Stress and coping across development 9781315825489, 1315825481, 0898599601

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STRESS AND COPING DEVELOPMENT

Edited by Tiffany M. Field Philip M. McCabe Neil Schneiderman

STRESS AND COPING ACROSS DEVELOPMENT

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STRESS AND COPING ACROSS DEVELOPMENT

Edited by T iffa n y M . F ie l d P h il ip M . M c C a b e N e il S c h n e id e r m a n

University o f Miami Medical School

V p Psychology Press A

Taylor & Francis Croup New York London

First Published by Lawrence Erlbaum Associates, Inc., Publishers 365 Broadway Hillsdale, New Jersey 07642 Transferred to Digital Printing 2009 by Psychology Press 270 Madison Avc, New York NY 10016 27 Church Road, Hove, East Sussex, BN3 2FA Copyright €> 1988 by Lawrence Erlbaum Associates, Inc. All rights reserved. No part of this book may be reproduced in any form, by photostat, microform, retrieval system, or any other means, without the prior written permission of the publisher.

Library of Congress Cataloging-in-Publication Data Stress and coping across development. Based on the annual University of Miami Symposia on Stress and Coping, held Feb. 20-21, 1984. Includes bibliographies and indexes. 1. Stress (Psychology)— Congresses. 2. Adjustment (Psychology)— Congresses. 3. Devel­ opmental psychology— Congresses. 4. Medicine and psychology— Congresses. I. Field, Tiffany. II. McCabe, Philip M. III. Schneiderman, Neil. IV. University of Miami Sym­ posia on Stress and Coping (2nd: 1984) [DNLM: I. Adaptation, Psychological-congresses. 2. Human Development— congresses. 3. Stress, Psychological— congresses. WM 172 S9127 1984J BF575.S75S765 1987 155.9 87-24526 ISBN 0-89859-960-1 Publisher’s Note The publisher has gone to great lengths to ensure the quality of this reprint but points out that some imperfections in the original may be apparent.

Contents

Preface

ix

P A R T I: IN FA N C Y 1.

Maternal Deprivation and Supplemental Stimulation Saul M. Schanberg and Tiffany M. Field

3

Maternal Separation Stress, Tactile Stimulation, and Growth in Rat Pups 4 Effects of Supplemental Stimulation on Premature Neonates 11 Weight Gain and Responsivity to Stimulation in Nonorganic Failure-to-Thrive Infants 17 Discussion 19 References 21

2.

Patterns of Infant Feeding, the Mother-Infant Interaction and Stress Managem ent C. Sue Carter Nutrition, Immunities and Breast Feeding 28 The Biology of Lactation 30 Nursing Patterns, Milk Production and the Mother-Infant Reaction 33 Nocturnal Nursing and Sleeping Through the Night Behavioral Consequences of Breastfeeding 36 The Consequences of Breast Versus Bottle-Feeding Speculations Regarding the Role of On-Demand Nursing in Stress Management 42 Conclusions 43 References 44

27

34 40

v

C O N T EN TS

The Mutual Regulation Model: The Infant’s Self and Interactive Regulation and Coping and Defensive Capacities A. Gianino and E. Tronick Coping with Interactive Stress in Infancy 47 The Mutual Regulation Model 48 Infant Coping in Response to the Still-Face, Simulated Depression, Clinical Depression, and the Strange Situation 53 The Interconnections Am ong Self and Mutual Regulation, Object Exploration, Coping, and Defense 60 References 65

P A R T II: C H ILD H O O D

Antecendents of the Coronary-Prone Behavior Pattern Barbara S. McCann and Karen A. Matthews Major Research Assum ptions 72 Assessm ent of Type A Behavior in Children and Adolescents 74 Psychophysiological Characteristics of Type A Children 78 Familial Factors in Type A Behavior 80 Current Research 85 References 85

Type A Behavior In Preschool Children Nitza Vega-Lahr, Tiffany Field, Sheri Goldstein, and Deborah Carran Method

95

Results 98 Discussion 102 Future Directions References 106

105

C O N T EN T S

6.

Coping Behaviors in Children Facing Medical Stress Barbara G. Melamed, Lawrence J. Siegel, and Robyn Ridley-Johnson

VÜ

109

Introduction 109 Response to Medical Stressors: A Prototype for Anxiety Management 109 Illness and Medical Concerns 112 Theories of the Development of Fear 113 Parenting Behaviors in Stressful Medical Settings 116 Factors Which Mediate the Impact of Medical Experiences 117 New Approaches to Studying Children’s Fears 123 Sum m ary and Conclusions 132 References 132 7.

Children with Diabetes and their Families: Coping and D isease Management Annette M. La Greca

139

Overview of Diabetes 139 Psychosocial Aspects of Treatment Adherence and Glycemic Control 142 Individual Differences in Physiological Functioning and Disease Pathogenesis 154 Conclusions 155 References 156 P A R T III: A D U L T H O O D 8.

Delay Behavior A m o ng W om en with Breast Sym ptom s Elizabeth M. Singer Introduction 163 Incidence of Breast Cancer 164 The Importance of Early Detection 164 Delay Behavior 165 Socio-Demographic and Historical Variables Procedure 171 Sam ple Characteristics 173 Results 173 Sum mary 183 References 185

167

163

vüi

9.

CONTENTS

Behavioral Influences on Immune Function: Evidence for the Interplay between Stre ss and Health Janice K. Kiecolt-Glaser and Ronald Glaser

189

Background Information: Immune System 189 Life Events, Distress, and Immune Function 190 Psychosocial Influences on Herpesvirus Latency 193 Relaxation and Hypnosis 795 Depression and Immune Function 197 Carcinogenesis 198 Distress, Morbidity, and Mortality 200 The Future of Psychoneuroimmunology Research 202 References 203 10.

Is There Life After Type A: Recent Developments in Research on Coronary-Prone Behavior Redford B. Williams, Jr., M.D. References

11.

212

The Effect of Depression on Cardiovascular Reactivity Joel E. Dimsdale, M.D. Introduction

221

Preventing Relapse Following Treatment for Depression: The Cognitive Pharmacotherapy Project Steven D. Hollon, Mark D. Evans, and Robert J. DeRubeis Nature of Depression 227 Interventions for Depression 228 Implications of Differential Prophylaxis 232 Three Models of Change in Cognitive Therapy for Depression 234 Sum mary 238 References 239 Author Index Subject Index

215

215

Behavioral Reactivity 215 Depressive Syndrom es 218 Physiological Alterations of Depression Conclusion 223 References 224 12.

207

245 261

227

Preface

This is the second volume based on the annual University o f Miami Symposia on Stress and Coping. These sym posia are focused on current research related to developm ental, physical, and m ental health aspects o f stress and coping. The first volum e, Stress and Coping, provided a general discussion o f the concept of stress, an overview o f psychophysiological processes involved in stress and coping, and research relating behavioral stresses to the im mune response, sleep disorders, depression, and cardiovascular disease. In addition, the volum e cov­ ered psychosocial aspects o f stress and coping involving anger, type A behavior, depression, hardiness and self-consciousness. The present volume is focused on some representative stresses and coping mechanisms that occur during different stages o f developm ent including infancy, childhood, and adulthood. Accordingly, the volume is divided into three sections for those three stages. The first section on infancy includes chapters on maternal deprivation stress, infant feeding, and mother-infant social interactions and how the infant is stressed by these as well as the coping mechanisms available to the young infant. In the opening chapter by Doctors Schanberg and Field, animal literature is first reviewed illustrating that maternal deprivation contributes to marked behavioral and physiological “ stress” responses in the offspring ranging from transient changes in body tem perature, heart rate, and locom otor activity following short periods o f separation to marked growth retardation, developm en­ tal delays, and immune dysfunction following more long-term separations. The authors then present data demonstrating that restriction o f active tactile stim ula­ tion by the mother during maternal separation produces at least three different alterations in biochem ical processes involved in the growth and developm ent o f rat pups. These included a decrease in ornithine decarboxylase activity, a fall in ix

X

PREFACE

growth hormone secretion, and a loss of tissue sensitivity to exogenous growth hormone. These alterations were then reversed by providing tactile stimulation that grossly approximated the m other’s tongue licking (brush stroking). The second group o f studies documented the facilitative effects o f tactile-kincsthctic stimulation on the growth and behavioral organization o f preterm intensive care neonates and nonorganic failure to thrive infants. A group o f intensive care preterm neonates who experienced maternal separation were provided with a tactile-kinesthetic stimulation program. The treated infants averaged 47% more weight gain, were more active, and showed more mature behavior on the neo­ natal behavioral assessment scale. The combined demonstrations that tactile stimulation restores normal growth physiology for maternally-deprived rat pups and facilitates weight gain and more mature behavioral organization in separated preterm neonates suggests that similar horm onal and biochemical mechanisms might be involved in these two conditions. The authors suggest that evaluation of sym pathoadrenal and adrenocortical function in understimulated and treated pre­ term neonates may allow us to distinguish between “ stress” and understim ula­ tion. In the second chapter entitled “ Patterns of infant-feeding, The mother-infant interaction and stress m anagem ent,” Dr. Sue Carter discusses the hypothesis that patterns o f infant feeding and related early experiences provide a foundation for stress management. Existing literature suggests that breast-feeding provides an early opportunity for the human infant to obtain both an optimal source o f food and some degree of environmental control as well as an opportunity to develop coping skills. The physiological systems that regulate lactation depend on behaviorally active substances such as dopamine and possibly the endogenous opiates. These same chemicals have been implicated in organismic responses to environ­ mental stressors, and lactating females may have attenuated or more efficient stress responses. Carter argues that further research is needed on the relationship between early breast-feeding experiences and later stress management. In the final chapter o f this section Doctors Gianino and Tronick present a system for describing the infant’s abilities to cope with stressful interactions and the developmental changes in stability of these abilities. Very young infants are seen to develop strategies for coping with stress during their interactions with people or objects. In addition to the infants’ ability to signal both positively and negatively with emotional expressions, infants are able to reject or push away a stressful object, they are able to withdraw from the stressor by turning or arching away and even by losing postural control, and they are able to decrease their perceptual receptivity to these stressful stimuli by “ looking without seeing.” These skills are employed w henever the flow o f the interaction is disrupted by a mismatch. Effectively, in attempting to redirect an interaction which has become distressing, the infant employs his affective displays to signal the partner to change her behavior. W hen the partner’s behavior is changed, the infant’s dis­ tress is typically alleviated. W hen interactive stresses are markedly prolonged,

