The Disorders: Specialty Articles from the Encyclopedia of Mental Health

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Specialty Articlesfrom the Encyclopedia of Mental Health Editor-in-Chief

HOWARD S. FRIEDMAN Department of Psychology University of California, Riverside

ACADEMIC PRESS A Harcourt Scienceand Technology Company

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Compilation copyright 9 2001 by ACADEMIC PRESS All Rights Reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher. Requests for permission to make copies of any part of the work should be mailed to: Permissions Department, Harcourt Inc., 6277 Sea Harbor Drive, Orlando, Florida 32887-6777 A c a d e m i c Press A Harcourt Science and Technology Company 525 B Street, Suite 1900, San Diego, California 92101-4495, USA http://www.academicpress.com A c a d e m i c Press Harcourt Place, 32 Jamestown Road, London NW1 7BY, UK http://www.academicpress.com Library of Congress Catalog Card Number: 2001088682 International Standard Book Number: 0-12-267805-2 PRINTED IN THE UNITED STATES OF AMERICA 01 02 03 04 05 06 QW 9 8 7 6

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Contents

About the Editor-in-Chief Preface How to Use This Reference

vii ix xi

Disorder (ADHD)

Russell A. Barkley and Gwenyth H. Edwards Autism and Pervasive Developmental Disorders Deborah Fein, LeeAnne Green, and Lynn Waterhouse

Agoraphobia Geoffrey L. Thorpe

83

Borderline Personality Disorder Jerome Kroll

97

107

Alcohol Problems Melanie E. Bennett and William R. Miller

15

Alzheimer's Disease Mark W. Bondi and Kelly L. Lange

27

Classifying Mental Disorders: Nontraditional Approaches Theodore R. Sarbin and Ernest Keen

117

Amnesia John F. Kihlstrom and Elizabeth L. Glisky

45

Conduct Disorder

131

Anorexia Nervosa and Bulimia Nervosa Melissa Pederson Mussell and James E. Mitchell

57

Dementia

147

Antisocial Personality Disorder Robert G. Meyer, Daniel Wolverton, and Sarah E. Deitsch

65

Dependent Personality Robert F. Bornstein

169 177

Anxiety Nader Amir and Michael J. Kozak

75

Depression Rick E. Ingram and Christine Scher Dissociative Disorders

187

Attention Deficit/Hyperactivity

Alan E. Kazdin

John L. Woodard

Richard P. Kluft

vi

Contents

DSM-IV John J. B. Allen

209

Posttraumatic Stress Lisa H. Jaycox and Edna B. Foa

337

Epilepsy Henry A. Buchtel

223

Premenstrual Syndrome (PMS) Katharina Dalton

347

Gambling Douglas Carroll and Frank F. Eves

235

Psychopathology Keith S. Dobson and Dennis Pusch

357

Mental Retardation and Mental Health Sharon A. Borthwick-Duffy

243

367

Mood Disorders Charles DeBattista, H. Brent Solvason, and Alan F. Schatzberg

259

Schizophrenia Jason Schiffman and Elaine Walker Sexual Disorders Ronald M. Doctor and Bryan Neff

379

Narcissistic Personality Disorder Salman Akhtar

271

Somatization and Hypochondriasis Javier I. Escobar and Michael A. Gara

393

Obsessive-Compulsive Disorder Randy O. Frost and Gail Steketee

277

Substance Abuse Thomas Ashby Wills

403

Panic Attacks Richard J. McNally

291

417

Paranoia Allan Fenigstein

Suicide Ronald W. Maris

301

Personality Disorders Robert G. Meyer

311

Phobias George A. Clum and Greg A. R. Febbraro

323

Encyclopediaof Mental Health Executive

Advisory Board

431

Contributors

433

Index

437

About the Editor-in-Chief

Social Science Citation Index. His books include two textbooks, Health Psychology and Personality; three edited scholarly volumes; and the authored comprehensive analysis titled The Self-Healing Personality. Dr. Friedman's research centers around the relations of mental and physical health, with a special focus on expressive style. He has taught undergraduates, graduate students, medical students, and postdocs. Professor Friedman has received the career Outstanding Contributions to Health Psychology Award from the Health Psychology Division of the American Psychological Association. He also received the Distinguished Teaching Award from the University of California, Riverside, and the Outstanding Teacher Award from the Western Psychological Association.

HOWARD S. FRIEDMAN is Distinguished Professor of Psychology at the University of California, Riverside. He also holds an adjunct appointment as Clinical Professor at the University of California, San Diego Medical School. Dr. Friedman attended Yale University, graduating magna cum laude with honors in psychology. He was awarded a National Science Foundation graduate fellowship at Harvard University, where he received his Ph.D. Professor Friedman is a thrice-elected Fellow of the American Psychological Association and an elected Fellow of the Society of Behavioral Medicine and the American Association for the Advancement of Science (AAAS). Friedman is author of many influential scientific articles in leading journals and was named a "most-cited psychologist" by the publishers of the

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VII

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Preface

A number of scientific and intellectual trends have converged to change our understanding of mental health. Conceptions of mental health and mental disorders have broadened significantly to take into account new knowledge about the genetic, biological, developmental, social, societal, and cultural nature of human beings. Our award-winning Encyclopedia of Mental Health was the first to bring together these emerging trends in one resource, and now the contributions primarily relevant to assessment and to the mental disorders are being made more accessible to those who desire a more concise and focused reference work. What are these mental health trends affecting our understanding of the disorders? First, our understanding has moved well beyond the artificial naturenurture dichotomy. We know more and more about the biological underpinnings of mental states and behavior, but we also better understand how these biological tendencies unfold in a family, social, and cultural environment. Second, we have moved beyond the old "mental" versus "physical" ("mind versus body") dichotomies. To a greater extent than previously imagined, there is a strong reciprocal relation between our health and activity and our cognitions, moods, and mental well-being. Third, the experts increasingly recognize the complementary importance of prevention and treatment. A simple model of treating mental "disease" is often ultimately futile without associated prevention efforts, yet prevention cannot sensibly ignore

the need for efficacious treatments. Fourth, we now emphasize primary mental health promotionmthe structural, environmental, family, and cultural context of mental health. Fifth, the best scholars now recognize meaningful variations across ages, genders, cultures, families, and societies. That is, to understand fully and improve significantly a person's mental health, we need to know not only about that person's biological and personal makeup, but also about his or her age, family, work, and position in society.

CONTENTS This volume on mental disorders thus encompasses various levels of analysis, from the molecular and biological, through the social and family, to the cultural. We have therefore included coverage of key topics not traditionally found in such a reference work. We of course include topics such as depression, conduct disorder, mood disorders, panic attacks, personality disorders, schizophrenia, phobias, and somatization and hypochondriasis. But we also examine such important matters as alcohol problems, Alzheimer's disease, anorexia and bulimia, premenstrual syndrome, gambling, substance abuse, suicide, and attention deficit/ hyperactivity disorder (ADHD). Also of note is that methodological issues receive attention throughout, including chapters on DSM-W and on nontraditional approaches to classifying mental disorders.

Preface

Finally, we have not neglected those fascinating topics that focus on the developmental context of mental disorders. For example, take a look at the articles on autism and pervasive developmental disorders and on mental retardation and mental health.

DISTINGUISHED SCHOLARS With the assistance of the outstanding editorial board, we have secured contributions by the most distin-

guished scholars and practitioners. Many are founders of their fields, and they are justly famous. But some contributors represent the brilliant new generation of mental health scholars. I have encouraged the contributors to write about what is most important. We thus have a reference work that is rooted in the present and looking toward the future, rather than bogged down in obsolete notions and topics. Emphasis has been placed on clarity and accessibility. Howard S. Friedman

How to Use This Reference

The Disorders is intended for use by students, research professionals, and practicing clinicians. Each article serves as a comprehensive overview of a given area, providing both breadth of coverage for students and depth of coverage for research and clinical professionals. We have designed this reference with the following features for maximum accessibility for all readers. Articles are arranged alphabetically by subject. Because the reader's topic of interest may be listed under a broader article title, we encourage use of the Index for access to a subject area, rather than use of the Table of Contents alone. Because a topic of study in mental health is often applicable to more than one article, the Index provides a complete listing of where a subject is covered and in what context. Each article contains an outline, a glossary, crossreferences, and a bibliography. The outline allows a quick scan of the major areas discussed within each article. The glossary contains terms that may be unfamiliar to the reader, with each term defined in the context of its use in that article. Thus, a term may appear in the glossary for another article defined in a

slightly different manner or with a subtle nuance specific to that article. For clarity, we have allowed these differences in definition to remain so that the terms are defined relative to the context of the particular article. The articles have been cross-referenced to other related articles in this reference. Cross-references are found at the first or predominant mention of a subject area covered elsewhere. Cross-references will always appear at the end of a paragraph. Where multiple cross-references apply to a single paragraph, the cross-references are listed in alphabetical order. We encourage readers to use the cross-references to locate other articles that will provide more detailed information about a subject. The Bibliography lists recent secondary sources to aid the reader in locating more detailed or technical information. Review articles and research articles that are considered of primary importance to the understanding of a given subject area are also listed. Bibliographies are not intended to provide a full reference listing of all material covered in the context of a given article, but are provided as guides to further reading.

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Agoraphobia Geoffrey L. Thorpe University of Maine

I. II. III. IV. V. VI.

Agoraphobia: Past and Present Descriptive Psychopathology and Epidemiology Etiological Theories Assessment and Diagnosis Treatment Conclusions and Prospects

Cognitive Therapy A system of psychotherapy focused upon identifying and restructuring dysfunctional thoughts and schemas linked to psychopathology. Exposure in Vivo The structured treatment of anxiety disorders by systematic confrontation of feared external situations to reduce avoidance behavior and anxiety. Exposure to Somatic Cues Extends the methods of exposure in vivo to those internal cues and bodily sensations associated with panic attacks. Limited Symptom Attack An anxiety episode with a few subjective anxiety symptoms, insufficient in number to qualify as a panic attack. Panic Attack A discrete period of intense fear, not explained by a continuing organic factor, that arises rapidly with at least 4 anxiety symptoms from a 13item list specified in the DSM-IV. Pharmacological Dissection The identification of qualitatively separate anxiety patterns by examining the differential effects of certain medications. AGORAPHOBIA is an anxiety disorder characterized by marked fear of entering crowded, public places; of traveling away from home, especially by public transportation; of feeling trapped or confined; and of being

separated from a place or person associated with safety. Sudden, brief episodes of extreme anxietym panic attacksmare commonly associated with agoraphobia, and may lead to avoidance of situations in which they occur. Often there is a "fear of fear" pattern, in which the bodily sensations of mounting panic are themselves a source of anxiety. Generally more debilitating than specific or social phobias, agoraphobia causes some people to remain entirely housebound. As a syndrome of anxiety elements in physiological, behavioral, and subjective domains, agoraphobia represents a distinct disorder with a typical clinical presentation and course. It usually arises in early adult life, with a prevalence in the Western world of approximately 2.5%; there is a significant preponderance of females in surveys of agoraphobia in clinical and community settings. Since about 1970, clinical researchers have developed effective pharmacological and psychological treatments to reduce or eliminate agoraphobic avoidance behavior and panic attacks.

I. AGORAPHOBIA: PAST AND PRESENT The term "agoraphobia" was introduced by the German psychiatrist C. F. O. Westphal (1822-1890) in a classic monograph of 1871, Die Agorapbobie. He chose the term to describe the abnormal fears of a series of three men who experienced anxiety episodes when walking alone in public places. Feared situations included city squares, concert halls, churches, open streets and fields, crowded rooms, and traveling by carriage, bus, or train; typical anxiety symptoms were trembling, heart palpitations, and "an immediCopyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

Agoraphobia

ate breakout of intense anxiety," or feeling "strange all at once, almost like a 'hangover.'" Westphal gave prominence to the patients' fear of walking alone in streets or across squares, and therefore used agoraphobia to denote "fear of spaces"; however, he acknowledged that the term was not exhaustive because it did not embrace all features of the disorder. Contemporary commentators have noted that the Greek "agora" refers to a marketplace or place of assembly, and find Westphal's choice of term felicitous in aptly describing the chief situational fears associated with agoraphobia today. Despite the enthusiasm of some American psychiatrists, interest in agoraphobia waned in the years following the publication of Die Agoraphobie. The taxonomist Emil Kraepelin later described a patient similar to those of Westphal, but referred neither to him nor to agoraphobia. The field of psychiatry rapidly became dominated by the psychoanalytic paradigm at the turn of the century, and, while agoraphobia received some attention from psychoanalysts, it was viewed as but one of many psychogenic disorders, not meriting particular notice. Sigmund Freud was more interested in all-encompassing theories of psychosexual development and neurotic symptom formation than in the classification of specific syndromes. The development of behavior therapy in the 1950s by Joseph Wolpe and others was closely connected with the study of phobias and other anxiety disorders; interest in agoraphobia revived with American and British research on systematic desensitization and related methods in the 1960s, and with the publication of Isaac Marks' Fears and Phobias in 1969. Systematic desensitization produced disappointing outcomes with agoraphobia, but treatment based on graduated or full-flooded real-life exposure to relevant situations was successful in reducing avoidance behavior and anticipatory anxiety. [See ANXIETY;PHOBIAS.] The work of Donald Klein on "pharmacological dissection" suggested that benzodiazepines are helpful in relieving anticipatory anxiety, whereas monoamine oxidase inhibitors and tricyclic compounds attenuate panic attacks. Such findings raise the question of different, co-existing anxiety patterns in agoraphobia. This progress in psychological and pharmacological treatment of agoraphobia in the 1970s influenced the diagnostic classification itself in the United States, so that in 1980 agoraphobia appeared for the first

time as a distinct category. Further developments in the 1980s gave prominence to the panic attack as the central feature of agoraphobia and, indeed, of panic disorder, a parallel syndrome not marked by phobic avoidance of situations. Psychological treatment of both syndromes focused on therapeutic exposure to panic sensations, and on encouraging patients to make more realistic and benign ascriptions as to the source of their anxiety; exposure to somatic cues and cognitive therapy have become the leading psychological interventions.

II. DESCRIPTIVE PSYCHOPATHOLOGY AND EPIDEMIOLOGY A. Description of Agoraphobia People with agoraphobia usually fear, and often avoid, situations in which it would be difficult or embarrassing to obtain help if overwhelmed by anxiety. Such situations include (a) traveling away from home, especially by bus, train, or car; (b)crowded, public places, such as government buildings, supermarkets, concert halls, shopping malls, and places of worship; and (c) confined places, such as elevators, the dentist's or beautician's chair, and---when driving~passing through tunnels, over bridges, or along a limited-access highway. Agoraphobia is commonly associated with highly distressing attacks of panic that appear to arise spontaneously and unpredictably, often~but not always~in the situations typically feared and avoided. When confronted by such typical agoraphobic situations as a large auditorium or a crowded shopping mall, a person with the disorder may experience rapid heartbeat, a compelling urge to escape from the situation, apprehensions about dying or losing control, and a sense of depersonalization or unreality. A "fear of fear" pattern often develops in which the appearance of any bodily sensation associated with anxiety engenders fear of an impending panic attack, thus arousing further anxiety. Some people with agoraphobia restrict their lives substantially, sometimes to the point of remaining housebound, in order to avoid the anxiety or panic aroused by entering public places. For many patients, dysphoric mood, somatoform disorders, interpersonal conflict, or substance abuse

Agoraphobia

accompany agoraphobia. Untreated, agoraphobia tends to follow a chronic, fluctuating course. It is common for people with agoraphobia to experience daily variations in anxiety severity; most describe having "good days" and "bad days." For some patients, there may be weeks or months of near-normal functioning followed by a resurgence of the original symptoms. For others, gradual improvement leading to complete recovery may occur without professional intervention, but this is not typical. In one study, patients interviewed 8 years following successful treatment reported general maintenance of improvement with some interim exacerbations. When agoraphobic problems had reappeared temporarily, the most common context was acute objective stress such as the loss of employment or a bereavement.

B. Diagnostic Classification The psychiatric taxonomy accepted in the United States is the Diagnostic and Statistical Manual of Mental Disorders (DSM), published since 1952 by the American Psychiatric Association and revised in 1968, 1980, 1987, and 1994. Before 1980, agoraphobia was not listed as a distinct disorder in the DSM classification, but could be found among lists of the Greek names for specific phobias in textbooks on psychiatry and abnormal psychology. By the time the third edition of the DSM was published in 1980 it had become clear that agoraphobia was in no sense a specific phobia-its prevalence, its resistance to treatment, its distressing and disabling consequences, and the broad range of its symptoms all clearly set it apart from such focal fears as phobias of heights, snakes, blood, or the number 13. Agoraphobia does include fear of situations (shopping malls, crowded buses, public meetings, etc.), but patients show varied patterns of specific fears, and there is no standard list of situations that must be feared for the diagnostic criteria to be met. Given that it is quite typical in agoraphobia for the patient to fear having a definite appointment, or even the ringing of the doorbell, it is difficult indeed to specify exactly what external situation constitutes the phobic stimulus. Some commentators note that what is chiefly feared in agoraphobia is the absence of safety signals, not the presence of disturbing objects. Most recently, "fear of the panic attack" (or, in patients who do not panic, fear of limited symptom attacks or circum-

scribed anxiety episodes) has been cited as a central feature of agoraphobia. The significance of the panic attack in many cases of agoraphobia further sets it apart from the specific phobias. In the 1980s, with such considerations in mind, the compilers of the DSM considered listing agoraphobia as a distinct diagnostic category. Renewed interest in agoraphobia in turn sparked interest in the panic phenomenon, and it was soon recognized that the overlapping of agoraphobia and panic attacks allowed several possible patterns: Agoraphobia with or without panic attacks, and panic attacks with or without agoraphobia. Accordingly, in the DSM-III of 1980 agoraphobia appeared in two forms, with and without panic attacks, and panic disorder was allotted a distinct category. The most recent changes were seen in the DSM-III-R of 1987 and the DSM-IV of 1994, both of which gave precedence to panic in the syndrome that includes panic attacks and agoraphobia.

C. The DSM-IV Classification Agoraphobia appears twice in the DSM-IV, as panic disorder with agoraphobia and as agoraphobia without history of panic disorder; both are found among the anxiety disorders. The DSM-IV lists separate criteria sets for "Panic Attack" and for "Agoraphobia." These are not diagnostic categories in themselves.

I. Panic Disorder with Agoraphobia The essential elements of this diagnosis are the presence of Panic Attacks and Agoraphobia, as defined in the criteria sets. Panic attacks are recurrent, distinct episodes of extreme anxiety or distress, not explained by the presence of a continuing organic factor. Panic attacks include at least 4 of a 13-item list of typical anxiety symptoms, which by definition are initially unexpected and are not produced in response to stimuli associated with specific or social phobias. The list of typical symptoms in a panic attack includes shortness of breath, dizziness, heart palpitations or rapid heart rate, trembling or shaking, sweating, the sensation of choking, depersonalization or derealization, and fear of dying, losing control, or developing an acute mental illness. By definition, the anxiety symptoms in a panic attack arise suddenly and rapidly increase in intensity. An organic factor may have been influential in early panic attacks (for example, the patient may have ex-

_

,

Agoraphobia

perienced dizziness as a result of a viral infection of the vestibular system, or depersonalization following ingestion of an illicit drug) but, by definition, the attacks will have continued despite successful treatment or removal of the initiating organic factor. [See PANIC

ATTACKS.] To meet criteria for panic disorder with agoraphobia, the patient with this diagnosis also has agoraphobia, of course, which is chiefly defined by fear of situations in which it could be difficult to obtain help if a panic attack arose, leading to avoidance or marked distress. The diagnosis applies even if the person's fear and avoidance of situations are not attributed to fear of having a panic attack.

2. Agoraphobia without History of Panic Disorder A person with this disorder has never had problems that meet criteria for panic disorder. Instead, he or she fears, and may avoid, situations in which it would be difficult or embarrassing to leave in the event of the sudden onset of anxiety, which may represent a "limited symptom attack" that would not include the range of symptoms associated with a panic attack. Agoraphobia entails difficulties with travel: either avoidance of travel altogether, or being able to travel only with the aid of a trusted companion, or despite significant discomfort. Finally, it should be noted that patterns meeting criteria for panic disorder but not agoraphobia are classified as panic disorder without agoraphobia; patterns consistent with panic disorder but in which an organic factor initiates and maintains the problems are classified as anxiety disorder due to a general medical condition.

D. Epidemiology Appropriate methodology requires assessing the prevalence and correlates of agoraphobia in the general community as well as in clinic samples (which tend to be unrepresentative). Because of recent changes in the taxonomy, allowance has to be made for the different terms and criteria in studies conducted in different decades. Accordingly, the most informative studies have separated the agoraphobic syndromes from panic disorder without history of agoraphobia and have used accurate community survey techniques. In the studies cited, about half of the respondents with agoraphobia

would be classified as having panic disorder with agoraphobia, and half as having agoraphobia without history of panic disorder. However, in clinical samples of agoraphobia, panic disorder with agoraphobia predominates, justifying extensive coverage of panic in discussions of treatment. The largest and most authoritative epidemiological investigation to include assessment of anxiety disorders was the Epidemiological Catchment Area study, reported in the 1980s. The fully structured Diagnostic Interview Schedule was used in a survey of 18,572 appropriately sampled adults in five communities in the United States (New Haven, Baltimore, St. Louis, Durham, and Los Angeles). The life-time prevalence of agoraphobia was estimated as 4.8%. A smaller study with similar methodology conducted in the former West Germany showed a life-time prevalence of 5.7% for agoraphobia; a similar Canadian study gave 2.9%. A rate of 6.9% was found for a Hispanic population in Puerto Rico with a Spanish form of the interview schedule. Generally, the estimates of the 6-month prevalence of agoraphobia in these studies were one or two percentage points lower than the life-time estimates. Overall, the findings on the prevalence of agoraphobia are consistent across countries and cultures in studies using the same instrument and careful sampling procedures. Across studies, the life-time prevalence of agoraphobia, with or without panic attacks, is about 5%; the 6-month prevalence is about 4%. However, by 1997 most experts, including the authors of the DSM-IV, had concluded that these estimates were inflated. A more realistic general prevalence estimate for agoraphobia is 2.5 %. Yet, whichever prevalence rate is accepted, these rates are markedly higher in women than in men; for the five sites in the Epidemiological Catchment Area study the ratio of women to men with agoraphobia was 2.7:1. Agoraphobia is associated with more severe impairment than other phobias and has a markedly higher comorbidity rate for depression. Substance abuse, hypochondriasis, somatization disorder, and personality disorders are often associated with agoraphobia. The usual course is chronic. The age of onset in agoraphobia varies but is usually in the 20s or 30s with a mean of about 28 years. There is no general agreement on an association between agoraphobia and specific childhood experiences. Maternal overprotection has been studied, but findings are mixed. [See PERSONALITY DISORDERS;SUBSTANCEABUSE.]

Agoraphobia

The estimated morbidity risk of anxiety disorders in the first-degree relatives of patients with agoraphobia is 32%; there is also a greater risk of an alcohol disorder. Concordance rates for panic disorder with and without agoraphobia are significantly higher in monozygotic than in dizygotic twins; a Norwegian study showed 31% concordance in 32 monozygotic twins but 0% in 53 dizygotic twins. Such results have been taken to indicate some genetic predisposition for agoraphobia and panic disorder.

III. ETIOLOGICAL THEORIES A. Biological Theories The observations that anxiety syndromes seem to run in families and that pharmacological treatment can be helpful have understandably led to considerable interest in biological mechanisms underlying agoraphobia and related disorders. Attention has been paid to the heritability of agoraphobia, to possible biological variables increasing vulnerability to agoraphobia, and to potential specific mechanisms that may explain agoraphobia. There is general agreement that a predisposition toward agoraphobia (and panic) may be inherited, but it is not possible to predict who will develop agoraphobia even among people with a number of close relatives with the disorder. (It is also widely accepted that mental disorders in general defy attempts to fit a classical model of single-gene heredity.) Agoraphobia probably conforms to a diathesis-stress model in which an inherited vulnerability is necessary, but not sufficient, for the eventual appearance of the syndrome. That would require the additional operation of certain environmental factors in interaction with the predisposing conditions. Physiological variables distinguishing agoraphobia from normal functioning, and from less pervasive anxiety disorders like specific phobia, include resting heart rate and forearm blood flow (both higher in agoraphobia) and skin conductance (higher and more variable in agoraphobia). However, such findings have not produced clear conclusions with implications for etiology or treatment. The most promising candidates for the inherited vulnerability factor (if there is but one) in people with agoraphobia can be described as personality traits such

as neuroticism, emotionality, trait anxiety, or "nervousness." Studies of animals and humans have consistently indicated a genetic component in emotionality; it is well known that rats can be bred for emotional reactivity, for example, and in the human studies, there is even stronger evidence for the heritability of trait anxiety or neuroticism than there is for the heritability of anxiety disorders. Neuroticism is thought to result from lability of the limbic system, of the autonomous nervous system, or of specific neurotransmitter processes. For example, one animal study showed that rats bred for emotionality had more brain benzodiazepine receptors than rats bred normally. Malcolm Lader has noted that many of the data on panic may be explained by positing an instability or hypersensitivity of central noradrenergic mechanisms centering on locus coeruleus function. Despite these observations, few definite conclusions may be drawn from the many physiological and endocrinological studies. The best-supported generalization is that patients with agoraphobia and related anxiety disorders have chronically overaroused central nervous systems and are slow to habituate to noxious stimuli. Several physiological processes and physical disorders produce symptoms like those of panic, arousing interest in possible mechanisms for agoraphobia. These include hyperventilation, asthma, limbic seizures, abnormalities of thyroid function, hypoglycemia, and mitral valve prolapse. Of particular interest has been the phenomenon of provocation of panic by sodium lactate infusions; people with a history of panic disorder, but not those without prior experience of panic, tend to react to the infusion with panic. Furthermore, pharmacological treatment by means of imipramine can abolish the lactate provocation of panic. Although such observations may appear to confirm a biological basis for panic disorder (and, therefore, of at least one of the agoraphobic syndromes), the mechanism is a subtle one that interacts with environmental and cognitive factors. The lactate provocation of panic can also be blocked by psychological treatment; hence, it would be misleading to focus exclusively on biological processes in interpreting panic phenomena. There is as yet no clear evidence of a particular biological variant that explains all of the features of agoraphobia. There is likely to be an inherited predisposition toward a labile limbic or autonomic nervous system, associated with chronic overarousal and slow habitu-

Agoraphobia

ation. This diathesis may in turn interact with certain behavioral and cognitive mechanisms to produce agoraphobic syndromes. David Barlow has pointed out that "The fact that language and meaning structures are the most common stimuli for anxiety in humans requires a complex neurobiological system."

B. Psychodynamicand Interpersonal Theories Psychoanalytic theory proposes that mental experience and behavior are influenced profoundly by the dynamic interaction of largely unconscious intrapsychic forces. All disorders are viewed as having important unconscious determinants, but this is particularly poignant in such disorders as agoraphobia because of the pivotal importance of anxiety to psychoanalytic theory. Early childhood experiences, particularly interactions with parents and other significant people, are given prominence not only because they form the prototypes for adult social interactions, but also because they influence the development of the mental apparatus itself. Particularly relevant to agoraphobia are the person's inner representations of other people. It is vital to one's sense of safety and security to develop stable "object relations," or internal representations of others. If object relations are disturbed, due, for example, to a poor quality or consistency of early actual relationships, then the person may be vulnerable to insecurity and anxiety later in life. Studies have shown that in humans and animals early separation from parents can be linked to agoraphobia-like behavior. Freud's initial theory of anxiety dealt with its somatic aspects. He described "anxiety neurosis" as an actual neurosis ("condition of the nerves"), not a psychoneurosis, because it results from undischarged neural excitation (caused by emotional trauma, for example). To Freud, such actual neuroses involve disturbed bodily processes, particularly difficulties in breathing. He later described psychoneuroses in which undischarged tension results from unacceptable ideas rather than from external stimulation. Eventually Freud turned his attention away from physical explanations of anxiety and emphasized its role as an ego function that is aroused in response to danger, a sense of helplessness when confronted by internal or external threat. Relevant to agoraphobia, Freud's ideas are consistent with the views that the ego

responds with anxiety to (1) real danger, (2) physiological processes involving the autonomic nervous system, and (3) the arousal of emotions like anger or frustration. An important issue for clinicians taking a psychodynamic approach is to separate manifestations of anxiety that stem from biological disturbances from those that stem from intrapsychic problems, such as an underlying conflict or a disorder of object relations. Psychodynamicists argue that, because environmental stimuli influence neurophysiological reactivity, and because the meaning of those stimuli mediates their impact, there is an important role for psychodynamic hypotheses and therapy in application to agoraphobia. An integrative theory put forward by Alan Goldstein and Dianne Chambless in 1978 uses behavioral and psychodynamic concepts to explain the various phenomena of agoraphobia, including typical personality factors and interpersonal styles. It is argued that the person with agoraphobia (a) fears panic attacks rather than particular places; (b) has difficulties with self-sufficiency, independence, and assertiveness; (c)is unable to trace the antecedents of emotional feelings when they arise; and (d) develops the initial symptoms of agoraphobia in a climate of interpersonal conflict. The interaction of these factors produces agoraphobia. The typical patient in this model is a woman who feels trapped in a troubled marriage. Although she wishes to leave, she lacks the necessary autonomy, independence, and self-sufficiency to make leaving a realistic option. Dealing directly with her feelings and asserting her opinions toward her husband are unfamiliar and difficult for her, so she attempts to tolerate this unsatisfactory situation. An argument with her husband early in the day elicits dysphoric mood but not a specific, identifiable emotion. Out in public later in the day, she still feels ill at ease, but is unsure of the origin of this feeling. Waiting in line somewhere (or using an elevator, traveling through an underpass, etc.), she feels trapped, and at some level this is reminiscent of being trapped in the unsatisfactory marriage. A panic attack suddenly arises. She later begins to avoid places similar to the site of the panic attack. Eventually becoming housebound, she is no longer able to contemplate leaving her husband, and this has the advantage of settling the matter so that she is no longer troubled by her mixed feelings about leaving. This view of agoraphobia draws attention to the potential role of adjunctive treatments like assertive-

Agoraphobia

ness training, marital therapy, or therapeutic work on recognizing and identifying feeling states. The work of some behavior therapists attests to the value of assertiveness training in programs for agoraphobia, and marital therapy has brought benefit to at least some patients with agoraphobia, as judged by anecdotal reports. However, marital distress has not been shown to have general etiological significance in agoraphobia.

C. Behavioral and Cognitive Theories I. Conditioning Theories The most familiar behavioral theory of the etiology of agoraphobia calls attention to classical conditioning as a possible mechanism. According to this view, previously innocuous stimuli such as streets, shops, and crowds acquire fear-eliciting properties through systematic pairing with noxious events. Although these noxious events are usually not specified, there are various plausible possibilities, such as witnessing an accident while in town, or being taken ill while shopping. Suddenly becoming ill, for example, creates reflex responses of distress and discomfort. By their pairing with the stimuli that elicit distress, certain stimuli in the immediate environment could become conditioned stimuli that on later occasions call forth anxiety as a conditioned response. An immediate objection to classical conditioning as an explanation of agoraphobia is that extinction of the acquired anxiety would be expected when the person encounters the newly feared situations without the original noxious stimuli. However, Mowrer's twofactor theory posits the operation of a second process, instrumental or operant learning, to explain the persistence of conditioned fear. Once fear is acquired by means of classical conditioning, avoiding the feared situations will be reinforced because avoiding these situations means removing anxiety. At the same time, avoidance of conditioned stimuli prevents the exposure to them that would be necessary to allow extinction to occur. So many objections have been raised to two-factor theory in this context that it can no longer be supported as a general explanation of agoraphobia. In agoraphobia, levels of fear and avoidance behavior are not closely correlated, yet two-factor theory explains avoidance behavior as motivated by conditioned fear. Conditioning does not explain the common phenomenon of daily fluctuations in anxiety severity, or the fact

that general stress is often associated with an exacerbation of agoraphobia. It is not clear from two-factor theory why agoraphobia so often represents a syndrome of fears of travel, crowds, confinement, and so forth, if indeed conditioning takes place haphazardly and involves whichever stimuli happen to be prepotent at the time. Conditioning theories do not obviously explain the comorbidity of agoraphobia with depression or hypochondriasis. Even the survivors of serious accidents or natural disasters do not necessarily develop an anxiety disorder, despite having been subjected to highly anxiety-provoking experiences. By contrast, most people with agoraphobia cannot recall having had an aversive experience with the situation or object they fear. Conditioned fear is very difficult to produce in humans in laboratory experiments, and there are many contradictory findings. Several attempts to replicate landmark studies of classical fear conditioning in humans were notorious failures. There is the paradox that, although unadorned conditioning accounts of agoraphobia have been discredited, treatments that seem based on extinction procedures have been quite successful. Exposure in vivo, in which the patient learns to confront agoraphobic situations without leaving at the onset of anxiety, can be helpful in overcoming a pattern of avoidance of situations and can attenuate panic attacks. However, the success of such treatment does not confirm a two-factor theory account of the etiology of agoraphobia. When the panic attack itself is considered to be the noxious event that allows classical conditioning of fear to external situations, the conditioning explanation becomes more credible. That leads to the proposition that it will be most helpful to explain the origin and maintenance of panic attacks. A panic attack may be viewed as the result of a vicious circle or upward spiral in which, at each point, stimuli associated with anxiety elicit conditioned anxiety responses, which in turn produce further anxiety-eliciting stimuli. This is an interoceptive conditioning view in which it is assumed that the conditioned stimuli are the bodily sensations that result from initial anxiety arousal, and that each conditioned response has a greater amplitude than its immediate predecessor. It follows from this view of panic attacks that it will be helpful therapeutically for the patient to confront anxiety sensations themselves rather than simply the external situations in which they commonly arise. If the patient

Agoraphobia

fears the bodily sensations of anxiety (heart pounding, dizziness, shortness of breath, and so forth), then the exposure principle would predict that systematic confrontation of these sensations will ultimately diminish their power to evoke anxiety. Problems with this view of panic attacks include the following. If any arousal of anxiety leads inexorably to a vicious circle that culminates in a panic attack, then people with panic disorder would never experience limited episodes of mild or moderate anxiety. However, it is usual for panic disorder patients to display moderate levels of generalized anxiety between their panic attacks. The theory also fails to explain who will be vulnerable to the escalation of mild anxiety into panic attacks. The cognitive therapy approach to which we turn next attempts to address this problem.

2. Cognitive Theories Aaron Beck's cognitive therapy rests upon several theoretical assumptions that center upon the individual's appraisal of events. Such appraisals range from fleeting "automatic thoughts" in the form of accessible, though covert, verbalizations (e.g., "Oh, no. I knew I'd get anxious if I came to the mall, and I feel slightly dizzy already!") to deeper and more enduring "cognitive schemas," not necessarily verbalized, reflecting a more fundamental attitude (e.g., strange feelings could indicate a serious medical catastrophe). Central to the application of cognitive therapy assumptions to panic attacks is the patient's appraisal of the bodily sensations or somatic cues connected with mounting anxiety. David Clark has argued that people with panic disorder have developed cognitive schemas concerning vulnerability to medical catastrophes, and he and others have demonstrated that people with panic disorder show cognitive biases in that direction. (The notion of fear of medical catastrophes as one variant of agoraphobia was introduced by Joseph Wolpe in 1970.) This model complements the conditioning of somatic cues model by indicating who is vulnerable to panic and why not all anxiety episodes culminate in panic. Variations in cognitive appraisals between and within individuals may account for the unpredictability of panic attacks. In Clark's model, the sequence begins when the client experiences sensations from a flushed face or pounding heart. It is immaterial to the model whether these sensations result from pathologi-

cal (developing a fever in response to an infection) or normal (having run up the stairs) processes. Next, the patient makes a "catastrophic misinterpretation" of the bodily sensations, viewing them as signals of a medical disaster such as a heart attack. The misinterpretation itself arouses increased anxiety, and the vicious circle continues when further alarming appraisals are made.

3. A Comprehensive Model Perhaps the most comprehensive contemporary theory is that of David Barlow, who suggests that panic results from activation of an ancient alarm system, and is the basic emotion of fear, while anxiety is a more general cognitive-affective structure. Panic occurs in response to three types of alarm. True alarms are panic attacks elicited by genuine danger. False alarms are panic attacks in the absence of objective danger, and result from a genetically determined predisposition in interaction with an accumulation of general stress. (Anyone may experience a false alarm, not only people with anxiety disorders.) Learned alarms are panic attacks that are triggered by cues, which may be particular objects, as in specific phobia, or internal physiological changes, as in panic disorder. Anxious apprehension also plays a part in explaining the development of anxiety disorders; a cognitive schema containing propositions concerning anxiety elicits negative affect when triggered, and the sequence of events that follows includes directing attention to internal self-evaluations, increased arousal, narrowing of attention, and hypervigilance concerning sources of apprehension. In summary, Barlow's model of agoraphobia is his model of panic disorder with the addition of the development of agoraphobic avoidance. Biological vulnerability interacts with objective stress to produce an initial uncued panic attack, or false alarm. The connection of the panic attack with interoceptive cues leads to the development of cued learned alarms. As a result, there is a psychological vulnerability characterized by anxious apprehension about future panic attacks. Next, panic attacks are triggered unpredictably by a combination of autonomic and cognitive symptoms of anxiety with additional somatic cues. Depending on the presence or absence of safety signals and various cultural and environmental factors, avoidance behavior may develop, giving rise to the panic disorder with agoraphobia syndrome.

Agoraphobia IV. ASSESSMENTAND DIAGNOSIS The assessment of agoraphobia in clinical practice proceeds through several stages. First, the diagnosis is established. Second, identification of the specifics of a patient's level of distress and disability allows development of an individualized treatment plan. Third, evaluating concomitant problems or issues, ranging from diagnosable disorders to matters of life circumstances, permits employment of adjunct treatments or influences the sequence in which treatments for agoraphobia are provided. Fourth, monitoring the patient's progress throughout the course of therapy is essential in determining response to treatment and alerting the clinician to needed procedural changes.

A. Diagnosis People with agoraphobia may be self-referred, referred by friends or relatives, or referred by other professionals. It is not uncommon for a patient to seek treatment having made a self-diagnosis of agoraphobia after reading a magazine article or viewing a television presentation about agoraphobia. It is also quite common for a patient to be referred to a mental health professional by emergency room staff after one or more visits for urgent treatment during panic attacks. Because many people with agoraphobia are either entirely housebound or have a limited range of travel, clinicians working with this disorder become accustomed to making home visits, at least in the early stages of assessment and treatment. Because there are several physical conditions that give rise to symptoms like those of agoraphobia, it is important that the patient receive a physical examination before mental health interventions begin. If anxiety persists despite successful treatment of a precipitating or complicating physical condition, then treatment of agoraphobia proceeds. It should be noted that having certain physical conditions is not incompatible with having agoraphobia, but accompanying physical disorders demand attention first. Assessment is needed to identify other psychiatric disorders that may co-exist with agoraphobia, including mood, somatoform, substance use, and personality disorders. Also relevant for assessment are issues like marital conflict, social skills deficits, and difficulty with personal autonomy that may not require a formal di-

agnosis but may yet be important foci for intervention. By no means do all people who experience anxiety when in public places or who have had panic attacks have problems that meet diagnostic criteria for agoraphobia syndromes. Social and specific phobias may center upon some of the situations commonly avoided in agoraphobia, and panic attacks may occur in mood disorders, psychosis, and in people without psychiatric disorders. Treatments usually employed with agoraphobia may be misdirected in these other diagnostic contexts.

B. Assessingthe Range and Extent of Agoraphobia Simply applying the appropriate diagnostic label is insufficient to guide treatment. The clinician seeks to know the patient as a unique individual and accordingly conducts the usual psychosocial history and mental status examination. Beyond that, the nature and extent of the agoraphobic problems will need to be charted in sufficient detail to allow formulation of an appropriate individual treatment plan and continued evaluation of progress toward treatment goals. The Anxiety Disorders Interview SchedulenlV (ADIS-IV) is the most widely used structured interview protocol in the assessment of agoraphobia and other anxiety disorders. Developed by Barlow and his colleagues, the ADIS-W allows detailed and accurate characterization of the person's anxiety problems and permits authoritative diagnosis in DSM-IV terms. The instrument is primarily employed in research trials to ensure uniformity of diagnostic practices. Although the complete protocol is too lengthy for routine clinical use, subsets of the ADIS-W may be used appropriately and conveniently in most clinical settings. Self-report questionnaires like the Fear Questionnaire, the Anxiety Sensitivity Index, and the Mobility Inventory are all useful for treatment planning and charting progress in respect of the specific agoraphobic symptoms. Questionnaires on other related issues, such as assertiveness, depression, or marital harmony, are generally helpful in initial evaluations and may be germane to the issues of particular clients throughout the course of treatment. It is highly desirable to have the patient self-monitor general anxiety, panic attacks, and agoraphobic avoidance daily. Individualized forms may be used so

10

Agoraphobia

that details of the specifics of the patient's situation may be accommodated therein. For example, daily ratings may be made of a patient's degree of avoidance of, fear in, and self-confidence about each item in a customized graded hierarchy of feared situations. Daily ratings of the frequency and intensity of panic attacks allow the patient to record the circumstances surrounding each episode, situational, cognitive, and interpersonal. The nature of agoraphobia allows the use of a hierarchically ordered behavioral test for most patients. This takes the form of an unaccompanied journey-walking, driving, or using public transportationmto take in as many situations relevant to the patient's fear and avoidance as is feasible. The clinician asks the patient to proceed as far as possible, and takes the distance actually traveled as a helpful datum in sampling current levels of agoraphobic avoidance. Physiological monitoring has been a customary component of research trials designed to provide generalizable information on treatment effectiveness, but is far less common in routine clinical practice. The typical finding that measures of anxiety in the different domains--self-report, behavioral observation, and psychophysiological~do not covary as might be predicted should not daunt the clinician unduly. When all such measures are available, it is recommended that treatment proceed until clear reductions have been seen in each measurement modality.

V. TREATMENT A. Pharmacological Treatment Pharmacological treatment has several advantages for the patient and significant progress has been made in this area since 1970, improving the general outlook for agoraphobia. Many people with agoraphobia have their first clinical contacts with physicians, either in emergency rooms following an initial panic attack or in family practice settings, and medication is readily available and convenient to use. (Despite this, surveys show that the general public and people with agoraphobia tend to disfavor drug therapy.) Agoraphobia subsumes anxiety and avoidance behavior, and is often associated with dysphoric mood if not clinical depression. The medications most commonly used, and extensively studied, in the treatment

of agoraphobia are those that are generally prescribed for anxiety and depressive symptoms.

I. Tricyclic Compounds Together with the monoamine oxidase inhibitors, the tricyclic compounds are chiefly used in treating depression, but the term "antidepressants" commonly applied to them may be misleading in this context because there is controversy about their role in agoraphobia treatment (do they attenuate dysphoric mood, facilitating other treatments, or do they act specifically to block panic attacks?). Imipramine has been the most extensively studied, but the related tricyclics desipramine and clomipramine may be similar in effectiveness. Early studies appeared to show that imipramine reduced panic attacks, but patients continued to avoid agoraphobic situations. Later studies demonstrated imipramine's superiority to placebo medication and indicated that it brought additional benefit when added to behavioral treatment. However, this additional benefit was not attributable to the blockade of panic. When imipramine is used in conjunction with the anti-therapeutic recommendation to avoid confronting feared situations, improvement in mood, but not in agoraphobia, is the resuit. Empirically, imipramine plus exposure therapy seems more effective than either treatment alone. It has been argued that inconsistencies in research findings with imipramine may result from marked differences in doseage across studies.

2. Monoamine Oxidase Inhibitors (MAOIs) The MAOIs phenelzine and iproniazid have received most attention. Whereas some studies have shown little if any difference between phenelzine and placebo in application to agoraphobia, another has shown that phenelzine reduces general disability and avoidance behavior. In that study phenelzine was more effective than imipramine. For reasons that are unclear, phenelzine appears to potentiate self-initiated exposure.

3. Benzodiazepinesand Triazolobenzodiazepines The benzodiazepines are minor tranquilizers that have been extensively prescribed for various forms of anxiety and stress reactions, clinical and subclinical, for decades. Donald Klein's initial work on imipramine had suggested that it is specific for blocking panic,

"

Agoraphobia

whereas the benzodiazepines are effective only with generalized or anticipatory anxiety. Later work suggests that high doses of benzodiazepines may be effective in treating panic attacks. The recent development of high-potency benzodiazepines like alprazolam and clonazepam has brought substantial benefit in the treatment of agoraphobia and panic. Alprazolam, a triazolobenzodiazepine, has been the subject of a multi-center world-wide double-blind study of people with panic disorder (with and without agoraphobia). Fifty percent of the alprazolam patients and 30% of placebo patients were panic-free 3 weeks after the start of the trial. Strong withdrawal reactions after discontinuance of alprazolam pose a significant problem, as does the phenomenon of "rebound panic" in which a minority of patients may experience even worse panic attacks after withdrawal from medication than before treatment.

4. Summary Imipramine, phenelzine, and alprazolam are helpful in the treatment of agoraphobia. The related medications desipramine, clomipramine, tranylcypromine (an MAOI), and clonazepam have received less attention but may be as helpful. Some medications not noted above, like the beta-blocker propranolol, have been shown ineffective for agoraphobia. By the late 1990s the selective serotonin reuptake inhibitors and other new medications have been widely prescribed for people with agoraphobia, and there is a ferment of pharmacological research activity. The mechanisms underlying successful pharmacological treatment are unclear.

B. Psychological Treatment Psychodynamic approaches to agoraphobia have received far less attention than biological, behavioral, and cognitive approaches in recent decades, and there is no corpus of empirical research on psychodynamic formulations of etiology or on the results of psychodynamic treatment. However, its proponents suggest that psychodynamic approaches are particularly germane to some of the common clinical issues in agoraphobia, and applying psychodynamic reasoning could be especially fruitful in this context. It is argued that these approaches may be particularly helpful with treatment-resistant patients, in guiding the strategy of supportive psychotherapy, and in using the therapeu-

II

tic relationship in a supportive context and as a potential therapeutic tool. Behavior therapists treating agoraphobia in the late 1950s and early 1960s emphasized its commonalities with the phobias, and sought to reduce situational fear and avoidance behavior by means of techniques effective for specific phobia. In the 1970s the differences between agoraphobia and other phobias began to be recognized, and treatment by systematic desensitization was replaced by imaginal flooding and exposure in vivo. Attention was paid to panic attacks as well as to avoidance behavior. Since the 1980s the focus has been on direct psychological treatment of panic attacks.

I. Treatment of Agoraphobic Avoidance Behavior Despite initial enthusiasm for Joseph Wolpe's technique of systematic desensitization as a therapeutic breakthrough for phobias, its application to agoraphobia in controlled clinical trials in the 1960s brought disappointing results. The technique was largely abandoned as treatment for agoraphobia when developments in the 1970s established flooding in fantasy and graded practice in real life as effective treatments. Researchers in Vermont led by Stuart Agras showed that graded practice--with or without praise for specific accomplishments--could quickly reduce agoraphobics' avoidance of unaccompanied journeys away from the clinic. This work converged with that of Isaac Marks in the United Kingdom to identify exposure in vivo as the central ingredient of psychological treatment for agoraphobic avoidance. Procedural variations such as brief or prolonged exposure duration, massing or spacing of treatment sessions, and terminating exposure at the point of increasing or decreasing anxiety were examined assiduously by clinical researchers, but the consensus is that these technical details are less important than the general recommendation to confront, rather than avoid, feared situations. This exposure principle is as well-founded as any in the entire field of mental health work. Improved functioning after exposure treatment for agoraphobia has been shown to persist for several years post-treatment. Not all patients accept or remain in exposure treatment; the attrition rate during therapy has been estimated at 12%. Of those who complete a course of treatment, approximately 70% have successful outcomes.

12

Agoraphobia

Exposure treatment may proceed intensively and rapidly. In some studies, an entire course of treatment was completed in 2 weeks of prolonged, daily sessions. While the data on adverse complications from rapid treatment are equivocal, particularly those concerning the possibility of social and marital disruptions, gradual treatment is recommended in order to facilitate patients' thorough consolidation of therapeutic gains at each step. Treatment of avoidance through exposure preferably includes weaning patients from "safety signals," items like written instructions from the therapist, bottles of minor tranquilizers (even empty ones), or canes or umbrellas that are carried more for their associations with a sense of security than for any more obviously practical benefit.

2. Treatment of Panic The current diagnostic classification assigns central importance to panic attacks in most cases of agoraphobia seen in clinical settings. If panic is primary, and avoidance behavior a secondary complication thereof, then treatment could logically be directed at panic phenomena. This is not incompatible with treatment of avoidance by exposure, which can itself reduce panic attacks. But, as David Barlow has put it, "treating avoidance behavior will always be necessary. Nevertheless, the primary goal should be the treatment of panic." The essential technique in the psychological treatment of panic is exposure to somatic cues, or reproduction of and confrontation by the bodily symptoms that the patient associates with panic attacks. The patient is asked to create sensations of panic deliberately in treatment sessions. Running in place, voluntary hyperventilation, and spinning around in a swivel chair are examples of procedures for creating such sensations. Clinicians match particular procedures to patient's most troublesome symptoms; someone who is most troubled by dizziness will practice spinning around, while someone disturbed by the sensations of a rapid heart-rate will run up and down the stairs. In early trials, this approach has brought the most impressive results yet seen in the treatment of panic and agoraphobia, the success rates approaching 100% in some studies. Advances in methodology that have allowed the daily monitoring of panic attacks have permitted accurate tracking of panic attack frequency. "Percentage of patients panic free" has become a standard datum to report in contemporary treatment trials. The success of exposure to somatic cues as treat-

ment for panic has prompted a reinterpretation of some early studies that lacked a theoretical context at the time. Inhalation of carbon dioxide as treatment for generalized anxiety, the "running treatment" for agoraphobia, the utility of imaginal flooding to phobiairrelevant themes in reducing phobic sensitivity, and the lactate provocation of panic as treatment for anxiety episodes--all found in the literature of the last few decadesmmay be readily understood today as consistent with the exposure principle in its most recent application to panic sensations. The efficacy of exposure to somatic cues has been attributed to various theoretical processes. These include the exposure principle, possibly resting upon the extinction or habituation of conditioned anxiety responses to panic sensations, or upon the development of coping skills by the patient. The success of the method is consistent with the specific hypothesis that chronic hyperventilation underlies panic disorder. It is also consistent with the cognitive therapy view that the patient makes catastrophic misinterpretations of the bodily sensations of panic, ascribing to them morbid significance as harbingers of a medical emergency. Parallel to exposure to somatic cues is cognitive therapy in the contemporary treatment approach to panic. Consistent with David Clark's model of an interaction of sensitivity to somatic cues and catastrophic misinterpretation thereof, patients are engaged in a cognitive treatment process of collaborative empiricism in which implicit schemas construing panic sensations as signals of dire illness are carefully assessed, gently challenged, and empirically tested. Cognitive therapy involves exploring, in a sympathetic and accepting way, the specific idiosyncratic cognitions that are assumed to underlie emotional distress. Wherever possible, real-life "experiments" are undertaken in attempting to challenge unrealistic assumptions. There is no standard, structured format that must be applied systematically to all patients; rather, the principles of cognitive therapy guide a creative treatment approach with each individual. The results of preliminary trials of cognitive therapy have been as encouraging as those of exposure to somatic cues, and the combination of these treatments has brought the best outcomes.

3. Comprehensive Treatment of Agoraphobia

In addition to the central psychological treatment approaches of exposure in vivo, exposure to somatic cues, and cognitive therapy, relaxation training and

13

Agoraphobia

breathing retraining have been found helpful in the treatment of agoraphobia and are recommended as optional components of a treatment plan. There is a consensus that in the typical case of panic disorder with agoraphobia treatment should proceed employing all of these techniques in sequence, beginning with self-paced exposure in vivo. Some authorities argue that, because it is not associated with deleterious sideeffects or complications from withdrawal, psychological treatment should be used first, and pharmacological treatment brought in as necessary subsequently.

many patients to gain access to psychological treatment, especially in rural areas. Innovations in service delivery are needed, and studies should address the viability of psychological treatment of agoraphobia from remote sites by means of the latest communications technology. Many communities are underserved by mental health professionals, and people who are housebound by agoraphobia have even greater difficulties than most people in gaining access to needed psychological services. This article has been reprinted from the Encyclopedia of Human

Behavior, Volume 1.

VI. CONCLUSIONSAND PROSPECTS Although it is fragmented by the current nomenclature into two distinct disorders, agoraphobia is a coherent syndrome with a range of symptomatology extending far beyond the limited compass of specific phobias. Recognized since 1871 as an unusually debilitating anxiety disorder, agoraphobia has only recently yielded to effective pharmacological, behavioral, and cognitive treatments. The conclusion of a recent Consensus Development Conference on the Treatment of Panic Disorder, sponsored by the National Institutes of Health and the National Institute of Mental Health in the United States, are pertinent and may be summarized as follows. Although perhaps most patients receiving psychological treatment are also taking medication, little is known about the effectiveness of combined pharmacological and psychological treatment. Not enough is known about the mechanisms of action of contemporary treatments, patient factors predicting success or permitting matching to the most appropriate treatment, the long-term effectiveness of the new treatments for panic, and the value of treatment for associated mental health problems and issues. Also in need of further attention by clinicians and researchers are the following. Whereas pharmacological treatment is readily available, it is difficult for

BIBLIOGRAPHY Barlow, D. H. (1988). "Anxiety and Its Disorders." Guilford Press, New York. Beck, A. T., Emery, G., & Greenberg, R. L. (1985). Anxiety disorders and phobias: A cognitive perspective. New York: Basic Books. Chambless, D. L., and Goldstein, A. J. (Eds.) (1982). "Agoraphobia: Multiple Perspectives on Theory and Treatment." Wiley, New York. Gournay, K. (Ed.)(1989). "Agoraphobia: Current Perspectives on Theory and Treatment." Routledge, London. Hecker, J. E., and Thorpe, G. L. (1992). "Agoraphobia and Panic: A Guide to Psychological Treatment." Allyn and Bacon, Boston. Hecker, J. E., Losee, M. C., Fritzler, B. K., & Fink, C. M. (1996). Selfdirected versus therapist-directed cognitive-behavioral treatment for panic disorder. Journal of Anxiety Disorders, 10, 253265. Knapp, T. J. (Ed.) and Schumacher, M. T. (Trans.) (1988). "Westphal's 'Die Agoraphobie'." University Press of America, Lanham, MD. Marks, I. M. (1987). "Fears, Phobias, and Rituals: Panic, Anxiety, and Their Disorders." Oxford University Press, New York. Mathews, A. M., Gelder, M. G., and Johnston, D. W. (1981 ). "Agoraphobia: Nature and Treatment." Guilford, New York. Thorpe, G. L., and Burns, L. E. (1983). "The Agoraphobic Syndrome: Behavioural Approaches to Evaluation and Treatment." Wiley, Chichester, UK. Walker, J. R., Norton, G. R., and Ross, C. A. (Eds.) (1991). "Panic Disorder and Agoraphobia: A Comprehensive Guide for the Practitioner." Brooks/Cole, Pacific Grove, CA.

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Alcohol Problems Melanie E. Bennett and William R. Miller The University of New Mexico

I. What Is Alcohol Health? II. Normal Development and Epidemiology of Alcohol Problems II!. Etiology of Alcohol Problems IV. The Changing Nature of Alcohol Problems over Time V. Risk and Protective Factors VI. Continuum of Intervention for Alcohol Problems VII. Conclusion

gies aimed at particular groups who are at high risk for developing alcohol problems. Universal Prevention Strategies Prevention strategies that target a large population such as all people in a particular city. ALCOHOL PROBLEMS represent several ways in which alcohol has a negative impact on an individual's life. Some alcohol problems are severe and involve substantial consumption of alcohol, which results in multiple physical and psychosocial problems. Other alcohol problems are less severe~an individual experiences some negative consequences as a result of his or her drinking, but these difficulties have not impacted the individual's overall functioning.

Alcohol Dependence Severe problem drinking that involves heavy use of alcohol despite the experience of serious alcohol-related consequences. The individual might drink more than intended, make unsuccessful attempts to stop drinking, spend substantial amounts of time drinking, and neglect other responsibilities due to drinking. Physiological symptoms of tolerance (need for more alcohol to feel intoxicated) and withdrawal (physiological reactions when alcohol is stopped or reduced) often develop. Harmful Drinking The use of alcohol that causes the drinker to experience negative consequences. Such consequences can be physical, legal, social, occupational, or interpersonal in nature. Public Health Model A model for describing how various factors interact to increase risk for alcohol problems. This model incorporates aspects of the agent, host, and environment in describing risk. Social Learning Theory A theory that emphasizes the role of individuals and experiences in the social world as important determinants of behavior. Targeted Prevention Strategies Preventionstrate-

I. WHAT IS ALCOHOL HEALTH? In order to understand the problematic use of alcohol, it is helpful first to consider what constitutes a state of health with regard to its use. Alcohol has held a common, even honored, place in the daily life of many cultures for thousands of years. It has been an element central to religious observances in JudeoChristian and other faiths, and has often been part of important social and cultural events as well. Wine has long been recommended to promote physical health, and indeed recent scientific evidence indicates a consistent association between moderate drinking and longevity, although the reasons for this link are still poorly understood.

15

Copyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

16

Alcohol Problems

At the same time, it is abundantly clear that heavier drinking is often associated with devastating consequences to the individual and to society. Alcohol is involved in about half of all traffic fatalities, and a substantial proportion of fatal falls, drownings, deaths by fire, homicides, and suicides. Excessive drinking is also closely linked to violence, crime, injuries, and a plethora of chronic diseases. The relationship of alcohol to health can thus be understood as a continuum. At one end of the continuum are abstainers, those who do not drink alcohol at all, who constitute more than one-third of adults in the United States. Such people obviously have no negative consequences related to their own drinking. Next are moderate problem-free ("normal")drinkers. The average consumption for this large group is about three or four drinks per week. They fall largely within the limits for safe drinking recommended by the National Institute on Alcohol Abuse and Alcoholism: not more than two drinks per day for men, and not more than one drink per day for women, with some alcohol-free days each week. Because alcoholic beverages differ in content, it is important here to define what constitutes "one drink." A useful definition is that one standard drink contains one-half ounce of ethyl alcohol. Table I shows how this alcohol content changes for different alcoholic beverages. When moderation is exceeded, or when one drinks at all in dangerous situations, one enters the realm of risky drinking, which includes both acute and chronic risk. Acute risk has to do with the immediate effects of intoxication. Even low levels of alcohol in the bloodstream, for example, can significantly impair driving ability. The only safe blood alcohol level behind the wheel is zero. A small amount of impairment from intoxication can also be lethal when combined with ac-

Table I

One drink is equal to: Alcoholic beverage

Alcohol Concentration Levels for Men .

.

.

.

.

.

Percent alcohol content

,,,

Number of drinks 120

Weight in pounds 140

160

180

200

220

240

260

1

2

2

2

1.5

1

1

1

1

2

4

3.5

3

3

2.5

2

2

2

3

6

5

3.5

4

3.5

3.5

3

3

4

8

7

6

5.5

5

4.5

4

3.5

5

10

8.5

7.5

6.5

6

5.5

5

4.5

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

One drink = 10 oz. of beer or 4 oz. of wine or 1 oz. of liquor ( 100 proof).

tivities such as water sports, skiing, hunting, climbing, or using power tools, where minor misjudgments can have major consequences. There is no known safe level of drinking during pregnancy. Perhaps one of the most dangerous aspects of intoxication is that above very moderate doses, perception and judgment are among the first abilities to be impaired. This can and does result in errors of perception regarding one's ability or (lack of) impairment, and in decisions and judgments that themselves lead to risky consequences. Tables II and III show how long it takes to eliminate alcohol completely from one's body, illustrating how even small amounts of alcohol can remain in and possibly impair functioning. Chronic risk, on the other hand, has to do with the long-term effects of drinking. Heavy drinking is closely linked to a wide range of health problems, at least doubling the risk for heart disease, cancers of

Table III

A p p r o x i m a t e H o u r s f r o m First D r i n k to Z e r o A l c o h o l C o n c e n t r a t i o n Levels for W o m e n

Number of drinks 120

Standard Drink Equivalents

Ounces of alcohol

Table II Approximate Hours from First Drink to Zero

Weight in pounds 140

160

180

200

220

240

260

1

3

2.5

2

2

2

1.5

1.5

1

2

6

5

4

3

3.5

3

3

2.5 4

10 ounces

beer

5%

3

9

7.5

6.5

5.5

5

4.5

4

4 ounces

table wine

12 %

4

12

9.5

8.5

7.5

6.5

6

5.5

5

2.5 ounces

fortified wine

20%

5

15

12

10.5

9.5

8

7.5

7

6

1.25 ounces

80 proof liquor

40%

1 ounce

100 proof liquor

50%

m,

One drink = 10 oz. of beer or 4 oz. of wine or 1 oz. of liquor ( 100 proof).

Alcohol Problems

many types, and hypertension. Risks for liver disease and for cancers of the mouth and gastrointestinal system are greatly increased by drinking above moderate levels. Harmful drinking is when negative consequences from drinking actually occur. In addition to adverse effects on physical health and appearance, common types include legal problems, social consequences, damage to relationships, financial problems, and emotional disturbance. Because alcohol is a depressant drug, depression is often caused or exacerbated by heavy drinking. In college students, drinking level has a strong and negative relationship to grade point average. Memory problems are common in heavy drinkers, and the occurrence of memory blackouts is associated with brain impairment from alcohol. A majority of crimes resulting in imprisonment are committed under the influence of alcohol, which is also associated with domestic violence. Alcohol dependence occurs as a person develops a pattern of alcohol use that results in substantial impairment in functioning. The person's life becomes more and more entangled with drinking. Typically, alcohol dependent people are quite able to "hold their liquor," showing less apparent intoxication from drinking than might be expected in the average person. Such tolerance is misleading, however, because while it appears that the person is unaffected, in fact he or she has a sufficiently high blood alcohol level to cause serious acute and chronic risk. Drinking occupies more of the person's time, and becomes increasingly important so that it is unpleasant to be away from alcohol. Gradually, the body adjusts to the presence of alcohol, so that sobering up results in unpleasant experiences such as hangovers, insomnia, agitation, or nervousness, sweating, and trembling. In the extreme, alcohol can produce a withdrawal syndrome stronger and considerably more life-threatening than that associated with heroin addiction. Other features of alcohol dependence include drinking more or for a longer time than intended, failed attempts to reduce or stop drinking, and foregoing other important activities in favor of drinking.

II. NORMAL DEVELOPMENT AND EPIDEMIOLOGY OF ALCOHOL PROBLEMS What is the normal course of human development with regard to alcohol? The answer to this question is

17

quite specific to culture. In some cultures, the normal course is lifelong abstention from alcohol. In France, on the other hand, heavy drinking is common among adults, resulting in one of the world's highest levels of alcohol-related health problems. In Mexico, binge drinking is common among males, whereas women are usually abstainers. Large general population surveys reveal that a majority of Americans drink alcohol. In 1992, researchers conducting the National Health Interview Survey interviewed more than 40,000 people about their alcohol consumption. At one end of the continuum, about one-third of men and one-half of women were classified as abstainers~individuals who drink less than once per year or not at all. Most individuals were classified as either light drinkers, consuming I to 13 drinks per month, or moderate drinkers, consuming 4 to 13 drinks per week. Fewer individuals were classified as heavier drinkers (14 or more drinks per week), although men were more likely to report heavier drinking than women (19% versus 7%, respectively). Although most Americans drink without negative consequences, a significant minority of individuals are found at the harmful end of the use continuum. Recent surveys estimate that 15.3 million individuals meet criteria for alcohol abuse ("harmful drinking"), dependence, or both. Drinking at these levels becomes increasingly dominated by men, who drink more often, in greater quantities, and report more frequent episodes of intoxication than women. In fact, studies find that men are more than three times more likely to be diagnosed with alcohol abuse or dependence at any age than are women. Table IV presents alcohol consumption norms for adults in the United States for both men and women. These figures illustrate women's greater likelihood of drinking moderately or not at all compared with men. In addition to gender, drinking patterns are affected by age. After little or no drinking during childhood, alcohol use increases sharply during adolescence and peaks in young adulthood. Young adults drink in greater quantities, show the highest rates of binge drinking and problems related to alcohol use, and show the highest rates of alcohol abuse and dependence of any age group. With adulthood, drinking tends to decrease, with most young adults "maturing out" of problem drinking in their later twenties. The percentage of abstainers increases with age, although it is thought that heavier drinkers may be more likely to

18

Alcohol Problems

Table IV

Alcohol Consumption Norms for U.S. Adults, in Percentages (Percentage of Adults Who Drink This Amount or More)

Drinks per week

Total

Men

Women

0

65 42 34 32 29 23 22 20 19 18 17 16 15 14 13 13 12 11 10 9 9 8 8 7 7 6 6 5 5 5 4 4 4 3 3 2 2 1 1 1 <0.5 <0.2

71 54 46 43 39 33 32 30 29 27 25 25 23 23 21 20 19 18 16 15 14 12 12 12 11 11 10 9 8 7 7 6 6 5 4 3 3 3 2 1 1 <0.5

59 32 23 22 18 14 13 11 11 10 9 9 8 7 6 6 6 5 4 4 4 4 4 3 2 2 2 2 2 2 2 2 1 1 1 1 1 <0.5 <0.4 <0.1 <0.1 <0.1

1

2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23-24 25 26-27 28 29 3O-33 34-35 36 37-39 40 41-46 47-48 49-50 51-62 63-64 65-84 85-101 102-159 160+

Source: National Alcohol Survey, Alcohol Research Group, Berkeley. Courtesy of Dr. Robin Room. One drink -- 10 oz. of beer, 4 oz. of wine, or I oz. of liquor (100 proof).

show stability of heavy drinking over time. This decrease in the number of people who use and abuse alcohol continues into older adulthood. Adults over age 65 have the lowest rates of alcohol abuse, dependence, and alcohol-related negative consequences of any age group. Some longitudinal research suggests that drinking patterns remain fairly stable over time, with the decreased rates of use and problems in older adulthood being attributable to increased mortality of heavy drinkers. Along with gender and age, a growing literature documents differences in alcohol use and problems across racial/ethnic groups. Although studies of general population samples indicate that consumption and problems are greatest during the young adult years, studies have found that minority groups do not always follow this pattern. For example, Blacks have been found to show low rates of heavy drinking in young adulthood, followed by increased rates of heavy drinking and problems in their adult years. Importantly, rates of abstinence are higher among Blacks of all ages, especially among Black females. Research has also found variations by age from general population samples in patterns of drinking among Hispanics. In a way that is similar to non-Hispanic Whites, heavy drinking and associated problems increase during the young adult years among Hispanics. Hispanic men, however, show a smaller decrease in heavy drinking and problems from young adulthood to adulthood than that found among general population samples. For Hispanic men, heavy drinking and negative consequences remain high into middle adulthood, and Hispanic men show higher rates of alcohol abuse and dependence than other racial/ethnic groups over this time as well. In addition, Hispanic women show higher rates of abstention at all ages than non-Hispanic White women. Importantly, research with Hispanic samples is complicated by the practice of studying individuals of Mexican, Cuban, and Puerto Rican descent together, ignoring the substantial cultural and geographic differences among these groups as well as their different rates of drinking and attitudes toward alcohol use. American Indians tend to show higher rates of alcohol problems than the general population, with a death rate from alcohol dependence that is more than five times higher than the rate for other races. Patterns vary widely by tribal affiliation, however, with some tribes drinking more than the general population average and others drinking less. Alcohol use among

19

Alcohol Problems

American Indians is highest and is associated with the greatest number of negative consequences through young and middle adulthood, with a decline in consumption in the forties.

III. ETIOLOGY OF ALCOHOL PROBLEMS Whatever the population, it is clear that a significant minority of individuals drink in an excessive or harmful way. What causes alcohol problems? Historically, this question too often has been answered by pointing to a single cause. In the nineteenth century, drunkenness was the mark of a sinful person who lacked morals or will power. More recently, alcohol problems have been attributed to genetics, an alcoholic personality, or a "dysfunctional" family. It is clear, however, that there are many causes of alcohol problems, which develop out of interacting biological, environmental, and cognitive factors that begin early in life and continue over the course of development. At various points in development, different factors have more or less of an influence on drinking behavior.

A. Biological Factors Much research has shown that genetics play a role in the development of alcohol problems. This research studies individuals with varying degrees of genetic relatedness to individuals with alcohol problems, and observes the rates at which these different relatives develop alcohol problems themselves. For example, family pedigree studies look at biological relatives of alcohol dependent adults; twin studies examine the rates at which identical and fraternal twins both develop alcohol problems; adoption studies follow children of alcohol dependent individuals who have been adopted by individuals without alcohol problems. The results of contemporary genetic studies strongly support a role for genetics in the development of alcohol problems, particularly among sons of alcohol dependent parents, who are three to four times more likely to develop alcohol problems than sons of nonalcohol dependent parents. Knowing that genetics plays a part in the development of alcohol problems, researchers have now turned their attention to identifying those processes or deficits that might be genetically transmitted and contribute to alcohol problems. Alcohol problems are

often conceptualized as stemming from biologically based difficulties in temperament and self-regulation, defined by Diaz and Fruhauf in 1991 as the ability to "plan, guide, and monitor one's own behavior flexibly according to changing circumstances." Self-regulation becomes more sophisticated over the course of development. As children are required to function more independently, they learn skills to help them evaluate situations and change behavior such as self-monitoring of functioning, evaluating functioning in comparison to a standard, and designing and implementing behavior change if needed. Some children make this transition readily, while others fail to become competent self-regulators. Temperamentally difficult child r e n - t h o s e showing poor behavioral control, hyperactivity, and impulsivity--are thought to have poor self-regulation. Such children can be difficult to parent. Their heightened activity interferes in the development of self-control skills, as well as in the formation of strong relationships with others such as parents who would help them develop these skills. As individuals develop and are required to behave more autonomously, individuals who are poor self-regulators may be less able to change their behaviors to meet new challenges. As a result, they rely on external sources of regulation such as alcohol and drugs, which in turn tend to impair self-regulation still further. A large body of research has shown that temperamentally difficult children show a greater likelihood of developing alcohol problems as adults.

B. Environmental Factors Although genetic and biological processes contribute to the development of alcohol problems, environmental factors are also strongly involved. Difficulties in temperament and self-regulation can be thought of as risk factors that interact with personal and environmental factors to lead to the development of alcohol problems. Social learning models of alcohol use and problems emphasize the importance of social reinforcers--reactions from others in the social world that either reward or punish particular behaviors. Positive reactions serve to reinforce drinking behavior, while negative reactions punish such behavior. Also important to such a model are personal, internal events that guide an individual's perception of the external world, such as attitudes and expectations about drinking.

20

Alcohol Problems

What environmental factors might be important to drinking behavior? There are multiple levels of environmental influence--more immediate influences include family members and peers, while farther removed factors include aspects of society, culture, and religion. Family and peers strongly influence drinking behaviors by setting examples, altering availability of alcohol, and by encouraging or discouraging alcohol use. Much evidence suggests that adolescents and young adults tend to hold attitudes toward alcohol and show drinking behaviors that are like those of their parents and peers: young individuals who drink tend to have parents and peers who drink. Through these links with drinking others, young people observe the positive features of drinking, learn how to drink, and receive positive feedback for their drinking. Similarly, peer influence appears to have a particularly strong impact on drinking in adolescence and young adulthood. Heavy-drinking youth typically are involved with similarly heavy-drinking peers. Such drinking networks may serve to teach adolescents and young adults how to drink, model appropriate (or inappropriate) drinking behavior, and reward such behavior with attention, movement into a higher social status, and an identity as a drinker. [See

ADOLESCENCE.] Along these lines, Jessor describes a problembehavior theory in which proneness both to problem drinking and to other problem behaviors in youth results from an interaction of personality, environmental, and behavioral systems. Personality proneness to problem behavior includes a low value on academic achievement, a high value on independence, and greater tolerance for deviance coupled with lower expectations of attaining goals and lower self-esteem. Environmental stressors include low parental support and control along with high peer engagement in and approval for deviance. Together these factors have been described as a style of unconventionality. This unconventionality makes for problematic behaviors and stressful interactions with others. Importantly, environment includes more than just an individual's home and peer experiences. Characteristics of the person and the immediate environment occur within a larger social context. Cultural ideas about alcohol use, societal attitudes toward intoxication, and laws about the purchase and consumption of alcohol all interact with an individual's biological, environmental, and cognitive makeup. For example, during

Prohibition in the United States, when attitudes were distinctly anti-alcohol and purchasing liquor was illegal, people drank less and experienced fewer alcohol problems. Patterns of alcohol use and problems vary by religious group affiliation. Jews tend to report a high prevalence of drinking but very low rates of alcohol problems, while Catholics tend to report higher rates of both drinking and heavy drinking. An especially important societal influence in modern society is the media. Both visual and print media provide a variety of models of and reinforcers for alcohol consumption. Messages about the positive effects of alcohol (it's fun and everyone is doing it) are delivered via television, movies, radio, billboards, and magazines. Drinkers are shown as attractive, socially adept, and healthy. In contrast, messages regarding the potentially harmful effects of alcohol on physical and psychological functioning are rarely shown.

C. Cognitive Factors Recently, the alcohol field has become interested in a third set of factors that influence and are influenced by an individual's biology and environment. Cognitive factors m beliefs about alcohol and its use, one's ability to cope with stress, and ideas about what sorts of things might help a person with their problemsA become increasingly important in decisions to engage in risky or harmful drinking. The young adult who has difficulty with self-regulation, is engaging in multiple problem behaviors, and experiences poor interactions with others is then faced with the more adult task of coping, a skill that has been found to be lacking in adolescents and young adults who drink heavily. In explaining differences between normaland problem-drinking adolescents, some researchers describe a stress-coping perspective in which adolescents who drink the most are using alcohol to cope with high levels of stress and few external rewards. Studies in this area have shown that teens who drink heavily report more life stressors along with poorer coping skills than teens who drink moderately. In making a decision about how to cope with a stressor or a problem, beliefs about the effects of alcohol appear to be another important cognitive factor. Alcohol expectancies are beliefs that alcohol use will have positive outcomes, such as increased feelings of relaxation, assertion, or general well-being. Alcohol expectancies have been found to be related to differences in drinking

Alcohol Problems

behavior in adolescents and adults~individuals who drink more report more positive expectations or beliefs about alcohol and its effects. Moreover, individuals who develop alcohol problems report stronger alcohol expectancies than normal drinking adults. Positive experiences have been found to exist before a child's direct experience with alcohol, suggesting a role for expectancies in developmental models of alcohol problems. Importantly, alcohol expectancies may connect coping and stress: problem drinking develops from using alcohol to cope with stress by those individuals who lack other means of coping and who perceive alcohol as being able to help resolve bad feelings. Research has shown some support for this view, finding that poor coping is linked to problem drinking in individuals with strong, positive alcohol expectancies. Thus at highest risk for problem drinking is the individual who, when faced with stress, shows low coping self-efficacy (I can't cope) and has strong positive expectancies about the effects of alcohol (Alcohol will help me cope). Rogers' protection-motivation theory emphasizes a person's perception of risk as crucial to the decision to engage in harmful behavior such as problem drinking. According to this view, health behaviors are guided by perceptions of threat and coping. First, a person must evaluate the likelihood of threat (Will drinking cause bad things to happen to me?) and the severity of the threat (If drinking causes bad things to happen to me, how bad will these things be?). Engaging in the maladaptive response, in this case harmful or risky drinking, is influenced by the interaction of rewards (feeling good, having fun, social approval) and consequences. Second, the individual makes a coping appraisal, a judgment about what alternatives are available and one's ability to engage in alternative behavior (Are there things to do besides drinking and can I do them effectively?). Rogers stresses the importance of selfefficacy, an individual's appraisal that he/she is capable of implementing and carrying out the behavior change. Problem-drinking individuals tend to evaluate the threat of problem drinking as low, the severity of potential consequences as low, the alternatives to drinking as unpleasant, and their ability to implement change as minimal. Thus multiple influences over the course of development interact to produce threats to alcohol health. Alcohol problems can evolve out of inherited difficulties in temperament and self-regulation that lead an

21

individual to engage in problem behaviors and poor interactions with others. With this foundation, a developing person is ill-equipped to cope with the stressors and problems that accompany the transition to adulthood. The balance of rewards that accompanies drinking and the perception of minimal threat contribute to an individual's maintaining problem alcohol use. Recently, researchers have become interested not only in the question of who is going to show alcohol problems at one point in time, but also in who is going to continue to have alcohol problems at many points in time. Remember that although young adults experience the highest rates of alcohol use and related problems, these rates decrease substantially in adulthood. These trends suggest that most young adults "mature out" of problem drinking upon entering adulthood. Different reasons for this "maturing out" have been suggested, most prominently that the assumption of adult roles such as work and marriage, along with a decrease in problem drinking among peers, leads young adults to moderate their use into patterns of typical social drinking. Individuals with alcohol problems, however, tend to report that they began drinking and experiencing negative consequences at a young age, so that rather than maturing out, some individuals will continue problem-drinking patterns from youth into adulthood. Some researchers have suggested that these patterns represent different problem-drinking typologies. According to this view, individuals who continue problem drinking over time are likely to be at the greatest risk for developing severe problems in adulthood; thus it is important to identify which young adults will be the ones to continue problem drinking into adulthood. Recent research suggests some qualities that may characterize individuals who will continue problem drinking from youth to adulthood, including having a higher degree of behavioral undercontrol, engaging in other problem behaviors in addition to problem drinking, and using alcohol to relieve negative feelings.

IV. THE CHANGING NATURE OF ALCOHOL PROBLEMS OVER TIME The above discussion highlights some of the many factors that influence the development and continuation of alcohol problems over time. It is important to re-

2

. . . Alcohol . . . Problems . . . . . . . . . . .

member that alcohol problems vary widely: some individuals develop risky, harmful, or dependent patterns, and some cycle in and out of these various use patterns. Rather than being stable, alcohol problems change and develop over time and show a range of outcomes. Vaillant has provided the clearest illustration of this variability in his research on the natural history of alcohol problems. He has followed a large sample of men for more than 50 years, 110 of whom had experienced alcohol abuse at some point in their lives. These men drifted in and out of alcohol problems: some were abstinent for long periods of time, others relapsed to heavy or risky drinking, and others returned to dependent patterns of drinking. In his most recent follow-up of these men, now in their 70s, Vaillant stressed that alcohol abuse can have different paths for different people, sometimes progressing to more severe drinking, sometimes remitting, and most often varying in severity over time. Vaillant's data illustrate that within an individual problem-drinking path there are many twists and turns, with periods of harmful and risky drinking interspersed with periods of moderate problem-free drinking or abstinence. V. RISK AND PROTECTIVE FACTORS What factors put individuals at increased risk for alcohol problems? A public health model offers a useful framework for describing different types of risk factors and illustrating how they interact to influence outcomes. As with other complex disease processes, this approach highlights three kinds of risk factors-- agent, host, and environment--to be considered in understanding the development of alcohol problems. The agent in infectious diseases is a bacterium or virus, but in this case the agent is alcohol. Alcohol has its own destructive properties, much like a particular virus can cause specific symptoms and damage. Yet in most diseases, only some individuals who are exposed to the agent actually come down with the disease. Similarly, only some individuals who are exposed to alcohol develop problems, highlighting the importance of host factors--individual characteristics that increase or decrease risk of alcohol problems. There are many such factors that are involved, including biological and psychological influences. One of the most important is gender. Men are more often drinkers and show a greater likelihood of drinking at a risky or harmful

level at all ages. A family history of alcohol problems also is a significant risk factor. Evidence from family, twin, and adoption studies suggests that a genetic vulnerability contributes to alcohol problems in some individuals, especially in sons of alcoholic fathers. Yet even identical twins may differ in whether or not they develop alcohol problems, indicating the role of environmental factors in addition to agent and host factors. Age also constitutes a significant risk factor for problem drinkingmyoung adults show the greatest use and greatest number of alcohol-related problems of any age group. In his study of the natural history of alcohol problems, Vaillant found that more than half of the individuals who would meet diagnostic criteria for alcohol abuse did so by age 31. Other host characteristics include temperament, coping skills, expectancies, and other psychopathology. As described earlier, temperamentally difficult children show a greater likelihood of developing alcohol problems as adults. Relatedly, individuals with alcohol problems tend to show poorer coping skills and to use alcohol to cope with the pressures and stresses that face them. As discussed earlier, individuals with strong, positive expectancies for alcohol (expecting alcohol will help relieve bad feelings) are more likely to drink and to develop alcohol problems. Finally, research shows that experiencing a psychological problem such as depression or anxiety, greatly increases risk for developing an alcohol problem. A third relevant domain is the environment. As discussed earlier, environment can be defined in a number of ways. Immediate environmental risk factors for alcohol problems include heavy or other problem-drinking family members who not only contribute possible genetic influences but also serve as role models for alcohol use and create a stressful home environment that may contribute to alcohol use. For adolescents and young adults, peer influences are among the most imp o r t a n t - - being part of an alcohol-using peer group increases risk for alcohol problems in these populations. Aspects of the larger environment are also relevant. Heavy-drinking communities show greater rates of alcohol-related problems. Cultures that sanction liberal use of alcohol likewise show higher rates of risky and harmful drinking. Stress may also be an important environmental risk factor: research suggests that severe and prolonged stress appears to be an important factor in problem drinkers returning to drinking after a period of abstinence.

Alcohol Problems

While there are characteristics that put people at increased risk for alcohol problems, there are also factors that protect individuals in the face of these risks. Protective factors are not merely the opposite or lack of risk factors. Rather, they are influences that moderate the links between risk factors and alcohol outcomes such that an individual may be exposed to risk but show resiliency and avoid problem alcohol use. Several protective factors have been identified in adolescents and young adults, including close and positive relationships with parents, adolescent conventionality, parental adjustment, and success in school. Religious affiliation and involvement appears to be a strong protective factor. Individuals who report strong religious beliefs or high levels of religious commitment consistently show lower levels of alcohol use and fewer alcohol-related problems. In contrast, individuals with alcohol problems are less likely to report firm religious beliefs or involvement. In addition, social support has been found to play an important protective role: individuals engaged in supportive relationships with others appear less likely to develop alcohol problems, and social resources are thought to offset other potentially harmful stressors and risks. It also makes a difference whether one's social group supports abstinence, moderation, or risky and heavy drinking.

VI. CONTINUUM OF INTERVENTION FOR ALCOHOL PROBLEMS From the previous discussion, it is clear that alcohol problems encompass a range of risk factors and difficulties that vary along a continuum of severity. All individuals are exposed to some risk factors; many individuals experience multiple risk factors that make them increasingly vulnerable. Some individuals are just beginning to develop problems with alcohol; others already have well-developed dependence. Such diversity necessitates a variety of intervention strategies. Any single type of prevention program is not likely to reach all who are at-risk, and one brand of treatment will not be effective for all problem drinkers. At one end of the continuum are universal prevention strategies, designed to target a large population with the goal of reducing the incidence of alcohol problems; for example, by increasing awareness of

23

risks and promoting alternatives to alcohol use. A target population might be all individuals in a particular city, school district, or university campus. An example of a universal prevention strategy is instituting an excise tax on alcoholic beverages that makes alcohol more expensive, with the result that people purchase less. Print and electronic media campaigns are also designed to reach large groups of people with their alcohol-related messages. Universal prevention strategies target everyone in a population, regardless of their level of risk for developing problems. Other interventions focus on individuals who are at high risk for developing problems. Termed targeted prevention strategies, such interventions are aimed at particular groups who have not yet developed a problem but are at increased risk due to their exposure to particular or multiple risk factors. Examples of such high-risk groups are children of parents with alcohol problems, adolescent boys with behavior problems, and college students with poor grades. The goal of targeted prevention is to stop a problem before it starts, or at least early in its development, by intervening with those at highest risk. For example, programs in college dormitories, fraternities, and sororities are aimed at providing information to individuals at high risk for drinking and related problems. Prevention is aimed at individuals who have not yet developed problems. Once an individual is identified as having an alcohol problem, the focus of intervention shifts toward treatment. Individuals identified as already having an alcohol problem may be referred for some sort of intervention or treatment. However, only a small percentage of individuals with alcohol problems ever receive formal treatment. A critical bridge between developing problems and receiving treatment is the person's motivation for change. Strengthening the commitment to change constitutes an important first step, and may need to be addressed before treatment takes place. Effective methods are available for enhancing motivation for change. Among the important elements of such interventions are providing personal feedback about drinking, empathic listening, acknowledging a range of alternatives for working toward behavior change, and emphasizing personal responsibility and ability to make change happen. Such motivational interventions are designed to help an individual become more aware of the impact of his/her drinking and to instill a commitment to change. This discussion has emphasized the diversity of al-

24

Alcohol Problems

cohol problems along a continuum of severity. The implication of this diversity is that what is helpful or appropriate for a drinker just beginning to develop an alcohol problem will differ from the most effective treatments for more severe, dependent drinkers. Individuals who are just beginning to show signs of problem alcohol use might fit the description of "risky' or "harmful" drinkers who are drinking heavily or in potentially dangerous situations. Intervention with these individuals is aimed at recognizing a problem early and preventing it from reaching diagnostic levels. For example, businesses have employee assistance programs where personnel are trained to recognize the early signs of alcohol problems in their employees. Other early identification strategies include urine drug-screening programs, justice system referrals, screening during routine health care, and programs for impaired drivers. Individuals at the beginning stages of problem development are often helped by brief interventions-motivational strategies that help individuals see their increasing involvement with alcohol and the negative consequences they may experience as a result. These interventions are usually one or two sessions of alcoholrelated counseling and advice to reduce drinking. Some brief interventions involve providing clients with reading and other educational materials that review drinking patterns and ways to reduce drinking. Studies have consistently found that such brief interventions help problem drinkers reduce their alcohol use. What about individuals who are far enough along the continuum to have developed more severe alcohol problems? There now exist a range of promising and effective approaches for use with different types of drinkers. As individuals with alcohol problems frequently have difficulties in many areas of functioning, several interventions are often combined. For drinkers with more severe problems, detoxification may be necessary to overcome the acute effects of alcohol withdrawal. With proper supervision, an addicted drinker is through the worst withdrawal within a week, and modern medical care can prevent the more uncomfortable and dangerous symptoms of alcohol withdrawal. Detoxification, however, is not treatment. Simply detoxifying a dependent drinker is unlikely to have any long-term effect on drinking. Various medications have been tested in treating alcohol problems. One of the most popular of these is disulfiram (Antabuse)--a medication that produces a negative physical reaction (nausea, vomiting) when alcohol is ingested. Naltrexone (ReVia) also appears to

be a promising agent in reducing relapse and craving. Medications, however, are only an aid in treatment, and are unlikely to be effective when given without other treatment. Some view alcohol problems as a lack of coping skills. Skills-training approaches view alcohol use as a maladaptive coping strategy, and teach appropriate coping skills as an alternative to drinking. Social skills training is used to help individuals with alcohol problems to interact effectively with other people, to cope with positive and negative feelings, and to handle stressful situations in the environment. The community reinforcement approach similarly emphasizes the need for the drinker to be prepared to cope with stress, and to establish a rewarding, alcohol-free life-style. Efforts are made to get individuals connected to community resources, social supports, employment, and other activities that would contribute to a rewarding life-style without alcohol. From this perspective, the focus is not only on stopping alcohol use but also on helping people to acquire skills and make changes that will support an alcohol-free life-style. Alcohol problems often affect family functioning. Behavioral marital therapy (BMT) regards the marital relationship as crucial in the maintenance and change of an individual's drinking behavior. BMT is designed to improve communication skills, teaching spouses how to reinforce changes in drinking behavior, and ways to cope with drinking-related situations and feelings. There are also effective approaches to help concerned family members and friends of individuals with alcohol problems, even if the drinker is unwilling to accept help. These concerned others often wish to help their loved one but lack the knowledge and skills to do so. Concerned family members can be helped to engage the problem drinker in treatment. Such treatments also attend to the needs of the family members themselves--to distance themselves from the drinker and to learn skills for coping with stress and other negative feelings. Recovery from alcohol problems typically involves relapse. Effective treatment often includes attention to the people, places, and things that are likely to trigger alcohol use in the future. Marlatt's relapse-prevention (RP) incorporates cognitive-behavioral strategies aimed at anticipating slips and considering how to handle high-risk situations. Specifically, RP stresses anticipating and working to prevent relapses and realistically considering how to recover and learn from relapses if they occur. To this end, clients identify specific

Alcohol Problems

high-risk situations and outline a plan for making it through without drinking. For individuals with less severe drinking problems, strategies to teach skills for moderate drinking are sometimes used. Moderation training programs are designed for risky or heavy drinkers who might not participate in treatment aimed at total abstinence, but who could benefit from reducing their alcohol use. For example, behavioral self-control training (BSCT) teaches clients skills for moderating their drinking. BSCT makes use of behavioral principles of self-control and teaches ways to self-monitor drinking, to set goals for decreasing consumption, and to implement alternative coping skills. BSCT and programs like it may be used with either abstinence or moderation goals. The above interventions all involve the individual with alcohol problems seeking assistance from a trained professional. Although outcome studies strongly support the efficacy of these treatment strategies, the fact remains that most individuals with alcohol problems never receive professional help and yet "recover" without formal intervention. Many of these drinkers will seek help not from professionals but from others with similar problems. Particularly in North America, mutual-help groups serve as a major source of help and support for many individuals with alcohol problems. The largest and best-known of these groups is Alcoholics Anonymous (AA), serving over two million members in 150 countries around the world. AA emphasizes commitment to abstinence and renewed spirituality recognizing the strength of a "higher power" as necessary to the change process. Other self-help groups, such as Women for Sobriety, SMART Recovery, Rational Recovery, and Moderation Management, emphasize personal control and responsibility in overcoming alcohol problems.

VII. CONCLUSION

Alcohol problems encompass a range of difficulties. Some individuals with alcohol problems experience minor difficulties in a one area of functioning. Other individuals experience substantial impairment in mul-

'-

25

tiple life areas due to their alcohol use. In this article, we have reviewed factors that put people at risk for alcohol problems, as well as theories that seek to explain how alcohol problems develop. There now exists a range of interventions for individuals at all levels of the alcohol problems spectrum. Future research will add to our knowledge of alcohol problems and yield important new information about how such problems develop and how they can be most effectively treated. ACKNOWLEDGMENT Preparation of this article was supported in part by National Institute on Alcohol Abuse and Alcoholism Grant K05-AA00133.

BIBLIOGRAPHY Blane, H. T., & Leonard, K. E. (Eds.). (1987). Psychological theories of drinking and alcoholism. New York: Guilford Press. Diaz, R. M., & Fruhauf, A. G. ( 1991 ). The origins and development of self-regulation: A developmental model on the risk for addictive behaviors. In N. Heather, W. R. Miller, & J. Greely (Eds.), Self-control and the addictive behaviors. Sydney: Maxwell Macmillan Publishing. Hester, R. K., & Miller, W. R. (Eds.). (1995). Handbook of alcoholism treatment approaches: Effective alternatives (2nd ed.). Boston, MA: Allyn & Bacon. Jessor, R. (1987). Problem-behavior theory, psychosocial development, and adolescent problem drinking. British Journal of Addiction, 82, 331-342. Marlatt, G. A., & Gordon, J. R. (1985). Relapse prevention. New York: Guilford Press. Miller, W. R., & Rollnick, S. (1991). Motivational interviewing: Preparing people to change addictive behavior. New York: Guilford Press. Monti, P. M., Abrams, D. B., Kadden, R. M., & Cooney, N. L. (1989). Treating alcohol dependence: A coping skills training guide. New York: Guilford Press. National Institute on Alcohol Abuse and Alcoholism. (1993). Eighth special report to the U.S. Congress on alcohol and health. Rockville, MD: U.S. Department of Health and Human Services. Rogers, R. W. (1983). Cognitive and physiological processes in fear appeals and attitude change: A revised theory of protection motivation. In J. T. Cacioppo & R. E. Petty (Eds.), Social Psychophysiology (pp. 153-176). New York: Guilford Press. Vaillant, G. E. (1983). The natural history of alcoholism. Paths to recovery. Cambridge, MA: Harvard University Press.

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Alzheimer's Disease Mark W. Bondi

Kelly L. Lange

California State Universi~ San Marcos, San Diego Veterans Affairs Medical Center, and University of California, San Diego

San Diego State University, and University of California, San Diego

I. II. III. IV. V.

Clinical Features Neuropathological Features Neuropsychological Deficits Affective and Personality Changes Differentiation of Alzheimer's Disease from Other Etiologies VI. Clinical Management of Alzheimer's Disease VII. Summary

Neurotransmitters Chemical substances in the brain that relay messages between neurons. Semantic Memory A general fund of knowledge, consisting of overlearned facts and concepts, which are not dependent upon contextual cues for retrieval.

ALZHEIMER'S DISEASE (AD) appears to be the most common cause of dementia, accounting for more than 50% of all dementia cases. AD is a progressive degenerative brain disorder that is characterized by neocortical atrophy, neuron and synapse loss, and the presence of senile plaques and neurofibrillary tangles. The plaques and tangles were first identified and reported in 1907 by the German physician and neuropathologist Alois Alzheimer. In his initial case he autopsied a 51-year-old patient who had recently died (from what we now term dementia) and discovered the presence of several histopathologic alterations, two of which were the neuritic plaques and the neurofibrillary tangles. Today they remain the two classic hallmarks of the disease and constitute the basis for the neuropathologic diagnosis of Alzheimer's disease. The dementia of AD is characterized by severe amnesia with additional deficits in language, "executive" functions, attention, and visuospatial and constructional abilities. Patients may also experience changes in affect or personality and impairment of judgment. This article will provide an overview of the clinical, pathological, neuropsychological, and affective features associated with AD.

Alzheimer's Disease Broadly characterized by a global and progressive deterioration of memory, cognition, and personality associated with neocortical atrophy, neuron and synapse loss, and the presence of neuritic plaques and neurofibrillary tangles. Dementia A syndrome of acquired intellectual impairment, of sufficient severity to interfere with social or occupational functioning, caused by brain dysfunction. Episodic Memory Knowledge of temporally dated autobiographical events that depend upon temporal and/or spatial contextual cues for their retrieval. Explicit Memory The conscious recollection of previously acquired information. Implicit Memory An unconscious trace of knowledge activated by previous experience with a stimulus. Neuritic Plaques Deposits of amyloid protein and glial cells that collect in intercellular space. Neurofibrillary Tangles Networks of insoluble protein that collect intracellularly and result in the disruption and eventual collapse of the neuronal cytoskeleton.

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Copyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

28

Alzheimer's Disease

I. CLINICAL FEATURES A. Definition of Dementia Dementia refers to a syndrome of acquired intellectual impairment of sufficient severity to interfere with social or occupational functioning, caused by brain dysfunction. According to the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, "Dementia of the Alzheimer's Type" involves m e m o r y impairment and cognitive deficits in at least one other domain, demonstrated by aphasia, apraxia, agnosia, or impaired executive functioning. These symptoms must not be due to other neurological disorders, medical conditions resulting in dementia, or substance abuse. The cognitive impairments must have a gradual onset and a progressive decline and be severe enough to significantly interfere with social or occupational functioning. Furthermore, the cognitive impairment must represent a significant decline from a previously higher level of functioning, and it must not occur exclusively during the course of delirium (see Table I). [See DEMENTIA.] Prior to the DSM, however, in 1984, the Work Group on the Diagnosis of Alzheimer's Disease, established by the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA), developed criteria for the clinical diagnosis of probable and possible AD (see Table II). Since then the N I N C D S - A D R D A clinical criteria have been tested against autopsy verified diagnoses and found to be quite effective.

B. Diagnosis and Course of Alzheimer's Disease Because dementia is associated with more than 50 different causes of brain dysfunction (see Table IlI), and there are no known peripheral markets for Alzheimer's disease, a definitive diagnosis continues to require histopathological verification of the presence of characteristic neurodegenerative abnormalities at autopsy (i.e., neuritic plaques and neurofibrillary tangles). However, documentation of the presence of dementia and the exclusion of all other known poten-

Table I

DSM-IV Diagnostic Criteria for Dementia of the Alzheimer's Type

A. The development of multiple cognitive deficits manifested by both 1. memory impairment (impaired ability to learn new information or to recall previously learned information); 2. one (or more) of the following cognitive disturbances: a. aphasia (language disturbance); b. apraxia (impaired ability to carry out motor activities despite intact motor function); c. agnosia (failure to recognize or identify objects despite intact sensory function); d. disturbance in executive functioning (i.e., planning, organizing, sequencing, abstracting). B. The cognitive deficits in Criteria A1 and A2 each cause significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning. C. The course is characterized by gradual onset and continuing cognitive decline. D. The cognitive deficits in Criteria A1 and A2 are not due to any of the following: 1. other central nervous system conditions that cause progressive deficits in memory and cognition (e.g., cerebrovascular disease, Parkinson's disease, Huntington's disease, subdural hematoma, normal-pressure hydrocephalus, brain tumor); 2. systemicconditions that are known to cause dementia (e.g., hypothyroidism, vitamin B~2or folic acid deficiency, niacin deficiency, hypercalcemia, neurosyphilis, HIV infection); 3. substance-induced conditions. E. The deficits do not occur exclusivelyduring the course of a delirium. F. The disturbance is not better accounted for by another Axis ! disorder (e.g., Major Depressive Disorder, Schizophrenia)

Note. DSM-IV refers to the Diagnostic and Statistical Manual for Mental Disorders, 4th edition. From American Psychiatric Associaiton, 1994.

tial causes allows probable or possible Alzheimer's disease to be clinically diagnosed during life with some certainty (i.e., current estimates are approximately 90% or better). Patients with Alzheimer's disease often live for many years following their diagnosis, dying eventually from conditions like pneumonia, sepsis, or other fatal conditions to which people of advanced age are prone. The duration of the disease from the time of diagnosis to death can be as little as 2 years or as long as 20 years or more, although the average length ranges between 7 and 10 years.

29

Alzheimer's Disease

Table II

N I N C D S - A D R D A Criteria for Definite, Probable and Possible Alzheimer's Disease

I. Definite Alzheimer's disease: Clinical criteria for Probable AD; Histopathologic evidence of AD (autopsy or biopsy). II. Probable Alzheimer's disease: Dementia established by clinical exam and documented by mental status testing; Dementia confirmed by neuropsychological testing; Deficits in two or more areas of cognition; Progressive worsening of memory and other cognitive functions; No disturbance of consciousness; Absence of systemic or other brain diseases capable of producing a dementia. III. Possible Alzheimer's disease: Atypical onset, presentation, or progression of a dementia syndrome with a known etiology; A systemic or other brain disease capable of producing dementia is present but not thought to be the cause of the dementia; A gradually progressive decline in a single intellectual function in the absence of any other identifiable cause. IV. Unlikely Alzheimer's disease: Sudden onset of symptoms; Focal neurological signs and symptoms; Seizures or gait disturbance early in the course of the illness. From McKhann et al. (1984). Clinical diagnosis of Alzheimer's disease: Report of the NINCDS-ADRDA Work Group, Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology, 34, 939-944.

C. Epidemiology I. Prevalence and Incidence of Alzheimer's Disease Estimates of the prevalence of dementia vary widely due to differences in definitions, sampling techniques, and the sensitivity of instruments used to identify cases. However, Cummings and Benson calculated the average of prevalence estimates across studies and suggested that approximately 6% of persons over the age of 65 have severe dementia, and an additional 10% to 15% have mild to moderate dementia. Also, the prevalence of the syndrome of dementia doubles approximately every 5 years after age 65. Not surprisingly, the prevalence of dementia is higher among hospital and nursing home residents than among those living within the community.

Table III

Causes of Dementia

I. Cerebral neuronaldegenerative disorders: Alzheimer's disease; Pick's disease; Parkinson's disease; Huntington's disease; Progressive supranuclear palsy; Dementia lacking distinctive histopathology. II. Acquired cerebral disorders (some of which may be reversible): Vascular dementia: Multi-infarct dementia; Binswanger's disease; Multiple sclerosis; Intracranial neoplasms; Trauma (e.g., subdural hematoma; dementia pugilistica; diffuse axonal injury); Hydrocephalus; Transmissible spongiform encephalopathies (e.g., Creutzfeldt-Jakob disease). III. Other potentially reversible dementias: Metabolic disorders; Chronic drug intoxication; Alcoholism; Malnutrition (e.g., vitamin B12deficiency); Infections: HIV (AIDS); Neurosyphilis; Tuberculous or bacterial meningitis; Cryptococcosis; Acute viral encephalitis; Dementia syndrome of depression.

Note: A complete listing would include many more disorders; those listed above serve to illustrate that dementia results from many different etiologies Adapted from Berg & Morris, in Terry, Katzman, & Bick (1994).

2. Risk Factors for Alzheimer's Disease A number of reliable risk factors for Alzheimer's disease have been identified. First, age is the single most important risk factor for dementia. Population-based studies in many different countries have confirmed that the prevalence of the most common causes of dementia (i.e., Alzheimer's disease and vascular dementia) rises in an approximately exponential fashion between the ages of 65 and 85. Second, it has been suggested that women have a slightly greater risk for Alzheimer's disease than men, due in part to its higher prevalence in women. The greater risk for women, however, may be a factor of their longer life expectancy, since incidence rates for Alzheimer's disease have not shown differences between men and women. Third, uneducated individuals over the age of 75 have about twice the risk for dementia as those who have completed at least a grade school education. Low lifetime occupational attainment, associated with little education, may also yield a greater risk for Alzheimer's

30

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Table IV Geneticsof Alzheimer's Disease Chromosome

Protein

21

Amyloid Precursor Protein

19 14

Apolipoprotein E Presenilin 1

1

Presenilin 2

.

Alzheimer's Disease

p---Latent Phase-t-

Percentage of AD

Age of Onset

<1

45-60

30-50 1-2

60+ 32-56

<1

4 0 - 85

Diffuse plaques A Initiation factors

9A I : ~ E4 9F a m i l y history 9H e a d trauma 9D o w l l ' s 9C o r o n a r y

d~,ease

90 1 f ) e r

Malignant Phase

Neuritic plaques, tangles, neuron and synapseloss Preclinical A A t<~-Phase--~ ~

Promoting factors Age 9

-

:

dath

Lo of independence Diagnosis Siqnificant fuTlctional decline Si~nificant c6gnitive aecline

disease. Education and occupational achievement may act as a surrogate for brain or cognitive reserve that helps to delay the onset of the usual clinical manifestations of the disease. Fourth, the risk of developing dementia is increased approximately fourfold by a family history of Alzheimer's disease in a first-degree relative (i.e., mother, father, brother, or sister). Given some of the findings of specific point mutations on the amyloid precursor protein gene of chromosome 21 and linkage studies identifying gene loci on chromosomes 1, 14 and 19, there is now little question that this familial association is genetically based (see Table IV). Furthermore, the epsilon-4 allele of the apolipoprotein E gene (ApoE-E4) located on chromosome 19 has recently been identified as another risk factor for dementia because of its over-representation in patients with Alzheimer's disease. Finally, the risk of developing Alzheimer's disease is doubled for individuals with a history of a single head injury that led to a loss of consciousness or hospitalization. This finding, however, may be confined to those Alzheimer's patients with previous head injuries who also carry at least one ApoE-E4 allele. Recent research has demonstrated that individuals with a history of head injury who lack the presence of the ApoE-E4 allele are not at increased risk for Alzheimer's disease. If one assumes that these aforementioned risk factors are simply additive at the population level, then the attributable risk of developing Alzheimer's disease from these known factors appears to be between 40% and 50% (and probably more given the recent addition of ApoE-associated risk). Thus, current views suggest that Alzheimer's disease is a chronic disease, much like cancer or heart disease, in which an individual is predisposed by ge-

Figure I

Chronic disease model of Alzheimer's disease. Adapted from Katzman and Kawas (1994), in Terry, Katzman, & Bick (Eds.), Alzheimer disease, with permission of Raven Press.

netic factors, traumatic events, or other unknown factors toward entering a malignant phase. Intracellular events will eventually lead to neuritic degeneration, the formation of neurofibrillary tangles, and neuron and synapse loss. Over a period of time, the neural degeneration gradually reaches a level that initiates the clinical symptoms of the dementia syndrome. This framework for understanding the development of AD suggests that cognitive deficits associated with the disease also appear gradually (see Fig. 1).

D. Neuroimaging in Alzheimer's Disease A variety of neuroimaging techniques have been used to study and characterize Alzheimer's disease. Some of the most recent techniques include structural and volumetric analysis of the brain with magnetic resonance imaging (MRI), computation of regional cerebral metabolism with positron emission tomography (PET), regional cerebral blood flow with single photon emission computed tomography (SPECT), and determination of regional biochemical concentrations with magnetic resonance spectroscopy (MRS). MRI studies of Alzheimer's disease patients reveal a decrease in brain volume, apparently due to gyral atrophy and ventricular dilatation. However, gyral atrophy and enlarged ventricles are also found in normally aging brains, lending minimal diagnostic value to structural images early in the course of the disease. Future research targeting hippocampal or entorhinal cortex, however, may yield more sensitivity to early stage Alzheimer's disease.

31

Alzheimer's Disease

Functional imaging studies with PET and SPECT have found significant differences between Alzheimer's disease patients and healthy older adult control subjects. Temporoparietal and frontal cortical regions have shown significant glucose metabolic reductions, with relative sparing of visual and sensorimotor cortex. Furthermore, significant relationships have been found between neuropsychological impairment in AD and the degree of hypometabolism found by PET. In addition, Haxby (in Rapoport, Petit, Lays, and Christen) measured cerebral metabolism with PET in Alzheimer's patients and found differing patterns of decreased metabolism in the association cortex. The individual patterns of decreased metabolism correlated with neuropsychological test scores purported to reflect processing in particular brain regions. The decreased neocortical metabolism was found even in patients in the earliest stages of dementia of the Alzheimer type, in whom neuropsychological testing revealed no deficits other than amnesia. This finding suggests that PET imaging can be useful in the early detection of AD. As a marker of cerebral blood flow in Alzheimer's disease, SPECT also demonstrates similar regional reductions to that of PET, although its spatial resolution is not as high. However, its significantly lower cost allows for its more widespread use. In addition, SPECT studies have attempted to trace neurotransmitter receptor changes in Alzheimer's disease patients (e.g., muscarinic receptors; dopaminergic D2 receptors), although results have been mixed to date. Findings in MRS studies suggest that this technique may also be sensitive to the early detection of Alzheimer's disease. For example, an increase in the biochemical concentration of myo-inositol has been found in patients with mild to moderate Alzheimer's disease. Myo-inositol serves several functions in the brain, one of which may involve the deposition of neuritic plaques characteristic of Alzheimer's disease. Increases in myo-inositol concentration have not been found in patients with other dementing illnesses or in normally aging individuals. Thus, preliminary findings from a number of recent studies suggest that MRI, PET, SPECT, and perhaps MRS can provide complementary information to the usual diagnostic procedures and may contribute to the early and more specific detection of the disease. It should be emphasized, however, that although the

usefulness of structural or functioning neuroimaging procedures appear promising, each of these costly techniques remains experimental and has not been shown to be as accurate as the clinician's judgment in the differential diagnosis of Alzheimer's disease. Future longitudinal studies are needed to determine the prospective accuracy of early diagnosis through structural and functional neuroimaging techniques, particularly studies that will be able to provide neuropathologic confirmation.

II. NEUROPATHOLOGICALFEATURES Alzheimer's disease is primarily characterized by two particular histological findings in the brain: neuritic plaques and neurofibrillary tangles (see Fig. 1). Other associated features include neurotransmitter reductions, particularly acetylcholine and norepinephrine, as well as neuron and synapse loss.

A. Neuritic Plaques Neuritic plaques are complex deposits of amyloid protein and glial cells. These extracellular deposits collect most heavily in portions of the entorhinal cortex and hippocampal formation, two brain areas critical for memory and learning of new information. Neuritic plaques are also found throughout the cortical mantle of the neocortex, with a predilection for association regions (see Fig. 2).

B. Neurofibrillary Tangles Neurofibrillary tangles are networks of insoluble proteins which collect inside neurons and result in a breakdown in the structure of the neuron's cytoskeleton (see Fig. 3). The protein networks become so complex over time that normal cell metabolism and nutrient flow become impossible and the cell eventually dies. As with plaques, tangles accumulate most densely in the entorhinal and limbic regions of the brain, although tangles are also found in many structures that project to the cerebral cortex such as the nucleus basalis of Meynert, locus ceruleus, midline thalamic nuclei, as well as in some hypothalamic nu-

32

,

m

,,,

Alzheimer's Disease

Figure 2 Microscopic stain of a neuritic plaque. Plaques consist of dystrophic neurites and glial elements with or without a dense central core of insoluble amyloid protein.

clei and the ventral tegmental area, and dorsal raph~ nucleus.

C. Distribution of Neuropathological Changes In addition to plaques and tangles, pathological changes in Alzheimer's disease include neocortical atrophy (see Fig. 4), neuron loss, and synapse loss (see Fig. 5). These changes occur primarily in the hippocampus, entorhinal cortex, and in the association cortices of the frontal, temporal, and parietal lobes. Although the temporal progression of the neuropathological changes of Alzheimer's disease are not fully known, recent studies suggest that the hippocampus and entorhinal cortex are involved in the earliest stage of the disease, and that frontal, temporal, and parietal association cortices become increasingly involved as the disease progresses.

D. Major Neurochemical Alterations In addition to these cortical changes, subcortical neuron losses occur in the nucleus basalis of Meynert and in the locus ceruleus, resulting in a decrement in neocortical levels of cholinergic and noradrenergic markers, respectively.

E. Lewy Body Variant of Alzheimer's Disease Another neuropathologic condition in demented patients is characterized by the typical cortical distribution of senile plaques and neurofibrillary tangles of Alzheimer's disease, the typical subcortical changes in the substantia nigra, locus ceruleus, and dorsal vagal nucleus of Parkinson's disease, and, in addition, Lewy bodies that are diffusely distributed throughout the

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.

Alzheimer's Disease

.

33

Figure 3 Microscopic stain of a neurofibrillary tangle. Tangles result from the accumulation of abnormal components of the neuronal cytoskeleton and create disruptions in the structure and function of the neuron.

neocortex. Although only recently identified, this neuropathologic condition is not rare and may occur in approximately 25 % of all demented patients. The clinical manifestation of this disorder, which is sometimes known as the Lewy body variant of Alzheimer's disease, is similar to that of Alzheimer's disease in many respects, and these patients are often diagnosed with probable or possible Alzheimer's disease during life. However, retrospective studies indicate that Lewy body variant of Alzheimer's disease may be clinically distinguishable from "pure" Alzheimer's disease. While both disorders are associated with a severe and progressive dementia, there may be an increased prevalence of mild extrapyramidal motor findings (e.g., bradykinesia, rigidity, masked facies)

and hallucinations in patients with Lewy body variant of Alzheimer's disease, as well as a more rapid course.

III. NEUROPSYCHOLOGICAL DEFICITS A. Memory Failure of recent memory is usually the most prominent feature during the early stages of Alzheimer's disease. Accordingly, much of the neuropsychological research concerning the early detection of Alzheimer's disease has focused on memory. Numerous studies have shown that measures of the ability to learn new information and retain it over time are quite sensitive

34

Alzheimer's Disease

.

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;

'~

f

Figure 4 Gross examination of the brain of a nondemented older adult (shown on left) and that of an Alzheimer's disease patient (shown on right) demonstrates sulcal widening and gyral atrophy.

p

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,

~

%

9

o

o o

Figure 5 Synaptic loss in Alzheimer's disease. With the advent of immunostaining techniques to label and image synapses, an area of frontal cortex of a nondemented older adult (shown on left) displays abundant numbers of synapses, whereas the frontal cortex of an Alzheimer's disease patient (shown on right) has significant reductions in synaptic density. Reprinted from Terry, Masliah, & Hansen (1994), in Terry, Katzman, & Bick (Eds.), Alzheimer disease, with permission of Raven Press.

~r

Alzheimer's Disease

in differentiating between mildly demented patients with clinically diagnosed AD and normal older adults.

I. Explicit Memory Explicit, or declarative, memory, which refers to the conscious recollection of previously acquired information, is the type of memory assessed by classic, clinical tests of recall and recognition. One common dichotomous classification of explicit memory, the distinction between episodic and semantic memory, is based on the type of information stored in memory. Episodic memory contains context-linked information in which retrieval depends upon spatial and temporal cues. For example, remembering whether one took one's last dose of a medication requires retrieval of an episodic memory (i.e., where and when one took the medicine). Semantic memory, in contrast, refers to information that is context-free and usually overlearned. Thus, recollection that 3 x 2 = 6, that Hawaii is in the Pacific, and that the colors of the American flag are red, white, and blue, can be achieved without recalling the episode (or spatiotemporal context) in which that information was acquired. Although of general heuristic value in understanding anterograde amnesia (i.e., impaired learning and retention of new information after occurrence of cerebral insult), the episodic-semantic distinction's application to retrograde amnesia (i.e., impaired recollections of information acquired before cerebral insult) is more problematic. For this reason, loss of remote memory (or retrograde amnesia) in Alzheimer's disease is discussed briefly before episodic and semantic memory are discussed.

2. Remote Memory Retrograde amnesia is temporally graded in early Alzheimer's disease. In other words, events from the distant past, such as the patient's childhood, are remembered more easily than events from more recent past, such as middle adulthood. As the disease progresses into later stages, the patients' retrograde amnesia loses its temporal gradient, and a deficit is seen in retrieval of all explicit memory, regardless of when the information was encoded.

3. EpisodicMemory Episodic memory involves the storage and recollection of temporally dated autobiographical events that depend upon temporal and/or spatial contextual cues

35

for their retrieval. Memory difficulties in the earliest stages of Alzheimer's disease become apparent when patients are confronted with everyday tasks requiring the use of episodic memory, such as tracking medication regimens, paying bills on schedule, and keeping abreast of recent events in the news. Because of its prevalence in the early stages of AD, episodic memory disturbance is considered to be a necessary (but not sufficient) feature for the clinical diagnosis (see Table I). Memory impairments, even in patients in the early stages of the disease, are apparent on clinical and experimental memory tasks that require the learning and retention of either verbal or nonverbal information over a series of trials. This severe anterograde amnesia appears to primarily result from a failure in consolidation that is mediated by damage to the hippocampus and entorhinal cortex, and neurotransmitter changes in the cholinergic system. This inability of Alzheimer's patients to transform to-be-remembered information into a form suitable for long-term retention cannot be circumvented by effortful or elaborative processing at the time of acquisition. This contrasts with normal elderly, who have been shown to benefit from engaging in elaborative or semantic processing of information during the study phase of free recall tasks. Further evidence of patients' deficiencies in storage (i.e., consolidation) is provided by their severe impairments on recognition as well as on recall tasks and by their very limited improvement in acquisition over repeated learning trials (see Fig. 6). The numerous observations that Alzheimer's patients tend to recall only the most recently presented stimuli (i.e., heightened recency effects) support the notion that these patients have great difficulty in transferring information from short- to long-term storage. In addition to their difficulties in storing new information, patients also tend to evidence rapid forgetting of what little they do initially learn. The rapid forgetting is apparent for both verbal and nonverbal information and has been shown to be even more rapid in Alzheimer's disease than in amnesia. Recent findings suggest that this feature of memory loss is most important for the early and differential diagnosis of Alzheimer's disease and can be obtained through measures of delayed recall (e.g., number of words recalled after a few minutes delay) and savings scores (e.g., percent retained over a period of time).

36

Alzheimer's Disease

' ~

Long Delay Free Recall

~

~

1

Recognition Discriminability

1

Response Bias

Discriminability - Trial 5 Recall

-5

-4

-2 -1 0 Standard Scores

1

2

Figure 6 Standard scores of patients with Alzheimer's disease and Huntington's disease on the California Verbal Learning Test, a standardized memory test. Despite comparable poor delayed recall between Alzheimer's and Huntington's patients, the two groups differ in recognition memory, response bias, and a third measure assessing both retention over time and potential benefits of a recognition format over free recall--the difference between recognition memory performance and recall on trial 5 of the initial learning trials. Adapted from Delis et al. (1991). Profiles of demented and amnesic patients on the California Verbal Learning Test: Implications for the assessment of memory disorders. Psychological Assessment, 3, 1926, with permission of the American Psychological Association. Intrusion errors, or errors representing the intrusion of previously learned information into the attempted recall of new material, represent a consistent behavioral marker of dementia in Alzheimer's disease and are evident on tests of memory for verbal and figural information. However, some caution should be exercised when using such errors in a clinical setting. Intrusion errors in isolation do not represent an exclusive finding in AD since they also occur in patients with other forms of dementia (e.g., Huntington's disease) and in some patients with circumscribed amnesia (e.g., Korsakoff's syndrome). Furthermore, measures of error types have not proven to be the most sensitive cognitive indices for the detection of dementia. Thus, the occurrence of intrusion errors on episodic memory tests should be considered one indicator of a significant memory disturbance and should serve to initiate a thorough search for the processes underlying the patient's impairments.

4. Semantic Memory While the episodic memory impairment in Alzheimer's disease has been studied in great detail, the semantic memory deficits associated with the disorder have only recently been extensively investigated. It has been

known for some time through clinical characterizations of Alzheimer's disease that language deficits, such as word-finding difficulties in spontaneous speech and mild anomia, often occur during the course of the disease. Similarly, decrements in patients' general fund of knowledge concerning common facts of history, geography, arithmetic, and science have been observed and reported. Despite these observations, systematic study of patients' semantic knowledge was lacking. Fortunately, investigators have now begun to examine the language and knowledge deficits in Alzheimer's disease within the framework of current models of the representation of semantic knowledge that were developed in the field of experimental cognitive psychology. It is often assumed that semantic knowledge is organized as a complex network of associated concepts, and that within the network, concepts that have many attributes in common are more strongly associated than those that share fewer attributes. These strongly related concepts are thought to form conceptual categories made up of exemplars that share many attributes. The attributes not only provide a means of grouping concepts into categories, but also provide a means of distinguishing among the various exemplars that constitute a given category. Thus, dog and lion are both categorized as animals because they share attributes such as being alive, being mobile, and being able to reproduce, but they can be distinguished from each other by such attributes as domesticity, size, and shape. A number of recent investigations suggest that this organization of semantic memory is disrupted in patients with AD, possibly due to damage to the association cortices that are thought to store the concepts and associations that constitute semantic knowledge (see Fig. 7). There are a number of characteristics of the semantic memory impairment in Alzheimer's patients. First, patients exhibit a disproportionately severe fluency deficit when generating exemplars from a semantic category (e.g., animals) as compared to generating words from a phonemic category (e.g., words beginning with "F"). Their category fluency performance is characterized by an increased propensity to produce category labels relative to specific exemplars. Second, AD patients are impaired on object-naming tasks and produce a significantly greater proportion of semantically based errors than normal older adults and patients with Huntington's disease. In particular, Alzheimer's patients tend to refer to specific objects by their superordinate category names (e.g., "bird" for peli-

Alzheimer's

ENC

[

w,d

~

I_ s~

,,

fSome,.,r

I

r Domestic

]

1

HD I

[

Wild

I

1

B

lion

t~ger-

~ COW )

Disease

37

can). Third, patients with Alzheimer's disease demonstrate a deficit in sorting items on the basis of subordinate, but not superordinate, attributes. Fourth, there is a correspondence in items missed by AD patients across tasks designed to access semantic knowledge through different modes of input and output. Lastly, there is a deterioration in the organization of semantic knowledge in patients that can be consistently demonstrated by alterations in cognitive maps that reflect the semantic relationships used in categorizing concepts. Taken together, these findings suggest that there is a true loss of semantic knowledge in Alzheimer's disease, and that the nature of semantic memory deterioration in AD is consistent with a bottom-up breakdown in which specific attributes of a semantic category are lost before more general superordinate knowledge. This loss of semantic knowledge disrupts the normal organization of semantic memory in AD patients and results in aberrations in their network of semantic representations.

5. Implicit Memory f- sAa,, ! DAT

cat

sheep

Figure 7 Cognitive maps of elderly normal controls (ENC), patients with Huntington's disease (HD), and patients with Alzheimer's disease (AD) obtained from multidimensional scaling analysis (MDS) and ADDTREE clustering analysis. The position of each animal is determined by MDS; animals in the same cluster, according to ADDTREE cluster analysis, are encircled together. ENC and HD maps have two clusters based on domesticity and size. The map for Alzheimer's patients contain three disorganized clusters. Reprinted from Chan et al. (1993). An assessment of the semantic network in patients with Alzheimer's disease. Journal of Cognitive Neuroscience, S, 254-261, with permission of MIT Press.

Tests of episodic and semantic memory generally require that prior episodes or events, or previously acquired knowledge, be explicitly and consciously recollected. However, recent research indicates that some forms of learning and memory occur implicitly, without conscious recollection. This implicit knowledge is expressed indirectly throughout the performance of the specific operations comprising a task. Classical conditioning, lexical and semantic priming, motor skill learning, and perceptual learning have all been considered forms of implicit memory. In all of these instances, individual's performances are facilitated "unconsciously" by the prior exposure of stimulus material. As is the case for episodic and semantic memory, the distinction between explicit and implicit memory receives neurobiological and neuropsychological support from studies of patients with amnesia. Severely amnesic patients are impaired on tests of explicit memory, but perform normally on implicit memory tests. For example, amnesic patients can acquire and retain motor skills (e.g., playing a series of notes or tune on a piano) without any memory for the training experiences. Similarly, amnesic patients will often evidence decreased visual identification thresholds for previously presented words they cannot recall or rec-

38

Alzheimer's Disease

C. Language

ognize on explicit memory tests. It is presumed that the initial visual presentation of the words activated some unconscious trace that later facilitated the visual identification of the stimuli without affecting conscious attempts to recollect the materials. Although the specific neurological substrates of explicit memory have been extensively described, little attention has been given to the brain structures responsible for various forms of implicit memory. While damage to the mesial region of the temporal lobes, the medial diencephalon, and the basal forebrain all result in severe impairments in explicit memory, little is known about the brain structures that mediate various forms of verbal and pictorial priming and skill learning. However, recent studies of the performances of Alzheimer's and Huntington's patients on lexical and pictorial priming as well as on skill-learning tasks have resulted in some new insights into this neuropsychological issue. The findings emanating from these studies have indicated that Alzheimer's and Huntington's patients matched for overall level of cognitive decline can be dissociated with implicit memory tasks that involve the priming of semantic knowledge and the initiation of central motor programs. This double dissociation suggests that portions of the association cortex and the basal ganglia mediate quite different forms of implicit memory. More specifically, the association cortices, which are damaged in Alzheimer's disease, appear to be vital for implicit tasks that seem to rely upon the integrity of semantic knowledge, whereas the basal ganglia, which are damaged in Huntington's disease, are most important for implicit tasks that involve the generation and modification of central motor programs to guide behavior.

Deficits in some aspects of language increase in severity throughout the course of Alzheimer's disease. Certain language abilities tend to remain intact, however. Patients exhibit little impairment in articulation abilities, and they also have little of the severe grammatical deficits seen in other neurological disorders, such as Broca's aphasia. With relatively few phonetic and syntactic deficits, the fluency of patients' spontaneous speech and oral reading typically remain intact. In the later stages of the disease, some patients have difficulty producing complex syntax in spontaneous speech. Similarly, patients' auditory comprehension of complex sentences with abstract components may become impaired as dementia increases in severity. Difficulty with word finding is seen early in Alzheimer's patients, although usually not as early as memory deficits. Patients experience a progressive anomia directly evident on tests of confrontation naming, such as the Boston Naming Test. Patients often circumlocute as they search for particular targets. They also make semantic errors, as described earlier, such as providing picture names that are actually the categories to which pictures belong (e.g., saying "bird" for the target "pelican") and providing names for pictures that are meaningfully associated to the target (e.g., saying "sweeping" for the target "broom"). Alzheimer's patients also exhibit semantic deficits on tests of category fluency. This is a disproportionately severe fluency impairment exhibited by patients when generating exemplars from a specific category compared to generating words that begin with a particular letter.

B. Attention/Concentration

D. Spatial Cognition

In addition to memory deficits, patients with Alzheimer's disease also experience deficits in attentional and concentration abilities. It has been hypothesized that impairment in working memory results in difficulty maintaining attention to complex or shifting sets. In fact, subtle impairments in the earliest stages of AD may be seen on complex attentional tasks depending upon divided and shifting attention. Some patients in the early disease stages do not have attentional problems, but such deficits typically emerge and increase in severity as the disease progresses.

Impairments in spatial cognition are evident in some patients with mild Alzheimer's disease, and in nearly all patients in the later stages of the disease. Degeneration of the parietal lobe is the likely cause of these deficits. Early in the disease, patients experience a more severe and progressive disorientation in space relative to time. This results in the wandering behavior and confusion about location seen frequently in patients. Spatial disorientation appears to be a result of combined impairment in both memory and visuospatial skills.

39

Alzheimer's Disease

E. Executive Function

o) pt 2119" DAT (command)

b) pt 2232: DAT (cornmond)

Although patients are typically aware of their earliest symptoms, such as memory problems, there is an increasing loss of insight as Alzheimer's disease progresses. Gradually patients are unable to recognize their cognitive impairments and to judge the quality of their own behavior. In addition, preservations and intrusions are evident in patients' daily behavior early in the disease. Progressive decline in patients' executive function is also seen in their ability to think abstractly and to solve problems, with deficits occurring early in the course of the disease.

IV. AFFECTIVE AND PERSONALITY CHANGES c) pt 2179: DAT (cornmond)

d) pt 2179" DAT (copy)

Figure 8 Examples (a) and (b) depict conceptual errors in the clock drawings of patients with Alzheimer's disease (DAT).Examples (c) and (d) represent a single patient's attempts to draw the clock to command (c) and to copy (d). Reprinted from Rouleau et al. (1992). Quantitative and qualitative analyses of clock drawings in Alzheimer's and Huntington's disease. Brain & Cognition, 18, 70-87, with permission of AcademicPress.

A progressive decline in drawing ability is also characteristic of patients with Alzheimer's disease. An early onset of impairment is often seen on complex tasks. For example, patients are significantly impaired compared to healthy older adults when asked to draw a clock or when copying complex geometric designs such as the Rey-Osterrieth Complex Figure. In their drawings, patients tend to make more omission, confabulatory, and perseverative errors, and when drawing a clock AD patients often make conceptual errors (see Fig. 8). Finally, qualitative differences in the types of errors made on tests of visuoperceptive ability may help differentiate normal aging from patients in the early stages of Alzheimer's disease.

Personality changes represent one of the most common alterations in Alzheimer's disease, affecting upward of 75% of patients at some time during the course of the disease. Changes can vary widely in a number of ways such as disengagement or disinterest in one's surroundings, disinhibition or inappropriate social behavior, psychosis, delusions, or other disruptive behaviors. Affective changes can occur as well. Although major depression is uncommon, dysphoric affect can occur with some regularity in Alzheimer's disease (e.g., 50% report symptoms of sadness or demoralization), and anxiety is reported in approximately 50% of patients as well. Hallucinations, which occur in approximately 25 % of Alzheimer's cases, are typically visual or auditory in nature, although gustatory, olfactory and haptic hallucinations have also been reported. Delusional preoccupation is not uncommon either. For example, "capgras syndrome," in which the individual believes that his or her family member has been replaced by an imposter, represents one of the most common types of delusional disturbances. Finally, agitation is also one of the most frequently cited symptoms in patients (up to 75 %), which creates tremendous burden for caregivers. In sum, abnormal behaviors as a consequence of affective or personality changes in Alzheimer's patients are quite common and typically give rise to more caregiverrelated burden than do the cognitive sequelae.

40

Alzh'eimer's Disease

V. DIFFERENTIATIONOF ALZHEIMER'S DISEASE FROM OTHER ETIOLOGIES A. Alzheimer's Disease Versus Normal Aging Individuals in the early stages of Alzheimer's disease are by definition impaired in two or more cognitive functions, although the most effective neuropsychological measures for distinguishing between these subjects and healthy older individuals are those that assess the ability to learn new information and retain it over time. For example, in direct comparisons of the effectiveness of measures of learning, retention, confrontation naming, verbal fluency, and constructional ability for differentiating between very mildly demented patients with probable AD and normal elderly individuals, a number of studies have demonstrated the highest diagnostic accuracy (approximately 90%) with delayed free recall measures. Similar results have also been obtained with confirmation by subsequent postmortem histopathologic evidence of Alzheimer's disease in patients who were psychometrically classified as mildly impaired and in none of those classified as normal elderly. Although measures of learning and retention are the most effective neuropsychological indices for differentiating between mildly demented and normal elderly individuals, measures of language, "executive" functions, and constructional abilities also have some diagnostic value. For example, performances of mildly demented patients with probable Alzheimer's disease and normal elderly control subjects on several types of verbal fluency tasks demonstrate that the semantic category fluency task has greater than 90% sensitivity and specificity for the diagnosis of dementia. Similarly high sensitivity and specificity rates for the differentiation of normal older adults from those patients with Ad has been shown on tests of executive function such as the Stroop Color-Word test, Trailmaking, and on a modified version of the Wisconsin Card Sorting Task. In addition to detecting subtle cognitive impairment in the early stages of a dementing illness, neuropsychological testing is important for tracking the progression of cognitive decline throughout the course of the disease. Several studies have shown that brief, standardized mental status examinations can effectively document general cognitive decline. Nevertheless, despite the effectiveness of mental status examinations

for assessing general cognitive decline, comprehensive neuropsychological testing is often required to track the progression of dementia, particularly when it is necessary to detect changes in specific cognitive domains, or to evaluate the efficacy of a potential treatment. A number of studies have shown that tests of memory and other neuropsychological functions are sensitive to the cognitive decline that occurs between the mild and moderate stages of dementia severity. However, these studies have also shown that neuropsychological measures other than memory are most effective in this regard. Because even mildly demented patients often have severe memory deficits that result in near floor performance on tests of free recall, measures of recognition memory, verbal fluency, confrontation naming, and praxis may be better studied for staging dementia severity or tracking its progression.

B. Alzheimer's Disease versus Depression A continuing problem for health care professionals involves the diagnosis of older adults who present with signs of both cognitive impairment and depression. In these individuals, a determination must be made whether the patient is experiencing cognitive difficulty secondary to a mood disorder or whether the patient has developed a depressive syndrome secondary to a dementing illness such as Alzheimer's disease. Kaszniak and Christenson (in Storandt and VandenBos) highlight that research findings concerning neuropsychological test performance of patients with depression and cognitive impairment remains small and difficult to interpret. The "dementia syndrome of depression" likely represents a heterogeneous mixture of different patient groups. Some of these patients may have a combination of a primary dementing illness and depression, and they will remain cognitively impaired following effective treatment of their depression. Others may have cognitive impairment secondary to their depression and will demonstrate improvement of both cognition and mood following effective treatment. However, even among this second group, some patients may manifest a clear progressive dementia over time despite initial improvements in mood. Thus, it is not surprising to find that depressed patients form clusters of different patterns of performance on various neuropsychological tests, such as the California Verbal Learning Test. In reviews of the research literature relevant to differentiation of dementia from

41

Alzheimer's Disease

Table V

C. Alzheimer's Disease versus Subcortical Dementia

Qualitative Features in Neuropsychological Test Data that are Helpful in Differentiating Alzheimer's Disease from Dementia Syndrome of Depression

Measure

Alzheimer's Disease

Dementia Syndrome of Depression

Recognition memory

Impaired

Relatively intact

False positive recognition memory errors "Don't know" errors (controversial) Performance on "automatic" encoding tasks Effort in attempting to perform tasks

Greater

Fewer

Unusual

Usual

Impaired

Intact

Good

Poor

Performance on tasks of similar difficulty

Consistent

Variable

Semantic organization

Unhelpful

Helpful

Prompting

Less helpful

Helpful

Awareness of impairment

Impared

Intact

Note. From Kaszniak VandenBos, 1994.

&

Christenson,

in Storandt

&

depression (see Kaszniak and Christenson), attempts have been made to determine those quantitative and qualitative aspects of neuropsychological test performance that may be helpful in this diagnostic task. Those features most frequently identified by these authors are listed in Table V. Kaszniak and Christenson caution that these neuropsychological test features should be viewed as guidelines for increasing or decreasing suspicion of a patient having Alzheimer's disease versus the dementia syndrome of depression, rather than as providing definitive diagnoses. Recent research suggests that differentiating patients with dementia syndrome of depression from those with vascular dementia due to subcortical infarctions, or other subcortical dementias, may be particularly difficult. Investigators have found that, among a group of depressed patients, the California Verbal Learning Test revealed a subgroup demonstrating the same pattern of deficits as those seen in patients with Huntington's disease, which is typically regarded as a prototypical subcortical dementing illness. [See DEPRESSION.]

A considerable amount of recent research has been directed toward identifying the pattern of cognitive changes that might distinguish between Alzheimer's disease and dementia associated with other neurodegenerative diseases. Much of this research has been carried out within the framework of a "corticalsubcortical" distinction, which holds that different patterns of primary neuropsychological deficits are associated with neurodegenerative diseases that predominately involve regions of the cerebral cortex (e.g., Alzheimer's disease, Pick's disease) or that have their primary locus in subcortical brain structures (e.g., Huntington's disease, Parkinson's disease, progressive supranuclear palsy). Studies that address this distinction usually compare and contrast neuropsychological test performance of patients with AD (a prototypical cortical dementia) and that of patients with Huntington's disease (a prototypical subcortical dementia) (see Table VI). In addition to these differences in the general neuropsychological features of Alzheimer's disease and dementia associated with Huntington's disease, numerous studies utilizing concepts and experimental procedures of cognitive psychology suggest that there is a fundamental difference in the nature of the memory impairment that occurs in each disorder. AlzTable VI Neuropsychological Features Associated with Cortical and Subcortical Dementia Cortical Dementia (e.g., Alzheimer's Disease) 9Failure in storage (amnesia) 9Severe retrograde amnesia 9Rapid forgetting 9Impaired recall and recognition memory 9Numerous intrusion errors 9Deterioration of semantic knowledge 9Intact skill learning

Subcortical Dementia (e.g., Huntington's Disease) 9Retrieval deficit (forgetfulness) 9Mild-to-moderate retrograde amnesia 9Relatively normal rate of forgetting 9Relatively normal recognition memory 9Few intrusion errors 9Intact structure of semantic knowledge 9Impaired skill learning

Note. Adapted from Butters, Salmon, & Butters, in Storandt & Vandenbos, 1994.

2

............... Alzheimer's Disease

heimer's patients exhibit a severe deficit in episodic memory (i.e., temporally dated autobiographical episodes that depend upon contextual cues for their retrieval) that appears to result from ineffective consolidation (i.e., storage) of new information, whereas the memory disorder of Huntington's patients is thought to result from a general difficulty in initiating a systematic retrieval strategy when recalling information from either episodic or semantic memory (i.e., overlearned facts and concepts that are not dependent on contextual cues for retrieval). Although Huntington's patients also exhibit difficulty in learning and recalling information on free recall tasks, evidence of a general retrieval deficit is provided by a marked improvement in their performance when memory is tested with a recognition format, and by their ability to retain information over a delay in near normal fashion, quite unlike that of AD patients (see Fig. 6). Patients with cortical and subcortical dementia syndromes can also be differentiated by their performances on tests of remote memory. Several studies indicate that in early stages of DAT, remote memory loss is temporally graded with memories from the distant past (i.e., childhood and early adulthood) better remembered than memories from the more remote past (i.e., mid and late adulthood). In contrast, patients with Huntington's disease or Parkinson's disease suffer only a mild degree of retrograde amnesia that is equally severe across all decades of their lives. These results suggest that the remote memory deficit of patients with subcortical dementia is another reflection of a general retrieval deficit that equally affects recollection of information from any decade of their lives, whereas the temporally graded remote memory loss of Alzheimer's patients is indicative of a failure to adequately consolidate information through repeated processing, rehearsal, or re-exposure. In addition to their distinct patterns of performance on tests of episodic and remote memory, patients with cortical and subcortical dementia syndromes differ markedly with regard to presence and severity of language deficits. AD patients, for example, are noted for mild anomia and word-finding difficulties in spontaneous speech, and evidence suggests that this deficit is indicative of a loss of semantic knowledge and a breakdown in the organization of semantic memory. In contrast, patients with Huntington's disease generally retain their language abilities. For example, these patients perform at near normal levels on tests of con-

frontation naming, and the errors they produce are often visuoperceptually based rather than semantically based. Although Huntington's patients perform poorly on tests of verbal fluency, they are equally impaired regardless of the semantic demands of the task, suggesting that their poor fluency performance is more likely to be related to their general deficiency in initiating an effective retrieval strategy than to a true language deficit. Another major distinction that can be drawn between patients with cortical and subcortical dementia syndromes is the different patterns of spared and impaired abilities they exhibit on various implicit memory tasks. Implicit memory has been described as being mediated by a distinct memory "system" independent from the conscious, episodic memory system. Neuropsychological and neurobiological evidence for this distinction is provided by numerous studies that have demonstrated preserved implicit memory in patients with severe amnesia arising from damage to hippocampal formation or to diencephalic brain regions. Studies comparing patients with cortical and subcortical dementia on various priming tasks have shown that Alzheimer's patients, but not Huntington's patients, are significantly impaired on lexical, semantic, and pictorial priming tests. In contrast to the priming results, Huntington's patients, but not Alzheimer's patients, are impaired on motor skill learning, prism adaptation, and weight biasing tasks that involve generation and refinement (i.e., learning) of motor programs to guide behavior.

VI. CLINICAL MANAGEMENT OF ALZHEIMER'S DISEASE A. Management of Behavioral Disturbances Alzheimer's patients experience a variety of behavioral disturbances, which place great demands on caregivers in finding ways to effectively manage them. Psychiatric symptoms, wandering, and aggressive behaviors, ranging in severity, are common in patients. Patients may also become frustrated with their own impairments, for example, when trying to communicate or remember things. More severe changes in behavior are evident in the later stages of the disease, when patients are no longer able to handle their daily

43

Alzheimer's Disease

functioning needs, like eating, bathing, and toileting. Management of these behavioral symptoms is often attempted by teaching caregivers behavioral modification techniques. Simplifying the stimulation available in patients' environments, offering frequent reminders and reassurances, abiding by a consistent routine, and providing patients with enjoyable activities also help to keep the patient comfortable and content. To aid in coping with the stress of managing these symptoms, support groups for caregivers of Alzheimer's patients are available nationwide. Because the responsibilities of caregiving for patients with AD are so great, however, the services offered by nursing homes often provide care for patients whose families are unable to handle the tasks on their own.

B. Pharmacologic Treatment Psychotropic medications may be used to manage behavioral disturbances in Alzheimer's patients. Antipsychotic drugs, such as Haldol, can minimize delusions, hallucinations, and agitation experienced by patients. Antidepressants, like Prozac, are used to improve patients' moods and energy level. Valium and other anti-anxiety medications are prescribed to manage agitation and anxiety. Unfortunately, many psychiatric medications can also further compromise cognitive functioning, especially those with strong anticholinergic properties. Recent research has focused on testing medications that may slow the progression of Alzheimer's disease. Tetrahydroaminoacridine (THA), or Cognex, is a drug that purportedly suppresses the breakdown of acetylcholine in the hopes of slowing patients' cognitive decline. Unfortunately, Cognex, the first drug approved for the treatment of Alzheimer's disease, has not appeared to be clinically effective in the majority of patients for whom it is prescribed. Other current research is focusing on the role of neurotrophic factors, estrogen, calcium, and antioxidants in the progression of Alzheimer's disease.

VII. SUMMARY Alzheimer's disease is the most common cause of dementia, currently affecting nearly 4 million people in the United States. Estimates project that its prevalence will rise to approximately 14 million by the year 2050. Whether one views AD from an individual, family, or

public health perspective, its devastating consequences will continue to escalate and affect us either directly or indirectly in many ways. In short, Alzheimer's disease will increasingly become the dominant disorder in late life. Cognitive changes associated with this dementia include progressive impairments in memory, attention, language, spatial cognition, and executive function, some of which occur in the earliest stages of the disease. Patients also experience changes in behavior, affect, and personality. The cognitive, behavioral, and affective changes result in an increasing dependency of Alzheimer's patients on others in their day-to-day functioning. The disease is characterized by a number of neuropathological changes, including the presence of neurofibrillary tangles and neuritic plaques, loss of neurons and synapes, neocortical atrophy, and alterations in neurotransmitter levels. A definitive diagnosis can be made only at autopsy or with a brain biopsy, upon detection of sufficient numbers of neurofibrillary tangles and neuritic plaques. As no effective treatment or cure for Alzheimer's disease is currently available, strategies for the management of disease symptoms focus on behavioral modification and the use of psychiatric medications where appropriate. Fortunately, sustained efforts on a number of research fronts (i.e., molecular biological, genetic, cognitive, and behavioral) have helped to improve our understanding of Alzheimer's disease and ultimately may lead to effective treatments for the prevention and cure of this complex and devastating disease.

ACKNOWLEDGMENTS Preparation of this chapter was supported in part by funds from the National Institute on Aging (AG12674) and the Medical Research Service of the Department of Veterans Affairs.

BIBLIOGRAPHY American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author. Birren, J. E., Sloane, R. B., & Cohen, G. D. (Eds.). (1992). Handbook of mental health and aging. San Diego: Academic Press. Craik, F. I. M., & Salthouse, T. A. (Eds.). (1992). The handbook of aging and cognition. Hillsdale, NJ: Lawrence Erlbaum Associates. Cummings, J. L., and Benson, D. F. (1992). Dementia: A clinical approach (2nd ed.). Boston: Butterworth-Heinemann. Grant, I., & Adams, K. M. (Eds.). (1996). Neuropsychological as-

44

Alzheimer's Disease

sessment of neuropsychiatric disorders (2nd ed.). New York: Oxford University Press. La Rue, A. (1992). Aging and neuropsychological assessment. New York: Plenum. Parks, R. W., Zec, R. F., and Wilson, R. S. (Eds.). (1993). Neuropsychology of Alzheimer's disease and other Dementias. New York: Oxford University Press. Rapoport, S. I., Petit, H., Leys, D., & Christen, Y. (Eds.). (1990).

Imaging, cerebral topography, and Alzheimer's disease. Berlin: Springer-Verlag. Storandt, M., & VandenBos, G. R. (Eds.). (1994). Neuropsychological assessment of dementia and depression in older adults: A clinician's guide. Washington, DC: American Psychological Association. Terry, R. D., Katzman, R., & Bick, K. L. (Eds.). (1994). Alzheimer disease. New York: Raven Press.

j Amnesia John F. Kihlstr0m* and Elizabeth L. Glisky University of Arizona

I. II. III. IV. V. VI.

The Amnesic Syndrome Traumatic Retrograde Amnesia Functional Amnesias Amnesia through the Lifespan Amnesias of Everyday Experience Theoretical and Practical Implications

riences occurring in the first 5 - 7 years of life. Infantile amnesia commonly covers the period before language and speech develop. Posthypnotic Amnesia A retrograde amnesia induced by means of hypnotic suggestion; it may be canceled by a prearranged reversibility cue. Transient Global Amnesia A benign and temporary amnesia characterized by sudden onset, apparently caused by momentary vascular insufficiencies affecting brain tissue. Traumatic Retrograde Amnesia A retrograde amnesia resulting from a concussive blow to the head; most of the affected memories are eventually recovered, except for a "final RA" affecting the accident itself.

Alcoholic Blackout Amnesia without loss of consciousness, in which the intoxicated person retains the ability to perform certain "automatized" behaviors without any subsequent memory for the episode. Amnesia A special case of forgetting in which the memory loss is greater than would be expected under ordinary circumstances. Anterograde amnesia affects memory for events occurring after the instigating event; retrograde amnesia affects memory for events occurring before the instigating event. Amnesic Syndrome A profound deficit in learning and memory usually associated with bilateral damage to the diencephalon or to the medial portions of the temporal lobe. It always involves an anterograde amnesia and may involve a retrograde amnesia as well. Functional Amnesia A significant loss of memory attributable to an instigating event, usually stressful, that does not result in insult, injury, or disease affecting brain tissue. Its most common forms are psychogenic amnesia, psychogenic fugue, and multiple personality disorder. Infantile and Childhood Amnesia An amnesia observed in adults, affecting memory for personal expe-

AMNESIA may be defined as a special case of forgetting, in which the loss of memory is greater than would be expected under ordinary circumstances. A head-injured patient is no longer able to learn things that he was once able to master easily; a patient with psychogenic fugue loses her identity as well as her fund of autobiographical memories. Amnesia includes frank pathologies encountered in neurological and psychiatric clinics, such as Korsakoff's syndrome, Alzheimer's disease, traumatic retrograde amnesia, and multiple personality disorder. But it also includes abnormalities of memory observed ubiquitously, such as infantile and childhood amnesia, the exaggerated forgetfulness associated with healthy aging, and the memory failures associated with sleep and general anesthesia. These naturally occurring pathologies of

*John F. Kihlstrom is presently at the Universityof California, Berkeley.

45

Copyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

46

Amnesia

memory have their counterparts in amnestic states induced in otherwise normal, intact individuals by means of experimental techniques, such as electroconvulsive shock in laboratory rats and posthypnotic amnesia in college sophomores. Experimental research on memory began with the publication of Ebbinghaus' Uber das Gedachtniss in 1885, but the clinical description of amnesia dates from even earlier. Korsakoff described the amnesic syndrome that bears his name in 1854. And in 1882 Ribot published Les Maladies de la memoire, with a detailed description of the consequences for memory of brain insult, injury, and disease, as well as a theory of memory and amnesia. On the basis of his observations, and Hughlings Jackson's principle that ontogeny recapitulates phylogeny, he concluded that brain disorder produces a progressive loss of memory that affects memories in the reverse order of their development. Thus, in traumatic retrograde amnesia, memories for events occurring immediately before the accident are most likely to be lost. This principle, now known as Ribot's Law, does not always hold, but it was an important first step in the journey from clinical description to scientific theory. For reasons that are not completely clear, clinical and experimental study of amnesia languished for the first half of the 20th century, but was revived by Talland's 1965 monograph Deranged Memory, which reported an extensive psychometric and experimental study of patients with Korsakoff syndrome. Talland's work ushered in a new age of research in which clinicians and experimentalists joined forces under the banner of cognitive neuropsychology~a discipline that attempts to integrate evidence obtained from the intensive study of brain-damaged patients with theories of normal cognitive function. In this article, we provide a summary of this research, as it pertains to the major disorders of memory~pathological and normal, natural and artificial~and discuss the role of this research in the contemporary psychology of memory.

I. THE AMNESIC SYNDROME The amnesic syndrome represents a profound deficit in learning and memory; it is by far the most commonly studied pathology of memory. Its characteristic

feature is a gross anterograde amnesia (AA), meaning that the person cannot remember events that have occurred since the time of the brain damage. Short-term memory (as measured by digit span, for example) is unimpaired; but after even a few moments' distraction, these patients cannot remember what they have said or done, or what has been said or done to them, just recently. In the classic cases, the patient's cognitive deficits are specific to long-term memory: general intelligence, perception, reasoning, and language functions are spread. But this anterograde amnesia is associated with several different etiologies, and careful examination indicates that these disparate origins are associated with somewhat different patterns of memory and cognitive deficit. One form of the amnesic syndrome, now known as diencephalic amnesia, was first described by Korsakoff in association with alcoholism. At the time, chronic alcoholics frequently suffered from a deficiency of vitamin B~ (thiamine) which results in bilateral damage to structures of the diencephalon, including the upper portion of the brainstem, the mammillary bodies, the dorsomedial nucleus of the thalamus, and the mammillothalamic tract (unilateral lesions produce "material-specific" amnesias for verbal or nonverbal memories, depending on which hemisphere is damaged). Although this disease is now effectively prevented by the introduction of vitamin-enriched commercial foods, other etiologies, including vascular insufficiencies, tumors, and fronto-temporal brain damage can have similar effects. These patients typically show a retrograde amnesia (RA) as well as AA, meaning that they also have difficulties in remembering events from their premorbid life, especially those from the years immediately preceding their disease. Remote memory, such as for childhood events, is apparently preserved. Note that such a pattern conforms to Ribot's Law. Another form of amnesic syndrome, known as temporal lobe amnesia, stems from bilateral lesions in the medial portion of the temporal lobe, and especially the hippocampus, entorhinal cortex, and surrounding structures (again, there are also material-specific amnesias resulting from unilateral damage to these structures). The most famous case is Patient H. M., who displayed a profound AA after surgical resection of his medial temporal lobes, including the hippocampus, in a desperate attempt to relieve intractable epileptic seizures. Other cases have been caused by brain tumors,

.

.

.

.

.Amnesia

ischemic episodes, head trauma, and herpes encephalitis. Temporal-lobe patients always show AA; when they show RA, it is not always as extensive as in diencephalic patients. There is also a frontal-lobe amnesia, which is qualitatively different from the amnesic syndrome. Frontallobe patients are not globally amnesic, but they frequently show deficits on tasks requiring memory for temporal order, as well as memory for the source of newly acquired knowledge. They also lack metamemory capabilities~they have little appreciation of the contents stored in their own memories, or in the availability of appropriate memory strategies. Patients who have frontal damage in addition to diencephalic or medial-temporal lobe damage experience their greatest difficulties on memory tasks requiring strategic planning and organization. Finally, transient global amnesia is a temporary (typically lasting several hours) condition characterized by sudden onset. It closely resembles the permanent diencephalic and medial~temporal lobe amnesias, in that it involves both AA and RA, but, as its name implies, it is brief. The condition, while frightening, is benign: after remission, there are no signs of permanent brain damage (and little risk of another episode in the future). Transient global amnesia appears to be caused by temporary vascular insufficiency affecting brain tissue; interestingly, many cases appear in association with physical exertion or mental stress. In the absence of permanent brain damage, something akin to the amnesic syndrome may be observed in cases of alcoholic blackout. Blackout involves amnesia without loss of consciousness. The intoxicated individual may engage in conversation or perform other actions normally, but after regaining sobriety, he or she will have no memory for the episode. Blackouts are most commonly observed in chronic alcoholics, though they do occur to nonalcoholics who are severely intoxicated. In any case, blackout is most likely to occur when the person ingests large quantities of alcohol rapidly, especially when fatigued or hungry. Alcohol folklore suggests that the amnesia is an instance of state-dependent retrieval~that the memories return when the person resumes drinking. However, laboratory research clearly indicates that the memories covered by blackout are unrecoverable, and thus that the amnesia reflects an encoding deficit.

.

47

Sedative drugs, such as the barbiturates and benzodiazepines, also produce irreversible AA. The different patterns of task performance offer clues about the nature of the memory deficit in the amnesic syndrome. In principle, any instance of forgetting may be attributed to a failure at one or more of three stages of memory processing: encoding (the creation of a memory trace of a new experience), storage (the retention of trace information over time), and retrieval (the recovery of trace information for use in ongoing experience, thought, and action). Logically, a syndrome that affects memory for postmorbid but not premorbid events is most likely due to encoding failure. And, in fact, it has been suggested on the basis of laboratory experiments with lesioned rats and monkeys that the hippocampus and other structures in the medial-temporal lobe mediate that consolidation and storage of new memories. An alternative formulation assumes that representations of the various elements of an event are distributed widely in the cortex, and that the hippocampus creates a "cognitive map" to index and bind them together. In either case, the occurrence of AA means that the hippocampus is crucial for memory formation, even though the memories themselves are not stored there. What about the RA? Some degree of RA is usually, but not always, observed in the amnesic syndrome. Logically, damage to a structure that consolidates and organizes new memories should have no effect on old memories. In some cases, RA may reflect the disruption of premorbid memories that were incompletely consolidated at the time of disease onset; this would produce a temporal gradient, but the extent of RA observed would seem to imply that proper consolidation requires weeks, months, or years instead of seconds, minutes, or hours. On the other hand, if the hippocampus serves a binding and indexing function, its destruction will create an RA by effectively preventing the retrieval of memories that remain available in storage; this would produce an amnesia for remote as well as recent memories and would not necessarily produce a temporal gradient. Finally, in some cases what appears as RA may in fact be AA, reflecting the slow onset of an insidious disease process and producing the appearance of a temporal gradient; this suggestion is particularly plausible in the case of diencephalic amnesia associated with chronic alcohol abuse, but cannot account for amnesias of sudden onset.

48

Amnesia

The nature of RA in the amnesic syndrome remains unresolved. In the final analysis, it is important to remember that in real life outside the laboratory, pure cases of amnesic syndrome are exceedingly rare. Patients may suffer primary damage to one area, but collateral damage to another, and the precise combination of lesions may determine the presence and extent of RA. Even conclusions about encoding deficits must be qualified to some extent. At first glance, the AA observed in the amnesic syndrome appears to be a complete inability to acquire new information. However, closer examination indicates that certain aspects of learning and memory are spared even in the densest cases of amnesia. Thus, Patient H. M. has learned to solve the Tower of Hanoi puzzle, but he does not recognize the puzzle as familiar. Amnesic patients who study the word ELATED do not remember it just minutes later; but when presented the stem ELA- and asked to complete it with the first word that comes to mind, they are more likely to produce ELATED (as opposed to ELASTIC or ELABORATE) than would be expected by chance. The ability of amnesic patients to acquire cognitive and motor skills, and to show priming effects in word-stem completion, shows that they are able to acquire new information through experience, although, somewhat paradoxically, they are not aware that they possess this knowledge. The limits of such learning are still being studied, but already they have motivated a distinction between two expressions of episodic memory, explicit and implicit. Explicit memory (EM) refers to the conscious recollection of a previous episode, as in recall or recognition. By contrast, implicit memory (IM) refers to any change in experience, thought, or action that is attributable to such an episode, such as skill learning or priming. The dissociation between EM and IM in amnesic patients indicates that some forms of learning and memory are preserved. According to one view, amnesics suffer from a specific inability to encode declarative knowledge about specific events, but retain an ability to acquire procedural (or other nondeclarative) knowledge. This would account for their ability to acquire new cognitive and motor skills. Preserved priming has been attributed to the automatic activation of declarative knowledge structures that were stored prior to the brain damage, or to the encoding of new episodic representations in a primitive perceptual memory system that lacks the kinds of in-

formation (e.g., about the meaning of an event, or its spatiotemporal context) that would support EM.

II. TRAUMATIC RETROGRADE AMNESIA Another form of amnesia occurs as a consequence of head trauma. A very severe blow to the head can bruise gray matter and shear white matter, producing both cortical and subcortical damage that may result in AA and RA similar to that observed in the amnesic syndrome. Even in the absence of such damage, some blows to the head can result in a concussion or temporary cessation of electrical activity in the cortex and loss of consciousness. The recovery of consciousness begins with the return of simple reflexes, then the gradual return of purposeful movement, and then speech (this pattern would be predicted by Ribot's Law). After the victim appears fully oriented, he or she will display an AA for some time, as well as an RA for the accident itself and the events leading up to the accident. Typically, the AA is immediate, i.e., it will start at the time of the trauma. But if the loss of consciousness is delayed, the onset of the AA will be delayed as well. Such lucid intervals suggest that the AA is a result of vascular complications that may take some time to develop. The RA is characterized by a temporal gradient, meaning that it is densest for events nearest the time of the accident--another example of Ribot's Law at work. However, the gradient is broken by islands of memory consisting of isolated events, not necessarily personally important, that are remembered relatively well. The extent of the RA is correlated with the extent of the AA. Although the memories covered by the AA are permanently lost, apparently reflecting an encoding deficit, the RA gradually remits. It was once thought that this recovery began with the earliest memories and proceeded forward, which again would be predicted by Ribot's Law. Although the most recent events are generally recovered last, more careful studies show that the shrinkage of amnesia is accomplished by filling in the gaps that surround the islands of memory, leaving a final RA covering the accident itself and the moments or minutes leading up to it, and perhaps a few islands of amnesia. The shrinkage of amnesia clearly indicates that traumatic RA is a disorder of retrieval, and that the islands of memory act as anchors to support the recovery process. However,

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Amnesia

the final RA may reflect either a loss of memory from storage or more likely a disruption of consolidation. A nontraumatic form of retrograde amnesia is observed in psychiatric patients who are administered electroconvulsive therapy (ECT) for acute affective disorder. In ECT, electrical stimulation (e.g., 100 V, 500 mA for 500 msec), delivered from surface electrodes applied over the temporal lobe, induces a convulsive, tonic-clonic seizure not unlike those of grand mal epilepsy; after a short series of such treatments (e.g., 6 - 1 0 sessions over 2 - 3 weeks), patients often experience a rapid return to their normal mood state (ECT is not a cure, as episodes of depression or mania may recur). Because they are anesthetized when the treatment is delivered, patients experience no pain or distress from the convulsions themselves; because they receive muscle relaxants, the convulsions do not result in bone trauma. However, the seizure does produce both AA and RA as adventitious consequences (i.e., unrelated to treatment success). The RA shows the same sort of temporal gradient observed following concussive blows to the head. Because there is less memory impairment (though no difference in treatment outcome) with unilateral than with bilateral electrode placement, ECT is usually delivered to the nondominant hemisphere. The RA gradually clears up (except for the moments before ECT is actually delivered), but memories affected by the AA cannot be recovered. The amnesia induced by ECT shows a dissociation between EM and IM similar to that observed in the amnesic syndrome. In one experiment, patients who studied a list of words within 90 minutes following administration of ECT showed a deficit in recognition, but no deficit in priming on a word-stern completion test. In another study, patients who read word strings presented in mirror-reversed fashion before delivery of ECT later showed an advantage in reading those words, even though they failed to recognize these words as familiar. What about the memories covered by the final RA? Although electroconvulsive shock may disrupt encoding processes, it does not appear to remove the memory traces from storage. The relevant evidence comes from studies of the effects on memory of electroconvulsive shock (ECS) administered to animals. A common research paradigm is called one-trial, step-down, passive avoidance learning. A rat is placed on a shelf above an electrified floor. If the animal steps down, it

receives a footshock and jumps back up on the shelf. Under ordinary circumstances, the animal will not return to the floor; it learns in one trial to avoid the shock by doing nothing. But in the experiment, the animal received a dose of ECS similar to that delivered to patients in ECT. After the animal recovers, it steps down onto the floor after being placed on the shelf-as if it has forgotten all about the shock. ECS-induced amnesia shows a temporal gradient similar to that observed in other forms of traumatic retrograde amnesia. If the ECS is delayed from the time of the original learning experience, there is less amnesia than if it is administered immediately afterward. But the extent of amnesia also depends on how memory is measured. The amnesic animal steps down immediately, as if the footshock never happened. At the same time, it shows a marked increase in heart rate. Moreover, if the animal receives reminder treatments, such as tail shock in another environment or immersion in circulating ice water, it will remain on the shelf and avoid the floor. The desynchrony between behavioral and psychophysiological indices of fear is analogous to the dissociation between EM and IM observed in human amnesic patients; and the effectiveness of reminder treatments shows that at least some aspects of the forgotten event have been preserved. Memories covered by the final RA may never be accessible to conscious recollection, but they may nonetheless be expressed as implicit memories.

III. FUNCTIONAL AMNESIAS Clinically significant amnesias are not confined to cases of organic brain syndrome. Psychiatrists and clinical psychologists also encounter forms of functional amnesia in a group of mental illnesses known as the dissociative disorders. Functional amnesia may be defined as a loss of memory that is attributable to an instigating event (often, mental stress) that does not result in insult, injury, or disease to the brain. For example, victims of violent crimes such as rape, or other sorts of traumatic stress, often display an amnesia for the event itself. Although this might be an AA reflecting encoding deficits caused by high levels of arousal, there is often an RA covering the events leading up to the trauma as well--sometimes extending to a large portion of the person's life. Because there is no evidence of head injury, such memory failures are labeled

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as psychogenic amnesia. Compared to traumatic retrograde amnesia, psychogenic amnesia appears to be more extensive and longer lasting. Clinical lore holds that psychogenic amnesia can be reversed by hypnosis or barbiturate sedation, but evidence for the reliability of recollections produced by these techniques is largely lacking. [See DISSOCIATIVE DISORDERS.] Another dissociative disorder, psychogenic fugue, entails a more extensive loss of autobiographical memory, covering the whole of the person's life, a loss and/ or change in identity, and sometimes physical relocation (from which symptom the syndrome derives its name). Such cases often come to the attention of police and health providers when a person cannot identify himself; or when she comes to herself in a strange place and does not know how she got there. Interestingly, fugue patients lose self-knowledge and autobiographical memory, but they do not seem to lose their fund of semantic memory, or their repertoire of procedural knowledge. Upon recovery the patient is left with an amnesia covering the events of the fugue state itself, and retains no knowledge of whatever identity he or she may have adopted in that state. Examination of such cases after they are resolved often reveals an instigating episode of psychological stress. Multiple personality disorder (MPD), in which two or more personalities appear to inhabit a single body, alternating control over experience and action, also involves a disruption of memory and identity. One of these personalities is often "primary," in that it is the one that has been manifest the longest and known by most other people. Most important in the present context, the various personalities appear to be separated by an amnesic barrier that prevents one alter ego from gaining access to the memories of another. In many cases, the amnesia is asymmetrical, in that Personality A may be aware of Personality B, but not the reverse. The amnesia largely affects identity and autobiographical memory; as a rule, the various personalities share semantic memory and procedural knowledge in common. The most widely accepted theory of MPD holds that it develops in defense against abuse, trauma, or deprivation in early childhood. [See PERSONALITY DISORDERS.] Reports of MPD were relatively common in the clinical literature before 1920, and then virtually disappeared. There has been a resurgence of MPD, bordering on epidemic, in recent years. However, it is not

clear how many of these are iatrogenic in nature or simply misdiagnosed. Where the alternate personalities are initially elicited through hypnosis or other special techniques, or when an amnesic barrier is absent, the case is suspect. MPD is sometimes offered as an insanity defense, claiming that a second personality is actually responsible for crimes of which the first personality is accused. MPD raises interesting issues of criminal law: in principle, the actions of one personality may be outside another personality's ability to control; interpersonality amnesia may prevent the accused from assisting in the defense; and techniques intended to elicit testimony from a personality may violate constitutional safeguards against selfincrimination. However, MPD has rarely proved successful as a defense against criminal charges. There are several experimental studies that confirm the existence of interpersonality amnesia in MPD. Thus, for example, one alter ego is often unable to recall or recognize a list of items studied by another. Interestingly, there is some evidence that IM may be spared in these cases. Thus, one alter ego may show savings in relearning, interference, transfer of training, or priming effects involving a list studied exclusively by another one. Although the available research is somewhat ambiguous, in general it seems that the amnesic barrier is permeable in the case of implicit memories. Just as the amnesic syndrome finds its experimental analog in drug-induced amnesia, and traumatic retrograde amnesia in ECT and ECS, the functional amnesias seen clinically have their laboratory parallel in posthypnotic amnesia. Following appropriate suggestions and the termination of hypnosis, many subjects cannot remember the events that transpired while they were hypnotized. After the hypnotist administers a prearranged cue, the critical memories become accessible again; the fact of reversibility marks posthypnotic amnesia as a disruption of memory retrieval. The amnesia does not occur unless it has been suggested (explicitly or implicitly), and memory is not reinstated merely by the induction of hypnosis; thus, posthypnotic amnesia is not an instance of statedependent memory. Response to the amnesia suggestion is highly correlated with individual differences in hypnotizability: while hypnotic "virtuosos" typically show a very dense amnesia, their insusceptible counterparts show little or no forgetting. Like the organic amnesias, posthypnotic amnesia is

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selective. The subject may forget which words appeared on a study list, but retains the ability to use these words in speech and writing. Skills acquired in hypnosis transfer to the posthypnotic state, and suggestions for amnesia have no impact on practice effects. Subjects who learn new factual information while hypnotized may retain it despite suggestions for amnesia, but these same subjects may well forget the circumstances in which this knowledge was acquired--a phenomenon of s o u r c e a m n e s i a that has also been observed in the amnesic syndrome. Finally, there is good evidence that priming effects are preserved in posthypnotic amnesia. That is, subjects who cannot remember words from a study list are more likely to use those words as free associations or category instances than would be expected by chance. Thus, posthypnotic amnesia shows the familiar dissociation between EM and IM. Because functional amnesia occurs in the absence of brain damage, and because posthypnotic amnesia occurs in response to suggestion, questions inevitably arise about malingering, simulation, and behavioral compliance. Unfortunately, it is difficult to distinguish between genuine and simulated amnesia in either clinical or experimental situations. Claims of amnesia are readily accepted when there is palpable evidence of brain damage. It should be understood, however, that evidence of a significant interpersonal or sociocultural component does not necessarily mean that functional amnesia is faked. Rather, it means that functional amnesia is complex. Hypnosis may be a state of altered consciousness, but it is also a social interaction; thus, it should not be surprising to discover that the subject's response to amnesia suggestions will be influenced by the precise wording of the suggestion, the discourse context in which it is embedded, the subject's interpretation of the hypnotist's words, and perceived social demands. The social context is probably important in the organic amnesias, but its role is magnified in their functional counterparts.

IV. AMNESIA THROUGH THE LIFESPAN

Some forms of amnesia occur naturally in the course of psychological development. For example, adults rarely remember much from their early childhoods; the earliest memory is typically dated between the

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third and fourth birthdays, and is limited to a relatively small number of isolated fragments until about 5 or 7 years of age. The appearance of childhood amnesia is not merely an artifact of the long retention interval between childhood encoding and adult retrieval; something special seems to happen to memories for childhood events. Infantile amnesia, covering the first year or two of life, may be attributed at least in part to the lack of language and to the immaturity of the neocortex and other critical brain structures. However, the exact mechanism for childhood amnesia, covering the years after the second birthday, remains uncertain. The classic explanation for childhood amnesia was proposed by Freud. In his view, during the phallic stage of psychosexual development the child resolves the Oedipus complex by repressing infantile sexual and aggressive impulses, as well as any thoughts, images, and memories that might be related to them. Since (according to the theory) all the young child's mental life is concerned with these topics, all of early childhood is repressed~except a couple of banal s c r e e n m e m o r i e s that aid repression by giving the person something to remember. Recall that the major goal of psychoanalysis is to lift the repressive barrier so that patients can acknowledge and cope realistically with their primitive instinctual urges. Other theories emphasize the relationship between cognitive processes employed at encoding and retrieval. For example, Schachtel proposed that memories encoded by preoedipal, primary-process modes of thought cannot be retrieved by post-oedipal, secondary-process schemata. A similar account can be offered from Piaget's perspective, emphasizing the incompatibility between sensory-motor and preoperational encodings and the retrieval processes characteristic of concrete and formal operations. Note that all these theories predict that memories of childhood experience should be accessible to young children, who have not undergone the "five-to-seven shift." In contrast, some theorists have argued that young children simply do not possess the information-processing capacity~specifically, the ability to pay attention to two things at once, like an event and its episodic context~required to encode retrievable memories. In this case, the prediction is that children will know little more about their childhood histories than adults do. It should be noted that infantile and childhood amnesias affect only memories for personal experiences.

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Children acquire a vast fund of information, and a considerable repertoire of cognitive and motor skills, which they carry into adulthood. Whether this selectivity reflects merely the effects of constant rehearsal, or reveals a dissociation between EM and IM similar to that observed in the clinical amnesias, is not clear. At the other end of the life cycle, it appears that even the healthy aged have difficulty learning new information and remembering recent events. Aging has little effect on primary or short-term memory, as reflected in digit span or the recency component of the serial-position curve; but it has substantial effects on secondary or long-term memory, especially after moderately long retention intervals. Again, the deficit primarily affects episodic memory: the elderly do not lose their fund of semantic information (although they may be slower on such tasks as word-finding) and their repertoire of procedural knowledge remains intact, provided that they have been able to maintain these skills through practice. At the same time, it should be noted that episodicsemantic comparisons almost inevitably confound type of memory with retention interval. Memories for recent experiences have, by definition, been encoded recently; most semantic knowledge was acquired while the individual was relatively young. Surprisingly, little is known about the ability of older individuals to learn new vocabulary or acquire new world knowledge. The aged do show an impairment in episodic memory for remote events, but it is not clear whether this reflects age differences in retrieval processes or simply the effects of the retention interval and opportunities for proactive and retroactive interference. A relatively recent topic in research on aging memory compares EM and IM. Compared to the young, the aged show definite impairments on EM (especially free recall, less so on recognition); but they show less deficit, or none at all, on IM tasks such as stemcompletion. Part of the reason for their problems with EM may lie in the difficulty that the elderly have in processing contextual information. Spatial context, temporal context, and source are necessary for distinguishing one event from another, and thus crucial to conscious recollection. Whether this difficulty is specific to contextual features of events, or merely a reflection of a more general limitation on cognitive resources, is unclear. Memory problems are confounded in the dementing illnesses often associated with aging, e.g., Alz-

heimer's disease fAD). The severe memory problems associated with AD are likely related to the increase of neuritic plaques and neurofibrillary tangles, particularly in medial temporal regions of the brain. These changes, as well as neuronal loss and depletion of neurotransmitters in other cortical and subcortical areas, contribute to the extensiveness of the disease process. Both AA and RA emerge early in the course of these diseases and progressively worsen. In contrast to the amnesic syndrome, however, the memory deficit in dementia affects primary as well as secondary memory and forms part of a larger cluster of deficits affecting a broad swath of cognitive and emotional life, including the loss of premorbid semantic and procedural knowledge as well as episodic memory. In the latter stages of their illness, demented patients may show anosognosia or a lack of awareness of their deficits. [See ALZHEIMER'S DISEASE; DEMENTIA.] Does the abnormal forgetting observed in aging and dementia extend to implicit as well as explicit memory? Research on this question is still at a very early stage, but already it seems fairly clear that implicit memory is relatively spared in normal aging. Thus, elderly subjects will fail to recognize studied words, but show priming effects on word-fragment completion. With respect to AD and other forms of dementia, however, some controversy remains. There is some evidence of intact motor-skill learning in AD patients, but there is also evidence of impaired performance on priming tasks. The issue is complicated by the fact that AD is a progressive illness. Although impairments in explicit memory may be observed quite early in the course of the disease, deterioration of implicit memory may wait until later stages.

V. AMNESIAS OF EVERYDAYEXPERIENCE Amnesia is a symptom of neurological or psychiatric disorder, but it is also something that occurs in the ordinary course of everyday living. The most familiar example is sleep. A great deal transpires while we are asleep, including events in the external environment and endogenous activity such as dreams, nightmares, and (in some cases) episodes of somnambulism (sleepwalking) and somniloquy (sleeptalking), but virtually none of this is remembered in the morning. In fact, our inability to remember what has been happening is of-

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ten the phenomenological basis for inferring that we have been asleep. Similarly, attempts at sleep learning have been almost uniformly unsuccessful, leading investigators to conclude that we are able to learn during sleep only to the extent that we stay awake. Most investigators explain sleep-induced amnesia in terms of an encoding deficit or consolidation failure. According to this view, the low levels of cortical arousal characteristic of sleep effectively impair complex information-processing functions. Thus, events in the environment are not noticed, relevant information in memory is not retrieved, and traces of new experiences are not encoded in retrievable form. Some evidence favoring this view comes from studies of memory for dreams. Sleepers who are awakened during REM sleep almost invariably report a dream, apparently by virtue of retrieval from primary memory; but dreams are rarely reported upon awakening in the morning, a task that requires access to trace information in secondary memory. However, subjects will remember a dream in the morning if they awaken directly out of REM sleep. And dreams reported during REM awakenings will be accessible in the morning, provided that the dreamer has remained awake long enough to rehearse the dream before returning to sleep. Most evidence of sleep-induced amnesia comes from studies of EM, leading to speculation that evidence of memory for sleep events, including successful sleep learning, might be obtained with measures of IM. Research on this topic has only just begun, but the available evidence is negative. When care is taken to ensure that there is no evidence of cortical arousal indicative of awakening, subjects show neither EM nor IM for events that occurred while they were sleeping. Even if positive evidence for sleep learning were obtained, it would almost certainly not be as efficient as learning in the normal waking state. Amnesia is also an important component of general anesthesia induced in surgical patients. Clinically, the success of general anesthesia is indicated by the patient's lack of response to instructions, suppression of autonomic and skeletal responses to incisions and other surgical stimuli, and absence of retrospective awareness of pain and other events occurring during surgery. Thus, by definition, amnesia is a consequence of adequate general anesthesia. But, as with sleep, the amnesia is always assessed in terms of EM, leaving open the possibility that even adequately anesthetized

patients might show IM for surgical events. Some anecdotal evidence favoring this proposition is provided by occasional cases in which patients awaken from surgery with an inexplicable dislike of their surgeon-an attitudinal change which is plausibly traced to unkind remarks made about the patient by members of the surgical team. In recent years, this question has been the object of considerable investigation, and in fact research employing paradigms derived from studies of the amnesic syndrome has sometimes, but not always, provided evidence of spared IM. Thus, patients who are presented a list of words during surgery sometimes show significant priming effects. Such effects are not always obtained, however; and even when they are obtained, they are relatively small. Certainly the scope of information processing during general anesthesia cannot compare to what is possible when the patient is awake and properly oriented; for example, IM after anesthesia may well be limited to the processing of the physical properties of stimuli, but not their meaning. What accounts for the different outcomes across the available research is not clear. Perhaps some anesthetic agents impair EM but spare IM, while others impair both. Such a result might yield interesting insights about the biological foundations of memory.

