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Fully revised to incorporate DSM-5(TM) criteria andinformed by the most current research in its discussions ofdiagnosis and treatment Now in a second edition, Psychopathology: History, Diagnosis,and Empirical Foundations thoroughly explores psychopathologywith contributions from leading scholars in psycho-pathology. TheSecond Edition offers an overview of various topics in thecontext of major changes included in the DSM-5(TM). With new chapters on contextual factors affecting diagnoses andnon-alcohol substance abuse, Psychopathology, Second Editioncovers the history, theory, and assessment of anxiety disorders,posttraumatic stress disorder, mood disorders, schizophrenia, thepsychotic spectrum disorders, eating disorders, borderlinepersonality disorder, alcohol use disorders, psychopathy, sexualdysfunction, and sleep disorders. In addition, each chapter of the Second Editioncontains: * A description of the disorder, including brief history, caseexample, and epidemiological findings * Empirical foundations of each disorder, including findingsregarding neurobiological, behavioral, cognitive, and emotionalfactors * Assessment of each disorder, including interviews,self-reports, neurobiological assessment, and clinical ratingscales * Brief description and evaluation of the current interventionsfor each disorder * Summary and future directions Practical and thorough, this text is an essential reference forall mental health professionals and a solid introduction forstudents in psychopathology courses.
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Seitenzahl: 2005
Veröffentlichungsjahr: 2013
Table of Contents
Title Page
Copyright
Dedication
Preface
Historical Perspective
Acknowledgments
References
List of Contributors
Chapter 1: Issues in Diagnosis
General Terminological Issues
Functions of Psychiatric Diagnosis
Misconceptions Regarding Psychiatric Diagnosis
What Is Mental Disorder?
Psychiatric Classification From DSM-I to the Present
Criticisms of the Current Classification System
The DSM: Quo Vadis?
Summary and Future Directions
References
Chapter 2: Strategies for Evidence-Based Assessment of Children and Adolescents
Background
A Snapshot of Current Assessment Training and Practice
The First P: Prediction
The Second P: Prescription
The Third P: Process
Priority Areas for Research, Training, and Practice
References
Chapter 3: Obsessive-Compulsive Disorder
Introduction
The Nature of OCD
Signs and Symptoms of OCD
Prevalence and Epidemiology of OCD
Psychological Models
Neurobiological Models of OCD
Assessment
Psychological Treatment
Biological Treatments
Summary and New Directions
References
Chapter 4: Generalized Anxiety Disorder
Introduction
Nature of Generalized Anxiety Disorder
Neurobiological and Psychological Underpinnings
Cognitive and Behavioral Correlates
Emotional Correlates
Assessment
Interventions
Summary and New Directions
References
Chapter 5: Social Anxiety Disorder
Description of the Disorder
Epidemiology and Comorbidity
Actual Dysfunction
Psychological and Psychosocial Dysfunction
Interaction With Environmental Factors
Assessment of Social Anxiety Disorder
Interventions
Summary and Future Directions
References
Chapter 6: Panic Disorder
Description of Panic Disorder
Psychological Models and Empirical Data on Panic Disorder
Interaction With Environmental Factors
Etiological Models of Panic Disorder
Biological Features of Panic Disorder
Assessment of Panic Disorder
Treatment of Panic Disorder
Summary and Future Directions
References
Chapter 7: Posttraumatic Stress Disorder
Introduction
Diagnostic Criteria
Prevalence and Epidemiology
Psychological Models
Assessment
Interventions
Summary and Future Directions
References
Chapter 8: Major Depressive Disorder
Diagnostic Criteria
Prevalence of Major Depressive Disorder
Psychology of Major Depression
Behavioral Models of Depression
Cognitive Models of Major Depressive Disorder
Biology of Major Depression
An Integrative Model
Assessment of Depression
Psychological Treatment of Major Depressive Disorder
Prevention of Depression
Summary and Future Directions
References
Chapter 9: Persistent Depressive Disorder
Description and Diagnostic Criteria
Epidemiology
Course and Prognosis
Chronic Depression in Youth and the Elderly
Psychosocial Factors
Genetic and Neurobiological Factors
Assessment
Treatment
Summary and Future Directions
References
Chapter 10: Bipolar Disorder
Description of the Disorder
Etiology, Risk Factors, and Protective Factors: The Biopsychosocial Perspective
Psychosocial Predictors of the Course of Bipolar Disorder
Diagnostic Assessment
Treatment: Pharmacotherapy
Treatment: Psychotherapy
Summary and New Directions
References
Chapter 11: Schizophrenia and the Psychosis Spectrum
A Contemporary Diathesis-Stress Model
The Nature of Schizophrenia: Historical Perspectives
Origins of Schizophrenia
Biological Factors
Prenatal and Obstetrical Factors
Cognitive Deficits in Schizophrenia: Signs of Brain Dysfunction
Biological Indicators of Vulnerability: The Nature of the Brain Impairment
Premorbid Development, Course, and Prognosis
Assessment and Treatment of Schizophrenia
Summary and Future Directions
References
Chapter 12: Bulimia Nervosa and Binge Eating Disorder
Introduction
Symptoms and Diagnostic Criteria
History and Diagnostic Models of Binge Eating
Epidemiology
Genetic and Neurobiological Influences
Psychosocial Variables
Cognitive Dysfunction
Risk Factors
Environmental Factors
Assessment
Treatment
Summary and Future Directions
References
Chapter 13: Anorexia Nervosa
Description
Case Example
History of Anorexia Nervosa
Dysfunction
Assessment
Interventions
Summary and Future Directions
References
Chapter 14: Borderline Personality Disorder
The Clinical Symptoms of BPD
Current Theoretical Perspectives
Factors Involved in the Pathogenesis and Maintenance of BPD
Structural Approaches
Psychosocial Aspects
Cognitive Aspects of Borderline Personality Disorder
Contemporary Issues in the Diagnosis and Assessment of BPD
Clinical Approaches to Assessing Borderline Personality Disorder
Clinical Course and Treatment
Treatment
Summary and Future Directions
References
Chapter 15: Alcohol Use Disorders
Introduction
Overview
History
Theory
Diagnosis
Treatment
Summary and Future Directions
References
Chapter 16: Psychopathy as Psychopathology
Diagnostic Criteria
Conclusions
Psychological Models and Somatic Factors
Treatment of Psychopathy
Summary and Future Directions
References
Chapter 17: Sexual Dysfunction
Sexual Desire Disorders
Sexual Arousal Disorders
Orgasm
Sexual Pain Disorders
Vaginismus
Summary and Future Directions
References
Chapter 18: Sleep Disorders
Sleep Basics
Description of the Disorder
Models of Insomnia
Assessment of Disorder
Interventions
Brief Overview of Other Sleep Disorders
Summary and New Directions
References
Author Index
Subject Index
Cover image: © iStockphoto.com/Sergey Yeremin
Cover design: David Riedy
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Library of Congress Cataloging-in-Publication Data:
Craighead, W. Edward.