PREFACE

Xi

exaggerated, or distorted, as in the depressed mother and still-face mother stud­ ies of these authors, the infant is unable to readjust the interaction. This results in greater negative affect which often compels the infant to use other coping strat­ egies such as self-comforting behavior. In addition, the authors present longitu­ dinal data that suggest individual differences in infant coping styles that stabilize during early infancy. These three chapters com bined suggest the im portant role o f adequate stimulation during early infancy. Inadequate or inappropriate stim­ ulation is seen as stressful to the infant, but the stressful mismatches in stimula­ tion appear to provide the infant an opportunity to develop coping strategies. If these early experiences are abnormally stressful or prolonged (as in maternal depression or early separation) the infant may not develop adequate coping skills. The childhood section o f this volum e features chapters on type A behavior (or coronary-prone behavior patterns) and coping behaviors in children facing m edi­ cal stress and children coping with diabetes. In the first chapter o f this section Doctors M cCann and M atthews discuss the antecedents o f the type A or the coronary-prone behavior pattern. They first describe how type A can be assessed in the developing individual, discussing the reliability and validity o f available methods. They then consider the relationship o f children’s type A behaviors and related psychophysiological processes to those exhibited by adults. And, finally, they evaluate familial factors affecting the developm ent o f type A behavior. Because type A behaviors such as competitiveness and im patience-aggression are noted in adults experiencing coronary heart disease and because there is some evidence for continuity o f these behaviors from childhood to adulthood, the question o f the early antecedents o f coronary-prone behaviors is receiving in­ creasing attention. A greater psychophysiologic responsivity among type A males in these authors’ and others’ studies suggest that the origins o f type A can be traced to very early childhood. Early familial and genetic factors might play a critical role in the early developm ent o f type A behavior. Data from monozygotic and dizygotic twins suggest that type A may have an inheritable component as well as an environmental component. The latter influence has been observed in parents’ modeling o f the behavior and in the parents’ differential treatm ent of type A-B children during stressful tasks, with type A children receiving more pressure to perform and more positive evaluations of their performance. Following this overview o f the literature on the antecedents o f type A behav­ ior, Vega-Lahr and her colleagues present a comprehensive study o f type A behavior in preschool children. In this study type A behaviors were explored in preschool children using questionnaires, observations, and competitive tasks. The results suggested that the MYTH is a reliable assessment o f type A behavior in preschool children. Type A ratings o f the children’s mothers and fathers were highly correlated as were fathers’ ratings o f their own type A behavior and that of their children. Very few differences were noted between type A and type B children in the freeplay situations except that the type A children were con-

xi i

PREFACE

sistently more active than the type B children. This relative absence of behavioral differences between the types suggests that the freeplay, unstructured classroom environment may not possess the necessary characteristics to elicit the salient components o f type A behavior. In contrast, competitive situations including an inflatable punching doll, a car race, and a tow er building contest elicited dif­ ferences in type A and B children, with the type A children showing more competitive and impatient-aggressive behavior as well as winning the contest. Thus, as in adults, type A behavior appears to emerge more consistently in competitive situations. Knowing the effects o f dyad configuration and degree of uncontrolability in both the behavioral and physiological responses (such as cardiovascular and cortisol activity) in preschool children would help clarify whether precursors o f the type A pattern noted in adults can be found in early childhood. The subsequent chapter entitled “ Coping behaviors in children facing medi­ cal stress’’ by Doctors Melamed and Siegel argues for the use o f medical settings as a prototype for the study o f the developm ent o f coping behaviors in children. Theoretical support for this approach is derived from a learning theory model which emphasizes both conditioned fear and observational learning. The existing literature was reviewed and found to be inadequate in predicting vulnerability to anxiety in children facing medical procedures. The authors thus suggested that individual differences o f the child be taken into account relative to the task demands as well as the social contexts. A num ber o f parent behaviors including disciplinary styles and anxiety level and child behaviors including the child’s attachment to the mother, tem peram ent, age, cognitive and behavioral style were considered for their contributions to the child’s coping with medical procedures and the stress o f chronic illness. In addition, situational factors such as controllability-predictability, information on procedures and previous experience were considered for their effects on the child’s coping style. A m ultivariate, longitudi­ nal approach to the study o f how these variables interact in determining chil­ dren’s individual coping style was recom mended. Throughout the chapter the authors use data from their own research on children’s coping with medical stress to illustrate the complexity of this problem. The last chapter in the section on childhood by Dr. LaGrecca is entitled “ Children with diabetes and their families: Coping and disease m anagem ent.” In this chapter a model is presented for organizing psychosocial findings on coping and disease management in children and adolescents with diabetes. The psychosocial factors included in this model are diabetes knowledge and manage­ ment, treatment adherence, stress and psychological functioning. Two major trends emerged in the discussion o f this model including the importance of adopting a developm ental perspective and a family framework for understanding diabetes management and promoting more effective coping skills in youngsters with diabetes. The final section on adulthood includes chapters on the physical and psycho­

PREFACE

Xiii

logical problems most frequently studied in the context of adults’ coping with stress. These include: predictors o f delay behavior among women with breast sym ptom s, behavioral influences on immune function, the effects o f hostility on hormones o f heart disease, and preventing relapse following treatment for depression. The first chapter by Dr. Singer includes a comprehensive review o f the literature on breast cancer stress followed by the author’s study on the effects of socio-demographic and historical variables, social network variables, psycholog­ ical variables, health behavior variables, and stressful life event variables as potential predictors o f delay behavior among women with breast sym ptom s. This study revealed that younger women w ith a prior history o f breast symptoms did not delay, although there was a tendency for older women w ith prior history to delay. Another major finding was that women who knew someone w ho had breast cancer delayed less often. No relationships were found between psycho­ logical variables such as repression-sensitization, m onitoring-blunting, and locus o f control and the length o f delay. Also, no relationships were found between the three health behavior variables— general health concern, knowledge o f breast disease, or practice of breast self-exam ination and length o f delay. Finally, no relationships were noted between stressful life events and delay behavior. Thus, the critical variables appeared to be the individual’s past exposure to the threat of cancer, either by having a prior history o f breast sym ptom s, or knowing someone who had breast cancer. In the chapter by Doctors Kiecolt-G laser and G laser on behavioral influences on immune function, evidence was provided for the inter play between stress and health. The authors first provide a very articulate background on the functioning o f the immune system followed by presentation of im munological evidence supporting the causal relationship between major and m inor stressful life events and infectious disease in humans. They present data suggesting that the increase in stress regularly linked with life events is also associated with poorer immune function. Based on these data, they argue that while declines in immune function are very frequent sequelae o f certain comm onplace life events, factors such as the prior health o f the individual (particularly in regard to immune system func­ tion) and recent exposure to pathogens are important in determining the actual organic disease outcomes. In addition, their data suggest that psychological resources which reduce stress (e .g ., supportive interpersonal relationships) also concurrently attenuate adverse immunological changes. The following chapter by Dr. W illiams is entitled “ Is there life after type A: Recent developments in research on coronary-prone behavior.” In this chapter the literature on relationships between type A and coronary atherosclerosis (CAD) is critically reviewed and considered flawed for inadequate sample size, inadequate type A assessm ents, and failing to consider the effects o f age. Data are presented suggesting that type A behavior, as manifested on the structured interview, is indeed associated with increased premature CAD severity— i.e .,

x iv

PREFACE

that occurring in younger patients. W illiams suggests that “ the fact that such well established risk factors as sm oking and hyperlipidemia also behave similar­ ly, in both epidem iologic and angiographic studies, increases our confidence that som ething that is being measured by the structured interview is associated with increased CAD severity.” The chapter by Dr. Dimsdale examines the increased risk o f cardiovascular disease among depressed parents. Literature is reviewed suggesting that de­ pressed patients have subtly different sym pathetic nervous system activity in basal conditions. Dimsdale argues that depression itself is a type o f stress re­ sponse and since little is known about blood pressure or catecholamine responses in depressed patients under stress, it is important to study dynamic measures of reactivity to stressors. Thus, the chapter first deals with the measurement o f cardiovascular reactivity to stressors. Epidemiological evidence is then reviewed concerning the relationship o f depression and cardiovascular disease. Finally, D imsdale reviews psychiatric research on the physiological alterations in depres­ sion. The final chapter in the section on adulthood by Dr. Hollon examines relapse following treatm ent for depression and the prophylactic consequences o f cognitive therapy. Three models o f cognitive change during treatment are evaluated; deac­ tivation, accom modation, and compensation. Activation-deactivation, which pre­ dicts sym ptom atic relief but no major change in underlying mechanisms may hold for some patients but cannot account for differential prophylaxis. Accommoda­ tion, the preferred explanatory mechanism for most cognitive intervention theo­ rists, would predict both symptom relief and change in underlying mechanisms for therapies producing a prophylactic effect. Compensation, the third m odel, would predict symptom relief and specific skills acquisition, but no change in causal mechanisms for those same prophylactic therapies. These three models are exam­ ined in light o f the author’s recently completed cognitive-pharmacotherapy project which found clear evidence o f relapse prevention following treatment with cog­ nitive therapy. This, then, is an overview o f our second volum e on stress and coping. W e hope that providing representative research on different stresses and coping mechanisms at different stages of developm ent will stimulate further exploration o f stress and coping mechanisms at different stages in the life span.

