Esquizofrenia, Apuntes de Psicología

¡Descarga Esquizofrenia y más Apuntes en PDF de Psicología solo en Docsity!

S CHI ZOPHR E N I A

© 2009 The Guilford Press A Division of Guilford Publications, Inc. 72 Spring Street, New York, NY 10012 www.guilford.com

All rights reserved

No part of this book may be reproduced, translated, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission from the Publisher.

Printed in the United States of America

This book is printed on acid-free paper.

Last digit is print number: 9 8 7 6 5 4 3 2 1

The authors have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards of practice that are accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the authors, nor the publisher, nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they are not responsible for any errors or omissions or the results obtained from the use of such information. Readers are encouraged to confirm the information contained in this book with other sources.

Library of Congress Cataloging-in-Publication Data Schizophrenia: cognitive theory, research, and therapy / Aaron T. Beck... [et al.]. p. ; cm. Includes bibliographical references and index. ISBN 978-1-60623-018-3 (hardcover: alk. paper)

1. Schizophrenia—Treatment. 2. Cognitive therapy. 3. Cognition.
2. Cognition disorders. I. Beck, Aaron T. [DNLM: 1. Schizophrenia—therapy. 2. Cognitive Therapy. WM 203 S337223 2009] RC514.S33468 2009 616.89`8—dc 2008034198

The characteristics of patients in the case examples are composites so as to prevent identification, and the details of the case histories and the dialogue were modified without detracting from their significance.

To my wife, children, and grandchildren

—A.T.B.

To Debora and Zoe

—N.A.R.

In memory of Cyrell,

and to Kyler, Eden, Brady, and Shannon

—N.S.

To Amy, Leone, and Greg

—P.G.

vii

About the Authors

Aaron T. Beck, MD, is University Professor Emeritus of Psychiatry at the University of Pennsylvania and President of the Beck Institute for Cognitive Therapy in Philadelphia. Dr. Beck developed cognitive therapy in the early 1960s as a psychiatrist at the University of Pennsylvania. He has published over 500 articles and 19 books and has lectured throughout the world. Dr. Beck is the recipient of many honors from professional and scientific organizations, including “America’s Nobel,” the Lasker Clinical Medical Research Award.

Neil A. Rector, PhD, is Director of Research in the Department of Psychia- try at the Sunnybrook Health Sciences Centre in Toronto and Associate Pro- fessor of Psychiatry at the University of Toronto. He is a Founding Fellow of the Academy of Cognitive Therapy, an editorial board member of several cognitive therapy journals, and a Canadian Institutes of Health Research and Social Sciences and Humanities Research Council of Canada-funded investigator for the study of cognitive mechanisms and cognitive therapy treatments for psychiatric disorders. In addition to having an active cogni- tive therapy practice, Dr. Rector is involved in the training and supervision of cognitive therapists.

Neal Stolar, MD-PhD, is a Medical Director and Director of the Cognitive Therapy for the Treatment of Psychosis Special Project at Project Transition in the Philadelphia area; a psychiatric consultant for Creative Health Ser-

viii About the Authors

vices and Penn Behavioral Health; a researcher at the University of Penn- sylvania’s Psychopathology Research Unit and Schizophrenia Research Center; and is in private practice. Dr. Stolar is a Founding Fellow of the Academy of Cognitive Therapy. He has lectured on cognitive therapy of schizophrenia in the United States, China, and Brazil.