VI. THEORETICALAND PRACTICAL IMPLICATIONS Research on amnesia is intrinsically interesting, but it also has theoretical and pragmatic implications. At the theoretical level, amnesia engages our attention because it seems to carve nature at its joints. Amnesia is selective, and the difference between those aspects of memory that are impaired in amnesia and those that are spared promises to provide information about the processes underlying memory functioning and the organization of memory into different systems. Such conclusions are based on the logic of dissociation. In single dissociations, variable A affects performance on task Y but not task Z; in double dissociations, variable A affects Y but not Z, while variable B affects Z but not u in reversed associations, changes in A increase Y and decrease Z, while changes in B decrease Y and increase Z; in stochastic independence, performance on task Y is uncorrelated with performance on

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task Z. All other things being equal, differences such as these suggest that the tasks in question differ in qualitative terms. If they were only quantitatively different, they would be correlated with each other and influenced by the same variables. Such dissociations are commonly observed in amnesia. For example, the fact that the amnesic syndrome affects the recency portion of the serial-position curve, but not the primacy component, has been cited as evidence that primary (short-term) and secondary (longterm) memory are qualitatively different memory systems, perhaps with different biological substrates (one affected by the brain lesion, the other not). Evidence from amnesia also has been used to support other structural distinctions: between declarative and procedural knowledge and, within the domain of declarative knowledge, between episodic and semantic memory. Thus, amnesic patients have difficulty learning new factual information, but retain an ability to acquire new cognitive and motor skills; and if they do retain new factual knowledge, they display an amnesia for the circumstances in which this information was acquired. Logic and experience tell us that when something breaks, it tends to do so along natural boundaries, which form lines of least resistance. When a disorder of memory separates past memory from new learning, procedural and declarative knowledge, or episodic and semantic memory, it tells us that these distinctions, conjured in the minds of theorists, actually mean something in the real world. The fact that these kinds of dissociations are observed in all sorts of a m n e s i a ~ n o t just the amnesic syndrome, but in traumatic retrograde amnesia, psychogenic amnesia, and posthypnotic amnesia as well--strengthens the conclusion that the theoretical distinctions are psychologically and biologically valid. Of particular interest in recent theory are the various dissociations between explicit and implicit expressions of episodic memory. To date, three broad classes of theories have been proposed to explain these dissociations; each has several exemplars. According to the activation view, the activation, by a current event, of pre-existing knowledge representations is sufficient for IM; but EM requires elaborative activity, in which individually activated structures are related to each other. According to the processing view, IM is an automatic consequence of environmental stimulation, while EM occurs by virtue of controlled processes that

are limited by attentional resources. According to the memory systems view, IM reflects the activity of a perceptual representation system, which holds information about the form and structure of the objects of perception, and EM reflects the activity of an episodic memory system that represents knowledge about the meaning of events and the context in which they occur.

Research on the amnesic syndrome, including studies of both human patients and animal models, indicates that the medial-temporal lobe, including the hippocampus, entorhinal cortex, and perirhinal and parahippocampal cortex, forms the biological substrate of explicit memory. But the diencephalic form of amnesic syndrome seems to indicate that the mammillary bodies and the dorsomedial nucleus of the thalamus are also critical for memory. As research continues, investigation of amnesia will make a unique and valuable contribution to understanding the relation between explicit and implicit memory, and the biological foundations of each. At the same time, evidence of preserved memory functioning offers new insights concerning amelioration and rehabilitation in cases of amnesia. Loss of explicit memory has debilitating consequences for afflicted individuals in everyday life. They are often unable to keep track of events, remember appointments or schedules, engage in educational or vocational pursuits, or manage home activities. Attempts at rehabilitation have frequently focused on restoration of damaged explicit memory processes either through the use of repetitive drills or by teaching patients mnemonic strategies such as visual imagery or verbal elaboration. These retraining attempts have met with limited success. There is no evidence that exercising damaged neural or cognitive mechanisms leads to positive outcomes; and although patients have sometimes been able to acquire a few pieces of information by using mnemonic techniques, they do not use the strategies spontaneously in everyday life. On the other hand, rehabilitation strategies that have focused on providing compensatory devices designed to bypass problems in daily life have been somewhat more promising. External aids such as notebooks, diaries, alarm watches, and environmental labels have enabled some amnesic patients to function somewhat more independently, although use of such devices often requires considerable amounts of train-

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ing and practice. The microcomputer, potentially a powerful prosthetic for people with memory impairments, has yet to be extensively used for this purpose. The finding that implicit and procedural memory often remain intact even in cases of severe amnesia has recently prompted researchers to begin to explore ways in which these preserved processes might be exploited beneficially for rehabilitation purposes. Cuing techniques, which take advantage of amnesic patients' ability to respond normally to word-stem or fragment cues, have been used successfully to teach individuals new factual information such as vocabulary as well as procedural tasks such as data-entry and wordprocessing. Continued research in this direction, paralleling more theoretically based research concerning preserved memory functions in amnesia, should enable further progress toward improving the ability of amnesic individuals to function effectively in their everyday lives. ACKNOWLEDGMENTS Preparation of this article, and the research that supports the point of view represented herein, was supported by Grants MH35856 from the National Institute of Mental Health and AG09195 from the National Institute of Aging, the McDonnell-Pew Program in Cognitive Neuroscience, and the Flinn Foundation. We thank Terrence Barnhardt, Jeffrey Bowers, Jennifer Dorfman, Martha

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Glisky, Michael Polster, Barbara Routhieaux, Victor Shames, Michael Valdiserri, and Susan Valdiserri for their comments. This article has been reprinted from the Encyclopedia of Human Behavior, Volume 1.

BIBLIOGRAPHY Eich, E. (1990). Learning during sleep. In "Sleep and Cognition" (R. R. Bootzin, J. F. Kihlstrom, and D. L. Schacter, Eds.). pp. 88-108. American Psychological Association, Washington, DC. Glisky, E. L., and Schacter, D. L. (1989). Models and methods of memory rehabilitation. In "Handbook of Neuropsychology" (F. Boiler and J. Grafman, Eds.), Vol. 3, Part 5, pp. 233-346. Elsevier, Amsterdam. Kihlstrom, J. F., and Schacter, D. L. (1990). Anaesthesia, amnesia, and the cognitive unconscious. In "Memory and Awareness in Anaesthesia" (B. Bonke, W. Fitch, and K. Millar, Eds.), pp. 2144. Swets & Zeitlinger, Amsterdam. Schacter, D. L., and Kihlstrom, J. F. (1989). Functional amnesia. In "Handbook of Neuropsychology" (F. Boiler and J. Grafman, Eds.), Vol. 3, pp. 209-231. Elsevier, Amsterdam. Shimamura, A. P. (1989). Disorders of memory: The cognitive science perspective. In "Handbook of Neuropsychology" (F. Boiler and J. Grafman, Eds.), Vol. 3, Part 5, pp. 35-74. Elsevier, Amsterdam. Squire, L. R., Knowlton, B. J., and Musen, G. (1993). The structure and organization of memory. Annu. Rev. Neurosci. 44, 453495. Tulving, E., and Schacter, D. L. (1990). Priming and human memory systems. Science 247, 301-306.

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Anorexia Nervosaand Bulimia Nervosa

I. II. III. IV. V. VI. VII. VIII. IX. X.

Melissa Peders0nMusseU

James E. Mitchell

University of St. Thomas University of Minnesota

University of North Dakota Medical School Neuropsychiatric Research Institute

Overview of Eating Disorder Terms Continuum of Health Related to Eating Disorders Diagnostic Criteria Epidemiology Psychological and Social Impairment Medical Complications Detection and Assessment Treatment Prevention Summary

disturbed eating patterns and attitudes toward food and body image. Unhealthy weight control practices and intense body image distortion or disparagement are central features of eating disorders.

I. OVERVIEW OF EATING DISORDER TERMS The word "nervosa" indicates that each of these conditions is a "nervous disorder." Psychological difficulties are likely to be involved in the development of these disorders, and also are likely to be exacerbated by the eating-disordered behavior. "Anorexia" means "lack of appetite." The hallmark feature of anorexia nervosa (AN) is failure to maintain a minimally normal body weight. The meaning of the term "bulimia" is "ox hunger," or "hungry as an ox." Bulimia nervosa (BN) is characterized by recurrent episodes of binge eating (i.e., eating large amounts of food accompanied by a sense of loss of control) and compensatory behaviors (e.g., purging, fasting, or excessive exercise). Overlap between the symptoms of these disorders occurs in some individuals. Furthermore, individuals may engage in disturbed eating behaviors and/ or indicate intense body image disparagement, but not meet full criteria for AN or BN. Detailed information about diagnostic criteria are provided later in this chapter. It is important to note that eating-related behaviors may be best conceptualized as existing along a continuum ranging from "healthy" to "unhealthy" eating-related behaviors and body image.

Anorexia Nervosa A type of eating disorder associated with failure to maintain a minimally healthy body weight. Binge Eating Eating large amounts of food in a discrete period of time accompanied by a sense of loss of control of food intake. Bulimia Nervosa A type of eating disorder involving recurrent episodes of binge eating and compensatory behaviors (e.g., purging, fasting, or excessive exercise). Eating Disorder A category of psychiatric disorders involving disturbances in eating patterns and attitudes toward food and body image. Purging A method of compensating for dietary intake, most commonly by self-induced vomiting, laxative abuse, or diuretic abuse. ANOREXIA NERVOSA AND BULIMIA NERVOSA are two of the most commonly recognized eating disorders. The term "eating disorder" encompasses a variety of psychological/psychiatric disorders involving

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Copyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

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Anorexia Nervosa and Bulimia Nervosa

II. CONTINUUM OF HEALTH RELATED TO EATING DISORDERS The pursuit of and preoccupation with beauty represent a central feature of the female sex-role stereotype. Therefore, it is possible that attractiveness, and specifically body image, have a greater influence on selfconcept for women than for men. Although standards of beauty have varied widely across time and cultures, the mass media have contributed to the development of a more uniform standard of beauty. Unfortunately, the current images of women that are portrayed in the media often represent unrealistic weights and shapes for most women. In a classic study, Garner and colleagues demonstrated a consistent decrease in body weights and measurements of two (albeit arguable) standards of beauty (e.g., Miss America pageant winners, and Playboy centerfolds) over two decades (1950s to 1970s). Fashion models are now 23 % thinner than average women, compared to 8% thinner than average woman three decades ago. Indeed, models who depict the in-vogue "waif" look are likely to have a body weight consistent with criteria for AN. Given the preponderance of images of thinness as the ideal for beauty that are depicted in the media, it is not surprising that many females would perceive their bodies as inadequate. Because women naturally have more body fat than men, even those who are of normal body weight may judge themselves as overweight. In a recent national survey, over 40% of females reported having a negative body image. Although almost onehalf of young girls reported wanting to lose weight in one survey, only 4% actually were found to be overweight. Women are far more likely to rate their ideal figure to be significantly thinner than actual size than are men. Therefore, perceptions that one is overweight may be potentially more distressing for women and may lead to attempts to control body weight and shape through methods such as dieting. Female college students report dieting at much higher ra:es than their male counterparts. In a recent large-scale national survey data from the Centers for Disease Control and Prevention, containing a sample of over 60,000 adults, 38% of female and 24% of male adults reported to be trying to lose weight, and 44% of females versus 15 % of males in high school sample of over 11,000 students

reported to be trying to lose weight. [SEEDIETING.] The high prevalence rates of negative body image attitudes and dietary behaviors found among females has been referred to as "normative discontent." Therefore, although not necessarily "healthy," it may in fact be "normal" for women in Western cultures to hold disparaging views toward their bodies and to engage in activites aimed at modifying their weight and shape. However, body image disparagement and dieting behaviors may pose as risk factors for the development of an eating disorder. Initial degree of body image disatisfaction has been found to predict increased eating disturbance in longitudinal studies of adolescent girls and to predict eating disordered behavior in adults. Similarly, the interaction between body image and other risk factors (e.g., pressure for thinness) increased probability of reporting eating disturbance in female athletes. In a study of adult ballet students, body dissatisfaction and dietary restriction were found to predict eating-disordered symptoms. Therefore, individuals who derive self-esteem primarily or exclusively based on the perception of body image may be at increased risk for development of an eating disorder. It has been argued that individuals who develop eating disorders unquestionably accept and internalize societal messages about thinness as the ideal for female attractiveness. Excessive dietary restraint, often used as a means to modify body weight and shape in an attempt to more closely correspond to a thin ideal of beauty, has been posited to increase the potential for development of binge eating. Secondary symptoms of semi-starvation resulting from prolonged dietary restriction or fasting, such as increases in preoccupation with food, urges to binge eat, and depressed mood, may lead to further exacerbation of body image disparagement and disturbed eating. Although body image concerns and dieting practices are commonplace for many women, when body image disparagement and eating disturbances become extreme and begin to interfere with functioning or to compromise health, an eating disorder may be diagnosed.

III. DIAGNOSTIC CRITERIA Although the symptoms of the various eating disorder syndromes overlap considerably and often are char-

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acterized as along a continuum, classification of specific eating disorders is based on criteria as outlined in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). [See DSM-1V.]

A. Anorexia Nervosa The primary distinguishing feature of anorexia nervosa (AN) is the refusal to maintain a minimally normal body weight (i.e., at least 85% of expected body weight considering age and height). Despite their excessively low-weight status, individuals with AN exhibit intense fear of gaining weight. Such individuals experience their body weight or shape in a distorted manner (e.g., size distortion) and often indicate intense distress regarding body image. Body weight or shape unduly influences self-evaluation, often being the primary determinant of self-esteem. Absence of three or more consecutive menstrual cycles (i.e., amenorrhea) is also required to make a diagnosis of AN. Perhaps the feature that presents the greatest challenge in accurately assessing and effectively treating this disorder is the adamant denial of the seriousness of maintaining an excessively low body weight. Individuals with AN may also engage in recurrent binge eating and purging (i.e., self-induced vomiting, abuse of laxatives, or diuretics), which is classified as the binge eating/purging subtype of AN. Absence of recurrent binge eating and purging characterizes the restricting type of AN.

B. Bulimia Nervosa Within the past two decades bulimia nervosa (BN) only has been recognized as a distinct clinical disorder. The primary feature of BN is recurrent binge eating (i.e., eating large amounts of food in a short time period accompanied by a sense of loss of control) followed by methods of inappropriate compensation. Compensatory methods include purging (i.e., self-induced vomiting, or abuse of laxatives, or diuretics), fasting, or excessive exercise. Symptom frequency for a diagnosis of BN entails binge eating and compensatory behavior(s) occurring on average at least twice a week for a 3-month period. Perception of body shape and weight unduly influencing self-evaluation also is required for the diagnosis of BN. A diagnosis of BN is not given to individuals who receive a diagnosis of AN, because

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that diagnosis takes precedence. Subclassification of BN is based on type of recurrent compensatory methods, referred to as purging and nonpurging types.

C. Eating Disorders Not Otherwise Specified A large number of individuals engage in disturbed eating behaviors, but do not meet strict diagnostic criteria for AN or BN, in which case a diagnosis of eating disorder not otherwise specified (ED-NOS) may be appropriate. Examples of symptom constellations that might meet the criteria for ED-NOS include bulimic behavior occuring less frequently than two times per week or purging in the absence of binge eating behavior. Another example of ED-NOS, binge eating disorder (BED), which is characterized by recurrent binge eating in the absence of compensatory behaviors, has been listed in the appendix of DSM-IV as a diagnosis warranting further research.

IV. EPIDEMIOLOGY Although increasing prevalence combined with increased recognition of eating disorder problems for women has contributed to the perception that eating disorders have become an "epidemic," this is not supported by epidemiological research. However, the high prevalence of eating disorders is well documented, with women representing the majority of those afflicted. Although these disorders are most commonly seen in women, approximately 5% to 10% of individuals who develop AN or BN are men. Research on AN and BN indicate that these disorders are most often found among Caucasian adolescent and young adult females in industrialized countries espousing the idealogy of Western culture. The most recent figures indicate that from .10% to 1.0% of young females have AN. Prevalence rates are higher for BN, ranging from 1% to 3 % of young women when using stringent diagnostic criteria. Increased rates of AN and BN have been associated with certain professions (e.g., fashion models, ballet dancers) that emphasize thinness. Elevated rates of eating disorders have also been found among individuals involved in competitive athletics, particularly those in which maintenance of a low body weight is

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competitively advantageous (e.g., gymnastics, running, wrestling). It is possible that participation in such activities poses as a risk factor in the development of an eating disorder. Alternatively, some individuals with established eating disorders (or body image disparagement) may be drawn to such activities, in order to use compulsive exercise as a socially condoned form of dietary compensation in efforts to maintain or achieve a low body weight.

V. PSYCHOLOGICALAND SOCIAL IMPAIRMENT Body image disturbance is a central feature of AN and BN. Body size overestimation among individuals with AN and BN has been empirically documented. Among individuals with AN and BN, marked fluctuations of body image disparagement frequently occur, which may precipitate and/or result from intensified eating disordered behavior. Increased psychological distress often is found among individuals with an eating disorder. Relatively high rates of comorbid psychopathology (especially affective disorders) have been reported for samples of individuals with AN. In addition, problems with past or present substance abuse are not uncommon among eating disordered samples. Individuals with eating disorders also display a pattern of cognitive abnormalities, such as a dichotomous thinking style. Low selfesteem and difficulties in interpersonal relationships are often reported by individuals seeking treatment for eating disorders. The extent to which these psychological and social difficulties may be involved in the development of eating disorders remains unclear and could be clarified by prospective, longitudinal studies. However, it is important to note that many of these symptoms are ameliorated with treatment that results in reduction or cessation of eating disordered behaviors.

VI. MEDICAL COMPLICATIONS Several thorough reviews are available providing detailed accounts of adverse medical sequale of eating disorders. Although prevalence rates for AN are relatively low, the medical consequences can be grave. Mortality rates for AN at long-term follow-up range

from 6% to 20% and up to one-fourth of anorectic individuals develop severe, chronic disabilities resulting from the disorder. The results of prolonged malnutrition found in AN include certain visably recognizable symptoms, including obvious weight loss, dry hair and skin, alopecia (i.e., hair loss), and excessive lanugo hair (e.g, fine, downy body hair). Cold intolerance, sleep disturbances, headaches, and fatigue are common among individuals with AN. Prolonged protein depletion resulting from chronic malnutrition resuits in additional symptoms, detectable through laboratory examinations. Abdominal pain and bloating, and constipation are often reported by individuals with AN, which may be due to delayed gastric emptying. Constipation also may result from laxative abuse and starvation. Among the most serious consequences of AN are osteoporosis, growth stunting, and cardiac complications. Although mortality rates for BN are low, fatalities have been documented as a result of gastric rupture after binge eating, esophageal perforations (i.e., Boerhooves syndrome), and cardiomyopathy due to chronic ingestion of Ipecac. Fluid loss due to recurrent purging can result in dehydration and electrolyte imbalance, potentially leading to cardiovascular disturbances. Recurrent vomiting may result in esophageal erosion. Constipation and abdominal bloating and pain may result from binge eating.

VII. DETECTION AND ASSESSMENT Several factors contribute to the secretive nature of eating disorders, including denial of the seriousness of symptoms, embarrassment regarding the symptoms, and/or fear of the consequences of relinquishing the disturbed behaviors (i.e., potential weight gain or increased anxiety). Consequently, eating disorders often go unnoticed and can be challenging to assess, although warning signs are often present. Secretive eating, refusal to eat in public, and frequent dieting may be indicative that an individual is struggling with some form of an eating disorder; these symptoms are usually found in individuals with either AN or BN. Behavioral indications of purging behavior include spending excessive amounts of time in bathrooms or frequently going to a bathroom immediately following eating. Excessive or compulsive physical activity

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may also indicate the use of exercising as a form of dietary compensation. The use of stringent diets or fasting for extended periods of time may signal the presence of an eating disorder. Substantial changes in body weight, including weight fluctuations, or continued weight gain or loss may also be indicative of an eating disorder. Emaciation is usually the primary physical indication of AN. Measurements of body weight obviously aids in determining if an individual is below 85% of expected weight; however, individuals with AN may drink excessive amounts of fluid or wear concealed weights in an attempt to manipulate assessment of body weight. Overactivity (e.g., continuous body movement or pacing) is often observed among individuals with AN. As described above, some of the additional detectable signs of AN include dry skin and hair, lanugo, and alopecia. Ammenorhea may also indicate the possibility of AN, although the use of oral contraceptives may complicate the detection of this symptom. Although frequent weight fluctuations may signal the presence of BN, many individuals with BN are of normal weight and appear relatively healthy. Although BN is usually less easily detected than AN, certain signs may aid in its detection. One indication of recurrent self-induced vomiting, sometimes referred to as a "Russell's sign," is the development of callouses or scarring on the back of the hand resulting from abrasion during self-induced vomiting. This symptom may not be present in those individuals who primarily use alternative forms of purging (i.e., laxative, diuretic, or enema abuse), who have nonpurging BN, or who after prolonged vomiting have come to do so reflexively. Self-induced vomiting may also contribute to hypertrophy of the salivary glands, creating a swollen appearance of the neck and face (i.e., "puffy cheeks"). Although this symptom may be fairly pronounced in some women, it is not detectable in the majority of individuals with BN. Additional signs include the presence of small skin hemorrhages (i.e., facial petechiae) or conjunctival hemorrhages that may result from forceful vomiting. Dental enamel erosion, most pronounced on the inside surface of the upper teeth, is another indication of purging that may produce protrusion of dental fillings or discoloration (i.e., darkening) of the teeth. This symptom, which is easily detected during dental examinations, may be overlooked during routine physical examinations unless

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specifically assessed. Edema may be present for those who abuse laxatives or diuretics. Individuals with BN often present with complaints of "bloating," constipation, or lethargy. Laboratory tests may be used to detect electrolyte imbalance, although such abnormalities are detected in only approximately 40% of individuals with BN.

VIII.

TREATMENT

A. Psychotherapy

Psychotherapy is commonly used in the treatment of eating disorders. One form of psychotherapeutic intervention, cognitive behavioral therapy (CBT) has been the most extensively studied. Based on the work of Beck for the treatment of depression, CBT is a timelimited, present-focused, solution-oriented form of therapy. This approach is based on "collaborative empiricism" in which the client and therapist actively work together using an experimental approach to resolve a specified problem. As applied to eating disorders, the primary focus is on modifying disordered eating behaviors and distorted cognitions about food, weight, and shape. A combination of behavioral techniques, cognitive interventions, and emphasis on relapse prevention are integrated in this approach. The efficacy of CBT has been demonstrated in several studies of BN. Favorable reduction rates of binge eating (ranging from 77% to 93%) and purging (74% to 94 %) have been reported for five of the most recent, large studies. Methods used in behavior therapy (BT) also are commonly integrated in CBT treatment for individuals with eating disorders. Studies comparing BT with CBT have generally demonstrated that the addition of cognitive interventions to behavioral methods are associated with similar or greater clinical gains. The efficacy of an alternative type of psychotherapy, Interpersonal Psychotherapy (IPT), recently has been demonstrated in treating individuals with BN, as well as BED. IPT is time-limited, present-focused, and solution-oriented. IPT differs from CBT in that the emphasis of treatment is on modification of interpersonal interactions, rather than eating disordered behavior or cognitions. Another therapeutic approach that has been investigated is supportive-expressive therapy, a short-

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term, nondirective, dynamically informed modality that conceptualizes core conflicts in terms of interpersonal issues. Although supportive-expressive therapy was found to be effective in reducing binge eating in this study, CBT was found to be associated with greater improvements in many aspects of eating disturbance and psychopathology, and a higher rate of remission in bulimic symptoms. Alternative psychotherapeutic approaches to treating individuals with eating disorders recently have been well articulated, although no controlled outcome studies have yet to be conducted. The relative efficacy of psychodynamic therapy is unclear given the absence of empirical data. However, this approach may be beneficial for clients who have not derived benefit from less intensive interventions, such as CBT. Feminist therapists have convincingly argued for the importance of considering sociocultural and political issues in designing interventions for individuals with eating disorders. The potential efficacy of psychotherapeutic interventions incorporating feminist perspectives warrant future empirical investigation. Although favorable results have been reported using psychotherapy, particularly CBT and IPT, several limitations of this body of research warrant discussion. Despite the substantial rates of symptom reduction and remission reported in these studies, it is important to note that approximately one-third to one-half of participants remained symptomatic at the end of treatment. Furthermore, strict inclusion criteria utilized in research studies such as these limit the generalizability of the findings, which may not be representative of the majority of individuals seeking treatment for BN. Data are not available regarding the relative efficacy of individual versus group administration of CBT or IPT. Additional research comparing the relative efficacy of alternative psychotherapeutic approaches is warranted. However, this body of literature provides support for the efficacy of using solution-focused psychotherapeutic interventions such as CBT and IPT in treating individuals with BN. Despite the fact that AN has received attention from clinical researchers for several decades, little empirical data are available regarding efficacy of psychotherapy for this disorder. To a large extent, the paucity of AN treatment research is attributable to the logistical difficulties involved in implementing controlled studies with this population. Only four outpatient psychotherapy studies of AN have been reported to

date, with some suggestions of effectiveness. The potential benefits of using behavioral modification programs (which overlap to a certain extent with CBT interventions) during inpatient hospitalization has received support in several studies. Although limited empirical data are available regarding the relative efficacy of individual versus family therapy in treating individuals with eating disorders, some therapists have convincingly articulated the potential benefits of using family approaches in working with eating disordered individuals. Some empirical support exists for using family therapy for younger individuals with AN. Additional research is needed to investigate various psychotherapeutic interventions for treating individuals with AN, and relapse prevention strategies, given the substantial rate of relapse in those who initially respond to treatment.

B. Medication Antidepressant medications have been found to effectively reduce binge eating and purging symptoms in several BN studies. Four controlled trials involving outpatient samples have demonstrated the superiority of serotonin-reuptake inhibitors (SRIs) in comparison to placebo in reducing bulimic symptoms, although one impatient trial failed to support added benefit for the drug. These medications generally have been found to be well-tolerated. Therefore, fluoxetine hydrochloride (Prozac) administered at daily doses of 60 mg (higher than the recommended dose of 20 mg used to treat individuals with major depressive disorder) is considered by some the first choice for pharmacotherapy for BN. The use of tricyclic antidepressants or monoamine oxidase inhibitors also is supported by research. Although the side effects of these classes of medications may be more problematic for many individuals than the SRIs, they may be beneficial treatment strategies for those individuals who do not respond to the use of SRIs. In addition, some clinicians prefer the second generation tricyclics, such as despiramine, as the initial intervention owing to the lower cost of the medication. Despite the relative efficacy of antidepressant medications compared to placebo in reducing bulimic symptoms, it is important to note that rates of bulimic symptom remission at end of treatment range from 4 % to 20% in most studies. These rates of symptom re-

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mission are lower than those reported in psychotherapy outcome studies. Augmenting psychotherapy with pharmacotherapy may seem indicated in some cases, although results from research on this are mixed. Three studies have reported no benefit to adding antidepressant treatment regimen to psychotherapy on outcome in eating variables, and the results are equivocal in one study. There is some suggestion that certain other symptoms, such as those of depression, may benefit from the combination of interventions. Little empirical data are available from investigations of the benefits of pharmacotherapy in promoting weight restoration in individuals with AN. Approximately a dozen controlled trials have been conducted on variety of medications, yielding often ambiguous results. Benefits have been demonstrated for the use of amitriptyline in one study and for cyproheptadine in two studies. However, the majority of placebocontrolled studies, investigiating the efficacy of these and other medications (e.g., antipsychotics, clonidine, cisapride, lithium, and tetrahydrocannabinol) have not demonstrated efficacy in promoting weight restoration.

C. Nutritional Counseling Nutritional counseling is often regarded as a necessary therapeutic component for treatment of individuals with eating disorders. Healthy meal planning is the cornerstone of this approach, which involves providing objective nutritional information about the types and amounts of food necessary to achieve or maintain adequate nutrition and healthy weight. Behavioral strategies are also employed to increase the likelihood of successfully adhering to nutritional recommendations. Nutritional counseling is essential for the treatment of AN, which requires an increase in caloric intake to promote gradual weight restoration at a rate of I to 3 pounds per week. Nutritional counseling is also useful for treating BN to help stabilize the dietary chaos that often promotes binge eating.

D. Hospitalization At times sufficient medical danger exists (e.g., dehydration, severe electrolyte imbalance, gastrointestinal bleeding, severe emaciation, suicidal ideation) to require inpatient hospitalization. Goals of hospitalization include interruption of weight loss (usually if less

than 70 to 75% of ideal body weight), progress toward restoration of healthy body weight, cessation of binge eating or vomiting, treatment of medical complications, and treatment of comorbid conditions (e.g., depression or substance abuse). Hospitalization also may be indicated if clinical benefits are not obtained from adequate outpatient therapy. This may be required for severely underweight individuals who, evidence starvation-induced impaired cognitive functioning. Day treatment, or partial hospitalization, may be recommended following inpatient discharge or as an alternative to hospitalization. This type of treatment allows patients to receive therapy during the day without requiring an overnight stay. This type of treatment is more economical than inpatient hospitalization and is less socially disruptive. Additional benefits of this type of treatment include allowing the patient to pursue work or education while obtaining intensive treatment, and providing a structured atmosphere during meal times.

IX. PREVENTION Given the prevalence of these disorders and the seriousness of the psychological and medical sequelae, the prevention of eating disorders is an important area that requires increased attention. Such efforts often involve providing psychoeducational information in school-based settings aimed at reducing unhealthy dieting behavior and enhancing body acceptance, often involving critical analysis of messages conveyed through mass media. A number of eating disorder studies have been conducted to investigate the effectiveness of primary prevention programs. However, an unfortunately consistent finding across such studies is that although knowledge about eating disorders often increases, behavioral changes (i.e., reductions in unhealthy dietary practices) have not been detected among participants. Failure to observe the desired behavioral outcomes of primary prevention programs may be attributable, in part, to a variety of methodological challenges, including the validity of self-report assessments and the relatively low baseline frequency of eating disordered behaviors (e.g., self-induced vomiting) among the general adolescent population. However, it is also possible that, in order to have a significant impact, prevention efforts may need to be de-

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livered to individuals at a younger age (i.e., elementary school). Increased understanding of the complex etiology of AN and BN may be required in order to develop more comprehensive and effective prevention strategies. In addition, relatively little attention has been devoted to investigating the effectiveness of secondary prevention of eating disorders. As such, effective strategies to assist in identifying individuals who are experiencing initial symptoms of an eating disorder and facilitating appropriate treatment remain an important area to be developed.

X. SUMMARY Stringent diagnostic criteria show that the prevalence for any single eating disorder is rather low. However, combining prevalence rates across various types of disorders reveals that up to 5 to 10% of women may be afflicted with a diagnosable eating disorder (i.e., AN, BN, or ED-NOS). Serious medical, psychological, and social consequences are associated with these disorders. The treatment of individuals with eating disorders often requires a multifaceted approach (e.g., psychotherapy, pharmacotherapy, nutritional counseling, medical management) involving members of several professional disciplines (e.g., dieticians, psychologists, psychiatrists, internists) and various settings (e.g., inpatient, outpatient, day treatment, residential).

Literature on the treatment of these disorders indicates that substantial progress has been made in the last few decades. However, a sizable subgroup of individuals with either AN or BN do not adequately respond to established therapies, or do respond but subsequently relapse. Much additional work is needed in predicting treatment response, matching individuals to treatments, and developing relapse prevention strategies. Furthermore, effective primary and secondary prevention strategies remain to be established.

BIBLIOGRAPHY Brownell, K. D., & Fairburn, C. G. (Eds.). (1995). Eating disorders and obesity. New York: Guilford Press. Fairburn, C. G. & Wilson, G. T. (Eds.). (1993). Binge eating: Nature, assessment and treatment. New York: Guilford Press. Fallon, P., Katzman, M. A., & Wolley, S. C. (Eds.). (1994).Feminist perspectives in eating disorders. New York: Guilford Press. Garner, D. M. & Garfinkel, P. E. (Eds.). (1997). Handbook oftreatment for eating disorders. (2nd ed.). New York: Guilford Press. Mitchell, J. E. (Ed.). (1990). Bulimia nervosa. Minneapolis, MN: University of Minnesota Press. Smolak, L., Levine, M. P., & Striegel-Moore, R. (Eds.). (1996). The developmental psychopathology of eating disorders: implications for research, prevention and treatment. Mahwah, NJ: Lawrence Erlbaum. Striegel-Moore, R.H., Silberstein, L.R., & Rodin, J. (1986). Toward an understanding of risk factors for bulimia. American Psychologist, 41,246-263. Thompson, J.K. (Ed.). (1996). Body image, eating disorders, and obesity. Washington, DC: American Psychiatric Association.

!

Antisocial Personality Disorder Robert G. Meyer and Daniel Wolverton

Sarah E. Deitsch

University of Louisville

University of Kentucky

I. Characteristics of the Criminal II. Antisocial Personality Disorder-Psychopath Terminology III. Characteristics of the Antisocial Personality (AP) IV. Heritability of Psychopathy V. Difficulties in Studying the Psychopath VI. AssessmentMeasures with AP VII. PCL-R-Generated Concepts VIII. The Psychopath and the Major Theoretical Orientations IX. Proposed "Common Path" for the Development of Psychopathy X. Intervention Issues XI. Summary

Recidivism The return to a prior criminal-antisocial behavior pattern. Sensation-Seeking A need for increased stimulation of various sorts, as well as an increased need for thrills and danger. ANTISOCIAL PERSONALITY is arguably the most important personality disorder, in terms of both impact on society and complexity of psychological and legal issues. The concept of the antisocial personality disorder is confused by the common usage of three overlapping terms: the criminal personality, the antisocial personality, and the psychopath (sociopath). The criminal personality is a sociological term, not a DSM category. As we will see, it includes a variety of different personalities who are involved in some way in criminal activity. Many different personality types function as criminals in our society; of these, the antisocial personality, or the related term "psychopath," is only one specific psychological syndrome. Antisocial personalities apparently account for no more than about 30% of the overall prison population.

Burnout The notion that the passage of time, repetition, or aging generates a behavior change. Criminal Personality A concept that overlaps with that of antisocial personality disorder. It is more inclusive as it refers to more criminal behavior patterns. Primary-Secondary Psychopathy A further delineation of the concept of psychopathy. Primary psychopaths show even lower levels of anxiety, avoidance learning, and remorse, and higher levels of violence and sensation-seeking. Psychopath A term that also overlaps but is more narrow in focus than the antisocial personality disorder. Psychopaths show even less remorse and ability to profit from experience, and more violence, glibness, callousness, and sensation-seeking. Psychopathy Checklist--Revised (PCL-R) The premier instrument for the assessment of psychopathy.

I. CHARACTERISTICS OF THE CRIMINAL Several overall patterns characterize the criminal. Four principal characteristics of the criminal lifestyle are (1) irresponsibility, (2) self-indulgence, (3)interpersonal intrusiveness, and (4) social rule breaking. The young or "apprentice" criminal is typically motivated by peer influence, combined with stimulation-

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seeking, which gradually give way to more antisocial components as the criminal career develops. More specifically, the majority of offenses are caused by individuals aged 21 and younger, and approximately 80% of adult chronic offenders were chronic offenders before age 18. Criminals tend to be male, at about a 5:1 ratio, up to as high as 50:1 in some specific categories of aggressive crime. With the rise in feminism, we are increasingly closer to gender parity in "whitecollar crime," but the high ratio of males has persisted in aggressive crimes. As to the general causes of crime, both poor sociocultural conditions and heredity are major factors, while more specific factors are cold, rejecting, harsh, inadequate, and/or inconsistent parenting; a high level of stimulation-seeking; psychopathy; impulsivity; low intelligence, especially low verbal intelligence; mesomorphic body type; and a history of hyperactivity, handicap, and/or being abused as a child. Psychodiagnostician Edwin Megargee and several colleagues have developed an ongoing research program that has generated an excellent typology of the criminal personality. Using data primarily from the MMPI, they differentiated 10 criminal types in one prison population. On the basis of behavioral observations, social history data, and other psychological tests, they obtained validation for this classification and subsequently extended its use to other prison populations. Most importantly from the perspective of good research design, researchers working indepenTable I

dently of Megargee established the validity of the system in other prisons, and others have independently validated similar patterns. It is clear from this and other data that there is no single criminal type. Their empirically derived and applicable system is likely to remain the standard one for many years. Another helpful way of conceptualizing different criminal "paths" is provided in Table I.

II. ANTISOCIAL PERSONALITY DISORDER-PSYCHOPATH TERMINOLOGY The term antisocial personality reflects an evolution through a number of terms, the most widely known of which has undoubtedly been "psychopath." In about 1800, Philippe Pinel coined the term Manie sans d~lire to reflect the fact that these individuals manifest extremely deviant behavior but show no evidence of delusions, hallucinations, or other cognitive disorders. While Pinel was certainly including several personality disorder categories other than the antisocial personality in his descriptions, James Prichard's label of "moral insanity," denoted in 1835, is a clear forerunner of the antisocial personality grouping. This general conceptualization grew in acceptance, and late in the 19th century the label psychopathic inferiority, introduced by Johann Koch, became the accepted term. Later variations included "psychopathic character, .... psychopathic personality," and "psychopath."

Tracks to Various Antisocial Patterns

The aggressive/versatile track leading to "cafeteria style" offending, including violent, property, and/or drug offenses/abuse

The nonaggressive antisocial track leading to more specialized offending including property and drug offenses/abuse

Characteristics Higher rate of genetic, prenatal and/or birth disorders Onset of conduct problems in preschool years Aggressive and concealing problem behaviors More hyperactive/impulsive/attention problems Poor social skills Poor peer relationships Academic problems High rate of instigation of offenses Low remission rate More males than females Higher rate of drug abuse Higher rate of stimulation-seeking

Characteristics Lower rate of genetic, prenatal and/or birth disorders Onset in late childhood or early to middle adolescence Mostly nonaggressive conduct problems No appreciable hyperactive/impulsive/attention problems Capable of social skills Association with deviant peers Sporadic or minimal academic problems Low rate of instigation of offenses Higher remission rate, at least for delinquency Higher proportion of females than in aggressive/versatile path Lower rate of drug abuse Lower rate of stimulation-seeking

Source: Adapted in part from R. Loeber (1990), Clin. Psychol. Rev. 10, 1-42.

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Expositions by a number of individuals, particularly by Hervey Cleckley, brought the term into common usage. Despite the foundation for the condition, the first (1952) edition of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-I), the generally accepted "bible" of mental disorder classifications, muddied the issue by substituting the term "sociopathic personality" to cover the patterns that had traditionally be subsumed under the psychopath label. "Sociopathic" was used to emphasize the environmental factors allegedly generating the disorder and to de-emphasize the moralistic connotations that had become encrusted on the old terminology. Nevertheless, both concepts remained in lay and professional usages. The confusion was further heightened with the 1968 revisions of the Diagnostic and Statistical Manual (DSM-II), which included neither term; instead, the DSM-II substituted the label "antisocial personality disorder." Although this new term carries an inherent implication of specifically criminal behavior, many professionals believed that it was a clear improvement in that it emphasized observable behavioral criteria: that is, to patterns of observable, definable behavior that conflict chronically with agreed-upon societal norms. The trend toward objective criteria for the application of the term continues in the latest revisions of the Diagnostic and Statistical Manual, and the term "antisocial personality" disorder is also retained. It would be helpful if a specific psychopathic disorder diagnosis was included in the DSM, especially if references to overt criminality were minimized. Incidentally, if the individual is younger than 18, the appropriate diagnosis is conduct disorder. From early on, studies have found that the term "psychopathic personality" is meaningful and useful in diagnosis. Also, in an early, landmark study, Spitzer and his associates (1967) checked for the diagnostic reliability of all of the standard mental health diagnostic categories, and found the highest level of agreement (r = .88) in the respondents' ability to label persons in the category of antisocial personality. As we see, there is considerable overlap between the terms "antisocial personality disorder" (the present official DSM term), the "psychopath," and the "sociopath." Throughout this article, we will use the overall term "antisocial personality," recognizing that the psychopath (or sociopath) is typically seen as a sub-

group of this category. [See DSM-IV; PERSONALITY

DISORDERS.] III. CHARACTERISTICSOF THE ANTISOCIAL PERSONALITY (AP) The essential characteristic of the antisocial personality disorder (AP) is the chronic manifestation of antisocial behavior patterns in amoral and impulsive persons. They are usually unable to delay gratification or to deal effectively with authority, and they show narcissism in interpersonal relationships. The pattern is apparent by the age of 15 (usually earlier) and continues into adult life with consistency across a wide performance spectrum, including school, vocational, and interpersonal behaviors. A consensus of the research on the specific characteristics of the antisocial personality (and this research typically focuses on that narrower range of individuals seen as psychopathic) presents the following, i.e., relative to normals, they are (a) less physiologically responsive (e.g., by EKG, GSR, and EMG measures) to fearful imagery; (b) less psychologically responsive to social disapproval; (c) less responsive psychologically to affect-laden words, i.e., they respond cognitively but not affectively; (d) perseverate in behaviors with negative consequences even when they are intellectually aware of these consequences; (e) show more evidence of "cortical immaturity" but not significantly greater indices of brain dysfunction; and (f) show higher levels of sensation- and thrill-seeking behaviors. Although the DSM-IV discusses only the overall category of AP, there is good evidence that it can be further subdivided into categories of primary psychopath and secondary psychopath. Primary psychopaths are distinguished by the following characteristics: (1) they have very low levels of anxiety, avoidance learning, or remorse; (2) they are even more refractory to standard social control procedures; (3) they are higher in sensation- and thrill-seeking behaviors, particularly the "disinhibition" factor that refers to extroverted, hedonistic pleasure seeking. Both the secondary and the primary psychopath are quite different from those individuals who are antisocial because they grew up in and adapted to a delinquent subculture. These delinquent individuals are normal in relation to the subculture they were reared in; they follow (often almost obsessively) the rules and

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mores of this group. They can be as conformist as the good middle class, middle management person. As we have already noted, not all criminals are psychopaths, and not all psychopaths are criminals. Cleckley (1955), a particularly influential early theorist, asserted that psychopaths are often intellectually superior, and this concept has unduly influenced attitudes toward the AP. However, Cleckley was clearly in error here; such a characterization best fits the unique subsample that he usually encountered with in his clinical practice. It is not surprising that those rare psychopaths who (a) were willing to participate and stay in therapy and, especially, who (b) could pay a private therapist's fees would be brighter than the average psychopath. As a whole, all subgroups of antisocial personalities actually show lower than average scores on intelligence tests. This is logical considering their inability to adjust to school, and is especially so if genetic dysfunction and/or brain immaturity are involved. Violent crimes of nonpsychopaths are often characterized by extreme emotional arousal and frequently occur in situations of domestic dispute. They are more often perpetrated against women who are known to the aggressor and can be loosely characterized as "crimes of passion." On the other hand, the violent crimes of psychopaths are less affectively laden, being perpetrated most commonly against men unknown to the aggressor. Violence of psychopaths is often callous and cold-blooded, frequently stemming from a dispassionate search for revenge or retribution and displays of machismo.

IV. HERITABILITY OF PSYCHOPATHY Cesare Lombroso's very early theory that one can tell a criminal by certain physical features, such as a low forehead, has been discarded. However, though some still believe the genetic effect is not very strong, most modern researchers have shown that criminal behavior is affected by heredity, thus providing strong, though indirect, support for the belief that the AP also is affected by heredity.

V. DIFFICULTIES IN STUDYING THE PSYCHOPATH There is a reasonable concern that some of the research data available on AP's are not based on ade-

quate sampling techniques. Two populations are a favorite target of researchers: (1) persons (often college students) who score high on the Psychopathic Deviate (Pd (4)) scale of the Minnesota Multiphasic Personality Inventory (MMPI) and (2)incarcerated criminals. There are problems with both groups. Individuals high on the Pd scale (as is true for a significant number of psychology graduate students and medical students) may be creative, productive individuals who are contributing positively to society even though they do not accept some of the standard social mores. The use of an incarcerated criminal population is also a questionable practice. First, it assumes that the great majority of AP's are unsuccessful and, second, that they are lodged in prisons. There are data (some cited earlier) that refute both of these assumptions, and logic would argue otherwise. The most critical error lies in the assumption that the criminal population is largely composed of AP's. Anyone familiar with prisons is all too aware of the polyglot of individuals in residence.

VI. ASSESSMENT MEASURESWITH AP Numerous tests, e.g., MMPI-2, provide a narrow or indirect evaluation of psychopathy. However, empirical evidence gathered over the course of the past 10 years indicates that Hare's Psychopathy Checklist (PCL) and its revised form (PCL-R) offer one of the most promising methods of assessing psychopathy directly and comprehensively, yet reliably. The PCL-R is a 20-item revision of the original 22-item scale (Hare, 1980) designed to measure not only behaviors, but also inferred personality traits central to the traditional clinical conceptualization of psychopathy. Assessment is based on a semistructured interview (about 9 0 - 1 2 0 minutes) and a review of file information. The interview serves not only as a source of information about the subject, but also allows the examiner an opportunity to observe the person's interpersonal style. Scoring is based on a three-point scale (0, 1, or 2). Scoring criteria are well delineated and allow satisfactory interrater reliability of .83 for a single rating and .92 for the average of two ratings. The total score can range from 0 to 40 with higher scores indicating a closer match to the psychopathic prototype. Although scores fall along a continuum, a cutting score of 30 is recommended as the best diagnostic indicator and this

Antisocial Personality Disorder

cutoff is currently being used in most studies of forensic populations. In such populations the mean score is usually between 20 and 25 with a standard deviation of approximately 7. The psychometric properties of the PCL-R have been well documented and there is extensive evidence to support the measure's reliability and validity. Also, the base rate of psychopathy and the psychometric properties of the PCL for adolescents are similar to those obtained with adult male offenders. In addition, it does not appear that shortening the test severely compromises the positive psychometric properties, especially in civil populations. The PCL:SV, a 12-item screening version of the PCL-R, has been tested on both criminal and civil populations and has shown good psychometric properties. It has slightly lower reliability than the full-length version, with which it correlates at about .80. Testing is based on a 30- to 45-minute interview and less extensive file information. Scores range from 0 to 24 with a score of 18 or higher being a good indicator of psychopathy. While this measure is easier to administer and flexible enough to be used in a variety of populations, the fulllength version is still the best measure in forensic populations and should be used whenever this is feasible.

VII. PCL-R-GENERATEDCONCEPTS There is substantial evidence that psychopathy, as measured by the PCL-R, consists of two stable, main factors, and both factors show good interrater reliability and internal consistency. The more behaviorally oriented Factor 2 demonstrates slightly higher reliability than Factor I which is not surprising since there is less subjectivity involved in the scoring of Factor 2 items. However, greater internal consistency is shown by items loading on Factor I which is consistent with the idea of a core set of psychopathic personality traits. The factor components are as follows: Factor 1:

(1) (2) (3) (4) (5) (6) (7) (8)

Glibness/superficial charm, egocentricity/grandiose sense of self-worth, pathological lying, conning/lack of sincerity, lack of remorse, shallow affect, callousness/lack of empathy, failure to accept responsibility.

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Factor 2:

(1) (2) (3) (4) (5) (6) (7) (8) (9)

Need for stimulation/proneness to boredom, parasitic lifestyle, poor behavioral controls, early behavior problems, lack of realistic long-term plans, impulsivity, irresponsibility, juvenile delinquency, revocation of conditional release.

Factor 1 is positively related to clinical ratings of psychopathy and with personality measures of narcissism, dominance, and Machiavellianism. It is negatively correlated with nurturance, agreeableness, empathy, anxiety, and DSM diagnoses of avoidant and dependent personality disorders. Factor 2 is related to disruptive prison behavior, drug and alcohol problems, and DSM-IV APD. It is negatively correlated with conscientiousness, socialization, SES, employment, education, and IQ. There is evidence that the diagnosis of psychopathy via the PCL-R predicts recidivism even after such variables as criminal history, previous conditional release violations, and relevant demographic characteristics have been controlled. The behavioral and lifestyle variables of Factor 2 are important in the prediction of general recidivism, while the personality characteristics that compose the first factor are more important in predicting violent recidivism. This finding is consistent with the view that violent psychopaths are more persistent and instrumental in their use of violence than nonpsychopaths. Yet, while the PCL-R demonstrates impressive incremental validity in predicting violence, especially considering the severe restriction of range under which it functions, the usefulness of the PCL-R should not be overgeneralized. One should not infer from extant supporting research that the PCL-R is able to consistently predict violent behavior in the general population. So far, it appears that the usefulness of the psychopathy construct in predicting violence presupposes some history of violent behavior.

VIII. THE PSYCHOPATHAND THE MAJOR THEORETICAL ORIENTATIONS This section presents conceptualizations of the psychopath within the framework of the dominant theoretical orientations in psychology, e.g., psychodynamic,

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learning/behavioral, cognitive, existential, and finally biological, followed by a proposed etiological model.

A. PsychodynamicConcepts Blending psychodynamic and ethological perspectives, psychodynamic theorists such as John Bowlby have argued for the selective advantage of strong emotional attachments on the part of young animals toward their primary caregivers. Studying children in orphanages who had been reunited with their parents after long separations, Bowlby extended these ethological theories to humans and elaborated on a number of pathological attachment styles, e.g., clingingdependent, anxious-ambivalent, and avoidant. Clearly the attachment style of the psychopath would be "avoidant," since an inability to form meaningful attachments with others is a cardinal symptom of psychopathy. Given the frequency of lax, inconsistent, and often violent parenting in the families of psychopaths, it is not surprising that a budding antisocial would learn that social independence, self-sufficiency, and even interpersonal manipulation are the best defenses in a hostile, unsupportive, unnurturing world. To remain unattached is the best prevention against frustrated attachment. [See ATTACHMENT.] This viewpoint may account for the psychopath's peculiar blend of affective blandness interspersed with occasional fits of angry, gratuitous violence. The great majority of the time, the psychopath is the ultimate "well-defended" person--cold, unfathomable, and unflappable. The angry, frustrated inner child is usually buried so deeply that it is seldom available to the others, or to the psychopath himself. His developmental needs for nurturance, trust, and acceptance gone sorely unmet in childhood, the psychopath rises above his blocked needs by developing a "moving against" interpersonal style. Feeling profoundly inferior at one psychological level, the psychopath "rises above" others by dragging them down-manipulating, exploiting, humiliating, and perhaps even physically tormenting them to this end. Generally lacking education and socially accepted skills, the psychopath may even come to take special pride in his talent for antisocial and criminal pursuits.

B. Learning/Behavioral Concepts The issue of conditionability is noted earlier in this chapter. To amplify, the learning viewpoint also em-

phasizes early experience with primary caregivers, but frames these interactions more in terms of reinforcement and punishment. The basic notions here are that the parents of psychopaths are inconsistent and punitive in their parenting behavior. The apparently random quality of the caregivers' behavior teaches the young psychopath that others' treatment of him is not contingent upon his behavior. Moreover, because he is so frequently punished, and most often on a noncontingent basis, he eventually becomes enured to punishing consequences in general. Child-rearing patterns such as these may contribute to the fact that adult psychopaths do not learn from the punishing consequences of life mistakes, as well as the finding that, in learning experiments, psychopaths ignore negative consequences and focus only on potential rewards.

C. Cognitive Concepts At first glance, the cognitive model seems to have little to add to the discussion of the origins of psychopathy. Especially as articulated in the early writings of Aaron Beck and Albert Ellis, this model has focused less on etiology and more on here-and-now intervention. However, the following existential model certainly provides a cognitive perspective. Also, consider the underlying cognitive schemas that Beck finds to be facilitative of psychopathic behavior, as discussed in the upcoming treatment section.

D. Existential Concepts It is interesting to view the psychopath from this perspective because of its heavy emphasis on such notions as guilt, anxiety, and freedom. From a point of view influenced by Friedrich Nietzsche's writings, the psychopath is the most free person in the world (this may sound odd given the frequency with which psychopaths are incarcerated). Because he has suppressed it, or is not capable of experiencing it, he is not encumbered by the guilt and anxiety which would interfere with free, self-determined action in the worldmhe is not a "lamb." He has transcended the conflict and discontent befalling most who struggle to have their needs met in the context of a prohibiting society. He is willing to live with "dirty hands." Existentialists often focus not only on freedom, but also on death, isolation, and meaninglessness. We might even admire the psychopath in terms of his

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ability to confront, accept, and embrace death in the form of reckless and dangerous behavior; we might admire his ability to embrace his ultimate isolation and "go it alone"; and we might even grudgingly come to respect his having grasped the purposelessness of existence and then choicefully imposed his own meaning on it, however cruel and perverse its manifestations might be. But upon closer examination, we see that the psychopath does not really comfortably fit within the existentialist model. He has not really grappled and struggled with the conflicts inherent in choicefulness, e.g., the anxiety which follows from passing up opportunities which will never come again, the guilt which comes with inadvertently hurting others by one's decisions (the psychopath is willing to live with dirty hands because he does not experience them as dirty). And, not having struggled, the psychopath can never experience the wholeness which comes from growth through pain. We see thathe is reacting against others rather than for himself. We see that he is a slave to his impulses, not master of his fate. From a gestalt point of view, we see that he is so hardened and defended that he does not really experience the world. He is not in touch with, or "aware" of the environment in a way that would allow him to act freely in accord with it, rather than haphazardly against it. We see that he is not only alienated from others, but almost completely alienated from his deeper self.

1. Biological (prenatal, birth) disruption 2. Low SES 3. Family history of vocational-social-interpersonal dysfunction 4. Family history of psychopathy

E. Biological Concepts

B. From Birth to School Age

This article already notes that heritability has a strong role in the development of psychopathy, and some authors have hypothesized a biological link with such childhood disorders as attention-deficit hyperactivity disorder (ADHD). Additionally research has noted several biologically based correlates, including reduced arousal to fear-inducing stimuli, minimized startle responses, restricted affective range, inability to respond affectively to emotion-laden words, reduced conditionability, and a tendency to perseverate in terms of attention allocation. But there is more to be said. [SeeATTENTIONDEFICITHYPERACTIVITYDIsORDER (ADHD).] Whereas learning and psychodynamic models emphasize the effects of parents' temperaments on children's behavior, biologically based models emphasize the effects of children's temperaments on parents' be-

1. Child temperament factors (a) Child's lack of emotional responsiveness and lack of social interest fosters rejecting responses from parents (b) Child's high activity levels may cause parental annoyance and elicit punitive responses 2. Parental factors (a) Inconsistent parenting results in child's failing to learn behavioral contingencies (b) Aggressive, punitive parenting results in child's modeling aggression, experiencing hostility, becoming enured to punishing consequences, and developing a repressive defensive style (emotional "hardness") 3. Parent-child interaction (a) Unreliable parenting results in insecure attachment (i.e., interpersonally "avoidant" at-

havior. For example, consistent with this thinking, research has shown that because of failure to obey, antisocial children were able to elicit punitive behavior from mothers of children who had never even met them before. Psychopaths apparently elicit relatively rejecting responses from parents by being underemotional and unresponsive, by being overly active and thereby annoying, and/or by having little natural tendency to engage their parents socially. Also, research supports the notion that some individuals (especially psychopaths) have lower baseline levels of arousal than others. In order to achieve optimal levels of arousal, these individuals require more frequent and intense environmental stimulation. It follows that in their attempts to seek out sensational experiences they would be more likely to engage in antisocial acts, i.e., low levels of conditionability and high needs for sensation-seeking combine to create high levels of antisociality and impulsivity.

IX. PROPOSED "COMMON PATH" FOR THE DEVELOPMENT OF PSYCHOPATHY A. Pre-existing Risk Factors

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tachment style); child "goes it alone" rather than risk rejection and disappointment associated with unreliable and/or abusive parents

C. School Age to Adolescence 1. Predisposing personality factors (a) Low baseline level of arousal (i.e., Eysenck's biological extraversion) contributes to impulsive, undercontrolled, and sensation-seeking behavior (b) A synergy of physiological underarousal, repressive psychodynamics, and habitual "numbness" to social contingencies results in child being insensitive to, and unable to, "condition" to environmental events; therefore, does not learn or "profit" from experience (c) ADHA/"soft" neurological disorder overlay may exacerbate behavior problems 2. Personality development (a) Peer/teacher labeling may result in self-fulfilling prophecy effects (b) School and social failure result in sense of inferiority and increased interpersonal hostility; child develops "moving against" interpersonal style (c) Initial forays into antisociality (e.g., theft, fire setting, interpersonal violence) occur; evidence for diagnosis of conduct disorder mounts

D. Adolescence 1. The young psychopath hones exploitative style in order to express hostility and "rise above" feelings of inferiority; "proves superiority" by hoodwinking and humiliating teachers, parents, peers 2. Continued antisocial behavior results in initial scrapes with the law 3. Physiological impulsivity, inability to profit from experience (exacerbated by a perseverative attentional style), and interpersonal hostility and antagonism combine to make repeated legal offenses highly probable 4. Contact with other antisocials in the context of juvenile-criminal camps or prison results in "criminal education"; increased criminality resuits; criminal and antisocial behavior become a lifestyle at which the psychopath can "excel"

E. Adulthood 1. Antisocial behavior escalates through the psychopath's late 20s; increasingly frequent incarceration results in increased hostility and hardened feelings 2. Unable to profit from experience, lacking in insight, and unable to form therapeutic bonds, the psychopath becomes a poor therapy-rehab risk and bad news for society 3. Antisocial behavior decreases or "burns out" in an uneven fashion beginning in the early 30s (less so with violent offenses); this may be due to lengthier incarcerations, to changes in age-related metabolic factors which formerly contributed to sensation-seeking and impulsive behavior, or perhaps to decrements in the strength and stamina required to engage in violent or felony-property crimes

X. INTERVENTION ISSUES Nearly all significant theorists and researchers suggest that psychopaths are poor therapy candidates, and there is some evidence that the more severe, or primary, psychopaths may get worse with psychotherapy, i.e., psychotherapy may provide a "finishing school" experience for them. The treatment problem with all the personality disorders--getting the client into therapy and meaningfully involved---is acute in the antisocial personality disorder. And, to the degree the person shows primary psychopathy, the poorer are the chances for any meaningful change, no matter what treatment is used. Most effective are (1) highly controlled settings, (2) with personnel who are firm and caring yet sophisticated in controlling manipulations, (3) and in which the antisocial client resides for a significant period of time (and these appear to be effective only while the psychopath is in residence). Any inpatient treatment program should include four major components: (1) supervision, manipulation of the environment, and provision of education by the staff to facilitate change; (2) a token economy system that requires successful participation for one to receive anything beyond the basic necessities; (3) medical-psychiatric treatments to deal with ancillary psychopathology, e.g., neurological disorders, depression; and (4) a system of necessary social cooperation to maximize conformity and encourage development of the group

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ethic. This last component is seldom a consideration. In such a program every task that can be found that can reasonably be performed by another and which is not essential to health should be required to be performed only by one inmate for another. This is truly an area where the psychopath is a neophyte. Attention should also be paid to the AP's high level of stimulation-seeking. This need can be interpreted to the person with an antisocial personality disorder as similar to that of the alcoholic, in that the person will be driven to fulfill this appetite in one way or another. Therapists should attempt to work with psychopaths to develop methods, e.g., developing a consistent pattern of engagement in sports and other strenuous and/ or exciting activities and jobs that provide for a high level of activity and stimulation. Overall, a therapist would generally need to 1. As noted, expect resistance to entering therapy, and then to staying in therapy. 2. As noted, consider their proneness to boredom and their high level of stimulation-seeking. 3. Expect such clients to be deceptive about their history and present status. To the degree feasible, independently corroborate any critical questions about history or present behaviors. Contract ahead of time that if you feel it necessary, you will obtain such data from significant others, etc. 4. In line with the above, clearly confront the individual's psychopathy and any record of deviant behavior. The presentation of "objective" profiles from tests like the MMPI-2 or 16 PF can be effective here. Confront the psychopathology as a lifestyle disorder that will require treatment of a significant duration (and cost); thus, one might contract for some financial penalty for early withdrawal. At the same time, avoid the role of judge, and stay as much as possible in the role of collaborator. Maintaining a degree of adequate rapport is critical. Any exercises that help to develop empathy or social sensitivity are useful. 5. Challenge the following underlying beliefs as adapted from Beck et al. (1990): (a) rationalization-"My desiring something justifies whatever actions I need to take"; (b) the devaluing of others--"The attitudes and needs of others don't effect me, unless responding to them will provide me an advantage, and if they are hurt by me, I need not feel responsible for what happens to them"; (c) low-impact consequences--"My choices are inherently good. As such, I won't experience undesirable consequences or if they

occur, they won't really matter to me"; (d) "I have to think of myself first; I'm entitled to what I want or feel I need, and if necessary, can use force or deception to obtain those goals"; (e) "rules constrict me from fulfilling my needs."

A. The Issue of Antisocial Burnout Some solace may be achieved in the notion that psychopathic-antisocial behavior may diminish with age, independent of intervention. Fortunately, there is some empirical validation of this notion. Usually the downward trend begins after age 40, but unfortunately there appears to be no significant dropoff in violent crime for the true (high on Factor 1) psychopaths. And, though often at a diminished rate in nonviolent crime, more recent research suggests that more than a third of psychopath offenders remain criminally active throughout their adulthood.

XI. SUMMARY The antisocial personality presents a murky conflux of five axioms: (1) an apparent rationality and social appropriateness; (2) an apparent inability to process experience effectively under standard social controls and punishments; (3) some evidence of behaviordetermining variables, such as genetic defect and/or brain dysfunction; (4) an absence of evidence of mediating variables between these possible causes and eventual antisocial behavior; and (5) a disinterest in changing oneself, and a lack of positive response to imposed treatment methods. However pessimistic the picture regarding treatment potential, more psychopathic treatment and outcome studies are warranted, even if they focus on only the small improvements which are made by that small percentage of psychopaths who would stay in treatment. Since psychopaths, as a relatively small percentage of the population, commit such a large percentage of violent and property crimes, even a 5 - 1 0 % success rate may pay dividends in terms of overall reduction of the most severe offenses. This article has been reprinted from the Encyclopedia of Human Behavior, Volume 1.

BIBLIOGRAPHY Beck, A., and Freeman,A., et al. (1990). "CognitiveTherapy of the PersonalityDisorders." Guilford,New York.

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Cleckley, H. (1955). "The Mask of Sanity." Mosby, St. Louis. Eysenck, H., and Gudjonsson, G. (1989). "The Causes and Cures of Criminality," Plenum, New York. Hare, R. (1991). "The Hare Psychopathy Checklist-Revised." Multi-Health Systems, Toronto. Hare, R., Harpur, T., Hakstian, A., Forth, A., Hart, S., and Newman, J. (1990). The Revised Psychopathy Checklist: Reliability and factor structure. Psycbol. Assess. 2, 338-341.

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Megargee, E., and Bohn, M. (1979). "Classifying Criminal Offenders." Sage, Beverly Hills. Meyer, R. (1992). "Abnormal Behavior and the Criminal Justice System." Lexington Books, Lexington, MA. Serin, R. (1991). Psychopathy and violence in criminals. J. Interpersonal Violence 6, 423-431. Spitzer, R., et al. (1967). Quantification of agreement in psychiatric diagnosis: A new approach. Arch. Gen. Psychiatry 17, 83-87.

III

Anxiety Nader Amir and Michael J. Kozak Allegheny University of the Health Sciences

I. Definition I1. Theories of Anxiety II1. Measurement

(2) Can anxiety be controlled? and (3) Should one try to control anxiety and if so should one use medication or psychotherapy?

IV. Epidemiology V. PathologicalAnxiety

VI. Summary

I. DEFINITION A. The Nature of Emotion

Anxiety

A state that serves to mobilize an organism to escape or to avoid danger. Fear The term fear is routinely used interchangeably with the term anxiety. However, some theorists distinguish the two, defining fear as distress about an identified threat, and anxiety as distress about a vague or unidentified threat. Panic Sudden intense anxiety that peaks quickly and is characterized by noticeable physical reactions such as tachycardia, hyperventilation, sweating, trembling, dizziness, and so on. Phobia Intense, persistent, and interfering anxiety about nondangerous objects or situations.

There has been much argument among philosophers, psychologists, and other theoreticians about the nature of emotion itself. Our approach here derives from the contemporarily influential idea that emotions are functional states. That is, emotions are states of the organism that can best be understood according to their functions. According to this idea, understanding the function of a state is a good start toward understanding whether that state is emotional in nature. According to this conceptualization, anxiety is any state that serves a particular function or purpose. What function does anxiety serve? It has become conventional in psychology to construe anxiety as a state that serves to escape or avoid danger. Mobilization of an organism to take actions to avoid harm can be a function that enhances survivability. This is our working hypothesis about the function of anxiety. Another idea that has garnered empirical support is that the function of anxiety is to warn others about danger, particularly via facial expressions. Both of these views constitute theories of the nature of anxiety, and are subject to continuing investigation and development or decline, depending on the accumulation of relevant evidence.

It is generally agreed that ANXIETY is a fundamental human emotion. Thus, our concept of anxiety is inextricably wed to our understanding of the nature of emotion itself. What is an emotion? More fundamentally, what kind of thing is emotion? If we agree that anxiety is an emotion, then anxiety is that kind of thing. Is emotion mental or physical? These questions may at first seem arcane, but their answers can help us think more clearly about more practical questions, like: (1) How can you tell if someone is anxious?

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Copyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

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B. Dimensions of Emotion Some researchers have argued that a limited number of basic emotions exist that cannot be analyzed into more fundamental emotions. These include anger, fear, sadness, disgust, and joy. Other emotions are said to be combinations of these basic emotions. For example, it has been suggested that anxiety can be conceptualized as a combination of fear, guilt, and anger. Another approach is to analyze emotions according to their position along certain basic dimensions. Watson and Tellegan have proposed one dimension anchored by excitement/elation at one point and drowsy/ dull at the other and another dimension anchored by distress/fear at one end and relaxation/calm at the other. These dimensions of positive and negative affectivity are hypothesized to encompass a variety of emotions. Particular emotions are usually depicted as points mapped onto the two-dimensional space. In this model, anxiety is characterized by excess negative affect. Another example of a dimensional approach is Mehrabian and Russell's three orthogonal axes: (1)valence (pleasant vs. unpleasant); (2)arousal (excited vs. relaxed); and (3) dominance (controlling vs. controlled).

C. Threat Meaning and Anxiety Because our approach is to view anxiety as a state that serves to escape or avoid danger, an essential element of an anxiety state must be a perception of danger by the organism. Note that there need not be any actual danger, but only the perception of danger. The sense of danger could be very specific, like "there is a tiger about to tear out my esophagus," or rather vague, like "something seems to be wrong." We call this sense of danger "threat meaning" and think that it must be part of any state that counts as anxiety. Unless there is some perception of danger by the organism, it is hard to make sense of anxiety as a state whose function is to mobilize the organism to escape or avoid danger. Cognitive psychology experiments have well established that there are both conscious and unconscious perceptual processes, and that perception of danger can be unconscious. Thus, a person could perceive danger but not be consciously aware of this "threat meaning." It follows that an anxious person may or may not recognize a perception of danger involved in the anxious state.

II. THEORIES OF ANXIETY A. Conditioning Mowrer's two-stage theory for the acquisition and maintenance of fear and avoidance behavior has greatly influenced thinking about anxiety. According to the two-stage theory, a neutral event comes to trigger anxiety if it has been experienced along with an event that itself causes anxiety. Furthermore, it is supposed that anxiety can be conditioned not only to physical events, such as snakes and spiders, but also to mental events, such as thoughts and images. This is the first stage: a process called classical conditioning whereby neutral stimuli are associated with danger cues. Once fear of a previously neutral situation is acquired in this way, methods of escape or avoidance are attempted, and successful methods are learned and maintained. This learning to escape and avoid is the second stage of the hypothesized two-stage process: instrumental, or "operant," conditioning. It has been argued that Mowrer's theory is too simple to account for fear acquisition and maintenance. For example, it fails to account for the disproportionately high frequency of certain fears (e.g., snakes and spiders) among humans, compared to, say, phobias about electric sockets. It also does not explain the particular ease with which some fears, like taste aversions, are learned and maintained. A useful addition to the two-stage theory is the theory of biologically prepared learning, that hypothesizes that certain conditioned learning is especially easy because of evolutionary developments in the nervous system that have had survival advantages. Although preparedness theory is a plausible elaboration of two-factor theory, its experimental exploration has yielded equivocal results. Despite the limitations of the basic two-stage theory, it maps well onto certain observations about the maintenance of phobic avoidance and escape. Specifically, it is generally consistent with the common observation that confrontation with phobic situations has been found to provoke reports of distress and elevated cardiac and electrodermal activity, and withdrawal from the situations leads to temporary relief. Another influential theory of anxiety emphasizes the anxiogenic role of uncontrollability and unpredictability. Accordingly, unpleasant events feel much

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worse and have more lasting effects if they are unpredictable and uncontrollable.

B. Cognitive These theories postulate that what people think influences how they feel. For example, Beck and his colleagues have hypothesized that unrealistic expectations and attitudes, represented as cognitive "schemas," predispose a person to emotional distress. A limitation of this sort of cognitive theory is that it does not specify what expectations and attitudes distinguish different emotions, such as fear versus anger or sadness. Another type of cognitive theory supposes that certain styles of thinking, for example, overestimating of threat, are involved in pathological anxiety, and that the perception of threat is an important determinant of anxiety. For example, Watts and his colleagues have argued that the way people pay attention to, remember, and interpret threat-relevant information is a crucial determinant of anxiety. Furthermore, different emotions may be associated with different types of information processing bias, for example, anxiety with attentional bias, and sadness with memory bias.

C. Biological Biological theories of anxiety emphasize the role of the nervous system in anxiety. Anxiety is routinely construed as a stress reaction, and it is generally understood that environmental stressors affect physical wellbeing. Hans Selye introduced the concept of a General Adaptation Syndrome(GAS)to describe physical reactions to stressors. Accordingly, there are three phases in the reaction to stress. During the first phase, the alarm reaction, the activity in the autonomic nervous system increases. In the second stage, resistance, some physiological adaptation occurs, but if the stressor persists, other physiological reactions ensue, such as ulcers and atrophy of the thymus. Finally, in the third phase, exhaustion, irreversible damage or death may result if the source of stress is not removed. Other researchers have emphasized the importance of interpretation of events in the environment. For example, Lazarus suggests that interpretation of threat is as important as the triggering event in causing stress. For example, it has been suggested that stress

occurs when a situation is appraised as exceeding the individual's adaptive resources. The above theories of stress often refer to neuroanatomical structure that may be involved in the stress reaction. Jeffrey Gray's theory postulated that the nervous system has subsystems serving different functions, and that there is a subsystem called the "behavioral inhibition system" whose prime function is to inhibit behavior in certain situations (e.g., novel situations, aversive situations). Gray has argued that the effects of certain anti-anxiety substances such as alcohol, and of lesions of certain brain areas (e.g., septohippocampal system) that reduce anxiety support this theory. Furthermore, Gray suggested that individual differences in anxiety stem from differences in the activation of the behavioral inhibition system and that these differences are determined genetically.

D. Genetic and Evolutionary As noted earlier, anxiety is believed to have survival value because it prepares the organism to avoid harm. While the avoidance of threat is essential for survival, chronic anxiety can involve hypervigilance and exaggerated perception of the number and severity of dangerous environmental stimuli. Such hypervigilance could impede, rather than enhance, the organism's survivability, by interfering with essential activities. If this genetic advantage is passed on to one's offspring, then anxiety should be especially prevalent in relatives of anxious individuals. Genetic and family studies have found some support for this notion. For example, elevated levels of panic have been found in relatives of individuals with panic disorder. Another way of understanding genetic influence is through comparisons of identical (monozygotic) twins, who have identical genetic makeup, and dizygotic twins, who have similar upbringing but different genetic makeup. The method is to compare their concordance for anxiety, that is, to compare the number of each type of twin pair who both have anxiety. Such concordance is higher in monozygotic twins. Together, the various genetic studies point to a component of heritability for anxiety. Notably, however, heritable vulnerability is not absolute: the concordance rate for monozygotic twins is closer to 40% rather than to 100%. This means that genetic makeup provides a limited explanation of vulnerability to

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anxiety disorder. Furthermore, what seems to run in families is a vulnerability to develop some kind of anxiety, rather than to develop a specific disorder.

E. Diathesis-Stressor Because of evidence that both person and environment are important in understanding anxiety, it has become commonplace to suggest that an interaction between stressors in the environment with predispositions (or diatheses) in the person cause anxiety. The predisposition could itself be environmentally caused, or it could be inherited. Hypothesized environmentally caused diatheses might be brain injury caused by prenatal hypoxia, or autonomic hyperreactivity stemming from years of child abuse or imprisonment and torture. Some theorists have suggested that individuals inherit predispositions to differing levels of anxiety and that environmental stressors are influential in determining its onset and course.

F. Animal Models Animals experience distress in threatening situations, and this has been compared to anxiety in humans. For example, when animals are forced to make difficult choices between danger and safety signals, they show agitation, restlessness, distraction, hypersensitivity, muscle tension, and stomach ulcers. This phenomenon has been termed experimental neurosis, and can also be produced by punishment of appetitive behavior, and by long periods of restraint and monotony. There are parallels between disturbances observed in animals who are exposed to unavoidable and unpredictable stressors, and human reaction to extreme harm or threats (e.g., violent assault, physical injury). These similarities suggest that animal models can be useful for studying human reactions to extreme stress. Although animal models do not illuminate every feature of anxiety, they can probably explain some of the more prominent features.

III. MEASUREMENT A. Indicators Methods of assessing anxiety include interviewing, questionnaires, physiological monitoring, and obser-

vations of behavior. These can be used to assess the full range of anxiety, from mild to intense. The primary technique used to assess pathological anxiety is the clinical interview addressing criterion symptoms as specified in DSM-IV or another diagnostic rubric. [See DSM-IV.] An approach to anxiety advocated by Peter Lang holds that it is variously evident in three behavioral systems: semantic (what people report about themselves), physiological (e.g., heart rate, brain electrical activity), and overt behavior (e.g., avoidance), and that there is routinely some dysynchrony among the three systems. The implication of this particular view is that a thorough assessment entails measurement of the three systems. Measurement of each system has advantages and disadvantages. Self-report indicators of anxiety require introspective description of feelings. An advantage of this indicator is that language can indicate fine nuances of meaning that are less easily accessible in other indicators. Also, self-report provides a relatively economical method of assessment, and can often be done by questionnaire. A disadvantage is that subjects are often inconsistent in their observations of themselves, and the usefulness of their report depends heavily on their limited powers of self-observation. An advantage of direct monitoring of physiological functioning is that the data do not rely on the selfobservational accuracy of the subject, but rather, on the quality of the measurement methods and monitoring equipment. There is a subspecialty of psychology: psychophysiology, which is devoted to psychological theorizing founded in physiological assessment. Disadvantages of physiological assessment are not only the technical burdens, but more fundamentally, the multiplicity of physiological determinants. To put it simply, the bodily organs do not operate just to tell us about anxiety. How much variation in a particular physiological function is irrelevant to anxiety is ambiguous, and complicates any assessment of anxiety via physiology. There is no one physiological response pattern associated with anxiety. For example, heart rate could increase or decrease in response to threat. Note also that with physiological assessment alone, one can not determine if a heart is pounding because a person is running an Olympic race, running from an assailant, or riding a roller coaster at an amusement park. Behavioral measurement entails identifying and

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quantifying overt behavior that is deemed relevant to anxiety. For example, number of errors during a 5minute typing test could be used as a performance indicator of anxiety. Distance in feet that a person is willing to approach a dangerous object also could constitute a behavioral measure, as could frequency of eye contact in a social situation. An advantage of direct observation is that it is not subject to inaccuracies of the subject's interpretation. Disadvantages are that people act very differently in different circumstances, so it is difficult to obtain a representative sampling of behavior, and watching a person during an action often influences the target behavior, so that the observation process itself distorts the obtained behavioral sample.

B. Psychometrics As mentioned above, individuals are often inconsistent in their observations of themselves, and the usefulness of their reports depends heavily on their limited powers of self-observation. A subfield of psychology called psychometrics concerns the technology of measurement, and includes techniques to enhance the usefulness of self-report data. These methods focus on increasing the consistency, that is, reliability, and accuracy, that is, validity of self-report data, and involve using mathematical statistics to develop selfreport scales. A number of psychometrically sophisticated scales are available to measure anxiety, and many are in the form of questionnaires. Traditional psychometric approaches classify anxiety into state (transitory feelings) and trait (stable personality) attributes. One method of evaluating the accuracy of an anxiety scale is to compare its results to other measures of anxiety, for example, interview, physiology, and observations of behavior. By assessing various aspects of anxiety, the investigator tries to gauge an emotion for which no single indicator offers a perfect yardstick.

IV. EPIDEMIOLOGY A. Anxiety Across the Life Span Anxiety can develop at any time in the individual's life span. However, some fears more especially characterize certain stages of development. For example, fears of heights, of loss of physical support, and of loud

noises are common in infancy, but fear of strangers develops between 6 and 12 months. Jerome Kagan and his colleagues have demonstrated that there are individual differences in the level of anxiety, inhibition, and physiological reactivity that are apparent at infancy. Furthermore, these individual differences may have long-lasting implications for individual development. From 1 to 3 years of age children develop other fears, including fears of darkness, injury, and animals. Kindergartners develop fears such as separation from parents, bodily harm, animals, and sleeping alone. Later, at elementary school age, common fears include test-taking anxiety, fear related to physical appearance, and illness. Fears common in adolescence include anxiety related to social interactions, physical health, sexual matters, and political and social concerns. In the general population, common fears include, snakes, spiders, heights, flying, blood, and dentists. Anxiety about physical health attains more prominence in the elderly.

B. Gender Differences Differences exist between men and women in felt anxiety: women report more anxiety. This difference is evident in children as well as in adults. Furthermore, the objects of anxiety differ among the sexes. Environmental, agoraphobic, and animal phobias are more common among women, whereas fears of social situations, bodily injury, and illness are approximately equal among men and women. There are also sex differences in response to interpersonal threat situations, with women more likely to respond with anxiety, and men with anger. This appears related to perception of potential control of the threat by the subject. Other factors, e.g., greater cultural acceptability of reports of distress for women, probably also contribute to observed sex differences.

C. Cross-Cultural Perspective Although anxiety is common to all cultures its expression varies. For example, as Barlow points out, the introspective interpretation of anxiety is culture dependent. For example, in China, medical treatments of emotional disorders are less successful than they are

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in Western cultures because of the belief that familial separation is the cause of emotional problems. Furthermore, in the third world countries, somatic symptoms appear to be the prevalent mode of anxious expression. In sum, although there are individuals in all cultures that seem anxious, the foci of anxiety and worry, and the attributions of causes of anxiety, are diverse.

V. PATHOLOGICALANXIETY A. Definition Because everyone feels anxious from time to time, it becomes useful to distinguish normal from pathological anxiety. Disabling anxiety in the absence of any actual danger is clearly pathological. As a rule, if anxiety interferes with routine functioning (e.g., work, social life, leisure) and persists when there is minimal real threat, then it is considered pathological.

established method for reducing excessive fear is by confronting the feared situation. For example, through gradual approach, an individual who is afraid of insects can handle some insects and reduce the fear. The various components of anxiety described above, however, typically change at different rates. Although the person may be handling an insect, and so seem by his or her behavior to no longer be afraid, heartrate may still be elevated, and there may still be a suspicion that the insect is dangerous. This is an example of the often observed desynchrony among different aspects of anxiety. With more practice, the idea of threat and the physical reaction may also change. Although it is clear that anxiety can sometimes be controlled, it is unclear to what extent vulnerability to develop anxiety can be changed. Some researchers believe that psychological and biological interventions can change vulnerability to anxiety, but this issue remains controversial.

D. Classification of Anxiety Disorders B. Expression versus Suppression of Anxiety Should anxiety be suppressed or expressed? This is a variant of the broader question of whether it is healthier to express or suppress emotions. Although a common response to unpleasant feelings is to try to control them, some theorists have proposed that attempts to suppress negative emotions can result in somatic problems, such as ulcers, asthma, arthritis, urticaria, and so on. Although there is certainly evidence for psychosomatic disease, its existence does not itself imply that emotions should always be immediately and completely expressed. Expressing intense anger at a police officer who is giving you a ticket for speeding, or at an armed combat soldier who confiscates your property, could lead to serious harm. A balanced analysis would weigh the potential disadvantages of a particular expression of anxiety against those of its suppression. An often practical alternative to either expressing or suppressing anxiety might be to identify and eliminate its source.

C. Control of Anxiety Because anxiety can interfere with an individual's functioning it is sometimes desirable to reduce it. The most

The Diagnostic and Statistical Manual of Mental Disorder, Fourth Edition (DSM-IV), delineates seven specific anxiety disorders. This classification is based on both theoretical and practical considerations, and reflects contemporary thinking. Some theorists have argued that such classifications are too arbitrary, do not reflect "natural" categories, and should be replaced by dimensional descriptive nomenclature. The DSM-IV categories are: Obsessive-Compulsive Disorder, Panic Disorder, Social Phobia, Posttraumatic Stress Disorder, Generalized Anxiety Disorder, and Acute Anxiety Reaction. They differ not only according to the nature of the feared situation (e.g., social situations), but also according to the cluster of associated symptoms. [See OBSESSIVE-COMPULSIVEDISORDER;PANIC ATTACKS;POSTTRAUMATICSTRESS.]

C. Treatment Treatments for anxiety disorders often mirror the underlying theories of anxiety discussed above. For example, a clinician who believes that biochemical abnormalities cause anxiety might favor pharmacotherapy with anxiolytic medicine. A clinician who believes that faulty learning or mistaken beliefs are responsible for pathological anxiety might prescribe corrective

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exercises, for example, facing the anxiety-provoking situation as opposed to avoiding it, or reevaluating the likelihood of danger in a given situation. Certain drug- and learning-based treatments have been studied scientifically and found helpful for various kinds of anxiety. Particular treatments have been found especially helpful for particular types of anxiety, so it is important to obtain a treatment that has been found to match the type of difficulty experienced. Unfortunately, clinicians sometimes focus too much on the treatments in which they are most expert: a physician tends to prescribe medicine and a psychologist or social worker tends to prescribe psychotherapy. The kind of psychotherapy given sometimes depends more on the kind of psychotherapist (cognitive, behavioral, family, hypnosis, psychoanalytic) than on the kind of treatment that is of established efficacy for a particular type of anxiety. Ideally, a clinician should be familiar with scientific findings on the comparative efficacy of the available treatments for different anxiety problems, regardless of whether that clinician is competent with each treatment, and should guide the anxious person accordingly to choose a treatment of established efficacy. Seekers of treatments for anxiety should be cautious about treatment providers who are unwilling to explain the advantages and disadvantages of alternative treatments, including the strength of the evidence for and against each treatment.

VI. SUMMARY Anxiety is a routine part of human existence but is incompletely understood. One way of trying to understand it is by what function it serves, for example, to prepare to escape or avoid harm. Many theories about various aspects of anxiety have been proposed, but there is no generally accepted comprehensive explanation. A number of methods of assessing anxiety are available, and each has advantages and disadvantages. The incidence and expression of anxiety varies across age and culture. Anxiety merits treatment if it is severe, persistent, and disabling. Different drugs and psychotherapies have been found helpful for different types of anxiety, and careful consideration of the scientific evidence for each treatment should guide selection.

BIBLIOGRAPHY Barlow, D. H. (1988). Anxiety and its disorders: The Nature and treatment of anxiety and panic. New York: Guilford Press. Eysenck, H. (1992). Anxiety the cognitive perspective. Hillsdale, NJ: Lawrence Earlbaum Associates. McNally, R. J. (1994). Panic disorder: A critical analysis. New York: Guilford Press. Tuma, A. H., & Maser, J. (1985). Anxiety and the anxiety disorders. Hillsdale, NJ: Earlbaum.

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Attention Deficit/

Hyperactivity Disorder(ADHD) Russell A. Barkley and Gwenyth H. Edwards University of Massachusetts Medical Center

I. Introduction II. Historical Context

Impulsivity Reduced ability to resist an impulse or temptation to perform some action. Impulsive actions are those that are directed at obtaining immediate gratification without regard for the delayed consequences of the behavior. Reinforcement The consequences of behavior that increase the probability that the behavior will occur again. Response Inhibition The capacity to: (a) inhibit prepotent responses, or those that gain immediate reinforcement either positive or negative; (b) terminate ongoing responses as a function of feedback concerning errors or response ineffectiveness; or (c) protect ongoing self-directed and often private (cognitive) actions (i.e., thinking) from disruption by competing response patterns.

III. Description and Diagnosis

IV. V. VI. VII. VIII. IX.

Theoretical Framework Potential Etiologies Epidemiology of ADHD Developmental Course and Adult Outcome Diagnostic Criteria Conclusion

Attention

A multidimensional construct that can refer to alertness, arousal, selectivity, sustained attention, distractibility, or span of apprehension. Contingency-Shaped Attention Continued responding in a situation or to a task as a function of the immediate consequences provided by the task or activity. Developmental Disorder Any condition arising in childhood thought to be intrinsic to the individual that is characterized by functioning that is substantially below that expected, given the person's chronological age. Goal-Directed Persistence The maintenance of responding that is controlled by the capacity to hold events, goals, and plans in mind and to adhere to those plans and other rules governing behavior. Hyperactivity Characterized by increased or excessive movement of the body and its extremities. May be manifested as constant restlessness, fidgetiness, motor overactivity, or excessive talkativeness.

ATTENTION DEFICIT/HYPERACTIVITY DISORDER (ADHD) is a pattern of behaviors believed to be primarily of a neurodevelopmental origin that affects approximately 3 to 5 % of the school-aged population. Children with ADHD experience delays relative to other children of the same age in three areas of their functioning: the ability to regulate behavior and excessive levels of activity (hyperactivity); impulse control or behavioral inhibition; and sustained attention to tasks that are not inherently interesting or rewarding. Although children diagnosed with ADHD will gradually mature and make gains in these areas as they grow older, many may always lag behind other

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Copyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

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Attention Deficit/Hyperactivity Disorder (ADHD)

children of the same age to a significant degree in their behavioral regulation, impulse control, and sustained attention.

I. INTRODUCTION

It is not unusual for young children to be energetic and active, or to become bored quickly and move from one activity to another as they explore their environment. A young child's desire for immediate gratification is to be expected, rather than the restraint or self-control that would be demanded of someone older. However, some children persistently display levels of activity that are far in excess of their age group. Some are unable to sustain their attention to activities, their interest in tasks assigned to them by others, or their persistence in achieving long-term goals as well as their peers. When a child's impulse control, sustained attention, and general self-regulation lag far behind expectations for their developmental level, they are likely to be diagnosed as having ADHD. Children with ADHD have a greater probability of experiencing a number of problems in their social, academic, and emotional development and daily adaptive functioning. Attention Deficit/Hyperactivity Disorder (ADHD) has captured public commentary and scientific interest for more than 100 years. While the diagnostic labels for disorders of inattention, hyperactivity, and impulsiveness have changed numerous times, the actual nature of the disorder has changed little, if at all, from descriptions provided at the turn of the century. During the past century, and especially during the last 30 years, thousands of published scientific papers have focused on ADHD, making it one of the most wellstudied childhood psychiatric disorders.

II. HISTORICAL CONTEXT

Serious clinical interest in children who have severe problems with inattention, hyperactivity, and poor impulse control is first found in three published lectures by the English physician, George Still, presented to the Royal Academy of Physicians in 1902. Still reported on a group of 20 children in his clinical practice whom he defined as having a deficit in "volitional

inhibition" or a "defect in moral control" over their own behavior. Still's observations described many of the associated features of ADHD that would be supported by research almost a century later, such as an overrepresentation of boys compared to girls, the greater incidence of alcoholism, criminal conduct, and depression among the biological relatives, and a familial predisposition to the disorder. Initial interest in children with these characteristics arose in North America around the time of the great encephalitis epidemics of 1917 and 1918. Children surviving these brain infections were noted to have many behavioral problems similar to those comprising contemporary ADHD. These cases, as well as others known to have arisen from birth trauma, head injury, toxin exposure, and infections, gave rise to the concept of a "brain-injured child syndrome," often associated with mental retardation. This term was eventually applied to children without a history of brain damage or evidence of retardation but who manifested behavioral problems such as hyperactivity or poor impulse control. This concept would later evolve into that of "minimal brain damage," and eventually "minimal brain dysfunction" (MBD), as challenges were raised to the label given the lack of evidence of brain injury in many of these cases. During the 1950s researchers became increasingly interested in hyperactivity. "Hyperkinetic impulse disorder" was attributed to cortical overstimulation resuiting from ineffective filtering of stimuli entering the brain. These studies gave rise to the notion of the "hyperactive child syndrome" typified by daily motor movement that was far in excess of that seen in normal children of the same age. By the 1970s research findings emphasized the importance of problems with sustained attention and impulse control in addition to hyperactivity in understanding the nature of the disorder. In 1983 Virginia Douglas proposed that the disorder was comprised of major deficits in four areas: (1) the investment, organization, and maintenance of attention and effort; (2) the ability to inhibit impulsive behavior; (3) the ability to modulate arousal levels to meet situational demands; and (4) an unusually strong inclination to seek immediate reinforcement. Douglas' work, along with numerous subsequent studies of attention, impulsiveness, and other cognitive factors, eventually led to renaming the disorder "Attention Deficit Disorder" (ADD) in 1980.

Attention Deficit/Hyperactivity Disorder (ADHD)

Just as significant as the renaming of the condition at that time was the distinction made between two types of ADD: those with hyperactivity and those without it. Little research existed at the time on the latter subtype. However, later research suggested that ADD without hyperactivity might be a separate and distinct disorder of a different component of attention (selective or focused) than was the type of inattention seen in those with ADD with hyperactivity (persistence and distractibility). Thus, rather than being related subtypes of a single disorder with a shared, common impairment in attention, future research may show these subtypes to constitute separate disorders of attention altogether. Within a few years of the creation of the label ADD, concern was raised by Barkley in 1990 and Weiss and Hechtman in 1993 that problems with hyperactivity and impulse control were features critically important to differentiating the disorder from other conditions and to predicting later developmental risks. In 1987 the disorder was renamed Attention Deficit Hyperactivity Disorder. Diagnostic symptoms were identified from a single list of items incorporating all three constructs: hyperactivity, impulsivity, and inattention. The subtype of ADD without Hyperactivity was now renamed Undifferentiated ADD and relegated to minor diagnostic status until further research could clarify its nature and relationship to ADHD. Around this same time (mid-1980s to 1990s) reports began to appear that challenged the notion that ADHD was primarily a disturbance in attention. Over the previous decade, researchers studying information-processing capacities in children with ADHD were having difficulty demonstrating that the problems these children had with attending to tasks were actually attentional in nature (i.e., related to the processing of incoming information). Problems in response inhibition and preparedness of the motor control system appeared to be more reliably demonstrated. Researchers, moreover, were finding that the problems with hyperactivity and impulsivity were not separate constructs but formed a single dimension of behavior. All of this led to the creation of two separate lists of symptoms for ADHD when the latest diagnostic manual for psychiatry, The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (also known as the DSM-IV) was published by the American Psychiatric Association in 1994. In the

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DSM-IV, one symptom list now existed for inattention and another for hyperactive-impulsive behavior. The inattention list once again permitted the diagnosis of a subtype of ADHD that consisted principally of problems with attention (ADHD Predominantly Inattentive Type). But two other subtypes were also identified (Predominantly Hyperactive-Impulsive and Combined Types). As of this writing, debate continues over the core deficit(s) involved in ADHD, with increasing emphasis being given to a central problem specifically with behavioral inhibition and more generally with self-regulation or executive functioning.

III. DESCRIPTION AND DIAGNOSIS: A. The Core Symptoms Problems with attention consist of the child's inability to sustain attention or respond to tasks or play activities as long as others of the same age or to follow through on rules and instructions as well as others. The child appears more disorganized, distracted, and forgetful than others of the same age. Parents and teachers frequently complain that these children do not seem to listen as well as they should for their age, cannot concentrate, are easily distracted, fail to finish assignments, daydream, and change activities more often than others. Research corroborates that, when compared to normal children, ADHD children are often more "offtask," less likely to complete as much work as others, look away more from the activities they are requested to do (including television), persist less in correctly performing boring activities, and are slower and less likely to return to an activity once interrupted. Yet objective research does not find children with ADHD to be generally more distracted by most forms of extraneous events occurring during their task performance, although distractors within the task may prove more disruptive to them than to normal children. Research instead documents that ADHD children are more active than other children, are less mature in controlling motor movements, and have considerable difficulties with stopping an ongoing behavior. They frequently talk more than others and interrupt others' conversations. They are less able to resist immediate temptations and delay gratification and respond too quickly and too often when they are required to wait and watch for events to happen.

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Attention Deficit/Hyperactivity Disorder (ADHD)

Recent research shows that the problems with behavioral or motor inhibition arise first, at age 3 to 4 years, with those related to inattention emerging somewhat later in the developmental course of ADHD, at age 5 to 7 years. Whereas the symptoms of disinhibition seem to decline with age, those of inattention remain relatively stable during the elementary grades. Yet even the inattentiveness may decline by adolescence in some cases. A number of factors have been noted to influence the ability of children with ADHD to sustain their attention to task performance, to control their impulses to act, to regulate their activity level, and to produce work consistently. They include: time of day or fatigue; increasing task complexity where organizational strategies are required; extent of restraint demanded for the context; level of stimulation within the setting; the schedule of immediate consequences associated with the task; and the absence of adult supervision during task performance. It has been shown that children with ADHD are most problematic in their behavior when persistence in work-related tasks is required (i.e., chores, homework, etc.) or where behavioral restraint is necessary, especially in settings involving reduced parental monitoring (i.e., in church, in restaurants, when a parent is on the phone, etc.). Such children are least likely to pose behavioral management problems during free play, when little self-control is required. Fluctuations in the severity of ADHD symptoms have also been documented across a variety of school contexts. In this case, classroom activities involving self-organization and task-directed persistence are the most problematic, with significantly fewer problems posed by contexts involving fewer performance demands (i.e., at lunch, in hallways, at recess, etc.), and even fewer problems posed during highly entertaining special events (i.e., field trips, assemblies, etc.).

B. Associated Cognitive Impairments Although ADHD is defined by the presence of the two major symptom dimensions of inattention and disinhibition (hyperactivity-impulsivity), research indicates that these children often demonstrate deficiencies in many other abilities. These include: motor coordination and sequencing; working memory and mental computation; planning and anticipation or preparedness for action; verbal fluency and confron-

tational communication; effort allocation; applying organization strategies; the internalization of selfdirected speech; adhering to restrictive instructions; the self-regulation of emotions; and self-motivation. Several studies have also demonstrated what both Still (1902) and Douglas (1983) noted anecdotally years ago--ADHD may be associated with less mature or diminished moral reasoning and the moral control of behavior. The commonality among most or all of these seemingly disparate abilities is that all fall within the neuropsychological domain described as executive functions. The neurologist Joaquim Fuster wrote in 1989 that these executive abilities are probably mediated by the frontal cortex of the brain, and particularly the prefrontal lobes. Barkley has recently defined executive functions as being those neuropsychological processes that permit or assist with human self-regulation. Self-regulation is then defined as any self-directed form of behavior (both overt and covert) that serves to modify the probability of a subsequent behavior by the individual so as to alter the probability of a later consequence. Such behavior may even involve forgoing immediate rewards for the sake of maximizing delayed outcomes or even exposing oneself to immediate aversive circumstances for this same purpose. Self-regulatory behavior, therefore, includes thinking within this realm of private or covert self-directed behavior. By appreciating the role of the frontal lobes and the prefrontal cortex in these executive abilities, it is easy to see why researchers have repeatedly speculated that ADHD probably arises out of some disturbance or dysfunction of this brain region.

IV. THEORETICALFRAMEWORK Many different hypotheses on the nature of ADHD have been proposed over the past century, such as Still's (1902) notion of defective volitional inhibition and moral regulation of behavior, and Douglas' (1983) theory of deficient attention, inhibition, arousal, and preference for immediate reward. Few of these have produced models of the disorder that were widely adopted by both scientists and clinicians or that served to drive further programmatic research initiatives. Some of these theories have suggested that ADHD is a deficit in sensitivity to reinforcement, a more general

Attention Deficit/Hyperactivity Disorder (ADHD)

motivational disorder, or a deficit in rule-governed behavior (i.e., the control of behavior by language). Most recently, several theorists working in this area have proposed that ADHD represents a deficit behavioral inhibition; an assertion for which there is substantial evidence, at least for those subtypes that involve hyperactive-impulsive symptoms. Consistent with these proposals, Barkley outlined a model of ADHD in 1994 that was based upon an earlier theory by Jacob Bronowski first set forth in 1966 on the evolution of the unique properties of human language and their relationship to response inhibition. Bronowski's model was subsequently combined with that of Juaquim Fuster published in 1989, which specified that the overarching role of the prefrontal cortex is the cross-temporal organization of behavior. Barkley's hybrid theoretical model of ADHD places behavioral inhibition at a central point and supportive point in relation to four other executive functions dependent upon it for their own effective execution. These functions are working memory, the self-regulation of emotion/motivation, the internalization of speech, and reconstitution (analysis and synthesis of behavioral structures in the service of goal-directed behavioral creativity). The four functions are believed to permit and subserve human selfregulation, bringing behavior progressively under the control of internally represented information, often about the future, and transferring it at least partially away from the control of behavior by more immediate consequences and external events. The executive control of behavior afforded by these functions is proposed to result in a greater capacity for predicting and controlling one's self and one's environment so as to maximize future consequences over immediate ones for the individual. And, more generally, the interaction of these executive functions permits far more organized and effective adaptive functioning. Several assumptions are important in understanding this model as it is applied to ADHD. First, the capacity for behavioral inhibition begins to emerge first in the child's development, prior to or corresponding with the emergence of the four executive functions. Second, inhibition does not directly cause the activation of these executive functions but sets the occasion for their occurrence and is necessary for their effective performance. Third, these functions probably emerge at different times in the child's development and may have relatively independent developmental trajecto-

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ries, although interactive. Fourth, the sweeping cognitive impairments that ADHD creates across these executive functions are secondary to the primary deficit in behavioral inhibition, implying that if inhibition were to be improved, these executive functions would likewise improve. The deficit in behavioral inhibition is thought to arise principally from genetic and neurodevelopmental origins, rather than from purely social ones, although its expression is certainly influenced by a variety of social factors. The secondary deficits in the executive functions and self-regulation created by the primary deficit in inhibition feedback to contribute to further deficits in behavioral inhibition because selfregulation is required for self-restraint. Behavioral inhibition is viewed in the model as comprising three related processes: (1) the capacity to inhibit "prepotent" responses prior to their initiation; (2) the capacity to cease ongoing response patterns once initiated such that both (1) and (2) create delays in responding to events; and (3) the protection of this delay and the self-directed (often private or cognitive) actions occurring within it from interference by competing events and their prepotent responses (interference control). Prepotent responses are defined as those for which immediate reinforcement (both positive and negative) is available for their performance or for which there is a strong history of reinforcement in this context. Through the postponement of the prepotent, automatic responses and the creation of this protected period of delay, the occasion is set for the four executive functions to act effectively in modifying the individual's eventual initial responding to events or modifying their ongoing responses to those events (creating a sensitivity to feedback or errors). The executive system described here may exist so as to achieve a net maximization of both temporally distant and immediate consequences rather than immediate consequences alone. The chain of goal-directed, futureoriented behaviors set in motion by these acts of selfregulation is then also protected from interference during its performance by this same process of inhibition (interference control). Even if disrupted, the individual retains the capacity or intention (via working memory) to return to the goal-directed actions until the outcome is successfully achieved or judged to be no longer necessary. Space permits here only a brief description of each of the four executive components of this new model of

Attention Deficit/Hyperactivity Disorder (ADHD)

ADHD. The first of these involves working memory, or the capacity for prolonging and manipulating mental representations of events and using such information to control motor behavior. This particular type of memory can be thought of as remembering so as to do and serves to sustain otherwise fleeting information that will be useful in controlling subsequent responding, such as is seen in privately rehearsing a telephone number in mind so as to later dial it accurately. One component of working memory may be related to self-speech (verbal working memory), while a second component is related to perceptual imagery (visualspatial) and probably involves self-directed sensing, as in visual imagery or covert audition. This retention of information related to past events (retrospection) gives rise to the conjecturing of future events (prospection), which sets in motion a preparedness to act in anticipation of the arrival of these future events (anticipatory set). Out of this continuous referencing or sensing of past and future probably arises the psychological sense of time. These activities taking place in working memory appear to be dependent upon behavioral inhibition. Such working memory processes have been shown to exist in rudimentary form even in young infants permitting them to successfully perform delayed response tasks to a limited degree. As the capacity for inhibition increases developmentally, it probably contributes to the further efficiency and effectiveness of working memory. According to this model of ADHD, behavioral inhibition also sets the stage for the development of the second executive component of this model, that being the self-regulation of emotion in children. The inhibition of the initial prepotent response includes the inhibition of the initial emotional reaction that it may have elicited. It is not that the child does not experience emotion; rather, the behavioral reaction to or expression of that emotion is delayed along with any motor behavior associated with it. The delay in responding this creates allows the child time to engage in self-directed behaviors that will modify both the eventual response to the event as well as the emotional reaction that may accompany it. Because emotions are themselves forms of both motivational and arousal states, the model argues that deficits in the self-regulation of emotion should be associated with deficits in self-motivation and the self-control of arousal, particularly in the service of goal-directed behavior. The internalization of self-directed speech, as origi-

nally described by Vygotsky, forms the third executive component of this model of ADHD. During the early preschool years, speech, once developed, is initially employed for communication with others. As behavioral inhibition progresses, language becomes turned on the self. It now is not just a means of influencing the behavior of others but provides a means of reflection as well as a means for controlling one's own behavior (instruction). The fourth component of this model involves the capacity to rapidly take apart and recombine units of behavior, including language. The delay in responding that behavioral inhibition permits allows time for information related to the event to be mentally prolonged and then dissassembled so as to extract more information about the event that will aid in preparing a response to it. In a related fashion, previously learned response patterns can also be broken down into smaller units of behavior. This internal decomposition of information and its associated response patterns permits the complementary process to occur, that being synthesis, or the invention of novel combinations of behavioral structures, including words and ideas, in the service of goal-directed action. This gives a highly creative or generative character as well as a hierarchically organized nature to human goaldirected behavior. Finally, the internally represented information and motivation generated by these four executive functions is used to control a separate unit within the model, that being motor behavior itself. Such information serves to program, execute, and sustain behavior directed toward goals and the future, giving human behavior an intentional or purposive quality. Task-irrelevant movement is now more effectively suppressed, goal-directed behavior better sustained, and this pattern of behavior more efficiently reengaged should disruption of the behavioral pattern occur because of the control afforded by the internal information being generated from the four executive functions. The impairment in behavioral inhibition occurring in ADHD is hypothesized to disrupt the efficient execution of these executive functions, thereby limiting the capacity of these individuals for self-regulation. The result is an impairment in the cross-temporal organization of behavior, in the prediction and control of one's own behavior and environment, and inevitably in the maximization of long-term consequences for the individual. How does this model account for the problems

Attention Deficit/Hyperactivity Disorder (ADHD)

with attention believed to exist in ADHD ? According to this model, it is critical to distinguish between two forms of sustained attention that are traditionally confused in the research literature on ADHD. The first is called contingency-shaped attention. This refers to continued responding in a situation or to a task as a function of the immediate available contingencies of reinforcement provided by the task or its context. Responding that is maintained under these conditions then is directly dependent on the immediate environmental contingencies. Many factors affect this form of sustained attention or responding: the novelty of the task, the intrinsic interest the activity may hold for the individual, the immediate reinforcement it provides for responding in the task, the state of fatigue of the individual, and the presence or absence of an adult supervisor (or other stimuli which signal other consequences for performance that are outside the task itself). The model predicts that this type of sustained attention relatively unaffected by ADHD as it is behavior under the control of external events. As children mature, however, a second form of sustained attention emerges described in the model as goal-directed persistence. This form of sustained responding arises as a direct consequence of the development of self-regulation or the control of behavior by internally represented information. Such persistence derives from the development of a progressively greater capacity by the child to hold events, goals, and plans in mind (working memory), to adhere to rules governing behavior and to formulate and follow such rules, to self-induce a motivational state supportive of the plans and goals formulated by the individual so as to maintain goal-directed behavior, and even to create novel behaviors in the service of the goal's attainment. The capacity to initiate and sustain chains of goaldirected behavior in spite of the absence of immediate environmental contingencies for their performance is predicted to be the form of sustained attention disrupted by ADHD. Apart from this heuristically valuable distinction in forms of sustained attention, this theoretical model of ADHD makes numerous predictions about the cognitive and behavioral deficits likely to be found in those with the disorder (i.e., impaired working memory and sense of time, delayed internalization of speech, etc.), many of which have received little or no attention in research on ADHD. It also provides a framework by which to better organize and understand the numerous cognitive deficits identified in previous studies of

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children with ADHD than does the current view of ADHD as being chiefly an attention deficit.

V. POTENTIAL ETIOLOGIES The precise causes of ADHD are unknown at the present time. Numerous causes have been proposed, but evidence for many has been weak or lacking entirely. However, a number of factors have been shown to be associated with a significantly increased risk for ADHD in children. The vast majority of the potentially causative factors associated with ADHD that are supported by empirical research seem to be biological in nature; that is, they are factors known to be related to or to have a direct effect on brain development and/or functioning. The precise causal pathways by which these factors lead to ADHD, however, are simply not known at this time. Even so, far less evidence is available to support any purely psychosocial etiology of ADHD. In the vast majority of cases where such psychosocial risks have been found to be significantly associated with ADHD or hyperactivity, more careful analysis has shown these to be either the result of ADHD in the child or, far more often, to be related to aggression or conduct disorder rather than to ADHD. For instance, the child management methods used by parents, parenting stress, marital conflict, or parental psychopathology have now been shown to be far more strongly associated with aggressive and antisocial behavior than with ADHD. The strong hereditary influence in ADHD may also contribute to an apparent link between ADHD and poor child management by a pare n t ~ a link that may be attributable to the parent's own ADHD. The environment in which the child is raised and schooled probably plays a larger role in determining the outcomes of children with the disorder and a much lesser role in primary causation. Throughout the century, investigators have repeatedly noted the similarities between symptoms of ADHD and those produced by lesions or injuries to the frontal lobes of the brain, particularly the prefrontal cortex. Both children and adults suffering injuries to the certain regions of prefrontal cortex demonstrate deficits in sustained attention, inhibition, working memory, the regulation of emotion and

913

Attention Deficit/Hyperactivity Disorder (ADHD)

motivation, and the capacity to organize behavior across time. Numerous other lines of evidence have been suggestive of a neurological origin to the disorder. Several studies have examined cerebral blood flow in ADHD and normal children. They have consistently shown decreased blood flow to the prefrontal regions of the brain and the striatum with which these regions are richly interconnected, particularly in its anterior portion. More recently, studies using positron emission tomography (PET) to assess cerebral glucose metabolism have found diminished metabolism in adults and adolescent females with ADHD although not in adolescent males with ADHD. However, significant correlations have been noted between diminished metabolic activity in the left anterior frontal region of the brain and severity of ADHD symptoms in adolescent males with ADHD. This demonstration of an association between the metabolic activity of certain brain regions and symptoms of ADHD is critical in demonstrating a connection between the findings pertaining to brain activation and the behavior comprising ADHD. More detailed analysis of brain structures using high resolution magnetic resonance imaging (MRI) devices has also suggested differences in some brain regions in those with ADHD. Initial studies that focused on reading-disabled children and used ADHD children as a contrast group examined the region of the left and right temporal lobes (the planum temporale). These regions are thought to be involved with auditory detection and analysis and, therefore, with certain subtypes of reading disabilities. For some time, researchers studying reading disorders have focused on these brain regions because of their connection to the rapid analysis of speech sounds. Children with ADHD and children with reading disabilities were found to have smaller right hemisphere plana temporale than the control group, while only the reading disabled children had a smaller left plana temporale. In another study, the corpus callosum was examined in subjects with ADHD. This structure assists with the interhemispheric transfer of information. Those with ADHD were found to have a smaller callosum, particularly in the area of the genu and splenium and that region just anterior to the splenium. An attempt to replicate this finding, however, failed to show any differences between ADHD and control children in the size or shape of the entire corpus callosum with the ex-

ception of the posterior portion of the splenium, which was significantly smaller in subjects with ADHD. Two additional studies examining the corpus callosum, however, documented smaller anterior (rostral) regions in children with ADHD; findings more consistent with prior studies of brain anatomy and functioning in children with ADHD. Most recently, two studies using larger samples of ADHD and normal children and MRI technology have both documented a smaller right prefrontal cortex and smaller right striatum and right basal ganglia (of which the striatum is a part) in ADHD children. Thus, despite some inconsistencies in findings across some of the earlier studies of brain morphology and functioning in ADHD, more recent studies are increasingly identifying the prefrontal regions of the brain and certain regions of the basal ganglia, such as the striatum, as probably being involved in the disorder. None of these studies found evidence of frank brain damage in any of these structures in those with ADHD. This is consistent with past reviews of the literature conducted by Michael Rutter in 1983 suggesting that brain damage was related to less than 5% of those with hyperactivity. It is also consistent with more recent studies of twins suggesting that nonshared environmental factors, such as pre-, peri-, and postnatal neurological insults, among other factors, account for approximately 15 to 20% of the differences among individuals in the behavioral pattern associated with ADHD (inattention and hyperactive-impulsive behavior). Where differences in brain structures are found, they are probably the result of abnormalities that arise in brain development (embryology) within these particular regions, the causes of which are not known but may have to do with particular genes responsible for the construction of these brain regions. No evidence exists to show that ADHD is the result of abnormal chromosomal structures (as in Down's Syndrome), their fragility (as in Fragile X) or transmutation, or of extra chromosomal material (as in XXY syndrome). Children with such chromosomal abnormalities may show greater problems with attention, but such abnormalities are very uncommon in children with ADHD. By far, the preponderance of research evidence suggests that ADHD is a trait that is highly hereditary in nature, making heredity one of the most well substantiated among the potential etiologies for ADHD. Multiple lines of research support such a conclusion. For

Attention Deficit/Hyperactivity Disorder (ADHD)

years, researchers have noted the higher prevalence of psychopathology in the parents and other relatives of children with ADHD. In particular, higher rates of ADHD, conduct problems, substance abuse, and depression have been repeatedly observed in these studies. Research such as that by Joseph Biederman and colleagues at the Harvard Medical School (Massachusetts General Hospital) shows that between 10 and 35% of the immediate family members of children with ADHD are also likely to have the disorder, with the risk to siblings of the ADHD children being approximately 32%. More recent studies even suggest that if either parent has ADHD, the risk to offspring for the disorder may be as high as 50%. [See CONDUCT DISORDERS;DEPRESSION;SUBSTANCEABUSE.] Another line of evidence for genetic involvement in ADHD has emerged from studies of adopted children, which have found higher rates of hyperactivity in the biological parents of hyperactive children than in adoptive parents of hyperactive children. Biologically related and unrelated pairs of international adoptees also identified a strong genetic component to the behavioral dimension underlying ADHD. Studies of twins conducted in the United States, Australia, and the United Kingdom provide a third avenue of evidence for a genetic contribution to ADHD. In general, these studies suggest that if one twin is diagnosed with ADHD, the concordance for the disorder in the second twin may be as high as 81 to 92% in monozygotic twins but only 29 to 35% in dizygotic twins. Quantitative genetic analyses of a large sample of families studied in Boston by Joseph Biederman and his colleagues suggest that a single gene may account for the expression of the disorder. The focus of research recently has been on the dopamine type 2 gene, given findings of its increased association with alcoholism, Tourette's Syndrome, and ADHD. However, difficulties have arisen in the replication of this finding. More recent studies have implicated the dopamine transporter gene as being involved in ADHD as might the D4D repeator gene, which has shown an association with novelty-seeking and risk-taking personality traits. Clearly, research into the genetic mechanisms involved in the transmission of ADHD across generations will prove an exciting and fruitful area of research endeavor over the next decade as the human genome is mapped and better understood and as more sophisticated genetic technologies arising from this

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project come to be applied to the study of the genetics of ADHD. Pre-, peri-, and postnatal complications, and malnutrition, diseases, trauma, and other neurologically compromising events may occur during the development of the nervous system before and after birth. Among these various biologically compromising events, several have been repeatedly linked to risks for inattention and hyperactive behavior. Elevated body lead burden has been shown to have a small but consistent and statistically significant relationship to the symptoms comprising ADHD. However, even at relatively high levels of lead, less than 38% of these children are rated as hyperactive on teacher rating scales, implying that most lead-poisoned children do not develop symptoms of ADHD. Other types of environmental toxins found to have some relationship to inattention and hyperactivity are prenatal exposure to alcohol and tobacco smoke.

VI. EPIDEMIOLOGY OF ADHD The prevalence of ADHD, as reviewed by Peter Szatmari in 1992, using large epidemiological studies ranges from a low of 2 % to a high of 6.3 %, with most falling within the range of 4.2 to 6.3 %. Most studies have found similar prevalence rates in elementary school-aged children. Differences in prevalence rates are due in part to different methods of selecting these populations, to the criteria used to define a case of ADHD, and to the age range of the samples. For instance, prevalence rates may be 2 to 3% in females but 6 to 9% in males during the 6 to 12-year-old age period, but fall to 1 to 2% in females and 3 to 4.5 % in males by adolescence. While the declining prevalence of ADHD with age may reflect real recovery from the disorder, it may also involve, at least in part, an artifact of methodology. This artifact results from the use of items in the diagnostic symptom lists across the life span that are were developed upon and chiefly applicable to young children. These items may reflect the underlying constructs of ADHD very well at younger ages but may be increasingly less appropriate for older age groups. This could create a situation where individuals remain impaired by ADHD characteristics as they mature, but outgrow the diagnostic symptom list for the dis-

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order, resulting in an illusory decline in prevalence over development. Until more age-appropriate symptoms are studied for adolescent and adult populations, this issue remains unresolved. Gender appears to play a significant role in determining prevalence of ADHD within a population. On average, males are between 2 and 6 times more likely than females to be diagnosed with ADHD in epidemiological samples of children, with the average being roughly 3:1. Within clinic-referred samples, the sex ratio can rise to 6:1 to 9:1, suggesting that males with ADHD are far more likely to be referred to clinics than females, especially if they have an associated oppositional or conduct disorder. It is unclear at this time why males should be more likely to have ADHD than females. This could result partly from an artifact of the relationship between male gender and more aggressive and oppositional behavior; such behavior is known to increase the probability of referral to mental health centers. Because such behavior is often associated with ADHD, clinic-referred males are also more likely to have ADHD. The greater preponderance of males might also, in part, be an artifact of applying a set of diagnostic criteria developed primarily on males to females. Using a predominantly male population to set diagnostic criteria as was done for the D S M - I V (see below) could create a higher threshold for diagnosis for females relative to other females than for males relative to other males. Such a circumstance argues for the eventual examination of whether separate diagnostic criteria (symptom thresholds) ought to be considered for each gender. ADHD occurs across all socioeconomic levels. Where differences in prevalence rates are found across levels of social class, they may be artifacts of the source used to define the disorder or of the association of ADHD with other disorders known to be related to social class, such as aggression and conduct disorder. No one, however, has made the argument that the nature or qualitative aspects of ADHD differ across social classes. Hyperactivity or ADHD is present in all countries studied so far, such as New Zealand, Japan, Italy, Germany, India, and Australia. While it may not receive the same diagnostic label in each country, the behavior pattern comprising the disorder appears to be present internationally. ADHD arises also in all ethnic groups studied so far.

VII. DEVELOPMENTALCOURSE AND ADULT OUTCOME Major follow-up studies of clinically referred hyperactive children have been ongoing during the last 25 years at five sites: Montreal, New York City, Iowa City, Los Angeles, and Milwaukee. Follow-up studies of children identified as hyperactive during epidemiological screenings of general populations have also been conducted in the United States, Australia, New Zealand, and England. The onset of ADHD symptoms has been found to be generally in the preschool years, typically by age 3 or 4, and usually by entry into formal schooling. First to arise in many cases is the pattern of hyperactiveimpulsive behavior and, in some cases, oppositional and aggressive conduct. Preschool-aged children with significant degrees of inattentive and hyperactive behavior who are difficult to manage for their parents or teachers and whose pattern of such behavior is persistent for at least a year or more are highly likely to have ADHD and to retain their symptoms into the elementary school years. By the time ADHD children move into the age range of 6 to 12 years, the problems with hyperactiveimpulsive behavior are increasingly associated with difficulties with the form of sustained attention referred to above as goal-directed persistence and distractibility (poor interference control). These symptoms of inattention appear to arise by the age of 5 to 7 years and may emerge out of the increasing difficulties ADHD children are having with self-regulation. The inattentiveness evident in children having ADD without Hyperactivity (Predominantly Inattentive Type of ADHD) may be of a qualitatively different form (focused or selective attention) and may not emerge or be impairing of the child's school performance until even later, such as mid-to-late childhood. When ADHD is present in clinic-referred children, the likelihood is that 50 to 80% will continue to have their disorder into adolescence. Although severity levels of symptoms are declining over development, this does not mean hyperactive children are necessarily outgrowing their disorder relative to normal children; like mental retardation, the disorder of ADHD is defined by a developmentally relative deficiency, rather than an absolute one, that persists in many children over time.

Attention Deficit/Hyperactivity Disorder (ADHD)

The persistence of ADHD symptoms across childhood as well as into early adolescence appears to be associated with the initial degree of hyperactive/impulsive behavior in childhood, the co-existence of conduct problems or oppositional/hostile behavior, poor family relations and conflict in parent-child interactions, as well as maternal depression. These predictors have also been associated with the development and persistence of oppositional and conduct disorder into adolescence. The Montreal follow-up study of Weiss and Hechtman reported in 1993 that at least half of their subjects were still impaired by some symptoms of the disorder in adulthood. The New York City longitudinal study by Salvatore Mannuzza and Rachel Klein suggested that 18 to 30% of hyperactive children continue to have significant symptoms of ADHD into adulthood. Most recently, the Milwaukee follow-up study by Barkley and Fischer suggests that the source of information about the symptoms may be a significant factor in establishing the persistence of the disorder into adulthood. Less than 25 % of ADHD children reported having significant symptom levels of the disorder in adulthood when asked about themselves as young adults while their parents indicated that more than 60% of these subjects continued to have clinically significant degrees of the disorder as young adults. Until more studies report adult outcomes for ADHD children using clinical diagnostic criteria appropriate for adults and collecting information not only from the adult but from a parent or an immediate family member who knows them well, the true persistence of the disorder into adulthood will remain a matter of some controversy. At the very least, current research suggests it may be 30 to 50%, although the percentage may be higher among clinic-referred children followed to adulthood.

VIII. DIAGNOSTIC CRITERIA

The most recent diagnostic criteria for ADHD as defined in the DSM-IV (1994) are set forth in Table I. They stipulate that individuals have had their symptoms of ADHD for at least 6 months, that these symptoms exist to a degree that is developmentally deviant, and that they have developed by 7 years of age. From the Inattention item list, six of nine items must be en-

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dorsed as developmentally inappropriate. Likewise, from the Hyperactive-Impulsive item list, six of nine items must be endorsed as deviant. Depending upon whether criteria are met for either or both symptom lists will determine the type of ADHD that is to be diagnosed: Predominantly Inattentive, Predominantly Hyperactive-Impulsive, or Combined Type. These diagnostic criteria are empirically derived and are the most rigorous ever available in the history of clinical diagnosis for this disorder. They were developed by a committee of some of the leading experts in the field, a literature review of research on ADHD, an informal survey of rating scales assessing the behavioral dimensions related to ADHD by the committee, and from statistical analyses of the results of a field trial of the items using a large sample of children from 10 different sites in North America. Controversy continues over whether ADHDmPredominantly Inattentive Type represents a true subtype of ADHD. It is unclear if these children share a common attentional disturbance with the Combined Type and are distinguished simply by the relative absence of significant hyperactivity-impulsivity or whether they have a qualitatively different impairment in attention from that seen in the Combined Type. Several recent reviews of the literature have suggested that this is not in fact a true subtype but actually a separate, distinct disorder having a different attentional disturbance than the one present in ADHDmCombined Type. However, evidence for this subtype's existence was at least strong enough to place it within the DSM-IV while awaiting more research on its course and treatment responsiveness to help clarify its status. The very limited research available to date suggests that Predominantly Inattentive ADHD children have more problems in the focused or selective component of attention, appear sluggish in their speed of information processing, and may have memory retrieval problems; in contrast, those with ADHD-Combined Type have more problems with persistence and distractibility as well as with poor inhibition. The research criteria from the International Classification of Diseases (ICD-10) for Hyperkinetic Disorders closely resemble the DSM-IV in stressing two lists of symptoms related to inattention and overactivity and in requiring that pervasiveness across settings be demonstrated. The specific item contents, manner of presenting these symptoms lists within the home and school setting, requirement for office observation of

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Attention Deficit/Hyperactivity Disorder (ADHD)

Table I

DSM-IV Criteria for ADHD

A. Either (1) or (2): (1) Six (or more) of the following symptoms of inattention have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level: Inattention (a) Often fails to give close attention to details or makes careless mistakes in schoolwork, work, or other activities; (b) Often has difficulty sustaining attention in tasks or play activities; (c) Often does not seem to listen when spoken to directly; (d) Often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the work place (not due to oppositional behavior or failure to understand instructions); (e) Often has difficulty organizing tasks and activities; (f) Often avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort (such as schoolwork or homework); (g) Often loses things necessary for tasks or activities (e.g., toys, school assignments, pencils, books, or tools); (h) Is often easily distracted by extraneous stimuli; (i) Is often forgetful in daily activities. (2) Six (or more) of the following symptoms of hyperactivityimpulsivity have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level: Hyperactivity (a) Often fidgets with hands or feet or squirms in seat; (b) Often leaves seat in classroom or in other situations in which remaining seated is expected; (c) Often runs about or climbs excessively in situations in which it is inappropriate (in adolescents or adults, may be limited to subjective feelings of restlessness); (d) Often has difficulty playing or engaging in leisure activities quietly; (e) Is often "on the go" or often acts as if "driven by a motor"; (f) Often talks excessively. Impulsivity (g) Often blurts out answers before the questions have been completed; (h) Often has difficulty awaiting turn; (i) Often interrupts or intrudes on others (e.g., butts into conversations or games); B. Some hyperactive-impulsive or inattentive symptoms that caused impairment were present before age 7 years. C. Some impairment from the symptoms is present in two or more settings (e.g., at school [or work] and at home).

Table I

Continued

D. There must be clear evidence of clinically significant impairment in social, academic, or occupational functioning. E. The symptoms do not occur exclusively during the course of a Pervasive Developmental Disorder, Schizophrenia, or other Psychotic Disorder, and are not better accounted for by another mental disorder (e.g., Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder). Code based on type: 314.01 Attention-Deficit/Hyperactivity Disorder, Combined Type: if both Criteria A 1 and A2 are met for the past six months. 314.00 Attention-Deficit/Hyperactivity Disorder, Predominantly Inattentive Type: if Criterion A1 is met but Criterion A2 is not met for the past 6 months. 314.01 Attention-Deficit/Hyperactivity Disorder, Predominantly Hyperactive-Impulsive Type: if Criterion A2 is met but Criterion A1 is not met for the past six months. Coding note: For individuals (especially adolescents and adults) who currently have symptoms that no longer meet full criteria, "In Partial Remission" should be specified. From the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders. Washington, DC: American Psychiatric Association, 1994. Copyright by American Psychiatric Association. Reprinted with permission.

the s y m p t o m s , a n d the earlier age of onset (age 6 years) clearly differs f r o m the D S M - I V , as does the specification of a lower b o u n d of I Q b e l o w w h i c h the diagnosis s h o u l d n o t be given. Social critics have c h a r g e d t h a t professionals have been t o o quick to label energetic a n d e x u b e r a n t child r e n as h a v i n g this m e n t a l d i s o r d e r a n d t h a t e d u c a t o r s also m a y be using these labels simply as an excuse for p o o r e d u c a t i o n a l e n v i r o n m e n t s . This w o u l d imply t h a t children w h o are h y p e r a c t i v e or are d i a g n o s e d w i t h A D H D are actually n o r m a l but are being labelled as m e n t a l l y d i s o r d e r e d because of p a r e n t a n d t e a c h e r intolerance. If this were actually true, t h e n we s h o u l d find no differences of a n y cognitive, b e h a v i o r a l , or social significance b e t w e e n A D H D children a n d n o r m a l children. We s h o u l d also find A D H D is n o t associated w i t h a n y significant later risks in d e v e l o p m e n t for mala d j u s t m e n t w i t h i n a n y d o m a i n s of a d a p t i v e f u n c t i o n ing, social, or school p e r f o r m a n c e . F u r t h e r m o r e , research on p o t e n t i a l etiologies for the d i s o r d e r s h o u l d also c o m e up e m p t y - h a n d e d . This is h a r d l y the case. It s h o u l d b e c o m e clear f r o m the totality of i n f o r m a tion on A D H D p r e s e n t e d here a n d elsewhere in re-

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views such as those by Barkley in 1990 and Hinshaw in 1994 that those with ADHD have significant deficits in behavioral inhibition and associated executive functions that are critical for effective self-regulation, that these deficits are significantly associated with various biological factors, and particularly genetic and neurodevelopmental ones, and that ADHD symptoms and other associated disorders pose substantial risks for these individuals over the life span.

IX. CONCLUSION Future research needs to address the nature of the attentional problems in ADHD given that current research seriously questions whether these problems are actually within the realm of attention at all. Most studies of ADHD point to impairment within the motor, output, or motivational systems of the brain being most closely affiliated with ADHD rather than deficiencies in the sensory processing systems where attention has been traditionally thought to reside. Even the problem with sustained attention may represent a deficiency in a more complex form of goal-directed persistence that arises out of poor self-regulation rather than representing a disturbance in the more primitive form of sustained responding that is contingency shaped. Our understanding of the very nature of the disorder of ADHD is at stake in how research comes to resolve these issues. Key to understanding ADHD is the notion that it is actually a disorder of behavioral performance and not one of skill; of how and when one's intelligence comes to be applied in everyday effective adaptive functioning and not in that knowledge itself; of doing what one knows how to do rather than of knowing what to do. The concepts of time, timing, and timeliness are likely to prove increasingly crucial in deepening our understanding of ADHD. In particular, psychological time, how it is sensed, and how it is used in the crosstemporal organizing of complex, goal-directed behavior and in self-regulation may come to be a critical element in models of ADHD. Undoubtedly, research on brain function and structure is likely to further our understanding of the unique role of the prefrontal cortex and the midbrain structures with which it is closely associated in ADHD. But advances in theoreti-

cal models must also occur in order to better understand the nature and organization of the executive functions subserved by these brain regions and even the relationship of genetics, which builds these brain regions in embryological development, to ADHD and the deficits it produces in behavioral performance. And the current body of twin studies further suggests that while such genetic influences are important, there exists a lesser but still important role for unique (nonshared) environmental influences on the differences among individuals in symptoms of ADHD and its underlying behavioral traits. Some of these influences are no doubt social in nature while others are likely to be nongenetic pre-, peri-, and postnatal factors affecting brain development. Such studies, not only on the basic psychological nature of ADHD but also on its basic neuroanatomic and neurogenetic origins and the influence of unique social factors upon them, forebode further significant and exciting advances to come in the understanding and treatment of this fascinating developmental disorder.

BIBLIOGRAPHY American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author. Barkley, R. A. (1997a). Behavioral inhibition, sustained attention, and executive functions: Constructing a unifying theory of ADHD. Psychological Bulletin, 121, 65-94. Barkley, R. A. (1977b). ADHD and the nature of self-controI. New York: Guilford. Barkley, R. A. (1994). Impaired delayed responding: A unified theory of attention deficit hyperactivity disorder. In D. K. Routh (Ed.), Disruptive behavior disorders: Essays in honor of Herbert Quay (pp. 11-57). New York: Plenum. Barkley, R. A. (1990). Attention deficit hyperactivity disorder: A handbook for diagnosis and treatment. New York: Guilford. Biederman, J., Faraone, S. V., Keenan, K., & Tsuang, M. T. (1991 ). Evidence of a familial association between attention deficit disorder and major affective disorders. Archives of General Psychiatry, 48, 633-642. Bronowski, J. (1977). Human and animal languages. A sense of the future (pp. 104-131 ). Cambridge, MA: MIT Press. Denckla, M. B. (1994). Measurement of executive function. In G. R. Lyon (Ed.), Frames of reference for the assessment of learning disabilities: New view on measurement issues (pp. 117142). Baltimore, MD: Paul H. Brookes. Douglas, V. I. (1983). Attention and cognitive problems. In M. Rutter (Ed.), Developmental neuropsychiatry (pp. 280329). New York: Guilford. Fuster, J. M. (1989). The prefrontal cortex. New York: Raven.

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Hinshaw, S. P. (1994). Attention deficits and hyperactivity in children. Thousand Oaks, CA: Sage. Rutter, M. (1983). Introduction: Concepts of brain dysfunction syndromes. In M. Rutter, (Ed.), Developmental neuropsychiatry (pp. 1-14). New York: Guilford.

Szatmari, P. (1992). The epidemiology of ADHD. In G. Weiss (Ed.), Child and adolescent psychiatric clinics of North America (Vol. 1, pp. 361-372). Philadelphia: W. B. Saunders. Weiss, G. & Hechtman, L. (1993). Hyperactive children grown up. New York: Guilford.

I

Autism and Pervasive Developmental Disorders

I. II. III. IV. V. VI. VII. VIII. IX.

Deborah Fein and LeeAnne Green

Lynn Waterhouse

University of Connecticut

The College of New Jersey

Historical Development of the Concept of Autism DSM-IV Criteria Behavioral and Cognitive Characteristics Developmental Course and Prognosis Epidemiology Boundary Conditions and Comorbidity Biological Factors Clinical Assessment Treatment

PERVASIVE DEVELOPMENTAL DISORDERS (PDD) is the current term for what is probably a group of related neurodevelopmental disorders characterized by similar behavioral profiles. Autistic Disorder is the most widely studied and best described of these disorders. It is characterized by deficits in social relatedness, deficits in language and communication, and stereotyped and restricted patterns of behavior, and is frequently but not always accompanied by mental retardation.

Echolalia Parrot-like repetition of utterances either immediately after hearing the utterance (immediate echolalia) or at a later time (delayed echolalia). Gaze Avoidance The tendency to avert one's eyes in order to avoid eye-to-eye contact with another. Mainstreaming The integration, or partial integration, of a child with special needs into a classroom of typically developing children. Metaphorical Language Idiosyncratic utterances whose meaning is clear only to those who are familiar with the child's history. Pragmatics The social aspects of language, or the communicative uses to which language is put. Stereotypies Repetitive and often unusual motor movements. Stimulus Overselectivity A tendency to attend to a restricted portion of a stimulus array or a complex stimulus. Theory of Mind An understanding or concept of the existence of mental representations, including knowledge and perspective, in others.

I. HISTORICAL DEVELOPMENT OF THE CONCEPT OF AUTISM Autism was first described by Leo Kanner in 1943 and became known as Infantile Autism or Autistic Disorder. The concept has expanded since that date, and the term "Kanner autism" is sometimes used to refer to cases with symptoms similar to those of Kanner's original sample; such cases are a subset of PDD. Kanner's original description remains influential, and there is a tendency in the literature to assume that persons with "Kanner autism" represent the "nuclear" or "core" form of PDD, an assumption that may not be warranted. Kanner identified symptoms in three main groups: an autistic aloneness, a failure to use language communicatively, and an obsessive insistence on sameness in the environment; these are still the three areas of symptomatology used in current diagnostic systems. Although Kanner originally viewed the autis-

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tic aloneness as probably representing a constitutional defect, the two decades following his original work were marked by an unfortunate shift toward a psychodynamic/environmental view of the causation of autism. This served to derail any significant progress in understanding the disorder, as well as to cause a great deal of additional anguish to parents of autistic children. Beginning with Rimland's seminal work on autism in 1964, psychology and psychiatry began to explore seriously the biological foundations of autism, and theories of autism as resulting from disturbances in attention, language, sensory integration, perceptual constancy, and other neurological functions were promulgated and tested. Beginning in the early to mid1980s, research attention also began to focus seriously on the social and affective aspects of autism, both to clarify the range of heterogeneity in autistic children's functioning, and to posit new core deficits in these areas. Currently, researchers stressing both cognitive and social/affective deficits as primary are in agreement that the fundamental problem is a neurological, and not an environmental, one. Differential diagnosis was a conceptual problem for early autism research. Some clinicians believed that autism was a variant of or precursor to schizophrenia. Only in the 1970s came an awareness that disorders beginning in infancy must be regarded as separate in kind from those with onset in later childhood, adolescence, or adulthood. Autistic-like disorders virtually always begin before age 3, while schizophrenic-like disorders virtually never begin before age 7. This realization revitalized interest in infantile autism as a distinct nosologic entity, leading to the development of more operationally precise diagnostic criteria and a reconceptualization of the syndrome as a pervasive developmental disorder, under which label it was incorporated by the American Psychiatric Association in the third edition of that body's Diagnostic and Statistical Manual of Mental Disorders (DSM-III ); this conceptualization has been retained in DSM-III-R and DSM-

IV. [See SCHIZOPHRENIA.]

II. DSM-IV CRITERIA Current diagnostic practice, as reflected in the DSMIV, classifies Autistic Disorder as one of four specific

entities within Pervasive Developmental Disorder. Autistic Disorder is marked by the presence of symptomatology in three areas: (1) qualitative impairment in social interaction, as manifested by such behaviors as abnormal or reduced eye contact with others, failure to develop peer relationships, lack of spontaneous sharing of interests with others (e.g., showing or pointing out objects of interest to the caregiver), (2) qualitative impairment in communication, as manifested by delayed or deviant language without attempts to compensate through nonverbal communication, poor conversational skills if speech is present, and repetitive and stereotyped language and play, and (3) a restricted and repetitive repertoire of behaviors and interests, including preoccupations and rituals, or severe resistance to environmental changes. The specific behavioral manifestations of these traits differ by degree of accompanying retardation and age. A high-functioning, older autistic individual, for example, may attempt to be social, but violate implicit rules of social behavior and be insensitive to unspoken social signals, while a low-functioning or much younger autistic individual may react to other people as if they were little different from inanimate objects. Similarly, a high-functioning, older autistic individual may have perseverative interests in such topics as constellations, train schedules, or dinosaurs, and attempt to engage others in conversations on these subjects, while a lower functioning or younger autistic individual might engage in repetitive motor rituals. The other specific syndromes classified as Pervasive Developmental Disorders include Rett's Disorder, Asperger's Disorder, and Childhood Disintegrative Disorder. Rett's Disorder has marked behavioral commonalities with Autistic Disorder, including poor social engagement and mental retardation, but differs from Autistic Disorder in several ways: in Rett's Disorder, the retardation is more invariant and more typically severe, the disorder seems to present only in girls, it is marked by a characteristic pattern of head growth deceleration and loss of purposeful hand movements, sometimes accompanied by hand wringing behavior, following a period of normal development. Many girls with Rett syndrome also have epilepsy and other neurologic abnormalities. Asperger's Disorder is often considered a mild form of Autistic Disorder, and there is still controversy about how distinct it is from autism;

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diagnostically, it can be distinguished from autism by normal development of language. Childhood Disintegrative Disorder differs from Autistic Disorder in that the former is marked by a distinctive pattern of developmental regression following at least two years of normal development. This disorder is much rarer than autism, and controversy exists here, too, about the etiological and phenomenological distinctiveness between Childhood Disintegrative Disorder and Autistic Disorder. [See MENTAL RETARDATION AND MENTAL HEALTH.]

III. BEHAVIORAL AND COGNITIVE CHARACTERISTICS A. Behavioral Characteristics in Autism I. Social Behavior Social behavior is considered by many as the hallmark of autism. As with all features of autism, social impairment is highly heterogeneous; it varies with age, with IQ, with setting, and with interactive partner, and is modifiable by treatment. Social impairment is generally most severe in the preschool years; it is in early childhood that genuine aloofness is seen. Older children may initiate interaction to get their needs met, or may be responsive but noninitiating to others. Older or higher-functioning autistic individuals may approach others in an idiosyncratic, intrusive, and socially insensitive way. These three general styles (aloof, passive, active-but-odd) form the basis of a social typology described by Lorna Wing, and validated by several later studies. Highly structured settings with enforced proximity to peers may elicit the best peer interactions. Relationships with other children are almost always more impaired than the corresponding behavior with adults; other children may be ignored when adults are not. Behavioral deficits in social interaction are varied; among the most important, especially in early life, are (1) poor spontaneous imitation of others' language and behavior, (2) gaze avoidance or other deficits in the use of eye-to-eye gaze to modulate or initiate interaction, and (3) deficits in various joint attention skills, including drawing an adult's attention to an object of interest by showing or pointing, and following an adult's attentional focus in order to share it. On the

other hand, the "pervasive lack of responsiveness" described in DSM-III is actually uncommon; many young autistic children are selectively attached to their parents, derive comfort from their presence, and enjoy physical affection.

2. Communication and Play Older studies were composed primarily of clinical descriptions of language features such as pronoun reversal, echolalia, and metaphorical language. More systematic studies have appeared, based on modern understanding of the separable components of language. The more severely affected autistic child may remain nonverbal or minimally verbal and poorly intelligible. In those who develop more language, phonology, syntax, and (more arguably) semantics are relatively spared, although still often at a lower level than nonverbal skills. Verbal memory, prosody, and pragmatics, on the other hand, represent areas of particular difficulty for the average autistic child. In the domain of pragmatics, it is noted that communicative functions are generally more need-oriented and less affiliative, and that violations of language use rules are common, such as violations of implicit rules concerning interpersonal distance while speaking, and the rules of turn-taking in conversational exchange, as well as word selection which is overly formal or pedantic. Symbolic play is also often observed to be lacking in young autistic children, who sometimes prefer nonsymbolic play activities such as puzzles or other manipulatives. When symbolic play develops, it can be unusually repetitive and inflexible in nature. Some recent evidence suggests that high-functioning autistic children may be not so much incapable as uninterested in engaging in frequent or complex symbolic play.

3. Preoccupations, Perseverations, and Resistance to Change These constitute the third symptom group. These behaviors range from simple or complex motor stereotypies, to "self-stimulatory" sensory behaviors such as watching fans or water, to long-term perseverative interests. The resistance to change is manifested by tantrums or other extreme reactions to changes in environmental features or in routines. Despite the equal role assigned to perseverations/preoccupations and resistance to change in diagnostic criteria, some

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recent data suggest that resistance to change is a less common feature of autism than perseverations/preoccupations.

B. Cognitive Characteristics Overall cognitive level, or presence of mental retardation, is an important feature of the individual autistic child, and powerfully predicts the functional outcome that can be expected for the child. Recent work by several research groups, such as the group headed by Rapin (see Bibliography) suggests that high- and low-functioning autism may be significantly different in behavioral manifestations, history, and prognosis, that approximately half of the autistic population falls into each group, and that an IQ cutoff of about 65 makes the most appropriate division between highand low-functioning autism. Beyond studies of overall cognitive level, many investigators have examined typical cognitive profiles in autism, that is, areas of relative sparing and impairment. Some autistic children, both those with severe impairment and those who are higher functioning, display unusual gifts, especially in rote memory, calculations, and music. A majority of autistic children are known to have relative strengths in visuospatial abilities, while tasks requiring verbal reasoning, social cognition, or flexibility pose relative difficulty for the autistic child. Although this description suggests a typical cognitive profile, studies have shown that there is great heterogeneity in the autistic population, and that no single cognitive deficit is universal in autistic individuals.

I. Language The autistic child's language profile is arguably the syndrome's most distinctive cognitive feature, which has earned it a central position in some theories of the etiology of autism. Many aspects of verbal functioning are impaired in autistic children, as many as 40 to 50% of whom are mute, although this figure is declining with the advent of aggressive early intervention. Those with speech often display echolalia, difficulties with prepositions and pronouns, and inappropriate conversational behaviors. Verbal autistic children generally are able to acquire normal grammatical morphology and syntax, although onset and development are delayed. Some autistic children learn

grapheme-phoneme correspondence, leading to early decoding of words; comprehension, however, lags far behind. Comprehension of oral language is significantly impaired relative to expression, and deficits in the semantic and pragmatic aspects of language are common. They are also deficient in interactive communication, including conversational behavior, nonverbal communication and speech prosody. In general, the more linguistic aspects of communication, including especially phonology and syntax, are spared relative to the pragmatic aspects; pragmatic deficits can be seen in the failure to use language functionally to share or request information, or perform other speech functions that serve social, rather than instrumental, functions.

2. Social Cognition A decade of research has documented substantial deficits in autistic children's ability to understand the behavior, emotions, and cognitive states of other people. They have difficulty in matching pictures of emotional facial expressions to emotion words, to emotional situations, to similar expressions, and to vocal expressions of the same emotion. Much recent interest has been stimulated by exploration of autistic performance on "theory of mind" tasks; in a typical theory of mind task, the subject is asked to predict behavior of a doll in a social scenario. The behavior can only be correctly predicted if the subject has a true theory of mind, that is, truly understands the concept of others' minds, with their own representational capacities, and their own limits on available knowledge. Autistic subjects have been shown to be impaired on these tasks in several studies. A cautionary note here, however, about all of these social cognitive tasks is that many higher functioning autistic individuals do well on them; the deficits are far from universal. Furthermore, verbal IQ explains much of the variance in performance. Therefore, it remains to be demonstrated that deficits in social cognition, including theory of mind, occupy a key causal role in the syndrome; they may be more a concomitant deficit related to the overall social impairment, although opinions differ widely on this.

3. Attention Unusual attentional processes are characteristic of autistic children. Autistic children are generally able to

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sustain attention in tasks adequately when given potent reinforcement or when the task is of interest to them, and higher functioning individuals are able to perform well on standard neuropsychological tests of sustained attention. In contrast, many autistic children appear to have difficulty with tasks requiring the focusing and shifting of attention. They are found to be overseiective in their attention to particular parts of stimuli, and studies indicate that they may have difficulties in shifting attention between stimuli, especially across sensory modalities, perhaps contributing to the perseveration so characteristic of their behavior.

4. Memory Memory abilities in autism have not been as fully investigated as other cognitive functions. Anecdotally, amazing feats of memory have been reported, where autistic individuals recall distant episodes with great clarity and detail; hyperdeveloped memory for stimuli such as routes, spatial arrays, schedules and calendars, and music have also been frequently reported. Tested memory for visual material in high-functioning autistic individuals is often normal. In contrast, memory for linguistic and social material is usually impaired. Autistic individuals appear not to be able to use the intrinsic semantic structure of discourse or stories to aid recall, and in this regard, are more impaired than children with specific language disorders.

5. Executive Functions Executive functioning refers to the higher level cognitive processes of abstract conceptualization, planning, problem solving, and self-monitoring, self-correction and self-control. These processes are thought to be localized to prefrontal cortex, and are assessed with standardized neuropsychological tests developed for evaluation of frontal functions. Some autistic individuals have great difficulty with these tasks, especially in switching from incorrect strategies during tasks. Some researchers have noted similarities between certain symptoms of autism and those of patients with frontal lobe damage (e.g., perseveration, lack of inhibition), and have proposed that frontal executive system impairment causes distinct social cognitive deficits. Furthermore, some findings suggest that executive system adequacy may predict outcome for autistic adolescents better than measures of IQ.

IV. DEVELOPMENTAL COURSE AND PROGNOSIS Autism, as a developmental disorder, cannot be fully described at a single developmental point. The typical description of the autistic child is that he or she lacks interest in relating to others and lacks communicative language. These symptoms are most characteristic of autistic children in the preschool years. Even during this period, there are often signs of increasing social relatedness, especially to caretakers. On the other hand, stereotypies and especially resistance to change, may appear in the preschool years or somewhat later. During middle childhood, autistic children often master some daily living and academic skills and make behavioral adjustments to their parents and teachers. Their behavior may come to resemble that of hyperactive and/or retarded children, or they may develop into socially motivated children, who relate in an odd or idiosyncratic way, with deficits in emotional reciprocity. Early and middle adolescence can be particularly difficult. Besides the onset of seizures that sometimes occurs in early adolescence, a significant minority of PDD children regress behaviorally and even cognitively at this time. Some autistic adolescents show increasing interest in developing peer relationships during these years. Higher functioning individuals with PDD are prone to psychiatric problems, especially anxiety and depression, as they realize the extent of their difference from peers. On the positive side, both social and language skills often continue to improve during adolescence, and even those children who regress during early adolescence may recover and make developmental progress toward the middle or end of adolescence. Increasing interest in relating to other people can also set the stage for psychosocial interventions or behavioral skill training to be more effective. Long-term follow-up studies indicate great variability in adult outcomes, but a generally guarded prognosis for good adjustment must be the rule. About half of all autistic adults require residential care; many of the remainder depend on relatives for daily assistance. Gainful employment and fully independent living may be achieved by about one in five. Even for the best-outcome group, social difficulties remain common, marriage or sexual relationships rare, and many social relationships revolve around work or struc-

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tured activities and interests. It should be noted, however, that the generation of children who have received the benefit of modern special education and behavioral interventions have not yet reached adulthood, and their outcomes, it is hoped, will be significantly better. Follow-up studies are consistent in demonstrating that higher IQ and communicative language by the age of 5 are strong predictors of better outcome, associated neurological signs and symptoms are predictors of poorer outcome.

V. EPIDEMIOLOGY Prevalence rates vary according to the definition of the syndrome. Earlier and more restrictive definitions of autism yielded prevalence estimates of 2-4/10,000. Broader definitions encompassing the full PDD spectrum suggested rates three or more times greater. Recent estimates have increased. This may be attributable to improved detection, more lenient diagnoses, or actual increases in prevalence. Most recent estimates are approximately 10/10,000 for PDD disorder, including autism, and another 10/10,000 with a more broadly defined triad of deficits in social relatedness, communication, and stereotyped behavior plus mental retardation. PDD spectrum disorders are more common in males than in females, with ratios found between 2:1 and 10:1, the higher ratios applying more to the Asperger-type clinical picture.

VI. BOUNDARYCONDITIONS AND COMORBIDITY Specifying the boundary between autism and other PDD spectrum disorder (such as Rett's and Asperger's Disorder), mixed language disorder, or severe mental retardation can be problematic, and differential diagnoses among these conditions can be difficult. Although diagnostic definitions of autism and language disorder appear distinct, in practice, the differential diagnosis can be unclear, especially in preschool children. Studies from Rutter and colleagues in the 1970's and from Rapin's group indicate that the diagnostic groups can be distinguished not only by the presence of autism-related behaviors, but by differences in the

language domain itself. The autistic children tend to have greater delays and deficits in language comprehension than the language-disordered children; in the expressive domain, delayed appearance of Wh-questions is highly discriminating. Regression of acquired language skills is also much more typical of autism, but also characterizes children with Landau-Kleffner syndrome. Landau-Kleffner syndrome, also referred to as acquired epileptic aphasia, refers to loss of language in a child in the context of clinical seizures or a frankly epileptiform EEG. There is disagreement as to whether the term should be reserved for children who have no serious associated behavior or cognitive disorders, or whether the term should be broadened so as to include those children who also develop autistic behaviors or become frankly autistic. Autism may also have increased comorbidity with specific additional disorders. Although still controversial, some investigators present evidence that there is a greater than chance coincidence of autism and Tourette's disorder. When tics occur in autism, they tend to occur in high-functioning autism. The relationship between autism and schizophrenia also remains a matter of debate. At one time, the two disorders were believed to be related, but different ages of onset, patterns of symptomatology, and family histories have convinced many investigators that they are unrelated. Nevertheless, reports exist of schizophrenia developing in previously autistic individuals at a greater than chance rate, and a small number of researchers believe that autism is a particularly early and severe form of childhood schizophrenia. Autism is also related to the presence of seizure disorders. About half of autistic individuals have clinical seizures and/or abnormal EEGs. Infancy and adolescence are high-risk periods for the appearance of seizures. All types of seizures occur; generalized tonicclonic are the most common.

VII. BIOLOGICAL FACTORS A. Associated Biomedical Conditions and Genetic Factors Several specific medical conditions are associated with autism, including phenylketonuria, rubella embryopathy, herpes encephalitis, fragile X syndrome, and neurocutaneous disorders such as tuberous sclerosis.

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Some studies estimate that between one-eighth and one-fourth of autistic children have an associated medical condition, but it is not known whether these conditions play a causal role in the development of autistic symptoms. Of possible prenatal factors, maternal rubella is most commonly associated with autism, the prevalence for which is 100 times that for the general population. Other obstetrical factors are found more frequently in autistic children than in other populations, particularly midpregnancy maternal bleeding. The fragile X genetic syndrome has been identified in an estimated 2 to 10% of the autistic population. Fragile X is a rare X-linked syndrome (most prevalent in boys) that involves intellectual impairment, attention deficits, and identifying physical features (prominent ears, long and narrow face, and macroorchidism). Within the fragile X population, it is estimated that 15 to 30% have autistic features, which are qualitatively distinct compared with those seen in the "typical" autistic child. Fragile X autistic children have been found to show perseverative speech as opposed to echolalia, and display active-but-odd social behaviors rather than aloofness. The specific route of pathology connecting fragile X to the expression of autistic symptoms is unknown. A genetic basis for at least some forms of autism has been demonstrated by family studies. Approximately 3 % of families with an autistic child will produce another child with autism, a prevalence rate which equals 50 to 100 times that of the general population. In addition, the concordance rate for autism in monozygotic twins has been found to range from 40 to 96%. Further support for genetic involvement is found in studies of characteristics in families of autistic children. Siblings of autistic children may be more likely to show superiority in visuospatial over verbal abilities (analogous to the autistic profile), cognitive difficulties such as language disorder, and social disengagement. A few studies have found that some parents of autistic children may be more likely to show unusual social behaviors. The search for specific genetic markers for autism thus far has uncovered two prospects: a marker for a gene that regulates neuron development, and abnormalities of chromosome 15. Taken together, studies suggest that at least a subset of autistic cases are attributable to genetic origin, either familial or mutational. The incidence of autistic

symptoms in medical conditions that are not genetic, however, suggests that the PDD spectrum may represent a variety of etiologies ultimately affecting common brain systems.

B. Neuroanatomical Findings Studies of neuroanatomical abnormalities in autistic patients have relied mainly upon postmortem neuropathology examinations and imaging techniques such as positron emission tomography (PET), computerized tomography (CT) and magnetic resonance imaging (MRI). They have generally focused on cortex, brainstem, limbic areas and cerebellum, and have found great variability in brain pathology. Gross cortical and ventricular abnormalities, for example, have been found in some cases and not others. Two structures of great interest are the amygdala and hippocampus, which are limbic structures involved in social/emotional behaviors and in memory. Abnormalities in limbic areas of the brain have been implicated in several studies, most notably in detailed postmortem examinations performed by Bauman and Kemper. These and other studies have also found abnormalities in the cerebellum, although the nature of these cerebellar abnormalities is not consistent across studies.

C. Neurophysiological Findings Findings from PET studies of regional cerebral blood flow have suggested diminished temporal lobe activity, and possible delayed frontal lobe maturation in autistic children. PET studies of regional glucose metabolism, which reflects brain energy utilization, have indicated abnormal patterns of regional activation. Several others have found global glucose hypermetabolism in autistic patients, which was thought to reflect inefficient processing. This feature, however, is not unique to autism. Studies examining brain waves and oculomotor activity in REM sleep have suggested a developmental immaturity of brain mechanisms controlling sleep and an abnormally suppressed inhibition of sensory responding in autistic children. Brainstem dysfunction has been suggested for a subgroup of autistic individuals by findings of abnormalities in brainstem ERPs, although some studies have failed to support this.

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Many ERP studies offer support for abnormalities of attention and information processing in autism. Highfunctioning autistic subjects of varying ages usually show abnormally small amplitudes for a longer latency wave of the ERP thought to reflect the detection and classification of stimuli. Deficiencies in voluntary selective attention and orientation to novel stimuli also have been shown by diminished amplitudes in waves associated with these functions. Several other neurophysiological studies relying on cerebral electrical recording have indicated disruptions in normal hemispheric lateralization in autism.

D. Neurochemical Findings Investigations of neurotransmitter function have produced inconsistent findings. The most replicated finding among autistic patients is that of elevated blood levels of the neurotransmitter serotonin, which occurs in an estimated one-third of this population, but also is observed in other patient populations. The reason for this elevation is not yet known. Treatments with the drug fenfluramine can greatly reduce levels of serotonin, and sometimes result in improvements in stereotypies and hyperactivity. Studies of the neurotransmitter dopamine are not in agreement, despite reported improvements in many symptoms after treatments with drugs that block dopamine. Overactivity of the opiate peptide beta-endorphin has been suggested by some studies, and supported by findings that opiate blockade improves autistic symptoms in some patients. The peptide oxytocin, shown to promote affiliation in animals, also may be reduced in autistic children. It has been suggested that excess opiates may render social contact unrewarding by producing a state of intrinsic contentment, and may also serve to dysregulate oxytocin.

VIII. CLINICAL ASSESSMENT A. Medical Assessment If the diagnosis is made by a nonphysician and the child has not yet had a medical work-up relative to his/ her autism, the following referrals should be considered. Assessment of hearing is important for successful language treatment; if behavior and cooperation are problematic, a brainstem evoked potential assessment should be done. Motor abnormalities are common;

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these should be assessed by a pediatric neurologist and a pediatric OT. Some physicians believe that a full medical work-up, including EEG, genetic and chromosomal testing, CT scan, and so on, is indicated; others feel that these investigations have a low yield unless there is a specific indication for their use.

B. Neuropsychological Assessment Children and adolescents with autism or PDD should also have periodic neuropsychological evaluations. These will describe the child's current level and profile of cognitive and language abilities, which will have implications for current education and for long-range goals. Periodic reevaluations to monitor the child's progress will help to detect any deterioration that might signal negative medical or psychological events, and will document the success of treatment and education.

C. Behavioral Assessment Thorough behavioral description is equally important. Included in the behavioral description should be a profile of the individual's adaptive abilities and problem behaviors, including those central to the syndrome (such as social incapacity and resistance to change), those associated with the syndrome (such as self-injury and abnormal motor behaviors) and those sometimes found in association with it (such as hyperactivity, aggressiveness, and passivity). Analysis of antecedent conditions and consequences of the behaviors may clarify the role or function of the behavior for the particular autistic individual, and may dictate changes in stimulus conditions and reinforcements to ameliorate problem behaviors, as well as to foster positive behaviors.

IX. TREATMENT A. Pharmacological Treatments Pharmacotherapy can be an effective tool in improving the behavior of some autistic children. Serotonergic agents are often used. Fenfluramine is sometimes prescribed, and has been found to reduce hyperactivity and stereotypies in some, but not all, studies. Clomipramine has been found to enhance social relatedness

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and decrease obsessional behavior and aggression. Fluoxetine and other serotonin reuptake inhibitors are also used with some autistic children. Opiate antagonists may help to diminish selfinjury, and reduce social withdrawal and stereotypies. Self-injury and aggression have also reported to be improved by fluoxetine, clomipramine, buspirone and beta-blockers. Neuroleptics, such as haloperidol, and chlorpromazine, have also been found to reduce agitation, aggression and emotional lability, but most physicians are reluctant to use these agents in young children because they can produce movement disorders that may not regress even when the medication is stopped. Lithium is sometimes used to decrease aggressive, perseverative, and hyperactive behavior, and may be tried especially when a family history of bipolar disorder is present. Other common pharmacological treatments are tricyclic antidepressants, which sometimes enhance language and social behavior. Stimulants have been administered for hyperactivity, but some autistic children experience a worsening of stereotypies or thought disorganization. Stimulants may work best in high-functioning autistic children with absent or mild stereotypies. Natural treatments, such as dietary interventions or high-dose vitamin regimens have been advocated by some. Empirical support for the claims rests on a small number of studies, and mainstream physicians generally do not advocate their use.

B. Behavioral and Educational Treatments Special education services and behavioral treatments are crucial in producing an optimal outcome. Recent work indicates that aggressive early intervention (as early as 15 to 18 months)can produce the best outcome. The leading proponent of intensive (ca. 40 hours/week) behavioral "drills" (O. I. Lovaas) has reported highly successful outcomes~almost half of the children being successfully included without support in a typical grade-school class. Others using his methods report results that do not replicate his degree of success, but that are nonetheless highly effective. These behavioral programs can be carried out in an educational setting or, especially for preschoolers, in the home. Other preschool programs emphasize a child-centered, developmentally oriented approach,

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which attempts to stimulate the child to move along a typical developmental trajectory. Any successful program must address each of the behavioral, social, language, and cognitive needs of the children specifically. To be effective, programs should be highly structured and should teach parents behavior management techniques that can be used in the home. Individual differences in the children partly predict outcome: higher IQ, and the presence of communicative language by the age of 5 are positive prognostic signs. The recent trend in special education has been strongly in favor of various forms of "mainstreaming, . . . . integration," and "inclusion," in which the child attends a class that is composed of a mixed group of special needs and typical peers, or of mainly typical peers, for part or all of the school day, sometimes with a one-on-one aide to facilitate participation. Although research has shown that exposure to normal peers can promote social behavior, the degree to which a severely autistic child can benefit from inclusion in a regular classroom remains to be demonstrated. It is clinically obvious that at least some autistic children need more intensive one-on-one teaching than is available in a mainstream setting before they can benefit from the teaching and social opportunities in a regular class. In addition to special education or behavioral treatment, the autistic child often needs additional speech and language therapy, occupational therapy, and adapted physical education. Clinicians must also help families to obtain other necessary services, such as respite care, extended day programs, and summer programs to prevent the behavioral and cognitive regression that can occur. They may also be able to suggest appropriate leisure activities, such as gymnastics, swimming, or play or social groups, that can provide constructive ways to spend after-school hours and opportunities for social interaction with typical children, and can promote selfesteem. Prescription of therapies and services for the autistic individual must always include sensitivity to the often devastating effect of the disability on the family. Social support from other affected families, and keeping abreast of the latest developments in treatment and other research can help families manage their affected children and their own emotional reactions. The Autism Society of America (8601 Georgia Ave.,

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Suite 503, Silver Spring, MD 20910) publishes a regular newsletter with much information useful to parents; another good source of information for parents and professionals on recent developments in autism is Rimland's newsletter Autism Research Review International (4182 Adams Ave., San Diego, CA 92116).

BIBLIOGRAPHY Bauman, M. L., & Kemper, T. L. (Eds.). (1994). The neurobiology of autism. Baltimore: The Johns Hopkins University Press.

Dawson, G. (Ed.). (1989). Autism: Nature, diagnosis and treatment. New York: Guilford Press. Gillberg, C., & Coleman, M. (1992). The biology of the autistic syndromes (2nd ed.). Clinics in Developmental Medicine, 126. London: Mac Keith Press. Rapin, I. (Ed.). (1996). Preschool children with inadequate communication: Developmental language disorder, autism, low IQ. Clinics in Developmental Medicine, 139. London: Mac Keith Press. Schopler, E., & Mesibov, G. (Eds.). (1995). Learning and cognition in autism. New York: Plenum Press. Schopler, E., Van-Bourgondien, M. E., & Bristol, M. (Eds.). (1993). Preschool issues in autism. New York: Plenum Press.

j Borderline Personality Disorder JeromeKroll University of Minnesota Medical School

I. II. III. IV. V. VI.

Historical Development of the Concept Core Symptoms and Character Styles Demographic and Data-Based Studies Etiology and Relationship to Other Disorders Course of Borderline Personality Disorder Treatment of BPD

I. HISTORICAL DEVELOPMENT OF THE CONCEPT More than one decade after the development and publication of DSM-III, borderline personality disorder (BPD) remains the most controversial category in the nomenclature. Disagreement persists regarding the term itself, the particular diagnostic criteria established for BPD by DSM-III and DSM-IV, the scope of applicability, and the extent of overlap with Axis I and other Axis II disorders. Ultimately, this degree and intensity of dispute reflect both the range of difficulties in identifying and working with those persons designated as borderline, as well as the more basic question of validity: whether the BPD construct describes a meaningful unitary syndrome that corresponds to an actually existing state of affairs. While this latter question can certainly be asked of any ofthe personality (Axis II) disorders, something about the borderline concept seems to have engendered the strongest controversy. At least one major reason for the ongoing disputes is the fact that the very concept of borderline was born out of attempts to explain the clinical observation that certain patients seemed to do very poorly in psychodynamic psychotherapy. Thus, from the very first, this category was used to describe a disparate group of patients who had two things in common: they responded to psychotherapy by developing transient psychotic symptoms and they did not meet classical definitions of schizophrenia. It is not that they

As-If Personality A type of personality lacking a stable core identity, which then takes on characteristics of persons in the environment. Cluster B The grouping of four personality disorders (narcissistic, borderline, histrionic, and antisocial) in Axis II of DSM-III-R. Dissociation An altered state of consciousness that appears split off from one's ongoing sense of awareness and self-consciousness. Rejection-Sensitive Dysphoria A transient form of depressed mood brought on by perception of rejection by others.

BORDERLINE PERSONALITY DISORDER is a term that identifies a heterogenous group of patients with serious character pathology and behavioral disturbances. The main features of this disorder are behavior that is impulsive, dramatic, and often selfdestructive; moods that are labile and reactive to life circumstances; interpersonal relationships that are stormy; and a sense of self-identity that is fragile and contradictory.

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did not necessarily improve; many obsessional patients, for example, did not improve with psychotherapy. Rather, it is that these patients worsened in psychotherapy with a fairly specific pattern of acting out that showed up most dramatically in the development of severe transference problems. The difficulty confronting the predominantly psychoanalytic theoreticians and skilled therapists was how to fathom the nature of these patients who gave promise of being good psychotherapeutic cases, yet deteriorated during the course of a psychotherapy. Thus, the very origins of the borderline concept arose in the context of a clinical puzzle. The solution to the puzzle, keeping in mind that American psychiatry held a much more encompassing concept of schizophrenia in the 1940s and 1950s than at present, was to conceptualize these patients who became worse in psychotherapy as having a schizophrenic core underlying the neurotic facade. This notion was given concrete expression in a paper by Hoch and Polatin in 1949 describing the new category of pseudoneurotic schizophrenia. The construct fit neatly into a psychoanalytic model that postulated a spectrum of psychopathology based upon increasing primitiveness of defense mechanisms, extending in an unbroken chain from mild neurotics at one end to deteriorated schizophrenics at the other. The pseudoneurotic patient served as the missing link, bridging neurosis and psychosis, and thus serving as visible proof of the continuity connecting mild and severe psychiatric disorders. [See SCHIZOPHRENIA.] The problem with the pseudoneurotic schizophrenia construct was that the patients did not go on to develop the more classical symptoms of hallucinations and delusions nor the deteriorating course that is the usual outcome of schizophrenia. Nevertheless, the observation that there existed a group of patients who appeared neurotic, but worsened with intensive psychotherapy, was a valid finding that outlived the misleading label attached to it. The focus of what might be wrong with these difficult-to-treat patients shifted away from schizophrenia to consideration of severe character pathology, described as borderline states by Knight in 1953 and as the psychotic character by Frosch in 1964. In addition, the joint U.S.U.K. diagnostic studies carried out in the mid-to-late 1960s demonstrated convincingly that many patients diagnosed as schizophrenic by American psychia-

trists fit much better with manic-depressive and personality disorder symptoms and outcome. This diagnostic realignment tightened the diagnostic criteria for schizophrenia, thereby further emphasizing the differences between borderline conditions and schizophrenia. In 1968, Grinker and colleagues published the results of their study of 58 hospitalized patients who fell into a broadly defined notion of borderline syndrome. These patients had difficulties in interpersonal relationships, transient losses of reality testing under stress, angry and depressive affects, and deficient selfidentities. Cluster analyses of the data, primarily of measurements of ego functions, produced four major clusters. There was a "core" borderline group, two groups defined as bordering upon the psychoses and neuroses, and a fourth group embodying certain "as-if" features, most notably absence of a core selfidentity. Grinker's study, the first to utilize psychometric instruments and statistical analyses, moved the borderline concept away from the realm of schizophrenic spectrum disorders and provided the basis for future empirical studies that continued the attempt to define the still vague borderline syndrome. It is instructive that in the next series of studies carried out by Gunderson and Singer in 1975, the primary diagnostic concern was still to demonstrate that borderlines were different than schizophrenics. At the same time that empirical studies were focusing on narrowing the construct of borderline, Kernberg developed a broader notion of borderline, based upon a fusion of ego psychology and object relations theory, to designate a form of personality organization that was characterized by the use of primitive ego defenses (denial, splitting, projective identification), intact reality testing (with transient regressions under stress), and identity diffusion. Kernberg's construct of borderline personality organization includes the milder as well as the more severe forms of character pathology, and, in essence, encompasses most of the patients presently grouped under the Cluster B (dramatic, unstable)personality disorders: histrionic, narcissistic, borderline, and antisocial. This was the state of affairs while the DSM-IV committee developed inclusion and exclusion criteria for the personality disorders. There were four competing and overlapping concepts of borderline, and the final result represented some degree of compromise be-

Borderline Personality Disorder

tween the various groups. Since ideological and economic considerations, in addition to empirical studies and clinical lore, influenced the final product, it is important to define these considerations in some detail. The four overlapping concepts of borderline were as follows: (1) A residual model based upon the schizophrenic spectrum concept, using the term borderline to designate those persons, usually relatives of schizophrenics, who displayed odd, eccentric thinking and schizoid interpersonal relationships; this group was given the term schizotypal personality disorder. (2) An affective disorder model, which considered BPD as an affective spectrum illness displaying prominent features of mood instability with a predominance of depression, anger, and preoccupations with suicide. (3) An empirically derived model based primarily on the research of Gunderson, with diagnostic symptoms placed into five major groupings: impulse/ action patterns (including self-destructive behaviors); ego-dystonic, transient psychotic episodes; mood instability with primarily negative affects; disturbed but intense interpersonal relationships; and an unstable sense of self. (4) A psychoanalytic concept based primarily on the work of Kernberg, but encompassing theoretical formulations by Mahler relating to difficulties in the separation/individuation phase of child development. The final configuration of BPD adopted was most influenced by Gunderson's work, but nevertheless showed the strains inherent in a compromise between points of view that are ideologically very divergent. The results were the creation of several new personality disorders within Axis II, not based upon empirical studies, but with each reflecting to some extent components that were once loosely connected to the borderline concept. Essentially, in dividing the broad territory of the borderline syndrome, as this concept evolved during a 40-year span, the cognitive disturbances that had long been noticed were placed in the schizotypal personality disorder, the milder dramatic and attention-seeking traits were placed into the histrionic personality disorder, self-centeredness and entitlement became the core of the narcissistic personality disorder, and the affective symptoms of mood instability and negative affectivity (depression, anger, anxiety), along with impulsivity, were given prominence in the borderline personality disorder. Borderline personality disorder was defined by

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DSM-III-R as a condition marked by a pervasive pattern of instability of mood, interpersonal relationships, and self-image, beginning by early adulthood and present in a variety of contexts, as indicated by at least five of the following:

1. A pattern of unstable and intense interpersonal relationships characterized by alternating between extremes of overidealization and devaluation. 2. Impulsiveness in at least two areas that are potentially self-damaging, e.g., spending, sex, substance use, shoplifting, reckless driving, binge eating. 3. Affective instability: marked shifts from baseline mood to depression, irritability, or anxiety, usually lasting a few hours and only rarely more than a few days. 4. Inappropriate, intense anger or lack of control of anger, e.g., frequent displays of temper, constant anger, physical fights. 5. Recurrent suicidal threats, gestures, or behavior, or self-mutilating behavior. 6. Marked and persistent identity disturbance manifested by uncertainty about at least two of the following: self-image, sexual orientation, long-term goals or career choice, type of friends desired, preferred values. 7. Chronic feeling of emptiness or boredom. 8. Frantic efforts to avoid real or imagined abandonment. The revision of DSM-III-R into DSM-IV was completed by late 1993. Although the BPD construct did not undergo any major alterations, several changes were instituted which served to correct the overemphasis in DSM-III on the close relationship between BPD and the affective disorders and the omission of cognitive deficits. Criterion 3 (Criterion 6 in DSM-IV), which outlined the affective symptoms seen in BPD was changed to reflect reactivity of mood; this serves to emphasize the difference between the mood disturbances seen in BPD and the relatively situationindependent mood disturbances characteristic of the endogenous affective disorders (major depression and manic-depressive illnesses). Complementing this more accurate delineation of the type of mood disorder seen in BPD was the inclusion of a new criterion to reflect the specific cognitive disturbances of BPD. The DSMIV calls for a ninth criterion as follows: Transient stress-related paranoid ideation or severe dissociative

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Borderline Personality Disorder

symptoms. There were a few additional changes to the original eight criteria, but these are relatively minor, either reflecting grammatical alterations in the interest of clarity or the result of low sensitivity/specificity ratings for a few items on further field testing. Thus, the description of the identity disturbance in Criterion 6 was reworded and the construct "boredom" was dropped from Criterion 7.

II. CORE SYMPTOMS AND CHARACTER STYLE The clinical description of a psychiatric disorder does not correspond exactly to that disorder's diagnostic criteria in DSM-III. The main reason for this is that a clinical description needs to be a full and rich portrayal of the condition under question, whereas the requirements for diagnostic criteria are vastly different. Diagnostic criteria must aim for those characteristics of an illness that capture a few of its core symptoms while avoiding overlap with neighboring conditions. For example, as indicated above, while boredom may very well be a characteristic mental state in BPD, it was also found in histrionic and narcissistic personality disorders and therefore was of little specific diagnostic value. It did not help discriminate between BPD and other Cluster B personality disorders. In addition, diagnostic criteria must have acceptable validity and reliability. The issue of validity of psychiatric disorders, especially of personality disorders, is a troublesome one, since there are not external validators. The construction of DSM-III had paid major attention, some would say excessively so, to reliability issues. For example, certain factors that most workers would agree are characteristic of a disorder, such as the psychological defense of splitting in BPD, were not included in the diagnostic criteria because of a preference for behavioral rather than psychological phenomena, presumably because assessment of behaviors permits greater agreement as to whether they are present or not as compared to psychological constructs. As indicated at the beginning of this article, there remains considerable controversy about the core characteristics and boundaries of BPD. Workers in the field have tended to bring to the evaluation of BPD their own theoretical and clinical perspectives in the evaluation of borderlines. In addition, some of the

core characteristics of BPD, such as an increase in dissociative phenomena, appear to be changing in the past decade, a possibility that raises the question of the cultural influences and even faddish quality of some of the symptoms. Most workers would agree that BPD is a relatively severe personality disorder, seen primarily in young adults, that presents with a characteristic cognitive style, mood disturbances, problematic interpersonal relationships, negative and deficient sense of self, and a variety of dramatic and impulsive behaviors usually of a self-injurious nature. These diagnostic features represent points distributed on a continuum of personality traits with somewhat arbitrary use of social norms to determine cut-off scores separating normal from pathological. Because of this, some workers in the field have advocated use of a dimensional rather than categorical model for the personality disorders, but a categorical model has always been adopted because it is easier to use in clinical work. The cognitive style seen in borderline individuals encompasses three overlapping features. First, borderlines tend to have altered states of consciousness; these are usually referred to as dissociative states, and vary in intensity, density, and duration. They run the gamut from brief periods of self-absorption to fugue states lasting hours. The person may be partially or fully amnestic for some of the dissociative episodes. Second, borderlines tend to split their universe into good and bad, black and white. They have difficulty conceptualizing a person, including themselves, or an event, as encompassing positive and negative features. They tend to swing between the opposite poles of idealization and devaluation in their affections toward others. Third, borderlines tend to have impressionistic and global rather than precise and focused perceptions. They tend to be intolerant of unpleasant thoughts and images and to interrupt these processes with impulsive action, dissociation, and drug and alcohol use. There is a tendency toward imprecision and exaggeration, with a loss of salient detail. All of these disturbances are increased under conditions of stress. The affective disturbances are characteristically mood instability or lability. Mood is typically reactive to environmental circumstances, but this must be taken to include the borderline's own thought processes too. Negative affects, such as sadness, anger, and anxiety predominate the emotional landscape,

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Borderline Personality Disorder

but too literal adherence to this description would belie the positive affects and interpersonal warmth that borderlines can exhibit. Problematic interpersonal relationships are a hallmark of borderlines. Their relationships are characteristically intense, stormy, and conflictual. Dependency needs, power struggles, and the idealization/ devaluation swings described earlier tend to complicate most meaningful relationships. Victimization and entitlement themes in which the borderline alternates between being exploited by others and demanding reparations from others for damages incurred are frequent patterns seen in this disorder. Borderline individuals tend to have a deficient sense of self, and what enduring image of themselves they may have is usually negative. A deficient sense of self refers to the absence of a stable sense of core identity, of knowing who you are. A certain degree of this is expected in adolescents and young adults in Western culture, but the borderline problem with identity, by definition, must go beyond the norm for this age group. Borderlines will take on different roles and personality characteristics, depending upon the dominant features of the group they are associating with. This has been referred to as the "as-if" personality, first described by Helene Deutsch in 1942. When not caught up in a persuasive group identity, borderlines tend to have very negative notions about themselves, ranging from dislike to contemptuous loathing. Finally, borderlines characteristically are dramatic and impulsive in their actions. The patterns of impulsivity include directly self-injurious behaviors as well as an assortment of either ill-considered or risk-taking behaviors that also may be seen as self-destructive. Alcohol and drug abuse, bulimic eating disorders, promiscuity, and attraction to predatory partners are among the impusive actions seen in borderlines. As with the other core features of borderlines, the selfinjurious behaviors range from infrequent and mild delicate cutting of the wrists to deep cutting of the limbs, torso, and genitals, as well as occasional ingenious use of cigarettes, lighters, caustic solutions, and hot irons to burn themselves. Suicide threats and attempts are also hallmarks of borderlines, most frequently but not exclusively with prescription as well as nonprescription medication overdoses. There are many more threats and gestures than serious attempts, leading to the use of the term "para-suicide" to de-

scribe these provocative actions of borderlines, but often the differentiation between manipulative and serious attempts is not at all clear.