Acknowledgments

Several individuals, groups and organizations helped make this symposium pos­ sible. First, we thank the participants, who gave freely o f themselves and helped carry out the sym posium on a modest budget. Second, we thank our postdoctoral fellows and graduate students, whose efforts attenuated the stress for all con­ cerned. Third, we thank Ellie Schneiderman for her gracious hospitality. Fourth, we thank Ira Licht and his staff for graciously allowing us to use the aesthetically pleasing surroundings o f the Lowe Art M useum for one day o f our conference. Fifth, we thank, for their support and encouragem ent, David L. W ilson, Dean of the College o f Arts and Sciences, Herbert C. Quay, Chair o f the Department of Psychology, Robert S. Stem pfel, J r ., Vice Chair o f the D epartm ent o f Pediatrics and Director of the M ailman Center for Child D evelopm ent, and Stephen W eiss, C hief o f Behavioral M edicine, National H eart, Lung and Blood Institute. We gratefully acknowledge financial support from the University o f M iami Graduate Student A ssociation, the College o f Arts and Sciences, The M ailman Center for Child Development, the Departm ent o f Psychology, and National H eart, Lung, and Blood Training grant HL07426.

T.F. P.M. N .S .

xv

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INFANCY

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Maternal Deprivation and Supplemental Stimulation

S a u l M . S c h a n b e rg

Duke University Medical School Tiffany M . Field

University of M iam i Medical School

Development in mammals is profoundly affected by environmental stimuli. Those stimuli provided by the m other appear to be most critical for survival and growth. Disruption o f the mother-infant relationship contributes to marked be­ havioral and physiological stress responses in the offspring ranging from tran­ sient changes in body tem perature, heart rate, and locom otor activity following short periods o f separation, to marked growth retardation, developm ental delays, and immune dysfunction following more long-term separations (Field, 1985; Field & Reite, 1984; Harlow & Zim m erm an, 1959; Hinde & Spencer-Booth, 1971; Hofer, 1984; Levine & Coe, 1985; Reite, Short, Seiler, & Pauley, 1981; Suomi, Collins, & H arlow , 1976). A number o f studies demonstrate that specific sensory cues from the mother induce different physiological and behavioral responses in young animals. For exam ple, nipple attachment in rats is promoted by specific organic substances on the ventral surface o f the mother, and thermal input from the mother modulates locom otor activity in weanling-age rat pups, while compounds secreted by the m other’s G I tract “ orient” pups to the nest (Compton, K och, & A rnold, 1977; Leon & M oltz, 1971,1972,1973). More recent studies by our group suggest that mother-pup interactions also have marked effects on biochemical processes in the developing pup (Schanberg, Evoniuk, & Kuhn, 1984). These biochemical processes, like behavior, respond to specific environmental cues suggesting that mother-pup interactions are important regulators o f physiological as well as behavioral functions. Sensory stimuli associated with the mother elicit coordinated physiological and bio­ chemical responses which vary with the nature o f the stim ulus. W hereas some environmental stimuli are important regulators o f growth and developm ent, oth­ ers subserve quite different functions, such as maintaining tissue sensitivity to specific hormones. 3

4

SC H A N B E R G A N D FIELD

Although studies on human infants are less definitive, growth failure and developmental delays are characteristic problems of human infants deprived of stimulation as, for example, the prem ature neonate and the nonorganic failure-tothrive infant (reactive attachment disorder). Inadequate stimulation has been implicated as a potential stressor and contributor to the delays in both o f these groups. Previous attempts to facilitate their growth and developm ent have yielded inconclusive data. H owever, recent research by our group suggests that supplemental stimulation contributes to weight gain and sleep/w ake behavioral organization in these infants (Field, Schanberg, Scafidi, Bauer, Vega-Lahr, Gar­ cia, Nystrom, & K uhn, 1986; Goldstein & Field, 1985). The first group o f studies we discuss are those demonstrating that active tactile stimulation o f preweanling rat pups by the mother provides specific senso­ ry cues that m aintain normal growth and developm ent. The data presented dem ­ onstrate that restriction o f active tactile stimulation by the mother during mater­ nal separation produces at least three different alterations in biochemical processes involved in the growth and developm ent of the rat pups. These altera­ tions can be reversed by providing supplemental stimulation. The second group of studies we review docum ent the facilitative effects o f supplemental stimula­ tion on the growth and behavioral organization o f preterm intensive care neo­ nates and nonorganic failure to thrive infants.

M A T ER N A L SEPA R A TIO N ST R ESS, TACTILE STIM U LA TIO N , A N D GROW TH IN RAT PUPS Ornithine decarboxylase (ODC), the first enzyme in the synthesis o f the poly­ amines putrescine, spermine, and sperm idine, is an important regulator of growth and differentiation that is affected by mother-pup interactions. The end products of this enzyme are intimately involved in the regulation of protein and nucleic acid synthesis (Bachrach, 1973; Raina & Janne, 1970), and activity of this enzyme is thought to be a sensitive index o f environmental effects on biochemical and physiological processes in the developing animal. W hile ODC activity in both neonatal and adult rats responds markedly to various stresses, the pattern of tissue response is determ ined by the nature o f the environmental stimulus, or stress. Separation of preweanling rat pups from the m other (maternal deprivation), is one stress that profoundly affects tissue polyamine systems in developing animals. Maternal deprivation causes an immediate and marked de­ crease in tissue ODC activity and in tissue putrescine concentration. These changes occur in all tissues that we have studied including brain, liver, heart, kidney, and spleen, and in all brain regions (Fig. 1.1, Table 1.1). ODC activity normalizes soon after rat pups are returned to the mother (Fig. 1.2). This marked effect of maternal deprivation is observed in preweanling pups, from postnatal Days 1 to 18 (Fig. 1.3). It then rapidly disappears over the next few days.

1.

MATERNAL DEPRIVATION

120r

1 60-

FIG. 1.1. Effect of maternal deprivation on O D C activity in different re gio ns of 10-day-old rat brain. All value s are expressed a s m eans + S E M . All differences are significant P < 0.05 or better.

TABLE 1.1 Effect

of

M aternal tn O r g a n s

Control

D e p r i v a t i o n o n ODC A c t i v i t y o f 8 Day O ld R a ts

N

Deprived

N (10)

Brain

100

-

10

(5)

48

-

5a

Heart

100

-

15

(15)

64

-

8a

(15)

Liver

100

-

18

(20)

31

-

3a

(20)

Kidney

100

-

4

(10)

66

-

IIa

(10)

Spleen

100

-

6

(10)

58

-

8a

(10)

Pups w ere m a t e r n a l l y d e p r i v e d and k i l l e d 2 h o u r s + l a t e r . R e s u l t s a r e e x p r e s s e d a s p e r c e n t a g e s o f c o n t r o l - sem. ap < . 0 5 o r b e t t e r r e l a t i v e t o c o n t r o l .

° B ram

• Heart

Hours R e lu m e d ro M other

FIG. 1.2. C o m p a riso n in 10-day-old rat brain and heart of the recovery of O D C activity after a 2-hr deprivation and return to the mother. All va lue s exp ressed a s m ean s ± S E M . N = 5 in each group. Brain and heart value s are significantly below control (P < 0.05) at 2 hr. Brain va lue s are significantly above control value s at each point after return

(P < 0.05).

6

SC H A N B E R G A N D FIELD 12.0 A Non -Dcpnv^d Pup*

i

10.0

o Deprived Pupi

I i 2.0

0 0

6

-1------------ » 8 10

■________ I 12 id

I 16

I 18

FIG. 1.3. Effect of a 2-hr maternal deprivation on preweanling rat brain ODC activity in pups of different ages. All values are expressed as means ± SEM . N = 5 in each group. All differences significant P < 0.05 or better.

The decline in ODC associated with maternal deprivation does not result from a change in body tem perature, exposure to an unfam iliar environment, or other nonmatemal stimuli (Butler & Schanberg, 1977). Sim ilarly, interruption o f feed­ ing does not mediate the fall in ODC, inasmuch as preweanling rat pups placed with a mother whose nipples have been ligated do not experience a similar decrease o f ODC activity in all tissues. The latter demonstration is extremely important, given that feeding is one o f the m ajor components o f the mother-pup interaction during the first 2 postnatal w eeks, with pups feeding an average of every 10 min (Lincoln & W akerly, 1974). Furthermore, auditory, visual, and olfactory stim ulation, which play a role in mother-pup interaction at various times during the developm ent o f preweanling rats, do not influence ODC activity (Kuhn & Schanberg, unpublished observations). Apparently those stimulus modalities are not involved in the ODC response o f preweanling rats to maternal deprivation. This is not surprising in that both the auditory and visual systems are not functional at birth, but mature during the First 2 to 3 weeks postpartum. Interruption o f active tactile interaction between m other and pup seems to trigger the decline in ODC activity during maternal separation. Placing pups with a mother rat that has been anesthetized (with urethane) to prevent active interac­ tion but not feeding (Lincoln & W akerly, 1974) changes tissue ODC activity in the same way that separating the pups from the mother alters ODC activity (Table 1.1). This Finding is striking, as the decrease in ODC activity occurs despite the presence o f many other sensory cues that are passively transferred by the mother (olfactory, gustatory, auditory, tactile, etc.) and actively emitted by the littermates. Furtherm ore, when deprived pups are given tactile stimulation grossly approximating that o f maternal grooming (i.e ., paint brush stroking simulating maternal licking motions) ODC activity returns to normal levels in all

1.