Psychopathology: History, Diagnosis, and Empirical Foundations/W. Edward Craighead, David J. Miklowitz, Linda W. Craighead—Second edition.
pages cm
Includes bibliographical references and index.
ISBN: 978-1-118-10677-8 (cloth); ISBN: 978-1-118-41915-1 (ebk); ISBN: 978-1-118-41630-3 (ebk)
1. Psychology, Pathological. I. Miklowitz, David Jay, 1957–. II. Craighead, Linda W. III. Title.
RC454.P7865 2013
616.89—dc23
2013016114
Preface
This book provides a basic description and evaluation of clinical theory and research regarding psychopathology. It is intended primarily as an advanced text for psychopathology courses taught to graduate students in clinical, counseling, and school psychology, as well as neuroscience, psychiatry, and social work. Some instructors may find it appropriate for an upper-level undergraduate course in abnormal psychology or psychopathology. The book also provides updated and refresher materials for mental health professionals engaged in assessment, diagnosis, and treatment of psychological disorders.
This first edition of this book emerged from our many discussions regarding how best to provide reading materials for the graduate psychopathology course when we were professors at the University of Colorado, Boulder. From time to time different faculty members had been called upon to teach this course, and each time this occurred we had lengthy discussions about the most appropriate reading lists and books. In addition to the standard materials regarding psychopathology, we wanted to include clinically relevant materials that focused on vulnerability and stress, genetic markers, human development, affective neuroscience, translational research, and empirically supported treatments including efficacy and effectiveness outcomes. We faced repeated difficulties in assembling such materials and requesting readings from colleagues around the world. We concluded that it was an appropriate time to ask several of our clinical science colleagues to help us create a resource that would incorporate these current and critical areas of interest. We asked them to provide a broad range of information drawn from psychopathology and related basic research for each disorder, so the reader would have a 30- to 40-page comprehensive view of each of the topics. Although we have now moved to other universities and venues for our work, we believe there is still a need in the psychopathology area for an integrative set of reading materials. In order to reflect enormous changes in psychopathology research, we have updated and revised and produced this second edition of the book. The biggest issue in the development of this edition of the book was the timing of the release of DSM-5. Should we wait until it is released or should the needed revision go ahead as planned? The initial version of DSM-5 was published in May 2013. Ultimately we and Wiley decided to publish this book in time for the 2013–2014 academic year because we could describe the history of the DSM developments, including DSM-5; the relevant psychopathology literature is based on earlier editions of DSM; and, yet, we could note any major changes included in DSM-5. Relevant DSM-5–based psychopathology research will supply the basis of future editions. Furthermore, psychopathology research is beginning to take a somewhat different focus. Future books on this topic may present a quite different organizational structure, perhaps surrounding constructs underlying DSM categories of psychopathology (see NIMH, at http://www.nimh.nih.gov/research-funding/rdoc.shtml).
Although the description of psychopathological disorders, at least on a nonscientific basis, has existed for hundreds of years, the first modern attempts to classify behaviors, thoughts, biology, and feelings within a formal classification system are usually attributed to the prominent German psychiatrist, Emil Kraepelin, who did most of his work at the end of the 19th century. Psychology emerged as a discipline at about that same time, and except for learning disabilities and a few of the childhood disorders, psychology was largely unconcerned with psychopathology. It was a half-century later that psychiatry (via the American Psychiatric Association [APA]) offered the first full-scale and systematic modern classification manual—the Diagnostic and Statistical Manual of Mental Disorders—in 1952. As Lilienfeld, Smith, and Watts note in the first chapter in this book, this diagnostic manual has undergone extensive revision and reorganizations over the past half-century.
In order to understand the slow development of psychology's role in the evolution of theories and research in psychopathology, it is important to have at least a glimpse of the history of professional developments within psychology. By the time of World War I (1914–1918), psychologists had emerged on mental health teams as professionals who primarily conducted formal clinical assessments. Psychologists' activities proliferated during World War I, though the emphasis remained on assessment. Psychologists had originally focused primarily on intellectual assessment, but during World War I this focus shifted to include assessment of personality, largely in order to assess and predict what is now known as posttraumatic stress disorder. Between World War I and World War II, clinical psychology continued to emphasize the development of intelligence tests and assessments of intelligence, but the discipline also began in earnest to develop instruments and methods to assess personality. It was only during World War II and subsequent years that psychology began conducting psychotherapy on more than a minimal basis, initially under the supervision of psychiatrists and only later, during the 1960–1970 era, as independent professionals. This movement toward broader involvement in clinical, counseling, and school intervention brought with it an interest in psychopathology as well as psychotherapy. A number of theoretical and practical developments (ranging from insurance reimbursement for clinical practice to National Institutes of Health funding for research) contributed to wide-scale acceptance of the DSM classification system, even though this framework has been associated with much controversy, as will be evident throughout this book.
During the preceding professional developments, it was psychiatry that first directed and led most mental health teams in child hygiene clinics and community mental health centers. As noted, psychologists only became genuinely concerned with more broadly defined psychopathology and its assessment as they became involved in the delivery of therapeutic services. The field of psychopathology has thus emerged over the past four to five decades to reflect advances in psychology, psychiatry, and neuroscience. There have been very few books since Maher's (1968) that have provided extensive, comprehensive, and scientifically based overviews of theories and empirical foundations of psychopathology at the graduate level. It is our hope that this tightly coordinated book will be a step toward filling that vacuum.
This book begins with a chapter that picks up where the preceding brief historical review leaves off; namely, Lilienfeld, Smith, and Watts present an overview of the major issues that arise in the study of psychopathology at an advanced level. Youngstrom and Frazier's advanced summary of the major issues associated with assessment of various forms of psychopathology comprises Chapter 2. These first two chapters are very timely and introduce the student or professional to the complex issues one encounters in studying psychopathology.