III. DEMOGRAPHIC AND DATA-BASED STUDIES There are no accurate measures of the prevalence of BPD in the community. Most estimates range from 0.5 to 1%, but may go higher as a broader concept of borderline, such as that used by Kernberg, is applied. The prevalence of the disorder in clinical settings is influenced by the type of clinical population under consideration. An average across studies indicates that the general prevalence of BPD is 1 0 - 1 5 % , in inpatient settings about 20%, among outpatients with a personality disorder 3 0 - 3 5 % , and among inpatients with a personality disorder 6 0 - 6 5 % . Prevalence figures alone may be deceptive; it is possible that borderlines in an inpatient setting may have little similarity to outpatients who have never needed hospitalization. In most studies, excepting those done in VA and prison settings, 6 0 - 7 5 % of BPD are women. Although DSM-III diagnostic rules do not permit differential weighting of the different criteria, most studies have demonstrated that several items contribute disproportionately to diagnostic efficiency. The presence of two, or at most three, specific criteria (impulsivity, unstable-intense interpersonal relationships, and self-injurious behaviors) predict most strongly the diagnosis of BPD, although once again, the type of clinical setting (inpatient or outpatient) will influence this finding. There is considerable overlap (20-60%) between BPD and the other personality disorders, especially those of Cluster B, as well as schizotypal and dependent personality disorders. This finding continues to raise the question of whether personality disorders are discrete entities truly different from each other or reflect points on a continuum of serious character pathology. There are several Axis I disorders that have substantial overlap with BPD. These are alcohol and substance abuse disorders, bulimia, and the mood disorders, primarily dysthymia and major depression. To some extent, this finding reflects overlapping criteria (e.g., substance abuse is listed as a criterion for BPD), the heterogeneity of the BPD concept, and the fact

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that traits such as impulsivity and mood lability do express themselves in a wide array of behaviors. [See

PERSONALITYDISORDERS.] IV. ETIOLOGY AND RELATIONSHIP TO OTHER DISORDERS Since it appears that BPD is not a unitary disorder, and since diagnostic threshold can be met in a polythetic system by fulfilling any five of eight (or nine, under DSM-IV) criteria, it is highly unlikely that a unitary etiology will be found for this or other Cluster B personality disorders. Theories about the etiology of BPD tend to follow major trends of interest in the behavioral sciences in general. Thus, the predominance of psychoanalytic constructs as explanatory hypotheses of human health and illness has given way to a variety of biological-genetic models in the past decade. Even the recent robust correlations between childhood sexual abuse and adult BPD symptoms are increasingly explained more in terms of long-lasting neurophysiological alterations of stress-response systems rather than in terms of psychodynamic mechanisms. The major theories of the etiology of BPD are as follow: A. Psychoanalytic model of stage-specific difficulties 1. Deficit model (Masterson; Adler) 2. Conflict model (Kernberg) B. BPD as an affective spectrum model C. BPD as post-traumatic stress disorder secondary to childhood sexual and physical abuse D. BPD as an impulse spectrum disorder

achieve age-appropriate separation and individuation, thereby resulting in the development of a borderline personality in the child. Adler has emphasized the borderline child's inability, under circumstances similar to those described by Masterson, to form internalized soothing, holding introjects, such that the borderline child (and adult) lacks basic ego functions such as frustration tolerance, stable self-object relationships, and methods for calming itself during periods of stress. Kernberg has postulated the likelihood of an excessive aggressive drive in the infant that interferes with the fusion of sexual and aggressive drives; Kernberg's model therefore sees borderline pathogenesis as the result of a complex interaction between infant and caregiver rather than as unilaterally caused by a "not-goodenough" mother. The basic problem with the psychoanalytic hypotheses regarding etiology of BPD is shared by psychodynamic explanations of behavior in general: first, difficulty in operationalizing and thereby in testing various theories and second, a lack of specificity whereby certain postulated mechanisms at best appear to be general risk factors (e.g., parental psychopathology) rather than the specific and inevitable cause of a particular outcome. This latter problem, of course, applies to all unitary theories of etiology. Finally, the nature of the psychodynamic hypotheses are such that supportive evidence comes primarily from retrospective rather than prospective studies, and from individual case studies in which the investigator testing the hypothesis is also the therapist commited to the hypothesis.

A. Psychoanalytic Hypotheses

B. BPD as an Affective Spectrum Disorder

Based upon Mahler's theories of the importance of successful resolution of the rapprochment subphase of the separation/individuation processes in toddlerhood (ages 15-30 months), several overlapping psychodynamic hypotheses were advanced to explain those BPD features that were thought to represent the consequences of rapprochment failure. These features were the mental operation and defense of splitting, identity diffusion, and deficiencies in object constancy and object relationships. Differences of opinion and emphasis exist between various psychodynamic theories: Masterson has suggested that the mother of the borderline is herself borderline and establishes emotionally impossible conditions for the toddler to

The observation that borderline patients are frequently depressed, and the prominence of mood instability in the symptom picture, have led to the hypothesis that an affective disorder underlies the borderline condition. Attempts to validate this hypothesis examined a variety of biological markers, familial patterns, follow-up data, and pharmacological responses. The initial findings, varying somewhat from study to study, were that from 20 to 60% of borderline patients met diagnostic criteria for an affective disorder, usually major depressive episode. This was not particularly surprising since the diagnostic criteria for BPD were slanted toward affective type symptoms. The studies have shown that patients with depression and borderline patients who

Borderline Personality Disorder

were concurrently depressed resembled each other in regard to several biological markers of depression, such as the dexamethasone suppression test, REM latency time, and thyroid stimulating hormone response to thyrotropin, but the resemblances fell away with "pure" borderline patients, i.e., borderline patients who were not depressed. [See DEPRESSION.] Similar results were found in the family pedigrees of borderline patients. Borderline patients with concurrent depressions had a greater prevalence of relatives with affective disorders. However, this finding is true for most of the Axis II disorders, namely, that there is a higher prevalence of depressed persons in the families of patients with any personality disorder and depression. On the other hand, borderline patients without depression tend to have increased familial linkages to other disorders, namely, borderline and antisocial personality disorders, and alcoholism and drug abuse. Studies of pharmacological efficacy with borderlines have demonstrated minimal benefit from antidepressants, even with depressed borderlines, except for some amelioration of depressive symptoms. Lithium therapy has not proven valuable in treating BPD. There have been some indications that monoamine oxidase inhibitors are effective in reducing core borderline symptoms, thereby supporting the atypical depression model of BPD, but these findings have never been sufficiently replicated to be more than suggestive. Finally, the long-term follow-up studies have shown that most borderline patients do not go on to develop depressive syndromes, again arguing against a causal linkage between BPD and affective disorders. Despite the fairly clear evidence that BPD is not a variant of affective disorders, most studies do show that a certain percentage of borderline patients have a recurrent affective disorder (either depressive or bipolar type II, i.e., depressions and hypomanias) and evolve into a typical affective disorder pattern after the dramatic borderline symptoms recede in the 30s. Thus, it seems likely that a subclass of borderlines has a primary affective disturbance.

C. BPD as Posttraumatic Stress Disorder Secondary to Childhood Sexual and Physical Abuse There has been an increasing awareness of the frequency of childhood sexual abuse in the life history of many psychiatric patients. This awareness has paral-

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leled a growing public consciousness of domestic violence of many types. The question remains unresolved as to whether child abuse and other forms of violence have indeed become more common recently, reaching epidemic proportions, or whether the social taboos that maintained silence over such assaults have been lifted, with the result of greater casefinding and reporting of such episodes. Among psychiatric patients, rates of childhood sexual abuse range between 25 and 80%, depending on the population surveyed and the survey methods. Surveys from such varied locations as state hospitals, community hospitals, outpatient clinics, and emergency rooms have been consistent in these findings. Reported rates are highest for borderline personality disorder, in the order of 5 0 - 8 0 % . In the borderline population, there also appears to be a correlation between severity of certain types of symptoms, such as self-injurious behaviors and dissociative episodes, and the severity of the childhood sexual abuse experiences, as judged by age of first abuse, frequency and duration of abuse, degree of force and violence employed, and absence of ameliorative factors in the life of the child. The correlations between abuse and borderline symptomatology have been robust enough to lead several workers to hypothesize that most patients who have been diagnosed BPD are really suffering from PTSD and that this latter diagnosis makes better scientific and social sense, removing the stigma that has been attached to a BPD label. The case is strengthened by the logic of borderline symptoms, such as dissociation, as a learned response of the abused child to the horrors of the abuse experience, a response that was once adaptive, but has now become generalized as a response to all emotional flooding. In a similar way, self-injurious behavior seems to make sense as an expression of the selfhatred that the abuse victim directs inwardly. [See POSTTRAUMATICSTRESS.] There are several obvious problems to the linear causal chain that links childhood abuse to borderline symptomatology. The major problems relate to specificity between abuse and outcome. Patients with many psychiatric diagnoses, as well as many persons who do not have psychiatric symptoms have histories of childhood sexual abuse. Only a percentage of abused persons develop the BPD or PTSD picture. Conversely, not everyone with BPD has a history of childhood abuse. In addition, the abused child was most likely raised in a chaotic home with many other dis-

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turbing features, such that it is not valid to single out the experience of sexual abuse as the cause of adult problems. There are also considerable methodological problems related to the very sensitive nature of the topic and the fact that most of the research and clinical work are based upon retrospective reports of abuse in childhood. The methodological problems slice both ways; there are persons who have been abused and who deny it, and there are patients who may distort, exaggerate or invent abuse histories. There is no easy resolution to these issues, but, in general, the detailed reports by patients about their abuse appear to have credibility and are accepted by most researchers and health care workers. The particular diagnostic question discussed here about the overlap of BPD and PTSD, however, is less an issue of data than definition of causal relationships in human behavior. Thus, it appears that childhood sexual abuse and the disturbed environment in which the abuse occurred function as general risk factors predisposing to increased severity of many types of psychiatric and physical illnesses. Within the BPD population, there does appear to be a large subgroup whose symptoms and personality styles were profoundly affected by the experiences of childhood sexual abuse and whose symptoms can be understood as a form of PTSD. It needs to be kept in mind that PTSD is still a fairly vague concept encompassing many types of traumas and responses, and that most persons suffering from PTSD do not show borderline symptoms.

D. BPD as an Impulse Spectrum Disorder Although it sounds tautological to say that a syndrome characterized by impulsivity may be an impulse spectrum disorder, more is implied in the statement than meets the eye. Essentially, such a hypothesis raises the question of whether there is a group of disorders that share some common features in addition to impulsivity, such as familial linkage, associated psychiatric disorders, and underlying neurophysiological mechanisms. Family studies have shown an increased rate of alcoholism, substance abuse, and antisocial personality in the relatives of borderline personality. Other disorders considered related to problems with impulsivity include compulsive gambling, bulimia, intermittent explosive disorder, and the other Axis II personality disorders within Cluster B (histrionic and narcissistic). Studies are presently under way to in-

vestigate serotonergic and dopaminergic mechanisms that may have some linkage to impulsive behaviors. It is well recognized that the notion of "impu|sivity" is very vague, such that the various conditions being considered as impulse disorders may turn out to have very little in common beyond surface appearances. Conceptual clarification concerning what the terms "impulsive" and "compulsive" mean, and how these relate to the notion of "addiction," will be necessary if the hypothesis regarding impulse spectrum disorder is to be of any practical use.

V. COURSEOF BORDERLINE PERSONALITY DISORDER The initial delineation of borderlines as encompassing a group of difficult treatment cases combined with the finding of a poor outcome on short-term follow-up led to a fairly pessimistic outlook for patients with this diagnosis. Patients who were diagnosed in their late teens or early 20s as borderline were still doing poorly 2 to 5 years later, with ongoing self-injurious behavior and suicide attempts leading to multiple hospitalizations. It was not until the late 1980s that follow-up studies covered the 10- to 20-year period after initial hospitalization. Surprisingly, the outcome was much more favorable than the early studies indicated. In several independent studies from different parts of the country, it became clear that between 50 and 60% of BPD patients were doing fairly well as they moved into their 30s. Another 3 0 - 4 0 % of patients showed varying levels of disability. Suicide rates ranged from 8 to 15 % on 10-year follow-up. The largest follow-up series of patients was reported by Stone, who traced 502 of 550 patients (of whom 193 met DSM-III criteria for BPD) who had been hospitalized on an intensive long-term psychotherapy ward at New York State Psychiatric Institute during the years 1963-1976. As judged by Global Outcome Scores (GAS), 63% of the BPD patients were in the good to recovered categories, another 16% had made a fair adjustment, 12% were doing poorly, and 9% suicided. Less favorable outcome was correlated with the presence of major affective disorder, antisocial personality, and a pattern of alcohol and drug abuse. Poor outcome was not correlated with self-mutilative behaviors in the early years of the illness. Patients with a history of childhood neglect or sexual abuse tended to do less well

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Borderline Personality Disorder

than patients without these histories. Finally, there was not a good overall correlation between outcome and psychiatric treatment; some patients with very good outcomes had minimal treatment following index hospitalization and some patients with extensive treatment had poor outcomes. It is possible that averaging the outcome data washes out a treatment effect, but this remains to be demonstrated. VI. TREATMENT OF BPD

Three has been as much controversy about the treatment of BPD as there has been about the diagnosis. To a large extent and with some overlap, treatment modalities have tended to follow etiological hypotheses. As one might expect with a condition that drew its initial delineation from a group of difficult-to-treat patients, no single modality has yet demonstrated clearcut superiority or even effectiveness. Studies designed to evaluate treatment of BPD have been plagued by the usual problems of therapy outcome research: differing characteristics of the patient population, despite use of DSM-III criteria; difficulty in determining what constitutes evidence of improvement; difficulty in establishing control groups. Psychodynamic psychotherapy has been the standard and accepted form of treatment of BPD, despite the many problems that arise in this form of treatment. In a sense, the BPD population, comprising primarily young verbal adults who are dysfunctional but nonpsychotic, have appeared to be the obvious if not ideal candidates for psychotherapy. Close to 50% of psychotherapy patients seen in private practice and at most outpatient clinics will have a diagnosis of BPD or a related Axis II Cluster B (narcissistic or histrionic) disorder. While there has been no canon defining a specific therapeutic protocol for BPD (or any other disorder), the work of Kernberg has been most influential in guiding the theory and practice of psychotherapy with borderlines. The therapy has tended to be a mix of supportive and exploratory work, with special attention paid to avoiding becoming enmeshed in ill-advised rescue attempts and other acting out features that are the hallmarks of borderline patients. The outcome results of the Menninger psychotherapy project reported by Wallerstein and Stone's follow-up study suggest that it is impossible to predict, from patient characteristics alone, which patients would bene-

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fit most from supportive and which from exploratory psychotherapy, nor is there evidence that ultimate outcome is better with exploratory than supportive psychotherapy. A single study by Stevenson and Meares employing a 12-month psychotherapy regimen that utilized a written protocol based upon self-psychology demonstrated significant improvements across a broad range of measurements. Patients served as their own controls (pre- and post-treatment measures); a separate control group of patients was not used. There has been increasing interest in cognitivebehavioral treatment (CBT) modalities for BPD. The essence of these modalities is a focus on recognizing and eliminating the factors that reinforce self-injurious behaviors, and learning and practicing new behaviors that will enhance the quality of life of the patient. Therapy is not directed toward underlying psychodynamic causes, since the assumption of CBT is that selfinjurious behavior is a learned behavior that has become relatively independent of the specific causes that originally inspired it. CBT is done individually and in groups. Techniques that are taught and practiced include behavioral skill training, contingency management, cognitive restructuring, exposure to emotional cues, distress tolerance, interpersonal skills, and emotional regulation. Linehan and colleagues reported significant improvement in self-injurious and parasuicidal behaviors in a group of SIB borderlines in CBT compared to a group receiving treatment as usual. The improvements were not accompanied by changes in severity of reported depression, suicidal ideation, or reasons for living. The relationship of BPD to PTSD in those borderlines who experienced sexual abuse in childhood suggests that a PTSD-oriented treatment program should be helpful. To date, this has not been the case, most likely because no overall effective program for the treatment of PTSD has been demonstrated. The treatment of PTSD usually includes group therapy, desensitization techniques, and pharmacological agents. There has been a proliferation of incest and sexual abuse treatment groups, some of which seem to be very helpful and some of which have a deleterious effect on some group members. No controlled studies have been reported. Pharmacological treatment of PTSD is in its infancy; different medications have been reported to be effective with particular components of PTSD, especially the sleep disturbance and depressions that accompany PTSD, but no agents appear to interrupt

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the flashbacks and intrusive imagery that form the hallmark of this disorder. The pharmacological treatment of PBD is widely used, but relatively disappointing. Tricyclic antidepressants are effective only in alleviating depressive symptoms in those borderlines who are also depressed. Monoamine oxidase inhibitors have been reported to reduce the target symptom of rejection-sensitive dysphoria, but a controlled study is still wanting. There have not been controlled studies of the efficacy of the specific serotonin reuptake blockers to date. Lithium has not appeared to be of special benefit. There are mixed reports on the benzodiazepine anti-anxiety agents; there may be some benefit to the anti-anxiety properties, but several studies have reported a worsening of impulsive behaviors in BPDs taking these agents. In addition, long-term use of benzodiazepines would not be indicated in patients with significant alcohol or drug abuse histories. The single class of medications that has demonstrated significant short-term effectiveness in several key borderline symptoms has been lowdose anti-psychotics, but here the benefits must be weighed against the serious long-term side effects of these agents. A study of Soloff and associates in 1993 failed to replicate the positive findings of their earlier study reporting improvement in borderline patients with the use of antipsychotic medications. There has been a recent trend away from long hospitalizations for borderline patients. While much of the driving force toward brief hospitalizations in all medical fields has been concern about rising medical costs, there has also been growing awareness of the deleterious rather than helpful effect of prolonged hospitalization of borderlines. Although there are undoubtedly some patients who benefit from a controlled hospital environment that prevents major selfdestructiveness, the general experience has been that borderline patients continue their self-injurious behaviors in the hospital. This behavior sets up major conflicts with staff regarding proper responses to patients who challenge staff to prevent them from hurt-

ing themselves. Placing patients on one-to-one or constant observation has seemed to encourage rather than discourage self-injurious acts. The broad, but not unanimous consensus recently is that hospitalizations should be kept as brief as possible within the boundaries of responsible patient care, with the option of brief rehospitalizations seen as preferable to lengthy hospital stays. This article has been reprinted from the Encyclopedia of Human Behavior, Volume 1.

BIBLIOGRAPHY Druck, A. (1989). "Four Therapeutic Approaches to the Borderline Patient." Jason Aronson, Northvale, NJ. Gunderson, J. G. (1984). "Borderline Personality Disorder." American Psychiatric Press, Washington, DC. Herman, J. L. (1992). "Trauma and Recovery." Basic Books, New York. Kernberg, O. (1984). "Severe Personality Disorders." Yale University Press, New Haven, CT. Kroll, J. (1988). "The Challenge of the Borderline Patient." WW Norton, New York. Kroll, J. (1993). "PTSD/Borderlines in Therapy: Finding the Balance," Norton, New York. Linehan, M. M., Armstrong, H. E., Suarez, A., Allmon, D., and Heard, H. L. (1991 ). Cognitive-behavioral treatment of chronically parasuicidal borderline patients. Arch. Gen. Psychiatry 48, 1060-1064. Links, P. S. (1990). "Family Environment and Borderline Personality Disorder." American Psychiatric Press, Washington, DC. Paris, J. (1992). "Borderline Personality Disorder: Etiology and Treatment." American Psychiatric Press, Washington, DC. Soloff, P. H., Cornelius, J., George, A., Nathan, S., Perel, J. M., and Ulrich, R. F. (1993). Efficacy of phenelzine and haloperidol in borderline personality disorder. Arch. Gen. Psychiatry 50, 377385. Stevenson, J., and Meares, R. (1992). An outcome study of psychotherapy for patients with borderline personality disorder. Am. J. Psychiatry 149, 358-362. Stone, M. (1990). "The Fate of Borderline Patients." Guilford, New York. Wallerstein, R. S. (1986). "Forty-Two Lives in Treatment." Guilford, New York.

ClassifyingMental Disorders: Nontraditional Approaches Theodore R. Sarbin

Ernest Keen

University of California, Santa Cruz

Bucknell University

Narrative The story, implicit or explicit, that contextualizes and gives meaning to human conduct; the story may be idiosyncratic but most often is borrowed from the stock of stories that comprise a culture. Nosology A classification system of diseases assumed to be discrete entities, such as tuberculosis or measles. Root Metaphor The basic concept, often implicit, of a particular worldview that facilitates some interpretations of the world and forecloses others. The machine and the historical act are root metaphors for, respectively, the mechanistic worldview and the contextualist worldview. Strategic Actions Intentional acts performed by a person directed toward solving identity and existential problems.

I. II. III. IV.

Introduction The Purposes of Classification The Traditional Approach to Classification The Contextualist Construction of Deviant Conduct V. Assumptions and Alternatives VI. Diagnosing within a Contextualist Framework VII. Coda

Contextualism A worldview that requires taking into account the entire context in which actors' behavior takes place. For human beings, the context is largely symbolic and languaged so that one must consider the meanings that persons assign to aspects of their worlds. Discourse Analysis Analysis of the verbal and nonverbal communication contexts within which meanings of the world and its events and objects are constructed. Historical Act The root metaphor of contextualism, the basic concept for interpreting conduct as addressing the world in its narrative flow, thus assuming a past and anticipating a future. Internality A characteristic of traditional diagnostic language that locates the crucial context for understanding the causes of conduct as internal to the actor, tending to neglect other contexts. Mechanistic A worldview for understanding conduct in terms of the properties of machines, such as the transmission of energy.

Classifying for purposes of research or intervention is a feature of the scientific method. Traditional methods for CLASSIFYING MENTAL DISORDERS emerged from 19th century advances in the biological sciences basic to the science and practice of medicine. Underlying such advances was the explicit adoption of the world view of mechanism, the root metaphor of which was the transmittal of forces. In this context, physicians constructed systems for classifying organic disease. These systems provided the model for traditional psychiatric diagnostic and classification systems. Nontraditional classification systems flow from an alternate worldview--contextualism, the root meta117

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phor of which is the historical act in all its complexities. Instead of relying on the medically inspired concept of psychopathology, nontraditional practitioners speak of "unwanted conduct." This practice explicitly recognizes that a moral judgment is being made on the strategic actions that people employ to solve their problems in living. In the nontraditional method described in this article, classification is not of disease processes but of interactional strategies and the conditions that influence the success or failure of such strategies.

I. INTRODUCTION As a preamble to an article on alternate ways of classifying mental disorders, we point to a built-in source of ambiguity. The use of the construction, "mental disorders," together with the phrase "mental health" in the title of the encyclopedia, reflects an implicit acceptance of a particular worldview from which the traditional approaches to classification are generated. The use of the word "mental" implies an assured and nonproblematic ontological status for the concept of mind, notwithstanding the many critiques of the concept, and by the claim that "mind" is an exemplar of the human tendency to transfigure a metaphor to a literal entity. Lost in the history of lexicography is the recognition that at one time mind was a verb, useful for talking about silent and unseen actions, such as thinking, imagining, and so on. For the most part, the traditional approach treats "mind" as a literal entity, often as a quasi-organ parallel to the brain, or as an epiphenomenon arising from the workings of the brain. In actual practice, mental health professionals do not deal with "minds," but with persons whose actions fail to meet a particular society's standards of propriety or fail to meet selfimposed standards. It is an illusion that therapists aid in reconstructing "minds," although they may be instrumental in modifying beliefs and values, in reinforcing strategies for managing interpersonal relations, in changing habits, and in acquiring self-knowledge. "Disorders" is also an unsettled concept. The term implies a departure or deviation from "ordered" conduct. It is important to note that the supraordinate concepts "ordered" and "disordered" (staples of mental health and mental illness doctrines) are derived

from a particular worldview, probably unrecognized by the vast majority of mental health workers. The worldview is that of the machine, the root metaphor of which is the transmission of forces. Being "in order" or "out of order" (disordered), although apt constructions for describing the condition of a clock, a motor, or a computer, are misleading when applied to the acts of human beings. As a descriptor for unacceptable conduct, "disorders" is derived from traditional practices for classifying absurd or unwanted conduct-such practices being consistent with the mechanistic worldview that the "mind" operates like other machinesmas a vehicle for the transformation of forces. Related to the mechanistic conception of order is another implicit meaning of "disorder." The concept of "social order" grew out of the belief in an orderly universe. Thus, "disorder" is applied to violations of the normative expectations for human conduct in everyday life. Shared constructions of the social order supply the context within which conduct may be classified as mentally disordered, deviant, nonconforming, abnormal, inept, or improper. Further, the shared constructions provide the background for legitimating interventions such as hospitalization, incarceration, or other systematic effort to restore order to the social group the equilibrium of which has been disrupted by the conduct of the "disorderly" or "disordered" person.

II. THE PURPOSES OF CLASSIFICATION Behind any classification system is one purpose or more that provides the basis for distinguishing and defining categories. In Western culture, classifications of "mental disorders" have been designed to serve the purposes of the science and practice of medicine: (1) to select and guide treatment and (2) to facilitate research. In medical science, classifications are employed as a means of identifying diseases. For historically documented reasons, the classification of unwanted conduct has followed the patterns laid down by medical science for classifying organic disease. In regard to treatment, there are marked differences in the goals of treatment of measles and treatment for unwanted conduct (such as phobias). For measles, the ministrations of the doctor are in the service of providing a c u r e . For the person seeking help to control

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unwanted conduct, "cure" may be a less apt term than one that describes helping an individual to achieve his or her purposes in ways that are less objectionable to relevant others or more acceptable to oneself. Medical research also explores the causes and treatments of diseases. Knowledge of treatment efficacy depends on research. However, in order to conduct research, particular instances must be located in classes in order to process data from a collection of similar cases. The literature of psychiatry and clinical psychology is replete with research reports that are indeterminate because traditional classification by "disorders," which, like diseases, are categories based on "symptoms," has not been sufficiently reliable nor valid. If we add to treatment another purpose of classification, prevention, then examining the contexts that influence persons to engage in unacceptable conduct will influence the choice of categories for distinguishing among kinds of unwanted behavior. Such a move in the purpose of classification would require abrogating pretensions to being "objective" and value-free. The problem with the value commitments that attend the notion of "disease" is not that they are value commitments, for example, that the patient is not responsible for behavior "caused" by some internal happening. Any intervention into the life of another person engages a value commitment. The problem rather is that practices based on the notion of "disease" or "disorder" follow from the profession's commitment to a counterproductive set of values that positions the person as without agency.

III. THE TRADITIONAL APPROACH TO CLASSIFICATION To write about nontraditional ways of classifying persons whose conduct fails to meet contemporary standards of propriety requires that we first lay out the boundaries of traditional classification systems the better to show contrasting features. We take as the prime exemplar of traditional classification systems the Di-

agnostic and Statistical Manual of Mental Disorders, Fourth Edition, published by the American Psychiatric Association, with the most recent edition (hereinafter referred to as DSM-IV) published in 1994. DSM-IV provides a detailed nosology, a critical analysis of which opens the door to an understanding of the un-

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derlying worldview that guides the practice of classifying deviant conduct. The claimed purpose of the nosology is to provide a means of establishing reliable diagnoses. [See DSM-IV.]

A. The Mechanistic Conception of Unwanted Conduct The history of science makes clear that the mid-nineteenth century witnessed tremendous progress in the science of biology. This progress was directly related to the mechanization of biology. All biological phenomena were to be explained in terms of the mechanistic transmission of physical and chemical forces. Scientific explorations sought principles that were invariant. During this period medical doctors took on the task of explaining abnormal behavior by extrapolating from the findings of the rapidly developing field of neuropathology. The context for this development was the surface resemblance of symptoms of neuropathology to unwanted conduct for which no neuropathology could be found. During this period Emil Kraepelin formulated his initial classification of psychiatric diseases, a classification that assumed all abnormal behavior to be related to organic causes, even in the absence of organic signs and symptoms. "Organic" and "functional" were the terms of convenience to identify whether or not neuropathology was demonstrable. The remote influence of the ideology that influenced Kraepelin's formulations can be deduced from the explicit claim in DSM-IV that "nonorganic" mental disorders have a biological basis. The mechanistic framework inherited from Kraepelin creates serious problems for professionals engaged in the therapeutic enterprise. First, DSM-IV continues to manifest only marginal reliability, in spite of Herculean efforts by its creators. Second, the validity of the categories all too often fails traditional scientific tests and settles for negotiation and consensus among professionals. And third, the tendency to expand both the number of diagnoses, as well as the number of criteria, yields a continuing expansion of the category "mental disorder" into what might, from a less mechanistic point of view, be seen as the necessary travails and tragedies of everyday life. (The first Manual, published in 1952, listed 106 categories. DSM-IV lists 357 diagnostic categories.)

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Beginning with the question of reliability, it has been convincingly demonstrated that the accumulation of more categories and more criteria adds only marginally to the reliability of diagnostic practice. The self-advertised theoretically neutral "descriptive" character of diagnostic language may minimize unproved explanatory hypotheses, but it can yield no more agreement among practitioners than the language it uses to describe persons or behavior. For example, the stipulation that something must have been present for "at least 6 months" offers precision in a fairly trivial way compared to the difficulties of reliably assessing whether a set of actions is "disabling" or "not disabling." No behavior exists as simply disabling or not disabling, independent of the social and psychological context, most of which is beyond the specifiable stipulations of diagnostic manuals. Marginal reliabilities compromise research by including in samples persons whose conduct is heterogeneous but who are lumped together into diagnostic categories. More serious is the questionable validity of diagnostic categories in the course of selecting treatment programs. Traditional classification manuals fail to deal with the question of whether a "mental disorder" exists apart from a culturally specific context-whether, in other words, the label for a disorder names a part of nature that is independent of the social constructions of clinicians and the authors of diagnostic manuals. The controversy of a quarter century ago, whether homosexuality is a "disorder," is not an exception in its clear dependency on normative judgments and negotiations that occur in a historical and cultural context. Most unacceptable conduct, even if reliably identified, is "disordered" only in terms of a culturally relative standard. Cross-cultural research has shown no consistency across cultures in the use of traditional diagnostic categories, for example, "schizophrenia." It is unclear whether this lack of consistency indicates different social constructions by clinicians or different causal antecedents. Professionals are not justified in construing that the meaning of a set of behaviors in one culture is the same in another culture, in the same way that diabetes in one culture is the same in other cultures. Finally, in addition to the expansive and fluid character of the catalogue of disorder through its five editions, the Manuals' tendency to medicalize all human discomfort inspires even more questionable logic. The latest such version is the creation of "shadow syn-

dromes," which are formulated to legitimate treatment for persons whose conduct fulfills only some of the Manual's criteria for a disorder. Extrapolating from the proliferation of diagnostic entities over the various editions of the Manual, one might predict that through the typical negotiation process of the experts, some of these syndromes will come out of the shadows and enter the next version of the Manual as certified "disorders."

IV. THE CONTEXTUALISTCONSTRUCTION OF DEVIANT CONDUCT But there are practitioners and scholars who operate from a different worldview, namely, contextualism-a worldview the root metaphor of which is the historical act in all its complexity. Novelty and change are features of this alternative worldview that provides the foundation for a nontraditional approach to the classification of intentional actions. Historical acts are engaged in by people. Further, historical acts are narrated, told as accounts, anecdotes, and stories in which men and women make choices to resolve their everyday problems of living. Because contextualists construct the world in terms of historical actions, they look for reasons for such actions, unlike the mechanistically inclined clinician who would look for causes.

The contextualist worldview directs us to see human beings not only as biological specimens, but as agents, as doers, as performers and problem solvers. In so doing, we are perforce obliged to develop understandings of how human beings employ narrative structure to shape their life histories.

A. Happenings and Doings Completely overlooked in the constructions of traditional psychiatric classification is a simple distinction, that of happenings and doings. Examples of happenings are ruptured spinal discs, toothaches, brain tumors, and carcinoma. Such happenings are attributable to causes, empirically established or hypothesized. As exemplified in DSM-IV, abnormal actions are caused by happeningswthe transmission of forces in the brain or in the metaphorical mind. Neurotransmitters, phrenological bulges, chemical anomalies have been sought as the causes of abnormal be-

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havior. The diagnostic drama guided by traditional classification has no room for the client as agent, as doer, as capable of intentional action. On the other hand, doings are the agential, intentional, purposeful actions of persons attempting to participate in a drama based on their self-defining narratives. Slapping a child, seeking a mystical experience, declaring that one is host to multiple personalities, avoiding a confrontation, are examples of doings, of actions. The distinction between happenings and doings is helpful in understanding how the traditional diagnostic system and its vocabulary of symptoms has contributed to the medicalization of distress. In the absence of a strong competitor, the language of the medical model was embraced by neighboring professions to describe unwanted conduct. To refer to an action as a "symptom" is to adopt a special linguistic system. The use of "symptom" carries the implication "symptom of something." The "something" is a happening that is the presumed cause of the symptom-in traditional medicine, a microbe, a tumor, a morphological anomaly, a toxin, a chemical imbalance, and so on. The application of the mechanistic worldview with its emphasis on causal happenings has worked well in organic medicine. A perusal of D S M - I V makes clear that the model was adopted in its entirety by modern biological psychiatry. The Manual is explicit in proclaiming that the diagnosis and treatment of "mental disorders" belong to the domain of medical practice. Classifications of any kind must follow from some articulated theory. Although the authors of D S M - I V claim to being atheoretical, it is apparent that the claim is a veiled cover for a weakly defined theoretical system that is reminiscent of Kraepelin's mechanistic framework, that is, that all deviant conduct is caused by anomalies in organic systems. On this framework, D S M - I V fails because of the large proportion of cases for which no biochemical or other organic substrate can be found.

B. Unwanted Conduct We employ "unwanted conduct" rather than "psychopathology" to emphasize the moral judgmental component of diagnosis. Every society creates procedures and practices for marginalizing persons whose public actions fail to meet propriety norms. Beginning

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in the mid-nineteenth century, the responsibility for controlling such marginalized persons was assigned to physicians practicing in institutions variously named mad houses, lunatic asylums, and mental hospitals. The criteria for detention included atypical imaginings ("hallucinations"), nonconforming beliefs ("delusions"), and incomprehensible or absurd gestural or speech behavior. Behind these criteria were implicit premises about maintaining public order. Authority figures (parents, police, magistrates, and doctors) made the initial judgment whether any particular item of conduct was to be classified as unwanted. Those whose nonconforming behavior was under scrutiny were labeled as mad, insane, lunatic, crazy, and more recently, mentally ill. In the twentieth century, the scope of psychiatric practice included diagnosing and treating men and women who were self-referred. Not regarded as mad or insane, such self-referred patients sought help from medical doctors on the belief that they were suffering from ill-defined but nonetheless genuine "nervous" ailments. Hysteria was the diagnostic label employed to denote a wide variety of such "nervous" conditions. In due course, clinicians sorted the presenting complaints into a number of classes identified by labels derived from Greek or Latin roots, such as neurasthenia, psychasthenia, anxiety, hypochondriasis, and depression. These terms sometimes reflected unwanted "feelings." Persons seeking help for dealing with unwanted "feelings" would verbalize their complaints with vague and ambiguous expressions, such as "I am anxious, .... I am depressed, .... I can't concentrate, .... I'm sitting on a volcano." Taken together, these complaints are subsumed under the general medical term "dysphoria." Clinicians who subscribe to the medical model regard dysphoric complaints as symptomatic of a bodily dysfunction. It has become common practice among physicians to prescribe medications to reduce the extent of the dysphoria by altering the body chemistry. A radically different approach would be taken by contextualist clinicians who are sensitive to the notion that distress follows from the failure of strategic actions to solve problems of living. The self-reports of distress that are expressed in the language of "feelings" are construed as the patient's sense-making of proprioceptive and interoceptive changes associated with failed strategies to solve existential or identity problems. Contextualist clinicians direct their attention to the reasons for the unresolved strains-in-knowing

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rather than to reports of "feelings" that are adjuncts to personal problem solving. Their focus is on understanding the antecedents of the unsatisfactory attempts at problem solving, or expanding the library of plots for interpreting distress, and on the exploration of alternative strategies for maintaining an acceptable self-narrative.

V. ASSUMPTIONSAND ALTERNATIVES The difficulties with traditional methods of diagnosis can be specified in terms of four assumptions routinely built into diagnostic manuals (1) internality; (2) physicality; (3) individuality; and (4) the value judgments accompanying the concept of disease. For each of the assumptions undergirding traditional modes of classification, we propose an alternative assumption that is consistent with the contextualist perspective.

A. Internality The current system envisions each abnormal psychological condition to be a malfunction generated from within the person. In a given situation, one person may behave in accordance with common sense expectations while another may not. The latter will be labeled abnormal, deviant, disordered, disturbed, and so on. The difference between the two cases does not come from the social context that traditional diagnosticians assume to be the same for both. What is taken to produce acceptable conduct from one and unwanted conduct from the other are processes internal to the person. The most elemental of diagnostic decisions, for example, that of orientation to time, place, and person, depends on this diagnostic procedure borrowed from the standard neurological examination. Like that examination, what is being assessed is assumed to be inside the person. More elaborate diagnostic judgments, such as deciding between "depression" identified as a disease, and "mourning a death in the family," which is not so identified, depend, for example, on sadness in the absence of mourning. Such a judgment influences the traditional clinician to locate the cause of the phenomenon inside the body rather than externally, in human relationships. It is clear that most human behavior is oriented to concrete immediate situations. Human behavior is

jointly produced not only by a person and a situation, but each of these factors also responds to the other over time to create a dialectical whole, such as a relationship. When a relationship contextualizes a behavior, as is always true even in diagnosis, the meanings of any behavior must take into account the dialectical determinants. The complex of avoidant actions identified by the label "agoraphobia," for example, does not exist inside the person. The actions are ways of coping with situations that have developed over time. Nontraditional approaches that depart from the disease model begin with the individual's history of trying various ways to cope with his or her environment. Traditional diagnosis underplays the agential character of human behavior because "diseases" are ordinarily understood to be happenings that take place inside the person.

B. Physicality The traditional diagnostic system construes a person as a complex biological machine the controlling mechanisms of which are the neurochemical patterns of the brain. Information processing is seen as the central function of the brain, a conception that extends from neural transmissions to perceptions of the environment. This information is selected for its relevance to a given stimulus situation. Such selection is not always without error. The result of acting on mistaken perceptions is conduct that may violate social norms, leading to a psychiatric diagnosis. Observing a person confounding imaginings, rememberings, and current perceptions, a clinician would invoke the diagnostic label "hallucinating schizophrenic." Or, observing a person confounding irrelevant sad feelings with nonpresent situations, the clinician might entertain the diagnosis "depression." In these instances, information appears to be scrambled, and there is a strong presumption that the brain, as the organ of information processing, is malfunctioning and the unwanted behaviors are thus believed to be caused by chemical imbalances in the brain. Information, however, is not merely physical. To be sure, information can be reduced to a "signal" that can be described in the vocabulary of physics, but the signal never embodies meaning. In this sense, meaning is not physical but is constructed--the achievement of human beings who have acquired linguistic and epistemic skills. To sustain the premise that abnormal behavior is

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the product of exclusively physical processes would be like saying that the science of acoustics can reveal to us the meanings carried by human speech. The concepts and theory of sound waves and temporal patterns can tell us about human speech in their own terms, and that is hardly trivial. But scientists who do such work make no claims that their instruments can tell us anything about the meanings of words and sentences, the logic of theory, or the motives of actors who try to communicate with one another. To extend physical science into realms of meanings and motives is to claim too much. It is to persevere in a metaphysical belief that the only reality is the reality of the physical world, a belief that ignores the arguments and demonstrations that realities are social constructions.

C. Individuality The current system envisions abnormal psychiatric conditions as affecting encapsulated individuals. While cultural differences in the incidence of unwanted conduct are well known, and some patterns of behavior are culturally specific, as anorexia is to modern industrially advanced cultures, the goals of treatment, as well as the interpretation of the problem, rarely extend beyond the distressed individual. Although the stresses of poverty, for example, may increase the incidence of many abnormal conditions, current practice assumes that abnormal behavior happens to individuals independent of social contexts. To take more seriously conditions such as poverty, and to make them medically relevant, one can of course add a note to the diagnostic statement, codified as the marginally salient Axis IV in DSM-IE An impartial examination of demographic data of persons diagnosed as psychopathological would suggest that the mental health professions should advocate as therapeutically relevant such conditions as full employment, adequate welfare safety nets, and a livable minimum wage. But this practice is marginal exactly because taking it seriously would require economic, political, and governmental intervention rather than psychiatric or psychological attention. The entry of the treatment professions into politics would undermine the value-flee pretenses of the diagnostic system. Such political involvement, especially since it pretends to be scientific rather than political, runs many risks already revealed to us in the awkwardness of courts of law where psychiatric (diagnostic) testimony becomes a part of society's decision

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to blame w r o n g d o e r s ~ o r to excuse them. The risks already incurred by our diagnostic pretenses to scientific accuracy could stretch wildly the current legitimacy of the treatment professions. There is, of course, no simple solution to these problems, but it is clear they are made much worse by the notion of discrete diseases, some of which traditionally supply an excuse, others of which do not. Empirically demonstrable is the fact that such socioeconomic variables as poverty can be relevant to diagnosis, a fact that cannot be acknowledged so long as mental illness is seen as an individualistic phenomenon. Behavior that has traditionally been labeled mental illness is hardly a private matter analogous to such patently medical conditions as diabetes or cancer where internality and physicality are demonstrable.

D. Value Judgments Accompanying the Concept of Disease The current system envisions mental illnesses, like other illnesses, as conditions to be eliminated. Diseases, in our current understanding, rarely have value and meaning beyond that of deserving the most concerted efforts to eliminate them. The more internal, physical, and individual the diagnostic concepts and procedures, the less are abnormal actions perceived as addressing some aspect of a person's effort to position himself or herself in the world of social norms and moral expectations. An individual's complaints of depression and anxiety are not valued for their indexing a struggle with a personal decision or with a moral dilemma. They are merely "symptoms" that, when sufficiently aggregated, indicate a disease, and a disease is to be cured. Just as the elimination of pain by analgesic drugs may mask a bodily ailment, so may the elimination of anxious or depressed behaviors mask a moral crisis. Furthermore, the individual diagnosed may, on the authority of the mechanistically oriented professional, misinterpret his or her own life narrative as internal happenings. Beyond that, the profession might address the possibilities for preventive measures. It can of course be argued that such a "public health" approach in psychiatry may have to pretend to know with some precision the societal and family conditions that engender contranormative behavior. The parameters of the ideal family or neighborhood or school have yet to be spelled out. The prevailing practice of

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dealing with instances of human distress as "diseases" removes from the profession any pressure to allocate research resources to filling gaps in knowledge necessary for implementing prevention programs.

VI. DIAGNOSING WITHIN A CONTEXTUALIST FRAMEWORK A. Early Efforts to Construct a Contextualist Framework The diagnostic procedures based on Kraepelinian doctrine have been the subject of earlier critical works. During the first four decades of the twentieth century, the Swiss-American psychiatrist, Adolf Meyer, promoted a contextualist view of unwanted conduct. He rejected the idea that the causes of deviant conduct would be discovered with advanced anatomical and histological technology. Instead, he urged his colleagues and students to attend to the whole person in his or her social and cultural milieu. His focus was not on purported biological happenings but on the person's ineptitude in adjusting to his or her life circumstances. The history of the first half of the twentieth century credits Meyer's contextual approach with having a widespread impact on the direction of American psychiatry. A number of well-known texts promoted Meyer's contextualist views. These texts made use of formulations drawn from the social sciences and the humanities, among them discourse analysis, roletaking, socialization, learning theory, pseudocommunity, overinclusion, and so on. Meyer's approach had a positive impact on the development of American psychiatry, but his contextualism faded into obscurity when the psychiatric profession enthusiastically adopted psychoanalysis as its quasi-official theory. The displacement of Meyer's contextualist framework by psychoanalytic doctrine may be attributed to the fact that the hydraulic model advanced by Freud was consistent with the mechanistic perspective that was already entrenched in the medical sciences. In addition, Meyer, unlike Freud, had no self-proclaimed disciples, no professional institutes to promote his contextualist formulations, and no organized corpus of writings. More recent challenges to the validity of the Kraepelinian-inspired D S M - I V have been made in critical

works by scholars working from contextualist behaviorism and from social psychological orientations.

B. The Narrative Framework The contextualist model sensitizes the clinician to focus on the master question: "what is the client or patient trying to do?" Answers to this question will inevitably be in the form of a narrative that includes the parts played by other actors in the client's drama. The constructed narrative provides clues for a diagnosis in terms of the class of strategic actions employed. The clinician's answer to the master question satisfies the original purpose of diagnosismnamely, to guide the therapist and the client in developing a treatment plan. Classification for purposes of scientific research should consider the narrative context within which a distressed person is trying to do something. Also relevant to scientific classification is the issue of how the client's narrative fits or fails to fit into the narratives of the client's family, social group, or subculture. Sorting cases into categories to explore differences and similarities requires attention to crucial attributes, including meanings, of the behavior itself. Science cannot ignore these narrative meanings and contexts in deciding whether cases are similar or different. Unwanted behavior, then, is performed by agents whose purposes are crucial, even if such purposes may not be clear to relevant others or to the agents themselves. The talk, actions, and expressions of feelings that are the results of failed strategies to fulfill the requirements of an ongoing self-narrative are the raw data from which the clinician formulates a diagnosis. This alternative approach assumes that the narrative context must be understood if the puzzling behavior is to be understood. The narrative that guides a particular failed effort must be specified, as well as the fit or lack of fit, between such a narrative and the larger narratives of the social context. Usually, there is a lack of fit, which appears as a violation of norms and values held by social groups and codified in cultural traditions. The narratives that fit these traditions may be referred to as "conventional," and those that do not, as "unconventional." Those people whose behavior issues from a life-narrative that is incomprehensible or grossly nonconforming become candidates for psychiatric diagnosis. These are not people without self-

Classifying Mental Disorders: Nontraditional Approaches

narratives; they are people with unconventional narratives, and/or an unwillingness to disclose them. For example, it is not comprehensible to most of us how someone might seriously suspect a man's unconventional narrative in which he identifies himself as Jesus Christ. In the case of such a client who is apparently convinced of the authenticity of his claims, diagnosticians have no way to understand this conviction and this narrative except to construct the inference: "the man is psychotic." The logic of that inference is consistent with DSM-IV criteria that qualifies the client's claim as a delusion and as sufficiently "bizarre" to assign the diagnosis of schizophrenia (if the belief had been held for 6 months or more). [See

SCHIZOPHRENIA.] While this diagnostic term ought scientifically be seen as a description of the patient's conviction, it is usually taken as an explanation. This elision of description to explanation is one of the outcomes of employing the disease model. It renders unnecessary any understanding of the narrative as a context for unwanted conduct, or understanding the social or moral circumstances that provided the context for the particular narrative. The illicit shift from description to explanation is in great measure responsible for the standard professional practice of ignoring the patient's life story. However, it is important to note that not all behavior that is subject to professional diagnosis is merely an unconventional narrative. In a case of homicide, a truck driver strangled his wife in the heat of an argument in which she declared she had been unfaithful and was about to leave him for her lover. This threat not only confirmed his prior suspicions, it enraged the client. "I couldn't control myself, I was so mad. The anger inside me had to come out. I exploded." While this case is not one of clinical diagnosis for purposes of treatment, it is one of legal diagnosis for purposes of adjudication. To call him "insane" at the time of the murder would be to say that his behavior was caused by stimuli the provocative power of which controlled his behavior. He himself was helpless, the argument would go (and has gone); his being an agent of his actions would not be considered a factor. At the same time, we recognize that the man was following a well-known and not unpopular narrative plot of "punishing an unfaithful wife." The narrative does not excuse his behavior, but it makes it intelligible. It collects those circumstantial factors together

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in a way that, in fact, is how we understand his behavior. It bears on why he did it, when we understand the "why" as searching for reasons, rather than causes. This kind of contextual understanding does not resolve the question of whether or to what degree the man should be excused for his actions. It certainly avoids the possibility that the extreme behavior was caused by a diagnosable disease. And yet such contextual understanding is absolutely essential in order to understand the action, which, given the circumstances and the stock of cultural narratives about unfaithful wives and angry husbands, is quite easy to understand. This understanding addresses the question of what this man was trying to do. It opens up a psychological investigation of his strategic actions, given a particularly vivid set of circumstances. This case, like most behaviors that come to professional attention, deals with a struggle in which both social and moral questions aboundwquestions about what one is to do, who one is to be. Except for behavior that is casual or genuinely accidental, human beings behave in such a way as to work toward achieving their goals, one of which is to be a certain kind of person. Was the truck driver to perceive himself as a cuckold? Was he to perceive himself as a failure in not controlling his wife? He not only wanted to punish her, but also likely wanted to persuade her, and he certainly did not want his manhood challenged. These themes are congruent with common narratives in certain pockets of society, and they are not without influence. Grasping such meanings is what clinicians must do in order to have any intelligent grasp of clients' conduct. Such interpretive psychological work certainly does not suggest that a disease was the proximate cause of a death, as traditional diagnostic thought could imply. Finding a basis for such interpretive work is the point of the alternative model to which we now turn.

C. Strategic Actions As an alternative construction to the implicit theory underlying DSM-IV--that unwanted conduct is caused by anomalous happenings in the biological machinerywthe contextual construction takes its point of departure from the premise that people are agents. They are performers, actors, doers, discourse partners. This premise turns attention to a person's actions, not to postulated happenings in the brain or in

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the metaphorical mind. The actions of interest are in the service of resolving strain-in-knowing, particularly those actions that give rise to self-judgments or to other-declarations that such actions are unwanted. Strain-in-knowing is a response to conditions that interfere with the continuity of the person's self narrative. These are the conditions that are ordinarily subsumed under the heading of emotional life. Strain-in-knowing occurs when there is a discrepancy between the demands of emotional life and the actor's current constructions (beliefs and values). An alternate way of formulating strain-in-knowing is the expenditure of effort to locate or position oneself in relation to the world of occurrences. Sometimes identified as anxiety, disequilibrium, threat, or unassimilated input, the center of the concept is "I have a problem." The implicit and explicit behaviors intended to resolve strain-in-knowing may be called "strategic action." Often intelligible to the actor, strategic actions are not necessarily intelligible to others, for only the actor is the potential beneficiary. In cases we call abnormal, such strategic actions may become habitual and automatic, a condition that makes it difficult for actors to explain their conduct in ways that are intelligible to others. Strategic actions to resolve strain-inknowing may appear to others as obscure or meaningless, or as potentially dangerous or embarrassing. It is important to add a disclaimer that strain-inknowing is not a passive phenomenon taking place in the metaphorical mind. The multifarious behaviors that are traditionally regarded as abnormal or incomprehensible may be parsimoniously classified as phases in the construction of a self-narrative. Whether successful or not, strategic actions in the service of resolving strain-in-knowing become a part of the lived narrative. We present herewith a brief sketch of a model that derives from various contextualist frameworks. The model returns personal agency to the matrix of constructions that are employed to understand human action. The central feature of the model is a list of "strategic actions" that can serve as the scaffolding for a contextualist classification system. Strategic actions may be classified as follows: 9 instrumental acts (including rituals); 9 tranquilizing and tension-releasing acts; 9 attention deployment acts;

9 acts to change beliefs and values; 9 nonaction. These classes of strategic actions are connected to antecedent events and subsequent effects, the latter having a feedback function. Strategic actions are employed to neutralize strain-in-knowing. Any particular strategic act has two potential effects: the first, if successful in satisfying the intentions of the actor, would eliminate or modify the perceived source of strain, the second would provide a relevant audience with opportunities to give warrants of social validation or invalidation for the particular strategic action. In this model, the persons and institutions that enforce values are part of the external world of occurrences. The moral judgments of others are inputs that must be instantiated, matched against the beliefs and values that make up the person's self-narrative. The antecedent events to strain-in-knowing require no detailed analysis--the cognitive psychology of the 1960s and 1970s has given us a template. The world of occurrences may be sorted into discrete domains or ecologies: the self-maintenance domain, the timespace domain, the social domain, the moral domain, and the transcendental domain. Sensory inputs are also generated within the body, the proximal world of occurrences. Human beings (and other sentient organisms) try to match sensory inputs with their systems of knowledge. In problematic situations, the actor directs his or her efforts to the world of occurrences to gain confirming or disconfirming inputs. During the interval when no match is made, the condition of strain-in-knowing prevails. In short, the actor strives to match the inputs against a construct i o n - - a self-narrativemderived from his or her prior experience. Of special interest is the observation that efforts to find a match are not always successful. The prototype for sense-making is the ethological concept of vigilance. When an animal, human or other, registers inputs through vision, hearing, olfaction, and so on, it tries to match the sensory inputs against its available constructions. In the primeval world, the construction might be represented by the question: Is the stimulus event to be instantiated as benign or hostile? The choice of subsequent actions follows from the type of instantiation. The problems in living that are the starting places for both traditional and nontraditional professionals are in the social, moral, and transcendental domains.

Classifying Mental Disorders: Nontraditional Approaches

Positioning oneself in these domains or ecologies involves mapping input against existing constructions, that is, against the beliefs and values that have become part of the actors' ongoing self-narratives. Any particular self-narrative is built up from answers to the social identity question: Who am I? to the moral identity question: What am I in relation to moral standards? and to the transcendental identity question: What am I in relation to such abstractions as God, the universe, departed ancestors, and so on. When inputs from the social, moral, or transcendental domains produce incompatible or conflicting answers to the identity question, the person experiences strain-inknowing, a condition that involves effort to match inputs with existing constructions and/or to seek confirming or disconfirming inputs for putative matches. This is a proactive process. Effort involves physiological participation that produces interoceptive and proprioceptive inputs. These inputs feed back into the proximal world of occurrences, thus, the actor's task includes attending to the additional sensory inputs generated in efforts at sense-making. The use of strategic actions is not exclusive to people in distress who are the clients and patients of mental health professionals. We are all strategists in order to deal with our everyday strains-in-knowing, in our need to make sense of the welter of inputs from the various domains. It is only when the strategies fail to resolve the strain and/or are not given warrants of validation by significant figures~parents, spouses, teachers, employers, doctors~that the person becomes a candidate for diagnosis and treatment. Each class of actions has a target: instrumental acts are directed to the external world, to change the relations between the person and some aspect of the world of occurrences. Inputs from the social domain, for example, that cannot be matched to one's selfnarrative lead to an unvoiced interpretation: my identity is at risk. The person may choose between the traditional fight-or-flight instrumentalities in their many attenuated forms. A particular instrumental act may reduce strain-in-knowing and simultaneously be validated (or invalidated) by persons who have the power to pass moral judgment. The alleged Oklahoma City bombers are said to have constructed a belief that "the government" was evil. They equated a federal building with "the government" and destroyed it. Other citizens engage in less extreme forms of instrumental action: they write letters to their senators or change

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the relation to the distal domains by withdrawing from social relations, or becoming a hermit. Ritual behavior is included in the strategy of instrumental acts because it is mediated by the belief that, like direct action, rituals and ceremonials can influence the world of occurrences. The tranquilizing and releasing strategy is directed toward changing bodily sensations that may be indirect effects of sense making efforts. Alcohol, drugs, sex, hot baths, cold showers, vigorous exercise, and the excitement of gambling are examples of the choices of actions that modify inputs from the internal ecology. The use of the strategy by itself does not certify that one is a candidate for a clinic or a sanitarium. The moral judgment of relevant others on the particular tranquilizing or releasing strategy is the act that identifies the strategy as acceptable or as not acceptable. Examples of the strategy of attention deployment are the acts that are subsumed under such traditional labels as hypochondriasis, conversion reactions, and participation in imaginary worlds. The person's attentional resources focus on inputs other than those from the social and moral domains that are the usual antecedents to strain-in-knowing among humans. A common deployment is to attend to bodily sensations, thus avoiding critical inputs from the social world. A variant of the strategy of attention deployment is involved participation in an invented set of selfnarratives, as in classic multiple personality. Changing one's beliefs and values is a strategy directed to influencing the structure of knowledge. It is the strategy of choice for clinicians who work in the tradition of cognitive psychology. For example, a suicidal client holds the belief that suicide (an instrumental act) will solve his or her problems. The clinician takes on the task of modifying that belief. For example, a sample of women who held suicidal beliefs repudiated such belief following individual and group therapy, skills training, and other interventions. As with other strategies, change in beliefs may neutralize strain. When the person acts on the beliefs, or makes them public, the possibility exists for others to declare the beliefs good or bad. Persons who claim to have been abducted by extraterrestrial aliens, for example, are likely not to receive warrants of validation from most professionals. The fifth category is labeled nonaction. The person may have tried the available strategies and they have not worked, either in the direct reduction of strain or

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in gaining social validation. Under these conditions, strain-in-knowing increases. Not succeeding in neutralizing strain, the person may strive to reduce involvement in the world, lest any actions may lead to inputs that would increase the strain. Traditional diagnosticians would scan the DSM categories for one of the 10 mood disorders, a procedure that would locate the individual's suffering as a happening. In this connection, an alternative approach to "depressive disorders" should be mentioned. The nonaction of the so-called depressed person is interpretable as a subtle form of strategic action, the goal of which is to convince others that one is a helpless, hopeless, or worthless figure in a self-narrative. Specific kinds of "depressed" actions influence others to respond in specific ways. The "helpless" person, for example, calls out responses from others that are qualitatively different from the responses called out by persons who claim to be "hopeless." This briefly sketched model is radically different from the medical model in that moral judgment is an acknowledged component. The appellation "unwanted conduct" and similar terms are moral judgments rendered either by relevant others or by self. This component is ordinarily omitted from psychiatric discourses that focus on hypothesized internal mechanisms only after the initial moral judgment has been rendered by relevant others or by self.

VII. CODA The dominance of DSM-IV has clouded the fact that a variety of alternative approaches have been, from time to time, put forth for diagnosing psychological problems. These approaches have been eclipsed by the attempt to standardize procedures ~ an effort driven more by bureaucratic and insurance pressures than by scientific goals. In a historical and critical analysis of DSM some of these motivations have been laid bare. At century's end, the economic goals of the therapeutic professions continue to favor quick categorization of patients. A convincing argument has been made that the DSMs have evolved into instruments that serve bureaucratic and financial functions more fully than they do scientific ones. When critically examined the DSM's claim to theoretical neutrality cannot be sustained. In fact, the DSM authors take pains not

to conceal a strong biological bias. Critics have argued that the current dominance of DSM prematurely closes off scientific analysis. More specifically, the authors of DSM have failed to examine their underlying assumptions, particularly those embedded in their unarticulated theoretical structure and in their choice of root metaphors. Given the state of knowledge, it is premature to posit a theoretical structure that would support the notion of clearly delineated diseaselike entities. The root metaphor of mechanistic causal forces defines not only the clinical reality but human behavior in general, and it does so in a way that transforms historical actions of persons in identifiable sociocultural contexts into physicalistic happenings like infections and mechanical breakdowns that occur independent of human intentionality. The narrowness of this perspective is obvious. It not only neglects most of the considerable advances made in social psychology and social anthropology in recent decades, it negates common sense views like those of Adolf Meyer half a century ago to be examined to construct systems for organizing the actions of people. "Problems in living" are neither "mental" in any simple distinction from somatic, nor are they "disorders" in any obvious contrast to an order we can identify as natural. The intellectual resources available to the task of classifying people's problems in living are rich, varied, and often very much more precise and elaborate than the DSMs, but they have been neglected for reasons other than their scientific relevance to the task. DSMs of the traditional kind are bound to become increasingly unworkable as the number of diagnoses approaches 500 and as the number of criteria approaches 2000. This development, together with the promulgation of critical inquiries that continue to illuminate the flaws in DSM systems, will direct professionals to entertain nontraditional theoretical premises. It is our belief that DSM systems will be replaced with systems based on the premise that human beings are agents that engage in intentional strategic actions to maintain their self-narratives. It is likely that scientists of the next century will look back at traditional DSMs with somewhat the same puzzlement that is now expressed about the claims of phrenology in the nineteenth century and the claims of lobotomists in the twentieth century.

Classifying Mental Disorders: Nontraditional Approaches

ACKNOWLEDGMENT We acknowledge with thanks critical readings of an earlier draft by Ralph M. Carney, James C. Mancuso, and Karl E. Scheibe.

BIBLIOGRAPHY Berger, P. L., & Luckman, T. (1967). The social construction of reality: A treatise on the sociology of knowledge. Garden City, NY: Doubleday. Borges, E. (1995). A social critique of biological psychiatry. In C. Ross & A. Pam, Psychology, 64, 1117-1119. Follette, W. C., & Houts, A. C. (1996). Models of scientific progress and the role of theory in taxonomy development: A case study of the DSM. Journal of Consulting and Clinical Psychology, 64, 1120-1132. Goffman, E. (1959). The presentation of self in everyday life. Garden City, NY: Doubleday. Kirk, S. A., & Kutchins, H. (1992). The selling of DSM: The rheto-

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ric of science in psychiatry. Hawthorne, NY: Walter deGruyter. Kleinman, A. (1988). Rethinking psychiatry: From cultural categories to personal experience. New York: Free Press. Lief, A. (Ed.). (1948). The commonsense psychiatry of Adolf Meyer. New York: McGraw-Hill. Mirowski, J., & Ross, C. E. (1989). The social causes of psychological distress. New York: Aldine de Gruyter. Sarbin, T. R. (1997). On the futility of psychiatric diagnostic manuals (DSMs) and the return of personal agency. Applied and Preventive Psychology, 6, 568-570. Sarbin, T. R. (1977). Contextualism: A world view for modern psychology. In Landfield, A. (Ed.), 1976 Nebraska symposium on motivation. Lincoln, NE: University of Nebraska Press. Sarbin, T. R., & Keen, E. (1997). Sanity and Madness: Conventional and Unconventional Narratives of Emotional Life. In W. Flack & J. Laird (Eds.), Emotions and psychopathology: Theory and research, pp. 130-142. New York: Oxford University Press. Wiener, M. (1989). Psychosocial transactional analysis of psychopathology: Depression as an exemplar. Clinical Psychology Review, 9, 295-321.

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Conduct Disorder Alan E. Kazdin Yale University

I. Conduct Disorder in Childhood and Adolescence II. Conduct Disorder over the Course of Development III. Issuesand Challenges of Developmental Perspectives IV. Interventions to Promote Prosocial and to Decrease Antisocial Behavior V. Conclusions

children, this is an early stage that leads to conduct disorder. P r e v a l e n c e The rate or proportion of cases of a particular characteristic or problem (such as conduct disorder) within the population at a given point in time. Prevention Systematic efforts to avert the onset of a problem and to decrease further problems among those who already show the problem. P r o t e c t i v e Factor Among individuals who are at risk for an outcome (e.g., conduct disorder), many will not develop that outcome. Characteristics, events, or processes that attenuate the impact of risk factors on the outcome are referred to as protective factors. These factors appear to increase resilience in the face of influences that ordinarily increase risk. Risk Factor Characteristics, events, or processes that increase the likelihood (risk) for the onset of a problem or disorder (e.g., conduct disorder). Risk factors are not necessarily causes of the problem, but rather are correlated features that can be identified in advance of the onset.

Antisocial Personality Disorder A set of symptoms recognized as a psychiatric disorder among adults that includes a pervasive pattern of disregard and violation of the rights of others. The main characteristics include criminal behavior, impulsivity, aggressive acts, consistent irresponsibility, and lack of remorse. This disorder reflects a continuation of conduct disorder into adulthood. Attention Deficit-Hyperactivity Disorder Asetof symptoms recognized as a psychiatric disorder among children that includes as its central characteristics impulsivity, inattentiveness, and overactivity. The disorder is usually first evident in childhood. Externalizing Symptoms Symptoms that are directed toward the environment and considered to reflect undercontrolled behaviors. Examples include aggressive, delinquent, and hyperactive behavior. Internalizing Symptoms Symptoms that are directed inward and considered to reflect overcontrolled behaviors. Examples include withdrawal, anxiety, and depression. Oppositional Defiant Disorder A set of symptoms recognized as a psychiatric disorder among children that includes as its central characteristics stubbornness, temper tantrums, and noncompliance. For some

CONDUCT DISORDER refers to antisocial behaviors in children and adolescents. These behaviors encompass a variety of acts that reflect social rule violations and actions against others. Such behaviors as fighting, lying, and stealing are common examples of behaviors evident among youth referred for conduct disorder. It is important to note that many of these behaviors are seen in most children over the course of development. Conduct disorder refers to antisocial

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Conduct Disorder

behavior that is clinically significant and clearly beyond the realm if "normal" functioning. 1Whether antisocial behaviors are sufficiently severe to constitute conduct disorder depends on several characteristics of the behaviors, including their frequency, intensity, and chronicity, and whether they are isolated acts or part of a larger "package" or syndrome with other deviant behaviors. Typically, conduct disorder is reserved for instances in which antisocial behaviors lead to impairment in everyday functioning, as reflected in unmanageability at home and at school or dangerous acts that affect others (peers, siblings). Conduct disorder is identified in childhood as a pattern of clinical dysfunction, usually during elementary school years. Yet, for many individuals, conduct disorder is a pattern of functioning over the life span. This article discusses characteristics of conduct disorder, continuities and discontinuities over the course of development, issues and challenge for research, and implications of selected findings for social policy.

I. CONDUCT DISORDER IN CHILDHOOD AND ADOLESCENCE A. Diagnosis and Prevalence Extremes of conduct problems are delineated in contemporary diagnosis, as represented by the Diagnostic and Statistical Manual of Mental Disorders. Conduct Disorder (CD) is the diagnostic category for coding antisocial behavior among children and adolescents. The essential feature is a pattern of behavior in which the child ignores the rights of others or violates ageappropriate norms and roles. Table I lists the main symptoms that conduct youths exhibit. In contempo1Two issues related to terminology and meaning warrant comment here. First, the term conduct disorder here is used generically to delineate clinically severe levels of dysfunction. The proper noun, Conduct Disorder, will be used to refer specifically to the formal psychiatric diagnosis with its associated criteria. Second, the terms "normal" and "normal development" will be used to refer to youths functioning in the community and who are not referred for mental health services. These terms do not necessarily refer to youths without clinical dysfunction. The reason is that a significant proportion of youths (e.g., 17 to 22% under age 18) functioning in everyday life and who are not clinically referred show clinical symptoms and impairment.

Table I

Symptoms Included in the Diagnosis of Conduct Disorder

1. Bullying or threatening others. 2. Fighting.

3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15.

Usinga weapon that can cause serious physical harm to others. Beingphysicallycruel to people. Beingphysicallycruel to animals. Stealingand confronting a victim (e.g., mugging, purse snatching, extortion, armed robbery). Forcingsomeone into sexual activity. Firesetting. Destroyingproperty of others. Breakinginto someone else's house, building, or car. Frequent lying or "conning" others. Stealingwithout confronting a victim. Stayingout late at night despite parental prohibitions. Runningaway from home. Beingtruant from school.

rary psychiatric diagnosis, a diagnosis of CD is provided if: (1) the individual shows at least 3 symptoms of those listed in Table I; (2) the symptoms were evident within the past 12 months; and (3) at least one of the symptoms was evident in the last 6 months. Using diagnostic criteria such as those in Table I or prior versions of the DSM, the prevalence of the disorder among community samples of school-age youth is approximately 2 to 6%. One of the most frequent findings is that boys show approximately 3 to 4 times higher rates of CD than girls. The sex differences may be explained by differences in predispositions toward responding in aggressive ways and in socialization through parent-child interactions in relation to aggression, expression of anger, experience of empathy and guilt. Differential responding on the part of parents may contribute to greater sensitivity of girls to the emotions of others, to their higher levels of empathy, and their reduced outward expression of aggression, compared to boys. Differences in the base rates of boys and girls for a number of behaviors such as engaging in rough and tumble play, bullying others, not complying with requests, and fighting have implications for the greater prevalence of conduct disorder. The symptoms that are listed in the diagnostic criteria emphasize confrontive and violent acts that are more likely in boys than girls. Because of low rates of these behaviors in girls, even a few instances, albeit below the threshold of ex-

Conduct Disorder .

isting diagnostic criteria, may be clinically important. These base-rate differences have raised the possibility of a sex bias in the diagnostic criteria which would also explain, or at least contribute to, the greater prevalence of CD in boys than in girls. In general, research on normative development has revealed qualitative and quantitative differences between boys and girls in behaviors related to aggression and antisocial acts, but the information has not yet influenced diagnostic practices. Age variations reveal interesting patterns in prevalence rates. Rates of conduct disorder tend to be higher for adolescents (approximately 7% for youths ages 12 to 16) than for children (approximately 4% for children age 4 to 11 years). The increase seems to be due to increases in onset among adolescent girls and among youths who engage in nonaggressive forms of antisocial behavior (e.g., truancy, running away). Sex differences are apparent in the age of onset of dysfunction. The median age of onset of dysfunction is 8 to 10 years of age. Most boys have an onset before age 10 (median = 7 years old). For girls, onset of antisocial behavior is concentrated in the 14-to-16 year age range (median = 13 years old). Characteristic symptom patterns are different as well. Theft and aggression are more likely to serve as a basis of referral among antisocial boys. For girls, antisocial behavior is much more likely to include sexual misbehavior.

B. Age of Onset and Subtypes of Conduct Disorder Conduct disorder includes a heterogeneous set of problem behaviors. Research has identified subtypes in an effort to find meaningful ways of grouping various sets of symptoms and to understand processes leading to onset and course of conduct disorder. Many different ways of delineating subtypes and patterns have emerged. Recent attention has focused on age of onset as a way of accounting for prevalence differences over the course of development and sex differences in symptom patterns. Child-onset conduct disorder consists of youths whose dysfunction is evident early in childhood, beginning with stubbornness, noncompliance (e.g., Oppositional Defiant Disorder [ODD]) and hyperactivity (e.g., Attention-Deficit/Hyperactivity Disorder

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[ADHD]). The symptoms may progress to those of CD, even though many of the youths retain the symptoms from these other diagnoses. Youths with child onset are more likely than those with adolescent onset to engage in aggressive and criminal behavior and are more likely to continue their dysfunction into adulthood. Thus, child-onset conduct disorder is the more severe form. [See ATTENTION DEFICIT HYPERACTIVITY DISORDER (ADHD).] Adolescent-onset conduct disorder is more common than child onset. During adolescence, many youths engage in criminal behavior. For many of these youths, the acts are isolated; for others, the pattern meets criteria for CD. Both child- and adolescentonset conduct disorder youths engage in illegal behavior during adolescence. However, those with child onset are more likely also to engage in aggressive acts and to be represented primarily by boys. Those with adolescent onset are more equally distributed between girls and boys. Peer group influences are considered to play a central role in emergence and onset of adolescent conduct disorder. Child onset has been particularly well studied in relation to parent-child interaction. Evidence suggests that parent child-rearing practices contribute to child onset by inadvertently promoting aversive behavior in the child. Reinforcement of deviant behavior, inattention to positive, prosocial behavior, and coercive interactions between parent and child lead to escalation of aggressive child behavior. This, in turn, leads to stable patterns of child aggression that has other consequences (e.g., poor peer relations, association with deviant peers, school failure). Child and adolescent onset subtypes, at this point in the research, do not yet offer an explanation of the different patterns. Even so, age of onset may be a useful point of departure for connecting subtypes of conduct disorder to specific developmental processes. Perhaps influences studied in developmental research (e.g., regulation and dysregulation of emotions, bonding to parents, peers relations) and transitions over the course of development (e.g., school entry) can be readily integrated with these different patterns. Also, developmental work on understanding peer socialization may provide clues regarding early patterns and how they lead to different trajectories. In this regard, work on child popularity and rejection may be important because peer reactions predict later dysfunction.

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C. Correlates and Associated Features I. Child Characteristics Children who meet diagnostic criteria for CD are likely to show a number of other problem behaviors than those included in the diagnosis. They are likely to argue with adults, lose their temper, actively defy and refuse to comply with requests, deliberately annoy others, and they are angry and resentful. These behaviors, as a group, are occasionally referred to as oppositional behavior and comprise their own diagnostic category (Oppositional Defiant Disorder), alluded to previously. Developmentally, oppositional behaviors are precursors to conduct disorder for many youths. Most children who evince conduct disorder probably have this early history of oppositional problems; but most children with oppositional problems are not likely to progress to conduct problems. Longitudinal research is critical in delineating the conditions leading to the continuation and escalation of behavioral problems. In addition to oppositional behavior, many youths with severe conduct problems are considered by their teachers and parents to be "hyperactive." There is a reasonable basis for this. A large percentage of children (e.g., 40-70%) diagnosed with CD also meet criteria for Attention-Deficit/Hyperactivity Disorder. The core symptoms of ADHD include inattention, impulsiveness, and hyperactivity. The general point to underscore here is that children and adolescents with the diagnosis of CD are likely to have many other symptoms. There are other characteristics that affect diverse facets of functioning as well. Children with conduct disorder are also likely to show academic deficiencies. They are more likely to repeat a grade, to show lower achievement levels, and to end their schooling sooner than their peers matched in age, socioeconomic status, and other demographic variables. Such children are often seen by their teachers as uninterested in school, unenthusiastic toward academic pursuits, and careless in their work. Poor interpersonal relations also are associated with conduct disorder. Youths with conduct disorder often are socially ineffective in their interactions with adults (e.g., parents, teachers, community members) and engage in behaviors that promote deleterious interpersonal consequences such as peer rejection. Con-

duct disorder youths are often deficient in attributional processes and cognitive problem-solving skills that underlie social behavior. For example, such youths are more likely than their peers to interpret gestures of others as hostile and are less able to identify solutions to interpersonal problem situations and to take the perspective of others.

2. Parent and Family Characteristics Several characteristics of the parents and families of conduct disorder children are relevant to conceptualization of the dysfunction. Among the salient characteristics are parent psychopathology and maladadjustment, criminal behavior, and alcoholism. Parent disciplinary practices and attitudes also are associated with conduct disorder. Parents are likely to show especially harsh, lax, erratic, and inconsistent discipline practices. Dysfunctional relations are also evident, as reflected in less acceptance of their children, and in less warmth, affection, and emotional support, compared to parents of nonreferred youths. At the level of family relations, less supportive and more defensive communications among family members, less participation in activities as a family, and more clear dominance of one family member are also evident. In addition, unhappy marital relations, interpersonal conflict, and aggression characterize the parental relations of antisocial children. These characteristics are correlated with, and often antecedent to, conduct problems, but do not, of course, necessarily cause or inevitably lead to those problems.

3. Contextual Conditions Conduct disorder youths are likely to live in conditions of overcrowding, poor housing, and high crime neighborhoods, and to attend schools that are in disadvantaged neighborhoods. Many of the untoward conditions in which families live place stress on the parent or diminish the threshold for coping with everyday stressors. The net effect can be evident in adverse parent-child interaction in which parents inadvertently engage in patterns that sustain or accelerate antisocial and aggressive interactions. Also, contextual factors (e.g., poor living conditions) are associated with other influences (e.g., deviant and aggressive peer group, poor supervision of the child) that can further affect the child.

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D. Factors that Influence Onset of Conduct Disorder

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predispose children and adolescents to conduct disorder have been studied extensively in the context of clinical referrals and adjudicated delinquents. Numerous factors have been implicated. Table II highlights several risk factors that have been studied along with a general statement of the relation that has been found. Merely enumerating risk factors is misleading without conveying some of the complexities in how they operate. These complexities have direct implications for interpreting the findings, for understanding the disorder, and for identifying at-risk children for preventive interventions. First, risk factors tend to come in

I. Risk Factors Risk factors refer to characteristics, events, or processes that increase the likelihood (risk) for the onset of a problem or dysfunction (e.g., conduct disorder). Risk factors, as antecedents to the dysfunction, may provide clues as to development and progression of conduct problems, possible mechanisms and processes through which the dysfunction comes about, and periods during development that might be used to identify cases at risk and to intervene. The factors that

Table II

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Factors that Place Youths at Risk for the Onset of Conduct Disorder .

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Child factors Child Temperament. A more difficult child temperament (on a dimension of "easy-to-difficult"), as characterized by more negative mood, lower levels of approach toward new stimuli, and less adaptability to change. Neuropsychological Deficits and Difficulties. Deficits in diverse functions related to language (e.g., verbal learning, verbal fluency, verbal IQ), memory, motor coordination, integration of auditory and visual cues, and "executive" functions of the brain (e.g., abstract reasoning, concept formation, planning, control of attention). Subclinical Levels of Conduct Disorder. Early signs (e.g., elementary school) of mild ("subclinical") levels of unmanageability and aggression, especially with early age of onset, multiple types of antisocial behaviors, and multiple situations in which they are evident (e.g., at home, school, the community). Academic and Intellectual Performance. Academic deficiencies and lower levels of intellectual functioning. Parent and family factors Prenatal and Perinatal Complications. Pregnancy and birth-related complications including maternal infection, prematurity and low birth weight, impaired respiration at birth, and minor birth injury. Psychopathology and Criminal Behavior in the Family. Criminal behavior, antisocial personality disorder, and alcoholism of the parent. Parent-Child Punishment. Harsh (e.g., severe corporal punishment) and inconsistent punishment increase risk. Monitoring of the Child. Poor supervision, lack of monitoring of whereabouts, and few rules about where youths can go and when they can return. Quality of the Family Relationships. Less parental acceptance of their children, less warmth, affection, and emotional support, and less attachment. Marital Discord. Unhappy marital relationships, interpersonal conflict, and aggression of the parents. Family Size. Larger family size, i.e., more children in the family. Sibling With Antisocial Behavior. Presence of a sibling, especially an older brother, with antisocial behavior. Socioeconomic Disadvantage. Poverty, overcrowding, unemployment, receipt of social assistance ("welfare"), and poor housing. School-related factors Characteristics of the Setting. Attending schools where there is little emphasis on academic work, little teacher time spent on lessons, infrequent teacher use of praise and appreciation for school work, little emphasis on individual responsibility of the students, poor working conditions for pupils (e.g., furniture in poor repair), unavailability of the teacher to deal with children's problems, and low teacher expectancies. Note. The list of risk factors highlights major influences. The number of factors and the relations of specific factors to risk are more complex than the summary statements noted here.

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"packages." Thus, at a given point in time several factors may be present such as low income, large family size, overcrowding, poor housing, poor parental supervision, parent criminality, and marital discord, to mention a few. Second, over time, several risk factors become interrelated, because the presence of one factor can augment the accumulation of other risk factors. For example, early academic dysfunction can lead to truancy and dropping out of school that further increases the risk for conduct disorder. Third, risk factors may interact with (i.e., be moderated or influenced by) each other and with other variables. As one example, large family size has been repeatedly shown to be a risk factor for conduct disorder. However, the importance of family size as a predictor is influenced by income. If family income and living accommodations are adequate, family size is less likely to be a risk factor. As another example, risk factors often interact with age of the child (e.g., infancy, early or middle childhood). For example, marital discord or separation appear to serve as risk factors primarily when they occur early in the child's life (e.g., within the first 4 or 5 years). How risk factors exert impact in childhood and why some periods of development are sensitive to particular influences underscore the importance of understanding "normal" developmental processes.

2. Protective Factors Research on risk factors leads naturally to the study of positive outcomes. The reason is that even under very adverse conditions with multiple risk factors present, many individuals will adapt and will not experience adverse outcomes. A conceptually interesting and potentially critical set of influences that may affect onset are referred to as protective factors. These are characteristics, events, or processes that decrease the impact of a risk factor and likelihood of an adverse outcome. Although protective factors have been less well studied than have risk factors, significant progress has been made. Researchers have identified protective factors by studying individuals known to be at risk (i.e., show several risk factors) and by delineating subgroups of those who do, versus those who do not, later show conduct disorder. Youths can be identified who are at risk for delinquency based on a number of factors. Yet, not all at-risk youths become delinquent. Those who do not evince delinquency by adolescence are

more likely to be first born, to be perceived by their mothers as affectionate, to show higher self-esteem and locus of control, and to have alternative caretakers in the family (than the parents) and a supportive same-sex model who played an important role in their development. Other factors that reduce or attenuate risk include above average intelligence, competence in various skill areas, getting along with peers, and having friends. In many cases, these protective factors seem to be the absence or inverse of a risk factor. For example, easy temperament, academic success, and good relations with parents reduce risk, as does a good relationship with an emotionally responsive, caregiving adult, whether a parent or nonparent figure. Among the many protective factors, three general categories help to organize current findings. The first is personal attributes of the child. Beginning in infancy and unfolding throughout development, these include such factors as easy temperament, sociability, and competencies at school. The second category is family factors and includes such characteristics as caretaking style, education of the parents, and parent social competence. The third category consists of external supports and includes friendships, peer relations, and support from another significant adult. The categories are useful ways to describe protective factors, but it is important to bear in mind that they tend to be interdependent and reciprocal. For example, child attachment to the parent is important as a protective factor and probably reflects personal attributes of the child in combination with characteristics of the parent. In general, it is useful to conceptualize many of the protective factors as part of transactions between the child and the environment.

3. General Comments Risk and protective factors refer to variables that influence the probability of onset of an outcome in a population. Although many risk and protective factors have been identified, we do not understand how most of the factors operate. In some cases, there are clues as to the processes and mechanisms that have direct influences on the outcome. For example, harsh punishment practices serve as a risk factor for conduct problems. Punishment is part of a broader set of inept child-rearing practices that have been shown to escalate coercive and aggressive behavior directly. How

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the parent responds (e.g., coercively or passively) in response to the demands of the child has been shown to increase systematically the level of aggressive child behavior. Moreover, intervening with special training programs that alter how the parents respond to their children decreases child aggression and antisocial behavior. Research on parent discipline practices has made significant gains in moving from identification of a descriptor (risk factor) to the process (means of operation). Understanding the processes leading to dysfunction provides an excellent basis for preventive interventions. Also, understanding discipline practices and their relation to conduct problems draws attention to broader developmental issues. For example, inept discipline practices do not invariably lead to behavior problems. Understanding influences that may attenuate the role of these practices in development could be important. Thus, the study of conduct problems draws attention to discipline practices more generally in development, as well as to the search for protective factors among youths who are subjected to those practices that promote antisocial behavior.

II. CONDUCT DISORDEROVER THE COURSE OF DEVELOPMENT The manifestations of conduct disorder are likely to change over the course of development. Even so, there may be a continuity in the inferred trait or characteristic that underlies these manifestations. For example, young children (3 to 4 years of age) with conduct problems may be mildly stubborn, break other children's toys, and "borrow" (take) things that belong to their friends. These behaviors may not predict these same behaviors 10 years later. Yet, these early behaviors may predict other behaviors, such as stealing from stores and confronting strangers with a weapon, that are conceptually related or that belong to the same general class of behaviors. A life-span perspective emphasizes continuities and discontinuities over time and paths and progressions. Behavioral and other manifestations may be discontinuous but still reflect continuity at a broader level of conceptualization. Charting the course over the life span begins with descriptive characterization of conduct problems at different points in development. The period of schoolage years through early adolescence has been especially well studied. The present discussion of conduct

disorder focuses on early development and adult outcomes, to fill out the life course of the problems.

A. Early Development: Infancy and Preschool Years Risk-factor research suggests that a number of signs may be evident in the child, parent, and family context beginning in infancy. Child characteristics (e.g., difficult temperament, neuropsychological deficits, high activity), parent characteristics (e.g., prenatal and perinatal birth complications, parental punishment of the child), contextual characteristics (e.g., stress, marital conflict), and other factors, noted earlier, are likely to be present. In addition, diverse psychological processes and experiences (e.g., development of affect, attachment, and cognition) are likely to be implicated. It is likely that a set of general factors may emerge in early development that increase vulnerability to dysfunction and some set of more specific factors that move the child more specifically to conduct disorder. Charting the influence of any single factor is difficult because characteristics of child, parent, and contexts are dynamic rather than static. The dynamic feature emphasizes complex interrelations such as the reciprocal and mutual influence of the child on the parent and the parent on the child. As the child interacts with others (e.g., peers), reciprocal and dynamic influences continue and have their own consequences (e.g., early aggression may lead to peer rejection). In addition to dynamic influences at a given point, there is a developmental progression over time. The influences can place children on a trajectory or path that refers to a course leading to a particular outcome such as conduct disorder and criminality. The trajectory or path is not necessarily a fixed or determined course, but rather a matter of increased likelihood (probability) that specific behaviors will unfold in the short run and lead to other outcomes in the long run. Some outcomes become more probable (e.g., being arrested, bonding with delinquent peers), and other outcomes become less probable (e.g., graduating high school, sustaining employment). A variety of influences can converge to alter the probabilities. The progression of characteristics in early development toward conduct disorder has been examined in longitudinal studies from birth through adolescence and young adulthood. In such research, the same indi-

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viduals are studied at multiple points in time (e.g., every few years) and then early predictors of later behavior can be identified. Through longitudinal studies, one can chart the course over short and long periods and identify transitions from one time to another and the relations among proximal and distal manifestations. Recent research has characterized progressions and different paths and how conduct disorder symptoms and their associated features emerge. Among the salient findings is a progression of severity of conduct problems over time. Trivial antisocial acts precede more severe acts in the child's repertoire. Youths who show the more serious behaviors (e.g., assault, firesetting) are likely to have progressed through the less severe behaviors (e.g., temper tantrums, noncompliance ) but, of course, not all youths who engage in less severe antisocial behaviors progress to more severe antisocial behaviors.

B. Adult Outcomes I. Antisocial Personality Disorder and Psychopathy Longitudinal studies show that conduct disorder in childhood predicts conduct disorder up to 10, 20, and 30 years later. Antisocial behavior when continued into adulthood falls into another diagnostic category, namely, Antisocial Personality Disorder (APD). The essential features include a pervasive pattern of disregard of others, violation of the rights of others. The main symptoms of APD include repeatedly engaging in unlawful behavior, deceitfulness (e.g., repeated lying, conning others), impulsivity, irritability, aggressiveness (repeated fighting), disregard for the safety of others, consistent irresponsibility (e.g., repeated failure to retain a job), and lack of remorse. 2The presence of CD in one's youth is a prerequisite for the diagnosis of APD. The criteria include many concrete behavioral acts of CD but also encompass more pervasive personality patterns, as reflected in deceit, manipulation, impulsivity, and irresponsibility. Large-scale epidemiological research has revealed ZThe symptoms noted here are based on the DSM-IV, referred to previously. The diagnosis of Antisocial Personality Disorder requires evidence of a pervasive pattern of disregard for and violation of the rights of others occurring since age 15 years, as indicated by 3 or more of the symptoms noted here. In addition, the individual must be at least 18 years of age and with evidence of a history of Conduct Disorder before the age of 15.

a life-time prevalence rate of APD of 2.1 to 3.3%. Males are approximately 4 to 8 times more likely to be diagnosed with the disorder. The greater prevalence of APD among males compared to females is in keeping with the sex-difference pattern evident in childhood. Follow-up of child conduct disorder has elaborated this sex difference. Boys are much more likely to continue conduct disorder into adulthood and show APD. In contrast, girls are likely to shift into more internalizing types of disorders (e.g., depression, anxiety) in adulthood. This pattern is especially interesting in light of research showing different reactions of boys and girls who are exposed to factors that might increase risk for conduct disorder. For example, exposure to family violence in childhood (ages 6 to 11) is associated with externalizing and internalizing symptoms in boys but primarily internalizing symptoms among girls. The process leading to symptom pattern differences have yet to be elaborated. [See ANXIETY; DEPRESSION.]

The symptoms required for a diagnosis of APD, noted previously, emphasize overt behavioral signs. Over the history of the study of antisocial behavior in adulthood, emphasis has also been accorded internal experience such as lack of guilt or remorse, lack of empathy, and egocentricity. A distinction has been drawn between APD, which emphasizes the behavioral components, and psychopathy, which focuses more on the motivational and interpersonal processes. APD has as its characteristics adverse family background (e.g., low socioeconomic status) and lower IQ. Psychopathy is correlated negatively with anxiety and positively with narcissism. Interestingly, individuals with both APD and psychopathy are those who exhibit the most severe and enduring patterns of antisocial behavior in adulthood. The distinction in the adult literature between behavioral and motivational/interpersonal components is important from a developmental perspective because it identifies different end points of earlier developmental trajectories. Unfortunately, to date there have been few efforts to connect the different outcomes of adulthood with characteristics of early development.

2. Other Outcomes Among youths who are severely antisocial during childhood, slightly less than 50% continue their conduct disorder into adulthood. What happens to the remainder of youths? If all diagnoses are considered,

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Table III

Long-Term Prognosis of Youths Identified as Conduct Disorder: Overview of Major Characteristics Likely to Be Evident in Adulthood Characteristics in adulthood

Psychiatric Status. Greater psychiatric impairment including anatisocial personality, alcohol and drug abuse, and isolated symptoms (e.g., anxiety, somatic complaints); also, greater history of psychiatric hospitalization. Criminal Behavior. Higher rates of driving while intoxicated, criminal behavior, arrest records, and conviction, and period of time spent in jail. Occupational Adjustment. Less likely to be employed; shorter history of employment, lower status jobs, more frequent change of jobs, lower wages, and depend more frequently on financial assistance (welfare). Served less frequently and performed less well in the armed services. Educational Attainment. Higher rates of dropping out of school, lower attainment among those who remain in school. Marital Status. Higher rates of divorce, remarriage and separation. Social Participation. Less contact with relatives, friends, and neighbors; little participation in organizations such as church. Physical Health. Higher mortality rate; higher rate of hospitalization for physical (as well as psychiatric) problems. .

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Note. These characteristics are based on comparisons of clinically referred children identified for conduct disorder relative to control

clinical referrals or normal controls or from comparisons of delinquent and nondelinquent youths.

rather than continuation of conduct disorder alone, 84% of the full sample received a diagnosis of psychiatric disorder as adults. Moreover, diagnosis of dysfunction does not adequately characterize the scope of adjustment difficulties in adulthood. There are many other outcomes identified by following conduct disorder children. As adults, multiple domains may show continued dysfunction, as reflected in psychiatric symptoms, criminal behavior, physical health, and social maladjustment. The characteristics that conduct disorder youths are likely to show when they become adults are presented in Table III. As the table indicates, individuals with a history of conduct disorder evince a broad range of untoward outcomes.

because conduct disorder extends across generations. For example, children are more likely to show antisocial behaviors if their grandparents have a history of these behaviors. Similarly, one of the best predictors of how aggressive a boy will be in childhood is how aggressive his father was when he was about the same age. Thus, the life-span perspective requires consideration of how the dysfunction is extended to one's offspring and whether there are different modes of transmission.

C. General Comments

A. Continua of Dysfunction and Risk

From a developmental standpoint, it is important to understand the continuities and discontinuities of conduct disorder over the life span. Longitudinal studies have identified intriguing patterns, yet to be explained. For example, the continuity of conduct disorder among boys (ages 7 to 12) is influenced by APD of a parent or child intelligence. With either an APD parent and lower level of intelligence, boys are likely to continue conduct disorder symptoms. How these characteristics operate and combine and the other variables with which each is associated has yet to be studied. The continuity of conduct disorder over the life span warrants mention in another light. The continuity extends beyond the life of the individual,

Research often focuses on youths who meet diagnostic criteria for CD. In principle, it is quite useful to specify criteria in this fashion so that diagnoses can be made reliably and that research on these samples can be replicated. Yet, the criteria themselves are difficult to defend. Where one draws the cutoff point to decide dysfunction (e.g., 3 symptoms rather than 4 or 8; duration of 12 months rather than 18, 24, or more) is likely to lead to different findings with regard to risk and protective factors, developmental trajectories, responsiveness to treatment, and prognosis. Clearly, youths who meet the criteria are likely to be significantly impaired. Yet to understand the nature of conduct disorder more generally, it would be im-

!11. ISSUES AND CHALLENGESOF DEVELOPMENTAL PERSPECTIVES

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portant to extend research to the full spectrum of severity of impairment and dysfunction. For example, youths who show symptoms of CD but who are below, at, and above threshold (e.g., fewer than 2 symptoms, 3 symptoms, or more than 4 symptoms, respectively, as only one way to operationalize threshold) for meeting the diagnosis would be important to study. This type of analysis would permit evaluation of factors that predict functioning across the spectrum of severity and frequency, as well as those that are only predictive of more severe levels or types of dysfunction. In general, conduct disorder is a "fuzzy" insofar as some individuals are at each extreme (clearly conduct disorder, and clearly not) with many shades in the middle. Presumably, there are points on the continuum at which there is a particularly poor prognosis, failure to respond to treatment, and so on. The full spectrum warrants much more attention to understand where the points are warranted to be delineated for intervention and for policy decisions as well. In a similar vein, many of the factors that contribute to conduct disorder can be conceived along continua. In much of the research that focus on risk factors, groups are selected and compared based on their exposure to and experience of an event. For example, the effects of abusive child-rearing practices on children and adolescents are often studied in this way. Typically in research, one selects abused and nonabused children and then identifies the other characteristics they might show at some later point in time (e.g., symptoms of psychopathology, poor school performance, dysfunctional peer relations). Identification of extreme groups is an excellent point of departure, but we wish to understand the continuum of the risk characteristic. Evaluation of the continua of discipline practices is required to understand the impact of various levels and types of punishment and the point at which these practices become risk factors for various outcomes. Studying multiple levels of a proposed risk factor is important to reveal the function (or relation) in a more fine-grained fashion than the study of two groups or the presence or absence of a particular characteristic. Many influences are likely to bear curvilinear relations to an outcome of interest, and assessment of different levels of the risk characteristic can reveal this. For example, parental efforts to control their adolescents is related to externalizing symptoms and drug use. However, the relation between

degree of parental control and symptoms is not linear. Extremely high or low parental control, but not intermediate control, is associated with adolescent dysfunction. Similarly, adolescent substance abuse is correlated with current dysfunction and predicts lack of academic pursuits, job instability, and disorganized thought processes years later. Yet, the relation of substance use and untoward consequences is not linear. Heavy alcohol or drug use predicts later problems; no alcohol or drug use or consumption whatsoever is associated with undesirable personal and social characteristics as well. Use of a small amount of alcohol or drugs (primarily marijuana) is associated with positive outcomes such as decreased loneliness, reduced self-derogation, improved relationships with family, and increased social support. [See SUBSTANCEABUSE.] The point of these examples is to convey the need to study multiple levels of factors presumed (or indeed known) to increase risk for dysfunction. There may be points at which a given factor has one effect (risk), another at which it has no effect, and another level at which it has an opposite (protective) effect for an outcome of interest. Developmental research examines continuities and discontinuities over time for individuals and groups. Research is needed that examines continuities and discontinuities over dimensions of behavior (e.g., conduct disorder), risk factors (e.g., childrearing practices), and contextual influences (e.g., socioeconomic status). How the dimensions influence development and the points at which risk and impairment are especially likely are not well known.

B. Packages of Influences and Outcomes A significant challenge for research is the finding that many influences and outcomes come in "packages." It is difficult to identify simple profile of risk factors that are associated with and are unique to conduct disorder. The reason is that many influences and outcomes come in "packages," that is, sets of factors that go together and have multiple deleterious outcomes. For example, socioeconomic disadvantage, adverse childrearing practices, parental neglect, and low parental interest in the child's academic accomplishments are interrelated. The presence of one or two of these risk factors increases the likelihood of a child accumulating more of them. Thus, early child aggression or academic retardation is often associated with peer rejection, association with deviant peers, and placement in

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a class designed for socially and emotionally disturbed youths. These qualities in turn can lead to a "snowbailing" of additional risk factors. "Packages" are also evident in the outcomes (e.g., problem behaviors, disorders). Although we are interested in understanding the development and course of specific emotional and behavioral patterns, many of these are embedded in, or are part of, larger packages. For example, antisocial acts often are part of a larger cluster involving multiple problem behaviors (e.g., substance abuse, early sexual activity, and academic dysfunction). A challenge is to explain how these behaviors come together developmentally. A prominent view, referred to as problem behavior theory, suggests that problem behaviors serve similar functions in relation to development. Autonomy from parents and bonding with peers are two of the functions that may be served by such behaviors. Another view is that there is a trait or pervasive tendency to engage in deviant, delinquent, and criminal behavior. The tendency, referred to as low self-control, reflects a propensity to seek pleasures of the moment and short-term solutions to problems. What has been well established is that multiple deviant behaviors co-occur. Evidence points to complex interrelations among behaviors and patterns that are idiosyncratic and that vary reliably across individuals, situations, and contexts. Understanding the organization of affect, cognition, and behavior and how they emerge and evolve developmentally are central to understanding problem behavioral patterns. No doubt specific factors (e.g., risk and protective) relate to specific outcomes (e.g., conduct disorder), and these are obviously important to identify. Yet from what we know so far, two general conclusions can be reached: (1) multiple paths (e.g., different packages of risk factors) can lead to a specific outcome (e.g., conduct disorder); and (2) a single path (e.g., single or seemingly identical packages of risk factors) can lead to multiple outcomes (e.g., diverse types of dysfunctions or other outcomes). Elaborating specific lines of development and exploring the bases for variation are rich in opportunities for both theory and research.

C. Variations in Patterns of Influence and Outcome A challenge for research stems from the prospect that some influences and relations may vary systematically

as a function of other variables. For example, the relation between characteristics of early development and outcome in relation to conduct problems varies as a function of child sex. It is not merely the case that boys and girls differ on a particular characteristic (e.g., degree of aggressiveness), but rather how the relations among other variables differ as a function of sex. We know, for example, that early signs of aggression in the school is a risk factor for conduct disorder, delinquency, and crime in adulthood for boys but not for girls. The issue in relation to the present discussion is not merely the fact that there are sex differences, but rather the relation between antecedents and outcomes and how and why they are influenced by sex. Race and ethnicity are also likely to influence relations among factors related to conduct disorder. Differences are known to exist among European American, African American, Asian American, and Hispanic American children in relation to prevalence, age of onset, and course of dysfunction. For example, among youths with substance abuse, one of many behaviors associated with conduct problems, ethnic variation exists in the specific substances used, degree of family monitoring, and amount of exposure to substance use. In addition, whether a particular influence emerges as a risk factor varies as a function of ethnicity. That is, a relation between a particular antecedent and outcome is moderated by ethnicity. Sex and ethnic differences are not the only factors that influence the relations among other variables. Yet, these two are important and serve as a basis for articulating the challenge for research. Investigators are often interested in developing theories of dysfunction with implied widespread generality of explaining conduct disorder. It is likely that key variables such as sex and ethnicity, but no doubt others as well, influence onset and course of conduct disorder and the suitability of various interventions.

IV. INTERVENTIONS TO PROMOTE PROSOCIALAND TO DECREASE ANTISOCIAL BEHAVIOR Conduct disorder represents a serious clinical problem for individuals and their families, as well as a major mental health problem for society at large. From a social perspective, conduct disorder is considered to

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be the most costly mental disorder, at least in the United States. The costs stem from the fact that for many youths conduct disorder is a life-long problem. Over the course of childhood and adolescence, youths are likely to enter into many systems and programs, including special education classes, mental health services (inpatient or outpatient treatment), and the juvenile justice system. As adults, entry into mental health services and the criminal justice system may continue. Thus, the costs that accrue to care for conduct problem individuals is exorbitant. These costs extend beyond the individual's lifetime, insofar as conduct disorder tends to be transmitted from one generation to the next. With these considerations in mind, identifying interventions to combat the problem is obviously important. Three broad levels of intervention can be delineated, namely, treatment, prevention, and social policy. An overview of each is presented next.

A. Treatment Treatment refers to a broad range of interventions that are applied to youths who have been identified as showing conduct disorder symptoms and who experience impairment in their everyday lives. Conduct problem symptoms constitute the most frequent basis for which children and adolescents are referred for treatment. Consequently, there is a need for effective interventions. Many different treatments have been applied to youths with conduct disorder, including psychotherapy, pharmacotherapy (medications), psychosurgery, home, school, and community-based programs, residential and hospital treatment, and assorted social services. Few treatments have been carefully evaluated in controlled studies and shown to reduce conduct disorder problems and to improve functioning of the child in everyday life (at home and at school). A few treatment approaches have been studied and show considerable promise in treating children and adolescents who are referred for treatment. Three of the more well studied treatments are highlighted here. Parent management training refers to a treatment in which parents are trained to interact with the child in ways that promote prosocial behavior. The treatment is based on learning research from psychology and focuses on the use of reinforcement (e.g., use of contingent consequences), mild punishment (e.g., very brief

time out, response cost), and a variety of related techniques (prompting, shaping) to develop child behavior. Extensive research has shown that many parent-child interaction patterns in the home unwittingly foster and escalate child aggressive behavior. Parent management training teaches skills to the parent, develops interactions between parents and the child that promote positive parent and child behavior, and in the process decreases aggressive and antisocial behavior. Several controlled studies have shown that parent management training reduces oppositional, aggressive, and antisocial behavior at home, at school, and in the community. The effects have been maintained in many studies up to 1 to 2 years. Few studies have evaluated the longer term impact of treatment, but evidence has been favorable for these studies. Another technique is cognitive problem-solving skills training. This technique is based on research showing that conduct problem youths often show distortions in various cognitive processes. Cognitive processes reflect how individuals perceive, code, and experience the world, as reflected in beliefs, attributions, and expectations. A variety of cognitive processes pertain to interactions with others, including the ability to generate solutions to interpersonal problems, to identify the means to obtain particular ends (e.g., making friends) or consequences of action (e.g., what would happen after a particular behavior), and to make attributions to others of the motivation of their actions. Distortions and deficits in these and related cognitive processes relate to conduct problems at home and at school. Problem-solving skills therapy develops skills in approaching interpersonal situations. Youths learn a series of steps or self-instruction statements that help identify prosocial or adaptive solutions and alternative consequences of actions. Children practice using the approach in treatment sessions and at home with their parents. Within the sessions, several techniques are used, including modeling by the therapist, practice, role playing, and reinforcement to shape appropriate behavior of the child. Several controlled studies have shown that problem-solving skills training can reduce aggressive and antisocial behavior in children and adolescents. The effects have been maintained up to one year after treatment. Multisystemic therapy is a family systems approach to antisocial behavior. The treatment focuses on the child behavior within the context of various systems

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(e.g., the family, peer group, schools) which may contribute to the child's problem behavior or could be used to help alter that behavior. Many different techniques are applied within the context of treatment to modify specific behaviors of the child and others whose behaviors may be affected by the child. Parent management training and problem-solving skills training, mentioned previously, often are incorporated into treatment. A focus on the family as a system is designed to build better communication, to reduce negative interactions, and to improve the ability of the parents to function. Factors that can affect these interactions and the child's problems, such as stress that the parent experiences, marital conflict, association of the child with a deviant peer group, are focused on as well. Several controlled studies have shown that multisystemic therapy reduces delinquency and antisocial behavior. The effects of treatment surpass the effects achieved with other types of treatment routinely provided to antisocial youths (e.g., counseling, probation) and have been maintained up to 5 years after treatment. There are other promising treatments for conduct disorder, but only a small number of techniques have been carefully evaluated. Although the promising treatments have evidence from controlled studies in their behalf, they still leave many questions unanswered. For example, we do not yet know the longterm effects of even the best available treatments, whether they influence adaptation into adulthood, and for whom they are likely to be most effective. Considerable attention in the field focuses on these questions with the goal of improving treatment.

B. Prevention Ideally we would like to prevent the onset of conduct disorder so there would be no need for treatment. Actually, prevention includes a number of goals. Primary, secondary, and tertiary prevention have been delineated to note whether the intervention is designed to prevent the onset of dysfunction (incidence), to reduce the severity, duration, or manifestations among cases with early signs (prevalence), and to delimit the disability or dysfunction and its complications among persons who have early signs or the dysfunction itself, respectively. A more recent classification distinguishes types of interventions and includes: universal interventions, which are designed

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for the general population, are low cost, and deemed beneficial for persons in general; selective interventions, which are targeted to subgroups that have elevated risk for the disorder; and indicated interventions, which are targeted to high-risk individuals who already show detectable signs or symptoms of developing the problem. Research on risk factors has been very helpful in guiding preventive efforts. Because many risk factors for conduct disorder are known, we can identify youths who are at high risk and provide preventive interventions. In addition, the risk factors may suggest processes through which antisocial behavior may emerge. For example, we know that harsh punishment practices can contribute to antisocial behavior and that altering these practices reduces antisocial behavior. Parenting is one of the foci of many early intervention programs. Prevention programs come in many different forms. Early intervention programs with the family have been effective in altering conduct problems. High-risk families are identified, usually by such factors as low socioeconomic status, low educational attainment, and high-stress living conditions. Intervention programs sometimes begin before the child is born to provide counseling regarding maternal care, to provide support in the home to reduce stress, and to prepare the parents for child-rearing demands. After the infant is born, the program may continue for a few years to help support parents, to develop cognitive skills of the child, and to enroll the child in a preschool program. Programs of this type can have broad impact beyond reducing the incidence of conduct problems. Adolescents who have received such programs when they were young, compared to those who did not, show lower arrest rates, higher educational attainment, less substance use and abuse. Prevention programs are often conducted in the schools because there are opportunities to provide programs to youths in larger numbers, in the context of peers, and on a regular basis for protracted periods. Programs often focus on developing positive skills and success experiences at home and at school. The reason for this focus is that bonding to deviant peers and poor connections with the family are risk factors for such behaviors as delinquency and substance abuse. Developing such success experiences in the schools among elementary school children has increased bond-

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ing to families and decreased rates of antisocial behavior and substance abuse. Prevention is an obviously critical focus. To date, the evidence shows that preventive interventions can have impact on child functioning and onset of conduct problem behaviors. At the same time, the very best and most effective programs show that the incidence of conduct problems can be reduced, but by no means eliminated. The long-term effects of prevention are not well studied. However, the value of preventive efforts is that m a n y outcomes may be improved by early intervention.

C. Social Policy and Action Social policy refers to governmental and legislative efforts to implement changes to benefit society or a particular segment of society and, in this sense, is a social intervention. In principle, the interventions rely on practices that have emanated from research on the nature of the problem (e.g., risk and protective factors) and intervention practices that are or appear to be promising. Thus, policy interventions are not necessarily different from those discussed in the context of treatment or prevention. As an example, Head Start has been implemented as an early preschool program to have broad impact on child development and families. M a n y of the practices are designed to improve

educational and social goals of the children and to improve conditions that in the long term will have impact on children. Efforts to influence policy are reflected in recommendations to alter or modify practices with the goal of decreasing aggression, violence, and other conduct problems on a large scale. As a recent example, a Commission on Violence and Youth of the American Psychological Association (1993) completed a 2-year study and concluded that, "society can intervene effectively in the lives of children and youth to reduce or prevent their involvement in violence" (p. 5). Several specific suggestions were elaborated to convey how this can be accomplished. Table IV summarizes the categories of actions that can be taken. Each of these was developed in detail to convey their connection to what is known from current research on risk factors, onset of dysfunction, and interventions. There are multiple opportunities within society to reduce influences that can contribute to conduct problems and aggression more generally. For example, the use of corporal punishment in child-rearing and school discipline, violence in the media, especially television and films, and social practices that permit, facilitate, or tacitly condone violence and aggression (e.g., availability of weapons), to mention salient issues, are some of the practices that are relevant to the issue of aggression and antisocial behavior in society. We take as giv-

TableIV Overview of Recommendations to Curb Violence 9Early childhood interventions directed toward parents, child-care providers, and health-care providers to help build the critical foundation of attitudes, knowledge, and behavior related to aggression. 9 School-based interventions to help schools provide a safe environment and effective programs to prevent violence. 9 Heightened awareness of cultural diversity and involvement of members of the community in planning, implementing,and evaluating intervention efforts. 9Development of the mass media's potential to be part of the solution to violence, not just a contributor to the problem. 9 Limiting access to firearms by children and youth and teaching them how to prevent firearm violence. 9 Reduction of youth involvement with alcohol and other drugs, known to be contributing factors to violence by youth and to family violence directed at youth. 9Psychologicalhealth services for young perpetrators, victims, and witnesses of violence to avert the trajectory toward later involvement in more serious violence. 9 Education programs to reduce prejudice and hostility, which are factors that lead to hate crimes and violence against social groups. 9 Efforts to strengthen the ability of police and community leaders to prevent mob violence by early and appropriate intervention. 9Efforts by psychologists acting as individuals and through professional organizations to reduce violence among youth. From the Executive Summary of the Report of the American Psychological Association Commission on Violence and Youth (1993). Violence and youth: Psycbology's response (Vol. 1). Washington, DC: American Psychological Association.

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ens a backdrop of factors and practices that contribute in significant ways to aggression and antisocial behavior in society. The factors need to be scrutinized in relation to policy regarding child management and care. As an illustration, the use of corporal punishment (e.g., physical aggression against children) is already implicated as a contributor to child aggression. The extensive use of corporal punishment is one of the givens in our society---a right that accompanies parenting and often teaching~that might be challenged if there is broad interest in delimiting aggression and antisocial behavior. Corporal punishment in child discipline at home and at school has been banned in a number of countries (e.g., Austria, Denmark, Finland, Norway, and Sweden). Large-scale efforts to reduce risk factors in this fashion are critically important in addition to the more common prevention and treatment efforts. It might be useful to conceptualize the full range of influences in terms of a risk-factor model in which there are multiple influences that contribute to the outcome. Yet, in a risk-factor model, multiple influences add and combine to increase the likelihood of the outcome (e.g., aggression). Small influences can combine (additively and synergistically) and have significant impact, even if their individual contribution would be nugatory. We want to reduce risk factors not because individually they are the cause or because they will eliminate the problem, but because they are likely to have a palpable impact. Limiting violence in the media can be seen as one influence likely to affect the level of violence and aggression in society. Efforts to quell gross displays of violence in the media are countered with arguments noting the benefits of television (e.g., education) and the responsibilities of others (e.g., parents) in policing what children watch. Yet, the significant impact of the media on antisocial and at-risk behaviors already has been well documented. Reducing aggression in the media is likely to have impact, even though media violence is not "the cause" of violence in society. A commitment at the policy level and at the level that can mobilize social forces that influence, express, or model aggression could have significant impact on the problem. Social influences involving the matrix of societal displays, encouragement, and implicit endorsement of aggression including the media at all levels ought to be mobilized more systematically for a

broad effort to ameliorate aggression and antisocial behavior. Again, this is not the solution nor a reflection on the cause of aggression in society, but rather a way to have impact in one more incremental way.

V. CONCLUSIONS Conduct disorder represents a special challenge given the multiple domains of functioning that are affected. For many individuals, severe antisocial behavior and associated dysfunction in multiple spheres represents a lifelong pattern. Advances have been made in understanding the characteristics and patterns evident in schoobage children and adolescents. Also, efforts have been made to chart the life course longitudinally, different paths leading to conduct disorder in childhood and adulthood, and the role that specific influences play (e.g., parent child-rearing practices, peers) at different points in development. Research has identified characteristics of the child, parent, family, and contexts that contribute to the emergence and maintenance of conduct disorder. The lifelong pattern of conduct disorder and the transmission of the problems within families from one generation to the next underscore the importance of a developmental and life-span perspective. It will be important to identify the course and various paths and to examine developmentally opportune points of intervention. Over the course of development, influences vary in their contribution to conduct disorder. For example, during adolescence, the influence of peers on the appearance of conduct problem behavior is marked. Peer influences have been implicated in the onset, maintenance, and therapeutic change of antisocial behaviors. Identifying how such influences operate and precursors to such influences has obviously important implications for intervening. Although many fundamental questions remain about conduct disorder over the course of development, sufficient information is available to advance policy recommendations, a few of which were noted previously. A broad range of social interventions are required to have impact on such conduct problems. Specific programs and interventions developed by mental health professionals play a major role, but these programs do not exhaust the options. Broader social practices warrant scrutiny in ways that balance

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individual freedoms and responsibilities. Recommendations from research on ways of reducing conduct problems require addressing these broader issues.

ACKNOWLEDGMENTS Completion of this article was supported in part by a Research Scientist Award (MH00353) and a grant (MH35408) from the National Institute of Mental Health.

BIBLIOGRAPHY American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders. (4th ed.). Washington, DC: Author. American Psychological Association, Commission on Violence and Youth (1993). Violence and youth: Psychology's response (Vol. 1). Washington, DC: American Psychological Association.

Kazdin, A. E. (1995). Conduct disorder in childhood and adolescence (2nd ed.). Thousand Oaks, CA: Sage. Ketterlinus, R. D., & Lamb, M. E. (Eds.) (1994). Adolescent problem behaviors: Issues and research. HiUsdale, NJ: Erlbaum. McCord, J., & Tremblay, R. E. (Eds.) (1992). Preventing antisocial behavior. New York: Guilford. Mrazek, P. J., & Haggerty, R. J. (Eds.) (1994). Reducing risks for mental disorders: Frontiers of preventive intervention research. Washington, DC: National Academy Press. Patterson, G. R., Reid, J. B., & Dishion, T. J. (1992). Antisocial boys. Eugene, OR: Castalia. Pepler, D. J., & Rubin, K. H. (Eds.) (1991). The development and treatment of childhood aggression. Hillsdale, NJ: Erlbaum. Peters, R. D., McMahon, R. J., & Qinsey, V. L. (Eds.) (1992). Aggression and violence throughout the life span. Newbury Park, CA: Sage. Robins, L. N. (1991). Conduct disorder. Journal of Child Psychology and Psychiatry, 32, 193-212. Robins, L., & Rutter, M. (Eds.) (1990). Straight and devious pathways from childhood to adulthood. Cambridge: Cambridge University Press.

Dementia John L. Wo0dard Emory University School of Medicine*

I. II. III. IV. V.

D e m e n t i a A persistent decline in intellectual functioning in multiple cognitive domains relative to a previous level of performance. Dysarthria Difficulty with articulation due to impairment of the oral musculature. Encephalitis Infection and inflammation of brain tissue. Encephalopathy Dysfunction of the brain due to any cause. General Paresis Chronic syphilitic meningoencephalitis, associated with a progressive dementia and generalized paralysis. Korsakoff's Syndrome Disturbance of orientation, confusion, delusions, and hallucinations associated with chronic alcoholism. Meningitis Inflammation of the meninges of the brain. Ophthalmoplegia Paralysis or weakness of the eye muscles. Prions Subviral, infectious, unencapsulated protein particles that are thought to be associated with diseases such as kuru, Creutzfeld-Jacob disease, GerstmannStraussler-Scheinker syndrome, and Fatal Familial Insomnia. Wernicke's Encephalopathy A clinical syndrome associated with thiamine deficiency (frequently related to alcoholism) resulting in ophthalmoplegia, ataxia, and dementia.

Degenerative Dementias Dementia Due to Cerebrovascular Disease Dementia Due to Infectious Agents Dementia Due to Toxic or Metabolic Disorders Dementia Due to Other Causes

Agnosia Inability to recognize the symbolic meaning of stimulus material.

Aphasia Impairment of expressive and/or receptive language skills producing communication difficulty.

Apraxia An acquired inability to perform learned, purposeful motor acts. Ataxia Impairment of smooth coordinated muscle movement. Athetosis Involuntary movements characterized by a continuous slow, writhing, dancelike quality, often seen in Huntington's disease. Basal Ganglia A collection of nuclei in the forebrain, typically considered to include the caudate nucleus, putamen, parts of the thalamus, and the lentiform nucleus. Bradykinesia A condition often seen in Parkinson's disease produced by muscular rigidity that results in slowed movement, particularly on tasks involving fine motor coordination (e.g., writing). Chorea Involuntary rapid, jerky, complex movements, often seen in Huntington's disease, together with athetosis. Delirium A state of clouded consciousness, typically associated with fluctuating alertness and confusion.

DEMENTIA, as it is used in this article, refers to a persistent decline in intellectual functioning in multiple cognitive domains relative to a previous level of performance. A separate article discusses Alzheimer's

*Present address: Memory Assessment Clinic and Alzheimer's Disease Program, Georgia State University.

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Disease. Although Alzheimer's disease (AD)accounts for 45 to 80% of all dementias, the absence of a definite biological marker of AD in living patients continues to necessitate the exclusion of less common but sometimes treatable dementing conditions and differentiation among degenerative dementias. Given that some non-Alzheimer's dementias are potentially treatable (i.e., further cognitive deterioration can be avoided or minimized) and/or reversible (i.e., cognitive functioning can be improved), a thorough consideration of all potential etiologies is imperative. This article will describe the non-Alzheimer's dementias along a continuum of relatively untreatable, progressive disorders to treatable and potentially reversible causes. Many of these conditions represent diagnostic challenges given their rarity, and clinical diagnostic criteria for these disorders are either nonexistent or highly variable. The degenerative, non-Alzheimer's dementias will be considered first, the majority of which have limited treatment options available. Next, dementias due to cerebrovascular disease will be surveyed, some of which may be treated to avoid further progression of cognitive impairment. Dementias due to infectious processes will be reviewed subsequently, many of which may also be treatable if discovered in their early stages. Dementia due to toxic or metabolic conditions may be among the most treatable etiologies and are potentially reversible if detected and corrected relatively early. Finally, dementia due to other causes, many of which are treatable and reversible, will be examined.

I. DEGENERATIVE DEMENTIAS A. Frontal Lobe Degeneration and Pick's Disease I. Clinical Features Patients with degenerative changes confined principally to bilateral frontal or fronto-temporal brain regions often demonstrate a characteristic clinical pattern with early onset of personality changes associated with inappropriate social or personal behavior, followed by cognitive deficits that are evident later in the course of the disorder. With the exception of elicitation of primitive reflexes (e.g., grasp, suck, snout), neurological signs are typically absent. Computed tomog-

raphy (CT) and magnetic resonance imaging (MRI) scans commonly reveal prominent atrophy of the frontal or fronto-temporal cerebral cortex. Positron emission tomography (PET) and SPECT (single photon emission computed tomography) typically reveal diminished glucose metabolism and cerebral blood flow in the frontal and fronto-temporal cortex. Frontal lobe dementia tends to first become manifest in younger individuals in their 50s or early 60s, although cases have been reported in patients as young as 20. Women are affected nearly twice as often as men. Approximately half of patients diagnosed with frontal lobe degeneration have a first-degree relative who has shown similar behavioral and cognitive changes. Because of the striking and frequently problematic personality changes, frontal lobe degeneration is often misdiagnosed as a psychiatric disorder. Impaired judgment and lack of insight commonly lead to inability to manage instrumental activities of daily living, together with occupational impairment. Personality changes may reflect prominent apathy and lack of motivation at one extreme, or disinhibited, reckless, and hyperactive behavior at the other extreme. Language changes sometimes reflect terse, stereotyped, repetitive phrases, gradually progressing to echolalia (repetition of phrases said by others) and palilalia (repetition of single syllables uttered by themselves or others). Memory and orientation, visuospatial skills, and basic language abilities are surprisingly wellpreserved during the early stages of this disorder, although neuropsychological measures of executive functioning may reveal perseveration, diminished word list generation, cognitive rigidity, and difficulty formulating and sequencing complex behaviors. Pick's disease is a specific type of frontal lobe degeneration that is characterized by the presence of distinctive neuropathological markers known as "Pick bodies" that disrupt neuronal cytoskeletal organization and displace the neuronal nucleus toward the periphery of the cell body. Approximately half of the patients diagnosed with frontal lobe degeneration show evidence of Pick bodies at biopsy or autopsy.

2. Treatment Frontal lobe degeneration may be treated only symptomatically. Behavioral agitation and aggression are

Dementia

typically treated pharmacologically with neuroleptics. Activities of daily living must be routinized, and frequent supportive guidance and reality orientation may be used in an attempt to minimize disruptive behavior.

B. Parkinson's Disease I. Clinical Features Parkinson's Disease (PD), a degenerative disorder mainly involving the pigmented cells in the substantia nigra and other pigmented brain stem nuclei, affects approximately 1% of all individuals over the age of 65. Dopamine depletion in the frontal cortex and striatum (particularly in the anterodorsal portion of the head of the caudate nucleus), is the major neurochemical deficit associated with PD, although reduced levels of norepinephrine, acetylcholine, and somatostatin, and diminished serotonin receptors have also been reported. The cause of PD is not known, although toxic agents such as manganese poisoning in industrial workers and injection of 1-methyl-4-phenyl 1,2,3,6 tetrahydropyridine (MPTP) in drug abusers, are known to produce PD symptoms and pathology, suggesting the possibility that an environmental factor could play a role in the etiology. Although CT and MRI exhibit little predictive value for diagnosis of PD in an individual case, PET studies using fluorodeoxyglucose may show hypometabolism in the basal ganglia and frontal cerebral cortex. Regional cerebral blood flow studies have shown reductions in frontal cortical blood flow. PD is most prominently associated with motor abnormalities involving a resting tremor, loss of postural reflexes, stooped posture, bradykinesia (slowed movement), cogwheel rigidity, and slow shuffling gait. Small handwriting, dysarthria, reduced vocal volume, and a tendency to speak in a monotone fashion may also be seen. Between 25 and 40% of PD patients may develop dementia. When present, PD dementia typically occurs during the later stages of the disorder. Bradyphrenia (cognitive slowing) is typically one of the earliest features of PD dementia. Language deficits tend to involve motor components of speech (e.g., dysarthria, diminished phrase length, dysprosody, micrographia) more severely than linguistic aspects of speech, such as naming and comprehension. Memory and learning deficits are also seen in the early stages of PD dementia. For example, procedural learning

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(ability to acquire a new perceptual-motor skill)tends to be impaired. Effortful memory and spontaneous free recall are also generally impaired in PD dementia, although recognition memory is often preserved. Deficits in visuospatial abilities involving both visuoperceptual and visuoconstructional aspects have been well documented. Executive functioning deficits involving establishing, maintaining, and shifting cognitive set also are common in PD dementia and are similar to deficits in patients with discrete lesions of the frontal lobes. Depression may occur in 25 to 40% of PD patients.

2. Treatment PD is most commonly treated with medication designed to ameliorate the central dopamine deficiency. Levodopa, a dopamine precursor that readily crosses the blood-brain barrier and is metabolized to dopamine, is the most common pharmacologic agent used to treat PD. Following levodopa administration, symptomatic improvement in movement abnormalities is seen in approximately 60% of patients, and cognitive impairment has also been shown to improve following pharmacotherapy. However, this form of treatment becomes ineffective after 1 to 4 years, presumably due to progressive neuronal loss and inability of remaining neurons to convert levodopa to dopamine. Depression in PD is not affected by levodopa therapy and sometimes may be a side effect of the medication. Tricyclic antidepressants and electroconvulsive therapy have been used successfully to improve mood and motor disability. Surgical treatment of PD has a long history and a promising future. Before dopaminergic medications were available, the accepted method of treatment involved surgical placement of a lesion in the ventrolateral thalamus. Although this procedure improved tremor and reduced rigidity, this procedure had little effect on the akinesia associated with PD. Surgical intervention using placement of a lesion in the globus pallidus (pallidotomy) had also been attempted, although wide variability in the accuracy of lesion placement produced inconsistent and often devastating results. Using new microelectrode-guided lesion placement techniques, pallidotomy has reemerged as a potential treatment for PD with much fewer complications. Pallidotomy produces relatively rapid and substantial improvement in the motor symptoms, al-

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though there tends to be little effect on neuropsychological and psychiatric status postsurgically.

C. Diffuse Lewy Body Disease I. Clinical Features This disorder has received considerable attention within recent years as an important cause of dementia with parkinsonian features, although it has also been considered by some to be a variant of Alzheirner's disease. The occurrence of diffuse Lewy body disease appears to be linked to a genetic mutation in the betaamyloid precursor protein gene on chromosome 21. Approximately 20% of patients with a clinical diagnosis of Alzheimer's disease are thought to have concomitant diffuse Lewy body disease. This disease thus appears to reflect an overlap between Parkinson's disease and Alzheimer's disease. A progressive dementia, consisting of impaired attention, memory, language (e.g., verbal fluency, praxis, and naming), and visuospatial/visuoperceptual skills, typically appears first, followed by parkinsonian features, including akinesia, tremor, and rigidity. A cognitive hallmark of early diffuse Lewy body disease is a fluctuating cognitive state in which patients can be cognitively impaired on one day and cognitively intact on the next day. Sensitivity to the effects of neuroleptic medications, sometimes resulting in obtundation or stupor, has also been reported in this dementia. Neuropsychiatric disturbances, including paranoid delusions and auditory and visual hallucinations, are present in approximately half of all patients with diffuse Lewy body disease and tend to occur early in the disease course. Histologically, Lewy bodies are inclusion bodies (similar to Pick bodies) that disrupt neuronal cytoskeletal organization. In diffuse Lewy body disease, Lewy bodies are diffusely present in surviving cortical neurons, although they tend to favor layers V and VI of cingulate and entorhinal cortex, and they are also found in the brain stem and substantia nigra. Spongioform changes restricted to the temporal lobe help to differentiate diffuse Lewy body disease from prion diseases (described later in this article) in which the spongioform changes are diffusely located. However, there is no current evidence that diffuse Lewy body disease is transmissible. Efforts are currently underway to understand the nature of different Lewy body disease

and its relationship with Alzheimer's disease and with Parkinson's disease.

2. Treatment Symptomatic pharmacological treatment of the Parkinsonian features of this disorder is the only therapeutic option at this time. The dementia associated with diffuse Lewy body disease currently is not amenable to treatment.

D. Huntington's Disease I. Clinical Features Huntington's disease is a genetically inherited autosomal dominant condition that affects approximately 5 out of 100,000 patients. Persons with an affected parent have a 50% chance of developing the disease. The genetic locus for the disease appears on the short arm of chromosome 4. Males and females are equally likely to inherit the disorder. The disorder typically becomes manifest in persons between the ages of 25 and 45, although juvenile forms of the disease also occur. The disorder is characterized by choreiform (dancelike) movements involving the limbs and trunk, bradykinesia, and psychiatric disturbances (particularly affective disorders). Neuropathologically, a characteristic loss of the medium-sized spiny neurons in the caudate and putamen, which project to the globus pallidus and pars reticulata of the substantia nigra, occurs in Huntington's disease. Neuronal loss also occurs in the globus pallidus, ventrolateral thalamus, and subthalamic nucleus. This neuronal loss is associated with marked neurotransmitter reductions in the GABA-synthetic enzyme glutamate decarboxylase, neuropeptides (enkephalin, substance P, cholecystokinin), acetylcholine, and choline acetyltransferase. CT and MRI scans generally show a bilateral "wasting" of the caudate nucleus (although the entire striaturn is typically involved), with concomitant dilatation of the anterior horns of the lateral ventricles. Cortical atrophy is also commonly present. SPECT scans show decreased blood flow in the basal ganglia and frontal cortex, and PET studies also demonstrate diminished glucose utilization in these regions. For a number of years, Huntington's disease was considered to be a prototypical "subcortical" dementia, with the greatest pathological changes occurring in subcortical structures such as the basal ganglia. However, it is now

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clear that pathological changes occur in cortical regions as well, thereby blurring the distinction between the terms "cortical" and "subcortical" dementia. Early signs of Huntington's disease include alterations in memory, affect, or movement. As the disease progresses, impaired attention and concentration and executive dysfunction become prominent. Memory is also impaired and is characterized by deficient retrieval of new information during the early stages. Cues are generally effective in facilitating patients' recognition performance, although deficient encoding of new information becomes evident as the diseases progresses. Procedural learning tends to be impaired. Language abilities (e.g., comprehension, naming) are usually unaffected until the later stages of the disorder, although impairment in the motor aspects of speech may be associated with dysarthria and impaired writing. Diminished word list generation is also commonly seen. Approximately 50% of patients with Huntington's disease may develop affective disturbances, and there is a high risk of depression and suicide in this population. Impulsive aggressive or sexual behavior, irritability, angry outbursts, and anxiety are also common psychiatric manifestations. A presymptomatic genetic test was recently developed to determine whether an individual carries the abnormal gene and hence will eventually manifest the disease. However, prior to undergoing such testing, genetic counseling is extremely important, as there is a high risk of suicide in persons who test positive.

2. Treatment Huntington's disease has a progressive course that cannot be altered, although some control can be gained over the choreiform movements. Neuroleptic medications and tetrabenazine (a dopamine antagonist) may be helpful in this regard. The findings of reduced GABA in the basal ganglia in Huntington's disease patients have prompted the use of GABA-ergic agents, such as isoniazid, which have also had limited success in treating choreiform movements. Intravenous injection of physostigmine has been demonstrated to reduce the movement abnormalities in Huntington's disease, although oral administration of cholinergic compounds has not shown significant efficacy. The dementia associated with Huntington's disease is not improved with medication. However, it is important to note that the affective disturbances, including depres-

sion, irritability, angry outbursts, and psychosis, are amenable to pharmacologic treatment. Electroconvulsive therapy has also been effective in treating the depression associated with Huntington's disease. Psychosocial interventions, including genetic counseling, personal counseling, patient and caregiver support groups, and management of psychiatric disturbances, play a significant role in the treatment of these patients.

E. Progressive Supranuclear Palsy I. Clinical Features Progressive supranuclear palsy (PSP) is a relatively rare disorder that shares many of the same motoric abnormalities seen in Parkinson's disease. However, PSP also affects brainstem nuclei, producing progressive loss of volitional eye movements, swallowing difficulties, and dysarthria associated with pseudobulbar palsy, together with rigidity in the neck and trunk, and hypererect posture with neck extension. Voluntary downward gaze is generally lost first, followed by loss of upward gaze, and finally loss of horizontal eye movements. Approximately 60 to 80% of PSP patients exhibit dementia. PET studies have shown prominent hypometabolism and hypoperfusion in the superior frontal lobes, and hypometabolism has also been observed in the caudate, putamen, thalamus, and pons. Cognitive changes associated with PSP dementia include bradyphrenia, impaired learning, memory consolidation, and retrieval, personality changes including apathy and depression, impaired motor aspects of speech (e.g., hypophonia, dysarthria, diminished verbal output), and impaired executive functioning on tasks such as word list generation. Aphasia, apraxia, and agnosia are typically not seen in PSP.

2. Treatment

PSP has a relatively rapid, progressive course that is minimally amenable to treatment. Motor abnormalities, such as dyskinesia and rigidity, and extraocular movements are occasionally responsive to treatment with dopamine precursors and dopamine receptor agonists, although the dementia associated with PSP is generally unaffected. As with Parkinson's disease, pharmacotherapy becomes less effective as the disease progresses.

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F. Cortical-Basal Ganglionic Degeneration I. Clinical Features This degenerative disorder is typically associated with asymmetric neurological findings together with an overlay of cortical and subcortical neuropsychological deficits. Asymmetric rigidity and akinesia of the arms is typically seen, together with myoclonic jerking, tremor, and dystonic movements. From a neuropsychological perspective, a profound apraxia is associated with the affected limb, which gradually progresses to a loss of all executive functions associated with limb movement. Cognitive slowing, perseveration, and difficulty with cognitive flexibility is also seen. Generalized cerebral atrophy is typically present on CT and MRI scans. Asymmetric metabolic and blood flow abnormalities are often observed in the basal ganglia and associated fronto-parietal cortex on PET and SPECT.

2. Treatment There are no effective treatments for this progressive disorder.

G. Hallervorden-Spatz Syndrome I. Clinical Features Hallervorden-Spatz syndrome is a rare autosomal recessive condition that first becomes manifest in late childhood or early adolescence. It is characterized by motoric spasticity and rigidity, dystonia, or chorea, together with a progressive dementia. Moodiness, depression, and angry outbursts may presage the cognitive decline. Increased deposition of iron in blood vessels and cells of the basal ganglia is associated with this disorder. The globus pallidus and pars reticulata of the substantia nigra are typically discolored, appearing rusty brown, and partially destroyed. Magnetic resonance imaging (MRI) may show hypodensity in the globus pallidus, putamen, or substantia nigra, or a gradual wasting of the basal ganglia similar to that found in Huntington's disease may also be seen.

2. Treatment There are no effective treatments for this condition.

H. Wilson's Disease I. Clinical Features Wilson's disease is another autosomal recessive condition that occurs in approximately 1/30,000 patients.

It typically becomes manifest in the late teens or early 20s and affects males and females equally. This disorder is associated with abnormal copper metabolism, and increased deposition of copper is found in the liver, brain, and eyes. Motor symptoms include tremor, rigidity, dystonia, chorea, and dysarthria. Progressive dementia, characterized by impaired memory, poor concentration, impaired abstract reasoning and concept formation, and bradyphrenia, and psychiatric disturbances, such as psychosis, emotional lability, and childishness, occur in Wilson's disease. Language functions are commonly spared. The cognitive and motor symptoms of Wilson's disease are likely to be the result of the toxic effects of copper on cerebral tissue. Characteristic features of Wilson's disease include the brownish-green Kayser-Fleischerring found in the limbus of the cornea, low serum ceruloplasmin (a coppercarrying protein) concentration, and elevated copper excretion. CT and MRI scans frequently reveal hypodensity in the lenticular nuclei. PET scans may also demonstrate diffuse hypometabolism, together with marked hypometabolism in the lenticular nuclei. 2.

Treatment

Early diagnosis is essential, as this disorder is one degenerative condition that can be effectively treated with reduction of dietary copper, administration of the copper chelating agent D-penicillamine, and administration of pyridoxine to prevent anemia, thereby inhibiting further progression and reversing both hepatic and neurological signs.

I. Cerebellar and Olivopontocerebellar Degeneration I. Clinical Features A heterogeneous spectrum of disorders involving progressive ataxia, some of which are genetically inherited, are also associated with dementia. Symptoms associated with cerebellar dysfunction, such as ataxic gait, hypotonia, limb unsteadiness, intention tremor, and dysarthria, are common. Extracerebellar signs, such as ophthalmoplegia, deafness, hyperreflexia, and extensor plantar responses, may also occur and tend to be more indicative of olivopontocerebellar atrophy. Cerebellar degeneration may be evident on CT or MRI scans, while PET scans may show hypometabolism in the cerebellar hemispheres, cerebellar vermis, and brain stem. The inferior olivary and pontine nuclei

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often appear atrophied. Choline acetyltransferase and acetylcholinesterase tend to be diminished in olivopontocerebeUar degeneration. The dementia syndrome is characterized by impaired attention and memory, apathy, and psychomotor retardation. 2. Treatment There are no effective treatments for this disorder.

II. DEMENTIA DUE TO CEREBROVASCULAR DISEASE In contrast to the degenerative dementias in which the specific etiology is generally uncertain, dementia due to ischemic, anoxic, or hemorrhagic events can often be traced to known risk factors, such as cigarette smoking, hyperlipidemia, cardiac arrhythmia, or platelet aggregation. Given knowledge of these risk factors, early diagnosis of vascular dementia may potentially minimize further cognitive deterioration. Vascular dementia can be attributed to the cumulative effect of cerebrovascular events largely confined to the cerebral cortex (multi-infarct dementia), vascular lesions in specific subcortical structures (thalamic vascular dementia and lacunar state), or to accumulated, small vessel vascular lesions confined mainly to the periventricular white matter regions (Binswanger's disease or subcortical arteriosclerotic encephalopathy).

A. Multi-Infarct Dementia I. Clinical Features Multi-infarct dementia is associated with accumulated vascular damage that preferentially affects cortical gray matter areas. Men are typically affected more often than women. A rapid disease onset and stepwise clinical course characterized by plateaus and sharp declines in functioning are both associated with multi-infarct dementia, although more gradual and progressive diminution in mentation may also be seen as well. Nocturnal confusion, previous hypertension, and a history of transient ischemic attacks are also associated with multi-infarct dementia. Neurological examination typically reveals focal or bilateral pyramidal or extrapyramidal signs, including plantar extensor response, limb rigidity or spasticity, hyperreflexia, gait disturbance, or urinary incontinence. There is wide variation in the types and severity of cognitive

deficits associated with multi-infarct dementia, depending on the location and number of infarcts. The prototypic neuropsychological profile is a "patchy" presentation, with relative preservation of some abilities and loss of other skills. Frequent deficits are seen in the areas of orientation and attention, recent memory, abstract reasoning and problem solving, and language deficits, such as impaired writing, frequent literal paraphasias (e.g., saying "tome" for comb), apraxia, and difficulty with complex comprehension. Coronary insufficiency with systemic hypotension tend to produce more diffuse deficits. Psychiatric features, most notably depression and emotional lability, are also common in cerebrovascular dementia. 2. Treatment Early diagnosis is important in order to prevent or retard further progression of the dementia. Recognition of the presence of multiple risk factors for vascular disease can also facilitate diagnosis and identify targets for treatment. Controllable risk factors include cigarette smoking, hyperlipidemia, diabetes, and hypertension. Agents that inhibit platelet aggregation, such as aspirin or warfarin, may also reduce the risk of thrombotic infarction. Speech therapy may be helpful for patients who have developed aphasia, and occupational and physical therapy are beneficial to maximize the potential for continued independent living.

B. Thalamic Vascular Dementia I. Clinical Features Vascular lesions to the thalamus may produce a range of neurological and neuropsychological deficits depending on the specific thalamic nuclei involved. From a neurological perspective, thalamic hemorrhage may be associated with greater sensory than motor loss, memory impairment, impaired vertical gaze, and aphasic symptoms, if the lesion occurred in the dominant hemisphere. Variable arousal, including hypersomnia and loss of consciousness, have been reported with lesions (usually bilateral) to the paramedian thalamus. Disturbed attention on less-structured tasks may also be seen in thalamic lesions. Deficits that are typically characteristic of frontal lobe lesions are frequently associated with thalamic lesions as well, possibly in the region of the dorsomedial nucleus. These deficits include perseveration, increased susceptibility to interference, difficulty in sequencing information,

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and personality changes such as apathy, abulia, lack of concern, and euphoria. Language following ventrolateral and ventroanterior thalamic lesions is generally characterized by intact repetition, comprehension, reading, and writing, contrasted with impaired speech initiation, diminished content of speech, reduced word list generation, dysprosody, dysarthria, perseveration, and hypophonia. Lesions in the pulvinat and posterolateral thalamus have been associated with anomia, normal or increased speech output, and impaired comprehension. Visuospatial deficits may follow bilateral or unilateral right thalamic damage. Memory impairment has been attributed to lesions affecting the dorsomedial nucleus, mammillary bodies, and/or mammilothalamic tract.

2. Treatment Thalamic vascular lesions are not reversible. Treatment involves reducing or eliminating modifiable vascular risk factors plus supportive measures including speech, occupational, or physical therapy, and managing neuropsychiatric conditions should they occur.

C. Lacunar State I. Clinical Features

Small infarctions ranging from 0.5 to 1.5 mm in diameter that are located primarily in the basal ganglia,

thalamus, internal capsule, and brain stem are referred to as lacunes. Lacunes are thought to result primarily from hypertension-related fibrinoid necrosis of arterioles resulting in occlusion, although some lacunes may be associated with hemorrhage. The lenticulostriate branches of the middle cerebral artery or the thalamogeniculate, choroidal, and thalamoperforator branches of the posterior communicating and posterior cerebral arteries are commonly involved. The term lacunar state describes the condition in which multiple lacunes are present. Hypertension, diabetes, and atherosclerotic emboli have been noted to contribute to the formation of lacunes. Lacunar state is generally associated with combined motoric and cognitive impairment. The motor symptoms include rigidity and bradykinesia (which are seen in Parkinson's disease), spasticity, hyperreflexia, limb weakness, pseudobulbar palsy, and extensor plantar responses. Given the many motor abnormalities that are similar to Parkinson's disease, the term "arteriosclerotic parkinsonism" was used until recently to describe deficits

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associated with lacunar state. Cognitive deficits typically involve impaired memory, apathy, psychomotor retardation, impaired mental control and orientation, and frontal-lobe type deficits. Mood changes and fluctuations in mental state are also observed. Lacunes may be evident on CT or MRI, although many lacunes are too small to be visualized using either imaging technique. PET scans may reveal areas of hypometabolism at the site of the lacune as well as in cortical locations receiving projections from the affected region.

2. Treatment Once present, the cognitive and motor impairment associated with lacunar state cannot be reversed, although preventative measures such as correction of modifiable risk factors will help to reduce or retard progression.

D. Binswanger's Disease (Subcortical Arteriosclerotic Encephalopathy) I. Clinical Features When ischemic damage is confined to the periventricular white matter regions, the term Binswanger's disease or subcortical arteriosclerotic encephalopathy is applied. Occlusion of small blood vessels is commonly associated with this condition. Binswanger's disease may resemble a degenerative dementia such as Alzheimer's disease by virtue of its insidious onset and gradual progression. It may lack the abrupt onset and stepwise decline associated with other vascular dementias. Hypertension and smoking are the most common risk factors for Binswanger's disease. Clinical deficits vary depending on the extent of the lesions, although incontinence, pseudobulbar palsy, asymmetric weakness, gait disturbance, parkinsonism, and dysarthria have been described. Mood disturbances include irritability, apathy, mania with hyperactivity, depression with suicidal ideation, and psychosis with paranoid delusions. From a cognitive perspective, memory deficits are usually only mild in Binswanger's disease, although poor judgment, perseveration, abulia, and increased response latency are seen more frequently. Loss of white matter is most severe in the frontal lobes. The short arcuate "U" fibers are generally spared. Lacunar state may coexist with Binswanger's disease. Enlarged ventricles and evidence of periventricular lucency associated with white matter ischemia are typically noted on CT and MRI.

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Varying degrees of periventricular lesions have been reported in "normal" asymptomatic elderly individuals without neurological complaints, suggesting that the amount of white matter ischemia has little correlation with the extent of cognitive impairment. This finding has stimulated controversy regarding the radiologic diagnosis of Binswanger's disease. However, there are also data to suggest that persons with radiologic evidence of white matter lesions have significantly lower intellectual performance and more motor abnormalities than persons without diffuse white matter lesions, suggesting that periventricular lucencies may be a harbinger of deficits associated with Binswanger's disease even in asymptomatic individuals.

2. Treatment As with the other vascular dementias, prevention of further deterioration through careful monitoring of vascular risk factors (particularly smoking and hypertension) and antiplatelet treatment with agents such as aspirin, warfarin, and ticlopidine are the only treatment strategies for this condition at this juncture. E. Vasculitis Dementia may also be associated with inflammation of the cranial arteries due to systemic illnesses, such as giant cell (temporal) arteritis, sarcoidosis, systemic lupus erythematosus, granulomatous arteritis, and polyarteritis nodosa, or to chemical arteritis associated with use of amphetamines, "crack" cocaine, or oral contraceptives. Amyloid angiopathy is often associated with hemorrhages but may also be associated with dementia. Dementia due to vasculitis generally presents acutely in a manner consistent with a confusional state, although gradually progressive dementia is not uncommon. Cerebral arteriography and brain biopsy are often necessary for diagnosis. Treatment with antiinflammatory agents is frequently prescribed.

III. DEMENTIA DUE TO INFECTIOUS AGENTS The central nervous system can be vulnerable to infection from a variety of agents. Infectious agents producing dementia include viruses, bacteria, fungi, parasites, and atypical proteinaceous infectious agents called prions. Given an intact immune system, infec-

tion of the central nervous system is relatively rare, although infection by herpes simplex or cryptococcus can occur in immunocompetent hosts. However, in cases of immune system compromise, the brain may become vulnerable to a variety of infectious agents, some of which may be treatable if discovered early in the course of the disorder. The term encephalitis refers to inflammation and infection of brain tissue associated with any of the infectious agents described above. The term encephalopathy is broader, encompassing dysfunction of the brain due to any cause.

A. Viral Infections A virus is a small particle of protein-encapsulated DNA or RNA that infects a host cell and replicates itself therein. Two groups of viruses that may produce dementia have been described. The first group is termed the neurotropic viruses, such as those causing rabies and poliomyelitis, which have a special affinity for central nervous system cells. The second group is known as the pantropic viruses, such as mumps, measles, and herpes simplex, which invade cells throughout the body, in addition to central nervous system cells.

I. HIV Encephalopathy a. Clinical Features The dementia associated with infection by the Human Immunodeficiency Virus (HIV) which produces Acquired Immunodeficiency Syndrome (AIDS) has been well-characterized, and central nervous system involvement is present in virtually all AIDS patients at autopsy. Central nervous system compromise is produced in two ways. First, by weakening the immune system, the brain becomes susceptible to rare infectious agents, such as parasites and fungi. On a second level, the virus invades and destroys neurons, glia, subcortical nuclear structures, and white matter of the brain. Numbness, tingling, muscular weakness, and coordination difficulty may frequently be indications of direct central nervous system involvement by HIV. Other early neurological manifestations may include ataxia, action tremor, dysarthria, and exaggerated lower extremity reflexes. Headache, seizures, incontinence, and rigidity may appear with later disease progression. Early cognitive features may include forgetfulness, fluctuations in attention and concentration, and difficulty maintaining a coherent stream of thought. Apathy and depression

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may also become prominent during the early stages of infection. Frank memory deficits emerge later, in addition to visuospatial impairment, diminished fine motor coordination, decreased cognitive flexibility, and intact simple reaction time contrasted with impaired choice reaction time. Naming and vocabulary are typically preserved throughout the disease. Confusion and disorientation, psychomotor slowing, mutism, and apathy are frequently seen in the preterminal stages. Some patients may exhibit psychotic features and/or prominent affective symptoms. Cortical atrophy with ventricular enlargement and sulcal widening is generally evident on CT or MRI scans, although MRI scans will typically also reveal deep white matter lesions. In the early stages of HIV infection, reduced cerebral glucose metabolism and cerebral blood flow is generally evident in subcortical structures, including the basal ganglia and thalamus on PET or SPECT. More prominent and focal cortical hypometabolism and hypoperfusion are noted in the later stages and is quite distinct from the pattern observed in primary degenerative dementias, such as Alzheimer's disease. b. Treatment Medical management of opportunistic infections with antimicrobials, control of affective disorders with psychotherapy and medication, and careful monitoring of potential toxic and/or metabolic disruptions is important for limiting progression due to these secondary causes of dementia. Although it has significant side effects, the drug azidothymidine (AZT) has been beneficial in limiting viral replication within the individual and improving cognitive function. Individuals with mild to moderate dementia associated with HIV infection have shown improvement in cognition and in cerebral glucose metabolism following AZT treatment. The benefits from AZT are time-limited, however, typically lasting several months before the virus continues to progress. Reduction of the risk factors associated with contraction of HIV through community education, particularly related to intravenous drug abuse and unprotected and promiscuous sexual relations, should also be helpful in reducing the spread of this disease.

2. Subacute Sclerosing Panencephalitis (SSPE) a. Clinical Features The measles virus may sometimes cause an acute encephalitis, although it may also produce a slowly developing degenerative process

known as subacute sclerosing panencephalitis (SSPE). Progressive Rubella Panencephalitis is another viral encephalitis that is clinically similar to SSPE. SSPE typically presents during childhood or adolescence several years following measles infection and produces a rapid deterioration leading to death in from 3 to 10 months. Boys are affected more frequently than girls. Behavioral changes, including oppositional behavior and angry outbursts, together with slow cognitive decline and a deterioration in school performance typically are the earliest features of SSPE. Onset of seizures and movement abnormalities, such as myoclonic jerking (short, rapid involuntary muscular contractions), gait disturbance, and rigidity, are also seen in SSPE. End stages of the disease are characterized by hypothalamic dysfunction and autonomic failure and decerebrate posturing. Cognitive features include visuospatial deficits, distractibility, inability to self-dress, apraxia, alexia, aphasia, and agnosia. General intellectual functioning declines steadily throughout the course of SSPE. The electroencephalogram (EEG) demonstrates a characteristic burst-suppression pattern exemplified by periodic high amplitude waveform complexes, making it particularly helpful in diagnosis. MRI scans may reveal hyperintensities on T2-weighted images in the basal ganglia. PET may show hypermetabolism in the basal ganglia contrasted with cortical hypometabolism in the early stages of the disorder. b. Treatment SSPE typically progresses to death within several months, although periods of remissions and exacerbations are common. Amantadine, isoprinosine, and intraventricular administration of interferon have been reported to be effective in prolonging life and in bringing about periods of remission. Fortunately, the number of SSPE cases has been significantly reduced by the introduction of the measles vaccine. Thus, this devastating childhood dementia is potentially preventable.

3. Herpes Simplex Encephalitis

a. Clinical Features The Herpes Simplex Virus (HSV I) can produce an acute, severe encephalitis that results in destruction of the medial temporal and orbitofrontal cortical regions, with relative sparing of white matter. Following initial infection, HSV resides in cell bodies of the trigeminal nerves innervating cutaneous regions of the face. Reactivation of the virus can lead to viral migration along the trigeminal nerve

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with subsequent encephalitis. Headache and fever may be associated with early stages of the HSV encephalitis, followed by acute mental status changes, seizures, and coma. The disease is often fatal. However, in survivors, there is usually prominent memory impairment, reflecting damage to the medial temporal regions. A human condition resembling the so-called Kluver-Bucy syndrome seen in monkeys, represented by diminished responsiveness to social and emotional stimuli, increased oral exploratory behavior, reduced aggression and fearfulness, and difficulty recognizing the meaning or significance of common objects ("psychic blindness"), is sometimes associated with bilateral temporal lobe destruction. Aphasia may also be a cognitive sequel of HSV encephalitis. CT or MRI scans may show areas of lucency in the temporal lobe, and EEG may reveal diffuse or focal slowing or periodic sharp and slow-wave complexes.

tarabine therapy, although clinical trials with other antiviral agents have produced mixed results.

5. Limbic Encephalitis

b. Treatment Early treatment with acyclovir and adenine arabinoside may substantially diminish the morbidity and mortality associated with HSV encephalitis.

a. Clinical Features Limbic Encephalitis involves a progressive cognitive decline over 1 to 2 years in individuals with an underlying malignancy. Oat cell carcinoma of the lung is one neoplasm that is frequently associated with limbic encephalitis, although the syndrome has been described in a variety of other cancers. Characteristic features include marked disturbance of affect, commonly involving anxiety and depression, in addition to prominent memory impairment. Hallucinations and variable alertness may also be seen. Pathological changes include neuronal loss and inflammatory changes concentrated in hippocampus and medial temporal lobe, although lateral temporal cortex, and other widespread brain regions may also be involved. Limbic encephalitis may result from an autoimmune response producing an attack on temporal lobe neurons, given the relatively acute presentation, inflammatory changes, and occasional presence of intranuclear inclusion bodies.

4. Viral Infections Associated with Underlying Systemic Illness

b. Treatment There are no effective treatments for this paraneoplastic dementia.

a. Clinical Features Progressive Muhifocal Leukoencephalopathy (PML) is associated with infection by the papova viruses in immunocompromised persons (e.g., AIDS) or individuals with chronic lymphoproliferative, myeloproliferative, or granulomatous diseases. This disease affects many different areas of cerebral and cerebellar white matter and may be associated with motor weakness, gait disturbance, dysarthria, blindness and other visual disorders, and seizures. The dementia associated with PML includes behavioral changes, memory deficits, poor concentration, and language deficits. MRI may show multifocal hyperintensities in the white matter associated with subcortical demyelination. Microscopic changes include abnormal oligodendrocytes that are large and contain intranuclear inclusion bodies. Abnormally shaped, multinuclear astrocytes are also found in the areas of the lesions. PET studies reveal cortical hypometabolism in regions associated with white matter changes. Simian virus 40 (SV 40) is one of the most common papova viruses associated with PML.

a. Clinical Features Most forms of bacterial meningitis (infectious inflammation of the meninges surrounding the brain) typically have a rapid onset and are associated with fever, headache, and stiff neck. Although not common, certain bacteria produce a chronic meningitis that is associated with a gradual or subacute cognitive decline. For example, tuberculosis can be associated with central nervous system involvement manifested by pyramidal, extrapyramidal, and cerebellar signs, involuntary movements, poor insight, impaired memory, and personality changes. Lyme disease is caused by a tick-transmitted spirochete (Borrelia burgdorferi). A red rash around the bite area is typically followed by mild flu-like symptoms. Arthritis, cardiac symptoms, and neurological symptoms, including meningoencephalitis may appear months later.

b. Treatment Treatment of PML remains uncertain. There are some reports of improvement following cy-

b. Treatment Although it was previously a fatal condition, tuberculosis meningitis is now generally treat-

B. Bacterial Infections

I. Bacterial Meningitis

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able and curable. Common treatments include combination therapy with isoniazid, streptomycin, and para-aminosalicylic acid or isoniazid and rifampin. However, some treatment-resistant strains of tuberculosis have been reported recently, posing a significant challenge for future treatment of this disease. Oral penicillin or tetracycline is typically used to treat Lyme disease in the early stages, although intravenous administration of antibiotics may be required in the later stages.

2. Syphilis a. Clinical Features The spirochete, Treponema pallidum, is responsible for syphilitic infection. If not treated, symptomatic neurosyphilis may develop in approximately 10% of cases. Symptomatic neurosyphilis tends to be more common in men. Meningovascular syphilis, a condition associated with multiple strokes, may appear approximately 2 to 10 years after the initial syphilitic infection. The condition known as general paresis may appear 7 to 15 years after the initial infection and is characterized by prominent dementia, either with or without psychiatric manifestations, such as mania, depression, or psychosis. In addition to impaired memory, some individuals with general paresis may become severely disoriented and may confabulate. Other cognitive deficits include anomia, apraxia, verbal paraphasias, and dysarthria. Coarse tremors of the jaw and tongue are common. Diagnosis of syphilitic infection is facilitated by serum detection of specific treponemal antibodies (fluorescent treponemal antibody absorption; FTA-abs), together with pleocytosis (white blood cells) present in the cerebrospinal fluid (CSF). On autopsy, significant frontotemporal cortical atrophy is evident. b. Treatment Standard treatment involves intravenous administration of penicillin G, although dosage recommendations and treatment duration vary. Close monitoring of CSF every three months for the first year and every six months during the second year following treatment is recommended.

3. Brain Abscesses a. Clinical Features A variety of bacteria may produce small pockets of pus known as abscesses in or around brain tissue. They are commonly the result of secondary infections and generally originate from middle ear infections, sinusitis, or pulmonary conditions. With increasing size, the abscess behaves as an

expanding mass and may produce elevated intracranial pressure. The abscess may also produce necrosis or cell death, destroying neural tissue in the vicinity of the abscess. b. Treatment Abscesses may be treated with antibiotics, and they often require surgical drainage.

C. Mycotic (Fungal) Infections I. Clinical Features Fungal CNS infections are relatively rare. They occur most commonly in immunocompromised individuals (e.g., HIV infection, immunosuppressant therapy, systemic malignancies). Examples of such infections include cryptococcal meningitis, histoplasmosis, aspergillus, blastomycosis, and candida. These fungi may produce a chronic meningitis that has an insidiously progressive course associated with compromised intellectual functioning, variable arousal, impaired attention and orientation, and poor memory. Cranial nerve palsies are often seen.

2. Treatment Once established, fungal infections are difficult to treat and often result in a high mortality.

D. Parasitic Infections I. Clinical Features

The parasite Entamoeba histolytica (responsible for producing amoebiasis or amoebic dysentery) and several other protozoan and helminthic parasites may produce encephalitis, chronic meningitis, and brain abscesses. The parasite Plasmodium falciparum, responsible for producing cerebral malaria, is associated with infection of capillaries within the brain producing local hemorrhages, demyelination, and neuronal degeneration.

2. Treatment Antimalarial agents and steroid therapy are effective in completely reversing the effects of cerebral malaria if they are administered early in the course of the infection.

E. Prion Disease Prions are subviral, infectious, unencapsulated protein particles that resist most known forms of inacti-

Dementia

vation. They are resistant to boiling, ultraviolet light, and formalin, but they are susceptible to proteolytic treatments, such as autoclaving or immersion in a strong alkali solution. Human prion diseases include Creutzfeldt-Jacob disease (CJD), GerstmannStraussler-Scheinker (GSS) syndrome, kuru and fatal familial insomnia (FFI). Animal prion diseases include bovine spongioform encephalopathy (BSE; "mad cow disease"), and scrapie (seen in sheep). These neurodegenerative diseases were previously thought to be due to "slow viruses." Prion disease can be infectious (kuru, infectious CJD), sporadic (CJD with or without apparent somatic DNA mutation), or familial due to prion protein gene mutation (familial CJD, GSS syndrome, and FFI). The common denominator among all of the prion diseases is an aberrant metabolism of the prion protein (PrP) usually leading to an accumulation of an abnormal isoform of intracellular PrP. All infectious prions are composed of this abnormal PrP isoform. The prion diseases are referred to as the "spongioform encephalopathies" by virtue of the characteristic "spongy" appearance of the postmortem cerebral tissue on microscopic examination. This appearance results from the formation of ubiquitous vacuoles induced by rupture of neuronal and glial membranes. The transmissibility of prion disease via intracerebral inoculation with fresh-frozen brain tissue from humans with spongioform encephalopathy to primates is well established. Human-to-human transmission of CJD has also been documented through corneal transplants, human pituitary growth hormone therapy, human pituitary gonadotropin therapy, dura mater grafts, contaminated electroencephalographic electrode implants, and other neurosurgical procedures. Kuru was once common and was the leading cause of death among the Fore tribe in New Guinea. This disease also is associated with human-to-human transmission, as it is thought to be related to the cannibalistic consumption of dead family members. In addition to dementia, kuru is associated with gait ataxia, followed by limb ataxia, a shiverlike tremor, and dysarthria. The recently reported epidemic of Bovine Spongioform Encephalopathy (BSE or prion disease affecting cattle) in the United Kingdom has caused increased attention to be focused on the intraspecies transmission of prion disease. There has been some speculation that byproducts of sheep infected with scrapie may have been incorporated into cattle feed and may be asso-

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ciated with the apparent increase of BSE in British cattle. Transmission of prion disease from cattle to humans is not well documented, although two cases of CJD in individuals who were occupationally exposed to BSE have been reported in England and Wales. Thus far, the concurrence of CJD and BSE is less than that which could have occurred by chance, and the incidence of CJD in Europe has remained static over recent years. CJD is perhaps the most prototypical of the prion diseases with an incidence of approximately 1 case per million. In a series of 230 neuropathologically verified cases of CJD, up to 8% of the cases appear to be familial. CJD typically presents with subacute, rapidly progressive dementia and myoclonus, and in most cases, eventually demonstrates a characteristic EEG pattern of periodic sharp wave complexes that are predominantly triphasic. Cognitive deficits include concentration difficulty, fatigue, forgetfulness and depression during the early stages of illness, followed by marked aphasia and other cortical signs of dementia such as amnesia, agnosia, apraxia, and rapid intellectual decline. CT and MRI may be normal, or generalized atrophy or focal hyperintensities may be observed. PET and SPECT studies show multifocal areas of hypometabolism and hypoperfusion. GSS is a familial disorder that typically occurs between the ages of 40 and 70, with a duration ranging from 4 to 10 years. It presents as a cerebellar syndrome and dementia. Early motor features are consistent with cerebellar dysfunction, including impaired smooth pursuit eye movements, coordination difficulty, ataxia, and ophthalmoplegia. Parkinsonian symptoms are also sometimes reported. Bradykinesia, rigidity, and extensor plantar responses are also observed during the later stages. Cognitive difficulties are more prominent toward the latter stages of the disease and typically include impaired memory, dysnomia, poor judgment, psychomotor slowing, and affective disorders. FFI is also a familial disorder that is associated with selective degeneration of specific regions of the thalamus. Individuals with FFI exhibit an untreatable insomnia and impaired regulation of the autonomic nervous system. FFI is sometimes referred to as "thalamic CJD." Familial CJD, GSS syndrome, and FFI have been associated with specific mutations on the short arm of chromosome 20 in the prion protein (PrP) gene. The mutations are tightly linked to the expression of the

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disease. The PrP is a normal cellular protein that is synthesized by neurons and glial cells throughout life. PrP has been referred to as a "housekeeping" gene that is necessary for basic cellular functioning. PrP is located in the cellular membrane and is present in evolutionarily diverse organisms. It is thought that prion diseases are associated with a conformational change in PrP, resulting in an abnormal, protease-resistant isoform that is referred to as PrPL PrP P may result from either a genetic mutation causing synthesis of this new isoform or from post-translational modification in the gene product. The abnormal PrP P is thought to lead to cellular death by producing vacuoles and amyloid deposition.

tropic medications, anticholinergic medications, antihypertensive agents), drugs of abuse (alcohol, barbiturates, solvent vapor, amphetamines), heavy metals, and industrial cleaners and solvents. If discovered early and treated aggressively, the progression of a large number of these conditions may be arrested or slowed, and the cognitive disorders may be reversed in some cases. These conditions represent perhaps the most treatable etiologies associated with cognitive impairment, although they are much less common than the degenerative or vascular dementias.

IV. DEMENTIA DUE TO TOXIC OR METABOLICCONDITIONS

a. Clinical Features Thyroid dysfunction accounts for a sizable number of metabolic disturbances, and most of these disorders are highly treatable. Hyperthyroidism tends to be most frequently seen in the late teens or early 20's, although it may also mimic a progressive dementia in the elderly. Idiopathic thyroid overactivity accounts for most cases of hyperthyroidism, although other causes may include thyroid cancer, goiter, or pituitary adenoma that results in overproduction of thyroid stimulating hormone. In younger persons, hyperthyroidism may first present with personality changes including depression, restlessness, anxiety, emotional lability, and irritability, together with concentration and memory deficits, tremor, and tachycardia. Weight loss, skin changes, shortness of breath, and heat intolerance may also occur. These symptoms may progress to cognitive deterioration, apathy, somnolence, and coma in advanced stages. In contrast, the initial personality changes (e.g., anxiety and restlessness), tremor, and tachycardia may be completely absent in elderly persons with hyperthyroidism, and they may instead present with apathy, lethargy, and psychomotor slowing. Hypothyroidism also has prominent neurobehavioral effects including variable attention and orientation, memory deficits, psychomotor slowing, paranoia, and hallucinations. Cold intolerance and weight gain are common. Psychosis may occur in as many as 5 to 15 % of individuals with hypothyroidism, while dementia may occur in 5 % of hypothyroid individuals.

Metabolic derangements and toxic exposure are frequently overlooked causes of dementia, possibly due to the fact that these conditions often present acutely as confusional states, characterized by a fluctuating level of arousal, distractibility, increased motor and verbal response latencies, disorientation, and hallucinations (predominantly visual). Tremor, myoclonus, and asterixis are the most common motor findings associated with these acute conditions. However, metabolic changes or toxic exposure may also occur very slowly, producing a symptom resembling dementia. There are many causes of toxic/metabolic disorders, and a thorough description of each cause is beyond the scope of this article. However, some of the more common systemic illnesses associated with dementia syndromes include endocrine (e.g., thyroid disease, parathyroid disease, disorders of the adrenal medulla and pituitary gland), cardiovascular (e.g., congestive heart failure, hyperviscosity states including polycythemia and hyperlipidemia, anemia), pulmonary (e.g., pulmonary insufficiency, sleep apnea, postanoxic states), renal (e.g., uremia, dialysis encephalopathy), and hepatic (e.g., cirrhosis) dysfunction. Metabolic deficiencies and excesses (e.g., alterations in serum sodium, calcium, magnesium), and vitamin deficiency states (e.g., thiamine (B1), niacin (Bz), cyanocobalamin (B12), folate) are also important considerations in the dementia evaluation. Finally, exposure to a variety of toxic agents may produce encephalopathies. These substances include medications (e.g., psycho-

A. Systemic Illnesses I. Thyroid Dysfunction

b. Treatment Restoration of normal levels of thyroid hormones, most frequently through oral administration of synthetic thyroid supplementation (hypo-

Demenda

thyroidism) or through surgical or radioactive ablation of the thyroid gland (hyperthyroidism), commonly leads to improved cognitive and physical functioning.

2. Parathyroid Dysfunction a. Clinical Features Hyperparathyroidism is frequently associated with elevated serum levels of calcium. Apathy, depression, weakness, and a tendency to tire easily are seen in the early stages. As progression ensues, disorientation, poor memory, fluctuations in attention, paranoia and hallucinations may occur. Hypoparathyroidism and associated low serum levels of calcium commonly result in basal ganglia calcification that may produce parkinsonian motor features (e.g., bradykinesia and limb rigidity) or choreic movement abnormalities. Dementia associated with hypoparathyroidism includes variable orientation and concentration, apathy, and hallucinations. b. Treatment Restoration of normal serum calcium levels in these two metabolic disorders can reverse the cognitive and motor abnormalities in some patients, particularly if discovered early.

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the brain, and an accumulation of cellular metabolic by-products (e.g., carbon dioxide) and a corresponding decrease in pH in surrounding neural tissue take place. Somnolence, irritability, disorientation and confusion, and memory deficits are common. Repeated, prolonged vascular events may result in a stepwise deterioration. Hyperviscosity and hypercoagulable conditions such as hyperlipidemia and polycythemia (a proliferation of red blood cells) may produce sluggish blood flow and occlusive microvascular infarctions. Anemia may also produce cerebral anoxia due to the low concentration of oxygen-carrying hemoglobin in the blood. Myoclonus, restlessness, generalized cognitive deficits, and inattention are associated with chronic anemia. b. Treatment Improvement in cardiac output and correction of hyperviscosity and hypercoagulable states often lead to improved cognitive functioning. Treatment of anemia, often through dietary iron supplementation, commonly leads to reversal of the associated neurological and cognitive symptoms.

5. Pulmonary Disease and Anoxic States 3. Cushing's Disease and Addison's Disease a. Clinical Features Overproduction (Cushing's disease) or underproduction (Addison's disease) of glucocorticoids from the adrenal gland may also produce symptoms of dementia. Cushing's disease most commonly results from pituitary tumors (adenomas), although adrenal tumors may also be associated with this disorder. Depression, psychomotor slowing, disturbed sleep patterns, irritability, and diminished attention, concentration, and memory are seen in this disease and are correlated with the degree of serum cortisol elevation. Addison's disease may produce apathy, impaired memory, depression, paranoia, and irritability, together with weight loss, easy fatigue, and electrolyte imbalances. b. Treatment Restoration of normal serum cortisol levels improves cognitive functioning in most cases.

4. Cardiovascular Disease a. Clinical Features Cardiac insufficiency resulting from congestive heart failure, chronic arrhythmias, or occlusion of the major cerebral arteries from atherosclerosis is associated with diminished cerebral perfusion. As a result, decreased oxygen can be supplied to

a. Clinical Features Chronic pulmonary encephalopathy may result from a variety of diseases that produce pulmonary insufficiency such as emphysema and chronic obstructive pulmonary disease. Tremor and asterixis, headache, and papilledema may reflect physical manifestations of pulmonary encephalopathy. Disorientation, drowsiness, forgetfulness, and variable attention are common mental status changes associated with this condition. As in cardiovascular disease, decreased cerebral oxygen and increased carbon dioxide buildup in neuronal tissue is thought to be associated with the clinical manifestations of the disorder. A similar cognitive presentation has been described in hypoxia associated with living at high altitudes for extended periods. Sleep apnea has been cited as a common cause of cognitive impairment, particularly in the elderly, by producing chronic hypoxia and sleep deprivation. Finally, postanoxic states caused by cardiopulmonary arrest, carbon monoxide poisoning, hanging, and strangulation may produce a gradient of cerebral damage ranging from complete brain death, persistent vegetative state characterized by return of autonomic functioning without apparent higher cognitive activity, or variable deficits of higher cognitive functions, depending on the extent of cerebral damage.

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Amnesia, aphasia, agnosia, visuospatial and visuoconstructional deficits, together with spasticity, dystonia, and ataxia have been described in variable combinations in postanoxic cases. Milder cases may present with impaired judgment, memory deficits, and disinhibition. b. Treatment If discovered early, improvement in pulmonary function may reverse neurological and cognitive deficits. Sleep apnea is highly responsive to treatment using a continuous positive airway pressure (CPAP) device during sleep. In survivors of postanoxic states, rehabilitation, including occupational, speech, and physical therapies, may often be necessary. 6. Renal Disease and Dialysis a. Clinical Features Any disease affecting renal function may produce a wide range of metabolic abnormalities. In addition to a spectrum of medical conditions, a variety of drugs may also impair renal functioning. Tremor, myoclonus, and asterixis are commonly associated with this condition. Disorientation, memory disturbance, variable arousal, irritability, hallucinations, and paranoia or affective lability occur as a result of the metabolic changes produced by chronic renal failure. Uremic encephalopathy is associated with increased serum creatinine and elevated blood urea nitrogen (BUN). The EEG can be a good index of uremic encephalopathy and is commonly characterized by background slowing and disorganization, although paroxysmal bilaterally synchronous bursts of slow wave activity may also be seen. Dialysis encephalopathy produces a progressive cognitive decline, myoclonus, depression, markedly abnormal EEG, and a distinctive progressive difficulty with expressive and motor aspects of speech (including difficulty with initiation, dysarthria, and anarthria) contrasted with relatively preserved naming and comprehension. Cognitive deficits may be seen on visuospatial and timed psychomotor tasks. Paroxysmal slow wave bursts and generalized background slowing are seen in the earlier stages of the disease, although bifrontal bursts of slow and sharp waves, and spike activity may be seen in later stages. The cause of dialysis dementia remains uncertain, although a variety of metabolic etiologies and aluminurn intoxication have been proposed as possibilities.

b. Treatment There have been no successful treatments for dialysis encephalopathy, and the condition

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typically progresses to death within one to two years. Benzodiazepine administration has been temporarily effective in ameliorating the EEG, cognitive, and speech abnormalities, although these benefits subsequently abate and deterioration resumes. Desfuroximes may sometimes be used as an aluminum chelating agent. 7. Hepatic Disease a. Clinical Features Elevated levels of ammonia and short-chain fatty acids are commonly associated with hepatic encephalopathy and may underlie the associated cognitive impairment. There are a variety of diseases associated with hepatic encephalopathy, although alcoholic cirrhosis is the most common of these disorders. Approximately 5% of patients with cirrhosis may develop hepatic encephalopathy. Neuropsychiatric manifestations are frequent in hepatic encephalopathy and may be associated with euphoria, depression, and bizarre behavior. Variable arousal, visuoconstructional deficits, impaired attention and concentration, and memory deficits, together with irregular action tremor, asterixis, gait ataxia, exaggerated reflexes, and motor impersistence are characteristic cognitive and neurological features.

b. Treatment Treatment typically involves strict dietary reduction of protein intake and absorption because proteins are commonly metabolized to ammonia.

B. Vitamin Deficiencies Vitamin deficiencies can be seen in persons with poor or variable diets due to severe depression, anorexia nervosa, bulimia, social isolation in elderly persons, starvation, appetite loss associated with systemic illness (e.g., cancer), Crohn's disease, and chronic alcoholism. Gastrointestinal malabsorption syndromes (e.g., sprue or celiac disease) is another major cause of vitamin deficiency. I. Thiamine (Vitamin B,) a. Clinical Features Thiamine deficiency is most common in chronic alcoholism, but it may be seen in other nutritionally deficient states, including gastrointestinal malabsorption syndromes. The deficiency is due to consumption of a poor diet rather than to the effects of alcohol itself. Chronic thiamine deficiency

Dementia

produces a condition known as Korsakoff's Psychosis. This syndrome presents with ocular movement abnormalities, ataxia (particularly of gait), and a confusional state. Impaired recent memory generally appears following resolution of the confusional state. Complete amnesia for new information is common, and existing memory exhibits a characteristic temporal gradient, with remote memory being relatively intact compared to recent memory. Confabulation (i.e., providing irrelevant, unnecessary information that was not part of the original to-be-recalled material) may be seen in the early stages of this disorder, but it tends to be less common in later stages. Personality changes are often present, and docility with relative lack of concern with their deficits (anosognosia) are common. Pathological changes are seen in the mammillary bodies and the dorsomedial nucleus of the thalamus, in addition to the periventricular gray matter surrounding the third and fourth ventricles. The mammillary bodies are often shrunken and discolored, and this structural change is sometimes evident on CT or MRI scan. b. Treatment Thiamine administration may reverse the eye movement abnormalities and ataxia, although it does little to reverse the memory deficit. However, thiamine supplementation is important to prevent further memory decline. Vasopressin, clonidine, and methylphenidate have been reported to improve memory performance in some patients, although there has been no treatment that has been consistently effective.

2. Vitamin B~2 a. Clinical Features Vitamin B12 (cyanocobalamin) deficiency is associated with pernicious anemia. A lack of intrinsic factor in the gastrointestinal tract resuits in deficient absorption of dietary B12 and is the most common cause of B12 deficiency. Prolonged B~2 deficiency can produce peripheral neuropathy, optic atrophy, and a dementia syndrome characterized by slowed mental processing, memory impairment, depression, and confusion. Neuropsychiatric manifestations, including delusions, hallucinations, paranoia, and agitation may also be seen. b. Treatment Monthly intramuscular vitamin B12 injections are used to treat this deficiency, and most of the neurological symptoms improve or resolve during

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the first month of treatment, if it is initiated relatively early.

3. Folate Deficiency a. Clinical Features This deficiency state is common in Western countries but only rarely produces dementia. Diminished dietary intake or gastrointestinal malabsorption of folate are the most common causes, although the deficiency may be seen following chronic phenytoin or primidone administration. The condition may mimic B12 deficiency in many ways. Poor concentration, disorientation, memory deficits, difficulty with cognitive flexibility, perseveration, and apathy have been reported to occur in folate deficiency. b. Treatment Maintenance oral folate administration generally reverses the cognitive deficits. 4. Niacin (Bz) Deficiency (Pellagra) a. Clinical Features Symptoms of this deficiency state have been referred to as the three D's: dermatitis, diarrhea, and dementia, indicating the prominent effects on the skin, gastrointestinal tract, and central nervous system. This deficiency can result from low dietary intake, malabsorption syndromes, or chronic systemic illnesses. The dementia associated with pellagra is manifested by apathy, confabulation, psychomotor slowing, irritability, and memory impairment. Cogwheel rigidity and frontal release signs (sucking and grasping signs) are seen in acute niacin deficiency.

b. Treatment Consumption of a diet with adequate niacin is a standard treatment, although niacin supplements may be necessary for several days in severe cases. Most symptoms resolve gradually over several weeks after initiating treatment. C. Toxic Conditions

There are numerous substances known to be toxic to the central nervous system, and exposure to such substances continues to increase as technology advances. Many industrial pollutants in the air and water, pesticides, herbicides, food additives, and household supplies such as cleaners, paints, and organic solvents have been reported to produce potentially toxic effects on the central nervous system. Although many of these substances require a prolonged, continuous exposure to be harmful, the long-term effects of a number of

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chemicals are not known. In addition, medications can produce toxicity if they are overused or if alterations in the individual's metabolism prevent toxic by-products from being adequately cleared from the body. The elderly are particularly susceptible to toxic effects of drugs, due to greater variability in metabolic rates, decreased body mass, and lower drug-binding protein levels. Thus, close monitoring for toxicity and modification of drug dosages are often necessary in older persons. Finally, drugs of abuse have frequently been associated with dementia, and the neurotoxic effects of alcohol reflect perhaps the most common dementia associated with substance abuse.