M A T E R N A L DEPRIVATIO N

7

tissues, although other forms o f sensory stim ulation of equal intensity are inef­ fective (Figs. 1.4 and 1.5). This finding is o f particular interest because tactile stimulation appears to be an important stimulus for growth and developm ent in a number of species, including humans (cf. Cornell & G ottfried, 1976; Field, 1980; Schaeffer, H atcher & Barglow, 1980 for reviews). The physiologic signal which triggers the decline in ODC activity following interruption o f m atem al-pup interaction is still unknown. The uniform decline in tissue ODC activity throughout the body suggests that som e general endocrine or metabolic response to the withdrawal o f maternal tactile stimulation mediates this fall. This hypothesis is strengthened by our finding that ODC decreases during maternal deprivation even when innervation o f peripheral tissues is not yet functional, or when innervation is blocked pharm acologically with pro­ pranolol or atropine (Butler, Suskind, & Schanberg, 1977; Schanberg, un­ published observations). ODC activity is such an accurate and sensitive index of cell growth and developm ent that its decline during maternal deprivation could represent a specific biochem ical mechanism through which environmental stim­ uli affect growth and developm ent. The change in ODC activity during maternal deprivation suggested that secre­ tion o f one or more o f the many horm onal regulators o f ODC was affected by this stress. In additional studies, we have shown that maternal deprivation elicits a marked and unusual neuroendocrine response. This response represents the sec-

FIG. 1.4. Pups were maternally deprived for 2 hours and either left untouched or stroked heavily, stroked lightly, or pinched as described in Methods and then killed. Controls were left undisturbed with the mother for 2 hours. Results are expressed as percent control ± SEM. Control ODC activity = 0.147, 0.188 and 0.048 nmoles ornithine/'g tissue/hour respectively for brain, heart and liver.* = p < .05 or better compared to controls.** = p < .001 or better compared to controls, n a 15 except pinched and light stroking n a 8.

8

SC H A N B E R G A N D FIELD

FIG. 1.5. Pups were maternally deprived and stimulated as described in Fig. 1. Results are expressed as percent control ± SEM . Control serum GH = 54 ng/ml.* = p < .002 or better compared to controls, n a 15 except pinched and light stroking n a 10.

ond mechanism controlling growth and development that is disrupted by mater­ nal deprivation. W hen preweanling rat pups are separated from the mother, there is an increase in corticosterone and a selective decrease in growth hormone secretion from the anterior pituitary, while serum levels o f other stress-respon­ sive horm ones including prolactin and TSH do not change if nutrition and other aspects of the environm ent are controlled, minimizing disruptive conditions. This selective decrease in growth hormone is somewhat unique as stress almost always elicits a complex pattern o f endocrine responses which in the rat usually involves decreased growth horm one and TSH and increased corticosterone and prolactin secretion. The inhibition o f growth horm one secretion during maternal deprivation could affect developm ent significantly over a prolonged period of deprivation, as circulating growth hormone is responsible for the generation of substances called som atom edins, which are among the major regulators o f mus­ cle and possibly organ growth. Growth horm one is a w ell-known regulator of ODC activity in brain as well as in peripheral tissues (R oger, Schanberg, & Fellows, 1974). Therefore, the finding that growth hormone secretion decreased during maternal deprivation provided a possible explanation for the fall in tissue ODC activity. To investigate this possibility, we injected pups with ovine growth hormone during the separa­ tion procedure to reverse the decrease in ODC activity. Rather than restoring

1.

MATERNAL DEPRIVATION

9

T A B L E I .2 E f f e c t o f H o r m o n e s o n L i v e r ODC A c t i v i t y In M a t e r n a l l y D e p riv e d Rat Pups

ODC

Activity

(1% C o n t r o l )

Dose D r u g ______________________ (¿¿g)

C o n t r o l ________N________D e p r i v e d _____ N

Vehicle

100 1 00

437

10 0

315

Dexamethasone

200

366

Dibutyryl

800

518

PGE-1

50

510

Insulin

10

1306

OGrowth

Hormone

OPlacental

Lactogen

cAmp

+ + + + + + +

22

(60)

11

1 36a

(20)

11

± 3b + 2ab

54a

(10)

10

±

62a

(10)

172a

(60) (20)

lab

(10)

532

± 51a

(10)

(10)

5 39

±

183a

(10)

66a

(10)

620

213a

(10)

422a

(15)

2040

± +

594a

(15)

Pups were m a t e r n a l l y d e p r i v e d f o r 2 h o u r s , i n j e c t e d SC w i t h v e h i c l e or hormone, and k i l l e d 4 hou rs l a t e r . R e su lts expressed as p ercen tage o f c o n t r o l ± sem. c o n t r o l ODC a c t i v i t y was 37 n C i/3 0 m in /g t i s s u e . ^ p c O .O S or b e t t e r r e l a t i v e t o v e h i c l e t r e a t e d c o n t r o l . p < 0 .001 r e l a t i v e t o paired c o n t r o l.

ODC activity to normal levels, as predicted, w e found that tissue ODC was completely and selectively unresponsive to growth hormone during maternal deprivation. Growth hormone was unable to induce ODC activity in liver or brain o f deprived rats, although a number o f other hormones including cyclic AM P, insulin, and the glucocorticoid hormone dexamethasone still would induce ODC activity normally (Tables 1.2, 1.3). This selective loss o f tissue response to growth hormone represents the third major defect in growth-regulating processes that is disrupted by maternal deprivation. These three effects o f maternal deprivation (decrease in tissue ODC activity, fall in growth hormone secretion, and loss o f tissue sensitivity to exogenous growth hormone) appear to be regulated by the same sensory stimulus: active

Effect in

TABLE 1.3 o f H o r m o n e s on B r a i n ODC A c t i v i t y M a t e r n a l l y D e p r i v e d Rat Pups

Control Vehicle GH

10 0

Camp

ug

N

Deprived

(10)

100

± 16

(10)

59

í

166

±

(10)

67

t 9ab

(10)

41 3

± 39a

(10)

3 52

±

(10)

7a

5a

N

53a

Pups were m a t e r n a l l y d e p r i v e d f o r 2 h o u r s , i n j e c t e d i n t r a c i s t e r n a l l y w i t h s a l i n e , GH or cAMP, r e t u r n e d t o t h e d e p r i ­ v a t i o n c a g e s and k i l l e d 4 hou rs l a t e r . C o n tr o l pups l e f t w ith t h e mother were i n j e c t e d a t t h e same t i m e . R esults a r e e x p r e s s e d a s % c o n t r o l ± sem. C ontr ol ODC a c t i v i t y was 40 n C i/3 0 m in /g t i s s u e . , p c .01 or l e s s r e l a t i v e t o v e h i c l e - t r e a t e d c o n t r o l . p c .O O l r e l a t i v e to G H -injected c o n t r o l .

10

S C H A N B E R G A N D FIELD

Live r

Response

TABLE 1 .4 t o GH F o l l o w i n g R e t u r n t o M o t h e r

ODC A c t i v i t y (% C o n t r o l ) Control Control

+

Growth

Hormone

t 25

(10)

597

±

132a

(10)

39

+

5a

(10)

25

+

3

(10)

Deprived Deprived

+

Returned

to Moth e r

Returned

to M o t h e r

+ Growth

Growth

Hormone

Hormone

N

100

2 03

+ 54

(10)

982

+ 186a

(10)

Pups were mater nall y deprived f o r 2 hours and k i l l e d or returned to the nothe r. Two hours a f t e r return pups were in j e c t e d SC with v e h i c l e or GH (100i/g). Live r ODC a c t i v i t y was determined 4 hours a f t e r hormone ad m in is tr a­ t i o n . R e su lts are ex pr es sed as per ce nt age o f c ontr ol ± Sem. Control ODC a c t i v i t y was 40 nCi/30 m i n / g . ap < 0 . 0 0 1 r e l a t i v e to c o n t r o l .

tactile stim ulation by the m other. T herefore, placing the pups w ith a urethaneanesthetized m other to elim inate m aternal tactile stim ulation o f the pups, while m aintaining food intake, effects a decrease in O D C activity in organ tissue, and decreases in serum grow th horm one and in liver O D C response to exogenous grow th horm one (Table 1.4). In contrast, tactile stim ulation (brush stroking) of m aternally deprived rat pups returns all three param eters to norm al (Figs. 1.4, 1.5, Tables 1.4, 1.5). T hese studies o f the biochem ical basis o f grow th retardation o f m aternally deprived rats have significant clinical im plications for the conditions called non­ organic failure-to-thrive or “ reactive attachm ent disorder” and “ psychosocial d w arfism .” Psychosocial dw arfism is a retardation o f grow th and behavioral developm ent in children that show s a startling sim ilarity to the anim al m odel we TABLE 1 .5 R e s p o n s e o f L i v e r ODC t o GH in Pu p s w i t h an A n e s t h e t i z e d M o t h e r

ODC A c t i v i t y (% C o n t r o l )

Control

± 11

(20)

1087

±

144a

(20)

38

±

4d

(20)

41

±

6db

(20)

100

Control + Growth

Hormone

Pups

with

Anesthetized

Mother

+ Vehicle

Pups

with

Anesthetized

Mother

+ Growth

Hormone

N

Pups were p la c e d with a u r e th a n e - a n e s t h e t iz e d mother f o r 2 hours, i n j e c t e d SC with v e h i c l e or growth hormone (100 jig) and k i l l e d 4 hours l a t e r . R e s u l ts exp res sed as % c o n tr o l ± Sem. Control a c t i v i t y = 10 nCi/30 min/g. j*p

normal

-

normal

=

normal

Mechanisns (or m e c h a n i s m correlates)

abnormal

“

abnormal

>

normal

=

normal

Stable Traits

abnormal

—

abnormal

—

abnormal

>

normal

would yield comparable differences between the groups across all the relevant variables. Likely candidates for further study as potential mechanisms in such designs would include those variables already shown not to norm alize with the assumption o f asym ptom aticity, such as REM sleep abnorm alities (Kupfer & Reynolds, 1983; Kupfer, Spiker, C oble, N eil, U lrich, & Shaw, 1980), marital and other intimate interpersonal relationships (W eissm an, Klerman, Prusoff, Sholom skas, & Padian, 1981; W eissman, Klerm an, Paykel, Prusoff, & H anson, 1974), cortisol regulation as indexed by dexamethasone suppression (Carroll et al., 1981), and attributional styles (DeRubeis, Evans, Hollon, & Tuason, 1986). Finally, any treatment which provides a prophylactic effect after termination may help further highlight those mechanisms by virtue o f norm alizing their values before such norm alization occurs in patients being successfully treated with drugs. That need not be the case, for reasons we return to in the following paragraph, but, if the intervention works by virtue o f affecting basic causal mechanism s, then these processes should norm alize in cognitive therapy before they norm alize in pharm acotherapy. It is possible that a treatm ent which has a prophylactic effect produces this effect not by directly affecting causal m echanism s, but by virtue of compensating for them by blocking the em ergence o f their sym ptomatic consequences. This possibility is discussed in greater detail in the subsequent section.

