Neurobiology and Treatment of Traumatic Dissociation: Towards an Embodied Self [Paperback ed.] 0826106315, 9780826106315

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Lanius Paulsen Corrigan

Neurobiology and Treatment of Traumatic Dissociation Toward an Embodied Self

T

his is the first book to synthesize emerging research in the neurobiology of attachment, trauma, and affect with new developments in effective clinical interventions. Encompassing the contributions of leading researchers and practitioners, it offers neuroscientifically based understanding and practical guidance for clinicians working to heal people affected by traumatic dissociation. The text discusses current neuroscientific research on dissociation and other types of traumatic stress including attachment, affective neuroscience, polyvagal theory, structural dissociation, and information processing theory. This includes the translation of important work with laboratory animals into clinical applications and the dissemination of research about all levels of the brain from the brainstem to the neocortex. The text integrates concepts from the affective and cognitive neurosciences and the study of consciousness. It describes a comprehensive model that guides treatment of traumatic sequelae, and integrates this model with stage-oriented treatment and such therapeutic interventions as EMDR, somatic and body psychotherapy approaches, ego state therapy, and adjunctive pharmacological interventions. Readers are given hands-on practical guidance regarding clinical decision making, enabling them to make sound choices about interventions that will facilitate optimal treatment outcomes.

Key Features: ◆ Offers a truly comprehensive treatment approach to traumatic stress syndromes and dissociation ◆ Provides accessible, leading-edge research in neuroscience relevant to our understanding of attachment, traumatic stress, and dissociation ◆ Contains hands-on suggestions about how to integrate EMDR and somatic and body psychotherapy approaches with ego state therapy, and adjunctive pharmacological interventions ◆ The only text to encompass all levels of the brain beginning at the brainstem ISBN 978-0-8261-0631-5

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9 780826 106315

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“Through a skilled blending of emerging neuroscientific knowledge about emotional processes of mammalian brains and emerging clinical insights, each of the 22 chapters of this exceptional book will repeatedly provoke ‘aha’ moments of discovery. . . . The future of the field lies in credible neuropsychological syntheses, as superbly represented in this book.” – From the Foreword by Jaak Panskeep, PhD

Neurobiology and Treatment Traumatic Dissociation

Ulrich F. Lanius, PhD, Sandra L. Paulsen, PhD, Frank M. Corrigan, MD, Editors

Neurobiology and T reatment of T raumatic Dissociation Toward an Embodied Self

Editors

Ulrich F. Lanius Sandra L. Paulsen Frank M. Corrigan

Neurobiology and Treatment of Traumatic Dissociation

Ulrich F. Lanius, PhD, is a registered psychologist in West Vancouver, British Columbia, Canada, with a practice in clinical and neuropsychology. He has a particular interest in brain–behavior relationships with regard to attachment, trauma, and dissociation. His training includes eye movement desensitization and reprocessing (EMDR; EMDR Institute facilitator and EMDRIA approved consultant), sensorimotor psychotherapy, as well as neurofeedback. He specializes in the treatment of trauma and attachment-related problems, working from a client-centered perspective, integrating EMDR, body therapy, ego state interventions, and neurotherapy. He has presented in North America as well as internationally, and has authored and coauthored a variety of book chapters and articles on both the treatment and the neurobiology of dissociation. Sandra L. Paulsen, PhD, is a clinical and consulting psychologist who has accompanied many people on their extraordinary healing journeys for over two decades. She is a senior practitioner and instructor of advanced EMDR procedures and ego state therapy. She received 2 years of training in somatic therapy. She has published and spoken widely on the use of ego state therapy and EMDR to resolve complex and dissociative conditions. She is an EMDR Institute facilitator and EMDR International Association certified practitioner, consultant, and advanced specialty workshop instructor. She is a fellow of the International Society for the Study of Trauma and Dissociation. She has trained hundreds of mental health professionals in these special procedures since 1993. Frank M. Corrigan, MD, is a consultant psychiatrist in Argyll, Scotland. Formerly full time, he now works part time in trauma therapy in Argyll and privately in Glasgow and at Manor Hall, Doune. His encounters in general psychiatry with the effects on suicidality of early trauma led to training in dialectical behavior therapy, clinical hypnosis, EMDR, sensorimotor psychotherapy, and, most recently, brainspotting. He has an interest in understanding the impact of trauma on clinical presentations through awareness of laboratory work on stress and trauma and how this can be integrated with neuroscientific enquiry in humans.

