Memory and Emotion (Series in Affective Science)

Memory and Emotion Series in Aﬀective Science Series Editors Richard J. Davidson Paul Ekman Klaus Scherer The Nature...

Author: Daniel Reisberg | Paula Hertel

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Memory and Emotion

Series in Aﬀective Science Series Editors Richard J. Davidson Paul Ekman Klaus Scherer The Nature of Emotion: Fundamental Questions Edited by Paul Ekman and Richard J. Davidson Boo! Culture, Experience, and the Startle Reﬂex By Ronald Simons Emotions in Psychopathology: Theory and Research Edited by William F. Flack Jr. and James D. Laird What the Face Reveals: Basic and Applied Studies of Spontaneous Expression Using the Facial Action Coding System (FACS) Edited by Paul Ekman and Erika Rosenberg Shame: Interpersonal Behavior, Psychopathology, and Culture Edited by Paul Gilbert and Bernice Andrews Aﬀective Neuroscience: The Foundations of Human and Animal Emotions By Jaak Panksepp Extreme Fear, Shyness, and Social Phobia: Origins, Biological Mechanisms, and Clinical Outcomes Edited by Louis A. Schmidt and Jay Schulkin Cognitive Neuroscience of Emotion Edited by Richard D. Lane and Lynn Nadel

The Neuropsychology of Emotion Edited by Joan C. Borod Anxiety, Depression, and Emotion Edited by Richard J. Davidson Persons, Situations, and Emotions: An Ecological Approach Edited by Hermann Brandstätter and Andrzej Eliasz Emotion, Social Relationships, and Health Edited by Carol D. Ryﬀ and Burton Singer Appraisal Processes in Emotion: Theory, Methods, Research Edited by Klaus R. Scherer, Angela Schorr, and Tom Johnstone Music and Emotion: Theory and Research Edited by Patrik N. Juslin and John A. Sloboda Handbook of Aﬀective Sciences Edited by Richard J. Davidson, Klaus Scherer, and H. Hill Goldsmith Nonverbal Behavior in Clinical Settings Edited by Pierre Philippot, Erik J. Coats, and Robert S. Feldman Thinking about Feeling: Contemporary Philosophers on Emotions Edited by Robert C. Solomon Memory and Emotion Edited by Daniel Reisberg and Paula Hertel

Memory and Emotion

Edited by Daniel Reisberg and Paula Hertel

1

2004

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Library of Congress Cataloging-in-Publication Data

Memory and emotion / edited by Daniel Reisberg and Paula Hertel.

p. cm.—(Series in aﬀective science)

Includes bibliographical references and index.

ISBN 0-19-515856-3

1. Autobiographical memory. 2. Emotions. 3. Psychophysiology. 4. Psychiatry. I. Reisberg, Daniel. II. Hertel, Paula. III. Series. BF378.A87 M46 2003 152.4—dc21 2003006595

2 4 6 8 9 7 5 3 1 Printed in the United States of America on acid-free paper

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he study of the interplay between emotion and memory inevitably involves a mixing of perspectives. After all, the study of emotion is an important and sophisticated research enterprise in its own right, and so, too, is the study of memory. But, in addition, each of these topics in turn has been studied from multiple perspectives—the nature of emotion in normal populations and in pathological populations, in children, in adults, and in the elderly; the nature of the biological changes, and then the psychological and subjective changes, that accompany (and perhaps constitute) emotion; the range of emotions common in day-to-day life, and also the range of emotions one experiences only in extreme circumstances. It should be obvious that each of these perspectives on emotion has its own value and asks questions that do not arise within these other contexts. But it should also be obvious that common themes—or points of dissonance—may emerge when we start putting these various perspectives side by side. Unfortunately, though, those common themes often do not come into view: After all, in our ﬁeld research tends to be published in specialized venues, and so there is less cross-talk among related specialties than one might wish. It is precisely this situation that creates a need for volumes like this one. In this volume, we have brought together some of the leading investigators in the broad area of emotion and memory, deliberately seeking to span as best we could the full range of approaches visible in the current scene. This juxtaposition should provide easy access to any reader, from any perspective, hoping to enter this broad research literature. In addition (and as we’d hoped), the juxtaposition highlighted a number of themes that cross research areas. For example, many authors have proposed that emotion promotes memory, so that materials one has experienced while emotional are better retained than materials experienced while one is calm. Indeed, some evidence suggests that emotional char-

acteristics of an event help to ameliorate memorial deﬁciencies of one sort or another (in elderly adults, for example, or in individuals diagnosed with schizophrenia). But a broader view of the literature makes it plain that the opposite pattern also appears in some circumstances, with emotion serving to undermine memory—even memory for nonemotional events, particularly in the case of anxiety and depression. How should we think about this contrast? Is one of the eﬀects artifactual? Or (as seems likely) are both eﬀects genuine, with other important variables guiding the direction of the event? And, if the latter, what are those variables? Is the nature of the emotion crucial? The strength of the emotion? The nature of the to-be-remembered materials? The way in which memory is assessed? Each of these proposals arises in one or more chapters in this volume, and each of the proposals has arguments in its favor. Our intention in this preface, therefore, is surely not to settle the question of contrast, or even to suggest that the question should be settled in any straightforward way. Instead, we raise this point simply as a reminder that investigators in this broad domain—despite their very diﬀerent methods, working assumptions, and forms of data—are often working on closely related questions, so that all may beneﬁt from cross-talk among these various approaches. It is that hope that provides the main impetus for this volume. The volume begins with a contribution by Daniel Reisberg and Friderike Heuer. Reisberg and Heuer celebrate the progress that has been made in our understanding of how people remember emotional events, but also highlight the substantial gaps in our knowledge. A prominent theme in their chapter is that, in a wide range of circumstances, emotion promotes memory for an event’s “central” materials, but seems to have the opposite eﬀect, undermining memory, for details at an event’s “periphery.” Reisberg and Heuer argue, however, that this latter eﬀect may be produced not by emotion itself but by the presence of powerful “attention magnets” found within some (but by no means all) emotional events. From this base, Reisberg and Heuer explore possible limits of this data pattern, with an eye on how diﬀerent types and diﬀerent strengths of emotion may inﬂuence memory diﬀerently. The second chapter, by Tony Buchanan and Ralph Adolphs, explores the neuroanatomy of emotional memory, arguing that the brain mechanisms that encode, consolidate, and retrieve memories may operate diﬀerentially in emotional and nonemotional contexts. Speciﬁcally, the chapter emphasizes the role of the amygdala in the enhancement of memory for emotional events, largely through the amygdala’s inﬂuence over brain areas (including the hippocampus and striatum) during the period of memory consolidation and also during the retrieval of emotional memories. Data are drawn from human studies and from studies of other species, from lesion evidence, and from neuroimaging. The speciﬁc eﬀects reported, however, are not uniform, and here, as in other chapters, we see evidence of emotion’s mixed eﬀects on memory. Thus, for example, bilateral amygdala damage seems to eliminate both emotion’s tendency to promote

vi 

memory for an event’s gist and also its tendency to undermine memory for an event’s periphery. At the same time, the eﬀects do seem general in other ways, and the chapter argues that the amygdala eﬀects (and, more broadly, emotion’s memory eﬀects) depend on arousal itself, not the emotion’s valence. While these ﬁrst two chapters acknowledge emotion’s mixed eﬀects on memory, there is no question that these chapters emphasize the ways in which emotional events seem to be remembered better than neutral (but otherwise comparable) events. This emphasis is reversed, however, in the third chapter, by Jessica Payne, Lynn Nadel, Willoughby Britton, and Jake Jacobs. They focus on the biopsychological eﬀects of trauma and how these inﬂuence memory. They argue that trauma (and, more precisely, the stress that usually accompanies trauma) has identiﬁable eﬀects on the hippocampus, impairing both the neuronal structure and the function of this brain region. As a direct consequence, stress (especially uncontrollable stressors) impairs various forms of memory. However, not all memories suﬀer this eﬀect, and the chapter seeks to explain this point by arguing that the experience of stress (through its impact on the hippocampus) causes stressful events to be recorded in a “fragmented” manner, with the elements of the event not woven into a coherent remembered episode. At the same time, emotion works (via the amygdala) to promote memory for the gist of an event, leading to well-encoded memories for the thematic content of an emotion event, but, again, without the coherent spatio-temporal framework needed to organize the memory (because this framework relies on hippocampal circuits disrupted by stress). In this fashion, the authors seek to explain both the positive eﬀects of emotionality on memory and its negative eﬀects—with an emphasis on diﬀerentiable neural structures and, with that, on diﬀerent types of remembered information. The fourth chapter, by Richard McNally, Susan Clancy, and Heidi Barrett, is also on trauma and, like the Payne et al. chapter, seeks to understand the conditions under which traumatic events are remembered or forgotten. The chapter’s focus, however, is on the frequently espoused belief that all trauma will be forgotten—a belief presumably based on the notion that too much emotion hurts memory. In particular, McNally et al. review the evidence relevant to the debate about the extent to which trauma victims typically repress and then later recover memories of the traumatic event. In examining the reported evidence—from victims of childhood sexual abuse, concentration-camp survivors, war veterans, and alien “abductees”—the authors distinguish among phenomena that have more often been collapsed in discussions of repressed and recovered memories. They invite us to consider that the forgetting of traumatic events can arise from quite “normal” phenomena—such as the absence of rehearsal or the initial lack of attention to some aspects of the event—instead of special mechanisms of motivated repression. Another important feature of the chapter is their review of the laboratory research on forgetting mechanisms employed by people who have suﬀered through various types of trauma. The pursuit of this line of research

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seems certain to shed light on the memory processes that distinguish those who remember from those who forget and, in turn, from those who forget and then remember. Chapter 5, by Colin MacLeod and Andrew Mathews, considers how memory might be inﬂuenced by a variety of emotional states and conditions experienced by people with anxiety disorders. This chapter represents a thorough review of research performed with people who describe themselves as generally anxious (without formal diagnosis), as well as with people who have been diagnosed as experiencing generalized anxiety disorder, post-traumatic stress disorder, phobias, obsessive-compulsive disorder, and panic disorder. In the context of research on “mood congruent” memory, one might expect that these individuals will better remember stimuli that “ﬁt” with their anxious thoughts and beliefs; this expectation, however, is clearly challenged by the results that MacLeod and Mathews review. In some cases, anxious people do show evidence of anxietyrelated biases in memory, but the chapter argues that these probably result from special instances of emotional interpretation of events with ambiguous meaning. Under conditions less prone to interpretive ambiguity, anxious people tend not to remember in emotionally special ways. Chapter 6, by Paula Hertel, addresses what is by far the largest research area in the examination of memory in clinical groups—research conducted with depressed or naturally unhappy (but possibly nondiagnosed) people. The chapter theme is the connection between memory phenomena and habits of thought. More so than most anxious people, depressed people ruminate about their troubles. The practiced thought patterns of rumination facilitate memory for emotionally consistent events and interfere with memory for other events. Moreover, as Hertel wants us to understand, these habits take over under conditions of poor cognitive control, the main feature of cognition in depression. Hertel argues that the negative consequences of habitual thinking can be overcome by external control or by the training of new habits of thought. The literature on emotional memory in individuals diagnosed as schizophrenic is much less extensive than the literatures in depression and anxiety, and it is often ignored in collections on cognition and emotion. Recently, however, it has been augmented by the research conducted by Jean-Marie Danion, Caroline Huron, and their colleagues. The chapter here (by Danion, Huron, Lydia Rizzo, and Pierre Vidailhet) ﬁrst reviews evidence that both memory disturbances and emotional disturbances characterize schizophrenia and then raises questions about their interaction. Danion et al. argue that memory for emotional material operates “normally” in schizophrenic states when emotional aspects of experience are genuinely noted. Of course, often these experiences are not interpreted by a person with schizophrenia in a fashion that accurately reﬂects the event’s emotionality, with a corresponding memory deﬁcit. But in many cases the emotional characteristics of an event require little controlled attention, and, under these conditions, we should expect to see intact

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emotional memory, even in this population disrupted in so many other ways. Finally, in a concluding section of the chapter, Danion and his coauthors make the provocative suggestion that intact emotional processing potentially plays a role in perpetuating delusional cognitions, through constructive memory processes. The eighth chapter continues the emphasis on emotional remembering in special populations, but the population at issue here is not pathological. Instead, Robyn Fivush and Jessica Sales examine emotional memory in children. They also focus on a theme that appears in many other chapters of the volume—the fact that the functional role of emotional remembering often depends on attributes of memories other than their historical accuracy. In particular, Fivush and Sales discuss the ways in which the structure and content of young children’s emotional memories is co-constructed by the children and their parents, a process, they argue, that varies from culture to culture and also depends on the child’s gender. This co-construction is important for many reasons; among them, it is one of the essential means through which children gain a foundation for understanding themselves and their autobiographies. Also crucial here are the ways in which parent-child reminiscing about stressful experiences can guide the child’s understanding of and coping with aversive events. Exploring this latter point demands a comparison of how parents and children reminisce about both aversive and pleasant events and also how they reminisce about both emotionally mild events and emotionally extreme ones, themes that provide another important point of contact between this chapter and other chapters in the volume. In chapter 9, Mara Mather discusses memory at the other end of the lifespan—in the elderly. She ﬁrst examines age-related changes in emotional processing—in mechanisms of emotional regulation and arousal, for example, considered both psychologically and in terms of their neural mechanisms— and from this base oﬀers an intriguing set of suggestions about how these changes should inﬂuence emotional memory. Among other issues, she considers whether the older person’s improved ability to regulate emotion implies that memories should become more emotionally gratifying, as well as whether the emotional qualities of experience might actually protect an individual against the age-related decline in memory. These suggestions are then evaluated in her subsequent review of the current literature on age diﬀerences in the eﬀects of emotion on memory. In the end, Mather argues that emotional memory does constitute a “somewhat surprising island of maintained functioning” in a sea of general decline in old age. Chapter 10, by Robin Edelstein, Kristen Alexander, Gail Goodman, and Jeremy Newton, covers topics that have arisen in many other chapters—the memory eﬀects of trauma, emotional remembering by children, the long-term durability of emotional memories, and so on—but covers these themes from the perspective of the legal system, asking how eyewitnesses to crimes remember the events they have observed (or, in many cases, the events in which they were vic-

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timized). Of special importance here is the question of whether laboratory ﬁndings taken as characterizing emotional memory can be reasonably applied to real-life crime situations. Also prominent in this chapter is the special case of memories for childhood sexual abuse, including memories that are apparently lost and then recovered. The chapter discusses the complexity that arises when one tries to assess these memories and also factors (including a tendency toward dissociation, or various forms of psychopathology) that play a role in determining when a traumatic event will be vividly remembered and when that event will (apparently) be forgotten. Finally, chapter 11, by Robert Kraft, focuses on a particularly important form of emotional memory: memory of the Holocaust by its survivors. Throughout this book, chapters have commented on the memory eﬀects of traumatic or otherwise horriﬁc events; chapters have likewise commented on the process of sharing emotional memories with others—and perhaps sharing again and again. Just as important is the fact of deliberately not sharing memories. How does this sharing (or not sharing) shape the recollection? Archives of Holocaust memories speak powerfully to these issues, and Kraft provides a close qualitative analysis of these memories in order to explore (among other topics) the general characteristics of traumatic memory, how emotion itself is recalled, and how the recall of a memory can lead to the re-experiencing of emotion. Also of interest here is the way in which these emotional memories can shape the survivors’ beliefs and emotions throughout their lives. All of these considerations lead Kraft to proposals about “multiple systems” of memory that in some ways echo, and in other ways may challenge, related multiple-systems proposals oﬀered in several other chapters. We end with the happy task of thanking those who have helped us in assembling this volume. First, we are grateful to Catharine Carlin, our editor at Oxford University Press, who persuaded us to launch this project, and who has been enthusiastically encouraging ever since. We are also grateful to John Rauschenberg, also at OUP, for his labors in putting the volume together. We also thank the Series Editors, Richard Davidson, Klaus Scherer, and Paul Ekman, for their support of this endeavor. Finally, we are grateful to Pat Ullmann, in Trinity University’s Instructional Media Service, for transcribing some ﬁgures.

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Contributors,

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1. Memory for Emotional Events, 3

Daniel Reisberg and Friderike Heuer 2. The Neuroanatomy of Emotional Memory in Humans, Tony W. Buchanan and Ralph Adolphs

42

3. The Biopsychology of Trauma and Memory, 76

Jessica D. Payne, Lynn Nadel, Willoughby B. Britton,

and W. Jake Jacobs

4. Forgetting Trauma? 129

Richard J. McNally, Susan A. Clancy, and Heidi M. Barrett 5. Selective Memory Eﬀects in Anxiety Disorders: An Overview of

Research Findings and Their Implications, 155

Colin MacLeod and Andrew Mathews 6. Memory for Emotional and Nonemotional Events in Depression:

A Question of Habit? 186

Paula Hertel 7. Emotion, Memory, and Conscious Awareness in

Schizophrenia, 217

Jean-Marie Danion, Caroline Huron, Lydia Rizzo,

and Pierre Vidailhet

8. Children’s Memories of Emotional Events, Robyn Fivush and Jessica McDermott Sales

242

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xi

9. Aging and Emotional Memory, Mara Mather

272

10. Emotion and Eyewitness Memory, 308

Robin S. Edelstein, Kristen Weede Alexander, Gail S. Goodman, and Jeremy W. Newton 11. Emotional Memory in Survivors of the Holocaust:

A Qualitative Study of Oral Testimony, 347

Robert N. Kraft Index,

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391

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Ralph Adolphs, Department of Neurology, University of Iowa, Iowa City, Iowa

Kristen Weede Alexander, University of California, Sacramento, California

Heidi M. Barrett, Department of Psychology, Harvard University, Cambridge,

Massachusetts

Willoughby B. Britton, Department of Psychology, University of Arizona, Tucson,

Arizona

Tony W. Buchanan, Department of Neurology, University of Iowa, Iowa City,

Iowa

Susan A. Clancy, Department of Psychology, Harvard University, Cambridge,

Massachusetts

Jean-Marie Danion, Unité INSERM 405, Hopital Universitaire, Strasbourg, France

Robin S. Edelstein, Department of Psychology, University of California, Davis,

California

Robyn Fivush, Department of Psychology, Emory University, Atlanta, Georgia

Gail S. Goodman, Department of Psychology, University of California, Davis,

California

Paula Hertel, Department of Psychology, Trinity University, San Antonio, Texas

Friderike Heuer, Lewis and Clark College, Portland, Oregon

Caroline Huron, INSERM, Paris, France

W. Jake Jacobs, Department of Psychology, University of Arizona, Tucson, Arizona

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Robert N. Kraft, Department of Psychology, Otterbein College, Westerville, Ohio

Colin MacLeod, Department of Psychology, University of Western Australia,

Perth, Australia

Mara Mather, Department of Psychology, University of California, Santa Cruz,

California

Andrew Mathews, MRC Cognition & Brain Sciences Unit, Cambridge, United

Kingdom

Richard J. McNally, Department of Psychology, Harvard University, Cambridge,

Massachusetts

Lynn Nadel, Department of Psychology, University of Arizona, Tucson, Arizona

Jeremy W. Newton, Department of Psychology, University of California, Davis,

California

Jessica D. Payne, Department of Psychology, University of Arizona, Tucson,

Arizona

Daniel Reisberg, Department of Psychology, Reed College, Portland, Oregon

Lydia Rizzo, Laboratoire Universitaire de Psychologie, Metz, France

Jessica McDermott Sales, Department of Psychology, Emory University, Atlanta,

Georgia

Pierre Vidailhet, Unité INSERM 405, Hopital Universitaire, Strasbourg, France

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Memory and Emotion

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ollege graduation. The death of a pet. A particularly romantic evening. A moment’s reﬂection will persuade most people that events like these—events that were emotional when they occurred—provide many of their most vivid, most detailed, most compelling autobiographical memories. For many of us, these emotional memories are a basis for engaging and sometimes enjoyable reminiscence. More important, though, these memories also matter for us in important ways. After all, these emotional events are likely to have been consequential for us in one way or another, and are, in most cases, closely linked to issues, goals, or people that we care deeply about. It seems certain, therefore, that the recollection of these crucial events is likely to shape our sense of who we are and also our broad perceptions of the world. This, in turn, will inﬂuence many aspects of our actions, perceptions, and beliefs. In addition, many of these emotional events are consequential for other people, and so we may be called on to report the event in one setting or another; when that happens, it is of obvious interest to ask how full and accurate that report will be. These broad issues provide the motivation for our inquiry into the nature of autobiographical recollection. As we will see in this chapter, research in this domain has made considerable progress, but on some key issues, the available data are still rather sparse. Hence, this chapter simultaneously celebrates our advances and highlights the points on which more work is urgently needed. 3

The Accuracy

of Emotional Memories

Setting the Issue: Vividness Versus

Memory Accuracy

There is no question that emotional memories tend to be quite vivid, and, in one early study, we reported a correlation of .71 between participants’ ratings of their memories’ vividness and their ratings of how emotional the original event had been (Reisberg, Heuer, McLean, & O’Shaughnessy, 1988). Interestingly, this relationship was observed no matter what emotion was attached to the event, so the correlation between vividness and emotionality ratings was .89 for sad events, .68 for angry events, .90 for fearful events, and .71 for happy events (Reisberg et al., 1988, Experiment 2). It also didn’t matter whether the event being recalled was a personal one (e.g., death of a parent, graduation from college) or a public one (e.g., ﬁrst moon landing). The personal events were more vividly recalled and were more emotional than the public events, but the relationship between vividness and strength of aﬀect was the same for both (.661 and .641, respectively). Other studies conﬁrm this pattern, observing extreme memory vividness both for memories of traumatic events and memories for extremely positive events (e.g., Pillemer, Goldsmith, Panter, & White, 1988; Rubin & Kozin, 1984). One recent illustration of this ﬁnding is provided in Walker, Vogl, and Thompson (1997), who found that the rated emotionality of an event was consistently a strong predictor of whether participants believed they could remember the event or not, and the same data pattern emerged when participants were recalling extremely pleasant events and when they were recalling extremely unpleasant ones. Likewise, Porter and Birt (2001) invited their participants to describe their most traumatic autobiographical memory and also their most positive emotional experience. In both cases, they found that strong emotion was reliably associated with a high degree of memory vividness. Similarly, Berntsen (2001) examined the highly vivid involuntary (spontaneously arising) memories often called ﬂashbacks; the data showed little diﬀerence between involuntary memories for trauma and those for extremely happy events. But are these emotional memories accurate? It would be easy to assume they must be, since, after all, an emotional event is likely to be important to us, virtually guaranteeing that we will pay close attention as the event unfolds. In addition, emotional events are often emotional precisely because they are related to issues we care about and have thought about in other contexts; this will foster the sort of memory connections that we know promote retention and recall. Moreover, we tend to mull over emotional events in the minutes (or

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hours) following the event, and this is tantamount to memory rehearsal (cf. Bower, 1992). Finally, we are likely to revisit emotional events periodically, in our own thoughts or in conversations with others, and this too should promote retention. Even with these considerations, however, it is certain that at least some of our emotional memories do contain errors, and some may be wholly mistaken. Plainly, therefore, the accuracy of emotional memories must be tested and cannot be taken for granted. Evidence relevant to this point comes from many sources, but most forcefully from the debate over “ﬂashbulb memories,” a debate prominent in the research literature in the 1980s and 1990s. The term “ﬂashbulb memory” was coined by Brown and Kulik (1977), and referred to the exceptionally clear and detailed recollection people seem to have for singular, emotional, and consequential events they have experienced. Brown and Kulik oﬀered the example of people’s memory for John Kennedy’s assassination, an event that was still remembered “as if it were yesterday” many years after the event; more current examples would include the memory that many people have for Princess Diana’s death (in 1997), the O. J. Simpson trial (in 1995), and the destruction of the World Trade Center (in 2001). We will return to the topic of ﬂashbulb memories later in this chapter; for present purposes, we wish only to make a simple point about these memories. Flashbulb recollections tend to be extraordinarily vivid and detailed, and these memories are recalled with enormous conﬁdence that the memory is, in fact, correct. But ﬂashbulb memories can be shown in some circumstances to be wrong, making it plain that we cannot equate memory vividness with memory accuracy or memory conﬁdence with accuracy. One compelling illustration of this point comes from Neisser and Harsch (1992), who interviewed people days after the 1986 space-shuttle disaster, to determine where they were when they heard the news of the disaster, who brought them the news, and so on. Neisser and Harsch then reinterviewed these same people roughly 3 years later (32–34 months after the initial data collection), to see how memories for the event had fared over this time span. They found that people still reported detailed, high-conﬁdence memories in this 3-year follow-up, but many of these memories were simply wrong, sometimes in important ways, completely misrepresenting the original event. We hasten to say that other studies have yielded rather diﬀerent results, with impressive accuracy in people’s ﬂashbulb recollection (e.g., Conway et al., 1994), and so, as we have noted, we will need to return to this topic before we are done in order to address the question of why some ﬂashbulb memories seem accurate and long-lasting, while others do not. For now, though, we draw from the Neisser and Harsch data only the moral that emotional memories can be extremely vivid, extremely compelling, and yet completely out of step with the historical facts. This demands that we test the accuracy of emotional memories and not assume it.

    5

Studying Emotional Memory

in the Laboratory

Studies of ﬂashbulb memory obviously provide insights into how people remember the genuinely emotional events that actually take place in their lives. The disadvantage of these studies, though, is that we often have no way of knowing exactly what happened within the target event and thus no means of assessing the accuracy of memory. For this reason, the study of memory accuracy has often been taken into the laboratory so that we now have full knowledge of, and full control over, the to-be-remembered event. These laboratory studies have employed a variety of to-be-remembered materials. Here our emphasis will be on memory for events, and so we will hold to the side studies of people’s memory for emotional pictures (e.g., Canli, Zhao, Brewer, Gabrieli, & Cahill, 2000), emotion-laden word lists (e.g., Dietrich et al., 2001; Jones, O’Gorman, & Byrne, 1987), and memory for humor (e.g., Schmidt & Williams, 2001). Even with this narrowed focus, however, the evidence derives from a diversity of studies. In some studies, participants have witnessed an event presented via a series of slides, depicting successive moments within a story, with an accompanying (tape-recorded) narrative telling the emotional tale. In a smaller number of cases, the to-be-remembered event has been presented as a video clip (or, in just a few studies, an animation). An even smaller number of studies have employed live events, witnessed by the study’s participants. In virtually all cases, though, the studies compare participants’ memory for emotional materials to their memory for neutral materials, with the assessment of memory typically provided by a ﬁne-grained test in four-alternative forcedchoice (4AFC) format. The experimental materials are usually claimed to be emotional on three bases: the content itself, speciﬁcally chosen (or designed) for its emotional themes; self-reported emotionality from participants viewing the content; and physiological measures of arousal (usually heart rate). The neutral materials are then matched as well as possible to the experimental materials in structure and content but, of course, are claimed not to be emotional (usually on the same three grounds). As an illustration, several diﬀerent laboratories have used the “doctor/mechanic” stimulus set ﬁrst developed by Heuer (1987). In both versions of this stimulus, participants see slides and hear a narration about a mother and son going to visit father at work. In the emotional version of the stimulus, the father is a surgeon, and the son watches as his father completes a diﬃcult surgical procedure. One slide for this sequence shows a scene of surgery with the patient’s viscera in plain view; another shows the severed and reattached legs of a child. In the neutral version of the stimulus, the father is an automobile mechanic, and the son watches as his father completes a diﬃcult repair. One slide shows a scene of the repair with the engine in view; another shows the supposedly damaged part.

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The Easterbrook Hypothesis Most of the laboratory studies of emotional remembering have been cast as tests of two intertwined hypotheses. One hypothesis concerns participants’ memory for the gist or “central” materials within the event. As we will see, the weight of the evidence on this point is reasonably clear: in general, emotion seems to promote memory for an event’s gist or center. A second hypothesis derives from claims oﬀered many years ago by Easterbrook (1959). Based on animal studies, Easterbrook proposed that arousal causes a narrowing of attention, so that an aroused organism becomes less sensitive to information at the “periphery” of an event. As a consequence, the organism is likely to become more sensitive to information at the center of the event, perhaps because of diminished distraction from the periphery, or perhaps because the organism’s attentional resources are more “concentrated” on the event’s center. In either case, the hypothesis implies that the memory advantage associated with arousal will be observed only for the event’s center. Arousal should produce a disadvantage in remembering the event’s periphery (relative to memory for otherwise comparable neutral materials). Easterbrook’s own studies manipulated arousal by depriving animals of food for various lengths of time; his measures then assessed the animal’s sensitivity to cues in its immediate environment. There is obviously some extrapolation needed, therefore, to apply his hypotheses to the situation of a human, aroused through anger or fear or joy, remembering a complex event. Even so, that extrapolation is invited by a pattern often observed among victims or witnesses to crimes, a pattern known as the weapon focus eﬀect. This term refers to the fact that the witnesses to crimes often seem to “lock” their attention onto the criminal’s weapon and seem oblivious to much else in the scene. As a result of this attentional pattern, later on the witness will remember the perpetrator’s gun or knife with great clarity but may remember little else about the crime, including such crucial details as what the perpetrator looked like! Weapon focus has often been alleged by those in law enforcement and has also been documented in a variety of laboratory studies (e.g., Loftus, Loftus, & Messo, 1987; Stanny & Johnson, 2000; Steblay, 1992). In obvious ways, this eﬀect parallels the pattern observed by Easterbrook, with good memory for items at the center of the crime (the gun or knife) but poor memory for items at the periphery. Could it be, therefore, that Easterbrook’s claim applies to emotional remembering in general?

Studies of Memory Narrowing Many studies have asked whether participants show the pattern of “memory narrowing” for emotional events that we might expect by extension of the weapon-focus data. Early evidence on this point was mixed, and, indeed, one can

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easily ﬁnd in the literature claims that emotion promotes memory, claims that emotion undermines memory, and also claims that emotion has diverse eﬀects. For example, and in keeping with the Easterbrook suggestion, Christianson and Loftus (1991) found improved memory for the central materials within an emotional event but impoverished memory for the peripheral materials, in comparison to memory for a neutral (but otherwise similar) event. However, both Cliﬀord and Scott (1978) and Loftus and Burns (1982) reported evidence suggesting that emotionality impaired memory, and, using a somewhat diﬀerent paradigm, Heuer and Reisberg (1990) found that emotion seemed uniformly to improve participants’ memory, a beneﬁt that emerged for both central and peripheral materials (in comparison to memory for a matched neutral event). Although confusing when they were ﬁrst published, these contrasting data patterns are in retrospect easily explained. If emotion does have opposite eﬀects on central and peripheral materials, it is essential that we deﬁne these categories with care. To the extent that items on the memory test are miscategorized, this could easily obscure the results pattern. Similarly, our ability to make comparisons across studies is obviously compromised if diﬀerent investigators use diﬀerent categorization schemes for central and peripheral materials; that was, in fact, a problem in this early literature. Christianson and Loftus (1991), for example, deﬁned their categories largely in spatial or perceptual terms; peripheral details were those that were truly in the background. Heuer and Reisberg (1990), on the other hand, used deﬁnitions that were more conceptual and counted as central any bits of information directly relevant to the plot, or in any way important for how the story unfolded. Peripheral information, in contrast, was information that could be changed without in any material way changing the story. Which of these categorization schemes “carves nature at the joints”? Burke, Heuer, and Reisberg (1992) decided to treat this as an empirical question and therefore used a very ﬁne-grained categorization scheme in order to ask, in a data-driven fashion, which of these distinctions were relevant to emotion’s memory eﬀects and which were not. In their data analysis, Burke et al. separated items that were relevant to how the story unfolded from items that were not (thus replicating Heuer and Reisberg’s relevance-based distinction). The plot-relevant items were then subdivided into “gist” items, items that essentially deﬁned the story, and “basic level visual information,” items that, in the broadest terms, described what each of the slides in the sequence showed. Likewise, the plotirrelevant items were also subdivided, into those (irrelevant) details that happened to be spatially associated with plot-relevant actors or objections and those truly in the background. Finally, all of these categories were subdivided once again, but this time temporally, with questions divided according to whether they probed memory for materials that happened before, during, or after the parts of the story that were, in fact, arousing. Figure 1.1 depicts the Burke et al. categorization scheme, and, in a rough fashion, describes their results. As can be seen, the diﬀerence between plot-relevant

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Figure 1.1. A schematic description of the Burke et al. design and findings.

and plot-irrelevant materials does matter, inasmuch as the pattern in the top half of the ﬁgure is diﬀerent from the pattern in the bottom half. Likewise, the spatial/perceptual distinction also matters, evident in the contrast between the ﬁgure’s third and fourth rows. Finally, the temporal dimension also matters, as shown in the contrast between the table’s middle column and its two outer columns. (For related data, showing a similar eﬀect of the temporal dimension, see, for example, Bornstein, Liebel, & Scarberry, 1998.) How to summarize this pattern? First, these data do conﬁrm the memorynarrowing pattern, with emotion improving memory for materials central to the event and hurting memory for more peripheral materials. Second, the deﬁnition of the event’s center is complex—with materials favored by emotion if they are in any fashion tied to the “action” in the story—either conceptually or spatio-temporally. Several other studies have since conﬁrmed this pattern, albeit not at the same ﬁne grain. Safer, Christianson, Autry, and Österlund (1998), for example, showed participants a sequence in which a woman was shown either gathering ﬂowers in a park (neutral version) or stabbed in the throat and lying on the ground, bleeding (emotional version). The participants’ memory was then tested with various photographs diﬀering only in how much of a “close-up” they were; par-

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ticipants were asked to select the exact photo they had seen in the earlier sequence. We know from other studies (e.g., Intraub & Richardson, 1989) that people often remember photographs as being less zoomed-in than they actually were and correspondingly remember the photo as including more of the background than it actually did, a pattern known as boundary extension. Safer et al., however, found precisely the opposite pattern, with the emotional photos remembered as more zoomed in. Apparently, the participants’ memories excluded the peripheral information and also excluded the fact that there even was peripheral information. Similarly Wessel and Merckelbach (1997, 1998) invited spider phobics to the laboratory and, in one procedure, showed them a large, live spider (contained within a glass jar) and, in another procedure, showed them pictures of spiders mounted on a bulletin board. In both cases, these were particularly arousing stimuli for these participants but not for control subjects. In a subsequent memory test, the more aroused (phobic) participants showed the expected pattern of narrowing, with better memory for the event’s center (the spider) and worse memory for the event’s periphery than control participants. It should be acknowledged, though, that not all studies conﬁrm this broad picture, and two studies, one by Libkuman, Nichols-Whitehead, Griﬃth, and Thomas (1999) and one by Wessel, van der Kooy, and Merckelbach (2000), have failed to replicate the memory narrowing result. (We return to these nonreplications later.) Even so, the memory-narrowing pattern associated with emotional events has been replicated often enough to be regarded as wellestablished—especially when it is joined with the separate but substantial body of research directly examining the closely related weapon eﬀect. Overall, then, where does this leave us? We began this section by asking whether emotional events are remembered not just vividly but also accurately. The answer depends on what aspects of the emotional event we are considering. If we focus on central materials within an event—the gist of the event and details that are spatially central and also associated with the gist—the data seem reasonably uniform, with emotion seeming rather reliably to improve memory; we will consider even more data on this point (and some complications) later in the chapter. If we look instead at more peripheral materials (plot-irrelevant details that are spatially removed from the ‘action’), the evidence is less clear, but, overall, the data seem to indicate that memory is impaired by emotion. Thus, emotional events seem to be remembered accurately but incompletely.

Could Memory Narrowing

Be Artifactual?

Emotional events are distinctive in many ways. Quite obviously, they are accompanied by the feelings and bodily changes that we call “emotion” and, for this reason alone, may be remembered diﬀerently from neutral events. But, as we

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have already mentioned, several other factors may also be crucial here. Emotional events typically receive closer scrutiny than neutral events, and it may be this scrutiny, not the emotion itself, that explains the data we have so far reviewed. Emotional events are also likely to be perceived as worth thinking about after the fact and so probably are rehearsed to a greater extent than neutral events are. Perhaps it is this that shapes how these events are remembered, rather than the emotionality per se. In addition, emotional events are likely to be somewhat unusual (if they were more familiar, it seems likely that they would lose their emotional power), and this, too, may inﬂuence how they are remembered. Finally, emotional events are usually related to important themes or goals in our lives; this is presumably what makes them emotional in the ﬁrst place. Perhaps it is this relation to important themes that is crucial for memory and, again, not the emotionality itself. These factors are diﬃcult to control in any study of emotional remembering, but, even so, at least some evidence suggests that it is the emotionality that matters, over and above the undeniable contribution of these other points. For example, it is important that, in the Wessel and Merckelbach (1997, 1998) studies of spider phobics, it is the same event that is being remembered by the aroused and less aroused (nonphobic) subjects. This allows us to set aside a range of concerns that focus on some aspect of the emotional events (their familiarity, their coherence, their plausibility, their intelligibility) other than their emotionality. Moreover, a number of studies have directly tackled some of these extraneous factors. Christianson and Loftus (1991), for example, compared participants’ memory for three types of stimuli: a neutral stimulus, an emotional stimulus, and a stimulus designed to be unusual and attention-grabbing but unemotional. Speciﬁcally, the neutral stimulus told a story about a woman riding her bicycle; the arousal story told of a woman injured while riding her bicycle; the unusual story showed the woman carrying her bicycle on her shoulder. The results showed similar patterns for the emotional and unusual story with regard to the peripheral aspects of the story (a car seen in the background), but, for central information (the color of the woman’s clothing), performance was markedly better for the emotional event than for the unusual event. In short, then, the emotional and unusual stories led to diﬀerent memory patterns, suggesting that the eﬀects of emotion must be diﬀerent from those of sheer distinctiveness or unfamiliarity. In a similar spirit, Heuer and Reisberg (1990) compared memory under four diﬀerent circumstances. One group of subjects viewed an emotional sequence, and one a neutral sequence. (The doctor/mechanic series, already described, was used in this study.) A third group viewed the neutral sequence but was speciﬁcally urged to memorize the story as best they could; this condition seemed likely to elicit extra rehearsal of the story and so could illuminate rehearsal’s eﬀects. A fourth group was urged to scrutinize the (neutral) story closely and was told speciﬁcally that the stimulus they were about to see paralleled a recent event in

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the news; their task was to discern what that event was. (In truth, there was no such deliberate parallel, but participants had no way to know this.) This group was included to provide a comparison between emotion’s eﬀects and the eﬀects of close scrutiny (without emotion) and postevent contemplation. The comparison of these conditions is important if we are to isolate and identify emotion’s memory eﬀects. It is unfortunate, therefore, that this study, done some years ago, relied on a relatively crude measure of memory, one resting on a categorization of central and peripheral materials that the investigators subsequently abandoned (cf. Burke et al., 1992). Nonetheless, it is notable that the memory data for the emotion group were easily distinguishable from the data for any of the other three groups. Thus, though some caution is needed here, this study does suggest that emotion’s memory eﬀects cannot be reduced to these other factors. Roughly the same conclusion follows from a number of studies that have sought to examine emotion’s biological impact on memory. For example, several investigators have suggested that the amygdala plays a crucial role in emotional memory, a claim supported, for example, by studies of patients with UrbachWeithe disease, a disease that damages the amygdala without harming other brain structures. Adolphs, Cahill, Schull, and Babinsky (1997; also chapter 2 in this volume) presented two such patients with the stimuli developed by Heuer and Reisberg (1990). The patients found the emotional slides initially arousing, but showed no memory beneﬁt from this arousal, in comparison to their memory for neutral materials. These data are interesting for what they say about the biological mechanisms underlying emotion’s memory eﬀects but are also important for our purposes in this section. Presumably, Urbach-Weithe disease makes these stimuli no less unusual and no less coherent; if it is these factors that made the stimuli memorable, then the patients with this disease would remember the stimuli just as ordinary participants do. The data, of course, suggest otherwise. A parallel argument can be made for a study by Cahill, Prins, Weber, and McGaugh (1994). They showed (their adaptation of) the doctor/mechanic stimuli to participants but, prior to the presentation, injected half of the participants with propanolol, a beta-adrenergic blocker chosen to diminish emotion’s bodily (arousal) eﬀects, and injected the remainder with a placebo. If the memory eﬀects of the emotional stimulus truly depend on emotion (and, in particular, on the arousal that accompanies emotion), then the beta-blocker would be expected to reduce or eliminate these memory eﬀects. If, on the other hand, the memory eﬀects depend on factors like rehearsal or the unusual nature of the story, then it is not obvious why the beta-blocker should have an eﬀect. Cahill et al.’s results indicate that beta-blockers do reduce (and may even eliminate) the memory diﬀerences between neutral and arousal stories, buttressing the claim that it is indeed emotion that matters for memory, and not some other attributes of these stimuli. Once again, though, caution is needed here,

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because Cahill et al.’s study did not distinguish between central and peripheral elements of the story and so may not provide a complete portrait of emotion’s eﬀects. In short, the evidence on these points is strongly suggestive, but not conclusive. The weight of the evidence suggests that emotion itself has an impact on memory, with the eﬀect plausibly depending on emotion’s arousing eﬀects (which are speciﬁcally diminished by the administration of beta-blockers). For reasons we have mentioned, however, this is certainly a point in need of further research scrutiny.

Does All Emotion Have

the Same Eﬀects on Memory?

Does the Source of

the Emotion Matter?

We have so far painted a relatively straightforward picture of emotion’s eﬀects. A large number of studies indicate that emotion improves memory for an event’s center; a somewhat smaller, but still substantial, group of studies indicate that emotion disrupts memory for an event’s periphery. There are, however, two conspicuous problems with this claim. One is the studies, already mentioned, that have explicitly tried, but failed, to replicate the memory-narrowing pattern (Libkuman et al., 1999; Wessel et al., 2000). A second, and perhaps broader, problem lies with the generalizability of the studies cited so far. Emotion’s capacity to promote memory for an event’s gist or center has been demonstrated in many settings, both inside the laboratory and out (e.g., Bohannon, 1988; Brewer, 1988; Linton & Melin, 1982; Pillemer, 1984). To mention just a few of the more recent studies, Bluck and Li (2001) showed that the strength of participants’ emotional feelings about the O. J. Simpson verdict was predictive of how fully the event was recalled 8 months later. Bornstein et al. (1998) reported that the emotional center of an R-rated commercially produced movie was better recalled than a comparable but neutral episode. Peterson and Whalen (2001) reported that high stress levels facilitated young children’s recall of an emergency trip to the hospital 5 years earlier. Davidson, Luo, and Burden (2001) reported that children are better able to remember emotional behaviors than unemotional ones. And so on. But what of the narrowing eﬀect and, speciﬁcally, the tendency for emotion to diminish memory for an event’s periphery? Here the diversity of evidence is actually rather limited, because virtually all of the studies relevant to this eﬀect have induced emotion in roughly the same way: by showing participants something gruesome, or gory, or anxiety-provoking. Examples include pictures of disﬁgured faces, a picture of a boy shot in the eye, a picture of a woman with her

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throat slit, a picture of the severed legs of a child, or the sight of a dangerouslooking spider. All of these manipulations produce strong reactions, evident both in heart rates and self-report, but one might worry that these studies do not represent emotion as it naturally occurs outside the laboratory. In particular, one might argue that the emotion experienced outside the laboratory is more often induced, not by a particular visual stimulus but instead by involvement and empathy with an unfolding event. We become emotional, in other words, when we encounter issues and information that are pertinent to our lives, goals, and values (or, perhaps, the lives and values of people we care about). We refer to this more common kind of emotion as thematically induced, in contrast to the visually induced reactions involved in most previous studies, produced by the presentation of a speciﬁcally deﬁned emotional visual stimulus. This distinction between thematically and visually induced emotion raises two concerns about the extant evidence. First, can we generalize from the prior studies, or does the evidence instead allow us only to characterize one type of emotional event, with a diﬀerent proﬁle needed for other events? Second, and more troubling, this distinction raises the speciﬁc possibility that the “narrowing” of memory, observed in many studies, may be artifactual. Recall that the Easterbrook claim attributes the pattern of memory narrowing to arousal, with the implication that this pattern would not be observed if the arousal were somehow avoided or diminished. An alternative possibility, however, is that this “narrowing” has nothing to do with arousal but is observed simply because the experimental stimuli provide a highly salient stimulus to focus on, a strong “attention magnet” that seizes participants’ concentration during the event and therefore dominates their subsequent recollection of that event. We note that essentially the same concerns have been raised by investigators examining the phenomenon of weapon focus, which we described in an earlier section. Many authors have attributed this pattern to the emotional arousal experienced by the eyewitness; on this view, weapon focus is just another manifestation of the eﬀect described by Easterbrook. Other authors have pointed out, however, that the eyewitness may focus on the weapon simply because it is by far the most important and interesting aspect of the visual input. After all, what could be more important to a crime witness than to know whether he or she is in immediate danger or not, and, to this end, nothing in the scene is more important than knowing whether the weapon is cocked and pointed at him or her, or whether the criminal’s ﬁnger is on the trigger? On this logic, even an entirely calm witness might still show the weapon focus pattern, zooming in on the weapon because looking toward the weapon provides crucial information! As it turns out, the available evidence suggests that both of these mechanisms—one hinging on arousal, and one hinging on the weapon’s visual importance—may play a role in producing weapon focus. In several studies, for example, weapon focus has been observed even in the absence of emotion, indi-

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cating the importance of the weapon’s potency as an attention magnet (Kramer, Buckhout, & Eugenio, 1990; Loftus et al., 1987; Maass & Köhnken, 1989). Other studies indicate that it may be the unusualness of the weapon, and not the threat, that produces weapon focus (Pickel, 1998). Still other studies, however, suggest that the strength of the weapon focus eﬀect increases as arousal increases, indicating that arousal also plays a role (e.g., Peters, 1988). To the best of our knowledge, though, this issue has rarely been raised in the study of emotional memory (i.e., in the absence of a weapon). In the next section, therefore, we describe four studies designed to explore these points.

Thematically Induced Versus

Visually Induced Emotion

As a ﬁrst step toward addressing the issues just raised, it seems sensible to ask about the nature of the emotional events that actually ﬁll our lives. Is the emotion in these events typically visually induced (in which case the laboratory studies might be representative of emotionality in our day-to-day lives), or is the emotion typically thematically induced? In a pair of studies, Laney, Heuer, and Reisberg (in press) asked participants simply to list a series of emotional events from their lives; in their ﬁrst study, the participants were all college undergraduates at a prestigious institution; in their second study, the participants were much more diverse in ages, professions, and educational backgrounds. In both cases, the participants were then interviewed about the events they had listed, and, based on these interviews, the events were coded as either thematically or visually arousing. These two studies yielded virtually identical data. Despite a coding scheme set up to bias things toward counting events as visually induced, the huge majority of events reported by participants were in fact thematically induced— 82% in the study with undergraduates and 71% with the broader population. These results strongly suggest that (as Laney et al. [in press] put it) human emotional memory is not like a blockbuster movie with great special eﬀects; it is instead like a docudrama with complex characters and an emotionally engaging plot. Thus, most laboratory studies of emotional remembering are considering a form of emotion that is neither typical nor representative, and that of course invites the next question. Can we explore in the laboratory how participants remember thematically arousing events? In two unpublished studies, Laney et al. pursued this issue, asking how participants remember events that are arousing for thematic, not visual, reasons. The ﬁrst of these studies evoked arousal by appealing to an issue clearly emotional for the college-age participants, namely, date rape. As in previous research, the stimuli involved a slide sequence plus tape-recorded narration. The sequence showed a man and woman on their ﬁrst date, and the neutral and arousal sequences were visually identical except for one slide, late in the series. Hence, the

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15

arousal manipulation was not contained within the slides themselves, but within the narration, ensuring that the arousal was not induced by a speciﬁc visual target. In the neutral version, subjects heard that the woman was relaxed and happy about the date, and the man was polite and friendly. In the arousal version, subjects heard that the woman was growing increasingly apprehensive as the date progressed, and these fears turn out to be well founded, as the man attacks the woman late in the sequence and has to be forcibly pushed away. The memory data in this study showed a robust eﬀect of story, with participants having more complete and more accurate memories for the arousal story. This conﬁrms the positive eﬀect of emotion on memory for central materials, even with story materials that are thematically, not visually, arousing. On this point, Laney et al.’s study (unpublished) conﬁrms the generality of prior ﬁndings. However (and crucially), there was no hint of an impairment in memory for peripheral aspects of the emotional story; instead, these were remembered better than peripheral aspects of the neutral story. Said diﬀerently, emotion seemed in this case to improve memory for all aspects of the story, and thus there was no indication at all, in these data, of memory narrowing. Another study conﬁrmed these ﬁndings. In this case, participants viewed a series of 33 photographs conveying a story about a college student named Megan. In the arousal version, subjects learned early on that Megan is doing badly in her classes and may lose the ﬁnancial support she’s been getting from her parents. In addition, Megan’s boyfriend just dumped her—on her birthday. As the story unfolds, Megan discusses the possibility of suicide and gets quite speciﬁc about it, contemplating the combination of pills and alcohol that is, in fact, one of the most common paths to suicide among college students. We emphasize, though, that all of this upsetting information was conveyed in the narrative that accompanied these slides; there was nothing in the visuals that was at all upsetting. Indeed, neutral subjects saw the exact same visuals and heard a story with it that paralleled the arousal story, but with some essential diﬀerences. They heard that Megan was doing well in her classes and that she and her boyfriend were getting along ﬁne. They also heard about Megan reaching for a pill bottle, but, this time, in response to a hangover caused by her birthday celebration. Again, the memory data showed a strong eﬀect of story, with better memory overall for the arousal story. But, as in the previous study, there was no indication in the data of memory narrowing; the positive eﬀect that emotion had on memory was as reliable for peripheral details as it was for central materials. These two studies obviously suggest that memory narrowing is not inevitably produced by emotionality, in clear contrast to Easterbrook’s suggestion, many years ago, that it is arousal per se that leads to narrowed attention. Instead, these studies suggest that we need separate hypotheses to account for emotion’s positive eﬀects on memory for central materials and its negative eﬀects on memory for peripheral materials. The former is surely an eﬀect of emotion and the arousal that accompanies it; this is suggested by the beta-blocker results and other ﬁnd-

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ings. But the latter eﬀect seems not to be produced by emotion. Instead, it is the result of an event containing a powerful attention magnet that summons attention and, correspondingly, draws attention away from other aspects of the event. We hasten to say, however, that these claims about thematic arousal must be tentative, and this is a point on which further data are surely needed. A number of studies have documented memory narrowing for emotional events, but few studies have speciﬁcally examined thematic arousal, and, until the data base is larger, we urge caution on this theme. Indeed, one of our own early studies indicated that thematically arousing events do produce memory narrowing (Heuer, Reisberg, & Rios, 1997). We now believe that this early result, with its relatively crude stimuli and test materials, should be set aside in favor of more recent data collected with improved procedures. Even so, we must not pretend the data are univocal on the memory eﬀects of thematic arousal, and replication studies are plainly required. Let us for the moment, however, assume that Laney et al.’s (unpublished) third and fourth studies can be taken at face value. Concretely, this is a claim that emotion improves memory for all aspects of a story, not just the center, and that the negative memory eﬀects observed in prior studies are not a consequence of emotion but are, instead, produced by powerful attention magnets embedded within the emotional story. Does this mean investigators interested in emotion should henceforth ignore the memory-narrowing pattern, realizing that it is not a pattern produced by emotion? We believe that this question should get a ﬁrm no for an answer, for three reasons. First, it simply is the case that many emotional events do have a visual focus, do have an attention magnet embedded within the event. Laney et al.’s data tell us that such events are atypical, far outnumbered by thematically arousing events, but even so at least some emotional events do contain visible wounds, horrifying scenes, threatening weapons, and the like. If we are to understand how these events are remembered, we must consider the role of these salient visual targets in shaping memory. Second, even if the narrowing pattern is not produced directly by emotion, it may be potentiated by emotion. After all, what makes a visual stimulus a powerful magnet for our attention? Arguably, the key lies (at least in part) in the emotional importance of that stimulus—whether as a source of threat (e.g., a weapon), a focus of horror (e.g., a gaping wound), or a source of joy (e.g., the sight of a long-absent friend’s face). Thus, as emotion grows, the visual salience of these stimuli grows (cf. Öhman, Flykt, & Esteves, 2001), and it is then the visual salience that produces memory narrowing. Evidence consistent with this conjecture comes from a study to which we alluded earlier, by Peters (1988), examining adults’ memory for an occasion on which they received a rubella injection. The data showed a weapon focus eﬀect, with the sight of the hypodermic needle apparently seizing the adult’s attention,

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leading to an inability, later on, to identify the nurse who had given the injection. Importantly, participants’ ability to make this identiﬁcation was negatively correlated with arousal (measured by heart rate), suggesting that arousal served to magnify the “threatening” quality of the “weapon” and thus to increase the “weapon’s” power to seize attention, thus undermining memory for other aspects of the event. Third, and more immediately, this separation of mechanisms may allow us to untangle some of the apparent contradictions in the empirical literature. We noted earlier that two studies, by Libkuman et al. (1999) and Wessel et al. (2000), have failed to obtain the “standard” memory-narrowing eﬀect, despite their use of stimuli and procedures that seemed fully appropriate. If we assume that their stimuli were arousing, and if we assume that memory narrowing is (as Easterbrook suggested) a direct consequence of arousal, then it is odd indeed that these studies did not replicate the narrowing pattern. However, the framework we are developing here oﬀers a path toward explaining this nonreplication. Memory narrowing, we are proposing, is not a direct consequence of arousal; instead, it is a consequence of how witnesses direct their attention during an emotional event. This allocation of attention is to some extent under strategic control; it is likely to be inﬂuenced by instructions and taskset; it is likely to diﬀer somewhat from one subject population to the next. For these reasons, our current hypothesis (unlike Easterbrook’s claim) leads us to expect some degree of unevenness in the data pattern, with some studies demonstrating the narrowing pattern and some not. To be sure, this line of argument contains a substantial promissory note, because we have provided no details about any of these factors guiding attention and so no ﬁrm predictions about when narrowing will or will not be observed. Even so, an account cast in terms of attention oﬀers ﬂexibility that an account cast in terms of arousal does not, and this by itself seems noteworthy, given the mixed pattern of evidence.

Emotion Intrinsic to the Event,

Emotion Extraneous to the Event

We have now argued that the source of emotion may matter in determining how an emotional event is remembered. Does the arousal arise from the themes and meaning inherent in the emotional event or from some salient visual stimulus within the scene, such as the sight of a wound or a weapon? A related question also concerns the source of the emotion. Sometimes we are emotional during an event because the event itself is emotional—uplifting, perhaps, or frightening, or anger-provoking. But sometimes we are emotional for reasons external to the event we are participating in. We might still be emotionally aroused from some earlier event, now done. Or we might be aroused for some reason other than emotion—exercise, perhaps, or an overlarge dose of caﬀeine, or perhaps even an experimenter’s injection. Does this contrast matter? Are the memory eﬀects of

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emotion intrinsic to an event the same as the eﬀects of emotion that merely accompanies the event? This issue is of interest for several reasons, including a question of how we should conceptualize emotion’s impact on memory. Many accounts describe this impact in terms of arousal mechanisms—increased norepinephrine levels in the bloodstream, for example, and increased serum glucose levels, and their eﬀect on brain mechanisms serving memory (cf. chapters 2 and 3). If these are the keys in producing emotion’s memory eﬀects, then the nature of the arousal (intrinsic to the event or extraneous) should not matter. But if, on the other hand, the content and meaning of an emotional event inﬂuence memory (as plausibly they would), then the contrast between intrinsic and extraneous arousal may be crucial. Over the last few years, a number of studies have pursued this issue. Christianson and Mjörndal (1985; also see Christianson, Nilsson, Mjörndal, Perris, & Tjellden, 1986) asked how injections of adrenaline inﬂuenced memory for pictures. They reported no eﬀects of the injection on memory for neutral pictures and a diﬀerence between how participants remembered emotional pictures (after a saline injection) and how they remembered neutral pictures after the injection of a stimulant. This result suggests that the source of the arousal does matter and that only arousal intrinsic to the to-be-remembered materials has memory eﬀects. (For a related, but somewhat more complex study, see Clark, Milberg, & Ross, 1983.) In contrast, though, we know that ingestion of glucose does improve memory in some circumstances. Hall, Gonder-Frederick, Chewning, Silveira, and Gold (1989) and Manning, Hall and Gold (1990) reported that ingestion of glucose (dissolved in a lemon-ﬂavored drink) improved performance on a number of memory measures, including recall of an earlier heard narrative. In this case, mimicking one of arousal’s eﬀects in a fashion entirely external to the to-beremembered material did improve memory. It is not obvious what to make of these mixed results, although we suspect that part of the problem lies with the arousal construct itself. There has been considerable dispute over whether arousal can be understood as a single, uniﬁed construct or whether, instead, we need to distinguish various types and multiple dimensions of arousal (for some “classic” statements on this issue, see Anderson, 1990; Neiss, 1990). With this point unsettled, it is diﬃcult to make any comparisons across procedures. In addition, and perhaps more important for our purposes, what about memory for events, rather than memory for word lists, picture series, or verbal narrative? To address this question, Libkuman et al. (1999) showed half of their participants an arousing story and half a neutral story (using Heuer and Reisberg’s doctor/mechanic stimulus, already described). Within each group, half of the participants viewed the slides after a minute of sitting quietly, and half viewed the slides after spending a minute energetically running in place, to produce a

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baseline of elevated arousal. Their results showed little or no eﬀect of exerciseproduced arousal on memory. A second study replicated this ﬁnding, using a cued recall measure in place of a recognition test. A third study yielded similar data but this time with the exercise maintained during the slide presentation. (Participants pedaled on an exercise bicycle while viewing the slides.) Where does all of this leave us? We know that arousal does play an important role in mediating emotion’s memory eﬀects. This is evident, for example, in Cahill et al.’s (1994, 2000) studies, showing that an interruption of arousal (via betablockers) disrupts emotion’s impact on memory. But, as we have now seen, at least some evidence suggests that this arousal must come from the “right” source and must somehow be tied to the to-be-remembered event; otherwise, the arousal seems to have no eﬀect on memory. How should we put these clues together? One obvious conjecture is that physiological arousal may be necessary for promoting event memory but is not by itself suﬃcient for producing this memory eﬀect. Also necessary is an emotional content to the event, something that engages participants’ attention, processing, and subsequent rehearsal. In essence, this cognitive work could provide the speciﬁc steps needed to establish an event memory and to link this memory to other bits of knowledge (making the target memory accessible after on). The physiological arousal could serve to facilitate these steps or to consolidate the memory once it is established through these steps. This position is fully compatible with the claim, already in the literature (e.g., McGaugh, 2000), that physiological arousal has its eﬀect on memory chieﬂy through its impact on postevent memory-consolidation processes. In this view, arousal might play little role in establishing the content of emotional memories; that would be determined by other factors (such as the nature and meaning of the emotional episode itself). Arousal would instead play its role by cementing the content (whatever it is) in place, so that the resulting memory would be more complete and more long-lasting. From this perspective, neither the cognitive work evoked by an emotional memory nor the arousal by itself would be suﬃcient to produce emotion’s full memory eﬀect; instead, both acting in concert would produce the eﬀects we have been describing.

Does the Valence of

the Emotion Matter?

We have now argued that the source of emotional arousal matters in shaping emotion’s memory eﬀects. Thematically induced emotion seems to produce diﬀerent memory eﬀects than visually induced, and emotional arousal intrinsic to the to-be-remembered event seems in several studies to produce diﬀerent eﬀects than extraneous arousal. But, of course, emotionality also varies in other ways, including the emotion’s valence. We saw earlier in the chapter that valence seems largely irrelevant to the relationship between emotion and memory vividness, so that sad memories are recalled just as vividly as happy memories, and traumatic

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memories are no more vivid than memories for intensely pleasant events. But what about memory accuracy or completeness? Relatively few studies have pursued this issue. We do know that humor promotes memory—both for verbally presented jokes and for cartoons (e.g., Schmidt & Williams, 2001). But what about more complex materials? There is some suggestion in the literature that emotion’s memory eﬀects are mediated by the release of stress hormones (Gold, 1989, 1992; McGaugh et al., 1993); one might draw from this the claim that only aversive, stressful events will show the memory beneﬁts of these hormones. But, of course, there are many similarities between the biological eﬀects of emotionally positive experiences and those of aversive experiences (e.g., Hamann & Ely, 1999), so, on this view, it may be the arousal itself that promotes memory, independent of the emotion’s valence. A recent study from our laboratory (Moyer, 2002) was designed to explore these issues, albeit using an unusual stimulus: the form of animation known as anime. This choice of stimulus was motivated by the fact that it is often diﬃcult to evoke an emotional response in the laboratory, especially with a relatively brief stimulus designed to experimental speciﬁcations. It is helpful, therefore, to rely on a genre and a medium that is already engaging to students, and anime, a style of Japanese animation immensely popular with many college students, oﬀered these advantages. We created three stimuli, each an edited version of commercially available animes, one depicting an emotionally neutral story, one depicting an emotionally negative story, and one a positive story. The emotionality of the stimuli was conﬁrmed by pilot testing, as was the comparability of the stimuli on several other dimensions (quality, complexity, duration, number of scene changes). The positive event was drawn from the Magic User’s Club (Takahashi & Asari, 1996) and begins with four student members of the club, discussing ﬂying on their brooms. One of the students attempts to launch her broom, and her eﬀorts are both comical and erotic. Later, the anime shows the friends ﬂying along, and one of the students zooms past them, unable to control her broom. She is forced to let go of the broom, and her rescue (by another of the students) is again both funny and sexy. Participants reliably rated this video as making them “amused” and, perhaps more impressive, many laughed out loud while viewing the video. How did they remember the video? Questions in the memory test had been classiﬁed as central or peripheral by a panel of judges, using criteria derived from the Burke et al. (1992) data. Items were central if they were either relevant to how the story unfolded or visually prominent within the anime (e.g., tied to a plot-relevant character or object). Items were peripheral if they were both irrelevant to the story and distant, in the judge’s assessment, from the ‘attention centers’ of the video. In the recognition test (Moyer, 2002), the participants remembered 65% of the central details in the comical anime, compared to 51% in the emotionally neutral stimulus. Thus, once again we see the broad advantage for emotional materials relative to neutral ones. In addition, participants remembered 34%

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of the details considered peripheral by the judges, compared to 46% for the neutral stimulus. These data therefore replicate the memory-narrowing pattern (with improved memory for central materials, impaired memory for peripheral materials, in the emotional condition) but show this eﬀect for the ﬁrst time, as far as we know, with an emotionally positive stimulus. Moyer’s (2002) study also included a negatively tinged anime, drawn from Nosaka, Takahata, and Sato’s (1988) Graveyard of the Fireﬂies. The clip begins with a view of American ﬁghter planes and a voice yelling “air raid.” The scene then shifts to a child (about 15 years old) and his sister, leaving their house for the air raid shelter. The anime shows them running among falling bombs and debris and eventually shows them at a school that has been converted to a hospital. A neighbor takes the young boy to see his mother, who is covered in bandages and obviously dying. Although we did not intend this, the negative anime lacks any speciﬁc visual target that can be construed as a focus for viewers’ attention or as an attention magnet (to use the term we introduced earlier). Instead, the aﬀect, demonstrated clearly in pilot testing, involves an overarching feeling of sadness over these two children trying to survive and ultimately losing their mother. Therefore, inadvertently, this stimulus is akin to the thematically arousing stimuli studied by Laney et al. (in press), and this is reﬂected in the data: Once again, the emotion improved memory, with 65% of the central details remembered for this negative stimulus, in comparison to 51% for the neutral stimulus. However, in keeping with Laney et al.’s results, this (thematically arousing) anime showed no evidence of memory narrowing, that is, no evidence of an emotion-produced impairment for peripheral materials. Concretely, participants remembered 48% of the peripheral details of this anime, in comparison to 46% for the neutral stimulus. This study provides an initial hint, therefore, that emotionally positive events are remembered in much the same way that emotionally negative events are. Positive emotion conveys a broad memory advantage for the story’s gist and central materials, but positive emotion can also be accompanied by its own version of memory narrowing, its own version of weapon focus. A recently published study, however, seems at ﬁrst pass to be inconsistent with Moyer’s (2002) data. Berntsen (2002) asked participants to think of the most traumatic experience they had ever experienced, and the happiest experience they had ever experienced, and then to record as many details of these events as they could. These details were then categorized as either central or peripheral. (In one experiment, external judges did this categorization; in another, the participants themselves did this.) Berntsen concludes from this study that “tunnel memories” (a pattern of memory narrowing) “are due to the combined eﬀects of high arousal and negative valence, whereas high positive arousal . . . is not able to create the eﬀect” (p. 1018, emphasis added). This seems to contradict Moyer’s ﬁnding, which did show memory narrowing with positively valenced events.

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However, this data contrast is diﬃcult to interpret. As one concern, Berntsen’s study (2002) does not assess memory accuracy, because there was no way to conﬁrm (or disconﬁrm) her respondents’ recollections. Second, with participants able to select their own events for recollection, there is no way to know if the positive and negative events in Bernsten’s study were truly comparable. In particular, it is hard to know whether visually evoked and thematically evoked events were equivalently represented in the positive and negative recalls, and, as we have discussed, this may well have shaped the pattern of memory narrowing. Third, and most important, Berntsen’s study (2002) does not include data for neutral events, and this makes her results, as valuable as they are for her own purposes, impossible to interpret for our purposes. Concretely, what her data actually show is that the proportion of central details (relative to peripheral details) is greater for “shocking” memories than it is for positive memories. However, this leaves open the possibility that the positive memories may nonetheless have contained a greater proportion of central details (and, more to the point, a smaller number of correctly recalled peripheral details) than a set of neutral memories would have. With no way to evaluate this possibility (and with the other concerns just mentioned), there is no way to know from these data whether the positive events produced a pattern of memory narrowing or not. If we hold Bernsten’s study (2002) aside, then, Moyer’s (2002) data suggest that it is emotionality per se that matters for memory, not the emotional valence. A diﬀerent line of data, however, raises questions about this proposal and suggests overall that we may need a more ﬁne-grained account of how diﬀerent qualities of emotion inﬂuence memory. Levine and Burgess (1997) have argued that the valence of emotion does matter for memory; they argue that the speciﬁc emotion will inﬂuence not just how much within an event is remembered but also what within the event is remembered. In their view, emotions enhance memory for information that is “functionally relevant” to the emotional state, and what information that is will vary from one emotion to another. Thus, a broad categorization of an episode’s elements as central and peripheral may be too crude, because information central for one emotional state may be less so for another state. To explore this claim, Levine and Burgess (1997) manipulated their participants’ initial mood by telling them they had received either an “A” or a “D” on a surprise quiz. Participants then took part in what they believed to be an unrelated study during which they heard a narrative that they subsequently had to recall. The results from this memory test were complex, with the content of participants’ recall inﬂuenced (as predicted) by the participants’ exact emotional state. Thus, for example, participants who were angry tended to have better recall for information that concerned goals of the individuals described in the narrative; there was no relation between degree of anger and recall of other types of information. Sadness, on the other hand, was associated with enhanced recall

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of information about outcomes for individuals described in the narrative but not with other aspects of recall. In our view, Levine and Burgess’s (1997) argument merits close consideration. It is not yet clear whether the details of their proposal (with regard to “goals” and “outcomes” and so on) are warranted by data, and it is also worrisome from our point of view that the arousal at stake in their experiment was produced by a source external to the to-be-remembered event. (That is, it was the report of a grade that produced the arousal, but this grade had nothing to do with the narrative the participants subsequently had to remember.) Nonetheless, Levine and Burgess’s more general proposal seems plausible and is surely consistent with themes we have developed in earlier sections of this chapter. For example, we have suggested that neither arousal nor emotion is enough itself to produce the pattern of memory narrowing; instead, this narrowing will be observed only if the emotional event contains a salient stimulus, drawing participants’ attention. Moreover, we have suggested that in many cases a stimulus will gain its salience, that is, will gain its power to draw attention, from its meaning within the emotional event. Let us now add that this emotional meaning may well depend on the particular emotion being experienced, so that a stimulus salient for someone who is afraid may well be less salient for someone who is angry. With this additional step, the position we have sketched blends smoothly into that presented by Levine and Burgess. With this said, however, the fact remains that the available data are rather sparse for exploring the memory eﬀects of diﬀerent qualities of emotion. In our view, this provides powerful reason for investigators to broaden the focus of their work, and, until that is done, any claims regarding these issues need to be couched with caution. In the meantime, though, we do have at least some indications that the memory pattern for emotionally positive materials will resemble the pattern for emotionally negative materials, with an advantage overall (primarily deriving from information at the event’s center) but also with a disadvantage for peripheral materials if the to-be-remembered event contains a suitable visual focus. Even so, we are mindful of Levine and Burgess’s (1997) potentially crucial point that diﬀerent emotions will favor memory for diﬀerent aspects of the target event, and this is a proposal that cries out for further research.

Does the Intensity of

the Emotion Matter?

We have now considered diﬀerence sources of emotion and diﬀerent qualities of emotion; what about diﬀerent intensities of emotion? For years, the answer to this question has been cast in terms of the Yerkes and Dodson (1908) inverted-U curve, with the proposal that there is some ‘optimal’ level of emotion for promoting memory and that poorer and poorer memory is observed as one moves further away (in either direction) from this optimum. This pro-

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posal seems intuitive enough and ﬁnds support in the fact that many studies have shown a positive relationship between memory and level of arousal, while other studies have shown a negative relationship. (Studies in the latter group are common, for example, in the research literature on stress and are also reported in the literature on trauma; for discussion of both, see chapter 3, this volume.) Plausibly, studies in the ﬁrst group are on the uphill side of the YerkesDodson function, so that increasing the level of arousal moves us toward the optimum; studies in the second group could then be understood as on the downhill side of the function, so that increasing the level of arousal moves us away from this optimum. However, it may well be time to retire the venerable Yerkes-Dodson function, at least as applied to emotional memory. Other chapters in this volume will pursue the issue of how people remember extremely emotional events, but, for now, we will simply note that these events should not be remembered on most construals of the Yerkes-Dodson function but that they often are remembered—for quite some time and in considerable detail (e.g., chapters 2, 4, and 11). To be sure, there are some complications here (see chapters 3 and 8), but in any case the data cannot be read as indicating the Yerkes-Dodson, no-memory-for-extreme-emotion pattern. In addition, and more directly, Christianson (1992) argued persuasively that there is very little direct evidence in favor of the Yerkes-Dodson pattern in emotional memory. Indeed, the Yerkes-Dodson claim may actually be untestable, since it can explain virtually any result. (Note, for example, how readily this claim accommodates both positive eﬀects of emotion on memory and their opposite.) With what should we replace the Yerkes-Dodson function? At the least, we should acknowledge that multiple mechanisms are likely to contribute to emotion’s memory eﬀects, and it is plausible that each will have its own ‘optimal’ operating circumstances (cf. chapter 3). If so, the function linking arousal level and memory may not be unimodal, as the Yerkes-Dodson function is, but more complex. Consistent with this suggestion, consider a result reported by White (1991). Using an animal model, White examined the rate of learning as a function of the sugar dose delivered to the animal via a posttraining injection. His data do not reveal anything like the inverted-U function suggested by Yerkes and Dodson. Instead, his data plots have two peaks, with the clear suggestion that multiple mechanisms are in play, each contributing to the overall performance but with its own optimal level. This result implies that the relation between arousal and memory will be more complex than Yerkes and Dodson envisioned but still a relation that can be understood in terms of a single predictor variable. Figure 1.2 oﬀers an appreciably more complex model, initially oﬀered as a proposal for describing sports performance by Fazey and Hardy (1988) and then applied to memory by Deﬀenbacher (1994). This model implies that the relation between arousal and performance may depend on other variables, such as the person’s level of anxiety. At low anxiety levels, Fazey

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Figure 1.2. The Yerkes-Dodson inverted-U function is often offered as a description of how memory performance will change as a function of increasing arousal. This figure, suggested by Fazey and Hardy (1988), provides a more complex and perhaps more realistic model. Whether the details of this model turn out to be correct or not, Fazey and Hardy remind us that the relationship between memory and arousal is likely to interact with other variables. They suggest that a key third is “cognitive anxiety.”

and Hardy forecast a pattern similar to the Yerkes-Dodson inverted-U. As anxiety increases, however, the pattern changes, with a sharp discontinuity in the curve and the level of performance depending on whether arousal is gradually being increased or decreased. Not enough data are available to evaluate this model (or variants on it), but it does remind us that the “optimal arousal level” for memory (if one can be deﬁned) is very likely to depend on other factors, much as ﬁgure 1.2 suggests. If so, the Yerkes-Dodson function is not just unproven and probably untestable, it may be on the wrong track altogether, conceptualizing the data pattern in a (unidimensional) fashion that is far too simple. Once again, though, we call attention to the fact that this theme is plainly underresearched.

“Lost Memories”? Before moving on, we need to address one further topic clearly related to the themes of the last two sections. What happens when the emotion associated with an event is extremely intense and also strongly negative in its valence, perhaps with the valence marked by anxiety, perhaps by a sense of betrayal? Many authors have suggested that, under these circumstances, the relation between emotion and memory changes dramatically. No longer does emotion promote

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memory, but, instead, in these circumstances, emotion will be associated with amnesia for the painful events. This is not the place to delve deeply into this diﬃcult and contentious issue, but we do wish to touch a few points related to themes elsewhere in this chapter. (For more on this broad issue, see chapters 3, 4, and 11.) In doing so, we believe it important to separate the empirical claims from the interpretations often oﬀered for the data; we begin, therefore, by considering the facts and (as we view it) the considerable ambiguity attached to those facts. Can one experience a highly emotional event but not remember it? The answer is yes, for several reasons. First, some emotional events discussed in the literature have been experienced by very young children (e.g., Williams, 1995) and so are open to the widespread pattern of childhood amnesia (cf. Shobe & Kihlstrom, 1997), a pattern that applies to all events in the ﬁrst years of life, emotional or not. Second, emotional memories, as strong as they tend to be, are still vulnerable to the same sorts of forgetting mechanisms as other memories, including interference from other remembered events and retrieval failure. This, too, can lead to apparent amnesia for emotional events, and there is at least some indication that the rate of forgetting is similar for emotional and nonemotional memories (Read & Lindsay, 2000). Third, there is reason to believe that extreme levels of emotion can, in some circumstances, have a catastrophic eﬀect on memory, causing relatively complete amnesia for horriﬁc events that happened just hours or days earlier (Arrigo & Pezdek, 1997). It seems likely in these cases that the amnesia is caused by the bodily changes associated with extreme stress, changes that could disrupt the biological processes of memory consolidation needed to establish a memory in the ﬁrst place. On this view, the high levels of stress have washed away the seeds of memory, so to speak, before they had a chance to take root. What about cases in which people report that they have long been amnesic about an emotional event but have now recovered the relevant memories? There is no doubt that these reports of memory discovery do occur, and here too there are many mechanisms that might contribute to such reports. First, we believe that some of these cases involve memories that have never been truly lost; the “recovery” merely refers to a new-found willingness to talk about this always remembered but never discussed episode. This willingness might emerge in the safety of a therapy setting; it might be encouraged by a social climate in which reports of previous traumas are supported and perhaps even encouraged. Second, we believe that some of these cases involve “recategorizations” of the relevant memory. “I always knew that he did X, but until recently I didn’t realize there was something blameworthy in what he did, and it’s only now, when I realize that the action is culpable, that I’m talking about it.” Third, there are some cases in which, remarkably, someone is convinced he was amnesic about an event at some prior time but, in truth, did remember the event all along. In other words, this is an example of a memory error, but what is being misremembered is the

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fact of amnesia itself! Several such cases have now been documented, cases that are, in a sense, the inverse of someone falsely claiming, “I knew it all along.” Hence, these cases are sometimes referred to as revealing the “I forgot it all along” eﬀect (Schooler, Bendriksen, & Amadar, 1997; also Padilla-Walker & Poole, 2002). Fourth, we have noted that at least some emotional memories will be forgotten for routine reasons such as retrieval failure; these cases of forgetting are likely to be reversed if suitable retrieval cues should present themselves. Fifth, and ﬁnally, it does seem sadly plausible that at least some recovered memories may turn out to be false memories, recalling events that never took place or events that unfolded diﬀerently from the way they are remembered. In light of all these comments, we believe it is unsurprising that some emotional memories do seem genuinely to be forgotten, and also unsurprising that there are many reports of emotional memories allegedly forgotten and then rediscovered. Moreover, we have suggested that many diﬀerent causal sequences could lead to these facts, and, notably, in most of these causal sequences, there is no reason at all to challenge the veracity of the allegedly recovered memory. Why, then, have recovered memories been so controversial? The debate, we believe, does not revolve around the facts themselves; those, we have just suggested, are relatively uncontentious but also open to multiple interpretations. Instead, the debate hinges on a particular claim about the facts, namely, that emotional memories are lost because of a special mechanism of “repression” or “dissociation,” a mechanism that involves mental processes markedly diﬀerent from those involved in ordinary emotional remembering. Our view is that the facts do not warrant these latter claims, because, as just discussed, the available facts are easily accommodated with no need for new and distinctive mechanisms. We stress, though, that this is in no way intended as a statement of blanket skepticism about these lost or recovered memories. Instead, it is simply an assertion that there are multiple non-exotic steps through which emotional memories might well be apparently lost and then rediscovered.

Alternative Approaches Beyond Accuracy:

Memory Detailedness and Coherence

We began this chapter by asking how accurately emotional events are remembered. The answer, it seems, is “it depends.” Overall, many studies show that emotion promotes memory for an event’s center and that at least part of this promotion depends on bodily arousal. But many studies also show that emotion impedes accurate memory if the to-be-remembered event contains a salient visual target, summoning attention; in this case, memory for the event’s center will be enhanced but at the cost of poorer memory for the event’s periphery. In addi-

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tion, we have at least some indications that this pattern can be observed for emotionally positive events (e.g., an event that is comical and somewhat erotic) as well as emotionally negative events. Beyond this, though, at least two complications are needed in this account. First, the pattern of what speciﬁc content is remembered and what is not may depend on the nature of the emotion (after Levine & Burgess, 1997), and this issue needs further exploration. Second, the relation between memory and emotional intensity remains to be fully explicated, and it does seem likely that there will be circumstances in which emotion (perhaps only extreme emotion) has none of the eﬀects we are describing but, instead, undercuts memory (see, for example, chapter 8). It should be acknowledged, though, that this account views emotional memory from a distinct perspective—one highlighting a memory’s accuracy and completeness as its most important attributes. To be sure, this concern with memory accuracy is easy to justify, especially in light of psychology’s increasing concern over the accuracy of eyewitness memory in the courts. But other perspectives on emotional memory should also be explored and have their own value. As just one example, consider a study by Williams et al. (1996). Their study begins with the fact that hopelessness is a key factor in leading a depressed person to contemplate suicide, and so Williams et al. ask: Where does hopelessness come from? They explore the proposal that one becomes hopeless when one cannot imagine future events in any detail, and this impairment in imagination, in turn, becomes likely when one does not recall past events in detail. Their study conﬁrms these claims, with both a correlational design (using hospitalized patients who had, in fact, recently attempted suicide) and an experimental design (to explore causal relations). The Williams et al. article is interesting for several reasons, including the fact that memory accuracy plays no role in their account. Instead, what matters is memory detailedness and, arguably, memory vividness, and, more, these attributes matter for functions of considerable interest—the use of memory in problem solving; the use of memory in gauging the likelihood of future events; and, prominently, the use of memory in generating hope for the future. Thus, this article provides a compelling reminder that these other dimensions of memory are well worth our scrutiny. What do we know about emotion’s inﬂuence on these other dimensions? As we mentioned at the very outset, memory vividness is strongly correlated with how emotional an event is recalled to have been (Reisberg et al., 1988), but there are two concerns about this result (and related ﬁndings in the literature). First, note that the predictor variable here is retrospective assessment of an event’s emotionality, and, as we will see in a moment, we may not be able to take this retrospection at face value. Hence, we cannot be certain that there is a relation between how emotional an event was at the time of its occurrence and subsequent memory vividness. Second, the Reisberg et al. data (and, again, more recent, related ﬁndings) are in any case correlational, leaving questions about

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causal relationships. Indeed, Reisberg et al. also reported a strong correlation between memory vividness and how consequential the event was judged to have been (and also a correlation between rated emotionality and rated consequentiality), and this obviously clouds causal interpretation. If we can set these cautions aside, though, it does seem that emotional events will be recalled more vividly than other events and, hence, following Williams et al. (1996), will be more inﬂuential and more compelling in gauging the future than other events. In addition, the content of emotional memories (whether accurate or not) may be somewhat diﬀerent from that for neutral memories, and this, too, may matter for the function of these memories in problem solving, predicting the future, and the like. This diﬀerence in content is suggested by a result reported by Heuer and Reisberg (1990). They found that the number of intrusion errors made by participants was the same for emotional and neutral events, but the type of errors was diﬀerent. Participants who had viewed the neutral stimulus (about the boy visiting his mechanic father) tended to recall plot elements that had, in fact, not been mentioned. Participants who had viewed the emotional stimulus (with the boy visiting his surgeon father) tended to recall ‘psychological elements’—about how upset the boy was, for example, or how angry the mother was that her son had seen such gruesome sights. All of this leads us, then, to a by-now familiar message. We know a lot about memory for emotional events, but it is not diﬃcult to ﬁnd gaps in our knowledge, including our knowledge of the relationship between the emotionality of an event and how detailed, vivid, compelling, or coherent the memory for the event will be later on. In this setting, it is interesting to set psychologists’ inquiries into memory (and autobiographical memory in particular) side by side with the literary study of the genre of autobiography. In the study of this genre, there is ample discussion of how a recollection shapes someone’s values or character and discussion of how the qualities of a remembered event can compel someone to action, or fail to. Notably absent from this study, though, is much concern about the historical correctness of these memories; it is not the correctness that makes the memories formative or compelling. Perhaps psychologists would be well-advised to learn from this tradition—certainly not abandoning our research on memory accuracy but supplementing it with a rich and (perhaps) equally important set of questions about how emotion shapes memories in a way that can, in turn, mold who we are, how we will act, and what we will believe in the future. (For an important psychological foray into these issues, see Pillemer, 1998.)

Remembering the Emotion Itself Our concern about alternative approaches to emotional memory also leads us to another issue. Not only do we remember the content of an emotional event, we also remember our assessment of, and reactions to, the event. In particular,

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we remember how emotional the event was or was not for us, and this memory, in turn, can also be more or less accurate. For many people, introspection suggests that recall of prior feelings is immediate, long-lasting, and quite compelling. One may not remember much about a particular speaker’s lecture, but one remembers that the talk was boring; one may not recall the plot of a movie, but one remembers that it was quite funny; and so on. Despite these intuitions, however, evidence suggests that retrospective reports of emotionality are often reconstructions, inﬂuenced heavily by current assessments, and, in some cases, inaccurate. Of course, some memory for past feelings is rather accurate. For example, Safer, Bonanno, and Field (2001) surveyed participants whose spouse had died 6 months prior to the study. The participants reported their level of grief at the time of the survey and, then, roughly 4.5 years later, tried to recall their level of grief at the time of the survey. Safer et al. report that this recall was impressively accurate, although participants whose grief diminished relatively little over time did tend to overestimate their prior grief. It is important, though, that participants’ contemporary assessment of prior emotional events does change, so that the sting of past mishaps gradually fades, as does the glow of past triumphs. This pattern was documented by Walker et al. (1997), who asked participants to rate how they currently felt about previously experienced emotional events; these ratings were collected 3 months, 1 year, and 4.5 years after the target event. Walker et al. report that all the ratings became less extreme as time went on, and, interestingly, the unpleasantness of past humiliations and defeats faded more quickly than the pleasantness of past joys and celebrations. How do these changes in current assessment of an event inﬂuence the memory for the event? Some insight is provided by Levine’s (1997) study of how supporters of Ross Perot’s presidential campaign (in 1992) recalled their feelings upon hearing that Perot had withdrawn from the race and also their feelings upon hearing about Perot’s subsequent decision to rejoin the race. Levine reports that her participants showed frequent errors in how they recalled their past emotions but not (as some have suggested) a general tendency to overestimate past emotion. Instead, she found systematic distortions in emotion recall, bringing emotions-as-remembered into closer proximity to current appraisals. In short, it appears that her participants were to some extent reconstructing what their past emotions were likely to have been and were basing this reconstruction on their current emotions. A follow-up study found similar results in students’ recollection of their emotional reactions when they ﬁrst heard that O. J. Simpson had been acquitted of accusations that he had murdered his wife (Levine, Prohaska, Burgess, Rise, & Laulhere, 2001; also Levine & Safer, 2002). As time passed after the acquittal, Levine et al. found systematic changes in how people remembered their own emotional reactions, with these changes tending quite strongly toward bring-

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ing past emotions (as remembered) into alignment with current assessments. Thus, participants who had gradually grown angrier about the acquittal recalled their initial reaction as being angrier than it was; participants who had grown less upset recalled their initial reaction accordingly. A diﬀerent form of reconstruction of emotion, based on other cues, can also be observed in a shorter time scale. In one laboratory study, participants viewed photographs of faces while listening to sentences spoken in either a positive or negative tone of voice (Ochsner, Schacter, & Edwards, 1997). The faces themselves conveyed either positive or negative affect, albeit in a subtle way. In a subsequent memory test, participants were shown the faces once again and asked to recall the tone of voice in which the pictured person had spoken. The participants tended to recall the voice as having the same aﬀect as the picture—a memory illusion in which remembered-aﬀect is apparently reconstructed from other information, both perceptually given and drawn from memory. Other results show similar patterns, with aﬀect associated with one aspect of a stimulus altering (and in some cases distorting) how one remembers other aspects of the stimulus. For example, in a study by Hertel and Narvaez (1986), participants watched videotapes of conversations; memory was then tested (via a recognition test in one procedure, recall in another) for the speciﬁc words uttered in the conversation. Memory was clearly inﬂuenced by the emotional valence of the nonverbal gestures and facial expressions visible in the videotape (with the actual script held constant) in a fashion that suggested that the (nonverbal) aﬀect had inﬂuenced how participants remembered the gist of the conversation. (For a related result, see Nygaard & Lunders, 2002.) Surely, then, our memory for prior emotion (either experienced or observed) is based to some extent on reconstruction, and our memory for prior emotion can, in turn, shape how we recall other aspects of the event. These facts must be part of our broader account of how emotional events are remembered, but note that these facts also have methodological implications. We mentioned in the previous section that the data linking emotion to memory vividness rest on retrospective assessments of emotion; we now see good reason to be cautious about those assessments. Similarly, we will, in a later section, return to the topic of ﬂashbulb memories, and one of the issues there will be the role of emotion in forming such memories; many of the relevant studies, however, have relied on retrospective assessments of this emotion. For all of these reasons, we would be well served by an improved understanding of how emotion itself is recalled. Finally, one other complication should also be mentioned. Many events are likely not to be uniformly emotional; instead, they will have a mix of intense moments and less intense ones, moments of strong feelings interwoven with moments of relative calm. How will this changing proﬁle be reﬂected in memory? One might think that the subsequent memory will reﬂect some sort of ‘average’ of the emotion felt over the course of an event, but several studies suggest that this is not the case. Instead, people seem to retain just a few ‘snapshots’ of the overall

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event, and memory for the whole is dominated by the contents of these few snapshots. One snapshot seems to record the emotional peak of the target event— not surprisingly, since that peak is likely to be salient both in perception and in memory. Another snapshot seems to record the emotional ending of the event— again, not surprisingly, given what we know about recency eﬀects in memory (e.g., Reisberg, 2001). These two snapshots—the peak and the end—are then weighted heavily in subsequent recall of the event’s emotional meaning, so much so that the subsequent evaluation can be predicted almost entirely from evaluations of these two moments (Fredrickson & Kahneman, 1993; Kahneman, 2000; Schreiber & Kahneman, 2000). Certainly, though, further work is needed to explore how one derives a summary evaluation from these snapshots and then how one’s broader recollection of the target event is shaped by this summary evaluation.

Working Backward

From an Emotional Memory

One last perspective on emotional memories invites our attention, but it is a perspective we have already touched in passing. In thinking about memory for emotional events, it is tempting to begin with the event itself and ask: If someone experiences an event that makes him angry, or happy, or afraid, how will he remember the event later on? But we could plausibly reverse this logic and begin instead with a bit of emotional recall. In this case, we might ask: If someone remembers an emotional event, then what can we conclude from this recollection? This shift in perspective is important for a simple reason. Some instances of emotional remembering may be false, recording events that unfolded rather diﬀerently from the way they are recalled, or perhaps recording events that never happened at all. In other words, it is true that, if an emotional event occurs, there will likely be a memory corresponding to that event later on, and this memory is likely to be detailed and reasonably accurate. (This is a consequence of the positive eﬀects of emotion on memory, already discussed.) But the converse is not true. If an emotional event is recalled in vivid detail, it does not follow that there is likely to have been a prior event corresponding to the memory. Or, to put this succinctly, if there is an emotional event, then there will probably be an emotional memory for it; but if there is an emotional memory, there may (or may not) have been an emotional event. As illustrations, we have already mentioned that the intensity of emotion in an event may well be diﬀerent from the intensity as it is recalled (Levine, 1997; Levine et al., 2001). We have also mentioned the Neisser and Harsch (1992) data, in which students’ very emotional recollections of the space-shuttle explosion turned out to be wrong not just in detail but in major elements as well. Presumably, Neisser and Harsch’s participants were the victims of their own errors in reconstructing the earlier episode, and, ironically, emotional recollec-

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tion may be particularly vulnerable to this sort of error. To see why, imagine an event that was not considered noteworthy when it occurred, but which was later deemed consequential. One example might be a ﬁrst (and quite unremarkable) encounter between two people that later grew into an intense romance. A diﬀerent example might be a political event that seemed small at the time, but which marked the beginning of a gradual slide (visible only later) toward some triumph or some tragedy. In such cases, there is little reason to have encoded the initial event with great care, no reason to have paid special attention, no reason to have rehearsed the event, no arousal to promote memory consolidation. Yet, after the fact, there is ample reason to want to recall the event, and this will spur extra eﬀort toward reconstruction. Of course, without much initial encoding, information actually in memory will provide slim support for this reconstruction, leaving a large potential for schema-based inferences (which may or may not be correct) and intrusions from other, related, episodes. To explore these points, one would want a design in which two groups of individuals are exposed to a minor and emotionally bland episode and then led to recall the episode as best they can later on. Prior to the recall, however, one group would be exposed to information persuading them that the episode was, in fact, emotionally important in some fashion; this would tell us how, and how fully, perceived emotion inﬂuences memory reconstruction (its vividness, its completeness, its accuracy). To the best of our knowledge, however, no study of this sort has been conducted, despite the relevance of such a study to the ferocious debate over (potentially) false memories. The literature does contain hints on this topic—the diﬀerent types of intrusion errors for emotional and neutral memories (e.g., Heuer & Reisberg, 1990) or the impact of diﬀerent story outcomes on how a story is recalled (e.g., Spiro, 1980)—but, unmistakably, this is another topic crying out for empirical pursuit.

Flashbulb Memories Revisited We began this chapter with a mention of ﬂashbulb memories, and it will be useful to return to this topic in light of the wide range of issues we have now considered. We know that these memories are vivid, detailed, and long-lasting, reasonably accurate in many circumstances (e.g., Conway et al., 1994; McCloskey, Wible, & Cohen, 1988) but also sometimes error-ﬁlled (e.g., Neisser & Harsch, 1992). What produces this pattern? Why are some ﬂashbulb events remembered accurately, while others are not? As a number of authors have noted, several factors are relevant (cf. Conway, 1995; Finkenauer et al., 1998). One is the timing of the memory tests—that is, when the initial recording of the event occurs and then when the follow-up testing takes place (e.g., Winningham, Hyman, & Dinnel, 2000). It may also matter whether, how, and how often the ﬂashbulb event is discussed—for example, as part of the routine “sharing” of special memories that people often do (e.g., Philippot & Rime, 1998; Rime, Philippot,

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Boca, & Mesquita, 1992). Another, and crucial, factor is the consequentiality of the remembered event, with consequential ﬂashbulb events (e.g., Margaret Thatcher’s resignation, for many in England, or the 1989 Santa Clara earthquake, for those living near the epicenter) remembered more accurately than less consequential events such as Thatcher’s resignation for those living in the United States or the earthquake for those living far from the epicenter (Conway et al., 1994; Neisser, 1996). This is perhaps an unsurprising result. Consequentiality will motivate close attention and will spur rehearsal; consequentiality is also likely to be associated with stronger emotion and thus will invite emotion’s overall positive contribution to remembering (see Finkenauer et al., 1998, for a more extensive discussion of emotion’s role in ﬂashbulb formation). In short, then, ﬂashbulb memories—like other memories—tend to be accurate but are not always accurate. Flashbulb memories, like other memories, fade with the passage of time, are promoted by rehearsal, are enhanced if the eventas-experienced is consequential. In these (and other) regards, ﬂashbulb memories seem qualitatively similar to other emotional memories and so, despite early claims to the contrary, are almost surely not in a class by themselves.

Conclusions The main points of this chapter are relatively easy to describe. In general, emotion seems to have a positive eﬀect on memory, increasing memory vividness, accuracy, completeness, and longevity. But emotion’s eﬀects are not uniformly positive. Many emotional events contain a prominent visual stimulus, and, if so, emotion seems to promote a focus on this stimulus in a fashion that impairs memory for the event’s periphery. Emotion assigned to an event after the fact may also spur memory reconstruction based on too little information, and this may foster reconstructive error. And, ﬁnally, extremely intense emotion may work against memory, perhaps by interrupting the biological processes needed for memory consolidation. This summary of the evidence reﬂects considerable progress over the last 50 years, progress that has included the accumulation of a large quantity of data and has also included questions that have arisen in the literature and then been resolved to the satisfaction of many investigators (e.g., the “special status” of ﬂashbulb memories). This progress has also included evidence that directly challenges some long-held and often-quoted claims, including the Yerkes-Dodson function and the Easterbrook notion that arousal directly leads to memory narrowing. At the same time, though, the progress on these various fronts has helped highlight the gaps in what we know about memory for emotional events. In this chapter, we have considered the distinction between events that are visually arousing and those that are thematically arousing, but in truth the data pertinent to this distinction are few. We have also considered how people remember

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events that are emotionally positive or how the exact content of an emotional memory might be inﬂuenced by the particular emotion in place during an event. On these points, too, we know far less than we might wish. Other issues are also largely untouched, including the nature of intrusion errors in memory for emotional events, emotion’s inﬂuence on our eﬀorts toward reconstructing a poorly remembered past event, and emotion’s role in shaping the sorts of memory detailedness that seem to matter for problem solving and the generation of hope. Finally, also in need of elaboration is the exact role that arousal plays in shaping emotional memories. We have considered evidence that arousal may be necessary but not suﬃcient for producing emotion’s memory eﬀects, and the mechanisms behind this pattern need to be speciﬁed. We close, therefore, simultaneously celebrating what we know about emotional remembering and showcasing the work still to be done. We have come a long way in the last 50 years, and the knowledge we have gained provides a rich base for now tackling the questions currently before us.

References Adolphs, R., Cahill, L., Schul, R., & Babinsky, R. (1997). Impaired declarative memory for emotional material following bilateral amygdala damage in humans. Learning & Memory, 4, 291–300. Anderson, K. J. (1990). Arousal and the inverted-U hypothesis: A critique of Neiss’s “Reconceptualizing arousal.” Psychological Bulletin, 107, 96–100. Arrigo, J. M., & Pezdek, K. (1997). Lessons from the study of psychogenic amnesia. Current Directions in Psychological Science, 6, 148–152. Berntsen, D. (2002). Tunnel memories for autobiographical events: Central details are remembered more frequently from shocking than happy experiences. Memory & Cognition, 30, 1010–1020. Bluck, S., & Li, K. Z. H. (2001). Predicting memory completeness and accuracy: Emotion and exposure in repeated autobiographical recall. Applied Cognitive Psychology, 15, 145–158. Bohannon, J. N. (1988). Flashbulb memories of the space shuttle disaster: A tale of two theories. Cognition, 29, 179–196. Bornstein, B. H., Liebel, L. M., & Scarberry, N. C. (1998). Repeated testing in eyewitness memory: A means to improve recall of a negative emotional event. Applied Cognitive Psychology, 12, 119–132. Bower, G. H. (1992). How might emotions aﬀect learning? In S.-Å. Christianson (Ed.), The handbook of emotion and memory: Research and theory (pp. 3–32). Hillsdale, NJ: Erlbaum. Brewer, W. F. (1988). Memory for randomly sampled autobiographical events. In U. Neisser & E. W. Winograd (Eds.), Remembering reconsidered (pp. 21–90). Cambridge: Cambridge University Press. Brown, R., & Kulik, J. (1977). Flashbulb memories. Cognition, 5, 73–99. Burke, A., Heuer, F., & Reisberg, D. (1992). Remembering emotional events. Memory & Cognition, 20, 277–290.

36

  

Cahill, L., Prins, B., Weber, M., & McGaugh, J. (1994). ß-Adrenergic activation and memory for emotional events. Nature, 371, 702–704. Canli, T., Zhao, Z., Brewer, J., Gabrieli, J. D. E., & Cahill, L. (2000). Event-related activation in the human amygdala associates with later memory for individual emotional response. Journal of Neuroscience, 20, RC99. Christianson, S.-Å. (1992). Emotional stress and eyewitness memory: A critical review. Psychological Bulletin, 112, 284–309. Christianson, S.-Å., & Loftus, E. (1991). Remembering emotional events: The fate of detailed information. Cognition & Emotion, 5, 81–108. Christianson, S.-Å., & Mjörndal, T. (1985). Adrenalin, emotional arousal, and memory. Scandinavian Journal of Psychology, 26, 237–248. Christianson, S.-Å., Nilsson, L.-G., Mjörndal, T., Perris, C., & Tjellden, G. (1986). Psychological versus physiological determinants of emotional arousal and its relation to laboratory induced amnesia. Scandinavian Journal of Psychology, 27, 300–310. Clark, M. S., Milberg, S., & Ross, J. (1983). Arousal cues arousal-related material in memory: Implications for understanding eﬀects of mood on memory. Journal of Verbal Learning and Verbal Behavior, 11, 671–684. Cliﬀord, B., & Scott, J. (1978). Individual and situational factors in eyewitness testimony. Journal of Applied Psychology, 63, 352–359. Conway, M., Anderson, S., Larsen, S., Donnelly, C., McDaniel, M., McClelland, A. G. R., et al. (1994). The formation of ﬂashbulb memories. Memory & Cognition, 22, 326–343. Conway, M. A. (1995). Flashbulb memories. Hillsdale, NJ: Erlbaum. Davidson, D., Luo, Z., & Burden, M. J. (2001). Children’s recall of emotional behaviours, emotional labels, and nonemotional behaviours: Does emotion enhance memory? Cognition & Emotion, 15, 1–26. Deﬀenbacher, K. (1994). Eﬀects of arousal on everyday memory. Human Performance, 7, 141–161. Dietrich, D. E., Waller, C., Johannes, S., Wieringa, B. M., Emrich, H. M., & Muente, T. F. (2001). Diﬀerential eﬀects of emotional content on event-related potentials in word recognition memory. Neuropsychobiology, 43, 96–101. Easterbrook, J. A. (1959). The eﬀect of emotion on cue utilization and the organization of behavior. Psychological Review, 66, 183–201. Fazey, J. A., & Hardy, L. (1988). The inverted-U hypothesis: A catastrophe for sport psychology. British Association for Sports Sciences Monograph No. 1. Leeds, England: National Coaching Foundation. Finkenauer, C., Luminet, O., Gisle, L., El-Ahmadi, A., van der Linden, M., & Philippot, P. (1998). Flashbulb memories and the underlying mechanisms of their formation: Toward an emotional-integrative model. Memory & Cognition, 26, 516–531. Fredrickson, B., & Kahneman, D. (1993). Duration neglect in retrospective evaluations of aﬀective episodes. Journal of Personality and Social Psychology, 65, 45–55. Gold, P. E. (1989). Neurobiological features common to memory modulation by many treatments. Animal Learning & Behavior, 17, 94–100. Gold, P. E. (1992). A proposed neurological basis for regulating memory storage for signiﬁcant events. In E. Winograd & U. Neisser (Eds.), Aﬀect and accuracy in re-

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call: Studies of ‘ﬂashbulb’ memories (pp. 141–161). New York: Cambridge University Press. Hall, J., Gonder-Frederick, L., Chewning, W., Silveira, J., & Gold, P. (1989). Glucose enhancement of memory in young and aged humans. Neuropsychologia, 27, 1129–1138. Hamann, S. B., & Ely, T. D. (1999). Amygdala activity related to enhanced memory for pleasant and aversive stimuli. Nature Neuroscience, 2, 289–293. Hertel, P. T., & Narvaez, A. (1986). Confusing memories for verbal and nonverbal communication. Journal of Personality and Social Psychology, 50(3), 474– 481. Heuer, F. (1987). Remembering detail: The role of emotion in long-term memory. Unpublished doctoral dissertation, New School for Social Research. Heuer, F., & Reisberg, D. (1990). Vivid memories of emotional events: The accuracy of remembered minutiae. Memory & Cognition, 18, 496–506. Heuer, F., Reisberg, D., & Rios, C. (1997). The memory eﬀects of thematically induced emotion. In D. G. Payne & F. Conrad (Eds.), Intersections in basic and applied memory research (pp. 113–132). Hillsdale, NJ: Erlbaum. Intraub, H., & Richardson, M. (1989). Wide-angle memories of close-up scenes. Journal of Experimental Psychology: Learning, Memory & Cognition, 15, 179–187. Jones, E. B., O’Gorman, J. G., & Byrne, B. (1987). Forgetting of word associates as a function of recall interval. British Journal of Psychology, 78, 79–89. Kahneman, D. (2000). Evaluation by moments: Past and future. In D. Kahneman & A. Tversky, A. (Eds.), Choices, values and frames (pp. 693–708). New York: Cambridge University Press. Kramer, T., Buckhout, R., & Eugenio, P. (1990). Weapon focus, arousal and eyewitness memory: Attention must be paid. Law and Human Behavior, 14, 167–184. Laney, C., Heuer, F., & Reisberg, D. (in press). Exploring the contrast between thematically-induced and visually-induced emotion. Applied Cognitive Psychology. Levine, L. J. (1997). Reconstructing memory for emotions. Journal of Experimental Psychology: General, 126, 165–177. Levine, L. J., & Burgess, S. L. (1997). Beyond general arousal: Eﬀects of speciﬁc emotions on memory. Social Cognition, 15, 157–181. Levine, L. J., Prohaska, V., Burgess, S. L., Rice, J. A., & Laulhere, T. M. (2001). Remembering past emotions: The role of current appraisals. Cognition & Emotion, 15(4), 393–417. Levine, L. J., & Safer, M. A. (2002). Sources of bias in memory for emotions. Current Directions in Psychological Science, 11, 169–173. Libkuman, T. M., Nichols-Whitenead, P., Griﬃth, J., & Thomas, R. (1999). Source of arousal and memory for detail. Memory & Cognition, 27, 166–190. Linton, S. J., & Melin, L. (1982). The accuracy of remembering chronic pain. Pain, 13, 281–285. Loftus, E., & Burns, T. (1982). Mental shock can reproduce retrograde amnesia. Memory & Cognition, 10, 318–323. Loftus, E., Loftus, G., & Messo, J. (1987). Some facts about “weapon focus.” Law and Human Behavior, 11, 55–62.

38

  

Maass, A., & Köhnken, G. (1989). Eyewitness identiﬁcation. Law and Human Behavior, 13, 397–408. Manning, C., Hall, J., & Gold, P. (1990). Glucose eﬀects on memory and other neuropsychological tests in elderly humans. Psychological Science, 1, 307–311. McCloskey, M., Wible, C. G., & Cohen, N. J. (1988). Is there a special ﬂashbulbmemory mechanism? Journal of Experimental Psychology: General, 117, 171– 181. McGaugh, J. L. (2000). Memory—A century of consolidation. Science, 287, 248–251. McGaugh, J. L., Intoini-Collision, I. B., Cahill, L. F., Castellenano, C., Dalmaz, C., Parent, M. B., et al. (1993). Neuromodulatory systems and memory storage: Role of the amygdala. Behavioral Brain Research, 58, 81–90. Moyer, M. (2002). Polyanna revisited: Do we remember equally the good and the bad? Unpublished B.A. thesis, Reed College, Portland, Oregon. Neiss, R. (1990). Ending arousal’s reign of error: A reply to Anderson. Psychological Bulletin, 107, 101–105. Neisser, U. (1996). Remembering the earthquake: Direct experience vs. hearing the news. Memory, 4, 337–358. Neisser, U., & Harsch, N. (1992). Phantom ﬂashbulbs: False recollections of hearing the news about Challenger. In E. Winograd & U. Neisser (Eds.), Aﬀect and accuracy in recall: Studies of ‘ﬂashbulb’ memories (pp. 9–31). Cambridge: Cambridge University Press. Nosaka, A. (Writer), Takahata, I. (Director), & Sato, R. (Producer). (1988). Graveyard of the ﬁreﬂies [DVD]. Central Park Media Corporation, USA. Nygaard, L. & Lunders, E. (2002). Resolution of lexical ambiguity by emotional tone of voice. Memory & Cognition, 30, 583–593. Ochsner, K. N., Schacter, D. L., & Edwards, K. (1997). Illusory recall of vocal aﬀect. Memory, 5, 433–455. Öhman, A., Flykt, A., & Esteves, F. (2001). Emotion drives attention: Detecting the snake in the grass. Journal of Experimental Psychology: General, 130, 466–478. Padilla-Walker, L. & Poole, D. (2002). Memory for previous recall: A comparison of free and cued recall. Applied Cognitive Psychology, 16, 515–524. Peters, D. (1988). Eyewitness memory and arousal in a natural setting. In M. Gruneberg, P. Morris, & R. Sykes (Eds.), Practical aspects of memory: Current research and issues (pp. 89–94). New York: John Wiley. Peterson, C., & Whalen, N. (2001). Five years later: Children’s memory for medical emergencies. Applied Cognitive Psychology, 15(7), S7–S24. Philippot, P., & Rime, B. (1998). Social and cognitive processing in emotion: A heuristic for psychopathology. In W. F. Flack, Jr. & J. D. Laird (Eds.), Emotions in psychopathology: Theory and research. Series in aﬀective science (pp. 114–129). New York: Oxford University Press. Pickel, K. L. (1998). Unusualness and threat as possible causes of “weapon focus.” Memory, 6, 277–295. Pillemer, D. B. (1984). Flashbulb memories of the assassination attempt on President Reagan. Cognition, 16, 63–80. Pillemer, D. B. (1998). Momentous events, vivid memories. Cambridge, MA: Harvard University Press.

   

39

Pillemer, D., Goldsmith, L. Panter, A., & White, S. (1988). Very long-term memories of the ﬁrst year in college. Journal of Experimental Psychology: Learning, Memory and Cognition, 14, 709–715. Porter, S., & Birt, A. (2001). Is traumatic memory special? A comparison of traumatic memory characteristics with memory for other emotional life experiences. Applied Cognitive Psychology, 15, S101–S117. Read, J. D., & Lindsay, D. S. (2000). “Amnesia” for summer camps and high school graduation: Memory work increases reports of prior periods of remembering less. Journal of Traumatic Stress, 13, 129–147. Reisberg, D. (2001). Cognition: Exploring the science of the mind. 2nd ed. New York: W. W. Norton. Reisberg, D., Heuer, F., McLean, J., & O’Shaughnessy, M. (1988). The quantity, not the quality, of aﬀect predicts memory vividness. Bulletin of the Psychonomic Society, 26, 100–103. Rime, B., Philippot, P., Boca, S., & Mesquita, B. (1992). Long-lasting cognitive and social consequences of emotion: Social sharing and rumination. In W. Stroebe & M. Hewstone (Eds.), European review of social psychology, Vol. 3 (pp. 225–258). New York: John Wiley. Rubin, D. C., & Kozin, M. (1984). Vivid memories. Cognition, 16, 81–95. Safer, M. A., Bonanno, G. A., & Field, N. P. (2001). “It was never that bad”: Biased recall of grief and long-term adjustment to the death of a spouse. Memory, 9, 195–204. Safer, M. A., Christianson, S.-Å., Autry, M. W., & Österlund, K. (1998). Tunnel memory for traumatic events. Applied Cognitive Psychology, 12, 99–118. Schmidt, S. R., & Williams, A. R. (2001). Memory for humorous cartoons. Memory & Cognition, 29, 305–311. Schooler, J., Bendriksen, M., & Amadar, Z. (1997). Recovered memories and false memories. Oxford: Oxford University Press. Schreiber, C., & Kahneman, D. (2000). Determinants of the remembered utility of aversive sounds. Journal of Experimental Psychology: General, 129, 27–42. Shobe, K. K., & Kihlstrom, J. F. (1997). Is traumatic memory special? Current Directions in Psychological Science, 6, 70–74. Spiro, R. J. (1980). Accommodative reconstruction in prose recall. Journal of Verbal Learning and Verbal Behavior, 19, 84–95. Stanny, C. J., & Johnson, T. C. (2000). Eﬀects of stress induced by a simulated shooting on recall by police and citizen witnesses. American Journal of Psychology, 113, 359–386. Steblay, N. J. (1992). A meta-analytic review of the weapon focus eﬀect. Law and Human Behavior, 16, 413–424. Takahashi, H. (Director), & Asari, S. W. (Producer). (1996). Magic User’s Club: I’ll follow you [DVD]. Bandai Visual Corporation, Inc. Walker, W. R., Vogl, R. J., & Thompson, C. P. (1997). Autobiographical memory: Unpleasantness fades faster than pleasantness. Applied Cognitive Psychology, 11, 399–414. Wessel, I., & Merckelbach, H. (1997). The impact of anxiety on memory for details in spider phobics. Applied Cognitive Psychology, 11, 223–232.

40

  

Wessel, I., & Merckelbach, H. (1998). Memory for threat-relevant and threatirrelevant cues in spider phobics. Cognition & Emotion, 12, 93–104. Wessel, I., van der Kooy, P., & Merckelbach, H. (2000). Diﬀerential recall of central and peripheral details of emotional slides is not a stable phenomenon. Memory, 8, 95–109. White, N. M. (1991). Peripheral and central memory-enhancing actions of glucose. In R. C. A. Frederickson, J. L. McGaugh, & D. L. Felten (Eds.), Peripheral signalling of the brain: Neural, immune and cognitive function (pp. 421–441). Toronto: Hogrefe and Huber. Williams, J. M. G., Ellis, N. C., Tyers, C., Healy, H., Rose, G., & MacLeod, A. (1996). The speciﬁcity of autobiographical memory and imageability of the future. Memory & Cognition, 24, 116–125. Williams, L. M. (1995). Recovered memories of abuse in women with documented child sexual victimization histories. Journal of Traumatic Stress, 8, 649–673. Winningham, R. G., Hyman, I. E., Jr., & Dinnel, D. L. (2000). Flashbulb memories? The eﬀects of when the initial memory report was obtained. Memory, 8, 209– 216. Yerkes, R., & Dodson, J. (1908). The relation of strength of stimulus to rapidity of habit-formation. Journal of Comparative Neurology of Psychology, 18, 459–482.

   

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2

        .    

A

re there special neural mechanisms to account for our memories for emotional events? In the service of a species’ survival, has evolution equipped organisms with a specialized set of mechanisms that encode, consolidate, and retrieve memories in a domain-speciﬁc manner, operating diﬀerentially in emotional and in nonemotional contexts? Indeed, evidence from cognitive psychology and neuroscience suggests that such distinct emotional memory mechanisms exist and depend on speciﬁc neural structures that we will review. The uncommon vividness and (presumed) accuracy of ﬂashbulb memories led Brown and Kulik (1977) to suggest that autobiographical memories surrounding the learning of emotionally arousing information relied on a unique memory process. These authors speculated that encountering emotionally salient events resulted in enhanced activity in the brainstem’s reticular formation, leading to a “now-print” mechanism that permanently ﬁxed memories of these events—in addition to autobiographical ephemera accompanying them— in memory (Brown & Kulick, 1977; Schooler & Eich, 2000). More recent research has revised this proposal somewhat and indicates that while such memories can indeed be vivid, their accuracy is modest at best and often distorted (see Schmolck, Buﬀalo, & Squire, 2000). Though “ﬂashbulb memories” are no longer held to be a qualitatively diﬀerent kind of memory, the broader notion of emotional memories complements earlier ideas that such memories are typically experienced with special vividness and personal meaning and that there is evidence for specialized processes that subserve them. The current taxonomy of memory systems describes distinct neural mechanisms for declarative and nondeclarative memory processing (Squire & Kandel, 2000). The medial temporal lobe memory system—including the hippocampal formation as well as the overlying cortex—is known to be integral to the forma-

42

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42

tion and consolidation of declarative memories (or relational memories; see Eichenbaum & Cohen, 2001), whereas nondeclarative memories depend on regions outside the medial temporal lobe. This classic taxonomy distinguishes memory systems on the basis of their mode of operation—in what way they are acquired and in what way they are accessible to guide behavior. Of the other ways of distinguishing memory systems, two are important to operationalizing the term “emotional memory”: (1) systems directly involved in memory versus those having a modulatory role and (2) systems diﬀerentially involved depending on the nature of the material processed (domain-speciﬁc). Emotional memory concerns a speciﬁc domain of declarative memory, namely, memory for events or stimuli that are themselves emotional or that occurred in an emotional context. Emotional memory encompasses the enhancement of memory (assessed by, for example, a recognition test) for stimuli that are emotionally arousing (e.g., pictures of mutilated faces) compared to memory for stimuli that are emotionally neutral (e.g., pictures of neutral faces); it also includes the enhancement of memory for neutral faces that were encoded in an emotionally arousing context compared to a neutral context; and it even includes the possible repression of memory for faces associated with extremely traumatic events (a controversial possibility). Our review focuses on the facilitative eﬀects of emotion on declarative memory rather than its possible suppressive eﬀects. As such, memory for the mutilated faces may be a particularly potent declarative memory, relying on the medial temporal lobe system just as in memory for neutral faces. This eﬀect, though well described, needs to be distinguished from the equally well-described eﬀects of chronic stress and severely traumatic context on memory; in those cases, declarative memory is also modulated but in a qualitatively diﬀerent way. We thus envision a nonmonotonic relationship of emotional arousal to memory accuracy. Mild to moderate, and transient, emotional arousal generally enhances memory; severe or chronic emotional arousal instead suppresses and distorts memory. Though emotional arousal can be mapped on a continuum, its eﬀects on declarative memory are not linear [see chapters 1, 3, and 8 for more discussion of this topic—Eds.]. Another important distinction concerns the eﬀects of emotional arousal triggered by properties that are intrinsic to the stimuli being encoded (e.g., memory for pictures of mutilations) versus eﬀects provided by a context (e.g., memory for neutral pictures encoded in a highly arousing context). Again, without going into detail, our view is that the two engage equivalent mechanisms and lead to similar eﬀects when the emotional arousal relates to the stimulus. They may lead to diﬀerent eﬀects when the emotional arousal is irrelevant to the stimulus (see chapter 1). As a ﬁnal note, and to avoid any confusion, we emphasize that we use “emotional memory” to refer to declarative memory for emotional stimuli (where “emotional stimuli” means stimuli that induce an emotion in those who perceive

      

43

the stimuli—either as a result of intrinsic properties of the stimuli themselves or as a result of an emotional context related to the stimuli). This usage diﬀers from another usage of the term, especially in animal studies, as a form of nondeclarative memory (e.g., fear conditioning). Thus, classical fear conditioning has been occasionally referred to as emotional memory, and in a sense, it is that. But we do not use the term that way here. What neural structures are involved in making emotionally arousing stimuli more memorable than neutral stimuli? Are these structures in some way specialized to process emotional memory? And what mechanisms do such structures implement—in particular, do they modulate declarative memory at the level of encoding, consolidation, or retrieval? These questions will be the focus of this chapter. We will emphasize the role of the human amygdala in the enhancement of memory for emotional events through its inﬂuence over medial temporal lobe structures and other neural regions; we will also survey several other structures that may participate in emotional memory.

Emotional Memory in

Nonhuman Animals

Much of the human research presented in this chapter is predicated on animal research, speciﬁcally work in rats and nonhuman primates. In this section, we review some of the studies in animals, but the breadth of this work is beyond the scope of this chapter. We encourage the reader to look elsewhere for a comprehensive review of the literature on the topic (Baxter & Murray, 2000; Eichenbaum & Cohen, 2001; LeDoux, 2000; McGaugh, 2000). By virtue of its location in the brain, for many years the amygdala has been the focus of much interest as a possible site of learning and memory (Squire, 1987). It was originally thought to play an integral role in the formation of declarative memories, together with other proximal structures in the medial temporal lobe. More careful study has revealed the role of the amygdala to be separate from the traditional ‘medial temporal lobe memory system’ that includes the hippocampus and adjacent cortex (Murray, 1992; Zola-Morgan, Squire, Alvarez-Royo, & Clower, 1991; Zola-Morgan, Squire, & Amaral, 1986). Following the initial characterization of the memory deﬁcits of the famous patient H. M. (Scoville & Milner, 1957), considerable work went into developing a nonhuman primate model of amnesia through lesions of the medial temporal lobe (see Eichenbaum & Cohen, 2001, for a review of these initial studies). Typically, these early studies used a surgical approach similar to that used in patient H. M. Namely, the entire medial temporal lobe of the monkeys was removed, including the amygdala, hippocampus, and surrounding cortical regions: the entorhinal, parahippocampal, and perirhinal cortices. After the successful development of a nonhuman primate model of

44

  

amnesia, work began on delineating the role of the individual anatomical components of the medial temporal lobe in the amnesic animal. This work led to the ﬁnding that circumscribed lesions of the amygdala (sparing the surrounding cortical areas) do not produce the amnesic eﬀects produced by damage to other medial temporal structures, such as the hippocampus and entorhinal cortex (Zola-Morgan et al., 1991; Zola-Morgan, Squire, & Amaral, 1989). This is not to say that these lesions have no behavioral or mnemonic eﬀects. Many of these animals displayed altered emotional behavior reminiscent of a subset of the symptoms described by Klüver and Bucy in the 1930s (1937; see also Brown & Schafer, 1888, and Weiskrantz, 1956), such as increased visual and oral inspection of potentially threatening objects and increased tameness. These studies by Zola-Morgan and colleagues showed that reduced declarative memory performance after damage to the medial temporal lobe cannot be due to amygdala damage per se. Whereas studies in nonhuman primates showed that the amygdala is not necessary for the formation of new declarative memories, earlier work in rats had begun to elucidate the modulatory role that the amygdala plays in memory formation. For the purposes of this review, we will focus on the role of the amygdala in the modulation of long-term declarative memories and refer the reader to other reviews (Davis, 1997; LeDoux, 2000) for coverage of the amygdala’s role in nondeclarative forms of emotional memory, such as Pavlovian fear conditioning. Perhaps the ﬁrst indication of the amygdala’s modulatory role in memory came from studies of the eﬀects of electrical stimulation of the rodent amygdala. Goddard (1964) demonstrated that amygdala stimulation following aversive training resulted in reduced memory for the training period, pointing to a role in the modulation of consolidation rather than a direct role in memory formation. Subsequent work showed that amygdala stimulation could either reduce or enhance the consolidation of previously learned materials depending on the intensity of the stimulation (Gold, Hankins, Edwards, Chester, & McGaugh, 1975; McGaugh, 2000), possibly analogous to the nonmonotonic relation between emotional arousal and human declarative memory that we brieﬂy alluded to in the introduction. The neurobiology of this phenomenon has subsequently been the focus of much research. Based on this work, we now know that key components through which the amygdala modulates declarative memory include the stress hormones epinephrine and corticosterone, as well as noradrenergic, GABAergic, glutamatergic, and peptidergic neurotransmission within the amygdala (McGaugh, 2000; Roozendaal, 2000; Tomaz et al., 1993). Hormonal modulation of memory storage has been a major focus of study in physiological psychology (McGaugh, 1983). Many of the behavioral paradigms used to study learning and memory in the rat are suﬃciently stressful to result in the release of the adrenal hormones epinephrine and corticosterone. Gold and van Buskirk (1975) showed that the administration of epinephrine after a learning episode enhanced memory for that episode. Numerous studies have replicated this ﬁnding using both endogenous and exogenous manipulation of epinephrine.

      

45

Similarly, corticosterone manipulation has shown that this hormone plays a modulatory role in memory (Roozendaal, 2000). The mechanism of action of these hormones on memory function appears to be at the level of the amygdala (McGaugh, 2000). Manipulations such as amygdala lesions or blockade of either the ß-adrenergic receptor (Liang, Juler, & McGaugh, 1986) or the glucocorticoid receptor (Oitzl & de Kloet, 1992) in the amygdala block the memory-enhancing eﬀects of emotional arousal. The ﬁnal common pathway of the eﬀects of these hormones on memory appears to be noradrenergic neurotransmission within and originating from the amygdala (McGaugh, 2000). Blockade of ß-adrenergic activity within the amygdala blocks the memory-enhancing eﬀects of both epinephrine (Liang et al., 1986) and corticosterone (Roozendaal, Williams, & McGaugh, 1999). The relationships among epinephrine, the amygdala, and memory are somewhat complicated, since peripheral epinephrine does not cross into the brain, but instead exerts its eﬀects via the release of glucose (Gold & van Buskirk, 1975) or via neural transmission of body-state information through the vagus nerve (Clark, Krahl, Smith, & Jensen, 1995; Clark, Naritoku, Smith, Browning, & Jensen, 1999). The amygdala is not involved in all aspects of the memory but only inﬂuences other regions, such as the hippocampus and striatum (Packard & Teather, 1998), during emotional arousal and during a speciﬁc time window in consolidation (Bianchin, Mello e Souza, Medina, & Izquierdo, 1999). Inactivation of the amygdala does not block the memory for an emotionally arousing event once established (Packard, Cahill, & McGaugh, 1994), suggesting that the memory trace per se does not depend on the amygdala. As we said in the introduction, an important issue in relation to the eﬀects of emotion on long-term memory is the well-documented deleterious eﬀects of stress on memory. (A full account of the eﬀects of stress on cognitive function is beyond the scope of this chapter; a brief explanation follows.) We think of emotion as a transient state (on the order of msec to seconds) during which physiological response systems are activated in preparation for action; stress, on the other hand, is a more prolonged physiological perturbation due to a challenge to homeostasis (see Lovallo, 1997; McEwen, 2000). The onset of a stressful experience likely involves the experience of negative emotion, often characterized by a lack of control (Lovallo, 1997). The more prolonged nature of stress may result in a completely diﬀerent pattern of eﬀects on physiology and behavior. One might think of this relationship as analogous to the Yerkes-Dodson law (1908), which is characterized by an inverted-U-shaped eﬀect wherein midrange levels of emotion are beneﬁcial to memory whereas higher, more prolonged emotional experience may result in stress and subsequently impaired memory performance. Considerable research has documented just such a relationship between stress and memory performance in animals and humans (see Lupien & Lepage, 2001; McEwen & Sapolsky, 1995). This inverted-U eﬀect likely does not operate within the realm of emotional memory that we refer to in this chapter (see chapter 1 for a discussion of this topic); instead, the descending limb of the inverted-U—at which point

46

  

memory would be deleteriously aﬀected—corresponds to the onset of stress eﬀects on memory. The relationships among emotion, stress, and memory are quite complicated and the focus of much research. Throughout this chapter, we focus primarily on the eﬀects of emotion on memory. We refer the reader to one of many recent reviews on the topic of stress and memory for full coverage of this fascinating topic (see de Kloet, Oitzl, & Joels, 1999; Kim & Diamond, 2002; Lupien & Lepage, 2001; see also chapter 3 in this volume). Results from these studies suggest that a special neurobiological system— relying on the amygdala and stress hormones—is active during arousing learning situations to enhance memory for these events. The role of the amygdala, then, is not in the storage of emotional memories but in the modulation of other neural structures that directly implement such storage. During emotional arousal, the amygdala increases its modulatory eﬀect and, together with the inﬂuence of peripheral stress hormones, modulates other neural structures such as the hippocampus and striatum to enhance the memory trace for emotional events. This animal research has served as a basis for much of the work in the neuropsychology of human emotional memory. Are the same neural mechanisms outlined in nonhuman primates and rodents applicable to the study of human emotional memory in the laboratory? The answer to this question will be the focus of the remainder of this chapter.

The Human Amygdala

and Emotional Memory

Lesion Studies For most brain-behavior relationships, our initial source of information on the role of the brain in human behavior, as well as on the relationship between the amygdala and emotional declarative memories, has come from patients with speciﬁc brain lesions. Though selective bilateral lesions of the amygdala are rare, the few reported cases are illustrative. In addition to bilateral temporal lobectomies—which are no longer performed due to the profound amnesia produced in patient H. M. (Scoville & Milner, 1957)—two disorders have been described that result in the bilateral destruction of the amygdala: Urbach-Wiethe disease and herpes simplex encephalitis. Urbach-Wiethe disease (also known as lipoid proteinosis) is a rare hereditary disorder characterized by the deposition of hyaline material in the skin and mouth areas and is associated with bilateral mineralization of medial temporal lobe structures in about half of the cases, with speciﬁc mineralization of the amygdala in some cases. Herpes simplex encephalitis is an inﬂammation of neural structures following viral infection. Even though this disease may result in widespread pathology throughout the nervous system, its earliest pathology almost invariably includes the amygdalae. Additionally,

      

47

unilateral temporal lobectomy is commonly employed in the surgical treatment of intractable epilepsy. Here, we report on studies of long-term declarative memory of emotional events from subjects with both bilateral and unilateral amygdala damage. Bilateral Amygdala Damage One well-characterized case of bilateral amygdala damage was originally reported by Tranel and Hyman (1990). The patient (SM046) had been diagnosed with Urbach-Wiethe disease. Computerized tomography (CT) and magnetic resonance imaging (MRI) conﬁrmed the mineralization of both amygdalae, as well as minimal damage to anterior entorhinal cortices, but no other structural abnormality, an anatomical picture conﬁrmed by functional imaging. Neuropsychological evaluation of this patient revealed normal general intellect, language, and verbal memory function. These results are in stark contrast to the profound declarative memory impairment following hippocampal damage (Squire, 1987). Follow-up research with patient SM046 and others with amygdala damage has highlighted the modulatory role in memory played by the amygdala. Markowitsch and colleagues examined emotional memory formation in two patients with Urbach-Wiethe disease, including bilateral mineralization of the amygdala (Babinsky et al., 1993; Markowitsch et al., 1994). Neuropsychological evaluation revealed that though neither patient was amnesic, they showed reduced performance on several standard neuropsychological tests of memory (e.g., Auditory Verbal Learning Test). Memory for emotional material was similarly depressed, with one patient (C. P.) showing more impairment than the other (B. P.). Speciﬁcally, in a word stem completion task of previously presented emotional or neutral words, C. P. remembered the neutral words better than the emotional words, whereas B. P. showed roughly equivalent performance for neutral and emotional stimuli, as compared to control subjects who tended to remember the emotional stimuli better. Similarly, in a recognition test of previously presented emotional pictures, C. P. recognized neutral pictures better than emotional pictures in contrast to normal controls who showed enhanced recognition performance of the emotional materials. Testing one of the same patients previously mentioned (B. P.), Cahill, Babinsky, Markowitsch, and McGaugh (1995) showed that this patient did not show the normal enhancement of memory for an emotionally arousing slide show. In the task used in this study, originally described in Cahill and McGaugh (1995; see also Heuer & Reisberg, 1990), all participants were exposed to a slide show that included both neutral and emotionally arousing slides. Age-matched control subjects recalled the emotionally arousing stimuli much better than the neutral stimuli, but patient B. P. showed equivalent memory for both types of stimuli. Patient B. P. rated his emotional reaction to the slide show similarly to control participants (B. P.’s rating: 8, control’s rating: 7.25 ± 1.2, on a scale of 0 to 10). Even though B. P. rated his emotional experience the same as

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that of control subjects, this emotional experience did not translate into enhanced memory. Using the same task, Adolphs, Cahil, Schul, and Babinsky (1997) also tested the performance of an additional patient with bilateral amygdala damage (SM046). This study featured analysis of memory for each individual slide for both SM046 and for B. P. Whereas normal participants remembered emotionally arousing slides signiﬁcantly better than the neutral slides, neither amygdaladamaged patient showed this pattern (see ﬁg. 2.1). Speciﬁcally, the slide remembered best by the control participants (a slide showing the surgically reattached legs of a car crash victim) was the one on which the two patients deviated most from the controls’ scores (see ﬁg. 2.1A). Like B. P., SM046 also endorsed normal ratings of subjective emotional arousal for the story. The pattern of impaired facilitation of memory for emotionally arousing material in the face of apparently normal memory performance for neutral material in subjects with bilateral amygdala damage contrasts sharply with the performances of amnesic subjects. Subjects with hippocampal or diencephalic amnesia are impaired in their overall memory performance, regardless of the nature of the material, but show a normal enhancement (albeit of smaller magnitude) when the subject matter is emotionally arousing (Hamann, Cahill, & Squire, 1997). Unilateral Amygdala Damage Using the same task, Adolphs, Tranel, and Denburg (2000) examined the pattern of emotional memory performance following unilateral amygdala damage. Eight subjects with unilateral amygdala damage consequent to temporal lobectomy (6 left; 2 right), 9 brain-damaged controls with no damage to the anterior temporal lobe, and 7 normal controls participated in the study. In this experiment, each slide in the story was rated on scales of emotional valence, arousal, unusualness, and complexity. There were no group diﬀerences in slide ratings. As in the previous study, both normal controls and brain-damaged controls showed enhanced memory for phase 2 of the slide/narrative story, speciﬁcally for the most highly arousing slide. By contrast, the group with left amygdala damage failed to show enhanced memory for this slide, showing the same pattern as previously reported for subjects with bilateral amygdala damage. (The two subjects with right amygdala damage appeared to perform normally, but these ﬁndings are inconclusive due to the small sample size of this group.) These ﬁndings point to a role for the left amygdala in the consolidation of declarative memory for emotionally arousing stimuli. Further studies have addressed the role of unilateral amygdala damage in the formation of memory for emotional words. Phelps, LaBar, and Spencer (1997) examined emotional memory formation in 26 subjects following unilateral temporal lobectomy. In this study, subjects were presented with a list of 27 words (9 positive, 9 negative, and 9 neutral) while skin conductance responses (SCRs) were recorded. A surprise recall test was administered 1 minute after the presentation of the word list. Results illustrated that the left temporal lobectomy

      

49

Figure 2.1. A. Plots of standard deviations from normal of patient SM046 across all 15 picture stimuli. B. Raw data for patient SM046 and normal controls. (Reprinted from “Impaired declarative memory for emotional material following bilateral amygdala damage in humans,” Adolphs, Cahill, Schul, & Babinsky, 1997, Learning & Memory, 4, 291–300. Copyright © 1997 by Cold Spring Harbor Laboratory Press.)

group had the worst recall of the word list, but this eﬀect was not statistically signiﬁcant. Each group (controls and both temporal lobectomy groups) recalled the negative and positive words better than the neutral words, but there was no diﬀerence among the groups in terms of the pattern of word recall. The authors noted that the words used in the negative and positive categories (e.g., victim, comedy) were perhaps not salient enough to produce the emotional arousal necessary to show any group diﬀerences in emotional memory performance. In

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fact, psychophysiological data from SCR, a measure of autonomic arousal, illustrated that the neutral word category elicited a greater response than did either emotion word category. In light of these ﬁndings, these investigators reported an additional study designed speciﬁcally to address the role of the arousal dimension in memory consolidation (LaBar & Phelps, 1998). In this follow-up study, 22 temporal lobectomy patients (10 left, 12 right) were presented with a list of 40 words (20 arousing, 20 neutral). The arousing words chosen in this study consisted of “profanities, sexually explicit words, and words depicting social taboos.” These words were successful in producing increased SCRs over neutral words and were rated as signiﬁcantly more arousing than neutral words in controls, as well as in both right and left temporal lobectomy groups. Free recall for the words was assessed both immediately and at 1–hour postencoding. The results were assessed in terms of forgetting rates between the immediate and delayed free recall tests. Only the control group showed a diﬀerential forgetting rate for the arousing versus neutral words, showing increased recall for the arousing words at the delayed recall test. Both the right and the left temporal lobectomy groups showed decreased memory for the arousing words at delayed recall. Consistent with the two previously reported studies, in this study the left temporal lobectomy group showed the poorest levels of recall; their performance was signiﬁcantly worse than that of both controls and the right temporal lobectomy group. This eﬀect was not, however, speciﬁc to emotionally arousing material, as the left temporal lobectomy group showed reduced overall performance but not a speciﬁc impairment on memory for emotional stimuli. Although these results are consistent with previous research showing a left-hemisphere dominance for verbal memory, they do not address a speciﬁc role of the right or left amygdala in memory for verbal or visual emotional stimuli. A recent study in our lab has attempted to address this issue (Buchanan, Denburg, Tranel, & Adolphs, 2001). Participants consisted of 20 subjects with unilateral amygdala damage following temporal lobectomy for treatment of epilepsy (11 left, 9 right) and 25 brain-damaged controls with unilateral lesions outside the temporal lobe. Additionally, 35 normal control volunteers were recruited for participation. Participants were tested on 2 days; on the ﬁrst session 15 pictures diﬀering in emotional salience (5 pleasant, 5 unpleasant, 5 neutral) were presented along with a one-sentence verbal narrative description (e.g., accompanying a picture of two parents with their new twin babies was the narrative: “After the babies were born, both parents were very happy, although a bit exhausted”). Subjects were told to watch attentively while the emotional responses to the stimuli were recorded; no mention of a follow-up memory test was made. Twenty-four hours after the ﬁrst session, subjects’ memory for the slides was assessed with free recall, multiple choice, and four-alternative forcedchoice recognition tests. Within both free recall and multiple choice tests, memory for narrative and picture information was assessed. The recognition

      

51

test assessed only recognition of visual detail. Results illustrated that the group with left amygdala damage was speciﬁcally impaired on memory for emotional narratives relative to memory for neutral narratives. Interestingly, this group was not impaired on memory for emotional picture information. The right amygdala group, on the other hand, was impaired on visual recognition memory; however, this impairment was not speciﬁc to emotional pictures (see ﬁg. 2.2). These ﬁndings support a material-speciﬁc role of the left amygdala in the processing of verbal emotional stimuli and a role of the right amygdala in processing visual emotional stimuli, corroborating previous work describing the separable language versus visuospatial processing roles for the left and right hemispheres, respectively (Dobbins, Kroll, Tulving, Knight, & Gazzaniga, 1998). These data replicate previous work illustrating a deﬁcit in verbal emotional memory in individuals with left amygdala damage (LaBar & Phelps, 1998; Phelps et al., 1997) while illustrating a lateralized pattern of the amygdala’s inﬂuence on emotional memory.

