagnoses, but to add a dimensional option tothe usual categorical diagnoses for DSM-V ”(Kraemer, 2008, p. 9). None of the mental
disorders, including even the personality disorders, converted to a dimensionalclassi ﬁcation. There was a shift toward the conceptualization of some disorders as
existing along a spectrum (e.g., autism and schizophrenia), and substance use disordercollapsed the problematic distinction between abuse and dependence into onedisorder that includes four levels of severity. However, with respect to the latter,there remains no acknowledgement of the continuum into normal substance usage.There will continue to be a reliance on the NOS category to identify subthresholdconditions (the threshold for a substance use diagnosis was, in fact, raised from onecriterion to two).
DSM-III is often said to have provided a signi ﬁcant paradigm shift in how
psychopathology is diagnosed (Kendell & Jablensky, 2003; Klerman, 1983; Regier,2008). Much of the credit for the innovative nature and success of DSM-III is due to the
foresight, resolve, and perhaps even courage of its Chair, Dr. Robert Spitzer. Theprimary authors of DSM-5 fully recognized the failure of the categorical model of
classi ﬁcation (Kupfer et al., 2002; Regier, 2008; Regier et al., 2010). They had the
empirical support and the opportunity to lead the ﬁeld of psychiatry to a comparably
bold new future in diagnosis and classiﬁ cation, but no true paradigm shift in the
classi ﬁcation of psychopathology has occurred.
There was never an intention though to actually shift the diagnostic manual into a
dimensional system. As acknowledged by Helzer, Kraemer, and Krueger (2006), “our
proposal [for DSM-5 ] not only preserves categorical de ﬁnitions but also does not alter
the process by which these de ﬁnitions would be developed. Those charged with
developing criteria for speci ﬁc mental disorders would operate just as their predeces-
sors have ”(p. 1675). In other words, work groups, for the most part, continued to
develop diagnostic criteria to describe prototypic cases in a manner that wouldmaximize homogeneity and differential diagnosis (Robins & Guze, 1970; Spitzeret al., 1980), thereby continuing to fail to adequately describe typical cases and againleaving many patients to receive the diagnosis of NOS. Dimensional proposals forDSM-5 were only to develop “supplementary dimensional approaches to the cate-
gorical de ﬁnitions that would also relate back to the categorical de ﬁnitions ”(Helzer,
Wittchen, et al., 2008, p. 116). It was the intention for these dimensions to only serve asancillary descriptions that lacked any of ﬁcial representation within a patient ’s medical
record. They have no of ﬁcial alphanumerical code and may then not even be
communicated to any public health care agency.
Kraemer, Noda, and O ’Hara (2004)
argued that in psychiatry “a categorical
diagnosis is necessary ”(p. 21). “Clinicians who must decide whether to treat or
not treat a patient, to hospitalize or not, to treat a patient with a drug or with22 OVERVIEW

3GC01 06/26/2014 8:10:5 Page 23
psychotherapy, or what type, must inevitably use a categorical approach to diagnosis”(Kraemer et al., 2004, p. 12). This is a not uncommon perception, but it is not anaccurate characterization of actual clinical practice (Mullins-Sweatt & Widiger, 2009).In many common clinical situations, the decision is not in fact black and white.Clinicians and social agencies make decisions with respect to a frequency of therapysessions, an extent of insurance coverage, a degree of medication dosage, and evendegrees of hospitalization (e.g., day hospital, partial hospitalization, residentialprogram, or traditional hospitalization).
It is evident that these different clinical decisions are not well informed by a single,
uniform diagnostic threshold. The current diagnostic thresholds are not set at a pointthat is optimal for any one particular social or clinical decision, and the singlediagnostic threshold is used to inform a wide variety of different decisions. Adimensional system has the ﬂexibility to provide different thresholds for different
social and clinical decisions and would then be considerably more useful for cliniciansand more credible for social agencies than the current system. A ﬂexible (dimensional)
classi ﬁcation would be preferable to governmental, social, and professional agencies
because it would provide a more reliable, valid, explicitly de ﬁned, and tailored means
for making each respective social and clinical concern. It is for this reason that theauthors of DSM-5 included the supplementary dimensional scales to facilitate partic-
ular clinical decisions (e.g., Shear, Bjelland, Beesdo, Gloster, & Wittchen, 2008).
The National Institute of Mental Health (NIMH) has largely rejected DSM-5 ,
indicating that they are no longer interested in funding studies that rely upon thisnomenclature. As expressed by the director of NIMH, “it is critical to realize that we
cannot succeed if we use DSM categories ”(Insel, 2013). NIMH has developed its own
nomenclature, referred to as the Research Domain Criteria (RdoC; Insel, 2009;Sanislow et al., 2010), consisting of ﬁve broad areas of research (i.e., negative valence
systems, positive valence systems, cognitive systems, systems for social processes, andarousal/modulatory systems) that cut across the existing DSM-5 diagnoses. The
RDoC nomenclature is described as dimensional, because it is concerned with under-lying mechanisms that are best described in terms of levels or degrees of functioningrather than distinct categories. “Each level of analysis needs to be understood across a
dimension of function ”(Insel, 2013). However, the primary distinction with DSM-5 is
that the RDoC system emphasizes a neurobiological model of psychopathology.“Mental disorders are biological disorders involving brain circuits that implicate
speciﬁc domains of cognition, emotion, or behavior ”(Insel, 2013). NIMH is primarily
critical of the DSM-5 for deriving its diagnoses on the basis of overt symptoms
(Craddock & Owen, 2010; Kapur, Phillips, & Insel, 2012). “Unlike our de ﬁnitions of
ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a
consensus about clusters of clinical symptoms, not any objective laboratory measure”(Insel, 2013). However, it is also unclear if a biological reductionism will be any moresuccessful (Kendler, 2005).
Most (if not all) mental disorders appear to be the result of a complex interaction
of an array of interacting biological vulnerabilities and dispositions with a numberof signi ﬁcant environmental, psychosocial events that often exert their effects over a
progressively developing period of time (Rutter, 2003). The most complete andcompelling explanation will not likely be achieved through a biological reduction-ism because much will be lost by a failure to appreciate that explanation andMental Disorders as Discrete Clinical Conditions 23

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understanding at the level of behavior and cognition remains fundamentally valid,and necessary (Kendler, 2005). The sympto ms and pathologies of mental disorders
appear to be highly responsive to a wide variety of neurobiological, interpersonal,cognitive, and other mediating and mode rating variables that help to develop,
shape, and form a particular individual’ sp s y c h o p a t h o l o g yp r o ﬁle. This complex
etiological history and individual psychopathology pro ﬁle are unlikely to be well
described by single diagnostic categor ies that attempt to make distinctions at
nonexistent discrete joints along the con tinuous distributions (Widiger & Samuel,
2005). The publication of DSM-III w a ss a i dt oh a v ep r o v i d e das i g n i ﬁcant, major
advance in the diagnosis and classi ﬁcation of psychopathology (Klerman, 1983). The
APA diagnostic nomenclat ure, however, is now beset by substantial criticism
(Frances, 2013; Greenberg, 2013), with NIMH openly rejecting it (Insel, 2013).Perhaps it is time for a paradigm shift.
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CHAPTER 2
The Problem of Dual Diagnosis
MELANIE E. BENNETT, JASON PEER, and SELVIJA GJONBALAJ-MAROVIC
RESEARCH INDICATES THAT a substantial percentage of the general population
with a lifetime psychiatric disorder has a history of some other disorder(Kessler, 1997; Kessler et al., 1994), and more than half of patients in
psychiatric treatment meet criteria for more than one diagnosis (Wolf, Schubert,P a t t e r s o n ,M a r i o n ,&G r a n d e ,1 9 8 8 ) .T h eissue of comorbidity broadly refers tocombinations of any types of psychiatric disorders that co-occur in the sameindividual. A diagnostic pair that has received signi ﬁcant attention over the past
two decades is that of mental illne ss and substance abuse. The term dual diagnosis
describes individuals who meet diagnostic criteria for an Axis I or Axis II mentaldisorder (or disorders) along with one or m ore substance use disorders. Although
dual diagnosis has likely been a prevalent and persistent condition for a long time, itbegan to receive attention as both a clinical problem and research domain some 25years ago. Today, we ﬁnd ourselves with many years of research and thinking about
the frequent association between mental and substance use disorders, how this
association complicates the provision of mental health and substance abuse treat-ment services, and the impact of this assoc iation on all aspects of psychopathology
research and clinical practice. In this c hapter, we review data on rates of dual
diagnosis, both generally and for speci ﬁc domains of disorder s, as well as discuss
some of the ways in which dual diagnosis impacts the course, prognosis, assess-ment, and treatment of adult psychopathology. Finally, we review current researchand thinking on the etiology of dual diagnosis and highlight clinical and researchdirections.
A recurring theme throughout this chapter is the many ways that the concep-
tualization of dual diagnosis can change depending on de ﬁnitions, diagnostic
frameworks, assessment tools, and the sa mple being evaluated. Over time and
as these domains have changed, thinking about what mental health and substance
use disorders should be included within th e conceptualization of dual diagnosis, as
well as how to think about the impact of dual diagnosis on outcomes, has evolvedand shifted. Our goal here is to review the literature on dual diagnosis, to presentideas that can challenge and perhaps expand the thinking on what constitutes dual
35

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diagnosis, and to provide consideration of how such expansion may impact think-ing on psychopathology and diagnosis.
METHODOLOGICAL ISSUES IN THE ASSESSMENT OF DUAL DIAGNOSIS
There are several methodological issues to consider when reviewing the literature ondual diagnosis and evaluating its ﬁndings. These include the way that the sample
under study shapes the ﬁndings, the range of methods used to assess psychiatric and
substance use disorders and how different methods and measures shape studyﬁndings, and the critical impact of one ’sd eﬁnition of dual diagnosis on study ﬁndings.
S
AMPLE SELECTION INFLUENCES FINDINGS
Data on the epidemiology of dual diagnosis come from both epidemiological andclinical studies, each of which has bene ﬁts and drawbacks. Several large-scale
epidemiological studies examining rates of dual diagnosis in general populationsamples have been carried out since the mid-1980s. These studies provide representa-tive information on rates of mental illness and substance use disorders, use structureddiagnostic interviews, and generate results that are reliable and relevant to thepopulation as a whole. Most of the information on rates of dual diagnosis comesfrom studies of clinical populations. Although such studies are not representative ofthe general population, they provide valuable information on the types of problemsthat are faced by individuals in treatment, as well as on the links between dualdiagnosis, service utilization, the impact on illness, and treatment outcome. Impor-tantly, individuals with multiple disorders are more likely to seek treatment, acondition known as Berkson ’s fallacy (Berkson, 1949), so that estimates of the
prevalence of comorbid disorders will be higher in clinical samples. Relatedly, factorssuch as inpatient or outpatient status and chronicity of illness may affect rates of dualdiagnosis found in clinical samples. For example, research on patients with schizo-phrenia has found that more severely impaired inpatients are less likely to abusesubstances than patients who are less ill (Mueser et al., 1990). Dual diagnosis rateshave also been found to differ by setting, with hospital emergency rooms re ﬂecting
higher estimates than other settings (Barbee, Clark, Crapanzano, Heintz, & Kehoe,1989; Galanter, Castaneda, & Ferman, 1988). In addition, several demographicvariables correlate with substance abuse, and differences in these variables in clinicalsamples can in ﬂuence prevalence rates. For example, gender and age both correlate
with substance abuse: Males and those of younger age are more likely to abusesubstances. Because studies of comorbidity in schizophrenia often use samples ofinpatients who are more likely to be male, the comorbidity rate in schizophrenia foundin research with clinical samples may be in ﬂated, because males are both more likely to
have substance use disorders and more likely to be inpatients in psychiatric hospitals.
Another sample-related methodological issue involves the split between the mental
health treatment system and the substance abuse treatment system, and the impactthat this separation has on dual diagnosis research. The literature on dual diagnosisreally includes two largely separate areas of investigation: research on substanceabuse in individuals with mental illness, and research on mental illness in primary36 OVERVIEW

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substance abusers. In order to get an accurate picture of dual diagnosis and its fullimpact on clinical functioning and research in psychopathology, both aspects of thisliterature must be examined.S
TUDY METHODS AND ASSESSMENT MEASURES INFLUENCE FINDINGS
The methods used to determine psychiatric and substance use diagnoses can in ﬂuence
ﬁndings. The types of diagnostic measures used include structured research inter-
views, nonstructured clinical interviews, self-report ratings, and reviews of medicalrecords. Although structured interviews are the most reliable method of diagnosis(Mueser, Bellack, & Blanchard, 1992), research with clinical samples will often employless well-standardized assessments. Relatedly, studies measure different substances intheir assessments of dual diagnosis, typically including alcohol, cocaine, heroin,hallucinogens, stimulants, and marijuana. Importantly, some substances are nottypically considered in assessments of dual diagnosis. For example, nicotine is usuallynot considered a substance of abuse in dual diagnosis research, despite the high ratesof use among individuals with both mental illness (Lasser et al., 2000) and substanceabuse (Bien & Burge, 1990), as well as a growing literature that suggests that nicotinedependence has links, perhaps biological in nature, to both major depression (Quat-trocki, Baird, & Yurgelun-Todd, 2000) and schizophrenia (Dalack & Meador-Wood-ruff, 1996; Ziedonis & George, 1997). Others have found elevated rates of psychiatricand substance use disorders in smokers (Keuthen et al., 2000). Taken together, factorssuch as the type of problematic substance use assessed, the measures that are used,and the speci ﬁc substances that are included in an assessment all contribute to varying
meanings of the term dual diagnosis .
T
HERE ISNOSINGLE DEFINITION OF DUALDIAGNOSIS
Deﬁnitions of what constitutes dual diagnosis are far from uniform. Studies often use
differing de ﬁnitions and measures of substance use disorders, making prevalence rates
diverse and dif ﬁcult to compare. For example, de ﬁnitions used to determine rates of
dual diagnosis vary, ranging from problem use of a substance based on the frequencyof use or the number of negative consequences experienced as a result of use, to abuseor dependence based on formal diagnostic criteria. This is a particularly importantissue when formal diagnostic criteria for substance use disorders are used to assessdual diagnosis.
Currently the two most widely used systems for psychiatric diagnosis and classi ﬁ-
cation are the Diagnostic and Statistical Manual (DSM ; American Psychiatric Associa-
tion [APA], 1994), used primarily in the United States, and the International
Classi ﬁcation of Diseases (ICD) (World Health Organization [WHO], 1993), used
primarily in other countries. There are several issues related to these diagnosticframeworks that are must be considered. Having different systems internationallymeans that studies done in different countries will use different de ﬁnitions of
psychiatric and substance use disorders, presenting a challenge when making com-parisons across studies.
Importantly, these diagnostic systems are similar but not identical, and there are
important features of each that in ﬂuence how substance use disorders are diagnosedThe Problem of Dual Diagnosis 37

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that can, in turn, in ﬂuence rates of dual disorders. The diagnostic criteria for alcohol
use disorders from the fourth edition of DSM (DSM-IV) and the 10th edition of the ICD
(ICD-10) provide a good example (see Hasin, 2003, for a complete review). Both
systems include a diagnosis of alcohol dependence that requires at least threesymptoms be present from a list of six ( ICD-10 ) or seven ( DSM-IV ) that include
both physiological symptoms such as tolerance and withdrawal as well as non-physiological symptoms such as impaired control, giving up other important activi-ties, and continued use in the face of physical or psychological consequences.
Research has shown good reliability between DSM and ICD for dependence
diagnoses (Hasin, 2003). In con trast, these systems differ with respect to diagnoses
of alcohol abuse (as it is called in DSM-IV ) or harmful use (as found in ICD-10 ).
DSM-IV requires “recurrent use ”that leads to at least one of four possible conse-
quences (failure to fulﬁ ll obligations, use in situations in which it is physically
hazardous, use-related legal problems, use despite recurrent social/interpersonal
problems) in order to meet a diagnosis of alcohol abuse. ICD-10 is more speci ﬁci ni t s
deﬁnition of “recurrent ”(“T h ep a t t e r no fu s eh a sp e r s i s t e df o ra tl e a s t1m o n t ho r
has occurred repeatedly within a 12-month period” ) but less speci ﬁc in describing
those consequences that are “harmful, ”requiring only “clear evidence that alcohol
use contributed to physical or psychological harm ”and that a “pattern of use has
persisted” (WHO, 1993). Such differences in crit eria have no doubt contributed to
ﬁndings of lower reliability between these categories (Hasin, 2003). Moreover, these
sorts of differences are especially important when considering how rates of dualdisorders compare across nations and cultures (see Room, 2006, for a review).
Another critical consideration is that both DSM and the ICDare changing systems.
The preceding example was based on diagnostic criteria found in DSM-IV andICD-
10. However, in May 2013, a new edition of DSM, DSM-5 (APA, 2013), was
published, with signi ﬁcant implications for dual diagnosis. DSM-5 includes new
disorders (for example, disruptive mood dysregulation disorder has been added tothec
hapter on Depressive Disorders), cha nges to the symptom requirements needed
to meet criteria for some disorders (for example, a diagnosis of schizophrenia nowrequires at least one positive symptom), and consolidation of related conditions intoa single diagnostic classi ﬁcation (for example, autistic disorder, Asperger ’sd i s o r d e r ,
childhood disintegrative disorder, and pervasive developmental disorder not oth-erwise speci ﬁed have been merged within Autism Spectrum Disorder). Overall,
DSM-5 now has fewer total diagnoses —the revisions yielded 15 new diagnoses, 2
diagnoses that were not continued, and 28 that were combined. These sorts ofchanges can impact de ﬁnitions and prevalence rates o f dual diagnosis. For example,
inDSM-5 , the bereavement exclusion for major depressive disorder has been
eliminated. This has the potential to yiel d some additional cases of major depression
or to identify major depression earlier following loss. Although it is not yet clear howsuch a change would de ﬁnitively impact rates of dual diagnosis, it is possible that this
change would yield additional cases of major depression that could, in turn, yieldmore individuals affected by dual diagnosis. As the changes to diagnosis codi ﬁed in
DSM-5 begin to be used, we will be able to examine whether and how dual diagnosis
is impacted.
There were also several changes in the diagnosis of substance use disorders. The
title of the chapter dedicated to alcohol and drug diagnoses was revised from38 OVERVIEW

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Substance Use Disorders (DSM-IV) to Substance-Related and Addictive Disorders
(DSM-5) ; this revision reﬂ ects several changes that will have a substantial impact both
on how disorders related to alcohol and drug use are diagnosed andin the inclusion of
other conditions as addictions. To begin with, whereas DSM-IV had separate diag-
nostic groups for substance abuse and dependence, DSM-5 combines abuse and
dependence into one diagnostic category (substance use disorder) that is rated on acontinuum from mild to severe, with the severity rating based on the number ofcriteria met (mild =two to three criteria met; moderate =four to ﬁve criteria met;
severe =six or more criteria met). There also have been changes to the diagnostic
criteria for substance use disorder. For example, the criterion of “recurrent legal
problems” that was part of the substance abuse diagnosis in DSM-IV was not retained
inDSM-5 , and a new criterion —“craving or a strong desire or urge to use a
substance ”—was added. In addition, while in DSM-IV one or more criteria needed
to be met to earn a diagnosis of substance abuse and three or more needed to be met forsubstance dependence, now in DSM-5 , a diagnosis of substance use disorder requires
that 2 criteria from a list of 11 be met.
These changes will have a substantial impact on dual diagnosis. Combining
abuse and dependence into one diagnostic category can have the effect of identify-ing what might have previously been thou ght of as a less problematic or separate
state (abuse) as a more serious condition that is potentially related to somethingmore serious (dependence), with rates of dual diagnosis increasing as a result.Importantly, the longer list of diagnosti c criteria and the severity rating symptom
are a visible indication of the thinking th at mild substance-related problems are
fundamentally related to more severe ones. That is, these are not separate diagnosticcategories but ones that are related, different not in the makeup of the conditions butby degree. This pathway from mild to moderate to severe substance use disorder hasthe potential to impact dual diagnosis b y including less severe substance use
problems within the dual diagnosis fram ework. Whereas problem or heavy sub-
stance use that did not meet the threshold for a dependence diagnosis previouslymay not have been considered as part of a de ﬁnition of dual diagnosis, now less
severe expressions of substance use are considered a disorder that would becaptured within the de ﬁnition of dual diagnosis.
The shift from conceptualizing subst ance use disorders from abuse versus
dependence categories to a continuou s dimension was informed by a growing
literature of psychometric analyses of DSM-IV substance use disorder criteria.
Studies using traditional factor analysis, latent trait modeling, and item responsetheory (IRT) analysis all point to a single continuous factor as the most parsimoniousrepresentation of substance-abuse and dependence symptom criteria. Speci ﬁcally,
several studies using exploratory factor analysis found that a single factor solutionincluding both abuse and dependence symptoms had the best ﬁtf o ra l c o h o lu s e
disorders (Borges et al., 2010; Harford, Yi, Faden, & Chen, 2009; Lagenbucher et al.,2004) and marijuana and cocaine use disorders (Lagenbucher et al., 2004). Inaddition, these ﬁndings remained consistent across different national contexts
(Borges et al., 2010) and age groups (Harford et al., 2009; Martin, Chung, Kirisci, &Lagenbucher, 2006). Further, studies utili zed an analysis of substance use criteria
b a s e do nI R Ta n df o u n dt h a tt h es u b s t a n c e abuse and dependence criteria did not
fall on a continuum of severity in a
manner consistent with the DSM-IVThe Problem of Dual Diagnosis 39

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conceptualization of abuse and depende nce typology for alcohol use disorders
(Borges et al., 2010; Lagenbucher et al., 2004; Harford et al., 2009) and cocaine andmarijuana use disorders (Lagenbucher e t al., 2004; Martin et al., 2006). Speci ﬁcally,
for each item, IRT quantiﬁ es where an item falls on a latent variable representing
severity of substance use disorders and the ability of each item to discriminate
between subsequent levels of that latent variable.
The DSM-IV typology would predict that those individuals with less severe
substance use disorders would be less likely to endorse items associated withsubstance dependence (e.g., those items with greater severity) and that these itemswould be more closely related with regard to severity. However, when models werespeciﬁed to order items in such a way, they tended to have poorer ﬁt (Lagenbucher
et al., 2004). Finally, these studies have found some evidence that criteria may beinterpreted differently by respondents depending on age or national context (Borgeset al., 2010; Lagenbucher et al., 2004). In sum, this greater psychometric scrutiny ofDSM symptom criteria has led to a reconceptualization of substance use disorders as acontinuum and it is likely that similar analysis in the future will lead to greaterreﬁnements and precision in diagnostic criteria. In turn, this notion of a continuum
from mild to moderate to severe substance use disorder has the potential to impactdeﬁnitions of dual diagnosis. Where, in the past, substance abuse diagnosis may not
have been considered in dual diagnosis, we may now instead need to consider dualdiagnosis as a continuous variable as opposed to a categorical one. We may need toconsider the correlation between the severity of substance use disorder and speciﬁ c
Axis I diagnostic categories to best understand how different disorders are interrelatedor interact with each other.
Another important change in DSM-5 is expansion of the chapter on substance use
disorders to include gambling disorder, based on a body of research that nowindicates that many of the same underlying neurobiological processes that areactivated and make substance use biologically reinforcing are found in problemgamblers, and that symptoms of problematic gambling are similar in many waysto those of substance use disorders (Petry, 2006). The inclusion of a non-substance-related addiction alongside substance-related ones provides an interesting set ofquestions. Should gambling disorders now be included in the thinking about dualdiagnosis? What does this mean for (the likely increase in) prevalence rates of dualdiagnosis that might accompany such a change, our understanding of the causes ofdual diagnosis, and implications for assessment and treatment? If the most widelyaccepted de ﬁnition of dual diagnosis involves meeting diagnostic criteria for an Axis I
or Axis II mental disorder (or disorders) along with one or more substance usedisorders, and gambling disorder is fundamentally similar in many ways to alcohol ordrug use disorders, does the de ﬁnition need to be broadened to include non-substance
addictions?
The inclusion of gambling disorder in DSM-5 and the questions this change raises
for de ﬁnitions of dual diagnosis illustrate a broader issue: What one identi ﬁes as a
diagnosis is key to any de ﬁnition of dual diagnosis. Gambling provides but one
example. Another example can be seen with tobacco dependence. Although there is alarge literature documenting higher rates of smoking among individuals with psy-chiatric disorders (Farrell et al., 2003), tobacco dependence has not traditionally beenincluded as part of the de ﬁnition of dual diagnosis. This is generally because with such40 O
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high rates of smoking among those with psychiatric disorders, including it wouldyield extremely high rates of dual diagnosis, potentially sapping the concept of itsmeaning (if everyone has dual diagnosis, does it become less important?). However,with growing evidence that smoking may be related to the neurophysiology of somepsychiatric disorders (Wing, Wass, Soh, & George, 2012), it may be that tobaccodependence represents an especially important substance use disorder to include aspart of a de ﬁnition of dual diagnosis. The greater attention to gambling disorder and
tobacco dependence illustrates the ways in which changing ideas about mental healthproblems and addictions can impact rates of dual diagnosis.
Aﬁnal issue here concerns the de ﬁnition of dual diagnosis itself. As noted earlier,
dual diagnosis has generally been used to describe the co-occurrence within anindividual of an Axis I or Axis II mental disorder (or disorders), with one or moresubstance use disorders. Within this de ﬁnition lie many combinations of psychiatric
and substance use disorders. It is important to keep in mind that the literature on dualdiagnosis is, by necessity, simpli ﬁed and compartmentalized by the de ﬁnitions used to
guide it.
FINDINGS FROM MAJOR EPIDEMIOLOGICAL STUDIES
Over the past 25 years, several large-scale e pidemiological studies of mental illness
have examined rates of dual diagnosis, including the Epidemiologic CatchmentArea Study (ECA; Regier et al., 1990), t he National Comorbidity Survey (NCS;
Kessler et al., 1994), the National Comorbidity Survey Replication (NCS-R; Kessler &Merikangas, 2004), and the National Longitudinal Alcohol Epidemiology Survey(NLAES; Grant et al., 1994). Although each s tudy differs somewhat from the others
in methodology, inclusion/exclusion criteria, and diagnostic categories assessed(see Table 2.1 for a brief description of methods for these studies), we can takeseveral points from this literature that can contribute to our thinking about andunderstanding of dual diagnosis.D
UALDIAGNOSIS ISHIGHLY PREVALENT IN COMMUNITY SAMPLES
First, epidemiological studies consistently show that dual diagnosis is highlyprevalent in community samples. Each of these studies ﬁnds that people with
mental illness are at greatly increased ri sk of having a co-occurring substance use
disorder, and people with a substance use disorder are likewise much more likely tomeet criteria for an Axis I mental disorder. For example, the EpidemiologicCatchment Area Study (ECA; Regier et al., 1990) was the ﬁrst large-scale study
of comorbidity of psychiatric and substance use disorders in the general population,a n dd o c u m e n t e dh i g hr a t e so fd u a ld i a g n o sis among both individuals with primary
mental disorders and those with primary su bstance use disorders. Overall, indi-
viduals with a lifetime history of a mental illness had an odds ratio of 2.3 for alifetime history of alcohol use disorder and 4.5 for drug use disorder, a clearillustration of how those with mental illne ss are at substantial ly increased risk of
having a comorbid subst ance use diagnosis.
When examined by type of disorder, antisocial personality disorder (ASP) showed
the highest comorbidity rate (83.6%), followed by bipolar disorder (60.7%),The Problem of Dual Diagnosis 41

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schizophrenia (47.0%), panic disorder (35.8%), obsessive-compulsive disorder (32.8%),and major depression (27.2%). Further analysis of ECA data (Helzer, Robbins, &McEvoy, 1987) found that men and women with posttraumatic stress disorder (PTSD)were 5 times and 1.4 times more likely, respectively, to have a drug use disorder aswere men and women without PTSD. Substantial rates of dual diagnosis were alsofound in primary substance abusers (Regier et al., 1990). Overall, 37% of individualswith an alcohol disorder and 53% of those with a drug use disorder had comorbidmental illness.
Further analyses (Helzer & Pryzbeck, 1988) found that among those with alcohol
use disorders, the strongest association was with ASP (odds ratio =21.0), followed
by mania (OR =6.2) and schizophrenia (OR =4.0). Like the ECA study, the NCS and
the NLAES found markedly high rates of du al diagnosis. NCS (Kessler et al., 1994)
ﬁndings showed that respondents with men tal illness had at least twice the risk of
lifetime alcohol or drug use disorder, with even greater risk for individuals withcertain types of mental illn esses. Findings were similar for primary substance
abusers: The majority of respondents with an alcohol or drug use disorder had ahistory of some nonsubstance use psychiat ric disorder (Kendler, Davis, & Kessler,
1997; Kessler, 1997). Overall, 56.8% of men and 72.4% of women with alcohol abuseTable 2.1
Methods of Several Major Epidemiological Studies on Dual Diagnosis
Study Years MethodsECA (Regier et al.,1990)1980 –1984 Surveyed more than 20,000 adults in ﬁve cities across the United
States both in the community and in institutions. Trainedinterviewers used the Diagnostic Interview Schedule to determineDSM-III diagnoses. Included affective, anxiety, and schizophrenia-
spectrum disorders.
NCS (Kessler et al.,1994)1990 –1992 Assessed 12-month and lifetime prevalence rates for a range of
psychiatric disorders in more than 8,000 noninstitutionalizedindividuals ages 15 –54 across 48 states using the Composite
International Diagnostic Interview (CIDI) and based on DSM-III-R
criteria.
NLAES (Grant et al.,1994)1991 –1992 Examined rates of co-occurrence of alcohol and drug use
disorders and affective disorders in a general population sample.The NLAES is a household survey of more than 42,000 adults inthe United States that utilized diagnostic interviews to assessDSM-IV diagnostic criteria for alcohol use disorders.
NCS-R (Kessler &Merikangas, 2004)2001 –2002 Nationally representative face-to-face household survey of more
than 9,000 noninstitutionalized people ages 18 years or older.Diagnoses based on DSM-IV criteria assessed via CIDI interviews.
NESARC (Grant et al.,2004)2001 –2002 Nationally representative face-to-face survey of 43,093
noninstitutionalized respondents, 18 years of age or older,conducted by NIAAA. DSM-IV criteria for substance use disorders
and nine independent mood and anxiety disorders were assessedwith the Alcohol Use Disorders and Associated DisabilitiesInterview Schedule-DSM-IV Version (AUDADIS-IV), a structureddiagnostic interview administered by lay interviewers.42 O VERVIEW

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m e td i a g n o s t i cc r i t e r i af o ra tl e a s to n ep s ychiatric disorder, as did 78.3% of men and
86.0% of women with alcohol dependence (K endler et al., 1997). Moreover, 59% of
those with a lifetime drug use disorder als o met criteria for a lif etime psychiatric
disorder (Kessler, 1997). Likewise, the NLAES (Grant et al., 1994; Grant & Harford,1995) found that, among respondents with major depression, 32.5% met criteria for
alcohol dependence during their lifeti me, as compared to 11.2% of those without
major depression. Those with primary alcohol use disorders were almost 4 timesmore likely to be diagnosed with lifetime depression, and the associations were evenstronger for drug use disorders: Individuals with drug dependence were nearly7 times more likely than those without drug dependence to report lifetime majordepression (see Bucholz, 1999, for a review). Such ﬁndings clearly illustrate that
rates of dual diagnosis are signi ﬁcant among individuals with mental illness and
primary substance abusers, and that many t ypes of psychiatric disorders confer an
increased risk of substance use disorder. Overall these studies ﬁnd that a psychiatric
diagnosis yields at least double the risk of a lifetime alcohol or drug use disorder.H
IGHPREVALENCE RATES OF DUALDIAGNOSIS PERSIST OVERTIME
A second important feature of rates of dual diagnosis is that they appear to bepersistent. Examining how rates persist or change over time is important for severalreasons. When the ECA and NCS ﬁndings were ﬁrst published, the ﬁndings of high
rates of both single and dual disorders were signi ﬁcant because they illustrated the
many ways in which the understanding, assessment, and treatment of mental illnessand substance use disorders were incomplete. The NCS in particular came underincreased scrutiny, given that the rates it found for mental illness were even higherthan those found by the ECA. Replications of these studies can demonstrate whetherthe high rates found in the ﬁrst studies persist over time. In addition, since the ﬁrst
epidemiologic studies were conducted, DSM criteria have changed, leading to
questions of how these diagnostic chang es might impact illness rates. Finally,
seeking treatment for mental distress, as well as use of medications for symptomsof depression and anxiety, are now more w idely discussed and accepted than they
were 10 to 20 years ago, and it is unclear how changing attitudes might impact ratesof dual disorders. Findings from several replications of large epidemiologic studiesindicate that even with changes in diagnostic criteria and attitudes about psycho-logical distress, rates of dual disorders remain high. For example, the NCS wasrecently replicated in the NCS-R. The NCS-R (Kessler & Merikangas, 2004) sharedm u c ho ft h es a m em e t h o d o l o g ya st h eo r i g i n a lN C S ,r e p e a t e dm a n yq u e s t i o n sf r o mthe original survey, and included additional questions to tap DSM-IV diagnostic
criteria. Conducting these studies 10 years apart allows for an examination of thestability in rates of dual diagnosis, as well as how changes in assessment anddiagnostic criteria impact the prevale nce of dual diagnosis and other comorbid
conditions.
Comparisons of data from both studies illustrate the persistent nature of dual
diagnosis. That is, although speci ﬁc values have changed from one interview to
another, the overall picture of dual diagnosis remains the same: Prevalence rates arehigh, and people with mental illness remain at greatly increased risk for developingsubstance use disorders. For example, for major depressive disorder (MDD; KesslerThe Problem of Dual Diagnosis 43

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et al., 1996) found that 38.6% of respondents who met criteria for lifetime MDD alsohad a diagnosis of substance use disorder based on NCS data, whereas 18.5% ofrespondents who met criteria for 12-month MDD also had a diagnosis of substance usedisorder. Results from the NCS-R con ﬁrmed the high prevalence rates of dual
diagnosis in people with MDD: 24.0% of those with lifetime MDD also met criteriafor a substance use disorder, and 27.1% of those who met criteria for 12-month MDDalso met criteria for a substance use disorder (Kessler, Berglund, et al., 2005). Althoughthe exact percentages change over time, the rates for dual MDD and substance usediagnoses remain strikingly high over the 10 years between studies.
Similar comparisons can be made betw een the NLAES and a more recent NIAAA
survey called the National Epidemiologic Survey on Alcohol and Related Conditions(NESARC; Grant et al., 2004). The NESARC stressed the need to ensure that diagnosesof mood and anxiety disorders were independent from substance use disorders. Acomparison of the two studies shows that dual mood/anxiety and substance used i s o r d e r sc o n t i n u et ob eh i g h l yp r e v a l e n t in community samples. For example, in the
NLAES (Grant & Harford, 1995), responden ts with a past-year diagnosis of major
depression had a 21.36% rate of a co-occurring alcohol use disorder, compared with6.92% of those without 12-month major depression (OR =3.65). Similarly, high
odds ratios were found for 12-month major depression and drug use disorders(Grant, 1995).
Importantly, results of the NESARC con ﬁrm the persistent association of substance
use disorders and affective disorders. People who met criteria for any 12-month mooddisorder were 4.5 times more likely to meet criteria for substance dependence (rangeof 3.4 to 6.4 for the four mood disorders assessed). People who met criteria for any12-month anxiety disorder were 2.8 times more likely to meet substance dependencecriteria (range of 2.2 to 4.2 for the ﬁve anxiety disorders assessed). Examining the
results in terms of prevalence rates is similar: 19.97% of those with any 12-month mooddisorder had at least one substance use disorder (SUD), and 14.96% of those with any12-month anxiety disorder had at least one SUD. Similarly, 19.67% of those with a12-month SUD had at least one mood disorder, and 17.71% had at least one anxietydisorder. Overall, comparisons from replications of large epidemiologic studiesillustrate the persistence of dual diagnosis over time.D
UALDIAGNOSIS ISONLYONEPART OF THE COMORBIDITY PUZZLE
A third issue that is highlighted in some epidemiological studies is the fact that theterm and typical understanding of dual diagnosis may not accurately re ﬂect the nature
and complexity of the problem of co-occurring mental and SUDs. That is, co-occurringdisorders can take many forms, and limiting attention to a particular number orcombination of problems may restrict what we can learn about the links andinteractions between mental illness and SUDs. As discussed previously, the termdual diagnosis has most often been used to refer to a combination of one mental illness
and one SUD. However, epidemiologic studies ﬁnd high prevalence rates of three or
more co-occurring disorders that include but are not limited to dual mental-SUDcombinations. For example, Kessler and colleagues (1994) found that 14% of the NCSsample met criteria for three or more comorbid DSM disorders, and that these
respondents accounted for well over half of the lifetime and 12-month diagnoses44 OVERVIEW

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found in the sample. Moreover, these respondents accounted for 89.5% of the severe12-month disorders, which included active mania, nonaffective psychosis, or otherdisorders requiring hospitalization or associated with severe role impairment.
Other data from the NCS (Kessler et al., 1996) showed that 31.9% of respondents with
lifetime MDD and 18.5% of those with 12-month MDD met criteria for three or morecomorbid conditions. In the NCS-R, Kessler, Berglund, et al. (2005) found that 17.3% ofrespondents met criteria for three or more lifetime disorders. In addition, in examiningprojected lifetime risk of developing different DSM disorders, these authors reported
that 80% of projected new onsets were estimated to occur in people who already haddisorders. In examining 12-month disorders in the NCS-R sample, Kessler, Chiu, et al.(2005) found similar results: 23% of the sample met criteria for three or more diagnoses.As these authors state, “Although mental disorders are widespread, serious cases are
concentrated among a relatively small proportion of cases with high comorbidity ”
(Kessler, Chiu, et al., 2005, p. 617). Taken together, these ﬁndings illustrate the impor-
tance of thinking about dual diagnosis in the context of the broader picture of comorbidconditions. People with dual mental and substance use disorders may in fact meetcriteria for a combination of multiple mental and substance use disorders.
Such aggregation of mental and SUDs in a small proportion of people should
inﬂuence conceptualizations regarding the processes underlying dual and comorbid
conditions. In addition, comorbidity appears to be in ﬂuenced by severity of mental
illness. Using data from the NCS-R, Kessler and colleagues (2003) examined differ-ences in rates of comorbid disorders (including but not limited to SUDs) in respon-dents with MDD of differing levels of severity. Speci ﬁcally, respondents who met
criteria for 12-month MDD were classi ﬁed as showing mild, moderate, severe, or very
severe symptoms, based on scores on the Quick Inventory of Depressive Symptoma-tology Self Report (QIDS-SR) for the worst month in the past year. As severity levelincreased, so did rates of comorbidity, de ﬁned as the percentage of respondents with
two or more comorbid 12-month disorders, including SUDs. Speci ﬁcally, 34.9% of
mild, 58.0% of moderate, 77.3% of severe, and 82.1% of very severe MDD cases metcriteria for two or more comorbid disorders. This ﬁnding of increased severity as
number of disorders increases was also found for 12-month diagnoses (Kessler, Chiu,et al., 2005). This trend is another reminder that dual diagnosis and comorbidity labelsrepresent heterogeneous groups of people who differ in meaningful ways that likelyhave signiﬁ cance in terms of assessment, treatment, and etiology of mental and SUDs.
In sum, epidemiological studies are now able to tell us not only that dual diagnosis
is highly prevalent but also that rates of dual disorders persist over time. In addition,we now have ample evidence to suggest that talking about dual disorders is actually asimpli ﬁcation of a complex problem in that patients often have more than two
psychiatric disorders as well as use, abuse, or are dependent on multiple substances.Such ﬁndings suggest that thinking about the causes of dual disorders may need to be
broadened in order to be able to explain this range of diversity among dual-disorderedpatients.T
HECONCEPT OF DUALDIAGNOSIS HASEXPANDED AND CHANGED
As noted earlier, how studies de ﬁne dual diagnosis has a major impact on prevalence
rates. In this section we review three developments that have had an important impactThe Problem of Dual Diagnosis 45

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on prevalence rates of dual diagnosis: including tobacco dependence when de ﬁning
dual diagnosis, cross-national epidemiological studies, and examination of generalpopulation data focused on speci ﬁc demographic subgroups.
Tobacco Dependence Tobacco is the most widely used substance of abuse among
individuals with mental health diagnoses (Farrell et al., 2003) and rates of smoking forindividuals with mental health disorders are 2 to 3 times higher what is found in thegeneral population (Lawrence, Mitrou, & Zubrick, 2009). Smokers with mental healthdisorders have longer smoking histories and, importantly, are less likely to quit:Whereas tobacco use and dependence has been on the decline in the generalpopulation, rates have generally remained stable among smokers with mental healthdisorders (Dickerson et al., 2012; Secades-Villa et al., 2013; Williams, Steinberg,Grifﬁths, & Cooperman, 2013).
Despite these high prevalence rates, tobacco dependence has not often been con-
sidered in research and thinking about dual diagnosis. There are several reasons for this.First, with such high rates of prevalence of tobacco dependence among those withmental health disorders, including tobacco dependence would serve to de ﬁne a great
number of people with a mental health disorder as having a dual diagnosis. Second,there is a complicated history of tolerance and even encouragement of smoking amongthose with mental health disorders, as many treatment providers believed that indi-viduals would experience symptom relapse or display increased disruptive behavior ifnot able to smoke, ideas that have since been found to be untrue (el-Guebaly, Cathcart,Currie, Brown, & Gloster, 2002). Third, in the past, tobacco dependence was not fullyconsidered an addiction in the same way that chronic and harmful use of alcohol orillicit drugs was seen. Indeed, for a long time, rates of smoking in the general populationwere similarly high and the negative consequences of smoking, because they were oftenfar removed from the time of the actual behavior (i.e., the health effects were more likelyto manifest after many years of smoking), were not thought about in the same way asthe consequences of disordered drinking or illicit drug use.
There are now a range of reasons to consider tobacco dependence when thinking
about and studying dual diagnosis. The addictive nature of tobacco/nicotine isnow widely known, and the negative healt h effects of tobacco dependence and other
negative consequences for individuals with mental health disorders —cost, stigma,
second-hand smoke —have been identi ﬁed (see Bennett, Wilson, Genderson, &
Saperstein, 2013, and Graham, Frost-Pineda, & Gold, 2007 for reviews). As informa-tion and knowledge about tobacco dependen ce has increased, rates of smoking in the
general population have decreased dramatically, making tobacco dependence adecreasing problem for many people but still an alarming problem for individualswith mental health disorders. Estimates suggest that individuals with mental healthd i s o r d e r ss m o k e5 0 %o fa l lc i g a r e t t e sc o n s u m e di nt h i sc o u n t r y( L a s s e re ta l . ,2 0 0 0 )and that individuals with mental health disorders have a disproportionately dif ﬁcult
time quitting smoking (see Mackowick, L ynch, Weinberger, & George, 2012 for a
review). Moreover, research suggests that nicotine may have a unique connectionwith genetics and brain functioning in some psychiatric disorders including depres-
sion and schizophrenia (de Leon & Diaz, 2 012; Wing et al., 2012), and that quitting
m i g h tb em o r ed i f ﬁcult for individuals with mental health disorders due to biological
factors that may make smoking more reinfor cing (Berg, Sentir, Cooley, Engleman, &46 O
VERVIEW

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Chambers, 2013) or withdrawal symptoms more problematic (Leventhal, Ameringer,Osborn, Zvolensky, & Langdon, 2013; Wein berger, Desai, & McKee, 2010) than what
is experienced by other smokers. For these reasons, we believe a comprehensivereview of dual diagnosis should include i n f o r m a t i o no nt o b a c c od e p e n d e n c e ,a n d
have provided this in the following sections.
The epidemiological studies just listed provide information on rates of tobacco
dependence among those with mental health disorders. Lawrence and colleagues(Lawrence et al., 2009) used data from the NCS-R to examine rates of comorbidtobacco dependence and mental health disorders (affective, anxiety, and substance usedisorders) as measured by the WHO CIDI. Among respondents with a mental healthdisorder in the past 12 months, 40.1% were current smokers (almost double the 21.3%smoking prevalence in adults without a mental health disorder in the past 12 months).Rates were highest among those with SUDs (63.6%), followed by individuals withaffective disorders (45.1%) and anxiety disorders (37.6%). Goodwin, Zvolensky,Keyes, & Hasin (2012) examined rates of tobacco dependence among those withmental health disorders in the NESARC sample. Diagnoses of speciﬁ c phobia,
personality disorder, major depressive disorder, and bipolar disorder were associatedwith increased odds of nicotine dependence, as well as with increased risk ofpersistent nicotine dependence over a 3-year follow-up (Goodwin, Pagura, Spiwak,Lemeshow, & Sareen, 2011). In an examination of associations between smoking andpersonality disorders using the NESARC sample, Pulay and colleagues (2010) foundthat the nicotine dependence had the strongest associations with schizotypal, border-line, narcissistic, and obsessive-compulsive personality disorder diagnoses.Cross-National Epidemiological Studies The preceding review of epidemiological stud-
ies focuses on ﬁndings from studies conducted in the United States. An interesting and
important complement to ﬁndings from the United States comes from ﬁndings from
the WHO World Mental Health Surveys (WMHS; Kessler, Haro, Heeringa, Pennell, &Üstün, 2006), an assessment of diagnosis of mental health disorders using the WHOComposite International Diagnostic Interview (CIDI) carried out in 28 countriesaround the world with a sample of over 150,000 respondents. Findings from thisinternational survey con ﬁrm results from the United States: Mental health disorders
are prevalent in all regions of the world, and rates of comorbid SUDs are substantiallyhigher among those with mental health disorders. For example, in an examination ofprevalence rates and correlates of bipolar spectrum disorder in a subset of the WHOWMHS sample ( n=61,392), Merikangas and colleagues (Merikangas et al., 2011)
found that 36.6% of those with a bipolar spectrum disorder met criteria for a co-occurring substance use disorder. Other ﬁndings from the WHO WMHS replicate
ﬁndings reviewed above: Comorbidity of multiple mental health disorders, including
diagnostic combinations that include psychiatric and SUDs, is associated with greaterimpairments such as higher risk for suicide (Nock et al., 2009). As more cross-nationaldata are collected and analyzed, it will be important to expand on this work toexamine if and how different processes and cultural factors in ﬂuence the development
and persistence of dual diagnosis.Prevalence of Dual Diagnosis in Older Adults A special population that is important to
consider when thinking about dual diagnosis is older adults. With people livingThe Problem of Dual Diagnosis 47

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longer, it is important to understand how rates of dual disorders persist or change overtime. Findings from the NCS-R show lower rates of diagnosis of mood, anxiety, andsubstance use disorders for those 65 and older compared to those 18 –64 (Gum, King-
Kallimanis, & Kohn, 2009). Results from the NESARC (Chou & Cheung, 2013) ﬁnd
that although the overall prevalence of major depressive disorder is low in older adults(2.95% for the past year and 8.82% lifetime), among those with lifetime majordepressive disorder, 20% met criteria for an alcohol use disorder.
In line with the idea of including gambling disorder within the de ﬁnition of dual
diagnosis, several studies using NESARC d ata have found high rates of dual mental
and gambling disorders among older adul ts (Chou & Cheung, 2013; Pilver, Libby,
Hoff, & Potenza, 2013), highlighting the way in which older age may impact thetraditional de ﬁnition of dual diagnosis. For example, Pietrzak and colleagues
(Pietrzak, Morasco, Blanco, Grant, Petry , 2006) examined over 10,000 older adults
in the NESARC survey and found signi ﬁcantly elevated rates of SUDs (alcohol,
tobacco, and drugs), as well as mood, anxiety, and personality disorders amongthose with disordered gambling.
Dual diagnosis may play an important role in a subset of older adults who
experience chronic mental health disorders. Mackenzie and colleagues (Mackenzie,El-Gabalawy, Chou, & Sareen, 2013) examined factors that may contribute to persist-ence of three mental health diagnoses —mood, anxiety, and substance use disorders —
over time in older adults surveyed in the NESARC study. Their ﬁndings showed that
although most disorders were not persistent from one assessment to a second one thatwas conducted 3 years later, comorbidity of another mental health disorder (includingSUDs) was a signi ﬁcant predictor of persistence of any disorder over time.
FINDINGS FROM STUDIES OF CLINICAL SAMPLES
The fact that dual diagnosis is fairly common in the general population serves tohighlight the even higher rates found in treatment settings. Clinical studies of dualdiagnosis have assessed general psychiatric patients, patients with speciﬁ c psychiatric
disorders, and primary substance abusing patients.D
UALDIAGNOSIS IN GENERAL PSYCHIATRIC PATIENTS
Clinical studies of dual diagnosis over the past 20 years indicate that one-third tothree-quarters of general psychiatric patients may meet criteria for comorbid psychi-atric and substance use disorders, depending on the diagnostic makeup of the sampleand the level of chronicity represented (Ananth et al., 1989; Galanter et al., 1988;McLellan, Druley, & Carson, 1978; Mezzich, Ahn, Fabrega, & Pilkonis, 1990; Safer,1987). Rates seem to fall in the higher end of this range for samples comprising moreimpaired patient populations. For example, Ananth and colleagues (1989) found that72.0% of a sample of patients with schizophrenia, bipolar disorder, and atypicalpsychosis received a comorbid substance use diagnosis. Mezzich et al. (1990) con-ducted a large-scale assessment of dual diagnosis in more than 4,000 patientspresenting for evaluation and referral for mental health problems over an 18-monthperiod and found substantial rates of dual diagnosis among several diagnosticsubsamples. The highest rates were seen among patients with severe mental illnesses48 OVERVIEW

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such as bipolar disorder (45% diagnosed with an alcohol use disorder and 39%diagnosed with a drug-use disorder) and schizophrenia or paranoid disorders (42%and 38% were diagnosed with alcohol and other SUDs, respectively). However, dualdiagnosis was also pronounced in other patient groups. Speci ﬁcally, 33% of patients
with major depression were diagnosed with an alcohol use disorder, and 18% werediagnosed with a drug use disorder. Among patients with anxiety disorders, 19% and11% were diagnosed with alcohol and other substance use disorders, respectively.D
UALDIAGNOSIS IN SAMPLES OF PATIENTS WITHSPECIFIC DISORDERS
Rates of dual diagnosis have been extensively studied among patients with severemental illness, including schizophrenia (Dixon, Haas, Weiden, Sweeney, & Frances,1991; Mueser et al., 1990), bipolar disorder (Bauer et al., 2005; McElroy et al., 2001;Salloum & Thase, 2000; Vieta et al., 2000), and major depression (Goodwin & Jamison,1990; Lynskey, 1998; Merikangas, Leckman, Prusoff, Pauls, & Weissman, 1985;Swendsen & Merikangas, 2000). Findings show that dual diagnosis is common insuch samples. Mueser et al. (1990) evaluated 149 patients with schizophrenia spectrumdisorders and found that 47% had a lifetime history of alcohol abuse, whereas manyhad abused stimulants (25%), cannabis (42%), and hallucinogens (18%). Dixon andcolleagues (1991) found that 48% of a sample of schizophrenia patients met criteria foran alcohol or drug use disorder. Chengappa, Levine, Gershon, and Kupfer (2000)evaluated the prevalence of substance abuse and dependence in patients with bipolardisorder.
Among patients with bipolar I, 58% met abuse or dependence criteria for at least
one substance, and 11% abused or were dependent on three or more substances. In thebipolar II group, the rate of dual diagnosis was approximately 39%. Baethge andcolleagues (2005) followed a group of ﬁrst-episode bipolar I patients and found that
about one-third of the sample had a SUD at the baseline assessment, and that patientsusing two or more substances showed poorer outcomes over the 2 years of the study.Bauer and colleagues (Bauer et al., 2005) conducted structured interviews with a largesample of inpatient veterans with bipolar disorder across 11 sites ( n=328) to examine
rates of comorbid anxiety and substance use disorders. Results showed high rates ofcurrent (33.8%) and lifetime (72.3%) SUDs in the sample, along with a rate of 29.8%meeting criteria for multiple current disorders.
Hasin, Endicott, and Lewis (1985) examined rates of comorbidity in a sample of
patients with affective disorder presenting for treatment as part of the NationalInstitute of Mental Health Collaborative Study of Depression and found that 24%of these patients reported serious problems with alcohol and 18% met diagnosticcriteria for an alcohol use disorder. In an examination of patients with major depres-sion, bipolar disorder, and controls participating in the National Institute of MentalHealth Collaborative Program on the Psychobiology of Depression, Winokur andcolleagues (1998) found that affective disorder patients had substantially higher ratesof dual SUDs than did controls.
Dual diagnosis is also common among patients with anxiety disorders. In their
review of studies of dual anxiety and SUDs, Kushner, Sher, and Beitman (1990) foundthat rates differ by type of anxiety disorder, with social phobia (ranging from 20% to36% rate of dual diagnosis) and agoraphobia (ranging from 7.0% to 27.0% rate of dualThe Problem of Dual Diagnosis 49

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diagnosis) showing the highest rates of substance abuse comorbidity. Others havefound a 22% rate of lifetime alcohol use disorder among patients with social phobia(Himle & Hill, 1991), a 10% to 20% rate for patients with agoraphobia (Bibb &Chambless, 1986), and up to a 12% rate of lifetime alcohol dependence among patientswith obsessive-compulsive disorder (Eisen & Rasmussen, 1989). In addition, moreattention is being given recently to dual substance abuse and PTSD in clinical samples.A growing literature examining this diagnostic combination ﬁnds high rates of dual
diagnosis among patients with PTSD, with some ﬁndings as high as 80% (Keane,
Gerardi, Lyons, & Wolfe, 1988). Research both with samples of veterans with PTSDand samples of women with assault- or trauma-related PTSD show strikingly highrates of comorbid substance abuse and dependence (see Stewart, Pihl, Conrod, &Dongier, 1998, for a review), as well as other disorders. Moreover, Breslau, Davis,Peterson, and Schultz (1997) interviewed a sample of 801 women and found that PTSDsigniﬁcantly increased the likelihood for later alcohol use disorder. Research with
community mental health patients with several mental illnesses shows extremely highrates of co-occurring PTSD (14% –53%, usually undiagnosed; Grubaugh, Zinzow, Paul,
Egede, & Frueh, 2011).
Research documents high rates of dual diagnosis among those with eating dis-
orders. Higher rates of drug use have been found in samples of individuals with eatingdisorders than in controls (Krug et al., 2008), and studies of clinical samples show highoverall rates of alcohol and drug use disorders. For example, Grilo, White, and Masheb(2009) assessed DSM-IV lifetime and current psychiatric disorder comorbidity in
patients with binge-eating disorder and found that more than 73% of respondents hadat least one lifetime diagnosis and 43% had at least one current psychiatric diagnosis,with almost 25% of the sample meeting criteria for a lifetime SUD. Several studies haveshown variation in rates of SUDs across the different types of eating disorders —
anorexia nervosa, bulimia nervosa, binge-eating disorder— and subsets of disorders
within these (Root et al., 2010). In addition, rates of comorbidity, including that withSUDs, may be associated with eating disorder severity, with those with more severesymptoms of eating disorder showing the highest rates of comorbid SUDs (Spindler &Milos, 2007).
Some of the highest rates of comorbidity are found for patients with personality
disorders, especially antisocial personality disorder (ASP). Studies show thatcomorbid ASP accelerates the development of alcoholism (Hesselbrock, Hesselbrock,& Workman-Daniels, 1986), and that 80% of patients with ASP have a history ofproblem use of alcohol (Schuckit, 1983). In a recent review of studies on dualSUDs and borderline personality disorder (BPD), Trull and colleagues (Trull,Sher, Minks-Brown, Durbin, & Burr, 2000) found that, across studies, more than48% of patients with BPD met criteria for alcohol use disorders, and 38% of thosewith BPD met criteria for a drug use disorder. In a recent reanalysis of the NESARCdata, Trull and colleagues (Trull, Jahng, Tomko, Wood, & Sher, 2010) found highrates of dual personality disorders and SUDs. More than one-quarter of those withASP (26.65%) met criteria for drug dependence, although even higher rates of drugdependence were found for those with histrionic (29.72%) and dependent (27.34%)personality disorders.
Important work is now illustrating the need to think more broadly about dual and
multiple comorbidities and how these span Axis I and Axis II disorders. For example,50 OVERVIEW

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a recent examination of data on generalized anxiety disorder from the NESARCstudy (Alegría et al., 2010) found a lifetime prevalence rate of generalized anxietydisorder with comorbid SUD of 2.04%. However, those with generalized anxietydisorder and comorbid SUD showed signi ﬁcantly higher rates of comorbidity of
other psychiatric disorders than did those with generalized anxiety disorder alone,including higher lifetime rates of bipolar disorder, panic disorder, and ASP. A similarpattern was found for social anxiety in the NESARC data (Schneier et al., 2010):Respondents with both social anxiety disorder and comorbid alcohol use disorderwere signi ﬁcantly more likely to earn diagnoses of mood, other anxiety, psychotic,
and personality disorders, as well as additional SUDs and pathological gambling.Goldstein, Compton, and Grant (2010) examined rates of ASP in individuals withPTSD and how this combination of disorders affected risk of further comorbidpsychiatric disorders. Compared to those with PTSD only, those with PTSD +ASP
showed much higher rates of additional comorbid diagnoses. Speci ﬁcally, those with
PTSD+ASP met criteria for, on average, 5.7 additional lifetime Axis I diagnoses,
whereas those with PTSD only met criteria for only 2.3 additional lifetime Axis Idiagnoses. Rates of additional Axis II diagnosis were similar (2.5 additional Axis IIdiagnoses for those with PTSD +ASP versus 0.7 for those with PTSD only).
Wildes, Marcus, and Fagiolini (2008) examined rates of eating disorders in indi-
viduals with bipolar disorder and found that a subset of individuals with bipolardisorder and loss of control over eating showed elevated rates of substance usedisorders. In another study of individuals with bipolar disorder, Bauer and colleagues(2005) interviewed inpatients using the Structured Clinical Interview for DSM-IV and
found that rates of comorbidity with SUDs were high (33.8% current, 72.3% lifetime),but that almost 30% of respondents had comorbid bipolar, SUD, and anxiety dis-orders. Such ﬁndings illustrate the importance of expanding our thinking regarding
dual diagnosis into multiple comorbidities.
As noted earlier, rates of tobacco dependence are high among individuals with
mental health disorders. Studies indicate that more than 60% of adults with schizo-phrenia, 40% with bipolar disorder, and 30% with major depression in the UnitedStates smoke, compared to fewer than 20% in the overall adult population (Dickersonet al., 2012; Heffner, Strawn, DelBello, Strakowski, & Anthenelli, 2011). Similarly,research has found higher rates of smoking among those with a range of anxietydisorders, although directionality is unclear —there is evidence to suggest that smok-
ing is a risk factor for panic disorder and generalized anxiety disorder (Moylan, Jacka,Pasco, & Berk, 2012).
Some speculate that those with mental health disorders who smoke may experience
a more severe subtype of disorder than those who do not smoke. For example, Strongand colleagues (2010) examined differences in smoking behavior between those withno history of major depressive disorder, those with a single episode, or those withrecurrent major episodes in 1,560 participants in the NCS-R. Those with comorbidrecurrent major depression reported more smoking, greater nicotine dependence,more comorbid mental health disorders, and greater impairment in functioning thanthose with no or a single episode of major depression. Saiyad and El-Mallakh (2012)studied the impact of smoking on symptoms of bipolar disorders ( n=134) and found
that those with bipolar disorder who smoked reported more severe symptoms ofanxiety, depression, and mania. Others have suggested that smoking may be a markerThe Problem of Dual Diagnosis 51

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for a more chronic form of schizophrenia (Dalack & Meador-Woodruff, 1996) or asubtype of bulimia nervosa characterized by more depression and alcohol abuse(Sandager et al., 2008).D
UALDIAGNOSIS IN PATIENTS WITHPRIMARY SUBSTANCE USEDISORDERS
Substance-abusing patients in treatment are a heterogeneous group, encompassing arange of substances and levels of severity. Nonetheless, researchers have found highrates of dual disorders across diverse samples of patients seeking substance abusetreatment (Arendt & Munk-Jorgensen, 2004; Falck, Wang, Siegal, & Carlson, 2004;Herz, Volicer, D ’Angelo, & Gadish, 1990; Mirin, Weiss, Grif ﬁn, & Michael, 1991; Mirin,
Weiss, & Michael, 1988; Penick et al., 1984; Powell, Penick, Othmer, Bingham, & Rice,1982; Ross, Glaser, & Stiasny, 1988; Rounsaville, Weissman, Kleber, & Wilber, 1982;Watkins et al., 2004; Weissman & Myers, 1980). Findings of lifetime rates of psychiatricdisorder range from 73.5% of a sample of cocaine abusers (Rounsaville et al., 1991) to77% of a sample of hospitalized alcoholics (Hesselbrock, Meyer, & Keener, 1985) to78% of a sample of patients in an alcohol and drug treatment facility (Ross, Glaser, &Germanson, 1988). Findings of current psychiatric disorder are similarly high, rangingfrom 55.7% of a group of cocaine abusers (Rounsaville et al., 1991) to 65% in a generalsubstance-abusing sample (Ross, Glaser, & Germanson, 1988).
Further re ﬂecting their diagnostic heterogeneity, substance abusers in treatment
experience a range of comorbid psychiatric disorders. Among the most widely studiedhave been affective disorders, and treatment-seeking substance abusers show highrates of both major depression (Hasin, Grant, & Endicott, 1988; Hesselbrock et al.,1985; Merikangas & Gelernter, 1990; Mezzich et al., 1990; Miller, Klamen, Hoffmann, &Flaherty, 1996; Rounsaville, Weissman, Wilber, Crits-Christoph, & Kleber, 1982;Weissman & Myers, 1980) and bipolar disorder (Strakowski & DelBello, 2000). Millerand colleagues (1996) surveyed a sample of more than 6,000 substance abuse treat-ment patients from 41 sites and found that 44% had a lifetime history of majordepression. In a review of comorbidity of affective and substance use disorders,Lynskey (1998) found that the prevalence of unipolar depression among patientsreceiving treatment for substance use disorders ranged from a low of 25.8% for lifetimedepression in a sample of 93 alcohol-dependent men (Sellman & Joyce, 1996) to a highof 67% meeting a lifetime diagnosis of major depression among a sample of 120inpatients (Grant, Hasin, & Harford, 1989). Busto, Romach, and Sellers (1996) eval-uated rates of dual diagnosis in a sample of 30 patients admitted to a medical facilityfor benzodiazepine detoxi ﬁcation and found that 33% met DSM-II-R criteria for
lifetime major depression.
Results from large studies of treatment-seeking substance abusers ﬁnd that these
patients show 5 to 8 times the risk of having a comorbid bipolar diagnosis (seeStrakowski & DelBello, 2000, for a review). The importance of dual mental illnessin substance-abusing samples lies in its link to functioning and treatment outcome.Burns, Teesson, and O ’Neill (2005) studied the impact of dual anxiety disorders
and/or depression on outcome of 71 patients seeking outpatient alcohol treatment.Comorbid patients showed greater problems at baseline (more disabled, drank moreheavily) than did substance-abuse-only patients, a difference that persisted at a follow-up assessment 3 months later.52 OVERVIEW

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An extensive literature documents high rates of comorbid personality disorders in
primary substance abusers (Khantzian & Treece, 1985; Nace, 1990; Nace, Davis, &Gaspari, 1991), especially ASP (Herz et al., 1990; Hesselbrock et al., 1985; Liskow,Powell, Nickel, & Penick, 1991; Morgenstern, Langenbucher, Labouvie, & Miller, 1997;Penick et al., 1984; Powell et al., 1982). In their evaluation of a large sample oftreatment-seeking substance abusers, Mezzich and colleagues (1990) found that 18%of those with alcohol use disorders and almost 25% of those with drug use disordersmet criteria for an Axis II disorder. Busto and colleagues (1996) found that 42% of theirsample of patients undergoing benzodiazepine detoxi ﬁcation met DSM-III-R criteria
for ASP. Morgenstern and colleagues (1997) assessed prevalence rates of personalitydisorders in a multisite sample of 366 substance abusers in treatment. Results showedthat more than 57% of the sample met criteria for at least one personality disorder. ASPwas the most prevalent (22.7% of the sample), followed by borderline (22.4%),paranoid (20.7%), and avoidant (18%) personality disorders. Moreover, the presenceof a personality disorder doubled the likelihood of meeting criteria for a comorbidAxis I disorder. Brooner and colleagues (Brooner, King, Kidorf, Schmidt, & Bigelow,1997) assessed psychiatric disorders in 716 opioid abusers on methadone maintenancetherapy and found that 47% of the sample met criteria for at least one disorder, withASP and major depression being the most common co-occurring diagnoses. Inaddition, psychiatric comorbidity was associated with more severe substance usedisorder. Kokkevi, Stephanis, Anastasopoulou, & Kostogianni (1998) surveyed 226treatment-seeking individuals with drug dependence in Greece and found a 59.5%prevalence rate of personality disorder, with more than 60% of these patients meetingcriteria for more than one personality disorder. Furthermore, those with personalitydisorders were at twice the risk for meeting an additional Axis I diagnosis.
Findings are similar with anxiety disorders, with high rates of comorbid phobias
(Bowen, Cipywnyk, D ’Arcy, & Keegan, 1984; Hasin et al., 1988; Ross, Glazer, &
Stiasny, 1988), panic disorder (Hasin et al., 1988; Penick et al., 1984), and obsessive-compulsive disorder (Eisen & Rasmussen, 1989) documented in substance-abusingpopulations. Thomas, Thevos, and Randall (1999) reported a 23% prevalence rateof social phobias in a large study of both inpatients and outpatients with alcoholdependence. Substance abusers also appear to be especially affected by PTSD (Cottler,Compton, Mager, Spitznagel, & Janca, 1992; Davis & Wood, 1999; Trif ﬂeman,
Marmar, Delucchi, & Ronfeldt, 1995).
In an analysis of cocaine-dependent patients in the National Institute on Drug
Abuse Collaborative Cocaine Treatment Study, Najavitis and colleagues (1998) foundthat 30.2% of women and 15.2% of men met DSM-II-R criteria for PTSD. Recently, Back
and colleagues (2000) found that 42.9% of a sample of cocaine-dependent indivi-duals met criteria for PTSD, and Bonin and colleagues (Bonin, Norton, Asmundson,Dicurzio, & Pidlubney, 2000) found a 37.4% rate of PTSD in a sample of patientsattending a community substance abuse treatment program. In sum, the literatureclearly documents high rates of dual substance abuse and psychiatric disorders fora variety of psychopathological conditions and in a range of patient populations.Findings from epidemiological studies show that dual diagnosis is relatively commonin the general population, and results of clinical studies illustrate the frequency of dualdiagnosis among individuals in treatment. That rates of dual diagnosis are similarlyhigh in both mentally ill and in primary substance-abusing populations serves toThe Problem of Dual Diagnosis 53

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highlight the serious dif ﬁculties in having two separate and independent systems of
care for mental illness and substance abuse (Grella, 1996; Ridgely, Lambert, Goodman,Chichester, & Ralph, 1998), because both populations of patients are quite likely to besuffering from both types of disorders.
CLINICAL IMPACT OF DUAL DISORDERS
The importance of dual diagnosis lies in its negative impact on the course andprognosis of both psychiatric and SUDs, as well as its in ﬂuence on assessment,
diagnosis, and treatment outcome. Individuals with dual disorders show moreadverse social, health, economic, and psychiatric consequences than do those withonly one disorder, and they show more severe dif ﬁculties, often a more chronic course
of psychiatric disorder, and a poorer response to both mental health and substanceabuse treatment. In the next section, we review the ways that dual diagnosis impactsthree general areas: patient functioning, clinical care, and research.I
MPACT OF DUALDIAGNOSIS ON FUNCTIONING
Dual diagnosis has a profound impact on many domains of functioning. This sectionreviews the many ways that dual diagnosis affects symptoms of mental illness, courseof mental illness over time, cognitive functioning, and compliance with treatment.Symptoms, Course of Illness, and Life Functioning Dual diagnosis severely impacts the
severity and course of many disorders, especially among patients with serious mentalillnesses such as schizophrenia, bipolar disorder, and recurrent major depression.Often these dually diagnosed individuals show a poorer and more chaotic course ofdisorder, with more severe symptoms (Alterman, Erdlen, Laporte, & Erdlen, 1982;Barbee et al., 1989; Hays & Aidroos, 1986; Negrete and Knapp, 1986), more frequenthospitalizations (Carpenter, Heinrichs, & Alphs, 1985; Drake & Wallach, 1989; Sonne,Brady, & Morton, 1994), and more frequent relapses than patients without co-occurring substance abuse (Linszen, Dingemans, & Lenior, 1994; O ’Connell, Mayo,
Flatow, Cuthbertson, & O ’Brien, 1991; Sokolski et al., 1994). Haywood et al. (1995)
found that substance abuse, along with medication noncompliance, was the mostimportant predictor of more frequent rehospitalization among schizophrenia patients.
Recently, Margolese and colleagues (Margolese, Malchy, Negrete, Tempier, &
Gill, 2004) compared three groups of schizophrenia patients: those with currentSUD, those with lifetime but not current SUD, and those with no current or historyof SUD. Patients with current SUD showed m ore positive symptoms than both other
patient groups, had higher scores on measures of depression as compared to thesingle diagnosis group, and were more likely than the single diagnosis group to benoncompliant with their medications. Winokur and colleagues (1998) found thatpatients with drug abuse and bipolar disorder had an earlier age of onset of bipolardisorder than those with bipolar disorder alone, as well as a stronger family history
of mania.
Nolen and colleagues (2004) rated patients with bipolar or schizoaffective disorder
on severity of manic symptoms, severity of depressive symptoms, and number ofillness episodes over a 1-year period ( n=258). Results showed that ratings for mania54 O
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severity were associated with comorbid substance abuse. Lehman, Myers, Thompson,and Corty (1993) compared individuals with dual mental illness and substance usediagnoses to those with just a primary mental illness and found that the dual diagnosisgroup had a higher rate of personality disorder and more legal problems. Hasin,Endicott, and Keller (1991) followed 135 individuals with dual mood and alcohol usedisorders who were originally studied as part of the National Institute of MentalHealth Collaborative Study on the Psychobiology of Depression. Although most hadexperienced at least one 6-month period of remission of the alcohol disorder at somepoint during the follow-up period, most had relapsed after 5 years. Mueller andcolleagues (1994) examined the impact of alcohol dependence on the course of majordepression over 10 years among individuals with depression who participated in theNational Institute of Mental Health Collaborative Depression Study. Those who werealcohol dependent at baseline had a much lower rate of recovery from majordepression than those with major depression alone, illustrating the negative impactof alcohol use disorders on the course of major depressive disorder.
Dual diagnosis is also a serious issue for patients with anxiety disorders such as
PTSD (Najavitis, Weiss, & Shaw, 1997; Ouimette, Brown, & Najavitis, 1998). Overall,the combination of substance abuse and PTSD appears to be linked to higher ratesof victimization, more severe PTSD symptoms in general, more severe subgroupsof PTSD symptoms, and higher rates of Axis II comorbidity (Ouimette, Wolfe, &Chrestman, 1996). Saladin, Brady, Dansky, and Kilpatrick (1995) compared 28 womenwith both substance abuse and PTSD to 28 women with PTSD only and found thatthe dual diagnosis group reported more symptoms of avoidance and arousal, moresleep disturbance, and greater traumatic-event exposure than the PTSD-only group.Back and colleagues (2000) similarly found higher rates of exposure to traumaticevents, more severe symptomatology, and higher rates of Axis I and Axis II disordersamong cocaine-dependent individuals with PTSD as compared to those withoutlifetime PTSD. Moreover, evidence suggests that the combination of PTSD and cocainedependence remains harmful over several years, with patients showing a greaterlikelihood of continued PTSD as well as revictimization several years after an initialsubstance abuse treatment episode (Dansky, Brady, & Saladin, 1998).
Dual diagnosis also exerts a profound impact on overall life functioning. Patients with
severe mental illnesses such as schizophrenia who abuse substances appear to beparticularly hard hit in this regard (see Bradizza & Stasiewicz, 1997, for a review;Kozaric-Kovacic, Folnegovic-Smalc, Folnegovic, & Marusic, 1995). Drake and colleaguesconsistently have found that individuals with schizophrenia and comorbid substanceabuse show substantially poorer life adjustment than do individuals with schizo-phrenia without substance abuse, and eat fewer regular meals (Drake, Osher, & Wallach,1989; Drake & Wallach, 1989). Havassy and Arns (1998) surveyed 160 frequentlyhospitalized adult psychiatric patients and found not only high rates of dual disorders(48% of patients had at least one current substance use disorder; of these, 55.1% metcriteria for polysubstance dependence) but also that dual diagnosis was related toincreased depressive symptoms, poor life functioning, lower life satisfaction, and agreater likelihood of being arrested or in jail. Research similarly shows that patients withdual affective and alcohol use disorders show greater dif ﬁculties in overall functioning
and social functioning than do patients with depression (Hirschfeld, Hasin, Keller,Endicott, & Wunder, 1990) or bipolar disorder (Singh, Mattoo, Sharan, & Basu, 2005).The Problem of Dual Diagnosis 55

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Newman, Mof ﬁtt, Caspi, & Silva (1998) examined the impact of different types of
comorbidity (including but not limited to substance abuse –psychiatric disorder
combinations) on life functioning in a large sample of young adults. Multiple-disordered cases showed poorer functioning than single-disordered cases in almostevery area measured, including health status, suicide attempts, disruption in per-formance of daily activities, the number of months disabled because of psychiatricillness, greater life dissatisfaction, less social stability (more residence changes, greateruse of welfare for support, greater rates of adult criminal conviction records), greateremployment problems, lower levels of educational attainment, and greater reports ofphysical health problems. Weiss and colleagues (2005) examined the interplaybetween bipolar disorder and recovery from substance use disorders on a range ofquality-of-life factors in a sample of 1,000 patients with current or lifetime bipolardisorder. Speci ﬁcally, three groups were compared: those with no history of SUDs,
those with past SUDs, and those with current SUDs. Results showed that the current-SUD group had the poorest functioning, and both SUD groups reported lower qualityof life and higher lifetime rates of suicide attempts than did the non-SUD group.Moreover, the toxic effects of psychoactive substances in individuals with schizo-phrenia and bipolar disorder may be present even at use levels that may not beproblematic in the general population (Lehman, Myers, Dixon, & Johnson, 1994;Mueser et al., 1990).Cognitive Functioning Increasingly, clinicians and researchers are focusing on
cognitive functioning in persons with dual disorders. There is a range of cognitiveimpairments associated with psychiatric disorders, particularly serious mentalillness (e.g., schizophrenia, bipolar disorder). Individuals with schizophrenia spec-trum disorders demonstrate cognitive i mpairments across a range of cognitive
domains when compared to normative comp arison samples (Heinrichs & Zakzanis,
1998). Although not as severe, individuals with affective disorders demonstratesimilar impairments across a range of cognitive domains (Depp et al., 2007;
Goldberg et al., 1993; Schretlen et al., 2007). These impairments are linked bymodest to strong correlations to functional outcomes in schizophrenia (Green,1996) and bipolar disorder (Dickerson et al., 2004; Dickerson, Sommerville, Origoni,Ringel, & Parente, 2001).
There is also evidence that, in samples of individuals with primary SUDs, chronic
or sustained substance use can contribute to cognitive impairment and resulting braindysfunction (Bowden, Crews, Bates, Fals-Stewart, & Ambrose, 2001; Rogers & Robbins,2001). Moreover, cognitive impairment has been implicated in substance-abuse-treatment outcomes in this population (Aharonovich, Nunes, & Hasin, 2003; Fals-Stewart & Schafer, 1992). Such ﬁndings suggest that substance use may exacerbate
existing cognitive impairment, which may, in part, contribute to the poorer outcomesexperienced by persons with co-occurring serious mental illness (SMI) and SUD.
Although this recognition has prompted clinical research efforts to adapt and
develop new substance abuse interventions designed to accommodate some ofthe cognitive and motivational impairments associated with SMI (e.g., Addington,el-Guebaly, Campbell, Hodgins, & Addington, 1998; Bellack, Bennett, Gearon,Brown, & Yang, 2006; Ziedonis & George, 1997), other research efforts have beendirected toward further description and explication of the role of cognitive56 OVERVIEW

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impairment in individuals with dual diagnosis. The majority of this work has focusedon SMI samples. On the one hand, there is concern about the possible exacerbation ofexisting cognitive impairment resulting from substance use among individuals withdual disorders, suggesting that these individuals would demonstrate poorer cognitivefunctioning when compared to those without SUD. On the other hand, some datasuggest that engaging in behaviors necessary to obtain access to substances requires ahigher level of functioning (Dixon, 1999; Mueser et al., 1990), and, thus, theseindividuals with dual disorders would have better cognitive functioning than indi-viduals without SUD.
With regard to cognitive functioning, the data are in fact mixed and overall suggest
that there are few differences between those with SMI who have a current or history ofSUD and those who do not. In a meta-analysis of 22 studies investigating neuro-cognitive functioning among individuals with schizophrenia, Potvin, Joyal, Pelletier,and Stip (2008) found that there was no difference on a composite score of cognitivefunctioning between those with SUD and those without. Furthermore, they found fewdifferences between groups on speci ﬁc cognitive domains or speci ﬁc cognitive
measures. Depp et al. (2007) also found no differences in cognitive functioning amonga sample of individuals with bipolar disorder with and without SUDs. In contrast,Carey, Carey, and Simons (2003), in a sample of individuals with schizophreniaspectrum and bipolar disorders, found that those with a current SUD or former SUDboth demonstrated better cognitive functioning than those who had never usedsubstances.
The interpretation of these data is complicated by several substantive and meth-
odological issues. First, there is some indication that impairment may vary dependingon primary substance of abuse. Across the meta-analytic data, alcohol use wasassociated with poorer working memory performance, whereas cannabis use wasassociated with better problem solving and visual memory performance (Potvin et al.,2008). This ﬁnding is consistent with neuropsychological data from SUD samples
without psychiatric diagnoses, where alcohol is associated with greater impairmentsthan other drugs such as cocaine (Goldstein et al., 2004). However, types of substancesare not always accounted for in dual disorder studies (e.g., Carey et al., 2003). Second,consistent with methodological limitations across the dual diagnosis research litera-ture, the rigor with which samples have been characterized has been quite variable.Some studies have relied on chart diagnoses as opposed to diagnostic interview toidentify SUD, few have veri ﬁed drug status with urinalysis, and others have failed
to characterize the severity, recency, or chronicity of substance use. With regard tothe latter, analyses included in the Potvin et al. (2008) study indicated that as ageincreased, so did the cognitive impairment among those with SUD, suggesting thatchronicity of use may be a moderating factor in cognitive functioning among dualdisorders. Similarly, Carpenter and Hittner (1997) found that lifetime use of alcohol orcocaine (i.e., number of years of regular use) were the strongest predictors of cognitiveimpairment among a sample of individuals with mixed psychiatric diagnoses (affec-tive and anxiety disorders) and SUDs.
These latter ﬁndings raise the related question of how cognitive impairment
changes over time as a result of substance use in individuals with dual disorders.Few investigations have addressed this question. Using a group comparison designwith carefully characterized samples, Carey et al. (2003) found no difference inThe Problem of Dual Diagnosis 57

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cognitive functioning between individuals with SMI and current SUD versus thosewith past history of SUD (de ﬁned as not meeting full criteria for the past 6 months).
Peer, Bennett, and Bellack (2009) compared individuals with schizophrenia who metDSM-IV criteria for current cocaine dependence and those who met criteria for
remission on a brief neuropsychological battery and found few differences. Thisstudy also included a parallel analysis of samples of individuals with affectivedisorders and cocaine dependence versus remission, which yielded similar results.Although these studies used rigorous diagnostic criteria to characterize the samples,they are limited by their cross-sectional nature. That is, they did not evaluate changewithin subjects in cognitive functioning as a result of discontinuation of substance use.
At least two longitudinal studies have been conducted that address this question. A
brief longitudinal study of inpatients with schizophrenia with or without currentcocaine dependence at admission found few changes in cognition as a result ofabstinence from cocaine over an 18-day study period (Cooper et al., 1999). Further-more, there were few differences in cognition between groups at baseline or at follow-up. McCleery, Addington, and Addington (2006) followed 183 individuals with a ﬁrst
episode of psychosis over a 2-year study period and assessed cognition and substanceuse. Results indicated that cognition largely remained stable over time, while sub-stance use declined over the study period. Together these ﬁndings suggest that
cognitive functioning may be relatively static among individuals with dual disorders.Indeed, in the general SUD literature, longitudinal data suggest there are only slightand/or inconsistent improvements in neurocognitive functioning after a period ofabstinence from substances (Bates, Voelbel, Buckman, Labouvie, & Barry, 2005; DiSclafani, Tolou-Shams, Price, & Fein, 2002; Horner, 1999).
There are at least two possible interpretations of these data: (1) given the signi ﬁcant
cognitive impairment associated with SMI, substance use causes only minimaladditional impairment; and (2) the toxic effects of substance use on cognition arenot easily resolved following abstinence. In part, this research may be limited by thelack of sensitivity of the neuropsychological measures used for these particularresearch questions. With further advances in cognitive neuroscience, more re ﬁned
measures that are more tightly linked to brain structures and functions impacted bychronic substance use will likely be developed (Rogers & Robbins, 2001). Althoughcandidate brain structures and neurotransmitter pathways are increasingly beingidenti ﬁed in the general SUD literature (e.g., Goldstein et al., 2004; Goldstein &
Volkow, 2002), signi ﬁcantly more work is needed to understand the speci ﬁcs of
cognitive functioning in dual disorders, both with regard to preexisting impairment aswell as a sequelae of chronic substance use.Treatment Noncompliance and Violence Substance abuse often interferes with compli-
ance with both behavioral and psychopharmacological treatments. Lambert, Grif ﬁth,
and Hendrickse (1996) surveyed patients on a general psychiatry unit in a VeteransAdministration medical center and found that discharges against medical advice(AMA) were more likely to occur among patients with alcohol and/or substance usedisorders. Pages and colleagues (1998) similarly assessed predictors of AMA dis-charge in psychiatric patients. The presence of SUD and a greater quantity andfrequency of substance use were among the most important predictors. Owen andcolleagues (Owen, Fischer, Booth, & Cuffel, 1996) followed a sample of 135 inpatients58 OVERVIEW

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after discharge and found that medication noncompliance was related to substanceabuse, and that this combination was signi ﬁcantly associated with lack of outpatient
contact in the follow-up period. Speci ﬁcally, those with dual diagnoses were more
than 8 times more likely to be noncompliant with their medication. In a large-scalestudy of factors related to medication adherence in schizophrenia patients, Gilmer andcolleagues (2004) found that substance abusers were less likely to be adherent toantipsychotic medication regimens than were schizophrenia patients who did notabuse substances.
Similar results were found in a review of factors that impede use of medication in
individuals with bipolar disorder (Velligan et al., 2009): Many studies have found thatsubstance use is a critical barrier to medication adherence. Such ﬁndings are especially
important when linked to functioning and service use. For example, schizophreniapatients who were nonadherent with their medications were more than 2.5 times morelikely to be hospitalized than those who were adherent (Gilmer et al., 2004). Verduin,Carter, Brady, Myrick, and Timmerman (2005) compared bipolar only, alcohol-dependent only, and comorbid bipolar and alcohol-dependent patients on severaltreatment variables, including number of outpatient psychiatric visits and length ofpsychiatric hospitalizations, in the year leading up to and including an indexhospitalization at a veterans ’hospital from 1999 through 2003. The comorbid group
had fewer outpatient psychiatric visits and shorter inpatient hospitalizations than dideither of the single disorder groups.
For many disorders, substance abuse and its associated noncompliance with
treatment is linked not only to poorer outcomes but also to greater risk for violence(Marzuk, 1996; Poldrugo, 1998; Sandberg, McNiel, & Binder, 1998; Scott et al., 1998;Soyka, 2000; Steadman et al., 1998; Swanson, Borum, Swartz, & Hiday, 1999; Swartzet al., 1998) and suicide (Cohen, Test, & Brown, 1990; Goodwin & Jamison, 1990;Karmali et al., 2000; Landmark, Cernovsky, & Merskey, 1987; Pages, Russo, Roy-Byrne, Ries, & Cowley, 1997; Verduin et al., 2005). In terms of violence, Fulwiler,Grossman, Forbes, and Ruthazer (1997) compared differences between two groups ofoutpatients with chronic mental illness: those with and without a history of violence.The only signi ﬁcant differences between the two groups involved alcohol or drug use.
McFall and colleagues (McFall, Fontana, Rasking, & Rosenheck, 1999) examined 228male Vietnam veterans seeking inpatient treatment for PTSD and found that levels ofsubstance abuse were positively correlated with violence and aggression. The combi-nation of schizophrenia and ASP appears to put people at high risk for violence,especially when they are drinking (Joyal, Putkonen, Paavola, & Tiihonen, 2004).
In their recent examination of population-based registers of hospital discharge
diagnoses and violent crime in a Swedish sample over 30 years, Fazel, Lichtenstein,Grann, Goodwin, and Langstrom (2010) found that risk for violent crime amongindividuals with bipolar disorders was almost entirely due to substance abusecomorbidity, with those with bipolar-only diagnoses showing extremely low riskfor violent crime. Such ﬁndings illustrate the problematic impact of substance use on
violence in individuals with psychiatric disorders.
Research also shows links between dual disorders and rate of suicide. In an analysis
of epidemiological data from the NESARC, Oquendo and colleagues found thatlifetime rates of suicide attempts were higher for those with dual bipolar disorderand alcohol use disorders (25.29%) than for respondents with bipolar disorder aloneThe Problem of Dual Diagnosis 59

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(14.78%) (Oquendo et al., 2010). Pages and colleagues (1997) surveyed 891 psychiatricinpatients with major depressive disorder and found that both substance use andsubstance dependence were associated with higher levels of suicidal ideation. Potashand colleagues (2000) examined the relationship between alcohol use disorders andsuicidality in bipolar patients and found that 38% of subjects with dual bipolar andalcohol use disorders had attempted suicide, as compared to 22% of those with bipolardisorder only. Recently, McCloud, Barnaby, Omu, Drummond, and Aboud (2004)examined alcohol disorders and suicidality (de ﬁned as any record of self-harm or
thoughts or plans of self-harm or suicide written in the medical record) in consecutiveadmissions to a psychiatric hospital. Problem drinking (as measured by the AlcoholUse Disorders Identi ﬁcation Test [AUDIT]) was strongly related to suicidality, with
higher AUDIT scores (representing greater severity of problems with alcohol) show-ing higher rates of suicidality.
Importantly, those with m ultiple comorbidities— patients who have more than
two comorbid diagnoses— are at even higher risk for suicide. In such cases, the added
impact on suicidality of trauma in general or comorbid PTSD in particular is great.Tarrier and Picken (2010) examined rates o f suicide in individuals with dual schizo-
phrenia and substance use disorders and found that rates of suicidality (based onscores on the Beck Suicidality Scale) wer e higher among those with comorbid PTSD.
Cacciola and colleagues (Cacciola, Koppen haver, Alterman, & McKay, 2009) identi-
ﬁed four groups among a sample of 466 male v eterans: (1) substance use disorder
only; (2) substance use disorder +PTSD; (3) substance use disorder +PTSD +another
Axis I disorder; and (4) substance use disorder +another Axis I disorder. Lifetime
rates of both suicidal ideation and suicide attempts were highest in the substance usedisorder +PTSD +another Axis I disorder group. Such ﬁndings illustrate the ways
that multiple comorbidities can further increase risk for suicidality.I
MPACT OF DUALDIAGNOSIS ON CLINICAL CARE AND RELATED FACTORS
Dual diagnosis impacts clinical care on many levels. This section reviews the manyways that dual diagnosis impacts service use and health-care costs, as well as relatedfactors such as medical illness, legal problems, and homelessness.Service Utilization and Health Care Costs The fact that clinical settings routinely
demonstrate higher rates of dual diagnosis patients points to the fact that havingboth psychiatric and SUDs increases rates of seeking treatment. Increased serviceutilization among the dually diagnosed has been borne out in both large-scalehousehold surveys and clinical studies. For example, Helzer and Pryzbeck (1988)examined data from the ECA study and found that, for respondents of both sexes withalcohol use disorders, the number of additional non-substance-use-disorder diagnoseshad a signi ﬁcant impact on seeking treatment: Those with more diagnoses reported
greater utilization of treatment services. Grant (1997) examined the inﬂ uence of
comorbid major depression and substance abuse on rates of seeking alcohol anddrug treatment in data collected from the National Longitudinal Alcohol Epidemio-logical Survey (NLAES; Grant et al., 1994). The percentage of individuals with alcoholuse disorders seeking treatment practically doubled, from 7.8% to 16.9%, when acomorbid major depressive disorder was also present. Interestingly, the greatest rate60 OVERVIEW

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of seeking treatment (35.3%) was found among respondents who met criteria for allthree disorders —alcohol, drug, and depression —illustrating how the term dual
diagnosis is somewhat misleading, because some individuals have two or more
substance use and psychiatric disorders, and each might have an additive effect onnegative outcomes.
Similarly, Wu, Kouzis, and Leaf (1999), analyzing data from the NCS, found that
although 14.5% of patients with a pure alcohol disorder reported using mental healthand substance abuse intervention services, more than 32% of patients with comorbidalcohol and mental disorders used such services. Menezes and colleagues (1996)studied the impact of substance use problems on service utilization over 1 year ina sample of 171 individuals with serious mental illness. Although the number ofinpatient admissions was equivalent for those with dual disorders and those withmental illness only, the dual diagnosis group used psychiatric emergency services1.3 times more frequently and spent 1.8 times as many days in the hospital as didthe single disorder group.
Given their increased rates of service utilization, it is not surprising that dual
diagnosis patients generally accrue greater health care costs than do patients with asingle diagnosis (Maynard & Cox, 1998; McCrone et al., 2000). Dickey and Azeni(1996) examined the costs of psychiatric treatment for more than 16,000 seriouslymentally ill individuals with and without comorbid SUDs. Patients with dual diag-noses had psychiatric treatment costs that were nearly 60% higher than the costs ofpsychiatrically impaired individuals without substance abuse. Interestingly, most ofthe increased cost was owing to greater rates of inpatient psychiatric treatment,suggesting that the impact of substance abuse on psychiatric symptoms and illnessrelapse is realized when patients require costly psychiatric hospitalization. Garnick,Hendricks, Comstock, and Horgan (1997) examined health insurance data ﬁles over 3
years from almost 40,000 employees and found that those with dual diagnosesroutinely accrued substantially higher health care costs than those with substanceabuse only. Such ﬁndings suggest that individuals with dual disorders access the most
expensive treatment options (inpatient hospitalization, visits to emergency rooms)that are short-term in order to manage acute distress and fail to get the comprehensiveand ongoing care they require.
These ﬁndings on rates of services use can be perplexing. For example, if dual
diagnosis patients are accessing more and more expensive services, why do theyconsistently have more severe psychiatri c symptoms, more substance-related prob-
lems, and poorer outcomes than do those w ith single disorders? As noted earlier,
dual diagnosis patients appear to access expensive but short-term or acute treatmentoptions more often while being noncompliant or not adhering to longer-termmedication and outpatient treatment regimens. Other factors include lack of inte-grated care, as well as problems associated with treating more than one disorder( W a t k i n s ,B u r n a m ,K u n g ,&P a d d o c k ,2 0 0 1 ) .I na d d i t i o n ,r e s e a r c h e r sr e c e n t l yh a v ebegun to more closely examine the qualit y of services accessed by dual diagnosis
patients. For example, in their study of patients with bipolar disorder with andwithout comorbid substance use disorders, Verduin and colleagues (2005) foundthat patients with bipolar disorder and comorbid substance abuse were less likelythan patients with substance abuse alone to be referred to intensive substanceabuse treatment.The Problem of Dual Diagnosis 61

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Watkins and colleagues (2001) looked at the delivery of appropriate care to
probable dual-diagnosis patients assessed as part of the Healthcare for CommunitiesSurvey (a study of a subset of respondents from the Community Tracking Study, anationally representative study of the civilian, noninstitutionalized people in theUnited States [see Kemper et al., 1996, for details]). Appropriate care includedmedications for severe mental illness (a mood stabilizer for bipolar disorder, anti-psychotic medication for a psychiatric disorder), medications and/or psychosocialinterventions for anxiety disorders or major depression, and at least four sessions ofany sort of treatment in the past year. In addition, variables addressed includedwhether patients are receiving integrated care for dual disorders (receiving bothmental health and substance abuse treatment from one provider) or comprehensivesubstance abuse treatment (deﬁ ned as including inpatient or outpatient substance use
treatment that included a physical examination, a mental health evaluation, or job orrelationship counseling). Results showed that 72% of dual-diagnosis patients did notreceive any specialty mental health or substance abuse services (i.e., services providedby a mental health or substance abuse professional rather than a primary carephysician), 8% received both mental health and substance abuse treatment (eitherintegrated or by different providers), 23% received appropriate mental health care,and 9% received comprehensive substance abuse treatment.
Other studies have found a disconnect between services accessed and services
needed in dual diagnosis samples (Najavits, Sullivan, Schmitz, Weiss, & Lee, 2004).Such ﬁndings suggest that the complicated clinical picture presented by dual diagno-
sis patients makes it dif ﬁcult for patients and providers to determine and administer
appropriate care.Physical Illness Dual diagnosis puts people at risk for different forms of illness and
disease. This is especially true in the case of dual mental health disorders and tobaccodependence. The negative health effects of smoking are well known, and those withmental health disorders who smoke similarly share these risks. However, somepopulations fare even worse when it comes to the negative effects of smoking. Forexample, people with serious mental illness (SMI) represent a special population thatis even more markedly affected by the negative effects of smoking than other groups ofsmokers. People with SMI are known to suffer from a range of life threatening medicalconditions at rates that are signi ﬁcantly higher than those in the general population
(Jeste, Gladsjo, Lindamer, & Lacro, 1996; Muir-Cochrane, 2006) and are also morelikely to have multiple chronic illnesses (Carney & Jones, 2006; Carney, Jones, &Woolson, 2006; Dickerson et al., 2006). This high rate of medical comorbidity results inworsened psychosis and psychiatric symptoms, lowered quality of life, and higherrates of mortality in people with SMI (Auquier, Lancon, Rouillon, Lader, & Holmes,2006; Dixon, Postrado, Delahanty, Fischer, & Lehman, 1999; Dixon et al., 2007).
Smoking and tobacco dependence signi ﬁcantly impacts, complicates, or is known
to be a primary cause of, the medical diseases that lead to signiﬁ cantly elevated rates of
mortality for people with SMI (Compton, Daumit, & Druss, 2006). In addition to thedevastating health effects, smoking and tobacco dependence confer other negativeconsequences for those with SMI. Smoking increases the metabolism of some anti-psychotic medications, producing reduced antipsychotic blood levels and requiringsubstantial increases in medication dosages in some cases (Goff, Henderson, & Amico,62 OVERVIEW

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1992; Ziedonis, Kosten, Glazer, & Frances, 1994). SMI smokers have been found toshow a poorer course of illness, with earlier onset and more psychiatric hospitaliza-tions (Goff et al., 1992; Sandyk & Kay, 1991; Ziedonis et al., 1994). Finally, otherimportant consequences of smoking for people with SMI include the high ﬁnancial
cost of smoking in people with limited income (Steinberg, Williams, & Ziedonis, 2004),as well as additional negative social perceptions in a population that is already subjectto signi ﬁcant social stigma.
One of the most signi ﬁcant health problems among those with dual diagnosis is
greatly increased risk for HIV and AIDS. People with schizophrenia and other severemental illness are now one of the highest-risk groups for HIV (Gottesman & Groome,1997; Krakow, Galanter, Dermatis, & Westreich, 1998), and data indicate that sub-stance use substantially increases the likelihood of unsafe sex practices (Carey,Carey, & Kalichman, 1997) and other high-risk behaviors in those with mental illness.For example, McKinnon and colleagues (McKinnon, Cournos, Sugden, Guido, &Herman, 1996) found that 17.5% of a sample of psychiatric patients had a history ofinjection drug use, 35% reported using drugs during sex, and 30% traded sex fordrugs —all substance use behaviors that are highly risky in terms of the transmission
of HIV and AIDS. In their sample of 145 psychiatric inpatients and outpatients inAustralia, Thompson and colleagues (1997) found that 15.9% of dual diagnosispatients reported injection drug use, a ﬁgure that is 10 times higher than that found
in the general population. Hoff, Beam-Goulet, and Rosenheck (1997) examined datafrom the 1992 National Survey of Veterans and found that the combination of PTSDand substance abuse increased the risk of HIV infection by almost 12 times overindividuals with either disorder alone.
There is increasing evidence that other physical illnesses and high-risk health habits
are also found more often in people with dual disorders. Stuyt (2004) found that 29.7%of a dual diagnosis sample had hepatitis C, a rate that is 16 times higher than thatfound in the general population. Salloum, Douaihy, Ndimbie, and Kirisci (2004)examined physical health and disorders in three groups of psychiatric patientshospitalized on a dual diagnosis treatment unit: a group with both alcohol andcocaine dependence, a group with alcohol dependence only, and a group with cocainedependence only. Results showed that the group with both alcohol and cocainedependence showed higher rates of a range of medical problems, including multiplehepatitis infections, than both single diagnosis groups.
Jones and colleagues (2004) examined ph ysical health problems among people
with severe mental illness and found that 74% of the sample was treated for onechronic health condition, and 50% was treated for two or more. The two most highlyprevalent chronic health conditions —pulmonary disease and infectious disease —
were both associated with substance use di s o r d e r si nt h i ss a m p l e .M o r e o v e r ,r e s u l t s
of regression analysis showed that substance abuse, along with age and obesity, wasas i g n i ﬁcant predictor of health problem severity. Ouimette, Goodwin, and Brown
(2007) identi ﬁed medical problems in SUD patients with and without PTSD. Those
with dual SUD +PTSD had more cardiovascular, ne urological, and total physical
symptoms than those with SUDs alone. Others have found high rates of mortalityand other dangerous health conditions a mong those with dual diagnosis (Batki
et al., 2009; Dickey, Dembling, Azeni, & Normand, 2004; Lambert, LePage, &Schmitt, 2003). Importantly, these higher rates of physical health problems canThe Problem of Dual Diagnosis 63

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serve as additional barriers to achieving important recovery goals (Conover, Arno,Weaver, Ang, & Ettner, 2006).Legal Problems There is also evidence that individuals with dual diagnoses have more
frequent contacts with the legal system. Clark, Ricketts, and McHugo (1999) followeda sample of individuals with mental illness and substance use disorders over 3 years tolongitudinally examine legal involvement and its correlates in this population. Thesample consisted of 203 patients receiving treatment in a dual diagnosis treatmentprogram. Cost and use data were collected from a range of sources, including police,defenders, prosecutors, and jails. Interestingly, while rates of arrest were certainlyhigh, patients were 4 times more likely to have encounters with the legal system thatdid not result in arrest. This suggests that frequency of arrest, although signi ﬁcant, is
an underrepresentation of the frequency of contact that dual diagnosis patients havewith the legal system. In addition, continued substance abuse over the follow-upperiod was signi ﬁcantly associated with a greater likelihood of arrest. Among samples
of incarcerated prisoners, rates of severe mental illnesses and co-occurring psychiatricdisorders are far higher than in the general U.S. population (Wolff et al., 2011).Homelessness The combination of mental illness and substance abuse also increases
risk for homelessness. In a study of patien ts with schizophrenia, Dixon (1999) found
that those who used substances experienced not only greater psychotic symptomsand relapses, a higher incidence of violent behavior and suicide, elevated rates of HIVinfection, increased mortality, and high er rates of treatment and medication non-
compliance, but they were also more likely to live in an unstable housing situationor be homeless. Caton and colleagues (1994) compared a sample of mentally illhomeless men to a sample of mentally ill men who were not homeless and foundhigher rates of drug use disorders among the homeless group. Leal, Galanter,
Dermatis, and Westreich (1999) assessed h omelessness in a sample of 147 patients
with dual diagnosis and found that those int h eg r o u pw i t hs o – c a l l e dp r o t r a c t e dhomelessness (no residence for 1 year or more) were signi ﬁcantly more likely
than those patients without protracted homelessness to report a history of injectiondrug use. Recently, Folsom et al. (2005) examined risk factors for homelessness andpatterns of service use among those who are homeless in a large sample ( n=10,340)
of patients with severe mental illness from a large public mental health system insouthern California. Homele ssness was associated with a range of variables, includ-
ing substance abuse —60.5% of the homeless mentally ill group showed a substance
use disorder as compared to 20.9% of the non -homeless mentally ill group. Moreover,
results of multivariate logistic regression showed that those with mental illness andsubstance abuse were more than 4 times as likely to be homeless as were patientswho did not abuse substances.Issues for Women With Serious Mental Illness and Substance Abuse Importantly, dual
diagnosis is often particularly problematic for individuals who are also otherwiseunderserved. As noted, individuals with schizophrenia appear to be particularly hardhit by the additional dif ﬁculties of SUD. Another such population is women with
severe mental illness and substance abuse. Research on women with dual diagnoseshas shown that those with comorbid severe mental illness and substance abuse show64 OVERVIEW

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poorer retention in treatment (Brown, Melchior, & Huba, 1999) and elevated levels ofanxiety, depression, and medical illness (Brunette & Drake, 1998), as well as beingmore difﬁ cult to engage in treatment and more under-represented in treatment overall
(Comtois & Ries, 1995). In addition, women with dual diagnoses appear to havealarming rates of sexual and physical victimization that are substantially higher thanthose observed among women in the general population (Gearon & Bellack, 1999;Goodman, Rosenburg, Mueser, & Drake, 1997). Prevalence rates for physical victim-ization for women with serious mental illness range between 42% and 64% (Jacobson,1989), and other research ﬁnds that 21% to 38% of women with serious mental
illness report adult sexual abuse (Goodman, Dutton, & Harris, 1995). Among womenreceiving treatment in a residential therapeutic community, 49% reported physicalabuse and 40% reported sexual abuse (Palacios, Urmann, Newel, & Hamilton, 1999).Data from 28 women and 24 men with serious mental illness and SUDs indicated that,when compared with men, women were more likely to report being physically (60%of women vs. 29% of men) and sexually (47% of women vs. 17% of men) victimized(Gearon, Bellack, Nidecker, & Bennett, 2003).
In addition, issues related to pregnancy and parenting often affect women with
dual diagnosis. Grella (1997) summarized some of the many dif ﬁculties in terms of
providing services for pregnant women with dual disorders, including receivingadequate prenatal care, use of substances and psychiatric medications while pregnant,and lack of coordinated treatment planning and provision among medical, psychiat-ric, and addictions professionals. Kelly and colleagues (1999) examined the medicalrecords of all women delivering babies in California hospitals in 1994 and 1995 andfound that women with both psychiatric and substance use diagnoses were at greatlyelevated risk of receiving inadequate prenatal care. There are also substantial barriersto treatment and medical care for these women, including fears of losing custody of theunborn child or their other children, lack of medical insurance, and the often disjointednature of available services for the medical and psychiatric care of these patients(Grella, 1997). Finally, when compared to men, women with dual diagnosis may havedifferent treatment needs. Grella (2003) compared differences in substance use andtreatment histories and perceptions of service needs between men and womendiagnosed with severe mental illness (mood or psychotic disorders) on admissionto inpatient drug treatment. Women reported greater needs for family and trauma-related services, and women with psychotic disorders had the greatest level of need ofall the groups for basic services.P
ROVISION OF TREATMENT AND TREATMENT OUTCOME
Co-occurring SUDs raise problems for interventions that have been designed toimpact speci ﬁc psychiatric symptoms, or ones that have been validated on samples
that have excluded dual diagnosis patients. In addition, clinicians often experiencedifﬁculties in making referrals for dual diagnosis patients in the current system of
single disorder treatment that effectively separates the treatment systems for mentalillness and substance abuse. The fact that patients must often be forced into singlediagnostic categories no doubt results in SUDs being overlooked or ignored bytreatment professionals who have expertise in treating only single conditions or indual diagnosis patients not receiving both the psychiatric and the substance abuseThe Problem of Dual Diagnosis 65

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treatment they require (Blanchard, 2000). Patients with dual diagnosis are moredifﬁcult to treat and show poorer retention in treatment as well as poorer treatment
outcomes as compared to single disorder patients. Such ﬁndings tend to be true
both for patients with primary mental illness and co-occurring substance abuse (seeDrake, Mercer-McFadden, Mueser, McHugo, & Bond, 1998, and Polcin, 1992 forreviews; Goldberg, Garno, Leon, Kocsis, & Portera, 1999), as well as for patientsidenti ﬁed through substance abuse treatment programs with comorbid mental illness
(Glenn & Parsons, 1991; Ouimette, Ahrens, Moos, & Finney, 1998; Rounsaville,Kosten, Weissman, & Kleber, 1986). An early study by McLellan, Luborsky, Woody,O’Brien, and Cruley (1983) found that higher psychiatric severity was associated
with poorer treatment outcome among alcohol and drug abuse treatment patients.Tomasson and Vaglum (1997) examined the impact of psychiatric comorbidity on 351treatment-seeking substance abusers over a 28-month period and found that patientswith comorbid psychiatric disorders at admission showed worse outcome in terms ofmental health functioning at follow-up.
Ouimette, Gima, Moos, and Finney (1999) reported ﬁndings of a 1-year follow-up of
three groups of patients with dual substance use and psychiatric disorders (psychoticdisorders, affective/anxiety disorders, and personality disorders) as compared to agroup of substance abuse –only patients. Although all the groups showed comparable
decreases in substance use at follow-up, patients with dual diagnoses showed greaterlevels of psychological distress and psychiatric symptoms and lower rates of employ-ment than did patients with only SUDs. In a 3-year follow-up of a sample of patientswith alcohol use disorders, Kranzler, Del Boca, and Rounsaville (1996) found that thepresence of comorbid psychiatric disorders, including depression and ASP, is gener-ally associated with worse 3-year outcomes.
Thomas, Melchert, and Banken (1999) exa mined treatment outcome in 252 patients
in substance abuse treatment and found the likelihood of relapse within the yearfollowing treatment was signi ﬁcantly increased in patients with dual personality
disorders. Speciﬁ cally, 6% of patients with personality disorders were abstinent
1-year posttreatment, as compared with 44 % of those with no diagnosed personality
disorders. A study by Havassy, Shopshire, a nd Quigley (2000) examined the effects of
substance dependence on treatment outcome in 268 psychiatric p atients following
two different case management programs. Regardless of program, dual diagnosispatients showed more negative outcomes than patients with only a psychiatricdisorder.
Such results illustrate that the dually diagnosed fare worse than patients with either
SUDs or psychiatric disorders alone following treatment. Importantly, the fact thatdual-diagnosis patients are often found to still be adversely affected by psychiatricsymptomatology following substance abuse treatment is a stark reminder thattreatment strategies have yet to evolve that effectively address symptoms of bothtypes of disorders.
IMPACT OF DUAL DISORDERS ON ASSESSMENT AND DIAGNOSIS
There are numerous ways that dual diagnosis affects assessment and diagnosis,including symptom overlap, multiple impairments owing to different disorders,and substance-induced disorders resembling psychiatric disorders.66 OVERVIEW

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SYMPTOM OVERLAP
Symptom overlap is a signi ﬁcant complication in terms of assessment and diagnosis.
The symptoms of many psychiatric disorders overlap with those of substance usedisorders, making diagnosis of either class of disorders dif ﬁcult. For example, DSM
lists problems in social functioning as symptoms of both schizophrenia and SUDs.That some criteria can count toward multiple diagnoses can potentially increasecomorbidity rates and can make diagnosis of substance abuse difﬁ cult. This overlap
can work against identi ﬁcation of the psychiatric disorder in some cases. For example,
high rates of dual substance use and bipolar disorders lead to an underdiagnosis ofbipolar disorder, because of the often incorrect assumption that the behavioralmanifestations of bipolar disorder are secondary to substance use (Evans, 2000).Others (Brady, Killeen, Brewerton, & Lucerini, 2000; Brunello et al., 2001) suggest thatunderdiagnosis can also be an issue with dual PTSD and substance use disorders.M
ULTIPLE IMPAIRMENTS OWING TO DIFFERENT DISORDERS
Substance use disorders are often overlooked in mental health settings in whichpatients present with a range of acute impairments that exert a negative impact onoverall functioning. There is often diagnostic confusion in terms of whether a givenimpairment results from substance abuse, psychiatric disorder, both, or neither. Forexample, it is exceedingly dif ﬁcult to determine the impact of substance abuse when
serious mental illness profoundly affects all areas of functioning. Patients with severemental illness in particular have a range of impairments in social, cognitive, occupa-tional, and psychological functioning, and evaluating the negative impact of substanceabuse is dif ﬁcult when the functioning of individuals in this patient population is so
poor to begin with. Moreover, DSM-IV diagnoses of substance abuse and dependence
are based for the most part on diagnostic criteria that re ﬂect substance use becoming
more pervasive in a person ’s life and interfering with normal functioning. For
example, criteria involve substance use impairing one ’s ability to work, engage in
relationships, complete responsibilities, and participate in activities. However, suchfactors often do not apply to many patients with mental illness whose substantial levelof impairment associated with the psychiatric disorder often precludes them fromhaving a job, being in relationships, or engaging in other activities. It becomes unclearhow to measure the negative impact of substance use when there are few competingdemands, activities, or responsibilities to be disrupted.S
UBSTANCE -INDUCED DISORDERS RESEMBLE PSYCHIATRIC DISORDERS
Diagnosis of psychopathology in the presence of substance abuse and dependence isespecially dif ﬁcult because symptoms of substance use and withdrawal can resemble
psychiatric disorders (Schuckit, 1983; Schuckit & Monteiro, 1988). Schuckit andMonteiro (1988) review several instances in which symptoms of substance abuseresemble or mimic psychiatric symptoms. For example, long-term alcohol use andwithdrawal can lead to psychotic symptoms, and abuse of amphetamines often resultsin psychotic symptoms that are identical to schizophrenia. Alcohol abuse andwithdrawal also resemble symptoms of anxiety disorders (Kushner, Sher, & Beitman,The Problem of Dual Diagnosis 67

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1990). Panic and obsessive behavior are often found with stimulant use and with-drawal from depressant drugs (Schuckit, 1983). Because symptoms of substance useand withdrawal can resemble psychiatric symptoms, differential diagnosis may beconfounded. The lack of clear rules for differential diagnosis has important implica-tions. Rates of dual diagnosis might be in ﬂated, with individuals experiencing
psychiatric disorders concurrent with alcohol or drug dependence being countedamong those with dual disorder, although many of these symptoms will likely fadefollowing a period of abstinence.
Incorrect treatment decisions may be made if interventions are aimed at what
appear to be acute symptoms of psychiatric disorder but are, in fact, substance-induced symptoms. For example, Rosenthal and Miner (1997) review the issue ofdifferential diagnosis of substance-induced psychosis and schizophrenia and stressthat medicating what appears to be acute psychosis due to schizophrenia but isactually substance-induced psychosis is not only incorrect but also ineffective treat-ment. Schuckit and colleagues (1997) suggest that too little attention has been paid tothe“independent versus concurrent distinction ”as it applies to dual diagnosis. Some
alcoholics suffer from long-term psychiatric disorders that are present before, during,and after alcohol dependence and require treatment independent of that for theiralcohol abuse or dependence.
On the other hand, many individuals present with substance-induced disorders,
including depression, anxiety, and psychosis, that will remit after several weeks ofabstinence. They suggest that much dual diagnosis, while distressing and clinicallyrelevant in the short-term, is temporary, likely to improve after several weeks, andthus holds different clinical and treatment implications from a true, independentpsychiatric disorder. Their data, taken from the Collaborative Study on the Genetics ofAlcoholism, shows that the majority of alcohol-dependent men and women did notmeet diagnostic criteria for an “independent ”mood or anxiety disorder that occurred
outside of the context of the alcohol dependence. Speci ﬁcally, there was no increased
risk of a range of disorders in the alcohol-dependent sample, including majordepression, obsessive-compulsive disorder, or agoraphobia. In contrast, there wasan increased risk of independent bipolar, panic disorder, and social phobia.
Others have also found that a majority of dual diagnosis patients have concurrent
psychiatric diagnoses that are likely owing to the effects of heavy substance use.Rosenblum and colleagues (1999) used an algorithm to determine whether individualswith co-occurring mood and cocaine use disorders have either an “autonomous ”
mood disorder— that is, one that either existed prior to the cocaine use disorder or
persists during times of abstinence (similar to Schuckit’ s independent distinction) —or
a“nonautonomous ”mood disorder that followed from the cocaine use disorder and
would remit during cocaine abstinence. Results showed that 27% of subjects wererated as having an autonomous mood disorder, whereas 73% were rated as having anonautonomous mood disorder.
At this point, differentiating independent from concurrent dual disorders requires
signiﬁcant investment in training interviewers and in interviewing patients. Such
requirements often cannot be met in the day-to-day operations of mental healthtreatment programs. Moreover, multiple assessments may be necessary. For example,Ramsey and colleagues (Ramsey, Kahler, Read, Stuart, & Brown, 2004) examinedchanges in classifying depressive episodes in alcohol-dependent patients as either68 OVERVIEW

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substance-induced depression or independent major depressive disorder. Patients in apartial hospital program for alcohol treatment were assessed ﬁve times over a year for
symptoms of MDD. Results showed that many (more than 25%) of the cases ﬁrst
categorized as substance-induced MDD were reclassi ﬁed as independent MDD at
some point during the year, owing to depressive symptoms that persisted once thepatients had achieved a long period of abstinence.I
MPLICATIONS FOR NOSOLOGY
The fact that two disorders co-occur with great regularity raises the question ofwhether both categories actually represent two distinct disorders at all (Sher & Trull,1996). For example, the literature regarding SUDS and ASP ﬁnds a high rate of
comorbidity between the two disorders, one that is likely enhanced by the symptomoverlap inherent in the ASP diagnosis. However, some suggest (Widiger & Shea, 1991)that such a high degree of co-occurrence between these two disorders may mean thatthese are not, in fact, unique diagnoses, but rather that such a pattern of comorbidityindicates the presence of a single disorder.
IMPACT OF DUAL DIAGNOSIS ON PSYCHOPATHOLOGY RESEARCH
Dual diagnosis affects several areas that are critical to psychopathology research,including diagnosis, sample selection, and interpretation of research ﬁndings.
D
IAGNOSTIC AND SAMPLE SELECTION ISSUES IN PSYCHOPATHOLOGY RESEARCH
An accurate diagnosis is a necessary starting point for any psychopathology study,and dual diagnosis presents an abundance of diagnostic challenges. Individuals withdual diagnoses may provide unreliable diagnostic information, or their data may beinaccurate because of greater severity of impairments. Alternatively, they may mini-mize their substance use and associated consequences, especially if they have much tolose by admitting to or honestly discussing their substance use, such as services,beneﬁts (Ridgely, Goldman, & Willenbring, 1990), or child custody. The timing of a
research diagnostic interview can also impact results, as answers and resultingdiagnostic decisions may vary depending on type of use, stage of treatment, andpsychiatric stabilization. The method of assessment also can impact diagnosticﬁndings (Regier et al., 1998), and diagnoses given in a clinical setting may vary
with those obtained through more structured methods (Fennig, Craig, Tanenberg-Karant, & Bromet, 1994). As presented previously, establishing an accurate diagnosisin individuals with active substance use or withdrawal can be problematic, as theeffects of substance use can imitate the symptoms of various psychiatric disorders.Most diagnostic systems used in psychopathology research contend with this dif ﬁ-
culty by asking if psychiatric symptoms have been experienced solely during thecourse of substance use, and may recommend assessment only after a sustained periodof abstinence. However, patient reports may be inaccurate, and histories may be tooextensive and complicated to allow for this level of precise understanding.
Finally, the issue of overlapping diagnostic criteria can pose a signi ﬁcant dif ﬁculty
for psychopathology research, as common diagnostic criteria may contribute to theThe Problem of Dual Diagnosis 69