Neurobiology and Treatment of Traumatic Dissociation Toward an Embodied Self

Ulrich F. Lanius, PhD, Sandra L. Paulsen, PhD, and Frank M. Corrigan, MD Editors

Copyright © 2014 Springer Publishing Company, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of Springer Publishing Company, LLC, or authorization through payment of the appropriate fees to the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, 978–750-8400, fax 978–646-8600, [email protected] or on the Web at www.copyright.com. Springer Publishing Company, LLC 11 West 42nd Street New York, NY10036 www.springerpub.com Acquisitions Editor: Sheri W. Sussman Production Editor: Shelby Peak Composition: Newgen Imaging ISBN: 978-0-8261-0631-5 e-book ISBN: 978-0-8261-0632-2 14 15 16 17 / 5 4 3 2 1 The author and the publisher of this work have made every effort to use sources believed to be reliable to provide information that is accurate and compatible with the standards generally accepted at the time of publication. The author and publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or in part, from the readers’ use of, or reliance on, the information contained in this book. The publisher has no responsibility for the persistence or accuracy of URLs for external or third-party Internet websites referred to in this publication and does not guarantee that any content on such websites is, or will remain, accurate or appropriate. Library of Congress Cataloging-in-Publication Data Neurobiology and treatment of traumatic dissociation : towards an embodied self / [edited by] Ulrich F. Lanius, Sandra L. Paulsen and Frank M. Corrigan. p. ; cm. Includes bibliographical references. ISBN 978-0-8261-0631-5—ISBN 978-0-8261-0632-2 (e-ISBN) I. Lanius, Ulrich F., editor. II. Paulsen, Sandra, editor. III. Corrigan, Frank M., editor. [DNLM: 1. Dissociative Disorders—therapy. 2. Brain—physiopathology. 3. Stress Disorders, Traumatic—   therapy. WM 173.6] RC553.D5 616.85’23–dc23 2014006322

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Contents

Contributors   ix Foreword by Jaak Panskepp, PhD   xi Preface   xv Introduction: The Ubiquity of Dissociation by Sandra L. Paulsen and Ulrich F. Lanius   xix

PART I. NEUROBIOLOGY Introduction: Dissociation and Neurobiology   1 Ulrich F. Lanius 1.  Dissociation: Cortical Deafferentation and the Loss of Self   5 Ulrich F. Lanius, Sandra L. Paulsen, and Frank M. Corrigan 2. Threat and Safety: The Neurobiology of Active and Passive Defense Responses   29 Frank M. Corrigan 3.  Peritraumatic Dissociation and Tonic Immobility: Clinical Findings   51 Michelle J. Bovin, Elise Ratchford, and Brian P. Marx 4. A Social–Cognitive–Neuroscience Approach to PTSD: Clinical and Research Perspectives   69 Ruth Lanius, Paul Frewen, Anthony Nazarov, and Margaret C. McKinnon 5.  Dissociation and Endogenous Opioids: A Foundational Role   81 Ulrich F. Lanius 6. Attachment, Neuropeptides, and Autonomic Regulation: A Vagal Shift Hypothesis   105 Ulrich F. Lanius

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  7. Defense Responses: Frozen, Suppressed, Truncated, Obstructed, and Malfunctioning   131 Frank M. Corrigan   8. The Clinical Sequelae of Dysfunctional Defense Responses: Dissociative Amnesia, Pain and Somatization, Emotional Motor Memory, and Interoceptive Loops   153 Frank M. Corrigan   9.  Shame and the Vestigial Midbrain Urge to Withdraw   173 Frank M. Corrigan 10.  Attachment and Attachment Repair   193 Frank M. Corrigan, Alistair Wilson, and Deirdre Fay 11. Dissociation, EMDR, and Adaptive Information Processing: The Role of Sensory Stimulation and Sensory Awareness   213 Ulrich F. Lanius and Uri Bergmann

PART II. TREATMENT Introduction: Dissociation and Psychotherapy   243 Sandra L. Paulsen and Ulrich F. Lanius 12. Seeing That Which Is Hidden: Identifying and Working With Dissociative Symptoms   247 Sandra L. Paulsen and Ulrich F. Lanius 13.  The Compassionate Self    269 Frank M. Corrigan, Alistair Wilson, and Deirdre Fay 14.  Stabilization Basics    289 Sandra L. Paulsen and Joan Golston 15.  Stabilizing the Relationship Among Self-States    321 Sandra L. Paulsen and Joan Golston 16. Alexithymia, Affective Dysregulation, and the Imaginal: Resetting the Subcortical Affective Circuits    341 Sandra L. Paulsen, Katie O’Shea, and Ulrich F. Lanius 17. Fractionating Trauma Processing: TOTEMSPOTS and Other Attenuating Tactics    367 Sandra L. Paulsen and Ulrich F. Lanius

Contents  vii

18.  Accelerating and Decelerating Access to Self-States    383 Sandra L. Paulsen 19. Integrating Body and Mind: Sensorimotor Psychotherapy and Treatment of Dissociation, Defense, and Dysregulation    399 Pat Ogden and Janina Fisher 20.  Temporal Integration of Early Trauma and Neglect    423 Sandra L. Paulsen 21.  Toward an Embodied Self: EMDR and Somatic Interventions    447 Ulrich F. Lanius and Sandra L. Paulsen 22. Opioid Antagonists and Dissociation: Adjunctive Pharmacological Interventions    471 Ulrich F. Lanius and Frank M. Corrigan