THREE M O D E L S OF C H A N G E IN CO GNITIVE THERAPY FOR D E P R ESSIO N A cognitive theory o f depression holds that dysfunctional beliefs and maladap­ tive information processing contributes to the etiology and maintenance o f de­ pression (Beck, 1967, 1970). The m odel, as originally proposed, is actually a

12.

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235

diathcsis-stress model, in which the dysfunctional cognitive processes provide the diathesis, and various negative (and significant) life events provide the stress (Beck, 1984). According to this formulation, an individual with a predisposition to hold certain beliefs and/or process information in a depressotypic fashion is at particular risk for developing an episode of depression in the face o f distressing life events. A cognitive theory o f change in the treatment o f depression would hold that interventions which focus on changing those dysfunctional beliefs and maladap­ tive information processing heuristics should result in a concomitant reduction in symptomatic depression (Beck, 1970; Beck, Rush, Shaw, & Emery, 1979; Hol­ lon & Beck, 1979). Attention has focused on several components o f thinking; automatic thoughts, the relatively accessible thoughts and beliefs which can be reported by the individual; underlying assumptions, the relatively inaccessible attitudes and beliefs seen by Beck (1967, 1970) as underlying and unifying the individual’s belief systems; cognitive errors, such as overgeneralization, magni­ fication, and selective abstraction, among others, which may well correspond to the logical heuristics noted by Kahneman and Tversky to operate in normal populations (Kahneman, Slovic, & Tversky, 1982), and schemata, the integrated clusters o f beliefs and processes which organize thinking, particularly in the absence o f certainty (Markus, 1977; Neisser, 1967, 1976; Nisbett & Ross, 1980). Depressotypic schemata refer to both existing negative content and sys­ tematic biases in the selection and processing o f novel content. When a de­ pressive schema is operating, the individual has difficulty recalling positive life events (Clark & Teasdale, 1982) or more positive self-descriptions (Derry & Kuiper, 1981), generating benign attributions for negative events (Seligman, Abramson, Semmel, & Von Baeyer, 1979), generating positive expectations for coming events, or perceiving his or her own impact on the world (Garber & Hollon, 1980). Although the precise role and operation o f cognitive processes in the etiology and maintenance o f depression remains controversial (Coyne & Gotlib, 1983), numerous authors have argued for the utility o f the constructs (Goldfried & Robins, 1982, 1983; Hollon & Kriss, 1984; Turk & Salovey, 1985a, 1985b; Turk & Speers, 1983). The following discussion assumes some validity for the cognitive model.

Activation— Deactivation Starting from that assumption, we can ask how cognitive therapy influences depressive schemata. At last three models can be identified, as presented in Table 12.2 and as articulated elsewhere (Ingram & Hollon, 1986). The first model, activation-deactivation refers to a situation in which cognitive therapy (and perhaps other therapies) exert their impact on depression by virtue o f deac­ tivating an operating depressive schema. Basic schema theory holds that any individual may possess a number of different schemata, only one or some of

236

HOLLON, EV A N S, A N D D eR U B EIS TABLE 12. 2 M o d e l s o f Change in C o g n i t i v e T he r a py f o r D e p r e s s i o n

Model

Description

Activation-Deactivation:

O p e r a t i v e d e p r e s s i v e s c h e m a is d e a c t i v a t e d , with nondepressive schema activated. No c h a n g e in c a u s a l m e c h a n i s m s ( s c h e m a ) a n d n o r e d u c t i o n i n l i k e l i h o o d of r e c u r r e n c e ( a l ­ t h o u g h p o s s i b l e d e c r e m e n t s in l i k e l i h o o d of r e l a p s e ) .

Ac c o m m o d a t ion :

O p e r a t i v e d e p r e s s i v e s c h e m a is m o d i f i e d in a p r o f o u n d way. B a s i c c h a n g e s in c a u s a l m e c h a n i s m s (s c h e m a ) a n d r e d u c e d l i k e l i h o o d of relapse/recurrence.

Compensatory

O p e r a t i v e d e p r e s s i v e s c h e m a is l e f t u n ­ c ha n g e d , b ut d e v e l o p m e n t of c o m p e n s a t o r y s k i l l s ( s c ript) c o m p e n s a t e s f o r o r o f f s e t s p e r n i c i o u s i n f l u e n c e of s chema. No change in c a u s a l m e c h a n i s m s ( s c h e m a ) , b u t r e d u c e d l i k e l i h o o d of r e l a p s e / r e c u r r e n c e .

skills:

which are active at any given moment. For exam ple, the senior author o f this manuscript is both a clinical researcher and a parent. At work, his scientist/aca­ demician schema is generally operating, but, given the appropriate cues (e .g ., a telephone call from home or a cow orker’s com m ent, etc.), he can readily begin thinking like a parent. The reverse happens at home, when the “ parent” schema is dom inant, but the academ ician schema can readily be triggered by an appropri­ ate stim ulus. It is logically possible that cognitive therapy works, when it works, by deactivating depressive schemata but not altering their basic nature. The implication o f this process would be that while treatm ent may be suc­ cessful, the risk o f recurrence should rem ain relatively unaffected. Relapse may be rendered less probable, if the diathesis-stress model is valid, since some new precipitating life event would need to occur to trigger the emergence of renewed symptomaticity. Two sets o f clinical observations, neither supported, as yet, by controlled studies, tend to support this activation-deactivation model. First, it is striking how similar the attitudes and beliefs are o f individuals experiencing a subsequent episode to the attitudes and beliefs that they evidenced at the beginning of the original episode. This observation suggests that the same beliefs simply resur­ face, even though they may not have been evident when the patient was euthym ic. Second, an examination o f the individual response curves for the pa­ tients treated with cognitive therapy in the CPT project suggestes that, for many, that process was more nearly discontinuous than smooth. While the group re­ sponse curve was negatively decelerated, the individual response curves were often discontinuous. O f the three models, activation-deactivation is the process most likely to be discontinuous, since it need not involve the gradual accumula­ tion o f learning processes.

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237

W orking against the activation-deactivation model is the already noted evi­ dence o f relapse prophylaxis. If no basic change in underlying structures was going on, why would a pattern be obtained in which pharm acotherapy term ina­ tion, but not cognitive therapy term ination, was followed by rapid relapse? Even though relapse would be rendered less probable by a deactivation process, there should be no difference in the relative likelihood o f relapse between two or more interventions that both stimulated deactivation. It m ay, o f course, be the case that the activation-deactivation model best describes the change process for some patients, but not all, within either modality. Clearly, detailed ideographic studies of the consistency o f them es across episodes would be desirable.

Accommodation The second m ajor m odel, accommodation, is the process most often invoked by cognitive theorists to explain change in treatm ent (Beck, 1967, 1970; Evans & H ollon, in press; Hollon & G arber, in press; Hollon & Kriss, 1984). Accom ­ modation refers to the process o f change in the basic cognitive schem ata, either content or process or both. One o f the major findings o f the last 2 decades is just how difficult accom modation is to achieve (N isbett & Ross, 1980, Ross, 1977). It appears that the presence o f existing beliefs tends to color the recognition of and search for new information (Snyder, 1981), and influences behaviors in the direction o f producing outcom es consistent with those beliefs, the self-fulfilling prophecy phenomenon (Darley & Fazio, 1980). N onetheless, it is apparent that cognitive change can and does occur, particularly in the face o f empirical disconfirmation o f existing beliefs, exposure to alternative conceptualizations, and insight into the processes followed to arrive at those judgm ents (Ross, 1977). W ith regard to depression, those who adhere to an accom modation model would argue that basic change in depressive schemata does occur during various therapies (e.g ., cognitive therapy). Evans and Hollon (in press) have suggested that the basic process o f change may not be one o f getting depressed patients to think like nondepressives. Rather, the process is seen as one o f encouraging the client to utilize relatively atypical, deliberate information-processing strategies, as opposed to automatic processes, as defined in Schneider and Shiffrin’s distinc­ tion (Schneider & Shiffrin, 1977; Shiffrin & Schneider, 1977). Thus, nonnormative strategies are used to shift the content o f cognition in the direction of greater realism. The optimal way to detect the presence of accom modation should be by contrasting interventions producing a prophylactic effect (e.g ., cognitive thera­ py) versus those producing no such effect (e .g ., pharm acotherapy). W ithin the context o f a larger design such as presented in Table 12.1, accommodation should appear as greater differential change in the appropriate cognitive “ causal m echanism s” for cognitively treated patients relative to pharm acologically treat­

238

HOLLON, E V A N S, A N D D eR U B EIS

ed patients. To date, no such studies have actually been executed, but the measurement technologies now exist to make such an effort feasible.

Compensatory Skills The third and final model involves the developm ent o f compensatory skills which block or suppress the emergence o f sym ptom aticity without affecting the underlying causal or maintaining mechanisms. Such compensatory skills might involve behavioral or cognitive self-m anagem ent skills that do not affect basic inference generation but which do modify its consequences. The analogy here would be to a disorder like diabetes in which insulin self-m anagement am elio­ rates many of the negative consequences o f the disease without affecting its basic nature. The operation of such a model would be detected by first establishing a differential relapse/recurrence phenom enon, then finding an absence of accom­ modation in the type o f design ju st described, but the presence of certain ac­ quired performance skills. N ote further that the test for accommodation would suggest that recently treated patients with a reduced risk o f relapse/recurrence should be more similar to the “ never depressed” controls in terms o f potential causal mechanisms. In the compensatory skills m odel, recently treated patients would still possess these depressive schem ata, but they would be unlike those in any of the other groups in that they would possess and demonstrate the relevant compensatory behaviors. As for designs capable o f detecting accom modation, we know o f no current studies which have examined these processes. Perhaps the closest approximations have been R ippere’s studies o f coping strategies in nor­ mal populations (Rippere, 1977a, 1977b, 1977c). M easurem ent technologies for the assessm ent of acquired coping skills are not as well developed as for the detection o f psychopathologic schemata. W ork adapting A belson’s (1981) con­ cept o f scripts, knowledge structures guiding goal-directed action sequences, may prove o f use in this regard. Clearly, work in the area of measurement technology developm ent needs to be done before these hypotheses can be explored.