These introductory chapters are followed by overviews of most of the major clinical disorders. In order to assure consistency in the material presented in each chapter, we asked authors to follow a specific format, though some chapter topics and the associated research fit less easily within that format than others. The general outline for each chapter is as follows: (1) description of the disorder, including a brief history, a case example, and epidemiological findings; (2) empirical foundations of the disorder, including findings regarding neurobiological, behavioral, cognitive, and emotion factors; (3) assessment of the disorder, including interviews, self-reports, neurobiological assessment, and clinical rating scales; (4) a brief description and evaluation of the current interventions for each disorders; and (5) a summary and future directions. We greatly appreciate the willingness of our authors to adhere to this requested uniform outline. This approach improved our ability to provide consistent coverage across disorders, which makes this volume particular suitable for coursework. It also makes it easier for readers to find the needed information if the volume is used as a reference or resource book.
Following a long tradition that dates back to Freud's view of the centrality of anxiety in psychopathology, the DSM traditional anxiety disorders are presented first. These include obsessive-compulsive disorder (Abramowitz, Fabricant, & Jacoby, Chapter 3), generalized anxiety disorder (Rowa, Hood, & Antony, Chapter 14), social anxiety disorder including avoidant personality disorder (Ledley, Erwin, Morrison, & Heimberg, Chapter 5), panic disorder (Arch, Landy, & Craske, Chapter 6), and posttraumatic stress disorder (PTSD; Resick, Monson, & Rizvi, Chapter 7). As will be seen in the respective chapters, DSM-5 (APA, 2013) has moved OCD and PTSD to separate categories. The book continues with three chapters related to what have previously been labeled mood disorders, including major depressive disorder (Ritschel, Gillespie, Arnarson, & W. E. Craighead, Chapter 8), dysthymia and chronic depression (Klein & Black, Chapter 9), and bipolar disorder (Miklowitz & Johnson, Chapter 10). Chapter 11, by Trotman, Mittal, Tessner, and Walker, provides a thorough discussion of schizophrenia and the psychotic spectrum disorders. This is followed by two chapters regarding eating disorders: bulimia nervosa and binge eating disorders (L. W. Craighead, Martinez, & Klump, Chapter 12) and anorexia nervosa (Lock & Kirz, Chapter 13). Borderline personality disorder (Chapter 14) by Hooley and St. Germain, and alcohol use disorders (Chapter 15) by Ray, Courtney, and Bacio, comprise the next two chapters. The remainder of the book includes chapters on psychopathy by Vitale and Newman (Chapter 16), sexual dysfunction by Meston and Pulverman (Chapter 17), and sleep disorders by Kanady and Harvey (Chapter 18). As is apparent from this list, the authors were chosen because of their and their colleagues' and students' major contributions to our knowledge of psychopathology; this is apparent in the materials included in each chapter.
A very large number of people have contributed to the development and publication of this book. First, we acknowledge our own mentors: Leonard Ullmann and Gordon Paul (WEC), Michael Goldstein (DJM), and Alan Kazdin and Carolyn Sherif (LWC) are greatly appreciated. Colleagues, students, and friends who have contributed to our understanding of psychopathology, assessment, and interventions are just too numerous to mention, but fortunately they know who they are. We are especially appreciative to the Craighead and Miklowitz families for their support and caring while we completed this project. Specifically, we thank Ben, Wade, and Daniel Craighead and Margaret Craighead Shuster (along with Justin and Lily Shuster), and Mary Yaeger and Ariana Miklowitz.
We would like to thank our staff members, especially Jacqueline Larson. Jackie has been very helpful, efficient, and punctual in her assistance during the many phases of the development of this edition of the book.
We cannot imagine a better editor than Wiley's Patricia Rossi, who has been of great help from our very earliest conceptualization of the first edition right through the production of this second edition. She has been involved in every phase of its production, and in this process we have come to appreciate her insights and professional expertise in every phase of the editing process. It is a pleasure to work with such a talented person and genuinely fine human being. We also appreciate the help of her assistant, Kara Borbely, and the other cooperative and helpful people at John Wiley & Sons.
Finally, we would like to express our gratitude to the authors of the various chapters in this book. Each chapter's author team includes at least one of the established international leaders studying the topic. Coauthors were carefully chosen in their areas of expertise. As planned, the chapters reflect not only the contributions of the authors but also detailed reviews of the larger literature pertinent to each disorder. Thus, the reader can enjoy the detailed review of the psychopathology of the disorder in each chapter as well as the interesting commentary and thoughts about future directions for research and clinical issues from the perspective of individuals who are intimately involved in ongoing clinical psychopathology research. Our hope is that this will inform readers and also simulate the thinking of developing research investigators and students to inspire them to ask important questions regarding psychopathology. These outstanding scholars, in composite, have done what no one individual (or even three) can do today—namely, provide a thorough and comprehensive summary of the current state of knowledge regarding psychopathology.
American Psychiatric Association. (1952). Diagnostic and statistical manual of mental disorders (1st ed.). Washington, DC: Author.
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: Author.
Maher, B. (1968). Principles of psychopathology: An experimental approach. New York, NY: McGraw-Hill.
List of Contributors
Scott O. Lilienfeld, Sarah Francis Smith, and Ashley L. Watts
Psychiatric diagnosis is fundamental to the understanding of mental illness. Without it, the study, assessment, and treatment of psychopathology would be in disarray. In this chapter, we examine (a) the raison d'être underlying psychiatric diagnosis, (b) widespread misconceptions regarding psychiatric diagnosis, (c) the present system of psychiatric diagnosis and its strengths and weaknesses, and (d) fruitful directions for improving this system.
A myriad of forms of abnormality are housed under the exceedingly broad umbrella of mental disorders. Indeed, the current psychiatric classification system contains well over 300 diagnoses (American Psychiatric Association [APA], 2013). The enormous heterogeneity of psychopathology makes a formal system of organization imperative. Just as in the biological sciences, where Linnaeus' hierarchical taxonomy categorizes fauna and flora, and in chemistry, where Mendeleev's periodic table orders the elements, a psychiatric classification system helps to organize the bewildering subforms of abnormality. Such a system, if effective, permits us to parse the variegated universe of psychological disorders into more homogeneous, and ideally more clinically meaningful, categories.
From the practitioner's initial inchoate impression that a patient's behavior is aberrant to later and better-elaborated case conceptualization, diagnosis plays an integral role in the clinical process. Indeed, the essential reason for initiating assessment and treatment is often the observer's sense that “something is just not quite right” about the person. Meehl (1973) commented that the mental health professional's core task is to answer the question: “What does this person have, or what befell him, that makes him different from those who have not developed clinical psychopathology?” (p. 248). Therein lies the basis for psychiatric diagnosis.
Before proceeding, a bit of terminology is in order. It is crucial at the outset to distinguish two frequently confused terms: classification and diagnosis. A system of classification is an overarching taxonomy of mental illness, whereas diagnosis is the act of placing an individual, based on a constellation of signs (observable indicators, like crying in a depressed patient), symptoms (subjective indicators, like feelings of guilt in a depressed patient), or both, into a category within that taxonomy. Classification is a prerequisite for diagnosis.