Index   499

Contributors

Uri Bergmann, PhD—Private Practice, Commack and Bellmore, New York Michelle J. Bovin, PhD—National Center for PTSD, VA Boston Healthcare System; Boston University School of Medicine, Boston, Massachusetts Frank M. Corrigan, MD—Consultant Psychiatrist, Argyll, Scotland Deirdre Fay, MSW, LICSW—Center for Integrative Healing, Boston, Massachusetts Janina Fisher, PhD—Trauma Center, Boston, Massachusetts; Sensorimotor Psychotherapy Institute, Boulder, Colorado Paul Frewen, PhD—Departments of Psychiatry, and Psychology, Western University of Canada, London, Ontario, Canada Joan Golston, DCSW, LCSW—Private Practice, Seattle, Washington; ISSTD Board of Directors, McLean, Virginia

Brian P. Marx, PhD—National Center for PTSD, VA Boston Healthcare System; Boston University School of Medicine, Boston, Massachusetts Margaret C. McKinnon, PhD—Department of Psychiatry and Behavioral Neurosciences, McMaster University, Hamilton, Ontario, Canada Anthony Nazarov, PhD Cand.—Department of Psychiatry and Behavioral Neurosciences, McMaster University, Hamilton, Ontario, Canada Pat Ogden, PhD—Founder and Director, Sensorimotor Psychotherapy Institute, Boulder, Colorado Katie O’Shea, MA—Private Practice, Nampa, Idaho; EMDR-HAP, Hamden, Connecticut Sandra L. Paulsen, PhD—Private Practice, Bainbridge Island, Washington

Ruth Lanius MD, PhD—Department of Psychiatry, Neuroscience, Western University of Canada, London, Ontario, Canada

Elise Ratchford, BA—National Center for PTSD, VA Boston Healthcare System, Boston, Massachusetts

Ulrich F. Lanius, PhD—Private Practice, West Vancouver, British Columbia, Canada

Alistair Wilson, MD—Consultant Psychiatrist, Glasgow, Scotland

ix

Foreword: Toward a Neuroaffective Understanding of Troubled Minds

The diverse contributions to this book share insightful, indeed profound, appreciations of neuropsychological dynamics of stressed minds and how they can be helped to emerge from the overwhelming effects of excessive negative affects. This exceptional volume integrates diverse neurobiological perspectives on understanding how minds succumb to trauma, in order to provide skilled guidance on how to coordinate our modern understandings of the diverse resulting brain–mind changes with novel therapeutic strategies to optimally manage the affective sequelae of excessive stress. An integrated understanding of the affective networks of human and animal brains and their imbalances is writ large in this interprofessional compendium. This book offers 22 chapters of productive integration between neuroscientific analyses (the focus of the first 11 chapters) and clinical insights (the next 11). In successive chapters we move from clear discussions of the emotional processes of the brain—knowledge arising from modern brain imaging as well as crossspecies analyses of the neuroanatomies and neurochemistries of affective brain circuits and their responses to stress—toward exceptionally insightful ways to deal with the varieties of posttraumatic stress disorders. Within this synthesis of modern neuroscientific and psychotherapeutic knowledge, we find insights about the patterns of disorganization within overstressed brains and new evidence-based therapeutics that may help troubled minds to heal—to emerge toward neuropsychological wholeness—more effectively than ever before. It has become clearer during the past few decades that for optimal understanding of human psychiatric issues we must concurrently understand the neurobiologies of mammalian brains and the accompanying affective dynamics of both human and animal minds, and how both need to be envisioned from modern evolutionary perspectives. Rarely have these lines of thought been blended as skillfully as here. To xi