I. Occupational and Environmental Toxic Exposure a. Clinical Features A number of metals may interfere with cellular metabolism, producing dementia after prolonged or accumulated exposure. Lead, inorganic and organic mercury, manganese, arsenic, thallium, tin, bismuth, nickel, and cadmium have all been associated with dementia syndromes. Organic solvents can enter the body through inhalation or skin contact. They are often used in various cleaning supplies and include carbon tetrachloride, trichloroethane, trichloroethylene, methyl chloride, and ethylene glycol. These substances may produce irritability, depression, impaired concentration, memory deficits, and peripheral neuropathy. Organochlorine insecticides may produce anxiety and irritability, but dementia syndromes are somewhat rarer. In contrast, prolonged or continuous exposure to organophosphate insecticides may produce memory impairment, sleep disturbance, distractibility and anxiety. b. Treatment/Prevention The use of protective clothing and devices may be effective in eliminating or minimizing exposure to these hazardous toxic substances, thereby preventing intoxication. 2. Toxic Effects of Medications a. Clinical Features Medications frequently have side effects that may produce dementia following prolonged use. Tricyclic antidepressants have anticholinergic properties that may exacerbate memory impairment in vulnerable persons, and their use in the elderly must be carefully monitored. Lithium has also been associated with a dementia syndrome manifested by disorientation, impaired attention and concentration,

and comprehension deficits. A high-frequency tremor is often associated with lithium use as well. Benzodiazepines (e.g., diazepam, lorazepam, and alprazolam) are associated with impairment in memory functioning that is characterized by an inability to learn new information. Neuroleptic medications (e.g., haloperidol and the phenothiazines) may also produce chronic confusional states and dementia syndromes following long term use. Use of benzodiazepines and neuroleptics are also associated with increased risk of falling and hip fracture in the elderly. Some dementia syndromes have occasionally been associated with antihypertensive medications such as alpha-methyldopa and propanolol presumably through disruption of catecholaminergic synaptic functioning. Recent studies of anticonvulsants suggest that the barbiturates have the greatest impact on cognitive functioning, while anticonvulsants such as phenytoin, carbamazepine, and valproic acid do not commonly produce major cognitive effects at therapeutic serum levels. Dementia syndromes have also been associated with several drugs used in chemotherapy for cancer.

3. Toxic Effects of Drugs of Abuse a. Clinical Features Chronic polydrug abuse has been associated with dementia syndromes, particularly when barbiturates and analgesics are combined. Intravenous drug use using unsterile needles may produce multi-infarct dementia through bacterial endocarditis, although spread of HIV through sharing needles constitutes a much greater risk. An irreversible parkinsonian syndrome was produced in a small group of intravenous drug users who injected themselves with the compound MPTP (described in Degenerative Dementias~Parkinson's Disease). Intentional solvent inhalation (e.g., "glue sniffing") is also associated with significant central nervous system effects resuiting in motor and cranial nerve abnormalities and dementia. [See SUBSTANCEABUSE.] Alcohol is the most common substance associated with abuse and consequently has been widely studied. At least three mechanisms are thought to underlie cognitive deficits in alcohol abuse: thiamine deficiency through dietary neglect (described in the section on vitamin deficiencies), hepatic dysfunction through cirrhosis (described in the section on systemic illnesses-hepatic disease), and direct neurotoxic effects of alcohol on the central nervous system. Alcoholic dementia accounts for approximately 7% of dementias among

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patients evaluated for cognitive decline, and it tends to be seen in older patients after a number of years of abuse. According to Cummings and Benson, daily alcohol intake of 150 ml of absolute alcohol constitutes the definition of excessive alcohol use, which corresponds to two bottles of wine, seven pints of beer, or one-half bottle of distilled spirits. Neuropsychological deficits are seen in the following cognitive domains: memory, visuospatial functioning, abstract reasoning, and verbal fluency. Disorientation, circumstantiality, perseveration, psychomotor slowing and impaired attentional deployment are also typical. CT and MRI scans show cerebral atrophy manifested by enlarged lateral ventricles and widening of the cortical sulci. Atrophy of the cerebellar vermis is also commonly seen. Abnormal EEG slowing is also common in this patient group. Atrophy of the white matter and of the cerebral cortex have been reported at autopsy, together with atrophy of the mammillary bodies, dorsomedial nucleus of the thalamus, the mammilothalamic tract, and the cerebellar vermis. [See ALCOHOL

PROBLEMS.]

lus). Intracranial pressure can be normal or high in any of these conditions. The clinical triad of gait disturbance, cognitive impairment, and urinary incontinence are commonly associated with communicating hydrocephalus. The cognitive impairment is manifested by disorientation, memory impairment, psychomotor slowing, poor abstract reasoning, and bradyphrenia.

2. Treatment Communicating hydrocephalus may be treated by placement of a shunt tube to divert CSF from intracranial spaces to an extracranial site. Maintaining patency of the shunt tube can be problematic and may require shunt replacement. Nonobstructive hydrocephalus (e.g., hydrocephalus ex vacuo) refers to ventricular enlargement due to cerebral atrophy typically due to degenerative conditions, and is not amenable to surgical intervention.

B. Head Trauma I. Closed Head Injury

b. Treatment Abstinence from alcohol, together with improved dietary nutrition, results in at least partial reversal of many cognitive deficits, with recovery being dependent both on the chronicity of abuse and on the length of abstinence. However, it is rare for an alcoholic to return to their baseline level of cognitive functioning.

V. DEMENTIA DUE TO OTHER CAUSES A. Hydrocephalus I. Clinical Features Although this condition is not a common cause of dementia, it can be effectively treated if discovered early. An accumulation of cerebrospinal fluid (CSF) in the brain leads to enlargement of the ventricles. The nature of this CSF accumulation is unclear, but possible causes include excessive CSF secretion from the choroid plexus (e.g., choroid plexus papilloma), obstruction of CSF outflow from the ventricles to the cerebral subarachnoid space (e.g., obstructive noncommunicating hydrocephalus), or obstruction of the CSF flow from the subarachnoid space to the saggital sinus region (e.g., obstructive communicating hydrocepha-

a. Clinical Features Severe closed head injury may produce a posttraumatic dementia. The cognitive deficits may be due to a variety of mechanisms, including diffuse axonal injury, subdural or intracerebral hematoma, and cerebral contusions. The range of deficits following head injury is dependent on the location of cerebral damage and on the severity and mechanism of the trauma. Degree and duration of coma have been shown to correlate with functional outcome. Following loss of consciousness, a period of posttraumatic confusion and disorientation typically ensues, which may last days to weeks. Delirium, agitation, irritability, apathy, or withdrawal may be seen during this period. The duration of posttraumatic and retrograde amnesia duration are sometimes useful prognostic indicators, with longer amnestic periods associated with poorer outcomes. The duration of posttraumatic amnesia refers to the period between the injury and the resumption of continuous memory. The duration of retrograde amnesia refers to the period between the accident and the first clear memory prior to the accident. Longer durations of posttraumatic amnesia have been found to correlate with poorer cognitive outcomes in some studies. Other indices of severity, such as oculocephalic disturbances, are also prognostic of return to work and cognitive

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recovery. Minor head injury with no or minimal (less than 20 minutes) loss of consciousness, no focal neurologic deficits, and no positive neuroradiologic findings typically does not result in significant cognitive sequelae longer than three months postinjury in persons with no pre-injury history of head trauma, neuropsychiatric disturbance, or drug or alcohol abuse. b. Treatment Rehabilitation programs are frequently helpful in developing strategies to compensate for cognitive and motor deficits.

2. Dementia Pugilistica a. Clinical Features Repeated minor head blows, such as those that occur in boxing, result in the condition known as dementia pugilistica. Degeneration of the substantia nigra, neuronal loss in the cortex and cerebellum, neurofibrillary tangle formation and diffuse deposition of beta-amyloid plaques are seen at autopsy. Initial clinical features include mild coordination difficulty and affective dyscontrol, followed by apraxia, aphasia, agnosia, apathy, blunted affect and focal neurologic signs. End stages of the disease are characterized by global cognitive deterioration and the development of parkinsonism. b. Treatment Anti-parkinsonian medications may be helpful in treating the movement abnormalities, although this condition is considered to be progressive.

C. Tumors I. Clinical Features Depending on their location and extent, tumors can cause only discrete cognitive deficits, or they may produce global cognitive impairment characteristic of a dementia syndrome. Tumors in the thalamus, hypothalamus, or frontal or temporal cortex are more often associated with dementia. As noted above, chemotherapy can sometimes be associated with development of dementia independent of the tumor.

2. Treatment The clinical course of patients with tumors is highly variable, depending on the pathology of the tumor and its location. However, with improved imaging methods, treatment can frequently be initiated early, thereby improving prognosis.

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D. Psychiatric Conditions I. Depression a. Clinical Features Severely depressed individuals may manifest impaired attention and concentration, disorientation, and memory deficits, which may frequently be difficult to differentiate from a dementia. In addition, a "dementia syndrome of depression" has been recognized. Some reports have suggested that individuals with this syndrome may exhibit greater cortical volume loss, greater anxiety, and more frequent delusions relative to depressed patients without cognitive impairment. Difficulty abstracting and grasping the meaning of situations, increased response latency, and impaired attention, concentration, and recall but relatively preserved recognition memory are common neuropsychological features. The memory deficit associated with depression is thought to be related to fluctuations in attention and concentration and is less severe than that seen in Alzheimer's disease. Aphasia, apraxia, and inability to name objects are generally not present. The etiology of depression and the dementia syndrome of depression remains elusive, but it is relatively clear that multiple neurotransmitter systems are involved. Disturbed functioning of nigrostriatal and frontal-limbic connections may also be involved in producing variable alertness and attention.

[SeeDEPRESSION.] b. Treatment Cognitive deficits associated with depression are highly treatable with conventional antidepressant pharmacotherapy, or with electroconvulsive therapy in the case of pharmacologic nonresponse. Cognitively oriented psychotherapy has also been a highly effective treatment for depression. Antidepressants with potent anticholinergic properties should be avoided, as these medications may potentially exacerbate the severity of memory impairment.

2. Schizophrenia a. Clinical Features Schizophrenia (dementia praecox) affects approximately 1% of the general population. Initial presentation is that of psychosis, which generally begins in adolescence or young adulthood. Clinical features include "positive" symptoms such as delusions, hallucinations, and formal thought disor-

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der, and "negative" symptoms such as apathy, blunted affect, and anhedonia. Negative symptoms tend to emerge later in the disorder and are associated with dementia ("deficit syndrome"). Exacerbations and remissions of psychotic features characterize the course of the illness. Cognitive deficits are more common during exacerbations of the disease and include difficulty with abstract reasoning, memory impairment, disorientation, perseveration, impaired judgment, and tangentiality. The mechanism of cognitive decline in schizophrenia has not been determined. Ventricular enlargement and sulcal widening on CT and MRI scans correlate with the severity of cognitive impairment, raising the possibility that neuronal loss may account for the dementia. However, disordered monoamine function has also been proposed to underlie the cognitive deficits in schizophrenia. [See SCHIZOPHRENIA.] b. Treatment Treatment with the phenothiazines, butyrophenones, and thioxanthenes has been used to reduce the positive symptoms. Negative symptoms

tend to be unaffected by these three classes of medications, although clozapine has shown some promise.

ACKNOWLEDGMENTS The author thanks Dr. Felicia C. Goldstein, Dr. Robert C. Green, and Dr. Alexander P. Auchus of Emory University School of Medicine for reviewing this manuscript. Support for this research was provided by the Emory Alzheimer's Disease Center (NIA Grant #P30AG10130).

BIBLIOGRAPHY Cummings, J. L., & Benson, D. F. (1992). Dementia: A clinical approach (2nd ed.). Boston: Butterworth-Heinemann. Heilman, K. M., & Valenstein, E. ( 1993). Clinical neuropsychology (3rd ed.). New York: Oxford. Kolb, B., & Whishaw, I. Q. (1990). Fundamentals of human neuropsychology (3rd ed.). New York: W. H. Freeman. Mann, D. M. A., Neary, D., & Testa, H. (1994). Color atlas and text of adult dementias. London: Mosby-Wolfe. Roberts, G. W., Leigh, P. N., & Weinberger, D. R. (1993). Neuropsychiatric disorders. London: Mosby-Wolfe.

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DependentPersonality Robert F. Bornstein Gettysburg College

I. Historical Overview of Dependency Theory and Research II. The Development of Dependency III. Interpersonal Correlates of Dependency IV. Dependencyand Psychopathology V. Dependencyand Physical Disorders VI. The Dependent Personality: Past, Present, and Future

Oral Dependency A psychoanalytic term referring to a set of traits which simultaneously reflect a passive, helpless outlook and a predisposition to cope with stress and anxiety via food- and mouth-related activities (e.g., cigarette smoking). Self-Concept One's mental representation of the self, which is relatively stable and not strongly affected by changes in mood state; the self-concept may have both conscious and unconscious components, and is often associated with a strong affective (i.e., emotional) response. Suggestibility The degree to which a person's attitudes or opinions are easily swayed by the expressed opinions of others.

Authoritarian Parenting A parenting style wherein the primary caretakers impose rigid and inflexible rules and expectations on the child, and the child is expected to conform completely and without question to these rules and expectations. Dependent Personality Disorder A psychiatric disorder characterized by long-standing, extreme dependency which causes significant interpersonal and/or occupational impairment for the afflicted individual. Diathesis Predisposition or risk factor; the term is typically used in psychiatric or medical settings to refer to any form of vulnerability which places an individual at increased risk for physical or psychological illness. Disease-Prone Personality A hypothetical construct referring to a set of personality traits, attitudes, and behaviors which place an individual at risk for disease. Interactionism A framework for conceptualizing personality dynamics wherein behavior is understood as reflecting the interaction of stable personality traits and immediate situational influences.

The term DEPENDENCY, as it is used in personality theory and research refers to a personality orientation (or "style") wherein an individual: (1) perceives himor herself as helpless, powerless, and ineffectual, and therefore (2) turns to others for support, advice, and reassurance rather than attempting to cope with tasks and challenges in an autonomous, self-directed manner. Individuals who consistently display a passive, help-seeking orientation in a variety of situations and circumstances are described as having a dependent personality. During the past several decades there have been hundreds of published studies examining the antecedents, correlates, and consequences of dependent personality traits. These investigations may be grouped into three broad areas: developmental, social, and clinical. Research in each of these areas is discussed in this article.

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I. HISTORICAL OVERVIEW OF DEPENDENCY THEORY AND RESEARCH Although Freud made little mention of the psychodynamics of dependent personality traits, several prominent psychoanalytic theorists (e.g., Karl Abraham, Otto Fenichel, Edward Glover) published papers on the dependent personality during the first few decades of the 20th century. These seminal papers stimulated clinicians' and researchers' interest in the topic of dependency, and not surprisingly, much of the early research on dependency came from a psychoanalytic perspective. Early psychoanalytic studies tested the hypothesis that a dependent personality orientation in adolescence or adulthood could be traced to events that occurred during the infantile "oral" period (i.e., during the first I to 2 years of life). Specifically, the psychoanalytic model hypothesized that high levels of dependency resulted from overgratification or frustration during breastfeeding and weaning. Infantile experiences of frustration or overgratification were presumed to result in "oral fixation" and an inability to accomplish the developmental tasks associated with the infantile, oral stage (i.e., the development of a stable self-concept, along with feelings of autonomy, self-efficacy, and self-sufficiency). Although later studies indicated that dependency in adulthood was not directly related to infantile feeding or weaning experiences, the psychoanalytic model played a central role in bringing dependency research into mainstream psychology. During the 1950s and 1960s, social learning models began to influence dependency theory and research, supplanting (to some degree) the classical psychoanalytic model. These social learning models differed in certain respects, although they shared the fundamental hypothesis that high levels of dependency result from the reinforcement of passive, dependent behavior in the context of the infant-caretaker relationship. Social learning models of dependency further hypothesized that--insofar as passive, help-seeking behavior was reinforced by the parents (and other authority figures) during early and middle childhood--the individual would continue to show high levels of dependency later in life. By the early 1970s, the social learning view of dependency began to give way to ethological (i.e., attachment) theory, which was becoming increasingly influ-

ential in a number of domains within psychology. In contrast to the classical psychoanalytic and social learning models of dependency, attachment theory emphasized the innate, biological underpinnings of the infant-mother relationship as a primary factor in the development of dependent personality traits. Attachment models of dependency have not yet achieved the same status and influence as have the psychoanalytic and social learning models. Nonetheless, attachment theory stimulated a great deal of research examining the etiology and development of dependent personality traits, including some noteworthy studies examining infant-mother bonding in infrahuman subjects. Recent research in this area has focused on exploring the similarities between dependency and various forms of attachment behavior (e.g., insecure attachment)in children and adults. During the 1980s researchers took a more eclectic view of dependent personality traits, combining aspects of the psychoanalytic, social learning, and attachment models in order to arrive at a more integrated, comprehensive perspective on dependency. Thus, relatively few studies during the past decade have focused exclusively on one theoretical framework. Rather, researchers have built upon the strengths of different theoretical models, integrating and synthesizing these models to formulate hypotheses that account for aspects of dependency which are best explained via attention to multiple theoretical perspectives. Recent research on dependency has emphasized the importance of unconscious, unexpressed dependency needs (a concept typically associated with the psychoanalytic model), along with an exploration of the impact of early learning and socialization experiences in the development dependent personality traits (an area of inquiry which originated in social learning theory). During the past decade there have also been increasing efforts to integrate the results of developmental, social, and clinical studies of dependency in order to understand the ways in which findings from these three areas of dependency research complement (and contradict) each other.

II. THE DEVELOPMENT OF DEPENDENCY Developmental studies of dependency can be divided into three areas: (1) studies of the acquisition of depen-

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dent personality traits in infancy and early childhood; (2) investigations of the development of dependency during adolescence and adulthood; and (3) studies of dependency in older adults.

A. Childhood Antecedents of Dependency The results of numerous studies indicate that overprotective, authoritarian parenting is a primary cause of exaggerated dependency needs during adolescence and adulthood. Prospective and retrospective studies of the parenting style-dependency link have produced highly similar results, allowing strong conclusions to be drawn regarding the etiology of dependent personality traits. Findings in this area confirm that when parents show one of these qualities (i.e., overprotectiveness or authoritarianism), the likelihood that their children will show high levels of dependency increases significantly. When parents show both of these qualities, high levels of dependency in their offspring are particularly likely to result. It appears that overprotective, authoritarian parenting produces high levels of dependency in children largely because overprotective, authoritarian parents prevent the child from engaging in the kinds of trialand-error learning that help to provide a sense of mastery, autonomy, and self-sufficiency in children. Consequently, the child of overprotective, authoritarian parents comes to perceive him- or herself as powerless and ineffectual, and continues to rely on others--especially figures of authoritywfor advice, guidance, and protection. As numerous researchers have noted, the child's inability (or unwillingness) to behave in an assertive, autonomous manner exacerbates the situation, in that behaving in a passive, helpless way encourages figures of authority (e.g., parents, teachers) to continue to perform tasks for the child which the child is actually capable of doing on his or her own. Thus, the child's expressions of dependency come to serve as cues which continue to elicit helping and caretaking behavior on the part of others, further reinforcing the child's passive, dependent behavior and ultimately resulting in even greater levels of helplessness and dependency. Recent research confirms that the overt expression of dependency strivings does in fact serve as a help-eliciting cue in both children and adults.

B. Dependency in Adolescence and Adulthood During adolescence, substantial sex differences in dependency emerge, with girls showing significantly higher levels of dependency than boys. This pattern of results is consistent across different cultures {e.g., American, British, Japanese, Indian, German, Israeli), and across different cultural groups within American society. Moreover, the finding that females show higher levels of dependency than do males has been replicated numerous times. Recent studies further suggest that traditional sex-role socialization practices may be largely responsible for the higher levels of dependency typically found in women relative to men. Insofar as traditional sex-role socialization practices tend to encourage passive, help-seeking behavior in girls to a greater extent than boys, these socialization practices would be expected to produce higher levels of dependency in women than in men. Not surprisingly, empirical studies confirm that--to the extent that a girl grows up in a household which emphasizes traditional sex-role socialization practices--she is likely to show high levels of dependency during adolescence and adulthood. Conversely, to the extent that a boy is exposed to traditional sex-role socialization practices (which emphasize assertive, autonomous behavior in boys), he is likely to show low levels of dependency later in life. Not only do sex-role socialization practices play an important role in determining the expression of dependency needs in adolescents, but studies confirm that the object of an individual's dependency strivings (i.e., the person toward whom dependency needs are expressed most readily) changes from childhood to adolescence. Although dependency needs in childhood are typically directed toward the parents and other authority figures (e.g., teachers), during adolescence the dependent individual directs his or her dependency strivings toward members of the peer group rather than toward figures of authority. This shift continues to occur throughout early adulthood, at which point romantic partners become primary outlets for the expression of an individual's dependency needs. In addition, adults often express dependency strivings toward various "pseudoparental" authority figures (e.g., supervisors, physicians, therapists), and (to a lesser extent) toward peers, parents, and siblings.

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C. Dependency in Older Adults There have been no published studies examining individual differences in level of dependency in older adults. However, research suggests that, in general, older adults tend to exhibit more pronounced dependency needs than do younger adults. To some extent, the higher levels of dependency shown by older adults relative to younger adults reflects the fact that older adults as a group are more dependent on others to carry out tasks associated with daily living (e.g., cooking, shopping, driving). In this context, it is not surprising to learn that those older adults who live in environments which encourage autonomy and independence tend to show lower levels of dependency than do those older adults who live in environments where passivity and dependency are permitted or encouraged. Several investigations have demonstrated that changes in older adults' frequency of dependent behaviors can be traced directly to the contingencies which characterize the environments in which they live: Environments that directly or indirectly encourage the overt expression of dependency needs (e.g., certain nursing home environments and residential treatment facilities) actually appear to cause significant, long-term increases in the dependency levels of older adults.

III. INTERPERSONALCORRELATES OF DEPENDENCY In general, studies of the interpersonal correlates of dependency indicate that dependent persons adopt a passive, helpless stance in interpersonal interactions. Specifically, laboratory and field investigations indicate that individuals with a dependent personality orientation show high levels of suggestibility, cooperativeness, compliance, and interpersonal yielding. These results are not surprising when one considers the underlying goals and motivations of the dependent person. Clearly, being helped, nurtured, and protected is very important to the dependent person. In this context, one would expect that the dependent individual would exhibit behaviors that serve to strengthen and reinforce ties to potential nurturers and caretakers. Thus, dependent persons (1) tend to yield to the opinions of others in laboratory conformity experiments; (2) show high levels of suggestibility in both laboratory

and field studies; and (3) are cooperative and compliant in social, academic, psychiatric, and medical settings. Although the dependent person is generally suggestible, cooperative, compliant, and yielding, it is noteworthy that these dependency-related behaviors are even more pronounced when the dependent person is interacting with a figure of authority than when he or she is interacting with a peer. Apparently, figures of authority are perceived by the dependent individual as being particularly good protectors and caretakers. Consequently, the kinds of ingratiation strategies used by the dependent person with peers (e.g., compliance and interpersonal yieldings) are exhibited even more readily around figures of authority. Dependent persons in social settings also show high levels of help-seeking behavior. The dependency-helpseeking relationship is found in both men and women, and is consistent across different age groups (i.e., children, adolescents, adults), and across different measures of help-seeking. The dependency-help-seeking relationship found in adults clearly reflects the early developmental experiences of the dependent person. To the extent that help-seeking behavior during childhood was reinforced by the parents and other authority figures, the dependent adolescent or adult will continue to show exaggerated help-seeking behaviors in a variety of situations and settings. Performance anxiety and fear of negative evaluation might also play a role in encouraging the dependent individual to behave in a help-seeking manner in social situations. Although there have been relatively few studies examining directly the dependencyperformance anxiety relationship, studies in this area indicate that (1) dependent persons show higher levels of performance anxiety (and fear of negative evaluation) than do nondependent persons; and (2)there is a positive relationship between the degree to which a dependent person reports high levels of performance anxiety and the degree to which that person shows high levels of help-seeking behavior in various situations and settings. One final set of findings regarding the interpersonal correlates of dependency warrants mention in the present context. In a series of investigations conducted during the 1970s and 1980s, researchers demonstrated that dependent persons exhibit higher levels of interpersonal sensitivity (i.e., sensitivity to subtle verbal and nonverbal cues) than do nondependent persons. In

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fact, dependent persons are able to infer with surprising accuracy the attitudes and personal beliefs of strangers, roommates, teachers, and therapists. Although at first glance these results seem inconsistent with the oft-reported finding that dependency is associated with passivity and helplessness, findings regarding the dependency-interpersonal sensitivity relationship are actually quite consistent with these other findings. Clearly, to the extent that a dependent person is able to infer accurately the attitudes and personal beliefs of teachers, roommates, and therapists, the dependent person will be better able to develop strong ties to these potential nurturers, protectors, and caretakers.

IV. DEPENDENCYAND PSYCHOPATHOLOGY Because dependency has typically been conceptualized as a flaw or deficit in functioning, numerous studies have examined the relationship between level of dependency and risk for psychopathology. Studies of the dependency-psychopathology relationship can be divided into four areas: (1) studies of dependency and depression; (2) investigations of the dependency-substance use disorders relationship; (3) studies of dependency, obesity, and eating disorders; and (4) research on dependent personality disorder.

A. Dependency and Depression Although laboratory and field studies confirm that there is a positive relationship between level of dependency and level of depression in children, adolescents, and adults, the dependency-depression relationship is more complex than early researchers had thought. On the one hand, exaggerated dependency needs do in fact place an individual at increased risk for the subsequent onset of depression. However, it is also the case that the onset of depressive symptoms results in increases in dependent thoughts, feelings, and behaviors in a variety of subject groups. Presumably, the feelings of helplessness, hopelessness, anhedonia, and anergia that are frequently associated with depression can manifest themselves in increases in overt dependent behaviors in depressed subjects [See DEPRESSION.] The mechanism by which dependent personality traits place an individual at risk for depression is not completely understood, but initial findings suggest that dependency increases risk for depression by causing

the dependent person to be particularly upset and threatened by experiences of interpersonal loss. To be sure, interpersonal stressors affect everyone to some degree. However, the dependent person's lifelong tendency to look to others for nurturance, guidance, and protection may cause him or her to become extremely sensitive to the possibility that a potential caretaker will no longer be available to fulfill their protective and nurturing role. In this respect, dependency represents a vulnerability (or diathesis) that--when combined with interpersonal stressors--places the dependent person at increased risk for depression.

B. Dependency and Substance Use Disorders Dozens of studies have examined the possibility that dependent persons might be at elevated risk for substance use disorders. The results of these investigations have been decidedly mixed. For example, although studies confirm that dependent persons are at increased risk for tobacco addiction, numerous investigations have failed to obtain the hypothesized relationship between dependency and risk for alcoholism. In fact, longitudinal studies of the dependency-alcoholism link indicate that the onset of alcoholism is followed by increases in dependent thoughts, feelings, and behaviors. However, there is no evidence that dependency actually places individuals at risk for alcohol abuse or dependence. [See SUBSTANCEABUSE.] Similar findings have emerged in studies of dependency and other types of substance use disorders. Researchers have examined possible links between dependency and risk of opiate, cocaine, barbiturate, marijuana, and poly-drug abuse. The results of these studies have been relatively clear-cut: Dependent individuals do not show elevated risk for these substance use disorders, although--consistent with earlier findings regarding the dependency-alcoholism link-research confirms that the onset of an addictive disorder is often associated with elevations in dependent feelings, thoughts, and behaviors.

C. Dependency, Obesity, and Eating Disorders The hypothesis that dependent personality traits would be associated with obesity and other eating disorders (i.e., anorexia and bulimia) can be traced to the

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classical psychoanalytic hypothesis (described earlier) that the etiology of dependency lies in "oral fixation." There have been numerous studies examining the dependency-obesity relationship, and in general these investigations have found only weak relationships between dependency and obesity. Moreover, the dependency-obesity link (when it occurs at all) is somewhat stronger in women than in men. The disappointing resuits obtained in this area have caused researchers to shift their attention from examining the dependencyobesity relationship to examining the relationship between dependency and eating disorders such as anorexia and bulimia. Studies of the relationship between dependency and anorexia and bulimia have produced much stronger and more consistent findings than did studies of the dependency-obesity link. Anorexic and bulimic subjects almost invariably show higher levels of dependency than do matched control subjects who do not have these disorders. The dependency-bulimia link appears to be somewhat stronger than the dependency-anorexia link, although additional studies will be needed to confirm and clarify these preliminary results. Studies in this area also suggest that interpersonal stressors (e.g., the breakup of a romantic relationship) might increase the dependent person's risk for anorexia and bulimia in much the same way as they increase the dependent person's risk for depression. Thus, a diathesis-stress conceptualization of the dependency-eating disorders relationship holds considerable promise for future research in this area. [See ANOREXIA NERVOSAAND BULIMIANERVOSA.]

D. Dependent Personality Disorder Although the vast majority of studies of the dependency-psychopathology relationship have explored possible links between dependency and other forms of psychopathology (e.g., depression), in recent years there has been an increasing emphasis on conceptualizing exaggerated dependency needs as a separate and distinct form of psychological illness. The most prominent framework used to examine the pathological aspects of the dependency is the concept of "dependent personality disorder" as this disorder is described in the Diagnostic and Statistical Manual of Mental Disorders (DSM). The DSM framework argues that individuals who show exaggerated, inflexible dependency needs which cause social or occupational impairment

may be diagnosed as having a dependent personality disorder. Unfortunately, because the diagnostic category of dependent personality disorder was first discussed in 1980, with the publication ofthe third edition of the DSM series, there has been relatively little research on this disorder. Initial findings regarding the correlates and consequences of dependent personality disorder can be grouped into three areas and summarized simply. [See PERSONALITYDISORDERS.] First, studies confirm that individuals with dependent personality disorder are at increased risk for a wide range of psychopathologies, including depression, anxiety disorders, eating disorders, and somatization disorders. Individuals diagnosed with dependent personality disorder also show elevated risk for certain other personality disorders (e.g., border-line, avoidant, passive-aggressive). To some extent, findings regarding the links between dependent personality disorder and other forms of psychopathology dovetail with findings regarding the dependencypsychopathology relationship in general: As discussed earlier, studies to date suggest that dependent individuals show increased risk for a wide range of psychopathologies. Second, epidemiological research suggests that the prevalence of dependent personality disorder in community samples is relatively low, with about 5% of community subjects showing clinically significant dependent personality disorder symptoms. As expected, the frequency of dependent personality disorder symptoms and diagnoses in clinical (i.e., psychiatric inpatient or outpatient) samples is somewhat higher, with many studies reporting base rates of this disorder in clinical subjects of about 10-15%. Although dependent personality disorder appears to be somewhat more prevalent in women than in men, the magnitude of the sex difference in dependent personality disorder diagnosis rates is not great. Third, studies confirm that dependent personality disorder symptoms predict some important aspects of psychological treatment. For example, clinicians report elevated rates of help-seeking behaviors (e.g., requests for emergency sessions, requests for feedback and advice) among dependent personality disorder patients relative to nondependent patients. Along slightly different lines, recent research in this area suggests that dependent personality disorder is associated with cooperativeness and compliance with therapeutic regimens. Finally, several studies indicate that patients di-

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agnosed with dependent personality disorder remain in psychological and medical treatment significantly longer than do nondependent patients, presumably because treatment termination involves giving up a relationship with an important caretaking figure, which the dependent person is reluctant to do.

V. DEPENDENCY AND PHYSICAL DISORDERS One of the most interesting and noteworthy findings to emerge from recent studies of the dependent personality has to do with risk for physical disorders. Research indicates that dependent persons are at increased risk for a wide variety of physical illnesses, including infectious diseases, ulcers, heart disease, and cancer. Longitudinal (i.e., prospective) studies and archival (retrospective) studies have produced highly consistent findings in this area. The dependency-disease link has been found in men and women, and in both children and adults. Furthermore, the magnitude of the dependency-disease relationship is quite substantial. In fact, a recent direct comparison of the magnitude of the disease risk associated with dependency and the magnitude of the disease risk associated with other "illness-related" personality variables (e.g., hostility, compulsiveness, introversion) revealed that the magnitude of the relationship between dependency and risk for physical illness is actually larger than the personality-illness risk relationship found for all other illness-related personality variables. Clearly, dependency must be regarded as an important component of the "disease-prone personality." The mechanism by which dependency increases an individual's risk for physical illness parallels closely the mechanism by which dependency increases an individual's risk for depression. Specifically, it appears that dependency acts as a diathesis which--when coupled with experiences of interpersonal stress or losswincreases an individual's risk for various forms of illness. Preliminary findings in this area further suggest that the dependency-interpersonal stress-illness relationship may be mediated by the immune system: Dependent persons who experience significant interpersonal stressors show measurable deficits in immune function. The diminished immunocompetence associated with dependency and interpersonal stress may represent the common pathway through which

the dependent individual is placed at increased risk for various forms of illness. However, additional studies will be needed to confirm and extend these initial results. Ironically, although the dependent person is at increased risk for physical illness, the personality traits associated with dependency (e.g., cooperativeness, compliance, help-seeking) may actually help the dependent person to respond well to various treatment regimens. Physicians and other healthcare professionals consistently report that dependent individuals are compliant, cooperative patients who adhere particularly well to difficult treatment regimens. In addition, the dependent person is inclined to seek the advice and help of a physician relatively quickly when physical symptoms appear. This "medical help-seeking" tendency is certainly consistent with findings regarding the help-seeking behaviors of dependent persons in social settings. In addition, the help-seeking tendencies of the dependent person clearly represent a positive, adaptive quality of dependency. To the extent that the dependent person seeks help relatively quickly when physical symptoms appear, the likelihood of successful treatment should increase.

VI. THE DEPENDENTPERSONALITY: PAST, PRESENT,AND FUTURE Early research on the dependent personality was concerned primarily with two issues: (1) the exploration of personality traits and behaviors that were hypothesized to be associated with dependency (e.g., passivity, low self-esteem); and (2) the examination of psychoanalytic hypotheses regarding the etiology and dynamics of dependency (i.e., studies of oral fixation and oral dependency). Needless to say, the focus of dependency research has changed considerably during the past several decades. It is worthwhile to review some of these changes in order to get a sense of the directions in which dependency research is likely to head during the coming years. One important shift in this area has occurred with respect to the focus of dependency research. Whereas early studies in this area tended to focus on understanding the antecedents of dependent personality traits, recent studies have instead focused on understanding the consequences of dependency. Many of these recent investigations have examined the inter-

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personal (i.e., social) consequences of dependency, although other studies have assessed the effects of dependent personality traits on risk for physical or psychological illness. A second shift characterizing the study of dependency has involved the research methodologies used in this area. Many early investigations of the dependent personality employed correlational designs. Moreover, many of these early studies took place in field settings (e.g., schools) rather than in the laboratory. In contrast, recent research in this area has tended to use experimental (rather than correlational) designs, and most recent investigations of dependency have taken place in laboratory rather than field settings. A third shift characterizing research in this area has to do with clinicians' and researchers' conceptualization of dependency. For most of this century, dependency has been regarded primarily as a flaw or deficit in functioning. However, in recent years researchers have begun to examine the positive, adaptive qualities of dependency (e.g., compliance with medical regimens, willingness to seek help when symptoms appear). Thus, psychologists have moved from conceptualizing dependency solely in terms of deficit and dysfunction to conceptualizing dependency in a way which recognizes that dependency is associated with both positive and negative qualities. Fourth, the emphasis in dependency research has shifted from a more-or-less exclusive focus on dependency-related behaviors (e.g., help-seeking), to the study of dependency-related emotions and cognitions. Recent studies in this area have suggested that the disparate behaviors of dependent individuals can be understood more completely (and predicted more accurately) if the dependent individual's cognitive style is assessed directly. As researchers have increasingly emphasized the ways in which the dependent person's selfconcept and perceptions of other people mediate his or her behavior, many apparent inconsistencies in previ-

ous studies of dependency-related behaviors have been resolved. Finally, researchers are beginning to examine more closely the interaction of dependent personality traits and aspects of the situation or setting in which behavior is exhibited. Although dependency is often associated with passivity and helplessness, recent studies suggest that situational variables (e.g., the status of the person with whom the dependent individual is interacting, the type of environment in which an interaction occurs) also play a significant role in directing the behavior of the dependent person. In this respect, traditional trait models are beginning to give way to interactionist models of dependency. This shift has already generated some noteworthy findings, and the interactionist perspective on dependency is likely to produce many more important advances in dependency theory and research during the coming years. This article has been reprinted from the Encyclopedia of Human Behavior, Volume 2.

BIBLIOGRAPHY Birtchnell, J. (1988). Defining dependence. Br. J. Med. Psychol. 61, 111-123. Birtchnell, J. (1991 ). The measurement of dependence by questionnaire. J. Pers. Disorders 5,281-295. Blatt, S. J., & Homann, E. (1992). Parent-child interaction in the etiology of dependent and self-critical depression. Clin. Psychol. Rev. 12, 47-91. Bornstein, R. F. (1992). The dependent personality: Developmental, social and clinical perspectives. Psychol. Bull. 112, 3-23. Bornstein, R. F. (1993). "The Dependent Personality." Guilford, New York. Hirschfeld, R. M. A., Shea, M. T., & Weise, R. (1991). Dependent personality disorder: Perspectives for DSM-IV.J. Pers. Disorders 5,135-149. Overholser, J. C. (1992). Interpersonal dependency and social loss. Pers. Individual Diff. 13, 17-23. Zuroff, D. C., Igrega, I., & Mongrain, M. (1990). Dysfunctional attitudes, dependency and self-criticism as predictors of depressive mood states. Cog. Tber. Res. 14, 315-326.

Depression Rick E. Ingram

Christine Scher

San Diego State University

San Diego State University

and University of California, San Diego

I. II. III. IV. V. VI.

Definition of Depression Diagnostic Classification Exploratory Categories of Depressive Disorders Epidemiology Etiological Theories of Depression Protective Factors

lusions (i.e., false beliefs) and hallucinations (i.e., sensory experiences which have no basis in reality). Negative Affectivity The tendency to be chronically distressed and to chronically view oneself negatively. Negative affectivity may be a precursor to both depression and anxiety.

Bipolar Disorder An affective disorder that is characterized by at least one episode of mania. Used to be referred to as manic-depression. Comorbidity The occurrence of more than one disorder at the same time. For example, depression and anxiety are often comorbid, meaning that an individual will experience both of these states simultaneously. Double Depression Refers to dysthymia and major depressive disorder occurring at the same time. Epidemiology Information about the prevalence of disorders in a population. In the case of disorders such as depression, a prevalence rate refers to the number of people who have the disorder during a particular time period (e.g., the percentage of people in given location diagnosed with Major Depressive Disorder within a 1-year period of time). Etiology References to the cause of the disorder. An etiological theory would be a theory about what causes a disorder. Hypomania Episodes characterized by the same symptoms as manic episodes, but that are shorter and are associated with less impairment. Melancholia A very severe form of depression that can be associated with psychotic features such as de-

proposal that there is a specific kind of depression that is caused by negative and dysfunctional thinking patterns. Nosology The diagnosis of disorders into discrete entities with the assumption that each disorder that is nosologically classified will have a different cause, course, prognosis, and treatment response. Unipolar Disorder An affective disorder that is characterized by depression without any evidence for the occurrence of manic episodes.

Negative Cognition Subtype of Depression A

DEPRESSION means different things to different people. For some, depression means feelings of unhappiness that are uncomfortable but do not seem to hinder daily activities. For others, the depression connotes a sickness characterized by severely depressed mood, loss of appetite, lack of concentration, and an inability to function on one's own. Even for professionals the use of the term depression can vary. In 1987, Kendall and colleagues noted that "The professional use of the term depression has several levels of reference: symptom, syndrome, nosologic disorder . . . . Depression itself can be a sympt o m - f o r example, being sad. As a syndrome, depression is a constellation of signs and symptoms that

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cluster together . . . . The syndrome of depression is itself a psychological dysfunction but can also be present, in secondary ways, in other diagnosed disorders. Finally, for depression to be a nosologic category careful diagnostic procedures are required during which other potential diagnostic categories are excluded. The presumption, of course, is that a discrete nosologic entity will ultimately prove to be etiologically distinct from other discrete entities, with associated differences likely in course, prognosis, and treatment response." It is this likely nosologic disorder of depression that we will discuss.

I. DEFINITION OF DEPRESSION A. Symptoms of Depression Any definition of depression must begin with the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). The DSM-IV represents the official diagnostic classification system of the American Psychiatric Association and provides the criteria that are used to diagnosis depression. These criteria consist of the symptoms of depression. In order to make a diagnosis of depression, at least five out of nine possible symptoms must be present. These include (1) depressed mood; (2) diminished pleasure or interest in activities; (3) significant weight loss or weight gain; (4) insomnia or hypersomnia; (5) agitation; (6) fatigue or loss of energy; (7) thoughts of worthlessness or inappropriate guilt; (8) diminished concentration ability; and (9) thoughts of death or suicide. Symptoms of depression may vary according to an individual's age and culture. Children who are depressed, for instance, may express symptoms of irritability rather than sadness. They may also fail to make expected weight gains rather than lose weight. On the other end of the age continuum, older adults are more likely than younger adults to experience symptoms such as loss of appetite, loss of interest, and thoughts of death. Cultural differences also exist in report of depressive symptoms. One study, for example, found that depressed Jewish patients reported more somatic symptoms, and less guilt, than did nonJewish patients. Another study that examined depressive symptomatology in American, Korean, Philippine, and Taiwanese college students found that Taiwanese students reported the lowest numbers of

somatic symptoms and the highest numbers of affective symptoms. The other ethnic groups reporting similar levels of these symptoms. One's age and culture thus seems to affect how depression is expressed.

B. Comorbidity: The Relationship between Depression and Anxiety Comorbidity refers to the occurrence of more than one disorder at the same time. Although researchers and clinicians generally acknowledge depression as a distinct disorder, it does overlap with a variety of other difficulties. Much current research on this overlap has focused on the relationship between anxiety and depression. This is not surprising, given the high rates of comorbidity found in studies of the two disorder types. For example, one study found that 63% of a group of patients with panic disorder also experienced major depression. One possible explanation provided for such overlap lies in the concept of "negative affectivity." In 1984, Watson and Clark described individuals with high levels of negative affectivity as having a tendency "to be distressed and upset and have a negative view of self, whereas those low on the dimension are relatively content and secure and satisfied with themselves." Other characteristics of high negative affectivity include nervousness, tension, worry, anger, scorn, revulsion, guilt, self-dissatisfaction, rejectedness, and sadness. Both anxiety and depression seem to consist of high negative affectivity. There are however, important differences between depression and anxiety. While both depression and anxiety are characterized by high levels of negative affect, only depression is related to lowered levels of positive affect. Thus, depressed individuals tend to display both high negative affect and low positive affect, whereas anxious individuals display high negative affect and may or may not have lowered positive affect--the level of positive affect is unrelated to one's anxiety state. Research on negative affect as a link between anxiety and depression is continuing at a rapid pace. [See ANXIETY.]

II. DIAGNOSTICCLASSIFICATION Earlier we noted the DSM-IV. The DSM-IV is the most widely used classification scheme for psychiatric disorders in North America. According to this

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manual, there are five types of mood disorders that include depression as a significant component. These are (1) Major Depressive Disorder; (2) Dysthymic Disorder; (3) Bipolar I Disorder; (4) Bipolar II Disorder; and (5) Cyclothymic Disorder. Each of these classifications differs in terms of etiology, course, and symptomatology. [See MOOD DISORDERS.]

A. Major Depressive Disorder For a diagnosis of Major Depressive Disorder (MDD), DSM-IV specifies that at least five symptoms must occur for a period of at least 2 weeks. Chief among these symptoms is depressed mood that occurs most of the day, nearly every day for at least 2 weeks, or significantly diminished interest or pleasure in virtually all activities most of the day, nearly every day for the 2-week period. MDD can be further classified according to severity (i.e., mild, moderate, severe without psychotic features, severe with psychotic features), course (e.g., single episode versus recurrent episodes), and presentation (e.g., with catatonic features, with melancholic features). Psychotic features of depression include such experiences as delusions (i.e., false beliefs) and hallucinations (i.e., sensory experiences that have no basis in reality). A delusion, for example, would be a person who believes that she is dead. Catatonic features of depression involve psychomotor disturbances such as excessive movement or stupor. Melancholic features include the inability to experience pleasure even when good things happen and a lack of interest in previously pleasurable activities. No matter what the specific characteristics of a given individual's disturbance, MDD is, by definition, extremely distressing to the sufferer and is associated with significant impairment in important areas of the person's life (e.g., at work, home or school).

B. Dysthymic Disorder Dysthymic Disorder is characterized by a chronic depressed mood that lasts at least 2 years in adults and at least 1 year in children and adolescents. This depressed mood is accompanied by at least two of the following six depressive symptoms: (1) poor appetite or overeating; (2) insomnia or hypersomnia; (3) low energy or fatigue; (4) low self-esteem; (5) poor concentration or difficulty making decisions; and (6) feel-

ings of hopelessness. As fewer depressive symptoms are required to make a diagnosis, Dysthymic Disorder is often considered a milder form of depression than MDD. However, it can be just as upsetting to the sufferer and can cause just as much impairment. In addition, Dysthymic Disorder may occur in combination with episodes of major depression. When Dysthymic Disorder occurs along with major depression, the individual is considered to be suffering from a "double depression." The cooccurrence of MDD and dysthymia is not uncommon.

C. Bipolar I Disorder The hallmark characteristic of Bipolar I Disorder is mania. According to DSM-IV, a manic episode is characterized by elevated, expansive, or irritable mood that is persistent and distinctly different from normal elevated or irritable moods. This period is accompanied by at least three of seven possible symptoms. These symptoms include (1) inflated self-esteem; (2) a decreased need for sleep; (3) unusual talkativeness; (4) the feeling that one's thoughts are racing; (5) increased distractibility; (6) increased activity; (7) involvement in pleasurable but potentially harmful activities (e.g., sexual indiscretions). Bipolar I Disorder is typically recurrent; according to DSM-IV, additional episodes occur in more than 90% of individuals who have had a single manic episode. The manic episodes of those with Bipolar I Disorder are often intermixed with periods of depression. Like those with MDD, people with Bipolar I Disorder may exhibit psychotic, catatonic, and melancholic features as part of either their mania or their depression.

D. Bipolar II Disorder Bipolar II Disorder is characterized by periods of hypomania intermixed with periods of depression. Hypomanic episodes are characterized by the same symptoms as manic episodes. However, hypomanic episodes are shorter (e.g., 4 days in duration) and are associated with less impairment. While manic episodes may include psychotic features, interrupt daily functioning, and require hospitalization, hypomanic episodes typically do not. The depression experienced as part of Bipolar II Disorder, however, can be just as severe as that experienced in MDD and Bipolar I Disorder.

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E. Cyclothymic Disorder

B. Minor Depressive Disorder

Cyclothymic disorder is characterized by hypomanic periods intermixed with depressive periods that are not as severe as those experienced in MDD, Bipolar I Disorder, and Bipolar II Disorder. In Cyclothymia, the periods of mood disturbance may alternate rapidly, with little respite from affective difficulties. For a diagnosis of Cyclothymia these periods of shifting moods must be problematic for at least 2 years in adults and at least i year in children and adolescents. In addition to the five official diagnoses, DSM-IV has denoted four classifications for further study that include depression as a significant component. Such classifications are not yet considered to be disorders and more information is needed on factors such as symptom presentation, etiology, and degree of impairment to sufferers before these might be considered disorders in their own right. Nevertheless, these may represent serious problems and even though they are currently exploratory, we describe them here. They are: (1) Premenstrual Dysphoric Disorder; (2) Minor Depressive Disorder; (3) Recurrent Brief Depressive Disorder; and (4) Mixed Anxiety-Depressive Disorder.

Minor Depressive Disorder is characterized by fewer depressive symptoms than are seen in MDD. The level of impairment is also less than that associated with MDD. To meet the proposed criteria for Minor Depressive Disorder, a person must demonstrate either a depressed mood or loss of interest and two additional symptoms of a Major Depressive Episode. If this classification were included in future DSM editions as a disorder, it would constitute a residual category to be used only after the other mood disorders have been ruled out.

III. EXPLORATORYCATEGORIES OF DEPRESSIVEDISORDERS A. Premenstrual Dysphoric Disorder Premenstrual Dysphoric Disorder is characterized by several hallmark symptoms of depression (e.g., decreased interest in usual activities, depressed mood, difficulty sleeping or sleeping too much) in addition to symptoms such as affective lability, feelings of being overwhelmed or out of control, and food cravings. In order to meet the criteria that have been proposed for this diagnosis, such symptoms must have occurred during the late luteal phase of most of a woman's menstrual cycles in the past year. As a number of authors have pointed out, such a classification has potentially serious social, political, and legal ramifications for women. For example, some have argued that if this classification is adopted as an orificial diagnosis then women might be stigmatized as more unstable than or inferior to men. Arguments such as this keep the classification of Premenstrual Dysphoric Disorder a topic of considerable debate. [See PREMVNSTRt3AL SYNDROME (PMS).]

C. Recurrent Brief Depressive Disorder The principle difference between Recurrent Brief Depressive Disorder and MDD is one of duration. Recurrent Brief Depressive Disorder is characterized by periods of depression that meet all of the criteria for a Major Depressive Episode except for the duration requirement. While in major depressive episodes, symptoms must last at least 2 weeks, in recurrent brief depressive episodes, symptoms must last at least 2 but less than 14 days. In addition, these brief episodes must occur at least once a month for 12 months to meet criteria for the classification of Recurrent Brief Depressive Disorder. Recurrent Brief Depressive Disorder is quite similar to MDD in its age of onset and family incidence rates, thus raising questions as to whether this should be considered a distinct disorder.

D. Mixed Anxiety-Depressive Disorder The impetus behind a mixed anxious-depressed category lies in the finding that there are many people suffering from symptoms of anxiety and depression who do not meet criteria for any DSM anxiety or mood disorder, but who are nonetheless significantly impaired by their difficulties. The classification of Mixed Anxiety-Depressive Disorder is characterized by a dysphoric mood for at least 1 month in addition to at least four additional symptoms that primarily reflect anxiety (e.g., mind going blank, worry, hypervigilance). The primary argument in favor of adopting this proposed disorder is that it would cover the large number of people who have significant impairment linked to depression and anxiety but who do not fall into any currently existing diagnostic category. The primary

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argument against this classification is that people suffering from both depression and anxiety could in fact be categorized into already existing disorders with the use of more precise assessment methods.

IV. EPIDEMIOLOGY Epidemiology refers to information about the incidence and prevalence of disorders in a population. A prevalence rate refers to the number of people who have a given disorder during a particular time period (e.g., the percentage of people in given location diagnosed with MDD within a 1-year period of time). An incidence rate refers to the number of new cases of a disorder which occur during a given time period (e.g., the number of people diagnosed with Dysthymic Disorder during April 1996). Because the distribution of a disorder can be examined to determine whether it correlates with other factors, epidemiological information can be important for understanding some of the possible causes and correlates of depression.

A. Prevalence I. National Prevalence Two recent large-scale surveys of psychopathology in the United States have provided differing prevalence data on depression. Using diagnostic criteria from the revised 3rd Edition of the DSM (DSM-III-R), the Epidemiologic Catchment Area (ECA) study examined the rates of depression in five sites: New Haven, Baltimore, St. Louis, Los Angeles, and Durham. The ECA study found the lifetime prevalence of major depression (i.e., the number of people experiencing major depression during any point in life) to be 4.9% and the lifetime prevalence of dysthymia to be 3.2%. Alternatively, the National Comorbidity Survey (NCS) reported much higher prevalence rates: 14.9% for lifetime major depression and 6.4% for dysthymia. The discrepancies between these two studies may be accounted for by the different assessment instruments used, slightly different diagnostic criteria employed, and different age ranges studied (i.e., the ECA sample was 18 years of age or older, whereas the NCS sample ranged in age from 15 to 54 years). According to the ECA study, prevalence rates for bipolar disorders were much lower; lifetime prevalence of these disorders was

.8% for Bipolar I and .5% for Bipolar II. The NCS lifetime prevalence for manic episode was somewhat higher: 1.6 %. Even though these epidemiological studies reported somewhat discrepant rates, they are in agreement that mood disorders are relatively common in the United States.

2. International Prevalence A number of studies have examined the community prevalence of major depression in countries besides the United States. International lifetime prevalence rates vary widely, from a low of 3.3% in Seoul to a high of 15.1% among New Zealand residents aged 25 to 46. While such differences may indeed reflect true international differences in the occurrence of depression, other factors such as cultural differences in the sensitivity of the instruments used to assess disorder and different sample ages may also account for this range. In prevalence studies focusing on bipolar illness, ranges from .07% in Sweden to 7% in Ireland have been reported. Most studies, however, place prevalence at about 1% for bipolar illnesses, consistent with data from the ECA and NCS studies.

B. Age Differences The ECA study also reported incidence rates of depression for various age groups. For men, major depression was highest among those aged 18 to 29. A large decline in incidence was noted for men aged 45 and older. For women, the incidence of major depression was highest in the group aged 30 to 44 and did not decline until age 65.

C. Sex and Ethnic Differences According to the ECA study, lifetime prevalence rates of major depression, dysthymia, and all mood disorders are approximately twice as high for women as for men. Women's lifetime rates were 7.0%, 4.1%, and 10.2%, respectively, while rates for men were 2.6%, 2.2 %, and 5.2 %, respectively. These differences occur across a variety of ethnic groups (e.g., African American, Hispanic, Caucasian) even when differences in education, income, and occupations are controlled. Sex differences are also found in countries besides the United States. While sex differences in depression are among the most stable of findings across studies, no

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sex differences in the rates of bipolar disorder are reliably found. Although sex difference in the incidence of depression occur across different ethnic groups, there are some differences among these groups overall. For instance, the ECA study found higher rates of Major Depression and Dysthymia among Caucasians and Hispanics than among African Americans. However, few difference in the rates of bipolar disorders among the three groups were found.

D. Environmental Correlates The ECA study also examined a number of environmental correlates of depression and bipolar disorders. This study found that people who were separated or divorced had higher 1-year prevalence rates of major depression (6.3%) than those who were never married (2.8%), currently married (2.1%), or widowed (2.1%). This was also true of those with bipolar disorders, although the rates for those separated or divorced versus never married were nearly identical (1.7% versus 1.6%). The 1-year prevalence rate of major depression was also higher among the unemployed than the employed (3.4% versus 2.2%), but the rate was nearly identical for those with bipolar disorders (1.1% versus 1.0%). In addition, the ECA study found higher rates of major depression among white-collar workers and those with at least 12 years of education, but lower rates of depression among those with annual incomes of $15,000 or more. Consistent with the major depression findings, bipolar disorders were also less prevalent among those with annual incomes of $15,000 or more. Bipolar disorders were also found to be the most prevalent among none-white-collar workers with less than 12 years of education. Overall, these socioeconomic status differences were quite small.

V. ETIOLOGICALTHEORIES OF DEPRESSION A variety of different psychological theories of the causes of depression have been proposed. These can be grouped in psychoanalytic, interpersonal, and cognitive.

A. Psychological Theories

I. Psychoanalytic Approaches The first psychoanalytic writers to theorize about the etiology of depression were Sigmund Freud and his student, Karl Abraham. As would be expected, there are a number of similarities in the theories proposed by Freud and Abraham. First, both Freud and Abraham believed that some people are predisposed to experience depression. For Abraham, this predisposition consisted of anatomical anomalies that allowed a person to experience a great deal of oral eroticism. For Freud, this predisposition consisted of narcissistic object choices (e.g., object choices which are so similar to the self that love of the object is truly love of self). Second, both believed that a predisposition to experience depression was not, in and of itself, enough to cause depression. In order to experience a depression, a predisposed individual must also experience the loss of a loved object (e.g., through death or rejection). Despite these basic similarities, the two theorists diverge somewhat on how depression occurs once a loss has been experienced. For Abraham, the loss of a loved object in a person predisposed to depression triggers a regression to the oral stage of psychosexual development. Such a regression is meant to achieve three purposes: (1) to increase pleasure; (2) to hold on to the object through oral incorporation; and (3) to discharge one's aggressive impulses on to the object. Such a regression manifests itself most saliently in the depressive symptoms of eating too much or too little. For Freud, the loss of a loved object possesses different implications. Since the lost object was a narcissistic choice and thus represented the self, loss of the object means loss of the self. This loss of self triggers feelings of anger and depression. The energy associated with these negative feelings is withdrawn from the lost object and brought inward, in a process called introjection. Thus, depression as conceptualized by Freud is often summarized as "anger turned inward." For Freud, the difference between sadness and "true" depression was the difference between "this is awful" and "I am awful." Freud further extended his theory to account for the mania characteristic of bipolar depressive disorders. He hypothesized that, once the feelings of anger and depression over loss of the object are resolved, the energy associated with these negative feelings is freed for other purposes. In a person with bipolar disorder, this freed energy is used to zealousy search for

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2. Interpersonal Approaches

All of these lines of research have found some support; interpersonal research highlights the fact that depression is caused by a multitude of factors in interplay with one another. Much of the research converges on the theoretical idea that depression is maintained by a vicious cycle that is caused by disruptions in interpersonal interactions. For instance, many depressed individuals quite understandably seek out social support from others. If this support does not alleviate the negative feelings, further support is sought. This intensified support seeking, however, has the paradoxical effect of pushing away those who have been supportive. That is, as individuals begin to feel that their support capacity has been exhausted they pull back from the depressed person, leading to an even further intensification of social support seeking, and the further distancing of potentially supportive people. Interpersonal factors in the etiology of bipolar depressive disorders have not received as much research attention as such factors in unipolar depressive disorders. Nonetheless, persons with both types of depressive disorders seem to have difficulties in retaining social support. Indeed, in one recent study, people with bipolar disorder perceived their social supports as less available to them and as less adequate in the amount of support received than people in a community sample. Furthermore, perceptions of social support availability seemed to decrease as the duration of illness increased. Thus, it seems likely that social support plays a role in bipolar as well as unipolar depressive disorders.

Interpersonal approaches to the etiology and maintenance of depression focus on the interplay between a depressed person and his or her relations with others. Empirical research in this area has taken several directions. For example, some researchers focus on the role of social skills in depression, asking such questions as whether depressed people have poor social skills and whether the lack of such skills results in decreased reinforcement from others and consequent depression. Other research has evaluated the types of communications depressed people emit (e.g., sadness, hopelessness) and the effects these communications have on others. If others find the communications of depressed persons aversive, they will likely avoid such persons, which may then exacerbate depressive symptoms such as isolation and loneliness. Still others address the interplay between stress, social support, and depression.

Currently, cognitive approaches are among the most widely studied theories in the etiology of depression. One of the most influential of these theories was proposed by Aaron Beck in 1967. Beck argued that all individuals possess cognitive structures called schemas that guide the ways information in the environment is attended to and interpreted. Such schemas are determined from childhood by our interactions with the external world. For example, a child who is constantly criticized may begin to believe she is worthless. She might then begin to interpret every failure experience as further evidence of her worthlessness. If this negative processing of information is not changed, it will become an enduring part of her cognitive organization, that is, a schema. When this schema is acti-

new objects, thus accounting for the symptoms of mania. More recent psychoanalytic theorists have focused on the superego's role in depression. Some theorists, for example, have suggested that depression is distinguished from other states such as shame, apathy, or resentment by the presence of guilt. As guilt results only from an intrapsychic conflict of the superego, the superego is necessarily implicated in depression. One result of these differences in etiological focus has been the proposition of two forms of depression: anaclitic and introjective. Anaclitic depression is characterized by feelings of helplessness, inferiority, and being unloved. Anaclitic depression is proposed to be associated with the earlier stages of development and is most closely associated with the theorizing of Abraham and Freud. Alternatively, introjective depression focuses on feelings of unworthiness and failure to measure up to expectations and standards. It is associated with later stages of development, and more closely aligned with the works of later psychoanalytic theorists. Although much of psychoanalytic theory has been criticized on grounds that it has not been empirically tested, the distinction between anaclitic and introjectire depressions has been empirically examined and found to be valid. Psychoanalytic theorists have accounted for the development of bipolar disorders as well. Most notable amongst these theorists is Melanie Klein, who expanded upon the work of Freud.

3. Cognitive Approaches

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vated (e.g., by a poor grade on a test or any other failure experience), it will predispose her to depressive feelings (e.g., I'm no good). Beck stated that, as a result of this faulty information processing, depressed persons demonstrate a cognitive triad of negative thoughts about themselves, the world, and the future. He further extended his argument to include the manic phases of bipolar depressive disorders. Beck stated that such phases are characterized by a manic triad of irrationally positive thoughts about oneself, the world, and the future. Like the depressive triad in unipolar depressive disorders, the manic triad in bipolar depressive disorders was hypothesized to lead to the symptoms of mania, such as inflated selfesteem and extremely elevated mood. There is widespread agreement that depression can be caused by different factors. Some theorists have argued that dysfunctional cognitions cause only a subset of depressions. Termed the "negative cognition" subtype, this type of depression is brought about by either the kinds of schemas discussed by Aaron Beck or by dysfunctional attributional patterns that lead depressed people to take responsibility for the occurrence of negative events, and to avoid taking responsibility for positive events. This dysfunctional attributional pattern can lead to a sense of hopelessness that results in a "hopelessness depression," a component of negative cognition depression.

B. Biological Theories Although there are a variety of biologically based theories of depression, they can be broken down into two general approaches: genetic and neurotransmitter.

I. Genetic Approaches Genetic approaches suggest that depression is the result of inheriting genes that predispose to occurrence of depression. Three types of studies that are used to investigate genetic inheritance of depression illustrate this approach. These studies consist of family studies, twin studies, and adoption studies. In a typical family study, families with a depressed member are interviewed to determine how many other family members have or had an affective disorder. In twin studies, the concordance rate of affective disorder between monozygotic and dizygotic twin pairs is compared. Because monozygotic twins have identical genes, if genetic theories are correct then concordance rates of depression should be higher than for dizygotic twins (who

have similar but not identical genes). In adoption studies, two strategies are most often used. In the first, the rate of depressive disorder in the biological parents of adopted persons with and without affective disorders is compared. In the second, the rate of depressive disorders is compared between adopted children with and without affectively disordered biological parents. Adoption studies have an advantage over family and twin studies, as the effects of environment on affective disorder are reduced in this design. However, adoption studies constitute the least-used approach to investigating genetic factors in depression; the difficulty of obtaining complete records on adoptees and their biological parents makes this design quite prohibitive. Despite design differences, all three genetic approaches to the etiology of depression have yielded similar results: depression is heritable to at least some degree. A recent review of the research literature, for example, found rates of affective disorders among first-degree relatives of unipolar-disordered individuals ranging from 11.8% to 32.2%. Rates of affective disorders among first-degree relatives of bipolardisordered individuals ranged from 10.6% to 33.1%. Rates of affective disorder among first-degree relatives of normal individuals ranged from 4.8% to 6.3. In twin studies of unipolar and bipolar depression, concordance rates ranged from .04 to 1.0 for monozygotic twins, and from 0.0 to .43 to dizygotic twins, with the majority of studies reviewed reporting no concordance for dizygotic twins. The results of genetic investigations clearly suggest that there is a genetic component to depression, although the exact nature and functioning of this component is thus far still unknown.

2. Neurotransmitter Approaches Research on brain chemistry as an etiological factor in unipolar depression has focused on two monoamine neurotransmitters: norepinephrine (NE) and serotonin (5-HT). Initially, researchers believed that depression was due to a lack of NE in the brain, and later, to a lack of both NE and 5-HT. However, several difficulties with these hypotheses arose: (1) While the effects of antidepressants on monoamine levels start within hours of taking the medication, decreased depression levels do not become apparent until weeks later. (2) Some drugs that do not affect monoamine levels alleviate depression. (3) Some drugs that increase monoamine levels do not alleviate depression.

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Thus, researchers have directed their efforts to investigating more complicated relations between these neurotransmitters and depression. Recent efforts have included the study of receptor site hyposensitivity, relationships between NE and 5-HT, and relationships between. 5-HT and the neurotransmitter dopamine (DA). Research on brain chemistry as in etiological factor in bipolar depression has followed much the same course as such research on unipolar depression. Initially, researchers believed that the mania characteristic of bipolar disorders was due to excesses of the neurotransmitters NE and 5-HT, exactly opposite the belief for depression. However, difficulties arose with this hypothesis, including findings that (1) lithium, the medical treatment of choice for bipolar disorder which seems to affect both NE and 5-HT, was effective at controlling both depression and mania, and (2) both depression and mania may be characterized by lower levels of 5-HT. Thus, as with unipolar depression, researchers of bipolar depression have begun investigating more complicated relationships between bipolar depression and neurotransmitters. Similar to the recent efforts concerning unipolar depression, researchers have investigated interactions between 5-HT and DA, interactions between NE and DA, and receptor site hypersensitivity. These types of investigations represent promising areas of research in elucidating the multifaceted etiology of depression. Certainly, biology and psychology are implicated in the causes of depression, both unipolar and bipolar forms.

VI. PROTECTIVE FACTORS Given the potentially devastating effects of depression, many researchers have devoted their efforts to studying factors that decrease the likelihood of becoming depressed or decrease the amount of time spent in depressive episodes. Among the most widely studied of such protective factors are social support and coping styles.

A. Social Support There are numerous facets to the concept of social support. For example, social support can be conceived as the number of persons one can rely on for support. Social support can also be conceived as the amount of support received, regardless of the number of persons

one receives support from. In addition, socially supportive relationships can be conceptualized on a continuum of quality from very poor to very good. Examination of all these facets has proven important in understanding relationships between depression and social support. Overall, people in contact with numerous socially supportive persons are less likely to have mental health difficulties, including depression. In addition, those who perceive a great deal of support from others are less likely to be negatively affected by stressors that might lead to depression. For people who have become depressed, having a confidant such as a spouse or best friend and a supportive family is related to greater success in treatment. The quality of such relationships is also important to treatment. In one study, for example, depressed persons with good-quality confidant relationships needed shorter periods of treatment than those with poor-quality confidant relationships. The effects of social support for people with bipolar depressive disorders have not been as well studied as the effects for people with unipolar depressive disorders. Nonetheless, research suggests that social support is indeed beneficial for people with bipolar disorders. In one study, for example, a great deal of available social support was related to fewer psychological symptoms, better social adjustment, and better overall functioning.

B. Coping Styles Ways of coping with stressors can be roughly divided into two categories: approach strategies and avoidance strategies. Approach strategies are characterized by identifying the problematic situation, devising reasonable solutions to it, an implementing those solutions. Avoidance strategies include trying not to think about the problem, wishing the problem did not exist, and fantasizing about life without the problem. Overall, approach strategies seem to help people cope with stressors that might otherwise lead to depression. In addition, use of approach strategies is associated with better treatment outcome for those who become depressed. Conversely, people who use avoidance strategies to cope with stress seem more likely to become depressed and to have poorer treatment outcomes. As with the effects of social support, research on coping styles among people with bipolar depressive disorders is scarce. Nonetheless, one recent study that

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examined differences in coping between high- and low-functioning people with bipolar disorders suggested that avoidant coping styles are associated with poorer functioning. Thus, relationships between coping styles and bipolar depressive disorders and coping and unipolar depressive disorders may be similar.

BIBLIOGRAPHY Beck, A. T. (1967). Depression: Causes and treatment. Philadelphia: University of Pennsylvania Press.

Beckham, E. E., & Leber W. R. (1995). (Eds.). Handbook of depression (2nd ed. ). New York: Guilford Press. Cicchetti, D., & Toth, S. L. (1992). (Eds.). Developmental perspectives on depression. Rochester, NY: University of Rochester Press. Craig, K. D., & Dobson, K. S. (1995). (Eds.). Anxiety and depression in children and adults. Thousand Oaks, CA: Sage. Kendall, P. C., Hollon, S. D., Beck, A. T., Hammen, C. L., & Ingram, R. E. (1987). Issues and recommendations regarding use of the Beck Depression Inventory. Cognitive Therapy and Research, 11,289-299. Ingrain, R. E., Miranda, J., & Segal, Z. V. (in press). Cognitive vulnerability to depression. New York: Guilford Press. Robins, L. N., & Regier, D. A. (1991). (Eds.). Psychiatric disorders in America. New York: The Free Press.

Dissociative Disorders Richard P. Kluft Temple University School of Medicine and Harvard Medical School

I. II. III. IV. V. VI. VII. VIII. IX. X.

Switching Changing from one personality state to another. Trance The capacity to sustain an attentive, receptive, and intensely focused concentration with diminished peripheral awareness. The more peripheral awareness fades in relation to focused attention, the deeper the trance.

Dissociation Dissociation as a Response to Trauma The Spectrum of Dissociative Symptomatology Depersonalization Disorder DissociativeAmnesia Dissociative Fugue Dissociative Identity Disorder Dissociative Disorder Not Otherwise Specified Dissociative Trance Disorder Dissociation and Memory

Dissociation and the DISSOCIATIVE DISORDERS constitute one of the most compelling and controversial fields of study in the mental health sciences. Dissociation is a failure or a disruption in the usually integrative functions of consciousness, memory, identity, or perception of the environment. Such symptoms and experiences challenge, indeed threaten, one's customary sense of one's self and one's experience. Dissociation includes both phenomena within the normal range, and phenomena that are distinctly psychopathological. Some dissociative manifestations have a relatively universal distribution, while others are more or less culture bound. Recent findings indicate that abnormal dissociative phenomena are most often associated with trauma, overwhelming stress, and/or intolerable intrapsychic conflict. Several distinct dissociative disorders have been identified as discrete conditions, while others are grouped in an overflow category called dissociative disorder not otherwise specified, or are under consideration for adoption, such as dissociative trance disorder. The distinct conditions are dissociative amnesia, dissociative fugue, depersonalization disorder, and dissociative identity disorder (formerly known as multiple personality dis-

Amnesia An inability to recall important personal information that is too extensive to be explained by ordinary forgetfulness. Depersonalization A feeling of detachment or estrangement from one's self, such as a feeling of detachment from one's self, the sensation one is an outside observer of one's body, or a feeling that one is like an automaton or is living in a dream. Derealization An alteration in the perception of one's surroundings so that a sense of the reality of the external world is lost. Dissociation A disruption in the usually integrative functions of consciousness, memory, identity, or perception of the environment. Fugue Sudden unexpected travel away from home or one's customary place of work, with inability to recall one's past. Identity, Personality State, Alter (synonyms) An entity with a relatively persistent and well-founded sense of self and a relatively characteristic and consistent pattern of behavior and feelings to given stimuli.

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order). Each will be explored in view of contemporary advances. Controversial areas will be dealt with as they arise, with one exception. The complex relationship between dissociation and memory will receive separate discussion.

I. DISSOCIATION The concept of dissociation appears in the mental health literature as early as the work of Benjamin Rush, but did not rise to prominence until the work of Pierre Janet, who first used the term ddsagregation. Broadly defined, dissociation indicates that two or more mental processes or contents are not associated or integrated in the normally expected manner. Disruptions of the integrative functions of consciousness, memory, identity, or perception of the environment fall under the rubric of dissociation in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Disruptions of motor behavior are included among the dissociative disorders in some other classification systems. Dissociation has proven an elusive concept to define, and has had different referents in different contexts. Dissociation has been understood as constituting a spectrum of phenomena. Within a normal spectrum are experiences of absorption, focused concentration, meditation, hypnosis, and some mild depersonalization. Within the pathological spectrum are disruptions of memory, identity, consciousness, and perception of the environment and self. Scholars disagree as to whether the normal and abnormal dissociative phenomena are on a single continuum, or whether there are two disjunctive continua. Dissociation has been used as an explanatory or descriptive concept for a wide array of phenomena, including hypnosis, automatic behaviors, a mechanism of defense, distinguishing certain forms of memory, describing some forms of psychopathology, a number of cognitive phenomena, and to account for many findings in psychology laboratories. In an attempt to move toward clarification, Cardena described several domains of dissociation. In the first, dissociation as nonconscious or nonintegrated mental modules or systems, he includes dissociation as (1) the absence of conscious awareness of impinging stimuli or ongoing behaviors; (2) the coexistence of separate men-

tal systems or identities that should be integrated in the person's consciousness, memory, or identity; and (3) ongoing behaviors or perceptions that are inconsistent with a person's introspective verbal report. It is important to appreciate that dissociation has as well both cognitive and often psychophysiologic aspects. Dissociation allows the segregation of some sets of data from other sets of data in a relatively rule-bound way. Numerous studies of dissociative identity disorder patients demonstrate that both the different identities and the switch process by which one is replaced by another have neuropsychophysiologic correlates. Dissociation appears to have a series of functions. It automatizes behavior so that some actions and thought processes can occur without direct conscious attention, and hence with increased efficiency. It may permit a form of resolution for irreconcilable conflicts by keeping dissonant issues in different areas or levels of consciousness. Dissociation may allow an escape from reality, giving the illusion of mastery or escape from intolerable circumstances. Dissociation can isolate catastrophic experiences until an individual is better able to integrate them into mainstream consciousness. Dissociation can facilitate cathartic discharge, by putting aside the prohibition against the expression of certain feelings under most circumstances in some cultures.

II. DISSOCIATION AS A RESPONSE TO TRAUMA Although dissociation may occur spontaneously or in response to deliberate efforts, such as meditation, pursuit of mystical experiences, mediumistic trance, culture-bound rituals and practices, and autohypnosis, and may result from profound intrapsychic conflict, in the modern literature there has been a deep interest in the connection of dissociation and trauma. Reviews of the literature demonstrate that dissociative phenomena have long been associated with the experience of trauma. For example, rape victims and persons experiencing beatings not infrequently see themselves from above, and may even feel sorry for the unfortunate victim of the assault. Combat soldiers not infrequently have considerable amnesia for their actual experience of combat. Survivors of childhood abuse may block out their recollection in whole or in

Dissociative Disorders .

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part. Victims of natural disasters commonly experience a variety of dissociative as well as posttraumatic symptoms. [See POSTTRAUMATIC STRESS.] Modern studies have confirmed and expanded upon clinical and anecdotal informations. In a series of studies, David Spiegel and several colleagues studied normal populations exposed to natural disasters such as an earthquake and a firestorm, and the reactions of witnesses to executions. They discovered that dissociative as well as anxiety symptoms are part of the trauma response for many individuals, and that the proximity of exposure to and degree of involvement with the trauma are determinants of the intensity of symptomatology. Dissociative responses to trauma are predictors for the development of posttraumatic stress disorder, and high hypnotizability, a construct different from but in some ways related to dissociation, is associated with chronicity of severe posttraumatic symptomatology. Spiegel observed that dissociative defenses, which allow the compartmentalization of perceptions and memories, both help victims separate themselves from the full impact of trauma while it is occurring, and may delay the necessary working through and putting into perspective of these experiences once they have occurred. They may help trauma victims maintain a sense of control while they are feeling helpless, but then they become a mechanism by which the individual feels psychologically helpless once physical control is reestablished. The short-term assistance afforded by dissociation may, if its mechanism persists in other circumstances, become a major disadvantage.

III. THE SPECTRUM OF DISSOCIATIVE SYMPTOMATOLOGY Many efforts have been made to describe the wide range of dissociative manifestations. Many are flawed by a failure to distinguish between the phenomenology of dissociation and those of hypnosis. Here only manifestations associated with dissociative psychopathology will be included. Detachment and/or withdrawal from one's present circumstances can occur when an individual either blocks out awareness of his or her environment, or narrows his or her focus very dramatically to focus on a particular stimulus to the exclusion of the rest of

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the environment. This is a common symptom in overwhelmed individuals, and constitutes the essential feature of some forms of dissociative trance disorder. Steinberg has offered a model of dissociation that includes five symptom areas: amnesia, depersonalization, derealization, identity confusion, and identity alteration. Amnesia is the forgetting of personal information that is more extensive than can be explained by ordinary forgetfulness. Typically it takes the form of either (1) the subjective awareness that one has lost or is missing time; (2) appreciation that there are periods of one's life for which one cannot account (e.g., "my memory begins when I was in high school"); or (3) a realization upon reflection or in response to questioning that one cannot recall particular aspects or time periods of one's life. Amnesia is a core phenomenon of all forms of dissociative disorder except some forms of dissociative disorder not otherwise specified and depersonalization disorder. Many consider it the quintessential dissociative symptom. Depersonalization occurs when one's experience and perception of one's self is disrupted and/or distorted. Those who suffer depersonalization may feel detached from their selves, experience their selves as strange or unreal, feel detached from parts of their bodies and/or their emotions, or may feel like automatons or robots. They may see themselves as if they were watching themselves at a distance, or in a movie. As Steinberg notes, common mild depersonalization occurs as a symptom, is an isolated event or one of a few episodes, and is brief, often seconds to minutes. It often is precipitated by fatigue, stress, sensory deprivation, intoxication, illness, or hypnogogic or hypnopompic states. Transient depersonalization is an isolated symptom occurring in a single episode in response to life-threatening danger or severe psychological trauma. It may last from minutes to weeks. Abnormal depersonalization occurs in a constellation of other psychological symptoms, is persistent or recurrent, and may be chronic and persistent, lasting for weeks to years. It may be precipitated by stress or a traumatic memory, but it persists and recurs in the absence of stressors. While depersonalization occurs in many dissociative disorders, abnormal depersonalization is the essence of depersonalization disorder. Derealization involves a sense of estrangement or detachment from the environment rather than the self. The environment may be experienced as unreal; fa-

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miliar locations and others may seem strange and/or unfamiliar. It usually occurs in connection with other dissociative phenomenology. When it occurs in isolation, it is a form of dissociative disorder not otherwise specified. Identity confusion is a subjective feeling of uncertainty, puzzlement, or conflict about one's own identity. It often is associated with considerable inner turmoil about struggles or even battles over one's identity. It usually occurs with other dissociative symptoms, and is not the core of any particular dissociative disorder. Identity alteration involves a person's shift in role or identity that is observable by others through changes in a person's observable behavior. Some manifestations involve the use of different names, possession of knowledge or skills for which one cannot account, and the discovery of strange or unfamiliar personal items in one's possession. Identity alteration is often accompanied by episodes of amnesia such that one has no recollection of the out-of-character behavior. It is quite developed in dissociative identity disorder. Identity alteration is an essential aspect of those forms of dissociative trance disorder in which another identity is enacted, and is the cardinal feature of dissociative identity disorder. It is found in many cases of dissociative fugue, and in many forms of dissociative disorder not otherwise specified that closely resemble dissociative identity disorder.

IV. DEPERSONALIZATIONDISORDER Although depersonalization is an extremely common experience and psychiatric symptom, it usually is encountered in connection with other disorders, such as anxiety disorders in phobic patients with panic attacks and agoraphobia, depression, schizophrenia, borderline personality disorder, substance abuse (and withdrawal), seizure disorders (especially partial complex seizures), organic illness, and medication side effects. Depersonalization is experienced transiently by many persons in connection with severe stress or danger. Depersonalization Disorder itself is rarely diagnosed, and has been little studied. Its diagnostic criteria are given in Table I. Depersonalization disorder is characterized by persistent or recurrent episodes of feeling of detachment

Table I

Diagnostic Criteria for Depersonalization Disorder

A.

Persistent or recurrent experiences of feeling detached from, and as if one is an outside observer of, one's mental processes or body (e.g., feeling like one is in a dream).

B.

During the depersonalization experience, reality testing remains intact.

C.

The depersonalization causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.

D.

The depersonalization experience does not occur exclusively during the course of another mental disorder, such as Schizophrenia, Panic Disorder, Acute Stress Disorder, or another Dissociative Disorder, and is not due to the direct physiological effects of a substance(e.g., a drug of abuse, a medication) or a general medical condition (e.g., temporal lobe epilepsy).

or estrangement from one's self. The afflicted person may feel detached from his/her body or mental processes, and may feel as if he/she were an external observer of his/her own life and actions, as if he or she were an automaton, or watching a movie of him/herself. Often his/her emotions are numb, with the exception of anxiety and depression, often related to the depersonalization experiences. He/she may feel as if in a fog or trance, have difficulty recognizing him/herself in the mirror, may feel that behavior and emotions are not under his/her control, and may experience body parts as detached or distorted in size or unreal. Others may seem unfamiliar or unreal. Derealization, the sense that the external world is strange or unreal, may be present. Because these experiences often are difficult to describe and understand, the sufferer may be unable or unwilling to communicate them, fearing that they mean that he/she is crazy. The course of depersonalization disorder is often chronic, marked by remissions and exacerbations. Exacerbations are often associated with stress, subjective, or in response to external events.

A. Epidemiology Although up to 50 to 80% of the population has experienced depersonalization, and this symptom is found in from 40 to 80% of psychiatric inpatients, depersonalization disorder remains uncommonly diagnosed, and of unknown incidence and prevalence. Many series indicate a 2 - 4 : 1 female to male ratio, but these studies antedate modern diagnostic criteria.

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Childhood cases have been reported, but most series indicate a mean age at diagnosis of 24 to 27 years. Most cases are diagnosed between ages 15 and 30. The late onset of depersonalization disorder is rare. Neither familial nor cultural factors have been identified.

B. Etiology The cause of depersonalization disorder, like that of depersonalization, remains obscure, with most authorities acknowledging several theories, and some speculating that all models must ultimately affect the temporal lobe and its cerebral connections. Steinberg noted five models: (1) physiologic or anatomical disturbances, as in temporal lobe disturbances, metabolic and toxic states; (2) a "preformed functional response of the brain" adaptive to overwhelming trauma, as in psychiatric disorders and stress responses; (3) defense against painful and conflictual affects; (4) splits between the observing and experiencing ego, so that the patient becomes a detached observer of the self; and (5) when a child is reared in an environment that fails to acknowledge some aspect of the child, who experiences that aspect as not quite real.

C. Diagnosis The differential diagnosis of depersonalization is complex, and includes a range of medical and psychological disorders. A complete review of records is indicated, as well as a physical examination, a mental status, and perhaps neurological consultation. Screening blood chemistries should include a complete blood count, electrolytes, thyroid studies, chemistries (including liver studies, blood sugar, etc.), and possibly toxicology studies. Electroencephalograms (with nasopharyngeal leads if temporal lobe epilepsy is suspected) and possibly brain imaging studies are indicated. The baseline mental status examination should be performed, but it is not a good screen for dissociative phenomena. An expanded dissociative mental status may be used. Depersonalization phenomena are inquired after in the Dissociative Experiences Scale (DES), but examination of individual items may be more revealing than the overall score, because de-

personalization is only one of the dissociative phenomena it explores. Steinberg's Revised Structured Clinical Interview for the Diagnosis of DSM-IV Dissociative Disorders (SCID-D) is an excellent structured interview for dissociative disorders, and has 95 % interrater reliability (weighted kappa of .88) for depersonalization items. In making the diagnosis it should be clear that the depersonalization is in fact severe and symptomatic rather than transient, and is not better explained by some more common mental disorder.

D. Treatment The treatment of depersonalization per se is the treatment of the underlying disorder. Depersonalization Disorder often proves difficult to treat. Although many therapies have been employed to treat one or more patients with this condition, the literature remains anecdotal, with no approach having achieved wide success. This probably speaks to the diversity of this group of patients, and the diversity of the etiology of their symptoms. The psychodynamic approach assumes the depersonalization is a defense from low self-esteem, with feelings of worthlessness and helplessness, and with traumatic memories. The origins of these feelings and issues, and of the depersonalization that has resulted, are explored and worked through. The patient becomes able to see that unrealistic expectations are related to these feelings, and more realistic standards, when accepted, can allow the patient's sense of and experience of self to become acceptable. Cognitive education about the symptoms may be helpful. Behavioral approaches, including flooding, performing aversive tasks when depersonalization occurs, and contingent rewards for symptom absence, have been successful or somewhat successful in studies of one or two patients. Hypnosis may be used to demonstrate to patients how to initiate and control depersonalization experiences. Some depersonalization has responded to single intravenous administration of amphetamines. Half responded, and half of the responders rapidly relapsed. Tricyclic antidepressants have occasionally been useful, as has fluoxetine in six female patients. Some patients respond to either clozapine or phenazepam. Patients have also responded to clonazepam.

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I. Example A 32-year-old woman sought treatment because she felt no connection with her body and her feelings. She often saw her body as if she were outside of herself, observing her actions as if she were watching a movie of her life. She had no reaction to situations that usually evoked strong emotional reactions. She was terrified that she never would feel again, and planned to kill herself if her situation could not be corrected. She withdrew from all social contacts because she did not know what she really felt about them. In fact, at times she felt that the people in her life had become strangers to her, and doubted if they were real. She experienced her home as having changed and become unfamiliar. Her parents were very controlling, and she was stifled and dependent. Initially doubtful that therapy could help her, she reluctantly accepted fluoxetine, which, at 60 mg/day, offered her much relief, although she still remained uncomfortably symptomatic. She allowed her therapist to recreate her dissociative symptoms with hypnosis, and learned to control many of her symptoms autohypnotically. Then she was able to allow a psychodynamic exploration of the circumstances that led to her becoming symptomatic. As she addressed these inner conflicts and family difficulties, her symptoms became progressively less frequent and less severe. She moved from her parents' home and developed a social life of her own. After having been without depersonalization symptoms for a year, she was tapered off of her medication and she was seen infrequently in follow-up sessions. She retained her gains and made many improvements in her life. After a mild recurrence, she was placed on fluoxetine again, and she was seen for a series of sessions. She has been asymptomatic for a year, maintained on fluoxetine and monthly visits.

V. DISSOCIATIVE AMNESIA Amnesia is both a symptom of mental disorders and a free-standing mental disorder, dissociative amnesia, in its own right. It is among the diagnostic criteria for dissociative fugue, dissociative identity disorder, so-

matization disorder, acute stress disorder, and posttraumatic stress disorder. An inability to recall important personal information is the core feature of dissociative amnesia. What is forgotten is usually traumatic or stressful, and is too extensive to be explained by normal forgetfulness. (Unfortunately, there is no consensus regarding the domain of normal forgetfulness.) The memory impairment is reversible. Autobiographic material cannot be retrieved in a verbal form; if temporarily accessed, it cannot be completely retained in awareness. The most common presentation of amnesia is a retrospectively reported gap or series of gaps of the individual's life history. In some cases, what has been forgotten may manifest itself in nightmares, reenactments, intrusive imagery, and somatoform symptoms. Although acute, florid and dramatic episodes of amnesia, often associated with wartime trauma or natural disasters, may be recognized at once, most patients ultimately given the dissociative amnesia diagnosis did not have their symptoms recognized as such, and may be in treatment an average of four years before the diagnosis is rendered. Diagnostic criteria are given in Table II. Several subtypes of amnesia are recognized in DSM-IV. In localized amnesia, there is an inability to recall events related to a circumscribed period of time, usually surrounding a disturbing event. In selective amnesia, an individual can recall some, but not all, of the events during a circumscribed period of time. Less common are some other forms. Generalized amnesia is a failure to recall one's whole life. Continuous amTable II

Diagnostic Criteria for Dissociative Amnesia

A.

The predominant disturbance is one or more episodes of inability to recall important personal information, usually of a traumatic or stressful nature, that is too extensive to be explained by ordinary forgetfulness. B. The disturbance does not occur exclusively during the course of Dissociative Identity Disorder, Dissociative Fugue, Posttraumatic Stress Disorder, Acute Stress Disorder, or Somatization Disorder and is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a neurological or other general medical condition (e.g., Amnestic Disorder Due to Head Trauma). C. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. ,,,

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nesia involves an ongoing inability to recall events after a particular time, including the present, such that the patient continues to fail to recall events even as they continue to occur. In systematized amnesia, there is a loss of memory for certain categories of information, such as memories relating to one's family or to a particular person. Until Coons' systematic 1992 study, it had been thought that the onset of amnesia was acute, of sudden onset, and that the condition resolved rapidly and rarely recurred. It now is clear that some amnesia is chronic--it involves the loss of large blocks of time and does not resolve rapidly. Furthermore, 24 to 40% have multiple episodes of amnesia. While older studies emphasized dramatic acute amnesias, Coons found 46% had amnesia for recent events, 60% had amnesia for remote events, and 24% had both recent and remote memory loss. Recent amnesias range from minutes to four hours (mean, 1.2 hours). Remote amnesias range from one month to many years (mean, 7.7 years). Remote amnesia is usually selective, but may be generalized. Dissociative amnesia patients may suffer from a number of other symptoms: depression (84%), headaches (64 % ), sexual dysfunction (60 % ), sornatization (44%), depersonalization (40%), and many others. The subjective experience of amnesia may include: blackouts or "time loss"; reports by others of disremembered behaviors; the appearance of unexplained possessions; perplexing changes in relationships; fragmentary recall of one's life history; evidence of unusual fluctuations in skills, habits, tastes, and knowledge; fuguelike episodes; recurrent, unexplained mistaken identity experiences; and brief, trancelike amnesia episodes ("microamnesias"). Not uncommonly, in acute amnesias, there may be a period of confusion before the individual realizes that he/she has suffered a memory loss, and is able to organize his/her understanding of his/her circumstances around that construct.

A. Epidemiology Many older studies report on amnesia as a symptom rather than dissociative amnesia as it is currently defined. Nonetheless, studies done in civilian academic hospital and clinic settings indicate a prevalence of amnesia as a serious symptom or primary diagnosis in

from 0.26% to 1.8% of cases, while studies of combat veterans have shown a prevalence of 5 to 14.4%, and suggest that the percentage increases with exposure to more severe and sustained combat. These suggest that dissociative amnesia will be more common in populations exposed to massive trauma. Recently Ross and his colleagues examined 1005 randomly selected citizens of Winnipeg, Canada, and followed up half with a structured interview. Seven percent of the interviewees fulfilled criteria for dissociative amnesia. Although it is conceivable that some organic amnesias may have been inadvertently included, this demonstrates that this condition is quite common, and usually goes undiagnosed.

B. Etiology Although some authorities continue to conceptualize amnesia as malingering, as an artifact of therapy, as a social role designed to escape responsibility, and so on, most experienced scholars and clinicians understand dissociative amnesia to be a basic aspect of the psychobiology of the human trauma response: a protective activation of altered states of consciousness in reaction to overwhelming psychological trauma. Memories, affects, sensations, and cognitions associated with trauma are encoded in an altered state; upon return to baseline conditions, access to this material is blocked in whole or in part. Nonetheless, as noted above, it may covertly influence behavior and mentation. Profound intrapsychic distress and conflict with or without exogenous trauma may play an etiologic role. Coons described possible precipitants in his series (some cases had multiple precipitants): child abuse (60%); marital trouble (24%); disavowed sexual behavior (16 %); suicide attempts (16 %); criminal behavior (12%); death of relative (4%); psychotherapy (4%); runaway behavior (4%); unknown (16%). He further noted that his dissociative amnesia patients had a strong history of childhood trauma. Seventytwo percent had childhood trauma: sexual abuse (52%); physical abuse (40%); neglect (16%); abandonment ( 12 %). Despite contemporary controversy about amnesia for trauma, virtually every systematic study and comprehensive review has demonstrated not only that trauma is extremely prevalent in the history of those

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with dissociative amnesia, and that studies of traumatized populations consistently document the presence of amnesia among their clinical phenomenology. This is further buttressed by numerous cross-cultural studies demonstrating that dissociative amnesia is a instead, widely-recognized response across cultures to psychological trauma. As of this writing there is considerable interest in studies demonstrating that there is a distinct psychophysiology to traumatic amnesia, and that there is a decrease in the size of the hippocampus in the brains of combat veterans with posttraumatic stress disorder and survivors of childhood abuse. It remains to be seen whether this line of research will cast further light on the origins and mechanisms of dissociative amnesia. There is also some interest in whether dissociative amnesia is related to the hypnotizability and dissociativity of traumatized individuals.

C. Diagnosis No particular test or examination can unequivocally demonstrate whether an impairment of memory is organic, malingered, associated with a mental disorder, or some combination of the above. The differential diagnosis of dissociative amnesia includes: dementia, delirium, and amnestic syndromes; discrete memory loss in organic disorders (posttraumatic amnesia, amnesia associated with seizure disorders, anmesia due to psychoactive substances, transient global amnesia); other dissociative disorders; other mental disorders of which dissociative amnesia is a symptom (posttraumatic stress disorder, somatoform disorder, borderline personality disorder, acute stress disorder); malingered amnesia. Therefore, a comprehensive examination is crucial. It must include a complete history, involving attention to developmental concerns and inquiry about trauma in childhood and adult life. When possible, it is useful to obtain prior medical records and collateral interviews. Assessment must include a complete physical and neurological examination with cognitive testing, and baseline laboratory studies with an electrocardiogram, toxicology, and blood alcohol level. Additional studies may be warranted: dementia workup, electroencephalogram, computed axial tomography, magnetic resonance imaging studies, and neuropsychological studies. On occasion prolonged electroencephalographic monitoring in a specialized teleme-

try unit may be needed to rule out occult seizure disorders. Most situations are relatively straightforward unless there are superimposed organic and psychogenic components. The relatively new Structured Clinical Interview for DSM-IV Dissociative Disorders-Revised is a useful diagnostic approach.

D. Treatment Treatment is facilitated by using a triphasic trauma therapy model. Herman speaks of a phase of safety followed by a phase of remembrance and mourning, and finally a phase of reintegration. The first stage attempts to make the individual safe, offers stabilizing interventions, and builds his or her strength as a therapeutic alliance with the clinician is formed. In the second, if it has been possible to achieve the goals of the first, the disowned material is accessed and processed. Then the patient is helped to reintegrate him or herself, and to reconnect with life, moving the patient beyond the focus on trauma into a renewed life. The therapy never is simply a matter of "getting out the trauma." The stressors that are powerful enough to sever the continuity of autobiographic memory are not simply the events or conflicts themselves. Overwhelming affects and the personal meaning of the trauma reinforce the persistence of the amnesia. Despair, grief, guilt, shame, self-hatred, helplessness, and terror often play powerful roles. Furthermore, the events shrouded by amnesia may have caused profound shifts in the patient's view of him/herself and others, and his/her view of the world. The meaning of the trauma and the amnesia for it must be explored and addressed in order to prevent the patient from remaining symptomatic. Uncovering efforts always must be undertaken cautiously, and paced carefully, with a profound respect for the patient's vulnerability. While usually recent amnesias can be resolved in short order, more chronic amnesias with childhood onsets must be approached with extreme circumspection. Some such patients can be retraumatized and destabilized if efforts to overcome amnesia are too hasty. If a supportive environment can be established in the treatment of recent acute amnesia, often spontaneous remission of the amnesia will occur, the material will return in the course of history taking or treatment, or permissive suggestions that memory recovery will occur when the patient is ready, and at a pace

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that the patient can tolerate, will be successful. With more chronic situations, it often is more important to establish a more long-term therapy that addresses the sequelae of whatever led to the amnesia. Such patients are often at considerable risk for self-harm, selfdestructive relationships, alcohol or substance abuse, and so on, as the treatment continues. Some hospital stays may prove necessary for restabilization or to address difficult issues in a safe environment. Uncovering dissociated memories may be contraindicated for patients with instabilities in their ego strength, personal circumstances, or therapeutic alliance. The use of hypnosis and drug-facilitated interviews have a venerable history in the resolution of dissociative amnesia. However, it is appreciated that many procedures designed to enhance the recovery of memory may also lead to the recovery of confabulated memories that the patient will subjectively experience as genuine and compelling. Therefore, in any circumstance in which a patient may be involved in legal proceedings, it is essential to withhold their use prior to assessing the implications of such interventions, lest the patient be considered to have had his/her memory distorted by these processes, and be compromised as a witness to his/her own circumstances. If there is no contraindication, hypnosis may be used to contain and titrate the experience of distressing symptoms, facilitate the recovery of memories in an orderly and titrated manner, offer ego-strengthening to the patient, and assist in the processing and integration of dissociated material. Permissive amnesia can be suggested for material that emerges prematurely or precipitously. Drug-facilitated interviews often can lower the inhibitions and defenses of the dissociative amnesia patient. Often the amnesia created by the barbiturate chemicals usually used allows revelations to be made without the patient's recalling the revelation. Such sessions are best taped or videotaped. I. Example A woman in her late twenties was admitted to a general hospital unit, acutely depressed. She had amnesia for a period of approximately 2 hours of the previous evening. She had gone over to her fiance's home planning to finalize some details of their upcoming wedding and returned home much earlier than she was expected. She went to bed with a severe headache, and awakened the next morning suicidally depressed. Antidepressants and suicide precautions

were begun. Medical and neurological workups and lab studies were normal, and an electroencephalogram was unremarkable. Her depression had come "out of a clear blue sky," with no antecedent psychobiological changes or known stressors. Her psychiatrist worked to establish a warm supportive relationship with her, and was successful in making her feel safe and cared about. On the third hospital day he happened to inquire about her visitors. When she sadly observed that her fiance had not come to see her, the psychiatrist began to inquire about their relationship. She became acutely upset, and began to strike her head with her fists, shouting "No!" repeatedly. The psychiatrist took her hands to prevent self-injury. After about 15 minutes of screaming "No!" and trying to attack herself, she collapsed, sobbing. Several minutes later she was able to whisper that she had just remembered that when she had gone to visit her fiance, she had found him in the company of a mutual female friend. Her lipstick was smudged and her blouse had been hastily and incorrectly buttoned. Confronted with clear evidence that her fiance had been with this other woman, she left, not having said a word. In therapy sessions it was discovered that her sense of shame and rejection (the wedding date was near, wedding invitations had already been printed) had generated an incredible rage in which she experienced strong homicidal urges, which were completely alien to her character. These had been turned against herself, a character style of the patient's, and the overwhelming experience and its profound implications for her life had been dissociated. Only the depression remained accessible to the conscious mind. After ventilating her grief and outrage, and making a safety contract not to harm herself or others, she was transferred to outpatient treatment.

VI. DISSOCIATIVEFUGUE The essential feature of dissociative fugue is sudden unexpected travel away from one's home or one's customary place of work, with an inability to recall one's past (Criterion A). There is either confusion about one's personal identity or the assumption of a new identity, either partial or complete (Criterion B). The diagnostic criteria are given in Table III. The travel and identity alteration may be brief, running its course in hours or days, with a minimal amount of travel.

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Table III

Dissociative Disorders

Dissociative Fugue .

.

.

.

.

,,,

A.

The predominant disturbance is sudden, unexpected travel away from home or one's customary place of work, with inability to recall one's past.

B.

Confusion about personal identity or assumption of a new identity (partial or complete).

C.

The disturbance does not occur exclusively during the course of Dissociative Identity Disorder and is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., temporal lobe epilepsy).

D.

The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

However, it may continue for weeks, months, or even years, and involve a complicated pattern of travel extending over thousands of miles and many national boundaries. Usually both the onset and recovery are rapid and sudden, and often the recovery occurs upon arising from sleep. Recurrences once were thought rare, but it is clear that some patients who suffer dissociative fugues may have recurrences, and many have other dissociative symptoms at other points in time. Most fugues do not involve the formation of elaborate alternate identities. When a new identity is formed, it often but not inevitably is more gregarious and uninhibited than was the baseline identity. This expectation may be based on the sociocultural aspects of the societies in which famous classic cases were discovered. The person may assume a new name, establish a new domicile, and develop a complex set of activities that appear well integrated. There may be no hint of mental illness. However, considerable agitation and distress may accompany the recovery of the baseline identity, coming to grips with the lost time and the behaviors attributed to the person in his/her alternate identity and/or the period for which he/she was amnestic, and the reactions of those effectively abandoned by the patient during the fugue. Often fugues occur in stressful situations in which remaining in one's baseline identity and occupation involves real risk and danger, such as in military settings.

A. Epidemiology It is virtually impossible to use older studies as a guide, because the boundaries between the dissocia-

tive and posttraumatic states with amnestic symptoms are not clearly drawn. In a modern study using DSM-HI-R criteria, Ross and colleagues found that approximately 1% of a nonpatient population acknowledged the symptoms of dissociative fugue on a structured interview. However, many times reports of fugue behavior ultimately is attributed to an underlying dissociative identity disorder; this may be an overestimation. There is general consensus that dissociative fugue is relatively uncommon compared to dissociative amnesia and dissociative identity disorder, and that it appears to be more common in war, natural disasters and in other settings in which violence and extreme social disruption are common.

B. Etiology The same factors that are associated with dissociative amnesia are relevant. In addition, the literature is divided as to the relevance of individual psychopathology and difficult family backgrounds. Dissociative fugue often occurs under circumstances that raise a suspicion of malingering, because the fugue may appear to reduce accountability, responsibility, or exposure to danger (such as evading combat). Psychodynamic factors often appear more relevant than trauma per se. Many patients with fugues have intense separation anxiety, suicidal or homicidal impulses, and primitive denial. Furthermore, many fugues have the quality of wish fulfillments. Many fugues begin in association with fatigue, sleep, or sleep deprivation; some observe that heavy alcohol use may be a predisposing factor.

C. Diagnosis The approach to diagnosis is similar to that for dissociative amnesia. It is useful to recall, however, that in the middle of a dissociative fugue, if the patient has developed another identity, he or she may not have either an awareness of the past or an awareness of amnesia for the past. Consequently, they may be without symptoms or distress, and are unlikely to come to the attention of the mental health professions. When they revert to their former identities they can become very distressed over their amnestic gaps and their circumstances. Malingering is often in the differential diagnosis, because many individuals in fugues leave situations that it would be desirable to leave for one's own safety or benefit.

DissociativeDisorders

D. Treatment The approach to treatment is similar to that for dissociative amnesia; when alternated identities are encountered, approaches similar to that for dissociative identity disorder may be useful. However, there may be considerable real world consequences associated with the life the person has led while in an alternate identity or a confused state, and these must be addressed. Often there are considerable issues with guilt and shame. In the unusual circumstance that the patient is still in a fugue when treated, one must recover information about the baseline identity, learn what led to its being abandoned, and facilitate its restoration. When the patient is encountered after having returned to the baseline identity, both the amnesia and the alternative identity (if it persists covertly) must be addressed.

I. Example The friendly and outgoing 32-year-old assistant manager of a fast food restaurant retired to his office saying he was beginning to feel "weird," and planned to take a nap. When a coworker went to check on him a few minutes later, he found the manager in an agitated state, wondering what he was doing there. When addressed by the name by which he was known, he corrected the coworker, claiming a different first name and a slightly different last name as his own. He claimed to be a fireman in a large city several states away. He thought the date was 3 months earlier than the calendar date. Having returned home, he entered psychotherapy. His psychiatrist learned that this man was known as a worried, fretful, and anxious but contained man, socially inhibited, but as a fireman, willing to take risks and highly regarded for his bravery in difficult situations. Under hypnosis, it emerged that his counterphobic behavior covered over a deeper pervasive insecurity. On the last shift before he vanished, he and a new firefighter had been briefly trapped in a dangerous situation that he had decided to enter. A roof had fallen in, injuring the rookie firefighter and narrowly missing the patient. He had been terribly frightened, and guilty that he had exposed the rookie to injury. He began to have profound uncertainty and insecurity. He suffered several panic attacks. However, he determined to continue his work and to disregard his concern. When he next drove to the station, he instead wound up several hundred miles away, and

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began an alternative life. Hypnosis never succeeded in obtaining more than a patchy recollection of the missing time period, and never could access any trace of the alternative identity under which he had lived. Psychotherapy helped him discover the sources of his insecurity and need to prove himself strong and brave over and over again. He found a different career and had no recurrent difficulties.

VII. DISSOCIATIVE IDENTITY DISORDER Dissociative identity disorder is a chronic complex dissociative psychopathology characterized by disturbances of memory and identity. Its manifestations are often polysymptomatic, pleiomorphic, and fluctuating. Often in the course of its natural history there are periods in which the condition is apparently latent and can only be diagnosed by history, and often the overt manifestations fall short of dissociative identity disorder criteria, and the condition's phenomenology is more appropriately described as dissociative disorder not otherwise specified. The essential features of dissociative identity disorder are the presence of two or more distinct identities or personality states that recurrently take control of the patient's behavior, accompanied by amnesia. The diagnostic criteria are presented in Table IV. This condition demonstrates a failure to integrate identity, memory, and consciousness. The personality states may vary considerably in their degrees of awareness of the existence, activities, and thoughts of one another. They may also differ considerably in their de-

Table IV Diagnostic Criteria for Dissociative Identity Disorder A. The presence of two or more distinct identities or personality states (each with its own relativelyenduring pattern of perceiving, relating to, and thinking about the environment and self). B. At least two of these identities or personality states recurrently take control of the person's behavior. C. Inabilityto recall important personal information that is too extensive to be explained by ordinary forgetfulness. D. The disturbance is not due to the direct physiologicaleffects of a substance (e.g., blackouts or chaotic behavior during alcohol intoxication) or a general medical condition (e.g., complex partial seizures). Note: In children, the symptomsare not attributable to imaginaryplaymates or other fantasy play.

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gree of elaboration and distinctness. Each personality state has its own identity, self-representation, autobiographical memory, and sense of ownership of its own activities. Separate names are commonly, but not inevitably present, and often are more a title than a name (e.g., "The Evil One, .... Rage," "Mother," etc.). Modern studies indicate that female patients have, on the average, from 16 to 18 alters, while males average approximately 8. Patients with very large numbers of personalities have been described. Approximately half of contemporary cases have 10 or fewer identities. The personalities are not separate people. In many ways it is more accurate to understand the dissociative identity disorder patient as deprived of a single identity than as in possession of many identities. All of the personality states and their interaction constitute the patient's personality in the conventional use of the term; i.e., the dissociative identity disorder patient's identity is to have multiple identities. Although the dramatic differences across the personality states often are the focus of curiosity about this condition, it is actually their common feature of being alternative ways of adapting to difficult circumstances that is more central. Usually the primary identity that carries the legal name is depressed, constricted, guilty, and somewhat masochistically passive. The alternate identities often have different names and contrasting characteristics. They commonly are represented as emerging in response to particular circumstances and/or stressors, and may differ in reported age, gender, knowledge, coping style, dominant affects and concerns, and so on. They not infrequently contain an inner world of alters that replicates significant aspects of the intrafamilial and/or interpersonal aspects of the patient's childhood circumstances. Typically, but not inevitably, the system of personality states will include parts designed to cope in general and with specific circumstances, parts based on abusers, parts based on real or wished-for protectors, and parts that hold the memory and experience of traumatic experiences. In complex cases personality states may be created to hold specific traumata and very specialized skills. Not infrequently the inner world of the personalities, in which they are imagined to interact, has a subjective reality equally or more compelling than the external world. In this world, the personality states are experienced as having complex relationships, involving both enmities and alliances of various sorts. On

occasion, the patient can mistake what has occurred in his or her inner world for what has occurred in the outer world, and vice versa. The personality states may take control to take advantage of one another, may make critical comments on one another (heard as internal voices), and may be in open conflict, sometimes so intense that one tries to kill the other, often inflicting harm on the body with the misapprehension that thereby they will kill the other, but not themselves. Their degree of conviction of their being genuinely separate may be intense enough to be considered delusional. Gaps in memory for both recent and remote events is characteristic. Often the amnesia is asymmetrical; that is, part A has a far greater degree of memory for the actions of part B than part B has for the actions of part A. Typically protective alters and alters that are identified with aggressors have more extensive memories. Some patients have personality states that have the role of maintaining a reasonably continuous memory, for the whole life or for some period of life. Although personality states' influences are most obvious when they actually take overt control, it is more common for them to influence from behind the scenes by producing hallucinations such as a voice giving instructions, or by imposing a feeling, thought, or action that is felt as an unwilled intrusion by the personality ostensibly in charge of the body at the time. The personality states take control from one another in response to psychosocial stressors, particular circumstances, or inner arrangements or conflicts among the personality states. The transfer of control need not be complete ~ situations in which more than one personality state is out and/or influencing behavior ("copresence") are commonplace. The process of transition, or "switch" phenomenon, may occur within seconds or less, but, it may occur gradually. When there is conflict between the personality state in apparent control with the effort of another personality state to emerge, the switch may be accompanied with much agitation and discomfort, and, not infrequently, headaches and physical gestures indicating conflict or distress (psychomotor agitation, facial features and expressions showing the two states in fluctuating degrees of presence, hands raised to the face, and expostulations, etc.). Dissociative identity disorder patients commonly have many depressive, somatoform, and posttraumatic

,,

,,

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,

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symptoms (such as nightmares, startle responses, and flashbacks). Self-mutilation, suicide attempts, and, less frequently, aggressive behavior, may occur. Numerous anxiety symptoms are common. Substance abuse, sexual dysfunction, conversion symptoms, eating disorders, and sleep disorders may cooccur. Many times the abusive relationships of their childhood are repeated in chronic experiences of revictimization. These patients are highly hypnotizable as a group, and have many capacities associated with this talent, such as the capacity to block out pain, and to hallucinate and to negatively hallucinate (e.g., to not see what is before them). Their many difficulties often lead to the picture of borderline personality disorder, but sophisticated psychological testing indicates that for most patients, the superficial picture of borderline features is not matched by a borderline structure.

A. Epidemiology Long considered rare, apocryphal, or iatrogenic, it now is clear that dissociative identity disorder is a relatively common condition, and that often its features are clearly apparent long before the diagnosis is made and treatment begun. Two types of studies have been done to assess its contemporary prevalence ~ studies of clinical populations and studies of nonpatient populations. Studies in the United States, Canada, the Netherlands, and Norway have used screening tests such as the Dissociative Experiences Scale to screen inpatient psychiatric populations from which known dissociative disorder patients have been excluded. They studied patients with screening test scores that suggested the possibility of a dissociative disorder with structured interviews such as the SCID-D or DDIS. These studies indicate that between 3 and 5 % of psychiatric inpatients have previously undiagnosed dissociative identity disorder. Similar studies of partial hospitalization and drug treatment settings have identified an even higher prevalence. Ross and his colleagues have studied a stratified sample (1055 persons) of the population of Winnipeg, Canada, with the Dissociative Experiences Scale, and followed up as many as possible (43 %) with DDIS interviews. They concluded that 3.1% fulfilled criteria for dissociative identity disorder. However, they determined that only approximately 1% were actually clinical dissociative identity disorder patients. It is unclear whether this reflects problems with the instrument or the diagnostic criteria, whether there

are nonpathological endogenous forms of dissociative identity disorder, or whether patients remaining completely amnestic for childhood abuse were less symptomatic. In modern clinical studies dissociative identity disorder is most commonly discovered in women among adult populations, at a ratio of 8 to 9:1 in most studies. However, among children the gender distribution is close to 1:1. It remains unclear whether females are harder to diagnose among youngsters and males among adults, or whether gender differences in adults seeking and remaining in treatment plays a role in this discrepancy. Many speculate that many males with this disorder enter the legal rather than the mental health treatment system, but there is no hard data to demonstrate this. Although the average age at diagnosis is in the early-to-mid 30s, this condition has been identified in patients ranging from 3 years to over 80 years of age. Much remains to be learned about its recognition in various age groups.

B. Etiology Many models for the development of dissociative identity disorder have been offered. Kluft noted 11 basic models: (1) supernatural/transpersonal; (2) psychological; (3 ) sociological; (4) role-playing/malingering/ iatrogenesis; (5) trance state/autohypnotic; (6) split brain/hemispheric laterality; (7) neurologic (temporal lobe/complex partial seizures/kindling); (8) behavioral states of consciousness; (9) neural network or memory/information processing; (10) neodissociation/ego states; and a (11) basic affects model. None essentially precludes the operation of another, and none explains dissociative identity disorder rather than illustrates a potential possible mechanism. Generally it is agreed by those who perceive dissociative identity disorder as a naturalistically occurring disorder that dissociative identity disorder occurs in connection with a child's being overwhelmed, usually repeatedly, and often by abuse. Those who dispute its legitimacy and/or dispute its origin in the context of childhood trauma emphasize the importance of an iatrogenesis model. As of this writing, the iatrogenesis hypothesis is a matter of opinion rather than a proven fact. However, a number of studies have documented that most patients who develop dissociative identity disorder were indeed abused. Surveys that accept the

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patients' accounts as data report childhood abuse in the histories of up to 97 or 98%. Studies that document abuse or investigate abuse allegations have documented abuse in 95% of children and adolescents and in up to 85 to 89% of adults. Kluft's four-factor theory holds that dissociative identity disorder occurs in (factor 1) a dissociationprone child (a biological capacity) who experiences (factor 2) overwhelming stressors that cannot be managed with nondissociative defenses. While child abuse is the most frequent stressor in North American studies, this may not be universally the case. Exposure to death, vicarious traumatization (by witnessing the intentional or accidental death or mistreatment of others), the loss of significant persons, cultural dislocation, dysfunctional family pressures (often in the context of divorce), childhood illness and injury, and repeated childhood surgeries have been cited as instrumental overwhelming stressors as well. The child makes use of (factor 3) various shaping influences and substrates to form the kernel of the various alters. These may include life experiences and crucial persons in the child's life space (via introjection, internalization, and identification), imaginary companionship, developmental lines, extrinsic interpersonal influences from childhood (encouragement of role-playing and acting, contradictory caretaker demands or reinforcement systems, or identification with a dissociative parent) and from contemporary sources (previous therapy, the media and literature, errors in technique, autohypnotic coping). Finally, the situation is reinforced by (factor 4) the inadequate provision of stimulus barriers and restorative experiences by significant others. This approach to etiology is consistent with clinical experience.

C. Diagnosis Numerous studies demonstrate that on the average dissociative identity disorder patients have been in treatment for just under 7 years before their condition is diagnosed, and have received over three inaccurate or comorbid diagnoses before it is recognized. Most standard mental status and interview schedules are not constructed to make adequate inquiry about the dissociative phenomena that play a role in the phenomenology of dissociative identity disorder. This is especially problematic because many of its manifestations are subtle and covert much of the time.

Until the last few years it had been customary to make inquiries about signs suggestive of dissociative identity disorder. These include: (1)prior treatment failure; (2) three or more prior diagnoses; (3) concurrent psychiatric and somatic symptoms; (4) fluctuating symptoms and levels of function; (5) severe headaches and/or other pain syndromes; (6) time distortion, time lapses, or frank amnesia; (7) being told of disremembered behaviors; (8) others noting observable changes; (9) the discovery of objects, productions, or handwriting in one's possession that one cannot account for or recognize; (10) the hearing of voices (80% experienced as within the head) that are experienced as separate, urging the patient toward some activity; (11) the patient's use of "we" in a collective sense and/or making self-referential statements in the third person; (12) the eliciting of other entities through hypnosis or a drug-facilitated interview; (13) a history of child abuse; and (14) an inability to recall childhood events from the years 6 t o 11. Recently Loewenstein published a special mental status that makes inquiry about six areas of symptomatology commonly demonstrated in dissociative identity disorder patients: (1) indications of the dissociative processes at work (e.g., differences in behavior, linguistic indications, switching; (2) signs of the patient's high hypnotic potential (e.g., enthrallment, trance logic, out-of-body experiences); (3) amnesia; (4) somatoform symptoms; (5) post-traumatic stress disorder symptoms; and (6) affective symptoms. Many clinicians ask directly to meet an alter if they have reason to believe that dissociative identity disorder is present. Other strategies involve: (1) asking the patient to journal for 20 to 30 minutes a day, because other personalities may make entries; (2) extending the interview to 2.5 to 3 hours, because often spontaneous dissociation will be observed. At times the use of hypnosis or drug-facilitated interviews is warranted and useful. The most modern strategy involves the use of structured diagnostic interviews if either there are clinical indications that dissociation may be present of if a screening test of dissociation, such as the Dissociative Experiences Scale indicates the need for further assessment. Clinicians generally use a score of 20 or more as suggestive, while researchers recently have advocated a score of 30. Two structured interviews are available, the Dissociative Disorders Interview Sched-

Dissociative Disorders

ule (DDIS) of Colin Ross, and the Structured Clinical Interview for DSM-IV Dissociative DisordersRevised (SCID-D-R) of Marlene Steinberg. The DDIS involves an array of forced choice questions that permit the interviewee to endorse the symptoms of many psychiatric disorders (including the dissociative disorders), the experience of abuse, and many symptoms associated with dissociative identity disorder. It takes from 45 to 75 minutes to administer. The SCID-D-R is a semistructured interview allowing the clinician considerable discretion and at times several options. It may take from 45 minutes to over 2 hours to administer. It includes items of observation made during the interview. Amnesia, depersonalization, derealization, identity confusion, and identity alteration are rated. Dissociative identity disorder patients generally score 3 or above in each category (although derealization may be weak), for a score of from 15 to 20. Both instruments are highly sensitive (over 90%) and have few false positives. The DDIS makes wider inquiries and asks for some history; the SCID-D-R gives a much richer and more comprehensive portrait of the patient's experience of his or her disorder.

D. Treatment A curious dichotomy pervades writing on the treatment of dissociative identity disorder. On the one hand, experienced clinicians have developed a form of therapy that has resulted in many successful outcomes. On the other, those skeptical of the condition's legitimacy fulminate against that treatment, and maintain it has the potential to create and/or worsen it. They opine that it should be treated by nonreinforcement of the dissociative psychopathology and by focusing on contemporary problems of living. The compelling weight of evidence is that dissociative identity disorder is a naturalistically occurring disorder that responds better to specific therapy for dissociative identity disorder than nonspecific therapy or a regimen of nonreinforcement and redirection. However, it is also clear that many patients have not prospered in specific treatments that were inattentive to their particular vulnerabilities and needs. The treatment of this group of patients must be individualized thoughtfully. Ideally, the treatment should address alleviating the problems of identity and memory; that is, they should attempt to bring the patient to a subjective sense of a

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unified identity by integrating the personality states, and amnesia should be relieved by achieving a confluent identity in the here and now, and by uncovering amnesia for past events. It is understood that what is uncovered in the treatment of the traumatized may not consist exclusively of material that is historically accurate and can be verified. Considerable controversy surrounds the nature and accuracy of traumatic memory. Some authorities hold that it is reconstructive and unreliable, while others hold that it involves both retrieved and reconstructive elements. Some demonstrations of the recovery of verifiable memories have been published, which appear to have only minor reconstructive elements. However, regardless of this controversy, which remains unresolved, it is understood that processing the mind's representation of its past appears essential to the achievement of an integrated identity and memory. While the unification of the dissociative identity disorder patient is the optimal goal, it is only one aspect of the treatment of a suffering individual, and may have a lower priority than other goals in many treatments, and even at many times in a treatment that is attempting to pursue integration. Integrationalist therapies set as their goal the integration of the individual in the course of resolving problematic symptoms and difficulties in living. Personality-focused therapies attempt a problem-solving approach among the personality states, which are encouraged to collaborate more harmoniously without necessarily ceding their separateness. Adaptationalism focuses primarily on managing here-and-now difficulties and maximizing function. Although a vocal minority of therapists and many patients oppose working toward integration, as of this writing, it appears that the longterm stability of integrated patients is superior to that of patients who do not integrate. The triphasic approach to the traumatized patient, described above, applies to the treatment of dissociative identity disorder. The stages of the treatment of dissociative identity disorder (Table V) are consistent with this model. Stages 1 to 3 are consistent with the phase of safety, stage 4 is consistent with the phase of remembrance and mourning, and stages 5 to 9 are consistent with the phase of reconnection. In practice, the stages discussed below as if they were discrete blend into and overlap with one another. For example, some identities may have integrated before others have even been discovered.

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Table V The Stages of the Psychotherapy of Dissociative Identity Disorder

1. 2. 3. 4. 5. 6. 7. 8. 9.

Establishingthe therapy Preliminaryinterventions Historygatheringand mapping Metabolismof the trauma Movingtoward integration/resolution Integration/resolution Learningnew coping skills Solidificationof gains and workingthrough Follow-up

Establishing the psychotherapy involves the creation of an atmosphere of safety in which the diagnosis can be made and confirmed, the security of the treatment frame can be established, the therapeutic alliance is begun, the patient is informed of the nature of the treatment, and sufficient hope and confidence is established. Preliminary interventions involve gaining access to the more readily reached personality states; establishing contracts against terminating treatment prematurely, self-harm, suicide, and so on; fostering communication and cooperation among the alters; expanding the therapeutic alliance; and maximizing symptomatic relief safely. New coping skills are taught, many of which may involve hypnotic or autohypnotic methods, in order to help the patient deal with intrusive traumatic material, calm unsettled personality states, and recover his/her equilibrium. In history-gathering and mapping one learns more about the personality states, their origins, and their relationships to one another. The inner world of the personalities is clarified. Working with this enhanced knowledge, further efforts are made to deal with the personality states' issues and interactions, and to gain more cooperation and collaboration. Without achieving the goals of these first three stages, it is not advisable to proceed to metabolism of the trauma, which involves accessing and dealing with the overwhelming events alleged to be at the sources of the dissociative identity disorder. A precipitous and/or premature entry into this work is often associated with the decompensation of the patient. Patients who cannot achieve the goals of the stages prior to metabolism of the trauma should remain in a supportive and preliminary therapy that builds ego

strength and focuses on adaptational and personalityoriented issues. Integration should not be pursued. When a patient is able to move into the trauma work, this work should be done in a very circumspect, cautious, and gradual fashion. Even in this stage, trauma work should not be the focus of every session, and care is given to restabilize the patient as much as possible at the end of each session. Some personality states will integrate spontaneously in this process. Moving toward integration~resolution involves working through the traumatic material across the personality states and facilitating still further cooperation, communication, mutual identification, and empathy among them. At this stage often the personality states may show signs that their identities are fading or blurring. Integration/resolution consists of the patient's coming to a new and more solid stance toward both self and the world. Integration is the blending of the personality states into a unity. Resolution is a smooth collaboration among personality states that retain their separateness. Learning new coping skills involves appreciating and mastering how to deal with life without dissociative defenses. Solidification of gains and working through is a long and difficult stage in which the patient must learn to live in the world. Often working through in the transference what has been learned about the past is quite helpful. Characterologic issues may become accessible for the first time. Relationship issues and stress management are crucial, as is dealing with intercurrent traumata. Follow-up rather than termination is advised in order to sequentially reassess the stability of the outcome, especially for those patients who achieved resolution rather than integration. It is not uncommon to find minor or partial relapses, or the discovery of personality states that were not accessible previously, in the first 27 months after integration. Several aspects of treatment require special consideration. Medication is useful for target symptoms or comorbid conditions, but is ineffective for the treatment of the core symptoms of dissociative identity disorder. Hospitalization may be required when a patient becomes self-destructive/suicidal or aggressive to others, overwhelmed by traumatic material to the point of dysfunction, or unable to contain alters' inappropriate activities. The creative arts therapies (movement therapy, art therapy, music therapy, etc.) are

Dissociative Disorders

very helpful for this group of patients. Although they often are disruptive to general therapy groups, carefully conducted groups specifically for this patient group have been very beneficial. Hypnosis plays a major role in the treatment of dissociative identity disorder, whether the therapist introduces it or not. Spontaneous trance and autohypnotic phenomena abound, even in the absence of trance induction. Many hypnotic techniques are useful for symptom relief, attenuating the impact of powerful events and affects, ego strengthening, giving comfort to overwhelmed or anxious alters, modulating abreactions, and accessing personality states to make them available to the therapy. This is in addition to the venerable use of hypnosis to retrieve dissociated materials, which is currently the source of some controversy. A recent study validated many memories that were retrieved with the use of hypnosis, but there is ample reason to be circumspect about material recovered in this manner, because it may be confabulated in whole or in part. Clinicians utilizing hypnosis for this purpose should have explained this concern prior to undertaking the procedure, and should have their patient's informed consent. Hypnosis should be avoided in instances in which the state of the patient's memory may be crucial for forensic matters. Often individuals who have been hypnotized may be held by the courts to have had their memories contaminated by the process; this may seriously damage the legal standing of the patient in court proceedings. Although no controlled studies of the treatment of dissociative identity disorder are available, there is an ample body of literature to indicate that most of those patients who can involve themselves in a definitive therapy with a therapist experienced in the treatment of this condition have a reasonably good prognosis. Recent studies demonstrate that there are three subgroups of dissociative identity disorder patients. One has relatively little comorbid pathology and relatively good ego strength, and usually gets well within a few years. A second has more ego weakness and comorbidity and runs a longer and often more crisisfilled treatment, but makes slow and gradual progress. Many in this group will integrate, and many others will ultimately have a good resolution. A third group has more ego weakness and comorbidity, and/or may remain enmeshed with alleged abusers. This group rarely can move toward definitive treatment and their treatment must remain adaptationalist

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and personality-oriented for long periods. Many may never integrate or reach stable resolutions, but a minority makes dramatic gains, even after long periods of instability.

I. Example Nancy, a 36-year-old nurse, had been in treatment for depression and posttraumatic stress for several years before her increasing complaints of headaches, hearing voices in her head, and amnesia led to an evaluation for dissociative identity disorder. She had given a history of father-daughter incest. Nancy's sisters and coworkers described out-of-character angry outbursts for which she had no memory. At times men she did not know called her or even arrived at her door maintaining they had a date for that night. Her closet contained several garments she did not recall buying, and their style was more revealing than her customary garb. Her diary contained entries in a handwriting she was sure was not hers. Her score on a dissociative experiences scale was 42. On an early version of the SCID-D interview she scored 18 (amnesia 4, depersonalization 4, derealization 3, identity confusion 3, identity alteration 4). During the SCID-D, an inquiry about internal dialogs (the voices heard within her head) prompted a spontaneous switch into another personality, Jill, which identified itself as the owner of the more revealing garments, and described an active social life unbeknownst to Nancy, whom she disparaged. This personality attributed the angry outbursts to still another personality, Liz, and mentioned the existence of several others as well. Liz emerged upon request and vociferously attacked Nancy as a "wimp" who had allowed herself to be abused as a child and dominated in contemporary work, family, and social situations. Liz stated that she punished Nancy for her failures by inflicting injuries to the body, and tried to prevent Jill from being sexual, because she considered all sex abusive. Nancy was transferred to the consultant for treatment. For several months her therapy focused on enhanced coping, safety, increased mutual tolerance and cooperation across the many personalities. Although the main thrust of her therapy was psychodynamic, she was taught many autohypnotic, cognitive, and behavioral approaches to stress and the management of painful material. Safety contracts with all known alters were obtained, and her personality system was explored without probing traumatic material in detail

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or in depth. Then, slowly, each personality was allowed to tell, abreact, and process its experiences. Some alters integrated spontaneously after doing their work, while others responded to suggestions to integrate employing hypnosis and imagery. Nancy had a few serious crises in which she became suicidal while she dealt with the traumatic material; she twice inflicted cuts on her forearms, and several times overused medication to "take away the pain." On one occasion she lost 2 weeks of work because she was so disorganized by work on her traumata. However, with some emergency sessions and telephone support, these crises were weathered. Her sisters and mother were able to confirm many of the memories of abuse recovered from her alters. In her fourth year of therapy she achieved complete integration. Treatment continued to work through her traumata in a unified self, and to enhance her coping. Two years after her integration, she visited her then terminally ill father, and told him she forgave him, even if he could not admit his transgressions. He admitted his misuse of her and begged her to pray for him lest he go to hell.

VIII. DISSOCIATIVE DISORDER NOT OTHERWISE SPECIFIED This category is utilized for those patients suffering from dissociative symptoms whose symptoms do not

fulfill the diagnostic criteria for the specific designated dissociative disorders. Currently it includes the research category, Dissociative Trance Disorder, which is discussed separately here. Typical examples are listed in Table VI. The natural history of many patients with Dissociative Identity Disorder involves many periods of time in which their overt symptoms are vague, and their phenomenology is more accurately described under this heading. In Coons' study of 50 patients with Dissociative Disorder N o t Otherwise Specified, 17 were found to have disorders with separate ego-states or identities, 16 had a spectrum of dissociative symptoms he termed "not further specified" (in which a wide variety of dissociative symptoms were present without any reaching a diagnosable threshold for a dissociative disorder), 10 suffered dissociative psychoses (many dissociative features with psychotic dimensions in association with another psychosis), 3 had gender identity disorders with dissociative features (personas with different genders, but without an amnestic barrier between them), one had the Ganser syndrome, and one a nocturnal dissociative disorder (in which separate identities are noted, but only nocturnally, arising from apparent sleep, but with wake electroencephalograms). As a group, 96% of these patients reported histories of childhood abuse or neglect. 82% suffered depression. In clinical practice, many patients who achieve this diagnosis appear to have autohypnotically based

Table VI Description of Dissociative Disorder Not Otherwise Specified This category is included for disorders in which the predominant feature is a dissociative symptom (i.e., a disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment) that does not meet criteria for any specific Dissociative Disorder. Examples include: 1. Clinical presentations similar to Dissociative Identity Disorder that fail to meet full criteria for this disorder. Examples include presentations in which a) there are not two or more distinct personality states, or b) amnesia for important personal information does not occur. 2. Derealization unaccompanied by depersonalization in adults. 3. States of dissociation that occur in individuals who have been subjected to periods of prolonged and intense coercive persuasion (e.g., brainwashing, thought reform, or indoctrination while captive). 4. Dissociativetrance disorder: single or episodic disturbances in the state of consciousness, identity, or memory that are indigenous to particular locations and cultures. Dissociative trance involves narrowing of awareness of immediate surroundings or stereotyped behaviors or movements that are experienced as being beyond one's control. Possession trance involves replacement of the customary sense of personal identity by a new identity, attributable to the influence of a spirit, power, deity, or other person, and associated with stereotyped "involuntary" movements or amnesia. Examples include Amok (Indonesia), bebainan (Indonesia), latah (Malaysia), pibloktoq (Arctic), ataque de nervios (Latin America), and possession (India). The dissociative or trance disorder is not a normal part of a broadly accepted collective cultural or religious practice. 5. Loss of consciousness, stupor, or coma not attributable to a general medical condition. 6. Ganser syndrome: The giving of approximate answers to questions (e.g., "2 plus 2 equals 5") when not associated with Dissociative Amnesia of Dissociative Fugue.

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symptoms resembling trance phenomena gone out of control.

I. Example I. (Ego-State Disorder)

Table VII ResearchCriteria for Dissociative Trance Disorder A.

Either (1) or (2): 1. Trance, i.e., temporary marked alteration in the state of consciousness or loss of customary sense of personal identity without replacement by an alternate identity, associated with at least one of the following: a. narrowing of awareness of immediate surroundings, or unusually narrow and selective focusing on environmental stimuli; b. Stereotyped behaviors or movements that are experienced as being beyond one's control. 2. Possession trance, a single or episodic alternation in the state of consciousness, characterized by the replacement of customary sense of personal identity by a new identity. This is attributed to the influences of a spirit, power, deity, or other person, as evidenced by one (or more) of the following: a. stereotypic and culturally determined behaviors or movements that are experienced as being controlled by the possessing agent; b. Full or partial amnesia for the event

B.

The trance or possession trance state is not accepted as a normal part of a collective cultural or religious practice.

C.

The trance or possession trance state causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.

D.

The trance or possession trance state does not occur exclusively during the course of a Psychotic Disorder (including M o o d Disorder With Psychotic Features and Brief Psychotic Disorder) or Dissociative Identity Disorder and is not due to the direct physiological effects of a substance or a general medical condition.

A woman presented with depersonalization, derealization, inner voices, and depression. Behind these voices were over a dozen apparent identities, most of which were not very elaborate. Usually she experienced their voices and feelings as intrusive symptoms. There was no contemporary amnesia, nor did the other identities directly assume executive control. In her predominant personality she had amnesia for documented childhood abuse.

2. Example 2. (Dissociative Disorder Not Further Specified) A woman with recurrent major depression had amnesia for some aspects of her childhood abuse, rare episodes of time loss, depersonalization, and one or two brief fugues. Several evaluations for Dissociative Identity Disorder were negative. As dissociative disorders continue making their way into the clinical mainstream, it is likely that some of these symptom complexes will be accorded recognition as separate mental disorders. The treatment of the various forms of Dissociative Disorder Not Otherwise Specified usually follows the approaches helpful for the types of dissociative disorder they most resemble. Ego-state disorders respond nicely to the therapy used for Dissociative Identity Disorders, for example. Patients whose symptoms resemble trance phenomena often respond well to approaches that teach them autohypnotic self-regulation, allowing the restructuring of their dysfunctional dissociative experiences.

IX. DISSOCIATIVE TRANCE DISORDER This diagnostic entity is included in D S M - I V among those conditions that have not been accepted, but are considered worthy of further study. Its essential feature is an involuntary state of trance that is not a normal aspect of cultural or religious practice that causes clinically significant distress or impairment. Those afflicted either manifest an altered response to their environment, or feel or appear to be possessed or taken over by some other identity, usually a spirit, power,

deity, or person. In the latter case, there usually is amnesia for the possession experience. Diagnostic criteria are in Table VII. These conditions tend to be episodic with a duration from minutes to hours. Although pathological trance phenomena appear to be ubiquitous and most aspects of them appear reasonably uniform across cultures, possession trance states often are profoundly influenced by culture both with regard to the identity of the entities encountered, the nature of the behaviors performed in the altered state, associated sensory alterations (such as anesthesia to pain, blindness, etc.), and the nature and degree of amnesia. Many have sufficient distinctness to be regarded as culture-bound syndromes. Trance phenomena often appear to have an autohypnotic or dissociative mechanism. They appear related to dissociated memories and/or intense intrapsychic conflicts out of conscious awareness. Trance

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possession states appear to share these substrates, but achieve their unique forms of expression from the patient's cultural and social surround.

A. Trance The patients are clearly out of contact with the environment and are preoccupied with inner experiences. In general they do not communicate with those who attempt to speak to them, do so in a rudimentary manner, or reveal that they are disoriented to the contemporary environment, and are reacting to events of the past or inner preoccupations. They often are still, and may be mistaken as catatonic. However, some rock, engage in stereotyped behaviors or movements, or appear to be reenacting a past scenario. Some verbalize, often with distress and/or agitation, and may be hard to understand. These episodes are self-limited, but may recur. The patient usually is amnestic for the trance; for some there is a dreamlike or depersonalized recollection.

I. Example A woman whose young son died tragically some years ago periodically lapses into altered states during which she appears to be rocking a baby in her arms and crooning a silent lullaby. At these times she is unresponsive to others' conversation and physical efforts to attract her attention.

B. Possession Trance State Here the manifestations dramatize the patient's experience of being taken over by another entity. Commonly, the patient is amnestic while another entity controls behavior, but cases exist in which the patient is aware of the entity's intrusion and contends with it for the control of behavior. Some such circumstances are ego-syntonic and sought out, such as when the patient speaks in the voice of a benign advisor or mentor, as in mediumistic trance, and do not come under the aegis of this condition if they do not cause dysfunction. However, in circumstances when the entities are not benign, the experience of the patient may be terrifying. The actions of the entity may lead to self-injury or suicide. Nemiah holds that those who feel they are possessed by evil spirits have guilt-laden conflicts over personal transgressions, but many cases demon-

strate other dynamics, such as identification with an aggressor. I. Example A professional man from Haiti was noted to periodically lapse into states in which his voice and behavior changed, and he spoke in a French dialect. At such times he assembled a series of objects, impervious to others' attempts to intervene, and chanted over them. He was amnestic for these episodes, which endangered his career. A physician who spoke French examined him under hypnosis and found that in these altered states he experienced himself as an evil spirit trying to call up still other evil spirits.

C. Treatment Dissociative trance disorder usually responds to the same sort of treatment strategies used for the more familiar dissociative disorders. A supportive therapeutic environment must be established, and the pace of the therapy must respect the vulnerability of the patient to being overwhelmed in the process of reacquiring access to the dissociated material. The dissociated mental contents must be explored with techniques that can reaccess them and manage the abreaction of whatever painful emotions are associated with them. Hypnosis and drug-facilitated interviews may prove useful. Patients are helped to gradually work through the traumata and/or conflicts, to retain what had been dissociated in conscious awareness, and to master new strategies of managing their residual impacts. Often autohypnotic strategies can restructure pathological dissociative trances, and teach patients to master them. When dealing with many possession trance states, the strategies useful in managing dissociative identity disorder, informed by a sensitivity to the cultural elements of the condition, are often effective.

D. Comment Often as traditional societies with indigenous possession trance states become industrialized, and as their citizens are educated to accept worldviews that are more universal and secular, the incidence of these conditions decreases except in remote areas and ethnic enclaves that preserve old beliefs and practices. When this occurs, often dissociative identity disorder, a lai-

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cized expression of the older trance possession states, and related forms of dissociative disorder not otherwise specified, begin to occupy the psychopathological niche once held by them.

X. DISSOCIATIONAND MEMORY One of the most complex and controversial aspects of the study of the dissociative disorders is the relationship between dissociation and memory. While many traumatized individuals remember what has befallen them, many individuals with dissociative disorders, posttraumatic stress, and related conditions have either blocked out memory of their traumatization or only have partial, fragmentary, and/or intermittent recollection. Williams demonstrated that as many as 38% of girls with documented childhood abuse did not report a documented episode of abuse when reinterviewed at 17-year follow-up. Kluft found many instances in which long-forgotten abuses recovered in psychotherapy, often with hypnosis, could be documented. Additionally, genuinely traumatized individuals may have and/or recover distorted and/or inaccurate recollections of abuse. Both relatively accurate and relatively inaccurate memories may be found in the same patient. As a consequence, although there is consensus that many dissociative disorder patients have suffered severe traumatization, the only test of the accuracy of an apparent recollection of abuse is external corroboration by some form of documentation or by some witness whose corroboration or failure to corroborate the allegation would not be patently self-serving. A denial by an alleged perpetrator has no more face validity than the accusation made against him/her.

The study of this area has been compromised by a failure to distinguish between the constructs of "truth" that are useful in psychotherapy, science, and the court of law. Neither of these constructs are necessarily consistent with historical truth, but all are useful in particular contexts.

BIBLIOGRAPHY Cardena, E. (1994). The domain of dissociation. In S. J. Lynn & J. w. Rhue (Eds.), Dissociation: Clinical and theoretical perspectives (pp. 15-31). New York: Guilford. Coons, P. M. (1992). Psychogenic amnesia: A clinical investigation of 25 cases. Dissociation, 5, 73-79. Coons, P. M. (1992). Dissociative disorder not otherwise specified: A clinical investigation of 50 cases with suggestions for typology and treatment. Dissociation, 5, 187-195. Hermon, J. L. (1992). Trauma and recovery. New York: Basic Books. Kluft, R. P. (1995). The confirmation and disconformation of memories of abuse in DIO patients: A naturalistic study. Dissociation, 8,253-258. Kluft, R. P., & Fine, C. G. (1993). Clinical perspectives on multiple personality disorder. Washington, DC: American Psychiatric Press. Michelson, L. K., & Ray, W. J. (Eds.).(1996). Handbook ofdissociation. New York: Plenum. Putnam, F. W. (1989). Diagnosis and treatment of multiple personality disorder. New York: Guilford. Ross, C. A. (1997). Dissociative identity disorder: Diagnosis, clinical features, and treatment of multiple personality disorder (2nd ed.). New York: Wiley. Spiegel, D. (Section Editor). (1991). Dissociative disorders. In A. Tasman & S. M. Goldfinger (Eds.), American Psychiatric Press review of psychiatry (Vol. 10) (pp. 141-275). Washington, DC: American Psychiatric Press. Steinberg, M. (1994). Interview guide to the Structured Clinical Interview for the Diagnosis or DSM-IV Dissociative Disorders-revised. Washington, DC: American Psychiatric Press.

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DSM-IV John J. B. Allen University of Arizona

I. The Purpose of Diagnosis II. A Brief History of the Development of the DSM-IV and Its Predecessors III. Organization and Contents of the DSM-IV IV. Evaluation of Diagnostic Systems: Reliability and Validity V. Challenges to Validity and Future Directions in Diagnosis

for those with a mental disorder. Reliability Consistency of diagnosis. If diagnoses can be assigned reliably, an individual will be assigned the same diagnosis across differing circumstances (e.g., different diagnosticians). Validity The extent to which a diagnosis is meaningful. A valid diagnosis allows that individuals with the diagnosis can be distinguished from individuals with other diagnoses and from individuals with no diagnosis. Valid diagnoses should also provide useful information about the etiology, treatment, or prognosis of the mental disorder.

Comorbidity The co-occurrence of two or more mental disorders in the same individual. Diagnosis The determination of the nature of a disease. Although in most branches of medicine this implies that the cause of the disorder has been identified, this is often not the case with psychiatric diagnosis using the DSM-IV, which involves assigning a diagnostic label on the basis of the observed and/or reported behaviors and symptoms. Etiology The cause of a disorder. Heterogeneity The situation where individuals who share the diagnosis of a particular disorder do not share all symptoms in common. A heterogeneous disorder is one where people with the disorder can present with a variety of different symptoms. Mental Disorder The DSM defines mental disorder as a pattern of behavior, or psychological features, occurring in an individual that are currently associated with any of the following: a subjective sense of distress; impairment in important areas of function, such as work, school, relationships; or a significantly increased risk of posing a danger to oneself or others, or of losing an important freedom. Prognosis Estimating the likely course and outcome

DSM-IV is the abbreviation for the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. The DSM-IV details the diagnostic criteria for nearly 300 mental disorders, and nearly 100 other psychological conditions that might be the focus of professional attention, thereby providing a standardized system of classification that is intended to be used internationally. The DSM-IV also provides systems for noting medical conditions and stressors that may be related to the psychological conditions, and for noting how the individual's functioning (for example, job performance or ability to care for one's self) may be affected.

I. THE PURPOSE OF DIAGNOSIS Diagnosis of psychological symptoms using the DSMIV entails classifying observable symptoms, or reports

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of such symptoms, into discrete categories termed mental disorders. A mental disorder (defined above) represents a pattern of behavior or psychological features that in some way causes the person distress or impairment. Moreover, a mental disorder is conceptualized in the DSM-IV as a problem or dysfunction that resides within an individual, rather than a problem that results from a conflict between that individual and society. This caveat is important because it is supposed to prevent the misuse of diagnostic labels for the purpose of social control, applying them to individuals whose values or beliefs differ from those of the majority. Assigning a diagnosis using the DSM-IV does not necessarily suggest that the etiology (cause) of the symptoms is known, but only than an individual's symptoms meet the criteria for the particular mental disorder. For example, two individuals might meet the criteria for a diagnosis of Major Depressive Disorder, but might develop these symptoms after a very different set of circumstances; one person might experience these symptoms only after a series of troubling setbacks (e.g., financial, legal, and relationship problems) while another might experience these symptoms after an apparently unstressful period. Although one might imagine that the etiology of the depression differs for these two individuals, they would both receive the same diagnosis using the DSM. Assigning a diagnostic label may have profound implications for the person receiving the diagnosis. On the one hand, diagnostic labels may allow individuals to receive the treatment they are seeking. On the other hand, such labels may have a stigmatizing effect for the person diagnosed. Consider, for example, how you might think about yourself, and how others might begin to think about you and to treat you, if they learned you had received a diagnosis of a severe psychosis--schizophrenia. Diagnostic labels convey a wealth of information, some of it intended, some of it not. Because assigning a diagnostic label may have profound effects on how people may view the person who receives the label, the diagnosis of mental disorders should be taken seriously, and should have the potential for some clear benefits for those diagnosed. What, then, is the purpose of diagnosing mental disorders? First, diagnosis should help us identify a homogeneous group of individuals. For example, many different disorders may entail delusions--beliefs that most persons in an individual's culture

DSM-IV

would regard as false, such as the belief that one can read verbatim another's thoughts. Yet despite similarity in this particular symptom, individuals with delusions may differ in important ways. Delusions are associated in some cases with the ingestion of psychoactive substances (e.g., amphetamines), in others with a disturbance in mood (e.g., mania or depression), and in others with hallucinations and disorganization of thought (e.g., schizophrenia). These different diagnoses, while sharing a symptom in common, may differ in other important ways. By identifying patterns of symptoms that tend to occur together, important differences between individuals with a common symptom may be identified, such as the cause of the disorder, the most effective treatments, or the prognosis for the future. Second, diagnosis should help in the planning of treatment. For example, the delusional behavior that can be seen in both mania and schizophrenia will typically be treated by different drugs. Similarly, knowing that the delusional behavior results from use of psychoactive substances suggests a different intervention; i.e., stopping use of the substance causing the symptom. Third, diagnosis can facilitate communication among professionals. A diagnostic label provides a succinct means of conveying information. For example, if, after an assessment interview, a mental health professional determines that an individual needs to be referred to another mental health professional or facility, the diagnostic label can summarize much of the information. Of course the diagnosis does not summarize all relevant information, but can reduce the amount of description required to round out the assessment picture. Another instance in which diagnostic labels facilitate communication is the case of communication between mental health professionals and insurance providers. Given particular diagnoses, insurance providers will authorize reimbursement for particular treatments, without the need to review the entire assessment interview.

II. A BRIEF HISTORY OF THE DEVELOPMENT OF THE DSM-IVAND ITS PREDECESSORS Over the last several thousand years, many systems have existed for diagnosing mental disorders. The DSM series is relatively recent, with the first edition of

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the Diagnostic and Statistical Manual (now referred to as DSM-I) appearing in 1952. The manual has been revised several times since, with the DSM-II appearing in 1968, the DSM-III appearing in 1979, a minor revision--the DSM-III-R~appearing in 1987, and the current version of the m a n u a l ~ t h e DSM-IV~ appearing in 1994. In contrast to the DSM series, most earlier systems detailed only a handful of diagnostic categories. Several categorization systems existed for use in the United States prior to the development of the DSM. These systems included: simple systems with between one and seven diagnostic categories to aid in collecting census data concerning mental illness during the nineteenth century; a system for statistically tallying information on patients in mental hospitals in the early twentieth century; a system developed by the U.S. Army, and modified by the Veteran's Administration, for use with servicemen; and several editions of a system developed by the World Health Organization (WHO). Since the latter part of the nineteenth century, the WHO had ben publishing the International Classification of Disease (ICD), a comprehensive listing of medical conditions. With the sixth edition (ICD-6), mental disorders were included for the first time. In each revision of the DSM series, an attempt was made to coordinate the system with the corresponding revision of the ICD system. Each of the disorders listed in the DSM-IV has a corresponding code in the most recent versions of the ICD, namely the ICD-9-CM and ICD-I O. The DSM-I was the product of The American Psychiatric Association Committee on Nomenclature and Statistics, and contained 106 mental disorders, with an emphasis on being clinically useful. DSM-II added 76 new disorders and, unlike its predecessor, encouraged rather than discouraged assigning multiple diagnoses to each patient. Both DSM-I and DSM-II were similar in format, providing a description of the disorder, but lacking detailed criteria by which to diagnose the disorder. DSM-III represented a major change, with each disorder possessing tangible, operational criteria. This change was inspired by research that showed that clinicians using the previous DSM versions failed to agree on a diagnosis for a surprisingly large percentage of the patients. Although inconsistency in information provided by the patients, and inconsistencies in the type of information gathered by clinicians could explain some of the disagree-

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ment, a vast majority of the problem lay with the diagnostic criteria themselves. The descriptions were overly broad, were often vague, sometimes included reference to unobservable processes, and often overlapped with descriptions of other diagnostic categories. The operational criteria of the DSM-III referred to observable or reportable symptoms, with specific numeric criteria for frequency and duration of symptoms. The DSM-III for the first time included a multiaxial system of diagnosis (see below), a feature that has been retained in subsequent revisions. In contrast to earlier systems, which contained only a few broad and severe diagnostic categories that were likely to be relevant to governmental and institutional interests, the DSM series was designed to be of use to the clinical psychiatrist; DSM therefore focused on a broader range of symptoms, including less severe forms of disturbance that might be treated outside of institutional settings. The origins of this trend began a decade prior to the publication of the DSM-I, as military and Veterans Administration psychiatrists found a need for additional diagnostic categories to cover the psychiatric conditions resulting from the stress of combat. These conditions were less severe and less chronic than the few severe categories that existed prior to World War II. Moreover, these conditions could be treated in an outpatient setting rather than through institutionalization. As a diagnostic system was developed to delineate these broader, less severe, diagnostic categories, it became impossible to unequivocally link each diagnostic category to a specific etiology. The DSM series, therefore, established diagnostic categories on the basis of the pattern of symptoms and their appearance over time, remaining largely agnostic with respect to etiology (with some clear exceptions). This descriptive categorical approach defines discrete categories of mental illness, based primarily on observable symptoms. In contrast to an etiologically based system, where each diagnostic category is included because a cause has been scientifically established, the decision to include a diagnostic category in the descriptive system must be based on informed judgments of experts as to whether the symptoms co-occur in such a manner to merit the inclusion of a discrete category defining those symptoms. Although such judgments will ideally be influenced by scientific research, some subjectivity is inevitable. The development of DSM-IV, in particular, in-

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volved many individuals chosen for their expertise in a variety of areas. A 27-member DSM-IV Task Force worked with 13 Work Groups, each comprised of up to a dozen members. Additionally, each task force relied on the advice of committees of up to 100 people. Members of these committees represented many different specializations and professions, with medical doctors having the largest representation. Over the course of 6 years, a three-step process was followed to increase the likelihood that changes would be based on the basis of research findings, rather than the whim of committee members. This three-step process involved literature reviews, reanalysis of previously collected data sets, and field trials to assess the reliability of several alternative criterion sets. New diagnostic categories were included when the Task Force considered that sufficient evidence existed to justify the addition of a new category in terms of antecedent indicators (e.g., family history or precipitating situations), concurrent indicators (e.g., physiological and psychological symptoms that co-occur), and predictive indicators (e.g., response to treatment, prognosis). Conversely, in a few instances, a category from the DSM-III-R was removed when insufficient evidence existed to merit retaining it. The DSM-IV, therefore, ideally represents the informed scientific judgment of many experts in the mental health field. On the other hand, these judgments are inevitably shaped and limited by the current scientific knowledge base, the previous diagnostic systems that form the basis for scientific research, the particular composition of the Task Force and Work Groups, and the idiosyncratic preferences of these various committee members. The DSM-IV, therefore, may best be viewed as one more chapter of a work in progress.

III. ORGANIZATION AND CONTENTS OF THE D$M.IV The DSM-IV details a multiaxial system of diagnosis, meaning that individuals are assessed in multiple areas, or along multiple dimensions or axes. Axis I contains 15 major classes of mental disorders. Axis II contains personality and developmental disorders. Axis III contains medical conditions. Axis IV provides for the notation of psychological, social, and environmental stressors that may affect diagnosis. Axis V provides for a measure of the individual's function in

areas such as work, social activities, and self-care. The multiaxial system is designed to encourage a comprehensive evaluation of biological, social, and psychological factors relevant to each person's presenting symptoms. The multiaxial system also provides a means for detailing differences between those with identical diagnoses. With respect to the example provided at the beginning of the chapter--two depressed individuals who developed symptoms after different life events--Axis IV would provide a way of summarizing that one individual developed depression only after a series of troubling setbacks while another developed depression in the absence of such events.

A. Axis I: Clinical Disorders and Other Conditions That May Be a Focus of Clinical Attention Almost all mental disorders or conditions that may be a focus of clinical attention appear on Axis I, with a few exceptions that appear on Axis II. Axis I organizes mental disorders into 15 major groups of disorders, as presented in Table I. Most of the groups in Table I were created based on the similarity of symptoms of disorders within that group, although in some cases disorders are grouped together because of the typical age at which symptoms first appear (Disorders Usually First Diagnosed in Infancy, Childhood or Adolescence), or because of common etiology (Mental Disorders due to a General Medical Condition, SubstanceRelated Disorders, Adjustment Disorders). In many cases, an individual may receive more than one Axis I diagnosis, although some diagnoses by definition will preclude another diagnosis. Each disorder on Axis I includes a set of diagnostic criteria, which are typically a combination of monothetic (i.e., all conditions of the criterion must be met) and polythetic (i.e., only some from among a larger set of conditions must be met) criteria. For example, to diagnosis Attention Deficit/Hyperactivity disorder, an individual must meet the following criteria: (a) either 6 or more symptoms (from among 9) of inattention, or 6 or more symptoms (from among 9) of hyperactivity-impulsivity (polythetic); (b) some symptoms are present and causing impairment before age 7 (monothetic); (c) impairment is seen in at least two settings, such as school and home (monothetic); (d) the symptoms clearly cause impairment in functioning (monothetic); and (e) the symptoms are not

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Table I

Examples of Disorders in Each of the 15 Major Groups Listed on Axis I of DSM-IV Group

Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence Delirium, Dementia, and Amnestic and Other Cognitive Disorders Mental Disorders Due to a General Medical Condition Substance-Related Disorders Schizophrenia and Other Psychotic Disorders Mood Disorders Anxiety Disorders Somatoform Disorders Factitious Disorders Dissociative Disorders Sexual and Gender Identity Disorders Eating Disorders Sleep Disorders Impulse-Control Disorders Not Elsewhere Classified

Examples of Disorders Attention Deficit/Hyperactivity Disorder, Autistic Disorder Dementia of the Alzheimer's Type, Vascular Dementia Mood Disorder Due to a General Medical Condition (e.g., stroke, hypothyroidism) Alcohol Abuse, Nicotine Dependence, Caffeine Intoxication, Cocaine Withdrawal Schizophrenia, Delusional Disorder, Schizoaffective Disorder Major Depressive Disorder, Bipolar I Disorder (aka Manic Depression), Dysthymic Disorder Agoraphobia, Social Phobia, Panic Disorder, Obsessive-Compulsive Disorder, Posttraumatic Stress Disorder Somatization Disorder, Hypochondriasis Factitious Disorder Dissociative Identity Disorder (formerly Multiple Personality Disorder), Dissociative Amnesia Sexual Dysfunctions (e.g., Male Erectile Disorder), Paraphilias (e.g., Exhibitionism, Pedophilia), Gender Identity Disorder Anorexia Nervosa, Bulimia Nervosa Primary Insomnia, Narcolepsy, Sleep Terror Disorder Kleptomania, Pyromania, Pathological Gambling .

better accounted for by another mental or physical disorder (monothetic). Polythetic criterion sets have advantages and disadvantages. The primary advantage is that polythetic sets reduce the number of diagnostic categories required, since people with highly similar but nonidentical symptoms can receive the same diagnosis. If, by contrast, each and every criterion were required, such highly similar people would require different diagnoses. The primary disadvantage to polythetic criterion sets is symptom heterogeneity, where people with the same diagnosis may be quite different in terms of their symptoms. In fact, in the case of some disorders, it is possible that two individuals with the same diagnosis may not share a single symptom in common. [See ATTENTION DEFICIT HYPERACTIVITY DISORDER (ADHD).] There are also disorders that appear on Axis I that do not have such clearly defined criterion sets. There are over 40 disorders that include "NOS" in their name, an abbreviation for Not Otherwise Specified. These disorders are diagnosed if the symptoms resemble those of another diagnosis but fail to meet the full criteria required for diagnosis. For example, Anxi-

.

.

.

.

.

.

.

,,

ety Disorder NOS is a diagnosis for cases in which there is "prominent anxiety or phobic avoidance that do not meet the criteria for any specific Anxiety Disorder" (p. 444) or meet criteria for Adjustment Disorder. [See ANXIETY.] Also found for each disorder (other than NOS disorders) listed on Axis I are other sections providing more detailed information that may be of use to clinicians. The Diagnostic Features section provides an overview of the essential features of the disorder, along with examples and definitions of criteria and terms that are part of the criterion set for that disorder. The Subtypes and~or Specifiers section delineates subtypes of the disorder (e.g., Catatonic Subtype of Schizophrenia) or specifiers of the disorder (e.g., Postpartum Onset for Major Depressive Disorder), where applicable. The Recording Procedures section includes information to assist in reporting the correct name of the disorder and the associated five-digit code that corresponds to the disorder. These five-digit codes correspond to the codes listed in the International Classification of Disease (9th edition, with clinical modification), the diagnostic system of the

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World Health Organization that includes both medical and mental disorders. The Associated Features and Disorders section describes symptoms that, while not necessary for the diagnosis of the disorder, are often seen in persons with the disorder. This section also includes a listing of other mental disorders that are commonly comorbid (likely to co-occur) with the disorder, and includes a listing of laboratory findings, clinical findings from examination, and medical conditions that may be associated with the disorder. The Specific Age, Culture, or Gender Features section details information concerning how the symptoms of a disorder may differ as a function of these demographic variables, including how symptoms may present differently in children and the elderly, how particular symptoms of the disorder may present differently in different cultures, and the proportion of women and men among those with the disorder. The Prevalence section provides information estimating how common the disorder is thought to be. These estimates are taken from largescale epidemiological studies when possible, and include estimates of point prevalence (prevalence at any point in time) as well as lifetime prevalence (the proportion of people that in their lifetimes will experience the disorder). The Course section details information concerning onset and progression of symptoms, as well as the prognosis for remission and for relapse. In this section are included the typical age (or ages) of onset, factors that may predispose one to develop the disorder, and information concerning whether symptoms may worsen or improve with age. Also included in this section are estimates of whether a disorder is likely to involve one episode, multiple episodes with symptom-free periods between episodes, or chronic unremitting symptoms. The Familial Pattern section summarizes evidence concerning whether the disorder and related disorders are more common in the firstdegree biological relatives of those with the disorder than members of the general population. This section also summarizes the results of twin or adoption studies, when available. Finally, the Differential Diagnosis section provides information to assist the diagnostician in distinguishing the disorder from other disorders that may appear similar or that may share symptoms in common. This section highlights the differences between disorders that could possibly be confused (e.g., Major Depressive Disorder versus Adjustment Disorder with Depressed Mood or, in the elderly, Dementia). [See DEPRESSION.]

DSM-IV

B. Axis I1: Personality Disorders and Mental Retardation On Axis II are listed Personality Disorders and Mental Retardation. These disorders, by definition, are present for a substantial period of time (i.e., years). Although Axis I disorders may also be present for similar lengths of time, enduring symptoms are fundamentally part of these Axis II disorders. Also listed on Axis II are other traits or prominent features of a person's personality that a clinician deems maladaptive (e.g., frequent use of denial, excessive impulsivity). In addition to the Personality Disorders, Mental Retardation appears on Axis II and is defined by (a) significantly below average intellectual abilities; (b) significant problems with adaptive functioning, defined as serious problems in carrying out duties expected for the person's age (e.g., self-care, interpersonal skills, work); and (c) an onset of these symptoms before the age of 18. Mental Retardation is placed on Axis II because of its pervasive and persistent effects on a person's function. It is worth noting that in the previous version of the DSM (DSM-III-R), other developmental disorders such as Autism and learning disorders were also listed on Axis II; these disorders, however, are listed on Axis I in DSM-IV. [See AUTISM AND PERVASIVE DEVELOPMENTAL DISORDERS; MENTAL RETARDATION AND MENTAL HEALTH.]

As the term Personality Disorder implies, people with these disorders have characterological features that create difficulties. DSM-IV defines a Personality Disorder as follows: A Personality Disorder is an enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual's culture, is pervasive and inflexible, has an onset in adolescence or early adulthood, is stable over time, and leads to distress or impairment (p. 629).

Upon a casual reading of the criteria for the various personality disorders, one may see many descriptions that may seem applicable to oneself or others at times. Symptoms of various personality disorders include, as examples, emotional lability, feelings of emptiness, bearing grudges, lacking close friends, suspiciousness, impulsivity, suggestibility, feeling envious, concern with criticism or rejection, difficulty in making everyday decisions, and perfectionism. In fact, many writers have criticized the DSM series' Personality Disorders for pathologizing anyone who simply may be different, or difficult. A Personality Disorder, how-

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ever, can (in theory) be distinguished from what might be considered normal variation in personality because a Personality Disorder is persistent, pervasive, and

pathological. By persistent, it is meant that the pattern of behavior in Personality Disorders is consistent over time. Whereas people without personality disorders may from time to time, after a bad day or following certain triggering events, display some of the features of certain personality disorders (e.g., difficulty controlling anger), such persons do not do so often or with any consistency. By pervasive, it is meant that the behavior in Personality Disorders is seen across many different situations in the person's life. Whereas people without personality disorders may demonstrate some features of certain personality disorders in restricted situations (e.g., one is extremely suspicious of a difficult coworker; e.g., one doubts the fidelity of a spouse or sexual partner after a previously difficult and unfaithful relationship), such persons do not do so across situations (e.g., with coworkers, with spouse or partner, and with neighbors). By pathological, it is meant that the severity of the symptom in Personality Disorders exceeds that which would be considered acceptable or normal by most people. Hot tempers, while not well-liked, are not necessarily pathological, but repeatedly getting into physical fights could be considered excessive. Daydreaming of a life more fantastic than one's own may be an occasional brief escape, but losing hours lost in fantasy could be considered excessive. Impulsive spontaneity can be fun, but impulsivity that results in overextended spending sprees, sexual indiscretions, or reckless driving could be considered excessive. Feeling empty and lonely are a part of the human condition, but suicide attempts that result from these feelings could be considered excessive. In each of these examples, what makes the behavior pathological in Personality Disorders involves the intensity of the subjective feeling, an impairment in judgment, and the degree to which the subjective feeling is translated into unacceptable or problematic behavior. The personality disorders are organized by their apparent similarity into three clusters. Cluster A, the odd and eccentric cluster, includes the Paranoid, Schizoid, and Schizotypal Personality Disorders. Cluster B, the dramatic, emotional, and erratic cluster, includes the Antisocial, Borderline, Histrionic, and Narcissistic Personality Disorders. Finally, Cluster C,

the anxious and fearful cluster, includes the Avoidant, Dependent, and Obsessive-Compulsive Personality Disorders. In addition to general criteria for Personality Disorders, each disorder has its own polythetic criterion where an individual must have some minimum number (ranging from 3 to 5 for various disorders) from among a larger number (ranging from 7 to 9 across disorders) of symptoms. [See OBSESSIVE-

COMPULSIVEDISORDERS;SCHIZOPHRENIA.]

C. Axis II1: General Medical Conditions On Axis III are listed general medical conditions that may be relevant to the disorder(s) listed on Axes I and II. The presence of Axis III should not be taken to suggest a mind-brain dualism, with Axes I and II representing problems of the mind in the absence of a physiological basis. On the contrary, mental experience is rooted in the function of the brain. Axis III is included in the DSM to encourage a comprehensive evaluation and a consideration of the various ways in which a general medical condition may be related to mental disorders. There are several ways in which medical conditions may be related to mental disorders. First, the medical condition may be the direct cause of the mental condition. For example, hypothyroidism (Axis III) can lead to a syndrome of depressed mood known as Mood Disorder due to Hypothyroidism (Axis I). Similarly, Alzheimer's Disease (Axis III) produces Dementia of the Alzheimer's type (Axis I), and systemic infections (Axis III) can produce a Delirium (Axis I). [See

ALZHEIMER'SDISEASE;DEMENTIA.] The second manner in which a general medical condition may be relevant to a mental disorder is that the medical condition may be related to the development of the mental disorder, but not through direct physiological means. For example, an Axis I disorder such as Major Depression or Adjustment Disorder with Depressed Mood might follow in reaction to learning of one is diagnosed with a malignant melanoma (Axis III). Finally, an Axis III medical condition, while not related to the appearance of the symptoms of a mental disorder, might be relevant in the treatment of a disorder. For example, certain antidepressant medications might be ill-advised in the presence of certain cardiovascular conditions. Alternatively, someone with a severe psychosis (Axis I) might have a medical condition (Axis III) that needs careful monitoring or

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treatment (e.g., diabetes), and might be unable to adhere to the treatment without assistance.

D. Axis IV: Psychosocial and Environmental Problems Axis W is included for detailing psychological, social, and environmental problems that may be relevant to the presenting mental disorder. Such problems may have influenced the development of the disorder, may have developed as a consequence of the disorder, may be relevant to the selection of an appropriate treatment, or may influence the prognosis for recovery. Although both positive (e.g., job promotion) and negative (e.g., job loss) life events can be perceived as stressful, typically only the negative events are detailed on Axis IV unless the positive event is clearly related to the mental disorder. Moreover, only events during the last year are typically noted, unless remote events still appear to be a significant influence on the mental disorder. Examples of problems that could be listed on Axis IV include death of a loved one, divorce, problems with school, unemployment or other job problems, homelessness or a difficult living situation, financial troubles, lack of insurance, legal troubles, or experiencing a natural disaster. A careful assessment of the problems listed on Axis IV may suggest that, in some cases, the most appropriate intervention will not focus on the individual (as is the case with psychological counseling or the prescription of psychotropic medication), but rather on the broader social environment in which the individual must exist. In such cases, the primary intervention could involve not only mental health professionals (e.g., providing family therapy), but teachers, landlords, lawyers, insurance companies, and so on. On the other hand, some mental disorders may arise in the relative absence of psychosocial and environmental problems and suggest that the treatment might most fruitfully focus on the individual.

tinuum of mental health to mental illness and range from 100 (exemplary) to I (inordinately poor). Taken into account in making the rating are the person's psychological, social, and occupational functioning. Limitations due to purely physical limitations (e.g., spinal cord injury) are not considered when making the rating. The severity of psychological symptoms and the potential for suicide or violence are important determinants of the person's functioning rating. Global functioning is typically rated for the period surrounding the current evaluation, although it may be useful to rate, in addition, previous time periods to provide an indication of how well or poorly the individual may function at other times. At the top end ofthe scale (81-100)are people who are models of mental health. These scores are reserved for those fortunate individuals who not only are without impairment, but exhibit many of the traits considered to be mentally healthy (superior functioning, wide range of interests, social effectiveness, warmth, and integrity). Just below this range (71-80) are individuals with no significant symptoms or impairment, but who lack the positive mental health features. Below this range are scores that will likely characterize a majority of individuals in need of psychological or psychiatric treatment. Those in the upper range (31-70) will most likely be capable of receiving outpatient treatment, whereas those in the lower range (1-40) will most likely require inpatient treatment.

F. Appendices to the DSM-IV Included in the DSM-IV are 10 appendices. The appendices include a guide to facilitate differential diagnosis, a glossary, alphabetical and numerical listings of the diagnoses described in the manual, a summary of changes between the DSM-IV and the previous version of the DSM, comparisons of DSM-IV codes to the codes in two editions of the International Classification of Diseases, and a listing of contributors. Worth special mention are two other appendices,

Criteria Sets and Axes Provided for Further Study,

E. Axis V: Global Assessment of Functioning Axis V provides a scale for the assessment of a person's overall level of functioning. Ratings reflect a con-

and an Outline for Cultural Formulation and Glossary of Culture-Bound Syndromes. The first of these lists entries that were considered for inclusion in the DSM-IV, but were not included due to insufficient evidence. The disorders or axes are listed in the appendix to encourage research that will provide sufficient evi-

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dence to include or exclude these entries from future editions of the DSM. The appendix encourages researchers to study refinements in these sets of criteria. Examples of entries in this appendix include Caffeine Withdrawal, alternative descriptions of Schizophrenia and other disorders related to Schizophrenia, other variants of depressive disorders, Premenstrual Dysphoric Disorder, Mixed Anxiety-Depressive Disorder, a series of Medication-Induced Movement Disorders, and Passive Aggressive Personality Disorder (which appeared as an Axis II disorder in the previous edition of the DSM). The proposed Axes include a scale to measure strategies for coping with emotional states, termed the Defensive Functioning Scale, and two scales modeled after Axis V to measure functioning in specific areas (relationships, and social/occupational). The appendix covering cultural variations in the presentation of mental disorders provides information that might be of assistance in evaluating individuals from cultures other than one's own. One could mistakenly label as mental illness behaviors that appear abnormal from one's own culture, but that would not be regarded as aberrant by members of the culture from which the individual originates. For example, hearing voices is typically considered a psychotic symptom by members of the mental health community, although within some religious groups the experience is supported and interpreted as an experience that is to be heeded or revered. When diagnosing, one needs to take into account how such symptoms would be viewed by fellow members of an individual's culture, which may be include religious, ethnic, racial, and geographic influences.

IV. EVALUATIONOF DIAGNOSTIC SYSTEMS: RELIABILITY AND VALIDITY A discussion of the validity of a diagnostic system must first assume that diagnoses can be assigned reliably. Reliability of diagnosis simply means that the same diagnoses will be assigned to individuals across different circumstances. Such different circumstances might involve the passage of time (in the case of testretest reliability) or different diagnosticians (in the case of inter-rater reliability). Because symptoms of mental illness often wax and wane, test-retest reliability may not be the most appropriate means of assessing the reliability of diagnosis, since we might

expect diagnoses to change over time. The standard method of assessing the reliability of the diagnosis of mental illness, therefore, is inter-rater reliability, or the extent to which two (or more) independent raters agree on the presence or on the absence of a mental illness.

A. Calculation of Inter-Rater Reliability In assessing inter-rater reliability, one could simply calculate the overall proportion of agreement between two independent raters. This approach, however, fails to account for the proportion of time that two raters would agree merely by chance. For example, imagine that two raters agree on the presence or absence of depression 70% of the time. Although this might appear promising, one needs to compute the likelihood that they would agree by chance alone. To illustrate, imagine that these two diagnosticians each "diagnose" 100 individuals for depression with the flip of a coin. Each diagnostician therefore labels 50 individuals depressed, and 50 nondepressed. Of the 50 individuals labeled depressed by the first diagnostician, half (25) will also be diagnosed as depressed by the second diagnostician (since the second diagnostician is independently "diagnosing" by a coin flip). Similarly, among the 50 individuals labeled nondepressed by the first diagnostician, 25 will be similarly labeled by the second diagnostician. Therefore, by chance alone, these two diagnosticians would agree for 50 (25 + 25) of the 100 individuals. Of course diagnosticians do not diagnose by coin flips, but the calculation of chance agreement follows in a similar fashion. Assume that in a particular clinic, based on the observation of symptoms, each diagnostician identifies half of the patients as depressed. Also assume, for the moment, that the diagnosticians' ratings agree only for reasons of chance. The raters would agree that 25 of the patients merit a diagnosis of depression, and would agree that 25 do not, yielding an overall agreement of 50/100 cases, or 50%. The actual agreement of 70%, while higher than that expected by chance, is not as promising as it initially appeared. To account for chance agreement, a corrected estimate of agreement, termed Kappa, is often calculated: PO m PC K

-1

--

Pc

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Kappa reflects the extent to which the observed proportion of agreement (Po; e.g., 70%) exceeds the proportion of agreement expected by chance (p~; e.g., 50%), expressed as a proportion of the difference between perfect agreement (1.0) and chance agreement (e.g., 50%). Stated differently, Kappa reflects the improvement beyond chance actually obtained by the diagnosticians, expressed as a proportion of the maximum possible improvement beyond chance. Kappa therefore ranges from 0 (chance agreement) to 1.0 (perfect agreement). A Kappa of .50, for example, would indicate that the agreement of the diagnosticians fell midway between chance and perfect agreement. In the hypothetical example above, where 70% agreement was obtained, but .50% was expected by chance: K.

P o - P~ . 1 -pc

.

.70 - .50 . 1 -.50

.20 .50

.40

For DSM-III diagnoses, Kappas range from near 0 to near 1. Reliability data, while provided as an appendix in DSM-III, have been conspicuously absent from DSM-HI-R and DSM-IV manuals. The reliability data from the DSM-IV field trials is promised to appear in Volume V of the DSM-IV Sourcebook, a compendium of the literature reviews and empirical research on which DSM-IV is based. Two years after the publication of the DSM-IV, however, only Volumes I and II of the Sourcebook have appeared in print. It is reasonable to assume that Kappas will again span a broad range, but on average be slightly higher than those associated with earlier versions of the DSM. While Kappa provides a simple metric for summarizing agreement beyond chance, Kappa is not a panacea. Kappa is influenced by base rates of diagnosis, and Kappa provides no direct evidence of validity. The base-rate problem results when diagnoses are assigned very frequently or virtually never. In such cases, even small increases beyond chance can result in an appreciable value of Kappa. This can be problematic since the rate of many mental disorders in the general population is rather low. Imagine that two diagnosticians agree on only 4 % more cases than would be expected by chance for a disorder that affects 5 % of the population. If each of these diagnosticians label 5% of the sample with the diagnosis, they will agree that 90.25% (.95 * .95) of the people do not have the disorder, and will agree that fewer than 1% (.05 * .05 =

.25 %) of the people have the disorder. In other words, by chance alone, they would agree 90.5 % of the time. If their actual agreement exceeds this by 4 % (94.5 %), Kappa would be .42. As can be seen from the preceding examples, it required agreement that was 20% higher than that expected by chance to achieve a Kappa in the range of .4 when the baserate of diagnosis was in the range of 50%, but it only required agreement that exceeded chance by 4% to achieve a similar Kappa when the base rate was quite low. The interpretation of Kappa is not absolute, as Kappa is considerably influenced by the base rate of diagnosis. A second form of the base-rate problem stems from the fact that the base rate of disorders may vary dramatically by setting. For example, while schizophrenia is quite rare in the general population, it is considerably more prevalent among patients in a psychiatric hospital. Because the value of Kappa is influenced by the baserate of the diagnosis, Kappa can vary by setting even when raters apply criteria consistently across these settings. The second caveat to consider is that Kappa provides no direct evidence of the validity of diagnosis. High values of Kappa merely indicate agreement. In fact, independent of any correspondence to the actual symptoms, perfect agreement (K = 1.0) would be obtained if both diagnosticians agreed that every individual had the diagnosis in question. Therefore, while high values of Kappa may be necessary to ensure validity, they are by no means sufficient. Moreover, it is possible to alter diagnostic criteria to improve interrater agreement as indexed by Kappa, but to sacrifice validity in the process. For example, by making the criteria for a disorder increasingly tangible, one might increase agreement at the expense of making the criteria so narrow that many individuals no longer meet the criteria, despite having symptoms that many people would consider to be essential features of the disorder. A final caution to keep in mind when considering the reliability of diagnosis, whether it be measured by Kappa or some other index, is that two raters can disagree for a variety of reasons, only some of which may reflect a poor system of diagnostic classification. For example, the particular method used to assess the symptoms (e.g., a standardized interview versus an unstructured interview) can determine what symptoms are elicited. Moreover, poor training of the diagnosticians can also lead to poor reliability. Research

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studies of mental illness, therefore, typically employ highly trained diagnosticians who use a standard structured interview to inquire about each of the symptoms of the disorder under study. Reliability, therefore, should not be the sole standard by which the adequacy of diagnostic criteria are judged. Although this sounds obvious, there is a tendency for researchers to use high reliability as evidence of the adequacy of diagnostic criteria; this may be tempting since a single number can provide a summary of reliability whereas establishing validity is considerably more complicated.