The Human Amygdala and Memory

for Gist Versus Detail

Memory for gist as well as for peripheral details has been a major topic in the study of the eﬀects of emotion on memory (Christianson & Loftus, 1991; Heuer & Reisberg, 1990). Despite discrepancies in the ﬁndings, several studies have shown that emotional arousal enhances memory for gist, but not memory for detail (Burke, Heuer, & Reisberg, 1992; Reisberg & Heuer, 1992; see also chapter 1 here). More work is needed in operationalizing these constructs; however, the basic idea is that gist or central information pertains to the most salient, relevant aspects of a stimulus (the aspects that one would focus on when describing it to someone else and whose alteration would change the meaning of the stimulus), whereas detail or peripheral information is everything else. Clearly, these categories do not form a strict dichotomy, but some features of a stimulus are almost unanimously deemed gist, whereas others are described as detail. Recent work in our lab has addressed the role of the amygdala in memory for the gist/central information versus the peripheral details of emotional stimuli. Using a task similar to that already described (Buchanan et al., 2001), Adolphs, Denburg, and Tranel (2001) assessed memory for the gist and details of emotionally negative and neutral slides and narratives from patient SM046 as well as from patients with unilateral temporal lobectomy (12 left, 8 right), braindamaged controls (n = 15), and age-matched controls (n = 47). Memory for gist was operationalized as salient, general information of the stimulus suﬃcient to distinguish that particular stimulus from all the other stimuli and that did not depend on remembering details of the scene; it was assessed with a fouralternative forced-choice written questionnaire. Detail memory was deﬁned as

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Figure 2.2. Free recall for narratives and pictures across valence categories. A. Mean (± standard error) of correctly recalled narratives across all subjects from each valence category. B. Mean (± standard error) of correctly recalled pictures across all subjects from each valence category. (Reprinted from “Verbal and nonverbal emotional memory following unilateral amygdala damage,” Buchanan, Denburg, Tranel, & Adolphs, 2001, Learning & Memory, 8, 326–335. Copyright © 2001 by Cold Spring Harbor Laboratory Press.)

      

53

information that could be accessed only from a detailed memory of the visual image and was assessed using a four-alternative forced-choice visual recognition task showing the original visual stimulus and three computer-manipulated foils that diﬀered only in their details. The study found that all groups (including those with unilateral temporal lobectomies) showed enhanced memory for the gist of negative rather than neutral stimuli, whereas patient SM046 showed the opposite pattern, with greater memory for the gist of the neutral than the negative stimuli. Performance on detail memory, on the other hand, showed a diﬀerent pattern. Both control groups (age-matched and brain-damaged controls), as well as the left temporal lobectomy group, showed greater detail memory for the neutral than the negative stimuli, whereas SM046 and the right temporal lobectomy group remembered the details of both the negative and neutral stimuli equivalently. The general pattern of memory performance on this task in the control subjects was that emotionally negative stimuli enhanced gist memory but reduced detail memory, compared to neutral stimuli. Bilateral amygdala damage, on the other hand, interfered with both of these eﬀects: SM046 remembered gist for unpleasant stimuli relatively worse than controls, and her detail memory performance for negative stimuli was better than that of controls (see ﬁg. 2.3). This study had an inherent confound precluding an unambiguous interpretation of the data; gist and detail memory were assessed with diﬀerent methods (questionnaire and visual recognition, respectively). Current studies under way in our laboratory are providing data conﬁrming that the eﬀects reported here can really be attributed to the amygdala’s role in processing gist and detail information. These ﬁndings provide evidence that the human amygdala modulates declarative memory for emotionally arousing stimuli through diﬀerential eﬀects on memory for gist and for visual detail. The data are consistent with the idea that the amygdala acts as a ﬁlter in the encoding of relevant information from emotional stimuli. Whereas the healthy amygdalae are able to enhance the memory processing of the gist of these stimuli and disregard the irrelevant details, damage to this structure impairs this ability. This pattern is consistent with recent work showing that the amygdala is involved in the enhancement of perception of emotionally salient events (Anderson & Phelps, 2001; Öhman & Mineka, 2001), suggesting that both perceptual and mnemonic processing of unpleasant events critically involve the amygdala. Findings from these studies indicate that the emotional arousal, not the pleasantness of the stimuli, most determines whether a stimulus will be remembered (see Bradley, Greenwald, Petry, & Lang, 1992). This arousal-mediated memory enhancement is the feature that appears to be most aﬀected following amygdala damage (it is also arousal that is most predictive of amygdala activity in functional imaging studies, as we discuss in the next section). These ﬁndings accord with recent neuroimaging work showing amygdala activity while viewing both negative and positive emotional stimuli, whether pictures (Hamann,

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Figure 2.3. A. Memory for gist. Mean (± standard error) number of questions (out of a maximum of two) answered correctly per stimulus, for the two emotion categories. All subjects except SM046 showed the same pattern: superior memory for emotionally aversive stimuli compared with neutral stimuli. B. Memory for visual detail. Subjects’ mean percentage correct on a four-alternative forced choice recognition memory task. The four stimuli consisted of the original stimulus and three computer manipulated foils that were identical in gist but diﬀered in detail. Whereas controls remembered the details of aversive stimuli less well than those of positive stimuli, subjects with amygdala damage remembered details about both types of stimuli equally well. (Reprinted from “The amygdala’s role in long-term declarative memory for gist and detail,” Adolphs, Denburg, & Tranel, 2001, Behavioral Neuroscience, 15, 983–992. Copyright © 2001 by the American Psychological Association, Inc.)

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55

Ely, Hoﬀman, & Kilts, 2002) or words (Hamann & Mao, 2002). Together, these lines of work suggest that the primary variable that determines memory for emotional material is arousal and also that this variable is the most salient instigator of amygdala activity. The principal diﬃculty here has been in constructing stimuli of pleasant valence that can be as arousing as those of negative valence.

Neuroimaging of the Amygdala

and Emotional Memory

Functional neuroimaging has provided another tool with which to examine the role of the human amygdala in the formation of emotional memories. Several recent studies have been able to test speciﬁc hypotheses derived from both animal research and studies in humans with amygdala lesions using positron emission tomography (PET) and functional magnetic resonance imaging (fMRI). The ﬁrst study to examine the role of the human amygdala in the formation of emotional memories using functional neuroimaging was conducted by Cahill et al. (1996). Healthy participants viewed emotionally arousing and neutral videos during PET scanning. Three weeks later, participants were asked to recall all the information that they could remember from each video. As expected, participants recalled signiﬁcantly more information from the emotionally arousing video than from the neutral video. Correlation analyses revealed a signiﬁcant positive correlation between the glucose metabolic rate of the right amygdala and the number of emotional ﬁlm clips recalled (r = 0.93; see section on gender diﬀerences for discussion of a lateralization of amygdala activity in a similar task). Further analyses showed no such association with recall of neutral ﬁlm clips. These ﬁndings suggest that the amygdala is activated during the encoding of emotionally arousing events and is involved in the translation of these events into long-term memory. A follow-up study corroborated the ﬁnding that amygdala activity is not involved in the formation of declarative memory for nonemotional material (Alkire, Haier, Fallon, & Cahill, 1998). This study did, however, document an association between hippocampal activity and the formation of memory for a nonemotional word list. These two studies further illustrate the dissociation of memory functions between the hippocampus and amygdala and highlight a speciﬁc role of the amygdala in the formation of emotional memories. Subsequent studies have extended these ﬁndings to show an association between bilateral amygdala activity during encoding and memory for both emotionally pleasant and unpleasant stimuli using both PET (Hamann, Ely, Grafton, & Kilts, 1999) and fMRI (Canli, Zhao, Desmond, Glover, & Gabrieli, 1999). The study by Hamann et al. additionally tested the emotional speciﬁcity of the amygdala’s inﬂuence on memory by including a stimulus category of interesting and unusual pictures. These interesting pictures included a chrome rhinoceros and a scene from a surrealist painting. Presumably, if the amygdala is involved in general memory enhancement, then amygdala activity should be

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associated with memory for unusual yet nonemotional stimuli. Results from this study illustrate that while these unusual pictures were better remembered than neutral (e.g., a book) and pleasant pictures (e.g., opposite-sex nudes) 4 weeks after encoding, this enhancement was unrelated to amygdala activity, which was instead speciﬁcally related only to memory for aversive and pleasant stimuli (a ﬁnding also consistent with studies in monkeys, which have failed to ﬁnd any eﬀect of amygdala lesions on the von Restorﬀ eﬀect—enhanced memory for especially unusual or distinctive stimuli in a set; Parker, Wilding, & Akerman, 1998). These results highlight the speciﬁc role of the amygdala in the enhancement of memories for emotionally signiﬁcant material regardless of valence (see ﬁg. 2.4). A recent event-related fMRI study has shown that stimuli rated as emotionally intense are associated with increased amygdala activity and increased memory performance (Canli, Zhao, Brewer, Gabrieli, & Cahill, 2000). In this study, 10 female volunteers were exposed to a selection of neutral and emotionally negative pictures (e.g., scenes of mutilation) while the fMRI response was recorded for each picture. Immediately after viewing each picture, subjects rated their emotional response on a scale from 0 (not emotionally intense at all) to 3 (extremely emotionally intense). Analysis of the fMRI response illustrated that bilateral amygdala activity was correlated with increased ratings of emotional intensity, such that the greater the emotional intensity, the greater the amygdala response. Three weeks later, subjects returned for a surprise memory test in which they were asked to report whether they were certain that they remembered a slide, whether the slide seemed familiar, or whether they did not remember the slide (in a remember/know recognition paradigm). Performance data illustrated that those slides rated as extremely emotionally intense were remembered signiﬁcantly better than those rated as less intense. Additionally, the degree of left amygdala activation during picture encoding was correlated with subsequent memory for the pictures (see section on gender diﬀerences for discussion of lateralization of amygdala activity related to memory performance). Those pictures that tended to produce the greatest response in the left amygdala were also remembered most often.

Autobiographical Memories and

the Amygdala

In addition to the evidence reviewed, that the amygdala plays a role in the encoding and consolidation of emotional memories, there is evidence that the retrieval of autobiographical memories may depend, in part, on the amygdala. Likely, the majority of our distant autobiographical memories are associated with an emotional response, suggesting that perhaps the amygdala plays a role both in the encoding and retrieval of these memories by virtue of their emotionally arousing nature. Mori et al. (1997) assessed memory for autobiographical events

      

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Figure 2.4. Top. Brain activity correlated with memory enhancement. Maps of pixels in which individual subject rCBF was signiﬁcantly correlated with individualsubject episodic memory enhancement superimposed on an axial MRI image. Left: correlation map for pleasant stimuli at z = -10.5. Right: correlation map for aversive stimuli at z = -16.5. Note that in this ﬁgure the right hemisphere is shown on the right. Bottom. Relationship between pleasant-picture memory and brain activity for individual subjects. Correlation scatterplots for the pleasant picture memory with rCBF. a. Left amygdala. b. Right amygdala. c. Left hippocampus. d. Right hippocampus. (Reprinted with permission from “Amygdala activity related to enhanced memory for pleasant and aversive stimuli,” Hamann, Ely, Grafton, & Kilts, 1999, Nature Neuroscience, 2, 289–294. Copyright © 1999 by Nature America Inc.)

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surrounding the 1995 Kobe earthquake in patients with probable Alzheimer’s disease. Neuropathological studies have shown that the characteristic plaques and neuroﬁbrillary tangles associated with Alzheimer’s disease are often located in the amygdala, and atrophy of this structure has been reported in both autopsied patients (Scott, DeKosky, & Scheﬀ, 1991) and in vivo in patients with early signs of the disease (Cuenod et al., 1993). Mori et al. examined the preexisting individual diﬀerences in the amygdala volume of a group of patients with putative Alzheimer’s disease (diagnosed prior to the earthquake) to determine whether changes in the size of this structure inﬂuenced emotional autobiographical memory. Results from this study illustrate that the volume of the amygdala was positively correlated with patients’ memories for their experiences during and after the earthquake (see ﬁg. 2.5). Hippocampal volume was also correlated with emotional memory but not as strongly as the relationship between amygdala volume and emotional memory. This association between amygdala volume and emotional memory was signiﬁcant even when controlling for factors such as age, education, whole brain volume, and ratings of dementia. There was no relationship between the size of the amygdala and memory for general (nonemotional) knowledge about the events surrounding the earthquake. These ﬁndings extend work from laboratory research focusing on the amygdala and emotional memory

8

Total Emotional Memory Score

Total Emotional Memory Score

8

6

4

2

0 600

1200 1600 2000 2400 Amygdalar Volume (mm3)

6

4

2

0 1600 2000 2400 2800 3200 3600 Hippocampal Volume (mm3)

Figure 2.5. Scatterplots of amygdala and hippocampal volumes with total emotional memory scores of 36 patients with Alzheimer’s disease. Pearson correlation analysis showed signiﬁcant correlations between amygdala volume and total emotional memory score and between hippocampal volume and total emotional memory score. After controlling for the eﬀects of age, sex, education, whole brain volume, and disease severity, the former correlation remained signiﬁcant, while the latter was no longer signiﬁcant. (Reprinted with permission from “Amygalar volume and emotional memory in Alzheimer’s disease,” Mori, Ikeda, Hirono, Kitagaki, Imamura, & Shimomura, 1999, American Journal of Psychiatry, 156, 216–222. Copyright © 1999 by the American Psychiatric Association, Inc.).

      

59

and suggest that memory for real-life emotional situations depends on the integrity of this structure. A hypothesis has been proposed suggesting that the temporofrontal cortical areas including the amygdala and uncinate fasciculus ﬁber bundle connecting these areas are speciﬁcally involved in the retrieval of autobiographical memories (Kroll, Markowitsch, Knight, & von Cramon, 1997; Markowitsch et al., 2000). More speciﬁcally, a right-sided temporofrontal network purportedly retrieves autobiographical memories, while a left-sided temporofrontal network encodes this information into memory (Tulving, Kapur, Craik, Moscovitch, & Houle, 1994; Tulving et al., 1994). This hypothesis has found support from studies of patients with lesions of these areas (Kroll et al., 1997; Levine et al., 1998), as well as functional neuroimaging studies of healthy participants (Fink et al., 1996; Markowitsch et al., 2000). Fink et al. showed that when subjects listened to transcripts of their own autobiographical memories, activity in areas including the right amygdala, right hippocampus, and right prefrontal cortex increased signiﬁcantly. The authors of several of these studies suggest that the role of these areas in the retrieval of memory is, in part, due to the emotional nature of autobiographical memories (Markowitsch et al., 2000). Memories from our lives that we are able to retrieve presumably have some aﬀective character, thus making these memories salient for recollection. These studies, in combination with previous work on emotional memory encoding, suggest that the amygdala may be involved not only in encoding emotional information but also in its retrieval. One note of caution regarding the studies reviewed in this last section is that they have not pinpointed the observed eﬀects solely to the amygdala but may reﬂect structures in the immediate vicinity of the amygdala including the temporal pole.

Gender Diﬀerences in

Amygdala Activity

Findings from several of these studies have suggested the possibility of gender diﬀerences related to lateralized amygdala activity in memory for emotional visual stimuli. In studies on men, results have shown a predominantly right-sided activation of the amygdala (Cahill et al., 1996; Hamann et al., 1999), whereas two studies documented more left lateralized activation in women (Canli et al., 1999, 2000). These gender diﬀerences have recently been investigated directly in a study including both men and women (Cahill et al., 2001) and using experimental conditions identical to those previously used with men only (described in the section on neuroimaging; Cahill et al., 1996). Results from this study illustrated the same gender-speciﬁc lateralized pattern of activation previously documented across separate studies, with enhanced emotional memory performance correlating with right amygdala activity in men but left amygdala activity in women (Cahill et al., 2001). Another interesting facet of this work is the ﬁnding that women show better memory for emotionally arousing material than do men

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(Seidlitz & Diener, 1998). Canli, Desmond, Zhao, and Gabrieli (2002) examined the possible neural mechanisms of women’s enhanced memory for emotional material. In a functional MRI study similar in methodology to previous experiments using emotional picture stimuli (Cahill et al., 2001; Canli et al., 2000), the authors replicated the ﬁnding of women’s enhanced memory for emotional stimuli. Additionally, they found that women showed a greater network of neural activity related to emotional memory (including the left amygdala, hippocampus, and frontal cortex) than men (whose activity was primarily located in the right amygdala). Subjective ratings of emotional arousal were equivalent between men and women, so this ﬁnding suggests that gender diﬀerences in emotional responsiveness alone are not responsible for this cognitive diﬀerence. The authors of these studies suggest that these gender diﬀerences may reﬂect diﬀerent cognitive strategies between men and women in the processing of these stimuli, perhaps related to diﬀerential attention to gist and to peripheral details, a cognitive phenomenon that also shows a gender diﬀerence (see Cahill & van Stegeren, 2003). These intriguing ﬁndings clearly warrant the inclusion of gender and laterality as factors in future work on the relationship between the amygdala and emotional memory. [For another perspective on gender diﬀerences in emotional memory, see chapter 8—Eds.]

The Human Hippocampus

and Emotional Memory

The role of the hippocampus in the enhancement of memory by emotion has been assessed in several studies. Two studies by Hamann, Cahill, McGaugh, and Squire (1997) and Hamann, Cahill, and Squire (1997b) assessed memory for emotionally arousing materials in amnesic patients with damage to either the hippocampus only, damage to the hippocampus and amygdala, or damage to the diencephalon. Results from these studies illustrated that damage to the hippocampus alone or damage to the diencephalon leaves the enhancement of declarative memory by emotional arousal intact, presumably by relying on the intact amygdala in the subjects included in these studies. Two patients with combined damage to the hippocampus and amygdala (including overlying cortices) showed no discernible memory for the emotionally arousing or neutral stimuli. A neuroimaging study (mentioned earlier in the section on the role of the amygdala; Alkire et al., 1998) has demonstrated that activity of the hippocampus, but not the amygdala, correlates with memory for nonemotional materials. In another neuroimaging study, Hamann et al. (1999) addressed the relationship between the amygdala and hippocampus in the enhancement of memory by emotion. Bilateral activity in both the amygdala and hippocampus was associated with memory enhancement for both pleasant and aversive stimuli in this study. Results from the studies with amnesics illustrate that the

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hippocampus, while necessary for the formation of new declarative memories, is not itself responsible for the modulation of memory by emotional arousal. The neuroimaging work shows that correlated activity between the amygdala and hippocampus may be a necessary mechanism for the enhancement of memory for emotionally arousing events. This work further demonstrates the modulatory role of the amygdala, which in combination with the hippocampus lays down a stronger memory trace for emotional situations than for nonemotional situations.

The Prefrontal Cortex

and Emotional Memory

The prefrontal cortex, notably its dorsolateral regions, is known to be involved in both the encoding and retrieval of memories (Buckner & Wheeler, 2001; Tulving, Kapur, Craik, et al., 1994) and is thought to provide “executive” strategies for recollecting, comparing, and ordering memories. Work from numerous investigators has also suggested a role of the orbitofrontal region in emotional processing (Bechara, Damasio, & Damasio, 2000; Rolls, 2000b). As dorsolateral and orbital sectors of the prefrontal cortex are intimately connected (Rolls, 2000a), and as orbitofrontal cortex is also massively connected with the amygdala, it is natural to hypothesize that networks within the prefrontal cortex participate in structuring emotional memories as well. Whether and how the prefrontal cortex may be involved in the modulation of memory by emotion has been less well studied than the case of the amygdala, but several studies have begun to provide some hints. Numerous studies have documented the eﬀects of orbitofrontal damage on decision making (Bechara et al., 2000; Bechara, Damasio, Damasio, & Lee, 1999; Bechara, Damasio, Tranel, & Damasio, 1997; Bechara, Tranel, Damasio, & Damasio, 1996). This work has outlined a model whereby the orbitofrontal cortex processes emotional signals from the body that aﬀect decision-making processes (Damasio, 1994). One study has sought to distinguish this decision-making bias from the enhancement of memory by emotion (Bechara et al., 2000). Patients with orbitofrontal damage were presented with a series of neutral and emotionally arousing picture stimuli in four sets. One set of pictures was presented only once, another set was presented twice, a third set was presented three times, and a fourth set was presented eight times. Memory for these stimuli was assessed immediately after all stimuli had been presented. Results from this study illustrated that while the orbitofrontal patients showed a reduced overall level of memory, these patients still showed enhanced memory for the emotionally arousing pictures rather than for the neutral pictures, and both groups showed improved memory for those stimuli that were repeated most often. This study suggests that the biasing of decision making by emotion that depends on the orbitofrontal cortex is separable from the inﬂuence of emotion on memory, which appears to rely less on the orbitofrontal cortex.

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Recent neuroimaging studies have documented a role of the prefrontal cortex in the memory for neutral material encoded in an emotionally arousing context (Maratos, Dolan, Morris, Henson, & Rugg, 2001; Maratos & Rugg, 2001). For example, these studies give the example of the word “corn” used in a negative context: “The farmer was shredded when he fell into the corn grinder,” and used in a positive context: “The farmer was overjoyed with his bountiful crop of corn.” Using electrophysiological recordings, the authors in these two studies showed that the areas that are normally activated during the retrieval of old neutral words (including the right prefrontal cortex) exhibited enhanced activity when these words were presented in a negative context (Maratos & Rugg, 2001). In an event-related fMRI study using a similar experimental design (with the addition of a positive emotional context), Maratos et al. (2001) demonstrated that the re-presentation of neutral words that had been presented in a positive emotional context resulted in heightened activity in the orbitofrontal cortex, the dorsolateral prefrontal cortex, and the medial temporal lobe areas such as the amygdala and hippocampus. Results from these studies suggest (1) that activity within areas normally involved in the retrieval of neutral information (including the prefrontal cortex) is enhanced by an emotionally arousing context and (2) that the same areas activated during encoding of emotionally arousing materials (including the amygdala) are active during the retrieval of these materials. These studies from both lesion and neuroimaging paradigms illustrate the complex relationship between the prefrontal cortex and the enhanced memory for emotional material. Though the role of the PFC in emotional memory has not been well documented in lesion patients, the neuroimaging data suggest a subtle role for this region in the encoding and recognition of emotional stimuli. It is worth emphasizing the close connectivity between the amygdala, orbitofrontal cortex, basal forebrain, and the dorsal prefrontal cortex. Studies in monkeys have demonstrated that the amygdala and orbitofrontal cortex are two essential components of a system for processing the emotional properties of stimuli; disconnection of the two structures can result in impairments on certain tasks of associative emotional memory that are as severe as lesions in either structure (Gaﬀan, Murray, & Fabre-Thorpe, 1993). It seems plausible to suggest the same systems-level architecture for declarative emotional memory.

Neurodegeneration

and Emotional Memory

A ﬁnal section to our review concerns the insights gleaned not from focal lesion or activation studies but from the more diﬀuse types of damage incurred by neurodegenerative diseases (see chapter 9 here for a discussion of these conditions in relation to aging). Alzheimer’s disease (AD) is initially characterized by memory

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complaints, often concomitant with alteration in emotional behavior. The plaques and neuroﬁbrillary tangles—the neuropathological hallmarks of AD—are often ﬁrst noted in medial temporal lobe structures including the amygdala, entorhinal cortex, and hippocampus (Hyman, Van Hoesen, & Damasio, 1990; Van Hoesen, Augustinack, & Redman, 1999). These ﬁndings have led several investigators recently to examine emotional memory in AD. Results from two studies have shown impairments in the enhancement of memory by emotion in patients with probable AD (Abrisqueta-Gomez, Bueno, Oliveira, & Bertolucci, 2002; Hamann, Monarch, & Goldstein, 2000), yet two other studies have shown no such impairment (Kazui et al., 2000; Moayeri, Cahill, Jin, & Potkin, 2000). The major diﬀerence between the studies showing impairment and those showing no impairment is that the latter studies used a slide show paradigm similar to that described in Cahill, Prins, Weber, and McGaugh (1994), whereas the former studies showing an impairment used individual emotional pictures devoid of a narrative. This diﬀerence in methodology deserves attention in future research in emotional memory. Perhaps a cohesive narrative structure is necessary to keep such patients’ attention, whereas the presentation of unrelated emotional pictures may not be salient enough (see discussion of the distinction between visually arousing and thematically arousing inﬂucences on memory in chapter 1 for a fuller explication of this possibility). The aforementioned study by Mori et al. (1999) that demonstrated an association between amygdala volume and emotional memories for the Kobe earthquake in AD patients suggests that, at least in some of these patients, the volumetric loss of the amygdala plays a role in the ability to remember emotional events (see previous section on autobiographical memories and the amygdala for fuller description of this study). The same neural structures (amygdala and hippocampus) that have been described as playing a role in emotional memory in neurodegenerative diseases are also known to be aﬀected in normal aging. Speciﬁcally, the volumes of both the amygdala (Jack et al., 1997; Mu, Xie, Wen, Weng, & Shuyan, 1999) and hippocampus (Golomb et al., 1993; Jernigan et al., 2001) diminish with age. In line with this reduction in brain volume are the well-documented memory impairments that accompany aging (Grady & Craik, 2000). The eﬀect of aging on memory for emotional material has not been well studied. A recent study from our laboratory has sought to examine this issue (Denburg, Buchanan, Tranel, & Adolphs, in press). In the study, 80 healthy adults between the ages of 35 and 85 years were presented with a series of pictures that ranged from pleasant to neutral to unpleasant scenes (the same ones mentioned in connection with the studies by Buchanan et al. [2001] and Adolphs et al. [2001] on pages 51 and 52). Memory for these pictures was then tested 24 hours later. Results from this study showed that regardless of the age of the subject, memory for the emotionally arousing pictures was better than that for neutral pictures. Though there was an overall decline in memory function with age, there was only a small diﬀerence in the degree of memory modulation by emotion across the age range. These

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ﬁndings indicate a sparing of the inﬂuence of emotion on memory with age, perhaps due to a more pronounced age-related degeneration of the hippocampus than for the amygdala. Studies designed to assess the relationship between age-related declines in brain volume and emotional memory function are necessary to test this hypothesis.

Summary and Integration The studies reviewed in this chapter illustrate the complex interrelationships among brain structures involved in the modulation of memory by emotion. Numerous brain structures—including the amygdala, hypothalamus, hippocampus, cingulate, insular and orbitofrontal cortices, among others—are involved in both the evaluation of and response to emotional stimuli. Findings from lesion studies and neuroimaging point to the amygdala as the most critical structure for the enhanced memory of stimuli encoded during emotional arousal. Our focus on the amygdala’s (and other structures’) role in modulation of declarative memory for stimuli does not exclude its role in other aspects of “emotional memory,” more broadly construed. In our view, the amygdala (together with structures like the ventral striatum and orbitofrontal cortex) helps to mount a coordinated, multisystem response to an emotional challenge. Such a response consists of concerted changes in many parameters of an organism’s body (autonomic, endocrine, and other changes) and brain. The changes in brain functioning are also multicomponent, and include, among others, changes in attention, alertness, and—the focus of this chapter—memory encoding and consolidation. The known neuroanatomical connectivity of the amygdala bears out this sketch; it receives rudimentary (LeDoux, 2000) as well as highly processed sensory information (Amaral, Price, Pitkanen, & Carmichael, 1992), which allows for quick and speciﬁc activation of response systems that inﬂuence behavior and subsequent memory formation. The speciﬁc role of the amygdala appears to be that of instigator, the catalyst that initially imbues incoming stimuli with emotional signiﬁcance and triggers other neural regions to react accordingly. The detection and experience of emotion increases the processing of the emotional stimuli by focusing attention and enacting response systems (Frijda, 1987; Lang, Bradley, & Cuthbert, 1990). The amygdala plays an integral role in this enhanced processing through inﬂuence over numerous brain structures, including the hippocampus, hypothalamus, brain stem arousal centers, basal forebrain, and bidirectional connections with neocortex (McGaugh, 2000; Packard & Teather, 1998; Pitkänen, 2000). Along with the integrative, multisystem role played by structures like the amygdala in coordinating emotional responses, its role in memory is equally diverse. We can think of the ways in which emotion inﬂuences memory as changes in memory for (1) the emotion-inducing sensory properties of stimuli themselves (e.g., remembering that a picture showed mutilated bodies), (2) the

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intrinsically neutral sensory properties of stimuli associated with a related emotional state (e.g., remembering that one saw a picture of landscape as part of story about a terrible disaster), (3) the emotional state itself in the perceiver (e.g., remembering that one felt upset), or (4) higher-order information about the emotion and the stimuli (e.g., remembering simply that there were some emotional stimuli or that one felt an emotion). None of these is mutually exclusive, and there is evidence to suggest that the amygdala may contribute to all of them. Interesting questions for the future remain about how these aspects of information are related and how they might depend diﬀerentially on certain brain structures. The ﬁndings we have reviewed place the amygdala in a modulatory position of the traditional medial temporal lobe memory system, its activity inﬂuencing memory formation only under conditions of emotional arousal. In response to emotion, the same brain structures are recruited in the service of both response output and memory formation. The ﬁnding that enhanced activity of response systems—autonomic, endocrine, and skeletal motor activity—accompanies increased mnemonic representation illustrates the coordinated activity of these brain structures in the service of survival. The lesion studies described suggest that the amygdala is necessary for the enhancement of memory for emotionally arousing stimuli. The dysfunction of one or both amygdalae (because of disease or surgery) results in reduced memory for emotionally arousing materials. The precise nature of such dysfunction—whether it is hyper- or hypoactivation— can lead either to compromised emotional memories or to the pathological exaggeration of such memories, as seen in traumatic and phobic memories that we have not reviewed here (Davis, Walker, & Lee, 1997; Öhman & Mineka, 2001). The nature of these studies has made it diﬃcult for the assessment of consolidation or retrieval eﬀects but clearly implicate the amygdala in the encoding of emotional material into memory. Similarly, functional neuroimaging studies have most consistently pointed to encoding as the memory stage at which the amygdala exerts its eﬀects (but see Dolan, Lane, Chua, & Fletcher, 2000). The most consistent ﬁnding from the discussed studies is an association between amygdala activity during encoding and the enhancement of subsequent memory. The activation of the amygdala would seem to be a potent predictor of memory performance. Another pathway through which the amygdala may inﬂuence memory performance is via hormonal output (see chapter 3 for a more thorough discussion of these issues). The previously described pharmacological studies in animals have illustrated the eﬀect of manipulations of both catecholamines and glucocorticoids on emotional memory performance. Direct connections between the amygdala and the hypothalamus mediate the release of both epinephrine and glucocorticoids during emotionally arousing situations (Davis, 1997). Following their release, these hormones exert actions throughout the central nervous system and speciﬁcally at the amygdala (Honkaniemi et al., 1992; Shepard,

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Barron, & Myers, 2000). A great deal of animal research has focused on the bidirectional nature of the relationship between the amygdala and stress hormones (McGaugh & Izquierdo, 2000; Roozendaal, 2000). Enhancement of either adrenergic or glucocorticoid activity improves, but blockade of these hormones reduces, memory performance. These ﬁndings have been documented in both animals (Roozendaal, 2000) and humans (Buchanan & Lovallo, 2001; Cahill et al., 1994). The ﬁnal common pathway of these hormones’ eﬀects on memory performance appears to be at the amygdala—speciﬁcally through noradrenergic neurotransmission in the lateral/basolateral nuclei (Quirarte, Roozendaal, & McGaugh, 1997). As previously mentioned, manipulations of this activity within these nuclei inﬂuence hippocampal and cortical function (Escobar, Chao, & Bermudez-Rattoni, 1998; Ikegaya, Nakanishi, Saito, & Abe, 1997), providing a potential mechanism whereby the actions of these hormones at the amygdala could inﬂuence the formation of emotional memories. Even though human research has yet to show a relationship among stress hormones, amygdala activity, and emotional memory, animal research suggests such a relationship; future work will no doubt focus on elucidating this topic. Consistent with the ﬁnding that systemic hormones inﬂuence subsequent amygdala activity, one mechanism through which an emotional response could inﬂuence memory is via perception of the physiological response in the body. Vagal stimulation in both animals (Clark et al., 1995) and humans (Clark et al., 1999) results in increased memory performance. In fact, the sensory role of the vagus nerve is proposed as one mechanism whereby peripherally released epinephrine—which does not readily pass the blood-brain barrier—inﬂuences amygdala function in the formation of emotional memories (McGaugh, 2000). These results illustrate that the inﬂuence of the amygdala on memory could occur at multiple stages: (1) through rapid initial responses inﬂuencing neural information processing with a short latency after the occurrence of a stimulus, or (2) indirectly, through ﬁrst triggering an emotional response in the body and subsequent central eﬀects of the body’s physiological state (of which some of the latter may then also be mediated by the amygdala, albeit at a later time than mechanism 1). Most current studies have not permitted a separation of the emotion depicted in the stimulus, from the emotional reactions and feelings of the subject, and an important goal for the future will be to disentangle these issues. In all likelihood, a variety of structures participate in modulating the encoding, consolidation, and retrieval of our memories for emotional events, with respect to diverse components of information and at multiple temporal scales. Structures such as the amygdala and the ventral striatum perhaps provide an initial, rapid, automatic evaluation of the emotional signiﬁcance of stimuli, or of the context within which they occur, and can then consequently modulate our attention to those stimuli (e.g., via basal forebrain), the strength of their memory consolidation (e.g., via hippocampus), or the nature of their contextual links to autobiographical information and to other items stored in memory (e.g.,

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via prefrontal regions). Perhaps, at a later point, many of the same structures can modulate memory through less direct mechanisms. Given the enormous and varied amount of declarative knowledge that humans store over their lifetime, it seems prudent to acknowledge that multiple, complex neural mechanisms would exist to encode, order, and eﬃciently store such knowledge.

Note We thank Antonio and Hanna Damasio, Daniel Tranel, and Natalie Denburg for their participation in some of the studies reviewed. Supported in part by an NRSA grant from the National Institute on Aging to T.W.B. and from the National Institute of Mental Health to R.A.

References Abrisqueta-Gomez, J., Bueno, O. F., Oliveira, M. G., & Bertolucci, P. H. (2002). Recognition memory for emotional pictures in Alzheimer’s patients. Acta Neurologica Scandinavica, 105, 51–54. Adolphs, R., Cahill, L., Schul, R., & Babinsky, R. (1997). Impaired declarative memory for emotional material following bilateral amygdala damage in humans. Learning & Memory, 4, 291–300. Adolphs, R., Denburg, N. L., & Tranel, D. (2001). The amygdala’s role in longterm declarative memory for gist and detail. Behavioral Neuroscience, 115, 983– 992. Adolphs, R., Tranel, D., & Denburg, N. (2000). Impaired emotional declarative memory following unilateral amygdala damage. Learning & Memory, 7, 180–186. Alkire, M. T., Haier, R. J., Fallon, J. H., & Cahill, L. (1998). Hippocampal, but not amygdala, activity at encoding correlates with long-term, free recall of nonemotional information. Proceedings of the National Academy of Science, USA, 95, 14506–14510. Amaral, D. G., Price, J. L., Pitkanen, A., & Carmichael, S. T. (1992). Anatomical organization of the primate amygdaloid complex. In J. P. Aggleton (Ed.), The amygdala: Neurobiological aspects of emotion, memory, and mental dysfunction (pp. 1–66). New York: Wiley-Liss. Anderson, A. K., & Phelps, E. A. (2001). Lesions of the human amygdala impair enhanced perception of emotionally salient events. Nature, 411, 305–309. Babinsky, R., Calabrese, P., Durwen, H. F., Markowitsch, H. J., Brechtelsbauer, D., Heuser, L., & Gehlen, W. (1993). The possible contribution of the amygdala to memory. Behavioural Neurology, 6, 167–170. Baxter, M. G., & Murray, E. A. (2000). Reinterpreting the behavioral eﬀects of amygdala lesions in non-human primates. In J. Aggleton (Ed.), The amygdala: A functional analysis (Vol. 2, pp. 545–568). Oxford: Oxford University Press. Bechara, A., Damasio, H., & Damasio, A. R. (2000). Emotion, decision making and the orbitofrontal cortex. Cerebral Cortex, 10, 295–307. Bechara, A., Damasio, H., Damasio, A. R., & Lee, G. P. (1999). Diﬀerent contributions of the human amygdala and ventromedial prefrontal cortex to decisionmaking. Journal of Neuroscience, 19, 5473–5481.

68

  

Bechara, A., Damasio, H., Tranel, D., & Damasio, A. R. (1997). Deciding advantageously before knowing the advantageous strategy. Science, 275, 1293– 1295. Bechara, A., Tranel, D., Damasio, H., & Damasio, A. R. (1996). Failure to respond autonomically to anticipated future outcomes following damage to prefrontal cortex. Cerebral Cortex, 6, 215–225. Bianchin, M., Mello e Souza, T., Medina, J. H., & Izquierdo, I. (1999). The amygdala is involved in the modulation of long-term memory, but not in working or shortterm memory. Neurobiology of Learning and Memory, 71, 127–131. Bradley, M. M., Greenwald, M. K., Petry, M. C., & Lang, P. J. (1992). Remembering pictures: Pleasure and arousal in memory. Journal of Experimental Psychology: Learning Memory and Cognition, 18, 379–390. Brown, R., & Kulick, J. (1977). Flashbulb memories. Cognition, 5, 73–99. Brown, S., & Schafer, A. (1888). An investigation in the functions of the occipital and temporal lobes of the monkey’s brain. Philosophical Transactions of the Royal Society of London, 179, 303–327. Buchanan, T. W., Denburg, N. L., Tranel, D., & Adolphs, R. (2001). Verbal and nonverbal emotional memory following unilateral amygdala damage. Learning & Memory, 8, 326–335. Buchanan, T. W., & Lovallo, W. R. (2001). Enhanced memory for emotional material following stress-level cortisol treatment in humans. Psychoneuroendocrinology, 26, 307–317. Buckner, R. L., & Wheeler, M. E. (2001). The cognitive neuroscience of remembering. Nature Reviews Neuroscience, 2, 624–634. Burke, A., Heuer, F., & Reisberg, D. (1992). Remembering emotional events. Memory & Cognition, 20, 277–290. Cahill, L., Babinsky, R., Markowitsch, H. J., & McGaugh, J. L. (1995). The amygdala and emotional memory. Nature, 377, 295–296. Cahill, L., Haier, R. J., Fallon, J., Alkire, M. T., Tang, C., Keator, D., Wu, J., & McGaugh, J. L. (1996). Amygdala activity at encoding correlated with long-term, free recall of emotional information. Proceedings of the National Academy of Science, USA, 93, 8016–8021. Cahill, L., Haier, R. J., White, N. S., Fallon, J., Kilpatrick, L., Lawrence, C., et al. (2001). Sex-related diﬀerence in amygdala activity during emotionally inﬂuenced memory storage. Neurobiology of Learning and Memory, 75, 1–9. Cahill, L., & McGaugh, J. L. (1995). A novel demonstration of enhanced memory associated with emotional arousal. Consciousness and Cognition, 4, 410– 421. Cahill, L., Prins, B., Weber, M., & McGaugh, J. L. (1994). Beta-adrenergic activation and memory for emotional events. Nature, 371, 702–704. Cahill, L., & van Stegeren, A. (2003). Sex-related impairment of memory for emotional events with beta-adrenergic blockade. Neurobiology of Learning and Memory, 79, 81–88. Canli, T., Desmond, J. E., Zhao, Z., & Gabrieli, J. D. (2002). Sex diﬀerences in the neural basis of emotional memories. Proceedings of the National Academy of Science, USA, 99, 10789–10794.

      

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Canli, T., Zhao, Z., Brewer, J., Gabrieli, J. D., & Cahill, L. (2000). Event-related activation in the human amygdala associates with later memory for individual emotional experience. Journal of Neuroscience, 20, RC99. Canli, T., Zhao, Z., Desmond, J., Glover, G., & Gabrieli, J. D. (1999). fMRI identiﬁes a network of structures correlated with retention of positive and negative emotional memory. Psychobiology, 27, 441–452. Christianson, S.-Å., & Loftus, E. F. (1991). Remembering emotional events: The fate of detailed information. Cognition and Emotion, 5, 81–108. Clark, K. B., Krahl, S. E., Smith, D. C., & Jensen, R. A. (1995). Post-training unilateral vagal stimulation enhances retention performance in the rat. Neurobiology of Learning and Memory, 63, 213–216. Clark, K. B., Naritoku, D. K., Smith, D. C., Browning, R. A., & Jensen, R. A. (1999). Enhanced recognition memory following vagus nerve stimulation in human subjects. Nature Neuroscience, 2, 94–98. Cuenod, C. A., Denys, A., Michot, J. L., Jehenson, P., Forette, F., Kaplan, D., et al. (1993). Amygdala atrophy in Alzheimer’s disease. An in vivo magnetic resonance imaging study. Archives of Neurology, 50, 941–945. Damasio, A. R. (1994). Descartes’ error and the future of human life. Scientiﬁc American, 271, 144. Davis, M. (1997). Neurobiology of fear responses: The role of the amygdala. Journal of Neuropsychiatry and Clinical Neuroscience, 9, 382–402. Davis, M., Walker, D. L., & Lee, Y. (1997). Roles of the amygdala and bed nucleus of the stria terminalis in fear and anxiety measured with the acoustic startle reﬂex. Possible relevance to PTSD. Annals of the New York Academy of Science, 821, 305–331. de Kloet, E. R., Oitzl, M. S., & Joels, M. (1999). Stress and cognition: Are corticosteroids good or bad guys? Trends in Neuroscience, 22, 422–426. Denburg, N. L., Buchanan, T. W., Tranel, D., & Adolphs, R. (in press). Evidence for preserved emotional memory in normal elderly persons. Emotion. Dobbins, I. G., Kroll, N. E., Tulving, E., Knight, R. T., & Gazzaniga, M. S. (1998). Unilateral medial temporal lobe memory impairment, type deﬁcit, function deﬁcit, or both? Neuropsychologia, 36, 115–127. Dolan, R. J., Lane, R., Chua, P., & Fletcher, P. (2000). Dissociable temporal lobe activations during emotional episodic memory retrieval. Neuroimage, 11, 203–209. Eichenbaum, H., & Cohen, N. J. (2001). From conditioning to conscious recollection, memory systems of the brain. Oxford: Oxford University Press. Escobar, M. L., Chao, V., & Bermudez-Rattoni, F. (1998). In vivo long-term potentiation in the insular cortex, NMDA receptor dependence. Brain Research, 779, 314–319. Fink, G. R., Markowitsch, H. J., Reinkemeier, M., Bruckbauer, T., Kessler, J., & Heiss, W. D. (1996). Cerebral representation of one’s own past, neural networks involved in autobiographical memory. Journal of Neuroscience, 16, 4275– 4282. Frijda, N. H. (1987). Emotion, cognitive structure, and action tendency. Cognition and Emotion, 1, 115–143.

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Gaﬀan, D., Murray, E. A., & Fabre-Thorpe, M. (1993). Interaction of the amygdala with the frontal lobe in reward memory. European Journal of Neuroscience, 5, 968–975. Goddard, G. V. (1964). Amygdaloid stimulation and learning in the rat. Journal of Comparative and Physiological Psychology, 58, 23–30. Gold, P. E., Hankins, L., Edwards, R. M., Chester, J., & McGaugh, J. L. (1975). Memory interference and facilitation with posttrial amygdala stimulation, eﬀect on memory varies with footshock level. Brain Research, 86, 509–513. Gold, P. E., & van Buskirk, R. (1975). Facilitation of time-dependent memory processes with posttrial epinephrine injections. Behavioral Biology, 23, 509– 520. Golomb, J., de Leon, M. J., Kluger, A., George, A. E., Tarshish, C., & Ferris, S. H. (1993). Hippocampal atrophy in normal aging. An association with recent memory impairment. Archives of Neurology, 50, 967–973. Grady, C. L., & Craik, F. I. (2000). Changes in memory processing with age. Current Opinion in Neurobiology, 10, 224–231. Hamann, S., & Mao, H. (2002). Positive and negative emotional verbal stimuli elicit activity in the left amygdala. Neuroreport, 13, 15–19. Hamann, S. B., Cahill, L., McGaugh, J. L., & Squire, L. R. (1997). Intact enhancement of declarative memory for emotional material in amnesia. Learning & Memory, 4, 301–309. Hamann, S. B., Cahill, L., & Squire, L. R. (1997). Emotional perception and memory in amnesia. Neuropsychology, 11, 104–113. Hamann, S. B., Ely, T. D., Grafton, S. T., & Kilts, C. D. (1999). Amygdala activity related to enhanced memory for pleasant and aversive stimuli. Nature Neuroscience, 2, 289–293. Hamann, S. B., Ely, T. D., Hoﬀman, J. M., & Kilts, C. D. (2002). Ecstasy and agony, activation of the human amygdala in positive and negative emotion. Psychological Science, 13, 135–141. Hamann, S. B., Monarch, E. S., & Goldstein, F. C. (2000). Memory enhancement for emotional stimuli is impaired in early Alzheimer’s disease. Neuropsychology, 14, 82–92. Heuer, F., & Reisberg, D. (1990). Vivid memories of emotional events, the accuracy of remembered minutiae. Memory & Cognition, 18, 496–506. Honkaniemi, J., Pelto-Huikko, M., Rechardt, L., Isola, J., Lammi, A., Fuxe, K., et al. (1992). Colocalization of peptide and glucocorticoid receptor immunoreactivities in rat central amygdaloid nucleus. Neuroendocrinology, 55, 451–459. Hyman, B. T., Van Hoesen, G. W., & Damasio, A. R. (1990). Memory-related neural systems in Alzheimer’s disease, an anatomic study. Neurology, 40, 1721– 1730. Ikegaya, Y., Nakanishi, K., Saito, H., & Abe, K. (1997). Amygdala betanoradrenergic inﬂuence on hippocampal long-term potentiation in vivo. Neuroreport, 8, 3143–3146. Jack, C. R., Jr., Petersen, R. C., Xu, Y. C., Waring, S. C., O’Brien, P. C., Tangalos, E. G., et al. (1997). Medial temporal atrophy on MRI in normal aging and very mild Alzheimer’s disease. Neurology, 49, 786–794.

      

71

Jernigan, T. L., Archibald, S. L., Fennema-Notestine, C., Gamst, A. C., Stout, J. C., Bonner, J., et al. (2001). Eﬀects of age on tissues and regions of the cerebrum and cerebellum. Neurobiology of Aging, 22, 581–594. Kazui, H., Mori, E., Hashimoto, M., Hirono, N., Imamura, T., Tanimukai, S., et al. (2000). Impact of emotion on memory, controlled study of the inﬂuence of emotionally charged material on declarative memory in Alzheimer’s disease. British Journal of Psychiatry, 177, 343–347. Kim, J. J., & Diamond, D. M. (2002). The stressed hippocampus, synaptic plasticity and lost memories. Nature Reviews Neuroscience, 3, 453–462. Klüver, H., & Bucy, P. C. (1938). ‘Psychic blindness’ and other symptoms following bilateral temporal lobectomy in rhesus monkeys. American Journal of Physiology, 5, 33–54. Kroll, N. E., Markowitsch, H. J., Knight, R. T., & von Cramon, D. Y. (1997). Retrieval of old memories, the temporofrontal hypothesis. Brain, 120, 1377–1399. LaBar, K. S., & Phelps, E. A. (1998). Arousal-mediated memory consolidation: Role of the medial temporal lobe in humans. Psychological Science, 9, 490–493. Lang, P. J., Bradley, M. M., & Cuthbert, B. N. (1990). Emotion, attention, and the startle reﬂex. Psychological Review, 97, 377–395. LeDoux, J. E. (2000). Emotion circuits in the brain. Annual Review of Neuroscience, 23, 155–184. Levine, B., Black, S. E., Cabeza, R., Sinden, M., McIntosh, A. R., Toth, J. P., et al. (1998). Episodic memory and the self in a case of isolated retrograde amnesia. Brain, 121, 1951–1973. Liang, K. C., Juler, R. G., & McGaugh, J. L. (1986). Modulating eﬀects of posttraining epinephrine on memory, involvement of the amygdala noradrenergic system. Brain Research, 368, 125–133. Lovallo, W. R. (1997). Stress and health: Biological and psychological interactions. Thousand Oaks, CA: Sage. Lupien, S. J., & Lepage, M. (2001). Stress, memory, and the hippocampus, can’t live with it, can’t live without it. Behavioral Brain Research, 127, 137–158. Maratos, E. J., Dolan, R. J., Morris, J. S., Henson, R. N. A., & Rugg, M. D. (2001). Neural activity associated with episodic memory for emotional context. Neuropsychologia, 39, 910–920. Maratos, E. J., & Rugg, M. D. (2001). Electrophysiological correlates of the retrieval of emotional and non-emotional context. Journal of Cognitive Neuroscience, 13, 877–891. Markowitsch, H. J., Calabrese, P., Wurker, M., Durwen, H. F., Kessler, J., Babinsky, R., Brechtelsbauer, D., Heuser, L., & Gehlen, W. (1994). The amygdala’s contribution to memory—A study on two patients with Urbach-Wiethe disease. Neuroreport, 5, 1349–1352. Markowitsch, H. J., Thiel, A., Reinkemeier, M., Kessler, J., Koyuncu, A., & Heiss, W. D. (2000). Right amygdalar and temporofrontal activation during autobiographic, but not during ﬁctitious memory retrieval. Behavioural Neurology, 12, 181–190. McEwen, B. S. (2000). The neurobiology of stress, from serendipity to clinical relevance. Brain Research, 886, 172–189.

72

  

McEwen, B. S., & Sapolsky, R. M. (1995). Stress and cognitive function. Current Opinion in Neurobiology, 5, 205–216. McGaugh, J. L. (1983). Hormonal inﬂuences on memory. Annual Review of Psychology, 34, 297–323. McGaugh, J. L. (2000). Memory—A century of consolidation. Science, 287, 248–251. McGaugh, J. L., & Izquierdo, I. (2000). The contribution of pharmacology to research on the mechanisms of memory formation. Trends in Pharmacological Science, 21, 208–210. Moayeri, S. E., Cahill, L., Jin, Y., & Potkin, S. G. (2000). Relative sparing of emotionally inﬂuenced memory in Alzheimer’s disease. Neuroreport, 11, 653–655. Mori, E., Yoneda, Y., Yamashita, H., Hirono, N., Ikeda, M., & Yamadori, A. (1997). Medial temporal structures relate to memory impairment in Alzheimer’s disease, an MRI volumetric study. Journal of Neurology, Neurosurgery, and Psychiatry, 63, 214–221. Mu, Q., Xie, J., Wen, Z., Weng, Y., & Shuyan Z. (1999). A quantitative MR study of the hippocampal formation, the amygdala, and the temporal horn of the lateral ventricle in healthy subjects 40 to 90 years of age. American Journal of Neuroradiology, 20, 207–211. Murray, E. A. (1992). Medial temporal lobe structures contributing to recognition memory: The amygdaloid complex versus the rhinal cortex. In J. P. Aggleton (Ed.), The amygdala: Neurobiological aspects of emotion, memory, and mental dysfunction (pp. 453–470). New York: Wiley-Liss. Öhman, A., & Mineka, S. (2001). Fears, phobias, and preparedness, toward an evolved module of fear and fear learning. Psychological Review, 108, 483–522. Oitzl, M. S., & de Kloet, E. R. (1992). Selective corticosteroid antagonists modulate speciﬁc aspects of spatial orientation learning. Behavioral Neuroscience, 106, 62–71. Packard, M. G., Cahill, L., & McGaugh, J. L. (1994). Amygdala modulation of hippocampal-dependent and caudate nucleus-dependent memory processes. Proceedings of the National Academy of Science, USA, 91, 8477–8481. Packard, M. G., & Teather, L. A. (1998). Amygdala modulation of multiple memory systems, hippocampus and caudate-putamen. Neurobiology of Learning and Memory, 69, 163–203. Parker, A., Wilding, E., & Akerman, C. (1998). The Von Restorﬀ eﬀect in visual object recognition memory in humans and monkeys. The role of frontal/perirhinal interaction. Journal of Cognitive Neuroscience, 10, 691–703. Phelps, E. A., LaBar, K. S., & Spencer, D. D. (1997). Memory for emotional words following unilateral temporal lobectomy. Brain and Cognition, 35, 85–109. Pitkänen, A. (2000). Connectivity of the rat amygdaloid complex. In J. P. Aggleton (Ed.), The amygdala: A functional analysis. Oxford: Oxford University Press. Quirarte, G. L., Roozendaal, B., & McGaugh, J. L. (1997). Glucocorticoid enhancement of memory storage involves noradrenergic activation in the basolateral amygdala. Proceedings of the National Academy of Science, USA, 94, 14048–14053. Reisberg, D., & Heuer, F. (1992). Remembering the details of emotional events. In E. Winograd & U. Neisser (Eds.), Aﬀect and accuracy in recall: Studies of “ﬂashbulb” memories (pp. 163–190). Cambridge, MA: Harvard University Press.

      

73

Rolls, E. T. (2000a). Memory systems in the brain. Annual Review of Psychology, 51, 599–630. Rolls, E. T. (2000b). The orbitofrontal cortex and reward. Cerebral Cortex, 10, 284– 294. Roozendaal, B. (2000). Glucocorticoids and the regulation of memory consolidation. Psychoneuroendocrinology, 25, 213–238. Roozendaal, B., Williams, C. L., & McGaugh, J. L. (1999). Glucocorticoid receptor activation in the rat nucleus of the solitary tract facilitates memory consolidation, involvement of the basolateral amygdala. European Journal of Neuroscience, 11, 1317–1323. Schmolck, H., Buﬀalo, E. A., & Squire, L. R. (2000). Memory distortions develop over time: Recollections of the O. J. Simpson trial verdict after 15 and 32 months. Psychological Science, 11, 39–45. Schooler, J. W., & Eich, E. (2000). Memory for emotional events. In E. Tulving & F. I. M. Craik (Eds.), The Oxford handbook of memory (pp. 379–392). Oxford: Oxford University Press. Scott, S. A., DeKosky, S. T., & Scheﬀ, S. W. (1991). Volumetric atrophy of the amygdala in Alzheimer’s disease, quantitative serial reconstruction. Neurology, 41, 351–356. Scoville, W. B., & Milner, B. (1957). Loss of recent memory after bilateral hippocampal lesions. Journal of Neurology, Neurosurgery, and Psychiatry, 20, 11–21. Seidlitz, L., & Diener, E. (1998). Sex diﬀerences in the recall of aﬀective experiences. Journal of Personality and Social Psychology, 74, 262–271. Shepard, J. D., Barron, K. W., & Myers, D. A. (2000). Corticosterone delivery to the amygdala increases corticotropin-releasing factor mRNA in the central amygdaloid nucleus and anxiety-like behavior. Brain Research, 861, 288–295. Squire, L. (1987). Memory and brain. New York: Oxford University Press. Squire, L. R., & Kandel, E. R. (2000). Memory: From mind to molecules. New York: Scientiﬁc American Library. Tomaz, C., Dickinson-Anson, H., McGaugh, J. L., Souza-Silva, M. A., Viana, M. B., & Graeﬀ, F. G. (1993). Localization in the amygdala of the amnestic action of diazepam on emotional memory. Behavioral Brain Research, 58, 99–105. Tranel, D. & Hyman, B. (1990). Neuropsychological correlates of bilateral amygdala damage. Archives of Neurology, 47, 349–355 Tulving, E., Kapur, S., Craik, F. I., Moscovitch, M., & Houle, S. (1994). Hemispheric encoding/retrieval asymmetry in episodic memory, positron emission tomography ﬁndings. Proceedings of the National Academy of Science, USA, 91, 2016–2020. Tulving, E., Kapur, S., Markowitsch, H. J., Craik, F. I., Habib, R., & Houle, S. (1994). Neuroanatomical correlates of retrieval in episodic memory, auditory sentence recognition. Proceedings of the National Academy of Science, USA, 91, 2012–2015. Van Hoesen, G. W., Augustinack, J. C., & Redman, S. J. (1999). Ventromedial temporal lobe pathology in dementia, brain trauma, and schizophrenia. Annals of the New York Academy of Science, 877, 575–594. Weiskrantz, L. (1956). Behavioral changes associated with ablation of the amygdaloid complex in monkeys. Journal of Comparative and Physiological Psychology, 49, 381–391.

74

  

Yerkes, R. M., & Dodson, J. D. (1908). The relation of strength of stimulus to rapidity of habit formation. Journal of Comparative Neurology and Psychology, 18, 31– 39. Zola-Morgan, S., Squire, L. R., Alvarez-Royo, P., & Clower, R. P. (1991). Independence of memory functions and emotional behavior, separate contributions of the hippocampal formation and the amygdala. Hippocampus, 1, 207–220. Zola-Morgan, S., Squire, L. R., & Amaral, D. G. (1986). Human amnesia and the medial temporal region, enduring memory impairment following a bilateral lesion limited to ﬁeld CA1 of the hippocampus. Journal of Neuroscience, 6, 2950– 2967. Zola-Morgan, S., Squire, L. R., & Amaral, D. G. (1989). Lesions of the amygdala that spare adjacent cortical regions do not impair memory or exacerbate the impairment following lesions of the hippocampal formation. Journal of Neuroscience, 9, 1922–1936.

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3

       . ,  ,  . ,  .  

T

rauma aﬀects memory. We have known that for millennia, but only recently have we been able to ask and answer pointed questions about why and how. Only by elucidating the neurological consequences of trauma, which until recently had been deemed a purely “psychological” event, can we unravel its impact on memory. In this chapter we (1) brieﬂy discuss the nature and organization of memory; (2) attempt to deﬁne the notion of trauma and the related phenomenon of stress; (3) consider the impact of trauma and stress on the brain and, by extension, on the memory functions subserved by the brain; (4) oﬀer an integrated account connecting these data with several clinical manifestations of trauma, stress, and memory; and (5) use this account to resolve an apparent tension between two parallel literatures: one describing a trauma- or stress-based impairment of memory and another describing an emotion-based enhancement of memory.

The Nature of Memory:

A Taxonomy

One of the key insights of recent cognitive- and neuroscience-based analyses of memory is that multiple systems underlie this function. Unlike earlier perspectives, which viewed memory as a single system, perhaps subserved by a restricted part of the brain, the modern consensus view is that several types of memory, each obeying rather diﬀerent rules of operation, and each subserved by discrete neural systems, interact to produce our subjective sense of remembering. This insight is critical if we are to understand the impact of any experience, normal or traumatic, on memory, because it raises the possibility that diﬀerent kinds of memory will face diﬀerent fates in the presence of trauma.

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We needn’t go into much detail about the nature of these multiple memory systems or the types of information they process. Various views suggest how to classify and arrange these systems (cf. Schacter & Tulving, 1994); most agree on a distinction between two broad classes of memory. First, there are memories of the events in our lives and the knowledge of the world that we obtain from those events. Typically, this class of memory, referred to as explicit memory, can be explicitly retrieved on demand. Second, there are memories for the skills, procedures, and habits we acquire through experience. These implicit memories are not so readily made explicit; indeed, in most instances these memories cannot be expressed explicitly and are evident only in behavior. A distinction between explicit and implicit memory is important but not suﬃcient for understanding the impact of trauma on remembering. Within explicit memory, there is a further crucial subdivision between episodic and semantic memories. Episodic memory incorporates the speciﬁc context of an experienced event, including the time and place of its occurrence. Semantic memory, on the other hand, is concerned with the knowledge one acquires during events but is itself separated from the speciﬁc event in question. Thus, our knowledge about the meaning of words, and facts about the world, though acquired in the context of some speciﬁc experience, appears to be stored in a form that is not bound to the originating context. The sensory features of experiences, their positive and negative attributes, other objects with which they might have been associated— knowledge of this kind constitutes a part of semantic memory. The exact relation between episodic and semantic memory remains to be unraveled; however, there is considerable agreement that they are separable in the brain. Evidence suggests a third, emotional memory, system that mediates the encoding and storage of emotionally charged events. This system pertains to learning about fearful and unpleasant stimuli, although some evidence suggests it plays a role in memory for pleasant information as well (see chapter 2, this volume; Hamann, Ely, Grafton, & Kilts, 1999). Apparently, each of these memory systems is subserved by a diﬀerent brain area, and, consequently, each is open to diﬀerential impact by exposure to stressors and to trauma. Episodic memory seems to be the most inﬂuenced by trauma and stress and is neuroanatomically linked to the hippocampal formation in the medial temporal lobe. But before embarking on a description of the hippocampal system and detailing its response to stress, we ﬁrst deﬁne stress and trauma.

What Are Stress and Trauma? Despite the widespread use of “stress” and “trauma,” these terms lack precise deﬁnitions. Although “stressor” is unambiguous according to the Oxford English Dictionary (OED), which gives it a single deﬁnition, “a single condition or agent that constitutes a stress for an organism,” the term “stress” is utterly ambiguous.

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The OED provides at least nine distinct senses of the word when it is used as a noun. These range from stress deﬁned as “emphasis,” to stress deﬁned as “physical hardship, strain or pressure.” Furthermore, the OED provides at least ﬁve distinct meanings for “stress” used as a verb. “Trauma” is similarly ambiguous. Although the OED considers it only as a noun, it gives ﬁve distinct senses for its use, including two that are germane here: 1. Pathology. A wound, or external bodily injury in general; also the condition caused by this. 2. Psychoanalysis and Psychiatry. A psychic injury, especially one caused by emotional shock the memory of which is repressed and remains unhealed; an internal injury, esp. to the brain, which may result in a behavioral disorder of organic origin. Also, the state or condition so caused.

In the scientiﬁc literature, both trauma and stress are often treated as static things, as if they were well-deﬁned entities characterized by psychophysiological measures that identify and quantify them (Kim & Diamond, 2002). Such is clearly not the case, at least not at this stage in our understanding. Both stress and trauma are events, that is, dynamic processes associated with various physical and psychological responses that can diﬀer in magnitude and expression. A common working deﬁnition of stress is any event that seriously disturbs the physiological or psychological homeostasis of an organism. Cannon (1929) was the ﬁrst to use ‘homeostasis’ to characterize processes that are essential to the maintenance of life and to highlight the body’s ability to control its internal environment within narrow limits. Selye (1956) initiated the ﬁrst major study of the eﬀects of stress on systemic regulation, deﬁning stress as any severe threat to homeostasis that could result in death. More recently, however, McEwen (2000, 2001) has suggested that because homeostasis applies to a limited number of systems (such as pH, body temperature) that are essential for survival, another term, “allostasis,” may better describe the processes disturbed during stress. Allostasis refers to the systems that actively maintain homeostasis even when life and death are not at stake. Kim and Diamond (2002) argue that a good deﬁnition of stress must address the following two facts. First, stress is determined not by a given environmental situation but by how an organism perceives and reacts to a situation. This deﬁnition permits individual diﬀerences in response to stressors, as well as variations in response to a ﬁxed stressor over time and experience within an individual. The need to take experience, personal biases, and temperament into account should be obvious to anyone who has learned to engage in public speaking; at ﬁrst a nerve-racking experience, for most, public speaking eventually becomes easier and less anxiety-provoking. Second, there is no physiological state that always deﬁnes stress. Although most investigators rely on elevations of stress hormones

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(e.g., glucocorticoids) as an indicator of stress, such hormones can also increase in response to physical exertion and daily changes in the sleep/wake cycle (e.g., Kanaley, Weltman, Pieper, Weltman, & Hartman, 2001; Plihal & Born, 1999; Van Cauter & Turek, 2001). With these limitations in mind, Kim and Diamond (2002) presented a threepart deﬁnition of stress, which they claim is broadly applicable across species and paradigms. They argue that, ﬁrst, stress is always accompanied by high levels of physiological arousal, as measured by behavior (motor behaviors) or neurochemistry (increased stress hormones). Second, stress must be perceived as threatening and something that would be avoided if possible. For example, giving a speech is considered threatening, and many people would avoid it if possible. When the speech cannot be avoided, however, the task is accompanied by increased physiological excitability (heart rate, sweating, glucocorticoid increases, etc.). Finally, stress depends on whether an organism perceives that it has control over the stressful experience. This component reﬂects evidence from animal and human studies demonstrating that perceived control can profoundly mitigate the experience of stress (e.g., Fox & Dwyer, 2000; Maier & Watkins, 1998; Prince & Anisman, 1990). We agree with the ﬁrst component of the deﬁnition but take issue with the second and third components. We suggest that “stressor” should not always mean something negative. Instead, it should simply designate a dynamic “strain” or “pressure” exerted on an individual. This strain or pressure could be pleasant (e.g., skydiving, sexual activity) or unpleasant (e.g., a loss of social status), but in both cases it disturbs the individual’s allostatic balance. Further, the data suggest that controllability can sometimes mitigate the action of a stressor but at other times has no impact at all. People often have control over events they experience as stressful; giving speeches and willingly jumping out of airplanes are two good examples. Thus, although controllability is certainly important and may, in some cases, both mitigate the perceived negativity of stress and determine its magnitude, we assert that stress reactions, even intense stress reactions, occur in the presence of perceived control. For our purposes, then, we use “stress” to designate activation of a dynamic physiological state—a system that, according to current knowledge, consists of the hypothalamic-pituitary-adrenal (HPA) axis. We use the activation of this system as a proxy for stress, bearing in mind the noted qualiﬁcation that the mere presence of this physiological state does not indicate inevitable stress. Further details of the physiology of stress will be provided in the section that follows. Moreover, we use the term “stressor” to designate the environmental conditions that elicit or inﬂuence this physiological system, recognizing the need to specify the formal relations between given environmental stressors and the stress response. We do not consider psychological trauma the equivalent of intense stress. Although stress coupled with environmental variables may produce a traumatic

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psychological state, and a traumatic psychological state may induce stress (i.e., serve as a stressor), a traumatic state is, by our reckoning, a quasi-independent mental state that systematically interacts with stress and stressors.1

Eﬀects of Stress: Brain Physiology

and Anatomy

As mentioned, stressors activate the HPA axis. Although the stress response system is complex, to date much of the research focus has been on the HPA axis and the hippocampus. Stress leads to the release of corticotropin-releasing factor (CRF) from the hypothalamus and subsequently triggers adrenocorticotropic hormone (ACTH) release from the pituitary gland. In response to ACTH, stress hormones called glucocorticoids are secreted and released from the adrenal glands. Circulating glucocorticoids then feed back onto the pituitary and hypothalamus to inhibit the secretion of CRF and ACTH. The hippocampus (and certain cortical areas, particularly the frontal cortex) plays an important role in this negative feedback system as well, helping the pituitary and hypothalamus inhibit HPA activity (Feldman & Conforti, 1980, 1985; Jacobson & Sapolsky, 1991; Sapolsky & Meaney, 1986). Hippocampal involvement in the regulation of the stress response turns out to be critically important to any discussion of stress and memory, because, as we noted, this structure has long been implicated in explicit memory. In particular, the hippocampal formation has been linked to episodic memory, to context, and to spatial maps (e.g., O’Keefe & Nadel, 1978). Debate rages over aspects of this story, but the link between the hippocampal system and episodic memory seems ﬁrm. The seminal studies of Scoville and Milner (1957), for example, made it clear that bilateral ablation of the hippocampal complex resulted in profound loss of memory. We now know that damage to the hippocampus results in a speciﬁc form of memory dysfunction, in particular that involving spatial/contextual and episodic memories (Hirsch, 1974; Nadel, 1991, 1994; Nadel & Willner, 1980; Rosenbaum et al., 2000), and, further, that stress appears to impair precisely these types of memory (see Lupien & McEwen, 1997). Together with the discovery of dense concentrations of stress hormone receptors in the hippocampus (e.g., McEwen, Weiss, & Schwartz, 1968), these ﬁndings provide a basis for the claim that stress hormone modulation of hippocampal activity underlies the damaging eﬀects of stress in animals and humans (see Bremner, 1999; McEwen, 2000, for reviews). Thus, increases in stress hormones not only trigger inhibition of HPA activity via hippocampal mediation but at high enough levels also impair the neuronal structure and function of the hippocampus. Glucocorticoids at abnormally high or abnormally low concentrations can, by changing the physiological characteristics of large populations of neurons, disrupt hippocampal function. Thus,

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a moderate level of circulating glucocorticoids appears to enhance memory, whereas maximal or minimal levels appear to disrupt it. The stress response typically involves a dramatic increase in the level of circulating glucocorticoids, which can produce changes in hippocampal neuronal physiology and anatomy. In short, stress appears to alter hippocampal morphology, disrupt neurogenesis, and block synaptic plasticity thought to underlie memory formation (see McEwen, 2000, 2001, for reviews). For example, both glucocorticoid exposure and restraint stress over 21 days have been shown to result in reduced dendritic branching in pyramidal neurons of the CA3 region of the rat hippocampus (Magarinos & McEwen, 1995; Watanabe, Gould, & McEwen, 1992; Woolley, Gould, & McEwen, 1990). Psychosocial stress leads to atrophy of dendrites as well, in the tree shrew (Magarinos, McEwen, Flugge, & Fuchs, 1996) and in rats (McKittrick et al., 2000). In addition, stress and glucocorticoid elevation can produce alterations in synaptic terminal structure in CA3 (Magarinos, Verdugo, & McEwen, 1997). With even longer periods of exposure to stress and glucocorticoids, initial evidence suggested that overt loss of hippocampal neurons occurred (e.g., Sapolsky, Krey, & McEwen, 1985; Uno, Ross, Else, Suleman, & Sapolsky, 1989). Such ﬁndings led to assumptions that neuronal death associated with glucocorticoid release might underlie the severe memory impairments seen in posttraumatic stress disorder (see later discussion). More recent work, however, raises questions about whether glucocorticoids are themselves toxic or simply create conditions for other factors to exert neurotoxic eﬀects (Sapolsky, 1996). Nonetheless, chronic exposure to stressors is undoubtedly associated with hippocampal impairment. For example, post-mortem analysis of chronically stressed monkeys showed extensive damage in the CA3 region of the hippocampus; subsequent research suggested that high levels of the glucocorticoid cortisol were responsible for the hippocampal damage, as cortisol-secreting pellets implanted in the monkey hippocampus resulted in the same pattern of damage. In addition to having neurotoxic eﬀects on hippocampal neurons, chronic exposure to stressors may also inhibit the growth of new neurons (granule cells) in the dentate gyrus, thereby changing its structure. A stress-induced decrease in neurogenesis has been demonstrated in the dentate gyrus of rats, tree shrews, and primates (Gould, Tanapat, McEwen, Flugge, & Fuchs, 1998; Gould & Tanapat, 1999; Tanapat, Hastings, Rydel, Galea, & Gould, 2001) and has been hypothesized as the primary mechanism of stress-related hippocampal impairment (Gould & Gross, 2002; Gould & Tanapat, 1999). Glucocorticoids appear to mediate these stress-induced changes in neurogenesis. For example, normalizing glucocorticoid levels was shown to prevent predator odor stress from inhibiting granule cell production (Tanapat et al., 2001). In addition, corticosterone treatment has been shown to decrease dentate cell proliferation, whereas adrenalectomy increases the production of new granule cells (Cameron & Gould, 1994; Cameron & McKay, 1999).

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In addition to these structural eﬀects, stress and stress hormones also modulate the excitability of hippocampal neurons. Acute stress and glucocorticoid release can impair hippocampal plasticity (Diamond, Fleshner, & Rose, 1994; Foy, Stanton, Levine, & Thompson, 1987). Long-term potentiation (LTP) and the related phenomenon of primed burst potentiation (PBP) are two processes by which hippocampal neuronal responsiveness changes in response to experience (McEwen, 2001). Thus, these forms of potentiation are often conceptualized as physiological models of memory. Studies show that hippocampal LTP can be impaired by the administration of glucocorticoids (e.g., Diamond & Rose, 1994; Filipini, Gijsbers, Birmingham, & Dubrovsky, 1991). Diamond, Bennet, Fleshner, and Rose (1992) reported an inverted U-shaped relationship between the level of circulating glucocorticoids and the extent of LTP, demonstrating that glucocorticoids facilitated LTP at low levels but disrupted it at high levels. Stressinduced disruption of LTP targets CA1 and the dentate gyrus and has been shown to last up to 48 hours in rats and 24 hours in mice (e.g., Garcia, Musleh, Tocco, Thompson, & Baudry, 1997; Shors, Gallegos, & Breindl, 1997). These studies show that LTP can be disrupted by stress and that changes can last for days after exposure to a single stressor; however, these changes are typically not permanent. More recent studies suggest that PBP may be even more sensitive to psychological stress (e.g., predator exposure) than is LTP (Mesches, Fleshner, Heman, Rose, & Diamond, 1999).

Stress and Brain Anatomy:

Evidence for Hippocampal

Volume Reduction

Given the evidence of hippocampal impairment in response to stress, one might expect to see gross structural changes in the hippocampi of certain patient populations. Indeed, the human hippocampus does appear to show signs of atrophy as a result of severe stress or persistently elevated glucocorticoids. Reductions have been noted in disorders associated with prolonged glucocorticoid elevations, such as Cushing’s syndrome, recurrent major depression, schizophrenia, posttraumatic stress disorder, and in some cases of normal aging (Starkman et al., 1999; Sheline et al., 1996; Bremner et al., 1993; Bremner, Randall, Capelli, et al., 1995; Gurvits et al., 1996; Fukuzako et al., 1996; Convit et al., 1995). For example, Cushing’s syndrome arises from adrenocorticotropic hormone or corticotropin-releasing hormone secreting tumors (Sapolsky, 2000). Those with the disorder thus have hypercortisolemia and often exhibit cognitive dysfunction (Sapolsky, 2000; Starkman et al., 1999). Using magnetic resonance imaging (MRI), researchers have reported selective hippocampal atrophy in individuals suﬀering from Cushing’s syndrome for approximately 1 to 4 years (Starkman, Gebarski, Berent, & Schteingart, 1992). Although a trauma control group was not tested in this study, hippocampal reduction was strongly correlated with cortisol levels.

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MRI studies of PTSD have revealed a pattern of evidence many consider indicative of hippocampal atrophy. When Vietnam veterans with combat-related PTSD were compared to healthy control subjects, the PTSD patients were found to have an 8% reduction in right hippocampal volume (Bremner, Randall, Scott, et al., 1995). This diﬀerence in volume was associated with short-term memory impairments as assessed by the WMS-Logical memory test. Similar results were obtained in childhood abuse survivors (physical and sexual) with PTSD (Bremner et al., 1997). In this sample, however, left hippocampal volume was 12% smaller than that of controls. Although right hippocampi were 3.8% smaller than those of controls, this diﬀerence did not reach statistical signiﬁcance. In both studies, control subjects were matched for sex, age, race, height, weight, socioeconomic status, education, and alcohol abuse. Other studies ﬁnding similar diﬀerences in hippocampal volume include Gurvits et al. (1996) (26% smaller bilateral volume in Vietnam combat veterans with PTSD compared to non-PTSD combat veterans) and Stein, Koverola, Hanna, Torchia, & McClarty (1997) (5% smaller left hippocampal volume in women who reported sexual abuse than in controls). Concerns about the reliability and interpretability of these studies, which center on the co-occurrence of hippocampal atrophy with other disorders (e.g., depression, substance abuse), led Bremner and other researchers to revisit their dataset and statistically exclude those subjects who had abused alcohol or other substances during the 6 months prior to their MRIs. Despite these changes, results remained suggestive of a relationship between PTSD and reduced hippocampal volume not explainable by alcohol or drug abuse (see Bremner, 2001b). Though in general MRI studies are suggestive of stress-related hippocampal atrophy, interpretation of the results is compromised by cross-sectional designs and the use only of subjects with chronic PTSD. Consequently, one cannot use these results to infer causality. Reduced hippocampal volume could either precede the traumatic event, making individuals vulnerable to developing PTSD, or could develop in the aftermath of the trauma as a consequence of prolonged exposure to stress hormones or other uncontrolled factors. To correct for these confounds, Bonne et al. (2001) conducted a prospective MRI study examining the hippocampal volume of individuals exposed to acute traumas (traumas experienced by subjects admitted to a hospital emergency room). The hippocampal volume of those who developed PTSD 6 months later did not diﬀer from those who had not developed PTSD at the 6-month followup. Although these results are inconsistent with earlier studies of hippocampal volume reductions and PTSD, they may be explained by diﬀerences in the nature or duration of trauma. The earlier studies tested individuals exposed to chronic traumatization, such as child abuse or war experience, whereas Bonne et al. tested individuals exposed to acute stressors, perhaps of lesser severity.2 Another possibility is that the earlier studies failed to screen tightly for confounding factors such as alcoholism and depression, although Bremner (2001b) attempted to do so. In any case, the conservative conclusion is that tentative evidence

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exists for reduced hippocampal volume in PTSD. Further studies that better control for comorbidity, type and duration of trauma, and duration of PTSD are needed. Nonetheless, stress-induced deﬁcits in memory may exist in the absence of gross neuroanatomical changes, reﬂecting either functional or subtle structural impairments.

Eﬀects of Stress on Memory: Data We have shown that exposure to trauma may result in damage to brain regions important for memory function. Now we turn to evidence supporting a relationship between stressors and memory function itself, a relationship with a long history. Stress-related memory impairments have been reported in a variety of clinical settings. As we mentioned, patient populations with chronically elevated levels of stress hormones, such as Cushing’s syndrome, schizophrenia, some forms of recurrent depression, PTSD,3 dementia of the Alzheimer’s type, and asthmatic patients treated with the glucocorticoid prednisone (Keenan, Jacobson, Soleymani, & Newcomer, 1995; Mauri et al., 1993; Rasmusson et al., 2001; Sapolsky, 2000; Sheline, Sanghavi, Mintun, & Gado, 1999; Starkman et al., 1999), are characterized by impaired memory function. However, despite consistent correlations between chronic elevations in stress hormones and memory impairment, these data are limited by the problems endemic to all naturalistic studies. Because nonrepresentative sampling, possible noncausal associations, and confounding variables such as extraneous disease factors may be responsible for memory impairments (e.g., Sapolsky, 2000), these observations must be treated with caution. The correlations do, however, serve as a starting point and encourage us to take a closer look at the nature of memory and its interactions with stress and trauma. A growing body of randomized, placebo-controlled studies, using reasonably precise deﬁnitions of stress, has demonstrated that exposure to uncontrollable stressors can impair memory. This research has proceeded along two separate but related paths, one dedicated to the study of relations between episodic memory and long-term/chronic stress and the other to relations between episodic memory and short-term/acute stress. The ethics inherent in human research make experimental studies of relations between memory and chronic stressors diﬃcult if not impossible, leaving the ﬁeld to naturalistic research designs. Experimental studies of relations between memory and acute stressors, such as stressful speeches or participation in highrisk tasks (e.g., skydiving), though diﬃcult ethically, are at least possible. Finally, the ethics governing animal research permit the induction of short-term (acute) and long-term or repeated (chronic) stress using stressors such as tail-shock, restraint, swimming in cold water, and more naturalistic stressors such as

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predator exposure. We consider each of these literatures brieﬂy in the following sections. The administration of stress-related hormones permits well-controlled studies of relations between memory and acute stress in humans. Acute doses of stress hormones such as glucocorticoids (e.g., cortisol) can be safely administered to humans over relatively brief periods. In some studies, agonists (corticocortisone) or antagonists (e.g., dexamethasone) of naturally occurring glucocorticoids are used instead of cortisol. Glucocorticoid antagonists reduce the level of circulating glucocorticoids, and both abnormally high and abnormally low levels of glucocorticoids have been shown to produce memory deﬁcits (Conrad & Roy, 1996; Luine, Villegas, Martinez, & McEwen, 1994; Vaher, Luine, Gould, & McEwen, 1994).

Acute Stressors: Memory in Humans Inducing acute stress in the laboratory typically involves exposing the subject, whether animal or human, to a brief, one-time stressor (e.g., a speech task, a predator’s odor) or administering a single dose of glucocorticoids. In both cases, glucocorticoid levels increase, usually for no longer than several hours in humans. However, the cognitive eﬀects of acute stress or glucocorticoid administration are often apparent for several hours to as long as a day; moreover, they are usually reversible and are often speciﬁc to the task or experimental situation (McEwen, 2001). These eﬀects are typically speciﬁc to memory function, with spatial and verbal-episodic memory often showing the greatest impairment. Wolkowitz, Reus, and Weingartner (1990) and Wolkowitz et al. (1993), for example, examined recall of previously learned verbal-episodic material after the administration of dexamethasone or prednisone and found that these glucocorticoids interfered with word recall. In the dexamethasone study, participants learned a list of 12 semantically associated words, which they were ﬁrst asked to recall following a 90-second distractor task and then asked to recognize in a larger list of related distractor words. Participants were tested 1 week before and 1 day after administration of 1 mg of dexamethasone. Although this single dose of dexamethasone did not change recall, it did increase errors of commission, or false recognition of related words not presented on the study list. The prednisone study used a similar test of memory, but here both recall and recognition of previously learned words were required 24 hours after presentation of the list, a manipulation that created a test of longer-term episodic memory. Participants were given 80 mg of prednisone daily for 5 days. Word recognition and recall were tested once during an initial 5-day placebo period, again after 4 days of prednisone administration, and once again 7 days after discontinuation of the treatment. Again, participants receiving prednisone showed no diﬀerences in free recall but falsely recognized more semantically related words than

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did controls. Thus, administration of dexamethasone and prednisone resulted in diﬃculties recognizing words presented in standard word lists (see also Bender, Lerner, & Poland, 1991), a diﬃculty characterized by an impaired ability to discriminate previously studied information from new, but similar, information. Newcomer, Craft, Hershey, Askins, and Bardgett (1994) also investigated the eﬀects of dexamethasone on measures of memory, as well as attention and perceptual function. Dexamethasone treatment administered over 4 days (in successive doses of 0.5, 1, 1, and 1 mg) was associated with impaired recall of verbal material originally presented in a paragraph (Wechsler, 1945). This impairment was strongest on the 4th day of treatment and was speciﬁc to memory for verbal material. The presence of dexamethasone did not aﬀect measures of attention or perception. Unlike Wolkowitz et al. (1990, 1993), Newcomer et al. (1994) found that dexamethasone treatment resulted in errors of omission (information in the paragraph was forgotten) but not errors of commission (related but nonpresented information was added to the material presented in the paragraph). The diﬀerences between the Wolkowitz et al. (1990) and Newcomer et al. studies are likely due to diﬀerences in the strategies required by the two tasks. The recall task Newcomer et al. used required the verbatim recall of story-like information presented in paragraph format. Given these instructions, normal subjects usually make more omission than commission errors, as thematically related intrusions errors rarely occur in this type of task. By comparison, semantically associated word lists, like the ones used in Wolkowitz et al. (1990), are known to produce commission errors at high rates (see Roediger & McDermott, 1995). We have recently shown that psychologically induced stress increases commission errors on semantically associated word lists (Payne, Nadel, Allen, Thomas, & Jacobs, 2002), a result we will discuss in more detail. Results of the ﬁrst few experimental studies indicate that pharmacological doses of the glucocorticoids dexamethasone and prednisone impair verbal episodic memory. However, caution should be used when thinking of this memory impairment as causally related to stress-induced increases in cortisol. Although changes in recall and recognition could result from increased glucocorticoid receptor binding in a manner similar to the direct administration of cortisol (the traditional explanation), an alternative explanation is possible. Dexamethasone suppresses cortisol, and because very high or very low levels of cortisol can aﬀect the biological structures on which memory depends, the observed changes could result from dexamethasone-induced decreases in cortisol secretion—and, hence, a failure to bind to glucocorticoid receptors. This uncertainty, along with diﬀerences in the binding of dexamethasone and cortisol to type I and type II glucocorticoid receptors in the hippocampus, limits our conﬁdence in the generality of conclusions reached when dexamethasone and similar ligands are used to examine the eﬀects of cortisol or stress in humans (Newcomer et al., 1999).

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Similar concerns motivated a second study by Newcomer et al. (1999), which examined interactions between hydrocortisone (cortisol) and explicit memory for words, again using a paragraph recall task. Two ﬁxed oral doses of hydrocortisone (160 mg/d or 40 mg/d) were administered over 4 days. The lower-dose treatment was selected to approximate physiological levels of cortisol associated with mild to moderate stress, and the higher-dose treatment was selected to approximate physiological levels of cortisol associated with severe stress. Sampling of plasma cortisol and memory testing were conducted at baseline (day 0), on days 1 and 4, and after a 6-day washout period (day 10). Impaired paragraph recall was reported in the presence of the higher, but not the lower, dose of hydrocortisone. As in their previous study (Newcomer et al., 1994), this eﬀect was maximal on the 4th day of treatment. Newcomer et al. (1999) did not observe the immediate eﬀects of glucocorticoids seen in some studies (e.g., Wolkowitz et al., 1990) but instead showed that several days of cortisol exposure at doses and plasma concentrations associated with high stress could impair the recall of verbal material presented in a paragraph format. An earlier study by Kirschbaum, Wolf, Wippich, and Hellhammer (1996), however, reported that a single, low dose of hydrocortisone (10 mg) led to a deﬁcit in verbal episodic memory. In this study, subjects who received hydrocortisone recalled fewer words (via a cued recall test) from a previously learned word list than did control subjects when recall occurred 60 minutes after receiving the drug. Thus, hydrocortisone apparently can produce a deﬁcit in at least one type of verbal memory (cued word recall) at smaller doses and with shorter delays between administration and test than suggested by the results of the Newcomer et al. (1999) experiment. Again, the diﬀerences in these two experiments might depend on the nature of the material recalled, the delay between learning and test, or diﬀerent task demands. Although the details vary from experiment to experiment, the administration of drugs simulating acute stress clearly changes the recall pattern of words presented in word lists or paragraphs, both of which measure aspects of explicit verbal memory. Many of the glucocorticoid-administration studies are limited in that the physiological eﬀects of cortisol are longer-lived than those of the standard memory experiment (which typically lasts no longer than an hour or two). Consider the designs used by Kirschbaum et al. (1996) and Newcomer et al. (1999) already described. In each case cortisol levels were probably elevated continuously throughout the study, making it diﬃcult to determine what aspect of memory was impaired. In an attempt to sort this out, de Quervain, Roozendaal, Nitsch, McGaugh, and Hock (2000) administered 25 mg doses of cortisone (which is quickly absorbed and transformed into cortisol) at diﬀerent stages of a verbal delayed free-recall experiment. In this way they could evaluate the impact of elevated cortisol on each of three distinct memory processes: acquisition, storage, and retrieval. Participants learned word lists composed of unrelated words and received cortisone either (1) before list learning, (2) immediately after

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list learning, or (3) 24 hours later, but immediately before recall. Impairment in recall was found only when cortisone was given immediately before recall, thus implicating retrieval as the memory stage most aﬀected by a low dose of cortisol. Although a 25 mg dose of hydrocortisone administered at encoding did not aﬀect recall of verbal material presented in paragraphs (Newcomer et al., 1999), the same low dose of cortisone did aﬀect the retrieval of words presented in lists (de Quervain et al., 2000). This discrepancy could have arisen from diﬀerences in the kind of information recalled (stories vs. word lists), or it might reﬂect a greater impact of stress on retrieval than on encoding or consolidation. In addition to explicit memory for words, spatial memory also appears to suﬀer in the presence of stress. To our knowledge, spatial memory in humans has not yet been assessed with the direct administration of glucocorticoids. However, Laurance, Hardt, Nadel, and Jacobs (2001) found that exposure to a social stressor (public speaking) slows the rate at which spatial information is acquired in a virtual environment. The impact of stress in this study was speciﬁc to spatial map-based performance, whereas performance based on individual cues, and therefore dependent on diﬀerent neural circuits, remained intact. Public speaking tasks have also resulted in verbal episodic deﬁcits, as measured by listlearning tasks, in healthy elderly subjects (Lupien et al., 1997) and in younger adults (Kirschbaum et al., 1996).

Acute and Chronic Stressors:

Memory in Animals

Animal studies of stress and memory yield results that are generally consistent with the human studies; exposure to glucocorticoids, acute or long-term, is often associated with deleterious eﬀects on memory tasks dependent on hippocampal integrity (e.g., Bodnoﬀ et al., 1995; Luine et al., 1994; Ohl & Fuchs, 1999; see Kim & Diamond, 2002; Lupien & Lepage, 2001, for reviews). As in humans, however, acute stress eﬀects are often short-term and reversible, whereas repeated or long-term stress eﬀects can lead to frank cognitive dysfunction (McEwen & Sapolsky, 1995) that may result from the changes in hippocampal morphology already described. Administering corticosterone to rats facilitates the extinction of forms of conditioned shock-avoidance that depend on the hippocampal formation (e.g., Bohus & Lissak, 1968; Greidanus, 1970; Roozendaal & McGaugh, 1996). Spatial memory, also known to depend on the hippocampus, is impaired in rats exposed to stressors or given corticosterone and in transgenic mice with elevated corticosterone levels. For example, 21 days of restraint was correlated with impairments in spatial memory as measured by performance in the radial arm maze task (Luine et al., 1994). Exposure to stressors has also been shown to disrupt hippocampal-dependent object recognition (e.g., Clark, Zola, & Squire, 2000) and

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working memory (Diamond, Fleshner, Ingersoll, & Rose, 1996; Diamond, Park, Heman, & Rose, 1999). Likewise, long-term subcutaneous implants of glucocorticoids, which mimic the eﬀects of chronic stress, impair new learning and memory for maze escape behaviors in rats. In one study, the severity of such deﬁcits was correlated with the number of damaged cells in the CA3 region of the hippocampus (Arbel, Kadar, Silberman, & Levy, 1994). A thorough review of the eﬀects of stress in animals is beyond the scope of this chapter, but the reader is directed to excellent reviews (de Kloet, Oitzl, & Joels, 1999; Kim & Diamond, 2002; Lupien & Lepage, 2001; Lupien & McEwen, 1997; McEwen, 2000). Collectively, ﬁndings from these studies converge on the idea that elevated levels of glucocorticoids released during stress disrupt normal hippocampal physiology, which, in turn, leads to changes in speciﬁc forms of memory. These eﬀects do not, however, occur alone. Instead, they occur in the context of a larger stress response. Other neurochemical systems interact with glucocorticoids to mediate the eﬀects of stress on memory and hippocampal function, including norepinephrine, serotonin, dopamine, amino acids (e.g., GABA, glutamate), and immune compounds. Because many reviews focus exclusively on the glucocorticoids, a brief mention of the other systems will be appropriate here. Exposure to stress causes the release of norepinephrine from the locus coeruleus (a nucleus in the pontine region of the brainstem), and this is often thought of as the “ﬁrst wave” response to stress. The norepinephrine system responds almost immediately to a stressor, whereas the HPA axis, or “second wave” response, reacts more slowly. Norepinephrine binds to receptors throughout the brain and facilitates motor responsiveness, thus governing the “ﬂight or ﬁght” response (e.g., Stoddard, Bergdall, Townsend, & Levin, 1986). Moreover, norepinephrine has potentiating eﬀects on memory for emotional experiences, a ﬁnding that may be mediated by the numerous norepinephrine receptors located in the amygdala (e.g., McGaugh, 2000). Norepinephrine can reach very high levels and still facilitate memory for emotion, even while similarly high levels of glucocorticoids impair contextual and verbal episodic memory. Exposure to stress also produces serotonin release in the hippocampus, medial prefrontal cortex (PFC), and amygdala, among other brain regions (e.g., Inoue, Tsuchiya, & Koyama, 1994; Kaehler, Singewald, Sinner, Thurnher, & Philippu, 2000), and stress-induced alterations in serotonin impact memory function. For example, substances that reduce extracellular serotonin levels appear to block the eﬀects of stress on memory and hippocampal function, suggesting that serotonin release during stress might contribute to hippocampal damage (McEwen et al., 1997; McEwen, 2000). Tianeptine, an antidepressant that works by enhancing serotonin reuptake (and therefore reducing extracellular serotonin levels), blocks both stress- and corticosterone-induced dendritic atrophy of neurons in the CA3 region of the hippocampus (Watanabe, Gould, Daniels, Cameron, & McEwen, 1992).

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Inhibition of hippocampal neurons and associated memory deﬁcits may also be mediated by a stress-induced increase in proinﬂammatory cytokines. Speciﬁcally, interleukin-1 (IL-1), which is released by macrophages in response to stress, may mediate stress-induced memory impairments by stimulating serotonin release in the hippocampus (Linthorst, Flachskamm, Holsboer, & Reul, 1994) or directly interfering with LTP (Bellinger, Madamba, & Siggins, 1993) by disrupting calcium inﬂux mechanisms (Cunningham, Murray, O’Neill, & O’Connor, 1996). In any case, IL-1 may play a key role in mediating hippocampusspeciﬁc memory impairments. For example, IL-1 induction has been found to impair performance on spatial (i.e., hippocampal-dependent) versions of the Morris water maze task but to leave performance on the nonspatial versions unaﬀected (Gibertini, Newton, Friedman, & Klein, 1995). IL-1 has also been shown to interfere with fear conditioning to contextual but not discrete cues (Aubert, Vega, Dantzer, & Goodall, 1995). The stress response also involves the dopaminergic system, primarily the system that innervates the medial PFC. This system appears to be vulnerable to mild and brief stress, and some studies suggest that stress has a negative eﬀect on dopaminergic function. This is important because this region, which appears essential for the normal functions associated with working memory, shares responsibility with the hippocampus for processing the source of information (source is a type of contextual information specifying where, or from whom, something was learned) and plays a role in episodic binding. Dopamine turnover is necessary to ensure proper PFC function; in line with this observation, recent evidence suggests that working memory is impaired by exposure to extreme or chronic stressors (Arnsten, 2000). Dopamine may play a role in emotional memory as well, perhaps mediating the cognitive modulation of fear responses (see Pani, Porcella, & Gessa, 2000). Benzodiazepines play a role in stress and memory by potentiating the eﬀects of the inhibitory neurotransmitter GABA. Blocking benzodiazepine receptors increases the experience of anxiety, while Valium, a benzodiazepine receptor agonist, decreases it. Results from several studies suggest that chronic stress reduces benzodiazepine receptor binding in the frontal cortex, not only increasing the subjective experience of stress and anxiety but also perhaps impairing hippocampal function (McEwen, 2000). Moreover, recent experiments in young animals show that inducing stress through maternal deprivation also reduces benzodiazepine receptor binding in the frontal lobes, as well as the amygdala and locus coeruleus (Caldji, Francis, Sharma, Plotsky, & Meaney, 2000; cf. Bremner & Vermetten, 2001). Finally, excitatory amino acids and endogenous opiate peptides may be involved in the stress-induced impairment of hippocampal function (Moghaddam, Bolinao, Stein-Behrens, & Sapolsky, 1994). In brief, excitatory amino acids (e.g., glutamate) may abet glucocorticoids in causing pyramidal cell loss in the hippocampus (e.g., Virgin et al., 1991). Stress- and glucocorticoid-induced atrophy

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of dendrites can be blocked by the anti-epileptic drug phenytoin (Dilantin), which works primarily by blocking the release of glutamate. Some evidence suggests that glucocorticoids and stress elevate levels of glutamate in the hippocampus and other brain areas (Stein-Behrens, Lin, & Sapolksy, 1994) and that a high concentration of glutamate is toxic to neurons. In addition, excitatory amino acids aid in the damage of hippocampal neurons in culture and appear to exacerbate kainic acid-induced damage, as well as ischemic damage, to the hippocampus (Stein-Behrens et al., 1992). NMDA receptors are thought to be involved, because blockade of such receptors is another eﬀective means of preventing stress-induced atrophy of dendrites (McEwen et al., 1995). Clearly, then, glucocorticoids are accompanied by, and in some cases modulated or mediated by, other neurochemicals that respond to stressors. This point is important because it suggests that any eﬀects of stress on memory may reﬂect complex cascades; thus, understanding stress- or trauma-induced memory impairments in humans, to which we now turn our attention, will not be a simple matter.

Chronic Stress: Memory in Humans As in animals, the memory-impairing eﬀects of acute stress or glucocorticoid administration are generally reversible in humans (Lupien & McEwen, 1997; McEwen, 2000).4 Whether the eﬀects of chronic stress are reversible, however, remains an open question. Research generally suggests that chronic glucocorticoid elevation is associated with memory dysfunction in humans (e.g., Mauri et al., 1993). Although some studies examining the long-lasting eﬀects of Cushing’s disease suggest that moderate recovery from cognitive deﬁcit after cortisol reduction may be possible (Starkman et al., 1999), other studies suggest more permanent damage (Sheline et al., 1996; see also Bremner, 2001b). Memory deﬁcits associated with aging in humans appear related to progressive dysregulation of HPA activity with increasing age. For instance, Lupien et al. (1994) reported that elderly individuals whose cortisol levels increased over a 4-year period performed signiﬁcantly poorer on tests of explicit memory than individuals whose cortisol levels declined over the same period (see also Lupien et al., 1998). These observations led to the clinically relevant idea that some individuals who endure life-threatening experiences with associated increases in stressrelated hormones might experience a dysregulation of their memory systems, perhaps for speciﬁc traumatic events and for autobiographical events in general. Traumatic Stress and Memory in Humans: The Special Case of Posttraumatic Stress Disorder For every 100 people who endure horrifying experiences (e.g., Holocaust survivors, victims of physical or sexual abuse or rape, war veterans, etc.), about 15 will develop posttraumatic stress disorder (American Psychiatric Association, 1994 [DSM-IV]), which characteristically involves a collection of memory

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problems (see Bremner, 1999; Lemieux & Coe, 1995; Yehuda et al., 1995). Diagnostic criteria for PTSD include previous exposure to “an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others.” In addition, the person’s response must have involved intense fear, helplessness, or horror (DSM-IV). PTSD is characterized by intrusive recollections of the traumatic experience, avoidance of the event and reminders of the event, hyperarousal, dissociation, sleep disturbance, emotional numbing, and, paradoxically, increased emotional responsivity and anxiety (Emilien et al., 2000; Golier, Yehuda, & Southwick, 1997; Saigh & Bremner, 1999). Epidemiological studies suggest that the lifetime prevalence of PTSD in the general population ranges from 8 to 9 per 100 and that roughly 60% of these cases become chronic (e.g., Breslau, Davis, Andreski, & Peterson, 1991; Davidson, Roth, & Newman, 1991; Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995). Prevalence rates may be even higher in children and adolescents and are twice as frequent in women as in men (e.g., Costello, Erkanli, Fairbank, & Angold, 2002; Kessler et al., 1995; see Fairbank, Ebert, & Caddell, 2001, for a more comprehensive review). Clinicians have long reported that memory diﬃculties are also associated with PTSD, noting that war veterans often forget appointments and what they had for breakfast yet describe the central aspects of their combat experiences in excruciating detail, as if those experiences happened yesterday (Bremner, 2001b). Although forgetting appointments was once understood as a psychoanalytical defense mechanism and treated as “resistance” on the part of the patient, a growing body of empirical research supports a more biological explanation for the memory problems seen in PTSD (Bremner, 2001b). Both short-term memory and episodic memory appear to suﬀer in those diagnosed with PTSD (Bremner et al., 1993; Bremner, 2001a, b; Torrie, 1944). Severe memory deﬁcits have been measured in PTSD using portions of the Wechsler Adult Intelligence Scale (WAIS), the Wechsler Memory Scale (WMS), and the Verbal Selective Reminding Test (vSRT). For example, veterans with PTSD performed more poorly than healthy controls on the logical memory component of the WMS (about 2 of 5 show impaired immediate recall and 1 of 2 show impaired delayed recall; Bremner et al., 1993). More recently, Vasterling et al. (2002), using the Rey Auditory Verbal Learning Test (AVLT), showed that Vietnam veterans with PTSD manifested greater deﬁcits on this working memory task than controls (Vietnam Veterans without diagnosed psychopathology). These authors demonstrated that the cognitive impairments associated with PTSD are independent of estimated verbal general intelligence (see, however, McNally & Shin, 1995). Similar results were obtained from a sample of adults reporting childhood sexual abuse (Bremner, Randall, Capelli, et al., 1995). These individuals performed more poorly than controls on the WMS Logical component for immediate and delayed recall, as well as percent retention. They also had diﬃculty with

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the immediate recall of words as measured with the vSRT. These impairments cannot be explained by diﬀerences in general intelligence as reﬂected by IQ, which did not diﬀer in either study. Vietnam veterans, Desert Storm veterans, and victims of rape diagnosed with PTSD all have impaired verbal episodic memory in comparison to control subjects (Jenkins, Langlais, Delis, & Cohen, 1998; Uddo, Vasterling, Brailey, & Sutker, 1993; Vasterling, Brailey, Constans, Borges, & Sutker, 1997; Vasterling, Brailey, Constans, & Sutker, 1998; Yehuda et al., 1995, but see Stein et al., 1997). Although these studies show that PTSD and memory deﬁcits are related, design limitations prevent unequivocal causal conclusions. The ﬁrst limitation is associated with the well-understood problems of quasi-experimental designs. The second concerns a failure to examine memory performance in the context of other neuropsychological functions, which leaves open the question of whether PTSD patients exhibit selective memory impairments or more general cognitive impairments. The third concerns lack of control over the potential relations among diﬀerent cognitive functions, leaving us asking, for example, if memory changes in PTSD can be explained more generally by changes in attention, concentration, visuospatial abilities, or other cognitive functions related to memory. The fourth concerns what accounts for changes in memory observed under these conditions; memory deﬁcits may be due to development of PTSD symptoms per se, to the result of trauma exposure generally, or to some unknown set of factors. A ﬁfth limitation concerns comorbidity, that is, whether other disorders associated with changes in memory (e.g., depression, alcoholism) might account for many of the memory eﬀects observed in PTSD. Horner and Hamner (2002) reviewed 19 studies examining cognitive function in PTSD and concluded that converging evidence for memory deﬁcits in PTSD does exist. They caution, however, that methodological problems, particularly comorbidity (e.g., substance abuse, mood disorders, and other anxiety disorders), were a problem in most studies. Sixteen of the 19 studies reported evidence of attention or memory diﬃculties, or both, in PTSD. However, 15 of these studies included patients with other comorbid disorders, reﬂecting the diﬃculty recruiting cases of “pure” PTSD—and raising the question of whether such a pure sample exists. An important study by Gilbertson, Gurvits, Lasko, Orr, and Pitman (2001), which was not discussed in the Horner and Hamner (2002) review, examined performance on a range of neuropsychological tests including memory, attention, visuo-spatial skills, and executive functioning. These authors reported that, although those meeting criteria for PTSD were impaired on all these tasks compared to controls, performance on the attention and memory tasks uniquely predicted a PTSD diagnosis. In addition, verbal memory emerged as distinguishable from generalized attentional diﬀerences, as well as from the severity of the triggering trauma, general intelligence, depression, alcohol use, or a history of

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developmental learning problems (Gilbertson et al.). This study provides some of the ﬁrst evidence for a speciﬁc association between changes in episodic memory and the presence of PTSD. Autobiographical memory also suﬀers in PTSD. Individuals diagnosed with PTSD often have overly general (i.e., nonspeciﬁc, lacking context and detail) memories of the past (McNally, Lasko, Macklin, & Pitman, 1995) and show selective deﬁcits when retrieving speciﬁc personal information in response to cue words having positive (e.g., “kindness”), neutral (e.g., “appearance”), or negative (e.g., “panic”) emotional valence (Kaspi, McNally, & Amir, 1995; McNally, Litz, Prassas, Shin, & West, 1994; McNally, 1998). When individuals with PTSD were asked to retrieve a personal event memory triggered by a cue, they tended to retrieve generic memories without reference to a speciﬁc event. That is, rather than reporting contextually speciﬁc memories with speciﬁc source (time, place) information, they appear to report schema- or knowledge-based narratives. Moreover, they report diﬃculty retrieving speciﬁc positively valenced personal memories, suggesting that trauma-related thoughts hamper access to positive or neutral memories. As these results clearly demonstrate, memory problems are a hallmark of PTSD. In addition to general memory eﬀects, those with the disorder tend to either vividly re-experience (i.e., “ﬂashbacks”), or fail to remember, information related to their traumas. PTSD can thus be characterized as a disorder that paradoxically includes excessive and uncontrolled memory retrieval (e.g., intrusive memories, nightmares, ﬂashbacks) and memory disruption (e.g., traumatic amnesia, fragmented memory).

Stress and Memory: What Is

Forgotten and Why

Although the foregoing discussion makes it clear that stress can impair memory, the data leave one wondering precisely what aspect(s) of memory are impacted by stress. All aspects, and all systems of memory, obviously are not entirely disrupted; if they were, researchers would be left with nothing to measure. So what, exactly, does stress cause us to fail to learn, fail to store, or fail to retrieve? In this section, we suggest that (1) contextual memories (i.e., memories of the spatial and environmental aspects of experience), (2) detailed memories (i.e., those details that allow episodic memories to be distinguished from one another), and (3) coherent, explicit autobiographical memories (i.e., the conscious, contextually, or episodically grounded recall of material with details that ﬁt together in sensible, meaningful ways) suﬀer in the presence of high levels of stress.5 What evidence is there that memory for stressful experiences lacks coherence, context, and episodic detail? Initial support came primarily from anecdotal clinical reports, which suggested that experiences encoded during high levels of stress

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are often fragmented (Bremner, 1999; Golier et al., 1997; Gray & Lombardo, 2001; van der Kolk, Hopper, & Osterman, 2001; van der Kolk, 1994). The bits and pieces of experience are not related to one another as a whole. That is, these pieces and patches are not bound together in a way that produces a “good gestalt,” or a coherent episode. Fragmentation is an important feature of PTSD. Patients sometimes describe “gaps” in recalled experiences, not only of trauma but also of other personal experiences (Bremner, 1999). Some laboratory evidence suggests that stress-induced fragmentation can emerge in experiments assessing memory for verbal material (e.g., Payne et al., 2002, described later); it is, however, most commonly observed in response to trauma. Rather than simply retrieving fragments and reporting them as such, some individuals who have experienced trauma appear to make educated guesses about memory in a process called “narrative smoothing.” Jacobs and Nadel (1998) oﬀered a neurobiological theory of reconstructed memory taking this phenomenon into account. Starting with the observation that multiple memory systems underlie the storage of episodic information, they suggested that retrieving an autobiographical memory entails accessing and integrating fragments of information stored in these diﬀerent systems. Many diﬀerent types of information go into the retrieval of a speciﬁc experience. There are the elements composing the episode: what happened; who engaged in which actions; what it all looked like, sounded like, smelled like; etc. In addition to this episodic “content,” there is also spatial or contextual information. This is a particularly important type of information because all episodes occur someplace and thus are deﬁned partly by the space or context in which they occur. It can be diﬃcult if not impossible to divorce memories of episodes from memories of context, a notion that led us to suppose that context serves as an organizing frame to which the elements of an episodic memory trace are attached (Jacobs & Nadel, 1998; Nadel & Payne, 2002; Nadel, Payne, & Jacobs, 2002). Consider a hypothetical traumatic war experience; a memory of this experience might include smells (the jungle, unwashed bodies), sounds (gunﬁre and cursing), sights (the ﬂash of a sniper’s weapon, the sight of a wounded combatant), tactile feelings (the humidity, thorns slashing skin), actions (diving for cover, returning ﬁre), and emotions (anger and fear). Each of these independent features is stored in the relevant part of the brain, typically, but not exclusively, in the neocortex. The hippocampus and adjacent medial temporal regions appear to be critical to a process by which these disparate fragments of information from multiple brain regions are bound into a uniﬁed memory trace at the time of retrieval (Mitchell, Johnson, Raye, Mather, & D’Esposito, 2000; Mitchell, Johnson, Raye, & D’Esposito, 2000). At the same time, the hippocampus appears to be critical for placing an autobiographical memory in time, place, and context. Hence, the disruption of hippocampal function by high levels of stress and glucocorticoids could disrupt the storage of information about place, time, and context during a

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traumatic experience, as well as the binding process that connects features of the experience to the context and to one another (Bremner, Krystal, Charney, & Southwick, 1996; Jacobs & Nadel, 1998). The idea that memories are disaggregated during storage and then reaggregated during retrieval has several implications in explaining interactions between extreme stress and memory (Jacobs & Nadel, 1998). By disrupting the hippocampally based binding function, stress may leave the pieces, patches, and context of a memory trace disconnected. So memories formed in the presence of stressors, and hence under the inﬂuence of high levels of glucocorticoids, will be disjointed and fragmented, lacking spatial or temporal context, and thus creating deﬁcits in episodic memory. Although traumatic stress appears to disrupt hippocampally based features of memory (e.g., context, episodic detail), quite the contrary appears to be the case for emotional features of memory based in other brain regions.6 The amygdala, a brain region adjacent to the hippocampus, is known to process, and perhaps store, emotional memories (Fanselow & LeDoux, 1999; LeDoux, 2000). The amygdala is active during emotionally charged conditions, and the emotional memories dependent on this region are highly resistant to forgetting (LeDoux, 1992). This “stamping in” of emotional memories is at least partly mediated by the stress hormone norepinephrine, which, as noted earlier, also reaches high levels during stressful experiences (see McGaugh, 2000, for a review). Hence, two prominent stress hormones, both released during intense stress, have opposite eﬀects on diﬀerent structures in the brain. High levels of cortisol disrupt hippocampal function, impairing episodic (e.g., de Quervain et al., 2000; Payne et al., 2002) and spatial memory (Laurance et al., 2001). In contrast, high levels of both norepinephrine and cortisol facilitate amygdalar functions and the emotional memories dependent on them (see Buchanan & Lovallo, 2001; Metcalfe & Jacobs, 1996, 1998, 2000). Jacobs and Nadel (1998) suggested that in the absence of an intact hippocampus-based memory system, the amygdala-based system stores emotional information unbound to the spatio-temporal context of the relevant events. This process results in a pool of emotional memories encoded without a coherent spatio-temporal frame to organize them. This pool is, essentially, a population of sensory and perceptual fragments acquired during the traumatic event (Jacobs, Laurance, Thomas, Luzcak, & Nadel, 1996). By this model, traumatic events do not typically lead to a complete eradication of memory but rather to the storage of fragments lacking an organizing framework. Devoid of this framework, traumatized individuals resort to “narrative smoothing”; retrieved memories are composed of re-aggregated representations cobbled together by a narrative based on gist, inference, and educated guesswork (Jacobs & Nadel, 1998; Nadel & Jacobs, 1998; see also Shimamura, 1997). By this model, a fragmentation of normally coherent elements of an experience resulting from disruption of hippocampally based contextual encoding,

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coupled with the sparing or even enhancement of amygdala-based emotional encoding, leads to a theoretically interesting clinical picture of trauma and memory. Van der Kolk and Fisler (1995) presented evidence that traumatic events are remembered initially as disconnected images and waves of disjointed sensations and emotions. The emotions can emerge as punctate waves (van der Kolk & Fisler, 1995) or as persistent anxiety without an apparent source (e.g., Freud, 1926). Clinicians sometimes suspect that clients presenting with such generalized (or “freeﬂoating”) anxiety—an emotional disturbance without obvious anchors in autobiographical memory—have suﬀered past traumas. Claims about generalized anxiety are supported by some empirical evidence, which suggests that memory disturbance in response to trauma may be associated with dysregulation of the autonomic nervous system, heightened arousal or vigilance, and increased startle reﬂex (Joseph, 1996). Indeed, emotional dysregulation is also characteristic of PTSD, and while patients often suﬀer from extreme anxiety, they may also exhibit isolation of aﬀect (described in the following) and describe emotional blunting and feelings of numbness. Cortisone therapy (a common treatment for rheumatoid arthritis) has been associated with both anxiety and panic, on the one hand, and with aﬀective dissociation, depersonalization, and emotional ﬂatness, on the other (Clark, Bauer, & Cobb, 1952). These observations are reminiscent of a defense mechanism proposed late in Freud’s career: defensive “undoing” (Freud, 1926). Freud thought of anxiety as a marker that emerges when the mind cannot cope with the threatening information assailing it. Thus, it pushes autobiographical information associated with the trauma out of awareness, and anxiety emerges instead. Like much of Freud’s work, defensive undoing is an intuitively appealing idea but diﬃcult to test. In contrast, the biological response to stress oﬀers a testable and more rigorous explanation of this phenomenon. If high levels of cortisol disrupt normal neuronal function of the structure responsible for the storage of critical contextual information (i.e., the hippocampus), then coherent memories of trauma will be rendered inaccessible.7 Moreover, if physiological processes impair cognitive but not emotional aspects of memory, as suggested by the opposite actions of catecholamines on amygdala function and cortisol on hippocampal function, then feelings of anxiety disconnected from the corresponding “factual” or autobiographical memory of a traumatic event might be expected. In other words, emotional memory for the traumatic event might continuously enter awareness in the form of generalized feelings of anger, fear, or uneasiness (referred to as “body memories” by van der Kolk, 1994) unbound to the originating episodic context. Without a contextual framework to relate emotional memories to associated traumatic events, these emotional memories surface as vague disconnected feelings of unease, anger, or fear that are troublesome. Anxiety is thus experienced as “generalized” and “freeﬂoating.”

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Isolation of Aﬀect in PTSD:

A Paradoxical Memory Deﬁcit

Perhaps the most common pattern of deﬁcit seen in PTSD involves what we described: a disruption of episodic memory, along with the experience of extreme anxiety apparently devoid of a source. Clinicians also describe cases exhibiting the opposite pattern of forgetting, however, when a person retains episodic information concerning a traumatic event but loses the corresponding emotional response (see chapter 11). Modern clinicians use the terms “emotional blunting” or “emotional numbing” to describe this pattern (e.g., Golier et al,, 1997; chapter 11). However, this observation is reminiscent of Freud’s concept of “isolation of aﬀect,” when people may recount traumatic experiences in the absence of the emotion that must have initially accompanied them; these individuals are, in fact, often overtly blasé about the upsetting information they recount (also called “splitting oﬀ of aﬀect”; Freud, 1926). Thus, isolation of aﬀect involves a lack of emotion and may contribute to experiential aspects of PTSD (Harvey & Bryant, 1998; van der Kolk, 1991). Freud speculated that individuals experiencing emotional numbness do not repress traumatic memories, thereby holding disturbing information out of awareness. Rather, unlike the failure to remember in “undoing,” individuals experiencing emotional numbness have no trouble recollecting the episodic aspects of the trauma. They do, however, have diﬃculty consciously accessing the emotion that originally belonged to it. By this conjecture, these individuals remember only the cognitive aspects of trauma (Mitchell & Black, 1995). To bring memory of the emotion into awareness would be too threatening, unduely straining the ego. Although there is little or no epidemiological data on which to rest the case, isolation of aﬀect (emotional blunting) lends itself to a biological explanation. One possibility (we speculate on it in the next section) is that stress disconnects normal chains of communication among normally interacting hippocampal, amygdala, and cortical networks. A Speculative Neurobiological Account of Isolation of Aﬀect Metcalfe and Jacobs (1996, 1998, 2000), working within the theoretical framework just outlined, explored interactions between two learning/memory systems, (1) a cool system, based in interactions between hippocampal and frontal regions, that is slow, emotionally neutral, ﬂexible, integrative, episodic, strategic, and highly contextualized and (2) a hot system, based in the amygdala, that is the basis of emotionality, fears, and passions, that is fast and impulsive and controlled by innate and acquired releasing stimuli. Stress has a diﬀerent impact on the cool hippocampal-based system and the hot amygdala-based system. Exposure to intense stressors or trauma disrupts the hippocampus, leaving disaggregated memories ruled by the cool system. Exposure to these same stressors, however,

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enhances the hot system, encoding context-free emotional memories rapidly and eﬃciently. This approach seems to account for many features of recovered memory, speciﬁc phobia, panic attacks, and PTSD (Jacobs & Nadel, 1985, 1998; Nadel & Jacobs, 1996; Metcalfe & Jacobs, 1996), with one glaring exception. As we have described, modern clinicians often describe an emotional blunting associated with the presence of PTSD; some even describe this as a “core deﬁning feature” of PTSD (e.g., Litz & Gray, 2002). To oﬀer an account of emotional blunting (i.e., isolation of aﬀect), we must consider two possibilities, neither well supported empirically. The ﬁrst possibility is that chronic exposure to glucocorticoids damages neurons in the amygdala, disrupting its processing of emotional information. The most serious weakness of this proposal is that chronic stress does not appear to damage the amygdala. Indeed, there is some evidence that, in the rat, predictable exposure to a stressor simultaneously disrupts dendritic arborization in the hippocampus but enhances this same process in the amygdala (Vyas, Mitra, Rao, & Chattarji, 2002). Under these conditions, one expects to observe disruption of hippocampal-mediated memory (e.g., contextualization) and enhancement of amygdala-mediated memory (e.g., emotional memory). In contrast, chronic exposure to unpredictable stressors leaves the dendritic arborization process relatively intact in the hippocampus but induces dendritic atrophy in the basolateral nucleus of the amygdala (Vyas et al., 2002). Under these conditions, one expects to observe highly contextualized episodic and emotional memories but greatly disrupted processing of emotional memories. That is, one expects broad emotional ﬂattening. In the presence of a damaged amygdala, however, one would expect a global disruption of emotional processing, yet this apparently does not happen to individuals who experience isolation of aﬀect. Instead, these individuals appear to be unaware of their emotional reactions while simultaneously showing enhanced behavioral and physiological reactivity (see, for example, Jacobs, Nadel, & Hayden, 1992). This ﬁnding recalls work reported by Peter Lang and his colleagues and introduces a second possible explanation of isolation of aﬀect. Lang and Cuthbert (1984) conceptualized anxiety as including three loosely coupled response systems (constellations) of overt behavior, verbal report (cognition), and physiological activation. Within this framework, those who experience isolation of aﬀect behave as if they do not experience subjective emotion (i.e., “feelings”) but do experience heightened arousal at the level of both behavioral and physiological constellations (Jacobs et al., 1992). It is as if the physiological concomitants of emotion do not enter awareness. The physiological changes occur but without corresponding emotional valence. More formally, aﬀect is not expressed in the cognitive constellation, while heightened emotion (e.g., hypervigilance, in-

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creased startle, etc.) remains expressed in both behavioral and physiological constellations. We account for this pattern of responding in isolation of aﬀect by making several potentially defensible assumptions about interactions among stress, stressors, and the functions of hippocampus, amygdala, and PFC.

Stress and the Frontal Cortex:

Stress-Induced Forgetting Beyond

the Hippocampus

We have focused almost exclusively on the hippocampus and amygdala. The frontal lobes, however, have received increasing attention in the stress literature. Recent experiments using functional magnetic resonance imaging (fMRI) (Henson, Shallice, & Dolan, 1999) and electrophysiological techniques (Otten & Rugg, 2002) have demonstrated an important role for the PFC in memory (Raye, Johnson, Mitchell, Nolde, & D’Esposito, 2000; Buckner, Logan, Donaldson, & Wheeler, 2000). Traditionally, the PFC was thought to contribute mainly to encoding processes through its presumed role in working memory, which allows information to be maintained temporarily in an active state (Baddeley, 1986). New evidence from PET and fMRI studies, however, shows that the PFC is also involved in memory retrieval (see Henson et al., 1999; Nyberg & Cabeza, 2000; Rugg, Flethcer, Chua, & Dolan, 1999) and that the PFC may share, with the hippocampus, responsibilities for binding episodic material (Mitchell, Johnson, Raye, & D’Esposito, 2000). The frontal cortex is also involved in the modulation of emotion and inhibitory responses (e.g., Arnsten, 2001; Rosenkranz & Grace, 2002). Moreover, damage to this area, particularly if it is conﬁned to the prefrontal region, leads to perseveration, diﬃculty choosing correct responses, and distortions and confabulations of memory. For example, patients with frontal lobe damage tend to make an abnormally large number of conﬁdent false recognition errors, in spite of good recall and recognition generally (Curran, Schacter, Norman, & Galluccio, 1997; Delbecq-Derouesne, Beauvois, & Shallice, 1990; Melo, Winocur, & Moscovitch, 1999; Parkin, Bindschaedler, Harsent, & Metzler, 1996). With the existence of glucocorticoid receptors in the frontal lobes (reviewed later), stressrelated increases in commission errors likely are not caused solely by a disrupted hippocampus. An important review by Lupien and Lepage (2001) underscores the contribution of frontal regions to stress-related eﬀects on episodic and emotional memory. These authors argue that the hippocampus has been studied at the expense of other brain regions likely involved in glucocorticoid action and that attempts to explain stress impairments on memory solely on the basis of the impact of stress on the hippocampus may be incomplete.

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Lupien and Lepage (2001) note that both Type I (mineralocorticoid, MR) and Type II (glucocorticoid, GR) stress receptors are present in cortical regions, with a preferential and dense distribution in the PFC. Hence, stress may exert eﬀects not only on hippocampal neurons but also on neurons critical for the normal functioning of the PFC. If one takes the inﬂuence of stress and corticosteroids on human memory to reﬂect the action of GRs, then one must acknowledge that both hippocampal and PFC function are likely involved. Diﬀerential MR and GR action in the hippocampus and PFC may underlie some of the diﬀerences in the magnitude and nature of memory impairments reviewed in this chapter. The hippocampus, mainly through MR, but also moderate GR, receptor binding, may be a primary site of short-term, reversible eﬀects that occur in response to stress (e.g., de Quervain et al., 2000; Newcomer et al., 1994, 1999; Payne et al., 2002; Wolkowitz et al., 1990, 1993). MRs must be totally saturated before GRs become activated, and signiﬁcant reductions in LTP do not take place until both MRs and GR receptors are occupied. Thus, experiments using humans (for obvious ethical reasons) likely rarely attain the levels of stress needed to produce lasting changes in memory. On the other hand, exposure to trauma may lead to the widespread and sustained saturation of both MR and GR receptors in the PFC and hippocampus. These conditions cannot be ethically reproduced in the laboratory and thus may emerge only in the context of naturally occurring chronic stress in the patient populations described earlier (e.g., Cushing’s syndrome, PTSD, major recurrent depression, etc.). In such cases, extensive binding of cortisol to both receptor types in the hippocampus and PFC may lead to long-lasting and harmful changes in neuronal functioning in the entire memory circuit, resulting in dramatic changes in how environmental information is encoded, stored, and retrieved. Evidence that excessively high levels of norepinephrine (e.g., during exposure to uncontrollable stress) impair cognitive functions of the PFC (Arnsten, 1998) makes this concept all the more feasible. Consequently, exposure to intense stress appears to aﬀect the PFC, as well as the hippocampus and amygdala. Models of stress and memory that focus solely on the hippocampus and amygdala cannot adequately account for isolation of aﬀect, but perhaps the addition of the PFC can explain this phenomenon. Does the PFC play a role in the modulation of emotions? What happens to that role under conditions of extreme stress? And, if we can specify that role adequately, how does this help us understand isolation of aﬀect? We start by assuming that the PFC plays two roles in emotional processing and regulation: (1) inhibitory control of emotional responses generated by an amygdala-centered system and (2) subjective awareness of that emotion (e.g., Amaral, Price, Pitkanen, & Carmichael, 1992; Reiman, Lane, Ahern, Schwartz, & Daivdson, 2000; Rosenkranz & Grace, 2002; Anderson, Bechara, Damasio, Tranel, & Damasio, 1999). Under the model outlined earlier, these assumptions have two important implications. First, disruption of the PFC should disinhibit

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the amygdala and thereby amplify the behavioral and physiological constellations of emotions controlled by it. Second, disruption of the PFC should disrupt the subjective experience of emotionality. Under these conditions, we expect individuals to experience high levels of emotional arousal in the behavioral and physiological constellations but not in awareness. This process would then account for narrow (or cognitive) emotional ﬂattening with enhanced reactivity in the behavioral and physiological constellations. Although the model remains to be rounded out and tested, the welldocumented processes that simultaneously impair PFC- and hippocampalbased memories and facilitate amygdala-based memories provide empirical physiological support for defensive undoing and emotional blunting, or the isolation of aﬀect.

Trauma and Memory:

What Is Remembered?

Intense stress is associated with memory disruption, either partial or complete, relating to the trauma itself or to episodic memory in general. Yet, paradoxically, other cases of trauma provoke an inability to forget (hypermnesia) and a desire to talk about the experiences constantly (e.g., Terr, 1991, 1993). Along similar lines, some individuals report spontaneous ﬂashbacks and hallucinations, as well as severe emotional upset in relation to the trauma. Sometimes these ﬂashbacks appear to be triggered by environmental stimuli (e.g., the sound of a ﬁrecracker or an engine backﬁring) and are reportedly so real that the person feels he or she is re-experiencing, rather than remembering, the event. The fact that people report ﬂashbacks suggests that some representation of traumatic events has been stored but is not always accessible. Interestingly, ﬂashbacks reportedly plague trauma survivors regardless of whether they report amnesia for traumatic events or experience hypermnesia and talk about them obsessively.8 Further, whether they experience ﬂashbacks may be unrelated to general level of memory function (e.g., Joseph, 1996). A thorough investigation of ﬂashbacks is beyond the scope of this chapter. Nonetheless, we brieﬂy note that an understanding of the neurobiological processes involved may help elucidate ﬂashback phenomena. Although fear is tied to speciﬁc stimuli in a person’s immediate environment, anxiety appears to be a secondary response (LeDoux, 1992). Pathways of fear involve interactions between cortical sensory processing areas and the amygdala, where emotionally neutral sensory signals are transmitted to receive their aﬀective connotation. Depending on whether the emotional processing mechanisms of the amygdala are activated directly by incoming sensory information or indirectly by cognitive processes organized elsewhere, a person will either experience fear, a primary response, or anxiety, a secondary response (Davis, 1992; Davis & Shui, 1999; Gray, 2000). The former pathway may initiate ﬂashbacks, which elicit fear di-

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rectly and are experienced in the here and now. The secondary pathway may characterize “normal” reactivation of trauma memories, which should elicit negative aﬀect and anxiety that are correctly referenced to the past. This latter pathway appears to be disrupted during the trauma, leading to decontextualized and fragmented memory for the experience. Acknowledging the diﬀering contributions of these two pathways, we might expect the content of ﬂashbacks to be highly emotional, as fear circuits become activated. The fact that amygdala function is preserved during intense stress ﬁts this suggestion. Moreover, due to stress-induced disruption of the structures underlying context and detail memory (i.e., hippocampus and PFC) during the trauma, we might expect ﬂashbacks to lack both contextual information and details outside the emotional center of the traumatic event. In the absence of contextual detail, ﬂashbacks should consist mainly of the central content or theme of the traumatic experience.9 In other words, we expect the content of ﬂashbacks to be rarely, if ever, about the peripheral details of a traumatic experience. Rather, we expect the images that emerge during a ﬂashback to be the most horrible, emotionally salient, and central features of the traumatic experience. These considerations force us to examine another literature, one that seemingly unfolded parallel to the trauma and memory literature.