xii  Foreword

do this well, there is no reasonable alternative but to devote equal consideration to the ancestral passions of our animal past and our uniquely human capacity to think and peer into the future. Our raw emotional feelings, which arise from ancient brain regions we share with other animals, energize and direct higher cognitive processes, which begin to flow in narrow, ruminative ways in overstressed minds. Throughout this book, one finds well-measured interprofessional arguments that concurrently avoid excessively ruthless neural reductionism as well as neurobiologically unbridled mentalizing. Rather, neural and psychological perspectives are blended to yield a rich tapestry of understanding, pregnant with therapeutic implications. By effectively using evidence from our brethren (animals), the discussions in this book avoid strict behavioristic perspectives, which have commonly ruled preclinical theorizing in the past, and move toward more nuanced visions of how our understanding of human and animal minds, brains, and behaviors can be harmoniously integrated. Contributions to this book offer rich and nuanced understandings of basic social emotions and attachment processes, allowing us to understand how higher order emotions such as guilt and shame arise from more fundamental substrates and how various developmental landscapes predispose minds and brains to become profoundly scarred. However, it is becoming increasingly clear that such wounds can be healed effectively if we apply our increasing understanding of the emotional processes of the brain with revolutionary therapeutic maneuvers, such as eye movement desensitization and reprocessing (EMDR) procedures, which have now been repeatedly found to be exceptionally effective in countering the devastating psychological effects of stress. Through a skilled blending of emerging neuroscientific knowledge about emotional processes of mammalian brains and emerging clinical insights, each of the 22 chapters of this exceptional book will repeatedly provoke “aha” moments of discovery. As this book blends brain and mind issues seamlessly, it illuminates the affective dynamics of human minds with clarity and wisdom. In passing, it is worth noting that throughout the history of modern biological psychiatry, there has yet to be a new psychiatric medicine that has been developed through an understanding of brain emotional processes rather than by mere serendipity. What is the cause of this failure? Surely, it is partly due to the lack of adequate tools and scientific perspectives. Among the latter, one of the most detrimental may have been the vast investment in behavioristic strategies that neglected the emotional mind of animals. As this book exemplifies, that is finally changing as clinical investigators are recognizing the enormous stretches of brain–mind evolution that we share with the other animals, especially in affective realms. Such perspectives have been placed front and center in this book, and they are effectively blended with our understanding of human emotional processes permitted by modern brain imaging. It is through such syntheses that a new era of understanding of psychiatric disorders, as well as the nature of human and animal minds, will emerge, which should fertilize more rapid progress than any other strategy so far considered. For instance, we can already envision how future psychotherapy facilitators may be constructed, such as d-cycloserine at the present time, which may further facilitate the emotional learning that must transpire during psychotherapies. We can envision neuroscientific insights that will

Foreword  xiii

reveal how EMDR and other reconsolidation therapies help restructure imbalanced emotional circuits, potentially providing not only an understanding of underlying mechanisms of action but also additional clinical insights as we reveal how each therapeutic modality works. In this context, I would share a personal experience with EMDR, facilitated by one of the editors of this book (SP). In 2009, my wife Anesa and I were concurrently diagnosed with lymphomas, with her prognosis, fortunately, less life threatening than mine. After many chemos, I was advised that the only treatment left that might save my life was tandem stem cell transplants—autologous followed by allogeneic. We proceeded to get treatment from the “Best in the West” at the “Fred Hutch” (more formally known as the Seattle Cancer Care Alliance). The first of my transplants was estimated to require 2 months of medical leave, but as successive life-threatening iatrogenic side effects emerged, the process stretched through 4 months. Suffice to say, abundant negative affect weighed on my mind. During this period, Sandra Paulsen kindly offered a sampler of EMDR therapy to see whether it might counteract and diminish/soften my negative feelings. She skillfully guided me through a sampler of EMDR procedures. As she systematically retrieved emotional feelings related to various medical problems/mistakes I had encountered, she applied her standard EMDR procedure. I easily retrieved emotional feelings under her clinical guidance, and I was amazed how rapidly those feelings dissolved once I started conjugate eye movement, following a smoothly flowing row of lights moving to the right and left on her EMDR apparatus. My negative feelings, whether anger, anxiety, or sadness, dissolved promptly once I initiated eye movements. The effect was repeatable in distinctly robust ways: Each time I evoked negative feelings from abundant autobiographical memories, the negative feelings faded promptly as soon as I initiated eye movements. We did this repeatedly with different primal affective states—rage, fear, and grief. The results were consistently clear. Repeatedly, with the onset of bilateral eye movements, the intensity of affect faded promptly. Each time! Surely, this should be an optimal way to reconsolidate affectively negative memories with less aversive hues. This is eminently testable and needs to be experimentally evaluated across a substantial set of clients. I assume it will replicate, and may be one of, perhaps “the” fundamental source of emotional relief obtained with EMDR, which may allow for the reconsolidation of troublesome memories with diminished negative-affective intensity. If this can be demonstrated, how might this occur neurodynamically? I would first note that exploratory eye movements represent a basic primate SEEKING response. Such scanning movements are organized in deep midbrain layers of the superior colliculi, just above the periaqueductal gray (PAG), which may be the most important brain region for engendering raw emotional affects since circuits for the most negative primal emotions—FEAR, RAGE, and PANIC/GRIEF—are concentrated in the dorsal PAG, very close to the exploratory eye-orientation maps at the neuronal seam between the superior colliculi and the PAG. There are neural connections between those eye-orienting response networks and the negative emotional primes, perhaps inhibitory gamma-aminobutyric acid (GABA) connections. This could provide a reasonable explanation for therapeutic