B. Validity When considering whether a set of diagnostic criteria have validity, one is asking whether assigning the diagnostic label provides valuable informationm beyond the specific symptoms that begot the diagn o s i s - a b o u t a person with a particular diagnosis. There may be many such external indicators of validity, but three of the most important would include etiology, treatment, and prognosis. Additionally, and perhaps most primary, a valid system of diagnosis should allow one to clearly make distinctions between one disorder and another, and between a disorder and the absence of a disorder. Individuals who share a diagnosis should be similar to one another (in terms of symptoms, etiology, response to treatment, or prognosis) and should be clearly different than individuals with other diagnoses or individuals with no diagnosis. If such a clear delineation is not possible, then there is insufficient evidence to justify the existence of the diagnostic category. The DSM-IV in particular has been criticized for inadequately distinguishing between mental disorders and normal variations in behavior. For example, although significant depressive symptoms that follow the death of a loved one are considered a normal reaction (for a period, incidentally, of up to 2 months), depressive symptoms following other major losses or setbacks (e.g., divorce, diagnosis with a terminal illness) are considered evidence of the mental disorder Major Depression. In terms of etiology, a valid system would ensure that people with the same diagnostic label would share a common etiology. In some instances in the DSM-IV, this is clearly the case (e.g., Alcohol Withdrawal Delirium, also known as "delirium tremens"); in other instances, it is likely that people with the same

diagnosis may have different etiological influences (e.g., Major Depressive Disorder). In terms of treatment, a valid system should suggest particular treatments that are likely to be effective for a particular disorder. Alternatively, since no treatments are 100% effective, a valid system should inform us of the likelihood that different treatments may be effective for the disorder. For example, given an episode of Major Depression that has lasted less than 2 years, there is a 50 to 70% chance that an individual will experience remission using one of several antidepressant medications, or by receiving one of two varieties of psychotherapy. In terms of prognosis, a valid system should provide an indication of what is likely to happen in the future given that a person has a particular diagnosis. For example, given that a person has experienced one episode of Major Depression, there is approximately a 50% chance that the person will experience another at some point in life. Given that one has a personality disorder diagnosis, it is likely that the pattern of behavior will continue for quite some time, if not indefinitely.

V. CHALLENGESTO VALIDITY AND FUTURE DIRECTIONS IN DIAGNOSIS The DSM-IV, like its predecessors, has adopted a descriptive categorical approach to diagnosis, which assumes that there exist discrete categories of mental illness that can be defined--for most diagnoses-primarily on the basis of observable symptoms. Discrete categories of illness dichotomize individuals into those who do, and those who do not, have the illness; borderline cases are categorized into one or the other category (or given one of the may NOS diagnoses). When the etiology of an illness is known, the categorical approach is defensible and is likely to provide useful information. For example, people either do or do not have a history of a stroke. Within the category of those with strokes, there are certainly gradations in severity, but there is a clear delineation between those who have, and those who have not, experienced a stroke. In the case of most mental disorders, by contrast, there are not such obvious distinctions between the presence and the absence of the condition. For example, DSM-IV requires that five of nine symptoms be present in order to make the diagnosis of a Major

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Depressive Episode. Certainly people who meet four of the nine symptoms are not free of depression, yet they would not be categorized as having a Major Depressive Episode. Strictly speaking, a categorical approach assumes that there exist necessary and sufficient features for categorical membership. Although the DSM-IV adopts a categorical approach, there are many instances of disorders that do not have necessary or sufficient criteria. Consider for example, the case of ObsessiveCompulsive Personality Disorder, for which an individual must meet at least four of eight possible criteria to receive the diagnosis. None of the individual criteria are necessary and, moreover, two individuals could both meet criteria and share not a single one of the criteria in common. In other words, there can exist considerable heterogeneity in symptoms among those who share a common diagnosis. Strictly speaking, a categorical approach also assumes that categories are either nested, or mutually exclusive. For example, a square is a special (nested) case of a rectangle, but is mutually exclusive with the category of circle. For diagnoses of mental illness, by contrast, there exists considerable overlap (comorbidity) of diagnoses. A recent large-scale community study found that, across the life span, about one-sixth of the population had three (or more) diagnoses, and that this group accounted for over half all diagnoses. Such high comorbidity certainly raises questions as to whether the categorical approach to diagnosis is justified. When comorbidity of diagnoses is observed, it is unclear whether the different disorders reflect different manifestations of the same underlying cause, whether one disorder served to facilitate the development of another, or whether the disorders resulted from different underlying causes and merely cooccurred by chance. Comorbidity can also present an enigma in terms of treatment, as it can be unclear which disorder to treat, or how to coordinate treatments for different disorders. A modification to the classical categorical approach is the prototype approach, in which exemplars (also known as prototypes) of a given diagnosis become the standard for comparison. Each individual is compared to the diagnostic prototypes, and assigned the diagnosis associated with the best-fitting prototype. Such a system has several advantages. Such a system eliminates the problem of borderline cases,

since such cases will receive a diagnosis if they are more similar to the diagnostic prototype than to any other prototype. Such a system also virtually eliminates the need for the NOS categories, which in the DSM seem to have become the "wastebasket" for many borderline or unusual cases. On the other hand, a prototype system has its drawbacks. Prototypes stem from the perceptions of the diagnosticians, and therefore may fail to reflect important features of a disorder that are not easily observable (e.g., lab findings). Moreover, the use of prototypes may make the identification of new disorders more difficult, and instead simply reify the implicit theories that people have about forms of mental illness. Finally, to distinguish mental health from mental illness, one would presumably require a prototype of mental health. Although it could be difficult to define a single prototype for each diagnostic category, it might be even more challenging to define the prototype(s) for mental health. Other modifications to the categorical approach of the DSM-IV have been proposed, including eliminating categories entirely. The dimensional approach involves assessing individuals along a set of relevant dimensions. Under such a system, an individual would receive a quantitative rating along each dimension in the diagnostic system. Although the conceptual simplicity of a category may be lost using such a system, such a system could possibly convey more information about each individual, would eliminate the problem of classifying borderline cases, and would have no problems of comorbidity. On the other hand, many diagnosticians prefer the yes-or-no simplicity of categorical diagnosis, and may be likely to establish idiosyncratic cutpoints on the dimensions, such that those individuals scoring above a certain value would be considered to have a particular categorical diagnosis. Additionally, it is no trivial matter to determine the relevant set of dimensions to use in such a system. In the final analysis, there may exist some types of problems for which a categorical system is well-suited, and others where a dimensional approach may hold greater utility. The DSM-IV is already an amalgam of different approaches to categorization, with some diagnoses clearly defined by etiology, and others defined solely by the presence of particular symptoms. This may reflect the nature of different forms of mental illness. Some forms may have a single causal factor that

DSM-IV

is more potent than all other contributing factors, and have a homogeneous set of symptoms that appear. Others, by contrast, may have multiple determinants, and may present with a heterogeneous set of symptoms that differ for each individual. The DSM-IV is the current version of the most widely-used diagnostic system for mental disorders. If history provides an accurate indication, many other revisions~some major, and some m i n o r ~ a r e likely to follow, with considerable controversy and debate surrounding each.

BIBLIOGRAPHY American Psychiatric Association (1987). Diagnostic and statistical manual of mental disorders (3rd ed., revised). Washington, DC: American Psychiatric Association. American Psychiatric Association (1994). Diagnostic and statistical

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manual of mental disorders (4th ed.). Washington, DC: American Psychiatric Association. Cantor, N., Smith, E. E., deSales French, R., & Mezzich, J. (1980). Psychiatric diagnosis as prototype categorization. Journal of Abnormal Psychology, 89, 181-193. Clark, L. A., Watson, D., & Reynolds, S. (1995). Diagnosis and classification of psychopathology: Challenges to the current system and future directions. Annual Review of Psychology, 46, 121-153. Kessler, R. C., McGonagle, K. A., Shanyang, Z., Nelson, C. B., Hughes, M., Eshlemen, S., Wittchen, H., Kendler, K. (1994). Lifetime and 12-month prevalence of DSM-III-R Psychiatric Disorders in the United States: Results from the National Comorbidity Study. Archives of General Psychkatry, 51, 8-19. Kirk, S. A., & Kutchins, H. (1992). The selling of DSM: The rhetoric of science in psychiatry. New York: Walter de Gruyter, Inc. Robins, L. N., & Barrett, J. E. (1989). The validity of psychiatric diagnosis. New York: Raven Press Ltd. Rosenhan, D. L. (1973). On being sane in insane places. Science, 179,250-258. Wakefield, J. C. (1996). DSM-IV: Are we making progress? Contemporary Psychology, 41,646-652.

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I

Epilepsy HenryA. Buchtel Ann Arbor Veterans Administration Medical Center and University of Michigan

I. II. III. IV. V. VI. VII. VIII. IX. X. XI.

Overview Prevalence and Incidence Classification of Epileptic Seizures Impact on the Individual with Epilepsy Causes and Diagnosis Nonepileptic Seizures Effects of Epilepsy on Cognition Personality Changes and Behavioral Problems Treatment Options Epilepsy Advocacy Groups Future Directions

considered pejorative and the term psychogenic seizures is preferred). Seizure An episode of abnormal activity in the brain that causes a disturbance of consciousness or of sensory/motor functions. Seizure Focus A defined area in the brain that is the origin of an epileptic seizure. EPILEPSY is a behavioral manifestation of a brain disturbance that causes synchronous firing of large numbers of neurons. Its incidence in the population and the severity of the disability in millions of individuals makes this a serious health problem worldwide. Diagnosis depends on a careful analysis of the person's behavior and the pattern of neuronal activity in the brain, sometimes supplemented by brain imaging studies. In some individuals, there is no discernible physiological cause of the seizures and a diagnosis of psychogenic seizures will be made, often with the help of someone in the mental health field. Psychologists and social workers often play a role in the choice of treatments and their implementation. Another role of the mental health worker is to point the person with epilepsy or that person's family to groups in the community and national groups that are dedicated to helping persons with this disorder.

Antiepilepsy Drug (AED) Medication prescribed to control seizures. Aura A feeling or sensation that frequently precedes the seizure. Electroencephalogram (EEG) Recording of electrical activity of the brain, usually with small flat electrodes glued to the scalp. Epilepsy Surgery Surgical removal of brain tissue that has been identified as responsible for the seizures, or cutting of the neural band connecting the two hemispheres (surgery is generally sought when the seizures cannot be controlled by antiepilepsy medication). Febrile Seizure A seizure that occurs during a high fever, experienced by about 5 % of children. Ictal Discharge Abnormal firing of neurons in synchrony during a seizure, frequently consisting of a repetitive "spike and wave" pattern. Pseudoseizures Nonepileptic episodes that otherwise resemble real ("organic") seizures (the term is

I. OVERVIEW Unlike most medical conditions, epilepsy is entirely defined by and diagnosed on the basis of publicly ob-

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Copyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

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servable behavior: the epileptic seizure. Purists will argue that epilepsy is not a disease but rather the symptom of an underlying neurological condition. Usually the seizure disorder is accompanied by an obvious abnormality in the electroencephalogram (EEG), but the presence of abnormal brain waves in the EEG is not a necessary condition for diagnosis. The condition has serious consequences for schooling, psychosocial development, and employment. Life expectancy is also reduced for persons with epilepsy, with mortality rates 2 to 4 times those of matched nonepilepsy persons. Treatment options have increased markedly in the past 50 years, and strictly behavioral treatments have been developed. Opportunities for a normal life with epilepsy are greatly improved compared with even a generation ago, and persons with seizures and their families are being involved increasingly in choosing treatments. The earliest known descriptions of epilepsy are in the writings of Hippocrates (ca. 460-ca. 377 BC), most notably in his essay titled "On the Sacred Disease," so named because in ancient Greece, the inexplicable cause of seizures had led to the common belief that the person with epilepsy was periodically possessed by spirits (in more recent times, demons). Hippocrates denounced such interpretations as charlatanism and argued that this was a human disease with physical causes. In this interesting essay he also refers to the shame that is felt by those who have seizures, although it is clear from the following quote that he thought children would seek comfort whereas adults would choose to be alone during the seizure: But such persons as are habituated to the disease know beforehand when they are about to be seized and flee from men [to a place] where as few persons as possible will see them falling . . . . This they do from shame of the affliction, and not from fear of the divinity, as many suppose. And little children at first fall down wherever they may happen to be, from inexperience. But when they have been often seized, and feel its approach beforehand, they flee to their mothers, or to any other person they are acquainted with, from terror and dread of the affliction, for being still infants they do not know yet what it is to be ashamed. (~15)

Many extraordinary individuals have had epilepsy, and writers have for centuries suggested a connection between genius and epilepsy. Although some of the early cases may be better classed as having episodes of insanity (Aristotle, who compiled a list of ancient epileptics, agreed with the Hippocratic view of a close relationship between epilepsy and insanity, which at

that time was attributed to black bile), the behaviors described often sound very much like seizures. Intriguingly, some have suggested that an aggressive drive needed for success may be caused by temporal lobe epilepsy. A partial listing of early famous persons with behaviors that may have been epileptic include Pythagoras (b580 BC), Socrates (b470 BC), Alexander the Great (b356 BC), Caesar (bl00 BC), Caligula (b12 AD), and Mohammed (b569). Some later figures for whom epilepsy is clearly established or very likely include Petrarch (b1304), Charles V of Spain (b1500), St. Teresa of Avila (b1515), Cardinal Richelieu (b1585), Louis XIII (b1601), Moliere (Childhood; b1622), Pascal (b1623), Peter the Great (b1672), Handel (b1685), Napoleon (b1769), Paganini (b1782), Byron (b1788), Shelley (b1792), Dickens (Childhood; b1812), Edward Lear (b1812), Dostoyevski (b1821), Flaubert (b1821), Nobel (b1833), William Morris (b1834), Swinburne (b1837), Tchaikovsky (b1840), de Maupassant (b1850), and van Gogh (b1853). Interestingly, epilepsy among Queen Victoria's relatives in the late nineteenth century led to the founding of the internationally renowned National Hospital for the Paralysed and Epileptic at Queen Square, London (now known as The National Hospital for Neurology and Neurosurgery). It is probably obvious that these famous individuals are mentioned frequently in essays and articles for the general public in order to demythologize the illness and to provide inspiration for persons with epilepsy by showing that a normal or even extraordinary life can be led by persons with the disorder.

II. PREVALENCE AND INCIDENCE Estimates of the prevalence of epilepsy in the general population, that is, the ratio of individuals affected to those unaffected, have varied from 2 per 1000 to 50 per 1000. The variability reflects the different definitions of what constitutes epilepsy (e.g., Does the diagnosis require a minimum seizure frequency? Are febrile seizures included? How accurate is the diagnosis?). On average, the most accurate estimates suggest that the prevalence is around 5 per 1000, meaning that in a city of 1,000,000 there would be 5000 individuals with seizures. Thus in the United States, with a population of around 250,000,000, there are approximately 1.5 million individuals with a seizure disorder. Twenty per-

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cent of these will have intractable seizures (uncontrollable using current treatments). Over a lifetime, I in 20 individuals (5 % ) will have at least one seizure; of those that have a seizure, 12 % will develop chronic epilepsy (this suggests that the prevalence should be .12 x .05 or 6/1000 rather than 5 / 1 0 0 0 - - t h e discrepancy probably reflects the increased death rate among persons with epilepsy, which is described in more detail in the next section. The incidence of epilepsy (new cases in a particular time period) has been estimated to be about 0.5 to 1.0 per 1000 per year, meaning that in a group of 1,000,000 individuals there would be about 500 to 1000 new cases each year. Data from studies in Great Britain indicate that most seizure disorders begin in the age range of 0 to 4 years (.75/1000). The next most common ages of onset are 15 to 19 years (.53/1000), 10 to 14 years (.44/1000), and 5 to 9 years (.33/1000). All other age groups have incidence rates below .23/1000. Males and females appear to be equally affected; there are more left-handers with epilepsy than would be expected by chance.

III. CLASSIFICATION OF EPILEPTIC SEIZURES In 1970, an international group established a classification scheme according to the type of seizure, consisting of four general classes, each with several subcategories, as shown in Table I.

IV. IMPACT ON THE INDIVIDUAL WITH EPILEPSY Seizures are not just unpleasant and embarrassing experiences for the person with seizures. Epilepsy entails a significant increase in morbidity and mortality. Particularly important for the mental health clinician is the increased risk for serious depression (around 5 % across all kinds of epilepsy and 3 to 4 times the national average; among persons with epilepsy, suicide is listed as cause of death in 7 to 22% of deaths). Studies since the turn of the century have consistently shown that the life expectancy of persons with epilepsy is shorter than in the rest of the population; the death rate of children with epilepsy 0 to 5 years of age is 1.3 times greater

Table I

International Classification of Epileptic Seizures .

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I. Partial seizures (seizures beginning locally) A. Partial seizures with elementary symptomatology (generally without impairment of consciousness) 1. With motor symptoms (includes Jacksonian seizures) 2. With special sensory or somatosensory symptoms 3. With autonomic symptoms 4. Compound forms B. Partial seizures with complex symptomology (generally with impairment of consciousness); temporal lobe or psychomotor seizures 1. With impairment of consciousness only 2. With cognitive symptomology 3. With affective symptomology 4. With "psychosensory" symptomatology 5. With "psychomotor" symptomatology (automatisms) 6. Compound forms C. Partial seizures secondarily generalized II. Generalized seizures (bilaterally symmetrical and without local onset) 1. Absences (petit mal) 2. Bilateral massive epileptic myoclonus 3. Infantile spasms 4. Clonic seizures 5. Tonic seizures 6. Tonic-clonic seizures (grand mal) 7. Atonic seizures 8. Akinetic seizures III. Unilateral seizures (or predominantly) IV. Unclassifiedepileptic seizures (owing to incomplete data) .

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than that of the general population; from 5 to 24 years of age, the rate is 6.6 times greater; and from 24 to 25 years of age, the rate is 3.7 times greater. During the period when persons with epilepsy were typically institutionalized, as many as 50% of them died of causes either directly or indirectly associated with their seizures. Among those whose deaths were directly attributed to seizures, about 12% died of status epilepticus (a continuous and uncontrollable seizure); many others died of the accumulative effects of multiple injuries sustained during seizures. Still important but not directly life-threatening, childhood epilepsy also negatively affects educational achievement and, regardless of the age of onset, has an impact on the person's eventual employment level. About one third of children with epilepsy receive special educational support, and IQ increases linearly as

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a function of age of onset (from 83 for adults whose seizures began in infancy to 102 for those with adult onset). Equally serious, and probably not unrelated to the person's educational experiences, a person's ability to find employment is greatly reduced by epilepsy. In a 1973 survey, almost one half of persons with epilepsy reported that they had been turned down for a job because of their epilepsy, and 30% reported that they had lost at least one job because of seizures. Various studies over this century have shown that the unemployment rate among working-age persons with epilepsy is between 2 and 7 times the rate of unemployment in the general population. In general, an employer has the right to ask a prospective employee if he or she has any medical condition that will interfere with successful carrying out of the duties, so the reduction in employment opportunities may not be entirely the product of a prejudice against epilepsy itself. Loss of the ability to drive a car is mentioned by most persons with epilepsy as a major loss (the period of being seizure-flee before driving again differs from place to place; e.g., in Michigan, it is 6 months, in Ontario, Canada, I year). There have been reported cases of birth defects for women who use antiepileptic drugs (AEDs). In the overall population, the rate of birth defects is 2 to 3 %, and the rate is slightly higher (0.5 %) for women with epilepsy who are not taking medication. Women taking a single AED have a risk of about 6 to 7%, with some medications being more problematic than others. Taking several AEDs increases the risk even more. Unfortunately, seizure frequency may go up during pregnancy, so the need for AEDs may even increase. In some cases, the person's physician may feel that the risks of pregnancy are too great for the mother and child, and recommend that pregnancy be avoided. Finally, some AEDs reduce the effectiveness of oral birth control pills. As discussed later, the genetics of epilepsy suggest that children may inherit a predisposition to epilepsy, but not epilepsy itself. This means, for example, that a head injury would more likely lead to a seizure disorder if the person has close relatives with epilepsy. Persons with epilepsy frequently suffer consequences when bystanders do not know what to do when they see a seizure occur. It was once believed that a soft object should be inserted between the person's teeth to prevent biting the tongue during a seizure. This is now highly discouraged. The proper re-

sponse, if any, depends on the kind of seizure. In general, only a person having a generalized tonicclonic seizure (grand mal) needs attention, and in this case the greatest help consists of remaining calm, helping the person gently to the floor, and loosening any tight clothing. Hot or sharp objects that could cause harm should be moved away. Placing a cushion or folded piece of clothing beneath the person's head can reduce the chance of a head injury, and turning the head to one side so the saliva can escape is a good idea. It is useless to try to interrupt the seizure; when the seizure is over, the person may need to rest or sleep. Seizures usually stop within several minutes, but if the seizure continues for 10 minutes or more, or if seizures follow in succession without a period of complete recovery, then medical attention should be sought (this could signal the beginning of status epilepticus). Focal (simple partial) seizures do not require any action on the part of observers. A person having a complex partial seizure should not be restrained unless the person is placing him/herself in danger. As in the case of a generalized seizure, hot or sharp objects should be removed. Partial seizures sometimes progress to a generalized seizure (secondarily generalized), so further precautions may be necessary.

V. CAUSESAND DIAGNOSIS When classified according to the known or putative origin of the seizure disorder, there are three etiological categories.

1. Symptomatic Epilepsy. Symptomatic epilepsy comprises cases in which the seizures are one of the clinical manifestations of a neurological disorder, such as tuberous sclerosis, Sturge-Weber syndrome, and cerebral degenerative diseases. Alcohol withdrawal seizures would also fit into this category. 2. Secondary or Organic Epilepsy. This type of epilepsy results from nonspecific cerebral changes or damage that is permanent and nonprogressive, such as head trauma or perinatal anoxia (i.e., temporary lack of oxygen during a difficult delivery). 3. Idiopathic Epilepsy. This epilepsy is also referred to as cryptogenic, essential, pure, primary, or true. These are cases in which the cause is unknown; genetic factors may be involved in the etiology. About 75 to 80% of all cases of epilepsy are of this type.

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An enormous amount of work has been dedicated to uncovering the biochemical events that are responsible for an epileptic seizure. It is likely that seizures are caused by a lack of inhibition in the region of the epileptogenic focus rather than by an increase of excitation of the neurons in that area, but both factors may need to be present for the initiation of many if not most seizures. An important factor thought to be involved in the development and expansion of an epileptogenic seizure focus is the so-called "kindling" phenomenon. This was discovered by Goddard at McGill in the 1960s while testing Hebb's theory of synaptic changes in learning and memory. Goddard found that if a restricted subcortical brain region of a rat was stimulated electrically over many days, an initially innocuous stimulus would eventually lead to seizures, presumably because of the establishment or strengthening of pathways that convey the excitation of the stimulus from a localized area to a more widespread region, and thereby eventually synchronous activity of the whole brain (a seizure). Although the causal connection is still controversial, the development of an epileptogenic focus in another part of the brain has been attributed to this kindling effect, with the "mirror focus" in the homologous position of the opposite hemisphere being a special candidate for this designation. There are two distinct steps in the process of diagnosing epilepsy. First, the neurologist or general physician has to be convinced that the spells, which are almost always described secondhand by someone not well trained in observation, are characteristic of epilepsy and not some other illness, organic or otherwise (Table II). Abnormal EEGs are very helpful in confirming that the seizures probably have a physiological (organic) rather than psychogenic cause, but epileptiform brain activity (i.e., EEG abnormalities characteristic of epilepsy) can also be found in indi-

Table II

Distinguishing Characteristics of Epileptic and Nonepileptic Seizures a

Epileptic seizure Usual onset <12 years Emotional but adequate description No "shortage of breath" as aura

Nonepileptic seizure Onset >12 years Patient evades direct questions Shortage of breath or hyperventilation

Table II

Continued

Epileptic seizure

Seldom visual aura Cannot resist beginning of seizure Often rising epigastric sensations in aura Status epilepticus not frequent Bilateral synchronous tonic and clonic jerks Seldom turning of head Incontinence occurs Bystanders not often hit With bilateral jerks, unconsciousness Short period of atonia after falling Understandable injuries, biting of tongue With bilateral tonic-clonic seizure, no speech No rapid shivering More flexion of trunk than extension Neurological signs often present After tonic-clonic seizures, minutes of coma Seldom crying afterward Malaise and passive afterward In focal epilepsy, seizures in sleep Usually some benefit from anticonvulsants Bystanders worried Seizures usually not seen by doctor Patient speaks about epilepsy only Seldom non-anticonvulsant co-meds

Nonepileptic seizure Often visual aura (twinkles/ colors) Often lengthy fights against the seizures No rising epigastric sensation Often very long seizures {up to hours) Alternating left and right jerks Alternating turning of head, often quick Incontinence very rare Bystanders often hit or kicked Can remember bilateral jerks Long periods of atonia Automutilation, strange injuries Massive jerks together with speech Rapid shivering Arching of back No neurological signs on examination Consciousness after massive jerks Often crying afterward Either relieved or complaining afterward No seizures during sleep No or inconsistent reaction to AEDs Bystanders often irritated by patient Doctors often see seizures Patient speaks of all kinds of complaints History of many other drugs taken

aThe presence of characteristics in the nonepileptic seizure column does not constitute sufficient evidence that the spells have a psychogenic origin. However, a preponderance of characteristics in this column would certainly raise the question that at least some of the person's spells may be nonorganic in origin.

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viduals without seizures, and some persons with epilepsy have an apparently normal EEG between seizures. In rare cases, the seizure focus is too deep in the brain to be discerned by scalp electrodes, and the EEG will remain normal even during a seizure. If the spells are determined to be epileptic in nature, their cause needs to be found as that will dictate the appropriate treatment (e.g., medication or surgery). Sometimes the seizure is the first manifestation of the presence of a brain tumor. In this case, the malignancy of the tumor will need to be determined so the benefits of surgery can be weighed. If the seizure occurs in childhood, both the child and the family will need to be educated about epilepsy and the importance of following a medication regimen. In some patient groups, the cessation of seizures under medication control for 2 to 5 years may mean that the medications can be safely stopped without a return to seizures (stopping the medication too soon can lead to a resumption of seizures, which may now be harder to stop, possibly because of kindling effects as described earlier).

VI. NONEPILEPTIC SEIZURES The vast majority of seizures have an organic basis, and mental health workers should assume that a patient or client with seizures has no control over their frequency, duration, or form. However, some seizures are nonorganic in origin and will need to be treated by nonmedical therapies. Nonepileptic seizures may be under conscious control (malingering), presumably because of secondary gain, or they may be outside the patient's control (e.g., Munchausen syndrome) and difficult to understand in terms of a supposed "reward" for the behavior. When the seizure is believed to be nonorganic in origin, it has been called a pseudoseizure or hysterical seizure, although these terms are generally discouraged because their pejorative connotations may interfere with effective communication with the individual and his or her family. One should also be aware of the fact that the majority of nonepileptic seizures occur in individuals who also have organically determined seizures (this probably explains why they are so good at mimicking the seizure behavior). Withdrawal symptoms from alcohol dependency may occur for several days after abstinence. It is thought that postsynaptic supersensitivity is caused by alcohol's prolonged inhibition of a particular trans-

mitter system in the brain (the glutamatergic system). With alcohol withdrawal, approximately 15% of individuals will experience seizures, which can be successfully treated or prevented with anticonvulsants and/or sedatives (e.g., diazepam [Valium] or chlordiazepoxide [Librium]). The seizures in such cases are not expected to continue beyond the acute withdrawal period. Of course, individuals with a history of frequent falls during intoxication are at increased risk of seizures from brain damage, and in such cases, seizures may occur as a consequence even without the added effect of withdrawal. Recurrent hospitalization and detoxification appears to lead to increased risk for seizures at a subsequent detoxification, suggesting a kindling effect.

VII. EFFECTSOF EPILEPSY ON COGNITION The performance of epilepsy patients on cognitive tests has been of great help in exploring the brain organization involved in perception, thinking, and reasoning. Memory functions of patients who have a seizure focus in the temporal lobe (or who have had an excision of part of their temporal lobe) have been particularly informative in breaking down memory functions into their component parts. A small number of patients have focal motor seizures that leave consciousness and cognitive abilities intact, but the vast majority of persons with epilepsy lose consciousness and are subsequently amnesic for the events that occurred during the episode. However, unlike the case of most psychiatric illnesses, these effects are discrete in time and the person can be entirely normal between seizures. Of significance for the mental health professional is that there can be lasting behavioral effects of the seizures (especially episodes of continuous seizure activity) and/or the effect of the brain damage that is the cause of the seizures in the first place. Factors to be considered when deciding whether a person is showing effects of a time-related decline in abilities include age of onset, the site of the focus or foci, treatment side effects (medication, surgery), effects of injuries sustained during a seizure (especially head injuries), and effects of status epilepticus or prolonged seizures with inefficient breathing. Age of onset has obvious effects on the acquisition of knowledge and on interpersonal relationships. Sometimes the effects of a seizure focus are direct (lowered attentional abilities), sometimes indirect (missing school for a school-

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age child). Overall, significant brain reorganization is much more likely if the brain damage and seizures onset occurs before the age of 6 years than after that age, with puberty providing a likely upper limit for the period of useful plasticity.

VIII. PERSONALITY CHANGES AND BEHAVIORAL PROBLEMS There has been much written about the so-called "epileptic personality," some sensible and some bordering on the ridiculous. Lennox and Lennox in their 1960 book, Epilepsy and Related Disorders, point out that many of the personality characteristics supposedly associated with epilepsy are actually frequently seen in many institutionalized patients suffering from a variety of debilitating chronic physical illnesses. Therefore they cautioned against an overarching assumption that the epilepsy itself may cause a personality disorder. Nevertheless, the particular characteristics of epilepsy (sudden loss of consciousness and other bodily functions, uncertainty about when a seizure will occur and what danger it may engender, the attendant problems dealing with family and friends, etc.) make it likely that individuals with seizures will be at increased risk for psychological problems. Joseph A. Schwartz, a psychiatrist who often works with epilepsy patients, has found that consultation requests by neurologists mention personality disorders about 10 times more often for epilepsy patients than for patients with other neurological disorders. He has proposed that the problems experienced by persons with epilepsy be referred to as "social apraxia" in order to remove the moral opprobrium usually associated with the term personality disorder. The auras themselves may resemble a psychotic experience (25% of auras involve a feeling or sensation; 15 % involve a change in mood). It is not uncommon to become fearful before, during, and after seizures. These emotional concomitants are naturally associated primarily with temporal lobe seizure foci (because of the connection with the limbic system), with mood disturbances being more associated with leftsided foci than with a right-hemisphere foci (approximately 65% vs. 45%). Interestingly, depressed mood is sometimes alleviated after a seizure in these patients, much as electroconvulsive shock has been shown to be helpful in cases of severe intractable de-

pression. Rarely, patients will experience a delayed psychotic episode 12 to 48 hours after a seizure. [See

DEPRESSION.] For these reasons and others, personality testing is often requested and may be used to help determine the origins of the various facets of the person's problem (especially in cases of possible nonorganic origins). Psychological assessments of epilepsy patients will naturally be tailored to reflect the needs of the patient and referral question. If the patient is being considered for epilepsy surgery, the assessment will include a full neuropsychological battery, with a focus on memory functions, but also assessing frontal, parietal, and occipital functions (prognosis for successful outcome is greatly improved if the neuropsychological findings point to a disturbance of functions of a single region of the brain). For psychosocial assessments, a commonly accepted instrument is Dodrill's 1977 Washington Psychosocial Seizure Inventory, a yes/no questionnaire of 132 questions about the epilepsy patient's feelings and attitudes concerning his or her seizure disorder (e.g., Do your seizures keep you from driving? Are you generally free from depression? Are you concerned people won't like you or want you around after a seizure?). There are 29 "Critical Items" that may suggest the need for further discussion or action (e.g., Do you often wish you were dead? Do you need vocational counseling?) and eight clinical scales assessing seven psychosocial areas and an overall index of adjustment: 1. Family Background (questions about relationships with family members, happiness, and security in the home, etc.) 2. Emotional Adjustment (questions about depression, feelings of hopelessness, fatigue, worry, etc.) 3. Interpersonal Adjustment (questions about the patient's relationships with people outside the family) 4. Vocational Adjustment (questions about problems at work) 5. Financial Status (questions about the patient's financial resources and feelings of financial security) 6. Adjustment to Seizures (questions about attitude toward the seizures, dread of the seizures, etc.) 7. Medicine and Medical Management (questions about the patient's perception of his or her doctors, compliance with medication regimen, etc.) 8. Overall Psychosocial Functioning

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After scoring the responses, the clinician plots the scores on each of the clinical scales, noting where the major concerns are focused and taking appropriate action if indicated.

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least in part the consequence of prejudice against the person with epilepsy, both by physicians and by the general public.

A. Medication (Drug) Therapies IX. TREATMENTOPTIONS In the fifth century BC, when Hippocrates wrote "The Sacred Disease," epilepsy was treated by purifications, incantations, and magical spells. Certain foods were forbidden, as were particular kinds of clothing (e.g., goat skin) and fabric colors. Hippocrates thought such "treatments" were fraudulent and argued convincingly (largely on philosophical grounds) that the disease should be treated as any other physical illnesses. He concluded that the disease was hereditary (as discussed earlier, a predisposing hereditary component is in fact present in some cases). Hippocrates' explanation for the onset of epilepsy seems absurd today, being based as it was on his theories on the effect of phlegm as it moves within the body and the brain (the weather, southerly winds in particular, also played a role in Hippocrates' explanation, mainly insofar as they affect the production of mucus). His prescribed treatment was vague and appears internally inconsistent: And in this disease as in all others, he [the physician] must strive not to feed the disease, but endeavor to wear it out by administering whatever is most opposed to each disease, and not that which favors and is allied to it. For by that which is allied to it, it gains vigor and increases, but it wears out and disappears under the use of that which is opposed to it. But whoever is acquainted with such a change in men, and can render a man humid and dry, hot and cold by regimen, could also cure this disease, if he recognizes the proper season for administering his remedies, without minding purifications, spells, and all other illiberal practices of a like kind. (721)

It is likely that further relevant details of treatment were passed from physician to student during medical apprenticeship (some have even suggested that the Hippocratic writings were meant only for lay people and were therefore purposefully uninformative, with treatment secrets reserved for one-on-one training). The prescription of treatments that are considered useless today continued well into this century. For reasons that are no longer clear, at the turn of the century even reputable physicians tried the so-called Corsican treatment, cauterization of the ears. Institutionalization of persons with epilepsy was common until the 1940s and they made up as much as 25% of the residents in institutional settings. This was at

Anticonvulsant medications are numerous and trials of new medications are common. Early attempts to find effective treatments do not sound very scientific by today's standards (Galen preferred mistletoe, reasoning that it is a plant that grows on oak and therefore resistant to falling, thus useful for the "falling disease," epilepsy). Bromides (sedatives made of compounds of bromine and another element, such as potassium) gained popularity in the second half of the nineteenth century and helped approximately half the patients, although side effects of long-term use (mental torpor) were unacceptable. The popularity of this drug was so great that around the turn of the century, over a ton of bromides were being delivered yearly to the main hospital treating epilepsy in London, England. In 1912, phenobarbital was found to control seizures better than any substance before it, and many of the current effective medications are variations on the molecular structure of this substance. All anticonvulsants will cause side effects if the dose is high enough, but none of these medications should have unacceptable side effects in the vast majority of patients if the serum levels are kept within the therapeutic range. Around 4% of pediatric patients will need to switch to another anticonvulsant because of the severity of the side effects of the medication. Table III

Common Antiepileptic Drugs (AEDs), Typical Effectiveness, and Relevant Common Side Effects (Registered names are for the United States unless otherwise notedp

Carbamazepine (1,2,3) b (Tegretol): Especially effective for partial seizures; behavioral side effects in approximately 30% of pediatric cases; useful in posttraumatic seizure disorders. Many cause mild sedation, ataxia, disequilibrium, and visual blurring. Clonazepam (4) (Klonopin, Rivotril): A benzodiazepine, often used as adjunctive therapy for absence seizures or generalized seizures; rarely the first choice except for myoclonic seizures (muscle jerks). May cause mild to severe sedation; rarely may cause ataxia, increased depression, or personality change. Ethosuximide (5) (Zarontin): Particularly effective for absence seizures; sedative and gastrointestinal side effects are common.

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Table III

Continued

Gabapentin (1,2,3)(Neurontin): Well tolerated; usually used as adjunctive therapy with other AEDs. May cause mild sedation, ataxia, and disequilibrium. Lamotrigine (1,2,3) (Lamictal): Usually used as adjunctive therapy with other AEDs. Side effects are less common than with carbamazepine and phenytoin. May cause mild sedation, ataxia, disequilibrium, and visual blurring.

Phenobarbital (1,2,3) (Luminal) Inexpensive, relatively safe. Previously used commonly with children, less commonly used with adults; behavioral side effects such as sedation or cognitive interference seen in up to 60% of pediatric cases. Rarely may cause increased depression and memory impairment. Phenytoin (1,2,3) (Dilantin): Especially effective for partial seizures; behavioral side effects in approximately 15 % of pediatric cases. May cause mild sedation, ataxia, disequilibrium, visual blurring, and sometimes gingival hyperplasia (swollen gums). Primidone (1,2,3) (Mysoline): Behavioral side effects in approximately 20% of pediatric cases. May cause mild to severe sedation, especially initially; rarely may cause increased depression and memory impairment.

Valproate (1,2,3,4,5) (Depakene, Depakote, Epival in Canada, Epilim in Great Britain): Gastrointestinal side effects at the beginning of therapy are common; behavioral side effects are seen in approximately 15 % of pediatric cases. May cause mild sedation, appetite stimulation (weight gain), and hair breakage. Less Common AEDs

Clobazam (1,2,3) (Frisium in Canada and Great Britain): May cause mild to severe sedation; rarely may cause ataxia, increased depression, or personality change. Diazepam (7) (Valium): A benzodiazepine. May cause mild to severe sedation; rarely may cause ataxia, increased depression, or personality change.

Felbamate (1,2,3,6) (Felbatol): May cause anorexia and weight loss, vomiting, and insomnia. Associated with unacceptably high incidence of aplastic anemia and hepatic failure. Nitrazepam (4) (Mogadon in Canada and Great Britain): See Clonazepam. Oxycarbazepine (1,2,3) Closely related to Carbamazepine, but with fewer interactions and possibly fewer side effects. Vigabatrin (1,2,3)(Sabril in Canada and Great Britain): May cause sedation and weight gain; rarely may cause encephalopathy and personality change. Zonisamide (1,2,3,4,6)(Excegran in Japan): May cause mild sedation and weight loss; rarely may cause memory impairment. aThe author thanks Linda Selwa and Thomas Henry for help in constructing this table. ~Typically used for: 1, simple partial; 2, complex partial; 3, tonic-clonic; 4, myoclonic; 5, absence; 6, atypical absence; 7, convulsive and nonconvulsive status epilepticus.

Table III gives common antiepileptic medications and descriptions of some of their side-effects.

B. Surgery Surgical removal of brain tissue or the cutting of intrahemispheric commissures (corpus callosotomy) to eliminate a seizure disorder may seem an extraordinary treatment, but as it has become clear that the origin of the seizure lies in the brain, it has in some cases become the most viable option. Because in most cases epilepsy surgery is elective (i.e., not necessary to preserve life), psychological and neuropsychological findings assume an unusual importance in the decisionmaking process. Psychologists, social workers, and others in mental health provide essential input into the decision about whether or not to proceed to surgery. For surgery to be considered, the following six conditions should be met: 1. The seizures are uncontrollable even with high doses of anticonvulsants. Or if the seizures a r e controllable with high doses of medication, the side effects at these levels are unacceptable or dangerous. A watershed decision is made at this step to establish candidacy for surgery. Even if condition 1 is satisfied, some patients and their families may not want to proceed further toward brain surgery because of the possible dangers of surgery or in the hope that an effective medication will be developed in the near future. 2. The seizures are intolerable to the person experiencing them (sometimes this means that the person may be unemployable or the seizures may be dangerous or extremely unpleasant). 3. All or most of the seizures arise from a single focal brain region (i.e., removal of the focus~usually scar tissue within the gray matter of the b r a i n ~ i s likely to eliminate or reduce the seizures because there is no other potential source of seizures). 4. This seizure focus is accessible (i.e., it is in a part of the brain that can be exposed during surgery without undue risk to the patient). 5. The tissue that would need to be excised can be removed without intolerable consequences for the person with epilepsy (i.e., surgery would not lead to severe loss of cognitive abilities, such as speech or memory). 6. The individual has the internal psychological resources and a support network in place to help with postsurgery recovery and a successful transition to nonepilepsy status.

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When the first two conditions are met, the patient begins a lengthy process to establish the remaining four conditions. Psychologists (usually neuropsychologists) are involved in conditions 3, 5, and 6. Condition 4 is the province of the neurosurgeon or neurologist. Condition 6 usually requires contributions from a social worker as well as the psychologist and nurse clinician working with the individual. On occasion, a patient will be told that before he or she can progress further toward surgery, an improvement in mood or a strengthening of the support network is needed. Different epilepsy surgery teams may differ in their threshold for this kind of problem. Condition 3 usually includes a neuropsychological evaluation designed to pinpoint which brain areas are functioning at levels below expectation. This is important because if the pattern of cognitive strengths and weaknesses indicates bilateral involvement or damage to areas outside the region thought to harbor the epileptogenic focus, the prognosis for seizure control after surgery is worse. In the case of temporal lobe epilepsy, the memory functions for verbal and pictorial materials are tested (tapping speech- and nonspeech-hemisphere functions, respectively). Other examinations are usually done at the same time: EEG localization, brain scans, including computerized tomography (CT) or magnetic resonance imaging (MRI), and metabolic positron emission tomography (PET) or single-photon emission computerized tomography (SPECT). The ideal candidate for surgery has findings from all of these examinations that point to the same area of the brain as the probable origin of the seizures. Magnetoencephalography (MEG) is being developed as an alternative to EEG; it is reported to have a localizing accuracy of approximately 8 mm, compared with 10 mm for EEG. The test measures the magnetic field generated by cortical activity by using extremely sensitive detectors (strength of the field is about one billionth that of the earth's gravitational field). If conditions 3 and 4 are satisfactorily answered, condition 5 is evaluated by using one or both of the following methods: (1) the Intracarotid Amobarbital Procedure (IAP; sometimes called the Wada Test, after Juhn Wada, the neurologist who introduced the technique at the Montreal Neurological Institute in the 1950s), or (2) speech mapping if the hemisphere to be operated on makes a contribution to normal language production and comprehension.

I. The Intracarotid Amobarbital Procedure This test is designed to determine the hemispheric organization of speech abilities and to prevent postsurgery amnesia by eliminating candidates whose memory abilities depend on the tissue in the area to be respected. Typically, a small amount of sodium amobarbital (Amytal) is injected into the internal carotid artery, which serves most of the cerebral hemisphere on the same side. After the injection, the neuropsychologist has approximately 5 minutes to test cognitive functions of the nonaffected hemisphere. Language abilities are tested and new information is presented to determine whether memory mechanisms of the noninjected hemisphere are capable of forming new memories. If the person can speak and learn new information after the injection, the noninjected hemisphere is considered able to support language and memory functions.

2. Speech Mapping If the epileptogenic focus is near regions of the brain that are required for language, the area near the proposed surgical removal needs to be mapped (mapping may also be needed for motor and sensory functions if the removal is near the primary sensory or motor cortices). Electrical stimulation is applied to the brain surface, usually during the surgery in the awake patient, although in some cases it may be preferable to stimulate the region using an implanted electrode array over an extended period before surgery. In the case of language functions, an interruption of speaking or comprehension during stimulation indicates that the underlying cortex should be left intact.

C. Nonmedical Therapies Physicians rely primarily on medication or surgery to treat their epilepsy patients, but nonmedical treatments of seizure disorders have played at least a peripheral role throughout the history of the illness. On the most superficial level, patients themselves often feel that something in their environment or a modification of their behavior can affect the frequency, duration, or severity of their seizures, both positively and negatively. This knowledge, either because it is accurate or through a superstitious process, leads to modifications in behavior. Rarely, patients actually like the feeling of the aura or seizure and so find ways to trigger one. Visual stimulation, such as passing the fingers

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back and forth in front of the eyes, can elicit seizures, and flashing lights (photic driving) are used as part of the diagnostic workup, because they can frequently produce abnormalities in the EEG or actual seizures. Patients with visually evoked seizures learn to avoid visual conditions with flashing lights (e.g., strobeilluminated dance halls) or repetitive moving patterns (e.g., a picket fence). Some people have their seizures elicited by any sudden stimulus that causes a mild startle reaction. Although it is difficult for a person to eliminate entirely the possibility of being startled, those around the patient can learn to reduce unexpected loud noises or sudden movements. Other non-medication/non-surgical treatments include:

1. Behavioral approaches, often used adjunctively. These treatments work best when the activities of the neurologist treating the patient are carried out in concert with the behavioral work. Three types are most common: (1) behavior modification, reward management or reinforcement-based strategies; (2) therapy, self-control or cognitive and psychodynamic-based strategies; and (3) conditioning, psychophysiological methods (desensitization and classical conditioning extinction, of greatest use in reflex epilepsy). 2. Biofeedback using the EEG (e.g., individuals with seizures having a motor component may be able to learn to normalize the cortical neural firing patterns and thereby dramatically reduce seizure frequency); biofeedback using exhaled CO2 (hyperventilation, which will cause a seizure in susceptible individuals, leads to a decrease in the CO2 in exhaled breath; learning to increase CO2 levels by means of biofeedback training may act in the opposite direction and decrease the frequency of seizures). 3. Special diet. One of these is the ketogenic diet, which is high in lipids (fats) and low in proteins and carbohydrates. This causes a condition in the body called ketosis, which appears to cause a rise in the threshold for seizures. This diet needs to be supervised closely by the person's physician. Fasting in the short term has the same effect. 4. Unconventional and as yet poorly studied treatments include the application of magnetic fields to the scalp over the seizure focus (applying to the brain a magnetic field within the same characteristics as seen when recording over the epileptogenic focus).

X. EPILEPSYADVOCACYGROUPS The Epilepsy Foundation of America (EFA) is an active group with hundreds of chapters and tens of thousands of members. The Foundation supports research into the causes and treatment of epilepsy and is a resource for professionals and patients and their families concerning new knowledge about epilepsy, treatment options, local experts, and support groups. Its Web Site contains much useful information for both professionals and lay persons. The National Tuberous Sclerosis Association also helps persons with epilepsy from tuberous sclerosis. Epilepsy Foundation of America (EFA) 4351 Garden City Drive Landover, MD 20785-2267 Local Phone: (301) 459-3700 Toll Free: (800) EFA- 1000 Fax: (301)377-2684 Web Site: http://www.efa.org National Tuberous Sclerosis Association 8181 Professional Place, Suite 110 Landover, MD 20785-2226 Phone: 1-800-225-NTSA or 301-459-9888 FAX: 301-459-3094 E-mail: [email protected] or [email protected] Web Site: http://www.ntsa.org In Canada, contact: Epilepsy Canada 1470 Peel Street, Suite 745 Montreal, Quebec, Canada H3A 1T1 (514) 845-7866 The International League Against Epilepsy publishes Epilepsia, a scientific journal containing articles on basic and applied research into causes and treatment of seizure disorders. The American Epilepsy Society (AES) has yearly meetings for its members, with scholarly presentations on all aspects of epilepsy. Additional information on the Ketogenic diet can be obtained from The Johns Hopkins Pediatric Epilepsy Center (410) 955-9100 or The Charlie Foundation to Help Cure Pediatric Epilepsy (800) 367-5386. Books for the general public include: Devinsky, O. (1994). A guide to understanding and living with epilepsy. Philadelphia: Davis.

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Evans, M. (1953). A ray ofdarkness. New York: Roy. Possibly the most readable description of the experience of an epileptic attack. Gumnit, R. J. (1990). Living well with epilepsy. New York: Demos. Gumnit, R. J. (1995). The epilepsy handbook: The practical management of seizures (2nd ed. ). New York: Raven. Gumnit, R. J. (1995). Your child and epilepsy: A guide to living well. New York: Demos. Lechtenberg, R. (1984). Epilepsy and the family. Cambridge, MA: Harvard University Press.

XI. FUTURE DIRECTIONS At the time of this writing, efforts are underway in a number of domains of importance to mental health workers concerned with epilepsy. Persons with epilepsy, after a long history of being fairly passive in their treatment, are beginning to be asked to play a more active or even a central role in the management of their illness. Toward this end, they and their family members are being asked about the impact of their illness with established questionnaires such a the WPSI and the Quality of Life in Epilepsy Inventory; similarly, families are being given a larger role when the physician considers the advisability of discontinuing antiepileptic medication after an interval without a seizure (usually more than 2 years). In cases of epilepsy, as well as other illnesses in which the person's behavior may modulate the progression of the disease process, the increasingly active role that members of the public are playing in determining the nature of their medical care is a positive one that should be encouraged by mental health professionals.

BIBLIOGRAPHY Dam, M. & Gram, L. (Eds.). (1991). Comprehensive epileptology. New York: Raven. Epilepsy Foundation of America (1975). Basic statistics on the epilepsies. Philadelphia: Davis. Hippocrates (1964). The sacred disease. In The theory and practice of medicine [reprint of Francis Adams (1849)translation] pp. 356-357. New York: Philosophical Library. Also available at http://www.mit/techclassics.html. Lennox, W. G. (1960). Epilepsy and related disorders (with the collaboration of Margaret Lennox). Boston: Little, Brown. Mostofsky, D. I., & Loyning, Y. (1993). The neurobehavioral treatment of epilepsy. Hillsdale, NJ: Lawrence Erlbaum. Sackellares, J. C., & Berent, S. (Eds.). (1996). Psychological disturbances in epilepsy. Boston: Butterworth-Heinemann. Sands, H. (1983) Epilepsy: A handbook for the mental health professional. New York: Bruner/Mazel. Temkin, O. (1971). The falling sickness: A history of epilepsy from the Greeks to the beginnings of modern neurology (2nd ed.). Baltimore: Johns Hopkins.

ImernetResources(accurateas of 10/97): Frequently asked questions about epilepsy: http://debra.dgbt.doc.ca/---andrew/epilepsy// FAQ.txt Massachusetts General Hospital information about epilepsy surgery: http://neurosurgery.mgh.harvard.edu/epil-nih.htm Information Guide from the National Institute of Neurological Disorders and Stroke: http://www.ninds.nih.gov/healinfo/disorder/ epilepsy/epilepfs.htm On-Line questions and answers from persons with epilepsy: http://dem0nmac.mgh.harvard.edu/neurowebforum/EpilepsyMenu.html (the "0" in the first part of this URL is a "zero", not the letter "0") For an up-to-date listing, search for "Epilepsy" using one of the Web Search pages.

i

J

Gambling Douglas Carroll and FrankF. Eves University of Birmingham

i. II. III. IV. V. VI.

Gambling Pathological Gambling Prevalence Explanations Treatment Conclusions

or drug addiction. This entry briefly describes the salient characteristics of the pathological gambler and indicates the current prevalence of the disorder. Explanations for pathological gambling are reviewed along with comments on treatment and intervention.

I. GAMBLING

Arousal A state of activation or excitement manifest by heightened affect and increased physiological activity. Cognitive Bias A term used to describe the biases in thinking that individuals may display. Gambling Wagering money or goods on a game or sport in which the outcome is uncertain. Pathological Gambling An impulsive disorder manifest by an addiction to gambling. Personality The stable attributes and dispositions that characterize an individual. Prevalence A measure of the rate of a particular phenomenon, such as pathological gambling, within a population at a particular time. Reinforcement Schedule The pattern of outcomes associated with an individual's responses or actions.

Gambling, in some form or another, is legally sanctioned in more than 90 countries worldwide and in 48 of the 50 states of the United States. In 1988, it was estimated that Americans legally wagered some $210 billion; by 1991, the estimated expenditure on gambling had soared by 50% to $304 billion. The proliferation of video lottery terminals and the establishment of casinos on Native American lands, consequent on passage of the federal Indian Gaming Regulation Act in 1988, are just the most recent manifestations of the progressive loosening of legislative restrictions on gambling. In this context, it is worth noting that in 1974, the total of legal wagers in the United States was $17 billion, a mere 5 % of the most recent expenditure estimates. Other countries have increasingly adopted similarly supportive legislative postures and have shown similar expenditure trajectories. For example, government revenue from gambling in Australia rose from $168 million (Australian dollars) in 1972-1973 to $2.02 billion in 1992-1993. Indeed, some countries began relaxing strictures against gambling much earlier than the United States. Although the United Kingdom was slow to appreciate the fiscal possibilities of lottery gambling, the Gaming Act, which legalized gaming for

GAMBLING is a strikingly ubiquitous human activity. For most people it constitutes a fairly casual pastime, amid a varied matrix of social and leisure pursuits. For some, however, gambling is anything but a casual activity: for the pathological gambler, gambling is preoccupying, consuming substantial time and money. The American Psychiatric Association regards pathological gambling as an impulsive disorder manifest as an addiction to gambling akin to alcohol 235

Copyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

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profit, became law in 1968. Among other things, it allowed licences to be granted for slot machine installations in cafes, leisure centers, or dedicated slot machine arcades, with access policed only by a voluntary code of conduct, devised by the British Amusement and Catering Trade Association (BACTA). The BACTA code prohibits those under 16 years of age from entering slot machine arcades. However, the code does not apply to seaside arcades, does not bind owners who are nor members of the association, and does not apply to nonarcade sites. Thus, while other European countries, Australia, and the states of the United States set the legal minimum age of access to slot machines at 18 or 21 years, the United Kingdom, in effect, exerts no legal restriction. Not surprisingly, the legislative arrangements that govern gambling have implications for behavior. For example, whereas other countries are not without problems related to slot machine gambling, it would appear that the heavy involvement of young people is a particularly British phenomenon. In the United Kingdom, organizations such as Gamblers Anonymous (GA) report an increasingly large number of under-18 youths seeking help for excessive or uncontrolled slot machine use. In 1964, the typical British GA member was a 40- to 50-year-old horse race gambler; by 1986, approximately 50% of new members were slot machine players, half of these being adolescents. Legislative relaxation in the United States has not only seen a massive increase in expenditure on gambling, it has also been associated with a substantial increase in participation. In 1974 in the United States, about 60% of the adult population were estimated to have participated in some form of gambling. By 1990, the figure had risen to just over 80%, and the most recent estimates, based on sampled states, suggest that the current lifetime participation rates may be even higher. These figures are cited only as illustration. Nevertheless, they are broadly representative. With increasing legislative laissez-faire has come increased access and participation rates, as well as massively increased expenditure on gambling, not to mention, in many cases, vast increases in government revenues. In addition, where legislation and cultural values permit, gambling appears to be a prevalent activity among the young. For example, surveys show that

between 3 % and 14% of British high school students are regular slot machine players. The figures for occasional use are more dramatic, with two thirds of British adolescents reporting use of gaming machines in arcades.

II. PATHOLOGICAL GAMBLING While for most people gambling represents an occasional distraction, for the pathological gambler it is anything but. In contrast to the occasional or recreational gambler, the pathological gambler has lost control over his or her gambling behavior. Gambling has, for such an individual, reached the point of disrupting not only his or her life, but also the lives of close family members and friends. In 1980, the American Psychiatric Association (APA) formally recognized pathological gambling as a disorder of impulse control, similar in many ways to other addictions. Save for "chasing" losses, the criteria used for defining gambling as pathological were very much modeled on those used to define alcohol and drug abuse. Like the substance addict, the pathological gambler is consumed by gambling, and will beg, borrow, cheat, and steal to support their addiction. Like the substance addict, the pathological gambler often shows tolerance, needing to increase the size or the frequency of the bet to achieve the desired excitement or "high." Similarly, withdrawal symptoms of disturbed mood and behavior are evident when gambling is curtailed. With regard to withdrawal, one study interrogated 222 pathological gamblers. Sixty-five percent reported at least one of the following: insomnia, headaches, upset stomach, loss of appetite, physical weakness, heart racing, muscle aches, breathing difficulties, sweating, and chills. Indeed, the pathological gamblers reported, if anything, more withdrawal symptoms than did substance-addicted control subjects. Finally, there are many instances of cross-addictions among pathological gamblers. Some studies have observed that as many as 50% of pathological gamblers had abused alcohol or drugs at some point in their lives. The following criteria are currently recommended by the APA as being characteristic. A diagnosis of pathological gambling is registered if an individual meets five or more of these criteria, with the proviso that the behavior is not better accounted for by a

Gambling

manic episode. A person may meet the criteria if he or she 1. Is preoccupied with gambling (e.g., preoccupied with reliving past gambling experiences, handicapping or planning the next venture, or thinking of ways to get money with which to gamble) 2. Needs to gamble with increasing amounts of money in order to achieve the desired excitement 3. Has repeated unsuccessful efforts to control, cut back, or stop gambling 4. Is restless or irritable when attempting to cut down or stop gambling 5. Gambles as a way of escaping from problems or of relieving a dysphoric mood (e.g., feelings of helplessness, guilt, anxiety, depression) 6. After losing money gambling, often returns another day to get even ("chasing" one's losses) 7. Lies to family members, therapist, or others to conceal the extent of involvement with gambling 8. Has committed illegal acts such as forgery, fraud, theft, or embezzlement to finance gambling 9. Has jeopardized or lost a significant relationship, job, or educational or career opportunity because of gambling 10. Relies on others to provide money to relieve a desperate financial situation caused by gambling

III. PREVALENCE Prevalence is the measure of the rate of a given phenomenon, such as pathological gambling, in a given population at a given time. Accordingly, the examples of prevalence rates cited here will necessarily be parochial. Although there are reasons for suspecting that the rates have increased in recent years, the data are circumstantial. As yet, there are no published reports of repeat prevalence surveys conducted on the same population. Nevertheless, there are clear trends apparent in research findings. Consider, for example, surveys of slot machine gambling among British high school students; in general, higher rates of pathological gambling appear in more recent surveys. Similarly, an escalation in pathological gambling can be inferred from the increase in treatment-seeking behavior. Consider the example of Holland and its alcohol and drug

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treatment centers. The number of individuals seeking treatment for gambling-related problems at these centers has increased strikingly over time. While only 10 individuals sought information or treatment in 198.5, 400 did so in 1986, 1200 in 1987, and 3883 in 1991. The only national survey in the United States was conducted in 1974. The authors concluded that 1.1 million Americans were probable pathological gamblers. More recently, researchers have relied for data on state-based prevalence surveys. Those carried out since 1990 report prevalence rates ranging from 1.4 to 2.8%. Surveys of gambling behaviors in Canadian provinces yield, if anything, slightly lower prevalence rates, but much depends on the definition of what constitutes pathological. One of the problems with the survey research is variation in the criteria used to define pathological gambling. For example, if one adheres to a strict definition of pathological gambling, the Canadian provincial rates range from 0.8 to 1.7%. However, if one relaxes the definition to include problem gamblers who possess almost, but not quite, a sufficient number of the defining characteristics to qualify as pathological gamblers, the prevalence rates range from 2.7% in Saskatchewan to 8.6% in Ontario. Other countries are gradually beginning to survey their populations. Rates of j~athological gambling in regions of Spain currently run at about 1.7%. In Australia, a partial national survey revealed pathological gambling rates of 1.2%, an identical figure to that which emerged from the recent national survey in New Zealand. Some appreciation of what these figures mean in social problem terms can be obtained by extrapolating from the case of New Zealand. A prevalence rate of 1.2 % implies that there are approximately 27,500 pathological gamblers in New Zealand. If we assume an overall current prevalence rate of 2 % in the United States, a reasonable assumption given recent individual state estimates, and an age structure similar to New Zealand, we can calculate that there are more than 3 million pathological gamblers in the United States. There are reasons for suspecting, however, that the prevalence rates revealed by many of these surveys are, if anything, underestimates. We have already alluded to the matter of the criteria used to identify pathological gambling; someone may have severe problems with gambling, yet fall just short of pathological status. Secondly, most of the prevalence surveys have re-

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. . . Gambling

lied on telephone data collection techniques. Such an approach has obvious pitfalls. Pathological gamblers may be underrepresented as they are more likely to have their telephones cut off periodically for nonpayment of bills, or to be too poor to possess telephones. Furthermore, telephone surveys have notoriously high nonresponse and refusal rates; pathological gamblers are less likely to be at home to telephone enquiries and, if they are, more likely to be reticent in the face of enquiries about gambling. This would again lead to pathological gamblers being undersampled. Problems also arise from unsampled groups, such as those in institutional care. Studies of patients in alcohol and drug treatment centers reveal prevalence rates of pathological gambling of 9 to 15 %. The exclusion of such individuals from surveys of pathological gambling will consequently lead to underestimates of prevalence. There is also emerging evidence of relatively high rates of pathological gambling among adolescents. For example, recent surveys among high school age individuals in Canada registered pathological gambling prevalence rates of about 3 %. Most general telephone surveys necessarily exclude adolescents and are, as a result, likely to yield prevalence estimates lower than the true figure. Finally, individual surveys in the United States usually show that pathological gambling prevalence rates are higher among those with low levels of education, as well as being higher among males, young adults, and nonwhites. It is worth noting that young adults and nonwhites tend to be underrepresented in treatment programs. Thus, treatment may not be reaching many of those who need it most.

IV. EXPLANATIONS Early attempts to account for pathological gambling relied either on psychodynamic metaphor or on a strict application of reinforcement theory. From a psychodynamic perspective, gambling was regarded as an attempt to resolve conflicts with parental figures through symbolic contests with a surrogate. Pathological gambling reflected an unconscious desire to lose such contests, thus appeasing the parental figures. Reinforcement theory regarded gambling as a learned response to intermittent schedules of financial reinforcement. Pathological gambling, from this perspective, was the result of repeated exposure to these pow-

.

erful schedules. Neither provide a satisfactory answer. While psychodynamic explanations are couched in a manner that renders empirical examination extremely difficult, strict reinforcement theory, with its emphasis on purely financial contingencies, gives improper regard to other motivating agencies and to intraindividual factors. Other, recent theoretical models of pathological gambling are much more multifactorial in character, and, although retaining variable financial reinforcement schedules as part of the explanatory matrix, have incorporated a range of other factors. Most prominent among these are cognitive bias, personal disposition, and arousal.

A. Cognitive Bias One of the most influential contributions to a cognitive psychology of gambling has been the work of Ellen Langer on the illusion of control. The illusion of control is defined as an expectancy of personal success inappropriately higher than the objective probability would warrant. In an elegant series of laboratory studies, Langer demonstrated that subjects' appropriate orientations toward chance events could be altered by a range of manipulations. For example, subjects who cut cards against a nervous competitor bet more than when playing against a confident competitor. Subjects would pitch the sale price of a lottery ticket that they had chosen themselves at a higher price than they would a ticket chosen for them. Subjects given the opportunity to practice a novel game of chance would bet more than those denied such an opportunity. Finally, subjects led to believe that they were particularly successful during the early trials of a cointossing task rated themselves as significantly better predictors of outcomes than subjects led to believe they performed poorly in the early stages of the task. In summary, if devices conventionally characteristic of skill situations are introduced into chance situations, individuals will inappropriately shift their expectations of success to levels better than chance. For example, provision of "feature" buttons which control aspects of slot machine behavior may enhance beliefs that skill is relevant to this form of gambling. Studies of gamblers in naturalistic settings yield confirmatory data. Regular gamblers frequently deny the importance of chance factors in their chosen pursuit, erroneously believing that they have devised a win-

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ning system. They display flexible attributions in that success is attributed to their own skill, whereas external factors such as bad luck or fluke circumstances are invoked to account for losses. It is also clear that individuals vary in the degree to which they generally attribute outcomes to internal factors, such as skill, or to external factors, such as luck. Thus, some individuals may be more likely to adopt a skill or control perspective in essentially chance situations. There is certainly evidence from studies of slot machine players that an internal locus of control may be particularly characteristic of young pathological slot machine gamblers.

B. Personality Aside from orientations regarding the locus of control, other personality factors have been implicated as predisposing a person to pathological gambling. Given the variety of personality questionnaires that have been deployed and the variations in the populations studied, it is perhaps hardly surprising that not all studies point in the same direction. Nevertheless, some consistent themes can be discerned. Sensationseeking, impulsivity, and lack of concern for others emerge as characteristic of pathological gamblers in a number of studies. Results from studies that have measured a disposition toward sensation-seeking have yielded equivocal results. However, perhaps sensation-seeking is best regarded in the context of prevailing levels of stimulation. Evidence seems to indicate that pathological gamblers, apart from their gambling, endure a lifestyle noticeably low in stimulation, and many report relief from boredom as a major motivating force. Accordingly, to the extent that sensation-seeking is implicated in pathological gambling, it is perhaps less as a personality trait, and more as a response to characteristically low levels of stimulation and arousal. While caution is appropriate, given the bias toward male subjects in research, impulsivity and a lack of concern for others emerge from a number of studies of pathological gamblers. Pathological gamblers score high on a range of questionnaires devised to measure disregard for others, lack of empathy, inability to form and sustain relationships, attraction to risk and danger, and preference for immediate stimulation regardless of the consequences. Further evidence on im-

pulsivity emerges from electroencephalographic studies. Drawing on the theory that brain hemispheric dysregulation is related to poor impulse control, hemispheric activation was measured in response to simple verbal versus nonverbal tasks. Pathological gamblers showed a pattern of activation dissimilar to normal control subjects, but similar in many ways to children with attention deficit disorder. Probably the major behavioral characteristic of such children is impulsivity. It has been speculated that at the neurochemical level, poor control of impulses may reflect a deficit in a particular brain neurotransmitting substance, serotonin. There is some recent evidence in line with this speculation. A serotonergic probe was used to measure the degree of activity of the serotonin system in pathological gamblers and matched control subjects. The pathological gamblers showed hypoactivity relative to the controls. It would appear that pathological gambling may share common neurochemical features with other behavioral disturbances characterized by poor impulse control.

C. Arousal A number of recent theories propose an important role for arousal in pathological gambling theories. Such theories add arousal, as a reinforcer on a fixed-interval schedule, to the more commonly hypothesized variable financial schedule to explain what sustains pathological gambling. Indeed, it has been argued that arousal as a reinforcer may be the most important determinant of loss of control. From this perspective, then, arousal in combination with irregular financial schedules is regarded as the driving force behind pathological gambling. Early laboratory investigations of heart rate as an index of arousal suggested that gambling was not particularly provocative. However, the ecological validity of these studies has been questioned. Tellingly, a key study found only modest increases in heart rate among students and regular gamblers in the context of a laboratory casino. For the regular gamblers in a real casino, however, substantial increases in heart rate accompanied gambling. Furthermore, the magnitude of the increase was related to the size of the wager. In subsequent studies, reliable increases in cardiovascular activity has been observed during slot machine play and horse race gambling. Nevertheless, there is still no strong evidence that

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individual variation in arousal underlies pathological gambling; that is, there is no evidence that pathological gamblers are any more aroused by gambling than recreational gamblers. Furthermore, a recent study comparing pathological and recreational slot machine gamblers suggested that it might be baseline levels of arousal that are discriminating, and not the magnitude of the increase provoked by gambling; pathological slot machine gamblers tended to register low baseline arousal levels.

V. TREATMENT

A variety of treatments have been applied to pathological gambling, but have not, on the whole, been subject to systematic and controlled evaluation. Because, for many, GA is the main or only recourse available, it is unfortunate that its mixture of disclosure and social support has received so little formal evaluation. In a study of 232 GA attenders in Scotland, 8% were abstinent at the 1-year follow-up; by the 2-year follow-up, 7% remained abstinent. The addition of behavior therapy to the usual GA provisions seemed to produce better results; in one study in the United States that used this combination, 54% reported gambling less than they did before treatment. This latter study raises an, as yet, unresolved issue: the appropriate outcome measure. Whereas earlier studies championed complete abstinence, there has been a shift toward moderated gambling as the preferred treatment outcome. Moderated gambling is not necessarily, as critics claim, associated with an increased probability of a return to pathological gambling. There is even evidence that intermittent relapses from complete abstinence can occur without gambling returning to pathological proportions. A number of earlier studies applied behavioral techniques to the treatment of pathological gambling. The underlying assumption of the behavioral approach is that pathological gambling constitutes a learned response to schedules of intermittent reinforcement by money and arousal. The most common treatment procedures have been aversive conditioning and covert sensitization. In the former, unpleasant, but not painful, electric shocks are administered while individuals engage in gambling behavior. In the latter, aversive imagery is substituted for the electric shocks; the gambler is guided through a sequence of imagined

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gambling scenes characterized by unpleasant physical (e.g., nausea) or social (e.g., discovered gambling by spouse) consequences. The application of both of these techniques has produced encouraging outcomes, with up to 40 to 50% of pathological gamblers reporting either complete abstinence or that gambling is under control at follow-up. Nevertheless, caution is warranted. None of the behavioral treatment studies to date has included proper control conditions, many have treated very small numbers of gamblers, and the follow-up period has often been of limited and insufficient duration. More recently, cognitive therapies have been tried. These are based on the assumption that faulty and erroneous cognitions are important determinants of pathological gambling. The aim of therapy is to replace dysfunctional cognitions with adaptive and rationale thinking. While there are fewer data available, cognitive therapies would seem to produce outcomes not wholly dissimilar to more purely behavioral approaches; that is, about 40 to 50% of pathological gamblers derive benefit from the therapy. Of the various behavioral and cognitive approaches that have been applied, currently the most promising is imaginal desensitization. In contrast to covert sensitization described earlier, imaginal desensitization promotes images in which the gambler is no longer excited by gambling and no longer thinks of it as a way of dealing with tension, stress, and boredom. Participants practice relaxation along with imaging four scheduled scenes. In the one published controlled treatment outcome study, imaginal desensitization was compared with aversive therapy. Whereas only 2 out of 10 of aversive therapy participants reported that they were abstinent from gambling at 1-year follow-up, 7 out of the 10 imaginal desensitization participants did so. As gambling has become more accessible, so the casualties have increased. While the development of effective treatment is very much in the early stages, the need is pressing. It is clear that our general understanding of pathological gambling is improving, and, accordingly, more recent therapeutic initiatives are being informed by more sophisticated theory. However, in this context, we would do well to pay more heed to the models of behavior change being deployed elsewhere. Most relevant are the therapeutic models being applied to changing unhealthy behaviors, such

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as cigarette smoking and poor dietary habits. In particular, the stages-of-change model, described first in 1984 by Prochaska and Di Clemente, is worth close consideration. The stages-of-change model has, as its starting point, a keen appreciation that people differ in their willingness to consider or to adopt behavioral changes. Furthermore, the process of change contains a series of stages through which individuals progress, reflecting the temporal dimension in which behavior change occurs. A stages-of-change model may be particularly applicable to changing gambling behavior in that it describes both the nature of change and the strategies most likely to facilitate change. Five stages of change are identified. The first stage is known as precontemplation. Here, no or only occasional thought is given to changing behavior. The next stage is known as contemplation, in which the individual begins to consider changing his or her behavior. However, contemplation does not guarantee action, and individuals can still slip back to the precontemplation stage. Nevertheless, contemplation may lead to active consideration, which is the necessary launching pad for behavioral change. These stages of active consideration and achievement of behavioral change are the planning and action stages. The final stage is one of consolidation and maintenance of behavioral change. From this perspective, intervention is about moving individuals from one stage to the next, from precontemplation to contemplation, from contemplation to active consideration, and so on. Thus, it is important that the therapist appreciates what stage the individual is at and also that different sorts of intervention are called for, dependent on stage. A number of researchers have identified phases in the career of a pathological gambler. At the very least, it has been argued, it is important to distinguish between acquisition and maintenance. Nevertheless, there has been, as yet, no systematic attempt to exploit a stages model in treating pathological gamblers. Preventive strategies have received limited attention, although there are encouraging preliminary resuits from a high school-based program in Quebec. However, given the evidence implicating early initiation into gambling in the development of pathological gambling and the high prevalence rates of pathological gambling among adolescents in many countries, substantially greater energies should be devoted to developing and evaluating preventive strategies.

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VI. CONCLUSIONS

It is clear that relaxation of legislative strictures and easing of access are associated with increased gambling. This is evident both in the numbers gambling and the monies wagered. It is almost certain that such changes have consequences for the numbers who gamble pathologically. While substantial progress has been made, the study of gambling has still to yield a definitive account of the mechanisms that lead some individuals to pathological gambling. A variety of factors are undoubtedly involved. It is also likely that these various factors assume a different importance during progression from acquisition to maintenance, that is, from induction to addiction. For example, at the induction stage, positive cultural attitudes toward gambling, legislative laissez-faire, and early age of initiation all undoubtedly increase risk. Subsequently, compelling schedules of monetary reinforcement, the consistently arousing nature of gambling in the context of an otherwise unfulfilling and unstimulating lifestyle, a tendency to presume control when it is chance that operates, and a personality high on impulsivity and low on social concern, are all likely to be significant factors. Nevertheless, this is merely the bare bones of a theory, and, aside from the proposed role of hemispheric dysregulation and serotonergic deficits in impulsivity, we are without any account of the mechanisms operating at a neurobiological level. Given that pathological gambling may not be phenomenally distinct from other addictive behaviors, it is perhaps to the neurobiology of other, more fully studied addictions that gambling researchers should look for clues. Both behavior and cognitive treatment techniques have been applied to pathological gamblers with some success. However, there is a dearth of properly controlled therapeutic trials. In addition, the treatment of pathological gambling could well benefit from adopting the therapeutic models that have been used successfully in other areas of behavior change. In particular, much could be gained from adopting a model that appreciates stages of change. Furthermore, more attention needs to be paid to preventive strategies. Given the prevalence rates of pathology gambling in young people, it is imperative that effective schoolbased preventive programs are developed. Finally, there may be a need to consider selective legislative

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intervention. Many of the substantial numbers of young people in the United Kingdom who fall afoul of slot machines could be helped by effective treatment regimes. However, simple legislative reform, restricting access to those 18 years or older, would undoubtedly yield more immediate and cost-effective dividends.

BIBLIOGRAPHY

Blaszczynski, A., & Silove, D. (1995). Cognitive and behavioral therapies for pathological gambling. Journal of Gambling Stud-

ies, 11,195-219. Carroll, D., & Huxley, J. A. A. (1994). Cognitive, dispositional and psychophysiological correlates of dependent slot machine gam-

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bling in young people. Journal of Applied Social Psychology, 24, 1070-1083. Galski, T. (Ed.). (1987). The handbook of pathological gambling. Springfield, IL: Charles C. Thomas. Langer, E. J. (1983). The psychology of control. Beverley Hills, CA: Sage. Lesieur, H. R. (1994). Epidemiological surveys of pathological gambling: Critique and suggestions for modification. Journal of Gambling Studies, 10, 385-398. Lesieur, H. R., & Rosenthal, R. J. ( 1991 ). Pathological gambling: A review of the literature. Journal of Gambling Studies, 7, 5-39. Prochaska, J. O., & Di Clemente, C. C. (1984). The transtheoretical approach: Crossing traditional foundations of change. Homewood, IL. Don Jones, Irwin. Rosenthal, R. J. (1992). Pathological gambling. PsychiatricAnnals, 22, 72- 78. Shaffer, H. J., Stein, S. A., Gambino, B., & Cummings, T. N. (Eds.). (1989). Compulsive gambling: Theory, research, and practice. Lexington, MA: Lexington Books. Volberg, R. A. (1996). Prevalence studies of problem gambling in the United States. Journal of Gambling Studies, 12, 111-128. Walker, M. B. (1992). The psychology of gambling. Oxford, UK: Pergamon Press.

Mental Retardation and Mental Health Sharon A. Borthwick-Duffy University of California, Riverside

I. II. III. IV. V. VI.

Definition of Mental Retardation Psychopathology and Behavior Problems Assessment of Mental Health Treatment and Intervention Promotion of Mental Health Implications of Mental Health Considerations

quences that are not contingent on reinforcement and are considered pathological. MENTAL RETARDATION is characterized by low intelligence and deficits in adaptive skills that are observed before the age of 18. The majority of people with mental retardation are mentally healthy and free of serious behavior problems, although the prevalence of psychiatric disorders is higher than in the general population. This entry discusses the factors that contribute to the risk of behavior problems and emotional disorders, as well as the assessment, treatment, and implications of mental health problems among persons with mental retardation.

Adaptive Skills An array of age-appropriate behavioral competencies required to function in and adapt to the environments encountered in daily living. Age-Appropriate Typical of one's chronological age peers. Aversive Intervention Any intervention that is applied in a behavior-contingent manner with the expected effect that the future rate of the behavior will decline as the individual seeks to avoid the stimulus. Diagnostic Overshadowing When the presence of mental retardation decreases the perceived significance of problem behavior and reduces the likelihood of the behavior being linked to a psychiatric disorder. Dual Diagnosis Individuals who have both mental retardation and a psychiatric disorder. Etiology Cause or causes of a given condition. Maladaptive Behavior Observed problem behavior that may or may not be symptomatic of a psychiatric disorder. Psychotropic Drug Any agent prescribed for the purpose of bringing about behavioral, cognitive, or emotional change. Self-Injurious Behaviors Acts directed toward oneself that result in tissue damage. Stereotyped Behaviors Self-stimulatory behaviors that are repetitious motor behaviors or action se-

I. DEFINITION OF MENTAL RETARDATION According to the most recent (1992) definition of the American Association on Mental Retardation (AAMR), people with mental retardation are characterized by significantly subaverage intellectual functioning (IQs lower than 70 or 75) and by concurrent limitations in two or more adaptive skill areas. Mental retardation is defined as a fundamental difficulty in learning (intellect) and an ensuing difficulty in performing daily life skills (adaptation). Consistent with a developmental perspective, mental retardation is manifested before age 18. Although certain aspects of this new definition depart from previous conceptions of mental retardation, the dual criteria of low IQ and deficits in adaptive behavior have been critical elements of most definitions for many years. Defining

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mental retardation in terms of adaptive behavior deficits is especially important when considering the presence of co-occurring mental health problems.

A. Evolution of the Definition of Mental Retardation There has never been a universal consensus as to what mental retardation actually is. Moreover, at any time in history, the definition of mental retardation has reflected the current status of scientific knowledge and prevailing views on social issues related to mental retardation. From the turn of the century until the first formal AAMR definition in 1959, mental retardation was widely believed to be a biologically based condition of the central nervous system, existing from birth, that was incurable and probably irremediable. The 1959 AAMR definition was less restrictive, focusing on current functioning rather than constitutionality, and not explicitly stating that mental retardation was incurable. The assumption of a theoretically normal distribution of intelligence suggests that most people will have IQs that are closer to the mean score of 100 (i.e., scores close to the cutoff) and that the number of people who are expected to have more severe forms of mental retardation decreases as IQs deviate farther from the mean. Thus, mild retardation comprises the largest group of people with mental retardation. The arbitrariness of the concept of mental retardation is illustrated by the AAMR definitional change in 1973, which moved the upper IQ limit from approximately 85 (one standard deviation from the mean of 100) down to 70 (two standard deviations from the mean). With this change, approximately 13% of the population "lost" their potential membership in the mental retardation category. For individuals with severe forms of mental retardation, these definitional differences were irrelevant; they would probably have been identified no matter what definition was used. But, for those with IQs between about 70 and 85, who had been previously identified as having mental retardation, this decision changed their diagnosis. Today, the majority of children with mild forms of retardation do not have known pathology (biologic origins). They are more likely to come from adverse economic and living situations that contain risk fac-

tors, such as poor nutrition, poor medical care, low motivation for personal achievement, and parents who have below average IQs. For some children, these factors will result in depressed intellectual functioning, poor development of adaptive skills, and a diagnosis of retardation. Most formal organizations (e.g., American Psychiatric Association, World Health Organization, state and federal agencies) have historically used approximations of the AAMR definitions in their definitions or eligibility criteria for mental retardation. But because the 1992 AAMR definition and classification system is still rather new and has introduced some conceptual shifts, its long-term impact on the definitional criteria used by other organizations is unknown.

B. Sociological Perspective on Deviant Behavior and Mental Retardation For those people whose IQs are close to the cutoff, adaptive functioning is the key determinant in their diagnosis. It is the lack of adaptive competence, rather than low IQ, that usually leads to referral for evaluation and diagnosis. Thus, many individuals with IQs below the cutoff will never be referred for evaluation if their levels of adaptive competence do not draw attention. The measurement of adaptive functioning is subjective, as it involves a determination of what constitutes "normal" or competent behavior within specific environments. From a sociological perspective, then, the values and expectations of each society determine how mental retardation is to be defined, that is, by identifying the types and degree of deviant behavior that is not tolerated. This suggests that a diagnosis of mental retardation is assigned when an individual with subaverage intelligence deviates too far from the behavior standards dictated by societal norms. Thus, two people with the same IQ score and the same repertoire of adaptive competencies could presumably end up with different diagnostic outcomes (with or without mental retardation) if their environments produce different demands and behavioral expectations.

C. Mental Retardation Distinguished from Mental Illness In the earliest civilizations mental retardation was not differentiated from other handicapping conditions, and it was common for adults with mental retardation

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to be institutionalized with people with mental illness. Both groups were believed to be insensitive to cold, heat, hunger, and pain, thus justifying the harsh treatment they often received in their confinement. Later attempts to distinguish between mental retardation and mental illness included Paracelsus's definition during the Renaissance period and Esquirol's classification system in the early nineteenth century, which designated mental retardation as amentia and mental illness as dementia. Despite the fact that mental retardation was scientifically acknowledged in the early 1800s to be an important social problem distinct from mental illness, many people today still do not recognize that the majority of persons with mental retardation are mentally healthy and are free of significant behavioral problems. The distinction that eventually was made, to associate mental retardation with low intelligence and to associate mental illness with emotional disorders, has been identified as one explanation for current tendencies toward dismissing the possible presence of behavior disturbance among persons with mental retardation. In other words, once it was clear that mental retardation was not synonymous with mental illness, the pendulum swung back such that these conditions were not even expected to co-occur.

D. Dual Diagnosis The term dual diagnosis is now applied to persons who have intellectual deficits (mental retardation) along with emotional impairment (psychiatric disorders). As noted previously, people with mental retardation experience difficulty functioning independently in their environments but they do not necessarily have psychological disturbances. When psychiatric disorders are present, they are usually of the same types and are diagnosed by the same criteria as for persons of normal intelligence. The dual diagnosis term grew out of the recognition that individuals with both conditions present unique needs to mental retardation and mental health service systems. Professionals have established the fact that the presence of these two conditions creates a complex set of issues that may complicate the diagnostic process and may require unique methods of treatment. The utility of the dual diagnosis term has been questioned by some clinicians who believe it adds another stigmatizing label to persons who already experience difficulties ob-

taining services from agencies that resist taking responsibility for them. Others suggest this reflects problems with the service systems, rather than with labels or assessment per se.

II. PSYCHOPATHOLOGY AND BEHAVIOR PROBLEMS Although mental retardation and psychopathology are believed to be functionally independent, studies of the prevalence of psychiatric disorders among individuals with mental retardation have shown, almost without exception, rates that are much higher than those found in the general population. The rates reported in the literature range from less than 10% to more than 80% for persons with mental retardation, depending on methods of sampling, eligibility criteria, and types of assessment. The two largest epidemiological population studies conducted in the Isle of Wight, Wales (Rutter & Graham, 1970) and in Aberdeen, Scotland (Koller, Richardson, Katz, & McLaren, 1982) concluded that the prevalence of psychiatric disorders among children with mental retardation was about four times greater than in the general population. The prevalence rates of psychiatric disorders for children with normal intelligence in those studies ranged from 5to 10%.

A. Specific Psychiatric Disorders with Mental Retardation Although the incidence of psychiatric disturbance has been found to be higher among persons with mental retardation, the literature consistently affirms that the majority of symptoms do not differ in kind from people without mental retardation who are referred for psychiatric evaluation. I. Affective Disorders Affective disorders, including depressive and bipolar disorders, have been found to occur with much greater frequency among children and adults with mental retardation than in the general population. Contrary to earlier hypotheses that people with mental retardation are devoid of feelings, the results of some studies suggest that adults with mild mental retardation appear to experience even higher rates of de-

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pression than their peers without mental retardation. [See DEPRESSION; MOOD DISORDERS.]

2. Schizophrenia Schizophrenia has been found to be present in about 2 to 39/0 of persons with mental retardation, a prevalence that is much higher than in the nonretarded population. The symptoms of schizophrenia are generally similar across groups, although they may be simpler in form among persons with mental retardation. [See SCHIZOPHRENIA.]

3. Autism It has been estimated that 75% of children with autism will perform at a level within the regarded range throughout their lives; however, less than 3 % of persons with mental retardation have autistic behavior. Contrary to early theories that autism was caused by "cold" parenting styles, a variety of biological problems are now thought to explain the central nervous system dysfunction that characterizes this disorder. [See AUTISM AND PERVASIVE DEVELOPMENTAL DISORDER.]

4. Anxiety Disorders Anxiety disorders have received less attention than other psychiatric disturbances among persons with mental retardation. Although prevalence estimates are scarce, several authors have reported higher rates of anxiety among persons with mental retardation than in the general population. A 22-year longitudinal population study conducted in Aberdeen, Scotland, for example, found that more than one fourth of the children exhibited problems with nerves and anxiety by early adulthood. No differences were observed between boys and girls, but a higher prevalence was found among those with more severe levels of retardation. [See ANXIETY.]

5. Phobias Studies have shown that persons with and without mental retardation experience the same types of fears. Several studies suggest that mental age is a factor in comparisons of fears across these groups, where fears of older people with mental retardation tend to be more similar to fears of younger nonretarded people. Social phobias are expected to be high among persons with mental retardation; in the presence of cognitive limitations, social skill deficits are common and lead to increased vulnerability for peer rejection, low levels of social support, and social anxiety. [See PHOBIAS.]

B. Estimating Prevalence of Psychopathology Two primary factors have been associated with the discrepancy (less than 10% to more than 80%) in prevalence rates of psychiatric disorders that have been reported for people with mental retardation. I. Assessment An accurate count of individuals who have a dual diagnosis is dependent on valid and reliable assessments of both mental retardation and psychiatric disorder. Difficulties associated with obtaining valid estimates of adaptive behavior deficits have been noted since this criterion was first included in the definition of mental retardation. Prevalence studies have also been based on definitions of mental retardation that vary from the AAMR definition. Some widely cited studies (e.g., Isle of Wight) have even used definitions that considered low IQ, but not adaptive behavior deficits, as the criterion for mental retardation. Reliable diagnosis of mental health problems in persons with mental retardation also presents a major challenge to clinicians. Identification of psychiatric disorders depends on the clinical method, the source of information, and the taxonomy of disorders used to assign diagnoses. For example, one multimethod study of people with mental retardation found that the prevalence rates of mental disorders ranged from about 12 to 59%, depending on the method of assessment that was used.

2. Sampling Bias Prevalence estimates are also affected by sampling bias. A large number of studies have been based on samples of individuals who have either been referred to clinics for psychiatric assessment or have resided in institutions where behavior problems led to their placement. Not surprisingly, these studies overestimate the presence of mental health problems among the population of persons with mental retardation. Service system registries comprise another major sampling source, wherein individuals receiving state-funded services are included in databases containing records of client characteristics and services provided. Because people with mild mental retardation are less likely to require state services if they do not have serious health or behavior-related problems, these databases probably overestimate the prevalence of dual diagnoses among people with mild mental retardation in the

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population. Finally, because many states have separate agencies providing services for persons with mental retardation and mental health problems, prevalence estimates may be affected by the determination of which agency tends to serve persons with both conditions.

C. Relationships with Age Although age has not been found to be related to the overall distribution of psychiatric impairment, studies of specific disorders suggest that some conditions may be age-related. Moreover, in studies of behavior problems that have not been restricted to those with formal psychiatric diagnoses, age differences have been identified in rates of observed problem behavior in people with mental retardation, with lower rates found for children than for adolescents and adults. [See AGING AND MENTALHEALTH.]

D. Relationships with Intellectual Level The relationship between the overall frequency of psychiatric disorder and severity of retardation has not been established; however, the available evidence suggests that specific types of psychiatric disorder appear to be more commonly found among certain levels of mental retardation. Most studies show that the types of psychiatric syndromes observed among children and adults with mild or moderate levels of mental retardation are similar to those found in the general population, for example, major affective disorders; schizophrenia; obsessive-compulsive disorder; disorders of conduct; anxiety, activity levels, and attention; and mood and affect disorders. In contrast, some disorders are more commonly manifested by persons with severe levels of mental retardation, such as autism and other pervasive developmental disorders, aggression, stereotypic behaviors, and self-injurious behavior. Stereotypy (repetitive motor behaviors) and self-injury may occur in isolation or in conjunction with major neuropsychiatric disorders among persons with severe or profound mental retardation.

E. Relationships with Gender Most studies have found no significant relationships between overall behavior disturbance and gender. However, gender differences have been observed within certain types of disturbance. For example, con-

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sistent with findings in the nonretarded population, antisocial behavior has been found to be more prevalent among males, while emotional disturbance has been observed more frequently among females.

F. Relationships with Etiology of Mental Retardation The evidence suggests that certain genetically related causes of mental retardation, such as Prader Willi syndrome, Cornelia de Lange syndrome, Lesch-Nyhan disease, fragile X syndrome, and Williams syndrome are associated with the presence of specific behavior problems and psychological disorders in persons with mental retardation. Lesch-Nyhan disease is best known for the manifestation of self-injurious biting. The minority of individuals with Lesch-Nyhan who do not bite indulge in some other form of selfinjurious behavior, such as head banging. Aggressive behavior is also directed against others, and most of these individuals vomit, which interferes with nutrition. Lower incidences of self-injurious behavior than those in Lesch-Nyhan have been observed among persons with Cornelia de Lange syndrome, Tourette's syndrome, and fragile X syndrome. The majority of self-injuring individuals, however, have nonspecific diagnoses of mental retardation and display this behavior in self-stimulating or stereotypic patterns. Fragile X syndrome is the most common known inherited cause of mental retardation and developmental disabilities. Attention deficit disorders, autistic disorders, and socially related and anxiety-based disorders appear to be associated with fragile X syndrome, although these disorders are not present in all persons who have fragile X. Food preoccupation, hyperphagia, and obesity are most often associated with Prader Willi syndrome. Recent studies have also linked maladaptive symptoms that are not related to food, such as obsessive-compulsive disorder, temper tantrums, internalizing problems, and oppositional-defiant disorders to individuals with Prader Willi syndrome. Recent data suggest increased risks of anxiety disorders and attention deficit hyperactivity disorder among people with Williams syndrome. Adults with Down syndrome appear to be at a higher risk of depression relative to other adults with mental retardation. Researchers have also discovered links between Down syndrome and Alzheimer's disease, with people with Down syndrome having a greater than average risk of developing this disease after the age of 45.

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G. Behavior Problems Distinguished from Psychiatric Disorders

A. Applicability of Taxonomies Used for the General Population

Observed behavior problems do not by themselves indicate psychopathology. Interrelationships between deficits in adaptive behavior, maladaptive or problem behavior, and psychiatric disorders among persons with mental retardation are complex. Maladaptive behavior is a term that has been used in the field of mental retardation to refer to problem behaviors that are sometimes categorized as personal (e.g., selfinjury, depression) or social (e.g., aggression, property destruction). In general, the terms maladaptive behavior and behavior problems are used interchangeably. Despite the definitional criteria that require deficits in adaptive skills to be present in persons with mental retardation, these deficits are not always associated with maladaptive behavior. Adaptive and maladaptive behavior represent two distinct, independent constructs and deficient interpersonal skill development (i.e., lack of adaptive skills) is not always associated with undesirable or pathological behavior. Psychopathology is only indicated when behavior problems are part of an overall pattern of behavior. Although persons with a dual diagnosis are at a higher risk of evincing destructive behavior patterns (e.g., self-injury, aggressive behavior, and property destruction), it is clear that these destructive behaviors are also present among a significant proportion of people whose only diagnosis is mental retardation.

There is a general consensus that the full range of mental disorders observed in the general population is found among persons with mental retardation. Psychopathology is typically reported according to established diagnostic systems, such as the American Psychiatric Association's Diagnostic and Statistical Manual (DSM-IV), that are also used to classify disorders in persons with normal intellectual ability. Early versions of the DSM classification system were thought to lack reliability and validity for persons with mental retardation, but the heightened awareness of dual diagnosis in the 1980s led to vast improvements in defining DSM categories that were appropriate for persons with mental retardation. Some clinicians still contend, however, that the expression of psychopathology among persons with severe and profound mental retardation may take on different forms and require separate classifications.

III. ASSESSMENTOF MENTAL HEALTH Although the diagnosis of mental retardation is determined in part by deficits in adaptive functioning, the behaviors that one must display in order to be considered competent cannot be clearly delineated for every situation and age group. Measures of social competence must, for practical reasons, sample only selected behaviors that are used to represent typical functioning. Decisions that rely on measurement of adaptive and maladaptive behavior are highly dependent on the method of assessment used. Moreover, behavior is not expected to be "normal" for persons with mental retardation. Because base rates of behavior may be compared either to the general population or to the subset of people with mental retardation, the selection of a comparison group can also influence the identification of pathology.

B. Consideration of Quality and Reliability of Mental Health Information I. Multimethod Approach to Assessment Multiple informants and multiple methods of data collection are typically used to provide a clinical picture of abnormal behavior among persons with mental retardation. These methods, which may include abstracting information from case records, systematic observations, interviews, formal instruments, and medical examinations, provide ratings that may differ according to the rater's familiarity with the individual, contexts in which behaviors are observed, rater or situational tolerance of the behavior, behavioral expectations, and response styles on rating scales.

2. ComplicationsCaused by Communication Deficits Communication deficits that are associated with low intelligence complicate the evaluation process in several important ways. The simplistic emotional expressions and concrete thought patterns that are characteristic of these individuals can lead to clinical misinterpretations of their behavior or mental health conditions. The identification of some syndromes also depends on information obtained by interview with the individual or observation of his or her speech (e.g., hallucinations, complaints of pain, or fears). With in-

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dividuals who are nonverbal or who lack expressive language, it may be impossible to diagnose reliably certain conditions. Finally, individuals who lack the communication skills necessary to make their needs known or to interact socially with others may develop problem behaviors that represent attempts to communicate and do not stem from emotional disturbance. 3. Effect of Behavior on IQ Test Performance Although the extent of its impact is difficult to determine, it is possible that severe behavior disorders, especially those present from early childhood, lead to poor performance on intelligence tests, which can result in a false diagnosis of mental retardation. The importance of knowing whether behavior disturbance has depressed a person's behavioral functioning to such a degree that his or her IQ falls within the retarded range, or whether in fact the person has both mental retardation and a severe emotional disorder, has been questioned in terms of its relevance to treatment. Nevertheless, this distinction affects prevalence rates of dual diagnosis and may also determine which bureaucratic system (mental retardation or mental health agency) will assume responsibility for the provision of services to that individual.

C. Diagnostic Overshadowing Diagnosticians are less likely to identify psychiatric illness in individuals with mental retardation, even when their observed behaviors are identical to those displayed by persons of average intelligence. This phenomenon, which has been referred to as diagnostic overshadowing, suggests that behavioral problems evinced by persons with mental retardation tend to be attributed to the retardation rather than to a concomitant behavior disorder. Because adaptive skill deficits partly define mental retardation, this attribution is understandable; however, it is likely to affect prevalence rates and may also lead to different profiles of persons with and without mental retardation who are given the same psychiatric diagnosis.

D. Measures Developed for Individuals with Mental Retardation Historically, attempts were made with limited success to adapt instruments developed for the general population for use with people with mental retardation. The

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1980s was a period in which the lack of adequate assessment instruments for identifying and classifying psychopathology among persons with mental retardation emerged as an important clinical and research priority. In 1991, Aman published a comprehensive review for the National Institute of Mental Health of instruments that had been specifically developed for or tested with samples of people with mental retardation. He identified 23 instruments that were appropriate as general purpose diagnostic tools. Of these, most were developed after 1984, indicating a flurry of activity in the past decade. Despite what appears to be a wide selection of available measures, however, the numbers are greatly reduced when they are broken down by relevant age groups, levels of mental retardation, specific conditions covered, type of rater used (self-ratings, other informant, or clinician), and whether adequate psychometric testing (e.g., reliability and validity) has been reported. I. Clinical Dimensions across Instruments A moderate degree of consistency has been found across factor analytic studies of the clinical dimensions of psychopathology, suggesting that similar dimensions are being tapped by different instruments. Aman noted, however, that the dimensions that emerge from factor analysis of items on an instrument are highly dependent on the collection of items or questions that it contains. For example, if an instrument contains few or no questions about self-injury, factor analyses cannot produce a separate dimension related to this problem. This point is particularly relevant if some behaviors that are unique to persons with severe and profound retardation are not included on measures that were originally developed for people with normal intelligence.

2. Validity of Instruments Many instruments have not been evaluated for their validity, that is, their ability to identify accurately the psychopathology, and especially specific diagnostic categories. When the correctness of classifications has been examined, the current version of the DSM has typically been used as the criterion or standard (i.e., representing the true diagnosis). If the concerns that have been noted with regard to the appropriateness of using DSM systems to identify all disorders found among persons with severe and profound mental retardation are valid, then using the current version of the DSM as the criteria to establish the validity of new instruments may be problematic. It is also possible

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that certain disorders might exist in such persons but may be presented quite differently than presented in the general population, which would further compromise use of the DSM. Future work in this area of assessment should focus on the need for adequate standardization samples, carefully designed studies of classification accuracy and reliability, developmentally appropriate measures for persons of all ages and levels of mental retardation, and establishment of validity with respect to external criteria (differential response to treatment, long-term outcome, etc.).

E. New Evaluation Techniques The development of neuroimaging technology in recent years presents new opportunities to understand certain psychiatric disorders and to provide rationales for treatment methods. Brain imaging techniques, for example, examine brain structure and anatomy, and include the use of computerized tomography (CT) and magnetic resonance imaging (MRI). Positron-emission tomography (PET) technology emphasizes brain function and provides sophisticated computer images of brain activity that can help to explain causes of emotional states in individuals with and without mental retardation.

IV. TREATMENT AND INTERVENTION A. Historical Perspective on the Treatment of Behavior Disorders With the recognition in recent years that a significant number of people with mental retardation have dual diagnoses, there has come a shift in approaches to treatment. Historically, maladaptive behavior was thought to be primarily a management of care issue and was treated by mental retardation professionals who used behavioral methods. Reduction of behavior problems meant more opportunities for educational, vocational, and residential placements in less restrictive settings, as well as increased involvement in community activities. Recent attention to dual diagnosis, combined with a broadened interest in affective and other internalizing behavior disturbances, has led to a greater involvement of mental health professionals in treatment efforts. Unlike behaviorally oriented therapists who view the specific diagnostic category as less

important than observable behaviors, mental health professionals are more likely to believe that the best possible treatment requires the identification of a specific disorder and an accurate psychiatric diagnosis.

B. Relationship of Causal Factors to Treatment Methods I. Causal Factors Selected treatments of problem behaviors and psychiatric disorders were historically determined in conjunction with specific causal theories (e.g., organic, behavioral, developmental, and sociocultural) that were assumed to explain the behavior. In contrast to this single-factor approach, more recent efforts have focused on the complex interactions of multiple causes (e.g., biological and psychosocial) and on interdisciplinary approaches to treatment. a. Low Intelligence and Environmental Factors Reduced intellectual capacity, along with a limited repertoire of skills for coping with environmental demands, expose children with mental retardation to a wide range of stressful experiences. Some situations, although not unique to persons with mental retardation, are exacerbated by intellectual disability. For example, individuals with mental retardation are more likely to encounter teasing, social rejection, communication handicaps, academic failure, parental guilt and overprotectiveness, and overall rejection than their nonhandicapped peers. Lower intelligence, combined with environmental demands to adapt to novel situations or to modify established patterns of behavior, may also result in higher levels of anxiety. It is not surprising that difficult social situations, combined with limited abilities to handle them, result in an increased vulnerability to develop emotional problems. b. Developmental Explanations Based on the premise that persons with mental retardation develop along the same general patterns but at slower rates than their nonhandicapped peers, behaviors of individuals who are at similar levels of cognitive development are expected to respond in similar ways to environmental events and demands. Moreover, some behaviors that are considered appropriate when displayed by young children could also be considered "appropriate" (not pathological) among older persons with mental retardation who function at lower cognitive levels. In gen-

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eral, current developmental theories of disordered behavior consider genetic background, family history, neurological conditions, and life experiences along with cognitive levels of development. c. Behavioral Theory As noted earlier, behavioral theory has tended to dominate the treatment of maladaptive behaviors that are disruptive or harmful. Behavioral models focus on observed behaviors and on the interactions between people and their environments. Operant conditioning models concentrate on the effects of various types of reinforcement on both prosocial and problem behaviors. The importance of reinforcing appropriate behavior and of discovering and removing unintentional reinforcement of problem behaviors is emphasized. Classical conditioning and social learning theories have been used to explain connections between fears, phobias, and past experiences among persons with and without mental retardation. Although behavioral methods used in isolation have been successful in the reduction of problem behaviors among many persons with mental retardation, the importance of considering possible interactions between specific organic problems and behavioral contingencies has been noted. d. Genetic Links to Behavior Current research efforts have focused on the relationship of psychopathology to psychosocial and genetic factors, suggesting that knowledge of behavioral phenotypes (behaviors associated with specific genetic mental retardation syndromes) may help the development of optimal therapy and intervention for people with different disorders. For example, studies linking molecular genetics to behavioral variables are finding associations between psychopathology, cognition, and specific aspects of the fragile X gene. Other work has shown promising resuits that relate skin-picking and other compulsions to features of chromosome 15. Although there appears to be a link between affective disorders and Down syndrome, researchers have not yet determined that it is the genetic disorder that leads to depression. Current findings in genetic research suggest that the identification of causal relations between specific genetic syndromes and problem behaviors will make rapid progress during the next decade. e. Family Influences The evidence suggests that family processes are contributory factors in some

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cases of behavioral disturbance in children with mental retardation. Notwithstanding the fact that many families with children with retardation function quite well and provide emotional support to their children, the additional stresses associated with the child's disability may lead to home environments and parent-child interactions that contribute to the development of behavior problems or more serious psychopathology. f. The "New Morbidity" Advances in medical care over the last several decades have greatly reduced the incidence of children's mortality and morbidity (illness) from serious infectious disease. At the same time, however, a "new morbidity" has been described that affects a significant number of children in the United States and it appears to be strongly related to socioeconomic status, family constellation, and other social characteristics. These behavioral, social, and schoolrelated problems in American society are thought to be health risks, because they are known to contribute to poor adjustment, handicaps, physical illness, mental retardation, and mental health problems in children. The risk factors associated with the new morbidity tend to operate interactively, causing children to become psychologically and biologically vulnerable to failure in environments that lack the supports necessary to promote their successful adaptation. The concept of a new morbidity has immediate implications for the prevention of dual diagnoses. For example, Fetal Alcohol Syndrome is a preventable condition that is known to be related to emotional disability. It is also one of the most commonly identified causes of mental retardation. Low birthweight babies, more common in poor economic and social environments, are also at high risk of mental retardation and emotional disorders. The concept of a new morbidity suggests that medical advances will not be sufficient to reduce the risk of dual diagnosis. A significant investment is also necessary in research and prevention efforts directed toward the social and behavioral aspects of the new morbidity.

g. Consideration of Multiple Causes: Self-Injury As an Example Causal theories of self-injurious behavior have been studied extensively and can illustrate the ways in which multiple pathways can result in the same observed behavior. Self-injury, which is associated with several types of psychiatric disorder but is

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also observed independent of mental illness, appears to result from a variety of mechanisms. Among the noted origins are direct biochemical causes such as metabolic error (e.g., in persons with Lesch-Nyhan disease), increased levels of B-endorphin that increase tolerance for self-injury, and environmental factors (e.g., inadvertent reinforcement from attention received during behavior-stopping efforts, attempts to communicate needs or feelings). Research studies have also noted that even though one mechanism may serve as the initial cause of self-injury, a shift may occur later to a different mechanism that maintains more serious forms of the behavior. These different origins of self-injurious behavior suggest different approaches to treatment. Therefore, researchers have suggested that the most effective prevention and treatment approaches for behavior problems are determined by an understanding of the history and sequence of causal factors in each individual.

2. Treatment Whereas clinical researchers studying treatment issues traditionally concentrated on problems affecting behavior management and treatment of severe behavior disorders (e.g., self-injurious behavior) in institutional settings, increased attention in recent years to such conditions as depression, schizophrenia, and anxiety disorders reflects a mental health movement that also considers the emotional well-being of all individuals with mental retardation, regardless of their residential placements. Current practices also reflect an interdisciplinary strategy that integrates behavioral, psychopharmacological, developmental, and other approaches to intervention. a. Matching Treatment to Genetic Causes of Mental Retardation The recent literature on syndromerelated differences in psychopathology suggests that improved accuracy in the identification of genetically caused mental retardation syndromes may have important implications for treatment. It has been suggested, for example, that "etiology-specific early intervention" may optimize treatment outcomes for some disorders. This approach assumes that some aspects of treatment are useful for all individuals with a given behavior; whereas other aspects of treatment may be unique to particular etiologies. It should be noted, however, that although certain genetically caused forms of mental retardation show associations with

certain behavioral patterns, the behaviors are usually not exhibited by every person with the syndrome. This area represents a relatively new area of study that is being conducted in connection with the identification of new genetic disorders. b. Behavior Therapies Behavioral procedures have been identified as one of the most effective techniques for eliminating problem behaviors and replacing them with alternative, acceptable, and functional behaviors. Behavioral interventions focus on specific observable behaviors, rather than on syndromes. In a functional analysis of a target problem behavior, the environmental conditions that serve as antecedents or consequences of that behavior are identified. For example, functional analysis might reveal that inappropriate behaviors serve a communication or social function, a self-regulatory function, or a self-reinforcing play function. Similar behaviors can serve different functions across and even within children. Knowledge of this type informs therapists about the design of behavioral interventions. Intervention plans may involve teaching alternate, more appropriate responses to antecedent conditions, improving communication skills, rearranging the environment by removing or reducing stimuli related to problem behavior, or rearranging contingencies associated with the behavior. Functional analyses can be used to modify instructional and environmental variables that affect student behavior at school. Altering antecedent stimuli, such as student choice and variation of tasks, instructional pace, sequencing tasks and breaking them into component parts, and modifying task difficulty have all been shown to reduce the occurrence of problem behavior among students with mental retardation. Although these methods may be less effective for more severe forms of disordered behavior, they are likely to promote learning and improved interpersonal relationships among a large percentage of students who exhibit behavior that is incompatible with effective instruction. Similar behaviors that have different causal factors have been found to be differentially responsive to behavioral treatments. In general, behavioral interventions will be appropriate for learned behaviors, but may not be effective with behaviors that are organically or biologically caused. For example, whereas self-injurious biting among persons with Cornelia de Lange syndrome has been successfully treated by

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operant conditioning, this same behavior in LeschNyhan patients tends to be resistant to behavioral approaches. Because Lesch-Nyhan disease is characterized by a defective enzyme that appears to influence the balance of neurotransmitters in the central nervous system, it is not surprising that behavioral methods are less effective in treating self-injury in these individuals. c. Ethics of Aversive Interventions Behavior reduction programs may use a combination of positive reinforcement and aversive procedures. Aversive interventions have been defined narrowly (e.g., interventions that cause physical or emotional pain or discomfort) and broadly (e.g., interventions that are not "positive," including timeout, physical, or chemical restraints). Although pain or discomfort is commonly associated with aversive interventions, an aversive stimulus is simply a stimulus that a person seeks to avoid, defined by its consequences on the targeted behavior. Questions about the moral justification for the use of these procedures has caused considerable controversy among direct-care workers, clinicians, and professional organizations. Whereas a "freedom from harm" position holds that aversive intervention is morally wrong in all instances, the "right to effective treatment" position contends that unpleasant or painful treatments are ethical if they lead to outcomes that involve less overall physical damage than would be the case without the intervention. The latter position suggests that aversiveness must be judged in the context of long-term suffering experienced by the individual, not just in relation to the immediate effects of the aversive program. In other words, nonaversive interventions that are ineffective or only effective for the short-term, may, in fact, result in more prolonged suffering. Those who support the right to effective treatment base their arguments on an assumption of the effectiveness of aversive interventions; if these procedures are more immediately effective, then their use is justified from the beginning. The argument becomes more complicated in the absence of compelling evidence on the expected efficacy of treatment or degree of harm for specific individuals. Yet, individual circumstances and ethical considerations in studies designed to gather this information make it extremely difficult to gather the information. Other concerns about aversive treatments have been noted regarding the powerful role of the therapist, maintenance and

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generalization issues, lack of social acceptability, and emotional side effects. d. Psychopharmacological Interventions Clinical experience and experimental studies have provided promising evidence that psychopharmacological interventions can effectively treat psychiatric disorders among persons with mental retardation. Moreover, researchers are now finding that many behavior problems that have been resistant to behavioral or other treatment efforts have biological etiologies. There is some optimism that this knowledge will lead to successful prevention and effective neurochemical treatments for at least some of these conditions. For example, self-injurious behavior has been reduced in some individuals by as much as 50% through treatment by drugs that inhibit endorphin release and that appear to lower pain thresholds. Research findings on vulnerable neurotransmitter systems in nonhandicapped adults with Alzheimer's disease have also led to pharmacological strategies that could alleviate cognitive impairments. Several studies have shown that behavioral symptoms associated with autistic disorders, including self-injury and stereotyped behavior, aggression, hyperactive behavior, and affective disorders, can be successfully treated with psychotropic medication. For some conditions, such as schizophrenia, responsiveness to pharmacological treatment has been found to be generally similar to that found among persons with mental retardation. Claims of overuse and misuse of psychotropic drugs in institutional settings (often prescribed without regard to diagnosis and without close monitoring), along with evidence of high rates of the tardive dyskinesia (involuntary movement) side effect during the 1960s and 1970s, created a heightened awareness and even fear of psychopharmacological treatment. Psychopharmacology tended to be directed at the suppression of behavioral symptoms, rather than at matching drug therapies to well-defined syndromes. The antidrug sentiment was probably exacerbated by the exposure of a prominent researcher who was found to have falsified his research on drug therapies. This period was followed by dramatic decreases in psychotropic drug treatment. Although still the subject of controversy, current attitudes are generally more favorable toward drug therapy. Many clinicians are now trained to (a) differentiate psychiatric symptoms from maladaptive behavior, (b) consider the implications of behav-

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ioral syndromes, (c) pay attention to the psychological and physical costs of drug therapy, and (d) plan drug withdrawal programs that monitor the effects of withdrawal. The importance of close monitoring of pharmacological treatments, especially for persons residing in community-based settings, is emphasized. Continued scientific study with controlled procedures and standardized assessments is also needed to answer questions about disorders and medications that have received less attention in previous research, potential side effects, identification of clinical factors that predict who will respond favorably to medical interventions, and the relative importance of linking pharmacological treatment to identified psychiatric disorders (rather than to isolated behavioral symptoms).

e. Skill Development Functional skill development, initiated at early ages, has been hypothesized to play an important role in the prevention of serious behavior problems among persons with mental retardation. State-of-the-art services providing infant and preschool training in communication and social skills represent a comprehensive approach to teaching functional responses that might otherwise be replaced by problem behaviors. This approach to understanding behavior problems focuses on the lack of functional skills, rather than on the presence of behavioral excesses. Researchers and clinicians advocating this approach acknowledge that it may not be applicable to some severe problem behaviors that have physiological origins. The communication function served by problem behaviors among many persons with mental retardation is well established. Communication training provides a mechanism for replacing inappropriate behavior with alternate means of expressing intentions and ideas. Research has demonstrated that even persons with severe degrees of mental retardation can be taught communication skills. Pragmatic theory, which focuses on the social function of language, has been emphasized to teach people with mental retardation to communicate. Social skills training, which is based on the theory that social competence relies on specific skills necessary for social interactions, has been used successfully with many individuals with mental retardation. The need for training in social skills has been emphasized

in numerous studies that have found people with mental retardation to lack the skills required to promote social acceptance and friendships in integrated settings. These studies have concluded that social skills training may be the key to the successful integration of people with mental retardation with their nonhandicapped peers. This training typically focuses on either context-specific skills (e.g., school, workplace, or residential setting) or on reducing social fears among persons with diagnosed social phobias.

V. PROMOTION OF MENTAL HEALTH The President's Committee on Mental Retardation has emphasized the need for national prevention programs in relation to mental health issues of people with mental retardation. Although national prevention programs have received less attention than other mental health issues in terms of federal support, research not specifically aimed at prevention has led to a sense of optimism about preventing or reducing the impact of mental health problems.

A. Prevention and the New Morbidity Recognition of social and economic factors that cause or influence degrees of mental retardation and psychiatric disorders, that is, the new morbidity, has important implications for prevention. Prevention efforts that focus on subgroups with characteristics (e.g., low socioeconomic status, high prevalence of drug and alcohol use) that place them at a high risk for mental retardation and mental health problems will have the greatest impact. For example, improved prenatal care and health-oriented treatment of drug and alcohol abuse during pregnancy are obvious targets of prevention efforts.

B. Genetic Mapping Recent scientific advances in the identification of causal factors related to mental health problems among persons with mental retardation have provided a sense of optimism about the eventual prevention of these conditions. More than 50% of severe and profound mental retardation is caused by genetically determined disorders. The application of DNA tech-

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nology to studies of mental retardation has made it possible to map abnormal genes to specific chromosome regions. Within the next decade or so, researchers expect to define all of the disorders that are associated with severe mental retardation. Ultimately, researchers hope to identify DNA alterations that cause abnormal genes to malfunction. This research is progressing quickly and there is a sense of great optimism, because the capacity to develop DNA markers for genetic causes of mental retardation has important implications for prevention. It will soon be possible to identify persons who are at risk of having children that will be affected with genetic conditions that can result in mental retardation. Moreover, it is possible that in the long range it will be possible to develop complex gene therapies to treat genetic disorders. These developments in genetic mapping have provided new hope with regard to future cures or reversals of effects of inherited diseases that cause both mental retardation and mental illness.

C. Early Intervention Programs Part H of the federal special education law, the Individuals with Disabilities Education Act, mandates that states provide coordinated early intervention services to children with disabilities from birth through 36 months. One component of Part H is the Individualized Family Service Plan, which identifies specific needs of the child and family and designates the services to be provided to meet those needs. Services can include psychological services, family training, counseling, and home training if their purpose is to prevent or reduce the impact of disabilities on the child and family. This recently mandated program, along with other federal and state-sponsored programs that target low income and disadvantaged children, should lead to reductions in the incidence of mental health problems among children with mental retardation.

VI. IMPLICATIONSOF MENTAL HEALTH CONSIDERATIONS A. Cost of Mental Health Care The cost of providing services to individuals in the United States with mental retardation who also dis-

play destructive behavior (e.g., aggression, self-injury, property destruction) was estimated in a 1991 study by the National Institute of Child Health and Human Development to exceed $3.5 billion per year.

B. Residential Placement The presence of behavior problems among people with mental retardation has a direct influence on how and where they will live. In the wake of the deinstitutionalization movement, the majority of people who still reside in large, segregated, residential facilities are either those who are medically fragile or whose behaviors are not tolerated in less restrictive settings. Thus, the presence of challenging behaviors, especially those that are harmful to self, others, or property, limits opportunities for individuals with mental retardation to live with their families or in smaller community placements that provide for increased levels of independence. Studies of individuals living in communitybased residences who are in jeopardy of being moved to more restrictive settings have noted that unmet needs for support, such as mental health services, professional counseling, and behavioral intervention services, contribute to the vulnerability of their residential status. Despite these systematic trends in placement selections, challenging behaviors are present among people in all types of living arrangements. The availability of resources, including well-trained and adequately paid staff, to serve the mental health needs of these individuals, will be a key to their living as independently as possible.

C. Family Issues Research on families of children with mental retardation has established the important role that families play in the development and adjustment of their children. Contrary to earlier stereotypes of these families as typically having serious marital problems, parental psychopathology, and psychosocial adjustment problems, more recent research indicates that families with children with mental retardation are equally likely to function well. Trends toward a more positive perception of these families have not ignored the fact, how-

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ever, that the presence of children with mental retardation adds additional parenting responsibilities and may contribute to higher levels of emotional and physical stress than is found in other families. Caregiving of children with mental retardation, who also have severe behavior problems or psychological disorders, presents additional responsibilities as families encounter more difficulties obtaining needed educational, medical, psychological, or other services. Depending on the condition that is identified as the primary diagnosis, the family may end up working with either or both mental health and mental retardation service systems, where professional attitudes toward parental involvement may differ and conceptual approaches toward treatment are also likely to differ. Although families are no longer implicated as the primary cause of psychological disturbance in their children, various factors related to the home and family context (e.g., marital relationships, parental depression, parent-child interactions, sibling relationships) have been identified as contributory factors for some children. Further research on these relationships is needed.

D. Educational Implications I. Guarantee of Public Education The Individuals with Disabilities Education Act (PL 94-142) requires public education systems to serve all children with mental retardation and severe behavior disorders. To the greatest extent possible, these students must be educated in what is believed to be the least restrictive environment, that is, by spending as much time as possible with their nonhandicapped peers. The law has also been interpreted in such a way as to limit the school system's power to expel a student whose behavior is thought to be part of his or her disability. Each student must have a written Individualized Education Plan (IEP) that describes the major goals of his or her educational program. For children with mental retardation and severe behavior problems, the IEP should address remediation of behavioral excesses and deficits. It should designate opportunities to learn appropriate behaviors and document methods of discipline to be used. The use of intrusive or restrictive disciplinary procedures is prohibited unless there is compelling evidence that they represent least restrictive alternatives.

2. Written Safeguards in Schools The legal guarantees for special education students have also led to the need for administrative procedures that safeguard both teachers and students in relation to responses to unacceptable behaviors exhibited in school. Constitutional rights and full informed parent/guardian consent required by PL 94-142 provide the basic protections to treatment of students. In addition, many schools have established behavioral specialist teams and human rights review committees, along with specific written safeguards that protect the rights of students, teachers, and educational administrators.

E. Service Delivery Systems: Two Handicaps--Two Service Delivery Systems In the 1970s, most states recognized that the servicerelated needs of individuals with mental retardation and mental illness are different and they created two separated bureaucracies to serve them, that is, a department of mental retardation and a department of mental health. Concerns were expressed at the time that the needs of individuals who had both mental retardation and mental health problems might be left unserved, as they fell through the cracks between service delivery systems. Concerns were also voiced about the importance of cross-training competent professionals who would understand the complex mental health issues of people with a dual diagnosis. These concerns remain a high priority today. Historically, efforts were made to distinguish between primary and secondary handicaps, thus determining the agency that would assume primary responsibility for provision of care. Services provided focused on the primary handicap, with little or no attention given to the secondary handicap. The concept of a dual diagnosis represents an alternative to the primary versus secondary handicap distinction, in which presumably all service needs can be addressed. This group of people requires specialized services that involve high levels of agency intercollaboration and interdisciplinary treatment programs; this is clearly an instance where the whole (dual diagnosis) is greater than the sum of its separate parts (mental retardation and mental health needs). Because doctors tend to be trained in either mental retardation o r mental illness, but not

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both, our service systems currently lack professionals specifically trained to treat individuals with dual diagnoses. The federal Department of Health and Human Services has recently recognized this, citing the mental health needs of individuals with developmental disabilities (including mental retardation) as one of its top funding priority areas.

F. Legal Issues The presence of both mental retardation and mental illness poses difficult legal and ethical issues. For example, individuals with mental retardation and serious mental illness may find it difficult, or even impossible, to make informed, legally appropriate decisions. In this case, a third-party decision maker may assume this responsibility. Although this is legally defensible and is intended to benefit the individual, ethical issues remain when personal autonomy is substituted for proxy consent. Thus, according to a "substitute judgment doctrine" invoked by the legal system, the task of the decision maker is to attempt to determine how the individual would have decided if he or she were competent in this role, rather than to judge what is best for him or her. Analysts of this doctrine explain that this rule treats people with dual diagnoses (who are determined incompetent in the legal sense) the same as it treats individuals who can decide for themselves, that is, with respect, autonomy, and dignity of choice. Individuals with dual diagnoses are protected by the due process clauses in the Fifth and Fourteenth Amendments. Therefore, they have the right to the same procedural safeguards as people without mental retardation. This right has particular relevance when individuals with dual diagnoses are accused of crimes, refuse medical treatment, or are placed in state residential facilities. Numerous court cases have confirmed the constitutional rights of this group; neither punishment, nor medication, nor residential confinement without

safety and personal freedom can be denied on the basis of a person's limited intellectual capacity.

BIBLIOGRAPHY Aman, M. G. (1991). Assessing psychopathology and behavior problems in persons with mental retardation: A review of available instruments. [DHHS Publication No. (ADM) 91-1712]. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service, Alcohol, Drug Abuse, and Mental Health Administration, National Institute of Mental Health. Bregman, J. D. (1991 ). Current developments in the understanding of mental retardation: 2. Psychopathology. Journal of the American Academy of Child and Adolescent Psychiatry, 30, 861872. Dibble, E., & Gray, D. B. (Eds.). (1988). Assessment of behavior problems in persons with mental retardation living in the community. Bethesda, MD: National Institute of Mental Health. Koller, H., Richardson, S. A., Katz, M., & McLaren, J. (1982). Behavior disturbance in childhood and the early adult years in populations who were and were not mentally retarded. Journal of Preventive Psychiatry, 87, 386-395. Luckasson, R. (Ed.). (1992). Mental retardation: Definition, classification, and systems of supports (9th ed.). Washington, DC: American Association on Mental Retardation. Matson, J. L., & Barrett, R. P. (Eds.). (1993). Psychopathology in the mentally retarded. Needham Heights, MA: Allyn & Bacon. Matson, J. L., & Mulick, J. A. (Eds.). (1991). Handbook ofmental retardation. New York: Pergamon Press. Nezu, A. M. (Ed.). (1994). Mental retardation and mental illness. Journal of Consulting and Clinical Psychology, 62, 4-62. Repp, A. C., & Singh, N. N. (Eds.). (1990). Perspectives on the use of nonaversive and aversive interventions for persons with developmental disabilities. Sycamore, IL: Sycamore. Rutter, M., & Graham, P. (1970). Epidemiology of psychiatric disorder. In M. Rutter, J. Tizard, & K. Whitmore (Eds.), Education, health, and behavior (pp. 178-201). London: Longman Group. Stark, J. A., Menolascino, F. J., Albarelli, M. H., & Gray, V. C. (Eds.). (1988). Mental retardation and mental health: Classification, diagnosis, treatment, services. New York: SpringerVerlag. Thompson, T., & Gray, D. (Eds.). (1994). Destructive behavior in developmental disabilities. Thousand Oaks, CA: Sage.

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i Mood Disorders Charles DeBattista, H. Brent S01vas0n,and Alan F. Schatzberg Stanford University School of Medicine

I. II. III. IV.

Clinical Syndromes Epidemiology of Mood Disorders Etiology Treatment

The symptom of depression most associated with depression is depressed mood. Depressed patients will often describe a gradually worsening sadness that becomes oppressive and unremitting. At times this dejection comes on abruptly after a significant stressor. However, some patients will develop depressive episodes that are cyclic in nature and seem to have little to do with external stressors. A few patients will not complain of depressed mood at all. They may describe other dysphoric states such as apathy, irritability, numbness, and so on. The description of mood states occurs within a specific social and cultural context. For instance, males in many cultures will be averse to endorsing depressed mood, but may describe other uncomfortable mood states. Anhedonia, or loss of interest or pleasure in usual activities, is the other symptom that occurs in most patients with Major Depression. Activities that were previously enjoyed hold no or little interest in the patient. Recreational activities often cease, and work activities become a struggle. Libido, or sexual interest, tends to diminish along with other interests. In addition to anhedonia and/or depressed mood, patients with Major Depression experience a variety of vegetative symptoms that affect energy, sleep, and appetite. Fatigue is experienced by most patients with Major Depression and is often the presenting symptom. The patient may feel that there is something physically wrong with them and seek advice from their general practitioner. Some patients describe a heaviness in the limbs and find that even small tasks are exhausting. Sleep disturbance in Major Depression can take any form but is classically characterized by early morning

M O O D DISORDERS represent a common and heterogeneous group of disorders. According to the third edition of the American Heritage Dictionary, mood refers to "an emotional state," while affect is a verb that means "to act on one's emotions." The clinician tends to regard mood as a subjective state described by the patient, while affect is objective evidence of the mood state observed clinically. Mood disorders and affective disorders have been used synonymously to describe the four major mood disorders and their variations: major depressive disorder, bipolar disorder, Dysthymia, and Cyclothymia. However the current nosology, DSMIV, uses the term "mood disorders" as a more encompassing class of psychopathology, since these disorders may not always be apparent as disorders of affect.

I. CLINICAL SYNDROMES A. Major Depressive Episode Major Depression represents a syndrome of both emotional and physical signs and symptoms lasting for at least two weeks (see Table I). Depression differs from sadness in its persistent quality, its physical manifestations, and by the fact that it significantly affects the ability of the patient to function normally. A major depressive episode can range from mild to incapacitating and life threatening. [See DEPRESSION.]

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Copyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

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Table I DSM-IV Criteria for Major Depressive Episode* A. Five or more of the symptoms listed below have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either depressed mood or loss of interest or pleasure. (1) Depressed mood most of the day nearly every day, as indicated either by subjective report (e.g., feels sad or empty) or observations of others (e.g., appears tearful). Note: In children and adolescents, can be irritable mood. (2) Markedly diminished interest or pleasure in all, or almost all, activities most of the day nearly every day, as indicated by subjective account or observations of others. (3) Significantweight loss when not dieting or weight gain (e.g., a change of more than 5% body weight in one month or decrease or increase in appetite nearly every day. Note: In children, failure to achieve expected weight gains. (4) Insomnia or hypersomnia nearly every day. (5) Psychomotor agitation or retardation nearly every day, as indicated not merely by subjective feelings of restlessness or being slowed down but by observations of others. (6) Fatigue or loss of energy nearly every day. (7) Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day, as indicated not merely by self-reproach or guilt about being sick. (8) Diminished ability to think or concentrate or indecisiveness nearly every day, as indicated either by subjective account or observations of others. (9) Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide. B. The symptoms do not meet criteria for a mixed episode. C. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. D. The symptoms are not due to the direct physiological effects of a substance (e.g., an abused drug, a medication) or a general medical condition (e.g., hypothyroidism). E. The symptoms are not better accounted for by bereavement (i.e., after the loss of a loved one) or the symptoms persist for longer than 2 months or are characterized by marked functional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation. * Reproduced with permission of APA Press. awakenings with an inability to fall back asleep (terminal insomnia). These awakenings occur at least 2 hours before usual awakening. Patients typically feel at their worst in the early morning, but may feel somew h a t better as the day progresses (diurnal variation of depression). Patients may have other types of sleep disturbance, including having trouble falling asleep (initial insomnia), trouble with waking up in the middle of the night (middle insomnia), or sleeping too much (hypersomnia). Appetite may be significantly impacted in depressed patients. Anorexia, or a loss of appetite, often occurs in depressed patients. The most severely depressed patients can require feeding tubes because they have lost all interest in food. Some loss of weight is c o m m o n . However, other depressed patients gain weight when they are depressed and will find not overeating to be a significant struggle. [See ANOREXIA NERVOSA AND BuLIMIA NERVOSA.] Feelings of worthlessness, hopelessness, and guilt are also very c o m m o n in M a j o r Depression. Patients may dwell on previous indiscretions long ignored before the depressive episode, and decide that they are

being punished for earlier sins. Sometimes, this guilt can take on delusional p r o p o r t i o n s and the patient is then said to have a psychotic depression. Those afflicted often feel hopeless that things will get any better and may feel they are a burden with nothing to contribute to their friends, family or society. M o s t depressed patients will entertain thoughts of death at some point in their illness. These thoughts are often passive in nature: wishing they w o u l d die in their sleep or cease to exist. However, depressed patients c o m m o n l y develop specific suicidal thoughts, and approximately 15 % of untreated patients succeed in eventually killing themselves. [See SUICIDE.] Patients with M a j o r Depression often have their first episode in early adulthood, but 5 0 % of patients experienced a first depressive episode after age 40. The mean age of onset for M a j o r Depression is a r o u n d age 40. An untreated episode tends to last from 6 to 12 months, but 2 0 % of patients will have episodes that last for more than 2 years. Recurrences are expected in M a j o r Depression, with at least 75 % of patients having a second episode within 10 years of the first episode.

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B. Bipolar Disorder Along with Major Depression, bipolar, or manic depressive disorder, represents a major mood disorder. "Bipolar" refers to the fact that patients may experience two clinical poles: depression, and mania or hypomania. Most bipolar patients experience multiple cycles of depression interspersed with mania or hypomania. Less than 10% of bipolar patients tend to only experience manic-type episodes and not depression. However, any patient who experiences at least one hypomanic episode, that is not explained by another disorder, is conventionally described as bipolar. A manic episode may be thought of as the flip side of a depressive episode. Instead of patients feeling depressed, they may feel euphoric and on top of the world. However, as the manic episode evolves, panic and dysphoria may be common features. Instead of feeling fatigued and lacking in energy, the manic patient has more energy than he can handle, and may need very little sleep or no sleep at all. Rather than feeling bad about himself like the patient in a depressive episode, the manic patient may be quite grandiose. Likewise, anhedonia in the depressed patient is replaced by an increase in goal-directed activity in which the patient may try to accomplish too much and have extremely unrealistic goals. There is often a certain impulsivity that may get manic patients into trouble in business and legal transactions as well as interpersonally. Their judgment tends to be impaired during manic states. For example, they may impulsively spend their life savings on a foolish business venture, or take a flight on the impulse that it would be nice to be in a different country. Manic patients may lose contact with reality, become floridly psychotic, and experience hallucinations as well as paranoid or grandiose delusions. A formal thought disorder characterized by disorganized, tangential, or circumstantial thought may be more common in mania than it is in schizophrenia. More rarely, impulsive criminal acts may occur during a manic state. Violent acts are sometimes carried out that are uncharacteristic of the patient. By convention, manic episodes must last at least i week but tend to average 8 to 16 weeks. Bipolar patients may have manic and depressive episodes that occur four or more times a year (rapid-cycling bipolar illness), but more commonly the episodes are separated by 6 months to a year as the illness progresses. Patients who experience

full manic episodes as opposed to hypomanic periods are said to suffer from Bipolar I Disorder. About 10 manic episodes in a lifetime is the mean for bipolar I patients, but many patients suffer from more frequent episodes. (See Table II.) Bipolar I Disorder may begin in childhood, but more commonly begins in early adulthood. The earlier the onset, the worse the prognosis tends to be. The mean age of onset is approximately 30 years old. The index or first mood disturbance in bipolar patients tends to be Major Depression. This depression can precede the advent of manic episodes by many years. Bipolar disorder is characterized by episodic cycles with a relative remission of symptoms between episodes. Sometimes, bipolar patients will have episodes with features of depression and mania simultaneously. For example, they may describe high energy and decreased need for sleep, but complain of severe depression and suicidal thoughts. These episodes are referred to as mixed episodes and appear less common than manic, hypomanic, or depressed episodes. A hypomanic episode, on the other hand is a grade below mania in its presentation. It may have a shorter duration than a typical manic episode (4 days or longer), is not characterized by psychosis, and is not of sufficient intensity that the patient requires hospitalization. The symptoms of hypomania are otherwise like the symptoms of mania including increased energy, hyperverbal speech, grandiosity, increase in goal directed activity, and so on, but of lower severity. Some bipolar disorders are characterized only by hypomanic episodes interspersed with Major Depression and are called Bipolar II Disorder, to distinguish them from classic or Bipolar I Disorder in which the patient has full blown manic episodes. Bipolar II Disorder, like Bipolar I, often begins in early adulthood with a major depressive episode. The hypomanic episodes tend to be briefer than manic episodes, and rapid cycling appears to be more common than in Bipolar I Disorder. Cyclothymia often evolves into Bipolar II Disorder, and in turn, bipolar II sometimes evolves into bipolar I.

C. Dysthymic Disorder Dysthymic Disorder is a low-grade depression lasting at least 2 years and often a lifetime. Like Major Depression, it is characterized by depressed mood. How-

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D S M - I V Criteria for Manic Episode .

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A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood, lasting at least one week (or any duration if hospitalization is necessary). B. During the period of mood disturbance, three (or more) of the following symptoms have persisted (four if the mood is only irritable) and have been present to a significant degree: 1. Inflated self-esteem or grandiosity; 2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep); 3. More talkative than usual or feels pressure to keep talking; 4. Flight of ideas or subjective experience that thoughts are racing; 5. Distractibility (i.e., attention to or easily drawn to unimportant or irrelevant external stimuli); 6. Increase in goal-directed avtivity (socially, at work or school, or sexually) or psychomotor agitation; 7. Excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments). C. The symptoms do not meet criteria from mixed episode. D. The mood disturbance is sufficiently severe to cause marked impairment in occupational functioning in usual social activities or relationships with others or to necessitate hospitalization to prevent harm to self or others, or there are psychotic features. E. The symptoms are not due to the direct physiological effects of a substance (e.g., an abused drug, a medication, or other treatment) or a general medical condition (e.g., hyperthyroidism). Note: Manic-like episodes that are clearly caused by somatic antidepressant treatment (e.g., medication, electroconvulsive therapy, light therapy) should not count toward a diagnosis of bipolar I disorder. D S M - I V Criteria for Hypomanic Episode A. A distinct period of persistently elevated, expansive, or irritable mood, lasting at least 4 days, that is clearly different from the usual nondepressed mood. B. During the period of mood disturbance, three (or more) of the following symptoms have persisted (four if the mood is only irritable) and have been present to a significant degree: 1. Inflated self-esteem or grandiosity; 2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep); 3. More talkative than usual or feels pressure to keep talking; 4. Flight of ideas or subjective experience that thoughts are racing; 5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli); 6. Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation; 7. Excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g., the person engages in unrestrained buying sprees, sexual indiscretions, or foolish business investments). C. The episode is associated with an unequivocal change in functioning that is uncharacteristic of the person when not symptomatic. D. The disturbance in mood and the change in functioning are observable by others. E. The episode is not severe enough to cause marked impairment in social or occupational functioning or to necessitate hospitalization, and there are no psychotic features. F. The symptoms are not due to the direct physiological effects of a substance (e.g., an abused drug, a medication, or other treatment) or a general medical condition (e.g., hyperthyroidism). Note: Hypomanic-like episodes that are clearly caused by somatic antidepressant treatment (e.g., medication, electroconvulsive therapy, light therapy) should not count toward a diagnosis of bipolar II disorder.

ever, the d e p r e s s e d m o o d need only be p r e s e n t m o r e days t h a n not, r a t h e r t h a n m o s t of the day every day as in M a j o r D e p r e s s i o n . Energy, appetite, a n d sleep d i s t u r b a n c e m a y be p r e s e n t but n o t in the incapacitating w a y t h a t is e v i d e n t in M a j o r D e p r e s s i o n . Dyst h y m i c D i s o r d e r tends to be m o r e c h a r a c t e r i z e d by chronic, lifelong p a t t e r n s of low self-esteem a n d pessimism, r a t h e r t h a n discrete episodes of m o r e severe depression. T h u s , a mild d e p r e s s i o n pervades the personality of the d y s t h y m i c p e r s o n to the e x t e n t t h a t

such a p e r s o n can often n o t recall n o t being depressed. (See Table III.) D y s t h y m i a usually begins g r a d u a l l y in adolescence or early a d u l t h o o d . Patients often describe themselves as being d e p r e s s e d since birth. T h e d i s o r d e r tends to define the p e r s o n to s o m e extent, a n d afflicted patients r e g a r d the D y s t h y m i a as p a r t of w h o they are. Dyst h y m i c D i s o r d e r a p p e a r s to be a risk factor for o t h e r m o o d disorders. For e x a m p l e , at least 2 0 % of dyst h y m i c patients go on to develop m a j o r depressive epi-

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Table III .

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DSM-IV Criteria for Dysthymia

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A. Depressed mood for most of the day more days than not for at least 2 years, as indicated either by subjective account or observations of others. Note: In children and adolescents, mood can be irritable, and duration must be at least 1 year. B. Presence,while depressed, of two (or more) of the following: 1. Poor appetite or overeating; 2. Insomnia or hypersomnia; 3. Low energy or fatigue; 4. Low self-esteem; 5. Poor concentration or difficulty making decisions; 6. Feelingsof hopelessness. C. During the past 2-year period (one year for children or adolescents) of the disturbance, the person has never been without the symptoms in Criteria A and B for more than 2 months at a time. D. No major depressive episode has been present during the first 2 years of the disturbance (1 year for children and adolescents), i.e., the disturbance is not better accounted for by chronic major depressive disorder or major depressive disorder in partial remission. E. There has never been a manic episode, a mixed episode, or a hypomanic episode; and criteria has not been met for cyclothymic disorder. F. The disturbance does not occur exclusivelyduring the course of a chronic psychotic disorder, such as schizophrenia or delusional disorder. G. The symptoms are not due to the direct psysiological effects of a substance (e.g., an abused drug or a medication) or a general medical condition (e.g., hypothyroidism). H. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

sodes. Such patients may have Dysthymia interspersed with discrete, more severe, major depressive episodes in which they are incapacitated. This pattern of Dysthymia with superimposed Major Depression is referred to as "double depression" and appears to be a more difficult type of depression to treat. In addition, as m a n y as 15% of dysthymic patients develop bipolar type I or II disorder.

D. Cyclothymic Disorder Cyclothymic Disorder, like Dysthymic Disorder, is a chronic disorder of at least 2 years' duration in which the afflicted person has multiple episodes of hypomania interspersed with mild depressive periods. The cycles in cyclothymic patients tend to be neither as robust nor as long as they are in bipolar illness. However, the changes in cycles are often abrupt and disruptive. If the patient ever has a full manic episode or meets criteria for Major Depression along with hypomanic episodes, the patient would then have an established bipolar I or II disorder. Cyclothymic Disorder appears to be on a spectrum with bipolar illness. In most cyclothymic patients, the disorder begins gradually in adolescence or early adulthood. Children who go on to be cyclothymic are sometimes described as irritable and moody. As one can imagine, the hy-

pomanic and depressive periods in cyclothymic disorder may significantly interfere with interpersonal relationships, careers, and general well-being. During hypomanic episodes, the patient's judgment may be somewhat impaired and irritability may be a significant problem. On the other hand, the patient may be very productive during the hypomania and achieve significant success in their field. The depressive episodes tend to be disruptive but not disabling. Cyclothymic Disorder tends to be lifelong, and may evolve into bipolar disorder. In some surveys, from 30 to 4 5 % of cyclothymic patients will eventually meet criteria for bipolar disorder.

II. EPIDEMIOLOGY OF MOOD DISORDERS M o o d disorders are quite prevalent in the United States and represent among the most c o m m o n reasons patients seek mental health treatment. For example, M a j o r Depression may occur in up to 26 % of women and 12% of men during their lives. At any point in time, as m a n y as 6% of the American population suffer from Major Depression; this is upwards of 11 million people. In all cultures, depression appears to be about twice as c o m m o n in women as it does in men. The prevalence of depression does not appear to be

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higher in any socioeconomic or racial group but is more common in single and divorced persons. Dysthymic disorder is also fairly common with around 3 % of the population suffering from this disorder. As with Major Depression, women are far more likely to be afflicted than men. Dysthymia also appears to be more common in lower socioeconomic groups and in unmarried adults. Bipolar I Disorder is equally found in men and women. About 1% of the population suffers from Bipolar I Disorder, but the incidence of Bipolar II Disorder appears to be several times higher. There is some evidence that bipolar disorder may be more evident in higher socioeconomic groups. In contrast, bipolar disorder may occur at higher rates in populations who are not college educated, perhaps because the earlier onset of the illness may interfere with the ability to pursue higher education. Cyclothymia may be somewhat more common in females than males. As in Bipolar I Disorder, the prevalence of Cyclothymia is estimated at about 1% of the population.

III. ETIOLOGY Mood disorders appear to have causes that defy simple explanations. In most cases there appears to be a complex interrelationship of biological, psychological, and social factors that contribute to the onset and maintenance of a mood disorder in a given person. The available data would suggest that Dysthymia is biologically related to Major Depression in many ways and the same is true for Cyclothymia and bipolar disorder. The etiology of Major Depression and bipolar spectrum disorders has been the object of intense investigation over the past 50 years. Biological factors have been demonstrated to be significant in the cause of depression spectrum illness. Among the biological factors most studied are genetic contributions to the mood disorders. Depression and bipolar illness tend to run in families, although the evidence for familial transmission is greater in bipolar disorder. Perhaps the greatest risk factor for developing a major mood disorder is having a biologic parent who also suffers from a mood disorder. In bipolar disorder, for example, the rate of bipolar illness in first degree relatives is 10 to 20 times higher than it is in the general

population. Major depression is also more prevalent in the first-degree relatives of both bipolar patients and unipolar depressed patients. If one parent suffers from Bipolar I Disorder, the children have approximately a I in 4 chance of developing the illness. If both parents are afflicted, the rate increases to as much as 75 % in some studies. One could argue that having parents or siblings afflicted with a major mood disorder presents a significant environmental stressor that may account for the increased prevalence of the disorder in other family members. However, adoption and twin studies would argue that environmental factors only partially explain the higher rate of mood disorders among family members. For example, adoption studies indicate that the rate of Major Depression and bipolar illness is much higher in the biological children of patients with major mood disorders, even if the children are raised from birth by parents who are not afflicted. Monozygotic twin studies provide even more substantial evidence that some form of genetic transmission appears to increase the vulnerability of some patients to mood disorders. Identical twins, including those raised apart from birth, have a high concordance rate for both Major Depression and bipolar illness. If one twin develops Bipolar I Disorder, for example, there is a 30 to 90% chance the other twin will also develop the disorder. The concordance rate among monozygotic twins with Major Depression appears to be about 50%. Just what is being genetically transmitted is not at all clear. Attempts to find specific genes for the mood disorders have so far not yielded clear-cut nor reproducible results. Abnormalities with monoamine neurotransmitters such as serotonin, norepinephrine, and dopamine have been implicated in the etiology of mood disorders. The evidence that mood disorders may be related to nonoamine abnormalities comes from several lines of evidence. The first is that drugs that deplete monoamines like reserpine appear to precipitate depression in some people. Likewise, in patients who respond to serotonergic antidepressants, depriving the diet of precursors necessary for the synthesis of serotonin quickly results in relapse of symptoms. Functional imaging studies suggest that there is a reduction in activity in ascending monoaminergic pathways in depressed patients and there is also some evidence of decreased activity of the monoamines from the evaluation of metabolites of monoamines in urine and cerebrospinal fluid. The

Mood Disorders

strongest evidence for monoamine involvement in major depressive episodes comes from antidepressants. All known effective antidepressants appear to enhance neurotransmission of the monoamines, particularly serotonin and norepinephrine. During manic episodes, there is evidence of overactivity of dopamine and other monoamines. Dopaminergic antagonists such as typical antipsychotics, in addition to mood stabilizing agents, appear to be very helpful in treating acute mania. Mood disorders are commonly associated with neuroendocrine abnormalities. Patients with Major Depression appear to have higher rates of abnormalities in the hypothalamic pituitary axis (HPA). For example, patients with Major Depression tend to have higher serum levels of the stress hormone cortisol. More severe depressions tend to be associated with higher levels of serum cortisol. Thus, depressed patients tend to show abnormalities in tests of the HPA axis such as the dexamethasone suppression test. This test is not specific nor sensitive enough, however, to make the diagnosis of Major Depression. Abnormalities in the thyroid axis are also quite common in Major Depression and depressive spectrum illness. Hypothyroidism often presents with symptoms of depression. In addition, about 40% of depressed patients with normal thyroid levels will show blunting of the thyroid axis with provocative tests, such as the administration of thyroid stimulating hormone. It is unclear whether thyroid abnormalities are associated with an increased vulnerability for depression, or the presence of depression increases the likelihood of thyroid abnormalities. Whatever biological vulnerability may be present in the etiology of mood disorders, psychosocial factors appear to be very important. Biological and psychological explanations need not be mutually exclusive. At least early in the natural course of a mood disorder, stresses and the social environment play a significant role. Major losses of various kinds, such as the death of loved one, the loss of a spouse through divorce, the loss of a career, and so on may precipitate either depression or mania in a susceptible patient. The loss of a parent before adolescence also appears to be a risk factor for developing Major Depression in adulthood. Real or imagined losses may be equally potent at precipitating mood disorders. Even in the case of a significant stressor such as the loss of a loved one, both biological and psychological

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factors can be posited. Psychological explanations would include the Freudian concept of anger being associated with object loss. Freud suggested that object loss results in a patient trying to become like the lost person (introjection) as a way of possessing part of the lost person within themselves. However, the patient also feels angry at the lost person for abandoning them and since they have introjected the lost object, the anger is directed at themselves. The depressed patient starts hating himself, feels worthless, and may ultimately kill himself out of anger toward the lost object. In variations of this theory, the introjection is not necessarily a lost object but an ambivalently held love object such as parent. The part of the parent that is introjected is punitive, critical, and becomes part of the superego or conscience. The patient is always trying to achieve a parental standard that is idealized and unobtainable. As a result, the patient feels guilty and worthless. The biological theorist, on the other hand, would argue that losses, particularly early in life, may result in lifelong changes including higher cortisol responses to stress. These enhanced biological reactions to stress may result in long-term changes in noradrenergic and serotonergic neurotransmitters and their receptors. The psychoanalytic theories of depression may be way of describing the psychological machinery and personal experience associated with the biological changes that may occur secondary to object loss. Freud himself noted some forms of depression were biological in etiology. In psychodynamic theory, mania and hypomania are considered a maladaptive defense to depression. As a way of defending against depression, a patient is occasionally able to throw off the shackles of an overly punitive superego. The neutralization of the superego may emerge from excessive denial or through the temporary merger of the ego with the superego. When this happens, self-criticism and self-loathing are replaced by euphoria and grandiosity. The patient believes that there is nothing he cannot accomplish and, with the absence or neutralization of the superego, guilt no longer is major factor. In this environment, sexual indiscretions, free spending, and other impulsive manic and hypomanic actions become possible. Other more recent psychological theories include the cognitive behavioral theory of depression proposed by Aaron Beck. Beck and his colleagues conceptualize depression and Dysthymia as resulting from

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cognitive distortions. The problem, in this theoretical framework, is not loss or other stressors, but how these stressors are perceived. A depressed patient is likely to make cognitive errors in his perception of events that result in a negative mood and perhaps feelings of hopeless and worthlessness. For example, a patient prone to depression might perceive a work evaluation that shows a deficiency in some area, in a maladaptive way. The patient may magnify the significance of the evaluation and overgeneralize that he is incompetent at all aspects of his work instead of the narrow aspect defined the evaluation. Catastrophic thinking may ensue that the patient will lose his job, be out on the street, and never be able to find another job. The accumulation of cognitive errors such as these may result in the patient developing a major depressive episode or Dysthymia. Social factors have also been implicated in the etiology of mood disorders. Early childhood deprivation in the form of grossly inadequate parenting or institutional care may be associated with developing depressive states in adulthood. While socioeconomic factors are not necessarily correlated with Major Depression, they are correlated with Dysthymia and bipolar illness. Lower socioeconomic status may be associated with Dysthymia and higher socioeconomic status with bipolar illness. These correlations may be the result of diagnostic bias, or may be a function of factors related to economic position. For example, economic success may be associated with increased motivation, perseverance, creativity and other factors. Some theorists have suggested that mania and hypomania may be the biological exaggeration of these traits and therefore would congregate in families in which these traits are present. There is little evidence for this theory but it remains an interesting idea. It is more intuitive that poverty can present a significant stressor that might be depressogenic in some people.

IV. TREATMENT A. Somatic Therapy Once the diagnosis has been secured, and medical or substance-induced mood disturbances have been

ruled out, the treatment of mood disorders will need to address the biological, interpersonal, and social dysfunction which cause such significant morbidity. Given our current knowledge of the biological basis for these disorders, a variety of somatic treatments are available. For depressive spectrum disorders physicians and mental health practitioners currently employ six classes of antidepressants. These are the selective serotonin reuptake inhibitors (SSRIs) such as Prozac (fluoxetines); the serotonin and norepinephrine reuptake inhibitors (SNRIs) such as Effexor (venlafaxine); agents which act at postsynaptic receptors such as the 5HT2 receptor antagonists, such as Serzone (nefazodone) and Deseryl (trazodone); monoamine oxidase inhibitors (MAOIs) such as Nardil (phenelzine); the large class of tricyclic drugs (TCAs) that include Tofranil (imipramine) and Pamelor (nortriptyline); and atypical agents, such as Remeron (mirtazapine) and Bupropion (wellbutrin). The available antidepressants differ in mechanism of action and side effects, but share a number of common features. For example, all of the antidepressants appear to work by enhancing the neurotransmission of monoamines in the brain. Overall, the antidepressants appear to be equally efficacious in the treatment of depression, but some subtypes may respond preferentially to one class over another. In general, a depressed patient has a 60 to 70% chance of responding to the first antidepressant they try, regardless of which agent that happens to be. The use of an antidepressant will double the likelihood that a patient will recover from an episode of Major Depression in the first 2 months. Therefore, atypical antidepressant trial is from 1 to 2 months, and patients who respond are kept on the medication for at least 6 months to reduce the risk of relapse. Patients who have had many recurrences of Major Depression may be kept on an antidepressant for many years or even a lifetime. Antidepressants do not carry the risk of tolerance and addiction that are common to mood-elevating street drugs, such as cocaine or amphetamine. Finally, none of the antidepressants work immediately. The maximum antidepressant effects may not be seen for 1 month or longer. Given the many drug classes which may be used to treat depression, the choice of a particular antidepressant rests on considerations of safety, severity, a constellation of symptoms suggestive of Major Depression

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versus Dysthymia, the presence of a bipolar spectrum illness including Cyclothymia, tolerability, and the risk of toxicity. In this regard clinicians consider the age of the patient, and concurrent medical illness. In addition, a past history in the individual or in the family of a response to a particular class of drug may direct the selection of an antidepressant. Patients with Major Depression who do not respond to an initial antidepressant trial have approximately an 80 to 90% chance of eventually responding to a subsequent trial of antidepressants. However, it may take several trials before an adequate medication is discovered. At least 10 to 20% of seriously depressed patients will fail to respond to all antidepressants. In such cases, approaches such as electroconvulsive therapy (ECT) are often considered. ECT is one of the oldest and most controversial procedures in psychiatry having been used since the 1930s. It involves passing small electric current through the cranium while a patient is under general anesthesia with their muscles relaxed. The stimulus results in a generalized seizure lasting for 30 to 120 seconds and a series of from 6 to 12 treatments given every other day often results in remission of the Major Depression. Compared to medications, ECT is probably more effective and faster acting. However, patients will typically have some problems with retrograde and anterograde memory that is typically short-lived, but may last for weeks or longer after a series of treatments. When a patient suffers from recurrent seasonal depressions, light therapy (phototherapy) is sometimes employed. Winter depressions usually begin in the fall as days shorten, tend to be at their worst in the winter, and improve in the spring. The depression is thought to be related to the shorter periods of light in the winter that may result in some hormonal and neurochemical changes in susceptible patients, which leads to depression. Such patients may respond to exposure to a light box with full spectrum light at the beginning or end of the day during the winter months. The pharmacological treatment of Dysthymia follows the treatment of Major Depression. Current strategies include SSRIs, MAOIIs, and TCAs. There are no "head-to-head" studies that define which treatments are more efficacious, but a first choice in treatment would be an SSRI, given its safety and ease of administration. Failure on one or more SSRIs may suggest trial of an MAOII, which in some studies show better improvement than TCAs. There is some

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anecdotal evidence that response, for instance to an SSRI, may require a longer treatment window, up to 16 weeks. More aggressive treatment, such as ECT, does not appear to be useful in the treatment of Dysthymia. In bipolar spectrum disorders, the depressive phase is treated with the agents described above, but concurrent with these agents, a mood stabilizer such as lithium, valproate, or carbamazepine will be used. There has recently been a surge of interest in valproate in the treatment of acute mania, with results suggesting it is more effective than the traditional agent lithium in patients with significant irritability and in mixed episodes. However, the data showing that valproate is also as effective as lithium in the prophylaxis of manic episodes has not yet been established. Lithium has been the standard mood stabilizer in bipolar disorder for more than 25 years. It is an effective prophylactic agent in approximately two-thirds of patients for mania and possibly for depression. Responders to lithium are characterized by the presence of euphoric mood, infrequent episodes, a family history of bipolar disorder and response to lithium, and a profile of mood changes consisting of depression to mania to euthymic interval pattern. It is effective in treating 30% of rapid cyclers, and 40% in mixed or dysphoric manic states. In classic bipolar patients the response rate is as high as 60 to 80%, although including the mixed states the response overall is about 50 % of patients. All currently used mood stabilizers have the potential for significant toxicity. For example, the mood stabilizers have a potential for neurotoxicity ranging from a mild tremor at the therapeutic doses to delirium, coma, and death in overdose. The chronic use of lithium is sometimes associated with changes in kidney function, while valproate can be toxic to the liver. Carbamazepine is sometimes associated changes in blood cell and platelets that can sometimes be quite toxic. The treatment of acute mania can include the use of a mood stabilizer, along with antipsychotic drugs and hypnotic agents such as diazepam (Valium) or lorezapam (Ativan). There is some suggestion that valproate alone can treat the acute manic symptoms as well as psychosis during the acute episode without an additional neuroleptic. The treatment of the depressive phase (bipolar major depressive episodes) is characterized by treatment

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during the depressive phase only, and caution with agents with a history of inducing manic episodes. Tricyclic antidepressants have been most implicated in induced mania and induction of rapid cycling, but all antidepressants have the potential to induce mania. MAOIIs and Bupropion have some support for being less likely to induce mania or rapid cycling. Currently, the strategy recommended by some experts starts with a MAOII, followed by Bupropion or an SSRI, followed by a TCA. Light therapy may be useful when a seasonal variation is observed. Neuroleptics play an uncertain role in the absence of psychosis, although as noted above clozaril may act as a mood stabilizer and risperidone may act as an antidepressant. Cyclothymia, a bipolar spectrum disorder, may be treated with lithium, valproate, or other mood stabilizer. There is some evidence that Cyclothymia responds at lower doses than those used to treat type I bipolar illness. Treatment with antidepressants risks a hypomanic or manic episode. About one-third of these patients become bipolar, and most often bipolar II. Therefore, in treatment of Cyclothymia, the presence of a developing bipolar disorder, and treatment strategies used in bipolar disorder, need to be considered.

B. Psychosocial Treatments A number of psychotherapy strategies have been employed in the treatment of Major Depression, Dysthymia, and the depressive phase of bipolar illness. The most common of these are cognitive behavioral therapy, interpersonal psychotherapy and psychodynamic psychotherapy. Cognitive Behavioral Therapy (CBT) is the beststudied psychotherapy for the treatment of depression. It appears to be as efficacious as medications in mild to moderate depression, and may have some prophylactic benefits as well. CBT is typically a timelimited psychotherapy of between 12 and 20 sessions. As described earlier, the underlying premise of CBT is that depression is caused and maintained by cognitive distortions in a susceptible person. A number of cognitive errors have been described in depression. These include the tendency to catastrophic and all-ornothing thinking. Depressed patients tend to amplify the negative aspects of their experience such that molehills are transformed into mountains. Depressed patients will dwell on minor events or flaws in their character to the extent that these take on undue importance in the patient's life. The emotional reaction

to amplifying these negative events or traits is for the depressed patient to feel increasingly helpless, worthless, guilty, and depressed. These cognitive errors are often of an automatic quality. They occur too rapidly for rational assessment and may be unconscious. For example, depressed patients will typically be quite self-critical in response to perceived shortcomings. But an assessment by the patient in response to a particular situation such as "I am so stupid" may be rapid and automatic that awareness of this assessment is lacking. However, the patient may be aware of the emotional reaction to this assessment: dysphoria. The goal of CBT is to increase the awareness of these automatic thoughts and cognitive distortions so that they may be rationally challenged. The CBT therapist use a variety of techniques to this end. Patients undergoing CBT are assigned homework in which they may have to keep a diary after each session. The diary is a tool for the patient to track their cognitive process that is associated with negative states and allow the patient to focus on these. The diary is reviewed in the subsequent CBT session and cognitive errors are pointed out by the therapist. In time the patient becomes aware of the distortions as they occur and can effectively challenge them. Behavioral techniques are also employed in CBT to mobilize the depressed patients. Social skills and assertiveness training are often used in CBT to help the depressed counter social isolation and feelings of inadequacy in interpersonal relationships. Patients are put on schedules of activities to further mobilize them. Patients are also assigned tasks in increasing order of complexity and challenge so that the depressed persons slowly develop a sense of mastery over tasks they felt they could not do. Another type of psychotherapy that is well studied in the treatment of depressive states is interpersonal psychology (IPT). This therapy is based on the work of Gerald Klerman and Myrna Weissman and based on the theory that depression results from deficiencies in social functioning, dependency, intimacy, and social isolation. Like CBT, IPT is time-limited and typically lasts for 12 to 20 sessions. The goals of IPT are to identify problem areas such as grief reactions, interpersonal disputes, and problems with interpersonal communication. IPT sessions revolve around clarifying the negative feeling associated with these problems and developing options for contending with these problems. Techniques used in

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IPT include reassuring the patient, testing the patient's perceptions of what happened interpersonally, and teaching techniques for improving communication. IPT appears to be effective in mild to moderate depression alone. However, the best results often have been obtained when IPT is combined with pharmacotherapy. Psychodynamic therapies are based on the work of Sigmund Freud and subsequent therapy, and has been used for almost 100 years in the treatment of depression. Psychodynamic therapy focuses on the childhood origins of depression as well as unconscious motives and defenses as they relate to current conflicts. Dynamic therapy tend to be more open-ended and less directive than IPT or CBT. Sessions may occur up to several times a week and may last for years. The relationship of the patient to the therapist is evaluated as a way of correcting problems that may occur or have occurred in past relationships. Sessions may have the goal of obtaining insight into the roots of the depression so they can be effectively dealt with. However, dynamic therapy may also be supportive in nature and have the goals of encouraging rest, taking active steps to reduce stressors, and allowing the patient a safe place to vent emotions. While the efficacy of dynamic therapy is less well established than that of IPT or CBT, there are patients who clearly benefit from this approach over others. Family and group therapies, as well as psychoeducation, are very important for patients with depression and bipolar spectrum illness. Depression does not occur in a vacuum, and tends to intimately affect family members. Families, in turn, can help buffer patients from stressors or increase their vulnerability. Table IV

Comparison of Individual Psychotherapies of Depression * .

Type: Premise Goal Approach Technique

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Cognitive/Behavioral Depression secondaryto cognitive distortion Correct cognitive distortions Directive Cognitivediary Homework assignments

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Depressionsecondaryto interpersonal problems Enhance current social functioning Directive Reassurance Improve interpersonal communication Role rehearse interpresonal solutions 12 to 20 sessions

12 to 20 sessions .

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Assertiveness training Duration

Family therapy, then, can be used to educate families about the course of a mood disorder, facilitate communication, and limit the effects of isolation. [See FAMILY THERAPY.] Group therapy allows patients with mood disorders to share their experiences with others who suffer from similar problems. Patients in group therapy derive considerable validation, support and insight from other group members as well as from the group therapist(s). Groups are very good settings for testing negative perceptions, comparing experiences about medications, and decreasing isolation. The group may help mobilize the patient to action, and most patients are tremendously comforted by knowing that they are not unique or alone in their suffering. Mood disorders groups tend to meet weekly and may be psychodynamic, supportive, or cognitively oriented among other forms. Group therapy usually lasts from 1 to 2 hours and may be time-limited or open-ended. Whatever the form of therapy that is pursued, psychotherapy, pharmacotherapy or a combination of the two, education tends to play an important role in the treatment of mood disorders. Patients and their families derive considerable benefit from learning about the signs and symptoms of the illness, the disorder's course, and what can be expected from the treatments. Side effects of biological therapies tend to be reviewed in detail and the time it takes to respond is discussed. Likewise the rationale for pursuing a particular psychotherapy is discussed with patients as well as what can be expected from pursuing a given therapy. (See Table IV.) We are currently in a period of rapid development for the treatment of mood disorders. Still, there is

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* DeBattista C, Glick I: MedicalManagementof Depression, EMIS, 1996.

Psychodynamic Depression secondaryto unconscious conflict Resolve conflict over loss Nondirective Interpret unconsciousmaterial Graded tasks Ventilation/catharsis Brief (12 sessions)

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much to be learned about biological, psychological, and social approaches to the treatment of mood disorders. While most people with mood disorders can be significantly helped by the treatment options available, there continues to be a need for more efficacious, cost-effective, and less toxic treatments. Such treatments await further research. BIBLIOGRAPHY

American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author.

Beck, A., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Cognitive therapy of depression. New York: Guilford Press. DeBattista, C., & Glick, I. D. (1996). The medical management of depression. Dallas, TX: Essential Medical Information Systems. Goodwin, F., & Jamison, K. (1980). Manic depressive illness. New York: Oxford Press. Kaplan, H. I., & Sadock, B. J. (1995). Comprehensive textbook of psychiatry (6th ed.). Baltimore: Williams & Wilkins. Kessler, R. C., et al. (1994). Lifetime and 12 month prevalence of DSM III-R psychiatric disorders in the United States: Results from the national comorbidity survey. Archives of General Psychiatry, 51, 8-19. Schatzberg, A. F., Cole, J. O., & DeBattista, C. (1996). Manual of clinical psychopharmacology (3rd ed.). Washington, DC: APA Press.

Narcissistic Personality Disorder Salman Akhtar

JeffersonMedicalCollege

I. II. III. IV.

Manifestations Distinction from Related Conditions Intrinsic Nature Treatment

beginning with Sigmund Freud's elucidation of the concept of narcissism. Freud published his seminal paper "On Narcissism" in 1914. He defined narcissism as the concentration of libidinal interest upon one's ego and distinguished primary from secondary narcissism. The former was a normal phenomenon of infancy, the latter a result of withdrawal of interest from the outer world. Freud noted that human attachments are of two types: anaclitic and narcissistic. The former are evident when we are involved with those who nourish and protect us and the latter when we are involved with those who merely reflect us (the way we are, or were, or will be). In essence, the narcissistic relationship is nothing but thinly veiled sell-affirmation. While avoiding character typology in this paper, Freud did refer to individuals who compel our interest by the narcissistic consistency with which they manage to keep away from their ego anything that would diminish it." However, it was not until 1931 that he described the "narcissistic character type."

Narcissism Emotional investment into the self. When normal, it leads to sustained self-regard and mature aspirations. When pathological, it is accompanied by inordinate demands upon the self, excessive dependence upon acclaim from others, and deteriorated capacity for interpersonal relations. Personality Disorder A pervasive pattern of chronically maladaptive behavior which is a source of constant interpersonal problems. Personality disorders are ego-syntonic, i.e., such individuals are not aware of their own personalities as being deviant or abnormal. They suffer from the interpersonal consequences of their behavior but they do not recognize their own role in the origin and perpetuation of these problems. Such individuals are therefore unlikely to seek professional advice although they may consent to it if this is urged by others or forced by social repercussions of their behavior.

The subject's main interest is directed to self-preservation:he is independent and not open to intimidation. His ego has a large amount of aggressiveness at its disposal, which also manifests itself in readiness for activity. In his erotic life loving is preferred above being loved. People belongingto this type impress others as being "personalities"; they are especially suited to act as a support for others, to take on the role of leaders and to give a fresh stimulus to cultural development or to damage the established state of affairs.

NARCISSISTIC PERSONALITY DISORDER is a newly recognized diagnostic entity in clinical psychiatry. It was introduced into "official" psychiatric nomenclature in 1980 with the publication of the third edition of the American Psychiatric Association's Di-

This description is generally viewed as the pioneering portrayal of narcissistic personality disorder. The fact, however, is that a 1913 paper by Ernest Jones, one of Freud's distinguished pupils, also contained signi-

agnostic and Statistical Manual of Mental Disorders (DSM-III). There is, however, evidence that the concept had been evolving since the turn of the century

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ficant details regarding the phenomenology of this condition. Using the term "God Complex" for their condition, Jones portrayed such individuals as excessively admiring of themselves, having omnipotent fantasies, being exhibitionistic, and scornful of others. Such grandiosity is, at times, masked by caricatured modesty, pseudohumility, and a pretended contempt for materialistic aspects of life. Over the subsequent decades, many other psychoanalysts contributed to the study of narcissistic personality. Prominent among these were Robert Waelder, Wilhem Reich, Christine Olden, Helen Tartakoff, and John Nemiah. These authors clearly recognized this condition though often without designating it as such. They noted that the central feature of this condition, grandiosity, is a defensive maneuver against feelings of inferiority which they traced to severe frustrations during early childhood. In the 1970s the publication of two psychoanalytic books breathed new life in the study of narcissistic personality disorder: The Analysis of the Self (1971) by Heinz Kohut and Borderline Conditions and Pathological Narcissism (1975) by Otto Kernberg. The views of Kohut and Kernberg are summarized below. Suffice it to say here that their works stirred up considerable controversy and mobilized further interest in investigating the true nature of narcissistic personality disorder. Among those who made subsequent major contributions are Sheldon Bach, Ben Bursten, Mardi Horowitz, Arnold Modell, Arnold Rothstein, and Vamik Volkan. Finally, when in 1980 the DSM-III included narcissistic personality disorder as a separate diagnostic entity, an official imprimatur was added to the evolving concept. The DSM-IV retained the condition with only minor modifications of its diagnostic criteria. I. MANIFESTATIONS

The cardinal feature of narcissistic personality disorder is heightened narcissism. Individuals with this disorder display grandiosity, intense ambition, and an insatiable craving for admiration. Their consuming self-interest renders them incapable of appreciating and understanding the independent motivations and needs of others. Consequently, they come across as cold, unempathic, exploitative, and having little concern for those around them.

The clinical features of narcissistic personality disorder involve six areas of psychosocial functioning: (i) self-concept, (ii) interpersonal relations, (iii) social adaptation, (iv) ethics, standards, and ideals, (v) love and sexuality, and (vi) cognitive style. In each of these areas there are "overt" and "covert" manifestations. These designations do not necessarily imply their conscious or unconscious existence although such topographical distribution might also exist. In general, however, the "overt" and "covert" designations denote seemingly contradictory phenomenological aspects that are more or less easily discernible. Moreover, these contradictions are not restricted to the individual's self-concept but permeate his interpersonal relations, social adaptation, love life, morality, and cognitive style. Narcissistic individuals have a grandiose selfconcept. They give an appearance of self-sufficiency and are preoccupied with achieving outstanding success. Covertly, however, they are fragile, vulnerable to shame, sensitive to criticism, and filled with morose self-doubts and feelings of inferiority. Their interpersonal relations are extensive but exploitative and driven by an intense need for tribute from others. They are unable to genuinely participate in group activities and, in family life, value children over the spouse. Inwardly, they are deeply envious of others' capacity for meaningful engagement with life. They attempt to hide such envy by scorn for others; this may, in turn, be masked by pseudo-humility. Capable of consistent hard work, narcissistic individuals often achieve professional success and high levels of social adaptation. However, they are preoccupied with appearances and their work is done mainly to seek admiration. The overly zealous vocational commitment masks a dilettante-like attitude, chronic boredom, and gnawing aimlessness. Their ethics, standards, and ideals display an apparent enthusiasm for sociopolitical affairs, a caricatured modesty, and pretended contempt for money in real life. At the same time, they are often quite materialistic, ready to shift values to gain favor, irreverent toward authority, and prone to pathologic lying and cutting ethical comers. A similar contradiction is evident in the realm of love and sexuality. Overtly, narcissistic individuals are charming, seductive, and given to extramarital affairs, even promiscuity. Covertly, however, they draw little gratification beyond physical pleasure from sexuality

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and are unable to have deep and sustained romantic relations. Moreover, they seem unable to genuinely accept the incest taboo and are vulnerable to sexual perversions. Superficially, their cognitive style suggests a decisive, opinionated, and strikingly supple intellect. However, their knowledge is often limited to trivia ("headline intelligence") and they are forgetful of details. Their capacity for learning is also compromised since learning forces one to acknowledge one's ignorance and they find this unacceptable. They are articulate but tend to use language and speaking for regulating self-esteem rather than communicating. In sum, narcissistic personality disorder is characterized by a defensively inflated self-concept which is fueled by fantasies of glory, protected by being constantly admired for social success, and buttressed by scornful devaluation of those who stir up envy. Underneath this grandiose self-concept (not infrequently built around some real talent or special aptitude) lie disturbing feelings of inferiority, self-doubt, boredom, alienation, and aimlessness.

II. DISTINCTION FROM RELATED CONDITIONS Individuals with narcissistic personality disorder have superficial resemblances to those with compulsive personality disorder. Both types of individuals display high ideals, great need for control, perfectionism, and a driven quality to their work. However, the compulsive seeks perfection while the narcissistic claims it. Consequently, the compulsive is modest, the narcissist haughty. The compulsive loves details that the narcissist casually disregards. The compulsive has a high regard for authority and strict inner morality, while the narcissist is often rebellious and prone to cutting ethical corners. [See OBSESSIVE--CoMPULSIVE

DISORDER.] Three other characterological constellations need to be distinguished from narcissistic personality disorder: borderline, antisocial, and paranoid personality disorders. Both borderline and narcissistic individuals are self-absorbed and vacillating in their relationships. Borderline individuals, however, show a greater propensity for disorganization into really regressed men-

tal states. They are less tolerant of aloneness, more angry, and have a poorer capacity for sustained work than narcissistic individuals. [See BORDERLINE PERSONALITYDISORDER.] Both antisocial and narcissistic individuals dream of glory and can lie, cheat, and indulge in ethically dubious acts to achieve success. However, in narcissistic personality such disregard of conventional morality is hidden, occasional, and cautious whereas in antisocial personality it is open, frequent, ruthless and calculated. [See ANTISOCIALPERSONALITYDISORDER.] Both paranoid and narcissistic individuals are grandiose, emotionally stilted, envious, sensitive to criticism, and highly entitled. However, the paranoid individual is pervasively mistrustful and lacks the attention-seeking charm and seductiveness of the narcissist. The cognitive style of the two types of individuals differs in a striking way. The narcissist is inattentive to real events and forgetful of details. The paranoid, in contrast, has a biased but acutely vigilant cognition. [See PARANOIA.]

III. INTRINSIC NATURE In the realm of probable causes and the intrinsic nature of narcissistic personality disorder the views of Heinz Kohut and Otto Kernberg form the two major, if sharply divergent, contemporary perspectives. According to Kohut, the origin of narcissistic personality disorder resides in faulty parental empathy with the child. Kohut posits that a growing child needs an enthusiastically responsive audience ("mirroring") for his or her activities and achievements. When such mirroring is deficient, the child's ordinary pride and associated healthy need to be affirmed take on an insistent and unhealthy exhibitionistic quality (the "grandiose self Kohut also proposes that, in addition to mirroring, the child needs the opportunity to idealize the parents and draw strength from this borrowed sense of importance. When parents either are truly not admirable or their weaknesses are prematurely or shockingly revealed to the child, the hunger for powerful figures goes unsatisfied and becomes a persistent feature of later, adult life. It is this paradoxical mixture of grandiosity and hunger to belong to prestigious others that forms the nucleus of narcissistic character. Inner fragility of self-esteem is hidden

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by these compensatory structures. Any threat to such self-regulation mobilizes shameful sense of imperfection and intense, vengeful anger ("narcissistic rage"). In contrast to Kohut, Kernberg regards narcissistic personality not as a developmental arrest but a specific pathological formation to begin with. Kernberg differentiates the normal narcissism of children (which retains a realistic quality and does not affect the capacity for mutuality) from the early development of pathological narcissism (which creates fantastically grandiose fantasies and impairs the capacity for mutuality). Kernberg agrees that narcissistic individuals were treated by their parents in a cold, even spiteful manner. However, he adds that they were also viewed as special since they possessed some outstanding attribute, e.g., talent, beauty, superior intelligence, etc. Using Kohut's term with a different formulation, Kernberg proposes that "grandiose self" is formed by the fusion of a highly idealized view of oneself (built around some truly good aspect of oneself) and a fantastically indulgent and admiring inner audience of imagined others. Such grandiose self is a defensive structure against the anger directed at the frustrating parents of childhood. Rage in narcissistic personality is therefore the inciting agent, not merely an epiphenomenon. The views of Kohut and Kernberg differ in many other ways but their most important differences involve (i) a developmental arrest versus a pathological formation view of grandiosity, and (ii) the reactive versus the fundamental view of aggression in narcissistic personality disorder. These differences affect the techniques which the two theoreticians propose as being suitable to treat this condition.

IV. TREATMENT The treatment of choice for narcissistic personality disorder is psychoanalysis, provided the patient is psychologically minded, has verbal facility, and is earnestly motivated for change. Within the psychoanalytic framework, however, the approaches outlined by Kohut and Kernberg (and developed further by their proponents) differ considerably. Kohut's approach aims at a full-blown reactivation, in vivo, of the frustrated childhood mirroring and idealizing needs. The analyst accepts the validity of such needs and helps

the patient see their persistence as emanating from childhood deprivations. The patient's rage, if it erupts in treatment, is interpreted as an understandable response to the inevitable empathic failures of the analyst. Such an experience is then shown to have connections with similar experiences caused by faulty parental empathy during childhood. Countless repetitions of feeling understood and seeing the present in the light of past gradually facilitate the relinquishment of grandiosity and idealizations. Kernberg's approach differs. He emphasizes that the experiences of narcissistic patients in analysis are not readily traceable to the actuality of their childhoods. Instead, these are multilayered and include in them early wishes, defenses against those wishes, real experiences, and unconscious distortions of them. Kernberg notes that the patient's disappointments in the analyst not only reveal his or her real or fantasied frustrations of childhood, now being repeated in the treatment situation, but also dramatically reveal the patient's psychic readiness for hate and total devaluation of others. Kernberg does not view the patient's rage as a reaction to the analyst's failures but as an inevitable manifestation of the patient's pathology. At its core, this involves seething rage against real and imagined hurts from parents, a rage that is also used defensively to ward-off dependent longings. Empathy, for Kernberg, is not a therapeutic measure but a technical necessity. The mainstay of treatment is working through the patient's rage and mistrust, anxiety about dependence, and, in later phases of treatment, the guilt over having exploited, devalued, and hurt others including the analyst. With diminution of rage and dread of true attachment, there emerges a capacity to empathize with others, a reduction in self-centeredness, an ability to give, and a dawning awareness of life's complex emotional offerings in the context of genuine affective involvement with fellow human beings. This article has been reprinted from the Encyclopedia of Human Behavior, Volume 3.