The Emotion and Memory Literature We have focused almost exclusively on memory impairment that results as a consequence of stress and trauma. Many readers, however, particularly those with a background in emotion, may be wondering how these data ﬁt with evidence seemingly pointing in the opposite direction—namely, that memory often improves in response to emotion, even intense emotion (see also chapter 2 here). A key ﬁnding in the emotion and memory literature is that memory for emotional events is superior to memory for similar, neutral events (e.g., Heuer & Reisberg, 1990; chapter 1 here). Most people have ready examples of emotional events that are remembered vividly “as if they happened yesterday,” and a substantial literature conﬁrms that some emotional experiences are unforgettable (see chapter 1). People also report vivid recollections for intensely negative experiences accompanied by strong negative emotion (e.g., Porter & Birt, 2001). So we now have one literature demonstrating that high levels of stress can disrupt memory for stressful experiences and another literature demonstrating that intense negative emotion can improve memory for negative experiences. The key to this apparent conﬂict, we think, is embedded in an as yet unacknowledged diﬀerence between strong negative emotion and stress. Although stressful experiences are usually negative, and although substantial overlap may connect negative emotion and stress, we claim that they are not the same. In the following pages, we try to address the tension between these two literatures directly. Although at ﬁrst blush data from the two research traditions seem

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contradictory, we suggest that a solution resides in the diﬀerential contributions of hippocampus-based circuits and amygdala-based circuits. Can intensely negative memories be vivid and intact in some cases and disrupted and fragmented in others? Can traumatic memories be both vivid and fragmented? The short answer to both questions, we think, is yes. The key to resolving this apparent paradox likely resides in (1) the magnitude of the stress, (2) the corresponding amount of stress hormones released during emotional experiences of diﬀerent intensities (i.e., the degree of stress inherent in a given emotional experience), and (3) the degree to which changes in these stress hormones aﬀect diﬀerent memory structures. The thrust of our argument resides in the (possibly nonlinear) relations between experienced emotion and the magnitude or intensity of the stress response. However, we brieﬂy point out two additional diﬃculties that may help account for the contradictory literatures. The ﬁrst diﬃculty is deﬁnitional. It concerns the often-overlooked fact that there are multiple memory systems. Memory is not a single entity that goes up or down in response to emotional arousal; rather, memory is an aggregate of many systems of which emotional memory is just one. If this is true, emotional arousal (even in the absence of stress) may facilitate some attributes of “memory” yet disrupt others. The second concerns how “emotion” is conceptualized and where and how it comes into play in memory experiments. In the stress/trauma literature, emotion (emotional memory) is a dependent variable, one of several types of memory diﬀerentially aﬀected by stress, the independent variable. Conversely, in the emotion literature, emotion (or emotional arousal) is often used as an independent variable, which inﬂuences diﬀerent types of memory (usually enhancing memory for emotional content: words, pictures, videos, experiences, etc.). Subtle diﬀerences between emotion and stress need untangling, but distinguishing between emotional content and emotional arousal that may be associated with that content is critical. We consider each of these problems. Something about emotionality leads to particularly vivid and long-lasting memories. Attempts to isolate mechanisms underlying this eﬀect have led to discoveries anchored in research techniques derived from cognitive theory (e.g., chapter 1) and in research techniques derived from learning/neuroscientiﬁc theory (e.g., McGaugh, 2000, 2002). The Learning/Neuroscientiﬁc Approach to Emotion and Memory Research A crucial contribution of the neuroscience approach is the unshakable notion that speciﬁc neural and hormonal mechanisms underlie the enhanced consolidation of memory for emotional materials. One group of researchers (Cahill, Babinsky, Markowitsch, & McGaugh, 1995; Cahill & McGaugh, 1998), for example, has demonstrated that stress hormones interact with the amygdala and, through that interaction, enhance the storage of explicit memories. This group has shown that adrenergic activity enhances (e.g., O’Carroll, Drysdale, Cahill, Shajahan,

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& Ebmeier, 1999; Southwick et al., 2002) and blockade of adrenergic activity reduces (e.g, Cahill, Prins, Weber, & McGaugh, 1994) the consolidation of explicit memory for emotional materials in humans. The activation of beta-adrenergic receptors, located on neurons in the basolateral nucleus of the amygdala, appears critical for this noradrenergic mediation of emotional memory consolidation (McGaugh, 2002; McGaugh & Roozendaal, 2002). In addition to adrenergic inﬂuences on memory, McGaugh, Cahill and their associates point out that low doses of glucocorticoids can enhance memory as well, suggesting that both epinephrine (and norepinephrine) and cortisol enhance memory consolidation (Cahill & McGaugh, 1998). Indeed, the enhancing eﬀects of cortisol on memory for emotional (i.e., nonhippocampal-dependent) information have been demonstrated in animal studies of aversive conditioning and in human studies that use emotional memory tasks (e.g., Buchanan & Lovallo, 2001; Roozendaal, 2000). For example, Buchanan and Lovallo showed that 20 mg of hydrocortisone facilitated memory for emotional pictures, but not neutral pictures, relative to a placebo control. Again, the basolateral amygdala (BLA) is the speciﬁc nucleus thought to underlie these eﬀects. The BLA is not only a locus of interaction between norepinephrine and cortisol (McEwen, 2000) but also a major hub of communication between the amygdala and hippocampus. As such, the BLA is thought to be a critical locus regulating norepinephrine and glucocorticoid inﬂuences on memory consolidation enhancement eﬀects (Roozendaal & McGaugh, 1997). These ﬁndings appear to contradict the stress data we reviewed. Yet a close examination of the designs, the data, and the measures to obtain them leads to a proposal that could resolve this apparent contradiction, given a clear understanding of features composing emotional memory. The design of a typical study examining “emotion and memory” goes something like this. Human subjects watch a series of slides depicting successive moments in a story that is either emotionally arousing or emotionally neutral. A tape-recorded narrative accompanies the slides, helping subjects interpret the scenes and synthesize them into a story. Many studies have used variations on the “doctor/mechanic” slide sequences originally developed by Heuer and Reisberg (1990). In both stories, a mother and young boy visit the father at work. In the emotional series, the father is a surgeon performing explicit surgeries (where viscera or severed legs are in plain view); in the neutral series, the father is a mechanic working on a broken car, and disconnected car parts are in plain view. Studies in this tradition focus mainly on consolidation processes, so after waiting for a time (usually minutes after viewing the slides; although see Cahill et al., 1994), participants receive a substance that either enhances or blocks adrenergic activity. The participants receive a single test of memory, usually after a long delay. The typical result shows enhanced memory for the emotional slide sequence with adrenergic facilitation and decreased memory for the emotional slide sequence under adrenergic blockade. Neutral slides,

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on the other hand, remain unaﬀected by adrenergic alterations (e.g., Cahill et al., 1994). These studies have made critical contributions to our understanding of the neural and hormonal mechanisms underlying emotional memory enhancement. Nevertheless, they tempt us to believe, perhaps prematurely, that emotional arousal improves emotional memory overall. Despite having borrowed emotional memory materials and designs from cognitive researchers, these researchers measure memory diﬀerently. Those from the learning-based tradition often obtain high-level aggregate measures of memory, measures that may not be sensitive to subtle nuances obtained when measuring the components of memory directly (although see Adolphs, Denburg, & Tranel, 2001). For example, Cahill and colleagues assess memory using traditional recall and recognition measures, focusing on the overall “amount” of memory preserved posttreatment. In contrast, cognitive researchers often examine qualitative diﬀerences within emotional memory—for example, diﬀerentiating memory for central or gist-like information from memory for peripheral detail (see chapter 1), often showing that only the former is enhanced by emotion. Hence, although arousal may lead to broad enhancement of emotional memory, we do not yet have the necessary data to draw such a conclusion. Until the eﬀects of emotion on gist-like information and peripheral detail are directly compared, it may be safest to assume that memory enhancement maps onto a fairly robust pattern of ﬁndings in the cognitive literature—that emotional arousal promotes memory for an event’s gist or center, often at the expense of other (contextual) details (Adolphs et al., 2001; Metcalfe & Jacobs, 1998, 2000; chapter 2 here). The Cognitive Approach to Emotion and Memory Research: Central Versus Peripheral Information Results anchored in the cognitive tradition are generally consistent with the notion that increased levels of norepineprhine (and arousal) enhance recall of memory for emotional events. An early ﬁnding in the emotion and memory literature was that individuals initially remember highly unpleasant events more poorly than neutral events but that, over time, the pattern reverses, with enhanced recall for arousing events after a delay (e.g., Goodman, Hirschman, Hepps, & Rudy, 1991; Osborne, 1972). Clark, Milberg, and Ross (1983) and Kleinsmith and Kaplan (1963, 1964) demonstrated that highly arousing events are initially less well remembered than low-arousal or neutral events, but a recovery eﬀect for the high-arousal events occurs after a delay. The eventual enhancement of memory by arousal is not surprising because such memories may be essential for survival. For instance, remembering to avoid a certain poisonous food could save one’s life (Bremner, Southwick, & Charney, 1997, 1999; McEwen, 2000). It seems safe to assume that negative emotional events lead to overall enhanced memory for these events, particularly after a delay. Recent research, however, suggests that the story isn’t quite so straightforward. First, newer studies show that emotional arousal can promote imme-

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diate memory enhancement, implicating an eﬀect of arousal on encoding, in addition to consolidation, processes (see Hamann, 2001, for a review). Second, and more important, many studies suggest that emotion enhances episodic memory but in a way often limited to the central and thematic features of such experiences (Burke, Heuer, & Reisberg, 1992; Christianson & Loftus, 1987, 1991; Loftus, Loftus, & Messo, 1987). People tend to remember the gist or aﬀective signiﬁcance of a stimulus or event at the expense of peripheral details (Christianson, 1992, Goodman et al., 1991; Ochsner & Schacter, 2000). This tendency may appear in the “weapon focus” phenomenon, when witnesses to crimes recall information about the weapon used during an assault at the expense of other important details (Stanny & Johnson, 2000). Loftus and Burns (1982), for example, reported that subjects who watched an emotionally arousing videotape of a violent bank robbery (in which a little boy is shot in the face) did not recall the events immediately preceding the attack as well as control subjects who watched a less emotional videotape (in which bank robbers simply ran past the little boy, leaving him unharmed). Similarly, Goodman et al. (1991) showed that receiving an unpleasant inoculation leads to enhanced memory for central information related to the procedure; likewise, Christianson and Loftus (1991) found enhanced memory for central information but impaired memory for peripheral information within an emotional event, as compared to a similar, neutral event. Burke, Heuer, and Reisberg (1992) demonstrated the same emotion-driven enhancement of central or gist-like information but added to our understanding of “centrality” by showing that memory improved both for visually central information and information associated with an event’s central theme or plot. As in other studies, however, memory suﬀered for details that were not associated with central events (see also Christianson & Loftus, 1991). Christianson and Loftus (1990) found that people describing their most traumatic memories reported more central than peripheral detail information. Study after study has shown that memory for peripheral detail suﬀers while memory for gist or thematic content improves with heightened emotionality (see chapter 1 for a comprehensive review and more detailed scrutiny of these data). There are several possible explanations for this phenomenon (see Heuer & Reisberg, 1992, also chapter 1 here). For example, central information may be better remembered simply because people attend to it longer. Increased memory for emotional information, however, can occur even when viewing time for emotional and nonemotional information is held constant (Christianson et al., 1991; Ochsner & Schacter, 2000). Another possibility is that the nature of attention may diﬀer for emotional and nonemotional events, leading to better memory. Emotional events could also be associated with more elaborate processing and more rehearsal of the information to which people attend (Ochsner & Schacter, 2000). For example, witnesses to emotional attention-grabbing episodes (e.g., accident, crime, assault), compared with a neutral attention-

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grabbing episode, may be more concerned with what they have just seen and think about (rehearse) it more often. According to Christianson and Safer (1995), this process of elaboration implies a psychological focusing on salient information that is the source of emotional stress, while at the same time limiting access to the information in the mental periphery. Although most discussion of these ﬁndings focuses on memory diﬀerences for central detail versus peripheral detail, there is another way to conceptualize the ﬁndings. As Christianson (1992) points out, central detail represents the source of the emotional arousal; it includes the most relevant information for extracting the emotional signiﬁcance of a stimulus or event. So there may be an alternative deﬁnition of what centrality is and what it means for traumatic memory. First, central information may represent a concentration of experience, where disproportionate emphasis is placed on emotion. Whatever is emotional about an experience will therefore be well remembered, whereas more neutral information will not fare as well. Thus, emotion, likely through the activation of the adrenergic system, may be responsible for the memory enhancement of central experiences, because centrality and the source of emotionality often overlap. Second, central information may also represent a schematization of experience, where peripheral details are not well remembered but the gist or essence of an event is particularly well preserved. The process of schematization occurs when preserved emotional details are woven into a meaningful narrative memory on the basis of schematic inference. The result is a gist-based memory that may be biased toward central and emotional features of experience. By this view, schematized memories are likely thematically consistent, but they may not be accurate. Our notion of schematized memories dovetails with evidence suggesting that emotional memories are prone to errors and can even be entirely false (see chapter 1). Due to the way they are formed, schematically consistent memories are not always accurate, especially if one believes that “the truth is in the details.” Centrality and gist are quite compatible within this interpretation and likely represent the same information. Gist memories, we say, are composed of preserved bits of central information, linked together by schemabased inferences. Glucocorticoid binding at hippocampal receptor sites may shed light on this process, particularly if one thinks of peripheral details as contextually important features (i.e., specifying source information, spatial and temporal relationships) that rely on a functional hippocampus and central information as gist-like and relatively noncontextual, capturing the essence of experience but missing many of the episodic details that would produce complete and veridical memories. By this view, then, central information represents not only the emotional tone but also the overall gist or theme of a stressful experience. Central or gist-like information may survive, whereas detail memory may suﬀer, in response to emotional stress.

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This claim brings us to the inevitable place where the words “emotion” and “stress” must be pulled apart. Despite obvious overlap between the two, emotional arousal is not always suﬃciently intense to elicit a stress response, and occasionally a stress response is elicited but is relatively mild (and thus may enhance memory; see Cahill & McGaugh, 1998). Thus, while the pattern of enhanced gist and impaired detail memory may be inﬂuenced by deﬁnitional problems with these terms and limits in memory measurement (i.e., in the neuroscientiﬁc experiments previously described), the most compelling reason for such a pattern concerns the magnitude of negative emotion and, critically, the degree of HPA-axis activity associated with negative emotion. Stress is distinct from ordinary emotion insofar as HPA-axis activity and cortisol reach high enough levels for memory impairment. Whether emotion promotes memory for gist and centrality while disrupting memory for noncentral details may depend on the level of stress elicited by an emotional experience.10 Along these lines, we suspect that HPA-axis activity may be associated with the viewing of emotional slides and videotapes used in most emotional memory experiments. This hypothesis is easy to test if cortisol measures are taken during these procedures. A study of this nature is currently under way in our laboratory, with the goal of testing our predictions about how gist and detail memory fare in response to stress. Our suggestion ﬁnds support in other studies as well. There is good evidence in the memory literature that gist and detail memory are diﬀerent (Neisser, 1981; Reyna & Kiernan, 1994; see also chapter 11 here, which distinguishes between “core memory” and “narrative memory”). The fuzzy trace theory of Brainerd and Reyna (1998), for example, posits two types of processing that eventually lead to two diﬀerent representations of experience. During encoding, verbatim and gist traces are formed in parallel, creating a hierarchy of independent representations at varying levels of precision. In many cases, gist representations are more easily retrieved than detail representations, and we suggest that stress is one such case. Interestingly, fuzzy trace theory has gained attention as a theoretical framework that could explain a variety of false memory errors, and we note here that preservation of gist at the expense of detail may inspire “ﬁlling in,” or narrative smoothing, setting the stage for emotional memories that are true to gist yet inaccurate (see Golier et al., 1997; Heuer & Reisberg, 1992). Studies demonstrating increased memory for central, thematic, and appraisalrelevant information (e.g., Burke et al., 1992) are consistent with the results of stress studies by Payne et al. (2002) and Lindsay and Jennings (2000). Both studies sought to determine the eﬀect of stress on false memory as assessed by the Deese-Roediger-McDermott (DRM) paradigm (Deese, 1959; Roediger & McDermott, 1995). In this work, participants studied a number of lists of semantically related nouns (e.g., candy, sour, sugar, bitter, chocolate, cake, etc.), followed by a four-item recognition task consisting of three types of words: words

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presented in the original list (e.g., candy), words not presented in the original list and not related to the theme of the list (e.g., hat), and “critical lure” words not presented in the original list but highly related to the them of the list (e.g., sweet). Payne et al. showed that experiencing an acute stressor followed by a brief waiting period dramatically increased false recognition of the critical lures. In particular, thematically related or gist-based false alarms (incorrect identiﬁcation of critical lures as present in the original list, or “commission errors”) were ampliﬁed by the psychologically induced stressor. This increase in false alarms using the DRM paradigm has also been observed in chronically anxious participants (Lindsay & Jennings, 2000), in traumatized patients with and without the diagnosis of PTSD (Zoellner, Foa, Brigidi, & Przeworski, 2000), and in sexually abused women with PTSD (Bremner, Shobe, & Kihlstrom, 2000). Both Payne et al. (2002) and Lindsay and Jennings (2000) concluded that elevated stress hormones increase the production of false memories in the DRM paradigm. One must, however, ask “false memory for what”? Only on very rare occasions did stressed subjects falsely recognize unrelated distractor words, and their rate of false recognition of these distractors did not diﬀer from that of nonstressed control subjects. Stressed subjects exhibited false memory of a particular type; they falsely remembered more words related to the thematic structure of the word list and therefore made more gist-based errors than their nonstressed counterparts. We suggest that this may be due to impaired contextual and detail memory and, as a result, an overreliance on gist memory (see Payne et al., 2002). These ﬁndings converge on the idea that stress disrupts memory for spatial and contextual details of experience, leading to an overreliance on thematic information.11 A closer look at the studies described earlier supports this idea. Recall that in Wolkowitz et al. (1990, 1993; see also Deptula, 1983), dexamethasone treatment was associated with signiﬁcantly greater rates of commission errors, or intrusions (self-generated words) into free recall, than control (placebo) treatment. It was also associated with greater rates of false recognition of semantically related distractor words. There was, however, no diﬀerence between the treatment and control groups on correct free recall or total hits on the recognition task. The same pattern emerged for people given prednisone, though the tendency to false alarm to related distractors disappeared 7 days after discontinuation of treatment. Although not conceptualized as false memory experiments, the work of Deptula (1983) and Wolkowitz et al. (1990, 1993) found the same false remembering of related but nonpresented information as did Lindsay and Jennings (2000) and Payne et al. (2002). Excessive reliance on gist information implies some “ﬁlling in” of missing context and details and leads to errors logically consistent with the theme of an experience but nonetheless incorrect. Indeed, “innocent confabulation” and “narrative smoothing” during traumatic memory retrieval may stem from an overreliance on gist information. When people face decontextualized fragments, they may infer thematic material based

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on gist to make sense of their experience. Thus, many memories formed under stress may in some sense be false, and many false memories may reﬂect gist-based narrative smoothing. Although the context and details of experience may be incorrect, the gist may well be accurate, an important consideration for the validity of memories for traumatic experience. The relation between emotional stress and memory for central or gist-like information clearly warrants further exploration. Nonetheless, the research reviewed here tempts one to conclude that focusing on the central or thematic features of an emotionally arousing event, perhaps at the expense of memory for context and detail, may be a characteristic reaction to stress.

Putting It All Together To summarize, stress, on the whole, appears to disrupt types of memory that depend on a functional hippocampus and PFC. Disruption of these structures is associated with impairment in episodic memory. Episodic memory, however, appears to be composed of diﬀerent parts: memory for context (spatial memory), memory for events that occur within the speciﬁc context, and thematic (gist) information, derived by inference. Trauma appears to disrupt memory for the context (e.g., Jacobs & Nadel, 1985, 1998) and the details of experienced events (e.g., Bartlett, 1932/1995). The thematic content of the memory, on the other hand, appears to survive intact, perhaps because it is facilitated by an amygdalabased modulation of emotional aspects of experience. We suggest, speculatively, that this same pattern of impairment and sparing might characterize how memory is disrupted in PTSD. We have also pointed out that traumatic memories can apparently suﬀer two rather diﬀerent fates: In one case, episodic information is disrupted while emotion is preserved; for example, emotion might be remembered in the form of intrusive fear and recurrent images of the trauma (ﬂashbacks) or as persistent anxiety (free-ﬂoating anxiety). All episodic information associated with the trauma is not necessarily forgotten. Rather, the memory survives in a fragmented form that renders those fragments susceptible to narrative smoothing. Narrative smoothing does not reﬂect intentional fabrication but an automatic and inferential use of preserved emotional and gist information that ﬁlls in gaps and smooths over inconsistencies. In the second case, described in detail in the previous section, memory for traumatic events is preserved, but the associated emotion is cut oﬀ (isolation of aﬀect). Based on the central idea that trauma results in abnormal functioning in various brain regions, with consequences for the memory roles these structures play, we have described patterns of disruption that account for the abnormal intrusion of traumatic memories into consciousness (i.e., ﬂashbacks), the lack of recall for traumatic memory (amnesia), and the fragmentation and subsequent ﬁlling in of traumatic memories, depending on the speciﬁc circumstances. We

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hope these ideas stimulate debate and experimentation and, with proper development, eﬀective intervention.

Notes The writing of this chapter was supported by grants to L. N. from the Flinn Foundation and the McDonnell-Pew Cognitive Neuroscience Program. Address correspondence to any of the authors at: Psychology Department, University of Arizona, Tucson, AZ 89719 ([email protected], [email protected], or wjj@u. arizona.edu). 1. But what is trauma? Trauma is an event that often has a speciﬁed role in the etiology of a mental disorder. But what is a mental disorder? Building on the work of Klein (1978) and Wakeﬁeld (1992), we use the term “mental disorder” to designate an authentic dysregulation of adaptive emotional, cognitive, or behavioral systems designed through natural or sexual selection to solve speciﬁc adaptive problems. A “disorder” becomes noticeable when a dysregulated system becomes maladaptive (dysfunctional), that is, consistently fails to solve the adaptive problem for which it was designed. Accordingly, the presence of a dysregulated system (a mental disorder) may be inferred from measurable maladaptive (dysfunctional) characteristics at an emotional, cognitive, behavioral, physiological, or anatomical level. Note that this deﬁnition of mental disorder diﬀers from that oﬀered by Klein (1978) and Wakeﬁeld (1992) in two ways. First, the term “harmful” has been removed from the phrase “harmful dysfunction.” The term has been a source of both controversy and confusion (see McNally [2001] for a brief summary). Second, the notion of sexual selection has been added to natural selection as a “gold standard” against which one might determine ‘normality’ (see Miller [2000] for a delightful introduction to the notion of sexual selection and the scope of its inﬂuence). It is far beyond the reach of this chapter to discuss the implications of these moves. Suﬃce it to say that these distinctions provide theoretically useful predictions about distinctions between extant judgments of disorder and nondisorder. 2. The nature of traumatic events leading to the emergency room visits was not described in the Bonne et al. (2001) article. However, subjects were not included in the study if they suﬀered head trauma or physical injury that required hospitalization. 3. Although PTSD has been associated with persistently low levels of cortisol (hypocortisolemia) (Yehuda, 1997; Yehuda, Southwick, Nussbaum, Giller, & Mason, 1991), some cases, particularly in the early stages of the disorder, show elevated levels of stress hormones (e.g., Pitman & Orr, 1990; see Bremner, 2001b). 4. “Reversible” here implies that memory function eventually returns to baseline in acute stress studies. 5. These three types of memory are not mutually exclusive. For example, “context” can be a part of detail memory, helping to distinguish one episode from another, and “coherence” is a direct outcome of contextual information and details being combined properly to yield a veridical representation of experience. 6. It behooves the reader to distinguish between the eﬀects of emotion on memories of various forms and the eﬀects of traumatic stress on emotional memories. The

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data we discuss here apply to the latter. In the section entitled “The Emotion and Memory Literature,” we discuss eﬀects of emotion on memory (traditionally conceptualized) and provide a brief critique of the methods and interpretations oﬀered by that literature. 7. This idea ﬁnds some support in the controversial evidence pointing to the existence of psychogenic amnesia, where trauma memories, or even memory for one’s entire identity, can be temporarily lost (Emilien et al., 2000; Markowitsch, 1999; but see Kihlstrom, 2001). 8. We do not know if these two reactions to trauma reﬂect diﬀerent underlying brain functions, individual diﬀerences wherein some talk about traumatic events and others attempt to forget them, the level of stress experienced, the nature of the stressor (events that inspire guilt, shame, or severe physical threat may be less likely to be discussed), or some combination of these factors. 9. See Nadel et al. (2002) and Nadel and Payne (2002) for deﬁnitions of context and detail and an explanation of how gist-based memories result from a lack of both. 10. An important distinction in the emotional memory literature is that some of the material we remember is itself emotional, while other material is emotionally neutral but encountered while one is emotionally aroused by some other experience. In our view, the source of emotional arousal is not critical for the pattern of enhanced gist/impaired detail memory to emerge because elevated stress and HPA activity determine the pattern. Given suﬃcient elevation, regardless of its source, this HPA activity will diﬀerentially inﬂuence hippocampus-based and amygdala-based memory function, provided that the stress response occurs within a speciﬁc timeline. 11. This information on “gist” and “thematic information” brings to mind work on schemas and scripts—representations that describe knowledge people can abstract from common, frequently occurring events (e.g., Abelson, 1981; Mandler, 1984)—and recalls the classic studies of Bartlett (1932/1995), who demonstrated that schemas can inﬂuence retrieval. His classic “War of the Ghosts” study showed that people reconstruct their memories based on schemas as they try to ﬁll in missing details and make sense out of incomprehensible information.

References Abelson, R. P. (1981). Psychological status of the script concept. American Psychologist, 36, 715–729. Adolphs, R., Denburg, N. L., & Tranel, D. (2001). The amygdala’s role in long-term declarative memory for gist and detail. Behavioral Neuroscience, 115, 983–992. Amaral, D. G., Price, J. L., Pitkanen, A., & Carmichael, S. T. (1992). Anatomical organization of the primate amygdaloid complex. In J. P. Aggleton (Ed.), The amygdala: Neurobiological aspects of emotion, memory and mental dysfunction (pp. 1–66). New York: Wiley-Liss. Anderson, S. W., Bechara, A., Damasio, H., Tranel, D., & Damasio, A. R. (1999). Impairment of social and moral behavior related to early damage in human prefrontal cortex. Nature Neuroscience, 2, 1032–1037. Arbel, I., Kadar, T., Silberman, M., & Levy, A. (1994). The eﬀects of long-term corticosterone administration on hippocampal morphology and cognitive performance of middle-aged rats. Brain Research, 657, 227–235.

     

113

Arnsten, A. (1998). Catecholamine modulation of prefrontal cortical cognitive function. Trends in Cognitive Sciences, 2, 436–447. Arnsten, A. (2000). Stress impairs prefrontal cortical function in rats and monkeys: Role of dopamine D1 and norepinephrine alpha-1 receptor mechanisms. Progress in Brain Research, 126, 183–192. Arnsten, A. F. T. (2001). Dopaminergic and noradrenergic inﬂuences on cognitive functions mediated by prefrontal cortex. In M. V. Solanto, A. F. T. Arnsten, & F. X. Castellanos (Eds.), Stimulant drugs and ADHD: Basic and clinical neuroscience (pp. 185–208). London: Oxford University Press. Aubert, A., Vega, C., Dantzer, R., & Goodall, G. (1995). Pyrogens speciﬁcally disrupt the acquisition of a task involving cognitive processing in the rat. Brain, Behavior and Immunity, 9, 129–148. Baddeley, A. (1986). Working memory. Oxford: Clarendon. Bartlett, F. C. (1932/1995). Remembering: A study in experimental and social psychology. New York: Cambridge University Press. Bellinger, F. P., Madamba, S., & Siggins, G. R. (1993). Interleukin 1 b inhibits synaptic strength and long-term potentiation in the rat CA1 hippocampus. Brain Research, 628, 227–234. Bender, B. G., Lerner, J. A., & Poland, J. E. (1991). Association between corticosteroids and psychologic change in hospitalized asthmatic children. Annals of Allergy, 66, 414–419. Bodnoﬀ, S. R., Humphreys, A. G., Lehman, J. C., Diamond, D. M., Rose, G. M., & Meaney, M. J. (1995). Enduring eﬀects of chronic corticosterone treatment on spatial learning, synaptic plasticity, and hippocampal neuropathology in young and mid-aged rats. Journal of Neuroscience, 15, 61–69. Bohus, B., & Lissak, K. (1968). Adrenocortical hormones and avoidance behaviour of rats. International Journal of Neuropharmacology, 7, 301–306. Bonne, O., Brandes, D., Gilboa, A., Gomori, J. M., Shenton, M. E., Pitman, R. K., et al. (2001). Longitudinal MRI study of hippocampal volume in trauma survivors with PTSD. American Journal of Psychiatry, 158, 1248–1251. Brainerd, C. J., & Reyna, V. F. (1998). Fuzzy-trace theory and children’s false memories. Journal of Experimental Child Psychology, 71, 81–129. Bremner, J. D. (1999). Does stress damage the brain? Biological Psychiatry, 45, 797– 805. Bremner, J. D.. (2001a). A biological model for delayed recall of childhood abuse. In J. Freyd & A. Deprince (Eds.), Trauma and cognitive science: A meeting of minds, science, and human experience (pp. 165–183). The Haworth Maltreatment & Trauma Press. Bremner, J. D. (2001b). Hypotheses and controversies related to eﬀects of stress on the hippocampus: An argument for stress-induced damage to the hippocampus in patients with posttraumatic stress disorder. Hippocampus, 11, 75–81. Bremner, J. D., Krystal, J. H., Charney, D. S., & Southwich, S. M. (1996). Neural mechanisms in dissociative amnesia for childhood abuse: Relevance to the current controversy surrounding the “False Memory Syndrome.” America Journal of Psychiatry, 153, FS71–82.

114

  

Bremner, J. D., Licinio, J., Darnell, A., Krystal, J. H., Owens, M., Southwick, S. M., et al. (1997). Elevated CSF corticotropin-releasing factor concentrations in posttraumatic stress disorder. American Journal of Psychiatry, 154, 624–629. Bremner, J. D., Randall, P. R., Capelli, S., Scott, T., McCarthy, G., & Charney, D. S. (1995). Deﬁcits in short-term memory in adult survivors of childhood abuse. Psychiatry Research, 59, 97–107. Bremner, J. D., Randall, P. R., Scott, T. M., Bronen, R. A., Delaney, R. C., Seibyl, J. P., et al. (1995). MRI-based measurement of hippocampal volume in posttraumatic stress disorder. American Journal of Psychiatry, 152, 973–981. Bremner, J. D., Randall, P., Vermetten, E., Staib, L., Bronen, R. A., Mazure, C. M., et al. (1997). MRI-based measurement of hippocampal volume in posttraumatic stress disorder related to childhood physical and sexual abuse: A preliminary report. Biological Psychiatry, 41, 23–32. Bremner, J. D., Scott, T. M., Delaney, R. C., Southwick, S. M., Mason, J. W., Johnson, D. R., et al. (1993). Deﬁcits in short-term memory in post-traumatic stress disorder. American Journal of Psychiatry, 150, 1015–1019. Bremner, J. D., Shobe, K. K., & Kihlstrom, J. F. (2000). False memories in women with self-reported childhood sexual abuse: An empirical study. Psychological Science, 11, 333–337. Bremner, J. D., Southwick, S. M., & Charney, D. S. (1997). Neuroanatomical correlates of the eﬀects of stress on memory: Relevance to the validity of memories of childhood abuse. In P. S. Appelbaum, L. A. Uyehara, & M. R. Elin (Eds.), Trauma and memory (pp. 61–92). London: Oxford. Bremner, J. D., Southwick, S. M., & Charney, D. S. (1999). The neurobiology of PTSD: An integration of animal and human research. In J. D. Bremner & P. Saigh (Eds.), Posttraumatic stress disorder: A comprehensive text (pp 103–143). New York: Allyn and Bacon. Bremner, J. D. Southwick, S. M., Johnson, D. R., Yehuda, R., & Charney, D. S. (1993). Childhood physical abuse in combat-related posttraumatic stress disorder. American Journal of Psychiatry, 150, 235–239. Bremner, J. D., & Vermetten, E. (2001). Stress and development: Behavioral and biological consequences. Development and Psychopathology, 13, 473–489. Breslau, N., Davis, G. C., Andreski, P., & Peterson, E. (1991). Traumatic events and post-traumatic stress disorder in an urban population of young adults. Archives in General Psychiatry, 48, 216–222. Buchanan, T. W., & Lovallo, W. R. (2001). Enhanced memory for emotional material following stress-level cortisol treatment in humans. Psychoneuroendocrinology, 26, 307–317. Buckner, R. L., Logan, J., Donaldson, D. I., & Wheeler, M. E. (2000). Cognitive neuroscience of episodic memory encoding. Acta Psychologica, 105, 127–139. Burke, A., Heuer, F., & Reisberg, D. (1992). Remembering emotional events. Memory & Cognition, 20, 277–290. Cahill, L., Babinsky, R., Markowitsch, H. J., & McGaugh, J. L. (1995). The amygdala and emotional memory. Nature, 377, 295–296. Cahill, L., & McGaugh, J. L. (1998). Mechanisms of emotional arousal and lasting declarative memory. Trends in Neuroscience, 21, 294–299.

     

115

Cahill, L., Prins, B., Weber, M., & McGaugh, J. L. (1994). Beta adrenergic activation and memory for emotional events. Nature, 371, 702–704. Caldji, C., Francis, D., Sharma, S., Plotsky, P. M., & Meaney, M. J. (2000). The eﬀects of early rearing environment on the development of GABA-A and central benzodiazepine receptor levels and novelty-induced fearfulness in the rat. Neuropsychopharmacology, 22, 219–229. Cameron, H. A., & Gould, E. (1994). Adult neurogenesis is regulated by adrenal steroids in the dentate gyrus. Neuroscience, 61, 203–209. Cameron, H. A., & McKay, R. (1999). Restoring production of hippocampal neurons in old age. Nature Neuroscience, 2, 894–897. Cannon, W. B. (1929). Bodily changes in pain, hunger, fear, and rage. 2nd ed. New York: Appleton. Christianson, S.-Å. (1992). Emotional stress and eyewitness memory: A critical review. Psychological Bulletin, 112, 284–309. Christianson, S.-Å., & Loftus, E. F. (1987). Memory for traumatic events. Applied Cognitive Psychology, 1, 225–239. Christianson, S.-ÅA, & Loftus, E. F. (1990). Some characteristics of people’s traumatic memories. Bulletin of the Psychonomic Society, 28, 195–198. Christianson, S.-Å., & Loftus, E. F. (1991). Remembering emotional events: The fate of detailed information. Cognition & Emotion, 5, 81–108. Christianson, S.-Å., Loftus, E. F., Hoﬀman, H., & Loftus, G. R. (1991). Eye ﬁxations and memory for emotional events. Journal of Experimental Psychology: Learning, Memory, and Cognition, 17, 693–701. Christianson, S.-Å., & Safer, M. A. (1995). Emotional events and emotions in autobiographical memories. In D. C. Rubin (Ed.), Remembering our past: Studies in autobiographical memory (pp. 218–243). Cambridge: Cambridge University Press. Clark, L. D., Bauer, W., & Cobb, S. (1952). Preliminary observations on mental disturbances occurring in patients under therapy with cortisone and ACTH. New England Journal of Medicine, 246, 205–216. Clark, M. S., Milberg, S., & Ross, J. (1983). Arousal cues arousal-related materials in memory: Implications for understanding eﬀects of mood on memory. Journal of Verbal Learning and Verbal Behavior, 22, 633–649. Clark, R. E., Zola, S. M., & Squire, L. R. (2000). Impaired recognition memory in rats after damage to the hippocampus. Journal of Neuroscience, 20, 8853–8860. Conrad, C. D., & Roy, E. J. (1996). Dentate gyrus destruction and spatial learning impairment after corticosteroid removal in young and middle-aged rats. Hippocampus, 5, 1–15. Convit, A., DeLeon, M. J., Tarshish, C., De Santi, S., Kluger, A., Rusinek, H., et al. (1995). Hippocampal volume losses in minimally impaired elderly. Lancet, 345, 266–266. Costello, E. J., Erkanli, A., Fairbank, J. A., & Angold, A. (2002). The prevalence of potentially traumatic events in childhood and adolescence. Journal of Traumatic Stress, 15, 99–112. Cunningham, A. J., Murray, C. A., O’Neill, L. A., & O’Connor, J .J. (1996). Interleukin 1-b (IL-1b) and tumor necrosis factor (TNF) inhibit long-term potentiation in the rat dentate gyrus in vitro. Neuroscience Letters, 203, 17–20.

116

  

Curran, T., Schacter, D. L., Norman, K. A., & Galluccio, L. (1997). False recognition after a right frontal lobe infarction: Memory for general and speciﬁc information. Neuropsychologia, 35, 1035–1049. Davidson, J. R. T., Roth, S., & Newman, E. (1991). Treatment of posttraumatic stress disorder with ﬂuxetine. Journal of Traumatic Stress, 4, 419–423. Davis, M. (1992). The role of the amygdala in fear and anxiety. Annual Review of Neuroscience, 15, 353–375. Davis, M., & Shui, C. (1999). The extended amygdala: Are the central nucleus of the amygdala and the bed nucleus of the stria terminalis diﬀerentially involved in fear versus anxiety? In: J. McGinty (Ed.), Advancing from the ventral striatum to the extended amygdala: Implications for neuropsychiatry and drug use: In honor of Lennart Heimer (pp. 281–291). New York: New York Academy of Sciences. Delbecq-Derouesne, J., Beauvois, M. F., & Shallice, T. (1990). Preserved recall versus impaired recognition. Brain, 113, 1045–1074. de Quervain, D. J.-F., Roozendaal, B., Nitsch, R. M., McGaugh, J. L., & Hock, C. (2000). Acute cortisone administration impairs retrieval of long-term declarative memory in humans. Nature Neuroscience, 3, 313–314. Deese, J. (1959). On the prediction of occurrence of particular verbal intrusions in immediate recall. Journal of Experimental Psychology, 58, 17–22. De Kloet, E. R., Oitzl, M. S., & Joels, M. (1999). Stress and cognition: Are corticosteroids good or bad guys? Trends in Neuroscience, 22, 422–426. Deptula, D. J. (1983). Lateralized brain dysfunction in depression: An analysis of memory. Dissertation Abstracts International. Diamond, D. M., Bennet, M. C., Fleshner, M., & Rose, G. M. (1992). Inverted U relationship between the level of peripheral corticosterone and the magnitude of hippocampal primed burst potentiation. Hippocampus, 2, 421–430. Diamond, D. M., Fleshner, M., Ingersoll, N. & Rose, G. M. (1996). Psychological stress impaires spatial working memory: Relevance to electrophysiological studies of hippocampal function. Behavioral Neuroscience, 110, 661–672. Diamond, D. M., Fleshner, M., & Rose, G. M. (1994). Psychological stress repeatedly blocks hippocampal primed burst potentiation in behaving rats. Behavioural Brain Research, 62, 1–9. Diamond, D. M., Park, C. R., Heman, K. L., & Rose, G. M. (1999). Exposing rats to a predator impairs spatial working memory in the radial arm water maze. Hippocampus, 9, 542–552. Diamond, D. M., & Rose, G. M. (1994). Stress impairs LTP and hippocampaldependent memory. Annals of New York Academy of Sciences, 746, 411–414. Emilien, G., Penasse, C., Charles, G., Martin, D., Lasseaux, L., & Waltregny, A. (2000). Post-traumatic stress disorder: Hypotheses from clinical neuropsychology and psychopharmacology research. International Journal of Psychiatry in Clinical Practice, 4, 3–18. Fairbank, J. A., Ebert, L., & Caddell, J. M. (2001). Posttraumatic stress disorder. In H. E. Adans & P. B. Sutker, (Eds.), (pp. 183–209). Comprehensive handbook of psychopathology (3rd ed., pp. 183–209). New York: Plenum. Fanselow, M. S., & LeDoux, J. E. (1999). Why we think plasticity underlying Pavlovian fear conditioning occurs in the basolateral amygdala. Neuron, 23, 229–232.

     

117

Feldman, S., & Conforti, N. (1980). Participation of the dorsal hippocampus in the glucocorticoid negative-feedback eﬀect on adrenocortical activity. Neuroendocrinology, 30, 52–55. Feldman, S., & Conforti, N. (1985). Modiﬁcations of adrenocortical responses following frontal cortex stimulation in rats with hypothalamic diﬀerentiations and medial forebrain bundle lesions. Neuroscience, 15, 1045–1047. Filipini, D., Gijsbers, K., Birminghan, M. K., & Dubrovsky, B. (1991). Eﬀects of adrenal steroids and their reduced metabolites on hippocampal long-term potentiation. Journal of Steroid Biochemistry and Molecular Biology, 40, 87–92. Fox, M. L., & Dwyer, D. J. (2000). Reducing stress by increasing control. Clinical Leadership and Management Reviews, 14, 114–117. Foy, M. R., Stanton, M. E., Levine, S., & Thompson, R. F. (1987). Behavioral stress impairs long-term potentiation in rodent hippocampus. Behavioral Neural Biology, 48, 138–149. Freud, S. (1926). Inhibitions, symptoms, and anxiety. London: Hogarth Press and the Institute of Psycho-analysis. Fukuzako, H., Fukuzako, T., Hashiguchi, T., Hokazono, Y., Takeuchi, K., Hirakawa, K., et al. (1996). Reduction in hippocampal formation volume is caused mainly by its shortening in chronic schizophrenia: Assessment by MRI. Biological Psychiatry, 39, 938–945. Garcia, R., Musleh, W., Tocco, G., Thompson, R. F., & Baudry, M. (1997). Timedependent blockade of STP and LTP in hippocampal slices following acute stress in mice. Neuroscience Letters, 233, 41–44. Gibertini, M., Newton, C., Friedman, H., & Klein, T. W. (1995). Spatial learning impairment in mice infected with Legionella pneumophila or administered exogenous interleukin-1–b. Brain, Behavior and Immunity, 9, 113–128. Gilbertson, M. W., Gurvits. T. V., Lasko, N. B., Orr, S. P., & Pitman, R. K. (2001). Multivariate assessment of explicit memory function in combat veterans with posttraumatic stress disorder. Journal of Traumatic Stress, 14, 413–432. Golier, J. A., Yehuda, R., & Southwick, S. M. (1997). Memory and posttraumatic stress disorder. In P. S. Appelbaum, L. A. Uyehara, & M. R. Elin (Eds.), Trauma and memory (pp. 225–242). London: Oxford. Goodman, G. G., Hirschman, J. E., Hepps, D. H., & Rudy, L. (1991). Children’s memory for stressful events. Merrill-Palmer Quarterly, 37, 109–158. Gould, E., & Gross, C. G. (2002). Neurogenesis in adult mammals: Some progress and problems. Journal of Neuroscience, 22, 619–623. Gould, E., & Tanapat, P. (1999). Stress and hippocampal neurogenesis. Biological Psychiatry, 46, 1472–1479. Gould, E., Tanapat, P., McEwen, B. S., Flugge, G., & Fuchs, E. (1998). Proliferation of granule cell precursors in the dentate gyrus of adult monkeys is diminished by stress. Proceedings of the National Academy of Science USA, 95, 3168–3171. Gray, J. A. (2000). The neuropsychology of anxiety: An enquiry into the function of the septo-hippocampal system. New York: Oxford. Gray, M. J., & Lombardo, T. W. (2001). Complexity of trauma narratives as an index of fragmented memory in PTSD: A critical analysis. [Special issue]. Applied Cognitive Psychology, 15, S171–S186.

118

  

Greidanus, T. J. B. (1970). Eﬀects of steroids on extinction of an avoidance response in rats. A structure-activity relationship study. Progress in Brain Research, 32, 185–191. Gurvits, T. G., Shenton, M. E., Hokama, H., Ohta, H., Lasko, N.B., Gilbertson, M.W., et al. (1996). Magnetic resonance imaging study of hippocampal volume in chronic, combat-related posttraumatic stress disorder. Biological Psychiatry, 40, 1091–1099. Hamann, S. (2001). Cognitive and neural mechanisms of emotional memory. Trends in Cognitive Sciences, 5, 394–400. Hamann, S. B., Ely, T. D., Grafton, S. T., & Kilts, C. D. (1999). Amygdala activity related to enhanced memory for pleasant and aversive stimuli. Nature Neuroscience, 2, 289–293. Harvey, A. G., & Bryant, R. A. (1998). Relationship of acute stress disorder and posttraumatic stress disorder following motor vehicle accidents. Journal of Consulting and Clinical Psychology, 66, 507–512. Henson, R. N. A., Shallice, T., & Dolan, R. J. (1999). Right prefrontal cortex and episodic memory retrieval: A functional MRI test of the monitoring hypothesis. Brain, 122, 1367–1381. Heuer, F., & Reisberg, D. (1990). Vivid memories of emotional events: The accuracy of remembered minutiae. Memory & Cognition, 18, 496–506. Heuer, F., & Reisberg, D. (1992). Emotion, arousal, and memory for detail. In S. Christianson (Ed.), The handbook of emotion and memory: Research and theory (pp. 151–180). Hillsdale, NJ: Erlbaum. Hirsh, R. (1974). The hippocampus and contextual retrieval of information from memory: A theory. Behavioral Biology, 12, 421–444. Horner, M. D., & Hamner, M. B. (2002). Neurocognitive functioning in posttraumatic stress disorder. Neuropsychology Review, 12, 15–30. Inoue, T., Tsuchiya, K., & Koyama, T. (1994). Regional changes in dopamine and serotonin activation with various intensity of physical and psychological stress in the rat brain. Pharmacology, Biochemistry, & Behavior, 49, 911–920. Jacobs, W. J., & Nadel, L. (1985). Stress-induced recovery of fears and phobias. Psychological Review, 92, 512–531. Jacobs, W. J., & Nadel, L. (1998). Neurobiology of reconstructed memory. Psychology, Public Policy and Law, 4, 1110. Jacobs, W. J., Nadel, L., & Hayden, V. (1992). Anxiety disorders. In D. J. Stein & J. Young (Eds.), Cognitive science and clinical disorders. (pp. 211–233) New York: Academic Press. Jacobs, W. J., Laurance, H. E., Thomas, K. G. F., Luzcak, S. E., & Nadel, L. (1996). On the veracity and variability of recovered traumatic memory. Traumatology, 2. Available http://www.rdz.stjohns.edu: 80/trauma/traumaj.html Jacobson, L., & Sapolsky, R. M. (1991). The role of the hippocampus in feedback regulation of the hypothalamic-pituitary-adrenal axis. Endocrinology Reviews, 12, 118–134. Jenkins, M. A., Langlais, P. J., Delis, D., & Cohen, R. (1998). Learning and memory in rape victims with posttraumatic stress disorder. American Journal of Psychiatry, 155, 278.

     

119

Joseph, R. (1996). Neuropsychiatry, neuropsychology, and clinical neuroscience. Baltimore: Williams & Wilkins. Kaehler, S. T., Singewald, N., Sinner, C., Thurnher, C., & Philippu, A. (2000). Conditioned fear and inescapable shock modify the release of serotonin in the locus coeruleus. Brain Research, 859, 249–254. Kanaley, J. A., Weltman, J. Y., Pieper, K. S., Weltman, A., & Hartman, M. L. (2001). Cortisol and growth hormone responses to exercise at diﬀerent times of day. Journal of Clinical Endocrinology and Metabolism, 86, 2881–2889. Kaspi, S. P., McNally, R. J., & Amir, N. (1995). Cognitive processing of emotional information in posttraumatic stress disorder. Cognitive Therapy and Research, 19, 319–330. Keenan, P. A., Jacobson, M. W., Soleymani, R. M., & Newcomer, J. W. (1995). Commonly used therapeutic doses of glucocorticoids impair explicit memory. Annals of the New York Academy of Sciences, 761, 400–402. Kessler, R. C., Sonnega, A., Bromet, E., Hughes, M., & Nelson, C. B. (1995). Posttraumatic stress disorder in the national comorbidity survey. Archives of General Psychiatry, 52, 1048–1060. Kihlstrom, J. F. (2001). Dissociative disorders. In P. B. Sutker & H. E. Adams (Eds.), Comprehensive handbook of psychopathology (3rd ed.). New York: Kluwer Academic/Plenum Publishers. Kim, J. J., & Diamond, D. M. (2002). The stressed hippocampus, synaptic plasticity and lost memories. Nature Reviews Neuroscience, 3, 453–462. Kirschbaum, C., Wolf, O. T., May, M., Wippich, W., & Hellhammer, D. H. (1996). Stress- and treatment-induced elevations of cortisol levels associated with impaired declarative memory in healthy adults. Life Sciences, 58, 1475–1483. Klein, D. F. (1978). A proposed deﬁnition of mental illness. In R. L. Spitzer & D. F. Klein(Eds.), Critical issues in psychiatric diagnosis (pp. 41–71). New York: Raven Press. Kleinsmith, L. J., & Kaplan, S. (1963). Paired-associate learning as a function of arousal and interpolated interval. Journal of Experimental Psychology, 65, 190–193. Kleinsmith, L. J., & Kaplan, S. (1964). The interaction of arousal and recall interval in nonsense syllable paired-associate learning. Journal of Experimental Psychology, 67, 124–126. Lang, P. J., & Cuthbert, B. N. (1984). Aﬀective information processing and the assessment of anxiety. Journal of Behavioral Assessment, 6, 369–395. Laurance, H. E., Hardt, O. M., Nadel, L., & Jacobs, W. J. (2001). Stress aﬀects spatiotemporal processing: Support for a model of traumatic memory. Poster session presented at the 109th meeting of the American Psychological Association. LeDoux, J. E. (1992). Emotion and the amygdala. In J. P. Aggleton (Ed.), The amygdala: Neurobiological aspects of emotion, memory, and mental dysfunction (pp. 339–351). New York: Wiley-Liss. LeDoux, J. E. (2000). Emotion circuits in the brain. Annual Review of Neuroscience, 23, 155–184. Lemieux, A. M., & Coe, C. L. (1995). Abuse-related posttraumatic stress disorder: Evidence for chronic neuroendocrine activation in women. Psychosomatic Medicine, 57, 105–115.

120

  

Lindsay, A. L., & Jennings, J. M. (2000). Chronic anxiety and false memory: Potential implications for medial temporal lobe functioning. Poster session presented at the 2000 meeting of the Society for Neuroscience. Linthorst, A. C., Flachskamm, C., Holsboer, F., & Reul, J. M. (1994). Local administration of recombinant human interleukin-1b in the rat hippocampus increases serotonergic neurotransmission, hypothalamic-pituitary-adrenocortical axis activity and body temperature. Endocrinology, 135, 520–532. Litz, B. T., & Gray, M. J. (2002). Emotional numbing in posttraumatic stress disorder: Current and future research directions. Australian and New Zealand Journal of Psychiatry, 36, 198–204. Loftus, E. F., & Burns, T. (1982). Mental shock can produce retrograde amnesia. Memory & Cognition, 10, 318–323. Loftus, E. F., Loftus, G., & Messo, J. (1987). Some facts about “weapon focus.” Law and Human Behavior, 11, 55–62. Luine, V., Villegas, M., Martinez, C., & McEwen, B. S. (1994). Repeated stress causes reversible impairments of spatial memory performance. Brain Research, 639, 167–170. Lupien, S. J., de Leon, M., de Santi, S., Convit, A., Tarshish, C., Nair, N.P.V., et al. (1998). Cortisol levels during human aging predict hippocampal atrophy and memory deﬁcits. Nature Neuroscience, 1, 69–73. Lupien, S. J., Gaudreau, S., Tchiteya, B. M., Maheu, F., Sharma, S., Nair, N. P. V., et al. (1997). Stress-induced declarative memory impairments in healthy elderly subjects: Relationship to cortisol reactivity. Journal of Clinical Endocrinology and Metabolism, 82, 2070–2075. Lupien, S. J., Lecours, A. R., Lussier, I., Schwartz, G., Nair, N. P. V., & Meaney, M. J. (1994). Basal cortisol levels and cognitive deﬁcits in human aging. Journal of Neuroscience, 14, 2893–2903. Lupien, S. J., & Lepage, M. (2001). Stress, memory, and the hippocampus: Can’t live with it, can’t live without it. Behavioural Brain Research, 127, 137–158. Lupien, S. J., & McEwen, B. S. (1997). The acute eﬀects of corticosteroids on cognition: Integration of animal and human model studies. Brain Research Reviews, 24, 1–27. Magarinos, A. M., & McEwen, B. S. (1995). Stress-induced atrophy of apical dendrites of hippocampal CA3c neurons: Involvement of glucocorticoid secretion and excitatory amino acid receptors. Neuroscience, 69, 89–98. Magarinos, A. M., McEwen, B. S., Flugge, G., & Fuchs, E. (1996). Chronic psychosocial stress causes apical dendritic atrophy of hippocampal CA3 pyramidal neurons in subordinate tree shrews. Journal of Neuroscience, 16, 3534– 3540. Magarinos, A. M., Verdugo, J. M., & McEwen, B. S. (1997). Chronic restraint stress alters synaptic terminal structure in hippocampus. Proceedings of the National Academy of Sciences, 94, 14002–14008. Maier, S. F., & Watkins, L. R. (1998). Stressor controllability, anxiety, and serotonin. Cognitive Therapy Research, 22, 595–613. Mandler, J. M. (1984). Stories, scripts, and scenes: Aspects of schema theory. Hillsdale, NJ: Erlbaum.

     

121

Markowitsch, H. J. (1999). Functional neuroimaging correlates of functional amnesia. Memory, 5/6, 561–583. Mauri, M., Sinforiani, E., Bono, G., Vignati, F., Berselli, M. E., Attanasio, R., et al. (1993). Memory impairment in Cushing’s disease. Acta Neurologica Scandinavica, 87, 52–55. McEwen, B. S. (2000). The neurobiology of stress: From serendipity to clinical relevance. Brain Research, 886, 172–189. McEwen, B. S. (2001). Neurobiology of interpreting and responding to stressful events: Paradigmatic role of the hippocampus. In B. S. McEwen (Ed.). Handbook of physiology. Section 7: The endocrine system. Volume 4: Coping with the environment: Neural and endocrine mechanisms. New York: Oxford University Press. McEwen, B. S., Albeck, D., Cameron, H., Chao, H. M., Gould, E., Hastings, N., et al. (1995b). Stress and the brain: A paradoxical role for adrenal steroids. In G. D. Litwack (Ed.), Vitamins and hormones (pp. 371–402). New York: Academic Press. McEwen, B. S., Conrad, C. D., Kuroda, Y., Frankfurt, M., Magarinos, A. M., & McKittrick, C. (1997). Prevention of stress-induced morphological and cognitive consequences. European Neuropsychopharmacology, 7(suppl.), 322–328. McEwen, B. S., & Sapolsky, R. M. (1995). Stress and cognitive function. Current Opinion in Neurobiology, 5, 205–216. McEwen, B. S., Weiss, J. M., & Schwartz, L. S. (1968). Selective retention of corticosterone by limbic structure in rat brain. Nature, 220, 911–912. McGaugh, J. L. (2000). Memory—A century of consolidation. Science, 287, 248–251. McGaugh, J. L. (2002). The amygdala regulates memory consolidation. In L. R. Squire & D. L. Schacter (Eds.), Neuropsychology of memory. 3rd ed. New York: Guilford Press. McGaugh, J. L., & Roozendaal, B. (2002). Role of adrenal stress hormones in forming lasting memories in the brain. Current Opinion in Neurobiology, 12, 205–210. McKittrick, C.nR., Magarinos, A. M., Blanchard, D. C., Blanchard, R. J., McEwen, B. S., & Sakai, R. R. (2000). Chronic social stress reduces dendritic arbors in CA3 of hippocampus and decreases binding to serotonin transporter sites. Synapse, 36, 85–94. McNally, R. J. (1998). Experimental approaches to cognitive abnormality in posttraumatic stress disorder. Clinical Psychology Review, 18, 971–982. McNally, R. J. (2001). On Wakeﬁeld’s harmful dysfunction analysis of mental disorder. Behaviour Research & Therapy 39, 309–314. McNally, R. J., Lasko, N. B., Macklin, M. L., & Pitman, R. K. (1995). Autobiographical memory disturbance in combat-related posttraumatic stress disorder. Behaviour Research and Therapy, 33, 619–630. McNally, R .J., Litz, B. T., Prassas, A., Shin, L. M., & West, F. W. (1994). Emotional priming of autobiographical memory in post-traumatic stress disorder. Cognition & Emotion, 8, 351–367. McNally, R. J., & Shin, L. M. (1995). Association of intelligence with severity of posttraumatic stress disorder symptoms in Vietnam combat veterans. American Journal of Psychiatry, 152, 936–938. Melo, B., Winocur, G., & Moscovitch, M. (1999). False recall and false recognition: An examination of the eﬀects of selective and combined lesions to the medial

122

  

temporal lobe/diencephalon and frontal lobe structures. Cognitive Neuropsychology, 16, 343–359. Mesches, M. H., Fleshner, M., Heman, K. L., Rose, G. M., & Diamond, D. M. (1999). Exposing rats to a predator blocks primed burst potentiation in the hippocampus in vitro. Journal of Neuroscience, 19, RC18(1–5). Metcalfe, J., & Jacobs, W. J. (1996). An interactive hot system/cool system view of memory under stress. PTSD Research Quarterly, 7, 1–6. Metcalfe, J., & Jacobs W. J. (1998). Emotional memory: The eﬀects of stress on ‘cool’ and ‘hot’ memory systems. In D. L. Medin (Ed.), The psychology of learning and motivation: Vol. 38. Advances in research and theory (pp. 187–222). San Diego, CA: Academic Press. Metcalfe, J., & Jacobs, W. J. (2000). Can ‘hot’ human emotions be captured by ‘cool’ mathematical models? In E. Tulving (Ed.), Memory, consciousness, and the brain: The Tallinn Conference (pp. 228–242). Philadelphia: Psychology Press. Miller, G. F. (2000). The mating mind: How sexual choice shaped the evolution of human nature. New York: Doubleday. Mitchell, K. J., Johnson, M. K., Raye, C. L., & D’Esposito, M. (2000). fMRI evidence of age-related hippocampal dysfunction in feature binding in working memory. Cognitive Brain Research, 10, 197–206. Mitchell, K. J., Johnson, M. K., Raye, C. L., Mather, M., & D’Esposito, M. (2000). Aging and reﬂective processes of working memory: Binding and test load deﬁcits. Psychology and Aging, 15, 527–541. Mitchell, S. A., & Black, M. J. (1995). Freud and beyond: A history of modern psychoanalytic thought. New York: BasicBooks. Moghaddam, B., Bolinao, M. L., Stein-Behrens, B., & Sapolsky, R. (1994). Glucocorticoids mediate the stress-induced extracellular accumulation of glutamate. Brain Research, 655, 251–254. Nadel, L. (1991). The hippocampus and space revisited. Hippocampus, 1, 221– 229. Nadel, L. (1994). Multiple memory systems: What and why. An update. In D. L. Schacter & E. Tulving (Eds.), Memory systems 1994 (pp. 39–63). Cambridge, MA: MIT Press. Nadel, L., & Jacobs, W. J. (1996). The role of the hippocampus in PTSD, panic, and phobia. In N. Kato (Ed.), The hippocampus: Functions and clinical relevance (pp. 455– 463). Amsterdam: Elsevier Science. Nadel, L., & Jacobs, W. J. (1998). Traumatic memory is special. Current Directions in Psychological Science, 7, 154–157. Nadel, L., & Payne, J. D. (2002). The hippocampus, wayﬁnding, and episodic memory. In P. Sharp (Ed.), The neural basis of navigation: Evidence from single cell recording (pp. 235–247). Boston: Kluwer Academic Publishers. Nadel, L., Payne, J. D., & Jacobs, W. J. (2002). The relationship between episodic memory and context: Clues from memory errors made while under stress. Physiological Research, 51, S3–S11. Nadel, L., & Willner, J. (1980). Context and conditioning: A place for space. Physiological Psychology, 8, 218–228. Neisser, U. (1981). John Dean’s memory: A case study. Cognition, 9, 1–22.

     

123

Newcomer, J. W., Craft, S., Hershey, T., Askins, K., & Bardgett, M. E. (1994). Glucocorticoid-induced impairment in declarative memory performance in adult humans. Journal of Neuroscience, 14, 2047–2053. Newcomer, J. W., Selke, G., Melson, A. K., Hershey, T., Craft, S., Richards, K., et al. (1999). Decreased memory performance in healthy humans induced by stresslevel cortisol treatment. Archives of General Psychiatry, 56, 527–533. Nyberg, L., & Cabeza, R. (2000). Brain imaging of memory. In E. Tulving & F. I. M. Craik (Eds.), The Oxford handbook of memory (pp. 501–519). Oxford: Oxford University Press. O’Carroll, R. E., Drysdale, E., Cahill, L., Shajahan, P., & Ebmeier, K. P. (1999). Stimulation of the noradrenergic system enhances and blockage reduces memory for emotional material in man. Psychological Medicine, 29, 1083–1088. Ochsner, K. N., & Schacter, D. L. (2000). A social cognitive neuroscience approach to emotion and memory. In J. C. Borod (Ed.), The neuropsychology of emotion (pp. 163–193). New York: Oxford University Press. Ohl, F., & Fuchs, E. (1999). Diﬀerential eﬀects of chronic stress on memory processes in the tree shrew. Cognitive Brain Research, 7, 379–387. O’Keefe, J., & Nadel, L. (1978). The hippocampus as a cognitive map. Oxford: Clarendon Press. Osborne, J. (1972). Short- and long-term memory as a function of individual diﬀerences in arousal. Perceptual and Motor Skills, 34, 587–593. Otten, L. J., & Rugg, M. D. (2002). The birth of memory. Trends in Neurosciences, 25, 279–281. Pani, L., Porcella, A., & Gessa, G. L. (2000). The role of stress in the pathophysiology of the dopaminergic system. Molecular Psychiatry, 5, 14–21. Parkin, A. J., Bindschaedler, C., Harsent, L., & Metzler, C. (1996). Pathological false alarm rates following damage to the left frontal cortex. Brain and Cognition, 32, 14–27. Payne, J. D., Nadel, L., Allen, J. J. B., Thomas, K. G. F., & Jacobs, W. J. (2002). The eﬀects of experimentally-induced stress on false recognition. Memory, 10, 1–6. Pitman, R., & Orr, S. (1990). Twenty-four hour urinary cortisol and catecholamine excretion in combat-related posttraumatic stress disorder. Biological Psychiatry, 27, 245–247. Plihal, W., & Born, J. (1999). Memory consolidation in human sleep depends on inhibition of glucocorticoid release. Neuroreport, 10, 2741–2747. Porter, S., & Birt, A. (2001). Is traumatic memory special? A comparison of traumatic memory characteristics with memory for other emotional life experiences. Applied Cognitive psychology, 15, S101–S117. Prince, C. R., & Anisman, H. (1990). Situation speciﬁc eﬀects of stressor controllability on plasma corticosterone changes in mice. Pharmacology, Biochemistry, and Behavior, 37, 613–621. Rasmusson, A. M., Lipschitz, D. S., Wang, S., Hu, S., Vojvoda, D., Bremner, J. D., et al. (2001). Increased pituitary and adrenal reactivity in premenopausal women with posttraumatic stress disorder. Biological Psychiatry, 50, 965–977.

124

  

Raye, C. L., Johnson, M. K., Mitchell, K. J., Nolde, S. F., & D’Esposito, M. (2000). fMRI investigations of left and right PFC contributions to episodic remembering. [Special issue]. Psychobiology, 28, 197–206. Reiman, E. M., Lane, R. D., Ahern, G. L., Schwartz, G. E., & Davidson, R. J. (2000). Positron emission tomography in the study of emotion, anxiety, and anxiety disorders. In R. D. Lane & L. Nadel (Eds.), Cognitive neuroscience of emotion (pp. 389–406). Oxford: Oxford University Press. Reyna, V. F., & Kiernan, B. (1994). Development of gist versus verbatim memory in sentence recognition: Eﬀects of lexical familiarity, semantic content, encoding instructions, and retention interval. Developmental Psychology, 30, 178–191. Roediger, H. L., & McDermott, K. B. (1995). Creating false memories: Remembering words not presented in lists. Journal of Experimental Psychology: Learning, Memory & Cognition, 21, 803–814. Roozendaal, B. (2000). Glucocorticoids and the regulation of memory consolidation. Psychoneuroendocrinology, 25, 213–238. Roozendaal, B., & McGaugh, J. L. (1996). Amygdaloid nuclei lesions diﬀerentially aﬀect glucocorticoid-induced memory enhancement in an inhibitory avoidance task. Neurobiology of Learning and Memory, 65, 1–8. Roozendaal, B., & McGaugh, J. L. (1997). Glucocorticoid receptor agonist and antagonist administration into the basolateral but not central amygdala modulates memory storage. Neurobiology of Learning and Memory, 67, 176–179. Rosenbaum, R. S., Priselac, S., Kohler, S., Black, S. E., Gao, F, Nadel, L., et al. (2000). Remote spatial memory in an amnesic person with extensive bilateral hippocampal lesions. Nature Neuroscience, 3, 1044–1048. Rosenkranz, J. A., & Grace, A. A. (2002). Cellular mechanisms of infralimbic and prelimbic prefrontal cortical inhibition and dopaminergic modulation of basolateral amygdala neurons in vivo. Journal of Neuroscience, 22, 324– 337. Rugg, M. D., Fletcher, P. C., Chua, P. M.-L., & Dolan, R. J. (1999). The role of the prefrontal cortex in recognition memory and memory for source: An fMRI study. NeuroImage, 10, 520–529. Saigh, P. A., & Bremner, J. D. (1999). The history of posttraumatic stress disorder. In P. A. Saigh & J. D. Bremner (Eds.), Posttraumatic stress disorder: A comprehensive text. Needham Heights, MA: Allen & Bacon. Sapolsky, R. M. (1996). Why stress is bad for your brain. Science, 273, 749–750. Sapolsky, R. M. (2000). Glucocorticoids and hippocampal atrophy in neuropsychiatric disorders. Archives of General Psychiatry, 57, 925–935. Sapolsky, R. M., Krey, L. C., & McEwen, B. S. (1985). Prolonged glucocorticoid exposure reduces hippocampal neuron number: implications for aging. Journal of Neuroscience, 5, 1222–1227. Sapolsky, R. M., & Meaney, M. J. (1986). Maturation of the adrenocortical stress response: Neuroendocrine control mechanisms and the stress hyporesponsive period. Brain Research, 396, 64–76. Schacter, D. L., & Tulving, E. (Eds.), (1994). Memory systems 1994. Cambridge, MA: MIT Press.

     

125

Scoville, W. B., & Milner, B. (1957). Loss of recent memory after bilateral hippocampal lesions. Journal of Neurology, Neurosurgery, and Psychiatry, 20, 11–21. Selye, H. (1956). The stress of life. New York: McGraw-Hill. Sheline, Y. I., Sanghavi, M., Mintun, M. A., & Gado, M. H. (1999). Depression duration but not age predicts hippocampal volume loss in medically healthy women with recurrent major depression. Journal of Neuroscience, 19, 5034–5043. Sheline, Y. I., Wang, P. W., Gado, M. H., Csernansky, J. C., & Vannier, M. W (1996). Hippocampal atrophy in recurrent major depression. Proceedings from the National Academy of Sciences USA, 93, 3908–3913. Shimamura, A. P. (1997). Recollection: Perspectives on reinstated memory and child trauma. In J. D. Read & D. S. Lindsay (Eds.), Recollections of trauma (pp. 253–266). New York: Plenum Press. Shors, T. J., Gallegos, R. A., & Breindl, A. (1997). Transient and persistent consequences of acute stress on long-term potentiation (LTP), synaptic eﬃcacy, theta rhythms and bursts in area CA1. Synapse, 26, 209–217. Southwick, S. M., Davis, M., Horner, B., Cahill, L., Morgan, C. A., Golc, P. E., et al. (2002). Relationship of enhanced norepinephrine activity during memory consolidation to enhanced long-term memory in humans. American Journal of Psychiatry, 159, 1420–1422. Stanny, C. J., & Johnson, T. C. (2000). Eﬀects of stress induced by a simulated shooting on recall by police and citizen witnesses. American Journal of Psychology, 113, 359–386. Starkman, M. N., Gebarski, S. S., Berent, S., & Schteingart, D. E. (1992). Hippocampal formation volume, memory dysfunction, and cortisol levels in patients with Cushing’s syndrome. Biological Psychiatry, 32, 756–765. Starkman, M. N., Giordani, B, Gebrski, S. S., Berent, S., Schork, M. A., & Schteingart, D. E. (1999). Decrease in cortisol reverses human hippocampal atrophy following treatment of Cushing’s disease. Biological Psychiatry, 46, 1595–1602. Stein-Behrens, B. A., Elliott, E. M., Miller, C. A., Schilling, J. W., Newcombe, R., & Sapolsky, R.M. (1992). Glucocorticoids exacerbate kainic acid-induced extracellular accumulation of excitatory amino acids in the rat hippocampus. Journal of Neurochemistry, 58, 1730–1735. Stein-Behrens, B. A., Lin, W. J., & Sapolsky, R. M. (1994). Physiological elevations of glucocorticoids potentiate glutamate accumulation in the hippocampus. Journal of Neurochemistry, 63, 596–602. Stein, M. B., Koverola, C., Hanna, C., Torchia, M. G., & McClarty, B. (1997). Hippocampal volume in women victimized by childhood sexual abuse. Psychological Medicine, 27, 951–959. Stoddard, S. L., Bergdall, V. K., Townsend, D. W., & Levin, B. E. (1986). Plasma catecholamines associated with hypothalamically-elicited ﬂight behavior. Physiology & Behavior, 37, 709–715. Tanapat, P., Hastings, N. B., Rydel, T. A., Galea, L. A., & Gould, E. (2001). Exposure to fox odor inhibits cell proliferation in the hippocampus of adult rats via an adrenal hormone-dependent mechanism. Journal of Comparative Neurology, 437, 496–504.

126

  

Terr, L. (1991). Childhood traumas: An outline and overview. American Journal of Psychiatry, 148, 10–20. Terr, L. (1993). Unchained memories. New York: Basic Books. Torrie, A. (1944). Psychosomatic casualties in the Middle East. Lancet, 29, 139– 143. Uddo, M., Vasterling, J. T., Brailey, K., & Sutker, P. B. (1993). Memory and attention in posttraumatic stress disorder. Journal of Psychopathology and Behavioral Assessment, 15, 43–52. Uno, H., Ross, T., Else, J., Suleman, M., & Sapolsky, R. (1989). Hippocampal damage associated with prolonged and fatal stress in primates. Journal of Neuroscience, 9, 1705–1711. Vaher, P., Luine, V., Gould, E., & McEwen, B. (1994). Eﬀects of adrenalectomy on spatial memory performance and dentate gyrus morphology. Brain Research, 656, 71–76. van Cauter, E., & Turek, F. W. (2001). Roles of sleep-wake and dark-light cycles in the control of endocrine, metabolic, cardiovascular, and cognitive function. In B. S. McEwen & H. M. Goodman (Eds.), Handbook of physiology: Section 7, The endocrine system. New York: Oxford University Press. van der Kolk, B. A. (1991). The biological response to psychic trauma: Mechanisms and treatment of intrusion and numbing. Anxiety Research, 4, 199–212. van der Kolk, B. A. (1994). The body keeps the score: Memory and the evolving psychobiology of posttraumatic stress. Harvard Reviews Psychiatry, 1, 253–265. van der Kolk, B. A., & Fisler, R. (1995). Dissociation and the fragmentary nature of traumatic memories: Review and experimental conﬁrmation. Journal of Traumatic Stress, 8, 505–525. van der Kolk, B. A., Hopper, J. W., & Osterman, J. E. (2001). Exploring the nature of traumatic memory: Combining clinical knowledge with laboratory methods. Journal of Aggression, Maltreatment & Trauma, 4, 9–31. Vasterling, J. J., Brailey, K., Allain, A. N., Duke, L. M., Constans, J. I., & Sutker, P. B. (2002). Attention, learning, and memory performances and intellectual resources in Vietnam veterans: PTSD and no disorder comparisons. Neuropsychology, 16, 5–14. Vasterling, J .J., Brailey, K., Constans, J. I., Borges, A., & Sutker, P. B. (1997). Assessment of intellectual resources in Gulf War veterans: Relationship to PTSD. Assessment, 4, 51–59. Vasterling, J. J., Brailey, K., Constans, J. I., & Sutker, P. B. (1998). Attention and memory dysfunction in posttraumatic stress disorder. Neuropsychology, 12, 125–133. Virgin, C. E., Taryn, P. T. H., Packan, D. R., Tombaugh, G. C., Yang, S. H., Horner, H. C., et al. (1991). Glucocorticoids inhibit glucose transport and glutamate uptake in hippocampal astrocytes: Implications for glucocorticoid neurotoxicity. Journal of Neurochemistry, 57, 1422–1428. Vyas, A., Mitra, R., Rao, S. B. S., & Chatterji, S. (2002). Chronic stress induces contrasting patterns of dendritic remodeling in hippocampal and amygdaloid neurons. Journal of Neuroscience, 22, 6810–6818.

     

127

Wakeﬁeld, J. C. (1992). Disorder as harmful dysfunction: A conceptual critique of DSM-III-R’s deﬁnition of mental disorder. Psychological Review, 99, 232–247. Watanabe, Y., Gould, E., Daniels, D. C., Cameron, H., & McEwen, B. S. (1992). Tianetine attenuates stress-induced morphological changes in the hippocampus. European Journal of Pharmacology, 222, 157–162. Watanabe, Y., Gould, E., & McEwen, B. S. (1992). Stress induces atrophy of apical dendrites of hippocampal CA3 pyramidal neurons. Brain Research, 588, 341– 345. Wechsler, D. (1945). A standardized memory scale for clinical use. Journal of Psychology, 19, 87–95. Wolkowitz, O. M., Reus, V. I., & Weingartner, H. (1990). Cognitive eﬀects of corticosteroids. American Journal of Psychiatry, 147, 1297–1303. Wolkowitz, O. M., Weingartner, H., Rubinow, D. R., Jimerson, D., Kling, M., Berretini, W., et al. (1993). Steroid modulation of human memory: Biochemical correlates. Biological Psychiatry, 33, 744–746. Wooley, C. S., Gould, E., & McEwen, B. S. (1990). Exposure to excess glucocorticoids alters dendritic morphology of adult hippocampal pyramidal neurons. Brain Research, 531, 225–231. Yehuda, R. (1997). Stress and glucocorticoid. Science, 275, 1662–1663. Yehuda, R., Keefe, R. S. E., Harvey, P. D., Levengood, R. A., Gerber, D. K., Geni, J., et al. (1995). Learning and memory in combat veterans with posttraumatic stress disorder. American Journal of Psychiatry, 152, 137–139. Yehuda, R., Southwick, S. M., Nussbaum, E. L., Giller, E. L., & Mason, J. W. (1991). Low urinary cortisol in PTSD. Journal of Nervous and Mental Disorders, 178, 366–369. Zoellner, L. A., Foa, E. B., Brigidi, B. D., & Przeworski, A. (2000). Are trauma victims susceptible to “false memories”? Journal of Abnormal Psychology, 109, 517– 524.

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4

   . ,  . , 

 . 

M

ost experts agree that people exposed to traumatic events remember them all too well. (For reviews, see McNally, 2003c; Pope, Oliva, & Hudson, 1999.) Indeed, survivors of trauma often report intrusive memories despite their eﬀorts to forget. But debate persists regarding whether a substantial subset of survivors repress, dissociate, or otherwise forget having been traumatized—and then remember it all later (McNally, 2003a). Consider the views of Brown, Scheﬂin, and Hammond (1998), who proclaim “overwhelming scientiﬁc support for the existence of repressed or dissociated memory” (pp. 538–539). Summarizing across studies, they conclude that “generally speaking, approximately a third of sexually abused victims report some period of their lives where they did not remember anything about the abuse and later recovered the memory of the abuse” (p. 196). Yet after considering much of the same evidence, Loftus and Ketcham (1994) published their diﬀerent conclusions in The Myth of Repressed Memory. How can scholars scrutinize the same evidence yet arrive at such diametrically opposed conclusions? To address this question, we examine the evidence adduced in support of repressed and recovered memory for traumatic experiences. To provide a fresh perspective on the debate, we also summarize our recent laboratory research on cognitive functioning in people who report repressed, recovered, or continuous memories of trauma.

Common Assumptions About

Forgetting Trauma

Some theorists distinguish between repression and dissociation, deﬁning the former as inhibition of taboo urges and the latter as inhibition of disturbing 129

memories. But in the recovered memory debate, this is a distinction without a diﬀerence. In fact, as Brown et al. indicate, “repressed memory” and “dissociated memory” are used interchangeably. Regardless of whether the theorist’s favored mechanism is repression or dissociation, he or she usually endorses the following assumptions about forgetting and trauma. First, people are motivated to forget unpleasant experiences. Second, they are especially likely to forget atrocious trauma: “The ordinary response to atrocities is to banish them from consciousness” (Herman, 1992, p. 1). Third, because sexual abuse, in particular, is so traumatic, if someone fails to think about the abuse for many years, then he or she must have repressed or dissociated it from awareness. That is, an active inhibitory force must be keeping it out of consciousness. Otherwise, why would someone not think about it for years? Fourth, the more frequently a person (especially a child) is traumatized, the more diﬃcult it will be for him or her to remember having been traumatized (Terr, 1991). That is, people exposed to repetitive trauma develop dissociative skills to cope with inescapable situations, making it diﬃcult to recall these experiences many years later. Fifth, children are more likely to forget having been traumatized if they were abused by their parents than if they were abused by strangers (Freyd, 1996). Sixth, forgotten trauma is neither inert nor benign; it is the silent source of diverse psychological problems (Blume, 1990). Accordingly, remembering forgotten trauma, emotionally processing it, and integrating it into one’s autobiography are important steps toward healing (Courtois, 1992). All assumptions except the ﬁrst have been ﬂashpoints for intense controversy.

Evidence Adduced for

Forgetting of Trauma

The trauma therapists Brown et al. (1998) have assembled evidence in support of the six assumptions. Many of the studies they cite were modeled on an inﬂuential survey conducted by Briere and Conte (1993). Recruiting subjects through a network of therapists specializing in the treatment of sexual abuse, these authors obtained questionnaire data on 450 patients who reported having been sexually abused as children. In response to the question, “Was there ever a time when you could not remember the forced sexual experience,” 59% of the subjects responded in the aﬃrmative. Many psychologists, such as Brown et al., interpreted these ﬁndings as evidence that many sexual abuse survivors experience amnesia for their traumatic experiences, only to remember them later in life. Scholars soon drew attention to the methodological limitations of this survey and others like it. First, the subjects were patients potentially exposed to therapeutic techniques likely to foster illusory memories of abuse (Poole, Lindsay, Memon, & Bull, 1995). As in many abuse recollections, external corrobo-

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ration was apparently unavailable, and the duration of “amnesia” for trauma was unspeciﬁed (a week? decades?). The most important issue concerned the key survey question about forgetting. Interpreted literally, this question seems to make little sense. An aﬃrmative response implies that the subject had repeatedly attempted to remember the abuse but failed to do so (i.e., could not remember). But if subjects were unaware of having been abused, on what basis would they attempt to recall it in the ﬁrst place? Indeed, the most sensible way to regard aﬃrmative responses to this question is to assume that subjects interpreted it to mean, “Was there ever a time when you did not think about your abuse?” A person who answered “yes” to this question might have experienced sexual abuse as a child, managed not to think about it for many years, but was reminded of the abuse in adulthood. But the long time when the person did not think about his or her abuse cannot be equated with “amnesia,” or an inability to recall something from memory when furnished with adequate retrieval cues. Just because a person did not remember (did not think about it) does not mean that the person could not remember. Moreover, as Schooler and others have shown, some people who believe they have not thought about their (documented) traumatic experiences for many years are surprised to learn that they had, in fact, discussed these events with family members when they thought the memories never came to mind (Schooler, Bendiksen, & Ambadar, 1997). That is, a person can forget having remembered (thought about) a traumatic event, producing an “illusion of amnesia.” A person might be especially likely to forget a previous instance of recalling abuse if the recollection was not accompanied by strong emotion. For example, in a conversation with her husband, a woman might mention that she was once molested by a distant relative. If this conversation occurs during an especially positive period in her life, she might not experience much emotion while recounting her abuse and therefore not recall the conversation with her husband. A key point in examining the literature on forgetting trauma is that one cannot equate amnesia for an event with merely not having thought about the event for a time. To conﬁrm amnesia, one must show that the person had encoded the event in the ﬁrst place and is now incapable of recalling it despite the adequate retrieval cues (e.g., such as being asked whether one had ever been abused). Failure to think about something for a time must not be confused with an inability to remember it. Moreover, as we have learned in our ongoing studies, many individuals report that the abuse was not experienced as traumatic when it occurred. Many of our subjects have told us that they felt it must be “wrong”—that something was not “right” about it. At the time, they often felt confused or embarrassed by the experience. Only years later did they grasp the full signiﬁcance of what had happened (i.e., that they were sexually abused). In fact, many of them rate the abuse as more traumatic now than it was at the time.

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These points also apply to the growing number of case reports concerning people who recall long-forgotten—and often corroborated—episodes of abuse (for reviews, see Cheit, 1998, 1999; McNally, 2003c, chapter 7). Some children are exposed to one (or sometimes more) episodes of molestation, often nonpenetrative (e.g., fondling) but abusive nevertheless. They ﬁnd the experiences confusing or upsetting but not necessarily terrifying. They avoid dwelling on the experience and may succeed in forgetting it, especially if reminders are no longer present (e.g., the perpetrator moves away). Then, many years later, they encounter retrieval cues (e.g., someone mentions the perpetrator, or they hear news reports on television regarding sexual abuse), and the memory suddenly pops back into awareness. Such cases clearly qualify as “recovered memories of sexual abuse,” but they do not count as amnesia (i.e., an inability to recall when provided adequate retrieval cues). In fact, sudden recollections of seemingly forgotten experiences are fairly common in the general population and are not conﬁned to adverse events like sexual abuse (Read, 1997). Most important, a failure to think about something for many years does not mean that active forces (repression, dissociation) are preventing these memories from entering awareness. An important study by Williams (1994) further illustrates these interpretive pitfalls. Her research team interviewed 129 women who had been assessed for suspected sexual abuse approximately 17 years earlier, when they were children. Medical evidence conﬁrmed the abuse in many cases. The main purpose of the study was to survey women about their health and experiences with the health care system. Embedded within the interview were questions about sexual abuse. Women who acknowledged having been abused were questioned about the event. Their narratives were compared with the hospital records that described the index event. Of the 129 women, 49 of them did not mention the index event (although 33 of them did describe other incidents of sexual abuse). Strikingly, 16 of the 49 women denied ever having been sexually abused. Some authors have interpreted these data as showing that victims can repress or dissociate all memory of their abuse rather than merely forget it (i.e., not think about it for a long time), but other interpretations are possible. Many of the subjects were younger than 5 when assessed for abuse. Because few memories from very early childhood survive into adulthood, memories of the index event may have undergone ordinary forgetting. Moreover, the younger the child was when abused, the more likely she might have failed to understand what the perpetrator was doing, thereby undermining encoding and later retrieval of the memory. Other subjects may have remembered the index event but may have been too embarrassed to disclose such personal matters to the interviewer. A study by Goodman et al. (2003) provides further data on failure to disclose abuse. They assessed 175 subjects (81% female) who had been involved in legal proceedings concerning sexual abuse. The proceedings occurred when the subjects were approximately 9 years old (range: 3 years to 16 years). Questions about sexual abuse were embedded in a longer survey concerning attitudes about the

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law and experiences with the legal system. The survey was administered 13 years after the subjects had been involved in the legal proceedings. The results revealed that 88% of the subjects mentioned the index event that led to the legal proceedings. Like some subjects in Williams’s study, 17 subjects denied ever having been abused. However, further analysis of the data undermines many popular explanations for why these nondisclosing individuals may have “forgotten” their abuse. Contrary to the notion that people prone to dissociation are most likely to forget their abuse, the higher a subject’s score on the Dissociative Experiences Scale (DES; Bernstein & Putnam, 1986), the more likely the subject was to disclose the abuse. Contrary to Freyd’s (1996) conjecture that children exposed to parental abuse are those most likely to be unable to remember it, there was no correlation between failure to disclose and relationship to the perpetrator. The studies by Williams (1994) and Goodman et al. (2003) do not provide clear support for any special repression or dissociation mechanism that actively inhibits recollection of the index event. The ﬁndings from these studies can be most parsimoniously interpreted as showing that a minority of adults with childhood abuse histories will deny having been abused when questioned by a survey interviewer. However, in neither study did researchers conduct subsequent clariﬁcation interviews to ascertain the basis for the discrepancy between documents concerning the abuse and the subject’s denial of it. In a study on young adults with documented histories of physical abuse, Femina, Yeager, and Lewis (1990) found that all subjects who had denied (or minimized) their abuse during an interview later acknowledged that they had not forgotten it when originally questioned by the interviewer. Subjects who had earlier denied their documented abuse later said that they did not wish to discuss such upsetting experiences or did not like the interviewer. None had repressed or forgotten the abuse. The ﬁndings of this study suggest that some of the nondisclosers in the studies of Williams and Goodman et al. may have been disinclined to discuss abuse they had, in fact, remembered. In any event, survey studies have not been the only source of evidence adduced in support of repressed memories of trauma (Brown et al., 1998; van der Kolk & Fisler, 1995). For example, Brown et al. wrote that “Dollinger (1985) found that two of the 38 children studied after watching lightning strike and kill a playmate had no memory of the event” (pp. 609–610). Although this trauma was well documented, the amnesia experienced by these two children for this horror has nothing to do with dissociation or repression. Brown et al. forgot to mention that both children had themselves been struck by side ﬂashes from the main lightning bolt, had been knocked unconscious, and had nearly died (Dollinger, 1985). Given the severe eﬀects on the central nervous system of a lightning strike (Kotagal, Rawlings, Chen, Burris, & Nouri, 1982), it is little wonder that these two children had amnesia for the episode. Obviously, their amnesia was entirely organic. Indeed, none of the other children who had not been struck by lightning forgot this horriﬁc event.

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Interpreting research on memory for trauma among former inmates of concentration Camp Erika (Wagenaar & Groeneweg, 1990), Brown et al. (1998) claimed that “amnesia for Nazi Holocaust camp experiences has also been reported” (p. 156). Wagenaar and Groeneweg assessed the memories of camp survivors 40 years after the survivors had provided testimony about their internment shortly after their release. Impressed by the strikingly accurate recollections of the former inmates, Wagenaar and Groeneweg emphasized that “there is no doubt that almost all witnesses remember Camp Erika in great detail, even after 40 years” (p. 84). Why, then, did Brown et al. cite this study as providing evidence for traumatic amnesia? As it turns out, several subjects claimed to have forgotten the name of an especially brutal guard or failed to mention several violent incidents that they had mentioned 40 years earlier. But even these isolated incidents of forgetting do not indicate amnesia. With one exception, subjects immediately recollected the forgotten details once they examined their original testimony. Given the “remarkable degree of remembering” (Wagenaar & Groeneweg, 1990, p. 80) exhibited by the former inmates, Brown et al.’s claim about amnesia regarding the Holocaust seems far-fetched. Because memory does not operate like a video recorder, it is hardly surprising that not every detail mentioned was instantly recalled 40 years later. [See chapter 11—Eds.] One of the most common blunders made by theorists of traumatic amnesia is to confuse general memory impairment in the wake of trauma with an inability to remember that one has been traumatized. Listing studies that supposedly support the notion of traumatic amnesia, Brown et al. (1998) mention Wilkinson’s (1983) study of individuals who had witnessed the horriﬁc collapse of the Hyatt Regency skywalks in Kansas City. Of those assessed, 27% endorsed the DSM-III symptom of “memory diﬃculties” while aﬃrming their intensely vivid recollections of the disaster itself. Indeed, intrusive memories of the disaster may have contributed to problems with forgetfulness in everyday life. In another often misinterpreted study (Brown et al., 1998; van der Kolk & Fisler, 1995), Archibald and Tuddenham (1965) reported that 65% of their World War II combat fatigue cases complained of “diﬃculty in memory” versus only 5% of psychiatrically healthy combat veterans. However, 60% of veterans who were not in combat and suﬀered from other psychiatric disorders endorsed the same complaint. Moreover, the authors themselves emphasized how unforgettable combat was for the traumatized patients, noting that these veterans “cannot blot out their painful memories” (p. 480). Obviously, the “memory problems” reported by these men concern everyday forgetfulness, not amnesia for their combat trauma. However, other studies on combat veterans have uncovered evidence of apparent amnesia for combat itself among groups of men referred for psychiatric evaluation and treatment. Eder (1917) reported that 2% of his psychiatric battle

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casualties could not recall certain combat events occurring in World War I. According to Sargant and Slater (1941), 14% of psychiatric casualties who had escaped from Dunkirk reported amnesia for events occurring during the chaotic retreat. World War II psychiatrists reported rates of amnesia for combat in 5% of patients in the Paciﬁc Theater (Henderson & Moore, 1944) and 8.6% in North Africa (Torrie, 1944). But as Pope et al. (1999) pointed out, these psychiatrists were often unable to rule out organic causes of amnesia (e.g., exhaustion, head injury) or malingering. Other more recent cases of amnesia for traumatic events provide an interesting contrast with the typical case of repressed and recovered memory of childhood sexual abuse. Swihart, Yuille, and Porter (1999) have described cases of “red-out” in which a person murders a loved one in a ﬁt of rage but experiences amnesia for the murder itself. Swihart et al. suspect that these cases may be genuine, not malingered. Indeed, the murderer often phones the police and immediately admits to committing the crime despite claiming not to have remembered the actual attack. There have been other cases of psychogenic amnesia in which an event, often shocking, triggers retrograde amnesia (see McNally, 2003c, chapter 7, for a review of this case study literature). Reviewing this literature, Arrigo and Pezdek (1997) connected it to the furor over recovered memories of sexual abuse. However, the phenomenon of psychogenic amnesia is drastically diﬀerent from the controversial cases in the child abuse ﬁeld. In cases of psychogenic amnesia, say, after the death of a loved one, the person develops complete retrograde amnesia shortly after the shocking event, accompanied by loss of personal identity. Psychogenic amnesia seldom lasts for more than a few hours to a few weeks. Typically, memory and personal identity return abruptly without any psychotherapy. In contrast, cases of traumatic amnesia, say, of repressed and recovered memories of childhood sexual abuse, have no clear onset, never involve identity loss, may last for years or decades, and often gradually return piece by piece during the course of psychotherapy. Moreover, the amnesia selectively blocks retrieval of trauma; it does not blot out the entire person’s life and identity. Accordingly, classic psychogenic amnesia has little to do with the controversy over repressed and recovered memories of childhood abuse. Finally, some theorists note that “inability to recall an important aspect of the trauma (psychogenic amnesia)” has been a diagnostic criterion of PTSD ever since DSM-III-R (American Psychiatric Association [APA], 1987, p. 250) and adduce this fact to support the notion that trauma survivors can repress or dissociate their memory for trauma. Unfortunately, this diagnostic criterion is fatally ambiguous because it does not distinguish between an inability to recall an aspect of the trauma that was never encoded into memory in the ﬁrst place and an inability to recall an aspect of the trauma because an inhibitory mechanism (e.g., repression) blocks its access to awareness. Because the mind is not a

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video recorder, there will inevitably be aspects of the traumatic event that never make it into memory. Encoding failure must not be confused with amnesia, let alone repression. In summary, extant data do not support the claim that unconscious repression or dissociation mechanisms expel traumatic memories from awareness and prevent them from entering consciousness. People often try not to think about their sexual abuse or other unpleasant experiences, and sometimes they succeed. But not thinking about something for a long time does not imply an inability to remember it (i.e., amnesia).

A View From the Cognitive

Psychology Laboratory

Cognitive psychologists have conducted considerable research on mechanisms of inhibition in memory retrieval (e.g., Anderson & Neely, 1996). And they have drawn on basic research to speculate about how false memories of trauma might be inadvertently fostered in clinical settings (e.g., Ceci & Loftus, 1994; Lindsay & Read, 1994). But this work is swiftly dismissed by repressed memory theorists, who assert that generalizations from laboratory studies with college students have questionable relevance for how abuse survivors might remember or forget their trauma (e.g., Brown et al., 1998, p. 98). In fact, one of the most striking features of the recovered memory debate has been the near absence of any research on cognitive functioning in people reporting repressed or recovered memories of abuse. This situation may have arisen because few clinicians possess expertise in laboratory research, and few cognitive psychologists have access to trauma populations. In any event, during the past few years our research group has been conducting laboratory studies designed to test hypotheses relevant to (1) mechanisms implicated in either the ability to repress and recover traumatic memories or (2) mechanisms relevant to proneness to forming false memories of trauma (McNally, 2001, 2003b). This line of research began quite by accident. The ﬁrst author was conducting psychiatric diagnostic interviews for a positron emission tomography (PET) study designed to map the functional neuroanatomy of autobiographical recollection of traumatic memories in women who had been sexually abused as children (Shin et al., 1999). We had posted advertisements seeking female adult survivors of childhood sexual abuse, and we planned to distinguish those with and without PTSD prior to the study. During the diagnostic interview, three women who expressed interest in the project turned out not to have any explicit autobiographical memories of molestation, despite considering themselves survivors of abuse. Further questioning revealed that they assumed that they harbored repressed memories of abuse because they were inexplicably tense in the presence of certain relatives, experienced diverse symptoms (e.g., depressed mood), and so forth; lacking a suit-

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able explanation, they assumed that their problems must be attributable to repressed memories of early abuse. Because they lacked autobiographical memories of trauma, these women did not qualify for the neuroimaging study. But their reports of repressed memories inspired us to recruit and study individuals who reported diverse memory manifestations of trauma. In our ﬁrst series of studies, we recruited four groups of women from the community. The repressed memory group included subjects who suspected they had been sexually abused as children but had no autobiographical memories of abuse. These subjects inferred their abuse history from a diverse range of symptoms (e.g., nightmares, depressed mood, bulimia). About a third of this group mentioned having acquired the belief in their repressed memories of abuse during psychotherapy. The recovered memory group included subjects who reported recollecting abuse after long periods of not having thought about it. Nearly half of them remembered their abuse during the course of psychotherapy, but only one mentioned recovering a memory in session. The continuous memory group reported never having forgotten their abuse. The control group included individuals who denied ever having been sexually abused. We were unable to corroborate reports of the abuse (although we are actively attempting to do so in our current set of studies). Accordingly, we do not know whether the recovered (or continuous) memories of abuse are genuine or whether those who suspected they harbored repressed memories of abuse were really abused. Of course, the absence of corroboration does not mean that the memories are false. To characterize our groups, we conducted a study on personality proﬁles and clinical symptoms (McNally, Clancy, Schacter, & Pitman, 2000b). Our subjects completed the Multidimensional Personality Questionnaire (MPQ; Tellegen, 1982), an inventory designed to characterize normal personality variation that includes an Absorption scale (Tellegen & Atkinson, 1974) that taps fantasy proneness. In addition to these personality measures, they also completed three psychiatric questionnaires. The Beck Depression Inventory (BDI; Beck & Steer, 1987) measured symptoms of depression, the Dissociative Experiences Scale (DES; Bernstein & Putnam, 1986) measured alterations in consciousness (e.g., memory lapses, depersonalization, episodes of “spacing out”), and the civilian version (Vreven, Gudanowski, King, & King, 1995) of the Mississippi Scale for Combat-Related Posttraumatic Stress Disorder (CMISS; Keane, Caddell, & Taylor, 1988) measured PTSD symptoms, as well as other problems (e.g., occupational diﬃculties, suicidal ideation) sometimes linked to PTSD. The MPQ uncovered striking similarities and diﬀerences in personality proﬁle among the groups. The continuous memory group and the control group were indistinguishable on every measure of personality. The same was true for the repressed and recovered memory groups, who did not diﬀer on any scale. Moreover, the four groups did not diﬀer on positive aﬀectivity, or proneness to experience joy and enthusiasm. In contrast, the groups did diﬀer in negative aﬀectivity, or proneness to experience sadness, anxiety, anger, and guilt. Re-

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pressed memory subjects scored higher than did either the continuous memory or control groups, whereas recovered memory subjects scored midway between the repressed subjects and subjects in the other two groups. Consistent with patterns of negative aﬀectivity, repressed memory subjects had more depressive, dissociative, and PTSD symptoms than did continuous memory and control subjects. Repressed memory subjects also had more depressive and PTSD symptoms than recovered memory subjects, who, in turn, had more dissociative and PTSD symptoms than did control subjects. Strikingly, continuous memory subjects were indistinguishable from control subjects in PTSD, dissociative, and depressive symptoms. Finally, the repressed and recovered memory groups did not diﬀer on the absorption scale, but both groups scored higher than the control group. The repressed memory group also scored signiﬁcantly higher than the continuous memory group. Table 4.1 summarizes these ﬁndings. These data indicate that people who believe they harbor repressed memories of sexual abuse are more psychologically distressed than those who have never forgotten their abuse. There are at least two explanations for this pattern. Heightened levels of distress among repressed memory subjects may reﬂect the psychic toll of blocking out memories of abuse. On the other hand, their distress may have arisen from diverse and poorly understood causes, motivating an “eﬀort after meaning” that led them to attribute their problems to repressed memories of abuse. As Bass and Davis (1988) emphasized in The Courage to Heal, “When you ﬁrst remember your abuse or acknowledge its eﬀects, you may feel tremendous relief. Finally there is a reason for your problems. There is someone, and something to blame” (p. 173). When confronted with a choice between being miserable and not knowing why and being miserable and knowing why, many people will choose the latter, especially if they can also blame others for their diﬃculties. To test Bass and Davis’s (1988) hypothesis, we recontacted 11 of our recovered memory subjects and asked them to complete a Child Abuse Survivor Questionnaire (Clancy, 2000). In this pilot study, subjects wrote brief responses to

table 4.1 Summary of Psychometric Results Variable Positive affectivity Negative affectivity Depression symptoms PTSD symptoms Dissociative symptoms Absorption

Repress a a a a a a

Group Recover Continuous a ab b b ab ab

a b b bc bc bc

Control a b b c c c

Note. Repress = repressed memory group; recover = recovered memory group. Means of groups sharing a letter do not differ significantly (p > .05). A mean value represented by a is greater than a mean value represented by b, which, in turn, is greater than a mean value represented by c (i.e., a > b > c).

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each question and then rated their strength of endorsement of each item on a 9-point Likert scale. The questions and anchors for each scale follow. 1. Since you recovered the memory, do you feel your self-esteem has changed? The anchors were 1 (“I feel much worse about myself ”) and 8 (“I feel much better about myself”). 2. Since you recovered the memory, do you ﬁnd that other people are more or less supportive of you? The anchors were 1 (“I have many less social supports since I recovered the memory”) and 8 (“I have many more social supports since I recovered the memory”). 3. Since you recovered the memory, has your level of happiness changed? The anchors were 1 (“I feel much less happy”) and 8 (“I feel much happier”). 4. Overall, since you recovered the memory, have things been better or worse for you? The anchors were 1 (“Things have been much worse”) and 8 (“Things have been much better”). 5. If you had to do it all over again, would you choose NOT to remember that you were abused? The anchors were 1 (“I would deﬁnitely choose not to remember”) and 8 (“I would deﬁnitely choose to remember”). 6. Do you feel that recovering the memory changed how you understand yourself? The anchors were 1 (“I understand myself much less now”) and 8 (“I understand myself much better now”).

The results revealed that 100% of the subjects reported at least some beneﬁts from recovering their memories of abuse, and 73% reported beneﬁts in response to all questions. After recovering their memories, 100% of the subjects reported increased self-esteem (M = 6.7), 82% reported increased social support (M = 5.4), 91% reported increased happiness (M = 5.8), 82% reported overall life improvement (M = 6.2), 91% said they would choose to remember their abuse if they could do it all over again (M = 7.2), and 100% reported increased self-understanding (M = 7.5). These pilot data suggest that Bass and Davis (1988) may be correct. Identifying oneself as an abuse survivor by recovering memories of abuse may yield psychological beneﬁts to already distressed individuals even if the eﬀects of the abuse itself have been clearly harmful.

Forgetting Trauma-Related Material Some trauma theorists assert that sexually abused children develop an avoidant (or dissociative) encoding style that enables them to disengage attention from terrifying stimuli during abuse episodes and redirect it elsewhere (e.g., Terr, 1991). Unable to escape physically from the perpetrator, abused children may endeavor to escape mentally. Although adaptive in the short run, a dissociative style of coping with threats presumably fosters long-term psychological problems.

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This hypothesized cognitive style ought to be evident in the laboratory and detectable through directed forgetting methods. There are two main directedforgetting paradigms, and each engages diﬀerent mechanisms (Golding, in press; Johnson, 1994). In the list method, the experimenter presents the subject with a list of words, halfway through the procedure, he or she tells the subject that the ﬁrst set of words was “only for practice” and hence can be forgotten. After this instruction to forget, the experimenter resumes presentation of the words to be remembered. In the item method, an instruction to remember or to forget follows the presentation of each word. For both paradigms, the experimenter asks the subject to recall as many words as possible, regardless of original instructions. Generally, subjects tend to recall more remember-words than forget-words, but the mechanisms underlying this eﬀect diﬀer for each paradigm. In the list paradigm, forget-words appear to have been encoded but areinhibited at retrieval. In the item paradigm, subjects appear to attenuate their encoding of a word as soon as the forget instruction occurs; hence, later recall failures seem chieﬂy attributable to poor encoding of the forget-words. In our ﬁrst experiment, we tested adult female survivors of childhood sexual abuse with PTSD, psychiatrically healthy survivors of childhood sexual abuse, and nonabused control subjects (McNally, Metzger, Lasko, Clancy, & Pitman, 1998). Subjects had experienced penetrative abuse, and most had always remembered it. The subject viewed a series of words on a computer screen that were either trauma-related (e.g., incest), positive (e.g., cheerful), or neutral (e.g., cupboard). After each word’s presentation, instructions appeared that told the subject either to remember or to forget the immediately preceding word. Immediately after this encoding phase, we asked subjects to write down all the words they could remember, regardless of whether a word had been followed by remember or forget instructions. The standard directed forgetting eﬀect emerging from basic research indicates that subjects abort encoding of forget-words and, accordingly, exhibit better recall for remember-words than for forget-words (Johnson, 1994). However, if psychologically traumatized survivors are characterized by a superior ability to disengage attention from trauma cues, then the PTSD group, compared to healthy survivors and controls, should exhibit superior forgetting of trauma words relative to other words. The results contradicted this hypothesis: childhood sexual abuse survivors with PTSD exhibited memory deﬁcits for positive and neutral words they had been instructed to remember, and they exhibited excellent memory for trauma words, including words they had been instructed to forget. Exhibiting the standard directed forgetting eﬀect, healthy survivors and control subjects recalled remember-words more often than forget-words, regardless of the word’s valence. Contrary to our original hypothesis, survivors with PTSD seemed to exhibit an impairment in the ability to banish trauma words from awareness. One limitation of the previous study was that our sexual abuse survivors were suﬀering from intrusive thoughts as part of their current PTSD. Perhaps indi-

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viduals reporting repressed or recovered memories of abuse would be most likely to exhibit superior forgetting of trauma words in the laboratory. To test this hypothesis, we used the same directed-forgetting protocol to compare the relative ability to forget trauma words in recovered memory subjects, repressed memory subjects, and nonabused control subjects (McNally, Clancy, & Schacter, 2001). If anyone should exhibit heightened ability to forget trauma words, it should be individuals who once repressed (or still have repressed) their memories of abuse. Contrary to this hypothesis, the memory performances of the repressed and recovered memory groups were entirely normal. Both groups recalled remember-words better than forget-words, regardless of valence. (Control subjects, however, exhibited diﬃculty forgetting trauma words.) The directed-forgetting paradigm involves the forgetting of trauma words, mere pale proxies for autobiographical memories of abuse. If these individuals developed a skill for repressing or dissociating genuine memories of trauma, it should easily be brought into play in the laboratory when they are asked to forget words linked to abuse. Yet we found no evidence of any superior ability to forget trauma words among our childhood sexual abuse groups, and those with PTSD appear to experience a breakdown in the ability to banish trauma words from awareness. The very fact that abuse survivors with PTSD have diﬃculty forgetting is fully consistent with the cardinal symptom of the disorder: intrusive recollection of traumatic memories. On the other hand, preoccupation with the possibility that one might have been sexually abused might heighten the salience of trauma words, making it diﬃcult for subjects to disengage attention from them and forget them in this paradigm.

Intrusion of Traumatic Material PTSD is characterized by intrusive recollection of traumatic memories. Assessment of this symptom has traditionally relied on introspective self-reports disclosed in interviews or questionnaires. The emotional Stroop color-naming paradigm provides a quantitative measure of intrusive cognition that does not rely on introspection (for reviews, see McNally, 1998; Williams, Mathews, & MacLeod, 1996). In this laboratory paradigm, subjects view words that vary in emotional signiﬁcance and are asked to name the colors of the words while ignoring their meanings. When the meaning of a word captures the subject’s attention, the subject exhibits a delay in naming its color. The intrusiveness of meaning is reﬂected in delayed color naming (Stroop interference). Psychiatrically disturbed trauma survivors who qualify for PTSD take longer to name the colors of words related to their trauma than to name the colors of neutral words or emotional words unrelated to their trauma (for a review, see McNally, 1998).

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Trauma survivors who do not suﬀer from PTSD seldom show much Stroop interference. Psychologically traumatized survivors of combat (e.g., McNally, Kaspi, Riemann, & Zeitlin, 1990), rape (e.g., Foa, Feske, Murdock, Kozak, & McCarthy, 1991), and sexual abuse (Dubner & Motta, 1999) exhibit Stroop interference for words related to their traumatic memories. Indeed, color naming of trauma words is more strongly associated with intrusive symptoms than with avoidance/numbing symptoms (Cassiday, McNally, & Zeitlin, 1992). We used the emotional Stroop paradigm to test whether subjects reporting either continuous, repressed, or recovered memories of sexual abuse, compared to nonabused control subjects, would exhibit interference for trauma words (McNally, Clancy, Schacter, & Pitman, 2000a). Although we did not conduct diagnostic interviews to assess for PTSD, the repressed memory group exhibited elevations on the CMISS. Moreover, if severity of trauma is what causes PTSD and what motivates repression of traumatic memories, subjects who cannot recall their presumably repressed memories may nevertheless exhibit interference on the emotional Stroop task—a measure of automatic (obligatory) emotional processing (McNally, 1995). Subjects named the colors of a series of trauma-related (e.g., molested), positive (e.g., elation), and neutral (e.g., carpet) words on a computer screen as quickly as possible. Unlike patients with PTSD, none of the groups exhibited delayed color naming of trauma words relative to neutral or positive ones. These data suggest that interference eﬀects for trauma-related material may be conﬁned to abuse survivors who qualify for PTSD (Dubner & Motta, 1999). Believing that one harbors repressed memories of abuse is not associated with patterns of interference that characterize survivors with PTSD.

Memory Distortion Many psychologists have warned that certain therapeutic techniques may inadvertently foster false memories of abuse in distressed patients (e.g., Poole et al., 1995). One such technique is guided imagery. Misguided therapists who believe that patients with certain symptom patterns harbor repressed memories of abuse will ask these patients to visualize abuse scenarios that might have happened, hoping that the content of guided imagery might trigger recollection of the blocked trauma. Unfortunately, repeated visualization of imagined events may increase conﬁdence that the events actually occurred (Garry, Manning, Loftus, & Sherman, 1996; Heaps & Nash, 1999). Using an imagination inﬂation paradigm developed by Garry et al. (1996), we tested whether recovered memory subjects are more susceptible than control subjects to this form of memory distortion (Clancy, McNally, & Schacter, 1999). Subjects rated their conﬁdence regarding whether they had experienced unusual, but

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nontraumatic, childhood events (e.g., getting stuck in a tree, ﬁnding a $10 bill in parking lot). During a subsequent visit to our laboratory, they performed a brief guided imagery task requiring them to visualize certain events but not others. Immediately thereafter, they rated their conﬁdence in whether any of these events had actually occurred during their childhoods. Perhaps because of modest statistical power, the increase in conﬁdence that imagined events had in fact happened fell short of signiﬁcance. However, the eﬀect size for this imagination inﬂation phenomenon was more than twice as large in the control group than in the recovered memory group. Several subjects in the recovered memory group later said that they thought the experiment was about creating false memories in the laboratory, perhaps indicating that the procedure was transparent. Continuing to explore whether recovered memory subjects are especially vulnerable to false memory eﬀects in the laboratory, we next applied a variant of the Deese/Roediger-McDermott (DRM) paradigm (Deese, 1959; Roediger & McDermott, 1995). This paradigm is less transparent than the guided imagery one. During the encoding phase, subjects hear a series of word lists, each consisting of semantically related items (e.g., sour, bitter, candy, sugar) that converge on a nonpresented word—the “false target”—that captures the theme of the list (e.g., sweet). The false memory eﬀect occurs when subjects “remember” having heard the false target on subsequent recognition tests. Research suggests that false memory eﬀects in this paradigm occur when people rely on their memory for the general semantic aspects (or gist) of the items they studied. We tested subjects who reported either repressed, recovered, or continuous memories of childhood sexual abuse and nonabused control subjects (Clancy, Schacter, McNally, & Pitman, 2000). None of the lists was trauma-related. The results revealed that the recovered memory group was more prone to “remember” false targets than were the other groups. This group exhibited no general memory impairment; material that had been presented was remembered as well by the recovered memory subjects as by the other subjects. Moreover, the higher a subject’s DES score, the more likely she was to exhibit the false memory eﬀect. (The DES also predicts this eﬀect among college students in the DRM paradigm; Winograd, Peluso, & Glover, 1998.) Thus, self-reported dissociation in everyday life was linked to remembering words never presented. This tendency for false memory formation notwithstanding, we do not know whether the eﬀect would be more or less pronounced for material directly related to abuse. What implications do these ﬁndings have for false memories of trauma? The fact that recovered memory subjects apparently relied on gist rather than memory for speciﬁc words suggests a processing style that might contribute to memory confusion later in life. Aﬃrming that something occurred based on general resemblance to events that did occur might lead one to suspect they were sexually abused if they did, in fact, experience other similar adverse events in childhood (e.g., emotional abuse, neglect).

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False Memory Eﬀects in

“Space Alien Abductees”

The DRM experiment suggested that individuals who report recovered memories of sexual abuse are prone to exhibit false memory eﬀects in the laboratory. But this does not mean that their recovered memories of abuse are false. We were unable to obtain independent evidence bearing on the veracity of their abuse reports, but external corroboration of abuse is often diﬃcult to obtain. In our next experiment, we extended our work to a group of subjects whose memories of trauma were likely inaccurate: people who report recovering memories of abduction by space aliens. Applying Robinson and Roediger’s (1997) DRM paradigm, we tested the false recognition and false recall propensities in three groups of subjects (Clancy, McNally, Schacter, Lenzenweger, & Pitman, 2002). One group reported recollections of alien abduction. A second group, similar to our repressed memory subjects, included individuals who believed they had been abducted but had no explicit memories of the trauma. They inferred a history of abduction from sources such as unexplained marks on their bodies, interpreted as evidence of alien medical probes; a passion for reading science ﬁction books; panic attacks triggered by seeing drawings of aliens on book covers; and so forth. They assumed that the aliens had control of their memories or that the abduction occurred in another dimension. A third (control) group included individuals who denied a history of alien abduction. Like subjects who report having recovered memories of sexual abuse, those reporting abduction by space aliens exhibited greater false memory eﬀects in the DRM paradigm than did either the control group or the group that had suspected (but had no memory) they had been abducted. The group that believed they had been abducted, but who had no conscious memories of abduction, exhibited greater false memory eﬀects than the control group but not as great eﬀects as the group that had recovered “memories” of abduction. Therefore, subjects who had recovered “memories” of abduction relied most on gist memory in the DRM paradigm, a propensity that may explain why they recall these experiences after having undergone quasi-hypnotic regression therapies, read books about abduction, and so forth. Accordingly, this pattern may explain why the recovered memory group went on to develop full-blown false memories of abduction, whereas others did not. People who have recovered memories of sexual abuse often experience intense emotion while remembering these long-forgotten events, tempting some therapists to credit the veracity of the accounts. Surely the memories must be genuine, some therapists believe; otherwise, how could these recollections trigger such extreme aﬀect? In fact, considerable research indicates that when people with PTSD recollect their traumatic experiences—more speciﬁcally, when they listen to

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audiotaped descriptions of them—they exhibit heightened psychophysiologic reactivity (for a review, see Orr & Roth, 2000). Indeed, Orr et al. (1998) found not only that female survivors of sexual abuse with PTSD exhibited greater physiological responding while listening to autobiographical trauma scripts than did abuse survivors without PTSD but also that those with PTSD who had recently recovered their memories tended to be more physiologically responsive than were those who had always remembered their abuse. Using this script-driven imagery procedure, we tested whether people reporting abduction by space aliens exhibit heightened psychophysiologic responding while listening to scripts describing their purported abduction experiences (McNally et al., 2002). If they did, then this ﬁnding would imply that belief that one has been traumatized can generate a physiologic proﬁle similar to that of PTSD patients who have endured traumatic conditioning experiences. Each of our 10 “abductees” traced contact with space aliens to an episode of apparent sleep paralysis accompanied by hyponopompic (upon-awakening) hallucinations. These episodes occur as the person is awakening from rapid eye movement (REM) sleep (Cheyne, Rueﬀer, & Newby-Clark, 1999). Dreams occur during REM sleep, and this stage of sleep is associated with full–body paralysis. However, during an episode of sleep paralysis, the cognitive and motoric aspects of REM become desynchronized for several seconds to several minutes. The sleeper awakens before paralysis has waned and becomes aware of an inability to move. No more pathological than a hiccup, sleep paralysis occurs at least once to approximately 30% of the general population (Cheyne, Newby-Clark, & Rueﬀer, 1999). About 5% of the population, however, has also experienced hallucinations during these episodes, including ﬂashing lights, buzzing sounds, feelings of levitating oﬀ the bed, electrical tingling sensations shooting through one’s body, and seeing threatening ﬁgures hovering near one’s bed. Within a few seconds or minutes, the person is entirely awake, can move again, and the hallucinations cease. None of our subjects realized that he or she was experiencing sleep paralysis, and all eventually interpreted the episode as an encounter with alien beings. Frightened by such experiences, some sought hypnosis to recover presumably repressed aspects of these episodes. During these sessions, they recalled additional “memories” of having been transported into spacecraft, where they endured medical and sexual experimentation at the hands of alien beings. For the script-driven imagery protocol, each abductee furnished material for ﬁve individualized, autobiographical scripts: two scripts related to abduction trauma; a script related to a diﬀerent, highly stressful event; a script related to a positive experience; and one related to an emotionally neutral experience. Our control group consisted of individuals who denied a history of alien abduction. Each control subject heard the scripts of one of the abductees. Compared with control subjects, abductees exhibited greater heart rate and skin conductance responses during imagery of abduction scripts than to imagery of the other scripts (ps < .06; eﬀect size rs = .40). Although none of the

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abductees ever met full criteria for PTSD, the magnitude of their heart rate and skin conductance responses to their abduction scripts matched or exceeded the reactivity exhibited by PTSD subjects to their trauma scripts in previous research. For example, abductees had a mean skin conductance response of 1.82 æS, whereas Vietnam combat veterans with PTSD in Keane et al.’s (1998) deﬁnitive study had a mean response of 0.8 æS. Likewise, the mean heart rate response of abductees was 7.8 bpm, whereas for Vietnam veterans with PTSD it was 3.2 bpm (Keane et al., 1998). Believing that one has been traumatized by space aliens produces heightened physiologic responding similar to that of people exposed to combat and other traumatic events. Therefore, emotional responding during recollection provides no guarantee that the memory is veridical.

Are Memories of Trauma Special? Some clinical theorists believe that memories of traumatic events diﬀer qualitatively from memories of other emotionally intense experiences. Consider the claim of Brown et al. (1998): Thus, across all studies, a robust ﬁnding is that narrative memory for the gist or central action of a negative emotionally arousing event is extremely well retained. The more involved the person is, the more likely the memory will be retained. Traumatic events are a signiﬁcant exception to this general rule. A signiﬁcant portion of traumatized individuals suﬀer from traumatic amnesia; even if their narrative memory for the traumatic event is retained, it may not be readily accessible. (p. 368)

Intensity of emotion, Brown et al. believe, is a key variable. “[W]hen emotional material reaches the point of being traumatic in intensity—something that cannot be replicated in artiﬁcial laboratories—in a certain subpopulation of individuals, material that is too intense may not be able to be consciously processed and so may become unconscious and amnesic” (p. 97). Others have made similar assertions (e.g., Joseph, 1999; van der Kolk, 1994), suggesting that memory for traumatic experience follows an inverted-U function (Yerkes & Dodson, 1908). That is, emotional arousal enhances memory, but only up to a point. After that point is reached, these theorists believe that intense emotion somehow undermines hippocampal function and impairs explicit memory for the trauma. This theory is riddled by many conceptual and empirical problems (see McNally, 2003c, chapter 6, for detailed critique). First, intense arousal does not block the formation of explicit narrative memory for traumatic experiences. As Langer’s (1991) work has shown, survivors of the Nazi concentration camps are haunted by detailed, explicit, vivid memories of the horrors they experienced. Indeed, the evidence overwhelmingly shows that traumatic experiences are remembered all too well (Pope et al., 1999). People tend not to forget the central aspects of trau-

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matic events, even if they fail to encode or remember details of these experiences. [as with nontraumatic emotional memories; see chapter 1—Eds.]. Second, abundant laboratory research shows that amygdala activation promotes encoding and hippocampus-mediated explicit memory for emotionally intense experiences (for a review, see McGaugh, Ferry, Vazdarjanova, & Roozendaal, 2000). To be sure, release of stress hormones can impair performance on certain explicit memory tasks mediated by the hippocampus (for a review, see Lupien & McEwen, 1997). But stress does not impair memory for the stress-producing experience itself. For example, Kirschbaum, Wolf, May, Wippich, & Hellhammer (1996) exposed subjects to a social stressor (giving a speech prior to trying to solve math problems out loud) before having them learn and recall a list of words. The higher the levels of stress hormone (cortisol) triggered by this stressor, the fewer words subjects recalled. Hence, stress can impair memory for an incidental activity, such as memorizing words. But it does not abolish memory for the stressor itself. Third, as Christianson’s (1992) review shows, studies on emotional stress and memory fail to support a Yerkes-Dodson–like (1908) notion that moderately high stress enhances memory and extreme stress impairs it. (Moreover, as some trauma theorists seem to have forgotten, Yerkes and Dodson studied visual discrimination learning in mice, not memory for trauma. Hence, the work of these two scientists has scant relevance for the recovered memory debate.) As Easterbrook’s (1959) theory implies, extreme stress enhances memory for the central aspects of the traumatic experience, sometimes at the expense of the peripheral details (McNally, 2003c, chapter 5). Fourth, some theorists have suggested that extreme stress establishes implicit memories of the traumatic experience while sometimes undermining explicit memories of it (e.g., van der Kolk, 1994). As Brown et al. (1998) asserted, “Much of the memory for trauma is retained as an implicit rather than explicit memory” (p. 483). In contrast to memory for ordinary events, dissociated trauma memory supposedly remains frozen and relatively impervious to distortion during the passage of time. These allegedly dissociated implicit memories of trauma are nevertheless manifested “in the form of body memories [conditioned emotional responses?], ﬂashbacks, fragments, sudden intense feelings, avoidant behaviors, images, sensory processes, and dreams” (p. 187). There are several problems with this formulation (McNally, 2003c, chapter 6). In the absence of explicit memory, one cannot reason backward and infer a repressed or dissociated memory from dreams, sudden feelings, and so forth. These alleged implicit markers of buried memories can arise from many causes. Moreover, implicit memories are just as subject to change and distortion as explicit ones are (Lustig & Hasher, 2001). Finally, the notion that people can undergo trauma yet retain only implicit traces (e.g., conditioned emotional responses) contradicts recent critiques of the literature on conditioning without awareness (Lovibond & Shanks, 2001; Shanks & Lovibond, 2001). The

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clinical implications are clear: if people are suﬃciently traumatized to acquire conditioned emotional responses and other implicit memories of the experience, they will retain explicit memories as well.

Dispelling Semantic Confusion The debate about repressed and recovered memories has been partly fueled by confusion concerning the meaning of basic concepts such as remembering and forgetting. At times, the debate has been inﬂamed by proponents on each side who use the same words for diﬀerent issues. Consider the verb forget. In accordance with everyday parlance, many of our research subjects say, “I was abused as a child, but then I forgot about it.” Further questioning clariﬁes what they mean. Many say they deliberately tried to push these experiences out of their minds after they occurred. Engaged by other matters, they often succeeded in their attempts not to think about their abuse, sometimes for long periods. Prior to their enrolling in our research program, they encountered cues that reminded them of their “forgotten” abuse—abuse that had not entered their mind for some time. Other subjects say, “I never forgot that I was abused as a child.” Obviously, memories of their abuse were often absent from awareness for hours, days, or perhaps even weeks at a time, only to pop into mind either spontaneously or when triggered by some reminder. Some traumatic amnesia theorists seem to believe that memories of sexual abuse ought to come to mind with reasonable frequency, and if someone does not think about the abuse for months or years at a time, some mechanism must be actively inhibiting its retrieval during these periods of “forgetting.” Because these theorists assume that sexual abuse memories are highly emotionally charged, they assume that a failure of these memories to enter the mind during long periods must be attributable to an active force keeping them out of awareness. The problem with this assumption is that the evidence for this postulated mechanism—repression or dissociation—is inferred from the very phenomena it is designed to explain. In these cases, there is no independent evidence of inhibitory mechanisms other than the mere absence of certain memories from awareness for periods of time. To be sure, cognitive psychologists have devised ingenious methods for conﬁrming active inhibitory processes in memory, at least for neutral words (e.g., Anderson & Green, 2001). But to defend a claim of active inhibition, one should show that people are unable to recall their abuse in the presence of adequate retrieval cues, such as the question: “Were you ever sexually abused as child?” An inability to recall abuse when it should be readily accessible provides a stronger basis for inferring inhibition than does the mere failure to think about it for periods of time (everyday forgetting), which does not require postulation of any inhibitory mechanism.

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Thus, merely because someone has not thought about something for a long time—has “forgotten” it—does not mean that the person has been unable to remember it. One need not postulate any special mechanisms to explain why someone tried not to think about something unpleasant and managed not to think about it for long stretches of time. Only an inability to remember when exposed to adequate retrieval cues can provide a reasonable basis for labeling the phenomenon as amnesia (assuming, of course, that the event was encoded in the ﬁrst place). Until such evidence is adduced, the most parsimonious explanation for not thinking about trauma for long periods of time—for forgetting it— must lie with the conventional memory and forgetting mechanisms of cognitive psychology, not repression or traumatic dissociation. Finally, some recovered memories may not correspond to genuine events. Some recovered memories are likely false. In our research, we have noted two strikingly diﬀerent types of recovered memory experience. In one type, subjects are suddenly reminded of events that they had not thought about in many years. They are surprised at their recollection but not at the content of the memory per se. For example, in one of our cases, the subject suddenly recalled her own abuse on learning that her daughter had just been molested. These individuals often remark, “My God! I can’t believe I forgot that.” In the other type, subjects realize that they are abuse survivors, sometimes gradually recalling new memories over a time. For example, one of our cases recovered memories of being involved in cult abuse and cannibalism. This kind of recollection diﬀers from those in which the person is surprised not by the content of the recollection but by not having thought about it for so long. The second type of experience, we suspect, may be more likely to involve false memory than the ﬁrst type.

Note Preparation of this chapter was supported in part by NIMH grant MH61268 awarded to the first author.

References American Psychiatric Association. (1987). Diagnostic and statistical manual of mental disorders. 3rd ed., rev. Washington, DC: APA. Anderson, M. C., & Green, C. (2001). Suppressing unwanted memories by executive control. Nature, 410, 366–369. Anderson, M. C., & Neely, J. H. (1996). Interference and inhibition in memory retrieval. In E. L. Bjork & R. A. Bjork (Eds.), Memory (pp. 237–313). San Diego, CA: Academic Press. Archibald, H. C., & Tuddenham, R. D. (1965). Persistent stress reaction after combat: A 20-year follow-up. Archives of General Psychiatry, 12, 475–481. Arrigo, J. M., & Pezdek, K. (1997). Lessons from the study of psychogenic amnesia. Current Directions in Psychological Science, 6, 148–152.

 

149

Bass, E., & Davis, L. (1988). The courage to heal: A guide for women survivors of child sexual abuse. New York: Harper and Row. Beck, A. T., & Steer, R. A. (1987). Beck Depression Inventory manual. San Antonio, TX: The Psychological Corporation. Bernstein, E. M., & Putnam, F. W. (1986). Development, reliability, and validity of a dissociation scale. Journal of Nervous and Mental Disease, 174, 727–735. Blume, E. S. (1990). Secret survivors: Uncovering incest and its aftereﬀects in women. New York: Wiley. Briere, J., & Conte, J. (1993). Self-reported amnesia for abuse in adults molested as children. Journal of Traumatic Stress, 6, 21–31. Brown, D., Scheﬂin, A. W., & Hammond, D. C. (1998). Memory, trauma treatment, and the law. New York: Norton. Cassiday, K. L., McNally, R. J., & Zeitlin, S. B. (1992). Cognitive processing of trauma cues in rape victims with post-traumatic stress disorder. Cognitive Therapy and Research, 16, 282–295. Ceci, S. J., & Loftus, E. F. (1994). “Memory work”: A royal road to false memories? Applied Cognitive Psychology, 8, 351–364. Cheit, R. E. (1998). Consider this, skeptics of recovered memory. Ethics and Behavior, 8, 141–160. Cheit, R. E. (1999). Junk skepticism and recovered memory: A reply to Piper. Ethics and Behavior, 9, 295–318. Cheyne, J. A., Newby-Clark, I. R., & Rueﬀer, S. D. (1999). Relations among hypnagogic and hypnopompic experiences associated with sleep paralysis. Journal of Sleep Research, 8, 313–317. Cheyne, J. A., Rueﬀer, S. D., & Newby-Clark, I. R. (1999). Hypnagogic and hypnopompic hallucinations during sleep paralysis: Neurological and cultural construction of the night-mare. Consciousness and Cognition, 8, 319–337. Christianson, S.-Å. (1992). Emotional stress and eyewitness memory: A critical review. Psychological Bulletin, 112, 284–309. Clancy, S. A. (2000). Child Abuse Survivor Questionnaire. Unpublished questionnaire, Department of Psychology, Harvard University, Cambridge, MA. Clancy, S. A., McNally, R. J., & Schacter, D. L. (1999). Eﬀects of guided imagery on memory distortion in women reporting recovered memories of childhood sexual abuse. Journal of Traumatic Stress, 12, 559–569. Clancy, S. A., McNally, R. J., Schacter, D. L., Lenzenweger, M. F., & Pitman, R. K. (2002). Memory distortion in people reporting abduction by aliens. Journal of Abnormal Psychology, 111, 455–461. Clancy, S. A., Schacter, D. L., McNally, R. J., & Pitman, R. K. (2000). False recognition in women reporting recovered memories of sexual abuse. Psychological Science, 11, 26–31. Courtois, C. A. (1992). The memory retrieval process in incest survivor therapy. Journal of Child Sexual Abuse, 1, 15–31. Deese, J. (1959). On the prediction of occurrence of particular verbal intrusions in immediate recall. Journal of Experimental Psychology, 58, 17–22. Dollinger, S. J. (1985). Lightning-strike disaster among children. British Journal of Medical Psychology, 58, 375–383.

150

  

Dubner, A. E., & Motta, R. W. (1999). Sexually and physically abused foster care children and posttraumatic stress disorder. Journal of Consulting and Clinical Psychology, 67, 367–373. Easterbrook, J. A. (1959). The eﬀect of emotion on cue utilization and the organization of behavior. Psychological Review, 66, 183–201. Eder, M. D. (1917). War-shock. London: William Heinemann. Femina, D. D., Yeager, C. A., & Lewis, D. O. (1990). Child abuse: Adolescent records vs. adult recall. Child Abuse and Neglect, 14, 227–231. Foa, E. B., Feske, U., Murdock, T. B., Kozak, M. J., & McCarthy, P. R. (1991). Processing of threat-related information in rape victims. Journal of Abnormal Psychology, 100, 156–162. Freyd, J. J. (1996). Betrayal trauma: The logic of forgetting childhood abuse. Cambridge, MA: Harvard University Press. Garry, M., Manning, C. G., Loftus, E. F., & Sherman, S. J. (1996). Imagination inﬂation: Imagining a childhood event inﬂates conﬁdence that it occurred. Psychonomic Bulletin & Review, 3, 208–214. Golding, J. M. (in press). Understanding directed forgetting. In A. Wenzel & D. C. Rubin (Eds.), Cognitive methods in psychopathology research. Washington, DC: American Psychological Association Press. Goodman, G. S., Ghetti, S., Quas, J. A., Edelstein, R. S., Alexander, K. W., Redlich, A. D., et al. (2003). A prospective study of memory for child sexual abuse: New ﬁndings relevant to the repressed-memory controversy. Psychological Science, 14, 113–118. Heaps, C., & Nash, M. (1999). Individual diﬀerences in imagination inﬂation. Psychonomic Bulletin and Review, 6, 313–318. Henderson, J. L., & Moore, M. (1944). The psychoneuroses of war. New England Journal of Medicine, 230, 273–278. Herman, J. L. (1992). Trauma and recovery. New York: Basic Books. Johnson, H. M. (1994). Processes of successful intentional forgetting. Psychological Bulletin, 116, 274–292. Joseph, R. (1999). The neurology of traumatic “dissociative” amnesia: Commentary and literature review. Child Abuse & Neglect, 23, 715–727. Keane, T. M., Caddell, J. M., & Taylor, K. L. (1988). Mississippi Scale for CombatRelated Posttraumatic Stress Disorder: Three studies in reliability and validity. Journal of Consulting and Clinical Psychology, 56, 85–90. Keane, T. M., Kolb, L. C., Kaloupek, D. G., Orr, S. P., Blanchard, E. B., Thomas, R. G., et al. (1998). Utility of psychophysiological measurement in the diagnosis of posttraumatic stress disorder: Results from a Department of Veterans Aﬀairs Cooperative Study. Journal of Consulting and Clinical Psychology, 66, 914–923. Kirschbaum, C., Wolf, O. T., May, M., Wippich, W., & Hellhammer, D. H. (1996). Stress- and treatment-induced elevations of cortisol levels associated with impaired declarative memory in healthy adults. Life Sciences, 58, 1475–1483. Kotagal, S., Rawlings, C. A., Chen, S.-C., Burris, G., & Nouri, S. (1982). Neurologic, psychiatric, and cardiovascular complications in children struck by lightning. Pediatrics, 70, 190–192.