SUM M ARY The preceding comments have been largely speculative in nature. Nonetheless, they may facilitate the developm ent o f research strategies that can better answer important questions o f etiology and m aintenance in depression, with the ultimate goal o f both refining treatm ent strategies and developing preventative programs. We began with the growing body o f literature suggesting a differential pro­ phylactic effect for cognitive therapy in the treatm ent o f depression. Such a phenom enon would be important in its own right for pragm atic clinical purposes,

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but its theoretical implications could prove even more important. Basically, such a phenomenon, if replicated, may provide a means of identifying the key pro­ cesses maintaining, if not causing, episodes o f depression. Suggestions are given for novel research comparisons that may facilitate such identification. Within the context of cognitive therapy, three models of change are presented and evaluated in light of this purported differential prophylactic effect. Activa­ tion-deactivation, which predicts symptomatic relief but no major change in underlying mechanisms, may hold for some patients, but cannot account for differential prophylaxis. Accommodation, the preferred explanatory mechanism for most cognitive intervention theorists, would predict both symptom relief and change in underlying mechanisms for therapies producing a prophylactic effect. Compensation, the third model, would predict symptom relief and specific skills acquisition, but no change in causal mechanisms for those same prophylactic therapies. Ultimately, it is hoped that such speculations as the preceding can help both solidify our understanding of depression and of the change process. If so, we should be able to enhance the efficacy of our existing interventions and, perhaps, develop new prophylactic and preventative strategies as well. It has long been known that theoretically relevant treatment outcome work can enhance our un­ derstanding of the psychopathologies of interest. It may well prove that differen­ tial prophylaxis can play the same role.

ACKN O W LEDG M EN T Preparation of this chapter was supported, in part, by a grant from the National Institutes o f Mental Health (R01-M H33209) to the Department o f Psychology, University of Minnesota, and the Department of Psychiatry at the St. PaulRamsey Medical Center, St. Paul, Minnesota. We would like to express our appreciation to Judy Garber for her comments on an earlier version of this chapter and to Bonnie Arant Ertelt and Barbara Ann Hendricks for their secre­ tarial assistance in the preparation of this manuscript. Requests for reprints should be sent to Steven D. Hollon, Department of Psychology, Vanderbilt University, 134 Wesley Hall, Nashville, TN 37240.

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Author Index N umbers in italics indicate pages with com plete bibliographic information.

A A belson, R. P ., 238, 239 A bram son, L. Y ., 235, 242 A chenbach, T . M ., 115, 132 A dam , E ., 195, 203 A dam son, L ., 48, 49, 50, 51, 53, 62, 64 , 65,

66 , 68 A dam s, D ., 217, 224 A der, R ., 197, 202, 203 A dler, E. M ., 32, 36, 4 3 , 4 4 A gras, W . S ., 113, 132 A histedt, S ., 28, 45 A hlqvist, J ., 190, 203 A insw orth, M ., 64, 65, 114, 115, 127, 132, 133 A itken-Sw an, J ., 163, 185 A kiskal, H. S ., 228, 239, 240 A lagna, S. W ., 171, 183, 185 A lbala, A . A ., 234, 240 A lexander, L ., 110, 134 A listair, G . S ., 12, 24 A llen, M. T ., 78,5(5 A lpem , G . D ., 113, 137 A ls, H ., 48, 49, 50, 51, 53, 54, 55, 62, 64, 65, 68 A lson, D ., 48, 65 A m sterdam , B ., 118, 136 A nderson, A . A ., 207, 213 A nderson, B. J ., 48, 65, 153, 154, 156 A nderson, G ., 12, 13, 23 A nderson, J ., 216, 224 A ndersson, B ., 28, 45 A ndrykowsky, M. A ., 122, 136 A ngelakos, E ., 217, 224 A ngulo, J ., 75, 76, 77, 87, 90, 91, 96, 98, 102, 104, 105. 107 A nism an, H ., 200, 205 A nson, O ., 167, 185 A ntonovsky, A ., 165, 167, 170, 176, 177, 182, 185 A ppels, A ., 220, 224 A rnold, W. J ., 3 ,2 2 A rohonka, K ., 198, 204

A sher, S ., 47, 67, 201, 203 A skenasy, A . R ., 168, 171, 183, 186 A tkins, A ., 120, 122, 134 A uerbach, S. M ., 110, 120, 132 A uslander, W ., 153, 154, 156 A very, D ., 228, 240 A vis, N . E ., 76, 87 A zaroff, P ., 113, 117, 134

B B abigian, H ., 201, 203 B achrach, U ., 4 , 21 Badia, P ., 119, 132 Bailey, P. M ., 127, 130, 133 Bakem an, R ., 47, 65 Baker, L ., 152, 153, 156, 158 Bancroft, J ., 32, 36, 43, 44 B andura, A ., 82, 85, 113, 117, 133, 180, 185 Barboriak, J. J ., 207, 213 Barcai, A ., 152, 153, 156 Barefoot, J. C ., 207, 210, 212, 213 Barglow , P. D ., 7 , 24, 151, 156 B arnard, K . E ., 11, 12, 13, 21, 22 Barratt, E. S ., 19, 24 Barrett, C. L ., 112, 135 Barrett, K ., 47, 49, 50, 66 B arry, J ., 169, 182, 185 B artrop, R. W ., 190, 203 B ass, C ., 207, 212 Bauer, C. R ., 4, 1 3 ,2 5 , 3 7 , 4 4 B eahrs, J. O ., 197, 203 B eck, A . T ., 228, 229, 232, 234, 235, 237, 240, 241, 242 B eck, P ., 113, 136 B eck, S ., 150, 157 B ecker, D ., 144, 145, 150, 157 B ecker, M. H ., 148, 156 B edrosian, R. C ., 228, 240 B ee, H . L ., 11, 22 B eebe, B ., 48, 52, 62, 65, 66 B ell, P. A ., 169, 185 B ell, R. Q ., 39, 44

245

246

A U T H O R IN D E X

Bell, S ., 64, 65 Bellack, A . S ., 228, 240 Bendell, D ., 12, 22 Bengston, D ., 110, 123, 137 B ennet, P. L ., 220, 224 B erenson, G . S ., 75, 88 B erg, I., 114, 133 B em al, J. F ., 37, 39, 46 B em baum , J ., 13, 22 B ertelson, A . D ., 142, 157 B erton, K ., 77, 87 B essm an, G . A ., 119, 133 B eyer, J ., 72, 86 B ieliauskas, L. A ., 201, 205 B ielski, R ., 228, 242 Birch, H. G ., 118, 137 Bird, J ., 200, 203 B ishop, S ., 228, 229, 240 Bistoletti, P ., 20, 21, 23 B ithoney, W . G ., 17, 22 B itm an, J ., 30, 45 Black, P. H ., 197, 204 Black, S ., 197, 203 Blackburn, H ., 216, 224 Blackburn, I. M ., 228, 229, 240 Blalock, J. E ., 190, 203 Blase, B ., 11, 12, 24 B lizard, P. J ., 163, 187 Blizzard, R. M ., 11, 17, 19, 20, 21, 24 B lock, J ., 73, 85 Block, P. C ., 207, 212 Bloom , B. L ., 201, 203 B loom , K ., 4 8 , 53, 66 B lot, J ., 184, 185 B lum enthal, J. A ., 152, 157, 207, 209, 210, 211, 212, 213 B lurton Jones, N ., 33, 44 B obik, A ., 223, 224 B onnell, G ., 196, 204 B ora, C ., 35, 36, 44 B orer, J . t 216, 224 B orkenstein, M ., 155, 158 Bortner, R. W ., 72 , 75, 78, 83, 85, 8 7 Borysenko, J ., 189, 203 Borysenko, M ., 189, 203 B overm an, H .t 11, 12, 23 B ow lby, J ., 33, 44, 49, 60, 62, 66, 114, 133 B oyle, H ., 36, 45 B radfield, R . B ., 16, 25 B radley, C ., 151, 156 Brady, J. V ., 119, 133

Brand, R. J ., 71, 87 Brank, R. J ., 90, 107 B rascl, J. A ., 11, 17, 19, 20, 21, 24 Bravem an, N ., 196, 203 B razelton, T . B ., 47, 48 , 50, 51, 52, 53, 54, 58, 62, 63, 64, 65, 66, 67 Breese, G . R ., 21, 22 B rennan, J ., 12, 13, 23 B reslau, N ., 110, 133, 219, 224 Bretherton, I., 114, 127, 133 B rew ster, D . P ., 41, 44 B ridger, W . M ., 12, 24 Briesem eister, L ., 33, 34, 45 Brightm an, U . J ., 193, 204 B riner, W ., 196, 204 Brodsky, I., 202, 205 Brooks, G . W ., 171, 185 Brow n, B ., 130, 131, 133 Brow n, J. V ., 47, 65, 163, 164, 187 Bruhn, J. G ., 77, 87, 220, 221, 224 B rozek, J ., 216, 224 Buckley, L ., 118, 136 Budenz, D ., 228, 240 Budzynski, T . H ., 152, 157 Buglass, D ., 114, 133 Bullow a, M ., 4 8 , 64, 66 B um am , M . A ., 77, 86, 91, 106 Burstein, S ., 120, 133 Bush, J. P ., 110, 127, 130, 133, 135 Butler, S. R ., 6 , 7 , 19, 20, 22, 23 B ym e, D ., 169, 182, 185