BIBLIOGRAPHY Akhtar, S. (1992). "Broken Structures: Severe Personality Disorders and Their Treatment." Jason Aronson, Northvale, NJ. Akhtar, S. (1989). Narcissistic personality disorder: Descriptive features

Narcissistic Personality Disorder

and differential diagnosis. Psychiatric Clinics of North America 12,505-529. Bach, S. (1977). On the narcissistic state of consciousness. In "Narcissistic States and the Therapeutic Process." Jason Aronson, New York. Kernberg, O. F. (1975). "Borderline Conditions and Pathological Narcissism." Jason Aronson, New York. Kernberg, O. F. (Ed.) (1989). Narcissistic personality disorder. The

Psychiatric Clinics of North America, xii (3). Kohut, H. (1971). "The Analysis of the Self." International Universities Press, New York.

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Kohut, H. (1977). "The Restoration of the Self." International Universities Press, New York. Mahler, M. S., & Kaplan, L. (1977). Developmental aspects in the assessment of narcissistic and so-called borderline personalities. In "Borderline Personality Disorders: (P. Hartocolis, Ed). International Universities Press, New York. Modell, A. (1984). "Psychoanalysis in a New Context." International Universities Press, New York. Volkan, V. D. (1982). Narcissistic personality disorder. In "Clinical Problems in Psychiatry" (J. O. Cavenar, and H. K. H. Brodie, Eds.). Lippincott, Philadelphia, PA.

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Obsessive-C0mpulsiveDisorder

I. II. III. IV.

Randy O. Frost

Gail Steketee

Smith College

Boston University

Diagnosisand Symptoms Family and Patient Characteristics Theory and Treatment Future Directions

of obsessions or compulsions, some degree of recognition of the irrationality of the behavior, and significant interference with everyday functioning. This article provides an up-to-date summary of the state of knowledge regarding obsessive-compulsive disorder.

Compulsions Behaviors or mental acts one feels driven to perform in response to an obsession or according to certain rules. DSM-III Diagnostic and Statistical Manual of Mental Disorders--Third Edition, published by the American Psychiatric Association. DSM-IV Diagnostic and Statistical Manual of Mental Disorders--Fourth Edition, published by the American Psychiatric Association. Obsessions Repetitive, unwelcome, and intrusive thoughts, images, or impulses that are inappropriate and cause distress. Schizotypal Personality Disorder A personality disorder characterized by social and interpersonal deficits as well as by cognitive or perceptual distortions. Tourette's Syndrome An Axis I disorder characterized by multiple motor and vocal tics. (YBOCS) Yale-Brown Obsessive-Compulsive Scale An assessment interview used in most current obsessive-compulsive disorder treatment outcome studies.

I. DIAGNOSIS AND SYMPTOMS Obsessions are recurring and persistent thoughts, images, or impulses that are experienced as intrusive, distressing, and, at least at times, unreasonable. Responding to these experiences, the individual may "neutralize" them, using some ritualistic thought or action, or attempt to ignore or suppress them. These repeated behaviors or mental acts are undertaken to relieve anxiety provoked by the obsessions and are called compulsions. Compulsions are usually applied rigidly or excessively. From the patient's perspective, they restore safety or prevent a dreaded event. The intent of the compulsion is often hidden from the casual observer or even close family members. These symptoms consume at least an hour a day and interfere with the person's normal activities. The symptoms of OCD are relatively common in the general population, but are not usually severe enough or do not interfere enough to meet diagnostic criteria. The content of clinical obsessive intrusions differs little from ordinary intrusive thoughts experienced by most people, but the former provoke much more anxiety and are more difficult to dismiss. The content of obsessions and compulsions vary considerably from patient to patient, sharing only the

OBSESSIVE-COMPULSIVE DISORDER (OCD) is an Axis I Anxiety Disorder in the American Psychiatric Association's (APA) Diagnostic and Statistical Manual of Mental Disorders--Fourth Edition (DSMIV). The primary diagnostic criteria are the existence

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disturbing nature of the intrusions and the ritualistic efforts to neutralize the obsessions. Often, patients report more than one type of obsession and ritual, and sometimes the content of the obsession or compulsion changes (e.g., cleaning to checking). The most common compulsions are checking rituals, which are usually designed to prevent catastrophes like fire, burglary, causing someone harm, or embarrassing oneself. Also common are washing rituals, which serve to remove "contamination" or "dirt" and thereby prevent a feared disaster (e.g., disease). Other common compulsions include repeating compulsions or magical rituals in which ordinary actions (such as crossing a threshold or lifting an object) are repeated to prevent harm from occurring (e.g., a loved one dying in an accident). Less common are ordering rituals, which involve arranging objects to produce symmetry or balance, and hoarding, the acquisition of and failure to discard seemingly useless objects like old magazines and receipts or empty containers. The APA's DSM-III defined obsessive-compulsive disorder (OCD) not only by the obsessions and compulsions, but by patients' recognition of the irrationality of obsessions. Individuals who did not recognize the irrationality of their thoughts were considered either psychotic or "overvalued" in their ideas about the obsessions. Recent research demonstrates that patients vary on this characteristic from complete awareness to complete lack of awareness of the rationality of the symptoms, with most having at least some insight. This criterion has changed somewhat in DSM-IV in that patients must have insight at least at some point in the disorder. DSM-IV added a category of "poor insight" for patients with OCD who do not recognize the unreasonableness of their behavior. Diagnostically, obsessions can be distinguished from symptoms of generalized anxiety disorder and hypochondriasis in that they are mental experiences that are not merely excessive worries about real-life problems (e.g., finances, family well-being, health, etc.). Also, obsessions are different in character from the guilty or depressive ruminations characteristic of people with major depression. Preoccupations with food, alcohol, drugs, gambling, and buying are readily distinguishable from obsessive fears of contamination, causing harm, preventing danger, and other anxietyprovoking concerns and rituals. The former symptoms are all appetitive preoccupations, while obsessive fears generally involve avoidance or escape responses.

A. Epidemiology and Clinical Course Epidemiological studies of community samples estimate the annual and lifetime prevalence rates to be considerably higher than previously thought (annual, 0.8 to 2.3%; lifetime, 1.9 to 3.3%). Prevalence rates in this range have been replicated in a variety of studies throughout the world. While some studies have shown a slightly higher percentage of women than men with OCD, other studies have failed to find this difference. When examining childhood onset of OCD, however, males outnumber females by up to 2 to 1. For males, the mean age of onset is 14 to 19 years, while for females it is 21.7 to 22.0 years. Most patients develop symptoms before age 25 (65%), and only a small number (15%) develop symptoms after age 35. Patients typically wait 7 to 8 years after the onset of symptoms before seeking treatment. While 40% of those with OCD can identify no clear precipitant, some research suggests that changes in life roles and demands (i.e., pregnancy, childbirth, etc.) may be precipitants. Recent prospective studies of the course of OCD indicate that despite significant advances in treatment, most OCD patients (at least 75 %) remain at least partially symptomatic over the long term. Between 43% and 75% of treated patients remain at least partially improved 2 to 5 years after treatment. Despite limited research on prediction of treatment outcome, mild or atypical symptoms, a short duration of symptoms, and a good premorbid personality appear to predict a good outcome. On the other hand, early onset in males, symmetry or exactness-related symptoms, symptoms of hopelessness, delusions or hallucinations, a family history of OCD, and the presence of tics suggest a poor prognosis. There is some indication that the expression of OCD symptomatology is at least partially influenced by cultural factors. Similarities exist between OCD rituals and religious or cultural rituals, and certain religious practices are associated with OCD symptomatology. Culture-specific beliefs, as illustrated by koro (a fear of penile shrinkage found exclusively in Chinese cultures), also suggest the influence culture has on the expression of OCD symptoms. However, while these cultural variables may influence the symptom expression in OCD, there is little evidence to suggest they contribute to the development of the disorder. There is also little evidence to suggest that race

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or socioeconomic status are associated with OCD, although at least one study suggests that AfricanAmericans may present with more severe OCD symptomatology. Given the lack of research in this area, however, any such conclusions must be tentative. Furthermore, different patterns of help-seeking among minority populations may mask potential differences between minority and nonminority groups.

B. Comorbidity Comorbidity of OCD with other disorders is as high as 60% or more. Anxiety disorders, depression, alcohol abuse (dependence), eating disorders, Tourette's syndrome, body dysmorphic disorder, hypochondriasis, and schizophrenia have all been found to be associated with OCD. Comorbidity with anxiety disorders is quite high, ranging from 25 to 60%, with the highest frequencies for specific phobias, followed by social phobia and panic disorder. Comorbidity and family study data have led some to suggest that OCD patients share a general genetic vulnerability with anxiety disorders. [See ANXIETY.] There may be a shared vulnerability for various forms of depression as well, with studies indicating concurrent prevalence rates of 12 to 80%. At least one third of patients with OCD report histories of clinical depression, although 25 to 33 % do not report depression. An important question concerning the relationship of OCD and depression is whether the depression that accompanies OCD is primary or secondary. The majority of patients report an onset of depressive symptoms that occurred after the onset of OCD, and several investigators have found that successful treatment of OCD resulted in the reduction of depressive symptoms. [See DEPRESSION.] Despite a wide range in the degree of insight shown by OCD patients, OCD is relatively rarely accompanied by schizophrenia, although some research suggests a link. Patients with OCD may have more schizotypal traits and less cognitive inhibition than other anxiety disorder patients, similar to schizotypal and schizophrenic patients. Further research is necessary to test the hypothesis that obsessional thoughts (like schizophrenic thoughts) result from a failure in the cognitive inhibition of associations to ongoing stimulation. [See SCHIZOPHRENIA.] Some impulse control disorders overlap with OCD

and, consequently, they have been labeled as OC Spectrum Disorders. Tourette's, Sydenham's chorea, and other tic disorders have shown an association with OCD. One form of Tourette's may be OCD-related and some OCD cases are Tourette's-related. This has led to speculation that OCD and Tourette's may be different expressions of a similar underlying genetic abnormality, for example, of the basal ganglia-frontal cortex pathway. Some investigators report associations between OCD and kleptomania, as well as exhibitionism. These reports are suggestive enough to warrant closer examination of a possible link with obsessive and compulsive symptoms. As mentioned earlier, if the content of obsessions or compulsions concerns primary symptoms of eating disorders, body dysmorphic disorder, or hypochondriasis, a diagnosis of OCD is ruled out. In each of these cases, similarity of symptoms, comorbidity evidence, and response to treatment suggest that these disorders are closely related to OCD. Some have even suggested that they are actually forms of OCD. Studies of comorbidity of OCD with Axis II disorders reveal that over one half of patients with OCD have at least one diagnosable personality disorder (PD). Unfortunately, the evidence fails to provide any clear indication of which co-occur most frequently. Despite its name, obsessive-compulsive personality disorder is no more closely related to OCD than avoidant, dependent, histrionic, or several other personality disorders. One observation from this literature deserves comment. Antisocial personality disorder often has the smallest overlap with OCD, which may reflect the importance of beliefs about excessive responsibility in patients with OCD. Questions remain about the role of personality disorders in OCD, as some evidence suggests that PD symptoms decline with successful treatment of OCD.

II. FAMILYAND PATIENT CHARACTERISTICS A. Family Factors Although marital satisfaction among OCD patients resembles that of the general population, OCD patients (especially males who have an early onset) have higher celibacy rates than the general population. When OCD symptoms occur within a family context,

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family members often involve themselves in the rituals or avoidance behaviors of the patients. In families where households are restructured to adapt to OCD symptoms, greater family dysfunction and negative attitudes toward the patient have been observed. A number of parental characteristics have been hypothesized to play a role in the development of OCD. The parents of OCD cleaners are hypothesized to be overcontrolling and overprotective and may model excessive cleaning behaviors. Parents of checkers are hypothesized to set higher standards for their children, to be overcontroUing and overcritical, as well as modeling meticulousness. Numerous cases report similar characteristics in the parents of OCD patients, including demanding or critical attitudes, overprotectiveness, perfectionism, and rejecting attitudes. Despite the frequency with which these characteristics have been informally observed, systematic research comparing parents of OCD patients and controls has been limited. A small number of controlled studies on this issue support the existence of these characteristics in the parents of OCD patients. In particular, parents of OCD patients and/or subclinical obsessive compulsives have been found to be overprotective, critical, perfectionistic, and risk aversive. In addition, the families of OCD patients show higher levels of expressed emotion (criticism and overinvolvement) than families of controls. Clinical observation and preliminary evidence on these issues suggest that the parents of people who develop OCD are more likely to show a constellation of behaviors, including perfectionism, overprotectiveness, overcritical and demanding attitudes, and high levels of risk avoidance. Further research must establish that these characteristics are more prominent in the families of OCD patients than in controls; then, the question of their role in the development of the disorder can be addressed.

B. Cognitive Characteristics Patients with OCD display a number of cognitive characteristics to a greater degree than other people. International experts have identified at least six such characteristics as being very important in OCD. These include overestimation of risk, excessive responsibility, controllability, overimportance of thoughts, intolerance of ambiguity, and perfectionism.

In the early 1970s, it was first noted that patients with OCD exaggerate the probability and severity of negative outcomes. Clinical and empirical studies indicate that people with OCD are risk-aversive, that is, they are less likely to engage in behavior that they consider risky. Threat overestimation can be defined as the exaggeration of the probability or severity of harm believed to result from or follow intrusive internal experiences. A second widely noted cognitive characteristic is an exaggerated sense of responsibility for harm that might befall oneself or others. Some investigators have argued that exaggerated responsibility is central to OCD. According to recent work on this issue by Salkovskis and others, obsessional responsibility refers to the belief that one has power to bring about or prevent subjectively crucial negative outcomes that may be actual (having real consequences) and/or moral. In normal cognitive processing, irrelevant and intrusive thoughts are simply ignored, whereas in cognitive processing by people with OCD these thoughts are attended to, believed important, and attempts to suppress them are undertaken. Efforts at suppression typically provoke a paradoxical increase in the intrusions and associated discomfort. When efforts to suppress these thoughts fail, sensitization and vigilance to similar thoughts occurs, and this process escalates into an obsessional pattern. Individuals with OCD appear to have a need for control, which can be defined as an overvaluation of the importance of exerting complete control over intrusive thoughts, images, and impulses, and the belief that this is possible and desirable. Such efforts at control are hypothesized to be evident in hypervigilance for mental events, in a moral attitude toward control as a virtue, and in feared psychological and behavioral consequences of the failure to control thoughts. People with OCD may believe that simply having an unwanted, objectionable thought is morally equivalent to engaging in the objectionable act, a form of moral "thought-action fusion." Furthermore, when OCD patients imagine negative events, they may come to believe that the events are more likely to actually occur. Recent research on thought-action fusion supports the importance of this construct. Overimportance of thoughts can be defined as a belief that the mere presence of an intrusive thought gives it significance.

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Related to this concept are possible problems that people with OCD have with Cartesian reasoning and magical thinking. Doubt about the veracity of one's experience and the need for absolute certainty are commonly noted features of OCD. Some suggest that doubt stems from a belief that every situation has a perfect solution and the person with OCD will not feel comfortable unless that perfect solution is found. Others have suggested that because of their need for certainty, OCD patients repeat actions in an attempt to achieve perfect certainty. Such doubt may be central to the indecision seen in people with obsessive-compulsive tendencies. Intolerance for ambiguity is evident in obsessional beliefs about the necessity of being certain, about poor capacity to cope with unpredictable change, and about inadequate functioning in situations that are inherently ambiguous. Perfectionism has been closely linked to OCD in both theory and clinical descriptions of the disorder. Recent research has found higher levels of perfectionism among OCD-diagnosed populations, as well as nonclinical populations, that exhibit obsessivecompulsive tendencies. Although it appears that high levels of perfectionism also characterize other disorders (e.g., social phobia, depression, and eating disorders), it appears to be important in shaping the course of OCD, and consequently international experts consider it a key cognitive component.

C. Information Processing in OCD Several information processing capabilities, including memory, categorization, and attention, have been hypothesized to distinguish OCD patients from nonpatients. Four types of memory deficits have been hypothesized: (a) memory for actions, (b) general memory, (c) confidence in memory, and (d) reality monitoring (distinguishing actual from imagined actions). Among subclinical compulsive checkers, several studies reported deficits in memory for actions performed. Among clinical patients, this finding is less consistent, however, with one study supportive and another failing to replicate. Similar findings have emerged for general memory deficits. Nonclinical subjects showed poorer overall memory functioning, whereas findings for clinical patients were mixed, although most studies reported poorer memory func-

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tioning, especially with regard to visual memory. One consistent finding in this literature has been the lowered confidence in memory capacity shown by OCD subjects. No reality-monitoring deficits have been found. Related to memory dysfunction in OCD, some argue that OCD patients also fail to categorize and integrate information properly. They categorize in an underinclusive way, such that many small categories are generated with narrow boundaries and overspecifled rules for category membership. Some clinical, as well as empirical, research supports this hypothesis. Because of a failure to recognize proper category boundaries, OCD patients create artificial structures that become rituals to determine the proper end of a sequence of behaviors. A related hypothesis suggests that OCD patients fail to adequately inhibit irrelevant stimuli during normal processing, interfering with their focus on relevant stimuli. Consequently, processing ordinary information requires more conscious effort and active suppression of irrelevant or unwanted thoughts. A similar attention or cognitive inhibition deficit is hypothesized to characterize schizophrenia and schizotypal personality disorder. Several studies support this hypothesis having used a negative priming paradigm. Another approach to studying attentional processes in OCD involves the use of the Stroop Color Word test. Subjects watch fearful and nonfearful words presented in different colors and are asked to name the color of the word. Fearful word meanings should be harder to inhibit and naming the color in which they are printed should take longer. Indeed, some studies have found that OCD washers take longer to name contamination words than neutral words, and that non-OCD patients do not. In other studies, OCD subjects have been found to attend selectively to negative OC-related words (e.g., disease, disaster) but to not show an attentional bias toward positive words (e.g., clean, precise). In another test of attentional processing, it has also been reported that after successful treatment, OCD patients no longer showed attentional bias toward contamination items in a dichotic listening task. The research on memory and OCD provides some confirmation of deficits in memory for actions, general memory, decreased confidence in memory functioning, problems with overspecification in categorization, and problems in inhibiting attention to irrelevant

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information and in attending to relevant information. The findings fail to support any difficulties in distinguishing actual from imagined actions. Specific causes for these deficits will require further research.

III. THEORY AND TREATMENT This section reviews the three major theoretical models for the development and maintenance of OCD and the treatment methods derived from these models, and summarizes evidence for the effectiveness of these treatments.

A. Behavioral Models Early behavioral treatments for OCD (thought stopping, aversion therapy) were based on contingent reinforcement and punishment models and worked for only a limited number of patients. Efforts to use conditioning models alone (e.g., systematic desensitization) improved the situation only slightly. In the early 1970s, a refinement in the conditioning model led to the development of a more promising treatment. Exposure and response prevention (ERP), the standard and most effective of the behavioral techniques, is derived from the two-stage theory of fear and avoidance. The first part of the two-stage theory posits that an otherwise neutral event acquires the capacity to provoke fear because of its pairing with an aversive stimulus, much as a dog phobia might develop in someone who has been bitten. While this can account for the onset of a number of cases, there is evidence that it does not account for all. Many patients cannot recall conditioning experiences associated with symptom onset. Also, although onset often follows stressful life events, it rarely does so immediately, as would be expected by the traumatic onset theory. Modifications of the acquisition portion of the two-stage theory suggest that stressful events sensitize some individuals to cues that have an innate tendency to elicit fear, were learned during early traumatic experiences, or have special cultural significance. Observational or informational learning also seems to account for the onset of some cases of OCD, particularly when patients report that their symptoms resemble their parents' behavior. In the second stage of this model, compulsions or escape/avoidance behaviors provide relief from the

obsessional anxiety or discomfort. This relief negatively reinforces the compulsions. Thus, the frequency of compulsive actions increases in future situations, which triggers an obsessional concern. Both external cues (objects or situations) and internal triggers (thoughts, images, or impulses) serve as fear stimuli and can produce obsessional discomfort. Many of these cues or triggers cannot be avoided (e.g., closing the front door when leaving the house). Therefore, the passive avoidance which allows phobics to manage their fears is often insufficient to control anxiety for those with OCD. More active strategies like compulsive behaviors are needed to prevent harm or restore a feeling of safety. Substantial evidence supports a behavioral account of OCD in which obsessions increase discomfort and compulsions reduce it. Obsessive thoughts increase heart rate and skin conductance more than normal thoughts, and contact with contaminants increases subjective and physiological anxiety reactions. In most instances, compulsions reduce anxiety in the short run. Although this model clearly accounts for the maintenance of OCD symptoms, it does not adequately account for many instances of onset, and expansion of this theory is necessary.

B. Behavioral Treatments Treatment strategies based on the behavioral model attempt to disconnect obsessions from the associated discomfort and to eliminate rituals that prevent habituation of obsessional fears. Behavioral treatment for obsessions and compulsions involves exposure to overt and covert cues that provoke obsessions, followed by prevention of the compulsion. Because compulsions interfere with habituation of the negative mood generated by obsessions, blocking the rituals prevents the premature reduction of fear. This program of ERP has been widely studied and has been found to be highly effective. Exposure and response prevention was developed by British researchers in the early 1970s to treat hospital patients who feared contamination and performed washing rituals. In the first attempt to use ERP, daily direct contact with contaminants and complete prevention of compulsions (turning off the plumbing in patients' rooms, having nurses observe all washing) resulted in 10 of 15 patients being much improved or symptom-free, and the remaining 5 being moderately

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improved. After 5 to 6 years, only 2 patients relapsed. Since then, approximately 30 open trials and controlled studies, representing more than 600 patients with OCD, have reported good outcomes with ERP and its variants. Numerous studies have shown that using from 10 to 20 sessions of ERP produces significant improvement in symptoms. After ERP, approximately 55% can be labeled "much" or "very much" improved, indicating that target symptoms improved by more than half; approximately 85 % show at least some degree of improvement. Improvement rates remain high at follow-up, with 50% of patients still in the "much" or "very much" improved categories and 75% in the "improved" category. With regard to the amount of symptom improvement, the average degree of benefit from ERP ranges from 40 to 75 %. At follow-ups ranging from 3 months to 6 years, treatment gains remain high, in the 45 to 70% range for target symptoms. The degree of benefit and the consistency of ERP results from multiple treatment sites and countries are quite impressive and clearly indicate that exposure and response prevention is an effective intervention. Support for the behavioral model from which ERP is derived can be found in studies examining the separate effects of exposure and response prevention on obsessions and compulsions. According to behavioral theory, exposure should reduce anxiety associated with obsessions, while response prevention should influence rituals more than obsessions. Several case series provide support for these hypotheses. When delivered independently, exposure reduces subjective anxiety more than rituals, although both decline. Response prevention reduces rituals more than it does obsessions. When exposure and response prevention are both given, patients show maximum improvement in symptoms. Foa and Kozak suggested that ERP allows for the processing of emotional information which is prevented by compulsions. Compulsions circumvent this processing by allowing the patient to escape from a fearful situation before they have had a chance to habituate to it. These theorists hypothesize that fearrelated memories are stored in fear structures that are activated by exposure to a fear stimulus. In the case of OCD, this may include any stimulus that prompts an obsession. Fear activated by exposure will dissipate unless neutralized by a compulsion. Exposure and re-

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sponse prevention activate the fear structure causing the patient to experience anxiety. When the ritual is prevented, habituation of anxiety will eventually occur. If habituation occurs within a session, then the fear structure is weakened and initial response to exposure should be lower at subsequent sessions. The new emotional information processed within such a session contains information about habituation, coping with anxiety, and so on, which is incompatible with a "fear" structure and therefore weakens the OC fear. Several parts of this process have been supported by research. As predicted by this model, attention-focusing instructions are associated with more anxiety during exposure and better habituation, whereas distracting instructions reduce initial anxiety and subsequent habituation, leading to poorer outcome. Therefore, standard clinical practice should focus attention on the exposure situation and avoid distracting conversation that might interfere with the processing of fearful information. Traditional ERP has been supplemented by varying the procedure to enhance benefits and reduce the cost of the treatment. Several investigations have found that imagery-based exposure is as effective as in vivo exposure. Furthermore, some evidence suggests that imaginal exposure may work better for patients with checking compulsions, perhaps because their fears can be more easily accessed by imagery. Other variants that have shown some promise include the use of therapist modeling and varying the duration of treatment and the spacing of ERP sessions. Additionally, several studies have found that self-controlled treatment is as effective as therapist directed, and may produce more durable gains. Recently, a number of self-help books have been published with background information and instructions to help in setting up self-directed ERP. Preliminary findings from one study suggest that using self-help texts can lead to significant improvement. Although it may be too early to tell whether completely self-directed ERP is effective, it may represent a significant development in the treatment of ERP. Another recent advance in the application of modified versions of ERP is group administration. Only one controlled trial of group ERP has been reported in the literature, however. This study compared group ERP, with or without imagined exposure, to comparable individual treatment and to an individual relaxation control treatment. After 12 weeks, both exposure treatment conditions showed significant

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improvement in OCD symptoms, while the control group did not. Average posttest Yale-Brown OC Scale (YBOCS) scores fell below the clinical range. The group treatment led to changes comparable to those of individual therapy, although group benefits occurred somewhat more slowly. This study demonstrates the potential for group administration of ERP. Several researchers have suggested the use of support groups for patients and family members. Some have used open-ended monthly group meetings for family members and patients to discuss the effect of OCD on the family and to plan coping strategies and rehearse behavioral exercises. Other reports have outlined psychoeducational groups for families that include sessions on diagnosis, assessment, theories of OCD, behavioral treatment, medications, and prevention of relapse. Goals for such groups include improving self-esteem, sharing feelings and experiences, accepting patients' realistic limitations, and learning strategies for coping with OCD symptoms. Most of these studies reported high participant satisfaction, but no outcome data. Further developments along these lines include using family members as treatment assistants. Evidence that spouse assistance in exposure treatment improves outcome, at least in the short run, has been reported by some investigators, although more research is needed to clarify the amount of added benefit over individual treatment. It appears that involving spouses and other family members in ERP leads to significant gains in OCD symptoms, mood state, and social and occupational functioning compared with unassisted treatment. Furthermore, family-treated patients continue to improve after treatment. Some studies suggest that nonanxious, consistent family members are more successful in providing support and supervision than anxious and inconsistent members, especially those who engage in argument and ridicule. Similar programs that teach relatives to reduce their involvement in rituals and to encourage self-exposure in noncritical ways have been found to be successful. Symptom decreases of 45% at discharge and 60% at 6-month follow-up indicate good success with family member involvement. Substantial reductions in YBOCS scores among patients in multiple family therapy groups that included spouses/partners, parents, and other relatives have been reported. The reductions are still significant I year later. Research on predictors of success with ERP has

failed to reveal consistent trends. Sex, age of onset, symptom severity, and duration have generally not been found to predict success in ERP. However, severity of avoidance behavior may be associated with poor ERP outcome. Some research also suggests that comorbid personality disorders, especially schizotypal personality disorder, are associated with poorer outcome in ERP. Greater insight regarding obsessions has been associated with positive ERP outcome in some studies, but not in others. The studies on group, self-directed, and familyassisted behavioral treatments guide the way for the future of OCD treatment. Cost-effective applications of the behavioral treatments known to work for OCD are sorely needed. Further research in these areas is vital.

C. Cognitive Models Models emphasizing the appraisal of threat form the backdrop for most of the cognitive theories of OCD. These models involve a two-step process. Identification of a potentially harmful situation (primary appraisal) creates an initial state of apprehension, and a secondary appraisal (of one's ability to cope with the threat) determines whether the anxiety will rise or decline. As noted earlier in discussing cognitive characteristics of OCD, obsessive-compulsive patients are thought to make abnormally high estimates of the probability of bad things happening to them. That is, they anticipate danger or misfortune more readily than nonobsessionals and may believe in the need to be concerned about danger and to dwell on its possible occurrence in order to protect themselves. This overestimation of threat is part of an inaccurate appraisal process which contributes to the development of OCD. From a cognitive perspective, several types of beliefs or assumptions contribute to inaccurate appraisal. These include beliefs described by rational emotive therapists (RET) and by other cognitive theorists. Perfectionistic beliefs may take the form that one should be thoroughly competent, adequate, and achieving in all possible respects (i.e., perfect) to consider oneself worthwhile and to avoid criticism, and that perfect solutions to all problems are available and should be found. Other hypothesized OCD beliefs include the notion that making mistakes or failing to reach one's ideals is unacceptable and should result in punishment, that one has the power to prevent disas-

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trous outcomes by magical rituals, and that certain thoughts and feelings are unacceptable. Related to the cognitive features described earlier is the need for certainty to avoid criticism and reduce risk. Coping with threats generated by these beliefs is thought to be difficult for people with OCD. These early theories are similar with respect to the role and content of specific irrational beliefs, although they have been largely subsumed by more recent cognitive theorizing. The most prominent cognitive theory of OCD was proposed by Salkovskis in 1985. He drew heavily from Beck's cognitive theory of emotional disorders. Salkovskis noted that extensive research shows that intrusive cognitions are normal phenomena experienced by more than 90% of the population. What distinguishes people with OCD is not the experience of intrusive thoughts, but the way in which their occurrence and content are interpreted. People with OCD give special importance to their intrusions, whereas people not suffering from OCD simply ignore them. According to Salkovskis, the reaction to negative intrusive experiences in people with OCD depends on a set of underlying beliefs. These beliefs are characterized by an exaggerated sense that one is responsible for harm to oneself or to others and that one must act to prevent it. The OCD patient seeks to reduce the discomfort produced by these thoughts by engaging in neutralization (i.e., compulsion, suppression, or avoidance). The first step in the process is an appraisal of an intrusive thought as an indication that they are in some way responsible for harm or its prevention. In the second step, this appraisal elicits neutralizing behavior (overt or covert). If negative appraisal occurs without the appraisal of responsibility, neutralization will not take place and the result will be anxiety and/ or depression, but not OCD. Thus, the core assumption of this model is that OCD symptoms are efforts to neutralize or ameliorate the appraisal of responsibility for harm. Neutralization includes overt behaviors (washing, checking, etc.) as well as mental events, attempts to put things right, thought suppression, and reassurance seeking. Salkovskis suggests that neutralization effectively reduces the level of perceived responsibility in the short run, but increases the probability of intrusive thoughts in the longer term. Research on the nature and measurement of obsessional responsibility, as well as experimental manipulations of responsibility, lend support to this theory,

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but there have been suggestions for modification. It has been proposed that in this theory, more emphasis should be given to dysfunctional beliefs about controlling thoughts and the costs of not doing so, as well as to the effect of depression in impairing the ability to control thoughts. Theorists also suggest that neutralization may develop only when other thought control efforts fail. An alternate cognitive theory of OCD proposed recently is quite different from the appraisal model that has characterized previous cognitive theories. This model focuses on the inference process. It suggests that people with OCD do not react to an actual feared stimulus nor to its perceived consequences. Instead, they react to what they imagine might be there despite a lack of sensory evidence to support the belief. In this model, a faulty inference process is responsible for OCD beliefs. Rather than forming an hypothesis about an obsessional fear (the table is dirty) and testing it (feeling the table), the person with OCD changes the evidence to fit the hypothesis (the table must be dirty because I can imagine it dirty). The rituals are attempts to change this "fictional narrative" by changing what is real. The reliance on superstition, or on magical or pseudoscientific justifications for obsessional beliefs also reflects attempts to make the reality fit the fiction. This theory is quite interesting and deserves further research. Although early cognitive treatments for OCD were not derived from these cognitive conceptualizations, more recently developed treatments have been. In particular, the use of rational emotive therapy (RET) and Beckian cognitive therapy tailored specifically for OCD have been investigated. Although still in the early stages of testing, these treatments show great promise. D. Cognitive Treatments

Some investigators have observed cognitive changes after ERP treatment, especially with respect to the overestimation of risk. They suggest that ERP may reduce the overestimation of risk experienced by people with OCD. If exposure-based treatments can change cognitions associated with OCD, and if, as is suggested by the cognitive theories just reviewed, these cognitions are important components of the disorder, then perhaps other ways of changing cognitions exist. The assumption underlying cognitive therapy is that

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changing cognitions will lead to reductions in OCD symptomatology. Early studies of the effects of cognitive therapy on OCD were hampered by the fact that the therapies were generic and not specifically tied to OCD cognitions. Not surprisingly, these treatments were not very successful. Subsequent studies in which the cognitive therapy was tailored to OCD have met with considerably more success. Several studies have compared RET focusing on OCD beliefs with self-controlled ERP. Both treatments led to substantial improvement in patient symptoms and RET was superior to ERP in improving mood. In subsequent studies, comparable improvement for RET and ERP treatments was seen among patients randomly assigned to treatment type and RET was also associated with a greater decline in irrational beliefs. The other cognitive treatment model used in treating OCD is Beck's cognitive model, in which faulty beliefs are identified, examined, and challenged. Case studies of the application of this type of therapy have been promising. Alternating cognitive therapy with response prevention resulted in improvement in a suicidal adolescent who previously refused exposure. Others have reported that this form of cognitive therapy altered unrealistic beliefs in a case with overvalued ideas. Furthermore, another investigation found that this type of therapy--focusing on excessive responsibility and without ERPmproved successful in treating four patients with checking rituals. The application of this model to OCD has been described by clinical researchers in the Netherlands and in Quebec, Canada. These researchers reported on two controlled trials that used this approach. The first of these studies compared cognitive therapy with exposure only in the context of behavioral experiments to an exposure-alone group. Both treatments resulted in substantially improved symptoms at posttest and follow-up. There was a trend for more favorable outcome for cognitive therapy, but the results were comparable to findings reported by others using ERP. A second study found cognitive therapy plus exposure significantly better than a waiting-list control for 29 obsessional ruminators. The treatment was successful for 85 % of the patients and the gains were maintained at 1-year follow-up. Although to date only a small number of studies have been completed, cognitive therapy for OCD shows clear promise with or without ERP. It may also

help in the reduction of relapse after treatment. In order for cognitive therapy to develop, however, research must identify which cognitions to target and how best to measure them. Research on the six cognitive characteristics associated with OCD identified by international experts in the field is an obvious place to start this process. E. Biological Models The discovery of the effectiveness of serotonin reuptake inhibitors (SRIs) in treating OCD produced a surge of speculation and theory about a biological basis for the disorder. Positron-emission tomography (PET) and related technology have generated dramatic advances in our knowledge of the biology of OCD. Two types of explanations have emerged. Neuropharmacological explanations have focused on the role of the serotonergic transmission system, and neuroanatomical explanations have concentrated on the orbitofrontal cortex, the basal ganglia, and their connections. These two types of explanations are by no means mutually exclusive. Studies of the effects of administering SRIs as a treatment for OCD constitute the most consistent evidence for a neurochemical explanation. The evidence clearly shows that treatment with SRIs reduces OCD symptoms (see the following treatment section). Although this provides strong evidence for the role of serotonin in the biology of OCD, drug response studies are not the best source of evidence for neurochemical processes. Direct evidence of the role of serotonin in OCD comes from two types of studies. First, concentrations of known metabolites of serotonin (5-hydroxyindoleacetic acid: 5-HIAA)in the blood or cerebrospinal fluid provide peripheral markers of serotonin in the brain. Administration of serotonin agonists provoke serotonergic responses in people whose serotonergic system is dysregulated. These pharmacologic challenge studies provide a second direct way of testing the role of serotonin in OCD. Unfortunately, peripheral marker studies have been inconsistent in establishing the role of serotonin function in OCD. It is possible that compensatory mechanisms in the body mask peripheral markers that would indicate serotonin dysregulation. Although the effectiveness of SRIs in treating OCD suggest that patients suffer from a functional deficit in serotonin, surprisingly, pharmacologic chal-

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lenge studies have suggested the opposite. Administration of serotonin agonists produce exacerbated OCD symptoms, suggesting that OCD patients have heightened sensitivity to serotonergic stimulation. Furthermore, administration of serotonin receptor antagonists reverses this effect. There is some inconsistency in the findings of these challenge studies, however. Neuroendocrine responses to pharmacologic challenge suggest a hyposensitivity, whereas behavioral responses suggest a hypersensitivity. This suggests that dysregulation of the serotonergic system is probable, but the nature of the dysregulation is not clear. A number of investigators suggest taking multiple transmitter systems into account in developing a more complex model of OCD. The basal ganglia, frontal cortex, and the limbic structures which connect them have been the focus of anatomical models of OCD. The basal ganglia assist in the regulation of movement and cognitive functioning. Within the basal ganglia, the three structures that make up the corpus striatum (caudate nucleus, putamen, and globus pallidus) have been the focus of attention with respect to OCD. The volume of the caudate nucleus appears to be smaller in OCD patients than in controls, as measured by computerized tomography (CT) studies. Increased metabolic activity has also been observed in the caudate nucleus of OCD patients during rest. Other PET scan studies have found increased metabolic activity in the striatum during exposure among OCD cleaners, but reduced metabolic activity among OCD checkers. The latter finding may reflect the ability of checkers to engage in covert neutralization during the PET scan procedure. In any case, there is clear evidence of a striatal abnormality in OCD, but whether it is primary or secondary is not clear. On the basis of evidence for basal ganglia involvement, some investigators postulate that OCD is a basal ganglia disorder. The function of the basal ganglia is to detect stimuli that activate fixed-action patterns and to allow their release. These fixed-action patterns are innate species-specific responses that are motor programs for action and take the form of grooming and safety rituals. The basal ganglia stores these programs and provides a gating mechanism for their release. In OCD patients, basal ganglia dysfunction allows the inappropriate release of fixed-action patterns (i.e., compulsive rituals). Neuropsychological testing and electroencephalo-

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gram (EEG) studies suggest that deficits in frontal lobe functioning also play a role in OCD. In addition, PET scan studies and single-photon-emission computed tomography (SPECT) studies have shown increased metabolic activity in the frontal cortex of OCD patients compared with controls. Increased metabolic activity in response to provocative stimulation (obsessional rumination) has been found in OCD patients and in normal controls. This suggests that the mental activity associated with obsessional thinking can be localized in the frontal lobe. Furthermore, elevations in metabolic activity in the frontal lobes are no longer present after successful treatment with medication or behavior therapy. Based on this evidence and that of basal ganglia involvement, in 1992, Insel suggested a hyperactive cortical-striatal-thalamic-corticalcircuit in OCD. According to this theory, the caudate nucleus sends erroneous inhibitory signals to the globus pallidus. As a result, the globus pallidus fails to inhibit the thalamus from sending signals to the cortex. Thus, the cortex receives signals that it would not have received if the circuit operated normally. Further erroneous signals from the caudate nucleus inhibit the interruption of the circuit and messages continue to reverberate. Baxter and colleagues suggested that the gating and screening activities of the striatum fail to inhibit impulses or thoughts that "leak" into consciousness and are experienced as obsessions. Fixed-action patterns (obsessions) occur automatically in response to obsessions and require effortful suppression and/or neutralization. This produces hyperactivity in the basal ganglia and frontal lobes. Similar models postulate a problem with the "comparator mechanism" in the limbic system or in the basal ganglia which matches sensory information with what is anticipated. When a mismatch occurs, arousal and corrective procedures are undertaken. A defective comparator mechanism might result in faulty evaluation of sensory input (i.e., hands feel dirty when they are not) and ineffective corrective action (washing hands to remove dirt that is not there). The dirt can only be felt but not removed. There is strong evidence for frontal-striatal circuit involvement in OCD. The etiologic significance of this circuit is unclear, however. It may cause the disorder or may simply be the biological expression of it. Future research along these lines will clarify the mechanisms and roles of biochemical substances and structures in OCD.

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Studies of genetic involvement in OCD have been inconsistent. Those using strict diagnostic criteria to define concordance have found only weak or inconsistent evidence for genetic transmission. Studies using subclinical OCD symptoms to establish concordance have found strong evidence of genetic involvement in OCD. However, some have suggested that what is transmitted is a diathesis for anxiety disorders rather than OCD specifically. Also along these lines, some researchers suggest that at least a subtype of OCD and Gilles de la Tourette's syndrome are different phenotypic expressions of a common underlying genotype.

F. Biological Treatments for OCD A substantial number of clinical and placebo controlled trials have now been conducted with the serotonin reuptake inhibitors, including clomipramine (Anafranil), fluvoxamine (Luvox), fluoxetine (Prozac), and sertraline (Zoloft). Qualitative and quantitative reviews of the treatment outcome literature generally conclude that all SRIs are effective in the treatment of OCD. Recent studies have also shown promise for a newer SRI, paroxetine (Paxil). At least moderate improvement occurs with SRIs in 55 to 70% of previously untreated patients. Although these drugs are also considered antidepressants, the SRIs appear to work for OCD patients whether or not they are depressed. Meta-analytic comparisons among the SRIs show a preference for clomipramine, although at least one such study was equivocal on this issue. More largescale direct comparisons of treatment efficacy are needed before drawing conclusions regarding differential effectiveness of these drugs. More research is also needed on the effects of method of administration. Intravenously administered clomipramine may work significantly faster than oral administration, as has been seen in several clinical series, and it may be effective for patients who do not respond to standard treatment. Dosage ranges have been partly tested for fluoxetine, with higher doses (up to 60 mg) producing better results, but additional research is needed to identify optimal dosage ranges for the SRIs. Despite the effectiveness of SRIs in the treatment of OCD, there are some drawbacks to their use. Patients treated with SRIs show only a modest (30 to 60%) reduction in their symptoms, and a significant number (30% or more) show no improvement at all. While the

side effects of newer SRIs are less severe than those of tricyclic antidepressants and clomipramine, they still represent a problem. The major side effects include sedation, sexual dysfunction, and weight changes. Although many patients may be willing to tolerate the side effects for the symptom relief they provide, these side effects can be a major cause of treatment dropout. Unfortunately, few studies report dropout or noncompliance rates for SRIs. In recent reports, from 10 to 27% of patients drop out of SRI treatment. Little information is available regarding relapse rates for the SRIs. Cessation of SRIs resulted in 89% and 90% relapse, respectively, in two studies. Relapse during continued SRI treatment has ranged from 18 to 23 %. Predictors of treatment response have been examined in a recent multicenter trial of more than 500 patients. Only age of onset predicted outcome. Later age of onset was associated with better response to SRIs. Other research suggests that patients with schizotypal personality disorder respond poorly to SRI treatment for OCD. There is some evidence that augmenting SRI treatment with neuroleptics may benefit those patients with schizotypal personality disorder and comorbid tic disorders. The development of sophisticated instrumentation, more precise lesion placement, and the increasing safety record make psychosurgery a viable treatment option for patients who have failed to respond to multiple medication trials and behavior therapy. Four types of such surgery are in use: cingulotomy, capsulotomy, limbic leucotomy, and subcaudate tractotomy. Few studies of psychosurgery outcome for patients who have failed to respond to medication or behavior therapy exist. One such study reported that 45% of cingulotomy patients who had failed at adequate trials of medication and behavior therapy were at least partial treatment responders. Reviews of the available literature have recommended cingulotomy as the first choice for psychosurgery with these patients. A newer method of psychosurgery, gamma knife, may also show promise for intractable OCD. Few studies offer a direct comparison of behavior therapy, SRIs, or a combination of the two. The first such comparison, in the early 1980s, found greater average improvement with exposure treatment compared with clomipramine. In a later study, 75 to 80% of ERP patients improved compared with 22 to 23 % of clomipramine patients. The combination of clomipramine and ERP resulted in more subjects in the

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"much" improved category after 1 year (73%). Others have reported a slight advantage for the combination of fluoxetine and behavior therapy at 6 months, but after 1 year the effects are minimal. Preliminary results from a multicenter trial suggests that ERP alone may be more effective than clomipramine and the combination of clomipramine and ERR Reviews of combined ERP and SRI efficacy are hampered by the small number of studies using both treatments and by the inconsistencies in outcome measures. Nonetheless, they provide some pertinent information. In a comprehensive 1993 review, Abel concludes that ERP is more effective than clomipramine, especially in the treatment of rituals. For patients with severe depression, obsessions only, and overvalued ideas about obsessions, however, clomipramine appears to be more effective. While SRIs have the advantage of less time and effort by therapist and patient, ERP has fewer dropouts, side effects, and risks, and better maintenance. Meta-analytic reviews have provided additional information about comparative efficacy. These reviews have found behavioral and pharmacologic treatments equivalent, or that ERP alone and ERP in combination with medication were both more effective than SRIs alone, according to self-report measures. No differences among the treatments have been observed when assessor-rated measures were used. So far, no studies examining the efficacy of SRIs compared to or combined with cognitive treatments have been reported.

IV. FUTURE DIRECTIONS Although our knowledge of the nature and treatment of this disorder is far greater than it was a decade ago, there remain significant gaps. For example, the level of insight into obsessions varies both between and within OCD patients. It is not yet understood how insight influences treatment or whether some treatments (e.g., cognitive therapy) can change insight. In addition to level of insight, other issues remain unsolved. A number of other disorders appear to be closely associated with OCD, including hypochondriasis, eating disorders, impulsive disorders, and more. Research is needed to identify the core overlapping features of these disorders.

There may be some utility to identifying subtypes of OCD. One subtype may be those with early onset (especially males), tics, and/or schizotypal traits. These patients have been found to respond poorly to treatment. Similarly, identification of cultural influences on symptomatology and treatment response is needed. The influence of family members on the maintenance of OCD symptoms also remains largely unexplored. Efforts to incorporate family members into the treatment process must be guided by such research. Attempts to develop cognitive treatments for OCD developed out of the realization of the importance of belief structures and cognitive processing in the disorder. Progress in this endeavor depends on the conceptualization and measurement of these phenomena. Thoughtful progression from conceptual models to treatment strategies is needed to ensure that newly developed treatments will be effective. Cooperative investigation offers the potential for speeding this process along.

BIBLIOGRAPHY Abel, J. L. (1993). Exposure with response prevention and serotonergic antidepressants in the treatment of obsessive compulsive disorder: A review and implications for interdisciplinary treatment. Behaviour Research and Therapy, 31,463-478. Baxter, L., Schwartz, J., Guze, B., Bergman, K., & Szuba, M. (1990). PET imagining in obsessive-compulsive disorder with and without depression. Journal of Clinical Psychiatry, 51, 61-69. Foa, E. B., & Kozak, M. (1986). Emotional processing of fear: Exposure to corrective information. Psychological Bulletin, 99, 20-35. Foa, E. B., & Wilson, R. (1991 ). Stop obsessing: How to overcome your obsessions and compulsions. New York: Bantam Books. Freeston, M., Rh~aume, J., & Ladouceur, R. (1996). Correcting faulty appraisals of obsessional thoughts. Behaviour Research and Therapy, 34, 433-446. Insel, T. (1992). Toward a neuroanatomy of obsessive compulsive disorder. Archives of General Psychiatry, 49, 739-744. Salkovskis, P. M. (1985). Obsessional-compulsive problems: A cognitive-behavioral analysis. Behaviour Research and Therapy, 23, 571-583. Steketee, G. (1993). Treatments of obsessive compulsive disorder. New York: Guilford Press. Steketee, G., & White, K. (1990). When once is not enough. Oakland, CA: New Harbinger. van Oppen, P., & Arntz, A. (1994). Cognitive therapy for obsessivecompulsive disorder. Behaviour Research and Therapy, 32, 79-87.

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i Panic Attacks Richard J. McNally Harvard University

I. II. III. IV. V. VI. VII. VIII. IX. X.

History of the Concept of Panic Attack Assessing Panic Attacks Panic Attack Variants The Development of Panic Disorder and Agoraphobia Epidemiology Biological Aspects of Panic Psychological Aspects of Panic Psychopharmacologic Treatments for Panic Psychological Treatments for Panic Conclusions

disorder than among more distant relatives of this person. Hyperventilation Occurs when minute ventilation exceeds metabolic needs (i.e., more carbon dioxide is exhaled than is produced by cellular metabolism). Minute ventilation is the product of respiration rate and tidal volume (i.e., amount of air inhaled per breath). Incidence The rate of new cases of a disorder that appear during a certain time period (e.g., annual incidence). Interoceptive Conditioning A form of Pavlovian (classical) conditioning in which the conditioned stimuli arise within the body (e.g., an increase in heart rate) rather than outside the body (e.g., a flashing light, a tone). Prevalence The percentage of a population that has a disorder during a certain time period (e.g., annual prevalence, lifetime prevalence).

Anxiety Neurosis A DSM-II diagnosis characterized by chronic, excessive anxiety not triggered by specific phobic stimuli. Anxiety Sensitivity Refers to fears of anxietyrelated symptoms that are based on beliefs that these symptoms have harmful consequences. Diagnostic and Statistical Manual of Mental Disorders (DSM) The manual that describes diagnostic criteria for diagnosing mental disorders. The fourth edition (DSM-IV) appeared in 1994.

PANIC ATTACKS are discrete episodes of terror that begin suddenly and are associated with intense physiological symptoms (e.g., breathlessness, rapid heart rate, dizziness) and thoughts that one is about to die, lose self-control, or "go crazy."

Epidemiologic Catchment Area (ECA) Study

The largest house-to-house survey of mental disorders ever conducted in the United States. Interviewers evaluated more than 18,000 adults in five geographical areas (Los Angeles, North Carolina Piedmont region, St. Louis, New Haven, Baltimore) to estimate the prevalence of DSM-III mental disorders. First-Degree Relatives First-degree relatives are one's parents, siblings, and children. If a disorder is influenced by genetic variables, it ought to occur more often among first-degree relatives of a person with the

I. HISTORY OF THE CONCEPT OF PANIC ATTACK In 1959, research psychiatrist Donald F. Klein was studying imipramine, a new drug synthesized by a minor alteration in the chemical structure of the "ma-

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jor tranquilizer" chlorpromazine. Researchers hoped that imipramine, like chlorpromazine, would help people with schizophrenia, whose psychotic symptoms were at that time believed to result from excessive anxiety. Unfortunately, imipramine did not attenuate delusions or hallucinations, but it did alleviate depressive symptoms in schizophrenic patients, and its mood-improving effects were notably dramatic in patients suffering from severe depression. As evidence for the antidepressant effects accumulated, Klein and his associates struggled to treat a group of highly anxious inpatients who had been diagnosed as "schizophrenic" but who exhibited neither delusions nor hallucinations. Not only had they failed to respond to sedatives and to psychotherapy, their anxiety was not reduced by chlorpromazine. These results were puzzling in light of prevailing theory: chlorpromazine helped typical schizophrenics whose psychotic symptoms supposedly resulted from extreme anxiety, yet it failed to help an atypical group of schizophrenics who were very anxious, but who were not psychotic. Klein's decision to prescribe imipramine for these atypical schizophrenics was born of frustration. Other approaches had failed, and the new drug was known to be safe and to have some anxiety-reducing properties. However, after taking imipramine for several weeks, the patients maintained that the drug was ineffective because it failed to attenuate their chronic anxiety. Their psychotherapist concurred, but the nursing staff did not. Before taking imipramine, these patients had been rushing to the nursing station several times a day, terrified, and exclaiming that they were dying. The nurses would reassure them that they were not dying, and their terror would pass after about 20 minutes or so. Despite their claims of lack of improvement, patients were no longer experiencing these terrifying episodes of suddenly feeling on the brink of death. Also, once their sudden, unpredictable episodes of terror (i.e., panic attacks) had ceased, patients became increasingly comfortable, moving freely throughout the hospital unaccompanied by others. Based on these observations, Klein inferred that imipramine was effective against acute panic attacks, but not against chronic anxiety. Indeed, their chronic anxiety was itself the consequence of panic; they lived in dread of these recurrent episodes of terror. These observations also suggested a qualitative distinction

between episodic panic attacks and chronic anticipatory anxiety. Klein reasoned that the effects of imipramine would make no sense if panic were just an extreme form of anxiety. Indeed, why should a drug be effective against the severe form of a disease, but not against its mild form? This paradox would disappear if panic and anxiety arose from different underlying processes rather than being two points on a quantitative continuum of severity. As Klein observed, such apparent paradoxes are common in nonpsychiatric medicine. Bacterial pneumonia and the common cold are respiratory disorders that share many symptoms, and although the former might be mistaken for a severe form of the latter, antibiotics are effective against bacterial pneumonia but are useless against the common cold. Therefore, reasoned Klein, just as bacterial pneumonia does not lie on a continuum of severity with the common cold, panic is not merely a severe form of ordinary anxiety. [See ANxi~:rY.] Klein's experience with imipramine not only motivated his distinction between panic and anxiety, it also led him to conclude that agoraphobia was chiefly a consequence of panic attacks. (The "schizophrenic" patients who first responded to imipramine would now be diagnosed as having "panic disorder with agoraphobia" because they fearfully avoided many activities in addition to having panic attacks.) Traditional views conceptualized agoraphobia as a fear of open or public places. But it became apparent that the motivation for avoidance was fear of panicking in situations where escape was not easy or help readily available. Klein subsequently delineated three types of panic attack. Spontaneous panic attacks are sudden, unexpected surges of terror accompanied by intense (especially cardiorespiratory) symptoms. Spontaneous panics are often accompanied by catastrophic thoughts that one is about to die, "go crazy," or lose selfcontrol. From the perspective of the panicker, the attacks seem to "come out of the blue," uncaused by any obvious environmental precipitant. "Spontaneous" does not imply "uncaused"; it implies only the absence of external triggers, not the absence of neurobiological dysregulation. Spontaneous panics are akin to other conditions in medicine that erupt without clear-cut external provocation, like paroxysmal tachycardia, migraine, and vertigo (i.e., rotational dizziness) arising from inner ear disease. Stimulus-bound panics refer to the sudden surge of

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intense fear experienced by people with specific phobias (e.g., of animals, of heights) when they encounter, or anticipate encountering, their feared object. These episodes are similar to spontaneous attacks except that the panicker is aware of the external precipitant and is less likely to misinterpret the attacks as a sign of impending insanity. [See PHOBIAS.] Situationally predisposed panics occur in some situations more than in others, but are not inevitably or immediately triggered by these external stimuli. For example, people with agoraphobia often panic while in crowded stores, but crowded stores do not inevitably trigger panic with the same predictability that snakes trigger panic in people with snake phobia. Klein's work greatly influenced the inclusion of panic disorder as a diagnostic category in the third edition of the Diagnostic and statistical manual of mental disorders (DSM-III), which appeared in 1980. Based partly on his work, DSM-III postulated two types of anxiety neurosis. One type was characterized by repeated spontaneous panic attacks (panic disorder), and the other was characterized by chronic high levels of anxiety that did not erupt into panic attacks (generalized anxiety disorder). In the revised version of DSM-III (DSM-III-R), which appeared in 1987, panic disorder was coded as either panic disorder without agoraphobia or panic disorder with agoraphobia. This important change acknowledged the consensus view among American psychopathologists that although some people with panic disorder do not extensively avoid situations and activities, when people do develop agoraphobia, their avoidance almost always develops as a consequence of panic disorder. Some people, however, develop agoraphobia after having experienced episodes of intense symptoms that do not qualify as full-blown panic attacks (e.g., sudden bouts of dizziness). Because research has indicated that spontaneous panic attacks occasionally occur in people with other disorders (e.g., social phobia, major depressive disorder), DSM-IV defines panic attacks separately from panic disorder. That is, recurrent spontaneous panics are insufficient for the diagnosis of panic disorder: the person must also alter his or her life to accommodate the attacks, develop a chronic fear of the attacks, or both. According to current DSM-IV criteria, panic attacks are discrete periods of intense fear or discomfort

that begin suddenly and reach peak intensity within 10 minutes. (Most research studies, however, indicate that panic attacks usually reach peak intensity well before 10 minutes have elapsed, and often seem to peak almost instantly.) To qualify as a panic attack, an episode of sudden-onset fear must be accompanied by at least four of the following symptoms: (1) palpitations, pounding heart, or accelerated heart rate; (2) sweating; (3) trembling or shaking; (4) sensations of shortness of breath or smothering; (5) feeling of choking; (6) chest pain or discomfort; (7) nausea or abdominal distress; (8) feeling dizzy, unsteady, lightheaded, or faint; (9) derealization (feelings of unreality) or depersonalization (being detached from oneself); (10)fear of losing control or going crazy; (11) fear of dying; (12) paresthesias (numbness or tingling sensations); and (13) chills or hot flushes. Rapid-onset attacks of fear that are characterized by fewer than four of these symptoms are called "limited-symptom attacks." DSM-IV distinguishes three types of panic attack that are approximately equivalent to Klein's spontaneous, stimulus bound, and situationally predisposed panics. Unexpected (uncued) panic attacks are not triggered by any obvious external stimulus, and seem to occur "out of the blue" for no apparent reason. Situationally bound (cued) panic attacks are triggered by an encounter with a feared (phobic) stimulus or in anticipation of such an encounter. For example, a person with a snake phobia will typically experience a situationally bound panic upon encountering a snake in the woods. Finally, situationally predisposed panic attacks are triggered by encounters with feared situational stimuli, but are not invariably triggered by such encounters. For example, a person with a fear of driving automobiles will tend to experience panic attacks more often while driving than while doing other things, but driving does not invariably cause panics.

II. ASSESSING PANIC ATTACKS Most research on spontaneous panic attacks has been based on the patients' retrospective self-report. Patients are often asked to recall their most recent, most severe, or most typical attack, and then indicate the presence and severity of the DSM symptoms on some scale. Regrettably, these ratings are subject to uninten-

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tional distortion. Research suggests that atypically intense, and therefore memorable, attacks are often described as "typical," and patients often overestimate the frequency and severity of their attacks when asked about them days or weeks later. To circumvent this problem, clinical researchers now have patients prospectively self-monitor their attacks and record them in structured diaries designed for this purpose shortly after the attack occurs. Because classic panic attacks occur unpredictably, they have rarely been captured in the psychophysiology laboratory. Indeed, most laboratory research on panic involves attacks provoked by biological challenges (see below). Nevertheless, about 20 unexpected attacks have been recorded while patients were undergoing various assessments while wired for psychophysiologic assessments. These recorded episodes have indicated that panics do, indeed, begin abruptly, as patients say, and are marked by increases in heart rate, skin conductance (i.e., sweating), facial muscle tension, and hyperventilation.

III. PANIC ATTACKVARIANTS During the mid-1980s, researchers noted that about one-third of the young adult (nonclinical)population reported having experienced a "panic attack" during the previous year. These nonclinical panic attacks seemed to suggest that a phenomenon so common might not be indicative of psychopathology. Subsequent studies revealed, however, that most of these attacks were not especially severe and nor were many the spontaneous, unexpected attacks that characterize panic disorder. Consensus now holds that between 2 % and 7% of the general young adult population experiences at least one spontaneous panic attack that meets DSM criteria each year. Occasional panic attacks may presage the development of panic disorder in people who also have elevated anxiety sensitivity. Researchers have described the seemingly oxymoronic condition of nonfearful panic attacks among cardiology patients seeking help for unexplained chest pain. These individuals complain of sudden rushes of somatic symptoms identical to those of panic attacks, but do not experience fearful thoughts about imminent death and so forth. Comparisons between typical panickers and nonfearful panickers on variables such

as age of onset, average number of symptoms per attack, duration of disorder, depressive, agoraphobic symptoms, and so forth indicate that the two groups are nearly indistinguishable except for the fact that typical panickers experience terror during their attacks, whereas nonfearful panickers do not. Nonfearful panic indicates that sudden rushes of autonomic symptoms are not equivalent to panic attacks, thereby raising the possibility that a person's interpretation of the symptoms as threatening may partly determine whether they experience the episode as terrifying. Although panic attacks most often occur during the daytime, they can also erupt while the person is sleeping. Nocturnal (or sleep) panics are characterized by abrupt awakening, terror, and intense physiological arousal. Because nocturnal attacks emerge during nonREM (rapid-eye-movement) sleep, they are rarely preceded by dreams (which occur during REM sleep). Most attacks occur during the transition from stage 2 to stage 3 sleep (i.e., as the person is going into a deeper stage of sleep). About 5% of college students report having had a nocturnal panic at some point in their lives, and about 69% of panic disorder patients have had at least one nocturnal panic. It is very unusual for a person with panic disorder to have only nocturnal panics, but those who experience nocturnal panics tend to experience more daytime panics as well. There are similarities and differences between nocturnal panics and night terrors (also known as payor nocturnus in children and incubus in adults). Both erupt during non-REM sleep; both are rarely preceded by dreams; and both are marked by abrupt awakenings, terror, and autonomic arousal. Yet night terrors are more common in children than in adults, and emerge after a sustained period of very deep (stage 4) sleep. Panic attacks, including nocturnal ones, are more common in adults than in children. Furthermore, night terrors begin with a blood-curdling scream, yet the person who experiences a night terror rarely remembers the episode, and easily returns to sleep. Also, a person experiencing a night terror may become combative or run out of the house. In contrast, nocturnal panickers vividly remember their attacks, and often experience difficulty returning to sleep. The causes of nocturnal attacks are unknown. One possibility is that physiological irregularities waken the person who then panics in response to perplexing

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symptoms like breathlessness, racing heart, and so forth. Another possibility is that the psychobiological substrate of the emotion of fear does, indeed, begin while the person is sleeping, consistent with patients' reports that they awoke already in the midst of fear.

IV. THE DEVELOPMENT OF PANIC DISORDER AND AGORAPHOBIA Panic attacks usually start in late adolescence or in early adulthood; they rarely begin before puberty or late in life. They typically emerge during periods of life stress such as after the death of a loved one, in anticipation of a major life event (e.g., wedding), after losing a job, and so forth. Occasional panic attacks are not uncommon in the general population, but if individuals become persistently fearful of them or alter their lives in response to them, panic disorder is diagnosed. The vast majority of people who develop agoraphobia do so as a consequence of their fear of panic attacks. It is very unusual for someone to become agoraphobic without first having had panic attacks. Rarely, clinicians encounter people who appear to have agoraphobia without a history of panic. But close inspection of these cases reveals that such patients fear other forms of sudden bodily incapacitation that do not qualify as panic per se (e.g., diarrhea, migraine headaches). Some panickers become agoraphobic within days of their first attack; others become increasingly agoraphobic over weeks, months, and years; and still others never become agoraphobic. Researchers have studied what factors predict which panickers develop agoraphobia by comparing panickers with and without agoraphobia. Avoiders and nonavoiders do not differ in their age of onset or duration of panic disorder, and there are few differences in the severity of the attacks themselves: agoraphobic panickers do not seem to have worse attacks than nonagoraphobic panickers. There are no differences in the frequency of attacks. The best predictors of avoidance are cognitive. Predictors of agoraphobic avoidance include expectations of panicking in certain situations, perceived negative consequences of panic, fears of dying or going crazy during attacks, and lack of confidence in one's ability to cope with panic.

V. EPIDEMIOLOGY Epidemiology is the study of the distribution and determinants of disease in the population. Interviewing more than 18,000 American adults, the Epidemiologic Catchment Area (ECA) team endeavored to determine the prevalence and incidence of panic disorder and other mental disorders. The ECA data indicated that the annual prevalence rate of DSM-HI panic disorder (without agoraphobia) was 1.2 % in women and 0.6 % in men, and the lifetime prevalence was 2.1% in women and 1.0% in men. Panic disorder was most common among people aged 30 to 44 years, and least common in people older than 65 years old. People with panic disorder sought the services of mental health professionals more than people with any other disorder, including alcoholism and schizophrenia. The ECA team reported annual prevalence rates for DSM-III agoraphobia of 5.9% for women and 2.1% for men. Surprisingly, however, the ECA team reported that only 7% of the subjects diagnosed with agoraphobia also had panic disorder. This result was dramatically at variance with the observations of clinicians who rarely see agoraphobics without panic disorder. Subsequent reexamination of the "agoraphobia without panic" cases strongly suggested that the ECA team had inadvertently classified many cases of specific phobias (e.g., of flying, driving, crossing bridges) as instances of agoraphobia. The ECA researchers estimated the annual incidence of panic disorder 2.4 new cases per 1000 persons per year. The estimated incidence of a severe panic attack was 9 per 1000 persons per year. The ECA team found that 20% of people with panic disorder reported having attempted suicide at some point in their lives. This finding was surprising because panic patients often fear dying in the midst of their attacks, and most studies on patients with the disorder indicate that they are not at high risk for attempting suicide. A reanalysis of the ECA data suggested that the presence of comorbid disorders that independently increase risk for suicide attempt (e.g., schizophrenia, alcoholism, depression) may have been the basis for the apparent connection between panic disorder and suicide attempts. Nevertheless, the presence of panic disorder in a person with, say, depression provides no guarantee that the person will not attempt suicide.

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The National Comorbidity Survey (NCS), a nationwide DSM-III-R assessment of mental disorders, revealed a lifetime prevalence rate for panic disorder of 3.5%; 1.5% of the respondents had panic disorder at the point of the survey. The NCS indicated that 1.5 % of the population develops panic disorder with agoraphobia at some point in their lives; 0.7% had it at the time of the survey. As in the ECA study, the rate was about twice as high for women as for men. The NCS team also found that those with less than a high school education were more than 10 times as likely to have panic disorder as those who had graduated from college. Because income level, unlike education, was unrelated to risk for panic disorder, the NCS team suggested that lower cognitive ability may be linked to panic. Race/ethnicity was unrelated to panic disorder. Being married (or living with someone) and being employed was associated with reduced risk.

VI. BIOLOGICAL ASPECTS OF PANIC

One early hypothesis was that chronic hyperventilators are prone to panic because they are more likely than other people to experience hyperventilationinduced sensations (e.g., dizziness) that may frighten them, causing further overbreathing, greater fear, and so forth until full-blown panic results. However, most subsequent research indicates that panic patients are usually not chronic hyperventilators. But excessive ventilation is a common accompaniment of panic attacks and can worsen the symptoms associated with panic. Therefore, hyperventilation does not seem to cause panic attacks, but it does seem to intensify attacks that do occur. An important tool for studying panic in the laboratory has been the biological challenge test. Biological challenge tests produce intense bodily sensations, and incite panic attacks far more often in panic patients than in patients with other disorders or in healthy subjects. They are designed to stress specific neurobiological systems, and if panic occurs, then dysfunction in the stress system may constitute a vulnerability to naturally occurring panic attacks. A purpose of this research is to identify procedures that will reliably initiate attacks in the laboratory that strongly resemble spontaneous panic attacks. These

procedures, in turn, enable researchers to investigate the mechanisms of panic in controlled experimental situations. However, panic attacks occurring in response to biological challenges have been interpreted in two principal ways. One interpretation holds that challenges directly incite panic by exacerbating a neurobiological dysfunction. The other interpretation holds that they incite attacks merely by generating intense bodily sensations that these patients are prone to fear. Several challenges have been used. Infusion of sodium lactate occasions panic in about 67% of panic patients, but in only about 13% of healthy control subjects. Controversy persists about whether the response of panic patients differs qualitatively from that of control subjects. For example, panic patients often are more anxious and more physiologically aroused than control subjects before the infusion begins. That is, the reactivity of panic patients is often not greater than that of control subjects (i.e., the magnitude of change is not greater), but patients begin the challenge at a higher baseline level of arousal and anxiety. Some psychopathologists believe that dysregulation in the noradrenergic system is involved in the genesis of panic attacks. This hypothesis stems partly from the phenomenology of panic itself. Panic attacks are characterized by symptoms indicative of massive autonomic arousal associated with norepinephrine surges, thereby implying an instability in the noradrenergic system. Consistent with this possibility, oral (or infused) yohimbine challenges, which stimulate noradrenergic activity, produce panic in about 63% of panic patients and in about 7% of control subjects. Carbon dioxide inhalations have also been used as biological challenge tests. One hypothesis is that panic disorder patients are characterized by hypersensitive carbon dioxide receptors in the brainstem such that increases in central carbon dioxide produce an excessive ventilatory response that can initiate panic attacks. A related hypothesis is that panic is attributable to a pathologically low threshold for firing of an evolved suffocation alarm. That is, carbon dioxide receptors in the brainstem may respond to relatively low increases in carbon dioxide as if the person is suffocating. When this alarm fires, the person begins hyperventilating and experiences the terror appropriate to one who cannot breathe. Physiological evidence in support of carbon dioxide receptor hypersensitivity is mixed. In some studies, panic patients have exhibited

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excessively vigorous ventilatory responses to carbon dioxide inhalation, whereas in others they have not. Panic disorder appears to run in families, suggesting the possibility of a genetic vulnerability. It is unclear whether this vulnerability is for panic attacks per se, for overactive physiological responding, or for personality traits that may predispose people to react fearfully to bodily symptoms. Rates of panic disorder are higher in the first-degree relatives of patients with panic disorder (17.3 %) than in the first-degree relatives of healthy control subjects (1.8%). Estimates of the heritability of panic attacks and panic disorder vary depending on the population from which the subjects are drawn. In one study involving patients, 31% of the identical twins with panic attacks had a co-twin with panic attacks as well, whereas none of the fraternal twins with panic attacks had a co-twin with panic attacks. In one population study, 23.9% of the identical twins were concordant for panic disorder as compared to 10.9% of the fraternal twins when a psychiatrist made the diagnosis based on the collected data, but the respective concordance rates were nearly identical (14.5 % vs. 14.6 %) when a computer algorithm evaluated the data.

VII. PSYCHOLOGICALASPECTS OF PANIC Psychological theorists hold that physiological symptoms are insufficient to produce the experience of panic. For panic qua panic to occur, the person must react to these bodily sensations with fear. Responding to one's own bodily sensations as if they were phobic stimuli, panickers worsen these symptoms, and thereby amplify their terror. Moreover, only those people who dread these symptoms will qualify for panic disorder. According to psychological theorists, panic disorder is in large part a "fear of fear" itself. There have been several versions of the fear-of-fear hypothesis of panic disorder. One view holds that Pavlovian interoceptive conditioning figures in development of panic disorder. Initial panic attacks establish certain bodily sensations (e.g., heart palpitations, breathlessness) as conditioned stimuli that evoke subsequent panic attacks. Another view holds that panic attacks occur because individuals catastrophically misinterpret certain

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benign bodily sensations as harbingers of imminent psychological or physical disaster. Thus, a person might misinterpret palpitations as an impending heart attack, become more anxious, and thereby intensifying these sensations until they culminate into a panic attack. According to this view, catastrophic misinterpretations of bodily sensations are necessary for a panic attack to occur. A third approach emphasizes that not everyone is equally likely to respond fearfully to their own bodily sensations. People who hold mistaken beliefs about rapid heartbeats, dizziness, and so forth are presumably more likely than other people to react fearfully when these sensations occur. This notion is embodied in the anxiety sensitivity hypothesis. Anxiety sensitivity is an individual difference variable that may constitute a cognitive risk factor for panic disorder. It is conceptually and empirically distinguishable from trait anxiety. Trait anxiety refers to a proneness to react fearfully to a wide range of potential stressors, whereas anxiety sensitivity refers to the specific tendency to react fearfully to bodily sensations associated with anxiety. Importantly, people with elevated scores on the Anxiety Sensitivity Index (ASI)~a questionnaire measure of this variable~respond just like panic patients to biological challenges (e.g., carbon dioxide inhalation) even if they have no history of panic attacks or panic disorder. These studies imply that a fearful response to challenge is a marker for the fear of symptoms rather than a marker for panic disorder per se. Longitudinal research indicates that people with elevated ASI scores are at enhanced risk for developing panic and other anxiety disorders. Implicit in the fear-of-fear construals of panic is the notion that people prone to experience panic attacks process arousal-related information differently than do people who are not prone to experience panic attacks. That is, people with panic disorder seem characterized by cognitive biases favoring the interpretation of threat. A growing body of experimental research indicates that panickers are characterized by interpretive, attentional, and memory biases favoring threat. For example, when asked to provide explanations for ambiguous scenarios (e.g., "You feel discomfort in your chest area. Why?"), panic patients are prone to interpret them in a catastrophic manner (e.g., reacting to chest discomfort as indicative of heart attack rather than indigestion). Panic patients are also characterized by attentional

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biases favoring threat, as evinced by their responses on "emotional Stroop" tasks. In these tasks, subjects are shown words of positive, neutral, and negative emotional significance, and are asked to name the colors in which the words appear (on a computer screen) while ignoring the meanings of the words. Delays in color-naming occur when the meaning of the word captures the subject's attention despite the subject's effort to attend to the color of the word. In one experiment, panic patients exhibited delayed color naming for words related to fear (e.g., panic), bodily sensations (e.g., breathless), and catastrophe (e.g., insane). In another experiment, they exhibited greater interference for catastrophe words than for positive words of equivalent but opposite valence (e.g., carefree). These studies suggest that panic disorder is characterized by biases for selectively attending to threat cues. Finally, other studies have shown that panic patients exhibit superior memory for words related to anxiety and threat. This memory bias for threat appears enhanced when patients are in a state of physiological arousal. Taken together, these results suggest that threat-related material may have preferential access to conscious mentation in these patients.

VIII. PSYCHOPHARMACOLOGIC TREATMENTS FOR PANIC As noted earlier, the tricyclic antidepressant, imipramine, was the first compound shown effective against panic attacks. Patients need not be depressed for this drug to work against panic. The effects of imipramine are potentiated by combining it with exposure in vivo, a behavior therapy method (see below). Unfortunately, a substantial minority of panic patients fail to tolerate the side effects of imipramine, which include increased heart rate and jitteriness. Some clinicians suggest slowly increasing dosage until a therapeutic effects are reached as a means of managing side effects. High-potency benzodiazepines, such as alprazolam, have been used to treat panic disorder. Their side effects are less disagreeable, and these medications begin to exert their antipanic effects within days of commencing treatment in contrast to imipramine, which often takes weeks before benefits begin to appear. Disadvantages of these compounds include their capacity to induce pharmacologic and psychological depen-

dence; panic patients often find it difficult to cease taking alprazolam. This can pose a problem for women who wish to become pregnant, and therefore need to be free of alprazolam. Moreover, cessation of these compounds often results in the return of panic attacks, and sometimes these rebound panics are more intense than the attacks that had been occurring before the patient began taking alprazolam. Some evidence suggests that panic patients with agoraphobia who undergo otherwise effective in vivo exposure treatments do worse at follow-up if they had been taking alprazolam than if they had been taking placebo. The selective serotonin reuptake inhibitors (SSRIs) have been widely prescribed for many psychiatric conditions in recent years. Originally developed as antidepressants, SSRIs, such as fluoxetine, have been recently used as antipanic agents. Indeed, the study reporting the most impressive evidence for the pharmacologic treatment of panic disorder tested the SSRI fluvoxamine. Although controlled research on the treatment of panic disorder with SSRIs has only recently begun, the consensus among psychopharmacologists is that SSRIs are the drug treatment of choice for panic disorder. The SSRIs appear to have more tolerable side effects than tricyclic antidepressants and they appear to be less likely to produce dependence than high-potency benzodiazepines. Limited data also suggest that relapse upon drug discontinuation may be less likely than relapse following discontinuation of alprazolam and similar compounds.

IX. PSYCHOLOGICALTREATMENTS FOR PANIC Despite differences in emphasis, most cognitivebehavior therapists treat panic as follows. Early sessions usually are designed to reduce the patient's anxiety sensitivity by providing the patient with basic information about panic attacks that counteracts the patient's catastrophizing tendencies. For example, one approach emphasizes that panic attacks reflect an adaptive, evolved fight-or-flight response that fires at inappropriate times. Under this view, panic attacks are not dangerous events but rather reflect an evolved mechanism for protecting against danger. Patients are also shown how they may inadvertently maintain their disorder by hypervigilantly monitoring their bodies

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for feared sensations and then misinterpreting them as harbingers of harm. Some clinicians next train patients to use symptom (or panic) management techniques. These include respiratory control procedures for counteracting patients' tendencies to hyperventilate during panic attacks (and thus worsening them). Patients are taught to breathe by using their abdomen rather than just their upper chest, and are taught to breathe at a comfortable pace instead of gasping for air and making things worse. They are taught to breathe through the nose, not the mouth, as an additional means of counteracting hyperventilation. Patients are taught a technique called applied relaxation as another means of managing symptoms. This method first involves teaching them how to tense and relax different muscle groups in the clinic and to detect signs of tension. They are then given practice in applying these procedures while they engage in everyday activities. It is unclear whether these methods are effective because they blunt symptoms during episodes of panic, or whether they enhance the patient's sense of restoring control. Inspired by the notion that panic attacks are akin to conditioned responses to the phobic stimuli of one's own bodily sensations, clinicians structure interoceptive exposure exercises. Interoceptive exposure refers to graduated, structured induction of feared bodily sensations done in a fashion so as to reduce the patient's fear of the sensations. Patients may be asked to run up stairs to increase heart rate, to breathe through a straw to increase breathlessness, and so forth. The rationale is that structured exposure to harmless bodily sensations reduces the patient's fear of them. Just as the fear-of-fear hypothesis inspired the development of interoceptive exposure, so has the catastrophic misinterpretation hypothesis inspired cognitive techniques for refuting patient's beliefs about the harmfulness of bodily sensations. These beliefs are treated as experimental hypotheses, and therapists work with patients to evaluate the evidence for and against their catastrophic hypotheses and noncatastrophic alternative interpretations of bodily sensations. This approach entails the conducting of behavioral experiments. If, for example, a patient hypothesizes that dizziness leads one to collapse, the therapist might have the patient hyperventilate while sitting and then have the patient stand up quickly. The failure of the patient to collapse disconfirms the cata-

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strophic hypothesis while confirming the noncatastrophic alternative that intense lightheadedness may produce unsteadiness, but not collapse. The basic notion behind these experiments is that patients often engage in subtle avoidance behavior in the midst of panic attacks that prevents their catastrophic beliefs from being tested and refuted. Thus, if patients always sit down when becoming dizzy and panicky, they will never learn that their feared catastrophe of collapse never occurs. The object of cognitive therapy is to provide these instructive learning experiences. Finally, most patients with panic disorder have developed varying degrees of agoraphobic avoidance behavior. Although few become entirely housebound, most have restricted their lives to a considerable extent. Therefore, patients are urged to undertake in vivo (i.e., real-life) exposure exercises whereby they practice entering previously avoided situations and engaging in previously avoided activities. The general rule is for patients to remain in these situations until their discomfort has diminished. Although it was once believed that exiting a feared situation in the midst of a panic would automatically worsen the patient's fear and avoidance, subsequent research has indicated that this is not necessarily true. Even if a patient leaves the feared situation, no lasting exacerbation of fear seems to occur if the patient reenters the situation soon afterward. The chief goal is to ensure that patients regularly practice engaging in feared activities. It is not essential that the therapist accompany the patient on these forays, but for highly avoidant patients, it is often helpful. Most early psychological research on the treatment of panic disorder and agoraphobia concentrated on the reduction of fear and avoidance via exposure therapies. Although in vivo exposure does not directly target panic, catastrophic misinterpretations, and so forth, it has been shown to reduce (but not always to eliminate) panic attacks. Some studies have shown that the combination of imipramine and exposure is better than either alone, whereas adding alprazolam to exposure seems to reduce the effectiveness of the latter. There are no data on combined SSRI and behavioral treatment. During the past several years, researchers have tested the efficacy of the cognitive-behavioral approach described above. This strategy eliminates panic attacks in approximately 80% to 90% of patients, and most retain their gains at follow-ups of 1 to 2

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years posttreatment. Indeed, the percentages of patients who are panic-free at posttreatment are comparable and often higher than the percentages of panicfree patients who receive medication. Moreover, rates of relapse are lower after cognitive-behavior therapy than after drug treatment, probably because patients have learned not to react fearfully to bodily sensations and have therefore learned how not to let fear spiral into panic. Moreover, cost-effectiveness analyses have confirmed that cognitive-behavioral treatment for panic is not only at least as effective in the short term as drug treatment, it is less expensive in the long term, and it does not generate side effects or pharmacologic dependence.

X. CONCLUSIONS Although most researchers agree that panic attacks constitute emotional phenomena distinct from anxiety, there is no consensus about their cause. Biological researchers have identified several possible pathways that may give rise to unusual bodily sensations (e.g., noradrenergic overreactivity, carbon dioxide hypersensitivity), it is unlikely that one physiologic cause is the source of sensations in all patients. More likely,

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several different biological abnormalities produce the sensations that patients fear. Most data indicate that surges of sensations do not produce the emotional phenomenon of panic unless the person reacts to them as threatening stimuli. Taken together, the data suggest that panic disorder comprises abnormalities in both biology and cognition. Fortunately, effective treatments, both pharmacologic and cognitive-behavioral, are available.

BIBLIOGRAPHY Barlow, D. H., & Craske, M. G. (1989). Mastery of your anxiety and panic. Albany, NY: Graywind. Clark, D. M. (1986). A cognitive approach to panic. Behav. Res. Ther., 24, 461-470. Eaton, W. W., Kessler, R. C., Wittchen, H. U., & Magee, W. J. (1994). Panic and panic disorder in the United States. Am. J. Psychiat., 151,413-420. Gould, R. A., Otto, M. W., & Pollack, M. H. (1995). Meta-analysis of treatment outcome for panic disorder. Clin. Psychol. Rev., 15, 819-844. Klein, D. F. (1981 ). Anxiety reconceptualized. In D. F. Klein & J. G. Rabkin (Eds.), Anxiety: New research and changing concepts (pp. 235-263). New York: Raven Press. Margraf, J., Barlow, D. H., Clark, D. M., & Telch, M. J. (1993). Psychological treatment of panic: Work in progress on outcome, active ingredients, and follow-up. Behav. Res. Ther., 31, 1-8. McNally, R. J. (1994). Panic disorder: A critical analysis. New York: Guilford Press.

Paranoia Allan Fenigstein Kenyon College

I. II. III. IV.

Paranoid Syndromes Prevalence Causes of Paranoia Treatment of Paranoia

aware of himself as an object of attention to others. Therapeutic Alliance A tactic frequently used in treating paranoids, in which the therapist acknowledges the patient's delusional beliefs as understandable, in an attempt to build trust.

Delusions Faulty interpretations of reality that cannot be shaken, despite clear evidence to the contrary, and that are not shared by other members of the community. Ideas of Reference The misperception of oneself as the target of others' thoughts and actions; for example, a person seeing others laughing might relate the event to himself, and see himself as the target of their laughter. Paranoia A disordered mode of thought that is dominated by a pervasive, exaggerated, and unwarranted suspiciousness and mistrust of people, and a corresponding tendency to interpret the actions of others as deliberately threatening or demeaning. Paranoid Illumination The point at which the paranoid realizes that he has been singled out for mistreatment, and others are working against him; suddenly, everything begins to make sense. Projection A psychological defense often associated with paranoid thinking, in which the individual attributes one's own unacceptable motives or characteristics to others. Pseudo-Community A delusional system in which the paranoid organizes a variety of unrelated persons into a structured group whose primary purpose is to engage in a conspiracy against him. Self-Focus A behavioral style characteristic of paranoia, in which the individual is especially prone to be

PARANOIA, although originally referring (in Greek) to almost any kind of mental aberration or bizarre thinking, is currently used to describe a disordered mode of thought that is dominated by an intense, irrational, but persistent mistrust or suspicion of people and a corresponding tendency to interpret the actions of others as deliberately threatening or demeaning. Because of the general expectation that others are against them or are somehow trying to exploit them, paranoid persons tend to be guarded, secretive, and ever vigilant, constantly looking for signs of disloyalty or malevolence in their associates. These expectations are easily confirmed: the hypersensitivity of paranoids turns minor slights into major insults, and even innocuous events are misinterpreted as harmful or vindictive. As a result, a pernicious cycle is set in motion whereby expectations of treachery and hostility often serve to elicit such reactions from others, thus confirming and justifying the paranoid's initial suspicion and animosity. Of all psychological disturbances, paranoia is among the least understood and most difficult to treat.

I. PARANOID SYNDROMES Paranoid features are found in a variety of different psychological conditions. Although these conditions

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are often regarded as distinct, the criteria for distinction are not entirely clear and the practical utility of the distinction, in terms of etiology or treatment implications, has not been established. Thus, it may be useful to consider the different paranoid disorders as related syndromes existing along a continuum which varies in terms of the frequency and severity of paranoid thoughts, the degree to which reality is allowed to influence perceptions, and the extent to which functioning is impaired. The continuum extends from paranoid personality disorder, which is nondelusional, but where suspicion and its sequelae occur so regularly that work and family life are often disrupted; to delusional (paranoid) disorder, involving a chronic, dysfunctional delusional system, although apart from the delusion, reality testing is good and behavior is not obviously odd; and finally, to paranoid schizophrenia, a severe, incapacitating psychosis, involving a serious loss of contact with reality in which all thought is affected by the delusion.

A. Delusional (Paranoid) Disorder The cardinal feature of this disorder is the presence of a delusion that is so systematic, logically developed, well-organized, and resistant to contradictory evidence, that others are often convinced by it. Delusions are faulty interpretations of reality that cannot be shaken, despite clear evidence to the contrary. Although the delusions in this disorder are nonbizarre (unlike those found in paranoid schizophrenia) and involve situations that may occur in real life, in fact they have no basis in reality, and are not shared by others in the culture. Delusional systems are usually idiosyncratic, but some themes or combination of themes are more frequently seen than others, and psychiatric diagnosis of this disorder is now specified by the predominant theme of the delusions present. Delusions of persecution, in which the paranoid believes that "others are out to get me," are the most common form of this disorder. While those with a paranoid personality disorder may be suspicious that colleagues are talking about them behind their backs, persons with delusional disorder may go one step further and suspect others of participating in elaborate master plots to persecute them. They often believe that they are being poisoned, drugged, spied upon, or are the targets of conspiracies to ruin their reputations. Many of them tend to be inveterate "injustice-

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detectors," inclined to take retributive actions of one sort or another, and are constantly embroiled in litigation or letter writing campaigns, in an attempt to redress imagined injustices. Persons with delusions of grandiosity have an exaggerated sense of their own importance. In some cases, these beliefs are related to persecutory delusions, in that the paranoid eventually comes to feel that all the attention he's receiving is indicative of his superiority or unique abilities. Such exalted ideas usually center around messianic missions, extremist political movements, or remarkable inventions. Persons suffering from delusions of grandeur often feel that they have been endowed with special gifts or powers and, if allowed to exercise these abilities, they could cure diseases, banish poverty, or ensure world peace. When these efforts are ignored or thwarted, as they almost inevitably are, the paranoid may become convinced of a conspiracy directed against him. Another theme frequently seen is that of delusional jealousy, in which any sign~even an apparent wrong number on the phone or a short delay in returning home--is summoned up as evidence that a spouse is being unfaithful. When the jealousy becomes irrationally pathological, and the paranoid becomes convinced beyond all reason that his spouse is cheating and plotting against him in an attempt to humiliate him, he may become violently dangerous. An erotic delusion (also known as erotomania) is based on the belief that one is romantically loved by another, usually someone of higher status or a wellknown public figure, although the other, presumably, cannot acknowledge it openly. Because of unrealistic expectations about the likelihood of living with the celebrity, these delusions often result in stalking or harassment of famous persons through incessant phone calls, letters, visits, and surveillance. When their love is not returned, these delusional individuals feel a sense of betrayal that may turn to rage and hatred. Although this disorder has been reported most often in women, it occurs in men as well (perhaps the best example being John Hinckley, whose erotomanic delusions involving the actress Jodie Foster led to his attempted assassination of then-President Ronald Reagan). Those with somatic delusions are convinced that there is something very wrong with their bodies----that they emit foul odors, or have bugs crawling inside of them, or are misshapen. These delusions often result in an avoidance of others, except for physicians who,

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despite being accused of conspiring to deny the problem, are consulted continuously regarding the imagined condition. The thinking and behavior of these individuals tend to become organized around the delusional theme in the form of a pathological "paranoid construction" that, for all its distortion of reality and loss of critical judgment, provides a sense of identity, importance, and meaning not otherwise available. The meaningfulness of delusions is also suggested by the fact that they often reflect the person's position in the social universe: Women and married men are most likely to have delusions with sexual content; foreign immigrants are most prone to have persecutory delusions; and people from higher socioeconomic levels are the most likely to have delusions of grandeur. Once the basic delusion is accepted, other aspects of behavior, including emotional responses, may be described as appropriate and more or less conventional. Delusionally disordered persons do not suffer hallucinations or indications of other mental disorders, and their personalities do not change drastically; there are few exacerbations or remissions. There is a relatively high level of cognitive integration skills in areas that do not impinge on the delusional thought structure. Despite their mistrust, defensiveness, and fear of being exploited, they can sometimes function adequately, especially when their suspicions are limited to one specific area; for example, if they suspect poisoners everywhere, they may be satisfied if they can prepare all their own food. Their lives may be very limited and isolated, but they are just as likely to be regarded as harmless cranks than as someone requiring the help of a mental health professional. Sometimes, however, the consequences of the delusions are debilitating and not so easy to manage; for example, a person suffering from delusions of persecution may assault an imagined persecutor or spend a fortune fleeing enemies and pursuing redress for imagined wrongs. In other instances, the disorder may be dangerous. In particular, paranoid delusional disorder may be overrepresented among fanatical reformers and self-styled prophets and cult leaders. These individuals may be especially attracted to an enterprise that encourages blaming others, regarding themselves as a victim, and putting themselves at the center of things. Especially in times of social cataclysm or uncertainty, their grandiosity and moralistic tendencies, as well as the logical and compelling presentation of their messi-

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anic or political delusions, can often attract disciples. In addition, their garrison mentality is quite capable of provoking events which then serve to confirm their apocalyptic prophecies. Much of the difficulty involved in diagnosing paranoid disorders is because of the slipperiness of the concept of delusion. Even in the real world, it is not always possible to determine the truth or falsity of an idea: Does the government keep track of unsuspecting individuals? Is our air and water filled with unseen toxins? Does our boss really have our best interests in mind? Some ideas that are patently false are held with sincere conviction by many; and even when an idea is held as preposterous by the majority, that majority may be wrong. How, then, do we evaluate the irrationality of an idea, or decide whether clearly eccentric and convoluted thinking merits the designation "delusional?" Although it may be difficult to distinguish reality from illusion, particularly when the belief system develops around a potentially real injustice, other indications may be diagnostically helpful. An inability to see facts in any other light or to place them in an appropriate context, a glaring lack of evidence for far-reaching conclusions, and a hostile, suspicious, and uncommunicative attitude when delusional ideas are questioned usually provides clues of pathology.

B. Paranoid Personality Disorder Anyone starting in a new situation or relationship may be cautious and somewhat guarded until they learn that their fears are unwarranted. Those with paranoid personality disorder cannot abandon those concerns. Although not of sufficient severity to be considered delusional, theirs is a rigid and maladaptive pattern of thinking, feeling, and behavior, usually beginning by early adulthood, that is built upon mistrust, vigilance, and hostility. The conviction that others "have it in for them" represents their most basic and unrelenting belief; they feel constantly mistreated, and have a high capacity for annoying and provoking others. Seeing the world as a threatening place, these individuals are preoccupied with hidden motives and the fear that someone may deceive or exploit them. They are inordinately quick to take offense, slow to forgive, and ready to counterattack at the first sign of imagined criticism, even in their personal relationships. Disordered paranoid personalities see references to them-

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selves in everything that happens. If people are seen talking, the paranoid knows they are talking about him. If someone else gets a promotion, that person's advancement is seen as a deliberate attempt to humiliate him and downgrade his achievements. Even offers of help and concern are taken as implied criticisms of weakness or as subtle manipulations of indebtedness. The constant suspicions and accusations eventually strain interpersonal relations to the point where these individuals are in continual conflict with spouses, friends, and legal authorities. Given their hypersensitivity, any speck of evidence that seems to confirm their suspicions is blown out of proportion, and any indication to the contrary is ignored or misinterpreted. Trivial incidents become accumulated and unconnected "facts" are fit together to create false, but unshakeable beliefs regarding their mistreatment. Because of their conviction that others are undermining their efforts or ruining their achievements, they tend to see themselves as blameless, instead finding fault for their own mistakes and failures in others, even to the point of ascribing evil motives to others. Those with disordered paranoid personalities also tend to overvalue their abilities, and have an inflated sense of their rationality and objectivity, making it extraordinarily difficult for them either to question their own beliefs or to accept or even appreciate another's point of view. Unable to recognize the possibility of genuine dissent, simple disagreement by others becomes a sign of disloyalty. The resulting obstinacy, defensiveness, and self-righteousness exasperates and infuriates others, and elicits responses that exacerbate the conflict and confirm the original paranoid expectations. In addition to being argumentative and uncompromising, paranoids appear cold and aloof, and emotionally cut off from others. They avoid intimacy, partly because they fear betrayal, partly in an attempt to maintain total control over their affairs, and partly because of profound deficits in their capacity for joy, warmth, and nurturance. The resulting social isolation, by limiting the opportunity to check social reality and learn from others, only reinforces their egocentric perspective. Compared to some other paranoid pathologies, those with disordered personalities tend not to progressively worsen, but rather reach a certain level of severity and stay there. They show considerably less disorganization of personality, and they do not de-

velop the kind of systematic and well-defined delusions found in delusional disorders. However, the proverbial kernel of truth is often greater in the suspicions of disordered paranoid personalities than in those with delusional disorders; their accusations have more plausibility and their paranoid attitudes are more diffuse. Because of the complexity and pervasiveness of personality disorders, these individuals may have more impoverished lives, although some do manage to function adequately in society, often by carving out a social niche in which a moralistic and punitive style is acceptable or at least tolerated.

C. Paranoid Schizophrenia This major mental illness is one of the most common types of psychotic disorders. Paranoid schizophrenics may be distinguished from those with delusional disorder on the basis of the extreme bizarreness of their paranoid delusions, such as the belief that their thoughts or actions are being controlled by external forces, and by the presence of hallucinations (e.g., hearing voices) and other indications of a serious break with reality. The delusions of schizophrenics are not organized and systematic, but fragmentary and unconnected. Although these individuals may be suspicious and very much threatened by outside influences, their reaction, unlike that of the disordered paranoid personality, is usually hesitant and confused; their anger has no concentrated intensity. The behavioral, cognitive, and perceptual disorders of paranoid schizophrenics are so dysfunctional that performance on the job or at home almost invariably deteriorates, and emotional expressiveness becomes severely diminished. These individuals commonly suffer from delusions of persecution, wherein they are convinced that they are constantly being watched or followed, and that strangers or government operatives or even alien beings are plotting against them with fantastic machines, undetectable poisons, or extraordinary mental powers. Of course, given the exceptional cunning and duplicity of these diabolical forces, virtually anything--a look, a sound, a bodily sensation, for that matter, even the absence of anything, a particularly shrewd maneuv e r - i s seen as confirmation of one's suspicions. When the schizophrenic experiences the "paranoid illumination," and recognizes that all this overwhelming evidence fits together, the sense of his own visibility and

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vulnerability is profoundly increased, as is the tendency to misperceive himself as the target of other people's stares, comments, and laughter. In some cases, persecutory beliefs are accompanied by delusions of grandeur: that they are the target of these forces is only because they are special or powerful or dangerous. They may recognize that others reject them and their message, but they interpret these negative reactions as persecution based on jealousy, hostility, or enemy conspiracies. Some paranoid schizophrenics avoid detection for long periods because their extreme suspiciousness encourages them to keep their "precious knowledge" secret. Moreover, although these individuals are deeply disturbed and are subject to intense panic (given their sense of imminent danger) and extreme excitement (over their irrational "discoveries"), many of them are not overtly bizarre or belligerent. [See SCHIZOPHRENIA.]

D. Other Paranoid Disorders Some paranoid thinking manifests itself in a less persistent form. Acute paranoid disorder, in which delusions develop quickly and last only a few months, sometimes appear after a sudden, stressful social change, such as emigration, prison, induction into military service, or even leaving a family home. Although these conditions are multifaceted, they all are associated with extreme social isolation, unfamiliarity with the appropriate customs and rules of behavior, a sense of vulnerability to exploitation, and a general loss of control over life, psychological factors which may play an important, albeit temporary, role in inducing episodes of paranoia. Paranoid symptoms may also be a byproduct of physical illness, organic brain disease, or drug intoxication. Among organic illnesses, hypothyroidism, multiple sclerosis, Huntington's disease, and epileptic disorders, as well as Alzheimer's disease and other forms of dementia, are common causes of paranoia. In some people, alcohol stimulates a paranoid reaction even in small doses, and paranoia is a common feature of alcohol hallucinosis and alcohol withdrawal delirium. Chronic abuse of drugs, such as amphetamines, cocaine, marijuana, PCP, LSD, or other stimulants or psychedelic compounds, may produce some of the symptoms of paranoid personality disorder, and in high doses, may cause an acute psychosis that is almost indistinguishable from paranoid schizophrenia.

These drugs may also exacerbate symptoms in persons already suffering from a paranoid disorder. [See

DEMENTIA.] II. PREVALENCE It is difficult to estimate the frequency of paranoia in the general population because many paranoids function well enough in society to avoid coming to the attention of professionals, and because their suspiciousness and intellectual arrogance usually prevent them from volunteering for treatment. While clinical diagnoses of paranoid disorders are rare, a more realistic picture of its actual occurrence is suggested by the many exploited inventors, morbidly jealous spouses, persecuted workers, fanatic reformers, and self-styled prophets who are often able to maintain themselves in the community without their paranoid condition being formally recognized. Estimates of prevalence are further complicated by the fact that almost everyone engages in paranoid thinking at one time or another. Most people can think of an occasion when they thought that they were being watched or talked about, or felt as if everything was going against them, or were suspicious of someone else's motives without adequate proof that such things had actually occurred. Recent studies have shown that for a significant number of people, these paranoid beliefs represent a relatively stable personality pattern. Such paranoid personalities--although characterized by suspiciousness, self-centeredness, scapegoating tendencies, and a generally hostile attitude-apparently are capable of functioning reasonably well in society.

III. CAUSES OF PARANOIA A. Biological Bases I. Genetic Contribution Although there is little research on the role of heredity in causing paranoia, there is some evidence from twin studies indicating that paranoid symptoms in schizophrenia may be genetically influenced. In addition, family studies suggest that features of the paranoid personality disorder occur disproportionately more often in families with members who have either delusional

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disorders or paranoid schizophrenia, suggesting that these syndromes may be genetically related.

2. Biochemistry No identifiable biochemical substrate or demonstrable neuropathology relates specifically to paranoid thought or delusions; that is, there is no brain system whose dysfunction would specifically produce the psychological characteristics associated with paranoia. Although the abuse of drugs, such as amphetamines, may lead to paranoid symptoms, thus suggesting a possible biochemical pathway, no such pathway has been identified; whatever drug effects have been found may be psychologically, and not biochemically, mediated.

B. Psychological Bases In the absence of a clear organic basis or effective drug treatment for paranoia, most researchers have sought to identify the psychological mechanisms that explain how paranoid ideas become fixed in the mind.

I. Psychodynamic Theory Of all psychological theories, Freud's is perhaps the best known, although it is increasingly challenged. He believed that paranoia was a form of repressed homosexual love. According to Freud, paranoia arises, at least in men, when a child's homosexual feelings for his father are preserved but driven into the unconscious, from which they re-emerge during an adult emotional crisis, converted into suspicions and delusions by projection~the attribution of one's own unacknowledged wishes and impulses to another person. That is, before reaching consciousness, the impulses undergo some kind of transformation that disguise their homosexual origin; for example, a man suffering from paranoid jealousy, unable to acknowledge that he himself loves another man, projects that feeling onto his wife and becomes convinced that it is his wife who loves the man. Although Freud's theory of unconscious homosexuality has been largely discredited, projection is still recognized as a basic mechanism used by paranoids to defend against their feelings. Paranoids will explain their sense of helplessness by pointing to the control exerted by others; or self-critical ideas are transformed into the belief that others are criticizing them. Viewing others as hostile not only justifies the paranoid's feeling of being threatened, it may actually elicit the other's anger,

thus confirming the paranoid's original assumption. As a result, paranoids are left feeling weakly vulnerable, but morally righteous.

2. Faulty Development Rather than emphasizing unconscious dynamics, other approaches have viewed paranoid thinking as the outcome of a complex interaction of personality traits, social skills, and environmental events, some of which may be traced to early family dynamics. Paranoids, even as children; were often described as aloof, suspicious, secretive, stubborn, and resentful of punishment. Rarely was there a history of normal play with other children, or good socialization with warm, affectionate relationships. Their family background was often authoritarian, and excessively dominating and critical. Paranoid persons may dread being watched and judged because, it has been suggested, that reminds them of their parents, who were distant, demanding, and capricious. This inadequate socialization may have kept them from learning to understand others' motives and points of view which, in turn, may have led to a pattern of suspicious misinterpretation of unintentional slights. Social relationships tended to be suffused with hostile, domineering attitudes that drove others away. These inevitable social failures further undermined self-esteem and led to deeper social isolation and mistrust. In essence, these individuals emerged from childhood with deeply internalized struggles involving issues of hostility, victimization, power, submission, weakness, and humiliation. In later development, these early trends merged to create self-important, egocentric, and arrogant individuals, who maintained their unrealistic self-image and a sense of control by projecting blame for their problems onto others, and seeing weaknesses in others that they could not acknowledge in themselves. Their suspicion and hypersensitivity were made even more problematic by their utter inability to see things from any viewpoint but their own.

3. The Paranoid "Illumination" and the Paranoid Pseudo-Community Other theorists have focused, not on early family history, but on the later emergence of a fixed, unyielding paranoid belief system. Given the paranoid's rigidity, self-importance, and suspiciousness, he is likely to become a target of actual discrimination and mistreatment; and ever alert to such occurrences, the paranoid

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is likely to find abundant "proof," both real and imagined, of persecution. The cycle of misunderstanding is then perpetuated by the paranoid's subsequent responses. The belief that others are plotting against him results in hostile, defensive behavior. This in turn elicits the others' anger and irritability in response to the paranoid's apparently unprovoked hostility, thus confirming the paranoid's original suspicion that they are out to get him. This cycle of aggression and counteraggression has also been offered as one explanation for the greater prevalence of paranoia among males than females. The paranoid's inability to consider the others' perspective--that the other may be operating out of defensiveness against the paranoid's antagonism and belligerence--only exacerbates the conflict. As failures and seeming betrayals mount, the paranoid, to avoid self-devaluation, searches for "logical" explanations. He becomes more vigilant in his scrutiny of the environment, looking for hidden meanings and asking leading questions. Eventually, a meaningful picture, in the form of the "paranoid illumination," crystallizes and everything begins to make sense: he has been singled out for some obscure reason, and others are working against him. Failure is not because of any inferiority on his part, but rather because of some conspiracy or plot directed at him. With this as his fundamental defensive premise, he proceeds to distort and falsify the facts to fit the premise, and gradually develops a logical, fixed delusional system, referred to as the "pseudocommunity," in which the paranoid organizes surrounding people (real and imaginary) into a structured group whose purpose is centered on his victimization. As each additional experience is misconstrued and interpreted in light of the delusional idea, more and more events, persons, and experiences become effectively incorporated into the delusional system. Because the delusion meaningfully integrates all the vague, disturbing, amorphous, and unrelated "facts" of his existence, the paranoid is unwilling to accept any other explanation and is impervious to reason or logic; any questioning of the delusion only convinces him that the interrogator has sold out to the enemy.

4. Anomalous Perceptions Another theory offers the intriguing hypothesis that delusions are the result of a cognitive attempt to account for aberrant or anomalous sensory experiences. For example, research has shown that persons with

visual or hearing loss--because of both heightened suspiciousness and an attempt to deny the loss--may conclude that others are conspiring to conceal things from them. The experience of many elderly people, who are a high risk group for paranoia, provides a particularly good example of this phenomena. These individuals, because of physical disability or social isolation, often feel especially vulnerable. These realistic feelings may be converted to paranoia by an unacknowledged loss of hearing. That is, an awareness of oneself as a potential victim of greedy relatives or petty criminals, together with an increased sense that others are whispering, may contribute to a growing suspicion that others are whispering about them, or harassing them, or perhaps planning to steal from them. When the others angrily deny the accusation, that only reinforces the conspiratorial delusion, and intensifies the cycle of hostility and suspicion. The occurrence of paranoia in those with degenerative brain disorders, such as Alzheimer's disease, may be explained through a similar process. These diseases commonly involve a disruption of memory that victims may be unwilling to acknowledge. As a result, failures of memory become an anomalous experience that needs to be explained. For example, not being able to locate one's keys is transformed into the belief that someone else has stolen or misplaced them. This suspicion may then be incorporated with actual perceptions, such as seeing one's child speaking to the doctor, to produce the conviction that others are conspiring to confuse the patient in order to put them away. [See ALZHEIMER'SDISEASE.] The general hypothesis that anomalous experience may be the basis for paranoia assumes that the process by which delusional beliefs are formed is very similar to the process that operates in the formation of normal beliefs; that is, delusions are not the result of a disturbed thought process, but arise because of abnormal sensory or perceptual experiences. Anomalous experiences demand an explanation, and in the course of developing hypotheses and testing them through observations, the delusional insight is confirmed through selective evidence. This explanation offers relief in the form of removing uncertainty, and the relief in turn works against abandonment of the explanation.

5. Stress A related explanation may account for the often observed association between paranoia and stressors

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such as social isolation, economic deprivation, and abrupt situational changes. These conditions generally involve feelings of confusion, vulnerability, and a loss of control, suggesting that, in some ways, paranoid thought may serve to impose meaning and control in an otherwise uncertain and threatening environment. The paranoid belief that others are responsible for one's own misfortune, although threatening and irrational, may still be preferable to the belief that one is responsible for one's own misfortune or that such misfortune is a purely random event. In this regard, it is possible that the paranoid thinking which often develops as a result of acute drug intoxication (for example, amphetamine abuse), or aging (and its concomitant sensory loss and social isolation), or degenerative brain disorders (such as Alzheimer's disease) may be mediated by the confusion and vulnerability often found in these conditions.

6. Biases in Information Processing Some of the approaches discussed thus far have emphasized the fact that, apart from the paranoid construction itself, the cognitive functioning of paranoids is essentially intact. In fact, given their delusional system, paranoid reactions are not unlike the biased tendencies of many individuals with strong belief systems, who are likely to exaggerate, distort, or selectively focus on events which are consistent with their beliefs. Once the paranoid suspects that others are working against him, he starts carefully noting the slightest signs pointing in the direction of his suspicions, and ignores all evidence to the contrary. With this flame of reference, it is quite easy, especially in a highly competitive, somewhat ruthless world, for any event, no matter how innocuous, to be selectively incorporated into the delusion. This, in turn, leads to a vicious cycle: suspicion, distrust, and criticism of others drives people away, keeps them in continual friction with others, and generates new incidents for the paranoid to magnify. Although these information processing biases serve to maintain the paranoid's beliefs once they are established, they do not address the question of the origin of paranoid beliefs. The essence of paranoia is a malfunctioning of the capacity to assign meanings and understand causes for events. Ordinarily, these cognitive processes operate in a reasonably logical and objective fashion. In paranoia, such objective assessments are overwhelmed by judgments and interpretations that bear little relation to what actu-

ally happened, but instead are perverted in accord with the paranoid's own concerns and interests. The persistent rnisperception of oneself as the target of others' thoughts and actions, referred to as an idea or delusion of reference, is the hallmark characteristic of almost all forms of paranoid thought. Even when there is no basis for making any connection, paranoids tend to perceive others' behavior as if it is more relevant to the self than is actually the case as, for example, when the laughter of others is assumed to be self-directed, or the appearance of a stranger on the street is taken to mean that one is being watched or plotted against. Why does the paranoid consistently feel singled out or targeted by others? a. Paranoia and Self-Focus Part of the answer may lie in the characterization of paranoia as a very selffocused style of functioning. Recent studies have suggested that self-awareness, or the ability of an individual to recognize itself as an object of attention, heightens the tendency to engage in paranoid inferences. In essence, to see oneself as an object of attention, particularly to others, leaves a person susceptible to the paranoid idea that he is being targeted by others. Apparently, as a result of recognizing the self as an object of attention, the self is more likely to be interjected into the interpretation of others' behavior, thus transforming insignificant and irrelevant events into ones that appear to have personal relevance for the self. Self-focus not only relates directly to paranoid ideas of reference, it has important implications for other critical aspects of paranoid thought. b. Personalism and Intent Unfortunate things happen to everyone, and usually they are dismissed as random or chance events. But paranoids rarely accept the idea that bad things just happen; instead they are likely to believe that it is someone else's doing. Why? Because events that are taken personally or are seen as uniquely targeted toward the self, are more likely to be understood in terms of others' personal characteristics or intentions. For the paranoid, the negative event itself is evidence for others' malevolent intentions toward them. Eventually, the accumulation of such events constitutes evidence for a fundamentally irrational view of the world as a hostile and threatening place. Once the assumption of ubiquitous danger is accepted, the other manifestations of paranoia become comprehensible: suspicion and guardedness; selective attention and memory for signs of trickery or

Paranoia

exploitation; misinterpretation of apparently harmless events as malevolent; and blaming others for all of one's difficulties. Moreover, when negative events are seen not as fortuitous occurrences, but as personally intended by others, hostilities become intensified and enemies are found everywhere. c. Egocentricity One of the critical elements of paranoid thinking is the utter inability to understand the motivations and perspectives of others. Not only are paranoids more likely to misinterpret the other's behavior, they are less likely to correct that misinterpretation by altering their point of view. The narrowness and rigidity of paranoid thoughtmthe failure to examine events critically or in a broader context, the ability to fit anything into one's belief system, the unwillingness to consider ever changing one's mindmis, in large part, the result of being locked into one's own perspective. Although social isolation may account, in part, for this deficit in role taking, self-focused attention may also contribute to the self-centeredness of paranoids. Attention directed toward the self interferes with the ability to take the role of another or appreciate the existence of alternative perspectives. As a result, paranoids are likely to assume that others share their own view of events, and fail to appreciate the way in which their own actions are viewed by others. Thus, in a typical encounter, they are unlikely to consider how their own behavior provokes the hostility of others, but instead are likely to see themselves as the innocent victim of the other's hostility. Self-focus may also play a role in the egocentric tendency of paranoids to project their own characteristics onto others. IV. TREATMENT OF PARANOIA

Treatment of paranoia is extraordinarily difficult for a number of reasons. First, little is known about the causes that presumably are to be treated. Second, it is difficult for the paranoid to recognize a problem when he is locked into his own perspective and is reluctant to accept another's viewpoint. Finally, it is nearly impossible for therapists to penetrate the barrier of suspiciousness. For all these reasons, paranoids are generally unlikely and unwilling to enter therapy; and once in therapy, their wariness often leads them to sabotage treatment, or break it off prematurely. Paranoids also generally refuse to take responsibility for their treatment, because the only problems they see

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are those created by the people intent upon harming them. In addition, the disclosure of personal information or other aspects of therapy may represent a loss of control, especially to male paranoids. Mistrust obviously serves to undermine the therapeutic relationship. Any expression of friendliness or concern by the therapist is likely to arouse suspicion or be taken as confirmation that others are trying to humiliate them. Any questions or suggestions are likely to be seen as criticisms or attacks. Even if therapy improves other aspects of the paranoid's functioning, their delusional system is so strenuously defended, and so easily confirmed by "clues" detected in the therapeutic situation, that it often remains intact, yielding a highly unfavorable prognosis for complete recovery. Because of the paranoid patient's guardedness and insistence on their own correctness, an effective therapeutic approach usually focuses on trust building rather than direct confrontation of the delusional beliefs. Perhaps the most powerful strategy is to establish rapport by forming a "therapeutic alliance" in which the therapist recognizes whatever kernel of trust exists in a paranoid system, and acknowledges the delusional beliefs as powerful, convincing, and understandable. The therapist can then try to identify the ways in which these beliefs may interfere with the patient's goals or create frustration for others as well as for the patient. The patient's paranoid reactions have usually driven others away or incited them to counterattack, heightening the cycle of suspicion and hostility. The therapist can sometimes bring about change by providing a different, empathic response that serves as a model of nonparanoid behavior. The task is then to help the paranoid become more competent at discriminating real threats from perceived ones, and the final step is the development of more adaptive responses to real or even ambiguous threats. Behavioral theory assumes that paranoids have learned to be hypersensitive to the judgments of others and, as a result, they behave in ways that invite just the sort of reaction they anticipate and fear. As others begin to avoid them, they become socially isolated and develop increasingly elaborate suspicions that maintain the isolation. Behavior therapy tries to break the cycle by first using relaxation and anxiety management to teach the patient to be less sensitive to criticism, and then improving social skills by training the patient to act in ways that will not invite attack or avoidance. The patient can also be given help with recognition and avoidance of situations that produce or increase

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delusions. Paranoid thinking can in some cases be altered by aversive conditioning or the removal of factors that reinforce maladaptive behavior. This article has been reprinted from the Encyclopedia of Human Behavior, Volume 3.

BIBLIOGRAPHY Akhtar, S. (1990). Paranoid personality disorder: A synthesis of developmental, dynamic, and descriptive features. Am. J. Psychother. 44, 5-25. Bentall, R. P., Kaney, S., & Dewey, M. E. (1991 ). Paranoia and social reasoning: An attribution theory analysis. Br. J. Clin. Psychol. 30, 13-23.

Cameron, N. (1943). The development of paranoic thinking. Psychol. Rev. 50, 219-233. Fenigstein, A., & Vanable, P. A. (1992). Paranoia and selfconsciousness. J. Pers. Soc. Psychol. 62, 129-138. Kaney, S., & Bentall, R. P. (1989). Persecutory delusions and attributional style. Br. J. Med. Psychol. 62, 191-198. Magaro, P. A. (1980). "Cognition in Schizophrenia and Paranoia: The Interpretation of Cognitive Processes." Erlbaum, Hillsdale,

N3. Maher, B. A. (1988). Anomalous experience and delusional thinking: The logic of explanations. In "Delusional Beliefs" (T. F. Oltmanns and B. A. Maher, Eds.), Wiley, New York. Shapiro, D. (1965). "Neurotic Styles." Basic Books, New York. Williams, J. G. (1988). Cognitive intervention for a paranoid personality disorder. Psychotherapy 25,570-575. Zimbardo, P. G., Andersen, S. M., & Kabat, L. G. (1981). Induced hearing deficit generates experimental paranoia. Science 212, 1529-1531.

J Personality Disorders Robert G. Meyer University at Louisville

I. Personality Types and Disorders II. Treatment Relationships and the Personality Disorders III. Summary

tern of behavior, or lack of behavior, that is troublesome to others or whose pleasure sources are socially defined as either harmful or illegal.

I. PERSONALITY TYPES AND DISORDERS

Paranoid Pseudocommunity The conspiracy network of persons a paranoid perceives as against him or her. Personality Disorder Chronic disruptive adjustment patterns, found as a formal diagnosis on Axis II of the DSM system. Personality Type Patterns of behavior found in normals that operate as a predisposition to a personality disorder. Underlying Beliefs The cognitive beliefs that help to generate, and maintain, a personality disorder.

The various personality disorders are generated because they are effective, at least in the short run, in coping with that person's individual environment. Of course, the more distorted or disturbed that environment is, the more likely it is that a distorted coping pattern will emerge and become reinforced. Within this perspective, a personality type (a behavior pattern seen as within the normal range of adjustment) is a way-station on the developmental road toward a fullblown personality disorder. Table I describes common personality types (which we all manifest to some degree), along with the personality disorder they are most likely to develop, if they are exaggerated and crystallized. The DSM-IV personality disorders have traditionally been grouped into three clusters in the DSM's. The first includes the paranoid, schizoid, and schizotypal personality disorders, as these are denoted by peculiar or eccentric behavior. The second cluster focuses on dramatic and emotionally labile behavior: It includes the histrionic, narcissistic, antisocial, and borderline personality disorders. The last cluster, which emphasizes chronic fearfulness and/or avoidance behaviors, includes the avoidant, dependent, obsessive-compulsive, and passive-aggressive personality disorders.

PERSONALITY DISORDERS are chronic, cognitivebehavioral patterns, generated from an early age, that the individual has developed in order to cope with his or her particular problems of living. These disorders are not so clearly bizarre as the psychoses, nor do they include the clear anxiety patterns of the neuroses. However, they are severely maladaptive, because (1) the psychopathology is pervasive and thoroughly integrated into the personality, (2) the patterns are chronic and often recognizable by the time of adolescence or earlier, and (3) such persons usually avoid treatment and are difficult to treat if for some reason they do enter treatment. Thus, a personality disorder describes a pat311

Copyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

Table I

Personality Types and Correlated Traits and Disorders Personality Types

Correlates Typical behaviors Interpersonal patterns Thinking styles Mood-affect expression View of self Probable personality disorders

Inhibited

Introverted

Organized, formal Polite

Watchful, preoccupied Shy

Passive, quiet Withdrawn

Energetic, engaging Provocative

Divergent

Respectful

Repressed

Vague

Distracted

Pessimistic, hurt Misunderstood Passiveaggressive, borderline avoidant

Restrained, content Reliable Compulsive, paranoid, passiveaggressive

Uneasy, wary

Bland, coolness Placid Schizoid, schizotypal, compulsive, avoidant

Intense, frenetic Interesting Borderline schizotypal, histrionic, narcissistic

Sensitive

Controlling

Aggressive

Confident

Sociable

Cooperative

Manipulative demanding Authoritarian

Bold, initiating Intimidating

Poised, distant Unempathic

Animated, engaging Demonstrative

Docile, submissive Compliant

Erratic, responsive Unpredictable

Calculating

Dogmatic

Imaginative

Superficial

Open

Disappointment resentment Unappreciated Passiveaggressive, sadistic, paranoid

Anger, distrust Assertive Antisocial, sadistic paranoid

Calm, unconcerned Self-assured Narcissistic, paranoid, antisocial

Dramatic, labile Charming Histrionic, borderline narcissistic

Tender, fearful Weak Dependent, compulsive, avoidant

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Source: Adapted in part from T. Millon and G. Everly, 1985, Personality and Its Disorders, Wiley, New York.

Respectful

Lonely Avoidant, schizotypal, selfdefeating

Emotional

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Personality Disorders

The following is a discussion of each individual personality disorder, from the perspective of both behavioral patterns and the more recently articulated cognitive patterns.

A. Paranoid Personality Disorder The paranoid personality disorder can be thought of as anchoring the other end of the continuum of paranoid disorders from the most disturbed and fragmented pattern, paranoid schizophrenia. However, since there is neither thought disorder nor even a well-formed delusional system in the paranoid personality disorder, it is not listed under the DSM paranoid disorders and is not a psychotic condition. Like the other personality disorders, it is a chronic, pervasive, and inflexible pattern of behavior that typically has been in evolution since childhood and is already recognizable in adolescence. Modeling of parental or other significant others is possibly even more important in this disorder than in the psychotic paranoid conditions. [See PARANOIA.]

I. Behavioral Patterns Paranoid personalities manifest hyperalertness toward the environment and have a chronic mistrust of most people. They see themselves as morally correct, yet vulnerable and envied, and see others as far less than perfect. As a result, their information base is continuously distorted and their affect is constricted. Consequently, they find it difficult to adapt adequately to new situations or relationships, which is paradoxical because of their hyperalertness to their environment. Paradoxically, they will frequently be correct in assuming that other people are against them. Yet the paranoia is usually a disabling overreaction to a low initial level of scrutiny by others. Unless these individuals have almost absolute trust in another person, they cannot develop intimacy and are continually seeking various ways to be selfsufficient. They avoid the emotional complexities of working out a meaningful relationship and tend to be litigious. For example, they may write negative letters to public figures or bring lawsuits on minimal grounds. It is rare for them to come into therapy without significant coercion from others. The disorder is more common in men. Both Nero and Robespierre displayed characteristics of the paranoid personality pattern. As with other individuals in this classification, these important historical figures were suspicious and oversensitive about

the behavior and intentions of other people. Each was very manipulative in his relationships so that the other person could not gain the advantage. Nero was a Roman emperor during the first century, and Robespierre was a leader of the French Revolution; each man had considerable power over large numbers of people. Unlike most paranoid personalities, therefore, their paranoid reactions had a significant impact on a great many lives; and their delusions or misperceptions may have caused them to unjustifiably imprison or execute many innocent people. Although most paranoid personalities are not dangerous or physically injurious, they are at best perceived as a nuisance, e.g., through perennial complaints and lawsuits against other persons. In order to relate to, or even treat the paranoid personality, it is essential to gain their trust through empathy, but not through participation in the disorder patterns. It is especially necessary to empathize with and articulate the consequences of such an individual's behavior, such as the sense of being isolated and not understood or the interpersonal rejection that appears unfair to the paranoid. The underlying beliefs that paranoids often struggle with are (a) I am unique and others are jealous; (b)others will exploit my mistakes; (c) it always pays to be wary, accusatory, and adversarial (some paranoids do make good trial lawyers); (d) people who are trusting or content are fools, i.e., I can't be that way; (e) negative events are generated purposefully by others. The concept of the paranoid pseudocommunity holds that the paranoid is unable to communicate freely with other persons and has a pattern of finding fault with others as a result of inadequate social development. This inability creates a problem when the paranoid is under stress, because he cannot corroborate his perceptions with those of other persons or cannot assume the perspectives of other individuals. Relying on his own devices, he continues in his misperceptions and reconstructs reality to make it consistent with them. The culmination of this behavior is the paranoid's conception of himself as the center of a community of persons who are in a conspiracy against him. Because the situation does not exist as the paranoid perceives it, he is said to be living in a pseudocommunity.

B. Schizoid Personality Disorder The essential feature of this disorder is impairment in the ability to form adequate social relationships. As a

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Personality Disorders

result, schizoid personalities are shy and socially withdrawn or, as novelist Joan Didion states in The White Album (p. 121), "only marginally engaged in the dailiness of life." They have difficulty expressing hostility and have withdrawn from most social contacts. But, unlike agoraphobia, the behavior is ego-syntonic, i.e., the individual is at least minimally comfortable with the behavior.

I. Behavioral Patterns In contrast to the personalities who relate to the environment, the schizoid personality is particularly characterized by distancing behaviors and alienation. The schizoid individual reacts to disturbing experiences and conflicts by apparent detachment from the environment rather than by manifesting normal coping responses. The schizoid personality is described in DSM as shy, oversensitive, seclusive, often eccentric, and likely to avoid close or especially competitive relationships. Walter Mitty is the schizoid hero of James Thurber's novel and the movie The Secret Life of Walter Mitty. Mitty is essentially detached from his environment and is much more absorbed in his elaborate, heroic fantasies. Given the situation of an idle moment or a disturbing experience, he plunges into his imaginings, rather than utilizing normal coping mechanisms. Most schizoid persons are considered to be cold and withdrawn because they do not seem to respond to their environment. Walter Mitty, however, seems more warm and likeable, although no more reachable, than other schizoid personalities.

C. Schizotypal Personality Disorder The reader is referred to the previous category, the schizoid personality disorder, since many of the features of that disorder are found here. The essential difference is that in addition to the disturbances in social functioning, the schizotypal personality manifests peculiarities in the communication process. Schizotypal individuals are much more likely than the schizoid to show dysphoria and anxiety, and because of the odd thinking patterns, they are more likely to have developed eccentric belief systems and become involved in fringe religious groups. The schizotypal personality is also more likely to be emotionally labile, overtly suspicious, and hostile of others than is the schizoid. Many schizotypal individuals also appear to meet the criteria for the borderline personality disorder. Any therapist's attention must be directed not only toward the interpersonal withdrawal processes, but also to the emergent disturbances in affect and thinking that are common.

D. Histrionic Personality Disorder These persons seek attention and are overreactive, with the response being expressed more dramatically and intensely than is appropriatemhence, the term "histrionic." This category has traditionally been labeled the "hysterical personality." However, "hysteric" wrongly suggests a disorder that parallels the causes and symptoms of what has been traditionally labeled "hysterical neurosis."

2. Cognitive Patterns

Like the person with an avoidant personality disorder (discussed later in this article), the schizoid has inadequate interpersonal relations. But unlike one with an avoidant personality disorder, the schizoid does not care, so therapy is quite difficult. Characteristic underlying cognitive assumptions are (a) any disruption of my emotional routine (however minimal the emotions are) is scary and messy-in that sense they are analogous to the obsessivecompulsive's fear of disruption of external routines; (b) I can survive alone (maybe not optimally, but at least predictably), and need space to do that; (c) it's necessary to be free and independent--other people are like Brer Rabbit's "Tar Baby"; if you relate to them, you get stuck to them.

I. Behavioral Patterns

Histrionic personalities may elicit new relationships with relative ease, as they appear to be empathic and socially able. However, they turn out to be temperamentally and emotionally insensitive and have little depth of insight into their own responsibilities in a relationship. Even though they may be flirtatious and seductive sexually, there is little mature response or true sensuality. If one accepts the apparent sexual overture in the behavior, the histrionic individual may act as if insulted or even attacked. There has been a continuing controversy as to whether this disorder occurs with any frequency in males. But, it is clear that this disorder is found in males, but because the symptoms are a caricature of

Personality Disorders

the traditional role expectations for women, it is more common in women. An excellent behavioral example of a histrionic personality pattern is seen in the character of Martha in Albee's play Who's Afraid of Virginia Woolf? The stormy relationship between Martha and her husband, George, alternating between wild physical and verbal abuse and tender affection, is not fiction created for the stage, as many couples live in what can be termed a "conflict-habituated" marriage. In such a marriage, there is private though sometimes unverbalized acknowledgment by both husband and wife as a rule that incompatibility is pervasive, that conflict is ever-potential, that an atmosphere of tension permeates the relationshipwnevertheless, the relationship will continue. It seems likely that at least one of the partners in this kind of marital situation would be labeled as a hysterical personality, and often, as is the case with the character George in Who's Afraid of Virginia Woolf?, the other partner is a passive-aggressive personality. Such people do not often seek treatment. Rather, they maintain the core around which the pretense and the conflict revolve, much as Martha and George maintained her fantasied pregnancy as well as their mythical child.

2. Cognitive Patterns Histrionics quickly avoid blame for any difficulties of interpersonal relationship and, in that sense, show a degree of the projection that is characteristic of paranoid disorders. Common underlying beliefs in histrionics are (a) being responsible or attending to details means the loss of "zest for life"; (b) rejection is disastrous; (c) people won't love me for what I do but what I pretend to be, or what I present to entertain/entice them; (d) being "special" means never having to say "I'm sorry" (or at least I don't have to feel it or mean it).

E. Narcissistic Personality Disorder This category, which was new in the DSM-III-R, centers on individuals who are to a degree products of our modern social-value systems. No doubt, such people have always existed, but it appears that this pattern has become more common recently. It is not a surprising development when there are advertisements about "The Arrogance of Excellence" and self-help seminars unequivocally urging people to live out the axiom "I'm

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number one" (with little evidence that there is much room for a number two or three close behind). [See NARCISSISTIC PERSONALITYDISORDER.] I. Behavioral P a t t e r n s

Narcissistic personalities are "flattery-operated"; more specifically, they manifest an unrealistic sense of selfimportance, exhibitionistic attention seeking, inability to take criticism, interpersonal manipulation, and lack of empathy resulting in substantial problems in interpersonal relationships. Narcissistic personalities are similar to antisocial personalities, except that they are not so aggressive or hostile and their value systems are more asocial and hedonic than antisocial. The prognosis for major change is moderate at best. In 1984, Otto Kernberg introduced the subdiagnosis of malignant narcissist. It was first applied to people like Adolf Hitler and Joseph Stalin, and more recently it has been suggested as fitting Saddam Hussein. The four characteristics of this pattern are (1) a strong suspiciousness, occasionally to the point of paranoia; (2) an extremely inflated sense of self, often grandiose; (3) sadistic cruelty (which in some individuals is turned inward as self-mutilation--"for a higher goal"); and (4) an utter lack of remorse. There are numerous productive narcissists in society. One night while we were on a fishing trip, my friend and I had dinner at a fine Chinese restaurant. The restaurant was named after the owner, an aging but still attractive Chinese woman. The walls were totally covered with formal photographs of her, there was a bulletin board filled with candid shots from throughout her life, the restaurant's cards had a photo of her as a young woman, and you could even purchase postcards with various pictures from her life. A short conversation with her quickly revealed her narcissism, but it should have been evident to any customer. She was not especially offensive (it was a short conversation); however, by narcissistically including her restaurant as a part of her "self," she had turned it into an excellent operation that she groomed as carefully as her hair. Certain media-created stars, "personalities," and politicians are also examples of extreme but at least occasionally productive narcissism.

2. Cognitive Patterns Underlying beliefs common to this disorder are (a) I am special, unique, elite; (b) I like to challenge or com-

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Personality Disorders

pete with others, but because of both "a" and the fact it is psychologically necessary for me to prevail, I may play by other rules (usually known only to me); (c) any defects I have come from my bad parents and/or background; (d) recognition, admiration, and respect are necessary and others exist to provide it, and indeed, promote it; (e) sharing, serving others, or selfless behaviors are signs of weakness and signal disintegration of my self.

F. Antisocial Personality Disorder The antisocial personality is an interesting category that deserves special consideration in light of its evolution as a concept. In the early 1800s Prichard suggested the term "moral insanity" or "moral imbecility" to designate persons who did not fit the psychiatric categories of that time. The first reference to the classic notation "psychopathic" occurred in 1891 with the introduction of the label "psychopathic inferiority." This classification was an attempt to place the disorder with other disturbances, such as retardation, that were believed to be congenital. Caesare Lombroso's classic conception of the criminal as showing consistent and significantly different facial characteristics was also a popular view. The Zeitgeist of that period therefore maintained that the psychopathic disorder was the result of genetic or hormonal defects rather than learning or environmental factors. Eventually, the term "psychopathic personality" was used, but in such a way that there was much confusion about the concept. In time the term "sociopathic personality pattern" was also adopted by the American Psychiatric Association for DSM-I (to emphasize, now apparently inaccurately, that this pattern is largely a result of social conditioning) and became the broad category under which several problematic social behaviors, such as sexual deviations, alcoholism, and drug addiction, were listed. Hervey Cleckley, a pioneer in this area, has described the antisocial personality (more specifically, psychopathy) as having a "mask of sanity," or the absence of the usual indicators of insanity. These are persons who discard meaningful relationships, goals, and success for reasons that others cannot understand. Cleckley's list of the following 16 indicators of psychopathy has been influential through the ensuing years:

1. Superficial charm and good "intelligence" 2. Absence of delusions and other signs of irrational "thinking" 3. Absence of "nervousness" or psychoneurotic manifestations 4. Unreliability 5. Untruthfulness and insincerity 6. Lack of remorse or shame 7. Inadequately motivated antisocial behavior 8. Poor judgment and failure to learn by experience 9. Pathologic egocentricity and incapacity for love 10. General poverty in major affective reactions 11. Specific loss of insight 12. Unresponsiveness in general interpersonal relations 13. Fantastic and uninviting behavior, with drink and sometimes without 14. Suicide rarely carried out 15. Sex life impersonal, trivial, and poorly integrated 16. Failure to follow any life plan There is good evidence that the category of antisocial personality can be further subdivided, e.g., into categories of primary psychopath and secondary psychopath. [See ANTISOCIALPERSONALITYDISORDER.]

G. Borderline Personality Disorder At first glance, this disorder may seem to overlap with the schizotypal personality disorder, as both imply an easy transition into a schizophrenic adjustment. However, individuals with borderline personality disorder are neither as consistently withdrawn socially nor as bizarre in symptomatology as are schizotypals, and the borderline diagnosis covaries most commonly in inpatients with a diagnosis of histrionic personality disorder. [See BORDERLINEPERSONALITYDISORDER.]

I. Behavioral Patterns Though the DSM does not specifically mention it, this category seems to be a resurrection of an old term at one time much favored by clinicians: "emotionally unstable personality." Persons in the borderline personality disorder category do show significant emotional instability, are impulsive and unpredictable in behavior, and are irritable and anxious. They also often show "soft" neurological signs, and avoid being alone or experiencing the psychological emptiness or boredom to

Personality Disorders

which they are prone. There is some evidence that as these individuals improve, they show more predictable behavior patterns, yet this is combined with increasingly evident narcissism. Glenn Close's character in the movie "Fatal Attraction" is a good example of this disorder. 2. Cognitive Patterns Borderlines are intense and labile emotionally and cognitively, and are draining to significant others (and therapists). Yet, paradoxically, they need to understand that they fear facing their own intense negative emotions over time, and so find it hard to grieve the many relationship losses they generate. They maintain a facade of competence and independence, yet desperately want various types of help, and then react negatively when it is not forthcoming. The following beliefs are common: (a) I'm afraid I'll be alone forever, as no one who really gets to know me will want to love me; (b) If I ignore my own needs, I can entrap some people into relationships, but, since I can't control my feelings, and I need the relationships, I'll be very unhappy; (c) though I need people, they will eventually hurt or reject me, so I must protect myself; (d) I deserve any bad things that happen to me; (e) my misery (and/or "badness") is how people recognize me as a unique self.

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In many ways, this disorder is close to the anxiety disorders, since there is a degree of anxiety and distress, and low self-esteem is common. However, the behaviors that produce the distress are relatively egosyntonic. Their depression and anxiety are more related to the perceived rejection and criticism of others. This common disorder is seen more often in women. Any disorder in childhood that focuses on shyness predisposes one to the avoidant personality disorder. 2. Cognitive Patterns Avoidant personalities are extremely sensitive to rejection and seem to need an advance guarantee that a relationship will work o u t ~ a relationship with an attached warranty. Thus, they resonate negatively to the refrain from W. B. Yeats: "Only God, my dear / Can love you for yourself alone / and not for your yellow hair." Other cognitions common to the avoidant personality include (a) if people really got to know me, they would see how inadequate (or odd) I really am, and they would reject me; (b) I am unable to cope with unpleasant people or situations; (c) not thinking about a problem or unpleasant situation or not trying to cope with it may allow it to go away; (d) you'll never leave me because I'll make sure I leave you first; (e) nothing ventured, nothing failed.

H. Avoidant Personality Disorder

I. Dependent Personality Disorder

These individuals are shy and inhibited interpersonally, yet at the same time desire to have interpersonal relationships, which distinguishes them from those with the schizotypal or schizoid personality disorders. They also do not show the degree of irritability and emotional instability seen in the borderline personality disorder. This is a common secondary diagnosis in inpatient populations.

In one way, dependent personality disorders can be seen as successful avoidant personality disorders. They have achieved a style that elicits the desired relationships, though at the cost of any consistent expression of their own personality. They show elements of agoraphobia, not crystallized, and they lack any real selfconfidence. [See DEPENDENTPERSONALITY.]

I. Behavioral Patterns A major feature of this chronic disorder is an unwillingness to tolerate risks in deepening interpersonal relationships. These persons are extremely sensitive to rejection and seem to need a guarantee ahead of time that a relationship will work out. Naturally, such guarantees are seldom available in healthy relationships. Thus, the friends they manage to make often show a degree of instability or are quite passive.

I. Behavioral Patterns People with the dependent personality disorder have a pervasive need to cling to stronger personalities who are allowed to make a wide range of decisions for them. They are naive and show little initiative. There is some suspiciousness of possible rejection, but not to the degree found in the avoidant personality disorder. Since this is an exaggeration of the traditional feminine role, it is not surprising that it is far more common in women. If the individual is not in a dependent rela-

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tionship, anxiety and upset are common. Even if enmeshed in a dependent relationship, there is still residual anxiety over the possibility of being abandoned. Dependent personalities may be getting many rewards for their behavior, in the midst of the negatives that may have led them into therapy, e.g., abusive relationships. Very often significant others only want very circumscribed changes, so once changes begin, they will likely subvert things. At the same time, the eventual termination of any therapy is always threatening with these clients.

2. Cognitive Patterns Underlying cognitive systems that are often included are (a) I am perpetually at risk of being alone in a cold and dangerous world; (b) I'm not able to cope with and/or enjoy life without a supportive other; (c) a loss of self is a fair price to pay in order to obtain a relationship with a supportive other, even if they periodically abuse me in some fashion; (d) I need constant access to this other, with as much intimacy as I can elicit, so I'll be as subservient and inoffensive as I need to be.

J. Obsessive-Compulsive Personality Disorder This disorder is occasionally confused with the obsessive-compulsive disorder (which is an anxiety disorder), but there are significant differences between the two syndromes. First, the obsessive-compulsive personality seldom becomes obsessed about issues. Second, for the obsessive-compulsive personality the term compulsive refers to a lifestyle in which compulsive features are pervasive and chronic, but it does not refer to a specific behavior such as persistent hand-washing. Third, the person with an obsessivecompulsive personality disorder is not upset, anxious, or distressed about his or her lifestyle, whereas anxiety is generic and often obvious at times in the functioning of the obsessive-compulsive disorder. [See OBSESSIVE-COMPULSIVE DISORDER.]

I. Behavioral Patterns According to Sigmund Freud, their essential characteristics are that they are "exceptionally orderly, parsimonious and obstinate." Obsessive-compulsive personalities are preoccupied with rules and duties, are unable to express warmth and caring except in lim-

ited situations, are highly oriented toward a lifestyle marked by productivity and efficiency, are temperamentally and emotionally insensitive, and are generally distant from other individuals. They are inclined to be excessively moralistic, litigious, and hyperalert to criticism and perceived slights from others. They can be described as workaholics without warmth. The extent to which the ritualistic and conforming behavior is generalized throughout the person's life and, more importantly, the degree to which it is functional must be taken into consideration before a diagnosis is made. For example, a pilot develops rituals for determining that his plane is safe before takeoff. If a part of the ritual is omitted by a copilot, the pilot may experience considerable distress and may actually risk alienation by insisting on the performance of the ritual. The pilot's insistence on carrying out a ritualistic check of the instruments makes him appear obsessive, but it also keeps him alive. Captain Queeg, in the novel and movie The Caine Mutiny, may be regarded as an obsessive-compulsive personality. Queeg continually insisted on order, cleanliness, and obedience; disruption of routine panicked him. However, because Captain Queeg's symptom pattern also included paranoid features, he does not completely fit the obsessive-compulsive category.

2. Cognitive Patterns It is true that a degree of compulsivity is effective, particularly in our society. It becomes a problem when it overwhelms the rest of the personality. Paradoxically, obsessive-compulsives are often indecisive in their thinking and poor planners of their time, a result of their narrow focus and concern with precision, even when precision may be irrelevant. Typical underlying beliefs such as (a) to err, or worse, to fail, is anxiety-provoking, will allow others to criticize me, and makes me feel less than a whole person; (b) to lose control is anxiety-provoking; (c) my obsessiveness and/or compulsivity are powerful enough to avoid errors, failure, or finding myself with nothing to do, yet; (d) as regards meaningful decisions, rather than "Better to have tried and failed than to never have tried at all," my motto is "Better to have not tried at all, than to have tried and failed"; (e) details are important, i.e., if you can see trees, no need to look for the forest; (f) I am responsible for myself and others; (g) I hate others when they don't follow

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"the rules," i.e., my rules, and especially if they get by with it.

K. Passive-Aggressive Personality Disorder Most parents have had the experience of a child pushing them to the limit of their control and then backing off. Like that child, the passive-aggressive becomes acutely sensitive to such limits and is consistently able to go so far but no further. When this pattern becomes an integral part of a social and vocational lifestyle, a passive-aggressive personality disorder exists. Although these patterns are commonly modeled and learned in childhood, such a family usually reaches a state of mutual d6tente. The pattern then causes severe problems when it is transferred into any new intimate, consistent contact relationship, such as marriage.

I. Behavioral Patterns The passive-aggressive pattern is characterized by pouting, procrastination, stubbornness, or intentional inefficiency that is designed to frustrate other people. The essential condition in this category is that there is a social context in which something has been requested from the individual exhibiting passive-aggressive behavior. The individual is apparently capable of complying with what is requested but does nothing. This inaction results in severe frustration for the observer rather than for the passive-aggressive individual. Typically, there is no overt opposition from the individual such as a blatant refusal to comply. Rather, there is an apparently cooperative attitude but no resulting action. For example, there may be stubborn insistence on procedural detail that effectively renders any actual achievement impossible. The classic example of this behavior pattern is seen in the character of Schweik in The Good Soldier Schweik (Hasek, 1930), the model for the cartoon character Beetle Bailey, who managed to infuriate his military commanders by carrying out each order to the ultimate detail, thereby revealing its absurdity. The passive-aggressive personality disorder often takes the standards and the belief system of significant others and turns them around to immobilize the others effectively. The strategy (which is not thought to be a conscious behavior) is to present the "enemy" (often a person depended on) with a choice that forces one ei-

ther to capitulate or to violate an individual belief system. That person is thus immobilized, with no adequate reason to justify retaliation.

2. Cognitive Patterns The automatic thought "I don't have to get there on time--nobody can tell me what to do" is common to passive-aggressives. Thus, they are inclined to be late for payments, sessions, etc., so clear contracts with detailed consequences are necessary. Passive-aggressives are also often late within a much longer perspective~the developmental tasks of life, e.g., establishing a career, or getting married or having children. This stems not only from their sense "You (in this case, society) can't make me do i t . . . " but also from an inability to tie responsibilities to time, and the fact that responsibility per se is often aversive because it is interpreted as a "society should." Analogously, there is often a passive refusal to accept the discipline and sacrifice needed to develop either vocational or interpersonal "careers." Attaining the required credentials and "putting in your time" in order to attain the payoff of an accrual process is seen as too restricting and demanding. In addition to the beliefs embedded in the prior points, beliefs common in the passive-aggressive are (a) I know I can really be self-sufficient, but I apparently do need others, at least now, and I resent that; (b) any control by others is aversive; (c) while I apparently have to accept some subjugation of my desires and/or loss of control, they'll pay a price for making me do so; (d) if the conditions were right (and/or I really tried), I would be outstanding; (e) following rules, expectations, deadlines, etc., makes me less of a whole person; (f) no one, including me, really deserves to have authority.

L. Sadistic Personality Disorder The term "sadistic personality disorder" does not officially appear in the DSM's, though it was made available in an Appendix of the DSM-III-R as an optional diagnosis for clinicians to add when they find it helpful. In any case, the concept has a long history. Kernberg (1984) terms the sadistic personality the "malignant narcissistic" and places it between the antisocial and the narcissistic personalities on this continuum. The personality might also be thought of

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as an antisocial pattern, though with better socialization and a more prominent quality of revenge. See the prior description of those disorders for the relevant cognitive patterns, as they are an amalgam of those two, combined with the cognitive schemata "Not only does pain in others not generate empathic emotions, it may result in pleasure or an enhanced sense of self for me." The DSM criteria were (1) uses violence or cruelty to establish a dominance relationship; (2) demeans or humiliates people in the presence of others; (3) takes pleasure in physical or psychological suffering of other humans or animals; (4) has, with unusual harshness, disciplined someone under his or her control; (5) has lied with the goal of inflicting pain or harm; (6) uses intimidation, or even terror, to get others to do what he or she wants; (7) restricts the autonomy of someone with whom he or she has a close relationship; or (8) is fascinated by weapons, martial arts, injury, torture, or violence in general. The dominant trend is a love of cruelty and an absence of remorse. There is a noteworthy distinction between sadism, which is a paraphilia and the sadistic personality disorder. While sadistic sexual patterns are common in the sadistic personality disorder, it is not a necessary part of the pattern. In essence, the sadistic personality disorder is marked by a very assertive lifestyle based on power motives, commonly accompanied by gender dominance, the inflicting of pain for pleasure, and extreme aggression with or without sexual motivation. Yet, the sadistic behavior is well rationalized, and the individual may even present a very self-righteous air.

II. TREATMENT RELATIONSHIPS AND THE PERSONALITY DISORDERS Modern theorists point out that treating the personality disorders, particularly those with antisocial, narcissistic, or borderline components, requires a rethinking of what are often termed transference issues. They note that such individuals often elicit an "objective counter-transference." This is usually a response of anger and frustration, even hate, but in some cases can be a type of protective affection. The important point is to recognize that these emotional reactions of the therapist are reasonable, and based on good data. This is in contrast to the traditional conception of the therapist's reactions to neurot-

ics. In the latter instance, such feelings would be seen as indicative of emotional blocks in the therapist, which would signal a need for more analysis for the therapist and/or a transfer of the patient to another therapist. However, in the "objective counter-transference" to the personality disordered client, the therapist needs to (a) recognize and "metabolize" such feelings, i.e., not act out toward the client in response to such feelings; (b) gradually let the client know that such reactions are occurring; (c) relate them to the eliciting behaviors; and (d) thus let the client know they can and are being controlled. Therefore, rather than allowing the client to project "onto" the therapist, as with a neurotic type in more classical analysis, this type of client is allowed to project "into" the therapist. Most such clients seem to use this as a means of communication, as well as control, almost as if it is the only way another can ever know the level of pain they went through.

III. SUMMARY Personality or character disorders, unlike other mental disorders, are manifested primarily in a social context. They are more like "us," and we would rather not think so. These disorders trouble society, over time, more than they trouble the individual. Rarely do such individuals experience the crippling anxiety that is characteristic of the neuroses, the loss of functioning due to thought disorder characteristic of the schizophrenic process, the incapacity of organic brain syndromes, or the consistently manifested extremes of mood found in the affective disorders. Instead, one finds an apparently intact organism, with little evident symptomatology, whom is unable to organize his or her behavior and relate interpersonally in an effective manner. These disorders present a life-long problem for the individual, the treater, and society as a whole. This article has been reprinted with updated references to DSMIV from the Encyclopedia of Human Behavior, Volume 3.

BIBLIOGRAPHY Beck, A., Freeman, A., et al. (1990). "Cognitive Therapy of Personality Disorders." Guilford, New York. Cleckley, H. (1982). "The Mask of Sanity," 5th ed. Mosby, St. Louis. Kernberg, O. (1984). "Severe Personality Disorders: Psychotherapeutic Strategies." Yale University Press, New Haven.

Personality Disorders .

Meyer, R. (1993). "The Clinician's Handbook," 3rd ed. Allyn and Bacon, Boston. Meyer, R. (1992). "Abnormal Behavior and the Criminal Justice System." Lexington Books, Lexington, MA. Millon, T. (1981). "Disorders of Personality. DSM-III Axis II." Wiley, New York.

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Oates, W. (1987). "Behind the Masks." Westminster, Philadelphia. Turkat, D. (1990). "The Personality Disorders." Pergamon, New York. Widiger, T., & Frances, A. (1985). The DSM-I]I personality disorders: Perspectives from psychology. Arch. Gem. Psych., 42, 615-623.

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Phobias George A. Clum

Greg A. R. Febbrar0

Virginia Polytechnic Institute and State University

Medical Universityof South Carolina

I. Specific Phobia II. Social Phobia III. Agoraphobia

general conduct of life. The current classification of phobias includes three types: specific phobia, social phobia, and agoraphobia. They tend to occur frequently, as approximately one in seven adults will experience a phobia at some point in their lives. While we think of the various types of phobias as separate entities, it is not uncommon for a given person to experience more than one type of phobia at the same time. Similarly, individuals who develop phobias are likely to experience other types of mental disorders, among them depression, and other anxiety disorders such as obsessive-compulsive disorder and generalized anxiety disorder. Phobic disorders, in addition to being relatively common, often have a profound effect on the lives of individuals who suffer with them. In this article, each of the three types of phobias will be examined. A definition of each type will be provided, followed by an examination of the associated features of the disorder, its typical course and prognosis. Several causal models of each phobia group will be evaluated, followed by a discussion of therapeutic approaches.

IV. Panic Disorder and Agoraphobia

Atypical Depression

Depression that is not related to a stressful event and does not meet criterion for a major depressive disorder. Cognitive Symptoms Specific thoughts or patterns of thoughts found to characterize certain mental disorders. Comorbidity Coexistence, in the same individual, of more than one diagnosable psychiatric disorder. Epidemiology The study of rates of an illness in different groups within a population. Etiology An approach to understanding the cause of a phenomenon. Obsessive-Compulsive Disorder A mental disorder characterized by the persistent intrusion of thoughts, images, or behaviors. Physiological Arousal Response of increased activation of the organism characterized by such things as increases in heart rate, respiration, and muscle tension. Prognosis The future course of a disorder.

I. SPECIFIC PHOBIA A. Definition

PHOBIA derives from the Greek word phobos, meaning "fear." Phobias are persistent, excessive fear responses to objects or situations that are for most people neutral or only mildly anxiety-arousing. Phobias typically involve fears of the commonplace situations involved in life and, if the feared situation is frequently encountered, can interfere greatly in the

The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, (DSM-IV, the primary source in the United States for defining the various mental disorders) defines specific phobias as irrational and persistent fears of certain objects or animals. Specific phobias have historically been known as "simple

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Copyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

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phobias," "monosymptomatic phobias," or "focal phobias." The phenomenon of specific phobias has been described for centuries. Hippocrates, for example, described a man displaying an irrational fear of bridges. Detailed discussions of phobic symptoms can be found in the writings of seventeenth- and eighteenth-century authors such as Descartes, Le Camus, and Sauvages. [See DSM-W.] DSM-IV identifies three central features of specific phobias: (1) fear is directed at a limited set of stimuli; (2) confrontation with these stimuli elicits fear and avoidance behavior; and (3) the fear is unreasonable and excessive to a degree that it interferes with daily life. In addition, the fear persists over an extended period of time. With the publication of DSM-IV, specific phobias were for the first time differentiated into four highly prevalent types: (1) animal type (e.g., spider phobia); (2) natural environment type (e.g., height phobia); (3) blood-injection-injury type (e.g., dental phobia); and (4) situational type (e.g., claustrophobia). In addition, DSM-IV introduces an "other type" that includes phobias of specific situations not covered above--choking phobia, for example. The validity of such distinctions is supported by data showing that these types tend to differ with respect to age of onset, familial aggregation, and physiological responses to the phobic stimulus.

B. Clinical Features I. Symptoms and Epidemiology When not confronting the feared object, individuals with specific phobias are not different from nonphobic individuals in their level of physiological arousal. When confronting the feared situation, however, phobic individuals reported a number of common anxiety-related somatic symptoms such as heart palpitations, trembling, and sweating. In addition, individuals with specific phobias demonstrate similar increases in indices of arousal upon exposure to cues associated with their phobia. Thus, a person with a fear of spiders might become fearful when looking at a picture of a spider or when entering a dusty place where spiders may be present. In addition to physiological arousal, phobic individuals also show increases in subjective level of fear and in their tendency to avoid the phobic object. However, this consistency is not always present as phobic individuals

may manifest increases in one or two of these domains and not the other(s). Blood-injection-injury phobics are characterized by a unique physiological response to their fear cues. These individuals exhibit an initial increase in heart rate and blood pressure, as do most other phobics, followed by a dramatic drop on these measures, often resulting in fainting. Not much is known about the cognitive symptoms in individuals with specific phobias due to an assumption that any thoughts individuals with specific phobias might have would be related to the feared object. Furthermore, cognitions have not been considered to be important in the etiology of specific phobias. This view~that cognitions are unimportant in the development of specific phobias--is changing. For example, 37% of individuals exposed to a phobic stimulus reported being equally or more concerned with their physical sensations than with the stimulus itself. In addition, many claustrophobics report thoughts of being trapped, suffocating, and losing control, thoughts characteristic of individuals who experience panic attacks. It was found in a recent national survey of mental disorders that 11.3% of the population will have a specific phobia in their lifetime. Situational and environmental phobias are the most common (13 % of the population), followed by animal phobias (8%), and blood-injection-injury phobias (3 %). Women are twice as likely as men to be diagnosed with a specific phobia. This is especially true for animal phobias and situational and environmental phobias, but less so for blood-injection-injury phobias.

2. Course/Prognosis and Comorbidity Issues Specific phobias develop at different points in the life cycle. Animal phobias develop earliest (average age around 7 years), followed by blood phobias (average age around 9 years), dental phobias (average age around 12 years), and claustrophobia (average age around 20 years). The differences in age of onset among the specific phobias suggest that different causal factors are at work in their development. The heterogeneity of the diagnostic group is further evidenced when one examines claustrophobia. Claustrophobia may well be descriptively and functionally a less constricting form of agoraphobia, a disorder described later. Support for a link between claustropho-

Phobias

bia and agoraphobia comes from (1) a similar age of onset with both developing around 20 years of age; (2) a similar mode of acquisition, with agoraphobia (81% of the time) and claustrophobia (69% of the time) developing after experiencing a stressful event; and (3)the co-occurrence in claustrophobia of uncued/ unexpected panic attacks, worry about becoming anxious and panicky, fear of bodily symptoms of arousal (e.g., "fear of fear"), and unpredictability of the fear response in claustrophobic situations, all of which are features of Panic Disorder with Agoraphobia. In contrast, other specific phobias have an earlier age at onset, are less likely to be acquired after experiencing a traumatic event, and are more consistently associated with fear of specific situations than of internal anxiety symptoms. The natural course of specific phobias is usually chronic and can be characterized by the persistence of mild rather than severe symptoms of anxiety over time. Only 16% of individuals with specific phobias have a complete remission of symptoms over a followup period of 7 years. While specific phobias appear to occur frequently in the general population, few sufferers seek treatment, even though this problem may seriously threaten their social or occupational functioning and in spite of the fact that treatment can be highly successful.

C. Etiology I. Genetic Factors The genetic hypothesis contends that a predisposition to develop specific phobias is inherited. Evidence indicates there is a consistent, modest contribution of genetic factors to the development of specific phobias. Furthermore, the genetic factors underlying specific fears appear to be of a general nature, such that what is inherited is a trait that predisposes to anxiety in general rather than inheritance of a specific fear. In some cases, the predisposition is expressed as a specific phobia; in other cases, the complaints may take the form of, for example, social phobia or agoraphobia. However, blood-injection-injury phobia may represent an exception to this pattern. Evidence suggests that in blood-injection-injury phobia, the genetic contribution is much stronger than in other phobias and that what is inherited is the specific vulnerability to develop this phobia.

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2. Biological Factors The preparedness hypothesis suggests specific phobias are an example of evolution-prepared learning. The concept of "preparedness" refers to the observation that anxiety responses are more easily learned to some stimuli than to others and that the ease of learning in any one instance varies from species to species. Most specific phobias involve stimuli that over the course of evolution might have been dangerous to man (e.g., snakes, heights) and are still reacted to as though intrinsically dangerous. Several human and animal studies have tested the preparedness hypothesis under laboratory conditions and found evidence to support it. In one such study, it was found that when conditioned responses to evolution-relevant cues are acquired, they continue to persist much longer than conditioned responses to evolution-neutral cues. A number of studies on monkeys lend further support to the preparedness hypothesis. In these studies, observer monkeys acquired an extremely persistent fear of snakes after they watched model monkeys reacting fearfully to snakes. In contrast, observer monkeys failed to acquire a fear of flowers after they had seen models exhibiting identical fear responses when presented with flowers. These various research studies provide support for the contention that fear responses to some stimuli are much easier to acquire if fear responses to these stimuli were adaptive to our ancestors' survival. The "Preparedness" hypothesis specifies that learning a phobic response will occur more easily for some stimuli than for others. An association with a negative unconditioned stimulus is still, however, required. An alternative, nonassociative hypothesis is that certain stimuli are hard-wired to produce fear, that is, they elicit a fear response without a previous negative experience with the stimulus. Darwin noted, after observing his 2-year-old's nonfearful response to caged animals, that fears are inherited effects of real dangers. When Darwin tried to control his fear response to the strike of a puff adder seated behind a solid glass barrier, he was unable to restrain his automatic recoil

from the barrier. Perhaps the best evidence for the biological basis of fear comes from examining the responses of infant rhesus monkeys. Shown slides of monkeys in various poses, these monkeys displayed clear fear responses when shown pictures of threatening, but not of nonthreatening, monkeys. Because these infant monkeys were reared in isolation, they could not have learned this fearful response by ex-

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periencing trauma themselves or by watching other monkeys display a fear response. Similar nonlearned fearful responses in human children develop at specific periods in the developmental cycle. Thus, human infants display a fear of strangers from around 4 to 9 months of age, peaking at 12.5 months. Human infants, after they develop locomotion, also display a fear of falling when placed on the edge of an apparatus that looks like a visual cliff. Infants will crawl away from mothers who call to them from across the cliff even after patting the surface to assure themselves of its solidity. Such data indicate that for at least some stimuli there is a built-in readiness to experience fear in their presence. There are critics of the biological hypothesis. These critics point out that the results of these studies are open to alternative interpretations. One such interpretation is that the tendency for learned responses to some stimuli to persist might be the product of expectancies rooted in culture rather than genes. Such an explanation fails to account for the automatic fear response of infants and of monkeys raised in isolation to specific fear stimuli.

3. Associative Learning Classical conditioning is a process by which different stimuli, which occur at the same time, come to be associated. The earliest demonstration that humans could learn a fear response via classical conditioning occurred in 1920 when Watson and Rayner produced a fearful response in an 11-month-old infant named Albert. Watson observed that Albert's response to a white laboratory rat was initially positive--Albert smiled and played with the animal. Subsequently, whenever the rat was present, a loud noise was sounded that startled Albert. The rat, through repeated presentations with the noise, came to be associated with the noise. This association of an initially neutral stimulus (rat) with an aversive unconditioned stimulus (UCS = loud noise) resulted in a conditioned fear response (CR) when only the rat was presented. For some time after this demonstration it was thought that all phobic reactions were obtained via aversive conditioning as in the "Little Albert" study. The classical conditioning model of phobias explains why people react with subjective and physiological fear when they are exposed to a learned phobic stimulus. However, it does not account for the persistent avoidance behavior phobics display. A

two-stage model explaining the development of the fear response and avoidance behavior was subsequently developed. Classical conditioning explained the learned fear response in the first stage, while instrumental conditioning explained the learned avoidance response in the second stage. Instrumental conditioning in this case refers to the reinforcement of the avoidance response produced by the decrease in anxiety. During classical conditioning, the pairing of a neutral CS and an aversive UCS results in a conditioned fear response to the CS. During instrumental learning, the person learns that the fear response to the CS can be reduced by escaping or avoiding the CS. The reduction in fear levels that follows avoidance reinforces this behavior (a process termed negative reinforcement) and, in time, avoidance behavior becomes an integral part of the phobia. This two-stage theory has been well-documented in the laboratory. However, the two-stage theory has several limitations. First, the conditioning approach fails to explain why specific fears are nonrandomly distributed, that is, why some individuals are more likely to develop phobias than are others. Second, individuals do not always acquire phobias as a result of confronting an aversive stimulus and pairing it with a neutral stimulus. Individuals who have specific phobias, for example, frequently are unable to remember a traumatic event during which they learned to fear the stimulus. Lastly, fearful behavior that is produced via classical conditioning in the laboratory requires repeated pairings of the unconditional and neutral stimuli, a circumstance inconsistent with reports of how specific phobias develop. Because of the failure of classical conditioning to explain how most specific fears developed, Rachman proposed two additional pathways: (1)vicarious learning (i.e., learning to fear by watching someone else act fearfully toward a stimulus) and (2) acquisition of negative information and the aforementioned associative learning. All three of these explanations for the development of specific fears have in common a cognitive expectancy of threat that is connected to the feared stimulus. People essentially learn through direct or indirect experience that some stimuli pose a threat to them and that fear is proportional to the likelihood and severity of that threat. The vicarious learning hypothesis has been supported by both animal and human laboratory studies that show individuals react fearfully after watching others act

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fearfully. Negative information provided by significant others, such as parents, or through the media of books or television may give rise to fear of stimuli that are subjects of the negative information. Support for the three modes of fear acquisition comes from studies that ask individuals with specific phobias to identify what they believe caused their disorder. A proportion of phobic individuals report their phobias began suddenly, following a fear-producing encounter with the stimulus, while a smaller proportion report their fear began when they viewed someone respond fearfully or learned indirectly of the potential danger associated with the object. These three avenues for acquiring phobias through learning occur with different frequencies in the four subtypes of specific phobias. Animal phobics and blood-injectioninjury phobics more often ascribe their fears to seeing others respond fearfully and to negative information that do claustrophobics. In contrast, the associative learning pathway is more pronounced in claustrophobia than in animal phobia, blood-injection-injury or height phobia. The acquisition of a fear through modeling or negative information is associated with phobias with an early age of onset. It is also likely that the acquisition of a specific phobia is overdetermined, that is, individuals who acquire a phobia often report negative learning experiences of more than one variety. There are even indications that subjects with "mixed" pathways (e.g., conditioning and modeling) have higher levels of fear.

4. Treatment It is generally accepted that the most successful treatments for specific phobias employ a reconditioning paradigm. In specific phobias, neutral stimuli such as animals, storms, or blood have become associated with an anxiety response, whether through direct association, vicarious learning, or anxiety-producing information. Presenting the phobic stimulus to the sufferer in the absence of a reinforcing or unconditioned stimulus leads to reductions in the fear response to the stimulus. This has been accomplished using a variety of treatment approaches, including systematic desensitization-both imaginal and "in vivo," that is, in "real life"--and vicarious learning techniques. Systematic desensitization refers to a process in which the phobic stimuli are arranged in hierarchical fashion from least anxiety-producing to most anxietyproducing, and these stimuli are systematically paired

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with a response incompatible with anxiety. Taking as an example an individual with a spider phobia, an item low on the hierarchy might be a picture of a small spider, while an item high on the hierarchy might be holding a jar containing a live tarantula. After constructing the hierarchy, the phobic individual would then be taught a method of inducing relaxation. The final step would involve the phobic individual sequentially confronting items in the hierarchy while remaining relaxed. Phobic items are presented repeatedly until the sufferer reports little or no anxiety when presented with the phobic cue. When this level of comfort is reached, the sufferer proceeds to the next item on the hierarchy until he is able to tolerate all phobic stimuli on the hierarchy with a minimal level of anxiety. In one version of this approach, all the stimuli are presented imaginally, while in another version the sufferer is exposed to the fearful stimuli in vivo. The in vivo approach has been found very successful with improvement rates in excess of 85 %. Vicarious learning techniques are used adjunctively to the above two approaches as well as alone. Vicarious learning is a phenomenon by which organisms learn a response by watching the emotional responses of others to these same stimuli. Children whose parents exhibit fearless responses to a variety of situations are themselves likely to show low fear responses to the same situations. On the other hand, children who observe their parents or peers responding fearfully to certain situations are themselves likely to respond fearfully to these same situations. Used therapeutically, vicarious learning involves corrective information, for example, "the spider is not harmful," skills on how to handle the feared object, and exposure to models who respond positively to the phobic stimuli. The sufferer is then encouraged to expose himself to the previously feared situations. Interestingly, individuals with blood-injury phobias can also be treated with exposure techniques, but in this case the phobic stimulus is paired with a muscle-tensing response that is incompatible with the drop in blood pressure characterizing this group of phobias. When this procedure is carried out repeatedly, both the fear of blood-injury and the drop in blood pressure experienced at the sight of blood diminish. All the above treatment techniques involve learning a new and incompatible response in place of the fearful response to the phobic stimulus. The process by

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which the new learning takes place is still a matter of some debate. One explanation is a simple reconditioning model in which either the old fearful response to the phobic stimulus is changed by prolonged exposure without the reinforcement provided by the presence of an aversive stimulus, or a new relaxation response is learned in the presence of the phobic stimulus. Another explanation is provided by the informationprocessing theory of fear reduction. In this model, phobic knowledge that exists in the brain consists of both stimulus (such as images associated with the phobic object) and response propositions, including the behavioral, verbal, and physiological reactions to the phobic object. Change is thought to occur when the individual processes the phobic stimulus and the response to that stimulus thoroughly, thereby altering the fearful images and anxious responses associated with that stimulus.

II. SOCIAL PHOBIA A. Definition Although fears in the presence of others have been described for centuries and have been addressed in the mental health literature since at least 1970, social phobia was not considered a diagnosable entity until the publication of the third Diagnostic and Statistical Manual of Mental Disorders, published in 1980. DSM-IV (the current system) identifies the essential feature of Social Phobia (also referred to as Social Anxiety Disorder) as a marked and persistent fear of social or performance situations in which embarrassment may occur. Social phobics fear and/or avoid a variety of situations in which they would be required to interact with others or to perform a task in front of other people. Typical social phobia situations include speaking, eating, or writing in public, using public bathrooms, and attending parties or interviews. In addition, a common fear of social phobics is that other individuals will identify and ridicule their anxiety in social situations. When a person fears a broad spectrum of social situations, it is referred to as Social Phobia, Generalized subtype, whereas fear of one or a few social situations is referred to as Social Phobia, Specific subtype. Individuals with social phobia are aware that their fears and social isolation are unreasonable

and excessive, but they feel unable to control these feelings.

B. Clinical Features: Symptomatology and Epidemiology As in specific phobia, the anxiety of social phobics is stimulus-bound, that is, it occurs only in the presence of the feared situation or when anticipating that situation. When in or anticipating a potentially embarrassing situation, the individual with social phobia experiences profound anxiety, accompanied by a variety of somatic symptoms including palpitations, muscle tension, nausea, and blurred vision. The person with a social phobia experiences symptoms that underscore the fear of public scrutiny, including symptoms such as trembling, shaking, blushing, twitching, and sweating. Social phobics also experience more negative selfevaluative thoughts and fewer positive thoughts prior to and during social situations than do individuals who do not experience anxiety. Not only do individuals with social phobia experience more negative arousal symptoms compared to nonphobic individuals, social phobics also perform less well in social situations and systematically underestimate their performance. Judging from their response to social situations, social phobics have a variety of information that serves to underpin their fears. Social anxiety and reports of shyness in the general population are relatively common, occurring in about 40% of college students. Furthermore, social anxiety is a common accompaniment of all anxiety disorders. The most recent National Comorbidity Survey found a given individual had a 13 % chance of developing a social phobia in his/her lifetime. The distinction between generalized and specific social phobia is a useful one. Individuals with generalized social phobia have a fear of and will avoid a wide variety of interpersonal and performance situations. These may include formal speaking to a group, informal interactions such as going to parties or meeting strangers, assertive interactions and being observed by others. Individuals with specific social phobia typically are afraid only in performance situations or in a limited number of interpersonal situations. Most individuals with social phobia experience anxiety in two or more different social situations. A lack

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of social skills has been found in the generalized type, with increases in subjective feelings of anxiety being found in the specific type. Individuals with generalized social phobia reported themselves as more shy and, especially for males, less likely to date during the late adolescent period. Differences between the two types are also indicated by treatment studies that attempt to match treatment type to type of social phobia, a distinction discussed further in the section on treatment of social phobias. Unlike agoraphobia and specific phobia, social phobia has repeatedly been found to have an essentially equal sex distribution or even a slight tendency to affect males more than females. A similar sex distribution has been found among socially anxious college students.

C. Course/Prognosis and Comorbidity Issues The consensus among individuals who study anxiety disorders is that social phobia typically begins in late childhood or early adolescence, with fewer individuals developing the disorder in early childhood. Onset is generally gradual and, clinically, most social phobics report they cannot specifically remember the beginning of their symptoms. Some social phobics report specific stressful experiences prior to the onset of the disorder. The course of social phobia is often continuous, with duration frequently being lifelong. Social phobia may fluctuate in severity or remit during adulthood, and severity of impairment may fluctuate with life stressors and demands. Social phobia is much more serious and disabling than previously thought and can have severe functional consequences. More than 50% of individuals diagnosed with social phobia are unable to complete high school, more than 70% of these individuals are in the lowest two socioeconomic quartiles, and 22 % of individuals with pure social phobia receive welfare. The majority of individuals with social phobia are unmarried. It is clear from the prevailing information that social phobia is a severe illness with numerous social consequences. In addition to the social and occupational consequences of social phobia, almost 19% of individuals with social phobia are likely to abuse alcohol, while 13% will likely develop some type of drug abuse. In addition, social phobia is also commonly associated

with major depression (16.6 %), dysthymia (chronic low-grade depression) (12.5), obsessive-compulsive disorder (11.1%), and anxiety disorders such as panic disorder (4.7), agoraphobia (4.9%), and specific phobia (59%). In the majority of cases, the onset of social phobia precedes the onset of the second psychiatric disorder, with the exception of specific phobias, by many years. Social phobia, generalized subtype, is viewed as being more severe than social phobia, specific subtype, and thus is associated with more frequent comorbidity.

D. Etiology I. Genetic It is likely there is a genetic predisposition to developing social anxiety and shyness. The rate for social phobia in first-degree relatives (parents, children, siblings) of individuals with pure social phobia is 16%, compared to 5% in individuals selected randomly from the population. Identical twins were also found to have a higher rate of social phobia (49%) if their cotwin had the disorder than did fraternal twins whose cotwin had the disorder (30%). Such findings have been reported by several different investigators, even when controlling for gender in various studies. It has been estimated that genetic factors account for 30% of the vulnerability for social phobia.

2. Biological Factors Little research has been conducted on the biological causes of social phobia. One line of research has examined biological differences between anxiety in social phobics and other anxiety disorders. When in social situations perceived as evaluative, 50% of individuals with social phobia symptoms experience a surge of epinephrine (a drug secreted in your body to prepare you for an emergency), distinguishing them from panic attacks in which an adrenaline surge is not regularly seen. Another line of investigation has assessed the relationship between sensitivity to social disapproval and neurotransmitters (chemicals necessary for efficient transmission of nerve signals). These studies have revealed a connection between depletion of specific neurotransmitters and mood responses to social approval and disapproval. The possibility exists that this transmission system is poorly regulated in social phobics and those with atypical

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depression. Both these groups overreact to criticism or rejection, and greatly benefit from a group of antidepressant drugs---monoamino oxidase inhibitors~ that reduce their sensitivity to rejection and also inhibit the metabolism of specific neurotransmitters.

3. Environmental Factors In addition to direct conditioning experiences, social phobics report parental behavior that tends to foster dependency and insecurity. Social phobics compared to nonphobic normals perceive their parents as overprotective and low in emotional support. Other research has replicated these findings and additionally found social phobics rated their parents as rejecting. These parental patterns could account for general feelings of insecurity, typical of most individuals who experience anxiety. Other research compared social phobics to agoraphobics. Social phobics reported their parents isolated them from social experiences, overemphasized the opinions of others, and de-emphasized socializing with others as a family. These additional patterns in the parents of social phobics could account for the specific manifestation of anxiety found in these individuals.

4. Psychological Factors Four types of concerns have been identified among social phobics: (1) perceptions of autonomic arousal; (2) concern with others' awareness; (3) feelings of social inadequacy; and (4) fear of negative evaluation. Of these, the last three have all been identified as important causal and/or maintaining factors in social phobia. Awareness of others' perceptions was one of the earliest areas to be investigated in social phobia. Research studies substantiated increased public selfconsciousness in socially anxious individuals accompanied by a fear of negative evaluation. Increases in self-consciousness led to increased autonomic arousal. Social phobics believe that compared to others they are deficient in social skills. They combine a belief that others hold high expectations for their performance with the perception of their own inadequacy. Consequently, they anticipate negative evaluations and are predisposed to interpret neutral feedback or even moderately positive feedback in negative terms. This bias in the manner in which information is processed by socially anxious individuals tends to maintain

these perceptions as socially phobic individuals tend to "find" the behaviors in others for which they search. When asked to recall their past evaluations, they are more likely to recall negative feedback than are non-socially anxious individuals.

E. Therapy I. Psychological Approaches Psychological treatment approaches are both effective and often preferred to medications by people who experience side effects from medications. Relapse rates for social phobics treated by specialized psychological treatments tend to be lower than for those treated with medications. Specific psychological techniques can be linked to the symptoms and characteristics of social phobias. Aspects of successful interactions that cut across a variety of approaches can be identified. These common elements constitute the basic ingredients of a successful approach. They include: 1. Education regarding the defining characteristics and treatment of the disorder. Social phobics are frequently ashamed of their problem, believe their problem to be unique, and thus have not discussed it with others. Informing such individuals that much is known about the problem and that many people share the problem is very reassuring and anxiety-reducing. 2. Anxiety-reduction techniques such as relaxation training and diaphragmatic breathing (breathing that begins in the diaphragm) can be used to diminish the anticipatory anxiety as well as anxiety within the phobic situation itself. Social phobics experience heightened arousal manifested in a variety of somatic experiences of anxiety. Anxiety-reduction techniques are effective in dealing with these symptoms and in restoring confidence in the ability to decrease arousal in phobic situations. 3. Cognitive-retraining techniques deal with the exaggerated beliefs of being humiliated or ridiculed for having anxiety symptoms. Techniques that challenge such beliefs, invite the sufferer to test his beliefs against reality, and even dismiss or reframe the perceived negative evaluations of others are a critical element of therapy. 4. Training in social interaction techniques and social skills is important for individuals with generalized

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social phobia. Sufferers of the generalized form are deficient in assertiveness techniques, in techniques for starting a conversation or engaging a stranger, as well as techniques for deepening intimacy. Training in the use of such approaches and practice with them serves to improve social skills and increase their confidence in the ability to engage in these behaviors. 5. Graduated exposure to the feared situation. It is in this context alone that the social phobic learns to apply the above techniques in real-life situations. Such self-exposure increases the belief that the feared situation can be faced and that the sufferer can reduce the anxiety and cognitions and engage actively in social situations.

2. Pharmacological Approaches The use of pharmacologic interventions in the treatment of social phobics has been relatively rare until recent times. Some drugs have achieved a high rate of acceptability, in part because of their effectiveness and in part because of their low rate of side effects. Beta-adrenergic blockers--beta blockers--have been widely accepted as a treatment for performance anxiety. Fast-acting and with a relatively short presence in the body, beta blockers are used by seasoned performers and amateurs facing their first public appearance as a way of reducing the physiological accompaniments of anxiety. Side effects from using these drugs are negligible. The effectiveness of beta blockers appears to be restricted to social phobics with specific fears such as stage fright. Generalized social phobias are less likely to be helped by this group of medications, perhaps because of the failure of these drugs to reduce the negative cognitions associated with this disorder. A second class of drugs--an antidepressant group known as monoamino oxidase inhibitors (MAOIs)-have the highest success rates in the treatment of social phobia. This class of drugs was initially found to be effective with a type of depression characterized by interpersonal sensitivity. They were then tried on social phobics who, as previously discussed, also display a high level of interpersonal sensitivity. This class of drugs is successful with both specific and generalized social phobics, and also has beneficial effects for a variety of disorders that frequently co-occur with social phobia, including panic disorder, obsessive-compulsive disorder, and depression. The principal drawback

of the MAOIs is that severe side effects are likely to occur, including hypertensive crisis, unless the individual taking the drug eliminates from his diet foods that contain tyramine (including cheeses, wines, beers, and some brans). For this reason, the use of MAOIs in the treatment of social phobia has been restricted. A new class of antidepressant medication called selective serotonin reuptake inhibitors (SSRIs) has also been used in the treatment of both specific and generalized social phobias. This class of drugs has been found effective with the advantage that the individual taking these drugs experiences few side effects. Because of the frequency with which this class of drugs is well-tolerated, it may well be the first choice of pharmacologic interventions. The level of effectiveness is high even when the social phobia is accompanied by other anxiety disorders or depression, all of which are also responsive to this class of medications.