 

151

Langer, L. L. (1991). Holocaust testimonies: The ruins of memory. New Haven, CT: Yale University Press. Lindsay, D. S., & Read, J. D. (1994). Psychotherapy and memories of childhood sexual

abuse: A cognitive perspective. Applied Cognitive Psychology, 8, 281–338.

Loftus, E., & Ketcham, K. (1994). The myth of repressed memory. New York: St. Martin’s.

Lovibond, P. F., & Shanks, D. R. (2002). The role of awareness in Pavlovian conditioning: Empirical evidence and theoretical implications. Journal of Experimental Psychology: Animal Behavior Processes, 28, 3–26. Lupien, S. J., & McEwen, B. S. (1997). The acute eﬀects of corticosteroids on cognition: Integration of animal and human model studies. Brain Research Reviews, 24, 1–27. Lustig, C., & Hasher, L. (2001). Implicit memory is not immune to interference. Psychological Bulletin, 127, 618–628. McGaugh, J. L., Ferry, B., Vazdarjanova, A., & Roozendaal, B. (2000). Amygdala: Role in modulation of memory storage. In J. P. Aggleton (Ed.), The amygdala: A functional analysis (2nd ed., pp. 391–423). Oxford: Oxford University Press. McNally, R. J. (1995). Automaticity and the anxiety disorders. Behaviour Research and Therapy, 33, 747–754. McNally, R. J. (1998). Experimental approaches to cognitive abnormality in posttraumatic stress disorder. Clinical Psychology Review, 18, 971–982. McNally, R. J. (2001). The cognitive psychology of repressed and recovered memories of childhood sexual abuse: Clinical implications. Psychiatric Annals, 31, 509–514. McNally, R. J. (2003a). Progress and controversy in the study of posttraumatic stress disorder. Annual Review of Psychology, 54, 229–252. McNally, R. J. (2003b). Recovering memories of trauma: A view from the laboratory. Current Directions in Psychological Science, 12, 32–35. McNally, R. J. (2003c). Remembering trauma. Cambridge, MA: Belknap Press/ Harvard University Press. McNally, R. J., Clancy, S. A., & Schacter, D. L. (2001). Directed forgetting of trauma cues in adults reporting repressed or recovered memories of childhood sexual abuse. Journal of Abnormal Psychology, 110, 151–156. McNally, R. J., Clancy, S. A., Schacter, D. L., & Pitman, R. K. (2000a). Cognitive processing of trauma cues in adults reporting repressed, recovered, or continuous memories of childhood sexual abuse. Journal of Abnormal Psychology, 109, 355–359. McNally, R. J., Clancy, S. A., Schacter, D. L., & Pitman, R. K. (2000b). Personality proﬁles, dissociation, and absorption in women reporting repressed, recovered, or continuous memories of childhood sexual abuse. Journal of Consulting and Clinical Psychology, 68, 1033–1037. McNally, R. J., Kaspi, S. P., Riemann, B. C., & Zeitlin, S. B. (1990). Selective processing of threat cues in posttraumatic stress disorder. Journal of Abnormal Psychology, 99, 398–402. McNally, R. J., Lasko, N. B., Clancy, S. A., Macklin, M. L., Pitman, R. K., & Orr, S. P. (2002). Psychophysiologic responding during script-driven imagery in people reporting abduction by space aliens. Manuscript submitted for publication. McNally, R. J., Metzger, L. J., Lasko, N. B., Clancy, S. A., & Pitman, R. K. (1998).

152

  

Directed forgetting of trauma cues in adult survivors of childhood sexual abuse with and without posttraumatic stress disorder. Journal of Abnormal Psychology, 107, 596–601. Orr, S. P., Lasko, N. B., Metzger, L. J., Berry, N. J., Ahern, C. E., & Pitman, R. K. (1998). Psychophysiologic assessment of women with posttraumatic stress disorder resulting from childhood sexual abuse. Journal of Consulting and Clinical Psychology, 66, 906–13. Orr, S. P., & Roth, W. T. (2000). Psychophysiological assessment: Clinical applications for PTSD. Journal of Aﬀective Disorders, 61, 225–240. Poole, D. A., Lindsay, D. S., Memon, A., & Bull, R. (1995). Psychotherapy and the recovery of memories of childhood sexual abuse: U.S. and British practitioners’ opinions, practices, and experiences. Journal of Consulting and Clinical Psychology, 63, 426–437. Pope, H. G., Jr., Oliva, P. S., & Hudson, J. I. (1999). Repressed memories: The scientiﬁc status. In D. L. Faigman, D. H. Kaye, M. J. Saks, & J. Sanders (Eds.), Modern scientiﬁc evidence: The law and science of expert testimony (Vol. 1), Pocket part (pp. 115–155). St. Paul, MN: West. Read, J. D. (1997). Memory issues in the diagnosis of unreported trauma. In J. D. Read & D. S. Lindsay (Eds.), Recollections of trauma: Scientiﬁc evidence and clinical practice (pp. 79–108). New York: Plenum. Robinson, K. J., & Roediger, H. L., III. (1997). Associative processes in false recall and false recognition. Psychological Science, 8, 231–237. Roediger, H. L., III, & McDermott, K. B. (1995). Creating false memories: Remembering words not presented in lists. Journal of Experimental Psychology: Learning, Memory, and Cognition, 21, 803–814. Sargant, W., & Slater, E. (1941). Amnesic syndromes in war. Proceedings of the Royal Society of Medicine, 34, 757–764. Schooler, J. W., Bendiksen, M., & Ambadar, Z. (1997). Taking the middle line: Can we accommodate both fabricated and recovered memories of sexual abuse? In M. A. Conway (Ed.), Recovered memories and false memories (pp. 251–292). Oxford: Oxford University Press. Shanks, D. R., & Lovibond, P. F. (2002). Autonomic and eyeblink conditioning are closely related to contingency awareness: Reply to Wiens and Öhman (2002) and Manns et al. (2002). Journal of ExperimentalPsychology: Animal Behavior Processes, 28, 38–42. Shin, L. M., McNally, R. J., Kosslyn, S. M., Thompson, W. L., Rauch, S. L., Alpert, N. M., et al. (1999). Regional cerebral blood ﬂow during script-driven imagery in childhood sexual abuse-related PTSD: A PET investigation. American Journal of Psychiatry, 156, 575–584. Swihart, G., Yuille, J., & Porter, S. (1999). The role of state-dependent memory in “red-outs.” International Journal of Law and Psychiatry, 22, 199–212. Tellegen, A. (1982). Brief manual for the Diﬀerential Personality Questionnaire. Minneapolis: Department of Psychology, University of Minnesota. Tellegen, A., & Atkinson, G. (1974). Openness to absorbing and self-altering experiences (“absorption”), a trait related to hypnotic susceptibility. Journal of Abnormal Psychology, 83, 268–277.

 

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Terr, L. C. (1991). Childhood traumas: An outline and overview. American Journal of Psychiatry, 148, 10–20. Torrie, A. (1944, January 29). Psychosomatic casualties in the Middle East. Lancet, 246, 139–143. van der Kolk, B. A. (1994). The body keeps the score: Memory and the evolving psychobiology of posttraumatic stress. Harvard Review of Psychiatry, 1, 253–265. van der Kolk, B. A., & Fisler, R. (1995). Dissociation and the fragmentary nature of traumatic memories: Overview and exploratory study. Journal of Traumatic Stress, 8, 505–525. Vreven, D. L., Gudanowski, D. M., King, L. A., & King, D. W. (1995). The civilian version of the Mississippi PTSD Scale: A psychometric evaluation. Journal of Traumatic Stress, 8, 91–109. Wagenaar, W. A., & Groeneweg, J. (1990). The memory of concentration camp survivors. Applied Cognitive Psychology, 4, 77–87. Wilkinson, C. B. (1983). Aftermath of a disaster: The collapse of the Hyatt Regency Hotel skywalks. American Journal of Psychiatry, 140, 1134–1139. Williams, J. M. G., Mathews, A., & MacLeod, C. (1996). The emotional Stroop task and psychopathology. Psychological Bulletin, 120, 3–24. Williams, L. M. (1994). Recall of childhood trauma: A prospective study of women’s memories of child sexual abuse. Journal of Consulting and Clinical Psychology, 62, 1167–1176. Winograd, E., Peluso, J. P., & Glover, T. A. (1998). Individual diﬀerences in susceptibility to memory illusions. Applied Cognitive Psychology, 12, S5–S27. Yerkes, R. M., & Dodson, J. D. (1908). The relation of strength of stimulus to rapidity of habit-formation. Journal of Comparative Neurology and Psychology, 18, 459–482.

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E

xperimental support for the idea that anxious individuals may display anomalous performance on cognitive tasks extends back many decades (Calvin, Koons, Bingham, & Fink, 1953). Early research focused primarily on investigating the patterns of cognitive impairment associated with anxiety. Now convincing evidence shows that anxious participants indeed demonstrate performance decrements across measures of cognitive functioning, especially diﬃcult and demanding memory tests (cf. Eysenck, 1982). However, contemporary accounts of such performance deﬁcits attribute them, in part, to anxious individuals’ tendency to process task-irrelevant information associated with their worries. Recently, many researchers have directly examined whether the emotional valence of stimulus materials can moderate anxiety-linked patterns of performance on cognitive tasks. One hypothesis suggests that anxious individuals may display memory biases that selectively favor the retrieval of emotionally threatening information. Following a brief review of research showing that anxiety can be associated with memory deﬁcits, we provide an overview of the extensive experimental work testing whether anxious participants preferentially retrieve threat-related memories. Support for this position is by no means compelling, though favorable evidence has been more apparent in certain populations of anxious individuals and for certain types of memory tasks.

Memory Deﬁcits in Anxiety Like other dysphoric states such as depression, anxiety is associated with cognitive performance deﬁcits, including those involving memory (Eysenck, 1982; Humphreys & Revelle, 1984; Mueller, 1992). In a highly inﬂuential account, 155

Eysenck and Calvo (1992) proposed that anxiety aﬀects information processing in two quite diﬀerent ways. First, by eliciting task-irrelevant cognitive activity such as worry, anxiety consumes processing resources within working memory (Baddeley, 1986). At the same time, however, their concern to avoid poor performance motivates anxious individuals to invest greater eﬀort in task performance to compensate for their capacity limitations. If the task is not too demanding, this additional eﬀort may lead anxious individuals to perform as well as, or even better than, nonanxious individuals. In contrast, if a task places high demands on temporary storage capacity, performance of anxious participants likely suﬀers. In general, research ﬁndings have supported predictions derived from Eysenck and Calvo’s (1992) account. For example, Darke (1988b) demonstrated that highly anxious participants display a lower digit span than do less anxious individuals and show poorer ability to intentionally recall words presented at the end of sentences. In another study, Darke (1988a) observed that, though highly anxious readers demonstrate a normal ability to draw the elementary inferences necessary to comprehend text, their performance is impaired on inference tasks that plausibly demand greater processing resources. Consistent with the hypothesis that anxiety is associated with restricted cognitive capacity, MacLeod and Donellan (1993) found that increases in mental load disproportionately impaired reasoning task performance in highly anxious individuals. One important but unresolved issue concerns whether performance deﬁcits in anxious individuals result from mood state at the time of testing or represent an enduring characteristic of individuals with high trait vulnerability to anxiety. Eysenck and Calvo’s (1992) hypothesis causally implicates anxious mood state in such cognitive impairment. Under many circumstances, the high correlation between trait and state anxiety can make dissociating their respective roles diﬃcult. However, state anxiety elevated by quite speciﬁc worries still causes impaired cognitive performance. For example, anxiety about mathematics is associated with temporary impairment of the ability to hold numbers in memory and with lesser ability to avoid distracting thoughts when one performs calculations (Ashcroft & Kirk, 2001). Although little direct evidence is available concerning longer-term memory consequences, Ashcroft and Kirk suggest that these temporary problems likely contribute to impaired long-term knowledge about mathematical operations. Such performance deﬁcits clearly need to be a part of discussion on memory in anxiety disorders. However, the bulk of research and theory to be reviewed here has focused on whether anxiety is associated with the relative enhancement of memory for threatening material. There are several reasons why this pattern of memory selectivity might be expected. One is that most people tend to remember the gist of emotional events, such as the content of threatening pictures, better over time (cf. chapter 1 here). Furthermore, people remember emotional events better than matched unemotional events perhaps because of individual

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diﬀerences in emotional arousal (see Andrews, cited in Reisberg & Heuer, 1992). Various explanations for this eﬀect have been proposed (Christianson, 1992; Wessel, van der Kooy, & Merckelbach, 2000). Selective attention to the emotional focus of a scene may lead to better encoding of information in that location, rather than in other less well–attended locations. Also, people may elaborate disproportionately on the meaning of emotional scenes, leading to more extensive memorial representations and consequently to improved retrieval. Additionally, emotional arousal at the time of processing the scene may directly enhance the durability of the memory trace (Revelle & Loftus, 1990; Cahill & McGaugh, 1995). Though these are not mutually exclusive possibilities, particularly strong evidence supports the ﬁrst suggestion, that the elevation of anxiety may be associated with an attentional focus on threat during encoding. People with heightened levels of anxiety are more likely than nonanxious individuals to let threatening words or pictures hold their attention (Fox, Russo, Bowles, & Dutton, 2001; Mathews & MacLeod, 1994; Yiend & Mathews, 2001). Even if anxiety exerts no direct eﬀect on the retrieval process itself, greater attention to threatening aspects of stimuli during encoding likely enhances later memory for such information. However, whether more attention to a threatening stimulus event results in better or worse memory for that event also may depend on the type of encoding, as well as the task used to assess memory. If attention to threat during encoding is accompanied by subsequent processing of the distinctive meaning of this emotional information, then its later recall is likely enhanced. On the other hand, if attention to threat during encoding results, for example, principally in registration only of the aversive quality of the feelings evoked, then there may be fewer distinctive features within the memory representation to help in its later recall. A memory test requiring retrieval of certain aspects of an event could thus reveal either good or poor recall, despite the greater allocation of attention resources to this event at the time of presentation, depending on how the event has been encoded. Therefore, an encoding bias for threatening information may result in preferential memory for such material, even when the retrieval process itself is not biased to favor this type of information. Conversely, if there is a memory advantage for threatening information or not, such information nevertheless may have recruited disproportionate attentional resources during encoding. The evidence we review here suggests that increased selective attention to threatening stimuli, demonstrated so reliably by highly anxious individuals, is not consistently associated with better subsequent memory for this information. In contrast to research on depressed participants, who demonstrate recall advantages for negative information that are easy to replicate, the bulk of research on memory bias in anxious individuals has proven surprisingly negative. Anxious individuals commonly display no greater tendency to recall emotionally threatening material than less anxious individuals exposed to the same material do. Exceptions to this general rule will be highlighted during our review and

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will be discussed at the end of this chapter. To anticipate, despite variable results across studies, greater evidence of a recall bias favoring threatening information has been obtained in studies examining panic disorder patients than in studies of other anxiety disorders or of nonclinical individuals with elevated levels of trait or state anxiety. Also, measures of implicit memory, especially those involving perceptually driven processes, may detect an anxiety-linked memory advantage for threatening information more often than measures of explicit memory, such as recall and recognition. In drawing conclusions, we distinguish between eﬀects that could arise solely from selective encoding and those attributable to biases aﬀecting subsequent access to, or retrieval of, emotionally valenced information. We suggest that an anxiety-linked recall advantage for threatening material is more likely when participants are free to initially encode emotional material without restrictions. Under such free encoding conditions, highly anxious groups are disproportionately likely to encode personally relevant meanings of threatening stimulus items, and this facilitates memory performance for such information, even without anxiety-linked bias in the retrieval process itself. The review that follows is organized into sections that separately describe research investigating the association between anxiety and tests of autobiographical memory, recall, recognition, and implicit memory. Within these main sections, we review studies carried out on nonclinical populations selected according to their scores on anxiety questionnaires, as well as studies that have assessed patients suﬀering from anxiety disorders, including generalized anxiety disorder (GAD), phobias, obsessive compulsive disorder (OCD), posttraumatic stress disorder, and panic disorder.

Memory for Emotional Information

in Anxiety Disorders

Recall of Autobiographical Memories A number of researchers have sought to establish whether autobiographical memory functioning is biased within anxious individuals. For example, Richards and Whittaker (1990) asked high and low trait-anxious individuals to recall a speciﬁc personal memory evoked by either happy cue words (e.g., pleased, lucky) or anxiety-related cue words (e.g., anger, pain). High trait-anxious participants, unlike low trait anxious individuals, were signiﬁcantly faster in retrieving autobiographical memories elicited by the anxiety-related cue words, suggesting that anxiety-related memories may be disproportionately accessible for such participants. However, because Richards and Whittaker did not examine the emotional content of the memories produced, their data instead could reﬂect high trait-anxious participants producing more memories with objectively neutral

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content in response to the anxiety-related cues. That is, high trait-anxious individuals may simply have associated more of their memories with the anxietyrelated cues, regardless of the emotional tone of the memories themselves. Subsequent studies by Burke and Mathews (1992), carried out on generalized anxiety disorder (GAD) patients and nonanxious control participants, employed independent raters to assess the emotional tone of memory content. GAD patients and controls were presented with emotionally neutral cue words and were instructed to recall the ﬁrst personal memory brought to mind by each item. Independent blind ratings revealed a nonsigniﬁcant trend for the GAD patients to report memories that were more threatening than those reported by controls. In a second study, GAD patients, unlike controls, produced signiﬁcantly more memories when directly instructed to recall anxious autobiographical memories to neutral cues. However, judges classiﬁed only 80% of these memories to be truly “anxious” in GAD patients, in comparison to 92% in the case of control participants. Thus, GAD patients may indeed use more liberal criteria when deﬁning recollected events as anxiety–relevant. More important, it has proven diﬃcult to replicate the early ﬁnding that anxiety is associated with biased autobiographical memory performance. Levy and Mineka (1998) obtained independent ratings of the emotional tone of memories elicited in response to neutral, positive, and threatening cue words in high and low trait-anxious participants. There were no group diﬀerences in the relative number of memories produced in response to each type of cue, in the emotional tone of these memories, or in the pattern of recall latencies across these three cue conditions. Rapee, McCallum, Melville, Ravenscroft, and Rodney (1994) presented social phobics and nonanxious participants with social-threat and neutral cue words and instructed them to retrieve associated memories of events either they or a close friend or relative experienced. Across all conditions, there was no evidence that the social phobics diﬀered from the nonanxious participants in their tendency to recall negative events. Wenzel, Jackson, and Holt (2002) also presented social phobics and nonanxious controls with social–threat and neutral cue words, instructing them to report the ﬁrst speciﬁc personal memory evoked by each cue. The social phobics showed no enhanced ability to recall memories in response to the threatening retrieval cues. Using a similar autobiographical memory task, with both happy and anxious cue words, Wilhelm, McNally, Baer, and Florin (1997) found an equivalent pattern of retrieval latencies across obsessive-compulsive disorder patients and control participants. Even in posttraumatic stress disorder, where patients might be expected to show better recall of trauma-related events, the experimental evidence provides little support for such an autobiographical memory bias. McNally, Litz, Prassas, Shin, and Weathers (1994) presented Vietnam combat veterans, some who suﬀered from PTSD, with negative, positive, and neutral words as retrieval cues, again instructing them to recollect personal memories elicited by each cue word. All participants were faster to retrieve memories in response to

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the negative cues than in response to the neutral or positive cues, but this eﬀect did not diﬀer across groups with or without PTSD. [For evidence concerning the forgetting of traumatic memories, see chapter 4—Eds.] Overall, the balance of evidence provides little support for the idea that anxiety disorders are associated with the facilitated recall of negative autobiographical material. In many ways, this ﬁnding is rather surprising, given the strong possibility that individuals who develop anxiety pathology may actually have experienced a disproportionate number of threatening events (Finlay-Jones & Brown, 1981). Indeed, the fact that one cannot assume equivalence of negative event frequency across anxious and control populations compromises interpretation of those few early studies that claimed to demonstrate evidence of an autobiographical memory bias. To overcome this methodological problem, many researchers have turned away from autobiographical memory tasks and instead have tested for memory bias following the presentation of to-be-recalled stimuli under controlled conditions. We now turn to these studies.

Recall of Experimentally

Presented Stimuli

The emotional stimuli presented in such controlled experiments usually have been single emotional words. Participants have either read these words or used them in an imagery or judgment task, before an unexpected recall test for the items. Following both reading and imagery tasks, Richards and French (1991) assessed recall of emotionally threatening stimulus words (e.g., trapped, humiliated) and neutral words in high and low trait-anxious participants. Regardless of whether these words had simply been read or had been employed to evoke imagined scenes, no diﬀerences in relative recall separated high and low traitanxious participants. Using a rather diﬀerent encoding task, Nugent and Mineka (1994) directed high and low trait-anxious participants to rate how much they liked or disliked presented threatening and nonthreatening words, then unexpectedly tested ability to recall these words. Although there was some evidence from an initial study to suggest relatively better recall of threat words in high trait-anxious participants, this eﬀect failed to emerge in a second experiment, leading these researchers to conclude that trait anxiety is not reliably associated with a recall advantage for threatening information. In contrast, three articles have reported ﬁnding that the recall of negative words is enhanced for high trait-anxious participants (Eysenck & Byrne, 1994; Reidy & Richards, 1997; Russo, Fox, Bellinger, & Nguyen-Van-Tam, 2001). Under certain combinations of encoding and recall tasks, Eysenck and Byrne observed relatively facilitated recall of negative stimulus words in their high traitanxious participants, though correlational analysis failed to disentangle the potential mediating roles of anxiety and depression, both elevated within this sample. Similarly, following a self-descriptive or other-descriptive encoding task,

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Reidy and Richards found that recall of self-encoded negative words was disproportionately good for high trait-anxious participants. However, this eﬀect proved to be correlated with depression rather than with anxiety level. Russo et al. (2001) observed no diﬀerences in the patterns of recall shown by high and low trait-anxious individuals following a semantic encoding task that required participants to rate the pleasantness of emotionally toned stimulus words. They suggest that this ﬁnding could reﬂect a ceiling eﬀect, given that the high level of overall recall left little scope for stimulus emotionality to inﬂuence memory performance. Consistent with this account, Russo et al. found greater evidence of an anxiety-linked recall bias following an alternative encoding task that required participants to make structural judgments about the stimulus words (i.e., counting the number of syllables). Although recall was poorer following this structural encoding task than in the semantic encoding task, threat words now were recalled disproportionately by the high trait participants. However, as the authors themselves acknowledge, this eﬀect might be attributed to diﬀerential encoding and so does not require the conclusion that anxiety is associated with a biased retrieval process. The structural encoding task instructed participants to attend to the syllabic format of each word while ignoring its semantic content. Previous research convincingly demonstrates that high traitanxious individuals display an impaired ability to direct attention away from the semantic content of threatening stimuli, even when explicitly instructed to do so (e.g., Williams, Mathews, & MacLeod, 1996; Wood, Mathews, & Dalgleish, 2001). Certainly, despite instructions to process syllabic structure, Russo et al.’s (2001) simple task permitted ample time for the processing of semantic content, as each word was exposed for 4 seconds. Under these circumstances, one would predict on the basis of established research ﬁndings that high trait-anxious participants would attend disproportionately to threat word content. Thus, although the net result was one of better memory for threat words in anxious participants, compared to nonanxious individuals, it seems more parsimonious to regard this result as further evidence of selective encoding, rather than of an anxiety-linked bias in the memory retrieval process. Those investigators who have examined memory for emotional stimulus words in clinical populations have not obtained consistent evidence of a recall advantage for threatening material in patients suﬀering from anxiety disorders. In an early study, Mogg, Mathews, and Weinman (1987) required patients with GAD, and nonanxious control participants, to judge whether positive and negative words were either self-descriptive or other-descriptive. In a subsequent unexpected memory test, there was no group diﬀerence in relative ability to recall these two classes of stimulus words. Indeed, a subsidiary analysis carried out on the subset of negative words judged to be most threatening revealed that they actually were recalled disproportionately poorly by the anxiety patients. In a virtually identical experiment, reported by Mogg and Mathews (1990), GAD patients did display a nonsigniﬁcant trend toward relatively better

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recall of negative words, compared to nonanxious control participants, across both encoding conditions. However, Mogg and Mathews noted that their GAD patients also generated a disproportionate number of negative words as intrusion errors while performing the recall task, suggesting that the observed eﬀects may result from a negative response bias, rather than from any enhanced ability to retrieve the negative material from memory. Becker, Roth, Andrich, and Margraf (1999) had GAD participants and nonanxious controls rate the ease with which they could imagine scenes evoked by emotionally valenced words, some closely related to the usual concerns of GAD patients, before giving them an unexpected recall test for these words. No group diﬀerences in pattern of recall performance were observed, leading Becker et al. to conclude that GAD is not associated with any memory advantage for threatening words, even when they are relevant to disorder-related concerns. In a study of cued recall in GAD patients and nonanxious controls, Mathews, Mogg, May, and Eysenck (1989) used a similar encoding method but then provided three-letter word stems that participants were directed to complete to yield one of the previously exposed words. There were no diﬀerences between groups in the observed pattern of cued recall accuracy. Otto, McNally, Pollack, Chen, and Rosenbaum (1994) replicated this null result. As noted, Russo et al. (2001) suggested that the failure to ﬁnd an anxietylinked memory bias in certain studies may reﬂect ceiling eﬀects, which render the task insensitive to group diﬀerences in the ability to recall valenced stimuli. However, in a study comparing patients suﬀering from GAD and those with clinical depression, Bradley, Mogg, and Williams (1995) also failed to obtain evidence of any anxiety-linked recall bias, while nevertheless conﬁrming their task’s sensitivity to individual diﬀerences in the selective recall of emotional materials. Participants ﬁrst rated depression-relevant words (e.g., discouraged, despair), anxiety-relevant words (e.g., embarrassed, assaulted), positive words (e.g., paradise, bliss), and neutral words (e.g., bench, cereal) for their relevance to personal concerns. In an unexpected subsequent memory test, the depressed patients showed evidence of a recall bias favoring depression-related words. However, once again there was no diﬀerence between the recall proﬁles of GAD patients and nonanxious controls. In contrast, Friedman, Thayer, and Borkovec (2000) did observe better recall of threat words in GAD patients than controls when they used a less directive approach to initial stimulus processing. Speciﬁcally, threat and neutral words were presented for 8 seconds each, during which time the participant was required simply to read each item aloud. When memory for these words then was tested, GAD patients recalled more threat than nonthreat words and more threat words than did control participants. The initial word processing task used by Friedman et al. was similar, in potentially important ways, to that employed by Russo et al. This task permitted, but did not require, the processing of semantic content, and the exposure time was long. These conditions likely allowed participants ample time and freedom to encode the words in quite

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diﬀerent ways, so an anxiety-linked tendency to selectively encode the aversive semantic content of the threat words may underlie the enhanced recall of such materials shown by the anxious patients. Studies that have investigated the memorial characteristics of social anxiety have failed to yield evidence that it is associated with any recall advantage for threatening information. Sanz (1996) found no diﬀerences between socially anxious students and nonanxious controls in their recall of neutral, positive, and negative trait words previously encountered in a self-descriptiveness rating task, even when these words were closely related to social anxiety. When comparing memory for words appraised earlier by participants for emotional tone, Rapee et al. (1994) likewise found no diﬀerence between clinical social phobics and nonanxious controls in the relative recall of neutral words, positive words, and negative words related either to general threat or speciﬁcally to social threat. In a second study, Rapee et al. modiﬁed their encoding task, now requiring socially phobic patients and control participants to imagine a scene involving themselves and the referent of each stimulus word and then to rate this scene for pleasantness. Afterward, Rapee et al. tested cued recall, rather than free recall, by instructing participants to complete three-letter word stems to produce previously encountered words. Once again, however, no group diﬀerence in the relative recall of neutral, positive, and negative words emerged. Finally, in a third experiment designed to increase ecological validity, Rapee et al. provided positive and negative feedback concerning participant performance on an initial task (e.g., your material was poorly organized) and then unexpectedly tested recall of this emotional feedback. Compared to nonanxious control participants, social phobic patients displayed no facilitated recall of the negative information. Indeed, these patients actually recalled a disproportionately small number of the negative feedback statements. Cloitre, Cancienne, Heimberg, Holt, and Liebowitz (1995) and Lundh and Ost (1997) also examined the ability of socially phobic patients to recall emotional stimuli, using free and cued recall procedures, respectively, and found no evidence of any anxiety-linked memory bias. Becker et al.’s (1999) study, cited earlier, included a group of social phobic as well as GAD patients. These social phobic patients, like the GAD patients, did not diﬀer from nonanxious control participants in terms of their relative ability to recall threat words associated with social concerns, general threat words, neutral words, and positive words. Amir, Coles, Brigidi, and Foa (2001) investigated whether practicing the recall of neutral, positive, or social threat words would reveal diﬀerences between socially phobic and nonanxious participants. Words initially were exposed together with a preceding category label, such as Fruit—Mango or Job—Stress. Subsequently, half of the participants were given cued retrieval practice, which involved presenting the category labels together with the initial fragment of the associated test word (e.g., Fruit—Ma- -), which had to be completed to produce the original item. Finally, all participants were given a cued recall test, within which they were shown parent category words and told to recall the words paired with them.

     

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Without retrieval practice, the groups did not diﬀer in their relative ability to recall the emotional categories of stimulus words. Retrieval practice did not elicit any relative recall advantage for negative words in the socially phobic patients. Indeed, the socially phobic patients gained less than controls from retrieval practice with socially threatening words. Collectively, therefore, these experimental studies provide no empirical support for the proposal that the recall of emotional information is enhanced in social phobia. Fewer experimental studies have investigated whether patients suﬀering from OCD or PTSD demonstrate preferential recall of threatening information. One problem that arises quite commonly in these studies is that supposedly emotional material may be neutral for control participants. For example, Radomsky and Rachman (1999) found better recall of “contaminated” than “clean” objects in OCD patients, relative to nonanxious control participants. However, contamination was manipulated by varying whether objects were touched by the experimenter, a distinction unlikely to aﬀect the control group emotionally. Within a directed forgetting paradigm, Wilhelm et al. (1996) exposed OCD patients and control participants to neutral words (e.g., spoon, curtain), positive words, (e.g., laugh, conﬁdent), and negative words often associated with obsessive concerns (e.g., danger, disease). In this experimental approach, after each word has been presented, a signal directs the participant to either remember or forget that item. Wilhelm et al. found that when participants were instructed to remember words, the two groups demonstrated equivalent subsequent recall across all three classes of stimuli. However, for those items they were directed to forget, the OCD patients subsequent recalled the negative words more often than the controls did. Using a similar paradigm, McNally, Metzger, Lakso, Clancy, and Pitman (1998), exposed survivors of childhood abuse, with or without PTSD, to neutral words, positive words, and negative words related to their traumatic experience (e.g., molested, abuse). Their results were similar to those obtained by Wilhelm et al. using OCD patients. Participants did not diﬀer in their patterns of recall for the words they had been instructed to remember, but for those they had been directed to forget, the PTSD patients recalled a disproportionate number of the negative items. Anxiety is associated with a reduced capacity to inhibit attention to threatening meanings during the encoding of stimulus words (Wood et al., 2001). Directing participants to forget a word, at the time of its initial exposure, means that they must try not to process the meaning of that stimulus, which is disproportionately diﬃcult for anxious individuals when this meaning is emotionally threatening. Thus, the relative diﬃculty PTSD and OCD patients appear to experience, when trying not to process threat words under such “forget” instructions, may reﬂect this well-established encoding eﬀect, rather than any anxiety-linked bias in the retrieval process itself. A related issue arises in a study by Vrana, Roodman, and Beckham (1995), who exposed Vietnam veterans with and without PTSD to neutral and threat-

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ening words (e.g., ﬁreﬁght, death), within an emotional Stroop task (Williams et al., 1996). Consistent with much previous research, PTSD participants were disproportionately slow to color-name the threatening words during their initial exposure, an eﬀect commonly attributed to anxious individuals’ diﬃculty in suppressing the processing of these words’ negative semantic content. Vrana et al. also found that the PTSD patients subsequently recalled a disproportionate number of the threatening words. However, because of the observed pattern of color-naming interference, these researchers quite reasonably ascribe this group diﬀerence to the PTSD patients’ tendency to selectively encode threat word meaning during the color-naming task, despite instructions to ignore word content. Thus, the few available studies of OCD or PTSD patients are either rendered problematic by the use of stimuli unlikely to be threatening for control participants or they invite explanation in terms of an anxiety-linked failure to inhibit the encoding of negative meanings, not in terms of an anxiety-linked bias in the retrieval of information from memory. In contrast, there is much more empirical support for the existence of a memory bias that favors the retrieval of threatening information in panic disorder patients. Of course, some of the relevant studies suﬀer from the methodological limitations already described, and null results sometimes have been obtained even in sound experimental designs. For example, in an early study of agoraphobia (now considered to be closely associated with panic disorder), Nunn, Stevenson, and Whalan (1984) assessed recall of words and short passages. Agoraphobic patients recalled more words and propositions from threatening passages than did nonanxious control participants. However, the threatening material described activities such as shopping and included words such as street, travel and cinema, which control participants probably would not consider emotionally negative. Furthermore, Pickles and van den Broek (1988) failed to replicate Nunn et al.’s original ﬁndings, despite employing a very similar experimental design. Otto et al. (1994) found no diﬀerences between the patterns of recall shown by panic disorder patients and nonanxious control participants for neutral, positive, general threat, and panic-related words that earlier had been rated for personal emotional signiﬁcance. Likewise, Rapee (1994) did not observe any diﬀerence in the patterns of recall shown by panic disorder patients and nonclinical controls for diﬀering classes of emotional words previously exposed within a free association task. However, these few negative reports are outweighed by a greater number of studies that have found that panic disorder patients demonstrate enhanced recall of threatening information. McNally, Foa, and Donnell (1989) required panic disorder patients and nonanxious control participants to rate anxietyrelated words (e.g., apprehensive, uptight) and other words unrelated to anxiety (e.g., charming, outgoing) for self-descriptiveness. In an unexpected subsequent memory test, control participants recalled fewer anxiety-related words than anxiety-unrelated words, whereas this pattern reversed in the panic disorder

     

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patients. Contrary to the ﬁndings of Mogg and Mathews (1990), the emotional valence of intrusion errors did not diﬀer between patients and controls, suggesting that these results reﬂect a genuine group diﬀerence in recall, rather than in response bias. Similar ﬁndings have been reported in studies that have employed diﬀerent encoding tasks. For example, Lundh, Czyzykow, and Ost (1997) required participants to imagine scenes evoked by each of their stimulus words and then tested memory using a cued recall test that required three-letter word stems to be completed to make previously exposed words. Control participants recalled similar numbers of threat and neutral words, whereas panic disorder patients recalled a disproportionate number of physically threatening words (but not socially threatening words), with the magnitude of this recall advantage for threat predicted by a measure of anxiety sensitivity. Using the same encoding task with panic disorder patients and control group participants, Becker, Rinck, and Margraf (1994) observed no group diﬀerence in the subsequent recall of positive and generally negative words (e.g., lonely, brutal) but found that panic disorder patients did recall more of the negative words speciﬁcally related to panic (e.g., fainting, madness). Once again, such words did not appear more commonly among the intrusion errors made by panic patients, mitigating against a response bias explanation of the eﬀect. In their subsequent research, Becker et al. (1999) included three types of panic-related words: somatic (e.g., palpitations, sweating), cognitive (e.g., helplessness, dying), and situational (e.g., tunnel, airplane). Panic disorder patients demonstrated enhanced recall of somatic and situational threat words but not of cognitive threat words, without showing increased representation of such items among their intrusion errors. Cloitre and Liebowitz (1991) employed two quite diﬀerent encoding tasks to expose panic disorder patients and nonclinical controls to neutral, positive, and threat words. One task required participants to decide whether each item described a feeling state, whereas the other task required them to decide only whether the item was a legitimate English word. The nonanxious group subsequently recalled a similar number of words from all three emotional categories, whereas the panic disorder patients recalled more threat words than either positive or neutral words, regardless of encoding task. Again, the patterns of intrusion errors were equivalent across groups, suggesting that the observed recall eﬀects could not be attributed to a group diﬀerence in response bias. Cloitre, Shear, Cancienne, and Zeitlin (1994) used another encoding task variant, in which panic disorder and control participants assessed the semantic association between members of word pairs, which could be neutral (e.g., gauge-metric), positive (e.g., smiles-elated), or panic-related (e.g., dizzy-faint). An unexpected cued recall test then was given, with participants shown the ﬁrst word of each pair followed by the ﬁrst three letters of the second word, which they were required to complete to yield the original item. Control participants displayed

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equivalent recall of the classes of emotional words, but panic disorder patients recalled a disproportionate number of the panic-related threat words. In summary, then, although recall studies have yielded little compelling experimental evidence to support a negative retrieval bias among individuals who report high levels of trait anxiety, or in patients suﬀering from most clinical anxiety disorders, they have provided ﬁrmer grounds for believing that such a retrieval bias may characterize panic disorder. The few studies that have demonstrated a recall advantage for threat stimuli among other anxious populations typically have tested memory following encoding tasks that have either instructed participants to ignore word content or permitted individuals considerable freedom to choose how they process stimulus content during encoding. When, instead, participants have been directed to process the semantic content of stimuli in a speciﬁed manner during encoding, typically no anxiety-linked bias in recall performance has been observed. This pattern of ﬁndings suggests that the occasionally observed superior recall of threatening words by such anxious participants likely results from their established tendency to selectively process threat stimulus content during encoding rather than from any bias in the retrieval process itself. The same is not true, however, for panic disorder patients, for whom encoding instructions appear to have little impact on observed patterns of selective recall. Across a wide range of studies, varying in both encoding and recall methodology, panic disorder patients repeatedly have displayed a recall bias favoring threatening stimuli, suggesting that the retrieval of such information may indeed be facilitated within this particular anxious population. We now will turn to the consideration of experiments that have employed measures of recognition, rather than recall, to test for selective memory bias in anxious participants. Such studies continue to provide little evidence that the retrieval of threatening information is generally enhanced across diﬀering populations of anxious participants.

Recognition Memory Recognition memory diﬀers from recall; for example, it does not need to engage the search component of memory retrieval that characterizes recall, which may make recognition measures less sensitive to emotional biases that exert their primary inﬂuence on this search process. However, recognition tasks have the advantage of permitting assessment of memory for types of stimuli that do not readily ﬁt within recall tasks, such as pictures of emotional faces. Furthermore, recognition data can be subjected to signal detection analysis, allowing a distinction between measures of memory sensitivity (d’) and response bias (B). Across two experiments, Nugent and Mineka (1994) assessed high and low trait-anxious participants’ recognition memory for threat and nonthreat words, which previously had been rated for likeability, and subjected their data to signal detection analysis. In one of these studies, high trait individuals were found

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to demonstrate a response bias favoring threat words. However, in neither of the experiments was any diﬀerence observed between the groups in their relative memory sensitivity for the two classes of stimulus words. Similarly, Dalgleish (1994) found no evidence from signal detection analysis to indicate that high and low trait-anxious participants diﬀered in relative ability to accurately recognize neutral, positive, or anxiety-related words that earlier had been encountered as solutions to an anagram task. A number of researchers have compared the ability of GAD patients and nonanxious controls to recognize threat and nonthreat words previously presented within an emotional Stroop task. Using signal detection analysis, both Mathews and MacLeod (1985) and Mogg, Mathews, and Weinman (1989) failed to ﬁnd any group diﬀerence in the sensitivity of recognition memory for these two word types. However, recognition performance was generally poor in these studies, probably because the encoding task invited little processing of word content. To counteract this limitation, MacLeod and McLaughlin (1995) modiﬁed the initial emotional Stroop task, by requiring participants to read each word aloud after it had been color-named. This did indeed improve recognition memory for the stimulus words, but still GAD patients and nonanxious controls did not diﬀer in relative recognition memory for the threat and nonthreat words. This failure to observe an anxiety-linked recognition memory advantage for threat words extends to other studies that have employed quite diﬀerent encoding tasks. Mogg et al. (1987) examined recognition memory for negative and positive trait adjectives that previously had been rated by participants for selfdescriptiveness or other-descriptiveness. Patients suﬀering from GAD showed no relative enhancement of recognition memory for threat words, compared to nonanxious control participants. Indeed, the anxiety patients tended to recognize fewer threat words, and more positive words, than the nonanxious participants did, although this group diﬀerence in recognition sensitivity was not statistically signiﬁcant. Rapee et al. (1994) included recognition measures to assess memory for words that participants previously had rated for likeability but observed no diﬀerences between social phobics and controls in ability to recognize threat and nonthreat words. Cloitre et al. (1995) also found equivalent patterns of recognition memory for emotional words in social phobics and nonanxious control participants. Lundh and Ost (1996a) assessed recognition memory for images of faces rather than word stimuli. These researchers required socially phobic patients and nonanxious controls initially to classify faces according to whether they would anticipate a high- or low-quality interaction with the person shown. Subsequently, both groups of participants demonstrated an equivalent ability to recognize the faces, regardless of the classiﬁcation imposed. However, in a second study, Lundh and Ost (1996b) had participants rate the faces as either critical or accepting. In a later memory task, the social phobics, unlike the control participants, recognized a disproportionate number of those faces they earlier had rated

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as critical. Although this may suggest that social phobics display a recognition memory advantage for emotionally negative faces, there are other possible interpretations. Because the experimenters did not directly manipulate the emotional valence of the faces, their ﬁndings may reﬂect anxiety-linked diﬀerences in rating task performance, rather than in recognition memory performance. For example, social phobics may have been disproportionately inclined to judge the more perceptually distinctive faces as critical. Even if all participants then ﬁnd these distinctive faces easier to subsequently recognize, to the same degree, this rating bias would lead to the social phobics recognizing a disproportionate number of the faces they deemed critical, though to construe this diﬀerence as a group diﬀerence in selective memory would be misleading. This problem was circumvented by Mansell, Clark, Ehlers, and Chen (1999), who presented social phobics and nonanxious individuals with equivalent arrays of diﬀering faces, some displaying neutral, some happy, and some negative emotional expressions (anger, disgust, fear, or sadness). Signal detection analysis revealed no subsequent group diﬀerences in relative recognition memory sensitivity for faces with diﬀering emotional expressions. Thus, to conclude that social phobics display a recognition memory advantage for negative faces would be premature. Similarly, measures of recognition memory for neutral and negative words do not reveal diﬀerences between nonanxious controls and participants suﬀering from OCD, PTSD, or phobic states. Using intentional memory instructions, Wilhelm et al. (1996) found that OCD patients and controls display an equivalent pattern of recognition memory for neutral, positive, and negative stimulus words. Even when textual stimuli have been employed, tailored to describe events closely related to typical OCD concerns, these anxiety patients do not demonstrate enhanced recognition memory for such emotionally negative information. Foa, Amir, Gershuny, Molnar, and Kozak (1997) presented OCD patients and nonanxious individuals with neutral sentences and others related to contamination concerns (“they soiled their clothes with blood”). Both groups subsequently displayed an equivalent pattern of recognition memory, with all participants recognizing the neutral sentences better than the contamination sentences. Vrana et al. (1995) exposed Vietnam veterans with and without PTSD to neutral, negative, and trauma-related words within an emotional Stroop task. Subsequent recognition memory was better for the negative than for the neutral words, but the observed pattern did not diﬀer between the anxiety patients and the control participants. Even when anxious participants are characterized by speciﬁc fears, they still do not generally show enhanced recognition memory for stimuli associated with these fears. Watts, Trezise, and Sharrock (1986) had spider-phobics and nonanxious controls look at a variety of dead spiders and then tested their capacity to subsequently recognize them. The phobics showed no overall superiority in recognition memory performance. Indeed, for the larger spider, which presumably represented the more highly feared stimuli, the phobics actually demonstrated poorer recognition memory than control participants did.

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We concluded earlier that good evidence indicates that panic disorder patients display relatively enhanced recall of emotionally negative material, yet such patients appear to show no parallel recognition memory advantage for negative information. Ehlers, Margraf, Davies, and Roth (1988) gave panic disorder patients and control participants a recognition memory test for words that had been presented within an earlier emotional Stroop task. Signal detection analysis revealed that threat words were recognized more accurately than neutral words, but this eﬀect was equivalent across both patient and control groups. Beck, Stanley, Averill, Baldwin, and Deagle (1992) assessed recognition memory, in panic disorder patients and control participants, for previously exposed neutral and emotional words. Overall, they found greater recognition memory sensitivity for socially threatening words than for neutral words, but once again this pattern did not distinguish the two groups. Across two experiments, Lundh, Thulin, Czyzykow, and Ost (1998) assessed recognition memory in panic disorder patients and nonanxious controls, using the face recognition methodology previously employed by Lundh and Ost (1996b) to test social phobics. There were no group diﬀerences in relative recognition memory for faces participants previously had classiﬁed as accepting or critical or for faces they had classiﬁed as high or low in degree of desired contact. Only when participants initially had classiﬁed faces according to whether they would consider the displayed person to be safe or unsafe were diﬀerent patterns of subsequent recognition memory observed between the patients and the controls. However, the nature of this eﬀect was that the panic disorder patients displayed disproportionately poor recognition memory for those faces that they previously rated unsafe. Clearly, therefore, these experiments provide no support for the proposal that recognition memory for negative information is enhanced in panic disorder patients. Only one study has found evidence to support the existence of such a bias, and it employed a rather unusual measure of recognition memory. Cloitre and Liebowitz (1991) ﬁrst exposed neutral, positive, or threatening words within a task that required panic disorder patients and control participants to judge whether the item described a feeling state or simply whether it was a legitimate English word. Participants subsequently were given a high-speed recognition memory task adapted from Jacoby and Dallas (1981). Previously seen and new words were displayed for only 35 ms each, and participants made a forced–choice decision concerning whether the word had been encountered earlier in the experiment. Although such a brief exposure likely restricted awareness of these test stimuli, Cloitre and Liebowitz nevertheless contend that their task assessed explicit memory, because participants were directed to identify which words they had previously seen. There was a trend toward greater recognition memory sensitivity for threat words in the panic disorder group alone, but this eﬀect reached signiﬁcance only when performance on negative and positive words was directly compared, after removing neutral word data from the analysis.

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Overall, research on recognition memory has provided little evidence that anxiety is associated with enhanced recognition memory for negative information. Most well-designed experiments have yielded null results. Only the unusual recognition task Cloitre and Liebowitz (1991) used has oﬀered limited support for the hypothesis, though the eﬀect was signiﬁcant only when an experimental condition was excluded within a post-hoc subsidiary analysis, so whether the ﬁnding will prove replicable remains uncertain. Nevertheless, the best evidence for an anxiety-linked recognition memory advantage for negative information comes from a task that imposed a substantial restriction on awareness. We turn now to the consideration of experiments designed speciﬁcally to assess implicit memory performance. The results of such studies have been very variable, and although they have yielded somewhat greater evidence for such an anxietylinked bias than explicit memory tasks, the phenomenon nevertheless remains elusive.

Implicit Memory Whereas recall and recognition tests require participants to consciously recollect previously encountered information, implicit tests infer memory indirectly, by examining how prior exposure to stimulus items inﬂuences later task performance. For example, when asked to complete word stems with the ﬁrst items that come to mind, people are disproportionately likely to generate words they have seen recently (Richardson-Klavehn & Bjork, 1988). Similarly, people are more likely to accurately identify a brieﬂy exposed word if this word has been recently encountered (Jacoby & Dallas, 1981). Evidence that measures of implicit memory, yielded by such indirect tests, can usefully be distinguished from the more common recall and recognition measures of explicit memory has come from work on amnesic patients, who typically show impaired performance on explicit memory tasks without demonstrating corresponding deﬁcits on implicit memory tasks (Jacoby & Witherspoon, 1982). In a study that compared the performance of high and low trait-anxious participants on several implicit tests, Russo, Fox, and Bowles (1999) failed to ﬁnd evidence that anxiety is associated with enhanced implicit memory for threatening words. No group diﬀerences were observed in the impact exerted by previously exposed emotional words (which had been simply read or used within an imagery task) on either subsequent word fragment completion or on the perceptual identiﬁcation of threat and nonthreat words. However, though null results of this type have not been uncommon, the pattern of ﬁndings has been highly inconsistent across studies, and a number of researchers also have presented evidence to support anxiety-linked bias on implicit memory tasks.1 Nugent and Mineka (1994) initially presented high and low trait-anxious participants with emotional words they were to rate for likeability and then assessed implicit memory for this information using a word stem completion task.

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As evidence of implicit memory, more of these stems were completed to yield previously exposed (primed) words than alternative (nonprimed) words. However, the relative magnitude of this eﬀect, across threat and nonthreat words, did not diﬀer between the groups. In contrast, using this same word stem completion task, Richards and French (1991) did ﬁnd a diﬀerent pattern of implicit memory for threat words and nonthreat words in high and low trait-anxious individuals, though only when these words initially had been processed in a selfreferential manner during their initial exposure. For high trait-anxious participants, but not for low trait-anxious individuals, the priming measure of implicit memory was signiﬁcantly greater for threat words than for non-threat words. Eysenck and Byrne (1994) also used a stem word completion task to compare high and low trait-anxious participants’ implicit memory for emotional words, encountered earlier in an encoding task that required either simple reading or the generation of the words from their deﬁnitions. Regardless of encoding task, Eysenck and Byrne observed that the priming index of implicit memory was greater for threat than for neutral words in high trait-anxious individuals but not in either medium for low trait-anxious participants. Mathews et al. (1989) found evidence that GAD patients also display disproportionately good implicit memory for threatening words. They presented neutral, positive, and threatening words to these anxiety patients, and to nonanxious controls, within an initial encoding task that required participants to generate a self-referent image using each stimulus item. Following this, implicit memory was assessed by measuring the magnitude of the priming eﬀects exerted by these stimuli on a subsequent word stem completion task. Control participants evidenced signiﬁcantly smaller priming eﬀects for the threat words than for the nonthreatening words, whereas GAD patients showed slightly greater priming eﬀects for the threat words than for the nonthreatening words. Although this pattern of ﬁndings is consistent with the presence of an anxiety-linked implicit memory advantage for threatening information, the eﬀect has not replicated consistently across other studies of GAD patients, possibly because of variations in the encoding tasks employed. Mathews, Mogg, Kentish, and Eysenck (1995) exposed GAD patients and controls to word sets similar to those used by Mathews et al. (1989), but instead of instructing participants to generate images from these words, they asked them to count occurrences of the letter e in each word. Under these encoding conditions, there was no tendency for the GAD and control participants to diﬀer in the relative degrees to which the threatening and nonthreatening words primed a later word stem completion, suggesting no diﬀerential pattern of implicit memory between the groups. Bradley et al. (1995) also employed fairly superﬁcial encoding tasks, requiring participants to judge personal usage frequency of words or simply exposing them very brieﬂy (14 ms), before inferring implicit memory for these word from the magnitude of repetition priming eﬀects observed on a subsequent lexical decision task. These researchers, too, failed to observe any diﬀerence between GAD patients and control participants

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in relative implicit memory for neutral, positive, and anxiety- or depressionrelevant words. Nevertheless, MacLeod and McLaughlin (1995) did ﬁnd evidence of an implicit memory advantage for threat words in GAD patients, without using a self-referential encoding task. GAD patients and controls were presented with threat and nonthreat words in an initial emotional Stroop task and were instructed ﬁrst to name the ink color and then to pronounce each word aloud. Subsequently, these words, together with matched new words, were exposed for a duration calibrated to permit around 70% accurate identiﬁcation, and implicit memory was inferred from participants’ increased ability to identify the old words relative to the new words. GAD patients, unlike nonanxious control participants, showed evidence of greater implicit memory for the threat words than for the neutral words. MacLeod and McLaughlin concluded that enhanced implicit memory for negative information is a replicable, even if not entirely reliable, characteristic of GAD patients. The results of studies designed to investigate implicit memory bias in social phobics also have been inconsistent. Using a word stem completion task to assess implicit memory for neutral and social threat words, previously encountered in a self-referential imagery task, Rapee et al. (1994) found no diﬀerences between the patterns of performance by social phobics and by nonclinical controls. However, using this same word stem completion procedure to assess implicit memory for emotionally toned stimuli following a similar encoding task, Lundh and Ost (1997) obtained more encouraging ﬁndings. Despite the absence of a signiﬁcant interaction of group by word type, hypothesis-driven tests revealed a trend toward disproportionately strong priming eﬀects for social threat words in the social phobics, compared to the control participants, consistent with an implicit memory advantage for such material. Amir, Foa, and Coles (2000) used a diﬀerent procedure to assess implicit memory, based on Jacoby, Allan, Collins, and Larwill’s (1988) ﬁnding that background noise is judged to be quieter when familiar material is embedded within it. Amir et al. ﬁrst had social phobics and nonanxious controls listen to, and repeat aloud, emotionally toned sentences. Later, the participants heard sentences, some previously presented and some new, embedded within white noise. Implicit memory was revealed by their tendency to rate the white noise intensity as lower when this embedded sentence had been exposed earlier. For social phobics, but not for control participants, the perceived intensity of this white noise was disproportionately low when it accompanied previously presented sentences with threatening emotional content. This ﬁnding was taken as evidence that implicit memory for such threatening sentences was enhanced in these anxious patients. An insuﬃcient number of studies have examined implicit memory for emotional information in either OCD or PTSD patients to permit clear conclusions. Only one such experiment has been carried out on each of these populations, and each used the white noise paradigm to assess implicit memory. Foa et al. (1997) exposed contamination-fearful OCD patients to contamination-related and neu-

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tral sentences before presenting these same sentences and matched new sentences embedded in white noise. Perceived noise intensity was lower when the noise accompanied old sentences, conﬁrming implicit memory for this material. However, the relative magnitude of this eﬀect across both emotional categories of sentences was equivalent for OCD patients and nonanxious individuals. In contrast, when Amir, McNally, and Wiegartz (1996) used the same approach to assess implicit memory for neutral and for combat-related sentences in Vietnam veterans with and without PTSD, evidence of a group diﬀerence was obtained, though only when white noise volume was high. Veterans with PTSD, unlike those without, judged subjective noise intensity as lower when it accompanied the old combat-related sentences. Thus, though only a few studies have addressed the issue, no evidence of an implicit memory advantage for negative information yet has been found in OCD patients, though some evidence indicates that such a bias may characterize PTSD patients. Amir, McNally, Riemann, and Clements (1996) used this same white-noise methodology to assess implicit memory for emotional sentences in panic disorder patients and control participants. Old and new sentences were embedded in a low level of white noise, and panic disorder patients demonstrated disproportionate attenuation of subjective noise intensity when it accompanied old sentences describing panic-related threat scenarios. Although this ﬁnding is consistent with an implicit memory advantage for threatening information in panic disorder, some studies using other measures of implicit memory to assess this same population of clinical patients have failed to support this conclusion. Rapee (1994) used the word stem completion task to measure implicit memory for neutral and threat words, initially exposed within a word association task, and found no diﬀerence in the patterns of performance shown by panic disorder patients and nonanxious control participants. Similarly, Lundh et al. (1997) failed to ﬁnd any diﬀerence between panic disorder patients and controls on a word stem completion measure of implicit memory for such emotional words, initially encoded in a self-referential imagery task. In a later experiment, Lundh, Wikstrom, Westerlund, and Ost (1999) employed a perceptual-identiﬁcation measure to assess implicit memory for these emotional words, following their initial exposure in an emotional Stroop task. Perceptual identiﬁcation was facilitated by prior exposure, conﬁrming the presence of implicit memory, but the magnitude of this eﬀect was equivalent across all three classes of words for both panic disorder patients and control participants. Nevertheless, Amir et al.’s claim that implicit memory for threat is enhanced in panic disorder patients gains some support from a study by Cloitre et al. (1994). In this experiment, emotional words ﬁrst were presented in pairs, and participants rated the strength of semantic association between items. They later were shown the ﬁrst word from each pair, together with the ﬁrst three letters of the second word, and were instructed to complete these stems to make the ﬁrst words that came to mind. A measure of memory was provided by degree to which the previously exposed words,

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rather than alternatives, appeared in these completions. Cloitre et al. observed that, among panic disorder patients, this priming eﬀect was disproportionately great for threat words and took this result as evidence of an implicit memory advantage for threatening information in patients with this anxiety disorder. As shown in this review, the overall pattern of implicit memory ﬁndings is not yet suﬃciently consistent to sustain ﬁrm conclusions. There are many possible reasons for this inconsistency, including the potential impurity of the memory measures. Though implicit memory tasks are designed to be sensitive to the inﬂuence of implicit memory, performance on most implicit memory tasks also can be inﬂuenced by explicit memory (Perruchet & Baveux, 1989), and the degree to which observed eﬀects reﬂect the impact of each type of memory may depend on subtle aspects of the experimental procedure. For example, the fact that word stems in Cloitre et al.’s (1994) study were accompanied by another word, which earlier had been paired with an item that could complete this stem, might encourage the use of explicit memory to identify this candidate completion. Thus, one might plausibly contend that Cloitre et al.’s ﬁnding could reﬂect the inﬂuence of enhanced explicit memory, rather than enhanced implicit memory, for threatening information in panic disorder. However, with the exception of panic disorder, evidence of an anxiety-linked explicit memory advantage for threat is conspicuously lacking. Therefore, it would seem unreasonable to argue that the more common appearance of such an anxiety-linked bias on implicit memory tasks should be attributed to the contaminating inﬂuence of explicit memory. Indeed, contamination from explicit memory might reduce the capacity of these tasks to detect an anxiety-linked bias in implicit memory. If so, perhaps task reﬁnements that increase the purity of the resulting implicit memory measures may result in more consistent evidence of such a bias. For the moment, however, we must concede that, whereas a greater proportion of implicit memory tasks than explicit memory have supported the idea that memory for threatening information may be enhanced in anxious individuals, neither approach has provided suﬃciently reliable evidence to conﬁrm the validity of this hypothesis.

Theoretical Implications The most obvious conclusion we draw from this review is that, from the wide range of studies that now have examined memory performance in high traitanxious groups and in patients suﬀering from most anxiety disorders, not enough evidence has been obtained to support the existence of a memory bias that consistently favors the retrieval of threatening information. Despite the wellestablished fact that both clinically anxious patients and high trait-anxious members of the normal population selectively direct attentional resources toward such

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information during encoding (cf. Mathews & MacLeod, 1994), they do not reliably display an enhanced ability to subsequently access this type of material from memory. Such ﬁndings contrast markedly with those observed in depressed participants, who do indeed commonly display disproportionately good recall of negative self-related information (e.g., Bradley et al., 1995). [See chapter 6— Eds.] Within the anxiety disorders, such a pattern of selective recall appears only in panic disorder. For this condition alone, the majority of experimental studies have supported the existence of an explicit recall bias favoring the retrieval of threatening or panic-related information.

Why Is There So Little Evidence

of a General Anxiety-Related

Memory Bias?

Elsewhere, we have suggested two possible reasons why anxiety-related memory advantages for threatening information typically are not observed (e.g., Mathews & MacLeod, 1994). First, although anxious individuals selectively attend to threat cues during encoding, this information may not be processed in a manner that produces representations that can readily be accessed during memory search. The success of such a search process likely depends highly on the degree to which stimulus information has undergone elaborative processing, thereby establishing associations between the new to-be-remembered information and prior knowledge (Graf & Mandler, 1984). If the aversive nature of threatening stimuli motivates highly anxious individuals to rapidly detect them, but also to limit their further processing, such elaboration will be restricted, countering any subsequent retrieval advantage that otherwise would result from increased attention (Eysenck & Mogg, 1992; Williams, Watts, MacLeod, & Mathews, 1997). Although many studies have instructed participants to process stimulus information during the encoding task, in ways that might counter such avoidance (such as relating word meanings to the self), highly anxious individuals may fail to comply fully with such instructions, perhaps to avoid a sustained aversive experience. There is little direct evidence to support the idea that anxious individuals avoid elaboratively processing threatening stimuli. Indeed, the widely recognized tendency for anxious individuals—particularly those suﬀering from GAD—to worry excessively suggests that extensive elaborative processing of threat occurs in some anxiety disorders, especially in the form of verbal propositions (Borkovec & Inz, 1990). One could argue that this type of elaboration would aid the recall of such information. However, elaborative processing in the form of worry may exert no beneﬁcial impact on recall performance, particularly if the worry involves stereotypical themes. Instead, if diﬀerent threat cues elicit similar worry content in anxious individuals, the distinctiveness of the representations resulting from this type of elaboration could be reduced, compromising retrieval of the original cues.

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The robust tendency to display relatively facilitated recall of negative information in depression often has been attributed to processing that establishes novel linkages with other self-related negative information, already represented within depressives’ memory. Depressive individuals typically demonstrate such a negative memory bias only for words encoded in tasks that encourage selfreferential processing (Bradley & Mathews, 1983). If depression alone is associated with particular negative ideation about the self, the apparent diﬀerence in the patterns of memory selectivity demonstrated by depressed and by anxious participants might be explained. For depressed individuals, the elaborative processing of new negative information links it to existing negative self-schema, which then functions as a retrieval aid during memory search. In contrast, although anxious individuals worry about future events, there is little evidence to suggest that they habitually ruminate about their own negative qualities (as do depressives), so there is no compelling reason to expect anxious individuals to display a negative recall bias following such commonly used self-referential encoding procedures (e.g., Mogg et al., 1989). Another reason that could explain the lack of an anxiety-linked recall bias is that anxious individuals may tend to represent threatening information perceptually rather than in a conceptual form based on verbal propositions. This contention is consistent with the supposition that threat can be processed within a primitive fear system (or module) that evolved prior to the development of language (Öhman & Mineka, 2001). If anxious participants are particularly inclined to represent threat using perceptual codes, perhaps because this primitive fear system is overly active, then according to the transfer-appropriate processing accounts of memory (Roediger & Blaxton, 1987), retrieving this information when performing memory tasks that encourage conceptual processing, such as free recall, would prove diﬃcult for them. In contrast, memory tasks that encourage perceptual processing should more eﬀectively tap anxious participants’ representations of previously encountered threat stimuli. This may explain why conventional implicit memory tasks, such as rapid word identiﬁcation, which characteristically encourage perceptual rather than conceptual processing, have more often revealed evidence of an anxiety-related memory advantage for threat. According to this account, the widespread tendency to use self-referential or other semantic encoding procedures may reduce the likelihood of ﬁnding such biases on this type of implicit memory task. Certainly, as we have shown, the evidence in support of an anxiety-linked implicit memory advantage for threat is very mixed, but it may not be fully explained by variations in encoding tasks. Several studies that have used structural encoding methods have failed to reveal any implicit memory advantage for threat in anxious participants, though others have yielded more supportive ﬁndings (e.g., MacLeod & McLaughlin, 1995). Perhaps the prevailing use of words as stimuli also may undermine the likelihood of ﬁnding enhanced perceptual memory for threat in anxious individuals, as the perceptual encoding of such stimuli seems less likely than would be ex-

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pected with pictorial materials. Though such a proposal is speculative at this stage, both the restricted elaboration hypothesis and the perceptual encoding hypothesis remain viable explanations for the absence of any general memory advantage for threat stimuli in anxious individuals, despite their tendency to selectively allocate attention to such information. Neither account, however, has been directly supported by experimental evidence; indeed, few experiments have been designed to test these hypothetical accounts.

Why Is There a Memory Bias

in Panic Disorder?

Despite the sparse evidence that anxiety is associated with a memory bias favoring threat, panic disorder patients tend to recall more panic-related threat words than nonanxious controls do. We cannot attribute this eﬀect to anxiety per se, given the absence of parallel eﬀects in other anxiety disorders, so it seems necessary to explain why panic disorder is an exception to the rule. One obvious possibility, already noted in our comments on the study by Nunn et al., (1984), is that the supposedly negative words in these studies often may be threatening only for the panic patients. For example, words describing common cues for the panic attacks experienced by such patients (e.g., street, crowd) frequently have been used in these experiments, even though such words are unlikely to be emotionally charged for nonanxious control participants. As we reported in the introduction, emotional information is more likely to be recalled than neutral information, regardless of anxiety level, and the ﬁnding that panic patients recall these words disproportionately well may reﬂect only this general eﬀect. The confound between clinical status and stimulus valence makes it diﬃcult to determine whether the panic disorder patients and the controls would have recalled diﬀerently stimulus materials that both groups had considered threatening. This problem is less evident within studies that have used stimulus materials likely to be emotionally threatening for all participants. Words such as torture and death presumably would have similar threat values for all readers, so any general recall advantage for emotional words would not produce group diﬀerences in recall. Nevertheless, as we have pointed out, likely group diﬀerences in the perceived threat value of stimulus materials have compromised at least one study of OCD patients (Radomsky & Rachman, 1999). In this study, discrepant patterns of memory performance arose perhaps because a contamination manipulation increased stimulus threat value for patients, but not for nonanxious controls. The more common ﬁnding is that OCD patients do not diﬀer from nonanxious controls in memory for threatening stimuli, even when these are related to their concerns, although they do often report less conﬁdence in their memory (e.g., Tolin et al., 2001). Thus, the anomalous memory advantage for threat-related words shown by panic disorder patients may reﬂect the fact that panic-related word cues possess more emotionally negative meaning for panic

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patients than for nonanxious controls. The use of stimulus words that have special emotional signiﬁcance only for one group of participants prevents the attribution of observed group diﬀerences in the recall of such material to a tendency to selectively remember emotional information.

Are Discrepancies in Memory Eﬀects

Due to Diﬀering Encoding Tasks?

We have suggested that some of the memory eﬀects shown by anxious participants can readily be attributed to anxiety-linked patterns of selective encoding, without the need to implicate a bias in the retrieval process itself. For example, in the experiments carried out by Friedman et al. (2000) and by Russo et al. (2001), words were exposed for durations that far exceeded the minimum time required to register their identity. Anxious individuals characteristically direct attention toward, and ﬁnd it disproportionately diﬃcult to disengage attention from, emotionally threatening words during such encoding procedures. Consequently, their enhanced subsequent ability to recall the threatening words can be attributed to the superior encoding of the threatening information, resulting from this reduced ability to inhibit attention to such aﬀective meanings (Williams et al., 1996; Wood et al., 2001). Further evidence to support this account comes from a series of experiments reported by Pury and Mineka (2001). In a typical study, participants were required to judge, as quickly as possible, whether a presented word (e.g., bleeding, conﬁdence) described something dangerous or safe or whether it described a physical or psychological state. When participants were not informed which decision was required until immediately prior to word presentation, highly anxious participants were slower than low anxious controls to make the physical versus psychological judgment but not to make the dangerous versus safe judgment. This ﬁnding, together with the results of other experiments from this same series, provides evidence that high anxious individuals are more likely than their low anxious counterparts to encode stimuli in terms of their aﬀective meaning. If anxious individuals’ infrequently observed threat-related bias in recall results from their heightened inclination to encode the emotionally threatening content of aﬀective stimulus words, then this recall bias should be particularly likely following encoding tasks that permit ample opportunities for participants to select how to process these stimuli. Under such encoding conditions, we suppose that increased attention paid to threatening aspects of meaning may help high anxious individuals to retain such words better. In contrast—again assuming that the enhanced memory for threat occasionally demonstrated by anxious participants reﬂects an anxiety-linked tendency to process the aﬀective meaning of such stimuli during encoding—this eﬀect should not be observed following encoding tasks that require all participants to process stimuli in terms of their aﬀective meaning. In general, as this review has indicated, anxious individuals more often show en-

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hanced relative recall of threatening information following encoding tasks that permit but do not require the encoding of aﬀective meaning. Technically, of course, the term “memory bias” is appropriate to describe the recall advantage for threat sometimes shown by anxious participants following free encoding conditions that employ long exposure durations (e.g., Friedman et al., 2000; Russo et al., 2001). However, we contend that it is not parsimonious to ascribe the eﬀect to a bias in the process of retrieving information from memory, when it can be explained by the well-established tendency for highly anxious individuals to attend to and selectively encode threatening meanings. We believe that the eﬀect may better be construed as an indirect consequence of the bias that favors the selective encoding of threatening stimulus content in anxiety. Nevertheless, the possibility that the patterns of selective attention and encoding associated with vulnerability to anxiety may, under certain circumstances, give rise to long-term memory eﬀects is clearly important. These patterns of encoding selectivity may aﬀect not only how old events are recalled but also how new events are understood. For example, our work on the experimental manipulation of such biases has shown that people trained to attend selectively to threatening meanings of stimulus information become more likely to store negatively disambiguated representations of newly presented ambiguous events in memory (Mathews & MacLeod, 2002). Distinctions between attention, interpretation, and memory thus can become blurred when life events are processed, given that initial encoding biases so readily can translate into diﬀerential patterns of interpretation and recall. In closing, however, we emphasize that, despite this potential capacity for encoding biases to inﬂuence memory performance, most experimental studies have failed to demonstrate that anxious individuals (with the possible exception of panic disorder patients) consistently display enhanced recall or recognition memory for emotionally threatening information. Though an implicit memory bias favoring threat stimuli sometimes has been observed in anxious participants, at best it is a fragile eﬀect that often has proven diﬃcult to replicate. It remains to be seen whether the future reﬁnement of experimental methodologies will identify particular conditions under which anxious participants will more reliably demonstrate a memory advantage for negative information. For the moment, the most appropriate conclusion is that such a memory bias does not represent a robust general characteristic of anxiety.

Note 1. Whereas methodological rigor has varied across these studies, and it sometimes is possible to criticize experimental decisions such as choice of appropriate baselines, the pattern of observed inconsistences cannot readily be explained in terms of such design variations.

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References Amir, N., Coles, M. E., Brigidi, B., & Foa, E. B. (2001). The eﬀect of practice on recall of emotional information in individuals with generalized social phobia. Journal of Abnormal Psychology, 110, 76–82. Amir, N., Foa, E.B., & Coles, M. (2000). Implicit memory bias for threat-relevant information in individuals with generalized social phobia. Journal of Abnormal Psychology, 109, 713–720. Amir, N., McNally, R. J., Riemann, B. C., & Clements, C. (1996). Implicit memory bias for threat in panic disorder: Application of the “white noise” paradigm. Behaviour Research and Therapy, 34, 157–162. Amir, N., McNally, R. J., & Wiegartz, P. S. (1996b). Implicit memory bias for threat in posttraumatic stress disorder. Cognitive Therapy and Research, 20, 625–635. Ashcraft, M. H., & Kirk, E. P. (2001). The relationship among working memory, math anxiety, and performance. Journal of Experimental Psychology: General, 130, 224–237. Baddeley, A. D. (1986). Working memory. Oxford: Oxford University Press. Beck, J. G., Stanley, M. A., Averill, P. M., Baldwin, L. E., & Deagle, E. A. (1992). Attention and memory for threat in panic disorder. Behaviour Research and Therapy, 30, 619–629. Becker, E., Rinck, M., & Margraf, J. (1994). Memory bias in panic disorder. Journal of Abnormal Psychology, 103, 396–399. Becker, E. S., Roth, W. T., Andrich, M., & Margraf, J. (1999). Explicit memory in anxiety disorders. Journal of Abnormal Psychology, 108, 153–163. Borkovec, T. B., & Inz, J. (1990). The nature of worry in generalized anxiety disorder: A predominance of thought activity. Behaviour Research and Therapy, 28, 153–158. Bradley, B. P., & Mathews, A. (1983). Negative self-schemata in clinical depression. British Journal of Clinical Psychology, 22, 173–181. Bradley, B. P., Mogg, K., & Williams, R. (1994). Implicit and explicit memory for emotional information in non-clinical subjects. Behaviour Research and Therapy, 32, 65–78. Bradley, B. P., Mogg, K., & Williams, R. (1995). Implicit and explicit memory for emotion-congruent information in clinical depression and anxiety. Behaviour Research and Therapy, 33, 755–770. Burke, M., & Mathews, A. (1992). Autobiographical memory and clinical anxiety. Cognition & Emotion, 6, 23–35. Cahill, L., & McGaugh, J. L. (1995). A novel demonstration of enhanced memory associated with emotional arousal. Consciousness and Cognition, 4, 410–421. Calvin, A. D., Koons, P. B., Bingam, J. L., & Fink, H. H. (1953). A further investigation of the relationship between manifest anxiety and intelligence. Journal of Consulting Psychology, 19, 280–282. Christianson, S-Å. (1992). Emotional stress and eyewitness memory: A critical review. Psychological Bulletin, 112, 284–309. Cloitre, M., Cancienne, J., Heimberg, R. G., Holt, C. S., & Liebowitz, M. R. (1995). Case histories and shorter communications: Memory bias does not generalize across anxiety disorders. Behaviour Research and Therapy, 33, 305–307.

     

181

Cloitre, M., & Liebowitz, M. R. (1991). Memory bias in panic disorder: An investigation of the cognitive avoidance hypothesis. Cognitive Therapy and Research, 15, 371–386. Cloitre, M., Shear, M. K., Cancienne, J., & Zeitlin, S. B. (1994). Implicit and explicit memory for catastrophic associations to bodily sensation words in panic disorder. Cognitive Therapy and Research, 18, 225–240. Dalgleish, T. (1994). The relationship between anxiety and memory biases for material that has been selectively processed in a prior task. Behaviour Research and Therapy, 32, 227–231. Darke, S. (1988a). Anxiety and working memory capacity. Cognition & Emotion, 2, 145–154. Darke, S. (1988b). Eﬀects of anxiety on inferential reasoning task performance. Journal of Personality and Social Psychology, 55, 499–505. Ehlers, A., Margraf, J., Davies, S., & Roth, W. T. (1988). Selective processing of threat cues in subjects with panic attacks. Cognition & Emotion, 2, 201–220. Eysenck, M. W. (1982). Attention and arousal: Cognition and performance. Berlin: Springer. Eysenck, M. W., & Byrne, A. (1994). Implicit memory bias, explicit memory bias, and anxiety. Cognition & Emotion, 8, 415–431. Eysenck, M. W., & Calvo, M. G. (1992). Anxiety and performance: The processing eﬃciency theory. Cognition & Emotion, 6, 409–434. Eysenck, M. W., & Mogg, K. (1992). Clinical anxiety, trait anxiety, and memory bias. In S-Å. Christianson (Ed.), Handbook of emotion and memory (pp. 429–450). Hillsdale, NJ: Erlbaum. Finlay-Jones, R., & Brown, G. W. (1981). Types of stressful life event and the onset of anxiety and depressive disorders. Psychological Medicine, 11, 803–815. Foa, E. B., Amir, N., Gershuny, B., Molnar, C., & Kozak, M. J. (1997). Implicit and explicit memory in obsessive-compulsive disorder. Journal of Anxiety Disorders, 11, 119–129. Fox, E., Russo, R., Bowles, R., & Dutton, K. (2001). Do threatening stimuli draw or hold visual attention in subclinical anxiety? Journal of Experimental Psychology: General, 130, 681–700. Friedman, B. H., Thayer, J. F., & Borkovec, T. D. (2000). Explicit memory bias for threat words in generalized anxiety disorder. Behavior Therapy, 31, 745–756. Graf, P., & Mandler, G. (1984). Activation makes words more accessible but not necessarily more retrievable. Journal of Verbal Learning and Verbal Behaviour, 23, 553–568. Humphreys, M. S., & Revelle, W. (1984). Personality, motivation, and performance: A theory of the relationship between individual diﬀerences and information processing. Psychological Review, 91, 153–184. Jacoby, L. L., Allan, L. G., Collins, J. C., & Larwill, L. K. (1988). Memory inﬂuences subjective experience: Noise judgments. Journal of Experimental Psychology: Learning, Memory, and Cognition, 14, 240–247. Jacoby, L. L., & Dallas, M. (1981). On the relationship between autobiographical memory and perceptual learning. Journal of Experimental Psychology: General, 110, 303–340.

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Jacoby, L. L., & Witherspoon, D. (1982). Remembering without awareness. Canadian Journal of Psychology, 36, 300–324. Levy, E. A., & Mineka, S. (1998). Anxiety and mood-congruent autobiographical memory: A conceptual failure to replicate. Cognition & Emotion, 12, 625–634. Lundh, L.-G., Czyzykow, S., & Ost, L.-G. (1997). Explicit and implicit memory bias in panic disorder with agoraphobia. Behaviour Research and Therapy, 35, 1003– 1014. Lundh, L.-G., & Ost, L.-G. (1996a). Face recognition in patients with social phobia. Scandinavian Journal of Behaviour Therapy, 25, 139–148. Lundh, L.-G., & Ost, L.-G. (1996b). Recognition bias for critical faces in social phobics. Behaviour Research and Therapy, 34, 787–794. Lundh, L.-G., & Ost, L.-G. (1997). Explicit and implicit memory bias in social phobia. The role of subdiagnostic type. Behaviour Research and Therapy, 35, 305–317. Lundh, L.-G., Thulin, U., Czyzykow, S., & Ost, L.-G. (1998). Recognition bias for safe faces in panic disorder with agoraphobia. Behaviour Research and Therapy, 36, 323–337. Lundh, L.-G., Wikstrom, J., Westerlund, J., & Ost, L.-G. (1999). Preattentive bias for emotional information in panic disorder with agoraphobia. Journal of Abnormal Psychology, 108, 222–232. MacLeod, C., & Donellan, A. M. (1993). Individual diﬀerences in anxiety and the restriction of working memory capacity. Personality and Individual Diﬀerences, 15, 163–173. MacLeod, C., & McLaughlin, K. (1995). Implicit and explicit memory bias in anxiety: A conceptual replication. Behaviour Research and Therapy, 33, 1–14. Mansell, W., Clark, D. M., Ehlers, A., & Chen, Y.-P. (1999). Social anxiety and attention away from emotional faces. Cognition & Emotion, 13, 673–690. Mathews, A., & MacLeod, C. (1985). Selective processing of threat cues in anxiety states. Behaviour Research and Therapy, 23, 563–569. Mathews, A., & MacLeod, C. (1994). Cognitive approaches to emotion and emotional disorders. Annual Review of Psychology, 45, 25–50. Mathews A., & MacLeod, C. (2002). Induced processing biases have causal eﬀects on anxiety. Cognition & Emotion, 16, 310–315. Mathews, A., Mogg, K., Kentish, J., & Eysenck, M. (1995). Eﬀect of psychological treatment on cognitive bias in generalized anxiety disorder. Behaviour Research and Therapy, 33, 293–303. Mathews, A., Mogg, K., May, J., & Eysenck, M. (1989). Implicit and explicit memory bias in anxiety. Journal of Abnormal Psychology, 98, 236–240. McNally, R. J., Foa, E. B., & Donnell, C. D. (1989). Memory bias for anxiety information in patients with panic disorder. Cognition & Emotion, 3, 27–44. McNally, R. J., Litz, B. T., Prassas, A., Shin, L. M., & Weathers, F. W. (1994). Emotional priming of autobiographical memory in post-traumatic stress disorder. Cognition & Emotion, 8, 351–367. McNally, R. J., Metzger, L. J., Lasko, N. B., Clancy, S. A., & Pitman, R. K. (1998). Directed forgetting of trauma cues in adult survivors of childhood sexual abuse with and without posttraumatic stress disorder. Journal of Abnormal Psychology, 107, 596–601.

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Mogg, K., & Mathews, A. (1990). Is there a self-referent mood-congruent recall bias in anxiety? Behaviour Research and Therapy, 28, 91–92. Mogg, K., Mathews, A., & Weinman, J. (1987). Memory bias in clinical anxiety. Journal of Abnormal Psychology, 96, 94–98. Mogg, K., Mathews, A., & Weinman, J. (1989). Selective processing of threat cues in anxiety states: A replication. Behaviour Research and Therapy, 27, 317–323. Mueller, J. H. (1992). Anxiety and performance. In A. P. Smith & D. M. Jones (Eds.), Factors aﬀecting human performance (Vol. 3, pp. 127–160). London: Academic Press. Nugent, K., & Mineka, S. (1994). The eﬀect of high and low trait anxiety on implicit and explicit memory tasks. Cognition & Emotion, 8, 147–163. Nunn, J. D., Stevenson, R., & Whalan, G. (1984). Selective memory eﬀects in agoraphobic patients. British Journal of Clinical Psychology, 23, 195–201. Öhman, A., & Mineka, S. (2001). Fears, phobias, and preparedness: Toward an evolved module of fear and fear learning. Psychological Review, 108, 483–522. Otto, M. W., McNally, R. J., Pollack, M. H., Chen, E., & Rosenbaum, J. F. (1994). Hemispheric laterality and memory bias for threat in anxiety disorder. Journal of Abnormal Psychology, 103, 828–831. Perruchet, P., & Baveux, P. (1989). Correlational analyses of explicit and implicit memory performance. Memory & Cognition, 17, 77–86. Pickles, A. J., & van den Broek, M. D. (1988). Failure to replicate evidence for phobic schemata in agoraphobic patients. British Journal of Clinical Psychology, 27, 271–272. Pury, C. L. S., & Mineka, S. (2001). Diﬀerential encoding of aﬀective and nonaﬀective content information in trait anxiety. Cognition & Emotion, 15, 659–693. Radomsky, A. S., & Rachman, S. (1999). Memory bias in obsessive-compulsive disorder (OCD). Behaviour Research and Therapy, 37, 605–618. Rapee, R. M. (1994). Failure to replicate a memory bias in panic disorder. Journal of Anxiety Disorders, 8, 291–300. Rapee, R. M., McCallum, S. L., Melville, L. F., Ravenscroft, H., & Rodney, J. M. (1994). Memory bias in social phobia. Behaviour Research and Therapy, 32, 89–99. Reidy, J., & Richards, A. (1997). Anxiety and memory: A recall bias for threatening words in high anxiety. Behaviour Research and Therapy, 35, 531–542. Reisberg, D., & Heuer, F. (1992). Remembering the details of emotional scenes. In E. Wingrad & U. Neisser (Eds.), Aﬀect and accuracy in recall: Studies of “ﬂashbulb” memory (pp. 162–190). New York: Cambridge University Press. Revelle, W., & Loftus, D. A. (1990). Individual diﬀerences and arousal: Implications for the study of mood and memory. Cognition & Emotion, 3, 209–237. Richards, A., & French, C. C. (1991). Eﬀects of encoding and anxiety on implicit and explicit memory performance. Personality and Individual Diﬀerences, 12, 131–139. Richards, A., & Whittaker, T. M. (1990). Eﬀects of anxiety and mood manipulation in autobiographical memory. British Journal of Clinical Psychology, 29, 145–153. Richardson-Klavehn, A., & Bjork, R. A. (1988). Measures of memory. In M. R. Rosenzweig & L. W. Porter (Eds.), Annual Review of Psychology, 9, 475–543. Roediger, H. L., & Blaxton, T. A. (1987). Retrieval modes produce dissociations in memory for surface information. In D. Gorfein & R. R. Hoﬀman (Eds.), Memory

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and cognitive processes: The Ebbinghaus Centennial Conference. Hillsdale, NJ: Erlbaum. Russo, R., Fox, E., Bellinger, L., & Nguyen-Van-Tam, D. P. (2001). Mood-congruent free recall bias in anxiety. Cognition & Emotion, 15, 419–433. Russo, R., Fox, E., & Bowles, R. J. (1999). On the status of implicit memory bias in anxiety. Cognition & Emotion, 13, 435–456. Sanz, J. (1996). Memory biases in social anxiety and depression. Cognition & Emotion, 10, 87–105. Tolin, D. F., Abramowitz, J. S., Brigidi, B. D., Amir, N., Street, G. P., & Foa, E. B. (2001). Memory and memory conﬁdence in obsessive-compulsive disorder. Behaviour Research and Therapy, 39, 913–927. Vrana, S. R., Roodman, A., & Beckham, J. C. (1995). Selective processing of traumarelevant words in posttraumatic stress disorder. Journal of Anxiety Disorders, 9, 515–530. Watts, F. N., Trezise, L., & Sharrock, R. (1986). Processing of phobic stimuli. British Journal of Clinical Psychology, 25, 253–261. Wenzel, A., Jackson, L. C., & Holt, C. S. (2002). Social phobia and the recall of autobiographical memories. Depression & Anxiety, 15, 186–189. Wessel, I., van der Kooy, P., & Merckelbach, H. (2000). Diﬀerential recall of central and peripheral details of emotional slides is not a stable phenomenon. Memory, 8, 95–109. Wilhelm, S., McNally, R. J., Baer, L., & Florin, I. (1996). Directed forgetting in obsessive-compulsive disorder. Behaviour Research and Therapy, 34, 633–641. Wilhelm, S., McNally, R. J., Baer, L., & Florin, I. (1997). Autobiographical memory in obsessive-compulsive disorder. British Journal of Clinical Psychology, 36, 21– 31. Williams, J. M. G., Mathews, A., & MacLeod, C. (1996). The emotional Stroop task and psychopathology. Psychological Bulletin, 120, 3–24. Williams, J. M. G., Watts, F. N., MacLeod, C., & Mathews, A. (1997). Cognitive psychology and emotional disorders. 2nd ed. Chichester, UK: Wiley. Wood, J., Mathews, A., & Dalgleish, T. (2001). Anxiety and cognitive inhibition. Emotion, 1, 166–181. Yiend, J., & Mathews, A. (2001). Anxiety and attention to threatening pictures. Quarterly Journal of Experimental Psychology, 54, 665–681.

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he truest claim that cognitive science can make might also be the least sophisticated: the mind tends to do what it has done before. In previous centuries philosophers and psychologists invented constructs such as associations, habit strength, and connectivity to formalize the truism, but others have known about it, too. In small towns in the Ozarks, for example, grandmothers have been overheard doling out warnings such as, “Don’t think those ugly thoughts; your mind will freeze that way.” Depressed persons, like most of us, usually don’t heed this advice. The thoughts frozen in their minds might not be “ugly,” but they often reﬂect disappointments, losses, failures, other unhappy events, and a generally negative interpretive stance toward ongoing experience. By considering these habits of thinking, we should better understand the nature of memory in depressed states. Deliberate attempts to remember are either impaired or facilitated in ways that appear related to habits of thinking. Even more commonly, memory is expressed indirectly through the content of current thoughts and interpretations. This chapter examines the relations among habitual thoughts—often called ruminations—and memory phenomena in depression. I use “depression” imprecisely, to refer to both diagnostic categories and the self-reported state of dysphoria. “Dysphoria” is used to denote undiagnosed negative aﬀect, of the sort that produces moderate-to-high scores on the Beck Depression Inventory (BDI: Beck, Ward, Mendelson, Mock, & Erbaugh, 1961). Although the patterns of performance associated with self-reported measures of depressed mood—such as BDI scores—are often similar to those obtained from diagnosed samples, occasional evidence for diﬀerences should be noted (see Burt, Zembar, & Niederehe, 1995). We should note the imprecision associated with diagnosis as well (e.g., the boundary problems for mood disorders and generalized anxiety disorders; see

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Brown, Di Nardo, Lehman, & Campbell, 2001). On the side of simplicity, however, many phenomena appear similar in form, if not extent, across studies measuring dysphoria and depression. (For a short review, see Wenzlaﬀ, Meier, & Salas, 2002.) Further caution about the use of “depression” is appropriate when considering the many studies performed with experimental mood inductions (e.g., through the use of sad or happy music) in an eﬀort to make causal statements about mood and memory. In some of these studies, the language of depression is used to describe the ﬁndings from negatively valenced inductions. (See Parrott & Hertel, 2000, for a description of these and other methodological issues.) Moodinduction studies sometimes reveal patterns similar to those in studies based on self-reports or diagnoses. But because habits of ruminating do not likely characterize students randomly assigned to listen to sad music, this chapter rarely addresses ﬁndings from mood inductions.

Habits of Thought Negative thinking has been such a prevalent feature of depression, as observed clinically, that Beck (1967) used “schema” to capture its habitual and interrelated qualities. These stable cognitive structures were proposed as one way of organizing and describing thought patterns in depression. “Rumination” is used as a process-oriented companion to the structural construct of a schema. Depressed people tend to ruminate. They ponder the episodes associated with sad feelings and imagine similar future occurrences. They focus on their feelings and wonder if they will ever change (see Ingram, 1990; Nolen-Hoeksema, 1991). Rumination can be an intensely attention-demanding process, yet the initiation of a ruminative episode is often thoughtless or automatic, even to the extent that the person can become so engaged without awareness. The draw toward rumination has a lot in common with the tendency to attend to external stimuli that are emotionally congruent with depressive concepts. For example, dysphoric students are slower to name the color of ink when it spells a word related to depression (e.g., Gotlib & McCann, 1984). On similar tasks nondepressed participants preferentially attend to positive members of word pairs and avoid the negative members, but clinically depressed and dysphoric participants lack this positive bias (McCabe & Gotlib, 1995; McCabe & Toman, 2000). Mood-related experience also encourages the tendency to ﬁnd negative meaning in ambiguous information, relatively automatically. Lawson, MacLeod, and Hammond (2002) devised a clever indirect measure of such interpretive biases by measuring the blink reﬂex to noise occurring as participants imaged situations evoked by auditorially presented ambiguous and nonambiguous words. Participants who had scored high on the BDI produced particularly ampliﬁed blink reﬂexes during the imaging of ambiguous words that lend themselves to

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negative interpretations, in a pattern similar to that for clearly negative words. Using a quite diﬀerent paradigm, Wenzlaﬀ and Bates (1998) presented strings of words that could be unscrambled to form either negative or non-negative sentences. Dysphoric students formed negative versions more often than others did. Even students who were formerly dysphoric displayed this bias under dual-task conditions. Although direct reports of beliefs and thoughts tend toward less negativity as depression lessens (Haaga, Dyck, & Ernst, 1991), ﬁndings such as those by Wenzlaﬀ and Bates (1998) reveal the enduring nature of depressive habits of thought (also see Wenzlaﬀ, Rude, Taylor, Stultz, & Sweatt, 2001). Depressive habits of thought seem, moreover, to exacerbate sad moods and predict future depressive episodes. In an extensive program of research by NolenHoeksema and her colleagues (e.g., Lyubomirsky, Caldwell, & Nolen-Hoeksema, 1998; Nolen-Hoeksema & Morrow, 1993), depressed and nondepressed participants have been asked to concentrate on either self-focused or distracting phrases. The self-focused phrases themselves do not suggest sad or depressed mood; in fact, the nondepressed participants typically report feeling no sadder after concentrating on them than they feel after entertaining thoughts about distracting phrases (e.g., geographical locations). But in study after study, the sad moods of depressed participants have increased following the self-focused statements and decreased following the distracting phrases. Similarly, Fennell, Teasdale, Jones, and Damle (1987) reported improvements in mood after depressed participants focused on distracting images of outdoor scenes. Therefore, habits of thought can aﬀect mood, and recent discoveries have shown that they can also predict future mood impairment (e.g., Alloy, Abramson, & Francis, 1999; Nolen-Hoeksema, 2000; Rude, Wenzlaﬀ, Gibbs, Vane, & Whitney, 2002). Measures of negative-thinking styles, demonstrated either through self-reports or by performance on laboratory tasks, predicted episodes of dysphoria and depression in weeks to come. So, just as depressed mood might establish habits of negative thinking, such habits at least portend, and perhaps help establish, not only temporary changes in mood but also future depressive episodes. Indeed, substantial empirical evidence now supports the concept of a vicious cycle of rumination and mood, described years ago by John Teasdale (1983).

Habits of Memory Separating habits of memory from habits of thinking is a somewhat arbitrary exercise. Obviously, ruminative episodes often include autobiographical memories that come to mind habitually. Less obviously, perhaps, even the acts of interpreting current experience in habitually negative ways are themselves instances of using memory implicitly or without intention. Jacoby and Kelley (1987, citing Polyani, 1958) distinguished the use of memory as an object for examination from the use of memory as a tool for perception and interpretation,

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a helpful distinction in the context of considering cognitive habits. Both uses of memory—object and tool—can become biased out of habit. To refer to memory as an object (explicit memory) is to communicate awareness that the content of one’s thoughts derives from a past event. Episodes from one’s personal past can come to mind habitually, sometimes uninvited (but with full awareness of their temporal status) and sometimes deliberately and repeatedly sought. At the end of this section, I examine the well-documented tendency for depressed persons to remember negative episodes from their biographical past. Depressed persons habitually remember the bad. Habits of remembering negative events also show up in the laboratory. On tests of explicit memory, the tendency to think negatively can facilitate the deliberate remembering of experimental materials from the same conceptual neighborhood. On tests ostensibly unrelated to memory (implicit or indirect tests of memory), performance can also reﬂect habits of prior preferential processing. The experimental goal in both cases is to control the initial experience intended to operate as tool or object on the test (i.e., the experience to be “remembered”); however, the autobiographical method obviously lacks such control over the initial experience. In experimental studies, at least we know the characteristics of the immediate experience to be remembered. Yet it is important to keep in mind that the power of any mood-congruent eﬀect—experimental or autobiographical—no doubt lies in uncontrolled, pre-experimental habits of thought.

Memory-as-Object in the Laboratory If we present positively and negatively aﬀective words in a ﬁrst experimental task and later ask the depressed and nondepressed participants to recall those words, chances are good that recall will in some way be congruent with mood. (See the meta-analysis by Matt, Vazquez, & Campbell, 1992.) Maybe the diﬀerences will be lopsided, especially in the case of dysphoria, with dysphoric participants recalling fewer positive words but the same number of negative words as nondysphoric participants do. Likely, the diﬀerences will obtain only for words encountered conceptually in the ﬁrst task. In fact, some evidence suggests further restrictions to words considered in relation to the self (e.g., Bradley & Mathews, 1983; Derry & Kuiper, 1981; Dobson & Shaw, 1987). These limitations support the claim that habits of thought play a role in producing moodcongruent recall. Habits likely play a large role during the test itself. An illustration is the experiments performed by Murray, Whitehouse, and Alloy (1999). They found evidence of mood-congruent recall following a self-referential task, but only when participants were not required to guess in order to produce a criterion number of words. When recall was “forced,” the mood-related diﬀerences vanished. These results should encourage researchers to use a forcing procedure more often. A reasonable hypothesis is that mood-congruent biases inﬂuence the

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ﬂuency or ease of remembering, but that materials with other meaning can be brought to mind with suﬃcient persistence or external aid. Such an outcome, however, does not reduce our interest in the ubiquitous ﬁndings of moodcongruent recall and their interpretation. Most acts of recall are probably ﬂuencydriven, without prolonged pursuit of additional material. Several theoretical frameworks have emphasized the greater degree of conceptual processing that depressed persons devote to negative materials. Some approaches propose that elaborative conceptual processing facilitates recall by establishing richer and more diverse retrieval routes (see Williams, Watts, MacLeod, & Mathews, 1988, and the network account by Bower, 1981). According to the framework of transfer-appropriate processing (Morris, Bransford, & Franks, 1977; see Roediger & McDermott, 1992), mood-congruent recall is established by the match between conceptual elaboration during the initial task and the conceptual basis of the attempt to remember. This account can be extended to include a third type of “occasion”: prior habits of thinking. Predated by such habits, negative self-referential material comes to mind with greater ﬂuency, either during the initial episode to be remembered, during the test itself, or on both occasions. Probably more often than we realize, however, evidence for mood-congruent recall of conceptually processed material is not obtained. Can a consideration of cognitive habits suggest boundary conditions for the mood-congruent eﬀect, at least on a post-hoc basis? Among others, Parrott and Spackman (2000) have written about the tendency for some people in negative moods to attempt mood repair by deliberately thinking positive thoughts. Indeed, evidence for moodincongruent recall might result from these attempts, as reconﬁrmed recently by Rusting and DeHart (2000). They instructed some participants to keep focusing on negative events (imagined vignettes for speciﬁed words or autobiographical episodes) used to induce negative mood, much like what one does in rumination. Other participants were instructed to engage in positive reappraisals of those events. Subsequent recall was mood-congruent for the former participants and mood-incongruent for the latter. These participants were not depressed; nevertheless, the results provide a model for what might happen naturally when depressed persons develop either set of cognitive habits.1 The literature on depression and mood-congruent recall is substantial. Many studies now conducted to examine depression-related biases in other types of cognitive tasks often include a demonstration of mood-congruent recall for comparison (e.g., Watkins, Mathews, Williamson, & Fuller, 1992). There are also published reports of mood-congruent recognition in depression (e.g., Wenzlaﬀ et al., 2002), even one that reports mood-related diﬀerences in eventrelated potentials during the initial task of rating pleasantness, as well as during the recognition test (Deldin, Keller, Gergen, & Miller, 2001). Diﬀerent levels of brain activity should indeed inform our understanding of mood-congruent memory, but they do not necessarily reveal the causal mechanisms underly-

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ing the dispositions for negative interpretations. Habits might serve as instigators, outcomes, or both.

Memory as Tool In the last decade of the 20th century, a number of experiments on implicit memory in depression were published (e.g., Bazin, Perruchet, De Bonis, & Féline, 1994; Danion et al., 1991; Denny & Hunt, 1992; Elliott & Greene, 1992; Hertel, 1994; Hertel & Hardin, 1990; Watkins et al., 1992). Some of these experiments were not designed to address mood-congruence. But others varied the emotional valence of the materials in attempts to determine whether mood-congruent memory would be revealed on indirect tests, in situations in which people presumably are not trying to remember. In the same experiments that produced mood-congruent recall, there was at ﬁrst a notable failure to ﬁnd moodcongruent diﬀerences on indirect tests. Some researchers anticipated this outcome, predicting that prior conceptual processing, so advantageous for strategic retrieval tasks, is unimportant for nonstrategic indirect tests (e.g., Williams et al., 1988). If mood-congruent memory relies on diﬀerences during initial conceptual processing, mood congruence—like other conceptual manipulations, in this line of reasoning—should not characterize performance on indirect tests (also see Denny & Hunt, 1992). An exception to the initial rule was reported by Ruiz-Caballero and González (1994), who found evidence of mood congruence on a stem-completion task. In this indirect test, beginning letters of both previously read words and new words are provided, along with instruction to complete the stems with the ﬁrst words that come to mind. Such a test can easily be turned into an explicit test of memory-as-object if participants begin to use the stems as cues for deliberate recall, even on occasional trials (see Watkins et al., 1992). Responding to these concerns about the process purity of the test, Ruiz-Caballero and González manipulated intention to learn in a second experiment. This manipulation aﬀected levels of free recall (which followed stem completion), but not levels of “priming” on stem completion, although performance on both tests showed evidence of mood congruence. If the participants engaged in deliberate recall on the stemcompletion test, the authors argued, performance on that test should have shown eﬀects of intention to learn. But, as Chapman and Chapman (1973) alerted us, the two memory tests might be diﬀerentially sensitive to the manipulation of intention to learn, while showing similar diﬀerences according to emotional valence. The provision of stems might compensate for the lack of intentionality in the unintentional condition and thereby overwhelm the eﬀect of intentional learning, while nevertheless cuing recall in mood-congruent ways. Therefore, doubts about mood-congruent uses of memory as tool remained. Evidence for mood-congruent memory from tests of stem completion is surprising, particularly to a reader in a transfer-appropriate-processing frame of

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mind. Among others, Roediger and McDermott (1992) discussed the importance of the match between types of processing at “study” and test. Moodcongruent thoughts during initial exposure should facilitate similar thoughts, but not perceptions, at the time of testing, regardless of whether memory is used as tool or object. Word-stem cues should function more perceptually than conceptually. Therefore, mood-congruent performance on stem completion should not occur. In hindsight, it now seems clear that prior habits of reading moodcongruent words can sometimes facilitate performance on so-called perceptually driven tests (e.g., unprimed word identiﬁcation, as used by Von Hippel, Hawkins, & Narayan, 1994, and stem completion of both old and new items, as reported by Bazin et al., 1994). Nevertheless, it was rare to see or to expect to see evidence of mood-congruent memory on tests lacking a substantial reliance on conceptual processing. Taking Roediger and McDermott’s (1992) suggestion to use conceptual indirect tests, Watkins and his associates (Watkins, Martin, & Stern, 2000; Watkins, Vache, Verney, Muller, & Mathews, 1996) have found mixed evidence of mood-congruent performance by clinically depressed participants. Watkins et al. (1996) found it on a test of free association, but there was no accompanying assurance against contamination by explicit remembering. Using both perceptual and conceptual indirect tests, Watkins et al. (2000) found evidence of mood congruence following a conceptual orienting task, but only on one conceptually driven test, the test they called word retrieval (in which one produces words when cued by dictionary deﬁnitions). Again, we can’t be sure that participants were unaware of the memorial nature of the task or that they did not attempt to remember deliberately if they were aware. Contamination on indirect tests by deliberate remembering should not undermine interest in the many ways that habits of thought can inﬂuence memory. No doubt, all tests that reﬂect prior experience do so through a mixture of automatic and recollective processes (see Jacoby, 1991). Even so, it is important to know whether instances in which memory is used primarily as a tool for understanding current experience are aﬀected by habits of negative thinking in depression, and in this regard more evidence is needed. Obtaining that evidence in the laboratory is likely made more diﬃcult by problems in controlling the thoughts that should come to mind on indirect tests. Finding conceptual tests that do not invite deliberate uses of memory as object and, at the same time, produce eﬀects that override other sources of ﬂuency from the past has been diﬃcult. Thinking of words from deﬁnitions might work because other words cannot be used, but tests of free associations may invite too many extra-experimental responses. In other words, memory-as-tool is hard to control experimentally. A general-purpose or prototypical tool might work better in experimental demonstrations of implicit bias. Past habits of thinking inﬂuence performance on current tasks not only because the exact thought keeps returning (the realworld analog for the indirect test of memory as tool) but also because past-

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related thoughts guide current thoughts. Recent experiments in my lab illustrate this point (Hertel, Mathews, Peterson, & Kintner, in press). An initial “training” phase was designed to encourage either negative or nonnegative interpretations of homographs as participants judged semantic relatedness (e.g., pursue vs. celery, in relation to stalk). The subsequent task directed participants to form images of individual words, none of which had been used during training and many of which were homographs with both negative and nonnegative interpretations; performance in this task reﬂected the bias established during training. The training phase in this line of research is intended to model what happens naturally when prior habits of thought inﬂuence current interpretations in emotionally biased ways. The inﬂuence itself is an example of memory, put to use as tool, although we tend not to think about it that way. Our typical impressions about memorial inﬂuences more often occur in conjunction with being reminded about our personal past.

Memory as Autobiographical Experience Habits of thought and rumination often include memories of events from the personal past. Some of the earliest evidence for mood-congruent memory in depression was obtained in autobiographical studies (e.g., Clark & Teasdale, 1982), with accompanying interpretations that related mood congruence to habits of thinking. Now, direct evidence of this linkage is available. Using the same set of ruminative or distracting procedures previously used to aﬀect the temporary mood of dysphoric students, Lyubomirsky et al. (1998) produced diﬀerentially negative biases in autobiographical recall. In experiment 1, Lyubormirsky et al. (1998) randomly assigned dysphoric and nondysphoric students to engage in 8 minutes of rumination or distraction and then requested free recall of events from their lives. Following recall, the students rated the hedonic tone of the memories they produced. Dysphoric students who had ruminated prior to recall rated their memories as less positive and more negative than students in the other three conditions did. The same pattern of results was obtained in experiment 2, in which the students were prompted to recall two happy and two unhappy events, and in experiment 3, in which the students judged frequency of occurrence in their lives for 10 positive and 10 negative events listed by the experimenter. In experiment 4, students were instructed to think aloud during the rumination or distraction phase, and their thoughts were recorded. The ﬁrst six autobiographical memories mentioned in the tapes were rated for negativity and unhappiness by independent judges. The same pattern of mood congruence occurred: dysphoric students who ruminated produced more negative memories, compared to those who were distracted and compared to nondysphoric students in both conditions. All experiments also produced the pattern of eﬀects on mood ratings described previously in this chapter: only the dysphoric students felt more or less sad and depressed as a function

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of rumination or distraction, respectively. In summary, ruminative thoughts not only aﬀected mood; they also invoked or contained more negatively toned memories from the dysphoric students’ personal pasts. The experiments by Lyubomirsky et al. (1998) could not address the precise nature of the mood-congruent ﬁnding. The authors acknowledge diﬃculties in concluding that the eﬀects in the ﬁrst three experiments pertained to memory instead of merely to ratings exaggerated by rumination. And, of course, in any autobiographical study, we cannot be sure that the memories are accurate (although accuracy issues do not trump all other interests in bias). So, with these qualiﬁcations, it is reasonable to conclude that ruminative habits encourage negative thoughts about the past. Especially those students with a reason for focusing on negative past events were led to do so by a brief ruminative episode. Making a similar point, Rothkopf and Blaney (1991) found clearer evidence of mood-congruent autobiographical recall when students ﬁlled out the BDI prior to the recall test rather than at other times. One interpretation of this type of result points to demand established by the statements on the BDI. Another interpretation, however, posits that a depressed person must become aware of her depressed state for the ruminative memories to be invoked. The self-schema must be “activated” (Beck, 1967). Caught unaware of self, he might sidestep habits of remembering the negative, and then other characteristics of the situation could more powerfully guide performance. The notion that a schema or prototype guides attempts to remember is consistent with a second major characteristic of autobiographical memory in depression, that is, its tendency to be overly general, as if attempts to remember events from one’s life stop short at the categorical level (see the review by Healy & Williams, 1999). Williams, Teasdale, Segal, and Soulsby (2000) provide the example of the cue word “kindness” eliciting the following memory: “My grandmother was always kind to me. She used to take me out when my father got cross” (p. 150). The response referred to a category of events instead of to a (requested) speciﬁc memory. Both positive and negative autobiographical memories tend to be described at this categorical level by depressed people (as well as by those who suﬀer from posttraumatic stress disorder; see chapter 4). This tendency might reﬂect an unconscious habit or a conscious strategy to avoid emotion associated with speciﬁc details (Williams et al., 2000).2 As with so many aspects of depressive cognition, the direction of cause is not at all clear. An overly categorical pattern of thinking and remembering might very well contribute to onset of depressive episodes, as suggested by Beck’s (1967) theory and by hopelessness formulations of depression (Abramson, Metalsky, & Alloy, 1989). Whatever the origin, the style is not so habitual that it cannot be modiﬁed (Williams et al., 2000). There is even evidence that a focus on speciﬁc experience (instead of abstract analysis) can at least temporarily reduce the categorical extent of autobiographical memory (Watkins & Teasdale, 2001). Building new habits to recruit speciﬁc instances can deﬂect a habitual dark-cloud schema and reveal a diﬀer-

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ent self to the rememberer. Of course, this assumption has long been incorporated into the techniques of cognitive-behavioral therapy.

Summary When past events serve as the objects of current thought, these thoughts are both more negative and more abstract for depressed people than for others. Habit’s role in explicit memory bias is depicted in results from manipulations of selfreferential processing and rumination. When memory is being used as a tool for other purposes, however, convincing evidence of similar bias has not yet been established for speciﬁc events, even though common sense tells us that these unintended eﬀects are ubiquitous. After all, these cognitive habits are nothing other than the nondeliberate inﬂuences of past conceptual experiences during current, similar conceptual acts. Interpretive biases, surely established primarily by past experience, are well documented in depression. A primary question about the inﬂuence of cognitive habits on both forms of memory concerns the extent to which the inﬂuence relies on awareness of one’s mood state. Tasks that occur prior to tests for mood-congruent recall include selfreferential judgments of trait words, self-referential images, ruminative training, and a variety of mood-related forms and inventories. These tasks are guaranteed to make one consider one’s mood state. The distracting phrases used by Lyubomirsky et al. (1998) might sidestep mood congruence not merely because mood is temporarily improved but also because other habits of thinking have not been recently exercised. A continuing task for future research is to ask whether negative biases can be invoked without awareness of self. Interpretive and memory biases are not always symmetrical with mood. Depending on the type of “depression” and on the nature of the materials, the depressed participants do not always recall more negative words than positive words, but they do fail to show the positive bias in the nondepressed group. Sometimes they recall negative materials at the same level as the nondepressed group (but fewer positive words). In part, these asymmetries reﬂect other diﬀerences associated with mood and memory—diﬀerences in the degree to which controlled, strategic thoughts are initiated and used. This is the other side of the “habit” coin.

Impaired Control

in Nonhabitual Tasks

Deﬁcient cognitive control sets the stage for habits to emerge. At the same time, thoughts that habitually occupy attention leave little mental room for thoughts about anything else. These assertions of a reciprocal relation between habits of thought and controlled attention characterize theoretical approaches to memory

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in depressed states, particularly when the topic pertains to impaired performance. Memory impairment is one of the frequent complaints of people in depressed states (Beck, 1967). “Control” refers to the operation of cognitive procedures at the opposite end of the continuum from habit (see Jacoby, Jennings, & Hay, 1996). Controlled procedures are initiated with awareness or intent, and their components are not well integrated. From a phenomenological perspective, an individual must decide what to do or think next—quite a strain in depression. No wonder that eﬀort metaphors have been used so often in descriptions of depressed participants’ diﬃculties in tasks that require or reﬂect control (see Hasher & Zacks, 1979; Weingartner, Cohen, Murphy, Martello, & Gerdt, 1981).

Eﬀortful Construction

of Memory as Object

The idea that depressed people have trouble carrying out eﬀortful mental procedures emerged ﬁrst in early studies of intellectual functioning. (See the review by Hartlage, Alloy, Vazquez, & Dykman, 1993.) Only after attention theorists (e.g., Posner & Snyder, 1975) began to write about the control of attention, however, did researchers begin to connect eﬀortful or controlled processing to performance on memory tests (Hasher & Zacks, 1979; Tyler, Hertel, McCallum, & Ellis, 1979). In a nutshell, the idea was that the more eﬀortful or attentiondemanding the process, the more likely that the product would be remembered. Like the levels-of-processing framework popular among memory researchers at that time (Craik & Lockhart, 1972), the connection of cognitive eﬀort to memory was based on assumptions about the strength of memory traces or links in an associative network. In the case of eﬀort, however, strength was thought to directly reﬂect the amount of attention or eﬀort expended during initial processing, instead of the type or level of processing. Orienting tasks vary in the degree of eﬀortful, attention-demanding processes required to complete them; those requiring more eﬀort supposedly produce a stronger memory. This idea was not unlike the idea of diﬃculty, but eﬀort referred to a characteristic of processing, not the task itself. Eﬀort-inducing tasks inspired or required more focused concentration, as revealed by longer latencies to perform a simple secondary task (e.g., Tyler et al., 1979). The applicability of the eﬀort-memory connection to depression was a central feature of Hasher and Zacks’s (1979) often-cited work. Since then, literature reviews and a meta-analysis have supported the idea that depression-related deﬁcits in memory occur primarily when the initial orientation task requires controlled concentration (Burt et al., 1995; Hartlage et al., 1993). Hartlage et al. also described the variety of theoretical accounts of eﬀort’s role in depression-related impairment. Condensed and simpliﬁed, one account connects the concept of reduced attentional control to abnormal frontal function. (See

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Davidson, 2000, for a more recent review.) Another claims that eﬀortful processing is limited by the allocation of resources to personal concerns, presumably for the duration of the depressive episode (e.g., Ellis & Ashbrook, 1988). Implicit or explicit in all eﬀort accounts is the assumption that greater eﬀort produces a memory trace that is more easily found when needed. This assumption, rarely stated quite so simply, is clearly too simple in any form. The ability to focus attention and concentrate—either because the neurotransmitters are fully supplied to the appropriate areas of the brain or because other matters are not more compelling—likely has beneﬁcial consequences for memory, but only when those particular procedures are subject to replication on the test. The intensity of concentration is important to memory only in the sense that it must be suﬃcient to carry out the procedures that will later, when replicated, beneﬁt performance on a memory test. According to a transferappropriate-processing perspective, research should examine that suﬃciency, as well as the match in attentional focus across the occasions of initial exposure and memory test. One obvious way to evaluate the transfer-appropriate claim is to examine the literature on memory as tool-versus-object in depressed states, because both the need for controlled attention and its focus varies across types of tests. If depressed people do not focus on aspects that will later guide performance on memory tests, and if they do not concentrate suﬃciently for later replication, performance should suﬀer, regardless of the “intentionality” of the test or its diﬃculty.

Appropriate Use of Memory

as Tool or Object

Indirect tests of memory are designed to elicit automatic or habitual use of prior experience and often do not require concentrated eﬀort during their performance. Spelling homophones is an example of such a test. It takes little concentration to spell common words read aloud by the experimenter at a fast pace (e.g., week/ weak). Similarly, the orienting tasks prior to the spelling test often require little concentration on one of the two alternative meanings (e.g., while listening to the question: Name the days of the week). Simple spelling and comprehension use habitual procedures. As expected, the dysphoric students’ spelling performance matched that of controls in eﬀects of question-biased meaning; yet in the same experiment, the subsequent use of recognition strategies was impaired in the dysphoric group (Hertel & Hardin, 1990). On the other hand, memory can operate as a tool in performing somewhat more attention-demanding tasks. Even stem- and fragment-completion tests, when not performed habitually, might function as puzzles that require at least momentary eﬀort and concentration, yet the available reports show no evidence of depression-related impairment (in the same experiments that revealed impaired free or cued recall of nonnegative words; e.g., Bazin et al., 1994; Denny

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& Hunt, 1992; Ruiz-Caballero & González, 1994; Watkins et al. 1992).3 Why should we not see occasional evidence of impairment? One possible reason is that it is suﬃcient to have focused attention on the look or sound of the words in the orienting task in order that memory operates as a tool during perceptual indirect tests—tests that might well demand concentration on seeing or hearing them again. Sustained processing of meaning does not boost performance, but any task that discourages attention to words as units might decrease it. For example, consider an experiment that used a word-identiﬁcation test, in which previously presented and nonpresented words were displayed very brieﬂy and back-masked, and the task was merely to try to name the words. Anyone who has tried these tests knows that they require focused attention to “see” the words. To what extent should identiﬁcation beneﬁt from prior exposure (memory as tool)? In the orienting task of one such experiment (Hertel, 1994), I asked participants to evaluate some words according to the degree of roundness in their letters. The words evaluated in this task were identiﬁed more frequently on the subsequent perceptual test than were words not previously exposed, but this eﬀect was smaller for the depressed participants! A reasonable postdiction is that during the orienting task the depressed participants attended less often to the words as integrated units and so were disadvantaged in naming them on the test. Word identiﬁcation beneﬁts from prior lexical processing, even as it requires concentration or eﬀort. Conceptual processing facilitates use of the same concepts later on. Conceptual implicit tests require prior attention to meaning and therefore should reﬂect the extent to which meaning has been fully attended. For example, Jenkins and McDowall (2001) found a depression-related impairment on both free recall and the indirect test of category association, but only for the words that had been generated from antonyms (vs. merely read) during the orienting phase. No clear evidence of impaired fragment completion was found for either the previously generated or previously read words. These results are not as unambiguous as I describe them; for example, baseline performance on the category-association test was low for the depressed group. Nevertheless, the pattern illustrates the importance of transfer-appropriate conceptual processing. And the results also suggest that the depressed participants’ conceptual processing during antonymgeneration was insuﬃcient to support the later production of those concepts during recall or category association. Whether category association functioned purely as a test of memory as a tool cannot be assured, of course. Like the freeassociation task used by Watkins et al. (1996), it might have been contaminated by attempts to remember, particularly in the nondepressed group. Because other category associates are available, the depressed participants could perform the test without concentrating on the past and, therefore, without showing the beneﬁt of prior generation of category members, and a mood-related impairment would thereby result. Depressed people are less likely to devote eﬀort to thinking about the past when the current task can be performed without doing so. This claim receives indirect

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support from a series of problem-solving experiments in which memory for similar past problems operated as tool or object in facilitating solutions for current problems (Hertel & Knoedler, 1996). The logic-based word problems were themselves attention–demanding and quite diﬃcult without prior experience in learning how to solve similar problems. During training, problems were presented for solution attempts, and each (almost always unsuccessful) attempt was followed by experimenter-provided instruction in how to solve that problem. Following the training phase, a series of structurally identical but superﬁcially dissimilar target problems was presented, always without such instruction. Because we were curious about how memory operates as a tool in problem solving, we included a condition to measure spontaneous transfer; in this condition, the training problems were not mentioned during the target series. We also included a condition in which we provided very speciﬁc cues and instructions for using memory for the structurally similar training problem “as object” just prior to presenting each target. In two experiments, these hints for recalling the prior analogy actually disrupted performance by the nondysphoric students. Focusing attention on the details of the past problem while solving a new one seemed to be a transfer-inappropriate use of prior experience; in comparison, more targets were solved when memory for the analogy was allowed to operate as a tool. The dysphoric students performed similarly well, with or without hints to think back, which led us to suspect that they did not sustain attention to the relevant past problem and therefore were not led astray in transfer-inappropriate ways. Attending to important features of the target problem itself beneﬁted from earlier attention to those features of the analog. In predicting performance in the problem-solving experiments, Knoedler and I initially reasoned that if the nondepressed students’ solution rates were similar with and without hints, they might have been using memory as object on their own initiative in the no-hint condition. If this pattern were obtained, we expected to ﬁnd depressive impairments. When the hints turned out to be detrimental for nondepressed students, we inferred that memory for training problems in the no-hint condition operated spontaneously as a tool. In reasoning this way, we did not truly believe that either use was “all or none.” Similarly, most researchers understand that memory usually operates as both tool and object in a variety of memory tasks and that memory tasks are not “process-pure” (Jacoby, 1991). Yet when no attempt is made to determine the degree to which one use of memory contaminates the other use, reasoning about the role of controlled attention in depressive memory is made more diﬃcult. Luckily, Jacoby’s process-dissociation procedure directly addressed the problem of how to examine the separate inﬂuences of tool and object memory. The central method used by Jacoby—and others, subsequently—entails two conditions of instructions: one in which automatic or habitual uses of memory operate in concert with controlled attention to the past and one in which they operate in opposition to each other in producing a response. In recognition tasks,

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for example, participants are instructed to endorse items that either feel familiar or are recollected from a speciﬁc prior task on inclusion trials, whereas on exclusion trials, they are instructed to reject items from that speciﬁc task while endorsing other old items. In the inclusion case, recognition hits are produced by both controlled memory for speciﬁc prior occurrences and habitual procedures of reading or thinking words that were earlier read or thought. The uses of memory operate in concert. In the exclusion case, however, items from the speciﬁc prior task are (erroneously) endorsed only if they produce a feeling of familiarity in the absence of memory for source as object. Habit and control operate in opposition to each other. When independence of the two classes of inﬂuences can be assumed, their estimates can be computed from the proportion of positive recognition responses under the two instructional conditions. The relevance of these procedures to depression-related impairment should be obvious: Unless habits are disrupted during orientation, habitual use of memory as tool should remain intact, and only the estimates of controlled uses of memory as object should reveal the impairment. This indeed is what we found on recognition tests following a conceptual orienting task (Hertel & Milan, 1994). The dissociation was replicated through similar procedures designed for conceptually cued fragment-completion tests (e.g., building-s_o_e) following the reading of meaningful cue-target pairs in the orienting task (e.g., building-stone), (Hertel, 1998; also see Hertel & Meiser, 2000, for a multinomial model applied to those results). Again, the importance of transfer-appropriate attention across orienting task and test is illustrated. To the extent that participants attended to the connection between the cue and target initially, they would be able to attend to it as an object in the past, including the target or excluding it when required by instruction. A less careful focus on the pair initially would make it harder to both exclude and include deliberately on the test. The component of memory that represents the past as the object of attention is the one that shows a deﬁcit associated with depression. However, the mere reading of the word pair during the orienting task makes the target available later, as a completion of the fragment, in the presence or absence of controlled recollection, and this habit-oriented component of memory was unimpaired. Thus, attentional control is indeed a factor in producing memory impairment in depression, when performance relies on the replication of focus across the two occasions.4

Habit as Detriment to Control Poor performance often reﬂects absence of habit in performing a cognitive act. This is why controlled attention is required—to do the nonhabitual and think about things one does not usually think about. Seemingly, all of the reported cases of depression-related impairment involved nonnegative materials—materials unrelated to the personal concerns thought to occupy attention habitually in depression. Habits of negative thinking beneﬁt the controlled use of memory

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for related stimuli, as is the case on tests of mood-congruent recall, but otherwise they can detract. Therefore, attentional control in depression should depend on the suppression of habitual thoughts in the service of focusing elsewhere. A line of research begun by Hasher and Zacks (1988) has shown evidence of inhibition diﬃculties associated with aging that might also characterize depression. Like eﬀort-related diﬃculties, inhibitory diﬃculties in depression could logically arise from fundamental frontal dysfunction, from speciﬁc concerns associated with the depressed state, or from both (see Hertel, 1997). Reliance on an inhibition construct is not the only way to represent the problem of impaired control in the context of habitual thinking. We might slightly shift perspective to propose that control is made more diﬃcult when other habits are strong. Habits of attending (e.g., to negatively toned events) might make the act of disengaging attention more diﬃcult than it otherwise might be in the course of turning attention to a diﬀerent event. At this stage of research, however, the aptness of the metaphor (inhibition vs. disengagement) is less important than gathering evidence for depression-related diﬃculties in turning away from habit-related stimuli in order to do something else. The “something else” in experimental studies has often been the task to respond to a dot or color patch in a screen location that diﬀers from the one occupied by a mood-relevant word (e.g., Bradley, Mogg, & Lee, 1997; McCabe & Gotlib, 1995). Bradley et al. found dysphoria-related biases under conditions of suprathreshold but not subthreshold exposures to the words. They argued that the problem was therefore one of disengaging attention, because a bias in allocating attention to relevant stimuli would pertain for both exposure conditions. Recently, investigators have used the negative-priming paradigm to examine depression-related diﬃculties in disengagement or inhibition. In the standard version of this paradigm, items to be attended and ignored are presented concurrently on each trial, with the attended item on trial X sometimes having served as the ignored item on trial X-1. When the ignored is subsequently attended, or even when the same category of the ignored is now the category of the attended, the judgment for trial X is slowed, compared to control conditions. This slowing (called negative priming) is attributed sometimes to inhibition of the ignored item or category and sometimes to transfer-inappropriate attention (Neill & Mathis, 1998). If depressed people have trouble disengaging from moodrelated thoughts, negative-priming eﬀects should be reduced or absent. Some suggestion of this diﬃculty has been demonstrated in a simple letter-identiﬁcation task after students were induced by music to feel sad (von Hecker, Conway, Meiser, & Holm, 2002). However, Joormann (in press) has used a more conceptually relevant task. She asked nondysphoric and mildly dysphoric students to judge the self-relevance of negative and positive targets while ignoring distractors of the same or opposite valence. All participants took longer to judge the selfrelevance of positive words when positive words had been ignored on the previous trial, compared to previous trials of ignored negative words. This ﬁnding

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roughly corresponds to the typical negative-priming eﬀect. The same pattern of negative priming was obtained for nondysphoric participants in judging negative items after having ignored negative (vs. positive) items, but it was not pertain obtained for mildly dysphoric participants or for those who reported prior episodes of depressed mood. The diﬀerence in these patterns suggests that the participants who tended currently to be in more negative mood states (or reported feeling depressed in the past) ignored the negative adjectives less successfully.5 Diﬃculty in disengaging attention from negative material is more clearly documented in connection with anxiety disorders or high levels of trait anxiety (see Fox, Russo, Bowles, & Dutton, 2001). Again, when researchers use scores on inventories like the BDI or even when they use diagnostic labels to form groups for experimental purposes, their dysphoric or depressed participants are likely to be anxious. In the other direction, ruminative habits more typically attributed to depression also typify anxious states or traits (Nolen-Hoeksema, 2000). Regardless of their lack of speciﬁcity to depression, however, habits of dwelling on the negative have consequences for memory beyond those reported in relation to evidence for mood-congruent memory, and these consequences are not always desirable. One consequence might be trouble in forgetting. Not only do depressed people have trouble ignoring mood-congruent material when they focus on other material presented concomitantly (as in Joormann’s negative-priming studies), they also less successfully suppress mood-congruent material in more sustained attempts. Evidence for diﬃculties in sustained thought suppression has been documented by Wegner, Wenzlaﬀ, and their colleagues (for review, see Wenzlaﬀ & Bates, 1998). Thought suppression, whether accomplished directly or indirectly in the service of thinking about something else, plays an important role in forgetting (see Anderson & Neely, 1996). And forgetting can be a valuable outcome, particularly for the depressed person who might prefer not to ruminate about past events beyond one’s control. Intentional forgetting has been studied in the lab by directing participants to forget items or lists of items.6 Clearly, instructions to forget lists can have their intended eﬀect, particularly when the participants are given something else to think about. To document eﬀects of direct suppression on individual items, Anderson and Green (2001) developed the “think/no-think” procedure. After learning pairs of unrelated words to a ﬁxed criterion, the participants were given a varied number of trials (0, 1, 8, or 16) to practice the retrieval of the second member of some pairs and to practice the suppression of the second member of other pairs. The ﬁrst member of each pair was presented as a cue for either retrieval or suppression. This practice phase was followed by a ﬁnal test of cued recall, in which participants were instructed to recall all of the response words, regardless of previous instruction. In several experiments, the main ﬁnding was increased forgetting as a function of practice in suppression, both when the original studied cues were used at test and when new cues related categorically to

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the response words were used at test. The simple story is that people can successfully suppress to the point of incurring forgetting. Can depressed people do this as well as others? Melissa Gerstle and I have recently conducted an experiment to answer that question (Hertel & Gerstle, in press). To investigate the possibility of mood-congruent suppression, we replicated the procedures developed by Anderson and Green (2001), but with one major change: The cues we used throughout the experiment were adjectives related to the target nouns. On half of the pairs, the adjectives gave the essentially neutral nouns a negative meaning, and on the other half, the meaning was positive. (The materials were fully counterbalanced, e.g., gloomy cottage vs. splendid cottage.) To encourage initial attention to the emotional valence of the materials, in the learning task we instructed participants to construct a self-referential image for each pair and to rate the meaningfulness of the image. These materials and instructions had been used earlier in a recall experiment without suppression instructions, together with other materials in which a third set of adjectives produced neutral concepts when paired with the same nouns (e.g., plain cottage; Hertel & Parks, 2002). In that experiment, dysphoric and nondysphoric participants alike recalled the nouns when they had been given emotional meanings (both positive and negative) more often than when they had been given neutral meanings. In the suppression experiment, Gerstle and I also found that recall was not signiﬁcantly associated with emotional valence for the dysphoric participants (although the controls showed more forgetting of nouns from positive pairs). More important, however, was our ﬁnding that the eﬀect of practicing suppression on later recall was signiﬁcantly reduced in the dysphoric group. The dysphoric participants recalled as many of the rehearsed items as did the nondepressed participant and signiﬁcantly more of the targets that they had practiced suppressing, regardless of the cues’ valence (see ﬁg. 6.1). Similarly, Power, Dalgleish, Claudio, Tata, and Kentish (2000) found evidence for depression-related diﬃculties in one of their three experiments on directed forgetting. Perhaps because their participants were clinically depressed (experiment 3), however, this diﬀerence was restricted to negative adjectives. Recall of positive adjectives—to be remembered or to be forgotten—was no better or worse than that of anxious participants and controls. At the same time that depressed people might have trouble deliberately forgetting self-referential thoughts, they also have trouble remembering what they had been thinking about prior to an episode of self-referential rumination. At least this is true for the controlled component of memory, as estimated through process-dissociation procedures on a test of cued fragment completion (Hertel, 1998). In the experiment previously mentioned, we inserted what might be seen as an interference phase between the initial orienting task of reading word pairs and the ﬁnal memory phase. We assigned a third of the dysphoric and control participants to merely sit and wait for 7 minutes, another third to ruminate, and the ﬁnal third to think about other matters, such as geographical locations. The

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Nondys Respond

Nondys Suppress

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Intervening Task Figure 6.1. The mean percentage of targets recalled on the final test, after depressed and nondepressed participants had practiced retrieving or suppressing them in response to cues. (Adapted from “Depressive Deficits in Forgetting,” by P. T. Hertel and M. Gerstle, in press, Psychological Science. Copyright © 2003 by the American Psychological Society.)

latter two groups actually underwent the rumination or distraction procedures used by Nolen-Hoeksema and Morrow (1993) that I described elsewhere in this chapter. Following the period of self-focus in the rumination condition, the dysphoric participants showed impaired control on the memory test (relative to the other participants), much like those who simply waited during the 7-minute interval. However, the participants who thought about objects and locations showed no depression-related impairment in control (see ﬁg. 6.2). In addition to improving mood under some conditions (e.g., Lyubormirsky et al., 1998), distraction also seems to improve controlled attention to the past when the rememberer is depressed. And because the distracted group showed no impairment, it is tempting to infer that even those who merely waited for 7 minutes focused on suﬃciently compelling matters that thinking back during the memory test was made more diﬃcult. Inherent in those results (Hertel, 1998) are the ﬁnal two points of this chapter: situations that permit mind wandering invite habitual thinking and impair memory for other matters. Deﬁcient performance is not, therefore, an inevitable outcome of depression, because habits can be opposed in ways that beneﬁt control.

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Mean Estimated Recollection

0.5

Nondysphoric Dysphoric

0.4 0.3 0.2 0.1 0 Wait

Ruminate

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Intervening Task Figure 6.2. The mean estimate of controlled retrieval by dysphoric and nondysphoric participants, following an intervening period of waiting for 7 minutes, entertaining ruminative thoughts, or entertaining distracting thoughts. Adapted from “The Relationship between Rumination and Impaired Memory in Dysphoric Moods,” by P. T. Hertel, 1998, Journal of Abnormal Psychology, 107, p. 170. Copyright © 1998 by the American Psychological Association.