xiv  Foreword

effects: Namely, as one dwells on negative affects, arousing the dorsal PAG, the rapid shift of attention toward external events may engender direct inhibition of primal dorsal PAG emotional circuits for various negative affects. The retrieval of negative emotional memories into active neuronal reprocessing can allow “memory reconsolidation” processes to promote lasting dampening of the emotional intensity of the retrieved memories. By having systematically retrieved troublesome memories, and rapidly establishing a euthymic affective state, the associated cognitive memories should be restored (i.e., reconsolidated) with a greatly diminished affective penumbra. Of course, this is currently just a working hypothesis, but an eminently testable one. This neuromental hypothesis may highlight how a little bit of idiographic “me-search” may help promote illuminating nomothetic research on the efficacy of EMDR, a treatment modality that is so far begging for a cogent neuroscientific explanation. In this context, it is worth noting a general principle of reciprocal controls between inwardly directly basic affective-emotional (subcortical) and externally directed higher cognitive (neocortical) processes. When strongly aroused, these two global brain functions often work in reciprocal inhibitory ways. When people are emotionally aroused, there is disruption and narrowing of cognitive activities (rumination on one’s woes); conversely, when one is intently focusing on externally directed cognitive tasks, there is typically a global inhibition of affective cortical and subcortical processes (for an overview, see the Liotti and Panksepp chapter in the Textbook of Biological Psychiatry I edited for Wiley in 2004 [pp. 33–74]): In other words, just as emotional arousals can disrupt cognitive processing, intense engagements with cognitive issues can inhibit affective arousals. But this is just a working hypothesis, not a definitive conclusion. This book is written in this same spirit. The diverse contributions to this volume provide up-to-date reviews of how emotional stressors operate within the brain and how stressed minds may be helped to emerge from the psychoneural ravages of excessively sustained negative affective arousals. This book helps to counter the all-too-common trend during the past century of separating neuroscientific and psychological issues in clinical discourse. The future of the field lies in credible neuro­ psychological syntheses, as superbly represented in this book. Jaak Panksepp Professor and Baily Endowed Chair of Animal Well-Being Science Department of Integrative Physiology and Neuroscience Washington State University

Preface

Most psychologists treat the mind as disembodied, a phenomenon with little or no connection to the physical body. Conversely, physicians treat the body with no regard to the mind or the emotions. But the body and the mind are not separate, and we cannot treat one without the other. —Candace Pert, in Molecules of Emotion (1999)

This book was conceived out of our shared vision that pivotal emerging developments from the neurobiology of attachment, trauma, and affect can inform the clinical practice and, in particular, the use of certain contemporary clinical methods. That vision was to synthesize key neurobiological developments with effective developments in clinical practice to offer both understanding and practical guidance for the many practitioners working to heal people burdened with traumatic sequelae. We feel we have achieved that vision to a large degree; though the fact that there must be two parts to the book, neurobiology and treatment, reflects the status of the fields of inquiry—divided by science and practice. We have attempted to integrate them herein by weaving together the view from the warp and weft of those two outlooks, punctuating each part of the book with relevant understandings from the other. We are pleased to have the chance to translate some of the important animal work from the laboratory studies to clinical applications. For example, the research on defense responses informs our understanding of human reactions under stress. The research on emotions informs all of human experience, including that encountered at times of traumatic stress. Also, much of the literature stops at the corticolimbic level and ignores the brainstem where the emotions, orienting, and defense responses are generated primarily—even if they are elaborated through thalamocortical projections. This volume is unique in bringing in all levels of the brain from the brainstem, through the thalamus and basal ganglia, to the limbic structures, including the older xv

xvi  Preface

forms of cortex, to the neocortex. We want to look at the neurochemistry of peritraumatic dissociation and explore the effects on neuroplasticity and the eventual structural dissociation. Further, we want to help clinicians lay a sound foundation to support contemporary treatment methods with neuroscience. We make an earnest plea about research conceptualization. Because of the difficulty doing randomized controlled trials for polysymptomatic, posttraumatic presentations such as major disorders of structural dissociation, it is essential that the concept of evidence be expanded to include that which is neuroscientifically feasible. If evidence for new treatments is based only on trials of manualized therapies in rigidly defined groups, application to the dissociative disorders will remain forever out of reach, or the research has to exclude those very individuals we most want to help, with their significant clinical problems such as chronic suicidality, fragility, and tendency to decompensate and disorganize. But of all people, those most fragile patients need psychotherapy that is informed by not only clinical tradition but also enriched by the most promising leading-edge treatments, explicable at a neuroscientific level as research advances. Moreover, of all people, their treatment must be provided, not by students with manuals and clipboards, but by practitioners rich with a range of knowledge and tools, and driven by commitment, compassion, flexibility, and creativity. Otherwise, they will be offered the same standardized treatment packages from which most will drop out or be excluded, their humanity again unseen, their complex nonverbal story again not heard as it reveals itself in a variety of symptoms. Those patients who were most severely traumatized at the most vulnerable developmental stages are being excluded by research and treatment systems that cannot cope with the complexity of the presentations and cannot adapt to the need for longterm, highly specialized input. It is our hope that the findings and revelations of this book will help to explain why narrowly defined manualized treatment protocols will inevitably fail. Multimodal, creative, compassionate psychotherapy rooted in neuroscience and in healing traditions is required. A word is in order about traditional versus contemporary treatments. While we surely appreciate and honor the traditions of our field, many of the recent publications in complex trauma and dissociation do not incorporate some of the revelations of the neurobiology of trauma and affect, or they rely too heavily on traditional treatments. While all three of us are steeped in traditional psychological interventions (the first two authors are psychologists and the third is a psychiatrist), we have been privileged to also acquire a range of leading-edge methods in the treatment of trauma. It was important to us to include these newer ways of working with the clinical sequelae of trauma with an understanding of the multiple levels of the brain, the short-term neurochemical effects, and the long-term neuroplastic circuitry effects. All of the treatment methods we discuss herein assume a theoretical basis of information processing that is blocked as a defensive and survival strategy. The treatments must both deal with the defensive blocking and enable information processing, which includes affect, soma, cognitive channels, and more, to resume processing for healing to occur. So, we incorporate herein not only psychoanalytic, cognitive behavioral, and hypnotic methods, but also specific ego state, somatic/sensorimotor methods, eye movement desensitization and reprocessing (EMDR), and variations of EMDR suitable for working with trauma in the attachment period, the latter methods being explicitly information-processing methods that address affective and