III. AGORAPHOBIA A. Definition The term agoraphobia, which literally means "fear of the marketplace," was initially used by Westphal in 1871 to reflect the frequent observation that individuals with this problem were afraid of venturing into public places. The diagnosis requires the existence of two primary features: (1) anxiety about being in places or situations from which escape might be difficult (or embarrassing) or in which help might not be available, and (2) avoidance of these situations, enduring them with marked distress or fear of having panic symptoms, or requiring the presence of a companion before entering the phobic situation. The agoraphobic individual fears the onset of panic attacks (a discrete period of intense fear or discomfort that develops abruptly and reaches its peak within 10 minutes) or panic symptoms and avoids situations associated with such attacks. Four feared situations typically yield the avoidance behavior that occurs in agoraphobia: (1) situations, typically social, from which escape might be difficult, including restaurants, shopping malls, hairdressers, dentist chairs, and so on; (2) travelling where escape is difficult, including strange cities, bridges, tunnels, planes; (3) traveling away from home; and (4) being home alone. The c o m -

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mon feature of these situations is the fear of being unable to obtain help in the event of a panic attack, or the possibility of embarrassment if one obtained help. This response has been referred to as the fear of fear.

B. Clinical Features: Symptomatology and Epidemiology The chief feature of agoraphobia is escape from or avoidance of situations where panic symptoms might occur. While agoraphobia is frequently accompanied by or preceded by panic attacks, many agoraphobics are unable to recall a distinct panic episode prior to developing avoidance behavior. In these individuals, limited-symptom panic attacks (attacks where fewer than four symptoms are present) or fears of putting themselves at risk by leaving their safe base appear to underlie the avoidance behavior. Thoughts of dying, losing control, becoming seriously ill, going insane, or acting in an embarrassing fashion are likely to precede the avoidance behavior. Recent evidence indicates that the lifetime prevalence for agoraphobia is 6.7%. Agoraphobia tends to develop later in life than specific or social phobias and occurs more than twice as frequently in women as in men. Individuals who are agoraphobic tend to have lower income and education levels, are frequently unemployed, and are more likely to live with someone other than a spouse. It is unknown whether agoraphobics, because of their illness, drift into these less productive circumstances or whether the stress of these circumstances produces agoraphobia. When individuals with agoraphobia are studied in the general community, they are often found to have at least one additional diagnosis, with major depressive disorder, specific phobia, and panic disorder among the most likely of these. While a number of mental disorders tend to co-occur with agoraphobia, it is often less related to substance abuse or dependence, indicating that agoraphobics tend not to medicate themselves with alcohol or street drugs. When unaccompanied by another disorder, agoraphobics tend to perceive little role impairment, which may account for the finding that only about one-fourth of these individuals seek help even when their agoraphobic avoidance is extensive. Having another diagnosable mental illness, and especially the existence of panic attacks, significantly

increases the likelihood that agoraphobics perceive themselves as being impaired socially or occupationally, with as many as 70% of these individuals reporting that they have sought help for their problem.

C. Course and Prognosis Agoraphobia develops from young adulthood through middle life with few instances of agoraphobia beginning in late life. The average age for the onset of this disorder is between 25 and 29. Panic attacks, which frequently are the precursor of agoraphobia, often begin with the onset of puberty. These findings indicate there is a lag between the onset of panic attacks and the development of avoidance behavior. When agoraphobia is accompanied by panic disorder, long-term outcome is poor. Studies up to 20 years in length reveal 50% of untreated individuals with this problem experience significant social and occupational impairment, with 80% at least occasionally symptomatic. A variety of additional problems either co-occur with this disorder or develop in response to it, including increased depression, suicidality, sexual and marital problems, tranquilizer addiction, unemployment, and financial difficulties. Treatment using one of several recognized approaches improves the long-term adjustment, although a significant portion of sufferers who receive treatment continue to experience symptoms or, in fact, relapse to the level of adjustment prior to treatment. Individuals who at the conclusion of treatment continue to experience occasional panic attacks, or who remain avoidant, are more likely to experience a relapse to their previous level of functioning. Likewise, individuals who experience low levels of social support, problems in their marital relationship, or significant stressors after treatment is completed are likely to suffer a relapse.

D. Causal Factors Agoraphobia is best viewed as the endpoint of a series of factors that contribute to the development of this disorder. Genetic factors produce a biological vulnerability that then interacts with stressors and other environmental factors that in turn increase the likelihood one will develop panic disorder and agoraphobia. A strong genetic and biological vulnerability will require fewer environmental factors to produce ago-

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raphobia, while a weak genetic and biological vulnerability will require more and stronger environmental factors before agoraphobia develops.

E. Heredity There is a demonstratable link between genetic factors and the development of panic disorder, a frequent precursor of agoraphobia. First-degree relatives of individuals with panic disorder are approximately seven times more likely to be diagnosed as panic disordered than are first-degree relatives of individuals with no panic disorder. Similarly, identical twins are twice as likely to share a common diagnosis of anxiety disorder than are fraternal twins, although they are unlikely to share the same diagnosis for the specific type of anxiety disorder. If one twin has a diagnosis of agoraphobia with panic attacks, their identical cotwin is likely to experience panic attacks as well, while their fraternal cotwin is not. It appears from the limited research in this area that a biological vulnerability exists for panic attacks but not necessarily agoraphobia. A stronger genetic relationship is likely to exist for anxiety problems in general such that what is inherited is a vulnerability to develop anxiety.

F. Biological Factors If genetic factors play a role in the development of panic, the question remains as to what type of vulnerability is inherited. One possibility is that panic disorder may involve a deficit in the metabolism of factors that inhibit the transmission of anxiety messages in the brain, while another possibility is that there is an increased sensitivity to certain substances. If the latter is true, the introduction of these substances to the bodies of individuals with panic disorder and agoraphobia should produce symptoms of panic, while this response would not be expected in individuals without panic attacks. These differences in sensitivity to certain substances have been demonstrated in a wide variety of studies. Panic disordered agoraphobics have been shown more sensitive to sodium lactate, adrenalin, caffeine, and hyperventilation. The first of these---sodium lactate~is similar to lactic acid, a substance that increases naturally in the body in response to

physical exercise. It is known that agoraphobic individuals possess a sensitivity to increases in physiological arousal such as increased heart rate, respiration, and sweating, body changes common to both exercise and panic attacks. Panic attacks, therefore, may be an alarm reaction to detected physiological changes produced by increases in lactic acid. People suffering from panic disorder show this increased sensitivity by developing panic attacks when injected with sodium lactate, while people who do not have this problem do not show this sensitivity. Similarly, panic-disordered agoraphobics respond with panic attack symptoms when administered a standard hyperventilation procedure, when they drink caffeine, or when they are injected with adrenalin. This response is not typically seen in nonpanickers, thus supporting the biological vulnerability hypothesis. The finding that panic-disordered agoraphobics have an increased sensitivity to symptoms of physiological arousal may help explain why there is an increase vulnerability to panic in individuals with certain cardiovascular problems. One such line of evidence has shown that individuals with mitral valve prolapse syndrome (MVPS), a problem characterized by chest pain, difficulty in breathing, dizziness, fatigue, and tachycardia are at risk for developing panic disorder. Individuals who experience such symptoms and are psychologically sensitized to them may come to fear them and develop catastrophic cognitions when they occur~the previously identified "fear of fear." Further evidence for the role of biological factors comes from panic-disordered individuals who report fluctuations in the frequency and severity of attacks they experience. Recent findings in women indicate increases in panic attacks of as much as 100% occur during the premenstrual period, while there is no change in the degree of anticipatory anxiety or avoidance behavior at these times. Again, the biological contribution is more apparent for panic attacks than for agoraphobia.

G. Psychological Factors The childhood backgrounds of agoraphobics suggest family experiences play a role in the development of this problem. Lack of maternal care and a general lack of social support, coupled with high intrafamily

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conflict, have been linked to the development of agoraphobia in adulthood. This deficiency in a warm, supportive parent-child relationship and frequent punishment and criticism produce individuals who view themselves as incompetent and unable to handle challenging situations. This self-view in turn leads to withdrawal and avoidance when faced with challenging situations as an adult. As many as 80% of agoraphobics report the onset of their panic symptoms was preceded by identifiable stressors or a period of prolonged stress. Interpersonal problems is a frequent precipitant of agoraphobia in adults. Rejection or loss have been reported by a majority of sufferers able to identify a precipitant. Also implicated are marital conflicts in which persons fail to assert themselves, or when they do assert themselves are threatened with loss of the relationship. Loss by death, divorce, or separation, either of a family member or a friend, has been reported as a factor that has led to the development of agoraphobia. The combination of low support and high conflict in childhood and threatened or actual loss of interpersonal relationships in adulthood produces a unique psychological vulnerability to agoraphobia. Some people who have panic attacks do not become agoraphobic. Women, who tend to value social relationships more than men do, may be uniquely vulnerable to losing such relationships, a fact that may help explain why so many more women with panic than men with panic develop agoraphobia. Two additional factors are predictive of who among panicdisordered individuals develops agoraphobia---how panickers think about their attacks, and how they cope with them. Those panickers who develop agoraphobia believe there is a connection between the situations they avoid and the likelihood they will suffer panic attacks in those situations, while nonavoiders are less likely to make such links. Further, individuals who become agoraphobic believe that if they do have a panic attack, there will be nothing they can do to control itmthe absence of a belief known as selfefficacy. The belief that coping strategies are available that will help control panic attacks is also associated with lower levels of avoidance. The use of coping strategies such as seeking out social support, reasoning out what is happening, controlling one's breathing and relaxing one's muscles are specific strategies linked to lower levels of avoidance, while wishful

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thinking is a strategy linked to higher levels of avoidance.

IV. PANIC DISORDERAND AGORAPHOBIA A. Psychological Approaches Psychological treatments for this disorder target each of the disorder's components m the panic attacks, anticipatory anxiety, and agoraphobic avoidance. Panic attacks themselves are comprised of several features, each of which is targeted within the treatment program. These features include physiological arousal symptoms and catastrophic cognitions. In addition, panic attacks develop from a baseline of chronically high anxiety and are preceded by high levels of anticipatory anxiety when sufferers face situations where panic attacks have previously occurred. Panic sufferers typically have little information about their problem and considerable misinformation. The first phase of treatment aims at providing an understanding of the disorder as well as factors that may have caused it and serve to maintain it. Subsequently, techniques that reduce the chronically high baseline anxietymsuch as applied relaxation--are taught to the panicker with instructions to frequently practice them. Reducing the level of generalized anxiety decreases the frequency of panic attacks but only infrequently eliminates them completely. Strategies for dealing with both the physiological and cognitive components of the panic attacks themselves have the greatest positive effects. The physiological symptoms are reduced by using a variety of coping strategies, including diaphragmatic breathing, distraction strategies, and social support strategies. Catastrophic cognitions, which are interpretations of the symptoms and inaccurate predictions of the likely consequences of the symptoms, are reduced by providing accurate information and by teaching the sufferer ways of challenging the negative thoughts. Because one of the principal symptoms that occurs during panic attacks is confusion of thought, and because the panic sufferer does not believe in his ability to use these techniques during the panic attack itself, the techniques are practiced in contexts similar to those experienced during an actual panic attack. As the sufferer gains confidence in the new coping strategies, he is encouraged to enter previously avoided situations and to practice

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strategies for dealing with attacks prior to entering the phobic situation and when in the situation itself. Mastery of the panic attacks is accompanied by a decrease in anticipatory anxiety and a willingness to enter phobic situations. As the phobic situations are entered absent the panic attacks, the agoraphobia decreases.

B. Pharmacologic Treatments A variety of classes of psychotropic medications have been evaluated as treatments for panic disorder and agoraphobia. These include (1) three classes of antidepressants--tricyclics, MAO inhibitors, and the SSRIs; (2) two classes of benzodiazepines~low-potency benzodiazepines such as valium and librium, and highpotency benzodiazepines such as alprazolam; and (3) beta-blockers. Both low-potency benzodiazepines and beta-blockers have limited effectiveness with panic attacks and are used infrequently in the treatment of this disorder. All three types of antidepressants have been studied as treatments for panic attacks. Tricyclics and MAO inhibitors are moderately effective in reducing panic attacks, but each is often accompanied by significant side effects. One principal side effect is an initial increase in paniclike symptoms, a response that leads from 30 to 40% of individuals given these drugs to discontinue their use. Similar problems are encountered with the SSRIs, but less frequently. Another problem occurs when panic sufferers attempt to discontinue their use of these drugs: panic attacks frequently return and the individual is faced with a choice between relapse of panic symptoms or remaining on the medication indefinitely. High-potency benzodiazepines such as alprozalam are the pharmacologic treatment of choice for panic disorder and agoraphobia. Side effects are few, and approximately 80% of those on a therapeutic dose experience an elimination of their panic attacks. As with the antidepressants, however, stopping use of this drug is frequently accompanied by a return of panic attacks. A comparison of the best psychological intervention with the antidepressants and high-potency benzodiazepines on the three criteria of treatment dropout, treatment improvement, and treatment relapse seems to favor the psychological approach. Antide-

pressants produce an unfavorable side effect profile with numerous treatment dropouts. Relapse rates are high after discontinuing treatment. Treatment success rates are comparable for the best psychological treatments and high-potency benzodiazepines---approximately 80% are significantly improved. Relapse rates after concluding treatment are considerably higher for the high-potency benzodiazepines than for the best psychological treatment, however, thus favoring the psychological approach. Another avenue is to combine pharmacologic and psychological treatments. This approach produces treatment improvement rates similar to the best psychological approach alone. Other considerations may lead to choosing this alternative, however, such as the necessity to produce a quick reduction in panic attacks. In typical clinical practice, panic-disordered and agoraphobic individuals are treated with a combination of medications and psychological interventions. There is some evidence that drugs interfere with the beneficial effects of psychotherapy techniques that involve exposure to phobic stimuli. The individual's choice of what approach to use--drugs or psychotherapy--often comes down to biases and expectations that exist prior to seeking help. Some who choose drugs do not want to spend the time or make the effort required by psychological treatments. Others do not want the stigma or side effects associated with the use of drugs. Future intervention strategies may take into consideration these basic attitudes and best available treatments in recommending a course of therapeutic action. [See PANIC ATTACKS.]

BIBLIOGRAPHY American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders (4th Ed.). Washington, CD: Author. Clum, G. A. (1989). Coping with panic: A drug-free approach for dealing with anxiety attacks. Pacific Grove, CA: Brooks-Cole Publishing Co. Markway, B. (1992). Dying of embarrassment: Help for social anxiety and social phobia. Oakland, CA: New Harbinger. Rosenbaum, J. F., Pollock, R. A., Otto, M. W., & Pollock, M. H. (1995). Integrated treatment of panic disorder. Bulletin of the Meninger Clinic, 59, A4-A27. Sheehan, D. (1983). The anxiety disease. New York: Charles Scribner's Sons.

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Posttraumatic Stress Lisa H. Jaycox and EdnaB. F0a Allegheny University of the Health Sciences

I. II. III. IV. V. VI.

Reactions to Traumatic Events Measures of PTSD Prevalence of PTSD Vulnerability and ResiliencyFactors Concomitant Problems Following Trauma Theories on the Development and Maintenance of PTSD VII. Psychologicaland PharmacologicalInterventions

POSTTRAUMATIC STRESS is a set of psychological and physical symptoms that follow a traumatic experience. In some cases, these symptoms persist beyond the immediate aftermath of the trauma and develop into Posttraumatic Stress Disorder (PTSD), an anxiety disorder that includes symptoms of arousal, avoidance, and reexperiencing, lasts for more than 1 month, and causes significant impairment in social or occupational functioning. This article discusses the stress symptoms that commonly follow trauma and describes PTSD and its prevalence. The theories underlying the development and maintenance of symptoms are discussed along with the treatments used for PTSD and their efficacy.

Arousal Cluster of Posttraumatic Stress Disorder symptoms that includes concentration problems, anger, exaggerated startle response, sleep disturbance, and overalertness. Avoidance Cluster of Posttraumatic Stress Disorder symptoms that includes behavioral and psychic avoidance, such as avoidance of thoughts, feelings, and reminders of the trauma, emotional numbing, loss of interest in activities, disconnection from others, psychogenic amnesia, and a sense of foreshortened future. Diagnostic and Statistical Manual of Mental Disorder (DSWI) A reference manual used by mental health professionals of descriptions and diagnostic criteria for psychiatric disorders. Reexperiencing Cluster of Posttraumatic Stress Disorder symptoms that includes experiencing the trauma in the form of nightmares, flashbacks, or intrusive distressing thoughts, or becoming intensely emotionally upset or having physiological arousal on exposure to reminders of the trauma. Trauma An event, witnessed or experienced, in which there is threat of death, injury, or physical integrity, and during which an individual feels terrified, horrified, or helpless.

I. REACTIONS TO TRAUMATIC EVENTS Psychologists and physicians have long been interested in vulnerability and resilience factors in reaction to extreme stress. Earlier accounts of posttrauma reactions focused on descriptions of cases. Spurred by inclusion of Post-traumatic Stress Disorder (PTSD) in the psychiatric diagnosis nomenclature in 1980, experimental research has examined many facets of the phenomenon. In the Diagnostic and Statistical Manual (DSM-IV) published by the American Psychiatric Association in 1994, a trauma is defined as an experienced or witnessed event that involves threat of death or serious injury, and which evokes feelings of terror, horror, or helplessness. Thus, events such as anticipated death of a loved one, job loss, or divorce would not qualify

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as a trauma in this formulation. The International Classification of Diseases (ICD-I O), published by the World Health Organization in 1992, describes a traumatic event as having an exceptionally threatening or catastrophic nature, which would be likely to cause pervasive distress in almost anyone. [See DSM-IV.] The most common traumas studied are combat, sexual assault, sexual abuse in childhood, criminal victimization, torture, accidents, and natural disasters. Larger-scale traumas, such as mass migration, refugee camp experiences, and holocausts, have not yet been thoroughly researched. Clearly, such mass traumas would be expected to have considerable impact on those individuals directly affected as well as on their children, communities, and cultures.

A. Acute Reactions A number of physical and psychological symptoms are considered common reactions immediately after a traumatic experience. Many trauma victims report being disoriented and anxious after a trauma and have difficulty sleeping and concentrating. Victims are often reluctant to talk about the trauma or deliberately contemplate it; nevertheless the traumatic memory intrudes on their thoughts quite frequently. In recognition of the severe distress and psychological dysfunction that often occur immediately after a trauma, a new diagnostic classification called Acute Stress Disorder (ASD) was adopted in the DSM-IV in 1994. The focus of this disorder is on dissociative features, and, consequently, the symptom criteria include at least three of the following: a sense of numbing, detachment, or lack of emotional responsiveness, a reduction in awareness of surroundings (e.g., being in a daze), derealization, depersonalization, and dissociative amnesia. Reexperiencing of the trauma, avoidance, and arousal, as defined in the criteria for PTSD, must also exist. A diagnosis of Acute Stress Disorder is warranted when such symptoms last between 2 days and 1 month, occur within 1 month of the trauma, and interfere significantly with daily functioning.

B. Posttraumatic Stress Disorder Posttraumatic Stress Disorder, as described in DSMIV, is a set of symptoms that begins after a trauma apA persists for at least 1 month. The symptoms fall into three clusters. First, the individual must reexperience

the trauma in one of the following ways: nightmares, flashbacks, or intrusive and distressing thoughts about the event; or intense emotional distress or physiological reactivity when reminded of the event. Second, the individual must have three of the following avoidance symptoms: avoidance of thoughts or feelings related to the trauma, avoidance of trauma reminders, psychogenic amnesia, emotional numbing, detachment or estrangement from others, decreased interest in leisure activities, or a sense of foreshortened future. Third, the individual must experience two of the following arousal symptoms: difficulty falling or staying asleep, difficulty concentrating, irritability or outbursts of anger, hypervigilance, or an exaggerated startle response. To meet diagnostic criteria for PTSD, the symptoms must cause significant impairment in daily functioning. These criteria provide a good operational definition of PTSD, as they describe the symptoms seen in most cases. However, the three categories of symptoms are not empirically validated as distinct symptom clusters. For instance, it is not clear that the symptoms of behavioral avoidance and emotional numbing are similar and belong in the same category. The ICD-IO criteria for PTSD also include some reexperiencing symptoms (nightmares, flashbacks, distress on exposure to reminders), actual or preferred avoidance of trauma reminders, and either an inability to recall important aspects of the trauma or sustained psychological sensitivity and arousal (sleep disturbance, hypervigilance, difficulty concentrating). These three criteria must all be met within 6 months of the traumatic event for a diagnosis to be given. Several differences between the two definitions can be identified. First, the DSM-IV specifies a minimal number of symptoms that need to be observed to receive the diagnosis, whereas the ICD-IO leaves more freedom for clinical judgment. The advantage of the former approach is its utility in clearly operationalizing the concept of PTSD. The disadvantage is its rigidity and the possibility that one symptom can determine diagnostic membership. Second, the ICD-IO does not recognize the numbing symptoms, which together with flashbacks and nightmares are thought to be cardinal features of PTSD. Third, arousal symptoms are optional in the ICD-IO but are required in the DSM-IE Clinical observation and theoretical accounts of PTSD support the importance of these symptoms and render the I CD-IO diagnostic criteria less satisfactory.

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C. Course of PTSD

B. Self-Report Measures

The course of PTSD is variable. For the majority of individuals, symptoms begin immediately after the trauma, although some appear to have a delayed reaction. During the first 3 months after the trauma, the individual is said to have acute PTSD, whereas chronic PTSD is defined as symptoms persisting beyond 3 months. Symptoms can fluctuate over time between diagnosis of PTSD, subthreshold symptoms, and few or no symptoms. Recovery is affected by a number of factors, including perception of oneself and one's surroundings, actual social support, life stress, coping style, and personality.

Several self-report scales have been developed to assess symptoms of PTSD. The first was the Revised Impact of Events Scale (RIES), which yields two factors: intrusion and avoidance. A revised version of the RIES added hyperarousal items, but has shown mixed resuits in reliability studies and, like its predecessor, does not correspond fully to the D S M - I V PTSD symptoms. Two scales, the Mississippi Scale and the Penn Inventory, have excellent psychometric properties in veteran samples but do not provide information about diagnostic status because they do not fully correspond to the D S M - I V defining symptoms. The PTSD Symptom Scale-Self-Report (PSS-SR) and its successor, the PTSD Diagnostic Scale (PDS), provide information about each of the 17 DSM-IV symptoms, yielding both diagnostic and severity information. The PDS is the only self-report instrument that assesses all D S M - I V criteria, including information about the nature of the traumatic event and the level of functional interference, in addition to information about PTSD diagnosis and symptom severity. It was validated in a sample of victims of a wide range of traumas and evidenced sound psychometric properties, and thus can be used in studies of various trauma populations.

II. MEASURES OF PTSD A number of measures have been developed to assess PTSD, including clinical interviews and self-report instruments. These measures vary widely in terms of the target symptoms, administration time, and the samples used for ascertaining psychometric properties. Adult assessment tools are reviewed in the next section. Although some measures have also been developed for children, they are outside the scope of this article.

A. Interviews The Structured Clinical Interview for DSM (SCID) is believed to be the most widely used diagnostic interview. Its major disadvantage, however, is that it does not provide a measure of symptom severity. Several other interviews that provide information of both diagnostic status and symptom severity are available. Two interviews are becoming quite widely used in PTSD research. The first is the Clinician-Administered PTSD Scale (CAPS) that yields separate scores for frequency and intensity for each symptom. Disadvantages of this interview include a long administration time and validation on military veterans only. The second interview, the PTSD Symptom Scale Interview (PSS-I), includes a combined frequency/severity rating for each of the 17 PTSD symptoms in the D S M - I V and thus yields both a diagnosis and a continuous severity rating. Unlike the CAPS, the PSS-I takes only about 15 to 20 minutes to administer and was validated on female assault victims.

III. PREVALENCE OF PTSD Lifetime prevalence of PTSD in the general population is estimated at 9%, with up to a third of these cases having chronic PTSD. Among trauma victims, the rate is much higher, estimated at 24 %. However, the rates of PTSD tend to vary considerably among different types of trauma. For instance, estimates of the lifetime prevalence of PTSD in Vietnam War veterans range from 27 to 65%; in civilian populations exposed to terrorism and torture, prevalence ranges from 33 to 54%. Between 35% and 94% of victims of violent assaults manifest PTSD. In contrast, accidents and natural disasters appear to produce lower rates of PTSD, 4.6 to 59%, depending on the event studied and the degree of exposure. Even individuals with little or no direct exposure to the trauma can develop PTSD; this phenomenon has been referred to as the "ripples outward" effect. Importantly, certain occupations are at risk for PTSD by virtue of increased probability of r e -

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peated direct exposure to trauma; between 9% and 26% of professionals such as police, nurses, and firefighters develop PTSD in reaction to stressors experienced on the job. Prevalence in certain vulnerable populations is much higher than in the general population, presumably because individuals in these groups have been exposed to more traumatic experiences. These include populations seeking outpatient psychotherapy and those in substance abuse clinics. Women appear to be somewhat more likely than men to develop PTSD after trauma, 10.4 % versus 5 %, respectively. As noted earlier, the prevalence of emotional difficulties after mass traumas, such as refugee camp experiences or holocausts, has not been systematically studied.

IV. VULNERABILITY AND RESILIENCY FACTORS Factors implicated in posttrauma reactions can be divided into three categories: pretrauma variables, variables related to the trauma itself, and posttrauma variables. Research on pretrauma demographic variables has not identified reliable predictors of who will develop chronic PTSD with one exception: women are somewhat more likely to manifest PTSD than men after experiencing a similar trauma. In contrast, it appears that poor psychological and social functioning prior to the trauma renders the individual vulnerable to developing chronic symptoms. For instance, prior hospitalization and a history of drug abuse were found to be associated with a more severe posttrauma reaction. Also, a history of traumatic events in childhood or adulthood predicts a more severe response to a new trauma. The nature of the trauma itself also appears to affect recovery. First, traumas differ in their likelihood of producing PTSD; rape, for example, is more likely to produce persistent symptoms than a natural disaster. Second, given a specific trauma (e.g., rape), injury and perceived threat of death produce more severe and persistent reactions. Several posttrauma factors have been found to exacerbate symptoms. It appears that dissociation (emotional numbing, amnesia, depersonalization) shortly after a trauma hinders recovery. Also, on average, assault victims who exhibit more severe initial reactions to the trauma also show more symptoms later on.

Thus, individuals seem to differ in how strongly they are affected by a similar trauma, and their initial reaction is associated with later psychopathology. Evidence on the role of social support as facilitating or hindering recovery is equivocal. It seems that negative reactions from others, such as blame, increase posttrauma psychopathology, but, unfortunately, positive reactions do not show the expected positive effects. Excessive anger or guilt after the trauma also appears to block readjustment. Additional longitudinal research on the factors that promote resilience to trauma are clearly needed.

V. CONCOMITANT PROBLEMS FOLLOWING TRAUMA Traumatized individuals not only exhibit ASD or PTSD symptoms, but also depression, substance abuse, anxiety, dissociation, and physical health problems. The rate of use and abuse of drugs and alcohol, including nicotine, in traumatized individuals is higher than in the general population. There are at least two explanations for this finding. First, traumatized individuals may choose to cope with their symptoms by increasing substance use. Second, substance abuse may increase the risk of being exposed to a traumatic experience. [See SUBSTANCEABUSE.] Many individuals report symptoms of depression after a traumatic event, such as sadness, lack of energy, diminished interest in leisure activities, hopelessness, sleeplessness, and eating disturbances. Although some of these symptoms overlap with the defining symptoms of PTSD (e.g., markedly diminished interest in activities), the two disorders are separate entities and both can develop independently as a response to a traumatic experience. [See DEPRESSION.] The incidence of comorbid anxiety disorders is also elevated among individuals with PTSD. For example, lifetime comorbidity of panic disorder in Vietnam veterans with PTSD was 21% in females and 8% in males, versus 1.5 to 3.5% in the general population. The lifetime prevalence of obsessive-compulsive disorder was found to be 13% in females and 10% in males, as compared with 2.5 % in the general population. [See OBSESSIVE-COMPULSIVEDISORDER; PANIC

ATTACKS.] There is a greater frequency of physical health prob-

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lems among trauma victims than in the general population, especially among those who develop chronic PTSD. Trauma victims have higher rates of gastrointestinal disorders and pelvic or abdominal pain, and visit the doctor more often than the general population. In the aftermath of rape and child sexual abuse, gynecological and psychosexual problems such as vaginal discharge, dysmennorhea, dyspareunia, vaginismus, and pelvic pain have also been noted.

VI. THEORIES ON THE DEVELOPMENT AND MAINTENANCE OF PTSD Reactions to trauma have long captured the interest of theorists of psychopathology. Janet's 1889 theory of reactions to trauma has influenced both early and contemporary conceptualizations. Janet proposed that when confronted with a traumatic event that besieges the victim with an overabundance of intense thoughts and feelings, too numerous or intense to integrate, some individuals selectively attend away from the trauma to trauma-irrelevant thoughts and feelings. Thus, ideas related to the trauma remain split off or dissociated from normal consciousness and become "fixed." Although out of consciousness, these "fixed ideas" remain part of the victim's ideational content, and therefore continue to exert influence over his or her thought, mood, and behavior in the form of fragmented reliving of the trauma such as visual images, somatic states, emotional conditions, or behavioral reenactment.

A. Psychoanalytic Theories Freud wrestled with understanding the influence of traumatic experiences on the individual's psyche. In early writings, he was influenced by Janet's theory on the strength of the emotional reactions that are produced by a traumatic experience and that force the victim to become fixated on the trauma. Later, Freud abandoned the dissociation view and proposed that the persistence of trauma reactions reflects an association between the traumatic event and childhood repressed conflicts, ideas, or impulses, and the efforts to prevent conscious awareness of them. He also coined the concept of "repetition compulsion" to explain trauma reexperiencing, proposing that because of the need to keep it away from consciousness, the individual is forced to repeat aspects of the trauma as a

contemporary experience rather than as a memory of it. Influenced by World War I experiences, Freud refocused on the external reality, and, in the spirit of Janet, viewed the emotional upheaval generated by the trauma as the source of traumatic neurosis. He suggested that the intensity of the trauma, the inability to find conscious expressions for it, and the unpreparedness of the individual cause a breach to the stimulus barrier and overwhelm the defense mechanisms. More recent theorists have proposed that the developmental level and ego resources available to the victim are central to the manner in which the trauma is experienced and to the production of symptoms. For instance, a young child, easily overwhelmed and flooded with emotion, may experience complete helplessness in the face of trauma, whereas a mature adult would be more likely to respond through emotional numbing and cognitive constriction. Psychoanalytic theorists and practitioners focus on the need to help the victim acknowledge and bear the trauma and the resulting psychic damage, and develop coping mechanisms such that the memories of the trauma are incorporated into his or her current experience.

B. Cognitive and Behavioral Theories Several schools of thought inspired cognitive-behavioral theories of PTSD. The first is learning theory, which explains PTSD symptoms in terms of instrumental and classical conditioning. The learning model that most directly influenced cognitive-behavioral treatments (CBT) aimed at anxiety reduction was Mowrer's two-factor theory. First, Mowrer proposed that fear is acquired through classical conditioning, where a neutral stimulus comes to evoke fear through its pairing with an aversive stimulus. Applying this theory to explain PTSD symptoms, neutral stimuli (e.g., supermarket) that were present during the trauma are presumed to acquire the ability to elicit fear through their associations with the danger stimuli (e.g., gun). Through the processes of generalization and second-order conditioning, stimuli similar to those present during the trauma also come to evoke fear. For instance, the stimuli all men, being alone, and the word rape can all acquire the capacity to cause anxiety. In Mowrer's second stage, avoidance behavior is established through the process of operant conditioning. That is, an individual learns to reduce trauma-related anxiety through avoidance of, or escape from, the feared stimuli. Escape and avoidance

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behaviors are negatively reinforced because avoidance diminishes the aversive fear state. Cognitive-behavioral therapy of PTSD has also been influenced by cognitive theory. Cognitive theory assumes that the interpretation of events, rather than events themselves, underlies emotional reactions. Accordingly, an event can be interpreted in different ways and consequently can evoke different emotions. Aaron Beck and colleagues suggest that trauma victims who manifest chronic persistent anxiety are unable to discriminate between safe and unsafe signals, and consequently their thinking is dominated by the perception of danger. They also suggest that traumatic fear can be maintained through a sense of incompetence to handle stressful events. Other cognitive theorists have postulated that cognitive schemas are disrupted after victimization. A schema is a meaning structure that guides the perception, organization, and interpretation of incoming information. Common to these theories is the supposition that a traumatic experience requires cognitive modification and that such modification is accomplished by assimilation and accommodation. Accordingly, the victim must either assimilate the traumatic experience into preexisting schemas, or, more often, change schemas to accommodate the traumatic experience. In her 1992 book, Janoff-Bulman took the position that people in general hold the assumptions: "the world is benevolent, the world is meaningful, and self is worthy," and these assumptions are incompatible with a traumatic experience. Building on Janoff-Bulman's ideas, other theorists suggest that the following areas are of particular relevance: safety, dependency/trust of self and others, power, esteem, intimacy, and independence. Coming from the psychoanalytic tradition, Horowitz integrated psychoanalytical and information processing notions in his 1986 book, suggesting that people have a basic need to match trauma-related information with their "inner models based on old information." The process of recovery entails the repeated revision of both trauma-related information and the inner models until they agree, which Horowitz referred to as the "completion tendency." Foa and Kozak integrated cognitive and learning theories to explain the development and maintenance of pathological anxiety in what they called emotional processing theory. In their 1986 paper, fear is conceived as a cognitive structure or a program for escaping danger which includes representations of fear

stimuli, fear responses, and their meaning. Pathological fear, they suggested, is distinguished from normal fear in that it includes erroneous associations and evaluations. Emotional processing theory views anxiety disorders as representing distinctive fear structures in memory, and the persistence of anxiety symptoms is conceived as reflecting impairment in emotional processing. Accordingly, PTSD is construed as reflecting a fear memory that contains erroneous associations and evaluations, whereas a normal trauma memory reflects associations and evaluations that better match reality. First, a pathological PTSD structure contains excessive response representations that are reflected in the PTSD symptoms. Second, this structure includes erroneous stimulus-stimulus associations that do not accurately represent the world. For example, the pathological fear structure of a woman who was raped at gunpoint by a bald man would contain an association between "bald men" and "gun." In reality, however, bald men are not more likely to carry guns or to rape than men with a full head of hair. Third, the structure also includes erroneous associations between harmless stimuli such as "bald," "home, .... suburbs," and the meaning of "dangerous." Being raped one time while at home in the suburbs does not tangibly increase the chance of encountering violence in that environment. Fourth, the structure includes erroneous associations between harmless stimuli and escape or avoidance responses. For example, the victim who was raped by the bald man would tend to run away from such men. In reality, however, running away from "bald men" is not likely to enhance safety. These erroneous associations would lead to mistakenly interpreting the world as entirely dangerous. Another set of erroneous associations and evaluations is the interpretation of the victim's response representations. It is thought that the victim's responses during and after the trauma, and in particular the PTSD symptoms, are interpreted to mean selfincompetence. In summary, emotional processing theory hypothesizes that two major pathological concepts underlie PTSD: the world as entirely dangerous, and the self as entirely inept.

C. PsychobiologicalApproaches Psychophysiological, neurohormonal, neuroanatomical, and immunological changes have been observed

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in animals exposed to extreme stress and in trauma victims who developed PTSD (van der Kolk, McFarlane, & Weisaeth, 1996). These changes have been hypothesized to disregulate responses to incoming information and to inhibit successful processing of traumatic memories. The normal stress response upon exposure to a high-magnitude stressor is a complex neurohormonal response, including the release of catecholamines (e.g., epinephrine and norepinephrine), serotonin, endogenous opioids, and hormones of the hypothalamus, pituitary, or adrenal gland (e.g., cortisol, vasopressin, oxytocin). Normally, the introduction of a stressor produces intense and rapid stress responses, and these dissipate quickly after the removal of the stressor. However, after prolonged exposure to stress, the stress responses become disregulated. Theorists propose that PTSD reflects a failure to regulate autonomic reactions to stimuli such that the individual either experiences hyperreactivity or "shutting down" and emotional numbing. Individuals with PTSD show hyperreactivity, as measured by heart rate, skin conductance, and blood pressure, in reaction to reminders of traumatic events. This disregulation of the emotional and physiological responsiveness occurs with specific reminders of the trauma as well as in reaction to intense but neutral stimuli, signifying a loss of stimulus discrimination. In addition, the individual may come to fear his or her emotional reactions because of being able to do little to control them. Neurohormonal changes in individuals with PTSD have also been found. First, prolonged stress causes depletion of the noradrenergic system, such that receptors become hypersensitive to any new release of norepinephrine. This noradrenergic hyperreactivity is linked to the increased arousal and startle of PTSD. The high levels of norepinephrine are proposed to inhibit the release of corticotrophin-releasing hormone and thereby inhibit the entire hypothalamic-pituitaryadrenocortical axis. This inhibition, in turn, produces a deficiency in endogenous opioids. Some theories postulate that the reexperiencing symptoms of PTSD cause a burst in the release of endogenous opioids and therefore make up for this deficiency. These endogenous opioids are thought to produce an artificial numbing or calmness, another hallmark of PTSD. Additional theories propose that cortisol responses are lowered in retraumatized individuals and that serotonin levels may decrease in response to prolonged inescapable stress.

In addition to psychophysiological and neurohormonal factors, specific brain abnormalities have recently been detected in individuals with PTSD. One system that is implicated in the disorder is the limbic system, which is thought to function in memory and in emotional reactions to incoming stimuli. One area in the limbic system, the hippocampus, is presumed to record spatial and temporal aspects of experiences in memory. Researchers have noted decreased hippocampal volume in trauma victims with PTSD compared with those without PTSD. One possible explanation for this finding is that individuals with smaller hippocampuses are more likely to develop PTSD; a more likely interpretation of these results is that increased cortisol activity causes shrinkage, because cortisol is toxic to the hippocampus. A second area in the limbic system, the amygdala, also appears to be altered in individuals with PTSD. The amygdala is thought to assign meaning to incoming stimulation by integrating memory images with emotional experiences associated with those memories, guiding emotional behavior. A single intense stimulation of the amygdala appears to alter the limbic physiology such that a "kindling" effect occurs. That is, the behavior that follows may be predominantly either "fight" or "flight," and a pattern of conditioned behavior is set up such that there is limited processing of incoming information before the response is initiated.

VII. PSYCHOLOGICALAND PHARMACOLOGICALINTERVENTIONS Several psychological interventions have been used with trauma victims, including supportive counseling individually or in groups, brief dynamic psychotherapy, hypnotherapy, pharmacotherapy, and cognitivebehavioral therapy. As recently reviewed by Foa and Meadows, although a variety of psychological interventions are used routinely with trauma victims, controlled outcome studies have tended to focus on cognitive-behavioral treatments such as systematic desensitization, exposure, and anxiety management. Nevertheless, hypnotherapy and psychodynamic therapy have also shown promise in the few studies examining their efficacy.

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A. Early Interventions The popular supposition among trauma theories is that for recovery to occur after a traumatic experience, special processing efforts should take place. This view has prompted the development of early intervention programs. These programs have focused on education, debriefing after trauma, and training professionals at risk (e.g., police). Usually, "critical incident stress debriefing" is conducted in groups, such as emergency workers, and focuses on education about common reactions to traumatic experiences, encouraging trauma victims to process their experiences in a group setting. Although such programs have become routine in many places, little is known about their efficacy. In fact, some experts have raised concerns that such programs could interfere with rather than facilitate the natural recovery process. The recognition that victims who exhibit severe reactions immediately after the trauma are more likely to develop chronic dysfunction has prompted researchers to implement interventions that aim to prevent chronic PTSD. Foa and colleagues conducted a study to compare PTSD severity of female assault victims, who received a brief prevention program (four individual therapy sessions), to that of victims who underwent an assessment procedure. Victims who received the brief prevention program had less severe PTSD and depressive symptoms 2 months after the assault. Clearly, more studies of this type are needed before confidence in prevention efforts can be established.

B. Cognitive-Behavioral Therapies Currently, five cognitive-behavioral interventions are in use for PTSD: Prolonged Exposure, cognitive therapy, Stress Inoculation Training, Cognitive Processing Therapy, and Eye Movement Desensitization and Reprocessing.

I. Prolonged Exposure (PE) This is a set of procedures that involves confrontation with feared stimuli, either in vivo or in imagination. With PTSD, exposure therapy typically includes repeated reliving of the traumatic event in imagination and actual confrontation with feared situations and objects that have been avoided because they are reminders of the trauma but are not intrinsically dangerous. As discussed earlier, the theoretical basis of PE lies

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in learning and emotional-processing theories. Foa and Kozak have proposed that successful therapy involves correcting the pathological elements of the fear structure, and that this corrective process is the essence of emotional processing. They further suggest that regardless of the type of therapeutic intervention used, two conditions are required for fear reduction. First, the fear structure must be activated through introduction of fear-relevant information. If the fear structure is not activated (fear is not evoked), the structure would not be available for modification. Second, during exposure, information that is incompatible with the existing pathological elements (e.g., fear reduction) must be provided so that the pathological fear structure can be corrected. Specifically, exposure researchers hypothesize that repeated reliving promotes several cognitive changes. First, it promotes habituation of anxiety associated with the trauma memory, and this habituation disconfirms the victim's erroneous belief that anxiety will stay forever and therefore lead to disastrous consequences. Second, reliving promotes discrimination between "remembering" the trauma and "encountering" it again, thus reinforcing the realization that remembering itself is not dangerous. Third, repeated exposure promotes differentiation between the trauma and similar but safe situations, disconfirming the idea that the world is extremely dangerous. Fourth, it promotes the association between PTSD symptoms and a sense of mastery, rather than incompetence. Finally, repeated recounting of the trauma narrative helps to organize the narrative and thereby to facilitate the integration of the trauma memory. Several controlled studies on exposure have shown their usefulness in treating PTSD. Whereas studies on veterans showed only modest improvement, two studies with female rape victims showed more improvement. Foa and colleagues found that exposure (imaginal and in vivo) was effective in eliminating PTSD in 55% of rape victims with chronic PTSD compared with 45% of those who received supportive counseling. Superior results were found in a second study: about 70% of victims who received Prolonged Exposure lost their PTSD diagnosis, and none of the women in a wait-list group lost their diagnosis. These treatment effects were maintained at 6-month follow-up.

2. Stress Inoculation Training (SIT) This intervention consists of training victims to handle anxiety with several skills for anxiety management:

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relaxation, thought stopping, assertiveness, cognitive therapy, coping self-statements, and guided imagery. Although the direct goal of anxiety management techniques is to teach patients techniques to manage their anxiety, the successful acquisition of such techniques can have indirect effects on the victim's schemas of self and the world. Specifically, the victim's experience of being able to control the anxiety fosters a more positive self-image and thereby modifies the perception of the world as overwhelmingly dangerous. Several studies point to the efficacy of this program used alone or in combination with other techniques. For example, the two studies on rape victims reported earlier found that SIT significantly reduced PTSD, to a degree comparable to that of exposure. Researchers believed that if PE and SIT are quite, but not completely, successful in ameliorating PTSD symptoms, a program that combined these two treatments would yield superior results. However, research does not support this view: combined programs were helpful for female assault victims, but not more than exposure or stress inoculation alone.

3. Cognitive Therapy Cognitive techniques are often incorporated into anxiety management programs that teach patients to examine and change systematically maladaptive thoughts that can lead to negative responses. Cognitive therapy involves the use of discourse, in which the patient is taught to identify the beliefs underlying the fear, to examine whether they are distorted or accurately reflect reality, and to replace mistaken or dysfunctional beliefs with more realistic, functional ideas about the ability of the patient to cope with stress and the dangerousness of the world. One possible benefit of cognitive restructuring is that it addresses directly beliefs underlying emotions other than fear, such as anger and guilt. Early investigations of this technique revealed some promise in the use of this therapy to reduce symptoms of PTSD in rape victims.

4. Cognitive Processing Therapy (CPT) Another cognitive-behavioral program called Cognitive Processing Therapy is described in Resick and Schnicke's 1992 book. It involves cognitive restructuring and exposure through writing about the trauma. The cognitive therapy is geared toward correcting maladaptive cognitions associated with rape, such as power, safety, and esteem. In one study, on the aver-

age, victims who received CPT reported 40% symptom reduction, and these gains were maintained over time. More studies are needed to establish the efficacy of this relatively new treatment.

5. Eye Movement Desensitization and Reprocessing(EMDR) This therapy, described by Shapiro in 1995, is a form of exposure with a cognitive emphasis, accompanied by guided eye movements. The studies that have evaluated the efficacy of this treatment produced equivocal results. Some show good results, but others show no improvement. Because these studies have many methodological problems, it is difficult to determine the validity of the findings. Further well-controlled studies are needed before a definite conclusion about the value of EMDR can be made.

C. Pharmacotherapy Many medications have been used for the treatment of PTSD, but only a few have been systematically studied. Most of these have used male combat veterans, and thus the efficacy of pharmacotherapy for other traumatized populations is largely unknown. Tricyclic antidepressants have been used in an attempt to reduce locus coeruleus overactivity and noradrenergic disregulation found in PTSD, with equivocal results. Amitriptyline and imipramine have shown modest reductions in PTSD symptoms in comparison with placebo in double-blind studies with male veterans. In contrast, desipramine failed to show efficacy. One study of fluoxetine, a selective serotonin reuptake inhibitor used to regulate serotonergic dysfunction in individuals with PTSD, found it to be effective in reducing symptoms of PTSD, especially in trauma victims other than Vietnam veterans. Other medications that have been tested include anticonvulsants such as carbamazepine and valproic acid; but no double-blind studies have been conducted to date. Beta-adrenergic blockers such as propanolol have shown promise in reducing aggressivity and arousal symptoms in open studies, and alpha2adrenergic agonists, such as clonidine, appear to be effective through their suppression of locus coeruleus activity. Finally, benzodiazepines have been widely used to suppress anxiety and are believed to reduce PTSD symptoms by reducing limbic system kindling and reversing neurochemical changes in the locus coeruleus

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and hypothalamus. However, the rebound anxiety and withdrawal symptoms associated with benzodiazepines can be problematic. In summary, most of our knowledge about efficacy of pharmacotherapy for PTSD is confounded by the restricted samples used in existing studies. Most were conducted on Vietnam veterans, whose symptoms are particularly resistant to all types of treatments, and therefore the present results may underestimate the efficacy of this treatment.

D. Hypnotherapy and PsychodynamicPsychotherapy Hypnotherapy uses heightened concentration and focused attention to facilitate treatment related to trauma. It is based on the supposition that individuals with PTSD are unknowingly entering trance states when they reexperience the trauma and that hypnotherapy can help them learn how to control their trance states and digest the dissociated traumatic experience in a controlled manner. One study found hypnosis to be as effective as psychodynamic psychotherapy and a type of exposure called systematic desensitization. More studies of this technique are needed before conclusions can be drawn about the usefulness of hypnotherapy. [See HYPNOSIS AND THE PSYCHOLOGICAL UNCONSCIOUS.]

Psychodynamic psychotherapy has also been used to help individuals recover from trauma. It focuses on intrapsychic conflict about the trauma rather than on resolution of specific symptoms of PTSD. The methods used are in some respects similar to those used in cognitive-behavioral therapy, as these interventions focus on helping the victims process the traumatic experience and on teaching them how to tolerate anxiety. Both individual and group therapies have been

used, and some preliminary studies suggest the utility of these interventions.

BIBLIOGRAPHY American Psychiatric Association. (1994). Diagnostic and statistical manual (4th ed.). Washington, DC: American Psychiatric Press. Davidson, J. R. T., & Foa, E. B. (Eds.). (1993). Post-traumaticstress disorder: DSM-IV and beyond. Washington, DC: American Psychiatric Press. Foa, E. B., & Kozak, M. J. (1986). Emotional processing of fear: Exposure to corrective information. Psychological Bulletin, 99, 20-35. Foa, E. B., & Meadows, E. A. (1997). Psychosocial treatments for post-traumatic stress disorder: A critical review. In J. Spence (Ed.), Annual review of psychology. Palo Alto, CA: Annual Reviews, Inc. Foa, E. B., & Riggs, D. S. (1993). Post-traumatic stress disorder in rape victims. In J. Oldham, M. B. Riba, & A. Tasman (Eds.), American psychiatric press review of psychiatry (Vol. 12, pp. 273-303). Washington, DC: American Psychiatric Press. Horowitz, M. J. (1986). Stress response syndromes (2nd edition). Northvale, NJ: Jason Aronson, Inc. Janet, P. (1889). L'Automatisme psychologique. Paris: Felix Alcan. (Reprinted 1973, Paris, Societe Pierre Janet.) Janoff-Bulman, R. (1992). Shattered assumptions: Towards a new psychology of trauma. New York: Free Press. Kessler, R. C., Sonnega, A., Bromet, E., Hughes, M., & Nelson, C. B. (1995). Post-traumatic stress disorder in the National Comorbidity Survey. Archives of General Psychiatry, 52, 10481060. Resick, P. A., & Schnicke, M. K. (1992). Cognitive processing therapy for sexual assault survivors: A treatment manual. Newbury Park, CA: Sage. Shapiro, F. (1995). Eye movement desensitization and reprocessing: Basic principles, protocols, and procedures. New York: Guilford Press. van der Kolk, B. A., McFarlane, A. C., & Weisaeth, L. (Eds.). (1996). Traumatic stress: The effect of overwhelming experience on mind, body, and society. New York: Guilford Press. World Health Organization. (1993). ICD- I O: The ICD- I O classification of mental and behavioural disorders: Diagnostic criteria for research. Geneva, Switzerland: Author.

PremenstrualSyndrome(PMS) Katharina Dalton University College Hospital, London, U.K.

I. II. III. IV. V. VI. VII. VIII.

Introduction Symptoms Signs Characteristics Diagnosis Diagnostic Pointer Checklist

confusion, or hallucinations), but may not last longer than 14 days, and there must be complete absence of all symptoms for at least 7 days before ovulation. The symptoms should be severely disabling and interfering with work capacity and/or social life, thus excluding the valuable warning symptoms marking the approach of menstruation. Occasionally only one symptom is present, but more frequently the women are polysymptomatic.

Etiology

Treatment

Follicular Phase Covers the days from menstruation until ovulation. Intermenstruum Covers those days of the menstrual cycle that are not included in the paramenstruum. Luteal Phase The days from ovulation until menstruation. Menstrual Cycle Measured from the first day of menstruation until the day before the next menstruation. Paramenstruum The four days immediately before menstruation and the first four days of menstruation. P r e m e n s t r u u m The days from ovulation until menstruation.

I. INTRODUCTION Before normal bodily functions there are valuable, warning sensations. For instance, these sensations inform the individual when the bladder is full, or when the bowels need emptying. There is a nasal tickling before sneezing, and thirst when dehydrated. In the same way there are valuable, warning sensations before menstruation. These sensations should not be considered premenstrual symptoms, but this does account for the findings of some surveys of an incidence of PMS exceeding 90%. On the other hand there are women whose premenstrual symptoms are disabling, interfering with normal working and social life, they suffer from PMS and are deserving of consideration and treatment. A normal menstrual cycle varies from 21 to 35 days, and is considered to be regular if variations, cycle to cycle, do not exceed 4 days. Normal menstruation may last from 2 to 8 days, with the bleeding being pink, bright red, or dark brown. The normal

PREMENSTRUAL SYNDROME (PMS) is the recurrence of disabling physical or psychological symptoms occurring in the premenstruum with complete relief in the postmenstruum. PMS has a precise definition requiring recurrence of the same symptoms at the same phase of the cycle for at least the last three menstrual cycles. The symptoms may last less than 1 day (e.g., epilepsy, migraine,

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Premenstrual Syndrome(PMS)

age of menarche is from 12 to 14 years, but the age does vary with race, economic, and social factors. Early menarche is usual in the blind, deaf, and congenitally physically handicapped (hydrocephalus, spina bifida, dislocated hip). The normal age of menopause is between 45 and 55 years, therefore if menstruation stops before the age of 45 years, or if bleeding becomes heavy then gynecological examination is indicated. Cyclical symptoms may occur for up to 2 years before the menarche, and up to 2 years after the menopause. Following recovery from the trauma of hysterectomy or bilateral oophorectomy, cyclical symptoms return.

II. SYMPTOMS There are no unique symptoms; all symptoms also recur in men, children, and postmenopausal women, and almost all organs are involved. The diagnosis depends entirely on the timing and severity of symptoms. Even women with diagnosed PMS may, under certain circumstances, suffer their typical premenstrual symptoms at other times of their menstrual cycle. During pregnancy, when menstruation is temporarily abolished, PMS disappears, and years later the patient will usually recall pregnancy as the time of exceptional good health. However, PMS often returns with increased severity after the pregnancy, especially if complicated by preeclampsia, postnatal depression, or puerperal psychosis. Cyclical symptoms disappear temporarily when ovulation is stopped with estrogen implants, Danazol, or GnHR agonists, but reappear if progestins are used to cause withdrawal bleeding. Cyclical monthly symptoms reappear after recovery from the trauma of hysterectomy or oophorectomy, which may take up to 3 years. More than 150 symptoms have been described, of which 33% are psychological. These include tension (with the triad of depression, irritability and lethargy), mood swings, anxiety, crying, self-mutilation, as well as psychosis with delusions, hallucinations, and paranoia. Common behavioral symptoms include food cravings, decreased motivation, increased alcohol urges, social isolation, increased libido, insomnia or hypersomnia, clumsiness and forgetfulness. Among the common physical symptoms are headaches, breast tenderness, asthma, sinusitis, epilepsy, skin lesions, conjunctivitis , and joint and muscle pains.

Symptoms never exceed 14 days, but may only last a few hours, for example, panic attacks, psychosis, epilepsy, migraine. Symptoms always increase in severity as menstruation approaches; thus, symptoms that occur a week before the onset of menstruation and then disappear are unlikely to be repeated at the same phase of the cycle month after month. Occasionally, symptoms start during menstruation. This occurs in women who have a slight menstrual bleed for a few days before the full menstrual flow, when symptoms are occurring in the physiological "premenstruum," although recorded as chronological "menstruation." A single severe symptom (e.g., epilepsy, migraine, aggressive outburst, self-mutilation) may occur in the morning, with menstruation starting in the evening, in which case the premenstrual event is recorded as occurring on the first day of menstruation. This is the reason most sociological surveys (accidents, criminal offenses, examination results, hospitalization) compare incidents during the paramenstruum with the other days of the menstrual cycle. Typically, patients are polysymptomatic, with six or more symptoms recurring during the premenstruum, and with symptoms tending to span more than one medical speciality. Neurologists, rheumatologists, dermatologists, otologists, chest physicians, urologists, and gastroenterologists are also frequently involved. Many workers prefer to limit the initial daily recording to the three priority symptoms, as when those are satisfactorily treated the other minor symptoms tend also to disappear. Depression is a common PMS symptom, but differs from major depression in that the timing is predictable and shorter, never more than 14 days, and is followed by days of complete normality. It is characterized by weight increase with food cravings and binges, in contrast to the weight loss and diminished appetite of typical depression. Those with PMS have a yearning for sleep and would like to stay in bed all day, as opposed to the early morning waking and restlessness of other depressives, who get up, wander round the house, make tea or even do the housework. Marked irritability and mood swings accompany the depressive days but are absent in the follicular phase. Nulliparous women may have nymphomania during the premenstruum, which differs from the complete loss of libido in other depressions. [See DEPRESSIOtq.] With PMS irritability there may be loss of self-

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control resulting in verbal abuse with shouting, yelling, and swearing, as well as violence with banging, slamming, throwing, and hitting. She may become impatient, irrational, illogical, hostile, and paranoidal. Her behavior may lead to criminal offenses for damage to property, grievous bodily harm, or attempted or actual murder. A cry for help during the premenstruum may be an attempted suicide, hoax telephone calls, or arson. PMS-related crimes tend to be committed alone, to the surprise of those near to them at the time; they do not appear to be premeditated; they are without apparent motive; and there is usually no attempt to escape detection. The headaches tend to be hemicranial or centered in, above, below, or behind one or both eyes, and they may describe the eye as being "stoney hard." Migrainologists recognize "tension headaches" as being occipital, with radiation of pain down the neck and across the shoulders, but this is not the most common type of PMS headache.

III. SIGNS There are few signs of PMS, although a partner may recognize darkening under and puffiness of the eyes. He is unlikely to recognize excessive weight gain during the premenstruum, unless alerted by the patient, for healthy normal women may also experience weight swings of up to five pounds each cycle. If one records daily blood pressure readings, there may be paramenstrual swings about 20 mm Hg in both the diastolic and systolic pressure compared with intermenstrual readings, but not reaching hypertensive levels. Those complaining of headaches centered on the eyes may, with daily recording, note an increase in intraocular tension of about 5 mm Hg during the paramenstruum compared with the intramenstruum, occurring both in those whose intraocular tension is normal and those with early or treated glaucoma. There may be proteinuria in catheter specimens of urine during the paramenstruum compared with the intramenstruum. The day-by-day changes in severity of a patient with asthma are easily shown by the peak flow meter. Investigation of these signs in individuals are not always necessary, although they are interesting findings for research.

IV. CHARACTERISTICS These characteristics of PMS are helpful at the initial screening of women who have not yet started regular recording of symptoms. If present they are accepted in English law as sufficient reason to delay sentencing or court appearances until a positive diagnosis can be made. PMS women are normal on gynecological examination. They have regular and painless menstruation, with normal loss, normal blood levels of estrogen, follicle stimulating hormone, luteinizing hormone, and prolactin, and do not have infertility problems. Cyclical symptoms may recur for 2 years before menarche, continue for about 2 years after the natural menopause, and also restart up to 3 years after recovery from the trauma of hysterectomy or oophorectomy. Pain with menstruation is n o t a presenting PMS symptom and always requires further investigation. Common causes of premenstrual and menstrual pain include spasmodic dysmenorrhea, which only occurs in ovulatory cycles and so disappears with the contraceptive pill; endometriosis, which is accompanied by dyspareunia and pain on moving the uterus at vaginal examination; and pelvic inflammatory disease, which causes pain throughout the cycle that is worse in the premenstruum and is usually accompanied by a vaginal discharge. PMS tends to start at times of hormonal uph e a v a l - 3 2 % at puberty and 33% after pregnancy-while others start on stopping the contraceptive pill, after amenorrhea (e.g., due to anorexia, head injury), after sterilization, and after unilateral oophorectomy. These are also the times when PMS may increase in severity. PMS follows recover from preeclampsia and postnatal depression in 80% of cases. Symptoms are increased at times of stress. One frequently hears a woman describe how she had a difficult time with PMS at puberty, but that it then eased for many years until after a pregnancy, or when she was under stress from an unsatisfactory relationship, a bereavement, redundancy, or a financial problem. PMS women have difficulty in tolerating progestin medication, whether administered orally, transdermally, or as long-term injections, in contraceptive pills, or HRT, for progestins lower the blood progesterone level. They have difficulty in tolerating long intervals without food, and easily become shaky, tired,

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anxious, or aggressive at such times. Symptoms tend to increase if there is sleep deficit, and they are poor jet-lag travelers. While they can tolerate normal alcohol intake during the intermenstruum, they may have uncontrollable alcohol urges premenstrually. Regardless of their poor premenstrual behavior, it is then that their libido is increased and may reach nymphomanic proportions. Monthly weight swings of up to five pounds occur in normal, healthy women, but during their adult years PMS women experience weight swings exceeding 28 pounds between their highest nonpregnant weight and their lowest weight since the age of 16 years. In common with most hormonal diseases a positive family history is frequent, with three or four generations suffering. This genetic factor has been demonstrated in twin studies, where if one monozygous twin suffers from PMS the other will also be suffering, whereas in female dizygous twins the incidence is similar to that found in sisters. Similarly, adoption studies have shown a statistically significant difference between the low incidence of PMS in mothers of adopted daughters compared with the high incidence in mothers of biological daughters. Finally, PMS can occur together with any chronic condition (e.g., schizophrenia, Down's syndrome, congenital mental handicap, rheumatoid arthritis, fibromyalgia, bronchitis, tuberculosis), in which case treatment of PMS will only improve premenstrual symptoms and not the underlying condition.

V. DIAGNOSIS The diagnosis of PMS depends on prospective, daily recording by the patient or responsible person of the days of symptoms and days of menstruation for a minimum of 2 months. This is easier when recording a specific symptom with a marked onset and end (e.g., migraine, new acne papules, epilepsy, sore throat), but it is more difficult when considering symptoms present throughout the cycle and while trying to record an increase or decrease in severity (tiredness, clumsiness, forgetfulness). Ideally, no more than the three most severe symptoms should be recorded; otherwise it makes the patient unduly introspective, or recording is made without full consideration. Therapists, including males working with PMS, should try to record

their symptoms daily for at least 2 months, for only then will they appreciate the difficulties of recording after a late night party, on holiday, or during a stressful event, and they will then understand the need to keep the recording as simple as possible. A simple menstrual chart, which gives the diagnosis of PMS at a glance, is shown in Table I. The patient is advised to keep it by her bed and to mark it with a pen each night before retiring. Many daily rating scales and visual analog scales have been developed; some demand daily body temperature and body weight, which may be helpful for clinical trials of mild to moderate cases, but will never be completed by desparate women demanding immediate help. Many daily symptom charts list some 30 different symptoms that patients may never have considered, but that they can easily manipulate. Questionnaires are of limited value, as the more often one is used, the less attention the patient pays in completing it. All too often patients completing certain questionnaires tend to confuse menstrual pain with PMS. In severe cases the partner, or other responsible person, may be able to note the days when symptoms are present. Otherwise it may be necessary to gather particulars of precise dates of specific incidents from other sources such as hospital emergency rooms in cases of suicide attempts or the suturing of slashed wrists; from police in relation to domestic violence or alcohol abuse; from prison for indicipline, causing a disturbance, or aggressive attacks; from schools or community centers where records are kept of disturbances covering instances of bodily harm or arson attempts; and from college registers showing absences. No blood tests are diagnostic of PMS. In particular progesterone blood level is of no importance, as progesterone level only rises in the luteal phase in ovular cycles, but PMS also occurs in anovular cycles. Progesterone is secreted in spurts, and is lower after meals. The sex hormone binding globulin (SHBG) level is frequently low in PMS, but the estimation must be done when the patient has been free of all medication (including analgesics, vitamins, minerals, laxatives) for at least 7 days and free of hormone medication (including the pill and HRT) for at least 1 month. Furthermore, it is not reliable in those with thyroid disorder, liver disease, obesity, or hirsuitism, and the blood must be kept frozen until analyzed. A ferritin estimation is worthwhile and is often sur-

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PremenstrualSyndrome(PMS)

Table I

Menstrual Charts Jan.

Feb.

Mar.

Oct.

Nov.

Dec.

X X X X

I

X X H

X X

H

MX

H

hM 1

MI

MX

H

M

MH

M

Mh

M

M

M

M M M M

1 X = tension hH = headache M = menstruation

prisingly low in PMS patients, w h o otherwise have a good hemoglobin level and normal hematology. It is a reflection of their iron store, and low levels are found in those w h o habitually allow their blood glucose lev-

els to drop. Restoring the patient's ferritin level to more than 3 0 / z g / l by giving an iron supplement or improving the diet, will improve their stamina and energy level.

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PremenscrualSyndrome(PMS)

Table II Diagnostic Checklist Irrelevant/positive/negative Hormonal time of onset. H o r m o n a l time of increased severity. Painless m e n s e s (2 -vesif painful). Increased libido in premenstruum. Pre-eclampsia. Postnatal depression. Side effectwith the pill. Adult weight swing exceeding 12 kg. Food craving in the premenstruum. Alcohol urges in the premenstruum. Family history of PMS. Total % Score =

positives x 100 positives + negatives

VI. DIAGNOSTIC POINTER CHECKLIST When a 2-month menstrual record is not immediately available a diagnostic pointer checklist, compiled from the characteristics mentioned earlier, is helpful. Items are scored "positive, .... negative," and "irrelevant," while those whose presenting symptom is pain with menstruation, or dysmenorrhea, score two negatives. The total positive scores are multiplied by 100, and divided by the sum of the positives and negatives. Women with a diagnostic pointer scores exceeding 66% are likely to produce a positive menstrual chart after charting for 2 months (Table II).

VII. ETIOLOGY The many hormonal and chemical interactions, which result in PMS, are not fully understood, although many etiological theories exist. An acceptable etiological theory must be able to explain at the molecular level the following facts known to occur in PMS: 1. Psychological and physical symptoms present in the luteal phase with absence in the follicular phase. 2. Absence of symptoms and general well-being in pregnancy. 3. High incidence after pregnancy, and particularly after postnatal depression.

............

4. Inability to tolerate progestins, and their failure to relieve PMS. 5. Increased intensity of symptoms at times of stress. 6. Inability to tolerate long food gaps, and symptom relief from the "three hourly starch diet." 7. Relief from high-dose natural progesterone. 8. Symptoms occur in both ovular and anovular cycles. 9. Persistence of symptoms after recovery from the trauma of hysterectomy and oophorectomy. 10. Cyclical symptoms can occur two years before menarche and continue for two years after the natural menopause. Critical to the diagnosis is the fact that PMS occurs in the luteal phase and not in the follicular phase. Estrogen, measured in picograms, is present in the blood in varying amounts throughout the menstrual cycle. Progesterone is only present in the luteal phase, and is absent in the follicular phase; it is measured in nanograms, which is 1000 times higher than picograms; thus, fluctuations of amplitude of estrogen relative to progesterone are minimal. During pregnancy, when there is a massive increase in progesterone from the placenta, PMS eases and there is a sense of well-being. At labor, when the placenta is also delivered, the progesterone blood level falls abruptly; postnatal blues and a high incidence of postnatal depression follow. The involvement of progesterone in the etiology of PMS is supported by facts 1, 2, and 3. Molecular biologists in the last decade have further supported the hypothesis that progesterone is involved in PMS by their discovery of progesterone receptors. Progesterone receptors are compounds, found in the hundreds, in those cells that require progesterone. The task of progesterone receptors is to bind to progesterone molecules and to transport the progesterone molecules to the nucleus. Using new technology and animal studies researchers have been able to recognize some of the unique characteristics of progesterone receptors. For instance, after an initial dose of progesterone the receptors become hyposensitive and require a high dose of progesterone to stimulate them again. Progesterone receptors do not accept progestins in the same way as progesterone molecules in the presence of adrenalin, such as occurs at times of stress and at low blood glucose level, for then the progesterone recep-

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Premenstrual Syndrome(PMS)

tors function as corticosterone receptors, correcting the adrenalin balance. Thus, unless current stress can be ameliorated and low blood glucose levels avoided, the administration of progesterone will not help PMS. Progesterone receptors are widespread throughout the body, with the highest concentration in the limbic area, the center of emotion, which may explain the predominance of psychological symptoms in PMS. Other areas of high concentration of progesterone receptors are the meninges, the nasopharyngeal passages and lungs, eyes, bones, and skin, which would account for headaches, sinusitis, asthma, conjunctivitis, sties, joint and muscle pains, and skin lesions, respectively. It has recently been shown that progesterone receptors are controlled within the cells by a specific stress protein, hspg0. Thus, a fault in the functioning of progesterone receptors, or of the stress proteins controlling them, would explain facts 4, 5, 6, and 7. The function of progesterone receptors in the systemic cells, where PMS symptoms originate, occurs whether or not ovulation is occurring, thus explaining facts 8, 9, and 10. PMS women do not have hypoglycemia, but a hyperefficient lower controlling mechanism that releases adrenalin whenever the blood glucose level nears the lower optimum level. This adrenalin release mobilizes glucose in cells, which passes into the blood, correcting the low blood glucose level. However, the empty cells soon fill with water, giving the bloatedness and weight gain so familiar to PMS subjects. Adrenalin is the hormone of fight, flight, and fright, which in turns is responsible for the tension and behavioral symptoms. It is easy to negate the involvement of progesterone in the etiology by recalling that there is no evidence that progesterone blood levels are low in PMS. Recognition of the function of progesterone receptors explains why the blood progesterone level is irrelevant, and also why low-dose progesterone, as used in current double-blind placebo controlled trials is doomed to failure. It is going to be difficult to arrange double-blind controlled trials of high-dose progesterone, which also control for the avoidance of stress and of transient episodes of low blood glucose levels. Both stress and low blood glucose levels stimulate adrenalin and inhibit the action of progesterone receptors. Progesterone is formed in the adrenals by both sexes and at all ages, and is then converted to estro-

gens, testosterones, and cortisones. The exact mechanism that controls the menstrual cycle remains unknown. It is though to be in the hypothalamus, at the base of the brain. Zuspan and his colleagues, using a culture of human placental cells, have demonstrated that progesterone has an inhibitory effect on monoamine oxidase activity; in short, progesterone is a natural MAOI antidepressant. Others have unsuccessfully suggested etiological theories that do not explain the 10 facts enumerated above. These include deficiency of pyridoxine, magnesium, essential fatty acids, dietary irregularities, allergies, and thyroid dysfunction.-Most of these studies have been done on LLPPD without consideration of the characteristics of PMS. Ashby and his coworkers noted low serotonin levels in LLPPD, and several reports have appeared of the beneficial effect of the selective serotonin reuptake inhibitors (SSRIs) in PMS. The action of SSRIs on the brain cells is similar to that of progesterone on brain cells, but in other parts of the body progesterone has other effects, such as building up bones, which are not shared by SSRIs.

VIII. TREATMENT A disease with no universally accepted etiology is always subject to numerous suggested treatments, some that have never been clinically tested and others that rely on symptomatic relief of the common symptoms of PMS. If one accepts the part played by progesterone receptors then the relief of stress and the maintenance of a stable blood sugar level are two imperatives in treatment.

A. Stress Relief In the past there may have been family members or religious leaders with whom one could openly discuss the day-to-day problems that cause stress. Today, members of our nuclear societies are often unable to unburden themselves. Counsellors or therapists are needed to help PMS women understand themselves and their problems, while some may need full psychotherapy, either cognitive or behavioral. Abnormal behavior in the premenstruum may be followed by ex-

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Premenstrual Syndrome(PMS)

cessive guilt, which is best handled by a therapist. Many benefit from relaxation, stress-relieving, or assertiveness classes. Life-style changes may be needed, through stopping smoking, drugs, or excess alcohol, preventing sleep deficit, and avoiding night work. The woman may need to be advised to change from hormonal contraception, all of which contains progestins, which exacerbates symptoms. Recording of dayto-day symptoms on a menstrual chart should be continued throughout treatment to assess progress.

B. Dietary Advice Too often one finds women who ensure that their children and partners have regular food while neglecting their own. One English survey found that half of PMS women did not stop for breakfast; in fact, they unknowingly started the day with a blood glucose drop. The "three hourly starch diet" has been found to be the most effective tool in easing PMS in 68% of sufferers. Women are advised to divide their usual day's starch intake (flour, potatoes, rice, rye, oats, and corn) into six or seven portions, and have a starchy snack every 3 hours throughout the day, always within 1 hour of waking and 1 hour of retiring. The diet should be continued throughout the cycle, and other nutrients (especially proteins, fruit, and vegetables), which they normally eat, should be continued. It is worth reminding patients that when they exceed 3 hours on only one occasion it may take up to 7 days before the normal utilization of progesterone can occur. It is a simple multicultural diet, and patients soon get into the habit of always eating little and often. There should be no weight gain if the individual is eating the same amount of starch each day, but in seven portions instead of the more usual three meals. Those who are initially overweight find they lose weight as bloating is eliminated. Taking a full dietary history is essential before teaching the patient the three hourly starch diet, so any other nutritional deficiencies can be corrected. It should not be necessary to add extra vitamins or minerals, which should be available in the normal diet. In particular, vitamin B6 (pyridoxine) should not be advised now that the possibility of causing pyridoxine overdose neuropathology is recognized.

C. Symptomatic Treatment If one premenstrual symptom predominates above all others, particularly in LLPPD where 30% of the symptom may be present throughout the cycle, then individual symptomatic treatment may be preferable. This applies to those likely to benefit from selected antidepressants, anxiolytics, tranquilizers, anticonvulsants, analgesics, or muscle relaxants. It applies even more with respect to physical symptoms, where headaches, asthma, skin lesions, conjunctivitis, and sinusitis are the only PMS symptom. Here, the most effective symptomatic treatment should be used in addition to training the patient on the three hourly starch diet and counseling her on avoiding hormonal contraception. Among the antidepressants most likely to be effective in PMS are the selective serotonin reuptake inhibitors (SSRIs) or the monoamine oxidase inhibitors (MAOIs).

D. Progesterone Therapy Only a few severe sufferers of PMS require progesterone therapy; the majority will benefit from treatments already suggested. Even if progesterone is needed, the three hourly starch diet is still required. Progesterone treatment is essentially prophylactic and needs to be started before symptoms develop, so it is usually started 14 days before the next expected menstruation and it is continued until the onset of bleeding. Progesterone cannot be utilized if administered orally or transdermally. The minimal dose is 400 mg suppositories used vaginally or rectally twice daily, but this may be increased to 400 mg used 6 times daily, or progesterone intramuscularly into the buttock in doses of 50 mg or 100 mg daily. It is not possible to overdose with our present methods of administration, which cannot reach the blood progesterone levels found in mid or late pregnancy. There are no interactions with other medications. If vaginal candidiasis is present, symptoms may be exacerbated by progesterone, but today candidiasis can be treated with a single capsule of fluconazole 150 mg given to both the patient and her partner. There is anecdotal evidence of the effectiveness of progesterone in PMS in the British National Health Service Tribunal on overspending in 1958, and in individual women charged in England with serious crimes, including murder and infanticide, but the only

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Premenstrual Syndrome(PMS)

successful double-blind placebo controlled trial was that by Magill in general practice using 400 mg twice daily. All other trials using a lower dose of progesterone have been unsuccessful. Progesterone can also be used as a contraceptive in cases of severe PMS by starting with a small daily dose of progesterone 100 mg from day 8, raising to the patient's normal progesterone dose on day 14, and continuing until menstruation.

BIBLIOGRAPHY Dalton, K., & Holton, D. (1994). PMS: The essential guide to Treatment Options. London & San Francisco: HarperCollins Publishers. Dalton, K. (1984). The Premenstrual Syndrome and Progesterone Therapy (2nd ed.). London: W. Heinemann Medical Books, Ltd., and Chicago: Year Book Medical Publishers, Inc. Smith, S., & Schiff, I. (1993). Modern management ofpremenstrual syndrome. New York and London: Norton Medical Books.

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Psychopathology Keith S. Dobson and Dennis Pusch Universityof Calgary, Canada

I. II. III. IV.

Definitional Issues Categorical Models of Psychopathology Dimensional Models of Psychopathology Future Issues in Psychopathology

sive discussions about how best to conceptualize and assess abnormal behavior, and how to minimize the potentially negative influences of labeling.

I. DEFINITIONAL ISSUES

Diagnosis The process of applying consistent labels to patterns of abnormal functioning. Insanity A legal term, meaning that a person is not legally responsible for his or her actions. Mental Health The absence of psychopathology, and the positive aspects of subjective well-being, development and use of abilities, social adaptation, and achievement of goals. Mental Illness Largely synonymous with psychopathology, although implying an underlying disease or illness process. Psychopathology An aberrant or dysfunctional way of functioning, defined in terms of behavioral, interpersonal, emotional, cognitive, and psychophysiological patterns.

A. Normalcy versus Abnormalcy Within the overall frame of reference of psychopathology a number of related concepts must be defined and distinguished. As a term, psychopathology refers to an aberrant or dysfunctional (i.e., pathological) way of functioning, where functioning is defined in terms of behavioral, interpersonal, emotional, cognitive, and psychophysiological patterns. Whether a particular way of functioning is aberrant can be judged by a number of criteria. Included in such criteria is whether that functioning causes personal distress, causes others in the person's social sphere to become distressed, falls outside of accepted social norms or values for functioning, falls within certain criteria for abnormal functioning, or is a statistically rare functional pattern. Each of these approaches to establishing an aberrant pattern of functioning has advantages and disadvantages. It is due to the presence of these approaches that different approaches to conceptualizing psychopathology exist. Mental illness is a term that is largely synonymous with psychopathology, although it carries the implication that the unusual or aberrant patterns of functioning seen in these conditions reflect some form of disease or illness. The medical model reflected in the illness term is rejected by some psychopathologists, as

The definition of PSYCHOPATHOLOGY has long been a matter of theoretical and practical importance to individuals involved in the mental health movement. It is primarily psychiatric and psychological professionals who have been involved in the conceptualization and definition of psychopathology. At the theoretical level, debates have centered around such issues as whether humans or their behavior is disordered or "ill," the different approaches that can be taken to define health and pathology, and the moral implications of defining some individuals as having a pathological condition. At the practical level, there have been exten-

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an inappropriate model for either all or some forms of psychopathology. Another term that is considered synonymous with psychopathology is abnormal behavior. This term is equally descriptive as psychopathology, as neither implies a belief in the cause of the unusual or aberrant patterns of functioning, but is more focused on the behavioral component of the dysfunction. A term that is sometimes confused with psychopathology is insanity. Although such terms as insane, mad, and lunatic were once used in much the same way modern society uses the terms psychopathology and mental illness, insanity has taken on a much more narrow definition. Specifically, insanity is a legal term that addresses the question of whether a particular person can be held criminally responsible for his or her actions. Several different tests of insanity exist, but in every case the decision as to whether a person is legally insane is made by a judge or jury, and is made with respect to the crime they are alleged to have committed. It is the case that many different forms of abnormal or psychopathological behavior do not meet the criterion for insanity. Further, it is possible that a person can be legally insane (i.e., not legally responsible for their actions) when they have no discernable form of psychopathology, as defined by mental health practitioners. A term that has relevance to psychopathology is mental health. While one can imagine mental health as the absence of psychopathology, it is also possible to conceptualize mental health in terms of its positive attributes. The World Health Organization has defined mental health as "inner experience linked to interpersonal group experience," and is associated with such characteristics as subjective well-being, optimal development and use of mental abilities, social adaptation, and achievement of goals. In summary, psychopathology is a concept that is similar to mental illness and abnormal behavior, but is distinct from insanity. Mental health can be conceptualized as the absence of psychopathology, but also has other positive components not related to the concept of psychopathology.

B. Conceptual Approaches to Psychopathology There are a large number of theoretical approaches to psychopathology, and these have steadily evolved over the centuries.

One dominant belief about the cause of abnormal behavior is that of possession; which is the idea that evil spirits or demons possess the mind and body of the person in question and cause them to behave in an aberrant fashion. There is fossil evidence that early humans believed in demonic possession as a cause of abnormal behavior, as there are skulls dating from prehistoric times which show purposeful cutting of the skull, or trephination. Trephination is often explained as an effort to release pressure in the skull, which may have been conceptualized by early humans as possession by an evil spirit. The idea of demonic possession as an explanation for abnormal behavior continues to persist (for example, the Roman Catholic Church still has procedures for exorcism as part of its accepted canon, and voodooism is still practised in some parts of the world today), but it has largely been supplanted by other explanations of abnormalcy. One early alternative model to possession was the humoral theory promoted by Hippocrates. The humoral model proposed that four humors, or fluids, are in the body, and that each is associated with a particular attitude and time of life. Blood, for example, is associated with growth, optimism, and good health, while black bile, or melancholia, is associated with death, depression, and darkness. The humoral theory was a prominent one in medicine for centuries, but has been since shown to be false. Contemporary conceptions of psychopathology can be broken down into the two major categories of categorical and dimensional types. Categorical conceptions of psychopathology view abnormal behavior as discontinuous with normal behavior; as something that has a qualitatively different sense to it. Such conceptions are apt to include ideas of illness or disease processes, as these processes are those that distinguish normal from abnormal functioning. Categorical approaches to psychopathology are consistent with the practise of diagnosing or labeling dysfunctional patterns of functioning. The categorical approach to psychopathology is very heavily subscribed to because diagnosis is often considered to be necessary prior to the provision of treatment in psychiatric settings. Dimensional approaches to psychopathology view aberrant functioning as falling on a continuum, with some types or levels of functioning being more or less dysfunctional than others. Within a dimensional approach diagnosis and labeling are less accepted, except to the extent that labels are applied to individuals at agreed upon points along a continuum. For

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example, if a person bites his or her nails more than three times a week, we might label that as "abnormal"; less than three times a week might be considered "normal." Dimensional approaches are often used in combination with statistical conceptions of what is "average" or normal, and abnormalcy is defined as being atypical or highly different from the "average" person.

II. CATEGORICALMODELS OF PSYCHOPATHOLOGY A. Historical Precursors to the Diagnosis of Psychopathology The labeling of abnormal behavior has taken place for centuries. In ancient Greek society, such disorders as melancholia (what we would today term depression), mania (agitated or excited behavior), and phrenitis (most other forms of psychopathology, including severe forms of thought and behavior dysfunction) were distinguished. Models for the onset (etiology) of these disorders were established, and these disorders had differentiated treatment programs. After the Dark Ages, the Renaissance and Enlightenment periods of Western civilization saw a renewed and more sophisticated approach to the diagnosis of psychopathology emerge. With the creation of asylums, large institutions designed for the holding and treatment of persons with mental illness, came the ability to study, differentiate, and more carefully assess abnormal conditions. Different systems for diagnosing psychopathology began to emerge, with different labels being proposed, debated, and either accepted or rejected. By the end of the 19th century, the number of divergent systems for diagnosis was recognized as a serious problem for the credibility and acceptability of any diagnostic system. The approach to diagnosis and labeling that has been generally accepted was formalized by a German physician, Emil Kraepelin, in 1883. Using an approach comparable to that used in the rest of medicine, his approach included the assessment of different symptoms that formed cohesive patterns called syndromes. These syndromes, once identified, could then be labeled. In the original Kraepelinian diagnostic system there were a relatively small number of syndromes and diagnoses, but each was conceptually distinct and had its own specific symptoms.

B. The International Classification of Diseases The World Health Organization (WHO) adopted Kraepelin's system for diagnosing psychopathology, and has listed mental disorders as potential causes of death since 1939. The list of mental disorders included in the WHO directory has been revised a number of times, and the 1969 revision in particular received some acceptance. In 1979 the WHO published the ninth revision and the current version of the International Classification of Diseases (ICD ). There are a total of 30 major categories of mental disorders in the ICD-9 (see Table I). As many of these categories contain more specific forms of psychopathology, there are a total of 563 diagnostic categories in the ICD-9. One of the principle features of the ICD is that it distinguishes organic from nonorganic forms and causes of abnormal behavior. For example, a major distinction is made between "organic psychotic conditions" and "other psychoses." This distinction has been severely examined in the diagnostic literature as potentially lacking validity. For example, it is sometimes the case that what appears to be the same type of abnormal behavior may have different etiological bases; it is often impossible, however, to know with certainty which of the different etiological possibilities is the correct one. A diagnostic system that requires the diagnostician to make etiological judgments may therefore force false decisions. Another aspect of the ICD is that it distinguishes "psychotic" from "nonpsychotic" (also referred to as "neurotic") conditions. The psychotic-neurotic distinction within the ICD is also problematic. For example, depressive conditions are found listed both as psychotic (major depressive disorder) and neurotic (depressive disorder) conditions, but the distinction between these two hypothetically distinct types of depression is not clear. Despite some problems with the ICD system for diagnosing mental disorder, it is a widely subscribed to international model for diagnosis. It is the dominant approach used in Europe, as well as countries that have been under European influence. The World Health Organization is currently at work on the ICD-IO.

C. Diagnostic and Statistical Manual Due to problems with earlier versions of the ICD, the American Psychiatric Association developed its own

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Table I

Psychopathology

Major Mental Disorder Diagnostic Categories from the International Classification of Diseases

A. Organic psychotic conditions 1. Senileand presenile organic psychotic conditions 2. Alcoholicpsychoses 3. Drug psychoses 4. Transient organic psychotic conditions 5. Other organic psychotic conditions B. Other psychoses 1. Schizophrenicdisorders 2. Affectivepsychoses 3. Paranoid states 4. Other nonorganic psychoses 5. Psychoseswith origin specific to childhood C. Neurotic disorders, personality disorders, and other nonpsychotic mental disorders 1. Neurotic disorders 2. Personalitydisorders 3. Sexual deviations and disorders 4. Alcohol dependence syndrome 5. Drug dependence 6. Nondependent abuse of drugs 7. Physiologicalmalfunction arising from mental factors 8. Specialsymptoms or syndromes, not elsewhere classified 9. Acute reaction to stress 10. Adjustmentreaction 11. Specificnonpsychotic mental disorders due to organic brain damage 12. Depressivedisorder, not elsewhere classified 13. Disturbance of conduct, not elsewhere classified 14. Disturbance of emotions specific to childhood and adolescence 15. Hyperkinetic syndrome of childhood 16. Specificdelays in development 17. Psychicfactors associated with diseases not elsewhere classified D. Mental retardation 1. Mild mental retardation 2. Other specified mental retardation 3. Unspecifiedmental retardation ....

system for diagnosis. Referred to as the Diagnostic and Statistical Manual (DSM), the system was first published in 1952, and has since been updated and republished three more times. The current DSM is the fourth version, which was published in 1994). The first two editions of the DSM had many similarities to the ICD. Distinctions were made between psychotic and nonpsychotic disorders, for example, and the diagnostic system included many etiological terms in the diagnoses. In 1980, with the publication of DSM-III, the American Psychiatric Associa-

tion made a major departure from this approach and deleted, as much as possible, all references to putative causes of disorder. Instead, the DSM became a more descriptive system that attempted to label disorders solely on their objective features, with as little inference as possible about the cause of the disorders. In addition to the more descriptive nature of the later editions of DSM, an additional feature was that it was multi-axial. The multi-axial nature of the DSM-IV meant that it examined different axes or dimensions of functioning within the person being diagnosed at a single time, in order to achieve a more rounded assessment of the person and their functioning. DSM-IV has continued the basic descriptive approach of the DSM-III. The DSM-IV, as was true for the DSM-III, has five major axes. The first two axes are those most analogous to the ICD diagnostic system. Axis I comprises the major psychopathology diagnoses (see Table II), while Axis II is used to diagnose personality disorders and mental retardation. Axis Ill is used to diagnose physical disorders and conditions. Some of these disorders or conditions may be relevant to the other psychopathology diagnoses, whereas other medical disorders or conditions may simply help to round out a picture of the person's current problems. Axis IV of the DSM-IV is used to rate the severity of psychosocial stressors, whereas Axis V consists Table II

Major Mental Diagnostic Categories from Axis I of the Diagnostic and Statistical Manual-IV

Disorders usually first evident in infancy, childhood, or adolescence Delirium, dementia, and amnestic and other cognitive disorders Mental disorders due to a general medical condition Substance-related disorders Schizophrenia and other psychotic disorders Mood disorders Anxiety disorders Somatoform disorders Factitious disorders Dissociative disorders Sexual and gender identity disorders Eating disorders Sleep disorders Impulse control disorders Adjustment disorders Other conditions that may be a focus of clinical attention

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of a global assessment rating of the individual's functioning for the past year. In order to diagnose a person using the DSM-IV, information should be provided on each of the five axes. Thus, whereas only Axes I and II are comparable to the ICD's diagnostic labels, the DSM system is more comprehensive than the ICD, and provides more of a complete context in terms of the patient's medical and psychosocial issues. [See DSM-IV.]

D. Future Issues and Developments A large number of conceptual, research, and ethical issues are relevant to the categorical approaches to psychopathology. At the conceptual level, issues of validity (i.e., accurate portrayal of reality) have been raised. These issues have taken a number of forms. For example, the fact that over time the total number of diagnostic categories has been increasing, and the fact that the ICD and the DSM systems have different numbers and types of diagnoses, leads to the question about which (if either) system best reflects the real range of psychopathology. Ideally, diagnostic systems should be both comprehensive (that is, include all potential diagnoses) and distinctive (that is, each diagnostic category should be distinct and minimally overlapping with other categories). It is not clear at present that either existing system meets these criteria. Nor is it easy to imagine how they could demonstrate that they are both comprehensive and distinctive. Another validity issue that has been raised with regard to the two major diagnostic systems is the extent to which a categorical system best represents psychopathology. This issue has been particularly raised in the case of the personality disorders, where it has been argued that rather than being discrete disorders they represent the extreme ends of personality dimensions. According to this view, rather than diagnosing personality disorders such as dependent personality disorder, psychopathologists should speak about the relative strength or weakness of certain personality dimensions such as dependency. Although the issue of whether disorders are dimensional or categorical in nature is most acute in the case of personality disorders, it is also clear that in other disorders judgments must be made about when a given behavioral pattern or other symptom falls outside the range of normal. Consider, for example, the diagnosis of anorexia nervosa (see Table III). Within that diag-

Table III

Diagnostic Criteria for Anorexia Nervosa

A. Refusal to maintain body weight at or above a minimally normal weight for age and height, e.g., weight loss leading to maintenance of body weight less than 85% of that expected; or failure to make expected weight gain during period of growth, leading to body weight less than 85% of that expected. B. Intense fear of gaining weight or becoming fat, even though underweight. C. Disturbance in the way in which one's body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight. D. In postmenarcheal females, amenorrhea, i.e., the absence of at least three consecutive menstrual cycles. (A woman is considered to have amenorrhea if her periods occur only following hormone, e.g., estrogen, administration.) Source: Adapted from the Diagnostic and Statistical ManualIV. Italics not in the original.

nosis are a number of judgments that a diagnostician would have to make, including what is an "expected body weight," when a fear of being overweight is "intense" and when thoughts about body size are "disturbed." While at the extremes of such judgments there would likely be high agreement across diagnosticians, less extreme fears and disturbances are more difficult to judge with certainty. Put otherwise, some of the symptoms are themselves not dichotomous, but reflect dimensions of disturbance, which are identified only if they cross some imaginal "line" of dysfunction. Decisions about how to recognize where that line has been crossed require some agreement among diagnosticians about what that line is, and how to recognize it is being breached. [See ANOREXIA NERVOSA AND BULIMIA NERVOSA.]

Similar arguments have been made with respect to most forms of childhood disorders, as these disorders are typically conceptualized in terms of extreme forms of behavior (for example, too much aggressive behavior) that might better be seen as extremes on a continuum rather than discrete forms of psychopathology. A third issue about diagnoses has been that to some extent they do not reflect the real world of psychopathology, but rather society's beliefs about and experience of abnormal behavior. Critics of diagnosis have pointed out that the "emergence" of new disorders and deletion of others reflect changing societal val-

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ues, rather than scientific advances that could validate such changes. For example, the diagnosis of homosexuality has had an interesting history within the DSM system. In the DSM-II, published in 1968, homosexuality was defined as a psychopathology diagnosis. By the time DSM-III was published in 1980 the system had changed, such that only ego-dystonic homosexuality (i.e., sexual preference for a same-sex person, but where the individual felt that this preference was inconsistent with their own wishes) was a recognized disorder; instances where the homosexual patterns were ego-syntonic (consistent with the persons's wishes) were not considered abnormal. Homosexuality has been totally deleted as a diagnostic label in the DSM-IV (ICD continues to include homosexuality). It has been pointed out that this evolution of approaches to homosexuality mirrors a growing recognition and acceptance of homosexuality in Western society. It has been argued, therefore, that the changing diagnoses related to homosexuality do not reflect changes in the scientific basis of that diagnosis, but rather reflect changes in the attitudes and biases that the developers of diagnostic systems share with society at large. It has been similarly argued that other disorders, such as anorexia nervosa, reflect societal beliefs and awareness about specific behaviors, rather than necessarily reflecting the "true" nature of psychopathology. At the scientific level, the major issues that face categorical systems of psychopathology are those related to the internal consistency and reliability of diagnostic categories. If a perfect diagnostic system existed, then every person with psychopathology should be captured in the system, and every trained diagnostician should recognize an individual's unique diagnoses in a manner consistent with other diagnosticians. Research on these issues suggests that our current systems, although better than their precursors, do not closely approximate these goals. Clearly, further research and development are needed to clarify why consistency and reliability have been elusive. Finally, there have been ethical arguments raised against the practice of diagnosis. It has been argued, for example, that diagnosis involves an artificial process of labeling people, and that once these labels are applied they become more than descriptions of the individual's current functioning, but become long-term crosses for the individual to bear. These abuses of the

diagnostic process have been used as a basis for arguing that the utility of diagnosis is more than offset by its costs, and should be abandoned.

III. DIMENSIONAL MODELS OF PSYCHOPATHOLOGY Dimensional models view psychopathology as deriving from underlying dimensional constructs that explain both normal and abnormal functioning. For example, it is possible to imagine a construct called interpersonal dependency. At one end of this construct is extreme dependency, as would be marked by such thoughts as being insufficient without others, having to have others around to feel comfortable, and marked by such behavior as constantly seeking out others to be with, talking to others, etc. At the other end of this construct is extreme interpersonal independency, which would be marked by such thoughts as never needing others, having to be alone to feel comfortable, and such behaviors as spending time alone, not starting conversations with others, etc. A person functioning at either of the extremes on this dimension would be considered dysfunctional or psychopathological; between these two extremes lies a wide range of normal dependency-independency options. Research has shown that most constructs are more common at their middle range, and less common at their extremes. As such, if those constructs related to personality or behavior that are related to psychopathology could be identified, then it would be possible to identify those points along the continua where abnormal or extreme patterns could be identified. For example, using the dimension of interpersonal dependency-independency, it might be possible to identify a point along that continuum where the person is either so dependent or independent it causes distress and/or interpersonal problems for the person. It would be at those points we would talk about the person crossing an imaginary line from normal to psychopathological functioning (see Fig. 1).

A. Trait versus Symptom Approaches Dimensional models of psychopathology can be viewed as typically being one of two major types. Some dimensional models focus on underlying theo-

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retical dimensions or traits that might explain abnormal behavior, while other focus more on the range of symptoms or descriptive features of the dysfunctional behaviors themselves. Trait approaches are more theoretical than symptom approaches, and typically have an associated theory of normal personality as well as psychopathology, while symptom approaches focus more on the elements of psychopathology alone. There are a number of trait approaches to psychopathology, and all cannot be described here. The work of Hans Eysenck is a good example of this approach, however, and will be used to provide an example. In Eysenck's earlier research, he identified two basic dimensions to normal and abnormal behavior. One of these was the dimension of introversion-extroversion, which had extremes of being highly introverted (shy, retiring, isolated) and highly extroverted (outgoing, sociable), while the other was neuroticism (which had two extremes of stable versus unstable patterns; where instability is marked by such attributes as anxiety, physical complaints, moodiness, etc.). According to Eysenck's research these two personality dimensions were unique from each other. An individual's placement on each dimension, according to Eysenck, reflects a basic disposition on the part of the individual which likely could be seen in different situations that the person finds him/herself in, and also lasts across time. Within Eysenck's model of functioning, psychopathology is identified at the extremes of each dimension. Thus, a person who is "too" extroverted could be said to be dysfunctional; similarly, a person "too" high on neuroticism could be said to be dysfunctional. Eysenck developed questionnaires to measure these dimensions which allowed clinicians to identify how much of these dimensions were represented by an in-

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dividual, and thereby identify if the person was in the normal range of functioning or not. A later addition to Eysenck's theory was a third dimension, referred to as psychoticism. This dimension was theoretically distinct from the other two, and reflected an underlying tendency toward more extreme forms of abnormal behavior, including insensitivity toward and lack of caring about others, and opposition of accepted social customs. A mental health professional using Eysenck's system to describe psychopathology would not talk about a given individual as "extroverted," "neurotic," or "psychotic," but would rather talk about an individual as being high on these dimensions. The mental health professional would know that certain forms of thought, emotion, and behavior are related to these dimensions, and would explain psychopathology in terms of these underlying trait dimensions. As stated previously, Eysenck's is just one of a number of trait approaches to psychopathology. One of the major issues that has been addressed by theorists who use these models has been that of trying to develop a comprehensive and exhaustive system. In recent years, there has been considerable discussion about what are referred to as the "Big Five" personality traits that might explain most human behavior. These five factors include neuroticism, extraversion, openness, agreeableness, and conscientiousness. While we will not discuss the adequacy of this model here, it is important to note two elements: first, that many theorists are beginning to converge on the importance of these five factors in personality, and second, that one of these dimensionsmneuroticism--is explicitly oriented toward identifying abnormal behavior of a neurotic type (anxiety, physical complaints, nervousness, edginess, etc.). As opposed to trait models of psychopathology, there are symptom dimensional approaches. One prominent example of this type of approach has been with regard to the personality disorders. Within the DSM-IV, there are 11 recognized personality disorder diagnoses. As is true for other diagnostic categories, DSM-IV lists the descriptive features of these disorders, and presents them as unique (although a given individual could have more than one diagnosis simultaneously). An alternative perspective to conceptualizing types of personality disorders is to conceptualize personality as having a number of dimensions, which

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at their extreme represent dysfunctional patterns of interpersonal relating. Such an alternative approach would view personality features in terms of their symptoms, as well as in terms of the severity of these symptoms. [See PERSONALITYDISORDERS.] Symptom-based approaches, as seen in the area of personality disorders, can be imagined for most types of psychopathology. In the area of depression, for example, one can imagine that rather than diagnosing an individual as depressed or not based upon whether they meet certain diagnostic criteria, a psychopathologist could describe the severity or depth of depression. Such an approach would require a psychopathologist to determine the key symptoms of depression, to evaluate the severity of each of these symptoms, and then determine the overall depth or severity of depression for a given individual. The fact that the end result is an index of severity, though, means that an underlying dimensional, rather than categorical, approach has been used to conceptual and describe depression. [See

DEPRESSION.] Dimensional approaches to most forms of psychopathology exist. Typically, the assessment of psychopathology using such approaches relies on questionnaires, which are self-report means to determine the number and severity of different symptoms the person may be experiencing. A large number of trait and symptom questionnaires have been developed, predominantly by psychologists working in the fields of personality and psychopathology. A listing of all published questionnaires and psychological tests can be gained by examining the Mental Measurements Yearbook, which is an annual publication of the Buros Institute.

B. Models of Psychopathology Psychopathologists are not content with conceptualizing and describing categorical and dimensional aspects of psychopathology. Another key activity of psychopathologists is to develop theoretical models that can potentially explain the cause, course, and required treatment of these disorders as well. A large number of theoretical models have been developed to attempt to explain psychopathology, many of which are very complex and well beyond the scope of this article. An excellent starting reference for interested readers is Abnormal Psychology, by Davison and Neale (1991).

Models of psychopathology fall into several major categories. One major dimension which can be used to think of these models is whether their focus is on factors that are external or internal to the person. Models that focus on external factors might place an emphasis on such issues as early childhood experiences, family dynamics, traumatic experiences, and even social and cultural issues that might lead to different forms of problematic behavior. These models are likely to focus on the need for changes external to the individual to correct psychopathology, including marital and family therapy. Some theorists who adopt this type of environmental or social perspective also focus on the need to change societal or cultural variables to lower the likelihood of some forms of psychopathology. For example, it has been argued that some eating disorders are encouraged by the value that society places on thinness, and that by changing societal values, we may actually be able to lower the future likelihood of some eating disorders. Theorists who focus on factors internal to the individual typically adopt either a biological or a psychological perspective. Biologically oriented theorists might focus on genetic contributions to psychopathology, structural problems in the nervous system that cause abnormal behavior, or neurological processes that can be disordered and lead to psychopathology. These theorists are likely to focus on biological treatments to psychopathology, including psychoactive medications. A large number of medications for treating psychological disorders exist, many of which have documented benefit. The third major theoretical approach to psychopathology is psychological in nature. Such approaches focus upon psychological models of both normal and abnormal personality, and try to explain psychopathology in terms of these processes. Within the psychological approaches are a number of discrete models, including psychoanalytic, behavioral, cognitive, humanistic, and other theoretical approaches. While all of these models share the assumption that there is something within the individual at the psychological level that explains abnormal behavior, the specifics of each model vary dramatically, as do the therapies they promote. In summary, psychopathology researchers not only classify, diagnose, and assess abnormal behavior, but also are interested in the causes, course, and treatment

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of these conditions. Different models are used in the effort to explain psychopathology. While some models appear to be better suited for some forms of abnormal behavior, others may be more appropriate for other conditions. It is also possible that a given form of psychopathology, such as anxiety, may have multiple causes, which may vary from person to person having that disorder. Humans are extremely complex, and the large number of approaches helps to encompass that complexity in the way psychopathologists conceptualize their subject field.

IV. FUTURE ISSUES IN PSYCHOPATHOLOGY As the above reveals, psychopathology is an intricate and often perplexing field of study. Although there are a large number of issues that face the field, major issues include the future of categorical and dimensional approaches, theoretical models, and treatment issues. Each is discussed in turn below.

A. Categorical and Dimensional Approaches Both of the categorical and dimensional approaches to psychopathology face the issues of comprehensiveness and distinctiveness. How many diagnoses or dimensions, respectively, adequately account for the range of human dysfunction? Are these distinct diagnoses and dimensions, or is their overlap such that they call into question the theoretical basis for the approach to psychopathology? Another question that both approaches face is how best to assess psychopathology. As has been stated, each of these approaches has its own methodology for assessment. Categorical approaches lend themselves to diagnoses, which are typically constructed as a result of interviews with individuals, and the decision as to whether the given individual qualifies for one or more diagnoses. Dimensional approaches are most often assessed using questionnaires that assess one or more dimensions of psychopathology, using traits or symptoms as the conceptual basis for assessment. Interview and questionnaire assessment strategies are not necessarily contradictory, and many psychopathologists believe that using both leads to a more

comprehensive understanding of the individual in question. It remains for the field to adequately address which strategy or strategies are best within each approach, and how best to integrate these two types of assessment.

B. Theories of Psychopathology Theories of psychopathology, as is true for all scientific theories, are tested against their explanatory power. Within psychopathology, many research methods exist to test theoretical models, including the ability to discriminate groups with different types of psychopathology, or the correlation between certain theoretical constructs and the severity of psychopathology. The field of psychopathology is rich with research questions. Psychopathology research is notoriously difficult to conduct for a number of reasons, including the large number of definitional, assessment and theoretical perspectives already discussed. Further, it is often difficult to easily obtain large numbers of research subjects that clearly have a distinct form of psychopathology, and for ethical reasons it is often not possible to conduct the experimental types of studies that might best test different theories of psychopathology. Finally, a good number of different forms of psychopathology need time to develop (indeed, sometimes it is the course of different disorders that itself is the object of scientific study), which requires long-term research funds and geographical stability of both researchers and research objects. Such control is not easy to obtain in the real world. Despite the above problems, research in the field of psychopathology is increasingly driven by strong theoretical questions, and the answers to these questions are slowly being accumulated. The field has begun to contrast competing theories, and the overall adequacy of some theoretical models is beginning to become clear. It can be expected that over the next decades some "best models" for different forms of psychopathology will emerge.

C. Treatment Issues in Psychopathology Many psychopathologists enter the field because of a desire not only to understand, but also to help people with behavioral problems. One hope is that with accurate assessment and diagnosis, treatment options

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may become clarified. Although there does not yet exist a clear correspondence between different forms of psychopathology and treatments, the field has advanced considerably in this direction. For a given disorder there likely are several viable treatments, some of which may have better success rates, but all of which have some potential for helping an individual in distress. With increasing sophistication of assessment, diagnosis, and conceptualization, it is likely that treatment of psychopathology will become an even more complex and successful enterprise in the future than now.

This article has been reprinted with updated references to DSMIV from the Encyclopedia of Human Behavior, Volume 3.

BIBLIOGRAPHY American Psychiatric Association (1994). "Diagnostic and Statistical Manual-IV." Washington, DC. Buros Institute (1992). "Mental Measurements Yearbook." Gryphen, Highland Park, NJ. Davison, G., and Neale (1991). "Abnormal Psychology," 5th ed. Wiley, New York. World Health Organization (1979). "International Classification of Diseases," 9th ed. Geneva, Switzerland.

Schizophrenia Jason Schiffman and Elaine Walker E m o r y University

I. II. III. IV. V. VI. VII.

Description and Classification History Demographic Characteristics of Schizophrenia Life Functioning and Prognosis Etiology: Theories and Research Findings Treatment and Therapy Summary

I. DESCRIPTION AND CLASSIFICATION Schizophrenia is a serious mental illness that afflicts about 1% of the population at some point in their lifetime. In the current Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), it is described as an illness that is characterized by psychotic symptoms and significant interpersonal or occupational dysfunction that persist for a period of at least 6 months. The term psychotic refers to symptoms that indicate an impairment in the patient's ability to comprehend reality. This includes beliefs that have no basis in reality and that are not susceptible to corrective feedback (delusions), and sensory perceptions that have no identifiable external source (hallucinations). In addition to hallucinations and delusions, the DSM lists three other key symptoms of schizophrenia: disorganized speech, disorganized or catatonic behavior, and negative symptoms. [See DSM-IV.]

Antipsychotics Medications that have been demonstrated to reduce the symptoms of schizophrenia. Behavioral Genetics The study of the extent to which individual differences in behavior are attributable to genetic factors as opposed to environmental influences. Dopamine A catecholamine neurotransmitter located throughout the brain, particularly the substantia nigra and basal ganglia. Frontal Lobes The portion of each cerebral hemisphere that is anterior to the central sulcus and above the lateral fissure, and is active in reasoning, planning, and other higher mental processes. Neuropsychology The study of the relation between brain function and behavior. Ventricles Cavities in the brain that are continuous with the central canal of the spinal cord and are filled with cerebrospinal fluid.

A. Symptoms I. Delusions Delusions are the primary example of abnormal thought content in schizophrenia. Delusional beliefs conflict with reality and are tenaciously held, despite evidence to the contrary. There are several types of delusions. Delusions of control is the belief that one is being manipulated by an external force, often a powerful individual or organization (e.g., the FBI) that has malevolent intent. Delusions of grancleur refers to patients' beliefs that they are especially important and have unique qualities or powers (e.g., the capacity to influence weather conditions). In contrast, some pa-

SCHIZOPHRENIA is a psychotic disorder characterized by disturbances in thought, emotion, and behavior. This article discusses the symptoms, etiology, treatment, and other pertinent issues concerning this mental illness.

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tients express the conviction that they are victims of persecution or an organized plot, and these beliefs are referred to as delusions of persecution. Examples of more specific delusions include thought broadcasting, the patient's belief that his or her thoughts are transmitted so that others know them, and thought withdrawal, the belief that an external force has stolen one's thoughts.

2. Hallucinations Hallucinations are among the most subjectively distressing symptoms experienced by schizophrenia patients. These perceptual distortions vary among patients and can be auditory, visual, olfactory, gustatory, or tactile. The majority of hallucinations are auditory in nature and typically involve voices. Examples include the patient hearing someone threatening or chastising him or her, a voice repeating the patient's own thoughts, two or more voices arguing, and voices commenting. The second most common form of hallucination is visual. Visual hallucinations often entail the perception of distortions in the physical environment, especially in the faces and bodies of other people. Other perceptual distortions that are commonly reported by schizophrenia patients include feeling as if parts of the body are distorted in size or shape, feeling as if an object is closer or farther away than it actually is, feeling numbness, tingling, or burning, being hypersensitive to sensory stimuli, and perceiving objects as flat and colorless. In addition to these distinctive perceptual abnormalities, persons suffering from schizophrenia often report difficulties in focusing their attention or sustaining concentration on a task. It is important to note that in order for an unsubstantiated belief or sensory experience to quality as a delusion or hallucination, the individual must experience it within a clear sensorium (e.g., unsubstantiated sensory experiences that occur only upon awaking from sleep or when falling asleep would not qualify as delusions). Thus, for example, if a patient reports hearing something that sounds like voices when alone, but adds that he or she is certain that this is a misinterpretation of a sound, such as the wind blowing leaves, this would not constitute an auditory hallucination.

3. Disorganized Speech The DSM uses the term disorganized speech to refer to abnormalities in the form or content of the indivi-

dual's verbalizations. It is assumed that these abnormalities reflect underlying distortions in the patient's thought processes. Thus the term thought disorder is frequently used by researchers and practitioners to refer to the disorganized speech that often occurs in schizophrenia. Problems in the form of speech are reflected in abnormalities in the organization and coherent expression of ideas to others. One common abnormality of form, incoherent speech, is characterized by seemingly unrelated images or fragments of thoughts that are incomprehensible to the listener. The term loose association refers to the tendency to abruptly shift to a topic that has no apparent association with the previous topic. In general, the overall content of loosely associated speech may be easier to comprehend than incoherent speech. In perseverative speech, words, ideas, or both are continuously repeated, as if the patient is unable to shift to another idea. Clang association is the utterance of rhyming words that follow each other (e.g., "a right, bright kite"). Patients choose words for their similarity in sound rather than their syntax, often producing a string of rhyming words.

4. Disorganized or Catatonic Behavior The overt behavioral symptoms of schizophrenia fall in two general areas: motor functions and interpersonal behavior. Motor abnormalities, including mannerisms, stereotyped movements, and unusual posture, are common among schizophrenia patients. Other common signs include bizarre facial expressions, such as repeated grimacing or staring, and repeated peculiar gestures that often involve complex behavioral sequences. As with other symptoms of the psychosis, the manifestation of motor abnormalities varies among individuals. Schizophrenia patients sometimes mimic the behavior of others, known as echopraxia, or repeat their own movements, known as stereotyped behaviors. Although a subgroup of patients demonstrate heightened levels of activity, including motoric excitement (e.g., agitation or flailing of the limbs), others suffer from a reduction of movement. At the latter extreme, some exhibit catatonic immobility and assume unusual postures that are maintained for extended periods of time. Some may also demonstrate waxy flexibility, a condition in which patients do not resist being placed into strange positions that they then maintain. Catatonia has decreased dramatically in recent decades, so that it is

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now rare. Several researchers have attributed this decline to the introduction of antipsychotic medication (described later). In the domain of interpersonal interactions, schizophrenia patients frequently demonstrate behaviors that are perceived as bizarre or inappropriate by others. For example, it is not uncommon for patients to use socially unacceptable language and unusual tones of voice, or to show overly dependent or intrusive behavior. Another common symptom, inappropriate affect, involves unusual emotional reactions to events and experiences. For example, patients may laugh at a sad or somber occasion, or be enraged by insignificant events. Finally, many patients manifest increasingly poor hygiene as their illness progresses. Their appearance may also be marked by disheveled clothing or inappropriate clothing, such as gloves and coats in the summer.

5. Negative Symptoms The symptoms of schizophrenia can be classified into the general categories of positive and negative. Positive symptoms involve behavioral excesses and most of the symptoms described earlier fall in to this category (e.g., delusions, hallucinations, and bizarre behaviors). In contrast, negative symptoms involve behavioral deficits. Examples include fiat affect (blunted expressions of emotion), apathy, and social withdrawal. In the domain of verbal expression, schizophrenia patients who manifest a very low rate of verbal output are described as showing poverty of speech. Patients whose speech is normal in quantity, but lacks meaning, suffer from poverty of content. Recently, some researchers have suggested that positive and negative symptoms may be caused by different neural mechanisms. It is important to mention that a reduction in overt displays of emotion does not necessarily imply that patients have less intense subjective emotional experiences than the average person. In fact, recent findings indicate that blunted emotional expressions can coexist with intense subjective feelings of emotion.

B. Variability of Symptoms among Patients According to DSM-IV, patients must show two or more of the preceding five symptoms to meet the diagnostic criteria for schizophrenia. Thus, no one of these symptoms is required for the diagnosis. Fur-

thermore, the following four criteria must also be met: (1) the patient shows marked deterioration in occupational, interpersonal, or domestic functioning; (2) the patient manifests continuous signs of symptoms or dysfunction for at least 6 months; (3) the patient does not manifest predominant signs of mood disturbance (e.g., depression or mania); and (4) the symptoms are not caused by substance abuse or a primary medical condition. Because the diagnostic criteria for schizophrenia are relatively broad, with no one essential symptom, there is a great deal of variability among patients in their symptom profiles. It has therefore been proposed that schizophrenia is a heterogeneous disorder with multiple causes. It is also the case, however, that patients must show a marked and persistent impairment to meet the diagnostic criteria for schizophrenia. Thus, those who meet criteria for the diagnosis are significantly impaired in everyday functioning. For many individuals who are diagnosed with schizophrenia, independent functioning is never achieved.

C. Subtypes of Schizophrenia The DSM lists five subtypes of schizophrenia. In schizophrenia of the paranoid type, delusional concerns about persecution and/or preoccupation with threat dominate the clinical presentation, although delusions of grandeur are also often present. Disorganized schizophrenia is distinguished by extremely incoherent speech and behavior, as well as blunted or inappropriate affect. In catatonic schizophrenia, the clinical picture is dominated by abnormalities in movement and posture, such as those described earlier. Patients classified as having undifferentiated schizophrenia do not meet criteria for any of the previous subtypes. Finally, the diagnosis of residual schizophrenia is applied to patients who have had at least one episode of schizophrenia and who continue to show functional impairment, but who do not currently manifest any positive symptoms.

II. HISTORY During the late 1800s and early 1900s, Emil Kraepelin and Eugen Bleuler provided the first conceptualizations of schizophrenia. Kraepelin defined "dementia praecox," the original term for schizophrenia, as an endogenous psychosis characterized by intellectual

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deterioration (dementia) and early onset (praecox). Kraepelin included negativism, hallucinations, delusions, stereotyped behaviors, attentional difficulties, and emotional dysfunction as major symptoms of the disorder. Kraepelin's work focused on description and phenomenology, leaving subsequent researchers to investigate the cause or causes of the disorder. In contrast to Kraepelin, Eugen Bleuler, a Swiss psychiatrist, proposed a broader view of dementia praecox, with a more theoretical emphasis. Bleuler contested two of Kraepelin's defining assumptions: specifically, that the psychosis was typically characterized by early onset and intellectual deterioration. Bleuler attempted to identify an underlying commonality among the diverse variations of what Kraepelin referred to as dementia praecox and concluded that all of the patients suffered from a "breaking of associative threads," causing a disharmony among communicative and thought processes. He believed this abnormality accounted for the problems of thought, emotional expression, decision making, and social interaction associated with schizophrenia. Guided by the defining principle of disharmonious mental structures, Bleuler renamed the disorder "schizophrenia," meaning "split mind." In the early to mid-1900s, American psychiatrists continued to use a broad definition of schizophrenia. The distinction between process and reactive schizophrenia was considered important, however, because it was assumed to distinguish between cases characterized by gradual deterioration (process) and cases that were precipitated by acute stress (reactive). During this time, some clinicians and researchers viewed the specific diagnostic criteria for the major mental illnesses (schizophrenia, bipolar disorder, major depression) as artificial and discretionary, and used instead flexible and inconsistent standards for diagnoses. Studies that compared the rates of disorder across nations revealed that schizophrenia was diagnosed at a much higher rate in the United States than in Great Britain and some other countries. This national difference resulted from the use of broader criteria for diagnosing schizophrenia in the United States. Many patients who were diagnosed as having depression or bipolar disorder in Britain were diagnosed with schizophrenia in the United States. Because subsequent revisions in the DSM have included more restrictive criteria for schizophrenia, U.S. diagnostic rates are now comparable with other countries.

In addition to a more restrictive definition of schizophrenia, subsequent editions of the DSM have included additional diagnostic categories that contain similar symptoms. Thus the range of "schizophreniaspectrum disorders" continue to broaden with the description of variants of schizophrenia, such as schizoaffective disorder, which is characterized by a mix of affective and psychotic symptoms. The diagnostic category of schizophreniform disorder was also added. This diagnosis is given when the patient shows the typical symptoms of schizophrenia, but does not meet the criterion of 6 months of continuous illness.

III. DEMOGRAPHIC CHARACTERISTICS OF SCHIZOPHRENIA Estimates of the prevalence of schizophrenia converge at around 1% of the population. Although there is evidence of cross-national differences in the rate of schizophrenia, the differences are not large (i.e., 1 to 2% difference). It is, in fact, striking that the rate of occurrence is so consistent across cultures. The modal age at onset of schizophrenia is in early adulthood, usually before 25 years of age. Thus most patients have not had the opportunity to marry or establish a stable work history before the onset of the illness. As a result of this, and the often chronic nature of the illness, many patients never attain financial independence. It is relatively rare for preadolescent children to receive a diagnosis of schizophrenia. Similarly, it is rare for individuals beyond the age of 40 to experience a first episode of the illness.

A. Sex Differences Although it has traditionally been assumed that there is no sex difference in the rates of schizophrenia, some recent research findings indicate that a somewhat larger proportion of males than females meet the DSM-IV criteria for the disorder. Nonetheless, the overall rates do not differ dramatically for men and women. It is well established, however, that women are more likely to have a later onset of illness, as well as a better prognosis. Women also show a higher level of interpersonal and occupational functioning during the period prior to illness onset. The reasons for this sex difference are not known, but it has been proposed by several theorists that the female sex hormone, es-

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trogen, may function in attenuating the severity of the illness.

B. Social Class Differences Compared with the general population averages, schizophrenia patients tend to have significantly lower incomes and educational levels. Poor urban inner city districts, inhabited by the lowest socioeconomic class, contain the largest proportion of schizophrenia patients. There is a sharp contrast between the rates of schizophrenia in the lowest socioeconomic class and all other levels, including the next higher level. Findings from various cultures suggest that rates of schizophrenia are almost two times higher in the lowest social class group compared with the next lowest. These social class differences appear to be a partial consequence of the debilitating nature of the illness. The social-drift theory suggests that during the development of schizophrenia, people drift into poverty. When the incomes and educational levels of the parents of patients are compared with those of the general population, the differences are not as striking. There is, nonetheless, evidence that patients do come from families where the incomes and educational backgrounds of the parents are slightly below the average. These findings have led researchers to conclude that there may be a causal link between social class and risk for the illness. The sociogenic hypothesis posits that situational factors associated with low social class, such as degrading treatment from society, low levels of education, and few opportunities for achievement and reward, produce stress that contributes to the risk for schizophrenia.

IV. LIFE FUNCTIONING AND PROGNOSIS Before the introduction of antipsychotic medications in 1950, the majority of patients spent most of their lives in institutional settings. There was little in the way of programs for rehabilitation. But contemporary, multifaceted treatment approaches have made it possible for most patients to live in community settings. Of course, during active episodes of the illness, schizophrenia patients are usually seriously function-

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ally impaired. They are typically unable to work or maintain a social network, and often require hospitalization. Even when in remission, some patients find it challenging to hold a job or to be self-sufficient. This is partially due to residual symptoms, as well as to the interruptions in educational attainment and occupational progress that result from the illness. However, there are many patients who are able to lead productive lives, hold stable jobs, and raise families. With the development of greater community awareness of mental illness, some of the stigma that kept patients from pursuing work or an education has diminished.

A. Long-Term Course For about one third of patients, the illness is chronic and is characterized by episodes of severe symptoms with intermittent periods when the symptoms subside but do not disappear. For others, there are multiple episodes with periods of substantial symptom remission. About one third of those who receive the diagnosis eventually show a partial or complete recovery after one or two episodes. Several factors have been linked with a more favorable prognosis for schizophrenia. Early treatment seems to be important in that the shorter the period between the onset of the patient's symptoms and the first prescribed medication, the better the clinical outcome. Another indicator of better prognosis is a high level of occupational and interpersonal functioning in the premorbid period. Also, as noted earlier, women and patients who have a later onset of symptoms have a better long-term outcome.

B. Premorbid Characteristics of Schizophrenia Some of the difficulties experienced by individuals with schizophrenia can be observed before the onset of the clinical symptoms. Deficits in social skills, concentration, emotional expression, motivation, and occupational or academic performance often precede the first clinical symptoms. This period of gradual decline in functioning before the first illness episode is referred to as the prodromal phase. However, there are often more subtle signs of dysfunction long before the onset of the prodromal period. Controlled studies using archival data sources, such as medical and school records or childhood

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home-movies, indicate that subtle differences are discernible as early as infancy in some patients. Individuals who succumb to schizophrenia in adulthood sometimes have abnormal motor development and show deficits in emotional expression and interpersonal relationships in early childhood. Cognitive impairment and difficult temperament have also been observed. During middle childhood and adolescence, researchers have found evidence of neurological abnormality, poor emotional control, social immaturity, and academic performance deficits. Premorbid behavioral problems often become marked through the adolescent years, and many exhibit behavioral disturbances and cognitive abnormalities that resemble the clinical symptoms of schizophrenia.

V. ETIOLOGY: THEORIES AND RESEARCH FINDINGS The causes of schizophrenia are unknown, but it is now widely accepted by both researchers and clinicians that schizophrenia is biologically determined. This is in striking contrast to the early and mid-1900s, when many subscribed to the theory that faulty parenting, especially cold and rejecting mothers, caused schizophrenia in offspring.

A. Brain Abnormalities in Schizophrenia There are several sources of evidence for the assumption that schizophrenia involves an abnormality in brain function. First, studies of schizophrenia patients have revealed a variety of behavioral signs of central nervous system impairment, including motor and cognitive dysfunctions. Second, when the brains of patients are examined with in vivo imaging techniques, such as magnetic resonance imaging (MRI), many show abnormalities in brain structure. Similarly, postmortem studies of brain tissue have revealed irregularities in nerve cell formation and interconnections. Laboratory studies of schizophrenia patients have revealed a variety of abnormalities, including irregularities in smooth pursuit eye movements, psychophysiological responses to sensory stimuli, and concentration. Research on the neuropsychological performance of schizophrenia patients was first conducted in the 1950s and continues to the present time. Individual neuropsychological tests are designed to measure functions subserved by specific regions or

systems of the brain. An early finding in this area was that schizophrenia patients were the one psychiatric group whose performance on neuropsychological tests was indistinguishable from people with known brain damage. The findings suggested a generalized cerebral dysfunction in schizophrenia. However, patients show the most consistent deficits on tests of attention and memory, indicating dysfunction of the frontal and temporal lobes and the hippocampus. Further evidence of dysfunction in these brain regions is derived from poor performance on tests of executive functions: the ability to formulate, maintain, and adapt appropriate responses to the environment. Brain-imaging studies of schizophrenia have yielded results that mirror those obtained from neuropsychological research. Some relatively consistent findings are that the brains of schizophrenia patients have abnormal frontal lobes and enlarged ventricles. Enlarged ventricles suggest decreased brain mass, particularly in the limbic regions, which are intimately involved in emotional processing. Furthermore, ventricular size correlates with negative symptoms, performance deficits on neuropsychological tests, poor response to medication, and poor premorbid adjustment. These associations between ventricular enlargement and both premorbid and postmorbid characteristics suggest that the brain abnormalities are long-standing, perhaps congenital. In addition to brain structure, investigators have examined biological indices of brain function in schizophrenia. Functional brain-imaging studies, with procedures such as positron emission tomography (PET) and measurement of regional cerebral blood flow, reveal that schizophrenia patients have decreased levels of blood flow to the frontal lobes, especially while performing cognitive tasks. Researchers are now pursuing the question of what causes the brain abnormalities observed in schizophrenia. Although as yet there are no definitive answers, investigators have made continuous progress in identifying factors that are associated with risk for the disorder.

B. Biochemical Factors The structural brain abnormalities that have been observed in schizophrenia support the assumption that it is a disorder of the central nervous system. But it has also been shown that similar structural abnormalities (i.e., ventricular enlargement and volume reductions)

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are present in other disorders, both neurological and psychiatric. It is therefore assumed that specific abnormalities in brain biochemistry may play a role in schizophrenia. The functioning of the central nervous system is dependent on a host of chemicals that serve as the "messenger substances" among neurons. These chemicals or neurotransmitters have been the subject of intense investigation. Among the various neurotransmitters that have been implicated in the neuropathophysiology of schizophrenia is dopamine. Dopamine is viewed as a likely candidate for two main reasons: (1) drugs that act to enhance the release or activity of dopamine can produce psychotic symptoms, and (2) drugs that have been established to have antipsychotic properties (i.e., reduce psychotic symptoms) reduce the activity of dopamine in the brain. Current theories of the role of dopamine in schizophrenia have focused on dopamine receptors. There is evidence that there may be an abnormality in the number or sensitivity of certain dopamine receptors in the brains of schizophrenia patients. To date, however, this evidence remains inconclusive. Several other neurotransmitters have also been hypothesized to play a role in schizophrenia. Current theories under investigation include a malfunction of the receptors for a neurotransmitter called glutamate and an abnormality in the balance between dopamine and serotonin (another neurotransmitter which, like dopamine, has been implicated in the pathogenesis of schizophrenia). As research findings on the biochemical aspects of schizophrenia accumulate, it increasingly appears that the illness may involve multiple neurotransmitters, with different biochemical profiles for different patients.

C. Genetics A convincing body of research supports the notion of a genetic predisposition to schizophrenia. Behavioral genetic studies of families, twins, and adopted offspring of schizophrenia patients indicate that an inherited vulnerability is involved in at least some cases of the disorder. There is an elevated risk of schizophrenia for individuals with a biological relative who suffers from the disorder, and the risk rates increase as a function of the genetic closeness of the relationship. For example, it has been estimated that children of schizophrenia patients have a 9 to 15 % likelihood of developing the

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illness, siblings of patients have an 8 to 14% likelihood, and cousins have a 2 to 6% likelihood of being diagnosed with schizophrenia. Given the general population rate of approximately 1%, relatives of patients are at statistically increased risk. It must be noted, however, that relatives share common experiences as well as common genes. Therefore, examinations of the prevalence of schizophrenia in the relatives of patients cannot elucidate the relative contributions of environmental and genetic factors. Some investigators have studied the development of adopted children whose biological mothers had schizophrenia. This approach has the potential to provide more conclusive information than family studies. The results of these investigations show that when biological offspring of schizophrenic mothers are reared from infancy in adoptive homes they are more likely to develop schizophrenia than are adopted children from healthy mothers. Furthermore, these children also exhibit a higher rate of other adjustment problems when compared with controls. Studies of this type have clearly illustrated that vulnerability to schizophrenia can be inherited. Research on twins examines differences in concordance rates between identical (monozygotic or MZ) and fraternal (dizygotic or DZ) twins. Twin studies rely on the fact that MZ twins essentially share 100% of their genes. Thus, environmental influences account for any behavioral differences between MZ twins. In contrast, DZ twins are no more genetically similar than regular siblings; DZ twins do, however, share more similar environmental factors than do nontwin siblings. To date, the results of twin studies have consistently shown that MZ twins are significantly more likely to be concordant for schizophrenia than are DZ twins. At the same time, it is important to note that in at least 50% of the cases in which one member of an MZ twin pair has schizophrenia, the other does not. Such "discordant" pairs have been the subject of a recent, comprehensive investigation in the United States. Among the most important findings from this research project are those from the MRI scans conducted on the twins. The ill twins in the pairs showed significantly more brain abnormalities than the healthy twins. Most notable were reductions in the volume of certain brain regions, especially the hippocampus, and increases in the size of the ventricles. These results clearly indicate the importance of environmental factors in the etiology of schizophrenia.

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D. Obstetrical Complications As is the case with many other disorders that involve brain dysfunction, there is evidence that schizophrenia is associated with exposure to prenatal and delivery complications. Obstetrical complications (OCs) are defined as physical deviations from the normal course of events during pregnancy, labor, or the neonatal period. Estimates of OCs in schizophrenics have been as high as 67%, significantly higher than the rate of OCs found in normal controls. Among the prenatal factors that have been found to be associated with increased risk for schizophrenia are prenatal maternal nutritional deficiency, viral infection, bleeding, and toxemia. Complications of delivery that can result in hypoxia have also been linked with heightened risk for the disorder. Hypoxia, a deficiency in the amount of oxygen available to the fetus, can affect the development of various parts of the brain. Some researchers argue that hypoxia results in hippocampal damage, thus contributing to vulnerability for schizophrenia. Low birth weight, a neonatal complication, is another potential early factor contributing to schizophrenia. There is evidence that low birth weight is related to increased ventricular size, which is a common characteristic of schizophrenia patients. The findings on prenatal complications support the notion that fetal brain development may be disrupted in individuals who later manifest schizophrenia. A central question raised by these findings concerns the nature of the etiologic role of OCs. Some hypothesize that OCs produce the neural predisposition to schizophrenia, whereas others posit that OCs exacerbate or interact with an existing genetic predisposition. Findings from prospective, high-risk research projects lend support to the hypothesis that OCs interact with genetic vulnerabilities in the etiology of schizophrenia. High-risk studies involve the repeated assessment of children of schizophrenia patients, based on the expectation that a larger percentage of these children will eventually develop the illness than individuals in the general population. The high-risk method offers some advantages when compared with retrospective studies of the precursors of schizophrenia. One advantage is that it allows for the direct assessment of subjects in the premorbid period, as well as the selection and study of variables that are thought

to have prognostic relevance. Furthermore, because a significant portion of the data collection takes place during the premorbid period, this reduces confounds that often occur in the study of diagnosed patients (e.g., medication and institutionalization). Studies using the high-risk method have shown an interactive effect of genetic risk and exposure to OCs in predicting adult psychiatric outcome. In other words, the correlation between OCs and adult psychiatric symptoms was greater for offspring of schizophrenia parents than for children of healthy parents. The same pattern was apparent for the relation between OCs and adult brain morphology, suggesting that pre- and perinatal factors contribute to brain abnormalities.

E. Viral Infection As noted earlier, prenatal exposure to maternal viral infection has also been linked with schizophrenia. Specifically, the rate of schizophrenia is increased for cohorts who were in the second trimester during flu epidemics. Another source of evidence for the viral hypothesis is the finding that the births of schizophrenia patients do not seem to be randomly distributed throughout the course of the year. Instead, the births of schizophrenia patients occur more frequently in winter months. Some researchers have suggested that postnatal viral infection may also be relevant to schizophrenia, and that the illness may be caused by a long-acting virus. This hypothesis claims that "slow viruses," which are active over a long period of time, interact with a genetic predisposition to produce schizophrenia. Various findings are cited in support of this hypothesis. Some researchers have identified a viral infection in fatal catatonia, a disorder characterized by schizophrenia-like symptoms, suggesting that a similar viral infection may be found for schizophrenia. Other researchers have found signs of viral activity in the cerebrospinal fluid of patients with schizophrenia.

F. Diathesis-Stress Model The diathesis-stress model has dominated theories about the etiology of schizophrenia for several de-

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cades. This model assumes that certain individuals inherit or acquire a vulnerability to schizophrenia (the diathesis), and that the behavioral expression of this vulnerability is determined or triggered by environmental stressors. Although "stress" was originally conceptualized as psychosocial in origin, contemporary versions of this model broaden the definition of stress to include prenatal and postnatal insults to the central nervous system. Thus the diathesis, combined with exposure to environmental stressors, can produce schizophrenia. Exposure to stress within the context of the family has been the focus of researchers in the field. Families in which there is a schizophrenia patient show more conflict and abnormalities in communication than do other families. However, it has also been shown that there is greater conflict and more abnormalities of communication in families in which any member has a severe debilitating illness. Thus, family communication styles are unlikely to play a unique causal role in schizophrenia. There is good evidence, however, that exposure to high levels of criticism from family members can increase the likelihood of relapse in schizophrenia patients. The number of critical comments, expressions of hostility, and emotional overinvolvement comprise a construct referred to as expressed emotion (EE). Recovering schizophrenia patients in families high in EE are much more likely to have a relapse compared with patients in families low in EE. There is also evidence from studies of the adopted offspring of schizophrenia patients suggesting that familial stress can hasten the onset of symptoms.

VI. TREATMENTAND THERAPY Before 1900, knowledge of the nature and causes of mental disorders was limited. Individuals with psychiatric symptoms, particularly psychotic symptoms, were typically viewed by others with disdain or amusement. However, social trends and advances in medical knowledge converged to produce greater sympathy for those with mental illness. This led, especially during the early part of the century, to the construction of public and private hospitals devoted to the care of the mentally ill. Today, most schizophrenia patients experience at

least one period of inpatient treatment. This is typically precipitated by the first psychotic episode. During this initial hospitalization, an extensive assessment is usually conducted to determine the most appropriate diagnosis. Treatment is then initiated to reduce symptoms and stabilize patients so that they can return to the community as soon as possible. In the past, periods of hospitalization were longer in duration than they are today. This is due, in part, to the availability today of better medical treatments. Another factor that has contributed to shorter hospital stays is the deinstitutionalization movement. Initially spurred by concerns that too many of the mentally ill were becoming "institutionalized" and were losing their ability to function in the community, financial support for state psychiatric hospitals was gradually cut. But community support services and transitional living arrangements were not readily available to many patients. As a result, former psychiatric inpatients now constitute a substantial proportion of the homeless found in U.S. cities.

A. Antipsychotic Medication Introduced in the 1950s, antipsychotic medication has since become the most effective and widely used treatment for schizophrenia. Research indicated that the "typical" antipsychotics, such as haloperidol, decreased the symptoms of schizophrenia, especially positive symptoms, and reduced the risk of relapse. However, they were not as effective in reducing the negative symptoms. Furthermore, some patients showed no response to antipsychotic drugs. Chlorpromazine (Thorazine) was among the first antipsychotic commonly used to treat schizophrenia. Since the 1950s, many other antipsychotic drugs have been introduced. Like chlorpromazine, these drugs reduce hallucinations, delusions, and thought disorder, and engender more calm, manageable, and socially appropriate behavior. As mentioned, all currently used antipsychotic drugs block dopamine neurotransmission. Thus it has been assumed that their efficacy is due to their capacity to reduce the overactivation of dopamine pathways in the brain. Unfortunately, the benefits of standard or typical antipsychotic drugs are often mitigated by side effects. Minor side effects include sensitivity to light, dryness of mouth, and drowsiness. The more severe effects are

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psychomotor dysfunction, skin discoloration, visual impairment, and tardive dyskinesia (an involuntary movement disorder that can appear after prolonged use of antipsychotics). It is especially unfortunate that tardive dyskinesia is sometimes irreversible when patients are withdrawn from neuroleptics. Many of these physical signs are known to be caused by chronic blockade of dopamine pathways. Although additional medications can counter some of the negative effects of the typical antipsychotics, schizophrenia patients often resist taking them because of an aversion to the side effects. Within the past decade, some new, "atypical" antipsychotic drugs have been introduced. It was hoped that these drugs would be effective in treating patients who had not responded to standard antipsychotics. Also, researchers hoped to identify medications that had fewer side effects. One example is Clozapine, released in 1990, which seems to reduce negative symptoms more effectively than typical antipsychotic drugs. Clozapine not only offers hope for patients who are nonresponsive to other medications, but it also has fewer side effects than typical antipsychotics. However, clozapine can produce one rare, but potentially fatal, side effect, agranulocytosis, a blood disorder. Consequently, patients who are on this medication must be monitored on a regular basis. It is fortunate that several other new antipsychotic medications have recently become available, and some of these appear to have no serious side effects. It appears that it is important to begin pharmacological treatment of schizophrenia as soon as possible after the symptoms are recognized. The longer patients go without treatment of illness episodes, the worse the long-term prognosis. Medication also has the benefit of lowering the rate of mortality, particularly suicide, among schizophrenia patients. Patients who are treated with antipsychotic medication generally require maintenance of the medication to obtain continued relief from symptoms. Medication withdrawal often results in relapse. At the same time, the associated long- and short-term side effects of antipsychotics, especially the typical antipsychotics, are of continuing concern to patients, their families, and physicians. It is possible that future research on the neural mechanisms involved in schizophrenia will lead to the development of novel treatments that eliminate the need for maintenance medication. Many schizophrenia patients also suffer from de-

pression and, as noted, are at elevated risk for suicide. The reason or reasons for the high rate of co-occurance of depression with schizophrenia is not known. Given the debilitating and potentially chronic nature of schizophrenia, however, it is likely that some patients experience depressive symptoms in response to their condition. For others, depressive symptoms may be medication side effects or a manifestation of a biologically based vulnerability to depression.

B. Psychological Treatment Clinicians have used various forms of psychological therapy in an effort to treat schizophrenia patients. Early attempts to provide therapy for schizophrenia patients relied on insight-oriented or psychodynamic techniques. The chief goal was to foster introspection and self-understanding in patients. Research findings provided no support for the efficacy of these therapies in the treatment of schizophrenia. It has been shown, however, that supportive therapy can be a useful adjunct to medication in the treatment of patients. Similarly, psychoeducational approaches that emphasize providing information about symptom management have proven effective in reducing relapse. Among the most beneficial forms of psychological treatment is behavioral therapy. Some psychiatric hospitals have established programs in which patients earn credits or "tokens" for appropriate behavior and then redeem these items for privileges or tangible rewards. These programs can increase punctuality, hygiene, and other socially acceptable behaviors in patients. In recent years, family therapy has become a standard component of the treatment of schizophrenia. These family therapy sessions are psychoeducational in nature and are intended to provide the family with support, information about schizophrenia, and constructive guidance in dealing with the illness in a family member. In this way, family members become a part of the treatment process and learn new ways to help their loved one cope with schizophrenia. Another critical component of effective treatment is the provision of rehabilitative services. These services take the form of structured residential settings, independent life-skills training, and vocational programs. Such programs often play a major role in helping patients recover from their illness.

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VII. SUMMARY It is now firmly established that schizophrenia is caused by an abnormality of brain function that in most cases has its origin in early brain insults, inherited vulnerabilities, or both. But the identification of the causal agents and the specific neural substrates responsible for schizophrenia must await the findings of future research. There is reason to be optimistic about future research progress. New technologies are available for examining brain structure and function. In addition, dramatic advances in neuroscience have expanded our understanding of the brain and the impact of brain abnormalities on behavior. We are likely to witness great strides in our understanding of the causes of all mental illnesses within the coming decades. It is hoped that advances will also be made in the treatment of schizophrenia. New drugs are being developed at a rapid pace, and more effective medications are likely to result. At the same time, advocacy efforts on the part of patients and their families have

resulted in improvements in services. But a further expansion of services is greatly needed to provide patients with the structured living situations and work environments they need to make the transition into independent community living.

BIBLIOGRAPHY Breier, A. (Ed.). (1996). The new pharmacotherapy of schizophren/a. Washington DC: American Psychiatric Press. Keefe, R. S., & Harvey, P. (1994). Understanding schizophrenia: A guide to the new research on causes and treatment. New York: Free Press. Miller, G. A. (Ed.). (1995). The behavioral high-risk paradigm in psychopathology. New York: Springer. Shriqui, C. L., & Nasrallah, H. A. (Eds.). (1995). Contemporary issues in the treatment of schizophrenia. Washington DC: American Psychiatric Press. Torrey, E. F. (1994). Schizophrenia and manic-depressive disorder: The biological roots of mental illness as revealed by the landmark study of identical twins. New York: Basic Books. Walker, E. F. (1991). Schizophrenia: A life-course developmental perspective. New York: Academic Press.

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Sexual Disorders R0nald M. Doctor and Bryan Neff California State University, Northridge

I. II. III. IV. V. VI. VII.

Introduction Gender Identity Disorders The Paraphilias Causal Models and Treatments Sexual Addiction Rape Homosexuality

Sexual Orientation One's emotional and physical attraction toward the same sex (homosexual), opposite sex (heterosexual), or both (bisexual). Transsexualism An extreme form of gender identity disorder in which a person exhibits a life-long sense of gender incongruence (e.g., feeling trapped in the body of the opposite sex) and an overriding desire to undergo reassignment surgery. Transvestism A paraphilia that is marked by a compulsion to cross-dress in clothing of the opposite sex. The amount of cross-dressing can be partial or regular. Most transvestites are heterosexual. Voyeurism A paraphilic condition characterized by a recurrent, intense, and sexually oriented act that involves the observation of unsuspecting people who are naked, disrobing, or engaged in sexual activity.

Biological Sex Refers to one's status as male or female in terms of basic physiological characteristics, e.g., chromosomes, hormones, genitalia, etc. Exhibitionism A paraphilic condition in which sexual gratification is obtained by inducing surprise, fear, or disgust in an unsuspecting person by the "flashing" of one's genitalia. Fetishism A paraphilia that involves sexual gratification through rubbing, fondling, or usage of body parts or nonhuman objects such as underwear, garters, shoes, silk, etc. Gender Identity Refers to a person's psychological identification with culturally defined traits and behaviors that constitute being a man (masculine) or woman (feminine). Gender Identity Disorders Sexual disorders in which a person experiences a psychological confusion or mismatch between their biological sexual characteristics and their culturally assigned gender identity. Paraphili~ Sexual disorders that are characterized by an intense focus upon ( 1 ) nonhuman objects, (2) the suffering or humiliation of oneself or a partner, or (3) children or other nonconsenting persons; and result in great personal distress or disturbance.

SEXUAL DISORDERS encompass the full range of human sexual thoughts, feelings, and actions that are generally regarded as abnormal, dysfunctional, or disordered. With three exceptions (homosexuality, sexual addictions, and rape), the disorders discussed here are listed in the Diagnostic and Statistical Manual Version IV (DSM-IV) used in psychiatry and psychology as a means of listing the various diagnostic categories treated with psychotherapy or medications. Since the DSM-IV represents our current cultural values regarding human sexuality, it will serve as the basis for identifying various "disorders" that we feel are unacceptable in mainstream society. The disorders discussed are listed under "sexual and gender identity disorders" in the DSM-IV. The gender identity disorders,

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while they begin in childhood, have a profound effect on adult behavior and the ways in which adults cope with this disorder. Homosexuality has been excluded from the DSM-IV but remains a topic in the sexual disorders literature and cannot be excluded as a form of sexual variation that has significant socio-cultural history. The sexual addictions are included in this discussion for information purposes since the terminology has been used extensively in the public literature and media. Finally, rape, which is not represented in the DSM-IV, is discussed in this article, although we emphasize its aggressive and violent nature rather than sexual nature. Rape, as with such crimes as murder, are usually considered symptoms of other underlying problems, not a disturbance in itself.

I. INTRODUCTION Few topics regarding human behavior hold as much interest and as much pathos as that of deviations and dysfunctions in human sexuality. What constitutes deviations and dysfunctions, however, are heavily dependent on contemporary cultural attitudes and values and these are often blind to the past history of sexuality in the culture. We know, for example, that sexuality was represented in the rock art of the earliest human cultures. Paleolithic (30,000 to 10,000 B.C.) rock art, for example, is replete with both human and animal fertility symbols that were thought to endow the represented forms with abundant offspring. The Egyptians (3000 B.C.) are thought to have added power to the concept of fertility as represented in their symbols. In Western culture, our sexual values came mostly from the JudeoChristian traditions. The Judaic tradition emphasized reproductive sexual behavior without guilt. The core concern was to protect the integrity of marriage with all other considerations of secondary value. Strict laws of adultery were applied to women but the husband was instructed only to "not covet your neighbor's w i f e . . . ," otherwise sex outside the marriage was tolerated. While the Jews were nomadic and their values emphasized family and procreation, sexual values for the Greeks emanated from their more settled agricultural lifestyle. Here family was still central but the Greeks allowed far more freedom of sexual expression in varied forms. For example, bisexuality was common among Greek males. Since beauty was the primary value or attraction, sexual behavior and arousal could arise in response to both boys and young or mature

women of beauty. With the rise of Christianity more ascetic beliefs began to emerge. In general, sex had a procreative function, not the pleasure role noted with the Greeks and Hebrews. By the 18th century, religious views of life shifted from emphasis on eternal life in heaven to attaining happiness on earth and romantic love was valued. Sexual "deviations" started to become cultural issues with particular emphasis on homosexuality and masturbation. As venereal diseases became widespread, cultural values shifted to the physician as the arbiter of sexual morality, and to the repression of sexual behavior, particularly that of males. In the 20th century sexual notions are clearly shifting towards a continuum of behaviors. Modern sexologists not only have described the physiological, emotional, and psychological aspects of sexual behavior but have also highlighted the various forms of sexual behavior that exist whether in overt or covert forms. This article deals with the full range of human sexual thoughts, feelings, and actions that are generally regarded as abnormal, deviant, or disordered. Our focus will be on these extremes but it should be noted that "deviant" and "disordered" are concepts that rest upon the assumption of a medical, disease, or psychiatric model of behavior that dichotomizes human actions into two qualitatively separate categories of "normal" and "abnormal." Some sexologists, on the other hand, view these sexual behavior variations not as diseases to be cured but as atypical expressions representing quantitative rather than qualitative differences. To them, sexual behavior falls on a broad continuum with the extremes being vulnerable to labels like "disordered" and "abnormal." Here we are dealing with differences in intensity and narrowness of behavior rather than qualitatively different behaviors. We can see this, for example, in the husband who might be aroused by his wife wearing lingerie versus the fetish individual who can only become sexually aroused by lingerie. Furthermore, the demarcation between abnormal and normal categories is not fixed or absolute. Rather, it consists of an ever changeable subjective value judgment derived from psychiatric, cultural, and political forces. For example, masturbation, once considered a sin then a disease, is now acceptable and understood. Likewise, homosexuality was actually removed from the psychiatric nomenclature due to political pressures and changes in culture norms. These are examples of the changeable nature of categorization and labeling and the subjective social value judgments they represent.

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Our discussion will follow closely the psychiatric nomenclature and diagnostic categories since these represent our current values regarding human sexuality and the types of behaviors that are considered unacceptable in mainstream society. We will use the terms or labels often used in psychiatry and law to denote these patterns. Although it is not a psychiatric disorder, we will discuss homosexuality since it is a form of sexual behavior that has socio-cultural historical relevance and is still a controversial topic among some peoples. We will also discuss rape, gender identity disorders, and sexual addictions which are listed in the psychiatric diagnostic system but not under sexual disorders. The behavioral area of sexual dysfunctions is not discussed since it usually represents inhibitions in sexual drive or performance and is not as comprehensive a manifestation of one's being as are the problems and stresses characteristic of sexual disorders. Finally, we will briefly discuss the topic of rape, emphasizing its aggressive and violent nature rather than sexual nature. Our starting place in discussing sexual disorders is to focus on the notion of "sexual identity." A person's sexual identity can be seen as an interrelationship among the three basic elements of human sexual behavior, namely, biological sexual characteristics, gender identity, and sexual orientation. In the diagram below you can see that sexual identity is formed from the interaction between biological sex characteristics (such as male and female sex organs, hormones, etc.), gender identity (or one's identification with or feeling of femininity or masculinity), and sexual orientation (homo-, bi-, heterosexual, or other objects of stimulation as found, for example, in the paraphilias). In examining the gender identity disorders we will be discussing biological sex and gender identity. On the other hand, when we discuss the paraphilias, we will be focusing in part upon sexual orientation. Sexual orientation (homo-, bi-, hetero., or other sexual objects)

Gender identity (feminine vs masculine)

Biological sexual characteristics

(male vs female)

II. GENDER IDENTITY DISORDERS A person with gender identity disorder (GID) experiences a confusion or mismatch between biological sexual characteristics and their culturally assigned gender identity. The identity problem is psychological in nature rather than a biological ambiguity. Biologically, they are dimorphic (male vs female) in terms of chromosomal, gonadal, genital development, and hormonal levels. The ambiguity exists in terms of the individual's identification with culturally defined traits that constitute being a woman or man, i.e., the degree of femininity or masculinity the person exhibits through thoughts, feelings, and their actions. Not all people are comfortable with what they feel is their true sense of being a woman or man and their biological sex. The amount of disturbance can range from a mild sense of inappropriateness, to feeling like a woman trapped in a male's body, and vice versa. GID should not be confused with transvestism, homosexuality, and hermaphroditism. Transvestites, as we will see later in more detail, cross-dress for fetishistic pleasure, and, with few exceptions, rarely find an incongruity between their sex and gender. A person who is emotionally and sexually attracted to a member of their same sex is, likewise, not inherently disturbed in regards to their gender identity. Finally, the hermaphrodite has to some degree the sexual organs for both sexes. Since this confusion stems from being biologically intersexed, the hermaphrodite's dilemma is not considered a psychological disorder. Once again, those with GID are unambiguously biologically formed in one sex, and their confusion is at the emotional and psychological levels. GIDs are conceptually divided into three categories: GID of childhood, GID of adolescence and adulthood (not transsexual), and transsexualism. Let us look at each of these three categories.

A. Gender Identity Disorder of Childhood GID of childhood is reserved for prepubescent children and is relatively uncommon. The sex ratio for the population in general is unknown, yet through clinical work it appears that there are many more boys than girls diagnosed with this condition. Generally, the age of onset for both sexes is age 4; however, in some cases it may appear as early as age 2. The majority of children will return to their expected gender roles by puberty, while the remaining minority will continue experiencing what is called "gender dysphoria" or role confu-

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sion. Reliable predictions of adult pathology, based upon nontypical childhood behavior have proved elusive. The primary symptoms needed to make a diagnosis are: (1) a persistent and severe discomfort regarding her or his own biological sex, and (2) a belief that they are, or desire to be, of the opposite sex. Such feelings and behaviors are chronic and problematic, thereby transcending any normal variation of stereotypical gender roles, such as being a "tomboy" or a "sissy." A female with this disorder exhibits intense feelings of frustration at being a girl with a corresponding desire to become a boy, or, in some cases, they may even believe that they are of the opposite gender already. They often seek male peers and are repulsed by traditional feminine toys, games, etc., preferring instead the masculine equivalents. Lastly, there is an intense disgust toward and rejection of their anatomy, often illustrated by beliefs that they will grow a penis or not go through normal female pubescent body changes. The overall pattern with males is identical to the female description except that the specifics are reverse. For example, GID boys typically show severe distress at being a boy, they engage in cross-dressing, and prefer female toys, peers, and so on. They are repulsed by their genitalia, often wishing that it would disappear or that they would grow up and become a woman. A major difference between the two sexes is found in the fact that many more boys than girls are treated for this condition. It is thought that differential socialization patterns may account for the discrepancy in prevalence rates. For example, boys are more often subjected to rigid parental expectations and therefore any nontypical gender behavior is often more apparent. Boys also tend to display more signs of secondary pathology, e.g., depression, anxiety, and withdrawal, perhaps due to harsher social consequences from peers for their feminine-like behavior. On the other hand, females who cross the gender line ("tomboys") tend to be more readily accepted than "sissies," or boys who violate gender expectations.

B. Gender Identity Disorder of Adolescence or Adulthood (Nontranssexual) A person with this condition must have reached puberty, exhibit reoccurring discomfort with their biological sex, and habitually cross-dress. Motivation for wearing the apparel of the opposite sex is for emulation

purposes, not for fetishistic pleasure. They are psychologically identified with the opposite sex and exhibit intermittent to constant cross-dressing. Despite the person's sense of discomfort, they usually have no preoccupations with changing their sex to match their gender identity. Some researchers theorize that GIDs should be conceptualized on a continuum rather than as separate diagnostic categories. Accordingly, they might prefer the term transgenderism, which can be seen as an intermediate stage between the two extremes of GID of childhood and secondary transsexualism, i.e., someone who after a period of time decides to make a sex change. The transgenderist is someone who is living permanently in the role of the opposite sex but does not have the desire for a complete sex change. Essentially, their change is in gender, not in sexual biological characteristics.

C. Transsexualism The transsexual condition can be distinguished from other GIDs essentially because of a life-long sense of gender incongruence or inappropriateness and a persistent preoccupation or obsessive quest for sex realignment or "reassignment" surgery. This preoccupation for sex change surgery must be present for at least 2 years to be diagnosed transsexualism. As you can see, we are now at the more extreme end of the GID continuum. Some theorists have attempted to distinguish between primary and secondary transsexualism, with the former evidencing a history of gender dysphoria since childhood while the latter may be long-term cross-dressers or transgenderists but they seek reassignment surgery later in life usually after experiencing a traumatic stressor. Secondary pathology for transsexuals is common and most often includes anxiety and depression. For those who are driven to change their sex, the difficulty in getting the funds to pay for surgery can result in self-mutilation and even suicide. In a culture that defines their dilemma as pathological and abnormal, transsexuals have many stories to relate about the pain and suffering they experience. This brief glimpse into the recollection of a girl "trapped" in a male body should partially convey their struggle for recognition as legitimate human beings: ... I wanted above all to walk down the hall at school and be looked at and respected as werethe normalgirls.Yes,nor-

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mal girls; for I was a girl with all my heart, but I was not a normal girl. I was a freak of a girl, one w h o had to look like a boy . . . . (Benjamin, 1966, p. 199)

It is generally believed that transsexualism is present in about 1 out of 30,000 males and 1 out of every 100,000 females. More males seek out treatment than females, with ratios as high as 8 to 1. In the United States alone, it is estimated that there are between six and ten thousand postoperative transsexuals, i.e., people who have had sex change operations.

D. Etiology of Gender Identity Disorders As the current body of knowledge now stands, the causal roots of GID remain undiscovered. The various approaches that attempt to explain this particular disorder can be broken down into the biological/medical, psychodynamic, and developmental/learning models. The first approach purposes genetic, hormonal, neurological, and chromosomal abnormalities as a causal factor. Despite a few leads, such as the effects of prenatal hormones on gender behavior, there is a meager amount of data to support the notion of biology as a sole or even major influence. The psychodynamic model emphasizes early childhood and personality development. Causal roles are attributed to difficulty with mother-child relations and the failure to psychologically identify with the parent of the opposite sex. Again, this is not a universal or even major phenomenon. Furthermore, it is very difficult to tease out what is the chicken and what is the egg. In other words, do parents shape children's behavior or does the child's behavior shape the parents' difficulty with the relationship ? Finally, the importance of socialization processes and the acquisition of atypical childhood behaviors via modeling or conditioning represents the learning and developmental point of view. Unfortunately, contrary to both the psychodynamic and learning models, there is very little indication that the family environment has any serious effect in the development of gender identity disorders for substantial numbers of cases. For example, in a study by R. Green (American Journal of Psychiatry, 1978), of 16 children who were raised by transsexuals all were found to have heterosexual orientation with no disturbance in their gender identity.

E. Treatment Approaches to Gender Identity Disorders The general consensus is that many or all behavioral and psychodynamic treatments for GID are ineffective.

Behavioral therapies have produced a few "successes" in strongly motivated clients, but even then some of the behavioral modification techniques used have raised disturbing moral questions. For example, reports of behavior therapies describe asking children to overemphasize the gender identity differences so as to produce aversive social reactions which, presumably, would diminish these opposite-sex behaviors and attitudes. In contrast, psychodynamic treatments aim at resolving childhood conflicts in the hope of producing acceptance of one's sex and the corresponding gender identity. After many case histories and grueling therapeutic hours, personality reorganization approaches have almost always ended in total failure. Both approaches subject children to personal pain in addition to the feelings of failure they must experience in therapies are ineffective. For transsexuals, sex reassignment treatment (sex change surgery) has proven in a majority of cases to be successful in bringing happiness and relief. After a careful screening process, a qualified individual must undergo intensive counseling and instruction on matters of grooming, vocation, legal rights, voice training, and the proper use of stereotypical gender role mannerisms. Then they may begin hormonal therapy in order to produce the desired secondary sex characteristics, e.g., breasts in males, facial/body hair modification, changes in body fat distribution, and some voice alteration. After living and working in one's new gender role for 1 to 2 years, only then can the candidate undergo genital reconstruction. The artificially constructed vagina is much more realistic in appearance and function than its male counterpart. While female genitalia is capable of lubrication and orgasm, the penis is less sensitive and lacks natural erectile capacities. Though limited in number and with sometimes inconclusive findings, some follow-up studies have indicated an 80 to 85% satisfaction rate for transsexual operations, with male-to-female transsexuals usually faring better than their counterparts. Dissatisfaction is usually the result of poor surgical techniques and personal and social instability that preceded surgery.

III. THE PARAPHILIAS The term parapbilia is derived from the notion of a deviation or separation (para-) from what most people are attracted to (-philia). Originally, these were called "perversions," but modern terminology generally

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describes them as "deviations" or, more recently, as "variations." The D S M - I V describes these deviations as " . . . recurrent sexually arousing fantasies, sexual urges, or behaviors generally involving either (1) nonhuman objects, (2) the suffering or humiliation of oneself or one's partner, or (3) children or other nonconsenting persons." The diagnosis, however, is made only if the person has acted on their urges or is greatly disturbed or distressed about them. Paraphilic fantasy (such as sex with animals, arousal from undergarments, sado-masochistic thoughts, cross-dressing, or sex with children, etc.) as such is not sufficient to warrant clinical diagnosis. These preoccupations must be intense and recurrent, or undesired and disturbing to the individual, the preferred or exclusive forms of sexual gratification, or acted out overtly to be considered pathological. The paraphilias are usually multiple in nature rather than singular. They are almost exclusively confined to men with the exception of masochism, in which we see a significant number of females. Current views of paraphilias have been heavily influenced by Freudian theory and analysis of sexual behavior. Within the psychodynamic model, a healthy or natural sexual relationship consists of opposite sexed partners whose object is coitus (sexual gratification through intercourse). These deviations in sexual orientation involve the use of an object other than the opposite sex partner, such as one of the same sex (homosexual), children (pedophilia), close relative (incest), animals (zoophilia), inanimate objects (fetish), or even dead people (necrophilia), as sexual objects. Likewise, instead of seeking coitus, departures include watching others (voyeurism), exposing genitals (exhibitionism), infliction of pain (sadism), or suffering pain (masochism) as deviant aims. In the paraphilias, the erotic object has a role or characteristic that is more important than their personality and personal characteristics of the object and the aim is to enact the paraphilic fantasy. Mainstream diagnostic systems have been strongly influenced by these two major departures from object and aim. Alternatively, others have argued that perhaps the impact on others should be used as the diagnostic criterion. Here, fetishes and transvestism, and perhaps gender identity disorders, would be excluded in that they usually have little or no direct negative impact on others. All this is brought to your attention to highlight the subjective and consequently changing nature of diagnosis and categorization. Basically, as with most other mental illness categories, we are dealing

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with social value judgments rather than specific "diseases" and as such cultural and political values and attitudes influence the diagnostic process.

A. Pedophilias The pedophile (derived from the Greek for "child lover") sexually prefers children of either sex for erotic gratification. It is usually thought that perpetrators must be at least 10 years older than their victims, but this age difference may differ considerably depending on circumstances. Pedophilia is also called "child sexual abuse" and "child molestation." Child molestation is most often perpetrated by males and usually involves such actions as manipulation of the child's genitalia, stroking of the body, forcing the child to manipulate the adult's genitalia, and, to a lesser degree, intromission. Pedophilia is the most common form of paraphilias and involves the most vulnerable victims~ children. Heterosexual men are responsible for most sex abuse against girls. Two out of three sexually abused children, however, are girls. Conservative estimates are that 10% of females and 2% of males were sexually abused as children. There is no well-delineated personality for the pedophilic. However, the concept of the "dirty old man" as perpetrator is misguided in that most pedophiles are in their late 30s with only about 5 % being aged men. If we had to generalize, we could say that pedophiles are generally immature developmentally even though they may have married and have children of their own. Second, we often see the behavior under stress, i.e., during stressful life periods often accompanied by marital and sexual problems. Alcohol is consistently involved in pedophilic encounters. The majority of victims are relatives, neighbors, or acquaintances; and encounters, while usually brief, occur in series of extended contacts. Generally the younger the child, the more immature the perpetrator. Actual penetration and coitus occur in only 4% of cases. Interestingly, the vast majority (80%) of perpetuators have themselves been abused as children.

B. Incest Incest is treated here as a subcategory of pedophilia. However, since pedophiles differ in age from their victims, incest may not necessarily meet the criteria. For example, the majority of incest cases seem to involve cousins and siblings who might be similar in age. Incest

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(from the Latin "impure") is a form of pedophilia involving close relatives, most commonly between cousins but parent-child or sibling-sibling incest is the most repugnant and most often the focus of treatment or criminal proceedings. Taboos against incest are present in all cultures, particularly against mother-son incest. Surveys among adults indicate that 14% of males reported having had sexual contact with a relative before adulthood (95% of which were heterosexual in nature) and 9% of females have had such contact. Most of these experiences were with cousins and essentially involved some form of "petting." Among a university sample, however, 10% of females reported incestuous relationships with their fathers (including stepfathers). Almost 90% of cases brought to court for incest involve father-daughter while only 5% are father-son incidents. Transgenerational incest seems to occur in about 10% of incest cases but probably has different dynamics than immediate parents and children or children and children. The studies of incest have concluded that these events occur within seriously disturbed or dysfunctional families and that a code of silence develops in which these events are not spoken about and often repressed by the victims. Furthermore, the parents in this unhappy marriage typically consist of a domineering, authoritative, and impulsive husband and a dependent and emotionally distant wife. The husbands often also abuse the wives as well as the children. Incest is a criminal as well as psychological disorder. The experience of incest is traumatic and psychologically damaging to the children involved (and even to those who know about it). Criminal prosecution does not erase the trauma of incest. These deep psychological scars must eventually be addressed in order for the victim to heal and live a fully mature life.

C. Voyeurism Voyeurs are also called "peepers" or "Peeping Toms." The psychiatric diagnostic system describes this condition as a recurrent, intense, and sexually oriented "act of observing unsuspecting people, usually strangers, who are either naked, in the process of disrobing, or engaging in sexual activity . . . . "Looking (or "peeping") provides sexual arousal but no actual sexual contact with the observed person is sought. Orgasm, usually produced by masturbation, may occur during the voyeuristic activity, or later in response to the memory

of what the person has witnessed. Often these people enjoy the fantasy of having a sexual experience with the observed person, but in reality this does not occur. In its severe form, peeping constitutes the exclusive form of sexual activity. Lady Godiva's ride through the streets of Coventry to remit an oppressive tax was watched by no one from the t o w n - - o u t of respect and gratitude for her actionsmwith the exception of Tom the tailor, who peeped through the curtains and for this act went blind. The "Peeping Tom" of today does not go blind literally but they are almost always men. To be considered a paraphilia, there must be a recurrent and intense preoccupation with looking from hiding or secret places. Just looking at live nudes or pictures of nudes is not a paraphilia. Voyeurs tend to be younger men (convicted age is 23.8 years), unmarried and with little or no alcohol, drug, or other mental illness problems. While they tend to be heterogeneous as a group, they do commonly have deficiencies in heterosexual relationships. As a matter of fact, it has been conjectured that the voyeuristic practices are a safe and protected way of avoiding a possible relationship with a woman.

D. Exhibitionism The legal term for exhibitionism is "indecent exposure" because of the shock or offensive value of the act to others. Again, this is mainly a male disorder. Like other paraphilias, it involves repetition, intensity, and sexual urges or arousing fantasies of at least 6 months duration. For the exhibitionist or "flasher" gratification seems to come from the disgust, shock, fear, and surprise of the unsuspecting usually female victims. There is usually a compulsive, driven quality to this behavior (as with most paraphilias) but they are also prone to be caught as they return to the same situation or place repeatedly. There is some evidence that at some level they may wish to be caught and that this consequence is deliberate and desired. The exhibitionists' behavior has a distinctive hostile air to it and this, coupled with the fact that they often have serious sexual problems might suggest intense, perhaps unconscious, hostility exists toward women. As a group they tend to be younger (30s) with about 30% married, 30% divorced or separated, and 40% never married. They are often above average in intelligence and do not have more serious forms of mental illness.

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Anxiety, which forms a part in all the paraphilias, is also apparent in exhibitionists both in terms of the excitement or anxiety associated with the act itself and with the desire for anxiety relief that results from the act. There is also evidence that exhibitionists are sexually aroused by stimuli that usually have little or no arousal potential for most people (such as seeing fully clothed women in normal activities) and thus may misread the motives and intentions of others (perhaps seeing them as sex crazed as they are). A fairly large percentage of women (between 45 and 50%) report having seen or had direct contact with a "flasher."

E. Fetishism Fetishism involves sexual arousal from some inanimate or nonliving object. Exposure to the object or preference for the object is usually necessary to maintain erectile states. Common objects include shoes, sheer stockings, gloves, toilet articles, undergarments particularly underpants, and many tactilely stimulating substances (soft fetishes) such as fur, velvet, and silk garments, and smooth solid objects (hard fetishes) that can be rubbed and fondled such as shoes, leather objects, and so on. In ancient cultures, fetishes were objects that had magical powers. For the fetishist the object itself is endowed with sexual power and the owner is of little or no interest. Panties, stockings, and garters may be alluring and channel excitement to the wearer but to the fetishist, the object itself is the allure and goal, not the user. Almost any object can acquire fetish properties. One mechanism for acquisition is classical conditioning in which a neutral object comes to acquire arousal properties by association with sexual arousal and stimulation (i.e., masturbating with the object present). By this process, any stimulus, even body parts, can become a fetish object. Orgasm may occur with the fetish alone or the fetish object may need to be present during intercourse in order to maintain stimulation toward orgasm. Again, poorly developed heterosexual relationships are found in fetishes as in other paraphilias. Here, however, there is usually a strong mother-son bond with the fetish individual. Fetishes usually develop during adolescence. Fetishists are seldom distraught enough by the behav-

ior to seek out psychotherapy and they are usually not overt or foolish enough to be arrested or detected.

F. Transvestism The Latin trans meaning "across" and vestia meaning "dress" for the term for "cross-dressing" or "transvestism." As pointed out earlier, transsexuals often manifest cross-dressing as a first expression of opposite sex feelings. This behavior, along with men who dress in "drag" to attract other men for sexual purposes, is not usually considered manifestations of transvestism. Likewise, female impersonators and actors who play female parts are not included under this diagnosis. To qualify as transvestism, there must be a compulsive desire to cross-dress and an intense frustration when the practice is interfered with. The transvestite is usually heterosexual in orientation, married, and otherwise masculine in appearance, demeanor, and sexual preference. The cross-dressing, while compulsive, is done in secret and does not lead to homosexuality or gender identity problems--although transvestites report feeling like a woman during the cross-dress episodes. Often wives will be overt or covert conspirators in the cross-dressing activities. Cross-dressers will often seek each other out for social occasions while made up as women. The compulsion to cross-dress begins by adolescence, although most children who cross-dress will "grow out of it" by adulthood. Some male transvestites recall their parents forcing them to wear girls clothing as a form of humiliation and punishment. As an adult, however, the wearing of women's clothing usually has more significance than just sexual arousal or punishment. It affords the transvestite male an opportunity to escape from pressures and responsibilities. Some males only partially cross-dress, usually by covertly wearing female undergarments under their male clothing. Others are complete cross-dressers, who overtly carry out this practice either occasionally or, for some, all the time.

G. Sadomasochism (S-M) The term sadomasochism is derived from the family names of two historical characters. The first is the French nobleman Marquis de Sade (Donatien Alphonse Francois was his "first" name, 1740-1814),

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whose writing consisted of vivid accounts of pain inflicted on one partner in sexual encounters of various kinds. Sexual sadism is defined as the infliction of physical pain and/or personal humiliation and degradation on a sexual partner. While de Sade portrayed infliction of excruciating pain on individuals, most sadism involves mild to moderate pain. It is estimated that about 5% of men and 2% of women have obtained sexual pleasure by inflicting pain on a regular basis. While sadists inflict pain on willing or nonconsenting partners, sexual masochists (from Leopold von Sacher-Masoch, a German novelist who described this behavior in the late 19th century) enjoy suffering for erotic excitement as a preferred form of sexual activity. While sadists overwhelmingly tend to be men, masochists are more often females. The study of sadomasochism has only just begun. What little is known about these practices comes mainly from case studies, i.e., examination of S-M activities at centers for such activities or through paid dominance and submission sexual surrogates hired for these purposes. Sadomasochistic activities center on use of dominance-aggression and submission in sexual activities. Terms that denote these activities abound such as bondage and domination (B-D), master-mistress, dominatrix, humiliation, restraints, whipping, leather/ rubber, slave, bottom or submissive, and so on. Activities often involve elaborate interactions, sometimes with predetermined code words that will lead to the immediate release of a victim if desired and often use fetishistic trappings such as leather/rubber garments, chains, whips, shackles, harnesses, and other props. Rarely do sadomasochistic practices lead to physical injury, mutilation, or death. Victims, however, may be nonconsenting or willing and, not infrequently, paid sexual partners. The most frequent S-M activities are spanking, master-slave bondage, humiliation situations, oral-anal S-M contexts, whipping, and to a lesser degree, verbal abuse, enemas, torture, "golden showers" (urinating on someone), and use of toilet articles. There is a well-defined S-M subculture that includes paraphernalia sex shops, stages for bondage scenes, magazines, prostitutes trained in S-M skills, and videos. Participants are predominantly heterosexual males with a greater concentration of bisexual female participants. Sadomasochistic activities are de-

fined as paraphilias if they are recurrent and intense. To just tie up a sexual partner occasionally is not S-M activity.

H. Miscellaneous Paraphilias Sexual arousal can become conditioned to a wide variety of eliciting stimuli. In this section, we will describe some relatively uncommon paraphilias that involve unusual and sometimes noxious objects of sexual arousal. The miscellaneous paraphilias described below not only occur rarely but are often not detected due to their secretive nature and the fact that persons who engage in these acts are rarely motivated to seek treatment for their behavior. A number of paraphilias are difficult to clarify. Some seem closely linked to fetishism but instead of body parts, body discharges take on erotic significance. Coprophilia, for example, involves erotic fascination with feces; klismaphilia with enemas; urophilia with urine; and mysophilia with filth. These stimuli may excite or be used for orgasm. Soiling othe r s - b y urinating or defecating on t h e m ~ c a n also serve sadomasochistic purposes and is sometimes seen in assaults and rape situations. Some paraphilias may have a sexual goal that is not immediately obvious. For example, pyromania (fire setting) and kleptomania (stealing for excitement)are thought to sometimes represent sexualized activities and thereby qualify as paraphilias. Frotteurism (or toucherism) is a paraphilia that involves sexual gratification or arousal by rubbing against or fondling an unsuspecting, nonconsenting person. The frotteur acts on urges to touch, rub, or fondle usually in crowed places, often accompanied by fantasies of having sex with the singled-out person. Contact is brief to avoid detection. Finally, the 20th century has brought a host of telephone scatologia, or efforts to seek sexual gratification by making obscene telephone calls. Anonymity and escape from detection are enhanced in use of this media for contact.

IV. CAUSALMODELS AND TREATMENTS Several key observations and assumptions should be noted before addressing the etiology and treatment

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of sexual disorders. First, contemporary sexologists have had little success in identifying specific causal factors and in designing and implementing successful treatment modalities. Such a state is due, in part, to limited theoretical models and problematic methodology. Criticism of existing causal models has been in terms of their myopic and/or reductionistic focus. In other words, most theories have focused solely on cognitive/emotional, behavioral, or environmental elements rather than on how all three elements interact and affect an individual's sexual identity. Another factor may be methodological problems, e.g., the difficulty in forming operational definitions for, and measuring such abstract concepts as, gender identity or sexual orientation. A more important and subtle point however, is the view that by separating the range of sexual behaviors into specific categories and calling these "abnormal," we are, by this process alone, not asking the critical questions about how sexual identity and orientation develop as a phenomenon. Instead, we are caught up in treating our categorizations as if they are real and true medical diseases or abnormalities. In fact, it appears that sexual expression can vary greatly and lies on a continuum. Even though experience and socialization can affect the location of one's position on the continuum, we know very little about how individuals get to a particular place on the continuum in the first place. Biological theories have predominated as causes of sexual disorders. The specific biological determinant or process would have to be in the male and not female structures. No absolute causative biological mechanisms have been identified. Most behavioral scientists see very little value in the psychoanalytic or psychodynamic theories. Both deficient psychosexual development and Oedipal fixations have been used to account for sexual disorders. Repressed hostility is thought to be at the roots of most paraphilias and the disorder allows a symbolic acting out of these repressed urges. Learning theory models emphasize classical conditioning or associative learning linking sexual arousal with previously neutral objects or situations, masturbation becoming a key activity for this linking to occur. Learning theory seems to account for some paraphilias and for some portion of the sexual disorders but it lacks sufficient empirical power and predictability. As mentioned previously, treatments for the paraphilias and other sexual disorders are very ineffective and positive effects seem to be confined to highly

motivated clients with milder forms of the disorders. Biological treatments essentially attempt to dull or reduce sexual drive. The behavior therapies utilize counter-conditioning and desensitization methods. Various forms of group therapies (structured in a selfhelp manner) seem to be effective with the motivated client.

V. SEXUAL ADDICTION How far do normal sexual activity levels extend? Where do we draw the line for pathological levels of sexual activity? Again, changes in social values have defined different patterns and points on the sexual activity continuum as pathological at different times. As a matter of fact, lack of precision in defining this category and the subjective nature of judgments resulted in the elimination of sexual addiction from the paraphilias in the DSM-III-R edition. The terms "sexual addiction" and "sexual compulsion" began to appear in the scientific and clinical literature in the 1970s. They soon became popular terms to describe individuals who seemed obsessed with sexual behavior, i.e., nymphomaniacs, etc. Usually, sexual activity had to reach a level where it interfered with their job, relationships, career, or even their health. The behavior was often described as uncontrolled sexual behavior but functional analysis showed that it tended to lower anxiety states and probably helped enhance self-esteem and the sense of power and control. Critics of the use of these concepts or diagnostic categories argued that they lacked precision and behavioral clarity, that they were often unreliable, and full of subjective judgments. Critics pointed out that the concepts did not fit our knowledge of the addictions nor of the compulsive processes. Furthermore, they were often applied to gay men with many partners and thus seemed discriminatory. Supporters of this category argued that frequency was not the issue, rather one had to look at the purpose and meaning to the individual as critical components. Here, seeking out transient relationships in an indiscriminate manner certainly had the ring of selfdefeating and self-destructive patterns of behavior that qualified as paraphilias. At this point, however, sexual addiction is an historical term.