C C affey, E. M ., 232, 242 C ahill, G . F ., Jr., 140, 141, 159 C aldw ell, B. M ., 39, 44 C aldw ell, S ., 131, 134 C am eron, A ., 169, 185 C am pbell, J. D ., 118, 133 C am pos, J ., 47, 49, 50, 66 C arlsson, B ., 28, 45 C arlsson, S. G ., 37, 44 C arroll, B. J ., 234, 240 C arter, W . A ., 202, 205 C arter, W . R ., 151, 156 Carvalho, M . D ., 33, 44 C arver, C. S ., 91, 106 C ase, N. B ., 207, 212 C ase, R. B ., 207, 212

A U T H O R IN D E X Caslcr, L ., 11, 22 C assell, S ., 121, 133 C assem , N. H ., 165, 186 C ataldo, M. F ., 110, 119, 133, 137 C atanzano, D. M., 207, 212 C ater, J ., 33, 46 C athcart, E. S ., 197, 204 Chance, J ., 170, 187 Chandler, B ., 220, 221, 224 C handra, R. K ., 29, 44, 197, 200, 203 C hapin, H ., 113, 132 Chapm an, D. P ., 83, 86 C herry. T ., 146, 158 Chess, S ., 118, 137 C hristie, H ., 220, 224 C hristie, J. E., 228, 240 C hristophersen, E. R ., 144, 158 C ipes, M., 110, 123, 137 C itrin, W . S ., 149, 153, 154, 156, 157, 158 C lark, D. M., 235, 240 C lark, L ., 216, 224 C larke, J ., 114, 133 C larke, W. L ., 151, 156 C luss, P. A ., 146, 156 Cobb, B ., 168, 182, 185 Cobb, S ., 168, 171, 185 C oble, P. A ., 234, 241 C obum , C ., 144, 145, 157 C oe, C. L ., 3, 19, 21, 22, 23 C ogen, A. B ., 200, 203 C ohen, F ., 124, 133, 169, 171, 185 C ohen, J ., 166, 173, 180, 185 C ohen, J. B ., 73, 86 C ohen, N ., 197, 203 Cohen, P ., 173, 180, 185 Cohen, S ., 82, 86 C ohen-C ole, S ., 200, 203 C ohn, J ., 47, 48, 50, 51, 52, 56, 58, 60, 61, 62, 63, 64, 66, 68 Cole, P ., 163, 164, 184, 185, 187 Cole, T ., 11, 12, 24 C olem an, A . E., 91, 106 Collector, M. I., 200, 201, 205 C ollins, C ., 78, 86 C ollins, H. L ., 3 ,2 5 Com pton, R. P ., 3, 22 Connell, D ., 56, 66 C onnelly, W . E., 171, 185 C onner, R. L ., 32, 36, 46 C ontrada, R ., 78 , 86, 93, 107 Cook, A ., 32, 36, 43, 44, 45

247

C ook, M ., 119, 135 Cook, W. W ., 209, 212 C ooksey, R ., 200, 203 C om blath, M ., 20, 22 Cornell, E. M ., 7 , 12, 22 Corrigan, S. A ., 77, 86, 90, 91, 92, 96, 102, 104, 106 C orse, C. D ., 77 , 86 C osta, P. T ., 210, 212 C ow an, R ., 216, 225 C oyne, J. C ., 168, 187, 228, 235, 240 Craig, M ., 219, 220, 224 C ritcher, E. C ., 78, 86 Crow ne. D . P ., 169, 185 Culbertson, S ., 119, 132 Cum m ings, M ., 47, 51, 68 Cuthbert, M ., 110, 121, 133, 134 C utting, R. T ., 72, 87

D D ahlstrom , G ., 210, 212 D ale, J ., I l l , 134 D allm an, M. F ., 21 , 22 D ’A m brosio, S. M ., 200, 204 Danem an, D ., 150, 157 D anielsson, B ., 37, 44 D arley, J. M ., 237, 240 D ash, J ., 112, 134 D avenport, Y. B ., 47, 51, 68 D avidson, D ., 32, 36, 43, 44 D avidson, M ., 119, 135 D avia, J. E ., 207 , 213 D avidson, J. M ., 21, 22 D avidson, R. J ., 169, 188 D avies, T . P ., 16, 24 D avis, G ., 219, 224 D avis, K . L ., 198, 201, 205 D avis, J. M ., 228, 241 D avis, K ., 221, 225 D earborn, M ., 119, 121, 122, 135 D eavers, D. R ., 16, 24 D eBoer, K. F ., 152, 158 D egrc, C ., 207, 213 D elam ater, A. M ., 142, 157 D em broski, T . M ., 81, 82, 86, 87, 90, 106, 152, 157, 207, 209, 212, 213, 223, 224 D em os, V ., 4 8 , 51, 53, 66 D em psey, J ., 16, 22 D enby, L ., 216, 224

AUTHOR INDEX

248

D ’Ercole, A. J ., 19, 20, 22 D erry, P. A ., 235, 240 D erryberry, D ., 52, 64, 66 D eRubeis, R. J ., 229, 234, 240, 241 D etre, K ., 220, 225 D etre, T ., 223, 224 D eV ellis, R ., 170, 188 D evereux, R ., 216, 224 de V igne, J. P ., 234, 240 D iam ond, G . R ., 48, 51, 53, 66 D iM ascio, A ., 228, 243 D im sdale, J. E ., 207, 209, 212, 2 1 3 , 216, 218, 220, 221, 224 D iPietro, J. A ., 40, 44 D istefano, G ., 20, 24 D ixon, S. D ., 48, 51, 66 D jeu, J., 192, 204 Dodd, D. A ., 33, 40, 45 D ohrenw end, B. P ., 168, 171, 183, 185, 186 D ohrenw end, B. S ., 168, 171, 183, 185, 186 D okechi, P. R ., 48, 65 D onnerberg, R ., 196, 204 D oughaday, W . H ., 20, 22 D oust, J ., 220, 224 D rachm an, R. H ., 148, 156 D rash, A ., 144, 145, 157 D reher, M ., 146, 147 D rotar, D ., 112, 124, 125, 133 D rum m , D. A ., 154, 158 D uckw orth, W . C ., 154, 158 D uffy, J. C ., 129, 133 D unbar, J ., 144, 157 D unn, J. B ., 38, 42, 44 D unn, S. M ., 142, 157 D upuis, A ., 154, 157 D utton, L ., 207 , 213

E E agle, C ., 120, 122, 134 E aston, P ., 33, 46 E aton, R. P ., 154, 158 E den, C. S ., 28, 45 E didin, D. V ., 151, 156 Eichler, A ., 17, 24 Ekm an, P ., 62, 66 Elias, M. F ., 35, 36, 44 Ellenberg, L ., 112, 134 Elliot, C. H ., 112, 126, 131, 134, 137 E llis, D. J ., 33, 44

E lting, E ., 78, 86 Em ery, G ., 235, 240 Engclm an, K ., 221, 225 Enos, W . F ., 72, 86 Epstein, L. H ., 142, 146, 150, 156, 157 Epstein, S ., 169, 186 E rbaugh, J. K ., 229, 240 E m ster, V. L ., 201, 203 E scalona, S ., I l l , 127, 131, 133 E sler, M ., 223, 224 Etzw iler, D. D ., 146, 157 E unson, K. M ., 229, 240 E vans, A . S ., 193, 204 E vans, M. D ., 229, 234, 237, 240, 241 Evans, N ., 120, 122, 134 E voniuk, G ., 3, 16, 19, 22, 23, 24, 37, 46

F Fafouti-M ilenkovic, M ., 50, 66 Fagerberg, H ., 37, 44 Falkner, B ., 217, 223, 224 Fallstrom , S. P ., 28, 45 Farkas, G ., 150, 157 Farquar B row n, M ., 35, 44 Faust, J ., 121, 133 Fazen, L . E ., 110, 111, 137 Fazio, R ., 237, 240 Feinberg, M ., 234, 240 Feinglos, M . N ., 142, 151, 152, 159 Feinleib, M ., 71, 86 Feiring, C ., 115, 135 Feldstein, S ., 48, 65 Fellow s, R. E ., 8 , 24 Fenz, W. D ., 169, 186 Fergusson, D. M ., 29, 44 Fernandez, J ., 111, 135 Field, T . M ., 3, 4 , 7 , 12, 13, 16, 18, 19, 22, 23, 37, 44, 47, 48, 50, 62, 66 Figueroa, J ., 150, 157 Fink, L. U ., 184, 186 F ink, M ., 155, 158 Finkeistein, J. W ., 120, 122, 134 Fischl, M. A ., 192, 205 Fischm an, S. E ., 127, 134 Fiselier, T ., 21 , 23 Fish, R. D ., 20, 23 F isher, E. B ., Jr., 142, 157 Fisher, S ., 184, 186 Fleece, L ., 121, 122, 135

AU THO R IN D EX Fogel, A., 48, 51, 53, 66 Foley, J., 110, 127, 137 Foilansbee, D. J., 149, 157 Folstcin, M ., 220, 225 Forbes, A. E ., 20, 22 Foucard, T ., 28, 44 Fowler, J. E., 152, 157 Fox, B. H., 164, 184, 186, 189, 197, 201, 203, 204 Frances, A., 114, 135 Frantz, A. G ., 35>46 Fraser, D. W., 28, 39, 42, 45 Frasier, S. D ., 19, 23 Freedman, D. G ., 11, 12, 23 Freedman, N ., 11, 12, 23 Freeman, A ., 200, 203 Friedman, A., 33, 44 Friedman, M., 71, 78, 83, 85, 86, 87, 89, 90, 96, 106, 107, 220, 224 Friedman, S. B ., 112, 133 Friedrich, G., 82, 88 Frohm, K. D., 210, 213 Frosch, E ., 58, 66 Fry, L., 197, 203 Fuchs, C. Z ., 228, 241 Fukushima, D., 120, 122, 134