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somatic modes of processing. Ego state therapy explicitly addresses defensive and dissociative structural blockages to information processing, adopted early in life. Our approach emphasizes decreasing internal conflict between the patient’s dissociated viewpoint and the viewpoint of the aggressor adopted via introjection, which assumes structural proportions in dissociative disorders and complex trauma. Ego state therapy is both old and newly important, with its inclusion in conjunction with EMDR and attachment trauma processing. It is impossible to be comprehensive in all the detail needed for full explication and treatment of dissociative disorders, but the structure of the approach—chemical, anatomical, and clinical—is novel and important. Even if a specific interpretation is disputed, there is in this volume a coherent framework in which research is understood. That framework can continue to provide a way of viewing the trauma disorders and can inform further discussion and research at the biological level as well as at the clinical. All three of us have leadership roles in training for the treatment of trauma using these leading-edge methods, and are excited to share our understandings and experience with the many people who have eagerly attended our trainings and consultation groups. We are grateful to the patients whose courage to free themselves from their heavy burden of suffering has required them to walk a long and arduous road, and we are privileged to have walked that road with them. We know how hard it is for them to trust anyone, and their trust in us requires an enormous act of faith on their part. We also are grateful to our students and consultees, whose questions have forced us to formulate our hypotheses and articulate explanations that might have otherwise remained gray. We are heartened by the gratitude and appreciation of so many. We are humbled and grateful for what we have learned from countless colleagues and contributors, and no list would be long enough to pay homage to those who have gone before. The ancient tradition of honoring our scholarly and clinical ancestors informs our gratitude, each in our own way. We particularly want to thank some of the people at the forefront of their respective fields who have inspired us: Candace Pert, Jaak Panksepp, Onno van der Hart, Bessel van der Kolk, Francine Shapiro, Alan Schore, John G. and Helen Watkins, Richard Kluft, Catherine Fine, and the countless others whose names are rarely far from our lips. We also thank the enduring support and patience of our friends and family who supported us during the creation of this work. Frank Corrigan is also specifically grateful to Pete Redgrave, Peter Carr, Rajiv Raju, David Finn, and Andrew Harkin for discussion of early drafts.

REFERENCE Pert, C. (1999). Molecules of emotion: The science between mind-body medicine. New York, NY: Scribner.

Introduction: The Ubiquity of Dissociation Sandra L. Paulsen and Ulrich F. Lanius

This book makes an attempt to embody both neuroscience and treatment in the field of dissociation, the dialectic of those two themes being reflected in Part I, Neurobiology, and Part II, Treatment. We try to provide our readers with a neurobiological framework that directly informs treatment and clinical practice. Let us briefly explore the neurobiology and treatment parts in turn.

PART I. TOWARD A NEUROBIOLOGICAL MODEL OF DISSOCIATION

What happens in the brain when an experience is overwhelming? Traumatic dissociation is a complex phenomenon that can be viewed from diverse clinical and scientific perspectives. This book attempts to integrate recent findings in cognitive and affective neuroscience, integrating neurobiological research to provide a comprehensive model of dissociation. Our understanding of these neurobiological processes has been strongly influenced by Jaak Panksepp’s (1998) work: Affective Neuroscience. Clinicians and researchers report that people show different experiential, psycho­physiological, and neurobiological responses to trauma. They hypothesize two subtypes of trauma response, one characterized predominantly by hyperarousal and the other primarily dissociative, each one representing unique pathways to chronic stress-related psychopathology (e.g., Lanius, Bluhm, Lanius, & Pain, 2005).