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VI. RAPE

VII. HOMOSEXUALITY

Rape (Latin, "to seize") or the actual act of seizing a person by physical force or threat is an extreme form of sexual aggression and coercion. Rape is technically a legal term but it can be viewed from a psychological perspective. Current definitions of rape have extended the violation to deliberate intrusion into the emotional, physical, or rational integrity of the individual and even debasement through voyeurism ("visual rape"). Legally, rape is divided into statutory (seduction of minor) and forcible seizure of an unwilling partner over age 18. Recent attention has been focused on "date rape" or the use of coercion by dates, acquaintances or even boyfriends. The victims are almost always women. No woman is entirely safe from rape. Almost 100,000 rapes are reported each year but estimates are the majority of rapes go unreported. Most occur outside or in the victim's home. National studies have found that the incidence of rape has increased more rapidly than any other type of violent crime. There are many factors and levels of causation to rape. Certainly, cultural and subcultural attitudes toward women and about men contribute to the setting for rape. Psychological studies of rapists have identified some broad typologies of rapists. These types were derived from a psychological examination of rape cases. In none of these cases was it found that rape was motivated by sexual satisfaction. All the cases were characterized by a predominance of power motive or anger. This led to the classification of rapists as (1) power assertive types (intimidation and control), (2) power reassurance types (to compensate for an underlying sense of weakness and inadequacy), (3) anger-retaliation type (rage, hatred, and violence predominate), and anger-excitation rape (the pathological sadist). Prediction of rape from psychological profiles is not possible even though a proportion of rapists are obviously disturbed. The literature in this area is replete with instances of rape, in which, prior to the attack, the rapist had given no hint whatsoever of being a dangerous person. Conviction rates for rape are low and treatment or therapeutic interventions have generally been ineffective and disappointing. In addition to the need to develop adequate predictive and therapeutic measures for rapists, there is a tremendous need to improve treatments for the traumatized victims of these violent crimes.

Sexual orientation, as it relates to homosexuality, is one's erotic attraction toward the same sex. Sexual orientation is a part of one's sexual identity, which, in turn, is primarily related to physical and emotional disposition, and is simultaneously interconnected yet distinct from biological and gender identity. In Western culture, the most prominent means of conceptualizing sexual orientation is in terms of hetero- versus homosexuality. Traditionally, such distinctions are oversimplified and create oppositional positions. For these reasons, some theorists would rather conceive of orientation as being on a continuum, with heterosexuality and homosexuality at either end and in between a vast gradation of overlap reflecting bisexuality. Dichotomous thinking, coupled with rigid cultural values biased in favor of the heterosexual majority have led to a lengthy history of intolerance towards and oppression of homosexual and bisexual individuals. Two forces helped shape negative and oppressive attitudes toward homosexuality. The first was JudeoChristian values and beliefs that held that nonprocreative sexual acts were regarded as "sins against nature" and consequently frowned on in the culture. The second force was the rise of medicine and psychology as powerful authorities and arbiters of social morality by defining and controlling "deviant" and "diseased" behaviors. This control led to the condemnation of many fringe or nontraditional sexual practices with homosexuality in the forefront. Psychiatry, for example, included homosexuality in their diagnostic manual thus sanctioning intervention and treatment. Sin was now replaced by pathology. Being identified as mentally ill meant that homosexuals could be stripped of their civil and human rights while the heterosexual population looked on. Under fire from within and outside their ranks, on December 15, 1973, the American Psychiatric Association board of trustees voted to remove homosexuality from the categories of mental illness. After much struggle and debate, homosexuality was replaced with a new category, ego-dystonic homosexuality, denoting those homosexual individuals who were distressed by their orientation and wanted to become heterosexual. This compromise category did not last for long, as many professionals and lay persons could see that it was just another more subtle means of per-

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petuating prejudice and oppression. Finally, all reference to homosexuality was removed from the official nomenclature. A. Prevalence

The problem in measuring the prevalence of homosexuality is that it must be operationally defined. Renowned sex researcher Alfred Kinsey chose to operationally define sexual orientation on a continuum in terms of behavior frequency of homo-, hetero-, and degree of combined sexual behaviors. The following scale was developed: 0. Exclusive heterosexual with no homosexual 1. Predominately heterosexual, only incidental homosexual 2. Predominately heterosexual, but more than incidental homosexual 3. Equally heterosexual and homosexual 4. Predominately homosexual, but more than incidental heterosexual 5. Predominately homosexual, but incidental heterosexual 6. Exclusively homosexual What resulted from his pioneering assessment of the sexual practices of the American public was surprising. Kinsey found that 37% of males surveyed had had physical contact to the point of orgasm, at least once, with another man. In addition, another 4 - 6 % were either primarily or exclusively homosexual. It was found that of the females questioned, 13 % had at least one such encounter with another female. To conceive of homosexuality in strict behavioral terms challenged the more prevalent practice of using the terms to represent a personality deficit. The latter approach, of course, leads to social stigmatization. Kinsey also avoided applying sexual orientation labels in an either/or manner, by conceiving of sexuality as a range of behaviors on a continuum. Despite his popularity, his results were criticized on methodological and theoretical grounds. Specifically, grave doubts were raised about the generalizability of his data from the limited sampling he used. Other researchers conducting surveys with better sampling methods found similar to much lesser rates of incidence; usually between 4 and 16% homosexual behavior of some kinds. Theoretically, Kinsey was criticized for being too reductionistic by trying to conceptualize the homosexual expe-

rience in terms of the frequency of same sex behaviors. Regardless of the precise percentages and how one exactly conceives of it, homosexuality is and has been a pervasive part of our culture and population. Since the early 1970s, there appears to have been a radical rethinking of how we treate those of homoor bisexual orientations. Still, some lay persons and professionals find these orientations pathological and must seek causes and roots for these disorders. Katchadourian responds to these efforts in the following manner: Those who accept homosexuality as an illness seek its causes. Those who do not, object to this approach. "Causes" implies that there is something wrong; why not seek the "causes" of heterosexuality? The search for the origins of sexual orientation--homosexual or heterosexual--is a more legitimate quest.

The causal agents responsible for producing any sexual orientation are basically unknown. If we hope to gain insight by relying on a single explanation, then we will surely miss the dynamic and interactive nature of sexual identity. Whether the theoretical model is based upon genetic inheritance, developmental influences, or psychodynamic conflict, the nature of sexual orientation, regardless of sexual preference, seems better understood as having multiple roots. B. Treatments

Contemporary thought rejects the outdated notion of homosexuality and bisexuality as diseases to be treated and cured. Attempts by professional to change or convert homosexuals into heterosexuals have almost always been exercises in futility. Despite long and intensive therapeutic hours, psychoanalysis has had no success. With their aversive counter-conditioning techniques, the behavioral therapies have only faired marginally better. Irrespective of the theoretical model, when a person (homosexual or not) is forced into the therapy room, not only is change highly unlikely but the chances for negative psychological consequences are greatly increased. An apparent exception to this lack of success was the Masters and Johnson sex therapy study, which reported to have "helped" two-thirds of those who volunteered for a 2-week treatment program. Criticisms of their work include the fact that the male and female participants were carefully screened to ensure that they

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exhibited high levels of desire to change and were the beneficiaries of very supportive partners. In addition to such biases in sampling, further analysis of the followup data revealed that the claimed failure rate of only 28% was probably too low. Perhaps a rate of about 45 % would be more accurate.

methodologically flawed clinical/nonclinical designs. Once corrected for biased sampling, such studies show that the differences in gender identity are minimal. Yes, "butch" lesbians and effeminate gays exist, but as a stereotype they are not representative of the homosexual and bisexual population as a whole.

C. Differences in Health and Personality

This article has been reprinted with updated references to DSMIV from the Encyclopedia of Human Behavior, Volume 4.

As pointed out earlier, psychiatrists have conceptualized the homosexual as inherently pathological and heterosexual as "normal." Numerous scientific studies have compared homosexuals who sought treatment against normal heterosexuals who were n o t in treatment. Differences were found between these groups on health and personality variables. More recent studies, with improved methodology, have shown that very few differences in pathology actually exist between equivalent heterosexual and homosexual samples. Differences in depression and suicide rates previously attributed to pathology or flaws in the individuals are now seen from a broader socio-psychological level of causation, i.e., environmental pressures to live up to one's societal status as deviant. Another area in which scientific bias has played a mystifying role is in the realm of personality differences between homo- and heterosexuals. Specifically, there have been studies showing gay men were more feminine than straight men and that lesbians were more masculine than their heterosexual counterparts. Once again, such findings have been shown to be based on

BIBLIOGRAPHY American Psychiatric Association. (1994). "Diagnostic and Statistical Manual," 4th ed. Washington, DC. Bancroft, J. (1983). "Human Sexuality and Its Problems." Churchill Livingston, London. Bayer, R. (1987). "Homosexuality and American Psychiatry: The Politics of Diagnosis." Princeton University Press, NJ. Benjamin, H. (1966). "The Transsexual Phenomenon." Julian Press, New York. Bullough, V. L., & Brundage, J. (1982). "Sexual Practices in the Medieval Church." Prometheus, Buffalo, NY. Carnes, P. J. (1983). "The Sexual Addiction." CompCase, Minneapolis. Doctor, R. F. (1988). "Transvestites and Transsexuals: Toward a Theory of Cross-Gender Behavior." Plenum, New York. Freeman, E. B. (1988). "Intimate Matters: A History of Sexuality in America." Harper and Row, New York. Finkelhor, D. (1984). "Child Sexual Abuse." Free Press, New York. Gonsiorek, J. C., & Weinrich, J. D. (Eds.)(1991). "Homosexuality: Research Implications for Public Policy." Sage, Newburry Park. Katchadourian, H. A. (1989). "Fundamentals of Human Sexuality," 5th ed. Holt-Rinehart and Winston, San Francisco.

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Somatizationand Hypochondriasis

I. II. III. IV. V. VI.

Javier I. Escobar

Michael A. Gara

UMDNJ-Robert Wood Johnson Medical School

UMDNJ-Robert Wood Johnson Medical School UMD NJ- University Behavioral Health Care

Introduction Systems of Classification Pathogenesis Detection, Recognition, Diagnosis Cross-Cultural Issues Clinical Management

(e.g., hypochondriasis) to common psychiatric disorders, such as depression and anxiety. There will also be a focus on systems of classifying somatoform disorders, as well as the epidemiology, pathogenesis, diagnosis, cross-cultural, and clinical management of somatoform disorders.

I. INTRODUCTION

Abridged Somatization Construct A method for classifying somatization disorder and subsyndromal somatization using a simple series of interview probes and the somatic symptom index (see below). Hypochondriasis A preoccupation with fears of having a serious, often life-threatening disease, despite overwhelming medical evidence to the contrary. Somatic Symptom Index A count of the number of unexplained physical symptoms. The presence of four unexplained symptoms in males, and six in females, suggests somatization. Somatization As a broad notion, the presentation of somatic complaints not explained by any known general medical condition or substance abuse, and that may represent a psychopathological state. Somatoform A label used to group clinical syndromes in which the patient presents with multiple physical symptoms that have no clear medical explanation.

A general conception in psychology and psychiatry that has been held for more than a century is that somatization represents negative emotions and/or rather intense psychological conflicts that have been unconsciously converted into physical symptoms or somatic sensations. The exact mechanism mediating this conversion process is unknown, although there is extensive speculation about its psychological, social, and biological underpinnings. Nonetheless, the subjective experience of having a physical illness is a compelling reality for the somatizing patient, which tends to persist despite reassurance from physicians that no medical explanation can be proffered for the patient's complaints. The somatizer vigorously resists any efforts that are made to reframe his or her distress as a consequence of psychiatric disorder, (i.e., depression, anxiety) or even psychosocial stressors. A conceptual difficulty in advancing the fields is the fact that somatization is a diagnosis always made by exclusion. Hence, there is always a chance that a heretofore undetected or yet-to-be discovered underlying physical disorder may account for the complaints. Medical disorders that pose the greatest difficulty for differential diagnosis obviously are those with mul-

SOMATIZATION refers to multiple physical complaints for which there are no medical explanations, and that may be related to coping mechanisms or psychopathological states. This article will discuss the links of somatization and other somatoform disorders

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Copyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

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tiple ambiguous symptoms (for example, lupus erythematosus or multiple sclerosis). In order to reduce the rate of "false positive" diagnoses of somatization, diagnostic criteria for somatization have emphasized issues of severity, a polysymptomatic presentation, and the absence of positive physical findings as key elements for the diagnosis. When presenting symptoms cut across many organs/ biological systems, the likelihood of a somatization diagnosis is much higher.

II. SYSTEMS OF CLASSIFICATION In the most recent psychiatric nosologies, the American Psychiatric Association's Diagnostic and Statistical Manual, 4th Edition (DSM-IV), and the International Classification of Diseases, 10th Edition (ICD-I O), the label "somatoform" is used to group clinical syndromes whose most distinguishing feature is the presentation of and preoccupation with physical symptoms or somatic sensations that remain without a clear medical explanation. The syndromes that have been grouped under the rubric "somatoform" in DSM-IV are somatization disorder, hypochondriasis, conversion disorder, body dysmorphic disorder, pain disorder and undifferentiated/not otherwise specified somatoform disorder. Somatization disorder is an entity that can be traced to older concepts in psychiatry, such as hysteria or Briquet's syndrome. The criteria for this disorder are fairly stringent, such as age of onset before 30, several years of unsuccessful medical treatment with significant loss of functioning in one or more domains (e.g., occupational), many unexplained symptoms (in DSM-IV at least eight unexplained symptoms are required) spread across different physical sites or systems. This diagnosis has high validity and reliability indexes and generally leads to poor outcomes. The other somatoform disorders in the DSM-IV have much less stringent criteria than does full-blown somatization disorder and their validity seems less clear. Undifferentiated somatoform disorder requires that the patient present with at least one unexplained symptom that persists beyond 6 months and causes significant functional impairment. Hypochondriasis requires that the patient be preoccupied with having a serious disease, such as cancer, for at least 6 months, which persists despite medical

reassurance. Body dysmorphic disorder is defined by a preoccupation with an imagined deficit in appearance, which at times may reach psychotic proportions. Table I compares the taxonomy of somatoform disorders that exists within DSM-IV with those in ICD-IO. Although DSM-IV and ICD-IO resemble each other more than did any of their predecessors, there are still significant differences between the two taxonomies in the case of several diagnostic categories, including dissociative and somatoform disorders. For example, the most pressing reason for mentioning "dissociation" in this article is the inclusion of "conversion disorders" under a superordinate dissociative class (F44)in the ICD-IO. In contrast, "conversion disorders" are subsumed under somatoform disorders in DSM-IE One additional reason to mention somatization/conversion in the context of dissociation acknowledges the historical cogenesis of dissociative and hysterical phenomena in nineteenth-century French psychiatry. In addition, DSM-IV highlights psychological elements thought to be at work in conversion disorder (e.g., temporal onset of conversion symptoms immediately after psychological trauma), whereas ICD-10 tends to elaborate the physical aspects of conversion symptoms. Because of the limitations of current diagnostic classifications, a number of proposals have been made to reframe somatoform syndromes in simpler, more practical ways. These proposals suggest a somewhat different taxonomy than that appearing in the DCM or ICD systems, albeit with discernable areas of overlap, at least for the symptoms more commonly seen in primary care settings. For example, in 1991 Kirmayer and Robbins at McGill University proposed three forms of somatization in primary care. These are (1) high levels of functional somatic distress measured by the somatic symptom index of Escobar; (2) hypochondriasis, measured by high scores in an "illness worry" scale; and (3) somatic manifestation seen exclusively in patients with current depression or anxiety. Over 25 % of patients attending a family medicine clinic met criteria for one or more of these forms of somatization. Interestingly, these forms were only mildly overlapping. G. Richard Smith's (1994) review of the literature on the course of somatization and other aspects of the disorder, proposes four categories in his classification: (1) clear somatization disorder or SD (essentially the same entity as in DSM-IV); (2) subthreshold somatiza-

Somatization and Hypochondriasis

Table I

ICD-IO and DSM-IVNosologies .

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ICD-IO Diagnostic Criteria for Research (DCR) F 44--Dissociative and Conversion Disorders (Primary symptom = "Physical"/Includes "stress" component) F 44.0 Dissociative amnesia F 44.1 Dissociative fugue F 44.2 Dissociative stupor F 44.3 Trance and possession disorders F 44.4 Dissociative motor disorders F 44.5 Dissociative convulsions F 44.6 Dissociative anesthesia, sensory loss F 44.7 Mixed dissociative/conversion disorder F 44.8 Other dissociative disorders (Ganser, multiple personality disorder, and so on) F 4 5 - - Somatoform Disorders F 45.0 Somatization disorder (Criteria = 6 or more symptoms from a list of 14, that includes 6 gastrointestinal, 2 cardiovascular, 3 genitourinary and 3 skin and pain symptoms) F 45.1 Undifferentiated somatoform disorder F 45.2 Hypochondriacal disorder F 45.3 Somatoform autonomic dysfunction F 45.4 Persistent somatoform pain disorder F 45.8 & 45.9 Other/unspecified somatoform disorders F 48.0 Neurasthenia (listed under F48 "Other neurotic disorders")

DSM-IV Criteria Dissociative Disorders (Primary symptoms = "Psychological ..... Disturbance of normal integration functions of identity, memory or consciousness") Dissociative amnesia Dissociative fugue Dissociative identity disorder (multiple personality) Depersonalization disorder Dissociative disorder not otherwise specified Somatoform Disorders Somatization disorder (8 symptoms - 4 pain, 2 gastrointestinal, 1 sexual, 1 pseudoneurologic, down from 13 in

DSM-III-R) Hypochondriasis Conversion disorder (either "motor deficit," "seizure," "sensory deficit," or "mixed") Body dysmorphic disorder Pain disorder Undifferentiated/not otherwise specified .

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tion (for patients with unexplained physical symptoms who do not meet all criteria for SD); (3) somatization with comorbid physical illness; and (4) somatization with comorbid psychiatric illness. Smith's review suggests that patients with fullblown SD perceive themselves as "sicker than very sick," spending, on average, 1 week per month in

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bed. In addition, these patients, relative to medical controls, present with a greater number and intensity of psychological symptoms (depression, panic) and greater work and social disability. Interestingly, the strong belief held by SD patients that their health is "extremely poor" is not corroborated by research evidence. For example, Smith cites the mortality rate of SD as being equal to that of patients in the general population and significantly lower than that found in major depression. Perhaps most telling of all statistics cited by Smith is the fact that SD patients evince health care utilization costs at nine times the U.S. per capita average. According to Escobar, parallel to patients with SD, those with subsyndromal SD also report increased sick leave, restricted activities, and avid use of nonpsychiatric medical services compared with the general population. Moreover, when somatization coexists with either physical or psychiatric illness (Categories 3 and 4 in Smith's taxonomy), there is a significant amplification of the discomfort and disability typically associated with either class of illness when occurring in isolation. Smith notes that it has also been established that high levels of psychiatric comorbidity are much higher for somatizing patients than for nonsomatizing controls, particularly with respect to major depression, generalized anxiety, phobia, and some Axis II personality disorders, such as avoidant, paranoid, and self-defeating disorders.

A. Escobar's Abridged Construct of Somatization Because more than one-fourth of all patients seeking primary care services are somatizers and many of these would not be captured by the SD diagnosis in current nosologies, the first author (JIE) and his colleagues sought to develop methods of identifying and classifying SD and subsyndroma| somatization phenomena that would be feasible for use by primary care providers. In this context Escobar proposed an "abridged" somatization construct, along with a relatively simple series of interview probes to be used by the physician or lay interviewer. Figure 1 is a flowchart that provides a practical example of the probing logic for chest pain, a common symptom in a primary care setting. Essentially, male patients satisfy criteria for Escobar's "abridged" somatization if they present with four or more unexplained physical symptoms that impair

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1

'?A[N IN THE CHEEr"

J

TYPICAL?

RISK FACTORS?

POSITIVEFINDINGSON ANGIOGRAPHY, EXERCISETEST

CARDIAC PAIN CORONARYARTERYDISEASE

NONCARDIAC PAIN

ANXIETY/DEPRF~SIONSYMPTOMS?

PANIC DISORDER , , MAJORDEpRESSIVEDISORDER ~ ~ O ~ Y c H O L ( x ~ I U N E X P L A

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CC SG~OMS?

i!ol VOCABUIDd~YOF DISTRESS?

Figure I Probinglogic for chest pain. some aspect of functioning and daily living, whereas females satisfy criteria with six or more unexplained symptoms. More recently, the WHO-sponsored international classification (ICD-IO) drafted a "primary

care version" of the diagnostic criteria for SD and subsyndromal somatization that uses this more generic definition of somatizing patients as those "presenting with many unexplained somatic complaints."

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Somatization and Hypochondriasis .

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According to Escobar, a somatization symptom should be coded individually on the basis of its severity, frequency, and the degree of functional interference and disability it conveys. A rigorous system of probes should be used to rule out alternative explanations for a given symptom, such as the use of medications, drugs, or alcohol, or the presence of a physical illness or injury. High levels of unexplained symptoms elicited in this manner (e.g., more than four lifetime symptoms for males) imply "somatization." Escobar's extensive program of research on both general populations and primary care samples has validated his method of identifying the disorder by showing that patients who satisfy these abridged criteria independently evidence elevated scores on standardized measures of psychopathology, show high levels of utilization of inpatient and outpatient medical services, and present with greater disability in work, family, and social domains. Put another way, the validity coefficients (correlates) of Escobar's abridged somatization construct have been observed to be similar both in direction and magnitude to the correlates of "full-blown" SD. These results are consistent with but do not prove a "dimensional" as opposed to a "discrete" view of the somatization phenomena. Interestingly, although the threshold for "full" somatization disorder required 13 or more unexplained symptoms in DSM-III-R, the threshold has been moved closer to that of Escobar's in ICD-IO and DSM-IV (Table 1). Thus, in the Diagnostic Criteria for Research in ICD10 only six symptoms are required, while in DSM-IV only eight symptoms are now required, with the caveat that at least two of these must be pseudoneurological (e.g., numbness, blindness, seizures).

B. Are "Medically Unexplained Somatic Symptoms" Always Psychiatric Symptoms? There seems to be some consensus, based on the reviews by Escobar, Noyes, Holt and Kathol, and Smith that prior to assuming that a somatic symptom that remains medically unexplained has a psychiatric basis, the symptom should have the following characteristics: la. The symptom is associated with a "primary" psychiatric disorder (e.g., major depression or panic disorder).

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1b. The symptom appears in close temporal proximity with certain life events such as overwhelming trauma or other severe stressors. 2. The symptom provides some sort of psychological "gratification" to the individual (e.g., "secondary gain" such as decreased work or family responsibilities) or represents a less-stigmatized (than mental illness) mode of expressing underlying chronic unhappiness (as in the personality "trait" of neuroticism). 3. The symptom becomes persistent, joins a conglomerate of other unexplained physical symptoms, setting in motion extensive use of health services and chronic dissatisfaction with medical care.

III. PATHOGENESIS The pathogenesis of somatization is unknown. A number of factors is thought to act in concert to produce somatization. One sociological explanation is that adoption of a "sick role" provides secondary gains to the person who adopts it (lowering of work responsibilities) while simultaneously shielding the individual from the stigma associated with mental illness. The "primary gain" associated with somatization, according to psychoanalytic theory, is the amelioration of intrapsychic conflict. There are also many other plausible psychological and biological explanations, some of which have been summarized by Noyes, Holt and Kathol. One of these factors is autonomic arousal. Under the influence of stress or anxiety, patients experience heightened arousal and, with it, a host of mediated symptoms. Palpitations, shortness of breath, dizziness, sweating and other symptoms may all become a focus of health concern. Excessive worry about health, regardless of its source, may be another factor. Worried persons are vigilant and scan their bodies for sensations that then become an object of worried concern. By focusing narrowly on a body part, a person may intensify sensations arising from it, sensations that may grow distressing or even painful. Still another factor has to do with communication of distress. Some somatizers are unable to distinguish between emotions and bodily sensations and have difficulty communicating feelings (p. 741).

Somatizers may also have lower thresholds and tolerance for physical discomfort. For example, in experimental situations, the same stimulus that elicits a simple sensation of "pressure" in the nonsomatizer

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can elicit "pain" in the somatizer. There is speculation that this lower threshold is constitutional in nature. The prevalence of SD or subsyndrornal somatization in general medical practice has risen over the last half century. This rise seems less attributable to an actual increase in mild, self-limiting physical symptoms (such as fatigue, headaches, and upper respiratory distress) than to a societal tendency to reclassify mild and benign bodily discomfort as symptoms of medical disease. In line with increased "medicalization" of benign transient symptoms is a growing list of "functional somatic syndromes" whose scientific status and medical basis remain unclear. These include chronic fatigue syndrome, total allergy syndrome, food hypersensitivity, reactive hypoglycemia, systemic yeast infection (Candida hypersensitivity syndrome), Gulf War syndrome, fibromyalgia, sick building syndrome, and mitral valve prolapse.

clude not only each reported symptom but also its intensity or severity, and the way in which it clusters with others symptoms and psychosocial attributes. Somatization may be an interesting exception to the trend of reducing psychiatric diagnostic process to symptom inventories, at least in DSM-IV. Since it rules that in order to score a physical complaint as a psychiatric symptom the probing needs to scrutinize severity issues in addition to documenting medical visits and lack of clear medical explanations for the symptom. In our opinion, high levels of somatic symptoms represent a reliable entity, akin to the sturdier disorders in psychiatry such as melancholia. As such, somatization may be much more accessible to empirical scrutiny than most other symptomatic constructs in psychiatry.

IV. DETECTION, RECOGNITION, DIAGNOSIS A. FROM "DISTRESS" TO "PSYCHOPATHOLOGY": IS THERE A "BRIDGE"? Theoretical formulations within a variety of social and behavioral science disciplines, such as sociology, anthropology, and psychology, invariably link psychiatric disorders with "stress." Because "distress," regardless of its source, commonly is expressed in psychological or behavioral terms (e.g., "demoralization," "anxiety, .... depression"), these formulations continue to hold significant influence on the mental health field. However, a distinction must be made between expressions of "distress" (or "stress-induced" states) and formal "psychopathologic" states. Psychiatric diagnoses that are distinct, reliably made, and predictable, such as endogenous/melancholic depression, do not seem to fit well the theoretical framework of the "stress spectrum disorder." Quite naturally, the theorizing that linked "distress" to psychiatric disorder was transported to the field of psychiatric epidemiology, and therefore, instruments used in these surveys tend to be simple self-report measures of "distress." In this zeitgeist, even a formal diagnostic system such as DSM-IV can be truncated to a mere symptom checklist, used by clinicians simply to elicit symptoms one by one. In the opinion of the authors, key elements in generating valid psychiatric diagnosis should in-

Somatization and its various syndromes, although well documented throughout the years, have baffled medical practitioners with their tendency to metamorphism as part of cultural evolution and the changing perspectives of the medical paradigms. For example, Barsky and Borus have argued that somatization is on the rise because "sociocultural currents reduce the public's tolerance of mild symptoms and benign infirmities and lower the threshold for seeking medical but not psychiatric (italics ours) attention for such complaints. These trends coincide with a progressive medicalization of physical distress in which uncomfortable bodily states and isolated symptoms are reclassified as diseases for which medical treatment is sought" (p. 1931). In clinical settings as well as in common parlance, somatizers tend to be labeled in a derogatory manner. Curiously, however, these vernacular terms (such as "hysterics, .... Gomers" [acronym for Go Out of My Emergency Room], "turkeys, .... hypochondriacs," and many others) seem to have more currency in describing the experience of dealing with these patients than do the more refined and euphemistic diagnostic labels. The fact that somatoform disorders lag far behind other psychiatric diagnoses in terms of their proper recognition and visible research activity may be explained by their rather ambiguous nosological status. Problems in classifying these syndromes include issues of diagnostic validity and the excessive comorbidity that exists with other types of psychopathology. Also,

Somatization and Hypochondriasis

since patients affected by these disorders believe their illness is "physical," they reject psychological labeling or referral and are rarely seen in psychiatric settings. Moreover, they are unlikely to form "advocacy groups" such as those seen in the case of people with anxiety or mood disorders. It is likely, however, that many somatizing patients readily joint patient groups with more "medicalized" labels such as functional somatic syndromes like "chronic fatigue, .... TMJ, .... Fibromyositis, .... Multiple Chemical Sensitivity," among numerous others. The current age of cost containment has brought new awareness about these patients, since they are avid consumers of services and technologies, thus taxing health care systems excessively. Following suit with tradition, newly found characterizations of these somatizing patients prove colorful though still highly pejorative. Thus, the traditional "hysterics" or "hypochondriacs" at the medical clinics are becoming the "frequent flyers" at the corporate health headquarters. Because of the ambiguity of their symptoms, treatment refractoriness and lack of psychological mindedness, somatizing patients use health services excessively, in pursuit of diagnostic confirmation or reassurance. This leads to heavy utilization of expensive technologies and often may result in unnecessary procedures being performed. It is as if medical care became an essential social support network and the patient role part of personal identity for these patients. Paradoxically, these patients also display chronic dissatisfaction with the care received, and may often seek financial compensation for their symptoms and "mishaps." This latter factor, when added to avid service use and disability inherent in the disorder, makes somatizing syndromes some of the most expensive entities in medicine. Indeed, somatization is on a collision course with cost-containing trends in managed care.

A. Somatizers and Hypochondriacs: A Profile Individuals affected with these traits, generally display a tendency to amplify physical symptoms and sensations. They also tend to endorse multiple physical symptoms involving various body areas. My impression (JIE) in working with many of these patients, is that there is a tendency to "overreport" not only physical symptoms, but also psychiatric ones, hence the high levels of psychiatric comorbidity that are well

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documented in the literature. In addition to over reporting physical symptoms, these patients also tend to overreport negative "experiences" (e.g., trauma, instances of being victimized, sexual abuse), relative to other clinical populations. Contrary to much theorizing, "somatizers" are not a good model for "masked" psychiatric disturbances since they report very high levels of psychological distress. High levels of these unexplained physical symptoms seem to be a good marker for affective and anxiety syndromes, and possibly several other psychiatric disorders. Anxiety syndromes would primarily imply unexplained cardiopulmonary symptoms, while depressive syndromes would coexist with unexplained somatic pain in many sites, muscular-skeletal weakness, and pseudoneurological symptoms (e.g., numbness, amnesia). In advancing the specificity of somatization indexes, the authors are currently exploring clustering of somatic symptoms for the various disorders. [See ANXIETY; DEVRESSION.]

B. Problems with the New Classifications A glance at some DSM-IV and ICD-IO categories leaves one with the impression that in trying to make larger numbers of individuals fit the criteria, the "net" has become much less discriminating, and the "catch" much less specific. In the hands of less experienced clinicians, many of these nosologic categories end up as mere "symptom checklists," simply eliciting symptoms as present or absent regardless of their severity or clustering attributes. Although this may be a convenient feature in the age of managed care, it flies in the face of traditional psychopathology that has relied on detailed anamnesis, natural course of illness, and precise dissection of symptom phenomenology in the creation of "valid" diagnoses. To counter the lack of specificity of many psychiatric syndromes, it is important to restore the Kraepelinian tenet, that the intensity or severity of the symptom, its temporal evolution, and its clustering, rather than the symptom per se, should remain the key elements in psychiatric diagnosis. Fortunately, in eliciting somatization symptoms, DSM-III-R and DSM-IV have drafted unambiguous rules. For example, the "probing" is expected to scrutinize severity issues in addition to documenting medical visits and lack of clear medical explanations for the symptom prior to scoring it as present. Thus, when elicited in this manner, high levels of med-

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ically unexplained somatic symptoms may represent more valid and reliable indexes than other symptom clusters. Besides, a medically unexplained symptom is more objective, more accessible to scrutiny, and, also, it may prove less intrusive, eliciting far less resistance from the individual affected than other psychopathologic concepts.

V. CROSS-CULTURALISSUES It is generally accepted that cultural influences may color the expression of somatization and hypochondriasis. Although it is often difficult to disentangle the contribution of ethnicity from other demographic factors (e.g., socioeconomic status: patients of lower socioeconomic status tend to somatize more than those of higher status), most studies reinforce the view that culture exerts a powerful influence in shaping symptom presentation and determining health-related attitudes. For example, in the United States the prevalence of somatization, based on counts of unexplained physical symptoms, is higher for some ethnic groups (e.g., Jewish and Italian Americans) than for others (e.g., Irish Americans). Also, relatively high levels of unexplained physical symptoms in the United States have been reported in the case of Middle Eastern, Southeast Asian, and Latino patients. However, there is also significant within-group variation among the different Southeast Asian ethnic groups and also among such Latino subgroups as Mexican American, Puerto Rican Americans and Cuban Americans. It is conceivable that the type of symptoms presented by "somatizing" patients may differ in various cultural settings. International research reports reveal rather pathognomonic symptom presentations for patients with somatoform disorders in various cultures. For example, in Africa (Nigeria), "feeling of heat," "peppery and crawling sensations," and "numbness"; in India, "burning hands and feet, .... hot, peppery sensations in head"; and in Puerto Rico, headache, trembling, stomach disturbances, palpitations, and dissociative symptoms, all components of a syndrome called "ataque de nervios." Moreover, even within similar countries, such as European and North American, there are unique differences. For example, in North America there is an emphasis on immunologically based symptoms.

VI. CLINICAL MANAGEMENT The clinical management of somatizing syndromes continues to be an area of active debate and improvisation. These disorders confront us both with diagnosis and therapeutic challenges because of their polysymptomatic (multiorgan) and polysyndromic (comorbid) features, their persistence, and their refractoriness to traditional interventions. The lack of psychological "mindedness" in somatizers poses serious hurdles to psychotherapeutic management and negatively affects adherence to psychiatric interventions. Because of the diagnostic dilemmas often faced, and possibly because these patients rarely present to mental health treatment settings, very few scientific data are available on how the various therapeutic interventions affect the most salient outcomes. One of the few exceptions is the study by Smith, Rost, and Kashner on the effects of a brief intervention on costs of care, level of functioning, and clinical outcome. The intervention was followed by primary physicians and had several distinct features. These included the adoption of an understanding and reassuring attitude, taking the patient's complaints seriously, performing a brief physical assessment during regularly scheduled visits, and an active avoidance of procedures and medications. The latter strategy prevents iatrogenic complications that often result from unnecessary medical and therapeutic interventions performed on these patients. It was found that when these procedures were followed, physical functioning improved and costs of care went down. Noyes, Holt, and Katho| also emphasize the importance of regularly scheduled visits in order to reassure the somatizing patient that the physician is concerned about his or her well-being. At the same time, unscheduled visits are actively discouraged, since these tend to reinforce the patient's well-honed tendency to amplify existing symptoms or to generate new ones. Physicians themselves may need the support of colleagues or consultants in order to deal with negative emotions that arise when treating somatizers. Common emotions experienced by treating physicians are guilt and anger. Guilt may accompany the clinician's attempt to set limits on frequent phone calls or unscheduled visits from demanding patients. It is not uncommon to experience anger when treating a particularly demanding and resentful patient, especially

"

Somatization and Hypochondriasis

when he or she begins to test already established limits, and the provider may need a means to vent this anger or talk to a colleague so as not to direct the anger at the patient. Regarding pharmacotherapy, the use of antidepressants has been proposed for a number of the somatizing syndromes including chronic pain, chronic fatigue, somatization, and hypochondriasis, whereas neuroleptic agents such as pimozide are advocated for delusional syndromes such as delusions of infestation and severe cases of dysmorphophobia. With very few exceptions, however, most of these claims are based on anecdotal reports. The first author (Escobar) is aware of two currently ongoing double-blind trials in this area, one on hypochondriasis and the other on dysmorphophobia. Results of these important studies were not available as of September 1997 (JIE). Secondary syndromes, such as the somatic equivalents of anxiety and depression, would be expected to respond to traditional treatments such as antianxiety and antidepressant agents such as selective serotonin reuptake inhibitors. Few systematic data, however, are currently available. Psychological treatments, such as cognitive-behavioral treatments aimed at enhancing emotional expression and correcting dysfunctional attitudes towards illness and patient roles have also received some empirical support of efficacy. Treatments based on the behavioral paradigm of exposure-response prevention have also been developed. These psychological treatments, while promising, are in need of further research and development. Finally, on the basis of clinical experience and the studies described in a previous section, one would

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strongly predict the relevance of ethnic background to the processes of treatment seeking, adherence, and response of somatizing patients. Once again, however, there are no scientific data to provide guidance in this regard. This should become an important priority for future studies.

BIBLIOGRAPHY

American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author. Barsky, A. J., & Borus, J. F. (1995). Somatization and medicalization in the era of managed care. J. Amer. Med. Assoc., 274, 1931-1934. Castillo, R., Waitzkin, H., Ramirez, Y., & Escobar, J. I. (1995). Somatization in primary care, with a focus on immigrants and refugees. Arch. Fam. Med., 4, 637-646. Escobar, J. I. (1995). Transcultural aspects of dissociative and somatoform disorders. The Psychiatric Clinics of North America, 18, 555-569. Kirmayer, L. J., & Robbins, J. M. (1991). Three forms of somatization in primary care: prevalence, co-occurrence, and sociodemographic characteristics. J. Nerv. Ment. Dis., 179, 647655. Noyes, R., Holt, C. S., & Kathol, R. G. (1995). Somatization: Diagnosis and Management, Arch. Fam. Med., 4, 790-795. Smith, G. Richard, Rost, K., & Kashner, T. M., (1995). A trial of the effect of a standard psychiatric consultation on health outcomes and costs in somatizing patients. Arch. Gen. Psychiatry, 52,238-243. Smith, G. Richard. (1994). The course of somatization and its effects on utilization of health care resources. Psychosomatics, 35, 263-267.

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J SubstanceAbuse Thomas AshbyWills Albert Einstein College of Medicine

I. II. III. IV.

Introduction Epidemiologic Findings on Substance Use and Abuse Protective and Risk Factors Summary

greater likelihood that a person will be a substance abuser at a later point in time. Substance Abuse A condition where the level of substance use causes significant problems for the individual in important life domains such as work performance or social relationships with significant others. Substance Dependence A condition where the individual uses a substance in increasingly larger amounts, spends much time getting it and using it, and experiences negative physiological or psychological states when the substance is reduced or withdrawn.

Buffering Effect A process in which a protective factor reduces the adverse impact of a risk factor; also termed resiliency effect. Chronicity The extent to which the disorder continues to affect the person over an extended period of time. Comorbidity A phenomenon in which having one disorder increases the likelihood that the person will have one or more other disorders. Executive Functions A set of interrelated abilities that involve planning and organization, sequencing of activity, and monitoring of ongoing behavior. Population Prevalence The proportion of the population that has a given mental disorder. This is subdivided into two types of prevalence. Lifetime prevalence is the proportion of the population that has had the disorder at some time in their life; current prevalence, also point prevalence, is the proportion that has the disorder within a defined recent time interval (e.g., past 6 to 12 months). Protective Factor An environmental, social, or personal variable that is related to a lower rate of substance abuse; a protective factor at one point in time indicates a lower likelihood that a person will be a substance abuser at a later point in time. Risk Factor An environmental, social, or personal variable that is related to a higher rate of substance abuse; a risk factor at one point in time indicates a

SUBSTANCE ABUSE is construed here as the use of one or more substances which may include tobacco, alcohol, and illicit drugs (marijuana, cocaine, or heroin). This entry addresses substance abuse and related life problems. The generic definition of substance abuse is based on several concepts. First is level of use: an individual uses the substance frequently. Second is the concept of abuse: using the substance causes significant problems for the individual in important life domains such as work performance or social relationships with significant others. Third is the concept of dependence: the individual may use the substance in increasingly larger amounts, spend much time getting it and using it, and experience negative physiological or psychological states when the substance is reduced or withdrawn. Although the application of these criteria varies somewhat for different life stages (e.g., adolescence vs. adulthood) and for different drugs of abuse, when all of the defining conditions are met, then the individual can be diagnosed as having the dis-

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Copyright 9 1998 by Academic Press. All rights of reproduction in any form reserved.

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order of substance abuse or substance dependence. It is recognized that there is heterogeneity within a group of persons who all meet sufficient diagnostic criteria for a substance abuse disorder, and for some disorders (particularly alcohol abuse), evidence for subtypes has been reported. However, in the Diagnos-

tic and Statistical Manual of the American Psychiatric Association (DSM-IV), the core conditions are similar across diagnoses for all drugs of abuse, and the only diagnostic distinction allowed is between substance dependence and substance abuse. This entry examines epidemiologic findings on the prevalence of substance use and current knowledge about protective and risk factors for substance abuse.

I. INTRODUCTION Within the general population there are many persons who have tried cigarettes, alcohol, or marijuana at some time in their lives. There is a substantial proportion of persons who use substances in a consistent but infrequent pattern, such as persons who occasionally have a glass of wine with meals or who drink beer on social occasions. The number of persons who exhibit frequent, high-intensity substance use, however, is a smaller proportion of the population. For example, if the overall amount of alcohol use in the population is broken down, it is evident that a large part of total consumption is attributable to a small part of the population; these are the persons who would be characterized as heavy users. From the group of heavy users, some persons who meet the necessary defining conditions would be described as affected by diagnosable alcohol abuse or (if more severe) alcohol dependence. The prevalence of persons who have tried a substance, and the relative proportions of occasional users, heavy users, and abusers, differ considerably across drugs of abuse. For example, the proportion of the population who have tried cocaine is relatively small, but cocaine (particularly smokable or "crack" cocaine) is sufficiently addictive that a large proportion of triers move rapidly to abuse-dependence status. Several themes about substance abuse emerge in this entry. First is the concept of multiple risk factors. One way to approach substance abuse is to think about finding the particular factor that is responsible, for example, having an "alcoholic gene," or being the child of a substance-abusing parent, or living in a

poor inner-city area. Although each of these factors has some relevance for predicting substance abuse, research does not support the notion that there is one single cause of substance abuse; for example, although having an alcoholic parent increases children's risk for alcoholism, the majority of adult alcoholics do not have a family history of alcoholism. Instead of indicating a single cause, research indicates that it is a combination of environmental, personal, and social factors that puts some persons on a trajectory of life experiences that ultimately involves an extent and type of use that are indicative of substance abuse disorder. To understand and predict substance abuse, it is essential to consider information about the total number of environmental, personal, and social risk factors and protective factors that impinge on an individual. A second theme is multiple use. It is possible to find individuals who show only a high level of cigarette smoking, or only a high level of alcohol use, or only the use of an illicit drug (e.g., heroin or cocaine) with nothing else. However, such individuals are statistically rare in the population. Instead, it is more common to find that an individual with a high level of one type of substance use also shows high levels of other types of substance use. Although people have a clear stereotypic picture for the kind of person labeled "alcoholic," they often miss the fact that persons diagnosed with alcohol abuse also tend to be cigarette smokers; correspondingly, the kinds of persons labeled as "drug abusers," because they inject heroin, also tend to have high rates of alcohol, cocaine, and other drug use. The phenomenon of multiple use has been identified consistently in both adolescent samples and adult samples. However, the causal basis for the co-occurrence of tobacco, alcohol, and illicit drug use has not been definitively established at this time. The third theme is comorbidity. Recent research with general population samples has found that individuals with a substance abuse disorder have elevated rates for other mental health disorders, including anxiety or depressive disorders. Demonstration of substantial comorbidity of substance abuse with mental health disorders is a relatively recent development. The reasons for the comorbidities are not completely understood, but the phenomenon is believed to have significant implications for treatment of substance abusers. In the context of these themes, this entry summarizes current knowledge about substance abuse from

Substance Abuse

the perspective of epidemiologic research, with epidemiologic data on the prevalence of substance abuse and the comorbidity of substance abuse with other disorders. Risk factors and protective factors, conditions that increase or decrease the likelihood that an individual will be affected by substance abuse, are explored because recent work has shown that it is the balance between risk and protective factors that may be crucial for helping to steer an individual toward or away from substance abuse. Risk and protective factors have been studied in both adolescent and adult populations, so findings from both types of research are considered.

II. EPIDEMIOLOGIC FINDINGS ON SUBSTANCE USE AND ABUSE A. Prevalence of Substance Use and Multiple Use What proportion of the population engages in substance use? This question is addressed by studies that inquire about whether a person has ever used, or currently uses, a given substance (population prevalence). Surveys administered to samples of adolescents or adults include questions about the extent to which the person has used the substance, for example, Have you ever smoked marijuana? or Have you smoked marijuana in the past 30 days? Additional questions may establish whether the adolescent is a regular user (e.g., smokes every day or usually drinks alcohol several times a month). For adolescents, detailed information on substance use prevalence is available from household surveys and studies of school students. A large study of high school seniors, Monitoring the Future (MF), conducts repeated annual surveys to track current trends in adolescent substance use. In thinking about substance abuse, it is important to note that substance use typically begins in adolescence. Around age 12 years, prevalence rates for regular tobacco and alcohol use are low, single-digit figures, but these rates increase steadily over adolescence; by age 18, rates of regular use for tobacco, alcohol, and marijuana range from 15 to 30% of the adolescent population. Use of illicit drugs (e.g., heroin and cocaine) is relatively infrequent in the general population of adolescents, but increases markedly during young adulthood (ages 18 to 25 years), with declines thereafter.

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However, users of illicit drugs in adulthood typically have a history of prior substance use in adolescence. Adolescent data show variation for rates of use across different substances. Survey data for high school seniors from 1994 show that for cigarette smoking, 62% have smoked a cigarette at some time in their lives and 19% are current daily smokers. For alcohol, 80% have tried alcohol at some time, 50% had alcohol in the past month, and 28% engaged in what is defined as heavy drinking (five or more drinks on one occasion) during the past 2 weeks. Rates of use of illicit substances are lower but not negligible. Among high school seniors, 38% have tried marijuana at some time in their lives and 19% have used it recently (past 30 days); 16% have tried amphetamines without a medical prescription and 4% have used them recently; 6 % have tried cocaine and 2% have used it recently; 1% have tried heroin and 0.3% have used it recently. Data from samples of the adult general population (ages 18 to 65) in some ways mirror the relative rates of use found in adolescence, with alcohol use fairly prevalent, cigarette smoking intermediate, and rates of illicit drug use relatively low in comparison. The 1995 National Household Survey (NHS) indicated that 29% of U.S. adults are regular smokers. For alcohol use, data from the Epidemiologic Catchment Area Study (ECA) showed that 12% of U.S. adults are total abstainers, 60% engage in social drinking, and 14 % can be characterized as heavy drinkers (seven or more drinks at least one evening a week for several months), but are not diagnosable as alcohol abusers. For the illegal substances, 5 % of adults are characterized in NHS data as marijuana users (used in past month), 1% as heroin users, and 0.7% as cocaine users. Other research, discussed subsequently, indicates that rates of substance use vary considerably across particular subgroups of the population. The phenomenon of multiple substance use begins in adolescence. Studies of adolescent samples show substantial interrelationships for tobacco, alcohol, and marijuana use from early ages. The correlation between continuous scores for involvement in various types of substance use is around r - .35 in early adolescence (age 12 years), and the magnitude of the correlations increases with age to r = .60 or more in later adolescence (age 16 years). These data indicate that the great majority of adolescents who use one substance also use others regularly.

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This pattern of multiple use continues into adulthood. In general population samples of adults there are substantial correlations among tobacco, alcohol, and caffeine use. The recent NHS data indicated similar findings, showing that persons who smoked cigarettes were more likely to use alcohol and illicit drugs (marijuana and cocaine). Alcohol use, particularly heavy use, was also correlated with several types of illicit drug use. The evidence on multiple use has important implications for treatment programs. Many substance abuse treatment programs are specifically focused on one substance (e.g., alcoholism treatment) and may not provide mechanisms for dealing with other types of substance use. In addition, there are significant clinical questions as to whether the therapist and client should try to address different issues in treatment (e.g., simultaneous alcohol abuse treatment and smoking cessation) versus whether treatment should focus on only one addiction problem and how that problem should be selected, that is, which problem should be dealt with first. These questions are beginning to be addressed in clinical research. B. Prevalence

of Substance

Abuse

What part of the population can be characterized as affected by substance abuse? This question has been addressed by several recent studies conducted in the United States. Researchers conducted interviews in homes with a large sample of persons who were selected randomly so that they are representative of the U.S. population. The respondents were given a lengthy interview that asked detailed questions about whether they recently experienced signs and symptoms relevant for diagnosis of various mental disorders. An individual's responses were combined to determine whether he or she met the diagnostic criteria for a given disorder, either at some time in his or her life (lifetime prevalence) or in the past 6 to 12 months (current prevalence ). General population research indicates that substance abuse affects a significant proportion of the adult population. The most recent U.S. study, the National Comorbidity Survey (NCS), showed that one in four persons in the population will experience a substance abuse disorder at some time in his or her life. Data from the ECA and NCS studies, which used somewhat different interviews, indicate that 17 to 27%

.

.

.

.

.

of the population met the criteria for having a substance abuse disorder at some time in their life, and 6 to 11% evidenced a substance abuse disorder within the past 6 months to 1 year. Thus, even with stringent diagnostic criteria, substance abuse is not a rare disorder. In relative terms, substance abuse has a prevalence comparable to other disorders. For example, NCS data showed that 19% of the population have had an affecrive disorder at some time in their life, and 25 % have had an anxiety disorder at some time; this compares with a lifetime prevalence of 27% for substance abuse. Considering only episodes within the last year, 11% of the population experienced a depressive disorder, 17% experienced an anxiety disorder, and 11% experienced a substance abuse disorder. Thus substance abuse represents a significant part of the mental health burden in the population. [See ANXIETY;DEPRESSION;MOOD

DISORDERS.] Within the several types of substance abuse disorders, alcohol abuse is the most frequent. The NCS showed a lifetime prevalence of 14% for alcohol dependence and a lifetime prevalence of other substance dependence for 8 % of the population. Data on specific dependence-abuse diagnoses from the ECA study showed lifetime prevalences of 4.3 % for marijuana, 1.7% for amphetamines, 0.7% for opiates, and 0.2% for cocaine. These studies did not report data for tobacco dependence, a recently added diagnostic category, so the relative prevalence for this substance is currently unclear. [See ALCOHOL PROBLEMS;SMOKING.] A noteworthy aspect of substance abuse is that it is episodic. The few studies that have made repeated observations of adult substance abusers (e.g., alcoholics) show that rates of use vary widely over time, including many periods of minimal use together with some episodes of heavy or "binge" drinking. This aspect is mirrored in findings from the prevalence studies, which show that many more persons have had a substance abuse disorder sometime in their lives compared with the number who have a current disorder. One may speculate that together these findings suggest that rates of substance use are partly responsive to environmental conditions that are relatively short-term (e.g., argument with a significant other) or longer term (e.g., unemployment). However, there has been little research involving longitudinal observations of substance abuse episodes, and interpretation of the available findings is somewhat inferential at this time.

Substance Abuse

C. Temporal Trends Is the prevalence of substance abuse increasing or decreasing in the population? Data from the NHS on prevalence of substance use have shown a steady decline in cigarette smoking among U.S. adults, from a prevalence around 44% in 1975 to a prevalence of around 299/0 in 1995. This was accompanied with substantial decreases in marijuana use (compared with a peak in the mid 1970s) and cocaine use (from a peak in the late 1980s) and a modest decline in current alcohol use. In contrast to population trends in overall use, however, is evidence from the recent ECA and NCS studies that concur in finding rates of mental health disorders to be elevated among persons born in more recent years. This has been interpreted as indicating that the prevalence of psychopathology is increasing in the general population. Regular studies of adolescents provide a more precise picture of how the frequency of particular types of substance use is changing over time. Although this research does not provide diagnostic indices, it does provide yearly standardized data on the prevalence of substance use among adolescents (which has implications for their use as adults). Cigarette smoking among high school seniors has steadily declined since 1975, paralleling the decline in smoking among adults, whereas rates of overall alcohol use have not shown large changes. Rates of adolescents' marijuana use were declining during the 1980s, but began to increase around 1992. This increase in marijuana use has been paralleled by increases in cigarette smoking among younger adolescents (age 13 years). This worrisome trend is currently the subject of considerable attention and public policy debate.

D. Variation by Gender, Socioeconomic Status, and Ethnicity Substance abuse is not randomly distributed in the population, and attention to how the prevalence of substance abuse differs across demographic subgroups of the population provides a valuable perspective on the nature of these disorders. The nature of the demographic differences, however, depends on the type of substance involved. With regard to gender, adult alcohol abuse is more common among males. For example, NCS data showed the lifetime prevalence of alcohol dependence was 20% for males and 8% for

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females; and although the rate of the disorder among females is not trivial, the disorder is 2.5 times more frequent among males. Similar findings are usually noted for substance abuse other than alcoholism; for example, in NCS data, the prevalence of other drug dependence was 9% for males and 6% for females. The only type of substance use consistently found greater for women is tranquilizer use, consistent with the female differential found for anxiety disorders. Even this picture is unclear, because much of the total consumption of anxiolytic drugs is from medical prescription; when studies distinguish between prescribed and nonprescribed tranquilizer use, males have higher rates of nonprescribed tranquilizer use (which often goes along with illicit drug use). It is difficult to know which aspect of these findings deserves more emphasis. On the one hand, the prevalence of alcohol abuse among males is substantial, and it can be anticipated that a considerable proportion of males will experience diagnosable alcohol abuse at some time in their lives. On the other hand, the rate of substance abuse among women is not zero, and considering the broad-band diagnosis of any substance abuse/dependence, NCS data showed that 18 % of women will have a substance abuse disorder at some time in their lives, compared with 35 % for males. Thus the risk for women is lower, but not negligible. Drug abuse is more prevalent among persons of lower socioeconomic status. The results of several large-scale studies show diagnoses of substance abuse to be more frequent among persons with lower income and education. This does not, of course, mean that substance abuse is absent among persons with high socioeconomic status, as shown, for example, in media portrayals of highly paid athletes and entertainment personalities who have used cocaine and other drugs. However, the greatest risk of substance abuse is at the lowest rungs of the socioeconomic ladder. Studies also indicate that the chronicity of substance abuse and other mental health disorders is greater for persons with low socioeconomic status, and that comorbid disorders are markedly more frequent for persons of low socioeconomic status. Thus, the burden of disorder is substantially greater for this part of the population. The picture is complicated a little by alcohol statistics; moderate drinking tends to be more frequent among persons of middle or higher education, but alcohol abuse is elevated for persons with lower income and occupational status.

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Current findings on ethnicity and substance abuse are consistent in showing a lower prevalence among African Americans for most types of substance abuse. Data from the NCS indicate that African American adults have a lower rate of any substance abuse disorder compared with whites. This finding is comparable to ECA data, which showed lower rates of substance and alcohol abuse dependence among young African Americans than among whites. In these studies, Hispanics approach non-Hispanic whites in rates of disorder but generally are not higher. These findings are parallel to findings from studies of adolescents' substance use, which consistently show African American adolescents as having the lowest rates of tobacco and alcohol use, Hispanic adolescents intermediate, and whites highest. These observations are balanced by studies of ethnic differentials in morbidity and mortality that show that adult African Americans are more affected by chronic disease, some of it substancerelated. These findings have been interpreted as reflecting a greater impact of health risk factors in minority populations because of greater environmental stressors and reduced access to screening programs and medical care.

E. Comorbidity of Substance Abuse and Mental Disorder The issue of comorbidity involves the following question: If a person has a substance abuse disorder, is he or she more likely also to have one or more other diagnoses of mental disorder compared with the base rate in the population? Recent epidemiologic studies have provided an answer to the question by studying the co-occurrence of diagnoses among persons in representative community samples. Results have shown that there is extensive comorbidity. For example, ECA data showed persons with alcohol abuse had twice the risk for mental disorder (compared with the population base rate), and persons with other drug abuse disorders showed a fourfold increase in risk for mental disorder. Among persons with alcohol abuse, the risk for other drug abuse disorder was 7 times greater, and there is also a high co-occurrence of substance abuse and antisocial personality. In other words, abuse of one substance increases by 7 times the risk of abusing another substance, and a person with alcohol or sub-

stance abuse has 2 to 4 times the risk of a mental disorder. Comorbidity with alcohol or other substance abuse was found for affective disorders (particularly bipolar depression), anxiety disorders (particularly panic and obsessive-compulsive disorder), and schizophrenia. The NCS data showed that of persons with any lifetime disorder, only one-fifth (21%) had one disorder; the rest had two or three disorders. This indicates that the great majority of mental disorder is comorbid disorder. Moreover, comorbidity was related to chronicity: persons with a comorbid disorder were more likely to have had a recent experience of disorder and to have had more severe disorder. The degree of comorbidity was high among both treated and untreated parts of the population, but was found to be even greater among persons who had sought treatment. The high degree of comorbidity found in these studies has major implications for treatment professionals. One implication is that clinicians who focus on treatment of mental health problems will actually be encountering a substantial number of persons with a co-occurring substance abuse problem. Another implication is that the high degree of comorbid mental disorders among substance abusers probably presents a significant impediment to treatment for this population. A number of clinical research studies are currently underway to investigate how the effectiveness of substance abuse treatment programs may be enhanced through recognition and treatment of other disorders.

F. Treatment Rate One of the contributions of psychiatric epidemiology has been to determine what proportion of persons with mental illness receive professional treatment (the treatment rate). After determining whether a person has had a mental health disorder, researchers can then determine whether the person has received treatment at some time from a mental health professional (psychologist or psychiatrist), from other medical personnel (e.g., primary care physician), or from community agents who provide counseling and guidance (e.g., clergy). Data on persons with affective disorders have indicated that only a minority receive professional treatment. The figure is usually around 25% for persons with depressive or anxiety disorder. The remainder of

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persons with clinical depression or anxiety either receive brief contact with a primary care physician or receive no professional treatment at all. The experience of persons with substance abuse disorders appears to be even worse. For example, of persons who had a substance abuse disorder within the past year, only 4% received treatment in any kind of substance abuse facility (either inpatient hospitalization, outpatient treatment, or a drop-in program). This low treatment rate may be the result of a range of factors, including limited availability of treatment, restrictions on insurance coverage for treatment of substance abuse, or personality characteristics associated with substance abuse (e.g., alienation and antisocial behavior) that discourage drug abusers from becoming involved with any kind of professional agency, but the evidence shows that only a small proportion of affected persons receives professional treatment. What encourages persons with substance abuse to seek treatment is an important question that has received relatively little attention. The ECA study, which showed that primary-care physicians are a major source of treatment for mental disorders, included questions on whether a person had ever talked with their physician about an emotional problem or about substance abuse. Results showed that persons with any kind of emotional problem were unlikely to talk about it with the physician, and persons with substance abuse problems were particularly unlikely to do so. These findings suggest that health care providers encounter a substantial number of persons who are experiencing substance abuse, but frequently do not learn of this from their patients. This indicates that studying ways to increase recognition of substance abuse in treatment settings could be an avenue to opening treatment accessibility. Given the evidence about the episodic nature of substance abuse and the relatively low utilization of professional treatment programs, a significant question has arisen: How do persons who are affected by alcohol or other substance abuse, but who do not receive formal treatment, deal with their problem? One possible answer to the question is that many persons draw on social support from significant others and learn to control the substance abuse problem on their own, either by reducing their use to a level where it is no longer problematic to themselves or others, or by ceasing it entirely. Another possible answer is that persons participate in informal self-help groups such as Alcoholics Anonymous, a widely available resource

that promotes abstinence as the route to recovery. Although there is some evidence for both avenues of coping with substance abuse, this issue has been controversial because of evidence from studies of selfquitters suggesting that some persons may recover from alcohol abuse by learning self-control skills to reduce their use to low levels (controlled drinking). Research has explored the extent of recovery in untreated samples and has followed alcoholics in formal treatment programs to determine their subsequent experiences with abstinence, controlled drinking, or relapse. The present evidence indicates that recovery through controlled drinking occurs for only a small proportion of serious alcohol abusers. However, research on the comparative efficacy of self-change and formal inpatient or outpatient treatment is continuing. This remains an area where well-designed scientific research is needed to obtain more definitive answers.

III. PROTECTIVE AND RISK FACTORS A. Definitions The concept of protective factors and risk factors for substance abuse requires some discussion. A protective factor is an environmental, personal, or social variable that is related to a lower rate of substance abuse, either at the same point in time or over time. Such a factor could deter a person from becoming involved in substance use in the first place, or prevent a person from progressing to a high frequency and intensity of use. A risk factor is an environmental, personal, or social variable that is related to a higher rate of substance use or abuse; in the context of longitudinal research, the level of a risk factor at one point in time would predict the likelihood that a person will be a substance abuser at a later point in time. The concepts are linked in the sense that the level of protective factors may be particularly relevant for individuals with a high level of risk factors, so that substance use could be greatly reduced among persons who had a high level of risk factors but also had a high level of protective factors. Overall levels of protective factors and risk factors are not highly correlated, and protective factors may reduce the potentially adverse effect of risk factors. This is alternately called a buffering effect, in the sense that protective factors buffer a person from the impact of risk factors, or a resiliency effect, in the sense that protective factors enable persons to

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be resilient in the face of pressures that otherwise would operate to encourage substance use or abuse. The ideal study of risk for substance abuse would use a wide range of biochemical, neurological, and psychological measures; obtain such measures from a large and representative sample; collect data on a range of outcomes, including psychiatric diagnosis, work performance, and social relationships; and follow the respondents from infancy through age 35. No single study exists that has all of these characteristics. Accordingly, current knowledge about protective and risk factors is derived from a variety of studies that were designed at different times over the past 40 years. They were conducted for differing periods with samples that span the range somewhere between childhood to young adulthood, and used a wide variety of measures. The discussion here is based on a composite of findings from studies of children, adolescents, and adults which have examined different aspects of risk for substance abuse. Researchers have generally given more weight to knowledge derived from variables obtained at earlier measurement time points as predictors of adult substance abuse. The reason is that results may be ambiguous when study variables are measured at the same point in time as substance abuse in adulthood. For example, the finding of a correlation between depression and substance abuse is ambiguous because the depression may be a result of adverse consequences caused by the abuse, not a predictor. Although it may sound paradoxical to discuss variables measured at age 12, when there is virtually no cocaine use, in relation to cocaine use at age 25, such findings have significant interest because they precede the onset of the substance abuse. In addition, it is common to find drug abuse occurring in a context of multiple substance use and a history of prior substance use. Although many persons who experiment with substances in adolescence reduce or cease their use as they move into adulthood (a phenomenon called "maturing out"), there is evidence for stability of heavy use over time and this is a primary risk factor for substance abuse in adulthood.

tween protective and risk factors can sometimes be arbitrary; for example, one could plausibly argue that high academic achievement is a protective factor or that low academic achievement is a risk factor. The discussion tries to classify factors according to observed main effects and buffering effects. I. Gender

Gender could be characterized as a protective factor in the sense that girls have lower rates of substance use throughout adolescence and women have a lower prevalence of alcohol and other substance abuse disorder in adulthood. In addition, effects of adverse early environments (e.g., parental poverty and alcoholism) on substance use appear to be less for girls than for boys.

2. Temperament Two dimensions of temperamentuprecursors of adult personality characteristics that are observable in childhood and adolescence--have been related to substance abuse liability. Attentional orientation, the ability to focus attention and concentrate on tasks, is greater among persons with low levels of substance use. Positive emotionality, the tendency to be generally cheerful and happy, is also a protective factor and has been shown to buffer the impact of risk factors.

3. Intelligence and Verbal Skills Although one might expect intelligence to be a protective factor, evidence on overall IQ is actually quite mixed. Rather, it is an advantage specifically on verbal ability in IQ tests that is consistently noted to be a protective factor. Whether verbal skills are protective because they facilitate the development of problemsolving ability or because they contribute to better interpersonal relationships with parents and peers is not currently known; it is recognized that both mechanisms are possible.

4. Executive Functions and Problem Solving

This concept refers to a set of interrelated abilities

B. Protective Factors The following section presents a summary of knowledge about protective factors. The distinction be-

measured at the neuropsychological level as functions for planning, organization, and sequencing of activity, and measured at the behavioral level as dealing with problem situations by getting information, considering alternative courses of action, and thoughtfully selecting an alternative before acting. Higher levels of

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these abilities are present in children and adolescents who do not use substances, and the abilities protect against escalation and multiple use that occur for some individuals who are low on these functions. Executive functions are not strongly correlated with fullscale IQ and this domain of cognitive functioning is not merely a proxy for general intelligence.

5. Family Support and Relationships with Significant Others A strong protective factor among adolescents is positive relationships with parents and other family members. The construct of family support includes feeling accepted and valued, and feeling that emotional support is available because one can talk to a parent when one has a problem and that one can receive advice and assistance from a parent for instrumental needs. To some extent this is independent of the number of parents in the home; although a single-parent household is a risk factor for substance use, the level of support in the household appears to be a more important factor. In adulthood, marriage is a protective factor with regard to substance abuse, and a supportive relationship (involving emotional and instrumental support) with a significant other is a protective factor--as long as the significant other is not a drug user.

6. Academic Achievement This is a simple term for a complex construct. The basic finding is that adolescents who get good grades in school are less likely to be substance abusers as adults, hence academic achievement is a protective factor. This probably involves a constellation of characteristics, with higher-achieving individuals having positive attitudes toward school and valuing conventional achievement as a goal; getting support and assistance from parents for doing well; performing better in task situations and organizing behavior to meet requirements (e.g., completing homework on time); and behaving appropriately to meet the demands of the setting (e.g., sitting still in class and not "talking back" to teachers).

7. Religiosity Substance use is lower among persons who hold religious beliefs. This construct is sometimes measured by asking respondents whether they belong to a church, temple, or other religious institution, and, if so, how often they attend; sometimes by asking whether

they hold religious beliefs; and sometimes by asking whether they engage in prayer or meditation. Findings are generally robust across different measures of the construct of religiosity. Moreover, the protective effect is generally found across a number of different religious denominations. Some theorists have suggested that the effect of religiosity is mediated through an individual's identification with conventional social values, but there have been few explicit tests of this proposition.

8. Perceived Harmfulness of Drugs Persons who perceive substances to have adverse consequences (for health, social acceptance, or interpersonal relationships) are less likely to be substance users. This has been shown, in data from the MF study, to account for long-term trends in adolescent substance use. Where these attitudes come from has not been completely established, but research suggests some combination of communications from parents, personal observation, and exposure to educational programs.

9. Perceived Disapproval for Use The perception that significant others (parents, friends, or spouse) disapprove of substance use is a deterrent to substance abuse. To some extent this may be a selfguided effect, because persons with relatively positive attitudes toward drugs will tend to gravitate toward persons who are drug users and who have favorable attitudes themselves; conversely, individuals who hold negative attitudes toward drugs will tend to select friends with similar views. However, the perceived attitudinal climate has been shown in longitudinal studies to be a deterrent to involvement in substance use.

C. Risk Factors Risk factors for substance abuse make up what seems like a longer list. This may to some extent reflect an imbalance in the literature, with researchers tending to concentrate on finding variables that predict bad outcomes rather than protective variables that are related to good outcomes. It may partially reflect the nature of substance use, if there are many different types of factors that produce escalation of substance use among individuals who have experimented. In the listing that follows, it should be recognized that several of the risk factors are correlated. For example, parental alcohol abuse is typically related to discord and conflict be-

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tween parents and children. The nature and reasons for correlations among risk factors is not well understood and is the subject of ongoing investigation, but the reader should keep in mind that the risk factors discussed here are not necessarily independent. In the following section, little attention is given to cultural issues. This is not because these issues are unimportant; cross-cultural work suggests that drug use rates, preferences, and practices vary widely across cultures. However, the epidemiologic studies have mostly been conducted in North American samples and the discussion is focused on this type of evidence.

I. Gender Male gender may be construed as a risk factor for substance abuse. Not only are rates of alcohol and illicit drug use higher among male adolescents, but the differential increases with age. In adulthood, the prevalence of alcohol and other substance abuse disorders is consistently greater among men compared with women.

2. White Ethnicity The prevalence of substance use and abuse is greater among whites, and the strength of relationships between predictive factors and substance use outcomes is consistently found to be greater among whites compared with African Americans. This does not necessarily mean that the predictors of drug abuse are different for whites and for members of ethnic groups, as predictive relationships for a given variable are often found to be significant in all ethnic groups, but predictive effects are typically greater for whites.

3. Lower Socioeconomic Status The risk of substance use or abuse is greater for persons with lower socioeconomic status. This effect is observable beginning in adolescence for teenagers from families with lower education, hence this is a true predictive relationship. There is evidence that persons with substance abuse problems beginning in later adolescence or early adulthood may experience downward mobility, but this does not contradict the risk status that occurs early on. Studies conducted in adolescence have also shown the impact of risk factors on substance use to be greater among adolescents from lower-income families.

4. Family History of Substance Abuse Persons with a history of alcoholism among parents and/or grandparents are at increased risk for alcohol-

ism as adults. Evidence that this is attributable to genetic transmission has been shown by studies of twins and studies of adopted children, each type of research indicating a heritable basis for substance abuse liability. History of paternal alcoholism provides about a fourfold increase in children's risk; for example, a study in Sweden showed that 18% of male children of alcoholic fathers became alcoholic as adults, compared with a rate of 4% for children of nonalcoholic fathers in the population studied. At the same time, it should be noted that the majority of children of alcoholic parents (over 80%) did not become alcoholic themselves, so the data indicate there may be many factors beside family history that contribute to influencing substance abuse.

5. Temperament Two dimensions of temperament have been linked to greater liability for substance abuse. One is physical activity level, the tendency to be physically active and to be unable to sit still for long. The second is negative emotionality, the tendency to be easily frustrated, irritated, and angered. These characteristics are related to substance use at early ages and are found to be more prevalent in the histories of adult substance abusers. Negative emotionality and high activity level are also more common among children of substance abusers, and current research is exploring the possibility that effects of family history are partly transmitted by influencing the development of these temperament dimensions.

6. Poor Parental Relationship and Supervision Discordant relationships between parents and children, with frequent arguments and conflict, predict adolescent substance use and are found to be more common in the life history of adult substance abusers. Accompanying family discord is poor parental monitoring and supervision of children, so that parents frequently do not know where the children are (when they are out of the home) or who they are with. A combination of poor relationship with parents and lax supervision may encourage a child to begin affiliating with deviance-prone peers who can introduce him or her to substances and encourage their use.

7. Early Onset The age at which a person begins using substances predicts future substance abuse risk. Retrospective studies have shown that individuals who began using

Substance Abuse

illicit substances before age 15 are more likely to be affected by substance abuse as adults, whereas persons who began substance use later in adolescence do not show this degree of risk. Although a considerable proportion of teenagers engage in minimal experimentation with tobacco and alcohol, it is the smaller proportion of individuals who engage in early, persistent substance use, including illicit drugs, who are at greatly increased risk.

8. Poor Self-Control Lower ability for self-regulation of emotions and behavior is a risk factor for substance use and has been demonstrated among both adolescents and adults. The construct of poor self-control is a generalized one involving areas such as poor control of behavior in everyday situations (e.g., cutting in line), impatience in social interactions, low dependability in meeting responsibilities, acting without thinking, and less ability to calm down when upset and recover from irritations or embarrassments. Alternate labels given for this construct in the literature are impulsivity, disinhibition, or behavioral undercontrol. Although many persons will display one or two of these behaviors at some time, it is a high level of poor self-control across many situations that is indicated as a risk factor. It is important to note that poor self-control is not simply the absence of good self-control. Although these two dimensions are inversely related, they are not redundant and appear to derive from two different developmental systems. Good self-control has been shown to buffer the impact of poor self-control on substance use.

9. Novelty Seeking and Risk Taking A personality constellation has been identified that involves constantly seeking novel experiences, trying new things for fun and thrills, becoming easily bored, and liking to be involved in risky or dangerous situations. This construct of novelty seeking (sometimes called sensation seeking or risk taking) has been linked to substance abuse liability in animal research and in human studies, with individuals who score high on novelty seeking shown to be at increased risk. There is evidence that this dimension has substantial heritability, and recent research with humans has suggested a linkage with dopamine, a neurotransmitter that is central for brain reward mechanisms. Thus, a psychobiological basis for the novelty-seeking dimension is credible at this time.

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I0. Anger, Hostility, and Aggression This set of interrelated attributes involves feelings of alienation from others, cynical perceptions of hostile intent and distrust of others' motives, and overt aggression toward others including verbal aggression such as teasing, blaming, and criticizing, and physical aggression such as damaging objects or hitting persons. Measures of anger are one of the strongest predictors of substance use in adolescence, and the temperament dimension of negative emotionality appears to be a precursor of this attribute. Irritability and anger are quite stable in childhood and adolescence, and these constructs have been shown to predict substance abuse liability over long time periods.

II. Avoidant and Helplessness Coping In contrast to active types of coping, some persons may cope with problems by trying in various ways to avoid dealing with the problem or by disengaging from coping efforts entirely and taking the view that there is nothing they can do to cope. Measures of coping through avoidance and helplessness are related to increased risk for substance use and abuse over a wide range of ages, from early adolescence through later adult years; more traitlike measures, indexing perceived lack of control over the important things in one's life, have also been related to substance use risk in prospective investigations. It is possible that avoidance and helplessness may be a consequence of poor self-control and low actual competence in domains such as academic or work performance; interrelations among these constructs are currently being investigated.

12. Tolerance for Deviance This attitudinal dimension represents devaluation of conventional values and routes to accomplishment; for example, the belief that school (for adolescents) or work (for young adults) is boring and irrelevant together with endorsement of the attitude that behaviors such as lying, stealing, or fighting are not really so bad and that rule-breaking behavior is all right if one can get away with it. This attitudinal dimension may not be independent of other risk factors; adolescents who are doing poorly in school and who feel angry and alienated from their parents and community might tend to endorse these kinds of attitudes. However, it has been shown that this attitudinal dimension contributes to escalating involvement in substance use.

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13. Conduct Disorder and Antisocial Personality Disorder Substance use is found empirically to co-occur with conduct disorder in adolescence and with antisocial personality (ASP) in adulthood; in the latter case, substance use is one of the diagnostic criteria for ASP because it is highly associated with fighting, stealing, and involvement in other illegal behaviors. Substance use in adolescence is also found to co-occur with other adolescent problem behaviors, such as drunk driving and precocious, frequent sexual relations. The extent to which the diagnostic label is merely a convenient summary for dimensions such as poor self-control, anger, and risk-taking orientation is not known at present because studies have approached the question from such different perspectives. A recent retrospective study by Robins and McEvoy in 1990, using ECA data, did show that adult substance abuse disorder was best predicted by the total number of behavior problems in childhood; the presence of a conduct disorder diagnosis did not add additional ability for prediction of substance abuse. [See CONDUCT DISORDER.]

14. Negative Life Events Negative life events have been shown to precede the onset and escalation of substance use. In adolescent samples, it has been shown that both events occurring to family members (e.g., illness, unemployment)and events occurring directly to children (e.g., serious accidents) predict substance use, and statistical analyses have shown that negative life events are not simply a proxy for demographic factors. Research has indicated that negative events can be a consequence of other variables, such as poor self-control and tolerance for deviance, and can also be a predictor of other variables, such as deviant peer affiliations. The mechanism through which negative events influence substance use has not been completely established. Emotional distress evoked by negative events may be a predisposing factor for high-intensity substance use motivated by self-regulation of negative emotions. It is also possible that feelings of helplessness evoked by negative life experiences make individuals disengage from active modes of coping and seek out deviant companions who can provide hedonistic activities that help dampen the impact of negative experiences in other areas. Some evidence is available for both mechanisms.

15. Affiliation with Peer Users Having friends who smoke, who engage in heavy drinking, and/or who use illicit drugs is generally indicated as being the final common pathway to substance use, predicted by many other risk factors and strongly related to an individual's level of substance use. "Hanging out" with peer smokers and drinkers in early adolescence predicts subsequent escalation to high-intensity substance use, and studies of adult drug abusers show heavy use encouraged by involvement in a drug subculture that features a group of drinking companions or "shooting buddies." It is unlikely that the operation of peer affiliations involves just overt social pressure; although this element is not absent in any group situation, the available evidence suggests that vulnerable persons experimenting with substances seek out affiliation with groups of known users and thereby involve themselves in a cyclical process that promotes higher levels of use and increasing identification with users over time.

IV. SUMMARY The statistics on the prevalence of substance abuse show that alcohol or other substance abuse occurs for a significant part of the population, often comorbid with other mental disorders. Whether substance abuse disorders are decreasing or increasing in the general population is not yet clear. Some evidence can be noted for promising trends, such as declines in tobacco and cocaine use, but this may be offset by other trends such as increases in marijuana use. The one clear conclusion from the current prevalence studies is that substance abuse is not going to go away soon, and continued prevention and treatment efforts are necessary and valuable for the health of the population. Development of substance abuse is a complex process that is rooted in many factors. Having a single risk factor does not indicate that a person is likely to develop substance abuse. It is only when multiple risk factors are present that an individual has a substantial increase in risk. These factors span a wide range of areas including socioeconomic status, family history of substance abuse, patterns of temperament and personality, the individual's own early history of use, patterns of stress and coping, attitudes about deviant behavior in general and substance use in particular, and choices of mates and companions. An individual's

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profile on all of these attributes produces a trajectory that over time may steer the individual toward or away from the rocky shore of substance abuse; but as the number of risk factors one has increases, the probability of substance abuse increases. Although substance abuse is expressed in adulthood, research suggests that liability is contributed by factors that are observable at early ages. Diagnosing an individual as alcoholic at age 30 does not explain how he or she ended up in that condition, and research conducted at younger ages indicates that dispositional attributes, learned ways of coping with situations and feelings, and relationships with parents and peers all are acting to influence an individual's likelihood of substance use. Thus the study of substance abuse has much to gain from studying individual trajectories of use or nonuse over time, identifying early factors that make a minority of persons particularly vulnerable when pressures accumulate in adulthood. All the evidence suggests that prevention programs should begin early, and research has shown a number of modifiable factors that can reduce the likelihood of substance abuse. Many persons with risk factors do not develop substance abuse. Protective factors such as supportive family relationships, self-regulation skills, and developed competencies (e.g., academic performance) serve to blunt the impact of adverse conditions. Again, the existence of a single factor does not guarantee a positive outcome, but persons whose environments contain several protective factors may be buffered against risk to a considerable extent. Research indicates it is the balance of protective and risk factors that is most important for understanding vulnerability versus resilience. ACKNOWLEDGMENTS Preparation of this article was supported by Research Scientist Development Award K02-DA00252 from the National Institute on Drug Abuse. The author thanks Sean Cleary, Marnie Filer, and Ori Shinar for assistance.

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Suicide Ronald W. Maris University of South Carolina Suicide Center

I. II. III. IV. V.

Types of Suicide Prevalence and Epidemiology

may be subintentioned), making up the so-called "NASH" classification of manners of death on death certificates (sometimes a fifth manner of "undetermined" or "pending" death is added). A more elaborate definition of suicide by the French Sociologist Emile Dirkheim is any death that is the direct or indirect result of a positive or negative act accomplished by the victim him(her) self, which he(she) knows or believes will produce this result. Several important consequences follow from this definition. First, suicide must be a death. Nonfatal suicide attempts, self-destructive thoughts or gestures, partial suicides, and so on, strictly speaking are not suicides. Second, suicides must be self-inflicted. The agent ("efficient" or "proximate" cause) must not be another person (murder), atrophy or disease of the human body (natural death), or an external, impersonal agent encountered capriciously (accidental death). Third, risk-taking that leads to death, if the indirect causal sequence can be specified and was intentional, is suicide. Indirect suicide is a common but neglected form of suicide. Fourth, not doing something, as well as positive action, can be suicidal. Obvious examples include not taking life-preserving medication or not moving from the path of an approaching vehicle (ceteris paribus). Fifth, suicide is an intentional death. If someone swallows fifty Seconal capsules and dies, but did not believe or know (e.g., was a child) they were lethal enough to kill, then the death was an accident. Problems of measurement of intentionality (especially after death) have led some investigators to focus on lethal behaviors and to ignore intentionality altogether. This

Predictors

Biological Factors Conclusion

Biological Fitness Being capable of reproducing and propagating one's own genes. Developmental Stagnation Inability to mature normally or the failure to acquire behavioral skills appropriate to chronological human life stages. Dexamethasone Suppression Test Relatively cheap, simple, and safe biological measure of depression that assesses the hypersection of cortisol. Hopelessness Despair over a future tolerable existence related to vulnerability, deprivation, cognitive constriction, and repeated stress and depression. Interdisciplinary Etiology Complex and interrelated mix of biological, psychological, social, anthropological, and economic factors in the production of a behavioral outcome, such as suicide. Serotonin Hypothesis Prediction that low levels of hydroxyindoleacetic acid (5-HIAA), a metabolite of serotonin (5-HT), is causative of suicide--especially of violent suicides. Minimally, "SUICIDE" is intentional self-murder. The concept derives from the Latin sui ("of oneself") and cide ("a killing"). In German, suicide is literally selfmurder (selbstmord). Suicide is usually distinguished from homicide (which is contraintentioned), natural death (which is unintentioned) and accident (which

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approach is unacceptable, since many lethal behaviors result in accidental deaths or even in murders. Finally, death must be certain or thought to be certain. The essential point here is negative. If someone does something (e.g., jumps out of a second-story apartment window) and does not believe that it will kill, but it does, then the outcome is an accidental death. In 1995 the National Institute of Mental Health held a conference to address issues of suicide nomenclature, which resulted in a publication entitled "Beyond the Tower of Babel--A Nomenclature for Suicidology." Suicide can be thought of as resulting from the inability or refusal to accept the terms of the human condition. As such, suicide is problem-solving behavior. In fact, suicide is a drastic solution to the problem of life itself, as well as to many other specific life problems. Edwin Shneidman describes suicide as "a conscious act of self-induced annihilation, best understood as a multidimensional malaise in a needful individual who defines an issue for which suicide is perceived as the best solution." Of course, suicide is often, even usually, not the preferred resolution to one's life problems. "Rational" suicides are usually committed by older adults, who are nonpsychotic, who wait until their depression remits, have a consistent wish-to-die over time, consider deleterious consequences for significant others (even involve them in the decision, particularly their children), explore nonsuicidal alternatives thoroughly, are often in hopeless, irreversible physical conditions, sometimes with unrelenting pain or discomfort, and have made all necessary preparations for death. Under these conditions and perhaps a few others, some (not many) suicides can be said to be rational. One of the problems with the spate of assisted suicides by Dr. Jack Kevorkian is that it is not clear that his clients were assessed or treated first for clinical depression. Although the types of suicides vary, there probably are some common traits of most suicides. In addition to being seen as problem-solving, according to Shneidman, many suicides: 9 wish to produce cessation of consciousness; 9 wish to reduce intolerable psychological pain; 9 have frustrated psychological needs; 9 feel helpless and/or hopeless; 9 are ambivalent about dying; 9 are perceptually constricted;

.

.

.

.

.

9 feel a need for egression or fugue; 9 interpersonally communicate their suicide ideas; 9 use self-destruction as life-long coping. The concept of suicide also needs to be differentiated carefully from attempted suicide. "Attempted suicide" usually implies a conscious intent to kill oneself. However, most suicide attempters never die suicidal deaths (perhaps 85 to 90% die nonsuicidal deaths) and some of them also wish to live (i.e., they are ambivalent). This fact seems to escape many physicians, clinical psychologists, and research psychiatrists who claim they are studying suicide but whose only samples are patients who have made nonfatal suicide attempts. To help resolve such conceptual problems Norman Kreitman recommends the term "parasuicide," that is, nonfatal acts of deliberate self-injury (ignoring one's intent to die). As Figs. I and 2 suggest, the concept of suicide is actually a continuum of related overlapping behaviors and attitudes, including attempts, plans, risk-taking, gestures, and ideas. Probably the most numerous of all self-destructive behaviors are those that are indirect. It will be recalled from Durkheim's definition that under carefully speci-

Figure

I Linehan's overlapping populations model of suicide. [From M. M. Linehan (1986). Suicidal people: One population or two? In "Psychobiology of Suicidal Behavior" (J. J. Mann and M. Stanley,eds.),p. 21. New YorkAcademyof Sciences,New York.]

419

Suicide

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2

A continuum of suicidality.

fled conditions indirect self-destructive behaviors are in fact suicides. Since the 1930s and the work of Karl Menninger, the following behaviors have sometimes been regarded as partially or chronically suicidal: 9 alcoholism and drug abuse; 9 chronic overeating and obesity; 9 smoking to excess; 9 reckless driving and accident proneness; 9 sexual promiscuity and prostitution; 9 ignoring needed medications (like insulin); 9 gambling; 9 risky sports; 9 certain crimes. (See part V in Table I.) Of course, not all behaviors that are self-destructive are suicidal. Some partial self-destruction is absolutely necessary for growth to occur. In fact the educational process itself requires giving up prior ideas and conditioning in the interest of intellectual growth. The word "pseudocide" could be coined to describe adaptive behaviors that are partially self-destructive. It has long been recognized that many nonfatal suicide attempts are cries for help or appeal behaviors. Some parasuicidal behaviors are attempts at self-transformation and not at all intended to end one's life. It must also be noted that not all suicides are individual suicides, nor do all individual suicides have purely individual causes. In 1978, 911 fundamentalist followers of Jim Jones committed suicide (some were murdered) in Guyana. In AD 72-73, 960 Jews sui-

cided at Masada, rather than become captives of the Romans. More recently, there were 48 Swiss suicides/ murders of the Order of the Solar Tradition (October 1994) and 39 suicides by members of the "Heaven's Gate" cult in California (March, 1997). It is not too far-fetched to consider even industrial pollution or nuclear war as social suicides. There are clearly socialstructural factors in what seem to be only personal motivations. One thinks of the economic anomie of the stock market crash in 1929 in the United States or the role of competition in some Japanese suicides. There can be mixtures of suicide and nonsuicides as well, such as mass murder followed by suicide. The concept of suicide is not new. Art and history reveal numerous suicides resulting from defeat in battle, dishonor, shame, social obligation, and depressive illness. Probably the first visual reference to suicide is Ajax falling on his sword in a painting done about 540 BC. We also think of Socrates (399 BC), Samson and Judas in the Judeo-Christian scriptures, Dido, Lucretia, Thomas Chatterton, and more recently Yukio Mishima and Marilyn Monroe. The Asian ritual of seppuku and the Indian custom of suttee should be noted as well.

I. T Y P E S OF S U I C I D E

Suicide is not one kind of behavior. Thus, the explanation of suicide cannot be by a single factor or the province solely of one professional discipline. Suicid-

420

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OVERLAP MODEL (Five Domains) Biology Psychiatric rder

Psychosocial Life Events, and Chronic Medical Illness kkN,~

.

.

.

Suicide

J F a m i l y History and Genetics

Personality Traits Figure 3 Overlap model for understanding suicidal behavior. [From S. J. Blumethal and D. J. Kupfer (eds.) (1990). "Suicide over the Life-Cycle" p. 693. American Psychiatric Press, Washington, D.C.]

ology cannot be reduced to biology, genetics, psychology, or sociology (Fig. 3). Suicidology is doomed to be an inexact science unless it carefully specifies and delineates its dependent variable. Predictor variables must be tailored to the type of suicide to be investigated, understood, and controlled. For example, some suicides have clear biological markers (especially low brain serotonin levels), whereas other suicides have few or none. Some suicides are interpersonal, but some others are largely intrapersonal. Every individual suicide or type of suicide shares some common predictors with most other suicides, but also has some relatively unique predictors of its own. Theoretically there can be as many or as few types of suicide as one wishes to specify. Most suicidologists define three or four basic suicide types and one to three subtypes for each basic type. When a suicide researcher goes beyond four to twelve suicide types, he or she runs the risk of having too small a sample to analyze meaningfully (which includes the statistical problem of low power), since suicide is a rare behavior (namely, 1 to 3 per 10,000 in the general U.S. population). For present purposes, the suicidal typologies of Durkheim, Freud and Menninger, Baechler, and Maris will be reviewed briefly. Biological types are sufficiently important to be examined separately (see

Section IV). It should be remembered that here we are focusing on completed suicides. Another important continuum of self-destructive types is suicide ideas, gestures, nonfatal suicide attempts, and suicide completions (see Fig. 2). Emile Durkheim was one of the founders of the scientific study of suicide and published a hallmark study in 1897. Durkheim believed that there were four basic types of suicidal behavior (with seven subtypes and six mixed types). The four basic (pure or ideal) types of suicide are: 1. 2. 3. 4.

egoistic altruistic anomic fatalistic.

Egoistic and altruistic suicides are polar types, as are anomic and fatalistic suicides. It must be remembered that Durkheim was interested in broad social conditions of suicide, not in the attributes of individual suicides, and that his pure types of suicide are in fact mixed in real life. Durkheim argued that suicide rates varied inversely with the degree of integration of the social groups of which the individual forms a part. For example, egoistic suicide results from excessive individuation or lack of social integration. Other things being equal, Protestants (who tend to advocate a "priesthood of all believers") should have higher suicide rates than Catholics or Jews (who are more socially homogeneous and bound by tradition, catechisms, the Torah, etc.). On an individual level, male skid-row outcasts would be close to the egoistic suicide type. Apathy characterizes egoistic suicides. Altruistic suicide, on the other hand, results from insufficient individuation and is characterized by energy or activity, rather than apathy. The altruistic suicide type typically finds the basis for existence beyond earthly life, as with religious martyrs (like the Jonestown, Waco, and Swiss cults), soldiers who die for their country (like the Japanese kamikaze pilots in World War II), or Indian widows who were sacrificed on their husband's funeral pyre (suttee). If egoistic and altruistic suicides refer to social participation or involvement, anomic and fatalistic suicides concern social deregulation or hyperregulation. In a sense then, ego-altruistic suicides operate on the level of horizontal or social restraint, whereas anomicfatalistic suicides result from vertical or normative

421

Suicide

restraint. In French, anomie literally means without norms and anomic suicide results from a temporary but abrupt disruption of normative restraint. Suicides following stock market crashes or high rates of divorce could be considered anomic. Fatalistic suicide (which Durkheim considers only in a footnote) refers to suicides generated by excessive regulation. One thinks of jail or prison suicides or suicides of very young married couples. Most real-world suicides have both anomic and egoistic traits (and to a lesser degree altruistic and fatalistic traits). Note, too, that suicide varies only negatively with social integration, if the society's or group's norms are against suicide. For example, in Jonestown, Guyana, or the Heaven's Gate cult suicide and social integration were positively related. Durkheim maintained that altruistic and fatalistic suicidal types were relatively rare. Psychiatric and psychological types of suicides were developed by the celebrated Viennese physician Sigmund Freud and the American psychiatrist Karl Menninger. For Freud and Menninger, suicides had three fundamental dimensions, namely, hate, depression (melancholia), and guilt. It followed that all suicides were of three interrelated types: 1. revenge (a "wish-to-kill") 2. depressed (a "wish-to-die") 3. guilty (a "wish-to-be-killed"). Freud thought that the loss of an important love object(s) (such as the death of one's father; see the example of American poet Sylvia Plath) who had been internalized as part of one's own ego ("introjection") often resulted in adult melancholia (depression). Freud claimed that all suicides concerned hostility or a death wish originally directed at an external object (father, lover, etc.). Accordingly, one component of (and one type of) suicide comprised anger, rage, hatred, revenge, or a "wish-to-kill." Menninger called such suicide "murder-in-the-180th degree" or retroflexed anger. Psychologically trying to kill an introjected object results in ego-splitting and regression. The suicide also feels guilty for harboring murderous wishes toward love objects. Thus, suicides are not only a "wishto-kill" but also a "wish-to-be-killed" or punished for one's murderous feelings. Finally, suicides are depressed, hopeless, and cognitively constricted. As one's ego is destroyed by self-hatred and guilt, a "wish-to-die" arises. Freud further thought that pro-

cesses of civilization required collected repression of sexuality and aggression, which in turn were channeled into a group superego, fragmenting and diminishing healthy egos even more. In a sense, higher suicide rates were one cost of civilization. In an interdisciplinary synthesis published in 1979, French social philosopher Jean Baechler contended that there were eleven types of suicide (including non-fatal suicide attempts) fitting into four broad categories: 1. 2. 3. 4.

escape aggressive oblative ludic.

With all escape suicides the central meaning is to take flight. There are three subtypes: flight (to avoid an intolerable situation), grief (to deal with a loss), and punishment (to atone for a fault). Aggressive suicides are directed against another person or persons and consist of four subtypes: vengeance (revenge suicides), crime (murder-suicides), blackmail (putting pressure on another person), and appeal (a cry for help or alarm signal). Oblative suicides are reminiscent of Durkheim's altruistic suicides. There are two subtypes: sacrificial (to gain a value greater than one's own life) or transfiguration (to obtain a state, like religious martyrdom). Finally, ludic suicides are either of the ordeal type (to prove something) or the game type (to play with or risk one's life). Except for the ludic suicidal types, Baechler's types are mainly an amalgam of Durkheim and Freud's types. It is a conceptual flaw that Baechler includes nonfatal suicide attempters in his typology of suicides. In my own view, most suicides (about 75 %) are of the escape or fugue variety. Usually suicides are trying to escape from pain, aging, shame, unhappiness, failure, loneliness, or fatigue. As such, suicide is problemsolving behavior. As much as we do not like to admit it, the only real solution to some life problems is to die. Hopelessness and repeated depressive illness figure prominently into escape suicides. Most other suicides (roughly 20% of all suicides and many nonfatal suicide attempts) are revenge or aggressive suicides. Such suicides have strong interpersonal components and include motivations of anger, retribution, or manipulation. A few suicides are self-sacrificing or self changing. Such suicides typically give their lives for

Table I

A Multiaxial Classification of Suicidal Behaviors and Ideation a,b

Suicidal behaviors/ideas

4. 5. 6. 1. 2. 3. CircumCheck Primary Cer- LethalIntent stances Method (d) type tainty ity

I. Completed suicides A. Escape, egotic, alone, no hope B. Revenge, hate, aggressive C. Altruistic, self-sacrificing, transfiguration D. Risk-taking, ordeal, game E. Mixed II. Nonfatal suicide attempts A. Escape, catharsis, tension reduction B. Interpersonal, manipulation, revenge C. Altruistic D. Risk-taking E. Mixed F. Single vs. multiple G. Parasuicide lB. Suicidal ideation A. Escape, etc. B. Revenge, interpersonal, etc. C. Altruistic, etc. D. Risk-taking, etc. E. Mixed IV. Mixed or uncertain mode A. Homicide-suicide B. Accident-suicide C. Natural-suicide D. Undetermined, pending E. Other mixed V. Indirect self-destructive behavior (not an exclusive category) A. Alcoholism B. Other drug abuse C. Tobacco use D. Self-mutilation E. Anorexia-bulimia F. Over- or underweight G. Sexual promiscuity H. Health management problem, medications I. Risky sports J. Stress K. Accident-proneness L. Other (specify)

7.

8.

Sex

Age

10. 11. Marital OccuRace status pation ,

!

I I

aFrom R. W. Maris et al. (eds.) (1992). "Assessment and Prediction of Suicide," p. 82. Guilford, New York. bCertainty: 0-100%. Lethality (medical danger to life): zero, low, medium, high (O, L, M, H). Intent: zero, low, medium, high. Mitigating circumstances (psychotic, impulsive, intoxicated, confused): zero, low, medium, high. Method: firearm (F); poison (solid and liquid) (P); poison (gas) (PG); hanging (H); cutting or piercing (C); jumping (J); drowning (D); crushing (CR); other (O); none (N). Sex: male (M) or female (F). Age: actual age at event. Race: white (W), black (B), Asian (A), other (O). Marital status: married (M), single (S), divorced (D), widowed (W), other (O). Occupation: manager, executive, administration (M); professional (P); technical worker iT); sales worker (S); clerical worker (C); worker in precision production (mechanic, repairer, construction worker) (PP); service worker (SW); operator, laborer (OL); worker in farming, forestry, fishing (F); other (0); none iN).

Suicide

others or for a higher cause. Lastly, a small number of suicides (and many nonfatal suicide attempters) are risk-related. These suicides lose their lives in attempts to live on the edge of life or to enhance the quality of their life. Most risk-taking suicides are willing to die but death is not their primary objective. Of course, there are subtypes to these four basic suicide types and actual suicides are a mixture of these ideal types (see Table I).

I!. PREVALENCEAND EPIDEMIOLOGY Suicide is and always has been a relatively rare behavior. In general population, one to three persons per 10,000 takes their lives each year. In 1991 in the United states (the latest year for which official statistics were available at this printing), there were 30,810 suicides. This amounts to a rate of suicide of 12.2 per 100,000 population (Table II). Suicide is now the ninth leading cause of death in America, ranking ahead of cirrhosis of the liver (tenth) and just behind AIDS

Table I!

Mortality from 10 Leading Causes of Death: United States, 1994 (Rates per 100,000 Population) a

Cause of death and rank order All causes 1. Diseases of the heart 2. Malignant neoplasms, including neoplasms of lymphatic and hematopoietic tissues 3. Cerebrovascular diseases 4. Chronic obstructive pulmonary diseases and allied conditions 5. Accidents and adverse effects Motor vehicle accidents All other accidents and adverse effects 6. Pneumonia and influenza 7. Diabetes mellitus 8. HIV infection 9. Suicide 10. Chronic liver disease and cirrhosis All other causes

Rate

Percentage of total deaths

875.4

100.0

281.3

33

205.2 58.9

24 24

39.0

5

35.1 31.3 21.8 16.2 12.0 9.8

4 4 3 2 2 2

164.8

19

"From National Center for Health Statistics (1996). "Vital Statistics of the United States, 1994, Vol. II, Mortality, Part A." U.S. Public Health Service, Washington, D.C.

423

(eighth) and pneumonia-flu (sixth). Among adolescents, suicide is the third leading cause of death after accidents and homicides (of course, most adolescents do not die at all). For the last several years, suicide has accounted for about 1.5% of all deaths in any given year. National suicide rates tend to drop in war times (especially during major wars) and rise in economic crises (such as the 1929 great depression in the United States). Suicide rates are highest in western mountain states, like Nevada, Arizona, New Mexico, Montana, and Alaska. Although heart diseases and cancers are still the leading causes of death in most age categories, until late middle-age (i.e., 35-44), three of the five leading causes of death are violent. Accidents, suicides, and homicides rank as the third, fourth, and fifth leading causes of death, respectively, among the middle-aged. Suicide rates also vary considerably by age, sex, race, marital status, and occupation. Generally, suicide rates increase gradually with age until about age 85, after which they drop off slightly. The increase in suicide rates by age is mainly a male trend. Typically, female suicide rates peak in midlife (about ages 45 to 54), then plateau or decline slightly (Table III). Overall, the ratio of male to female suicide rates is three or four to one. The highest suicide rates are consistently observed among white males, followed in declining order by black males, white females, and black females. In 1989, 72% of all suicides were by white males and 18 % were by white females (note that 90% of all suicides in the United States are committed by whites). It is estimated that there are eight to twenty nonfatal suicide attempts for every completed suicide. Thus, there could be as many as 600,000 suicide attempts in the United States each year (not all attempts, as opposed to the legal requirement to report all deaths, are reported to emergency rooms). The ratio of nonfatal suicide attempts to suicide completion is thought to be especially high among young people. Between 1960 and about 1977 (the peak year for which teen suicide rate increased), the suicide rate among 15- to 24-year-olds (largely males) rose dramatically (roughly 230 to 250%; see Table III). Typically, marriage (and having children) protects one against suicide, especially among whites. Suicide rates are higher for the widowed, followed by the divorced and the never-married or single. Studies of the relationships of occupations, social class, and suicide

424

Table III

Suicide

Table III

Death Rates for Suicide, According to Sex, Race, and Age: United States, Selected Years 1950-1989 a

Continued

Sex, race, andage

White female 3 5 - 4 4 years 45-54 years 55-64 years 65-74 years 75-84 years 85 years and over

1950 b

1960 b

1970

1980

1989

8.2 10.5 10.7 10.6 8.4 8.9

8.1 10.9 10.9 8.8 9.2 6.1

13.0 13.5 12.3 9.6 7.2 5.8

9.1 10.2 9.1 7.0 5.7 5.8

7.1 8.0 7.9 6.4 6.3 6.2

2.4 2.2

2.4 2.4

0.1 r 2.3 4.1 4.6 2.8 2.3 1.7 r 1.4 r --r

0.3 r 2.8 3.7 3.9 3.0 2.5 2.1 r 1.7 r 0.6 r

Sex, race, andage

1950 b

1960 b

1970

1980

1989

All races All ages, age adjusted All ages, crude Under 1 year 1-4 years 5-14 years 15-24 years 25-34 years 3 5 - 4 4 years 45-54 years 55-64 years 65-74 years 75-84 years 85 years and over

11.0 11.4 . . 0.2 4.5 9.1 14.3 20.9 27.0 29.3 31.1 28.8

10.6 10.6

11.8 11.6 . . 0.3 8.8 14.1 16.9 20.0 21.4 20.8 21.2 19.0

11.4 11.9 . . 0.4 12.3 16.0 15.4 15.9 15.9 16.9 19.1 19.2

11.3 12.2

White male All ages, age adjusted All ages, crude Under I year 1-4 years 5-14 years 15-24 years 25-34 years 3 5 - 4 4 years 45-54 years 55-64 years 65-74 years 75-84 years 85 years and over

18.1 19.0 . . 0.3 6.6 13.8 22.4 34.1 45.9 53.2 61.9 61.9

18.2 18.0 . . 0.5 13.9 19.9 23.3 29.5 35.0 38.7 45.5 45.8

18.9 19.9 . . 0.7 21.4 25.6 23.5 24.2 25.8 32.5 45.5 52.8

19.6 21.4

Black male All ages, age adjusted All ages, crude Under 1 year 1-4 years 5-14 years 15-24 years 25-34 years 3 5 - 4 4 years 45-54 years 55-64 years 65-74 years 75-84 years 85 years and over

7.0 6.3 . . . . 4.9 9.3 10.4 10.4 16.5 10.0 ~ --

11.1 10.3 . . 0.9 12.3 21.8 15.6 12.0 11.7 11.1 10.5 18.9 r

12.5 12.2

0.9 16.7 22.0 18.1 10.9 10.4 15.4 14.7 22.2 r

5.7 5.9

4.8 5.2

Mondays.

0.3 4.4 5.9

a special and s o m e w h a t

White female All ages, age adjusted All ages, crude Under I year 1-4 years 5-14 years 15-24 years 25-34 years

. .

. . 0.3 5.2 10.0 14.2 20.7 23.7 23.0 27.9 26.0

17.5 17.6 . .

. . 0.5 8.6 14.9 21.9 33.7 40.2 42.0 55.7 61.3

7.8 6.4 . . .

. 4.1 12.4 12.8 10.8 16.2 11.3 6.6 6.9

. . . .

9.9 8.0 . . 10.5 19.2 12.6 13.8 10.6 8.7 8.9 8.7"

0.7 13.3 15.0 14.6 14.6 15.5 18.0 23.1 22.8

1.0 23.2 24.9 23.8 24.2 26.6 35.1 55.3 71.9

Black female All ages, age adjusted All ages, crude Under I year 1-4 years 5-14 years 15-24 years 25-34 years 3 5 - 4 4 years 45-54 years 55-64 years 65-74 years 75-84 years 85 years and over

1.7 1.9 1.5 1.6 . . . . . . ~" 0.0 * 1.8 r 1.3 r 2.6 3.0 2.0 3.0 3.5 3.1 1.1 r 3.0 1.9 r 2.3 r ~ 1.3 r __ mr

2.9 2.6 . . 0.2 3.8 5.7 3.7 3.7 2.0 ~ 2.9 r 1.7 r 2.8 r

. .

,,

a Data are based on the National Vital Statistics program. For data years shown, the code numbers for cause of death are based on the then current International Classification of Diseases which are described in Appendix II, Tables IV and V. bIncludes deaths of nonresidents of the United States. r Based on fewer than 20 deaths.

rates have been equivocal. Some (Durkheim) have f o u n d s u i c i d e r a t e s t o be h i g h e s t in t h e u p p e r s o c i a l classes a n d in t h e p r o f e s s i o n a l a n d m a n a g e r i a l o c c u pations. O t h e r s (Warren Breed and R o n a l d Maris) h a v e f o u n d j u s t t h e o p p o s i t e . It is n o w a p p a r e n t t h a t within each broad census occupational category there a r e j o b t y p e s w i t h b o t h h i g h a n d l o w s u i c i d e rates. F o r example, among physicians, psychiatrists tend to have the highest suicide rates, w h e r e a s surgeons a n d pediat r i c i a n s t y p i c a l l y h a v e l o w s u i c i d e rates. T h e p r e d o m i n a n t m e t h o d of suicide for b o t h males a n d females is f i r e a r m s (see T a b l e IV). S u i c i d e r a t e s a r e s l i g h t l y h i g h e r in t h e m o n t h s of M a r c h t h r o u g h M a y a n d o n

5.3 5.3 5.5 5.3 . . . . . . 0.1 r 0.1 r 2.7 2.3 5.2 5.8

7.2 7.1 . . 0.1 4.2 9.0

. .

T h e r e h a s b e e n a s p a t e of r e c e n t b o o k s

f o c u s i n g o n s u i c i d e a n d t h e life s p a n . S u i c i d e varies b y e a c h m a j o r a g e o r d e v e l o p m e n t a l g r o u p . S u i c i d e is

0.2 4.6 7.5

d i f f e r e n t p r o b l e m f o r chil-

dren, adolescents, y o u n g adults, the middle-aged, the y o u n g - o l d , and the old-old.

.

Table IV

.

.

Suicide

Completed Suicides (1987, 1991) by Method and Gendera

Percentage of

Gender Male (%) Method Firearms (E955.0-955.4) Drugs/medications (E950.0-950.5) Hanging (E953.0) Carbon monoxide (E952.0-952.1) Jumping from a high place (E957) Drowning (E954) Suffocation by plastic bag (E953.1) Cutting/piercing instruments (E956) Poisons (E950.6-950.9) Other" Totals

Female (%)

1987

1991

1987

1991

64.0 5.2 13.5 9.6 1.8 1.1 0.4 1.3 0.6 2.5

65 -15 b --------

39.8 25.0 9.4 12.6 3.0 2.8 1.8 1.4 1.0 3.2

40 -13 b

100.0

- -

1 0 0 . 0

- -

aData from National Center for Health Statistics (1990) and Statistical Abstract, U.S. (1994). bIncludes suffocation. tOther: Includes gases in domestic use (E951), other specified and unspecified gases and vapors (E952.8-952.9), explosives (E955.5), unspecified firearms and explosives (E955.9), and other specified or unspecified means of hanging, strangulation, or suffocation (E953.8-953.9).

III. PREDICTORS Prediction of suicide is such a complicated process that some scholars believe that accurate identification of suicidal individuals before the fact is impossible. As with many rare events, the major problem is one of too many false positives, that is, identifying someone as a suicide when they are in fact a nonsuicide. Correctly identifying true suicides (positive cases) is referred to as "sensitivity" and correctly identifying true nonsuicides (negative cases) is called "specificity." In one study of 4800 psychiatric patients, Alex Pokorny was able to predict 15 of 67 completed suicides. However, he also got 279 false positives. Ten major sets of predictors of suicide will now be examined. However, the reader should be cautioned that single-variable predictors seldom explain suicides or suicide rates well. Most suicides exhibit comorbidity (i.e., have multiple psychiatric diagnoses) or polymorbidity. There are in fact several different key predictors involved in most suicides. Often predictors interact with each other and vary in relative impor-

425

.

tance or weight depending on the type of suicide one is attempting to predict. Most prediction of suicide takes the form of specific scales.

A. Depression, Hopelessness, and Mental Disorders It should be self-evident that very few happy people take their own lives. We now know that about 15% of those with primary depressive illness will eventually suicide, at a rate of roughly 1% per year. Notice, however, that it follows that 85% of depressives will die a nonsuicidal death. There are also many specific types of depressive illnesses (probably the most common suicide-related diagnosis is major depressive episode). George Murphy and Eli Robins state that 47% of completed suicides in their St. Louis sample were manic-depressives. In another study in England, Brian Barraclough found that 64% of completed suicides had a primary depressive illness. Schizophrenics are also overrepresented among suicides, especially among hospital suicides. Still, the suicide rate among schizophrenics is relatively low compared to that of depressives. Ronald Maris found that several specific depression items were particularly related to completed suicide. These predictors included sleep disturbances, feelings of hopelessness, dissatisfaction, wanting to die, and loss of interest in other people. Aaron T. Beck claims that hopelessness is a better predictor of current suicidal intent than depression. [See DEVRESSION.]

B. Alcoholism and Drug Abuse George Murphy and Eli Robins state that 72% of all completed suicides are depressed (47%) and/or alcoholic (25%). No other single variable was present in even 5% of their St. Louis suicide completers. In a thorough review of many research studies on suicide and alcoholism, Alec Roy and Markku Linnoila concluded that, on average, 18% of all alcoholics will eventually die a suicidal death. Curiously, alcohol abuse may actually protect against suicide early on (perhaps in part by transiently raising hydroxyindoleacetic acid levels). Alcoholic suicides tend to be older males who have been alcoholic for 5 years. Some alcoholics may be using alcohol as self-treatment of depressive illness. Alcoholism aggravates other predictors of suicide as well. For example, alcoholism usually leads to loss of important social relationships.

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One study of adolescent suicide attempters discovered that 43% had serious drug problems.

and, use projective tests or even hypnosis to get at suicidal ideation.

C. Age, Sex, and Race

E. Lethal Methods

It is important to remember that the typical suicide tends to be an older white male. Some biological researchers have argued that maleness is more lethal than femaleness at all ages (even in utero). Males are more likely to die from most causes (except from obvious sex-linked illnesses and injuries, such as reproductive problems) than females are. Males usually make more violent suicide attempt than females. Perhaps part of these differences is related to male hormones and chromosomal differences. Although the patterns of suicide over the life span are changing, it is still true that suicides tend to develop slowly over a period of years. Everywhere in the world the lowest suicide rates are among the young. Suicides have developmental careers that peak around the ages 40 to 50 in most groups.

D. Prior Suicide Attempts, Ideation, and Suicide Talk Obviously one has to make a suicide attempt in order to complete suicide. Roughly 15 % of all nonfatal suicide attempters go on to complete suicide sometime in their lives. However, most (85 to 90%) older males (over 45 years) make only one fatal suicide attempt. Thus, a suicide attempt can be used to predict suicide in such cases but not to prevent suicide. Younger women are more likely than other groups to make repeated suicide attempts, but even they seldom make more than five nonfatal attempts before completing suicide. Only about 15 to 25% of suicides leave suicide notes. In the general population (such as random surveys taken in shopping malls), as many as 20% have considered suicide at some time in their lives. Most suicides do talk about suicide and death before their suicides, if you listen carefully. Of course, the trick is to know which of these suicide comments to take seriously. It is very useful to ask directly if an individual is suicidal, although often the individual will deny suicidal intent. If one should get a positive response to such questions, it is wise to follow-up with questions about the individual's specific plan, method, timing, and other detailed preparations for death. A skilled clinician can also consider a patient's dreams

Often a life or death outcome in a suicidal crisis is largely predicted by the availability of a lethal method. Indeed, "suicide proofing" in hospitals, jails, and prisons focuses on removing sharp or protruding objects, clothing and bedsheets that could be torn and made into nooses, and large supplies of medicines that could be used to overdose. In Great Britain, toxic gas supplies to homes were a primary method of suicide. When home gas was detoxified, the suicide rate went down. Potential suicides did not just switch to another method, like hanging or shooting themselves. Although in 1970 in the United States, poisons were the leading method for female completed suicides, by 1987 firearms were the single most common suicide method for both men (64-75%) and women (40%). Many observers have concluded that suicide control in effect amounts mainly to gun control. Hanging is the second most common suicide method (14-15%) for males (especially in jails and hospitals) and poisoning is the second most common method for females (25 %).

F. Social Isolation and Negative Interaction Numerous experiments (e.g., with mice or in confined human sea travel) have demonstrated that prolonged social isolation raises levels of irritability, hostility, and aggression. In Ronald Maris's Chicago research about 50% of completed suicides reported having no close friends at all. Whereas 71% of natural deaths had been "very or fairly close" to their parents, only 41% of nonfatal suicide attempters and 29% of suicide completers were close to their parents. Completed suicides were also much more likely than natural deaths (even though the natural deaths on average were 20 years older) to be unemployed at the time of their deaths (33 % versus 16 %). In another study, 42% of suicidal depressives lived alone compared to only 7% of nonsuicidal depressives. However, social involvement can increase suicide potential if one's social relations are negative and disruptive (as in many revenge suicides). How one came to be alone is probably just as important as the simple fact of social isolation.

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G. Suicide in Families and Imitation It is well known that suicides tend to run in families. Maris discovered that 11% of Chicago suicides had other antecedent first-degree relatives who suicided, whereas none of the natural death controls had suicides in their families. This pattern could be the result of genetic factors or of modeling. For example, the Journal of the American Medical Association (1985) investigated suicide and manic-depressive illness in Amish families and claimed that both outcomes were related to a defect in a narrow portion of chromosome 11. Contagion influences on suicide seem to be greatest among the young. The New England Journal of Medicine reported in 1986 that the adolescent suicide rate rose about 7% in New York City roughly up to a week after the broadcasting of television network films on adolescent suicide. In the same time frame, adult suicide rates rose only 0.5 %.

H. Stress and Negative Life Events Most suicides are chronic and develop over a period of 40 to 50 years, but against this backdrop acute stress or negative life events can "trigger" a suicide. This is especially the case if stressors have been repeated, as in the third or fourth hospitalization for depressive illness. It must be remembered that stress operates in concert with other predictive factors (i.e., there are interactive effects). Shneidman (in reviewing the Stanford Terman data) found that suicide was especially probable if a key supporting person (a "significant other") was lost, such as a midlife male losing a wife through death or divorce. Other acute negative life events that have shown to exacerbate suicide potential include having to go to prison or jail, shame, major financial failure, and terminal or painful irreversible physical illness.

I. Anger, Irritation, and Dissatisfaction It must never be forgotten that most suicides are violent aggressive acts. Anger and irritation are frequently the catalytic agents that ignite depression and hopelessness into a suicide attempt. Psychiatrists argue that suicide is in many cases thinly disguised murderous rage that gets turned back upon the eventual suicide. Gerald Brown and Frederick Goodman claim that aggression may in fact be a more basic affectual response to frustration than depression is (since ag-

gression clearly occurs in animals, but depression may not). It is interesting to speculate on the role of lithium carbonate in the treatment of suicidal behavior among manic-depressives. For example, does it treat the depression or the libidinal and aggressive energy? Anger is particularly suicidogenic when coupled with conceptual rigidity. Shneidman says the "four letter word" in suicidology is "only," as in "suicide was the only thing I could do." Suicide has a purging or cathartic effect. Survivors of serious suicide attempts often report feeling in effect that a valve has been opened and their anger or pain level has now been reduced to a tolerable level. There is also an element of atonement o r expiation in aggressive self-destructive acting out.

J. Physical Illness Thirty-five to forty percent of all suicides have significant physical illness. Since most suicides are older males, this is not too surprising. Certainly physical illness in and of itself seldom causes suicide. Maris found that his natural death control group had far more physical illness than his Chicago suicides, but of course none of the natural deaths suicided. Most physically ill individuals (even terminal cancer or AIDS patients) do not suicide. Like other single predictors, physical illness has a complicated relationship to suicide outcomes. Having pronounced these caveats, it does seem that some diseases are more related to suicidal outcomes than others. Suicide is more common among individuals suffering from epilepsy, malignancies, gastroenterological problems, and musculoskeletal disorders (like arthritis or chronic lower back pain).

IV. BIOLOGICAL FACTORS The biology of suicide is primarily a derivative of the phychobiology and psychopharmacology of depression and is clearly still in its infancy, although a promising beginning has been made. Perhaps the major finding is a disturbance of the metabolism of central monamines in suicides and depressives. Herman Van Praag hypothesizes that disturbances of central serotonergic functions form the root for disturbances of mood and aggressions. Following the work of Marie Asberg et al., van Praag argues that low levels (below 92.5 nmol/liter) of hydroxyindoleacetic acid (5-HIAA; a metabolite of the neurotransmitter serotonin or 5-HT) in cerebrospinal

428

Suicide

fluid (CSF) are predictive of suicidal acts, especially of violent suicides. The best-fitting Diagnostic and Statistical Manual of Mental Disorders-IV (DSM-IV) diagnoses to low levels of 5-HIAA appears to be "major depressive episode" and "dysthymic disorder." The correlation between 5-HIAA and suicidal behavior

-

occurs primarily in unipolar depressions. Some of the selective serotonin reuptake inhibitors (SSRIs), like fluoxetine hydrochloride (Prozac), have been thought to paradoxically increase suicide ideation and akathisia in some patients (see Fig. 4). The dexamethasone suppression test (DST) is probably the best-known

can Fluoxetine (Prozaci/~nticlepressant Pharmacology Cause Suicidal Ideation or Suicidal Behavior? Yes :

Martin H. Teicher, Carol Glod, and Jonathan Cole. American Journal of Psychiatry 147"2, February, 1990: 207-210.

No:

J. John Mann and Shitji Kaput. Archives of General P s y c h i a t r y 48, November 1991: 1027-1033.

I s s u e Summary: Yes: Five depressed outpatients and one inpatient (five females and one male 19-62 years of age) developed intense suicidal thoughts a mean of 26 days (range was 1250 days) after the initiation of fluoxetine treatment. Upon discontinuing fluoxetine the self-destructive thoughts faded after about 27 days (range 3-49 days). Four patients were receiving 60-80 mg of fluoxetine each day and two received 20-40 mg/day. No patient was actively suicidal at the time fluoxetine treatment began. Fluoxetine is known to be a potent and selective serotonergic uptake inhibitor. Serotonin may well be related to violent suicidal ideation or action and to obsessional thinking...fluoxetine may exert a paradoxical response in some patients (e.g., akathisia or motor restlessness, anxiety, nervousness, and insomnia might be special problems with fluoxetine treatment of some patients). No: The hypothesized association (of fluoxetine and suicidal ideation or acts) is surprising because there is considerable evidence of serotonin deficiency in patients who attempt or complete suicide and fluoxetine salective!y enhances serotonergic transmission...In cases like Teicher's the presence of comorbid disorders, previous suicidal tendencies or attempts, and a highly variable time interval between the development of suicidal ideation and the initiation of fluoxetine treatment...make it difficult to draw any clear conclusions...If suicidal ideation or behavior emerges with fluoxetine administration, it is not simply a complication of higher doses of fluoxetine...One hypothesis is that increased suicidality is secondary to the disorganization of certain vulnerable individuals in response to drug-induced activation and akathisia...the emergence of intensification of suicidal ideation and behavior...has not been proven to be associated with any specific type of antidepressant.

Figure 4 Can Fluoxetine (Prozac) Antidepressant Pharmacology Cause Suicide Ideation or Suicidal Behavior?

.....

Suicide

biological measure of depression. In nondepressed persons the synthetic steroid dexamethasone will cause suppression of cortisol secretion for about 24 hr, whereas in roughly 50% of primary unipolar depressives the suppression does not occur. This test is most specific for endogenous depression. Typically patients who are depressed hypersecrete cortisol. [See

DEPRESSION.] In a related set of studies by Brown and Goodwin it is argued that while it is commonly assumed in human self-injury that thought initiates the act, the order in fact may be reversed, with thought being used to elaborate and transform suicidal behaviors rather than to initiate them. Brown and Goodwin claim that aggression is a more primitive response to the environment than depression, since aggression is found at all ages and in all species, but significant depression and suicide are not. Another major biological factor in suicide is clearly alcoholism. As mentioned earlier, Roy and Linnoila surveyed follow-up studies of 27,956 alcoholics, and on the average 18% of all alcoholics in these studies died by suicide. Alcoholic suicides are much more likely to be men rather than women: almost 90% of alcoholic suicide victims are men. The mean age of alcoholic suicides is about 47 years old, with a mean duration of alcoholism of about 25 years. J. B. Ballenger et al. suggest that alcoholics have preexisting low brain serotonin levels that are transiently raised by alcohol consumption, but that in turn eventually lead to further depletion of brain serotonin levels. This may in part account for the paradoxical relation of alcoholism to suicide. That is, alcohol raises low brain 5-HT levels, but in the long run it lowers them. Of course, development of physical problems like cirrhosis of the liver also takes time. One of the earliest biological markers of suicide risk was developed by W. F. Bunney and Jan Fawcett. They discovered that 3 of their 36 depressed research subjects who committed suicide had very high levels of urinary 17-OHCS (hydroxycorticosterone), namely, 94- mg/24 hr for women and 14 4- mg/24 hr for men. Subsequent efforts to replicate 17-OHCS findings have been frustrated by the need for recording long-term elevated levels and the difficulty of collecting 24-hr urine samples from confused, uncooperative psychiatric patients. As a result, Krieger recommends measuring a precursor of 17-OHCS, namely, plasma cortiso|. In one study, Krieger found that 13 patients

429

who committed suicide had significantly higher serum cortisol levels than did 39 matched patients who did not suicide. In 1983, Agren found that subjects with a history of serious suicide attempts earlier in life had higher plasma cortisol levels. The sociobiology of suicide suggests that individuals are especially vulnerable to suicide when they experience severe coping impasses related to relationships to the opposite sex, health, and socially productive behavior. These factors are related to diminished capacities to reproduce and/or to produce for the welfare of one's kin (i.e., to being less biologically fit). Frederick Struve contents that suicide attempts are positively related to paroxysmal electroencephalogram (EEG) dysrhymthmia. Paroxysmal abnormalities are those that occur suddenly and episodically during a tracing. His research shows that both males and females with suicide ideation had more than twice the incidence of paroxysmal EEG dysrhythmias than did control patients, who were free of suicide and assaultive behaviors. The data suggest further that paroxysmal EEGs are associated with suicidal behavior that is impulsive. Cerebral dysrhythmia may impair emotional and behavioral control during periods of high situational stress. Finally, Bryan Tanney argues that electroconvulsive therapy (ECT) is very effective in the rapid amelioration of depressive disorders of biological origin, especially the delusional depressives or acutely suicidal patients who cannot wait for antidepressant medications to take effect. The side effects and dangers of ECT are minimal. ECT's action to increase 5-HT2 receptor activity offers support for the diminished 5-HT function in those with suicidal predispositions. This review of the biology of suicide has left some factors out. Little has been said about genetics, drugs used to suicide or treat suicides, hormones, urinary norepinephrine, CSF magnesium, symptomless autoimmune thyroiditis, and newer diagnostic tools like positron emission tomography (PET), nuclear magnetic resonance (NMR), and other brain imaging. In closing, it should be remembered that suicidal behaviors require a complex multidimensional model (like that in Fig. 3). Biological markers are only one part of this complex etiology. They are not yet specific or predictive of just suicidal behaviors. The accuracy of biological predictors of suicide when used alone is quite weak and, as with other single predictors, produces many false positives.

430

Suicide

V. CONCLUSION

BIBLIOGRAPHY

Suicide is a conscious act of self-induced annihilation, best understood as a multidimensional malaise in a needful individual who defines an issue for which suicide is perceived as the best solution. Suicide is not one behavior but in fact consists of several discrete but overlapping types, each with its own relatively unique etiology and predictors. Some of the basic types of suicide are escape, revenge, altruistic, and risk-taking. These basic types can be further specified by age, sex, race, and a few other variables. Suicide is a rare behavior, namely, 1 to 3 per 10,000 in the general population. Suicide is a behavior characteristic of older white males, at least in the Western world. Other relevant factors in the prediction of suicide include depressive illness, alcoholism, suicide ideation and nonfatal attempts, lethality of method, social isolation, suicide in the family, stress, anger, and certain types of mental illness (e.g., schizophrenia and borderline personality disorder). The predominant biological market of suicide at this time is low CSF 5-HIAA, a metabolite of serotonin.

Blumenthal, S. J., & Kupfer, D. J. (Eds.) (1990). "Suicide over the Life-Cycle." American Psychiatric Press, Washington, D.C. deCatanzaro, D. (1981). "Suicide and Self-Damaging Behavior: A Sociobiological Perspective." Academic Press, New York. Evans, G., & Farberow, N. L. (1988). "The Encyclopedia of Suicide." Facts on File, New York/Oxford, England. Jacobs, D., & Brown, H. N. (Eds.) (1989). "Suicide, Understanding and Responding: Harvard Medical School Perspectives." International Universities Press, Madison, Connecticut. Kushner, H. I. (1989). "Self-Destruction in the Promised Land: A Psychocultural Biology of American Suicide." Rutgers Univ. Press, New Brunswick, New Jersey. Mann, J. J., & Stanley, M. (Eds.) (1988). Suicide. In "Review of Psychiatry," Vol. 7. American Psychiatric Press, Washington, D.C. Maris, R. W. (1981). "Pathways to Suicide: A Survey of SelfDestructive Behaviors." Johns Hopkins Univ. Press, Baltimore. Maris. R. W. (Ed.) (1986). "The Biology of Suicide." Guilford, New York/London. Maris, W., et al. (Eds.) (1992). "Assessment and Prediction of Suicide." Guilford, New York/London. Murphy, G. (1992). "Suicide in Alcoholism." Oxford Univ. Press, New York. O'Carroll, P., et al. (1996). Beyond the tower of Babel--A nomenclature for suicidology. Suicide and Life-Threatening Bebav. 26(3). Pokorny, A. (1993). Suicide prediction revisited. Suicide and LilCeThreatening Behavior 23(1) (Spring), 1-10. Shneidman, E. S. (1985). "Definition of Suicide." WileyInterscience, New York

This article has been reprinted from the Encyclopedia of Human Biology, Second Edition, Volume 8.

Encyclopediaof Mental Health Editor-in-Chief Howard S. Friedman University of California, Riverside

Executive Advisory Board Nancy E. Adler University of California, San Francisco

Ross D. Parke University of California, Riverside

Christopher Peterson University of Michigan, Ann Arbor

Robert Rosenthal Harvard University

Ralf Schwarzer Freie Universit/it Berlin

Roxane Cohen Silver University of California, Irvine

David Spiegel Stanford University School of Medicine

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Contributors

Mark W. Ilondi

Salman Akhtar

Narcissistic Personality Disorder Department of Adult Outpatient Psychiatry Jefferson Medical College Philadelphia, Pennsylvania 19107

Alzheimer's Disease Department of Psychology California State University, San Marcos San Marcos, California 92096

JohnJ. B. Allen

Dependent Personality Department of Psychology Gettysburg College Gettysburg, Pennsylvania 17325

Robert F. Bornstein

DSM-IV Department of Psychology University of Arizona Tucson, Arizona 85721

Sharon A. Borthwick-Duffy

Mental Retardation and Mental Health School of Education University of California, Riverside Riverside, California 92521

Nader Amir

Anxiety Department of Psychiatry Allegheny University of the Health Sciences Philadelphia, Pennsylvania 19129

Henry A. Buchtel

Epilepsy Psychology Service of the Veteran's Administration Medical Center and Departments of Psychiatry and Psychology University of Michigan, Ann Arbor Ann Arbor, Michigan 48105 Douglas Carroll Gambling School of Sport and Exercise Sciences The University of Birmingham Edgbaston, Birmingham B15 2TT United Kingdom

RussellA. Barkley

Attention Deficit~Hyperactivity Disorder (ADHD) Department of Psychiatry University of Massachusetts Medical Center Worcester, Massachusetts 01581 Melanie E. Bennett

Alcohol Problems Department of Psychology University of New Mexico Albuquerque, New Mexico 87131 433

434

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'.

.

George A. Clum

Phobias Department of Psychology Virginia Polytechnic Institute and State University Blacksburg, Virginia 24061 KatharinaDalton

Premenstrual Syndrome (PMS) PMS Clinic University College Hospital London W1M 7TD United Kingdom Charles DeBattista

Mood Disorders Department of Psychiatry and Behavioral Sciences Stanford University School of Medicine Stanford, California 94305

SarahE. Deitsch Antisocial Personality Disorder Department of Psychology University of Kentucky Lexington, Kentucky 40506 Keith S. Dobson

.

Contributors

.

.

Frank F. Eves

Gambling School of Sport and Exercise Sciences The University of Birmingham Edgbaston, Birmingham B15 2TT United Kingdom GregklL Febbrar0

Phobias Medical University of South Carolina Charleston, South Carolina 29425 DeborahFein

Autism and Pervasive Developmental Disorders Department of Psychology University of Connecticut Storrs, Connecticut 06269

AllanFenigstein Paranoia Department of Psychology Kenyon College Gambier, Ohio 43022 Edna B. Foa

Psychopathology Department of Psychology University of Calgary Calgary, Alberta T2N 1N4, Canada

Posttraumatic Stress Department of Psychiatry Allegheny University of the Health Sciences Philadelphia, Pennsylvania 19129

Ronald M. Doctor

Randy O. Frost

Sexual Disorders Department of Psychology California State University, Northridge Northridge, California 91331

Obsessive-Compulsive Disorder Department of Psychology Clark Science Center Smith College Northampton, Massachusetts 01063

Gwenyth H. Edwards

Attention Deficit~Hyperactivity Disorder (AD HD) Department of Psychiatry University of Massachusetts Medical Center Worcester, Massachusetts 01581 Javier I. Escobar

Somatization and Hypochondriasis Department of Psychiatry Robert Wood Johnson Medical School University of Medicine and Dentistry of New Jersey Piscataway, New Jersey 08854

Michael k Gala

Somatization and Hypochondriasis Department of Psychiatry Robert Wood Johnson Medical School and University of Behavioral Health Care University of Medicine and Dentistry of New Jersey piscataway, New Jersey 08854 Elizabeth L Glislr/

Amnesia University of Arizona Tucson, Arizona 85721

435

Contributors

LeeAnneGreen

Autism and Pervasive Developmental Disorders Department of Psychology University of Connecticut Storrs, Connecticut 06269 Rick E. Ingrain

Depression Department of Psychology San Diego State University San Diego, California 92120 Usa H. Jaycox

Posttraumatic Stress RAND Corporation Santa Monica, California 90401 Alan E. Kazdin Conduct Disorder

Department of Psychology Yale University New Haven, Connecticut 06520 Ernest Keen

Classifying Mental Disorders: Nontraditional Approaches Bucknell University Lewisburg, Pennsylvania 17837 John F.Kihlstrom Amnesia

Department of Psychology University of California, Berkeley Berkeley, California 94720 Richard P. Kluft

Dissociative Disorders Clinical Professor of Psychiatry Temple University School of Medicine Philadelphia, Pennsylvania 19122 and in private practice in Bala Cynwyd, Pennsylvania 19004 Michael J. Kozak

Anxiety Department of Psychiatry Allegheny University of the Health Sciences Philadelphia, Pennsylvania 19129 Jerome KroU

Borderline Personality Disorder Department of Psychiatry University of Minnesota Medical School Minneapolis, Minnesota 55455

Kelly L. Lange Alzheimer's Disease San Diego State University/ University of California, San Diego, Joint Doctoral Program in Clinical Psychology San Diego, California 92120 Ronald W. Marls Suicide University of South Carolina Suicide Center Columbia, South Carolina 29208

RkhardI. NcHally Panic Attacks Department of Psychology Harvard University Cambridge, Massachusetts 02138 Robert G. Meyer

Antisocial Personality Disorder Personality Disorders Department of Psychology University of Louisville Louisville, Kentucky 40292 William R. Miller

Alcohol Problems Department of Psychology University of New Mexico Albuquerque, New Mexico 87131 lames E. Mitchell Anorexia Nervosa and Bulimia Nervosa

University of North Dakota Medical School Fargo, North Dakota 58102 and Neuropsychiatric Research Institute Fargo, North Dakota 58103 Melissa Pederson Mussell

Anorexia Nervosa and Bulimia Nervosa University of St. Thomas St. Paul, Minnesota 55105 and University of Minnesota Eating Disorders Research Program Minneapolis, Minnesota 55414 Bryan Neff Sexual Disorders

Department of Psychology California State University, Northridge Northridge, California 91331

436

Contributors

............

DennisPusch

Geoffrey L. Thorpe

Psychopathology Department of Psychology University of Calgary Calgary, Alberta T2N 1N4, Canada

Agoraphobia Department of Psychology University of Maine, Orono Orono, Maine 04469

Theodore R. Sarbin

Classifying Mental Disorders: Nontraditional Approaches University of California, Santa Cruz Santa Cruz, California 95064 Alan F. Schatzberg

Mood Disorders Department of Psychiatry and Behavioral Sciences Stanford University School of Medicine Stanford, California 94305 Christine Scher

Depression San Diego State University/ University of California, San Diego, Joint Doctoral Program in Clinical Psychology San Diego, California 92120 JasonSchUlman

Schizophrenia Department of Psychology Emory University Atlanta, Georgia 30322 H. Brent Solvason

Mood Disorders Department of Psychiatry and Behavioral Sciences Stanford University School of Medicine Stanford, California 94305 Gail Steketee

Obsessive-Compulsive Disorder Boston University Boston, Massachusetts 02215

Elaine F. Walker

Schizophrenia Department of Psychology Emory University Atlanta, Georgia 30322 Lynn Waterhouse

Autism and Pervasive Developmental Disorders Child Behavior Studies The College of New Jersey Ewing, New Jersey 08628 ThomasAshbyWills

Substance Abuse Ferkauf Graduate School of Psychology and Department of Epidemiology and Social Medicine Albert Einstein College of Medicine Yeshiva University Bronx, New York 10461 Daniel Wolverton

Antisocial Personality Disorder Department of Psychology University of Louisville Louisville, Kentucky 40292 John L. Woodard

Dementia Memory Assessment Clinic and Alzheimer's Disease Program Georgia State University Atlanta, Georgia 30303

Index

Acute stress disorder (ASD), diagnosis, 338 AD, see Alzheimer's disease Addison's disease dementia, 161 ADHD, see Attenton-deficit hyperactivity disorder ADIS-W, see Anxiety Disorders Interview Schedule-IV Affective disorder, see Mood disorder Agnosia, definition, 147 Agoraphobia assessment, 9-10 clinical presentation, 1-3 comorbidity risks, 4-5 course and prognosis, 332 definition, 331 development following panic attack, 295, 331,334 diagnosis, 9 diagnostic classification DSM-III, 3 DSM-III-R, 3 DSM-IV

with panic disorder, 3 - 4 without panic disorder, 4 epidemiology studies, 4-5,332 etiology biological theories, 5-6, 332-333 cognitive theories, 8 comprehensive model, 8 conditioning theories, 7-8 interpersonal theories, 6-7 psychodynamic theory, 6 psychological factors, 333- 334 heredity, 333 historical perspective, 1-2 pharmacotherapy advantages, 10 benzodiazepines, 10, 335 beta-blockers, 335 monoamine oxidase inhibitors, 10, 335 selective serotonin reuptake inhibitors, 335 tricyclic antidepressants, 10, 335

prevalence, 1, 4, 332 psychotherapy avoidance behavior, 11-12 cognitive therapy, 12 comprehensive treatment, 12-13 overview, 11,334-335 panic attacks, 12, 334-335 Alcohol problems, see also Substance abuse behavioral marital therapy, 24 behavioral self-control training, 25 blackout, 45, 47 body elimination time, 16 consequences, 16-17 consumption norms, 17-18 dementia, 164-165 dependence, 15, 17 detoxification, 24 epidemiology, 17-19 etiology biological factors, 19 cognitive factors, 20-21 environmental factors, 19-20 harmful drinking, 15 health continuum, 15-16 pharmacotherapy, 24 prevention strategies, 15, 23 protective factors, 23 relapse-prevention, 24-25 risk factors, 22 safe drinking recommendations, 16 skills training, 24 standard drink equivalents, 16 support groups, 25 trends, 21-22 Alzheimer's disease (AD) attention and concentration deficits, 38 course, 28 diagnostic criteria D S M - I V , 28 437

438

Alzheimer's disease (continued) NINCDS-ADRDA, 29 differential diagnosis depression, 40-41 normal aging, 40 subcortical dementia, 41-42 epidemiology frequency, 29, 43 risk factors, 29-30 executive function impairment, 39 genetics, 30 historical perspective, 27 language deficits, 38 Lewy body variant, 32-33 management behavioral disturbances, 42-43 pharmacotherapy, 43 memory types and impairment episodic, 27, 35-36 explicit, 27, 35 implicit, 27, 37-38 remote, 35 semantic, 27, 36-37 neocortical atrophy, 32 neurochemical alterations, 32 neurofibrillary tangles, 27, 31-32 neuroimaging, 30-31 personality changes, 39 plaques, 27, 31 spatial cognition impairment, 38-39 synaptic loss, 32 Amnesia aging and dementia, 52 alcoholic blackout, 45, 47 amnesic syndrome anterograde amnesia, 46-48 diencephalic amnesia, 46 frontal lobe amnesia, 47 temporal lobe amnesia, 46-47 transient global amnesia, 45, 47 anesthesia patients, 53 childhood amnesia, 45, 51-52 definition, 187 dissociative disorders, 189, 192-195 explicit and explicit memory dissociation, 48, 52-54 functional amnesia definition, 45, 49 multiple personality disorder, 50 posthypnotic amnesia, 45, 50-51 psychogenic amnesia, 50 psychogenic fugue, 50 historical perspective, 46 infantile amnesia, 45, 51-52

.....

Index

pathologies, 45-46 rehabilitation, 54-55 sleep-induced amnesia, 52-53 subtypes, 192-193 traumatic retrograde amnesia electroconvulsive shock studies in animals, 49 electroconvulsive therapy induction, 49 islands of amnesia, 48 Anorexia nervosa body image, 58, 60 definition, 57 detection and assessment, 60-61 DSM-IV criteria, 59, 361 epidemiology, 59-60 hospitalization, 63 medical complications, 60 nutritional counseling, 63 pharmacotherapy, 62-63 prevention, 63-64 psychological and social impairment, 60 psychotherapy cognitive behavioral therapy, 61-62 interpersonal psychotherapy, 61-62 Antisocial personality disorder, see also Psychopath assessment measures, 68-69 burnout, 65, 73 conduct disorder and psychopathy in adults, 138139 criminal personality characteristics, 65-66 definition, 65, 131 DSM criteria, 67 historical perspective, 316 indicators of psychopathy, 316 intervention issues, 72-73 paths to criminal behavior, 66 prevalence, 65 sensation-seeking, 65, 73 terminology, 65-67 Anxiety definition, 75 depression comorbidity, 178, 180-181 epidemiology cross-cultural perspective, 79- 80 life span changes, 79 sex differences, 79 measurement indicators, 78-79 psychometrics, 79 mental retardation dual diagnosis, 246 obsessive-compulsive disorder comorbidity, 279 pathological anxiety control, 80 definition, 80

Index

DSM-IV classification, 80

expression versus suppression, 80 treatment, 80- 81 theories animal models, 78 biological theories, 77 cognitive theories, 77 conditioning theories, 76-77 diathesis-stressor theory, 78 genetics, 77-78 threat meaning, 76 Anxiety Disorders Interview Schedule-IV (ADIS-IV), 9 Anxiety neurosis, definition, 291 Anxiety sensitivity, definition, 291 Anxiety Sensitivity Index, agoraphobia assessment, 9 Aphasia, definition, 14 7 Apraxia, definition, 147 ASD, see Acute stress disorder Ataxia, definition, 147 Athetosis, definition, 147 Attention deficit hyperactivity disorder (ADHD) adult outcome, 83-84, 92-93 behavioral inhibition deficit, 87-88 clinical presentation associated cognitive impairments, 86 core symptoms, 85-86 conduct disorder association, 133-134 definition, 131 developmental course, 92-93 diagnostic criteria deficits compared with hyperactive children, 94-93 DSM-IV, 85, 93-94 ICD-1 O, 93-94 epidemiology age distribution, 91-92 geographic distribution, 92 prevalence, 83, 91 sex differences, 91-92 twin studies, 91 etiology environmental factors, 91 heredity, 89-91 neuroimaging, 90 historical perspective, 84- 85 hyperactivity, 83 impulsivity, 83-84, 93 psychopathy, 71 reinforcement, 83 response inhibition, 83 subtypes, 85 sustained attention types contigency-shaped attention, 83, 89

goal-directed persistence, 83, 89 theory, 86-89 Autism assessment, 104 behavioral characteristics communication, 99 play, 99 preoccupations, perseverations, and resistance to change, 99-100 social behavior, 99 behavioral programs, 105 biological factors associated conditions, 102-103 genetics, 103 boundary conditions, 102 brainstem dysfunction, 103-104 cognitive characteristics attention, 100-101 executive function, 101 high- versus low-functioning autism, 100 language, 100 memory, 101 social cognition, 100 comorbidity, 102 developmental course, 101 DSM-IV criteria, 98-99 historical perspective, 97-98 mental retardation dual diagnosis, 246 neurochemical findings, 104 neuroimaging, 103-104 pharmacotherapy, 104-105 prevalence, 102 prognosis, 101-102 resources for patients, 105-106 special education, 97, 105 stereotypies, 97 Aversive intervention, definition, 243 Avoidant personality disorder, features, 317 Azidothymidine (AZT), human immunodeficiency viru encephalopathy management, 156 AZT, see Azidothymidine

Behavioral marital therapy (BMT), alcohol problems, i Behavioral self-control training (BSCT), alcohol proble 25 Benzodiazepines agoraphobia management, 10 panic attack management, 10, 298, 335

440

Beta-blockers panic attack management, 335 social phobia management, 331 Binge eating, definition, 57 Binswanger's disease clinical features, 154-155 treatment, 155 Bipolar disorder definition, 177, 261 epidemiology, 264 etiology, 264 treatment, 267-268 Bipolar I disorder, features, 179, 261 Bipolar H disorder, features, 179, 261 BMT, see Behavioral marital therapy Borderline personality disorder (BPD) as-if personality, 107, 111 behavioral patterns, 316-317 cognitive behavioral therapy, 115 cognitive patterns, 317 comorbidity, 111-112 core symptoms and character styles, 110-111 course, 114-115 dissociation, 107 DSM classification cluster B, 107-108, 110-112 DSM-III, 107, 110 DSM-III-R, 109 DSM-IV, 107, 109-110 etiology affective spectrum disorder, 112-113 impulse spectrum disorder, 114 posttraumatic stress disorder secondary to child abuse, 113-114 psychoanalytic hypothesis, 112 historical perspective, 107-110 pharmacotherapy, 116 prevalence, 111 psychoanalysis, 115 rejection-sensitive dysphoria, 107 BPD, see Borderline personality disorder Bradykinesia, definition, 147 Brain abscess, features and treatment, 158 Brain imaging, see Neuroimaging BSCT, see Behavioral self-control training Buffering effect, definition, 403,409 Bulimia nervosa body image, 58, 60 definition, 57 detection and assessment, 60-61 DSM-IV criteria, 59 epidemiology, 59-60

Index

hospitalization, 63 medical complications, 60 nutritional counseling, 63 pharmacotherapy, 62-63 prevention, 63-64 psychological and social impairment, 60 psychotherapy cognitive behavioral therapy, 61-62 interpersonal psychotherapy, 61-62

Catatonic behavior, schizophrenia association, 368-369 CBT, see Cognitive behavioral therapy CD, see Conduct disorder Cerebellar degeneration, features, 152-153 Childhood amnesia, 45, 51-52 Chlorpromazine, schizophrenia management, 375 Chorea, definition, 147 CJD, see Creutzfeldt-Jacob disease Classification, nontraditional approaches for mental disorders assumptions and alternatives to traditional diagnostics individuality, 123 internality, 117, 122 physicality, 122-123 value judgements accompanying disease concept, 123-124 contextualism construction of deviant conduct early efforts in construction, 124 happenings versus doings, 120-121 narrative framework, 124-125 overview, 117, 120 strategic actions, 125-128 unwanted conduct, 121-122 discourse analysis, 117 historical perspective of classification, 359 nosology, 117, 119 overview, 117-118 purpose, 118-119 root metaphor, 117 traditional approaches, see Diagnostic and Statistical Manual o f Mental Disorders; International Classification o f Diseases

Clozapine, schizophrenia management, 376 Cognitive behavioral therapy (CBT) agoraphobia, 12 borderline personality disorder, 115 definition, 1 eating disorders, 61-62

Index

mood disorders, 268-269 panic attack, 298-300 posttraumatic stress disorder treatment cognitive processing therapy, 345 cognitive therapy, 345 eye movement desensitization and reprocessing, 345 prolonged exposure, 344 stress inoculation training, 344-345 Comorbidity, definition, 177, 209, 323,403 Compulsion, definition, 277 Conduct disorder (CD) age of onset and subtypes, 133 attenton-deficit hyperactivity disorder association, 133134 behavioral overview, 131-132 continua of dysfunction and risk, 139-140 correlates and associated features child characteristics, 134 contextual conditions, 134 parent and family characteristics, 134, 136-137 costs on society, 141-142 course antisocial personality disorder and psychopathy in adults, 138-139 childhood, 137-138 continuity over life span, 139, 145 infancy, 137 long-term prognosis, 138-139 diagnosis, 132 influences and outcomes packages, 140-141 variations in patterns, 141 oppositional defiant disorder association, 131, 133 prevalence, 132-133 prevention, 143-144 protective factors, 136 risk factors, 135-136 social policy and action, 144-145 symptom externalization versus internalization, 131 treatment cognitive problem-solving skills training, 142 multisystemic therapy, 142-143 parent management training, 142 Coping, depression protection factor, 185-186 Cortical-basal ganglionic degeneration, features, 152 Creutzfeldt-Jacob disease (CJD), features, 159 Criminal personality, characteristics, 65-66 Cushing's disease dementia, 161 Cyclothymic disorder epidemiology, 264 features, 180, 263 treatment, 267-268

441

Delirium, definition, 147 Delusion definition, 301 paranoid delusional disorder, 302-303 schizophrenia association, 367-368 Dementia, see also Alzheimer's disease; specific dementias causes, 28-29, 148 cerebrovascular disease etiology Binswanger's disease clinical features, 154-155 treatment, 155 lacunar state clinical features, 154 treatment, 154 multi-infarct dementia clinical features, 153 treatment, 153 thalamic vascular dementia clinical features, 153-154 treatment, 154 vasculitis, 155 definition, 27-28, 147 depression association, 166 frontal lobe degeneration clinical features, 148 treatment, 148-149 fungal infection, 158 head trauma closed head injury, 165-166 dementia pugilistica, 166 hydrocephalus, 165 parasitic infection, 158 schizophrenia association, 166-167 subcortical dementia, Alzheimer's disease differential diagnosis, 41-42 systemic illness association Addison's disease, 161 cardiovascular disease, 161 Cushing's disease, 161 hepatic disease, 162 parathyroid dysfunction, 161 pulmonary disease and anoxic states, 161-162 renal disease and dialysis, 162 thyroid dysfunction, 160-161 toxic conditions drugs of abuse, 164-165 medications, 164 occupational and environmental exposure, 164 overview, 163 - 164 tumors as cause, 166

442

Dementia (continued) vitamin deficiency association folic acid, 163 niacin, 163 thiamine, 162-163 vitamin B12, 163 Dependency definition, 169 dependent personality disorder, 169, 174-175, 317318 development of dependency adolescence, 171 adults, 171 childhood antecedents, 171 elderly, 172 historical overview of dependency theory and research, 170 interpersonal correlates, 172-173 oral dependency, 169 physical illness risks, 175 prospects for research, 175-176 psychopathology relationships depression, 173 eating disorders, 173-174 personality disorder, 174-175 substance abuse, 173 Depersonalization disorder case study, 192 diagnostic criteria, 190-191 differential diagnosis, 191 epidemiology, 190-191 etiology, 191 overview, 187, 189 treatment, 191-192 Depression, see also Mood disorder age differences, 181 Alzheimer's disease differential diagnosis, 40-41 anxiety comorbidity, 178 atypical depression, 323 definition, 177-178 dementia association, 166 dependency psychopathology, 173 dexamethasone suppression test, 417, 428-429 double depression, 177 DSM-IV criteria, 178-180 environmental correlates, 182 ethnic differences, 181-182 exploratory categories minor depressive disorder, 180 mixed anxiety-depressive disorder, 180-181 premenstrual dysphoric disorder, 180 recurrent brief depressive disorder, 180

Index

genetic factors and heredity, 184 mental retardation dual diagnosis, 245-246 negative cognition subtype, 177 neurotransmitter roles norepinephrine, 184-185 serotonin, 184-185 obsessive-compulsive disorder comorbidity, 279 posttraumatic stress disorder comorbidity, 340 prevalence international, 181 United States, 181 protective factors coping styles, 185-186 social support, 185 psychological theories of etiology cognitive approaches, 183-184 interpersonal approaches, 183 psychoanalytic approaches, 182-183 sex differences, 181 suicide risk factor, 425 symptoms, 178 types bipolar I disorder, 179 bipolar II disorder, 179 cyclothymic disorder, 180 dysthymic disorder, 179 Major Depressive Disorder, 179 Derealization definition, 187 dissociative disorders, 189-190 Developmental stagnation, definition, 417 Dexamethasone suppression test, depression screening, 417, 428-429 Diagnosis, defmition, 209 Diagnostic overshadowing, definition, 243 Diagnostic and Statistical Manual of Mental Disorders (DSM) alternative diagnostic approaches, see Classification,

nontraditional approaches for mental disorders categorical approach modification prospects, 219-221 criteria for specific disorders, see specific disorders DSM-IVTask Force, 212 historical perspective, 210 - 212, 359- 360 limitations, 128, 361 mechanistic conception of unwanted conduct, 117, 119120 organization and content appendices, 216-217 Axis I features, 212-214, 360 Axis II features, 214-215 Axis HI features, 215-216 Axis IV features, 216

443

Index

Axis V features, 216 multiaxial system, 212, 360-361 purposes of diagnosis, 209-210 reliability of diagnosis definition, 209 Kappa calculation of inter-rater relability, 217-219 validity challenges in DSM-IV, 219-220 definition, 209, 361 external indicators, 219 Diathesis, definition, 169 Diathesis-stressor theory anxiety, 78 schizophrenia, 374-375 Diffuse Lewy body disease, features and treatment, 150 Dissociative disorders, see also Depersonalization disorder amnesia case study, 195 comorbidity, 193 diagnosis, 194 diagnostic criteria, 192-193 epidemiology, 193 etiology, 193-194 treatment, 194-195 disorders not otherwise specified, 204-205 dissociation definition, 187 domains, 188 functions, 188 historical perspective, 188 memory relationship, 207 fugue case study, 197 diagnostic criteria, 195-196 epidemiology, 196 etiology, 196 treatment, 197 identity disorder alternate identity features, 198 amnesia features, 198 comorbidity, 199 diagnosis criteria, 197-198 interviews, 200-201 signs, 200 epidemiology, 199 etiology, 199-200 stressors in personality switching, 198 treatment case study, 203-204 goals, 201

hypnosis, 203 psychotherapy, 201-203 symptoms amnesia, 189 depersonalization, 189 derealization, 189-190 identity alteration, 190 identity confusion, 190 trance disorder diagnostic criteria, 205 example of trance state, 206 possession trance state, 206 treatment, 206-207 trauma response, 188-189 Disulfiram, alcohol problem treatment, 24 Drinking, see Alcohol problems DSM, see Diagnostic and Statistical Manual o f Mental Disorders

Dysarthria, definition, 147 Dysthymic disorder epidemiology, 264 etiology, 266 features, 179, 261-263 treatment, 267

Eating disorder, see also Anorexia nervosa; Bulimia nervosa dependency psychopathology, 173-174 D S M - I V criteria, 59 health continuum, 58 terminology, 57, 64 Echolalia, autism, 97 ECT, see Electroconvulsive therapy Ego-state disorder, case study, 205 Egocentricity, paranoia, 309 Electroconvulsive therapy (ECT) amnesia induction, 49 Major Depression treatment, 267 suicide rate effects, 429 EMDR, see Eye movement desensitization and reprocessing Emotion dimensions, 76 nature, 75 Encephalitis definition, 147, 155 herpes simplex virus, see Herpes simplex encephalitis limbic encephalitis features and treatment, 157 measles, see Subacute sclerosing panencephalitis

44

Encephalopathy definition, 147 H I V , see Human immunodeficiency virus encephalopathy Epidemiologic Catchment Area Study, findings, 291,295, 409 Epidemiology, definition, 177, 323 Epilepsy advocacy group, 233-234 aura, 223, 229 behavioral problems, 229-230 cognition effects, 228-229 differential diagnosis, 227-228 electrencephalography, 223-224, 227-228 etiological categories, 226 historical perspective, 224, 230 ictal discharge, 223 incidence, 225 kindling phenomenon, 227 morbidity and mortality, 225-226 personality changes, 229-230 prevalence, 224-225 seizure classification, 225 focus, 223,227 management, 226 nonepileptic causes, 228 prevention, 233 triggers, 232-233 treatment antepileptic drug types, 223,230-231 historical perspective, 230 nonmedical therapies, 232-233 prospects, 234 side effects of antiepileptic drugs, 226, 230 surgery intracarotid amobarbital test, 232 neuroimaging, 232 overview, 223, 231 patient selection, 231-232 speech mapping, 232 ERP, see Exposure and response prevention Etiology, definition, 177, 323 Executive function, definition, 403 Exhibitionism, features, 379, 385-386 Exposure and response prevention (ERP), obsessive-compulsive disorder treatment, 282-285, 288-289 Eye movement desensitization and reprocessing (EMDR), posttraumatic stress disorder treatment, 345 Eysenck's model of functioning, 363

Index

Familial fatal insomnia (FFI), features, 159 Fear, definition, 75 Fear Questionnaire, agoraphobia assessment, 9 Febrile seizure, definition, 223 Ferritin, premenstrual syndrome levels, 350-351 Fetishism, features, 379, 386 FFI, see Familial fatal insomnia Fluoxetine, see also Selective serotonin reuptake inhibitors antidepressant efficacy, 266 eating disorder treatment, 62 Folic acid, deficiency and dementia, 163 Fugue case study, 197 definition, 187 diagnostic criteria, 195-196 epidemiology, 196 etiology, 196 treatment, 197

Gambling definition, 235 government revenue and regulation, 235-236, 241 pathological gambling comorbidity, 238 diagnostic criteria, 236-237 prevalence, 237-238 prospects for prevention and treatment, 241-242 theory arousal, 239-240 cognitive bias, 238-239 personality, 239 treatment behavior therapy, 240 cognitive therapy, 240 Gambler's Anonymous, 236, 240 stages-of-change model, 241 popularity, 235 Gaze avoidance, autism, 97 Gender identity disorder (GID) adolescence or adulthood (nontranssexual), 382 childhood disorder, 381-382 definition, 379, 381 etiology, 383 transsexualism comorbidity, 382 definition, 379

445

Index

features, 382 prevalence, 383 treatment, 383 General paresis, definition, 147 Gerstmann-Straussler-Scheinker syndrome (GSS), features, 159 GID, see Gender identity disorder GSS, see Gerstmann-Straussler-Scheinker syndrome

Hallucination, schizophrenia association, 368 HD, see Huntington's disease Head trauma, dementia association closed head injury, 165-166 dementia pugilistica, 166 Herpes simplex encephalitis clinical features, 156-157 treatment, 157 Histrionic personality disorder behavioral patterns, 314-315 cognitive patterns, 315 HIV encephalopathy, see Human immunodeficiency virus encephalopathy Homosexuality definition, 389 D S M classification history, 362 etiology, 390 prevalence, 390 status as sexual disorder, 389-391 treatments, 390- 391 Hopelessness, definition, 417 Human immunodeficiency virus (HIV) encephalopathy clinical features, 155-156 neuroimaging, 156 pathology, 155 treatment, 156 Huntington's disease (HD) clinical features, 151 epidemiology, 150 neuroimaging, 150 pathology, 150-151 treatment, 151 Hydrocephalus, dementia association, 165 Hypnotherapy dissociative identity disorder, 203 posttraumatic stress disorder, 346 Hypochondriasis, see also Somatization disorder definition, 393 detection, recognition, and diagnosis, 398-400

D S M - I V versus ICD-IO classification, 394-395, 399-

400 management, 400-401 Hypomania definition, 177 D S M - I V criteria, 262

ICD, see International Classification o f Diseases Identity disorder, see Dissociative disorders Imaging, see Neuroimaging

Imipramine, panic attack effects, 291-292 Incest, features, 384-385 Incidence, definition, 291 Infantile amnesia, 45, 51-52 Insanity, definition, 357-358 International Classification o f Diseases (ICD) criteria for specific disorders, see specific disorders

features, 359 historical perspective, 211,359 popularity, 359 Interoceptive conditioning, definition, 291 Interpersonal psychotherapy (IPT) eating disorders, 61-62 mood disorders, 268-269 IPT, see Interpersonal psychotherapy

Kappa, calculation of inter-rater relability, 217-219 Korsakoff's syndrome, definition, 147

Lacunar state clinical features, 154 treatment, 154 Lallervorden-Spatz syndrome, features, 152 Language Alzheimer's disease deficits, 38 autism, 100 metaphorical language, 97 pragmatics, 97 schizophrenia and disorganized speech, 368 Limbic encephalitis, features and treatment, 157 Limited symptom attack, definition, 1 Lithium, mood stabilization, 267

446

Index

M Major Depression age of onset, 260 D S M - I V criteria, 259-260 epidemiology, 263-264 etiology, 2 6 4 - 2 6 6 features of disorder, 179 symptoms, 259-260 treatment, 266-267 Maladaptive behavior, definition, 243 Mania, D S M - I V criteria, 262 MAOIs, see Monoamine oxidase inhibitors Melancholia, definition, 177 Memory aging effects, 52 Alzheimer's disease memory types and impairment episodic, 27, 35-36 explicit, 27, 35 implicit, 27, 37- 38 remote, 35 semantic, 27, 36-37 amnesia, explicit and explicit memory dissociation, 48, 52-54 autism, 101 dissociation relationship, 207 Meningitis bacterial meningitis features, 157 treatment, 157-158 definition, 147 Menstruation, see Premenstrual syndrome Mental disorder, definition, 209 Mental retardation assessment of mental health behavior effect on IQ test performance, 249 communication deficit complications, 248-249 diagnostic overshadowing, 243,249 D S M - I V applicability, 248 instruments, 249-250 multimethod approach, 248 neuroimaging, 250 definition, 243-244 deviant behavior, sociological perspective, 244 genetic mapping prospects, 254-255 mental illness distinguishment, 244-245 psychopathology comorbidity affective disorders, 245-246 age differences, 247 anxiety disorder, 246 autism, 246 behavior problem distingushment from psychiatric disorders, 248

causal factor relationship to treatment methods behavioral theory, 251 developmental explanations, 250-251 environmental factors, 250 family influences, 251 genetic links to behavior, 251 new morbidity concept, 251,254 self-injurious behavior, 251-252 costs, 255 dual diagnosis, 243,245,250 educational implications, 256 etiology of mental retardation factors, 247 family issues, 2 5 5 - 2 5 6 intellectual level relationships, 247 phobia, 246 prevalence assessment and sampling bias, 246-247 prevention, 254-255 residential placement, 255 schizophrenia, 246 service delivery systems, 256 sex differences, 247 treatment of behavior disorders aversive intervention ethics, 253 behavior therapy, 252-253 historical perspective, 250 matching to genetic causes of retardation, 252 pharmacotherapy, 253-254 skills training, 254 Minor depressive disorder, features, 180 Mobility Inventory, agoraphobia assessment, 9 Monoamine oxidase inhibitors (MAOIs) agoraphobia management, 10 antidepressant efficacy, 266 panic attack management, 335 social phobia management, 331 Mood disorder, see also Depression bipolar disorder features, 261 cyclothymic disorder features, 180, 263 dysthymic disorder features, 179, 261-263 epidemiology, 263-264 etiology, 264-266 Major Depression age of onset, 260 D S M - I V criteria, 259-260 symptoms, 259-260 treatment pharmacotherapy, 266-268 psychotherapy, 268-270 MPD, see Multiple personality disorder Multiple personality disorder (MPD), amnesia, 50

Index

Naltrexone, alcohol problem treatment, 24 Narcissistic personality disorder behavioral patterns, 315 cognitive patterns, 315-316 definition, 271 differential diagnosis, 273 historical perspective, 271-272 intrinsic nature and etiology, 273-274 manifestations, 272-273 treatment, 274 National Comorbidity Survey (NCS), findings, 296 NCS, see National Comorbidity Survey Negative affectivity, definition, 177 Neuroimaging Alzheimer's disease, 30-31 attenton-deficit hyperactivity disorder, 90 autism, 103-104 epilepsy surgery, 232 human immunodeficiency virus encephalopathy, 156 Huntington's disease, 150 mental retardation comorbidities, 250 obsessive-compulsive disorder, 287 Parkinson's disease, 149 schizophrenia, 372 Niacin, deficiency and dementia, 163 Nosology, definition, 177

Obsessive-compulsive disorder (OCD) basal ganglia dysfunction, 287 cognitive characterisics, 280-281 comorbidity anxiety, 279 depression, 279 personality disorders, 279 schizophrenia, 279 Tourette's syndrome, 279 compulsions, 2 7 7 - 2 7 8 course, 278 cultural factors, 278-279 diagnosis, 277-278 D S M - I V criteria, 2 7 7 - 2 7 8 epidemiology, 278 family factors, 279-280 genetics, 288 information processing, 281-282 neuroimaging, 287 obsessions, 277-278

....

447

posttraumatic stress disorder comorbidity, 340 prospects for research, 289 theory behavioral models, 282 biological models, 286-288 cognitive models, 284-285 treatment cognitive therapy, 285-286 exposure and response prevention, 282-285,288289 rational emotive therapy, 284, 286 selective serotonin reuptake inhibitors, 286-289 surgery, 288 Obsessive-compulsive personality disorder behavioral patterns, 318 cognitive patterns, 318- 319 obsessive-compulsive disorder comparison, 318 Obstetrical complications, schizophrenia association, 374 OCD, see Obsessive-compulsive disorder Ophthalmoplegia, definition, 147

Panic attack agoraphobia association, 3-4 agoraphobia development, 295 anxiety sensitivity, 291,297 assessment, 293-294 biological challenge tests carbon dioxide, 296-297 lactate, 296 yohimbine, 296 cardiac patients, 294 definition, 1, 75,291 D S M - I V criteria, 293 epidemiology, 295-296 genetics and heredity, 297 historical perspective, 291-293 hyperventilation, 291 mitral valve prolapse association, 333 nocturnal attacks, 294-295 pharmacotherapy benzodiazepines, 10, 298,335 beta-blockers, 335 imipramine effects, 291-292 monoamine oxidase inhibitors, 335 selective serotonin reuptake inhibitors, 298, 335 tricyclic antidepressants, 335 psychotherapy, 298-300 threat bias, 297-298

448

Paranoia definition, 301 genetics, 305 prevalence, 305 psychological theory anomalous perception, 307 faulty development, 306 information processing biases egocentricity, 309 overview, 308 personalism and intent, 308-309 self-focus, 301,308 paranoid illumination, 301,306-30 pseudo-community, 301,306-307 psychodynamic theory, 306 stress role, 307-308 syndromes delusional disorder, 302-303 overview, 301-302 personality disorder, 303-304, 313 schizophrenia, 304- 305 substance abuse association, 305-306 systemic illness as cause, 305 treatment behavioral therapy, 309-310 difficulty, 309 Paraphilia definition, 379, 383 diagnosis, 384 exhibitionism, 379, 385-386 fetishism, 379, 386 incest, 384-385 miscellaneous deviations, 387 pedophilia, 384 sadomasochism, 386-387 transvestism, 379, 386 voyeurism, 379, 385 Parkinson's disease (PD) causes, 149 clinical features, 149 neuroimaging, 149 treatment levodopa, 149 pallidotomy, 149-150 Passive-aggressive personality disorder behavioral patterns, 319 cognitive patterns, 319 PCL-R, see Psychopathy Checklist-Revised PD, see Parkinson's disease PDD, see Pervasive developmental disorder PE, see Prolonged exposure Pedophilia, features, 384 Personality disorder, see also specific p e r s o n a l i t y

Index

disorders

definition, 311 dependency psychopathology, 174-175 D S M - I V clusters, 311 objective counter-transference and treatment, 320 obsessive-compulsive disorder comorbidity, 279 paranoid personality disorder, 303-304, 313 Personality types, table, 312 Pervasive developmental disorder (PDD), see also Autism boundary conditions, 102 definition, 97 developmental course, 101 prevalence, 102 types of syndromes, 98-99 Pharmacological dissection, anxiety patterns, 1-2 Phobia, see also Agoraphobia; Social phobia; Specific phobia definition, 75, 323 mental retardation dual diagnosis, 246 Pick's disease clinical features, 148 treatment, 148-149 PML, see Progressive muhifocal leukoencephalopathy PMS, see Premenstrual syndrome Posttraumatic stress disorder (PTSD) arousal, 337 avoidance, 337 borderline personality disorder etiology child abuse, 113-114 treatment, 115-116 comorbidity depression, 340 obsessive-compulsive disorder, 340 physical health problems, 340-341 substance abuse, 340 course, 339 diagnostic classification D S M - I V , 337-338 I C D - I O, 338 dissociation, 188-189 measures interviews, 339 self-report measures, 339 prevalence, 339-340 reexperiencing, 337 resiliency factors, 340 stress response role, 343 theory behavioral theory, 341-342 cognitive therapy, 341-342 psychoanalytic theories, 341 psychobiological approaches, 342-343 treatment cognitive-behavioral therapy

"

Index

cognitive processing therapy, 345 cognitive therapy, 345 eye movement desensitization and reprocessing, 345 prolonged exposure, 344 stress inoculation training, 344-345 early intervention, 344 hypnotherapy, 346 pharmacotherapy, 345-346 psychodynamic psychotherapy, 346 vulnerability factors, 340 Premenstrual syndrome (PMS) age of menarche, 348 clinical characteristics, 349-350 diagnosis blood tests, 350-351 checklist, 352 questionnaires, 350 etiology, 352-353 menstruation phases, 347 premenstrual dysphoric disorder, 180 signs, 349 symptoms, 347-349 treatment diet, 354 progesterone therapy, 3 5 4 - 3 5 5 stress relief, 353-354 symptomatic treatment, 354 Prevalence, definition, 131,235,291,403 Prevention, definition, 131 Prion definition, 147, 155, 158 human diseases, 159 normal function of prion protein, 160 pathology, 159-160 transmission, 159 Progesterone, premenstrual syndrome management, 354355 Prognosis, definition, 209, 323 Progressive muhifocal leukoencephalopathy (PML), features and treatment, 157 Progressive supranuclear palsy (PSP) clinical features, 151 treatment, 151 Projection, definition, 301 Prolonged exposure (PE), posttraumatic stress disorder treatment, 344 Protective factor, definition, 131,403,409 Pseudo-community, definition, 301 PSP, see Progressive supranuclear palsy Psychoanalysis, borderline personality disorder, 115 Psychogenic seizure, definition, 223 Psychopath, see also Antisocial personality disorder assessment measures, 68-69

449

characteristics, 67-68 classification, 67-68 definition, 65, 67 heritability of psychopathy, 68 path to psychopathy development adolescence, 72 adulthood, 72 birth to school age, 7 1 - 7 2 pre-existing risk factors, 71 school age to adolescence, 72 research difficulty, 68 theory biological concepts, 71 cognitive concepts, 70 existential concepts, 70-71 learning/behavioral concepts, 70 psychodynamic concepts, 70 treatment, 7 2 - 7 3 Psychopathology conceptual approaches, 358-359 definition, 357 diagnostics history, 359 prospects, 361-362, 365 dimensional models model categories, 364-365 overview, 362 prospects, 365 symptom approaches, 362-364 trait models, 362-363 normalcy versus abnormalcy, 3 5 7 - 3 5 8 treatment prospects, 365-366 Psychopathy Checklist-Revised (PCL-R), antisocial personality disorder assessment, 65, 68-69 PTSD, see Posttraumatic stress disorder Purging, definition, 57

Rape causation in rapists, 389 incidence, 389 management, 389 Rational emotive therapy (RET), obsessive-compulsive disorder, 284, 286 Recurrent brief depressive disorder, features, 180 Relapse-prevention (RP), alcohol problems, 24-25 RET, see Rational emotive therapy Risk factor, definition, 131,403,409 RP, see Relapse-prevention

450

Sadistic personality disorder D S M classification, 319-320 sadism comparison, 319-320 Sadomasochism, features, 386-387 Schizoid personality disorder, features, 313-314 Schizophrenia course and prognosis, 371 dementia association, 166-167 D S M - I V classification, 367, 369 epidemiology prevalence, 370 sex differences, 370- 371 social class differences, 371 etiology brain abnormalities and neuroimaging, 3 72 diathesis-stress model, 3 74-3 75 genetics and heredity, 373-374 neurotransmitter abnormalities, 372-373 obstetrical complication role, 374 viral infection, 374 historical perspective, 369-370 mental retardation dual diagnosis, 246 obsessive-compulsive disorder comorbidity, 279 paranoid schizophrenia, 304-305, 369 premorbid characteristics, 371-372 prospects for research, 377 subtypes, 369 symptoms catatonic behavior, 368-369 delusions, 367-368 disorganized speech, 368 hallucinations, 368 inappropriate affect, 369 negative symptoms, 369 variability of symptoms, 369 treatment antipsychotic medication, 375-376 historical perspective, 375 psychotherapy, 376 Schizotypal personality disorder definition, 277 features, 314 Seizure, see also Epilepsy definition, 223 differential diagnosis, 227-228 nonepileptic causes, 228 Selective serotonin reuptake inhibitors (SSRIs), see also Fluoxetine antidepressant efficacy, 266 obsessive-compulsive disorder treatment, 286-289 panic attack management, 298, 335

Index

social phobia management, 331 Self-focus definition, 301 paranoia, 308 Serotonin hypothesis definition, 417 suicide, 427-428, 430 Sexual addiction, features, 388 Sexual disorders, see also specific disorders biological sex, 379 D S M - I V classification, 379-380 etiology, 387-388 historical perspective, 380 mormalcy versus abnormalcy, 380 Sexual orientation, definition, 379 SIT, see Stress inoculation training Sleep-induced amnesia, 5 2 - 5 3 Social phobia comorbidity, 329 course, 329 D S M - I V criteria, 328 epidemiology, 328-329 etiology biological factors, 329-330 environmental factors, 330 genetics, 329 psychological factors, 330 generalized versus specific phobias, 328 symptoms, 328-329 treatment pharmacotherapy, 331 psychotherapy, 330-331 Social support, depression protection factor, 185 Somatization disorder abridged somatization construct, 393, 395-397 bridge from distress to psychopathology, 398 cross-cultural studies, 400 definition, 393 detection, recognition, and diagnosis, 398-400 diagnosis, 393-394 D S M - I V versus ICD-10 classification, 394-395, 397, 399-400 management, 400-401 pathogenesis, 397-398 prevalence, 398 somatic system characteristics, 397 Somatoform definition, 393 diagnostic classification, 394-395 Specific phobia age of onset, 324-325 biological factors, 325-326 classical conditioning and associative learning, 326-327

Index

course, 325 D S M - I V criteria, 323-324 epidemiology, 324 genetics, 325 symptoms, 324 treatment, 327-328 types, 324 SSPE, see Subacute sclerosing panencephalitis SSRIs, see Selective serotonin reuptake inhibitors Stress inoculation training (SIT), posttraumatic stress disorder treatment, 344-345 Stroke dementia, see Dementia Subacute sclerosing panencephalitis (SSPE), features and treatment, 156 Substance abuse, see also Alcohol problems comorbidity, 404 definition, 403 dependence versus abuse, 403 dependency psychopathology, 173 D S M - I V criteria, 404 epidemiology ethnicity effects, 408 multiple use prevalence, 404-406 sex differences, 407 socioeconomic status effects, 407-408 substance abuse prevalence, 406 substance use prevalence, 404-405 temporal trends, 407, 414 intervention, 415 paranoia association, 305-306 posttraumatic stress disorder comorbidity with mental disorder, 340, 408 protective factors education, 411 executive functions, 404, 410-411 intelligence, 410 overview, 304, 409-410 perception of drug use, 411 religiosity, 411 sex differences, 410 supportive relationships, 411 temperament, 410 risk factors aggression, 413 antisocial personality disorder, 414 avoidant coping, 413 conduct disorder, 414 early onset, 412-413 family history, 412 negative life events, 414 overview, 304, 409-412 peer affiliation, 414 poor parental relations, 412

451

race, 12 risk taking, 413 self-control deficits, 413 sex differences, 412 socioeconomic status, 412 temperament, 412 tolerance for deviance, 413 suicide risk factor, 425-426, 429 treatment rate, 408-409 Suggestibility, definition, 169 Suicide attempted suicide, 418 definition and characteristics, 417-418 dexamethasone suppression test for depression screening, 417, 428-429 epidemiology prevalence, 420, 423,430 protective factors, 423 risk factors, 423-424 sex, race, and age effects, 423-424 mass suicide, 419 method and gender, 424-425 overlap model, 420 parasuicide, 418 paroxysmal electroencephalogram dysrhythmia, 429 predictors age, 426 anger and irritation, 427 depression and mental disorders, 425 genetics, 427 imitation, 427 lethal method availability, 426 physical illness, 427 prior attempts and ideation, 426 race, 426 sex, 426 social isolation and negative interaction, 426 stress, 427 substance abuse, 425-426,429 rational suicide, 418 serotonin levels, 427-428,430 types Baechler classification, 421 Durkheim classification, 420-421 Freud classification, 421 incidence by type, 421,423 multiaxial classification of suicidal behaviors and ideation, 422 urinary hydroxycorticosterone levels, 429 Syphilis, features and treatment, 158

452

TCAs, s e e Tricyclic antidepressants Tetrahydroaminoacridine (THA), Alzheimer's disease management, 43 T H A , s e e Tetrahydroaminoacridine Thalamic vascular dementia clinical features, 153-154 treatment, 154 Therapeutic alliance, definition, 301 Thiamine, deficiency and dementia, 162-163 Thyroid dysfunction dementia association, 160-161 Major Depression association, 265 Tourette's syndrome, obsessive-compulsive disorder comorbidity, 279 Trance definition, 187 dissociative disorder, s e e Dissociative disorders Transsexualism, see Gender identity disorder Transvestism, features, 379, 386 Trauma, see Head trauma; Posttraumatic stress disorder Traumatic retrograde amnesia, see Amnesia Tricyclic antidepressants (TCAs) agoraphobia management, 10 efficacy, 266 panic attack management, 335

Index

Unipolar disorder, definition, 177

Vasculitis, dementia, 155 Vitamin B12,deficiency and dementia, 163 Voyeurism, features, 379, 385

W Wernicke's encephalopathy, definition, 147 Wilson's disease, features and treatment, 152

Yale-Brown Obsessive-Compulsive Scale (YBOCS), 277, 284 YBOCS, s e e Yale-Brown Obsessive-Compulsive Scale