Another key set of terminological issues concerns the distinctions among syndrome, disorder, and disease. As Kazdin (1983) observed, we can differentiate among these three concepts based on our levels of understanding of their pathology—the underlying physiological changes that may accompany the condition—and etiology, that is, causation (Gough, 1971; Lilienfeld, Waldman, & Israel, 1994).
At the lowest rung of the hierarchy of understanding there are syndromes, which are typically constellations of signs and symptoms that co-occur across individuals (syndrome means “running together” in Greek). In syndromes, neither pathology nor etiology is well understood, nor is the syndrome's causal relation to other conditions established. Antisocial personality disorder is a relatively clear example of a syndrome because its signs (e.g., the use of an alias) and symptoms (e.g., lack of remorse) tend to covary across individuals. Nevertheless, its pathology and etiology are largely unknown, and its causal relation to other conditions is poorly understood (Lykken, 1995). In contrast, some authors (e.g., Lilienfeld, 2013; but see Lynam & Miller, 2012) argue that psychopathic personality (psychopathy) may not be a classical syndrome. These researchers contend that psychopathy is instead a configuration of several largely independent constructs, such as boldness, coldness, and disinhibition, that come together in an interpersonally malignant fashion (Patrick, Fowles, & Krueger, 2009; see also Vitale & Newman, Chapter 16, this book).
In other cases, syndromes may also constitute groupings of signs and symptoms that exhibit minimal covariation across individuals but that point to an underlying etiology (Lilienfeld et al., 1994). For example, Gerstmann's syndrome in neurology (Benton, 1992) is marked by four major features: agraphia (inability to write), acalculia (inability to perform mental computation), finger agnosia (inability to differentiate among fingers on the hand), and left-right disorientation. Although these indicators are negligibly correlated across individuals in the general population, they co-occur dependably following certain instances of parietal lobe damage.
At the second rung of the hierarchy of understanding there are disorders, which are syndromes that cannot be readily explained by other conditions. For example, in the present diagnostic system, obsessive-compulsive disorder (OCD) can be diagnosed only if its symptoms (e.g., recurrent fears of contamination) and signs (e.g., recurrent hand washing) cannot be accounted for by a specific phobia (e.g., irrational fear of dirt). Once we rule out other potential causes of OCD symptoms, such as specific phobia, anorexia nervosa, and trichotillomania (compulsive hair pulling) we can be reasonably certain that an individual exhibiting marked obsessions, compulsions, or both, suffers from a well-defined disorder (APA, 2000, p. 463).
At the third and highest rung of the hierarchy of understanding there are diseases, which are disorders in which pathology and etiology are reasonably well understood (Kazdin, 1983; McHugh & Slavney, 1998). Sickle-cell anemia is a prototypical disease because its pathology (crescent-shaped erythrocytes containing hemoglobin S) and etiology (two autosomal recessive alleles) have been conclusively identified (Sutton, 1980). For other conditions that approach the status of bona fide diseases, such as Alzheimer's disease, the primary pathology (senile plaques, neurofibrillary tangles, and granulovacuolar degeneration) has been identified, while their etiology is evolving but incomplete (Selkoe, 1992).
With the possible exception of Alzheimer's disease and a handful of other organic conditions, the diagnoses in our present system of psychiatric classifications are almost exclusively syndromes or, in rare cases, disorders (Kendell & Jablensky, 2003). This fact is a sobering reminder that the pathology in most cases of psychopathology is largely unknown, and their etiology is poorly understood. Therefore, although we genuflect to hallowed tradition in this chapter by referring to the major entities within the current psychiatric classification system as mental “disorders,” readers should bear in mind that few are disorders in the strict sense of the term.
Diagnosis serves three principal functions for practitioners and researchers alike. We discuss each in turn.
Diagnosis furnishes a convenient vehicle for communication about an individual's condition. It allows professionals to be reasonably confident that when they use a diagnosis (such as dysthymic disorder) to describe a patient, other professionals will recognize it as referring to the same condition. Moreover, a diagnosis (such as borderline personality disorder) distills relevant information, such as frantic efforts to avoid abandonment and chronic feelings of emptiness, in a shorthand form that aids in other professionals' understanding of a case. Blashfield and Burgess (2007) described this role as “information retrieval.” Just as botanists use the name of a species to summarize distinctive features of a specific plant, psychologists and psychiatrists rely on a diagnosis to summarize distinctive features of a specific mental disorder (Blashfield & Burgess, 2007). Diagnoses succinctly convey important information about a patient to clinicians, investigators, family members, managed care organizations, and others.
Psychiatric diagnoses are organized within the overarching nosological structure of other diagnoses. Nosology is the branch of science that deals with the systematic classification of diseases. Within this system, most diagnostic categories are arranged in relation to other conditions; the nearer in the network two conditions are, the more closely related they ostensibly are as disorders. For example, social anxiety disorder (social phobia) and specific phobia are both classified as anxiety disorders in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; APA, 2013), and are presumably more closely linked etiologically than are social anxiety disorder and narcissistic personality disorder, the latter of which is classified as a personality disorder in DSM-5. Thus, diagnoses help to locate the patient's presenting problems within the context of both more and less related diagnostic categories.
Perhaps most important, a diagnosis helps us to learn new things; it affords us surplus information that we did not have previously. Among other things, a diagnosis allows us to generate predictions regarding case trajectory. As Goodwin and Guze (1996) noted, perhaps hyperbolically, “diagnosis is prognosis” (Kendler, 1980). The diagnostic label of bipolar I disorder describes a distinctive constellation of indicators (e.g., one or more manic or mixed episodes) that discriminates the course, rate of recovery, and treatment response from such related conditions as major depression and bipolar II disorder, the latter of which is marked by one or more episodes of hypomania and disabling depression. But a valid diagnosis does considerably more than predict prognosis. Robins and Guze's (1970) landmark article delineated formal criteria for ascertaining whether a diagnosis is valid. Validity refers to the extent to which a diagnosis measures what it purports to measure. More colloquially, validity is truth in advertising: A valid diagnosis is true to its name in that it correlates in expected directions with external criteria. Specifically, Robins and Guze outlined four requirements for the validity of psychiatric diagnoses. According to them, a valid diagnosis offers information regarding:
As a further desideratum, some authors have suggested that a valid diagnosis should ideally be able to predict the individual's response to treatment (Waldman, Lilienfeld, & Lahey, 1995). Nevertheless, this criterion should probably not be mandatory given that the treatment of a condition bears no necessary implications for its etiology. For example, although both schizophrenia and nausea induced by food poisoning generally respond to psychopharmacological agents that block the action of the neurotransmitter dopamine, these two conditions spring from entirely distinct causal mechanisms. Some authors (e.g., Ross & Pam, 1996) have invoked the felicitous phrase ex juvantibus reasoning (reasoning backward from what works) to describe the error of inferring a disorder's etiology from its treatment. Headaches, as the hoary example goes, are not caused by a deficiency of aspirin in the bloodstream.