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diagnosis of multiple disorders when in fact the psychopathology is better understoodas a single pathological process rather than two distinct disorders (Blash ﬁeld, 1990;
Sher & Trull, 1996). The overlap of SUDs with ASP is notably problematic, and thisfrequent comorbidity has long been recognized (Widiger & Shea, 1991). Krueger(1999) examined 10 common mental disorders using structural equation modeling andfound that ASP loads onto a common “externalizing ”factor along with alcohol and
drug dependence, suggesting that substance dependence and ASP may share certainunderlying features. Whether this overlap is indeed because of common conceptualcharacteristics or is an artifact of similar diagnostic criteria is unknown. All of thesediagnostic issues impact research ﬁndings, in that poor diagnoses will necessarily lead
to poor-quality data. Researchers can improve diagnostic reliability by conductingstructured interviews, using collateral information and behavioral observation toinform diagnostic decisions, and assessing the patient at multiple time points (Carey &Correia, 1998).
In terms of sample selection, psychopat hology and treatment outcome research
tends to focus on single or pure disorder s and routinely excludes dual diagnosis
cases, a practice that has several implications for research. First , screening out dual
diagnosis patients yields samples that are atypical. Most patients with one psychi-atric disorder meet criteria for some other d isorder. Eliminating patients with dual
disorders means that the resulting sample is less impaired and less representative of
patients who present for treatment, resulti ng in limited generalizability of research
ﬁndings (Krueger, 1999). In addition, du al diagnosis patients often have other
characteristics that are not adequately r epresented in the resultant study sample.
For example, Partonen, Sihvo, and Lönnqvist (1996) report descriptive data onpatients excluded from an antidepressant ef ﬁcacy that screened out individuals with
“chronic alcohol or drug misuse.” As a result, younger male patients were likely to
be excluded, with current substance a buse as the strongest excluding in ﬂuence.
Second, dual diagnosis impacts required sample sizes. In their examination of the
impact of comorbid disorders on sample selection, Newman and colleagues (1998)discuss ﬁndings related to effect sizes of examining only single disorder cases versus
the inclusion of dual disorder cases when analyzing group differences. Resultsshowed that when dual disorder cases are excluded, larger sample sizes are requiredin order to detect small effect sizes. In contrast, retaining dual disorder cases yieldedgreater variance on study measures, resulting in larger effect sizes requiring smallersample sizes.
Third, psychopathology and treatment outcome research most often combines
those with dual diagnoses together without classi ﬁcation by the speci ﬁc type of drug
use disorder. Whereas some might limit the scope of the study to alcohol only, mostcast a wide net and include patients with alcohol, drug, and polysubstance-usedisorders. For example, research on substance abuse among patients with severemental illness typically includes disorders of any number or combination of sub-stances, including alcohol, marijuana, cocaine, and heroin. The impact of grouping allsubstance use disorders together is unclear, but it certainly raises the possibility thatresearch may miss important issues potentially particular to one substance. Forexample, it would not be surprising if interventions for patients with a greater numberof drug use disorders or with both alcohol and drug use disorders required adapta-tions that are not necessary for patients with single-drug or alcohol-use disorders.70 OVERVIEW

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Similarly, there are likely meaningful differences between patients who inject drugsand those who do not, patients who have long histories of substance dependence andthose who do not, or patients who are dependent on cocaine or heroin versus thosewho are abusing marijuana.I
NTERPRETATION OF PSYCHOPATHOLOGY AND TREATMENT OUTCOME RESEARCH
The overall result of screening out those with substance use disorders from psycho-pathology and treatment outcome research is that there are very few data to informtreatment. For example, following completion of an antidepressant ef ﬁcacy trial,
Partonen and colleagues (1996) point out that they were left without informationregarding the efﬁ cacy of antidepressants among patients with dual disorders. Given
the signi ﬁcant rates of dual disorders found in clinical samples, such an omission is
clearly problematic. In their discussion of the many complex issues surroundingcomorbidity and psychopathology research, Sher and Trull (1996) question theadvantage of studying pure cases when certain disorders occur together with suchgreat frequency that there really may be no ultimate bene ﬁt of studying either one
alone. It also is unclear how well ﬁndings from psychopathology and treatment
outcome research will generalize to the larger population of individuals with aparticular disorder if patients with dual diagnoses are not included. The epidemio-logical studies reviewed earlier clearly illustrate that a signi ﬁcant number of those
with mental illness or substance abuse experience dual disorders. The relevance ofsingle disorder research to this substantial population of dually impaired individualsis highly suspect, and excluding dual-diagnosis cases yields samples that are notrepresentative of those presenting for treatment.
However, routinely including dual-diagnosis cases in psychopathology and treat-
ment outcome research has its drawbacks. Sher and Trull (1996) and Krueger (1999)discuss the fact that if dual diagnosis cases are included in psychopathology research,understanding of both mental and substance use disorders is compromised, in thatsamples would be less well-de ﬁned. As a result, it would be unclear whether results
could be attributed to the disorder under study or to comorbid disorders representedin the sample. In addition, comorbidity complicates longitudinal data because differ-ent patterns of comorbidity may emerge over time within individuals (Sher & Trull,1996). One possible strategy for dealing with dual disorders in psychopathology andtreatment outcome research is the use of samples that include comorbid cases inpercentages found in the general population in order to increase the generalizability ofﬁndings (Newman et al., 1998; Sher & Trull, 1996). Widiger and Shea (1991) offer
additional options, including having one diagnosis take precedence over another,adding criteria in order to make a differential diagnosis, or removing criteria shared bydisorders. Sher and Trull (1996) additionally suggest statistically controlling forcomorbidity via regression techniques but acknowledge that this practice can maskimportant common features of disorders.
THEORIES OF DUAL DIAGNOSIS
This review makes two points clear: Dual diagnosis is highly prevalent, and it has apervasive impact on both clinical and research domains. There now is generalThe Problem of Dual Diagnosis 71

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agreement that the time has come to de ﬁne more precisely the mechanisms underlying
dual diagnosis, which is a complex task for several reasons. Most important, there is agreat degree of heterogeneity found in dual diagnosis populations. The numeroustypes of psychopathological disorders and substances of abuse ensure many dualdiagnosis combinations. In addition, although the term dualis meant to describe cases
with both mental illness and substance use problems, it can in actuality re ﬂect more
than two disorders (for example, an individual might meet criteria for an affectivedisorder, an anxiety disorder, and a substance use disorder). Thus, it is unlikely thatone explanation or causal model for dual diagnosis can explain the diversity of casesand experiences that are found.
Models to explain dual diagnoses tend to fall into one of four general categories (see
Mueser, Drake, & Wallach, 1998, for a review). Third variable or common factorsmodels suggest that some shared in ﬂuence is responsible for the development of both
psychiatric and substance use disorders. The two types of causal models— secondary
substance use disorder models and secondary psychiatric disorder models— posit that
either type of disorder causes the other. Bidirectional models suggest that eitherpsychiatric or substance use disorders can increase risk for and exacerbate the impactof the other. These models have been more or less described depending on theparticular area of psychopathology. Examination of this literature ﬁnds that models
of dual diagnosis are typically organized by disorder, with research focused onspeciﬁc combinations of dual disorders rather than on the issue of dual diagnosis
across disorders. Extensive reviews of models in each of these categories can be found(Blanchard, 2000; Mueser et al., 1998). The following section provides a review of somemodels of dual diagnosis in their respective domains of psychopathology.C
OMMON FACTORS MODELS
Common factors models suggest a shared etiological basis for psychiatric andsubstance use disorders. Most research has focused on genetics as the likely commonfactor. Results of numerous twin, adoption, and family studies clearly show that bothmental illness and substance abuse run in families, and that familial aggregation ofsingle disorders is substantial (Kendler et al., 1997; Kushner et al., 1990; Merikangaset al., 1985; Merikangas & Gelernter, 1990). Such ﬁndings have led to the hypothesis
that commonly co-occurring disorders might be linked via common genetic factors.However, for genetics to serve as a viable common factor, family studies must showhigh rates of transmission of pure forms of both substance use and psychiatricdisorders. For example, a proband with depression only should have an increasedrate of alcoholism only in the individual ’s relatives in order to provide evidence of
shared genetic etiology.
Studies of familial transmission of a range of comorbid psychiatric and substance
use disorders ﬁnd that the evidence for a common genetic factor is lacking.
Merikangas and Gelernter (1990) reviewed family, twin, and adoption studies ofalcoholism and depression and concluded that familial transmission of pure forms ofthe disorders was not supported: “Depressed only ”probands did not have increased
rates of “alcoholism only ”in their relatives, and “alcoholism only ”probands did not
have increased rates of “depression only ”in their relatives. These authors stress that
although familial aggregation of disorders is evident, the notion of a common genetic72 OVERVIEW

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factor underlying the two is not supported, and the disorders appear to be transmittedseparately.
In subsequent analyses of familial transmission of comorbid depression and
substance use disorders using data from the Yale Family Study of Comorbidity ofSubstance Disorders, Swendsen and Merikangas (2000) similarly found that there wasno support for a common factors model: Mood disorders in the proband were notassociated with an increased risk of alcohol dependence in relatives. Similar resultshave been reported with schizophrenia (Kendler, 1985), ASP (Hesselbrock, 1986), andpatients with schizoaffective and bipolar disorders (Gershon et al., 1982).
Importantly, common factors other than genetics may exist. Several possible
common factors might link substance use disorders and severe mental illness,including comorbid ASP, low socioeconomic status, and poor cognitive functioning(Mueser et al., 1998). For example, ASP is associated with both substance use disordersand severe mental illness. Mueser and colleagues (1999) examined the links betweenconduct disorder, ASP, and substance use disorders in patients with severe mentalillness and found that both childhood conduct disorder and adult ASP were signi ﬁ-
cant risk factors for SUDs. However, the status of ASP as a risk factor is unclear, giventhat problem substance use is part of the diagnosis of ASP, raising the possibility thatASP may be a byproduct of substance use disorder. Also, ASP is based in large part oncriminality and socioeconomic status, both of which are dif ﬁculties that often go along
with both substance use disorder and severe mental illness (Mueser et al., 1998).
Other researchers are proposing multivariate approaches to identifying common
factors of dual disorders. One such model is described by Trull and colleagues (2000)to explain the high prevalence of dual substance use disorders and borderlinepersonality disorder. These authors suggest that a family history of psychopathologyinspires both dysfunctional family interactions and the inheritance of deviant per-sonality traits that are associated with the development of both borderline personalitydisorder and substance use disorders. Speci ﬁcally, the personality traits of affective
instability and impulsivity are central to both disorders and are conceptualized asstemming from a combination of “constitutional and environmental factors ”(Trull
et al., 2000) that include inherited de ﬁciencies in serotonergic functioning, in combi-
nation with a deviant family environment that may include associated childhoodtrauma. These factors in turn impact the development of borderline personalitydisorder and SUD, both alone and in combination. These authors stress that althoughthis model is currently speculative, more prospective, longitudinal studies with adevelopmental and multivariate focus will enable the pieces of the models to beevaluated simultaneously. This model provides an example of combining strategiesfrom family studies and psychopathology research into a multivariate framework thatprovides rich details as to how two disorders could be developmentally related.
In fact, the description and measurement of multivariate inﬂ uences in the devel-
opment and maintenance of dual disorders are becoming increasingly sophisticated,spanning from neurophysiology to postnatal development factors such as familystress (Fishbein & Tarter, 2009). Several studies have focused on the identi ﬁcation of
neurocognitive and neurophysiological vulnerability indicators for substance use andpsychiatric disorders. The P3 event-related potential (ERP) is a neurophysiologicalmeasure of brain activity that occurs between 300 and 600 milliseconds after stimuluspresentation and is implicated in cognitive information processing, responseThe Problem of Dual Diagnosis 73

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inhibition, and self-regulation (Begleiter & Porjesz, 1995; Fishbein & Tarter, 2009).Reduced P3 amplitude has been fairly consistently identi ﬁed among individuals with
an alcohol SUD who are abstinent, as well as in populations at high risk for SUD (e.g.,sons of fathers with alcohol dependence) suggesting that it is a heritable preexistingvulnerability marker, or endophenotype, for alcohol use disorders (Begleiter &Porjesz, 1995).
As discussed previously, conduct disorder or, more generally, externalizing dis-
orders often co-occur with SUDs. Reduced P3 has also been associated with external-izing disorders (e.g., ADD; Klorman, 1991), which suggests it may represent acommon factor to both of these disorders (Iacono, Carlson, Malone, & McGue,2002). In a large longitudinal community-based sample, Iacono and colleagues(2002) measured P3 amplitude and assessed for a series of disorders includingattention-de ﬁcit/hyperactivity disorder, conduct disorder, ASP, and SUD in a sample
of 502 male adolescents and their parents. Participants were assessed at age 17 andthen reassessed 3 years later. Results indicated that reduced P3 amplitude wasassociated with not only a paternal history of SUD but also paternal history ofASP. It was also associated with childhood disorders of disinhibition includingSUDs, and P3 amplitude at age 17 predicted the development of several disordersof disinhibition including SUD. The authors conclude that reduced P3 amplitude maybe a common, genetically transmitted risk factor for a broad range of psychiatricdisorders including SUD that share the common feature of behavioral disinhibition. Itis anticipated that with continued advancements in cognitive neuroscience, similarendophenotypes will be identi ﬁed that will facilitate the identi ﬁcation of common
genetic risk factors for dual disorders.S
ECONDARY SUBSTANCE ABUSEMODELS
Secondary substance abuse models contend that mental illness increases vulnerabilityto SUDs. Probably the most widely discussed model of this type is the self-medicationmodel, which asserts that individuals with psychiatric disorders use substances as away to self-medicate psychopathological symptoms and relieve discomfort associatedwith the primary psychiatric disorder.
There are several types of studies used to examine applicability of a self-medication
model to different forms of psychopathology. Some determine the ages of onset ofdual disorders, with the idea being that SUDs developing after other Axis I psycho-pathology support the self-medication hypothesis. Some examine subjective reasonsfor use among patients with different disorders, while others correlate levels ofsymptoms with levels of substance abuse (from a self-medication perspective, greatersymptoms should correlate with greater substance abuse). Another line of self-medication research involves investigating the types of substances used by differentpatient groups. According to a self-medication hypothesis, patients with certainpsychopathological conditions should preferentially seek out and use substancesthat will directly impact symptoms associated with their speci ﬁc psychopathology.
Support for a self-medication model varies depending on the type of mental illness
under investigation. For example, although the model is popular among treatmentproviders working with patients with severe mental illness, empirical support for aself-medication model has not been compelling (see Mueser et al., 1998, for a review).74 OVERVIEW

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Although it has been suggested that schizophrenia patients preferentially abusestimulants to self-medicate negative symptoms (Schneier & Siris, 1987), this ﬁnding
has not been replicated in other studies (Mueser, Yarnold, & Bellack, 1992). Mostimportant, studies fail to ﬁnd evidence that speciﬁ c substances are used in response to
speciﬁc symptoms. Rather, patterns of drug use appear to be strongly associated with
demographic factors and drug availability (Mueser, Yarnold, et al., 1992). In addition,a self-medication model of SUDs in severe mental illness would predict that the moresymptomatic patients would be at higher risk for substance use disorders (Mueser,Bellack, et al., 1992). Several studies, however, have found the opposite to be true:More severely ill patients are less likely to abuse substances (Chen et al., 1992; Cohen &Klein, 1970; Mueser, Yarnold, et al., 1992), and patients with SUDs have betterpremorbid social functioning (Dixon et al., 1991).
Although individuals with schizophrenia and other severe mental illnesses report a
range of reasons for substance use —to alleviate social problems, insomnia, or
depression; to get high; to relieve boredom; and to increase energy —few endorse
using speci ﬁc substances to combat particular psychiatric symptoms (see Brunette,
Mueser, Xie, & Drake, 1997, for a review). Moreover, many studies have found thatpatients with schizophrenia report worsening of symptoms with substance abuse,including increased hallucinations, delusions, and paranoia (Barbee et al., 1989;Cleghorn et al., 1991; Dixon et al., 1991; Drake et al., 1989), and others have foundthat more severe symptoms of schizophrenia are not linked to more severe substanceabuse (Brunette et al., 1997). Similarly, ﬁndings of increased rates of cocaine use
among patients with bipolar disorder, interpreted by some to indicate self-medicationof depressive symptoms, have been found upon review to more likely reﬂ ect attempts
to prolong euphoric feelings associated with mania (Goodwin & Jamison, 1990).
Other secondary substance abuse models may be more relevant to patients with
severe mental illness. A social facilitation model suggests that patients with severemental illness may have fewer available opportunities for social interaction, and thatsubstance abuse helps smooth the process of social engagement in patients who lackappropriate social and interpersonal skills. Finding that a large portion of substanceuse/abuse by individuals with schizophrenia occurs in a public setting, Dixon, Haas,Weiden, Sweeney, and Frances (1990) suggest that drug use may provide “isolated,
socially handicapped individuals with an identity and a social group ”(p. 74) or to
fulﬁll needs for contact and acceptance (Mueser, Bellack, et al., 1992).
Others offer an alleviation of dysphoria model; substance abuse represents an
attempt to alleviate these negative mood states. Evidence for self-medication may bemore relevant to dual diagnosis within other psychopathological disorders. Forexample, several reviews have found that self-medication may apply to dual PTSDand SUDs, especially among women with trauma-related PTSD. Three main theories(Chilcoat & Breslau, 1998) are (1) the self-medication hypothesis, which suggests thatdrugs are used to medicate PTSD symptoms; (2) the high-risk hypothesis, whichsuggests that drug use puts individuals at heightened risk for trauma that can lead toPTSD; and (3) the susceptibility hypothesis, which suggests that drug users are morelikely to develop PTSD following exposure to a traumatic event. They then use datafrom a sample of more than 1,000 young adults who were randomly selected fromenrollees in a large health maintenance organization and were followed longitudinallyover 5 years in order to examine the timing of the development of both PTSD andThe Problem of Dual Diagnosis 75

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substance use disorders. Those with a history of PTSD at baseline were 4 times morelikely than those without PTSD to develop drug abuse or dependence at some pointduring the 5 years of the study. In contrast, baseline drug abuse/dependence did notconfer any increased risk of subsequent exposure to trauma or to developing PTSD inthose who did experience some traumatic event during the follow-up period.
Other data on dual SUD and PTSD (Stewart et al., 1998) that also lend support to a
self-medication model include: (a) development of substance abuse most often followsdevelopment of PTSD; (b) patients often report that they perceive substance use to beeffective in controlling PTSD symptoms; (c) patients with both PTSD and substanceuse disorder report more severe trauma and a greater severity of PTSD symptoms,suggesting that substances are used in an effort to control greater psychiatricsymptomatology; and (d) drugs of abuse may be related to different clusters ofPTSD symptoms, suggesting that substance abuse may be linked to attempts tocontrol intrusion or arousal symptoms of PTSD. These authors stress that although aself-medication model is likely too simplistic to explain all forms of PTSD –SUD
comorbidity, at this point it provides a good ﬁt for the current literature.
Recently there has been increased interest in neurobiological mechanisms that
underlie dual diagnosis, particularly with respect to the ways in which mental illnessand addiction share common neurological pathways. The foundation for this researchis that neurobiological de ﬁcits and abnormalities that provide the basis for different
forms of mental illness may predispose those with mental illness to substance abuse.
This literature includes animal studies of dual diagnosis, where brain lesions are
produced to simulate different forms of psychopathology. Factors such as the ability toexperience reinforcement from drug use and differential patterns of use and/orcravings are examined. A good summary of this approach to dual diagnosis inschizophrenia is presented by Chambers, Krystal, and Self (2001). Brie ﬂy, increased
vulnerability to substance use disorders in schizophrenia results from impairment inbrain systems that are central to schizophrenia —the most important of which may be
the mesolimbic dopamine system (MDS). According to this model, the MDS isimplicated in the reinforcing effects of drug use (drug use increases dopamine levels),as well as in the development of schizophrenia (high dopamine levels are implicatedas a major factor in the development of schizophrenia). In other words, these authorssuggest that the neuropathology of schizophrenia may contribute to the vulnerabilityto addiction by facilitating neural substrates that mediate positive reinforcement. Theputative neuropathology underlying schizophrenia involves alterations in neuro-anatomic circuitry that regulate positive reinforcement, incentive motivation, behav-ioral inhibition, and addictive behavior (Chambers et al., 2001, p. 71).
Thus, the neurobiological problems that give rise to schizophrenia also put the
individual at heightened risk for developing SUDs. Several studies have foundsupport for this sort of neurological linkage in schizophrenia. Chambers and Self(2002) studied rats with neonatal ventral hippocampal lesions (NVHL rats), a proce-dure that produces behavioral disturbances in rats that resemble the psycho-pathological behaviors seen in schizophrenia, including positive and negativesymptoms and abnormal cognitive functioning (see Chambers & Self, 2002, andChambers & Taylor, 2004, for details of the procedure and its effects). In comparisonto controls (rats with sham lesions), NVHL rats showed faster rates of cocaine self-administration, higher degree of binge cocaine use, and faster relapse to cocaine use76 OVERVIEW

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following a period of nonuse. Other studies using this and similar methodologies havegenerated similar ﬁndings (Chambers & Taylor, 2004).
Similar animal models are available for depression and substance use. In one model
for depression, rats undergo bilateral olfactory bulbectomy (OBX), creating behaviorthat is biologically and behaviorally similar to depression in humans, includingdecreased pleasure seeking, disruptions in sleep, agitation, and other cognitiveproblems that respond only to chronic (and not acute) antidepressant treatment(see Holmes et al., 2002, for a thorough review). Importantly, this procedure alsocauses dopamine dysregulation in areas of the brain implicated in the reinforcingeffects of drugs of abuse, again similar to those found in humans. In comparison to ratswith sham lesions (Holmes et al., 2002), those with OBX lesions were more sensitive tothe reinforcing effects of amphetamine. Speci ﬁcally, they learned to self-administer
amphetamine more quickly and had higher levels of stable amphetamineadministration.
Other studies have used rats genetically bred for signs of learned helplessness as an
operational de ﬁnition of depression in rats. For example, Vengeliene and colleagues
(Vengeliene, Vollmayr, Henn, & Spanagel, 2005) examined differences in alcoholintake between congenital learned helplessness rats (cLH) and congenital nonlearnedhelplessness rats (cNLH) —two lines of rats selectively bred for different escape
reactions following inescapable shock (cLH rats do not try to escape the shock,even though they have not been exposed to it before, whereas cNLH rats will tryto escape the shock). In this study, these two groups of rats were given access toalcohol and tap water for self-administration for 6 weeks and then underwent 2 weeksof no alcohol access followed by renewed access to alcohol for 4 days. Although resultsshowed no differences in males, female cLH rats consumed greater amounts of alcoholthan cNLH rats during the self-administration portion of the study and showed amore pronounced alcohol deprivation effect (greater consumption of alcohol follow-ing a period with no alcohol consumption). The authors suggest that inborn “depres-
sive-like ”behavior in female rats is associated with increase alcohol intake. These and
other animal models of depression (Fagergren, Overstreet, Goiny, & Hurd, 2005)appear to be a useful avenue for the study of dual diagnosis involving depression andsubstance abuse. Such studies are ﬁnding that “depressed ”animals respond differ-
ently than other animals to drugs and alcohol, providing interesting new leads in thesearch for biological mechanisms that lead to dual diagnosis.
The high rate of smoking among individuals with schizophrenia is another possible
instance in which a neurophysiological de ﬁcit predisposes individuals to engage in
substance use. Rates of smoking among individuals with schizophrenia are exceed-ingly high when compared to the general population (de Leon et al., 1995; Hughes,Hatsukami, Mitchell, & Dahlgren, 1986). Individuals with schizophrenia tend tosmoke more cigarettes (de Leon et al., 1995), smoke higher nicotine content cigarettes,and smoke harder in an attempt to extract higher doses of nicotine from cigarettes(Olincy, Young, & Freedman, 1997).
Somewhat different than the self-medication of symptoms of schizophrenia dis-
cussed previously, intriguing data suggest that, for some individuals with schizo-phrenia, smoking may be an attempt to adapt to a neurophysiological de ﬁcit related to
sensory gating. Speci ﬁcally, Adler, Hoffer, Wiser, and Freedman (1993) investigated
the impact of cigarette smoking on the P50 ERP. This ERP is involved in habituation toThe Problem of Dual Diagnosis 77

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stimuli and functions to screen out irrelevant information. It is typically elicited with asensory gating paradigm where two auditory clicks are presented in close temporalsequence. In intact sensory gating there is a diminished neurophysiological responseto the second click. Functionally, this represents a screening out of less relevantinformation, thus allowing for the availability of more cognitive resources for theprocessing of new salient stimuli.
Consistent with other research, Adler et al. (1993) found that in the case of
individuals with schizophrenia, there is a failure to inhibit the response to the secondclick. However, when allowed to smoke freely, there was a normalization (i.e., greaterinhibition in response to the second click), albeit lasting only brie ﬂy. In a second
experiment, Adler, Hoffer, Grif ﬁth, Waldo, and Freedman (1992) investigated the
impact of nicotine gum in ﬁrst-degree relatives of individuals with schizophrenia who
were nonsmokers and had a demonstrated sensory gating de ﬁcit (as measured by
P50). Results were similar to the patient sample: Relatives demonstrated a transientimprovement in P50 ERP. Interestingly, these effects were only found with a higherdose of nicotine gum (6 mg); pilot testing with lower doses failed to yield an effect(Adler et al., 1992).
Another well-documented psychophysiological de ﬁcit in individuals with schizo-
phrenia that has also been identi ﬁed in ﬁrst-degree relatives is that of eye tracking
dysfunction, namely smooth pursuit eye movement (SPEM; e.g., Holzman, 1987).Brieﬂy, when required to visually track a moving object, impaired individuals
demonstrate an increase in “catch-up ”(due to tracking too slowly) and “leading”
eye saccades (due to tracking too quickly or visually “jumping” ahead of the stimuli;
Olincy, Ross, Young, Roath, & Freedman, 1998). Essentially, these saccades decreasethe accuracy and ef ﬁciency with which individuals visually track a moving object.
Olincy et al. (1998) found that in individuals with schizophrenia, performance on aSPEM task signi ﬁcantly improved when patients were allowed to smoke freely
(compared to task performance after a 10-hour period of abstinence from smoking).
Notably, after smoking, there was a signi ﬁcant decrease in leading saccades, which
the authors postulated was an indication of enhanced inhibition and similar tonicotine ’s normalizing effect in the P50 ERP. These neurophysiological ﬁndings
have been linked to the alpha-7 nicotinic receptor, a low-af ﬁnity receptor that requires
high doses of nicotine for activation, which may partially explain heavy smoking (i.e.,extracting higher doses of nicotine) among individuals with schizophrenia (Adleret al., 1998). In addition to furthering our understanding of the impact of nicotine onthe pathophysiology of schizophrenia, these ﬁndings have also helped contribute to
the development of new cognitive-enhancing medications for individuals with thedisorder (e.g., Olincy et al., 2006).S
ECONDARY PSYCHIATRIC DISORDER MODELS
With some speciﬁ c differences, these models suggest that substance abuse causes
psychopathology. Schuckit and Monteiro (1988; Schuckit, 1983) stress that the use of orwithdrawal from many psychoactive substances causes reactions that appearindistinguishable from psychiatric disorder. As reviewed earlier, these authors con-tend that substance use disorders are often mistakenly diagnosed as psychiatricdisorders because of similar symptomatology, and that, although serious78 OVERVIEW

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psychopathology can be expected in the course of substance use disorder, substance-induced disorders are likely to remit following several weeks of abstinence.
The case for substance-induced psychiatric disorder appears to be particularly
relevant to dual SUDs and major depression. Raimo and Schuckit (1998) review theevidence in support of the idea that most cases of comorbid depression and alcoholdependence are substance-induced, including ﬁndings that (a) drinking can cause
severe depressive symptoms; (b) treatment-seeking substance abusers show increasedrates of depression that often remit following abstinence and in the absence of speci ﬁc
treatments for depression; (c) individuals with substance-induced depression do notshow elevated rates of depression in family members; and (d) children of alcoholicsshow higher rates of alcohol use disorders but do not show elevated rates of majordepression. These authors stress that, although having independent depression inaddition to alcohol abuse or dependence is certainly possible, most of the depressionthat is comorbid with alcohol use disorders is substance-induced and not independentin nature.
Following this example, Swendson and Merikangas (2000) reviewed ﬁndings that
are relevant to an etiological model of dual substance abuse and depression: (a) Theonset of alcohol dependence typically precedes the onset of unipolar depression;(b) symptoms of depression often remit following several weeks of abstinence fromalcohol; and (c) genetic studies do not support a shared genetic basis for comorbidityof depression and alcohol dependence. They suggest that the association betweenunipolar depression and alcohol dependence may best be described via a secondarypsychiatric disorder model, in which chronic alcohol use causes unipolar depression,through either the considerable life stress that alcohol dependence promotes for thedrinker in many important domains of functioning, or through the pharmacologicalproperties of alcohol as a depressant substance.B
IDIRECTIONAL MODELS
Bidirectional models propose that ongoing, interactional effects account for increasedrates of comorbidity. Support for a bidirectional model for anxiety and alcoholdependence (Kushner, Abrams, & Borchardt, 2000) includes the following: (a) mostpatients with anxiety and alcohol use disorders report drinking to control fears andreduce tension; (b) drinking can cause anxiety (i.e., anxiety can result from long-termalcohol use, patients report increased anxiety after drinking, and withdrawal fromalcohol can cause physiological symptoms of anxiety); (c) alcohol dependence can leadto anxiety disorders (i.e., alcohol dependence puts one at increased risk for laterdevelopment of an anxiety disorder, and chronic drinking can cause neurochemicalchanges that cause anxiety and panic); and (d) anxiety disorders can lead to alcoholdependence (i.e., having an anxiety disorder puts one at increased risk for laterdevelopment of alcohol dependence, alcohol provides stress-response dampening andreduces the clinical symptoms of anxiety, and many people use alcohol to self-medicate anxiety symptoms).
The authors conclude that alcohol and anxiety interact to produce an exacerbation
of both anxiety symptoms and drinking. Whereas initial use of alcohol provides short-term relief of anxiety symptoms, it negatively reinforces further drinking, leading toincreased physiological symptoms of anxiety. They then propose a so-called feed-The Problem of Dual Diagnosis 79

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forward cycle wherein drinking is promoted by its short-term anxiety-reducing effectsof alcohol, whereas anxiety symptoms are worsened by heavy drinking, leading tocontinued drinking in response to these worsened anxiety symptoms.
Although several caveats and issues remain to be clari ﬁed (i.e., the model seems to
bestﬁt with comorbid alcohol dependence and its relevance to drug use disorders is
unknown; those for whom the anxiety disorder begins ﬁrst would not necessarily
experience the anxiety-reducing properties of alcohol in a way that would initiate thefeed-forward cycle), the authors suggest that a bidirectional model can best explainexisting ﬁndings and can focus future research on comorbidity of anxiety and
substance use disorders. Moreover, this sort of bidirectional model highlights thepossibility that unidirectional causal models are likely too simplistic an approach inexplaining comorbidity. Rather, the relationship between psychiatric and substanceuse disorders is more likely characterized by complex interactions between the twodisorders.
SUMMARY AND FUTURE DIRECTIONS
We are at a critical juncture in the ﬁeld of dual diagnosis and its impact both clinically
and in research. Over the past three decades, efforts have focused primarily onidentifying the problem of dual diagnosis —including its rates and consequences —
and getting clinicians and researchers to think about dual disorders when pursuingtheir clinical or research work. We have learned much about the prevalence andimpact of dual disorders from general population and clinical studies over the lastseveral decades.
Currently we can say with certainty that dual diagnosis is common, both in the
general population and among clients in mental health and substance abuse treat-ment. Comorbid psychiatric and substance use disorders impact a large percentage ofpeople, and dual disorders persist over time. These patterns are likely to shift as abroadened de ﬁnition of substance use disorder that routinely includes tobacco
dependence makes its way into the mainstream of thinking around dual diagnosis.It will be interesting to see how the new de ﬁnitions and conceptualizations that are
part of DSM-5 impact dual diagnosis. As noted previously, changes in the diagnosis of
substance use disorders that include merging abuse and dependence into onedisorder, the addition of gambling disorder, and changes to the diagnostic require-ments for other disorders could lead to higher rates of dual diagnosis. Individualswith less severe problems (abuse) who may have been overlooked or not includedpreviously may now be counted.
Importantly, we are now beginning to see that patients who present with multiple
diagnoses are the most difﬁ cult and complex patients to understand and treat. The
notion of dual disorders may require reconceptualization as the frequency of indi-viduals with two, three, or more comorbid psychiatric and substance use disorderscontinues to climb. Such ﬁndings highlight the potential need to adjust our thinking
about dualdiagnosis and whether the term should be updated from dualtomultiple as
a way to more accurately capture the reality that many cases of dual diagnosis reallyreﬂect multiple comorbid conditions.
The issue of multiple comorbidities —multiple substance use, psychiatric, and even
medical disorders within individuals— is probably the most critical issue facing80 O
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assessment and diagnosis of dual disorders. Research is starting to examine theinterrelationships among mental health, somatic disease, and addiction. The inclusionof tobacco dependence within the framework of dual diagnosis plays an importantrole in this shift. For example, work on the relationships among mood disorders,smoking and tobacco dependence, and the presence of and recovery from physicalillnesses such as heart disease is ﬁnding complex associations that impact treatment,
recovery, and relapse (Stafford, Berk, & Jackson, 2013). Findings that individuals withmental health disorders have more health risk factors such as diabetes, obesity, andsmoking but receive less medical treatment for them (Briskman, Bar, Boaz, & Shar-gorodsky, 2012) highlight the need for more attention to the public health impacts ofmultiple comorbidities.
Second, it is clear that research on psychopathology and its treatments is compli-
cated by questions of dual diagnosis. Dual diagnosis impacts basic questions ofresearch methodology and impact: Who is included and excluded in dual diagnosisresearch? How are dual disorders handled in data collection and analysis? How areresearch ﬁndings to be understood when individuals have multiple disorders?
Although acknowledging and adapting to the reality of multiple comorbidites withinindividuals will further complicate treatment research, it is essential that researchexplore ways to include and be applicable to individuals with multiple conditions.That is, it is increasingly less useful to explore the relationships between only twodisorders, or to limit the development of treatments to individuals with two disorders,when many of those with comorbid conditions have more than two problems.Practically speaking, issues of mood, anxiety, and substance use are intertwinedfor many people, and research will need to address the understanding and treatmentof these syndromes together rather than separately.
Finally, several models that explain dual diagnosis take into account the
different types of psychopathology an d substances of abuse, as well as the
differences in disorder severity. Research linking neurobiological developmentof psychiatric disorders to substance abuse vulnerability highlights the need toincorporate biological and psychological constructs as we proceed in trying tounderstand dual diagnosis. The next step is to further examine causal mechanismsand determine how these mo dels work given the signiﬁ cant heterogeneity seen in
the dual diagnosis population. Although a range of theories has been proposed,more speci ﬁc work is required to fully examine the links between mental illness
and substance use disorders. Here again, r esearch will have to adapt to the current
reality of multiple comorbidities. At present it is unclear how prevailing models ofdual disorders that are organized around a pair of problems are going to berelevant to individuals with three or more diagnoses. Overall, moving forward inour understanding of dual disorders will require that we focus on comorbidity andthe connections among multiple problemsa saw a yt ob e s tl e a r na b o u ta n dt r e a tindividuals.
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CHAPTER 3
Structured and Semistructured
Interviews for Differential Diagnosis
Fundamental Issues, Applications, and Features
DANIEL L. SEGAL and KADIJA N. WILLIAMS
STRUCTURED AND SEMISTRUCTURED interviews were developed to address the dif ﬁ-
culties that clinicians and researchers historically have had in making accuratediagnoses of mental disorders with trad itional unstructured clinical inter-
views. A major contributing factor to diagnostic imprecision was the lack ofuniformity or standardization of questio ns asked of respondents to evaluate the
nature and extent of their psychiatric symptoms and to arrive at a formal diagnosis.Structured and semistructured interview s solve this problem by their very nature.
A ss u c h ,t h e yh a v eb e c o m ei n c r e a s i n g l yp o p u l a ra n de f f e c t i v ei nt h em e n t a lh e a l t hﬁeld, leading to vastly improved diagnostic clarity and precision. The purpose of
this chapter is to provide a basic introduction to structured and semistructuredinterviews used to assess and diagnose psychopathology among adults. We beginwith a discussion of the basic types of appli cations of structured and semistructured
interviews followed by an exploration of their major features, advantages, anddrawbacks. We conclude this chapter w ith a discussion of the most popular
multidisorder structured and semistruct ured interviews used to diagnose clinical
disorders and personality disorders.
With the recent publication of the Diagnostic and Statistical Manual of Mental
Disorders ,ﬁfth edition ( DSM-5 ; American Psychiatric Association [APA], 2013),
many changes have occurred, especially regarding the classi ﬁcation and organization
for many clinical disorders. One major change was the removal of the multiaxialsystem, which previously denoted an important distinction between clinical disordersand personality disorders on separate diagnostic axes. Notably, no changes weremade to the classi ﬁcation and diagnostic criteria for the personality disorders. In this
chapter, we describe the anticipated changes to some of the major structured andsemistructured interviews as these measures become updated from their linkage to theDSM-IV-TR (APA, 2000) to the DSM-5 .
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BASIC ISSUES REGARDING STRUCTURED AND
SEMISTRUCTURED INTERVIEWS
The most common method among mental health professionals to evaluate anddiagnose their clients is the direct clinical interview (Segal & Hersen, 2010). Suchinterviews, however, can vary tremendously, especially regarding the amount ofstructure that is imposed. Indeed, some important differences exist between less
structured interviews and more structured ones. Unstructured clinical interviewsare dependent on the clinician ’s unique background, knowledge base, theoretical
model, and interpersonal style, and thus are highly ﬂexible. Within this unstructured
approach, clinicians are entirely responsible for asking whatever questions they decideare necessary to reach a diagnostic conclusion. In fact, any type of question or topic(relevant or not) can be pursued in any way that ﬁts the mood, preferences, training,
speciﬁc interests, or philosophy of the clinician. As a consequence, one can imagine the
variability across interviews from one clinician to another. On the other hand,structured interviews conform to a standardized list of questions (including fol-low-up questions), a uniform sequence of questioning, and systematized ratings ofthe client ’s responses. These questions are designed to measure the speci ﬁc criteria for
many mental disorders as presented in the DSM . These essential elements of struc-
tured interviews serve several important purposes, most notably that their use:
Increases coverage of many mental disorders that otherwise might be overlooked.
Enhances the diagnostician ’s ability to accurately determine whether particular
symptoms are present or absent.
Reduces variability among interviewers, which improves reliability.
These features of structured interviews add much in developing clinical psychologyinto a true science. For example, structured interviews are subject to evaluation andstatistical analysis, and they can be modi ﬁed and improved based on the published
literature regarding their psychometric properties.
Not all structured interviews are the same. In fact, the term structured interview is
broad, and the actual amount of structure provided by an interview varies considera-bly. Structured interviews can be divided into one of two types: fully structured or
semistructured . In a fully structured interview, questions are asked verbatim to the
respondent, the wording of probes used to follow up on initial questions is speci ﬁed,
and interviewers are trained to not deviate from this rigid format. In a semistructuredinterview, although initial questions for each symptom are speci ﬁed and are typically
asked verbatim to the respondent, the interviewer has substantial latitude to follow upon responses. The interviewer can modify or augment the standard inquiries withindividualized and contextualized probes to more accurately rate speci ﬁc symptoms.
The amount of structure provided in an interview clearly impacts the extent of clinicalexperience and judgment that are required to administer the interview appropriately:Semistructured interviews require clinically experienced examiners to administer theinterview and to make diagnoses, whereas fully structured interviews can be admin-istered by nonclinicians who receive training on the speciﬁ c instrument. This latter
difference makes fully structured interviews popular and economical, especially inlarge-scale research studies in which accurate diagnoses are essential.104 OVERVIEW

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Structured and semistructured interviews have been created to assist with the
differential diagnosis of all major clinical disorders (formerly de ﬁned on Axis I of the
DSM-IV ) and all standard personality disorders (formerly de ﬁned on Axis II of
theDSM-IV ). Interviews used for psychiatric diagnosis are typically aligned with
theDSM system and, therefore, assess the formal diagnostic criteria speci ﬁed in the
manual. However, structured interviews exist beyond those designed for DSM
differential diagnosis. Other structured interviews are narrower in focus; for example,to assess a speci ﬁc problem or form of psychopathology (e.g., eating disorders,
substance abuse, borderline personality disorder features) in great depth. An excellentresource for information about a host of specialized interviews is provided by Rogers(2001). Our focus now turns to a discussion of some common functions of structuredand semistructured interviews.
APPLICATIONS OF STRUCTURED AND SEMISTRUCTURED INTERVIEWS
Whereas structured and semistructured interviews are used in many different venuesand for many different purposes, their application falls into three broad areas:research, clinical practice, and clinical training.
Research. T h er e s e a r c hd o m a i ni st h em o s tc o m m o na p p l i c a t i o n ,i nw h i c hs t r u c –
tured or semistructured interviews are used to formally diagnose participants forinclusion into a study so that etiology, comorbidity, and treatment approaches(among other topics) can be explored for a par ticular diagnosis or group of diagnoses.
Sound empirical research on mental disord ers certainly requires that individuals
assigned a diagnosis truly meet full crite ria for that diagnosis. Another research
application for structured interviews is to provide a standardized method for
assessing change in one ’s clinical status over time. As noted by Rogers (2003), these
types of longitudinal comparisons are essential for establishing outcome criteria,which is vital to diagnostic validity.
Clinical Practice. In clinical settings, administration of a structured or semistructured
interview may be used as part of a comprehensive and standardized intake evalua-tion. Routine and complete administration of a structured interview is increasinglycommon in psychology training clinics, but doing so requires considerable training forclinicians and time for full administration. A variation on this theme is that sections ofa structured interview may be administered subsequent to a traditional unstructuredinterview to clarify and con ﬁrm the diagnostic impressions. Widiger and Samuel
(2005) provide another thoughtful alternative especially regarding the assessment ofpersonality disorders in clinical practice. They recommend the strategy of adminis-tering an objective self-report inventory, which is followed by a semistructuredinterview that focuses on the personality disorders that received elevated scoresfrom the testing. This strategy is responsive to time constraints in clinical practice butalso allows for collection of standardized, systematic, and objective data from thestructured interview. Finally, we wish to emphasize that in clinical settings, structuredinterviews should not take the place of traditional clinical interviews. Both can beperformed, although at different times and for different purposes. The combination ofthe two approaches, integrated ﬂexibly to meet the needs of the individual clinician
and his or her clients, reﬂ ects the best of the scientist-practitioner model in which the
science and art of assessment are both valued and valuable (Rogers, 2003).Structured and Semistructured Interviews for Differential Diagnosis 105

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Clinical Training. Use of structured or semistructured interviews for training
mental health professionals is an increasin gly popular and ideal application, because
interviewers have the opportunity to learn (through repeated administrations)speciﬁc questions and follow-up probes used to elicit information and evaluate
speciﬁc diagnostic criteria provided by the DSM. Modeling the questions, sequence,
andﬂow from a structured interview can be a ni n v a l u a b l es o u r c eo ft r a i n i n gf o r
beginning clinicians.A
DVANTAGES AND DISADVANTAGES OF STRUCTURED AND SEMISTRUCTURED INTERVIEWS
No assessment device in the mental health ﬁeld is perfect, and structured and semi-
structured interviews are no exception to this truism. In this section, the strengths andweaknesses of structured interviews are discussed. Our intention is to give readersan appreciation of the major issues to be considered when deciding whether to usethe structured interview approach to assessment. A brief summary of the advantagesand disadvantages is presented in Table 3.1.Advantage: Increased Reliability Perhaps the most important advantage of structured
interviews centers on their ability to increase diagnostic reliability (reliability de ﬁned
in this context refers to consistency or agreement about diagnoses assigned by
Table 3.1
Advantages and Disadvantages of Structured and Semistructured Interviews
Advantages Disadvantages
Increased Reliability: Because questions are
standardized, structured interviews decreasevariability among interviewers, which enhancesinterrater reliability. Structured interviews alsoincrease the reliability of assessment for a client ’s
symptoms across time, as well as the reliabilitybetween client report and collateral information.May Hinder Rapport: Use of structured interviews
may damage rapport because they are problem-centered, not person-centered, and poorly trainedinterviewers may neglect to use their basic clinicalskills during the assessment.
Increased Validity: Structured interviews assure
that diagnostic criteria are covered systematicallyand completely. This is important because it servesto increase the validity of diagnosis.Limited by the Validity of the Classi ﬁcation
System Itself: Structured interviews used for
diagnosis are inherently tied to diagnostic systems.Thus, they are only as valid as the systems uponwhich they are based. Furthermore, it is dif ﬁcult to
establish the validity of particular structuredinterviews because there is no gold standard inpsychiatric diagnosis.
Utility as Training Tools: Structured interviews are
excellent training tools for clinicians in trainingbecause structured interviews promote the learningof speci ﬁc diagnostic questions and probes used by
experienced clinical interviewers. In addition,nonclinicians can easily be trained to administer fullystructured interviews, which can be cost effective inboth research and clinical settings.The Trade-Off of Breadth Versus Depth:Structured interviews are limited because theycannot cover all disorders or topic areas. Whenchoosing a structured interview, one must evaluatecarefully the tradeoffs of breadth versus depth ofassessment.106 O VERVIEW

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different raters; Coolidge & Segal, 2010a). By systemizing and standardizing thequestions interviewers ask, and the way answers to those questions are recorded andinterpreted, structured interviews decrease the amount of information variance indiagnostic evaluations (e.g., Rogers, 2001). That is, structured interviews decrease thechances that two different interviewers will elicit different information from the sameclient, which may result in different diagnoses. Thus, interrater reliability, or thelikelihood that two different interviewers examining the same individual will arrive atthe same diagnosis, is greatly increased.
Increased interrater reliability has broad implications in clinical and research
settings. Because many psychological and p sychopharmacological treatments are
intimately tied to speci ﬁc diagnoses, it is imperative that those diagnoses be accurate
(Segal & Coolidge, 2001). Thus, if differen t clinicians interviewing the same client
arrive at different diagnostic conclusions, it would be challenging to make a de ﬁnitive
decision about treatment. Similarly, accurate diagnosis is also essential for manytypes of clinical research, for example, stu dies that address causes and treatments of
speciﬁc forms of psychopathology (Segal & Coolidge). Imagine a study examining
different treatments for bipolar disorder .I ns u c has t u d y ,i tw o u l db ei m p e r a t i v et o
be certain that those individuals in the tr eatment groups actually have accurate
diagnoses of bipolar disorder. Researchers must be able to accurately and de ﬁnitively
diagnose participants with the disorder being studied before researchers can evenbegin to examine theories of etiology or the effectiveness of treatment for that parti-cular mental disorder.
In addition to increasing interrater reliability, structured interviews increase the
likelihood that the diagnosis is reliable across time and across different sources ofinformation (Rogers, 2001). In many clinical and research settings, individuals are infact assessed on different occasions. Making multiple assessments could be dangerousif an interviewer evaluates a client in a different manner with different questions ondifferent occasions. The client ’s presentation may be substantially altered because
the manner in which the client is asked about those symptoms has changed insteadof the client ’s symptoms or diagnosis being different. Using a standardized interview
for multiple assessments helps ensure that if a client ’s presentation has changed, it
is because his or her symptoms are actually different, not because of variance ininterviews (Rogers). Likewise, in many settings, clinicians conduct collateral inter-views with signi ﬁcant people in the client ’s life to glean a broader picture of the
client ’s symptoms, problems, and experiences. Using a structured interview for both a
client and a collateral source will likely increase the chances that discrepanciesbetween the client and collateral informant are real, rather than a consequence ofdifferent interviewing styles (Rogers).Advantage: Increased Validity Validity of psychiatric diagnosis refers to the meaning-
fulness or usefulness of the diagnosis (Coolidge & Segal, 2010b). A required pre-requisite for validity is reliability. Thus, by virtue of the fact that structured interviewsgreatly increase reliability of diagnosis, they also increase the likelihood that thediagnosis is valid. Structured interviews also improve the validity of diagnoses inother ways. The systematic construction of structured interviews lends a methodo-logical validity to these types of assessments compared to unstructured approaches.Because structured interviews are designed to thoroughly and accurately assessStructured and Semistructured Interviews for Differential Diagnosis 107

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well-de ﬁned diagnostic criteria, they are often better assessments of those criteria than
unstructured interviews (Rogers, 2001). According to Rogers, clinicians who useunstructured interviews sometimes diagnose too quickly, narrow their diagnosticoptions too early, and miss comorbid diagnoses. Because structured interviewsessentially force clinicians to assess all of the speci ﬁed criteria for a broad range of
diagnoses, they offer a more thorough and valid assessment of many disorderscompared to unstructured interviews.
In our experience, it is common for beginning clinicians who are performing an
unstructured clinical interview to gather information about the presence or absence ofonly a few common mental disorders. Coverage of other disorders may be neglectedduring an unstructured interview if the interviewer is unfamiliar with the speciﬁ c
criteria of some disorders. Some unstructured interviews may also provide limitedinformation about whether comorbid psychopathology exists or about the severity ofthe psychopathology. Because they incorporate systematic ratings, structured andsemistructured interviews easily provide information that allows for the determina-tion of the level of severity and the level of impairment associated with a particulardiagnosis. Structured interviews provide the same information about comorbiddisorders as well.Advantage: Utility as Training Tools Structured interviews can be invaluable training
tools for beginning mental health professionals as well as experienced clinicians whodesire to enhance their diagnostic skills. Use of structured interviews in the trainingcontext may help clinicians develop or enhance their understanding of the ﬂow,
format, and questions inherent in a comprehensive diagnostic interview. Withrepeated administrations, much of a structured interview can be internalized bythe clinician. In addition, use of structured interviews for training may reduce anxiety,especially among neophyte clinicians, because the format and ﬂow of the interview is
laid out clearly outlined for the interviewer. This type of structure can be helpful andcalming for beginning clinicians, who may be initially overwhelmed by the diagnosticprocess and its inherent complexity.
Structured interviews can also be a useful means of training those who make
preliminary mental health assessments, for example, intake staff at hospitals, so thatclients are thoroughly and accurately evaluated in preparation for treatment planning.In the case of nonclinician interviewers, fully structured interviews are advisablebecause they minimize the amount of clinical judgment needed for accurate adminis-tration. Use of these trained paraprofessionals can make large-scale research studiescost effective.Disadvantage: May Hinder Rapport Despite the advantages of structured interviews,
their application is not without controversy. The most common criticism of struc-tured interviews is that their use may damage rapport or the therapeutic alliance(Segal, Max ﬁeld, & Coolidge, 2008), which is widely viewed as an essential
component of effective psychotherapy. Attaining a reliable and accurate diagnosisof a client achieves a hollow victory if the p rocess prevents the therapeutic alliance
from forming, or in a more dramatic example of clinical failure, the client does notreturn for continued treatment. The well-known joke poking fun at medicine, “the
operation was a success but the patient died, ”m i g h tb er e c a s ti nt e r m so fs t r u c t u r e d108 O
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interviews as “the diagnosis was impeccable but the client never came back for
another session.”
How exactly might structured interviews damage rapport? Perhaps most impor-
tantly, structured interviews may impede the connection between client and clini-
cian because interviews are problem-centered rather than person-centered. There isa danger that interviewers may get so conce rned with the protocol of their interview
that they fail to demonstrate the warmth, empathy, and genuine regard necessaryto form a therapeutic alliance. Indeed, the standardization of the interview mayplay out as “routinization ”(Rogers, 2003). In addition, interviewers who are overly
focused on the questions that they must “get through ”in an interview may, as a
consequence, miss important behavioral c ues or other information that could prove
essential to the case.
Proponents of structured interviews note that the problem of rapport-building
during a structured interview can be overcome with training, experience, and ﬂexibility
(Rogers, 2003). We concur and emphasize the observation that “rapid inquiries or
monotonous questioning represents clear misuses of structured interviews ”(Rogers,
2003, p. 22). If interviewers make an effort to use their basic clinical skills, structuredinterviews can and should be conducted in such a way that establishes rapport andenhances understanding of the client. To ensure that this is the case, however, inter-viewers must be aware of the potential negative effects of structured interviews onrapport-building and make the nurturance of the therapeutic alliance a prominent goalduring an interview, even when they are also focused on following the protocol. Itbehooves those who use structured interviews to engage their respondents in ameaningful way during the interview and to avoid a rote-like interviewing style thatmay alienate. On the other hand, not all clients have a negative perception of a structuredinterview that must be intentionally overcome. Some clients actually like the structuredapproach to assessment because it is perceived as thorough and detailed, and in thesecases, rapport is easily attained.Disadvantage: Limited by the Validity of the Classi ﬁcation System Itself Earlier, we noted
that proponents of structured interviews claim structured interviews may rendermore valid diagnoses in general. The assumption inherent in this argument is that theDSM diagnostic criteria are inherently valid, which is a debatable point. One should
recognize that DSM diagnostic criteria were developed to operationalize theoretical
constructs (e.g., depression, panic disorder, schizophrenia) so there is no absolutebasis on which criteria were created. Furthermore, mental disorders are socialconstructions, which implies that they evolve over time as societies evolve.
Although successive editions of the DSM have been better grounded in empirical
research, and the criteria for some disorders (e.g., major depression) have solidresearch support, other disorders (e.g., most of the personality disorders) and theircriteria have not been examined as consistently or as completely, therefore leavingquestions about their validity (Widiger & Trull, 2007). This point is also bolstered bythe fact that the criteria for some disorders have changed signi ﬁcantly from one edition
to another in the evolution of the DSM (Coolidge & Segal, 1998; Segal, 2010).
Furthermore, criteria for many disorders in the DSM are impacted by cultural and
subcultural variations in the respondent (see Chapter 4 in this book), as well as by theage of the respondent. Indeed, the diagnostic criteria for many mental disorders do notStructured and Semistructured Interviews for Differential Diagnosis 109

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ﬁt the context of later life and, therefore, some criteria do not adequately capture the
presentation of the disorders among many older adults (e.g., Segal, Coolidge, &Rosowsky, 2006; Segal, Qualls, & Smyer, 2011). Thus, certain criteria may be valid onlyfor a particular group of individuals, at a particular point in time, at a particular age.The primary method clinicians currently use to conceptualize diagnoses (the DSM ),
while improving, is far from perfect. Because the DSM generally does poorly in
attending to these issues of age and diversity, interviews based on poor- ﬁtting
diagnostic criteria are similarly limited.
In addition to potential problems with DSM diagnostic criteria, another issue
regarding structured interviews is that it is challenging to establish ﬁrmly the validity
of any particular structured interview. The quandary is that our best means of establish-ing the validity of a structured interview is to compare diagnoses obtained from suchinterviews to diagnoses obtained by expert clinicians or by other structured interviews.This is inherently problematic because we cannot be certain that diagnoses by experts orother structured interviews are in fact valid in the ﬁrst place (Segal et al., 2008).
Disadvantage: The Trade-Off of Breadth Versus Depth Aﬁnal criticism of structured
interviews centers on the fact that no one structured interview can be all things in allsituations, covering all disorders and eventualities. For example, if a structuredinterview has been designed to cover an entire diagnostic system (like the DSM ,
which identi ﬁes several hundred speci ﬁc mental disorders), then inquiries about each
disorder must be limited to a few inclusion criteria. In this case, the ﬁdelity of the
ofﬁcial diagnostic criteria has been compromised for the sake of a comprehensive
interview. If the ﬁdelity of the criteria is not compromised, then the structured
interview becomes unwieldy in terms of time and effort required for its full adminis-tration. Most structured interviews attempt some kind of compromise between thesetwo points of tension.
Thus, regarding breadth versus depth of approach, users of structured interviews
are forced to make a choice about what is most useful in a given situation. Both choiceshave their limitations. If clinicians or researchers decide to use an interview thatprovides great breadth of information, they ensure that a wide range of disorders anda great many different areas of a respondent ’s life are assessed. However, one may not
have the depth of information needed to fully conceptualize a case. On the other hand,deciding to use an interview focused on a few speci ﬁc areas will provide clinicians and
researchers with a wealth of information about those speci ﬁc areas, but it may result in
missing information that could lead to additional diagnoses or a different caseconceptualization. Thus, it is essential to understand that when choosing a particularstructured or semistructured interview, there are often tradeoffs regarding breadthand depth of information.W
EIGHING ADVANTAGES AND DISADVANTAGES
Our examination of the strengths and limitations of structured interviews highlightsthe importance of carefully contemplating what is needed in a particular clinical orresearch situation before choosing a structured interview. Structured interviews canbe invaluable tools in both clinical and research work; however, it is essential that onedoes not use such tools without accounting for some of the problems inherent in their110 OVERVIEW

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use. Rogers (2001) voiced the helpful perspective that it would be unwise to view theinterviewing process as an either/or proposition (i.e., unstructured vs. structuredinterview). In certain situations, unstructured interviews may meet the objectives of aparticular clinical inquiry more ef ﬁciently than a structured interview. For example, in
a crisis situation, ﬂexibility on the part of the clinician is required to meet the pressing
demands of this ﬂuid and potentially volatile interaction. However, in other cases,
greater assurances that the diagnostic conclusions are valid and meaningful wouldtake priority, for example, in clinical research or in the delivery of clearly de ﬁned
psychotherapeutic intervention protocols. As noted earlier, the integration of a non-standardized or clinical interview with a structured or semistructured interview mayalso be an excellent option for clinicians and researchers.
Finally, despite some potential limitations to the use of structured and semistruc-
tured interviews, their use has clearly revolutionized the diagnostic process, vastlyimproving diagnostic reliability and validity. Such interviews have greatly improvedclinical and research endeavors by providing a more standardized, scienti ﬁc, and
quantitative approach to the evaluation of speci ﬁc symptoms and mental disorders.
As such, it is likely that the use of structured and semistructured interviews willincrease in the coming decades.
STRUCTURED AND SEMISTRUCTURED INTERVIEWS
FOR DIFFERENTIAL DIAGNOSIS
In this section, we examine several popular structured an ds e m i s t r u c t u r e di n t e r –
views. These interviews can be divided into those that focus on either clinicaldisorders or personality disorders. As noted earlier, although the DSM-5 no longer
makes a distinction between clinical disorders and personality disorders (with thereplacement of the multiaxial coding system with a nonaxial coding system), thedistinction is still relevant to the curre nt crop of structured and semistructured
interviews that were developed with this d ifference in mind. Instruments that focus
on clinical disorders include the Anxiety Disorders Interview Schedule for DSM-IV ,
Diagnostic Interview Schedule for DSM-IV , the Schedule for Affective Disorders and
Schizophrenia, and the Structured Clinical Interview for DSM-IV Axis I Disorders.
Instruments that measure personality disorders include the Diagnostic Interview forDSM Personality Disorders, the International Personality Disorder Examination, the
Structured Clinical Interview for DSM-IV Axis II Personality Disorders, and the
Structured Interview for DSM-IV Personality.
Where possible, we describe forthcoming updates to some of these instruments as
they are revised to conform to the current DSM-5 system. A general overview of each
instrument is provided in Table 3.2. Each instrument assesses a variety of mentaldisorders and, therefore, can assist in the important task of differential diagnosis (i.e., asystematic way of discriminating among numerous possible disorders to identifyspeciﬁc ones for which the client meets the diagnostic threshold). Each interview also
allows for an assessment of many comorbid mental disorders. The instrumentspresented in this chapter do not represent an exhaustive list of structured andsemistructured interviews, but they are among the most common and well-validatedones. Interested readers are referred to Rogers (2001) and Summerfeldt, Kloosterman,and Antony (2010) for coverage of instruments not reviewed in this chapter.Structured and Semistructured Interviews for Differential Diagnosis 111

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Table 3.2
Comparison of Major Diagnostic Interviews
Name Time Required Format Comment
Anxiety Disorders InterviewSchedule for DSM-IV(Brown, DiNardo, & Barlow,1994a)45 to 60 minutes Semistructured,
interviewer administeredProvides in-depth assessmentof anxiety disorders and otherfrequently comorbidconditions (e.g., mooddisorders, substance abuse).Designed to be administeredby trained mental healthprofessionals with training inadministration. Available inseparate current and lifetimeversions.
Diagnostic InterviewSchedule for DSM-IV
(Robins et al., 2000)90 to 150minutesFully structured,computerized, closed-ended questionsDesigned for epidemiologicalresearch. Includes all possiblediagnoses in DSM-IV . Can be
administered by nonclinicians,although interviewers mustreceive specialized training.
Schedule for AffectiveDisorders and Schizophrenia(Endicott & Spitzer, 1978)90 to 150minutesSemistructured,interviewer administeredProvides in-depth coverageon clinical disorders, namelymood and psychoticdisorders. Designed foradministration by trainedmental health professionals,and additional training inadministration is required.
Structured Clinical InterviewforDSM-IV Axis I Disorders
(First, Spitzer, Gibbon, &Williams, 1997a)45 to 90 minutes Semistructured,
interviewer administeredCovers DSM-IV clinical
disorders most commonlyseen in clinical settings.Designed for use byprofessionals with knowledgeof psychopathology, DSM-IV
diagnostic criteria, and basicinterviewing skills. ResearchVersion and Clinical Versionavailable.
Diagnostic Interview forDSM-IV Personality
Disorders (Zanarini,Frankenburg, Sickel, & Yong,1996)90 minutes Semistructured,
interviewer administeredDesigned to assess the 10standard DSM-IV personality
disorders. Requirements foradministration include atminimum a bachelor ’s degree,
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STRUCTURED AND SEMISTRUCTURED INTERVIEWS FOR CLINICAL DISORDERS
Anxiety Disorders Interview Schedule for DSM-IV The Anxiety Disorders Interview
Schedule for DSM-IV (ADIS-IV; Brown, DiNardo, & Barlow, 1994a) is a semistruc-tured clinician-administered interview designed to measure current episodes ofanxiety disorders as de ﬁned by the DSM-IV . It provides differential diagnosis among
anxiety disorders and includes sections on mood, somatoform, and substance usedisorders, as anxiety disorders are frequently comorbid with such conditions. Thereare two versions of the adult ADIS-IV: the Standard Version, which provides onlycurrent diagnostic information, and the Lifetime Version (ADIS-IV-L; DiNardo,Brown, & Barlow, 1994), which offers both past and current diagnostic information.The ADIS-IV-L is similar in structure to the ADIS-IV, but contains separate sectionsthat assess the occurrence of disorders in the past. The ADIS-IV can be used in bothclinical and research settings.
At the beginning of the ADIS-IV, basic demographic information is collected as well
as a short description of the presenting problem. This information gives the examineran idea of which topics should be pursued in more detail throughout the interview.Following the presenting problem, the examiner asks the respondent, “What would
you say is the main reason that brought you here today? ”and the response is recorded
verbatim. Next, the respondent is asked to describe any recent struggles in functioningwithin the past year (e.g., school, work, relationships). The interview then continuesInternational PersonalityDisorder Examination(Loranger, 1999)15 minutes (self-administeredscreen), 90minutes(interview)Contains self-administered pencil-and-paper questionnaire andsemistructured interviewEvaluates personalitydisorders for both the DSM-IV
and the International
Classi ﬁcation of Diseases ,
10th ed. ( ICD-10 ). Intended
for use by experiencedclinicians with specializedtraining in administration.
Structured Clinical InterviewforDSM-IV Axis II
Personality Disorders (First,Gibbon, Spitzer, Williams, &Benjamin, 1997)20 minutes (self-administeredscreen), 60minutes(interview)Contains self-reportscreening questionnaireand semistructuredinterviewAssesses the 10 standardDSM-IV personality disorders.
Designed for administrationby professionals withknowledge ofpsychopathology, DSM-IV
diagnostic criteria, and basicinterviewing skills.
Structured Interview forDSM-IV Personality (Pfohl,
Blum, & Zimmerman, 1997)60 to 90 minutes Semistructured interview Comprehensive interview for
DSM-IV personality disorders.
Collateral sourcesencouraged. Requirementsfor administration include anundergraduate degree in thesocial sciences and 6 months ’
experience with diagnosticinterviewing in addition tospecialized training.
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with the assessment of anxiety disorders. This section begins with the more prevalentanxiety disorders (e.g., panic disorder, agoraphobia, social phobia) and is organizedlogically to re ﬂect the shared symptoms among many anxiety disorders. Subsequent
to this segment are sections assessing mood disorders, somatoform disorders, mixedanxiety/depression disorders, alcohol and substance use/dependence, and psychoticand conversion symptoms. A segment assessing the individual ’s family history of
psychological disorders is also included. At the end of the ADIS-IV, the examineradministers the Hamilton Rating Scale for Depression and the Hamilton AnxietyRating Scale. The clinician manual (Brown, DiNardo, & Barlow, 1994b) notes thatthese scales are useful as they provide a general assessment of current depressive andanxious symptoms.
Each section on the ADIS-IV includes items assessing diagnostic criteria for the
given disorder. The examiner begins with several dichotomous yes/no initial inquiryquestions, and answers of “yes”warrant asking more extensive questions to gauge the
presence or absence of the particular disorder. In some sections, these dichotomousitems are considered skip-out points in which, pending negative ratings, continuationis not necessary. Dimensional ratings are also obtained regarding both current andpast experiences of major symptoms of the given disorder. As noted previously, theADIS-IV-L contains separate sections for current and past occurrences of disorders,whereas the ADIS-IV assesses only current disorders. However, the ADIS-IV containsscreening questions for past episodes in the initial inquiry items. If the respondentdenotes a positive response to these particular screening questions, the clinician ’s
manual recommends that the interviewer adapt other items in that section to obtaininformation about previous disorders. The manual notes that this information may beuseful in differential diagnosis.
After the initial inquiry section, the clinician continues with the current episode
segment of the interview, which provides items that collectively assess all diagnosticcriteria for a particular disorder. The questions in the current episode section arearranged so that they begin as open-ended and are followed by more speci ﬁc inquiries.
The need for the more speci ﬁc inquiries is contingent upon the response to the initial
open-ended question. For instance, if the respondent provides a speci ﬁc response to a
question regarding the timeline of a given symptom (e.g., “The symptom began
around one month ago”), then follow-up questions may not be needed. The currentepisode section also contains questions that assess the onset of the disorder andetiological factors. At the conclusion of the current episode section, the administratoragain inquires about past episodes of the disorder. The purpose of this repeated item isthat the interviewer can reassess the previous occurrence of the disorder given thewealth of diagnostic information collected in that section. In the ADIS-IV-L, thecurrent episode portion of the interview is followed by the past episode section, whichis similar in structure to the current episode segment.
The ADIS-IV contains a score sheet in which the interviewer records diagnoses
(including dates of onset) in addition to a diagnostic con ﬁdence rating (0 –100, 100
indicating complete certainty). If the diagnostic con ﬁdence rating is less than 100, the
interviewer must indicate why. Each disorder listed is given a rating of clinical severityranging from 0 to 8, with higher numbers indicating more distress. Ratings of 0indicate that there are no features of a given disorder present. These ratings are used toidentify clinical versus subclinical disorders, such that ratings of 3 or below indicate114 OVERVIEW

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subsyndromal symptomatology, and ratings of 4 and above indicate the presence of adisorder (as per the DSM-IV criteria). The ADIS-IV-L also contains a “diagnostic
timeline ”page that synthesizes information regarding the temporal sequence of
disorders as well as etiology.
The ADIS-IV is designed for use by experienced clinicians who are familiar with the
DSM-IV as well as the ADIS-IV. Examiners are encouraged to use clinical judgment to
determine whether an item should be read verbatim or re-worded as needed (e.g.,shortening length and complexity of questions for those with lower levels of educa-tion). Examiners are also encouraged to use their clinical judgment to gather furtherclarifying information from respondents, and to decide when to skip certain sectionsof the interview.
Overall, both the ADIS-IV and ADIS-IV-L are popular and valuable tools in
diagnosing anxiety disorders as well as frequently comorbid conditions. Studieshave indicated empirical support regarding the reliability and validity of theADIS-IV and ADIS-IV-L, and interested readers are referred to Grisham, Brown,and Campbell (2004) for a summary of the psychometric properties of both instru-ments. The ADIS-IV and ADIS-IV-L have been translated into at least ﬁve other
languages, and they also have been adapted into a version for use with children.
The ADIS was recently signi ﬁcantly updated to match changes in DSM-5 .T h e
interview name changed slightly, and is called the Anxiety and Related DisordersInterview Schedule for DSM-5 (ADIS-5; Brown & Barlow, 2014a). A lifetime version of
the ADIS-5 is also available (Brown & Barlow, 2014b). The ADIS-5 interview andmanual are available from Oxford University Press (www.us.oup.com).Diagnostic Interview Schedule for DSM-IV The Diagnostic Interview Schedule for
DSM-IV (DIS-IV; Robins et al., 2000) is designed to ascertain the presence or absence
of major mental disorders of the DSM-IV (APA, 1994). It is unique among the
multidisorder diagnostic interviews in that it is a fully structured interview speci ﬁcally
designed for use by nonclinician interviewers, whereas the other interviews aresemistructured. By de ﬁnition, a fully structured interview clearly speci ﬁes all ques-
tions and probes and does not permit deviations.
The original DIS was developed in 1978 at the request of the National Institute of
Mental Health Division of Biometry and Epidemiology, which was commencing aseries of large-scale, multicenter epidemiological investigations of mental disorders inthe general adult population in the United States. The development of a structuredinterview that could be administered by nonclinicians was imperative because of theprohibitive cost of using professional clinicians as interviewers. As a result, the DISwas designed as a fully structured diagnostic interview explicitly crafted so that itcould be administered and scored by nonclinician interviewers.
To ensure standardized administration of the DIS-IV, computerized administration
is required, which may be administered by the interviewer or it may be self-administered. In both formats, the exact wording of all questions and probes ispresented to the respondent in a ﬁxed order on a computer screen. Rephrasing of
questions is discouraged, although DIS-IV interviewers can repeat questions asnecessary to ensure that the respondent understands them. All questions areclosed-ended, and replies are coded with a forced-choice yes-or-no response format.The DIS-IV gathers all necessary information about the person from his or herStructured and Semistructured Interviews for Differential Diagnosis 115

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self-report. Collateral sources of information are not used. The DIS-IV is self-containedand covers all necessary symptoms to make many DSM-IV diagnoses. To this end, the
DSM-IV diagnostic criteria for the disorders have been faithfully turned into speci ﬁc
questions on the DIS-IV. The coded responses are directly entered into a databaseduring the interview, and the diagnosis is made according to the explicit rules of theDSM-IV diagnostic system.
Because the DIS-IV was designed for epidemiological research with normative
samples, interviewers do not elicit a presenting problem from the respondent, as wouldbe typical in unstructured clinical interviews. Rather, interviewers begin by askingquestions about symptoms in a standardized order. Like most of the other structuredinterviews examined here, the DIS-IV has sections that cover different disorders.Each diagnostic section is independent, except where one diagnosis preempts another.Once a symptom is reported to be present, further closed-ended questions areasked about diagnostically relevant information, such as severity, frequency, timeframe, and possibility of organic etiology of the symptom. The DIS-IV includes a setof core questions that are asked of each respondent. Core questions are followed bycontingent questions that are administered only if the preceding core question isendorsed. Interviewers use a probe ﬂowchart that indicates which probes to select
in which circumstances.
For each symptom, the respondent is asked to state whether it has ever been present
and how recently. All data about the presence or absence of symptoms and timeframes of occurrence are coded and entered into the computer. Consistent with its useof nonclinician interviewers who may not be overly familiar with the DSM-IV or
psychiatric diagnosis, the diagnostic output of the DIS-IV is generated by a computerprogram that analyzes data from the completed interview. The output providesestimates of prevalence for two time periods: current and lifetime.
Due to its highly structured format, full administration of the DIS-IV typically
requires between 90 and 150 minutes. To shorten administration time, the modularformat makes it possible to drop evaluation of disorders that are not of interest in aparticular study. Another option is to drop further questioning for a particulardisorder once it is clear that the threshold number of symptoms needed for diagnosiswill not be met. Although designed for use by nonclinician administrators, trainingfor competent administration of the DIS-IV is necessary. Trainees typically attend a1-week training program at Washington University (St. Louis, Missouri), duringwhich they review the DIS-IV manual, listen to didactic presentations about thestructure and conventions of the DIS-IV, view recorded vignettes, complete workbookexercises, and conduct several practice interviews followed by feedback and review.Additional supervised practice is also recommended.
The psychometric properties of the original DIS and its revisions are excellent, and
such data has been documented in an impressive array of studies. Interested readersare referred to Compton and Cottler (2004) for an excellent summary of the psycho-metric characteristics of the DIS-IV. Overall, the DIS-IV has proven to be a popular anduseful diagnostic assessment tool, especially for large-scale epidemiological research.The DIS-IV has been translated into more than a dozen languages, is used in countriesacross the globe for epidemiological research, and served as the basis for theComposite International Diagnostic Interview used by the World Health Organiza-tion. The lead authors of the DIS are working on updating the DIS-IV to include116 OVERVIEW

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changes reﬂ ected in the DSM-5 . It is anticipated that the updated modules will follow
the criteria for new diagnoses and will offer a more streamlined probe ﬂowchart
(L. Cottler, personal communication, July 20, 2013). For further information on DIS-IVmaterials, training, and developments, refer to the DIS website (http://epi.wustl.edu).Schedule for Affective Disorders and Schizophrenia The Schedule for Affective Disorders
and Schizophrenia (SADS; Endicott & Spitzer, 1978) is a semistructured diagnosticinterview designed to evaluate a range of clinical disorders, with a focus on mood andpsychotic disorders. Ancillary coverage is provided for anxiety symptoms, substanceabuse, psychosocial treatment history, and antisocial personality features. The SADSprovides in-depth but focused coverage of the mood and psychotic disorders andalso supplies meaningful distinctions of impairment in the clinical range for thesedisorders. The SADS can be used to make many DSM-IV diagnoses, but it is not
completely aligned with the DSM system representing a signi ﬁcant point of concern.
With substantive changes made in DSM-5 , the SADS is at risk for becoming more
outdated if it is not revised substantially.
The SADS is intended to be administered to adult respondents by trained mental
health professionals. It focuses heavily on the differential diagnosis of mood andpsychotic disorders, with great depth of assessment in these areas. In the beginning ofthe interview, a brief overview of the respondent ’s background and psychiatric
problems is elicited in an open-ended inquiry. The SADS is then divided into twoparts, each focusing on a different time period. Part I provides for a thoroughevaluation of current psychiatric problems and concomitant functional impairment.A unique feature of the SADS is that, for the current episode, symptoms are ratedwhen they were at their worst levels to increase diagnostic sensitivity and validity. Incontrast, Part II provides a broad overview of past episodes of psychopathology andtreatment. Overall, the SADS covers more than 20 diagnoses in a systematic andcomprehensive fashion and provides for diagnosis of both current and lifetimepsychiatric disorders. Some examples include schizophrenia (with 6 subtypes),schizoaffective disorder, manic disorder, hypomanic disorder, major depressivedisorder (with 11 subtypes), minor depressive disorder, panic disorder, obsessive-compulsive disorder, phobic disorder, alcoholism, and antisocial personality disorder(Endicott & Spitzer, 1978). In DSM-5 , the subtypes of schizophrenia have been deleted
(due to poor validity and clinical utility) so the distinction made by the SADS in thisarea may not be of much use in the future.
In the SADS, questions are clustered according to speci ﬁc diagnoses. For each
disorder, standard questions are speci ﬁed to evaluate speci ﬁc symptoms of that
disorder. Questions are either dichotomous or rated on a Likert-type scale, whichallows for uniform documentation of levels of severity, persistence, and functionalimpairment associated with each symptom. To supplement client self-report andobtain the most accurate symptom picture, the SADS allows for consideration of allavailable sources of information (i.e., chart records, input from relatives). In additionto the standard questions asked of each respondent, optional probes may be selec-tively used to clarify responses, and unstructured questions may be generated by theinterviewer to augment answers to the optional probes. Thus, considerable clinicalexperience and judgment are needed to administer the SADS. To reduce length ofadministration and evaluation of symptoms that are not diagnostically signi ﬁcant,Structured and Semistructured Interviews for Differential Diagnosis 117

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many diagnostic sections begin with screening questions that provide for skip-outs tothe next section if the respondent shows no evidence of having the disorder.Administration of the SADS typically takes between 90 and 150 minutes. Theinterviewer makes formal diagnostic appraisals after the interview is completed.No computer scoring applications have been designed for the SADS because of thecomplex nature of the diagnostic process and the strong reliance on clinical judgment.
As noted earlier, the SADS was designed for use by trained clinicians. Considerable
clinical judgment, interviewing skills, and familiarity with diagnostic criteria andpsychiatric symptoms are requisite for competent administration. As such, it isrecommended that the SADS only be administered by professionals with graduatedegrees and clinical experience, such as clinical psychologists, psychiatrists, andpsychiatric social workers (Endicott & Spitzer, 1978). Training in the SADS is intensiveand can encompass several weeks. The process includes reviewing the most recentSADS manual and practice in rating written case vignettes and videotaped SADSinterviews. Additionally, trainees typically watch and score live interviews as ifparticipating in a reliability study with a simultaneous-rating design. Throughout,discussion and clari ﬁcation with expert interviewers regarding diagnostic disagree-
ments or dif ﬁculties add to the experience. Finally, trainees conduct their own SADS
interviews that are observed and critiqued by the expert trainers.
Numerous additional versions of the SADS have been devised, each with a distinct
focus and purpose. Perhaps the most common is the SADS-L (Lifetime version), whichcan be used to make both current and lifetime diagnoses but has signi ﬁcantly fewer
details about current psychopathology than the full SADS and results in a quickeradministration time. The SADS-L generally is used with nonpsychiatric samples inwhich there is no assumption of a signi ﬁcant current psychiatric problem. The SADS-
Change Version is also popular and consists of 45 key symptoms from the SADS Part1. Extensive study of the SADS suggests that it possesses excellent psychometriccharacteristics. See Rogers, Jackson, and Cashel (2004) for a comprehensive review ofthese data.
The SADS has been translated into several languages, but its primary use has been
in North America. The SADS has been widely used in clinical research over the pastthree decades, and consequently has a large body of empirical data associated with it.As such, it is often the instrument of choice for clinical researchers desiring in-depthassessment of depression and schizophrenia. The extensive subtyping of disordersprovided by the SADS is also highly valued by clinical researchers. However, owing toits length and complexity, the SADS is infrequently chosen for use in many traditional,pure clinical settings (e.g., community mental health centers). Because the SADS ismost closely aligned with the Research Diagnostic Criteria (and not the DSM criteria),
there are no plans to update the measure to ﬁt the DSM-5 (J. Endicott, personal
communication, July 17, 2013).Structured Clinical Interview for DSM-IV Axis I Disorders The Structured Clinical
Interview for DSM-IV Axis I Disorders (SCID-I) is a ﬂexible, semistructured diagnostic
interview designed for use by trained clinicians to diagnose many adult DSM-IV
clinical disorders. The SCID-I has widespread popularity as an instrument to obtainreliable and valid psychiatric diagnoses for clinical, research, and training purposes,and it has been used in more than 1,000 studies.118 OVERVIEW

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The original SCID was designed for application in both research and clinical
settings. Recently, the SCID has been split into two distinct versions: the ResearchVersion and the Clinician Version. The Research Version covers more disorders,subtypes, and course speci ﬁers than the Clinician Version and, therefore, takes longer
to complete. The bene ﬁt, however, is that it provides for a wealth of diagnostic data
that is particularly valued by clinical researchers. The research version is distributedby the Biometrics Research Department of the New York State Psychiatric Institute(http://nyspi.org).
The Clinician Version of the SCID (SCID-CV; First, Spitzer, Gibbon, & Williams,
1997a) is designed for use in clinical setti ngs. It has been trimmed to encompass
only those DSM-IV disorders that are most typically seen in clinical practice and
can further be abbreviated on a module-by- module basis. The SCID-CV contains six
self-contained modules of major diagnost ic categories (Mood Episodes, Psychotic
Symptoms, Psychotic Disorders, Mood Di sorders, Substance Use Disorders, and
Anxiety and Other Disorders).
The modular design of the SCID represents a major strength of the instrument,
because administration can be customized easily to meet the unique needs of the user.For example, the SCID can be shortened or lengthened to include only those categoriesof interest, and the order of modules can be altered. The format and sequence of theSCID was designed to approximate the ﬂowcharts and decision trees followed by
experienced diagnostic interviewers. The SCID begins with an open-ended overviewportion, during which the development and history of the present psychologicaldisturbance are elicited and tentative diagnostic hypotheses are generated. Then, theSCID systematically presents modules that allow for assessment of speci ﬁc disorders
and symptoms. Most disorders are evaluated for two time periods: current (meetscriteria for the past month) and lifetime (ever-met criteria).
Consistent with its linkage with DSM-IV , formal diagnostic c riteria are included
in the SCID booklet, thus permitting interv iewers to see the exact criteria to which
the SCID questions pertain. This unique feature makes the SCID an outstanding
training tool for clinicians because it facilit ates the learning of diagnostic criteria and
presents excellent questions to assess th e criteria. The SCID has many open-ended
prompts that encourage respondents to elaborate freely about their symptoms. Attimes, open-ended prompts are followed by closed-ended questions to clarify fully aparticular symptom. Although the SCID pro vides structure to cover criteria for each
disorder, its semistructured format provides signi ﬁcant latitude for interviewers
to restate questions, ask for further clari ﬁcation, probe, and challenge if the initial
prompt was misunderstood by the interviewee or clari ﬁcation is needed to rate a
symptom. SCID interviewers are encouraged to use all sources of information abouta respondent, and gentle challenging of th e respondent is encouraged if discrepant
information is suspected.
During administration, each symptom is rated as either absent (or below threshold)
or present (and clinically signi ﬁcant). A question mark (?) denotes that inadequate
information was obtained to code the symptom. The SCID ﬂowchart instructs
interviewers to skip out of a particular diagnostic section when essential symptomsare judged to be below threshold or absent. These skip-outs result in decreased time ofadministration as well as the skipping of items with no diagnostic signi ﬁcance.
Administration of the SCID is typically completed in one session and takes fromStructured and Semistructured Interviews for Differential Diagnosis 119

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45 to 90 minutes. Once administration is completed, all current and past disorders forwhich criteria are met are listed on a Diagnostic Summary sheet.
The SCID is optimally administered by trained clinicians. Because of the semi-
structured format of the SCID, proper administration often requires that interviewersrestate or clarify questions in ways that are sometimes not clearly outlined in themanual to judge accurately if a particular diagnostic criterion has been met. The taskrequires that SCID assessors have a working knowledge of psychopathology, DSM-IV
diagnostic criteria, and basic interviewing skills. Standard procedures for training touse the SCID include carefully reading the Users Guide to the SCID (First, Spitzer,
Gibbon, & Williams, 1997b), reviewing the SCID administration booklet and scoresheet, viewing SCID videotape training materials that are available from the SCIDauthors, and conducting role-played practice administrations with extensive feedbackdiscussions. Next, trainees may administer the SCID to representative participantswho are jointly rated so that a discussion about sources of disagreements can ensue. Inresearch settings, a formal reliability study is advantageous. The reliability andvalidity of the SCID in adult populations with diverse disorders has been evaluatedin several investigations, with generally excellent results among widely variedparticipant samples and experimental designs (see review by First & Gibbon, 2004;Segal, Hersen & Van Hasselt, 1994).
Overall, the SCID is a widely used and respected assessment instrument. It has been
translated into 12 languages and has been applied successfully in research studies andclinical practice in many countries. Computer-assisted clinician-administered versionsof the SCID-CV and SCID Research Version are available. A self-administered com-puterized screening version of the SCID, called the SCID-Screen-PQ, is also available,but it does not produce ﬁnal diagnoses. Rather, likely diagnoses are further evaluated
by a full SCID interview or a clinical evaluation.
The SCID is currently being modi ﬁed to re ﬂect changes in the DSM-5 . The new
measure will be called the Structured Clinical Interview for DSM-5 Disorders.
Developers of the instrument are adding several new disorders including hoarding,premenstrual dysphoric disorder, trichotillomania, excoriation (skin picking) dis-order, intermittent explosive disorder, gambling disorder, and attention-de ﬁcit/
hyperactivity disorder (M. First, personal communication, May 9, 2013). In addition,screening for substance abuse will occur prior to the diagnostic modules of the SCID sothat the effects of the client ’s substance use can be clari ﬁed from the beginning of the
interview. For more information on the SCID, visit the SCID website (www.scid4.org).S
EMISTRUCTURED INTERVIEWS FOR PERSONALITY DISORDERS
Diagnostic Interview for Personality Disorders The Diagnostic Interview for DSM-IV
Personality Disorders (DIPD-IV; Zanar ini, Frankenburg, Sickel, & Yong, 1996) is
a semistructured interview designed to assess the presence or absence of the 10standard DSM-IV personality disorders as well as depressive personality disorder
and passive-aggressive pe rsonality disorder in the DSM-IV appendix. Prior to
personality disorder assessment, a full screening for clinical disorders is recom-mended. Additionally, an assessment of the respondent’ s general functioning (e.g.,
in the domains of work, school, and social li fe) is advised before administration of
the DIPD-IV (Zanarini et al., 1996).120 OVERVIEW

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The interview is conducted on a disorder-by-disorder basis. The interview contains
108 sets of questions, each designed to assess a speci ﬁcDSM-IV personality disorder
diagnostic criterion. The DSM-IV criterion is provided in bold below each set of
questions for easy cross-reference. The initial question for each criterion typically hasa yes-no format that is followed by open-ended questions to explore more fullyclients ’experiences. Clients are informed that the interview pertains to the past 2 years
of their life and that the interviewer wants to learn about the thoughts, feelings, andbehaviors that have been typical for them during the 2-year period. Whereas clientsare the sole source of information for rating most of the diagnostic criteria, behaviorexhibited during the interview is valued and may override client self-report if thereare contradictions. The administrator is encouraged to probe further if responsesappear incomplete or fallacious.
Each diagnostic criterion is rated on the following scale: 0 indicates absent or
clinically insigniﬁ cant, 1 indicates present but of uncertain clinical signi ﬁcance,
2 indicates present and clinically signi ﬁcant, and NA indicates not applicable. After
all 108 criteria are evaluated, ﬁnal categorical diagnosis for each personality disorder
is made based on the number of criteria met. The ﬁnal output is recorded as 2,
indicating yes or met full criteria, 1 indicating subthreshold (one less than requirednumber of criteria), or 0 indicating no.
Information about administration and sco ring of the DIPD-IV is relatively sparse,
at least compared to the other interview s focusing on personality disorders. The
training requirements include at minimum a bachelor ’s degree, at least one year of
clinical experience with personality-disordered clients, and several training inter-views in which the person observes skilled administrators and then administers the
interview. Training tapes and workshops are available, as is a Spanish version.Administration time is typically about 90 minutes. Most notably, the DIPD-IV hasbeen chosen as the primary diagnostic me asure for personality disorders in the
Collaborative Longitudinal Personality Disorders Study, which is a large, multisite,prospective naturalistic longitudinal study of personality disorders and comorbidmental health problems. Because personality disorder criteria have not changed inthe DSM-5 there will be no changes to the DIPD-IV (M.C. Zanarini, personal
communication, July 18, 2013). For furthe r information on the DIPD-IV, contact
Dr. Mary C. Zanarini ( zanarini@mclean.harvard.edu).
International Personality Disorder Examination The International Personality Disorder
Examination (IPDE; Loranger, 1999) is an e xtensive, semistructured diagnostic
interview administered by experienced clin icians to evaluate personality disorders
for both the DSM-IV and the International Classi ﬁcation of Diseases, 10th ed. (ICD-10 )
classi ﬁcation systems. The IPDE was develo ped within the Joint Program for the
Diagnosis and Classi ﬁcation of Mental Disorders of t he World Health Organization
and U.S. National Institutes of Health aimed at producing a standardized assess-ment instrument to measure personality disorders on a worldwide basis. As such,the IPDE is the only personality dis order interview based on worldwide ﬁeld trials.
The IPDE manual contains the interview questions to assess either the 11 DSM-IV or
the 10 ICD-10 personality disorders. The two IPDE modules ( DSM-IV and ICD-10 )
contain both a self-administered screeni ng questionnaire and a semistructured
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The Screening Questionnaire is a self-administered form that contains 77 DSM-IV
or 59 ICD-10 items written at a fourth-grade reading level. Items are answered either
“true ”or“false, ”and the questionnaire is typically completed in about 15 minutes.
The clinician can quickly score the questionnaire and identify those respondentswhose scores suggest the presence of a personality disorder. Subsequently, the IPDEclinical interview is administered.
The IPDE Interview modules (for either the DSM-IV orICD-10 systems) contain
questions, each re ﬂecting a personality disorder criterion, that are grouped into six
thematic headings: work, self, interpersonal relationships, affects, reality testing,and impulse control (Loranger, 1999). Because disorders are not covered on a one-by-one basis, the intent of the evaluation is less transparent, similar to the SIDP-IV.At the beginning of each section, open-e nded inquiries are provided to enable a
smooth transition from the previous section and to encourage respondents toelaborate about themselves in a less structured fashion. Then, speci ﬁcq u e s t i o n s
are asked to evaluate each personality dis order criterion. For each question, the
corresponding personality disorder and the speci ﬁcd i a g n o s t i cc r i t e r i o na r ei d e n t i –
ﬁed with speci ﬁc scoring guidelines.
Respondents are encouraged to report their typical or usual functioning, rather than
their personality functioning during times of episodic psychiatric disturbance. TheIPDE requires that a trait be prominent during the past 5 years to be considered a partof the respondent ’s personality. Information about age of onset of particular behaviors
is explored to determine if a late-onset diagnosis (after age 25 years) is appropriate.When a respondent acknowledges a particular trait, interviewers follow up by askingfor examples and anecdotes to clarify the trait or behavior, gauge the impact of the traiton the person ’s functioning, and fully substantiate the rating. Such probing requires
signiﬁcant clinical judgment and knowledge on the part of interviewers about each
criterion. Items may also be rated based on observation of the respondent ’s behavior
during the session, and this too requires a certain level of clinical expertise. Tosupplement self-report, an interview of informants is encouraged. Clinical judgmentis needed to ascertain which source is more reliable if inconsistencies arise.
Each criterion is rated on a scale with the following de ﬁnitions: 0 indicates that
the behavior or trait is absent or within normal limits, 1 refers to exaggerated oraccentuated degree of the trait, 2 signi ﬁes criterion level or pathological, and ?
indicates the respondent refuses or is unable to answer. Comprehensive item-by-item scoring guidelines are provided in the manual (Loranger, 1999). At the end of
the interview, the clinicia n records the scores for each response on the appropriate
IPDE Answer Sheet. Ratings are then col lated either by hand or computer. The
ultimate output is extensive, including pre sence or absence of each criterion, number
of criteria met for each personality disorder, a dimensional score (sum of individualscores for each criterion for each disor der), and a categorical diagnosis (de ﬁnite,
p r o b a b l e ,o rn e g a t i v e )f o re a c hp e r s o n a l i ty disorder (Loranger, 1999). Such compre-
hensive output is often of value to clinical researchers.
The IPDE is intended to be administered by experienced clinicians who have also
received speci ﬁc training in the use of the IPDE. Such training typically involves a
workshop with demonstration videotapes, discussions, and practice. Averageadministration time is 90 minutes for the interview, which can be reduced by usingthe screening questionnaire (omitting interview items associated with unlikely122 OVERVIEW

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personality disorders). Because the IPDE has been selected by the WHO for interna-tional application, it has been translated into numerous languages to facilitate cross-cultural research. Ample evidence of reliability and validity of the IPDE has beendocumented (Loranger, 1999; Loranger et al., 1994). Because of the instrument ’s ties
to the DSM-IV and ICD-10 classi ﬁcation systems and adoption by the WHO, the
IPDE is widely used for international and cross-cultural investigations of personalitydisorders. No major updates to the IPDE are planned at present.Structured Clinical Interview for DSM-IV Axis II Personality Disorders To complement
the clinical disorder I version of the SCID, a version focusing on personality disordersaccording to DSM-IV has been developed, and it is called the Structured Clinical
Interview for DSM-IV Axis II Personality Disorders (SCID-II; First, Gibbon, Spitzer,
Williams, & Benjamin, 1997). The SCID-II has a similar semistructured format as theoriginal SCID but it covers the 10 standard DSM-IV personality disorders, as well as
depressive personality disorder and passive-aggressive personality disorder (whichwere listed as disorders to be studied further in an appendix of the DSM-IV ).
For comprehensive assessment, the SCID-II may be easily used in conjunction with
the original SCID that would be administered prior to personality disorder assess-ment. This is encouraged so that the respondent ’s present mental state can be
considered when judging accuracy of self-reported personality traits. The basicstructure and conventions of the SCID-II closely resemble those of the SCID-I. Anadditional feature of the SCID-II is that it includes a 119-item self-report screeningcomponent called the Personality Questionnaire that may be administered prior to theinterview portion and takes about 20 minutes. The purpose of the PersonalityQuestionnaire is to reduce overall administration time, because only those itemsthat are scored in the pathological direction are further evaluated during the struc-tured interview portion.
During the structured interview component, the pathologically endorsed screening
responses are further pursued to determine whether the symptoms are actuallyexperienced at clinically signi ﬁcant levels. Here, the respondent is asked to elaborate
about each suspected personality disorder criteria and speci ﬁed prompts are pro-
vided. Like the original SCID, the DSM-IV diagnostic criteria are printed on the
interview page for easy review, and responses are coded as follows: ? indicatesinadequate information, 1 indicates absent or false, 2 indicates subthreshold, and 3indicates threshold or true. Each personality disorder is assessed completely, anddiagnoses are completed before proceeding to the next disorder. The modular formatpermits researchers and clinicians to tailor the SCID-II to their speci ﬁc needs and
reduce administration time. Clinicians who administer the SCID-II are expected to usetheir clinical judgment to clarify responses, gently challenge inconsistencies, and askfor additional information as required to rate accurately each criterion. Collection ofdiagnostic information from ancillary sources is permitted. Complete administrationof the SCID-II typically takes less than 60 minutes.
Training requirements and interviewer quali ﬁcations are similar to that of the
original SCID. There is no Clinician Version of the SCID-II. The psychometricproperties of the SCID-II are strong (see comprehensive review by First and Gibbon,2004). Given the extensive coverage of the personality disorders, modular approach,and strong operating characteristics, the SCID-II should remain a popular andStructured and Semistructured Interviews for Differential Diagnosis 123

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effective tool for personality disorder assessment. To be consistent with the removal ofthe multiaxial system in the DSM-5 , the SCID-II will be renamed the SCID-Personality
Disorders (SCID-PD) but no other changes are imminent. The SCID-II website is thesame as for the original SCID (www.scid4.org).Structured Interview for DSM-IV Personality The Structured Interview for DSM-IV
Personality (SIDP-IV; Pfohl, Blum, & Zimmerman, 1997) is a comprehensive semi-structured diagnostic interview for DSM-IV personality disorders. It covers 14 DSM-
IVpersonality disorder diagnoses, including the 10 standard personality disorders,
self-defeating personality disorder, depressive personality disorder, negativistic per-sonality disorder, and mixed personality disorder. Prior to the SIDP-IV structuredinterview, a full evaluation of the respondent ’s current mental state is required (Pfohl
et al., 1997). This is not surprising given that self-report of enduring personalitycharacteristics can be seriously compromised in a respondent who is experiencingacute psychopathology. Indeed, the aim of all personality assessment measures is torate the respondent ’s typical, habitual, and lifelong personal functioning rather than
acute or temporary states.
Interestingly, the SIDP-IV does not cover DSM personality categories on a disorder-
by-disorder basis. Rather, DSM-IV personality disorder criteria are re ﬂected in items
that are grouped according to 10 topical sections that re ﬂect a different dimension of
personality functioning. These sections include interests and activities, work style, closerelationships, social relationships, emotions, observational criteria, self-perception,perception of others, stress and anger, and social conformity. These categories are notscored; rather, they re ﬂect broad areas of personal functioning under which personality
disorder items can logically be subsumed (Pfohl et al., 1997).
Each SIDP-IV question corresponds to a unique DSM-IV personality disorder
criterion, except that one item addresses two criteria. An attractive feature is thatthe speci ﬁcDSM-IV criterion associated with each question is provided for interviewers
to easily view. All questions are administered, and there are no options to skip out. Mostquestions are conversational in tone and open-ended to encourage respondents to talkabout their usual behaviors and long-term functioning. In fact, respondents are speci ﬁ-
cally instructed to focus on their typical or habitual behavior when addressing each itemand are prompted to “remember what you are like when you are your usual self. ”Based
on client responses, each criterion is rated on a scale with four anchor points. A rating of0 indicates that the criterion was not present, 1 corresponds to a subthreshold levelwhere there is some evidence of the trait but it is not suf ﬁciently prominent, 2 refers to
the criterion being present for most of the past 5 years, and 3 signi ﬁes a strongly present
and debilitating level. The SIDP-IV requires that a trait be prominent for most of the past5 years to be considered a part of the respondent ’s personality. This 5-year rule helps
ensure that the particular personality characteristic is stable and of long duration, asrequired by the General Diagnostic Criteria for Personality Disorders.
A strong point of the organizational format by personality dimensions (rather than
by disorders) is that data for speci ﬁc diagnoses are minimized until ﬁnal ratings have
been collated on the summary sheet. This feature can potentially reduce interviewerbiases, such as the halo effect or changing thresholds, if it is obvious that a respondentneeds to meet one additional criterion to make the diagnosis. This topical organizationalso makes the interview ’s intent less transparent compared to the disorder-by-
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Signiﬁcant clinical judgment is required to properly administer the SIDP-IV,
because interviewers are expected to ask additional questions to clarify clientresponses when necessary. Also, data are not limited to self-report; rather, chartrecords and signi ﬁcant others such as relatives and friends who know the client well
should be consulted when available, and a standard informed consent is included forinformant interviews. Such collateral information is particularly prized when eval-uating personality-disordered individuals who may lack insight into their ownmaladaptive personality traits and distort facts about their strengths and limitations.Moreover, informants can also provide diagnostic data that can help resolve the state/trait distinction about speci ﬁc criterion behaviors.
If discrepancies between sources of information are noted, interviewers must con-
sider all data and use their own judgment to determine the veracity of each source.Making this distinction can be one of the challenges faced by SIDP-IV administrators.Given the multiple sources of diagnostic data, ﬁnal ratings are made after all sources of
information are considered. Such ratings are then transcribed onto a summary sheet thatlists each criterion organized by personality disorder, and formal diagnoses areassigned. As required by the DSM , diagnoses are made only if the minimum number
of criteria (or threshold) has been met for that particular disorder.
Minimum quali ﬁcations for competent administration consist of an interviewer with
an undergraduate degree in the social sciences and 6 months of experience withdiagnostic interviewing. Moreover, an additional month of specialized training andpractice with the SIDP is required to become a competent interviewer (Pfohl et al., 1997).Administrators are required to possess an understanding of manifest psychopathologyand the typical presentation and course of clinical and personality disorders. Trainingtapes and workshop information are available from the instrument authors. The SIDPtypically requires 60 to 90 minutes for the client interview, 20 minutes for interview ofsigniﬁcant informants, and approximately 20 minutes to ﬁll out the summary score
sheet. Studies documenting the strong psychometric properties of the SIDP are plenti-ful, and they are summarized in the manual for the instrument (Pfohl et al., 1997).
THE CULTURAL FORMULATION INTERVIEW (CFI) OF DSM-5
New to DSM-5 is the Cultural Formulation Interview (CFI), which is a 16-question
semistructured interview designed to assess the impact of cultural factors on anindividual ’s mental health. The CFI is based on the Outline for Cultural Formulation, a
framework for assessing cultural factors as they relate to individuals ’mental health
that was ﬁrst introduced in the DSM-IV . Although the CFI is not used to diagnose
mental disorders per se, we included it in this chapter because the CFI can be used tounderstand important cultural issues that can impact the expression and diagnosis ofmental disorders in diverse populations.
According to the DSM-5 , cultural concepts are essential to effective diagnostic
assessment and clinical management for several reasons such as:
Aiding in avoiding misdiagnosis.
Obtaining useful clinical information.
Improving clinical rapport and engagement as well as therapeutic ef ﬁcacy.
Clarifying cultural epidemiology.
Guiding clinical research (APA, 2013, p. 759).Structured and Semistructured Interviews for Differential Diagnosis 125

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The purpose of the CFI is to provide a guide for cultural assessment that improves“cultural validity of diagnostic assessment, ”aids in treatment planning, and fosters
the individual ’s commitment and satisfaction (APA, 2013). There are two versions of
the CFI: the core CFI, which is used to interview the individual, and the CFI-InformantVersion, which is used when the individual is unable to answer the question forthemselves such as with children, or with persons who are cognitively impaired orpsychotic. Information for the CFI-Informant version is collected from a person whoknows the individual well and is knowledgeable about the individual ’s clinical
problems, and the person ’s important life circumstances. The information gathered
from the CFI-Informant version can be used as a supplement to, or a replacement for,the core CFI.
The CFI is rooted in a person-centered approach focusing on the individual ’s
perspective of their cultural experiences a nd social contexts. It is suggested that the
C F Ib eu s e di nc o n j u n c t i o nw i t hp r e v i o u s l y obtained demographic information in
order to tailor the questions to the individual’ s current cultural context (APA, 2013).
The information collected from the CFI a nd or the CFI-Informant version along
with all other clinical information should be integrated to create a comprehensiveevaluation.
The CFI is composed of four main sections, each focusing on a different aspect of
cultural factors encountered in diagnostic assessment. The ﬁrst section (questions 1 –3)
focuses on the cultural de ﬁnition of the problem; the second section (questions 4 –10)
concentrates on cultural perceptions of cause, contacts, and support; the third section(questions 11 –13) focuses on cultural factors affecting self-coping and past help
seeking; and ﬁnally the fourth section (questions 14– 16) focuses on cultural factors
affecting current help seeking. The CFI is formatted into two columns. The left-handcolumn provides information to the interviewer on both how to administer the CFIand the goals of the section. The right-hand column offers suggested questions thatcan be used in the interview. The CFI is a semistructured interview so the questionsareﬂexible and may be rephrased. Clinicians are also encouraged to ask follow-up
questions as needed to clarify individuals ’answers. The DSM-5 suggests that the
CFI be used ﬂexibly to maintain a natural ﬂow during the interview and therapeutic
rapport (APA, 2013). Additional modules have been created to both guide clinicianswho wish to expand on any of the sections and explore them further during theinterview and for speciﬁ c populations such as older adults, children, and immigrants.
Supplemental modules can be found online at www.psychiatry.org/dsm5.
SUMMARY AND CONCLUSIONS
This chapter highlights the fact that structured and semistructured interviews havegreatly facilitated psychiatric diagnosis, objective measurement of symptoms, andproblem clari ﬁcation in a diverse range of clinical and research settings. Reliability of
diagnosis is much improved with the use of structured interviews compared to thenonstandardized approach that is common in clinical practice, and improved reliabil-ity provides the foundation for enhanced validity and utility of diagnosis. Given theﬁeld’s recent emphasis on empirically supported psychotherapeutic interventions and
processes (e.g., Barlow, 2014; Castonguay & Beutler, 2006; McHugh & Barlow, 2010;Nathan & Gorman, 2007), we hope that a concomitant focus on clinically relevant,126 OVERVIEW

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standardized, objective, and validated assessment procedures will be realized as well.Structured and semistructured interviews play an important role in the advancementof the science of clinical psychology.
This chapter provided a broad overview of t he basic issues surrounding structured
a n ds e m i s t r u c t u r e di n t e r v i e w s ,a n di td escribed many interviews available to
clinicians and researchers. We hope that this information enables clinicians andresearchers to choose instruments that w ill most appropriately suit their needs.
Finally, as noted earlier, with the recent publication of DSM-5 ,m a n yo ft h es t r u c t u r e d
and semistructured interviews described in this chapter will need to undergosigniﬁcant revisions to match the classi ﬁcation changes that occurred for many
diagnostic categories. The structured and semistructured interviews that are usedto diagnose personality disorders do not require imminent revisions because theclassi ﬁcation and criteria for the personality disorders did not change from DSM-IV-
TRtoDSM-5 . The areas of classi ﬁcation and clinical assessment will undoubtedly
continue to evolve and change in the coming years. As such, this is an exciting timefor researchers and clinicians who use str uctured and semistructured interviews
and other empirically based assessment tools.
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CHAPTER 4
Impact of Race, Ethnicity, and Culture
on the Expression and Assessment
of Psychopathology
L. KEVIN CHAPMAN, RYAN C. T. DELAPP, and MONNICA T. WILLIAMS
THIS CHAPTER PROVIDES an overview and framework for understanding race,
ethnicity, and culture as factors that affect adult psychopathology. Of primaryinterest are the assessment and treatment of psychopathology that integrates
culturally salient values, ideologies, and behaviors into the mental health care of ethnicminorities. Moreover, the chapter is organized into two sections. In the ﬁrst section, we
present a model that highlights relevant multicultural factors that should be consid-ered when working with ethnic minorities. The second section provides a discussionof how to effectively apply the knowledge of these multicultural factors whenassessing or treating individuals with diverse ethnic backgrounds. Ultimately, themain objective of this chapter is to encourage mental health professionals to acknowl-edge the impact of race, ethnicity, and culture on adult psychopathology in order tooptimize the ef ﬁcaciousness of mental health services provided to ethnic minority
individuals.
Existing literature has clearly demonstrated the importance of multicultural com-
petency in the assessment and treatment of ethnic minorities. Particularly, the rele-vance of ethnicity (or “a voluntaristic self-identi ﬁcation with a group culture,
identi ﬁed in terms of language, religion, marriage patterns and real or imaginary
origins ”; Bradby, 2012, p. 955) in adult psychopathology has been substantiated by
evidence identifying disparities in prevalence rates, symptom presentation, andseverity, as well as mental health service utilization across diverse ethnic groups.For example, Himle et al. (2009) found that most anxiety disorders (with the exceptionof PTSD) were more prevalent among non-Hispanic Whites in comparison to AfricanAmericans and Caribbean Blacks. However, despite their lower prevalence rates,researchers reported that African Americans and Caribbean Blacks experiencedanxiety disorders that were greater in severity and more functionally impairing,which demonstrates how experiences with mental illness can vary by ethnicity.
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Moreover, ethnicity has been implicated as a differentiating factor in the diagnosis andtreatment of schizophrenia (Fabrega et al., 1994; Gara et al., 2012).
These studies highlight the susceptibility of misdiagnosed schizophrenia in African
American patients due to the tendency for African Americans to endorse morepsychotic symptoms during diagnostic assessments. As a result, Gara and colleagues(2012) emphasize the importance of culturally sensitive diagnostic assessment tools byexplaining how an inability to effectively discriminate schizophrenia and schizoaf-fective disorders can lead to poor treatment outcomes. Additionally, the relevance ofethnicity in adult psychopathology is bolstered by the ﬁndings of Alegría and
colleagues (2007), who used data from the National Latino and Asian Study (NLAAS)to identify factors that inﬂ uence the treatment seeking behaviors of Latino individuals.
Speci ﬁcally, researchers found that the age of migration, Latino ethnicity (e.g.,
Mexican, Puerto Rican), birth origin (e.g., U.S.-born, foreign-born), primary languagespoken, and years of residency in the United States were all in ﬂuential factors in the
use of mental health services and the satisfaction with care received. Most notably,these ﬁndings highlight the impact of varied immigration statuses on the perspectives
that ethnic minority individuals bring to the mental health arena. Overall, theaforementioned studies clearly underscore the need for multicultural competencyin mental health professionals given that one ’s self-identi ﬁcation with an ethnic
heritage has proven to be a vital differentiating factor in the presentation of symptomsand treatment outcomes across diverse adult samples.
RELEVANCE OF ETHNIC IDENTITY AND ACCULTURATION
IN ADULT PSYCHOPATHOLOGY
An understanding of the interaction between multicultural factors (e.g., ethnicidentity, acculturation) and sociocultural factors (e.g., socioeconomic status, life stress)in ethnic minority patients has become undeniably germane to providing theseindividuals with effective mental health care. Prior to learning “how”to integrate
the understanding of this interaction within assessment, diagnostic, and treatmentpractices, mental health professionals must possess the knowledge of “what ”multi-
cultural factors exist. Accordingly, Carter, Sbrocco, and Carter (1996) have proposed atheoretical model that acknowledges the role of ethnicity, or a “shared culture and
lifestyle, ”as a pivotal underlying construct in the epidemiology, symptom expression,
and treatment of psychopathology in ethnic minority individuals (p. 456). Thoughinitially created to explain variations of anxiety disorders in African Americans, theCarter et al. (1996) model can be utilized to more broadly understand the relationshipbetween ethnicity and adult psychopathology by comprehending the salience ofethnic identity and acculturation in all ethnic minorities.
In particular, ethnic identity is a multifarious construct characterized by how
people develop and maintain a sense of belonging to their ethnic heritage (Robertset al., 1999). Important factors in ﬂuencing a person ’s ethnic identity include whether
they personally identify as a member of an ethnic group, their sentiments andevaluations of the ethnic group, their self-perception of their group membership,their knowledge and commitment to the group, and their ethnic-related behaviors andpractices (Burnett-Zeigler, Bohnert, & Ilgen, 2013). Extant literature has providedseveral models explaining the developmental stages of ethnic identity (Cross, 1978;132 OVERVIEW

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Cross & Vandiver, 2001; Phinney, 1989). Collectively, each model describes identityshifts between ethnic ambivalence (lack of interest or pride in one ’s ethnic back-
ground), ethnic exploration (curiosity in one ’s ethnic background potentially accom-
panied by a devaluing of other ethnic heritages), and multicultural acceptance(integration of one ’s commitment to their ethnic background and an appreciation
for other ethnic heritages). Evidence supports that individuals high in ethnic identity(i.e., closer to multicultural acceptance) typically have higher levels of self-esteem,develop more protective coping mechanisms, experience more optimism, and reportfewer psychological symptoms (Roberts et al., 1999; Smith, Walker, Fields, Brookins, &Seay, 1999; McMahon & Watts, 2002). Notably, Williams, Chapman, Wong, andTurkheimer (2012) compared the relationship between ethnic identity and the psy-chological symptoms of African American and European American adult samples.Researchers found that higher levels of ethnic identity were related to lower depres-sive and anxious symptoms in African Americans yet associated with a slightelevation in anxious symptoms for European Americans. Such ﬁndings illustrate
the protective nature of a strong ethnic identity for minority members. However, somestudies suggest that individuals with a strong sense of belonging to their nativeheritage can amplify the impact of culturally speci ﬁc stressors (e.g., discrimination;
social inequalities), thereby enhancing their focus on their difference from majorityculture (Yip, Gee, & Takeuchi, 2008). Past literature has found that the stage of ethnicidentity development, age, and level of perceived stress can attenuate the bufferinginﬂuence of high ethnic identity (see review by Burnett-Zeigler et al., 2013).
Another relevant construct implicat ed in the Carter et al. (1996) model is
acculturation, traditionally de ﬁned as the extent to which ethnic minorities adopt
the values and participate in the traditional activities of mainstream culture. Recentreconceptualizations of the acculturation process utilize a multidimensional per-spective where ethnic minorities must reconcile discrepancies in one ’s identities (the
salience of one ’s ethnic versus national identity), one ’s value system (individualism
versus collectivism), one ’sl a n g u a g ep r o ﬁciency, one ’s cultural attitudes and knowl-
edge, as well as one’ s cultural practices (Park & Rubin, 2012; Schwartz et al., 2013;
Yoon et al., 2013).
According to a meta-analysis of 325 studies about the relationship between
acculturation and mental health, Yoon and colleagues (2013) found that mainstreamlanguage pro ﬁciency was negatively associated with negative mental health, whereas
endorsing an ethnic identity was positively related to positive mental health. Mostimportantly, these ﬁndings demonstrate how complex the relationship between
acculturation and psychopathology can be, which emphasizes the need for mentalhealth professionals to consider the relevance of each acculturation dimension (e.g.,identity, language, value system, behaviors) when working with ethnic minorities.Furthermore, the acculturative stress of integrating disparities in ethnic and main-stream culture across these dimensions can result in dif ﬁculties adapting to main-
stream culture and/or perceived rejection from one ’s native heritage (Schwartz et al.,
2013), which has been associated with psychopathology in ethnic minority adults (e.g.,more eating-disorder symptoms [Van Diest, Tartakovsky, Stachon, Pettit, & Perez,2013]; greater levels of depression [Driscoll & Torres, 2013; Park & Rubin, 2012]).When confronted with such cultural disparities, extant literature has identi ﬁed
biculturalism, or the ability for ethnic minorities to effectively integrate elements ofImpact of Race, Ethnicity, and Culture 133

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two cultural streams, as one of the most protective acculturation statuses againstnegative health outcomes (Schwartz et al., 2013).
Alternative acculturative statuses include strongly adhering to the mainstream
culture and devaluing native heritage (assimilation), strongly adhering to the nativeheritage and devaluing the mainstream culture (separation), and exhibiting littleinterest in adhering to either cultural stream (marginalization; see Matsunaga, Hecht,Elek, & Ndiaye, 2010; Yoon et al., 2013). Overall, existing literature has yieldedinconclusive ﬁndings clarifying the impact of acculturation on the mental health of
ethnic minorities (see Concepcion, Kohatsu, & Yeh, 2013), which has been accreditedto the multiple de ﬁnitions of acculturation (e.g., time since immigration, language
ﬂuency, acculturation status) and examining this construct in few ethnic minority
groups (Burnett-Zeigler et al., 2013; Yoon et al., 2013).
Aside from having knowledge of ethnic identity and acculturation, mental health
professionals must also understand how these constructs interact to in ﬂuence the
psychopathology expressed in many ethnic minority individuals (Yoon et al., 2013). Inreferencing the Carter et al. (1996) model, African Americans who maintain a strongethnic identity and are highly assimilated in the dominant culture are believed toendorse traditional beliefs of mainstream society (e.g., individualism) and exhibitsymptoms presentations consistent with the current diagnostic nomenclature. Nota-bly, it is theorized that these individuals may feel con ﬂicted by being acculturated to
believe psychological treatment is effective while embodying a mistrust of societalsystems in mainstream culture as a result of historically signi ﬁcant cultural experi-
ences (e.g., perceived discrimination from individuals of the dominant culture).Similarly, Carter et al. (1996) conceptualized that African Americans low in ethnicidentity yet highly assimilated will exhibit a traditional symptom presentation, but bemore willing to seek, persist through, and bene ﬁt from traditional treatment practices.
In contrast, individuals high in ethnic identity who strongly de-identify with main-stream culture (separation acculturation status) represent a subset of ethnic minoritieswho may display unique symptom presentations and utilize culturally speci ﬁc
explanations for their symptoms, thereby resulting in a greater likelihood for mis-diagnosed psychopathology. Further, these individuals are theorized to be less likelyto seek treatment due to mistrust in and/or a limited knowledge of mental health care.
Although there is a dearth of literature devoted to examining the additive impact of
ethnic identity and acculturation on adult psychopathology (Chae & Foley, 2010),several studies provide evidence supporting the broad application of the Carter et al.(1996) model across diverse ethnic minority groups. Burnett-Zeigler et al. (2013)examined the relationship between ethnic identity, acculturation, and the lifetimeprevalence of mental illness and substance use in African American, Latino, and Asiansamples. Results indicated that higher levels of ethnic identity, and not higheracculturation, were related to decreased lifetime prevalence of psychiatric illnessand substance use for each minority group. Notably, higher acculturation (e.g., use ofEnglish language or social preference for individuals not in ethnic group) wasassociated with increased prevalence of depression in African Americans andHispanics, increased bipolar diagnoses in Hispanics, and increased anxiety disorderdiagnoses for all minority groups. Regarding substance use, higher acculturation wasrelated to increased lifetime prevalence of alcohol and drug use among the Hispanicand Asian sample. These ﬁndings suggest that having a strong sense of pride and134 O
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belonging to an ethnic heritage is protective; however, nondominant individuals whoare unable to maintain cultural ties with their native heritage (e.g., ﬁrst language,
relationships with members of ethnic group) may be more susceptible to negativehealth outcomes.
Nascent literature has provided a more speci ﬁc understanding of the interaction
between these two constructs by utilizing acculturation statuses (e.g., integration,assimilation, separation) instead of a broad de ﬁnition of acculturation (e.g., English
literacy; time of residency). In particular, Matsunga and colleagues examined theinteraction between ethnic identity and acculturation status in Mexican-heritageadolescents living in the southwest region of the United States and found that anintegration acculturation status was more prevalent than assimilation as well as morepredictive of a strong ethnic identi ﬁcation (Matsunaga et al., 2010), which suggests
that a strong ethnic identity and a successful integration of two cultures are closelyassociated. Furthermore, Chae and Foley (2010) found that high ethnic identitystrongly predicted positive psychological well-being among Chinese, Japanese, andKorean Americans whereas an assimilation acculturation status predicted poorerpsychological well-being among Korean Americans. Also, researchers found thatAsian Americans with an integration acculturation status experienced signi ﬁcantly
higher psychological well-being compared to other acculturation statuses. Mostimportantly, these ﬁndings suggest that ethnic minorities who maintain a strong
sense of belonging to their ethnic heritage (high ethnic identity) and who havesuccessfully integrated the identities, value systems, and cultural practices of theirnative and mainstream heritages (integration) exhibit fewer clinical symptoms andmore life satisfaction.
RELEVANCE OF SOCIOCULTURAL FACTORS
IN ADULT PSYCHOPATHOLOGY
Though an understanding of the aforementioned constructs is essential, it is equallyimportant to examine the impact of other sociocultural variables that also exert aconsiderable degree of in ﬂuence over the symptom presentation and treatment
outcomes of ethnic minorities. Although extant literature has identi ﬁed a myriad
of variables that impact minority mental health, the current chapter solely focuses onsocioeconomic status (SES), stressful life events, and age cohort, which were eachidenti ﬁed by the Carter et al. (1996) model as important contributors to the mental
health of ethnic minorities.
Researchers propose that SES can provide a more precise understanding of the
relationship between ethnicity and adult psychopathology by focusing on the speci ﬁc
environmental elements that characterize each social class. Past literature has shownthat high SES is related to better health outcomes. One study by Shen and Takeuchi(2001) examining the relationship between acculturation, SES, and depression inChinese Americans found that SES was a better indicator of depressive symptomsthan acculturation and that high SES individuals (i.e., high educational attainmentand increased income) were related to better mental health outcome (i.e., fewerdepressive symptoms) compared to low SES individuals. These ﬁndings suggest
that it is through the variance in SES and related variables (e.g., perceptions of stress,social support, and physical health) that acculturation may impact the mental healthImpact of Race, Ethnicity, and Culture 135