Opposing Habit Through Control Here is the prototype of the depressed rememberer as constructed by the ﬁndings described thus far: she (well, yes, she) is someone who habitually ruminates about personal concerns and other negative events and whose interpretations and perceptions reﬂect those habits; someone who tends to remember negatively aﬀective events more often or remembers events as more negatively toned; and someone whose memory for neutral or positive events is occasionally impaired, at least when attention is allowed to stray to habitual patterns. This person seems to have little cognitive self-control. (One can almost hear her grandmother’s admonishments.) I use “self-control” to imply that the most important aspect of impaired control in depression is control initiated by the self. Controlled attention to any stimulus can be facilitated by the environment; the structure of the task, stimulus salience, and its interest value are some of the relevant dimensions. Cognitive self-control is merely a convenient term for referring to the focusing, switching, and sustaining of attention under conditions where stimulus and task dimensions do not play obvious roles. In structural terms, self-control is loosely analogous to the central executive component of working memory (Baddeley & Hitch, 1974). Its physical components are frontal functions; indeed, much of the evidence for depression-related diﬀerences in brain activity implicates activity in the prefrontal cortex (see Davidson, 2000; Heller & Nitschke, 1998). Similar

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behavioral evidence is supplied by Channon (1996), who found impairments on a neuropsychological test of frontal function—the Wisconsin Card Sorting Test (WCST)—even in a sample of dysphoric college students. Furthermore, by statistically controlling for correlations with BDI scores, Davis and Nolen-Hoeksema (2000) found WCST diﬀerences associated with the tendency to ruminate. Selfreported ruminators made more perseverative errors on the WCST and failed to maintain set more often than did nonruminators. In a basic sense, then, cognitive self-control is a problem in depression, as well as a problem for people who tend to ruminate. A good simple example of the memory problems associated with depressive deﬁcits in self-control or initiation is impaired prospective memory in the absence of reminding cues (Rude, Hertel, Jarrold, Covich, & Hedlund, 1999). Depressed and control participants were instructed at the start of the session to press a function key every 5 minutes during their performance of an ongoing test of general knowledge. The depressed participants checked the time less often and thereby made more errors on the prospective task. Reduced self-control aﬀects performance in memory experiments under conditions of poor external control. For example, dysphoric students’ performance yielded lowerestimates of controlled recollection in my cued-fragment-completion study (1998) after a period of lax external control. Doing nothing for 7 minutes presented ample opportunity for mind wandering, because the dysphoric students had more trouble subsequently turning attention to the task of remembering. Although this depression-related impairment in controlled recollection was closely mimicked by data from participants in the rumination condition, it is not certain that the “waiting” students also ruminated during that period. For some, the break from the ongoing experiment might have invited mind blanking. As a learned response to stress, the habit to “tune out” might be just as reﬂective of poor self-control as the habit to ruminate. Watts, MacLeod, and Morris (1988) found that blanking tended to occur in tasks that involve planning (tapping frontal functions). Although we know too little about blanking in comparison to mind wandering or rumination, either type of habit should take over during periods of lax external control of the procedures to be performed. As I have argued previously (1997, 2000), lax external control often typiﬁes real-world thinking, and it sometimes characterizes the trials that constitute the orienting task in laboratory experiments. The orienting task is, according to eﬀort metaphors and other processing frameworks, the critical period in determining whether the material will be recalled later. Therefore, in allowing suﬃcient time on each trial for the elaborative processing that beneﬁts recall, memory researchers also encourage habits of mind wandering or blanking. Years ago, Stephanie Rude and I used a simple manipulation of either allowing an orienting decision to be made at any time during an 8-second exposure or requiring the decision at the end of the trial, along with a repetition of the target word. (The decision concerned whether a target word ﬁt sensibly into a sentence frame.) We called the

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two conditions unfocused and focused, respectively (Hertel & Rude, 1991a). Inthe focused condition, the materials did not stay on the screen for the 8-second period, as they did in the unfocused condition. To perform each trial in the focused condition, the participants had to hold the word and decision in mind for the duration of the trial, but their minds could wander in the unfocused condition because decisions could be reported early on during the 8 seconds. On the subsequent test of free recall, depressed participants from the unfocused condition performed poorly, compared to their nondepressed counterparts. This deﬁcit, however, was eliminated for participants who had been required to focus during the orienting task. The depressed participants’ ability to perform the task could not ever have been at issue. The task was not diﬃcult in either condition (even though it had been used previously as an example of an eﬀortful orienting task by Tyler et al., 1979, and Ellis, Thomas, & Rodriguez, 1984). Indeed, the more diﬃcult condition clearly was the focused one, because it required sustained attention. Therefore, instead of making the task easier to accomplish, the focusing instruction structured the task transfer-appropriately. Participants were required to attend to the recent past (a few seconds earlier) in the same way that they were later required to attend to the past during the recall test. Moreover, external control compensated for poor self-control by not allowing habits of thought (or no-thought) to carry the day. There were a number of variations of this attention-focusing procedure (Hertel & Rude, 1991b). We also tried to stiﬀen the requirements at the time of the test by using a forced-recall procedure. Although “forcing” the participants to write a certain number of words on the recall test merely increased levels of recall for everyone in our experiments, others have found that this procedure eliminated the depression-related deﬁcit (e.g., Murray et al., 1999). The forcing procedure counteracts a possibly conservative response tendency, but it does so by asking the participant to refocus attention on the past events, which might be at least as important as overcoming hesitancy or conservatism. Other methods of improving performance by providing external support have not always been successful. For example, in the recognition experiment with process-dissociation procedures, Milan and I reinstated the original context word in some test conditions. That procedure boosted estimates of controlled recollection for both dysphoric and nondysphoric participants (Hertel & Milan, 1994). Clearly, the nondysphoric students had done something that we had failed to capture by the manipulation. This was also true when recognition was much more strategically dependent (Hertel & Hardin, 1990). Hardin and I noticed that the nondysphoric students seemed to be using their performance on the prior indirect test of homophone-spelling to decide whether the recognition item had occurred in the original set of questions (e.g., Week/Weak? Did I just spell that word? How did I spell it? And was that word in a question? Oh, name the days of the week? Yes.). In a subsequent experiment, we asked participants to answer a similar set of questions before making each recognition judgment. By doing so,

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we found a pattern of dependency in the dysphoric group that mimicked the pattern of nondysphoric judgments under unassisted conditions, but the nondysphoric participants who got the set of question cues outwitted us. Their performance improved even for those items that they had spelled in the opposite way (e.g., Week/Weak? Did I just spell that word? Weak? Is there another way to spell it?). These and similar diﬀerences illustrate the diﬃculty in predicting exactly what people do under conditions of lax external control, but the ﬁndings also show that performance in depressed states can be improved by at least some version of external support. And the main point is that this support works because it forestalls the emergence of cognitive habits in depression—habits that interfere under poorly controlled conditions and make it diﬃcult for the depressed person to take control and show cognitive initiative (see Hertel, 2000). Habits of thought are diﬃcult to oppose. The historically important construct of habit strength in Hull’s theory of learning (1943) was opposed by the construct of inhibition, but Hull’s rats experienced immediate consequences—missing reward—that led to the orderly development of inhibitory strength. The consequences of thought are often much farther removed, so suppressing a turn of the mind is perhaps much harder to learn than is suppressing a turn in the maze. Modern approaches to thought suppression acknowledge this diﬃculty. Wegner’s ironic-processes theory (1994), for example, includes a construct called a monitor that checks whether thoughts are being successfully suppressed. According to this point of view, the depressed person’s need to suppress self-concerns, particularly during tasks that require self-control and initiative, presumably “activates” the monitor and ironically brings those concerns back to mind. At the very least, any attention devoted to the task of suppression likely disrupts procedures that require sustained attention or planning. Instructions to suppress are therefore much harder to follow when not accompanied by a task that directs attention through external means. The short version of that argument is that simple self-controlled thought suppression likely does not work well for depressed people, both in the sense of potentiating later forgetting (Hertel & Gerstle, in press) or freeing attention to focus in ways that later beneﬁt remembering. In the latter case, what works best is environmental support, but the world is not often arranged to be helpful. What also seems to work in the sense of improving both memory and momentary mood is a good distraction procedure (e.g., Hertel, 1998; Lyubormirsky et al., 1998). Distraction at least interrupts ongoing habitual thoughts so that the depressed person begins the recall task on even footing. There is even some reason to wonder if reappraisals of intrusive thoughts, under some circumstances, might aid recall of nonnegative events through temporary mood improvement or altered perspective (in the manner found by Rusting & DeHart, 2000; also see Parrott & Spackman, 2000). However, are these measures enough? According to Teasdale et al. (2000) and others, approximately 80% of people diagnosed with major depressive disorder experience recurrent depressive epi-

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sodes. Practical considerations therefore encourage us to consider not merely the opposition of habitual thinking by controlled procedures but the training of new habits through practice in control. Virtually the only line of research with that general aim is the research on mindfulness training, adapted from the meditation work of Kabat-Zinn by Teasdale, Williams, and Segal. The training consists of a sustained focus on some simple act (typically breathing). When attention wanders, the individual acknowledges the new thought or feeling but then redirects attention to the simple act. It diﬀers from simple thought suppression in two main respects: acknowledgment of the thought and practice in redirection. Do the beneﬁts of such training extend to long-term habits of control? So far, Williams et al. (2000) have found that mindfulness training boosts the eﬀects of cognitive-behavioral therapy in reducing overly general autobiographical memory by formerly depressed participants. Moreover, for people with at least three prior episodes of depression, the addition of mindfulness training to cognitive-behavioral therapy signiﬁcantly reduced recurrence during the subsequent year (Teasdale et al., 2000). These studies, of course, are merely a beginning. In short, the best antidote to maladaptive habits is a new set of habits—not the opposite sort of habits recommended by Pollyanna and the teachings of Norman Vincent Peale (1956) and not the habits of suppression as recommended by certain grandmothers but the habits of thought control. Cognitive control, as conceived by cognitive psychologists, is a concept that opposes habit, in that habitual procedures require little attention. But if the necessary control procedures—awareness of the wandering stream of thought and subsequent disengagement, for example—are practiced “religiously,” they too can become habitual. In the absence of mind wandering and rumination, memory biases are less extreme, and memory impairment is repaired.

Notes 1. Induction procedures are particularly useful when it is diﬃcult to determine the content of natural thought, although some procedures do not produce memorial eﬀects that mimic patterns in natural depression. For a case in which they fail to show mood-congruent recall in the same study in which it was obtained for dysphoric students, see Kwiatkowski and Parkinson (1994; also see Eich & McCaulay, 2000; Perrig & Perrig, 1988). Inductions have also been used to study mood-dependent memory: better memory when mood at initial encounter matches mood at test. Mood-dependent memory has also been studied with participants diagnosed with bipolar disorder. When the “mood” during initial encounter (mania or depression) matched the mood at test, higher levels of recall or recognition were found (Eich, Macaulay, & Lam, 1997; Weingartner, Miller, & Murphy, 1977). See Blaney (1986, p. 237) for a discussion of how mood-dependent memory can be seen as a special case of mood-congruent memory. 2. Ironically, overgeneral tendencies have also been correlated with spontaneous

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intrusions of stressful memories (Brewin, Reynolds, & Tata, 1999; Wessel, Merckelbach, & Dekkers, 2002). 3. In one exception to the early rule, Elliott and Greene (1992) did show impaired word-stem completion and homophone spelling but omitted unprimed items on the test, which might have encouraged participants’ awareness of the memorial goal and a concomitant use of memory as object. (See Bazin et al., 1994, and Roediger & McDermott, 1992, for full discussions of their design.) 4. Of course, attention might well be impaired during initial exposure. Consider a report by Rokke, Arnell, Koch, and Andrews (2002), who investigated the size of attentional blinks in a rapid-serial-visual-presentation paradigm (RSVP) administered to students with varying degrees of dysphoria. Moderately to severely dysphoric participants performed relatively well when the only task was to detect the presence of a single letter in the stream of rapidly presented letters. However, their performance suﬀered more, compared to that of nondysphoric or mildly dysphoric participants, when the task also involved attention to a letter occurring earlier in the stream (a deeper attentional blink). This outcome implicates fundamental deﬁcits in redirecting attention. 5. Some of the results reported in this section should be viewed cautiously, given either unexpected diﬀerences on baseline trials (e.g., Joormann, in press) or lack of information about baseline (e.g., Bradley et al., 1997). 6. Studies using this directed forgetting paradigm have revealed interesting diﬀerences associated with clinical disorders. For example, Sonntag et al. (2003) have shown that schizophrenics fail to show eﬀects of directed forgetting on measures of recollection (see chapter 7). McNally, Metzger, Lasko, Clancy, and Pitman (1998) found poor directed forgetting of trauma words by women with posttraumatic stress disorder, as well as deﬁcits in remembering neutral and positive words on the lists to be remembered (see chapter 4).

References Abramson, L. Y., Metalsky, G. I., & Alloy, L. B. (1989). Hopelessness depression: A theory-based subtype of depression. Psychological Review, 96, 358–372. Alloy, L. B., Abramson, L. Y., & Francis, E. L. (1999). Do negative cognitive styles confer vulnerability to depression? Current Directions in Psychological Science, 8, 128–132. Anderson, M. C., & Green, C. (2001). Suppressing unwanted memories by executive control. Nature, 410, 366–369. Anderson, M. C., & Neely, J. H. (1996). Interference and inhibition in memory retrieval. In E. L. Bjork & R. A. Bjork (Eds.), Memory (pp. 237–313). New York: Academic Press. Baddeley, A., & Hitch, G. J. (1974). Working memory. In G. Bower (Ed.), The psychology of learning and motivation (Vol. 7, pp. 47–89). New York: Academic Press. Bazin, N., Perruchet, P., De Bonis, M., & Féline, A. (1994). The dissociation of explicit and implicit memory in depressed patients. Psychological Medicine, 24, 239–245.

210

  

Beck, A. T. (1967). Depression: Clinical, experimental and theoretical aspects. New York: Harper & Row. Beck, A. T., Ward, C., Mendelson, M., Mock, J., & Erbaugh, J. (1961). An inventory for measuring depression. Archives of General Psychiatry, 4, 561–571. Blaney, P. H. (1986). Aﬀect and memory: A review. Psychological Bulletin, 99, 229– 246. Bower, G. H. (1981). Mood and memory. American Psychologist, 36, 129–148. Bradley, B., & Mathews, A. (1983). Negative self-schemata in clinical depression. British Journal of Clinical Psychology, 22, 173–181. Bradley, B. P., Mogg, K., & Lee, S. C. (1997). Attentional biases for negative information in induced and naturally occurring dysphoria. Behaviour Research and Therapy, 35, 911–927. Brewin, C. R., Reynolds, M., & Tata, P. (1999). Autobiographical memory processes and the course of depression. Journal of Abnormal Psychology, 108, 511–517. Brown, T. A., Di Nardo, P. A., Lehman, C. L., & Campbell, L. A. (2001). Reliability of DSM-IV anxiety and mood disorders: Implications for the classiﬁcation of emotional disorders. Journal of Abnormal Psychology, 110, 49–58. Burt, D. B., Zembar, M. J., & Niederehe, G. (1995). Depression and memory impairment: A meta-analysis of the association, its pattern, and speciﬁcity. Psychological Bulletin, 117, 285–305. Channon, S. (1996). Executive dysfunction in depression: The Wisconsin Card Sorting Test. Journal of Aﬀective Disorders, 39, 107–114. Chapman, L. J., & Chapman, J. P. (1973). Problems in the measurement of cognitive deﬁcits. Psychological Bulletin, 79, 380–385. Clark, D. M., & Teasdale, J. D. (1982). Diurnal variation in clinical depression and accessibility of memories of positive and negative experiences. Journal of Abnormal Psychology, 91, 87–95. Craik, F. I. M., & Lockhart, R. S. (1972). Levels of processing: A framework for memory research. Journal of Verbal Learning and Verbal Behavior, 11, 671–684. Danion, J.-M., Willard-Schroeder, D., Zimmermann, M.-A., Grange, D., Schlienger, J.-L., & Singer, L. (1991). Explicit memory and repetition priming in depression. Archives of General Psychiatry, 48, 707–711. Davidson, R. J. (2000). Aﬀective style, mood, and anxiety disorders: An aﬀective neuroscience approach. In R. J. Davidson (Ed.), Anxiety, depression, and emotion (pp. 88–108). New York: Oxford University Press. Davis, R. N., & Nolen-Hoeksema, S. (2000). Cognitive inﬂexibility among ruminators and nonruminators. Cognitive Therapy and Research, 24, 699–711. Deldin, P. J., Keller, J., Gergen, J. A., & Miller, G. A. (2001). Cognitive bias and emotion in neuropsychological models of depression. Cognition & Emotion, 15, 787–802. Denny, E. B., & Hunt, R. R. (1992). Aﬀective valence and meory in depression: Dissociation of recall and fragment completion. Journal of Abnormal Psychology, 101, 575–580. Derry, P. A., & Kuiper, N. A. (1981). Schematic processing and self-reference in clinical depression. Journal of Abnormal Psychology, 90, 286–297. Dobson, K. S., & Shaw, B. F. (1987). Speciﬁcity and stability of self-referent encoding in clinical depression. Journal of Abnormal Psychology, 96, 36–40.

     

211

Eich, E., & Macaulay, D. (2000). Are real moods required to reveal mood-congruent and mood-dependent memory? Psychological Science, 11, 244–248 Eich, E., Macaulay, D., & Lam, R. W. (1997). Mania, depression, and mood dependent memory. Cognition & Emotion, 11, 607–618. Elliott, C. L., & Greene, R. L. (1992). Clinical depression and implicit memory. Journal of Abnormal Psychology, 101, 572–574. Ellis, H. C., & Ashbrook, P. W. (1988). Resource allocation model of the eﬀects of depressed mood states on memory. In K. Fiedler & J. Forgas (Eds.), Aﬀect, cognition and social behavior (pp. 25–43). Toronto: Hogrefe. Ellis, H. C., Thomas, R. L., & Rodriguez, I. A. (1984). Emotional mood states and memory: Elaborative encoding, semantic processing, and cognitive eﬀort. Journal of Experimental Psychology: Learning, Memory, and Cognition, 10, 470– 482. Fennell, M. J. V., Teasdale, J. D., Jones, S., & Damle, A. (1987). Distraction in neurotic and endogenous depression: An investigation of negative thinking in major depressive disorder. Psychological Medicine, 17, 441–452. Fox, E., Russo, R., Bowles, R., & Dutton, K. (2001). Do threatening stimuli draw or hold attention in subclinical anxiety? Journal of Experimental Psychology: General, 130, 681–700. Gotlib, I. H., & McCann, C. D. (1984). Construct accessibility and depression: An examination of cognitive and aﬀective factors. Journal of Personality and Social Psychology, 47, 427–439. Haaga, D. A., Dyck, M. J., & Ernst, D. (1991). Empirical status of the cognitive theory of depression. Psychological Bulletin, 110, 215–236. Hartlage, S., Alloy, L. B., Vazquez, C., & Dykman, B. (1993). Automatic and eﬀortful processing in depression. Psychological Bulletin, 113, 247–278. Hasher, L., & Zacks, R. T. (1979). Automatic and eﬀortful processes in memory. Journal of Experimental Psychology: General, 108, 356–388. Hasher, L., & Zacks, R. T. (1988). Working memory, comprehension, and aging: A review and a new view. In G. H. Bower (Ed.), The psychology of learning and motivation (Vol. 22, pp. 193–225). San Diego, CA: Academic Press. Healy, H., & Williams, J. M. G. (1999). Autobiographical memory. In T. Dalgleish & M. Power (Eds.), The handbook of cognition and emotion (pp. 229–242). Chichester: Wiley. Heller, W., & Nitschke, J. B. (1998). The puzzle of regional brain activity in depression and anxiety: The importance of subtypes and comorbidity. Cognition & Emotion, 12, 421–447. Hertel, P. T. (1994). Depressive deﬁcits in word identiﬁcation and recall. Cognition & Emotion, 8, 313–327. Hertel, P. T. (1997). On the contributions of deﬁcient cognitive control to memory impairments in depression. Cognition & Emotion, 11, 569–584. Hertel, P. T. (1998). The relationship between rumination and impaired memory in dysphoric moods. Journal of Abnormal Psychology, 107, 166–172. Hertel, P. T. (2000). The cognitive-initiative account of depression-related impairments in memory. In D. Medin (Ed.), The psychology of learning and motivation (Vol. 39, pp. 47–71). New York: Academic Press.

212

  

Hertel, P. T., & Gerstle, M. (in press). Depression-related deﬁcits in forgetting. Psychological Science. Hertel, P. T., & Hardin, T. S. (1990). Remembering with and without awareness in a depressed mood: Evidence of deﬁcits in initiative. Journal of Experimental Psychology: General, 119, 45–59. Hertel, P. T., & Knoedler, A. J. (1996). Solving problems by analogy: The beneﬁts and detriments of hints and depressed moods. Memory & Cognition, 24, 16–25. Hertel, P. T., Mathews, A., Peterson, S., & Kintner, K. (in press). Transfer of training emotionally biases interpretations. Applied Cognitive Psychology. Hertel, P. T., & Meiser, T. (2000). Capacity and procedural accounts of impaired memory in depression. In U. von Hecker, S. Dutke, & G. Sedek (Eds.), Generative mental processes and cognitive resources: Integrative research on adaptation and control (pp. 283–308). Dordrecht, The Netherlands: Kluwer Academic Publishers. Hertel, P. T., & Milan, S. (1994). Depressive deﬁcits in recognition: Dissociation of recollection and familiarity. Journal of Abnormal Psychology, 103, 736–742. Hertel, P. T., & Parks, C. (2002). Emotional episodes facilitate word recall. Cognition & Emotion, 16, 685–694. Hertel, P. T., & Rude, S. S. (1991a). Depressive deﬁcits in memory: Focusing attention improves subsequent recall. Journal of Experimental Psychology: General, 120, 301–309. Hertel, P. T., & Rude, S. S. (1991b). Recalling in a state of natural or induced depression. Cognitive Therapy and Research, 15, 103–127. Hull, C. L. (1943). Principles of behavior. New York: Appleton-Century-Crofts. Ingram, R. E. (1990). Self-focused attention in clinical disorders: Review and a conceptual model. Psychological Bulletin, 107, 156–176. Jacoby, L. L. (1991). A process dissociation framework: Separating automatic from intentional uses of memory. Journal of Memory and Language, 30, 513–541. Jacoby, L. L., Jennings, J. M., & Hay, J. F. (1996). Dissociating automatic and consciously controlled processes: Implications for diagnosis and rehabilitation of memory deﬁcits. In D. Herrmann, C. McEvoy, C. Herzog, P. T. Hertel, & M. K. Johnson (Eds.), Basic and applied memory research: Theory in context (pp. 161– 194). Mahwah, NJ: Erlbaum. Jacoby, L. L., & Kelley, C. M. (1987). Unconscious inﬂuences of memory for a prior event. Personality and Social Psychology Bulletin, 13, 314–336. Jenkins, W., & McDowall, J. (2001). Implicit memory and depression: An analysis of perceptual and conceptual processes. Cognition & Emotion, 15, 803–812. Joormann, J. (in press). Attentional bias in dysphoria: The role of inhibitory processes. Cognition & Emotion. Kwiatkowski, S. J., & Parkinson, S. R. (1994). Depression, elaboration, and mood congruence: Diﬀerences between natural and induced mood. Memory & Cognition, 22, 225–233. Lawson, C., MacLeod, C., & Hammond, G. (2002). Interpretation revealed in the blink of an eye: Depressive bias in the resolution of ambiguity. Journal of Abnormal Psychology, 111, 321–328. Lyubomirsky, S., Caldwell, N. D., & Nolen-Hoeksema, S. (1998). Eﬀects of rumina-

     

213

tive and distracting responses to depressed mood on retrieval of autobiographical memories. Journal of Personality and Social Psychology, 75, 166–177. Matt, G. E., Vazquez, C., & Campbell, W. K. (1992). Mood-congruent recall of aﬀectively toned stimuli: A meta-analytic review. Clinical Psychology Review, 12, 227–255. McCabe, S. B., & Gotlib, I. H. (1995). Selective attention and clinical depression: Performance on a deployment-of-attention task. Journal of Abnormal Psychology, 104, 241–245. McCabe, S. B., & Toman, P. E. (2000). Stimulus exposure duration in a deploymentof-attention task: Eﬀects on dysphoric, recently dysphoric, and nondysphoric individuals. Cognition & Emotion, 14, 125–142. McNally, R. J., Metzger, L. J., Lasko, N. B., Clancy, S. A., & Pitman, R. K. (1998). Directed forgetting of trauma cues in adult survivors of childhood sexual abuse with and without posttraumatic stress disorder. Journal of Abnormal Psychology, 107, 596–601. Morris, C. D., Bransford, J. P., & Franks, J. J. (1977). Levels of processing versus transfer-appropriate processing. Journal of Verbal Learning and Verbal Behavior, 16, 519–533. Murray, L. A., Whitehouse, W. G., & Alloy, L. B. (1999). Mood congruence and depressive deﬁcits in memory: A forced-recall analysis. Memory, 7, 175–196. Neill, W. T., & Mathis, K. M. (1998). Transfer-inappropriate processing: Negative priming and related phenomena. In D. Medin (Ed.), The psychology of learning and motivation (Vol. 38, pp. 1–44). New York: Academic Press. Nolen-Hoeksema, S. (1991). Responses to depression and their eﬀects on the duration of depressive episodes. Journal of Abnormal Psychology, 100, 569–582. Nolen-Hoeksema, S. (2000). The role of rumination in depressive disorders and mixed anxiety/depressive symptoms. Journal of Abnormal Psychology, 109, 504–511. Nolen-Hoeksema, S., & Morrow, J. (1993). The eﬀects of rumination and distraction on naturally occurring depressed moods. Cognition & Emotion, 7, 561–570. Parrott, W. G., & Hertel, P. T. (1999). Research methods in cognition and emotion. In T. Dalgleish & M. Power (Eds.), The handbook of cognition and emotion (pp. 61– 81). Chichester: Wiley. Parrott, W. G., & Spackman, M. P. (2000). Emotion and memory. In M. Lewis & J. Haviland-Jones (Eds.), Handbook of emotions (2nd ed., pp. 476–490). New York: Guilford. Peale, N. V. (1956). The power of positive thinking. Englewood Cliﬀs, NJ. Perrig, W. J., & Perrig, P. (1988). Mood and memory: Mood-congruity eﬀects in absence of mood. Memory & Cognition, 16, 102–109. Polyani, M. (1958). Personal knowledge: Toward a post-critical philosophy. Chicago: University of Chicago Press. Posner, M. I., & Snyder, C. R. R. (1975). Attention and cognitive control. In R. L. Solso (Ed.), Information processing and cognition: The Loyola Symposium (pp. 55– 85). Hillsdale, NJ: Erlbaum. Powers, M. J., Dalgleish, T., Claudio, V., Tata, P., & Kentish, J. (2000). The directed forgetting task: Application to emotionally valent material. Journal of Aﬀective Disorders, 57, 147–157.

214

  

Roediger, H. L., & McDermott, K. B. (1992). Depression and implicit memory: A commentary. Journal of Abnormal Psychology, 101, 587–591. Rokke, P. D., Arnell, K. M., Koch, M. D., & Andrews, J. T. (2002). Dual-task attention deﬁcits in dysphoric mood. Journal of Abnormal Psychology, 111, 370–379, Rothkopf, J. S., & Blaney, P. H. (1991). Mood congruent memory: The role of aﬀective focus and gender. Cognition & Emotion, 5, 53–64. Rude, S. S., Hertel, P. T., Jarrold, W., Covich, J., & Hedlund, S. (1999). Remembering to remember: A diﬃculty for depressed individuals? Cognition & Emotion, 13, 267–276. Rude, S. S., Wenzlaﬀ, R. M., Gibbs, B., Vane, J., & Whitney, T. (2002). Negative processing biases predict subsequent depressive symptoms. Cognition & Emotion, 16, 423–440. Ruiz-Caballero, J. A., & González, P. (1994). Implicit and explicit memory bias in depressed and nondepressed subjects. Cognition & Emotion, 8, 555–569. Rusting, C. L., & DeHart, T. (2000). Retrieving positive memories to regulate negative mood: Consequences for mood-congruent memory. Journal of Personality and Social Psychology, 78, 737–752. Sonntag, P., Gokalsing, E., Olivier, C., Robert, P., Burglen, F., Kauﬀmann-Muller, F., et al. (2003). Impaired strategic regulation of contents of conscious awareness in schizophrenia. Consciousness and Cognition, 12, 190–200. Teasdale, J. D. (1983). Negative thinking in depression: Cause, eﬀect, or reciprocal relationship? Advances in Behavior Research and Therapy, 5, 3–26. Teasdale, J. D., Segal, Z. V., Williams, J. M. G., Ridgeway, V. A., Soulsby, J. M., & Lau, M. A. (2000). Prevention of relapse/recurrence in major depression by mindfulness-based cognitive therapy. Journal of Consulting and Clinical Psychology, 68, 615–623. Tyler, S. W., Hertel, P. T., McCallum, M. C., & Ellis, H. C. (1979). Cognitive eﬀort and memory. Journal of Experimental Psychology: Human Learning and Memory, 5, 607–617. Von Hecker, U., Conway, M., Meiser, T., & Holm, S. (2002). Inhibition deﬁcits in dysphoric mood. Manuscript submitted for publication. Von Hippel, W., Hawkins, C., & Narayan, S. (1994). Personality and perceptual expertise: Individual diﬀerences in perceptual identiﬁcation. Psychological Science, 5, 401–406. Watkins, E., & Teasdale, J. D. (2001). Rumination and overgeneral memory in depression: Eﬀects of self-focus and analytic thinking. Journal of Abnormal Psychology, 110, 333–357. Watkins, P. C., Martin, C. K., & Stern, L. D. (2000). Unconscious memory bias in depression: Perceptual and conceptual processes. Journal of Abnormal Psychology, 109, 282–289. Watkins, P. C., Mathews, A., Williamson, D. A., & Fuller, R. D. (1992). Mood-congruent memory in depression: Emotional priming or elaboration? Journal of Abnormal Psychology, 101, 581–586. Watkins, P. C., Vache, K., Verney, S. P., Muller, S., & Mathews, A. (1996). Unconscious mood-congruent memory bias in depression. Journal of Abnormal Psychology, 105, 34–41.

     

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Watts, F. N., MacLeod, A. K., & Morris, L. (1988). Association between phenomenal and objective measures of concentration problems in depressed patients. British Journal of Psychology, 79, 241–250. Weingartner, H., Cohen, R. M., Murphy, D. L., Martello, J., & Gerdt, C. (1981). Cognitive processes in depression. Archives of General Psychiatry, 38, 42–47. Weingartner, H., Miller, H., & Murphy, D. L. (1977). Mood-state-dependent retrieval of verbal associations. Journal of Abnormal Psychology, 86, 276–284. Wegner, D. M. (1994). Ironic processes of mental control. Psychological Review, 101, 34–52. Wenzlaﬀ, R. M., & Bates, D. E. (1998). Unmasking a cognitive vulnerability to depression: How lapses in mental control reveal depressive thinking. Journal of Personality and Social Psychology, 75, 1559–1571. Wenzlaﬀ, R. M., Meier, J., & Salas D. M. (2002). Thought suppression and memory biases during and after depressive moods. Cognition & Emotion, 16, 403–422. Wenzlaﬀ, R. M., Rude, S. S., Taylor, C. J., Stultz, C. H., & Sweatt, R. A. (2001). Beneath the veil of thought suppression: Attentional bias and depression risk. Cognition & Emotion, 15, 435–452. Wessel, I., Merckelbach, H., & Dekkers, T. (2002). Autobiographical memory specificity, intrusive memory, and general memory skills in Dutch-Indonesian survivors of the World War II era. Journal of Traumatic Stress, 15, 227–234. Williams, J. M. G., Teasdale, J. D., Segal, Z. V., & Soulsby, J. (2000). Mindfulnessbased cognitive therapy reduces overgeneral autobiographical memory in formerly depressed patients. Journal of Abnormal Psychology, 109, 150–155. Williams, J. M. G., Watts, F. N., MacLeod, C., & Mathews, A. (1988). Cognitive psychology and emotional disorders. New York: Wiley.

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7

, ,      - ,  ,  ,   

T

he conceptualization of schizophrenia has changed radically over the past decade. Cognitive deﬁcits are now viewed as core symptoms and major disabilities of the disease (Green, 1996); virtually all cognitive functions are considered defective (Aleman, Hijman, de Haan, & Kahn, 1999; Heinrichs & Zakzanis, 1998). Among these deﬁcits, memory impairments likely play a crucial role. Not all cognitive abilities are equally aﬀected; several studies have shown that memory functions are disproportionately impaired (e.g., Bilder et al., 2000; Gold, Randolph, Carpenter, Goldberg, & Weinberger, 1992; Heinrichs & Zakzanis, 1998; Palmer et al., 1997; Saykin et al., 1991, 1994). Moreover, memory impairments are strongly correlated with disturbed functioning in everyday life (Green, 1996), and a large part of clinical work (e.g., collecting historical information; conducting psychodynamic, behavioral, or cognitive therapies; ensuring medication compliance) relies on the ability of the patient to learn and remember. In normal subjects, the evidence that memory is strongly inﬂuenced by emotions is overwhelming (e.g., Blaney, 1986; Bower, 1981; Conway & Pleydell-Pearce, 2000). Memory for emotional events is better than memory for neutral events, a phenomenon known as the emotionality eﬀect (e.g., Dutta & Kanungo, 1975; Rubin & Friendly, 1986). Moreover, memory for positive events is often better than memory for negative events—a diﬀerence attributed to the Pollyanna tendency (Boucher & Osgood, 1969), a disposition for normal subjects to construct an aﬀectively positive world view. Finally, normal subjects exhibit better memory for events whose emotional valence is congruent with their current mood (mood-congruent memory). How do memory and emotion interact in patients with schizophrenia? Do these patients exhibit a particular diﬃculty in remembering emotional events? Do they still show the Pollyanna tendency? Is there any impairment of the subjective experience of retrieving 217

emotional memories? Because emotional disturbances, which interfere dramatically with behavior control and with social interaction, are another major aspect of schizophrenia (Taylor & Liberzon, 1999), the answers to these questions are crucial for the development of cognitive models of schizophrenia that take emotions into account. They may help us identify the mechanisms underlying the formation and the persistence of poorly understood symptoms comprising a strong emotional component, such as delusional experience. In this chapter, we begin by reviewing the studies of memory impairment and emotion disturbances in schizophrenia. Then we discuss experimental investigations of how memory and emotion interact in schizophrenia. Because conscious awareness, which plays a crucial role both in memory and emotion, may represent the fundamental impairment in schizophrenia (Andreasen, 1999; Danion, Huron, & Robert, 2001; Frith, 1992), we emphasize not only objective accuracy of memory but also states of awareness associated with emotional memories.

Memory Impairment in

Schizophrenia

The Dissociation of Performance in

Explicit and Implicit Memory Tasks

The long-term memory impairment associated with schizophrenia is selective. Whether patients with schizophrenia display a deﬁcit of performance depends on the task. Several studies have shown that patients display normal or quasinormal performance in implicit memory tasks—that is, when participants are not asked to retrieve material consciously. This pattern has been demonstrated in tasks exploring perceptual priming (Clare, McKenna, Mortimer, & Baddeley, 1993; Doniger, Silipo, Rabinowicz, Snodgrass, & Javitt, 2001; Gras-Vincendon et al., 1994), conceptual priming (Schwartz & Winstead, 1985), and procedural memory (Clare et al., 1993; Dominey & Georgieﬀ, 1997; Michel, Danion, Grangé, & Sandner, 1998; Schwartz, Rosse, Veazey, & Deutsch, 1996). It has also been demonstrated in implicit learning tasks (Danion, Meulemans, KauﬀmannMuller, & Vermaat, 2001). In accordance with these ﬁndings, Kazès et al. (1999), who used the process dissociation procedure (Jacoby, 1991) to obtain uncontaminated estimates of memory processes, found that automatic inﬂuences of memory, but not consciously controlled uses of memory, were intact in schizophrenia. In contrast to normal performance in implicit memory tasks, impaired performance is typically observed in explicit or episodic memory tasks. This impairment has been consistently demonstrated in free-recall (Koh & Peterson, 1978), cuedrecall (Schwartz, Rosse, & Deutsch, 1993), and, to a lesser degree, recognition tasks (Aleman et al., 1999; Calev, 1984a, 1984b). Episodic memory impairment

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occurs for verbal material, such as words, sentences (Koh & Peterson, 1978), and stories (Abbruzzese & Scarone, 1993); visual material, such as faces (Addington & Addington, 1998); and contextual information, such as space and time (Rizzo, Danion, Van der Linden, & Grangé, 1996; Rizzo, Danion, Van Der Linden, Grangé, & Rohmer, 1996). Autobiographical memories (memories for personal events and facts from one’s life) are also aﬀected. Patients with schizophrenia display an abnormal pattern of memories when theirs are compared to those of healthy individuals: the most severe impairment occurs for early adulthood memories, childhood memories are quasi-normal, and recent past memories are deﬁcient to a lesser extent (Feinstein, Goldberg, Nowlin, & Weinberger, 1998). Finally, despite diﬃculties with explicit memory, patients with schizophrenia remain able to learn (Goldberg, Weinberger, Pliskin, Berman, & Podd, 1989; Hawkins, 1999), although their learning curve is lower than normal (Aleman et al., 1999).

Recognition Memory

and Associated Subjective States

of Conscious Awareness

Most of the memory investigations carried out in normal controls and patients with schizophrenia primarily concern the objective accuracy of recall and recognition of stimuli. However, what often matters most is not the objective fact that we can say an event occurred but what it feels like and means to us to remember what took place. Recently, in recognition of the importance of subjective experience, many researchers have shifted their focus from questions about the absolute accuracy of memories and toward questions about the states of awareness accompanying memories. The notion of conscious awareness is pivotal to the distinction between explicit and implicit tasks. Therefore, we can infer from the pattern of learning and memory dysfunction observed in schizophrenia that memory is impaired when conscious awareness is required at encoding or at retrieval and is spared when conscious awareness is not required. In other words, conscious awareness might be the critical determinant of memory impairment both at encoding and at retrieval. However, this inference can be questioned because explicit and implicit memory tasks assess conscious awareness only indirectly, from an objective, or third-person, perspective. To obtain direct evidence of impaired conscious awareness, we should investigate the experiences of an individual from a subjective, or ﬁrst-person, perspective. Tulving (1985) was the ﬁrst to propose a ﬁrst-person approach to conscious awareness associated with recognition memory. According to Tulving, conscious awareness associated with recognition memory is not a unitary phenomenon. It includes at least two distinct subjective states that may be investigated experimentally using the Remember/Know procedure (R/K; Gardiner, Java, & RichardsonKlavehn, 1996; Tulving, 1985). In a recognition task, the participants are asked

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to report their subjective state of awareness at the time they recognize each individual item. They are instructed to make a Remember response if they consciously recollect something they experienced when they learned the item, that is, if they relive mentally the learning episode. This qualitatively rich mental experience includes perceptual, spatial, temporal, semantic, and emotional details that are attributed to a past event (Johnson, Hashtroudi, & Lindsay, 1993; Johnson & Raye, 1981). The participants are instructed to make a Know response if recognition is accompanied by feelings of familiarity yet no speciﬁc memories for the learning episode. Many experiments carried out with normal controls and the R/K procedure have shown functional dissociations between Remember and Know responses; these ﬁndings indicate that the two responses index two distinct states of conscious awareness (Gardiner et al., 1996; Gardiner & RichardsonKlavehn, 2000; Rajaram & Roediger, 1997; Yonelinas, Kroll, Dobbins, Lazzara, & Knight, 1998). Remember responses are inﬂuenced by variables that increase the salience of the events, or make them more distinctive: For instance, a deeper level of processing enhances the frequency of Remember, but not Know, responses (Gardiner, 1988). Know responses, on the other hand, depend on the ease with which an item can be processed either perceptually or conceptually: Repetition test priming increases Know responses, without inﬂuencing Remember responses (Rajaram, 1993). Moreover, neuropsychological data from brain-lesioned patients and brain imaging studies carried out in normal controls indicate that Remember and Know responses rely on diﬀerent neural correlates (Duzel, Yonelinas, Mangun, Heinze, & Tulving, 1997; Henson, Rugg, Shallice, Josephs, & Dolan, 1999; Smith, 1993). Using the R/K procedure, Huron et al. (1995; also see Huron, Danion, Rizzo, Killofer, & Damiens, in press) and Danion, Rizzo, and Bruant (1999) studied patients with schizophrenia. They showed that recognition performance of patients was associated with low levels of Remember, but not Know, responses, as compared to performance of normal controls. Impairment of conscious recollection was attributed to a failure of strategic processes at encoding, at retrieval, or at both points. Episodic memories are not a literal reproduction of the past but instead depend on constructive and reconstructive processes that are sometimes prone to errors, distortions, and illusions (e.g., Schacter, Norman, & Koutstaal, 1998). Recently developed paradigms for investigating false memories (memories for events that never happened) have been used to address issues in constructive memory. Using both the R/K procedure and the procedure initially introduced by Deese (1959) and subsequently modiﬁed by Roediger and McDermott (1995) to investigate false memories, Huron and Danion (2002) showed that the frequency of false memories was lower in patients with schizophrenia than in normal controls. These low levels of false memories were associated with a reduced frequency of Remember, but not Know, responses. Danion, Gokalsing, Robert, Massin-Krauss, and Bacon (2001) also showed that schizophrenia impairs the relationship between subjective experience and behavior, suggesting that pa-

220

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tients’ behavior is less determined by subjective experience, and less controlled by intentions, than that of normal controls. This is reminiscent of the traditional view that schizophrenia is characterized by a dissociation between thought and action (Bleuler, 1911). Because conscious recollection provides a basis for decision and action and a foundation for social relationships, these ﬁndings may have important clinical implications. Reduced conscious recollection leads to poor ability to apprehend subjective experiences in all their richness and may account for many behavioral disturbances exhibited by patients with schizophrenia (Danion, Huron, et al., 2001).

Emotional Disturbances

in Schizophrenia

According to a number of authors (e.g., Damasio, 1995; Ekman, 1993; Lazarus, 1991; Mandler, 1984; Zajonc, 1984), emotions are best conceptualized as a concatenation of cognitive evaluation with changes in body and brain state, arising in response to particular events or mental images. As the consequences of how people construe situations, emotions diﬀer according to the complexity of the cognitive evaluation from which they stem. In some situations, this evaluation may be rudimentary, whereas in others the full complex emotion can develop only with substantial reasoning about the situation and its implications. Body state changes correspond to physiological modiﬁcations, many perceptible to an external observer; examples include changes in skin color, facial expression, or skin conductance. Brain changes correspond to the activation of speciﬁc cerebral regions and produce cognitive processing modiﬁcations; some of these modiﬁcations—such as the rate at which images are produced or the ﬂuency with which aﬀective stimuli are processed—are perceptible to the individual in whom they are enacted. In addition to these evaluative and physiological components, emotions may involve consciousness when the subject becomes aware of the link between emotion and the causal event. The implication of conscious awareness and its experiential dimension explains why, in humans, emotions are not only closely related to adaptive behavior at an automated level but also oﬀer the ﬂexibility of response based on memory for emotional events from the personal past. A primary function of emotions is to make thought, action, and social interaction more eﬀective (Lazarus, 1991).

Inappropriate or Flat Aﬀect Emotional disturbances such as inappropriate or ﬂat aﬀect are a cardinal symptom of schizophrenia. An inappropriate aﬀect is one that is discordant with the content of the patient’s speech or ideation; sudden and unpredictable changes in aﬀect may also occur. In ﬂat aﬀect, there is little or no aﬀective expression in

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general and a reduced range of facial expression in particular. The mechanism underlying this symptom has long been controversial. On the one hand, ﬂat aﬀect has been taken as evidence that the primary emotional disturbance in schizophrenia is an inability to experience pleasure, that is, anhedonia (e.g., Rado, 1962). According to this view, the absence of pleasure is a central feature of schizophrenia; hence, the diminished expression of positive emotions is secondary to anhedonia. On the other hand, classical authors such as Bleuler (1911) noticed that, although patients often report that they experience strong emotions, observers do not always conﬁrm their reports. He believed that patients do experience emotions but that expression is blunted. Experimental evidence relevant to this debate has been obtained from laboratory studies. A disjunction between expressed and subjectively experienced emotions has been shown using emotion-eliciting ﬁlms: patients with schizophrenia experience as many positive and negative emotions as normal controls, but they are less facially expressive of both positive and negative emotions (Kring, Kerr, Smith, & Neale, 1993; Kring & Neale, 1996). Myin-Germeys, Delespaul, and deVries (2000) recently assessed emotional experience of patients with schizophrenia and normal controls in daily life. They used a structured time-sampling technique to collect the data. Participants received a digital wristwatch and a set of assessment forms. Ten times a day on 6 consecutive days, the watch emitted a beep at unpredictable moments between 7:30 AM and 10:30 PM. After every beep, reports of thoughts, current activity, moods, and severity of symptoms were collected. The assessment forms contained 10 Likert-type items about positive and negative emotions. Patients were divided into blunted and nonblunted subgroups on the basis of Brief Psychiatric Rating Scale behavioral ratings of ﬂat aﬀect. Patients with schizophrenia experienced more intense and more variable negative emotions than normal controls did. In contrast, they experienced less intense and less variable positive emotions. This ﬁnding, at variance with evidence from laboratory studies that patients experience the same intensities of positive emotions as normal controls do, may be explained by the absence of social context in laboratory studies. Patients with schizophrenia may indeed be capable of experiencing the same positive emotions as normal controls but, in the naturalistic context of daily life, engage less often in situations likely to elicit positive experiences. These patterns of emotion were observed whether the patients were emotionally blunted or not. In another study that used the same structured time-sampling technique, Myin-Germeys, van Os, Schwartz, Stone, and Delespaul (2001) provided additional evidence that patients with psychotic illness reacted with more intense negative emotions to subjective appraisals of stress in daily life than did controls. In summary, these results bear out the view that patients with schizophrenia are more emotionally active and responsive than what is usually assumed on the basis of behavioral observations and facial modiﬁcations perceptible to an external observer. In some circumstances, patients may experience more intense negative emotions and,

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possibly, less intense positive emotions than controls do. Therefore, the identiﬁcation of the circumstances in which patients with schizophrenia do experience emotions like controls and those in which they do not is a prerequisite for the investigation of how memory and emotion interact.

Cognitive Evaluation

of Emotional Events

A large body of experimental evidence shows that patients with schizophrenia fail to recognize emotion in others (see the review by Bryson, Bell, & Lysaker, 1997; Walker, Marwit, & Emory, 1980). Whether this deﬁcit reﬂects speciﬁc disturbances or is part of a more generalized impairment, such as, for instance, attentional, executive or evaluative functions, is a matter of debate. Kerr and Neal (1993) have shown that patients with schizophrenia do not exhibit greater impairment in aﬀect recognition than in nonemotional perception tasks. However, evidence from two studies that varied the emotional valence of words in working memory tasks suggests that patients with schizophrenia may still be sensitive to the emotional salience of stimuli. Koh, Szoc, and Peterson (1977) used pleasant, unpleasant, and neutral words in a Sternberg task.1 Despite their overall poorer performance, patients, like normal controls, were faster for neutral words than for pleasant and unpleasant words. Moreover, in both groups, there was no diﬀerence between pleasant and unpleasant words. Kay (1982) used a modiﬁcation of the Brown-Peterson task (Wickens, 1970) to investigate whether patients with schizophrenia were sensitive to the emotional salience of to-be-learned words. Participants were presented with three trials involving word triads (e.g., love, excellent, rest) drawn from a single aﬀective valence (e.g., positive) and then switched to the opposite aﬀective valence on the fourth trial (e.g., negative). After each trial, participants performed a distractor task over a short retention interval before recalling the word triads. Patients with schizophrenia performed progressively worse across trials but returned to the level of the ﬁrst trial for the fourth trial, namely, when the aﬀective valence shifted. This increase in performance induced by the shift of aﬀective valence indicates a release of proactive interference, suggesting that patients with schizophrenia were still sensitive to the aﬀective salience of the to-be-learned words. This ﬁnding is consistent with evidence from studies conducted in normal controls showing that words elicit an emotional evaluation automatically or with minimal strategic processes and conscious cognitive eﬀort (review in Ochsner, 2000). In summary, these ﬁndings suggest that patients with schizophrenia exhibit defective emotional processing when a highly complex or very speciﬁc cognitive evaluation of the emotional stimuli is required, such as recognizing, discriminating, and interpreting emotions in others. In contrast, patients remain sensitive to the emotional valence of stimuli when cognitive evaluation is more automatic.

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Body State Changes Body state changes arising in response to emotional events have been widely investigated in schizophrenia with measurements of skin conductance. Forty to 50% of patients with schizophrenia exhibit a reduced phasic response of skin conductance to orienting stimuli (review in Bernstein, 1987). But patients may also exhibit a tonic hyperactivity of skin conductance (Dawson, Nuechterlein, Schell, Gitlin, & Ventura, 1994). Finally, in the study using emotion-eliciting ﬁlms, Kring and Neale (1996) showed that, compared to normal controls, patients with schizophrenia evidenced greater reactivity of skin conductance to positive and negative ﬁlms. Yet they also exhibited greater reactivity to neutral ﬁlms than controls did. Thus, while they were reporting comparable levels of subjectively experienced emotions, the patients were more electrodermally aroused. The pattern of ﬁndings provided by these studies is complex: the level of physiological responses to emotional events is sometimes lower and sometimes higher in patients with schizophrenia than in normal controls. It suggests that schizophrenia is associated with a dysregulation of body responses, rather than a reduced reactivity to emotional events (Taylor & Liberzon, 1999).

Brain State Changes Advances in functional brain imaging have recently made it possible to investigate the functional brain correlates of mood changes in schizophrenia. Schneider et al. (1998) used functional magnetic resonance imaging to examine brain activity in patients with schizophrenia and normal controls during happy and sad mood induction. To induce happy and sad mood, researchers presented the participants with stimuli that consisted of happy and sad facial expressions. They were required to look at each face and use it to help them to feel happy or sad. In line with previous ﬁndings, results show brain activity in the amygdala of normal controls during negative aﬀect. Unlike controls, patients with schizophrenia did not demonstrate amygdala activation during sadness, despite similar subjective ratings of negative aﬀect. Using morphological procedures, researchers have reported structural abnormalities of the amygdala in schizophrenia (Bogerts, 1993). The absence of amygdala activation is consistent with the hypothesis that the inappropriate behavior displayed by patients with schizophrenia in an emotional context is related to a dysregulation of dopamine systems resulting from functional impairment of the amygdala (Louilot & Besson, 2000). Interestingly, three independent studies of patients with schizophrenia have recently shown that the response of dopamine terminals to systemic administration of amphetamine, a dopaminergic agonist, is enhanced (Abi-Dargham et al., 1998; Breier et al., 1997; Laruelle et al., 1996). However, to the best of our knowledge, there is no published study in which brain imaging techniques were used to investigate in patients with schizophrenia the functional brain cor-

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relates of emotions arising speciﬁcally in responses to discrete emotional events. In particular, in view of the dopamine hypothesis about schizophrenia and of the role putatively played by dopamine in response to emotional stimuli, investigating the inﬂuence of emotional stimuli on dopamine responses in patients with schizophrenia should be revealing (Taylor & Liberzon, 1999). Moreover, because most patients are treated with neuroleptic drugs, that is, dopamine blockers, evaluating the inﬂuence of treatment on the diﬀerent components of emotion should be worthwhile.

Implications for Research Both clinical and experimental ﬁndings show that schizophrenia is associated with an impairment of diﬀerent components of emotions, including evaluative processes and body and brain correlates. They also show that patients with schizophrenia often exhibit a disjunctive relationship among expressive, subjective, and biological dimensions of emotions, indicating that the diﬀerent components of emotion may not be defective altogether. In particular, the impairment of the expressive and biological dimensions does not necessarily imply a disturbance of the emotions subjectively experienced by the patient, which seem to be preserved in some situations. Moreover, patients are still sensitive to the emotional salience of events, provided that the cognitive evaluation of emotional valence is relatively automatic. Whether the subjective experience of emotion is intact depends on the type of information processing each emotional event requires. How emotion and memory interact in patients with schizophrenia should depend primarily on whether the sensitivity to the emotional salience of stimuli is intact. We can therefore conclude from these studies that emotional words, which elicit a cognitive evaluation of the emotional valence that can take place automatically, may represent appropriate stimuli for investigating the relationship between emotion and memory. Moreover, full-blown investigations of this relationship should include not only memory assessments but also measurements of body and brain changes induced by emotional memories.

Interaction of Emotion and

Memory in Schizophrenia

In comparison to the numerous studies that have addressed the issue of emotional disturbances, experimental evidence pertaining to the interaction of emotion and memory in schizophrenia is rare. With the exception of one study (Koh, Grinker, Marusarz, & Forman, 1981) that used photographs as to-be-memorized stimuli, all others used emotional words. None of them investigated the body and brain correlates of emotional memories. A series of studies (Kayton & Koh, 1975;

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Koh et al., 1981; Koh, Kayton, & Peterson, 1976) compared the impact of the emotional valence of to-be-learned words on recall performance in patients with schizophrenia and normal controls. As a collection, these studies consistently showed that normal controls recalled signiﬁcantly more pleasant words than unpleasant words, therefore exhibiting a Pollyanna tendency. In contrast, the studies did not provide consistent results in schizophrenia. Kayton and Koh used a free-recall task involving pleasant, unpleasant, and neutral words in 17 patients with schizophrenia and 12 normal controls. The results showed an absence of the Pollyanna tendency in schizophrenia: patients recalled pleasant words to the same extent as unpleasant words. Moreover, in comparison with the performance of normal controls, their recall performance for pleasant words, but not for unpleasant and neutral words, was impaired. In a second study, Koh, Kayton, and Peterson used a set of recall tasks to investigate the recall performance of patients with schizophrenia when they were asked to rate the pleasantness of words during the encoding phase. This orienting task was used to make sure that all participants encoded the aﬀective valence of words to be recalled. The set of recall tasks included an incidental free-recall task in which participants assessed the pleasantness of the words but were not aware that they would have to recall them; an intentional free-recall task, in which participants were instructed to learn the words that they rated; and a cued recall task in which recall was cued by diﬀerent emotional categories (e.g., pleasant or unpleasant). For all these recall tasks, the results showed that patients, like normal controls, tended to recall pleasant words more often than unpleasant words. However, this Pollyanna tendency was not statistically signiﬁcant in incidental free recall by the group of patients with schizophrenia. Interestingly, across all these tasks, the recall performance of patients with schizophrenia was not defective: they recalled as many words as did the controls. This pattern of results led the authors to conclude that both the recall deﬁcit and the absence of a Pollyanna tendency observed in their previous study of patients with schizophrenia was remediable when patients encoded the words according to their emotional features. Unfortunately, numerous methodological ﬂaws marred the study by Koh et al. (1976). For instance, the words used in the incidental free-recall task were the same words participants had to recall in the subsequent cued-recall task. Similarly, the words that they had to recall in the intentional free-recall task had been used previously as distractors in a recognition task. These methodological concerns limit the conclusions that can be drawn from these ﬁndings. Moreover, another study (Koh et al., 1981) using the same orienting task produced inconsistent results: Although overall recall performance was comparable in patients with schizophrenia and normal controls, the Pollyanna tendency was absent in patients. In a second experiment, Koh et al. investigated the interaction between memory and emotion in schizophrenia using items characterized by a separation of target (photographs of faces) and emotional information (favorable or unfavorable personality-trait words). They conﬁrmed the absence of a Pollyanna

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tendency in schizophrenia: controls recognized signiﬁcantly more favorably than unfavorably encoded faces, but this asymmetry was absent in patients. Finally, in a more recent study, Calev and Edelist (1993) investigated the eﬀect of the emotional valence of words on the rate of forgetting. They compared immediate and delayed recall of neutral, positive, and negative words in patients with schizophrenia and normal controls. The results showed that patients, like normal controls, forgot neutral words more rapidly than emotional words but forgot negative words less rapidly than positive words, whereas normal controls exhibited equivalent forgetting rates for positive and negative words. Moreover, patients with schizophrenia recalled fewer words than normal controls in both immediate and delayed recall tasks. These ﬁndings do not provide a clear picture of the impact of emotion on memory in schizophrenia. Indeed, some studies (Kayton & Koh, 1975; Koh et al., 1981) that revealed a defective Pollyanna tendency in schizophrenia suggest that the memory performance of patients with schizophrenia might be less inﬂuenced by the emotional valence of stimuli than that of normal controls. In contrast, Koh et al. (1976) reported an intact Pollyanna tendency that suggests that the memory performance of patients remains inﬂuenced by the emotional valence of words.2 Similarly, the more rapid forgetting of positive than negative words in schizophrenia reported by Calev and Edelist (1993) suggests that the emotional valence of the words to-be-learned still has an inﬂuence on patients’ memory.

An Investigation of the Inﬂuence

of Emotional Words on Recall

Performance in Schizophrenia

In view of these inconsistent results, we investigated the emotionality eﬀect in schizophrenia using words as emotional stimuli. Because patients with schizophrenia are sensitive to the emotional salience of words (Kay, 1982; Koh et al., 1977), we predicted that they should recall more emotional words than neutral words, even though they might recall fewer words overall in comparison to controls. However, to investigate whether a putative impairment of the emotionality eﬀect could be remediable, we asked each subject to complete two sessions. In the ﬁrst session, participants were asked to remember the words, no mention being made of their emotional component. The second session was identical to the ﬁrst one, with the exception that it included an additional orienting task in which we explicitly asked participants to assess the emotional dimension of words (Koh et al., 1981; Koh et al., 1976). Method Twenty-four clinically stabilized patients (10 men, 14 women) fulﬁlling DSM-III-R criteria for schizophrenia took part in the study. Twenty-two patients were receiving a long-term neuroleptic treatment (M = 561 mg of chlorpromazine or equivalent, SD = 410 mg), whereas 2 patients were drug free.

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Global psychiatric symptomatology (36.4, SD = 24.5) was assessed using the Brief Psychiatric Rating Scale (BPRS). Positive (24.5, SD = 27.6) and negative (38.4, SD = 31.1) symptoms were assessed using the Scale for the Assessment of Positive Symptoms (SAPS) and the Scale for the Assessment of Negative Symptoms (SANS), respectively (Andreasen, 1982). The normal control group comprised 24 participants (10 men, 14 women). The groups did not diﬀer signiﬁcantly in age (31.3 years, SD = 24.5, and 31.8 years, SD = 8.0, respectively) or education (11.0 years, SD = 4.8, and 11.4 years, SD = 3.0). Words were selected on the basis of their emotional valence (details of word selection procedure can be found in Danion, Kauﬀmann-Muller, Grangé, Zimmermann, & Greth, 1995; Grangé, Greth, & Danion, 1991). There were two lists of 30 words, each with 10 positive, 10 negative, and 10 neutral words, randomly selected from each of the three valence categories. Positive, negative, and neutral words were mixed in each list. The participants completed two sessions, separated by at least 24 hours. In the study phase of each session, the participants were exposed to the words of one list. The lists were counterbalanced across sessions within each group. The two sessions diﬀered in study instructions. In the ﬁrst session, we asked the participants to read the words aloud and remember them, no mention being made of the emotional component of words. We attempted to equalize recall performance for neutral words in both groups by giving more opportunity to patients than controls to learn the words and by shortening the delay between the study and test phases of the recall task. Normal controls were given 2 seconds per word and patients 5 seconds. In the second session, they were asked to read the words aloud, to remember them, and to perform an orienting task that required them to rate the words on a 100 mm visual analogue scale according to their subjective feelings of pleasantness and unpleasantness. Normal controls were given 5 seconds and patients 10 seconds per word. The test phases were conducted 10 minutes after the study phases in the control group and 3 minutes after in the patients group. In each of the two test phases, the participants were asked to write in 3 minutes as many words from the study list as possible. Finally, at the end of the second test phase, they were asked to rate the emotional valence of the words of the list presented in the ﬁrst study phase. Results and Discussion For each subject, we computed the mean ratings of positive, negative, and neutral words. Patients and normal controls discriminated among positive, negative, and neutral words to the same extent. In normal controls, the mean ratings for positive words (70.6, SD = 10.8) were higher than those for neutral words (52.8, SD = 7.2), which were higher than those for negative words (28.3, SD = 14.3). A similar proﬁle was observed in patients (67.5, SD = 14.4; 56.9, SD = 10.1; 32.2, SD = 17.7, respectively). An analysis of variance (ANOVA) carried out on these ratings yielded a signiﬁcant word type eﬀect,

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Mean Percent Recalled

F(2, 88) = 91.2, p < .0001, but neither the group eﬀect nor the interaction between group and word type was signiﬁcant. The mean proportions of words recalled were subjected to an ANOVA, with word type (positive vs. negative vs. neutral) and encoding condition as withinsubject factors and group as a between-subject factor. Figure 7.1 displays the results pooled across the two sessions; recall performance was not aﬀected by the orienting task, as indicated by a lack of a signiﬁcant eﬀect of encoding conditions or interactions (all Fs < 1). Patients recalled fewer words than controls, F(1, 46) = 9.80, p < .005. This result indicated that the attempt to equalize recall performance in the two groups failed, probably as a consequence of the severity of the memory impairment that characterized the patients. There was a signiﬁcant word-type eﬀect, F(2, 92) = 5.98, p < .005; the mean proportion of recalled words was signiﬁcantly higher for positive words compared to neutral words, t(47) = 3.35, p < .002, and for negative words compared to neutral words, t(47) = 2.81, p = .007. The diﬀerence between positive and negative words was not signiﬁcant, nor was the interaction between group and word type. Therefore, as we predicted, while patients’ recall performance was poor, both groups recalled emotional words better than neutral words. This pattern of performance was observed under conditions in which patients and normal controls discriminated between positive, negative, and neutral words to the same degree. It was independent of whether emotional encoding was induced by an orienting task forcing the participants to process the emotional valence of words. Although the hypothesis that participants deliberately noticed valence in the ﬁrst task, regardless of instructions, cannot be excluded, this ﬁnding is consistent with the assumption that the encoding of emotional valence

Controls Patients

25 20 15 10 5 0

Positive

Neutral

Negative

Materials Figure 7.1. Free-recall performance as a function of affective valence of words in patients with schizophrenia and normal participants.

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of words does not require any controlled, strategic processes but involves more automatic processes (e.g., Hasher & Zacks, 1979). It is also consistent with evidence that automatic memory processes are intact in schizophrenia (GrasVincendon et al., 1994; Kazès et al., 1999). To investigate whether aﬀective ﬂattening (limited outward expression of positive and negative emotions in face, voice, and gestures) blunted the emotionality eﬀect on memory performance, we carried out a complementary ANOVA of memory performance on two subgroups of 12 patients. We categorized these patients according to the score (below or above the median of the group) of the “aﬀective ﬂattening” item of the SADS, a clinical scale measuring the intensity of negative symptoms of schizophrenia. There was neither a signiﬁcant group eﬀect nor an interaction between group and word type. Therefore, our experiment suggests that the enhancement of memory performance for emotional words is not attenuated by aﬀective ﬂattening; it provides evidence of a disjunction between the expressed dimension of emotion, which is reduced, and emotions experienced at encoding and re-experienced at retrieval, which are preserved. Discrepancies between our results and those from previous studies suggesting that the emotionality eﬀect on memory is disturbed in schizophrenia may be linked to their methodological diﬀerences: diﬀerences in the emotional stimuli used and diﬀerences in samples of patients. Some former studies did not use explicit diagnostic criteria of schizophrenia.

Interaction of Emotion and

Conscious Awareness Associated

With Recognition Memory in

Normal Controls

Most of the previous investigations of the interaction of emotion and memory carried out in normal controls and in patients with schizophrenia primarily concerned the objective accuracy of memory for emotional stimuli. However, as we said, what often matters most is not the objective fact that an event occurred but what it feels like and how it is re-experienced. This is particularly important for emotional memories experienced by patients suﬀering from psychiatric diseases, such as schizophrenia, that are accompanied by major disturbances of emotion. However, most of the studies carried out in normal controls with the R/K procedure used neutral material (review in Gardiner & Java, 1993). On the other hand, studies that have addressed the issue of the subjective experience associated with emotional memories in normal controls shared a common approach: The participants were simply asked to rate the vividness of their memories at retrieval. These studies found that memories for emotional events are more vivid than memories for neutral events (Ochsner, 2000). Recently, Ochsner (2000) conducted three experiments using the R/K procedure with student participants to investigate the subjective states of aware-

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ness accompanying recognition of emotional events. He reasoned that emotional events possess unique attributes that make them more distinctive than neutral events. They elicit evaluative and physiological responses not generated by neutral events, and they induce semantic processing and emotional subjective states not evoked by neutral events. Because the distinctiveness with which stimuli are encoded enhances the frequency of conscious recollection (Dewhurst & Conway, 1994; Huron et al., in press; Rajaram, 1993), Ochsner postulated that emotional events should be consciously recollected more often than neutral events. Because familiarity is thought to rely on how easily a stimulus is processed, Ochsner also predicted that Know responses (which reﬂect familiarity) would be more frequent for emotional, and especially negative, stimuli than for neutral stimuli. Several lines of evidence suggest that without prior study, emotional stimuli are processed more ﬂuently than neutral stimuli. Speeded perceptual or conceptual access for emotionally arousing stimuli has been shown in various tasks (review in Ochsner, 2000). Increased ﬂuency seems to be more reliably found for negative stimuli than for positive stimuli. However, by considering that nonstudied aﬀective stimuli seen at test should be processed more ﬂuently as well, Ochsner reasoned that increases in familiarity for negative stimuli should be expected only if encoding signiﬁcantly boosts ﬂuency above an already elevated baseline ﬂuency. Photographs of scenes and objects selected from the International Aﬀective Picture System (IAPS; Lang, Greenwald, Bradley, & Hamm, 1993) were used as emotional stimuli. In experiment 1, the participants were presented with these photos and asked to rate each one according to its valence, arousal, and visual complexity. Experiment 2 was a replication of experiment 1, but the participants were not asked explicitly to attend and to rate the stimuli along these dimensions. In experiment 3, the participants were asked to encode stimuli by judging their subjective brightness. Ochsner conducted two series of analyses. Considering that the subjective states of awareness as assessed by Remember and Know responses are mutually exclusive, he ﬁrst computed the proportions of Remember and Know responses for old and new items as a function of word type. Computed values are measures of discrete states of awareness. However, whether these values reﬂect the underlying processes is a matter of debate. Initially, it was suggested that the states of awareness captured by the R/K procedure map onto the underlying processes of conscious recollection and familiarity (Gardiner & Java, 1993). According to this view, an item either could be recollected, or familiar, but not both. However, several authors have argued against such a direct mapping (e.g., Jacoby, 1991; Yonelinas et al., 1998). They have suggested that the underlying processes of conscious recollection and familiarity are independent, rather than mutually exclusive. According to their view, some items can be exclusively recollected, some can be exclusively familiar, and some can be both recollected and familiar. In other words, whether a given stimulus is consciously recollected does not constrain whether it is familiar. Therefore, in a second series of analyses, Ochsner

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used the independence model recently proposed by Yonelinas et al. to estimate the respective contributions of conscious recollection and familiarity to recognition memory. Conscious recollection is an estimate of how often words were correctly recollected relative to the number of opportunities participants had to do so. Familiarity is derived from the participants’ tendencies to give a correct Know response to old words and an incorrect Know response to new words. The results of the three experiments conﬁrmed most of Ochsner’s predictions. Remember responses were more frequent for emotional than for neutral stimuli and for negative than for positive stimuli; estimates of conscious recollection followed the same pattern. However, contrary to Ochsner’s prediction, diﬀerences in familiarity were slight and nonsigniﬁcant. These ﬁndings are consistent with the notion that emotional events are better recalled or recognized than neutral events, but they go further by demonstrating that greater accuracy is due primarily to better conscious recollection of emotional stimuli. The results also support the hypothesis that emotion leads to increases in the distinctiveness with which stimuli are encoded and re-experienced in memory later on. Moreover, the results indicated that the emotionality eﬀect obtained even when participants did not explicitly evaluate the emotional valence of stimuli (Experiment 2) or evaluated the subjective brightness of stimuli (Experiment 3). They thereby reconﬁrmed the hypothesis that the emotionality eﬀect does not depend on being instructed explicitly to attend to emotional aspects of words. Finally, the pattern of diﬀerences observed in this study with positive and negative photographs is opposite to the Pollyanna tendency usually observed with positive and negative words. In keeping with Conway and Dewhurst (1995), Ochsner suggested that a more general factor underlying the emotionality eﬀect on conscious recollection might be the personal signiﬁcance of a stimulus and not its absolute emotional valence. This interpretation is also supported by an investigation of autobiographical memories in normal controls that Conway, Collins, Gathercole, and Anderson (1996) conducted. This experiment showed that the personal signiﬁcance attributed to autobiographical events interacts with emotion to form a major determinant of conscious recollection for autobiographical memories.

An Investigation of the Inﬂuence of

Emotional Words on Recognition

Memory and Associated Conscious

Awareness in Schizophrenia

Ochsner’s results suggest that the R/K procedure is a more sensitive tool than traditional recall and recognition tasks for investigating the relationship between emotion and memory. The fact that emotional stimuli diﬀerentially inﬂuenced conscious recollection and familiarity may explain why some previous studies failed to ﬁnd a clear relationship between emotion and memory in normal con-

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trols. This may also account for some of the inconsistent results obtained by investigations of the interaction of memory and emotion in schizophrenia. However, the studies of conscious awareness in patients with schizophrenia were conducted using neutral stimuli, leaving unexplored the states of awareness that accompany memory for emotional events. Danion, Kazès, Huron, and Karchouni (in press) addressed this issue recently. They used the R/K procedure and the recognition model of Yonelinas et al. (1998) to investigate the inﬂuence of emotional words both on the subjective states of awareness accompanying recognition memory and the processes of conscious recollection and familiarity that might underlie Remember and Know responses. During the study phase of a recognition task, 24 patients with schizophrenia and 24 normal controls were presented with positive, negative, and neutral words. They were asked to remember the words and to perform an orienting task that required them to rate the words according to their subjective feelings of pleasantness and unpleasantness. In the test phase, the participants were presented with a list of studied and nonstudied words, and they were asked to recognize words from the study list. In addition, they were told to make a R/K judgment. Because patients with schizophrenia remain sensitive to the emotional salience of words, the researchers predicted that remember responses and conscious recollection should be more frequent for emotional than for neutral events. Results conﬁrmed this prediction. During the study phase of the task, patients evaluated the emotional valence of words just as normal controls did. At test, patients produced fewer Remember responses and exhibited lower levels of conscious recollection than normal controls did. They gave more Know responses than controls but familiarity, as estimated using the model of Yonelinas et al., was slightly reduced. Their Remember responses were more frequent for emotional than for neutral words and for positive than for negative words, with parallel variations in conscious recollection. This pattern of responses was similar to the one observed in normal controls. The levels of Know responses and familiarity for emotional and neutral words were similar. Therefore, provided that the cognitive evaluation of emotional valence is intact, patients, like controls, consciously recollected emotional words better than neutral words.

Concluding Comments This review of the investigations of conscious awareness in schizophrenia shows that, whereas several determinants of conscious recollection such as word frequency (Huron et al., 1995), picture superiority (Huron & Danion, 2002), and directed-forgetting eﬀects (Sonntag et al., 2003) are impaired in patients with schizophrenia, the emotionality eﬀect is preserved when words are used. However, this review leaves numerous questions unanswered. For instance, are the body correlates and the brain correlates of this emotionality eﬀect similar in

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patients with schizophrenia and in normal controls? Studies of the emotionality eﬀect of words in schizophrenia using psychophysiological and brain imaging techniques would be worth carrying out to answer this question. Are patients with schizophrenia still able to re-experience at retrieval the speciﬁc attributes that make an event emotional at encoding, such as particular emotional details or aspects of the event, components of the cognitive evaluation of the emotional valence, and physiological changes? One way to investigate this issue might be to use the R/K procedure to evaluate the subjective states of awareness that characterize the emotional component of the event. Another, complementary way to investigate this issue might be to compare the qualitative characteristics of the subjective experiences associated with emotional memories in patients with schizophrenia and in normal controls. The Memory Characteristics Questionnaire (MCQ), designed by Johnson, Foley, Suengas, and Raye (1988) to assess attributes of memories, could be used to achieve this goal. The MCQ asks the participants to rate the speciﬁc qualitative characteristics of their subjective experiences, such as visual details, mental images, and emotional reactions. These approaches to experiential aspects of emotions should provide information about not only the inﬂuence of emotional events on the frequency of conscious recollection in patients with schizophrenia but also the ability of patients to relive what makes this event distinctive, its emotional dimension. It is plausible that the relationship between emotion, memory, and conscious awareness depends on the type of information processing required by the emotional items at encoding and at retrieval. For instance, Koh et al. (1981) failed to observe a Pollyanna tendency, as noted earlier; the experiment used items characterized by a separation of target (photographs of faces) and emotional information (favorable or unfavorable personality-trait words). This failure may be related to a defective binding of target and emotional information. If so, whether this defective binding is speciﬁc to emotional information is not clear. Instead, it could simply be a special case of a generalized defect in binding separate dimensions of items. Such a deﬁcit has been described in schizophrenia for items that comprise several spatially, temporally, or cognitively separated components (Danion et al., 1999; Rizzo, Danion, Van der Linden, & Grangé, 1996; Rizzo, Danion, Van Der Linden, Grangé, & Rohmer, 1996). These results raise the issue of the inﬂuence of emotion on conscious recollection in schizophrenia when emotional stimuli other than words are used—such as stimuli that induce stronger emotional responses; stimuli that are associated with primary, innate emotions (instead of secondary, acquired emotions; e.g., Damasio, 1995); or stimuli that require a more controlled, strategic evaluation of emotional valence. Finally, patients with schizophrenia often suﬀer from depressive symptoms, and Brebion, Gorman, Malaspina, Sharif, and Amador (2001) have suggested that the deﬁcit of verbal memory observed in schizophrenia may be related to these symptoms. It would therefore be worthwhile to investigate whether schizophrenic patients suﬀering from

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depressive symptoms exhibit a mood congruency eﬀect, that is, better memory performance for negative than for positive stimuli [see chapter 6—Eds.]. All the investigations of emotion and memory in schizophrenia reviewed in this chapter shared a primary concern with episodic memory, as assessed in the laboratory using experimental procedures far removed from real-life situations. A crucial issue, albeit virtually unexplored in schizophrenia, is the relationship between emotion and autobiographical memories, that is, memories for personal events and facts from one’s life. There is converging evidence that emotional experience at the time of an event can inﬂuence memory and associated conscious recollection for that event (Conway et al., 1996). Because autobiographical memories are emotional in essence and act as organizers of autobiographical knowledge, a crucial function of the interaction of emotion and autobiographical memory is the development of the self and of personal identity (Conway & Pleydell-Pearce, 2000). Investigating the interaction of emotion and autobiographical memories may thus provide insights into the current abnormalities of personal identity, as well as the formation of the abnormal personal identity that characterizes schizophrenia. Abnormalities in personal identity emerge at the onset of schizophrenia, which occurs in adolescence and early adulthood, that is, when autobiographical knowledge is being acquired and organized to form personal identity. What are the clinical implications of the investigations of emotion and memory in schizophrenia? Evidence that the emotionality eﬀect on memory and subjective experience may be preserved in patients with schizophrenia has positive clinical implications. Emotions are closely related to adaptive behavior at an automated level. But because emotions enhance conscious recollection, they also oﬀer the ﬂexibility of response based on memory for emotional events from the subject’s personal past. Evidence of a preserved emotionality eﬀect therefore suggests that patients may still beneﬁt from such ﬂexibility, at least in some situations. Other clinical implications may be negative. As emotion is the consequence of how people construe situations, some neutral events or experiences may become emotional by virtue of false beliefs or delusions. Because these events will be more easily recollectable later and, hence, more richly and vividly experienced in memory, they could contribute to the persistence and the enrichment of delusional experiences. According to this view, symptoms of schizophrenia such as delusions may arise as a consequence of a combination of impaired and spared aspects of emotions and cognition.

Notes 1. In a typical Sternberg task, subjects are presented with a short list of items (memory set) to remember. After a short delay (retention interval), they are presented with a probe item and instructed to decide as quickly as possible whether the probe belongs to the previously presented memory set. Performance is measured by the time to respond and the number of errors.

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2. This conclusion implies that the nonaﬀective characteristics (e.g., frequency, imagery) of words to-be-learned can be considered equivalent.

References Abbruzzese, M., & Scarone, S. (1993). Memory and attention dysfunctions in story recall in schizophrenia: Evidence of a possible frontal malfunctioning. Biological Psychology, 35, 51–58. Abi-Dargham, A., Gil, R., Krystal, J., Baldwin, R. M., Seibyl, J. P., Bowers, M., et al. (1998). Increased striatal dopamine transmission in schizophrenia: Conﬁrmation in a second cohort. American Journal of Psychiatry, 155, 761–767. Addington, J., & Addington, D. (1998). Facial aﬀect recognition and information processing in schizophrenia and bipolar disorder. Schizophrenia Research, 32, 171–181. Aleman, A., Hijman, R., de Haan, E. H., & Kahn, R. S. (1999). Memory impairment in schizophrenia: A meta-analysis. American Journal of Psychiatry, 156, 1358–1366. Andreasen, N. C. (1982). Negative symptoms in schizophrenia. Deﬁnition and reliability. Archives of General Psychiatry, 39, 784–788. Andreasen, N. C. (1999). A unitary model of schizophrenia. Archives of General Psychiatry, 56, 781–787. Bernstein, A. S. (1987). Orienting response research in schizophrenia: Where we have come and where we might go. Schizophrenia Bulletin, 13, 623–641. Bilder, R. M., Goldman, R. S., Robinson, D., Reiter, G., Bell, L., Bates, J. A., et al. (2000). Neuropsychology of ﬁrst-episode schizophrenia: Initial characterization and clinical correlates. American Journal of Psychiatry, 157, 549–559. Blaney, P. H. (1986). Aﬀect and memory: A review. Psychological Bulletin, 99, 229– 246. Bleuler, E. (1911). Dementia Praecox ou groupe des schizophrénies. Paris: E.P.E.L. Bogerts, B. (1993). Recent advances in the neuropathology of schizophrenia. Schizophrenia Bulletin, 19, 431–445. Boucher, J., & Osgood, C. E. (1969). The Pollyanna hypothesis. Journal of Verbal Learning and Verbal Behavior, 8, 1–8. Bower, G. H. (1981). Mood and memory. American Psychologist, 36, 129–148. Brebion, G., Gorman, J. M., Malaspina, D., Sharif, Z., & Amador, X. (2001). Clinical and cognitive factors associated with verbal memory task performance in patients with schizophrenia. American Journal of Psychiatry, 158, 758–764. Breier, A., Su, T. P., Saunders, R., Carson, R. E., Kolachana, B. S., de Bartolomeis, A., et al. (1997). Schizophrenia is associated with elevated amphetamine-induced synaptic dopamine concentrations: Evidence from a novel positron emission tomography method. Proceedings of the National Academy of Sciences of the USA, 94, 2569–2574. Bryson, G., Bell, M., & Lysaker, P. (1997). Aﬀect recognition in schizophrenia: A function of global impairment or a speciﬁc cognitive deﬁcit. Psychiatry Research, 71, 105–113. Calev, A. (1984a). Recall and recognition in chronic nondemented schizophrenics: Use of matched tasks. Journal of Abnormal Psychology, 93, 172–177.

236

  

Calev, A. (1984b). Recall and recognition in mildly disturbed schizophrenics: The use of matched tasks. Psychological Medicine, 14, 425–429. Calev, A., & Edelist, S. (1993). Aﬀect and memory in schizophrenia: Negative emotion words are forgotten less rapidly than other words by long-hospitalized schizophrenics. Psychopathology, 26(5–6), 229–235. Clare, L., McKenna, P. J., Mortimer, A. M., & Baddeley, A. D. (1993). Memory in schizophrenia: What is impaired and what is preserved? Neuropsychologia, 31(11), 1225–1241. Conway, M. A., Collins, A. F., Gathercole, S. E., & Anderson, S. J. (1996). Recollections of true and false autobiographical memories. Journal of Experimental Psychology: General, 125, 69–95. Conway, M. A., & Dewhurst, S. A. (1995). Remembering, familiarity, and source monitoring. Quarterly Journal of Experimental Psychology, 48, 125–140. Conway, M. A., & Pleydell-Pearce, C. W. (2000). The construction of autobiographical memories in the self-memory system. Psychological Review, 107, 261–288. Damasio, A. R. (1995). Toward a neurobiology of emotion and feeling: Operational concepts and hypotheses. Neuroscientist, 1, 19–25. Danion, J., Gokalsing, E., Robert, P., Massin-Krauss, M., & Bacon, E. (2001). Defective relationship between subjective experience and behavior in schizophrenia. American Journal of Psychiatry, 158(12), 2064–2066. Danion, J. M., Huron, C., & Robert, P. (2001). Schizophrenia and autonoetic awareness. European Neuropsychopharmacology, S133–S134. Danion, J. M., Kauﬀmann-Muller, F., Grangé, D., Zimmermann, M. A., & Greth, P. (1995). Aﬀective valence of words, explicit and implicit memory in clinical depression. Journal of Aﬀective Disorder, 34, 227–234. Danion, J. M., Kazès, M., Huron, C., & Karchouni, N. (in press). Do patients with schizophrenia consciously recollect emotional events better than neutral events? American Journal of Psychiatry. Danion, J. M., Meulemans, T., Kauﬀmann-Muller, F., & Vermaat, H. (2001). Intact implicit learning in schizophrenia. American Journal of Psychiatry, 158, 944–948. Danion, J. M., Rizzo, L., & Bruant, A. (1999). Functional mechanisms underlying impaired recognition memory and conscious awareness in patients with schizophrenia. Archives of General Psychiatry, 56, 639–644. Dawson, M. E., Nuechterlein, K. H., Schell, A. M., Gitlin, M., & Ventura, J. (1994). Autonomic abnormalities in schizophrenia. State or trait indicators? Archives of General Psychiatry, 51(10), 813–824. Deese, J. (1959). On the prediction of occurrence of particular verbal intrusions in immediate recall. Journal of Experimental Psychology, 58, 17–22. Dewhurst, S. A., & Conway, M. A. (1994). Pictures, images, and recollective experience. Journal of Experimental Psychology: Learning, Memory, and Cognition, 20, 1088–1098. Dominey, P. F., & Georgieﬀ, N. (1997). Schizophrenics learn surface but not abstract structure in a serial reaction time task. Neuroreport, 8(13), 2877–2882. Doniger, G. M., Silipo, G., Rabinowicz, E. F., Snodgrass, J. G., & Javitt, D. C. (2001). Impaired sensory processing as a basis for object-recognition deﬁcits in schizophrenia. American Journal of Psychiatry, 158, 1818–1826.

, ,   

237

Dutta, S., & Kanungo, R. N. (1975). Aﬀect and memory: A reformulation. New York: Pergamon Press. Duzel, E., Yonelinas, A. P., Mangun, G. R., Heinze, H. J., & Tulving, E. (1997). Eventrelated brain potential correlates of two states of conscious awareness in memory. Proceedings of the National Academy of Sciences of the USA, 94(11), 5973–5978. Ekman, P. (1993). Facial expression and emotion. American Psychologist, 48, 384– 392. Feinstein, A., Goldberg, T. E., Nowlin, B., & Weinberger, D. R. (1998). Types and characteristics of remote memory impairment in schizophrenia. Schizophrenia Research, 30, 155–163. Frith, C. D. (1992). The cognitive neuropsychology of schizophrenia. East Sussex, England: Erlbaum. Gardiner, J. M. (1988). Functional aspects of recollective experience. Memory & Cognition, 16, 309–313. Gardiner, J. M., & Java, R. I. (1993). Recognising and remembering. In A. Collins, M. A. Conway, S. E. Gathercole, & P. Morris (Eds.), Theories of memory (pp. 163– 188). Hillsdale, NJ: Erlbaum. Gardiner, J. M., Java, R. I., & Richardson-Klavehn, A. (1996). How level of processing really inﬂuences awareness in recognition memory. Canadian Journal of Experimental Psychology, 50, 114–122. Gardiner, J. M., & Richardson-Klavehn, A. (2000). Remembering and Knowing. In E. Tulving & F. I. M. Craik (Eds.), The Oxford handbook of memory (pp. 229–244). New York: Oxford University Press. Gold, J. M., Randolph, C., Carpenter, C. J., Goldberg, T. E., & Weinberger, D. R. (1992). Forms of memory failure in schizophrenia. Journal of Abnormal Psychology, 101, 487–494. Goldberg, T. E., Weinberger, D. R., Pliskin, N. H., Berman, K. F., & Podd, M. H. (1989). Recall memory deﬁcit in schizophrenia. A possible manifestation of prefrontal dysfunction. Schizophrenia Research, 2, 251–257. Grangé, D., Greth, P., & Danion, J. M. (1991). Application des méthodes de classiﬁcation à la construction d’un test de mémoire. La Revue de Modulad, 8, 31–43. Gras-Vincendon, A., Danion, J. M., Grangé, D., Bilik, M., Willard-Schroeder, D., Sichel, J. P., et al. (1994). Explicit memory, repetition priming and cognitive skill learning in schizophrenia. Schizophrenia Research, 13, 117–126. Green, M. F. (1996). What are the functional consequences of neurocognitive deﬁcits in schizophrenia? American Journal of Psychiatry, 153, 321–330. Hasher, L., & Zacks, R. T. (1979). Automatic and eﬀortful processes in memory. Journal of Experimental Psychology: General, 108, 356–388. Hawkins, K. A. (1999). Memory deﬁcits in patients with schizophrenia: Preliminary data from the Wechsler Memory Scale-Third Edition support earlier ﬁndings. Journal of Psychiatry and Neuroscience, 24, 341–347. Heinrichs, R. W., & Zakzanis, K. K. (1998). Neurocognitive deﬁcit in schizophrenia: A quantitative review of the evidence. Neuropsychology, 12, 426–445. Henson, R. N., Rugg, M. D., Shallice, T., Josephs, O., & Dolan, R. J. (1999). Recollection and familiarity in recognition memory: An event-related functional magnetic resonance imaging study. Journal of Neurosciences, 19(10), 3962–3972.

238

  

Huron, C., & Danion, J. M. (2002). Impairment of constructive memory in schizophrenia. International Clinical Psychopharmacology, 17, 127–133. Huron, C., Danion, J. M., Giacomoni, F., Grangé, D., Robert, P., & Rizzo, L. (1995). Impairment of recognition memory with, but not without, conscious recollection in schizophrenia. American Journal of Psychiatry, 152(12), 1737– 1742. Huron, C., Danion, J. M., Rizzo, L., Killofer, V., & Damiens, A. (in press). Subjective qualities of memories with the picture superiority eﬀect in schizophrenia. Journal of Abormal Psychology. Jacoby, L. L. (1991). A process dissociation framework: Separating automatic from intentional uses of memory. Journal of Memory and Language, 110, 306–340. Johnson, M. K., Foley, M. A., Suengas, A. G., & Raye, C. L. (1988). Phenomenal characteristics of memories for perceived and imagined autobiographical events. Journal of Experimental Psychology: General, 117, 371–376. Johnson, M. K., Hashtroudi, S., & Lindsay, D. S. (1993). Source monitoring. Psychological Bulletin, 114, 3–28. Johnson, M. K., & Raye, C. L. (1981). Reality monitoring. Psychological Review, 88, 67–85. Kay, S. R. (1982). Conceptual disorder in schizophrenia as a function of encoding orientation. Journal of Nervous and Mental Diseases, 170, 154–163. Kayton, L., & Koh, S. D. (1975). Hypohedonia in schizophrenia. Journal of Nervous and Mental Diseases, 161, 412–420. Kazès, M., Berthet, L., Danion, J. M., Amado, I., Willard, D., Robert, P., et al. (1999). Impairment of consciously controlled use of memory in schizophrenia. Neuropsychology, 13, 54–61. Kerr, S. L., & Neale, J. M. (1993). Emotion perception in schizophrenia: Speciﬁc deﬁcit or further evidence of generalized poor performance? Journal of Abnormal Psychology, 102, 312–318. Koh, S. D., Grinker, R. R., Marusarz, T. Z., & Forman, P. L. (1981). Aﬀective memory and schizophrenia anhedonia. Schizophrenia Bulletin, 7, 292–307. Koh, S. D., Kayton, L., & Peterson, R. A. (1976). Aﬀective encoding and consequent remembering in schizophrenic young adults. Journal of Abnormal Psychology, 85, 156–166. Koh, S. D., & Peterson, R. A. (1978). Encoding orientation and the remembering of schizophrenic young adults. Journal of Abnormal Psychology, 87, 303–313. Koh, S. D., Szoc, R., & Peterson, R. A. (1977). Short-term memory scanning in schizophrenic young adults. Journal of Abnormal Psychology, 86, 451–460. Kring, A. M., Kerr, S. L, Smith, D. A. & Neale, J. M. (1993). Flat aﬀect in schizophrenia does not reﬂect diminished subjective experience of emotion. Journal of Abnormal Psychology, 102, 507–517. Kring, A. M., & Neale, J. M. (1996). Do schizophrenic patients show a disjunctive relationship among expressive, experiential, and psychophysiological components of emotion? Journal of Abnormal Psychology, 105, 249–257. Lang, P. J., Greenwald, M. K., Bradley, M. M., & Hamm, A. O. (1993). Looking at pictures: Aﬀective, visceral, and behavioral reactions. Psychophysiology, 30, 261–273.

, ,   

239

Laruelle, M., Abi-Dargham, A., Van Dyck, C. H., Gil, R., D’Souza, C. D., & Erdos, J. (1996). Single photon emisssion computerized tomography imaging of amphetamine-induced dopamine release in drug-free schizophrenic subjects. Proceedings of the National Academy of Sciences of the USA, 93, 9235–9240. Lazarus, R. S. (1991). Cognition and motivation in emotion. American Psychologist, 46, 352–367. Louilot, A., & Besson, C. (2000). Speciﬁcity of amygdalostriatal interactions in the involvement of mesencephalic dopaminergic neurons in aﬀective perception. Neuroscience, 96, 73–82. Mandler, G. (1984). Mind and body: Psychology of emotion and stress. New York: Norton. Michel, L., Danion, J. M., Grangé, D., & Sandner, G. (1998). Cognitive skill learning and schizophrenia: Implications for cognitive remediation. Neuropsychology, 12, 590–599. Myin-Germeys, I., Delespaul, P. A., & deVries, M. W. (2000). Schizophrenia patients are more emotionally active than is assumed based on their behavior. Schizophrenia Bulletin, 26, 847–854. Myin-Germeys, I., van Os, J., Schwartz, J. E., Stone, A. A., & Delespaul, P. A. (2001). Emotional reactivity to daily life stress in psychosis. Archives of General Psychiatry, 58(12), 1137–1144. Ochsner, K. N. (2000). Are aﬀective events richly recollected or simply familiar? The experience and process of recognizing feelings past. Journal of Experimental Psychology: General, 129, 242–261. Palmer, B. W., Heaton, R. K., Paulsen, J. S., Kuck, J., Braﬀ, D., Harris, M. J., et al. (1997). Is it possible to be schizophrenic yet neuropsychologically normal? Neuropsychology, 11, 437–446. Rado, S. (1962). Psychoanalysis of behavior. Vol. 2. New York: Grune & Stratton. Rajaram, S. (1993). Remembering and knowing: Two means of access to the personal past. Memory & Cognition, 21, 89–102. Rajaram, S., & Roediger, H. L. III. (1997). Remembering and knowing as states of consciousness during retrieval. In J. D. Cohen & J. W. Schooler (Eds.), Scientiﬁc approaches to consciousness: Carnegie Mellon symposia on cognition (pp. 213– 240). Mahwah, NJ: Erlbaum. Rizzo, L., Danion, J. M., van der Linden, M., & Grangé, D. (1996). Patients with schizophrenia remember that an event has occurred, but not when. British Journal of Psychiatry, 168, 427–431. Rizzo, L., Danion, J.-M., Van Der Linden, M., Grangé, D., & Rohmer, J. G. (1996). Impairment of memory for spatial context in schizophrenia. Neuropsychology, 10, 376–384. Roediger, H. L., & McDermott, K. B. (1995). Creating false memories: Remembering words not presented in lists. Journal of Experimental Psychology: Learning, Memory, and Cognition, 21, 803–814. Rubin, D. C., & Friendly, M. (1986). Predicting which words get recalled: Measures of free recall, availability, goodness, emotionality, and pronunciability for 925 nouns. Memory & Cognition, 14, 79–94. Saykin, A. J., Gur, R. C., Gur, R. E., Mozley, P. D., Mozley, L. H., Resnick, S. M., et al.

240

  

(1991). Neuropsychological function in schizophrenia. Selective impairment in memory and learning. Archives of General Psychiatry, 48, 618–624. Saykin, A. J., Shtasel, D. L., Gur, R. E., Kester, D. B., Mozley, L. H., Staﬁniak, P., et al. (1994). Neuropsychological deﬁcits in neuroleptic naive patients with ﬁrstepisode schizophrenia. Archives of General Psychiatry, 51, 124–131. Schacter, D. L., Norman K. A., & Koutstaal, W. (1998). The cognitive neurosciences of constructive memory. Annual Review of Psychology, 49, 289–318. Schneider, F., Weiss, U., Kessler, C., Salloum, J. B., Posse, S., Grodd, W., et al. (1998). Diﬀerential amygdala activation in schizophrenia during sadness. Schizophrenia Research, 34, 133–142. Schwartz, B. D., & Winstead, D. K. (1985). Icon formation in chronic schizophrenics. Biological Psychiatry, 20, 1015–1018. Schwartz, B. L., Rosse, R. B., & Deutsch, S. I. (1993). Limits of the processing view in accounting for dissociations among memory measures in a clinical population. Memory & Cognition, 21, 63–72. Schwartz, B. L., Rosse, R. B., Veazey, C., & Deutsch, S. I. (1996). Impaired motor skill learning in schizophrenia: Implications for corticostriatal dysfunction. Biological Psychiatry, 39, 241–248. Smith, M. E. (1993). Neurophysiological manifestations of recollective experience during recognition memory judgments. Journal of Cognitive Neuroscience, 5, 1– 13. Sonntag, P., Gokalsing, E., Olivier, C., Robert, P., Burglen, F., Kauﬀmann-Muller, F., et al. (2003). Impaired strategic regulation of contents of conscious awareness in schizophrenia. Consciousness and Cognition, 12, 190–200. Taylor, S. F., & Liberzon, I. (1999). Paying attention to emotion in schizophrenia. British Journal of Psychiatry, 174, 6–8. Tulving, E. (1985). Memory and consciousness. Canadian Psychology, 26, 1–12. Walker, E., Marwit, S. J., & Emory, E. (1980). A cross-sectional study of emotion recognition in schizophrenics. Journal of Abnormal Psychology, 89, 428–436. Wickens, D. D. (1970). Encoding categories of words: An empirical approach to meaning. Psychological Review, 77, 1–15. Yonelinas, A. P., Kroll, N. E. A., Dobbins, I., Lazzara, M., & Knight, R. T. (1998). Recollection and familiarity deﬁcits in amnesia: Convergence of rememberknow, process dissociation, and receiver operating characteristic data. Neuropsychology, 12, 323–339. Zajonc, R. B. (1984). On the primacy of aﬀect. American Journal of Psychology, 39, 117–123.

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

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T

he events of our lives are imbued with emotion. In the everyday ups and downs of daily life, the cyclical joys and sorrows, or the heart-stopping ecstasy, grief, or fear that comes just a few times in a lifetime, emotion is woven deep into the fabric of our personal past. Moreover, we don’t simply experience emotional events; we share them with others, both as they are occurring and in retrospect. How we experience and reminisce with others about the meaningful and emotional events of our lives plays a critical role in how we come to understand and evaluate our past and ourselves. For young children who are just beginning to construct an autobiographical memory, the way in which emotion and memory are intertwined provides a foundation for understanding of self and other (Fivush & Buckner, 2000; Fivush, Berlin, et al., 2003). Most important, early autobiographical memory is co-constructed in the context of parent-child reminiscing; parents inﬂuence both the structure and the content of young children’s emerging autobiography (Fivush, Haden, & Reese, 1996; Haden, Didow, Ornstein, & Eckerman, 2001; Nelson, 1993; Nelson & Fivush, 2002). In this chapter, we discuss two aspects of children’s developing memories of emotional events. First, we examine parent-child reminiscing about everyday emotional experiences. We argue that through participating in parent-guided reminiscing, children develop an emotional self-concept that simultaneously inﬂuences the way in which the past is remembered and forms the basis for understanding self in the present. We then turn to an examination of children’s memories of highly emotional and stressful experiences and how these memories may diﬀer from memories of highly positive experiences. Given our perspective on the role of parent guided reminiscing in children’s developing autobiographical memories, we also discuss the role of parent-child reminiscing about these kinds of stressful experiences and how parents might help or hinder young

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children in understanding and coping with aversive events. Throughout, we take a functional perspective on autobiographical memory (Bluck & Alea, 2002; Fivush, 1988). Our focus is on how autobiographical memories are used to link the past with current understanding of self through the creation of an autobiographical narrative, help deﬁne self in relation to others through time, and contribute to understanding, regulating, and coping with aversive experiences. Thus, we emphasize meaning making rather than accuracy; how do individuals make sense of their past experiences and how does this process emerge developmentally within joint reminiscing? To place this research in perspective, we ﬁrst brieﬂy review the development of children’s autobiographical memory and emotional understanding more broadly.

Autobiographical Memory

Development

Although memory functions from birth, autobiographical memory—deﬁned as consciously available and socially shareable memories of speciﬁc events experienced by the self at a speciﬁed time and place—emerges slowly across the preschool years (Nelson & Fivush, 2002; Pillemer & White, 1989). Children begin to converse about speciﬁc past experiences at about 16 to 18 months of age (Eisenberg, 1985; Harley & Reese, 1999). However, at this early point, adults provide much of the content and structure of what happened; children participate by conﬁrming, denying, or repeating what the adult says. Very quickly, children become more competent participants in autobiographical reminiscing, and by 3 years of age, children are able to give accurate detailed accounts of their personal past (Fivush, Gray, & Fromhoﬀ, 1987), although they still rely on adults to provide much of the coherence, or narrative structure (Hamond & Fivush, 1990; Ornstein, 1995). By the end of the preschool years, children can provide relatively clear and organized narratives of their past (Fivush, Haden, & Adam, 1995), and these skills continue to develop throughout childhood (Hudson & Shapiro, 1991; McCabe & Peterson, 1991). Extensive research conﬁrms that children are learning the forms and functions for talking about the past through participating in adult-guided reminiscing. In accord with Vygotsky’s (1978) social-cultural theory of development, adults provide the structure, or “scaﬀold,” for children’s early reminiscing; over time, children begin to internalize the forms used by adults and begin to provide the structure for themselves. More speciﬁcally, children learn the canonical narrative forms and the culturally appropriate content to include when recalling the past (see Fivush, 1994, and Fivush & Haden, 2003, for a review). Importantly, there are clear and enduring individual diﬀerences in both parents’ and children’s autobiographical reminiscing (Fivush & Fromhoﬀ, 1988; Hudson, 1990; McCabe & Peterson, 1991). Some parents display a highly elaborative

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reminiscing style, talking about the past in great detail and encouraging their children’s participation. In contrast, some parents display a less elaborative reminiscing style, taking about the past in sparse detail, often simply asking the same questions over and over. Not only is parental reminiscing style consistent over time but highly elaborative parents facilitate their children’s developing autobiographical memory skills. Children of more elaborative parents eventually come to tell more richly embellished narratives of their own past experience than children of less elaborative parents (Harley & Reese, 1999; McCabe & Peterson, 1992; Reese, Haden, & Fivush, 1993). In addition to individual diﬀerences within cultures, there are also substantial diﬀerences among cultures in parent-child reminiscing. Within Asian cultures, in which self is conceptualized as interdependent and integrated into a social and moral community (Oyserman & Markus, 1993), there is less focus overall on the past; parents in these cultures are less elaborative than Caucasian parents (Leichtman, Wang, & Pillemer, 2003). Provocatively, there are also diﬀerences within middle-class American culture between boys and girls. Parents are more elaborative and more evaluative overall when reminiscing with daughters than with sons (Reese, Haden, & Fivush, 1996). By middle childhood, the eﬀects of these diﬀerences in early parent-child reminiscing become apparent. Caucasian children tell longer and more elaborated narratives of their personal past than do Asian children (Han, Leichtman, & Wang, 1998), and middle-class Caucasian girls tell longer and more elaborated personal narratives than boys (Buckner & Fivush, 1998). And as adults, Caucasians and women provide longer and more detailed narratives of their personal past than do Asians and adult men (see Pillemer, 1998, for a review). The emerging eﬀects of culture and gender diﬀerences indicate that parental reminiscing style is an important avenue for the socialization of self and other, as well as for the construction of a culturally “appropriate” autobiography (Fivush & Haden, 2003).

Emotional Development Children begin talking about their emotions as well as their past early in development. By about 13 months of age, children begin referencing their emotional states, and by 2 years of age, children are integrating information about their own and others’ emotions into their everyday conversations (Bretherton, Fritz, ZahnWaxler, & Ridgeway, 1986). Further, and again similar to the development of autobiographical memory, the way in which parents incorporate emotion into conversations plays a critical role in children’s developing understanding of emotion. Mothers who talk more about emotion early in development have children who talk more about emotion later in development (Denham, Zoller, & Couchoud, 1994; Dunn, Bretherton, & Munn, 1987). More broadly, families that discuss emotional experiences in more open and integrative ways have children

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who develop better prosocial skills, have more positive peer relations, and show better psychological adjustment (see Halberstadt, Denham, & Dunsmore, 2001, for a review). And just as there are gender diﬀerences in parent-child reminiscing, there are also gender diﬀerences in emotion socialization. Mothers talk more about emotions overall with girls than with boys, and girls begin to talk more about emotion than boys do as early as the preschool years (Dunn et al., 1987; Zahn-Waxler, Cole, & Barrett, 1991). To summarize, early socialization patterns mirror adult patterns of emotional expression and understanding. Adult women express more emotion than men and report experiencing emotions more frequently and intensely than do men (see Fischer, 2000, for a review). Speciﬁc to autobiography, adult women include more emotion when narrating their past than do adult men (Bauer, Stennes, & Haight, in press; Davis, 1990).

Parent-Child Reminiscing About

Emotional Events

The developments in autobiographical memory and emotional development suggest that children may be socialized in both domains in parallel ways and along similar timelines. Not surprisingly, when reminiscing about the past, parents and children include information about the emotional aspects of their shared experiences. Reminiscing about past emotional experiences diﬀers in important ways from talking about emotions experienced in the present (Dunn, Brown, & Beardsall, 1991; Fivush, 1993). First, parents and children are not in the immediate heat of the emotional moment when reminiscing about past emotions and therefore may be better able to reﬂect on and interpret emotional experience. Second, in reminiscing, parents can choose to talk about particular emotions rather than others; for example, they can emphasize times when their children were sad but downplay times when their children were angry. Finally, parents can choose to talk about various aspects of emotional experience; they can focus on the emotion itself and the way it is expressed; they can focus on the causes of emotional experience, or on how negative emotion is resolved; and they can talk about both the child’s and others’ emotional experiences and explain similarities or diﬀerences. Thus, in the context of reminiscing about emotional experiences, parents can provide a framework for children’s developing understanding of how and why they and others experience emotion. Through parent-guided interpretation and evaluation of emotional experiences, children begin to develop an “emotional self-concept” (Fivush & Buckner, 2003; Fivush, Berlin, et al., 2003), composed of three functions: self-deﬁning (the kind of emotional person I am), self-in-relation (how I express and share my emotions with others), and self-regulation (how I cope with and resolve negative emotion).

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In line with gender diﬀerences in many other aspects of emotional processing (Fischer, 2000), several studies have documented gender diﬀerences in the emotional content of mother-child reminiscing (Adams, Kuebli, Boyle, & Fivush, 1995; Fivush, 1989, 1991; Kuebli, Butler, & Fivush, 1995; Kuebli & Fivush, 1992). In these studies, mothers and their preschool children are visited in their homes and asked to talk about several past experiences they have shared. No further instructions are given. Tape-recorded conversation are transcribed and coded for various dimensions. Across studies, mothers talk more about emotion with their preschool daughters than sons, especially about sadness. Mothers also use a wider variety of emotion words with girls than with boys, for example, talking about being “sad” and “upset” and “crabby” rather than simply “sad.” As children grow older, mothers talk increasingly of other people’s emotions as well as the child’s, especially with girls. Mothers also place emotions in a more social and relational context with girls than with boys. In reminiscing with daughters, mothers talk about how emotions emerge from, and are modulated by, interactions with other people, whereas with sons, they are more likely to discuss emotions as internal and autonomous experiences. These patterns suggest that mothers are providing a more embellished and diﬀerentiated understanding of emotion with daughter than with sons. Although there are no diﬀerences in how girls and boys talk about past emotions early in the preschool years, by the end of the preschool years, girls are taking signiﬁcantly more about their past emotional experience than are boys (see Fivush & Buckner, 2000, for a review). These ﬁndings, along with previous ﬁndings of diﬀerences in adults’ autobiographical narratives, raise the question of possible diﬀerences between mothers and fathers reminiscing with daughters and sons. To explore this issue, we asked mothers and fathers to independently discuss four speciﬁc past experiences with their 4–year-old children when the child experienced happiness, sadness, anger, and fear (Fivush, Brotman, Buckner, & Goodman, 2000). Overall, mothers talked more about emotion (M = 5.23 emotion words per event discussed) than fathers (M = 3.99 emotion words), but both mothers and fathers talked about sadness, especially the causes of sadness, more with daughters (M = 4.05 mentions) than with sons (1.95 mentions). In this study, girls talked more about being scared than did boys, but there were no diﬀerences in conversations about feeling happy, sad, or angry. Finally, as in previous research, both mothers and fathers placed emotions in a more social and relational context with daughters than with sons. Thus, overall, this body of research indicates that emotional experiences are discussed diﬀerently depending on both the gender of the parent and the child. Parents, especially mothers, talk about emotional experiences more, use a wider variety of emotional language, and place past emotions in a more social and relational context with their preschool daughters than with their sons. In turn, by the end of the preschool years, girls are talking more about the emotional

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aspects of their past experiences and using a wider variety of emotion terms than boys. These patterns suggest that children are being socialized into “genderappropriate” ways of understanding their emotional experience. Parents facilitate the development of a more complex and more diﬀerentiated emotional sense of self in the past with daughters than with sons (Fivush, 1998b). Whereas previous research on the development of autobiographical memory has demonstrated distinct parental reminiscing styles that vary in elaborativeness, research on reminiscing about emotional events focuses on diﬀerences in the emotional content of parent-child reminiscing. To integrate these research ﬁndings, we examined whether level of maternal elaboration is related to the type of emotional event discussed (Fivush, Berlin, et al., 2003). We were particularly interested in how mothers reminisce about emotionally negative events, because negative emotions are often diﬃcult to cope with, and children must learn how to express and resolve negative aﬀect in culturally appropriate ways. Are mothers more elaborative when reminiscing about fear rather than sadness or anger? Further, does content vary depending on the type of emotion discussed? Do mothers diﬀer in their focus on the emotion itself, the causes of emotional experience, or resolution of negative aﬀect depending on the type of emotional event under discussion or the gender of the child? Mothers reminisced with their 4-year-old children about three speciﬁc events, a time the child was scared, angry, and sad. With daughters, mothers were more elaborative overall, talking in more embellished detail about emotional experiences than with sons. Mothers were also more evaluative with daughters than with sons, providing more feedback and more conﬁrmation of their daughters’ contributions to the conversations than their sons’. Similarly, girls were more elaborative than boys. But there were also diﬀerences depending on the type of emotion discussed. Across all three emotions, mothers discussed the causes of the emotional experiences to a greater extent than the emotion itself or its resolution, suggesting that mothers are helping their children to understand how emotional experiences arise. However, when discussing fearful events, mothers elaborated more, and they talked more about the facts concerning the event itself than when discussing sadness or anger. Mothers also focused on resolving fear more so than anger (but not sadness). Children also seemed to be more concerned with fearful experiences than with sadness or anger. They talked more about fear overall, and they provided more evaluations and resolutions when discussing fear than when discussing sadness or anger. In contrast, in conversations about anger, mothers did not elaborate, they did not discuss the facts surrounding the event itself, and they did not resolve anger as much as they did in conversations about fear. Rather, when discussing anger, mothers focused on emotional attributions. Children also did not talk as much about anger, they did not evaluate information about anger, and they did not discuss emotional resolutions of anger to the same extent as

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resolutions of fear or sadness. Finally, sadness falls between these two extremes. Conversations about sadness were not as elaborative overall as conversations about fear, nor did mothers focus on the event itself, as they did for fear, or on emotional attributions, as they did for anger. Rather, mothers focused on evaluating and resolving sad feelings. Children also focused on resolving sadness. These conversational patterns are illustrated in table 8.1, which presents excerpts from conversations between one mother-daughter dyad and one mother-son dyad, each reminiscing about three emotional events. Mothers’ focus on the causes of their children’s emotions is apparent, as are the gender diﬀerences. Across all three emotional events, the mother and daughter talk more about the emotional event, and the mother uses more nuanced emotion language and talks in more detail about the daughter’s experience and expression of emotion than in the mother-son dyad. These patterns conﬁrm the previous suggestion that girls are socialized into a more elaborated and diﬀerentiated understanding of their past emotions. Perhaps most important, research on parent-child reminiscing underscores that even when recalling the everyday events of our lives, emotion is an integral aspect of what we remember. Beginning very early in development, parents and children are co-constructing personal narratives replete with emotional experience; through these narratives, parents are helping their children to interpret and evaluate their experience. Mothers seem to reminisce more about emotions than do fathers, and both mothers and fathers reminisce about emotions more with daughters than with sons. Through participating in richly emotional reminiscing, girls may be constructing a more emotionally laden and emotionally nuanced sense of self in the past. Further, by placing emotions in a more interpersonal context with daughters than with sons, parents may be teaching girls to integrate emotions into relationships with others to a greater extent than are boys. Thus, girls may be developing a more embellished, more diﬀerentiated, and more relational emotional self-concept than are boys. However, there are also important diﬀerences depending on the type of emotion discussed. These patterns suggest that parents are inﬂuencing the way in which their children are learning to understand, express, and perhaps even experience speciﬁc emotions. An important limitation of this research is the focus on white middle-class American families. Emotional expression is clearly culturally mediated (Lutz & White, 1986); therefore, it is not surprising that there are cultural diﬀerences in parent-child reminiscing about emotional events (see Leichtman et al., 2003, for a review). For example, Wang (2002) asked American and Chinese mothers to reminisce about times when their preschool child was happy, scared, angry, and sad. American mothers used what Wang labeled an “emotion-explaining” style, a pattern similar to what we have just described, whereas Chinese mothers used an “emotion-criticizing” style. An emotion-explaining style helps create shared emotional experiences that deﬁne one in relation to others; an emotion-

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 . Excerpts From Mother-Child Conversations About Everyday Emotional Events (“. . .” indicates some missing dialogue) Mother-daughter dyad

Mother-son dyad

Conversations about fear M: And what happens when there’s a big thunder and lightening storm? C: I’d want to be with my mom and dad [whispering]. M: Yes, you want to be with your mom and dad. And what happens if you’re sleeping, and sleeping and there’s a big bunch of thunder in the middle of the night? What happens sometimes? C: Scared M: Scared, do you tremble like that? Do you shake? Huh? Then what do you do? C: I get up and go to my mom and dad [whispering]. M: You get up and go to your mom and dad. And what do we do? C: Say don’t worry. M: Say don’t worry. Do we hold you? Yes, does holding you help you when you’re scared? Yes.

M: . . . why did you come in bed with mommy and daddy? Cause how did you feel, how did that storm make you feel? C: Umm, I feel really scared. M: A little bit scared? C: Really scared. M: You were really scared. What scares you about the thunderstorm honey? C: . . . brokes the TV. M: Yeah, that scared you because the TV went oﬀ.

Conversations about anger M: Well, I seem to remember that yesterday you and Patrick were swinging on the swings and he was doing something that really annoyed you. . . . Do you remember? C: He wouldn’t give me a swing. M: Oh! That’s right . . . and did you wait patiently for a long time, hmm? C: Yes. M: And is that when you started to get really angry? Uh-huh, how do you feel inside when you get angry? C: . . . Mad. M: Mad! And did your mouth turn down at the corners? And do you feel like going grrrr? Conversations about sadness ... M: Well, one thing that made you really sad was when your best friend Shena moved away, right? Yeah, and did we watch all her things go on the moving truck? Uh-huh, and do you remember why she had to move away? C: . . . Because Shena’s Dad had to work.

M: Now how do you feel when Mommy makes you take you vitamins in the morning and you don’t want to take them? C: I feel mad. M: You do! And what do you do? C: I hide. M: . . . Uh-huh, then what happens to Mommy? How does Mommy feel when you didn’t take your vitamins and your calcium? C: Mad. M: Then what happens to [you]? C: Get in trouble. M: Yeah.

M: How did you feel when Mandy wouldn’t let you play the other day, when she was playing with Jess and she told you boys to go away? How did that make you feel? C: Umm, sad. M: And why does Mandy do that? (continued)

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 . (continued) Mother-daughter dyad

Mother-son dyad

Conversations about sadness M: Shena’s Daddy was going to start working at a new job . . . And do you still miss Shena when you think about it? Yes? C: Yes. M: It makes you sad, doesn’t it? But is she still your friend even far away? Yes! What can you do even though she’s far away? C: Give her a happy letter with a [drawing] on it. M: Give her a happy letter, right, and we have a drawing, don’t we?

C: Because she’s mean. M: [laughing] Is she mean? Is she mean all the time? When she doesn’t let you play, you’re not very happy, are you? C: Umm.

criticizing style uses emotion to instill proper behavior and values. Wang argues that these diﬀerent styles emerge from larger cultural constructions of self as independent or interdependent, as discussed earlier. Independent selves own and express their emotional experience, whereas interdependent selves use emotions to regulate appropriate social behavior (see also Mullin & Yi, 1995). Obviously, these are not orthogonal functions, and mothers and children from both cultures likely show elements of both styles, but Wang’s research highlights that children may be developing diﬀerent understandings of self and emotion depending on the larger social and cultural context within which reminiscing is embedded. Thus far, we have discussed how parent-child reminiscing modulates children’s developing understanding of their everyday emotional experiences. But what of more stressful and traumatic events? How do extreme levels of stress aﬀect children’s memories, and how might parent-guided reminiscing play a role in helping children to understand and cope with aversive experiences?

Memories of Stressful

and Traumatic Events

Intertwined with everyday emotional experiences are the unfortunate accidents, disasters, and other stressful experiences that occur over the course of a lifetime. The concept of stress is familiar to both laypersons and professionals. In fact, it is not uncommon to hear the words stress or trauma in everyday conversations. However, as Mason (1975) notes, “The single most remarkable historical fact concerning the term ‘stress’ is its persistent, widespread usage in biology and medicine in spite of almost chaotic disagreement over

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its deﬁnition” (p. 9). Despite the lack of a universal deﬁnition, the topic of stress and memory has been of interest to researchers from many areas of study. Because much of the developmental research stems from forensic issues involving children as witnesses or victims of violence, the focus has been on how stress aﬀects the amount, accuracy, and suggestibility of children’s recall of past experiences (see Ceci & Bruck, 1993, and chapter 10, this volume). Although not the focus in this chapter, the consensus on accuracy is clear (see Westcott, Davies, & Bull, 2002, for an overview). Even quite young children can respond to open-ended free-recall questions (e.g., “What was the man wearing?”) with accurate details of their past experiences. Moreover, repeatedly interviewing children about the same event does not compromise accuracy in the absence of suggestive and misleading questions (Fivush, Peterson, & Schwartzmueller, 2002). The problem is that preschoolers, though accurate, provide little information in response to these open-ended questions, and errors increase dramatically as questions become more close-ended. Accuracy is compromised in young children’s memory reports in two ways. First, responses to speciﬁc close-ended questions (e.g., “What was the man wearing on his head?”), especially yes/no questions (e.g., “Was the man wearing a hat on his head?”), are vulnerable to error during the preschool years (Fivush et al., 2002). Second, preschoolers are substantially more susceptible to misleading and suggestive questions (e.g., “What color was the man’s jacket?” when no jacket was worn) than older children and adults (Ceci & Bruck, 1993). And suggestive questions asked over repeated interviews can induce many errors into young children’s memory reports (Leichtman & Ceci, 1995). What is still in question is the extent to which these kinds of misleading questions change the actual memory representation or whether children are responding to the implicit social demands of the interviewer’s questions. Related to this, although children change their responses to speciﬁc questions, it is not clear that these errors are incorporated into children’s subsequent free recall (Cassal & Bjorkland, 1995; Fivush et al., 2002). Moreover, the extent to which stress interacts with accuracy of recall is still controversial. First and foremost, this research domain is plagued by the problem of operationalizing stress. Several methods have been devised to assess children’s stress levels, including self-report, global ratings of stress level by parents or doctors, objective stress ratings based on speciﬁc behavioral indices, and physiological measures such as heart rate, skin conductance, and hormonal levels. When directly compared, the diﬀerent measures of stress do not correlate highly with one another (Eisen, Goodman, Ghetti, & Qin, 1999; Ornstein, 1995; Parker, Bahrick, Merrit, Lundy, & Fivush, 1998); thus, it is not surprising that they do not correlate systematically with memory measures. In addition, diﬀerent measures of memory have been used across studies, some studies assessing free recall and other studies assessing cued recall or recognition. Also, diﬀerent aspects of the

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event are targeted for recall, such as central or peripheral information. Moreover, studies have examined events ranging from mildly stressful, such as getting an inoculation, to highly traumatic, such as witnessing the murder of a parent. Finally, stress may inﬂuence memory diﬀerently at diﬀerent developmental points, further complicating comparisons across studies. Several clinical case studies describe children’s memories of truly horrendous experiences, such as being kidnapped and buried alive or witnessing the murder of a parent (Malmquist, 1986; Terr, 1979, 1988). Terr (1979) reports that school-age children who were kidnapped from a school bus and essentially buried alive overnight were able to recall the horriﬁc event in vivid detail up to 4 years later. Similarly, in describing long-term memories of children traumatized during the preschool years, Terr (1988) reports that children 3 years of age or older at time of traumatization continue to report vivid and elaborated memories of events such as abuse, kidnapping, and other violent acts. However, children under the age of 3 at the time of the event do not develop the ability to recall the event verbally as they grow older, although aspects of the traumatic experiences may be present in their behavior. These ﬁndings suggest that real-life traumatic events are remembered in great detail over long periods of time, at least in children 3 or older at the time of the event. Although clinical studies allow rich description of memories of real-life trauma, they do not allow for systematic comparisons across children or type of event. To examine this question, developmental researchers have taken advantage of necessary but painful medical procedures that many children must endure. Studies use one of two approaches. One approach compares one group of children’s memories of stressful events, such as inoculations, to another group of children’s memories of more mundane events such as a routine doctor examination. Children in the stressful situation generally show enhanced memory for the event in comparison to the participants experiencing a more neutral event, suggesting that stressful events are better recalled than emotionally neutral events (see Pezdek & Taylor, 2001, for a review). The other methodological approach has been to select a single stress-producing event and examine individual diﬀerences in stress level. For instance, Merritt, Ornstein, and Spicker (1994) examined children’s recall of a stressful medical procedure, a voiding cystourethrogram. They found that children who experienced more stress during this procedure, as measured by behavioral ratings, recalled less accurate information than children who displayed less stress during the procedure. Similarly, Vandermass, Hess, and Baker-Ward (1993) found that high anxiety or stress had a debilitative eﬀect on older children’s recall of a dental operation but not on younger children’s, suggesting developmental diﬀerences in the stress-memory relation. More speciﬁcally, preschool children may experience and recall stressful events diﬀerently than older children. In a systematic, longitudinal research program examining children’s memories of a stressful event, Peterson and others have examined children’s memories

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of an injury resulting in emergency room treatment (Peterson, 1999; Peterson & Bell, 1996; Peterson & Whalen, 2001). Injuries were relatively minor, requiring only outpatient procedures, and included mostly lacerations requiring stitches, severe burns, and broken bones. Children recalled their injury and treatment within 2 weeks of the event and again at 6 months, 1 year, 2 years, and 5 years after the event. Although there are several nuances to the results, the basic ﬁnding is that children 3 years of age or older at the time of the experience recalled this event extremely well over the 5–year period. In fact, Peterson and Whalen report virtually no forgetting of the injury itself and little forgetting of the hospital treatment. However, there were no relations between stress, as assessed by maternal and child report on a Likert scale, and either amount or accuracy of recall. These results conﬁrm that children recall stressful events extremely well over long time periods, although they also contribute to the mixed ﬁndings in the literature over possible relations between stress and memory. Importantly, children under the age of 3 at the time of experience showed a somewhat diﬀerent pattern (Peterson & Rideout, 1998). One- and 2-year-old children who were not able to verbally recall the event when it occurred did not show accurate recall as they grew older. Although many of these children did respond to the interviewer’s questions about what happened at later interviews, about 50% of what they reported was wrong. Thus, similar to the clinical descriptions provided by Terr (1988), more systematically controlled research conﬁrms that children under the age of 3 may have particular diﬃculty verbally recalling events even as they grow older and develop the required language skills. Most important, Peterson and Rideout present evidence suggesting that it is not age per se that is critical, but rather children’s ability to verbally recall the event when it occurred. Those 2-year-olds who were able to give a coherent, although obviously still limited, verbal report of what happened when ﬁrst interviewed remained able to recall the event accurately as they grew older. Thus, it seems that language or narrative skill at the time of experience is a critical factor in predicting whether children will remain able to recall events accurately as they grow older (see Fivush, 1998a, and Fivush, Pipe, Murachver, & Reese, 1997, for review and further discussion of this issue). One of the limitations of this body of research is the focus on memories of medical procedures. Whereas many of these procedures are quite painful and stressful for young children, it is not clear that they approach the level of stress experienced during traumatic events. Further, children often take their emotional cues from the adults around them as to the meaning and severity of the event; in the case of medical procedures, parents may be stressed, but they are not in fear of either their own or their children’s lives (at least for the events that have been studied thus far). One of the prevalent theories about the relation between memory and stress comes from the Yerkes-Dodson law that predicts an inverted-U function (see Christianson, 1992, for an overview). Basically, it is postulated that as stress increases to moderate levels, memory will be enhanced

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due to increased attention and processing, but as stress increases to extreme levels, memory will be hindered because the system will be overwhelmed. Although this theory is widely cited, little evidence shows that this function holds. One problem in assessing this function is that control for level of stress while holding the event to be recalled constant is diﬃcult. And, of course, creating extremely high levels of stress in the laboratory is not ethical. Only one study has systematically examined relations between children’s levels of stress and memory for a naturally occurring life-threatening traumatic event. Bahrick, Parker, Fivush, and Levitt (1998) examined how stress aﬀected preschool children’s memories for Hurricane Andrew, a devastating storm that hit the Florida coast in 1992. Stress was deﬁned by the amount of property damage to the family’s home. Children were placed into either a low, moderate, or high damage group. Families who prepared for the hurricane, but sustained little property damage, were placed in the low damage group. If they experienced substantial damage to the perimeter of their home, such as the yard, windows, or roof, but the house itself remained intact, they were placed into the moderate damage group. Families who experienced a severe storm that penetrated the home, often resulting in partial collapse of the roof and multiple broken windows or doors, were placed into the high damage group. Three- and 4-year-old children were interviewed about their experiences within 2 to 6 months of the storm. Interviews began with an open-ended question about the hurricane, followed by nondirective prompts until the child did not recall any additional information. Then the experimenter asked a series of more speciﬁc questions about preparing for the storm, the storm itself, and the aftermath of the storm. Children’s recall was related to the amount of stress experienced, such that the children exposed to a moderate amount of damage recalled more than children who experienced high or low damage did. This pattern would seem to support the proposed inverted-U function between memory and stress. However, 6 years later, when the children were 9 and 10 years old, we interviewed them again about their hurricane experiences (Fivush, Sales, Goldberg, Bahrick, & Parker, in press). Figure 8.1 displays the mean amount of information children recalled at each interview by stress group. All children were able to recall the event in vivid detail 6 years later, and there were no diﬀerences in overall amount recalled among children in the low, moderate, or high damage groups. Thus, there is no longer an inverted-U function. In fact, children now reported more than twice as much information about the experiences as they had at the initial interview. We do not want to argue that no forgetting occurs; we argue that children are now able to verbally report much more of what they remember than they could when they were younger. In this situation, children were able to recall the event when it occurred, and, as their language skills increased, their verbal report of the event increased as well (see Peterson & Whalen, 2001, for similar ﬁndings and arguments). This conﬁrms our earlier discussion of Peterson’s research (Peterson & Rideout,

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Mean propositions recalled

140 120 100 80

Low Moderate High

60 40 20 0 Immediate Recall

6 year follow-up Recall

Figure 8.1. Mean number of propositions recalled by children in each stress group over time.

1998). In that research, children who were unable to recall the event at the time of occurrence were not able to subsequently recall the event with any accuracy, but like that research, we also found that children who could recall the core aspects of the event when it occurred remained able to recall the event in vivid detail over extended time, indicating that memory of stressful events is quite long lived. Importantly, amount of recall was not related to either retention interval or amount of rehearsal at either interview time. However, there were still eﬀects of stress on memory 6 years later. Children in the high damage group needed more prompts and cues to recall as much information as children in the moderate and low damage groups, as shown in ﬁgure 8.2. This changes the interpretation of the original ﬁndings. Obviously, if children in the high stress group are now recalling as much information as children in the other two groups, arguing that stress interferes with memory per se becomes diﬃcult. Rather, stress may interfere with either the ability or the willingness to retrieve information for recall. If we interpret the lower recall in the high damage group at the ﬁrst interview as a form of avoidance, in that highly stressed children simply did not want to talk about their experiences, then 6 years later children in the high damage group may express avoidance as being less willing to respond freely to the experimenter because they found it stressful to recall their experiences openly. However, when directly questioned and prompted, these children demonstrated that they do indeed recall as much as the children who experienced lesser damage. Thus, stress may interfere with retrieval in diﬀerent ways at diﬀerent developmental ages or as time since the stressful experience increases.

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Mean Amount Recalled

120 100 80 60

Free Recall Cued Recall

40 20 0 Low Stress

Moderate Stress

High Stress

Figure 8.2. Mean number of propositions recalled by children in each stress group in free and cued recall.

Although stress aﬀected recall at both interviews, children in all three damage groups recalled detailed information about their hurricane experience. Though we were unable to compare amount of recall about this event directly to other events recalled by these same children, comparing across studies of children’s memory, we found that children recalled substantially more about the hurricane event than their age-peers recall about more mundane or even mildly stressful events (see Fivush, 1998a, for a review). Further, although only a subset of the children’s recall was judged for accuracy by mothers, ratings of accuracy were extremely high, above 90%. Thus, it appears that highly stressful events are well recalled overall, although as stress increases, children may be less willing to think about and talk about their experiences. To illustrate the richness and detail of children’s recall, table 8.2 presents excerpts from a child in the high damage group and a child in the moderate damage group at each interview. These are children’s responses to the ﬁrst openended question, “What do you remember about Hurricane Andrew?” and the nondirective prompts that followed this question. As shown, both children recalled the event in great detail at each interview. Even 6 years later, children were able to narrate a detailed, coherent account of the storm and its consequences. These excerpts also illustrate how emotionally compelling the memories are, especially for children who experienced extensive damage to their homes. Children seem to remain highly aﬀected by their experience even years later. As we already mentioned, most of the research on stress and memory has focused on accuracy and overall amount of information children recall. However, relations between memory and stress are important not only for forensic reasons but also

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table 8.2 Excerpts of Children’s Recall of Hurricane Andrew Immediate interview

Follow-up interview

Child who experienced high damage E: Can you think really hard about the hurricane and tell me everything you remember about it? C: [Child nods yes] E: Yeah? What do you remember ﬁrst? C: Um, I remember we had friends over. E: You had friends over, yeah, what else? C: Um, I was, um, stuﬀed in a corner. E: You were stuﬀed in a corner, yeah, what else can you remember? C: I was in my bedroom. E: In your bedroom, yeah. C: And um . . . and um, during the hurricane, there was a window in my bedroom, and um, well we, I was stuﬀed in the corner and then we, then we, um, we had the Farmigan’s over and they, um, stayed at our house for a little bit longer after the hurricane. E: Yeah, what else can remember about that? C: Um, that they were sitting on the furniture and I wasn’t. E: And you weren’t. O.K. Can you remember anything else about the hurricane? C: [Child shakes head no]

E: Can you tell me everything you can remember about Hurricane Andrew? C: Okay. Um, I remember the hurricane was the day after my fourth birthday party. And we were scared. My grand—, grandparents came over. And our neighbors Sue and Terry. And it was me, my mom and my dad. And we were in my room and my grandparents were sleeping in my mom and dad’s room. And I remember I had on, I sat, I wanted to go close to the window because we had a mattress over our window, because there’s only one window in my room. And I sat and then this big lightening bolt came I was scared a lot and I remember half way through the night, part, a corner of our roof blew oﬀ. And our grandparents came and told us that it was oﬀ and we put two or three trashcans under it to catch it. And Terry, he had out little weather radio and he said he was sorry because there were no cartoons on, there was only weather about the hurricane. And I remember, I had my bed is in the corner of the room and about ﬁve feet before my closet and they made me, my mom and my dad made me stay there the whole night. Cause they were afraid if the window blew oﬀ, the mattress would hit me [she goes on like this for several more sentences]. . . . And I was really scared because I had never been through anything like that, and um, I don’t remember a lot.

Child who experienced moderate damage E: So, can you think really hard and tell me what you remember about Hurricane Andrew? C: Ah. . . . You know, in my neighbor’s house. E: Ah. C: All the screens ‘cause she has a column of screens . . . when . . . when the screen was knocked over, they had to get new screen, and there was all trees. My next door neighbor had to go all [makes noise] like that.

E: Can you think really hard about the hurricane and tell me everything that you can remember about it. We want to hear anything and everything that you can think of. C: Well, I remember we had a coconut palm in our backyard, and my dad had to cut all the coconuts oﬀ to make sure none of the windows broke or anything. E: Uh-huh. C: And, well, and that coconut palm broke in the Hurricane Andrew so now that’s (continued)

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table 8.2 (continued) Immediate interview

Follow-up interview

Child who experienced moderate damage E: Anything else you remember about that? C: Only this . . . only my little screen fell oﬀ and nothing else. And all the trees fell oﬀ, a lot a lot, but not all. E: Right. C: Any you know what, and even when it was almost the hurricane we were cutting coconuts, and then, then we got back inside, and then, and my dad, and then he is all sweaty and he has ants all over. That’s it. E: Ok. Anything else that you remember about the hurricane C: Um, I think nothing else.

not there anymore. But we didn’t, we were pretty lucky and we didn’t have much happen. All it was was, like, fences and stuﬀ. E: Uh-huh. C: And our pool was very dirty. E: Really? C: Yeah. We, uh, stayed in our, what used to be our play room, which is now our computer room, and we had little shutters that we put over the glass so no glass would break there so we were very safe there. And we had a, we had a patio by the pool. E: Uh-huh. C: And we have some sort of electrical shutters to close everything up in the patio, so we can put lots of our stuﬀ in there. And I don’t remember much of the hurricane because I don’t know how, but I fell asleep in the middle of it. E: Really? C: Uh-huh. So that’s about it.