Paul Grant, PhD, is Director of Schizophrenia Research and a Fellow in the Psychopathology Research Unit in the Department of Psychiatry at the University of Pennsylvania. Dr. Grant’s research interests include cogni- tive psychopathological models of positive and negative symptoms as well as cognitive therapy of schizophrenia. He is the author of several journal articles and book chapters.

x Preface

on an in-depth understanding of its phenomenology and causes. Further, the therapist needs a conceptual framework to serve as a guide, just as a builder needs a blueprint. In this volume we have attempted to provide, first, an understanding of the origin, development, and maintenance of the symptoms (delusions, hallucinations, thinking disorder, and negative symptoms). Second, we have used our understanding of the symptomatol- ogy and our therapeutic experience fortified by the research in this area to present our suggestions for the treatment of this disorder. Finally, we have attempted to integrate the vast amount of research on the biology of schizo- phrenia with the relatively sparse work on its psychological aspects into a comprehensive psychobiological model of schizophrenia. Following an overview of schizophrenia in Chapter 1 and a review of the disorder’s complex and intriguing neurobiology in Chapter 2, we pro- vide a broad survey of the clinical and psychological aspects of delusions (Chapter 3). What struck us are the commonalities across all types of delu- sions. Most crucially, the hypersalient beliefs (whether paranoid or grandi- ose) usurp the information processing of the afflicted individuals. Further, the patients’ capacity to view their aberrant thoughts, interpretations, and beliefs as mental products subject to evaluation is attenuated. They view their paranoid or grandiose ideas as facts and perceive their fantasies as reality. A number of biases are present in all of the delusions. When the patients slip into the paranoid mode, for example, all their experiences are subjected to the triad of egocentric, externalizing, and internalizing biases: they are the object of other people’s investment, their unexpected or unusual experiences are caused by external entities, and these entities are motivated to affect their well-being or autonomy. Chapter 4, on hallucinations, indicates how these experiences are related to the patients’ own thoughts and ideas, which are transformed into auditory images. The key problem is the patients’ delusion that the voices are externally produced (often by some inimical entity) and that they are omnipotent, omniscient, and uncontrollable. The hallucinatory experience is often embedded in paranoid delusions and indeed is on a continuum with delusions of mind control (thought insertion, thought capture, and mind reading). Chapter 5, on negative symptoms, addresses the problem of why impairments in attention, memory, and mental flexibility are related to loss of productivity, anhedonia, and social withdrawal. The missing link, as we describe it, is the patients’ negative attitudes about their abilities, expec- tations of pleasure, and interpersonal competencies—all resulting from a history of frustrations related to actual neurocognitive dysfunction. Our

Preface xi

formulation of formal thought disorder (Chapter 6) explains the rambling characteristics as a function of deficient inhibitory mechanisms and the alo- gia as an attempt to spare resources. The disorganized thinking is triggered when highly charged cognitions are activated and consequently disrupt the normal flow of ideas. We present data from our own studies to support the hypotheses regarding negative symptoms and thought disorders. The section on treatment begins with a comprehensive discussion of the various techniques used in assessment (Chapter 7). Chapter 8 deals with problems in fostering the therapeutic relationship and provides guide- lines for dealing with patients’ reticence, poor attention span, many defi- cits, and suspiciousness. Specific problems in the assessment and thera- peutic approaches to delusions are described in Chapter 9, and concrete examples for dealing with them are provided. Similarly, Chapter 10, on assessment and therapy of hallucinations, describes a variety of strategies to help the patient reduce the distress associated with voices and, in some cases, eliminate them completely. The therapy of negative symptoms is described in Chapter 11, and various approaches to neutralize the defeatist attitudes and negative expectancies are detailed. In particular, the goal of improving the quality of life is formulated, and strategies for achieving it are reviewed. Because thought disorder can be a rate-limiting factor on interpersonal efficacy and engagement, Chapter 12 describes a therapeutic approach that helps patients to better assess their communicative difficulties and, impor- tantly, to decrease stress-inducing thinking and behavior that leads to the disorganization of speech. Questions are often raised regarding the rela- tion of psychotherapy to the pharmacotherapy of schizophrenia. Chapter 13 describes these two approaches as blended. The final chapter (Chapter