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of nondominant individuals (Shen & Takeuchi, 2001). Contrarily, nascent literaturehas begun to propose that the association between social class and mental health ismuch more complex in that evidence has supported that low SES and/or foreign-bornindividuals are not automatically guaranteed poor health outcomes (John, de Castro,Martin, Duran, & Takeuchi, 2012). Given such ﬁndings, it suggests that mental health
professionals should acknowledge the detrimental as well as the protective elementsof one ’s social class.
Also, the Carter et al. (1996) model identi ﬁes stressful life events as a contributor to
the variability in the psychopathology of ethnic minorities. Though a comprehensiveunderstanding of the multiple forms of stress (e.g., violence exposures, neighborhoodcontext, poverty, etc.) is beyond the scope of this chapter, extant literature pinpointsrace/ethnic-based stress as inﬂ uential to the mental health of ethnic minority indi-
viduals. In particular, Greer (2011) describes racism as “complex systems of privilege
and power, which ultimately serve to threaten and/or exclude racial and ethnicminorities from access to societal resources and other civil liberties ”(p. 215). As a
result of such racial/ethnic injustice, many ethnic minorities are subjected to damag-ing race/ethnic-focused attitudinal appraisals (i.e., prejudice), race/ethnic-focusedassumptions (i.e., stereotypes), and unjust treatment based upon their race/ethnicity(Greer, 2011).
Past studies have indicated that exposure to such race/ethnic-based experiences are
strong indicators of mental health outcomes across diverse ethnic minority groups(e.g., discrimination was related to increased lifetime prevalence of generalizedanxiety disorder in African Americans [Soto, Dawson-Andoh, & BeLue, 2011];perceived discrimination was associated with increased anxiety, affective, substanceabuse disorders among African Americans, Hispanic Americans, and Asian Amer-icans [Chou, Asnaani, & Hofmann, 2012]). Notably, empirical evidence suggests thatperceived discrimination may be particularly salient to African American clients,given that several studies have found African Americans to endorse greater degrees ofperceived discrimination in comparison to other ethnic minority groups in the UnitedStates (Cokley, Hall-Clark, & Hicks, 2011; Donovan, Huynh, Park, Kim, Lee, &Robertson, 2013). Overall, when utilizing ethnic identity and acculturation to gaininsight into the culturally speciﬁ c worldviews of nondominant individuals, it is
imperative that mental health professionals also examine the occurrence and impactof race/ethnic-based stressors on the psychopathology of ethnic minorities.
Finally, the Carter et al. (1996) model discusses the relevance of age cohort in the
manifestation of psychopathology in ethnic minorities. The evolution of the “social,
economic, and political climate ”in the United States has yielded diverse experiences
across generations of ethnic minorities in this country, thereby impacting the meaningof ethnicity for each generation (Carter et al., 1996, p. 460). In the context of each ethnicgroup, there are different historical details separating each generation; however, theimpact of age cohort on psychopathology remains a relevant consideration. In general,existing literature has implicated intergenerational disparities in perceived racialdiscrimination (Yip et al., 2008), ethnic identity (Yip et al., 2008), acculturation status(Buscemi, Williams, Tappen, & Blais, 2012), and lifetime prevalence of psychiatricillness (Breslau, Aguilar-Gaxiola, Kendler, Su, Williams, & Kessler, 2006) across theadult lifespan. One study particularly relevant to this chapter ’s discussion of the
Carter et al. (1996) model examined the protective and/or exacerbating nature of136 OVERVIEW

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ethnic identity in the relationship between racial discrimination and psychologicaldistress in Asian adults (Yip et al., 2008). Results indicated that ethnic identityappeared to buffer the negative impact of racial discrimination on the psychologicaldistress for adults ages 41 to 50 yet exacerbate the effects of racial discrimination foradults ages 31 to 40 and 51 and older. In an attempt to explain these ﬁndings, Yip and
colleagues (2008) theorize that the former age cohort is more likely to have a stablelifestyle with more coping mechanisms for stress, whereas the latter age cohorts maycharacterize adults who are in the exploration phase of their ethnic identity, which,therefore, heightens their sensitivity to being unfairly treated on the basis of their race/ethnicity. Furthermore, the parent-child relationship is another important way thatintergenerational differences can impact adult psychopathology, especially for immi-grant families (Kim, 2011; Vu & Rook, 2012).
In a study examining intergenerational acculturation con ﬂict and depressive
symptoms among Korean American parents, Kim (2011) found that greater discrep-ancies in cultural values between parent and child (greater intergenerational con ﬂict)
was related to increased parental depressive symptoms; an association more pro-nounced in mothers compared to fathers. It was proposed that the cultural expect-ations of the Korean mother (e.g., to be a “wise and benevolent ”primary care giver)
was con ﬂicted by an incongruence with the value system of mainstream culture (Kim,
2011, p. 691). Collectively, such ﬁndings provide evidence that the Carter et al. (1996)
model elucidates culturally speci ﬁc considerations for psychological distress among
diverse ethnic minorities.
SECTION 2: APPLICATION OF MULTICULTURAL FACTORS
Prior to addressing how the aforementioned factors can be applied to enhance theefﬁciency and effectiveness of treatment in ethnic minority patients, it is equally
important to understand how culture, race, and ethnicity impact the evaluation ofpsychopathology within such populations. In the following section, the pertinence ofvalidating assessment tools among ethnic minority groups is discussed. In particular,there is a general overview of common statistical methods used to establish measure-ment equivalence across diverse groups as well as important considerations whentranslating the results of such statistical methods to the in vivo assessment of ethnicminority clients.A
SSESSMENT
Historically, there has been a ubiquitous disconnect between investigating variousfacets of theoretical models that are endemic to ethnic minority populations, andthe subsequent application of these constructs in practice. As mentioned earlier, thereare a number of unique, culturally speciﬁ c factors that undoubtedly in ﬂuence the
manifestation (and subsequent treatment) of various forms of psychopathology.There is a substantive literature underscoring the exigency for conducting translationalresearch in ethnic minority populations that are beyond the scope of this chapter (for areview, see Hofmann & Parron, 1996; Nagayama Hall, 2001). Worth noting, however,are two relatively salient implications from the empirical literature. First, the need forculturally sensitive assessment tools that aid in the diagnosis of psychopathology inImpact of Race, Ethnicity, and Culture 137

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ethnic minority individuals. Second, the need for investigators to delineate ingredientsfor culturally sensitive interventions, presumably as a result of uncovering culturallyspeciﬁc factors through rigorous assessment in ethnic-minority populations.
As noted in the previous edition of this chapter, establishing measurement equiv-
alence (or lack thereof) is paramount before proceeding with effective translationalresearch, particularly as it relates to ethnic minority populations. In the previousedition, the authors described (a) linguistic/translation equivalence (accuracy oftranslation/understanding from the perspective of the ethnic minority individual),(b) conceptual equivalence (whether the underlying construct maintains the samemeaning in ethnic minority individuals as in European Americans), and (c) psycho-metric equivalence (whether the construct is measured the same across groups). Giventhat the previous edition provided readers with a thorough overview of the variouscomponents of measurement equivalence, the scope of the current chapter is tohighlight more recent work in the area of measurement equivalence with the aimof delineating potential “ingredients ”for culturally sensitive assessment tools in
ethnic minority populations. Only a brief summary is provided in this edition.
The most important prerequisite to assessment with ethnic minority populations is
taking a multicultural perspective rather than an ethnocentric one. In short, multicul-turalism refers to the recognition of equality of various cultural groups and the right ofindividuals to follow their own speci ﬁed paths (Shiraev & Levy, 2013). Ethnocentrism,
on the other hand, refers to a cognitive bias that supports “judgment about other
ethnic, national and cultural groups from the observer ’s perspective” (Shiraev & Levy,
2013, p. 19). Along these lines, when considering linguistic translation equivalence,one point worth noting is that evaluators must remain cognizant of the cognitivebiases that we all possess and subsequently acknowledge that our literacy is culturallybased (Shiraev & Levy, 2013).
Although many concepts translate naturally across cultures (e.g., numbers), scien-
tists and practitioners need to be increasingly mindful of the interplay between culture,race, and ethnicity during alltypes of assessment. As previously noted, differences in
racial identity, age, participation in acculturation experiences, and environment couldsigniﬁcantly impact how many ethnic minority individuals respond to questions on a
particular measure. Generally agreed upon standards have been established whenlanguage differences exist, particularly as it relates to forward and backward transla-tion (e.g., Butcher, 1996). Appropriately trained, bilingual administrators are criticallyimportant when establishing linguistic translation equivalence.
More recently, signi ﬁcant strides have been made in the realm of conceptual and
psychometric equivalence across racial and ethnic minority groups. Beyond basictheory, the question of conceptual equivalence can most accurately be investigated bydetermining psychometric equivalence. As such, it should be noted that the lack ofeither conceptual or psychometric equivalence neither precludes the elimination of anassessment tool nor suggests that the measure is not useful with a given ethnicminority population. Depending on the properties of the given measure, results ofstatistical analyses may suggest the necessity to modify the assessment tool into amore effective screener as a precursor for further diagnostic assessment (detailedlater). Nonetheless, psychometric equivalence is arguably the most important stan-dard to establish in order to fully understand how to proceed with assessment andsubsequent treatment geared toward ethnic minority individuals.138 OVERVIEW

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Before proceeding, it is important to reemphasize the importance of heterogeneity
in ethnic minority individuals and the relative differences in racial identity, accultur-ation, and the other previously described sociocultural constructs that in ﬂuence the
assessment experience. Historically, the exception during assessment has been to bemindful of cultural heterogeneity prior to assessment when, in fact, the understandingof this heterogeneity is most accurately described as the rule. Moreover, we are re-emphasizing the importance of assessing relevant sociocultural variables as a pream-ble to the discussion of a very promising area of investigation in ethnic minorityassessment and treatment, speci ﬁcally, factor pattern analyses with certain measures.
F
ACTOR PATTERN INVESTIGATIONS IN ETHNIC MINORITIES
Perhaps the most promising investigations in this area are the nascent, factor analyticstudies that examine factor patterns across racial and ethnic minority groups, particu-larly in the realm of anxiety and related disorders. The majority of these investigationshave utilized structural equation modeling (SEM), a comprehensive yet ﬂexible
approach that allows the investigator to examine various relationships among var-iables while controlling for measurement error (see Bentler, 1990; Hu & Bentler, 1999).The ability of an investigator to control for measurement area when examiningmeasurement equivalence while simultaneously examining various components ofthe general linear model makes this approach very attractive over traditional analyticmethods.
Many investigators interested in the assessment and treatment of ethnic minority
individuals have employed SEM in order to determine whether commonly usedassessment tools are equivalent (or contain invariant factor patterns) across EuropeanAmerican individuals (the majority in the United States) and ethnic minority indi-viduals. The most commonly used method for making this determination is one facetof the SEM, con ﬁrmatory factor analysis (CFA) also referred to as the “measurement
model ”(Hoyle & Smith, 1994). In other words, does the construct that is purportedly
measured by “X”tool in European Americans yield the same results in a speci ﬁc
ethnic minority population? Several studies have yielded promising results related topsychometric equivalence for various tools in the anxiety disorders literature for usewith ethnic minority populations. For instance, Chapman, Petrie, and Vines (2012)found that the factor structure of the Symptom Checklist 90 –Revised (SCL-90-R), a
commonly utilized measure of psychological distress, was equivalent in a sample ofAfrican American females. These results suggest that the SCL-90-R in its current formhas established empirical support for utilization in a community sample of AfricanAmerican females.
Other studies have examined measurement equivalence using similar methodology
with disparate ﬁndings when utilizing different measures. As mentioned earlier,
factor variance does not preclude the elimination of a measure; rather it may suggest
the need for a modi ﬁedversion of the measure. For instance, Melka and colleagues
(Melka, Lancaster, Adams, Howarth, & Rodriguez, 2010) examined the Fear ofNegative Evaluation Scale (FNE) and the Social Avoidance and Distress Scale(SAD) in a sample of non-Hispanic White and African American young adults andfound that several items on both measures needed to be omitted for the AfricanAmerican sample. Similarly, Chapman, Williams, Mast, and Woodruff-Borden (2009)Impact of Race, Ethnicity, and Culture 139

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investigated the original and other extant factor structures of the Beck AnxietyInventory (BAI), arguably the most widely used self-report measure for anxietysymptoms in general, in a sample of African American and non-Hispanic Whiteadults. Results revealed that the original factor structure was not equivalent in theAfrican American sample and that a 19-item version of the BAI best ﬁt the African
American sample (Chapman et al., 2009). Similar results have been obtained withother, widely utilized measures of family functioning (Family Assessment Device;Chapman & Woodruff-Borden, 2009), speci ﬁc phobias (Chapman, Kertz, Zurlage, &
Woodruff-Borden, 2008; Chapman, Vines, & Petrie, 2011), and perceived control overanxiety (Chapman, Kertz, & Woodruff-Borden, 2009), further underscoring theimportance of understanding cultural factors related to assessment in ethnic minorityindividuals.C
LINICAL UTILITY ASSESSMENT IN ETHNIC MINORITIES
In attempts to further understand which assessment tools have adequate clinicalutility in ethnic minority samples, other investigators have employed statisticaltechniques aimed at predicting the presence of psychopathology from screening tools.The extent to which screening tools are sensitive at predicting the presence or absenceof a speci ﬁc disorder, particularly in ethnic minority populations, has a number of
implications for clinical work. In short, the assessment process may be streamlinedthrough early detection of disorders, which in turn allows the clinician to spend moretime in (a) building rapport with ethnic minority clients and (b) engaging in time-limited, clinical intervention. Along these lines, a receiver operating characteristicanalysis (ROC) is one such method that has been heavily utilized to predict thepresence of various medical conditions (e.g., diagnosing breast cancer via digitalmammograms [Cole et al., 2004]; pneumonia detection [Lynch, Platt, Gouin, Larson, &Patenaude, 2004]) and psychiatric conditions (e.g., dexamethosone suppression testfor predicting major depressive disorder [Mossman & Somoza, 1989]; harm avoidancescores predicting generalized anxiety disorder [Rettew, Doyle, Kwan, Stanger, &Hudziak, 2006]; predicting PTSD with PTSD Checklist in female veterans [Lang,Laffaye, Satz, Dresselhaus, & Stein, 2003]).
Although a description of a ROC analysis is beyond the scope of this chapter, worth
noting is that the ROC analysis calculates an area under the curve (AUC), whichdetermines the suitability of a given measure as a screening tool, because it re ﬂects the
likelihood that a participant who meets criteria for a diagnosis selected at randomwill score higher on a measure than a randomly selected control participant (seeBredemeier et al., 2010). Moreover, a ROC analysis provides optimal cut scores forspeciﬁc measures in predicting the presence of particular disorders. In a more recent
investigation, Petrie, Chapman, and Vines (2013) investigated the sensitivity andspeciﬁcity of the Positive and Negative Affect Scales Expanded Form (PANAS-X)
at detecting social anxiety disorder in a sample of African American women. Resultssuggest that the PANAS-X is a clinically useful measure at predicting social anxietydisorder in African American females. More speci ﬁcally, a score above 11 on
the Negative Affect Scale of the PANAS-X indicates further examination (e.g.,a diagnostic interview) is warranted to assess the presence of social-anxiety disorder,whereas a score below 35 on the Positive Affect Scale reveals the need for further140 OVERVIEW

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examination to determine the presence of anyanxiety disorder. Chapman, Petrie, and
Richards (under review) yielded similar results with other measures predicting socialanxiety disorder, speci ﬁcally for the Social Phobia Scale (SPS; cut score of 6 >), Albany
Panic and Phobia Questionnaire (APPQ; score of 7 >), Social Interaction Scale (SIAS; cut
score of 15 >), and a social “fear factor ”from the Fear Survey Schedule –Second Edition
(FSS-II; cut score of 7 >). It should be noted that the social “fear factor ”(see Chapman
et al., 2008; Chapman et al., 2011) is composed of only four items.
Taken together, these results suggest that the assessment of sociocultural factors at
the beginning of treatment in addition to the utilization of assessment measures thatdemonstrate clinical utility in ethnic minority samples (or when modi ﬁcation is
necessary) is critically important to effective assessment. Readers are encouragedto further explore the aforementioned measures to further determine their clinicalutility in ethnic minority samples.
EXPRESSION/ASSESSMENT OF PSYCHOPATHOLOGY
Aside from the administration of culturally sensitive assessment tools to aid in theaccurate diagnosis of psychopathology among ethnic minority patients, extant litera-ture has implicated cultural factors endemic to ethnic groups that may in ﬂuence the
expression of their symptomology. In the following section, a general overview of howfactors, such as perceived discrimination and stigma of mental illness, impact variousforms of symptom expression among non-Western and Western ethnic groups ispresented.E
XPRESSION OF PSYCHOPATHOLOGY DIFFERS ACROSS CULTURAL GROUPS
It is often unclear how symptom proﬁ les may differ between ethnic groups when
typical research studies use structured instruments, based on an a priori set ofquestions believed to exemplify the disorder under investigation (Guarnaccia,1997). Measures based on Western notions of prototypical symptoms will fail tocapture cultural differences in the expression of all disorders. Thus, variations insymptom patterns are often overlooked or misunderstood. Such misunderstandingsaffect how we, in turn, conceptualize even seemingly well-de ﬁned disorders.
TheDSM-5 recognizes several cultural concepts of distress, or mental disorders that
are generally limited to speci ﬁc cultural groups for certain dysfunctional and/
or distressing behaviors, experiences, and observations (American Psychiatric Asso-ciation, 2013). However, many culture-bound syndromes are likely unrecognizedvariations of common Western ailments. For example, susto is a Latin American folkillness attributed to having an extremely frightening experience, thought to include“soul loss ”as part of the syndrome. People af ﬂicted with susto may have symptoms
that include nervousness, loss of appetite, insomnia, listlessness, despondency,involuntary muscle tics, and diarrhea. The symptoms of susto are actually quitesimilar to posttraumatic stress disorder (PTSD), which includes anxiety, avoidance,dissociation, jumpiness, sleep disturbances, and depression. When referring to soulloss within susto, a closer meaning to this may actually be loss of “vital force, “as the
soul is typically not thought to have actually left the body until death (Glazer, Baer,Weller, Garcia de Alba, & Liebowitz, 2004). This could resemble the fatigue andImpact of Race, Ethnicity, and Culture 141

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anhedonia, which may be a part of depressive symptoms within PTSD. Additionally,feeling as if one ’s soul has been lost may be an idiom of distress for dissociation.
Therefore, the concept of susto as a culture-bound syndrome may be better concep-tualized as a culture-speci ﬁc description of PTSD itself.
Interestingly, folk treatments for the disorder include elements of exposure-based
therapies for PTSD (e.g., Williams, Cahill, & Foa, 2010). During the treatment ritual,the individual af ﬂicted with susto must recount their terrifying experience while lying
on the axis of a cruci ﬁx on the ﬂoor. Fresh herbs are swept over the af ﬂicted
individual ’s body while the folk healer says a series of prayers (Gillette, 2013). Sugar,
water, and tea may also be used (Glazer et al., 2004). If the ﬁrst session is not effective,
the process is repeated every third day until the patient is recovered. This repeatedrecounting process is a critical active ingredient in prolonged exposure, a highlyeffective treatment for PTSD developed by Foa, Hembree, and Rothbaum (2007), andlikely accounts for the effectiveness of the folk remedy.
Another example of the connection between DSM disorders and culture-bound
syndromes can be seen in the enigmatic ailment called koro. Though uncommon inWestern cultures, koro is characterized by anxiety over the possibility of one ’s
genitalia receding into the body, resulting in infertility or death (Chowdhury,1990). To prevent any envisioned shrinkage or retraction of the genitals, a korosufferer will perform certain behaviors (i.e., pulling of genitals, spiritual rituals,securing genitals to prevent retraction) intended to reduce or eliminate this risk.
Obsessive-compulsive disorder (OCD) is characterized by distressing and typically
implausible obsessions, with compulsions designed to reduce the anxiety caused bythe obsessions. Davis, Steever, Terwilliger, & Williams (2012) note the possibility thatkoro is simply a form of OCD, as an alternative to the current classi ﬁcation as a culture-
bound syndrome. The most salient feature of koro concerns the anxiety surroundingthe retraction and shrinkage of genitalia. The degree to which this distress can impairthe daily functioning of those with koro has marked similarities to the construct ofobsessions in OCD. This, coupled with the improbability of one ’s genitalia actually
receding into one ’s body, makes it possible to categorize this fear as an obsession.
Sexual obsessions are extremely common in OCD worldwide (Williams & Steever,
in press), but these types of thoughts are considered taboo or embarrassing in mostcultures. Thus, the stigma and shame attached to the experience of sexual symptoms ofOCD is highly distressing (Gordon, 2002). Furthermore, Bernstein and Gaw (1990)note that sexual identity questions and con ﬂicting feelings about sexuality are
common in the experience of koro. Similarly, approximately 10% of treatment-seekingOCD patients report concerns about their sexual identity as a main concern(Williams & Farris, 2011). In OCD, these worries often manifest as fears of experienc-ing a change in sexual orientation, which is strikingly similar to the worries reported tounderlie many cases of koro. Finally, koro has been shown to respond well tobehavioral psychotherapy and medications like selective serotonin reuptake inhibitors(SSRIs; Buckle, Chuah, Fones, & Wong, 2007). These same treatments have long beenthe preferred method of treatment for OCD and its subtypes (e.g., NICE, 2005). Thus,koro is likely simply a cultural variant of OCD.
Although listed in DSM-5 as a culture-bound syndrome, neurasthenia, or shenjing
shuairuo, is currently a recognized mental disorder in the World Health Organiza-tion’sICD-10 and in the Chinese Classi ﬁcation of Mental Disorders. Traditional142 O
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Chinese medicine describes shenjing shuairuo as a depletion of vital energy andreduced functioning in critical internal organs. The Chinese Classi ﬁcation of Mental
Disorders considers it a mental disorder that may include weakness, emotionalsymptoms, excitement symptoms, tension-induced pain, and sleep disturbances.Neurasthenia has been considered a somatic illness, similar to or the same as majordepressive disorder, but involving culturally sanctioned idioms of distress (Shiraev &Levy, 2013).
Likewise, there are many conditions that may be considered Western culture-
bound syndromes, due to their infrequency or absence in other cultures. These mayinclude: anorexia nervosa, adolescence, drug abuse, chronic fatigue syndrome,animal hoarding, ADHD, Munchhausen by proxy, premenstrual syndromes, disso-ciative identity disorder, and even Typ e A personality. Many maintain that all
psychiatric disorders, regardless of culture, are always culturally in ﬂuenced con-
structs. Still oth ers assert that the DSM is in itself a culture-bound document and
question whether it should be used at all outside its country of origin (Nadkarni &Santhouse, 2012).E
XPRESSION OF PSYCHOPATHOLOGY DIFFERS WITHIN NATIONAL BORDERS
It may be misleading to present cultural differences in psychopathology as an issueonly applicable to those in non-Western or developing nations. The expression ofpsychopathology can and does differ among U.S. ethnic groups that may be consid-ered fairly acculturated (i.e., that share a common language and national borders).
For example, African Americans have been an integral part of American life for
centuries, yet notable differences in psychopathology are nonetheless evident. Arecent investigation of OCD in African Americans (Williams, Elstein, Buckner,Abelson, & Himle, 2012) found obsessive-compulsive concerns in six major areas,including (1) contamination and washing, (2) hoarding, (3) sexual obsessions andreassurance, (4) aggression and mental compulsions, (5) symmetry and perfectionism,and (6) doubt and checking. These dimensions are similar to ﬁndings of studies in
primarily White samples (i.e., Bloch et al., 2008). However, African Americans withOCD report more contamination symptoms and were twice as likely to reportexcessive concerns with animals compared to European Americans with OCD.This indicates notable cultural differences, which is consistent with ﬁndings among
nonclinical samples (e.g., Thomas, Turkheimer, & Oltmanns, 2000).
Williams and Turkheimer (2007) studied racial differences in OCD symptoms and
found that a nonclinical sample of African Americans scored signi ﬁcantly higher on an
animal attitude factor than European Americans, meaning they had greater concernsabout animals, and it was determined that cultural factors explained this difference. Itwas hypothesized that the Western perspective of animals as pets is more sociallyacceptable among European Americans than other cultures that are more likely toregard animals as a source of food or vehicle for labor. Other cultural differences mayrelate to the historic practices such as the use of dogs as a means to hunt slaves orattack protesters during the Civil Rights era. This is consistent with recent worksuggesting that African Americans may experience greater phobias of animals(Chapman et al., 2008). As such, cultural differences are plausible contributing factorsfor increased animal sensitivity among those with OCD.Impact of Race, Ethnicity, and Culture 143

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Fear of being misunderstood was also more frequently endorsed by African
Americans with OCD (Williams et al., 2012). An obsessive need to be perfectlyunderstood could be a unique ﬁnding for African Americans related to fears of
appearing unintelligent, resulting in stereotype compensation —an intentional effort to
present oneself in a counterstereotypical manner (Williams, Turkheimer, Magee, &Guterbock, 2008).P
REVALENCE RATESMAYDIFFER FOR CULTURAL REASONS
Prevalence rates of various disorders a lso may differ for cultural reasons. For
example, the National Survey of American Life (NSAL) conducted a comprehensivenationwide study of African American and Caribbean Blacks. They interviewed alarge number of adults ( n=5,191) and adolescents ( n=1,170) in their homes, using
professionally trained, ethnically matched interviewers. Their study was the ﬁrst to
examine the prevalence, age of onset, and g ender differences in a number of mental
disorders in a nationally representative Black sample (Taylor, Caldwell, Baser,
Faison, & Jackson, 2007).
Findings were consistent with previous research indicating that anorexia nervosa is
rare among African Americans. In fact, not a single woman in the study met criteria foranorexia in the previous 12 months, and there were no reports at all of anorexia inCaribbean adults. These ﬁndings indicate that Black Americans are at lower risk of
anorexia than their White counterparts. Likewise, a related study found that Hispanicand Asian American female adults experienced similarly low rates of anorexia nervosa(Franko, 2007). The authors of that study suggested that detection and barriers totreatment may be a factor in the lower rates, but there has been very little researchfocused on what cultural factors may differentially protect minorities from thisdisorder and yet promote it in European Americans.
Another way that culture may impact psychopathology can be found in the
frequencies of speciﬁ c symptoms within a disorder. For example, Chapman and
colleagues (Chapman et al., 2008; Chapman et al., 2011) found that both AfricanAmerican college students (2008) and African American adults from the community(2011) reported more animal and social fears than their European American counter-parts. These results indicate the need for further exploration of cultural factors andtheir impact on psychopathology.S
TIGMA AND SOMATIZATION OF DISTRESS ACROSS CULTURES
Although there is a general tendency toward somatization across all cultures, ethnicminority individuals in the United States appear more likely to express psychologicaldistress through bodily symptoms for two primary reasons: (1) as compared toEuropean Americans, there is a higher level of stigma associated with mental illnessand, therefore, physical symptoms are more socially acceptable, and (2) there is moreholistic conceptualization of the person, and, therefore, less of a distinction betweenmind and body among ethnic minorities (USDHHS, 2001).
For many groups there is considerable stigma attached to being af ﬂicted by mental
illness, and thus clients from these groups may be more comfortable reportingphysical symptoms over affective and cognitive symptoms. One study of African144 OVERVIEW

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Americans found that concerns about stigma prompted most mental health careconsumers to initially avoid or delay treatment, and once in treatment, they commonlyfaced stigmatizing reactions from others (Alvidrez, Snowden, & Kaiser, 2008). Hunterand Schmidt (2010) developed a model that incorporates stigma, racism, and somati-zation into the expression of anxiety in African Americans. The emphasis on physicalillnesses over mental illness in African American communities is thought to be relatedto physical explanations of somatic symptoms of anxiety, including attributing theseto conditions like cardiovascular disease, and subsequent help seeking oriented tothese explanations. In particular, anxiety disorders among African Americans arelikely to include both fears related to minority status and catastrophic interpretationsof somatic symptoms. They propose that these differences, because of their implica-tions for measurement and diagnosis, can explain reduced detection of certain anxietydisorders in African Americans compared with European Americans.
Western models of health and illness often depict a fragmented representation of
the person to conceptualize mental and p hysical processes. For example the mind
and body are regarded as separate (called dualism ), and then the mind is even further
divided in many common models (e.g., psychodynamic personality model of id,ego, and superego; cognitive behavioral therapy ’s affective, behavioral, and cogni-
tive components). However, many cultures do not make a distinction between themind and body. Additionally, many cultural traditions recognize the spirit as anintegral part of the person, inseparable f rom the mind and body (e.g., Parham, 2002).
Thus, omitting this component will reduce the salience of the treatment in suchclients.S
PIRITUALITY AND RELIGION
Spirituality and religious beliefs can be the most important facets of a person ’s
identity, thus appreciating spiritual and religious diversity is essential to multiculturalcompetency. In North America, 97% of adults profess spiritual beliefs, and 85% of thepopulation is Christian; of these, 65% say their beliefs are central to their lives(Shiraev & Levy, 2013). When help is sought, clients typically look for someonewho shares the same values. Thus, therapists will be viewed as more credible in thecommunity if competent in religious/spiritual issues.
Devout or orthodox members of most religious traditions tend to have negative
perceptions of the mental health profession s, distrust therapists, and underutilize
mental health services. This is in part because traditionally the ﬁeld of psychology
has been hostile toward religion. Psychologists are more secular and less religiousthan the population at large, and therapis ts have tended to reject organized religious
involvement; thus, there is a religiosity gap between mental health providers and
the U.S. majority. As a result, building tr ust may be challenging when working with
devout clients, and, in such cases, learning about a client ’s religious tradition is
essential to building rapport. At the very least, it is essential for therapists to avoidinterventions that conﬂ ict with normative religious beliefs. Therapists need to be
able to understand individuals and thei r beliefs within their cultural context
(Richards, Keller, & Smith, 2004).
Over the past few years, an uneasy truce has developed between psychology and
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mental health and well-being. For example, meditation and prayer are correlated withreduced blood pressure and pulse, lower endocrine activity, and lower metabolism.Religious involvement has also been shown to buffer against emotional dif ﬁculties,
such as depression and anger. Thus a variety of psychological and spiritual interven-tions may be appropriate with religious clients, depending on the client, the nature ofthe problem, and the therapist’ s religious af ﬁliation.
R
ACISM AND DISCRIMINATION
As previously noted, the experience of being a stigmatized ethnoracial minority is acommon phenomenon across cultures, with profound implications for mental health.This includes visible minorities in the United States and Canada, as well as ethnic andcultural groups in other countries, such as Blacks in the United Kingdom, Turks inGermany, and the Dalit in India. Many studies have established a link betweendiscrimination and mental health outcomes. In the United States, African Americansexperience the most racial discrimination, followed by Asian Americans and HispanicAmericans (Chou et al., 2012). Perceived discrimination has been found to benegatively correlated with mental health, and the effects seem to be strongest(most detrimental) for Asian Americans, followed by Hispanic Americans, followedby African Americans (Cokley, Hall-Clark, & Hicks, 2011).
In addition to overall psychological distress, racism and discrimination have been
associated with several speci ﬁc mental health problems, including stress (Clark,
Anderson, Clark, & Williams, 1999), depression (Banks & Kohn-Wood, 2007; Torres,Driscoll, & Burrow, 2010), anxiety (Hunter & Schmidt, 2010), binge drinking (Blume,Lovato, Thyken, & Denny, 2012), and PTSD (Carter, 2007; Pieterse, Todd, Neville, &Carter, 2012). A strong, positive ethnic identity has been shown to be a potentialprotective factor against psychopathology among minorities (e.g., Williams,Chapman, et al., 2012), except when discriminatory events are severe (Chae, Lincoln, &Jackson, 2011). Failure to understand the role of racism and discrimination limits ourunderstanding of mental health in stigmatized people groups.
Focusing speci ﬁcally on the link between racism and PTSD can help us understand
how Eurocentric models may sometimes be inadequate for identifying distress inminority populations. The criteria for a PTSD diagnosis implies that a traumatizingevent must be negative and uncontrollable, whereby an individual ’s physical well-
being is threatened (American Psychiatric Association, 2000). Although this descrip-tion may address many forms of ethnoracially motivated traumatic events, it does nottake into account ongoing low levels of racism that can lead to a general sense ofdistress and uncontrollability (Carter, 2007). These experiences, though they maynot be physical in nature, attack the individual ’s identity and force the person to
re-experience traumas associated with their culture ’s history (Helms, Nicholas, &
Green, 2010).
Previous editions of the DSM recognized racism as trauma only when an individual
met criteria for PTSD in relation to a discrete racist event. This is problematic giventhat many minorities experience cumulative experiences of racism as traumatic, with adiscrete event acting as “the last straw ”triggering trauma reactions (Carter, 2007).
Thus, current conceptualizations of trauma as a discrete horri ﬁc event may be limiting
for minorities. Recent changes to the DSM may open the door for wider recognition of146 O
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racism-related trauma. It is now within criteria that a person can have PTSD fromlearning about a traumatic event involving a close friend or family member, or if aperson is repeatedly exposed to details about trauma (APA, 2013). This couldencompass trauma resulting from ongoing racial stressors (Malcoun, Williams, &Bahojb Nouri, in press).
Moreover, existing PTSD measures aimed at identifying an index trauma fail to
include racism among listed choice response options, leaving such events to bereported as “other ”or made to ﬁt into an existing category that may not fully capture
the nature of the trauma (e.g., physical assault). This can be especially problematicsince minorities may be reluctant to report experiences of racism to EuropeanAmerican therapists (Carter, 2007), who comprise the majority of mental healthclinicians in the United States (U.S. Department of Labor, 2012). Minority clientsalso may not link current PTSD symptoms to a single experience of racism if theirsymptoms relate to cumulative experiences of discrimination.
Bryant-Davis and Ocampo (2005) noted the similar courses of psychopathology
between rape victims and victims of racism. Similar to rape victims, race-relatedtrauma victims may respond with dissociation or shock, which can prevent them fromresponding to the incident in a functional manner. Victims may then feel shame andself-blame because they were unable to respond or defend themselves, which maylead to poor self-concept or self-destructive behaviors (Bryant-Davis & Ocampo, 2005).In the same investigation, a parallel was drawn between race-related trauma victimsand victims of domestic violence. In both situations, survivors may feel shame overallowing themselves to be victimized.L
ANGUAGE AND SYMPTOM EXPRESSION
Another in ﬂuence on symptom expression is the language used by clinician and client
(Diaz et al., 2009). Malgady and Constantino (1998) examined the in ﬂuence of
language by experimentally varying the language spoken during an assessmentinterview with Hispanic clinicians. They found that severity of psychopathologywas found to be highest in the bilingual condition, followed by the Spanish-speakingcondition, and then the English-speaking condition. There was a tendency for clini-cians to rate Latino clients speaking Spanish or Spanish and English as having moresevere psychopathology and as functioning less well than Latino clients speakingEnglish only. It was not clear whether this bias was in the form of overpathologizingon the clinicians ’part or whether they are more sensitive to clients ’presenting
symptoms when assessing in Spanish. Nevertheless, there appears to be an importanteffect of language on diagnosis of psychopathology.
TREATMENT ISSUES
The understanding of the role of culture, race, and ethnicity on treatment isconsiderably important when working with ethnic minority patients. In the follow-ing section, a discussion of how such factors can in ﬂuence various domains of the
treatment process (e.g., therapeutic allianc e, clinical judgments, and client perspec-
tives) is presented. It is worth noting that the following treatment considerations arenot comprehensive, but rather a general overview of how acknowledging the impactImpact of Race, Ethnicity, and Culture 147

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of certain cultural factors when working with ethnic minority p atients can enhance
the ef ﬁciency and effectiven ess of treatment.
CLINICIAN AND CLIENT INTERPLAY
Many clients feel more comfortable discussing psychological problems with someoneof the same ethnoracial background (e.g., Jackson et al., 2004), and they may answerquestions about symptoms differently when ethnoracially matched (e.g., Williams &Turkheimer, 2007). Research shows that most people prefer to be matched to someoneof the same ethnicity. Ethnic minority clients may perceive their counseling experienceto be more effective when they are ethnoracially matched (Lee, Sutton, France, &Uhlemann, 1983), and European American clients may feel more comfortable withsomeone of the same ethnoracial group (Davis, Williams, & Chapman, 2011). Match-ing has been shown to strengthen the therapeutic alliance and improve retention(Flicker, Waldron, Turner, Brody, & Hops, 2008). However, cultural matching is notalways possible due to a lack of availability of a clinician of the same ethnicity as theclient, and it may not be desirable from the client ’s perspective (e.g., could be perceived
as“forced segregation ”; Pole, Gone, & Kulkarni, 2008). Furthermore, unmatched dyads
provide an opportunity for expanded awareness and greater cross-cultural under-standing in both the client and therapist. Thus cross-cultural training is essential for allclinicians (Williams, Tellawi, Wetterneck, & Chapman, in press).
Cultural traditions vary about the manner in which clinicians are regarded. Many
consider therapists authority ﬁgures and will feel uncomfortable challenging or
disagreeing with their clinician. For example, when a Japanese client enters aconsulting room, it is common for the client to just sit very tensely in front of thetherapist and calmly answer questions. Japanese clients typically want to performideally, and this is re ﬂected in therapist-client relationship. Clients tell the therapist
their issues, and then just wait for the therapist to analyze them. Clients expect thetherapist to tell them what to do. From a Western viewpoint, this can be seen asdependent, but it is actually a way for Japanese people to show respect by givingpower to those in authority. European American therapists can ﬁnd it dif ﬁcult to work
with Japanese clients if the therapist is not aware of the power dynamics within theJapanese culture. When the Japanese utilize psychotherapy services, they generallyapply Japanese methods of forming relationships, creating a hierarchical relationshipbetween client and therapist. A Japanese client was assessed by a Western therapistwithout this understanding and the therapist believed the client had no sense of self,describing the client as passive, needy, and repressed. Japanese clients sometimesappear helpless and this might be misinterpreted as playing a victim role. However,from the client ’s view, it is considered culturally appropriate (Nipoda, 2002).
This example also illustrates how cultures differ in terms of what they consider to be
the role of the therapist or healer. For example, within the Afrocentric framework, theessence of all things is spiritual. The spirit is energy and life force in each person, whichconstitutes a self-healing power. Thus, therapy becomes a process or vehicle in whichindividuals are helped to access their own self-healing power (Parham, 2002). This wasillustrated in a recent study of male African American outpatients being treated fordepression. Psychotherapy was viewed helpful only in that therapists helped clientsto identify methods for improving their individual will and agency. For example,148 OVERVIEW

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psychotherapy may help one to express feelings, discuss consequences of one ’s
actions, or understand why past events occurred or how past events impact reactionsto current dif ﬁcult life situations. The therapist was regarded as a vehicle for change
rather than an agent of change (Casiano, McMickens, Williams, & Epperson, underreview). Clients had learned to access their own self-healing power.R
OLE OF STEREOTYPES ,BIASES,AND THE CLINICIAN ’SCULTURE
Although most clinicians are now receiving some multicultural education in theirtraining programs (Green, Callands, Radcliffe, Luebbe, & Klonoff, 2009), practicalskills for working with members of speci ﬁc minority groups are often not included.
When clinicians and researchers lack the needed skills and education for effectivecross-cultural interactions, they may rely on a colorblind approach. Colorblindness is
the ideology that different ethnoracia l groups should all be treated the same,
without regard to cultural differences (Terwilliger, Bach, Bryan, & Williams,2013). Minorities are often treated as if th ey lack characteristics that make them
different from the dominant majority. Alth o u g ht h ei n t e n to fc o l o r b l i n d n e s si st o
promote fairness, it often cau ses confusion and can paradoxically increase prejudice
(e.g., Richeson & Nussbaum, 2004). When the idea of “treating everyone the same ”
is proposed, it is typically from the perspective of the dominant majority, implyingthat clients should be treated as if they were culturally European American(Terwilliger et al., 2013).
From a clinical standpoint, colorblindness could result in negative consequences for
an ethnic minority client if a therapist were to suggest that the client engage inbehaviors that are generally considered adaptive within European American psycho-logical tradition but that may in fact be culturally incongruent outside of that tradition.For example, a therapist may encourage an adult client to move out of the parents ’
home and ﬁnd his or her own apartment to assert autonomy. But in more collectivistic
cultures, it may be abnormal for unmarried children to move out. Thus such an eventcould potentially result in a family crisis, con ﬂict, and loss of needed emotional
support. The goal, therefore, is not to treat participants as if they were EuropeanAmerican, but as they should be treated based on the norms and customs of theirparticular culture. This approach, called multiculturalism , embraces the differences,
strengths, and uniqueness of each cultural group (Terwilliger et al., 2013; Williamset al., in press).
Another issue of which clinicians must be aware concerns preconceived notions
about clients based solely on ethnic group membership, or pathological stereotypes(Williams, Gooden, & Davis, 2012). These are generalizations about people used as ameans of explaining and justifying differences between groups and thereby usingthese differences to oppress the “out-group. ”Social status or group position deter-
mines the content of stereotypes, and not actual personal characteristics of groupmembers (Jost & Banaji, 1994). Groups that have fewer social and economic advan-tages will be stereotyped in a way that seemingly explains disparities, such as loweremployment or higher illiteracy rates. Although disadvantaged group members mayhave greater difﬁ culty ﬁnding a job due to in-group favoritism, discrimination, and
institutional racism, the disadvantaged group member is characterized asunmotivated (could have found a job if he looked hard enough), unintelligent (notImpact of Race, Ethnicity, and Culture 149

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smart enough to have that job), lazy (would rather take handouts than work), andcriminal (will steal rather than work) (Williams, Gooden, & Davis, 2012).
It is important to understand that pathological stereotypes about cultural groups
are unfair and inaccurate. Furthermore, all members of a society are affected by thenegative social messages that espouse these stereotypes, casting disadvantagedgroups in a negative light (Devine & Elliot, 1995). When we uncritically accept thesenegative messages, racism follows, even from professionals who mean well. This canlead to harmful, discriminatory behaviors toward clients, which may be conscious orunconscious, and overt or covert.
Perhaps the most common act of discrimination by clinicians is what is termed as
themicroaggression (Sue et al., 2007). A microaggression is a brief, everyday exchange
that sends denigrating messages to a target simply because they belong to a racialminority group. Microaggressions are often unconsciously delivered in the form ofslights or subtle dismissive behaviors. The target of a microaggression is often forcedto ascertain whether another individual did, in fact, perpetrate a discriminatory act.This attributional ambiguity is inherently stressful and is different from an overtdiscriminatory act, which is more easily identi ﬁed and explained. As such, the
inﬂuence of racial microaggressions on stress and anxiety may lie in the uncertainty
generated from such interactions (Torres et al., 2010). One study found that racialmicroaggressions directed against African American clients was predictive of aweaker therapeutic alliance with White therapists. This, in turn, predicted lowerratings of general competence and multicultural counseling competence, andunsurprisingly lower counseling satisfaction ratings. Racial microaggressions had asigniﬁcant indirect effect on client ratings of White counselors ’counseling competence
through the therapeutic working alliance (Constantine, 2007).
It is important to understand that microagressions can be particularly harmful to
vulnerable clients, who may already feel stigmatized and exposed even attemptingtherapy. Minority clients may ﬁnd it dif ﬁcult to respond to such remarks in counseling
situations due to self-doubt and power dynamics. These problems contribute tofeelings of distance from the therapist, unwillingness to disclose sensitive information,and early termination from treatment. Thus, clients may be unable to overcome thecondition for which they sought help due to undesirable therapist factors. The degreeof harm therapists may cause in this manner is unknown and likely underestimated(Constantine, 2007).C
ULTURE AS AN INTEGRAL PART OF ASSESSMENT
Americans are socialized not to acknowledge race and ethnicity, due in part toconcerns of appearing biased or racist (Gaertner & Dovidio, 2005). However, thisavoidance contributes to dif ﬁculty recognizing, discussing, and adapting to cultural
differences (Terwilliger et al., 2013). Many European American therapists areuncomfortable discussing race in cross-racial therapeutic dyads (Knox, Burkard,Johnson, Suzuki, & Ponterotto, 2003). However, therapists actually have more successworking cross-culturally when they address differences directly. Raising the issue ofrace early in the therapeutic relationship conveys cultural sensitivity and may addressclients ’concerns about a racially different counselor. When counselors communicate
their own cultural background and acknowledge their client ’s cultural values, clients150 O
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are more likely to see their counselor as credible and feel more relaxed in therapy(Owen, Tao, Leach, & Rodolfa, 2011). Culturally competent counselors are aware ofhow their own cultural backgrounds and experiences in ﬂuence their attitudes and
values surrounding psychological processes, and this recognition enables them tobetter access the client ’s needs (Delsignore, Petrova, Harper, Stowe, Mu’ Min, &
Middleton, 2010).
Thus, it is important that clinicians understand culture-speci ﬁc differences, which
can range from amount of eye contact to speci ﬁc idioms of psychological distress.
Mental health professionals must make culture an integral part of each assessment as itinﬂuences patterns of communication between clinician and patient and subsequent
diagnostic and treatment outcomes (Alarcón et al., 2009; Williams et al., in press).There are too many different groups for any one person to have an in-depth under-standing of all, so clinicians should at least receive training speci ﬁc to the ethnoracial
groups most commonly served, and seek additional information and consultationwhen confronted with clients from completely foreign cultures.
In its ongoing effort to more widely recognize cultural context, the DSM-5 now
includes a cultural formulation interview guide designed to help clinicians assesscultural factors inﬂ uencing client perspectives on their symptoms and treatment
options. It includes questions about client background in terms of culture, race,ethnicity, religion, and geographical origin. The interview facilitates the process forindividuals to describe distress in their own words and then relate this to how others,who may not share their culture, see their dif ﬁculties. This gives the clinician a more
comprehensive basis for diagnosis and care, and may be a good starting point for thoseclinicians working with ethnically different clients.M
ISTRUST OF MEDICAL INSTITUTIONS AND ESTABLISHMENT
According to the U.S. Surgeon General, “research documents that many members of
minority groups fear, or feel ill at ease, with the mental health system ”(NIH, 1999).
African Americans have greater distrust of the medical establishment and mentalhealth care, many believing that medical institutions hold racist attitudes (Gamble,1993; Whaley, 2001). Negative perceptions may be rooted in historical abuses of slaves,who were often used to test and perfect medical procedures before they wereattempted on Whites (Gamble, 1997).
The most well-known example of such abuses is The Tuskegee Study of Untreated
Syphilis in the African American Male. This is the longest nontherapeutic experimenton human beings in medical history. Begun in 1932 by the United States Public HealthService (USPHS), the study was designed to determine the natural course of untreatedsyphilis in 400 African American men in Tuskegee, Alabama. The research subjects,who had syphilis when they were enrolled in the study, were matched against 200uninfected subjects who served as controls (Heintzelman, 2003).
The subjects were recruited with misleading promises of “special free treatment, ”
which were actually spinal taps done without anesthesia to study the neurologicaleffects of syphilis, and they were enrolled without informed consent. The subjectswere denied antibiotic therapy when it became clear in the 1940s that penicillin was aneffective treatment for the disease. On several occasions, the USPHS actually interferedto prevent subjects from obtaining treatment elsewhere (Heintzelman, 2003).Impact of Race, Ethnicity, and Culture 151

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In many cases, the infected subjects passed the disease to their wives and subse-
quently newborn babies. Over 100 people died directly from advanced syphilis. InAugust 1972 an investigatory panel found the study was ethically unjustiﬁ ed and that
penicillin should have been provided. The National Research Act, passed in 1974,mandated that all federally funded proposed research with human subjects beapproved by an institutional review board (IRB). By 1992, settlement payments ofapproximately $40,000 were made to survivors. President Clinton publicly apologizedon behalf of the federal government to the handful of study survivors in April 1997(Heintzelman, 2003).
Many African Americans see the Tuskegee Study as representative of much current
medical research even today (Freimuth et al., 2001). For instance, one study examinedattitudes toward biomedical research across four ethnically diverse adult samplesand found that African Americans endorsed more fear of participation in researchthan non-Hispanic White adults, which suggests that a cultural mistrust of researchremains salient among African Americans (Katz et al., 2006). Most importantly, incases where ethnic minorities appear hesitant or distrusting of mental health care, it isimportant for mental health professionals to remember the historical signi ﬁcance of a
cultural mistrust in health care systems. Cultural knowledge of institutional abuses,combined with regular experiences of racism, maintains cultural mistrust surroundinghealth care.L
ACK OF AWARENESS CANRESULT IN MISDIAGNOSIS
Evidence shows that minorities are often misdiagnosed, due to the factors describedpreviously. These include:
Misuse of assessment instruments that are considered to be “gold standards. ”
Diagnostic criteria based on Eurocentric observations and conceptualizations,resulting in missed or misunderstood symptoms.
Research ﬁndings based on Eurocentric diagnostic criteria, providing less
helpful information about psychopathology in non-White populations.
Lack of adequate multicultural training for clinicians, often resulting in aproblematic colorblind approach.
Pathological stereotypes about members of speci ﬁc cultural groups that affect
clinician judgments.
Poor therapeutic working alliance due to lack of cultural awareness and micro-aggressions against clients.
These problems are not simply academic, but result in substandard care,
inappropriate treatments, and premature termination from treatment. For example,research shows that African Americans and Hispanic Americans are often over-diagnosed with psychotic disorders, and underdiagnosed with mood disorders. Inparticular, African Americans are more often given the diagnosis of paranoid schizo-phrenia than European Americans with similar symptoms (Snowden & Pingitore,2002). This could be due in part to misinterpretation by clinicians of “healthy cultural
paranoia ”—a defensive posture taken by African Americans when approaching a new
situation that could involve racism or discrimination (Whaley, 2001). This paranoia isnot completely unfounded given the reality of discrimination and racial tensions in the152 OVERVIEW

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United States. Additionally, African Americans are more likely to be admitted asinpatients, even after controlling for severity of illness and demographic variables(Snowden, Hastings, & Alvidrez, 2009).
For Hispanic Americans the research results are mixed. Chui (1996) ﬁnds that
Hispanics receive a diagnosis of schizophrenia less often than African Americans andnon-Hispanic Whites, but they more often receive diagnoses of other mental illnesses.Solomon (1992) reports that more Puerto Ricans are diagnosed schizophrenic than anyother group, including other Hispanics. This could be due to the intersection of raceand ethnicity as many Puerto Ricans are both Black and Hispanic. Furthermore, whenminorities are diagnosed with psychotic or affective disorders the conditions are morelikely to be considered chronic, rather than acute when compared to EuropeanAmericans with the same diagnoses.
Likewise, assessments of dangerousness and potential for violence are overesti-
mated for African American inpatients, in accordance with violent and criminalstereotypes (Good, 1996; Wood, Garb, Lilienfeld, & Nezworski, 2002). One resultof this bias is the overmedication of Black psychiatric patients (Wood et al., 2002). Thisis compounded by the fact African Americans, like many other ethnic minorities,metabolize antidepressants and antipsychotic medications more slowly than Whitesand may be more sensitive to the medications. This higher sensitivity is manifested in afaster and higher rate of response and more severe side effects, including deliriumwhen treated with doses commonly used for White patients (Munoz & Hilgenberg,2006). Thus, African Americans may exhibit poorer medication compliance, whichthen may be misinterpreted as resistance to treatment.
Interestingly, Hispanic Americans are less likely to be medicated at all (Hodgkin,
Volpe-Vartanian, & Alegría, 2007). Aside from limited health care access amongLatino populations (Perez-Escamilla, 2010), another potential explanation could be alack of adherence to medication throughout the course of mental illness (Hodgkinet al., 2007; Colby, Wang, Chhabra, & Pérez-Escamilla, 2012). In particular, Hodgkinand colleagues (2007) utilized data from the National Latino and Asian AmericanStudy (NLAAS) and found that 18.9% of Hispanic Americans who discontinuedantidepressant medication decided to do so without consulting a health professional.Researchers noted that possessing English-language pro ﬁciency, older age, being
married, having insurance, and consistent visits to see a therapist were related to betterantidepressant adherence in this sample.
African Americans are diagnosed less accurately than European Americans when
they are suffering from depression and seen in primary care (Borowsky et al., 2000), orwhen they are seen for psychiatric evaluation in an emergency room (Strakowski et al.,1997). One study found that African Americans were less likely than Whites to receivean antidepressant when their depression was ﬁrst diagnosed (27% versus 44%), and
among those who did receive antidepressant medications, African Americans wereless likely to receive the newer SSRI medications than were the White patients (Mel ﬁ,
Croghan, & Hanna, 2000).
In terms of substance abuse, 15% of the general population will abuse a substance in
their lifetime and 4% will abuse a substance within 12 months (Kessler et al., 2005a;Kessler et al., 2005b). Negative social stereotypes dictate that drug users are largelyBlack and Hispanic. Most people are surprised to learn that African American youthare signi ﬁcantly less likely to use tobacco, alcohol, or drugs than European AmericansImpact of Race, Ethnicity, and Culture 153

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or Hispanic Americans (Centers for Disease Control, 2000). In fact, African Americansspend 25% less than Whites on alcohol (U.S. Department of Labor, 2002). The NationalLongitudinal Alcohol Epidemiological Survey indicated that Whites were more likelyto use drugs over their lifetime but Blacks were more dependent than Whites,underscoring differential access to effective treatments (Grant, 1996). Blacks andWhites tend to abuse different drugs (e.g., crack versus cocaine), and the drugs usedby African Americans carry harsher penalties and are more likely to be the targets oflaw enforcement efforts (e.g., Beckett, Nyrop, & P ﬁngst, 2006). Thus, institutionalized
racism may play a role in drug abuse outcomes and access to treatment.
CONCLUSIONS
This chapter represents a charge to mental health professionals to fully consider andsubsequently integrate racial, ethnic, and cultural variables into inevitable work withethnic minority individuals. The importance of such integration undoubtedly has aprofound impact on several areas including but not limited to the following: assess-ment, expression of psychopathology, diagnostic practices, mental health disparities,treatment outcome studies, continued dearth of ethnic minorities involved in researchstudies, and a continued paucity of researchers and practitioners of color. Explicitacknowledgment of inherent biases that we all possess in addition to understanding theimportance of incorporating cultural variables throughout allportions of our work with
ethnic minority populations are important ﬁrst steps to decreasing mental health
disparities. Additionally, we continue to underscore the importance of reviewingthe empirical literature as it pertains to ethnic minority populations since “all measures
arenotcreated equal. ”Moreover, there continues to be a disconnect between much of
our scienti ﬁc training with regard to making decisions about assessment measures, how
psychopathology is expressed in many ethnic minority individuals, which often devi-ates from “traditional ”expressions, and our subsequent implementation of treatment.
Although signi ﬁcant strides have been made in the more recent empirical literature
endemic to ethnic minority individuals, we as mental health professionals have to beincreasingly cognizant of integrating identi ﬁed cultural factors throughout all facets of
both our own work and in training the next generation. Ethnoracial minorities arecurrently 36.6% of the U.S. population, and 50.4% of all births (U.S. Census Bureau,2011, 2012), with non-Hispanic Whites projected to be a minority in the United Statesby 2050 (Nagayama Hall, 2001). Thus, much of the work that we have highlighted isvitally important to our cultural competence in the 21st century.
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Annual Review of Psychology ,53,519–543.
Yip, T.,
Gee, G. C., & Takeuchi, D. T. (2008). Racial discrimination and psychological distress:
The impact of ethnic identity and age among immigrant and United States-born Asian adults.Developmental Psychology ,44(3), 787 –800.
Yoon, E., Chang, C., Kim, S., Clawson, A., Cleary, S. E., Hansen, M., . . . Gomes, A. M. (2013). A
meta-analysis of acculturation/enculturation and mental health. Journal of Counseling Psy-
chology ,60(1), 15 –30.162 O VERVIEW

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PART II
SPECIFIC DISORDERS

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CHAPTER 5
Schizophrenia
DENNIS R. COMBS, KIM T. MUESER, and EMILY DRAKE
INTRODUCTION
Schizophrenia is the most debilitating and costly of all adult psychiatric illnesses.Despite the recent trend toward community-oriented treatment, about 25% of allpsychiatric hospital beds are occupied by persons with schizophrenia. The costs oftreating schizophrenia are signi ﬁcant in terms of both ﬁnancial and personal costs.
It was estimated that the ﬁscal cost of schizophrenia in the United States was
$62.7 billion in 2002 (Wu et al., 2005) and $6.85 billion in Canada in 2004 (Goereeet al., 2005). About one-third (roughly 22.7 billion) of the U.S. dollars spent onschizophrenia is directed to the treatment and medical needs of this population.Despite the economic costs, the impact on the person ’s social and occupational
functioning over a lifetime may be even more devastating (Knapp, Mangalore, &Simon, 2004). In fact, the largest indirect cost associated with schizophrenia is the lossof productivity over the lifetime. The burden of schizophrenia places the disorder asone of the top 10 most disabling conditions in the world in terms of illness-adjusted lifeyears (Mueser & McGurk, 2004; Murray & Lopez, 1996). Even when persons withschizophrenia receive optimal treatments, many continue to experience substantialimpairments throughout most of their lives.
Since schizophrenia was ﬁrst described more than 100 years ago, the nature of the
disorder has been hotly debated, and public misconceptions about it have beencommonplace. In recent years, there has been a growing consensus among cliniciansand researchers to more rigorously de ﬁne the psychopathology and diagnostic
features of this disorder. Once referred to as a “wastebasket diagnosis, ”the term
schizophrenia is now used to describe a speciﬁ c clinical syndrome. Current arguments
about the disorder have focused on the validity of the diagnostic category ofschizophrenia, and alternative models argue that it is more bene ﬁcial to focus on
psychotic symptoms (e.g., paranoia, hallucinations, and delusions) (Bentall, Jackson, &Pilgrim, 1988). Nonetheless, an understanding of the core clinical features of schizo-phrenia is necessary for diagnosis and treatment planning. After many years ofstruggling to improve the long-term course of schizophrenia, there is now abundantevidence that combined pharmacological and psychosocial interventions can have amajor impact on improving functioning. This chapter provides an up-to-date review
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of schizophrenia, with a particular focus on the psychopathology of the illness and itsimpact on other domains of functioning.
DESCRIPTION OF THE DISORDER
Schizophrenia is characterized by impairments in social functioning, including dif ﬁ-
culty establishing and maintaining interpersonal relationships, problems working orfulﬁlling other instrumental roles (e.g., student, homemaker, employee), and dif ﬁcul-
ties caring for oneself (e.g., poor grooming and hygiene). These problems in dailyliving, in the absence of signi ﬁcant impairment in intellectual functioning, are the most
distinguishing characteristics of schizophrenia and are a necessary criterion for itsdiagnosis according to most diagnostic systems (e.g., American Psychiatric Associa-tion [APA], 2013). Consequently, many individuals with the illness depend on othersto meet their daily living needs. For example, estimates suggest that between 25% and60% of persons with schizophrenia live with relatives, and an even higher percentagerely on relatives for caregiving (Goldman, 1982; Torrey, 2001). Time spent providingsupport and care for a person with schizophrenia can be substantial (with reports ashigh as 6 to 9 hours per day for some families; Magliano et al., 1998). It appears that theemotional and physical burden on caregivers is found across cultures (Breitborde,Lopez, Chang, Kopelowicz, & Zarate, 2009; Huang, Hung, Sun, Lin, & Chen, 2009;Zahid & Ohaeri, 2010). Individuals without family support typically rely on mentalhealth, residential, and case management services to get their basic needs met. In theworst-case scenario, persons with schizophrenia who have insuf ﬁcient contact with
relatives and who fall between the cracks of the social service delivery system end upin jail (Torrey et al., 1992) or become homeless, with between 10% and 20% of homelesspersons having schizophrenia (Susser, Stuening, & Conover, 1989).
In addition to the problems of daily living that characterize schizophrenia, individ-
uals with the illness experience a range of different symptoms. The most commonsymptoms include positive symptoms (e.g., hallucinations, delusions, disorganization),negative symptoms (e.g., social withdrawal, apathy, anhedonia, poverty of speech),cognitive impairments (e.g., memory dif ﬁculties, planning ability, abstract thinking),
and problems with mood (e.g., depression, anxiety, anger). The speci ﬁc nature of these
symptoms is described in greater detail in the following section. The symptoms ofschizophrenia appear to account for some, but not all, of the problems in socialfunctioning (Glynn, 1998).
The various impairments associated with schizophrenia tend to be long term,
punctuated by ﬂuctuations in severity (i.e., relapse) over time. For this reason,
schizophrenia has a broad impact on the family, and individuals are often impededfrom pursuing personal life goals. Despite the severity of the disorder, advances in thetreatment of schizophrenia provide solid hope for improving the outcome.
CLINICAL PICTURE
Most studies on the dimensions of schizophrenia agree on at least three major groupsof symptoms (Liddle, 1987; Mueser, Curran, & McHugo, 1997; Van Der Does,Dingemans, Linszen, Nugter, & Scholte, 1993), including positive symptoms, negativesymptoms, and cognitive impairments. Positive symptoms refer to thoughts, sensory166 SPECIFIC DISORDERS

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experiences, and behaviors that are present in persons with the disorder but areordinarily absent in persons without the illness. Common examples of positivesymptoms include hallucinations (e.g., hearing voices, seeing visions), delusions(e.g., believing that others are persecuting the person), and bizarre, disorganizedbehavior (e.g., maintaining a peculiar posture for no apparent reason, wearingmultiple layers of clothes). Persecutory delusions (i.e., belief that some entity, group,or person has clear ongoing or future intentions to harm the person) are the mostcommon type of delusion found in schizophrenia (Appelbaum, Robbins, & Roth, 1999;as reviewed in Bentall, Corcoran, Howard, Blackwood, & Kinderman, 2001). About75% of persons with schizophrenia report hallucinations (Cutting, 1995). Auditoryhallucinations are the most common form and are frequently derogatory, negative, orabusive, although some can be benevolent, comforting, and kind (Chadwick &Birchwood, 1995; Copolov, Mackinnon, & Trauer, 2004; Cutting, 1995). Less frequent,but more speci ﬁc to schizophrenia, are voices that keep a running commentary on the
person ’s actions or consist of two or more voices having a conversation. Auditory
hallucinations can range from inaudible sounds (buzzing sounds, noises, muf ﬂed
speech) or clearly perceived voices of either gender and can occur intermittently or ona continuous basis. It has been assumed that visual hallucinations were infrequent inschizophrenia and were more re ﬂective of a medical condition (prevalence of 10% to
15% in schizophrenia), but recent evidence suggests that these symptoms are morecommon than initially believed, especially in more severe forms of the disorder(Bracha, Wolkowitz, Lohr, Karson, & Bigelow, 1989; Mueser, Bellack, & Brady, 1990).
Negative symptoms, conversely, refer to the absence or diminution of cognitions,
feelings, or behaviors that are ordinarily present in persons without the illness.Common negative symptoms include blunted or ﬂattened affect (e.g., diminished
facial expressiveness), poverty of speech (i.e., diminished verbal communication),anhedonia (i.e., inability to experience pleasure), apathy, psychomotor retardation(e.g., slow rate of speech), and physical inertia. The positive symptoms of schizophre-nia tend to ﬂuctuate over the course of the disorder and are often in remission between
episodes of the illness. In addition, positive symptoms tend to be responsive to theeffects of antipsychotic medication (Kane & Marder, 1993). In contrast, negativesymptoms and cognitive impairments tend to be stable over time and are lessresponsive to antipsychotic medications (Greden & Tandon, 1991). However, thereis some evidence that atypical antipsychotic medications, such as clozapine, risper-idone, and olanzapine, have a bene ﬁcial impact on negative symptoms and cognitive
functioning (Breier, 2005; Green et al., 1997; Tollefson & Sanger, 1997; Wahlbeck,Cheine, Essali, & Adams, 1999).
Aside from the core symptoms of schizophrenia, many persons with schizophrenia
experience negative emotions (e.g., depression, anxiety, and anger) as a consequenceof their illness (Freeman & Garety, 2003). Depression is quite common (estimatedcomorbidity rate of 45%; Leff, Tress, & Edwards, 1988) among people with schizo-phrenia and has been associated with poor outcomes (e.g., increased hospital use,lower employment rates) and suicidal tendencies (Sands & Harrow, 1999). Depressivesymptoms can occur during all phases of the illness (prepsychotic, prodrome, acute,and remission), but they tend to attenuate as the active psychotic symptoms remit(Birchwood, Iqbal, Chadwick, & Trower, 2000). In addition, it was generally estimatedthat approximately 10% of the persons with this illness die from suicide (Bromet, Naz,Schizophrenia 167

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Fochtmann, Carlson, & Tanenberg-Karant, 2005; Drake, Gates, Whitaker, & Cotton,1985; Jobe & Harrow, 2005; Roy, 1986), but recent research examining suicide rates haslowered this estimate to around 4.0% to 5.6% (Inskip, Harris, & Barraclough, 1998;Palmer, Pankratz, & Bostwick, 2005). Risk of suicide is greater in the presence of moodsymptoms and substance use, if previous suicide attempts were made, during theinitial onset of the disorder (Hawton, Sutton, Haw, Sinclair, & Deeks, 2005; ﬁrst
psychotic episode; rates 11% to 26%, as reviewed in Malla & Payne, 2005), and in timeimmediately preceding and following inpatient hospitalization (Qin & Nordentoft,2005). Anxiety is also common in schizophrenia (estimated comorbidity rate of 43%)and is a frequent precursor to psychosis (Argyle, 1990; Braga, Mendlowicz,Marrocos, & Figueria, 2005; Cosoff & Hafner, 1998; Penn, Hope, Spaulding, & Kucera,1994; Tien & Eaton, 1992). Speci ﬁcally, there is evidence for the role of anxiety in both
the formation and maintenance of persecutory delusions (threat beliefs) as well ashallucinations (Freeman et al., 2002; Freeman & Garety, 2003). Finally, anger, hostility,and social avoidance may also be present, especially when the person is paranoid(Bartels, Drake, Wallach, & Freeman, 1991; Freeman, Garety, & Kuipers, 2001; Gay &Combs, 2005). Interestingly, as paranoia increases, so does the tendency to perceiveambiguous interactions in a negative, threatening manner (Combs & Penn, 2004;Freeman et al., 2005).
In addition to the positive symptoms and negative emotions commonly present in
schizophrenia, individuals with this diagnosis often have comorbid substance usedisorders. Epidemiological surveys have repeatedly found that persons with psychi-atric disorders are at increased risk for alcohol and drug abuse (Mueser et al., 1990;Mueser, Yarnold, & Bellack, 1992). This risk is highest for persons with the most severepsychiatric disorders, including schizophrenia and bipolar disorder. For example,individuals with schizophrenia are more than 4 times as likely to have a substanceabuse disorder as are individuals in the general population (Regier et al., 1990). Ingeneral, approximately 50% of all persons with schizophrenia have a lifetime historyof substance use disorder, and 25% to 35% have a recent history of such a disorder(Mueser, Bennett, & Kushner, 1995). The presence of comorbid substance use dis-orders in schizophrenia has consistently been found to be associated with a worsecourse of the illness, including increased vulnerability to relapses and hospitalizations,housing instability and homelessness, violence, economic family burden, and treat-ment noncompliance (Drake & Brunette, 1998). For these reasons, the recognition andtreatment of substance use disorders in persons with schizophrenia is crucial to theoverall management of the illness.
Another important clinical feature o f schizophrenia is lack of insight and
compliance with treatment (Amador & Go rman, 1998; Amador, Strauss, Yale, &
Gorman, 1991). Many individuals with sch izophrenia have little or no insight into
the fact that they have a psychiatric illne ss or even that they have any problems at
all. This denial of illness can lead to noncompliance with recommended treatments,such as psychotropic medications and psychosocial therapies (McEvoy et al., 1989).Furthermore, fostering insight into the illness is a dif ﬁcult and often impossible task
with these persons.
Noncompliance with treatment is a related problem, but it can also occur because of
the severe negativity often present in the illness, independent of poor insight.Problems with paranoia and distrust may contribute to noncompliance, in that168 SPECIFIC DISORDERS

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some persons may believe medications or treatment providers are dangerous to them.Furthermore, the side effects of some medications (e.g., sedation, dry mouth, motorside effects), particularly the conventional antipsychotics, are unpleasant and can alsolead to noncompliance. Medication noncompliance increases the risk of relapse, andbetween 50% and 75% of individuals who discontinue their medication will relapsewithin 1 year. Therefore, treatment compliance is a major concern to clinical treatmentproviders (Buchanan, 1992). It has been argued that the newer atypical antipsychoticsmay lead to higher rates of compliance owing to better side effect pro ﬁles (Breier,
2005). However, a recent study of 63,000 individuals with schizophrenia in theVeteran ’s Affairs medical system found widespread noncompliance (compliance
measured in terms of ﬁlling needed prescriptions) across both conventional and
atypical antipsychotics (Valenstein et al., 2004). Strategies for enhancing complianceinvolve helping the person become a more active participant in his or her treatment,identifying personal goals of treatment that have high relevance for that individual,and helping the person to develop strategies for taking medications into thedaily routines (Azrin & Teichner, 1998; Corrigan, Liberman, & Engle, 1990; Kemp,Hayward, Applewhaite, Everitt, & David, 1996; Kemp, Kirov, Everitt, Hayward, &David, 1998).
People with schizophrenia are sometimes assumed to be violent or otherwise
dangerous. Indeed, rates of violence have been found to be relatively higher in peoplewith schizophrenia and other severe mental illnesses compared to the generalpopulation (Hodgins, Mednick, Brennan, Schulsinger, & Engberg, 1996; Swanson,Holzer, Ganju, & Jono, 1990). However, a more accurate comparison may be toexamine the rates of violence between schizophrenia and other psychiatric disorders.Data from the MacArthur Risk Assessment Study found that the actual rates ofviolence for persons with schizophrenia was 8% for the ﬁrst 20 weeks following
discharge (most violent events occur in the ﬁrst 20 weeks) and 14% over the course of a
1-year period (Monahan et al., 2001). In comparison, the rates of violence for personswith schizophrenia were actually lower than those for persons with depression andbipolar disorder for the same time period. A prospective study of violent behaviorsin females with severe mental illness reported a prevalence rate of 17% over a 2-yearperiod (Dean et al., 2006). Rates vary widely depending upon source of information(e.g., self-report vs. collateral reports), de ﬁnition of violence, population studied (e.g.,
inpatients versus outpatients), and where the research takes place (e.g., country).However, it should be emphasized that the majority of people with schizophrenia andother mental illnesses are not violent (Swanson, 1994). When violence does occur, it isoften associated with substance abuse (Steadman et al., 1998) or the combination ofsubstance abuse and medication noncompliance (Swartz et al., 1998). Other factorssuch as psychopathy (Nolan, Volavka, Mohr, & Czobor, 1999) or antisocial personalitydisorder (Hodgins & Côté, 1993, 1996) also have been implicated. Finally, targets ofviolence tend to be family members or friends rather than strangers, which is notunexpected given that most persons with schizophrenia rely heavily on familymembers for support (Steadman et al., 1998).
Although there is an increased rate of violence in schizophrenia, people with
schizophrenia are much more likely to be the victims of violence and violent crime(Hiday, Swartz, Swanson, Borum, & Wagner, 1999). About 34% to 53% of individualswith severe mental illness report childhood sexual or physical abuse (Green ﬁeld,Schizophrenia 169

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Strakowski, Tohen, Batson, & Kolbrener, 1994; Jacobson & Herald, 1990; Rose,Peabody, & Stratigeas, 1991; Ross, Anderson, & Clark, 1994), and 43% to 81% reportsome type of victimization over their lives (Carmen, Rieker, & Mills, 1984; Hutchings &Dutton, 1993; Jacobson, 1989; Jacobson & Richardson, 1987; Lipschitz et al., 1996). Tworecent surveys of a large number of people with severe mental illness found high ratesof severe physical or sexual assault in the past year (Goodman et al., 2001; Silver,Arseneault, Langley, Caspi, & Mof ﬁtt, 2005). These numbers are striking compared to
estimates of the general population, in which 0.3% of women and 3.5% of menreported assault in the past year (Tjaden & Thoennes, 1998). Studies of the prevalenceof interpersonal trauma in women with severe mental illness indicate especially highvulnerability to victimization, with rates ranging as high as 77% to 97% for episodi-cally homeless women (Davies-Netzley, Hurlburt, & Hough, 1996; Goodman,Dutton, & Harris, 1995).
The prevalence of posttraumatic stress disorder (PTSD) among people with
schizophrenia and other severe mental illnesses in various samples has rangedfrom 14% to 43% (Cascardi, Mueser, DeGirolomo, & Murrin, 1996; Craine, Henson,Colliver, & MacLean, 1988; Grubaugh, Zinzow, Paul, Egede, & Frueh, 2011; Mueser,Bond, Drake, & Resnick, 1998; Mueser et al., 2004; Switzer et al., 1999), but has been aslow as 3.8% (Braga et al., 2005). These current rates of PTSD are far in excess of thelifetime prevalence of PTSD in the general population, with estimates ranging between8% and 12% (Breslau, Davis, Andreski, & Peterson, 1991; Kessler, Sonnega, Bromet,Hughes, & Nelson, 1995; Resnick, Kilpatrick, Dansky, Saunders, & Best, 1993). Thus,interpersonal violence is so common in the serious mental illness population that itmust sadly be considered a normative experience (Goodman, Dutton, & Harris, 1997).
DIAGNOSTIC CONSIDERATIONS
The diagnostic criteria for schizophrenia are fairly similar across a variety of differentdiagnostic systems. In general, the diagnostic criteria specify some degree of work,social, or self-care impairment, combined with positive and negative symptomslasting a signi ﬁcant duration (e.g., 6 months or more). The diagnostic criteria for
schizophrenia according to DSM-V (APA, 2013) must include the presence of two or
more of the following ﬁve symptoms: delusions, hallucinations, disorganized speech,
grossly disorganized or catatonic behavior, or negative symptoms. One of thesymptoms must be delusions, hallucinations, or disorganized speech. The symptomsmust have been present at least for a month, unless successfully treated. Since thedisorder’ s onset, the symptoms must be accompanied by a decrease in functioning
such as work or social interaction, or self-care must be below the level that existedprior to the disorder ’s onset. Also, for a diagnosis of schizophrenia, there must be
continuous signs of the disturbance for at least 6 months.
The diagnosis of schizophrenia requires a clinical interview with the patient, a
thorough review of all available records, and standard medical evaluations to rule outthe possible role of organic factors (e.g., CAT scan to rule out a brain tumor). Inaddition, because many persons with schizophrenia are poor historians or may notprovide accurate accounts of their behavior, information from signi ﬁcant others, such
as family members, is often critical to establish a diagnosis of schizophrenia. The use offamily and other informants is especially important in the assessment of prodromal170 SPECIFIC DISORDERS

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and prepsychotic states. Because of the wide variety of symptoms characteristic ofschizophrenia and variations in interviewing style and format across different clinicalinterviewers, the use of structured clinical interviews, such as the Structured ClinicalInterview for DSM (SCID; First, Spitzer, Gibbon, & Williams, 1996) can greatly
enhance the reliability and validity of psychiatric diagnosis.
Structured clinical interviews have two main advantages over more open clinical
interviews. First, structured interviews provide de ﬁnitions of the key symptoms,
agreed upon by experts, thus making explicit the speci ﬁc symptoms required for
diagnosis. Second, by conducting the interview in a standardized format, including aspeciﬁc sequence of asking questions, variations in interviewing style are minimized,
thus enhancing the comparability of diagnostic assessments across different clinicians.The second point is especially crucial considering that most research studies ofschizophrenia employ structured interviews to establish diagnoses. It is importantthat interviewers are properly trained and interrater reliability with a criterion-trainedor expert rater is established before the use of structured interviews are initiated. If theﬁndings of clinical research studies are to be generalized into clinical practice, efforts
must be taken to ensure the comparability of the patient populations and theassessment techniques employed.
The symptoms of schizophrenia overlap with many other psychiatric disorders.
Establishing a diagnosis of schizophrenia requires particularly close consideration offour other overlapping disorders: substance use disorders, affective disorders, schiz-oaffective disorder, and delusional disorder. We discuss issues related to each of thesedisorders and the diagnosis of schizophrenia in the following sections.S
UBSTANCE USEDISORDERS
Substance use disorder, such as alcohol dependence or drug abuse, can either be adifferential diagnosis to schizophrenia or a comorbid disorder (i.e., the individual canhave both schizophrenia and a substance use disorder). With respect to differentialdiagnosis, substance use disorders can interfere with a clinician ’s ability to diagnosis
schizophrenia and can lead to misdiagnosis if the substance abuse is covert, denied,or not reported accurately (Corty, Lehman, & Myers, 1993; Kranzler et al., 1995).Psychoactive substances, such as alcohol, marijuana, cocaine, and amphetamines, canproduce symptoms that mimic those found in schizophrenia, such as hallucinations,delusions, and social withdrawal (Schuckit, 1995). In those cases in which thesubstance is involved in the etiology of psychosis, a diagnosis of substance-inducedpsychotic disorder would be appropriate. Further complicating matters, the use ofthese substances can exacerbate psychotic symptoms and in many cases lead to areturn of acute psychosis.
Because the diagnosis of schizophrenia requires the presence of speci ﬁc symptoms
in the absence of identi ﬁable organic factors, schizophrenia can only be diagnosed in
persons with a history of substance use disorder by examining the individual ’s
functioning during sustained periods of abstinence from drugs or alcohol. Whensuch periods of abstinence can be identi ﬁed, a reliable diagnosis of schizophrenia can
be made. However, persons with schizophrenia who have a long history of substanceabuse, with few or no periods of abstinence, are more dif ﬁcult to assess. For example,
in a sample of 461 individuals admitted to a psychiatric hospital, a psychiatricSchizophrenia 171

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diagnosis could be neither con ﬁrmed nor ruled out because of history of substance
abuse in 71 persons (15%; Lehman, Myers, Dixon, & Johnson, 1994).
Substance use disorder is the most common comorbid diagnosis for persons with
schizophrenia. Because substance abuse can worsen the course and outcome ofschizophrenia, recognition and treatment of substance abuse in schizophrenia is acritical goal of treatment. The diagnosis of substance abuse in schizophrenia iscomplicated by several factors. Substance abuse, as in the general population, isoften denied because of social and legal sanctions (Galletly, Field, & Prior, 1993; Stone,Greenstein, Gamble, & McLellan, 1993), a problem that may be worsened in thispopulation because of a fear of losing bene ﬁts. Denial of problems associated with
substance abuse, a core feature of primary substance use disorders, may be furtherheightened by psychotic distortions and cognitive impairments present in schizo-phrenia. Furthermore, the criteria used to establish a substance use disorder inthe general population are less useful for diagnosis in schizophrenia (Corse,Hirschinger, & Zanis, 1995). For example, the common consequences of substanceabuse in the general population of loss of employment, driving under the in ﬂuence of
alcohol, and relationship problems are less often experienced by people with schizo-phrenia, who are often unemployed, do not own cars, and have limited interpersonalrelationships. Rather, persons with schizophrenia more often experience increasedsymptoms and rehospitalizations, legal problems, and housing instability because ofsubstance abuse (Drake & Brunette, 1998).
Individuals with schizophrenia tend to use smaller quantities of drugs and alcohol
(Cohen & Klein, 1970; Crowley, Chesluk, Dilts, & Hart, 1974; Lehman et al., 1994) andrarely develop the full physical dependence syndrome that is often present in personswith a primary substance use disorder (Corse et al., 1995; Drake et al., 1990; Test,Wallisch, Allness, & Ripp, 1989) or show other physical consequences of alcohol suchas stigmata (Mueser et al., 1999). Even very low scores on instruments developed forthe primary substance use disorder population, such as the Addiction SeverityInventory, may be indicative of substance use disorder in persons with schizophrenia(Appleby, Dyson, Altman, & Luchins, 1997; Corse et al., 1995; Lehman, Myers,Dixon, & Johnson, 1996). Because of the difﬁ culties in using existing measures of
substance abuse for people with schizophrenia and other severe mental illnesses, ascreening tool was developed speci ﬁcally for these populations: the Dartmouth
Assessment of Lifestyle Instrument (DALI; Rosenberg et al., 1998). The DALI is an18-item questionnaire that has high classi ﬁcation accuracy for current substance use
disorders of alcohol, cannabis, and cocaine for people with severe mental illness.
Despite the difﬁ culties involved in assessing comorbid substance abuse in persons
with schizophrenia, recent developments in this area indicate that if appropriate stepsare taken, reliable diagnoses can be made (Drake, Rosenberg, & Mueser, 1996; Maisto,Carey, Carey, Gordon, & Gleason, 2000). The most critical recommendations fordiagnosing substance abuse in schizophrenia include (a) maintain a high index ofsuspicion of current substance abuse, especially if a person has a past history ofsubstance abuse; (b) use multiple assessment techniques, including self-report instru-ments, interviews, clinician reports, reports of signi ﬁcant others, and biological assays
for the presence of substances, which are routinely collected on admission to inpatienttreatment; and (c) be alert to signs that may be subtle indicators of the presence of asubstance use disorder, such as unexplained symptom relapses, familial con ﬂict,172 S
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money management problems, and sudden depression or suicidality. Once a sub-stance use disorder has been diagnosed, integrated treatment that addresses both theschizophrenia and the substance use disorder (co-occurring disorders) is necessary toachieve a favorable clinical outcome (Drake, Mercer-McFadden, Mueser, McHugo, &Bond, 1998).M
OODDISORDERS
Schizophrenia overlaps more prominently with the major mood disorders than anyother psychiatric disorder. The differential diagnosis of schizophrenia from mooddisorders is critical, because the disorders respond to different treatments, particularlypharmacological interventions. Two different mood disorders can be especiallydifﬁcult to distinguish from schizophrenia: bipolar disorder with psychotic features
and major depression. The differential diagnosis of these disorders from schizophre-nia is complicated by the fact that mood symptoms are frequently present in all phasesof schizophrenia (prodrome, acute, and remission), and psychotic symptoms (e.g.,hallucinations, delusions) may be present in persons with severe mood disorders(APA, 2013; Pope & Lipinski, 1978).
The crux of making a differential diagnosis between schizophrenia and a major
mood disorder is determining whether psychotic symptoms are present in the absenceof mood symptoms. If there is strong evidence that psychotic symptoms persist evenwhen the person is not experiencing symptoms of mania or depression, then thediagnosis is either schizophrenia or the closely related disorder of schizoaffectivedisorder (discussed in the following section). If, on the other hand, symptoms ofpsychosis are present only during a mood episode, but disappear when the person ’s
mood is stable, then the appropriate diagnosis is either major depression or bipolardisorder. For example, it is common for people with bipolar disorder to havehallucinations and delusions during the height of a manic episode, but for thesepsychotic symptoms to remit when the person ’s mood becomes stable again. Simi-
larly, persons with major depression often experience hallucinations or delusionsduring a severe depressive episode, which subside as their mood improves. If thepatient experiences chronic mood problems, meeting criteria for manic, depressive, ormixed episodes, it may be dif ﬁcult or impossible to establish a diagnosis of schizo-
phrenia, because there are no sustained periods of stable mood.S
CHIZOAFFECTIVE DISORDER
Schizoaffective disorder is a diagnostic entity that overlaps with both the mooddisorders and schizophrenia (APA, 2013). Three conditions must be met for a personto be diagnosed with schizoaffective disord er: (1) the person must meet criteria for a
major mood episode (depressive or manic mood episodes) along with symptomsfrom criterion A from schizophrenia; (2) t he person has delusions or hallucinations
for 2 or more weeks in the absence of a major mood episode; and (3) the moodsymptoms have to be present for a majority of the illness ’sd u r a t i o n( i . e . ,ap e r s o n
who experiences brief, transient mood stat e sa n dw h oi sc h r o n i c a l l yp s y c h o t i ca n dhas other long-standing impairments woul d be diagnosed with schizophrenia, rather
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Schizoaffective disorder and major mood disorder are frequently mistaken for one
another because it is incorrectly assumed that schizoaffective disorder simply requiresthe presence of both psychotic and mood symptoms at the same time. Rather, asdescribed in the preceding section, if psychotic symptoms always coincide with moodsymptoms, the person has a mood disorder, whereas if psychotic symptoms arepresent in the absence of a mood episode, the person meets criteria for eitherschizoaffective disorder or schizophrenia. Thus, schizoaffective disorder requireslongitudinal information about the relationship between mood and psychosis tomake a diagnosis. This information is often obtained from the individual but issubject to memory and self-reporting biases (poor insight, or lack of awareness ofmood states). The distinction between schizophrenia and schizoaffective disorder canbe more dif ﬁcult to make, because judgment must be made as to whether the affective
symptoms have been present for a substantial part of the person ’s illness. Decision
rules for determining the extent to which mood symptoms must be present todiagnose a schizoaffective disorder have not been clearly established.
Although the differential diagnosis between schizophrenia and schizoaffective
disorder is dif ﬁcult to make, the clinical implications of this distinction are less
important than between the mood disorders and either schizophrenia or schizoaf-fective disorder. Research on family history and treatment response suggest thatschizophrenia and schizoaffective disorder are similar disorders and respond to thesame interventions (Kramer et al., 1989; Levinson & Levitt, 1987; Levinson & Mowry,1991; Mattes & Nayak, 1984). In fact, many studies of schizophrenia routinely includepersons with schizoaffective disorder and ﬁnd few differences. Therefore, the infor-
mation provided in this chapter on schizophrenia also pertains to schizoaffectivedisorder, and the differential diagnosis between the two disorders is not of majorimportance from a clinical perspective.D
ELUSIONAL DISORDER
Delusions can be found in schizophrenia, schizoaffective disorder, severe mooddisorders, organic conditions, and delusional disorder and are a nonspeci ﬁc symptom
in many cases. Persons with delusional disorder develop ﬁxed delusions and do not
show the other symptoms of schizophrenia (prominent auditory hallucinations,disorganization, odd or bizarre behaviors, negative symptoms). The delusion maylead to problems with others, but in general the person has good social, educational,and occupational functioning. Tactile and olfactory hallucinations can be present andwill usually be incorporated into the delusional belief. Delusional disorder is morecommon in females (3:1 female-to-male ratio) and has a later age of onset (mean age of40; Evans, Paulsen, Harris, Heaton, & Jeste, 1996; Manschreck, 1996; Yamada,Nakajima, & Noguchi, 1998). Delusional disorder accounts for 1% to 4% of allinpatient admissions and is relatively rare in clinical practice (Kendler, 1982).
In previous editions of the DSM , the differential diagnosis between delusional
disorder and schizophrenia is based on the presence of nonbizarre delusions andabsence of other symptoms of schizophrenia. Nonbizarre delusions are based onevents or situations that could occur in real life but are highly improbable and lacksupporting evidence (Sedler, 1995). Examples of nonbizarre delusions include beingwatched, followed, spied upon, harassed, loved, or poisoned. In contrast, bizarre174 SPECIFIC DISORDERS

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delusions involve mechanisms not believed to exist in an individual ’s culture, such as
beliefs of thought insertion, control, and broadcasting. In reality, the distinctionbetween nonbizarre and bizarre beliefs is highly subjective and difﬁ cult (Junginger,
Barker, & Coe, 1992; Sammons, 2005). However, in the DSM-5 the issue of nonbizarre
versus bizarre delusions has been removed and it emphasizes the presence of ﬁxed
delusions of any type that are present for 1 month. Many persons with delusions willprovide convincing arguments that their beliefs are true, and a decision on whether thebelief is plausible must often be made with very little corroborating evidence (Flaum,Arndt, & Andreasen, 1991; Jones, 1999). An examination of the person ’s history,
premorbid and current functioning, and symptom pro ﬁle can be useful in distin-
guishing delusional disorder from schizophrenia. A structured interview, such as theSCID, can be useful in assessing delusional beliefs along with the other symptoms ofschizophrenia.
EPIDEMIOLOGY
It is estimated that approximately 2.2 million persons in the United States haveschizophrenia at any given time (Narrow, Rae, Robins, & Regier, 2002; Torrey, 2001). Itis believed that 51 million persons have schizophrenia worldwide. The annualincidence of new cases of schizophrenia ranges from 8 to 40 per 100,000 persons(Jablensky, 2000; McGrath et al., 2004, as cited in Tandon, Kesavan, & Nasrallah,2008a). Point prevalence for any given time period ranges between 3% and 7% per1,000 persons, with some estimates as high as 10% (Goldner, Hsu, Waraich, & Somers,2002; Jablensky, 2000; Saha, Chant, Welham, & McGrath, 2005). The lifetime risk fordeveloping schizophrenia appears to be about 0.7% on average (see Saha et al., 2005,as reviewed in Tandon et al., 2008a).
In general, the prevalence of schizophr enia is believed to be remarkably stable
across a wide range of different population s and cultures (Crow, 2008; Saha, Welham,
Chant, & McGrath, 2006; Tandon et al., 200 8a). There has been little difference in the
rates of schizophrenia according to gender, ra ce, religion, or level of industrialization
(Jablensky, 1999). Similar incidence rates and symptom patterns were found across10 countries in a study sponsored by the World Health Organization (WHO;Jablensky et al., 1992). However, a more rec ent review of prevalence studies showed
considerable heterogeneity in the rates of s chizophrenia among different countries
that may be partly owing to variations in diagnostic criteria (Goldner et al., 2002).Furthermore, there is evidence that schiz ophrenia is more heavily concentrated in
urban areas of industrialized countries and , in fact, persons from developing countr-
ies may have a better prognosis and course of illness (Jablensky, 2000; Jablensky et al.,2000; Peen & Dekker, 1997; Takei, Sham, O ’Callaghan, Glover, & Murray, 1995;
Torrey, Bowler, & Clark, 1997). This increas ed risk appears to be related not only to the
likelihood of people with schizophrenia drifting to urban areas, but to being born inurban areas as well, which suggests that “urbanicity ”h a sa ne f f e c to ns c h i z o p h r e n i a
(Torrey et al., 1997).
Because schizophrenia frequently has an onset during early adulthood when
important educational, social, and occupational milestones are often achieved, per-sons with the illness are especially affected in that they are less likely to marry orremain married, particularly males (Eaton, 1975; Munk-Jørgensen, 1987), and they areSchizophrenia 175

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less likely to complete higher levels of education (Kessler, Foster, Saunders, & Stang,1995) and have problems in occupational performance (Marwaha & Johnson, 2004). Interms of employment rates, only 14% to 20% of persons with schizophrenia holdcompetitive employment despite reporting a desire to work (Mueser, Salyers, &Mueser, 2001; Rosenheck et al., 2006). It has long been known that there is anassociation between poverty and schizophrenia, with people belonging to lowersocioeconomic classes more likely to develop the disorder (Hollingshead & Redlich,1958; Salokangas, 1978).
Historically, two theories have been adva nced to account for this association. The
social drift hypothesis postulates that the debilitating effects of schizophrenia on
capacity to work result in a lowering of socioeconomic means, and hence poverty(Aro, Aro, & Keskimäki, 1995). The environm ental stress hypothesis proposes that
the high levels of stress associated with poverty precipitate schizophrenia in someindividuals who would not otherwise devel op the illness (Bruce, Takeuchi, & Leaf,
1991). Recently, attention has been aimed a t different ethnic and migratory groups,
such as second-generation Afro-Caribbe ans living in the United Kingdom, who
show higher incidence rates of schizophrenia (Boydell et al., 2001; Cantor-Graae &Selten, 2005).
It is believed that being a minority in a po tentially hostile social environment
where racism and discrimination are pre sent may lead to increased stress and
potentially higher rates of symptoms (Clark, Anderson, Clark, & Williams, 1999;Combs et al., 2006). Both of these explanations may be partly true, and longitudinalresearch on changes in socioeconomic clas s status (SES) and schizophrenia provide
conﬂicting results. For example, Fox (1990) re analyzed data from several longitudi-
nal studies and found that afte r controlling for initial levels of socioeconomic class,
downward drift was not evident. Further more, Samele et al. (2001) found that a
downward drift in occupational function ing over a 2-year period was not linked to
illness course or prognosis. However, Dohrenwend et al. (1992) did ﬁnd evidence for
social drift, even after controlling for soc ioeconomic class. Also, it is possible that
SES level may interact with gender, as males from higher SES homes show poorerclinical outcomes (Parrott & Lewine, 2005). Thus, more work is needed to sort outthe relationships between SES and schizophrenia.
PSYCHOLOGICAL AND BIOLOGICAL ASSESSMENT
Diagnostic assessment provides important information about the potential utility ofinterventions for schizophrenia (e.g., antipsychotic medications). However, assessmentdoes not end with a diagnosis. It must be supplemented with additional psychologicaland biological assessments.P
SYCHOLOGICAL ASSESSMENT
A wide range of different psychological formulations have been proposed for under-standing schizophrenia. For example, there are extensive writings about psycho-dynamic and psychoanalytic interpretations of schizophrenia. Although this work hasmade contributions to the further development of these theories, these formulationsdo not appear to have improved the ability of clinicians to understand persons with176 SPECIFIC DISORDERS

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this disorder or led to more effective interventions (Mueser & Berenbaum, 1990).Therefore, the use of projective assessment techniques based on psychodynamicconcepts of personality, such as the Rorschach and Thematic Apperception Test, isnot considered here.
One of the primary areas to assess is severity of psychotic symptoms, because
treatment progression is mainly judged by a reduction of symptoms (Andreasen et al.,2005). This includes an assessment of positive and negative symptoms and generalpsychopathology due to the high co-morbidity with anxiety and mood disorders.Measures such as the Positive and Negative Syndrome Scale (PANN S; Kay,Fiszbein, & Opler, 1987), the Brief Psychiatric Rating Scale (BPR S; Overall & Gorham,1962), and the Psychotic Rating Scale (PSYRATS; Haddock, McCarron, Tarrier, &Faragher, 1999) have been frequently used in schizophrenia research and have goodpsychometric properties. Scales speci ﬁc to positive (Scale for the Assessment of
Positive Symptoms; Andreasen & Olsen, 1982) and negative symptoms (Scale forthe Assessment of Negative Symptoms; Andreasen, 1982) can be used for a more in-depth and detailed assessment of these areas. There are also self-report and interview-based measures of insight available as well (see Amador & David, 2004). Commonly,these symptom measures are used in conjunction with a structured diagnosticinterview in the assessment of schizophrenia.
As noted earlier, schizophrenia is often associated with a variety of neuro-
psychological impairments. Core areas to assess in terms of cognitive functioningare verbal and visual learning and memory, working memory, attention/vigilance,abstract reasoning/executive functioning, speed of information processing, and socialcognition. These areas are part of the National Institute of Mental Health —Measure-
ment and Treatment Research to Improve Cognition in Schizophrenia cognitivebattery (NIMH-MATRICS; Green et al., 2004). Having information on cognitivefunctioning in these areas will aid in examining the bene ﬁcial effects of antipsychotic
medication on cognition. It also is important to consider the generalization of theseimpairments to different situations (i.e., transfer of training problems). Thus, assess-ment needs to be conducted in the environments in which the skills are to be used inorder to provide a more ecologically valid assessment. For example, successfulemployment interventions incorporate assessment on the job on an ongoing basisrather than extensive prevocational testing batteries that do not generalize to real-world settings (Bond, 1998; Drake & Becker, 1996). Similarly, when assessing inde-pendent living skills, it is important that these be measured directly in the livingenvironment of the patient or in simulated tests (Wallace, Liberman, Tauber, &Wallace, 2000).
A great deal of research has been done on the functional assessment of social skills
in people with schizophrenia. Social skills refer to the individual behavioral compo-nents, such as eye contact, voice loudness, and the speci ﬁc choice of words, which in
combination are necessary for effective communication with others (Mueser & Bellack,1998). As previously described, poor social competence is a hallmark of schizophrenia.Although not all problems in social functioning are the consequence of poor socialskills, many social impairments appear to be related to skill de ﬁcits (Bellack, Morrison,
Wixted, & Mueser, 1990).
Several different strategies can be used to assess social competence. Clinical inter-
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These interviews can focus on answering questions such as: Is the patient lonely?Would the patient like more or closer friends? Is the patient able to stand up for his or herrights? Is the patient able to get others to respond positively to him or her? Patientinterviews are most informative when combined with interviews with signi ﬁcant
others, such as family members and clinicians who are familiar with the nature andquality of the patient ’s social interactions, as well as naturalistic observations of the
patient ’s social interactions. The combination of these sources of information is useful
for identifying speci ﬁc areas in need of social skills training.
One strategy for assessing social skills that yields the most speci ﬁc type of
information is role-play assessments. Role-plays usually involve brief simulated socialinteractions between the person and a confederate taking the role of an interactivepartner. During role-plays, individuals are instructed to act as though the situationwere actually happening in real life. Role-plays can be as brief as 15 to 30 seconds toassess skill areas such as initiating conversations, or they can be as long as severalminutes to assess skills such as problem-solving ability. Role-plays can be audiotapedor videotaped and later rated on speci ﬁc dimensions of social skill. Alternatively, role-
playing can be embedded into the procedures of social skills training, in which personswith schizophrenia practice targeted social skills in role-plays, followed by positiveand corrective feedback and additional role-play rehearsal. In the latter instance, theassessment of social skills is integrated into the training of new skills, rather thanpreceding skills training.
A commonly used assessment measure for social skill is the Maryland Assessment
of Social Competence (MASC; Bellack & Thomas-Lohrman, 2003). The MASC is astructured role-play assessment that consists of four 3-minute interactions. Followingeach role-play, ratings on verbal and nonverbal skill and effectiveness are made, thusallowing the clinician to examine social skill across different situations and contexts.
Recent research on the reliability and validity of social skill assessments, and the
beneﬁts of social skills training for persons with schizophrenia, has demonstrated the
utility of the social skills construct. Persons with schizophrenia have consistently beenfound to have worse social skills than persons with other psychiatric disorders(Bellack, Morrison, Wixted, et al., 1990; Bellack, Mueser, Wade, Sayers, & Morrison,1992; Mueser, Bellack, Douglas, & Wade, 1991), and approximately half of the personswith schizophrenia demonstrate stable de ﬁcits in basic social skills compared to the
nonpsychiatric population (Mueser, Bellack, Douglas, & Morrison, 1991). In theabsence of skills training, social skills tend to be stable over periods of time aslong as 6 months to 1 year (Mueser, Bellack, Douglas, & Morrison, 1991). Social skillin persons with schizophrenia is moderately correlated with level of premorbid socialfunctioning, current role functioning, and qu ality of life (Mueser, Bellack, Morrison, &
Wixted, 1990). Social skills tend to be asso ciated with negative symptoms (Appelo
et al., 1992; Bellack, Morrison, Wixted, et al., 1990; Lysaker, Bell, Zito, & Bioty, 1995;Penn, Mueser, Spaulding, Hope, & Reed, 1995), but not with positive symptoms(Mueser, Douglas, Bellack, & Morrison, 19 91; Penn et al., 1995). Furthermore, role-
play assessments of social skill are also s trongly related with social skill in more
natural contexts, such as interactions with signi ﬁcant others (Bellack, Morrison,
Mueser, et al., 1990).
Persons with schizophrenia show a wide range of impairments in social skills,
including areas such as conversational skill, con ﬂict resolution, assertiveness, and178 S
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problem solving (Bellack, Sayers, Mueser, & Bennett, 1994; Douglas & Mueser, 1990).Thus, ample research demonstrates that social skills are impaired with persons withschizophrenia, tend to be stable over time in the absence of intervention, and arestrongly related to other measures of social functioning. Furthermore, there is growingevidence supporting the ef ﬁcacy of social skills training for schizophrenia (Bellack,
2004; Heinssen, Liberman, & Kopelowicz, 2000).
The broadest area of psychological assessment is community functioning, and
improvement in this area is linked to the concept of recovery (see “Course and
Prognosis ”). Persons with schizophrenia show not only poor social skills but also poor
adaptive functioning in the community. Ideally, treatment programs should aim toimprove the person ’s quality of life and satisfaction. Independent living skills, quality
of life, and social functioning may need to be assessed in order to examine the person ’s
current functional capacity level. The Social Functioning Scale (Birchwood, Smith,Cochrane, Wetton, & Copstake, 1990) and UCSD Performance-Based Skills Assess-ment (UPSA; Patterson, Goldman, McKibbin, Hughs, & Jeste, 2001) are widely usedmeasures of adaptive and community functioning.F
AMILY ASSESSMENT
The assessment of family functioning has high relevance in schizophrenia for tworeasons. First, Expressed Emotion (EE), which refers to the presence of hostile, critical,or emotionally overinvolved attitudes and behaviors on the part of close relatives ofpersons with schizophrenia, is an important stressor that can increase the chance ofrelapse and rehospitalization (Butzlaff & Hooley, 1998). Second, caring for an indi-vidual with a psychiatric illness can lead to a signi ﬁcant burden on relatives (Webb
et al., 1998), which ultimately can threaten their ability to continue to provideemotional and material support to the individual. Family burden has its own negativeconsequences and can be related to EE and the ability of the family to care for theperson with schizophrenia. Thus, a thorough assessment of these family factors isimportant in order to identify targets for family intervention.
Several speci ﬁc methods can be used to assess a negative emotional climate in the
family and the burden of the illness. Interviews with individual family members,including the person with schizophrenia, as well as with the entire family, coupledwith observation of more naturalistic family interactions, can provide invaluableinformation about the quality of family functioning. The vast majority of research onfamily EE has employed a semistructured interview with individual family members,the Camberwell Family Interview (Leff & Vaughn, 1985). This instrument is primarilya research instrument, and it is too time-consuming to be used in clinical practice.Alternatives to the Camberwell Family Interview have been proposed (e.g., Magañaet al., 1986), although none has gained widespread acceptance yet. Several studieshave successfully employed the Family Environment Scale (Moos & Moos, 1981), aself-report instrument completed by family members, which has been found to berelated to symptoms and outcome in patients with schizophrenia (Halford, Schweit-zer, & Varghese, 1991).
Many instruments have been developed for the assessment of family burden. The
most comprehensive instrument, with well-established psychometric properties, isthe Family Experiences Interview Schedule (Tessler & Gamache, 1995). This measureSchizophrenia 179

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provides information regarding both dimensions of subjective burden (e.g., emotionalstrain) and objective burden (e.g., economic impact), as well as speci ﬁc areas in which
the burden is most severe (e.g., household tasks). The importance of evaluating familyfunctioning is supported by research demonstrating clinical bene ﬁts of family inter-
vention for schizophrenia. Numerous controlled studies of family treatment forschizophrenia have shown that family intervention has a signi ﬁcant impact on
reducing relapse rates and rehospitalizations (Dixon et al., 2001; Pitschel-Walz,Leucht, Bäuml, Kissling, & Engel, 2001). The critical elements shared across differentmodels of family intervention are education about schizophrenia, the provision ofongoing support, improved communication skills, and a focus on helping all familymembers improve the quality of their lives (Dixon & Lehman, 1995; Glynn, 1992;Lam, 1991).B
IOLOGICAL ASSESSMENT
Biological assessments are becoming more common in the clinical management ofschizophrenia. For diagnosis, biological assessments may be used to rule out possibleorganic factors such as a tumor, stroke, or covert substance abuse. Urine and bloodspecimens are sometimes obtained in order to evaluate the presence of substanceabuse. Similarly, blood samples may be obtained in order to determine whether theperson is compliant with the prescribed antipsychotic medication, although thespeciﬁc level of medication in the blood has not been conclusively linked to clinical
response. Blood levels may also be monitored to ensure appropriate levels of moodstabilizers (e.g., lithium). Some newer medications (e.g., Clozaril) also require ongoingblood tests to detect very rare, but potentially lethal, blood disorders (Alvir, Lieber-man, & Safferman, 1995; Young, Bowers, & Mazure, 1998). Client participation in thistype of medical monitoring is crucial when using these medications.
Biological measures are sometimes used to characterize impairments in brain
functioning associated with schizophrenia, although these assessments do not haveclear implications for treatment of the illness at this time and are expensive. Inaddition, many clinicians do not have access to imaging technology, and its usehas been speci ﬁc to research settings. In terms of brain function and structure,
computerized axial tomography (CAT) scans indicate that between one-half andtwo-thirds of all persons with schizophrenia display enlarged cerebral ventricles,particularly the lateral and third ventricles, which is indicative of cortical atrophy(Liddle, 1995).
Magnetic resonance imaging (MRI) studies have found structural changes and a
reduction in gray matter volumes in the prefrontal, superior temporal, amygdala,hippocampus, and thalamus (Lawrie & Abukmeil, 1998; Wright et al., 2000). Theseﬁndings have also been found in ﬁrst-episode and nonill relatives as well and may be a
pathophysiological marker for the disorder (Fannon et al., 2000; McDonald et al.,2002). These gross structural impairments in brain functioning, such as enlargedventricles, tend to be associated with a wide range of neuropsychological impairmentsand negative symptoms often present in schizophrenia (Andreasen, Flaum, Swayze,Tyrrell, & Arndt, 1990; Buchanan et al., 1993; Merriam, Kay, Opler, Kushner, & vanPraag, 1990). In addition, positron emission tomography (PET) and single photonemission computerized tomography (SPECT) have shown reduced metabolism and180 SPECIFIC DISORDERS

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blood ﬂow in several of the prefrontal and temporal cortexes, and abnormal activation
of the thalamus (Kindermann, Karimi, Symonds, Brown, & Jeste, 1997; Liddle, 1997;McClure, Keshavan, & Pettegrew, 1998; Miyamoto et al., 2003). Functional MRI (fMRI)studies have found less activation in the prefrontal cortex and anterior cingulate cortexduring working memory tasks (Carter, MacDonald, Ross, & Stenger, 2001; Perlstein,Carter, Noll, & Cohen, 2001). Finally, diffuse tensor imaging methods, which assessthe integrity of white matter pathways in the brain, have found problems in myeli-nated neurons in the prefrontal lobes speci ﬁcally and in the connections between the
frontal, temporal, and parietal lobes (Burns et al., 2003; Lim, Hedehus, deCrespigny,Menon, & Moseley, 1998).
To date, most of the advances in the treatment of schizophrenia have been in
psychopharmacology. Biological assessments are still not useful for diagnosing theillness or for guiding treatment. However, the clinical utility of biological assessment islikely to increase in the years to come as advances continue to be made in theunderstanding of the biological roots of schizophrenia.
ETIOLOGICAL CONSIDERATIONS
B
EHAVIORAL GENETICS AND MOLECULAR GENETICS
The etiology of schizophrenia has been a topic of much debate over the past 100 years.Kraepelin (1919/1971) and Bleuler (1911/1950) clearly viewed the illness as having abiological origin. However, from the 1920s to the 1960s, alternative theories gainedprominence, speculating that the disease was the result of disturbed family inter-actions (Bateson, Jackson, Haley, & Weakland, 1956). Psychogenic theories of theetiology of schizophrenia, positing that the illness was psychological in nature ratherthan biological, played a dominant role in shaping the attitudes and behaviorof professionals toward persons with schizophrenia and their relatives (Fromm-Reichmann, 1950; Searles, 1965). These theories have not been supported empirically(Jacob, 1975; Waxler & Mishler, 1971). Moreover, in many cases, psychogenic theoriesfostered poor relationships between mental health professionals and relatives(Terkelsen, 1983), which have only begun to mend in recent years (Mueser & Glynn,1999). For more than a century, clinicians have often noted that schizophrenia tends to“run in families. ”However, the clustering of schizophrenia in family members could
reﬂect learned behavior that is passed on from one generation to the next, rather than
predisposing biological factors.
In the 1950s and 1960s, two paradigms were developed for evaluating the genetic
contributions to the illness. The ﬁrst approach, the high-risk paradigm, involves
examining the rate of schizophrenia in adopted-away or biological offspring ofmothers with schizophrenia. If the rate of schizophrenia in children of biologicalparents with schizophrenia is higher than in the general population, then even in theabsence of contact with those parents, a role for genetic factors in developing theillness is supported. The second approach, the monozygotic/dizygotic twin para-digm, involves comparing the concordance rate of schizophrenia in identical twins(monozygotic) compared to fraternal twins (dizygotic). Because monozygotic twinsshare the exact same gene pool, whereas dizygotic twins share only approximatelyhalf their genes, a higher concordance rate of schizophrenia among monozygoticSchizophrenia 181

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twins than dizygotic twins, even reared in the same environment, would support arole for genetic factors in the etiology of schizophrenia.
Over the past 30 years, numerous studies employing either the high-risk or twin
paradigm have been conducted examining the role of genetic factors in schizophrenia.There has been almost uniform agreement across studies indicating that the risk ofdeveloping schizophrenia in biological relatives of persons with schizophrenia isgreater than in the general population, even in the absence of any contact between therelatives (Kendler & Diehl, 1993). Thus, support exists for the role of genetic factors inthe etiology of at least some cases of schizophrenia. For example, the odds ofdeveloping schizophrenia if one parent has the disorder is 13% and rises to about50% if both parents have the disorder, compared to only 1% risk in the generalpopulation (Gottesman, 1991, 2001; McGuf ﬁn, Owen, & Farmer, 1995). Similarly, the
concordance rate of one identical twin developing schizophrenia if his or her co-twinalso has schizophrenia is between 25% and 50%, compared to about 6% and 15% forfraternal twins (Cardno et al., 1999; Faraone & Tsuang, 1985; Torrey, 1992; Walker,Downey, & Caspi, 1991). It also appears that the risk of developing schizophrenia isgreater in more severe types of schizophrenia (average 20% for disorgranized andcatatonic types; see Gottesman & Shields, 1982).
The fact that identical twins do not have a 100% concordance rate of schizophrenia
(heritability rates =0.80 on average), as might be expected if the disorder were purely
genetic, has raised intriguing questions about the etiology of schizophrenia. In areview of 40 studies on genetic risk, it was found that 80% of persons with psychoticsymptoms do not have a single parent with the disorder, and 60% have a negativefamily history (Gottesman, 2001). It is likely that the development of schizophreniaresults from an interaction between genetic and environmental factors. The results of aseries of longitudinal studies support this case. Tienari (1991; Tienari et al., 1987;Tienari et al., 2004) compared the likelihood of developing schizophrenia in threegroups of children raised by adoptive families. Two groups of children had biologicalmothers with schizophrenia, and the third group had biological mothers with nopsychiatric disorder. The researchers divided the adoptive families of the children intotwo broad groups based on the level of disturbance present in the family: healthyadoptive families and disturbed adoptive families. Follow-up assessments wereconducted to determine the presence of schizophrenia and other severe psychiatricdisorders in the adopted children raised in all three groups. The researchers found thatbiological children of mothers with schizophrenia who were raised by adoptivefamilies with high levels of disturbance were signi ﬁcantly more likely to develop
schizophrenia or another psychotic disorder (46%) than either similarly vulnerablechildren raised in families with low levels of disturbance (5%) or children with nobiological vulnerability raised in either disturbed (24%) or healthy (3%) adoptivefamilies. This study raises the intriguing possibility that some cases of schizophreniadevelop as a result of the interaction between biological vulnerability and environ-mental stress.
Although families do not cause schizophrenia, there are important interactions
between the family and person with schizophrenia that deserve consideration. First,as previously mentioned, it has repeatedly been found that critical attitudes andhigh levels of emotional overinvolvement (Expressed Emotion [EE]) on the part ofthe relatives toward the individual with schizophrenia are strong predictors of182 SPECIFIC DISORDERS

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the likelihood that persons with schizophrenia will relapse and be rehospitalized(Butzlaff & Hooley, 1998). The importance of family factors is underscored by the factthat the severity of persons ’psychiatric illness or their social skill impairments is not
related to family EE (Mueser et al., 1993). Rather, family EE seems to act as a stressor,increasing the vulnerability of persons with schizophrenia to relapse.
A second important family consideration is the amount of burden on relatives
caring for a mentally ill person. Family members of persons with schizophreniatypically experience a wide range of negative emotions related to coping with theillness, such as anxiety, depression, guilt, and anger (Hat ﬁeld & Le ﬂey, 1987, 1993;
Oldridge & Hughes, 1992). Burden is even associated with negative health conse-quences for relatives (Dyck, Short, & Vitaliano, 1999). Family burden may be related tolevels of EE, ability to cope with the illness, and ultimately the ability of the family tosuccessfully monitor and manage the schizophrenia in a family member (Mueser &Glynn, 1999). Thus, EE and family burden are important areas for assessment andintervention. Finally, researchers have been interested in discovering genes andchromosomal areas involved in schizophrenia.
Current research has focused on nine chromosomes (i.e., most important appear to
be areas 8p and 22q) and seven candidate genes, which may be important inschizophrenia (see Harrison & Owen, 2003). In particular, researchers are particularlyinterested in identifying genes found across family members with the disorder(linkage studies) or directly related to the underlying pathophysiology of schizophre-nia (e.g., genes that affect neurotransmitter functioning such as dopamine, serotonin,or glutamate). This area of research has been hampered by the lack of independentreplication of these genetic markers. The exact mechanism for genetic transmission ofthe disorder is unknown, but it appears that schizophrenia does not follow aMendelian single gene pattern of inheritance. It is more likely that schizophrenia isa polygenetic condition or that it arises from an interaction of multiple genes, whichincrease the susceptibility to the disorder (Craddock, O ’Donovan, & Owen, 2006;
Miyamoto et al., 2003). Regardless, genes and gene-environment interactions areestimated to account for 80% of the risk for schizophrenia, according to a review of theliterature (as reviewed in Tandon et al., 2008b).N
EUROANATOMY AND NEUROBIOLOGY
Although there is clear evidence that genetic factors can play a role in the developmentof schizophrenia, there is also a growing body of evidence pointing to the in ﬂuence of
other biological, nongenetic factors playing a critical role. For example, obstetriccomplications, maternal exposure to the in ﬂuenza virus, and other environmental-
based insults to the developing fetus (e.g., maternal starvation) are all associated withan increased risk of developing schizophrenia (Geddes & Lawrie, 1995; Kirch, 1993;Rodrigo, Lusiardo, Briggs, & Ulmer, 1991; Susser & Lin, 1992; Susser et al., 1996; Takeiet al., 1996; Thomas et al., 2001; Torrey, Bowler, Rawlings, & Terrazas, 1993). Thus,there is a growing consensus that the etiology of schizophrenia may be heterogeneous,with genetic factors playing a role in the development of some cases and earlyenvironmental-based factors playing a role in the development of other cases. Thisheterogeneity may account for the fact that the genetic contribution to schizophreniahas consistently been found to be lower than the genetic contribution to bipolarSchizophrenia 183

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disorder (Goodwin & Jamison, 1990). Other biological and physiological factorsinclude alterations in brain chemistry and structure.
Pharmacological research has identi ﬁed many neurochemical changes associated
with schizophrenia. By far, the neurotransmitter most commonly implicated in theonset of schizophrenia is dopamine. The dopamine hypothesis proposes that alter-ations in levels of dopamine are responsible for the symptoms of schizophrenia.Originally, this hypothesis was based on ﬁndings that substances that increase
dopamine (e.g., levadopa used to treat Parkinson ’s disease) increase psychotic
symptoms, and substances that decrease dopamine reduce psychotic symptoms.Current versions of this hypothesis suggest that an overabundance of dopamine incertain limbic areas of the brain may be responsible for positive symptoms, whereas alack of dopamine in cortical areas may be responsible for negative symptoms (Davis,Kahn, Ko, & Davidson, 1991; Moore, West, & Grace, 1999). Other neurochemicals alsoappear to be implicated in schizophrenia. In particular, serotonin may directly orindirectly (e.g., by mediating dopamine) affect symptoms of schizophrenia, becauseseveral of the newer antipsychotic medications impact serotonin levels (Liebermanet al., 1998). In addition, glutamate and GABA may be altered in schizophrenia(Pearlson, 2000).
As discussed in the section “Biological Assessment, ”abnormalities in several brain
structures have also been identi ﬁed. In particular, enlarged ventricles and decreased
brain volume and blood ﬂow to cortical areas have been associated with a wide range
of cognitive impairments and negative symptoms of schizophrenia (Andreasen et al.,1990; Buchanan et al., 1993; Merriam et al., 1990).L
EARNING ,MODELING ,ANDLIFEEVENTS
Although schizophrenia is broadly accepted to be a biologically based disorder andnot a learned one, learning and modeling may play a role in the course, outcome, andsymptom expression of the disorder. In terms of symptom expression, there isempirical support for the role of operant conditioning in delusions and hallucinations(e.g., hallucinations increase when reinforced). Furthermore, research has shown thatpsychotic behavior can be modi ﬁed using differential reinforcement (i.e., attention for
any other behavior besides the expression of delusional statements) or punishmentprinciples (Jimenez, Todman, Perez, Godoy, & Landon-Jimenez, 1996; Schock, Clay, &Cipani, 1998). However, these processes are probably more relevant for the mainte-nance of psychotic symptoms than for etiology. Haynes (1986) proposed a behavioralmodel of paranoia in which suspiciousness partially stems from the reinforcement ofparanoid statements and parental modeling, but this theory has been largely untested.
As described in the following section, the stress-vulnerability model of schizophre-
nia posits that coping skills mediate the noxious effects of stress on psychobiologicalvulnerability to symptoms and relapses (Liberman et al., 1986; Nuechterlein &Dawson, 1984). Coping skills, such as social skills for developing and maintainingclose relationships with others and strategies for managing negative emotions anddistorted thinking processes, can be acquired either naturalistically through access togood role models (e.g., family, friends) or through social learning-based programs,such as social skills training (Bellack, Mueser, Gingerich, & Agresta, 1997) or cognitive-behavior therapy (Chadwick & Birchwood, 1995; Fowler, Garety, & Kuipers, 1995).184 SPECIFIC DISORDERS