Note. C stands for Child, E stands for Experimenter

because how we remember and incorporate the stressful occurrences of our lives has implications for future coping and physical and emotional well-being (Pennebaker, 1997). What we remember and how we come to understand the events of our lives may be more important for our everyday functioning than whether our memories are perfect replicas of the actual event (Fivush et al., in press). As the excerpts illustrate, children do not simply recall what happened during the hurricane; they are actively trying to understand and process what occurred, as indicated by the many references to their thoughts and emotions. Thus, we were interested in examining the content of children’s recall of Hurricane Andrew in relation to stress in more detail (Sales, Fivush, Parker, & Bahrick, 2002). In particular, based on research on expressive writing about negative events with adults (see Pennebaker, 1997, for a review), we focused on the inclusion of cognition and emotion words that have been related to higher levels of stress and coping with aversive events. Further, given the mixed ﬁndings in previous research, we were interested in examining relations among multiple measures of stress and memory. We included two diﬀerent types of stress measures at the initial interview: Likert scale ratings by mother and child assessing global assessment of experienced stress and more concrete, behaviorally based measures of stress, including the Frederick

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Posttraumatic Stress Disorder Reaction Index (Frederick, 1985), which asks mothers and children to rate 20 speciﬁc behaviors associated with stress (e.g., “Do thoughts about the hurricane make you feel afraid or upset?” and “Have you had bad dreams since the hurricane?”); a child well-being score, which assessed 35 speciﬁc behaviors associated with stress (e.g., “Wants to sleep with adults” and “Laughs easily”); and the damage groupings, as previously deﬁned. Only the PTSD Reaction Index was completed at the follow-up interview. As shown seen in table 8.3, the damage assessment, the child well-being survey and the PTSD Reaction Index, which all rate speciﬁc physical events or speciﬁc child behaviors, were highly correlated with one another, but not related to the more global and subjective Likert scale stress measures. Thus, the most reliable measures of stress seem to be those that decrease the amount of subjective interpretation of the rater and depend instead on more observable events and behaviors. Furthermore, only the objective ratings of stress were related to the content of children’s recall. As shown in table 8.4, which displays correlations among the stress and memory measures, highly stressed children initially included less positive emotion, fewer cognitive processing words, and less information overall than less stressed children. The inclusion of less language indicative of cognitive and emotional processing of the event, as well as shorter narratives, suggests that the highly stressed children had diﬃculty processing the event immediately following the storm. However, 6 years later they included more negative emotion words and more cognitive words in their recall than less stressed children, indicating that these highly stressed children are still trying to process and understand the event they experienced when they were only 3 and 4 years old to a greater extent than children who were less stressed at the time. In contrast, children who exhibited more emotional and cognitive processing indicative of better coping during their initial interview had better psychological outcomes 6 years later, as indicated by lower PTSD scores. These patterns accord with our previous interpretation that children who were highly stressed by Hurricane Andrew actively tried to avoid thinking about and processing the event. However, this table 8.3 Correlations Between Stress Variables Dmg MSR CSR CWB PTSD1 PTSD2

.43*

.03 -.36* .43** .13

MSR

CSR

CWB

.09

-.25 .19 .16

.16

-.07 .21

-.79**

-.13

PTSD1

.24

Note: Dmg = damage rating; MSR = mother’s rating of child’s stress; CSR = child’s rating of own stress; CWB = child wellbeing score; PTSD1 = Time 1 total PTSD score; PTSD2 = Time 2 total PTSD score. **p<.05. **p<.01.

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table 8.4 Correlations Between Stress and Content Variables

Damage rating Mom’s stress rating Child’s stress rating Child well-being PTSD Total Time 1 PTSD Total Time 2

Time 1 content variables

Time 2 content variables

Pos Neg Cog Total words words words recall

Pos Neg Cog Total words words words recall

-.37* -.24 .07 .27 -.17 -.37*

-.06 -.12 .02 .51** -.30 -.11

-.53** -.19 -.09 .08 -.09 -.01

-.37* -.25 -.18 .27 -.38* -.37*

.21 .03 .06 -.06 .11 .14

.46** .01 .04 -.16 .31 .26

.45** .06 -.18 -.16 .29 .26

.02 -.29 -.26 -.11 .11 .14

*p<.05 **p <.01

early avoidance led to later diﬃculty, and 6 years later, these children still seem to be struggling with trying to process their experience. In contrast, those children who were able to talk about their hurricane experience in more cognitively and emotionally integrative ways showed fewer stress symptoms related to the hurricane 6 years later. Consistent with these ﬁndings, Wolitzky, Fivush, Zimand, Hodges, and Rothbaum (2001) found that children who included more internal state language indicative of cognitive and emotional processing in their narratives about a cancer-related medical procedure had lower anxiety levels. Thus, across two types of stressful experiences the same pattern emerges between stress levels and content of children’s recall. Children who are less anxious and stressed immediately following an aversive event are able to express more about their thoughts and emotions concerning the event than children who are more anxious and stressed, and these children show fewer symptoms of stress over time. However, over time, more highly stressed children seem to include more of their thoughts and emotions in their recall. More detailed longitudinal research is needed to elucidate temporal patterns, as well as to establish causal relations. Still, the ﬁndings thus far indicate that it is not just amount of recall that may be aﬀected by stress but also the content of what children focus on when they report traumatic experiences. A major limitation of this research is the focus on negative events. Researchers tend to use the terms arousal and stress interchangeably and ignore emotional valence. It is possible that memory is aﬀected by higher arousal in similar ways for both positive and negative experiences, or there may be diﬀerences depending on valence of the event. Few studies systematically compare memory of events that are equally arousing but diﬀer in valence. The few experimental studies that have manipulated both of these dimensions found that arousal, not valence, accounts for better memory in adults, at least for static images of events presented in a laboratory setting (Hamann, Ely, Grafton, & Kilts, 1999). In the ﬁrst study to compare children’s memories of positive experiences directly to negative stressful life events, we examined narratives produced by

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5- to 12-year-old children growing up in a violent community (Fivush, Hazzard, Sales, Sarfati, & Brown, 2003).Because of the nature of these children’s living environments, many of the negative events narrated were highly traumatic and involved interpersonal violence, including witnessing a gun ﬁght between relatives, seeing one’s mother arrested and taken away by the police, and seeing an assault victim. However, other children narrated negative events that fall well within the range of “normal” childhood stressors, including serious illnesses and invasive medical procedures. Most of the positive events were family and school excursions to parks and beaches and church retreats. Because we allowed families to nominate the positive and negative events of their lives, it is not clear that the positive and negative events selected were equally arousing. We were speciﬁcally interested in the type of information children recalled, and we coded all unique units of information into one of seven categories: mention of persons, places, objects, actions, descriptions, and internal states including thoughts and emotions. As shown in ﬁgure 8.3, children recalled a

40 35

Mean Units

30 25 20 15

Positive Negative

10 5 0 l t e n n n on ora ec at io io io s j t t t t r c b a S p ip A O Pe m oc al cr e n s L r e

T D te In Codes

Figure 8.3. Mean amount of information recalled in each category for positive and negative events.

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great deal of information about both types of events. Overall amount of recall did not diﬀer between positive and negative events, but the content diﬀered. When recounting negative experiences, children included more information about their thoughts and emotions than when they recounted positive experiences. In contrast, when recalling positive experiences, they recalled more information about people, actions, and descriptions. Intriguingly, children’s narratives of the negative events were also more coherent than the positive event narratives. Coherence may emerge as children try to think through and process aversive experiences.There were no diﬀerences in parental reports of how often the positive or negative events had been talked about, nor was time since occurrence a factor in amount or type of recall. This pattern suggests that, even though children report similar amounts of information quantitatively, their reports of negative events diﬀer in content from their reports of positive events. The inclusion of thoughts and emotions in children’s narratives likely is related to how aversive the event is and may reﬂect the way in which children are trying to process, understand, and possibly cope with these negative experiences. Given that parent-guided conversations about everyday emotional experiences may help children in understanding and coping with negative emotion, we ask how parents may discuss highly stressful events with their young children and how this may aﬀect how children remember and cope with stress.

Parent-Child Reminiscing About

Stressful Events

To date, only two studies have examined how parents and children discuss highly stressful experiences. Ackil, Waters, Dropnik, Dunisch, and Bauer (1999) compared mother-child conversations about a devastating tornado that leveled their town to conversations about a nontraumatic event. Tornado conversations included more mention of negative emotion and information about the causes and consequences of the event than did the conversations about the nontraumatic events, suggesting that mothers are using the negative conversations as an opportunity to facilitate their children’s understanding of this overwhelming event. However, this study focused on the content of mothers’ and children’s conversations and did not assess parental reminiscing style. As we discussed earlier, elaborative parents facilitate the development of more detailed and embellished autobiographical narratives in their children. If parental reminiscing style remains consistent across positive and negative events, children of elaborative parents should produce more detailed narratives about negative past events as well. Findings in the adult literature indicate that detailed and coherent narratives of stressful events are related to higher levels of coping and well-being (Foa, Molnar, & Cashman, 1995; Pennebaker, 1997). As with adults, a more

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detailed memory of negative events may facilitate children’s coping with such events. Thus, an elaborative parental reminiscing style may help children cope with stressful life experiences. We examined both reminiscing style and content of parent-child conversations about two emotionally laden events: an injury requiring emergency room treatment and an individually nominated positively valenced experience (Sales, Fivush, & Peterson, 2003). As in previous research, we deﬁned parental style as extent of elaboration. Parental reminiscing style was consistent across the two emotional conversations, such that parents who were more highly elaborative when reminiscing about the positive experience were also more elaborative when reminiscing about the negative experience. Further, parents with a highly elaborative style had children who reported more new information during the conversations. However, there were also diﬀerences in parental reminiscing style for positive and negative events. When reminiscing about stressful events, parents asked a higher proportion of open-ended memory questions to their children, which require children to provide information in response, whereas when reminiscing about the positive experiences, parents asked a higher proportion of yes/ no questions, which require children only to conﬁrm or negate the questions. Parents also focused more on emotion when discussing positive experiences with their children and more on causal explanations when discussing the stressful experiences. These diﬀerences suggest that parents may have diﬀerent underlying goals in these two diﬀerent emotional contexts. Reminiscing about shared positive experiences serves to create, maintain, and strengthen emotional bonds, as well as to create a shared history, which is a basis for family identity (Fivush et al., 1996). Thus, in emotionally positive conversations, parents engage in coconstructing the experience with their children, with each conversational partner contributing information about the shared event. Furthermore, a greater focus on emotion, and especially positive emotion, may highlight how the event was meaningful to the parent-child relationship. In contrast, discussing stressful experiences may serve more of a didactic function. Parents are concerned with teaching their children how to cope with life’s stressful experiences and to avoid similar situations in the future. To facilitate their children’s thinking about what happened and why, parents may try harder to elicit their children’s recall of details of the event, rather than providing this information themselves and asking for conﬁrmation. Moreover, as in Ackil et al. (1999), parents focused on the causes of negative events more so than of positive events. Interestingly, parents focus on causes of emotion even when reminiscing about everyday negative events, as we noted earlier. Focusing on causal information helps children understand how and why stressful events occurred, thereby making the event more comprehensible and perhaps providing a lesson on how to cope with similar events. Thus, the functions of reminiscing about

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negative events, whether they are the everyday ups and downs or more serious and even traumatic experiences, seem to diﬀer from the functions of reminiscing about more positive experiences. Most intriguing, we are now exploring whether parental reminiscing style predicts children’s independent recall of stressful events in interviews with an unfamiliar adult (Peterson, Sales, & Fivush, 2002). Regression analyses on the amount and accuracy of children’s recall of their injury and hospital treatment indicates that parental education level, parental report of amount of family discussion of the event, parental report of the children’s stress level, and children’s language skills do not predict children’s’ recall, but parental reminiscing style does. Children of highly elaborative parents recall the hospital treatment more accurately and in more detail than children of less elaborative parents. Recall of the injury is more variable, with parental reminiscing style predicting level of detail but not accuracy. These ﬁndings indicate that parents who discuss emotionally diﬃcult events with their young children in elaborative ways may help facilitate their children’s understanding and memory of these events. Future analyses will allow us to examine whether parental style continues to facilitate children’s memories for stressful events over time.

Narratives and Coping Perhaps most intriguing, our research points to the close connection between memory and coping. The ways in which we recall the negative events of our lives is critical for subsequent physical and psychological well-being (Pennebaker, 1997). Adults who narrate stressful events more coherently, and include more emotion words and more words indicative of causal and cognitive processing (e.g., realize, understand, because) subsequently show lower levels of anxiety, a higher sense of well-being, and better immune system functioning than adults who narrate stressful events less coherently, and use fewer emotion and causal/ cognitive words. Our results suggest that, for young children, who are not yet able to create a coherent account of a stressful event for themselves, the ways in which adults, and particularly parents, help them to organize and remember these events may have important implications for children’s coping. Highly elaborative parents, who help their children construct a coherent and emotionally detailed narrative and help provide a causal-explanatory framework for the event, may facilitate their children’s coping eﬀorts. In turn, children of highly elaborative parents come to be able to construct coherent and emotionally detailed narratives of past experiences for themselves and thus may also come to develop better coping strategies to handle aversive events. Thus, we posit a dialectical developmental relation between parental reminiscing style and the development of children’s coping strategies (see Bretherton, 1996, for related arguments).

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Gender diﬀerences in parental reminiscing may also have implications for coping. Because parents are more elaborative and more emotional when reminiscing with their young daughters than with their sons, girls seem to develop more detailed and emotionally dense narratives of their personal past than do boys. This, in turn, suggests that girls may also develop better coping strategies than boys. Little is known about the development of coping strategies in children in general, and little attention has been paid to possible gender diﬀerences. We are currently examining these issues in our laboratory.

Remembering Interpersonal

Violence

Finally, we emphasize that virtually all of the research on children’s memories for stressful events has focused on medical procedures and natural disasters, and this limitation may aﬀect conclusions. First, these events do not involve interpersonal violence. Even though children may not understand the necessity of painful and invasive medical procedures, these events may not approach the interpersonal betrayal involved when one individual intentionally harms another. Interpersonal violence shatters basic assumptions about human interaction (Janoﬀ-Bulman, 1992). Second, and equally important, children too often experience violence at the hands of trusted adults. Physical abuse and sexual abuse are not simply stressful experiences; they fundamentally undermine a child’s belief in a safe world. In this way, interpersonal violence, speciﬁcally abusive experiences, may be remembered very diﬀerently from other kinds of stressful experiences (Fivush, 1998a; Freyd, 1996). Moreover, given the role of parent-child reminiscing in helping children to make sense of stressful experiences, and the posited relation to coping, children who experience violence and abuse may not have the opportunity to talk about these experiences with adults who can help them resolve and cope with the aversive aﬀect. Often violence and abuse occurs within silenced communities, where children are implicitly or explicitly not allowed to speak of their experiences. Thus, children are left on their own to make sense out of what is essentially senseless. It is not clear from the research ﬁndings thus far what might happen to these kinds of memories (see Fivush, 1998a, for a full discussion of this issue). Certainly, this is a critical topic for future research.

Conclusions and Implications We began this chapter with the assertion that emotion and memory are inseparable; the events of our lives are imbued with emotion, both at the time of experience and in retrospect. In the process of reminiscing with others, our life

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experiences take on deep emotional and evaluative meaning that aﬀects our sense of our self and our autobiographical history. The research we reviewed supports this assertion. Beginning very early in development, parents and children are already reminiscing in emotionally rich ways about their shared experiences. Parents who reminisce with their preschool children in elaborative and emotional ways have children who begin to tell the stories of their own lives in greater and more nuanced emotional detail. Further, these patterns are related to gender. Both mothers and fathers reminisce in more emotionally embellished ways with their preschool daughters than with their sons, and by the end of the preschool years, girls are including more emotion and more diﬀerentiated emotion in their own autobiographical narratives. This research demonstrates that even when recalling and reminiscing about the everyday events of our lives, emotion is an integral part of our experience. We do not simply remember what happened; we remember what these events meant to us in the past and continue to mean to us in the present. Moreover, our review points to the importance of examining how emotional events are recalled, examining issues that go beyond accuracy. Although stress is a diﬃcult concept to deﬁne and measure, the research indicates that highly stressful events are well recalled even over long periods. Our emphasis on content provides important new information about how and why stressful events are remembered. Stress and memory are intricately interrelated, such that level of experienced stress inﬂuences the emotional and cognitive content of children’s recall, and the content of children’s recall is related to continuing levels of stress as time since the experience passes. What children are remembering about the stressful events of their lives is important not just for understanding memory but for understanding coping and emotional resilience. The way in which children make sense of their stressful experiences, often through participating in joint reminiscing with their parents, helps them to place these stressful experiences in an appropriate context, in which children develop a sense of control over their life experiences through the ability to understand and regulate their emotional reactions. A functional approach to memory for emotional events expands the focus of research from addressing accuracy and retention to examining relations between parent-guided reminiscing, children’s developing narratives, and coping with aversive events.

References Ackil, J., Waters, J., Dropnik, P., Dunisch, D., & Bauer, P. (1999). From the eyes of the storm: Mother-child conversations about a devastating tornado. Poster session presented at the biennial meetings of the Society for Research in Child Development, Albuquerque, NM. Adams, S., Kuebli, J., Boyle, P., & Fivush, R. (1995). Gender diﬀerences in parentchild conversations about past emotions: A longitudinal investigation. Sex Roles, 33, 309–323.

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Bahrick, L. E., Parker, J. F., Fivush, R., & Levitt, M. (1998). The eﬀects of stress on young children’s memory for a natural disaster. Journal of Experimental Psychology: Applied, 4, 308–331. Bauer, P. J., Stennes, L., & Haight, J. (in press). Representation of the inner self in autobiography: Women’s and men’s use of internal state language in personal narratives. Memory. Bluck, S., & Alea, N. (2002). Exploring the functions of autobiographical memory. In J. D. Webster & B. K. Haight (Eds.), Critical advances in reminiscing work: From theory to application (pp. 61–75). New York: Springer. Bretherton, I. (1996). Internal working models of attachment relationships as related to resilient coping. In G. G. Noam & K. W. Fischer (Eds.), Development and vulnerability in close relationships (pp. 3–27). Mahwah, NJ: Erlbaum. Bretherton, I., Fritz, J., Zahn-Waxler, C., & Ridgeway, D. (1986). Learning to talk about emotions: A functionalist perspective. Child Development, 57, 529–548. Buckner, J. P., & Fivush, R. (1998). Gender and self in children’s autobiographical narratives. Applied Cognitive Psychology, 12, 407–429. Cassel, W. S., & Bjorkland, D. F. (1995). Developmental patterns of eyewitness memory and suggestibility: An ecologically based short-term longitudinal study. Law and Human Behavior, 19, 507–532. Ceci, S. J., & Bruck, M. (1993). Suggestibility of the child witness: A historical review and synthesis. Psychological Bulletin, 113, 403–439. Christianson, S.-Å. (1992). Emotional stress and eyewitness memory: A critical review. Psychological Bulletin, 112, 284–309. Davis, P. J. (1990). Gender diﬀerences in autobiographical memories for childhood emotional experiences. Journal of Personality and Social Psychology, 76, 498–510. Denham, S. A., Zoller, D., & Couchoud, E. A. (1994). Socialization of preschoolers’ emotion understanding. Developmental Psychology, 30, 928–936. Dunn, J., Bretherton, I., & Munn, P. (1987). Conversations about feeling states between mothers and their young children. Developmental Psychology, 23, 132– 139. Dunn, J., Brown, J., & Beardsall, L. (1991). Family talk about feeling states and children’s later understanding of others’ emotions. Developmental Psychology, 27, 448–455. Eisen, M., Goodman, G. S., Ghetti, S., & Qin, J. (1999, July). An examination of abuse disclosures in maltreated children. Paper presented at the meetings of the Society for Applied Research in Memory and Cognition, Boulder, Colorado. Eisenberg, A. (1985). Learning to describe past experience in conversation. Discourse Processes, 8, 177–204. Fischer, A. H. (2000). Gender and emotion: Social psychological perspectives. New York: Cambridge University Press. Fivush, R. (1988). The functions of event memory: Some comments on Nelson and Barsalou. In U. Neisser & E. Winograd (Eds.), Remembering reconsidered: Ecological and traditional approaches to memory (pp. 277–282). New York: Cambridge University Press. Fivush, R. (1989). Exploring sex diﬀerences in the emotional content of mother-child talk about the past. Sex Roles, 20, 675–691.

 ’     

267

Fivush, R. (1991). Gender and emotion in mother-child conversations about the past. Journal of Narrative and Life History, 1, 325–341. Fivush, R. (1993). Emotional content of parent-child conversations about the past. In C. A. Nelson (Ed.), The Minnesota Symposium on Child Psychology: Memory and aﬀect in development (pp. 39–77). Hillsdale, NJ: Erlbaum. Fivush, R. (1994). Constructing narrative, emotion and self in parent-child conversations about the past. In U. Neisser & R. Fivush (Eds.), The remembering self: Accuracy and construction in the life narrative (pp. 136–157). New York: Cambridge University Press. Fivush, R. (1998a). Children’s memories for traumatic and non-traumatic events. Development and Psychopathology, 10, 699–716. Fivush, R. (1998b). Gendered narratives: Elaboration, structure and emotion in parent-child reminiscing across the preschool years. In C. P. Thompson, D. J. Herrmann, D. Bruce, J. D. Read, D. G. Payne, & M. P. Toglia (Eds.), Autobiographical memory: Theoretical and applied perspectives (pp. 79–104). Hillsdale, NJ: Erlbaum. Fivush, R., Berlin, L., Sales, J. M., Mennuti-Washburn, J., & Casidy, J. (2003). Functions of parent-child reminiscing about negative events. Memory, 11, 179–192. Fivush, R., Brotman, M., Buckner, J. P., & Goodman, S. (2000). Gender diﬀerences in parent-child emotion narratives. Sex Roles, 42, 233–254. Fivush, R., & Buckner, J. P. (2000). Gender, sadness and depression: Developmental and socio-cultural perspectives. In A. H. Fischer (Ed.). Gender and emotion: Social psychological perspectives (pp. 232–253). Cambridge: Cambridge University Press. Fivush, R., & Buckner, J. P. (2003). Constructing gender and identity through autobiographical narratives. In R. Fivush & C. Haden (Eds.), Autobiographical memory and the construction of a narrative self: Developmental and cultural perspectives (pp. 149–168). Hillsdale, NJ: Erlbaum. Fivush, R., & Fromhoﬀ, F. (1988). Style and structure in mother-child conversations about the past. Discourse Processes, 11, 337–355. Fivush, R., Gray, J. T., & Fromhoﬀ, F. A. (1987). Two year olds’ talk about the past. Cognitive Development, 2, 393–409. Fivush, R., & Haden, C. (1997). Narrating and representing experience: Preschoolers’ developing autobiographical recounts. In P. van den Broek, P. A. Bauer, & T. Bourg (Eds.), Developmental spans in event comprehension and representation: Bridging ﬁctional and actual events. Hillsdale, NJ: Erlbaum. Fivush, R., & Haden, C. (2003). Autobiographical memory and the development of a narrative self: Developmental and cultural perspectives. Hillsdale, NJ: Erlbaum. Fivush, R., Haden, C., & Adam, S. (1995). Structure and coherence of preschoolers’ personal narratives over time: Implications for childhood amnesia. Journal of Experimental Child Psychology, 60, 32–56. Fivush, R., Haden, C., & Reese, E. (1996). Remembering, recounting and reminiscing: The development of autobiographical memory in social context. In D. Rubin (Ed.), Reconstructing our past: An overview of autobiographical memory (pp. 341– 359). New York: Cambridge University Press. Fivush, R., Hazzard, A., Sales, J., Sarfati, D., & Brown, T. (2003). Creating coher-

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  

ence out of chaos? Children’s narratives of emotionally negative and positive events. Applied Cognitive Psychology, 17, 1–19. Fivush, R., Peterson, C., & Schwarzmueller, A. (2002). Questions and answers: The credibility of child testimony in the context of speciﬁc questions. In M. Eisen, G. S. Goodman, & J. Quas (Eds.), Memory and suggestibility in the forensic interview (pp. 331–354). Hillsdale, NJ: Erlbaum. Fivush, R., Pipe, M.-E., Murachver, T., & Reese, E. (1997). Events spoken and unspoken: Implications of language and memory development for the recovered memory debate. In M. Conway (Ed.), True and false memories (pp. 34–62). Oxford: Oxford University Press. Fivush, R., Sales, J. M., Goldberg, A., Bahrick, L., & Parker, J. (in press). Weathering the storm: Children’s long-term recall of Hurricane Andrew. Memory. Foa, E. B., Molnar, C., & Cashman, L. (1995). Change in rape narratives during exposure therapy for posttraumatic stress disorder. Journal of Traumatic Stress, 8, 675–690. Frederick, C. J. (1985). Children traumatized by catastrophic situations. In S. Eth & D.F. Ross (Eds.), Children’s eyewitness memory (pp. 1–23). New York: Springer. Freyd, J. (1996). Betrayal trauma: The logic of forgetting childhood abuse. Cambridge, MA: Harvard University Press. Haden, C. A., Didow, S. M., Ornstein, P. A., & Eckerman C. O. (2001). Mother-child talk about the here-and now: Linkages to subsequent remembering. Child Development, 72, 1016–1031. Halberstadt, A. G., Denham, S. A., & Dunsmore, J. (2001). Aﬀective social competence. Social Development, 10, 79–119. Hamann, S. B., Ely, T. D., Grafton, S. T., & Kilts, C. D. (1999). Amydala activity related to enhanced memory for pleasant and aversive stimuli. Nature Neuroscience, 2, 289–293. Hamond, N. R., & Fivush, R. (1991). Memories of Mickey Mouse: Young children recount their trip to Disney World. Cognitive Development, 6, 433–448. Han, J. J., Leichtman, M. D., & Wang, Q. (1998). Autobiographical memory in Korean, Chinese, and American children. Developmental Psychology, 34, 701–713. Harley, K., & Reese, E. (1999). Origins of autobiographical memory. Developmental Psychology, 35, 1338–1348. Hudson, J. A. (1990). The emergence of autobiographic memory in mother-child conversation. In R. Fivush, & J. A. Hudson (Eds.), Knowing and remembering in young children (pp. 166–196). New York: Cambridge University Press. Hudson, J. A., & Shapiro, L. (1991). Eﬀects of task and topic on children’s narratives. In A. McCabe & C. Peterson (Eds.), New directions in developing narrative structure (pp. 89–136). Hillsdale, NJ: Erlbaum. Janoﬀ-Bulman, R. (1992). Shattered assumptions. New York: Free Press. Kuebli, J., Butler, S., & Fivush, R. (1995). Mother-child talk about past events: Relations of maternal language and child gender over time. Cognition & Emotion, 9, 265–293. Kuebli, J., & Fivush, R. (1992). Gender diﬀerences in parent-child conversations about past emotions. Sex Roles, 12, 683–698.

 ’     

269

Leichtman, M. D., & Ceci, S. J. (1995). The eﬀects of stereotypes and suggestions on preschoolers reports. Developmental Psychology, 31, 558–578. Leichtman, M., Wang, Q., & Pillemer, D. P. (2003). Cultural variation in interdependence and autobiographical memory. In R. Fivush & C. Haden (Eds.), Autobiographical memory and the construction of a narrative self: Developmental and cultural perspectives (pp. 73–98). Hillsdale, NJ: Erlbaum. Lutz, C. A., & White, G. M. (1986). The anthropology of emotion. Annual Review of Anthropology, 15, 405–436. Malmquist, C. P. (1986). Children who witness parental murder: Post-traumatic aspects. Journal of the American Academy of Child Psychiatry, 25, 320–325. Mason, J. W. (1975). A historical view of the stress ﬁeld. Part 1. Journal of Human Stress, 1, 6–12. McCabe, A., & Peterson, C. (1991). Getting the story: A longitudinal study of parental styles in eliciting narratives and developing narrative skill. In A. McCabe & C. Peterson (Eds.), Developing narrative structure (pp. 217–253). Hillsdale, NJ: Erlbaum. Merritt, K. A., Ornstein, P. A., & Spicker, B. (1994). Children’s memory for a salient medical procedure: Implications for testimony. Pediatrics, 94, 17–23. Mullen, M., & Yi, S. (1995). The cultural context of talk about the past: Implications for the development of autobiographical memory. Cognitive Development, 10, 407–419. Nelson, K. (1993). The psychological and social origins of autobiographical memory. Psychological Science, 1, 1–8. Nelson, K., & Fivush, R. (2002). The emergence of autobiographical memory. Manuscript submitted for publication. Ornstein, P.A. (1995). Children’s long-term retention of salient personal experiences. Journal of Traumatic Stress, 8, 581–606. Oyserman, D., & Markus, H. (1993). The sociocultural self. In J. Suls (Ed.), Psychological perspectives on the self: The self in social perspective (Vol. 4, pp. 187–220). Hillsdale, NJ: Erlbaum. Parker, J., Bahrick, L., Merrit. K., Lundy, B., & Fivush, R. (1998). Eﬀects of stress on children’s memory for a natural disaster. In C. P. Thompson, D. J. Herrmann, J. D. Read, D. Bruce, D. G. Payne, & M. P. Toglia (Eds.), Eyewitness memory: Theoretical and applied perspectives (pp. 31–54). Hillsdale, NJ: Erlbaum. Pennebaker, J. W. (1997). Opening up. New York: Guilford. Peterson, C. (1999). Children’s memories for medical emergencies: 2 years later. Developmental Psychology, 35, 1493–1506 Peterson, C., & Bell, M. (1996). Children’s memory for traumatic injury. Child Development, 67, 3045–3070. Peterson, C., & McCabe, A. (1982). Developmental psycholinguistics: Three ways of looking at a narrative. New York: Plenum. Peterson, C. & Rideout, R. (1998). One- and two-year-olds remember medical emergencies. Developmental Psychology, 34, 1059–1072. Peterson, C., Sales, J. M., & Fivush, R. (2002). Predicting children’s recall of emotionally negative events. Paper submitted to the biennial meetings of the Society for Research in Child Development, Tampa, FL.

270

  

Peterson, C., & Whalen, N. (2001). Five years later: Children’s memories for medical emergencies. Applied Cognitive Psychology, 15, 1–18. Pezdek, K., & Taylor, J. (2001). Memories of traumatic events. In M. Eisen, G. S. Goodman, & J. S. Quas (Eds.), Memory and suggestibility in the forensic interview (pp. 165–184). Hillsdale, NJ: Erlbaum. Pillemer, D. (1998). Momentous events, vivid memories. Cambridge, MA: Harvard University Press. Pillemer, D., & White, S.H. (1989). Childhood events recalled by children and adults. In H. W. Reese (Ed.), Advances in child development and behavior, Vol. 22. New York: Academic Press. Reese, E., Haden, C. A., & Fivush, R. (1993). Mother-child conversations about the past: Relationships of style and memory over time. Cognitive Development, 8, 403–430. Reese, E., Haden, C. A., & Fivush, R. (1996). Mothers, fathers, daughters and sons: Gender diﬀerences in reminiscing. Research on Language and Social Interactions, 29, 27–56. Sales, J. M., Fivush, R., Parker, J., & Bahrick, L. (2002). Stressing memory: Long term relations among children’s stress, recall and psychological outcome following Hurricane Andrew. Manuscript submitted for publication. Sales, J. M., Fivush, R., & Peterson, C. (2003). Parental reminiscing about positive and negative events. Journal of Cognition and Development, 4, 185–209. Terr, L. C. (1979). Children of Chowchilla: A study of psychic trauma. Psychoanalytic Study of the Child, 34, 547–623. Terr, L. C. (1988). What happens to early memories of trauma? A study of twenty children under age ﬁve at the time of documented traumatic events. Journal of the American Academy of Child and Adolescent Psychiatry, 27, 96–104. Vandermass, M. O., Hess, T. M., & Baker-Ward, L. (1993). Does anxiety aﬀect children’s reports of memory for a stressful event? Journal of Applied Psychology, 7, 109–128. Vygotsky, L. S. (1978). Mind in society: The development of higher psychological processes. Cambridge, MA: Harvard University Press. Wang, Q. (2002). “Did you have fun?”: American and Chinese mother-child conversations about shared emotional experiences. Cognitive Development, 16, 693–715. Westcott, H., Davies, G., & Bull, R. (Eds.). (2002). Children’s testimony in context. New York: Wiley. Wolitzky, K. Fivush, R., Zimand, E., Hodges, L., & Rothbaum, B. O. (2001). Coping with cancer: Relations among parent and child coping, anxiety and distress, and eﬀectivenes of virtual reality during invasive medical procedures. Manuscript submitted for publication. Zahn-Waxler, C., Cole, P., & Barrett, K. (1991). Guilt and empathy: Sex diﬀerences and implications for the development of depression. In J. Garber & K. Dodge (Eds.), The development of emotion regulation and deregulation: Cambridge studies in social and emotional development (pp. 243–272). New York: Cambridge University Press.

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M

ost studies investigating the relationship between emotion and memory in adults have used college students as participants. However, the impact of emotion on memory may change across the adult life span. Compared with younger adults, older adults exhibit deﬁcits in many types of memory tasks (for reviews, see Light, 1996; Prull, Gabrieli, & Bunge, 2000; Zacks, Hasher, & Li, 2000). In contrast, older adults actually improve rather than decline in emotional well-being and regulation (e.g., Carstensen & Charles, 1998). Emotions gain centrality in everyday information processing with age (Blanchard-Fields, 1998; Labouvie-Vief, 1998), and there is evidence that brain regions associated with emotional processes deteriorate less with age than many other regions. As outlined in the ﬁrst part of this chapter, this research on emotion and aging predicts that the relationship between emotion and memory should change as people age. In the second part of the chapter, I review studies examining age diﬀerences in memory for emotional information. These studies reveal that emotion becomes more salient in memory and that emotional goals have more of an inﬂuence as one grows older.

Age-Related Changes in Emotional

Processes and Their Implications

for Memory

Emotional Well-Being Improves

Across the Adult Life Span

Emotional well-being remains stable or even is enhanced with age. Younger adults are at higher risk for depression than older adults (Lawton, Kleban, & Dean, 1993; Weissman, Leaf, Bruce, & Florio, 1988). Even among patients di-

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agnosed with dysthymia (a milder, chronic form of depression), older adults have higher ratings for emotional well-being and seem to be in better mental health (Oxman, Barrett, Sengupta, & Williams, 2000). Almost all mental disorders are more prevalent among younger than older adults (Regier et al., 1988). A longitudinal study found that clinician-rated psychological health shows a steady improvement from age 30 to 62 (Jones & Meredith, 2000), indicating that these mental health diﬀerences do not simply reﬂect a cohort eﬀect. Many studies have also found that normal everyday subjective emotional experience either remains steady or actually improves across the life span—a quite remarkable ﬁnding considering that physical health tends to decline and social networks tend to contract in old age. On questionnaires, older adults respond that they experience fewer negative emotions than younger adults (Gross et al., 1997). Life satisfaction remains constant (Diener & Suh, 1998) or increases (Lawton et al., 1993) with age. When asked to look back and rate how satisﬁed they were at diﬀerent points in their lives, people tend to report that they are most satisﬁed at the current moment (Field, 1997), suggesting that people also have a subjective sense that their own satisfaction increases across the life span. In one experience sampling study including participants from 18 to 94 years old, the frequency and duration of negative emotions experienced in daily life decreased with age (Carstensen, Pasupathi, Mayr, & Nesselroade, 2000). Positive aﬀect appears to remain mostly constant (Carstensen et al., 2000) or increase (Mroczek, 2001) across the life span. In very old age (after the age of 85), crosssectional data indicate that positive aﬀect may decrease again (Smith, Fleeson, Geiselmann, Settersten, & Kunzmann, 1999), although a longitudinal study found that positive outlook increased from ages 85 to 92 (Agren, 1998). Another longitudinal study spanning 23 years revealed that negative aﬀect decreased over time in multiple age cohorts, whereas positive aﬀect remained stable until about age 60, when it decreased slightly (Charles, Reynolds, & Gatz, 2001). Among younger adults, negative mood increases the likelihood of remembering negative information (Blaney, 1986; Bower, 1981). Depression also increases the likelihood of remembering negative information (Bradley, Mogg, & Williams, 1995; Gilboa, Roberts, & Gotlib, 1997; Johnson & Magaro, 1987; Mineka & Nugent, 1995; Watkins, Mathews, Williamson, & Fuller, 1992). [Also see chapter 6—Eds.] Older adults’ lower levels of negative aﬀect suggest that they may be less likely to recall negative information than younger adults. Thus, across the life span, the likelihood of remembering negative information may decrease relative to the likelihood of remembering positive or neutral information, as a result of decreasing negative mood.

Emotion Regulation Eﬀectiveness Increases Emotions often seem to be beyond our control, coming and going whether we choose to experience them or not. Nevertheless, we actually have considerable

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control over our emotions (e.g., Gross, 2001). Furthermore, there is evidence that the ability to regulate emotions improves with age. Older adults are more likely than younger adults to maintain positive emotional states and to maintain the absence of negative states (Carstensen et al., 2000). They are more likely than younger or middle-aged adults to endorse statements suggesting increased emotional control, such as “I try hard to stay in a neutral state and to avoid emotional situations” and “Detachment or cool judgment is my best way to meet life situations” (Lawton, Kleban, Rajagopal, & Dean, 1992). They are also less likely to ruminate about emotionally upsetting events (McConatha & Huba, 1999). In addition, their coping and defense strategies tend to reﬂect more impulse control (Diehl, Coyle, & Labouvie-Vief, 1996). Across an ethnically and culturally diverse set of samples, older adults consistently reported being better able to control their emotions than younger adults (Gross et al., 1997). Ratings of emotional control and emotional experience were correlated; higher ratings of emotional control were associated with higher frequencies of happiness and lower frequencies of sadness and fear. This pattern suggests that changes in emotion regulation processes contribute to the improvement in emotional experience across the life span. People use a variety of strategies to regulate emotion. For example, reappraisal and suppression are both eﬀective ways to regulate emotion, but they have quite distinct mechanisms and side eﬀects (e.g., Gross, 2001). In general, these strategies can be classiﬁed as either response-focused or antecedent-focused (Gross, 2001, 2002). Response-focused strategies attempt to manage emotion after it is already under way, whereas antecedent-focused strategies attempt to inﬂuence emotion before it occurs. Initial research suggests that older adults’ increased ability to regulate emotion relies more on antecedent-focused strategies, such as reappraising an event to alter its emotional impact, than on response-focused strategies, such as suppressing the expression of an emotion (Carstensen, Gross, & Fung, 1998). For example, compared with younger adults, older adults report using less confrontative coping, greater distancing, and more positive reappraisal (Folkman, Lazarus, Pimley, & Novacek, 1987). In general, older adults seem to be better able to reappraise events cognitively (Diehl et al., 1996; Labouvie-Vief, DeVoe, & Bulka, 1989). Laura Carstensen’s socioemotional selectivity theory posits that the increasing eﬀectiveness of emotion regulation results from the increasing salience of emotional goals as people approach the end of life (Carstensen, 1992, 1995; Carstensen, Isaacowitz, & Charles, 1999). According to her theory, perceived limitations on time direct attention toward emotional goals. Thus, older adults prefer to spend time with emotionally meaningful social partners (Fredrickson & Carstensen, 1990; Fung, Carstensen, & Lutz, 1999; Fung, Lai, & Ng, 2001), and younger people mimic this preference under experimental conditions where time is limited (Fung et al., 1999). Older adults emphasize emotional dimensions more than other personal dimensions in their mental representations of social

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partners (Fredrickson & Carstensen, 1990), a pattern also evident in younger adults facing the end of their lives because of terminal illness (Carstensen & Fredrickson, 1998). Older adults are also more likely to adopt emotion-focused strategies when attempting to solve interpersonal problems (Blanchard-Fields & Camp, 1990; Blanchard-Fields, Camp, & Casper Jahnke, 1995). Thus, it appears that aging, because it brings people continually closer to the ultimate end, shifts goal priorities so that emotional goals gain importance and have more of an impact on behavior. The research demonstrating improved emotion regulation and increasing importance of emotional goals with age suggests several age diﬀerences in memory for emotional information. First, the increased importance of emotional goals may increase the salience of all emotionally relevant information relative to neutral information for older adults. Second, because one way to regulate emotion is to avoid attending to or remembering negative information—focusing instead on positive information—older adults may have a bias against negative information in their memories. Thus, older adults’ memories may be more emotionally gratifying. Third, insofar as older adults are more likely to use reappraisal strategies, they may remember originally negative events in a more positive light. I review studies addressing these possibilities later in the chapter.

Decreasing Physiological Arousal

Associated With Emotion

Physiological reactions to emotion-eliciting events rely on the cardiovascular system, which changes with age (Cacioppo, Berntsen, Klein, & Poehlmann, 1998). The muscle mass of the heart decreases, leading to a decline in the heart’s stroke volume. In addition, both blood ﬂow resistance and resting blood pressure increase. Thus, it is perhaps not surprising that cardiovascular reactivity (heart rate and pulse transmission time) associated with emotional responding decreases with age (Levenson, Carstensen, & Gottman, 1994; Levenson, Friesen, Ekman, & Carstensen, 1991; Tsai, Levenson, & Carstensen, 2000). This age diﬀerence in physiological reactivity appears when participants are asked to generate and relive past emotional episodes from their own lives (Levenson et al., 1991), discuss marital problems with their spouses (Levenson et al., 1994), or watch emotional ﬁlm clips (Tsai et al., 2000). These physiological diﬀerences occur despite similar subjective emotional experience and expressive behavior among younger and adult participants. According to the Easterbrook hypothesis (1959), physiological arousal leads to a narrowing of attention. Many studies have examined this claim in the context of the relationship between emotional arousal and memory in younger adults, but the results are mixed. Typically, these studies ﬁnd a positive eﬀect of arousal when the level of arousal is moderate and a negative eﬀect when the it is relatively high (Baddeley, 1998). [Also see chapter 1—Eds.] Using these stud-

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ies to make predictions about the implications of age-related changes in physiological arousal is further complicated because older adults’ lower levels of physiological reactivity are not associated with lower levels of emotional experience relative to younger adults. Thus, the age diﬀerences in physiological reactivity do not lead to any clear predictions about how the relationship of emotion and memory might change across the life span.

Relatively Well-Maintained Neural

Mechanisms of Emotion

Amygdala The emotional systems in the brain consist of interacting circuits involving the prefrontal cortex, amygdala, and anterior cingulate. The amygdala seems to play the most critical role in terms of the interaction between emotion and memory—at least for younger adults. [For a general review of emotion, memory, and the brain, also see chapter 2—Eds.] Neural and hormonal mechanisms mediated by the amygdala enhance memory for emotional stimuli (Hamann, 2001). It is highly interconnected with both cortical and subcortical regions (Young, Scannell, Burns, & Blakemore, 1994) and so is in a position to integrate disparate sources of information and aﬀect a wide range of functions. In particular, with its numerous connections to the hippocampus and other medial temporal regions, the amygdala is ideally situated to inﬂuence memory processes. Nevertheless, an intact amygdala is not needed to remember emotionally neutral material (e.g., Bechara, Tranel, Damasio, & Adolphs, 1995; Scoville & Milner, 1957). Instead, the amygdala plays a modulatory role, enhancing memory associated with emotionally arousing material, especially during the consolidation period after the emotional event (McGaugh, 2000). Animal studies indicate that adrenal stress hormones and the amygdala interact to modulate consolidation of recently acquired information (McGaugh, Ferry, & Vazdarjanova, 2000). Case studies of patients with bilateral lesions in the amygdala have found that they do not show the normal enhancement in memory for emotional material, although they remember nonemotional information as well as normal controls (Adolphs, Cahill, Schul, & Babinsky, 1997; Cahill, Babinsky, Markowitsch, & McGaugh, 1995). Conversely, amnesic patients with intact amygdalae show an enhancement in memory for emotional material despite their overall memory impairment (Hamann, Cahill, McGaugh, & Squire, 1997). Brain imaging studies also provide evidence that the amygdala plays a critical role in enhanced long-term memory for emotionally arousing events (Cahill et al., 1996; Canli, Zhao, Brewer, Gabrieli, & Cahill, 2000; Canli, Zhao, Desmond, Glover, & Gabrieli, 1999). For example, in one study, participants received a PET

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scan while watching either emotionally negative or emotionally neutral ﬁlms. Greater amygdala activity while watching the negative ﬁlms predicted better memory for these ﬁlms later, whereas there was no such correlation for neutral ﬁlms (Cahill et al., 1996). Recent ﬁndings indicate that the amygdala is also associated with enhanced memory for emotionally positive information (Hamann, Ely, Grafton, & Kilts, 1999). With age, brain volume decreases (for reviews, see Kemper, 1994; Raz, 2000). This decrease, however, does not occur at an equal rate across all regions of the brain. Aging has relatively little impact on the amygdala volume, especially when compared with the atrophy in other regions such as the prefrontal cortex. Although MRI studies focusing on the hippocampus or amygdala often ﬁnd decreases in volume with age (e.g., Bigler, Anderson, & Blatter, 2002; Jack, Petersen, O’Brien, & Tangalos, 1992; Jack et al., 1997; cf. Lim, Zipursky, Murphy, & Pfeﬀerbaum, 1990; Mu, Xie, Wen, Weng, & Shuyun, 1999; Smith, Malcein, et al., 1999), studies that include a broader selection of brain regions ﬁnd that the amygdala-hippocampus complex shows little or no change relative to other regions of the brain (e.g., Coﬀey et al., 1992; Good et al., 2001; Ohnishi, Matsuda, Tabira, Asada, & Uno, 2001; Raz et al., 1997; Sullivan, Marsh, Mathalon, Lim, & Pfeﬀerbaum, 1995) or decreases at a rate no greater than that of the volume of the whole brain (Tisserand, Visser, van Boxtel, & Jolles, 2000). Furthermore, postmortem studies using stereologically based cell-counting techniques ﬁnd almost no changes with normal aging in the hippocampus (Raz, 2000; West, Coleman, Flood, & Troncoso, 1994) or in the entorhinal cortex (Gomez-Isla et al., 1996), which is closely connected to the hippocampus and limbic system. This pattern suggests that the enhancement in memory for emotional material due to the interaction of the amygdala and hippocampus should remain relatively intact in older adults. Prefrontal Cortex Researchers investigating memory and aging have become interested in the role of the prefrontal cortex (PFC). The PFC shows a disproportionately large decrease in volume with age, compared with other regions involved in memory processes, such as medial temporal regions (Coﬀey et al., 1992; Cowell et al., 1994; DeCarli et al., 1994; Raz, 2000; Raz et al., 1997; West, 1996). Patients with lesions in the frontal lobes show deﬁcits in strategic memory tasks that are striking in contrast with their intact performance on nonstrategic memory tasks (Shimamura, 1995). Older adults show a similar, although less pronounced, disproportionate deﬁcit for strategic memory tasks (for reviews, see Johnson & Raye, 2000; Light, 2000; Moscovitch & Winocur, 1995; Prull et al., 2000). Furthermore, older adults’ performance on such tasks is correlated with their performance on neuropsychological tests usually associated with frontal lobe damage (Craik, Morris, Morris, & Loewen, 1990; Fabiani & Friedman, 1997; Glisky, Polster, & Routhieaux, 1995; Henkel, Johnson, & De Leonardis,

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1998; Mather, Johnson, & De Leonardis, 1999; McDaniel, Glisky, Rubin, Guynn, & Routhieaux, 1999; Schacter, Kazniak, Kihlstrom, & Valdiserri, 1991). The PFC also plays an important role in aﬀective processing (for a review, see Davidson & Irwin, 1999). Brain imaging studies reveal activity in the PFC during the normal experience of positive and negative emotions (George et al., 1995; Kimbrell et al., 1999; Lane, Reiman, Ahern, Schwartz, & Davidson, 1997; Lane, Reiman, Bradley, et al., 1997). Patient data going back to the famous case of Phineas Gage indicate that dysfunction of the prefrontal cortex disrupts the regulation of emotion and social conduct (Damasio, Grabowski, Frank, Galaburda, & Damasio, 1994; Dimitrov, Phipps, Zahn, & Grafman, 1999). An extreme example of a failure of social and emotional regulation is the act of killing someone—in particular, when this murder is not an act of self-defense. A positron emission tomography (PET) study of 41 murderers who had pleaded not guilty by reason of insanity found that, compared with normal controls, the murderers showed reduced glucose metabolism in the PFC (Raine, Buschbaum, & LaCasse, 1997). On the face of it, this pattern seems paradoxical. Normal aging leads to disproportionate declines in the PFC yet is not associated with the types of problems regulating emotions and social behavior that are the hallmark of many patients with frontal lobe damage. In fact, in addition to being better able to regulate their own emotional experience, older adults are also better able to control their expressions of negative emotions. For example, they are less likely than younger adults to report having a tendency to lose their temper quickly (McConatha & Huba, 1999). This pattern suggests that some prefrontal regions are more critical for the regulation of emotion and that prefrontal regions specialized for emotional processing are less subject to age-related decline than other regions of the PFC. Considering that the frontal lobes occupy about a third of the human cortex, it is not surprising that thinking about the PFC as a monolithic unit can be misleading. In terms of the role of the PFC in aging, emotion, and memory, it seems especially important to consider the dorsolateral PFC and the orbital PFC as discrete regions (Phillips & Della Sala, 1998). These two regions have separate anatomical pathways to communicate with subcortical regions and seem to mediate very diﬀerent processes (Masterman & Cummings, 1997). The orbital PFC seems to be essential for regulating emotion (see Davidson, Putnam, & Larson, 2000, for a review). Patients with lesions in orbitofrontal regions have diﬃculty reversing responses previously rewarded but no longer rewarded (Rolls, 2000) and show disinhibited behavior (Bechara, Damasio, Tranel, & Anderson, 1998). They also show emotion regulation deﬁcits in gambling tasks, as they are driven by short-term emotional payoﬀs, ignoring more signiﬁcant future emotional consequences (Bechara, Damasio, Damasio, & Anderson, 1994; Bechara, Damasio, & Damasio, 2000). On the other hand, the dorsolateral PFC seems particularly important for strategic memory processes. Declines in the volume and activity

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of the dorsolateral PFC in it have been associated with older adults’ deﬁcit in strategic memory tasks (for a review, see Raz, 2000). Unfortunately, there is little information about which areas of the PFC are most aﬀected by normal aging. Most studies examining age-related changes in the frontal lobes have not considered subdivisions within the frontal lobes. Recent evidence, however, indicates that the orbital PFC may be selectively spared in comparison to other areas of the PFC (Salat, Kaye, & Janowsky, 2001). In contrast, the study by Salat et al. (2001) suggests that regions in the medial and lateral PFC and anterior cingulate are more likely to be aﬀected by aging. Thus, preliminary evidence suggests that at least one region in the PFC that is important for regulating emotion is comparatively spared by aging. Hemispheric Asymmetry Indirect techniques for examining laterality and emotion suggest that the right hemisphere plays a larger role than the left hemisphere in processing emotions (for a review, see Kolb & Whishaw, 1990). For example, people tend to make eye movements toward the left during emotional tasks and to the right during nonemotional tasks (Schwartz, Davidson, & Maer, 1975), and the emotional aspect of facial expressions tend to be more pronounced on the left side of the face (Moscovitch & Olds, 1982). There is also evidence of laterality eﬀects for emotional valence, as people have a more negative response to ﬁlms shown to the right than left hemisphere (Dimond, Farrington, & Johnson, 1976). Data from case studies of patients with lesions suggest that this laterality eﬀect occurs in the frontal lobes, with the left frontal lobe normally mediating positive emotions and the right frontal cortex mediating negative emotions (Grafman, Vance, Weingartner, Salazar, & Amin, 1986). Furthermore, neuroimaging and electrophysiological studies with normal younger adults reveal right PFC activation during negative emotional states (Davidson & Irwin, 1999). Some researchers have proposed that certain age-related cognitive deﬁcits occur because in aging the right hemisphere deteriorates faster than the left hemisphere (Ellis & Oscar-Berman, 1989; Evert & Oscar-Berman, 2001; Goldstein & Shelly, 1981; Johnson et al., 1979; Nebes, 1990; Schaie & Schaie, 1977). Researchers suspect that the right hemisphere is more aﬀected by aging because older adults score as well as younger adults on verbal subtests of intelligence tests but are impaired on subtests measuring visuospatial skills. This dissociation is consistent with the lateralization of verbal and spatial functions to the left and right hemispheres, respectively. Furthermore, the performance of normal elderly persons on intelligence tests is similar to that of patients with damage restricted to the right hemisphere (Schaie & Schaie, 1977). A major problem with this hypothesis, however, is that the tests sensitive to right-hemisphere damage tend to require more complex problem solving than those sensitive to left-hemisphere damage. It may be the complexity of the tests that leads to older adults’ pattern of performance, rather than their reliance on the right hemisphere. Thus, a number of investigators have attempted direct tests

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of the right-hemisphere hypothesis by comparing younger and older adults’ performance on tasks in which the stimuli are tachistoscopically presented to either the right or left visual ﬁeld. Most visual half-ﬁeld experiments have not found age diﬀerences in hemispheric asymmetry (e.g., Hutner & Oscar-Berman, 1996; Mittenberg, Seidenberg, Oleary, & Digiulio, 1989; Nebes, 1990; Nebes, Madden, & Berg, 1983; Obler, Woodward, & Albert, 1984). In addition, studies speciﬁcally examining hemispheric asymmetry for the perception of emotional stimuli have not found age diﬀerences in how dominant the right hemisphere is for processing emotions (Cherry, Hellige, & McDowd, 1995; Hutner & OscarBerman, 1996; Moreno, Borod, Welkowitz, & Alpert, 1990; Reminger, Kaszniak, & Dalby, 2000). Finally, measurements of the volume of the right and left hemispheres have failed to ﬁnd evidence for greater age-related decreases in the right hemisphere (e.g., Good et al., 2001). Thus, there is little evidence to show that older adults have a selective decline in the right hemisphere that aﬀects emotional processing. In contrast, there is substantial evidence showing that prefrontal activity associated with memory and other cognitive processes becomes less lateralized with age (Cabeza, 2002). For example, brain activity associated with episodic retrieval is right-lateralized among younger adults (Nyberg, Cabeza, & Tulving, 1996) but becomes more bilateral with age. This decreased lateralization may reﬂect dediﬀerentiation of brain regions, changes in strategy, or compensatory mechanisms (in which analogous regions on the contralateral side are recruited to assist processing). In any case, this reduction in lateralization for memory processes does not lead to any strong predictions about changes in the impact of emotion on memory. One possibility, however, is that it interacts with the lateralization of positive and negative aﬀect also seen in the PFC (Davidson & Irwin, 1999). The decrease seen with age in the right lateralization of memory processes may lead to decreases in the degree to which memories are negative. Because we do not know whether laterality eﬀects for valence also decrease with age, this possibility is only speculative. Overview of Emotion and the Aging Brain In summary, studies investigating age-related changes in the brain suggest that brain regions typically associated with emotional processes are relatively well preserved in older adults. The amygdala shows little deterioration, and there does not appear to be greater right than left hemisphere decline with aging. There is also some indication that orbitofrontal regions associated with emotional control in the PFC are less aﬀected by aging than other parts of the PFC. Altogether, these ﬁndings suggest that the impact of emotion on memory will still occur among older adults. In fact, the impact of emotion might even be ampliﬁed, as emotional processes may gain more inﬂuence than other processes supported by brain regions that deteriorate faster.

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Summary of Predictions for

Memory Based on Research

on Emotion and Aging

The behavioral studies reviewed in the preceding sections indicate that emotional processes gain centrality and eﬀectiveness with age. In addition, the neurological studies indicate that the brain regions supporting emotional processing are relatively spared the eﬀects of age. The one major exception to this pattern of maintenance is that physiological intensity of emotion in the peripheral nervous system, as measured by heart rate, declines with age. Nevertheless, the reduced physiological responsiveness in older adults does not seem to aﬀect their subjective emotional reactions or experience (Levenson et al., 1991, 1994; Tsai et al., 2000). The ﬁndings regarding emotional functioning in these diﬀerent domains lead to two major hypotheses about how the impact of emotion may diﬀer for older and younger adults. First is the emotional compensation hypothesis: well-maintained emotional processes can help older adults remember information they otherwise would have forgotten. Second is the goal-directed emotional memory hypothesis: in general, memory should become more emotionally gratifying, as older adults focus on regulating emotion more than younger adults. In the following section, I review ﬁndings from studies examining age diﬀerences in the eﬀects of emotion on memory to see if either or both of these predictions hold.

Evidence for Changes in the Role

of Emotion in Remembering

as We Age

Memory for Emotional Versus

Neutral Information

Our most vivid and powerful memories involve emotional events (e.g., Brown & Kulik, 1977; Reisberg, Heuer, McLean, & Oshaughnessy, 1988; Rubin & Kozin, 1984). Several studies that look at memory for emotional information (but do not distinguish positive from negative information) suggest that memory accuracy for emotional information does not decrease with age as much as memory for neutral information. In one study, older and younger participants participated in scripted situations (such as packing a picnic basket) and imagined participating in others (Hashtroudi, Johnson, & Chrosniak, 1990). After intervening tasks, they rated their memories for half the situations they had experienced, using a memory characteristics questionnaire that assessed the amount of perceptual and contextual detail and thoughts and feelings associated with their memories. The following day, they rated their memories of each situation and then recalled

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as much as they could about them. After this 1-day delay, older adults rated thoughts and feelings as more memorable than younger adults did. In contrast, this age diﬀerence did not appear when participants rated situations immediately after they experienced them. This pattern suggests that, for older adults, the salience of thoughts and feelings increases over time. In addition, in their actual recall of the situations, older adults reported more thoughts and feelings and evaluative statements than did younger adults, whereas younger adults reported more colors, objects, actions, spatial references, and nonvisual sensory references than did older adults. Days later, Hashtroudi et al. (1990) asked the older and younger adults to make source attributions for each situation, indicating whether they participated in it or just imagined participating in it. Older adults seemed to emphasize their thoughts and feelings when making these source judgments, as their conﬁdence in their recollections correlated more highly with their ratings of associated thoughts and feelings for each event than those of younger adults (Johnson & Multhaup, 1992). Externally generated emotional information also seems to gain advantage in memory as one ages. One study suggesting that emotional information gains salience examined memory for a narrative that contained equivalent numbers of neutral (e.g., “Celia sipped some more sherry”) and emotional (e.g., “and looked very searchingly at Mrs. Oliver”) phrases (Carstensen & Turk-Charles, 1994). Four age groups from 20 to 83 years old were tested. Each successive age group recalled a greater portion of emotional information, so that a signiﬁcant linear trend across the life span emerged. Older adults also recalled a larger proportion of emotional information than younger adults in a study that examined memory for advertisements (Fung & Carstensen, in press). Participants saw a series of advertisements (such as a picture of a camera identiﬁed with a brand name and accompanied by a slogan). Some participants saw a particular advertisement picture and brand name with a slogan that appealed to emotional goals (e.g., “Capture those special moments”), whereas others saw it with a slogan that suggested expanding horizons or achieving success in the future (e.g., “Capture the unexplored world”). Younger adults remembered these diﬀerent types of slogans equally well, but older adults remembered the emotional slogans better than the expanding horizons slogans. One of the challenges of doing research on emotion and memory is counterbalancing emotional and neutral material. Diﬀerences between memory for the two types of stimuli can sometimes result from something other than the diﬀerence in emotionality. The age diﬀerences in Fung and Carstensen’s (in press) study, however, occurred not only for the slogans but also for the brand names— even though the brand names themselves were not emotional, and each brand name appeared equally often with each type of slogan. In addition, another recent study suggests that older adults remember the same information better if it is presented in an emotionally evaluative frame

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(Rahhal, May, & Hasher, 2002). Older and younger participants listened to a tape of a male and a female speaker reading trivia. They were told that all of the statements read by the female speaker were true and all of the statements read by the male speaker were false (or vice versa). After a short delay, they completed a source memory test in which they were given a list of the statements that had been read and were asked either who said the statements (a perceptual source task) or whether they were true or false (a conceptual, emotionally valenced source task). As many studies have shown, older adults were less able than younger adults to indicate who said each statement. Nevertheless, they were just as accurate as the younger adults at indicating whether the statements were true or false, even though this information had been conveyed by the gender of the speaker. This pattern was replicated when the conceptual, emotionally valenced task changed to one of evaluating the character of a person (good or evil) (Rahhal et al., 2002) or the safety of an item (May, Rahhal, Leighton, & Berry, 2002). Thus, for example, participants would be told that everyone the female speaker described was good and everyone the male speaker described was evil. If they heard the female speaker describe someone named Sally and were later asked if Sally was good or evil, they were as good as younger adults at making this judgment—but if asked whether Sally was described by the male or female, they were less accurate than younger adults. Each of the studies reviewed in this section suggests that older adults remember emotional aspects of events better than neutral events and thus conﬁrm a prediction generated from both the research on emotional goals and on brain regions associated with emotional processes. None of these studies distinguished positive from negative information, however, so the predictions regarding emotionally gratifying information were not addressed. I address studies that examine age diﬀerences in memory by valence in a subsequent section.

A Diﬀerent Story: Alzheimer’s Disease

and Emotional Memory

Unlike normal aging, Alzheimer’s disease has a dramatic impact on the amygdala. Compared with age-matched controls, Alzheimer’s patients show a signiﬁcant reduction in volume of their amygdalae, with estimates ranging from 20% to 35% (Callen, Black, Gao, Caldwell, & Szalai, 2001; Cuenod et al., 1993; Herzog & Kemper, 1980; Smith, Malcein, et al., 1999) to as much as 55% (Scott, DeKosky, & Scheﬀ, 1991). In addition, Alzheimer’s disease reduces amygdalar volume more dramatically than it reduces brain volume overall (Scott et al., 1991) or other individual structures (Cuenod et al., 1993; Kemper, 1994). Not surprisingly, this degeneration of the amygdala has an impact on emotional memory. A study examining memory for the Kobe earthquake (which measured 7.2 on the Richter scale and caused more than 6,000 deaths) found that among Japanese Alzheimer’s patients, the accuracy of autobiographical

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memory for the earthquake was positively correlated with the volume of their amygdala as measured by an MRI (Mori et al., 1999). Furthermore, compared with other older adults, patients with Alzheimer’s disease do not show the enhancement in memory for emotional rather than neutral pictures (AbrisquetaGomez, Bueno, Oliveira, & Bertolucci, 2002; Hamann, Monarch, & Goldstein, 2000; Kensinger, Brierley, Medford, Growdon, & Corkin, 2002) or the enhancement in memory for emotional words (Kensinger et al., 2002). Alzheimer’s patients are also impaired when learning to associate a neutral stimuli with an aversive outcome (Hamann, Monarch, & Goldstein, 2002).1 Thus, older adults with Alzheimer’s disease show a very diﬀerent memory pattern than that seen with normal aging. Whereas emotion enhances memory as much as or more for older adults than it does for younger adults, this emotional enhancement decreases or disappears altogether for Alzheimer’s patients.

Impact of an Aﬀective Focus on

Nonaﬀective Information

Many researchers have noted that older adults’ memories are more inﬂuenced by the gist or schematic information about an event than are younger adults’ memories. Older adults are more likely to falsely recognize new words that are semantically associated with studied words (Balota et al., 1999; Isingrini, Fontaine, Taconnat, & Duportal, 1995; Kensinger & Schacter, 1999; Norman & Schacter, 1997; Rankin & Kausler, 1979; Smith, 1975; Tun, Wingﬁeld, Rosen, & Blanchard, 1998), to falsely recognize new pictures that are categorically related to studied pictures (Koutstaal, Schacter, & Brenner, 2001; Koutstaal, Schacter, Galluccio, & Stofer, 1999), to falsely recognize schema-consistent objects as having been in a scene (Hess & Slaughter, 1990), and to incorrectly attribute schematically related statements to a speaker associated with that schema (Mather et al., 1999). Perhaps older adults’ greater schema reliance occurs because they engage more often in emotion-focused memory processes. For two reasons, we may assume that being more emotion focused will increase reliance on schematic knowledge. First, an emotional self-focus seems to shift people’s focus away from the event itself, instead emphasizing connections between the event and oneself. That is, asking people to rate how they feel when hearing statements enhances memory for the semantic content but impairs memory for associated contextual details, such as who made the statement (Johnson, Nolde, & De Leonardis, 1996; Mather et al., 1999; Suengas & Johnson, 1988). Lacking memory of speciﬁc perceptual and contextual details associated with the event in memory, people may rely more on their schematic knowledge about the event to help reconstruct it later. In addition, the thoughts and inferences generated while thinking about one’s reactions to an event may draw on schematic knowledge about the event and may then later become confused with the event itself. In summary, an emo-

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tional self-focus may increase how schematically an event is remembered, as a result of how attention is allocated and how related information becomes associated with the event. One study that supports the hypothesis that an emotional focus can lead related thoughts and inferences to be confused in memory with the event itself asked older and younger adults to participate in a play and then review it (Hashtroudi, Johnson, Vnek, & Ferguson, 1994). In the ﬁrst part of the experiment, two participants were prompted to repeat or think about lines of a play. The experimenter read each line of the play to the pair of participants and then indicated which one should say or think the line. There were three review conditions. In the factual focus condition, participants were asked to talk and then think about what had been said by both participants in each scene. In the aﬀective focus condition, participants were asked to talk and then think about how they felt during each scene. Finally, in the control condition, participants were asked to talk and then think about anything regarding the play. After rehearsing the scenes, half of the participants in each review condition were given a source-monitoring test, in which individual statements from the play were presented, as well as semantically related distractors. These participants were asked to indicate whether the statement had been said or thought and which person had said or thought it—or whether the statement had not been in the play. Examining participants’ source-monitoring accuracy revealed a signiﬁcant interaction between age and type of focus. Whereas the type of focus did not aﬀect younger adults’ source-monitoring accuracy, older adults were signiﬁcantly less accurate in the aﬀective and control conditions than in the factual focus condition. The other half of the participants recalled the play. Both older and younger participants in the aﬀective focus condition remembered less of the play. In addition, participants in the aﬀective focus condition recalled more inferences about and elaborations on the play. In fact, 51% of what the older adults recalled and 38% of what the younger adults recalled in the aﬀective focus condition included elaborative information (compared to less than 30% in both other conditions). Thus, an emotional focus can lead one’s inferences and related thoughts about an event to become confused with the event itself when one is remembering. This combination of greater recall of inferences and reduced recall of perceptual information after focusing on the emotional aspects of events may lead to more schema-reliant memories after focusing on one’s feelings. A study examining memory for choices is consistent with this possibility (Mather & Johnson, 2000). In this study, older and younger adults made a series of two-option choices (e.g., a choice between two job candidates). Each option had positive and negative features (e.g., “Seemed quite motivated,” “Has little professional experience”). After making the choices, one group of participants reviewed how they felt about each choice, another group reviewed the details of the choice options, and a third did an unrelated task. After a delay, participants were given memory tests for each decision that included the features from each option intermixed with new features.

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They were asked whether each feature had been associated with the ﬁrst option, the second option, or neither option. One piece of schematic knowledge about the decisions that might have inﬂuenced memory is the belief that chosen options were better than rejected options. If this belief were to aﬀect memory, it should do so by increasing the number of choice-supportive memory attributions. Positive features should more likely be attributed to the chosen than to the rejected options, and negative features should show the opposite pattern. In averages across conditions, older adults were more choice-supportive than younger adults. The focusing condition did not aﬀect how choice-supportive older adults were. Younger adults, however, were signiﬁcantly more choice-supportive in the emotional-review condition than in the other two conditions and were as choice-supportive as the older adults only in the emotional-review condition. However, increased inﬂuence of general knowledge or beliefs on memory after engaging in aﬀective focus may occur only for aﬀectively signiﬁcant situations such as choices. Remembering that the option you chose was the better option should make you feel less regret and more pleasure. Reviewing a choice may therefore activate emotional goals that would not be activated in other contexts. To investigate whether an aﬀective review would increase the inﬂuence of schematic knowledge on memory, even when the schema should not lead to more positive emotion, Mather and Johnson (2003) conducted a similar study with diﬀerent materials. They used a story that included several unstated inferences as the to-be-remembered material rather than choice options. Participants read the story and then were asked either to review how they felt about it, to review its details, or to do an unrelated task. Both older and younger adults in the aﬀective-review condition were very likely to falsely recognize the unstated inferences from the story. The factual review, however, helped reduce younger adults’ schema reliance much more than it reduced older adults’ schema reliance. Thus, across two studies, older adults were more schema-reliant than younger adults, except when participants were told to focus on their feelings. This pattern suggests that emotional processing increases schema reliance. Interestingly, the amygdala may help mediate this eﬀect, as patients with amygdala damage have poorer memory for gist and superior memory for detail (Adolphs, Denburg, & Tranel, 2001). In the Adolphs et al. study, participants were shown a series of photographs accompanied by brief descriptions. Normal controls and patients with unilateral amygdala damage all showed better memory for general information associated with aversive photographs than for their visual details. In contrast, a patient with bilateral amygdala damage had better memory for the detail than for the general information. Along these same lines, studies with undergraduates have found that emotional stimuli enhance memory for central information but have a detrimental eﬀect on peripheral details (Burke, Heuer, & Reisberg, 1992; Christianson, 1992; Reisberg & Heuer, 1992). As outlined earlier, the amygdala shows relatively little decline with age;

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thus, the enhancement it provides for memory for general information about emotional scenes is probably maintained.

Flashbulb Memories and Aging People often remember the circumstances of learning about shocking events with great vividness and detail. Brown and Kulik (1977) called these “ﬂashbulb memories” because they often seem as clear and vivid as if a ﬂashbulb camera went oﬀ and recorded every detail of the news. To help explain their ﬁndings of extremely vivid memories for surprising and emotionally arousing events, Brown and Kulik suggested that on recognizing that an event is unexpected and important, the limbic system issues a “Now print!” order for memory (Livingston, 1967). Subsequent research has conﬁrmed that, although ﬂashbulb memories are far from exact snapshots of the surprising moment, one remembers the circumstances of learning about shocking events better than those of ordinary events (e.g., Christianson, 1989). The strength of emotional reactions helps predict how accurate later recall will be (Conway et al., 1994; Pillemer, 1984), especially over a longer delay (Schmolck, Buﬀalo, & Squire, 2000). Most of what we know about aging and memory predicts that older adults will be less likely to have accurate and vividly remembered ﬂashbulb memories. According to Brown and Kulik’s (1977) original formulation, a ﬂashbulb memory includes information for contextual information associated with when the person ﬁrst learned about the event, such as the source of the information, the place, the other people present at the time, and what else was happening at the time. Older adults have particular diﬃculty remembering this type of contextual and source information (e.g., Hashtroudi, Johnson, & Chrosniak, 1989; McIntyre & Craik, 1987; Spencer & Raz, 1995), suggesting that they will be less likely to have ﬂashbulb memories. Nevertheless, evidence about age diﬀerences in the vividness and accuracy of ﬂashbulb memories is mixed. Wright, Gaskell, and O’Muircheartaigh (1998) conducted surveys that included several thousand British participants representative of the larger population. Participants were asked about their memories for Margaret Thatcher’s resignation as prime minister of Great Britain and for their memories of a semi-ﬁnal England Football Association Cup match in which 96 people were crushed to death in full view of a national television audience. To the surprise of the researchers, 19 months after Thatcher’s resignation and 36 months after the football tragedy, self-ratings for memory clarity for these events were greater the older the respondent was, until after age 75, when they returned to the levels in the younger adult cohort. In contrast, 12 years after President Kennedy’s assassination, Yarmey and Bull (1978) found less detailed accounts of the circumstances of learning of the assassination in people older than 66.

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Neither the Wright et al. (1998) nor the Yarmey and Bull (1978) studies included objective measures of accuracy. Studies of younger adults’ ﬂashbulb memories show that objective measures are essential because many highly conﬁdently recalled ﬂashbulb memories include quite inaccurate vivid details (e.g., Neisser & Harsch, 1992; Schmolck et al., 2000). In particular, among younger adults, ﬂashbulb memories are quite susceptible to distortion in which memory for the original circumstances becomes confused with other related memories. For example, when recalling how they learned about the space shuttle Challenger disaster 3 years after it occurred, many undergraduates remembered learning about it from a TV broadcast, even though they actually had learned about it from a friend or some other source (Neisser & Harsch, 1992). Older adults are more likely than younger adults to exhibit memory distortion as a result of misattributing information they learned from one source to another source (e.g., Henkel et al., 1998; Mather & Johnson, 2000; Mather et al., 1999; Mitchell, Johnson, & Mather, 2003). So older adults’ ﬂashbulb memories likely will be more susceptible to memory distortion caused by source monitoring errors. Thus, although the participants in the Wright et al. study remembered the shocking events more vividly the older they were, they also probably remembered them less accurately. Two additional studies examining age diﬀerences in ﬂashbulb memories measured recall within a few weeks of the event and again some months later (Cohen, Conway, & Maylor, 1994; Davidson & Glisky, 2002). Though participants’ ﬁrst memory reports were probably not exact representations of what happened, these studies could at least assess the consistency of the ﬂashbulb memories over time—a reasonable proxy for measuring objective accuracy. These studies provide mixed evidence for the hypothesis that older adults have less accurate ﬂashbulb memories. In the ﬁrst study, groups of younger and older adults recounted how they heard the news of Thatcher’s resignation (Cohen et al., 1994). They were tested within 2 weeks of the resignation and again 11 months later. Older adults’ responses at the two test points were signiﬁcantly less likely to be consistent than those of younger adults. In the second study examining age diﬀerences in ﬂashbulb memory consistency, groups of younger and older adults recounted how they learned about the deaths of Princess Diana and Mother Theresa within 3 weeks of each incident and again about 6 months later (Davidson & Glisky, 2002). In this study, there were no signiﬁcant diﬀerences between the consistency of younger and older adults’ memories. In addition, among the older adults, there were no signiﬁcant correlations between the consistency of their memories for the deaths and scores on a battery of tests associated with medial temporal lobe function or a battery of tests associated with frontal lobe function. In contrast, memory consistency for a control event (the most interesting event in their own lives that occurred on the same weekend when Princess Diana died) was correlated with performance on these batteries (although only marginally with

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the frontal battery). A number of studies examining older adults’ source memory performance have found signiﬁcant positive correlations between source attribution accuracy and performance on tests of frontal lobe function (Craik et al., 1990; Glisky et al., 1995; Mather et al., 1999) and sometimes also between source accuracy and performance on tests of medial temporal lobe function (Henkel et al., 1998; Mather et al., 1999). The fact that memories were as accurate for the surprising public events among older adults with low frontal function as among those with high frontal function suggests that other brain regions (such as the amygdala) may be involved in forming and consolidating memories of surprising events. Processes mediated by these regions may compensate for decline in frontal regions. In summary, the research on older adults and ﬂashbulb memories is somewhat surprising because older adults do not always show less accurate memories than younger adults, as one might expect from their memory performance in similar contexts. The emotional aspect of shocking events may be a critical component of this greater-than-expected accuracy. More research is needed, however, in which older and younger adults’ memory for shocking events is compared with memory for interesting but nonemotional events. The emotional compensation hypothesis outlined earlier in the chapter predicts that age diﬀerences in forgetting and distortion should be greater for the control events than for the shocking events. Also of interest is whether the valence of the event interacts with age diﬀerences at all. Most ﬂashbulb memory studies have looked at memories for negative events, but memories for positive surprising events can also have ﬂashbulb-like qualities (Scott & Ponsoda, 1996). As outlined in the following section, valence seems to have a diﬀerent impact on younger and older adults’ memories.

Evidence for Increasingly Gratifying

Memories With Age

For younger adults, negative information dominates positive information in many contexts (for reviews, see Baumeister, Bratslavsky, Fickenauer, & Vohs, 2001; Rozin & Royzman, 2001). Negative information is processed more thoroughly, negative impressions are more diﬃcult to disconﬁrm, and negative emotions have more impact. Nevertheless, the evidence is mixed for younger adults’ memory, with some studies ﬁnding a bias for negative and some for positive information. There is growing evidence, however, that with age comes a shift toward favoring positive rather than negative information in memory. As I show in this section, evidence for this shift has been seen both in longitudinal studies investigating personal autobiographical memories and in lab studies investigating memory for emotional pictures or verbal stimuli. Among younger adults, memories for highly negative events seem to be accessible for a longer time than memories of highly positive events (Berntsen,

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2001, 2002). A survey of over a thousand Danish citizens, however, revealed that this pattern in which negative memories last longer than positive memories reverses itself in the late 30s (Berntsen & Rubin, 2002). By age 60, there is dramatically reduced recall of remote negative events compared to recall of remote positive events. When asked to describe memory for an extremely happy event, older adults tended to pick events from their 20s, whereas when asked to describe a memory for an extremely sad or traumatic event, they picked more recent events. This pattern of recall for sad and traumatic events is contrary to ﬁndings indicating that, in general, people remember information encoded during adolescence and early adulthood better than information encountered earlier or later in life (Rubin, Rahhal, & Poon, 1998). Berntsen and Rubin (2002) conclude that the likely explanations of the reduced recall of remote sad and traumatic events are reduced rehearsal of negative events or repression. The decreasing accessibility of negative long-term personal memories across the life span may help explain an intriguing ﬁnding from a longitudinal study (Field, 1981). Sixty adults were interviewed four times over a 44-year period and were asked during each interview to rate how happy their childhood had been. There was a highly signiﬁcant trend over time, as participants rated their childhood as increasingly happier the older they became. A study of political supporters of Ross Perot indicates that memory for the intensity of past sadness decreases with age (Levine & Bluck, 1997). After Perot abruptly withdrew from the presidential race in July 1992, some of his supporters were asked to rate their initial emotional reactions. After the elections that November, they were asked to recall their initial emotional reactions. There were no age diﬀerences in the initial reports of emotion intensity. Nevertheless, the follow-up questionnaire revealed that, among those participants who still wished that Perot had been elected, older adults remembered experiencing less intense sadness than younger adults did. The older the participants, the more they underestimated how sad they had been when Perot withdrew from the race. Interestingly, there were no age diﬀerences for supporters who no longer wished that Perot had been elected—these supporters all tended to underestimate how sad they had been. A study in which older and younger adults were asked about recent memories also found that younger adults remember negative emotions more intensely than older adults. Older and younger adults carried electronic pagers for a week and ﬁlled out a questionnaire about their current emotions each time they were paged at random intervals throughout each day (Carstensen et al., 2000). At the end of the week, they were asked to recall the percentage of time they had experienced positive and negative emotions and their concomitant intensities (Kennedy, 2002). There were no age diﬀerences in the accuracy of estimates for the percentage of time emotions had been experienced, but younger adults were signiﬁcantly more likely than older adults to overestimate how intense their negative aﬀect had been.

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Decreases for negative information are also seen in memory for emotional pictures (Charles, Mather, & Carstensen, 2003). Younger (18–29 years), middleaged (41–53 years), and older (65–80 years) adults watched a slide show of negative, positive, and neutral pictures displayed in a random order. Half the pictures were of people (e.g., a couple mourning at a tombstone, a happy family, scuba divers) and half did not contain people (e.g., a slice of pizza with a cockroach on it, two bunnies, a chair). The participants included equal numbers of men and women, European Americans and African Americans, and white- and bluecollar workers within each condition. After seeing the pictures and completing a 15-minute ﬁller task, participants were asked to recall as many of the pictures as they could. Then, they completed a recognition memory test in which they saw a series of pictures and indicated which ones they had seen before. The proportion of total recall that consisted of negative pictures decreased across the life span, whereas the proportion that consisted of positive pictures increased. Recognition accuracy for negative pictures similarly decreased. These age diﬀerences were consistent across the diﬀerent genders, ethnicities, and socioeconomic statuses represented among the participants.2 Another study focusing on memory for emotional pictures examined whether there are age diﬀerences in brain activity at the time of encoding the pictures (Mather et al., 2001). Younger and older adults watched positive, negative, and neutral pictures while in a functional magnetic resonance imaging scanner. For each picture, they rated how emotionally arousing it was for them. After their scan, they were given a recognition memory test for the pictures in which they were asked whether they had seen each test picture while they were in the scanner. They were then asked to indicate whether they remembered it vividly or just knew it had been shown in the scanner (R/K; e.g., Gardiner & Java, 1993). Older adults rated the negative pictures as less arousing and rated the positive pictures as more arousing than the younger adults did. As in the study by Charles et al. (2003), there was a signiﬁcant age by valence interaction in recognition memory performance, indicating that older adults showed a disproportionate disadvantage in recognizing the negative pictures. Furthermore, when older adults did actually recognize a negative picture from the scanner session, they were less likely to say they vividly remembered it than they were for the positive pictures they recognized. As I said earlier, the amygdala appears to be relatively unscathed by aging. Mather et al. (2001) found that for both older and younger adults, the amygdala was more active while emotional pictures were displayed than while neutral pictures were displayed. There was an interaction, however. Older adults had greater amygdala activity while seeing positive pictures, whereas the younger adults had equivalent activation for the two types of emotional pictures. In addition, older adults showed more prefrontal activity while viewing positive pictures. These diﬀerences in brain activity at the time of encoding suggest that older adults’ bias to remember less negative information is at least partially a result of processes operating at the time of encoding.

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Another study suggests that biased attention at the time of encoding contributes to the increasingly emotionally gratifying memories seen with age (Mather & Carstensen, in press). On each trial, older and younger adults were shown an emotional and a neutral face side by side for 1 second. Then the faces disappeared, and a dot probe appeared behind one of the faces. Participants had to indicate the side of the screen the dot was on. In two experiments, older adults responded faster if the dot was behind a neutral face than if it was behind a negative face. They also showed a trend to respond faster if the dot was behind a positive face than if it was behind a neutral face. Younger adults did not show any attentional biases. In a later forced-choice recognition memory test, older adults were more accurate at identifying which positive faces they had seen before than which negative faces they had seen before, whereas this was not the case for younger adults. Increasingly emotionally gratifying memory with age was also found in two studies focusing on memory for choices (Mather & Carstensen, 2003; Mather & Johnson, 2000). These studies suggest that processes operating at the time of retention and retrieval also contribute to older adults’ emotionally gratifying memory biases. In the ﬁrst study, as described earlier in this chapter, older adults were more choice-supportive than younger adults when attributing features to options from past choices (Mather & Johnson, 2000). They were more likely to attribute positive features to the options they had chosen than to the other options and were more likely to attribute negative features to the rejected options. The age diﬀerence in choice-supportiveness obtained even when older and younger adults were equated for overall recognition and source attribution accuracy by decreasing the delay between encoding and test for the older adults. Older adults’ choice-supportive biases obtained not only for features actually associated with the options but also for new features misattributed to one of the two options. Older adults’ choice-supportive biases for new features indicate that at least some of the processes supporting emotionally gratifying memories operate at the time of retrieval. The importance of retrieval processes is further highlighted by the second study of age diﬀerences in memory for decisions (Mather & Carstensen, 2003). Half the participants were asked to recall the features from their choices before completing a recognition and source attribution test for the features, whereas the other half took the recognition test ﬁrst. Overall, there were age by valence interactions for both recall and recognition. Younger adults remembered negative features from the choice options much better than positive features. Older adults showed a less extreme advantage for the negative features than the positive features. Particularly interesting, however, was the diﬀerential impact of taking a recall test on later recognition of positive and negative features for older and younger adults. Younger adults were less likely to recognize positive features if they received the recall test ﬁrst, whereas the test order did not have much of an impact on older adults’ recognition of positive features. Taking a recall test ﬁrst had the opposite eﬀect for

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recognition accuracy of negative features. Younger adults’ accuracy for negative features was not aﬀected by having taken the test, whereas older adults were less likely to correctly recognize negative features if they had done the recall test ﬁrst. This pattern suggests that for younger adults, attempting to recall information that includes both positive and negative aspects may inhibit later memory for the positive aspects, whereas for older adults, recall may inhibit later memory for the negative aspects. Repeated retrieval may make older adults’ memories more positive and younger adults’ memories more negative. In addition, half of the participants in each condition completed the memory tests after 10 minutes, whereas the other half completed the tests after 2 days. Comparisons across these two delay groups revealed that older adults’ recognition accuracy for negative features declined more than did that of younger adults, whereas their decline in accuracy for positive features was not much greater than that of younger adults. Thus, older adults tended to forget the negative features more quickly than the positive features. Thus, factors operating over the retention interval also play a role in making older adults’ memories more gratifying. Apparently, the salience of emotional goals also plays an important role in making memories more gratifying. Mather and Johnson (2000) found that younger adults were more choice-supportive in their memories of their recent decisions if they had been asked to review their feelings than if they had been asked to review the details or to do an unrelated task. Only the emotion-focused younger adults were as choice-supportive as the older adults were across all of the conditions, suggesting that older adults were more likely to focus on emotion even when not explicitly told to think about their feelings. Kennedy, Mather, and Carstensen (in press) also found that making emotional goals salient increases gratiﬁcation. In their study, 300 nuns between the ages of 47 and 102 completed a questionnaire in which they were asked to remember their responses to a questionnaire they had completed 14 years earlier about their health practices and medical history. Participants in the emotion-focus condition completed a retrospective questionnaire in which they were asked to rate their current feelings after each subset of questions. At the same points in the questionnaire, participants in the accuracy-focus condition were reminded to answer the questions as accurately as they could and asked to complete ratings regarding their subjective sense of remembering. There was also a control condition questionnaire without any reminders. For age comparisons, the control group was divided into middle-aged (47–65) and older (79–102) groups. Older adults showed a positive bias when remembering their past health practices and illnesses, whereas middle-aged adults showed a negative bias. Both older and younger participants in the emotion-focused condition had a positive retrospective memory bias, whereas both older and younger participants in the accuracy-focused condition had a negative bias. Thus, older adults and emotionfocused participants showed the same pattern in their retrospective biases. These ﬁndings remained signiﬁcant after controlling for current mood and current

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ratings of physical and mental health and emotional experience. Furthermore, making emotional goals salient not only led to a positive memory bias but also led emotion-focused participants to be in a better mood than accuracy–focused participants after completing the questionnaire. Further evidence that older adults’ positive memory biases contribute to their enhanced well-being comes from a study comparing emotion while one is reminiscing with others about past events to emotion while one is engaged in other social activities (Pasupathi & Carstensen, in press). In contexts in which participants were engaged in mutual reminiscing, older adults experienced signiﬁcantly more positive emotion than younger adults. In contrast, in social contexts that did not involve reminiscing, age was not signiﬁcantly correlated with positive emotion. A second study found that age was associated with improved emotional experience only during reminiscing about positive experiences. These ﬁndings suggest that, for older adults, remembering positive events can be an eﬀective way to regulate emotion.

Summary: Aging, Emotion,

and Memory

In contrast with functioning in the physical and cognitive domains, emotional functioning does not deteriorate with age. Instead, if anything, it actually grows more eﬀective across the life span. Changing time perspective (Carstensen et al., 1999), greater experience and maturity (Labouvie-Vief, 1998), and relatively well-maintained brain regions associated with emotional processing may all contribute to this intact functioning and help older adults remember emotional information better than neutral information. Similarly, the pattern of fewer neurological changes in brain regions associated with emotion than in other regions suggests that emotional processes may be available to compensate for decline in other processes that contribute to memory formation and retention. This emotional compensation hypothesis is supported by studies in which memory for emotional information is maintained better in old age than memory for neutral information. For example, older adults remember their own internal emotional reactions more vividly than younger adults do (Hashtroudi et al., 1990), and a larger proportion of the externally perceived information they remember consists of emotional information (Carstensen & Turk-Charles, 1994; Charles et al., 2003; Fung & Carstensen, in press). Furthermore, at the time of retrieval, older adults can remember the source of information as well as younger adults if the source is identiﬁed through its emotional rather than nonemotional aspects (May et al., 2002; Rahhal et al., 2002). In addition, older adults’ errors and biases resemble those of younger adults under emotional conditions (Kennedy et al., 2002; Mather & Johnson, 2000, 2003), suggesting that, in general, older adults are more likely to engage in an emotional focus when encoding or retrieving events.

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Studies that focus on memory for positive and negative information separately, however, indicate only partial support for the emotional compensation hypothesis, as aging does not lead to a relative enhancement for all types of emotional information. Instead, the enhancement in memory for emotional material among older adults seems to be driven by enhanced memory for positive information. In fact, memory for negative information declines with age (e.g., Charles et al., 2003; Mather et al., 2001). This bias to remember positive relatively better than negative events with age is consistent with the hypothesis that older adults should remember information consistent with their emotional goals. Both in lab studies with controlled stimuli and in ﬁeld studies examining memories for real-life events, older adults’ memories are more emotionally gratifying than younger adults’ memories. In comparison with memories of younger adults, a larger proportion of what older adults remember is positive and a smaller proportion is negative (Charles et al., 2003; Mather et al., 2001; Mather & Carstensen, 2003). Older adults’ memories for speciﬁc events or time periods are also more likely than younger adults’ memories to be distorted in an emotionally gratifying direction (Field, 1981; Levine & Bluck, 1997; Mather & Carstensen, 2003; Mather & Johnson, 2000). For older adults, negative memories fade faster than positive memories, whereas this is not the case for younger adults (Berntsen & Rubin, in press; Mather & Carstensen, 2003). These gratifying memories seem to be a critical component of older adults’ successful emotion regulation processes. For example, older adults experience more positive emotion than younger adults while reminiscing with other people, but there is no signiﬁcant age diﬀerence in positive emotion in other social contexts (Pasupathi & Carstensen, in press). Thus, memory and emotional functioning seem to interact in mutually beneﬁcial ways. Emotional processes can help older adults remember information they might otherwise have forgotten—and, in turn, emotionally gratifying biases in memory enhance emotional well-being.

Notes Thanks to Laura Carstensen, Faye Crosby, Paula Hertel, Marcia Johnson, Noah Mercer, Karen Mitchell, Jennifer Taylor, and Avril Thorne for their comments on previous versions of this chapter. 1. Contrasting with these ﬁndings, one study found that Alzheimer’s patients showed as much of a memory beneﬁt for emotional stories as did normal older controls (Kazui et al., 2000). However, the control participants were at ceiling in their memory accuracy for the emotional aspects of the story, and the patients had relatively mild dementia (their average Mini-Mental State Examination score was 22.6). 2. However, a study testing older and younger adults using a similar set of emotional pictures did not ﬁnd an age by valence interaction (Kensinger et al., 2002). It is not clear why the results of these studies diﬀer.

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References Abrisqueta-Gomez, J., Bueno, O. F. A., Oliveira, M. G. M., & Bertolucci, P. H. F. (2002). Recognition memory for emotional pictures in Alzheimer’s patients. Acta Neurologica Scandinavica, 105, 51–54. Adolphs, R., Cahill, L., Schul, R., & Babinsky, R. (1997). Impaired declarative memory for emotional material following bilateral amygdala damage in humans. Learning and Memory, 4, 291–300. Adolphs, R., Denburg, N. L., & Tranel, D. (2001). The amygdala’s role in long-term declarative memory for gist and detail. Behavioral Neuroscience, 115, 983–992. Agren, M. (1998). Life at 85 and 92: A qualitative longitudinal study of how the oldest old experience and adjust to the increasing uncertainty of existence. International Journal of Aging and Human Development, 47, 105–117. Baddeley, A. (1998). Human memory: Theory and practice. Rev. ed. Boston: Allyn and Bacon. Balota, D. A., Cortese, M. J., Duchek, J. M., Adams, D., Roediger, H. L., McDermott, K. B., et al. (1999). Veridical and false memories in healthy older adults and in dementia of the Alzheimer’s type. Cognitive Neuropsychology, 16, 361–384. Baumeister, R. F., Bratslavsky, E., Fickenauer, C., & Vohs, K. D. (2001). Bad is stronger than good. Review of General Psychology, 5, 323–370. Bechara, A., Damasio, A. R., Damasio, H., & Anderson, S. W. (1994). Insensitivity to future consequences following damage to human prefrontal cortex. Cognition, 50, 7–15. Bechara, A., Damasio, H., & Damasio, A. R. (2000). Emotion, decision making and the orbitofrontal cortex. Cerebral Cortex, 10, 295–307. Bechara, A., Damasio, H., Tranel, D., & Anderson, S. W. (1998). Dissociation of working memory from decision making within the human prefrontal cortex. Journal of Neuroscience, 18, 428–437. Bechara, A., Tranel, D., Damasio, H., & Adolphs, R. (1995). Double dissociation of conditioning and declarative knowledge relative to the amygdala and hippocampus in humans. Science, 269, 1115–1118. Berntsen, D. (2001). Involuntary memories of emotional events: Do memories of traumas and extremely happy events diﬀer? Applied Cognitive Psychology, 15, 135–158. Berntsen, D. (2002). Tunnel memories for autobiographical events: Central details are remembered more frequently from shocking than from happy experiences. Memory & Cognition, 30, 1010–1020. Berntsen, D., & Rubin, D. C. (2002). Emotionally charged autobiographical memories across the lifespan: The recall of happy, sad, traumatic, and involuntary memories. Psychology and Aging, 17, 636–652. Bigler, E. D., Anderson, C. V., & Blatter, D. D. (2002). Temporal lobe morphology in normal aging and traumatic brain injury. American Journal of Neuroradiology, 23, 255–266. Blanchard-Fields, F. (1998). The role of emotion in social cognition across the adult life span. In K. W. Schaie & M. P. Lawton (Eds.), Annual review of gerontology and geriatrics: Focus on emotion and adult development (Vol. 17, pp. 238–265). New York: Springer.

296

  

Blanchard-Fields, F., Camp, C., & Casper Jahnke, H. (1995). Age diﬀerences in problem-solving style: The role of emotional salience. Psychology and Aging, 10, 173–180. Blanchard-Fields, F., & Camp, C. J. (1990). Aﬀect, individual diﬀerences, and real world problem solving across the adult life span. In T. Hess (Ed.), Aging and cognition: Knowledge organization and utilization (pp. 461–497). Amsterdam: North-Holland. Blaney, P. H. (1986). Aﬀect and memory: A review. Psychological Bulletin, 99, 229– 246. Bower, G. H. (1981). Mood and memory. American Psychologist, 36, 129–148. Bradley, B. P., Mogg, K., & Williams, R. (1995). Implicit and explicit memory for emotion-congruent information in clinical depression and anxiety. Behaviour Research & Therapy, 33, 755–770. Brown, R., & Kulik, J. (1977). Flashbulb memories. Cognition, 5, 73–99. Burke, A., Heuer, F., & Reisberg, D. (1992). Remembering emotional events. Memory & Cognition, 20, 277–290. Cabeza, R. (2002). Hemispheric asymmetry reduction in older adults: The HAROLD model. Psychology and Aging, 17, 85–100. Cacioppo, J. T., Berntsen, G. B., Klein, D. J., & Poehlmann, K. M. (1998). Psychophysiology of emotion across the life span. In K. W. Schaie & M. P. Lawton (Eds.), Annual review of gerontology and geriatrics: Focus on emotion and adult development (Vol. 17, pp. 27–74). New York: Springer. Cahill, L., Babinsky, R., Markowitsch, H. J., & McGaugh, J. L. (1995). The amygdala and emotional memory. Nature, 377, 295–296. Cahill, L., Haier, R. J., Fallon, J., Alkire, M. T., Tang, C., Keator, D., et al. (1996). Amygdala activity at encoding correlated with long-term, free recall of emotional information. Proceedings of the National Academy of Sciences, USA, 93, 8016–8021. Callen, D. J. A., Black, S. E., Gao, F., Caldwell, C. B., & Szalai, J. P. (2001). Beyond the hippocampus: MRI volumetry conﬁrms widespread limbic atrophy in AD. Neurology, 57, 1669–1674. Canli, T., Zhao, Z., Brewer, J. B., Gabrieli, J. D. E., & Cahill, L. (2000). Event-related activation in the human amygdala associates with later memory for individual emotional response. Journal of Neuroscience, 20, RC99. Canli, T., Zhao, Z., Desmond, J. E., Glover, G. H., & Gabrieli, J. D. E. (1999). fMRI identiﬁes a network of structures correlated with retention of positive and negative emotional memory. Psychobiology, 27, 441–452. Carstensen, L. L. (1992). Social and emotional patterns in adulthood: Support for socioemotional selectivity theory. Psychology and Aging, 7, 331–338. Carstensen, L. L. (1995). Evidence for a life-span theory of socioemotional selectivity. Current Directions in Psychological Science, 4, 151–156. Carstensen, L. L., & Charles, S. T. (1998). Emotion in the second half of life. Current Directions in Psychological Science, 7, 144–149. Carstensen, L. L., & Fredrickson, B. L. (1998). Inﬂuence of HIV status and age on cognitive representations of others. Health Psychology, 17, 494–503. Carstensen, L. L., Gross, J. J., & Fung, H. H. (1998). The social context of emotional

   

297

experience. In K. W. Schaie & M. P. Lawton (Eds.), Annual review of gerontology and geriatrics: Focus on emotion and adult development (Vol. 17, pp. 325–352). New York: Springer. Carstensen, L. L., Isaacowitz, D. M., & Charles, S. T. (1999). Taking time seriously: A theory of socioemotional selectivity. American Psychologist, 54, 165–181. Carstensen, L. L., Pasupathi, M., Mayr, U., & Nesselroade, J. R. (2000). Emotional experience in everyday life across the adult life span. Journal of Personality and Social Psychology, 79, 644–655. Carstensen, L. L., & Turk-Charles, S. (1994). The salience of emotion across the adult life course. Psychology and Aging, 9, 259–264. Charles, S. T., Mather, M., & Carstensen, L. L. (2003). Aging and emotional memory: The forgettable nature of negative images for older adults. Journal of Experimental Psychology: General, 132, 310–324. Charles, S. T., Reynolds, C. A., & Gatz, M. (2001). Age-related diﬀerences and change in positive and negative aﬀect over 23 years. Journal of Personality and Social Psychology, 80, 136–151. Cherry, B. J., Hellige, J. B., & McDowd, J. M. (1995). Age diﬀerences and similarities in patterns of cerebral hemispheric asymmetry. Psychology and Aging, 10, 191– 203. Christianson, S.-Å. (1989). Flashbulb memories: Special, but not so special. Memory & Cognition, 17, 435–443. Christianson, S.-Å. (1992). Emotional stress and eyewitness memory: A critical review. Psychological Bulletin, 112, 284–309. Coﬀey, C. E., Wilkenson, W. E., Parashos, I. A., Soady, S. A., Sullivan, R. J., Patterson, L. J., et al. (1992). Quantitative cerebral anatomy of the aging human brain: A cross-sectional study using magnetic resonance imaging. Neurology, 42, 527–536. Cohen, G., Conway, M. A., & Maylor, E. A. (1994). Flashbulb memories in older adults. Psychology and Aging, 9, 454–463. Conway, M. A., Anderson, S. J., Larsen, S. F., Donnelly, C. M., McDaniel, M. A., McClelland, A. G., et al. (1994). The formation of ﬂashbulb memories. Memory & Cognition, 22, 326–343. Cowell, P. E., Turetsky, B. I., Gur, R. C., Grossman, R. I., Shtasel, D. L., & Gur, R. E. (1994). Sex diﬀerences in aging of the human frontal and temporal lobes. Journal of Neuroscience, 14, 4748–4755. Craik, F. I. M., Morris, L. W., Morris, R. G., & Loewen, E. R. (1990). Relations between source amnesia and frontal lobe functioning in older adults. Psychology and Aging, 5, 148–151. Cuenod, C. A., Denys, A., Michot, J. L., Jehenson, P., Forette, F., Kaplan, D., et al. (1993). Amygdala atrophy in Alzheimer’s disease—An in-vivo magnetic-resonance-imaging study. Archives of Neurology, 50, 941–945. Damasio, H., Grabowski, T., Frank, R., Galaburda, A. M., & Damasio, A. R. (1994). The return of Phineas Gage: Clues about the brain from the skull of a famous patient. Science, 264, 1102–1105. Davidson, P. S. R., & Glisky, E. L. (2002). Is ﬂashbulb memory a special instance of source memory? Evidence from older adults. Memory, 10, 99–111.

298

  

Davidson, R. J., & Irwin, W. (1999). The functional neuroanatomy of emotion and aﬀective style. Trends in Cognitive Sciences, 3, 11–21. Davidson, R. J., Putnam, K. M., & Larson, C. L. (2000). Dysfunction in the neural circuitry of emotion regulation—A possible prelude to violence. Science, 289, 591–594. DeCarli, C., Murphy, D. G., Gillette, J. A., Haxby, J. V., Teichberg, D., Schapiro, M. B., et al. (1994). Lack of age-related diﬀerences in temporal lobe volume of very healthy adults. American Journal of Neuroradiology, 15, 689–696. Diehl, M., Coyle, N., & Labouvie-Vief, G. (1996). Age and sex diﬀerences in strategies of coping and defense across the life span. Psychology and Aging, 11, 127–139. Diener, E., & Suh, M. E. (1998). Subjective well-being and age: An international analysis. In B. Tucker & J. Libby (Eds.), Annual review of gerontology and geriatrics (Vol. 17, pp. 304–324). New York: Springer. Dimitrov, M., Phipps, M., Zahn, T. P., & Grafman, J. (1999). A thoroughly modern Gage. Neurocase, 5, 345–354. Dimond, S. J., Farrington, L., & Johnson, P. (1976). Diﬀering emotional response from right and left hemispheres. Nature, 261, 690–692. Easterbrook, J. A. (1959). The eﬀect of emotion on cue utilization and the organization of behavior. Psychological Review, 66, 183–201. Ellis, R. J., & Oscar-Berman, M. (1989). Alcoholism, aging, and functional cerebral asymmetries. Psychological Bulletin, 106, 128–147. Evert, D. L., & Oscar-Berman, M. (2001). Selective attentional processing and the right hemisphere: Eﬀects of aging and alcoholism. Neuropsychology, 15, 452–461. Fabiani, M., & Friedman, D. (1997). Dissociations between memory for temporal order and recognition memory in aging. Neuropsychologia, 35, 129–141. Field, D. (1981). Retrospective reports by healthy intelligent elderly people of personal events of their adult lives. International Journal of Behavioral Development, 4, 77–97. Field, D. (1997). Looking back, what period of your life brought you the most satisfaction? International Journal of Aging & Human Development, 45, 169–194. Folkman, S., Lazarus, R. S., Pimley, S., & Novacek, J. (1987). Age diﬀerences in stress and coping processes. Psychology and Aging, 2, 171–184. Fredrickson, B. L., & Carstensen, L. L. (1990). Choosing social partners: How old age and anticipated endings make people more selective. Psychology and Aging, 5, 335–347. Fung, H. H., & Carstensen, L. L. (in press). Sending memorable messages to the old: Age diﬀerences in preferences and memory for emotionally meaningful advertisements. Journal of Personality and Social Psychology. Fung, H. H., Carstensen, L. L., & Lutz, A. M. (1999). Inﬂuence of time on social preferences: Implications for life-span development. Psychology and Aging, 14, 595– 604. Fung, H. H., Lai, P., & Ng, R. (2001). Age diﬀerences in social preferences among Taiwanese and mainland Chinese: The role of perceived time. Psychology and Aging, 16, 351–356. Gardiner, J. M., & Java, R. I. (1993). Recognition memory and awareness: An experiential approach. European Journal of Cognitive Psychology, 5, 337–346.

   

299

George, M. S., Ketter, T. A., Parekh, P. I., Horwitz, B., Herscovitch, P., & Post, R. M. (1995). Brain activity during transient sadness and happiness in healthy women. American Journal of Psychiatry, 152, 341–351. Gilboa, E., Roberts, J. E., & Gotlib, I. H. (1997). The eﬀects of induced and naturally occurring dysphoric mood on biases in self-evaluation and memory. Cognition & Emotion, 11, 65–82. Glisky, E. L., Polster, M. R., & Routhieaux, B. C. (1995). Double dissociation between item and source memory. Neuropsychology, 9, 229–235. Goldstein, G., & Shelly, C. (1981). Does the right hemisphere age more rapidly than the left? Journal of Clinical Neuropsychology, 3, 65–78. Gomez-Isla, T., Price, J. L., McKeel Jr., D. W., Morris, J. C., Growdon, J. H., & Hyman, B. T. (1996). Profound loss of layer II entorhinal cortex neurons occurs in very mild Alzheimer’s disease. Journal of Neuroscience, 16, 4491–4500. Good, C. D., Johnsrude, I. S., Ashburner, J., Henson, R. N. A., Friston, K. J., & Frackowiak, R. S. J. (2001). A voxel-based morphometric study of aging in 465 normal adult human brains. NeuroImage, 14, 21–36. Grafman, J., Vance, S. C., Weingartner, H., Salazar, A. M., & Amin, D. (1986). The eﬀects of lateralized frontal lesions on mood regulation. Brain, 109, 1127–1148. Gross, J. J. (2001). Emotion regulation in adulthood: Timing is everything. Current Directions in Psychological Science, 10, 214–219. Gross, J. J. (2002). Emotion regulation: Aﬀective, cognitive, and social consequences. Psychophysiology, 39, 281–291. Gross, J. J., Carstensen, L. L., Pasupathi, M., Tsai, J., Skorpen, C. G., & Hsu, A. Y. C. (1997). Emotion and aging: Experience, expression, and control. Psychology and Aging, 12, 590–599. Hamann, S. B. (2001). Cognitive and neural mechanisms of emotional memory. Trends in Cognitive Sciences, 5, 394–400. Hamann, S. B., Cahill, L., McGaugh, J. L., & Squire, L. R. (1997). Intact enhancement of declarative memory for emotional material in amnesia. Learning & Memory, 4, 301–309. Hamann, S. B., Ely, T. D., Grafton, S. T., & Kilts, C. D. (1999). Amygdala activity related to enhanced memory for pleasant and aversive stimuli. Nature Neuroscience, 2, 289–293. Hamann, S. B., Monarch, E. S., & Goldstein, F. C. (2000). Memory enhancement for emotional stimuli is impaired in early Alzheimer’s disease. Neuropsychology, 14, 82–92. Hamann, S. B., Monarch, E. S., & Goldstein, F. C. (2002). Impaired fear conditioning in Alzheimer’s disease. Neuropsychologia, 40, 1187–1195. Hashtroudi, S., Johnson, M. K., & Chrosniak, L. D. (1989). Aging and source monitoring. Psychology and Aging, 4, 106–112. Hashtroudi, S., Johnson, M. K., & Chrosniak, L. D. (1990). Aging and qualitative characteristics of memories for perceived and imagined complex events. Psychology and Aging, 5, 119–126. Hashtroudi, S., Johnson, M. K., Vnek, N., & Ferguson, S. A. (1994). Aging and the eﬀects of aﬀective and factual focus on source monitoring and recall. Psychology and Aging, 9, 160–170.

300

  

Henkel, L. A., Johnson, M. K., & De Leonardis, D. M. (1998). Aging and source monitoring: Cognitive processes and neuropsychological correlates. Journal of Experimental Psychology: General, 127, 1–18. Herzog, A. G., & Kemper, T. L. (1980). Amygdaloid changes in aging and dementia. Archives of Neurology, 37, 625–629. Hess, T. M., & Slaughter, S. J. (1990). Schematic knowledge inﬂuences on memory for scene information in young and older adults. Developmental Psychology, 26, 855–865. Hutner, N., & Oscar-Berman, M. (1996). Visual laterality patterns for the perception of emotional words in alcoholic and aging individuals. Journal of Studies on Alcohol, 57, 144–154. Isingrini, M., Fontaine, R., Taconnat, L., & Duportal, A. (1995). Aging and encoding in memory: False alarms and decision criteria in a word-pair recognition task. International Journal of Aging and Human Development, 41, 79–88. Jack, C. R. Jr, Petersen, R. C., O’Brien, P. C., & Tangalos, E. G. (1992). MR-based hippocampal volumetry in the diagnosis of Alzheimer’s disease. Neurology, 42, 183–188. Jack, C. R. Jr, Petersen, R. C., Xu, Y. C., Waring, S. C., O’Brien, P. C., Tangalos, E. G., et al. (1997). Medial temporal atrophy on MRI in normal aging and very mild Alzheimer’s disease. Neurology, 49, 786–794. Johnson, H. M., & Magaro, P. A. (1987). Eﬀects of mood and severity on memory processes in depression and mania. Psychological Bulletin, 101, 28–40. Johnson, M. K., & Multhaup, K. S. (1992). Emotion and MEM. In S.-Å. Christianson (Ed.), The handbook of emotion and memory: Current research and theory (pp. 33– 66). Hillsdale, NJ: Erlbaum. Johnson, M. K., Nolde, S. F., & De Leonardis, D. M. (1996). Emotional focus and source monitoring. Journal of Memory and Language, 35, 135–156. Johnson, M. K., & Raye, C. L. (2000). Cognitive and brain mechanisms of false memories and beliefs. In D. L. Schacter & E. Scarry (Eds.), Memory, brain, and belief (pp. 25–86). Cambridge, MA: Harvard University Press. Johnson, R. C., Cole, R. E., Bowers, J. K., Foiles, S. V., Nikaido, A. M., Patrick, J. W., et al. (1979). Hemispheric eﬃciency in middle and later adulthood. Cortex, 15, 109–119. Jones, C. J., & Meredith, W. (2000). Developmental paths of psychological health from early adolescence to later adulthood. Psychology and Aging, 15, 351– 360. Kazui, H., Mori, E., Hashimoto, M., Hirono, N., Imamura, T., Tanimukai, S., et al. (2000). Impact of emotion on memory: Controlled study of the inﬂuence of emotionally charged material on declarative memory in Alzheimer’s disease. British Journal of Psychiatry, 177, 343–347. Kemper, T. L. (1994). Neuroanatomical and neuropathological changes during aging and dementia. In M. L. Albert & E. J. E. Knoepfel (Eds.), Clinical neurology of aging (2nd ed., pp. 3–67). New York: Oxford University Press. Kennedy, Q. (2002). Age diﬀerences in the reconstruction of long-term autobiographical memory: Testing a motivational hypothesis. Unpublished dissertation, Stanford University, Stanford, CA.

   

301

Kennedy, Q., Mather, M., & Carstensen, L. L. (in press). The role of motivation in the age-related positive bias in autobiographical memory. Psychological Science. Kensinger, E. A., Brierley, B., Medford, N., Growdon, J. H., & Corkin, S. (2002). Eﬀects of normal aging and Alzheimer’s disease on emotional memory. Emotion, 2, 118–134. Kensinger, E. A., & Schacter, D. L. (1999). When true memories suppress false memories: Eﬀects of aging. Cognitive Neuropsychology, 16, 399–415. Kimbrell, T. A., George, M. S., Parekh, P. I., Ketter, T. A., Podell, D. M., Danielson, A. L., et al. (1999). Regional brain activity during transient self-induced anxiety and anger in healthy adults. Biological Psychiatry, 15, 454–465. Kolb, B., & Whishaw, I. Q. (1990). Fundamentals of human neuropsychology. New York: W. H. Freeman. Koutstaal, W., Schacter, D. L., & Brenner, C. (2001). Dual task demands and gistbased false recognition of pictures in younger and older adults. Journal of Memory and Language, 44, 399–426. Koutstaal, W., Schacter, D. L., Galluccio, L., & Stofer, K. A. (1999). Reducing gistbased false recognition in older adults: Encoding and retrieval manipulations. Psychology and Aging, 14, 220–237. Labouvie-Vief, G. (1998). Cognitive-emotional integration in adulthood. In K. W. Schaie & M. P. Lawton (Eds.), Annual review of gerontology and geriatrics: Focus on emotion and adult development (Vol. 17, pp. 206–237). New York: Springer. Labouvie-Vief, G., DeVoe, M., & Bulka, D. (1989). Speaking about feelings: Conceptions of emotion across the life span. Psychology and Aging, 4, 425–437. Lane, R. D., Reiman, E. M., Ahern, G. L., Schwartz, G. E., & Davidson, R. J. (1997). Neuroanatomical correlates of happiness, sadness, and disgust. American Journal of Psychiatry, 154, 926–933. Lane, R. D., Reiman, E. M., Bradley, M. M., Lang, P. J., Ahern, G. L., Davidson, R. J., et al. (1997). Neuroanatomical correlates of pleasant and unpleasant emotion. Neuropsychologia, 35, 1437–1444. Lawton, M. P., Kleban, M. H., & Dean, J. (1993). Aﬀect and age: Cross-sectional comparisons of structure and prevalence. Psychology and Aging, 8, 165–175. Lawton, M. P., Kleban, M. H., Rajagopal, D., & Dean, J. (1992). Dimensions of aﬀective experience in three age groups. Psychology and Aging, 7, 171–184. Levenson, R. W., Carstensen, L. L., & Gottman, J. M. (1994). The inﬂuence of age and gender on aﬀect, physiology, and their interrelations: A study of long-term marriages. Journal of Personality and Social Psychology, 67, 56–68. Levenson, R. W., Friesen, W. V., Ekman, P., & Carstensen, L. L. (1991). Emotion, physiology, and expression in old age. Psychology and Aging, 6, 28–35. Levine, L. J., & Bluck, S. (1997). Experienced and remembered emotional intensity in older adults. Psychology and Aging, 12, 514–523. Light, L. L. (1996). Memory and aging. In E. L. Bjork & R. A. Bjork (Eds.), Memory (pp. 444–490). San Diego: Academic Press. Light, L. L. (2000). Memory changes in adulthood. In S. H. Qualls & N. Abeles (Eds.), Psychology and the aging revolution: How we adapt to longer life (pp. 73–97). Washington, DC: American Psychological Association. Lim, K. O., Zipursky, R. B., Murphy, G. M. Jr, & Pfeﬀerbaum, A. (1990). In vivo

302

  

quantiﬁcation of the limbic system using MRI: Eﬀects of normal aging. Psychiatry Research, 35, 15–26. Livingston, R. B. (1967). Reinforcement. In G. C. Quarton, T. Melnechuck, & F. O. Schmitt (Eds.), The neurosciences: A study program (pp. 568–576). New York: Rockefeller University Press. Masterman, D. L., & Cummings, J. L. (1997). Frontal-subcortical circuits: The anatomic basis of executive, social and motivated behaviors. Journal of Psychopharmacology, 11, 107–114. Mather, M., Canli, T., English, T., Golarai, G., Fleischman, D., Gabrieli, J. D. E., et al. (2001, November). An fMRI study of age-related changes in encoding and remembering emotional material. Paper presented at the annual conference of the Society for Neuroscience, San Diego, CA. Mather, M., & Carstensen, L. L. (2003). Implications of the positivity effect for older people’s memories about health care decisions. Manuscript submitted for publication. Mather, M., & Carstensen, L. L. (in press). Aging and attentional biases for emotional faces. Psychological Science. Mather, M., & Johnson, M. K. (2000). Choice-supportive source monitoring: Do our decisions seem better to us as we age? Psychology and Aging, 15, 596–606. Mather, M., & Johnson, M. K. (2003). Aﬀective review and schema reliance in older and younger adults. American Journal of Psychology, 116, 169–189. Mather, M., Johnson, M. K., & De Leonardis, D. M. (1999). Stereotype reliance in source monitoring: Age diﬀerences and neuropsychological test correlates. Cognitive Neuropsychology, 16, 437–458. May, C. P., Rahhal, T., Leighton, E., & Berry, E. (2002, April). Aging, source memory, and emotional cues. Paper presented at the Cognitive Aging Conference, Atlanta, GA. McConatha, J. T., & Huba, H. M. (1999). Primary, secondary, and emotional control across adulthood. Current Psychology, 18, 164–170. McDaniel, M. A., Glisky, E. L., Rubin, S. R., Guynn, M. J., & Routhieaux, B. C. (1999). Prospective memory: A neuropsychological study. Neuropsychology, 13, 103– 110. McGaugh, J. L. (2000). Memory—A century of consolidation. Science, 287, 248–251. McGaugh, J. L., Ferry, B., & Vazdarjanova, A. (2000). Amygdala: Role in modulation of memory storage. In J. P. Aggleton (Ed.), The amygdala (pp. 391–423). New York: Oxford University Press. McIntyre, J. S., & Craik, F. I. M. (1987). Age diﬀerences in memory for item and source information. Canadian Journal of Psychology, 41, 175–192. Mineka, S., & Nugent, K. (1995). Mood-congruent memory biases in anxiety and depression. In D. L. Schacter (Ed.), Memory distortions: How minds, brains, and societies reconstruct the past (pp. 173–193). Cambridge, MA: Harvard University Press. Mitchell, K. J., Johnson, M. K., & Mather, M. (2003). Source monitoring and suggestibility to misinformation: Adult age-related diﬀerences. Applied Cognitive Psychology, 17, 107–119. Mittenberg, W., Seidenberg, M., Oleary, D. S., & Digiulio, D. V. (1989). Changes in

   

303

cerebral functioning associated with normal aging. Journal of Clinical and Experimental Neuropsychology, 11, 918–932. Moreno, C. R., Borod, J. C., Welkowitz, J., & Alpert, M. (1990). Lateralization for the expression and perception of facial emotion as a function of age. Neuropsychologia, 28, 199–209. Mori, E., Ikeda, M., Hirono, N., Kitagaki, H., Imamura, T., & Shimomura, T. (1999). Amygdalar volume and emotional memory in Alzheimer’s disease. American Journal of Psychiatry, 156, 216–222. Moscovitch, M., & Olds, J. (1982). Asymmetries in spontaneous facial expressions and their possible relation to hemispheric specialization. Neuropsychologia, 20, 71–82. Moscovitch, M., & Winocur, G. (1995). Frontal lobes, memory, and aging. Annals of the New York Academy of Sciences, 769, 119–150. Mroczek, D. K. (2001). Age and emotion in adulthood. Current Directions in Psychological Science, 10, 87–90. Mu, Q., Xie, J., Wen, Z., Weng, Y., & Shuyun, Z. (1999). A quantitative MR study of the hippocampal formation, the amygdala, and the temporal horn of the lateral ventricle in healthy subjects 40 to 90 years of age. American Journal of Neuroradiology, 20, 207–211. Nebes, R. D. (1990). Hemispheric specialization in the aged brain. In C. B. Trevarthen (Ed.), Brain circuits and functions of the mind: Essays in honor of Roger W. Sperry (pp. 364–370). New York: Cambridge University Press. Nebes, R. D., Madden, D. J., & Berg, W. D. (1983). The eﬀect of age on hemispheric asymmetry in visual and auditory identiﬁcation. Experimental Aging Research, 9, 87–91. Neisser, U., & Harsch, N. (1992). Phantom ﬂashbulbs: False recollections of hearing the news about Challenger. In E. Winograd & U. Neisser (Eds.), Aﬀect and accuracy in recall: Studies of “ﬂashbulb” memories (pp. 9–31). Cambridge: Cambridge University Press. Norman, K. A., & Schacter, D. L. (1997). False recognition in younger and older adults: Exploring the characteristics of illusory memories. Memory & Cognition, 25, 838–848. Nyberg, L., Cabeza, R., & Tulving, E. (1996). PET studies of encoding and retrieval: The HERA model. Psychonomic Bulletin & Review, 3, 135–148. Obler, L. K., Woodward, S., & Albert, M. L. (1984). Changes in cerebral lateralization in aging. Neuropsychologia, 22, 235–240. Ohnishi, T., Matsuda, H., Tabira, T., Asada, T., & Uno, M. (2001). Changes in brain morphology in Alzheimer disease and normal aging: Is Alzheimer disease an exaggerated aging process? American Journal of Neuroradiology, 22, 1680–1685. Oxman, T. E., Barrett, J. E., Sengupta, A., & Williams, J. W. (2000). The relationship of aging and dysthymia in primary care. American Journal of Geriatric Psychiatry, 8, 318–326. Pasupathi, M., & Carstensen, L. L. (in press). Age and emotional experience during mutual reminiscing. Psychology and Aging. Phillips, L. H., & Della Sala, S. (1998). Aging, intelligence, and anatomical segregation in the frontal lobes. Learning and Individual Diﬀerences, 10, 217–243.

304

  

Pillemer, D. B. (1984). Flashbulb memories of the assassination attempt on President Reagan. Cognition, 16, 63–80. Prull, M. W., Gabrieli, J. D. E., & Bunge, S. A. (2000). Age-related changes in memory: A cognitive neuroscience perspective. In F. I. M. Craik & T. A. Salthouse (Eds.), The handbook of aging and cognition (2nd ed., pp. 91–153). Mahwah, NJ: Erlbaum. Rahhal, T., May, C. P., & Hasher, L. (2002). Truth and character: Sources that older adults can remember. Psychological Science, 13, 101–105. Raine, A., Buschbaum, M., & LaCasse, L. (1997). Brain abnormalities in murderers indicated by positron emission tomography. Biological Psychiatry, 42, 495– 508. Rankin, J. L., & Kausler, D. H. (1979). Adult age diﬀerences in false recognitions. Journal of Gerontology, 34, 58–65. Raz, N. (2000). Aging of the brain and its impact on cognitive performance: Integration of structural and functional ﬁndings. In F. I. M. Craik & T. A. Salthouse (Eds.), Handbook of aging and cognition (2nd ed., pp. 1–90). Mahwah, NJ: Erlbaum. Raz, N., Gunning, F. M., Head, D., Dupuis, J. H., McQuain, J., Briggs, S. D., et al. (1997). Selective aging of the human cerebral cortex observed in vivo: Diﬀerential vulnerability of the prefrontal gray matter. Cerebral Cortex, 7, 268–282. Regier, D. A., Boyd, J. H., Burke, J. D., Rae, D. S., Myers, J. K., Kramer, M., et al. (1988). One-month prevalence of mental disorders in the United States: Based on 5 epidemiologic catchment-area sites. Archives of General Psychiatry, 45, 977–986. Reisberg, D., & Heuer, F. (1992). Remembering the details of emotional events. In E. Winograd & U. Neisser (Eds.), Aﬀect and accuracy in recall: Studies of “ﬂashbulb” memories (pp. 163–190). Cambridge, MA: Harvard University Press. Reisberg, D., Heuer, F., McLean, J., & Oshaughnessy, M. (1988). The quantity, not the quality, of aﬀect predicts memory vividness. Bulletin of the Psychonomic Society, 26, 100–103. Reminger, S. L., Kaszniak, A. W., & Dalby, P. R. (2000). Age-invariance in the asymmetry of stimulus-evoked emotional facial muscle activity. Aging, Neuropsychology, & Cognition, 7, 156–168. Rolls, E. T. (2000). The orbitofrontal cortex and reward. Cerebral Cortex, 10, 284– 294. Rozin, P., & Royzman, E. B. (2001). Negativity bias, negativity dominance, and contagion. Personality and Social Psychology Review, 5, 296–320. Rubin, D. C., & Kozin, M. (1984). Vivid memories. Cognition, 16, 1–15. Rubin, D. C., Rahhal, T., & Poon, L. W. (1998). Things learned in early adulthood are remembered best. Memory & Cognition, 26, 3–19. Salat, D. H., Kaye, J. A., & Janowsky, J. S. (2001). Selective preservation and degeneration within the prefrontal cortex in aging and Alzheimer’s Disease. Archives of Neurology, 58, 1403–1408. Schacter, D. L., Kazniak, A. W., Kihlstrom, J. F., & Valdiserri, M. (1991). The relation between source memory and aging. Psychology and Aging, 6, 559–568. Schaie, K. W., & Schaie, J. P. (1977). Clinical assessment and aging. In J. E. Birren & K. W. Schaie (Eds.), Handbook of the psychology of aging (pp. 692–723). New York: Van Nostrand Reinhold.

   

305

Schmolck, H., Buﬀalo, E. A., & Squire, L. R. (2000). Memory distortions develop over time: Recollections of the O. J. Simpson trial verdict after 15 and 32 months. Psychological Science, 11, 39–45. Schwartz, G. E., Davidson, R. J., & Maer, F. (1975). Right hemisphere lateralization for emotion in the human brain. Science, 190, 186–288. Scott, D., & Ponsoda, V. (1996). The role of positive and negative aﬀect in ﬂashbulb memory. Psychological Reports, 79, 467–473. Scott, S. A., DeKosky, S. T., & Scheﬀ, S. W. (1991). Volumetric atrophy of the amygdala in Alzheimer’s disease: Quantitative serial reconstruction. Neurology, 41, 351–356. Scoville, W. B., & Milner, B. (1957). Loss of recent memory after bilateral hippocampal lesions. Journal of Neurology, Neurosurgery and Psychiatry, 20, 11–21. Shimamura, A. P. (1995). Memory and frontal lobe function. In M. S. Gazzaniga (Ed.), The cognitive neurosciences (pp. 803–813). Cambridge, MA: MIT Press. Smith, A. D. (1975). Partial learning and recognition memory in the aged. International Journal of Aging and Human Development, 6, 359–365. Smith, C. D., Malcein, M., Meurer, K., Schmitt, F. A., Markesbery, W. R., & Pettigrew, L. C. (1999). MRI temporal lobe volume measures and neuropsychologic function in Alzheimer’s disease. Journal of Neuroimaging, 9, 2–9. Smith, J., Fleeson, W., Geiselmann, B., Settersten, R. A., & Kunzmann, U. (1999). Sources of well-being in very old age. In P. B. Baltes & K. U. Mayer (Eds.), The Berlin Aging Study: Aging from 70 to 100 (pp. 450–471). New York: Cambridge University Press. Spencer, W. D., & Raz, N. (1995). Diﬀerential eﬀects of aging on memory for content and context: A meta-analysis. Psychology and Aging, 10, 527–539. Suengas, A. G., & Johnson, M. K. (1988). Qualitative eﬀects of rehearsal on memories for perceived and imagined complex events. Journal of Experimental Psychology: General, 117, 377–389. Sullivan, E. V., Marsh, L., Mathalon, D. H., Lim, K. O., & Pfeﬀerbaum, A. (1995). Age-related decline in MRI volumes of temporal lobe gray matter but not hippocampus. Neurobiology of Aging, 16, 591–606. Tisserand, D. J., Visser, P. J., van Boxtel, M. P. J., & Jolles, J. (2000). The relation between global and limbic brain volumes on MRI and cognitive performance in healthy individuals across the age range. Neurobiology of Aging, 21, 569–576. Tsai, J. L., Levenson, R. W., & Carstensen, L. L. (2000). Autonomic, subjective, and expressive responses to emotional ﬁlms in older and younger Chinese Americans and European Americans. Psychology and Aging, 15, 684–693. Tun, P. A., Wingﬁeld, A., Rosen, M. J., & Blanchard, L. (1998). Response latencies for false memories: Gist-based processes in normal aging. Psychology and Aging, 13, 230–241. Watkins, P. C., Mathews, A., Williamson, D. A., & Fuller, R. D. (1992). Mood-congruent memory in depression: Emotional priming or elaboration? Journal of Abnormal Psychology, 101, 581–586. Weissman, M. M., Leaf, P. J., Bruce, M. L., & Florio, L. (1988). The epidemiology of dysthymia in ﬁve communities: Rates, risks, co-morbidity, and treatment. American Journal of Psychiatry, 145, 815–819.

306

  

West, M. J., Coleman, P. D., Flood, D. G., & Troncoso, J. C. (1994). Diﬀerences in the pattern of hippocampal neuronal loss in normal ageing and Alzheimer’s disease. Lancet, 17, 769–772. West, R. L. (1996). An application of prefrontal cortex function theory to cognitive aging. Psychological Bulletin, 120, 272–292. Wright, D. B., Gaskell, G. D., & O’Muircheartaigh, C. A. (1998). Flashbulb memory assumptions: Using national surveys to explore cognitive phenomena. British Journal of Psychology, 89, 103–121. Yarmey, A. D., & Bull, M. P. (1978). Where were you when President Kennedy was assassinated? Bulletin of the Psychonomic Society, 11, 133–135. Young, M. P., Scannell, J. W., Burns, G. A., & Blakemore, C. (1994). Analysis of connectivity: Neural systems in the cerebral cortex. Reviews in the Neurosciences, 5, 227–250. Zacks, R. T., Hasher, L., & Li, K. Z. H. (2000). Human memory. In F. I. M. Craik & T. A. Salthouse (Eds.), The handbook of aging and cognition (pp. 293–357). Mahwah, NJ: Erlbaum.

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10

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L

ate one afternoon in Abilene, Texas, Margarita Chavez was piling her three children, ages 1 month, 2 years, and 6 years, into the car after a shopping trip. As Margarita went to return her shopping cart, an unfamiliar woman rushed to the car, removed the infant, and put her into her own car. When Margarita turned around, just a few seconds later, the woman had started to drive away. The frantic mother tried to stop the car and was dragged nearly 40 feet through the parking lot, sustaining minor injuries. Meanwhile, a bystander, 13-year-old Robert Gann, also tried to stop the car by slamming his ﬁst into the windshield. Despite their eﬀorts, the woman drove away, abducting the infant (“Baby snatched, ” 2002). The witnesses to this crime, Margarita, the two children, and Robert then faced the problem of explaining to the police what had just happened and describing the kidnapper and her car. Could they provide an accurate description of this highly emotional experience? How would their emotional state at the time of the event inﬂuence their subsequent memory? How might the children’s eyewitness memory diﬀer from that of Margarita, an adult? Questions such as these are central to the forensic evaluation of eyewitness accounts. The answers to these questions, moreover, often have critical implications for all involved, including victims, defendants, and legal professionals. Fortunately, psychological science can provide highly pertinent insight into these issues. In this chapter, we address these questions and others in light of current theory and research on emotion and memory. We focus primarily on memory for negative emotional events because of the centrality of negative emotions to the forensic context. We begin by reviewing research on the inﬂuence of emotion on eyewitness memory and the implications of this research for the legal system. Then, we discuss research on memory for highly emotional, or traumatic, events, including studies of repressed and recovered memories. Because the experience of trauma is often associated with clinical symptomatology, such

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as posttraumatic stress disorder and dissociation, we also consider the inﬂuence of psychopathology on eyewitness memory capabilities. Finally, we address developmental considerations in the study of emotion and eyewitness memory. We conclude with a discussion of potential avenues for future research.

Emotion and Eyewitness Memory Individuals who become involved in the legal system are often asked to recall highly emotional and negative information. Witnesses to a murder or victims of an assault, for instance, may be asked to recount the details of that crime to police oﬃcers, attorneys, or jurors. Moreover, both victims and witnesses may be under considerable emotional distress when encoding these details. How is negative emotional information remembered, and what is the inﬂuence of an individual’s emotional state (i.e., distress) on his or her memory? In this section, we consider the inﬂuence of negative emotion on eyewitness memory. Topics include the accuracy of emotional memories, memory for central versus peripheral details of an emotional event, the durability of emotional memories over long delays, and the potentially biasing eﬀect of emotion on memory.