There is reasonably strong evidence that many mental disorders fulfill Robins and Guze's (1970) criteria for validity. When these criteria are met, the diagnosis offers additional information about the patient, information that was not available before this diagnosis was made. For example, if we correctly diagnose a patient with schizophrenia, we have learned that this patient:
Is likely to exhibit psychotic symptoms that are not solely a consequence of a severe mood disturbance.
Has a higher than expected likelihood of exhibiting abnormalities on several laboratory measures, including indices of sustained attention, smooth pursuit eye tracking, and detection of biological motion (Kim, Park, & Blake, 2011).
Has a higher than average probability of having close biological relatives with schizophrenia and schizophrenia-spectrum disorders, such as schizotypal and paranoid personality disorders.
Is likely to exhibit a chronic course, with few or no periods of entirely normal functioning, but approximately a 30% chance of overall improvement.
Is likely to respond positively to medications that block the action of dopamine, although this is most likely to be the case for the positive symptoms (e.g., delusions, hallucinations) of the disorder (Subotnick et al., 2011).
Andreasen (1995) extended the Robins and Guze (1970) framework to incorporate indicators from molecular genetics, neurochemistry, and functional and structural brain imaging as additional validating indicators for psychiatric diagnoses (Kendell & Jablensky, 2003). Her friendly amendment to the Robins and Guze criteria allows us to use endophenotypic indicators to assist in the validation of a diagnosis. Endophenotypes are typically biomarkers or laboratory indicators, that is, “measurable components unseen by the unaided eye along the pathway between disease and distal genotype” (Gottesman & Gould, 2003, p. 636; Waldman, 2005). They are often contrasted with exophenotypes, the traditional signs and symptoms of a disorder.
We can view the process of validating psychiatric diagnoses within the overarching framework of construct validity (Cronbach & Meehl, 1955; Loevinger, 1957; Messick, 1995; but see Borsboom, Cramer, Kievit, Zand Scholten, & Franic, 2009, for a different perspective on construct validity), which refers to the extent to which a measure assesses a hypothesized attribute of individuals. As Morey (1991) noted, psychiatric classification systems are collections of hypothetical constructs; thus, the process of validating psychiatric diagnoses is also a process of construct validation. More broadly, we can conceptualize most or even all psychiatric diagnoses as open concepts (Meehl, 1977, 1990). Open concepts are marked by (a) fuzzy boundaries, (b) a list of indicators (signs and symptoms) that are indefinitely extendable, and (c) an unclear inner nature.
Recalling that psychiatric diagnoses are open concepts helps us to avoid the perils of premature reification of diagnostic entities (Faust & Miner, 1986). For example, the present diagnostic criteria for schizophrenia are not isomorphic with the latent construct of schizophrenia; they are merely fallible, albeit somewhat valid, indicators of this construct. Yet, the past few decades have occasionally witnessed a troubling tendency to reify and deify the categories within the current classification system, with some authors regarding them as fixed Platonic essences rather than as rough approximations to the true state of nature (Ghaemi, 2003; Michels, 1984). This error is manifested, for example, when journal or grant reviewers criticize researchers for examining alternative operationalizations of mental disorders that depart from those in the current diagnostic manual (see section Psychiatric Classification from DSM-I to the Present, later in this chapter). It is also manifested by the common error of referring to measures of certain psychiatric conditions as “gold standards” (see Skeem & Cooke, 2010, for a discussion of this tendency in the field of psychopathy), a phrasing that is erroneous in view of the fact that all indicators of psychopathology are at present fallible and provisional.
In a classic article, Cronbach and Meehl (1955) adopted from neopositivist philosophers of science the term nomological network to designate the system of lawful relationships conjectured to hold between theoretical entities (states, structures, events, dispositions) and observable indicators. They selected the network metaphor to emphasize the structure of such systems in which the nodes of the network, representing the postulated theoretical entities, are connected by the strands of the network, representing the lawful relationships hypothesized to hold among the entities (Garber & Strassberg, 1991).
For Cronbach and Meehl (1955), construct validation is a progressive and never-ending process of testing the links between hypothesized strands of the nomological network, especially those that connect latent constructs, which include psychiatric diagnoses (e.g., schizophrenia and major depression), to manifest indicators, which include the external criteria (e.g., laboratory tests and family history) laid out by Robins and Guze (1970). The more such construct-to-manifest indicator links are corroborated, the more certain we can be that our conception of the diagnosis in question is accurate. From this perspective, the approach to diagnostic validation outlined by Robins and Guze is merely one specific instantiation of construct validation.
One limitation of the Robins and Guze (1970) approach to construct validation is its exclusive emphasis on external validation, that is, the process of ascertaining the construct's associations with correlates that lie outside of the construct itself. As Skinner (1981, 1986; also Loevinger, 1957) observed, internal validation, ascertaining the construct's inner structure, is also a key component of construct validation. Internal validation can help investigators to test hypotheses regarding a construct's homogeneity (versus heterogeneity) and factor structure (Waldman et al., 1995). For example, if analyses suggest that a diagnosis consists of multiple and largely independent subtypes, the validity of the diagnosis would be called into question. Alternatively, factorial validity (i.e., the extent to which the factor structure of a diagnosis comports with theoretical predictions) can inform debates regarding the validity of a diagnosis. For example, factor analyses of attention-deficit/hyperactivity disorder (ADHD) generally support the separation of inattention from impulsivity and hyperactivity, as implied by the DSM criteria for this disorder (Martel, Von Eye, & Nigg, 2010).
In summary, valid psychiatric diagnoses serve three primary functions:
Beginning psychology graduate students and much of the general public hold a plethora of misconceptions regarding psychiatric diagnosis; we examine five such misconceptions here. Doing so will also permit us to introduce a number of key principles of psychiatric diagnosis. As we will discover, refuting each misconception regarding psychiatric diagnosis affirms at least one important principle.