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Thus, improving coping skills, as well as other life skills, through the systematicapplication of social learning methods is a common treatment goal in schizophrenia.
Although stressful life events alone are not the cause of schizophrenia, some
theories hypothesize that life events may contribute to the development of thedisorder and can play an important role in the course of schizophrenia. The stress-vulnerability model (Liberman et al., 1986; Zubin & Spring, 1977) assumes thatsymptom severity and related impairments of psychiatric disorders such as schizo-phrenia have a biological basis (psychobiological vulnerability) determined by acombination of genetic and early environmental factors. This vulnerability can bedecreased by medications and worsened by substance use disorder. Stress, includingdiscrete events such as traumas and exposure to ongoing conditions such as a hostileenvironment, can impinge on vulnerability, precipitating relapses and worse out-comes. Finally, coping resources, such as coping skills or the ability to obtain socialsupport, can minimize the effects of stress on relapse and the need for acute care.
As described earlier, EE represents a stressful familial environment that may
increase relapse and hospitalization in people with schizophrenia. In addition, inthe“Clinical Picture ”section, we discussed that people with schizophrenia are often
the targets of violence and have frequently been exposed to physical and/or sexualassault. Exposure to traumatic events may lead to PTSD, a condition characterized byreliving the traumatic experience (e.g., nightmares, intrusive memories), avoidance ofpeople, places, and things that remind the person of the event, and increased arousalsymptoms (e.g., irritability, sleep problems). Exposure to trauma and the presence ofPTSD are likely to worsen the course of schizophrenia and complicate treatment(Mueser, Rosenberg, Goodman, & Trumbetta, 2002). For example, research shows thatboth discrete stressors (e.g., life events) and exposure to a stressful environment canworsen psychotic disorders (Butzlaff & Hooley, 1998). PTSD is also associated withsubstance abuse (Chilcoat & Breslau, 1998), which, as described earlier, can havesevere consequences for people with schizophrenia.C
OGNITIVE INFLUENCES
Cognitive impairments refer to dif ﬁculties in verbal and visual learning and memory,
working memory, attention/vigilance, abstract reasoning/executive functioning (i.e.,understanding a concept, planning, organizing), and speed of information processing(Green et al., 2004). These cognitive de ﬁcits have been observed in unmedicated,
medicated, ﬁrst-episode, remitted, and high-risk children prior to developing the
disorder. Thus, cognitive impairments are so commonplace that they are nowconsidered a core feature of schizophrenia (Palmer et al., 1997; Wilk et al., 2005). Arecent meta-analysis of cognitive performance found that normal controls without ahistory of schizophrenia perform consistently better (about 1 standard deviation) thanpersons with schizophrenia on most cognitive tasks, which suggests that a generalizedcognitive de ﬁcit is present (Heinrichs, 2005). These de ﬁcits also appear to be relatively
stable over time and do not appear to re ﬂect a progressive deterioration (Heaton et al.,
2001). These cognitive impairments may interfere with the person ’s ability to focus for
sustained periods on work or recreational pursuits, interact effectively with others,perform basic activities of daily living, or participate in conventional psycho-therapeutic interventions (Bellack, Gold, & Buchanan, 1999; Brekke, Raine, Ansel,Schizophrenia 185

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Lencz, & Bird, 1997; Green, Kern, Braff, & Mintz, 2000; Sevy & Davidson, 1995;Velligan et al., 1997). Cognitive impairments also result in dif ﬁculties with generaliz-
ing training or knowledge to other areas (i.e., transfer of training problems) (Mueser,Bellack, Douglas, & Morrison, 1991; Smith, Hull, Romanelli, Fertuck, & Weiss, 1999).Thus, many rehabilitative efforts focus on teaching persons with schizophreniadirectly in the environment in which skills will be used or involve specialized teachingmethods, such as errorless learning procedures (Kern, Liberman, Kopelowicz,Mintz, & Green, 2002).
In addition to cognitive de ﬁcits, it has become apparent that impairments in social
cognition (de ﬁned as the way people perceive, in terpret, and understand social
information) are also found in schizophrenia (Penn, Corrigan, Bentall, Racenstein, &Newman, 1997). De ﬁcits in emotion and social cue perception, problems inferring the
intentions and motivations of others (The ory of Mind), and impairments in social
knowledge and schemata have all been found in schizophrenia (Brune, 2005;Corrigan & Penn, 2001; Edwards, Jackso n, & Pattison, 2002). More speci ﬁcally,
persons with persecutory delusions exhib it an attributional style in which they
tend to blame others rather than situations f or negative events (e.g., personalizing
attributional style; see Garety & Freeman, 1999). De ﬁcits in social cognition appear
to be independent from nonsocial cognit ion (e.g., memory, attention) in that
they predict incremental variance in social functioning and social skill andmay arise from distinct brain structures involved in social information processing(Penn, Combs, & Mohamed, 2001; Penn et al., 1997; Pinkham, Penn, Perkins, &Lieberman, 2003). The exact nature of the r elationship between social cognition
and cognitive functioning is unclear, but social cognition appears to be important
in the social functioning of persons with s chizophrenia (Green, Oliver, Crawley,
Penn, & Silverstein, 2005).S
EX AND RACIAL -ETHNIC CONSIDERATIONS
Several issues related to gender are important for understanding the psychopathologyin the course of schizophrenia. As described in the section on course and prognosis,women tend to have a milder overall course and later onset of schizophrenia than domen. The net consequence of this is that, although similar numbers of men and womenhave schizophrenia, men are more likely to receive treatment for the disorder. In fact,most research on the treatment of schizophrenia is conducted on samples rangingfrom 60% to 100% male.
Because treatment studies usually sample persons with schizophrenia who are
currently receiving treatment, often inpatient treatment, the ef ﬁcacy of widely studied
psychosocial interventions, such as social skills training and family therapy, has beenless adequately demonstrated in women. For example, some research suggests thatsocial skills training may be more helpful to men than to women (Mueser, Levine,Bellack, Douglas, & Brady, 1990; Schaub, Behrendt, Brenner, Mueser, & Liberman,1998; Smith et al., 1997). There is a need for more research on the effects of treatmentsfor women with schizophrenia. At the same time, further consideration needs to begiven to the different needs of women with this illness. For example, women withschizophrenia are much more likely than men to marry and have children. It is crucial,therefore, that psychosocial interventions be developed to address the relationship,186 SPECIFIC DISORDERS

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family planning, and parenting needs of women with schizophrenia (Apfel & Handel,1993; Brunette & Dean, 2002; Coverdale & Grunebaum, 1998).
Another issue related to gender in need of further consideration is exposure to
trauma. As described earlier, people with schizophrenia are at risk for being thevictims of violence. Although both men and women with schizophrenia reporthistories of abuse and assault, women report more sexual assault (Goodman et al.,2001; Mueser et al., 1998). Furthermore, in the general population, women are morelikely to be abused than men, are more likely to sustain injuries, and are more likely tobe economically dependent upon perpetrators of domestic violence. Thus, there is aparticular need to recognize and address trauma in the lives of women withschizophrenia. Accurate detection of trauma is further complicated by the fact thatmost severely mentally ill persons who have been physically or sexually assaulteddeny that they have been abused (Cascardi et al., 1996). The development of programsthat address both the causes of domestic violence and their sequelae, especiallyfor women with schizophrenia, is a priority in this area (Harris, 1996; Rosenberget al., 2001).
Research on the relationships between race, ethnicity, and severe psychiatric
disorders demonstrates that cultural factors are critical to understanding how personswith schizophrenia are perceived by others in their social milieu, as well as the courseof the illness. Although the prevalence of schizophrenia is comparable across differentcultures, several studies have shown that the course of the illness is more benign indeveloping countries compared to industrialized nations (Lo & Lo, 1977; Murphy &Raman, 1971; Sartorius et al., 1986). Westermeyer (1989) has raised questions about thecomparability of clinical samples in cross-cultural studies, but a consensus remainsthat the course of schizophrenia tends to be milder in nonindustrialized countries(Jablensky, 1989).
A variety of different interpretations have been offered to account for the better
prognosis of schizophrenia in some cultures (Le ﬂey, 1990). It is possible that the strong
stigma and social rejection that results from serious mental illness and poses anobstacle to the ability of persons with schizophrenia to cope effectively with theirdisorder and assimilate into society (Fink & Tasman, 1992) is less prominent in somecultures (Parra, 1985). Greater cultural, familial, and societal acceptance of the socialdeviations present in schizophrenia may enable these persons to live less stressful andmore productive lives. This may be especially true for Hispanic families, who showless expressed emotion as compared to White families (Dorian, Garcia, Lopez, &Hernandez, 2008; Lopez et al., 2009). Hispanic families are typically characterized asmore accepting and less blaming of persons with schizophrenia (Kymalainen &Weisman de Mamani, 2008). This is important given the link between EE and relapseand, in fact, lower rates of relapse have been found in minority families (Aguilera,Lopez, Breitborde, Kopelowicz, & Zarate, 2010).
Cultures with a stronger degree of family ties, in particular, may be less vulnerable
to the effects of mental illness (Lin & Kleinman, 1988). For example, Liberman (1994)has described how the strong functional ties of seriously mentally ill persons to theirfamilies and work foster the reintegration of persons with schizophrenia back intoChinese society following psychiatric hospitalization. In contrast, until recently,families of persons with schizophrenia in many Western societies were viewed bymental health professionals as either irrelevant, or worse, as causal agents in theSchizophrenia 187

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development of the illness (Leﬂ ey, 1990; Mueser & Glynn, 1999), thus precluding them
from a role in psychiatric rehabilitation. Furthermore, the use of other social supportsmay vary across different ethnic groups or cultures, such as the importance of thechurch to the African American community and its potential therapeutic bene ﬁts
(Grifﬁth, Young, & Smith, 1984; Lincoln & Mamiya, 1990).
Some have hypothesized that different cultural interpretations of the individual ’s
role in society and of the causes of mental illness may interact to determine course andoutcome. Estroff (1989) has suggested that the emphasis on the self in Westerncountries, compared to a more family or societally based identi ﬁcation, has an
especially disabling effect on persons with schizophrenia, whose sense of self is oftenfragile or fragmented. Another important consideration is the availability of adaptiveconcepts for understanding mental illness. For example, espiritismo in Puerto Rican
culture is a system of beliefs involving the interactions between the invisible spiritworld and the visible world, in which spirits can attach themselves to persons (Comas-Díaz, 1981; Morales-Dorta, 1976). Spirits are hierarchically ordered in terms of theirmoral perfection, and the practice of espiritismo is guided by helping individuals who
are spiritually ill to achieve higher levels of this perfection. Troubled persons are notidenti ﬁed as sick, nor are they blamed for their dif ﬁculties; in some cases, symptoms
such as hallucinations may be interpreted favorably as signs that the person isadvanced in his or her spiritual development, resulting in some prestige (Comas-Díaz, 1981). Thus, certain cultural interpretations of schizophrenia may promote moreacceptance of persons who display the symptoms of schizophrenia, as well asavoiding the common assumption that these phenomenological experiences are theconsequence of a chronic, unremitting condition.
Understanding different cultural beliefs, values, and social structures can have
important implications for the diagnosis o f schizophrenia. Religious practices and
beliefs may complicate diagnosis. For example, high levels of religiosity have beenfound in people with schizophrenia (Brewerton, 1994). Without a clear under-standing of the religious and cultural background, patients may be misdiagnosed(May, 1997). Ethnic groups may differ in th eir willingness to report symptoms, as
illustrated by one study that reported that African American persons were lesslikely than Hispanics or non-Hispanic Whites to report symptoms (Skilbeck,Acosta, Yamamoto, & Evans, 1984). Several studies have shown that ethnicdifferences in diagnosis vary a saf u n c t i o no fb o t ht h ec l i e n t ’s and the interviewer ’s
ethnicity (Baskin, Bluestone, & Nelson, 1 981; Loring & Powell, 1988). Misdiagnosis
of mood disorders as schizophrenia is the most common problem with thediagnosis of ethnic minorities in the United States (e.g., Jones, Gray, & Parsons,1981, 1983).
Other studies have found that African Americans are more likely than Whites to be
inappropriately diagnosed with paranoid schizophrenia, which has been viewed as aclinician bias in the interpretation of mistrust (Adams, Dworkin, & Rosenberg, 1984;Combs, Penn, & Fenigstein, 2002; Combs et al., 2006; Whaley, 1997, 2001). Alterna-tively, this ﬁnding may also represent the effects of stress and poverty in the
development of schizophrenia given the numbers of minorities who live in poverty(Bruce, Takeuchi, & Leaf, 1991; as discussed in “Epidemiology ”). Knowledge of
cultural norms appears critical to avoid the possible misinterpretation of culturallybound beliefs, experiences, and practices when arriving at a diagnosis.188 SPECIFIC DISORDERS

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Cultural differences are also critical in the treatment of schizophrenia, both with
respect to service utilization and the nature of treatment provided. There is a growingbody of information documenting that ethnic groups differ in their use of psychiatricservices. Several studies have indicated that Hispanics and Asian Americans use fewerpsychiatric services than non-Hispanic Whites, whereas Blacks use more emergencyand inpatient services (Cheung & Snowden, 1990; Hough et al., 1987; Hu, Snowden,Jerrell, & Nguyen, 1991; Padgett, Patrick, Burns, & Schlesinger, 1994; Sue, Fujino, Hu,Takeuchi, & Zane, 1991). Aside from cultural-based practices that may cause someindividuals to seek assistance outside the mental health system (e.g., practitioners ofsantería; González-Wippler, 1992), access to and retention in mental health servicesmay be in ﬂuenced by the proximity of mental health services (Dworkin & Adams,
1987) and by the ethnicity of treatment providers. Sue et al. (1991) reported thatmatching clinician and client ethnicity resulted in higher retention of ethnic minoritiesin mental health services. Increasing access to needed services for racial/ethnicminorities may require a range of strategies, including ensuring that services areavailable in the communities where clients live, working with the natural socialsupports in the community, awareness of relevant cultural norms, and adequaterepresentation of ethnic minorities as treatment providers.
Cultural factors may have an important bearing on psychotherapeutic treatments
provided for schizophrenia. Sue and Sue (1990) have described the importance ofproviding psychotherapy driven by goals that are compatible with clients ’cultural
norms. This requires both knowledge of subcultural norms and familiarity with theother social support mechanisms typically available to those individuals. Interven-tions developed for one cultural group may need substantial modi ﬁcation to be
effective in other groups. For example, Telles et al. (1995) reported that behavioralfamily therapy, which has been found to be effective at reducing relapse in schizo-phrenia for samples of non-Hispanic White and African American individuals(Mueser & Glynn, 1999), was signi ﬁcantly less effective for Hispanic Americans (of
Mexican, Guatemalan, and Salvadoran descent) with low levels of acculturation thanfor more acculturated individuals. In addition, behavioral family therapy has beenfound to be effective when implemented in Spain and China (Montero et al., 2001;Xiong et al., 1994; Zhang, Wang, Li, & Phillips, 1994). These ﬁndings underscore the
importance of tailoring psychosocial interventions to meet the unique needs of clientsfrom different cultural backgrounds.
Aﬁnal cultural factor is stigma —that is, negative attitudes that lead to prejudice
and discrimination against people with schizophrenia. Although stigma can bepresent for a variety of disabilities, attitudes toward people with serious mentalillness tend to be more negative (Corrigan & Penn, 1999). Stigma may stem fromcharacteristics of the disorder itself, such as poor social skills, bizarre behavior, andunkempt appearance, and stigma may develop and be maintained through negativemedia portrayals and myths (e.g., dangerousness, unpredictability) (Farina, 1998).Stigma and discrimination can greatly undermine the person ’s ability to recover from
the effects of schizophrenia and integrate into society. For example, people withserious mental illness identify role functioning, such as employment, developing andmaintaining friendships and intimate relationships, and regular activities as critical totheir recovery (Uttaro & Mechanic, 1994). However, many studies have shown thatthese are the very areas most affected by stigma (Farina, 1998). Much is being done toSchizophrenia 189

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try to reduce stigma associated with schizophrenia and other mental illness. Inparticular, strategies that involve active education and increased contact with peoplewith mental illness (best if same status and background) may be most effective foreradicating this serious problem (Corrigan & Penn, 1999).
COURSE AND PROGNOSIS
Schizophrenia usually has an onset in late adolescence or early adulthood, most oftenbetween the ages of 16 and 25. However, there is evidence that signs of the disorder arepresent long before the clinical symptoms of psychosis appear. Children who laterdevelop schizophrenia show impairments in sociability, emotional expressiveness(less positive and more negative facial expressions), and neuromotor functioning(Schiffman et al., 2004; Walker, Grimes, Davis, & Smith, 1993). Data from the NewYork High Risk Project, which followed a cohort of children at high risk for schizo-phrenia, found that de ﬁcits in verbal memory, attentional vigilance, and gross motor
skills in childhood (ages 7 to 12) predicted the development of schizophrenia later inlife (Erlenmeyer-Kimling et al., 2000).
Some individuals display a maladaptive pattern of behaviors, including disruptive
behavior, problems in school, poor interpersonal relationships, and impulsivity(Amminger et al., 1999; Baum & Walker, 1995; Fuller et al., 2002; Hans, Marcus,Henson, Auerbach, & Mirsky, 1992). Similarly, symptoms of conduct disorder inchildhood, such as repeated ﬁghting, truancy, and lying, have been found to be
predictive of the later development of schizophrenia (Asarnow, 1988; Cannon et al.,1993; Neumann, Grimes, Walker, & Baum, 1995; Robins, 1966; Robins & Price, 1991;Rutter, 1984; Watt, 1978). However, other persons with schizophrenia display nounusual characteristics in their premorbid functioning or competence (Zigler & Glick,1986). The signs of schizophrenia in childhood may be subtle, irregular, and gradual inonset, but they become increasingly more apparent as adolescence approaches(Dworkin et al., 1991).
Prior to the emergence of schizophrenia, many persons enter a prodromal period of
the illness, which is characterized by changes in mood and behavior (Yung &McGorry, 1996). The prodrome is an intensi ﬁcation of the core features of the disorder
that can last up to 5 years. Prodromal symptoms are subclinical or attenuatedsymptoms that fail to reach the threshold for a clinical diagnosis but becomeincreasingly apparent to others. Disruptions in sleep, anxiety, depression, aggres-sion/irritability, paranoia, and odd beliefs are common in the prodromal phase(Häfner, Maurer, Trendler, an der Heiden, & Schmidt, 2005; Malla & Payne, 2005;Norman, Scholten, Malla, & Ballageer, 2005; Yung & McGorry, 1996). Social isolation,withdrawal, changes in role functioning, and avolition may be present during thisstage as well.
The initial emergence of clinical symptoms ( ﬁrst-episode or ﬁrst break) is a crucial
time for treatment and intervention (Lincoln & McGorry, 1995). It is widely believedthat the earlier antipsychotic medications are initiated, the better the long-termoutcome becomes (Penn, Waldheter, Perkins, Mueser, & Lieberman, 2005). In fact,a critical time for treatment appears to be during the ﬁrst 5 years of the disorder (Malla,
Norman, & Joober, 2005). This ﬁnding, combined with the ef ﬁcacy of antipsychotic
medications (50% show remission after 3 months and 80% show remission at 1 year; as190 SPECIFIC DISORDERS

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reviewed in Penn et al., 2005) in ﬁrst-episode individuals, makes early intervention
programs a crucial aspect of treatment. Unfortunately, even after symptom remissionis attained, most individuals with schizophrenia still have de ﬁcits in social, vocational,
and community functioning (Tohen et al., 2000). Negative symptoms in ﬁrst-episode
individuals have been linked to poor cognitive functioning and longer durations ofuntreated psychosis (Malla & Payne, 2005).
It is extremely rare for the ﬁrst onset of schizophrenia to occur before adolescence
(e.g., before the age of 12), with most diagnostic systems considering childhood-onsetschizophrenia to be a different disorder than adolescent or adult onset. More commonthan childhood schizophrenia, but nevertheless rare in the total population of personswith schizophrenia, are individuals who develop the illness later in life, such as afterthe age of 40 (late-onset schizophrenia) or after the age of 60 (very-late-onsetschizophrenia) (Cohen, 1990; Howard, Rabins, Seeman, Jeste, & the InternationalLate-Onset Schizophrenia Group, 2000). It is estimated that approximately 23% ofindividuals with schizophrenia develop symptoms after the age of 40 (Harris & Jeste,1988). Late-onset schizophrenia is more common in women, and there is evidence ofbetter social, educational, and occupational functioning as compared to early-onsetschizophrenia (Howard et al., 2000).
Late-onset schizophrenia is more likely to involve positive symptoms (visual,
tactile, and olfactory hallucinations; persecutory delusions) and less likely to involveformal thought disorder or negative symptoms (Bartels, Mueser, & Miles, 1998). Late-onset schizophrenia is further complicated by the lack of clear-cut distinguishingcharacteristics that discriminate this disorder from a variety of other disorders thatdevelop later in old age such as dementia (Howard, Almeida, & Levy, 1994). Thus, it isimportant to emphasize that the symptoms of schizophrenia can arise at any point inlife and are a developmental phenomenon.
The onset, course, and prognosis of the illness are closely tied to gender (Haas &
Garratt, 1998). Women tend to have later age o f onset of the illness (average onset is
between 25 to 29 years), spend less time in hospitals, have fewer negative symp-toms, demonstrate less cognitive impairment, and have better social competenceand social functioning than men with the illness (Goldstein, 1988; Häfner et al., 1993;Leung & Chue, 2000; Mueser, Bellack, Morrison, & Wade, 1990; Salem & Kring,1998). The bene ﬁts experienced by women do not appear to be explained by societal
differences in tolerance for deviant behavior. A variety of different hypotheses havebeen advanced to account for the superior outcome of women with schizophrenia
(e.g., role of estrogen on dopamine receptors, more adaptive coping with socio-environmental stressors, improved social networks and competence [Castle &Murray, 1991; Flor-Henry, 1985; Halari et al., 2004]), but no single theory has
received strong support.
In general, the onset of schizophrenia can be described as either gradual or acute.
The gradual onset of schizophrenia can take place over many months or years, and itmay be dif ﬁcult for family members and others to clearly distinguish onset of the
illness (prepsychotic and prodromal signs). In other cases, the symptoms developrapidly over a period of a few weeks with dramatic and easily observed changesoccurring over this time. People with acute onset of schizophrenia have a somewhatbetter prognosis than those with a more insidious illness (Fenton & McGlashan, 1991;Kay & Lindenmayer, 1987).Schizophrenia 191

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Although schizophrenia is a long-term and severe psychiatric illness, there is
considerable interindividual variability in the course and outcome of the illnessover time (Marengo, 1994). Generally, though, once schizophrenia has developed,the illness usually continues to be present at varying degrees of severity throughoutmost of the person ’s life. Schizophrenia is usually an episodic illness with periods of
acute symptom exacerbation (i.e., relapse) requiring more intensive, often inpatient,treatment interspersed by periods of higher functioning between episodes (i.e.,remission). Preventing relapse is a signi ﬁcant clinical concern, because each relapse
leads to more persistent symptoms and greater cognitive and psychosocial impair-ment. Although most persons with schizophrenia live in the community, it iscomparatively rare, at least in the short term, for individuals to return to theirpremorbid levels of functioning between episodes.
Remission is the reduction of active symptoms to nonproblematic, less severe levels
(Andreasen et al., 2005). Recovery is much broader and includes both symptomremission and an improvement in social, community, occupational, and adaptivefunctioning. Recovery is also largely based on consumer perceptions of improvement.A recent review of 10 longitudinal studies on outcome in schizophrenia, some of whichfollowed individuals for more than 20 years, reported that between 21% and 57% ofpersons with schizophrenia showed periodic episodes of recovery (improved symp-toms; greater social, educational, and occupational functioning; Jobe & Harrow, 2005).In fact, some of these individuals showed extended periods of recovery without mentalhealth treatment (Harrow, Grossman, Jobe, & Herbener, 2005; Jobe & Harrow, 2005).
Some general predictors of the course and outcome of schizophrenia have been
identi ﬁed, such as premorbid functioning, but overall, the ability to predict outcome is
rather poor (Avison & Speechley, 1987; Tsuang, 1986). The primary reason for this isthat symptom severity and functioning are determined by the dynamic interplaybetween biological vulnerability, environmental factors, and coping skills (Nuechter-lein & Dawson, 1984; Liberman et al., 1986). Factors such as compliance withmedication (Buchanan, 1992), substance abuse (Drake, Osher, & Wallach, 1989),exposure to a hostile or critical environment (Butzlaff & Hooley, 1998), the availabilityof psychosocial programming (Bellack & Mueser, 1993), and assertive case manage-ment and outreach (Mueser, Bond, Drake, & Resnick, 1998; Mueser, Drake, & Bond,1997; Phillips et al., 2001; Quinlivan et al., 1995) are all environmental factors that incombination play a large role in determining outcome.
The importance of environmental factors and rehabilitation programs in determin-
ing the outcome of schizophrenia is illustrated by two long-term outcome studiesconducted by Harding and associates (DeSisto, Harding, McCormick, Ashikaga, &Brooks, 1995; Harding, Brooks, Ashikaga, Strauss, & Breier, 1987a, 1987b). The ﬁrst
study was conducted in Vermont, which had a highly developed system of commu-nity-based rehabilitation programs for persons with severe mental illness. Personswith schizophrenia in this study demonstrated surprisingly positive outcomes (60%recovery rate) over the 20- to 40-year follow-up period. In contrast, similar individualsin Maine, where more traditional hospital-based treatment programs existed, faredsubstantially worse over the long-term course of their illness. Thus, the outcome ofmost cases of schizophrenia is not predetermined by speciﬁ c biological factors, but
rather is in ﬂuenced by the interaction between biological and environmental factors.192 S
PECIFIC DISORDERS

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In summary, the prognosis of schizophrenia is usually considered poor to fair, and
there is general agreement that it is worse than that for other major psychiatricdisorders, such as bipolar disorder or major depression (Jobe & Harrow, 2005). Despitethe widespread acceptance that schizophrenia is usually a lifelong disability, recentresearch on the long-term outcome of schizophrenia has challenged this assumption.Many persons with schizophrenia can attain symptom remission and recovery withthe appropriate pharmacological and psychosocial treatment (Ciompi, 1980; Hardinget al., 1987a, 1987b; Harrow et al., 2005).
CASE STUDY
C
ASEIDENTIFICATION
Isaac is a 30-year-old, never-married man who lives independently and receives SocialSecurity Supplemental Income because of impaired functioning due to schizophrenia,which developed approximately 10 years ago. Isaac maintains close contact with hisparents, who live in the same town, and has occasional contact with his two olderbrothers and a younger sister. Isaac receives outpatient treatment at his local com-munity mental health center, including antipsychotic medications, involvement in agroup program aimed at teaching him how to manage his illness, and participation ina supported employment program that helps him maintain a part-time competitivejob at a local grocery store.P
RESENTING COMPLAINTS
Isaac is dissatis ﬁed with several areas of his life that are the focus of treatment.
Although medication signi ﬁcantly reduced many of his paranoid symptoms, he
c o n t i n u e st oh a v es u s p i c i o u st h o u g h t si ns o m es o c i a ls i t u a t i o n sa n df e e l sa n x i o u saround other people. He has few friends, none of them women, and he would like tohave more friends, including a girlfriend. Although his hygiene is generally good,when his psychotic symptoms increase, h e becomes more disheveled, smokes more
cigarettes, and becomes agitated. In addition to Isaac ’s mild paranoia and social
anxiety, his social skills are not stron g. For example, Isaac maintains poor eye
contact and speaks in a low tone of voice when talking with other people, he rarelysmiles spontaneously, and he has dif ﬁc u l t yc o m i n gu pw i t hi n t e r e s t i n gc o n v e r s a –
tional topics. Isaac is also dissatis ﬁed with not completing his college degree because
his three siblings have all graduated college, but he doesn’ tw a n tt or e t u r nt os c h o o l
until he has proved to himself that he can hold down his part-time job. He has a verylow energy level and sometimes has trouble following through regularly on hisgoals, including his part-time job. Isaac recognizes that he has problems and needs
help, but he lacks basic insight into his psychiatric disorder, and he does not believehe has schizophrenia. Isaac also does not like having to take medications, partlybecause of the weight gain he has experienc ed from his antipsychotic medication.
He periodically stops taking his medications when he feels better, which often leadsto relapses in his symptoms, a deterioration in functioning, and sometimesrehospitalization.Schizophrenia 193

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HISTORY
Isaac ﬁrst began to experience psychiatric problems 10 years ago. During the summer
before his junior year in college, he was working in a busy of ﬁce. He became
increasingly concerned that his of ﬁcemates were “out to get him ”and that there
was an intricate plot to discredit him. He also believed that his coworkers were secretlycommunicating with each other about him through certain facial expressions, choiceof clothing, and the con ﬁguration of items on their desks. As his paranoia escalated, he
became more disorganized in his thinking and behavior, he was less able to take careof his daily activities, and he experienced increased dif ﬁculties performing his job
because of a combination of dif ﬁculties with attention and fear of his co-workers, and
he eventually stopped coming to work. Isaac began to believe he was dying andattributed a variety of factors that were playing a role in his demise, including beingpoisoned by indoor air pollution. Isaac moved back home with his parents andinformed them that he would not be returning to school in the fall. As a result of Isaac ’s
symptoms, combined with the deterioration in his ability to take care of himself andmeet role expectations at work and school, his parents took him to a mental healthprofessional, who arranged for him to be hospitalized due to the extent of hisfunctional impairment.
During this hospitalization, Isaac was ﬁrst diagnosed with provisional schizophre-
niform disorder and treated with antipsychotic medication. Isaac bene ﬁted from his
treatment, and his most ﬂagrant symptoms improved substantially, including his
belief that others were plotting against him. He was discharged after a 4-week periodand referred to his local community mental health center for follow-up treatment andrehabilitation. Although Isaac ’s symptoms were improved, he continued to have
impairments in his functioning, including his self-care skills, limited social relation-ships, and decreased ability to work or attend school in his previous capacity. Whenthese impairments in psychosocial functioning had persisted for 6 months, hisdiagnosis was changed to schizophrenia.
Although Isaac continued to have symptoms and impairments of schizophrenia since
heﬁrst developed the disorder 10 years ago, he also made some positive steps toward
improving the quality of his life, with the help of his treatment team and his family. Afterseveral years of living at home, Isaac moved out 2 years ago to his own apartment. Isaachas been able to live on his own with the support of his family members and his casemanager, who coordinates his care with Isaac ’s treatment team. At ﬁrst when Isaac
moved back home, there was a signi ﬁcant amount of tension in the household, as his
parents and younger sister did not understand the nature of his illness and were upset byhis occasionally disruptive living habits, such as staying up much of the night. With thehelp of a clinician who worked with Isaac and his family for 15 months after he returnedhome, his family was able to learn more about schizophrenia, the principles of itstreatment, and strategies for solving problems together.
Last, after attending a local day treatment program, Isaac became interested in
working. The mental health center where he receives his treatment had a supportedemployment program in which an employment specialist was assigned to Isaac tohelp him ﬁnd a job in his area of interest and to provide supports to help him keep that
job. Isaac said that he was interested in working with animals, so his employmentspecialist helped him get a part-time job at a local pet store, where he cares for the194 SPECIFIC DISORDERS

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animals, feeds them, and cleans their cages. Isaac has kept this job for almost 2 years;on two occasions he has had to take some time off when he had a relapse of hissymptoms and had to return to the hospital. Isaac ’s employment specialist arranged
with his employer for him to be able to return to his job when he had recovered fromhis relapse. Isaac ’s case manager and employment specialist also worked together to
motivate Isaac to participate in a program designed to teach him more about hispsychiatric disorder and how to manage it in collaboration with others, in order toachieve his recovery goal of returning to school and completing his college degree.A
SSESSMENT
A diagnosis of schizophrenia was con ﬁrmed using the Structured Interview for DSM
(SCID). Many of the symptoms described in this vignette are highlighted in DSM-5
criteria for schizophrenia. Regarding the A criteria, Isaac clearly experienced three“characteristic symptoms, ”including delusions (e.g., his beliefs about his coworkers
and being poisoned by air pollution), disorganized speech and behavior, and negativesymptoms (e.g., ﬂattened affect, apathy). In terms of the B criteria, Isaac has expe-
rienced clear impairments in his social and occupational functioning—at the time ofdiagnosis, he was no longer able to care for himself or go to work, and he had droppedout of school. The duration criteria of DSM-5 were met because these dif ﬁculties lasted
longer than 6 months. In addition, with respect to the D and E diagnostic criteria forschizophrenia, other diagnoses were ruled out (e.g., mood disorders, substance abuse,developmental disorders). In addition to illustrating some of the symptoms andcharacteristic impairments of schizophrenia, this vignette illustrates that peoplewith this illness are often able to lead rewarding and productive lives, usuallywith the help of pharmacological and psychological treatment, as well as socialsupports, despite continued symptoms and impairment due to the illness.
SUMMARY
Schizophrenia is a severe, long-term psychiatric illness characterized by impairmentsin social functioning, the ability to work, self-care skills, positive symptoms (halluci-nations, delusions), negative symptoms (social withdrawal, apathy), and cognitiveimpairments. Schizophrenia is a relatively common illness, af ﬂicting approximately
1% of the population, and tends to have an episodic course over the lifetime, withsymptoms gradually improving over the long term. Most evidence indicates thatschizophrenia is a biological illness that may be caused by a variety of factors, such asgenetic contributions and early environmental in ﬂuences (e.g., insults to the develop-
ing fetus).
Despite the biological nature of schizophrenia, environmental stress can either
precipitate the onset of the illness or symptom relapses. Schizophrenia can be reliablydiagnosed with structured clinical interviews, with particular attention paid to thedifferential diagnosis of affective disorders. There is a high comorbidity of substanceuse disorders in persons with schizophrenia, which must be treated if positiveoutcomes are to accrue. Psychological assessment of schizophrenia is most usefulwhen it focuses on behavioral, rather than dynamic, dimensions of the illness. Thus,Schizophrenia 195

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assessments and interventions focused on social skill de ﬁcits and family functioning
have yielded promising treatment results. Biological assessments are useful at thistime primarily for descriptive rather than clinical purposes. Finally, there are a greatmany issues related to gender and racial or ethnic factors that remain unexplored.
Although schizophrenia remains one of the most challenging psychiatric illnesses
to treat, substantial advances have been made in recent years in developing reliablediagnostic systems, understanding the role of various etiological factors, developmentof effective pharmacological and psychosocial treatments, and the identi ﬁcation of
factors that mediate the long-term outcome of the illness, such as stress and substanceabuse. These developments bode well for the ability of researchers and clinicians tocontinue to make headway in treating this serious illness.
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CHAPTER 6
Bipolar and Related Disorders
DAVID J. MIKLOWITZ and SHERI L. JOHNSON
OVER THE PAST two decades, there has been a considerable resurgence of
interest in bipolar disorder (BD; formerly known as manic-depressiveillness). This resurgence is attributable in part to the availability of new
pharmacological agents, disorder-speci ﬁc psychosocial treatments, and data on
genetic mechanisms and neurophysiolog ical and neuroanatomical correlates. It
has also been driven by the increasing recognition that the onset of the disorder isoften in childhood or adolescence.
In this chapter we describe the disorder from the vantage points of diagnostic
criteria, diagnostic controversies, epidemiology, and course and prognosis, withparticular attention to developmental considerations pertinent to early-onset bipolarillness. A case study illustrates these issues.
We discuss the etiology and prognosis of BD from both a genetic and a
psychosocial viewpoint. Current etiological models view bipolar disorder as aprimarily genetic illness whose onset can be elicited by environmental stressors,
although the nature of the inherited biological vulnerability is unclear. Althoughfew studies have examined psychosocial st ressors relevant to the onset of bipolar
disorder, there is now a considerable literat ure on psychosocial stressors that affect
the course and outcome of the disease. In the ﬁnal sections, we summarize the major
recent ﬁndings concerning the treatment of the disorder and offer directions for
further research.
DESCRIPTION OF THE DISORDER
The core symptoms believed to constitute bipolar mania —elation, grandiosity, and
hyperactivation —have not fundamentally changed from one edition of the Diag-
nostic and Statistical Manual of Mental Disorders (DSM ) to the next. In this section, we
d e s c r i b et h ec o r ef e a t u r e so fm a n i a / h ypomania and depression and provide an
update on the rules of classi ﬁcation according to DSM-5 (American Psychiatric
Association [APA], 2013).
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MANIC,HYPOMANIC ,DEPRESSIVE ,ANDMIXEDEPISODES
Bipolar disorder (BD) is de ﬁned by manic symptoms. According to the DSM-5 (APA,
2013), people with bipolar, manic episodes ex perience elated, expansive, or irritable
mood (or any combination of these) and increa sed activity, plus at least three (four if
the mood is only irritable) of the following symptoms: decreased need for sleep;racing thoughts or ﬂight of ideas; rapid speech; inﬂ ated self-esteem (also called
grandiosity); impulsive, reckless behavio r (e.g., spending sprees, hypersexuality);
and distractibility. These symptoms must be present for at least 1 week or inter-rupted by hospitalization or emergency treatment. They must also cause functionalimpairment. Hypomania is characterize d by parallel symptoms, but the criteria
specify only that the symptoms last at least 4 days and result in a distinct, observable
change in functioning rather than severe impairment. Although persons withbipolar disorder often experience both depression and mania, a person who hasonly had one lifetime manic episode and no depression is still diagnosed withbipolar I disorder.
DSM-5 criteria differ from DSM-IV-TR (APA, 2000) in listing increased activity as
one of the cardinal symptoms of mania and hypomania. It has been argued thatchanges in activity may be more easily recognized than changes in subjective moodstate. As such, it is hoped that the DSM-5 criteria may provide for better accuracy and
reliability in the detection of manic and hypomanic episodes.
Depressive episodes, when present, last for at least 2 weeks and are characterized
by at least ﬁve symptoms, of which sad mood or loss of interest or pleasure in daily
activities must be one (criterion A symptoms), plus insomnia or hypersomnia,psychomotor agitation or retardation, increases or decreases in weight or appetite,loss of energy, dif ﬁculty concentrating or making decisions, feelings of worthlessness,
and suicidal ideation or behavior (criterion B symptoms). Depression must also beassociated with functional impairment. Manic or depressive episodes that are clearlyrelated to an ingested substance or to biological treatments —including antidepressant
medications —are classi ﬁed as substance-induced mood disorders.
A major change in the DSM-5 is the classi ﬁcation of episodes in which manic and
depressive symptoms occur simultaneously —what used to be called a mixed episode.
The DSM-5 refers to mixed features as a course speciﬁ er that can occur in mania or
depression, whether of the unipolar or bipolar variety. A patient with mania hasmixed features if he or she has three co-occurring symptoms of depression. If he or shehas major depressive disorder, the mixed speci ﬁer is met by having three simulta-
neous manic or hypomanic symptoms. Thus, a manic patient meets the mixedspeciﬁer criteria if he or she has irritable mood, increased activity, decreased need
for sleep, impulsive behavior, grandiosity, and pressure of speech (all manic symp-toms) along with loss of interests, suicidal thinking, and feelings of worthlessness(depressive symptoms). The new criteria, although more complicated than those in theDSM-IV , are intended to match what clinicians see in practice.
B
IPOLAR SUBTYPES
Bipolar I disorder is de ﬁned by the presence of a single manic episode that is not
substance-induced (see the following case study). In other words, patients need not218 SPECIFIC DISORDERS

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have experienced a major depressive episode to be called bipolar I. Rates of unipolarmania are between 25% and 33% in community samples but only about 10% inclinical samples (Depue & Monroe, 1978; Karkowski & Kendler, 1997; Kessler,Chiu, Demler, & Walters, 2005; Weissman & Myers, 1978). There is some evidence,
however, that most patients with unipolar mania eventually develop depressiveepisodes. In a 20-year study of unipolar m ania, 20 of 27 patients had episodes of
depression during the follow-up period (Solomon et al., 2003).
Bipolar II disorder is characterized by major depressive episodes alternating with
hypomanic episodes. Both must be present; one cannot be diagnosed with bipolar IIdisorder on the basis of hypomanic episodes alone. About 1 in 10 bipolar II patientseventually develops a full manic or mixed episode over a 10-year follow-up, and, thus,converts to bipolar I disorder (Coryell et al., 1995).
Cyclothymia is a variant of bipolar disorder characterized by 2 or more years
(or 1 year among adolescents) of alternations between hypomanic and depressivesymptoms, but none of these alternations meet the full DSM-5 criteria for a hypomanic
or major depressive episode. Bipolar disorder, not elsewhere classi ﬁed (previously
“not otherwise speci ﬁed”) is reserved for patients whose disorder meets the minimum
number of required symptoms but not the duration requirements for a full manic,hypomanic, or depressive, episode. Many childhood-onset patients receive thissubthreshold diagnosis, and up to 50% “convert ”to bipolar I or II disorder over
5 years (Axelson, Birmaher, Strober, et al., 2011).
EPIDEMIOLOGY
Differences in epidemiological estimates vary across studies, depending in part onculture and on how broadly the bipolar spectrum is de ﬁned.
A multinational study conducted by th e World Health Organization reported
lifetime prevalence rates in 61,392 adults in 11 countries: 0.6% for bipolar I disorder,
0.4% for bipolar II disorder, and 1.4% fo rs u b t h r e s h o l db i p o l a rd i s o r d e r .T h e
highest rates were observed in the United States; lifetime prevalence rates were1.0% for bipolar I disorders, 1.1% for bipolar II, and 2.4% for “subthreshold ”BD
(Merikangas et al., 2007). Although the re are fewer epidemiological data on
cyclothymic disorder, it is believed to affect as much as 4.2% of the generalpopulation (Regeer et al., 2004).A
GE AT ONSET
The onset of mood disorders appears to be getting younger in successive birthcohorts (Kessler et al., 2005; Wickrama ratne, Weissman, Leaf, & Holford, 1989).
Kessler et al. (2005) reported that the lifetim e risk of bipolar I or II disorders in 18-
to 29-year-olds was 22 times higher than in persons over 60. It is possible,however, that younger persons feel less stigmatized by psychiatric symptomsand are more likely than older persons to report mood disorder (notably manic)symptoms.
In a large ( N=10,123) community sample of adolescents in the United States,
2.5% met lifetime DSM-IV criteria for bipolar I or II disorder (Merikangas et al.,Bipolar and Related Disorders 219

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2012). Although many investigators suspect that bipolar disorder is more likely tobe diagnosed by practitioners in U.S. ch ildren (e.g., Reichart & Nolen, 2004), the
base rates of the disorder appear comparab le across countries when standardized
diagnostic interviews are used. An aggregate analysis of 12 clinical studies of 16,222children (ages 7 to 21) across the world rep orted a rate of bipola rs p e c t r u md i s o r d e r
(1.8%) that did not signi ﬁcantly differ across countries (Van Meter, Moreira, &
Youngstrom, 2011). The prev alence of bipolar spectrum d isorders (i.e., bipolar
disorder not elsewhere classi ﬁed, bipolar I, and bipolar II) may be as high as 6%
in U. S. treatment-seeking samples of yout h (Youngstrom, Findling, Youngstrom, &
Calabrese, 2005).
The mean age of onset of bipolar I disorder averages 18.2 years, and 20.3 years
for bipolar II (Merikangas et al., 2007), but there is substantial variability. Between
50% and 67% of patients develop the disease by age 18, and between 15% and 28%before age 13 (Perlis et al., 2004). Earlier a ge at onset is associated with rapid cycling
and other negative outcomes in adulthood (Coryell et al., 2003; Schneck et al., 2004).G
ENDER AND RACIAL -ETHNIC ISSUES
Women and men are equally likely to develop bipolar I disorder. Women, however,report more depressive episodes than men and, correspondingly, are more likely tobe diagnosed with bipolar II disorder (e.g., Leibenluft, 1997; Schneck et al., 2004).Women are also more likely to meet experience rapid-cycling BD (at least fourepisodes per year), again potentially related to the greater vulnerability to depression(Schneck et al., 2004).
Less is known about racial and ethnic differences in the diagnosis and treatment
of BD. In the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD), African American and Latino patients received fewer prescriptions for psychiatricmedications than European American patients (Gonzalez et al., 2007). Moreover,African American bipolar patients were less likely than Caucasian patients to havean outpatient follow-up visit within 3 months of the initial diagnosis (Kilbourneet al., 2005).
Evidence suggests major racial disparitie s in the treatment of bipolar disorder.
In the NCS-R major epidemiological study, none of the African American personswho were diagnosed with bipolar disorder were receiving adequate treatment(Johnson & Johnson, 2014). One study fou nd that adult African American patients
were less likely than Caucasians to be prescribed mood stabilizers or benzodiaze-pines and more likely to have been given antipsychotic medications (Kupfer,
Frank, Grochocinski, Houck, & Brown, 2005). African American adolescents withbipolar disorder are treated for longer pe riods than Caucasian adolescents with
atypical antipsychotics, even after adjusting for the severity of psychotic symptoms(Patel, DelBello, Keck, & Strakowski, 2 005). Not surprisingly given the treat-
ment de ﬁcits, the course of BD illness may be worse among African American
p a t i e n t s ,w h oa r em o r el i k e l yt oh a v ea t t empted suicide and been hospitalized
than Caucasian patients. The reasons for t hese racial disparit ies in treatment are
unclear, but are not explained by lack of in surance, lack of treatment-seeking, or
lack of acknowledgment of symptoms among African American patients (Johnson &Johnson, 2014).220 SPECIFIC DISORDERS

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CLINICAL PICTURE
Recent studies have examined the factor structure of the manic syndrome. A principalcomponent analysis of data from 576 diagnosed manic patients identi ﬁed seven
stable underlying factors: depressive mood, irritable aggression, insomnia, depressiveinhibition, pure manic symptoms, emotional lability/agitation, and psychosis (Sato,Bottlender, Kleindienst, & Moller, 2002). Through cluster analysis, Sato et al. identi ﬁed
four phenomenological subtypes of acute mania: pure, aggressive, psychotic, anddepressive-mixed mania.
The pattern of manic symptoms has been investigated in youths with bipolar
disorder. A meta-analysis of seven studies examining the phenomenological charac-teristics of mania among children and adolescents (aged 5 to 18; Kowatch, Young-strom, Danielyan, & Findling, 2005) found that the most common symptoms duringmanic episodes were increased energy, distractibility, and pressure of speech. Approx-imately 80% showed irritability and grandiosity, whereas 70% had the “cardinal ”
manic symptoms of elated mood, decreased need for sleep, or racing thoughts. Lesscommon symptoms included hypersexuality and psychotic symptoms. Thus, mostmanic children showed symptoms that also characterize adult mania.S
UICIDE
Bipolar disorder is associated with multiple threats to health and livelihood, but themost fundamental concern is the risk of suicide. The true prevalence of suicide in BDis unclear. Early estimates suggested tha t rates of completed suicide in BD were 12
to 15 times higher than in the general popul ation (Angst, Angst, Gerber-Werder, &
Gamma, 2005; Harris & Barraclough, 1997; Jamison & Baldessarini, 1999) and 4times higher than rates among patients with recurrent major depression (Brown,Beck, Steer, & Grisham, 2000). In a 44-y ear follow-up of patients with major
depressive disorder and BD, 11% died by su icide (Angst et al., 2005). Rates are
especially high among younger, recent-onset male patients and those who havecomorbid alcohol or substance abuse, social isolation, depression, signi ﬁcant anxi-
ety, aggression, impulsivene ss, a family history of suicide, or combinations of these
(Angst et al., 2005; Fawcett, Golden, & Rosenfeld, 2000; Jamison, 2000).
Some of these ﬁgures may overestimate the true suicide prevalence in BD (Bost-
wick & Pankratz, 2000). First, estimates based on “proportionate mortality preva-
lence ”(percentage of the dead who died by suicide) tend to be higher than the “case
fatality prevalence ”(proportion of people who died by suicide). The former method is
particularly error-prone for younger samples, who less commonly die from medicalcauses. Second, some studies base their estimates on hospitalized samples, who are atmuch higher risk than outpatient samples. In one study 4% of inpatients with affectivedisorders eventually committed suicide, compared to 2.2% of mixed inpatient/outpatient samples (Bostwick & Pankratz, 2000).F
UNCTIONAL IMPAIRMENT
Many patients with bipolar disorder experience ongoing impairments in social,occupational, and familial functioning even between episodes, especially if theyBipolar and Related Disorders 221

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have unresolved depressive symptoms (Altshuler et al., 2006; Fagiolini et al., 2005;Gitlin, Mintz, Sokolski, Hammen, & Altshuler, 2011). In a Stanley Foundation Net-work study of 253 adult patients with bipolar I or II disorder, only about one in threeworked full-time outside of the home (Suppes et al., 2001). More than half (57%) wereunable to work or worked only in sheltered settings. Only 42% of bipolar I, manicpatients show “steady ”work performance an average of 1.7 years after hospital
discharge (Harrow, Goldberg, Grossman, & Meltzer, 1990). In community samples,people with bipolar disorder are at 4 times greater likelihood of work disabilitycompared to the general population (Mitchell, Slade, & Andrews, 2004).
There is considerable variability in functional impairment, however. For example,
there appears to be a link between BD and creativity or productivity: Many famousartists, musicians, writers, and politicians probably had the disorder (Jamison, 1993).Patients with bipolar disorder and highly creative persons without psychiatricdisorder appear to have temperamental commonalities, such as high levels of drive,ambition, openness to new experiences and novelty seeking (Johnson, Edge,Holmes, & Carver, 2012; Nowakowska, Strong, Santosa, Wang, & Ketter, 2005).Children diagnosed with bipolar disorder and children who are the offspring ofbipolar parents scored higher than healthy control children on a creativity index(Simeonova, Chang, Strong, & Ketter, 2005). Interestingly, the unaffected familymembers of patients with bipolar disorder demonstrate higher accomplishmentand creativity than do their affected relatives.
COURSE AND PROGNOSIS
Virtually all patients with bipolar disorder have illness recurrences. The rates ofrecurrence, even when patients are treated with mood stabilizers, average 37% in1 year, 60% over 2 years, and 73% over 5 years (Gitlin, Swendsen, Heller, & Hammen,1995). Approximately one in ﬁve patients meets criteria for rapid cycling, de ﬁned by
four or more distinct episodes of mania, hypomania, mixed, or depressive disorderwithin 1 year (Schneck et al., 2004). Biological and psychosocial factors that predictillness recurrences are discussed further in the next section.
Even more signi ﬁcant are the persistent, mild-to-moderate residual symptoms
that most patients experience between episodes, even when undergoing pharmaco-therapy (Judd et al., 2002; Keller, Lavori, Coryell, Endicott, & Mueller, 1993; Post et al.,2003). Over a 13-year follow-up, subsyndromal symptoms were present duringapproximately half the weeks of follow-up (Judd et al., 2002). These symptomswere predominantly depressive rather than manic. A study of children with bipolarI, II, and NOS disorders observed similar patterns of residual symptoms over a15-month follow-up (Birmaher et al., 2009). Indeed, one of the most formidable issuesin the treatment of the disorder is the stabilization of depressive symptoms (e.g., Perliset al., 2006).P
SYCHOSOCIAL PREDICTORS OF THE COURSE OF BIPOLAR DISORDER
By the end of the 1980s, researchers began to acknowledge that biological andgenetic models of BD did not explain the eno rmous heterogeneity in the course of the
illness over time (Prien & Potter, 1990). Thi s recognition contributed to a renewed222 S
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emphasis on psychosocial predictors in the course of the disorder. For example,Ellicott, Hammen, Gitlin, Brown, and Ja mison (1990) found that BD patients with
high life-events-st ress scores were at 4.5 times greater risk for relapse in a 2-year
follow-up than patients with medium or low life-events-stress scores. Miklowitz,
Goldstein, Nuechterlein, Snyder, and M intz (1988) found that BD I manic patients
who returned after a hospitalization to families rated high on expressed emotion(EE) attitudes (criticism, hostility, or em otional overinvolvement) or who showed
high levels of caregiver-to-patient affectiv e negativity (criticism, hostility, or guilt
induction) during face-to-face interactions were at high risk for relapse. Those whosefamilies had both high EE and high affective negativity were highly likely to relapsewithin 9 months (94%), whereas those whose families rated low on both attributeswere unlikely to relapse within this time frame (17%).
Although these ﬁrst-generation studies established the prognostic role of psy-
chosocial factors, they did not address how psychosocial variables inﬂ uence depres-
sion versus mania. A second generat ion of research has examined which
psychosocial variables in ﬂuence the course of BD depression and which in ﬂuence
t h ec o u r s eo fm a n i a .P
SYCHOSOCIAL PREDICTORS OF DEPRESSION WITHIN BIPOLAR DISORDER
The symptomatology and neurobiology of unipolar and BD depression have manystrong parallels (Cuellar, Johnson, & Winters, 2005). Given these parallels, one mightexpect that psychosocial predictors of unipolar depression would in ﬂuence BD
depression. Here, we focus on well-established predictors of unipolar depression,including negative life events (Monroe, Harkness, Simons, & Thase, 2001), low socialsupport (Brown & Andrews, 1986), EE (Butzlaff & Hooley, 1998), neuroticism(Gunderson, Triebwasser, Phillips, & Sullivan, 1999), and negative cognitive styles(Alloy, Reilly-Harrington, Fresco, Whitehouse, & Zechmeister, 1999).
Negative life events are perhaps the most comprehensively examined predictors
of bipolar depression. Fortunately, a body of BD studies have now used interview-based measures of life events. As reviewed by Johnson (2005a), three of thesecross-sectional studies found that negative life events are equally common beforeepisodes of BD depression and unipolar depression (Malkoff-Schwartz et al., 2000;Pardoen et al., 1996; Perris, 1984). Finding so fp r o s p e c t i v es t u d i e sw i t hi n t e r v i e w –
based measures also indicate that stressful life events are correlated with slowrecovery from depression (Johnson & Miller, 1997) and predict increases in BDdepression over several m onths (Johnson et al., 2008). Thus, the most methodo-
logically rigorous studies suggest that ne gative life events are precipitants of
bipolar depression.
Other variables involved in unipolar depression also appear to have validity as
predictors of bipolar depression. For example, neuroticism (Heerlein, Richter,Gonzalez, & Santander, 1998; Lozano & Jo hnson, 2001), low social support (Johnson,
Winett, Meyer, Greenhouse, & Miller, 1999), family EE (Kim & Miklowitz, 2004;Yan, Hammen, Cohen, Daley, & Henry, 2004), and rejection sensitivity (Ng &Johnson, 2013) have been found to predict increases in depressive symptoms but notmanic symptoms over time. Although negative cognitive styles are often docu-mented in BD (see Cuellar et al., 2005, for review), they (a) are most likely to beBipolar and Related Disorders 223

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found during depression compared with well periods (Johnson & Kizer, 2002),
(b) predict depression better than mania (Johnson & Fingerhut, 2004; Johnson,Meyer, Winett, & Small, 2000), and (c) c an be explained by the presence of de-
pressive history rather than man ic history (Alloy et al., 1999).
In sum, variables that in ﬂuence the course of unipolar depression also in ﬂuence
BD depression, including negative life events, poor social support, family EE, negativecognitive styles, and low self-esteem. Few studies have examined the additive orinteractive effects of these risk variables in the course of BD.P
SYCHOSOCIAL PREDICTORS OF MANIA
Compared with BD depression, less is known about the psychosocial predictors ofmania. Available models highlight two sets of predictors: goal engagement and sleep/schedule disruption.Goal Dysregulation Drawing on biological models of overly sensitive reward path-
ways, the goal dysregulation model suggests that people with BD may show moreextreme responses to rewarding stimuli (Johnson et al., 2012). A large number of
studies indicate that people with a history of mania and students who are vulnerableto mania describe themselves as more sensitive to rewards (Johnson et al., 2012).People with BD also place a stably high em phasis on goal pursuit, even when they
are not in an episode (Johnson, Eisner, & C a r v e r ,2 0 0 9 ) .T h i sr eward sensitivity
w o u l db ee x p e c t e dt oi n ﬂuence reactions to life events that involve major successes.
Consistent with this idea, life events involving goal attainments (such as newrelationships, births of children, or care er successes) predict increases in manic
symptoms but not depressive symptoms (John son et al., 2000; Johnson et al., 2008).
Such effects were apparent even after controlling for baseline levels of manicsymptoms and excluding life events that c ould have been caused by the patients ’
symptoms.
Why might attaining an important goal trigger manic symptoms? A set of
studies suggest that for people with BD, cognition becomes much more positiveduring good moods than it does for other peo ple. Available evidence suggests that
mood states are associated with di stinct positive shifts in con ﬁdence (Johnson et al.,
2012; Stern & Berrenberg, 1979 ), autobiographical recall (Eich, Macaulay, & Lam,
1997), and attention to valenced stimuli (Murphy et al., 1999). Impulsivity, or thetendency to pursue rewards without awaren ess of potential negative consequences,
also becomes elevated as people become m anic (Swann, Dougherty, Pazzaglia,
Pham, & Moeller, 2004) or even more mild ly happy (Muhtadie, Johnson, Carver,
Gotlib, & Ketter, 2014). Mood-state-dependent shifts in con ﬁdence may contribute to
increased goal setting (Johnson, 2005b). In turn, investment in goal pursuit predicts
increases in manic symptoms over seve ral months (Lozano & Johnson, 2001).
Consistent with these ﬁndings, experience sampling d ata suggest that goal attain-
ments trigger increased goal engagement fort h o s ew i t hb i p o l a rd i s o r d e r( F u l f o r d ,Johnson, Llabre, & Carver, 2010), which, in turn, may trigger manic symptoms(Johnson, Carver, & Gotlib, 2012).
Reward engages con ﬁdence and goal pursuit but may also bring to mind memories
of failure or feelings of low self-worth (Eisner, Johnson, & Carver, 2008). In one study224 SPECIFIC DISORDERS

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(Miklowitz, Alatiq, Geddes, Goodwin, & Williams, 2010), remitted or partiallyremitted patients with BD, patients with MDD, and healthy controls unscrambledsix-word strings into ﬁve-word sentences, leaving out one word. The extra word
allowed the sentences to be completed in a negative, neutral, or “hyperpositive”
(manic/goal-oriented) way. Under conditions of reward (a pleasing bell tone for everyfour sentences completed), all subjects completed more sentences than in the non-reward conditions. However, patients with BD unscrambled more negative sentencesunder conditions of reward than did patients with MDD. Thus, a simple reward mayincrease the accessibility of negative thoughts among bipolar patients, consistent withearlier notions of mania as a defense against threat or low self-esteem (Adler, 1964;Lyon, Startup, & Bentall, 1999).Sleep and Schedule Disruption Experimental studies (Barbini et al., 1998) as well as
longitudinal studies (Leibenluft, Albert, Rosenthal, & Wehr, 1996) suggest that sleepdeprivation is an important trigger of manic symptoms. Wehr, Sack, and Rosenthal(1987) hypothesized that sleep disruption might be one way in which life events triggerepisodes of BD, noting that illness episodes are often preceded by life events interferingwith the ability to sleep (e.g., transmeridian ﬂights, childbearing). This theory was
broadened by Ehlers and colleagues (Ehlers, Frank, & Kupfer, 1988; Ehlers, Kupfer,Frank, & Monk, 1993), who suggested that social disruptions to other aspects ofcircadian rhythms could trigger symptoms (the “social zeitgebers model ”). Consistent
with this idea, Jones, Hare, and Evershed (2005) have documented that people withbipolar disorder demonstrate more variability in their daily schedules than do healthycontrols. In two studies, Malkoff-Schwartz et al. (1998; 2000) found that bipolar patientsreported more life events involving social-rhythm disruption (events that affect sleep orwake times, patterns of social stimulation, or daily routines) in the weeks precedingmanic episodes compared to the weeks preceding depressive episodes.
Laboratory mice with mutations in “CLOCK ”genes behave in ways that resemble
people with mania (e.g., increases in activity, decreased sleep, reward-seeking behav-ior). These changes are reversed when mice are given lithium (Roybal et al., 2007).These animal models may inform the role of sleep disruptions and possibly broaderschedule disruptions in the onset and course of mania.
In sum, sleep or schedule disruption is proposed to trigger manic symptoms. As
with research on the predictors of bipolar depression, very few longitudinal studies ofsleep disruption are available. As discussed next, some of these risk factors areamenable to modi ﬁcation through psychosocial intervention.
T
REATMENT OF BIPOLAR DISORDER :CURRENT TRENDS
Optimally, treatments for BD should involve combinations of pharmacological andpsychosocial interventions. Unfortunatel y, in the era of managed care cost contain-
ment, drug treatments are often the only tr eatment provided. Perhaps as a result,
the average duration of lithium treatment for patients in community settings is only76 days (Johnson & McFarland, 1996).Pharmacological Treatments Distinctions are usually made between acute pharmaco-
logical treatment and maintenance treatment. The goal of acute treatment is toBipolar and Related Disorders 225

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stabilize an existing manic or depressive episode (for recent reviews of acutepharmacotherapy studies, see Malhi, Adams, & Berk [2009] and Geddes & Miklowitz[2013]). Adjunctive psychotherapy is usually introduced during the postepisodestabilization phase and continued throughout maintenance treatment. The goals ofadjunctive psychotherapy are to minimize residual symptoms and prevent recur-rences. Untreated residual symptoms of mania or depression are prospectivelyassociated with illness recurrences (Perlis et al., 2006).
Current pharmacotherapy algorithms for mania for adult and childhood-onset
patients (e.g., Kowatch, Fristad, et al., 2005; McAllister-Williams, 2006) combine moodstabilizers (e.g., lithium carbonate, divalproex sodium, carbamazepine) with atypicalantipsychotic medications (e.g., olanzapine, quetiapine, risperidone, aripiprazole,ziprasidone, and less frequently, clozapine). Adjunctive antidepressant agents areoften recommended for bipolar depression. When given alone, antidepressant medi-cations can cause manic switching and acceleration of cycles in a signi ﬁcant number of
patients (Ghaemi, Lenox, & Baldessarini, 2001). When given with mood stabilizers,however, antidepressants do not appear to cause an increase in cycling (Altshuleret al., 2003; Sachs et al., 2007). The anticonvulsant lamotrigine is an option for manypatients given its antidepressant properties and lower propensity to cause cycleacceleration (Malhi et al., 2009).
Despite the clear effectiveness of many forms of pharmacotherapy, patients with
BD are prone to discontinuing their medications, with as many as 60% being fullyor partially noncompliant after a major episode of illness (Keck et al., 1998; Strakowskiet al., 1998). Patients who discontinue their pharmacotherapy abruptly are at a highrisk for recurrence and suicide attempts (Keck, McElroy, Strakowski, Bourne, & West,1997; Suppes, Baldessarini, Faedda, Tondo, & Tohen, 1993; Tondo & Baldessarini,2000). For example, in a naturalistic study of adolescent BD patients followed18 months after a hospitalization, relapse was 3 times more likely among patientswho discontinued lithium than among patients who remained on it. Patients describebarriers to compliance that include missing high periods, objecting to having one ’s
moods controlled by medications, lack of information about the disorder, or lack ofsocial or familial supports (for review, see Colom et al., 2000).Psychotherapy as an Adjunct to Medication Maintenance Randomized controlled trials
of psychotherapy indicate positive bene ﬁts for psychoeducational, skill-oriented, and
interpersonal treatments. The modalities investigated in the trials have includedindividual, family, and group formats.
Table 6.1 lists some of the key components of empirically supported treatments
for BD. Treatments supported by at least one randomized controlled trial includeindividual psychoeducation (Perry, Tarrier, Morriss, McCarthy, & Limb, 1999),group psychoeducation (e.g., Colom et al. , 2003; Simon et al., 2005), family-focused
therapy (FFT; e.g., Miklowitz, George, Richards, Simoneau, & Suddath, 2003; Reaet al., 2003), cognitive-behavioral therapy (CBT; e.g., Lam et al., 2003), and inter-personal and social rhythm therapy (IPSRT ; e.g., Frank et al., 2005) (for review, see
Miklowitz & Scott, 2009).
These treatments have several elements in common. First, all include an active
psychoeducational component, which often involves teaching patients (and in somecases, family members) to recognize and obtain early treatment for manic episodes226 SPECIFIC DISORDERS

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before they develop fully. All emphasize medication adherence, avoiding alcohol andstreet drugs, and the use of skills to cope more effectively with stress triggers. Theydiffer in the emphasis on speci ﬁc strategies, including involvement of family members
in psychoeducation (FFT), stabilizing sleep/wake rhythms (interpersonal and socialrhythm therapy), and cognitive restructuring (CBT; Miklowitz, Goodwin, Bauer, &Geddes, 2008).
The treatments listed in Table 6.1 have all been found in at least one study to
delay relapses of BD when combined with pha rmacotherapy. The control conditions
v a r ya n dh a v ei n c l u d e dt r e a t m e n ta su s ual, individual supportive therapy,
unstructured group support, and active clinical management. There are failed
replication studies as well: In a large-scale multicenter study, Scott et al. (2006)found that CBT was no more effective than treatment as usual in delaying recur-rences. Post-hoc analyses, however, revealed that relative to treatment as usual, CBTwas associated with longer time to recurrence among patients who had had fewerthan 12 lifetime episodes, and less time to recurrence among patients with 12 ormore prior episodes.
The large-scale Systematic Treatment Enhancement Program for BD (STEP-BD)
attempted to examine the effects of psychosocial interventions in a practical clinicaltrial across 15 U.S. treatment centers (Miklowitz et al., 2007). In this trial, 293 bipolar Iand II patients were randomly assigned to one of three intensive psychosocialinterventions (30 sessions over 9 months of family-focused treatment, IPSRT, orCBT, or a control treatment called collaborative care [CC]). The CC involved threepsychotherapy sessions over 6 weeks and focused on developing a relapse preventionplan. All patients were in an acute episode of bipolar depression at the time ofrandomization. All received “best practice ”pharmacotherapy (i.e., mood stabilizers,
atypical antipsychotic agents, or antidepressants, in various combinations) in combi-nation with psychotherapy.
Over 1 year, being in any of the intensive psychotherapies was associated with a
faster recovery from depression than being in CC. On average, patients in intensivetreatment recovered within 169 days, as compared to 279 days in the CC condition.Patients in intensive treatment were also 1.6 times more likely than patients in CC to beclinically well in any given study month. Rates of recovery over 1 year were as follows:FFT, 77%; IPSRT, 65%; CBT, 60%; and CC, 52%. The differences among the threeintensive modalities were not signi ﬁcant.Table 6.1
Key Therapeutic Elements of Psychoeducational Treatment
Teach emotion-regulation skills when challenged by stressors.
Encourage daily monitoring of moods and sleep cycles.
Enhance patient ’s (or family members ’) ability to identify and intervene early with relapses.
Track and encourage medication adherence.
Assist patient in stabilizing sleep/wake rhythms and other daily or nightly routines.
Educate family members about the disorder and enhance intrafamilial communication.
Increase access to social and treatment supports.
Help patient acquire balanced attitudes toward the self in relation to the illness.
Encourage acceptance of the disorder.Bipolar and Related Disorders 227

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There are still many gaps in research on psychosocial treatment. For example, effect
sizes for depression have been larger than those for mania prevention, and it remainsunclear whether particular subgroups of patients respond more completely to indi-vidual, family, or group treatment. Few studies have identi ﬁed the mechanisms of
action of psychosocial interventions (for example, whether they enhance medicationadherence, improve the patient ’s ability to recognize prodromal symptoms of recur-
rence, or increase insight or self-awareness).
The applicability of psychosocial interventions to early-onset BD, or children at risk
for developing the illness, has begun to be investigated systematically. Severalrandomized trials ﬁnd that family-based treatments are effective in reducing symptom
severity in children with bipolar spectrum disorders (Fristad et al., 2009) andadolescents with bipolar I or II disorder (Miklowitz et al., 2008). FFT has also beenfound to protect against the worsening of depressive and manic symptoms in childrenat high genetic risk for developing bipolar disorder (Miklowitz et al., 2013).
DIAGNOSTIC CONSIDERATIONS
Although the diagnosis of BD appears straightforward by DSM-5 , there is considera-
ble controversy as to its diagnostic boundaries with other conditions. Possibly,conceiving of bipolar disorder as a series of dimensions may enhance the reliabilityof diagnoses. Here, we address controversies regarding the de ﬁnition of the bipolar
spectrum, diagnosis in pediatric populations, and dual diagnosis (comorbidity)considerations.T
HEBIPOLAR SPECTRUM
Although it has traditionally been conceptualized as a disease involving shiftsbetween the dramatic poles of mania and depression, there is increasing recognitionthat many patients have bipolar spectru md i s o r d e r s ,w h i c h ,d e p e n d i n go nt h e
deﬁnition, may include subsyndromal manic episodes, manic or hypomanic epi-
sodes triggered by antidepressants, subs yndromal mixed episodes, or agitated
d e p r e s s i o n( A k i s k a l ,B e n a z z i ,P e r u g i ,&R i h m e r ,2 0 0 5 ;A k i s k a le ta l . ,2 0 0 0 ) .F o rexample, Smith, Harrison, Muir, and Bla ckwood (2005) observed that many young
adults with recurrent depression have symptoms that would be best consideredwithin the bipolar spectrum. In a sample of young adults treated for recurrentdepression at a university health service, only 16% met the DSM-IV criteria for
b i p o l a rd i s o r d e ra n d8 3 %f o rr e c u r r e n tm a j o rd e p r e s s i v ei l l n e s s .W h e nb r o a d e rdeﬁnitions of the bipolar spectrum were used, between 47% and 77% received
bipolar diagnoses. Caution is warranted in i nterpreting these re sults, as the inter-
rater reliability of interviews designed to assess milder spectrum forms of bipolar
disorder is relatively low (Kessler et al., 2006).
What is the evidence that spectrum patients are really bipolar in the classic sense?
Although they do not necessarily follow the same course of illness patterns aspatients with BD I or II, patients with subsyndromal forms of BD are more likelyto have family histories of BD and higher rates of hypomania induced by anti-depressants than people without subsyndromal BD symptoms. They also have highrates of suicide, marital disruption, and mental health service utilization compared228 SPECIFIC DISORDERS

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to those with no history of mental illness (Judd & Akiskal, 2003; Nusslock &Frank, 2011).
Some researchers have examined the bi polar spectrum as a risk factor for the
development of fully syndromal BD. Assessment instruments designed to identifypersons at risk include the Temperament Evaluation of Memphis, Pisa, Paris, and
San Diego —autoquestionnaire version (TEMPS -A; Akiskal et al., 2005). The TEMPS-
A is a self- or parent-rated assessment of t emperaments believed to precede the
o n s e to ff u l lB Da n dt op e r s i s td u r i n gt h e euthymic states. Although the TEMPS-A
measures a range of mood-related symptoms and tendencies, a speci ﬁct e n d e n c y
toward high moods and mood variability, as captured on the cyclothymia subscale,predicted onset of BD in a 2-year follow-up of 80 children and adolescents withdepression (Kochman et al., 2005).
The 79-item General Behavior Inven tory (GBI; Depue, Kleinman, Davis,
Hutchinson, & Krauss, 1985) evaluates life time experiences of depressive and manic
symptoms, as well as mood variability, on 1 –4 scales of frequency. High scores on
the GBI during adolescence are associated with psychosocial impairment in adult-
hood (Klein & Depue, 1984), and a childhood version rated by parents discriminatedpediatric BD from attention de ﬁcit hyperactivity diso rder (ADHD; Danielson,
Youngstrom, Findling, & Calabrese, 2003) . Whereas the Klein et al. studies focused
on the prognostic value of cyclothymic tem perament, Reichart et al. (2005) found
that higher scores on the GBI depression subscale were the best predictors of BD
onset at 5-year follow-up among a dolescents with depression.
Finally, the Hypomanic Personality Scale (Eckblad & Chapman, 1986) has been
used to assess subsyndromal manic symptoms and related traits. Kwapil et al. (2000)found that high scores on this scale predicted the onset of bipolar spectrum dis-orders over a 13-year follow-up of a large sample of college students. Thus, self-
report measures of spectrum symptoms and t emperamental characteristics predict
the onset of BDs in longitudinal studies.D
IAGNOSIS IN CHILDREN AND ADOLESCENTS
Perhaps the most controversial diagnostic dilemma is where to draw the boundariesof the bipolar diagnosis in children. Before about 1980, belief was widespread thatneither mania nor depression could occur before puberty, although individualcase reports of the phenomenon existed ( e.g., Anthony & Scott, 1960; Strecker,
1921). This belief has changed signi ﬁcantly in the past two decades (for review, see
Luby & Navsaria, 2010). Unfortunately, no s eparate diagnostic c riteria exist for
juvenile BD patients, and, as a result, there is little agreement on the operationaldeﬁnition of a manic or mixed episode, wheth er well-demarcated episodes of mania
a n dd e p r e s s i o nm u s to c c u ro rw h e t h e rt h es y m p t o m sc a nb ec h r o n i ca n du n r e -mitting, the minimum duration of epis odes, and what constitutes a symptom
(Biederman et al., 2003; Leibenluft, Charney, Towbin, Bhangoo, & Pine, 2003;McClellan, 2005). The reliability of the diagnosis appears to decrease with age(Meyer & Carlson, 2010).
Unfortunately, DSM-5 has done little to improve the situation. One diagnosis,
disruptive mood dysregulation disorder (DMDD), has been added to the mooddisorders section to give a “diagnostic home” to children and adolescents whoBipolar and Related Disorders 229

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have recurrent irritable outbursts as well as chronic negative affectivity. These youthhave often been called bipolar in community settings. Unfortunately, the DMDDdiagnosis has signi ﬁcant problems, such as the lack of distinction with oppositional
deﬁant disorder, the lack of a distinctive set of associated symptoms, and few data to
guide treatment (Axelson, Birmaher, Findling, et al., 2011).
One research group, led by Geller and colleagues (2002), has recommended that BD
not be diagnosed in children unless elevated mood and grandiosity are present.Another group (Leibenluft et al., 2003) has recommended that BD in children bedivided into three phenotypes: (1) a narrow phenotype (meets DSM-IV criteria for
mania or hypomania with elated mood and grandiosity); (2) an intermediate pheno-type (meets DSM-IV criteria but with irritable mood only); and (3) a broad phenotype
(e.g., mania that does not meet the duration criteria for bipolar I or II or is onesymptom short).
Does childhood-onset BD develop into adult BD, or are they separate conditions?
T h eN I M HC o u r s ea n dO u t c o m eo fB i p o l a rY o u t h( C O B Y )s t u d yp r o v i d e ss t r o n gempirical support for one approach to phenotyping high-risk youth. This long-termprospective study showed that youth with b ipolar disorder, NOS characterized by
(a) one DSM-IV symptom less than full criteria for a manic or hypomanic episode,
(b) a clear change in functioning, and (c ) a minimum symptom duration of 4 hours
within a day and a minimum of four lifetime episodes, were at substantiallyelevated risk for “converting ”t oB DIo rI Ib y4 -t o5 – y e a rf o l l o w – u p( B i r m a h e r
et al., 2009). A family history of bipolar I or bipolar II disorder also appearsimportant in predicting conversion rates among those with a BD-NOS pro ﬁle.
Among patients presenting with a BD-NOS phenotype, the risk of conversion toB DIo rB DI Iw a s5 2 %o v e r4y e a r sa m o n gt h o s ew i t h ﬁrst- or second-degree family
members who had a lifetime manic episo de, compared to 32% in BD-NOS patients
with a negative family history for mania (Axelson, Birmaher, Strober, et al., 2011;Birmaher et al., 2009). Thus, transient man ic episodes, when present in a child with
ab i p o l a r ﬁrst- or second-degree relative, are a high-risk phenotype for later
bipolar onset.
Another long-term study found develo pmental continuity for a narrow BD
phenotype from late adolescence to early adulthood, but not for a broader BDphenotype marked by irritab ility and euphoria without the associated manic symp-
toms (Lewinsohn, Seeley, Buckley, & Klein, 2002). A follow-up of manic children(mean age 11) who met strict DSM-IV criteria revealed th at 73.3% relapsed into
mania over 8 years. Most importantly, youth spent 60% of the weeks in theirlives with mood episodes, 40% in manic states. Between the ages of 18 and 21,44% had a recurrence of mania and 35% had developed substance use disorders(Geller, Tillman, Bolhofner, & Zimerman, 2008).
In a reanalysis of a large-scale longitudinal study of youths in semirural parts of
New York ( N=776, mean age 13.8), two categories of risk were de ﬁned: (1) episodic
irritability (based on the parents ’and child ’s answer to questions such as “Are there
times when [the child] feels irritable or jumpy? ”and“Do these times last for a week
or more? ”) and (2) chronic irritability (pers istent arguing and temper tantrums
across the home and school settings). Femal es exhibited higher levels of episodic
and chronic irritability than males. Epi sodic irritability was stable over time.
Moreover, episodic irritability in adolescence predicted the onset of a mania by230 SPECIFIC DISORDERS

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age 16 (Leibenluft, Cohen, Gorrindo, Brook, & Pine, 2006). Episodic irritability wasalso a unique predictor of mania by age 22, a lthough this relationship was mediated
by the cross-sectional correlation betwee n episodic irritability and depression in
early adolescence. In contrast, chroni c irritability was associated with ADHD by
mid-adolescence and major depressive il lness in early adulthood. Clearly, the
episodicity of symptoms is an important feature to assess when attempting todistinguish risk for BD from risk for other psychiatric disorders, notably ADHD.
D
UALDIAGNOSIS
BD patients are highly likely to be diagnos ed with one or more comorbid disorders.
When 12-month prevalence rates in a community epidemiological sample areconsidered, the highest associations are found between mania/hypomania,ADHD, and anxiety disorders (e.g., Kessler et al., 2005). The prevalence of anxietydisorders in clinical and epidemiologic studies ranges from 10.6% to 62.5% forpanic disorder, 7.8% to 47.2% for social anxiety disorder, 7% to 40% for post-traumatic stress disorder, 3.2% to 35% for obsessive-compulsive disorder, and 7% to32% for generalized anxiety disorder (Simo n et al., 2004). Taken together, at least
some form of comorbid anxiety disorder is present for the majority of persons withbipolar disorder.
Community and clinical population studies (Brady, Casto, Lydiard, Malcolm, &
Arana, 1991; Goldberg, Garno, Leon, Kocsis, & Portera, 1999; Kessler et al., 1997)have documented rates of lifetime subst ance use disorder ranging from 21% to
45%. This represents a sixfold increase in s ubstance use disorders among patients
with BD relative to the general population. One study found that patients were morelikely to use alcohol during depressive episodes and more likely to use cocaine andmarijuana during manic episodes (Strakowski, DelBello, Fleck, & Arndt, 2000).
Comorbid diagnoses —and even subsyndromal symptoms of comorbid disor-
ders—are associated with a poor prognosis of child and adult BD (Feske et al.,
2000; Frank et al., 2002; Masi et al., 2004; Otto et al., 2006; Tohen, Waternaux, &Tsuang, 1990). For example, anxiety comorbidity has been linked with younger onsetof BD, lower likelihood of recovery, poorer role functioning and quality of life, agreater likelihood of suicide attempts, and poorer response to medications (Henryet al., 2003; Simon et al., 2004). Studies have also documented lower recovery ratesamong patients with BD with a comorbid substance use disorder (Keller et al., 1986;Tohen et al., 1990) and a greater likelihood of rehospitalization (Brady et al., 1991;Reich, Davies, & Himmelhoch, 1974).
A separate issue is how to distinguish BD from comorbid disorders. A case in
p o i n ti sA D H D .I nas a m p l eo fc h i l d r e n, Geller et al. (1998) compared the
frequency of symptoms that are considered classic or pathognomonic of maniaversus those typically seen in either mania or ADHD. Elated mood, grandiosity,hypersexuality, decreased need for sleep, daredevil acts, and uninhibited people-
seeking were far more common in mania than ADHD. Distractibility, increasedactivity, and increased energy were observed in both disorders (see also Kim &Miklowitz, 2002). It has been argued that the presence of major depressiveepisodes among children with ADHD is a risk factor for developing BD (Chang,Steiner, & Ketter, 2000; Faraone, Bieder man, Mennin, Wozniak, & Spencer, 1997;Bipolar and Related Disorders 231

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Faraone, Biederman, Wozniak, et al., 1997 ;L e i b e n l u f te ta l . ,2 0 0 6 ) .H o w e v e r ,l o n g –
term longitudinal studies of girls with ADHD ﬁnd high rates of depression and
suicidal behavior at follow-up, and low rates of BD (Hinshaw et al., 2012; Turgay &Ansari, 2006).
DIAGNOSTIC ASSESSMENT METHODS
Most patients with BD are diagnosed by a clin ical interview; there are no biological
tests that verify the diagnosis. The most p rominent is the Structured Diagnostic
Interview for DSM-IV (SCID; First, Spitzer, Gibbon, & Williams, 1995). Despite
impressive reliability and validity statist ics for bipolar I disorder, the SCID and the
Kiddie Schedule for Affective Disorders a nd Schizophrenia (KSADS) are not sensi-
tive in identifying the milder forms of BD (Chambers et al., 1985; Kaufman et al.,1997). For example, the SCID may underestimate identi ﬁcation of hypomanic
episodes when comparing with diagnos es based on interviews by experienced
clinicians (Dunner & Tay, 1993).
Current thinking about diagnostic assessm ents is that instruments like the SCID
and KSADS should be supplemented by da ta from self-report questionnaires
(especially those that examine subsyndromal forms of mania) as well as a thoroughhistory of prior episodes involving an episode timeline, such as the National Instituteof Mental Health (NIMH) Life Charting method (Leverich & Post, 1998). Lifecharting enables the clinician to investigate the frequency, severity, and timing ofprior episodes; whether depressive, mixed, or manic episodes have dominated theclinical picture; whether other disorder s (e.g., substance dependence) preceded,
coincided with, or developed after the ons et of the mood disorde r; and to identify
triggers of episodes.
ETIOLOGICAL CONSIDERATIONS
Current models of bipolar disorder are multifactorial. It is well-established that thedisorder is highly heritable. The genetic and neurobiological vulnerability to bipolardisorder is believed to increase reactivity to socioenvironmental factors.H
ERITABILITY
Although heritability estimates for BD have ranged from 59% to 87%, newerstudies are available that estimate the prevalence of representative community
samples (McGuf ﬁn et al., 2003). These studies are particularly important as they are
less likely to be biased by the focus on more s evere, hospitalized samples. A Finnish
community-based twin sample that used stru ctured interviews to verify diagnoses
obtained a heritability estimate of 93% (Ki e s e p p ä ,P a r t o n e n ,H a u k k a ,K a p r i o ,&Lönnqvist, 2004). A British study with a similar design yielded a heritabilityestimate of 85% (McGuf ﬁn et al., 2003).
The risk of BD among children of bipolar parents is 4 times greater than the risk
among children of healthy parents. Children of bipolar parents, however, are also atapproximately 2.7 times higher risk for developing nonaffective disorders (including232 SPECIFIC DISORDERS

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ADHD and conduct disorder) than are the children of well parents. Thus, a proportionof the familial risk is not speciﬁ c to bipolar illness (Hodgins et al., 2002; LaPalme,
Hodgins, & LaRoche, 1997).
Several genomic regions relevant to BD have been identi ﬁed, including 13q32,
22q11, 8p22, and 10p14 (Badner & Gersho n, 2002; Berrettini, 2003), but effects
have generally been small and ﬁndings have not been entirely consistent from study
to study (Sullivan, Daly, & O ’Donovan, 2012). One model (Murray et al., 2004)
emphasizes the genetic overlap between BD and schizophrenia and commonsusceptibility genes that predispose ind ividuals to dopamine dysregulation and
psychosis. In addition to common suscepti bilities, there are probably other genes
whose expression affects neurodevelopment, illness-speci ﬁc neurological changes,
the likelihood of exposure to certain types of environments, and the eventualoutcome of BD, schizoaffect ive disorder, or schizophrenia (Murray et al., 2004).
N
EUROTRANSMITTER DYSREGULATION
Increasingly, BD is being described as an “impairment of synaptic and cellular plastic-
ity”(Manji, 2009, p. 2). This means that people with BD have genetically in ﬂuenced
problems with information processing in synapses and circuits (the neuronal connec-tions between one brain structure and others).
Traditional neurotransmitter models of mood disorders have focused on nor-
epinephrine, dopamine, and serotonin (Ch arney, Menkes, & Heninger, 1981; Thase,
Jindal, & Howland, 2002). It is now widely b elieved that dysregulations in these
systems interact with de ﬁcits in other neurotransmitter systems, such as gamma-
aminobutyric acid (GABA) and Substance P, to produce symptoms of mooddisorders (Stockmeier, 2003). Current research focuses on the functioning of neuro-transmitter systems rather than on simple models of neurotransmitter levels being
either high or low. Current paradigms include measuring sensitivity of the post-synaptic receptors through pharmacological challenges or neuroimaging. Moleculargenetic research has also informed resear chers about key neurotransmitter systems
to investigate. This type of research has p rogressed particularly rapidly in under-
standing dysregulation in ser otonin and dopamine systems.
Dopamine Among people without BD, several diff erent dopamine agonists, includ-
ing stimulants, have been found to trigger manic symptoms, including increases inm o o d ,e n e r g y ,a n dt a l k a t i v e n e s s( W i l l n e r ,1 9 9 5 ) .P e o p l ew i t hB Ds h o wp r o n o u n c e db e h a v i o r a le f f e c t st os t i m u l a n t s( A n a n d et al., 2000). Several paradigms have
been used to challenge the dopamine system, including behavioral sensitization(the study of how repeated administra tion of dopamine agonists changes the
sensitivity of dopaminergic reward pathw ays; Kalivas, Duffy, DuMars, & Skinner,
1988; Robinson & Becker, 1986) and sleep d eprivation (which ap pears to interfere
with normalizing the sensitivity of dopamine receptors; Ebert, Feistel, Barocks,Kaschka, & Pirner, 1994). Results obtaine d using these paradigms are consistent
with the idea that BD is characterized by hy persensitivity of the dopamine system
(Strakowski, Sax, Setters, & Keck, 1996; Strakowski, Sax, Setters, Stanton, & Keck,1997). Consistent with the idea of dopamine dysfunction, a large meta-analysisBipolar and Related Disorders 233

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suggested a link with the A1 polymorphism of the DRD2 gene Taq IA1 (Zou et al.,2012). In animal models, a set of cand idate genes for BD have been identi ﬁed
that relate to modulating dopamine signaling within reward pathways (Ogdenet al., 2004).
Molecular genetic studies in humans have not yet identi ﬁed other polymorphisms
that could explain these effects. For example, BD has not been found to consistentlyrelate to polymorphisms in the d1, d3, and d4 receptor genes or the dopaminetransporter genes (Chiaroni et al., 2000; Georgieva et al., 2002; Gorwood, Bellivier,Ades, & Leboyer, 2000; Lopez et al., 2005; Manki, Kanba, Muramatsu, & Higuchi,1996; Muglia et al., 2002).Serotonin Neuroimaging studies indicate that mood disorders are generally associ-
ated with decreased sensitivity of the serotonin receptors (Stockmeier, 2003). Thefunctioning of the serotonin system can also be tested by manipulating levels oftryptophan, the precursor to serotonin (Staley, Malison, & Innis, 1998). Findings oftryptophan-manipulation studies are consistent with the idea of serotonin receptordysfunction among persons with a family history of BD (Sobczak, Honig, Schmitt, &Riedel, 2003; Sobczak et al., 2002). Meta-analyses of the more than 20 studies of theserotonin transporter region in BD have yielded positive but small effects (e.g., Choet al., 2005; Lasky-Su, Faraone, Glatt, & Tsuang, 2005). Unfortunately, studies to datehave not examined interactions of the serotonin transporter gene with environmentalrisk in predicting vulnerability to BD.
BRAIN REGIONS INVOLVED IN BIPOLAR DISORDER
Although ﬁndings are not entirely consistent, neuroimaging studies implicate a set of
structures in the pathophysiology of BD. Many of these regions overlap substantiallywith those involved in emotional reactivity and regulation, and as such, manyparallels are present with the brain correlates of unipolar depression (Davidson,Pizzagalli, & Nitschke, 2002; Mayberg, Keightley, Mahurin, & Brannan, 2004). Differ-ences between bipolar and unipolar depression are also found (Delvecchio et al., 2012).Key structures relevant to bipolar disorder include the amygdala, which is involved inthe detection of the signi ﬁcance of emotionally salient stimuli; regions involved in
effective cognitive regulation of emotions and goal pursuit, such as regions of theprefrontal cortex, anterior cingulate, and hippocampus; and structures relevant toreward sensitivity (e.g., basal ganglia). One model suggests that mood disorders arecharacterized by increased activity in regions involved in emotional sensitivity,combined with diminished activity in regions involved in effective thinking andplanning in response to emotional cues (Phillips, Drevets, Rauch, & Lane, 2003).
More speci ﬁcally, several Positron Emission Tomography (PET) and functional
Magnetic Resonance Imaging (fMRI) studies of neural activity during cognitive oremotional tasks have shown a pattern of amygdala hyperactivity among people withbipolar I disorder (Altshuler, Bookheimer, Proenza, et al., 2005; Chang et al., 2004;Kruger, Seminowicz, Goldapple, Kennedy, & Mayberg, 2003; Lawrence et al., 2004).Some adult studies correspondingly suggest above-average volume of the amygdala(Phillips et al., 2003).234 SPECIFIC DISORDERS

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People with BD also appear to demonstrate diminished activity of the hippocampus
and some regions of the prefrontal cortex (Kruger et al., 2003). In parallel with theﬁndings of functional studies, structural studies have found that BD is associated with
a smaller-than-average volume in the prefrontal cortex, basal ganglia, hippocampus,and anterior cingulate (Phillips et al., 2003). Findings regarding diminished volumeof the hippocampus have been identi ﬁed in juvenile BD (Frazier et al., 2005).
Diminished function of the prefrontal cortex and related circuits might interferewith effective planning and goal pursuit in the context of emotion, leading to alow capacity to regulate emotion. Although prefrontal cortical deﬁ cits have been
implicated in schizophrenia as well (Barch, 2005), recent research suggests that theprefrontal de ﬁcits in BD compared to schizophrenia may be more speci ﬁc to the
orbitofrontal cortex (Altshuler, Bookheimer, Townsend, et al., 2005; Cotter, Hudson, &Landau, 2005). Several recent studies have suggested diminished connectivity ofregions of the prefrontal cortex with the amygdala when persons with bipolar disorderare viewing positive stimuli, although ﬁndings have not been congruent regarding
which regions of the prefrontal cortex are implicated (Almeida et al., 2009; Versaceet al., 2010; Wang et al., 2009).
Patterns of neural activation appear to shift with mood episodes. During depres-
sion, diminished activity in the anterior cingulate is observed (Mayberg et al., 2004).During mania, persons with BD may show diminished reactivity to negative stimulicompared with healthy or euthymic persons. For example, after viewing faces withdifferent negative emotional expressions, patients with mania showed decreasesin amygdala and subgenual anterior cingulate cortex activity compared to controls(Lennox, Jacob, Calder, Lupson, & Bullmore, 2004). Hence, brain regions involved inidentifying the importance of negative stimuli appear to become less active duringmanic episodes.
Finally, given models of reward sensitiv ity in BD, the role of structures within
the basal ganglia, including the nucleus accumbens (Knutson, Adams, Fong, &Hommer, 2001), has become an important focus of research. Both at rest and duringmotor tasks, the level of activity in the basal ganglia is positively correlated with theconcurrent level of manic symptoms (Blumb erg et al., 1999; Caligiuri et al., 2003;
Delvecchio et al., 2012).
Hence, one theory is that BD is related to dysregulation in brain regions relevant
to emotional reactivity, such as the amygdala, as well as regions in the prefrontalcortex involved in the regulation of emotion and cognitive control. Much of thisresearch demonstrates strong parallels with unipolar depression. Evidence suggeststhat neural activation is somewhat mood-state dependent. Regions involved inreward motivation are an important focus for research.
CASE STUDY
C
ASEIDENTIFICATION AND PRESENTING COMPLAINTS
Leonard, a 57-year-old White male, lived with his wife, Helen, and 15-year-old
son in a rented house in the suburbs of a major metropolitan area. His wiferequested treatment because of his angry o utbursts, sleep disturbance, and bizarreBipolar and Related Disorders 235

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preoccupations. He had become preoccupied with kickboxing and was spendinghours on the Internet examining relevant websites and writing about it. Shediscovered that he had written a 500-pag e manuscript describing the mechanics
of kickboxing, containing sections that were rambling, philosophical, and at timesincoherent. She explained that he was frequently awake until 4
A.M.a n dw e n tt o
bed smelling of alcohol. For nearly 5 years he had been unable to hold a job.
Leonard presented in his ﬁrst interview as combative and oppositional. He
admitted that he had been feeling “revved ”over the past 2 weeks, that he felt
full of energy and ideas, and that he needed little sleep, but he denied any negative
effects of his symptoms. He described an in cident that appeared to be related to his
recent manic behavior. He had made contact with a kickboxing champion in anotherstate and had started writing to this man about setting up a new television networkdevoted to kickboxing. He also claimed he was going to start his own studio. Theplans seemed unrealistic given that he had little formal training in this sport and had
no money to rent a studio. The kickboxing champion had stopped responding toLeonard’ s emails, which, Leonard claimed, might be because “he’sr a i s i n gm o n e y
and wants to surprise me. ”
Leonard had one manic episode accompanied by hospitalization when he was in
college. He had become entranced by a female professor and believed that she wasrelated to him by blood. He began calling her continually and ﬁnally followed her out
to a parking lot and tried to block her from getting into her car. A passerby called thepolice, and Leonard was taken to the hospital. He was admitted with the diagnosis ofbipolar I, manic episode.
Since this time Leonard had functioned poorly. His work had been intermittent,
and he had been ﬁred several times because, as he explained, “My bosses are
always idiots and I ’mm o r et h a nh a p p yt ot e l lt h e ms o . ”He had tried to set up a
web-based business selling automobile window shields but had made little money.He met Helen during a hiking excursion for singles. They had married approxi-
mately 1 year after they met (a period of r elative stability for Leonard) and had a
child 1 year later.
Leonard had begun medication shortly after his son was born, explaining that he
wanted to become a stable father. His psych iatrist recommended lithium carbonate
1,200 mg and divalproex sodium (Depakote) at 2,000 mg. Although Leonard didnot have further manic episodes, he had several hypomanic periods and complainedof an ongoing depression that never ful l yr e m i t t e d .H eh a dt h o u g h to fs u i c i d e
several times, and these fantasies usually had a dramatic quality. For example, hefantasized about setting himself on ﬁre and then jumping from a tall building.
He never made an attempt.
The clinician who evaluated Leonard admin istered the Structured Clinical Inter-
view for DSM-IV (First et al., 1995), which involved an individual interview with
him, followed by a separate interview with his wife. The interview con ﬁrmed the
presence of elated and irritable m ood for the past 2 weeks, along with in ﬂated self-
esteem, increased activity, decreased need for sleep, ﬂight of ideas and racing
thoughts, pressure of speech, and increased spending. His behavior did not requirehospitalization but clearly interfered wit h his functioning. He was given a diagnosis
of bipolar disorder I, manic episode and st arted on a regimen of lithium, divalproex,
and an atypical antipsychotic ag ent, quetiapine (Seroquel).236 S
PECIFIC DISORDERS

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SUMMARY
Much progress has been made in clarifying the diagnostic boundaries, genetic path-ways, and neurobiological mechanisms relevant to bipolar illness. New studiesrecognize the strong in ﬂuence of psychosocial variables against this background of
biological and genetic vulnerability. Psychotherapy is an effective adjunct to phar-macotherapy in the long-term maintenance treatment of the illness, notably interven-tions that focus on enhancing the patient ’s understanding of the disorder and
effectiveness in coping with its cycling.
Major focal areas for future studies include clarifying the validity of the bipolar
spectrum. It is unclear whether bipolar illness should include only DSM-5 -deﬁned
bipolar I or bipolar II disorder or whether it should also include subsyndromal mixedpresentations (e.g., depression with signi ﬁcant anxious-agitation), cyclothymia, or
episodes of mania, hypomania, or depression that do not meet the full severity orduration criteria. Nowhere are these questions more critical than in de ﬁning childhood-
onset BD, which is being diagnosed with increasing frequency. In the future, it may bethat fMRI or other imaging techniques will identify brain changes uniquely associatedwith bipolar illness, but until that time we must rely on clinical interviews andsupplemental questionnaires to diagnose these conditions. Research that improvesthe reliability, clinical utility, and consumer acceptance of existing diagnostic methods istherefore critical.
The interface between psychosocial and biological risk factors deserves considera-
ble study, especially as these factors relate to different poles of the disorder. As wehave summarized, life events involving goal attainment and factors that disrupt sleepare strongly correlated with the onset of manic episodes, although their role inpredicting illness onset has not been established in longitudinal studies. High intra-familial EE and negative life events stress are most consistently associated withdepressive episodes. Laboratory-based translational research may help clarify theavenues from speci ﬁc stressors to biological changes to manic versus depressive
symptom exacerbations.
The optimal combinations of psychotherapy and pharmacotherapy must be iden-
tiﬁed in trials that sample populations of diverse ethnicity, socioeconomic status,
psychiatric and medical comorbidity, and chronicity. Large-scale studies such asSTEP-BD are a move in this direction, but even studies of this size can be under-powered for examining treatment effects within speciﬁ c subgroups (e.g., patients with
comorbid substance dependence, rapid-cycling patients, patients of African Americanor Latino heritage). Studies that adapt treatment methods to the cultural needs ofspeciﬁc populations are essential to moving the ﬁeld forward.
Last, treatment studies should consider the synergy between biological and
psychosocial interventions, and under what conditions combining one with the otherwill produce the most enduring effects. For example, drugs that stabilize moodsymptoms may also energize patients to the extent that they become more amenableto the skill-oriented tasks of cognitive-behavioral treatment. Psychoeducational treat-ments may increase medication adherence, which in turn may allow patients toremain stable on fewer medications or on lower dosages. Interpersonal or familyinterventions that increase the patient’ s ability to bene ﬁt from social support and
decrease the impact of family or life stressors may decrease the need for adjunctiveBipolar and Related Disorders 237

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antidepressants in long-term maintenance. Ideally, the next generation of clinicalresearch in BD will address these questions.
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CHAPTER 7
Mood Disorders:
Depressive Disorders
LEILANI FELICIANO and BRENNA N. RENN
DESCRIPTION OF THE DISORDER
Depressive disorders are among the most common psychiatric disorders occurring inadulthood (Waraich, Goldner, Somers, & Hsu, 2004). They are characterized byfeelings of sadness, lack of interest in formerly enjoyable pursuits, sleep and appetitedisturbances, feelings of worthlessness, and at times thoughts of death and dying. Inolder adults, depressive disorders may present differently, with less reported sadnessand depression and more somatic complaints (Hybels, Blazer, Pieper, Landerman, &Steffens, 2009).
All depressive disorders are extremely debilitating and negatively impact the
quality of life of those af ﬂicted. At the beginning of this millennium, depressive
disorders were second only to heart disease as the illness most responsible for poorquality of life and disability (Pincus & Pettit, 2001). By the year 2030, major depressivedisorder (MDD) is predicted to be among the leading causes of disability globally,comparable to heart disease and second only to HIV/AIDS (Mathers & Loncar, 2006).Depression is also associated with increased suicide risk. In a recent cross-nationalsample of 17 countries, individuals with a mood disorder had an odds ratio of 3.4to 5.9 over that of individuals without a mood disorder, even after controlling for suchfactors as age, education, and relationship status (Nock et al., 2008). In terms of suicidecompletion, early statistics indicated that 15% of people with major depressioncompleted suicide (Guze & Robins, 1970), although recent estimates are moreconservative and place the lifetime risk of completed suicide between 2.2%(Bostwick & Pankratz, 2000) and 4.2% (Coryell & Young, 2005) in individuals withdepressive disorders. Comorbid substance use and personality disorders (borderlinepersonality disorder in particular) increase the risk of attempted and completedsuicide in people with depressive disorders (Bolton, Pagura, Enns, Grant, & Sareen,2010). Fortunately, depressive disorders can be treated successfully with psycho-therapy, antidepressant medication, or both (Norman & Burrows, 2007).
The research on these disorders continues to grow, and we know quite a bit about
how depressive disorders are presented, their etiology, and their course and progno-sis. The purpose of this chapter is to describe the depressive disorders and the revised
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diagnostic criteria, discuss their prevalence and effects on people who have thesedisorders, examine the best methods for assessing depressive disorders, and presentthe latest research on their etiology.D
IAGNOSIS AND DESCRIPTION
According to the ﬁfth edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5 ; American Psychiatric Association [APA], 2013), depressive disorders now
include several categories of illnesses: disruptive mood dysregulation disorder (appli-cable to children up to age 18 only), major depressive disorder (MDD), persistentdepressive disorder (formerly dysthymic disorder), premenstrual dysphoric disorder,substance/medication-induced depressive disorder, and depressive disorder due to amedical condition. The previous catchall category Depressive Disorder Not OtherwiseSpeci ﬁed (Depression NOS) has been replaced with a choice of other speciﬁ ed
depressive disorder and unspeci ﬁed depressive disorder, which allows for more
clinical speci ﬁcity. Using three of the diagnostic categories as an example, Table 7.1
illustrates how mood disorders in adulthood share common symptoms and clinicalfeatures. First, all disorders consist of mood symptoms, which include feeling “sad,
empty, or irritable. ”Second, these disorders are characterized by vegetative symp-
toms, which include fatigue, social withdrawal, and agitation. As with all mental
Table 7.1
Sample Diagnostic Criteria
SymptomsMajor Depressive
DisorderPersistent Depressive
Disorder (previously
Dysthymic Disorder)Other Speci ﬁed
Depressive Disorder
(previously
Depression NOS)
Depression Either depressed moodor anhedonia along withat least four othersymptoms must bepresent for no less than2 weeks, all day nearlyevery day.Depressed mood, plustwo or more symptomsmust be present for atleast 2 years, occurringmore days than not.Either depression oranhedonia plus othersymptoms speci ﬁct o
disorder speci ﬁed.
Duration is variabledepending on disorderspeci ﬁed.
AnhedoniaChange in appetiteChange in sleepAgitation or slowingLoss of energyDecreased concentration/trouble making decisionsThoughts of death/suicideFeeling guilty orworthless254 S PECIFIC DISORDERS

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disorders, these symptoms must cause signi ﬁcant distress and affect the person ’s
functioning.
Disturbances in sleep and appetite are also common, with lack of sleep and
appetite being more typical with depressi on, although patients with an atypical
presentation (discussed later) will complain of hypersomnia (increased sleep) orweight gain caused by frequent eating/overeating. Finally, all disorders consist ofc o g n i t i v es y m p t o m s .T h e s ei n c l u d et r o u b l ec o n c e n t r a t i n g ;d i f ﬁculty making deci-
sions; low self-esteem; negative thoughts about oneself, the world, and others;guilt; and suicidal ideation. The degree to which these features occur and thenumber of symptoms present will determi ne which type of depressive disorder a
person may be experiencing. Next we discuss each mood disorder that occurs inadulthood to clarify how it can be d istinguished from the others.
M
AJORDEPRESSIVE DISORDER
Major depressive disorder (MDD) is the most serious and most widely studied depres-
sive disorder. It is characterized by at least one major depressive episode (MDE), with no
history of mania (period of intense energy, euphoria, distorted thinking, and behav-ioral excesses). To qualify as an MDE, either depressed mood or lack of interest orpleasure in usual activities (anhedonia) must be present, most of the day, nearly everyday, and the episode must last at least 2 weeks. In addition, at least ﬁve out of nine
possible symptoms (listed in Table 7.1) must be present during that same period. Thesymptoms must be severe enough to interfere with the individual ’s social, educa-
tional, or occupational functioning. Lastly, the symptom picture should not be betteraccounted for by another condition (e.g., a medical condition, directly related to use orwithdrawal of a substance, a psychotic disorder).Speci ﬁers Major depressive disorder is further quali ﬁed as to its severity, chronicity,
and remission status. Severity is generally determined by the degree of disabilityexperienced by the affected person. If the person can continue to pursue obligations(work, family, and social activities), then the depression is rated as mild. If the person
has trouble getting out of bed and can no longer engage in any obligated activities,then the depression is rated as moderate . If a person is thinking of death or dying; is so
vegetative that he or she has not gotten out of bed, eaten, or engaged in any self-management activities, then the depression is rated as severe . With severe cases, if the
person is exhibiting psychotic behavior, the speciﬁ er of with psychotic features would be
designated, as well. Although it is rare, an individual with depression can exhibitsymptoms of catatonia, which is characterized by immobility, excessive motoractivity, extreme negativism or mutism, and bizarre posturing. In these cases, thequaliﬁerwith catatonia would be most appropriate. See the Diagnostic Speci ﬁers
section for more details.
A person will be diagnosed as having MDD, recurrent type if there has been more
than one episode of MDD with a minimum period of two consecutive months (inwhich the person no longer quali ﬁes for an MDE) between the episodes. Because
research has found MDD to be a recurrent disorder (single episodes are rare), if aperson has had an episode of MDD but is no longer experiencing any depressivesymptoms, that person is considered to be in remission .Mood Disorders: Depressive Disorders 255

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In addition to these quali ﬁers, clinicians should also note features of the disorder
related to its presentation (e.g., with anxious distress, mixed features, atypicalpresentation) (discussed in detail later in the Diagnostic Speci ﬁers section).
P
ERSISTENT DEPRESSIVE DISORDER
Persistent depressive disorder (previously Dysthymic Disorder or Dysthymia) encom-
passes two disorders from DSM-IV-TR (APA, 2000), Chronic Major Depressive Disorder
and Dysthymic Disorder, and regrouped them into a single disorder. Persistent
depressive disorder is generally not considered to be as severe as MDD as it requiresfewer symptoms for diagnosis. However, given that the duration required fordiagnosis of persistent depressive disorder is longer (2 years versus 2 weeks), theseverity differential between the two diagnostic categories may be debatable.
For diagnosis, the symptoms of persistent depressive disorder (listed in Table 7.1)
must be present for 2 years, during which time there should be no more than a 2-m o n t hp e r i o di nw h i c ht h ep e r s o ni ss y m p t o mf r e e .I nt h e DSM-IV-TR ,ad i a g n o s i s
of dysthymic disorder used to carry an additional requirement that no MDE bepresent during the ﬁr s t2y e a r so fd y s t h y m i cd i s o r d e r ,a l t h o u g ho n ec o u l do c c u r
after the 2-year period. If MDD occurred after the 2-year period, it was commonlydescribed as double depression . However, in the DSM-5 , this requirement has been
dropped. Thus, the criteria for an MDD ma y be met continuously during the 2-year
span. However, because the criteria for persistent depressive disorder requiresfewer symptoms, if a person ever meets full criteria for an MDE, the diagnosisshould be amended to include MDD as a quali ﬁer. In the DSM-IV-TR ,t h i sw a s
previously designated as Chronic MDD ,b u ti n DSM-5 this has been folded into the
persistent depressive disorder category. O f course, symptoms of persistent depres-
sive disorder must not be due exclusivel y to other disorders (including medical
conditions) or to the direct physiological effects of a substance (including medica-tion). As in MDD, the person must not ever have met criteria for manic episode,
hypomanic episode, or cyclothymic disorder, and the disorder should not be betteraccounted for by any of the psychotic disor ders (e.g., occur only during the course of
ap s y c h o t i cd i s o r d e r ) .Speci ﬁers If persistent depressive disorder occurs before age 21, it is described as
having early onset ; otherwise, it is described as having late onset. In addition to onset
qualiﬁers, clinicians should note the speci ﬁc features of the disorder (e.g., with
anxious distress, mixed features, atypical presentation, psychotic features) (dis-
cussed in the Diagnostic Speci ﬁers section). Clinicians sh ould also note whether the
disorder has a pure dysthymic syndrome, where the full criteria for an MDE have
never been met in the 2-year span. However, if the full criteria for an MDE have beenmet consistently during this 2-year span, then clinicians would specify that apersistent MDE was present. If there were 2-mo nth periods within the current
episode in which symptoms were subthreshold for an MDE but some depressivesymptoms were present, then a speci ﬁer of intermittent MDE, within current episode
would be given. Similarly, if intermittent MDEs have occurred previously, but notwithin the context of the current episode, a speci ﬁer of intermittent MDE, without
current episode would be noted.256 S
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PREMENSTRUAL DYSPHORIC DISORDER
Previously categorized as a provisional disorder under the DSM-IV (found under
Appendix B, “Criteria Sets and Axes Provided for Further Study”), premenstrual
dysphoric disorder has been instituted under the mood disorder section of DSM-5.
This mood disorder is thought to be caused by hormonal ﬂuctuations in the female
menstrual cycle (with symptoms more severe than what is typically seen withpremenstrual syndrome). The distinguishing characteristics of premenstrual dys-phoric disorder include the presence of ﬁve or more mood symptoms (i.e., signi ﬁcant
depressed mood, signi ﬁcant mood swings, irritability, anxiety, decreased interest in
activities, dif ﬁculty concentrating, lethargy, appetite changes, sleep dif ﬁculties, feeling
overwhelmed and physical symptoms) that occur in the majority of menstrual cycles(minimally over two cycles) and are tied to the course of the menstrual cycle. Thus,onset of symptoms begins during the premenstrual phase (approximately 1 weekbefore menses), begins to remit during or shortly after menses, and is absent orminimally present in the week postmenses. As with all mood disorders, the symptomsof premenstrual dysphoric disorder are associated with signi ﬁcant distress and
impairment in meaningful activity (e.g., negatively impacts or interferes withwork, school, or social performance). The mood disturbance should not be betteraccounted for by another disorder (e.g., MDD, panic disorder), although it may becomorbid with other disorders.S
UBSTANCE /M EDICATION -INDUCED DEPRESSIVE DISORDER
Substance/medication-induced depressive disorder is diagnosed when an individual expe-
riences depressed mood and/or anhedonia after exposure to a substance or medica-tion capable of producing such effects (e.g., alcohol, hallucinogens, opioids;medications such as antiviral agents, cardiovascular agents, hormonal agents, andimmunological agents, and psychotropic medications; see Botts & Ryan, 2010 for areview). This diagnosis is based on ﬁndings from the individual ’s history, physical
examination, and/or laboratory tests that provide evidence for a temporal linkbetween the depressive symptoms and medication/substance use or intoxication.For example, the mood disturbance should not precede the use of the substance ormedication. Like other depressive disorders, symptoms of substance/medication-induced depressive disorder must be severe enough to result in clinically signi ﬁcant
distress and/or impairment in important areas of functioning.
Although the symptoms of depression seen in this disorder may be similar to those
of MDD and other depressive disorders, the disturbance seen in this diagnosis shouldnot be better explained by another depressive disorder. Like all diagnoses, clinicaljudgment is essential. The clinician should evaluate whether the medication orsubstance is truly causative of the mood symptoms, or whether an independentdepressive disorder happened to co-occur with the use of medication or substances.The symptoms of this disorder often remit within days to weeks, depending on thehalf-life of the substance; mood disturbances that carry this diagnosis should notpersist for a substantial length of time (e.g., 1 month) after discontinuation ofsubstance or medication use. The clinician must also rule out delirium as a causefor this mood disturbance.Mood Disorders: Depressive Disorders 257

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DEPRESSIVE DISORDER DUE TO ANOTHER MEDICAL CONDITION
In the DSM-5, this diagnostic category has been removed from its previous designa-
tion under Depressive Disorder, NOS and recategorized as a full depressive disorder.Depressive disorder due to another medical condition refers to circumstances in which
depressed mood or anhedonia is present and there is clear “evidence from the history,
physical examination, or laboratory ﬁndings that the disturbance is the direct path-
ophysiological consequence of another medical condition ”(APA, 2013). That is, the
clinician determines that a medical condition is present and that it is causally related tothe mood disorder through a physiological pathway. For example, the clinician shouldevaluate the temporal relationship between any changes in the medication condition(i.e., onset, worsening, or remission) and the onset of depressive symptoms. Exampleswould include Depressive Disorders due to problems with the thyroid, poststroke,postsurgery, and so forth. This disorder must be distinguished from those disorders inwhich the symptoms are caused indirectly as when there are insuf ﬁcient resources to
cope with/manage the stressor (e.g., adjustment disorder with depressed mood) orare likely caused by a delirium process.O
THER SPECIFIED AND UNSPECIFIED DEPRESSIVE DISORDERS
Previously in the DSM-IV-TR, the Depressive Disorder, Not Otherwise Speci ﬁed
category was treated as a catchall for depressive conditions that were provisionaryand had not been studied in depth. In the DSM-5 , this category has been phased out
and replaced by two options: other speci ﬁed disorder and unspeci ﬁed depressive
disorder.Other Speci ﬁed Disorder This category of disorders is characterized by depressive
disorders that are s ubclinical in that they do not meet the full criteria for any of the other
depressive disorders mentioned here, yet the symptoms cause signi ﬁcant distress or
impairment in functioning. The DSM-5 describes three examples of disorders that
would ﬁt under this category including recurrent brief depression, short-duration
depressive episode, and depressive episode with insuf ﬁcient symptoms, although this
is not an exhaustive list. Recurrent brief depressive disorder is characterized by repeated
episodes of depression that last for at least 2 days, but less than 2 weeks. Speci ﬁcally an
individual would need to present with depressed mood and at least four othersymptoms for the speci ﬁed time period, once per month, for 12 consecutive months
in order to qualify for this diagnosis. Short-duration depressive episode is also character-
ized by depressed mood and at least four of eight symptoms of an MDE over aminimum of 4 days, but lasting less than 2 weeks. However, this diagnosis does nothave the chronicity of recurrent brief depressive disorder or the severity of MDD.Lastly, depressive episode with insuf ﬁcient symptoms requires depressed mood and at
least one of eight symptoms of an MDE that persists for at least 2 weeks.Unspeci ﬁed Depressive Disorder This category is reserved for those situations in which
the clinician determines that the individual ’s symptom presentation is characteristic of
a depressive disorder (e.g., depressed mood, signi ﬁcant distress, or impairment in
functioning), but the symptoms do not meet criteria for any other diagnostic category258 SPECIFIC DISORDERS