Accuracy of Negative

Emotional Memories

Does negative emotion enhance or impair memory? Findings across many studies, using a variety of methodologies, suggest that the answer to this question partially depends on how emotion is assessed (e.g., emotional stimuli vs. emotional distress of participants, self-report vs. physiological measures) and the kind of information being recalled (e.g., central vs. peripheral details of an event). In one line of research, participants are presented with a series of objectively rated stimuli (e.g., words, pictures, stories) ranging in emotionality, and their memory for these stimuli is assessed. Researchers can then determine how emotional valence (i.e., positive vs. negative vs. neutral) inﬂuences memory. The majority of research on memory for emotional stimuli suggests that adults remember negatively valenced stimuli better than emotionally neutral stimuli and sometimes better than positively valenced stimuli (e.g., Anooshian & Hertel, 1994; Bradley, Greenwald, Petry, & Lang, 1992; Canli, Desmond, Zhao, & Gabrieli, 2002; Doerksen & Shimamura, 2001; Heuer & Reisberg, 1990; LaBar & Phelps, 1998; Nagae & Moscovitch, 2002; Ochsner, 2000). Thus, individuals who witness (or experience) a negative event, such as an assault, may be particularly accurate when recalling that event. In one study, Ochsner (2000) examined recognition memory for pictures of negative, positive, and neutral emotional valence. Results across three experiments consistently indicated that negative pictures were remembered more accurately than either neutral or positive pictures. Moreover, correct recognition

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of negative pictures was more likely to be associated with a conscious recollective experience (i.e., a “remember” judgment; Tulving, 1985) than were neutral or positive pictures. These ﬁndings suggest that negative emotion may enhance memory by increasing the distinctiveness of emotional stimuli and/or the vividness with which they are recollected. In a second line of research, participants’ memory for an emotional event is assessed in relation to their emotional state (i.e., distress) during that event. In these studies, distress is measured in diﬀerent ways, including self-report (e.g., Christianson & Hubinette, 1993), observer report (e.g., Alexander, Goodman, Schaaf, et al., 2002), and physiological indices (e.g., Kirschbaum, Wolf, May, Wippich, & Hellhammer, 1996). Because victims and witnesses to a crime likely experience distress during the event, it is important to understand how distress inﬂuences eyewitness memory. For instance, if distress enhances (or impairs) memory for an event, the emotional state of a victim or witness is one factor that could be used to evaluate the credibility of his or her report. Perhaps because of diﬀering methodologies, research ﬁndings are sometimes inconsistent regarding the relation between experienced (or observed) distress and memory. A number of studies suggest that memory is enhanced both by selfreported distress (Yuille & Cutshall, 1986) and distress rated (or inferred) by observers (e.g., Alexander, Goodman, Schaaf, et al., 2002; Goodman, Hirschman, Hepps, & Rudy, 1991; Quas et al., 2001; Yuille, Davies, Gibling, Marxsen, & Porter, 1994), thus complementing ﬁndings from studies of memory for emotional stimuli. Other studies, however, suggest that both self-reported (e.g., Christianson & Hubinette, 1993) and observer-reported (e.g., Quas et al., 1999) distress may be unrelated to memory. Observer-rated distress has also been negatively related to memory (Vandermaas, Hess, & Baker-Ward, 1993). Studies using physiological measures of stress have yielded similarly mixed ﬁndings: Kirschbaum et al. (1996) administered cortisol, which causes physiological changes indicative of stress, to half of a sample of 40 male adults. Participants then studied a list of (not necessarily emotional) nouns. Compared to those given a placebo, individuals given cortisol showed decrements on a subsequent memory test. In other studies, however, adrenal stress hormones have facilitated emotional memory (e.g., Cahill, Prins, Weber, & McGaugh, 1994; van Stegeren, Everaerd, Cahill, McGaugh, & Gooren, 1998). Finally, additional studies suggest that, consistent with the Yerkes-Dodson law (Yerkes & Dodson, 1908), only moderate levels of stress hormones may enhance memory, whereas very high or low levels may impair memory (e.g., chapters 2 and 3, this volume; Lupien & McEwen, 1997; Quirarte, Roozendaal, & McGaugh, 1997). Thus, although most studies suggest that memory is enhanced for aﬀectively negative compared to neutral (and sometimes positive) stimuli, research is less consistent regarding the inﬂuence of an individual’s emotional state on his or her memory for a stressful event. In fact, in a recent survey of experts in psychology and law, only 50% indicated that they would testify in court about the eﬀects

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of stress on memory, yet over 75% would testify about other topics, such as the eﬀects of line-up instructions and the inﬂuence of postevent information (Kassin, Tubb, Hosch, & Memon, 2001). Thus, when evaluating eyewitness reports of stressful events, legal factﬁnders may not have a consensus of research to inform their judgments. Given the forensic importance of the inﬂuence of emotion on memory, further research is crucial to reconcile inconsistencies in ﬁndings and methodologies from previous studies.

Memory for Central Versus

Peripheral Details

In an attempt to account for previous inconsistent ﬁndings in the emotion and memory literature, Christianson (1992) proposed that emotion results in a narrowing of attention (Easterbrook, 1959), which enhances memory for central details of an event while impairing memory for peripheral details. A number of studies support this hypothesis (e.g., Berntsen, 2002; Bornstein, Liebel, & Scarberry, 1998; Burke, Heuer, & Reisberg, 1992; Christianson & Loftus, 1991; Safer, Christianson, Autry, & Osterlund, 1998; Wessel & Merckelbach, 1994, 1997, 1998; but see Wessel, van der Kooy, & Merckelbach, 2000), including those of real-life crime victims (e.g., Christianson & Hubinette, 1993), suggesting that the inﬂuence of stress on memory may depend in part on the type of information being recalled. Christianson and Hubinette, for instance, interviewed witnesses to a bank robbery and compared their accounts with information obtained from police reports. Some individuals had been bystanders during the robbery, whereas the robbers had threatened others (i.e., “victims”) with guns. Although accuracy was relatively high for both groups, the victims, who presumably experienced greater stress during the robbery, recounted the central details of the event more accurately than the bystanders. Participants were also asked to report their level of stress experienced during the crime; however, their ratings were unrelated to memory for the event, perhaps because both bystanders and victims reported relatively high levels of stress. The trade-oﬀ between central and peripheral details may also explain the phenomenon of weapon focus, in which victims of a crime involving a weapon tend to focus on that weapon at the expense of other details of the crime, such as the perpetrator’s face (e.g., Loftus, Loftus, & Messo, 1987; Pickel, 1999; Shaw & Skolnick, 1999; Stanny & Johnson, 2000). As a result, a victim’s ability to correctly identify a brieﬂy glimpsed stranger in a line-up may be compromised when a weapon is involved (see Steblay, 1992, for a meta-analytic review), at least in simulated crime situations. However, the extrapolation of weapon focus to reallife crime situations may be more complicated. A meta-analysis of studies on weapon focus suggests that, although the eﬀect is relatively small, it is more pronounced when stress is high and in contexts that more closely approximate real-life situations (Steblay, 1992). Although this

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ﬁnding suggests that weapon focus may be more prevalent among actual crime victims than is indicated by laboratory studies, more recent studies of real-life crimes suggest an opposite pattern of results, in which victims of crimes involving a weapon recall more information about the perpetrator than do victims of weaponless crimes (Cooper, Kennedy, Hervé, & Yuille, 2002; Tollestrup, Turtle, & Yuille, 1994). Cooper et al. (2002), for instance, examined memories of sexual assault among female prostitutes; those who were assaulted with a weapon provided more detail about the crime than those assaulted without a weapon. Although these ﬁndings seemingly contradict the weapon-focus hypothesis, because the accuracy of the information provided by the real-life victims could not be veriﬁed, the possibility remains that the presence of a weapon increases only the amount (as opposed to the accuracy) of the information provided. Thus, future research should examine the applicability of weapon-focus research to real-life crime situations, particularly given the consensus in the scientiﬁc community that a weapon impairs a victim’s ability to identify the perpetrator (Kassin et al., 2001): Kassin et al. reported that 87% of experts agreed that weapon focus was a reliable ﬁnding, and 77% indicated that they would testify to that eﬀect in court. It is also important to note that, according to the weapon-focus hypothesis, insofar as victims focus on the weapon at the expense of the perpetrator’s face, their memory for that weapon should be enhanced (e.g., Kramer, Buckhout, & Eugenio, 1990). That is, compromised memory for the perpetrator should coincide with improved memory for the weapon. Most studies of weapon focus, however, have not examined memory for the weapon (but see, e.g., Shaw & Skolnick, 1999), making it somewhat diﬃcult to interpret previous ﬁndings of impaired memory for the perpetrator. Although individuals purportedly orient toward a weapon, stress induced by the weapon may compromise memory in general, for both the perpetrator and the weapon. Nevertheless, the idea that emotion enhances memory for central details at the expense of memory for peripheral details has received considerable empirical support. Further research needs to be conducted, however, on real-life crime victims to determine whether these ﬁndings extend beyond the laboratory. Clarifying the mechanism underlying weapon focus is important not only to address theoretical issues surrounding distress and memory but also to evaluate eyewitness accounts of actual crimes involving weapons.

Long-Term Durability

of Emotional Memories

In many instances, victims or witnesses of a crime may not be asked to recount their experience for several days, weeks, or even years after the crime. The durability of emotional memories over time is thus an important concern in forensic settings. Several studies of memory for emotional experiences, after delays ranging from a few months to more than 10 years, suggest that such memories

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can be highly accurate (e.g., Burgwyn-Bailes, Baker-Ward, Gordon, & Ornstein, 2001; Christianson & Hubinette, 1993; Pillemer, 1984; Quas et al., 1999, 2001; Shrimpton, Oates, & Hayes, 1998; Yuille et al., 1994). Moreover, distress experienced during the event may continue to facilitate memory even after long delays. One study examined young adults’ memories of abuse-related legal involvement after a delay of approximately 13 years (Quas et al., 2001). As children, the young adults had been observed while waiting to testify at the courthouse, and their visible level of distress had been rated. In addition, details about each child’s legal experience (e.g., whether he or she actually testiﬁed, who else was in the courtroom) had been documented and thus could be compared to his or her current report. The accuracy of the young adults’ reports of their experience in court, including details about testifying (for those who took the stand), was positively related to their level of distress rated at the time of legal involvement. That is, individuals who were more distressed during the initial experience provided more accurate details about it after a delay, suggesting that emotion may facilitate memory retention over time. In another study, police trainees participated in a simulated crime event that was either stressful or nonstressful (Yuille et al., 1994). When their memory for the event was tested after a delay of either 1 or 12 weeks, trainees in the stressful condition provided more accurate information than those in the nonstressful condition. Moreover, memory for the stressful event was more resistant to decay over time. These ﬁndings reinforce the notion that the enhancing eﬀect of emotion on memory increases over time. Neurological research suggests that this eﬀect may be due to physiological processes involving the amygdala that support the consolidation of emotional memories (chapter 2, this volume; Cahill & McGaugh, 1998; Hamann, 2001). Another possibility is that individuals who are stressed during an event are more likely to discuss their experience with others, a process that often facilitates memory (e.g., Fivush, Haden, & Reese, 1996; Quas et al., 1999). Thus, emotion appears to enhance memory retention, as suggested by evidence that individuals who are more stressed during an event are less likely to forget that event over time. Not only can emotional events be remembered after a relatively long delay but they may be remembered more accurately than less emotional events. However, there is less consensus about the long-term durability of memory for events that are highly emotional, or traumatic.

Emotional Memory Biases Although many studies indicate that emotion enhances memory, others suggest the opposite, and this discrepancy may reﬂect diﬀerences across studies in the types of information for which memory is assessed (i.e., central vs. peripheral details; Christianson, 1992). Discrepancies may also result from diﬀerences in the type of eyewitness response considered (i.e., correct vs. incorrect). Some studies have revealed that emotional stimuli may be associated with increased rates of incorrect

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responses, or false alarms, as well as increased rates of correct responses, when recognition memory is assessed (e.g., Windmann & Krüger, 1998; Windmann & Kutas, 2001). Thus, in response to negative emotional information, individuals may relax the criterion they use to decide whether information is old or new. Recent event-related brain potential (ERP) data suggest that this phenomenon, the emotion-induced recognition bias (Windmann & Kutas, 2001), occurs automatically, rather than through a strategic, deliberate mnemonic process. Nevertheless, it may be possible to reduce this bias through practice or training. Limited evidence suggests that the experience of stress prior to encoding may also increase false-alarm rates for neutral information (Payne, Nadel, Allen, Thomas, & Jacobs, 2002). This idea may be particularly relevant to real-life crime situations, in which a victim or witness experiences stress during an event and then may be asked not only about details regarding the crime itself but also about details following the crime. Payne et al. induced stress by instructing participants to give an extemporaneous speech, about which they believed they would later be evaluated. After the stress induction, participants studied several lists of words. When their memory for those words was then tested, participants who had experienced the stress induction were more likely than those who had not to falsely recognize words semantically related to those they had studied. Correct recognition, however, was unaﬀected by stress. (False recognition of unrelated words occurred infrequently and was unrelated to stress condition.) According to the authors, increased rates of false alarms may result from the impact of stress on brain regions involved in long-term memory, such as the hippocampus. As we discuss later, some evidence suggests that chronic exposure to stress, as evidenced by PTSD symptomatology, may be similarly associated with increased false alarms. [See chapter 3—Eds.] Heightened false alarm rates may also result from the inﬂuence of emotion on source-monitoring processes (Johnson, Nolde, & Leonardis, 1996). According to Johnson et al., focusing on one’s own emotions while encoding an event (which may occur during real-life stressful situations; Gross, 2002) can impair an individual’s ability to discriminate the source of a particular memory. Sourcemonitoring diﬃculties, in turn, are associated with more false alarms (Johnson, Hashtroudi, & Lindsay, 1993). A possible emotion-induced recognition bias may have important implications for the forensic context. For instance, in forensic interviews, individuals may be asked yes/no questions (e.g., “Did he hit you?”) about a stressful experience. If negative experiences bias respondents to respond aﬃrmatively to such questions, open-ended questions (e.g., “What did he do?”), which are less likely to result in false alarms, may be more useful. For similar reasons, an emotioninduced bias may inﬂuence the outcome of a line-up if, for example, victims are biased to falsely recognize potential perpetrators. This possibility highlights the importance of constructing scientiﬁcally sound line-ups that limit false identiﬁcations (see Wells et al., 1998). In addition, the potentially stress-inducing

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nature of forensic situations themselves may be relevant. That is, eyewitnesses may be stressed during a line-up or while testifying not only because of their past experiences but also because of the stress associated with recounting those experiences to others.

Summary and Conclusions In summary, emotion inﬂuences eyewitness memory in a variety of ways. Whereas research on memory for emotional stimuli generally suggests that memory for central information is enhanced by emotion, particularly negative emotion, research on emotional stress and memory has yielded mixed ﬁndings. Other research, however, suggests that these inconsistent ﬁndings may be due, in part, to diﬀerences across studies in the type of information recalled (i.e., central vs. peripheral details) or to the type of eyewitness responses considered (i.e., correct or false alarms). In addition, the few long-term studies of distress and memory suggest that emotion may enhance memory consolidation over time and thus preserve long-term memory. Many of these ﬁndings have been used to inform forensic practice. To improve the forensic applicability of this research, however, future research should (1) clarify inconsistencies in the stress and memory literature, including the applicability of weapon-focus research to reallife crime situations; (2) further investigate the long-term durability of emotional memories; and (3) examine the prevalence of emotion-induced recognition biases outside the laboratory.

Memory for Traumatic Events The majority of research we have discussed concerns memory for events or stimuli that range in emotionality. However, whether these ﬁndings apply to memory for events that are highly emotional, or traumatic, is currently a topic of considerable debate (e.g., American Psychological Association [APA] Working Group, 1998; Williams & Banyard, 1999). Some researchers have hypothesized that memory for trauma is governed by special mechanisms (e.g., dissociation, repression; Freyd, 1996; Terr, 1994) that are not involved in the processing of nontraumatic information and that may cause traumatic memories to be inaccessible for extended periods. In the following sections, we consider the argument that special mechanisms underlie memory for traumatic events, as well as research on repressed and recovered memories.

Trauma and Memory: A Case

for Special Mechanisms?

At the upper end of the stress continuum are highly emotional, often traumatic, events (Metcalfe & Jacobs, 2000). A traumatic experience is threatening to the

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life or well-being of an individual (Brewin, Dalgleish, & Joseph, 1996), engenders feelings of helplessness or fear (Foa, Zinbarg, & Rothbaum, 1992), and results in altered levels of stress hormones, such as cortisol, epinephrine, and norepinephrine (American Psychiatric Association, 1994; Cooper, 1986). Examples of traumatic events include (but are not limited to) physical or sexual assault, automobile accidents, witnessing a violent crime, and military combat. Although some would predict enhanced memory for at least the central details of even very traumatic events, due to their highly stressful nature (e.g., Christianson, 1992; Goodman et al., 1991; Metcalfe & Jacobs, 2000; Shobe & Kilhstrom, 1997), others have argued that special mechanisms, such as repression, may be invoked when processing traumatic experiences (e.g., S. Freud, 1915; Freyd, 1996; Terr, 1994). Unfortunately, because it is diﬃcult to study memory for traumatic events in the laboratory, relatively little empirical evidence exists to evaluate either of these claims; however, a few studies have assessed participants’ memories for real-life traumatic events, such as child sexual abuse (CSA; e.g., Goodman et al., 2003; Williams, 1994). [Also see chapter 4—Eds.] According to the trauma-speciﬁc mechanisms view, events that are particularly traumatic (e.g., severe assault, abuse perpetrated by a close family member) are less likely to be recalled due to psychological defense mechanisms that inhibit conscious awareness of the experience (e.g., A. Freud, 1936; Freyd, 1996). Some support for this prediction comes from a study of women’s disclosure of CSA (Williams, 1994). Williams interviewed 129 women who had been seen at a hospital in the early 1970s because of alleged sexual abuse. When questioned approximately 17 years later about a variety of personal topics, including CSA, 38% of the women failed to disclose the documented abuse. Individuals who did not disclose were more closely related to the perpetrator of the abuse than were individuals who disclosed. Although nondisclosure could reﬂect psychological processes other than repression, such as reluctance to discuss sensitive topics, these ﬁndings are consistent with the idea that the more severe the abuse, the less likely it is to be remembered. Furthermore, based on the rate of nondisclosure in her sample, Williams concluded that forgetting CSA is relatively common (see also Widom & Morris, 1997). In a more recent study, however, Goodman et al. (2003) examined CSA disclosure in a sample of men and women with documented sexual abuse histories, after a delay of approximately 13 years. Only 19% of this sample failed to disclose the documented abuse, a rate considerably lower than that Williams (1994) obtained. Moreover, Goodman et al. found that abuse severity was positively related to disclosure, indicating that more severe abuse was less likely to be forgotten. The positive relation between abuse severity and disclosure is consistent with the idea that salient events are more likely to be remembered (Howe, 1997, 2000), despite their traumatic nature. Also consistent with the similar mechanisms idea is the ﬁnding of age-related diﬀerences in CSA disclosure (Goodman et al., 2003; Williams, 1994); individuals who were younger at the

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time of the abuse, particularly those who experienced the abuse before the oﬀset of infantile amnesia (i.e., 3–5 years of age), were less likely to disclose. Yet, additional predictors of disclosure may be unique to traumatic events. For instance, higher scores on the Dissociative Experiences Scale (DES; Bernstein & Putnam, 1986) were associated with a decreased likelihood of disclosure (Goodman et al., 2003), which may reﬂect memory impairment resulting from coping mechanisms associated with trauma. Despite evidence that many adults can recall traumatic childhood experiences, the accuracy of those recollections has rarely been investigated. In one exception, Alexander, Goodman, Quas, et al. (2002) compared participants’ current reports of the abuse with information obtained when the abuse was initially reported. Results indicated that abuse severity was positively related to the accuracy of participants’ memories for details of the abuse. That is, individuals who experienced more severe abuse made fewer commission errors in an interview about their documented CSA experience approximately 12 to 21 years after the abuse. In addition, participants who nominated CSA as their most traumatic lifetime event had better memory for the abuse, independent of abuse severity. These ﬁndings, like those regarding CSA disclosure, are consistent with the idea that similar memory mechanisms (e.g., event salience) may be operating for both traumatic and nontraumtic events (Shobe & Kihlstrom, 1997). However, Alexander, Goodman, Quas, et al. also identiﬁed potentially trauma-speciﬁc predictors of CSA memory, related to the severity of posttraumatic stress disorder symptomatology. Thus, although many adults can recall traumatic events they experienced in childhood, some individuals do appear to lack conscious recollection of such experiences, and some potential trauma-speciﬁc predictors of memory have been identiﬁed (e.g., dissociation; Goodman et al., 2003). The possibility therefore remains that repression or other psychological defenses could be operating, at least in some cases. In the following section, we review research on repressed memories, including research on memories that have been repressed and later recovered.

Repressed and Recovered Memories That some individuals fail to disclose documented CSA or other traumatic experiences (e.g., Goodman et al., in press; Williams, 1994) suggests that the memories for these experiences could have been repressed. This possibility is further bolstered by ﬁndings from retrospective studies, in which sizeable percentages of individuals reporting histories of CSA also report having had complete to partial amnesia for their abusive experience for some time (e.g., Briere & Conte, 1993; Epstein & Bottoms, 1998; Elliott & Briere, 1995). Briere and Conte, for instance, found that nearly 60% of their clinical sample described time periods when they had no memory for self-reported CSA experiences. Unfortunately, in these studies, no independent corroboration of the crime (or lack of memory for

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it) exists, so the data must be interpreted cautiously (Schooler & Eich, 2000). Moreover, ﬁndings from prospective studies (Edelstein, Ghetti, Redlich, Cordón, & Raskauskas, 2003; Williams, 1995) suggest that forgetting rates may be considerably lower than those reported in retrospective accounts. Retrospective studies are also limited by their reliance on participants’ assessments of prior memory states, which may be fallible (Henry, Moﬃtt, Caspi, Langley, & Silva, 1994; Hyman & Loftus, 1998; Read, 1999; Schooler, Ambadar, & Bendiksen, 1997). To illustrate this point, Schooler et al. interviewed four women who reported having forgotten a sexual abuse experience. Friends and family members of these women were then questioned to obtain independent corroboration of the abuse and subsequent forgetting. In at least two of the cases, these corroborative interviews suggested that the women had not entirely forgotten the abuse; instead, they appeared to have forgotten having previously remembered it. Moreover, somewhat ironically, estimates of amnesia may increase with active eﬀorts at reconstruction (Read & Lindsay, 2000). Read and Lindsay asked adult participants to characterize their memories of childhood events, such as going to summer camp and high school graduation. They were asked whether there was ever a time when they had less memory for the event than they had currently. One group of participants was asked to spend as much time as possible during the next month thinking about an assigned event and attempting to recall as many details of that event as possible (reminiscence group). The second group received the same instructions but was also asked to speak to family members about the event, to try to ﬁnd photographs of it, and to return to the site of the event if possible (enhanced group). Results indicated that, when memory characterizations were assessed after a 1–month delay, the enhanced group was more likely to report prior periods of poor memory for the assigned event (70%) than the reminiscence group (35%). These ﬁndings suggest that attempts to reconstruct a memory, which may occur during the process of therapy (Lindsay & Read, 1995), may alter participants’ perceptions of past memory states. In fact, some researchers have argued that false “recovered” memories of CSA can be evoked in therapy (Bottoms, Shaver, & Goodman, 1996; Poole, Lindsay, Memon, & Bull, 1995), particularly when suggestive therapeutic techniques are used, such as the examination of the client’s self-reported dreams (Mazzoni & Loftus, 1998; Mazzoni, Lombardo, Malvagia, & Loftus, 1999) or hypnosis (Loftus & Ketcham, 1991; Woodall, 1999). Because corroborating memories recovered during therapy is diﬃcult, however, the veracity of such reports remains a highly controversial topic (e.g., Alpert, Brown, & Courtois, 1998; Ornstein, Ceci, & Loftus, 1998). Recognizing the division in the scientiﬁc community over repressed and recovered memories of childhood abuse (APA Working Group, 1998), many state courts have refused to admit recovered memories as evidence (e.g., Engstrom v.

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Engstrom, 1997; Kohout v. Charter Peachford Hospital, 1998). In other states, however, individuals reporting recovered memories have been allowed to testify about their experiences (Brown, Scheﬂin, & Whitﬁeld, 1999; Woodall, 1999). In fact, some states have extended the statute of limitations for cases involving repressed memories, such that the time period for ﬁling charges starts from the time the memory is recovered, rather than from the time the abuse allegedly occurred (Bowman & Mertz, 1996; Brown, Scheﬂin, & Hammond, 1998; Gothard & Ivker, 2000).

Summary and Conclusions In summary, although further research is clearly needed, extant ﬁndings indicate that many adults can remember traumatic childhood events. Moreover, recall of these traumatic events and the accuracy of the reports are often predicted by factors such as age and the salience of the event that also predict memory for nontraumatic events. Additional predictors have been identiﬁed, however, such as dissociation (Goodman et al., 2003), which may be speciﬁc to memory for trauma. In addition, because some individuals do not appear to remember their traumatic experiences, and because others report prior periods of no memory, we cannot rule out the possibility that these memories were repressed. This possibility, and the phenomena of repressed and recovered memories, warrants further research. As the intense debate over repressed and recovered memories continues, a challenge for future research will be to clarify the conditions under which traumatic memories may be lost and later recovered and to develop criteria to evaluate the validity of such memories.

Symptoms of Psychopathology:

Implications for Eyewitness Memory

As we discussed earlier, individuals who become involved in the legal system often have experienced or witnessed a distressing or even traumatic event. Because a number of studies suggest associations between traumatic experiences and a variety of emotional problems, such as PTSD (e.g., Bremner et al., 1992; Feeny, Zoellner, & Foa, 2000) and high levels of dissociation (e.g., Chu, 1998; Putnam & Trickett, 1997), we must consider the inﬂuence of psychopathology on eyewitness memory. That is, how might clinical symptomatology aﬀect an individual’s ability to recount his or her past emotional experiences or to process new emotional information? We focus our attention on PTSD and dissociation because of their strong links with both trauma and memory; however, other emotional problems likely inﬂuence eyewitness memory capabilities, including depression (chapter 6) and panic disorder (Coles & Heimberg, 2002; chapter 5, this volume).

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PTSD and Eyewitness Memory PTSD is characterized by a reaction of intense fear, helplessness, or horror to a traumatic event (e.g., rape, assault), accompanied by persistent intrusive recall of the experience, avoidance of reminders of the event, and heightened anxiety (American Psychiatric Association, 1994). Individuals with PTSD often relive the traumatic event through intrusive thoughts, ﬂashbacks, and nightmares, so that, according to network models of memory (Bower, 1992), trauma-related information is easily activated in memory. Increased activation may, in turn, enhance memory for trauma-related information. Reliving a traumatic event via intrusive thoughts and ﬂashbacks may also enhance memory by facilitating rehearsal of the event. Thus, PTSD may be associated with memory biases for trauma-related information (e.g., Coles & Heimberg, 2002). In line with this hypothesis, PTSD has been associated with heightened activation of trauma-related information in an emotional Stroop paradigm (see Williams, Mathews, & MacLeod, 1996, for a review). In this paradigm, participants are shown a word (e.g., assault) printed in color, and their task is to say aloud the color of the word. Longer latencies to respond presumably reﬂect increased activation of or attention to the printed word, which interferes with color naming. Findings indicate that individuals with PTSD, compared to those without PTSD (who are often matched on trauma experience, age, or education level, or more than one of these), tend to take longer to name the color of the word when emotional or trauma-related words are presented (Bryant & Harvey, 1995; Cassiday, McNally, & Zeitlin, 1992; McNally, Amir, & Lipke, 1996; McNally, Clancy, Schacter, & Pitman, 2000; McNally, Kaspi, Riemann, & Zeitlin, 1990; McNally, Metzger, Lasko, Clancy, & Pitman, 1998; Moradi, Taghavi, NeshatDoost, Yule, & Dalgleish, 1999). Thus, individuals with PTSD may have diﬃculty inhibiting the activation of emotional or trauma-related words, which increases their response time on the emotional Stroop task. This heightened activation should, in turn, enhance memory for trauma-related information. To examine directly the hypothesis that PTSD symptomatology enhances memory for trauma-related information, Vrana, Roodman, and Beckham (1995) compared the performance of Vietnam veterans with and without PTSD on a memory task involving emotional words (some of which were related to combat) and neutral words. Individuals with PTSD remembered more emotional words than those without PTSD; however, there was no diﬀerence in memory for the neutral words. These ﬁndings suggest that individuals with PTSD have a memory bias in favor of emotional words, at least when trauma-related words are included. Furthermore, PTSD has been associated with enhanced memory for real-life traumatic events. In a study of long-term memory for documented CSA experiences, Alexander, Goodman, Quas, et al. (2002) found that individuals who nominated CSA as their most traumatic experience remembered the documented

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case relatively accurately. For individuals who nominated an event other than CSA (e.g., death of a loved one) as their most traumatic experience, memory accuracy was positively related to the number of PTSD criteria met. One interpretation of these ﬁndings is that, for individuals who selected CSA as their most traumatic event, the experience was particularly salient and emotional, so that long–term memory accuracy was preserved. This may not have been the case for victims who reported a non-CSA event as their most traumatic experience and met few PTSD criteria; for these individuals, the CSA experience may not have been particularly salient or emotional, and, as a result, their memory was less accurate. Individuals who nominated a non-CSA event and met more PTSD criteria, however, evinced memory as accurate as those nominating a CSA event. For these individuals, greater PTSD symptomatology may be associated with hypervigilance to trauma cues, which would facilitate CSA memory. In addition, although memory for traumatic events other than CSA was not investigated in this study, individuals nominating other events could show enhanced memory for that particular event. Despite the potentially memory-enhancing eﬀects of PTSD, additional research suggests that PTSD may also be associated with inconsistency of memory reports for traumatic experiences (Southwick, Morgan, Nicolaou, & Charney, 1997). Southwick et al. examined memories for combat experience among Operation Desert Storm veterans and found that, compared to veterans with fewer symptoms, those with more PTSD symptoms had less consistent memory reports for their combat experience over a 2-year period. Because inconsistent reports often are deemed less credible (Berman & Cutler, 1996; Fisher & Cutler, 1992), individuals with PTSD may be at a disadvantage when recalling their traumatic experiences in a forensic setting, even if their accounts are accurate. However, Southwick et al. did not examine memory accuracy per se. In contrast to research on memory for traumatic or emotional information, research on memory for nonemotional information suggests that PTSD may be associated with a variety of mnemonic deﬁcits. For instance, PTSD symptoms, particularly the chronic intrusion of traumatic memories, may interfere with working memory functioning (Galletly, Clark, McFarlane, & Weber, 2001; Uddo, Vasterling, Brailey, & Sutker, 1993), which is critical for making inferences, reasoning, and thinking abstractly (Baddeley, 1986; Miyake & Shah, 1999). Galletly et al. suggest that chronic processing of trauma-related memories may deplete cognitive resources necessary for other functions, including working memory. Alternatively, the chronic intrusion of unwanted memories may reﬂect a failure to inhibit irrelevant information (McNally, 1998), which may, in turn, impair working memory. Long-term memory deﬁcits have also been demonstrated among individuals with PTSD (Jenkins, Langlais, Delis, & Cohen, 1998; Moradi, Taghavi, NeshatDoost, Yule, & Dalgleish, 2000). Jenkins et al. found that rape victims with PTSD performed more poorly on a delayed free-recall task compared to rape victims,

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matched on age and education level, without PTSD. These memory deﬁcits were reduced, however, when participants were provided with retrieval cues, suggesting that PTSD symptomatology may impede the retrieval of nontraumatic memories by making them less accessible. Individuals with the disorder may thus have greater diﬃculty than other individuals when asked to recount their experiences, particularly when few retrieval cues are provided. However, these ﬁndings have not been replicated using trauma-related information, which is arguably more directly relevant to forensic settings. Recent ﬁndings suggest that these memory diﬃculties may be the result of physiological processes associated with trauma. Some evidence indicates that the hippocampus, a brain region centrally involved in memory consolidation (Brewer, Zhao, Desmond, Glover, & Gabrieli, 1998; Otten & Rugg, 2002; Wagner et al., 1998; chapter 3, this volume), is reduced in volume among adults with PTSD, including combat veterans (Bremner et al., 1995; Gurvits et al., 1996; Villarreal et al., 2002) and abuse victims (Bremner et al., 1997; but see Bonne et al., 2001; De Bellis, Hall, Boring, Frustaci, & Moritz, 2001; see Hull, 2002, for a review of studies linking PTSD and hippocampal volume). Moreover, animal studies indicate that hippocampal atrophy may result from the chronic stress (Magarinos, McEwen, Flugge, & Fuchs, 1996; McEwen & Magarinos, 1997; Uno, Tarara, Else, Suleman, & Sapolsky, 1989), that many trauma victims likely experience, and that may at least partially explain the link between trauma and hippocampal volume. As a whole, these ﬁndings suggest that the experience of trauma can lead to physiological processes (e.g., stress) that may aﬀect neurological functioning (Magarinos et al., 1996; McEwen & Magarinos, 1997; Uno et al., 1989). Neurological changes, in turn, may impair a traumatized individual’s ability to form new memories (Bremner, 2001). Although further research is necessary to test this model, particularly given the lack of prospective data linking trauma and hippocampal damage in humans (but see Gilbertson et al., 2002), it may ultimately provide a comprehensive explanation for the memory alterations observed among traumatized individuals. Now, however, it is unclear whether this model can adequately explain the ﬁndings that PTSD may enhance memory for trauma-related stimuli and experiences. Thus, the inﬂuence of PTSD on memory appears to depend on the nature of the to-be-remembered information. Preliminary evidence suggests that individuals with PTSD may be more attentive to trauma-related (or emotional) information and may remember that information better than individuals without PTSD. Research on memory for nonemotional information, however, indicates that PTSD is associated with deﬁcits in working memory, as well as long-term memory. Given the contrast between these sets of ﬁndings, future research should investigate conditions in which PTSD may compromise memory as well as those in which PTSD may enhance memory. Further research is also warranted to examine the role of the hippocampus in PTSD-related mnemonic functioning. In the following section,

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we turn to dissociation (believed by some to be linked to PTSD), which has also been linked with trauma, mnemonic functioning, and hippocampal volume.

Dissociation and Eyewitness Memory Dissociation is deﬁned by DSM-IV as a “disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment. The disturbance may be sudden or gradual, transient, or chronic”(American Psychiatric Association, 1994, p. 477). Dissociation has been associated with the experience of childhood trauma, such as CSA (e.g., Chu, 1998; Putnam & Trickett, 1997) and with memory diﬃculties (see Eisen & Lynn, 2001, for a review). Although some kinds of dissociative experiences are relatively common, even in nonclinical populations, more severe and frequent experiences may be considered pathological. In the majority of studies discussed here, dissociation is measured on a continuum, reﬂecting individual diﬀerences in dissociative tendencies, as opposed to dissociation as a clinical disorder per se. Recent research suggests that individuals with dissociative tendencies may have diﬃculty maintaining sustained attention to nonemotional stimuli (Freyd, Martorello, Alvarado, Hayes, & Christman, 1998) and may also show deﬁcits in long-term memory (DePrince & Freyd, 1999; Goodman et al., 2003), both of which have implications for the veracity of eyewitness reports. Sustained attention, for instance, plays an important role in both the encoding and retrieval of information (e.g., Craik, Govoni, Naveh-Benjamin, & Anderson, 1999). Regarding long-term memory, DePrince and Freyd (1999) found that DES scores were negatively related to the number of trauma-related words (e.g., incest, victim) remembered in a free-recall task. Memory for neutral words, however, was unrelated to DES scores. These ﬁndings suggest that dissociation may limit the processing of certain types of material (e.g., that which is emotional or threatening) and that dissociative individuals may not necessarily be impaired when processing aﬀectively neutral information. Yet, as we will describe in later sections, dissociation has also been linked with increased false-memory rates in tasks using neutral stimuli. In addition, Goodman et al. (2003) found that DES scores predicted failure to disclose CSA after a delay of approximately 13 years. In a sample of young adults with documented sexual abuse histories, individuals scoring high on the DES (measured concurrently with disclosure) were less likely to disclose the abuse during an interview about childhood trauma. Although there are a number of potential explanations for the link between dissociation and disclosure, including an unwillingness to talk about the abuse, one possibility is that highly dissociative individuals had poorer memory for the experience (or poorer memory in general). Consistent with this idea is evidence that, among participants who did disclose, those with higher dissociation scores were more likely to report having forgotten the abusive experience for some time (Edelstein et al., 2003).

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Recent ﬁndings indicate that, like PTSD, dissociation may be associated with a reduction in hippocampal volume among CSA victims (Stein, Koverola, Hanna, Torchia, & McClarty, 1997). Although further research is warranted, these ﬁndings, together with those related to PTSD, suggest that trauma may inﬂuence memory in a variety of ways. First, the stress inherent during the experience of a traumatic event can aﬀect later memory for it. Second, that stress, particularly if chronic, can inﬂuence physiological processes related to the hippocampus, which may then aﬀect memory for both the traumatic event and subsequent events. Third, trauma may result in the development of clinical disorders such as PTSD and dissociation, which may in turn aﬀect memory directly, or indirectly through the inﬂuence of the hippocampus (or other psychological means) on mnemonic functioning. Finally, some combination of these processes may increase an individual’s susceptibility to false-memory formation.

Dissociative Tendencies, PTSD,

and False-Memory Formation

Both PTSD and dissociation have also been associated with increased falsememory rates. Concerns about false memories are particularly relevant to forensic settings, because false memories for traumatic experiences could potentially result in mistaken accusations, and even imprisonment of innocent individuals. Yet misclassifying a true memory as false could hinder the prosecution of oﬀenders and further traumatize victims. Thus, if we can understand factors that may lead to false-memory formation, we may be able to eliminate them. To investigate false memories in the laboratory, many researchers have employed the “DRM” paradigm, an experimental procedure commonly used to study false recall and recognition. In this paradigm, introduced by Deese (1959) and modiﬁed by Roediger and McDermott (1995) and Read (1996), participants are presented with a series of semantically associated words (e.g., bed, pillow, dream) organized into lists, the majority of which are aﬀectively neutral. At test, large numbers of participants falsely recall and recognize words that were not studied (e.g., sleep) but are semantically related to the studied words (e.g., Roediger & McDermott, 1995; Roediger, McDermott, & Robinson, 1998). Several studies using the DRM paradigm suggest that trauma victims, particularly those with associated psychopathology, are more prone to false memories than are nontraumatized individuals (Bremner, Shobe, & Kihlstrom, 2000; Clancy, Schacter, McNally, & Pitman, 2000; Zoellner, Foa, Brigidi, & Przeworski, 2000). Bremner et al., for instance, compared women with self-reported histories of CSA, both with and without a diagnosis of PTSD, to a control group of nonabused men and women without PTSD (matched on age and education). Women with sexual abuse histories and a diagnosis of PTSD were more likely to falsely recognize nonpresented words than were individuals in the other two

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groups. In fact, women with PTSD were more likely than other participants to falsely recall and recognize unstudied words regardless of their semantic relation to the studied items, a result that perhaps reﬂects an overly liberal criterion for distinguishing between studied and unstudied items. Findings from DRM studies also suggest that high scorers on the DES are more prone to false-memory formation (Clancy et al., 2000; Winograd, Peluso, & Glover, 1998). Although the DRM paradigm has been criticized for lacking external validity (e.g., Freyd & Gleaves, 1996), the ﬁndings just discussed are bolstered by results from other studies, using other false-memory paradigms, that indicate a positive relation between DES scores and the tendency to assent to false autobiographical events (Hyman & Billings, 1998; Qin, 1999). Hyman and Billings presented college students with information about their childhood, obtained from the students’ parents, and asked participants to recall as many details about the events as possible. One of the events described, however, had not actually occurred. Results indicated that high scorers on the DES were more likely than low scorers to assent to the false autobiographical event. According to the authors, DES scores may reﬂect willingness to engage in constructive memory processes. That is, individuals scoring high on this measure may have made more eﬀorts to remember details about events from the past, some of which did not occur. Attempts at reconstruction, in turn, may have increased the likelihood of assenting to a false event. Alternatively, false memories may result from a lax criterion used to decide whether items are old or new (Hekkanen & McEvoy, 2002; Roediger & McDermott, 1999). That is, as individuals become more willing to characterize items as old, they are more likely to falsely endorse unstudied items as studied. Interestingly, Hekkanen and McEvoy found that DES scores were positively related to the criterion used by participants to discriminate between old and new items: Highly dissociative individuals, more so than those with lower dissociation scores, tended to adopt a more lax criterion, resulting in a greater number of items characterized as old. Thus, dissociation may predict false memory rates because of the inﬂuence of dissociative tendencies on decision-making criteria. Of course, a lax criterion also may be responsible for responses to the DES and false-memory rates. Nevertheless, it is interesting to reconsider the emotion-induced recognition bias (Windmann & Kutas, 2001) discussed earlier, in which emotional stimuli are associated with higher false-alarm rates (i.e., a more liberal criterion). Perhaps the heightened rates of false memories among dissociative individuals (or those with PTSD) is the result of a similar aﬀective process, in which even neutral stimuli are perceived in emotional terms. Windmann and Krüger (1998) and Windmann, Sakhavat, and Kutas (2002) have proposed that this kind of process may underlie the memory performance of individuals with panic disorder. Another potential explanation for the link between psychopathology and false-memory formation comes from research suggesting that trauma history

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is associated with “overgeneral” memories (McNally, Lasko, Macklin, & Pitman, 1995; McNally, Litz, Prassas, Shin, & Weathers, 1994). McNally et al. have found that traumatized individuals with PTSD have more diﬃculty than other individuals recalling speciﬁc personal memories (e.g., “the ﬁrst time I went to Hawaii”) in response to cue words (e.g., happy, angry). Instead, participants with PTSD are more likely to recall general memories (e.g., “the yearly vacations I took”), perhaps reﬂecting a reliance on categorical or “gist” memory traces. Insofar as PTSD is related to a tendency to rely on gist memories, and reliance on gist is associated with false-memory formation (Brainerd & Reyna, 1998; Brainerd, Reyna, & Poole, 2000), individuals with PTSD may be more susceptible to false memories. Thus, both PTSD and dissociative tendencies have been associated with increased false-memory rates, possibly as a result of the criterion used to discriminate between old and new information or because of a tendency to recall overgeneral memories. Insofar as these ﬁndings extend to real-life situations, individuals with PTSD and dissociative tendencies may at times have diﬃculty discriminating between details of events that did and did not occur, so their eyewitness memory capabilities could be impaired. This possibility highlights the importance of forensic interview techniques that limit false-memory formation, particularly when individuals with PTSD or dissociation are interviewed. Perhaps false-alarm rates could be reduced by teaching individuals to shift their response criterion. However, few studies have examined the extent to which PTSD and dissociation are associated with false memories for traumatic or even emotional information; thus, further research is necessary to examine the applicability of extant ﬁndings to the forensic domain.

Summary and Conclusions In summary, recent evidence links PTSD with enhanced memory for trauma-related information, as well as increased activation of such information, which may serve a memory-enhancing function. With respect to memory for nontraumarelated information, a growing area of research indicates that both PTSD and dissociative tendencies are associated with deﬁcits in working memory, long-term memory, and susceptibility to false memories. Together, these ﬁndings suggest that the relation between psychopathology and eyewitness memory may be complex and that, in some cases, considering the nature of the to-be-remembered information may be important. In a forensic setting, an individual’s legal involvement may have been precipitated by a traumatic event, which may, in turn, result in psychopathology. Despite recent advances, however, many questions remain about the association between psychopathology and memory. First, only a handful of studies have examined the inﬂuence of PTSD or dissociation on memory for emotional material,

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including memory for the precipitating traumatic event, and even fewer of these have examined false-memory formation. Because memory for a particular traumatic experience may be central to a legal prosecution (or defense), future research should investigate the inﬂuence of PTSD on memory for trauma. Second, research linking PTSD and dissociation with false-memory formation has often employed the DRM paradigm, which may have limited external validity. Further research is necessary to examine the applicability of DRM ﬁndings to real-life situations. Third, studies of CSA-related memory functioning have predominantly included female participants. Although this practice may be warranted, given that women are reportedly sexually abused more often than are men (Finkelhor, 1984), it is unclear how current ﬁndings may extend to sexually abused men. If men and women process emotional information diﬀerently (e.g., Canli et al., 2002), considering gender diﬀerences in this area, as well as in the context of emotion and memory research more generally, may be important.

Developmental Considerations A potential inﬂuence on eyewitness memory capabilities is the age of the individual whose memory is being examined. Because children’s developing cognitive and emotional abilities may aﬀect the way they process and remember emotional events, we focus now on children’s eyewitness memory and the developmental implications of stressful and traumatic life experiences on memory. Extant research suggests that, like adults, children can remember stressful personal experiences quite accurately (e.g., Alexander, Goodman, Schaaf, et al., 2002; Peterson & Bell, 1996), even over relatively long delays (e.g., Peterson & Whalen, 2001); however, developmental factors may play a role in the veracity of their reports. The quality of children’s memories for negative emotional experiences may diﬀer from that of adults because of developmental diﬀerences in biological processes (e.g., brain development; Bremner & Vermetten, 2001), social-emotional abilities (e.g., understanding and interpretation of emotions and emotional events; Stein & Liwag, 1997; Campos, Mumme, Kermoian, & Campos, 1994), and cognitive skills (e.g., speed of processing: Kail, 2000; knowledge base: Bjorklund, 1987; strategy use: Miller & Seier, 1994; executive function: Diamond, Prevor, Callender, & Druin, 1997). These important developments contribute to diﬀerences in how children process and recall emotional information, how they cope with and report particularly traumatic experiences, and how clinical disorders may inﬂuence their memory accuracy. In the following sections, we discuss children’s memory for emotional and traumatic events and the inﬂuence of clinical disorders on children’s eyewitness memory. We focus on similarities and diﬀerences between the memory performance of children and that of adults, as well on potential reasons for observed diﬀerences.

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Emotion and the Accuracy

of Children’s Eyewitness Memory

Few published studies have examined children’s memory for emotional versus nonemotional information. Existing research indicates that, like adults, children are more likely to remember emotional than nonemotional information (Davidson & Jergovic, 1996; Davidson, Luo, & Burden, 2001; but see Moradi et al., 2000). For instance, in one investigation of children’s ability to recall stories ranging in emotionality (Davidson et al., 2001), 6- to 11-yearold children heard four stories, two highly emotional and two less so. Each story consisted of three emotional incidents (i.e., happiness, sadness, anger); the stories diﬀered in the intensity with which the emotion was evoked. The results of two experiments showed that, across age groups, children recalled more highly emotional behaviors than less emotional behaviors from the stories, suggesting that emotional content enhanced memory. No signiﬁcant diﬀerences were found between recall for positive and negative information. These ﬁndings are consistent with those obtained with adults (e.g., Heuer & Reisberg, 1990; Ochsner, 2000), in which emotional stories and other stimuli are associated with better memory than are nonemotional stimuli. [For related arguments, see chapters 1and 8—Eds.] Although Davidson et al. (2001) found that emotional content enhanced memory for both older and younger children, age diﬀerences were nevertheless evident. For the shorter stories, older children remembered more low-emotion information than did younger children, yet there were fewer developmental diﬀerences between older and younger children’s memory for the highly emotional information. For the longer stories, older children remembered more emotional and nonemotional information than younger children. One explanation for these ﬁndings is that both older and younger children attend preferentially to the highly emotional information, resulting in enhanced recall. For the younger children, because of their more limited cognitive abilities, greater attention to emotional information may hamper recall of the less emotional information. In contrast, because of their greater processing/memory capacities, older children may have less diﬃculty processing and remembering both emotional and nonemotional information. These diﬀerences may have been magniﬁed for the longer stories. The degree of stress experienced by children during an emotional event has also been associated with their later memory for that event (e.g., Alexander, Goodman, Schaaf, et al., 2002; Bahrick, Parker, Fivush, & Levitt, 1998; Goodman et al., 1991; Vandermaas et al., 1993); however, ﬁndings have been somewhat inconsistent regarding the nature of this relation. Vandermaas et al., for instance, examined children’s memory for a dental procedure and found that high levels of anxiety, as rated by the researchers, impaired the memory performance of 7- to 8-year-olds, but not 4- to 5-year-olds. Children’s

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self-reports and parental reports of anxiety, however, were unrelated to children’s memory. In contrast, several studies of children’s memory for inoculations indicate that observer-rated stress is associated with better memory (e.g., Alexander, Goodman, Schaaf, et al., 2002; Goodman et al., 1991; Shrimpton et al., 1998; also chapter 8 here). As with studies of memory for emotional stimuli, however, age diﬀerences characterize children’s abilities to recount stressful experiences (e.g., Bahrick et al., 1998; Goodman et al., 1991). Age-related improvements in both the amount of information recalled and the accuracy of that information have been found in studies of children’s memory for inoculations (e.g., Alexander, Goodman, Schaaf, et al., 2002; Goodman et al., 1991), natural disasters (Bahrick et al., 1998), and sniper attacks (Pynoos & Nader, 1989). Moreover, children who are older at the time of the event remember central details more accurately than do younger children (Goodman et al., 1991). In summary, although some studies suggest that children’s memory is enhanced by negative emotion, others suggest that negative emotion impairs (or is unrelated to) children’s memory. This inconsistency, mirrored in the adult literature, may be due to the many diﬀerent ways that emotion is assessed and the variety of events for which memory is tested. Thus, further research is clearly needed before a deﬁnitive answer can be reached about the inﬂuence of emotion on children’s memory. Further research is also needed to address the similarities and diﬀerences in children’s and adults’ emotional memories. For instance, do children exhibit emotional memory biases (e.g., Windmann & Kutas, 2001) similar to those of adults? Investigation of developmental diﬀerences in the tendency to falsely recognize emotional stimuli may provide insight into the mechanisms underlying this bias. In addition, it is unclear whether the gender diﬀerences found in adults’ emotional memory (e.g., Canli et al., 2002) apply also to children. In general, gender diﬀerences in emotional memory have not been demonstrated with children; however, there are several reasons to believe that they may exist. For example, mothers talk more about emotions with female than with male children (e.g., Fivush, 1998; Kuebli, Butler, & Fivush, 1995), and parent-child conversation has been found to facilitate children’s memory (chapter 8 here). Also, female children elaborate more when discussing emotional experiences than do boys (e.g., Fivush, Brotman, Buckner, & Goodman, 2000), which may facilitate memory retention over time.

Children’s Memory

for Traumatic Events

As discussed earlier, research suggests that most adults can remember traumatic childhood experiences, such as CSA, even after long delays (Goodman et al.,

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2003; Williams, 1994). In this section, we will consider children’s memory for traumatic experiences. Children’s memory may be particularly vulnerable to distortion or loss because they do not have the cognitive capacity to cope with such highly stressful experiences. Thus, when children experience traumas, they may be more likely than adults to put up defenses such as dissociation or repression, which could result in memory distortions (Armsworth & Holaday, 1993). Alternatively, although memories for traumatic events may diﬀer signiﬁcantly from memories for nontraumatic events, many of the same memory principles may apply for both children and adults (Pezdek & Taylor, 2002). That is, like adults, children may remember traumatic experiences quite accurately, and their memory may be facilitated by factors such as the salience of the event and the age at which it was experienced. In the following sections, we discuss two lines of research that have examined children’s memories for documented traumatic experiences. The ﬁrst concerns children’s memory for highly stressful medical procedures, and the second concerns children’s memory for abuse. Children’s Memory for Medical Procedures Several studies have examined children’s memory for a highly stressful and invasive medical procedure, voiding cystourethrogram ﬂuoroscopy (VCUG; Brown et al., 1999; Goodman, Quas, Batterman-Faunce, Riddlesberger, & Kuhn, 1994, 1997; Merritt, Ornstein, & Spicker, 1994; Ornstein, Baker-Ward, Myers, Principe, & Gordon, 1995; Quas et al., 1999). Results from these studies indicate that children as young as 3 years old can remember these experiences relatively well, even after a delay of several years. As with studies of less stressful events (e.g., laboratory play sessions: Price & Goodman, 1990; classroom demonstrations: Powell & Thompson, 1996), however, children’s age at the time of the event is an important predictor of their later memory (e.g., Brown et al., 1999; Quas et al., 1999). Quas et al., for instance, found that most children who experienced the VCUG procedure at age 3 or older evinced at least some memory for it, even after a delay of 3 years. In contrast, most children who experienced the procedure before age 3 were unable to demonstrate a clear memory for the event. Studies of children’s memories for stressful injuries and resulting emergency room procedures have also yielded age diﬀerences (e.g., Burgwyn-Bailes et al., 2001; Peterson, 1999; Peterson & Bell, 1996; Peterson & Rideout, 1998; Peterson & Whalen, 2001; Terr, 1988). Like adults, however, children were more accurate about central than peripheral details of the injury experience (Peterson & Bell, 1996; Peterson & Whalen, 2001), and, consistent with adult research indicating that stress enhances memory for central details, children who were highly stressed during the injury had better memory for central details of the hospital event (Peterson & Whalen, 2001). Moreover, children’s memories for central details of highly stressful events are relatively well retained over time (e.g., Burgwyn-Bailes et al., 2001; Peterson, 1999; Peterson & Whalen, 2001). Burgwyn-Bailes et al., for in-

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stance, examined 3- to 7-year-old children’s memory for emergency room procedures shortly following their injury and again after a 1-year delay. Children’s recall after 1 year was nearly as accurate as it had been right after the procedure: 72% of speciﬁed features of the procedure were remembered accurately after 1 year, compared to 78% shortly after the procedure (but see Goodman et al., 1991). Even after a delay of approximately 5 years, Peterson and Whalen found that children’s recall of the central components of their injury experience was highly accurate. Children who were as young as 2 years old at the time of the injury fairly accurately remembered the event, although they were still less accurate than the older children. Memory for the hospital visit, however, was less accurate after the delay. Children’s Memory for Abuse Although few studies of children’s memory for documented abuse exist, extant research suggests that children can accurately (though not necessarily completely) remember their experiences (e.g., Bidrose & Goodman, 2000; Orbach & Lamb, 1999; Terr, 1988). Bidrose and Goodman, for instance, examined the memory of four girls (ages 8 to 15) who had been involved in sexually abusive acts with several men. The acts were documented by one of the perpetrators, who photographed or audiotaped (or both) many of the abusive incidents. The girls’ testimony, obtained from police interviews and court transcripts, could thus be compared to the photographs and audiotapes to determine the accuracy of the victims’ accounts. Overall, about 80% of the girls’ allegations could be veriﬁed, so their memory for the abuse was highly accurate, especially as some acts may not have been documented. Omissions of information (i.e., failing to disclose a particular documented act) were more likely than were allegations of nonveriﬁable acts. In another case study, Orbach and Lamb (1999) examined the accuracy of a 13-year-old victim’s report of a sexual abuse incident. The victim’s account was obtained from an investigative interview and was compared to an audiotaped record of the abuse incident and to the victim’s sister’s account of what happened immediately prior to and after the abuse. Over 50% of the details the victim reported were corroborated by the audiotaped evidence, and additional details were conﬁrmed by the perpetrator’s or sister’s reports. Thus, although this study included only one child, the ﬁndings support those of Bidrose and Goodman (2000) in suggesting that children’s eyewitness memories for abuse experiences can be quite accurate (see also Jones & Krugman, 1986). In addition, consistent with previous research on memory for emotional experiences, most of the corroborated details were determined to be central (as opposed to peripheral) to the event (i.e., plot-related details that speciﬁed the outline of the sexual event). In summary, although only limited research exists, ﬁndings consistently suggest that, like adults, children can remember highly distressing, and perhaps even traumatic, events. In addition, in some studies, children have remembered central details of traumatic experiences more accurately than peripheral details, a

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ﬁnding paralleled in the adult literature. However, research suggests that, as with less traumatic events, age diﬀerences are evident in the accuracy of children’s recall, with older children demonstrating better memory. As we describe in the next section, trauma may also have a more indirect inﬂuence on children’s memory, through clinical disorders such as PTSD and dissociation.

Clinical Disorders and Children’s

Eyewitness Memory

Despite some children’s resilience in the face of trauma, other children may develop clinical symptomatology, such as PTSD and dissociation, as a result of their early experiences (e.g., Putnam, 1996, 1997). These emotional problems, in turn, may have implications for children’s memory accuracy (Eisen & Goodman, 1998; Eisen & Lynn, 2001). For instance, like adults, children with PTSD may have enhanced memory for trauma-related information but impaired memory for nontrauma-related information, whereas dissociative children may show impaired memory for both types of information. Or the relation between psychopathology and memory may change with age. To examine the inﬂuence of emotional content and PTSD on children’s memory, Moradi and colleagues (2000) compared memory for words that were negative, positive, or neutral in children with and without PTSD. The clinical group was diagnosed with nonabuse-related PTSD and was matched to a control group on age, verbal intelligence, and reading ability. Participants were presented with a series of words on a computer screen and were then administered a recall test, followed by a recognition test. Findings showed that participants with PTSD recalled fewer words than controls; however, this main eﬀect was qualiﬁed by an interaction between group and word type, such that control participants recalled more neutral than positive and negative words. In contrast, PTSD participants recalled more neutral and negative compared to positive words. Thus, compared to the control participants, individuals with PTSD showed better memory for the negative words than the neutral words. Measures of recall bias (i.e., preferential memory for negative vs. neutral or positive words) were unrelated to participants’ age. In addition, although some of the negative words were trauma-related, no reliable diﬀerences in memory were found between trauma-related and nontrauma-related words for either group. Regarding recognition, signal detection analyses revealed that participants recognized neutral words more accurately than positive words and positive words more accurately than negative words, but there were no group diﬀerences. Thus, as in studies of adults’ memory for nonemotional information, when group diﬀerences were evident, participants with PTSD remembered fewer words than controls. Also consistent with the adult literature, PTSD participants evinced a negative emotion bias in recall. In an investigation of general cognitive functioning, Beers and DeBellis (2002) compared the performance of children with maltreatment-related PTSD

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with a matched group of non-PTSD, nonmaltreatment controls. Results showed that children with PTSD performed more poorly on tasks measuring attention and executive function. A similar study compared the cognitive performance of adolescents with and without PTSD (Moradi et al., 1999). Results indicated that adolescents with PTSD evinced deﬁcits in overall memory performance, including immediate and delayed story recall. These ﬁndings, consistent with those obtained in research with adults, suggest that PTSD may impair general memory functioning. Few studies of children’s dissociation and memory exist. In one study (Eisen, Goodman, Qin, & Davis, 1998; Eisen, Qin, Goodman, & Davis, 2002), children were questioned about a medical exam they had experienced as a result of suspected child physical or sexual abuse. Children’s memories and suggestibility for the exam were investigated in relation to their level of dissociation, as assessed by the Children’s Perceptual Alteration Scale (CPAS; Evers-Szostak & Sanders, 1992), the Adolescent-Dissociative Experiences Scale (A-DES; Armstrong, Putnam, Carlson, Libero, & Smith, 1997), or the Child Dissociative Checklist (CDC; Putnam, Helmers, & Trickett, 1993), or more than one of these. In contrast to research with adults, this study found no signiﬁcant relation between dissociation and children’s memories or suggestibility for the exam (but see Eisen, Qin, Goodman, & Davis, 1999). Thus, further research is clearly needed to examine the inﬂuence of PTSD and dissociation on children’s memories for emotional and nonemotional information. Extant studies indicate that, similar to ﬁndings with adults, PTSD is associated with impairments in general memory functioning. Findings are less clear, however, regarding the relation between PTSD and children’s memories for emotional information. Similarly, whether dissociation in children is associated with memory for emotional or nonemotional information remains unknown. Finally, because some studies linking PTSD and dissociation with memory, in either child or adult populations, have not fully considered the role of other clinical disorders (e.g., depression, general anxiety), separating the inﬂuence of one form of psychopathology from that of another is diﬃcult.

Summary and Conclusions In summary, despite their less than fully developed emotional and cognitive abilities, children can provide accurate reports about highly stressful and even traumatic experiences. In addition, their accuracy, like that of adults, is aﬀected by factors such as behavioral stress and emotional content of the event. Developmental change in the relation between emotion and memory has rarely been investigated, however. Further research in this area can focus on developmental diﬀerences in the eﬀects of emotion, stress, and concomitant clinical disorders on information processing and, ultimately, memory reports.

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Conclusions and Implications for

Future Research

We began this chapter by describing victims/witnesses of a crime—the abduction of an infant—and asking about their ability to recount the details of that crime in a forensic setting. Fortunately, in this example, the witnesses were able to provide enough information to local police to apprehend the kidnapper, and the infant was returned quickly and safely to her mother. Thus, as in many crimes, the testimony of eyewitnesses was critical to police eﬀorts. And, although the kidnapper in this case confessed to the abduction, such is not always the case. Eyewitness accounts are often extremely important for factﬁnders’ determinations in a variety of forensic settings, including criminal trials. Given the inherent emotional nature of many crimes, we need to understand how emotion inﬂuences eyewitness accounts. As a whole, the research throughout this chapter clearly indicates that emotion can powerfully inﬂuence eyewitness memory. Findings from studies of emotion and memory thus have the potential to inform the forensic community, including police oﬃcers, attorneys, judges, and jurors. Based on our review of the literature, we recommend several avenues for forensically relevant research: First, examining the extent to which the emotioninduced recognition bias found for negative stimuli extends to real-life negative emotional experiences is important. Are victims or witnesses of crimes, for instance, more prone to false recognition about a previously experienced stressful or traumatic event? Second, because recovered memories have been allowed as evidence in some states, researchers should evaluate the extent to which traumatic experiences may be forgotten and the conditions under which they may be later recalled. Third, further research should examine the inﬂuence of trauma on memory for emotional information, including links between PTSD, dissociation, and true versus false (emotional) memories. In particular, whether PTSD enhances memory for trauma-related information should be determined. Finally, longitudinal research on emotion and memory is needed. Many of these issues have not been adequately examined from a developmental perspective, including the ways in which the relation between emotion and memory may change with development. Expanding the scope of current emotion and memory research in these directions, and continuing to accurately and cautiously disseminate relevant ﬁndings to the legal community, will be important challenges for current and future researchers.

Note This material is based upon work supported by the National Science Foundation under Grant No. 9602125. Any opinions, findings, and conclusions or recommendations expressed in this material are those of the authors and do not necessarily reflect the views of the National Science Foundation.

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References Alexander, K. W., Goodman, G. S., Quas, J. A., Ghetti, S., Edelstein, R. S., Redlich, A. D., et al., (2002, September). Long-term memory for child sexual abuse and legal experiences. Paper presented at the European Conference on Psychology and Law, Leuven, Belgium. Alexander, K. W., Goodman, G. S., Schaaf, J. M., Edelstein, R. S., Quas, J. A., & Shaver, P. R. (2002). Children’s memory and suggestibility: Relations with attachment and cognitive inhibition. Journal of Experimental Child Psychology, 83, 262–290. Alpert, J. L., Brown, L. S., & Courtois, C. A. (1998). Comment on Ornstein, Ceci, and Loftus (1998): Adult recollections of childhood abuse. Psychology, Public Policy, and Law, 4, 1052–1067. American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: American Psychiatric Association. Anooshian, L. J., & Hertel, P. T. (1994). Emotionality in free recall: Language speciﬁcity in bilingual memory. Cognition & Emotion, 8, 503–514. APA Working Group. (1998). Final conclusions of the American Psychological Association Working Group on investigation of memories of childhood abuse. Psychology, Public Policy, and Law, 4, 933–940. Armstrong, J., Putnam, F., Carlson, E., Libero, D., & Smith, S. (1997). Development and validation of a measure of adolescent dissociation: The Adolescent Dissociative Experiences Scale. Journal of Nervous and Mental Disease, 185, 1–7 Armsworth, M. W., & Holaday, M. (1993). The eﬀects of psychological trauma on children and adolescents. Journal of Counseling and Development, 72, 49–56. Baby girl snatched at Texas Wal-Mart. (2002, August 15). Cable News Network. Retrieved August 15, 2002, fromhttp://www.cnn.com/2002/US/08/13/ texas.infant.abduction. Baddeley, A. D. (1986). Working memory. Oxford: Oxford University Press. Bahrick, L. E., Parker, J. F., Fivush, R., & Levitt, M. (1998). The eﬀects of stress on young children’s memory for a natural disaster. Journal of Experimental Psychology: Applied, 4, 308–331. Beers, S. R., & DeBellis, M. D. (2002). Neuropsychological function in children with maltreatment-related posttraumatic stress disorder. American Journal of Psychiatry, 159, 483–486. Berman, G. L., & Cutler, B. L. (1996). Eﬀects of inconsistencies in eyewitness testimony on mock-juror decision making. Journal of Applied Psychology, 81, 170–177. Bernstein, E. M., & Putnam, F. W. (1986). Development, reliability, and validity of a dissociation scale. Journal of Nervous and Mental Disease, 174, 727–735. Berntsen, D. (2002). Tunnel memories for autobiographical events: Central details are remembered more frequently from shocking than happy experiences. Memory & Cognition, 16, 1010–1020. Bidrose, S., & Goodman, G. S. (2000). Testimony and evidence: A scientiﬁc case study of memory for child sexual abuse. Applied Cognitive Psychology, 14, 197–213. Bjorklund, D. F. (1987). How age changes in knowledge base contribute to the development of children’s memory: An interpretive review. Developmental Review, 7, 93–130.

   

335

Bonne, O., Brandes, D., Gilboa, A., Gomori, J. M., Shenton, M. E., Pitman, R. K., et al. (2001). Longitudinal MRI study of hippocampal volume in trauma survivors with PTSD. American Journal of Psychiatry, 158, 1248–1251. Bornstein, B. H., Liebel, L. M., & Scarberry, N. C. (1998). Repeated testing in eyewitness memory: A means to improve recall of a negative emotional event. Applied Cognitive Psychology, 12, 119–131. Bottoms, B. L., Shaver, P. R., & Goodman, G. S. (1996). An analysis of ritualistic and religion-related child abuse allegations. Law and Human Behavior, 20, 1–34. Bower, G. H. (1992). How might emotions aﬀect learning? In S.-Å. Christianson (Ed.), Handbook of emotion and memory: Research and theory (pp. 3–31). Hillsdale, NJ: Erlbaum. Bowman, C. G., & Mertz, E. (1996). A dangerous direction: Legal intervention in sexual abuse survivor therapy. Harvard Law Review, 190, 549–639. Bradley, M. M., Greenwald, M. K., Petry, M. C., & Lang, P. J. (1992). Remembering pictures: Pleasure and arousal in memory. Journal of Experimental Psychology: Learning, Memory, and Cognition, 18, 379–390. Brainerd, C. J., & Reyna, V. F. (1998). Fuzzy-trace theory and children’s false memories. Journal of Experimental Child Psychology, 71, 81–129. Brainerd, C. J., Reyna, V. F., & Poole, D. A. (2000). Fuzzy-trace theory and false memory: Memory theory in the courtroom. In D. F. Bjorklund (Ed.). Falsememory creation in children and adults: Theory, research, and implications (pp. 93– 127). Mahwah, NJ: Erlbaum. Bremner, J. D. (2001). Hypotheses and controversies related to eﬀects of stress on the hippocampus: An argument for stress-induced damage to the hippocampus in patients with posttraumatic stress disorder. Hippocampus, 11, 75–81. Bremner, J. D., Randall, P., Scott, T. M., Bronen, R. A., Seibyl, J. P., Southwick, S. M., et al. (1995). MRI-based measurement of hippocampal volume in combat-related posttraumatic stress disorder. American Journal of Psychiatry, 152, 973–981. Bremner, J. D., Randall, P., Vermetten, E., Staib, L., Bronen, R. A., Mazure, C., et al. (1997). Magnetic resonance imaging-based measurement of hippocampal volume in posttraumatic stress disorder related to childhood physical and sexual abuse: A preliminary study. Biological Psychiatry, 41, 23–32. Bremner, J. D., Shobe, K. K., & Kihlstrom, J. F. (2000). False memories in women with self-reported childhood sexual abuse: An empirical study. Psychological Science, 11, 333–337. Bremner, J. D., Southwick, S., Brett, E., Fontana, A., Rosenheck, R., & Charney, D. (1992). Dissociation and posttraumatic stress disorder in Vietnam combat veterans. American Journal of Psychiatry, 149, 328–332. Bremner, J. D., & Vermetten, E. (2001). Stress and development: Behavioral and biological consequences. Development and Psychopathology, 13, 473–489. Brewer, J. B., Zhao, Z., Desmond, J. E., Glover, G. H., & Gabrieli, J. D. E. (1998). Making .memories: Brain activity that predicts how well visual experience will be remembered. Science, 281, 1185–1187. Brewin, C. R., Dalgleish, T., & Joseph, S. (1996). A dual representation theory of posttraumatic stress disorder. Psychological Review, 103, 670–686.

336

  

Briere, J., & Conte, J. R. (1993). Self-reported amnesia for abuse in adults molested as children. Journal of Traumatic Stress, 6, 21–31. Brown, D. A., Salmon, K., Pipe, M.-E., Rutter, M., Craw, S., & Taylor, B. (1999). Children’s recall of medical experiences: The impact of stress. Child Abuse and Neglect, 23, 209–216. Brown, D., Scheﬂin, A. W., & Hammond, D. C. (1998). Memory, trauma treatment, and the law. New York: W. W. Norton. Brown, D., Scheﬂin, A. W., & Whitﬁeld, C. L. (1999). Recovered memories: The current weight of the evidence in science and in the courts. Journal of Psychiatry and Law, 27, 5–156. Bryant, R. A., & Harvey, A. G. (1995). Processing threatening information in posttraumatic stress disorder. Journal of Abnormal Psychology, 104, 537–541. Burgwyn-Bailes, E., Baker-Ward, L., Gordon, B. N., & Ornstein, P. A. (2001). Children’s memory for emergency medical treatment after one year: The impact of individual diﬀerence variables on recall and suggestibility. Applied Cognitive Psychology, 15, S25–S48. Burke, A., Heuer, F., & Reisberg, D. (1992). Remembering emotional events. Memory & Cognition, 20, 277–290. Cahill, L, & McGaugh, J. L. (1998). Mechanisms of emotional arousal and lasting declarative memory. Trends in Neuroscience, 21, 294–299. Cahill, L., Prins, B., Weber, M., & McGaugh, J. L. (1994). ß-Adrenergic activation and memory for emotional events. Nature, 371, 702–704. Campos, J. J., Mumme, D. L., Kermoian, R., & Campos, R. G. (1994). A functionalist perspective on the nature of emotion. Monographs of the Society for Research in Child Development, 59, 284–303. Canli, T., Desmond, J. E., Zhao, Z., & Gabrieli, J. D. E. (2002). Sex diﬀerences in the neural basis of emotional memories. Proceedings of the National Academy of Sciences, 99, 10789–10794. Cassiday, K. L., McNally, R. J., & Zeitlin, S. B. (1992). Cognitive processing of trauma cues in rape victims with post-traumatic stress disorder. Cognitive Therapy and Research, 16, 283–295. Christianson, S.-Å. (1992). Emotional stress and eyewitness memory: A critical review. Psychological Bulletin, 112, 284–309. Christianson, S.-Å., & Hubinette, B. (1993). Hands up: A study of witnesses’ emotional reactions and memories associated with bank robberies. Applied Cognitive Psychology, 7, 365–379. Christianson, S.-Å., & Loftus, E. (1991). Remembering emotional events: The fate of detailed information. Cognition & Emotion, 5, 81–108. Chu, J. A. (1998). Dissociative symptomatology in adult patients with histories of childhood physical and sexual abuse. In J. D. Bremner & C. R. Marmar (Eds.), Trauma, memory, and dissociation (pp. 179–203). Washington, DC: American Psychiatric Press. Clancy, S. A., Schacter, D. L., McNally, R. J., & Pitman, R. K. (2000). False recognition in women reporting recovered memories of sexual abuse. Psychological Science, 11, 26–31.

   

337

Coles, M. E., & Heimberg, R. G. (2002). Memory biases in the anxiety disorders: Current status. Clinical Psychology Review, 22, 587–627. Cooper, A. M. (1986). Toward a limited deﬁnition of psychic trauma. In A. Rothstein (Ed.), The reconstruction of trauma: Its signiﬁcance in clinical work (pp. 41–56). Madison, CT: International Universities Press. Cooper, B. S., Kennedy, M. A., Hervé, H. F., & Yuille, J. C. (2002). Weapon focus in sexual assault memories of prostitutes. International Journal of Law and Psychiatry, 25, 181–191. Craik, F. I. M., Govoni, R., Naveh-Benjamin, M., & Anderson, N. D., (1999). The eﬀects of divided attention on encoding and retrieval processes in human memory. Journal of Experimental Psychology: General, 12, 159–180. Davidson, D., & Jergovic, D. (1996). Children’s memory for typical and atypical actions in script-based stories. Journal of Experimental Child Psychology, 55, 104–126. Davidson, D., Luo, Z., & Burden, M. J. (2001). Children’s recall of emotional behaviours, emotional labels, and nonemotional behaviours: Does emotion enhance memory? Cognition & Emotion, 15, 1–26. De Bellis, M. D., Hall, J., Boring, A. M., Frustaci, K., & Moritz, G. (2001). A pilot longitudinal study of hippocampal volumes in pediatric maltreatment-related posttraumatic stress disorder. Biological Psychiatry 50, 305–309. Deese, J. (1959). On the prediction of occurrence of particular verbal intrusions in immediate recall. Journal of Experimental Psychology, 58, 17–22. DePrince, A. P., & Freyd, J. J. (1999). Dissociative tendencies, attention, and memory. Psychological Science, 10, 449–452. Doerksen, S., & Shimamura, A. P. (2001). Source memory enhancement for emotional words. Emotion, 1, 5–11. Diamond, A., Prevor, M. B., Callender, G., & Druin, D. P. (1997). Prefrontal cortex cognitive deﬁcits in children treated early and continuously for PKU. Monographs of the Society for Research in Child Development, 62, 1–205. Easterbrook, J. A. (1959). The eﬀect of emotion on cue utilization and the organization of behavior. Psychological Review, 66, 183–201. Edelstein, R. S., Ghetti, S., Redlich, A. D., Cordón, I. M., & Raskauskas, J. L. (2003, April). Do child sexual abuse victims forget their experiences? Poster presented at the Biennial Society for Research in Child Development Conference, Tampa, FL. Eisen, M. L., & Goodman, G. S. (1998). Trauma, memory, and suggestibility in children. Development and Psychopathology, 10, 717–738. Eisen, M. L., Goodman, G. S., Qin, J., & Davis, S. (1998). Memory and suggestibility in maltreated children: New research relevant to evaluating allegations of abuse. In S. Lynn & K. McConkey (Eds.), Truth in memory (pp. 163–189). New York: Guilford Press. Eisen, M. L., & Lynn, S. J. (2001). Dissociation, memory, and suggestibility in adults and children. Applied Cognitive Psychology, 15, S49–S73. Eisen, M., Qin, J. J., Goodman, G. S., & Davis, S. (1999). The impact of dissociation, trauma, and stress arousal on the memory and suggestibility of physically and sexually abused, and neglected children. Washington, DC: National Center on Child Abuse and Neglect. Eisen, M. L., Qin, J., Goodman, G. S., & Davis, S. (2002). Memory and suggestibility

338

  

in maltreated children: Age, stress arousal, dissociation, and psychopathology. Journal of Experimental Child Psychology, 83, 167–212. Elliott, D. M., & Briere, J. (1995). Posttraumatic stress associated with delayed recall of sexual abuse: A general population study. Journal of Traumatic Stress, 8, 629–647. Engstrom v. Engstrom, Second Appellate District, California, Case No. VC016157, March, 1997. Epstein, M. A., & Bottoms, B. L. (1998). Memories of childhood sexual abuse: A survey of young adults. Child Abuse and Neglect, 22, 1217–1238. Evers-Szostak, M., & Sanders, S. (1992). The Children’s Perceptual Alteration Scale (CPAS): A measure of children’s dissociation. Dissociation, 1, 91–97. Feeny, N. C., Zoellner, L. A., & Foa, E. B. (2000). Anger, dissociation, and posttraumatic stress disorder among female assault victims. Journal of Traumatic Stress, 13, 89–100. Finkelhor, D. (1984). Child sexual abuse: New theory and research. New York: Free Press. Fisher, R. P., & Cutler, B. L. (1992, September). The relation between consistency and accuracy of witness testimony. Paper presented at the Third European Conference on Law and Psychology, Oxford, England. Fivush, R. (1998). Children’s recollections of traumatic and nontraumatic events. Development and Psychopathology, 10, 699–716. Fivush, R., Brotman, M., Buckner, J. P., & Goodman, S. H. (2000). Gender diﬀerences in parent-child emotion narratives. Sex Roles, 42, 233–253. Fivush, R., Haden, C. A. & Reese, E. (1996). Remembering, recounting and reminiscing: The development of autobiographical memory in social context. In D. Rubin (Ed.), Remembering our past: An overview of autobiographical memory (pp. 377–397). New York: Cambridge University Press. Foa, E. B., Zinbarg, R., & Rothbaum, B. O. (1992). Uncontrollability and unpredictability in post-traumatic stress disorder: An animal model. Psychological Bulletin, 112, 218–238. Freud, A. (1936). The ego and the mechanisms of defense (C. Baines, Trans.). New York: International Universities Press. Freud, S. (1915/1957). Repression. In J. Strachey (Ed.), The standard edition of the complete psychological works of Sigmund Freud. Vol. 14. London: Hogarth. Freyd, J. J. (1996). Betrayal trauma: The logic of forgetting childhood abuse. Cambridge, MA: Harvard University Press. Freyd, J. J., & Gleaves, D. H. (1996). Remembering words not presented in lists: Implications for the recovered/false memory controversy? Journal of Experimental Psychology: Learning, Memory, and Cognition, 22, 811–813. Freyd, J. J., Martorello, S. R., Alvarado, J. S., Hayes, A. E., & Christman, J. C. (1998). Cognitive environments and dissociative tendencies: Performance on the Standard Stroop Task for high versus low dissociators. Applied Cognitive Psychology, 12, S91–S103. Galletly, C., Clark, C. R., McFarlane, A. C., & Weber, D. L. (2001). Working memory in posttraumatic stress disorder: An event-related potential study. Journal of Traumatic Stress, 14, 295–309.

   

339

Gilbertson, M. W., Shenton, M. E., Ciszewski, A., Kasai, K., Lasko, N. B., Orr, S. P., et al. (2002). Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Nature Neuroscience, 5, 1242–1247. Goodman, G. S., Ghetti, S., Quas, J. A., Edelstein, R. S., Alexander, K. W., Redlich, A. D., et al. (2003). A prospective study of memory for child sexual abuse: New ﬁndings relevant to the repressed/lost memory controversy. Psychological Science, 14, 113–118. Goodman, G. S., Hirschman, J. E., Hepps, D., & Rudy, L. (1991). Children’s memory for stressful events. Merrill-Palmer Quarterly, 37, 109–157. Goodman, G. S., Quas, J. A., Batterman-Faunce, J. M., Riddlesberger, M. M., & Kuhn, J. (1994). Predictors of accurate and inaccurate memories of traumatic events experienced in childhood. Consciousness and Cognition, 3, 269–294. Goodman, G. S., Quas, J. A., Batterman-Faunce, J. M., Riddlesberger, M. M., & Kuhn, J. (1997). Children’s reactions to and memory for a stressful event: Inﬂuences of age, anatomical dolls, knowledge, and parental attachment. Applied Developmental Science, 1, 54–75. Gothard, S., & Ivker, N. A. C. (2000). The evolving law of alleged delayed memories of childhood sexual abuse. Child Maltreatment, 5, 176–189. Gross, J. J. (2002). Emotion regulation: Aﬀective, cognitive, and social consequences. Psychophysiology, 39, 281–291. Gurvits, T. V., Shenton, M. E., Hokama, H., Ohta, H., Lasko, N. B., Gilbertson, M. W., et al. (1996). Magnetic resonance imaging study of hippocampal volume in chronic, combat-related posttraumatic stress disorder. Biological Psychiatry, 40, 1091–1099. Hamann, S. (2001). Cognitive and neural mechanisms of emotional memory. Trends in Cognitive Science, 5, 394–400. Hekkanen, S. T., & McEvoy, C. (2002). False memories and source-monitoring problems: Criterion diﬀerences. Applied Cognitive Psychology, 16, 73–85. Henry, B., Moﬃtt, T. E., Caspi, A., Langley, J., & Silva, P. A. (1994). On the “remembrance of things past”: A longitudinal evaluation of the retrospective method. Psychological Assessment, 6, 92–101. Heuer, F., & Reisberg, D. (1990). Vivid memories of emotional events: The accuracy of remembered minutiae. Memory & Cognition, 18, 496–506. Howe, M. L. (1997). Children’s memory for traumatic experiences. Learning and Individual Diﬀerences, 9, 153–174. Howe, M. L. (2000). The fate of early memories: Developmental science and the retention of childhood experiences. Washington, DC: American Psychological Association. Hull, A. M. (2002). Neuroimaging ﬁndings in post-traumatic stress. British Journal of Psychiatry, 181, 102–110. Hyman, I. E., & Billings, F. J. (1998). Individual diﬀerences and the creation of false childhood memories. Memory, 6, 1–20. Hyman, I. E., & Loftus, E. F. (1998). Errors in autobiographical memory. Clinical Psychology Review, 18, 933–947. Jenkins, M. A., Langlais, P. J., Delis, D., & Cohen, R. (1998). Learning and memory

340

  

in rape victims with posttraumatic stress disorder. American Journal of Psychiatry, 155, 278–279. Johnson, M. K., Hashtroudi, S., & Lindsay, D. S. (1993). Source monitoring. Psychological Bulletin, 114, 3–28. Johnson, M. K., Nolde, S. F., & De Leonardis, D. M. (1996). Emotional focus and source-monitoring. Journal of Memory and Language, 35, 135–156. Jones, D., & Krugman, R. (1986). Can a 3-year-old bear witness to her own assault? Child Abuse and Neglect, 10, 253–258. Kail, R. (2000). Speed of information processing: Developmental change and links to intelligence. Journal of School Psychology, 38, 51–61. Kassin, S. M., Tubb, V. A., Hosch, H. M., & Memon, A. (2001). On the “general acceptance” of eyewitness testimony research. American Psychologist, 56, 405–416. Kirschbaum, C., Wolf, O. T., May, M., Wippich, W., & Hellhammer, D. H. (1996). Stress- and treatment-induced elevations of cortisol levels associated with impaired declarative memory in healthy adults. Life Sciences, 58, 1475–1483. Kohout v. Charter Peachford Hospital, Georgia Supreme Court, Case No. S98C1773, September 1998. Kramer, T. H., Buckhout, R., & Eugenio, P. (1990). Weapon focus, arousal, and eyewitness memory: Attention must be paid. Law and Human Behavior, 14, 167–184. Kuebli, J., Butler, S., & Fivush, R. (1995). Mother-child talk about past emotions: Relations of maternal language and child gender over time. Cognition & Emotion, 9, 265–283. LaBar, K. S., & Phelps, E. A. (1998). Arousal-mediated memory consolidation: Role of the medial temporal lobe in humans. Psychological Science, 9, 490–493. Lindsay, D. S., & Read, J. D. (1995). “Memory work” and recovered memories of childhood sexual abuse: Scientiﬁc evidence and public, professional, and personal issues. Psychology, Public Policy, and the Law, 1, 846–908. Loftus, E. F., & Ketcham, K. (1991). Witness for the defense: The accused, the eyewitness and the expert who puts the memory on trial. New York: St. Martin’s Press. Loftus, E. F., Loftus, G. R., & Messo, J. (1987). Some facts about “weapon focus.” Law and Human Behavior, 11, 55–62. Lupien, S. J., & McEwen, B. S. (1997). The acute eﬀects of corticosteroids on cognition: Integration of animal and human model studies. Brain Research Reviews, 24, 1–27. Magarinos, A. M., McEwen, B. S., Flugge, G., & Fuchs, E. (1996). Chronic psychosocial stress causes apical dendritic atrophy of hippocampal CA3 pyramidal neurons in subordinate tree shrews. Journal of Neuroscience, 16, 3534–3540. Mazzoni, G. A., & Loftus, E. F. (1998). Dream interpretation can change beliefs about the past. Psychotherapy: Theory, Research, Practice, Training, 35, 177–187. Mazzoni, G. A., Lombardo, P., Malvagia, S., & Loftus, E. F. (1999). Dream interpretation and false beliefs. Professional Psychology: Research and Practice, 30, 45–50. McEwen, B. S., & Magarinos, A. M. (1997). Stress eﬀects on morphology and function of the hippocampus. Annals of the New York Academy of Sciences, 821, 271–284. McNally, R. J. (1998). Experimental approaches to cognitive abnormality in posttraumatic stress disorder. Clinical Psychology Review, 18, 971–982.

   

341

McNally, R. J., Amir, N., & Lipke, H. J. (1996). Subliminal processing of threat cues in posttraumatic stress disorder? Journal of Anxiety Disorders, 10, 115–128. McNally, R. J., Clancy, S. A., Schacter, D. L., & Pittman, R. K. (2000). Cognitive processing of trauma cues in adults reporting repressed, recovered, or continuous memories of childhood sexual abuse. Journal of Abnormal Psychology, 109, 355–359. McNally, R. J., Kaspi, S. P., Riemann, B. C., & Zeitlin, S. B. (1990). Selective processing of threat cues in posttraumatic stress disorder. Journal of Abnormal Psychology, 99, 398–402. McNally, R. J., Lasko, N. B., Macklin, M. L., & Pitman, R. K. (1995). Autobiographical memory disturbance in combat-related posttraumatic stress disorder. Behavior Research and Therapy, 33, 619–630. McNally, R. J., Litz, B. T., Prassas, A., Shin, L. M., & Weathers, F. W. (1994). Emotional priming of autobiographical memory in post-traumatic stress disorder. Cognition & Emotion, 8, 351–367. McNally, R. J., Metzger, L. J., Lasko, N. B., Clancy, S. A., & Pitman, R. K. (1998). Directed forgetting of trauma cues in adult survivors of childhood sexual abuse with and without posttraumatic stress disorder. Journal of Abnormal Psychology, 107, 596–601. Merritt, K. A., Ornstein, P. A., & Spicker, B. (1994). Children’s memory for a salient medical procedure: Implications for children’s testimony. Pediatrics, 94, 17–23. Metcalfe, J., & Jacobs, W. J. (2000). ‘Hot’ emotions in human recollection: Toward a model of traumatic memory. In E. Tulving (Ed.), Memory, consciousness, and the brain: The Tallinn Conference (pp. 228–242). Philadelphia: Taylor and Francis. Miller, P. H., & Seier, W. L. (1994). Strategy utilization deﬁciencies in children: When, where, and why. In H. W. Reese (Ed.), Advances in child development and behavior (Vol. 25, 107–156), San Diego: Academic Press. Miyake, A., & Shah, P. (1999). Models of working memory: Mechanisms of active maintenance and executive control. Cambridge: University Press. Moradi, A. R., Taghavi, R., Neshat-Doost, H. T., Yule, W., & Dalgleish, R. (1999). Performance of children and adolescents with PTSD on the Stroop colour-naming task. Psychological Medicine, 29, 415–419. Moradi, A. R., Taghavi, R., Neshat-Doost, H. T., Yule, W., & Dalgleish, T. (2000). Memory bias for emotional information in children and adolescents with posttraumatic stress disorder: A preliminary study. Journal of Anxiety Disorders, 14, 521–534. Nagae, S., & Moscovitch, M. (2002). Cerebral hemispheric diﬀerences in memory of emotional and nonemotional words in normal individuals. Neuropsychologia, 40, 1601–1607. Ochsner, K. N. (2000). Are aﬀective events richly recollected or simply familiar? The experience and process of recognizing feelings past. Journal of Experimental Psychology: General, 129, 242–261. Orbach, Y., & Lamb, M. E. (1999). Assessing the accuracy of a child’s account of sexual abuse: A case study. Child Abuse and Neglect, 23, 91–98. Ornstein, P. A., Baker-Ward, L., Myers, J., Principe, G. F., & Gordon, B. N. (1995). Young children’s long-term retention of medical experiences: Implications for

342

  

testimony. In F. E. Weinert & W. Schneider (Eds.), Memory performance and competencies: Issues in growth and development (pp. 349–371), Hillsdale, NJ: Erlbaum. Ornstein, P. A., Ceci, S. J., & Loftus, E. F. (1998). Adult recollections of childhood abuse: Cognitive and developmental perspectives. Psychology, Public Policy, and Law, 4, 1025–1051. Otten, L. J., & Rugg, M. D. (2002). The birth of a memory. Trends in Neurosciences, 25, 279–281. Payne, J. D., Nadel, L., Allen, J. J. B., Thomas, K. G. G., & Jacobs, W. J. (2002). The eﬀects of experimentally induced stress on false recognition. Memory, 10, 1–6. Peterson, C. (1999). Children’s memory for medical emergencies: Two years later. Developmental Psychology, 35, 1493–1506. Peterson, C., & Bell, M. (1996). Children’s memory for traumatic injury. Child Development, 67, 3045–3070. Peterson, C., & Rideout, R. (1998). Memory for medical emergencies experienced by 1– and 2–year-olds. Developmental Psychology, 34, 1059–1072. Peterson, C., & Whalen, N. (2001). Five years later: Children’s memory for medical emergencies. Applied Cognitive Psychology, 15, 17–24. Pezdek, K., & Taylor, J. (2002). Memory for traumatic events in children and adults. In M. L. Eisen, J. A. Quas, & G. S. Goodman (Eds.), Memory and suggestibility in the forensic interview (pp. 165–183). Mahwah, NJ: Erlbaum. Pickel, K. L. (1999). The inﬂuence of context on the “weapon focus” eﬀect. Law and Human Behavior, 23, 299–311. Pillemer, D. B. (1984). Flashbulb memories of the assassination attempt on President Reagan. Cognition, 16, 63–80. Poole, D. A., Lindsay, D. S., Memon, A., & Bull, R. (1995). Psychotherapy and the recovery of memories of childhood sexual abuse: U.S. and British practitioners’ beliefs, practices, and experiences. Journal of Consulting and Clinical Psychology, 63, 426–437. Powell, M. B., & Thomson, D. M. (1996). Children’s memory of an occurrence of a repeated event: Eﬀects of age, repetition, and retention interval across three question types. Child Development, 67, 1988–2004. Price, D. W., & Goodman, G. S. (1990). Visiting the wizard: Children’s memory for a recurring event. Child Development, 61, 664–680. Putnam, F. W. (1996). Posttraumatic stress disorder in children and adolescents. In L. Dickstein, M. Riba, & J. Oldham (Eds.), Review of psychiatry (Vol. 15, pp. 447–467). Washington, DC: American Psychiatric Press. Putnam, F. W. (1997). Dissociation in childhood adolescents: A developmental perspective. New York: Guilford Press. Putnam, F. W., Helmers, K., & Trickett, P. K. (1993). Development, reliability, and validity of a child dissociation scale. Child Abuse and Neglect, 17, 731–741. Putnam, F. W., & Trickett, P. K. (1997). The psychobiological eﬀects of sexual abuse: A longitudinal study. Annals of the New York Academy of Sciences, 821, 150–159. Pynoos, R. S., & Nader, K. (1989). Children’s memory and proximity to violence. Journal of the American Academy of Child and Adolescent Psychiatry, 28, 236– 241.

   

343

Qin, J. (1999). Adults’ memories of childhood: True versus false reports. Unpublished doctoral dissertation, University of California, Davis. Quas, J. A., Goodman, G. S., Bidrose, S., Pipe, M.-E., Craw, S., & Ablin, D. (1999). Emotion and memory: Children’s long-term remembering, forgetting, and suggestibility. Journal of Experimental Child Psychology, 72, 235–270. Quas, J. A., Goodman, G. S., Redlich, A. D., Ghetti, S., Cordón, I. M., & Jones, D. P. H. (2001, April). Long-term memory for testifying in criminal court as children. Paper presented at the Biennial Meeting Society for Research in Child Development, Minneapolis, MN. Quirarte, G. L., Roozendaal, B., & McGaugh, J. L. (1997). Glucocorticoid enhancement of memory storage involves noradrenergic activation in the basolateral amygdala. Proceedings of the National Academy of Sciences of the United States of America, 94, 14048–14053. Read, J. D. (1996). From passing thoughts to false memories in 2 minutes: Confusing real and illusory events. Psychonomic Bulletin & Review, 3, 105–111. Read, J. D. (1999). The recovered/false memory debate: Three steps forward, two steps back? Expert Evidence, 7, 1–24. Read, J. D., & Lindsay, D. S. (2000). “Amnesia” for summer camps and high school graduation: Memory work increases reports of prior periods of remembering less. Journal of Traumatic Stress, 13, 129–147. Roediger, H. L. III, & McDermott, K. B. (1995). Creating false memories: Remembering words not presented in lists. Journal of Experimental Psychology: Learning, Memory, and Cognition, 21, 803–814. Roediger, H. L. III, & McDermott, K. B. (1999). False alarms and false memories. Psychological Review, 106, 406–410. Roediger, H. L. III, McDermott, K. B., & Robinson, K. J. (1998). The role of associative processes in creating false memories. In M. A. Conway, S. E. Gathercole, & C. Cornoldi (Eds.), Theories of memory (Vol. 2, pp. 187–245). Sussex, UK: Psychology Press. Safer, M. A., Christianson, S., Autry, M. W., & Osterlund, K. (1998). Tunnel memory for traumatic events. Applied Cognitive Psychology, 12, 99–117. Schooler, J. W., Ambadar, Z., & Bendiksen, M. (1997). A cognitive corroborative case study approach for investigating discovered memories of sexual abuse. In J. D. Read & D. S. Lindsay (Eds.), Recollections of trauma: Scientiﬁc evidence and clinical practice (pp. 379–387). New York: Plenum Press. Schooler, J. W., & Eich, E. (2000). Memory for emotional events. In E. Tulving & F. I. M. Craik (Eds.), The Oxford handbook of memory (pp. 379–392). New York: Oxford University Press. Shaw, J. I., & Skolnick, P. (1999). Weapon focus and gender diﬀerences in eyewitness accuracy: Arousal versus salience. Journal of Applied Social Psychology, 29, 2328–2341. Shobe, K. K., & Kihlstrom, J. F. (1997). Is traumatic memory special? Current Directions in Psychological Science, 6, 70–74. Shrimpton, S., Oates, K., & Hayes, S. (1998). Children’s memory of events: Eﬀects of stress, age, time delay, and location of interview. Applied Cognitive Psychology, 12, 133–143.

344

  

Southwick, S. M., Morgan, C. A., Nicolaou, A. L., & Charney, D. S. (1997). Consistency of memory for combat-related traumatic events in veterans of Operation Desert Storm. American Journal of Psychiatry, 154, 173–177. Stanny, C. J., & Johnson, T. C. (2000). Eﬀects of stress induced by a simulated shooting on recall by police and citizen witnesses. American Journal of Psychology, 113, 359–386. Steblay, N. M. (1992). A meta-analytic review of the weapon focus eﬀect. Law and Human Behavior, 16, 413–424. Stein, M. B., Koverola, C., Hanna, C., Torchia, M. G., & McClarty, B. (1997). Hippocampal volume in women victimized by childhood sexual abuse. Psychological Medicine, 27, 951–959. Stein, N. L., & Liwag, M. D. (1997). Children’s understanding, evaluation, and memory for emotional events. In P. W. van den Broek & P. J. Bauer (Eds.), Developmental spans in event comprehension and representation: Bridging ﬁctional and actual events (pp. 199–235), Hillsdale, NJ: Erlbaum. Terr, L. C. (1988). What happens to early memories of trauma? A study of twenty children under age ﬁve at the time of the documented traumatic events. American Journal of Psychiatry, 148, 10–20. Terr, L. C. (1994). Unchained memories. New York: Basic Books. Tollestrup, P. A., Turtle, J. W., & Yuille, J. C. (1994). Actual victims and witnesses to robbery and fraud: An archival analysis. In D. F. Ross, J. D. Read, & M. P. Toglia (Eds.), Adult eyewitness testimony: Current trends and developments. New York: Press Syndicate of the University of Cambridge. Tulving, E. (1985). Memory and consciousness. Canadian Psychologist, 26, 1–12. Uddo, M., Vasterling, J. J., Brailey, K., & Sutker, P. B. (1993). Memory and attention in combat-related post-traumatic stress disorder. Journal of Psychopathology and Behavioral Assessment, 15, 43–52. Uno, H., Tarara, R., Else, J. G., Suleman, M. A., & Sapolsky, R. M. (1989). Hippocampal damage associated with prolonged and fatal stress in primates. Journal of Neuroscience, 9, 1705–1711. van Stegeren, A. H., Everaerd, W., Cahill, L., McGaugh, J. L., & Gooren, L. J. (1998). Memory for emotional events: Diﬀerential eﬀects of centrally versus peripherally acting beta-blocking agents. Psychopharmacology, 138, 305–310. Vandermaas, M. O., Hess, T. M., & Baker-Ward, L. (1993). Does anxiety aﬀect children’s reports of memory for a stressful event? Applied Cognitive Psychology, 7, 109–127. Villarreal, G., Hamilton, D. A., Petropoulos, H., Driscoll, I., Rowland, L. M., Griego, J. A., et al. (2002). Reduced hippocampal volume and total white matter volume in posttraumatic stress disorder. Biological Psychiatry, 52, 119–125. Vrana, S. R., Roodman, A., & Beckham, J. C. (1995). Selective processing of traumarelevant words in posttraumatic stress disorder. Journal of Anxiety Disorders, 9, 515–530. Wagner, A. D., Schacter, D. L., Rotte, M., Koutstaal, W., Maril, A., Dale, A. M., et al. (1998). Building memories: Remembering and forgetting of verbal experiences as predicted by brain activity. Science, 281, 1188–1191. Wells, G. L., Small, M., Penrod, S., Malpass, R. S., Fulero, S. M., & Brimacombe,

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345

C. A. E. (1998). Eyewitness identiﬁcation procedures: Recommendations for lineups and photospreads. Law and Human Behavior, 22, 603–648. Wessel, I., & Merckelbach, H. (1994). Characteristics of traumatic memories in normal subjects. Behavioral and Cognitive Psychotherapy, 22, 315–324. Wessel, I., & Merckelbach, H. (1997). The impact of anxiety on memory for details in spider phobics. Applied Cognitive Psychology, 11, 223–232. Wessel, I., & Merckelbach, H. (1998). Memory for threat-relevant and threatirrelevant cues in spider phobics. Cognition & Emotion, 12, 93–104. Wessel, I., van der Kooy, P., & Merckelbach, H. (2000). Diﬀerential recall of central and peripheral details of emotional slides is not a stable phenomenon. Memory, 8, 95–109. Widom, C. S., & Morris, S. (1997). Accuracy of adult recollections of childhood victimization, Part 2: Childhood sexual abuse. Psychological Assessment, 9, 34–46. Williams, L. M. (1994). Recall of childhood trauma: A prospective study of women’s memories of child sexual abuse. Journal of Consulting and Clinical Psychology, 62, 1167–1176. Williams, L. M. (1995). Recovered memories of abuse in women with documented sexual victimization histories. Journal of Traumatic Stress, 8, 649–673. Williams, L. M., & Banyard, V. L. (1999). Trauma and memory. Thousand Oaks, CA: Sage. Williams, M., Mathews, A., & MacLeod, C. (1996). The emotional Stroop task and psychopathology. Psychological Bulletin, 120, 3–24. Windmann, S., & Krüger, T. (1998). Subconscious detection of threat as reﬂected by an enhanced response bias. Consciousness and Cognition, 7, 603–633. Windmann, S., & Kutas, M. (2001). Electrophysiological correlates of emotioninduced recognition bias. Journal of Cognitive Neuroscience, 13, 577–592. Windmann, S. Sakhavat, Z., & Kutas, M. (2002). Electrophysical evidence reveals aﬀective evaluation deﬁcits early in stimulus processing in patients with panic disorder. Journal of Abnormal Psychology, 111, 357–369. Winograd, E., Peluso, J. P., & Glover, T. A. (1998). Individual diﬀerences in susceptibility to memory illusions. Applied Cognitive Psychology, 12, S5–S27. Woodall, J. (1999). The nature of memory: Controversies about retrieved memories and the law of evidence. Journal of Psychiatry and Law, 26, 151–218. Yerkes, R., & Dodson, J. (1908). The relation of strength of stimulus to rapidity of habit-formation. Journal of Comparative Neurology of Psychology, 18, 459–482. Yuille, J. C., & Cutshall, J. L. (1986). A case study of eyewitness memory of a crime. Journal of Applied Psychology, 71, 291–301. Yuille, J. C., Davies, G., Gibling, F., Marxsen, D., & Porter, S. (1994). Eyewitness memory of police trainees for realistic role plays. Journal of Applied Psychology, 79, 931–936. Zoellner, L. A., Foa, E. B., Brigidi, B. D., & Przeworski, A. (2000). Are trauma victims more susceptible to “false memories”? Journal of Abnormal Psychology, 109, 517–524.

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oused in archives throughout the world are videotaped oral testimonies documenting the memories of individuals who have lived through prolonged trauma. The testimonies in these archives consist of unconstrained recall of personal experiences in the context of larger historical events. The most extensive of these collections have been provided by survivors of the Holocaust, though sizeable collections in this country are from veterans of World War II and the Vietnam War.1 The testimonies in these archives support research in oral history, but they also constitute a valuable resource for cognitive researchers studying memory for traumatic events. My research took place at the Fortunoﬀ Video Archive for Holocaust testimonies at Yale University, a collection of more than 4,000 testimonies from survivors of the Holocaust. Each testimony typically consists of a single Holocaust survivor spontaneously recalling events in the presence of two nonintrusive interviewers. Though there are no time limits, the length of most testimonies is between 40 minutes and 3 hours, with an average length of 2 hours. Survivors speak from memory, and, in many cases, their testimony is their ﬁrst extended recall for more than 40 years. In the testimonies I studied, survivors came from 12 diﬀerent European countries, varying in economic background, level of education, religiousness, language, and culture. They ranged in age from infancy to 43 when World War II started and from 40 to 95 when giving testimony. I focus in this chapter on emotional memory in survivors of prolonged trauma. To describe and explain the characteristics of emotional memory, I called on my analysis of more than 200 hours of oral testimony given by Holocaust survivors. My general strategy was to study and categorize the phenomenal experience of the survivors: their memories of emotional events, their emotional experiences, and their observations about memory and emotion. 347

A Summary of the Methods My methodology is rooted in the inductive methods of ethology and population biology (Hubbell, 1999; Linton, 1986). More recently, I have drawn on techniques elaborated over the past decade for the qualitative study of complex psychological phenomena in natural settings (Tolman & Brydon-Miller, 2001). In analyzing the testimonies, I used a repeated study procedure, viewing each testimony in its entirety twice. During the Wrst viewing, I attended to the general content and organization of the memories and to the observations of the survivor. I then re-viewed the testimony, annotating passages and describing the remembered episodes. I selectively viewed the testimony up to 10 more times, focusing on the annotated passages, transcribing the words, and detailing the contextual and extra-linguistic features. After viewing the videotaped testimonies, I categorized the content and structure of the transcribed testimony. I parsed the transcribed portions into passages that were comparable to paragraphs in a written text and labeled each passage with the categorical terms that characterized the passage. I then tabulated each category. As the analysis proceeded, the number of categories grew and I subdivided the categories into more precisely deﬁned and more detailed units. Through this inductive analysis, the particulars from the individual testimonies coalesced into general patterns of traumatic memory and the relationships between traumatic memory and strong emotion (Kraft, 2002).

Concepts of Accuracy My approach to studying traumatic memory assumes that the witnesses who provided the oral testimony tried to communicate their memories honestly. In fact, the data collection procedures at the Yale Archive are especially conducive to unconstrained and detailed testimony. This chapter does not address issues of accuracy at length because my focus is on the phenomenal experience of traumatic memory and not on the correspondence between historical events and memory for those events. Nonetheless, oral testimony can contribute to theoretical and practical discussions of accuracy and can support assessments of accuracy in long-term traumatic memory. Thus, it is important to introduce and delineate the diﬀerent methods that can be employed with oral testimony to assess the accuracy of memory. Over the past 30 years, myriad facts about the Holocaust have been extensively described and meticulously documented. By comparing the information in the testimonies to these documented facts, one can assess the historical truth of information in oral testimony (Spence, 1982). As an outgrowth of this assessment, memory researchers could also categorize the types of information reliably remembered in testimony. In such an assessment, one must separate documented instances in which the initial encoding of events was ﬂawed.2

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In a seminal study, Wagenaar and Groeneweg (1990) conducted an assessment of historical accuracy in testimony provided by survivors from Camp Erika in the Netherlands. Some of these survivors were interviewed twice, once in the mid-1940s and again in the mid-1980s; other survivors were interviewed just once in the mid-1980s, primarily in the context of trials of camp guards. Wagenaar and Groeneweg compared the recall of inmates interviewed once with known facts, and they compared the two sets of testimony provided by the survivors interviewed twice. They found a high level of remembering across the 40-year interval between events and interviews. The ﬁrst sentence of the Results section makes this ﬁnding clear: “The most striking aspect of the testimonies is that witnesses agreed about the basic facts, which is demonstrated by a comparison of 55 longer interviews” (p. 80). After noting the “remarkable degree of remembering,” the authors then identify and tabulate speciﬁc kinds of errors witnesses made (p. 80). In fact, sometimes oral testimony can identify existing errors in historical documents. Hoﬀman and Hoﬀman (1994) described how oral testimony corrected an inaccurately captioned photograph on display at Yad Vashem, the oﬃcial Holocaust museum in Israel. The photograph was labeled “Gardelegen, a concentration camp in which 150 inmates were killed.” The oral testimony of the second author proved that the photograph was not of Gardelegen. Rather, it depicted a barn near Hannover into which Nazis herded prisoners, then burned them to death. A variation of the method used in Wagenaar and Groeneweg (1990) is to compare selected testimonies to other, corroborating testimonies. In my study of child survivors, I assessed the accuracy of Holocaust testimony by comparing the memories of the child survivors to those of older witnesses, in the few cases that permitted it. As with other memory-based methods of verifying accuracy, this method assumes the accuracy of the corroborating (or refuting) memories (Kraft, 1996, 2002). Categorizing the metamemory statements of witnesses constitutes another assessment method. While providing testimony, witnesses make direct statements about what they can and cannot remember about particular events. They also use probabilistic terms and qualifying statements, which indicate uncertainty (Kraft, 2000, 2002). These metamemory statements and the probabilistic terms can then be used to identify the types of information that are clear and accessible to the witnesses and the types that are unclear and inaccessible. In fact, Winograd (1994) has concluded that rather than debating the general question of accuracy, memory researchers should focus on identifying the conditions conducive to accuracy and those likely to lead to distortion. A third assessment of accuracy involves examining the consistency and inconsistency of information in the testimonies. Though this approach does not assess accuracy per se, consistency in the testimonies is a suggestive indicator of accuracy. When Winograd (1992) considered the relationship between accuracy and

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consistency in ﬂashbulb memories, he concluded, “If people are inconsistent in reporting the same memory on two occasions, it is diﬃcult to argue for accuracy” (p. 1). This method arises from the obverse of Winograd’s conclusion—admittedly a more tentative one: if people consistently report the same memory on two occasions, it is diﬃcult to argue for inaccuracy. In my study of oral testimony, I assessed consistency by comparing the information in diﬀerent testimonies provided by the same witness—with the diﬀerent testimonies separated by 8 years in most cases. In a variation of this approach, I also examined consistencies and inconsistencies within each testimony (Kraft, 2002). One diﬃculty with naturalistic studies of accuracy is the problem of deciding a priori what someone else will or should remember. In the laboratory, of course, such decisions can be made on the basis of the speciﬁc materials to be remembered. With traumatic events in the world, social or forensic considerations may determine what information is helpful to remember, but failure to recall such information only indicates the incompleteness of memory, not inaccuracy. In general, what people do remember from traumatic events, they remember vividly, consistently, and permanently. For an introduction to experimentation and theory on accuracy and emotional memory, refer to Aﬀect and Accuracy in Recall (Winograd & Neisser, 1992), Memory Distortions and Their Prevention (Intons-Peterson & Best, 1998), and, more recently, a comprehensive investigation of research on eyewitness testimony conducted by Wells et al. (2000), and the 2000 edition of The Annual Review of Psychology, which contains a concise history of research approaches in experimental psychology that pertain to accuracy and distortion in memory, including a section on autobiographical memory (Koriat, Goldsmith, & Pansky, 2000).

Excerpts From the Testimonies My plan in this chapter is to describe, exemplify, and explain the characteristics of emotion and memory that emerged from qualitative analysis of more than 130 diﬀerent testimonies of Holocaust survivors. To provide a sense of the inductive process in this study, I begin by presenting a set of excerpts from these testimonies. For some reason . . . I could not get any tears. . . . Why weren’t we screaming maniacs at that point, those of us who saw it daily? (Testimony of Irene W., 1982) There is one thing I have to say: that throughout my experience then, I don’t remember feeling fear. . . . What I remember feeling is numbness. (Testimony of Meir V., 1992) I didn’t feel anything. I didn’t even feel the elation that I thought I was going to feel. . . . It really didn’t make any diﬀerence. So we are liberated, so what? (Testimony of Daniel F., 1980)

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You was indiﬀerent to everything. You was like a vegetable. . . . I didn’t care. . . . I didn’t care if they would kill me in a minute. (Testimony of Zoltan G., 1979) Only very highly charged, painful memories are with me. Speciﬁc memories. (Testimony of Clemens L., 1990) To this day, I cannot really hear German. I have not changed about that at all. When I hear the language . . . it does something to my insides. They turn over. (Testimony of Eva B., 1979) I don’t want to think about it because I can’t bear to think about it. (Testimony of Zezette L., 1980) I am going over it if I am speaking about it or not. There is not really one day of my life or one night that I don’t think about it. (Testimony of Nadia R., 1995) I think the problem is . . . I’m afraid if I open it up, I’m going to have nightmares that I had for years and years, and I will not allow this, . . . I’m afraid it might destroy me. (Testimony of Martin S., 1988) It is diﬃcult to talk about feelings. . . . Now I feel more horrible than I felt at the time. (Testimony of Alex H., 1983) The tortures days and nights. It’s something that we have. It’s in our mind. You can’t forget. . . . I don’t want to live with that pain. But it’s there. It’s there. It forms its own entity. And it surfaces whenever it wants to. I go on a train and I will cry. I will read something and I’ll be right back there where I came from. And I can’t erase it. I’m not asking for it. It comes by itself. (Jacob K. in the Testimony of Bessie and Jacob K., 1983) Flashes come through about . . . my experiences. I still have dreams. (Testimony of Abraham P., 1984) The screams when they took away the babies, I can never forget this. This is with me constantly. Walking and taking away babies from a mother’s hands. (Testimony of Nina S., 1996) It’s still ﬁfty years since it was the end of the war, and many things, because of such time elapsed, are somewhere in the back of my mind. Now, I could never forget the things that happened there, but they are somewhere in the back. And suddenly everything comes to the front. (Testimony of Henry S., 1996) How can you tell a child? How can I tell my child? My young son, to tell him that another human being burned his grandparents. How can you tell such horror? (Testimony of Violet S., 1991) What we learned was rage. . . . I don’t know where—how all that takes shape. What surprises me is that we’re able to contain it. (Testimony of Robert K., 1984)

As I studied the relationships between traumatic memory and strong emotion, broad categories emerged that became the organizing topics of this chapter: (1) general characteristics of traumatic memory that inform the study of emotion and memory, (2) recall of emotions that occurred at the time of the

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events, (3) the re-experiencing of emotion in the present, (4) emotions that endure over the course of people’s lives, and (5) the palliative eﬀects of distraction.

Characteristics of

Traumatic Memory

Analysis of oral testimony reveals two general characteristics of traumatic memory pertinent to the study of emotion and memory: episodic structure and duality of representation. With oral testimony, the primary unit of remembering is the episode: a discrete event with a start and a ﬁnish, a small story. The episode is usually a narrative, although it can be impressionistic, and the episode may be placed within a precisely described spatial layout. The basic elements of the episode are vivid perceptual images, deeply felt emotions, and physiological experiences (Kraft, 1998a). These basic elements are then used to construct the episodic testimony. Martin S. precisely summarizes the structure of his thinking: “I just know episodes. Speciﬁcs. That comes back to mind repeatedly” (Testimony of Martin S., 1988). Typically, survivors recall individual episodes one at a time, proceeding from one episode to the next. During testimony, these encapsulated episodes are organized in sequences, like beads on a string, with diﬀerent sequences of episodes connected to one another by thin strands that are either chronological and geographic or thematic or rhetorical (Kraft, 2002). The elements of episodic memory and the episodes themselves constitute two separate levels of memorial representation. At one level, memory represents the original phenomenal experience in the form of images, emotions, and bodily sensations. These original memories are then integrated into a narrative, episodic construction of events, creating memory’s second level. In their seminal article, Brown and Kulik (1977) posited a “ﬂashbulb memory” for highly consequential events that is “ﬁxed for a very long time, and conceivably permanently, varying in complexity with consequentiality but, once created, always there, and in need of no further strengthening. . . . The memory is not narrative and not even in verbal form, but represented in other, perhaps imaginal, ways” (p. 85). The term “ﬂashbulb memory” quickly migrated into the lexicon of cognitive psychology, and the underlying concept became the subject of considerable debate and research, especially about accuracy, durability, and status as a distinctive memory system. Arising from this debate a decade later was the elaboration of a fundamentally diﬀerent, nonnarrative, and “imaginal” level of memory. Diﬀerent pairs of terms introduced in the literature on memory reﬂect the two distinct levels of memory suggested by Brown and Kulik (1977). Flashbulb memory corresponds to “deep memory,” to be distinguished from “common memory” (Langer, 1991, pp. 5–6). It is “situationally accessible memory” as distinguished from “verbally accessible memory” (Brewin, Dalgleish, & Joseph,

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1996, p. 676). Similarly, Nadel (1994) proposed two separate memory systems on the basis of task-driven, computational diﬀerences and rates of learning: (1) a system with rapid acquisition of information about speciﬁc episodes that preserves spatial information as a primary way of distinguishing one episode from another and (2) a slower system that learns incrementally and generalizes across diﬀerent instances. According to Nadel, the episodic system represents speciﬁc episodes “sparsely,” so that they do not interfere with one another, and provides a “rapidly forming template” (p. 57) to serve as a basis for gradually changing the representations in the longer-lasting general system. To formalize the distinction in the two types of memory, Reyna and her colleagues introduced fuzzy-trace theory, which posits verbatim memory and gist memory (Reyna, 1998; Reyna & Titcomb, 1997). Verbatim memory is the original representation of the events; gist memory structures and summarizes verbatim memory and is in linguistic form. Distortions, errors, and intrusions do occur, but they occur within gist memory, not within verbatim memory. Verbatim memory endures, resistant to distortion and assimilation (Reyna & Titcomb, 1997). I refer to the two levels of memory as core memory and narrative memory (Kraft, 2002). Core memory is the representation of the original phenomenal experience in the form of perceptual, emotional, and physiological experience: visual images, sounds, smells, tastes, emotions, and bodily sensations. I chose “core” because the word speciﬁcally refers to the most basic and activating elements in a structure, whereas “verbatim” applies speciﬁcally to language and does not describe the powerful images, emotions, and physiological experiences represented in this basic level of memory. Core memory is both explicit and implicit, consisting of representations of imagery and emotion that can be consciously—though not deliberately—experienced during extended recall, as well as implicit representations of emotional, physiological, and bodily responses that can be triggered by external cues.3 Narrative memory is constructed from the images in core memory, shaped in accordance with narrative conventions and conveyed primarily in language. The word “narrative” characterizes how people structure episodes in personal memory for the purpose of thinking about oneself in silent remembering and communicating with others to tell the events of the past (Sarbin, 1986). The following excerpt illustrates how narrative memory draws on imagery in core memory and how testimony can be analyzed to learn about the underlying sources of information. In testimony, Renee G. describes an incident that occurred while she was a teenager surviving as a slave laborer in a small ghetto: At one point, I bent down because I found a picture of my family, so I must have stopped to look at it and all of a sudden I heard a big whip over my legs and I just remember the sting of it. And I just froze for a minute and got up and stood straight. . . . I was probably by that time, completely bereft of emo-

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tion . . . sort of half-dead, not here and not there. . . . And I just stared at the German into the face. I remember big, red face. I would probably recognize him today. (Testimony of Renee G., 1980)

The excerpt suggests contributions from core memory as well as narrative constructions. Based on images provided by core memory, Renee G. clearly remembers the “sting” of the whip and the German guard’s “big, red face.” The statements that she “must have” stopped to look at the photograph and that she was “probably” bereft of emotion indicate that she is constructing a reason for stopping her work and for freezing after being whipped. The reason for the uncharacteristic pause in her work appears to be constructed from general knowledge of her actions at the time and not based in core memory. Renee’s assessment that she was bereft of emotion also appears to be based on a schematized representation of her general emotional state while subsisting in the ghetto (Testimony of Renee G., 1980). Those who give oral testimony about the Holocaust usually call on narrative memory to tell of the horrible events, and the testimony is structured and coherent. Sometimes, though, when describing a scene, the survivor may be drawn into core memory, losing contact with narrative memory. While providing testimony, these survivors appear immersed in visualizing the events, where the outside world dissolves and the survivors re-experience the events of the past. When a person is fully visualizing, or “back there,” as survivors often say, the images are conveyed in raw form, unstructured, and testimony can seem incoherent to the listener. In terms of subjective experience, back there refers to a level of consciousness similar to hypnagogic sleep, with the images of memory possessing the ﬁerce vividness of dreams. As the observer of a movie experiences being in the scene while simultaneously maintaining a disconnected awareness of the surrounding theater, the survivor experiences a loss of self within the immediate environment and an immersion in the past, while only vaguely aware of the present. After an hour of testimony, Jolly Z. says, “I’m sure we are guided by inner needs to see or to deny things around us. Um, but, um. [She shakes her head and looks down for ﬁve seconds.] I lost my thought. I’m back there again. [She gestures backwards with her ﬁnger.] . . . I’m just back there.” Jolly is asked what she sees when she is “back there,” and she replies: “Mud. And just grey, and mud. [She shakes her head.] Mmm, bodies. [She sighs.] Oh, I know what I was trying to say.” During this testimony, Jolly loses the present, momentarily slipping into the horrors of the remembered past. Jolly describes the experience of being back there: “I feel myself to be there. I see the mud around me. I smell it. Smell is very important. I smell it. I see the bodies, dead and alive. I’m there. I see all the details. I’m there. I’m very visual. I’m there. I see the sun or the rain. I feel the wet clothes. I’m there.” Jolly explains that she is “seventeen or eighteen” years old when she submerges in this

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memory, a diﬀerent self: “I’m not here. . . . I don’t even know about myself now. I’m there. . . . Somebody else talks out of me. . . . You see it’s not me. It’s that person who experienced it who is talking about those experiences. And maybe that’s what I am referring to. Because I am there. It is that part of me. Not now” (Testimony of Jolly Z., 1988). Hanna F. accesses core memory while describing an episode at Auschwitz. When inmates died during the night, they were taken out of the barracks and dumped onto a pile of bodies. One night, Hanna had to go to the latrine, which meant walking past this pile of corpses. She says, “And the rats were standing and eating the people’s faces. Eating. They were having a—. [She stops and does not ﬁnish her sentence. After 13 seconds of silence, she abruptly begins again.] Anyway, I had to do my job. I was just looking [at] what’s happening to a human being” (Testimony of Hanna F., 1987). During the silence in her testimony, Hanna appears to be immersed in the images of core memory, reliving the events of the past. Other survivors experience similar immersion into the altered reality of atrocity, and they refer to this experiential change in their testimony. Myra L. interrupts her own testimony to comment: “I’m talking a little incoherent because these things, these things. I’m coming back to the transports from the ghetto” (Testimony of Myra L., 1984). In comparing laboratory research on trauma with naturalistic studies of trauma outside the laboratory, one fact is clear: simulations of traumatic events fortunately lack many of the essential characteristics of trauma: the suddenness, the overwhelming emotion—including shock, helplessness, and terror, the violation of one’s body and psyche, physical pain, confusion, betrayal, and humiliation, a ﬂood of information that has not been perceived before and that is not attended to eﬀectively, an inability of existing schemas to predict outcomes, a ﬂight response that cannot be enacted, a hyperaroused state of mind, and a complex of neurophysiological responses. Terr (1994) wrote succinctly, “You can’t replicate trauma in an experimental lab. You can’t simulate murders without terrorizing your research subjects” (p. 52). In terms of subjective experience, the initial exposure to trauma leaves people bereft of understanding, unable to apply prior learning, and unable to comprehend. Contact between ongoing events and existing knowledge breaks apart, resulting in unguided perception of the events. Those who are victimized see an unbelievable reality of horror in ﬂeeting moments of painful clarity, ultimately creating memories that are sensory and relivable, in the form of smells, sounds, scenes, emotions, and physiological sensations (Kraft, 1998b). One emerging consensus from the vast clinical literature on PTSD is that severe trauma leads to memories qualitatively diﬀerent from memories for events that do not threaten one’s health and well-being. Memories from severe trauma are distinctively fragmented, intrusive, and durable and can be accompanied by recurrent nightmares and ﬂashbacks that involve vivid sensory experiences and high physiological arousal. Moreover, some aspects of traumatic memories ap-

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pear to remain distinct from other memories and to be constant over time (Brewin et al., 1996; Kraft, 2002; Terr, 1994; van der Kolk, 1996). In terms of Nadel’s (1994) two-system framework, the fundamental diﬀerence in episodic memory between the formation of traumatic memories and the formation of nontraumatic memories is that traumatic events are not represented sparsely. They are learned quickly and represented in persistent detail, creating a disruption in the process of assimilating speciﬁc memories into more general representations.

Recall of Emotional Experiences For Holocaust survivors, the most frequently recalled emotional experiences are fear and numbness. The survivors remember experiencing extreme emotion— or the absence of emotion. Both meanings of the word “petrify” accurately convey the victim’s remembered emotional state during severe trauma: to paralyze with terror and to convert organic matter into a stony replica.

Fear Survivors clearly recall their fear within speciﬁc episodes. Blanche H. remembers being sent into hiding after her older sister was taken away by the Nazis. Accompanied by an older woman, Blanche took a train to her uncle’s house, and she and the woman were the only two civilian passengers on the train. The rest were uniformed German soldiers. Blanche says, “That was about a three-hour train ride, and I am thinking . . . I was going to die. I shook like a leaf and the mere fact that I was shaking I felt would give myself away to them” (Testimony of Blanche H., 1992). Similarly, Esther W. describes standing appell at Skarzysko, lining up and being counted for hours every morning, while German guards berated them: “The fear. The fear. You could have died from the fear alone” (Testimony of Esther W., 1994). Performing slave labor as a young boy, Martin S. proved his worth by operating four machines by himself, tooling bullets. He excelled at his labor, but he felt guilty because others were doing what they could to sabotage the German war eﬀort. So Martin began making defective bullets, cutting them so they would jam in the riﬂes. One day, after making boxes and boxes of defective bullets, Martin noticed the camp inspector approaching, so he quickly adjusted the machines, turning out several dozen good bullets. By chance, when the inspector examined Martin’s work, he chose one of the properly engineered bullets. Martin describes how he felt: “Oh, the fear was unbelievable. I thought I had had it.” He continues: “We all went through many terrifying moments” (Testimony of Martin S., 1986). Sabina S. tells of her childhood hiding from the Nazis. “And we heard above us the Germans yelling, searching for us and looking for us. . . . You couldn’t

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breathe. You couldn’t talk. You were always afraid they were going to discover you. So there was always that fear that they’re there to kill you” (Testimony of Sabina S., 1985). Kluger (2001) provides a metaphoric description of her emotions while waiting in a special barracks at Auschwitz, either to be gassed or sent to a labor camp: “Fear infected me like a poisonous illness. My mind was like a theater in which a ﬁre alarm had gone oﬀ and panic has broken out” (p. 111).

Numbness In recalling her arrival at Auschwitz, Jolly Z. provides a glimpse of the unthinking and unfeeling response when people confront unprecedented horrors: “When these things actually happen, you don’t think, you just act. Your feelings, the reactions, come later. When the selection took place, you probably just think, which way did he say to go, so I’ll go right or left. There are no emotions. There is no observing reaction. There’s just action. The rest comes later” (Testimony Jolly Z., 1988). In the testimonies I studied, more than 75% of the survivors who describe their emotional state during the horrors say that they were “numb” (Kraft, 1998b). They use a variety of phrases to elaborate this state of numbness: “in a trance,” “like a piece of wood,” “frosted over,” “frozen,” “like a stone,” “hibernating,” “like a vegetable,” “like robots,” “in a catatonic state.” Eva L. describes her initial memory of leaving the freight car at Auschwitz and being immediately separated from her mother: We couldn’t believe that everything was happening so fast. And then, we just didn’t feel anything, didn’t feel anything. Was just like in a trance. I just didn’t feel anything. They pushed me into a bath, they stripped me, they shaved my hair. They took—stripped me of my clothes. They just gave me a little rag, just a little blouse that covered my front. The back was ripped. The rest was naked. And I was just pushed, like in a trance, I didn’t care (Testimony of Eva L., 1982).

The numbness is so alien and so pervasive that some survivors say they were given drugs. Nina S. describes the aftermath of her arrival at Auschwitz, after losing her mother during the initial selection. She says, “They gave us tranquilizers because the next day nobody was crying.” She explains: “Suddenly we became all calm at the same time. They gave us some soup. And everybody said there was something in it because we became like diﬀerent people. The next day nobody missed their parents. Nobody was crying” (Testimony of Nina S., 1996). Chana F. describes the quick steps to chronic numbness: If you ask people about feelings, I ask myself in the beginning the same thing. The ﬁrst ordinance was tragic: we cried, we pulled our hair, what’s going to be. The second was bad. The third you take already, and then it just comes to

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you. . . . We were numb. We were already numb. We were numb the ﬁve years. There were no feelings (Testimony of Chana F. and Henry F., 1980).

The persistent numbness caused by constant horror showed itself clearly at liberation. After struggling to live through the camps, some survivors expected to feel elation when liberated, but that expectation often could not override their adaptive numbness. In fact, liberation only highlighted the survivors’ blunted emotional state. Emina N. describes her feeling of being drugged and her subsequent response to liberation: It was a day before the liberation. . . . I was walking through the dead [bodies]. I wanted to go to the toilet. I have to walk through all the piles of dead people and I don’t believe that I had any feelings. It didn’t bother me at all. I didn’t—. Either way, like it would be some dirt or something, I walked away. I think it was either something wrong with me, with us, with everybody, or maybe they gave us something, like medication, or something that you were just numb. And, in fact, when I was liberated, I didn’t even want to go out. (Emina N. in the Testimony of Emina N. and Miriam W., 1979).

Celia K. summarizes her emotional experience just after liberation: “There weren’t any emotions at all. You couldn’t hate. You couldn’t feel” (Testimony of Celia K., 1980). Leon W. agrees: “I don’t think I was happy. . . . I don’t think we had any feelings for dancing or joy or smiling” (Testimony of Leon W., 1979).

Associated Emotions Although fear and numbness are often the only emotional states that survivors talk about, they were not the only emotions to be experienced. People may not remember other emotions during horriﬁc events because shock may have prevented them from being aware of these emotions or because the strong memory of fear and numbness obscures memory for other emotions. In particular, adaptive numbness can remain long after the horrors end, so the experience of other strong emotions may arise only after many years. Clemens L. describes an image from early childhood, just before he went into hiding. While he was playing with other children in a courtyard near his apartment, the owner of the apartment building came over to him and demanded that he pull down his pants. Clemens complied, and the owner saw he was circumcised. After Clemens told his mother about the incident, the two of them quickly escaped. Clemens goes on to describe his emotions then and now: “It seems like I don’t remember the feelings at the time. I think when I speak about those images, I have—. I’m speaking from the point of view of a stunned person. I have feelings now of course. . . . I do have very strong feelings about it. And I think I guess I have more feelings about it than I thought I did” (Testimony of Clemens L., 1990). Izzard (1991) describes “patterns of emotion,” combinations of fundamental emotions that occur together with the same motivational impact. Although fear

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and numbness predominate in the memories of Holocaust survivors, sometimes complex emotions are remembered, even within the conﬁnes of atrocity. After being transported by truck to a large building, Esther W. and others were forced to undress and were told they were going to the showers. They had all heard rumors about gas chambers, so there was the fear that they were about to die. Esther says, “Once we went in, naked, the things were put aside. Everything was taken away from us, and the doors were locked. And there were little windows and the Germans stood, looked in the windows. And we were waiting for the gas to come. And all of a sudden, hot water came. Hot water came, so, of course, I wouldn’t say joy, but at least you weren’t gassed” (Testimony of Esther W., 1994). After adapting to the routine of horror, some survivors remember the reemergence of motivating emotion growing out of their numbness and helplessness. Eva L. worked to maintain cooperation within her group of ﬁve prisoners at Auschwitz, using hatred and creative thoughts of revenge to sustain her: We started building hatred. Hatred, and all kinds of ideas what we going to do to the Germans when we live through this. And that hatred made us survive and made us live. The thoughts that we had . . . were sickening. . . . We said we going to cut them into pieces. We going to put salt on them. We going to tie them to two horses and let the two horses run. The most horrible, horrible things that could come to mind. We fed ourselves with that hatred, and that made us go. (Testimony of Eva L., 1982)

Separation of Emotional Memory

and Event Memory

Analysis of oral testimony indicates that emotional experience is represented separately from other event information, such as location, time, people, and sequences of action. With child survivors in particular, memory for strong emotion and memory of speciﬁc events can be unconnected. They can recall emotional events without remembering the emotional experience, and they can recall emotional experience without recalling the events themselves (Kraft, 1996). Susan S. talks about separating from her mother as a child and going into hiding: “To be very honest I must have repressed a lot of the feelings. I really don’t remember missing my mother.” Susan knows that she must have felt strong emotions, and she clearly remembers not knowing where her mother was, but she does not recall the emotions she felt (Testimony of Susan S., 1991). Conversely, Clemens L. says, “My emotions are so powerful. I’m surprised I’m feeling them as much as I am here. So that’s there. But the placement of it, the speciﬁc memory of it, that’s diﬃcult” (Testimony of Clemens L., 1990). Similarly, Hilda S. primarily recalls emotion but is unsure about the associated events. From her early childhood, Hilda describes her memory of Kristallnacht (the night of the broken glass), which began November 9, 1938, a night during which synagogues and Jewish businesses throughout Germany were damaged and burned: “There

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were ﬁres all over the city and obviously we all knew about that and there was talk in the family about these events. Whether I saw it or whether I heard it, I really can’t remember. But I do clearly recall being very frightened—being ‘terriﬁed’ is more the word for it—by what was happening” (Testimony of Hilda S., 1993). Amelia B. describes what she remembers of the 3 days when she was in a cattle car being transported to Auschwitz: “The funny part is I don’t recollect the train ride so clearly. I mean I remember going into the train and coming out from the train. But for the three days really forgot what really happened. But I remember seeing my father. He was so scared, he was so—. And somehow we were sitting around and it was like utter despair” (Testimony of Amelia B., 1994). For Amelia, the emotions inside the cattle car are accessible, though the events that gave rise to these emotions are not.