The person most closely associated with this position is the late psychiatrist Thomas Szasz (1960), who argued famously for over 40 years that the term mental illness is a false and misleading metaphor (Schaler, 2004). For Szasz, individuals whom psychologists and psychiatrists term mentally ill actually suffer from problems in living (that is, difficulties in adjusting their behaviors to the demands of society). Moreover, Szasz contended that mental health professionals often apply the mental illness label to nonconformists who jeopardize the status quo (Sarbin, 1969; Szasz, 1960). This label serves as a convenient justification for forcing maladjusted, malcontented, and maverick members of society to comply with prevailing societal norms.
Specifically, Szasz maintained that medical disorders can be clearly recognized by a lesion to the anatomical structure of the body, but that the disorder concept cannot be imported to the mental realm because there is no such lesion to indicate deviation from the norm. According to him only the body can become diseased, so mentally ill people do not suffer from an illness akin to a medical disorder.
It is undeniable that psychiatric diagnoses are sometimes misapplied. Nevertheless, this legitimate pragmatic concern must be logically separated from the question of whether the mental illness concept itself exists (Wakefield, 1992). We should recall the logical principle of abusus non tollit usum (abuse does not take away use): Historical and sociological misuses of a concept do not negate its validity.
Wakefield (1992) and others (e.g., Kendell, 1975) have observed that the Szaszian argument is problematic on several fronts. Among others, it assumes that medical disorders are in every case traceable to discernible lesions in an anatomical structure, and that all lesions give rise to medical disorders. Yet identifiable lesions cannot be found in certain clear-cut medical diseases—such as trigeminal neuralgia and senile pruritis—and certain identifiable lesions, such as albinism, are not regarded as medical disorders (Kendell, 1975; Wakefield, 1992). Szasz's assertion that identifiable lesions are essentially synonymous with medical disorders is false; therefore, his corollary argument that mental disorders cannot exist because they are not invariably associated with identifiable lesions is similarly false.
According to this criticism, when we diagnose people with a mental disorder, we deprive them of their uniqueness: We imply that all people within the same diagnostic category are alike in all important respects.
To the contrary, a psychiatric diagnosis does nothing of the sort; it implies only that all people with that diagnosis are alike in at least one important way. Psychologists and psychiatrists are well aware that even within a given diagnostic category, such as schizophrenia or bipolar I disorder, people differ dramatically in their race and cultural background, personality traits, interests, and cognitive skills (APA, 2013).
Reliability refers to the consistency of a diagnosis. As many textbooks in psychometrics remind us, reliability is a prerequisite for validity but not vice versa. Just as a bathroom scale cannot validly measure weight if it yields dramatically different weight estimates for the same person over brief periods of time, a diagnosis cannot validly measure a mental disorder if it yields dramatically different scores on measures of psychopathology across times, situations, and raters.
Because validity is not a prerequisite for reliability, extremely high reliability can exist without validity. A researcher who based diagnoses of schizophrenia on patients' heights would end up with extremely reliable but entirely invalid diagnoses of schizophrenia.
There are three major subtypes of reliability. Contrary to popular (mis)conception, these subtypes are frequently discrepant with one another, so high levels of reliability for one metric do not necessary imply high levels for the others.
Test-retest reliability refers to the stability of a diagnosis following a relatively brief time interval, typically about a month. In other words, after a short time lapse, will patients receive the same diagnoses? Note that we wrote brief and short in the previous sentences; marked changes following lengthy time lapses, such as several years, may reflect genuine changes in patient status rather than the measurement error associated with test-retest unreliability.
In general, we assess test-retest reliability using either a Pearson correlation coefficient or, more rigorously, an intraclass correlation coefficient. Intraclass correlations tend to provide the most stringent estimates of test-retest reliability because, in contrast to Pearson correlations, they are influenced not merely by the rank ordering and differences among people's scores, but by their absolute magnitude.
Our evaluation of the test-retest reliability of a diagnosis hinges on our conceptualization of the disorder. We should anticipate high test-retest reliability only for diagnoses that are traitlike, such as personality disorders, or that tend to be chronic (long-lasting), such as schizophrenia. In contrast, we should not necessarily anticipate high levels of test-retest reliability for diagnoses that tend to be episodic (intermittent), such as major depression.
Internal consistency refers to the extent to which the signs and symptoms comprising a diagnosis hang together—that is, correlate highly with one another. We generally assess internal consistency using such metrics as coefficient alpha (Cronbach, 1951) or the mean interitem correlation. Cronbach's alpha can overestimate the homogeneity of a diagnosis, however, if this diagnosis contains numerous signs and symptoms, because this statistic is affected by test length (Schmidt, Le, & Ilies, 2003). We should anticipate high levels of internal consistency for most conditions in the current classification system given that most are syndromes, which are typically constellations of signs and symptoms that covary across people.
Interrater reliability is the degree to which two or more observers, such as different psychologists or psychiatrists, agree on the diagnosis of a set of individuals. High interrater reliability is a prerequisite for all psychiatric diagnoses, because different observers must agree on the presence or absence of a condition before valid research on that condition can proceed.
Many early studies of psychiatric diagnosis operationalized interrater reliability in terms of percentage agreement, that is, the proportion of cases on which two or more raters agree on the presence or absence of a given diagnosis. Nevertheless, measures of percentage agreement tend to overestimate interrater reliability. Here's why: Imagine two diagnosticians working in a setting (e.g., an outpatient phobia clinic) in which the base rate (prevalence) of the diagnosis of specific phobia is 95%. The finding that they agree with each other on the diagnosis of specific phobia 95% of the time would hardly be impressive and could readily be attributed to chance. As a consequence, most investigators today operationalize interrater reliability in terms of the kappa coefficient, which assesses the degree to which raters agree on a diagnosis after correcting for chance, with chance being the base rate of the disorder in question. Nevertheless, the kappa coefficient often provides a conservative estimate of interrater reliability, as the correction for chance sometimes penalizes raters for their independent expertise (Meyer, 1997).
Many laypersons and even political pundits believe that psychiatric diagnoses possess low levels of reliability, especially interrater reliability. This perception is probably fueled by high-profile media coverage of dueling expert witnesses in criminal trials in which one expert diagnoses a defendant as schizophrenic, for example, and another diagnoses him as normal. After the widely publicized 1982 trial of John Hinckley, who was acquitted on the basis of insanity for his attempted assassination of then-president Ronald Reagan, political commentator George Will maintained (on national television) that the disagreements among expert witnesses regarding Hinckley's diagnosis merely bore out what most people already knew: that psychiatric diagnosis is wildly unreliable (Lilienfeld, 1995).
Yet there is a straightforward explanation for such disagreement: Given the adversarial nature of our legal system, the prosecution and defense typically go out of their way to find expert witnesses who will support their point of view. This inherently antagonistic arrangement virtually guarantees that the interrater reliabilities of experts in criminal trials will be modest at best.