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of mood disorder. This category allows for clinical judgment and the ﬂexibility of
diagnosing the presence of a mood disorder when there is inadequate informationavailable to make a differential (e.g., in short-term, integrated care settings in whichthere is more emphasis on solutions rather than conducting a full comprehensiveintake, in emergency room settings, in situations where the individual is a poorhistorian and no collateral informants are available).D
IAGNOSTIC SPECIFIERS
Clinicians add speci ﬁers as appropriate to provide more information about an
individual ’s unique presentation. The DSM-5 added several new speciﬁ ers to the
previous ones available under earlier editions. Speci ﬁers can be thought of as subtypes
of depressive disorders and are classi ﬁed with the following: (a) anxious distress,
(b) mixed features, (c) melancholic features, (d) atypical features, (e) mood-congruentpsychotic features, (f) mood-incongruent psychotic features, (g) catatonia, (h) peri-partum onset, and (i) seasonal pattern. Anxious distress may be used to describe an
MDE or persistent depressive disorder characterized by psychomotor agitation suchas tenseness or restless behavior, or anxious thoughts such as worry, fear, or sense oflosing control. Mixed features refer to an MDE that presents with at least three
hypomanic/manic symptoms such as expansive mood or increased psychomotoractivity (e.g., decreased need for sleep, ﬂight of ideas, pressured speech).
MDE and persistent depressive disorders can also present with melancholic features,
such that the mood disturbance is characterized by a near-absence of the capacity forpleasure and/or an inability to feel better, even brie ﬂy, when something good
happens (mood reactivity). This melancholic presentation is further classiﬁ ed by a
sense of despondency and despair, psychomotor symptoms, early morning awaken-ing, and depression that is worse in the morning. Some researchers have suggestedthat this subtype is more typically associated with biological etiology and that it maybe more responsive to psychopharmacological intervention than to psychotherapies(Andrus et al., 2012; Simons & Thase, 1992).
Conversely, atypical features are speci ﬁed during a depressive disorder in which
mood reactivity is notable (i.e., the individual ’s mood brightens in response to
something positive) and occurs in conjunction with psychomotor symptoms of weightgain or increased appetite, hypersomnia, and/or leaden paralysis (i.e., feeling asthough one ’s limbs are heavy, leaden, or weighed down). These individuals may
also present with a long-standing pattern of sensitivity to “interpersonal rejection. ”
This depressive subtype is thought to be primarily triggered by stressful life eventsor a speci ﬁc psychosocial problem. Although most researchers agree there is likely to
be some genetic component to this subtype as well, depression would only beexpressed in the face of a major problem that a person could not solve immediately(e.g., loss of employment). This tends to be interpreted as suggesting a depressivedisorder that is more likely to respond to psychosocial interventions than to medica-tions (Nutt et al., 2010).
Speci ﬁers related to psychotic features provide information about whether the
depressive disorder presents with delusions and/or hallucinations, and whetherthese symptoms are congruent orincongruent with depressed mood (i.e., content of
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punishment, or guilt). If catatonic features occur during an MDE, the catatonia speciﬁer
is used to describe this marked decrease in reactivity to the environment. Althoughhistorically associated with schizophrenia, catatonia can occur in other disorders, suchas severe MDD.
Finally, two other speci ﬁers provide information about mood disturbances that are
related to context-speci ﬁc factors. First, peripartum onset is speci ﬁed when onset of
symptoms in an MDE occurring during pregnancy (prepartum) or within the ﬁrst 4
weeks following delivery (postpartum). These symptoms can occur with or withoutpsychotic features. If an individual experiences recurrent MDEs that are temporallyassociated with a particular time of year (e.g., in the winter), his/her depression isspeciﬁedwith seasonal pattern.
In addition to providing more information about a context for a depressive
disorder, these speciﬁ ers have clinical and prognostic utility. For example, individuals
with a mixed feature presentation are at risk of receiving a bipolar disorder diagnosisin the future. Melancholic features are more frequently seen on an inpatient rather thanoutpatient basis and may co-occur with psychotic features. Psychotic features areassociated with lower recovery rates compared to depressive episodes not compli-cated by psychotic presentation. Peripartum onset of an MDE with psychotic featuresis associated with infanticide when the mother experiences command hallucinationsto kill the infant or delusions of the infant ’s possession.
W
HENDEPRESSION ISNOT ADEPRESSIVE DISORDER
Sometimes symptoms of depression may be present but may not be diagnosed as oneof the depressive disorders. People who develop depression after a signi ﬁcant life
stressor for a short time are more likely to be suffering from an adjustment disorder
rather than a mood disorder (in the DSM-5 adjustment disorders are found under the
new Trauma- and Stressor-Related Disorders section). In addition, a previous manicepisode will also exclude a diagnosis of MDD or persistent depressive disorder.Finally, if the individual with depression has symptoms that are better accounted forby another diagnostic category, then that diagnostic category should be assigned inlieu of a depressive disorder (e.g., schizoaffective disorder). See the section ondisorders due to another psychiatric condition.
Everyone experiences feelings of sadness from time to time. This is a normal
experience that should not be pathologized. Depressive symptoms are consideredproblematic when they persist for 2 weeks or more and are accompanied by distressand considerable dif ﬁculty managing day-to-day activities. In the next section, we
provide examples of these disorders.
CLINICAL PICTURE
Major depressive disorder, dysthymic disorder, and other speciﬁ ed and unspeci ﬁed
depressive disorders all vary to a degree in their presentation but share severalfeatures that distinguish these disorders from other mental illnesses. People withdepressive disorders can be identi ﬁed by their pessimism and negativistic thinking,
difﬁculty solving even everyday problems, and lack of initiative. People with260 S
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depressive disorders are also quite disabled by the illness and often report havingmultiple somatic symptoms.
Most people with a depressive disorder exhibit what is called negativistic thinking .
This term was coined by Aaron Beck (Beck, 1961) and has since been used extensivelyto describe the cognitive style of people suffering from depressive disorders. Nega-tivistic thinking is best described as a style of thinking that is overly pessimistic andcritical. People with depression tend to expect failure and disappointment at everyturn and will focus only on their past failures as a way to con ﬁrm these beliefs (Alloy
et al., 2000). People with negativistic thinking also have poor self-esteem and are morelikely than people without this cognitive bias to experience depressive symptoms(Verplanken, Friborg, Wang, Traﬁ mow, & Woolf, 2007). The presence of negativistic
thinking in depression is a bit of a “chicken or egg ”problem: Does depression cause
negativistic thinking, or does negativistic thinking cause depression? Recent researchsuggests that the cause of depression is more likely an imbalanced thinking style andthat negativistic thinking may have a clearer association with repeated exposure tofailure and disappointment. In a study by Issacowitz and Seligman (2001), people withpessimistic thinking as well as those with optimistic thinking were at risk fordeveloping depressive symptoms after exposure to stressful life events. In fact,optimists were at higher risk for depression than pessimists were, although pessimiststended to have more persistent depression. Therefore, objective perceptions of one ’s
abilities, of one ’s environment, and of other people are likely to be more protective
than overly optimistic or pessimistic styles of thinking.
Negativistic thinking is primarily responsible for why individuals with depression
ﬁnd it dif ﬁcult to engage in and enjoy activities that once gave them pleasure, and thus
social isolation is a common feature of depressive disorders (Cacioppo, Hawkley, &Thisted, 2010). Many people with a depressive disorder will report that they havestopped socializing or engaging in pleasant activities, largely because they anticipateno enjoyment from the activity (Chentsova-Dutton & Hanley, 2010). As will bediscussed in the section on etiology, it is felt that repeated exposure to stress willinﬂuence the reward centers of the brain; animal studies have demonstrated that
repeated exposure to negative events will result in the adoption of avoidancemotivation over appetitive motivation; in other words, people who experience toomany negative experiences begin to anticipate that all experiences will be negative andtherefore, they will be motivated by pain reduction rather than by need for pleasure(Ho & Wang, 2010).
It is important that people who have depression attempt to reengage in social
activities. Increased social isolation puts the individual with depression at greater riskof severe depression. Several studies show that social support can offset the occurrenceor worsening of depression, and thus increasing exposure to socialization is animportant process in recovering from depression (Barros-Loscertales et al., 2010;Dichter, Felder, & Smoski, 2010; Jakupcak, Wagner, Paulson, Varra, & McFall,2010; Mazzucchelli, Kane, & Rees, 2010).
People with a depressive disorder also tend to use passive coping skills, or they
avoid solving problems (Nolen-Hoeksema, Larson, & Grayson, 1999). This is some-times due to a preexisting skills de ﬁcit or to learned helplessness, a condition caused
by repeated attempts and failures to cope with problems (Folkman & Lazarus, 1986).Most often, after people develop depression, they avoid proactive attempts to solveMood Disorders: Depressive Disorders 261

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problems because they anticipate that they are not capable of implementing asuccessful solution (Nezu, 1986). This avoidance often results in more problems;for instance, avoiding marital problems potentially results in divorce.
A relatively recent movement, positive psychology , focuses on an individual ’s
strengths (virtues) as well as any skills de ﬁcits in the treatment of depression
(Sin & Lyubomirsky, 2009). Seligman and Csikszentmihalyi (2000) discuss positivepsychology as an adjunct to treatment of mental health problems to provide treatmentto the whole person rather than a focus on treating the depressive symptoms only. Themain tenets involve putting our strengths to work in achieving a balance of three lives:the pleasant life, the good life, and the meaningful life. Seligman and colleagues havedesigned and researched a series of Internet exercises designed to increase happinessand decrease suffering. For a more detailed review, see Seligman, Steen, Park, andPeterson (2005).
Many people are often surprised to discover how disabling depression can be.
People who have depression will complain of somatic problems, such as fatigue,stomach upset, headaches, and joint pain (Viinamaeki et al., 2000). These symptoms,coupled with the pessimism and avoidant style associated with depression, are relatedto the increased number of disability days reported by people with depressivedisorders (Pincus & Pettit, 2001). In the National Comorbidity Survey (NCS; Kessler &Frank, 1997), people with depression reported a ﬁvefold increase in time lost from
work than did those without depression. In fact, individuals treated for depressionincurred greater disability costs to employers than did people needing treatment forhypertension and had costs comparable to those with more severe chronic illness likediabetes (Conti & Burton, 1995; Druss, Rosenheck, & Sledge, 2000). Data from theNCS-R (Greenberg et al., 2003) suggested that the economic burden of depressionstabilized somewhat between 1990 and 2000, rising from $77.4 billion to $83.1 billion(adjusted for in ﬂation). The majority of this burden was associated with workplace
costs (e.g., lost productivity). Interestingly, costs related to treating depression arealmost as great as the costs due to disability days from depression (Kessler et al., 1999),and some studies have found the treatment of depression to decrease disability days(Simon et al., 2000).
DIAGNOSTIC CONSIDERATIONS
Although the DSM-5 provides guidelines for the diagnosis of depressive disorders, the
comorbidity of other medical and psychiatric disorders can complicate a diagnosticdecision. To make an accurate diagnosis of depression, the provider must considerphysical health and medical history, medications, family and personal history, andpsychosocial stressors. With regard to the latter, the DSM-IV-TR previously required
that an individual with bereavement be excluded from an MDE diagnosis, regardless of
symptom presentation, unless their symptoms lasted more than 2 months or resultedin marked impairment, suicidality, or psychotic features.
As discussed in more detail later (see Grief and Bereavement), the DSM-5 has
instituted a change in that bereavement is no longer an exclusion criteria for adiagnosis of depression; people who are suffering from the loss of a signi ﬁcant other
could be diagnosed with a depressive disorder, if they meet the clinical characteristicsof MDE (Corruble, Falissard, & Gorwood, 2011). This is not to say that bereavement262 SPECIFIC DISORDERS

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automatically results in depression; rather, this change re ﬂects the clinical under-
standing that the loss of a loved one, as well as other stressful life events, can trigger agenuine mood disorder when out of proportion to a “normal ”response (Kendler et al.,
2003). Clinicians are urged to consider the culture of the individual in determiningwhat is a normal or expected response to grief/loss, as grief may be expresseddifferently across cultures.M
EDICAL ILLNESS
Theﬁrst important step in diagnosing depressive disorders is to have the patient get a
complete physical. Depression commonly co-occurs with other mental disorders (e.g.,anxiety disorders) and physical disorders (King-Kallimanis, Gum, & Kohn, 2009),which can further exacerbate distress and disability, and can challenge treatmentefforts. Because many medical illnesses are related to the onset of a depressive episode,at times treating both the illness and the depression is a more ef ﬁcient way to effect
symptom change (Gupta, Bahadur, Gupta, & Bhugra, 2006; Katon, 2003; Simon, VonKorff, & Lin, 2005; Stover, Fenton, Rosenfeld, & Insel, 2003; Trivedi, Clayton, & Frank,2007). For example, in endocrinological disorders like hyperthyroidism and hypo-thyroidism, one of the diagnostic signs is a change in affect and mood. People who aretreated for these disorders experience radical changes in mood. Moreover, people withchronic illnesses like diabetes mellitus have high rates of depressive symptoms (deGroot, Jacobson, Samson, & Welch, 1999; Renn, Steers, Jay, & Feliciano, 2013), but notnecessarily higher rates of MDD or persistent depressive disorder (Fisher, Glasgow, &Strycker, 2010; Fisher, Mullan, et al., 2010).
Acute medical illnesses such as stroke (Sagen et al., 2010), Parkinson ’sd i s e a s e
(Caap-Ahlgren & Dehlin, 2001), pancreati c cancer (Jia et al., 2010; Mayr & Schmid,
2010), coronary heart disease (Kubzansky & Kawachi, 2000), and myocardialinfarction (Martens, Hoen, Mittelhaeuser, de Jonge, & Denollet, 2010) are alsoassociated with depressive symptoms. Neurological ﬁndings suggest that cerebro-
vascular disease (particularly ischemic small-vessel disease) may be related to theonset of late-life depression (Rapp et al., 2005). Although it is unclear whether theseillnesses directly cause depression or the depression is the result of the life changesbrought on by the illness, recovery from these diseases (when possible) will helpalleviate depressive symptoms.D
RUG AND ALCOHOL ABUSE
The next step in establishing a diagnosis is to determine to what extent the persondrinks alcohol or uses drugs. Often substance abuse or dependence disordersare strongly associated with depressive symptoms (Gunnarsdottir et al., 2000;Merikangas & Avenevoli, 2000; Ostacher, 2007). Scientists have debated whetherdepressive symptoms are a consequence of substance abuse and the problems relatedto this disorder, or whether the substance use is a means of self-medicating depressivesymptoms. The psychiatric and substance abuse ﬁelds are slowly moving toward the
co-management of depression and substance abuse, and while abstaining fromsubstances does often clarify the diagnostic picture, it is often very unlikely thatsomeone who is abusing substances and has depression will be able to abstain withoutMood Disorders: Depressive Disorders 263

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treatment. Therefore, when these two conditions do present together, cliniciansgenerally ascribe a dual diagnosis and attempt to untangle which disorder wasapparent ﬁrst through gathering a thorough diagnostic history.
In determining the best course of action regarding treatment, it is crucial to get a list
of all medications (both prescribed and over-the-counter) the person uses, given thatthe side effects of many medications can cause or contribute to the depressivesymptoms observed. This is particularly true with older adults, who are morevulnerable to the side effects of medication. For example, in a review of late-lifedepression, Dick, Gallagher-Thompson, and Thompson (1996) note that some medi-cations, such as antihistamines, antihypertensives, some antiparkinsonian drugs, andsome pain medications, commonly cause symptoms of depression. In addition,diuretics, synthetic hormones, and benzodiazepines have also been noted to contrib-ute to depressive symptomatology (Cooper, Peters, & Andrews, 1998). The higher thenumber of drugs the person takes, the higher the risk for medication side effects anddrug –drug interactions —a situation that emphasizes the need for good assessment of
drug regimens.G
RIEF AND BEREAVEMENT
Grief over the loss of a special person or the presence of a major life stress or changecan also complicate attempts to diagnose depressive disorders. Although bereavement
may produce a grief response that mimics symptoms of depression, it was previouslyan exclusion for a diagnosis of MDE or a mood disorder (bereavement in the DSM-IV-
TRwas assigned a V-Code falling under Additional Conditions that may be a Focus of
Clinical Attention). This exclusion was originally intended to prevent misdiagnosing“normal ”grief as depression (Maj, 2008). Therefore, the removal of the bereavement
exclusion has created controversies in the ﬁeld; some clinicians criticized that bereave-
ment was the only psychosocial stressor to exclude an individual from an MDEdiagnosis (Wake ﬁeld et al., 2007), whereas others conceptualize grief as a normal
reaction to loss and are loathe to pathologize it.
The DSM-5 recognizes that a signi ﬁcant psychosocial stressor, such as a loss of a
loved one, can trigger a mood disorder. Because of the overlap between “normal ”
grieving and depression, careful consideration is given to delineate what is a normal orappropriate response, with consideration given to the person ’s history and cultural
norms. In making this distinction, clinicians must use their judgment to decidewhether symptoms (e.g., sadness, weight loss) are appropriate for the loss or whetherthe symptoms more resemble those associated with a depressive episode. Forexample, grieving is typically classi ﬁed by feelings of emptiness and loss, whereas
depression is associated with a persistent sadness and an inability to experiencepleasure or happiness. Also, grief is often experienced in waves of dysphoria, longing,and/or yearning, typically brought on by reminders of the deceased. These pangs ofgrief might also include positive emotions associated with these memories. In contrast,the unhappiness of depression is persistent and pervasive, and not associated withspeciﬁc thoughts or memories.
Although it is possible that those with uncomplicated bereavement or adjustment
disorder can develop a depressive disorder, little is known about the extent to whichgrief can develop into depression (Boelen, van de Schoot, van den Hout, de Keijser, &264 SPECIFIC DISORDERS

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van den Bout, 2010; Wellen, 2010). However, when bereavement and a depressiveepisode co-occur, the individual often experiences more severe functional impairmentand a worse prognosis (Shear et al., 2011; Zisook, Simon, et al., 2010) than bereavementnot accompanied by depression. Individuals with other vulnerabilities to depression(e.g., poor social support, trauma history, increased stressors) may be more apt toexperience a major depressive episode with bereavement (Ellifritt, Nelson, & Walsh,2003; Shear et al., 2011).D
EPRESSION DUE TO OTHER PSYCHIATRIC DISORDERS
Adults with other psychiatric disorders can have co-occurring depressive symptoms,and thus establishing a differential rule-out for these other disorders is often impor-tant. For instance, people with anxiety disorders, particularly generalized anxietydisorder, report feelings of sadness and hopelessness (Hopko et al., 2000). Co-occurring mood and anxiety disorders are also more commonly reported in mid-dle-aged and older women than men (Byers et al, 2009). When under stress, peoplewith personality disorders will also report signi ﬁcant symptoms of depression
(Petersen et al., 2002). In fact, they can become quite acutely depressed. Speci ﬁcally,
depressive episodes are most prevalent with avoidant, borderline, and obsessive-compulsive personality disorders (Rossi et al., 2001). Furthermore, personality dis-orders have an association with a longer remission onset from a depressive episode(O’Leary & Costello, 2001). Finally, depression is common in prodromal phases of
schizophrenia and is a recurrent feature in bipolar disorder.L
ATE-LIFEDEPRESSION
Depression, although not a natural consequence of aging, is one of the most commonmental health disorders that older adults experience. Prevalence rates differ depend-ing on the population surveyed and the settings observed (see Epidemiology section).Older adults present differently than younger populations in that they are less likely toreport feeling sad or depressed (Fiske, Wetherall, & Gatz, 2009) or symptoms of guilt(Gallagher et al., 2010) and may report more anhedonia, memory problems (in theabsence of dementia), and somatic symptoms such as fatigue, decreased appetite, andmuscle pain (Kim, Shin, Yoon, & Stewart, 2002). In addition, because older adults aremore likely to have chronic illnesses, the presence of physical illnesses as well as theside effects of medications taken to treat these conditions can overshadow or worsensymptoms of depression (Areán & Reynolds, 2005), which can further complicatediagnosis. In older populations, depression is also associated with increased mortalityand health service usage. This association highlights the importance of earlyrecognition, differential diagnosis, and treatment of this disabling illness.
EPIDEMIOLOGY
The patients described in this chapter are representative of a growing number ofpeople in the United States suffering from depressive disorders. Several large-scaleepidemiological studies on mental illness have taken place in the United States. TheEpidemiological Catchment Area Study (ECA) was conducted in the 1980s (Regier,Mood Disorders: Depressive Disorders 265

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1988) and was the ﬁrst to de ﬁnitively determine the prevalence of psychiatric
problems in the United States. However, the generalizability of the ECA was limited,as data was collected at ﬁve sites. The second study, called the National Comorbidity
Survey (NCS; Kessler, McGonagle, Zhao, et al., 1994), was carried out on a nationallyrepresentative sample of the United States at the time of data collection. The NCSfocused speci ﬁcally on English-speaking adults between the ages of 18 and 65 and was
mostly concerned with the prevalence of co-occurring DSM-III-R psychiatric disorders
in the United States.
The NCS was replicated a decade later to examine the prevalence for the DSM-IV
and the International Classi ﬁcation of Disease, version 10 (ICD-10) psychiatric disorders
and to provide age-of-onset estimates for me ntal health disorder si nar e p r e s e n t a t i v e
U.S. sample (NCS-R; Kessler et al., 2004; Kessler & Merikangas, 2004). The data from
these studies demonstrate that the prevalence of depressive disorders varies frompopulation to population; therefore, the following discussion will present theprevalence of depressive disorder s by different populations. As the DSM-5 was
released in May 2013, no updated national prevalence data were yet available at thetime of this writing.C
OMMUNITY SAMPLES
Depressive disorders are serious and relatively common. Based on DSM-IV-TR
criteria, the lifetime prevalence, or the number of persons who have ever experiencedany type of mood disorder, is 20.8% (Kessler et al., 2005). The NCS-R (Kessler et al.,2005) found a lifetime prevalence for an episode of major depression to be 16.6% in acommunity-dwelling sample, with a 12-month prevalence of 6.6% (Kessler et al.,2003). Previous estimates of MDE were as low as 5.8% (Regier, 1988) using DSM-III-R
diagnostic criteria. These studies also indicate that in a given 6-month period,approximately 3% to 9% of the general population will experience an episode ofmajor depression (Kessler, McGonagle, Zhao, et al., 1994; Regier, 1988). The lifetimeprevalence for dysthymic disorder is lower than the rates for MDD. According to theNCS and the NCS-R (Kilzieh, Rastam, Ward, & Maziak, 2010), between 2.5% and 6%of the general population has had a period of Persistent Depressive Disorder, puredysthymic syndrome in their lifetimes. No nationally representative prevalence dataare yet available for the new DSM-5 diagnostic label of persistent depressive disorder.
P
REVALENCE BY GENDER
The ECA and the NCS show differential prevalence by gender. In the ECA studies,lifetime prevalence of affective disorders for adult women average 6.6%, whereas inthe NCS, prevalence is signi ﬁcantly higher at 21.3% (Kessler, McGonagle, Nelson,
et al., 1994; Regier, 1988). The lifetime prevalence for men was 8.2% in the ECA and12.7% in the NCS. Although prevalence for depression varied between these twostudies, a consistent theme emerges: More women than men report having depressiveepisodes. The most recent nationally representative prevalence data from the NCS-Rfound that women are at a 1.5-fold increased risk (compared to their male counter-parts) of developing a mood disorder over their lifetime, and a 1.7-fold increased riskof developing MDD speci ﬁcally (Kessler et al., 2003; Kessler et al., 2005). This266 S
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difference between men and women has been found repeatedly throughout theworld and thus appears to be accurate re ﬂections of true differences in the preva-
lence of the disorder between men and women (Kessler, 2003). Although the reasonsfor these differences are relatively unknown, some speculate that sex differences inbiological makeup, differences in cognitiv e and behavioral patterns of mood control
(Nolen-Hoeksema, 2000), and social inﬂ uences, including differential expectations
for the two genders, account for the difference in prevalence (Kilzieh et al., 2010).P
REVALENCE BY AGECOHORT
The prevalence of depressive disorders in the United States varies by age, with theNCS-R reporting a peak in 12-month prevalence of MDD during the ages 18 –29
(Kessler et al., 2003). Prevalence in this age group is threefold higher than theprevalence in individuals 60 years or older; rates drop to a 1.8-fold and 1.2-foldincreased risk for adults aged 30 –44 and 45 –59, respectively (Kessler et al. 2003). The
NCS-R included individuals over the age of 60 and up to the age of 75, which is animprovement over the demographics in the previous ECA and NCS samples(Kessler & Merikangas, 2004). As Burke, Burke, Rae, and Regier (1991) ﬁrst pointed
out, rates for all psychiatric disorders are increasing with each decade, indicating thatdisorders like depression may be in ﬂuenced by cohort effects, including willingness to
self-disclose symptoms and differences in measures utilized (Richards, 2011). How-ever, the information presented by the NCS-R on the differential prevalence rates ofdepression between younger and older people is limited and does not include ourfastest-growing segment of the population, the “oldest-old ”(those age 85 and older).
With the preceding caveat in mind, it is important to highlight what is known aboutthe prevalence of depression in older adults.
The prevalence of depression among older adult populations is one of the highest of
any mental disorder (Baldwin, 2000; Kessler et al., 2005). The NCS-R reports lifetimeprevalence of mood disorders for individuals over the age of 60 to be 11.9%, with themajority of these cases accounted for with the diagnosis of MDD (10.6%; Kessler et al.,2005). However, it is important to keep in mind that the prevalence of depressionvaries substantially by population studied (e.g., NCS-R study did not include institu-tionalized older adults), and is affected by other sociodemographic variables such asgender, socioeconomic status, and race/ethnicity. Also, the difﬁ culties in detecting
depression in older adults (see Late-Life Depression) make this a difﬁ cult population
from which to obtain precise epidemiological data.P
REVALENCE IN MINORITIES
Rates of depression also vary by ethnic group. According to the NCS data, AfricanAmericans have rates of depression similar to those of the Caucasian population.Approximately 3.1% of African Americans have had an MDD episode, and 3.2% havehad persistent depressive disorder, pure dysthymic syndrome (Jackson-Triche et al.,2000). However, Asian Americans have the lowest rates, with only 0.8% reporting thatthey had experienced an MDE and 0.8% experiencing persistent depressive disorder,pure dysthymic syndrome (Jackson-Triche et al., 2000). Hispanics/Latinos were foundto have an interesting presentation of prevalence that depended on immigrationMood Disorders: Depressive Disorders 267

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status. According to Alderete, Vega, Kolody, and Aguilar-Gaxiola (1999), Hispanics/Latinos who recently emigrated from Latin America were less likely to have depres-sion than Hispanics/Latinos who were born and raised in the United States.Hispanics/Latinos who were U.S.-born had rates of depression much like the ratesof Caucasians (3.5% for MDD and 5% for persistent depressive disorder, puredysthymic syndrome), whereas immigrants reported only half the prevalence ofU.S.-born Hispanics. Although uncon ﬁrmed empirically, Vega, Kolody, Valle, and
Hough (1986) believe that lower rates in immigrants result from a heartiness factor;those who are able to withstand the stress related to immigration are more likely tocope with stress related to depression.
There are two relatively new studies aimed at capturing higher numbers of
minorities in epidemiological research: First, the National Latino and Asian AmericanStudy (NLAAS), is a household survey that includes nationally represented samples ofadults from various ethnic groups (i.e., eight different ethnic and subethnic groupsincluding Latinos, Asian-Americans, African Americans, and non-Latino Whites)(Alegría et al., 2004). Second, National Survey of American Life (NSAL), a householdsurvey of community dwelling African-American and Black adults (Caribbean). In arecent study, the data from the NLAAS, the NCS-R, and the NSAL were statisticallytreated and combined into a single dataset ( n=8762). This study found the 12-month
prevalence rates of depressive disorders was higher than that found in earlierepidemiological studies; 5.4% for Asians, 10.8% for Latinos, and 8% for African-Americans compared to 11.2% for non-Latino Whites (Alegría et al., 2008). This studyalso con ﬁrmed that of those with depressive disorders, an alarming number did not
receive any kind of mental health treatment or received inadequate treatment (Alegríaet al., 2008), highlighting the need for better assessment and treatment of depressionfor diverse groups.P
REVALENCE IN SPECIAL SETTINGS
Prevalence of depression in certain settings is greater than what has been found in thegeneral community. For instance, people who have depression are more likely to seekhelp in primary care settings (Wagner et al., 2000). Estimates vary, but most studiesindicate that what used to be referred to as minor depression is the most commondepressive disorder, with as many as 25% of patients meeting diagnostic criteria(Wagner et al., 2000). Although the prevalence of depressive disorders may be high,recurrence is lower in these settings than in the community. According to van Weel-Baumgarten, Schers, van den Bosch, van den Hoogen, and Zitma (2000), patientstreated in primary care medicine are less likely to suffer a relapse or remission thanthose treated in psychiatric settings. However, psychiatry tends to manage moreseverely depressed patients, and thus this ﬁnding is likely an artifact of the popula-
tions served in each setting.
Another setting with high rates for depression is long-term care. Approximately
32% of people living in assisted living facilities experience MDD (Waraich et al., 2004),with new episodes occurring in 31.6% of patients within the ﬁrst 12 months of
admittance (Hoover et al., 2010). The causes for higher prevalence of depressivedisorders in nursing home facilities may vary but most likely include loss of functionalindependence, loss of familiar surroundings, decreased access to pleasant activities or268 SPECIFIC DISORDERS

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loved ones, and comorbid physical illnesses. Given the impact that depressivedisorders have on rehabilitation, the high rate of these disorders in these settingsis cause for concern and argues for more vigilant and proactive treatment of depres-sion in long-term care.
PSYCHOLOGICAL AND BIOLOGICAL ASSESSMENT
The assessment of depression has evolved over the decades, but many issues andcontroversies about the most adequate means of detecting this disorder still remain.Controversies over cultural differences, age differences, and the setting in which aclient is being evaluated are still under investigation. This section focuses on thestrengths and weaknesses of different methods for assessing depression, ranging fromscreening instruments to structured clinical interviews.
ASSESSING THE INDIVIDUAL WITH DEPRESSION
The most common way to assess for depressive disorders is by conducting in-personinterviews with patients. The interviewers, usually mental health professionals ortrained clinic workers, ask patients questions regarding the current episode ofdepression, including the symptoms patients are experiencing, how long they havebeen experiencing them, what they think caused the depression, and what they wouldlike to do about the depressive episode. In addition, intake clinicians will also askabout family and personal history, past and current medical history, previouspsychiatric history, and the impact of the depression on day-to-day functioning.All this information is compiled to determine whether patients have a depressivedisorder, the type of disorder they have, and the degree to which they are suffering.This information is then used to determine the appropriate treatment.
Most mental health professionals use their own methods o f assessment. Some
will conduct an open-ended interview that is guided not by any instrumentation,b u to n l yb yp a t i e n t s ’responses to questions. Although this method is most
commonly practiced, it also carries the greatest risk of misdiagnosis, particularlyif the interviewer is not an expert in depress ive disorders. Because of this risk, many
mental health organizations prefer to use a combination of an open-ended inter-
view with a screening instrument or a guide, such as a semistructured interviewform, to help remind clinicians to ask for all relevant information. In using ascreening instrument or semistructured int erview, it is imperative that the instru-
ments chosen be highly reliable and valid. Other than a medical examination to ruleout physical causes for depressive symptoms, there is no biological test to diagnosedepression, so accurate diagnosis rests with clinicians and the instrumentation usedto conﬁ rm a diagnosis.
S
CREENING INSTRUMENTS
In many health settings, practitioners are concerned with identifying as many peopleas possible who have the disorder so that quick and effective interventions can takeplace. This tradition comes from medical practice, where physicians routinely conductmedical tests when they suspect a particular illness. These screening tests help theMood Disorders: Depressive Disorders 269

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doctor determine whether further tests are needed to make a speci ﬁc diagnosis. For
instance, when a patient sees a doctor about symptoms of fatigue, the physician willlikely order blood and urine screens to determine whether the fatigue is due to anemia,diabetes, or mononucleosis. Standardized screening instruments are used for similarpurposes in mental health. Screening instruments should be highly sensitive; that is,they should detect depression in everyone with the disorder. Otherwise, their utility islimited. Once someone screens positive for depression, further assessment is requiredto con ﬁrm a diagnosis.
The most common mechanism for diagnosing depression in adults is through self-
report measures. The DSM-5 proposed that one such measure, the Nine-Item Patient
Health Questionnaire (PHQ-9; Spitzer, Williams, Kroenke, Hornyak, & McMurray,2000; see below for more detail) be used as an “emerging measure ”for future research
and clinical evaluation to monitor treatment progress. However, there are numerousother self-report measures that are well-represented in the literature and clinicalpractice, including the Beck Depression Inventory (BDI; Beck, 1961; also, BDI-II; Beck,Steer, & Brown, 1996), the Center for Epidemiological Studies —Depression Scale
(CES-D; Radloff, 1977), the Zung Depression Scale (Zung, 1972), the MontgomeryAsberg Depression Rating Scale (MADRS-S; Montgomery & Asberg, 1979), and theProﬁ le of Mood States (POMS; Plutchik, Platman, & Fieve, 1968). Because some of
these measures contain items that are related to somatic symptoms (e.g., fatigue) andare frequently scored in a depressed direction by older adults who have acute physicalor chronic illnesses (Street, O ’Connor, & Robinson, 2007), some self-report measures
have been designed speci ﬁcally for detecting depression in older adults, such as the
Geriatric Depression Scale (GDS; Yesavage et al., 1982). A patient completes theseinstruments and indicates the degree to which he or she has experienced symptomsover a speci ﬁed period (e.g., 1 week, 2 weeks), and then the instrument is hand-scored
by the person administering the scale. A patient ’s score on the instrument re ﬂects the
severity of depressive symptoms.
These instruments are considered cost-effective and ef ﬁcient. They are useful in
primary care settings in making quick diagnoses, especially when followed with asecond-stage interview (Schmitz, Kruse, Heckrath, Alberti, & Tress, 1999). However,they are often too inclusive in that they tend to identify some people as havingdepressive symptoms who do not. They also differ in their assessments of depressionand speci ﬁcations within the diagnosis. For example, the BDI and the MADRS-S are
equivalent in their assessment of depression, but the MADRS-S has a greater focus oncore depressive symptoms than does the BDI (Svanborg & Asberg, 2001). Addition-ally, and of late, many health-care providers are using these instruments for deter-mining a diagnosis. An issue that arises here is that these instruments are designed tobe screening devices and not diagnostic tools. Furthering the problem, researchindicates that such scales may be ef ﬁcient in identifying psychological distress
that might then be erroneously identi ﬁed as major depression (Wake ﬁeld, Baer, &
Schmitz, 2010).
Because of the prevalence of depression in primary care medicine, several instru-
ments have been created speci ﬁcally for use in that environment. These instruments
are meant to raise a red ﬂag to the provider so that a more thorough assessment of
depression can be conducted. The Primary Care Evaluation of Mental Disorders(PRIME-MD; Spitzer et al., 1994) is a good example. The patient completes a brief270 SPECIFIC DISORDERS

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questionnaire in which two questions are red ﬂags for depression. If the patient
endorses one of the two red- ﬂag questions, then the provider asks more speci ﬁc
questions to ﬁnalize the diagnosis. The PRIME-MD has satisfactory reliability and
validity (Spitzer, Kroenke, & Williams, 1999). The Nine-Item Patient Health Ques-tionnaire (PHQ-9; Spitzer, Williams, Kroenke, Hornyak, & McMurray, 2000) is a self-administered depression module adapted from the PRIME-MD. Like the PRIME-MD,it has strong internal reliability in a primary care setting (Cronbach ’s alpha =0.89),
excellent test-retest reliability, as well as good criterion and construct validity(Kroenke, Spitzer, & Williams, 2001). In addition, the PHQ-9 has validity in individ-uals of different ages and from diverse cultural backgrounds, such as Latinos, AfricanAmericans, and people of Asian descent including Thai, Korean, and Chinese, as wellas individuals from Nigeria and Kenya (Adewuya et al., 2006; Diez-Quevedo, Rangil,Sanchez-Planell, Kroenke, & Spitzer, 2001; Han et al., 2008; Huang et al., 2006;Lotrakul et al., 2008; Omoro et al., 2006; Yeung et al., 2008).
Another brief self-report questionnaire for medical patients is the Beck Depression
Inventory —Primary Care (BDI-PC; Beck, Guth, Steer, & Ball, 1997). This seven-item
questionnaire consists of some of the same items from the full BDI and instructs thepatient to rate symptoms occurring over the past 2 weeks on a 4-point scale. Inresearch examining the BDI-PC as a screening measure for MDD, it has been shown tohave high internal consistency in primary care outpatient settings (Cronbach ’s alpha =
0.85; Steer, Cavalieri, Leonard, & Beck, 1999) and in medical inpatients as well(Cronbach ’s alpha =0.86; Beck et al., 1997; Parker, Hilton, Hadzi-Pavlovi, & Bains,
2001). When using a cut score of 4 and greater, it yielded excellent sensitivity (97%)and speci ﬁcity (99%; Steer et al., 1999). Researchers noted that an advantage of the
BDI-PC is that it has not been found to be correlated with age, sex, or ethnicity/racialstatus (Beck et al., 1997; Winter, Steer, Jones-Hicks, & Beck, 1999).
Other structured screening instruments designed for primary care include the
Hospital Anxiety and Depression Scale (HADS; Zigmond & Snaith, 1983) and theMini-International Neuropsychiatric Interview-Screen (MINI-Screen), a shorter ver-sion of the MINI that is available and described in more detail in the following section.The HADS is used in medical and community populations as a quick screen foranxiety and depressive symptoms in patients with physical illness. In an attempt toreduce confounds of depression diagnoses in the medically unwell population, thescreen does not assess somatic symptoms. However, the trade-off is that this renders itless sensitive than other measures at screening for depression (Brennan, Worrall-Davies, McMillan, Gillbody, & House, 2010) and for detecting depression in someminority groups that tend to report more somatic symptoms than affective symptoms.
Another measure used to assess depressive symptom severity in a time-ef ﬁcient
manner is the Quick Inventory of Depressive Symptomatology (QIDS; Rush et al.,2003). The QIDS is a 16-item inventory developed to assess the nine DSM-IV-TR
criterion symptom domains (i.e., sad mood, energy/fatigue, appetite and sleepdysfunction, etc.). The inventory is available in both self-report (QIDS-SR16) andclinician-rating forms (QIDS-C16), and both forms have demonstrated a high degreeof internal consistency (Cronbach ’s alpha =0.86 and 0.86 respectively) and acceptable
psychometric properties (Trivedi et al., 2004).
Two additional screening measures for depression are the General Health Ques-
tionnaire (GHQ; Goldberg, 1972) and the World Health Organization ’s Well-BeingMood Disorders: Depressive Disorders 271

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Index (WHO-5; World Health Organization [WHO], 1990). Both measures are used incommunity and nonpsychiatric clinical settings, such as primary care. The GHQ is ascreening instrument used in primary care and general practice to detect psychiatricdisorders. The original scale included 60 questions intended to capture the patient ’s
somatic and psychiatric symptoms in less than 10 minutes. The test creators found a0.80 correlation between clinical assessment and GHQ score (Goldberg & Blackwell,1970). More recent modi ﬁcations of the scale include 12-item, 20-item, 28-item, and 30-
item questionnaires. The WHO-5 was adapted from the original 28-item questionnaireof quality of life in patients with diabetes. The ﬁve items chosen cover positive mood,
vitality, and general interest. Although originally developed as a well-being index, theWHO-5 has been validated as a depression-screening tool for use with older adults(Bonsignore, Barkow, Jessen, & Heun, 2001).S
TRUCTURED AND SEMISTRUCTURED CLINICAL INTERVIEWS
Once a person screens positive for a depressive disorder, the next step is to con ﬁrm the
diagnosis, which is best done by using a structured or semistructured interview. Asstated earlier, most people who are expert in the diagnosis of depression disorders donot need the assistance of a structured instrument. However, because experts are notalways available and employing them can be quite costly, structured and semi-structured interviews have been developed for use by less-experienced personnelor for use in research or facility protocols to increase consistency in assessment. Toaddress the concerns of managed-care systems, these interviews have utility in thatthey increase standardization in service delivery, increase consistency in diagnosis,and allow for tracking outcomes (Rogers, 2001). The best-known instruments are theStructured Clinical Interview for DSM-IV and the Composite International Diagnostic
Interview. Another short structured diagnostic interview is the Mini-InternationalNeuropsychiatric Interview. The Diagnostic Interview for DSM (DIS) has also been
used widely but has been largely replaced by the CIDI and so will not be discussed inthis chapter.The Structured Clinical Interview for DSM-IV The Structured Clinical Interview for
DSM-IV (SCID; First, Spitzer, Gibbon, & Williams, 2002) was developed for clinical
research to determine the presence of DSM-IV disorders. It is a semistructured
interview to be used by formally trained staff. Although interviewers use the instru-ment as a guide to structure the interview, the interviewer can also rely on his or herjudgment in interpreting a patient ’s answers to questions. Because there is a reliance
on clinical judgment, the SCID functions best when administered by a trained mentalhealth professional.
The SCID interview is divided into three sections: (1) a historical overview of the
presenting complaint; (2) a screening list to determine beforehand whether the patienthas symptoms of MDD, alcohol or substance abuse, obsessive-compulsive disorder,and anxiety disorders; and (3) the different diagnostic modules to re ﬂect all the Axis I
diagnoses of DSM-IV . Although the SCID has been used extensively in research
studies, it has only fair validity and reliability. According to the SCID ’s creators, this
instrument has a kappa coef ﬁcient of agreement equal to only 0.31 in nonpatient
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The utility of the SCID compared to physician diagnoses of depression has been
demonstrated (Sanchez-Villegas et al., 2008). The main advantage to the SCID is itsstructured nature, which decreases the amount of variation of diagnosis from
clinician to clinician. Howev er, it is still a costly instrument in that staff administer-
ing the SCID must be trained in its use and must be of a professional level. However,costs can be lowered while maintaining the effectiveness of the assessment by theuse of trained research assistants rather th an senior investigators to administer the
test (Miller et al., 1999).Composite International Diagnostic Interview The Composite International Diagnostic
Interview (CIDI) was developed by WHO for the purpose of providing a variety ofdiagnoses that are in accord with de ﬁnitions from the DSM-IV . This structured clinical
interview is a fully computerized interview and so is able to attain a complexity anddepth of diagnosis with carefully programmed skip patterns and ﬂowcharts. Its great
advantage is that it does not require a mental health professional to administer theinstrument —in fact, the CIDI can be used as a patient-only-administered instrument,
although it is also common for a researcher to administer it. Because the programmakes the diagnosis, the researcher giving the interview does not need to make anyindependent clinical judgments (Kessler & Üstün, 2004).
The obvious beneﬁ ts of the CIDI are that it is computerized and thus cuts down on
costs of training interviewers and of using health practitioners to make diagnoses. Thereare, however, some drawbacks to the use of the CIDI. One important one is that becauseit is computerized, certain disorders may be more dif ﬁcult to diagnose because of
individuals ’desire to maintain secrecy or denial of mental disorders (Thornton,
Russell, & Hudson, 1998). Additionally, because it is computerized, differences amongindividuals that the program does not account for cannot be adjusted within theinterview. However, the CIDI can be a useful tool provided that it is used with afollow-up interview with a clinician.The Mini-International Neuropsychiatric Interview The Mini-International Neuro-
psychiatric Interview (MINI) was developed by Sheehan and colleagues (1998) toassess the most common DSM-IV andICD-10 psychiatric disorders. With a 15-minute
administration time, the MINI is purported to be shorter than the typical interviewsused in research settings but is more thorough than screening tests. Like the CIDI, theMINI is advantageous in that it does not require a mental health professional toadminister the instrument, thus saving costs and freeing time for mental healthprofessionals to focus on other critical issues. The interview items focus on currentsymptoms (except for bipolar disorder) that are most routinely asked about byclinicians. This allows for a shorter administration time than other interviews, suchas the SCID, that probe for past symptomatology as well.
Research testing the validity of the clinician-rated MINI has shown good to very good
concordance with other clinician-rated diagnostic interviews (SCID and the CIDI), and ithas excellent interrater reliability (kappa >0.79) for all diagnostic categories and good
test-retest reliability (kappa >0.63) for all diagnostic categories except simple phobia
and current mania. The MINI also demonstrated very good speci ﬁcity (>0.86 with
SCID; >0.72 with CIDI) and very good positive and negative predictive values for most
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The MINI is also available in other formats, including a longer version for the
academic researcher called the MINI-Plus that includes 23 psychiatric disorders (asopposed to 19); a patient-rated version for use in outpatient settings (the MINI-PR); aversion for children and adolescents (the MINI-Kid); and a shorter screening instru-ment, the MINI-Screen (as previously discussed), for primary care. There are alsomultiple translated-language versions and a computerized version now availablewhose properties are currently being investigated.C
OMMENT
Determining the presence of a depressive disorder requires skill and effort in gatheringinformation about the depression and its potential causes. The most ef ﬁcient method
to determine the presence of a depressive disorder is to ﬁrst screen the patient and
then, if the screening is positive, to perform an in-depth interview.
ETIOLOGICAL CONSIDERATIONS
The most debated topic in depression research is etiology. To date the majority ofresearch in this area has focused on MDD, with very little research on dysthymicdisorder. Other speci ﬁed or unspeci ﬁed depressive disorder appears to be related to
whatever is thought to be the comorbid cause. Most scientists now believe thatdepressive disorders are multifaceted, with causes resulting from the interactionsof psychological, social, and biological factors (Kendler, Thornton, & Prescott, 2001;O’Keane, 2000). For example, stressful life events have been found to increase the risk
for developing depression (Kendler & Gardner, 2010; McIntosh, Gillanders, & Rodg-ers, 2010). However, the person ’s coping style, social support, and genetic makeup all
mediate the impact that stress has on depression (Fountoulakis, Iacovides, Kaprinis, &Kaprinis, 2006; Vergne & Nemeroff, 2006). A person who loses his job but has goodsocial support and coping skills will be less likely to develop depression than anotherunemployed person who has limited coping skills and no social support. Thoughdepression is related to many variables, their intermingling can most clearly predictthe development of depression, rather than any single factor determining the onset.Genetics, learning, and life experiences all work together to cause depression.F
AMILIAL AND GENETIC
The most fascinating research on the etiology of depression has been the recent workon the role of genetics in mental health. With the mapping of the human genome, theprospect of clearly identifying the inﬂ uence of genetics on mental health is within
reach. However, with depressive disorders, the contribution of genetics may takelonger to uncover than for other disorders that have already demonstrated a cleargenetic and biological cause (i.e., schizophrenia). Although past evidence from twinstudies has been able to demonstrate some genetic involvement in depressive dis-orders, those links have thus far been weak.
Historically, the principal method for studying the in ﬂuence of genetics on
psychopathology was to compare the concordance of depression in identical twins(MZ; monozygotic twins), who originate from the same gene and are effectively274 SPECIFIC DISORDERS

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genetically identical individuals, to that of fraternal twins (DZ; dizygotic), who shareonly half of their genes and thus are genetically similar to siblings. Because thefrequency of twin births is low, genetic researchers also observe the rates of depressivedisorder in ﬁrst-degree relatives (often parents and children). According to the twin
studies, MZ twins have greater concordance rates for depressive disorders than do DZtwins (Englund & Klein, 1990). More recent work by Kendler and Prescott (1999)evaluated MDD in DZ and MZ twins according to sex, and estimates the odds ratiosfor a lifetime diagnosis of MDD to be equal to 39% and is approximately the same formale and female twins. Family studies also ﬁnd that the onset of depression is more
likely in people with relatives with depression than in those who do not have familymembers with depression (Byers et al., 2009). The rates are not that compelling,however, with relatives having only a 21% risk for developing depression (Kupfer,Frank, Carpenter, & Neiswanger, 1989). Overall, the aggregate estimated rate ofheritability for depression is between 31% and 42% (Sullivan, Neale, & Kendler, 2000).
However, recent research in MZ and DZ twins suggests that there is higher
heritability for all unipolar depressive disorders combined compared to MDD alone.Additionally, recurrent early-onset MDD seems to be the most heritable form of theunipolar depressive disorders, with research estimating that approximately half ofﬁrst-degree relatives and one-quarter of extended relatives of individuals with
recurrent, early-onset MDD suffer from at least one mood disorder (Zubenko,Zubenko, Spiker, Giles, & Kaplan, 2001). Rates of heritability for MDD, whencorrelated with other unipolar depressive disorders (e.g., atypical depression, dys-thymic disorder, and adjustment disorder with depressive features), were moderatelyhigher than heritability of MDD alone. These ﬁndings suggest that some depressive
disorders (e.g., MDD, persistent depressive disorder, pure dysthymic syndrome) maybe reﬂections of the same underlying genetic liability (Edvardsen et al., 2009).
Direct genetic comparisons are becoming a more popular method for determining
genetic links to mood. These methods are considered superior to the methodsdiscussed previously, because DNA is a speci ﬁc measure that is unlikely to be
modi ﬁed by environmental in ﬂuences. The results from twin and family studies
cannot account for the impact of learning on development of depression, whereasDNA is less likely to be in ﬂuenced by personal experience. Additionally, molecular
genetic analysis allows for speciﬁ c genetic hypotheses to be tested. DNA studies are
able to compare depressed with nondepressed controls on characteristics of certaingenes that are associated with neurotransmitters related to depressive disorders.Although still in its infancy, this research has been very helpful in con ﬁrming the role
of genetics in the development of depressive disorders. For instance, Dikeos andcolleagues (1999) studied whether the genetic location of the D3 dopamine receptordiffered in patients with MDD as compared to those with no history or current MDD.The investigators observed that genotypes carrying the allele (DNA structure) associ-ated with D3 polymorphisms were found in 75% of the MDD patients and in 50% ofthe controls, suggesting genetic in ﬂuences in MDD. Other studies, however, have not
found such robust effects (Frisch et al., 1999; Neiswanger et al., 1998; Qian et al., 1999).More recently, Green and associates (2010) demonstrated an increased risk forrecurrent MDD in individuals who have a variation in a gene that provides instruc-tions to cells for making calcium channels. These channels are an important feature ofcells, as they are involved in intercellular communication and generating andMood Disorders: Depressive Disorders 275

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transmitting electrical signals, although their exact role in brain tissue is still unclear(Splawski et al., 2004). At best, the literature on the genetics of depressive disorderssuggests a propensity to develop these disorders but that this propensity can be offsetby learning and environmental in ﬂuences.
N
EUROANATOMY AND NEUROBIOLOGY
Over the past 5 years, there has been considerable advancement in our understandingof the neuroanatomy and biology of depression. In the quest to uncover biologicalmarkers of mental disorders, much research effort has gone into determining biologi-cal determinants of depression, with a speci ﬁc focus on the brain structures that
appear to be associated with depression, neurocircuitry, and neurotransmitters.However, to date no laboratory test has been uncovered as a valid diagnostic toolfor depressive disorders.Neuroanatomy and Neurocircuitry Research into brain regions associated with depres-
sion is ongoing, but current brain theories of depression argue that several brainsystems interact to regulate mood in response to stress. Research data from functionalneuroimaging (fMRI) studies, research on people with brain damage, and positronemission tomography (PET) suggest that four brain regions are associated withdepression. The ﬁrst is the amygdala, which is responsible for memory of emotional
reactions to stimuli. This part of the brain interprets the emotional salience of stimuli,and when there is a threatening stimulus, it produces an emotional reaction thattriggers the brain into action. Next is the orbitofrontal cortex , which is responsible for
cognitive processing and decision making. This part of the brain is in part responsiblefor putting logical meaning to the stimulus and for determining what should be doneabout the stimulus. The dorsolateral prefrontal cortex is responsible for affect regulation,
planning, decision making, intentionality, and social judgment. Finally, the anterior
cingulate cortex is also involved with depression and is responsible for error detection,
anticipation of tasks, motivation, and modulation of emotional responses (Koenigs &Grafman, 2009).
These systems work together to help us navigate our environment, and when they
work well and in concert, we are able to manage most problems that come our way.When we are faced with a problem to solve, whether it is social, ﬁnancial, or
environmental, these systems work together to ﬁrst let us know there is a problem
in the environment, to assess the degree of threat the problem presents with, tomodulate our emotions in reaction to the problem, to decide among a series ofpotential solutions to solve the problem, and then to initiate behavior to eithercope with or solve the problem. When any of these systems is not working properly,whether due to brain damage, congenital anomalies, or learned behavioral patterns,our chances for developing depression are increased. For instance, if the moodregulation systems in the dorsolateral cortex are not working properly, they fail toregulate the emotional reaction to the problem. This failure prevents the orbitofrontalcortex from being able to create an action plan to solve the problem. What results is thetendency to avoid, rather than solve, the problem or to overreact to the problem.
Several functional imaging studies are beginning to support the role these systems
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depression is a rather heterogeneous disorder (people with the same diagnosis, evenhistory, can have a very different clinical presentation), scientists are often coming upwith different explanations for how these systems work, even about which systemsare most important. This is partly because the expense of conducting this research isso high, and therefore the number of research participants in these studies tends tobe quite small; given the heterogeneity of the illness, it is no surprise that under-sampled studies would yield heterogeneous results. Finally, although technologiessuch as fMRI have revolutionized the ﬁeld, many scientists are now claiming that
results from these experiments should be viewed with caution (Logothetis, 2008).Neurochemistry and Transmitters Clinicians initially believed that depression was
caused in part by lack of the two neurotransmitters norepinephrine andserotonin . Now,
however, it is known that the dysregulation rather than the de ﬁciency of these
neurotransmitters causes depression (Moore & Bona, 2001). Antidepressants toregulate the production and distribution of norepinephrine and serotonin are effectivein their ability to increase the availability of receptor sites rather than increase theproduction of the neurotransmitters (Veenstra-VanderWeele, Anderson, & Cook,2000). Neurotransmitters provide an important but still only partial picture of thebiological origin of depression, because abnormalities in neurotransmitter regulationdo not necessarily lead to a depressed mood.
Neuroendocrinology also adds to a more complete understanding of the biological
causes of depression. The most heavily researched of this area has been the linkbetween the hypothalamic-pituitary-adrenal (HPA) axis functioning and adult depres-
sion over the past 40 years (Lopez-Duran, Kovacs, & George, 2009). The HPA axis is amajor part of the neuroendocrine system that regulates bodily processes, including thestress response; not surprisingly, abnormal HPA axis functioning has been implicatedin numerous psychiatric disorders, most notably major depressive disorder(Pariante & Lightman, 2008). Speci ﬁcally, evidence points to an overabundance of
cortisol in the systems of patients with depression. Additionally, abnormalities in
thyroid functions are often related to symptoms of depression, further indicating animportant role for the neuroendocrine system in depression. In a study by Ghaziuddinand colleagues (2000), neuroendocrine imbalances in adolescents with MDD ascompared to their nondepressed counterparts demonstrated that depression is asso-ciated with abnormal baseline levels of prolactin as well as sharper prolactin andcortisol responses to serotonergic challenges. Evidence for such abnormalities not onlyyields a more complete understanding of causation but also aids in the development ofmore effective drug treatments.L
EARNING AND MODELING
There is a tremendous amount of research investigating and supporting behavioral,social, and environmental in ﬂuences in the development of depression. A review of
this literature suggests that depressive disorders appear to be related to threepsychological variables and the individual ’s learning history (life experiences):
1. People ’s cognitive appraisals of themselves, their lives, and others (Alloy et al.,
2000; Beck, Rush, Shaw, & Emery, 1979).Mood Disorders: Depressive Disorders 277

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2. Whether people proactively solve problems or avoid them (D ’Zurilla & Nezu,
1999).
3. The degree to which proactive attempts to cope with stress have been successful
(Folkman & Lazarus, 1988).
4. An individual ’s learning history could lead to the development of depressive
symptoms or serve to maintain depression/dysphoria.
In this paradigm, people who have negative expectations about their ability to cope
with problems generally acquire these expectations through past learning experience.Repeated failed attempts to solve problems (learning history), for instance, leave aperson feeling hopeless and helpless, abandoning his or her usual methods for solvingproblems, and becoming depressed (Seligman, Weiss, Weinraub, & Schulman, 1980).These factors —cognitive attributions, coping skills, and learned helplessness —have
all been found to be predictive of depression.
People with negative expectations or cognitive vulnerabilities are more likely to
develop depression when faced with a stressor than are people who do not possesscognitive vulnerabilities. Grazioli and Terry (2000) found that in women withpostpartum depression, both general and maternal-speci ﬁc dysfunctional attitudes
were associated with self-reported depression, particularly in women who hadchildren who were found to be temperamentally difﬁ cult. Another study found
that individuals with negative cognitive styles had higher lifetime prevalence ofdepression than people who were not cognitively vulnerable (Alloy et al., 2000).Therefore, people with negative perceptions of themselves and their environment areat risk for becoming depressed.
Coping skills have also been found to be related to depression. Most research has
found that people who use active forms of coping, such as problem solving, are lesslikely to develop depression than are people who use passive forms of coping, such asavoidance. In fact, in one study, people who used an avoidant coping style were morelikely to develop depression when faced with psychosocial stressors (Welch & Austin,2001). Rumination, a repetitive pattern of thoughts and behaviors focused on one ’s
depressed state, can also result in less effective problem solving (Donaldson & Lam,2004). Although coping skills de ﬁcits and cognitive style contribute to depression, the
interaction of these two factors seems to have the biggest impact on the developmentof depression. Several studies have supported this interaction in learned helplessness .
Originally, these theories were tested in animal models, where unsolvable prob-
lems were presented to animals and all attempts to solve the problem were met withunpleasant consequences, such as an electric shock. After repeated attempts to solvethe problem failed, these animals would exhibit depressogenic behavior —with-
drawal, acting as if they were in pain —and, even after a solution was presented to
them, the animals would refuse to try the solution (Altenor, Volpicelli, & Seligman,1979). Scientists have been able to draw a relationship between learned helplessnessand depression in research with people. For instance, Swendsen (1997) found thatpeople with high-risk attributional styles were more likely to experience depressedmood after exposure to negative stressful events.
A person ’s learning history may also play a role in the development of depression.
Since the 1970s there has been a tremendous amount of interest in investigating therole that learning principles play in the development of depression. Ferster (1973)278 SPECIFIC DISORDERS

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postulated that individuals with depression did not engage in enough activities andmay even avoid activities, thus leading to insuf ﬁcient reinforcement for those activi-
ties. This limited engagement in activities also results in fewer opportunities to learnthrough experiencing those activities (contingencies of reinforcement). Lewinsohn(1974) expanded upon this theory, emphasizing depression as being the result of lowlevels of reinforcement contingent upon behavior. This lack of reinforcement that aperson would obtain from doing something proactive would lead to less engagementin those types of behaviors in the future, eventually leading to withdrawal andisolation. According to this model, depression results from either a decrease inpleasant events or an increase in unpleasant events and speaks to the importanceof considering context in the development of depression (Jacobson, Martell, &Dimidjian, 2001).
Jacobson and colleagues developed the behavioral activation model (which grew
from these theories and further developed them), emphasizing that when life is lessrewarding or stressful, people sometimes pull away from the world around them andﬁnd that basic routines in their life become disrupted. This disruption in routines can
increase depressive symptoms and make it dif ﬁcult to solve life problems effectively.
In turn, this can lead to secondary problems (e.g., relationships, occupational dif ﬁ-
culties), which maintain or further exacerbate depression. Support for these models isstrong and can be found in the depression treatment literature.L
IFEEVENTS
The literature is replete with data indicating that stressful life events contribute to thedevelopment of a depressive episode. Although not everyone who faces dif ﬁcult
problems develops depression, it is evident that prolonged exposure to psychosocialstress can precipitate a depressive episode (Hammen, Kim, Eberhart, & Brennan,2009). Several studies have found that most depressive episodes are preceded by asevere life event or dif ﬁculty in the 6 months before onset of the episode (Kendler &
Gardner, 2010). Kapci and Cramer (2000) also found that people were more likely todevelop depression when they were exposed to numerous negative life events, butonly if their belief in their ability to solve problems was impaired. Thus, the interactionof negative life events, coping skills, and attributions about coping skills in ﬂuences
whether a person will experience depression. In addition, patients with more long-term or chronic depression were more likely to report past abuse, although the causalrelationship is unclear (Keitner et al., 1997).
Because depression is a multifaceted disorder, it is dif ﬁcult to pinpoint the speci ﬁc
role life events have on the development of a depressive disorder. Most people willhave to face severe life stress at some point in their lives, yet not everyone developsdepression. How an individual views severe life events and the perceived control he orshe feels over the situation both play an important role in determining one ’s
vulnerability to depression. For instance, several studies ﬁnd that the relationship
of life events to depression is mediated by other factors such as social support,cognitive style, and coping abilities (Alloy et al., 2000; Cacioppo, Hughes, Waite,Hawkley, & Thisted, 2006). Severe life events are signi ﬁcantly more likely to provoke a
major depressive episode in individuals without social support (Leskelä et al., 2006).Support systems give an individual external support when internal coping skills areMood Disorders: Depressive Disorders 279

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put to the test. Without the external support, however, an individual must relyexclusively on his or her own internal resources, which under severe duress might notbe entirely effective. Therefore, although negative life events do in ﬂuence the occur-
rence of depressive disorders, the social and psychological resources available to theperson facing the stressful life event generally mediate the impact on mood.G
ENDER ,RACE,ANDETHNICITY
Many researchers have been trying to determine the reasons for the discrepant ratesof depressive disorders across gender and racial-ethnic lines. Are the reasonsgenetic or biological? Is it that these populations are exposed to more stress andhave fewer resources to cope with stress and therefore are more vulnerable thanmen and nonminority groups? Or is depression presented differently across thesegroups, and therefore the estimates in the prevalence for depressive disorders inthese populations are inaccurate? Mental he alth researchers are still struggling with
these questions and have only been able to give a partial explanation of why thediscrepancy exists.
Some theorists believe that the reason minorities have differing rates of depressive
disorder is that they present their symptoms of depression differently than doCaucasians (Escalante, del Rincon, & Mulrow, 2000; Ryder et al., 2008). Manyresearchers have spent years trying to discern the most appropriate way to assessdepression in different cultures. Although research from the WHO indicates thatdepression is similar across cultures, how people from one culture report the symp-toms and their cultural attitude about mental health (and its treatment) can clouddiagnoses. Screening instruments and scales that were developed for Caucasianpopulations can be problematic if they are simply translated without regard fortranslation bias. Additionally, many studies have found that the factor structures andreliabilities of these instruments tend to differ across ethnic groups, indicating thatgroups vary in their reports of depressive symptoms (Azocar, Areán, Miranda, &Muñoz, 2001). For instance, lower rates of depression in Asians may be attributable totheir tendency to underreport affective symptoms of depression and to rely more onsomatic presentation (Ryder et al., 2008).
Others have hypothesized that the different rates of depression in ethnic groups are
associated with the fact that in this country, minority groups such as AfricanAmericans and Hispanics are more likely to be impoverished and to have to copewith ﬁnancial and urban stress (Alexopoulos, 2005). Studies have demonstrated that
socioeconomic status and exposure to trauma related to racism, urban living, andﬁnancial strain are correlated with depression and other mental illnesses such as
anxiety and substance abuse (Caron & Liu, 2010; Gottlieb, Waitzkin, & Miranda, 2011;Kiima & Jenkins, 2010; Rhodes et al., 2010). Other studies have found that the rates fordepression in middle class and af ﬂuent minorities are more similar to the national
rates of depression as compared to middle-class and af ﬂuent Caucasians. These
studies seem to argue that in the case of minority populations, increased exposureto stress is the reason for the differing rates of depressive disorder (Olfson et al., 2000).
The differing rate of depressive disorders between men and women is an interest-
ing yet complicated ﬁnding. Researchers initially thought that the different prevalence
rates resulted from reluctance on the part of men to admit feelings of depression, as280 SPECIFIC DISORDERS

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well as men ’s tendency to cope with stress through substance use (Shorey et al., 2011).
Others suggest that the increased prevalence of depression in women is becausewomen tend to be victims of sexual abuse and therefore suffer a signi ﬁcant psycho-
social stressor that is not as common in men (Gaudiano & Zimmerman, 2010;Ghassemi, Sadeghi, Asadollahi, Yousefy, & Mallik, 2010; Plaza et al., 2010). Stillothers suggest that the willingness of women over men to seek treatment servicesmight account for the difference in prevalence (Fikretoglu, Liu, Pedlar, & Brunet,2010). However, because the discrepancy between men and women seems to beuniversal, others claim that hormonal and biological differences account for thedifferential prevalence rates. Whatever the differential effect, the fact remains thatdepression is more commonly reported in women than in men, and this issue stillneeds to be resolved.
COURSE AND PROGNOSIS
Research has begun to identify variables that can predict toward better or worsecourse and outcome, but a great deal of uncertainty still exists. Here we present thedescriptive data regarding length, severity, and prognosis of depressive disorders.C
OURSE
Beyond the basic diagnostic criteria, MDD has several delineating features. Early-onset depression tends to appear before age 20 and has a more malignant course thanlate-onset depression (Devanand et al., 2004; Papakostas, Crawford, Scalia, & Fava,2007). It is also associated with a family history of depression and other mooddisorders (Bergemann & Boles, 2010; Wermter et al., 2010). Late-onset depressiontends to emerge in the mid-30s and is associated with fewer recurrent episodes,comorbid personality disorders, and substance abuse disorders relative to early-onsetdepression (Chui, Cheung, & Lam, 2011). However, there is a much greater variationin the age of onset with depression than in disorders such as schizophrenia. Second,the course of MDD tends to be time limited. The average episode lasts 6 months,although this varies greatly from person to person (Rhebergen et al., 2010). Third,MDD tends to be a recurrent disorder. Patients who have one major depressiveepisode have a 36.7% chance of experiencing a second; those who have two previousepisodes have a 48% chance of developing a third episode. With each additionalepisode, chances for another additional episode increase by approximately 15%(Seemuller et al., 2010).
Persistent depressive disorder is a more chronic, long-lastin g illness. The mean
duration of dysthymic disorder is 30 years, and given that the symptom presenta-tion for persistent depressive disorder has not changed much, it is thought that thisstatistic still holds for the newer persistent depressive disorder category. Almosthalf of those patients who were previously classi ﬁed as dysthymic disorder will
develop a major depressive episode in their lifetimes (Rhebergen et al., 2010). Thosewith persistent depressive disorder (pure dysthymic syndrome) have been found tohave worse clinical prognosis than people with either MDD or depressive disorder,N O S( n o wc l a s s i ﬁed as other speci ﬁed or unspeci ﬁed depressive disorder) and are
as disabled as those with MDD (Grif ﬁths, Ravindran, Merali, & Anisman, 2000).Mood Disorders: Depressive Disorders 281

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Thankfully, persistent depressive disord er (pure dysthymic syndrome) is respon-
sive to both psychotherapy and medication treatment, at least in the short term,with some studies suggesting that the most robust intervention is a combination of
psychotherapy and medication (Barrett et al., 2001). Unfortunately, few people
with persistent depressive disorder ever receive treatment. Fewer than half will
ever receive any kind of mental health treatment unless they have also experienceda major depressive episod e (Rhebergen et al., 2010).
P
ROGNOSIS
Early diagnosis and treatment with therapy, medication, or both result in a betterchance of recovery from MDD, persistent depressive disorder, pure dysthymicsyndrome, and other speci ﬁed or unspeci ﬁed depressive disorder (depression
NOS) (Rhebergen et al., 2010). The ease of recovery from depression, however, isrelated to several factors. Prognosis is best when the patient is facing few stressful lifeevents (Sherrington, Hawton, Fagg, Andrew, & Smith, 2001) and has a solid supportnetwork on which to rely (Rubenstein et al., 2007). Furthermore, individuals with aninitial early recovery are less likely to develop recurring symptoms. Early improve-ments indicate that the patient has access to coping mechanisms that allow for a quickrecovery, and this often suggests an overall positive long-term prognosis. Theprognosis for persistent depressive disorder, pure dysthymic syndrome is less certain.For example, Ciechanowski and colleagues (2004) demonstrated a 50% reduction atthe end of a 12-month period in depressive symptoms and functional improvementusing problem-solving therapy in home-based intervention for older adults withmedical illnesses, minor depression, and persistent depressive disorder, pure dysthy-mic syndrome. However, Klein and colleagues (Klein, Shankman, & Rose, 2006) foundthat adults with persistent depressive disorder, pure dysthymic syndrome improvedat a much slower rate and were more symptomatic at a 10-year follow-up than wereindividuals with MDD. As of this writing, few treatment studies have demonstratedany long-lasting positive effect for any intervention for persistent depressive disorder,pure dysthymic syndrome.
Another factor involved in the prognosis for both MDD and persistent depressive
disorder are levels of self-esteem. A higher self-esteem predicts an increasinglypositive prognosis (Sherrington et al., 2001). Poor self-esteem, on the other hand,predicts a longer and more delayed recovery. The prognosis of depressive disorders ispoor when they have an early onset, a premorbid personality disorder exists, and therehas been a previous episode (Ryder, Quilty, Vachon, & Bagby, 2010). More intensiveand extended treatment can improve the remission and maintenance of remissionfrom MDD episodes, even with high severity of the depression, although the evidenceon persistent depressive disorder is limited.
CASE STUDIES
M
AJORDEPRESSION
Case Identi ﬁcation R. J. was a single, 32-year-old African American woman who self-
referred to mental health services for what she called “depression. ”282 S PECIFIC DISORDERS

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Presenting Complaints Before seeking services, R. J. had contemplated getting gastric
bypass surgery and was extremely unhappy with her employment. She was managingseveral large projects for the company she worked for and felt that she was the onlymember of her staff who was doing any work. She felt that she was not trusted to doher job, was not respected for the work she did, and was being taken for granted. Shewas also concerned about getting the surgery, because she would need recovery timeand would be unable to care for her family members. Her symptoms included feelingdepressed nearly all day, every day, for the past 12 months; feeling a lack of interest inher usual activities (in this case walking and attending a weight-loss program); andincreased irritability. For the past 12 months, she reported insomnia, increasedappetite, and feelings of worthlessness and hopelessness about the future. Shereported feelings of guilt, believed that she was being punished, and constantlyworried that she was not doing enough for her family. In addition, she reportedhaving dif ﬁculty concentrating and making decisions. Although she had occasionally
felt that she would be better off dead, she was not suicidal. She did not feel that suicidewas an option and had no plan to harm herself.History R. J. was the younger of two female siblings from the northwestern section of
the United States. As a child, she did not have time for friends, because she was oftencaring for her sick mother. She was a good student but had dropped out of high schoolto care for her mother. Her father had left her mother and moved out of state shortlybefore her mother became ill. R. J. had a large extended family but acutely felt the loss ofa father ﬁgure. Her uncle had problems with drugs and was incarcerated. Subse-
quently, she had taken on the care of her younger niece and nephews. As an adult, R. J.had success in school (she was able to achieve her GED and was successfully takingcollege courses) and in her work. She believed that she had suffered from depressiontwice before in her adult life but had always been able to overcome the depression onher own. However, she had often turned to food for comfort and was suffering fromobesity. She explained that she had never sought help for her depression before becauseshe was busy caring for her family and did not take time for herself. Furthermore, sheindicated that it was not like her to talk with someone about her feelings. She believedher mother was depressed following the loss of her husband and subsequent medicalproblems but was unsure of these facts, because these issues were never discussed.Assessment R. J. presents with several interesting issues related to depression. First, she
reports having no less than nine symptoms of depression, six for more than a year; shealso reports having these symptoms nearly every day and that they are impairing herability to function at work and socially. R. J. also indicates having had two previousdepressive episodes that spontaneously remitted, and that her mother may havesuffered from depression as well. Based on this assessment, R. J. met criteria for recurrentmajor depressive disorder and may have an endogenous form of the disorder.P
ERSISTENT DEPRESSIVE DISORDER ,W ITHPUREDYSTHYMIC SYNDROME
Case Identi ﬁcation B.G. was a retired, 55-year-old Caucasian man who sought
services for depression after a doctor recommended he talk to a mental healthprofessional.Mood Disorders: Depressive Disorders 283

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Presenting Complaints B.G. stated that for the past 3 years, he occasionally felt
worthless, depressed, and irritable. He reported that some days he often found itdifﬁcult to get himself going to complete his chores for the day but would somehow
manage to do so. He indicated that he was unsure of whether he needed treatment,because he had “good days, ”but upon further probing he reported that these days
were infrequent (no more than 1 or 2 days per week). Although he said he and his wifedid not have marital problems, he felt guilty that she worked and he did not. Theprimary symptoms he complained about were occasional sadness, lack of energy,irritability, feelings of worthlessness, and guilt.History B. G. was the oldest of ﬁve children in his family and was currently married
with three children, all of whom were grown and living in other parts of the country.He completed high school and trade school afterward. He had been employed withone construction company his entire adult life. He was living with his wife at the timeof his intake. He had no serious health problems other than chronic pain resulting froma back injury. B.G. retired because the back injury prevented him from performing hisjob. Three years ago, his wife took on a part-time job to make extra money, and B. G.began looking after the house. Prior to this visit, he had never sought mental healthservices, nor had he ever felt depressed.Assessment B. G. presents with some classic symptoms of dysthymic disorder, now
subsumed under the category in DSM-5 of persistent depressive disorder; he reports
having depressed mood for more days than not for more than the required 2-yearperiod. He denied a history of manic episodes and did not meet criteria for an MDEduring this 2-year period. He also met the two or more additional symptom require-ments, which included such symptoms as lack of energy and low self-esteem.Although B. G. did report brief periods in which he felt “good,” these symptom-
free periods only occurred on average 1 to 2 days per week, and, therefore, he met theadditional speciﬁ cation of not having been symptom free for more than 2 months at a
time during the current episode. Based on our assessment, B. G. met criteriafor a diagnosis of persistent depressive disorder, with pure dysthymic syndrome,late onset.U
NSPECIFIED DEPRESSIVE DISORDER
Case Identi ﬁcation T. J. was a 40-year-old woman who was referred by her physician
for treatment of depression. According to the physician, T. J. was struggling withplacing her elderly mother in a nursing home, and this struggle made her quitedepressed. The provider indicated that T. J. had a recent diagnosis of hyperthyroidismand was being treated with medication.Presenting Complaints T. J. stated that she had been feeling depressed for several
months, ever since her mother had become more seriously ill and T. J. began trying toﬁnd a nursing home for her. Her primary complaints were depression and sadness
nearly all day, every day; feeling slowed down; and trouble with concentration. Shealso indicated that having had a recent diagnosis of hyperthyroidism complicatedmatters for her and that she had been unable to take her medication regularly.284 SPECIFIC DISORDERS

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History T. J. was an only child who was living with her mother at the time of referral.
She had a college education and had been employed as an administrative assistant for10 years. She was divorced with no children. T. J. indicated that she had been hermother ’s caregiver for most of her life and that they had a “love-hate ”relationship.
Her mother was being verbally abusive to T. J. regarding the placement, making T. J.feel guilty. T. J. indicated that she would normally be able to let her mother ’s abuse roll
off her back, having long ago accepted that her mother was a dif ﬁcult person.
However, the last 4 months were hard to cope with, even though she had a goodcaseworker helping her, and her mother would be placed in a pleasant assisted-livingfacility within the next month.Assessment/Treatment After consideration of her symptoms, T. J. ’s symptoms did not
appear to meet full criteria for MDD, but it was clear to the therapist that a depressivedisorder was present. What was unclear was whether the depression was primary,whether her medical symptoms were the cause of the depression, or if the client ’s
depressive symptoms were related to a psychosocial stressor, thus a diagnosis ofunspeci ﬁed depressive disorder was assigned.
T. J. was encouraged to start taking her medication for hyperthyroidism and was
educated about the link between the illness and depressive symptoms. T. J. and hertherapist agreed to meet again in 2 weeks. At that meeting, T. J. reported that hermother had been placed in the assisted-living facility and that while she felt guilty for afew days, she found that her mother was actually quite happy at the facility. She alsoreported taking the medication regularly and stated she already felt much better ( “like
my old self ”), although she was still somewhat symptomatic of depression (occasional
sadness and poor energy). Now that her mother had been successfully placed, T. J.indicated that she would like to work on rebuilding her social life.
SUMMARY
Depressive disorders are common and widely studied. Given the extent of ourknowledge of MDD and what was previously classi ﬁed as dysthymic disorder,
research continues to address the best me ans of recognizing depression, how to
treat depression in different settings an d in different cultures, and further clari ﬁ-
cation of the etiology of these disorder s. The causes and symptoms of depressive
disorders are extremely variable and intermingled. The causes include both physi-ological and environmental factors, and the expressions of depression vary from
short, severe episodes to chronic symptomatology. Because of the immense com-plexity of the depressive disorders, further research will aid in the ability to tailordiagnosis and therapy to each particular manifestation, to better address thesedisorders with medical comorbidities, and explore cross-cultural concerns inassessment and treatment.
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CHAPTER 8
Anxiety Disorders
DAVID P. VALENTINER, THOMAS A. FERGUS, EVELYN BEHAR,
and DANIEL J. CONYBEARE
MUCH OF WHAT we know about panic disorder, agoraphobia, generalized
anxiety disorder, social anxiety disorder, and speciﬁ c phobias is based on
studies using diagnostic criteria that predate the Diagnostic and Statistical
Manual of Mental Disorders ,ﬁfth edition ( DSM-5 ; American Psychiatric Association
[APA], 2013). De ﬁnitions of these disorders have generally shown small changes over
recent editions of the DSM , allowing for reasonable inferences about disorders, as
currently de ﬁned, to be drawn using past studies. With this caveat in mind, these
disorders are prevalent and often quite debilitating.
Anxiety disorders are commonly diagnosed in the United States, with almost one-
third of individuals meeting criteria for at least one anxiety disorder at some time intheir lives —a prevalence rate second only to substance use disorders (Aalto-Setälä,
Marttunen, Tuulio-Henriksson, & Lönnqvist, 2001; Beekman et al., 1998; Kessler et al.,1994). In addition, these disorders lead to poor educational outcomes (Kessler, Foster,Saunders, & Stang, 1995). Goisman et al. (1994) found that about 50% of patients withpanic disorder and/or agoraphobia were receiving unemployment, disability, wel-fare, social security payments, or some other form of ﬁnancial assistance. Generalized
anxiety disorder is also associated with signi ﬁcant costs to society due to decreased
work productivity and increased use of services, particularly primary health care(Wittchen, 2002). Social anxiety disorder is associated with compromised functioningin school and at work (Liebowitz, Gorman, Fyer, & Klein, 1985; Turner, Beidel,Dancu, & Keys, 1986; Van Ameringen, Mancini, & Streiner, 1993; Wittchen & Beloch,1996; Zhang, Ross, & Davidson, 2004). Anxiety disorders create an enormous burdenon society, with annual costs estimated at $42.3 billion, or $1,542 per individualmeeting the criteria for an anxiety disorder (Greenberg et al., 1999). Clearly, thesedisorders are common and substantially interfere with quality of life (Olatunji,Cisler, & Tolin, 2007).
299

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DESCRIPTION OF THE DISORDER
PANIC DISORDER
Panic attacks are de ﬁned as discrete periods of intense fear or discomfort that begin
abruptly and reach their peak within 10 minutes. The DSM-5 requires that at least 4 of
the following 13 symptoms be present: palpitations, pounding heart, or acceleratedheart rate; sweating; trembling or shaking; sensations of shortness of breath orsmothering; feelings of choking; chest pain or discomfort; nausea or abdominal distress;feeling dizzy, unsteady, lightheaded, or faint; derealization or depersonalization; fearof losing control or going crazy; fear of dying; paresthesias; and chills or hot ﬂushes.
Panic attacks occur in nonclinical populations, with about 6.3% of a community samplereporting having experienced a full-blown panic attack some time during their lives(Norton, Zvolensky, Bonn-Miller, Cox, & Norton, 2008) without debilitating conse-quences, development of a disorder, or treatment-seeking behavior.
Panic attacks also occur in the context of many psychiatric conditions, especially
anxiety disorders. For example, the acute fear responses that individuals with speci ﬁc
phobias experience in the presence of feared objects or situations (e.g., spider phobics ’
responses to spiders) sometimes meet the criteria for a panic attack. When a panicattack is triggered by exposure to or anticipation of a feared object or situation, it isconsidered to be an expected panic attack (also known as a cued panic attack).Expected panic attacks are most common among individuals with other anxietydisorders, including social anxiety disorder and speci ﬁc phobias.
In addition to expected panic attacks, panic attacks can also be unexpected (or
uncued); these panic attacks are not associated with any speciﬁ c object or situation.
Anyone, including individuals with no diagnoses, can experience expected orunexpected panic attacks. Expected panic attacks are not uncommon among indi-viduals with social anxiety disorder or speci ﬁc phobias, but they also occur in a
substantial number of patients with panic disorder (Craske et al., 2010). One issue thatshould be considered when diagnosing panic disorder is that the term unexpected may
have different meanings across various cultural contexts (Lewis-Fernández et al.,2010).
The diagnosis of panic disorder requires recurrent and unexpected (uncued) panic
attacks, followed by at least 1 month of concern about (a) additional attacks or theimplications of the attack, or (b) changes in behavior (APA, 2013). The DSM-5 does not
recognize subtypes of panic disorder (e.g., respiratory, nocturnal, nonfearful, cogni-tive, and vestibular subtypes), although some investigators have recently explored thepossibility of categorizing panic disorder in this way (see Kircanski, Craske, Epstein, &Wittchen, 2010).A
GORAPHOBIA
Agoraphobia is a fear of being in public places or situations in which escape might bedifﬁcult or in which help may be unavailable if a panic attack occurred. Patients with
agoraphobia avoid (or endure with marked distress) certain situations, including largestores; open or crowded public spaces; traveling on buses, trains, or cars; and being faror away from home (APA, 2013).300 SPECIFIC DISORDERS

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TheDSM-III-R (APA, 1987) viewed agoraphobia as primary and panic attacks as a
frequent but secondary feature. It included the diagnostic categories of “agoraphobia
with panic attacks ”and“agoraphobia without panic attacks. ”Subsequent revisions
of the DSM have reversed this view and have included diagnostic categories of
“panic disorder with agoraphobia, ”“panic disorder without agoraphobia, ”and an
infrequently used category of “agoraphobia without panic disorder. ”This last
category is used for patients who deny or have an unclear history of panic attacks,or who merely report histories of panic-like experiences (e.g., limited symptom panicattacks). Such cases may be dif ﬁcult to differentiate from speci ﬁc phobias, obsessive-
compulsive disorder, and posttraumatic s tress disorder. Although agoraphobia was
seen as a frequent but secondary feature of panic disorder in the DSM-III-R and
DSM-IV , the view that it is a distinctive condition independent of panic disorder
(Wittchen, Gloster, Beesdo-Baum, Fava, & Craske, 2010) is now incorporated into theDSM-5.G
ENERALIZED ANXIETY DISORDER
Generalized anxiety disorder (GAD) is characterized by worry (APA, 2013), which istypically de ﬁned as repetitive thinking about potential future threat, imagined
catastrophes, uncertainties, and risks (Wa tkins, 2008). Individuals with GAD spend
an excessive amount of time worrying and feeling anxious about a variety of topics,and they ﬁnd it dif ﬁcult to control the worry. The diagnosis also requires three or
more of the following six symptoms: (1) res tlessness or feeling keyed up or on edge;
(2) being easily fatigued; (3) difﬁ culty concentrating or mind going blank; (4)
irritability; (5) muscle tension; and (6) sleep disturbance. Fi nally, the worry and
anxiety are not conﬁ ned to another disorder (e.g., worry about social evaluation
only in the context of so cial anxiety disorder), and they lead to signi ﬁcant distress or
impairment.
The diagnosis of GAD ﬁrst appeared in the DSM-III (APA, 1980), but it was poorly
deﬁned, unreliable, and assigned only in the absence of other disorders (Mennin,
Heimberg, & Turk, 2004). With publication of the DSM-III-R (APA, 1987), the
diagnostic criteria for GAD were revised to include worry as the primary featureand to allow for primary diagnoses of GAD in the presence of other disorders. Despitethese improvements, diagnostic reliability remained poor due to overly broad criteriafor associated symptoms (Marten et al., 1993). The DSM-IV (APA, 1994) added the
uncontrollability criterion and reduced the set of associated symptoms to re ﬂect
empirical ﬁndings and to improve speci ﬁcity. As a result, diagnostic reliability
improved but remained low relative to most of the other anxiety disorders (Brown,Di Nardo, Lehman, & Campbell, 2001). The DSM-5 continues to use the same
diagnostic criteria.
Although worry is the primary diagnostic and clinical feature of GAD, the majority
of high worriers do not meet criteria for the disorder (Ruscio, 2002). However,compared to high worriers without GAD, high worriers with GAD report greaterdistress and impairment associated with worry, indicating that worry is more harmfulat clinical levels. High worriers with GAD are also more likely to perceive their worryas uncontrollable (Ruscio & Borkovec, 2004). Individuals who do not meet theAnxiety Disorders 301

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“excessiveness of worry ”criterion may present a milder form of GAD; they are less
symptomatic overall and report fewer comorbid disorders compared to individualswith full GAD (Ruscio et al., 2005). Nonetheless, GAD without “excessive ”worry is
associated with considerable impairment, high rates of treatment seeking, and highrates of comorbidity.
GAD was initially conceptualized as a “nonphobic anxiety disorder” and was
instead classi ﬁed (alongside panic disorder) under the umbrella of “anxiety neurosis ”
(DSM-II ; APA, 1968). Although it remains unclear whether GAD is indeed a “non-
phobic ”condition in which no speci ﬁc feared stimulus exists, several theoretical
conceptualizations of GAD converge on the idea that worry serves an avoidantfunction. These conceptualizations include the avoidance theory, the intolerance ofuncertainty model, the meta-cognitive model, and emotion regulation models (for adetailed review, see Behar, DiMarco, Hekler, Mohlman, & Staples, 2009).
The avoidance theory (Borkovec, Alcaine, & Behar, 2004) holds that the verbal-
linguistic properties of worry preclude emotional processing.Worry is primarilyverbal-linguistic as opposed to imagery based in nature (Behar, Zuellig, & Borkovec,2005; Borkovec & Inz, 1990; Stöber, Tepperwien, & Staak, 2000), and it inhibits somaticarousal during a subsequent anxiety-inducing task (Borkovec & Hu, 1990; Borkovec,Lyon ﬁelds, Wiser, & Deihl, 1993; Peasley-Miklus & Vrana, 2000). Moreover, worry is
associated with decreased anxious affect during subsequent periods of trauma recall(Behar et al., 2005) and depressive rumination (McLaughlin, Borkovec, & Sibrava,2007). Lastly, individuals with GAD often report that worry serves as a distractionfrom more emotional topics (Borkovec & Roemer, 1995). Thus, it seems that worryprecludes the somatic and emotional activation required for habituation to anxiety-provoking stimuli. Moreover, worry may be negatively reinforced via the removal ofaversive and evocative images and emotional experiences (Borkovec et al., 2004).
Intolerance of uncertainty (IU) is de ﬁned as the tendency to respond negatively to
uncertain situations in ter ms of cognition, affect, and behavior (Dugas, Buhr, &
Ladouceur, 2004). IU is further de ﬁned as a schema through which an individual
with GAD perceives the environment; for the individual with GAD, uncertainsituations are unacceptable and distre ssing and may lead to worry (Dugas et al.,
2004). Individuals with GAD consistently report greater levels of IU compared tononclinical controls (Dugas, Gagnon, Ladouceur, & Freeston, 1998; Ladouceur,Blais, Freeston, & Dugas, 1998) and individ uals with other anxiety disorders (Dugas,
Marchand, & Ladouceur, 2005; Ladouceur et al., 1999). Finally, worry partiallystatistically mediates the relationshi pb e t w e e nI Ua n da n x i e t y( Y o o k ,K i m ,S u h ,&
Lee, 2010).
The premise of the metacognitive model of GAD is that individuals with GAD
experience two types of worry: Type 1 worry refers to worry about external threatsand noncognitive internal triggers (e.g., physical symptoms), whereas Type 2 worryrefers to meta-worry, or worry about worry (Wells, 1995, 2004). Positive beliefs aboutworry (e.g., that worrying will help avoid a catastrophe) give rise to Type 1 worry,whereas negative beliefs about worry (e.g., the belief that worry is uncontrollable)prompt Type 2 worry. Negative beliefs about worry may be more speci ﬁc to GAD
compared to positive beliefs about worry. Individuals with GAD perceive worry asmore dangerous and uncontrollable than do individuals with other anxiety disordersand controls, even when controlling for Type 1 worry (Davis & Valentiner, 2000;302 SPECIFIC DISORDERS

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Wells & Carter, 2001). Type 2 worry, on the other hand, may not be speci ﬁct o
GAD; individuals with GAD do not report greater positive beliefs about worrycompared to anxious nonworriers (Davis & Valentiner, 2000), high worriers withoutGAD (Ruscio & Borkovec, 2004), and individuals with other anxiety disorders (Wells &Carter, 2001).
Emotion dysregulation models propose that individuals with GAD have difﬁ culties
understanding and modulating their emotions, and they may instead rely on sup-pression and control strategies (e.g., worry; Mennin, Heimberg, Turk, & Fresco, 2002).The model further describes speci ﬁc components of emotion dysregulation in GAD,
including heightened intensity of emotions (both positive and negative, but particu-larly negative; Turk, Heimberg, Luterek, Mennin, & Fresco, 2005), poor understandingof emotions, negative reactivity to emotions, and maladaptive management ofemotions (Mennin, Heimberg, Turk, & Fresco, 2005; Mennin, Holaway, Fresco,Moore, & Heimberg, 2007). Both analogue and clinical GAD samples report higheremotion dysregulation compared to nonanxious participants, although individualswith depression report similar de ﬁcits. Moreover, self-reported emotion dysregula-
tion predicts severity of trait worry and analogue GAD status when controlling fornegative affect (Salters-Pedneault, Roemer, Tull, Rucker, & Mennin, 2006), as well asdimensional GAD-Q-IV scores when controlling for symptoms of depression andanxious arousal (Roemer et al., 2009). The acceptance-based model also positsdifﬁculties with emotional experiences in GAD, but instead focuses on fear and
avoidance of internal experiences (Roemer, Salters, Raffa, & Orsillo, 2005). Indeed,deﬁcits in mindfulness account for unique variance in GAD symptom severity, even
after controlling for emotion regulation and depressive and anxious symptoms(Roemer et al., 2009).S
OCIAL ANXIETY DISORDER
Social anxiety disorder, sometimes referred to as social phobia, is a marked andpersistent fear of social or performance situations in which embarrassment may occur.Exposure to or anticipation of the feared social situation almost invariably provokesanxiety or fear. Acute fear responses can take the form of situationally bound orpredisposed panic attacks. Feared situations include performing certain activities inthe presence of others (such as speaking, eating, drinking, or writing), or fearing thatone may do something that will cause humiliation or embarrassment, such as sayingsomething stupid or not knowing what to say, behaving inappropriately, or appearingoverly anxious. The diagnosis requires that these feared situations are either avoidedor endured with signi ﬁcant distress (APA, 2013). The insight criterion found in prior
versions of the DSM (i.e., that the individual recognizes that the fear is irrational) has
been replaced with the criterion that the clinician judges the fear to be out ofproportion to actual danger (APA, 2013). Cultural factors are likely to affect theassessment of this requirement, as it implies a comparison to the patient ’s social
reference group (Lewis-Fernández et al., 2010).
If an individual fears many or most social interactions, the generalized subtype
should be speciﬁ ed. Generalized social anxiety disorder overlaps considerably with
avoidant personality disorder, “so much so that they may be alternative conceptuali-
zations of the same or similar conditions ”(APA, 2000, p. 720). Individuals notAnxiety Disorders 303

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assigned to the generalized subtype are commonly viewed as belonging to a non-generalized or speci ﬁc subtype. Compared to the nongeneralized subtype, the
generalized subtype is associated with greater comorbidity, earlier age of onset,and greater heritability, and is generally an indicator of greater severity, as is theoverlapping diagnosis of avoidant personality disorder (Bögels et al., 2010).
Social anxiety disorder may subsume three other possible disorders. First, the
separate diagnostic category of selective mutism may be an expression of socialanxiety disorder during childhood (Bögels et al., 2010). This conceptualization ofselective mutism treats the refusal to talk as a form of social avoidance. Second, theDSM-5 recognizes a culturally bound syndrome, Taijin Kyofusho, found mainly in
Japan and Korea. The Korean term Taein-kongpo is used interchangeably with social
anxiety disorder (Kim, personal communication, 2010). These conditions appear to bethe same as anthropophobia, a condition recognized in the ICD-10 (World HealthOrganization, 1992). These conditions involve a fear of offending and making othersuncomfortable, such as through poor manners or bad odors, and have also beendocumented in Western cultures (Kim, Rapee, & Gaston, 2008; McNally, Cassiday, &Calamari, 1990). Lewis-Fernández et al. (2010) have suggested that the de ﬁnition of
social anxiety disorder could be broadened to subsume Taijin Kyofusho and equiv-alent conditions. Third, the DSM-5 does not recognize test anxiety as a separate
disorder but subsumes it within social anxiety disorder. LeBeau et al. (2010) suggestedthat one form of test anxiety may be a form of social anxiety disorder in that it involvessocial evaluative concerns and acute fear reactions, whereas a second form may be aform of generalized anxiety disorder in that it involves anticipatory anxiety andworry. The DSM-5 requires a speci ﬁcation when “performance anxiety only ”applies,
implying that there may be two distinct conditions within the diagnostic category ofsocial anxiety disorder.S
PECIFIC PHOBIAS
Speci ﬁc phobias are marked and persistent fears of clearly discernible, circumscribed
objects or situations. Exposure or anticipation of exposure to the feared object orsituation almost invariably provokes anxiety or fear. Acute fear responses can take theform of expected (situationally bound or cued) panic attacks. Five subtypes of speciﬁ c
phobia are recognized by the DSM-5 and are speci ﬁed based on the type of object or
situation that is feared: animals (e.g., dogs, snakes, spiders), natural environment (e.g.,storms, water, heights), blood-injection-injury (BII; e.g., seeing blood, getting aninjection with a syringe), situations (e.g., elevators, ﬂying), and other (e.g., situations
related to choking, vomiting, illness, falling without means of physical support). Thediagnosis requires that these feared situations are either avoided or endured withsigniﬁcant distress (APA, 2013).
Although many individuals meet criteria for a speci ﬁc phobia, very few seek
treatment (Barlow, DiNardo, Vermilyea, Vermilyea, & Blanchard, 1986), althoughindividuals with comorbid diagnoses might be more likely to seek treatment (Barlow,1988). Animal phobia and height phobia are the most frequently diagnosed forms(Curtis, Magee, Eaton, Wittchen, & Kessler, 1998; Stinson et al., 2007). Althoughsubtypes of speci ﬁc phobia appear to have relatively distinctive ages of onset (Öst,
1987), they are generally accepted as constituting a single category. An exception is304 SPECIFIC DISORDERS

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that the BII subtype may be or may subsume a disorder with distinct features andetiological factors (LeBeau et al., 2010; Page, 1994).D
IAGNOSTIC CONSIDERATIONS
Anxiety disorders identi ﬁed in the DSM-5 show considerable overlap and high rates of
comorbidity. These observations suggest that a categorical approach to understandingthese problems is not optimal. In addition, these problems do not appear to bediscontinuous from normal (nonclinical) variation. Dimensional methods may moreaccurately model the nature of these problems (Krueger, 1999; Watson, 2005) and mayeventually come into use. Given the usefulness of the diagnostic categories of panicdisorder, GAD, social anxiety disorder, and speci ﬁc phobias, it is not surprising that
the de ﬁnitions of these diagnoses have not changed substantially since the publication
of the DSM-III-R.
One model for organizing internalizi ng problems involves distinguishing
between distress and fear disorders (Kr ueger, 1999; Watson, 2005). Panic disorder
and speci ﬁc phobias involve acute fear reaction s and avoidance behaviors that occur
in response to speci ﬁc stimuli. In panic disorder, the feared stimulus is an internal
physiological sensation, such as a racing heart or dizziness. Each subtype of speci ﬁc
phobia is cued by a class of feared stimul i (e.g., snakes, heights). These fear
disorders can be distinguished from distress disorders that include major depres-sive disorder, GAD, and other internalizing disorders not characterized by an acutefear response.
The anxiety associated with GAD does not appear to occur in response to speci ﬁc
feared stimuli, but rather can be thought of as “anxious expectation ”(APA, 2013).
Elsewhere it has been described as “a chain of thoughts and images, negatively affect-
laden and relatively uncontrollable; it is an attempt to engage in mental problem-solving on an issue whose outcome is uncertain but contains the possibility of one ormore negative outcomes” (Borkovec, Robinson, Pruzinsky, & DePree, 1983; p. 10).
Interpersonal concerns are the most commonly reported worry topic, regardless ofGAD status (Roemer, Molina, & Borkovec, 1997). However, individuals with GAD aremore likely than those without GAD to worry about minor or routine issues, as well ashealth or illness (Craske, Rapee, Jackel, & Barlow, 1989; Roemer, Molina, Litz, &Borkovec, 1997). They also report more worry topics overall and that their worry is lesscontrollable and more realistic. Finally, although the diagnosis of GAD is categorical,taxometric analyses have indicated that worry exists on a continuum and may occur toa greater or lesser extent in a given individual (Olatunji, Broman-Fulks, Bergman,Green, & Zlomke, 2010; Ruscio, Borkovec, & Ruscio, 2001). Given that worry is thecore diagnostic feature of GAD, these ﬁndings support a dimensional classi ﬁcation of
the disorder.
Although many of the physiological symptoms of GAD overlap with depression,
theDSM-5 criteria for GAD include those symptoms that show unique associations
with worry after controlling for depression. These symptoms include muscle tension(Joormann & Stöber, 1999), gastrointestinal symptoms, and aches and pains (Aldao,Mennin, Linardatos, & Fresco, 2010).
Watson (2005) found that social anxiety disorder shows closer relationships with
depression and GAD than it does with panic disorder, suggesting that it might beAnxiety Disorders 305

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conceptualized as a distress disorder. However, for the nongeneralized subtype, acutefear reactions (including cued panic attacks) are often triggered by social situations,such as having to give a speech to an audience. Thus, generalized social anxietydisorder may be a distress disorder, whereas the nongeneralized subtype may be afear disorder (Carter & Wu, 2010).
Although the DSM-5 does not recognize higher-order classes of distress and fear
disorders, there is good evidence for these superordinate classes because of patterns ofcomorbidity or co-occurrence of symptoms and patterns of shared heritable risk(Krueger, 1999). Presence (versus absence) of an acute fear response and avoidancebehavior may be the key diagnostic distinction for fear disorders (versus distressdisorders). Differential diagnosis within the fear disorder category (e.g., panic dis-order versus animal phobia versus natural environment phobia) requires identi ﬁca-
tion of the feared stimuli. For example, if panic attacks only occur upon exposure to oranticipation of a speciﬁ c stimulus, then panic disorder is not indicated and the speci ﬁc
stimulus provides a clue as to the subtype of speci ﬁc phobia that best describes the
condition.
Despite such questions about the best way to conceptualize these types of problems,
theDSM-5 categories have proven to be quite useful, especially with regard to
predicting prognosis and treatment response. These disorders are quite recognizable,with relatively good reliability of diagnosis when using a semistructured interview(Brown, Campbell, Lehman, Grisham, & Mancill, 2001). Additionally, given theavailability of a host of treatment manuals, treatment planning is greatly facilitatedwhen working with patients seeking treatment for panic disorder, GAD, social anxietydisorder, or speci ﬁc phobias. Finally, it should be noted that anxiety disorders present
risk of suicide, especially when comorbid diagnoses (e.g., depression, personalitydisorders) are present (Cox, Direnfeld, Swinson, & Norton, 1994; Khan, Leventhal,Khan, & Brown, 2002; Warshaw, Dolan, & Keller, 2000).
EPIDEMIOLOGY
P
ANIC DISORDER
Prevalence The lifetime prevalence rate of panic disorder with agoraphobia is
estimated to be between approximately 1.5% and 5%, whereas the 12-month preva-lence rate is estimated to be between approximately 1% and 2.7% (Barlow, 2002; Grantet al., 2006; Kessler, Berglund et al., 2005; Kessler, Chiu, Demler, & Walters, 2005).Gender The incidence rate of panic disorder is approximately 2 times higher in
women than in men (Barlow, 2002; Bland, Orn, & Newman, 1988; Mathews, Gelder, &Johnson, 1981; Wittchen, Essau, von Zerssen, Krieg, & Zaudig, 1992). Differenthypotheses have been proposed to account for observed gender differences in relationto the incidence of panic disorder. For example, it is possible that women are simplymore likely to report fear, or it is possible that men are more likely than women toengage in self-medication for their anxiety and, thus, are less likely to report problemswith panic (Barlow, 2002). The gender distribution of panic disorder with agoraphobiais even more unbalanced, with the greater incidence in women again potentially beingdue to gender role socialization (Bekker, 1996).306 SPECIFIC DISORDERS

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Age of Onset The average age of onset for panic disorder is 26.5 years of age
(range =19.732) (Burke, Burke, Regier, & Rae, 1990; Grant et al., 2006; McNally,
2001; Öst, 1987). Panic disorder typically ﬁrst appears during adulthood, although it
also appears in prepubescent children and older adults (Barlow, 2002).Comorbidity Approximately half of individuals currently suffering from panic dis-
order also suffer from a comorbid psychological disorder, with comorbidity estimatesranging from 51% to 60% (Brown, Antony, & Barlow, 1995; Brown et al., 2001). Amongthe most commonly co-occurring disorders, approximately 59% of individuals withpanic disorder have a comorbid mood or anxiety disorder and 46% have a comorbidanxiety disorder alone. Among speciﬁ c disorders, approximately 23% of individuals
with panic disorder suffer from co-occurring major depressive disorder, 16% sufferfrom co-occurring GAD, 15% suffer from co-occurring social anxiety disorder, and15% suffer from co-occurring speci ﬁc phobia (Brown et al., 2001). Panic disorder is also
often accompanied by substance use disorders (Barlow, 2002), and this comorbidityappears to substantially re ﬂect attempts at self-medication, and, to a lesser degree,
common genetic vulnerability (Kushner, Abrams, & Borchardt, 2000).Clinical Course The clinical course for panic disorder is chronic and disabling without
treatment. The 12-month remission rate for panic disorder is estimated to be approxi-mately 17%, and the 5-year remission rate is estimated to be approximately 39%(Keller et al., 1994; Yonkers et al., 1998). Panic disorder is also associated withsubstantial social, occupational, and physical disability, including especially highrates of medical utilization (Barlow, 2002).G
ENERALIZED ANXIETY DISORDER
Prevalence The lifetime prevalence rate of GAD is 5.7% (Kessler, Berglund et al.,
2005), whereas the 12-month prevalence rate is 3.1% (Kessler, Chiu et al., 2005).Gender GAD is more prevalent among women compared to men. In a nationally
representative sample, women were approximately twice as likely as men to reportlifetime and 12-month diagnoses of GAD, and reported greater disability from GAD(Vesga-López et al., 2008). Given that the genetic contribution to GAD is equivalentamong men and women, gender differences in prevalence are likely due to cognitiveand environmental in ﬂuences (Hettema, Prescott, & Kendler, 2001). Finally, although
prevalence and severity differ between genders, rates of relapse and remission aresimilar (Yonkers, Bruce, Dyck, & Keller, 2003).Age of Onset GAD is associated with a later age of onset compared to the other
anxiety disorders, with 50% of lifetime cases beginning by age 31 (Kessler, Berglund,et al., 2005). This later age of onset may re ﬂect the fact that the symptoms of GAD and
associated impairment are recognized later during the course of the disorder.Comorbidity Correctly classifying GAD may be particularly dif ﬁcult due to high rates
of comorbidity and symptom overlap with other disorders, especially major depres-sive disorder (Kessler, Chiu, et al., 2005). Twenty-six percent of those with a primaryAnxiety Disorders 307

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diagnosis of GAD also meet criteria for current major depressive disorder (Brown,et al., 2001). Moreover, when disregarding the DSM-IV hierarchy rule that prohibits
the diagnosis of GAD when symptoms occur only during the course of a mooddisorder, 67% of those with a primary diagnosis of major depressive disorder alsomeet diagnostic criteria for current GAD. In a longitudinal birth-cohort study, Mof ﬁtt
et al. (2007) found that 12% of the sample had lifetime diagnoses of both GAD andmajor depressive disorder. Among those comorbid cases, 37% reported that GADtemporally preceded major depressive disorder, whereas 32% reported that majordepressive disorder temporally preceded GAD.
Despite substantial comorbidity between GAD and major depressive disorder, a
recent study found evidence that GAD was more similar to other anxiety disordersthan it was to depression with respect to risk factors and temporal patterns (Beesdo,Pine, Lieb, & Wittchen, 2010). Furthermore, a substantial proportion of GAD diag-noses occur without comorbid depression, and levels of impairment between the twodisorders are comparable (Kessler, DuPont, Berglund, & Wittchen, 1999). Thus,although GAD and major depressive disorder overlap considerably, evidence sug-gests that they occur independently and likely represent unique syndromes.Clinical Course A naturalistic longitudinal study found that 42% of participants who
had GAD at baseline were still symptomatic at 12-year follow-up (Bruce et al., 2005).Although cognitive-behavioral therapy is effective for treating GAD (Borkovec &Ruscio, 2001) and reducing symptoms of comorbid Axis I disorders (Borkovec,Abel, & Newman, 1995), only 50% of patients achieve high end-state functioningas a result of treatment (Borkovec, Newman, Pincus, & Lytle, 2002).S
OCIAL ANXIETY DISORDER
Prevalence The lifetime prevalence rate of social anxiety disorder is estimated to be
between 5.0% and 13.3%, whereas the 12-month prevalence rate is estimated to bebetween 2.8% and 6.8% (Grant et al., 2005; Kessler et al., 1994; Kessler, Berglund, et al.,2005; Kessler, Chiu, et al., 2005).Gender The incidence rate of social anxiety disorder is relatively equally represented
between genders, with the sex ratio (1.4:1) only somewhat favoring women relative tomen (Kessler, Berglund, et al., 2005).Age of Onset The average age of onset for social anxiety disorder is approximately
15 years of age, with a median age of onset of approximately 12.5 years of age (Grantet al., 2005). Social anxiety disorder is typically especially prevalent among youngadults between the ages of 18 and 29 (Kessler, Berglund, et al., 2005).Comorbidity Approximately 46% of individuals currently suffering from social
anxiety disorder also suffer from a comorbid Axis I disorder (Brown et al., 2001).Among the most commonly co-occurring disorders, approximately 45% of individualswith social anxiety disorder have a comorbid mood or anxiety disorder, and approxi-mately 28% of individuals have a comorbid anxiety disorder alone. Among speciﬁ c
disorders, approximately 14% of individuals with social anxiety disorder suffer from308 SPECIFIC DISORDERS

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co-occurring major depressive disorder, and 13% of individuals suffer from co-occurring GAD (Brown et al., 2001). Other commonly comorbid disorders includesubstance use disorders (Grant et al., 2005).Clinical Course The clinical course for social anxiety disorder is chronic and disabling
without treatment. The 12-month remission rate for social anxiety disorder is esti-mated to be approximately 7%, and the 5-year remission rate is estimated to beapproximately 27% (Yonkers, Bruce, Dyck, & Keller, 2003). Social anxiety disorder isalso associated with substantial social, occupational, and physical disability, includingespecially high levels of scholastic dif ﬁculties (Stein & Kean, 2000).
S
PECIFIC PHOBIA
Prevalence The lifetime prevalence rate for speci ﬁc phobia is estimated to be between
2% and 12.5%, whereas the 12-month prevalence rate is estimated to be between 1.8%and 8.7% (Bland et al., 1988; Eaton, Dryman, & Weissman, 1991; Kessler, Berglund,et al., 2005; Kessler, Chiu, et al., 2005; Lindal & Stefansson, 1993; Stinson et al., 2007;Wittchen, Nelson, & Lachner, 1998). Among the speciﬁ c phobias, animal phobia and
height phobia are the most frequently diagnosed forms (Curtis et al., 1998; Stinsonet al., 2007).Gender Speci ﬁc phobia is approximately 4 times more common in women than in
men (Kessler, Berglund, et al., 2005). However, research indicates that the incidence ofphobias of heights, ﬂying, injections, dentists, and injury do not signi ﬁcantly differ
between women and men (Fredrikson, Annas, Fischer, & Wik, 1996). Differenthypotheses have been put forth to account for observed gender differences in relationto the incidence of speci ﬁc phobia. These hypotheses include differences relating to the
reporting of fear between genders, as well as differences in the ways women and menare taught to deal with threatening stimuli (Barlow, 2002).Age of Onset The average age of onset for speci ﬁc phobia is between 9.1 and 16.1 years
of age (Stinson et al., 2007; Thyer, Parrish, Curtis, Nesse, & Cameron, 1985), with amedian age of onset of approximately 15 years (Magee, Eaton, Wittchen, McGonagle, &Kessler, 1996). Moreover, results suggest that particular speci ﬁc phobias may have
differential ages of onset. For example, animal phobia and BII phobia tend to begin inchildhood, whereas situational phobia and height phobia tend to develop in adolescenceor adulthood (e.g., Antony, Brown, & Barlow, 1997; Barlow, 2002; Himle, McPhee,Cameron, & Curtis, 1989; Marks & Gelder, 1966; Öst, 1987).Comorbidity Speci ﬁc phobias are likely to co-occur with other speci ﬁc phobias, with
only 24.4% of phobic individuals having a single speci ﬁc phobia (Curtis et al., 1998).
However, other ﬁndings suggest that the presence of multiple speci ﬁc phobias is
relatively rare (Fredrikson et al., 1996). Moreover, approximately 34% of individualscurrently suffering from a speci ﬁc phobia meet the criteria for an additional Axis I
disorder, with mood and anxiety disorders being the most common co-occurringdisorders (Brown et al., 2001). Among mood and anxiety disorders, some research hasfound especially high rates of co-occurring panic disorder in individuals sufferingAnxiety Disorders 309

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from speci ﬁc phobias (Stinson et al., 2007). Other data suggest that speci ﬁc phobias are
rarely the principle diagnosis when they co-occur with other disorders, but they areoften a secondary diagnosis (Barlow, 2002; Sanderson, Di Nardo, Rapee, & Barlow,1990).Clinical Course The clinical course for speci ﬁc phobia is relatively chronic and
disabling without treatment. The 15-month full remission rate is estimated to beapproximately 19% (Trumpf, Becker, Vriends, Meyer, & Margraf, 2009). Speci ﬁc
phobia is also often associated with substantial social, occupational, and physicaldisability, including avoidance of medical procedures (Wolitzky-Taylor, Horowitz,Powers, & Telch, 2008).
TREATMENT
P
HARMACOLOGICAL TREATMENTS
Panic Disorder Many pharmacological agents have been used for the treatment of
panic disorder with and without agoraphobia, including benzodiazepines, selectiveserotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors(SNRIs), monoamine oxidase inhibitors (MAOIs), and tricyclic antidepressants (e.g.,Ballenger et al., 1988; Barlow, Gorman, Shear, & Woods, 2000; Marks et al., 1993;Mavissakalian & Perel, 1999; Tesar et al., 1991; van Vliet, Westenberg, & den Boer,1993). Among these agents, a growing body of research suggests that SSRIs and SNRIsshould be considered the front-line pharmacological agents for the treatment of panicdisorder (Hoffman & Mathew, 2008; McHugh, Smits, & Otto, 2009; Pollack et al.,2007). Although benzodiazepines have been shown to be effective in the treatment ofpanic, they are associated with abuse potential and may interfere with psychologicalinterventions; speci ﬁcally, they interfere with the experience of anxiety during
exposure to feared situations (Jorstad-Stein & Heimberg, 2009) and are thus notconsidered ﬁrst-line pharmacological agents for panic disorder.
Generalized Anxiety Disorder A host of pharmacological interventions have been used
in the treatment of GAD, including benzodiazepines, SSRIs, SNRIs, tricyclic anti-depressants, Buspirone, and Pregabalin (Baldwin, Waldman, & Allgulander, 2011;Hidalgo, Tupler, & Davidson, 2007; Katzman, 2009; Mitte, Noack, Steil, & Hautzinger,2005; Mula, Pini, & Cassano, 2007; Rickels & Rynn, 2002). When GAD is comorbidwith depression, SSRIs and tricyclic antidepressants may evidence greater ef ﬁcacy
relative to benzodiazepines (Davidson, 2009) by targeting symptoms of both GAD anddepression uniquely (Olatunji et al., 2008). It should be noted that benzodiazepinesmay be associated with high dropout rates (Martin et al., 2007). Furthermore, becausebenzodiazepines, tricyclic antidepressants, and SSRIs are associated with adverse sideeffects that may limit their utility, Buspirone and Pregabalin are often relied upon asﬁrst-line pharmacological treatments for GAD (Mitte et al., 2005).
Social Anxiety Disorder Efﬁcacious pharmacological agents for the treatment of social
anxiety disorder include benzodiazepines, SSRIs, SNRIs, and MAOIs (e.g., Blackmore,Erwin, Heimberg, Magee, & Fresco, 2009; Blanco et al., 2003; Clark et al., 2003;310 SPECIFIC DISORDERS

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Davidson et al., 2004; Gerlernter et al., 1991; Kobak, Greist, Jefferson, & Katzelnick,2002; Ledley & Heimberg, 2005; Otto et al., 2000). Given the noted concerns surround-ing benzodiazepines, the SSRIs, SNRIs, and MAOIs are considered the ﬁrst-line
pharmacological agents for the treatment of social anxiety disorder (Jorstad-Stein &Heimberg, 2009).Speci ﬁc Phobia Extant data suggest that use of pharmacological agents, such as
benzodiazepines and sedatives, in the treatment of speci ﬁc phobias is limited.
Moreover, there exists a paucity of data relating to the ef ﬁcacy of antidepressant
medications as they relate to the treatment of speciﬁ c phobias (Grös & Antony, 2006;
Hamm, 2009). Pharmacological agents are not standard treatments for speciﬁ c
phobias, and many individuals with speciﬁ c phobia do not seek treatment, likely
managing their fears using avoidance and self-medication (Bandelow et al., 2012).C
OGNITIVE -BEHAVIORAL TREATMENTS
Panic Disorder Often considered to be a ﬁrst-line treatment, cognitive-behavioral
therapy (CBT) that incorporates psychoeducation, interoceptive and in vivo exposures,
and cognitive restructuring has been shown to be ef ﬁcacious in both individual and
group format, with 80% to 90% of patients showing marked improvement (e.g.,Barlow et al., 2000; Clark et al., 2003; Hofmann & Smits, 2008; McHugh et al., 2009;Olatunji, Cisler, & Deacon, 2010; Öst, Thulin, & Ramnero, 2004; Penava, Otto, Maki, &Pollack, 1998; Telch et al., 1993). Interoceptive exposures entail provoking fearedarousal-related sensations in order to facilitate habituation of fear and discon ﬁrmation
of feared catastrophic outcomes of such sensations. Treatment gains associated withCBT for panic disorder have shown excellent maintenance, including at 2 yearsposttreatment (e.g., Craske, Brown, & Barlow, 1991).Generalized Anxiety Disorder Cognitive-behavioral therapy for GAD has also been
shown to be ef ﬁcacious (Borkovec & Ruscio, 2001). Because GAD is not characterized by
motoric avoidanceof disorder-speci ﬁc stimuli (as are other anxiety disorders), traditional
behavioral exposure techniques that are so effective in the treatment of other anxietysyndromes are not used in the treatment of worry. Instead, approaches to treating GADrely on targeting nonadaptive patterns of awareness, physiology, behavior, and cogni-tion (Behar & Borkovec, 2005, 2009; Borkovec, Newman, Pincus, & Lytle, 2002; Newmanet al., 2011). This approach evidences relatively lower rates of success than do otherCBT-based treatments for anxiety, with only 50% of patients reaching high end-statefunctioning at post-therapy (Borkovec et al., 2002). More recently, an investigation wascompleted examining the additive value of therapy focusing on interpersonal processesand emotional avoidance above and beyond the effects of CBT; the results of that studyfailed to indicate that this augmented treatment was associated with superior ef ﬁcacy
relative to CBT alone (Newman et al., 2011).Social Anxiety Disorder Cognitive-behavioral therapy for social anxiety disorder
includes engagement in psychoeducation, exposure to feared social-evaluative situa-tions, and cognitive restructuring in an attempt to modify appraisals and reactions tosocial situations. Exposures, in which individuals engage in feared social situations,Anxiety Disorders 311