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Dissociation—Multiple Phenomena

Dissociation includes a wide variety of phenomena like depersonalization, derealization, amnesia, and identity disturbances. Further, dissociative symptoms can occur in a wide variety of disorders, such as dissociative disorders; posttraumatic stress disorder (PTSD), including the more complex posttraumatic presentations (e.g., complex PTSD; disorder of extreme stress not otherwise specified); somatoform disorders; personality disorders (e.g., borderline personality disorder); attachment disorders; and many others. Moreover, dissociative experiences are not only reported by a considerable proportion of psychiatric patients but also by “healthy” people.

The Autonomic Nervous System (ANS)—Sympathetic, Dorsal Vagal, and Ventral Vagal

The hyperarousal response in PTSD—also referred to as fight-or-flight response—has been studied in great detail. It is understood to be mediated by sympathetic nervous system arousal, which involves a release of catecholamines, especially adrenaline (epinephrine) and noradrenaline (norepinephrine). The release of these neurotransmitters is commonly associated with a narrowing of consciousness, that is, a specific focus on the threatening event associated with the mobilization of active defensive responses (also see Chapter  2, Threat and Safety: The Neurobiology of Defense Responses). However, the nature of the ANS is such that an activation of the sympathetic nervous system is complemented by an activation of the parasympathetic nervous system, commonly dorsovagal activation. It is this parasympathetic activation that is the underpinning of the dissociative response. This parasympathetic activation is a normal neurobiological mechanism that is evident not only in lower animals like reptiles but also in mammals and humans. It is commonly associated with a passive defensive response (also see Chapter 7, Defense Responses: Frozen, Suppressed, Truncated, Obstructed, and Malfunctioning; as well as Chapter 8, The Clinical Sequelae of Dysfunctional Defense Responses: Dissociative Amnesia, Pain and Somatization, Emotional Motor Memory, and Interoceptive Loops). These passive defensive responses are at least in part mediated by anesthetic and dissociative neurochemicals, namely, endogenous opioids and endocannabinoids that reduce the perception of physical pain as well as emotional pain. Moreover, the release of these anesthetic neurochemicals results in a lowering of consciousness and interferes with the integration of information, for example, information processing. The organism is concerned with survival and minimizing the use of energy, and reflects the core of the dissociative experience.

Ubiquity Is Hardwired—Everybody Can Dissociate

It has been documented that even what can be considered innocuous and minor stressors like giving students an unsolvable math task will result in significant analgesia (Bandura, Cioffi, Taylor, & Brouillard, 1988). That is, a dissociative response

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like anesthesia occurs in nonclinical populations that are exposed to what are normal everyday stressors. Now, this dissociative response, under normal circumstances, will not result in significant posttraumatic sequelae. For this to happen, there likely needs to be concurrent cholinergic activation associated with hyperarousal and a narrowing of attention as well reduced opioid receptor density that is attributable to prior attachment experience (also see Chapter  5). We suggest that dissociation reflects a normal underlying neurobiological mechanism that is present not only in humans. Rather, it is a basic hardwired neurobiological mechanism that occurs in mammals and humans.

Learned Helplessness (LH), Tonic Immobility (TI), and Anesthetic Neurochemicals

In humans, the alteration and lowering of consciousness due to anesthetic neurochemicals is commonly described as peritraumatic dissociation, a phenomenon that has been associated with the severity of PTSD. Relevant animal models in this regard are LH and TI. The relevance of these animal models to dissociation is discussed in Part I of the book, specifically in Chapter 3, Peritraumatic Dissociation and Tonic Immobility: Clinical Findings and in Chapter 5, Dissociation and Endogenous Opioids: A Foundational Role. In Chapter  1, Dissociation: Cortical Deafferentation and the Loss of Self, we describe how the narrowed focus with regard to sensory input in conjunction with a lowering of consciousness results in the decreased capacity to integrate this information across multiple levels in the brain, giving rise to what has been referred to as “structural dissociation” or fragmented self-states, as well as other dissociative symptoms that are commonly considered pathological; both positive, for example, hypermnesias, flashbacks, somatization; as well as negative, for example, amnesia, alexithymia, numbing, paresthesias, and so forth.

Severity of Peritraumatic Dissociation and Attachment

We suggest that increased severity of peritraumatic dissociation will give rise to increasingly pathological dissociative symptoms. The severity of the peritraumatic response in turn is likely attributable to alterations in brain functioning, both at the receptor and synaptic level that are influenced by a history of prior trauma as well as affected by an individual’s prior attachment history (see Chapter 10, Attachment and Attachment Repair). This conceptualization makes evolutionary sense, in that offspring that is not initially protected by its mother or father is more likely to become killed, eaten, or victimized by a predator. Thus, an increased availability of a passive defense response like immobility, freezing, diminished perception of pain, and peritraumatic dissociation potentially not only confers a survival advantage but also reduces suffering. Further, in Chapter  6, Attachment, Neuropeptides, and Autonomic Regulation: A Vagal Shift Hypothesis, we suggest how some possible neurobiological underpinnings with regard to ventral engagement are intrinsic to the

xxii  Introduction

attachment relationship on one hand, but also how we can potentially shift our clients or patients from states of sympathetic hyperarousal or dorsovagal shutdown toward social engagement and a ventral vagal state. By drawing on the ventral vagal system, we can maximize affective regulation and information processing in trauma-focused interventions. Finally, in Chapter  9, Shame and the Vestigal Midbrain Urge to Withdraw, we discuss the specific role of the emotion of shame and its contribution to dissociation.

