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

_~

.

.

"D o B

I

._

~

.

.

I

cn . 2D ~:

I

.

u~

~ t-

--c-

~

--

"o . o 5

I

"5

-

(/)

". -~ ._

~

D ._o

~

"o o B

~ ~ t-o

D o -~ ~

E o

I

I

I

--

I

Lowest

D

.,~

Highest +

Figure

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

.

.

.

.

.

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