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allow for habituation of fear and discon ﬁrmation of feared catastrophes in the absence
of maladaptive responses such as escape and avoidance (e.g., see Clark & Wells, 1995).CBT for social anxiety disorder has been shown to be ef ﬁcacious in both individual
and group formats (Clark et al., 2006; Feske & Chambless, 1995; Heimberg & Becker,2002; Jorstad-Stein & Heimberg, 2009; Olatunji, Cisler, et al., 2010; Ponniah & Hollon,2008; Powers, Sigmarsson, & Emmelkamp, 2008). Moreover, treatment gains associ-ated with CBT for social anxiety disorder show excellent maintenance, including at 5years posttreatment (e.g., Heimberg, Salzman, Holt, & Blendell, 1993). Newer formu-lations of CBT (e.g., Clark, 2001; Clark & Wells, 1995; Hofmann & Otto, 2008)incorporate manipulation of self-focused attention, elimination of safety behaviors,reevaluation of social costs, and change in self-perceptions.Speci ﬁc Phobia Cognitive-behavioral therapy for speci ﬁc phobia typically involves
exposure to feared stimuli. In the absence of avoidance responses, such exposureallows for habituation of fear and discon ﬁrmation of the expected catastrophes
associated with coming into contact with feared stimuli (e.g., see Antony & Swinson,2000). Cognitive-behavio ral treatments for speci ﬁc phobia have been shown to be
efﬁcacious (e.g., Choy, Fyer, & Lipsitz, 2007; Hamm, 2009; Muhlberger, Herrmann,
Wiedemann, Ellgring, & Pauli, 2001; Olatunji, Cisler, et al., 2010; Öst, 1989;Rothbaum, Hodges, Smith, Lee, & Price, 2 000; Van Gerwen, Spinhoven, Diekstra, &
Van Dyck, 2002; Wolitzky-Taylor et al., 2008). One version of this treatment,delivered during a single session lastin g 2 to 4 hours, has been shown to be highly
effective, with about 90% of patients sh owing marked improvement (Öst, 1989).
Treatment gains associated with CBT for speci ﬁc phobia have shown excellent
maintenance, including at 14 months pos ttreatment (e.g., Choy et al., 2007).
O
THER PSYCHOLOGICAL TREATMENTS
Acceptance and commitment therapy (ACT ; Hayes, Luoma, Bond, Masuda, & Lillis,
2006) is another psychological treatment for anxiety disorders that has garneredrecent interest. Broadly speaking, ACT seeks to reduce the extent to which indi-viduals respond to thoughts and other inner experiences in ways that maintain andexacerbate emotional distress. Preliminary data indicate that ACT is an ef ﬁcacious
treatment for reducing anxiety symptom s (e.g., see Öst, 2008). Moreover, ACT-
based treatments for panic disorder (Lopez & Salas, 2009) and social anxietydisorder (Dalrymple & Herbert, 2007) have been examined.
Mindfulness-based approaches have also received attention recently, particularly
in the treatment of GAD. Mindfulness is de ﬁned as “paying attention in a particular
way, on purpose, in the present moment, and nonjudgmentally” (Kabat-Zinn, 1994,
p. 4) and “bringing one ’s complete attention to the present experience on a moment-
to-moment basis ”(Marlatt & Kristeller, 1999, p. 68). Thus, mindfulness-based
treatments for GAD aim to increase clients ’awareness and acceptance through
practicing mindfulness of internal and external experiences, nonjudgmental obser-vation of those experiences, relaxation, meditation, and a focus on the presentmoment (Roemer, Salters-Pedneault, & Orsillo, 2006). Mindfulness-based interven-tions have been shown to be ef ﬁcacious as stand-alone treatments (e.g., Roemer,312 S
PECIFIC DISORDERS

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Orsillo, & Salters-Pedneault, 2008), an d can also be added to traditional CBT
techniques (Behar, Goldwin, & Borkovec, in press) in an attempt to increase ef ﬁcacy.
Other psychological treatments that have garnered some interest in the treatment of
panic disorder, GAD, social anxiety disorder, and speci ﬁc phobias include inter-
personal therapy, psychoanalytic psychotherapy, and eye movement desensitizationand reprocessing (EMDR) therapy. High-quality randomized and controlled clinicaltrials have generally not yet been conducted, or have found no support for treatingthese disorders with these alternate psychological approaches. For example, anexamination of the ef ﬁcacy of EMDR in the treatment of panic disorder with
agoraphobia indicated that EMDR was not signiﬁ cantly different from a credible
attention placebo condition (e.g., Goldstein, de Beurs, Chambless, & Wilson, 2000).These treatments are, therefore, not widely considered to be ﬁrst-line treatments
(Hamm, 2009; Jorstad-Stein & Heimberg, 2009; McHugh et al., 2009).C
OMBINED PHARMACOLOGICAL AND PSYCHOLOGICAL TREATMENTS
Traditional Pharmacological Agents Several studies have examined the combined
effects of traditional pharmacological agents and cognitive-behavioral treatments forpanic disorder (e.g., Azhar, 2000; Barlow et al., 2000; Berger et al., 2004; Spinhoven,Onstein, Klinkhamer, Knoppert-van der Klein, 1996; Stein, Norton, Walker, Chartier, &Graham, 2000). In a review of such studies, Furukawa, Watanabe, and Churchill (2006)concluded that combined traditional pharmacological and psychological treatments inthe treatment of panic disorder is modestly more ef ﬁcacious relative to either pharma-
cological treatment or CBT for panic disorder alone. However, such a combinedapproach is associated with greater dropouts and side effects relative to CBT alonefor panic disorder (e.g., Barlow et al., 2000).
Likewise, only a few investigations have examined the efﬁ cacy of a combined
treatment approach for GAD. Power et al. (1990) failed to ﬁnd superiority of a
combined CBT +diazepam approach over CBT-alone, and Crits-Cristoph et al.
(2011) failed to ﬁnd superiority of a combined CBT +venlafaxine approach over
venlafaxine-alone, suggesting that combination treatments are not superior to mono-therapies in the treatment of GAD.
Only a few known studies have examined whether a combined approach is
efﬁcacious for social anxiety disorder. Such ﬁndings have been mixed: One study
found that a combined approach was superior to a psychological approach alone andpharmacological treatment alone (Blanco et al., 2010), one study found that acombined approach was not superior to a psychological approach alone or a phar-macological approach alone (Davidson et al., 2004), and one study found thepsychological treatment alone to be especially bene ﬁcial at 1-year follow-up (Blomhoff
et al., 2001).
No known studies have examined the efﬁ cacy of a combined approach in the
treatment of speci ﬁc phobias, although advantages of such an approach have been
posited (e.g., Cottraux, 2004). Some researchers view the use of medications, particu-larly benzodiazepines, as antithetical to the mechanisms of change in CBT if they areused to reduce feared somatic sensations (Bruce, Spiegel, & Hegel, 1999; Deacon &Abramowitz, 2005).Anxiety Disorders 313

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D-cycloserine (DCS) and Related Issues Among nontraditional pharmacological
agents, D-cycloserine (DCS) has emerged as a potentially important supplementto traditional cognitive-behavioral treat ments for panic disorder, social anxiety
disorder, and speci ﬁcp h o b i a s .D C S ,a nN M D Aa g o n i s t ,s e e m st oa u g m e n tl e a r n i n g
and memory (Schwartz, Hashtroudi, Hertin g, Schwartz, & Deutsch, 1996; Tsai, Falk,
Gunther, & Coyle, 1999) and has been shown t o facilitate conditioned fear extinction
in animal studies (Ledgerwood, Richardson, & Cranney, 2003; Walker, Ressler,Lu, & Davis, 2000). Such evidence led inves tigators to examine whether DCS might
enhance the effects of exposure-based cogni tive-behavioral interventions in a host
of anxiety disorders (e.g., Guastella et a l., 2008; Hofmann et al., 2006; Norberg,
Krystal, & Tolin, 2008; Ressler et al., 2004) . Thus far, evidence indicates that DCS
does indeed enhance the effects of CBT for panic disorder, social anxiety disorder,and speci ﬁc phobias at posttreatment and follow -up; its potential enhancing effects
in the treatment of GAD have not been explored.
Behavioral treatments for most anxiety disorders utilize procedures that incorpo-
rate exposure to conditioned stimuli, an approach that mirrors the process of fearextinction as studied most extensively in rats. As laboratory investigations usinganimal models identify agents and procedures that enhance extinction processes,translational applications of these ﬁndings to research on humans will hopefully lead
to innovative changes to behavior therapy protocols that are used for panic disorder,GAD, social anxiety disorder, and speci ﬁc phobias. For example, extinction has
traditionally entailed learning of safety associations that compete with fear associa-tions; however, alternate procedures might be used to erase fear associations alto-
gether, such as through speci ﬁc chemical agents or behavioral procedures that
interfere with reconsolidation (see Quirk et al., 2010). In addition, such researchmay lead to knowledge regarding the degree to which factors such as sleep and timingbetween therapy sessions might in ﬂuence therapeutic effectiveness.
P
REDICTORS OF TREATMENT OUTCOME
A host of variables may predict enhanced or compromised response to treatmentacross anxiety disorders. One commonly examined predictor of treatment outcomeis symptom severity. In panic disorder, higher levels of agoraphobia are associatedwith poorer treatment outcome (e.g., Cowley, Flick, & Roy-Byrne, 1996; Warshaw,Massion, Shea, Allsworth, & Keller, 1997). However, in GAD, the evidence is mixed.Some investigations have shown that patients with more severe anxiety at pretreat-ment respond less well to therapy (Butler, 1993; Butler & Anastasiades, 1988; Yonkers,Dyck, Warshaw, & Keller, 2000), whereas others have failed to ﬁnd such relation-
ships (e.g., Barlow, Rapee, & Brown, 1992; Biswas & Chattopadhyay, 2001; Durham,Allan, & Hackett, 1997). In social anxiety disorder, greater severity of depression andgreater severity of avoidant personality traits are related to poorer treatment outcome(Chambless, Tran, & Glass, 1997).
Overall, there are mixed ﬁndings regarding the impact of comorbid conditions on
treatment outcome. For example, some research indicates that individuals with panicdisorder who have comorbid major depressive disorder evidence poorer treatmentoutcome (Cowley et al., 1996), whereas other research has found that such comorbid-ity does not negatively impact treatment outcome in panic (McLean, Woody, Taylor, &314 SPECIFIC DISORDERS

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Koch, 1998; Tsao, Mystkowski, Zucker, & Craske, 2002). In GAD, the presence of acomorbid Axis I disorder generally (Durham et al., 1997), and comorbid dysthymia orpanic disorder speci ﬁcally (Tyrer, Seivewright, Simmonds, & Johnson, 2001), predict
relapse of symptoms. In speci ﬁc phobias, the presence of additional comorbid anxiety
disorders does not seem to affect treatment outcome (Ollendick, Öst, Reuterskiöld, &Costa, 2010).
Interpersonal problems seem to predict a poor response to treatment among
individuals with GAD patients. For example, Borkovec et al. (2002) found thatinterpersonal problems remaining at treatment termination predicted poorer function-ing at post-therapy and follow-up assessments. Likewise, personality disorder traits areassociated with poorer response to cognitive therapy and self-help treatments amongGAD patients (Tyrer, Seivewright, Ferguson, Murphy, & Johnson, 1993).
Finally, several treatment process variables (e.g., therapeutic alliance, treatment
compliance) have also been examined as predictors of treatment outcome. The degreeto which patients expect to change seems to be especially important (Jorstad-Stein &Heimberg, 2009). For example, research indicates that lower levels of treatmentexpectancy are related to poorer outcome in social anxiety disorder (Chamblesset al., 1997).
ASSESSMENT
Multimodal approaches are generally recommended in the assessment of panicdisorder, GAD, social anxiety disorder, and speci ﬁc phobias. These approaches often
include the use of a clinical interview, self-report measures, and behavioral tests (e.g.,see Antony, 1997; Barlow, 2002; Grös & Antony, 2006). In addition, the emergence ofbiological assessments may lead to enhanced knowledge of these conditions in thefuture.C
LINICAL INTERVIEWS
Clinical interviews provide detailed i nformation relating to an individual ’sp s y c h i –
atric history and current functioning. Clinical interviews can differ with respect totheir format: Some clinical interviews are highly structured and directive, whereasother clinical interviews use an unstruct ured and conversational approach. When
seeking a diagnosis, the use of structured clinical interviews is recommended due
to their increased standardization and reliability (Summerfeldt, Kloosterman, &Antony, 2010).
Two of the most commonly used semistructured clinical interviews for diagnosing
anxiety disorders include the Anxiety Disorders Interview Schedule for DSM-IV –
Lifetime (ADIS-IV-L; Di Nardo, Brown, & Barlow, 1994) and the Structured ClinicalInterview for DSM-IV Axis I Disorders (SCID; First, Spitzer, Gibbon, & Williams,1996). Although these interviews can be used to reach a diagnosis relating to a widerange of psychological disorders, both the ADIS-IV-L and the SCID can also be used tospeciﬁcally assess whether an individual meets the diagnostic criteria for panic
disorder, GAD, social anxiety disorder, or speci ﬁc phobia. The ADIS-IV-L and the
SCID both explicitly provide questions for clinicians to ask when administering theinterview. This structured format ensures that each individual is asked the sameAnxiety Disorders 315

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questions, in the same order, using the same terminology. However, subsequentquestions, which may deviate from the standardized questions, can be used tofurther probe an individual ’s presenting problem(s). Both the ADIS-IV-L and the
SCID have been shown to have good psychometric properties in prior studies (e.g., seeSummerfeldt et al., 2010).
Despite the ADIS-IV-L and the SCID providing a standardized, systematic, and
valid assessment of panic disorder, GAD, social anxiety disorder, and speci ﬁc
phobia, both interviews require training and can be time-consuming to administer.
Nonetheless, the use of such interviews is recommended when assessing for these
three disorders. Inter-rater reliability e stimates using the ADIS-IV-L are adequate
for GAD ( κ=.65) and good for panic disorder with or without agoraphobia ( κ=.79),
social anxiety disorder ( κ=.77), and speci ﬁcp h o b i a( κ=.71) (Brown et al., 2001).
S
ELF-REPORT MEASURES
Self-report measures provide an ef ﬁcient and cost-effective method to assess for panic
disorder, GAD, social anxiety disorder, or speci ﬁc phobia, as well as their associated
symptoms. There are several well-validated self-report measures (see Antony,Orsillo, & Roemer, 2001). We present some of the most commonly used self-reportmeasures to assess each disorder.
For panic disorder, well-validated and frequently used self-report measures
include the Panic Disorder Severity Scale (PDSS; Shear et al., 1997) and the Panic
and Agoraphobia Scale (PAS; Bandelow, 1 999). The Agoraphobic Cognitions Ques-
tionnaire (ACQ; Chambless, Caputo, Br ight, & Gallagher, 1984) and the Anxiety
Sensitivity Index-3 (ASI-3; Taylor et al., 2007) are two frequently used measures toassess for panic-related cognitions and anxiety focuse d on physical sensations,
respectively.
For GAD, the most commonly used self-report measure is the Generalized
Anxiety Disorder Questionnaire —DSM-IV (GAD-Q-IV; Newman et al., 2002).
The GAD-Q-IV is a nine-item self-report measure of the symptoms of GAD asoutlined in the DSM-IV-TR and DSM-5. Trait worry, the central symptom dimen-
sion underlying generalized anxiety disord er, can also be assessed with existing self-
report measures, most notably the Penn S tate Worry Questionnaire (PSWQ; Meyer,
Miller, Metzger, & Borkovec, 1990). The PSWQ is a 16-item self-report trait measureo ft h ef r e q u e n c ya n di n t e n s i t yo fw o r r y .T h eP S W Qh a sd e m o n s t r a t e dh i g hi n t e r n a lconsistency and good retest reliability ( Meyer et al., 1990), correlates well with
diagnostic measures of GAD (Behar, Zuel lig, & Borkovec, 2005), is distinct from
anxiety and depression in clinical sample s (Meyer et al., 1990), and discriminates
individuals with GAD from those with oth er anxiety disorders (Brown, Antony, &
Barlow, 1992).
For social anxiety disorder, well-validated and frequently used self-report mea-
sures include the Social Phobia and Anxiety Inventory (SPAI; Turner, Beidel, Dancu, &Stanley, 1989), the Social Interaction Anxiety Scale (SIAS; Mattick & Clarke, 1998), andthe Social Phobia Scale (SPS; Mattick & Clarke, 1998). The Brief Fear of NegativeEvaluation Scale (BFNES; Leary, 1983a) is a frequently used self-report measure toassess for the core cognition purported to underlie social anxiety disorder. In addition,the Social Phobia and Anxiety Inventory for Children (SPAI-C; Beidel, Turner,316 SPECIFIC DISORDERS

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Hamlin, Morris, 2000) is a well-validated self-report measure for assessing socialanxiety symptoms in children and adolescents.
For speci ﬁc phobias, the Fear Survey Schedule (FSS-II; Geer, 1965) is well validated
and commonly used, although other promising self-report measures exist as well (e.g.,Phobic Stimuli Response Scales; Cutshall & Watson, 2004). Whereas the FSS-II assessesa broad range of speci ﬁc phobias, self-report measures designed to assess certain types
of speci ﬁc phobias exist as well (e.g., Fear of Spider Questionnaire [Szymanski &
O’Donohue, 1995]; Blood-Injection Symptom Scale [Page, Bennett, Carter, Smith, &
Woodmore, 1997). The Spence Child Anxiety Scale (Spence, 1997, 1998; Spence,Barrett, & Turner, 2003) includes both self-report and parent informant versionsfor assessment of anxiety disorder symptoms in children and adolescents.B
EHAVIORAL ASSESSMENTS
Although less frequently used in clinical practice, behavioral assessment strategiesoffer unique insights into the nature and expression of an individual ’s symptoms. The
chief goal of behavioral assessments is to evaluate an individual ’s distress during
exposure to and avoidance of his/her feared stimulus. Such an assessment iscommonly referred to as a behavioral approach test (BAT). BATs can differ in theirorientations, with multiple-task BATs (i.e. BATs that require individuals to completeseveral fear-related tasks) generally being favored relative to single-task BATs. BATsare idiographic in nature, such that the feared stimulus is chosen based on anindividual ’s speci ﬁc symptom pro ﬁle. For example, an individual with spider phobia
would likely be exposed to different stimuli relating to spiders, whereas an individualwith social anxiety disorder would likely be exposed to situations relating to social orperformance situations. In the case of panic disorder, behavioral assessments includephysiological symptom inductions that trigger anxiety or fear. Subjective units ofdistress are often assessed during BATs, with higher units indicating higher levels ofdistress (e.g., Antony, 1997; Barlow, 2002; Grös & Antony, 2006).
Self-monitoring is another behavioral assessment strategy that is important in
the assessment of anxiety disorders. Self-monitoring involves recording thoughts,emotions, and behaviors in response to speci ﬁc situations. In panic disorder, self-
monitoring typically entails recording the time of onset, intensity, antecedents,consequences, and location of panic attacks, as well as cognitions experienced duringthe attacks. If accompanied by agoraphobia, additional information might include thefrequency and duration of excursions from home, distance traveled, escape behaviors,safety behaviors, and level of anxiety (Barlow, 2002).
In GAD, self-monitoring entails recording levels of anxiety and associated behaviors
and cognitions at many points throughout the day; the resulting enhanced awarenessis then used to help clients catch the anxiety spiral early enough to intervene usingprescribed interventions before anxiety becomes excessive (e.g., Behar & Borkovec,2005, 2009). In social anxiety disorder, self-monitoring typically includes recording thefrequency and duration of social interactions, antecedents and consequences of theseinteractions, cognitions during the interactions, and level of anxiety experienced (e.g.,Heimberg, Madsen, Montgomery, & McNabb, 1980). In speci ﬁc phobia, self-monitoring
entails recording thoughts, behaviors, and fear levels upon coming into contact withthe feared stimulus.Anxiety Disorders 317

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Despite the potentially useful information that accompanies behavioral assessment
strategies, it is important to note that such strategies have been broadly criticized forpoorer reliability and validity relative to structured clinical interviews and self-reportmeasures. Moreover, behavioral assessment strategies can be prone to bias (e.g.,observer bias, con ﬁrmation bias; Groth-Marnat, 2003). In addition to having potential
assessment value, self-monitoring may also have therapeutic value by helpingindividuals become more aware of the automatic cognitions and behaviors thatmaintain their disorders.B
IOLOGICAL ASSESSMENT
Neuroanatomical differences are not suf ﬁciently established to warrant routine
assessment of neuroanatomy in individuals suffering from panic disorder, GAD,social anxiety disorder, and speci ﬁc phobia (e.g., Britton & Rauch, 2009). Although
their diagnostic value is limited at prese nt, neuroanatomical assessment techniques
are a promising area of research. Approaches used to assess the neuroanatomy ofindividuals suffering from panic disorder, GAD, social anxiety disorder, and speci ﬁc
phobias, as well as psychopathology more broadly, can be divided into two diffe-rent methods: structural (anatomical) te chniques and functional (physiological/
neurochemical) techniques.
Computerized tomography (CT) and magnetic resonance imaging (MRI) are two of
the most common structural techniques used to examine how various parts of thebrain relate to one another spatially. Of these two techniques, MRI produces betterresolution than does CT and is thus used more often. The most commonly usedfunctional techniques include single photon emission computed tomography(SPECT), functional MRI (fMRI), and positron emission tomography (PET). Suchfunctional techniques allow for the examination of changes in the brain ’s metabolism
and blood ﬂow.
Both SPECT and PET use trace amounts of ligands that are labeled with radioactive
isotopes, which in turn allow measurement of cerebral metabolism or cerebral bloodﬂow. This radioactive dye is injected into the bloodstream, and SPECT or PET scanners
detect the radiation emitted by the isotopes. PET allows for more precision and betterresolution than does SPECT and is thus used more often. fMRI assesses cerebral bloodﬂow in a similar fashion as the other two functional techniques, but fMRI has the
advantage of not requiring any exposure to ionizing radiation. It is also important tonote that structural and functional methods can be combined, such that a functionalimage can be placed on top of a structural image (i.e., image registration) to determinethe exact structural location of the functional change (Andreasen, 2001).
ETIOLOGY
B
EHAVIORAL GENETICS
Behavioral genetic studies (e.g., studies of identical twins, studies of adopted siblings)estimate that about 20% of the variance in panic disorder, social anxiety disorder,and speci ﬁc phobias is attributable to genetic factors (e.g., Hettema, Neale, Myers,
Prescott, & Kendler, 2006). Familial factors (i.e. environmental factors shared by twins318 SPECIFIC DISORDERS

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and siblings) account for less than 10% of the variance in the occurrence of the disorders,and the majority of the variance (perhaps as much as 70%) is attributed to uniqueenvironmental factors and measurement error. Although some behavioral geneticsstudies have resulted in higher estimates of the contribution of heritable genetics(perhaps as high as about 50% when correcting for measurement error; Kendler,Karkowski, & Prescott, 1999; Kendler, Myers, Prescott, & Neale, 2001), it is generallyagreed that compared to most other psychological conditions, these anxiety disordersappear to be relatively less in ﬂuenced by heritable genetics and more in ﬂuenced by
environment or by gene-environment interactions. A notable exception to these ﬁndings
is that the BII subtype of speci ﬁc phobia appears to be relatively more heritable (Kendler
et al., 1999, 2001). In addition, when social anxiety disorder subtypes are examined, thegeneralized subtype appears to involve somewhat greater heritable genetic risk than thenongeneralized subtype (Mannuzza et al., 1995; Stein et al., 1998).
Some of the heritable genetic risk for panic disorder and speci ﬁc phobias appears to
be due to a general factor (perhaps neuroticism; Gray & McNaughton, 2000; Hettemaet al., 2006) underlying most internalizing disorders (Krueger, 1999). A substantialpart of the heritable genetic risk is speci ﬁc to the group of disorders that involves acute
fear reactions (Krueger, 1999). A modest amount of disorder-speci ﬁc heritable genetic
risk has been found for panic disorder (Hettema et al., 2006). It is also noteworthy thatanxiety sensitivity (Stein, Lang, & Livesley, 1999), which is a risk factor for panicdisorder (see Personality and Temperament: Anxiety Sensitivity), and behavioralinhibition (Hirsch ﬁeld-Becker, Biederman, & Rosenbaum, 2004), which is a risk factor
for social anxiety disorder (see Personality and Temperament: Behavioral Inhibitionand Shy Temperament), are heritable. Although the largest portion of heritable geneticrisk appears to involve a general factor underlying the entire class of disorders thatinvolve acute fear reactions, unique environmental factors appear to play a consider-able role, particularly with regard to which type of acute fear disorder develops.
A meta-analysis of family and twin studies found that genetic factors account for
approximately 32% of the variance in liability to GAD (Hettema, Neale, & Kendler,2001). Not surprisingly, there is considerable overlap in genetic liability for GAD andmajor depressive disorder, 25% of which is accounted for by neuroticism (Kendler,Gardner, Gatz, & Pedersen, 2007). Furthermore, a large twin study found that GADand depression were linked to one genetic factor termed “anxious-misery,” whereas
the phobias were linked to another factor termed “fear”(panic disorder was linked to
both factors, but less strongly; Kendler, Prescott, Myers, & Neale, 2003). A similarstudy examining only anxiety disorders found that GAD is linked to the same geneticfactor as panic disorder and agoraphobia, whereas a different genetic factor wasassociated with situational and animal phobias (Hettema, Prescott, Myers, Neale, &Kendler, 2005). Despite genetic overlap, family studies suggest that GAD and panicdisorder are somewhat distinct. For example, rates of GAD are higher among relativesof individuals with GAD compared to relatives of individuals with panic disorder(Noyes et al., 1992; Weissman, 1990).B
IOLOGICAL CONSIDERATIONS
The neuroanatomy, neurochemistry, and endocrinology underlying normal fearprocesses have been studied extensively (see Meaney, LeDoux, & Liebowitz, 2008).Anxiety Disorders 319

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Normal fear and panic responses are often understood as part of a complex physicalsystem involving neural, endocrinological, circulatory, muscular, and behavioralsystems. This ﬁght-or- ﬂight system is designed to prevent or avoid physical danger
and harm, and involves a fast and efﬁ cient response. Perceptions of immediate danger
trigger a cascade of physical reactions that begin in the amygdala, which projects to thehypothalamus. The hypothalamus releases corticotropin-releasing factor (CRF),which triggers the pituitary to release adrenocorticotropic hormone (ACTH), whichin turn triggers the adrenal cortex to release hormones, including cortisol. Thesehormones play a central role in regulating the body ’s preparation for stress.
The hypothalamus also activates the sympathetic nervous system, resulting in a
variety of bodily changes including the release of glucose from the liver; increases inheart rate, breathing, and blood pressure; a pattern of vasodilation and vaso-constriction that increases blood ﬂow to the major muscles; and other changes
associated with preparation for the ﬁght-or- ﬂight response.
These physiological changes constitute the physical symptoms of panic attacks.
Numbing and tingling in the ﬁngers and toes and sensations in the stomach (nausea)
and bladder are sometimes experienced as less blood reaches these nonvital areas;shaking and trembling are by-products of the readiness of the major muscles toexpend energy; sweating is release of heat in preparation for physical exertion.
Fear appears to be a preparation for a full panic response and involves a similar,
though less dramatic, pro ﬁle of physiological changes and symptoms. Thus, although
we consider panic attacks and acute fear responses in the context of anxiety disordersto reﬂect pathology, the pathology does not appear to be due to the manner in which
the hypothalamic-pituitary-adrenal (HPA) axis system is carrying out its function.Rather, the pathology appears to be due to the inappropriate triggering of the HPAaxis, which typically works well to avoid physical danger and harm, even inindividuals with panic disorder, social anxiety disorder, and speciﬁ c phobias.
Consistent with this view, no abnormalities in the cardiovascular and vestibular
systems have been consistently established for panic disorder (Jacob, Furman,Durrant, & Turner, 1996; Kathol et al., 1980; Shear, Devereaux, Kranier-Fox, Mann,& Frances, 1984). Anxiety disorders in general do, however, appear to be associatedwith greater reactivity in the amygdala (see Britton & Rauch, 2009; Meaney et al.,2008). For example, compared to nonanxious controls, children with anxiety disordershave increased amygdala activity when viewing fearful versus neutral faces (Pineet al., 2005). There is evidence that hyperventilation in patients with panic disordermay lead to decreased blood ﬂow and changes in metabolism in and around the
hippocampus, but it is not clear whether these observations constitute differentialprocessing compared to nondisordered individuals (Uhde & Singareddy, 2002).Overall, researchers have not identi ﬁed neuroanatomical or neurochemical features
that are speci ﬁc to panic disorder, social anxiety disorder, or speci ﬁc phobias (see
Britton & Rauch, 2009).
Physiology of GAD is characterized by autonomic in ﬂexibility; chronic tension and
anxiety may lead to a restricted range of autonomic responses to environmentaltriggers (Thayer, Friedman, & Borkovec, 1996). GAD is associated with decreasedvagal tone (an index of parasympathetic activity) and heart rate (Lyon ﬁelds,
Borkovec, & Thayer, 1995; Thayer et al., 1996). Importantly, physiological variablesdiffer among individuals with GAD; only those high in baseline sympathetic arousal320 SPECIFIC DISORDERS

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displayed reduced sympathetic response to a lab stressor (Fisher, Granger, &Newman, 2010).
Autonomic in ﬂexibility has also been linked to panic disorder, and, thus, the
physiological pro ﬁle of GAD overlaps with other disorders (Hoehn-Saric, Schlund, &
Wong, 2004). Nonetheless, research suggests that the physiological pro ﬁle of GAD
is related to a physiological-inhibitory effect of worry, the primary feature of thedisorder. Relative to neutral thinking or relaxation, worrying prior to exposure to aphobic image is associated with decreased heart rate response during that subsequentimage (Borkovec & Hu, 1990; Borkovec et al., 1993). Moreover, compared to neutralthinking, experimentally induced worry is also associated with decreased vagal tone,heart rate, and heart rate variability among individuals with and without GAD(Thayer et al., 1996; Lyon ﬁelds et al., 1995). Worry is also associated with decreased
heart rate response during subsequent anxiety-eliciting tasks (increased heart rateduring exposure is a marker of emotional processing; Foa & Kozak, 1986) whileincreasing subjective distress (e.g., Borkovec & Hu, 1990).
Patterns of connectivity between the amygdala, the medial prefrontal cortices, and
other associated areas suggest the engagement of a compensatory, cognitive controlsystem among individuals with GAD (Etkin, Prater, Schatzberg, Menon, & Greicius,2009). Moreover, individuals with GAD fail to use the pregenual anterior cingulate todampen amygdala activity and regulate emotions during laboratory emotional con ﬂict
tasks (Etkin, Prater, Hoeft, Menon, & Schatzberg, 2010). Interestingly, the medialprefrontal and anterior cingulate regions are associated with worry both in individualswith GAD and in normal controls, but only individuals with GAD show persistentactivation in these areas following experimental worry periods (Paulesu et al., 2010).GAD is also associated with increased brain activity in response to both neutral andworry-related verbal statements, and reductions in that increased activity correspond toreductions in anxiety during treatment with citalopram (Hoehn-Saric et al., 2004).Lastly, compared to individuals without GAD, those with GAD show increasedgamma-band EEG activity in areas associated with negative emotion, as well asincreased subjective negative emotion while worrying (Oathes et al., 2008). Moreover,both of these were attenuated following treatment for generalized anxiety disorder.
The amygdala has also been implicated in GAD, but the ﬁndings are not entirely
clear. For example, individuals with GAD show increased activity in the amygdala inresponse to neutral and aversive pictures (relative to healthy controls; Nitschke et al.,2009). In response to fearful faces, however, individuals with GAD show decreasedamygdala activity (relative to individuals with social anxiety disorder and healthycontrols; Blair et al., 2008). Finally, the neurochemical underpinnings of GAD likelyinvolve abnormalities in several neurotransmitters, including gamma-aminobutyricacid (GABA), which is thought to mediate anxiety; norepinephrine (NE), a mediator ofthe sympathetic nervous system; and serotonin (5-HT), a target of ef ﬁcacious phar-
macologic treatment of GAD (Sinha, Mohlman, & Gorman, 2004).
Unlike other phobias, the BII subtype of speci ﬁc phobia involves a parasympathetic
response to feared stimuli. This response is distinct from fear responses in otherphobias in that there is decreased blood pressure and vasodilation that results inpooling of the blood in the extremities. Page (1994) has suggested that this subtype canbe further split into two distinct disorders, one that involves blood reactions, aparasympathetic response, and feelings of nausea and disgust; and another thatAnxiety Disorders 321

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has a similar physiological reaction to that of other speci ﬁc phobias and is character-
ized by fear of pain associated with needles and injury.S
PECIFIC GENES
Research on speci ﬁc genes that confer risk for panic disorder has led to con ﬂicting
ﬁndings (see Maron et al., 2008; Schmidt et al., 2000). Linkage and association studies
have examined several candidate genes known to be involved in the development ofthe brain structures associated with fear and fear learning. One gene (COMT) involvedin the inactivation of dopamine in the prefrontal cortex appears to be associated withpanic disorder (see Meaney et al., 2008). Also implicated are speci ﬁc alleles of the
serotonin transporter (5HTT) gene, which appear to play an important role in fearlearning (Risbrough & Geyer, 2008). For example, in individuals who are carriers ofparticular alleles of 5HTT, the nonspeci ﬁc experience of childhood maltreatment may
lead to high levels of anxiety sensitivity (Stein, Schork, & Gelernter, 2008), a risk factorfor panic disorder (see Personality and Temperament: Anxiety Sensitivity). Fewerinvestigations examined speci ﬁc genes that confer risk for social anxiety disorder and
speciﬁc phobias. The development of new gene technologies is quite likely to facilitate
the search for speci ﬁc genes and to clarify the ways in which genetic risk is conferred.
Although this work is in its early stages, research on speciﬁ c genes and gene-
environment interactions holds promise for elucidating the development of theseconditions and for informing approaches to prevention.
Some studies have found associations between speci ﬁc genes and GAD. For
example, variation in the monoamine oxidase A (MAOA) serotonin transporter genesmay confer increased risk for GAD. In one study, a polymorphism in the MAOA genewas associated with GAD but not with panic disorder or major depressive disorder,whereas a different MAOA polymorphism was associated with GAD, panic attacks,and possibly speciﬁ c phobia and agoraphobia (Tadic et al., 2003). Similarly, a variant
in the serotonin transporter linked polymorphic region (5-HTTLPR) is overrepre-sented among individuals with GAD compared to normal controls (You, Hu, Chen, &Zhang, 2005). However, another study failed to replicate this ﬁnding (Samochowiec
et al., 2004). Overall, speci ﬁc genetic polymorphisms may increase risk for GAD and
anxiety-related traits (e.g., neuroticism and anxiety sensitivity).P
ERSONALITY AND TEMPERAMENT
Anxiety Sensitivity Anxiety sensitivity is a dispositional trait that is characterized by
a fear of autonomic arousal and the physical sensations associated with anxiety states(e.g., increased heart rate, dizziness, nausea, shortness of breath; Reiss & McNally,1985; Reiss, Peterson, Gursky, & McNally, 1986). Anxiety sensitivity, sometimes calledthe fear of fear, is conceptualized as the key feature of panic disorder (McNally, 1990;Taylor, 1999). Several investigations have indicated that individuals with panicdisorder evidence high levels of anxiety sensitivity (e.g., Rapee, Brown, Antony, &Barlow, 1992), and individuals with panic disorder seem to have higher levels ofanxiety disorders than do individuals with other anxiety disorders (Taylor, Koch, &McNally, 1992). It is important to note, however, that anxiety sensitivity is not uniqueto panic disorder; it is also an important construct in PTSD (McNally, Luedke, Besyner,322 SPECIFIC DISORDERS

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Peterson, Bohm, & Lips, 1987), depression (Schmidt, Lerew, & Jackson, 1997), andother anxiety disorders (Taylor et al., 1992).
Anxiety sensitivity also seems to be especially elevated in agoraphobia (Reiss et al.,
1986). In a meta-analysis examining anxiety sensitivity across diagnostic groups,Olatunji and Wolitzky-Taylor (2009) concluded that anxiety sensitivity is substantiallyhigher among individuals with panic disorder, GAD, social anxiety disorder, andPTSD compared to nonclinical controls (see also Naragon-Gainey, 2010), and thatthis difference is greater among females compared to males. In terms of differencesbetween anxiety disorders, they found that (a) panic disorder was associated withgreater levels of anxiety sensitivity compared to all other anxiety disorders except forPTSD; (b) PTSD was associated with greater levels of anxiety sensitivity compared toGAD and social anxiety disorder; and (c) levels of anxiety sensitivity among the otheranxiety disorders (and mood disorders) generally did not differ from one another.
Evidence for anxiety sensitivity as a risk factor for the development of panic attacks
comes from work by Schmidt, Lerew, and Jackson (1997, 1999), who conducted aprospective longitudinal study of Air Force recruits before and after a stressful 5-weekcadet training program. Anxiety sensitivity before cadet training predicted frequencyof panic attacks during boot camp, even after controlling for previous panic symptomsand trait anxiety. Although more research is needed to better understand how anxietysensitivity develops and how it contributes to the development of panic disorder,anxiety sensitivity does seem to uniquely predict panic attacks and related symptoms(Maller & Reiss, 1992; Schmidt et al., 1997, 1999) as well as the development of anxietydisorders (Calkins et al., 2009; Maller & Reiss, 1992).Behavioral Inhibition and Shy Temperament Behavioral inhibition has been proposed
as an enduring tendency to respond to unfamiliar events with anxiety (Kagan,Reznick, & Snidman, 1987), and thus has obvious conceptual similarities to bothshyness and social anxiety. Beha vioral inhibition during the ﬁr s tf e wy e a r so fl i f e
predicts inhibited behavior with peers la ter in childhood (Aksan & Kochanska, 2004)
and social anxiety disorder in adolescence (Chronis-Tuscan et al., 2009; Hayward,Killen, Kraemer, & Taylor, 1998; Schwartz, Snidman, & Kagan, 1999) and adulthood(Kagan & Snidman, 1999).
The relative stability of socially inhibited behavior from the ﬁrst years of life until
adulthood is consistent with the view of social anxiety disorder as rooted in relativelyunchangeable, biologically based behavioral tendencies (i.e., temperament). It isnotable, however, that a substantial number of children classi ﬁed as having behavioral
inhibition do not go on to develop social anxiety disorder (Hayward et al., 1998;Kagan & Snidman, 1999; Schwartz et al., 1999; Wittchen, Stein, & Kessler, 1999).Studies of behavioral inhibition might also provide a means for understanding howparental variables contribute to the development of social anxiety disorder (Moehleret al., 2007) and how chronic inhibition in social behavior may develop through adynamic interplay between child characteristics and parenting.B
EHAVIORAL CONSIDERATIONS
Classical Conditioning Drawing upon the observation that fears can be acquired
through a repeated process of paired learning, early behaviorists proposed thatAnxiety Disorders 323

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phobias are acquired through classical conditioning (Mowrer, 1947). An early andfamous demonstration of this approach involves the story of Little Albert, a 4-year-oldboy who was conditioned to fear white rabbits after only a few conditioning trials(Watson & Rayner, 1920). Following this line of reasoning, a single conditioning trialwith a suf ﬁciently severe unconditioned stimulus could result in learned fear.
Although classical conditioning of fear represents one way that fear can be acquired,it does not account for the fact that most individuals with speci ﬁc phobias have not
experienced such events. Inconsistent with the classical conditioning model, manyindividuals with no prior experience with the feared object or situation meet thecriteria for speci ﬁc phobia, and many individuals with seemingly traumatic condi-
tioning experiences do not develop phobias (Rachman, 1989). Nevertheless, the viewof speci ﬁc phobias as a learned association has persisted and is consistent with views
of exposure therapy as extinction.
Conditioning has also been applied to understanding the development of panic
disorder. These efforts have sometimes been criticized as tautological because panicand anxiety are considered to be responses that become conditioned, but the con-ditioned stimuli are interoceptive symptoms associated with panic and anxiety (e.g.,McNally, 1990). Bouton, Mineka, and Barlow (2001), however, point out that thetautology is resolved because panic and anxiety are distinct: Panic becomes condi-tioned to the symptoms of anxiety. Panic attacks in the context of panic disorder can beviewed as a highly generalized fear response, one in which one interoceptive stimulus(e.g., accelerated heart rate) may be suf ﬁcient to trigger an acute fear reaction even in
the absence of any speciﬁ c external stimulus.
Operant Conditioning Mowrer (1947) proposed that whereas fear is acquired via
classical conditioning, it is maintained via operant conditioning. Speci ﬁcally, he
posited that the avoidance and escape behaviors that accompany phobic fear aremaintained through a process of negative reinforcement in that they remove orprevent negative affective states. This position has become very in ﬂuential in treat-
ment models for anxiety disorders, providing a compelling rationale for the reductionor elimination of avoidance and safety behaviors in panic disorder, social anxietydisorder, and speci ﬁc phobias (e.g., Bennet-Levy et al., 2004). Escape and avoidance
behaviors are thought to maintain fear either through their prevention of fearactivation (which is theorized to be a necessary precursor to habituation; Foa &Kozak, 1986) or through their prevention of discon ﬁrmation of erroneous threat
beliefs. In addition to escape from and avoidance of feared situations, subtle in-situation avoidance behaviors (also known as safety behaviors) have been identi ﬁed as
an important feature of these disorders (Helbig-Lang & Petermann, 2010). Operantbehaviors are widely recognized as involved in the maintenance of anxiety disorders,but they are not usually seen as playing a substantial role in the early development ofpanic disorder, social anxiety disorder, or speci ﬁc phobia.
Current theoretical conceptualizations of GAD posit that worry is in itself a type of
avoidant response. Worry is predominantly a verbal-linguistic (as opposed to imag-ery-based) activity (Borkovec & Inz, 1990), and this predominance of verbal activityinhibits the somatic reactivity (Vrana, Cuthbert, & Lang, 1986) that is necessary foremotional processing of fear cues (Foa & Kozak, 1986). Although this inhibition ofsomatic activation reduces undesired distress in the short term, it prevents the324 SPECIFIC DISORDERS

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emotional processing of fear that is theoretically necessary for successful habituationand extinction to eventually take place (Foa & Kozak, 1986). The avoidance theory ofworry (Borkovec, Alcaine, & Behar, 2004) thus argues that worry is an ineffectivecognitive strategy that is maladaptively used to reduce threat that exists in the form ofsomatic, physiological fear.Vicarious Conditioning In addition to classical conditi oning, vicarious conditioning
(sometimes called observational learning or learning by modeling) is now widelyrecognized as a means for developing a learned association, functionally equivalentto learning by classical conditioning. Acquisition of fear by vicarious conditioning iswell-illustrated in a study by Cook and Mineka (1990). In that study, lab-rearedmonkeys who had never seen a snake we re shown a videotape of wild-reared
monkeys displaying fear of live and toy snakes. This vicarious conditioningexperience was suf ﬁcient for the lab-reared monkeys to acquire a fear of snakes.
Such processes are widely accepted to be relevant to human learning processes(Mineka & Zinbarg, 2006).
Vicarious conditioning may interact with temperament to predict the development
of social anxiety disorder (Rapee & Spence, 2004). For example, de Rosnay, Cooper,Tsigaras, and Murray (2006) trained mothers to act in shy and nonshy manners withstrangers. Their 12- to 14 month-old infants acted shyly in subsequent encounters withstrangers following shy modeling (demonstrating vicarious learning), and this effectwas particularly pronounced for those infants with an inhibited temperament.Informational Acquisition Rachman (1977) suggested that phobias might be acquired
in three ways: (1) classical conditioning, (2) vicarious conditioning, and (3) informa-tional acquisition. Information acquisition involves the development of a fear as aresult of receiving information, such as from a parent or doctor. Both vicariousand informational learning has also been documented for social anxiety disorder(Mulkins & Bögels, 1999). For example, Barrett, Rapee, Dadds, and Ryan (1996) foundthat when presented with threatening scenarios, children with anxiety disorders andtheir parents independently chose avoidant responses and that children ’s selection of
avoidant responses increased after they interacted with their parents; such a patternwas not apparent among aggressive children. This familial enhancement of avoidantresponding in children with anxiety disorders is consistent with informationalacquisition. The three-pathways model proposed by Rachman (1977) has also beenapplied to understand the retrospective accounts of the onset of many types of speci ﬁc
phobias (King, Eleonora, & Ollendick, 1998).Preparedness Theory One observation that challenges the behavioral view of phobias
as learned associations is that common fears are not randomly distributed but aremore frequently associated with stimuli that are objectively evolutionarily dangerous.To account for this observation, Seligman (1971) proposed the “preparedness theory, ”
which posits that during the Paleolithic period of the evolution of the human species,survival and reproductive ﬁtness were increased by fear and avoidance of objects and
situations that were dangerous. Drawing upon preparedness theory, Mineka andÖhman (2001, 2002) proposed that humans are prepared to fear stimuli that arerelevant to survival because we have evolved a module for fear learning that isAnxiety Disorders 325

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encapsulated and relatively independent of cognitive processing. This view proposesthat fears of survival-relevant stimuli are relatively automatic and involve centralbrain regions. There is evidence for several aspects of this model (see Mineka &Öhman, 2001; Mineka & Zinbarg, 2006), including evidence of slower extinction tosurvival-relevant stimuli and limited penetrability to conscious cognitive control forfear of stimuli that are relevant to survival (Öhman & Soares, 1998).
Work by Cook and Mineka (1990, 1991, discussed earlier) illustrates preparedness
to acquire fear of stimuli relevant to survival. Although lab-reared monkeys who hadnever seen a snake quickly acquired fear when presented with a videotape model,illustrating vicarious learning, no such learning took place when they were presentedwith a videotape model of a monkey displaying fear of stimuli that are irrelevant tosurvival, such as ﬂowers and toy rabbits. Also, this preferential conditioning did not
occur with learning of other responses (e.g., appetitive). Although such enhanced fearconditioning to evolutionarily dangerous stimuli has been displayed in monkeys,applicability of preferential conditioning in humans is somewhat less well-established(see Mineka & Zinbarg, 2006).
Another observation that is consistent with preparedness theory is the distribution
of age of onset as a function of different types of speci ﬁc phobia (Öst, 1987). Animal
phobias tend to develop early (mean age of onset of 7 years of age), during an agewhen animals present the greatest objective threat. In contrast, claustrophobia tends todevelop much later (mean age of onset of 20 years of age), during an age when takingrefuge in an enclosed hiding place may be less advantageous.
Related to preparedness theory, an evolutionary view of blood reactions has also
been proposed (Thyer, Himle, & Curtis, 1985). Fainting appears to be an adaptiveresponse to injury, because decreased blood pressure and raising the wound siterelative to the heart reduces and slows blood loss. The high heritability of bloodreactions might help explain the higher and relatively more speci ﬁc heritability of the
BII subtype of speci ﬁc phobia (see Merckelbach & de Jong, 1997).
Disgust has been implicated as a distinct emotional state that is involved in many
anxiety disorders (Woody & Teachman, 2000). For example, animal phobias can bedifferentiated into those that involve contamination threat and disgust reactions (e.g.,fear of rats) and those that involve predators and do not include disgust reactions (e.g.,fear of dogs; Matchett & Davey, 1991). Disgust also appears to be relevant to otherspeciﬁc phobias (e.g., BII phobias), to obsessive-compulsive washers, and perhaps to
social anxiety disorder in the form of self-disgust (Amir, Najmi, Bomyea, & Burns,2010). The role of disgust in these anxiety disorders appears to re ﬂect an avoidance of
disease that is also evolutionarily advantageous (Matchett & Davey, 1991; Woody &Teachman, 2000).C
OGNITIVE CONSIDERATIONS
Cognitive biases have often been noted in individuals diagnosed with panic disorder,GAD, social anxiety disorder, and speciﬁ c phobias. These phenomena are usually
described using an information-processing framework (Lang, 1979) for understandingpathological fear (Foa & Kozak, 1986; Rachman, 1980). Studies of these biases can bedivided into those that focus on content (e.g., beliefs, expectancies, appraisals) andthose that focus on process (e.g., attention, interpretation, memory). A key task in326 SPECIFIC DISORDERS

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evaluating cognitive approaches to understanding the etiology of these disorders is toidentify which biases play a causal role and which are simply features or by-productsof the disorders.Situation-Speci ﬁc Cognitions and Related Variables Approaches to understanding
cognitive biases can be further divided into those that emphasize relatively endur-ing individual difference factors and situation-speci ﬁc cognitions. Individual dif-
ference factors include anxiety sensitivity, which can be viewed as a tendency toengage in the situation-speci ﬁc cognitions that cause panic attacks in the context of
panic disorder (McNally, 1990). In addition, individual difference factors includecore beliefs, which can be viewed as the laten t variables that interact with situational
variables to produce the automatic cognit ions that are the proximal determinants of
fear, anxiety, and avoidance behavior (Beck & Emery, 2005). The individual differ-ence variable of fear of negative evaluation (Leary, 1983b), which can be viewed asthe tendency to overestimate the likelihood and importance of being negativelyevaluated when in a social situation, has b ecome the axiomatic dimension associated
with social anxi ety disorder.
Regarding situation-speci ﬁc cognitions, panic disorder, GAD, social anxiety dis-
order, and speci ﬁc phobias have been characterized by overestimations of fear and
danger. Evolutionarily, underestimation of fear and danger could be very costly toindividuals, whereas overestimation of fear and danger were advantageous. Examiningsituation-speci ﬁc cognitions under a variety of names (including expectancies, con-
cerns, automatic thoughts, catastrophic thoughts, and catastrophic misinterpretations),researchers have generally found that situation-speci ﬁc cognitions are predictors of
fear, anxiety, and avoidance behavior. For example, expectancies appear to be proximalcognitive determinants of fear and fear behavior (e.g., Valentiner, Telch, Petruzzi, &Bolte, 1996). The types of expectancies and concerns that are most important arebelieved to vary across different types of fear stimuli: Acrophobia is believed to involveexpectances of falling (Menzies & Clarke, 1995), whereas claustrophobia is believed toinvolve expectancies of suffocation and entrapment (Radomsky, Rachman, Thordarson,McIsaac, & Teachman, 2001; Valentiner et al., 1996). Panic attacks in the context of panicdisorder are believed to involve misinterpretation of bodily sensations, resulting incatastrophic thoughts related to heart dysfunction, suffocation, and mental control(Cox, 1996).
Another situation-speci ﬁc cognitive variable that has been implicated for these
disorders is self-ef ﬁcacy, which is conceptualized as a higher-order cognitive process
that incorporates lower-order cognitions, including estimates of one ’s coping capaci-
ties in addition to expectancies of anxiety and expectancies of danger (Bandura &Adams, 1977). Although there are methodological concerns about how the self-efﬁcacy construct is typically operationalized, there is some evidence for self-ef ﬁcacy
as a unique predictor of fear and fear behavior for panic disorder (Cho, Smits,Powers, & Telch, 2007) and speci ﬁc phobias (Valentiner et al., 1996). Furthermore,
individuals with GAD overestimate the likelihood of negative future events andunderestimate their ability to cope with negative outcomes should they occur(Borkovec, Hazlett-Stevens, & Diaz, 1999).
Situation-speci ﬁc cognitions and individual differences in the tendency to engage
in situation-speci ﬁc cognitions have proven to be useful to understanding panicAnxiety Disorders 327

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disorder, GAD, social anxiety disorder, and speci ﬁc phobias. These content variables
predict changes in functioning over time and during treatment (e.g., Hoffman, 2004;Wilson & Rapee, 2005), and manipulations that target these cognitions appear toimprove the ability of behavioral treatment techniques in reducing symptoms of panicdisorder (e.g., Murphy, Michelson, Marchione, Marchione, & Testa, 1998), socialanxiety disorder (e.g., Kim, 2005), GAD (Borkovec, Newman, Pincus, & Lytle,2002), and speciﬁ c phobias (e.g., Kamphuis & Telch, 2000).
Attentional Biases and Related Cognitive Processes Regarding studies of cognitive biases
that focus on process, a good deal of research has examined attentional processes (Bar-Haim, Lamy, Pergamin, Bakermans-Kranenburg, & van IJzendoorn, 2007). Anxietyhas been found to be associated with biases in various attentional processes, namelyorienting, engagement, and disengagement (see Ouimet, Gawronski, & Dozois, 2009).In addition, attentional biases have been found, using a variety of tasks, to occur in allanxiety disorders (see Cisler & Koster, 2010), including panic disorder (e.g., Buckley,Blanchard, & Hickling, 2002), social anxiety disorder (e.g., Amir, Elias, Klumpp, &Przeworski, 2003), GAD (e.g., Bradley, Mogg, White, Groom, & de Bono, 1999) andspeciﬁc phobias (e.g., Watts, McKenna, Sharrock, & Trezise, 1986).
Some researchers (Bögels & Mansell, 2004), however, have viewed the evidence for
attentional biases in social anxiety disorder as somewhat mixed. In addition, theremay be differences in attentional biases as a function of social anxiety disordersubtype. McNeil et al. (1995) found evidence for cognitive interference (using theemotional Stoop task) on general social words and speech-speci ﬁc words for the
generalized subtypes of social anxiety disorder, but only for speech-speci ﬁc words for
the nongeneralized subtype.
The overall picture that emerges is one in which attentional biases are strongly
implicated in anxiety disorders, including panic disorder, GAD, social anxietydisorder, and speci ﬁc phobias (Bar-Haim et al., 2007; Ouimet et al., 2009). The
attentional bias appears to be content-speciﬁ c, with, for example, spider phobics
showing attentional biases to spiders (Watts et al., 1986). The pattern that emergesinvolves an attentional bias toward threatening stimuli evident early in the attentionalprocess, followed by dif ﬁculty disengaging from threatening stimuli, and then later
avoidance of threatening stimuli (Cisler & Koster, 2010). In addition, retraining ofattentional bias appears to reduce fear and avoidance (Amir, Weber, Beard, Bomyea, &Taylor, 2008; Bar-Haim, 2010). This emerging approach is attractive because relativelybrief interventions that modify attention biases may undermine the development ormaintenance of anxiety conditions. Thus, attention bias modi ﬁcation might be deliv-
ered as an adjunct to enhance exposure-based treatments or as stand-alone approachesfor prevention in high-risk populations (Bar-Haim, 2010).
A variety of other cognitive process variables have been proposed as being
involved in the development and maintenance of these disorders. For example,interpretation biases have been demonstrated for panic disorder (Westling & Öst,1995) and social anxiety disorder (Amir, Foa, & Coles, 1998). Implicit memory bias hasbeen found in panic disorder (Amir, McNally, Riemann, & Clements, 1996). Evidencefor a memory bias in social anxiety disorder is weak, although some authors suggestthat such a bias might only be evident in the context of an imminent social threat(Hirsch & Clark, 2004).328 SPECIFIC DISORDERS

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One cognitive process that has been shown to play a role in social anxiety disorder
is postevent processing (cf. rumination), repetitive self-focused thought in which one’ s
social performance is reconstructed and distorted to be consistent with the pathologi-cal beliefs underlying social anxiety (see Brozovich & Heimberg, 2008). Similarprocesses may be involved in the development of panic disorder and speci ﬁc phobias,
as Davey and Matchett (1994) have demonstrated that mental rehearsal of a con-ditioning trial can enhance conditioned fears.Self-Focused Attention A cognitive process variable that appears to be particularly
relevant to social anxiety is that of self-focused attention, or the tendency for sociallyanxious individuals to attend to internal stimuli rather than external, social stimuli.These internal stimuli are believed to include both interoceptive sensations (e.g.,racing heart) and negative images of the self and behavior. Consistent with the socialanxiety disorder model proposed by Clark and Wells (1995; see also Clark, 2001), self-focused attention when in social situations appears to be an important cognitivefeature of the disorder, as well as an important factor in the maintenance of socialanxiety (Bögels & Mansell, 2004), leading to an increased awareness of anxietyresponses (Alden & Mellings, 2004) and a disruption of the realistic processing ofthe situation and other people ’s behaviors (Bögels & Lamers, 2002). Targeting self-
focused attention appears to improve outcomes during exposure-based treatment forsocial anxiety disorder (Wells & Papageorgiou, 1998).C
ULTURE ,SOCIALIZATION ,AND THE SOCIAL ENVIRONMENT
Messages that parents give to their children about the meaning and importance oftheir interoceptive sensations, through parental reinforcement of illness behavior, mayplay a role in the development of panic attacks and panic disorder. A retrospectivestudy by Stewart et al. (2001) provides evidence that childhood learning experienceswith respect to arousing-reactive symptoms (e.g., racing heart, shortness of breath,etc.) but not arousing-nonreactive symptoms (e.g., colds, aches, rashes, etc.) contrib-uted to the frequency and intensity of panic attacks. This effect appeared to be partiallymediated by anxiety sensitivity.
Compared to control participants, individuals with GAD report a history of
rejection and neglect from their mothers, along with more frequent role-reversed/enmeshed relationships (in which the child must take care of the mother), as well ascurrent feelings of vulnerability toward their mothers (Cassidy, Lichtenstein-Phelps,Sibrava, Thomas, & Borkovec, 2009).
Social factors also appear to play an important role in the development and course
of social anxiety disorder. For example, poorer social relationships have been observedin shy children (Gazelle & Ladd, 2003; Rubin, Wojslawowicz, Rose-Krasnor, Booth-LaForce, & Burgess, 2006) and among children (Alden & Taylor, 2004) and adults(Lampe, Slade, Issakidis, & Andrews, 2003; Whisman, Sheldon, & Goering, 2000)diagnosed with social anxiety disorder. The social de ﬁcits associated with social
anxiety disorder and shyness include peer neglect (Gazelle & Ladd, 2003), fewerpositive responses (Spence, Donovan, & Brechman-Toussaint, 2000), and peer victim-ization (Hawker & Boulton, 2000; La Greca & Harrison, 2005; McCabe, Antony,Summerfeldt, Liss, & Swinson, 2003; Siegel, La Greca, & Harrison, 2009; Storch &Anxiety Disorders 329

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Masia-Warner, 2004). Social de ﬁcits, such as peer rejection, appear to be mediated by
poor social skills (Greco & Morris, 2005), although individuals with social anxietydisorder do not always show poor social skills (e.g., Beidel, Turner, & Jacob, 1989). Itshould also be noted that peer victimization may be both a cause (Bond, Carlin,Thomas, Rubin, & Patton, 2001) and a consequence of social anxiety, as social anxietypredicts subsequent victimization (Siegel et al., 2009).
In a study by Daniels and Plomin (1985), mothers ’sociability was signi ﬁcantly
associated with the shyness of their adopted infants, and genetic in ﬂuences were ruled
out given that the infants in the study had been adopted. In addition, the effect wasstill evident after controlling for maternal shyness, largely ruling out modeling orsocial learning interpretations.
Culture may also play a role in the expression of panic disorder and other anxiety
conditions. Ataque de nervios is an acute set of symptoms and behaviors that shares some
similarities with a panic attack, although typically experienced in response to a stressfulfamily event and incorporating a volitional behavior component (APA, 2000). It is notclear whether this and other culture-speci ﬁc anxiety conditions represent an inappli-
cability of our nosological system to Latin American and Caribbean cultures, a culture-speciﬁc expression of known anxiety disorders such as panic disorder, or something else
(Guarnaccia, Lewis-Fernández, & Marano, 2003). In addition, the de ﬁnitional require-
ment that panic attacks reach a peak within 10 minutes and the duration of panic attacksmay vary as a function of culture (Lewis-Fernández et al., 2010).
Cultural factors likely play a role in the development of social anxiety as well.
For example, culture-speciﬁ c norms appear to impact the acceptability of socially
inhibited behavior and affect the expression of social anxiety (Heinrichs et al., 2006).In addition, culture likely affects the expression of social anxiety. As discussed earlier,Taijin Kyofusho has been viewed as a culturally bound syndrome thought to appearonly in Japan and Korea (APA, 2000; cf. anthropophobia, WHO, 1992). More infor-mation about the likely role of cultural attitudes, beliefs, norms, and practices on thedevelopment and expression of social anxiety is needed.L
IFEEVENTS
Stress, including life events and chronic conditions such as maltreatment duringchildhood, appears to increase risk for a variety of mental disorders, including anxietydisorders (Allen, Rapee, & Sandberg, 2008; Kessler, Davis, & Kendler, 1997; Phillips,Hammen, Brennan, Najman, & Bor, 2005). Past traumatic events may contribute tofeelings of anxious apprehension and the perception that the world is a dangerousplace (Borkovec, Alcaine, & Behar, 2004). Stressful events also impact the maintenanceand course of panic disorder (Craske, Rapee, & Barlow, 1988), agoraphobia (Rachman,1984), GAD (Roemer, Molina, Litz, & Borkovec, 1997), social anxiety disorder(Mineka & Zinbarg, 1996), and speci ﬁc phobias (Craske, 1991).
Individuals with GAD are more likely to h ave experienced the death of a parent
before the age of 16 compared to individu als with panic disorder and controls
(Torgersen, 1986). Furthermore, life events that contribute to GAD may differ fromthose that contribute to depression; eve nts characterized by loss and danger may
convey speci ﬁc vulnerability to noncomorbid GAD, whereas loss and humiliation
m a yb em o r es p e c i ﬁc to major depressive disorder (Kendler, Hettema, Butera,330 S
PECIFIC DISORDERS

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Gardner, & Prescott, 2003). A 32-year longi tudinal study found several risk factors
associated with GAD but not with major depressive disorder, including lowsocioeconomic status, maternal internal izing symptoms, maltreatment, inhibited
temperament, internalizing and conduct problems, and negative emotionality(Mofﬁtt et al., 2007).
Consistent with a conditioning model, individuals with social anxiety disorder
retrospectively report greater incidence of traumatic social events than do healthycontrols, and this greater incidence appears to be higher for those with the non-generalized subtype compared to the generalized subtype (Stemberger, Turner,Beidel, & Calhoun, 1995).
Early studies suggest that onset of panic di s o r d e r ,G A D ,s o c i a la n x i e t yd i s o r d e r ,
and speci ﬁc phobias are sometimes triggered b y the occurrence of a stressful life
event. This phenomenon may re ﬂect fear in ﬂation (Mineka & Zinbarg, 1996;
Rescorla, 1974), which takes place when a person or animal undergoes conditioningof mild fear, such as through cl assical conditioning, and then experiences an intense,
unpaired exposure to the unconditioned st imulus, so that the previously mild fear
increases in strength. More recent evidence has found no greater rates of stressful lifeevents prior to anxiety disorder onset than at other times (Calkins et al., 2009).
The phenomenon of latent inhibition, in which prior benign (nonfearful) exposure
to a stimulus inhibits fear acquisition, is a well-established ﬁnding in the animal
literature that informs how we think about fear learning in humans (see Mineka &Zinbarg, 2006). Prior exposure also reduces generalization of fear (Vervliet, Kindt,Vansteenwegen, & Hermans, 2010), an observation that may be especially relevant tothe development of panic disorder, which is sometimes viewed as involving highlygeneralized fear responses (Gorman et al., 2001). Related to these ideas, positivecontrol experiences early in life appear to provide protection against fear conditioningand the development of anxiety disorders (see Chorpita & Barlow, 1998).
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CHAPTER 9
Obsessive-Compulsive and
Related Disorders
SANDRA M. NEER and KATIE A. RAGSDALE
OBSESSIVE -COMPULSIVE AND RELATED DISORDERS is a new category in the ﬁfth edition
of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5 ; American
Psychiatric Association [APA], 2013) and includes obsessive-compulsive
disorder (OCD), body dysmorphic disorder (BDD), hoarding disorder (HD), tricho-tillomania (TTM), and excoriation (skin-picking) disorder (ED). The new DSM-5
category includes disorders previously categorized elsewhere within the DSM-IV-
TR(APA, 2000) (e.g., anxiety disorders [OCD], somatoform disorders [BDD], and
impulse-control disorders not elsewhere classi ﬁed [TTM]), as well as two new
diagnoses (HD and ED). The disorders were reclassi ﬁed within this new category
to reﬂ ect their diagnostic and clinical relatedness (APA, 2013).
Diagnostically, OCD is characterized by obsessions and/or compulsions that
consume more than 1 hour per day or cause clinically signi ﬁcant distress or impair-
ment (APA, 2013). Obsessions include recurrent and persistent thoughts, urges, orimages (e.g., thoughts of contamination or urges to kill someone) of an intrusive orunwanted nature, which individuals attempt to suppress, ignore, or neutralize (e.g.,by performing a compulsion). Compulsions are repetitive behaviors or mental acts(e.g., counting or washing) individuals engage in to prevent or reduce anxiety ordistress. Compulsions do not need to be logically connected to the obsessions they areattempting to neutralize, although they often are.
BDD is de ﬁned by a preoccupation with perceived physical defects or ﬂaws that, at
some point during the course of the disorder, result in repetitive behaviors (e.g., mirrorchecking) or mental acts (e.g., appearance comparisons) (APA, 2013). Preoccupationcan occur with any part of the body (e.g., hair, face shape, or nose) but is mostcommonly associated with the skin (e.g., wrinkles or scars). Although the perceiveddefects or ﬂaws cause clinically signi ﬁcant distress or impairment to the individual,
they appear minor or unrecognizable to others. Individuals who are preoccupied withbody build, believing that the body is too small or insuf ﬁciently muscular, would meet
criteria for the speci ﬁcation of BDD with muscle dysmorphia. Additionally, clinicians
can specify whether an individual ’s level of insight is good, fair, poor, or absent. In a
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case where an individual is completely convinced of their defect, absent insight/delusional beliefs may be speci ﬁed.
HD, a new diagnosis of the DSM-5 ,r eﬂects persistent dif ﬁculty parting with
possessions to the point that it causes clinically signi ﬁcant distress or impairment
(APA, 2013). Dif ﬁculty discarding an item is unrelated to the item ’s actual value;
rather, it is related to both the distress associated with discarding the item and aperceived need to save it. As a result, accumulation of possessions causes congestionand clutter in living areas, which substantially compromises their intended uses. Inaddition, individuals who excessively acquire additional possessions which are notneeded or for which there is no room would meet criteria for the speci ﬁcation of HD
with excessive acquisition.
TTM (hair-pulling disorder) is de ﬁned by recurrent hair pulling that results in hair
loss. Although hair pulling typically results in visible hair loss, individuals whowidely pull hair from various body regions may not evidence this clinical marker(APA, 2013). The scalp, eyelids, and eyebrows are the most common sites; however,hair pulling may occur at any region of the body where hair grows. In addition to hairpulling, individuals suffering from TTM repeatedly attempt to decrease or stop hairpulling, and endorse signi ﬁcant associated distress or impairment.
ED (skin picking), also a new disorder to the DSM-5 , is characterized by recurrent
skin picking which results in skin lesions (APA, 2013). Skin picking commonly occurson the face, arms, and hands; however, individuals may pick various body regions(APA, 2013). Although individuals typically use ﬁngernails to pick, other objects (e.g.,
tweezers) and techniques (e.g., squeezing or rubbing) may be used. Individuals maypick at a variety of sites including healthy skin, scabs, or skin irregularities, andrepeatedly attempt to decrease or stop skin picking. As with all other psychiatricdisorders, individuals must experience clinically signi ﬁcant distress or impairment to
meet diagnostic criteria.C
LINICAL FEATURES
OCD is a clinically heterogeneous disorder with various presentations of obsessionsand/or compulsions. Although individuals do not need to endorse both obsessionsand compulsions to meet diagnostic criteria (APA, 2013), 96% of outpatients withOCD report experiencing both, whereas 2% endorse predominant obsessions and 2%report predominant compulsions (Foa & Kozak, 1995). Among this large sample ofindividuals from the DSM-IV ﬁeld trials, the most common obsession reported was
contamination (37.8%), followed by fear of harming self or others (23.6%) andsymmetry (10%). The most common compulsions reported were checking (28.2%)and cleaning/washing (26.6%). Other obsessions included somatic, religious, andsexual obsessions, whereas other compulsions included repeating, mental rituals,ordering, and counting.
A meta-analysis of factor analytic studies of OCD symptom categories revealed
four factors, which explained nearly 80% of the variance in 17 studies of adults withOCD (Bloch, Landeros-Weisenberger, Rosario, Pittenger, & Leckman, 2008). The fourfactors included symmetry (symmetry obsessions and repeating, counting, and order-ing compulsions), cleaning (contamination obsessions and cleaning compulsions),forbidden thoughts (aggressive, religious, and sexual obsessions), and hoarding356 SPECIFIC DISORDERS

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(hoarding obsessions and compulsions) .O f t e n ,o b s e s s i o n sa n dc o m p u l s i o n sa r e
functionally related (e.g., contaminati on fears accompanied by cleaning rituals or
self-doubt and dread accompanied by rep etitive checking; Turner & Beidel, 1988).
For instance, strong associations exist between some similar obsessions and com-pulsions (e.g., contamination obsessions a nd cleaning compulsions), whereas others
are less speci ﬁc (e.g., checking compulsions are related to a variety of obsessions)
(Bloch et al., 2008).
OCD is a debilitating disorder with signi ﬁcant functional impairment and
reduced quality of life (Norberg, Calam ari, Cohen, & Riemann, 2008). In fact, a
recent review found that quality of life in OCD is signi ﬁcantly lower than quality of
life in community controls and individua ls with other psychiatric and medical
disorders (Macy et al., 2013). Unfortunately, despite the associated impairment anddistress, few individuals with the disorder initiate treatment (Levy, McLean,Yadin, & Foa, 2013).
Clinically, BDD is marked by preoccupation with physical appearance that
results in repetitive behavioral or mental a cts. On average, preoccupation is focused
onﬁve to seven areas of the body (Phillips, Menard, Fay, & Weisberg, 2005).
Although the clinical presentation in men a nd women is more similar than different,
implicated body regions differ signi ﬁcantly (Phillips, Mena rd, & Fay, 2006). Men are
more likely to be preoccupied with body build, genitals, and hair thinning orbalding, whereas women are more likely to be preoccupied with a wider variety ofb o d ya r e a s( i . e . ,s k i n ,s t o m a c h ,w e i g h t ,b r e a s t s ,b u t t o c k s ,t h i g h s ,l e g s ,h i p s ,t o e s ,a n dexcessive body or facial hair). Repetitive or safety behaviors in response to bodypreoccupation may include co mparison to others, camou ﬂaging (i.e., using body
posture or position, clothes, and makeup, among others, to hide the perceiveddefect), mirror checking, grooming, reassurance seeking, dieting, and tanning(Phillips et al., 2005).
Individuals with BDD endorse high rates of both suicidal ideation and suicide
attempts due to appearance concerns (Rief, Buhlmann, Wilhelm, Borkenhagen, &Brähler, 2006). For instance, in a sample of 200 individuals with BDD, 81.3% of treatedsubjects and 71.2% of untreated subjects endorsed suicidal ideation, and over a quarterof all subjects had attempted suicide (Phillips et al., 2005). Further, individuals withthe disorder are more likely to be divorced, unmarried, unemployed, and have lowerincomes than individuals without the disorder (Rief et al., 2006) and may be house-bound, miss work and school, drop out of school, and receive disability (Phillips et al.,2005). Despite the associated distress and impairment, few individuals with BDDdisclose their body image concerns to clinicians, most often due to feelings ofembarrassment or fears of being negatively evaluated (Conroy et al., 2008). Instead,many individuals with the disorder receive nonpsychiatric treatment (i.e., dermatol-ogy and cosmetic surgery) (Phillips et al., 2005).
The typical clinical presentation of HD involves an individual who has signi ﬁcant
difﬁculty parting with possessions and associated distress and impairment. Over two-
thirds of individuals with the disorder may also exhibit excessive acquisition of items,which has been found to be a clinical predictor of distress and/or impairment(Timpano et al., 2011). Individuals with the disorder most frequently accumulateitems through purchase (64.4%) and obtaining free things (53.4%); however, asubsample of those who engage in excessive acquisition may also steal (25.3%).Obsessive-Compulsive and Related Disorders 357

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Clinically signi ﬁcant hoarding may lead to work impairment, eviction from the home,
and/or removal of others from the home, and is a signi ﬁcant public health burden
(Tolin, Frost, Steketee, Gray, & Fitch, 2008).
The hallmark symptom of TTM is clinically signi ﬁcant hair pulling. Individuals
usually pull hair from multiple sites, most frequently being the scalp, followedby eyelashes, eyebrows, and pubic hair (Flessner, Woods, Franklin, Keuthen, &Piacentini, 2009). Although it is not necessary for diagnosis, many adults with thedisorder report an urge, need, or drive to pull hair, as well as a sense of grati ﬁcation or
relief during or after pulling (Lochner et al., 2012). Most individuals pull out singlehairs (68%); however, some may pull out clumps (5%), or a combination of single hairsand clumps (27%) (Christenson, MacKenzie, & Mitchell, 1991). Additionally, indi-viduals may target speci ﬁc types of hair based on thickness, texture, or color and may
manipulate hair after it is pulled (e.g., suck on hairs or scrape off roots) (Walsh &McDougle, 2001). Finally, individuals with TTM may express associated negativeaffective states, including feeling unattractive (87%), secretiveness (83%), shame (75%),irritability (71%), low self-esteem (77%), and depressed mood (81%) (Stemberger,Thomas, Mansueto, & Carter, 2000).
ED describes clinically signi ﬁcant picking of the skin that results in skin lesions. An
examination of 60 individuals with pathologic skin picking suggests that the disorderis time-consuming and associated with various complications (Odlaug & Grant, 2008).Results of this study also suggest that individuals often begin picking in response totriggers, such as feel (55%) or sight (26.7%) of the skin, boredom/downtime (25%), andstress (20%). The face and head (60%) are the most common sights for picking,followed by the legs and feet (33.3%), arms (30%), torso (23.3%), and hands and ﬁngers
(21.7%). Most individuals (68.8%) pick from multiple sites of the body, often switchingareas in order for other sites to heal. In fact, 35% of this sample experienced infectionsrequiring antibiotics as a result of skin picking.D
IAGNOSTIC CONSIDERATIONS
The National Comorbidity Survey Replication (NCS-R; Kessler et al., 2004) found that90% of individuals with a lifetime diagnosis of OCD met criteria for an additionalDSM-IV disorder (Ruscio, Stein, Chiu, & Kessler, 2010). The most common comorbid
disorders were anxiety disorders (75.8%), followed by mood disorders (63.3%),impulse-control disorders (55.9%), and ﬁnally substance use disorders (38.6%). Within
anxiety disorders, the highest comorbidity rates were found for lifetime social phobia(43.5%), speci ﬁc phobia (42.7%), and separation anxiety disorder (37.1%); whereas
major depressive disorder (40.7%) was the most frequent comorbid mood disorder.Another study that examined a wider variety of DSM-IV disorders also found high
rates of lifetime anxiety and depression comorbidity, as well as high rates of lifetimecomorbid obsessive-compulsive personality disorder (24.7%) in individuals with OCD(Pinto, Mancebo, Eisen, Pagano, & Rasmussen, 2006).
In a sample of 200 individuals with BDD, lifetime comorbidity was compared in
treated and untreated individuals (Phillips et al., 2005). Comorbidity rates werehighest for mood (88.1% in treated individuals and 75.8% in untreated individuals),anxiety (73.1% and 62.1%, respectively), substance use (50.0% and 43.9%, respec-tively), and personality disorders (47.9% and 39%, respectively). The highest rate of358 SPECIFIC DISORDERS

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comorbidity for both samples was major depression (75.4% and 72.7%, respectively);however, rates were relatively high for social phobia (40.3% and 34.8%, respectively)and avoidant personality disorder (26.9% and 22.0%, respectively), which are likelyrelated to appearance concerns associated with BDD.
Literature on the comorbidity rates of HD is sparse, likely due to its introduction as
a stand-alone disorder in the DSM-5 . However, one recent study did examine current
comorbidity of HD (de ﬁned by the then-proposed DSM-5 criteria) in 217 individuals
with the diagnosis (Frost, Steketee, & Tolin, 2011). Major depression was the mostcommon comorbid mood disorder (50.7%); however, comorbidity rates were also highfor attention-de ﬁcit/hyperactivity disorder inattentive type (27.8%), generalized
anxiety disorder (24.4%), social phobia (23.5%), and OCD (18%).
Similarly, research examining comorbidities of TTM is limited. A recent review
suggests mood, anxiety, and substance use disorders are the most commonly identi-ﬁed comorbidities (Duke, Keeley, Geffken, & Storch, 2010). In addition, TTM is related
to skin-picking disorder (Snorrason, Belleau, Woods, 2012), which is discussed in moredetail next.
Although no literature exists at this time that examines comorbidities of DSM-5 ED,
earlier studies examining pathologic skin picking do exist. In one study, comorbiditywas examined in a small sample ( n=60) of individuals who engaged in pathologic
skin picking, de ﬁned similarly to the DSM-5 criteria (with the exception of inclusion of
preoccupation, tension, and relief criteria). Results found that 38.3% of individuals metcurrent criteria for an additional DSM-IV disorder, whereas 56.7% met lifetime criteria
for another disorder (Odlaug & Grant, 2008). Speci ﬁcally, 36.7% of individuals met
current criteria for TTM (with a similar rate for lifetime diagnosis [38.3%]), 15.0% metcriteria for current OCD (16.7% for lifetime), and 15.0% met current criteria for majordepressive disorder (31.7% for lifetime). Indeed, the comorbidity of TTM and skin-picking disorder appears to be high, with an average of 20.8% of TTM outpatientsamples endorsing skin picking, and an average of 15.5% of skin-picking disorderoutpatient samples endorsing TTM, indicating relatedness between the two disorders(Snorrason et al., 2012).E
PIDEMIOLOGY
Due to the recent advent of the DSM-5, current epidemiological studies re ﬂect
diagnoses largely based on DSM-IV-TR criteria. Diagnostic changes introduced in
theDSM-5, as well as inclusion of new disorders, will likely generate new research that
may elucidate changes in prevalence rates re ﬂective of new diagnostic criteria. Thus,
epidemiological data re ﬂected here are based on DSM-IV-TR criteria and in samples of
U.S. adults, unless otherwise noted.
Although over one-fourth of individuals report experiencing obsessions or com-
pulsions at some point in their lives, meeting diagnostic criteria for OCD occurs in amuch smaller percentage of individuals (Ruscio et al., 2010). Speci ﬁcally, the 12-month
prevalence rate of OCD is 1.2% and the lifetime prevalence rate is 2.3%. As a result,OCD is a relatively rare disorder.
In a nationally representative study, the point prevalence of BDD was 2.4% (Koran,
Abujaoude, Large, & Serpe, 2008); however, rates vary widely depending on thesetting. In one study, 1.8% of outpatient adults met criteria for BDD (van der MeerObsessive-Compulsive and Related Disorders 359

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et al., 2012), whereas rates in inpatient samples range from 13.1% to 16% (Conroy et al.,2008; Grant, Kim, & Crow, 2001).
Using the DSM-IV hoarding criterion of obsessive-compulsive personality disorder
(i.e., being “unable to discard worn-out or worthless objects even when they have no
sentimental value ”) (APA, 1994), the weighted community prevalence was 5.3%
(Samuels et al., 2008). Similarly, in a large German community sample, 5.8% ofindividuals endorsed current hoarding according to (then proposed) DSM-V criteria
(Timpano et al., 2011).
In a community sample, 0.6% of individuals met DSM-IV-TR criteria for TTM;
however, the prevalence increased to 1.2% when the prior diagnostic criteria ofbuilding tension or release were ignored (Duke, Bodzin, Tavares, Geffken, & Storch,2009), suggesting that the DSM-5 criteria may be less restrictive and produce larger
prevalence rates. Among a psychiatric inpatient sample, the point prevalence of TTMwas 3.4% and the lifetime prevalence was 4.4% (Grant, Levine, Kim, & Potenza, 2005).Interestingly, a similar rate of TTM (3.9%) was found for a sample of college students;however, the latter rate was based on a modi ﬁed self-report measure of the clinical
interview administered to the inpatient sample (Odlaug & Grant, 2010).
Although ED was not an of ﬁcial diagnosis within the DSM-IV-TR (APA, 2000),
prevalence rates based on various diagnostic criteria do exist. For instance, in non-clinical community samples, 1.4% to 5.4% of individuals endorsed clinically signi ﬁ-
cant skin picking with associated distress or impairment (Hayes, Storch, & Berlanga,2009). In a recent study examining prevalence based on (then proposed) DSM-5
criteria, 4.2% of college students met diagnostic criteria for ED (Odlaug et al., 2013).P
SYCHOLOGICAL AND BIOLOGICAL ASSESSMENT
Various clinician-administered measures for the assessment of OCD exist. Forinstance, the Anxiety Disorders Interview Schedule for DSM-IV (ADIS-IV; Brown,
DiNardo, & Barlow, 1994) and the Structured Clinical Interview for DSM-IV-TR Axis I
Disorders (SCID-CV; First, Spitzer, Gibbon, & Williams, 1996) are semistructureddiagnostic interviews that assess for OCD and other disorders. Additionally, the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS; Goodman et al., 1989a; Goodman et al.,1989b) is considered the “gold standard ”for assessing OCD symptom severity and
now includes a revised second edition (Y-BOCS-II; Storch, Rasmussen, et al., 2010).The Y-BOCS-II is a semi-structured, clinician-administered measure that assesses forthe frequency and severity of OCD symptoms over the past week, with good toexcellent psychometric properties (Storch, Larson, et al., 2010; Storch, Rasmussen,et al., 2010).
Although OCD is typically assessed using semi-structured clinical interviews,
various self-report measures with established reliability and validity exist, includingthe Y-BOCS-Self Report (Baer, Brown-Beasley, Sorce, & Henriques, 1993; Steketee,Frost, & Bogart, 1996) and Obsessive-Compulsive Inventory (OCI; Foa et al., 2002).Finally, behavioral avoidance tests (BATs), or observational tasks in which individualsare exposed to feared stimuli while rating their distress, have recently been used toassess OCD (Grabill et al., 2008). Speci ﬁcally, BATs are often administered before
treatment to assess the severity of avoidance and distress, and after treatment to assessfunctional change. Although BATs provide additional clinical information, they are360 SPECIFIC DISORDERS

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generally considered an adjunct to traditional clinical interviewing, providing partic-ularly helpful information for development of exposure hierarchies. For recentcomprehensive reviews of assessment measures for OCD, see Benito and Storch(2011) and Grabill et al. (2008).
Although the SCID-CV (First et al., 1996) screens for BDD, more thorough assess-
ments are needed for diagnosis. For example, the BDD Examination (BDDE; Rosen &Reiter, 1996), a 34-item semi-structured clinical interview, is designed speci ﬁcally to
diagnosis BDD. The BDDE has acceptable reliability and validity, and measures notonly the various aspects of preoccupation, but also the level of conviction theindividual holds regarding the perceived defect (Cororve & Gleaves, 2001). Inaddition, the Y-BOCS (Goodman et al., 1989a; Goodman et al., 1989b) was modi ﬁed
for the assessment of BDD (Y-BOCS-BDD; Phillips et al., 1997); however, the measurehas been criticized for a narrow focus of obsessive compulsive type symptomatology(Rosen & Reiter, 1996).
The majority of current measures that assess for hoarding are based on DSM-IV-TR
criteria (APA, 2000), which conceptualized hoarding as a symptom of OCD or acriterion of obsessive-compulsive personality disorder (Frost, Steketee, & Tolin, 2012).Although hoarding subscales exist on some measures of OCD, more recent measuresdesigned speci ﬁcally for hoarding have been created and may more accurately assess
the diagnostic criteria of the disorder. For instance, the Hoarding Rating Scale-Interview (HRS-I; Tolin, Frost, & Steketee, 2010) is a ﬁve-item semi-structured clinical
interview used to assess compulsive hoarding and related impairment and distress.The HRS-I exhibits excellent reliability, is sensitive to treatment changes, and candistinguish individuals with hoarding from both OCD patients without hoarding andcommunity controls (Tolin et al., 2010). Additionally, the Saving Inventory –Revised
(SI-R; Frost, Steketee, & Grisham, 2004) is a 23-item self-report measure that assessesfor clutter, dif ﬁculty discarding, and excessive acquisition, which exhibits appropriate
reliability and validity. For more comprehensive reviews of assessment of hoarding,see Frost et al. (2012) and Frost and Hristova (2011).
Although no gold standard assessment f or TTM exists, there are some measures
designed to assess for the disorder (Duke e t al., 2010). Measures with acceptable
psychometric properties include the Massa chusetts General Hospital Hairpulling
Scale (MGH-HPS; Keuthen et al., 1995; O'Sullivan et al., 1995), a seven-item self-report scale, and the Milwaukee Inventory for Subtypes of Trichotillomania-Adult
Version (MIST-A; Flessner, Woods, Franklin, Cashin, & Keuthen, 2008), a 15-itemscale that provides two distinct scale scores (i.e., automatic pulling and focusedpulling scores).
There does not appear to be an assessment measure yet developed for the DSM-5
diagnosis of ED; however, some measures do assess for factors related to earlierconceptualizations of skin picking. For instance, the Skin Picking Scale (SPS; Keuthenet al., 2001) is a six-item self-report measure modeled after the original Y-BOCS(Goodman et al., 1989a; Goodman et al., 1989b); however, the measure only assessesfor severity of skin picking. Further, similar to the MIST-A (Flessner et al., 2008), theMilwaukee Inventory for the Dimensions of Adult Skin Picking (MIDAS; Walther,Flessner, Conelea, & Woods, 2009) is a reliable and valid assessment of automatic andfocused skin picking for individuals who engage in the behavior. Even so, assessmentof ED is currently lacking due to the recent advent of the disorder in the latest DSM-5 .Obsessive-Compulsive and Related Disorders 361

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Clinical interviews or self-report measures that assess for the presence of DSM-5
criteria are of particular need.
ETIOLOGICAL CONSIDERATIONS
BEHAVIORAL AND MOLECULAR GENETICS
OCD has a complex etiology involving both genetic and environmental factors.Evidence from family, twin, and segregation studies shows that heredity plays amajor role in the etiology of OCD. In a meta-analytic study, Hettema, Neale, andKendler (2001) found an average prevalence rate of 8.2% for ﬁrst-degree relatives of
OCD probands compared to 2% in comparison relatives, suggesting heritability. Twinstudies of OCD patients also support the presence of signi ﬁcant genetic in ﬂuence, with
estimates of 45% to 65% in children, and 27% to 47% in adults (Jonnal, Gardner,Prescott, & Kendler, 2000). In a large twin study examining heritability of dimensionsof OCD, including rumination, contamination, and checking, genetic factorsaccounted for 36% of the variance for an overall factor of OCD symptoms (vanGroothest, Boomsma, Hettema, & Kendler, 2008). The remaining 64% was explainedby environmental factors. Only the contamination dimension appeared to be in ﬂu-
enced by speci ﬁc genes and to be an independent dimension.
In another study of OCD symptom dimensions, ﬁve major symptom dimensions
(checking, hoarding, obsessing, ordering, and washing) were analyzed in a sample offemale twins (Iervolino, Rijsdijk, Cherkas, Fullana, & Mataix-Cols, 2011). The authorsconcluded that no single underlying factor could explain the heterogeneity of OCD.However, the majority of the genetic variance was due to shared genetic factors(62.5% –100%), whereas the nonshared environmental variance was due to dimension-
speciﬁc factors (Iervolino et al., 2011). In this study, the hoarding dimension had the
lowest loading on the common factor and was more in ﬂuenced by speci ﬁc genetic
effects (54.5%). Future research is needed to help identify speci ﬁc genetic and
environmental factors underlying the dimensions of this heterogeneous disorder.
The speci ﬁc genetic markers for OCD are largely unknown; however, genome-wide
linkage studies that attempt to identify regions that may contain vulnerability geneshave been conducted in patients with OCD. Early studies were conducted with smallsample sizes and produced mixed results. Taken together, however, these earlystudies suggest that regions containing chromosome 9 may be of particular impor-tance (Hanna et al., 2002; Shugart et al., 2006; Willour et al., 2004). Although theseresults are far from de ﬁnitive, it is interesting to note that several studies have reported
an association between OCD and a glutamate transporter gene (SLC1A1), which islocated in the area of chromosome 9p (Chakrabarty, Bhattacharyya, Christopher, &Khanna, 2005; Ting & Feng, 2008; Rotge et al., 2010). More recently, however,Mathews and colleagues (2012) conducted a genome-wide linkage analysis using33 families that had two or more individuals with childhood-onset OCD. Authorsidenti ﬁedﬁve areas of interest on chromosomes, with the strongest result on chro-
mosome 1p36. Future studies are needed to replicate this genomic area of interest.
The etiology of BDD is also complex; however, extant research suggests that
heritability is an important part of the variance of BDD etiology. A family studyinvestigating the relationship between OCD and possible spectrum disorders revealed362 SPECIFIC DISORDERS

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that 8% of individuals with BDD have a ﬁrst-degree relative with a lifetime diagnosis
of BDD, which is 3 to 8 times greater than the prevalence in the general population(Bienvenu et al., 2000). Interestingly, 7% of patients with BDD also have a ﬁrst-degree
relative with OCD (Phillips, Gunderson, Mallya, McElroy, & Carter, 1998), and ﬁrst-
degree relatives of OCD patients have 6 times the lifetime prevalence of BDDcompared to controls. Taken together, these studies suggest a shared heritabilitybetween BDD and OCD.
A recent twin study of BDD revealed that genetic factors accounted for 44% of the
variance in dysmorphic concerns, whereas nonshared environmental factorsaccounted for the remaining variance (Monzani et al., 2012). Although there is limitedresearch regarding speciﬁ c genetic markers for BDD, one candidate gene study found
association for GABA (A)-gamma-2 (5q31.1-q33.2) with the 1 (A) allele occurring morefrequently in BDD subjects than controls (Phillips & Kaye, 2007). The GABA (A)receptor-y2 gene was also associated with BDD, but not OCD patients, in a subsequentgenetic investigation (Richter et al., 2009).
Information regarding the etiology of HD is primarily derived from research on
patients with OCD who have been divided into hoarding or nonhoarding subgroups.Within this framework, hoarding has been shown to have a strong familial association(Pertusa, Fullana, Singh, Menchon, & Mataix-Cols, 2008). In a study of monozygoticand dizygotic twins from the UK twin registry, “caseness ”of hoarding was deter-
mined by completion of the Hoarding Rating Scale– Self Report (HRS-SR), with 2.3% of
the sample reporting symptoms severe enough to be included (Iervolino et al., 2009).The authors found that heritability of hoarding in female twins was associated withboth genetic (50%) and nonshared environmental factors (as well as measurementerror). Shared environmental factors did not contribute to the liability. It is interestingto add that a signi ﬁcantly higher rate of severe hoarding, as well as any hoarding
symptoms (compared to no symptoms), was observed for male twins, compared tofemale twins.
Given the recent inclusion of hoarding as a diagnostic category, there is little
research in the area of genetic etiology of HD. Using data from a large collaborativegenetics study of OCD, Samuels and colleagues (2007) found signi ﬁcant linkage of
compulsive hoarding to Chromosome 14 in families with OCD. These investigatorsalso found that hoarding and indecision were more prevalent in relatives of hoardingthan nonhoarding OCD patients. Future research that focuses on HD as a separatediagnostic entity may help to increase understanding of etiological factors.
The etiology of TTM for any particular patient is most likely an interaction between
biological, psychological, and social factors (Diefenbach, Reitman, & Williamson,2000). Early genetic research indicates that hair-pulling behavior occurs at increasedrates (5% –8%) in family members of TTM probands relative to normal controls
(Christenson, Mackenzie, & Reeve, 1992; Lenane et al., 1992). Heritability has alsobeen suggested by results of a twin study in which concordance rate for TTM (asdeﬁned by DSM-IV-TR criteria) was 38.1% for monozygotic twins compared to 0% for
dizygotic twins (Novak, Keuthen, Stewart, & Pauls, 2009). Taken together, thesestudies suggest heritability is an important component in the etiology of TTM.
ED also appears to have a familial component. In a study with 60 patients with skin-
picking disorder, Odlaug & Grant (2012) found 28.3% of ﬁrst-degree family members
also met criteria for the disorder. Another study found that 43% of 40 patients with EDObsessive-Compulsive and Related Disorders 363

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had ﬁrst-degree relatives with skin-picking symptoms (Neziroglu, Rabinowitz,
Breytman, & Jacofsky, 2008). Further in support of a heritability component in theetiology of ED, Monzani and colleagues (2012) found that clinically signi ﬁcant skin
picking was reported by 1.2% of twins, with higher concordance for monozygotic thandizygotic twins. Within this female sample, genetic factors accounted for 40% of thevariance, with the remaining variance attributable to nonshared environmentalfactors. Future studies are needed with homogenous samples, diagnosed withDSM-5 criteria, to establish heritability of ED.
N
EUROANATOMY AND NEUROBIOLOGY
Extant literature supports an association between OCD and impairments of the brain ’s
corticostriatal systems, which include organized neural circuits that connect the basalganglia, thalamus, and cortex. For instance, fMRI ﬁndings suggest that patients with
OCD exhibit impairments in functional connectivity of both the ventral and dorsalcorticostriatal systems, with a direct link between ventral corticostriatal connectivityand symptom severity (Harrison et al., 2009). Although these authors were able toshow system-wide differences in connectivity, the sample size was too small todetermine the effects of speci ﬁc symptom dimensions. More recent research has
focused on a multidimensional model that examines direct links between majorOCD symptom dimensions and structural and functional brain indicators (Menzieset al., 2010).
In a recent study, investigators evaluated the in ﬂuence of OCD symptom dimen-
sions on brain corticostriatal functional systems (Harrison et al., 2013). Results found ashared connectivity involving the ventral striatum and orbitofrontal cortex that wasrelated to overall severity level, but independent of speci ﬁc symptom dimensions.
Rather, distinct anatomical relationships between the severity of symptom dimensionsand connectivity were observed, with aggression symptoms moderating connectivityin the ventral striatum, amygdala, and ventromedial frontal cortex, and sexual/religious symptoms affecting ventral striatal-insular connectivity. This recent datasuggests common pathophysiological changes in orbitofrontal-striatal regions acrossvarious forms of OCD. Further, Beucke and colleagues (2013) examined abnormalconnectivity in the orbitofrontal cortex in medicated and nonmedicated OCD patientsand matched normal controls. Consistent with previous research, the orbitofrontalcortex and the basal ganglia showed greater connectivity in unmedicated OCDpatients, suggesting that antidepressant medication may reduce brain connectivityin OCD patients. It is also interesting to note that more distant connectivity wasobserved in this study, highlighting the need for future research to determine theextent of hyper connectivity outside of corticostriatal circuitry (Beucke et al., 2013).
Structural magnetic resonance imaging (MRI) studies with BDD patients have
shown caudate nucleus asymmetry (Rauch et al., 2003) and orbitofrontal cortexvolume abnormalities (Atmaca et al., 2010), with both studies ﬁnding an increase
in white matter volume in patients with BDD. White matter microstructure wasrecently evaluated by diffusion weighted MRI to examine connectivity amongstructures thought to be involved in BDD (Feusner et al., 2013). Results of the studysuggest a relationship between impairments in insight and ﬁber disorganization in
tracts connecting visual with emotional and memory processing. Arienzo and364 SPECIFIC DISORDERS

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colleagues (2013) also conducted a brain network analysis and found disturbances inwhole brain organization. Speci ﬁcally, abnormal connectivity between regions
involved in lower-order visual processing and higher-order visual and emotionalprocessing was observed. Further, a study using single photon emission computedtopography (SPECT) imaging found occipital perfusion and parietal abnormalities inBDD (Carey, Seedat, Warwick, van Heerden, & Stein, 2004), which is interesting asparietal dysfunction has also been shown to be associated with disturbances in bodyimage (Trimble, 1988). Although more research is needed, these studies suggestdisturbances in information processing in patients with BDD.
Given the perceived defects that patients with BDD report about their appearance,
and the visuospatial processing de ﬁcits found within neuropsychological research, it
is likely that disturbances in visual perceptual or visuospatial processing may bepresent in patients with BDD. In a neuroimaging study investigating visual processingof others ’faces in patients with BDD compared to controls, fMRI was used to scan
while subjects looked at photographs of unknown faces that were unaltered or alteredto contain primarily low or high detail information (Feusner, Townsend, Bystritsky, &Bookheimer, 2007). BDD patients evidenced greater left hemisphere activity relative tocontrols for all image types but particularly to the low-detail faces. This lateralityimbalance may suggest greater detailed facial processing and less holistic processing.In a more recent fMRI study, BDD subjects viewed photographs of their own face anda familiar face that had been altered or unaltered to include high or low detailinformation (Feusner, Neziroglu, Wilhelm, Mancusi, & Bohon, 2010). Again, BDDsubjects showed relative hypoactivity in visual cortical systems for low detail photo-graphs. To investigate if BDD patients have a more general abnormality in visualprocessing, BDD patients were scanned while looking at pictures of houses (asopposed to faces). The BDD group showed abnormal relative hypoactivity in leftvisual association areas for low detail images and hyperactivity of prefrontal systemsfor high detail images (Feusner et al., 2010). Thus, it appears that BDD patients mayexhibit general abnormalities in lower and higher order visual processing.
Preliminary evidence suggests that hoarding symptoms may have a different
neural substrate than OCD. Studies of animal hoarding and hoarding due to braindamage or dementia have implicated the subcortical limbic structures and theventromedial prefrontal cortex as important in hoarding behavior (see Mataix-Cols, Pertusa, & Snowdon, 2011 for a review). Studies of humans with compulsivehoarding have focused on the same brain areas and found similar results. Saxena andcolleagues (2004) found that compulsive hoarders show a unique pattern of abnormalresting-state brain function relative to that of normal controls and nonhoarding OCDpatients. Speci ﬁcally, the hoarding group evidenced abnormally low activity (reduced
glucose metabolism) in the posterior cingulate cortex compared to normal controlsand the dorsal anterior cingulate when compared to nonhoarding OCD patients.
Brain activity of hoarding and nonhoarding OCD patients was compared to normal
controls in a symptom-provocation study (An et al., 2009). During an fMRI assess-ment, these subjects were asked to imagine throwing away objects that belonged tothem while shown pictures of the items. The OCD patients with hoarding symptomsshowed more reactivity in the ventromedial prefrontal cortex (VMPFC) than the othergroups. In an exploratory study, Tolin, Kiehl, Worhunsky, Book, & Maltby (2009)conducted fMRI assessment of a small group of severe hoarders ( n=12; only 2 withObsessive-Compulsive and Related Disorders 365

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OCD diagnosis) and normal controls. When deciding whether to keep or discard realpersonal items, individuals with hoarding symptoms showed greater activity in theleft lateral orbitofrontal cortex and parahippocampal gyrus compared to controls.
In a more recent study, neural activity was measured by fMRI in patients with well-
deﬁned primary HD (as proposed for DSM-5 in Mataix-Cols et al., 2010) and
compared to patients with OCD and normal controls (Tolin et al., 2012). The taskinvolved real-time, binding decisions that had to be made about whether to keep orabandon actual belongings compared to control items. The HD group discardedsigniﬁcantly fewer personal items than the OCD and control groups with no differ-
ences in decisions to discard control items. With regard to neural activity, the HDgroup differed from OCD and normal controls in the anterior cingulate cortex and theleft and right insular cortex. Taken together, these studies suggest that the ventro-medial prefrontal/cingulate and medial temporal regions may be involved in hoard-ing behavior.
Imaging studies of TTM have been somewhat inconsistent. Early studies of hair
pulling (then de ﬁned as an impulse control disorder NOS in DSM-IV ) found evidence
of fronto-striatal abnormalities (O ’Sullivan et al., 1997; Keuthen et al., 2007) and
fronto-striatal-thalamic pathways (Chamberlain et al., 2008). Structural abnormalitiesimplicated increased grey matter densities in extensive areas including the prefrontallobe, anterior cingulate, striatum, amygdala, and hippocampus (Chamberlain et al.,2008). In a subsequent study, Chamberlain and colleagues (2010) looked at whitematter integrity, rather than gray matter abnormalities, using diffusion tensor imaging(DTI). Results indicated a disruption in white matter integrity in the anterior cingulate,orbitofrontal cortex, presupplementary motor areas, and temporal lobe compared tonormal controls. These ﬁndings are, in part, similar to the ﬁndings in OCD patients
described previously. In a recent study, white matter integrity was explored inpatients with TTM and normal controls (Roos, Fouche, Stein, & Lochner, 2013).Although there were no differences between patients with TTM and controls onDTI measures, these investigators reported increased mean density (global average ofall diffusion directions) in white matter tracts of the frontostriatal-thalamic pathway inpatients with longer hair-pulling duration and increased TTM severity.
White matter abnormalities have also been shown in ED. Neurocognitive ﬁndings
indicate that ED is related to impairment in prepotent motor responses and that thisfunction is dependent on the integrity of the right frontal gyrus and the anteriorcingulate cortices as well as the white-matter tracts that connect them. To examinewhether these regions are impaired, Grant, Odlaug, Hampshire, Schreiber, &Chamberlain (2013) conducted a diffusion tensor imaging study with 13 subjectsmeeting proposed DSM-5 criteria for ED. Results were as expected, with patients with
ED showing signi ﬁcantly reduced fractional anisotropy in tracts distributed bilater-
ally, which included the anterior cingulate cortices. The ﬁndings support dis-
organization of white matter tracts involved in motor generation and suppressionin the pathophysiology of excoriation in patients with ED.L
EARNING ,M ODELING ,ANDLIFEEVENTS
There is some evidence that trauma may be associated with increased symptomseverity in OCD (Cromer, Schmidt, & Murphy, 2007). Among children and366 SPECIFIC DISORDERS

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adolescents, OCD is related to an increased number of lifetime traumatic events aswell as more events in the year preceding onset, compared to those with any otheranxiety disorder (Gothelf, Aharonovsky, Horesh, Carty, & Apter, 2004). The severityof childhood trauma also appears to be greater for patients with OCD comparedto normal controls (Lochner, du Toit, et al., 2002). Other life events associatedwith OCD onset include accidents and serious mistakes (Rheaume, Freeston,Leger, & Ladouceur, 1998) as well as pregnancy and childbirth (Wisner, Peindl,Gigliotti, & Hanusa, 1999).
Developmental factors, particularly sexual, emotional, and physical abuse, may be
associated with BDD. Although no longitudinal data is available, two cross-sectionalstudies found frequent reports of childhood maltreatment in BDD cases. Neziroglu,Khemlani-Patel, and Yaryura-Tobias (2006) found that 19 of 50 BDD patients (38%)reported some type of abuse during childhood (28% emotional abuse, 22% sexualabuse, and 14% physical abuse) compared to 14% of a group of 50 patients with OCD.Early abuse was shown to be associated with BDD in another study (Didie et al., 2006)with nearly 79% of 75 BDD subjects reporting a history of maltreatment (68% emo-tional neglect, 56% emotional abuse, 33.3% physical neglect, and 28% sexual abuse).
Early social interactions with peers may also be associated with BDD. In one study,
individuals with BDD reported more teasing by peers, especially about appearance,compared to healthy control subjects (Buhlman, Cook, Fama, & Wilhelm, 2006). In arecent study appearance-related social-evaluative concerns were higher in BDDpatients than healthy controls (Anson, Veal, & de Silva, 2012). Speci ﬁcally, BDD
participants reported higher levels of importance and anxiety associated with percep-tions of others ’view of their appearance as well as their own view.
It has been suggested that HD may develop as a conditioned emotional response
related to thoughts or beliefs concerning items or possessions (Grisham & Barlow,2005). Anxiety experienced with discarding and decision-making is avoided byacquisition and hoarding of items. Furthermore, the hoarding behavior is reinforcedbecause the possessions take on pleasurable or soothing characteristics; however,more research is needed in this area.
TTM and ED may have similar environmental risk factors. Lack of stimulation or
boredom has been suggested as a factor in both experimental (Teng, Woods, Marcks, &Twohig, 2004) and self-report studies (Shusterman, Feld, Baer, & Keuthen, 2009;Snorrason, Smári, & Olafsson, 2010). Early case reports also suggested that severeactivity restriction may be implicated in the development of TTM and ED (Evans,1976; Gupta, Gupta, & Haberman, 1986). Further, a number of case studies havesuggested a relationship between history of trauma and skin picking/hair pulling butlongitudinal data are needed to determine whether traumatic events play a causal rolein these disorders (Snorrason, Belleau, Woods, 2012).C
OGNITIVE INFLUENCES
A cognitive model of OCD (Rachman, 1997) proposes that it is not the content of theintrusive thought per se, but the interpretation of the thought that leads to pre-occupation and anxiety in patients with OCD. In this model, dysfunctional beliefsabout the inability to tolerate the negative emotions associated with the intrusivethoughts are thought to lead to the development and maintenance of OCD. ThreeObsessive-Compulsive and Related Disorders 367

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types of dysfunctional beliefs have been proposed to contribute to OCD: (1) over-estimated responsibility and exaggerated threat; (2) perfectionism and intolerance ofuncertainty; and (3) overimportance of thoughts and need to control thoughts(Calkins, Berman, & Wilhelm, 2013).
In a large, nonclinical sample, Taylor and colleagues (2010) used structural equation
modeling and found that responsibility and threat estimation beliefs predicted alltypes of OCD (checking, hoarding, ordering, washing) above and beyond the othertwo types of beliefs. Using an assessment instrument that conceptualizes OCD from amultidimensional perspective, Wheaton, Abramowitz, Berman, Riemann, and Hale(2010) replicated this ﬁnding in a clinical sample, with beliefs related to in ﬂated
responsibility and threat predicting contamination and responsibility for harmdimensions. However, other symptom dimensions were predicted by other beliefs,with each dimension of OCD uniquely predicted by a single belief domain. The resultsof this study and others indicate intolerance of uncertainty to predict OC symptoms(Boelen & Carleton, 2012; Carleton et al., 2012), which highlights the importance ofinvestigating OCD as a multidimensional, heterogeneous disorder.
Neurocognitive performance in OCD patients has received considerable attention,
with impairment in executive functioning a common ﬁnding. Early examples of
executive dysfunction include studies that showed decreased cognitive ﬂexibility
and set shifting (Henry, 2006; Lawrence et al., 2006) and impaired decision-makingand planning (Shin et al., 2004). Memory impairments in tests requiring implicitorganization have also been demonstrated (Greisberg & McKay, 2003). In a recentstudy, Kashyap, Kumar, Kandavel, and Reddy (2013) tested neuropsychologicalfunctions in 150 patients with OCD compared to 205 healthy control subjects. Patientswith OCD showed de ﬁcits in scanning, planning time, concept formation, decision-
making and encoding of nonverbal memory. Thus, these results con ﬁrm executive
dysfunction, with particular dif ﬁculties in strategizing and organizing. Of note, this
neuropsychological pro ﬁle involves the prefrontal cortex and striatum, suggesting
that OCD may not be just an orbitofronto-striatal disorder.
Cognitions in BDD are similar to those in OCD in that patients with BDD experience
recurrent, persistent, and intrusive preoccupations. In BDD, however, these thoughtsare speci ﬁcally related to perceived physical defects. There have been fewer studies
that have examined neurocognitive functioning in patients with BDD. However, likepatients with OCD, most studies have suggested executive dysfunction. Speci ﬁcally,
Hanes (1998) compared patients with BDD, OCD, and schizophrenia to normalcontrols on tests of executive function, memory, and motor function. BDD andOCD patients showed more impaired performance on executive function tasks(New Tower of London and Stroop) compared to controls, suggesting impairmentin the frontal cortex. Similarly, patients with BDD showed both nonverbal (ReyComplex Figure Test) and verbal (California Verbal Learning Test) memory impair-ments when compared to healthy controls (Deckersbach et al., 2000). The authorssuggest that the memory impairments may be mediated by poor organizationalstrategies, possibly as a result of executive dysfunction.
More recently, Dunai, Labuschagne, Castle, Kyrios, and Rossell (2010) again
demonstrated executive functioning de ﬁcits in patients with BDD, speci ﬁcally de ﬁcits
related to spatial working memory and thinking speed. However, in this study,patients with BDD did not show de ﬁcits in short-term memory capacity, motor speed,368 S
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or visual memory, which may be due to heterogeneous executive function measuresused in the different studies. In a recent study, authors compared executive function inBDD and OCD patients using the same cognitive tasks for both groups (Spatial Span,Spatial Working Memory, Stockings of Cambridge, and Pattern Recognition). Ingeneral, results suggest that both groups evidence impaired executive functioningcompared to controls (Labuschagne, Rossell, Dunai, Castle, & Kyrios, 2013); however,there was also an interesting difference between groups, as BDD patients showedgreater de ﬁcits on a planning task that assesses spatial planning ability, compared to
both OCD patients and controls.
There is less known about the signi ﬁcance of cognitions in HD. Most research has
focused on indecisiveness and emotional attachment to objects. In general, impair-ment in decision-making has been thought to be a core feature of HD. Results of earlyneuropsychological research are mixed and interpretation is dif ﬁcult, as different tasks
with homogeneous groups have been used (Grisham, Brown, Savage, Steketee, &Barlow, 2007; Hartl et al., 2004; Lawrence et al., 2006). More recently, Grisham,Norberg, Williams, Ceroma, and Kadib (2010) used a well-standardized neuro-psychological battery to assess severe hoarders, matched anxious, and matchednormal controls. In this study, severe hoarders showed de ﬁcits on only the plan-
ning/problem-solving task and did not differ on tasks of decision-making, cognitiveﬂexibility, or response inhibition. Further, Frost, Tolin, Steketee, and Oh (2011)
examined indecisiveness in a large sample of adults who self-referred as havingsevere hoarding. Interestingly, they also examined hoarding in adult children andspouses of these individuals. Individuals with hoarding problems reported moredecision-making problems than children or spouses and substantially more thannormal controls. In addition, adult children reported more indecisiveness thanspouses, suggesting a familial characteristic.
Memory problems have also been implicated in this population, as compulsive
hoarders have been shown to score signi ﬁcantly worse on tasks of implicit memory
(Blom et al., 2011). Tolin and colleagues (2011) found decreased ability to sustainattention and poorer adaptive memory strategies in patients with HD relative to OCDand normal controls. The authors note that true impairment on any neuro-psychological task was rather low across all groups; however, 67% of hoarders(compared to 58% of OCD and 42% of normal controls) scored in the impaired rangeon at least one measure (Tolin et al., 2011). Finally, executive functioning has beenassessed in older adults with HD (Ayers et al., 2013). Matched for age with healthycontrols, older adults showed impaired functioning in executive function includingworking memory, mental control, inhibition, and set shifting. More research is neededto replicate these ﬁndings with homogeneous groups under similar conditions.
With regard to ED, research regarding cognitive in ﬂuences and neuropsychological
functioning is needed due to its recent inclusion in the DSM-5 .
S
EX AND RACIAL -ETHNIC CONSIDERATIONS
Men and women are equally likely to suffer from OCD, although community samplesevidence higher rates in women, whereas clinical samples evidence higher rates of OCDin men (Karno, Golding, Sorenson, & Burnam, 1988). These contradictory ﬁndings
suggest that men may experience more impairment related to OCD symptomology,Obsessive-Compulsive and Related Disorders 369

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which may lead to increased help-seekin g behavior. In a recent comprehensive
cross-sectional study conducted in Brazil, phenomenological characteristics of men
and women with OCD were evaluated (Torresan et al., 2013). The sample included504 women (58.7%) and 354 men (41.3%) with a mean age of 35.4 years old (18-77).Men were found to be younger, more frequently single, and with symptominterference at a younger age. In addition to these differences, the obsessionalcontent in men was more likely to encompa ss sexual/religious themes, whereas
women were more likely to present with sy mptoms related to aggression, contami-
nation/cleaning, and hoarding. Results of this study support results found instudies previously conducted in Italy (Lensi et al., 1996) and India (Khandelwal,Aggarwal, Garg, & Jiloha, 2009).
Contamination and checking are OCD themes most consistently found across
cultures (Matsunaga & Seed at, 2007). Other speci ﬁc themes or content of OCD
symptoms may be more prevalent in certain cultures, such as fear of leprosyamong those who live in Africa (Steket ee & Barlow, 2002) or religion themes
among those from the Middle East (Fontenelle, Mendlowicz, Marques, & Versiani,2004). There is some data that suggests l ower prevalence of OCD among African
Americans (Karno et al., 1988) although this may re ﬂect lower numbers of African
Americans seeking evidence-based treatme nts in mental health settings. An under-
representation of minorities in clinical tr ials of evidence-based treatments suggests
that ef ﬁcacy in non-White populations is not known (Williams, Powers, Yun, &
Foa, 2010).
In an early study of BDD, Bohne, Keuthen, Wilhelm, Deckersbach, & Jenike (2002)
found similar rates of body dysmorphic concerns in German (5.3%) and American(4%) students, which may be expected due to somewhat similar cultures of the twocountries. In a cross-sectional study of BDD in undergraduates in the southeast UnitedStates, differences in gender, race/ethnicity, and sexual orientation were evaluated. Inthis population, an overall BDD prevalence of 4.9% was obtained, with womenendorsing more symptoms of BDD than men. In addition, among women, Caucasiansand Latinas endorsed more symptoms than African Americans, and sexual minoritiesof both genders endorsed more symptoms than heterosexuals (Boroughs, Krawczyk, &Thompson, 2010). Further, racial/ethnic factors in BDD were assessed in an onlinesurvey (Marques et al., 2011). In this study, no signi ﬁcant differences were found
between Caucasian, Latino, or African American participants. However, there was asigniﬁcant difference between Caucasian and Asian participants, with Asians report-
ing more concern with straight hair and dark skin, but fewer body shape concerns. Inaddition, Asian respondents reported lower rates of grooming, touching body parts,and camou ﬂaging, as well as higher rates of exercise. It is important to note that this
research is in the early stages and has focused on BDD symptoms rather than BDD inclinical settings.
Two studies have shown compulsive hoarding to be more prevalent in women
(Iervolino et al., 2009; Samuels et al., 2008); however, the phenomenology of hoardingis very similar in men and women. Although most research has been done with OCDpopulations, subdivided into hoarding and nonhoarding groups, there is no datasuggesting that hoarding is different across cultures (Mataix-Cols et al., 2010).Obviously more research is needed in this area now that HD is a standalone diagnosisinDSM-5 .370 S
PECIFIC DISORDERS

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Existing literature indicates that 88 to 94% of patients with TTM are female (Odlaug,
Kim, & Grant, 2010). The reason for this large gender bias is unclear, but may berelated to societal values of beauty, and related distress, and greater drive to seek helpdue to hair loss in women. There is very little research regarding racial/ethnicdifferences in TTM. In a survey of American college students, there was no differencefound between African-American and non-African students (McCarley, Spirrison, &Ceminsky, 2002). In a more recent study, ethnic differences in TTM symptoms wereevaluated among minority and Caucasian participants (Neal-Barnett et al., 2010).Overall, results indicate that the minority sample was less likely to report pulling fromeyebrows and eyelashes, as well as less likely to report tension prior to pulling. Therewas also a difference in interference, in which minorities reported more problems withhome management related to pulling, and Caucasians reported more interference withacademic endeavors. In addition, Caucasians reported more daily stress and treatmentutilization, although treatment ef ﬁcacy did not differ among ethnic groups.
ED is more frequent in females with higher rates of co-occurring grooming
disorders (Grant et al., 2012). The clinical characteristics have been shown to bethe same across age ranges as well as cultures (Bohne et al., 2002; Lochner, Simeon,Niehaus, & Stein, 2002).C
OURSE AND PROGNOSIS
OCD is a chronic and disabling disorder that rarely remits without treatment. Thedevelopment of OCD usually begins between late adolescence and early adulthood.Symptoms of OCD are typically stable over time, with changes occurring withinsymptom dimensions rather than between sy mptom dimensions (Mataix-Cols et al.,
2002). In a recent multicenter naturalisti c study from the International College of
Obsessive Compulsive Spectrum Disorder s (ICOCS), early onset and long duration
of illness were identiﬁ ed as negative predictors of long-term outcome (Dell ’Osso
et al., 2013).
Both biological and behavioral therapies have been shown to be effective. Positive
treatment outcome has been shown with SSRIs (such as Prozac or Zoloft) as well ascognitive-behavioral treatments, such as exposure with response-prevention (ERP)(NICE, 2006). In a recent meta-analysis, Olatunji, Davis, Powers, and Smits (2013)evaluated 16 randomized controlled trials (RCTs) of CBT for OCD and found that CBToutperformed control conditions across the studies. Of greater interest, perhaps, is thatfew moderator variables affected ef ﬁcacy. Speci ﬁcally, outcome was not associated
with greater severity of OCD or level of depression at pretreatment. There weresmaller effect sizes for adult RCTs and older age, suggesting greater efﬁ cacy in
younger patients with OCD. CBT should be considered a ﬁrst-line treatment for
OCD, with or without adjunctive pharmacotherapy.
BDD typically begins in adolescence (Phillips et al., 2005), which is a stage of
development marked by hormonal changes and accelerated growth. Adolescence isalso a period in which acne may develop and lead to peer rejection. These factors maybe related to, or trigger, the development of BDD, but research is needed to addressthese factors. A recent study compared patients with early onset BDD (before age 18)to later onset BDD (Bjornsson et al., 2013). In general, early onset was associated withmore gradual onset, a lifetime history of attempted suicide, and greater comorbidity.Obsessive-Compulsive and Related Disorders 371