G Gaitan, E., 200, 203 Gale, E., 140, 141, 159 Gale, M ., 207, 210, 213 Gallo, J. S ., 165, 187 Garber, J., 235, 241 Garcia, R., 4, 13, 23, 37, 44 Garland, F. N ., 77, 86, 91, 107 Gamer, A. M ., 146, 158 Gamer, W ., 190, 192, 204 Garron, D. C ., 201, 205 Garvey, M. J., 229, 241 Gavlin-Kremer, E ., 116, 137 Gaull, G. E ., 30, 45 Gayton, W. F ., 112, 133 Gewirtz, J. L ., 12, 23 Gianino, A., 47, 51, 52, 54, 58, 64, 66, 67 Gibber, J. R ., 35, 45 Gilbertson, V. A ., 168, 187 Glaser, R., 190, 192, 193, 194, 195, 196, 198, 199, 200, 201, 203, 204 Glasgow, R. E., 146, 147, 150, 158

249

Glasier, A ., 35, 45, 72, 75, 77, 78, 83, 86, 87, 89, 90, 91, 92, 93, 104, 106, 107, 152, 157 Glen, A. I. M ., 228, 231, 240, 241 Goklaney, M., 228, 243 Goldfried, M. R ., 229, 235, 241 Goldman, L ., 32, 46 Goldmeier, D., 193, 204 Goldsen, R. K., 165, 169, 186 Goldsmith, H., 47, 49, 50, 66 Goldstein, D., 154, 155, 158 Goldstein, S ., 4, 18, 19, 23 Gonder-Frederick, L. A ., 151, 156 Good, R. A., 197, 204 Goodwin, F. K., 228, 243 Gotlib, I. H., 235, 240 Gotlieb-Stematsky, T ., 193, 195, 203 Gottfried, A. W., 7, 12, 22 Gotthold, J., 112, 133 Gottman, J. M ., 62, 67 Grandstaff, N. W ., 169, 186 Grannose, C., 32, 36, 37, 40, 43, 46 Grant, I., 151 >157 Grasso, S., 20, 24 Greden, J. F ., 234, 240 Green, L. W ., 168, 186 Greenbaum, P. E ., 130, 133 Greenberg, R., 12, 13, 23 Greenspan, S ., 47, 67 Greer, S., 163, 182, 186 Grim, C. E., 82, 87 Grobstein, R., 127, 134 Gross, A. M., I l l , 134, 149, 157 Gundewall, C ., 37, 44 Gunnar, M. R ., 20, 23 Gussler, J., 33, 34, 45

H

Hackett, R. F., 234, 240 Hackett, T. P., 165, 186, 207, 209, 212, 213 Hagman, E ., 113, 134 Hakstian, A. R., 228, 241 Halonen, P. E., 198, 204 Haiton, A ., 50, 67 Hamilton, M ., 229, 241 Hammerschlag, C. A., 167, 186 Hamosh, M ., 30, 45 Hamosh, P., 30, 45 Hampe, E ., 112, 135

250

AU THO R IN D EX

Haney, T. L ., 152, 157, 209, 212, 207, 209, 210, 211, 213 Hanlon, T. E ., 228, 242 Hanna, N. C ., 147, 158 Hannallah, R. S., 116, 134 Hanshaw, J. B ., 195, 205 Hanson, B., 234, 243 Hanson, L. A ., 28, 45 Haque, N ., 153, 156 Harbeck, R ., 42, 46 Harkavy, J., 121, 122, 136, 144, 145, 157 Harlow, H. F., 3, 23, 25, 37, 45 Harper, L ., 84, 86 Harris, D. R., 197, 203 Harris, E. L ., 81, 87 Harsh, J., 119, 132 Harshfield, G ., 216, 224, 225 Hartman, H ., 165, 170, 176, 177, 182, 185 Hasselmeyer, E. G ., 11, 12, 13, 23 Hatcher, R. P., 7, 24, 151, 156 Hawes, R ., 121, 122, 135 Haykal, R. F., 228, 239, 240 Haynes, S. G ., 71, 86 Hazzard, W ., 220, 225 Heding, L. G ., 155, 158 Hefferman, M ., 113, 117, 134 Heller, S. S., 207, 2/2 Henderson, A. S., 114, 133 Henderson, J. G ., 168, 186 Henderson, R. W ., 38, 45 Henle, G ., 195 , 204 Henle, W., 195, 204 Herberman, R. B ., 192, 204 Hermecz, D ., 119, 121, 122, 134, 135 Hersch, P. D ., 170, 186 Hersen, M ., 228, 240 Hershman, I. H ., 119, 122, 123, 134 Hervig, L ., 78, 87 Hewat, R. J., 33, 44 Hilgard, E. R., 197, 203 Hilpert, P., 122, 134 Hilton, W. F., 78, 86 Himmelhoch, J., 228, 240 Hinde, R. A., 3, 23 Hines, P., 118, 136 Hinkle, L ., 151, 157 Hinton, J., 169, 185 Hodapp, R ., 47, 67 Hofer, M. A., 3, 19, 23 Hoffman, A ., 42, 46 Hoffman, J., 62, 67

Hoffman, R. G ., 207, 213 Holleb, A. 1., 164, 186 Hollenbeck, A. R., 12, 23 Hollenberg, N ., 217, 224 Holliday, J. E ., 190, 192, 193, 195, 196, 198, 203, 204 Hollis, J., 91, 107 Hollon, S. D ., 228, 229, 234, 235, 237, 240, 241, 242 Holmes, R. H ., 72, 86 Hopwood, N. J., 19, 24 Homeman, G ., 37, 44 Homer, M. S ., 73, 86 Horwood, L. J., 29, 44 Houston, B. K ., 73, 78, 86 Houston, M. J., 36, 45 Howard, J. L ., 2 1 ,2 2 Howie, P. W ., 35, 36, 45 Hubley, P ., 63, 68 Hügel, R., 113, 136 Hughes, J. R ., 83, 86 Hulley, S. G ., 207, 213 Hunter, S. M ., 75, 88 Huston, A. C ., 180, 185 Hutcherson, S ., 121, 122, 135 Hutter, A. M ., 207, 212 Hwang, C-P., 37, 44 Hyson, M. C ., 123, 134

I Ignatoff, E ., 12, 13, 23 Ingram, R. E ., 235, 241 Isaacs, C. E., 30, 45 Izard, C. E ., 49, 67

J Jacklin, C. N ., 76, 86 Jackman, G ., 223, 224 Jacobs, D. R ., 77, 83, 86, 87 Jaffe, J., 48, 65 James, N. M d ., 234, 240 Janne, J., 4, 24 Jansen, M ., 21, 23 Jantti, V ., 198, 204 Jaskir, J., 115, 135 Jason, J. M ., 29, 42, 45 Jason, M ., 216, 224

AUTHOR INDEX Jay, S. M ., 112, 126, 131, 134 Jelliffe, D. B ., 28, 29, 30, 40, 43, 45 Jelliffe, E. F. P ., 28, 29, 30, 45 Jenkins, C. D ., 71, 73, 86, 87, 90, 98, 107 Jennings, J. R ., 75, 79, 87 Johnson, A ., 193, 204 Johnson, A. L ., 231, 241 Johnson, C . A ., 83, 86 Johnson, P ., 121, 134 Johnson, R ., 130, 134 Johnson, S. B ., 139, 142, 144, 145, 157 Johnson, W . E ., 231, 242 Johnson, W. G ., 149, 157 Johnston, J ., 35, 36, 44 Jones, M ., 228, 242 Jones, R. L ., 154, 157 Jovanovic, L ., 140, 157 Jura, M. B.» 17, 18, 24

K K afka, M ., 223, 224 Kagan, A ., 73, 86 Kagan, J ., 73, 87, 114, 115, 134 K ahnem an, D ., 183, 184, 186, 188, 235, 241 K annel, W. B ., 71, 86 Kapen, S ., 35, 46 K aplan, B. H .t 82, 86 K aplan, G ., 220, 224 K aplan, P. M ., 127, 134 K asl, S. V ., 171, 185, 193, 204 K ästner, L. S ., 112, 136, 137 K atcher, A. H ., 193, 204 Katz, E. R ., 110, 119, 122, 123, 134 Katz, J ., 120, 122,'134 K ay, R ., 153, 156 K azdin, A. E ., 150, 157 Kegeles, S ., 165, 186 K ehoe, K ., 78, 86 K eir, R ., 119, 135 K eller, S. E ., 190, 198, 201, 205 K ellerm an, J ., 110, 119, 122, 123, 134 K elley, N . H ., 165, 186 K elsey, J. L ., 163, 164, 186 K ennell, J. H ., 36, 37, 45 K eys, A ., 216, 224 K iecolt-G laser, J. K ., 190, 192, 193, 194, 195, 196, 198, 199, 201, 203, 204 K ilm an, P. R ., 120, 132 K iloh, L. G ., 190, 203

251

K im zey, S. L ., 190, 204 K irk, K ., 200, 203 K irklcy, B. G ., 142, 157 K irscht, J. P ., 148, 156 Klaus, M. H ., 33, 36, 37, 44, 45 K lein, D . F ., 114, 134, 228, 241 K leiner, B ., 216, 224 K leinert, H ., 216, 224, 225 K leinknecht, R ., 110, 134 K lepac, R ., 110, 113 K lerm an, G. L ., 228, 234, 241, 242, 243 K lingm an, A ., 121, 134 K lorm an, R ., 122, 134 K night, R ., 120, 122, 134 K och, M. D ., 3, 22 K oenigsberg, S ., 130, 134 K oltcrm an, O . G ., 140, 158 Kong, Y ., 207, 209, 210, 211, 213 K onner, M . J ., 33, 36, 39, 45 K om itzer, M ., 207, 213 K oslow ski, B ., 4 7 , 48, 52, 53, 54, 63,