Certainly, the interrater reliability of psychiatric diagnoses is far from perfect. Yet for most major mental disorders, such as schizophrenia, mood disorders, anxiety disorders, and alcohol use disorder (alcoholism), interrater reliabilities are typically about as high—intraclass correlations between raters of 0.8 or above, out of a maximum of 1.0—as those for most well-established medical disorders (Lobbestael, Leurgans, & Arntz, 2011; Matarazzo, 1983). Still, the picture is not entirely rosy. For many personality disorders in particular, interrater reliabilities tend to be considerably lower than for other conditions (Maffei et al., 1997; Zimmerman, 1994), probably because most of these disorders comprise highly inferential constructs (e.g., lack of empathy) that raters find difficult to assess during the course of brief interviews.
From the standpoint of Szasz (1960) and other critics of psychiatric diagnosis (Eysenck, Wakefield, & Friedman, 1983), psychiatric diagnoses are largely useless because they do not provide us with new information. According to them, diagnoses are merely descriptive labels for behaviors we do not like. Millon (1975) proposed a helpful distinction between psychiatric labels and diagnoses; a label simply describes behaviors, whereas a diagnosis helps to explain them.
When it comes to a host of informal pop psychology labels, like sexual addiction, Peter Pan syndrome, codependency, shopping disorder, Internet addiction, and road rage disorder, Szasz and his fellow critics probably have a point. Most of these labels merely describe collections of socially problematic behavior and do not provide us with much, if any, new information (McCann, Shindler, & Hammond, 2003). The same may hold for some personality disorders in the current classification system. For example, the diagnosis of dependent personality disorder, which has been retained in DSM-5 (APA, 2013), arguably appears to do little more than describe ways in which people are pathologically dependent on others, such as relying excessively on others for reassurance and expecting others to make everyday life decisions for them.
Yet, as we have already seen, many psychiatric diagnoses, such as schizophrenia, bipolar I disorder, and panic disorder, do yield surplus information (Robins & Guze, 1970; Waldman et al., 1995) and, therefore, possess adequate levels of validity. Nevertheless, because construct validation, like all forms of theory testing in science, is a never-ending process, the validity of these diagnoses is likely to improve over time with subsequent revisions to the present classification system.
According to advocates of labeling theory, including Szasz (1960), Sarbin (1969), and Scheff (1975), psychiatric diagnoses produce adverse effects on labeled individuals. They argue that diagnostic labels not only stigmatize patients, but also frequently become self-fulfilling prophecies, leading observers to interpret ambiguous and relatively mild behaviors (e.g., occasional outbursts of anger) as reflecting serious mental illness.
A sensational 1973 and widely cited (over 2,300 citations as of this writing) study by Rosenhan appeared to offer impressive support for labeling theory. Rosenhan, along with seven other normal individuals, posed as pseudopatients (fake patients) in 12 U.S. psychiatric hospitals (some of the pseudopatients presented at more than one hospital). They informed the admitting psychiatrist only that they were hearing a voice saying, “empty,” “hollow,” and “thud.” All were promptly admitted to the hospital and remained there for an average of 3 weeks, despite displaying no further symptoms or signs of psychopathology. In 11 of 12 cases, they were discharged with diagnoses of schizophrenia in remission (the 12th pseudopatient was discharged with a diagnosis of manic depression in remission).
Rosenhan (1973) noted that the hospital staff frequently interpreted pseudopatients' innocuous behaviors, such as note taking, as indicative of abnormality. In case summaries, these staff also construed entirely run-of-the-mill details of pseudopatients' life histories, such as emotional conflicts with parents during adolescence, as consistent with their present illness. These striking results led Rosenhan to conclude that psychiatric labels color observers' perceptions of behavior, often to the point that they can no longer distinguish mental illness from normality.
Even today, some writers interpret Rosenhan's findings as a resounding affirmation of labeling theory (e.g., Slater, 2004; but see Spitzer, Lilienfeld, & Miller, 2005, for a critique of Slater, 2004). Yet, the evidence for labeling theory is less impressive than it appears. As Spitzer (1975) observed, the fact that all 12 of Rosenhan's pseudopatients were released with diagnoses in remission (meaning showing no indications of illness) demonstrates that the psychiatrists who treated them were in all cases able to distinguish mental illness from normality. Spitzer went further, demonstrating in a survey of psychiatric hospitals that in-remission diagnoses of previously psychotic patients are exceedingly infrequent, showing that the psychiatrists in Rosenhan's study successfully made an extremely rare judgment with perfect consensus.
Although incorrect psychiatric diagnoses can engender stigma, at least in the short run (Harris, Milich, Corbitt, Hoover, & Brady, 1992; Milich, McAninich, & Harris, 1992), there is scant evidence to support the popular claim that correctly applied psychiatric diagnoses do so. The lion's share of the research suggests that stigma is a consequence not of diagnostic labels, but rather of disturbed and sometimes disturbing behavior that precedes labeling (Link & Cullen, 1990; Ruscio, 2004). For example, within 30 minutes or less, children begin to react negatively to children with attention-deficit/hyperactivity disorder (ADHD) who have joined their peer group (Milich et al., 1992; Pelham & Bender, 1982).
Contrary to the tenets of labeling theory, there is evidence that accurate psychiatric diagnoses sometimes reduce stigma, because they provide observers with at least a partial explanation for otherwise inexplicable behaviors (Ruscio, 2004). For example, adults tend to evaluate mentally retarded children more positively when these children are labeled as mentally retarded than when they are not (Seitz & Geske, 1976), and peers rate the essays of children with ADHD more positively when these children are labeled with ADHD than when they are not (Cornez-Ruiz & Hendricks, 1993).
Our discussion up to this point presupposes that the boundaries of the higher-order concept of “disorder,” including mental disorder, are clear-cut or at least reasonably well delineated.1 To develop a classification system of disorders, one must first be able to ascertain whether a given condition is or is not a disorder. Yet the answer to the question of how best to define disorder, including mental disorder, remains elusive (Gorenstein, 1992). The issues here are of more than academic interest, because each revision of psychiatry's diagnostic manual has been marked by contentious disputes regarding whether such conditions as ADHD, premenstrual dysphoric disorder, and, more recently, binge eating disorder, attenuated psychosis syndrome, and hypersexual disorder are genuine disorders (Frances & Widiger, 2012; Wakefield, 1992). The fact that homosexuality was removed from the formal psychiatric classification system in 1974 by a majority vote of the membership of the American Psychiatric Association (Bayer & Spitzer, 1982) further demonstrates that these debates are frequently resolved more by group consensus than by scientific research.