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With regard to treatment, ef ﬁcacy of cognitive behavior therapy for BDD has recently
been reviewed (Prazeres, Nascimento, & Fontenelle, 2013). Authors indicate that bothindividual and group cognitive behavioral therapies, that include psychoeducation,cognitive restructuring, and ERP, are superior to no treatment.
It has been suggested that HD may develop in response to early deprivation, both
emotional and material, but this has not been largely supported (Frost & Gross, 1993).Studies have shown abnormally high levels of trauma or stressful life events that, insome cases, occur prior to the onset or worsening of symptoms (Cromer, Schmidt,Murphy, 2007; Samuels et al., 2008). However, hoarding is a chronic disorder andthere is no evidence that hoarding can be explained as a response to stressors or losses(Mataix-Cols et al., 2010). The course of compulsive hoarding is typically chronic withhoarding behavior beginning decades before symptoms reach a clinical level (Samuelset al., 2008). No prospective studies have been completed but retrospective datasuggest that hoarding symptoms begin in childhood or early adolescence (Ayers,Saxena, Golsha, & Wetherell, 2009) and begin interfering with daily life by the mid-30s(Pertusa et al., 2008). It has also been suggested that acquisition has a later onset thandifﬁculty discarding or clutter (Grisham, Frost, Steketee, Kim, & Hood, 2006), possibly
due to means to acquire and a place to store possessions.
Treatment of compulsive hoarding has been described as challenging due to low
levels of insight, little motivation for treatment, and impaired cognitive functioning(Grisham & Barlow, 2005). In patients wit h OCD, the presence of hoarding symp-
toms is typically associated with refusal of treatment and higher dropout rates.Cognitive behavioral treatment, usually involving psychoeducation, practice in
decision making, and exposure components , is generally though to fa st h et r e a t m e n t
of choice for hoarding. Randomized contro lled trials are needed for this recently
deﬁned disorder.
TTM may occur at any age, from infancy through later life. Most research, however,
indicates an average age of onset at 12.9 years (Cohen et al., 1995; Grant, Odlaug &Kim, 2010; Lochner et al., 2010; Odlaug & Grant, 2008). TTM may interfere with socialrelationships, family life, and work, and has been associated with signi ﬁcant impair-
ment (Woods et al., 2006). Although there are studies on the long-term course of thedisorder, most data suggest that the course is chronic, with waxing and waningsymptom severity (Snorrason, Belleau, Woods, 2012). With regard to treatment,Flessner, Penzel, and Keuthen (2010) have identi ﬁed cognitive-behavioral treatment
as the treatment of choice for TTM. Although Habit Reversal Training (Azrin, Nunn, &Frantz, 1980) was initially posited as effective for TTM, failure to achieve greatersymptom reduction, with longer lasting effects, has led researchers to look at innerexperiences that may trigger hair pulling.
Experiential avoidance has been associated with more severe hair pulling and fear
of negative evaluation (Norberg, Wetterneck, Woods, & Conelea, 2007). Woods andcolleagues have evaluated the addition of Acceptance and Commitment Therapy(ACT) to traditional habit reversal and have shown signi ﬁcant reductions in
hair pulling that persisted to 3-month follow-up (Twohig & Woods, 2004; Woods,Wetterneck, & Flessner, 2006). Affective dysregulation has also been evaluated asplaying a role in TTM (Shusterman et al., 2009). Dialectical Behavior Therapy (DBT;Linehan, 1993a, 1993b) has also been combined with habit reversal training withpositive results. In a series of trials, Keuthen and colleagues have demonstrated an372 SPECIFIC DISORDERS

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inverse relationship between hair pulling severity and emotional regulation that haspersisted at both 3- and 6-month follow-up (Keuthen et al., 2010; Keuthen et al., 2011;Keuthen et al., 2012). Given these promising results, DBT-enhanced CBT for TTM shouldbe evaluated against other credible treatment interventions and at longer follow-up.
Research suggests that the age of onset for s kin picking varies considerably, with
onset from childhood through adulthood . Most research has shown an age of onset
from 12 to 16 years, with an average age across studies of 13.5 years (Flessner &Woods, 2006; Grant et al., 2007; Grant, Odlaug & Kim, 2010; Lochner et al., 2002).Symptoms appear to be similar regardless of age and no differences have beenreported in different cultures (Grant et al., 2012). The course of the disorder is alsovariable with most cases being chronic in nature with ﬂuctuating intensity. Patients
usually pick on a daily basis, often for a signi ﬁcant amount of time, and severity
tends to vary with life stressors (Snorraso n, Stein, Woods, 2013). Skin problems may
occur, including bleeding and soreness, wi th possibility of infection or permanent
skin damage.
Individuals with ED may experience mild to severe impairment in social, academic,
or occupational functioning. Treatment has largely focused on cognitive-behavioralinterventions and pharmacology (SSRIs). Habit reversal training has been used(Deckersbach et al., 2002), as well as habit reversal combined with acceptance andcommitment therapy (Siev, Reese, Timpano, & Wilhelm, 2012; Woods, Wetterneck,et al., 2006), both with promising results. Emotion dysregulation has been suggested tobe a factor in ED, which may lead to future research on treatment using DBTprocedures in conjunction with traditional CBT.C
ASESTUDIES
Ann is a 34-year-old female who is consumed by thoughts of germs, contamination,and sickness. She is constantly fearful that she may encounter bacteria or a virus thatwill cause her to become ill and ultimately lead to her death. She experiences intrusiveimages of herself lying in a hospital bed and of her own funeral. Despite attempting todisregard these thoughts and images, Ann is unable to control her need to clean andsterilize her surroundings to ensure she does not come into contact with germs. Annspends hours each day cleaning and disinfecting her home, often recleaning areas shehas just cleaned. She no longer allows friends or family to enter the home in an effort toprotect herself. Ann rarely leaves the house, except to purchase cleaning supplies or goto medical appointments. She is no longer able to work, experiences signi ﬁcant
ﬁnancial strain, and has little to no social life.
Tanya is a 22-year-old female who is preoccupied with the shape of her face. She
spends hours per day gazing into the mirror criticizing the odd shape of her face,mentally commenting on the asymmetrical angles of her cheekbones, the sharp pointof her chin, and the uneven hairline above her forehead. Friends and family areunaware of her preoccupation and believe that she is an ordinary, even attractive,looking female. Aside from spending hours critiquing herself in the mirror, Tanya isconstantly comparing her facial features to others around her, noting how pronouncedher perceived defects are compared to the perfection of others ’facial shapes. Despite
her attempts to hide the perceived ﬂaws using hairstyles, scarves, and makeup, Tanya
begins to experience passive suicidal ideation.Obsessive-Compulsive and Related Disorders 373

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Jack is a 67-year-old retired, widowed male. He spends the majority of his time
shopping at garage sales, exploring dumpsters for what he calls “treasures, ”and
shopping online. Despite an excessive accumulation of items, Jack is unable to discardanything in his home to make room for his new purchases. In fact, he experiences suchdifﬁculty parting with items, even boxes, newspapers, and broken tools, that he has
little room left in his home to live. Despite the urging of his family to de-clutter hishome and curb his shopping, Jack is unable to make the necessary changes due to thedistress he experiences attempting to make the changes. As a result, he is experiencingsigniﬁcant strain in his familial relationships and is at risk of losing his home due to his
inability to maintain city health codes.
Jess is a 29-year-old female who presented to her primary care doctor due to
frequent hair pulling. Speci ﬁcally, Jess reported that she ﬁnds herself pulling hairs out
of her scalp throughout the day, most frequently when engaged in stressful activitiessuch as dif ﬁcult work assignments. Initially, Jess was pulling out her hair infrequently;
however, she has begun to notice bald spots above her ears, where she pulls mostfrequently. People at work have begun to comment on the hair loss, asking if she isokay. She is very distressed by her behavior, and the attention it brings from others,but is experiencing dif ﬁculty stopping.
Tim is an 18-year-old male who frequently engages in skin picking. Speci ﬁcally,
Tim began by picking at an ingrown hair on his leg, which quickly progressed topicking at normal skin, lesions, and scabs all over his body. Initially, Tim used hisﬁngernails to pick, but has recently begun using tweezers, knives, and toothpicks.
Although he feels embarrassed by the scars, some of which are infected, Tim feels asthough he is unable to stop picking. His girlfriend of 2 years has been threatening tobreak up if he does not get some help.
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CHAPTER 10
Trauma and Stressor-Related
Disorders
Posttraumatic Stress Disorder, Acute Stress
Disorder, and Adjustment Disorders
ANOUK L. GRUBAUGH
THEDIAGNOSTIC AND Statistical Manual of Mental Disorders ,ﬁfth edition ( DSM-5 ;
American Psychiatric Association [APA], 2013) includes a chapter titled“Trauma and Stress-Related Disorders, ”which contains posttraumatic stress
disorder (PTSD), acute stress disorder (ASD), and the adjustment disorders. BothPTSD and ASD were previously classi ﬁed under the “Anxiety Disorders ”chapter of
theDSM-IV , whereas adjustment disorders were classi ﬁed separately as a residual
diagnostic category (APA, 1994). PTSD is broadly characterized as a psychiatricdisorder resulting from a life-threatening event and requires a history of exposureto a traumatic event (Criterion A) that results in a minimum threshold of symptomsacross four symptom clusters: intrusion, avoidance, negative alterations in cognitionsand mood, and alterations in arousal and reactivity (Criterion B through E). Addi-tional criteria concern duration of symptoms (Criterion F), functioning (Criterion G),and differential diagnosis due to a substance or other co-occurring condition(Criterion H).
For Criterion A, an event associated with PTSD must include actual or threatened
death, serious injury, or sexual violation resulting from one or more of the followingscenarios:
Directly experiencing the traumatic event.
Witnessing the traumatic event in person.
Experiencing the actual or threatened death of a close family member or friendthat is either violent or accidental.
Directly experiencing repeated and extreme exposure to aversive details of theevent (i.e., the type of exposures frequently encountered by police of ﬁcers and
ﬁrst responders).
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With regard to criteria B through E, an individual must report symptoms from each
of the four symptom clusters. Intrusion symptoms (Criterion B) include repetitive,
involuntary, and intrusive memories of the event; traumatic nightmares; dissociativereactions (i.e., ﬂashbacks) along a broad continuum; intense prolonged distress after
exposure to reminders of the trauma; and heightened physiological reactivity toreminders of the trauma. Avoidance symptoms (Criterion C) include avoidance of
trauma-related thoughts or feelings; and avoidance of people, places, activities,and so forth that cue distressing thoughts or feelings about the traumatic event.Negative alterations in cognitions and mood symptoms (Criterion D) include a persistent
and distorted sense of self or the world; blame of self or others; persistent trauma-related emotions such as anger, guilt, shame; feeling estranged or detached fromothers; marked lack of interest in pretrauma activities; restricted range of affect; anddifﬁculty or inability remembering important parts of the traumatic event. Finally,
alterations in arousal and reactivity symptoms (Criterion E) include irritability and
aggressiveness self-destructive or reckless behaviors, sleep dif ﬁculties, hyper-
vigilance, marked startle response, concentration dif ﬁculties, and sleep disturbance.
For a diagnosis of PTSD an individual must exhibit at least one symptom from
Criterion B, one symptom from Criterion C, two symptoms from Criterion D, and twosymptoms from Criterion E, and the symptoms endorsed in categories B through Emust persist for 1 month or longer (Criterion F). The symptoms must also beaccompanied by signi ﬁcant distress or impairment in social, occupational, or other
important life domains (Criterion G), and symptoms cannot be better explained byanother medical or psychiatric illness (Criterion H).
The DSM-5 includes two additional speci ﬁers or associated features that can be
added to a PTSD diagnosis: “with dissociated symptoms ”and“with delayed expres-
sion.”The dissociated symptoms speci ﬁer includes either depersonalization (i.e., expe-
rience of being an outside observer to one’ s experience or feeling detached from
oneself) or derealization (i.e., experience of unreality or distortion) in response to
trauma-related cues. The delayed onset speciﬁ er includes an onset of symptoms that
can occur immediately after the trauma, but that may not meet full criteria for PTSDuntil at least six months after the trauma.
Some notable changes were made to the diagnostic criteria for PTSD from DSM-IV
(APA, 1994) to DSM-5 . In addition to the inclusion of speci ﬁers for depersonalization
and derealization, the DSM-5 provides greater speci ﬁcation regarding what events
constitute a traumatic event (i.e., what events constitute a Criterion A event); andexcludes the need for an individual to have experienced intense fear, helplessness, orhorror at the time of the trauma due to its lack of predictive utility. Additionally, theavoidance/numbing symptom cluster found in the DSM-IV is divided into two
distinct clusters in the DSM-5 :avoidance and negative alterations in cognitions and
mood . The latter of these clusters retain most of the DSM-IV numbing symptoms
while also including a broader range of emotional reactions. Last, Criterion E,alterations in arousal and reactivity, retains the majority of DSM-IV arousal symptoms
but also includes additional symptoms regarding aggressive or reckless behavior.
A diagnosis of acute stress disorder (ASD) requires an antecedent event (Criterion
A event) in which the person:
Experienced an event or events that involved a threat of death, actual orthreatened serious injury, or actual or threatened physical or sexual violation.388 S
PECIFIC DISORDERS

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Witnessed an event or events that involved the actual or threatened death,serious injury, or physical or sexual violation of others.
Learned of such harm coming to a close relative or friend.
Experienced repeated or extreme exposure to aversive details of unnatural death,serious injury, or serious assault or sexual violation of others that were notlimited to electronic media, television, video games, and so forth.
Individuals must then exhibit a minimum of 9 out of 14 symptoms across a broad
spectrum of posttraumatic reactions (Criterion B). This spectrum includes symptomsrelated to negative mood, intrusive thoughts, dissociation, avoidance, and anxiety.Aside from a greater emphasis on dissociative symptoms, the other Criterion Bsymptoms for ASD largely mirror the Criterion B through E symptoms for PTSD.Additional criteria for ASD concern duration of symptoms (Criterion C), functioning(Criterion D), and differential diagnosis due to a substance or other co-occurringcondition (Criterion E).
Changes to the diagnostic criteria of ASD from DSM-IV toDSM-5 include less
emphasis on dissociative criteria (i.e., feeling detached from one’ s body, emotions, or
the world). Rather than being required for a diagnosis as was the case in the DSM-IV ,
dissociative symptoms in DSM-5 are viewed as one of several possible posttraumatic
reactions that an individual may experience. Comparable to changes to the diagnosticcriteria for PTSD, the DSM-5 provides more speci ﬁcation regarding the qualifying
traumatic event for ASD; and the criterion requiring a subjective reaction to the trauma(i.e., fear, helplessness, horror) was eliminated.
Adjustment disorders are classi ﬁed in the DSM-5 as a range of stress response
syndromes. This differs from the DSM-IV in which adjustment disorders were part of
a residual category for individuals experiencing clinically signi ﬁcant distress that did
notﬁt diagnostic criteria for other psychiatric disorders. Speci ﬁcDSM-5 criteria for an
adjustment disorder include: (a) the development of emotional or behavioral problemsin response to an identi ﬁable stressor occurring within 3 months of exposure to the
stressor (this feature is considered the core feature of adjustment disorders;(b) symptoms or behaviors are clinically signi ﬁcant and out of proportion to the
severity of the stressor once cultural and contextual factors are taken into account.Additionally, the stress response (a) cannot be better accounted for by anotherdisorder and is not an exacerbation of a preexisting condition; (b) is not indicativeof normal bereavement (if this is the precipitating event); and (c) once the stressor isremoved, the symptoms do not persist for more than 6 additional months. Diagnosticspeciﬁers for the adjustment disorders include depressed mood, anxiety, mixed
anxiety and depressed mood, disturbance of conduct, mixed disturbance of emotionsand conduct, and unspeci ﬁed.
Whereas PTSD and ASD emphasize fear and anxiety responses, adjustment
disorders can accommodate a broader range of stress reactions. Second, althoughthere is an explicit potential for ASD to predict subsequent impairment (i.e., to predictthe development of PTSD), an adjustment disorder is typically viewed as a discretedisorder that has a fairly immediate onset and is relatively short in duration. A thirddistinction between PTSD, ASD, and adjustment disorders regards the timing ofdiagnosis. Adjustment disorders can be diagnosed immediately after the event, ASDcan be diagnosed from 2 days to up to 1 month after the event, and PTSD can bediagnosed from 1 month to several years after the trauma.Trauma and Stressor-Related Disorders 389

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CLINICAL FEATURES
The clinical expression of PTSD can vary signi ﬁcantly in terms of severity. Although
the diagnosis is categorical, there is evidence of a dimensional structure to PTSD(Broman-Fulks et al., 2006; Forbes, Haslam, Williams, & Creamer, 2005; Ruscio,Ruscio, & Keane, 2002). An implication of this dimensional structure is that mildersymptoms of PTSD may cause signi ﬁcant distress and impairment. Indeed, one study
found that veterans with subthreshold PTSD underutilize mental health care, despiteincreased psychiatric comorbidity and impairment relative to veterans without PTSD(Grubaugh et al., 2005). Yet other studies using samples of Operation Iraqi Freedom(OIF) and Operation Enduring Freedom (OEF) veterans have found an associationbetween subthreshold PTSD and elevated levels of anger and hostility, physical healthfunctioning, and an increased likelihood of hopelessness and suicidal ideation relativeto those without PTSD (Jakupcak et al., 2011). Among civilians, subthreshold PTSDhas likewise been associated with levels of impairment and suicidality that areequivalent to those with full PTSD (Zlotnick, Franklin, & Zimmerman, 2002).
Suicidality is elevated among individuals with PTSD (Panagioti, Gooding, &
Tarrier, 2009; Jakupcak et al., 2011), and particular types of trauma, such as childhoodabuse, military sexual trauma, and combat, may be more strongly associated withsuicidality than others (A ﬁﬁet al., 2008; Kimerling, Gima, Smith, Street, & Frayne,
2007). Additionally, increased risk of suicidality is uniquely associated with PTSD(Sareen, Houlahan, Cox, & Asmundson, 2005; Sareen et al., 2007). That is, thisassociation is not solely accounted for by the presence of other psychiatric conditionscommonly found with PTSD. Of course, an increased risk of suicidality is present in anumber of other psychiatric conditions to a comparable or greater degree than thatfound in PTSD (Nock, Hwang, Sampson, & Kessler, 2010).
The clinical picture of acute stress disorder (ASD) is similar to that of PTSD.
Additionally, a review on the topic found that at least half of trauma survivors withASD subsequently met criteria for PTSD (Bryant, Friedman, Spiegel, Ursano, & Starin,2011). This ﬁnding suggests that individuals with ASD are, in fact, at higher risk of
subsequently developing PTSD. Conversely, however, the majority of individualswho subsequently develop PTSD do not initially meet criteria for ASD, suggesting thatASD (using DSM-IV criteria) is not highly speci ﬁc with regard to its predictive utility.
Additional ﬁndings suggest that the predictive power of ASD is increased when
subthreshold symptoms are used and the dissociative symptoms required for DSM-IV
are relaxed (Bryant et al., 2011). These and similar ﬁndings likely in ﬂuenced the
decreased emphasis in DSM-5 on dissociation symptoms in favor of accepting a
broader symptom presentation and one that more closely mirrors the symptomsassociated with PTSD.
Due to the conceptualization of adjustment disorders as fairly time limited, as well
as their history as a nebulous, catch-all diagnostic category, they have not been wellstudied in the psychiatric literature. The ﬁndings that do exist largely consist of non-
U.S. samples, focus on children or adolescents, and/or were published in the 1980sand early 1990s. Some commonly agreed upon emotional signs of adjustment dis-orders are sadness, hopelessness, lack of enjoyment, crying spells, nervousness,anxiety, worry, trouble sleeping, dif ﬁculty concentrating, feeling overwhelmed,
and thoughts of suicide. Some behavioral signs of adjustment disorders include390 SPECIFIC DISORDERS

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ﬁghting, reckless behaviors, neglecting important tasks or responsibilities, and avoid-
ing family or friends. Although the presence of an adjustment disorder has been linkedto increased suicidal ideation and risk of suicide (e.g., Portzky, Audenaert, & Van-heeringen, 2005; Taggart et al., 2006), they are often considered less severe than otherpsychiatric disorders. Supporting this view, one study found that adjustment dis-orders range in severity between no psychiatric disorder and the presence of a moodor anxiety disorder (Fernandez et al., 2012).
DIAGNOSTIC CONSIDERATIONS
Comorbidity is a concern when diagnosing PTSD. Large nationally representativesamples have found that PTSD is signi ﬁcantly correlated with the majority of mood
and anxiety disorders, as well as alcohol use disorders (National Comorbidity SurveyReplication [NCS-R]; Kessler, Chiu, Demler, & Walters, 2005; National ComorbiditySurvey [NCS]; Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995). Data from theNCS-R found that approximately half of those who met criteria for PTSD also metcriteria for at least three additional psychiatric diagnoses (Kessler et al., 1995).
Although there is some degree of symptom overlap between PTSD and otherpsychiatric diagnoses (e.g., sleep and concentration difﬁ culties and diminished
interest in activities are common to both depression and PTSD), this overlap doesnot account for the high rate of comorbidity (Elhai, Grubaugh, Kashdan, & Frueh,2008). When comorbid with mood disorders, PTSD is more likely to be primary,whereas it is more likely to be secondary when comorbid with anxiety disorders(Kessler et al., 1995). Importantly, PTSD and comorbid diagnoses may change overtime within a given individual. A study of trauma survivors found that half of thosewho reported PTSD only at 3-month follow-up reported depression only at 12-monthfollow-up; likewise, half of those with depression only at 3-month follow-up reportedPTSD only at 12-month follow-up (O ’Donnell, Creamer, & Pattison, 2004).
Due to the lack of epidemiological studies speciﬁ c to ASD or the adjustment
disorders, there are few reliable data on the clinical comorbidity associated with thesedisorders. Given the conceptual overlap between ASD and PTSD, it is likely thatindividuals with ASD experience high rates of mood, anxiety, and substance disordersrelative to the general population, as well as an increased risk of suicidality. As notedelsewhere, adjustment disorders in the DSM-IV served as a residual “catch-all ”
diagnostic category once other psychiatric conditions were ruled out. As such,they are seldom diagnosed with other psychiatric conditions. With this restrictionin mind, adjustment disorders have most often been linked in adult samples to acomorbid diagnosis of a personality disorder, substance use disorder, and increasedsuicidality (Dowrick et al., 1998; Greenberg, Rosenfeld, & Ortega, 1995; Polyakova,Knobler, Ambrumova, & Lerner, 1998; Strain et al., 1998).
EPIDEMIOLOGY
In the general population, the 12-month and lifetime prevalence of PTSD is 3.5 and6.8%, respectively (Kessler, Burglund, Demler, et al., 2005; Kessler et al., 2005). Pointprevalence of PTSD among U.S. combat veterans is estimated to be between 2% andTrauma and Stressor-Related Disorders 391

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17%, depending on the characteristics of the sample and the measurement strategiesthat were used (Richardson, Frueh, & Acierno, 2010). There are different conditionalprobabilities of developing PTSD by trauma type. For example, combat exposure andphysical and sexual abuse are more often associated with PTSD than other types oftrauma. Despite this variability, the symptom expression of PTSD remains fairlyconsistent regardless of the type of trauma experienced.
Little is known regarding the prevalence of ASD and the adjustment disorders in
the general population. Large-scale epidemiological studies, such as the World HealthOrganization (WHO) Mental Health Epidemiologic Survey, the Epidemiologic Catch-ment Area study, and the National Comorbidity Survey Replication, did not report onthese disorders. Rates of ASD in community and clinical samples range from 7% to ashigh as 28% with a mean rate of 13% (Bryant et al., 2011), and rates of ASD are typicallyhigher among victims of violent versus nonviolent traumas. When subsyndromalcases of ASD are included, estimates of the disorder increase from 10% to 32% with amean rate of 23% (Bryant et al., 2011).
There are few reliable ﬁndings on the prevalence of adjustment disorders. This gap
in knowledge is likely in ﬂuenced by the poor delineation between adjustment
disorders and normal or adaptive stress responses, as well as the use of adjustmentdisorders as a residual “last resort ”diagnostic category in the DSM-IV . One epide-
miological study, the European Outcome of Depression International Network, founda 1% prevalence of adjustment disorder with depressed mood (ODIN; Ayuso-Mateoset al., 2001). More circumscribed samples of adults suggest adjustment disorders aremore common in hospital psychiatric consultation settings (12%; Strain et al., 1998;18.5%; Foster & Oxman, 1994) and among psychiatric inpatient admissions (Koranet al., 2002). A recent meta-analysis found prevalence rates of 15.4% and 19.4% inpalliative care and oncology settings, respectively (Mitchell et al., 2011).
PSYCHOLOGICAL AND BIOLOGICAL ASSESSMENT
There are a number of diagnostic measures for assessing PTSD.
Although revisions are underway, these measures re ﬂectDSM-IV , rather than
DSM-5, criteria for PTSD. The Clinician-Administered PTSD Scale (CAPS; Weathers,
Keane, & Davidson, 2001) is the most common interviewer-based instrument for PTSDand has robust psychometric properties (Weathers et al., 2001). The CAPS includes adetailed assessment of each traumatic event, frequency and severity ratings for eachsymptom, and overall distress and impairment ratings. Several CAPS scoring algo-rithms have demonstrated good diagnostic utility (Weathers, Ruscio, & Keane, 1999).A common scoring method is to score a symptom as present if the frequency is greaterthan or equal to 1 and the intensity is greater than or equal to 2, and to further requirethe endorsement of a suf ﬁcient number of symptoms for each symptom cluster. This
method favors sensitivity (0.91) over speciﬁ city (0.71), and thus may be better for
screening purposes. Using a total dimensional cut-score of greater than or equal to 65,on the other hand, favors speciﬁ city (0.91) over sensitivity (0.82), and thus may be
better for con ﬁrming a diagnosis (Weathers et al., 1999). Other interview measures
include the PTSD Symptom Scale –Interview (PSS-I; Foa & Tolin, 2000) and the
Structured Interview for PTSD (SI-PTSD; Davison, Smith, & Kudler, 1989).392 SPECIFIC DISORDERS

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Additionally, the Structured Clinical Interview for DSM-IV (SCID-IV; First, Spitzer,
Gibbon, & Williams, 1996) and the Anxiety Disorders Interview Schedule (ADIS-IV;Brown, Di Nardo, & Barlow, 1994) contain a module for assessing the presence orabsence of PTSD.
Self-report questionnaires may also be used to assess PTSD. Commonly used
measures include the PTSD Checklist (Blanchard, Jones-Alexander, Buckley, &Forneris, 1996), the PTSD Symptom Scale –Self-Report (PSS-SR; Foa, Riggs, Dancu, &
Rothbaum, 1993), and the Posttraumatic Diagnostic Scale (PDS; Foa, Cashman,Jaycox, & Perry, 1997). An extensive list of measures used to assess PTSD is availablefrom the National Center for PTSD (www.ptsd.va.gov). As already noted, thesemeasures are being revised to re ﬂect recent changes to the diagnostic criteria of
PTSD in DSM-5.
Aside from interview and self-report measures of PTSD, several physiological
variables have been found to distinguish current PTSD from lifetime PTSD and theabsence of PTSD. These include an increased resting heart rate, an increased responseto non-trauma-related stressors, and increased heart rate, skin conductance, anddiastolic blood pressure in response to trauma cues (Pole, 2007). However, thediagnostic utility of these physiological variables is limited in that they tend to beless accurate in predicting PTSD than interview-based and self-report assessments.
There are few empirically validated diagnostic measures for ASD or adjustment
disorders. Measures designed speci ﬁcally for ASD include the Acute Stress Disorder
Interview and the Acute Stress Disorder Scale, both developed by the same group ofinvestigators (ASDI, ASDS; Bryant, Harvey, Dang, Sackville, & Basten, 1998). TheSCID-IV contains an optional module for ASD, as well as a section on adjustmentdisorders that speci ﬁes the diagnosis should not be made if the criteria for any other
psychiatric disorders are met (First et al., 1996). With regard to physiological mea-sures, there are some data indicating that individuals who subsequently developPTSD have higher heart and respiration rates immediately post-trauma relative tothose who do not (Bryant et al., 2011). However, these data are not limited toindividuals with ASD, and are likely hampered by the same classi ﬁcation precision
of these measures for PTSD.
ETIOLOGICAL CONSIDERATIONS
A number of causal mechanisms have been implicated in the development of PTSD.These include genetic factors, brain structure and neurochemical abnormalities, pre-and post-trauma life events, cognitive appraisals and attentional biases, and socio-demographic variables such as gender.B
EHAVIORAL AND MOLECULAR GENETICS
Among Vietnam era veterans, the risk of developing PTSD has been explained by (a) agenetic factor common to alcohol use and PTSD, (b) a genetic factor associated withPTSD but not with alcohol use, and (c) unique environmental effects (Xian et al., 2000).Yet another twin study of Vietnam era veterans found that the genetic factors thataccounted for the relationship between combat exposure and PTSD also accounted forthe relationship between combat exposure and alcohol use (McLeod et al., 2001).Trauma and Stressor-Related Disorders 393

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Genetic factors contributed more to the relationship between combat exposure andPTSD as compared to environmental factors, whereas genetic and environmentalfactors contributed equally to the relationship between combat exposure and alcoholuse. Interestingly, the genetic factors that account for the presence of PTSD may alsoinﬂuence exposure to certain types of traumatic events. Concordance of both inter-
personal violence and PTSD is higher among monozygotic twins compared todizygotic twins, whereas other types of trauma (i.e., natural disasters, motor vehicleaccidents) are not accounted for by genetic factors (Stein, Jang, Taylor, Vernon, &Livesley, 2002).
In terms of speciﬁ c genetic markers, the 5-HTTLPR polymorphism has been
associated with an increased risk of developing PTSD in speciﬁ c groups of trauma
survivors including hurricane survivors with a high degree of exposure (Kilpatricket al., 2003) and individuals reporting a traumatic event in childhood as well asadulthood (Xie et al., 2009). A similar interaction has been reported for variants ofpolymorphisms in the FK506 binding protein 5 (FKBP5) gene, which is involved inregulating the intracellular effects of cortisol. Individuals with these variants, whoreported severe child abuse, were found to be at increased risk for developing PTSDafter experiencing a traumatic event in adulthood (Binder et al., 2008; Xie et al., 2009).This gene was underexpressed among survivors of the September 11, 2001 attacks onthe World Trade Center who developed PTSD compared to those who did not(Yehuda et al., 2009). There is evidence for candidate genes in other systems (e.g.,the dopamine system), but ﬁndings have been limited or inconsistent (Broekman,
Olff, & Boer, 2007; Koenen, 2007; Nugent, Amstadter, & Koenen, 2008). Geneticresearch on the trauma and stress related disorders of the DSM-5 are limited to PTSD.
N
EUROANATOMY AND NEUROBIOLOGY
Several brain structures have been implicated in PTSD, including the amygdala, themedial prefrontal cortex, and the hippo campus. First, PTSD is associated with
increased activation in the amygdala in respo nse to trauma-related stimuli (Francati,
Vermetten, & Bremner, 2007). This increased activity likely represents the neuralsubstrates of exaggerated fear acquisition and expression and may explain thesalience of trauma memories in PTSD (Rauc h, Shin, & Phelps, 2006). Importantly,
hyperactivity in the amygdala is not unique to PTSD; increased activity in responseto disorder-related stimuli has also been noted in speci ﬁcp h o b i aa n ds o c i a la n x i e t y
disorder (Etkin & Wagner, 2007; Shin & Liberzon, 2010). Second, PTSD is associatedwith de ﬁcient functioning in the medial prefrontal cortex (Francati et al., 2007;
Shin & Liberzon, 2010). This de ﬁciency is thought to underlie inadequate top-down
modulation of the amygdala (Rauch et al., 2 006). Moreover, the medial prefrontal
c o r t e xi st h o u g h tt or e g u l a t ep r o c e s s e st h a ta r ei m p o r t a n tf o rh a b i t u a t i o na n dextinction of fear responses, including emotional appraisal (Liberzon & Sripada,2008). Third, PTSD is associated with abnormalities in the hippocampus. Theseabnormalities may underlie dif ﬁculties contextualizing memories (e.g., recognizing
that certain contexts are safe; Liberzon & Spirada, 2008; Rauch et al., 2006). A meta-
analysis concluded that increased PTSD severity is associat ed with decreased
volume of the hippocampus, as well as decreased volume in the amygdala andthe anterior cingulate, a stru cture in the medial prefrontal cortex (Karl et al., 2006).394 S
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Decreased hippocampal volume likely represents a risk factor for developing PTSD,as opposed to a neurobiological effect of trauma (McNally, 2003). Consistent withthis, hippocampal volume does not change over time following trauma exposure(Bonne et al., 2001). Moreover, a study of v eteran twin pairs discordant for combat
exposure and PTSD found that PTSD severity among affected twins was negativelycorrelated with not only their own hippocampal volume but also that of theirnonexposed twin (Gilbertson et al., 2002).
The neurochemical underpinnings of P TSD likely involve catecholamines
(epinephrine, norepinephrine, and dop amine) and cortisol, a hormone involved
in the neuroendocrine response to stress, as well as a variety of other neuro-transmitters (Yehuda, 2006). PTSD may a lso be characterized by disturbance of
the hypothalamic-pituitary-adrenal axis, arising primarily from hypersensitivity
of glucocorticoid (i.e., cortisol) recepto rs (Yehuda et al., 2009). This may represent
a risk factor, although the research ﬁndings are not yet clearly integrated into a
cohesive model.
There are few data speciﬁ cally reporting on neurobiological models of ASD or
adjustment disorders. When viewed as a stress reaction conceptually related to PTSD,ASD in particular may also involve a dysregulation of the neurotransmitter andneuroendocrine systems implicated in PTSD. Quite possibly as well, ASD may involvedeﬁcits in certain brain regions such as the hippocampus, which are implicated as a
risk factor for PTSD.L
EARNING ,MODELING ,ANDLIFEEVENTS
Clearly, traumatic life events contrib ute to PTSD. Less clear is whether trauma
exposure and PTSD share a dose-response relationship in which frequency and/or
intensity of trauma correspond with sym ptom severity. Rates of PTSD vary based
o nt h et y p eo ft r a u m a t i ce v e n t ,w i t ha s s a ultive violence and sexual assault being
associated with the highest rates (Breslau et al., 1998; Norris, 1992). Furthermore,
rates of PTSD among Vietnam era veterans roughly correspond to degree ofcombat exposure (Dohrenwend et al., 2006). However, PTSD severity has notb e e nf o u n dt oc o r r e s p o n dt os e v e r i t yo fe xposure in other trauma samples such as
motor vehicle accident survivor s and political prisoners (Bas ̧og ̆lu et al., 1994;
Schnyder, Moergeli, Klaghofer, & Buddeberg, 2001). Importantly, a dose-responserelationship between trauma exposure and PTSD may be nonlinear. That is, after acertain degree of trauma exposure, symptom exacerbation may reach a plateau(McNally, 2003).
PTSD may also be related to degree of trauma exposure prior to the traumatic event.
Exposure to childhood physical or sexual abuse is associated with an increased risk offuture trauma exposure, as well as the development of PTSD in response to thosesubsequent traumas (Koenen, Mof ﬁtt, Poulton, Martin, & Caspi, 2007). In addition to
previous childhood abuse or neglect, meta-analyses on the topic have identi ﬁed other
pre-trauma risk factors for PTSD, such as level of prior psychological adjustment and/or the presence of a previous personal or family history of psychiatric illness. Post-trauma risk factors include a lack of social support and additional life stressors(Brewin, Andrews, & Valentine, 2000; Keane, Marshall, & Taft, 2006; Ozer, Best,Lipsey, & Weiss, 2008).Trauma and Stressor-Related Disorders 395

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Few studies have examined risk factors speci ﬁcally in relation to the development
ASD or adjustment disorders. However, given the conceptual overlap between PTSDand ASD, they likely share similar pre- and post-trauma risk factors. Supporting thisline of reasoning, one study found that individuals with a previous history of traumaexposure or PTSD and those with more psychiatric dysfunction were at greater risk fordeveloping ASD when experiencing a new trauma (Barton, Blanchard, & Hickling,1996). Speci ﬁc to adjustment disorders, there is some indication of a greater risk of the
disorder among individuals from disadvantaged backgrounds, but virtually nosystematic data on the topic (APA, 1994).C
OGNITIVE INFLUENCES
Cognitive in ﬂuences of PTSD include maladaptive beliefs that one holds about the
meaning of the traumatic event that is experienced (e.g., self-blame, guilt).Consistent with this view, cognitive pro cessing therapy (CPT) emphasizes the
importance of identifying and revising ma ladaptive beliefs about the trauma and
promoting a more balanced integration o f the traumatic event (Resick & Schnicke,
1993). Other possible cognitive mechan isms of PTSD include attentional or mem-
ory related biases toward threat-related st imuli or trauma-related material, which
may speci ﬁcally re ﬂect a cognitive vulnerability to developing PTSD (Brewin &
Homes, 2003; Thrasher & Dalgleish, 1999; Weber, 2008). PTSD may also beinﬂuenced by perceived seriousness of threat, which in turn may be in ﬂuenced
by cognitive variables such as poor contex tualization of autobiographical memory
(Ehlers & Clark, 2000). Although not speci ﬁct oA S D ,an u m b e ro fs t u d i e sh a v e
found that maladaptive or negative appraisals and beliefs predict the subsequentdevelopment of PTSD (Bryant, Salmon, Sinclair, & Davidson, 2007; Mayou,Bryant, & Ehlers, 2001).S
EX AND RACIAL -ETHNIC CONSIDERATIONS
Epidemiological surveys suggest that women are more likely to report sexual assaultor child molestation and men are more likely to report physical assault, combatexposure, or being threatened or attacked with a weapon (Norris et al., 1992).Prevalence studies of PTSD further indicate that women are more likely to developPTSD relative to men (at a 2:1 ratio) given exposure to a traumatic event (Norris et al.,2002). That is, women have a higher conditional risk of developing PTSD relative tomen. Traumas associated with ASD are similar to those for PTSD. However, system-atic efforts are needed to con ﬁrm whether gender differences in rates of ASD are
comparable to those associated with PTSD.
Findings regarding the interplay between trauma exposure, PTSD, and race/
ethnicity are often mixed (Pole, Gone, & Kulkarni, 2008). Overall, however, moststudies have found comparable rates of PTSD between African Americans andCaucasians. The few studies that have found signi ﬁcant racial/ethnic differences
report higher base rates of PTSD among African Americans relative to Caucasians thatlargely disappear once severity of trauma exposure is controlled for. The mostconsistent ﬁndings regarding PTSD and race/ethnicity pertain to Hispanics. Relative396 S
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to non-Hispanic Caucasians, Hispanics often have higher rates of PTSD in bothcommunity and clinical samples (Pole et al., 2008). Cultural context may in ﬂuence
some aspects of PTSD, but the disorder generally presents as a coherent group ofsymptoms across cultures. Parallel efforts to study the relationship between race/ethnicity in both ASD and adjustment disorders are lacking.
COURSE, PROGNOSIS, AND TREATMENT
According to the DSM-5 , symptoms consistent with a diagnosis of PTSD may begin
immediately following or long after a traumatic event, and there is suf ﬁcient evidence
that PTSD can persist for several years after the index trauma. The diagnostic speci ﬁer
“with delayed expression ”allows for a diagnosis of PTSD when all of the criteria for
the disorder are not met for 6 months or longer after the traumatic event. Althoughcases of delayed onset PTSD have been noted in the literature, these ﬁndings are likely
due to an exacerbation of prior symptoms over time. Supporting this view, a review onthe topic found that delayed-onset PTSD in the complete absence of prior symptomswas rare (Andrews, Brewin, Philpott, & Stewart, 2007), a conclusion that otherempirical studies have since supported (Frueh, Grubaugh, Yeager, & Magruder, 2009).
Parallel with its theoretical underpinnings, clinical practice guidelines generally
recommend cognitive behavioral interventions as the most effective treatmentapproach for PTSD (DVA, 2010; Foa, Keane, & Friedman, 2009; IOM, 2007; NICE,2005). Treatments that fall under this umbrella typically include elements of psycho-education, stress reduction, exposure to trauma-related cues and memories, andcognitive restructuring, with the latter two components being considered the “active
ingredients ”for PTSD symptom reduction.
Although there are a number of interventions that emphasize exposure and/or
cognitive restructuring, the empirical data weigh heavily in support of two speci ﬁc
manualized treatments for adults with PTSD: Prolonged Exposure (PE; an exposure-based intervention; Foa, Hembree, & Rothbaum, 2007) and Cognitive ProcessingTherapy (CPT; predominantly a cognitive restructuring intervention that includeselements of exposure; Resick & Schnicke, 1993). The focus in PE is on habituation tograded fear exposures, whereas the focus in CPT is on modiﬁ cation of maladaptive
trauma-related beliefs (e.g., denial or self-blame). However, CPT often includesexposure exercises, and PE often includes elements of cognitive restructuring. Addingcognitive restructuring to PE does not appear to increase its ef ﬁcacy (Foa et al., 2005),
nor does adding writing exposure exercises to CPT (Resick et al., 2008), indicating thatthe therapies are ef ﬁcacious in both their combined and component forms. Reviews on
the topic suggest the average patient receiving PE or CPT fares better than 86% to 90%of patients who are assigned to a control group (i.e., do not receive what is consideredan active treatment) (Bradley, Greene, Russ, Dutra, & Westen, 2005; Powers, Halpern,Ferenschak, Gillihan, & Foa, 2010). Despite the overall ef ﬁcacy of PTSD interventions,
18% to 35% of individuals who complete treatment retain the diagnosis at follow-up,with civilians showing dramatically greater improvement than military veterans(Bradley et al., 2005). Disability incentives to remain ill have been posited as onepossible reason why veterans evidence less clinical improvement than civilians (Frueh,Grubaugh, Elhai, & Buckley, 2007), as have other characteristics unique to veteranTrauma and Stressor-Related Disorders 397

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populations (e.g., nature of combat trauma). Additionally, treatment dropout rateshover around 30% across clinical populations (Cloitre, 2009).
Reﬂecting neurobiological models of the di sorder, pharmacological treatments
for PTSD act primarily on the neurotransmit ters associated with fear and anxiety,
which include serotonin, norepinephri ne, GABA, and dopamine. Selective sero-
tonin reuptake inhibitors (SSRIs) are gen erally considered the pharmacological
treatment of choice for PTSD (DVA, 2010; Stein, Ipser, & McAnda, 2009), and thisclass of drugs include the only two medic ations that are currently FDA approved
for the treatment of PTSD —sertraline (Zoloft) and paroxetine (Paxil). Although
there is some support for the ef ﬁcacy of psychotropic medications for the treatment
of PTSD, not all practice guidelines support their use. For example, after a review of37 PTSD pharmacotherapy trials, the Institute of Medicine determined that therewas insuf ﬁcient evidence in support of any psychotropic medications for PTSD
including SSRIs (IOM, 2007). Additionally, psychotropic medications do nottypically alleviate all the symptoms associated with this disorder and it is generallyrecommended that patients take medications in conjunction with a psychotherapyspeciﬁcally developed to treat PTSD, part icularly with more complex symptom
presentations.
Brief cognitive behavioral interventions immediately posttrauma have yielded
promising results in terms of preventing the subsequent development of PTSD amongthose with ASD (Bryant, Sackville, Dang, Moulds, & Guthrie, 1999; Bryant, Moulds,Nixon, & Basten, 2003; Echeburua, deCorral, Sarasua, & Zubizarreta, 1996; Gidronet al., 2001). These interventions generally consist of education about symptoms,relaxation training, exposure exercises, and cognitive therapy. In contrast, psycholog-ical debrie ﬁng interventions, which were sometimes used in the aftermath of trau-
matic events like natural disasters, have failed to demonstrate suf ﬁcient ef ﬁcacy and
are generally contraindicated with more severe traumas or posttraumatic reactions(Forneris et al., 2013; North & Pfefferbaum, 2013).
Due to the acute nature of most adjustment disorders, they often do not require
treatment or require limited treatment. A dditionally, however, the high degree of
variability in the symptom expression of adjustment disorders has likely compli-cated the development of standardized treatment approaches. Consistent with this,systematic investigations on the ef ﬁcacy of speciﬁ c interventions for adjustment
disorders are limited to two randomized controlled trials, one targeting adjustmentdisorder with depressed mood secondary t o myocardial infarction (Gonzales-
Jaimes & Turnbull-Plaza, 2003) and another targeting adjustment disorder resultingin occupational dysfunction (van der Klin k, Blonk, Schene, & van Dijk, 2003). Both of
these interventions were tailored for a speci ﬁc target population and anticipated
deﬁcits, with the ﬁrst demonstrating ef ﬁcacy of the intervention in terms of
symptom reduction and the latter in terms of decreasing absenteeism but notsymptom reduction. Pharmacotherapy trials for the treatment of adjustment dis-orders are likewise few in number and have not established the superiority ofantidepressants versus placebo for symptom reduction (Casey, 2009; Casey, Pillay,Wilson, et al., 2013). Less systematic effor ts and clinical wisdom would suggest that
psychosocial treatments for adjustment disorders should be relatively brief induration and focus on decreasing or remo ving the stressor as well as improving
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IMPLICATIONS OF THE DSM-5
The development of a trauma and stress-related chapter in the DSM-5 will help
emphasize PTSD, ASD, and adjustment disorders as stress responses along a contin-uum that are clearly linked to an antecedent event. It is unlikely that prevalence ratesof PTSD or ASD will change signi ﬁcantly as a result of changes made to their
diagnostic criteria in DSM-5. However, the decreased emphasis in the DSM-5 on
dissociation symptoms for ASD will likely improve the disorder ’s ability to predict the
subsequent development of PTSD. Re ﬁnements to the diagnostic criteria of adjust-
ment disorders and its placement in a chapter with other stress reactions, rather than aresidual diagnostic category, may increase providers ’use of the diagnosis in clinical
practice. Additionally, it may encourage more systematic research on adjustmentdisorders, both as an independent diagnosis and in relation to PTSD and ASD.
CASE STUDIES
Paul is a 26-year-old African American Iraq War veteran who presented to his local VAprimary care clinic due to feelings of anxiety. Paul served two tours of duty in Iraq andwitnessed multiple roadside bombings in which members of his unit were injured andkilled. His ﬁnal tour ended 2 years ago. He reports symptoms that began shortly after
theﬁrst roadside bombing he witnessed while overseas and an increase in the severity
and frequency of these symptoms since his return to the U.S. He experiences frequentnightmares and intrusive memories about Iraq, including nightmares and unwantedthoughts related to a bombing in which he witnessed the death of two of his comradeswith whom he was particularly close. Paul questions in his mind why he lived whilehis comrades died and feels certain that he should have been able to prevent whathappened. He avoids internal and external reminders of the event, which includethinking about the bombings and other graphic scenes from his service, as well asdriving. Last, he is experiencing marked irritability, anger, and hypervigilance,especially while driving. Paul often catches himself gripping the steering wheel ofhis car, anticipating an intermittent explosive device. Because of his symptoms, Paul ’s
relationships have suffered, most notably his relationship with his girlfriend of severalyears who has made a number of comments to him that he has changed sincecoming back from Iraq and is not the same “easygoing” guy she met. Paul is enrolled
in college under the GI Bill and is having dif ﬁculty studying due to problems
concentrating and a persistent lack of sleep. He fears he may have to withdrawfrom the semester.
Paul’s experiences in Iraq are consistent with the de ﬁnition of a traumatic event,
and his symptoms re ﬂect chronic PTSD with acute onset.
Claudia is a 45-year-old Hispanic woman who presented to her primary-care
physician for her annual appointment. During the course of the appointment, Claudiaadmitted to her physician that she has been struggling emotionally since her recentdivorce (9 months prior) and her son leaving for college (2 months prior). Since both ofthese events, but to a much greater extent since her son moved out of the home,Claudia describes feeling a mixture of depression and sadness about her failure as awife, her loneliness since her son ’s departure, as well as general feelings of anxiety and
fear about her future. She reports feeling at a loss as to how to manage her time andTrauma and Stressor-Related Disorders 399

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feels overwhelming sadness at being 45 and alone, with few friends or family to relyon. She acknowledged calling in sick from work a few times a month for the past fewmonths and then ruminating about the potential consequences of having not gone into work. She reports watching television several hours a day followed by periods ofanxious and somewhat obsessive housecleaning. She also reports having crying spells“over just about anything ”and was tearful while discussing her symptoms during her
primary-care appointment.
Claudia ’s clinical presentation is consistent with a diagnosis of adjustment disorder
with mixed anxiety and depressed mood.
SUMMARY
PTSD, ASD, and adjustment disorders are classi ﬁed in the DSM-5 as trauma- and
stress-related disorders that were precipitated by a stressful or traumatic event. Thevalue of classifying these disorders together will enable clinicians to better differenti-ate normal and mild stress reactions from more severe and pathological stressreactions. It also more clearly highlights the temporal and symptom requirementdistinctions between PTSD, ASD, and adjustment disorders. Whereas PTSD and ASDemphasize fear and anxiety responses, adjustment disorder symptoms can accommo-date a broader range of stress reactions. Second, although there is an explicit potentialfor ASD to predict subsequent impairment (i.e., to predict PTSD), an adjustmentdisorder is typically viewed as a discrete disorder that has a fairly immediate and timelimited symptom duration. A third distinction between PTSD, ASD, and adjustmentdisorders regards the timing of diagnosis. Adjustment disorders can be diagnosedimmediately after the event, ASD can be diagnosed from two days to up to one monthafter the event, and PTSD can be diagnosed from one month to several years afterthe trauma.
In conclusion, based on being linked to a cl ear precipitating stressful or traumatic
event, PTSD, ASD, and adjustment disorder s are viewed as stress reactions along a
continuum that are differentiated by the se verity of the initial stressor, an anxiety
focused or broader set of symptoms in reaction to the event, and the onset andduration of the symptoms. PTSD and ASD share many of the same symptoms, withASD being limited in duration to one month, and in some but not all cases predictingthe subsequent development of PTSD. The relationship between adjustment dis-orders, PTSD, and ASD is poorly understood as there has been little systematicstudy on the topic. The placement of adju stment disorders in the same chapter as
PTSD and ASD in the DSM-5 will likely prompt a better understanding of the
unique and overlapping features of these disorders in relation to PTSD and ASD.Future studies will likely shed light on the similarities and differences between thesethree disorders with regard to prevalence, diagnosis, clinical presentation, corre-lates, and treatment.
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CHAPTER 11
Dissociative Disorders
STEVEN JAY LYNN, JOANNA M. BERG, SCOTT O. LILIENFELD,
HARALD MERCKELBACH, TIMO GIESBRECHT,
MICHELLE ACCARDI, and COLLEEN CLEERE
“THE MOST RECENT edition of the Diagnostic and Statistical Manual of Mental
Disorders (DSM-5; American Psychiatric Association [APA], 2013) de ﬁnes
dissociative disorders as conditions marked by a disruption of and/or
discontinuity in the normal integration of consciousness, memory, identity, emo-tion, perception, body representa tion, motor control, and behavior ”(p. 291). The
presentation of dissociative disorders is often dramatic, per plexing, and highly
variable, both within and across individuals. The hallmarks of dissociation areprofound and often unpredictable shifts in consciousness, the sense of self, andperceptions of the environment.
DSM-5 asserts that the dissociative disorders share a common feature: They are
frequently manifested in the wake of trauma and are in ﬂuenced by their proximity to
trauma (p. 291). Later in the chapter, we contrast the posttraumatic theory that isﬁrmly embedded in the DSM-5 account of dissociation with a competing theory that
does not conceptualize trauma as a necessary precursor to dissociation. In the courseof our discussion, we will present a case study that illustrates the treatment of a patientwith dissociative identity disorder (DID) and highlight controversies that havedogged the ﬁeld of dissociation since the time of Janet ’s seminal writings on the
topic (1889/1973).
The DSM-5 (APA, 2013) identi ﬁes three major dissociative disorders that we
discuss in turn —dissociative amnesia, depersonalization/derealization, and dissocia-
tive identity disorder. We then present an overview of dissociation in general,followed by a more detailed discussion of diagnostic considerations, prevalence,assessment, and etiology speci ﬁc to each of the dissociative disorders.
1.Dissociative amnesia is marked by an inability to recall important autobiographi-
cal information, usually of a traumatic or stressful nature inconsistent withordinary forgetting. This condition most often “consists of localized or selective
amnesia for a speci ﬁc event or events, or generalized amnesia for identity and life
history” (APA, 2013, p. 298).
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2.Depersonalization/derealization disorder (DDD) , formerly known as depersonali-
zation disorder, is diagnosed on the basis of symptoms of persistentdepersonalization, derealization, or both. Depersonalization symptoms includeexperiences of unreality; feelings of detachment or being an outside observer ofone’s thoughts, feelings, sensations, or actions; an unreal or absent sense of self;
physical and emotional numbing; and time distortion. In contrast, derealizationexperiences involve feelings of unreality or detachment with respect to one ’s
surroundings that include the experience of individuals or objects as unreal,dreamlike, foggy, visually distorted, or lifeless.
3.Dissociative identity disorder (DID; formerly called multiple personality disorder)
is marked by a disruption of identity characterized by two or more distinctpersonality states and recurrent gaps in the recall of everyday events, personalinformation, and/or traumatic events that are inconsistent with ordinary for-getting (APA, 2013, p. 292).
DSM-5 also includes a fourth category of other speci ﬁed dissociative disorder,
which does not meet full criteria for any dissociative disorder and includes chronicand recurrent syndromes of mixed dissociative symptoms, identity disturbance due toprolonged and intense coercive persuasion, acute dissociative reactions to stressors,and dissociative trance. Additionally, DSM-5 includes a ﬁfth category of unspeci ﬁed
dissociative disorder in which criteria are not met for a speci ﬁc dissociative disorder
and there is insuf ﬁcient information to make a more speci ﬁc diagnosis. Finally, DSM-5
currently describes a dissociative subtype of posttraumatic stress disorder in whichpersistent or recurring feelings of depersonalization and/or derealization are man-ifested in reaction to trauma-related stimuli. DSM-5 requires that the symptoms of all
dissociative disorders must cause signi ﬁcant distress, impairment of functioning in
major aspects of daily life, or both, and must not be attributable to the effects of asubstance or another medical condition.
Some epidemiological studies among psychiatric inpatients and outpatients have
reported prevalence rates of dissociative disorders exceeding 10% (Ross, Anderson,Fleischer, & Norton, 1991; Sar, Tutkun, Alyanak, Bakim, & Barai, 2000; Tutkun, Sar,Yargiç, Özpulat, Yank, & Kiziltan, 1998), and a study among community women inTurkey even reported a prevalence rate of 18.3% for lifetime diagnoses of a dissocia-tive disorder (Sar, Akyüz, & Dogan, 2007). In contrast, many authors would take issuewith these high prevalence rates in both clinical and nonclinical samples. Indeed, asour discussion will reveal, estimates of the prevalence of dissociative disorders varywidely and are associated with considerable controversy.
Although many authors regard symptoms of depersonalization/derealization and
dissociative amnesia as core features of dissociation, the concept of dissociation issemantically open and lacks a precise and generally accepted de ﬁnition (Giesbrecht,
Lynn, Lilienfeld, & Merckelbach, 2008). This de ﬁnitional ambiguity is related, in no
small measure, to the substantial diversity of experiences that fall under the rubric of“dissociation. ”Dissociative symptoms range in their manifestation from common
cognitive failures (e.g., lapses in attention), to nonpathological absorption and day-dreaming, to more pathological manifestations of dissociation, as represented by thedissociative disorders (Holmes et al., 2005).408 SPECIFIC DISORDERS

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This variability raises the possibility that some of these symptoms are milder
manifestations of the same etiology or have different etiologies and biological sub-strates, raising questions about whether dissociation is a unitary conceptual domain(Hacking, 1995; Holmes et al., 2005; Jureidini, 2003). Indeed, van der Hart and hiscolleagues (van der Hart, Nijenhuis, Steele, & Brown, 2004, 2006) have distinguishedostensibly trauma-related or pathological dissociation, which they term structuraldissociation of the personality, from nonpathological dissociative experiences (e.g.,altered sense of time, absorption). Structural dissociation, in turn, can be subdividedinto levels that encompass primary dissociation, which is thought to involve onepurportedly apparently normal part of the personality (ANP) and one emotional part ofthe personality (EP), secondary structural dissociation, supposedly associated with asingle ANP and further division of the EP, and tertiary dissociation, ostensibly limitedto DID and characterized by several ANPs and EPs. Nevertheless, as our review willdemonstrate, researchers ’attempts to discriminate pathological from nonpathological
dissociative experiences psychometrically have been subject to criticism and have beenless than uniformly successful (Giesbrecht, Lynn, Lilienfeld, & Merckelbach, 2008;Modestin & Erni, 2004; Waller, Putnam, & Carlson, 1996; Waller & Ross, 1997).
Other researchers (Allen, 2001; Cardeña, 1994; Holmes et al., 2005) have proposed
two distinct forms of dissociation: detachment and compartmentalization. Detachmentconsists of depersonalization and derealization, which we describe in some detail later,and related phenomena, like out-of-body experiences. Psychopathological conditionsthat re ﬂect symptoms of detachment include depersonalization disorder and feelings of
detachment that occur during ﬂashbacks in posttraumatic stress disorder (PTSD).
Compartmentalization, in contrast, ostensibly encompasses dissociative amnesia,marked by extensive forgetting of autobiographical material, and somatoform dissoci-ation, such as sensory loss and “unexplained ”neurological symptoms (Nijenhuis,
Spinhoven, Van Dyck, Van der Hart, & Vanderlinden, 1998). The core feature ofcompartmentalization is a de ﬁcit in deliberate control of processes or actions that
would normally be amenable to control, as is evident in DID or somatization disorder.Although clinicians may ﬁnd it helpful to subdivide dissociative symptoms into
different symptom clusters (Bernstein-Carlson & Putnam, 1993), attempts to differenti-ate such clusters on a psychometric basis have not been consistently successful.
Dissociation is often presumed to re ﬂect a splitting of consciousness, although it
must be distinguished from the super ﬁcially similar but much debated concept of
Freudian repression. Speci ﬁcally, dissociation can be described as a “horizontal ”split;
that is, consciousness is split in two or more parts that operate in parallel. In contrast,repression is more akin to a “vertical ”split, in which consciousness is arranged in
levels, and traumatic or otherwise undesirable memories are ostensibly pusheddownwards and rendered more or less inaccessible.
Although the existence of dissociation as a clinical symptom is not much in dispute,
dissociative disorders are among the most controversial psychiatric diagnoses. Dis-agreement generally centers on the etiology of these disorders, with advocates oftenarguing for largely trauma-based origins (e.g., Dalenberg et al., 2012; Gleaves, 1996).In this light, dissociative symptoms are regarded as manifestations of a copingmechanism that serves to mitigate the impact of highly aversive or traumatic events(Gershuny & Thayer, 1999; Nijenhuis, van der Hart, & Steel, 2010). In contrast, skepticsDissociative Disorders 409

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often emphasize the role of social in ﬂuences, including cultural expectancies and
inadvertent therapist cueing of symptoms (e.g., Lilienfeld et al., 1999; Lynn et al., inpress; McHugh, 2008). As we will learn later in the chapter, the controversiesstemming from etiology and classi ﬁcation of dissociative disorders extend to their
assessment and treatment. We will focus our discussion on chronic dissociativesymptoms, rather than dissociation at the time of a highly aversive event (i.e.,peritraumatic dissociation). Also, we will not elaborate on the dissociative subtypeof PTSD described in DSM-5 . However, we will present a number of “state ”measures
of dissociation because researchers not infrequently consider temporary changes indissociation in the context of research on more chronic presentations of dissociation.
DISSOCIATIVE AMNESIA
The diagnosis of dissociative amnesia requires that the memory loss is extensive andnot attributable to substance use or to a neurological or other medical condition suchas age-related cognitive loss, complex partial seizures, or closed-head brain injury andthat the symptoms are not better explained by DID, PTSD, acute stress disorder,somatic symptom disorder, or major or mild neurocognitive disorder (APA, 2013,p. 298). This disorder, formerly referred to as psychogenic amnesia, often presentsas retrospective amnesia for some period or series of periods in a person ’s life,
frequently involving a traumatic experience.
DSM-5 lists several subtypes of dissociative amnesia. In localized amnesia, the
individual cannot recall any information from a speci ﬁc period of time, such as total
forgetting of a holiday week. Selective amnesia involves the loss of memories for some,but not all, events from a speci ﬁc period of time. In generalized amnesia, individuals
cannot recall anything about their entire lives, and in continuous amnesia, individualsforget each new event as it occurs. Finally, systematized amnesia consists of the “loss
of memory for speci ﬁc categories of information ”(e.g., sexual abuse, a particular
person). These last three types of dissociative amnesia —generalized, continuous, and
systematized —are much less common than the others, and may be manifestations of
more complex dissociative disorders, such as DID rather than dissociative amnesiaalone.
Lynn et al. (2014) argued that the central diagnostic criterion for dissociative
amnesia is vague and subjective in stipulating that one or more episodes of inabilityto recall important information must be “. . . inconsistent with ordinary forgetting ”
(Dahlenberg et al., p. 522). The reliability of judgments of what constitutes “ordinary
forgetfulness ”is questionable, and what is “ordinary ”hinges on a variety of factors,
including the situational context and presence of comorbid conditions. A similar pointwas raised by Read and Lindsay (2000), who demonstrated that when people areencouraged to remember more about a selected target event, they report theirforgetting to be more extensive, compared with individuals who are asked to simplyreminisce about a target event.E
PIDEMIOLOGY
Because rates of reporting vary so widely, it is dif ﬁcult to obtain reliable epidemio-
logical information regarding dissociative amnesia. Questions concerning the validity410 SPECIFIC DISORDERS

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of dissociative amnesia as a diagnostic entity are supported by markedly differentprevalence rates in the general population across cultures: 0.2% in China, 0.9% and7.3% in Turkey, and 3.0% in Canada (Dell, 2009). These varying prevalence estimatescould re ﬂect genuine cultural differences, but they could just as plausibly re ﬂect
different interviewer criteria for evaluating amnesia.
The DSM-5 states that dissociative amnesia can present in any age group,
although it is more difﬁ cult to diagnose in younger children due to their dif ﬁculty
in answering questions about periods of forgetting and possible confusion with a
number of other disorders and conditions, including inattention, anxiety, opposi-
tional behavior, and learning disorders. There may be just one episode of amnesia,or there may be multiple episodes, wit he a c he p i s o d el a s t i n ga n y w h e r ef r o m
minutes to decades. Other sources (e.g., Coons, 1998) suggest that most cases occurin individuals in their 30s or 40s, and that 75% of cases last between 24 hours and5d a y s .T h ep r e v a l e n c eo fd i s s o c i a t i v ea mnesia is approximately equal between
genders. Still others argue that the scienti ﬁc evidence for the existence of dissociative
amnesia is unconvincing, and that barri ng brain injury or substance abuse or
dependence, individuals who have experienced trauma do not forget those events(e.g., McNally, 2003; Pope, Hudson, Bodkin, & Oliva, 1998).
Certain cases of purported traumatic amne sia are in fact attributable to organic or
other nondissociative causes. For example, when critiquing a “convincing demon-
stration of dissociative amnesia ”(Brown, Sche ﬂi n ,&H a m m o n d ,1 9 9 7 ) ,M c N a l l y
(2004) discussed a study (Dollinger, 1985) of two children who witnessed a playmatestruck and killed by lightning, and who were later diagnosed with dissociativeamnesia. Yet as McNally noted, this diagnosis was clearly mistaken, because thechildren had also been struck by lightning and knocked unconscious.
Amusingly, and perhaps tellingly, Pope, Poliakoff, Parker, Boynes, and Hudson
(2007) offered a reward of $1,000 to “theﬁrst individual who could ﬁnd a case
of dissociative amnesia for a traumatic event in any ﬁctional or non- ﬁctional work
before 1800 ”(p. 225) on the basis that, whereas the vast majority of psychological
symptoms can be found in literature or records dating back centuries, dissociativeamnesia appears only in more modern literature beginning in the late 1800s. Over 100individuals came forward with examples, but none met the diagnostic criteria for thedisorder (although the prize later went to someone who discovered a case of dissocia-tive amnesia in a 1786 opera, Nina, by the French composer Nicholas Dalayrac).
Although Pope and colleagues ’challenge does not “prove ”anything regarding the
validity of the disorder, its relative scarcity, and apparently recent (perhaps post late18th century) development, raise troubling questions about its existence as a naturalcategory or entity.
A special form of dissociative amnesia is crime-related amnesia. Many perpetrators
of violent crimes claim to experience great dif ﬁculty remembering the essential details
of the crime they committed (Moskowitz, 2004). Memory loss for crime has beenreported in 25% –40% of homicide cases and severe sex offenses. Nevertheless, skeptics
believe that genuine dissociative amnesia in these cases is rare. They have pointedout that trauma victims (e.g., concentration camp survivors) almost never reportdissociative amnesia (Merckelbach, Dekkers, Wessel, & Roefs, 2003). For example,Rivard, Dietz, Matell, and Widawski (2002) examined a large sample of policeofﬁcers involved in critical shooting incidents and found no reports of amnesia.Dissociative Disorders 411

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Also, recent laboratory research shows that when participants encode informationwhile in a “survival mode, ”this manipulation yields superior memory effects
(Nairne & Pandeirada, 2008). This ﬁnding is dif ﬁcult to reconcile with the idea of
dissociative amnesia while committing a crime. Thus, it is likely that feigning under-lies most claims of crime-related amnesia (Van Oorsouw & Merckelbach, 2010).
DISSOCIATIVE FUGUE
Dissociative fugue (previously called psychogenic fugue) is arguably the mostcontroversial dissociative phenomenon after dissociative identity disorder. InDSM-IV-TR, dissociative fugue (i.e., short-lived reversible amnesia for personal
identity, involving unplanned travel or wandering) was listed as a separate diagnosis.InDSM-5 , dissociative fugue —deﬁned therein as apparently purposeful travel or
bewildered wandering associated with amnesia for identity or other importantautobiographical information —is no longer diagnosed as a disorder in its own right,
but is instead coded as a condition that can accompany dissociative amnesia. In afugue ( “fugue ”has the same etymology as the word “fugitive ”) episode, amnesia for
identity may be so extreme that a person physically escapes his or her presentsurroundings and adopts an entirely new identity. If and when this identity develops,it is often characterized by higher levels of extraversion than the individual displayedprefugue, and he or she usually presents as well integrated and nondisordered.
Periods of fugue vary considerably across individuals, both in duration and in
distance traveled. In some cases, the travel can be a brief and relatively short trip,whereas, in more extreme cases, it can involve traveling thousands of miles and evencrossing national borders. While in the dissociative fugue state, individuals oftenappear to be devoid of psychopathology; if they attract attention at all, it is usuallybecause of amnesia or confusion about personal identity. Again, it is doubtful thatfugues constitute a ﬁxed and cross-cultural diagnostic category. Hacking (1995)
provides a detailed historical and critical analysis of fugue showing that they ﬁrst
appeared in the 19th century and since that time ﬂuctuated in apparent prevalence and
acceptance by the psychiatric community.D
IAGNOSTIC CONSIDERATIONS
Although DSM-5 notes that dissociative fugue, with travel, is not uncommon in DID,
dissociative fugue may manifest with other symptoms, including depression, anxiety,dysphoria, grief, shame, guilt, stress, and aggressive or suicidal impulses (APA, 2013).Reportedly, the condition often develops as a result of traumatic or stressful events,which has led to controversy and ambiguity regarding the relation between dissocia-tive fugue and PTSD. Precipitants associated with the development of dissociativefugue include war or natural disasters, as well as the avoidance of various stressors,such as marital discord or ﬁnancial or legal problems (Coons, 1998). Such avoidance
suggests that clinicians must be certain to rule out malingering and factitious disordersbefore diagnosing dissociative fugue.
Certain culture-bound syndromes exhibit similar symptoms to dissociative fugue.
These include amok , present in Western Paci ﬁc cultures (which has given rise to the
colloquialism “running amok” );pibloktok , present in native cultures of the Arctic, and412 S
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Navajo “frenzy ”witchcraft, all of which are marked by “a sudden onset of a high level
of activity, a trancelike state, potentially dangerous behavior in the form of running orﬂeeing, and ensuing exhaustion, sleep, and amnesia ”for the duration of the episode
(APA, 2000, p. 524; Simons & Hughes, 1985).E
PIDEMIOLOGY
DSM-IV-TR places the population prevalence estimate of dissociative fugue at .02%,
with the majority of cases occurring in adults (APA, 2000, p. 524). Ross (2009b)observed that in the approximately 3,000 individuals he treated in his trauma programover a 12-year period, he encountered fewer than 10 individuals with pure dissociativeamnesia or pure dissociative fugue, although he noted that symptoms of amnesia andfugue were common in the patients he admitted.
DEPERSONALIZATION/DEREALIZATION DISORDER
Depersonalization/derealization disorder (DDD) is one of the most common disso-ciative disorders and perhaps the least controversial. In DDD, reality testing remainsintact (APA, 2013, p. 302): Individuals are aware that the sensations are not real andthat they are not experiencing a break from reality akin to psychosis. In a departurefrom DSM-IV, in which depersonalization and derealization were diagnosed sepa-
rately, DSM-5 created a new diagnostic category of depersonalization/derealization
disorder. This “lumping ”of formerly separate conditions is supported by ﬁndings
(Simeon, 2009a) that individuals with derealization symptoms do not differ signiﬁ –
cantly from those with depersonalization accompanied with derealization in salientrespects (e.g., illness characteristics, comorbidity, demographics).
Greatly contributing to our knowledge about depersonalization symptoms has
been the development of well-validated screening instruments, notably the CambridgeDepersonalization Scale (CDS; Sierra & Berrios, 2000; Sierra, Baker, Medford, & David,2005). Depersonalization episodes are not uncommonly triggered by intense stress andare often associated with high levels of interpersonal impairment (Simeon et al., 1997).Episodes of depersonalization or derealization are also frequently associated with panicattacks, unfamiliar environments, perceived threatening social interactions, the inges-tion of hallucinogens, depression, and PTSD (Simeon, Knutelska, Nelson, & Guralnik,2003). Individuals with DDD are also more likely than healthy individuals to report ahistory of emotional abuse. In contrast, general dissociation scores are better predictedby a history of combined emotional and sexual abuse (Simeon, Guralnik, Schmeidler,Sirof, & Knutelska, 2001).D
IAGNOSTIC CONSIDERATIONS
Nearly 50% of adults have experienced at least one episode of depersonalization intheir lifetimes, usually in adolescence, although a single episode is not suf ﬁcient to
meet criteria for the disorder (Aderibigbe, Bloch, & Walker, 2001). Becausedepersonalization and derealization are common, DDD should be diagnosed onlyif these symptoms are persistent or recurrent and are severe enough to cause distress,impairment in functioning, or both. The distress associated with DDD may beDissociative Disorders 413

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extreme, with sufferers reporting they feel robotic, unreal, and “unalive. ”They may
fear becoming psychotic, losing control, and suffering permanent brain damage(Simeon, 2009a). Individuals with DDD may perceive an alteration in the size orshape of objects around them. Other people may appear mechanical or unfamiliar, andaffected individuals may experience a disturbance in their sense of time (Simeon &Abugel, 2006).
A diagnosis of DDD requires that the symptoms do not occur exclusively in the
course of another mental disorder, nor can they be attributable to substance abuse ordependence or to a general medical condition. Furthermore, DDD should not bediagnosed solely in the context of meditative or trance practices. Symptoms of otherdisorders, such as anxiety disorders, major/unipolar depression, and hypochondria-sis and certain personality disorders, especially avoidant, borderline, and obsessive-compulsive, may also be present (Simeon et al., 1997). Depersonalization andderealization symptoms are often also part of the symptom picture of acute stressdisorder (ASD; APA, 2013), which is often a precursor to PTSD.E
PIDEMIOLOGY
DSM-5 estimates the lifetime prevalence of DDD in the United States as 2%, with a
range of 0.8% to 2.8% (see also Ross, 1991), suggesting that DDD might be as commonas or more common than schizophrenia and bipolar disorder. DDD is diagnosedalmost equally often in women as in men (Simeon et al., 2003). It frequently presentsfor treatment in adolescence or adulthood, even as late as the 40s, though its onset maybe earlier. Estimates of the age of onset of DDD range from 16.1 (Simeon et al., 1997) to22 years (Baker et al., 2003).
The onset and course of DDD vary widely across individuals. Some people
experience a sudden onset and others a more gradual onset; some experience achronic form of the disorder, whereas others experience it episodically. In about two-
thirds of people with DDD, the course is chronic, and symptoms of depersonalizationare present most of the time, if not continu ally. Episodes of depersonalization may
last from hours to weeks or months, and in more extreme cases, years or decades(Simeon, 2009a).
DISSOCIATIVE IDENTITY DISORDER
According to DSM-5 ,“the de ﬁning feature of dissociative identity disorder is the
presence of two or more distinct personality states or experiences of possession ”(APA,
2013, p. 292). Thus, the requirement that people diagnosed with DID must experiencedistinct identities that recurrently take control over one ’s behavior is no longer
present. Importantly, in DSM-5 “distinct personality states ”replaces the term identi-
ties. The diagnostic language in DSM-5 represents a distinct departure from DSM-II
(APA, 1968), which used the term multiple personalities, and from DSM-IV (APA,
1994), which labeled the condition dissociative identity disorder to underscore alter-ations in identity, rather than ﬁxed and/or complete “personalities. ”
These shifts in diagnostic criteria may prove to be problematic and result in changes
in the prevalence rates of DID. For example, what constitutes a personality state or anexperience of possession may be open to greater interpretation compared with414 SPECIFIC DISORDERS

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previous iterations of DSM . Moreover, in DSM-5 , signs and symptoms of personality
alteration may be not merely “observed by others, ”but also “reported by the
individual ”(APA, 2013; p. 292), further expanding opportunities for the diagnosis
of DID. In cases in which alternate personality states are not witnessed, in DSM-5 it is
still possible to diagnose the disorder when there are “sudden alterations or dis-
continuities in sense of self or agency . . . and recurrent dissociative amnesias ”(APA,
2013; p. 293), creating even more latitude and subjectivity in the diagnosis of DID.Moreover, amnesia is no longer restricted to traumatic events and may now bediagnosed in relation to everyday events, which may also increase the base ratesof diagnosed DID. Although DSM-5 no longer de ﬁnes DID in terms of “distinct
identities that recurrently take control of the individual ’s behavior ( DSM-IV, p. 519), ”
in the remainder of the chapter, we will not refrain from using the terms personalities
and identities, insofar as these terms (a) continue to be widely used in the extant
literature and (b) encompass “personality states.”
D
IAGNOSTIC CONSIDERATIONS
To meet diagnostic criteria for DID, an individual ’s symptoms cannot be attributable
to substance use or to a medical condition, and the “disturbance is not a normal part of
a broadly accepted cultural or religious practice” (APA, 2013; p. 292). When the
disorder is assessed in children, the symptoms must not be confused with imaginaryplay. To recognize cultural variants of dissociative phenomena, DSM-5 refers to a
“possession form ”of DID, which is “typically manifest as behaviors that appear as if a
‘spirit, ’supernatural being, or outside person has taken control, such that the
individual begins speaking or acting in a distinctly different manner” (APA, 2013,
p. 293). Because such manifestations are not uncommon in different cultures (seeCardeña, van Duijl, Weiner, & Terhune, 2009 for a discussion of trance/possessionphenomena), to warrant a diagnosis of DID, the identities must be present recurrently,be unwanted or involuntary, engender signi ﬁcant distress or impairment, and not be a
part of accepted cultural/religious practices.
In nonpossession forms of DID, there is typically considerable variation in the
presentation of symptoms. Nevertheless, the primary identity or personality state inan individual with DID often carries the individual ’s given name and tends to be
“passive, dependent, guilty, and depressed. ”Other personalities, often called “alters, ”
may be assertive or even aggressive and hostile, and these more dominant identitiesusually possess more complete memories regarding the individual ’s actions and history.
Within one individual, there can often be anywhere between 2 and 100 or morepersonalities, with approximately 50% of individuals reporting 10 or fewer distinctidentities, although extreme cases of many as 4,500 alters have been reported (Acocella,1999). Reported identities are usually just “regular ”people, but more extreme and
bizarre cases exist. There have been reports of identities claiming to be Mr. Spock fromStar Trek , the rock star Madonna, the bride of Satan, and even a lobster.
Researchers have documen ted substantial comorbidity of DID with other dis-
orders. For example, Ellason, Ross, and Fuchs (1996) reported that DID patients metcriteria for an average of 8 Axis I disorders and 4.5 Axis II disorders. One-half totwo-thirds of patients with DID meet diagno stic criteria for borderline personality
disorder (BPD; Coons, Bowman, & Milstein, 1988; Horevitz & Braun, 1984). Conversely,Dissociative Disorders 415

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Sar, Akyuz, Kugu, Ozturk, and Ertem-Vehid (2006) found that 72.5% of patientsscreened for BPD had a dissociative disorder. In one study, researchers (Kemp,Gilbertson, & Torem, 1988) reported no signi ﬁcant differences between BPD and
DID patients on measures of personality traits, cognitive and adaptive functioning,and clinician ratings, suggesting noteworthy commonalities between the two condi-tions. Histories of sexual and physical abuse are also commonly reported in both patientgroups, and BPD patients score well above general population norms on measures ofdissociation (Lauer, Black, & Keen, 1993). Indeed, Lauer and his colleagues (Lauer,Black, & Keen, 1993) suggested that DID is an epiphenomenon of the combination ofBPD with high suggestibility.
Individuals with DID often experience additional symptoms, including self-muti-
lation; suicidal or aggressive behavior; as well as major depression; substance abuse;and sexual, eating, and sleep disorders (Fullerton et al., 2000; North, Ryall, Ricci, &Wetzel, 1993; Ross, 1997). Accordingly, some clinicians have argued that the DIDdiagnosis really is a severity marker identifying extreme variants of a host of otherdisorders (for an extensive discussion see North et al., 1993).
Many DID patients meet the criteria for schizoaffective disorder (Lauer et al., 1993),
and as many as half have received a previous diagnosis of schizophrenia (Ross &Norton, 1988). Indeed, auditory and visual hallucinations are common in both DIDand schizophrenia. However, patients with DID commonly report that hallucinatedvoices originate inside of their heads, whereas patients with schizophrenia tend toperceive the origin of voices outside of their heads and possess less insight into thenature of their symptoms (Coons, 1998; Kluft, 1993).
DID patients have been reported to endorse more positive symptoms (e.g., delu-
sions, hallucinations, and suspiciousness) and Schneiderian ﬁrst-rank symptoms,
which include themes of passivity, than schizophrenic patients (Ellason & Ross,1995; Steinberg, Rounsaville, & Cichetti, 1990). Ellason and Ross (1995) argued thatthe presence of positive symptoms can be used to formulate an accurate differentialdiagnosis between the two disorders, although further research regarding this possi-bility is necessary (for further diagnostic considerations see Steinberg & Siegel, 2008).
PTSD is one of the most commonly comorbid conditions with DID (Loewenstein,
1991). Moreover, PTSD patients are more likely to present with symptoms ofdissociation (e.g., numbing, amnesia, ﬂashback phenomena) than patients with major
depression, schizophrenia, and schizoaffective disorder (Bremner, Steinberg, South-wick, Johnson, & Charney, 1993).E
PIDEMIOLOGY
DID may be episodic or continuous, and in some cases may remit after the late 40s(APA, 2000). There are documented cases of DID extending decades, and the conceptof fragmented or multiple personalities is an ancient one. That said, the number ofcases has increased exponentially in the past few decades. Prior to 1970, there wereapproximately 80 reported cases, but by 1986 that number had ballooned to approxi-mately 6,000. As of 1998, there were approximately 40,000 cases (Lilienfeld & Lynn, inpress).
Population prevalence estimates vary widely, from extremely rare (e.g., Piper,
1997; Rifkin, Ghisalbert, Dimatou, Jin, & Sethi, 1998) to rates approximating that of416 SPECIFIC DISORDERS

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schizophrenia (1 –2%; Coons, 1998; Ross, 1997). Estimates of DID in inpatient settings
range from 1– 9.6% (Rifkin et al., 1998; Ross, Duffy, & Ellason, 2002). In addition to the
dramatic increase in DID ’s prevalence over the past few decades, there has been an
increase in the number of “alters ”reported, from only two or three separate identities
to an average of approximately 16 (interestingly, the exact number reported by Sybil;see below) by 1990.
DID is between 3 and 9 times more common in women than men, and women also
tend to have more identities (an average of 15, as compared with the male averageof 8; APA, 2000). Nevertheless, this imbalanced sex ratio may be an artifact ofselection and referral biases (Lynn, Fassler, Knox, & Lilienfeld, 2009). In particular,a larger proportion of males with DID may end up in prisons (or other forensicsettings) than in clinical settings (Putnam & Loewenstein, 2000).
DID is the most controversial dissociative disorder, and easily among the most
controversial disorders in DSM-5 . Skeptics of the disorder (Paris, 2012; Piper &
Merskey, 2004) argue that its proliferation is in part a function of media exposure.In 1976, the movie Sybil was released, documenting the real-life story of a woman who
had supposedly experienced severe child abuse and later developed 16 personalities(but see “Etiological Considerations ”section for evidence calling into question
signiﬁcant details of the Sybil case). In addition to the number of cases increasing
after the release of this movie, the number of individuals reporting child abuse as acause of DID also rose drastically (Lilienfeld & Lynn, in press; Spanos, 1996). Incontrast, proponents of the disorder respond that clinicians now are simply betterequipped to identify the disorder (Gleaves, May, & Cardena, 2001). We elaborate onthis etiological debate later in the chapter.
PSYCHOLOGICAL ASSESSMENT
A variety of assessment instruments are available to evaluate dissociation anddissociative disorders. In this section, we review commonly used structured interviewand self-report measures.S
TRUCTURED INTERVIEW MEASURES
The Structured Clinical Interview for DSM-IV (SCID-D; Steinberg, 1985) and its
revision (SCID-D-R; Steinberg, 1994) are semistructured interviews that systematicallyassess ﬁve core symptoms of dissociation: amnesia, depersonalization, derealization,
identity confusion, and identity alteration. The SCID-D incorporates the DSM-IV
criteria for dissociative disorders. The full 250-item administration may take 2 –3 hours
for psychiatric patients with dissociative symptoms; however, nondissociative psy-chiatric patients may complete the interview in 30 to 90 minutes, and nonpsychiatricparticipants in 30 minutes. The severity of each of the ﬁve core symptoms is scored in
terms of distress, dysfunctionality, frequency, duration, and course. The revised scalewas administered in NIMH ﬁeld trials that encompassed 350 interviews of dissocia-
tive and nondissociative adults. Reports from the ﬁeld trials ( N=141 mixed
psychiatric patients) revealed that the interexaminer and temporal reliability of theSCID-D-R ranges from very good to excellent (weighted kappa 0.77 –0.86) for both the
presence and extent of dissociative symptoms over three time periods. For type ofDissociative Disorders 417

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dissociative disorder, interexaminer agreement ranged from 0.72 –0.86, and test-retest
reliability for the overall presence of a dissociative disorder was good (0.88 over 7-dayperiod). The SCID-D-R possesses good convergent validity, and is capable of distin-guishing DID patients from patients with anxiety disorders, substance abuse, per-sonality disorders, eating disorders, and psychotic disorders (Cardena, 2008). TheSCID-D may be helpful in discriminating DID from feigning. It also appears todistinguish DID from schizophrenia (Wellburn et al., 2003). Nevertheless, Kihlstrom(2005, p. 3) countered that “even with relatively strict criteria in place, it can be dif ﬁcult
to discriminate between dissociative disorders and bipolar disorder, borderlinepersonality disorder, and even schizophrenia.”
The Dissociative Disorders Interview Schedule (DDIS; Ross et al., 1989) is a
structured interview used to assist in the diagnosis of dissociative disorders, aswell as conditions that often co-occur with it, including somatization disorder, majordepressive disorder, and borderline personality disorder. The interview has been usedfor clinical and research purposes and consists of 16 sections with a total of 131questions. The interview is highly structured to minimize interviewer con ﬁrmation
bias and sequenced so that indirect questions about secondary features of DID precedeincreasingly speci ﬁc questions.
In the original validation study, 80 psychiatric patients from specialized research
clinics were interviewed. Patients diagnosed with DID ( n=20) were compared with
patients with panic disorder ( n=20), eating disorder ( n=20), and schizophrenia ( n=
20). For DID, the DDIS yielded a sensitivity of 90% and a speciﬁ city of 100% [see also
Ross et al. (1992) who demonstrated high agreement (94.1%) of DDIS classi ﬁcation
using the DDIS with independent clinical evaluation]. The authors reported thatinterrater reliability was adequate ( r=.68; Ross et al., 1989). The DDIS has demon-
strated good convergent validity, as indexed by high correlations of DID diagnosisscores with the DES ( r=.67–.78; Cardena, 2008). Nevertheless, the authors (Ross et al.,
1989) cautioned that depersonalization disorder cannot be reliably diagnosed usingthe DDIS (interrater reliability =.56).
The Clinician Administered Dissociation State Scale (CADSS; Bremner et al., 1998)
was developed to assess dissociative states. The clinician verbally administers 19“subject-rated ”items on a Likert-type scale ranging from 0 (not at all) to 4 (extremely).
Three subscales subsume the subject-rated items: amnesia, depersonalization, andderealization. The clinician also observes the participant’ s behavior during the inter-
view and rates eight behaviors presumed to indicate the presence of a dissociativestate on the same Likert-type scale as the subject-rated items.
In the original study, the CADSS was administered to patients with combat-
related PTSD and a comorbid dissociat ive disorder (PTSD/dissociative) ( n=68).
These patients were compared with patients with schizophrenia ( n=22), mood
disorders ( n=15), healthy controls (n =8), and combat veterans without PTSD
(n=11). The CADSS discriminated betwe en patients with PTSD and comorbid
dissociative disorders (86% of cases) and p atients with the comparison conditions.
Furthermore, the CADSS detected changesi nd i s s o c i a t i v es y m p t o m sb e f o r ea n dafter patients with PTSD participated in a traumatic memories group. These patients
showed a signi ﬁcant increase in symptoms compared with baseline, suggesting that
the
CADSS may be sensitive enough to capture changes in repeated measures
designs. Interrater reliability was excellent for the total scale (ICC =.92) and for the418 S PECIFIC DISORDERS

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subject-rated portion (ICC =.99), but was markedly lower for the observer ratings
(ICC=.34). The internal consistency of the CA DSS was good to excellent for the total
scale ( α=.94), subjective portion ( α=.94), observer ratings ( α=.90), and the
individual subscales ( α=.74–.90). Recently, Condon and Lynn (in press) reported
that the CADSS correlated at r=.63 with the DES-II and reported the internal
consistency of the CADSS to be α=.80 in a sample of undergraduates.
SELF-REPORT MEASURES
The Dissociative Experiences Scale (DES; Bernstein & Putnam, 1986) and its revision(DES-II; Bernstein-Carlson & Putnam, 1993) are brief self-report measures of dissoci-ation that can be used in both research and clinical settings to assess individuals withinnormal and psychiatric populations. Participants rate 28 items pertaining to dissocia-tion in terms of the frequency they are experienced, from 0% to 100%. In the originalsample, the test-retest reliability among 192 participants was .84 over a period of 4 to8 weeks, and split half reliability coef ﬁcients ranged from .71 to .96, indicating good
internal consistency. In addition, DES scores differentiated participants with a disso-ciative disorder (e.g., DID) from those without a dissociative disorder (e.g., normaladults, late adolescent college students, alcoholics, phobics). A cutoff of 30 correctlyidenti ﬁed 74% of patients with DID and 80% of subjects without DID in a multicenter
study (Carlson, Putnam, Ross, Torem, et al., 1991).
The DES is the most frequently used self-report measure of dissociation (Brand,
Armstrong, & Loewenstein, 2006). Nevertheless, researchers have questioned whetherthe scale is unidimensional, as would be expected of a factorially pure measure ofdissociation. Carlson et al. (1991) reported a three-factor solution —amnesia, absorption
(related to openness to experience), and depersonalization (also see Ross, Ellason, &Anderson, 1995; Sanders & Green, 1994) —and others (Ray & Faith, 1994) have identi ﬁed
four factors. In contrast, Waller (1995) reanalyzed Carlson et al. ’s (1991) data and
concluded that their three-factor solution could re ﬂect the skewed distribution of the
items, and thus might be a statistical artifact re ﬂecting the presence of dif ﬁculty factors
(that is, factors induced by similar levels of skewness across the items; see also Holmeset al., 2005; Wright & Loftus, 1999).
Waller, Putnam, and Carlson (1996) responded to criticisms that the DES contains a
substantial number of nonpathological items that tap absorption (e.g., “Some people
ﬁnd that when they are watching television or a movie they become so absorbed in the
story that they are unaware of other events happening around them. ”) by developing
the DES-Taxon (DES-T) scale. This 8-item scale contains items from the original DESthat measure pathological dissociation, including derealization, depersonalization,psychogenic amnesia, and identity alteration. Waller and Ross (1997) estimated thatthe general population base rate of pathological dissociation is 3.3%. Of course, beingclassi ﬁed as a taxon member (i.e., distinct type or latent class) cannot be equated with
DID (Modestin & Erni, 2004), as the prevalence of DID in the general population isalmost certainly much lower than 3%. Although the resulting scale was stricter in thecriteria for establishing evidence of pathologic dissociation, the data supporting itsvalidity are mixed. Simeon and colleagues (Simeon et al., 1998) found that the DES-Tsum score is superior to the standard DES at distinguishing patients withdepersonalization disorders (DDD) from control subjects. Nevertheless, later studiesDissociative Disorders 419

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revealed that the DES-T: (a) classi ﬁed only 64% of patients with DDD as having a
dissociative disorder (Simeon et al., 2003), (b) produced high false positive rates(Giesbrecht, Merckelbach, & Geraerts, 2007), and (c) lacked temporal stability fortaxon membership probability (Watson, 2003). Nevertheless, many studies havedocumented signi ﬁcant differences between people who score high versus low on
both the DES and the DES-T with respect to a variety of measures of memory andcognition (Giesbrecht et al., 2008).
The Adolescent Dissociative Experiences Scale (A-DES; Armstrong, Putnam,
Carlson, Libero, & Smith, 1997) is a 30-item self-report measure designed exclusivelyfor use with adolescent populations. The scale is intended to serve as a screening toolfor dissociative disorders among adolescents and trace the developmental trajectoriesof normal and pathological dissociation over time. The A-DES items are rated on an11-point Likert-type scale, and comprise the following subscales: dissociative amnesia,absorption and imaginative involvement, passive inﬂ uence, and depersonalization
and derealization. The A-DES was normed using a group of healthy adolescents injunior-high and high school populations (Smith & Carlson, 1996) and a group ofadolescent clinical patients (Armstrong et al., 1997). The authors reported excellentinternal consistency for the total score ( α=.93) and subscales ( α=.72–85). Never-
theless, there are questions concerning the A-DES ’s convergent validity. In a sample of
331 nonreferred youths, Muris, Merckelbach, and Peeters (2003) reported that A-DESscores are not only signi ﬁcantly related to PTSD symptoms and fantasy proneness, but
also to other anxiety symptoms.
The Multidimensional Inventory of Dissociation (MID 5.0; Dell, 2006) is a recently
developed self-report measure created to assess the symptom-domain of DID and thephenomenological domain of dissociation. The MID 5.0 contains 168 dissociationitems and 50 validity items rated on a 0 –10 Likert-type scale. The MID shows
promising convergent validity with other psychiatric diagnoses (e.g., it distinguishesamong individuals with DID, dissociative disorder not otherwise speci ﬁed, mixed
psychiatric, and nonclinical adults; Dell, 2002) and self-report measures (e.g., correla-tions with the DES =.90; Dell, 2006), as well as structural validity (e.g., factor analyses
isolated a single overarching factor of pathological dissociation; see Dell, 2006).Nevertheless, these ﬁndings have yet to be replicated by independent research groups.
The author reported good-to-excellent internal consistency of the 23 dissociation scales(α=0.84–0.96) and temporal stability (4- to 8-week test-retest interval; rs=.82–.97) in a
large clinical sample. These latter results were replicated in Israel and Germany (seeDell, 2006).
The Somatoform Dissociation Questionnaire (SDQ-20; Nijenhuis, Spinhoven, Van
Dyck, Van der Hart, & Vanderlinden, 1996) is a self-report measure designed toevaluate the presence of somatoform responses associated with dissociative states thatcannot be medically explained. Participants rate items on a 5-point Likert-type scale.Twenty of the 75 original items discriminated outpatients with dissociative disordersfrom nondissociative psychiatric outpatients and comprised the ﬁnal scale. The
authors reported excellent internal consistency ( α=0.95) and higher scores among
patients with DID compared with patients with dissociative disorder not otherwisespeciﬁed. The authors also reduced the SDQ-20 to a ﬁve-item screen for dissociative
disorders (SDQ-5; Nijenhuis, Spinhoven, Van Dyck, Van der Hart, & Vanderlinden,1997). For dissociative disorders among psychiatric patients, the SDQ-5 exhibited a420 SPECIFIC DISORDERS

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sensitivity of 94% and a speci ﬁcity of 98% (Nijenhuis et al., 1998). A study in which
DES, MID, and SDQ-20 were compared to SCID-D outcomes in psychiatric out-patients found that these self-report instruments have comparable diagnostic accuracyand are equivalently suitable as screening tools for dissociative disorders (Mueller-Pfeiffer et al., 2013).
The Dissociation Questionnaire (DIS-Q; Vanderlinden, Van Dyck, Vandereycken, &
Vertommen, 1991) was developed to account for sociocultural differences in Europeanpopulations as well as to assess a broad spectrum of dissociative experiences. Theauthors generated items from existing dissociation questionnaires and clinical expe-rience. Participants rate items on a 1 –5 Likert-type scale; the ﬁnal 63-item scale was
normed on 374 participants from the general population in Belgium and the Nether-lands. Four factors constitute the DIS-Q (i.e., identity confusion, loss of control,amnesia, and absorption). Internal consistency of the subscales ( α=0.67–0.94) and
the overall scale ( α=0.96) were good to excellent, as was test-retest reliability over a
period of 3 –4 weeks. The authors report successful discrimination of patients with
dissociative disorders and nondissociative disorders with the exception of PTSD.Within the dissociative disorders, the DIS-Q successfully discriminated DID fromdissociative disorder– not otherwise speciﬁ ed.
The State Scale of Dissociation (SSD; Kruger & Mace, 2002) is a self-report inventory
designed to detect changes in dissociative states, rather than traits. The SSD wasdeveloped using existing scales, the DSM-IV, and the ICD-10, along with the aid ofclinical experts. The 56-item scale is scored on a Likert-type scale from 0 –9 and broken
down into seven subscales: derealization, depersonalization, identity confusion,identity alteration, conversion, amnesia, and hypermnesia (remembering things toowell). In the original study, the SSD was administered to 130 patients with majordepression ( n=19), schizophrenia ( n=18), alcohol withdrawal ( n=20), dissociative
disorders ( n=10), and healthy controls ( n=63). A score of >3.9 nearly doubled the
certainty of a diagnosis of a dissociative disorder, although an important limitation isthe small sample of dissociative patients. The internal consistency of the SSD was goodto excellent for the total scale ( α=0.97), and correlations between the SSD and the DES
among people with a dissociative disorder were r=.81, and r=.57 in healthy controls.
Following a brief grounding activity (53 minutes, during which participants com-pleted a number of other scales), the SSD scores among all participants decreasedsigniﬁcantly on retest, suggesting that the SSD is sensitive to short-term changes in
dissociative states across diagnostic groups.
The Cambridge Depersonalization Scale (CDS ; Sierra & Berrios, 2000) consists of 29
items that ask respondents to rate recent depersonalization symptoms on a 5-pointfrequency scale (anchors: 0 =never; 4 =all the time) and a 6-point duration scale
(anchors: 1 =few seconds; 6 =more than a week). The scale differentiates patients with
DDD from other patient groups (e.g., patients with epilepsy, anxiety disorders) andfrom healthy controls (Sierra & Berrios, 2000). Sierra and Berrios (2000, 2001) reportedsound internal consistency for the CDS (e.g., α=0.89). An exploratory factor analysis
identi ﬁed four factors that accounted for 73.3% of the variance: anomalous body
experience, emotional numbing, anomalous subjective recall, and alienation fromsurrou ndings
(Sierra et al., 2005).
Assessment is often an ongoing process in psychotherapy, and much information
can be gleaned in the absence of standardized tests of dissociative experiences andDissociative Disorders 421

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symptoms. In this regard, a number of caveats are in order. Less formal assessmentprocedures that even subtly suggest a history of abuse or validate the manifestation ofalters with separate histories (e.g., personality “system mapping ”to establish contact
with nonforthcoming alters, providing names to alters, prompting or suggesting theemergence appearance of alters) should be avoided. A concern is that therapists whorepeatedly ask leading questions such as “Is it possible that there is another part of you
with whom I haven ’t yet spoken? ”may elicit via suggestion imagined-believed-in
alter personalities that ostensibly account for their clients ’otherwise enigmatic
behaviors (e.g., self-mutilation, and rapid and intense mood shifts). Repeated ques-tioning about historical events is not helpful, as it can lead patients to mistakenlybelieve that they have signi ﬁcant gaps (e.g., amnesia) in their autobiographical
memories of childhood (Belli, Winkielman, Read, Schwartz, & Lynn, 1998; Read &Lindsay, 2000). Assessors should also eschew the use of hypnosis to recover allegedlydissociated or repressed memories given that hypnosis does not enhance the overallaccuracy of memories and is associated with a heightened risk for confabulation(Lynn, Knox, Fassler, Lilienfeld, & Loftus, 2004).
CASE EXAMPLE
C
ASEIDENTIFICATION AND PRESENTING COMPLAINTS
The patient, a 47-year old Caucasian female, ﬁrst presented with dissociative symp-
toms to a health professional during a routine pelvic examination (see Colletti, Lynn, &Laurence, 2010 for a more complete description). During the exam, she exhibiteddramatic changes in her demeanor. In quick succession, her emotions vacillatedunpredictably, ranging from calm and composed, to scared and vulnerable, to angryand aggressive. The physician referred her for psychotherapy, insofar as her histrionicpresentation was at sharp variance with what he observed during prior of ﬁce visits.
H
ISTORY
When the patient initiated treatment with a psychotherapist, she insisted that herproblems were the product of stress at work related to serious medical concerns (e.g.,lupus, peripheral neuralgia, among others) that interfered with her job performance.Nevertheless, the therapist, a graduate student at a psychological clinic, noted that hermood and behavior ﬂuctuated dramatically both within and between sessions, with
episodes of anger and anxiety ﬂaring up frequently and unpredictably within sessions.
Over the next 2 years, the patient recounted a history of sexual assault 7 years prior totreatment, the death of a sibling, intense and sometimes unstable interpersonalrelationships, and sexual abuse in childhood. Emotional outbursts during sessionsescalated; seemingly innocuous statements by the therapist could trigger memories ofhighly aversive events. The patient began to experience more frequent crises in andout of sessions as well as emotional lability, often alternating between speaking in achildlike voice and an angry adult, only to later apologize and express deep regret. Hermemory for what transpired when she appeared to be enacting different “identities ”
was spotty and at times devoid of meaningful content.
After 2 years of treatment, the graduate student transferred the case to his supervisor,
who witnessed increased irritability, vitriolic anger, and ﬂashback-like experiences422 S
PECIFIC DISORDERS

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in session that were followed by amnesia, depersonalization, derealization, and prob-lems in focusing attention. The patient reported feeling “spaced out ”in session, and
reported that she often was aware of “missing time ”at home, and experienced
difﬁculties recalling anything beyond the gist of the previous session. At the start of
treatment with her second therapist, she met the criteria for borderline personalitydisorder, and DID was considered a rule-out diagnosis. She reported hearing “voices in
my head ”and experienced herself as “splitting off ”into an angry “adult protector ”or
defender of others and childlike aspects of herself that required protection. One majordiathesis for her dissociative symptoms appeared to be a history of fantasy versusreality-based coping originating in childhood. She became aware of this style ofcoping when her sister died when the patient was 5 years old, and she experiencedguilt for not somehow preventing her death. She stated that she began, from that timeforward, to think of herself as split into angry and protective “parts. ”As therapy
progressed, she reported more frequent episodes of depersonalization and disturbingepisodes of amnesia, as well as disorientation at times of high stress. She also reportedmore incidents of abuse during childhood, and her therapist felt her presentation nowmet criteria for DID.
At this time, Steven Jay Lynn, one of the authors of this chapter, was invited to serve
as a consultant and co-therapist. The therapists conveyed the consistent message thatalthough at times she felt as if she housed distinct personalities, she truly embodiedonly one personality. The therapists implemented a multifaceted treatment thatincluded: (a) elements of affect management and problem-solving to contend withanger; (b) cognitive behavioral therapy (CBT techniques including activity schedulingfor depressed mood, progressive muscle and hypnosis-based relaxation, and rationaldisputation of maladaptive thoughts); (c) mindfulness-based techniques for detachingfrom negative and self-deprecating cognitions and moods; and (d) affect containmentmethods derived from dialectical behavior therapy. After 4 years of treatment, thepatient exhibited no signs of “personality split” and only occasional episodes of
depersonalization, with improved functioning and mood stabilization.A
SSESSMENT
The patient met all the diagnostic criteria for DID, including her enacting distinct“identities ”during sessions and reports of such alterations outside of sessions. She
also reported amnesia associated with dissociative episodes, and was troubled by herfailure to recall key interpersonal interactions that others remembered well. Thepatient was not assessed at the outset of treatment, although when SJL came onboard,she was evaluated with the DES and scored in the clinical range (i.e., 39) and metdiagnostic criteria for DID based on the SCID-D (Steinberg, 1994).
ETIOLOGICAL CONSIDERATIONS
B
EHAVIORAL GENETICS
Limited research is available on the behavioral genetics of dissociative disorders. Theevidence indicates that DID co-aggregates within biological families (APA, 1994),although data on intact family members are indeterminate with regard to geneticDissociative Disorders 423

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versus shared environmental causation. Using twin registry data, Jang, Paris, Zweig-Frank, and Livesley (1998) reported that 48% of the variability in DES-T scores isattributable to genes, and that the other 52% of the variance can be attributed tononshared environments. When the researchers considered nonpathological dissoci-ation scores, excluding taxon items, genetic in ﬂuences accounted for 55% of the
variance, whereas nonshared environmental in ﬂuences accounted for 45% of the
variance. Similarly, a study of children and adolescents found a substantial genetic(59% genes, 41% nonshared environments) contribution to dissociation scores (Becker-Blease et al., 2004). In contrast, a study (Waller & Ross, 1997) based on 280 identicaltwins and 148 fraternal twins found no evidence for genetic in ﬂuences. Approximately
45% of the variance on a measure of pathological dissociation (DES-T) was attributableto shared environmental in ﬂuences, with the remaining variance due to nonshared
environmental in ﬂuences. Adoption studies would help to clarify the extent to which
the familial clustering of dissociative disorders is due to genes, shared environment,or both.B
IOLOGY
Drugs, notably low doses of the anesthetic ketamine, often produce dream-like statesand dissociative symptoms, suggesting that dissociative experiences need not neces-sarily arise in the aftermath of trauma. Krystal et al. (1994) found that ketamineproduces alterations in the perception of time (i.e., slowing) and alterations in thevividness, form, and context of sensory experiences, all possibly attributable todiminished NMDA-related neurotransmission (Simeon, 2004). Interestingly, cannabi-noids, including marijuana, which induce dissociative experiences, may similarlyaffect NMDA receptors (Simeon et al., 2003). The fact that hallucinogens (e.g., LSD),which frequently elicit depersonalization reactions in healthy participants, are ago-nists of serotonin 5-HT
2Aand 5-HT 2Creceptors implies that serotonin also may
mediate dissociation (Simeon, 2004). Research that establishes links between drugsthat produce dissociative symptoms in conjunction with changes in speci ﬁc neuro-
transmitter systems hold the potential to shed light on the neurobiological basisof these dissociative symptoms (Giesbrecht et al., 2008). The pharmacological study ofdissociation is important because it may shed light on the paradoxical phenomenonthat detoxiﬁed opiate users exhibit higher dissociation scores than patients who are ona methadone maintenance regimen (Somer, Altus, & Ginzburg, 2010). One possibleexplanation for this pattern is the chemical dissociation hypothesis, that is, the notionthat substance abuse patients achieve dissociative-like states through chemicals (e.g.,alcohol, opiates), and in the absence of chemicals, they feel compelled to produce thedissociative symptoms themselves. This line of reasoning is consistent with pilotdata suggesting that the opioid blocking drug naloxone is effective in reducingdepersonalization experiences (Nuller, Morozova, Kushnir, & Hamper, 2001; butsee Somer, Amos-Williams, & Stein, 2013).
Studies examining daytime EEG activity in highly dissociative individuals have
generally found evidence that dissociative experiences are related to parameterssignaling reduced attentional control (e.g., attenuated P300, Kirino, 2006; decreasedtheta activity; Krüger, Bartel, & Fletcher, in press). Sleep EEG recordings obtained ininsomnia patients found suggestive evidence that dissociative psychopathology is424 SPECIFIC DISORDERS

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related to extended REM sleep (van der Kloet et al., 2013). It is tempting to relate lackof attentional control and extended REM to structural sleep disturbances, as suggestedlater in our discussion.
Simeon et al. (2000) used PET and MRI brain imaging to compare 8 participants
with DDD with 24 healthy participants. The researchers found that depersona-lization is associated with functional abnormalities in sequential hierarchicalareas —secondary and cross modal —of the sensory cortex (visual, auditory, and
somatosensory), as well as areas responsible for integrated body schemas. Speci ﬁ-
cally, DDD patients showed lower metabolic activity in right Brodmann areas 21 and22 of the superior and middle temporal gy ri, and higher metabolism in parietal
Brodmann areas 7B and 39 and left occipital Brodmann area 19. The researcherscontended that these ﬁndings are compatible with the phenomenological concep-
tualization of depersonalizat ion as a dissociation of perceptions, as well as with the
subjective symptoms of DDD.
In a fascinating study, Sang, Jáuregui-Renaud, Green, Bronstein, and Gresty (2006)
showed that disorienting vestibular stimulation produced by caloric irrigation of theear labyrinths engendered depersonalization in healthy participants and symptoms(e.g., feeling spaced out, body feels strange/not in control of self) similar to thoseexperienced by patients with vestibular disease. The researchers suggested thatdepersonalization/derealization experiences may “occur because distorted vestibular
signals mismatch with sensory input to create an incoherent frame of spatial referencewhich makes the patient feel that he or she is detached or separated from the world ”
(p. 760).
In a later study, the researchers (Jáuregui-Renaud, Sang, Gresty, Green, &
Bronstein, 2008) found that patients with peripheral vestibular disease reported a
higher prevalence of depersonalization/de realization symptoms and greater errors
on a body rotation test of updating spatial orientation compared with healthycontrol participants. The investigators claimed that their ﬁndings support their
theory that DDD symptoms sometimes re ﬂect a mismatch between disordered
vestibular input and other sensory signals of orientation. This claim was supported
in a study in which patients with vestibular disease and patients with retinal diseasereported more symptoms of depersonalizat ion than patients with hearing loss and
healthy participants (Jáuregui-Renaud, Ra mos-Toledo, Aguilar-Bolaños, Montaño-
Velazquez, & Pliego-Maldonado, 2008). Depersonalization and derealization expe-riences may well be the product of mism atches or lack of integration between
multisensory inputs (e.g., vestibular, visual, proprioceptive) that produces dys-functional neural representations that i n turn generate an altered sense of self and
reality (Aspell & Blanke, 2009).
Out-of-body experiences (OBEs), which are intimately related to depersonalization,
are increasingly being studied in the laboratory (e.g., Ehrsson, 2007; Lenggenhager,Tadi, Metzinger, & Blanke, 2007) and are coming to be understood in terms of thescrambling of the senses (e.g., touch and vision) when people ’s usual experience of
their physical body becomes disrupted. In addition, scientists are identifying the brainlocation of OBEs by stimulating the vestibular cortex, the superior temporal gyrus, andthe place where the brain ’s right temporal and parietal lobes join (Blanke, Ortigue,
Landis, & Seeck, 2002; Blanke & Thut, 2007; Cheyne & Girard, 2009; De Ridder, VanLaere, Dupont, Menovsky, & Van de Heyning, 2007; Persinger, 2001).Dissociative Disorders 425

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Ehrrson (2007) provided participants with goggles that perm itted them to view a
video display of themselves relayed by a camera placed behind them. This set-up
created the illusion that their bodies, viewed from the rear, were standing in frontof them. Ehrrson touched participants with a rod on the chest while he used camerasto make it appear that the visual image was being touched at the same time.Participants reported the eerie sensatio n that their video double was also being
touched. In short, they reported that they could experience the touch in a location
outside their physical bodies (see also Aspell, Lenggenhager, & Blanke, 2009;
Lenggenhager et al., 2007). When visual sen sory impressions combine with physical
sensations, they can deceive people into believing that their physical selves areseparate from their bodies (Cheyne & Girard, 2009; Terhune, 2009), suggesting aphysiological genesis of at least some depersonalization experiences. Relatedly,disruptions in somatosensory signals may explain why some people experienceOBEs during sleep paralysis (Nelson, Matt ingly, Lee, & Schmitt, 2006) and during
general anesthesia when they retain partial awareness (Bunning & Blanke, 2005).Nevertheless, researchers have little understanding of how stressors and otherprecipitants of depersonalization and derealization create and maintain the symp-toms of dissociative disorders.
Researchers have devoted considerable attention to describing physiological dif-
ferences among alters in DID and have reported interidentity differences in heart rates,voice pitch, eyeglass prescriptions, handedness, handwriting, allergies, or pain toler-ance (see Lilienfeld & Lynn, in press). Nevertheless, it is unclear whether suchdifferences validate the existence of alters, as many of these differences may merelyreﬂect differences in mood, differences stemming from the unconscious role-playing
of different identities, or both. Also, some authors have pointed out that one mayobtain similar intra-individual differences when healthy actors are instructed to role-play alters (Boysen & VanBergen, in press; Merckelbach, Devilly & Rassin, 2002).Moreover, Allen and Movius (2000) suggested that some of these apparent differencesmight re ﬂect Type I errors given the large number of psychophysiological variables
analyzed in many of these studies.
Tsai, Condie, Wu, and Chang (1999) used MRI with a 47-year-old female with DID
in an attempt to corroborate a history of childhood abuse. The authors drew uponprevious investigations that had reported a reduction in hippocampal volume fol-lowing combat trauma (e.g., Bremner, Randall, Scott, & Bronen, 1995) and early abuse(Bremner, Randall, Vermetten, & Staib, 1997; Stein, Koverola, Hanna, & Torchia, 1997)to hypothesize that DID patients —given their presumed history of early abuse —
would similarly exhibit decreased hippocampal volume. As predicted, they foundsigniﬁcant bilateral reductions in hippocampal volume in their patient with DID.
Nevertheless, this ﬁnding must be interpreted cautiously for two major reasons
(Lilienfeld & Lynn, in press). First, because it is based on only one patient, itsgeneralizability to other individuals with DID is unclear. Second, decreased hippo-campal volume is not speci ﬁc to PTSD or to other conditions secondary to trauma, and
has also been reported in schizophrenia (Nelson, Saykin, Flashman, & Riordan, 1988)and depression (Bremner et al., 2000). Consequently, decreased hippocampal volumemay be a nonspeci ﬁc marker of long-term stress (Sapolsky, 2000) that is present in
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LEARNING ,M ODELING AND LIFEEVENTS
Some cases of (mis)diagnosed dissociative disorders are probably a product ofmalingering. Estimates suggest that malingering or other forms of feigning (e.g.,the faking seen in factitious disorders) account for 2% –10% of diagnoses of inpatient
dissociative disorders (Friedl & Draijer, 2000). There is widespread agreement thatDID can be successfully malingered. For example, Kenneth Bianchi, one of the twoHillside Strangler murderers, is widely believed to have faked DID to escape criminalresponsibility (Orne, Dinges, & Orne, 1984). In one survey, experienced neuropsy-chologists estimated the prevalence of feigned dissociative symptoms in casesinvolved in litigation to be about 10% (Mittenberg, Patton, Canyock, & Condit,2002). Nevertheless, cases of malingered DID are believed to be quite rare outsideof forensic settings, and the substantial majority of individuals with this condition donot appear to be intentionally fabricating their symptoms. Malingerers strive foradvantages (e.g., ﬁnancial, legal), but dissociative disorders are known to be associ-
ated with functional impairments that are so severe that they qualify as serious andoften debilitating mental illnesses (Mueller-Pfeiffer et al., 2012).
THE POSTTRAUMATIC VERSUS THE SOCIOCOGNITIVE
MODELS OF DISSOCIATION
There is little dispute that some individu als meet the diagnostic criteria for DID,
display unpredictable and sometimes bizarre shifts in mood and behavior, and areconvinced that they house compartmentalized “personalities” engendered by severe
early physical abuse, sexual abuse, or bot h. Nevertheless, over the past 25 years,
controversy has swirled around the question of whether the symptoms of DID arenaturally occurring responses to early trauma (Dalenberg et al., 2012; Gleaves, 1996),as the posttraumatic model (PTM) of disso ciation holds, or are largely socially
constructed and culturally in ﬂuenced, as the sociocognitive model (SCM) —called
by some the fantasy model (Dalenberg et al., 2012) —of dissociation holds (Spanos,
1994). One commentator (Paris, 2012) has gone so far as to claim that DID is a fadthat is now declining in interest in the psychiatric community, whereas othershave vigorously challenged this assertion (Brand, Loewenstein, & Spiegel, 2013b;Martinez-Taboas, Dorahy, Sar, Middleton, & Krüger, 2013).
Proponents of the PTM (Gleaves, 1996; Gleaves et al., 2001; Ross, 1997) argue that
DID is a posttraumatic condition that ar ises primarily from a history of severe
physical and/or sexual abuse in childhood. Advocates of the PTM contend that suchabuse is a crucial contributor to DID: The child compartmentalizes the abuse so thathe or she feels as though it is happening to someone else (Ross, 1997). Moreover,alters or ego states supposedly arise as a means of coping with the intense emotionalpain of the trauma [see Lilienfeld & Lynn (in press), for an explanation and critique].PTM theories variously emphasize the effects of childhood abuse and early traumaticexperiences on producing (a) patterns of disorganized interpersonal attachment(Liotti, 1999; 2009) that engender dissociati on; (b) structural dissociation (i.e., the
d e v e l o p m e n to fd i f f e r e n t“ parts” of the personality to handle different functions in
“defense ”and everyday life; Steele, van der Hart, Nijenhuis, 2009); (c) disturbancesDissociative Disorders 427

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in the self-system that integrates “identity-mind-body-world-time ”into a coherent
whole; in this view, alters are conceptualized as “younger self-systems (ego-states)
that are ‘trapped’ in a past trauma ”(p. 283, Beere, 2009); (d) developmental de ﬁcits
that degrade self-regulation and promote fra gmentation of the self (Carlson, Yates, &
Sroufe, 2009); and (e) a dissociative informa tion processing style related to feelings of
being betrayed by a trusted caregiver (Barlow & Freyd, 2009; Freyd, 1996).
These diverse theories are ostensibly supported by very high rates— sometimes
exceeding 90% —of reported histories of severe child abuse among patients diagnosed
with DID and other severe dissociative disorders (Dalenberg et al., 2012; Gleaves,1996). Nevertheless, critics of the PTM (see Giesbrecht et al., 2008; Giesbrecht et al.,2010; Lilienfeld et al., 1999; Lynn et al., in press; Merckelbach & Muris, 2001; Spanos,1994, 1996) have questioned the notion that DID is invariably linked to child abuse ormaltreatment for the following ﬁve reasons:
1. Many studies that purport to con ﬁrm this association lack objective corrobora-
tion of child abuse (e.g., Coons, Bowman, & Milstein, 1988). For example,Sanders and Giolas (1991) found a correlation of r=.44 between the DES
and scores on a child-abuse questionnaire. Yet when a psychiatrist (unaware ofthe dissociative status of participants) provided more objective ratings of traumabased on hospital records, the authors found a nonsigni ﬁcant negative correlation
between ratings of traumatic experiences and dissociation ( r=.21).
2. The overwhelming majority of studies investigating the link between self-
reported trauma and dissociation are ba sed on cross-sectional designs that do
not permit causal inferences (Merckelb ach & Muris, 2001) and that are subject
to retrospective biases. Prospective studies that circumvent the pitfalls ofretrospective reporting often fail to substantiat e a consistent link between
childhood abuse and dissociation in a dulthood (Dutra, Bureau, Holmes,
Lyubchik, & Lyons-Ruth, 2009; Noll, Trickett, & Putnam, 2003; Ogawa, Sroufe,Wein ﬁeld, Carlson, & Egeland, 1997; but see Bremner, 2010; Dalenberg et al.,
2012).
3. Researchers rarely control for potentially comorbid psychopathological syn-
dromes and symptoms known to be related to dissociative disorders (e.g.,anxiety, eating, personality disorders, impulsivity, schizotypal traits; seeGiesbrecht et al., 2008; Lynn et al., in press).
4. The reported high levels of child abuse among DID patients may be attributable
to selection and referral biases common in psychiatric samples. For example,patients who are abused are more likely than other patients to enter treatment(Pope & Hudson, 1995).
5. Correlations between abuse and psychopathology tend to decrease substantially
or disappear when participants ’perception of family pathology is controlled
statistically (Nash, Hulsey, Sexton, Harralson, & Lambert, 1993). Based on theseﬁve points of contention, Lilienfeld and Lynn (in press) noted that the available
evidence provides little or no warrant for concluding that early abuse is anecessary causal antecedent of DID (see also Lynn et al., 2014).
In contrast to the PTM, proponents of the sociocognitive model (SCM; Spanos, 1994,
1996; see also Aldridge-Morris, 1989; Lilienfeld et al., 1999; Lynn et al., 2014; Lynn &428 SPECIFIC DISORDERS