14. attempts to present a broad model of schizophrenia, integrating con- stitutional, stress, and psychological factors. In particular, it attempts to show the role of cognitive biases in producing excessive reactions to life experiences and as the missing link between neurological impairments and clinical symptoms. The reduction of cognitive resources is postulated as a major factor leading to the disruption of the coordination of brain func- tions essential for reality testing and other complex processes. The various chapters in this volume represent the combined efforts of each author. Typically, one or more of us assumed the responsibility for preparing an outline for a specific chapter. After discussions with the other authors, the designated authors proposed a preliminary draft. We all reviewed and made suggestions for successive drafts. Thus, the final version of each of the chapters include contributions from all of us.

xiii

Contents

CHAPTER 1 Overview of Schizophrenia 1

CHAPTER 2 Biological Contributions 30

CHAPTER 3 A Cognitive Conceptualization of Delusions 62

CHAPTER 4 A Cognitive Conceptualization of Auditory Hallucinations 102

CHAPTER 5 A Cognitive Conceptualization of Negative Symptoms 142

CHAPTER 6 A Cognitive Conceptualization of Formal Thought Disorder 159

CHAPTER 7 Assessment 176

CHAPTER 8 Engagement and Fostering the Therapeutic Relationship 192

CHAPTER 9 Cognitive Assessment and Therapy of Delusions 206

CHAPTER 10 Cognitive Assessment and Therapy of Auditory Hallucinations

CHAPTER 11 Cognitive Assessment and Therapy of Negative Symptoms 257

CHAPTER 12 Cognitive Assessment and Therapy of Formal Thought Disorder

xiv Contents

CHAPTER 13 Cognitive Therapy and Pharmacotherapy 305

CHAPTER 14 An Integrative Cognitive Model of Schizophrenia 324

APPENDICES

APPENDIX A Beck Cognitive Insight Scale (BCIS) 351

APPENDIX B Scoring and Interpretation of the Beck Cognitive Insight Scale (BCIS)

352

APPENDIX C Suggested Outline for Initial Psychological/Psychiatric Evaluation 353

APPENDIX D Cognitive Assessment of Psychosis Inventory (CAPI) 357

APPENDIX E Cognitive Triads for Delusional Beliefs 358

APPENDIX F Cognitive Distortions Seen in Patients with Psychosis 359

APPENDIX G Cognitive Distortions Specific to Psychosis 361

APPENDIX H Thought Disorder Rating Scale (THORATS) 362

References 363

Index 409

2 S C H I ZO PH R E N I A

sonal, social, and vocational havoc, leading to decades of cyclical encoun- ters with psychiatric services. Highlighting the link between symptoms and functional disability, Nash’s pervasive difficulty in day-to-day living appears rooted in the positive symptoms of schizophrenia (Andreasen, 1984b; Cutting, 2003), which include hallucinations (he hears “voices”^1 ), delusions (he believes that the New York Times contains special codes sent to him from space), bizarre behavior (he is disheveled and behaves inap- propriately), and positive formal thought disorder (his language is difficult to understand). Nash does not appear to have suffered from the negative symptoms of schizophrenia, which include reduced verbal (alogia) and nonverbal expressivity (affective flattening), as well as limited engagement in constructive (avolition), pleasurable (anhedonia), and social (asociality) activity (Andreasen, 1984a; Kirkpatrick, Fenton, Carpenter, & Marder, 2006). Ultimately, Nash’s story is one of hope:

Without warning, Nash started to show signs of recovery in the late 1980s. The reasons for his recovery are still unclear; he was neither tak- ing medications nor seeking help. He started to interact more with math- ematicians at Princeton, including several who were old friends. Then in 1994 he won the Nobel Prize in economics.... (Green, 2003, p. 87)

In the face of florid symptomatology, behavioral disorganization, and disability, Nash regained much of his lost interpersonal and work-related functioning. Recovery from schizophrenia has been described as an ongo- ing process of managing symptoms and establishing a sense of purpose (Ralph & Corrigan, 2005); in this respect, Nash certainly has recovered. While Green characterizes Nash’s turnaround with the evenhanded caution of a veteran schizophrenia researcher, Nash attributes his own improve- ment to several factors, the primary cause being acts of reasoning (Beck & Nash, 2005). To illustrate this point, Nash has described, first, convincing himself that the hallucinated voices he was hearing were a product of his own mind, and, later, persuading himself of the improbability and ultimate grandiosity of many of his most cherished beliefs. By adjusting his thinking regarding hallucinations and delusions, Nash diminished symptomatic dis- ruption and brought about considerable improvement in everyday function- ing. Nash, thus, exemplifies the cognitive approach to schizophrenia that we advocate in the current volume.