Here we evaluate several influential attempts to delineate the boundaries of disorder. As we will discover, each approach has its limitations but each captures something important about the concept of disorder. As we will also discover, these approaches differ in the extent to which they embrace an essentialist as opposed to a nominalist view of disorder (Ghaemi, 2003; Scadding, 1996). Advocates of an essentialist view (Widiger & Trull, 1985) believe that all disorders share some essence or underlying property, whereas advocates of a nominalist view (Lilienfeld & Marino, 1995, 1999; Rosenhan & Seligman, 1995) believe that the higher-order concept of disorder is a social construction that groups together a variety of largely unrelated conditions for the purposes of social or semantic convenience.
Advocates of a statistical model, such as Cohen (1981), equate disorder with statistical rarity. According to this view, disorders are abnormal because they are infrequent in the general population. This definition accords with findings that many mental disorders are indeed rare; schizophrenia, for example, is found in about 1% of the population across much of the world (APA, 2013).
Yet, a purely statistical model falls short on at least three grounds. First, it offers no guidance for where to draw cutoffs between normality and abnormality. In many cases, these cutoffs are scientifically arbitrary. Second, it is silent on the crucial question of which dimensions are relevant to abnormality. As a consequence, a statistical model misclassifies high scores on certain adaptive dimensions (like intelligence, creativity, and altruism) as inherently abnormal. Moreover, it does not explain why high scores on certain dimensions (e.g., anxiety) but not on others (e.g., hair length) are pertinent to psychopathology. Third, by definition a statistical model assumes that all common conditions are normal (Wakefield, 1992). Yet the common cold is still an illness despite its essentially 100% lifetime prevalence in the population, and the Black Death (bubonic plague) was still an illness in the mid-1300s despite wiping out approximately one third of the European population.
Proponents of a subjective distress model maintain that the core feature distinguishing disorder from nondisorder is psychological pain. This model unquestionably contains a large kernel of truth; many serious mental illnesses (such as major depression, obsessive-compulsive disorder, generalized anxiety disorder, and gender identity disorder) are marked by considerable distress, even anguish.
The subjective distress model also falls short of an adequate definition of mental illness, because it fails to distinguish ego-dystonic conditions (those that conflict with one's self-concept) from ego-syntonic conditions (those that are consistent with one's self-concept). Although most mental disorders (such as major depression and generalized anxiety disorder) are typically ego-dystonic, some (such as antisocial personality disorder and bipolar I disorder, at least in its manic phase) are largely or entirely ego-syntonic, because individuals with these conditions frequently see little or nothing wrong with their behavior. They experience little or no distress in conjunction with their condition, and frequently seek treatment only when demanded by courts or significant others, or when their condition is complicated by a secondary condition that generates interpersonal difficulties (e.g., alcohol use disorder). Moreover, approximately half of patients with schizophrenia and other severe psychotic conditions are afflicted with anosognosia, meaning that they are unaware of the fact that they are ill (Amador & Paul-Odouard, 2000).
Proponents of a biological model (Kendell, 1975) contend that disorder can be defined in terms of a biological or evolutionary disadvantage to the organism, such as reduced life span or fitness (i.e., the ability to pass on genes to subsequent generations). Indeed, some mental disorders are associated with biological disadvantages; for example, major depression is associated with a dramatically increased risk for completed suicide (Joiner, 2006), and between 5% and 10% of patients with anorexia nervosa eventually die from complications due to starvation (Goodwin & Guze, 1996).
A biological model, however, also falls prey to numerous counterexamples. For example, being a soldier in front-line combat is not a disorder despite its average adverse effect on longevity and fitness. Conversely, some relatively mild psychological conditions, such as specific phobia, are probably not associated with decreased longevity or fitness, yet are still mental disorders.
One parsimonious definition is simply that disorders are a heterogeneous class of conditions all characterized by a perceived need for medical intervention on the part of health (including mental health) professionals (Kraupl Taylor, 1971). Like other definitions, this definition captures an important truth: Many or most mental disorders, such as schizophrenia, bipolar I disorder, and obsessive-compulsive disorder, are indeed viewed by society as necessitating treatment. Nevertheless, this definition also falls victim to counterexamples. For example, pregnancy clearly is associated with a perceived need for medical intervention, yet it is not regarded as a disorder.
In an effort to remedy the shortcomings of extant models of disorder, Wakefield (1992) proposed a hybrid definition that incorporates both essentialist and nominalist features.
According to Wakefield, all disorders, including all mental disorders, are harmful dysfunctions: socially devalued (harmful) breakdowns of evolutionarily selected systems (dysfunctions). For example, according to Wakefield, panic disorder is a mental disorder because it (a) is negatively valued by society and often by the individual afflicted with it, and (b) reflects the activation of the fight-flight system in situations for which it was not evolutionary selected, namely those in which objective danger is absent. In other words, panic attacks are false alarms (Barlow, 2001). Wakefield's operationalization of disorder has its strengths; for example, it acknowledges (correctly) that most and perhaps all disorders are viewed negatively by others. The concept of disorder, including mental disorder, is clearly associated with social values. As Wakefield (1992) noted, however, social devaluation is not sufficient to demarcate disorder from nondisorder, claims by Szasz (1960) to the contrary. For example, rudeness, laziness, slovenliness, and even racism are viewed negatively by society, but are not disorders (for a dissenting view regarding racism, see Poussaint, 2002). Therefore, Wakefield contends that something else is necessary to distinguish disorder from nondisorder, namely evolutionary dysfunction.
Nevertheless, the dysfunction component of Wakefield's analysis appears to fall prey to counterexamples. In particular, many medical disorders appear to be adaptive defenses against threat or insult. For instance, the symptoms of influenza (flu), such as vomiting, coughing, sneezing, and fever, are all adaptive efforts to expel an infectious agent rather than failures or breakdowns in an evolutionarily selected system (Lilienfeld & Marino, 1999; Neese & Williams, 1994). Such counterexamples appear to falsify the harmful dysfunction analysis. Similarly, many psychological conditions appear to be adaptive reactions to perceived threat. For example, in contrast to other forms of specific phobia, blood/injection/injury phobia is marked by a coordinated set of dramatic parasympathetic reactions—especially rapid decreases in heart rate and blood pressure—that were almost surely evolutionarily selected to minimize blood loss (Barlow, 2001). Although these responses may not be especially adaptive in the early 21st century, they were adaptive prior to the advent of Band-Aids, tourniquets, and anticoagulants (Lilienfeld & Marino, 1995).