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Pintar, 1997; McHugh, 1993; Merskey, 1992; Sarbin, 1995) contend that DID resultsfrom inadvertent therapist cueing (e.g., suggestive questioning regarding the existenceof possible alters, hypnosis, sodium amytal), media in ﬂuences (e.g., television and ﬁlm
portrayals of DID, such as “Sybil ”), and broader sociocultural expectations regarding
the presumed clinical features of DID.
Advocates of the SCM cite the following ﬁndings (Lilienfeld et al., 1999; Lilienfeld &
Lynn, in press) as consistent with the SCM or as challenges to the PTM:
1. The number of patients with DID, along with the number of alters per DID
individual, have increased dramatically over the past few decades (Elzinga, vanDyck, & Spinhoven, 1998; North et al., 1993), although the number of alters at thetime of initial diagnosis appears to have remained constant (Ross, Norton, &Wozney et al., 1989).
2. The massive increase in reported cases of DID followed closely upon the release
of the best-selling book Sybil (Schreiber, 1973) in the mid 1970s, which told the
story of a young woman with 16 personalities who reported a history of severechild abuse at the hands of her mother. As noted earlier, in 1976, this book wasturned into a widely viewed television ﬁlm starring Sally Fields. Interestingly,
however, a well-known psychiatrist who was involved closely with the Sybilcase later contended that Sybil’ s presentation of DID was largely or entirely the
product of therapeutic suggestion. Herbert Spiegel, who served as a backuptherapist for Sybil, maintained that Sybil ’s primary therapist, Cornelia Wilbur,
frequently encouraged her to develop an d display differen t personalities in
therapy. According to Rieber (2006), who possessed tapes of conversations
between Sybil and Cornelia Wilbur, Spiegel referred to Sybil as a “brilliant
hysteric, ”with multiple identities fabricated to please the all too credulous
Wilbur. Spiegel further maintained that Wilbur and Flora Schreiber, whoauthored the best-selling book about Sybil, insisted that Sybil be described inthe book as a “multiple ”to make the book more appealing (Acocella, 1999).
Rieber concluded “the three women —Wilbur, Schreiber, and Sybil —are respon-
sible for shaping the modern myth of multiple personality disorder ”(Rieber,
2006, p. 109). In short, increases in the d iagnosis of DID and the number of alters
per DID patient coincide with dramatically increased therapist and publicawareness of the major features of DID (Fahy, 1988).
3. Mainstream treatment techniques for DID often reinforce patients ’displays of
multiplicity (e.g., asking questions like, “Is there another part of you with whom I
have not spoken? ”), reify alters as distinct personalities (e.g., therapists calling
different alters by different names, mapping their “personality systems ”), and
encourage patients to establish contact and dialogue with presumed latent alters(Spanos, 1994, 1996). A case in point is the N=1 within-subject study by
Kohlenberg (1973), who showed that the behavioral displays of alter personalitiescan depend on reinforcement contingencies: The patient ’s alters soon “disap-
peared ”after hospital staff stopped attending to them.
4. Many or most DID patients show few or no clear-cut signs of this condition (e.g.,
alters) prior to psychotherapy (Kluft, 1984).
5. The number of alters per DID individual tends to increase substantially over
the course of DID-oriented psychotherapy (Piper, 1997) and there are indicationsDissociative Disorders 429

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that this type of therapy might exacerbate symptoms (Fetkewicz, Sharma, &Merskey, 2000).
6. Psychotherapists who use hypnosis tend to have more DID patients in their
caseloads than do psychotherapists who do not use hypnosis (Powell & Gee, 1999).
7. The majority of diagnoses of DID derive from a relatively small number
of psychotherapists, many of whom are specialists in DID (Mai, 1995) andfrom a relatively small number of people in treatment (Boysen, 2011; Boysen &VanBergen, 2013; but see Brand, Loewenstein, & Spiegel, 2013b).
8. Laboratory studies suggest that nonclinical participants who are provided with
appropriate cues and prompts can reproduce many of the overt features of DID(Spanos, Weekes, & Bertrand, 1985; Stafford & Lynn, 2002).
9. Until 20 years ago, diagnoses of DID were limited largely to North America, where
the condition has received widespread media publicity (Spanos, 1996), althoughDID is now being diagnosed with considerable frequency in some countries (e.g.,Holland) in which it has become more widely publicized since the 1990s. Mani-festations of DID symptoms also vary across cultures. For example, in India, thetransition period as the individual shifts between alter personalities is typicallypreceded by sleep, a presentation that re ﬂects common media portrayals of DID
in India (North et al., 1993). There are indications that both research interestin DID and media coverage of the condition are waning, and so it will beinteresting to see whether this change heralds drops in prevalence rates (Pope,Barry, Bodkin & Hudson, 2006).
10. Laboratory research summarized below challenges the assertion that conscious-
ness can be separated into multiple streams by amnesic barriers to form indepen-dently functioning alter personalities (Huntjens, Verschuere, & McNally, 2012;Kong, Allen, & Glisky, 2008; Lynn et al., 2004).
These 10 sources of evidence do not imply that DID can typically be created in vacuo
by iatrogenic (therapist-induced) or sociocultural in ﬂuences. SCM theorists acknowl-
edge that iatrogenic and sociocultural in ﬂuences typically operate on a backdrop of
preexisting psychopathology, and exert their impact primarily on individuals who areseeking a causal explanation for their instability, identity problems, and impulsiveand seemingly inexplicable behaviors. Indeed, the SCM is entirely consistent withﬁndings, reviewed earlier, that many or most patients with DID meet criteria for
borderline personality disorder, a condition marked by extremely labile behaviors.C
OGNITIVE MECHANISMS OF DISSOCIATION
Despite subjective reports of profound cognitive disturbances like amnesia, feelings ofunreality, and identity alterations, researchers have found evidence for only relativelysubtle and speci ﬁc cognitive de ﬁcits in highly dissociative individuals. Such individ-
uals usually fall within the normative range on tests of intellectual ability and standardneuropsychological tests (Giesbrecht et al. 2008; Schurle, Ray, Bruce, Arnett, &Carlson, 2007). Indeed, whereas most studies, with few exceptions (but see Prohl,Resch, Parzer, & Brunner, 2001), fail to report any link between dissociation andworking memory capacity, some report that dissociative individuals exhibit superior
verbal working memory capacity or performance (Giesbrecht et al., 2008).430 SPECIFIC DISORDERS

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When cognitive de ﬁcits in dissociative patients are identi ﬁed, they tend to be quite
speciﬁc. For example, Guralnik, Schmeidler, and Simeon (2000) found that DDD
patients exhibited de ﬁcits in visual perception and visual-spatial reasoning for both
two- and three- dimensional stimuli. Patients’ visual and verbal short-term memory
capacity was also compromised, for both abstract and meaningful information,
especially under information overload co nditions. DDD participants experienced
difﬁculty with early stimulus-encoding tasks under conditions of heightened dis-
traction, to which they responded with m ore omission errors. Accordingly, DDD
appears to be characterized by vulnerability in early information processing atthe level of perception and attention (for r eplications, see Guralnik, Giesbrecht,
Knutelska, Sirroff, & Simeon, 2007; Quaed ﬂieg et al., 2012).
Simeon and colleagues (Simeon, Hwu, & Knutelska, 2007) found evidence for a
relationship between the dissociative symptoms of DDD patients, temporal dis-integration (i.e., problems in memory regarding the chronology and dating of events),and total DES scores. They concluded that the dissociative dimension of absorption isa signi ﬁcant predictor of temporal disintegration.
The relative absence of a measurable general neuropsychological de ﬁcit in the
dissociative disorders is noteworthy, as it differentiates them from most othersevere psychiatric disorders, such as schizophrenia and bipolar disorder. These otherconditions overlap with the dissociative disorders, but unlike them, are marked by awide range of neuropsychological de ﬁcits (Heinrichs & Zakzanis, 1998). In addition,
different dissociative disorders appear related to different cognitive de ﬁciencies. DID
is characterized mainly by performance ﬂuctuations [e.g., increased scatter on the
Wechsler Adult Intelligence Scale (Wechsler, 1981); Rossini, Schwartz, & Braun, 1996;reduced P300 amplitudes, but only during acute dissociative episodes in DID patients;Kirino, 2006], whereas DDD is associated with disruptions in early stages of informa-tion processing (Guralnik et al., 2000). Nevertheless, few investigations have con-trolled for general distress and psychopathology, or for scores on opennessto experience, which is moderately associated with both dissociative tendencies(Kihlstrom, Glisky, & Angiulo, 1994) and with crystallized intelligence (DeYoung,Peterson, & Higgins, 2005). Interestingly, as we have noted earlier, dissociativeindividuals sometimes exhibit a performance advantage relative to nondissociativeindividuals (e.g., Chiu, Yeh, Huang, Wu, & Chiu, 2009).
Much of the literature on cognitive mechanisms of dissociation is more consistent
with the SCM rather than the PTM. As already noted, proponents of the PTM typicallyargue that individuals who undergo horri ﬁc trauma in early life often dissociate or
compartmentalize their personalities into discrete alters, segregated by amnesicbarriers, as a means of coping with the intense emotional pain of the trauma. However,studies of amnesia among patients with DID have generally not reported ﬁndings
commensurate with the existence of true amnesia among so-called alter personalities(Giesbrecht et al., 2010). For example, researchers have found little or no evidence forinteridentity amnesia using objective measures (e.g., behavioral tasks or event relatedpotentials) of memory (e.g., Allen & Movius, 2000; Huntjens et al., 2006; Huntjenset al., 2012; Huntjens, Peters, Woertman, van der Hart, & Postma, 2007; Kong et al.,2008).
If dissociative symptoms attenuate the impact of traumatic events, individuals with
heightened levels of dissociation should exhibit slower or impaired processing ofDissociative Disorders 431

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threat-related information. Nevertheless, patients with DID and other “high disso-
ciators ”display better memory for to-be-forgotten sexual words in directed forgetting
tasks (Elzinga, de Beurs, Sergeant, Van Dyck, & Phaf, 2000; see also Cloitre, Cancienne,Brodsky, Dulit, & Perry, 1996), a ﬁnding strikingly discrepant with the presumed
defensive function of dissociation. Research on nonclinical samples (e.g., Candel,Merckelbach, & Kuijpers, 2003) showing that dissociation is not associated withinferior memory performance has been replicated in patients with DDD (Montagneet al., 2007). Studies of cognitive inhibition in high dissociative clinical (Dorahy,Irwin, & Middleton, 2002; Dorahy, Middleton, & Irwin, 2005; Dorahy, McCusker,Loewenstein, Colbert, & Mulholland, 2006) and nonclinical (Giesbrecht, Merckel-bach, & Smeets, 2006) samples typically ﬁnd a breakdown in such inhibition, which
stands in sharp contrast with the widespread idea that amnesia (i.e., extremeinhibitory effect on memory) is a core feature of dissociation (Anderson et al.,2004). Research also ﬁnds mixed support at best for the contention that highly
dissociative individuals are superior to low dissociators in dividing their attention.In two samples, Devilly et al. (2007) failed to replicate DePrince and Freyd ’s (2001)
ﬁndings of superior forgetting of trauma-related words in high- versus low-disso-
ciator college students in a divided attention task (see also Giesbrecht & Merckelbach,2009). Giesbrecht et al., (2010) contended that the ﬁndings we have reviewed challenge
the widespread assumption that dissociation is related to avoidant informationprocessing and suggested that apparent gaps in memory in interidentity amnesia,or dissociative amnesia more generally, could re ﬂect intentional failures to report
(McNally, 2003; Pope et al., 2006).
Giesbrecht and colleagues (Giesbrecht et al., 2008; Giesbrecht et al., 2010) further
argued that dissociation is marked by a propensity toward pseudomemories, possiblymediated by heightened levels of suggestibility, fantasy proneness, and cognitivefailures. They noted that at least 10 studies from diverse laboratories have con ﬁrmed a
link between dissociation and fantasy proneness (Giesbrecht, Merckelbach, Kater, &Sluis, 2007), and that heightened levels of fantasy proneness are associated with boththe tendency to overreport autobiographical memories (Merckelbach, Muris, Horse-lenberg, & Stougie, 2000) and the false recall of aversive memory material (Giesbrecht,Geraerts, & Merckelbach, 2007).
These authors contended that the relation between dissociation and fantasy prone-
ness may explain why individuals with high levels of dissociation are more prone thanother individuals to develop false memories of emotional childhood events (e.g., asevere animal attack; Porter, Birt, Yuille, & Lehman, 2000), and further pointed to datarevealing links between hypnotizability, dissociative symptoms (Frischholz, Lipman,Braun, & Sachs, 1992), and high scores on the Gudjonsson Suggestibility Scale (GSS:Gudjonnson, 1984; Merckelbach, Muris, Rassin, & Horselenberg, 2000; Wofradt &Meyer, 1998). Similarly, some researchers have shown that dissociation increases therisk of commission (e.g., confabulations/false positives, problems discriminating per-ception from vivid imagery, errors in response to misleading questions) rather thanomission memory errors; the latter type of error is presumably associated withdissociative amnesia (Giesbrecht et al., 2008; Holmes et al., 2005). Nevertheless, ﬁndings
pertinent to the relation between trait dissociation and false memory susceptibility areoften mixed and not invariably strong in magnitude (see Dalenberg et al., 2012; Lynnet al., 2014).432 SPECIFIC DISORDERS

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T a k e nt o g e t h e rw i t hr e s e a r c hd e m o n s t rating a consistent link between dis-
sociation and cognitive failures (Merc kelbach, Horselenberg, & Schmidt, 2002;
Merckelbach, Muris, & Rassin, 1999; Wright & Osborne, 2005), the ﬁndings sum-
marized above point to an association be tween heightened risk of confabulation
and possibly pseudomemories that raise questions regarding the accuracy of
retrospective reports of traumatic experiences. In addition, these ﬁndings limit
the inferences that we can draw from studie s that rely exclusively on self-reports
to establish a connection between trauma and dissociation (Merckelbach & Jelicic,2004; Merckelbach et al., 2000).
Still, these ﬁndings do not exclude some role for trauma in the genesis of
dissociation and dissociative disorders. Suggestibility, cognitive failures, and fantasyproneness might contribute to an overestimation of a genuine, although perhaps weakor modest, link between dissociation and trauma. Alternatively, early trauma mightpredispose individuals to develop high levels of fantasy proneness (Lynn, Rhue, &Green, 1988), absorption (Tellegen & Atkinson, 1974), or related traits. In turn, suchtraits may render individuals susceptible to the iatrogenic and cultural in ﬂuences
posited by the SCM, thereby increasing the likelihood that they will develop DIDfollowing exposure to these in ﬂuences. This and even more sophisticated etiological
models of DID have yet to be subjected to direct empirical tests. In the next section, weexamine a novel theory that provides a possible basis of rapprochement between thePTM and the SCM.S
LEEP,MEMORY ,ANDDISSOCIATION
A theory originally formulated by Watson (2001) linking sleep, memory failure, anddissociation may provide a conceptual bridge between the PTM and the SCM. In areview of 19 studies, van der Kloet, Merckelbach, Giesbrecht, and Lynn (2012)concluded that the extant research provides strong support for a link betweendissociative experiences and a labile sleep-wake cycle that is evident across a rangeof phenomena, including waking dreams, nightmares, and hypnogogic (occurringwhile falling asleep) and hypnopompic (occurring after falling sleep) hallucinations.Studies that offered evidence for a link between dissociative experiences and sleepdisturbances relied on clinical and nonclinical samples, and, with only one exception,yielded correlations in the range of 0.30 –0.55, suggesting that unusual sleep experi-
ences and dissociation are discriminable yet related constructs. Moreover, researchers(Giesbrecht, Smeets, Leppink, Jelicic, & Merckelbach, 2007) have shown that sleep lossinduced in the laboratory intensi ﬁes dissociative symptoms, suggesting a possible
causal link between sleep experiences and dissociation.
These ﬁndings suggest an intriguing interpretation of the link between dissocia-
tive symptoms and deviant sleep phenome na (see also Watson, 2001). Individuals
with a labile sleep-wake cycle —perhaps associated with a genetic propensity or
perhaps a byproduct of intrusions of trauma related memories —experience intru-
sions of sleep phenomena (e.g., dreamlike e xperiences) into waking consciousness,
which in turn foster fantasy proneness, depersonalization, and derealization. Thesedisruptions of the sleep-wake cycle, in turn, degrade memory (Hairston & Knight,2004) and attentional control (Williamson, F eyer, Mattick, Friswell, & Finlay-Brown,
2001), thereby accounting for, or co ntributing to, the attention de ﬁcits and cognitiveDissociative Disorders 433

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failures evidenced by highly dissociative individuals (Giesbrecht, Merckelbach,Geraerts, & Smeets, 2004) and dissociative patients (Dorahy et al., 2006; Guralniket al., 2007).
Accordingly, the sleep-dissociation per spective may explain both (a) how highly
aversive events disrupt the s leep-cycle and increase vulnerability to dissociative
symptoms, and (b) why dissociation, trau ma, fantasy proneness, and cognitive
failures overlap. Thus, the sleep-dissociation perspective is commensurate withthe possibility that trauma mediated by sleep disturbances plays a pivotal role in thegenesis of dissociation, and suggests that p reviously competing theoretical perspec-
tives may be amenable to integration. The SCM holds that patients becomeconvinced they possess separate indwelli ng identities as a byproduct of suggestive
media, sociocultural, and psychotherapeutic in ﬂuences. These patients ’sensitivity
to suggestive in ﬂuences may arise from their propensity to fantasize, memory
errors, increased salience of negative memories, and dif ﬁculties in distinguishing
fantasy and reality brought about by disruptions in the sleep cycle.S
IGNS OF THEORETICAL CONVERGENCE
Recently, signs are emerging of a modi cum of convergence or rapprochement
between competing theoretical perspectives. On the one hand, adherents of thePTM (Dalenberg et al., 2012) acknowledge that (a) “DID is a disorder of self-
understanding” (p. 568) and that “those with DID have the inaccurate idea that they
are more than one person ”(p. 568); (b) the potential effe cts of trauma on dissociation
are difﬁ cult to completely parcel out from harms caused by a pathogenic family
environment; (c) biological vulnerabilities, psychiatric history, social support, andprenatal factors probably contribute to the genesis of dissociation; and (d) fantasy
proneness may lead to inaccurate trauma reports. On the other hand, proponents ofthe SCM (Lynn et al., 2014) currently a cknowledge that (a) trauma may play a
nonspeci ﬁc role in dissociation (e.g., by increasing stress levels); (b) laboratory
support for the link between false mem ories and dissociation is mixed and not
consistently impressive in magnitude; (c) traumatic events may produce memoryfragmentation due to failures to encode signi ﬁcant events; and (d) therapeutic
approaches to treat dissociation may be helpful, although the mechanisms by whichimprovement occurs have yet to be delineated and isolated from nonspeci ﬁce f f e c t s
of psychotherapy in the context of randomize d clinical trials. The fact that divergent
perspectives concur that multiple causal antecedents, and not merely early trauma,need to be considered to provide a comprehensive account of dissociation anddissociative disorders is a welcome development.T
REATMENT
Depersonalization and Derealization The available research evidence provides few
guidelines for the treatment of dissociative disorders. Pharmacological treatmentshave proven to be of little help in improving symptoms of DDD or other dissociativedisorders (Somer, Amos-Williams, & Stein, 2013). For example, only a small pro-portion of people with DDD exhibit a clinic ally meaningful or even partial response
to selective serotonin reuptake inhibitors or benzodiazepines. Although stimulant434 S
PECIFIC DISORDERS

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medications may improve con centration in individuals with DDD, they have little
effect on the core symptoms of depersonalization (Simeon, et al., 1997, 2003).Moreover, the symptoms of depersonalization are no more responsive to ﬂuoxetine
(Simeon, Guralnik, Schmeidler, & Knutels ka, 2004) or lamotrigine (Sierra, Phillips,
Krystal, & David, 2003) than they are to a placebo. According to Simeon (2009b), thewell-documented lack of response to anxiolytics or mood stabilizers among DDDpatients suggests that this condition cannot be reduced to a mood or anxiety
spectrum disorder, “despite being often triggere d by, or co-occurring with, the
latter ”(p. 439). Nevertheless, the fact that treatment response differs across dis-
orders does not necessarily preclude commonalities in etiology.
The literature on psychotherapy with patients with DDD is similarly scant. An open
study conducted by Hunter, Baker, Phillips, Sierra, and David (2005) examined theeffects of cognitive-behavioral therapy (CBT) in DDD. The investigators taughtpatients to interpret their symptoms in a nonthreatening way. Although therewere dramatic improvements in the patient sample and follow-up results were onthe whole promising, the results must be interpreted with caution given the absence ofa randomized control group. More rigorous trials are needed to con ﬁrm the merits of
CBT and other psychotherapeutic approaches in patients with DDD.Dissociative Identity Disorder Individuals with DID typically are in treatment for an
average of 6 to 7 years before being diagnosed with this condition (Gleaves, 1996).Advocates of the PTM see this ﬁnding as evidence that individuals with DID are
underdiagnosed, whereas advocates of the SCM see it as evidence that patients whoare later diagnosed with DID typically en ter treatment with few or no symptoms
of the disorder. The treatment outcome literature for DID is sparse. According toBrand, Classen, McNary, and Zaveri (2009), only eight studies have examinedtreatment outcomes for DID and other di ssociative disorders. More recently,
Brand ’s research team (Brand, Classen, Lanius, et al., 2009) reported a naturalistic
study of DID and DD-NOS treatment by community clinicians. Nevertheless, thereare no randomized controlled trials on DID .F u r t h e r m o r e ,s t u d i e sd on o tp e r m i ta n
evaluation of the extent to which sympto m reduction in dissociative patients is
due to regression to the mean, the passage of ti me, placebo effects, or other artifacts.
Other methodological problems include vari ability in treatments offered to patients
(e.g., Choe & Kluft, 1995), lack of controls for nonspeci ﬁc effects (e.g., Ellason &
Ross, 1997), dropout rates as high as 68% (Gantt & Tinnin, 2007), and the failure todocument clinically meaningful changes f ollowing treatment. As a consequence,
one cannot draw con ﬁdent conclusions regarding treatment ef ﬁcacy from the
extant literature.
Importantly, some literature suggests that patients treated with commonly used
DID interventions that involve identifying alters, addressing “parts, ”and recovering
memories deteriorate signi ﬁcantly over the course of treatment. In one study, the
majority of patients developed “ﬂorid posttraumatic stress disorder during treatment ”
(Dell & Eisenhower, 1990, p. 361). Moreover, after treatment commences, patientsreport increased suicide attempts (Fetkewicz et al., 2000), hallucinations, severedysphoria, and chronic crises (Piper & Merskey, 2004). Nevertheless, Brand andLoewenstein (in press) contended that their analysis of treatment outcomes indicatesthat DID treatment, including interacting with “dissociated self states,” improvesDissociative Disorders 435

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clinical outcomes and that depriving DID patients of treatment may cause “iatrogenic
harm. ”Studies that compare negative sequelae across DID and conventional therapies
are a priority.
Assuming that future studies establish that certain sleep deviations serve
as causal antecedents of dissociative symptoms, it will be imperative to studythe effects of treatment interventions focus e do ns l e e pn o r m a l i z a t i o ni nd i s s o c i a t i v epatients (Hamner, Broderick, & Labbate, 2 001; Merckelbach & Giesbrecht, 2006).
Previous studies that have examined the effectiveness of sleep medication inPTSD (Van Liempt, Vermetten, Geuze, & Westenberg, 2006), DID (Loewenstein,Hornstein, & Farber, 1988) and dissociat ive symptoms in a mixed inpatient group
(van der Kloet, Giesbrecht, Lynn, Merck elbach, & de Zutter, 2012) have yielded
promising results.
CONCLUSION
Dissociative disorders and conditions, especially DID and dissociative fugue, areamong the most controversial in all of descriptive psychopathology, and for goodreason. Although dissociation is unquestionably a genuine subjective experience,serious questions remain concerning the assessment, etiology, and treatment of mostdissociative disorders. The dif ﬁculties of diagnosing DID have led some workers in the
ﬁeld to question whether the disorder can be reliably diagnosed. Piper and Merskey
(2004), for example, went so far as to write that patients “. . . with manifestations that
are visible to only some clinicians and on only some occasions; with symptoms thatcannot be distinguished from other psychiatric disorders or from malingering; withunacceptably vague diagnostic criteria; and with patients who initially deny theirsymptoms, show no signs of the condition ’s essential feature, and know nothing of
either their traumatic histories or the presence of alters —simply cannot be reliably
diagnosed” (p. 681; but see Gleaves et al., 2001, for a competing view). Although this
might prove to be an extreme or unwarranted conclusion with respect to DSM-5 ,
studies ascertaining the reliability and validity of dissociative disorder diagnoses areobviously a high priority.
Etiological issues are a particular sticking point, and appear no closer to
resolution with the publication of DSM-5. Although some authors (e.g., Dalenberg
et al., 2012; Gleaves, 1996) maintain th at DID and perhaps other dissociative
disorders stem primarily from early child abuse and maltreatment, others(e.g., Spanos, 1994) maintain that these condi tions are largely socially and culturally
inﬂuenced products that are aided and abetted by therapist prompting and
cueing of symptoms —a view that is supported by multiple sources of circumstan-
tial evidence (Lilienfeld et al., 1999). It remains to be seen whether new andpromising models, such as those linking sl eep deprivation to dissociative symptoms
(van der Kloet et al., 2012), may provide common ground between these competingtheories of the genesis of dissociative disorders. In the meantime, clinicians whowork with dissociative patients should bear in mind the powerful historical lessonimparted by the literature on DID: in their well-meaning efforts to unearthpsychopathology, assessors and therapi sts may inadvertently end up creating it
(Lilienfeld et al., 1999).436 SPECIFIC DISORDERS

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CHAPTER 12
Somatic Symptom and
Related Disorders
GORDON J. G. ASMUNDSON, MICHEL A. THIBODEAU, and DANIEL L. PELUSO
DESCRIPTION OF THE DISORDERS
The somatic symptom and related disorders, as described in the Diagnostic and
Statistical Manual of Mental Disorders ,ﬁfth edition ( DSM-5 , American Psychiatric
Association [APA], 2013), include somatic symptom disorder, illness anxiety disorder,conversion disorder (functional neurological symptom disorder), psychological fac-tors affecting other medical conditions, factitious disorder, other speci ﬁed somatic
symptom and related disorder, and unspeci ﬁed somatic symptom and related
disorder. The somatic symptom and related disorders reconceptualize and replacetheDiagnostic and Statistical Manual of Mental Disorders , fourth edition, text revision
(DSM-IV-TR ; APA, 2000) somatoform disorders. Changes were made in an effort to
eliminate overlap and clarify boundaries between diagnosable disorders, and torecognize that people meeting diagnostic criteria for one of these disorders may ormay not have an identi ﬁable medical condition.
The following changes were made in the DSM-5 : (a) conversion disorder (functional
neurological symptom disorder) remains but now emphasizes the importance of theneurological exam; (b) body dysmorphic disorder was reconceptualized as a DSM-5
obsessive-compulsive and related disorder (thereby moving it to a different category);(c) psychological factors affecting other medical conditions and factitious disorder, eachincluded in different sections of the DSM-IV , have been added to this category; and (d)
each of somatization disorder, undifferentiated somatization disorder, pain disorder,and hypochondriasis have been removed as diagnosable conditions and are subsumedunder one of somatic symptom disorder, illness anxiety disorder, or psychologicalfactors affecting other medical conditions. Importantly, unlike somatization disorderand hypochondriasis as de ﬁned in the DSM-IV-TR , the key disorder included in this
new category (i.e., somatic symptom disorder) no longer requires medicallyunexplained symptoms as a core feature; instead, emphasis is placed on the impactof symptoms on cognition, emotion, and behavior. Although not without controversy(e.g., Frances, 2013; Frances & Chapman, 2013; Sirri & Fava, 2013; Starcevic, 2013), theSomatic Symptom Workgroup has suggested that aforementioned changes were made
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in an effort to increase utility for the prima ry care and other medical (nonpsychiatric)
clinicians to whom patients with somatic sensations or changes often present, toreduce stigma, to reduce promotion of mind -body dualism, to improve therapeutic
alliance, and to facilitate correct diagnosis and good treatment outcomes (e.g.,Dimsdale et al., 2013).
The common feature of the somatic symptom and related disorders is prominent
somatic sensations (e.g., dyspnea, pain) or changes (e.g., subcutaneous lumps, rash) —
called “symptoms ”inDSM-5 terminology —that are associated with signi ﬁcant
emotional distress and functional impairment and often interpreted by the personas being symptomatic of some disease process or physical anomaly. Bodily sensationsand changes are a common experience of day-to-day living for most people, and theytypically remit without medical attention; however, about 25% of the population seeksmedical attention when these sensations and changes persist (Kroenke, 2003). Up to30% of those seeking medical attention will exhibit clinically signi ﬁcant distress about
having an unidenti ﬁed disease when there is no medical explanation for presenting
“symptoms ”(Fink, Sørensen, Engberg, Holm, & Munk-Jørgensen, 1999); yet, many
remain distressed despite identi ﬁable medical explanation (APA, 2013; Taylor &
Asmundson, 2004). This distress is associated with substantial impairment of per-sonal, social, and professional functioning as well as considerable costs to health care(Hessel, Geyer, Hinz, & Brahier, 2005), even after controlling for medical andpsychiatric comorbidity (Barsky, Orav, & Bates, 2005).
Despite prevalence and cost of distressing somatic sensations and changes, as well
as a substantive increase in empirical attention during the past decade, their presen-tation remains not well understood. Likewise, although there are some data on thevalidity, reliability, and clinical utility of somatic symptom disorder (Dimsdale et al.,2013), there have been few studies on the diagnostic category as a whole. In thesections that follow, we provide an overview of the general clinical pro ﬁle, diagnostic
considerations, and epidemiology of the DSM-5 somatic symptom and related dis-
orders. We then turn attention to issues of assessment, etiological considerations, andcourse and prognosis. In each of these latter sections, we touch on issues germane tothe collective category as well as its speciﬁ c disorders. In the case study, we focus more
speciﬁcally on an illustration of uncomplicated somatic symptom disorder. As there is
currently little data on epidemiology, etiology, course, prognosis, assessment, ortreatment of the disorders included in this new DSM-5 category, much of the
data presented below is borrowed from pre- DSM-5 knowledge of related conditions
and disorders.
CLINICAL PICTURE
The clinical pro ﬁle for each somatic symptom and related disorder is unique, although
each disorder is predicated on the prominence of somatic sensations or changes associ-ated with distress and impairment. A brief overview of the clinical pro ﬁle of each somatic
symptom disorder is provided, along with reference to DSM-5 diagnostic criteria.
S
OMATIC SYMPTOM DISORDER
Somatic symptom disorder is the cornerstone diagnosis of the somatic symptom andrelated disorders category. The main feature of somatic symptom disorder is the452 SPECIFIC DISORDERS

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presence of one or more somatic symptoms or features that cause distress andimpairment in daily living (Criterion A). The concern ranges from highly speci ﬁc
(e.g., “This pain in my gut is so bad. I must have stomach cancer ”) to vague and diffuse
(e.g., “My whole body is aching. What could it be? Maybe it ’s ALS. ”). Individuals with
somatic symptom disorder exhibit excessive thoughts, feelings, or behaviors related totheir somatic symptoms (Criterion B). An individual meets Criterion B if he or she: (a)exhibits disproportionate thoughts about the seriousness of their symptoms, (b)experiences persistently high levels of anxiety regarding their symptoms or abouttheir health, or (c) devotes an excessive amount of time to their health (e.g., seekingreassurance from health professionals, doing research about their somatic sensationsor changes, perusing body parts to ﬁnd potential lumps). Excessive somatic concerns
must persist for at least 6 months (Criterion C), although somatic symptoms do notneed to be present for this entire period. Individuals with somatic symptom disordermay often resist the idea that they are suffering from a mental health disorder and maycome to rely on reassurance seeking and checking behaviors (e.g., palpating sub-cutaneous lumps, searching for information about disease in medical textbooks and onthe Internet) to placate concerns about having a serious disease. Although thesebehaviors can be effective in providing short-term relief, they perpetuate the conditionin the long term (Taylor & Asmundson, 2004).
Somatic symptom disorder can be associated with a few diagnostic speci ﬁers. An
individual whose somatic complaints revolve largely around pain can receive a with
predominant pain speciﬁer. This speci ﬁer replaces the pain disorder diagnosis from DSM-
IV.Apersistent speciﬁer can apply in cases wherein severe symptoms and impairment
last for longer than 6 months. Finally, severity can be speci ﬁed as mild,moderate ,o r
severe when an individual meets one, two, or three of the Criterion B symptoms,
respectively. For example, a moderate severity speciﬁer could be assigned to an
individual who reports debilitating anxiety due to bodily symptoms and who checkstheir body for hours a day to ensure no new blemishes have appeared.I
LLNESS ANXIETY DISORDER
Illness anxiety disorder involves preoccupation with having or acquiring a seriousillness (Criterion A). For example, an individual may fear contracting HIV or havingrecently contracted the virus. Illness anxiety disorder differs from somatic symptomdisorder in that somatic symptoms are not present or are only minor (Criterion B). Ifminor somatic symptoms are present (e.g., light pain, minor bruising), the individual ’s
distress is clearly out of proportion to the actual threat and focuses more on themeaning of the symptoms (e.g., consequences of having diabetes) rather than thesomatic symptoms themselves. Individuals with illness anxiety disorder experience agreat deal of distress rooted in their disease-related preoccupations and are easilyalarmed about health-related matters (Criterion C). To illustrate, an individual withillness anxiety disorder may be excessively distressed when learning that a colleagueor stranger has contracted cancer. Individuals with illness anxiety disorder participatein excessive behaviors aimed at reducing their anxiety (Criterion D), often bodilychecking (e.g., looking for lesions that could be signs of an infection), reassuranceseeking (e.g., repeatedly seeking medical testing), health-related research (e.g., read-ing about HIV on the Internet), and avoidance (e.g., avoiding hospitals as these couldhouse harmful germs). These behaviors may placate concerns in the short term but,Somatic Symptom and Related Disorders 453

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ultimately, serve to reinforce disease-related preoccupation (Taylor & Asmundson,2004). A diagnosis of illness anxiety disorder is contingent on illness anxiety lasting atleast 6 months (Criterion E), although the focus of the anxiety may change during thistime (e.g., from HIV to syphilis). Finally, the symptoms of illness anxiety disordermust not be better explained by another diagnosis (Criterion F), such as somaticsymptom disorder, panic disorder, or obsessive-compulsive disorder. Illness anxietydisorder can be associated with one of two contrasting speci ﬁers. The care-seeking type
speciﬁer can be applied when individuals frequently seek medical care. The care-
avoidant type speciﬁer can be applied when individuals rarely use medical care.
C
ONVERSION DISORDER (FUNCTIONAL NEUROLOGICAL SYMPTOM DISORDER )
Conversion disorder involves the manifestation of altered voluntary motor or sensoryfunctioning (Criterion A). Motor symptoms can include paralysis, paresthesia, trem-ors, convulsions, and abnormal movements or posture. Sensory symptoms caninclude blindness, altered or reduced hearing, unusual or inconsistent skin sensations,and altered speech patterns. The hallmark of conversion disorder is a lack ofcorrespondence between signs and symptoms and medical understanding of thepossible neurological condition (Criterion B). For example, an individual may displaysymptoms very consistent with epileptic seizures, but lack electrical activity in thebrain consistent with epilepsy. Such an inconsistency is needed for a diagnosis. A lackof neurological evidence for reported or observed symptoms is not suf ﬁcient (e.g.,
trembling without any apparent brain damage). Symptoms of conversion disordermust not be better explained by another mental health or medical disorder (CriterionC) and the symptoms must cause clinically signi ﬁcant distress or impairment or
warrant medical evaluation (Criterion D).
People with conversion disorder are often unaware of psychological factors
associated with their condition, and many report an inability to control their symp-toms. Although not a criterion for diagnosis of conversion disorder, lack of worry orconcern about symptoms (i.e., la belle indifference ) is mentioned in the DSM-5 list of
associated features. The available literature, however, fails to support the use of la belle
indifference as a means of discriminating between conversion disorder and symptoms
of organic pathology (Stone, Smyth, Carson, Warlow, & Sharpe, 2006).
Observed signs and symptoms of conversion disorder often appear to represent
patient beliefs about how neurological de ﬁcits should present, rather than how
neurological diseases actually function (Hurwitz, 2004). Onset typically followsa period of distress, such as that stemming from trauma (McFarlane, Atchison,Rafalowicz, & Papay, 1994; Roelofs, Keijsers, Hoogduin, Naring, & Moene, 2002;Van der Kolk et al., 1996) or physical injury (Stone et al., 2009). Diagnosis of conversiondisorder can be associated with the speci ﬁerswith psychological stressor orwithout
psychological stressor . Moreover, a speci ﬁer of acute episode orpersistent can be applied
when an individual ’s symptoms present for less or more than six months, respectively.
P
SYCHOLOGICAL FACTORS AFFECTING OTHER MEDICAL CONDITIONS
A diagnosis of psychological factors affecting other medical conditions can apply inindividuals who suffer from a medical condition (Criterion A) that is adversely454 SPECIFIC DISORDERS

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affected by psychological or behavioral factors (Criterion B). The effects on the medicalcondition can increase the odds of suffering, disability, or death. Psychological orbehavioral factors can be deemed as detrimental if meeting one of the followingconditions: (a) the psychological or behavioral factors preceded the development orworsening of the medical condition, or delayed recovery from the condition (e.g.,repeatedly exacerbating an injury following discharge from hospital), (b) the factorsinterfere with treatment, (c) the factors are well established health-risks, or (d) thefactors in ﬂuence medical pathology, thereby exacerbating symptoms or requiring
medical attention. Psychological or behavioral factors can include distress, mal-adaptive interpersonal patterns, and poor treatment adherence. The psychologicalor behavioral factors must not be subsumed within another mental disorder (CriterionC); thus, worsening of a medical condition due to panic disorder or due to substanceabuse would not meet criteria for psychological factors affecting other medicalconditions. Clinicians can apply speci ﬁers re ﬂecting mild (increases medical risk),
moderate (aggravates medical condition), severe (results in hospitalization or emer-
gency attention), or extreme (life threatening risk) in ﬂuence of psychological factors on
a medical condition.F
ACTITIOUS DISORDER
Factitious disorder imposed on self is a condition wherein an individual acts as if theyhave physical or psychological signs of an illness by producing, feigning, or exag-gerating symptoms (Criterion A). The individual must present himself or herself as illor impaired (Criterion B) and a diagnosis is contingent on identifying that theindividual is actively misrepresenting their condition. Moreover, the deceptive behav-ior must occur without any obvious external rewards (Criterion C), such as monetarycompensation or reduced responsibilities. A diagnosis of factitious disorder can beassigned to individuals who have a medical condition; but, in this case, the deceptivebehavior is intended to make the person appear even more ill. The deceptive behaviorcannot be better explained by another disorder, such as schizophrenia or delusionaldisorder (Criterion D). Individuals with factitious disorder may produce or exaggeratesymptoms by consuming drugs (e.g., insulin, hallucinogens), injecting themselveswith noxious substances (e.g., bacteria), contaminating blood and urine samples, orreporting symptoms that have never occurred (e.g., seizures). A speci ﬁer of recurrent
episodes applies in cases wherein individuals have exhibited deceptive behavior more
than once.
A separate diagnosis, referred to as factitious disorder imposed on another, can also
be assigned. The criteria for this diagnosis are the same as factitious disorder, but aperson other than the victim conducts the deceptive behavior. For example, a fathermay tamper with the urine sample of his child to misrepresent the child ’s health status.
In this case, the parent would be assigned the diagnosis, not the child.O
THER SPECIFIED SOMATIC SYMPTOM AND RELATED DISORDER AND
UNSPECIFIED SOMATIC SYMPTOM AND RELATED DISORDER
Other speci ﬁed somatic symptom and related disorder applies to individuals who
present with distressing or impairing symptoms that are similar to one of the somaticSomatic Symptom and Related Disorders 455

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symptom and related disorders but that do not fully satisfy the criteria for a diagnosis.TheDSM-5 presents four examples of speci ﬁc disorders that can be used with the other
speci ﬁeddisorder diagnosis. These include brief somatic symptom disorder, which can
be assigned when an individual meets diagnostic criteria for somatic symptomdisorder, but for less than 6 months; brief illness anxiety disorder, which can beassigned when symptoms of illness anxiety disorder last for less than 6 months; illnessanxiety disorder without excessive health-related behaviors, which can be assignedwhen an individual meets all criteria for illness anxiety disorder except Criterion D;and, pseudocyesis, which can be assigned in individuals with a false belief of beingpregnant that is associated with objective and reported signs of pregnancy (e.g.,morning sickness, breast tenderness). A diagnosis of unspeci ﬁed somatic symptom
and related disorder can be applied when an individual presents with distressingor impairing symptoms that are similar to a somatic symptom and related disorder,but that do not meet the diagnostic criteria for any of the somatic symptom andrelated disorders.
DIAGNOSTIC CONSIDERATIONS (INCLUDING DUAL DIAGNOSIS)
To qualify for a somatoform disorder diagnosis under the DSM-IV-TR , somatic signs
and symptoms were required to be medically unexplained; that is, somatic signs andsymptoms could not be explained by organic pathology or physical de ﬁcit (APA,
2000). Sykes (2006) has argued that default attribution of medically unexplainedsomatic symptoms to psychopathology is untenable and has contributed to unjusti ﬁed
diagnoses of conditions characterized by somatic complaints as mental rather thanphysical disorders. In addition to supporting the perspective offered by Sykes (2006),and suggesting that diagnoses based on the absence of medically explained symptomspromoted stigma, the Somatic Symptom Workgroup pointed out that the reliability ofestablishing that somatic symptoms are not due to a general medical condition is low(e.g., Dimsdale et al., 2013). In the new classi ﬁcation system, somatic symptom
disorder is now de ﬁned on the basis of positive symptoms (i.e., distressing somatic
symptoms that present along with “observable ”cognitions, emotions, and behaviors
in response to the somatic symptoms); consequently, it is possible for people present-ing with and without a diagnosable general medical condition to satisfy diagnosticcriteria for the disorder. Medically unexplained symptoms only remain relevant toconversion disorder and other speci ﬁed somatic symptom and related disorder (i.e.,
pseudocyesis) where it is possible to demonstrate inconsistency between presentingsymptoms and medical pathology.
In arriving at a diagnosis of one of the somatic symptom and related disorders it is
important to consider that there are multiple sources of distressing somatic sensationand changes. First, a number of mental health disorders are characterized by somaticsymptoms (e.g., depression, panic disorder, posttraumatic stress disorder) and mayeither account for or accompany the somatic symptoms. In the former case a somaticsymptom and related disorder diagnosis would not be warranted, whereas in thelatter case a dual diagnosis would be warranted. Likewise, given that distressingsomatic symptoms often occur in response to a general medical condition such ascancer or multiple sclerosis, considerable care is warranted in establishing whether theresponse is psychopathological in nature. Some critics of the DSM-5 fear that456 S
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diagnostic thresholds have been loosened to the point where clinicians will bechallenged in distinguishing normal from psychopathological responses in thosewith distressing somatic symptoms stemming from a medical condition, resultingin overdiagnosis of somatic symptom disorders (Frances, 2013). Finally, it isimportant to recognize that many benign ph ysical factors can give rise to somatic
signs and symptoms. Consider, for example, physical deconditioning. Peopleconcerned by somatic sensations often avo id physical exertion, including aerobic
and anaerobic exercise, for fear that it w ill have harmful consequences. As a result,
they become physically deconditioned. Physical deconditioning is associated withpostural hypotension, muscle atrophy, and exertion-related breathlessness andfatigue, all of which can promote further i nactivity and reinforce beliefs that one
is ill (Taylor & Asmundson, 2004).
Further research is required to determine whether the modi ﬁcations made in the
DSM-5 will facilitate accuracy of diagnoses relative to that attainable with the DSM-
IV-TR somatoform disorders. The importance of diagnosis cannot be overstated, as
any diagnosis carries signi ﬁcant implications for individuals receiving the diagnosis
and their related experiences (e.g., stigmatization, interpretation of symptoms, natureof treatment, response to treatment). As Kirmayer and Looper (2007) note, diagnosisis a form of intervention and, as such, is a crucial element in shaping treatmentand outcome.
EPIDEMIOLOGY
Somatic symptom and related disorders are often associated with true or perceivedorganic pathology; consequently, this class of disorders is a challenge to diagnose andto study from an epidemiological standpoint due to difﬁ culties in thoroughly assess-
ing the mind and body. Given the substantial changes in diagnostic criteria betweentheDSM-III and DSM-5 , providing precise epidemiological prevalence rates for
somatic symptom and related disorders is extremely challenging. Indeed, the somato-form disorders were not included in the large-scale national comorbidity surveysbased on DSM-III-R (Kessler, 1994) and DSM-IV-TR criteria (Kessler, Chiu, Demler,
Merikangas, & Walters, 2005), nor were they examined in the World Health Organi-zation World Mental Health Surveys initiative (Kessler & Üstün, 2008), which furtherlimits inferences regarding the somatic symptom and related disorders. Moreover,epidemiological researchers have often paired somatoform disorders with otherdisorders (e.g., anxiety disorders; Bland, Orn, & Newman, 1988) or have excludedspeciﬁc disorders from analyses due to low or high base rates or differences in
classi ﬁcation methodologies (Leiknes, Finset, Moum, & Sandanger, 2008). As such,
the prevalence of somatic symptom and related disorders as a class of disordersremains almost entirely unstudied and our knowledge at this time can only beextrapolated from earlier research on the somatoform disorders.
The somatic symptom and related disorders are substantially different from the
somatoform disorders described in DSM-IV-TR ; however, some of the broader
epidemiological ﬁndings likely still hold true. For example, presentation of somatic
concerns that do not meet diagnostic crite ria for a somatoform disorder or medical
condition account for approximately half of all physician visits (Nimnuan, Hotopf,& Wessely, 2001), suggesting that subsyndromal somatic symptoms are highlySomatic Symptom and Related Disorders 457

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prevalent and costly (Barsky et al., 2005; Kirmayer & Robbins, 1991). Somaticsymptom and related disorders are lik ely more common in women (Wittchen &
Jacobi, 2005), with perhaps the excepti on of somatic sympt om disorder, which
appears to have similar prevalence in both genders based on the rates of hypochon-driasis (Asmundson, Taylor, Sevgur, & C ox, 2001; Bleichhardt & Hiller, 2007).
People with a somatic symptom and related disorder are also very likely tofrequently experience co-occurring mood disorders (Leiknes et al., 2008), anxiety
disorders (Lowe et al., 2008), personality disorders (Bornstein & Gold, 2008; Sakai,
Nestoriuc, Nolido, & Barsky, 2010), as well as other somatic symptom and relateddisorders (Leiknes et al., 2008).
Somatic symptom disorder encapsulates approximately 75% of individuals who
previously met diagnostic criteria for hypochondriasis (APA, 2013), and likelyrepresents the most prevalent of the somatic symptom and related disorders. Somaticsymptom disorder has a prevalence of approximately 5% to 7% in the generalpopulation (APA, 2013), which is consistent with the 12-month prevalence rate of4.5% for hypochondriasis (Faravelli et al., 1997). Research on hypochondriasis sug-gests that somatic symptom disorder is likely more common in primary care settings.Reported prevalence rates of hypochondriasis in primary care settings have variedconsiderably based on methodology. Studies using diagnostic interviews havereported a point prevalence of 3% (Escobar et al., 1998) and a 12-month prevalenceof 0.8% (Gureje, Üstün, & Simon, 1997), whereas a study using cutoff scores from self-report measures followed by interviews suggests a 12-month prevalence of 8.5%(Noyes et al., 1993). The inclusion of the with predominant pain speciﬁer to somatic
symptom disorder, which subsumes a portion of the DSM-IV pain disorder diagnosis,
may increase the prevalence of somatic symptom disorder beyond the prevalence ofhypochondriasis.
The prevalence of illness anxiety disorder is relatively unknown, but can be
estimated based on other phenomena. The 1- to 2-year prevalence of health anxietyand disease conviction (i.e., the belief that one has a disease) in community-basedsamples ranges from 1.3% to 10% (APA, 2013). A strong fear of contracting a disease,which is relatively similar to illness anxiety disorder, has a point prevalence ofapproximately 3% to 4% (Agras, Sylvester, & Oliveau, 1969; Malis, Hartz, Doebbeling,& Noyes, 2002). Together these ﬁndings suggest that illness anxiety disorder is
relatively common.
The point and 12-month prevalence rates of conversion disorder in the general
population are less than 0.1% (Akagi & House, 2001). Point prevalence in neurologyand primary care settings has been reported as 1% (Smith, Clarke, Handrinos,Dunsis, & McKenzie, 2000) and 0.2% (de Waal, Arnold, Eekhof, & van Hemert,2004), respectively. Despite low prevalence of conversion disorder, medicallyunexplained neurological symptoms are present in approximately 11% to 35% ofneurology patients (Carson et al., 2000; Snijders, de Leeuw, Klumpers, Kappelle, & vanGijn, 2004), suggesting that subsyndromal conversion may be more common thanalmost all neurological diseases.
The prevalence of other somatic symptom and related disorders are unknown,
partially because they are new diagnoses (e.g., psychological factors affecting othermedical conditions) and are very dif ﬁcult to study (e.g., factitious disorder,
unspeci ﬁed somatic symptom and related disorder).458 S
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PSYCHOLOGICAL AND BIOLOGICAL ASSESSMENT
Individuals with somatic symptom and related disorders will typically present inprimary care and other medical (nonpsychiatric) clinics rather than in mental healthsettings; indeed, they may often refuse a mental health referral because of a belief thattheir condition is purely organic. Cooperation between medical and mental healthprofessionals aids the referral process and, due to the complexity of the factorsinvolved (e.g., possibility of co-occurring organic pathology), is typically necessaryin making an accurate diagnosis. Throughout the course of assessing a person with apossible somatic symptom and related disorder, the mental health professional mustseek to establish and maintain rapport and should clearly relay an understanding that,although a disease process may or may not be present, the symptoms are real and notfeigned or “in the head ”(Taylor & Asmundson, 2004). The general goals of assessment
for the somatic symptom and related disorders are to rule out organic pathology-based, substance-based, or other psychopathology-based explanations of presentingsigns and symptoms, to determine the type and severity of signs and symptoms, andto facilitate appropriate treatment planning.
Ruling out organic pathology is no longer requisite to diagnosis of somatic
symptom and related disorders, as it was in the DSM-IV-TR somatoform disorders.
This aspect of the diagnostic process was c onsidered problematic for two primary
reasons. First, it relied heavily on the excl usion of general medical conditions, and
100% certainty was rarely if ever possible (Taylor & Asmundson, 2004; Woolfolk &Allen, 2007). Second, diagnosis is not us ually based on the absence of something
but, rather, according to the presence of p ositive features of a condition (Dimsdale
et al., 2013). Gathering a detailed history of somatic complaints, past and currentmedical conditions, and med ical professionals consulted is a crucial part of a
comprehensive diagnostic process and may provide insight regarding the natureof the presenting condition. A consult with the family physician may be necessaryto determine the need for further medica l assessments; however, caution is war-
ranted, because further assessments may reinforce maladaptive coping (e.g.,reassurance seeking) while also increasing the costs and potential risks associated
with medical care.
Structured clinical interviews have proven to be the gold standard in the diagnosis
of mental disorders, including somatoform disorders, and will likely remain so for thesomatic symptom and related disorders. Broad structured interviews that includesections on numerous mental disorders are the most commonly utilized. The Struc-tured Clinical Interview for the DSM-IV (First, Spitzer, Gibbon, & Williams, 1996) and
the Composite International Diagnostic Interview (CIDI; World Health Organization,1990) based on the International Statistical Classi ﬁcation of Diseases , 10th edition, criteria
(ICD-10 ; World Health Organization, 2007) were both used widely and demonstrated
efﬁcacy and reliability in diagnosing somatoform disorders. Other useful structured
interviews for diagnosing somatoform disorders included the Somatoform DisordersSchedule (World Health Organization, 1994), the Schedules for Clinical Assessment inNeuropsychiatry (Wing et al., 1990), and the Diagnostic Interview Schedule (Robins,Helzer, Croughan, & Ratcliff, 1981). At the time of writing this chapter, no revisions ofthese structured diagnostic interviews speci ﬁc to the DSM-5 criteria for the somatic
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Structured clinical interviews can be supplemented with diarized monitoring of
catastrophic thinking and maladaptive coping behaviors as well as informationgleaned from standardized self-report measures. Self-report measures are ef ﬁcient
and effective screening tools that can provide invaluable information for case con-ceptualization and regular monitoring of treatment progress. The Screening forSomatoform Symptoms (Rief, Hiller, & Heuser, 1997), the Symptom Checklist –90,
Revised (Derogatis, 1975), or the Patient Health Questionnaire –15 (Kroenke, Spitzer, &
Williams, 2002) have been used to assess a broad range of somatic symptoms. Morespeciﬁc information can be derived from a wide array of self-report measures that
have been developed to assess the severity of speci ﬁc somatic symptoms. It is beyond
the scope of this chapter to provide a comprehensive list of these measures; examplesinclude the Health Attitude Survey (Noyes, Langbehn, Happel, Sieren, & Muller, 1999)for use in assessing attitudes and perceptions associated with multiple somaticsymptoms, the Health Anxiety Questionnaire (Lucock & Morley, 1996) for use inassessing reassurance-seeking behavior and the extent to which symptoms interferewith a person ’s life, and the Whiteley Index (Pilowsky, 1967) for use in assessing
cognitions associated with health anxiety. Whether such measures, or revisionsthereof, prove to be of continuing value in the context of the DSM-5 somatic symptom
and related disorders remains to be determined. Medical service utilization and visualanalogue scales pertaining to distressing thoughts and maladaptive coping behaviorscan also be used to assess emotional and functional impact and to monitor treatmentprogress. Finally, measures of mood and anxiety can be useful in case conceptualiza-tion and monitoring and might include the Beck Depression Inventory –II (Beck,
Steer, & Brown, 1996), the Beck Anxiety Inventory (Beck & Steer, 1993), andthe original or recent 18-item expanded version of the Anxiety Sensitivity Index(Peterson & Reiss, 1987; Taylor et al., 2007).
ETIOLOGICAL CONSIDERATIONS
B
EHAVIORAL GENETICS AND MOLECULAR GENETICS
Heritability of somatoform disorders has been suggested by ﬁndings from behavioral
(e.g., Kendler et al., 2011; Torgersen, 1986) and molecular (e.g., Hennings, Zill, & Rief,2009) genetics studies. Somatic symptom concordance rates between monozygotictwins are higher than between dizygotic twins, even when controlling for co-occurringpsychiatric symptoms (Lembo, Zaman, Krueger, Tomenson, & Creed, 2009). Althoughmood and somatoform disorders share common genetic factors (e.g., deregulation ofserotonergic pathways), there are numerous genetic features unique to somatoformdisorders (e.g., immunological deregulation, hypothalamic-pituitary-adrenal [HPA]axis responses; Rief, Hennings, Riemer, & Euteneuer, 2010). The role of speci ﬁc genetic
markers in the development of somatic symptoms remains unclear; however, researchin this area is ongoing, and genetic factors are now being considered within the contextof psychological models of various somatoform disorders (e.g., Taylor, Jang, Stein, &Asmundson, 2008; Veale, 2004). Whether these ﬁndings generalize to the somatic
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NEUROANATOMY AND NEUROBIOLOGY
Neurological research on the DSM- 5 somatic symptom and related disorders remains
in its infancy; but, research using DSM-IV-TR criteria has demonstrated neurological
correlates for conversion disorder (e.g., Vuilleumier, 2005), hypochondriasis (e.g.,Atmaca, Sec, Yildirim, Kayali, & Korkmaz, 2010), and other related disorders (e.g.,somatization disorder, Hakala, Vahlberg, Niemi, & Karlsson, 2006; pain disorder andﬁbromyalgia, Wood, Glabus, Simpson, & Patterson, 2009). The HPA axis has been a
focus of research in this area. A recent longitudinal study reported preliminaryevidence that cortisol deregulation in the HPA axis may predate the developmentof somatic symptoms in some people (Tak & Rosmalen, 2010). The HPA axis controlsglandular and hormonal responses to stress and, when stressors (e.g., chronic pain,anxiety) have a chronic course, may lead to hypocortisolism (i.e., adrenal insuf ﬁ-
ciency), which induces greater stress and enhances experiences of pain and fatigue(Fries, Hesse, Hellhammer, & Hellhammer, 2005). Increases in these experiencestypically exacerbate somatic symptoms or lead to behaviors that exacerbate ormaintain them (Taylor & Asmundson, 2004). The second somatosensory area (SII)of the cerebral cortex, which is involved in the analysis and evaluation of complexpatterns of somesthetic input (e.g., perception of pain, sensations from visceralstructures, gastric sensations), has also been implicated as a source of the somaticperturbation associated with the somatoform disorders (Miller, 1984); however,despite its appeal as a neural structure underlying this class of disorders, peoplepresenting with concerns about somatic symptoms do not typically show abnormali-ties in sensory acuity.L
EARNING ,MODELING ,ANDLIFEEVENTS
Childhood physical and sexual abuse and neglect have been associated with increasedphysician visits during adulthood (Fiddler, Jackson, Kapur, Wells, & Creed, 2004) andwith hypochondriasis (Barsky, Wool, Barnett, & Cleary, 1994), as have other stressfullife events unrelated to disease; however, it is noteworthy that increased prevalence ofabuse and other stressful life events are characteristic of people with a variety ofpsychiatric conditions (e.g., panic disorder; Taylor, 2000), not just those presentingwith concerns regarding somatic symptoms.
E a r l yc h i l d h o o de x p e r i e n c e so fi l l n e s sa n dp e r c e p t i o n so fs i g n i ﬁcant illness in
others are associated with the experience of medically unexplained symptoms inadulthood (Hotopf, Wilson-Jones, Mayou ,W a d s w o r t h ,&W e s s e l y ,2 0 0 0 ) .L i k e w i s e ,
parents who fear disease, who are preoccupied with their bodies, and who overreactto minor ailments experienced by their children are more likely to have childrenwith the same tendencies, both during ch ildhood and adulthood (Craig, Boardman,
Mills, Daly-Jones, & Drake, 1993; Hotop f, Mayou, Wadsworth, & Wessely, 1999;
Marshall, Jones, Ramchandani, Stein, & Bass, 2007). That being said, a recent twinstudy suggests that environmental factor s not shared by twins (e.g., an ailment in
one of the twins), rather than shared environmental factors (e.g., parental style),seem most important in the development of DSM-IV-TR deﬁned hypochondriasis
(Taylor & Asmundson, 2012).Somatic Symptom and Related Disorders 461

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COGNITIVE INFLUENCES
Greater focus on somatic sensations is associated with greater experiences of thosesensations (Brown, 2004; Ursin, 2005). When attention is directed to the body, theintensity of perceived sensations increases (Mechanic, 1983; Pennebaker, 1980). Peoplewith somatoform disorders have been shown to spend a considerable amount of timefocusing on their bodies, thereby increasing their chances of noticing somatic sensa-tions and changes. They also tend to believe that somatic sensations and changes areindicative of disease or are otherwise harmful in some way (Barsky, 1992; Taylor &Asmundson, 2004; Vervoort, Goubert, Eccleston, Bijttebier, & Crombez, 2006). Thesebeliefs increase the attention directed to somatic sensations and changes and, in turn,increase associated distress. It is likely that similar cognitive in ﬂuences will be
identi ﬁed in the various somatic symptom and related disorders diagnoses.
S
EX AND RACIAL -ETHNIC CONSIDERATIONS
As noted in the Epidemiology section, the somatoform disorders were more prevalentin women than in men, perhaps with the exception of hypochondriasis. There areseveral possible explanations for this difference. Because women are more likely toseek medical services (Corney, 1990; Kessler et al., 2008), they may be more prone todiagnostic biases wherein physicians consider somatic symptoms presented by awoman as more likely to be psychological than organic in nature (e.g., Martin,Gordon, & Lounsbury, 1998). Women also tend to experience higher rates of psycho-pathology (Kessler et al., 2008). Shared etiological or maintenance factors betweenmental disorders may make it more likely that women are at a higher risk ofdeveloping a somatic symptom and related disorder. There is evidence that womentend to focus more on their bodies (Beebe, 1995) and are more fearful of some of theirbodily sensations (Stewart, Taylor, & Baker, 1997), further increasing their risk fordeveloping somatic symptom and related disorders. Other putative sex differenceshave been proposed (e.g., differential experiences of abuse; HPA axis dysregulation)but warrant further empirical scrutiny in the context of their role in somatic symptomand related disorders etiology.
Somatic sensations and changes are common in all cultural groups; however,
presentation varies widely depending on sociocultural norms (Kirmayer & Young,1998). Cultural factors, such as socially transmitted values, beliefs, and expectations,can in ﬂuence how a person interprets somatic sensations and changes, and whether
treatment seeking is initiated. Some cultures appear to be more distressed by gastro-intestinal sensations (e.g., excessive concerns about constipation in the United King-dom), whereas others are more distressed by cardiopulmonary (e.g., excessiveconcerns about low blood pressure in Germany) and immunologically based (e.g.,excessive concerns about viruses and their effects in the United States and Canada)symptoms (Escobar, Allen, Hoyos Nervi, & Gara, 2001). Whether one seeks care forsomatic concerns also appears to vary as a function of culture, with those of Chinese,African American, Puerto Rican, and other Latin American descent presentingwith more medically unexplained somatic symptoms than those from other groups(Escobar et al., 2001). Whether concern over somatic sensations and changes areexcessive needs to be judged in the context of the individual ’s cultural background.462 S
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COURSE AND PROGNOSIS (INCLUDING ISSUES OF TREATMENT)
As a diagnostic category, somatic symptom and related disorders share somaticfeatures and concerns as a prominent aspect of clinical presentation. That said,each disorder does not necessarily share a similar course and prognosis. Like thesomatoform disorders, course and prognosis may vary considerably, because thedisorders are heterogeneous in presentation and involve substantial comorbidity withmood and anxiety disorders, personality disorders, and, in some cases, generalmedical conditions. Certain prognostic indicators have been shown to be commonacross somatoform disorders; for example, comorbidity with other psychiatricdisorders contributes to a more chronic and persistent course (e.g., Rief, Hiller,Geissner, & Fichter, 1995). More somatic symptoms, sensitization to bodily sensationsand pain, as well as presence of a medical condition all contribute to greater severityand chronic course (APA, 2013). The presence of fewer somatic symptoms, few or nocomorbid conditions, identi ﬁable stressors at the time of onset, high intellectual
functioning, as well as sound social support networks are typically associated withgood prognosis. Also indicative of good prognosis is the development of a strongtherapeutic alliance between the patient and care provider, wherein the patientbelieves that the care provider views the patient ’s presenting signs and symptoms
as legitimate, albeit possibly not due to an organic pathology or physical defect(Taylor & Asmundson, 2004).
Research on psychological interventions does not yet exist for somatic symptom
disorders; but, psychosocial interventions have demonstrated ef ﬁcacy across the
DSM-IV-TR somatoform disorders. Cognitive behavior therapy (CBT) has demon-
strated to be superior to standard medical care in reducing health-related anxiety(Barsky & Ahern, 2004) and improving somatic complaints/somatization (Allen,Woolfolk, Escobar, Gara, & Hamer, 2006; Speckens, van Hemert, Bolk, Rooijmans, &Hengeveld, 1996). Psychiatric consultation letters to primary-care physicians describ-ing somatization and providing recommendations for primary care have also beenshown to signi ﬁcantly improve physical functioning and reduce cost of medical care
(Rost, Kashner, & Smith, 1994). Similar interventions will likely prove effective withthe somatic symptom and related disorders.
CASE STUDY
C
ASEIDENTIFICATION
The basic features of this case are undisguised; however, in line with Clifft ’s (1986)
guidelines, identifying information has been altered or omitted to protect con ﬁden-
tiality and privacy.
Jacob is a 37-year-old Caucasian male who has been married for 10 years and has a
5-year-old daughter and a 6-month-old son. He currently resides with his wife andchildren in an upper-middle-class suburban neighborhood. His family is ﬁnancially
secure, and he is not involved in any legal proceedings. Jacob is employed full time asan electrical engineer for a large company, a job he has held for the past 6 years. Heenjoys a variety of sports, walking the family dog, and spending time with his family.Until recently, he was active as a competitive triathlete. His job requires that he travelperiodically, with absences from home and his family for up to 1 month at a time. HeSomatic Symptom and Related Disorders 463

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reports that job demands increase in the months prior to extended travel and that hisnext lengthy trip is fast approaching in 10 weeks.P
RESENTING COMPLAINTS
Jacob was referred by his family physician for assessment and, if appropriate,treatment of increasing anxiety over his physical well-being that was negativelyimpacting on his work (e.g., spending excessive amounts of time searching medicalinformation on the Internet instead of working) as well as leisure and familyfunctioning (e.g., withdrawing from physical activity and shared leisure activities).These concerns started 9 months ago, when his father died of heart complicationsassociated with amyloidosis, a disease wherein amyloid proteins build up in speci ﬁc
organs and, over time, disrupt organ function and eventually lead to failure of theaffected organs. There is a rare form —hereditary amyloidosis —that is most frequently
passed from father to son and for which there are no preventive measures other thannot having children. There is no cure for amyloidosis, and the effects do not becomeapparent until later in life (i.e., over the age of 50 years). Beginning shortly after hisfather ’s death, Jacob became increasingly aware of and concerned by somatic sensa-
tions in his body —heart palpitations and racing, upper body aches and pain, dizzi-
ness, and blurred vision —all of which were similar to those initially experienced by his
father. He feared that he may also have amyloidosis and might die from it. His fearswere exacerbated upon the birth of his son, with speci ﬁc concerns that he had passed
on the condition and that his son would eventually succumb as well.H
ISTORY
Jacob had no prior history of mental health problems or treatment and, aside fromchicken pox and tonsillitis as a child, had been physically healthy throughout his
life. The report from his physician indicated that, despite numerous visits regardingvarious somatic complaints over the past months, there was no evidence of anorganic basis for Jacob ’s concerns. The physician report also indicated that Jacob was
physically healthy and that he and his son had a pending appointment for genetict e s t i n gt or u l eo u tt h eg e n e t i cp r o ﬁle for hereditary amyloidosis. Jacob reported
having a loving and supportive relationship with his wife, although she wasbecoming increasingly concerned by his condition and, at times, annoyed at hisgrowing reluctance to actively play with their children. Until recently, he wasexercising ﬁve or six times per week and had com peted in numerous triathlons;
however, because of growing concerns about his health, he had signiﬁ cantly cut
down his frequency of training and was not competing in order to “avoid physical
exertion ”f o rf e a rt h a th i sh e a r tw o u l d “explode. ”In place of training, he was
spending hours checking the Internet for medical information.A
SSESSMENT (RELATED TO DSM-5 CRITERIA )
Jacob was assessed using a semistructured interview that included probes pertinent tothe diagnostic criteria for DSM-5 somatic symptom and related disorders and a battery
of self-report questionnaires. The former was drafted for use in place of the Structured464 SPECIFIC DISORDERS

3GC12 06/26/2014 9:43:4 Page 465
Clinical Interview for the DSM-5 , which was not yet availab le at time of assessment.
The latter included (a) the Beck Depression Inventory –II, a measure of depression
over the past 2 weeks (Beck et al., 1996), (b) the Beck Anxiety Inventory, a measure of
general anxiety over the past week (Beck & St eer, 1993), (c) the Anxiety Sensitivity
Index (Peterson & Reiss, 1987), a measure of the fear of arousal-related bodilysensations, and (d) the Whiteley Inde x (Pilowsky, 1967), a measure of the core
features of health anxiety, including disease fear, disease conviction, and bodilypreoccupation. The structured interview and self-report data provided detailed data
regarding general features of Jacob ’s distress, as well as speci ﬁcf e a t u r e so fh i s
health-related concerns.
Jacob met the DSM-5 diagnostic criteria for somatic symptom disorder. He
presented with several speci ﬁc concerns, including daily worry that somatic changes
and sensations (e.g., heart palpitations and racing, upper body aches and pain,dizziness, blurred vision) were signs of physical disease as well as increasing inabilityto focus on work-related tasks and to be involved in family activities (somaticsymptom disorder Criterion A). He also presented with considerable worry andanxiety about his personal health and the future-oriented health and well-being of his6-month-old son, and reported spending hours on the Internet checking medicalinformation (somatic symptom disorder Criterion B). His concerns had, as notedpreviously, begun around the time of his father ’s death 9 months prior and had
persisted since (somatic symptom disorder Criterion C).
Given that the effects of amyloidosis are typically not evident until later in life,
and that Jacob was in his mid-30s, it was deemed unlikely that amyloid depositswere responsible for the bod ily sensations he was experiencing; however, since
Jacob (and his son) had not yet completed genetic testing and did not know whetherthey had the genetic pro ﬁle for hereditary amyloidosis at the time of assessment, we
remained cautious in our opinion whether his thoughts about the seriousness ofsymptoms were disproportionate. At the time of assessment, Jacob ’ss c o r eo nt h e
Whiteley Index was moderate overall (score =8; possible range 0 –14), characterized
by signi ﬁcant disease fear (score =3; possible range 0 –4) and bodily preoccupation
(score =3; possible range 0– 3) but little disease conviction (score =0; possible range
0–3), the latter of which is indicative of good prognosis with treatment (Taylor &
Asmundson, 2004). The moderately high le vels of health anxiety combined with
excessive checking behavior, in our opinion, were suf ﬁcient to warrant a moderate
severity speci ﬁer.
Jacob did not meet diagnostic criteria for other diagnosis. Scores on the Beck
Depression Inventory (score =13; possible range 0 –63) and Beck Anxiety Inventory
(score =26; possible range 0 –63) suggested a mildly depressed mood and moderate
general anxiety, respectively. The absence of comorbid diagnoses, along with depres-sion and general anxiety in the mild to moderate range, are also indicative of goodprognosis with treatment (Taylor & Asmundson, 2004). His score on the AnxietySensitivity Index (score =26; possible range 0 –64) indicated strong beliefs that arousal-
related bodily sensations have harmful consequences, which, when considered in thecontext of his signi ﬁcant disease fear and bodily preoccupation, suggest that attention-
focusing exercises (e.g., Furer, Walker, & Stein, 2007; Wells, 1997) and interoceptiveexposure (Taylor & Asmundson, 2004) may prove to be particularly bene ﬁcial
additi ons
to treatment.Somatic Symptom and Related Disorders 465

3GC12 06/26/2014 9:43:4 Page 466
SUMMARY
Conditions characterized by signi ﬁcant concern over somatic signs and symptoms,
often presenting as medically unexpl ainable, are associated with signi ﬁcant emo-
tional distress, cognitions characterize d by catastrophic thinking, maladaptive
coping behaviors typically manifest as exce ssive checking and reassurance seeking,
limitations in social and occupational func tioning, and excessive use of health care
resources. These conditions are represen ted by the disorders subsumed under the
current DSM-5 somatic symptom and related disorders. It remains to be determined
whether the changes from the DSM-IV-TR somatoform disorder to the DSM-5
somatic symptom and related disorders will promote more accurate diagnosis ofpeople concerned and functionally disabled by somatic sensations and changes and,if so, whether this will direct appropriate treatment resources to optimize outcomes.It also remains unclear if, or how, the changes to classi ﬁcation will facilitate efforts to
identify underlying mechanisms. The bu rden on the health-care system and the
personal distress associated with somatic symptoms highlight the need for appro-priate reconceptualization of disorders characterized by somatic symptom presen-tation; however, some investigators have suggested that there was insuf ﬁcient
empirical evidence to warrant change, t hat important evidence may have been
overlooked, and that the changes in the DSM-5 may have been premature (Taylor,
2009; Sirri & Fava, 2013; Starcevic, 2013), and that the new changes will increase,rather than decrease, diagnostic misclassi ﬁcation (Frances, 2013). Answers to these
questions await the accumulation of empirical evidence based on the new DSM-5
diagnostic criteria.
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with dopamine metabolism. The Journal of Pain ,10, 609 –618.
Woolfolk, R. L., & Allen, L. A. (2007). Treating Somatization: A cognitive-behavioral approach . New
York, NY: Guilford Press.
World Health Organization. (1990). The composite international diagnostic interview (CIDI) .
Geneva, Switzerland: Author.
World Health Organization. (1994). Somatoform disorders schedule (SDS) . Geneva, Switzerland:
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health problems , 10th revision. Geneva, Switzerland: Author.Somatic Symptom and Related Disorders 471

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CHAPTER 13
Feeding and Eating Disorders
CYNTHIA M. BULIK, SARA E. TRACE, SUSAN C. KLEIMAN, and SUZANNE E. MAZZEO
DESCRIPTION OF THE DISORDERS
Eating disorders represent a category of partially overlapping syndromes, all of whichhave some clinical features marked by eating dysregulation. We will focus ourdiscussion on anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder(BED), which represent the primary eating disorders listed in DSM-5 . Feeding
disorders, such as pica, rumination disorder, and avoidant/restrictive food intakedisorder— all more common in, but not exclusive to children —will not be covered
here. Eating disorders are serious mental illnesses that are in ﬂuenced by both genetic
and environmental factors. The syndromes are partially overlapping, as considerablediagnostic ﬂux occurs over time, with individuals migrating from one clinical
presentation to another, and because several diagnostic features are shared acrossdisorders. Nonetheless, pure forms of each of the presentations also exist.
CLINICAL PICTURE
AN, the most visible eating disorder, is a serious psychiatric illness characterized by aninability to maintain a normal healthy body weight or, in individuals who are stillgrowing, failure to make expected increases in weight (and often height) and bonedensity. Despite increasing weight loss and frank emaciation, individuals with ANstrive for additional weight loss, see themselves as fat even when they are severelyunderweight, and often engage in unhealthy weight-loss behaviors (e.g., purging,dieting, excessive exercise, and fasting).
AN is characterized by low weight; however, how one de ﬁnes low weight is
somewhat complicated. DSM-5 highlights restriction of energy intake relative to
requirements, leading to a signi ﬁcantly low body weight, and embeds that in the
context of the individual ’s age, sex, developmental trajectory, and physical health.
Even when at low weight, people with AN experience an intense fear of gainingweight or of becoming fat, or they engage in persistent behavior that interferes withweight gain. The behavior and cognitions of individuals with AN vigorously defendlow body weight. Other aspects of the diagnostic criteria include a three-part criterionof which only one component is necessary: disturbance in the way in which one ’s body
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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 currentlow body weight.
In the past, amenorrhea of 3 months or longer duration was a diagnostic criterion
for AN. Wisely, this has been eliminated, as there are no meaningful differencesbetween individuals with AN who do and do not menstruate (Gendall et al., 2006;Watson & Andersen, 2003). Although not diagnostic, cessation of menstruation can bea useful indicator of severity and resumption of menses a factor in determiningrecovery. AN presents either as the restricting subtype, in which low weight isachieved and maintained through energy restriction and increased physical activityonly, or as the binge-eating/purging subtype, in which the individual has beenregularly engaging in binge eating or purging behavior (i.e., self-induced vomitingor the misuse of laxatives, diuretics, or enemas) over the past 3 months.
BN is characterized by recurrent binge eating episodes, de ﬁned as eating an
unusually large amount of food in a short period of time ( ∼2 hours) while experienc-
ing a sense of loss of control over the eating episode. In addition, bulimia includesrecurrent inappropriate compensatory behaviors (e.g., self-induced vomiting, laxa-tive, diuretic, or other medication misuse, fasting, or excessive exercise). In individualswith BN, self-evaluation is unduly in ﬂuenced by body shape and weight. Binge eating
and compensatory episodes occur on average once a week for at least 3 months. BN isonly diagnosed if AN criteria are not met. Thus, to be diagnosed with BN, individualsshould have a body mass index (BMI) greater than 18.5 kg/m
2in adults (i.e., the lower
bound of normal weight according to the World Health Organization [1992] and theCenters for Disease Control).
BN onset most frequently occurs in adolescence or early adulthood, although it can
occur at any point across the life span (American Psychiatric Association [APA], 2013).BN can occur at any body weight (with the exception of the requirement to diagnoseAN binge-eating/purging type if criteria for AN are met). BN tends to be over-represented in women; however, it has been argued that BN diagnostic criteria aregender-biased, leading to underdetection in men. Men who seek treatment for BNtend to manifest a greater reliance on nonpurging forms of compensatory behavior,such as excessive exercise (Anderson & Bulik, 2003; Lewinsohn, Seeley, Moerk, &Striegel-Moore, 2002). It is important to consider such gender differences in theclinical presentation of BN to revise prevalence estimates of this diagnosis (Anderson &Bulik, 2003).
InDSM-5 , BED ﬁnally received recognition as a stand-alone disorder after years of
being categorized as a disorder “worthy of further study. ”Binge eating was ﬁrst noted
in a subset of obese individuals by Stunkard in 1959 (Stunkard, 1959). BED has had aslow and controversial evolution in the psychiatric nosology for eating disorders(Fairburn, Welch, & Hay, 1993; Spitzer et al., 1993; Walsh, 1992).
BED is marked by recurrent binge eating (at least weekly for 3 months, as in BN)
and a sense of lack of control over eating during the episode, but in the absence ofregular compensatory behaviors. Unlike BN, the diagnostic criteria for BED includedescriptions of the binge experience. To meet criteria, an individual must experiencedistress regarding the binge eating and at least three of the following: eating muchmore rapidly than normal, eating until feeling uncomfortably full, eating largeamounts of food when not feeling physically hungry, eating alone because of feeling474 SPECIFIC DISORDERS

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embarrassed by how much one is eating, or feeling disgusted with oneself, depressed,or very guilty afterward. It remains a curiosity why these descriptors remained in theBED criteria when they are not in the BN criteria; presumably, this was related toensuring that individuals who simply overeat were not misdiagnosed as having BED.BED can occur at any body weight and is only diagnosed if neither AN nor BN criteriaare met.
Other Speci ﬁed Feeding or Eating Disorder (OSFED) is a new category in DSM-5 ,
which replaces the historical Eating Disorder Not Otherwise Speci ﬁed (EDNOS). The
reorganization in DSM-5 occurred in part because BED became a stand-alone diag-
nosis and in part because, historically, far too many individuals with eating disordersreceived a diagnosis of EDNOS, rendering it the most frequently diagnosed eatingdisorder. This alerted many researchers and clinicians to the fact that the diagnosticsystem was in need of revision so that a greater number of individuals could becaptured under the hallmark categories of AN, BN, and BED. OSFED applies topresentations with symptoms characteristic of a feeding and eating disorder but topresentation where full diagnostic criteria are not met. Given that this is indeed a newcategory, we have very little epidemiologic data that re ﬂect the new diagnosis.
Research over the next several years will reveal how the transformation of thediagnostic schema has reshuf ﬂed the prevalences of the various disorders.
OSFED includes a useful category of atypical AN, in which an individual meets all
criteria for AN except that their weight falls within or above the normal weight range.This would capture, for example, an individual who was obese who precipitously losta large amount of weight and exhibited all of the psychological features of AN, butbecause of the weight at which the weight loss started, still fell in the normal weightrange. Other presentations under OSFED include BN and BED of low frequency orlimited duration, purging disorder (which is purging behavior in the absence of bingeeating), and night eating syndrome, in which individuals report recurrent episodes ofnight eating, marked by eating after awakening from sleep or by excessive foodconsumption after the evening meal.
Based on previous research with EDNOS, what we do not expect to change is that
being in the OSFED category in no way implies that an individual has a less seriousdisorder. The severity of pathology and psychosocial impairment is comparableamong individuals with EDNOS, AN, and BN (Fairburn & Bohn, 2005; Keel, Grave-ner, Joiner, & Haedt, 2010). Clinical descriptions of EDNOS are consistent in statingthat most cases have features similar to AN and BN (Crow, Agras, Halmi, Mitchell, &Kraemer, 2002; Waller, 1993; Walsh & Garner, 1997). Three studies (Fairburn &Cooper, 2007; Ricca et al., 2001; Turner & Bryant-Waugh, 2003) using the EatingDisorder Examination (EDE; Cooper & Fairburn, 1987) found that individuals withEDNOS presented with signi ﬁcant cognitive symptomatology related to eating,
shape, and weight, suggesting that these syndromes are clinically signi ﬁcant.
DIAGNOSTIC CONSIDERATIONS
With the publication of DSM-5 in 2013, investigation of the validity of the new
classi ﬁcation system is an important research focus. Some advances of the DSM-5
system include attention to stages of illness. In the past, for example, if someone hadmet criteria for AN and then began to recover, she or he might have received a newFeeding and Eating Disorders 475

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diagnosis of EDNOS. In DSM-5 , there is now the option to include the speci ﬁer of “in
partial remission ”if, after having met full criteria, weight has normalized but the
psychological features remain, and “full remission ”if, after having met full criteria, no
criteria have been met for a sustained period of time. In addition, severity speci ﬁers
also exist, and are currently based on body mass index (BMI), with mild AN being 17
kg/m2, moderate 16 –16.99 kg/m2, severe 15 –15.99 kg/m2, and extreme <15 kg/m2.
In addition to the core diagnostic features, individuals with AN often manifest a
speciﬁc cluster of personality traits, including perfectionism, obsessionality, anxiety,
harm avoidance, and low self-esteem (Cassin & von Ranson, 2005; Fassino, Amianto,Gramaglia, Facchini, & Abbate Daga, 2004; Klump et al., 2000). Furthermore, boththese personality characteristics and anxiety disorders often precede AN onset (Bulik,Sullivan, Fear, & Joyce, 1997; Kaye et al., 2004). Major depression and anxietydisorders frequently co-occur with AN (Bulik et al., 1997; Fernandez-Aranda et al.,2007; Godart, Flament, Perdereau, & Jeammet, 2002; Godart, Flament, Lecrubier, &Jeammet, 2000; Kaye et al., 2004), and longitudinal research suggests that depressionoften persists following recovery from AN (Sullivan, Bulik, Fear, & Pickering, 1998).
Some personality features common among individuals with AN are also man-
ifested by many women with BN, such as high harm avoidance, perfectionism, andlow self-esteem. However, other personality features appear more speciﬁ ct oB N ,
including elevated novelty seeking and impulsivity, low self-directedness, and lowcooperativeness (Bulik, Sullivan, Carter, & Joyce, 1995; Fassino et al., 2004; Steigeret al., 2004). Further reﬁ nements of the components of impulsivity suggest that
negative urgency, or the tendency to act rashly when distressed, is the facet ofimpulsivity most strongly associated with bulimia (Fischer, Smith, & Cyders, 2008).
Comorbid psychiatric disorders are very common among individuals with BN,
occurring among nearly 80% of patients (Fichter & Quad ﬂieg, 1997). These comor-
bidities include anxiety disorders, major depression, dysthymia, substance use, andpersonality disorders (Braun, Sunday, & Halmi, 1994; Brewerton et al., 1995; Buliket al., 2004; Perez, Joiner, & Lewinsohn, 2004).
Finally, BED also commonly co-occurs with numerous other psychiatric diagnoses,
including mood, anxiety, and substance abuse disorders (Grucza & Beirut, 2007;Johnson, Spitzer, & Williams, 2001; Marcus, Wing, & Fairburn, 1995; Striegel-Mooreet al., 2001; Wil ﬂey, Freidman, et al., 2000). Data from the National Comorbidity
Survey Replication (Hudson, Hiripi, Pope, & Kessler, 2007) indicate that BED is achronic condition associated with signi ﬁcant impairment in daily functioning. Global
data from the World Heath Organization World Mental Health Surveys indicate thatBED and BN are associated with signi ﬁcantly increased education in women. Early-
onset BED predicted reduced odds of marriage in women and reduced odds ofemployment in men, while early-onset BN predicted increased odds of current workdisability in both sexes. Both BED and BN were associated with signi ﬁcantly increased
days of role impairment, although much of the role impairment was accounted for bythe presence of comorbid disorders (Kessler, Shahly, et al., 2013).
Finally, those individuals with BED who are overweight or obese are at risk for
medical complications (Hudson et al., 2007). Yet, the negative psychological impact ofBED does not appear to be attributable to obesity. Obese individuals with BED reportsubstantially poorer psychological functioning than do obese individuals withoutBED (Grucza, Przybeck, & Cloninger, 2007), and normal weight and overweight476 SPECIFIC DISORDERS

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individuals with BED report equivalent psychological features of disordered eatingand depression (Dingemans & van Furth, 2012).
EPIDEMIOLOGY
Available epidemiologic data on eating disorders re ﬂectDSM-IV diagnostic criteria,
because suf ﬁcient time has not yet elapsed for studies to be conducted on the new
classi ﬁcations. Lifetime prevalence estimates of DSM-IV AN, BN, and BED from a
nationally representative population sample over age 18 are 0.9%, 1.5%, and 3.5% inwomen, and 0.3%, 0.5%, and 2.0% in men, respectively (Hudson et al., 2007). Theprevalence of subthreshold AN, de ﬁned as at least one criterion short of threshold, is
greater and ranges from 0.37% to 1.3% (Hoek, 1991). The gender ratio for AN isapproximately 9:1, women to men (APA, 1994). Awareness of these disorders hasincreased; however, the data on changing incidence are con ﬂicting. Some studies
report increasing incidence of AN or increases in disordered eating behavior (such asstrict dieting or fasting for weight or shape control) that are associated with AN (e.g.,Hay, Mond, Buttner, & Darby, 2008; Lucas, Crowson, O ’Fallon, & Melton, 1999;
Eagles, Johnston, Hunter, Lobban, & Millar, 1995; Jones, Fox, Babigan, & Hutton, 1980;Møller-Madsen & Nystrup, 1992), whereas others describe stable prevalence (e.g.,Smink, van Hoeken, & Hoek, 2012; Hoek, 2006; Currin, Schmidt, Treasure, & Jick,2005; Pawluck & Gorey, 1998; Hall & Hay, 1991; Hoek et al., 1995). The peak age ofonset for AN is between 15 and 19 years (Lucas, Beard, O ’Fallon, & Kurland, 1988), an
age group for which incidence has been increasing (Smink et al., 2012). However,reports suggest new-onset cases in mid- and late life (Gagne et al., 2012; Mangweth-Matzek et al., 2006; Beck, Casper, & Andersen, 1996; Inagaki et al., 2002) andincreasing presentations in children (Rosen, 2010).
The prevalence of BN in the United States is estimated to be 1.5% for women and
0.5% for men (Hudson et al., 2007). The prevalence of subthreshold behaviors isconsiderably higher, with 4.9% of women and 4% of men endorsing any binge eating.Similar to AN, reports suggest that more children and older adults are presenting withBN (Marcus et al., 2007; Rosen, 2010).
The prevalence of BED in the United States has been estimated at 3.5% for women
and 2% for men (Hudson et al., 2007), while community surveys across 12 countriesestimate the lifetime prevalence across both genders at 1.9% (Kessler, Shahly, et al.,2013). In a population-based study of female twins, 37% of obese women (BMI 30)
reported binge eating (Bulik, Sullivan, & Kendler, 2002), representing 2.7% of thefemale population studied. Community studies of obese individuals have found aprevalence of BED between 5% and 8% (Bruce & Agras, 1992; Bruce & Wil ﬂey, 1996).
The sex distribution in BED is more equal than in AN or BN (Hudson et al., 2007) withfew differences in prevalence across races or ethnic groups (Alegria et al., 2007; Marcuset al., 2007).
PSYCHOLOGICAL AND BIOLOGICAL ASSESSMENT
Careful and accurate assessment of eating disorders, which are frequently complexand have multiple presentations, is critical for effective treatment and research. Thegeneral goal of psychological assessment is to elicit information that accuratelyFeeding and Eating Disorders 477

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describes symptomatology, accurately characterizes diagnostic pro ﬁle, and indicates
appropriate treatment recommendations (Peterson & Mitchell, 2005). Assessing indi-viduals with eating disorders is often challenging secondary to denial of the illness andhidden signs and symptoms (Palmer, 2003; Schacter, 1999; Tury, Gulec, & Kohls, 2010;Vitousek, Daly, & Heiser, 1991). The use of active listening skills is important fordeveloping rapport (Keel, 2001), and motivational interviewing techniques (Miller &Rollnick, 2002), which encourage rolling with resistance, avoiding arguments, andexpressing empathy, are often helpful for conducting a successful assessment.
Clinical interviews in eating disorders are used to elicit the patient ’s perspective of
the development of his or her dif ﬁculties and frequently include the reason for the
assessment/primary complaint, history of present illness, medical complications,treatment history, and coexisting conditions (Peterson, 2005). A combination ofstructured interviews, self-report measures, and medical assessments may also beemployed to obtain a more complete clinical picture. In the case of minors, corrobo-rating information, such as reports from parents or school of ﬁcials, is additionally
informative (Lock, Le Grange, Agras, & Dare, 2001).S
TRUCTURED INTERVIEWS
Structured interviews are essential for clarifying differential diagnostic issues andassessing psychiatric comorbidity. Structured interviews are advantageous in thatthey allow for active involvement of the interviewer, who can help clarify concepts oranswer questions that may arise during the assessment. Obvious drawbacks tostructured interviews include greater ﬁnancial cost and clinician burden (Grilo, 2005).
For untrained interviewers, the two dominant instruments for assessing Axis I
pathology are the Diagnostic Interview Schedule (DIS; Robins, Helzer, Croughan, &Ratcliff, 1981) and the Composite International Diagnostic Interview (CIDI; WorldHealth Organization, 1990). The various versions of the Structured Clinical InterviewforDSM-IV (SCID; First, Spitzer, Gibbon, & Williams, 2002), which has excellent
validity and reliability (Grilo, 2005; Zanarini et al., 2000), are recommended forassessing Axis I pathology in adults by trained interviewers.
Several clinician-based structured or semistructured interviews have been devel-
oped speci ﬁcally for assessing eating disorder symptomatology. The Eating Disorder
Examination (EDE; Cooper & Fairburn, 1987) is well-established (Wil ﬂey, Schwartz,
Spurrell, & Fairburn, 2000) and widely used. It includes 33 items that measurebehavioral and psychological traits in AN and BN and, with the exception of thediagnostic items, focuses on the 28 days preceding the assessment. Items are rated on a7-point Likert-type scale, with higher scores indicating greater pathology, and com-prise the following scales: dietary restraint, eating concern, weight concern, and shapeconcern. The EDE has high interrater reliability (Cooper & Fairburn, 1987; Grilo,Masheb, Lozano-Blanco, & Barry, 2004; Rizvi, Peterson, Crow, & Agras, 2000),adequate internal consistency (Beumont, Kopec-Schrader, Talbot, & Touyz, 1993;Cooper, Cooper, & Fairburn, 1989), and good discriminative validity for distinguish-ing those with eating disorders from healthy individuals (Cooper et al., 1989; Wilson &Smith, 1989). Other popular structured interviews for assessing disordered eatinginclude the Interview for Diagnosis of Eating Disorders (IDED; Williamson, 1990) andthe Structured Interview for Anorexic and Bulimic Disorders (SIAB-EX; Fichter et al.,478 SPECIFIC DISORDERS

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1998). For a full review of these and other structured interviews in eating disorders,see Grilo, 2005.
The IDED-IV (Kutlesic, Williamson, Gleaves, Barbin, & Murphy-Eberenz, 1998) is
another semistructured interview primarily used for differential diagnosis of DSM-IV
AN, BN, and EDNOS. The IDED-IV differs from the EDE in that it does not focus onfrequency and severity data, but rather on differential diagnosis. Four studies supportthe psychometric properties of this instrument (Kutlesic et al., 1998).
The current version of the SIAB-EX (Fichter et al., 1998) assesses speci ﬁcc r i t e r i af o r
AN and BN (including subtype s), consistent with both the DSM-IV and the ICD-10 .
There is also an algorithm that allows the data to be used to generate the BEDresearch diagnosis and other eating disor der syndromes under the EDNOS category.
The SIAB-EX has demonstrated good internal consistency, factor structure, interraterreliability, and convergent and discrim inant construct validity (Fichter & Quad ﬂieg,
2000, 2001). Overall, the EDE and the SIAB-EX have been shown to produce generallysimilar ﬁndings. However, areas of divergence do exist, many of which could be
attributable to the differences in criter ia and time frames for assessment (Fichter &
Quad ﬂieg, 2001).
S
ELF-REPORTS
Many self-report measures are available for assessing disordered eating both inresearch and clinical settings. Self-report assessments can be used for a variety ofpurposes, including identifying clinical features, quantifying symptoms, and verifyingdiagnoses. They are particularly useful for assessing change over time and are timeand cost effective because they can be completed independently by the patient(Peterson & Mitchell, 2005). Two of the most widely used self-report questionnairesfor assessing disordered eating include the Eating Disorder Inventory (EDI) and theEating Disorder Examination –Questionnaire (EDE-Q).
The EDI (Garner, Olmsted, & Polivy, 1983, 1984), which assesses eating disorder
symptoms and associated psychological traits, is useful for differentiating levels ofeating disorder severity and for assessing treatment outcome (Williamson, Anderson,Jackman, & Jackson, 1995). This assessment is described by the authors as “investiga-
tor-based, ”emphasizing that it is the investigator ’s job to make ﬁnal judgments about
what symptoms and behaviors are present (e.g., to determine what constitutes abinge). The EDI has 64 questions answered on a 6-point Likert-type scale andcomprises the following eight subscales: drive for thinness, bulimia, body dis-satisfaction, ineffectiveness, perfectionism, interpersonal distress, interoceptiveawareness, and maturity fears. A revised version of the EDI, the EDI-2, was publishedin 1991 and includes 27 additional questions. The eight scales from the EDI wereretained, and three additional scales— asceticism, impulse regulation, and social
insecurity —were incorporated (Garner, 1991).
The third version of the scale, EDI-3 (Garner, 2004), retained the same items as the
EDI-2 but has a slightly different factor structure (Garner, Olmsted, & Polivy, 2008). Itcontains 91 items rated on a 0 –4 point scoring system. The three subscales assessing
eating pathology added in the EDI-2 (drive for thinness, bulimia, and body dis-satisfaction) remain largely unchanged, and the general psychology subscales includelow self-esteem, personal alienation, interpersonal insecurity, interpersonal alienation,Feeding and Eating Disorders 479

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interoceptive de ﬁcits, emotional dysregulation, perf ectionism, asceticism, and matu-
rity fears. Scoring for the EDI-3 includes the following six composite scores: (1) eatingdisorder risk, (2) ineffectiveness, (3) interpersonal problems, (4) affective problems,(5) over control, and (6) general psychologi cal maladjustment, as well as infrequency
and negative impression scores. The EDI-3 has yielded reliable and valid scores(Garner, 2004).
The EDE-Q (Fairburn & Beglin, 1994), another widely used self-report measure of
eating disorder symptoms, assesses severity of eating pathology and associateddisturbances over the past 28 days. It is most often used in research, but it can beapplied in clinical settings as well (Peterson & Mitchell, 2005). The EDE-Q was adaptedfrom the structured interview EDE (Cooper & Fairburn, 1987), and like the EDE, itconsists of 33 items and four subscales (restraint, eating concern, shape concern, andweight concern). The subscales and total scores are based on averages from 0 to 6, withhigher scores indicating greater pathology. The EDE-Q has been described as anaccurate method for assessing binge eating (Wilson, Nonas, & Rosenbaum, 1993) andshows acceptable reliability and validity (Fairburn & Cooper, 1993).
There are numerous other self-report assessments for eating disorders, including
the Multiaxial Assessment of Eating Disorder Symptoms (MAEDS; Anderson,Williamson, Duchmann, Gleaves, & Barbin, 1999), the Stirling Eating Disorder Scales(SEDS; Williams et al., 1994), the Anorexia Nervosa Inventory for Self-Rating (ANIS;Fichter & Keeser, 1980), the Three Factor Eating Questionnaire (TFEQ; Stunkard &Messick, 1985), the Binge Eating Scale (BES; Gormally, Black, Daston, & Rardin, 1982),and the Questionnaire for Eating and Weight Patterns-Revised (QEWP-R; Yanovski,1993). A full review of these and other self-report measures for assessing disorderedeating can be found in Peterson and Mitchell (2005) or Tury, Gulec, and Kohls (2010).M
EDICAL ASSESSMENT
Careful medical assessment, both initially and as indicated throughout the duration ofeating disorder treatment, is critical for effective treatment (Crow, 2005). It is alsoimportant for Emergency Medicine physicians to be able to screen for and recognizepatients with eating disorders, and to be aware of their medical complications andpsychiatric comorbidities, in order to carry out a successful therapeutic intervention(Trent, Moreira, Colwell, & Mehler, 2013; Mascolo, Trent, Colwell, & Mehler, 2012).Documentation of medical complications is imperative, not only for treatment plan-ning but also for service authorization by insurance companies. Although all eating-disorder presentations require medical monitoring, low-weight patients, individualswith purging behaviors, and obese individuals with binge-eating behavior (or acombination of these behaviors) are typically at the greatest risk for medical compli-cations (e.g., Crow, Salisbury, Crosby, & Mitchell, 1997; Harris & Barraclough, 1998;Kohn, Golden, & Shenker, 1998).
Low-weight individuals are particularly vulnerable to medical morbidity and
mortality (Harris & Barraclough, 1998). A BMI below 13 is associated with lessfavorable outcome (Hebebrand et al., 1997), and low weight is associated withincreased likelihood of sudden cardiac death. AN, BN, and EDNOS are all associatedwith increased mortality (Crow et al., 2009). Evidence of medical complications mightalso encourage otherwise resistant patients to enter treatment. A standard initial480 SPECIFIC DISORDERS

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assessment for low-weight individuals should include a complete blood count, anelectrolyte battery (including phosphorus, calcium, and magnesium), an electrocar-diogram, liver function tests, and a dual-energy X-ray absorptiometry (DEXA) scan(Crow, 2005). Blood pressure and pulse should also be documented, as dehydrationcan lead to orthostatic hypotension. The patient should be monitored carefullythrough the re-feeding process, because provision of adequate calories may lead toa drop in serum phosphorus, which is associated with mortality (Kohn et al., 1998)both in hospital (Ornstein, Golden, Jacobson, & Shenker, 2003) and outpatient settings(Winston & Wells, 2002).
Electrolyte disturbance is the most commonly recognized complication of purging
behaviors (Crow et al., 1997). Although not sensitive to vomiting frequency, hypoka-lemia is a marker of vomiting behavior (Crow et al., 1997). Another commoncomplication of self-induced vomiting is parotid hypertrophy, or painless swellingof the parotid glands, which may persist for months following cessation of purging(Ogren, Huerter, Pearson, Antonson, & Moore, 1987). Dental complications, includingdental enamel erosion on the lingual surfaces of teeth (Little, 2002), may occur inindividuals who vomit frequently and, thus, continued dental monitoring is impor-tant. A smaller number of individuals with purging behaviors report gastrointestinalsymptoms, including intestinal bleeding, hematemesis (vomiting blood), the passingof melanotic stools, or blood in the stools. Although rare, esophageal tears, gastricerosions, hemorrhoids, and gastric rupture may also occur (Cuellar, Kaye, Hsu, & VanThiel, 1988; Cuellar & Van Thiel, 1986). Abuse of laxatives and emetics are alsoassociated with signi ﬁcant medical morbidity. The use of syrup of Ipecac should signal
a medical and cardiac evaluation, as it is associated with severe cardiac effects.
BED, which is among the most common of eating disorder presentations, is often
associated with co-occurring conditions (Crow, 2005), including Type II diabetesmellitus and obesity. There is some evidence to suggest that obese individuals withType II diabetes mellitus who also binge eat experience worse outcomes than theirnon-binge-eating peers (Goodwin, Hoven, & Spitzer, 2003; Mannucci et al., 2002).Binge eating appears to be associated with medical problems independent of obesity(Bulik et al., 2002). Moreover, BED may confer a risk of developing metabolicsyndrome (a cluster of related risk factors for atherosclerotic cardiovascular disease,including abdominal obesity, dyslipidemia, hypertension, and abnormal glucosemetabolism) beyond the risk attributable to obesity alone (Hudson et al., 2010). Itis critical to remember that not all individuals with BED are overweight or obese. Weawait further data on the health impact of BED in normal weight individuals.
The growing interest in eating disorders over the past 20 years has resulted in
the development of numerous assessment t ools for research and clinical purposes.
Accurate assessment of individuals with dis ordered eating requires a multidisci-
plinary approach to address both the psych ological and biological factors under-
lying etiology.
ETIOLOGICAL CONSIDERATIONS
Although numerous psychological, social, and biological factors have been implicatedas potential causes of eating disorders, few speciﬁ c risk factors have been consistently
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(Jacobi, Hayward, de Zwaan, Kraemer, & A gras, 2004; Striegel-Moore & Bulik,
2007). Common risk factors across eating disorders include female sex, race, orethnicity, childhood eating and gastrointestinal problems, elevated concerns aboutshape and weight, negative s elf-evaluation, prior hist ory of sexual abuse and other
adverse events, and presence of additional ps ychiatric diagnoses (Jacobi et al., 2004).
Developmentally, prematurity, smallnes s for gestational age, and cephalohema-
toma have been identi ﬁed as possible risk factors for AN (Cnattingius, Hultman,
Dahl, & Sparen, 1999).
Current studies suggest that eating disorders are caused by a variety of factors,
including both genetic (e.g., Trace, Baker, Peñas-Lledó, & Bulik, 2013; Bulik, Slof-Op ’t
Landt, van Furth, & Sullivan, 2007) and environmental in ﬂuences (e.g., Becker &
Hamburg, 1996; Garner & Garﬁ nkel, 1980; Striegel-Moore & Bulik, 2007). Contempo-
rary understanding of eating disorders incorporates both genetic and environmentalfactors into causal models. Previously, an overemphasis on sociocultural factorsignored the fact that, although social pressures toward thinness are ubiquitous,only a fraction of individuals exposed to these factors develop eating disorders.Therefore, a clearer understanding of vulnerability has led to the model that indi-viduals who are more genetically predisposed to eating disorders are those who arealso more vulnerable to environmental triggers of illness —typically ones that result in
dieting, drive for thinness, and persistent negative energy balance.
Environmental in ﬂuences that might serve as eating disorder triggers include the
media ’s idealization of the thin body ideal and pressure to achieve an unrealistically
thin body type (Irving, 1990; Levine & Harrison, 2004). Sociocultural models of dis-ordered eating (Polivy & Herman, 1985; Striegel-Moore, Silberstein, & Rodin, 1986)suggest that the perception of a discrepancy between the self and the thin ideal leads topsychological discomfort. In turn, a desire to ameliorate this discomfort might result ineating disordered behavior. Striegel-Moore and Bulik (2007) report that cultural modelsof eating disorders are supported by the following: (a) the high percentage of femalecases of disordered eating; (b) the increase in incidence of eating disorders in womencoinciding with the decreasing body-weight ideal for women; (c) the reported higherincidence of eating disorders in cultures that emphasize thinness; and (d) the signi ﬁcant
association between thin ideal internalization and disordered eating.
In a community-based case-control study, Fairburn et al. (1998) found signi ﬁcant
differences in exposure to risk factors between women with BED and healthy controls,but surprisingly few differences between women with BED and BN. Speci ﬁcally,
compared with controls, women with BED reported more adverse childhood expe-riences, parental depression, personal vulnerability to depression, and exposure tonegative comments about weight, shape, and eating.
Other studies have indicated that environmental factors, including parental and
peer behaviors, contribute to both risk and protection from eating pathology (Enten &Golan, 2009; Twamley & Davis, 1999). For example, Twamley and Davis reported thatlow family pressures to control weight moderated the relation between exposure tothin norms and internalization of these messages. In addition, other environmentalvariables, including social pressure, could amplify or mitigate the risk of eatingdisorders (Striegel-Moore et al., 1986). For example, individuals exposed to peerteasing might be more likely to develop disordered eating (Thompson, Coovert,Richards, Johnson, & Cattarin, 1995; Thompson & Heinberg, 1993). Similarly,482 SPECIFIC DISORDERS

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individuals from higher social classes might be more prone to develop disorderedeating, as they presumably have more time, attention, and resources available to focuson the achievement of cultural beauty ideals (Striegel-Moore & Bulik, 2007). Althoughthese factors might in ﬂuence eating disorder etiology, they are likely not solely
responsible for their development (Striegel-Moore & Bulik, 2007). Personality traitssuch as perfectionism, as well as social anxiety, elevated weight, and high impulsivity,might also play important etiological roles. These sociocultural and environmentalfactors likely combine with genetic in ﬂuences (Strober, Freeman, Lampert, Dia-
mond, & Kaye, 2000) to contribute to the development of disordered eating, as isdescribed in the next section.B
EHAVIORAL GENETICS AND MOLECULAR GENETICS
The conceptualization of eating disorders has evolved rather radically across time(Vemuri & Steiner, 2007). Previously dominant sociocutural and psychodynamictheories have been supplanted by a biopsychosocial model. This evolution can beattributed in part to a systematic series of family twin and molecular geneticsinvestigations of eating disorders, which have supported the role of familial andgenetic factors in liability to eating disorders (Bulik et al., 2006; Klump, Miller, Keel,McGue, & Iacono, 2001). In this section, we review results of family, twin, andmolecular genetic studies (for a more thorough review see Trace et al., 2013).
Family studies investigate the degree to which a particular trait runs in families.
Although they are a valuable tool, family studies cannot tell us why a trait runs infamilies —whether due to genetic factors, environmental factors, or some combination
of both. The familial nature of AN is well-established. For example, ﬁrst-degree
relatives of patients with AN (parents, children, and siblings) are 11 times more likelyto have AN during their lifetime than ﬁrst-degree relatives of individuals who have
never had AN (Strober et al., 2000). Population-based twin studies have providedadditional support for the familiality of AN.
Twin studies allow us to examine familial components of disordered eating by
comparing similarities and differences in eating problems between monozygotic
twins (MZ) and dizygotic twins (DZ). MZ twins are generally assumed to share100% of their genetic material, whereas DZ twins, on average, share 50% of theirgenetic material (like brothers and sisters). Variance in liability to a disorder can bedissected into additive genetic factors, shared environmenta lf a c t o r s ,a n du n i q u e
environmental factors. Additive genetic factors refer to the cumulative effects of
many genes, each of which makes a small to moderate contribution. Sharedenvironmental factors re ﬂect environmental in ﬂuences that affect both members
of a twin pair and are believed to make twins more similar. Unique environmentalfactors (including measurement error), on the other hand, re ﬂect environmental
factors that only one twin is exposed to. Unique environmental factors are believedto make twins dissimilar. Twin studies hav e yielded heritability estimates between
28% and 74% for AN, with the remaining vari ability largely attributed to unique
environmental factors (Klump et al., 2001; Kortegaard et al., 2001; Bulik et al., 2006).Although twin studies can reveal the proportion of individual differences in adisorder that are due to genetic factors , they are unable to identify which speciﬁ c
genes are involved.Feeding and Eating Disorders 483

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Molecular genetic studies provide greater clarity regarding which genes in ﬂuence
risk for a trait or disorder. Association studies examine a genetic variant ’s association
with a trait; if the variant and trait are correlated, there is said to be an associationbetween the two. Association studies that involve a single gene or set of genes thathave a hypothesized association with the trait under study are referred to as candidategene studies. Molecular genetic designs that do not focus on one particular gene or setof genes include linkage and genome-wide association studies (GWAS). Linkageidenti ﬁes chromosomal regions that house predisposing or protective genes and allow
us to narrow the search from the entire human genome to speci ﬁc regions. GWAS
examines 300,000 to 1,000,000 genetic markers scattered across the genome, compar-ing cases with the trait to controls. If a genetic variant is more frequent in cases, thevariant is said to be associated with the trait. GWAS represents an agnostic search ofthe human genome and as such is a genetic discovery tool.
Decades of candidate gene association studies for AN have examined primarily
genes involved in the serotonergic, catecholaminergic, and dopaminergic systems andthose affecting appetite and weight regulation. The practice of preselecting a singlegene based on presumed biological involvement has fallen out of favor, and it hasgiven way to genome-wide approaches (described next).
Historically, using candidate gene approaches, the serotonergic system received
signiﬁcant attention, and results regarding its importance to eating disorders are
inconclusive. One meta-analysis of studies investigating 5-HTTLPR and AN suggests
that carriers of the short allele are at increased risk for this eating disorder (Calati, DeRonchi, Bellini, & Serretti, 2011). A comprehensive review of all candidate geneassociation studies conducted for AN (175 association studies of 128 polymorphismsrelated to 43 genes) points to promising although not conclusive evidence for genesrelated to mood regulation [brain-derived neurotrophic factor (BDNF) and SK3
channel], the hedonic reward system [catecholamine-O-methyltransferase (COMT)
and opioid receptor-1 (OPRD1 )], and appetite [agouti-related protein (AGRP)] (Rask-
Andersen, Olszewski, Levine, & Schiöth, 2010).
Linkage studies identi ﬁed chromosomes 1, 4, 11, 13, and 15 as possible regions of
interest in AN (Bacanu et al., 2005; Devlin et al., 2002; Grice et al., 2002). A follow-upstudy of candidate genes on chromosome 1 revealed associations with the serotoner-gic (5-HTR1D ) and opioidergic ( OPRD1 ) neurotransmitter system (Bergen et al., 2003).
Genome-wide approaches have been conducted. One Japanese study used deoxy-ribonucleic acid (DNA) pooling and included only 23K microsatellite markers(Nakabayashi et al., 2009); Wang et al. (2011), conducted GWAS in 1,033 femaleAN cases and 3,733 pediatric controls; however, no single nucleotide polymorphisms(SNPs), or DNA sequence variation, reached genome-wide signi ﬁcance, which is
typical in samples this small. A GWAS conducted under the auspices of the WellcomeTrust Case Control Consortium 3, also underpowered, failed to identify SNPS thatreached genome-wide signi ﬁcance (Boraska, in press). Large global efforts are under-
way to boost sample size in order to identify variants that in ﬂuence risk for AN
(Sullivan, Daly, & O ’Donovan, 2012).
Like AN, BN runs in families. First-degree relatives of individuals with BN are 4 to
10 times more likely to have the disorder themselves (Lilenfeld et al., 1998). In studiesof female twins, the estimated heritability of BN ranges between 54% and 83% infemales (see Slof-Op ’t Landt et al., 2005, for a review). As is the case in AN, molecular484 S
PECIFIC DISORDERS

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genetic studies of BN have generally focused on the serotonergic, dopaminergic,catecholamineric, and appetite systems. Signi ﬁcant associations have emerged
between BN and 5-HT2A and 5-HTTLPR .
Several meta-analyses (Calati et al., 2011; Lee & Lin, 2010; Polsinelli, Levitan, & De
Luca, 2012) have examined the association between 5-HTTLPR polymorphisms and
BN, with the large majority suggesting no signi ﬁcant association between 5-HTTLPR
polymorphisms and BN. Investigations exploring associations between other sero-tonin receptor genes and BN have yielded mixed results (see Scherag, Hebebrand, &Hinney, 2010, for a review). However, associations have been identi ﬁed between
several traits related to BN and the serotonin system, including minimum lifetime BMI(5-HT1B ), impulsiveness ( 5-HT2A and 5-HTTLPR), and affective dysregulation in
females ( 5-HTTLPR) (see Scherag et al., 2010, for a review). Furthermore, a gene –
environment interaction was identi ﬁed in one study; within a sample of individuals
with BN, carriers of the 5-HTTLPR short allele who reported physical or sexual abuse
also manifested greater sensation seeking, insecure attachment, and dissocial behavior(Steiger et al., 2007, 2008). The existence of this type of gene –environment interaction
might explain some of the inconsistent results regarding serotonin to date.
Studies investigating genes within the dopamine and catecholamine systems and
those genes involved in appetite have also yielded inconsistent ﬁndings. Nisoli et al.
(2007) examined the prevalence of TaqA1 polymorphisms of the DRD2 gene in
individuals with eating disorders, including BN, and in controls. No signi ﬁcant
associations were found between the A1 +allele in BN for either the A1/A1 or
A1/A2 genotypes. Sporadic associations were found between BN and the dopaminetransporter gene ( DAT1 ) (Shinohara et al., 2004) and COMT (Mikolajczyk, Grzy-
wacz, & Samochowiec, 2010), respectively. In addition, a few studies have identi ﬁed
an association between BN and preproghrelin (Miyasaka et al., 2006) and BDNF , yet
these results require replication.
Only one linkage study has been conducted for BN, which examined 308 multiplex
families identi ﬁed through a patient with BN. Signi ﬁcant linkage was found on
chromosome 10 and another region on chromosome 14 met criteria for genome-wide-suggestive linkage (Bulik et al., 2003). No GWAS of BN have been conducted todate. In sum, results of molecular genetic studies of BN remain inconclusive and arelimited by the use of small samples, which provide relatively low power.
The study of BED has burgeoned in the past decade. However, as the disorder has
been more recently operationalized than AN and BN, less research on the genetics ofBED has emerged. Nonetheless, extant family, twin, and molecular research largelysuggests that familial and genetic factors in ﬂuence risk for BED. A small number of
family studies have been conducted (Fowler & Bulik, 1997; Hudson et al., 2006; Leeet al., 1999). With the exception of the Lee et al. investigation, these studies suggest thatBED is familial. This has been further corroborated by twin studies. Two population-based twin studies have examined the heritability of BED (Javaras et al., 2008; Mitchellet al., 2010) and reported heritability estimates ranging from 39% to 45%.
Candidate gene association studies of binge eating and BED have focused on
neurotransmitter systems, such as the 5-HT and DA systems, and genetic variantsimplicated in appetite and obesity. One small case control investigation, comparingwomen with BED to normal women without BED, was conducted exploring the role ofthe 5-HTTLPR polymorphism in BED (Monteleone, Tortorella, Castaldo, & Maj, 2006).Feeding and Eating Disorders 485

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The homozygous long-allele and the heterozygous long-allele genotypes were foundto be more prevalent in individuals with BED than those without BED. Results maysuggest a role of the 5-HTTLPR polymorphism in BED; however, results should beconsidered preliminary, as the sample sizes in this study were small. Several investi-gations have also examined the role of DA polymorphisms, and particularly poly-morphisms of the DRD2 gene, in BED (Davis et al., 2008; Davis et al., 2009; Davis et al.,2012). Overall, studies exploring the association of between BED and polymorphismsof the DRD2 gene have been inconsistent, likely due to small sample sizes and a lack ofstatistical power. The largest study to date (Davis et al., 2012) suggests a potential roleof the DRD2 polymorphism Taq1A and C958T in BED; however, additional large-sample replication studies are needed.
Genes associated with obesity have also been investigated for their potential role in
BED, given the positive correlation between these conditions. MC4R (which is
associated with obesity) was examined as an early candidate for BED (Bransonet al., 2003), although this ﬁnding is not consistently replicated across studies
(Hebebrand et al., 2004). Positive associations with 5-HTTLPR and DAT1, BDNF,
and ghrelin have also been identi ﬁed in BED (Davis et al., 2007; Monteleone,
Tortorella, Castaldo, Di Filippo, & Maj, 2007; Monteleone, Tortorella, et al., 2006;Monteleone, Zanardini, et al., 2006; Shinohara et al., 2004); however, these resultsrequire con ﬁrmation and replication, and the ﬁeld awaits more comprehensive
genome-wide approaches.N
EUROANATOMY AND NEUROBIOLOGY
Neurobiological vulnerabilities contribute to eating disorder pathogenesis (Kaye,2008; Kaye, Wierenga, Bailer, Simmons & Bischoff-Grethe, 2013; Treasure & Campbell,1994), and brain structural and functional abnormalities are consistently found inindividuals with eating disorders (Frank, Bailer, Henry, Wagner, & Kaye, 2004; Kaye,Fudge, & Paulus, 2009). In addition, numerous behavioral traits associated with AN,including premorbid anxiety, obsessive behaviors, negative emotionality, impairedcognitive ﬂexibility, increased harm avoidance and perfectionism, and altered intero-
ceptive awareness, are hypothesized to be related to underlying abnormalities oralterations in brain structure and function (Kaye et al., 2013). Marsh et al. (2011)reported evidence of deactivation in the inferior frontal gyrus and neural systemencompassing the posterior cingulate cortex and superior frontal gyrus in femaleadolescents with bulimia in comparison to controls during the Simon spatialincompatibility task. This paradigm allowed them to observe abnormal patterns offrontostriatal activation in adolescents with bulimia when engaging in self-regulatoryprocesses associated with con ﬂict resolution. They suggested that this pattern could
explain how feeding behaviors might be “released ”from regulatory control in con ﬂict
situations, thereby perpetuating bulimic behaviors.
Brain structural abnormalities in eating disorders have been investigated using
computerized tomography (CT) and magnetic resonance imaging (MRI). Functionalimaging studies, including positron emission tomography (PET), single photonemission computer tomography (SPECT), and functional magnetic resonance imaging(fMRI), have also been employed to provide information about the cerebral activity ofa system or receptor being studied. Improvements in technology over the last decade,486 SPECIFIC DISORDERS

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