(^1) Nash reports that “voices” were a prominent aspect of his experience of schizophrenia beginning in 1959 (Beck & Nash, 2005).

Overview 3

Pioneered in the 1960s (Beck, 1963), cognitive-behavioral models that explain emotional and behavioral responses as products of thoughts, inter- pretations, and beliefs have proven highly successful in the understanding and treatment of a variety of psychiatric psychopathology—for example, mood disorders, anxiety disorders, substance abuse, and eating disorders (Grant, Young, & DeRubeis, 2005)—as well as somatic pathology—for example chronic pain (Winterowd, Beck, & Gruener, 2003). Further- more, hundreds of studies now support the basic cognitive model in which beliefs precede and, to a large degree, determine emotional and behavioral reactions (Clark, Beck, & Alford, 1999). Building on preliminary work in the United States (Beck, 1952; Hole, Rush, & Beck, 1979), investiga- tors in the United Kingdom successfully extended the cognitive model into schizophrenia in the 1980s and 1990s (Chadwick, Birchwood, & Trower, 1996; Fowler, Garety, & Kuipers, 1995; Kingdon & Turkington, 2005), producing promising adjunctive psychosocial treatment protocols target- ing delusions, hallucinations, and medication compliance (Rector & Beck, 2001). Cognitive approaches to schizophrenia, of this sort, have certainly advanced the treatment of this very serious condition. We believe that it is important to adapt our knowledge of nonpsychotic conditions to the understanding and treatment of schizophrenia. In a way, the formula- tion and treatment strategies we advocate are an extension of those that have been successfully applied to depression (Beck, Rush, Shaw, & Emery, 1979), anxiety disorders (Beck, Emery, & Greenberg, 1985), and personal- ity disorders (Beck, Freeman, Davis, & Associates, 2003). However, one size does not fit all, and there are important revisions that we must make in the way we approach patients with schizophrenia. Basically, it is crucial to understand the neurocognitive and psychological– cognitive aspect of schizophrenia as well as the uniqueness of schizophrenia as a psychiatric condition. Perhaps there is a continuum in terms of neuropathology and cognitive distortions as we move from the neuroses to the psychoses. But just as water changes character when it goes below the freezing point into ice, so the usual neurotic phenomena do evidence a kind of “deep change” when they become frozen into schizophrenia. The current volume is intended as an elaboration of the cognitive approach to schizophrenia. We believe that the best psychotherapeutic prac- tice derives from cognitive theory that is grounded in the existing scientific evidence base (Beck, 1976); therefore, the volume is organized into theoret- ical (Chapters 2–6) and treatment sections (Chapters 7–13), each contain- ing chapters that address the four primary psychopathological dimensions