Repression Survivors can remember emotions without speciﬁc event information and speciﬁc event information without the associated emotions. It is also the case that both kinds of information can be inaccessible. As Bessie K. was transported from the ghetto in Kovno to a concentration camp in Estonia, her baby was taken from her. She details the shock and dissociation: As I look back, I think that for a while I was in a daze. I didn’t know what was happening, actually. I saw they [were] taking away the men separate, the children separate, and the women separate. So, I had the baby, and I took the coats what I had with the bundles, and I wrapped around the baby and I put it on my left side because I saw the Germans were saying “left and right.” And I went through with the baby. But the baby was short of breath, started to choke, to choke, it started to cry. So the German called me back. He says “What do you have there?” in German. Now, I didn’t know what to do because everything was so fast. Everything happened so suddenly. I wasn’t prepared for it. To look back, the experience, was I think I was numb. Or something happened to me, I don’t know. But I wasn’t there even. And he stretched out his arms I should hand him over the bundle. And I hand him over the bundle. And this was the last time I had the bundle with me. (Bessie K. in the Testimony of Bessie K. and Jacob K., 1983)

As a result of this dissociative horror, Bessie K. repressed the memory of losing her child. She was taken from the camp in Estonia, detained in a ﬁeld for 2 weeks with other inmates, then placed on a ship to Stutthof in Danzig. In Stutthof, Bessie happened to see the doctor who operated on her in the ghetto following the birth of her baby. She describes their meeting: And when she saw me there, she was so happy to see me. Right away she said, “What happened—where’s the baby? What happened to the baby?” And right

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there I said, “What baby?” [Bessie pauses.] I said to the doctor, “What baby? I didn’t have a baby. I don’t know of any baby.” That’s what it did to me. [She points to her head with her index ﬁnger.] (Bessie K. in the Testimony of Bessie K. and Jacob K. 1983).

Repressing a memory is not simply forgetting, nor is it the failure to recall a speciﬁc horrible and consequential incident in the context of numerous similar incidents. Repression involves memory for a complex event that is inaccessible but potentially retrievable. Repression can then be deﬁned as the inability to recall a distinctive event represented in memory that is generally agreed to be consequential even after repeated prompts to remember. Moreover, the distinctive experience of dissociation appears to be a necessary factor for the occurrence of repression (van der Kolk, 1996). Using this deﬁnition, I have identiﬁed four documented cases of repression, the most dramatic being that of Bessie K. and her baby. It should be noted, however, that the study of oral testimony is not well suited for uncovering repressed memories. Simply put, if survivors are repressing important events, by deﬁnition, they are unable to describe these events in testimony, and the repression remains concealed (W. Banks, personal communication, November 12, 1994). Identiﬁcation of repression occurs when the repressed event is remembered before testimony is given or when historical documents or other survivors independently identify the event in question. For more information on methods for studying repressed memories, refer to the debated methodology of Williams (Williams, 1994a, 1994b; Loftus, Garry, & Feldman, 1994); the research of Briere and Conte (1993), Herman and Schatzow (1987), Loftus (1993), Terr (1994, 1996), and van der Kolk and Fisler (1995); and the reviews and comments of van der Kolk (1996), Burgess, Hartman, and Baker (1995), Loftus (1994), and Olio (1994).

Re-experiencing Emotion Multiple Systems Based on the representation of emotion in memory, Robinson (1995) outlined two broad explanations for recalling and re-experiencing emotions. The ﬁrst proposes that information about emotion is a part of the overall cognitive representation of an event in personal memory. The emotional information must then be decoded and described for the emotion to be re-experienced by the rememberer. In fact, this approach is similar to that of William James (1890/ 1950), who conjectured that emotions cannot be directly revived from memory, but must be recreated. Reliving of emotion during a particular event follows retrieval of memory for that event and subsequent thoughts about the memory. Robinson (1995) discusses a contrasting explanation that begins with the idea

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that emotional experience involves complex states consisting of physiological arousal, perceptual representations, knowledge, and evaluation, with diﬀerent representational systems for each type of information. Within this “multiple systems” framework, re-experienced emotions can be the direct result of accessing an implicit emotional representation, separate from constructive processes. The multiple systems framework posits that emotional experiences can be remembered in four ways: (1) remembering how one felt but not re-experiencing the feeling, (2) cognitively generated aﬀect, (3) spontaneous aﬀect, and (4) implicit memory. Within this framework, people re-experience emotions for three reasons: (1) the interpretation of a speciﬁc memory in such a way that emotions are cognitively generated, (2) the direct accessing of core memory representations of past emotions, and (3) the triggering of implicit memories.

Re-experiencing Emotion

During Recall

During testimony, emotional experience that follows from a description of one’s thought processes suggests cognitive generation based on the interpretation of a speciﬁc memory. Emotional experience that is sudden and surprising suggests the direct accessing of a core representation within a speciﬁc memory. Even when people do not initially recall strong emotions, the process of extended, detailed recall can expose core memories and lead to the experiencing of the represented emotions. Many times the recalling of a speciﬁc event produces sudden emotion—usually grief or anger. The display of emotion can seem abrupt and unexpected until one realizes that the emotions are released with the disclosure of a speciﬁc episode in memory. Judith G., a young survivor of the Vilna ghetto and Riga, explains: “The scars are there. You don’t talk about it as much. You don’t discuss it. But when you think about it, there is a great emotional charge that carries forward” (Testimony of Judith G., 1992). After 9 minutes of ﬂat, dispassionate description, Sally H. tells of a speciﬁc incident in the ghetto when a rabbi is humiliated and tortured. “It was horrible. . . . They were pulling his beard, and blood was coming out. And no one would help him.” She then cries, abruptly and unexpectedly (Testimony of Sally H., 1979). After 40 minutes of testimony, Amelia B. cries for the ﬁrst time as she talks about a friend who was walking behind her at Auschwitz: “I had a little friend. She’s here. And she walked behind me. [Amelia starts crying suddenly, then composes herself.] And she said, ‘We’ll never come out from here.’ She didn’t.” [Amelia cries again.] (Testimony of Amelia B., 1994). When survivors like Sally H. and Amelia B. cry while giving testimony, they often apologize, indicating that they cannot control the pain of the memory and that the speciﬁc episodic memories are the source of the emotion.4 In these examples and others with sudden grief, the emotional experience appears to arise directly from emotional representations in core memory.

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Leon H. gave testimony in 1985, 40 years after the end of World War II. After testifying for more than 2 hours, describing one atrocity after another, Leon concludes: “Angry all the time. Face looks angry. I don’t know how to straighten my face out.” He tells of his mother who was partially paralyzed from a stroke, though she still worked in the Lodz ghetto, weaving rags. One day, two SS men broke into their apartment and demanded that she tear up the ﬂoorboards so they could search for valuables. She was physically unable to do so quickly enough, so the SS men brutally kicked her, and she died soon after. “Kicked her so hard, she hardly could breathe,” Leon says. “That was my anger!” His face shakes, and he cries. Then he stops (Testimony of Leon H., 1985). Leon’s sudden display of emotion appears to be the result of accessing a core emotional representation in memory, formed at the time he witnessed the beating of his mother. Other displays of anger during testimony appear to be cognitively generated. Clemens L. describes hiding in a convent near the end of the war: I remember my mother coming to visit me on Sundays. I remember one time she came to visit me, she brought me an egg. [He pauses, becoming emotional.] I seem like I’m more sad now, thinking about it, than I was then. But to bring a goddamn—to be thankful for a fucking egg is really preposterous to me. It really pisses me oﬀ, to think about it that way. But, I must have been eternally thankful to get this one fucking egg (Testimony of Clemens L., 1990).

The abrupt coarseness of the language seems out of character for this witness, and the anger appears to erupt without warning. But based on what Clemens says, his anger arises only after he evaluates the deprived conditions of his own childhood in terms of present schemas of decency and responsibility in the care of children. When relating a speciﬁc incident during which she experienced humiliation, Esther W. cries suddenly, her emotion emerging in concert with the remembered humiliation. While in the slave labor camp of Skarzysko, Esther performed 12-hour shifts with two other women, working a machine that engineered bullets. She recalls the time that she and the other two women were accused of sabotage: One day the three of us were called, taken away from the machine, brought into a shed. . . . We had to bend down [she gestures] and were beaten [one] by one. And two oﬃcers were standing and waiting and looking while we were beaten. And when it came to me to be beaten, unfortunately I made in my pants, or whatever. And they stopped. From fear, I urinated. I’m not ashamed to say it but—. [She cries.] . . . It’s a funny thing. I’m not crying because I was beaten, but the humiliation (Testimony of Esther W., 1994).

Esther W. shows emotionally generated emotion, crying in response to the remembered humiliation at the hands of her tormentors. In contrast, some survivors recall their experiences dispassionately, describing gruesome events and cruelties that they personally witnessed, without ex-

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pressing emotion while recalling. Arnold C. ﬂatly describes the aftermath of allied bombing at Zeldenlager: “In the morning, there were arms and legs all over the place, on the wires, on the barbed wire, got caught. I must admit that it was the ﬁrst and only place where I saw cannibalism. I saw two people take a piece of meat from a body and try to make a ﬁre and cook it. The German oﬃcer who walked by, who saw it, shot them immediately.” [He then gives an aﬃrming nod to the camera, as if to say, I witnessed this and I can talk about it.] (Testimony of Arnold C., 1983). In telling the events, Arnold C. calls on narrative memory, not core memory. He does not access core emotional representations, nor does he show cognitively generated disgust or anger. His motivation is to tell the events clearly and directly. Repeated Testimony Fourteen survivors gave testimony at the Fortunoﬀ Video Archive more than once, and analysis of their later testimony reveals the emotional aftermath of extended recall itself. All the survivors say that giving testimony is profoundly distressing and that they are surprised at the strength of their distress. Daniel F. evaluates his ﬁrst testimony: “I didn’t realize that it’s going to just take me to the depths of depression for months. I didn’t realize it” (Testimony of Daniel F., 1988). Eva B. agrees: “When I did the ﬁrst tape here, I didn’t expect to get as upset as I did get . . . I can’t imagine what the reaction would be” (Testimony of Eva B., 1988). Hanna F. says that she needed to be tranquilized afterward because of the powerful emotion released during her testimony (Testimony of Hanna F., 1988). In fact, little is remembered from the testimony itself except the emotional pain. In her second testimony, Dori K. succinctly summarizes this pattern of recall. She says, “I remember very well how I felt. And I remember the interview. But I don’t remember, really, what I said” (Testimony of Dori K., 1988). What accounts for this emotional response to extended recall of trauma? The survivors themselves theorize that the emotional pain is caused by the length of the testimony, the concentration on a long sequence of events. Daniel F. explains: It’s the segment. It was a lengthy, in-depth kind of thing, where I felt that I was back there. And I was depressed for quite a while afterwards. . . . Your mind starts to focus on a particular segment of time, and you’re trying to pick out all the events in that segment of time. And then after the interview ﬁnishes, you continue trying to ﬁnd pieces of memory of those events (Testimony of Daniel F., 1988).

For Daniel F., recalling the details of an event accessed core emotional memories while also encouraging rumination about the memories afterward. Alan Z. said he does not cry when he talks to individuals and to larger groups about the loss of his family during the Holocaust: “Only when I go back that far is there a lot of detail. You see, when you go to speak somewhere to a school or to the synagogue, I don’t go into these details where it makes me emotional” (Testimony of Alan Z., 1984).

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Though a subset of traumatic memories remains painfully active, other core memories lie dormant, below the surface of consciousness. Linton (1986) drew a similar distinction with normal memories between “what pours out of memory and what can be elicited” (p. 65). Accessible with eﬀort, these dormant traumatic memories can be the most threatening to the survivor, and awareness that such memories exist leads to a reluctance to give testimony. Once retrieved into consciousness, these memories engender emotional pain. Detailed recall can mean experiencing the pain of core memory in accessible memories and opening associated memories that are otherwise not immediately accessible. As survivors engage in extended recall, they relate episodes recalled only because they are directly connected to immediately accessible episodes. Sally H. says, “Took me quite a while to come down from that interview. . . . You dig up memories you want to bury” (Testimony of Sally H., 1989). Eva B. says, “It was much more alive in me and much more burdensome to me than I had realized. I really thought I had it good and buried and it wasn’t going to ever come up again or bother me again” (Testimony of Eva B., 1988). Dori K. says, “It was the ﬁrst time I had spoken at such length. . . . It was a very painful experience” (Testimony of Dori K., 1988). Lengthy testimony can revive dormant memories of horror, which can remain active long after the testimony ends and create new emotional disturbance. Martin S. worries that his dreaded nightmares will return because of memories reactivated during testimony (Testimony of Martin S., 1988). Some survivors avoid the pain of memory by omitting details, talking about their lives in cryptic labels. Ruth A. ﬁrst encountered this avoidance of detail during initial contact with survivors after the war: The only question was, “Where were you during the war?” “I was in a concentration camp.” That’s it. “I was in the partisans.” That’s it. “I was hiding in the—some place.” That’s it. Nobody spoke any details. It seems that the people wanted to block it out from their mind. They did not want to talk about it, just vaguely question: “What is your name? Where did you live before the war? Where were you during the war?” And that was the whole conversation. (Testimony of Ruth A., 1994)

Renee G. says that her ﬁrst testimony was the ﬁrst time her memories came out “full force,” explaining, “It was almost like a release of emotions, with tension and fear and crying.” By saying “almost,” Renee carefully qualiﬁes the process of release; there was tension and fear and crying, but not catharsis (Testimony of Renee G., 1988). Eva B. agrees: “I don’t know that I ever will really get it out of my system, but at least, to live with it more peacefully” (Testimony of Eva B., 1988). Traumatic memory seems to be a self-generating source of emotional pain. Speciﬁc memories release emotional disturbance in the form of depression and nightmares, especially when an extended sequence of episodes has been recalled, but the power of emotional memory is not diminished through the release of emotions during testimony.

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Clinical psychologists who work with survivors of trauma promote the therapeutic value of talking about the trauma, allowing the victimized to examine their emotions in detail and to regain control of their own individual narratives (Harber & Pennebaker, 1992; Janoﬀ-Bulman, 1985). For Holocaust survivors, however, the therapeutic value of speaking their memories is not a given. Survivors themselves disagree: some avoid opportunities to talk and others carefully welcome the opportunity to communicate the horrors to receptive listeners. Although obvious almost to the point of tautology, if imposed silence is exacerbating emotional disturbance, then talking can be therapeutic. In such cases, conditions should enable these survivors to communicate their memories, without social discouragements, with listeners recognizing and helping to manage the inevitable pain of remembrance. Depending on the desired audience, survivors could actively seek out environments that are receptive to remembering: family meetings among survivors and their children, mediated by family therapists; oﬃcial gatherings of Holocaust survivors; instructional programs for teaching young people about the Holocaust; archives for collecting oral testimony. To force the reticent to talk is not helpful, but encouraging them to enter settings that are conducive to talking can be therapeutic.

Re-experiencing Emotion Due

to External Cues

Emotions can be experienced suddenly during the course of daily life. Particular events and situations in the world today can trigger retrieval of past emotional experience, producing strong emotional responses. Many survivors give examples of fears connected to speciﬁc Holocaust memories, many arising from what was lost in the traumatic past—the most pervasive fear concerning the safety of their children. In her testimony, Nina S. evinces this fear while revealing its source in memory: “I sometimes look out there and I say, ‘God All Mighty, it might happen again. What’s going to happen to the babies?’ I used to say when my children were born. I used to pray nothing should happen until they are six years old because in my mind, up to six years old, they going to take them, they going to kill them.The source of Nina’s fear resides in her speciﬁc memories of the Lodz Ghetto, which she explains: “They tore the children, the babies away from the mothers. And there were screams. Could you imagine? Babies. Up to six years old they tore them away from mothers’ hands. Mothers were crazy. But they had no choice. . . . They were going from one house to the next. And we sat there and we listened to it.” (Testimony of Nina S., 1996). For Nina, fears about the well-being of her children—and later her grandchildren—grow from these memories. Many years later, when Nina became a mother, these memories evoked insuppressible fear. Oral testimony reveals speciﬁc fears that are nearly universal among Holocaust survivors. Jolly Z. describes one such fear: “When I came over to this country, even on the railroads, even a conductor, I suspected. Because he had a uniform” (Testi-

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mony of Jolly Z., 1988). Martin S. concurs, providing more detail: “A sharp, black, dark-blue, black type uniform still makes me freeze no matter where I see it.” He adds, “Uniforms, to this day, especially when they’re very sharply dressed, is something that changes my attitude immediately” (Testimony of Martin S., 1988). Survivors fear that food will no longer be available, they fear dogs, they fear being trapped, and they fear abduction, with each fear linked to speciﬁc memories. News of current catastrophes can revive emotional memories of the traumatic past. Leon H. summarizes: “If I look at you it reminds me of something. If I look at world, reminds me of something” (Testimony of Leon H., 1985). When those in the United States and Europe belatedly learned of the genocide in Cambodia, survivors reacted. Edith P. says, “When I learned about Cambodia, I went into a depression. It pains me terribly that the world has not learned” (Testimony of Edith P., 1980). When President Reagan visited Bitburg, Jolly Z. says she was physically sick for the ﬁrst time since the war. She concludes that the emotion in Holocaust memory does not pale, “especially when it is triggered by something” (Testimony of Jolly Z., 1983). Reports in newspapers and on television summon past atrocities. Leo G. says, “You do open up a paper and you do listen to the radio and you watch it and it hits you from every side, and everything is constantly back. Your mind walks back and names and places and faces, and then you translate all this to your family” (Testimony of Leo G., 1988). Sabina G. says, “Any little news, political news, can disturb me. And can bring thoughts: What’s going to be? How it’s going to be? Will we, will we have it again?” (Testimony of Sabina G., 1984). Prolonged trauma splits the self-concept, creating the experience of two separate selves, each supported by memories that remain irreconcilable. When events in the world connect these two sets of memories—Holocaust and post-Holocaust— this connection is profoundly threatening to the survivor’s current self-concept and can cause a strong emotional response. Current events perceived as similar to the events of the Holocaust can create deep despair—events such as the cruelty and devastation in Cambodia, Bosnia, and Rwanda. Seeing people in uniform or seeing large dogs can generate fear. When events in the present lives of the survivors make contact with the traumatic memories of the Holocaust, emotional responses can result, in the form of fear and depression. Sometimes, events in the world tap into the well of implicit core memories, suddenly and without warning. When this happens, Holocaust memories can ﬂood into consciousness, unwanted and unrestrained, with responses that are unavoidable and physical. Sally H. tells about a panic attack she suﬀered while visiting the Holocaust museum in Detroit. When she saw the ﬂame in the museum, she became disoriented and frightened, and then she panicked and ran (Testimony of Sally H., 1989). Celia K. is clear about the extent and power of her memories. “I keep on just, not rehashing it. I’m not looking for it. It’s just automatically keeps on coming to me. And somehow everything is vivid, very much alive, very much.” Celia

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relates a recent incident. A bonﬁre had been built to burn garbage in her back yard. Unfortunately, the ﬁre vividly retrieved the memory of her cousins who were burned alive in a small synagogue. “I became so hysterical. Was screaming nonstop. I could not stop. . . . I was screaming until my jaw came out. I could not put my jaw back in. And I could not control myself.” Celia then had to be restrained (Testimony of Celia K., 1987). Celina R. talks of overwhelming emotion the one time she visited Auschwitz: “Then we went—. In Auschwitz there is one place that they collect hair and glasses, eyeglasses [She gestures], and I saw that mountain of glasses. My little brother wore glasses . . . and when I saw those glasses I was hysterical. I was so hysterical. I just couldn’t stop crying. All those things come back” (Testimony of Celina R., 1995). Many survivors also speak of automatic physical responses of disgust when hearing the language of their tormentors. Ernest R. says, “When I do travel in Europe and I hear Germans speaking, it does bother my ear. . . . Even until this date, I cannot forget it . . . I will never forget it” (Testimony of Ernest R., 1987). Celia K. says, “Today, after so many years, if I hear Ukrainian spoken or Lithuanian, I cringe. I get very sick. I can’t be in the same room with them . . . everything opens up all over again” (Testimony of Celia K., 1980). These responses are not the result of thoughtful resentment, and they are not the result of attitudes learned over time. They arise from connections in core memory between the survivors’ speciﬁc memories of trauma and the language of their tormentors. Kluger (2001) observed that the strongest bond between an individual and a place is the language of that place (p. 205). Events in the world that trigger emotional responses can also be temporal. Isabella L. describes a recurring change in mood every May, the time of year she was deported from the ghetto in Kisvarda, Hungary, to Auschwitz: For decades, the end of May, which is coming upon us soon, was an unbearable time for me. I never knew why suddenly I got terribly depressed and I couldn’t cope with the days in May. And I never quite remembered why. And then it would dawn on me. . . . Then in June, I would have a diﬀerent outlook on life. I would be more hopeful. But it would hit me like a clock. It reappeared every May (Testimony of Isabella L., 1989).

For Isabella, the time of year retrieves a representation of the original events, which in turn connects to core memory, leading to a release of emotion and the resulting eﬀects on her mood. For many years, the mood change came without her conscious awareness of its source. Hilda S. says, “I lived through some very diﬃcult periods. For instance, when my oldest daughter was eight, the age I was when I left home, I had a real tough time. [She cries for the ﬁrst time, then stops.] I was always very—. I guess, I guess, I was always very obsessed with what my mother went through. Sending two children away” (Testimony of Hilda S., 1993).

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According to Holocaust survivors, strong emotional and physical responses can occur during daily life without warning and without reason. These emotional and bodily responses appear to arise from implicit representations in core memory; to the survivors, the responses seem automatic and immutable. However, after repeatedly experiencing these unbidden responses, the survivors are able to attribute their responses to speciﬁc memories of the traumatic events. They do not use the language of cognitive psychology, but their meaning is clear. Beatrice S. describes witnessing the absolute horror of family members being brutally murdered. She hid with her father in a small cellar, watching as a Gestapo oﬃcer shot her mother and crushed her younger brother to death beneath his boots. As she witnessed the murder, Beatrice’s father clamped his hand over her mouth to prevent her from screaming. In her testimony, Beatrice describes the continuing physiological eﬀects of this horror: “To this day, I have trouble breathing, and I think it’s because what happened” (Testimony of Beatrice S., 1982). After surviving the war, Nadia R. discovered that she experienced powerful waves of panic in the company of other Jewish people. She says, “For the ﬁrst time . . . after the concentration camp, I was surrounded with Jews. It brought me such an anxiety attack . . . I started to hyperventilate” (Testimony of Nadia R., 1995). The implicit, somatic representations of suﬀocation for Beatrice S. and fear for Nadia R. are repeatedly activated and become evident to the survivors, who then can attribute these responses to their memories of speciﬁc events. When a current event (spatial or temporal) causes a survivor to access implicit representations in core memory, the represented emotional and bodily responses can be triggered and experienced. The activating event acts as a tuning fork causing an implicit memory representation to resonate, generating strong responses. Survivors are initially surprised by the triggered responses, but after becoming aware of the connection to particular worldly conditions, they construct intuitive theories to account for their overwhelming emotional and bodily responses. These theories provide an explanation for the emotional ﬂooding, but they do not make contact with the implicit memories and do not alleviate the problem of uncontrollable responses. Awareness of this connection does not prevent the overwhelming emotions any more than awareness of the physics of pressure waves and resonant frequencies can prevent unwanted resonant vibration. About the persistence of such responses, Martin S. concludes, “Things like that, I just cannot seem to shake—and probably never will” (Testimony of Martin S., 1986).

Enduring Emotion Some emotions endure for the remainder of the survivors’ lives. Though not constant, these emotions are repeated and persistent over many years. When

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discussing long-term emotional eﬀects, survivors frequently refer to their sadness and occasionally their anger, but the enduring emotion that they analyze most elaborately and question most intensely is guilt. In the literature on survivors of widespread catastrophes, there is considerable discussion and disagreement about guilt (e.g., Danieli, 1988; Hartman, 1994, Hass, 1995; Levi, 1986/1989). From the oral testimony in this study, it is clear that Holocaust survivors experience guilt for extended time, often beginning shortly after liberation and continuing for many years. Many talk about current feelings of guilt. As described by the survivors, guilt assumes several forms, with multiple causes and diﬀerent developmental paths. Many survivors evince a questioning, retrospective “why me” guilt, most often deemed survivor guilt. Menachem S. was 1 of only 2 children out of possibly 4,000 who survived his concentration camp; all the others were killed. As a result, Menachem experiences a questioning guilt, which he expresses in its most concise form: “You ask yourself the questions: Why? Why did I survive?” (Testimony of Menachem S., 1979). Similarly, Nina S. asks, “Why are we the ones to live? And so many wonderful people did not survive?” (Testimony of Nina S., 1996). Michael G. lost his family during the Holocaust, and memories of the events that led to his family’s murder continue to interrogate him: “To live with it and to justify your living. I feel, at many times, I feel guilty. I live with the guilt. And it’s not because I’ve done anything wrong. It’s just a guilt there: why. I’ve lived with that guilt for a long time. I ask myself many times when I do certain things and I say, well, I could have helped . . . if. If whatever” (Testimony of Michael G., 1992). Survivors describe this kind of guilt as arising from attempts to make sense of events that make no sense—events that violate moral principles as well as the laws of probability. Their very existence is based on surviving in an environment without morality and for no reason other than luck. Danieli (1988) suggested that this type of survivor guilt is, in part, an unconscious attempt to prevent oneself from remembering the absolute helplessness experienced during the Holocaust. According to Danieli, guilt presupposes choice and the ability to decide one’s fate. The unyielding pain of guilt is thus more acceptable to the survivor’s belief system than the experience of intolerable passivity and helplessness, and guilt serves as a defense against the memory of a nightmare world devoid of choice. In some cases, guilt assumes a form that many observers can imagine: an intense regret for failing to prevent the deaths of others. After the brother of Abe L. escaped the ghetto, Abe rescued his brother’s young daughters but was unable to save his brother’s two sons, ages 6 and 7. Abe confesses: “These two boys, I can’t get over it, until this moment. Day and night, I can’t go over it. Not being melodramatic, these two boys are killing me” (Testimony of Abe L., 1990). Abe persists in thinking about what he could have done diﬀerently to save his brother’s sons.

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Survivors sometimes try to diminish the impact of guilt with conceptual knowledge. Some survivors have learned to resolve the conﬂict of living while so many others died by emphasizing the concept of destiny. Samuel B. explains: This stupid feeling of guilt. . . . How is this: if I am alive, that somebody died because of me? Because I was supposed to be alive? All these things were very, very heavy somewhere sitting in me. And it took me years and years to understand, to liberate myself somehow from all this. It was a very crippling feeling. Trying to understand that nothing of all that was my own personal choice. It was all imposed on me by some games of destiny. (Testimony of Samuel B., 1995)

After years of inner conﬂict, many survivors ultimately incorporate the knowledge that responsibility lies with those who imposed the desperate conditions and not with their own seemingly cowardly or selﬁsh responses. As with Samuel B., Clara L. shed her conﬂict and replaced it with a strong belief in destiny. She says, “I was one of those who was destined to survive. And I feel no guilt feelings. I did whatever I could for my parents. I did whatever I could for my sister. And whoever was around me. More I could not do. So I don’t feel guilty about it to remain alive” (Testimony of Clara L., 1993). Eva L. understands the impossible conditions that killed others in her family, and she assimilates the concept of destiny, yet feelings of guilt persist. In the Lodz ghetto, Eva lay in a coma for 5 weeks with typhus before ﬁnally reviving. To aid her recovery, Eva’s father sold his food ration for medicine, and she credits him for saving her life. Soon after, her father died of starvation. She says, “He swell up, and he died. And I could not help him. I couldn’t do anything for him.” After describing her father’s death, Eva reveals a resolution of her underlying feelings of helplessness: “It was meant for me to live. Because under such circumstances, nobody can survive.” But Eva also describes the persistent, lingering eﬀects of her family’s death: “Sometimes I feel like guilt. Why am I the one, that I am here? . . . And the rest of my family is not?” She laments, “I can never push it away. I can never chase it away” (Testimony of Eva L., 1982). Horowitz and Reidbord (1992) provided one explanation for the etiology of feeling simultaneously guilty and not guilty. When a person is victimized by overwhelming trauma, the trauma destabilizes his or her normal experience of a single self-concept. To accommodate the traumatic events, the normally coherent sense of self splits into multiple self-concepts, and these multiple selves then permit people to process the traumatic events along “several parallel streams” (p. 353). In fact, many survivors speak of split selves, simultaneously experiencing the reality of the traumatic past as well as the normal present, as reﬂected in their emotional experience. The result many years later of these parallel streams of encoding is the experience of simultaneous conﬂicting emotions: guilty and not guilty, happy and not happy.

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For survivors who were eyewitnesses to the murder of their own families, strong feelings of guilt arose at the time of the murder and are represented with the events. As I described earlier, Beatrice S. witnessed such an atrocity while hiding from the Gestapo with her family: It was very cold and dark and my brother started crying and my mother said, “Because of him we’ll all get killed.” So she went out with him and she covered us. She covered the top up in the cellar, so they wouldn’t see there’s an opening. And she went to our next door neighbor, who was Christian— Polish, and the Gestapo shot her. And my brother was wounded. And I saw through the little window there, and my father put his hand on my mouth [she gestures], I shouldn’t scream. . . . And he was wounded, and the Gestapo came with his boots and just stepped on him.

Beatrice’s memory of this atrocity splits her self, causing her to feel simultaneously guilty and not guilty for the rest of her life. As a result, Beatrice says, “It’s like there are two of me. There’s one that wants to have a zest for life, wants to live and enjoy. And there’s another part of me that I have guilt feelings” (Testimony of Beatrice S., 1982). Kochevit P. relates a similar atrocity for which she claims partial responsibility, consequently suﬀering overwhelming guilt. As a young child, Kochevit was taken in by a neighbor who saw the SS soldiers coming with dogs looking for Jews: And I saw the family, my mother, my brother, my grandmother, and my aunt, and they shoot them down, on the place. . . . I saw this. . . . I was in the cellar and I saw through a small window. [She gestures, ducking her head down and peering out.] And my brother was begging, “Please.” And he tried to run away. He said, “Please. Don’t shoot me.” And he put his [She gestures with her right hand in front of her head, then stops talking.] I can’t speak about this.

Kochevit then struggles to ﬁnish her account: Was a very long—. It took me a very long time to believe what happened. I was a little girl. I said that they shot them, but they will never come back? And I saw this with my eyes. [She looks down and pauses.] I suﬀered a lot after this. I was very sorry that I run away, as a child. Because I was blaming myself that everybody is dead. Only I am alive. I was very much disturbed. (Testimony of Kochevit P., 1979)

For those who were eyewitnesses to their own family’s murder, the concept of destiny fails because of the persistent memory of useless proximity. These survivors describe experiencing guilt at the time of the events, guilt that is represented in the memory for these events.

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Other guilt feelings seem cognitively generated, arising from interpretations of past behavior. Abraham P. vividly describes his arrival at Auschwitz. After getting oﬀ the train transport, Abraham told his younger brother to go with his mother, and they were both sent to the gas chamber. “I feel like I killed him,” Abraham says. “I can’t get it out of my head. It hurts me. It bothers me and I don’t know what to do. I feel that I am responsible for that.” He then describes his long-term thought processes: “In one day . . . there were so many things have happened to us, we really couldn’t sort them out. And I’m still trying to sort out that day” (Testimony of Abraham P., 1984). Some survivors feel guilt for what they consider their own unfairness to other victims. Edith P. confesses intense guilt about a single insulting comment she made to an inmate at Auschwitz, an older woman who shoved Edith as they entered their barracks. After years of suﬀering from extreme deprivation, brutal beatings, and daily humiliations, Edith refers to this brief insult as “one of my most painful episodes from Auschwitz.” An oﬀense that in normal times might demand an apology intensiﬁes into an enduring insult, with Holocaust survivors interpreting their thoughtlessness or selﬁshness as contributing to the misery of their fellow victims, however excusable and transitory. The interpretation of the insult alters their self-concept by placing these survivors in the role of victimizer, along with its associated characteristics. To this day, Edith’s rudeness haunts her, and every year at Yom Kippur, Edith asks forgiveness from the woman (Testimony of Edith P, 1987).

Enduring Emotion as the Result

of Cognitive Discontinuity

In part, the persistence of emotion stems from discrepancies between fundamental expectations and the actual events, the eﬀort to account for these discrepancies, and the inability to resolve them in the case of extended atrocity. According to the schema-based framework of Harber and Pennebaker (1992), emotions arise when there is a conﬂict between our expectations and our direct encounters with events in the world. Emotions then direct attention to the unsuspecting schemas so they can be restructured to accommodate the discordant events. When expectations are realigned to account for the violating events, the emotions dissipate. When expectations and the remembered events are not aligned, emotions remain. With survivors of extended atrocity, the gulf between schema-based expectations and remembered experience is so wide that the discrepancy remains unresolved, and the emotions persist. Violet S. tries to take on the untenable perspective of the architects of genocide, but she is unable to, and the irreconcilable diﬀerence between her own view and that of the murderers generates great anger: “Children. Children. Imagine children to be alive? I mean this is—. To this day I mean, it wasn’t just a mess of, bunch of, hoodlums that run them. These were the top intelligence, scientiﬁcally,

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who planned to burn our children alive. I never, never forgive them. Never. I tried” (Testimony of Violet S., 1991). Hilda S. presents the same pattern. Her fundamental beliefs about the treatment of human beings cannot be restructured to account for the unprecedented cruelties she experienced, and her emotion persists. Hilda says, “I have always obviously been very bitter about what happened to the Jewish people. I carry a lot of hatred. And I think I’m always trying to understand how could it have happened” (Testimony of Hilda S., 1993). After the war, after survivors re-entered stable social settings, their emotional state conﬂicted with the emotional state of others around them. This interpersonal disparity paralleled and reinforced the cognitive disparity within the individual survivor. For example, after Julien E. immigrated to the United States and began attending high school, his own emotional state conﬂicted with that of his peers. Julien says he was unable to take part in the “seemingly frivolous” experiences of his fellow classmates because of his “sense of continuing mourning,” which, he says, “made it impossible to partake fully in the lighter side of life enjoyed by peers in school and elsewhere” (Testimony of Julien E., 1995).

Distracting Emotional Memory Instead of asking why survivors of atrocity experience strong emotion, perhaps we should ask how they manage not to. Certainly, survivors can avoid talking about their traumatic memories, but to avoid thinking about these memories is another matter. What survivors discuss most frequently is the importance of meaningful distraction in their daily lives. Such distraction eﬀectively decreases the pain of emotional memory in four ways: by focusing one’s thinking on activities in the present, by diverting attention away from potential triggers of traumatic memories, by decreasing the likelihood of cognitively generated emotion, and by allowing recent memories to overlay older, traumatic memories, helping to redeﬁne the remembered self in normal life. Raising children, building careers, establishing friendships, and carrying out civic responsibilities direct the attention of Holocaust survivors away from the traumatic past and toward the challenges of normal life. Alan Z. says that he suﬀered great fears and nightmares after liberation, but these fears and nightmares went away with the distraction of work and family. He says, “After I came to the United States, and I started to work, everything disappeared. I mean, my life changed drastically, when I was in the United States. My work, I was involved in my business. And raising my family. And it just moved away from me” (Testimony of Alan Z., 1984). Many survivors make similar observations about the relationship between the emotional pain of traumatic memory and the distractions of normal life. Intuitively, survivors distinguish between the cognitive and the emotional. Rena C. says, “Intellectually I manage very well. I went to college and so on.

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Work-wise I’m okay. But emotionally, I am not okay” (Testimony of Rena C., 1992). Karl S. says, “I believe I am a successful professional in my ﬁeld, as a technician. But as a person, as a Jew, I feel I’m sitting on a volcano” (Testimony of Karl S., 1980). Survivors do not use the same terminology as memory researchers, but they clearly distinguish between cognitive strategies for managing emotional pain and the experience of emotion. Some survivors describe overriding their emotional distress with resolute cognitive strategies. Near the end of his testimony, Harry F. says, “I had to make a decision. Is this going to bother me for the rest of my life, or what? And I decided that I couldn’t let it bother me for the rest of my life because that would be an admission that the other side had won the war.” He says, “I stopped suﬀering from the consequences one week after it was over. It’s something you never ever forget. It’s impossible. But we have to educate the next generations about man’s inhumanity to man and then go on from there” (Testimony of Harry F., 1995). While living in Czechoslovakia after the war, Nadia R. actively suppressed her memories and hid her Jewish identity, which she interpreted as a sign of wellbeing. “It was totally buried in me,” she says, “and I felt that is a good thing. That, I thought, was my proof how well I came across the whole trauma.” During the 23 years that Nadia lived in Czechoslovakia after the war, her closest friends were unaware of her background or her religion (Testimony of Nadia R., 1995).

Emotional Memory “Getting Worse” The power of distraction becomes most evident when it diminishes. Later in life, when the healthy distractions of work and raising children go away, many survivors experience this loss of distraction by experiencing their memories as growing stronger and more distressing. Near the end of his testimony, Abe L. says: But the worst of all, certain people, for some reason, some reason, certain ﬁgures, certain people is in you, in your brain. Certain people, they stay with you and they can’t get away, they can’t, they just can’t get away. Anyone, if he thinks, he sees the hole in his heart, is—is not getting smaller, is getting bigger. And the Holocaust itself, I thought when years go by, passes by, these will go away. We will have forgotten. No way. It’s getting closer. The Holocaust is getting nearer, and not farer [sic]. It’s getting nearer. (Testimony of Abe L., 1990).

Isabella L. says, “It’s much harder now. I feel my head is ﬁlled with garbage. All these images and sounds. And my nostrils are ﬁlled with the stench of burning ﬂesh” (Testimony of Isabella L., 1989). Eva B. agrees: “It’s going to be there until the day I die.” She says, “It’s more painful; it’s more alive rather than less so” (Testimony of Eva B., 1988). Leon W. explains why the torment of memory is worse: “I think about it more now, maybe because I get older . . . I think a lot about it. Too much I think.” Alex

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H. says that for many years after the war, he was so involved in the ﬁght for a new existence that he did not think about the past. Beginning with no family, no schooling, and the wrong language, Alex says the daily ﬁght to establish himself used all his energy. In fact, he suppressed his time in the concentration camp until 3 years before he came in to give testimony. He describes the result of having accomplished his goals: “My past is starting to haunt me . . . and I feel so depressed, very often. That I actually feel that I—, very often feel that I lived long enough.” [He speaks softly and slowly, looking down] (Testimony of Alex H., 1985). In the laboratory, Reisberg and Heuer (1992) showed the importance of retention interval in assessing emotional memory, with strong emotion slowing the process of forgetting with memory tests delayed between 1 and 2 weeks. Outside the laboratory in naturalistic studies of emotional memory, retention intervals can be considerably longer. Using the birth of a younger sibling, Sheingold and Tenney (1982) examined retention intervals from 1 month up to 16 years, with the results showing only a slight decrease in memory over this interval. Over longer periods of time, some emotional memories appear virtually permanent, showing no decline. In my study of oral testimony, recall intervals ranged from 35 to 55 years, with witnesses reporting no loss of memory for traumatic events (Kraft, 2002). Over these longer intervals, changes in the thoughts about one’s emotional memories can be experienced as changes in the memories themselves. After looking back over the terrain of normal life and recent world events and realizing the implications of the past atrocities, one’s interpretation of memory changes. The images remain, but the memories seem more horrifying. Eva L. ruminates about why she survived, with her focus on memory. First, she talks of her memories of the Holocaust: “The older I get, the more memories are haunting me. I keep asking myself, why, what is it? Is it fate that I am here, of the whole family, of the whole wonderful culture, only I am here from a whole family? . . . It’s getting harder, it’s getting worse with age. I sit and I work, and I think about things that I went through and I wonder.” Later Eva says, “I think when I was younger, it was easier because I was occupied with the children. I was busy with them. And I try, I try to push away those thoughts, but now they come more often, and it . . . haunts me” (Testimony of Eva L., 1982). Eva L. assesses her life raising children after the war, and she cannot reconcile the two sets of memories: “I myself cannot believe that I was there and I was able to live through a horror like this and yet come here to this country and have a family and live a normal life, more or less, a normal life, and bring up my children a normal way. And I wonder and I lay awake. And when I lay awake, I relive lot of things” (Testimony of Eva L., 1982). A contributing factor to the increasing pain of Holocaust memory is the loss of normal, pre-Holocaust memories. When Eva tries to recapture her preHolocaust memories of times when she was happy, she fails. She says, “Nights

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that I am up and I cannot sleep, I try to see my parents. It’s kind of like, so many years, the picture’s fading away and I won’t remember them. Comes a holiday, I try to copy, and remember how it was at home. I can never copy” (Testimony of Eva L., 1982). A fading happier childhood, a decrease in worldly distraction, and the laser clarity of the remembered horrors combine to worsen the torment of traumatic memory. Eva works at remembering the faces of her parents and the rituals of Jewish holidays, but these general personal memories formed long ago during normal times are not strong enough to endure. Memory for neutral events strengthens when rehearsed through thoughts or actions, yet these events were simply not repeated enough to endure. Prevented from recreating past rituals as they were in the world, Eva endeavors to reconstruct them in her thoughts, but the faded images of these comforting rituals lack the singular emotional and perceptual vividness of traumatic memories. She has no diﬃculty remembering the atrocities that followed, and she can no longer distract herself from these memories.

Rebound Eﬀects In their summary of research on thought suppression, Wegner and Schneider (1989) documented the fact that distraction from thinking about unwanted thoughts can produce rebound eﬀects. After participants actively suppressed thinking about a particular image (e.g., a white bear) by distracting themselves with thoughts of a variety of other topics, they later experienced more thoughts about the suppressed image than a control group who did not suppress. Wenzlaﬀ and Wegner (2000) summarized three processes that may be pertinent to suppression of thoughts about real-world traumatic events and subsequent increases in the frequency, intensity, and duration of these thoughts. First, images used to distract can become associated with the unwanted thoughts of trauma and can later serve as reminders of these thoughts. For Holocaust survivors, many years of actively suppressing images of the ghettos and the camps by distracting themselves with thoughts of other events may return the images with more frequency and more force many years later. Moreover, when attention is focused on one’s children, there may be associated thoughts of the children who were lost, either one’s own children or siblings, nieces, nephews, and cousins. Raising children simultaneously serves as an eﬀective distractor and a reminder of the children who never had the chance to live. Wenzlaﬀ and Wegner (2000) also describe ironic process theory, which involves two strategies: (1) actively seeking out other thoughts in an attempt to suppress unwanted thoughts and (2) a monitoring process that remains vigilant for failures in the suppression of unwanted memories and thoughts. Although this monitoring process serves a useful function, notifying the individual when to expend more cognitive eﬀort on suppression, when active suppression diminishes or goes away entirely, the monitoring process continues, highlighting the

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unwanted memories and thoughts. Wenzlaﬀ and Wegner propose a metacognitive process that depends on the underlying belief that suppression should be successful. When it is not, people become even more focused on suppressing and even more critical of themselves when suppression fails. This view is supported by testimony from survivors who say that they felt “successful” when hiding their past, that hiding the past from oneself and others was a sign of having endured the trauma. Associated with the belief that suppression should be successful is the corollary that a reversal in the eﬀectiveness of thought suppression is a sign of declining emotional health and personal failure. Holocaust survivors repeatedly demonstrate the pattern of distracting or suppressing traumatic memories for many years and then experiencing a strong return or reformation of painful emotion. Fifty years after the end of the war, Aladar M. talks of his nightmares: “Even more lately than in the beginning . . . because in the beginning, it was more like I have to work, I have to make a living, I have to do things. I did not have the time to think about it. There was no time” (Testimony of Aladar M., 1995). After 23 years, Nadia R. actively reversed her initial decision to suppress memories of the Holocaust and chose to accept her past. With that acceptance, she says her former self-concept returned, a self-concept deﬁned immediately after liberation from the concentration camp of Terezin and laden with fears and anxiety (Testimony of Nadia R., 1995). Sybilla F. decided to “be positive” and not dwell on her suﬀering during the war. She says that this attitude did not come quickly but that she was able to use strategies to overcome her emotions. After the war, after Sybilla came out of hiding, her remaining family did not talk about her brother’s death or the deaths of her mother’s family. She says, “To break down and then to feel terrible would not have been the way forward.” A few years before her testimony in 1991, however, Sybilla went through serious depression for a year and a half, which she describes: “Everything went black. [She gestures, with her hands spread wide.] And everything negative. And it just happened. . . . It was just something that happened” (Testimony of Sybilla F., 1991).

Conclusions The most pervasive ﬁnding in the study of Holocaust testimony is the extraordinary persistence of emotional memory. More than 50 years after the events, emotional memory remains vivid and powerful, with speciﬁc memories causing survivors to cry suddenly, to break down uncontrollably, to become enraged. Recent memory does not weaken or conceal older memories of atrocity, and time does not diminish their potency. Recalling past traumatic experiences does not reduce emotional pain, and there is no cathartic release.

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During testimony, survivors appear to experience emotion through cognitive generation or through direct accessing of core emotional representations. Cognitive generation is suggested if emotions are displayed after interpretation of the memories on the part of the survivor—typically a comparison of the remembered events with events in normal life or an assessment of the choices the perpetrators made. Core representations are implicated if emotion occurs suddenly in the testimony and is followed by an apology or by the survivor’s observations that the emotion was unexpected. When the poet Theodore Roethke wrote, “We think by feeling. What is there to know?” he embraced both the concept of core emotional representations and their primacy. In daily life, emotions can be reexperienced suddenly and without warning if events in the world activate implicit core memories of trauma, releasing emotional and bodily responses. One puzzling pattern in the testimony concerns numbness. So predominant in the remembered emotions of survivors, it is largely absent during recall and diﬀuse in the daily lives of the survivors. Numbness is remembered as an allencompassing feeling inhabiting one’s entire self. Survivors sometimes say that the source of the numbness was external—in some cases incorrectly attributing it to an ingested substance—but they remember the numbness as an experience involving the entire self. For such numbness to be re-experienced fully, similar external conditions need to be reinstated, conditions that are impossible during testimony and unlikely in the present lives of the survivors. Complicating the re-experience of numbness is the duality of the survivors’ self-concepts in their lives today. Consider a few phrases that survivors use to describe their experience of self: “a double existence,” “another world,” “a schizophrenic division,” “two worlds,” “two diﬀerent planets,” “double lives.” Many years after the events, survivors have the phenomenal experience of two separate selves, with residual numbness in the past traumatized self. The child survivor, Renee H., explicitly addresses this split in her self before and after the war: What is left is . . . two separate units in one’s experience. And so there is the me that is the wartime and prewartime me and me that is the postwartime. It’s like having an era before and after. And that—while they are all connected in myself—they are not reconcilable. And it took me a long, long time to realize that not only are they not reconcilable, I don’t want them to be reconcilable. That I wanted them to be separate. (Testimony of Renee H., 1979)

The diﬀuse experience of numbness in daily life shows itself in the duality of self after prolonged trauma, in the self-concept constructed during the period of extended trauma. When survivors speak of numbness later in life, they refer to the self-concepts they constructed during the Holocaust. The experience of Alina Z. is representative: “I was like stone. I couldn’t believe. And something stay in me. I’m very happy, but I can’t show a lot. I can’t cry with tragedy.” Now, she says her children cannot tell when she is happy: “I said I’m happy. I’m very happy,

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but I just can’t show the feeling. Can’t show. When I’m happy, they think I’m not happy” (Testimony of Alina Z., 1993). When survivors speak of “emotional masks,” they are referring to hiding their Holocaust selves. Recalling her time in Auschwitz, Violet S. says, “Many times, people that don’t know me, they look . . . they have no idea.” After describing her escape to Prague during a death march from Gross-Rosen to Bergen-Belsen, Beatrice S. admits in her testimony that her children do not know the “real me,” conceding that she is playing the part that is expected of her: “You put on a smile and you go. You just become an actress” (Testimony of Beatrice S., 1982). For all survivors, grief persists throughout their lives. For many, guilt and anger remain. For some survivors, nightmares continue even to this day. One strategy that survivors use to reduce this emotional pain is distraction. But the palliative eﬀects of distraction are temporary, and the emotional pain of deeply traumatic memory remains, often growing stronger as distractions diminish. According to these survivors, an eﬀective long-term strategy for accommodating the emotional pain of traumatic memory is to ﬁnd meaning through communication of their memories. The child survivor and psychiatrist Robert K. presents a symposium for high school students every year. In his testimony he asserts, “Nothing that I have ever heard from any psychiatrist or psychoanalyst in the world . . . matches one twenty-minute presentation by one of my survivor panelists in terms of their therapeutic well-being.” He points out that these survivors have guarded their memories for decades, hiding the memories within themselves. He then describes the survivors’ therapeutic revelation when speaking in public: They discover that there are ﬁve hundred students there who listen to them— and you should see the listening that goes on when they speak. And they see perhaps, perhaps they’re doing something with their experience that some of those ﬁve hundred will be touched by them, to perhaps make even this much [He holds his thumb and foreﬁnger, one inch apart.] of a shift in their perception of life, their philosophy. That gives the survivor great hope. And I’ve seen [them] go through it and get depressed and break down and be in tears and stay depressed for two weeks. And tell me that it was the best day of their lives. (Testimony of Robert K., 1984).

Fivush, Haden, and Reese (1995) documented the importance of children talking about their experiences to develop their skills in recounting memory and in learning the value of reminiscing. They proposed that language and memory can become “inextricably intertwined in the development of autobiographical memory” (p. 355). In chapter 8 in this volume, Fivush and Sales document complex linguistic interactions between parents and children that are speciﬁcally directed at the children’s memories for personal events. In stark contrast, those who are repeatedly traumatized in childhood learn the value of not talking about the past. They learn not to reminisce. According to the

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testimony of child survivors of the Holocaust, much remembering is unspoken, often insistent and unbidden. Very often, memories come to mind without being narrated or expressed. Later in life, these survivors discover that it can be therapeutic to unlearn the lesson of silent remembering and to ﬁnd ways to communicate their memories. Recalling traumatic events in public exposes painful emotion but does not diminish it. Documenting the traumatic events does not ease the pain of memory, nor does it provide meaning to the memories of suﬀering. Change occurs when survivors reinterpret the function of memory. No longer meant to be hidden, traumatic memories are meant to be communicated: to educate others and to commemorate the lives of those who were lost. Translating memories of atrocity into understandable narratives gives meaning to the act of recalling—an act that formerly provided only torment. Narrating the traumatic events of the past provides meaning to the telling of these events, allowing the survivors to coexist with the emotional pain of their memories.

Notes I thank Daniel Reisberg, whose thoughtful suggestions and skillful editing strengthened and clariﬁed this chapter. I gratefully acknowledge permission from the Yale University Library to reproduce oral testimonies from the Fortunoﬀ Video Archive for Holocaust Testimonies. Permission must be obtained before reproducing any of the testimony quoted in this chapter. Please contact Manuscripts and Archives, Yale University Library, and cite the speciﬁc testimony to be reproduced. 1. A list of archives, primarily in the United States, can be obtained from the Oral History Association at the following ground address: James Sleight, Associate Director, H-Net, Humanities and Social Sciences OnLine, Michigan State University, East Lansing, Michigan 48824-1120; or at the following Web page: www2.hnet.msu.edu/~oralhist/projects.html. 2. If the original interpretation of events is faulty in some way, memory can accurately represent this faulty interpretation. For example, Jolly Z. insists incorrectly, “They put a chemical in our food so that we did not menstruate later. There was a chemical in our food and we did not have menstrual periods” (Testimony of Jolly Z. and Rosalie W., 1979). Adele W. draws the same conclusion: “And you know how we suﬀered until we got back our periods. We were—. They gave us some certain pills to lose our periods. . . . I was very, very skinny, but I was like a balloon. Blown up. Because we didn’t have our periods” (Testimony of Adele W., 1982). These witnesses remember accurately that their periods went away, but they misinterpret the reason and accurately remember this misinterpretation. 3. The concepts of ﬂashbulb memory (Brown and Kulik, 1977), deep memory (Langer, 1991), situationally accessible memory (Brewin et al., 1996), verbatim memory (Reyna, 1998), core memory (Kraft, 2002), and emotional memory (chapter 3 here) all converge on the idea of two distinct representational systems in personal event memory. Although the diﬀerent systemic distinctions do not ﬁt together cleanly, the gist is that two levels of memory can be distinguished on the basis of phenomenal

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experience, clinical analysis, laboratory studies, and neurophysiological processes. A case can be made for further subdividing personal event memory, but in the context of Ockham’s razor, the results of my analysis of oral testimony encourage an integration of these distinctions to support a dual representation theory. 4. The following are characteristic examples of survivors crying during testimony and then expressing surprise at their emotion. Renee G. describes how her younger brother desperately pleaded for a hiding place to save his life. She then surprises herself when she begins to cry: “I didn’t think I would cry today. Sorry” (Testimony of Renee G., 1988). Josephine B. describes how her father escaped to England during the war and how the family was reunited afterward. When she talks of the reunion, she unexpectedly cries: “And then he was there. And he had a suitcase with him. I always—. I mean I love that in my memory. Big suitcase. And there was a pair of shoes he had for each of us.” Josephine then begins to cry and says to herself, “Stupid,” for breaking down (Testimony of Josephine B., 1992). Zezette L. discusses how she never talks with her brother about the Holocaust: “He knows I went back to Auschwitz. He cannot talk. He knows that I now talk, and forgive me. [Zezette begins to cry.] I don’t— I don’t usually become—.Thank God, learned not to cry this way. But, I guess I’m talking a little more than usual” (Testimony of Zezette L., 1980).

References Briere, J., & Conte, J. (1993). Self-reported amnesia for abuse in adults molested as children. Journal of Traumatic Stress, 6, 21–31. Brewin, C., Dalgleish, T., & Joseph, S. (1996). A dual representation theory of posttraumatic stress. Psychological Review, 103, 670–686. Brown, R., & Kulik, J. (1997). Flashbulb memories. Cognition, 5, 73–99. Burgess, A. W., Hartman, C. R., & Baker, T. (1995). Memory presentations of childhood sexual abuse. Journal of Psychosocial Nursing, 33, 9–16. Danieli, Y. (1988). Treating survivors and children of survivors of the Nazi Holocaust. In F. M. Ochberg (Ed.), Post-traumatic therapy and victims of violence (pp. 278–294). New York: Brunner/Mazel. Fivush, R., Haden, C., & Reese, E. (1995). Remembering, recounting, and reminiscing: The development of autobiographical memory in social context. In D. C. Rubin (Ed.), Remembering our past: Studies in autobiographical memory (pp. 341– 359). New York: Cambridge University Press. Harber, K. D. & Pennebaker, J. W. (1992). Overcoming traumatic memories In S.-Å. Christianson (Ed.), The handbook of emotion and memory: Research and theory (pp. 359–387). Hillsdale, NJ: Erlbaum. Hartman, G. H. (Ed.). (1994). Holocaust remembrance: The shapes of memory. Cambridge, MA: Blackwell. Hass, A. (1995). The aftermath: Living with the Holocaust. New York: Cambridge University Press. Herman, J. L. (1993). Sequelae of prolonged and repeated trauma: Evidence for a complex posttraumatic syndrome (DESNOS). In J. Davidson & E. Foa (Eds.), Posttraumatic stress disorder: DSM-IV and beyond (pp. 213–228). Washington, DC: American Psychiatric Press.

382

  

Herman, J. H., & Schatzow, E. (1987). Recovery and veriﬁcation of memories of childhood sexual trauma. Psychoanalytic Psychology, 4, 1–14. Hoﬀman, A., & Hoﬀman, H. (1994). Reliability and validity in oral history, In J. Jeﬀrey & G. Edwall (Eds.), Memory and History (pp. 107–130). Lantham, MD: University Press of America. Horowitz, M. J., & Reidbord, S. P. (1992). Memory, emotion, and response to trauma. In S.-Å. Christianson (Ed.), The handbook of emotion and memory: Research and theory (pp. 343–358). Hillsdale, NJ: Erlbaum. Hubbell, S. (1999). Waiting for Aphrodite. New York: Houghton Miﬄin. Intons-Peterson, M. J., & Best, D. L. (Eds.). (1998). Memory distortions and their prevention. New York: Wiley. Izzard, C. E. (1991). The psychology of emotions. New York: Plenum. James, W. (1890/1950). The principles of psychology. Vol. 2. New York: Dover. Janoﬀ-Bulman, R. (1985). The aftermath of victimization: Rebuilding shattered assumptions. In C. Figley (Ed.), Trauma and its wake (pp. 15–35). New York: Brunner/Mazel. Kluger, R. (2001). Still alive: A Holocaust girlhood remembered. New York: The Feminist Press at the City University of New York. Koriat, A., Goldsmith, M., & Pansky, A. (2000). Toward a psychology of memory accuracy. In S. T. Fiske, D. L. Schacter, & C. Zahn-Waxler (Eds.), The Annual Review of Psychology, 51, (pp. 481–537), Palo Alto, CA: Annual Reviews. Kotre, J. (1995). White gloves. New York: Free Press. Kraft, R. N. (1996, November). Memory in young children who survived the Holocaust. Paper presented at the 37th annual meeting of the Psychonomic Society, Chicago. Kraft, R. N. (1998a). Holocaust memory: Persistent recall of traumatic events. In R. R. Hoﬀman, M. F. Sherrick, & J. S. Warm (Eds.), Viewing psychology as a whole (pp. 375– 398). Washington, DC: American Psychological Association. Kraft, R. N. (1998b, November). Levels of awareness during traumatic events. Paper presented at the 39th Annual Meeting of the Psychonomic Society, Dallas. Kraft, R. N. (2000, November). Revealing mistakes in personal memory. Paper presented at the 41st Annual Meeting of the Psychonomic Society, New Orleans. Kraft, R. N. (2002). Memory perceived: Recalling the Holocaust. Westport, CT: Praeger. Langer, L. L. (1991). Holocaust testimonies: The ruins of memory. New Haven, CT: Yale University Press. Levi, P. (1989). The drowned and the saved (R. Rosenthal, Trans.). New York: Vintage. (Original work published 1986). Linton, M. (1986). Ways of searching and the contents of memory. In David C. Rubin (Ed.), Autobiographical memory (pp. 50–67). New York: Cambridge University Press. Loftus, E. F. (1993). The reality of repressed memories, American Psychologist, 48, 518–537. Loftus, E. F. (1994). The repressed memory controversy. American Psychologist, 49, 443–445. Loftus, E. F., Garry, M., & Feldman, J. (1994). Forgetting sexual trauma: What does

      

383

it mean when 38% forget? Journal of Consulting and Clinical Psychology, 62, 1177–1181. Nadel, L. (1994). Multiple memory systems: What and why, an update. In D. Schacter & E. Tulving (Eds.), Memory systems (pp. 39–63). Cambridge, MA: MIT Press. Olio, K. A. (1994). Truth in memory. American Psychologist, 49, 442–443. Reisberg, D., & Heuer, F. (1992). Remembering the details of emotional events. In E. Winograd & U. Neisser (Eds.), Aﬀect and accuracy in recall: Studies of “ﬂashbulb” memories (pp. 162–189). New York: Cambridge University Press. Reyna, V. F. (1998). Fuzzy-trace theory and false memory. In M. J. Intons-Peterson & D. L. Best (Eds.), Memory distortions and their prevention (pp. 15–27). New York: Wiley. Reyna, V. F., & Titcomb, A. L. (1997). Constraints on the suggestability of eyewitness testimony: A fuzzy-trace theory analysis. In D. G. Payne & F. G. Conrad (Eds.), Intersections in basic and applied memory research (pp. 157–174). Mahwah, NJ: Erlbaum. Robinson, J. A. (1995). Perspective, meaning, and remembering. In D. C. Rubin (Ed.), Remembering our past: Studies in autobiographical memory (pp. 199–217). New York: Cambridge University Press. Sarbin, T. R. (1986). The narrative as a root metaphor for psychology. In T. R. Sarbin (Ed.), Narrative psychology: The storied nature of human conduct (pp. 3–21), New York: Praeger. Sheingold, K., & Tenney, Y. T. (1982). Memory for a salient childhood event. In U. Neisser (Ed.), Memory observed: Remembering in natural contexts (pp. 201– 212). San Francisco: Freeman. Spence, D. P. (1982). Narrative truth and historical truth: Meaning and interpretation in psychoanalysis. New York: Wiley. Terr, L. (1994). Unchained memories: True stories of traumatic memories, lost and found. New York: Basic Books. Terr, L. (1996). True memories of childhood trauma: Flaws, absences, and returns. In K. Pezdek & W. P. Banks (Eds.) The recovered memory/false memory debate (pp. 69–80). San Diego: Academic Press. Testimony of Abe L. (1990, May). Videotape recording number T-1394, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Abraham P. (1984, August). Videotape recording number T-731, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Adele W. (1982, October). Videotape recording number T-213, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Aladar M. (1995, May). Videotape recording number T-2854, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Alan Z. (1984, June). Videotape recording number T-284, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Alex H. (1983, July). Videotape recording number T-210, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University.

384

  

Testimony of Alina Z. (1993, April). Videotape recording number T-2045, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Amelia B. (1994, December). Videotape recording number T-2740, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Arnold C. (1983, March). Videotape recording number T-363, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Beatrice S. (1982). Videotape recording number T-72, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Bessie K. & Jacob K. (1983, May). Videotape recording number T-206, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Blanche H. (1992, April). Videotape recording number T-2068, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Celia K. (1980, February). Videotape recording number T-36, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Celia K. (1987, October). Videotape recording number T-970, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Celina R. (1995, September). Videotape recording number T-3131, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Chana F. and Henry F. (1980, March). Videotape recording number T-81, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Clara L. (1993, May). Videotape recording number T-1850, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Clemens L. (1990, March). Videotape recording number T-1315, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Daniel F. (1980, February). Videotape recording number T-153, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Daniel F. (1988, April). Videotape recording number T-978, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Dori K. (1988, January). Videotape recording number T-969, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Edith P. (1980, February). Videotape recording number T-107, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Edith P. (1987, December). Videotape recording number T-974, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Emina N. and Miriam W. (1979). Videotape recording number T-144, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University.

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Testimony of Ernest R. (1987, May). Videotape recording number T-897, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Esther W. (1994, August). Videotape recording number T-2609, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Eva B. (1979, May). Videotape recording number T-1, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Eva B. (1988, April). Videotape recording number T-1101, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Eva L. (1982, May). Videotape recording number T-71, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Hanna F. (1980, February). Videotape recording number T-18, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Hanna F. (1987, October). Videotape recording number T-971, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Harry F. (1995, March). Videotape recording number T-2761, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Henry S. (1996, July) Videotape recording number T-3380, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Hilda S. (1993, June). Videotape recording number T-2148, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Irene W. (1982, November). Videotape recording number T-65, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Isabella L. (1989, May). Videotape recording number T-1270, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Jolly Z. (1983, January). Videotape recording number T-220, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Jolly Z. (1988, January). Videotape recording number T-971, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Jolly Z. & Rosalie W. (1979, August). Videotape recording number T-34, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Josephine B. (1992, May). Videotape recording number T-869, Fortunoﬀ Video Archive for Holocaust Testimonies,.New Haven, CT: Yale University. Testimony of Judith G. (1992, September). Videotape recording number T-1879, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Julien E. (1995, January). Videotape recording number T-2742, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Karl S. (1980, April). Videotape recording number T-173, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University.

386

  

Testimony of Kochevit P. (1979). Videotape recording number T-85, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Leo G. (1980, March). Videotape recording number T-158, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Leo G. (1988, March). Videotape recording number T-977, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Leon H. (1985, November). Videotape recording number T-628, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Leon W. (1979, May). Videotape recording number T-2, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Martin S. (1986, January). Videotape recording number T-641, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Martin S. (1988, May). Videotape recording number T-1091, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Mary E. (1984, March). Videotape recording number T-260, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Meir V. (1992, December). Videotape recording number T-1892, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Menachem S. (1979, July). Videotape recording number T-152, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Michael G. (1992, August). Videotape recording number T-1880, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Myra L. (1984). Videotape recording number T-299, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Nadia R. (1995, September). Videotape recording number T-3132, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Nina S. (1996, March). Videotape recording number T-3260, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Rena C. (1992, March). Videotape recording number T-2293, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Renee G. (1980, March). Videotape recording number T-5, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Renee G. (1988, March). Videotape recording number T-976, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Renee H. (1979, August). Videotape recording number T-50, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Robert K. (1984, May). Videotape recording number T-318, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Ruth A. (1994, October). Videotape recording number T-2678, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Sabina G. (1984, June). Videotape recording number T-287, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University.

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387

Testimony of Sabina S. (1985, November). Videotape recording number T-623, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Sally H. (1979, August). Videotape recording number T-3, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Sally H. (1989, March). Videotape recording number T-1154, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Samuel B. (1995, October). Videotape recording number T-618, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Susan S. (1991, November). Videotape recording number T-876, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Sybilla F. (1991, May). Videotape recording number T-1855, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Violet S. (1991, September). Videotape recording number T-1650, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Zezette L. (1980, July). Videotape recording number T-100, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Testimony of Zoltan G. (1979, August). Videotape recording number T-35, Fortunoﬀ Video Archive for Holocaust Testimonies. New Haven, CT: Yale University. Tolman, D. L., & Brydon-Miller, M. (Eds.). (2001). From subjects to subjectivities. New York: New York University Press. van der Kolk, B. A. (1994). The body keeps the score: Memory and the evolving psychobiology of posttraumatic stress. Harvard Review of Psychiatry, 1, 253–265. van der Kolk, B. A. (1996). Trauma and memory. In B. A. van der Kolk, A. C. McFarlane, & L. Weisaeth (Eds.), Traumatic stress: The eﬀects of overwhelming experience on mind, body, and society (pp. 279–302). New York: Guilford. van der Kolk, B. A., & Fisler, R. (1995). Dissociation and the fragmentary nature of traumatic memories: Overview and exploratory study. Journal of Traumatic Stress, 8, 505–525. Wagenaar, W., & Groeneweg, J. (1990). The memory of concentration camp survivors. Applied Cognitive Psychology, 4, 77–87. Wegner, D. M., & Schneider, D. J. (1989). Mental control: The war of the ghosts in the machine. In J. S. Uleman & J. A. Bargh (Eds.), Unintended thought (pp. 287– 305). New York: Guilford. Wells, G. L., Malpass, R. S., Lindsay, R. C. L., Fisher, R. P., Turtle, J. W., & Fulero, S. M. (2000). From the lab to the police station: A successful application of eyewitness research. American Psychologist, 55, 581–598. Wenzlaﬀ, R. M. & Wegner, D. M. (2000). Thought suppression. Annual Review of Psychology, 51, 59–91. Williams, L. M. (1994a). Recall of childhood trauma: A prospective study of women’s memories of child sexual abuse. Journal of Consulting and Clinical Psychology, 62, 1167–1176. Williams, L. M. (1994b). What does it mean to forget child abuse? A reply to Loftus,

388

  

Garry, and Feldman (1994). Journal of Consulting and Clinical Psychology, 62, 1182–1186. Winograd, E. (1992). Introduction. In E. Winograd & U. Neisser (Eds.) Aﬀect and accuracy in recall: Studies of “ﬂashbulb” memories (pp. 1–5). New York: Cambridge University Press. Winograd, E. (1994). The authenticity and utility of memories. In U. Neisser & R. Fivush (Eds.), The remembering self: Construction and accuracy in the selfnarrative (pp. 243–251). New York: Cambridge University Press. Winograd, E., & Neisser, U. (Eds.). (1992). Aﬀect and accuracy in recall: Studies of “ﬂashbulb” memories. New York: Cambridge University Press.

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abuse victims, physical memory retrieval in, 133, 265, 333 See also child sexual abuse (CSA) accessible memory in episodic memory, 352–353, 362, 381n.3 in Holocaust survivors, 360, 362, 365 accuracy-focused strategies, for aging memory, 293–294 adaptive numbness, in Holocaust survivors, 358–359, 379–380 adrenaline. See epinephrine adrenergic activity, in memory, 19, 104–105, 108 adrenocorticotrophic hormone (ACTH), release with stress, 80, 82 adult-guided reminiscing. See parentchild reminiscing affect emotional valence of, 4, 21–24; in elderly, 274–275, 284–287; visual vs. verbal, 32, 279–280, 286 with PTSD: as extreme, 144, 325; isolation of, 95, 97–99, 101, 111; negative vs. positive, 137– 138 in re-experiencing emotion, 362, 382n.4 with schizophrenia, 221–224

aging, emotional memory with, 272– 295 affective focus and nonaffective information, 284–287 Alzheimer’s disease, 59–60, 63–64, 283–284, 295n.1 deficits of, 59, 63, 82, 91, 272 emotional compensation hypothesis of, 273–274, 281–282, 289, 294– 295 flashbulb memories and, 287–289 goal-directed emotional memory hypothesis of, 272, 274–275, 281, 286, 293–294 as increasingly gratifying, 265n.2, 272–273, 275, 289–295 neurodegeneration in, 59–60, 63– 65 neutral vs. emotional information, 260–264, 273, 275–276, 281–284 processing changes with, 272–281; arousal decreases, 275–276; neural mechanism maintenance, 276–281; regulation effectiveness increases, 273–275; well-being improvement, 272–273 of shocking events, 287–289 summary of predictions for, 281, 294 valence factor, 274–275, 279, 281– 287, 295n.2 allostasis, stress and, 78–79



Alzheimer’s disease (AD) amygdala role in, 59–60 emotional memory and, 283–284, 295n.1 hippocampus role in, 59–60 neurodegenerative characteristics of, 63–64 ambiguity, role in emotional memory,

187

amino acids, excitatory, mediation of

stress, 45, 89–91 amnesia with amygdala damage, 48–49 of child sexual abuse, 317–319 forgetting as illusion of, 130–136, 149

misremembering of, 27–28 nonhuman primate model of, 44–45 psychogenic, 134–135 stress-induced (see forgetting)

amygdala, role in emotional memory, 12 autobiographical, 57, 59–60 in elderly, 276–277, 283, 286–287 emotion influence, 105, 147 gender differences in, 60–61 for gist vs. detail, 52–56 in humans, 47–61, 66 as integrative, 65–68 isolation of affect and, 98–100 lesion studies of, 46–52, 66 neurodegenerative characteristics

of, 64–65 neuroimaging of, 48, 56–58, 61, 63 in nonhuman animals, 44–47 in schizophrenia, 224 stress impact on, 96, 98–100 amygdala lesions, 46–52 disorders associated with, 46–47 memory damage from, 66; bilateral, 48–49; unilateral, 49–52 anger

in Holocaust survivors, 363, 380 influence on memory, 23–24, 30; impact of accurate remembering, 31–32 parent-child reminiscing about, 246–249 animals acute and chronic memory stressors in, 88–91 emotional memory in, 44–47





anime, for stimuli emotionality study, 21–22 antecedent-focused strategies, for

emotional control, 274 anxiety and anxiety disorders, 155–180 defense mechanisms for, 97–98, 102 encoding with, 156–158, 161–163, 167, 172–173, 176–177, 179–180 implicit memory in, 171–175, 180n.1

influence on memory: as bias, 93, 155, 157–158, 161–162, 176–179; for emotional information, 158– 175; encoding tasks and, 179– 180; intensity variable, 25–26; theoretical implications of, 175– 180

memory deficits in, 155–158 recall and: of autobiographical

memories, 158–160; of experimentally presented stimuli,

160–167 recognition memory in, 167–171 selective memory effects in, 155–180 trait: high level, 158–161, 167, 171– 172, 175; low level, 171–172; vs. state, 156 trauma-induced, 97, 102–103, 111 arousal, role in memory, 13, 36 in children, 254–255, 260–262 cognitive research on, 106–107, 109, 113n.10 context of, 18–20, 24, 43–44 in elderly, 275–276 in emotional continuum with

nonlinear effects, 43, 45, 54, 56, 106, 109 emotional valence vs., 22–23, 54, 56, 146, 156 heightened with PTSD, 97, 99–100, 146, 320–321 as increasing function, 24–26, 35 interruption of, 12–13, 16, 20 intrinsic vs. extraneous, 19–20, 24, 43–44 as narrowing attention, 7, 17–18, 35 physiological, 18–20, 275 selective in anxiety disorders, 156– 157, 161, 167 visual vs. thematic, 8–9, 14–18, 35– 36

artifact, in memory narrowing, 10–13 atrocity(ies). See trauma and traumatic memory attention affective focus of, by elderly, 284– 287 avoidant, by abuse victims, 139–141 control of: habit as detriment to, 200–205, 210n.4–n.5; impaired in nonhabitual tasks, 195–200, 210n.3; opposing habit through, 205–209 narrowing of, 7, 14–18, 35 selective, with anxiety disorders, 156–157, 161, 167, 179–180 stimulus salience and, 24 with traumatic events, 320; sustained vs. dissociative, 323–324 See also memory narrowing “attention magnets,” 15, 17, 21 autobiographical memory, 243 amygdala and, 57, 59–60 with anxiety disorders, 158–160 depressed states and, 187, 189, 193– 195; in Holocaust survivors, 364, 367, 380 detailedness and coherency of, 3–4, 30, 94–97, 262, 264 dysregulation factors of, 59, 63–64, 91, 112n.1 emotional development and, 244– 245 parent-child reminiscing and, 243– 244 PTSD impact on, 94, 97, 130, 136– 137 in schizophrenia, 235 as unique process, 42, 67–68, 95 autonomic nervous system, PTSD impact on, 97–99 aversive experiences. See negative experiences avoidance in children’s traumatic memory, 255–256, 260 in sexual abuse encoding, 139–141 awareness of previous trauma, in forgetting vs. remembering, 132, 134, 148–149 in schizophrenia (see conscious awareness)

subjective: in normal controls, 230– 232; prefrontal cortex role in, 101–102; in schizophrenia, 219– 221, 233 background details, in memory categorization, 8–10 basolateral amygdala (BLA), emotional memory role, 105 behavioral guilt, in Holocaust survivors, 373 benzodiazepines, influence on memory, 90 beta-blockers, impact on emotional memory, 12–13, 16, 20, 46, 105– 106 bias. See memory bias biopsychology, of trauma, 76–113 definitions for, 77–80 effects on brain, 80–84 effects on forgetting: hippocampus and, 94–100; prefrontal cortex and, 100–111 effects on memory, 12, 20–21, 45, 84–94 isolation of affect with, 95, 98–101, 111 overview of, 21, 76, 111–112 taxonomy for, 76–77 “body memories,” 97 body state changes, in schizophrenia, 221, 224 boundary extension, 10 brain aging effects on, 280; amygdala, 276–277, 283, 286–287; hemispheric asymmetry of, 279–280; prefrontal cortex, 277–279 effects of stress on, 80–84; forgetting as, 94–111; memory manifestations of, 84–94 See also specific anatomy brain imaging studies. See specific imaging technique brain lesion(s), impact on memory, 46–52, 66 brain state changes with aging, hemispheric asymmetry of 279–280, 221, 224–225 in schizophrenia, 221, 224–225





catecholamines, memory modulation and, 66–67, 97 categorization schemes for emotional memory research, 8– 10, 13, 108, 326 for relevant traumatic memory, 27– 28 causal relations, of emotion and memory vividness, 29–30 in children, 263–264 central details, of events (centrality) aging and, 272, 281, 286 cognitive research on, 106–111 in eyewitness memory, 311–312; of children, 330–332 role in memory, 7–10, 16 valence factor of, 21–22, 28–29 child sexual abuse (CSA), memory retrieval of accuracy of, 331–332 after repression, 317–319 avoidant encoding impact on, 139– 141 cognitive studies of, 136–139, 143 dissociation impact on, 323–325, 327 mechanisms of, 91–93, 110, 130– 132, 135, 316 reminiscing factor, 265, 318, 321 severity-disclosure correlation in, 316–317 children’s memories, 242–266 autobiographical, development of, 242–244 cognitive functioning and, 327–328, 330, 333 coping factors: developmental aspects of, 244–245, 328–333; gender socialization as, 245–250, 265, 329; narrative skills as, 264– 265; stressful memory and, 258, 262–264 emotional development and, 244– 245; in eyewitness memory, 327– 333 of emotional events: co-construction of, 242–243, 248, 263–264; parent-child reminiscing about, 245–250 of medical procedures, 252–253, 260, 264–265, 328, 330–331





of negative vs. positive experiences, 242–243, 246, 260–264, 328– 329; clinical disorders and, 330, 332–333 research strategies for, 265–266 of stressful and traumatic events, 250–262; accuracy of, 241, 251– 252, 330–332; arousal role, 254– 255, 260–262; avoidance in, 255–256, 260; cognitive functioning and, 253, 258–260, 264–265; emotional processing in, 245, 247–250, 258–260, 262– 264; Hurricane Andrew, 250, 254–260; interpersonal, 265; interviewing strategies, 251, 263– 264; parent-child reminiscing about, 242–243, 262–264; valence and, 242–243, 260–262 choice-supportive attributes, of memory in elderly, 286, 292–293 closed-ended questions, for interviewing children, 251 co-construction, of emotional memory in children, 242–243, 248, 263– 264 cognition and cognitive functioning with anxiety disorders, 155–158 attention control with: habit as detriment to, 200–205, 210n.4– n.5; impaired in nonhabitual tasks, 195–200, 210n.3; opposing habit through, 204–209, 366 in children, 327–328, 330, 333 in elderly, 279–280, 286–287 emotional memory and, 155; in oral testimonies, 347, 361, 381n.1; in re-experiencing emotion, 361– 363, 382n.4; research on, 106– 111, 113n.10–n.11 habitual: as control factor, 200– 209, 210n.4–n.5; in depressed states, 4–5, 186–188; in Holocaust survivors, 364, 366, 369 in Holocaust survivors: discontinuity of, 373–374; distraction strategies for, 374– 378, 380–381; habitual vs. controlled, 364, 366, 369 intrusive, color-naming paradigm for, 141–142, 165

in schizophrenia, 217, 221, 223, 235n.1

traumatic memory and, 93, 97–99, 362; in children, 253, 258–260; control factor, 79, 84; research on, 136–139, 143 coherence. See memory coherence color-naming paradigm, for intrusive

cognition, 141–142, 165 commission errors, in traumatic

memory, 86, 100, 110, 317 computerized tomography (CT), of

amygdala, 48 concentration ability, with depression, 196–197 concentration camps. See Holocaust survivors conscious awareness, in schizophrenia

emotional influence on, 218, 221, 230–232; normal controls of, 230–232 recognition memory with

subjective, 219–221, 232–233 research implications, 233–235 conscious recollection, 230–232, 234 in Holocaust survivors, 354–355, 365, 368 consistent memory, in Holocaust

survivors, 349–350, 355–356 context

of arousal stimulus, 18–20, 24; affective processing by elderly,

284–287; neural mechanism links to, 43–44, 67 in episodic memory, 77; stress impact on, 94–97, 99, 103, 110– 111, 112n.5 control and controllability

of cognitive attention: habit as

detriment to, 200–205, 210n.4– n.5; impaired in nonhabitual tasks, 195–200, 210n.3; opposing habit through, 204–209, 366 of stress, 79, 84, 101 coping mechanism(s)

in children: developmental aspects

of, 244–245, 328–333; gender socialization impact on, 245–250, 265, 329; narrative skills impact on, 264–265; stressful memory and, 258, 262–264

for threats: avoidant encoding as,

139–141; selective attention as, 156–158, 161, 167 core memory, 109 in episodic memory, 352–353, 381n.3 in Holocaust survivors, 353–354; reexperiencing emotions and, 362– 365, 382n.4 corticosterone, memory modulation

and, 45–46, 85 in animals, 88–89 corticotropin-releasing factor (CRF),

release with stress, 80, 82 cortisol level

in emotional memory, 105, 109 stress impact on, 82, 85–87, 112n.3; memory coherence and, 96–97, 101, 147 cortisone

anxiety disorders with, 97 impact on memory retrieval, 86–88 crime, influence on memory

in children, 251, 261 legal system and, 132–133, 309, 312–315, 318–319, 324, 334 in perpetrators, 135 prefrontal cortex role, 278 See also eyewitness memory

crying, by Holocaust survivors

re-experiencing during recall, 362– 365, 382n.4 re-experiencing with external cues,

368, 379 recall of, 357–358 culture. See social-cultural theory Cushing’s syndrome, stress hormones and, 82, 84, 101, 112n.3 cytokines, proinflammatory, influence

on memory, 90 date rape, 15–16 decision making, emotional

prefrontal cortex role in, 62 with PTSD dissociative tendencies,

325

declarative memory as emotional memory, 43–44 neural processing mechanisms for, 42–43, 45; as integrated, 65–68 deep memory, in episodic memory, 352, 381n.3





Deese-Roediger-McDermott (DRM) paradigm, for stress effect on false memory, 109–110, 143–144, 327 defense mechanisms, for memory with anxiety, 97–98, 102 delusions, role of emotional processing in. See schizophrenia dementia. See Alzheimer’s disease (AD) dendrites, stress-induced atrophy of, 81, 90, 99 prevention of, 89, 91 dentate gyrus, effects of stress on, 81– 82 depression and depressed mood, 186– 210 in elderly, 272–273 habits of memory with, 186, 188– 195; in autobiographical experience, 193–195, 364, 367, 380; congruency of, 191–193 habits of thought with, 186–188 influence on memory, 29, 93, 101, 186 memory as object in, 189, 195; appropriate use of, 197–200, 209n.2; effortful construction of, 196–197; for mood-congruency, 191–193 mood-congruent recall with, 189– 193, 209n.1 mood-congruent suppression with, 201–203, 208, 210n.5 negative thinking associated with, 186–188, 192 with PTSD, 137–138 self-control with: as impaired in

nonhabitual tasks, 195–205, 210n.3–n.5; opposing habit through, 205–209 detailedness, of memory. See memory detail details, of events background, 8–10 central (see central details) peripheral (see peripheral details) dexamethasone, impact on memory retrieval, 85–86, 110 directed-forgetting paradigm for anxiety disorders, 164 for depressed states, 202–203, 210n.5





for trauma-related material, 139– 141 disasters. See natural disasters; shocking events disengagement, impaired, in depressed states, 201–205, 210n.4–n.5 dissociation of memory tasks in schizophrenia, 218–219, 221 with traumatic memory, 28, 129– 130, 132–133, 135; avoidant encoding with, 139–141; avoidant recall for, 255; in children, 330, 332–333; cognitive studies of, 136–139, 143; false-memory formation and, 318–319, 324– 326; semantic confusion about, 148–149; in witnesses and victims, 317, 319, 323–324, 330 distinctiveness, role in memory construction, 11 distraction for emotional memory in Holocaust survivors, 374–378; as “getting worse,” 375–377; importance of meaningful, 374–375, 380–381; rebound effects of, 377–378 for habitual thoughts, 188, 196– 197, 208 distress. See stress doctor/mechanic stimuli, memory construction and, 6, 12, 19, 105 domain-specific material, memory system for, 43, 52 dopamine influence on memory, 89–90 in schizophrenic state, 224–225 dual representation theory, of episodic memory, 352–353, 356, 381n.3 durability, of emotional memory. See long-term memory dysphoria, 186 habits of memory with, 186, 188– 195, 209n.1 habits of thought with, 187–188 self-control with: as impaired in nonhabitual tasks, 195–205, 210n.3–n.5; opposing habit through, 205–209 dysthymia, 273

Easterbrook hypothesis, of arousal and memory, 7, 14, 16–18, 35 aging and, 275–276 elaboration hypothesis in parent-child reminiscing: autobiographical memory and, 243–244, 246–248, 262; impact on coping, 258, 262–264, 318 of threats and anxiety disorders,

174, 176–178 See also memory enhancement elderly’s memories. See aging emotion and emotionality in eyewitness memory, 308–315, 334 in Holocaust survivors, 351–352, 354–359, 381; with liberation, 357; re-living of, 352, 355, 361– 369, 382n.4 impact on memory: biological, 12, 20–21; in children, 327–329; detailedness and coherency in, 28–30, 94–97, 112n.5, 264; in elderly, 281–284; intensely negative variable, 26–28; intensity factor, 4, 24–26, 32–33; as positive promotion, 7–8, 10, 33, 35; prefrontal cortex role in, 100– 102; reaction assessment in, 30– 33; in schizophrenia, 222–223, 225; socialization factor, 244– 245; source factor, 11, 13–15, 282, 314; type factor, 18–20, 97, 111, 112n.6; as undermining, 10, 35; valence factor, 20–24, 28, 54, 146, 156, 203; visual vs. thematic, 8–9, 14–18, 35–36 emotion-criticizing style, 248, 250 emotion-explaining style, 248 emotion-focused strategies, of elderly impact on nonaffective information, 284–287 as increasingly gratifying, 265n.2, 272–273, 275, 289–295 for interpersonal problem-solving, 274–275 emotion-induced recognition bias, 314–315, 325 emotional blunting in schizophrenia, 222–223; word free-recall investigation of, 227– 230

stress-induced, 97–100, 102; in Holocaust survivors, 357–358, 379–380 emotional compensation hypothesis, for aging, 273–274, 281–282, 289, 294–295 emotional control. See self-regulation emotional development, in children, 244–245 eyewitness memory and, 327–333 emotional disturbances, in schizophrenia, 221–225 of affect, 221–224 of body state, 221, 224 of brain state, 221, 224–225 cognitive evaluation of, 217, 221, 223, 235n.1 research implications, 225 emotional goals, with aging, 272, 274–275, 281, 286, 293– 294 emotional masks, of Holocaust survivors, 380 emotional memory accuracy of, 4–13, 35–36; detailedness and coherency vs., 28–30, 94–97, 112n.5, 262 anxiety disorders and, 155–175 in children, 242–266 in depression, 186–210 durability of (see long-term memory) in elderly, 272–295 eyewitness, 308–334 in Holocaust survivors, 347–382 literature review of, 103–111 neuroanatomy of, 12, 42–68 in nonhuman animals, 44–47 research perspectives for (see research)

in schizophrenia, 217–236 traumatic stress impact on, 98– 100, 112n.6–113n.8 (see also stress; trauma and traumatic memory) emotional numbing/numbness in Holocaust survivors, 357–358, 379; as adaptive, 358–359, 379– 380 with PTSD, 97–100 emotional pain, in Holocaust survivors, 365–366, 381





emotional processing by children, 258–260; of negative experiences, 245, 247–250, 258– 260 by elderly, 272–281; arousal decrease, 275–276; neural mechanisms for, 276–281; regulation effectiveness increase, 273–275; well-being improvement, 272–273 in schizophrenia, 217, 221, 223, 235n.1

emotional reaction(s)

as extreme, with traumatic memory

retrieval, 144, 146–148 inhibition of: frontal cortex role in,

100–102; during stress, 79, 84, 101

remembering: accurate assessment with, 31–33; influence on memory, 30–31 emotional scenes, as threatening, 156– 157

emotional self-concept

in children, development of, 245, 248, 250 in elderly, 273–275 in Holocaust survivors, 367, 371, 373, 378–380 emotional stimuli/events, memory for,

3–36 with amygdala damage, 48–53 arousal continuum with nonlinear

effects, 43, 45, 54, 56, 106, 109 in children, 327–333 cognitive research on, 106–111, 113n.10

construction of, 6, 8–10 declarative, 43–44 in elderly, 273, 275–276, 281–283 intrinsic vs. extraneous, 18–20, 24, 43–44 neural processing in: in humans,

47–63; as integrative, 65–68, 76– 77; in nonhuman animals, 44–47 parent-child reminiscing about,

245–250, 318 prefrontal cortex role, 62–63 PTSD and dissociation impact on, 327 Sternberg task for evaluation of,

217, 223, 235n.1





emotional valence in children, 260–264, 281–283 in elderly, 274–275, 279, 281–287, 295n.2

in eyewitness memory, 309–311, 321

impact on memory, 20–24, 28–29, 54, 146, 156, 203 in schizophrenia, 222–223, 225– 230, 236n.2 in survivors (see Holocaust

survivors)

emotional well-being in elderly, 272–273, 294–295 in Holocaust survivors, 355–356 emotionality effect in memory, 4, 24–26, 32–33 in schizophrenia, 217, 227–230; conscious awareness and, 232– 233; research implications, 233– 235

encoding, of memory

with aging, 291–292, 294 in amnesia confirmation, 131–132, 135–136, 149 amygdala role in, 66, 147 arousal impact on, 106–107 avoidant style for coping, 139–141 as flawed in Holocaust survivors,

348, 353, 381n.2 initial, 34, 56, 60 integrative modulation of, 65–68, 76–77 prefrontal cortex role in, 63, 100 in schizophrenia, 219, 226 as selective in anxiety disorders,

156–158, 161–163, 167, 172–173, 176–177, 179–180 stress impact on, 88, 94–97, 99, 109, 139, 149, 323 epilepsy, intractable, temporal

lobectomy for, 48 epinephrine, memory modulation and,

19, 45–46, 66 episode(s), basic elements of

remembering, 352 episodic memory, 77 cognitive research on, 106–111 disruption of: with PTSD, 98–99, 102–103, 111, 113n.8; in schizophrenia, 218–220

hippocampal function and, 80 retrieval process of, 95; in Holocaust survivors, 134, 146, 356–361, 365–366 stress impact on, 84, 111; acute, 85– 88; chronic, 91–94, 99, 112n.4 in traumatic memory, 352, 362 event material(s), in emotional memory

ambiguity of, 187 comparisons across studies, 8–9 role of nature of, 4, 6–7 trauma-related, 139–141 exercise, influence on memory, 19–20 explicit memory, 77 dissociation of in schizophrenia, 218–219 in habits of thought, 189, 195; appropriate use of, 197–200, 209n.2; effortful construction of, 196–197 hippocampal function and, 80 stress impact on, 147–148, 171, 175 expression, of emotions, parent-child reminiscing impact on, 245–250 external arousal/cues in episodic memory, 353; of Holocaust survivors, 361, 366–369 in memory construction, 18–20, 24 rumination and, 187, 364, 376 extraneous emotion, in memory construction, 18–20, 24, 43–44 eyewitness memory, 308–334 in children, 251–252, 261–262; accuracy of, 328–329; age as factor, 327–328; clinical disorders and, 332–333; of medical procedures, 252–253, 260, 264– 265, 328, 330–331; of sexual abuse, 91–93, 110, 130–132, 135, 265, 316–319, 331–332; for traumatic events, 330–332 of crime, 7, 107, 135, 251, 261, 278 developmental considerations of, 327–333 emotion and, 308–315, 334; accuracy of negative events, 308– 311, 328–329; biases in, 313–315, 325, 329; central vs. peripheral details in, 311–312; long-term durability of, 312–313

as false, with dissociation, 318–319, 324–326 legal system impact on, 132–133, 309, 312–315, 319, 324, 334 psychopathology implications for, 319–327; in children, 330, 332– 333; dissociative tendencies and, 318–319, 323–326, 330, 332; PTSD and, 319–324, 332 research strategies for, 308–309, 315, 319, 327, 333 survivor guilt with, 372 for traumatic events, 315–319; in children, 330–332; repression and recovery of, 317–319; special mechanisms in, 316–317 fading aging and, 289–291, 295 of mishaps and triumphs, 31–32, 34–35 false alarms, memory biases in, 314– 315, 325 false memory of emotional vs. neutral events, 33– 34, 109–111 in schizophrenia, 220–221 in “space alien abductees,” 144–146 of traumatic events, 142–143; cognitive studies on, 136–139, 143; with dissociative tendencies, 318–319, 324–326 fear in Holocaust survivors, 356–367; associated emotions of, 358–360; re-experiencing with external cues, 366–369 parent-child reminiscing about, 246–249 trauma-induced, 102–103 See also phobia(s)

fear conditioning, classical, 44–45 feelings, toward emotional event accuracy in remembering, 4–5, 10, 20, 30–31, 103 influence on memory, 31–32 flashbacks, trauma-induced, 4, 94, 102–103 flashbulb memories accuracy of, 34–35, 42, 289 aging and, 287–289





flashbulb memories (continued)

consequentiality of, 35 in Holocaust survivors, 352, 381n.3 role of emotion in, 5–6, 32, 111 specialized production process for,

34, 42 forebrain

role in emotional memory, 63, 65, 67 see also prefrontal cortex (PFC)

forensic context, of emotional memory

emotion-induced recognition bias

in, 314–315, 325 eyewitness, 251, 256, 258, 308–309, 311, 321 false-memory in, 315, 324, 326 forgetting

difficulty of: with depressed states,

186, 202–203; for trauma-related material, 26–27, 94–100, 139– 140, 164, 210n.5 in schizophrenia, 227, 233 stress-induced, 100–111; cognitive approach to, 106–111; emotion and memory literature on, 103– 111; frontal cortex models of, 100–103; learning/ neuroscientific approach to, 104– 106

of traumatic events, 129–149; amnesia vs., 130–136, 149, 318; cognitive research on, 136–139, 143; complex mechanisms of, 26– 27, 94–100, 164, 210n.5; dispelling semantic confusion,

148–149; distortion with, 141– 143; evidence adduced for, 130– 136; flashbacks and, 4, 94, 102–103; of material related to, 139–141; recovery mechanisms of, 27–28; repression vs., 361; sexual abuse and, 317–319; in “space alien abductees,” 144–146; types of memory in, 94, 96, 111, 112n.5–113n.7 fragmentation, of memory

emotion influence on, 103–104 stress-induced, 94–95, 102–103, 111 functional relevance. See plot-relevant items funny memories. See positive experiences





fuzzy trace theory, 109 of episodic memory, 353 GABA, mediation of stress on memory, 45, 89–90 gender differences, in memory

amygdala activity and, 60–61 in children, 244–250, 265, 329 in elderly, 283 generalized anxiety disorder (GAD)

selective memory in, 158–159, 161– 163, 168, 172–173, 176 trauma-induced, 97, 111 gist information

amygdala and memory of, 52–56 cognitive research on, 107–111, 113n.10–n.11, 143 emotional valence of, 2, 108, 143, 146, 156; in elderly, 284–287 in episodic memory, 353, 381n.3 gender differences and, 61 in memory categorization, 8–10, 13, 108, 326 glucocorticoid-administration studies

in animals, 88–89, 91 in humans, 85–87; limitations of, 87–88 glucocorticoid antagonists, impact on

memory, 85 glucocorticoids

hippocampal function and:

disruption of, 80–81, 95–96; evidence for volume reduction,

82–83; potentiation of, 82, 90 as indicator of stress, 79–80 memory modulation and: in

animals, 88–91; emotion influence on, 108–109; in humans, 66–67, 85–86, 99 prefrontal cortex function and, 101 glucose

influence on memory: amygdala

metabolism, 56; serum level, 19, 25, 46 influence on mental health, 278 glutamate, mediation of stress on

memory, 45, 89–91 goal-directed emotional memory

hypothesis, for aging, 272, 274– 275, 281, 286, 293–294 granule cells, effects of stress on, 81

gratification, emotional, as increasing with aging, 265n.2, 272–273, 275, 289–295 grief accurate recall of, 31 in Holocaust survivors (see crying) guided imagery protocol memory distortion with, 142–143 for memory distraction, 377 guilt, in Holocaust survivors behavioral, 373 survivor, 369–373 habits of memory in depressed states, 188–195, 364 in Holocaust survivors, 364, 376; distraction strategies for, 366, 374–378, 380–381 self-control with: as detriment to, 200–205, 210n.4–n.5; as strategy to oppose, 205–209, 366 habits of thought cognitive control for, 205–209; in Holocaust survivors, 366, 374– 378; as impaired in nonhabitual tasks, 195–205, 209n.2–210n.3 as depression feature, 187–188 influence on memory, 4–5, 186 hallucinations neurobiology of, 102–103 in “space alien abductees,” 145 happiness in Holocaust survivors, 350, 358, 376–377 parent-child reminiscing about, 246 recall of: with amygdala damage, 50–53; vividness vs. accuracy of, 4–5, 10, 20, 103 See also positive experiences hatred, in Holocaust survivors, 359, 374 hemispheric asymmetry, of emotion, with aging, 279–280 herpes simplex encephalitis, 47 hippocampus effects of stress on, 80–82; evidence for atrophy, 82–84, 112n.2; fragmentation and, 95–97; glucocorticoid-administration studies of, 85–89, 91; hormonal mediation of, 80–81, 88–91

role in emotional memory: in elderly, 276–277; in humans, 61– 62, 147; as integrative, 65–68, 77; isolation of affect and, 98–100; neurodegenerative characteristics of, 64–65; in nonhuman animals, 44; stress impact on, 98–100 Holocaust survivors, emotional memory in, 347–382 destiny and, 371 distraction for, 374–378; as “getting worse,” 375–377; importance of meaningful, 374–375, 380–381; rebound effects of, 377–378 as enduring: guilt, 369–373; as result of cognitive discontinuity, 373–374 impact of sharing vs. not sharing, 366, 380–381 physiological arousal with, 355, 361–362, 368–369, 375, 382n.4 qualitative study of, 347–381; accuracy concepts, 348–350, 381n.2; conclusions from, 378– 381; of distraction, 374–378; of endurance, 369–374, 378; methodology, 347–350, 381n.1; of re-experiencing, 352, 355, 361– 369, 382n.4; of recall, 356–361; testimony excerpts, 350–352; trauma, 352–356, 381n.3 re-experiencing emotion through, 361–369; due to external cues, 366–369; examples of, 352, 355; multiple systems for, 361–362; during recall, 362–366, 382n.4; in repeated testimony, 364–366 recall of, 134, 146, 356–361, 381; associated emotions, 358–359; events separate from emotions, 359–360; fear, 356–357, 360, 366–369; forgetting vs., 360–361; numbness with, 357–359, 379– 380; re-experiencing emotion during, 362–366, 382n.4 repression of, 360–361 self-concept with, 367, 371, 373, 378–380 homeostasis, stress and, 78 hope, emotional memory for generation of, 36





hopelessness, 29 hormonal modulation, of memory system emotions and, 104–106 in humans, 66–67, 80–81 in nonhuman animals, 45–46, 88–91 horrific events. See trauma and traumatic memory humor

accurate recall of, 31 influence on memory, 21 Hurricane Andrew, children’s recall of, 250, 254–260 hydrocortisone, impact on memory retrieval, 86–88 hyperarousal, in Holocaust survivors, with re-living emotional memory, 355, 361–362, 368–369, 382n.4 hypermnesia, with trauma, 102 hypervigilance, with PTSD, 97, 99– 100, 321 hypothalamic-pituitary-adrenal (HPA)

axis

cognitive research on, 109, 113n.10 impact of aging on, 91 stressor activation of, 79–80, 89 imagery protocol

guided: memory distortion with, 142– 143; for memory distraction, 377 script-driven, for “space alien

abductees, 145–146 imagination inflation paradigm, for

memory distortion, 142–143, 352 imaging studies, of brain. See specific

imaging technique

implicit memory, 77 anxiety disorders and, 171–175, 180n.1

dissociation of in schizophrenia,

218–219 stress impact on, 147–148, 362 incomplete memory, in Holocaust

survivors, 349 inferences

anxiety disorders and ability to

draw, 156, 321 schema-based: for memory recall in

elderly, 284–287; for memory reconstruction, 34, 108, 110–111, 113n.11, 194





inhibition

of emotional response, frontal cortex

role in, 100–102 impaired, in depressed states, 200– 205, 210n.4–n.5 of traumatic memory recovery, 148– 149

intensity factor, of emotional memory,

4, 24–26, 32–33 intentionality

of forgetting, 139–140, 164, 202– 203, 210n.5 in habits of thought, 187, 189, 195, 197

interleukin-I (IL-I), influence on

memory, 90 interpersonal problems, emotionfocused strategies for solving, 274–275 interpersonal violence, children’s

recall of, 130, 265 interpretative memory, in Holocaust

survivors, 376, 379, 381 interviewing strategies

for children’s memories, 251, 263– 264

for forensics, 314, 326 intrinsic emotion, in memory

construction, 18–20, 43–44 intrusion errors, in traumatic memory,

30, 34, 110, 166, 321, 353 intrusive recollection, of traumatic

material, 140–142, 166, 321, 353

inverted-U function, of memory and

stress. See Yerkes-Dodson law

ironic-process theory, 208 for memory distraction, 377–378 Jewish persecution. See Holocaust survivors laboratory studies

of emotional memory, 6–7; induction methods, 15–18 of traumatic memory, 136–139, 355 language, as children’s trauma recall

factor, 253, 258–260, 264 impact on coping, 264–265 lateralization, of emotional cognition,

with aging, 279–280

learning theory of habits of thought, 187, 189, 195, 197, 208 of stress-induced forgetting, 104– 106 legal system, influence on traumatic memory construction, 132–133, 309, 312–315, 318–319, 324, 334 lipoid proteinosis, 47 long-term memory, emotional dissociation impact on, 323–327 eyewitness, 312–313 in Holocaust survivors, 352, 355– 356, 378 mechanisms of, 59–60, 63–65, 82, 90, 157 with PTSD, 322–323 long-term potentiation (LTP), as hippocampal response, 82, 90 “lost memories,” 26–28 magnetic resonance imaging (MRI) of amygdala, 48, 56–58, 61, 277, 284 of hippocampal atrophy, 82–83, 112n.2, 277 of prefrontal cortex, 63, 100 for research on aging, 284, 291 malingering, 135 material, for memories. See event material(s) media, influence of, 5 medial temporal lobe memory system in humans, 42–43, 47–61; cool vs. hot, 98–100 integrative mechanisms of, 65–68, 77 neurodegenerative characteristics of, 64–65 in nonhuman animals, 44–47 medical procedures, children’s memory for, 328, 330–331 recall of, 252–253, 260, 264–265 memory age-related decline in, 59, 63, 82, 91 effects of stress on (see stress; trauma and traumatic memory) as object, 189, 195; appropriate use of, 197–200, 209n.2; effortful construction of, 196–197; in mood-congruency, 191–193; in mood-suppression, 201–202, 208, 210n.5

physiological models of, 18–20, 45, 82, 107, 275 taxonomy for nature of, 76–77 memory accuracy in children: of child sexual abuse, 331–332; of stressful events, 241, 251–252, 330–332 of emotional events, 4–13, 21, 35– 36; detailedness and coherency vs., 28–30, 94–97, 112n.5, 262; in feelings toward, 4–5, 10, 20, 30– 31, 103 in eyewitness memory, 308–311, 328–329 in flashbulb memories, 34–35, 42, 289, 352 of happiness vs. sadness, 4–5, 10, 20, 103 in Holocaust survivors, 348–350, 381n.2 of personal vs. public events, 4–5, 13, 31, 33 strategies for, in aging memory, 293–294 in traumatic memory, 4–5, 34–35, 42, 289 vividness vs., with negative experiences, 5, 308–311 memory assessment role in emotions, 30–33 white-noise method of, 173–174 memory bias anxiety-related, 155, 157–158; encoding tasks contribution to, 179–180; with experimentally presented stimuli, 160–167; limited evidence for, 176–178; with panic, 178–179 decision making and, 62, 325– 326 in depressed states, 186–195, 201 in elderly, 275, 289–294 in eyewitness memory, 313–315, 325, 329 research coding schemes, 15 memory coherence, 28–30 autobiographical, 3–4, 30, 94–97, 262, 264 stress impact on, 94–97, 101, 112n.5, 112n.7, 147, 262, 264





memory-consolidation, postevent

glucocorticoid impact on, 88, 105 neural mechanisms for, 44, 49, 67– 68

physiological arousal impact on, 20, 45, 107 memory construction emotional context of, 4–5 role in perpetuating schizophrenia, 217–218, 221, 230–233 role of scrutiny in, 11–12 memory deficits

in anxiety disorders, 155–158 in depressed states, 196, 198, 209n.2; self-control for improving, 205–209 in elderly, 59, 63, 82, 91, 272 in schizophrenia, 218–221; subjective states of, 219–221, 233; task dissociation, 218–219, 221

with stress: acute, 85–88; in animals, 46–47, 88–91; chronic, 91–94, 99, 112n.4; correlation to severity, 317, 322; frontal cortex role in, 100–103; in humans, 66– 67, 112n.4–n.5, 113n.9–n.11; mnemonic, 321–323; paradoxical with PTSD, 92–94, 98–99, 110– 111, 129–136; as selective vs. general, 93–94 with trauma, 12, 20–21, 45; biopsychology of, 84–94, 102– 103, 112n.1–n.3, 112n.6–n.8 See also forgetting memory detail

amygdala role in, 52, 54–56 background, 8–10 coherence with, 28–30, 262, 264; autobiographical, 3–4, 30, 94– 97, 262, 264; of emotional events, 28–30, 94–97, 112n.5, 262

emotion influence on, 28–30, 109– 110

gender differences in, 61, 244–250, 265, 329 stress impact on, 7, 94–97, 112n.5 memory distortion, with trauma, 142– 143, 352–353





memory enhancement

in anxiety disorders, 156–157 human neural mechanisms for, 43, 61–62; hormonal, 80–81; as integrative, 65–68, 106, 109; with PTSD, 99–100 with PTSD, 320–323 See also elaboration hypothesis

memory errors in episodic memory, 352–353 of traumatic events: in children, 251–252; emotion influence on, 106–107, 109, 111; initial encoding of, 348–349, 353, 381n.2; intrusion, 30, 34, 36, 110, 166, 321, 353; omission vs. commission, 86, 100, 110, 317; reconstruction, 5, 27–28, 35–36, 95

memory narrowing

arousal role in, 7, 15–18, 35 as artifactual, 10–13 emotion source impact on, 11, 13–15 emotion valence impact on, 21–22, 203

studies of, 7–10 memory organization, temporal

framework for, 8–10, 96 See also spatio-temporal memory

memory reconstruction

schema-based inferences for, 34, 108, 110–111, 113n.11; with aging, 284–287; with depression, 194

of traumatic events, errors in, 5, 27– 28, 35–36, 95 memory recovery. See recall and

recollection

memory rehearsal with emotional events, 107–108 of flashbulb events, 34–35 promotion of retention, 4–5, 376– 377

with traumatic event, 320, 376 memory suppression

as emotional control, 274 for Holocaust survivors, 374–378; as “getting worse,” 375–377; importance of meaningful, 374– 375; rebound effects of, 377–378

mental disorders. See psychopathology; specific disorder metamemory, in Holocaust survivors, 349 mineralization, in amygdala lesions, 47–48 mineralocorticoids, in memory modulation, 101 misleading questions, for interviewing children, 251 mood-congruency, with depression indirect tests of, 191–193, 198, 209n.1 memory suppression and, 201–203, 208, 210n.5 recall and, 186, 189–193; induction of, 190, 209n.1 mood disorders habits of memory with, 186, 188– 195 habits of thought with, 187–188 influence on memory, 93, 156, 186, 273 narrative memory, 109, 146 in episodic memory of Holocaust, 352–354, 364, 366, 380–381 narrative skill, in children impact on coping, 264–265 as trauma recall factor, 253, 258– 260 narrative smoothing, 109–111 narrowing of attention, 7, 14–18, 35 See also memory narrowing natural disasters recall by children, 250, 254–260, 265; parent-child reminiscing impact on, 262–264 recall by elderly, 283–284 negative experiences amnesia for, 26–28 biological effects of, 21 cognitive research on, 106–111, 136–139, 143 emotional resolution of, by children, 245, 247–250, 258–260 emotional valence of, 22–24, 29, 54, 56, 203; in children, 242–243, 246, 260–264, 328–329, 332– 333; conscious awareness and,

230–232; in elderly, 273–275, 289–291, 295, 295n.1; in schizophrenia, 222–223, 225, 227–230, 233 eyewitness memory accuracy of, 308–311 fading memory of, 31–32; in elderly, 289–291, 295 habitual memory of, 188–195 parental-child reminiscing about, 242–243, 246–250 recall of, 103–104, 106; with amygdala damage, 50–53; with anxiety disorders, 156–167, 170– 171; by children, 250–262; vividness vs. accuracy of, 4–5, 10, 20, 308–311 See also stress; trauma and

traumatic memory

negative-priming paradigm, of inhibition in depressed states, 201–202, 210n.4 negative thinking, associated with depression, 186–188, 192 neural modulation, of memory system cool vs. hot, 98–100 in elderly, 276–281 emotions and, 104–106, 109, 113n.10, 147 in humans, 43, 61–62, 100 integrative mechanisms of, 65–68, 76–77 in nonhuman animals, 45–47 neuroanatomy, of emotional memory, 12, 42–68 cool vs. hot systems in, 98–100 fragmentation role, 95–97, 113n.7– n.8 gender differences in, 60–61 human amygdala in, 47–61 human hippocampus in, 61–62 impact of aging on, 276–280 integrative systems, 65–68, 76–77 literature review of, 103–111 neurodegeneration and, 63–65 in nonhuman animals, 44–47 prefrontal cortex in, 44, 61–63 processing systems, 42–44 stress impact on, 21, 45–47, 78–79, 82–85, 112n.3, 316, 323–324





neurobiology

of isolation of affect, 95, 98–101, 111 of trauma-induced flashbacks, 102– 103

neurodegeneration amygdala and, 59–60 emotional memory and, 63–65 hippocampus and, 59–60 neurogenesis, stress-induced, 81 neuroimaging

in emotional memory research: of

amygdala, 48, 56–58, 61; of prefrontal cortex, 63 See also specific imaging technique

neurons, effects of stress on, 81–82 neuropsychological evaluation

of amygdala: for gist vs. detail

memory, 52, 54–56; with lesion damage, 48–53, 66; neuroimaging correlation to, 56– 58, 61, 63 for emotional memory, 104–106 for PTSD, 92–94 neuroscientific research, on emotion and memory, 104–106 neutral stimuli/events emotional valence of, 21–23, 30, 107–108, 203; in children, 242– 243, 246, 260–264, 328–329, 332–333; conscious awareness and, 230–233; in elderly, 260– 264, 273, 275–276, 281–284; in Holocaust survivors, 376–377 eyewitness memory accuracy of, 308–311 false memories of, 33–34, 109 memory construction of, 6, 8–9, 11 recall with amygdala damage, 48– 53, 59 NMDA receptor blockade, for

prevention of dendrite atrophy,

91

nonaffective information, affective processing by elderly, 284–287 nondeclarative memory, neural processing mechanism for, 42–43 in animals, 44–45 nonemotional events. See neutral stimuli/events nonhabitual tasks, impaired cognitive control in, 195–200, 210n.3





noradrenergic neurotransmitters,

memory modulation and, 45–46, 67, 89 norepinephrine, influence on memory,

19, 89, 96, 101 emotion and, 105 numbness. See emotional blunting;

emotional numbing/numbness

obsessive compulsive disorder (OCD),

selective memory in, 158, 164– 165, 169, 173–174, 178 omission errors, in traumatic memory,

86, 100, 110, 317 open-ended questions

for forensics, 314 for interviewing children, 251, 263 oral testimony(ies) of Holocaust survivors, qualitative study of, 347–381, 381n.2– 382n.4 traumatic memory characteristics of, 352–356, 381n.3 of war survivors, 347, 381n.1 orbitofrontal cortex

emotional memory and, 62–63, 65 impact of aging on, 278–280 original phenomenal experience, in episodic memory, 352–353, 381n.3 overgeneral memories, with PTSD,

326

panic disorder

memory bias in, 158, 167, 178–179 retrieval of threatening information

in, 165–166, 170, 174 parent-child reminiscing about emotional events, 245–250 about stressful events, 242–243, 262–264, 318 autobiographical memory and, 243– 244

style vs. content in, 244, 247, 262– 264

parents

as abusers, 130, 265 as co-constructors of children’s

memory, 242–243, 248, 263–264 Pavlovian conditioning, classical, 44– 45

perceptual encoding hypothesis, of threats and anxiety disorders, 176–178 perceptual priming, for memory in schizophrenia, 218–220, 223 peripheral details, of events cognitive research on, 106–111, 286 in eyewitness memory, 311–312; of children, 330–332 role in memory, 7–10, 16 valence factor of, 21–22, 28 perpetrators, of crime memory retrieval in, 135 parents as, 130, 265 personal events, memory accuracy of, 4 personality profile, in traumatic memory retrieval, 137–139 phenytoin (Dilantin), for prevention of dendrite atrophy, 91 phobia(s) social, selective memory in, 158– 159, 163–165, 168–169, 173 spider, memory research on, 10–11 physical abuse victims, memory retrieval in, 133, 265, 333 physiological arousal as decreasing with aging, 275–276 emotion intensity variable, 25–26 intensely negative variable, 26–28 in memory construction, 18–20, 45, 82, 107, 275 with re-experiencing emotion in Holocaust survivors, 355, 361– 362, 368–369, 375, 382n.4 with stress, 79, 98–100, 102 pleasant memories. See positive experiences plot-relevant items emotional valence of, 21, 23 in memory categorization, 8–9, 107 Pollyanna tendency, in schizophrenia, 217, 226–227, 232, 234, 236n.2 positive experiences accurate remembering of feelings about, 4–5, 10, 20, 31, 103 biological effects of, 21 emotional valence of, 21–24, 29, 54, 56, 203; in children, 242–243, 246, 260–264, 328–329, 332– 333; conscious awareness and,

230–232; in elderly, 273–275, 289–295; in schizophrenia, 217, 222–233, 236n.2 eyewitness memory accuracy of, 308–311 fading memory of, 31–32 parent-child reminiscing about,

246

positron emission tomography (PET) of aging brain, 276–277 research applications of, 56–57, 100, 136 post-traumatic stress disorder (PTSD) affect with: as extreme, 144, 146– 148; isolation of, 97–99, 101, 111; negative vs. positive, 137–138 cognitive studies of, 136–139 diagnostic criteria for, 91–92, 135, 320 eyewitness memory and, 319–323; with dissociation, 318–319, 324– 326 false memory in, 136–139, 142–146, 318–319, 324–326 heightened arousal with, 97–100, 146, 320–321 hippocampal atrophy with, 83–84, 112n.2 material-related to: forgetting, 139– 141; intrusion of, 140–142, 166, 321, 353 memory deficits with, 92–94, 110– 111, 129–136; in children, 332– 333; correlation to severity, 317, 322; dissociative tendencies impact on, 318–319, 323–327; mnemonic, 321–323; as paradoxical, 98–99 memory enhancement with, 320– 323 prevalence rates of, 92 selective memory in, 158–160, 164– 165, 169, 173–174 stress hormone levels with, 84, 112n.3 potentiation, stress-induced forms of, 82, 90 predictions, of future, emotional memory for, 36 prednisone, impact on memory retrieval, 85–86, 110

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

prefrontal cortex (PFC) role in emotional memory: in elderly, 277–279; in humans, 61– 63, 100; as integrative, 65–68; isolation of affect and, 98–101; in nonhuman animals, 44; stress impact on, 100–111 stress-induced forgetting in, 100– 111; cognitive approach to, 106– 111; emotion and memory literature on, 103–111; learning/ neuroscientific approach to, 104–106; theoretical models of, 100–102; trauma-related, 102– 103 primed burst potentiation (PBP), by hippocampus, 82 problem solving by elderly, 274–275, 279–280 emotional memory for generation of, 30, 36 psychiatric questionnaires, in traumatic memory retrieval, 137– 138 psychopathology, impact on emotional memory in children, 330, 332–333 as dysfunctional dysregulation, 91, 112n.1 See also specific disorder public events, memory accuracy of, 4– 5, 13, 31, 33 reappraisal, as emotional control, 274–275 recall and recollection with anxiety disorders, as selective, 157–158, 167; of autobiographical memories, 158–160; of experimentally presented stimuli, 160–167 conscious, 230–232 of emotional memory: accuracy of, 4–13, 21, 35–36; autobiographical, 57, 59–60; as biased by elderly, 279, 289–294; with bilateral amygdala damage, 48–49, 66; by children, 250–262; cognitive studies on, 136–139, 143; failure with intensely negative, 26–28; with frontal cortex damage, 100–





102; hippocampal atrophy and, 83–84, 112n.2; impairment with stress, 83–94, 112n.2, 112n.4– 113n.11; intrusive, 140–142; semantic confusion about, 148– 149; sharing vs. not sharing impact on, 102, 113n.8, 366, 380– 381; with unilateral amygdala damage, 49–52; vividness vs., 4–5, 10, 20, 29, 103; working backward from, 33–34 of emotional reactions, 30–33 of explicit vs. implicit memory, 77, 147–148, 175 habitual, of negative experiences, 189–195 in Holocaust survivors: associated emotions, 358–359; of emotions, 134, 146, 356–361, 381; events separate from emotions, 359– 360; of fear, 356–357, 360, 366– 369; forgetting vs., 360–361; numbness with, 357–359, 379– 380; re-experiencing emotion during, 362–366, 382n.4 mood-congruent, 186, 189–193, 209n.1 of nonaffective information, by elderly, 284–287 in schizophrenia: emotion and, 226– 230; memory task dissociation and, 218–219, 221; subjective states of consciousness and, 219– 221, 233 of traumatic memory, 27, 94–100, 110–111, 129–139, 250; after repression of, 27–28, 132, 317– 319; in witnesses, 315–319 recall error. See memory errors recognition memory anxiety disorders and, 167–171 in children, 251–252 in depressed states, 197–200, 210n.3 in schizophrenia: conscious awareness and, 219–221; emotional words influence on, 232–233 reconstruction errors, in traumatic memory, 5, 27–28, 35–36, 95 “red-out,” 135

re-experiencing, of emotional reality in Holocaust survivors, 352, 355, 361–369, 382n.4 sharing vs. not sharing impact on, 102, 113n.8, 366, 380–381 rehearsal. See memory rehearsal relational memories as elderly focus, 274–275 neural processing mechanism for, 43 parent-child reminiscing and, 245– 246, 248–250, 263 Remember/Know (R/K) procedure, for memory impairment in normal controls, 230–232 in schizophrenia, 219–220, 232–234 reminiscing of child sexual abuse, 265, 318, 320–321 by elderly, 294–295 by Holocaust survivors, 364, 376; distraction strategies for, 364, 376, 380–381 vs. talking about present emotions, 3, 245 See also parent-child reminiscing repression, of traumatic memory in children, 317, 330, 332–333 cognitive studies on, 136–139, 143 forgetting vs., 361 in Holocaust survivors, 360–361 mechanisms of, 43, 98, 129–130, 133, 135 recall after, 27–28, 132, 317–319 semantic confusion about, 148– 149 research, on emotional memory categorization schemes for, 8–10, 13, 15, 27–28, 108, 236 children and, 265–266 cognitive approach to, 106–111, 113n.10–n.11, 286; on forgetting trauma, 136–139, 143 eyewitness, 308–309, 315, 317–319, 327, 333–334 further needs for, 13, 24, 26, 33, 111, 289 generalizability of, 13–15, 86 in Holocaust survivors, 360–361 learning approach to, 104–106 neuroimaging in, 48, 56–58, 61, 63, 100, 136, 284, 291

neuroscientific approach to, 104– 106 oral testimonies used in, 347, 381n.1 perspectives for, 3, 6–7, 13, 15–18 schizophrenia and, 225, 233–236 response-focused strategies, for emotional control, 274 retention factors influencing, 4–5 in Holocaust survivors, 376–377 retention interval, in assessing emotional memory, 376 retrieval, of memory. See recall and recollection retrieval cues for memory: with anxiety disorders, 159–167, 178; in children, 251– 254; semantic confusion with traumatic, 148–149, 159 in mood-congruent memory, 186– 187, 191–193, 202 right-hemisphere hypothesis, of problem solving by elderly, 279– 280 rumination. See habits of thought sadness parent-child reminiscing about, 246–250 recall of, 23–24, 290; vividness vs. accuracy of, 4–5, 10, 20 in survivors (see crying)

See also negative experiences

satisfaction, emotional, in elderly, 273 as increasingly gratifying, 265n.2, 272–273, 275, 289–295 schematization, for memory reconstruction, 34, 108, 110–111, 113n.11 with depression, 194 in elderly, 284–287 in Holocaust survivors, 373–374 schizophrenia, 217–236 conscious awareness in, 218, 233– 235; emotional influence on, 221, 230–232; normal controls of emotional influence, 230–232; recognition memory and, 219– 221, 232–233

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

schizophrenia (continued) emotional disturbances in, 221–225; of affect, 221–224; of body state, 221, 224; of brain state, 221, 224– 225; cognitive evaluation of, 217, 221, 223, 235n.1; research implications, 225 emotional memory interaction with, 225–233; conclusions about, 233– 235; conscious awareness influence on, 221, 230–233; as influential, 217–218; literature review of, 225–227, 236n.2; recall performance in, 227–230 memory impairment in, 218–221; subjective states of, 219–221, 233; task dissociation, 218–219, 221 scripts for memory reconstruction, 110– 111, 113n.11 by “space alien abductees,” 145–146 selective memory in anxiety disorders, 155–180 in schizophrenia, 218–219 self-concept. See emotional selfconcept self-control. See self-regulation self-defining, in emotional selfconcept, 245, 248 self-focus, emotional, in elderly, 284– 287 self-in-relation, in emotional selfconcept, 245, 248 self-referential tasks of habitual memory, 189–190, 194– 195, 203 in selective memory with anxiety, 172–177 self-regulation, of emotions by children, 245, 248, 250 by elderly, 273–275 impaired: with habits of thinking, 200– 205, 210n.4–n.5; in nonhabitual tasks, 195–200, 210n.3 opposing habit through, 205–209 semantic memory in anxiety disorders, 161, 166, 174, 177 in elderly, 284–285 with PTSD dissociative tendencies, 324–326

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

recall implications of, 77, 193, 220, 231 serotonin, influence on memory, 89 sexual abuse victims children as (see child sexual abuse (CSA)) memory in, 15–16 sharing, of traumatic memories, impact on recollection, 102, 113n.8, 366, 380–381 shocking events, flashbulb memories of

accuracy of, 5, 34–35, 42, 289 aging and, 287–289 role of emotion in, 5–6, 32, 111 short-term memory, impairment of, hippocampal atrophy with, 83– 84, 112n.2 signal detection analysis, in selective memory, 168–169 simulation. See laboratory studies situationally accessible memory, in episodic memory, 352–353, 381n.3 social-cultural theory of children’s memories, 243–244; emotional development, 243–244, 327, 329; parent-child reminiscing context, 245–250 Holocaust applications of, 373–374, 376–377 social phobias, selective memory in, 158–159, 163–165, 168–169, 173 socialization, in emotional development of children, 244–245, 327, 329 of elderly, 274–275, 294 gender impact on, 245–250, 265, 329 socioemotional selectivity theory, 274–275 source-monitoring, in emotional memory, 11, 13–15 with aging, 282–283, 285, 287–289 eyewitness, 314–315 “space alien abductees,” emotional memory in, 144–146 spatio-temporal memory with aging, 279–280 in episodic memory, 352–353, 369 framework for organization, 8–10, 96

glucocorticoid impact on, 85, 88, 96 hippocampal function in, 80, 95–96 spider phobics, memory research on, 10–11 startle reflex, with PTSD, 97, 99–100 Sternberg task, for cognitive evaluation, of emotional events, 217, 223, 235n.1 stimuli doctor/mechanic, memory construction and, 6, 12, 19, 105 emotional (see emotional stimuli/ events) emotional valence of (see negative experiences; positive experiences) experimentally presented, selective recall with anxiety, 160–167 nonemotional (see neutral stimuli/ events) stimuli emotionality study, animation for, 21–22 stress biopsychology of: effects on brain, 80–84; effects on forgetting in hippocampus, 94–100; effects on forgetting in prefrontal cortex, 101–102; effects on memory, 84– 94 chronic, 314; comorbidities impact, 29, 93–94, 101; episodic memory and, 91–94, 99, 112n.4; intensity variable, 25–26 coping mechanisms for: avoidance as, 139–141, 156–158, 161, 167; in children, 244–250, 258, 262– 265, 328–333 definition of, 77–80, 250–251 effects on memory, 84–94; acute, 85–88, 110, 314; in animals, 46– 47, 88–91; in children, 250–264, 328–332; chronic, 25–26, 29, 91–94, 101, 314; data review, 84–85, 112n.3; emotion influence on, 103–111, 113n.10; eyewitness, 309–313; in humans, 66–67, 321–322; long-term durability, 312–313, 322–323; as reversible, 88, 91, 112n.4; schizophrenia and, 222–223; traumatic, 12, 20–21, 45, 84– 94

physiological arousal with, 79, 98– 100, 102 See also trauma and traumatic memory stress hormones as indicator of stress, 78–79, 82 memory modulation and, 21, 45–47, 85; emotion influence on, 104– 106, 110, 147; in witnesses and victims, 316 with PTSD, 84, 112n.3 stress receptors, in frontal cortex, 101 stressor, definition of, 78–80, 112n.1 Stroop color-naming paradigm anxiety disorders and, 165, 168 for intrusive cognition, 141–142 PTSD memory bias in, 320–321 subjectivity, of emotionality in normal controls, 230–232 prefrontal cortex role in, 101–102 research implications, 234–235 in schizophrenia, 219–221, 233– 235 suicide, 16, 29 survivor guilt, 369–373 survivors. See Holocaust survivors; victims target event emotions differential favor of, 24, 28 peak vs. end snapshots of, 33 temporal lobectomy for intractable epilepsy, 48 memory impact of, 49–51, 54 temporal memory in Holocaust survivors, 368–369 See also spatio-temporal memory thematic information cognitive research on, 106–111, 113n.10–n.11 emotional valence of, 22–23 in memory construction, 8–9, 14– 18, 35–36 thought suppression. See habits of thought; memory suppression threat(s) anxiety disorders and: information retrieval with, 160–168, 171–172, 174–175; memory elaboration with, 176–178; panic as bias for, 178–179

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

threat(s) (continued) coping mechanisms for: avoidant encoding as, 139–141; in children, 245–250, 258, 262–265; selective attention as, 156–158, 161, 167 memory bias with, 178–179, 313– 315, 325 transfer-appropriateness, in habitual memory, 196–197, 199, 207 trauma and traumatic memory biopsychology of, 76–113; effects on brain, 80–84; effects on forgetting, 112n.5–113n.8; hippocampus and, 94–100; prefrontal cortex and, 100–111; effects on memory, 84–94, 112n.5; emotional memory in, 12, 20–21, 45; hippocampal atrophy studies, 83–84, 112n.2; overview of, 21, 76, 111–112, 112n.1; taxonomy for, 76–77 construction of: avoidant encoding, 139–141; emotion influence, 106– 111, 112n.6–113n.8; legal system and, 132–133, 309, 312–315, 318–319, 324, 334; sharing and, 102, 113n.8, 366, 380–381 definitions of, 78–80, 112n.1 dissociation with, 28, 129–130, 132–133, 135; avoidance and, 139–141, 255; cognitive studies of, 136–139, 143; false-memory formation and, 136–139, 142– 146, 318–319, 324–326; semantic confusion about, 148–149; in witnesses and victims, 317, 319, 323–324 eyewitness, 315–319; amnesia research on, 317–319; special mechanisms of, 316–317 flashbacks of, 4, 94, 102–103 forgetting, 129–149; amnesia vs., 130–136, 149; cognitive research on, 136–139; common assumptions about, 129–130; complex mechanisms of, 26–27, 94–100; dispelling semantic confusion, 148–149; evidence adduced for, 130–136; later recovery of, 27–28, 132, 317–319;





of material related to, 139–141; in “space alien abductees,” 144–146; types of memory in, 94, 96, 111, 112n.5–113n.7 in Holocaust survivors: characteristics of, 352–356, 381n.3; qualitative study methods for, 347–352, 381n.1–n.2 intrusion of, 140–142, 166, 321, 353 memory distortion with, 142–143 neurobiological account of, 97–100 prolonged (see Holocaust survivors) recall and recovery of: after repression, 27–28, 132, 317–319; in children, 250–262, 330–332; cognitive studies on, 136–139, 143; disruptive reactions and, 98–99, 102–103, 111, 113n.8; in elderly, 287–289; errors in, 5, 30, 33, 35–36, 166, 251; filling in with, 110–111; as healing, 130; with repetitive events, 130; as special, 146–148; vividness vs. accuracy of, 4–5, 10, 20 recategorization of relevant, 27–28 repression of, 43, 98, 129–130, 133, 135–139; recovery mechanisms, 28, 132, 317–319 survivor guilt in, 369–373 See also post-traumatic stress disorder (PTSD) “tunnel memories,” 22 uncinate fasciculus fiber bundle, in autobiographical memory retrieval, 60 “undoing,” as anxiety defense, 97–98, 102 unfamiliar/unusual stimulus, memory construction of, 11, 15 unpleasant memories. See negative experiences Urbach-Weithe disease, 12, 47–48 vagus nerve, body-state information transmission through, 46, 67 valence, of emotion. See emotional valence ventral striatum, role in emotional memory, 65, 67

verbatim memory in episodic memory, 352–353, 381n.3 stress impact on, 85, 87–88 victims, emotional memory in

amnesia research on, 317–319 children as, 130, 251–252, 261, 265 (see also child sexual abuse [CSA])

distress impact on, 309–311, 313 legal system impact on, 132–133, 309, 312–315, 318–319, 324, 334 of persecution (see Holocaust

survivors)

of sexual abuse, 91–93, 110, 130– 132, 135–141, 265 “space alien abductees” as, 144–146 special mechanisms of, 316–317 of trauma (see trauma and traumatic

memory) weapon impact on, 311–312 violence, children’s recall of, 251–252, 261–262 interpersonal, 265 (see also child sexual abuse [CSA]) visual information basic-level, in memory categorization, 8–9 processing of with aging, 279–280, 286 visually induced emotion in memory construction, 8–9, 14– 18, 35–36 valence factor of, 22–23, 28

vividness emotion influence on, 29–30; in children, 263–264 memory accuracy vs., 4–5, 10, 20; with negative experiences, 5, 308–311 war veterans, emotional memory in,

91–93, 95, 146 cognitive studies on, 137, 142, 320–321 oral testimonies of, 347, 381n.1 recall of, 134–135, 159, 174 weapon focus effect

hypodermic needle example, 17– 18

on memory construction:

eyewitness, 311–312; negative, 7, 10, 14, 107; positive, 22

white-noise method, of implicit

memory assessment, 173–174 witnesses, emotional memory of. See

eyewitness memory

working memory, 100 PTSD impact on, 320–322 Yerkes-Dodson law, of arousal and memory, 24–26, 35 challenges to, 25–26, 254 in children, 254–255 stress effect as, 46–47, 146–147, 253

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