Overview 5

deningly varying symptomatology of insanity into a bicameral and heuris- tic framework vis-à-vis normality. Elaborations and distortions of normal perception, belief, and behavior are brought together under the umbrella term positive mental symptoms ; these symptoms are embellishments of normal experience. Likewise, deficits in speech, motivation, emotion, and pleasure are grouped as negative mental symptoms ; these symptoms repre- sent losses relative to normal experience. Third, and perhaps most impor- tant, Hughlings Jackson proposes an intuitive causal interface of biology and manifest symptomatology: Negative symptoms are deficit states and naturally suggest underlying, disease- compromised brain structures (i.e., neuropathology); positive symptoms are elaborations on what is normal and naturally suggest an underlying cognitive process (i.e., failure of inhi- bition). Although Hughlings Jackson didn’t speculate regarding progno- sis and outcome of insane patients, it might be inferred that the “broken brain” disease process he postulated for negative symptoms might augur particularly unfavorably. Crow’s (1980) highly influential type I/type II model of schizophrenia, which is essentially a modern elaboration of Hughlings Jackson’s frame- work, sparked renewed interest in the negative symptoms of schizophrenia (Morrison, Renton, Dunn, Williams, & Bentall, 2004). Compelled by new findings in the neurobiology of schizophrenia emerging at the time, Crow proposed splitting schizophrenia into two distinct disorders. Individuals collected under type I schizophrenia manifest marked positive symptoms, respond well to psychoactive medication, and have an illness course char- acterized by sudden onset and favorable long-term outcome. Individuals grouped as having type II schizophrenia, by contrast, manifest predomi- nantly negative symptomatology, do not respond well to medications, and have an illness course characterized by insidious onset and poor long-term outcome. Crow argued, further, that neurochemical imbalance related to the neurostransmitter dopamine underlies type I schizophrenia, whereas structural brain abnormality such as reduced cerebral volume underlies type II schizophrenia. The impact of Crow’s model has been considerable (Bentall, 2004), as the Hughlings Jackson-inspired conceptual parameterization of posi- tive and negative symptom groupings has come to dominate schizophrenia theory and research (Healy, 2002). Of primary importance, investigators developed operationalized rating scales focused upon the positive and nega- tive symptoms of schizophrenia—for example, the Scale for the Assessment of Positive Symptoms (SAPS; Andreasen, 1984c), the Scale for the Assess-

6 S C H I ZO PH R E N I A

ment of Negative Symptoms (SANS; Andreasen, 1984b), and the Positive and Negative Syndrome Scale (PANSS; Kay, Fiszbein, & Opler, 1987). Andreasen’s scales (i.e., SAPS and SANS), in particular, are comprehensive, standardized instruments, in which a sizeable array of symptoms is identi- fied in observable terms (see Chapter 7). Psychometrically, these scales have been shown to be reliable and sensitive to change (Andreasen, 1990a). 2

Kraepelin’s Heterogeneous Category

Whereas Hughlings Jackson produced a framework that guides brain– behavior theory and research, it is the German psychiatrist Emil Kraepelin who devised the modern classificatory system, or nosology, for schizophre- nia (Healy, 2002; Wing & Agrawal, 2003). Based upon extensive patient observation, Kraepelin (1971) collected three diverse manifestations of insanity— hebephrenia (aimless, disorganized, and incongruous behav- ior), catatonia (lack of movement and stupor, on the one hand; agitated, incoherent behavior, on the other), and paranoia (delusions of persecu- tion and grandeur)—and placed them into a single disease category that he termed dementia praecox. Characteristic symptoms included some that Hughlings Jackson would have termed positive (i.e., hallucinations, disor- ganized speech, and delusions). However, dementia praecox was ultimately a deficit state, making symptoms Hughlings Jackson might have termed negative central to the condition, that is, “emotional dullness, failure of mental activities, loss of mastery over volition, of endeavor, and ability for independent action” (as cited in Fuller, Schultz, & Andreasen, 2003, p. 25). It is this fundamental illness chronicity combined with a progres- sively degenerative course that lead Kraepelin to categorize dementia praecox distinct from cyclical, mood-related psychotic conditions such as mania and melancholia, which he aggregated into a second disease cat- egory, manic– depressive psychosis. Course and long-term outcome, in this manner, guided Kraepelin’s nosological efforts more than manifest symptomatology (Healy, 2002). Although he believed that patients could recover from manic– depression, Kraepelin was deeply pessimistic regard- ing recovery from dementia praecox (Calabrese & Corrigan, 2005; War- ner, 2004).

(^2) We note that there is debate regarding the limitations of the SAPS and SANS to capture the symptoms of schizophrenia (e.g., Horan, Kring, & Blanchard, 2006).