Integrative Capacity

Moreover, both peritraumatic dissociation as well as structural dissociation interfere with the integrative capacity of the brain as well as information processing. Chapter 11, Dissociation, EMDR, and Adaptive Information Processing: The Role of Sensory Stimulation and Sensory Awareness, discusses the role of sensory awareness and stimulation in the experience of an embodied self as it relates to our understanding of treatment interventions like EMDR, specifically, but also other somatically oriented interventions like sensorimotor psychotherapy.

PART II. TREATMENT: BEING EMBODIED AND SAFELY TELLING THE TRUTH

When dissociation is a significant part of the clinical presentation, it often presents a barrier to effective treatment. It tends to interfere with clients’ sense of their own body, their ability to experience emotion, and emotional regulation. Moreover, dissociation tends to result in unpredictable ego state shifts and the continuity of self. In Part II, we describe a neurobiologically informed treatment approach that incorporates numerous elements from the armamentarium of contemporary psychotherapeutic procedures that address the key elements of dissociative disorders. This approach is intended to guide the client in a safe and paced manner to experience an embodied sense of self, one that is truthful to oneself, allowing an integrated self-system that operates with mutual cooperation and compassion. Chapter  12, Seeing That Which Is Hidden: Identifying and Working With Dissociative Symptoms, discusses some of the basic skills required for identifying and treating dissociative spectrum disorders. Chapter 13, The Compassionate Self, discusses the foundational role of safe embodiment, mindfulness, and reparative interventions in the treatment of dissociative symptoms as well as how that relates to attachment experience.

Ebb and Flow, Affect Modulation, and the Window of Tolerance

Most dissociative clients have lived their lives by disconnecting from intolerable realities and emotions. Since the material was too painful to process and integrate, and the child had little or no assistance with handling emotions, any waves of emotion then tend to become truncated at the peak of the wave. The child never experiences

Introduction  xxiii

the natural ebb and flow of emotion as facilitated in Mom’s or Dad’s loving arms. As a result, the client has both limited affect tolerance and a great deal of emotional intensity that is commonly held in the body, an intensity from which our clients naturally disconnect. The challenge and art of therapy is in finding a means to assist the integration of such intense emotional experience into the client’s sense of self, without overwhelming the client. Chapter 20, Temporal Integration of Early Trauma and Neglect, discusses the use of the time domain in titrating traumatic overwhelm, particularly using an approach that targets developmental time sequence. Indeed, if the intensity of painful experience is too great, the client will be flooded and ultimately shut down. No information processing or integration of experience takes place. We suggest that the integration of experience can be facilitated by one or more of the following strategies: (a) increasing client resources: It is necessary to increase the client’s resources so that the tolerance for affect can be greater than the magnitude of the pain. Chapter  14, Stabilization Basics, focuses on providing therapists with a conceptual understanding of different aspects of resourcing and stabilization and how that relates to therapeutic interventions; (b) decreasing client pain: Titrating the intensity of experience that the pain is manageable; (c) staying within the window of tolerance. These strategies can be summarized in the concept of the “window of tolerance” (Ogden, Minton, & Pain, 2006; Siegel, 1999). Trauma processing and therapy itself can only take place in the midrange of activation, neither extremely high nor extremely low. This midrange describes an area, the window of tolerance, in which the client can tolerate affect, bodily sensation, and painful awareness, while at the same time remaining aware of the present context: “I am safe now . . . it’s no longer happening.” All of the methods described in this book are designed to increase resources, on one hand, or titrate emotional intensity on the other.

Association and Dissociation—Accelerator and Brakes

The organizing principle for this book and all the therapies in it is dissociation and, conversely, association. Dissociation results when one doesn’t keep up with one’s associative housekeeping, the synthesis of experience that we all engage in, sometimes in REM sleep. The fragmented sensory channels of experience remain unintegrated and separate from ordinary consciousness. Through information processing, whether facilitated by EMDR or other therapeutic methods like sensorimotor psychotherapy, those channels become associated, synthesized, and integrated, thus “processed to an adaptive resolution” (Shapiro, 1995, 2001). The association of that which had been dissociated pathologically is the path to mental health for the trauma-related conditions, and for those conditions that result when developmental milestones couldn’t be successfully navigated because a child didn’t have sufficient help from caretakers. Adaptive information processing, the theory behind EMDR, postulates that as long as there is an adaptive neural network available to associatively link to, processing can occur, leading to an adaptive resolution. For dissociative clients, blocked processing can occur for several reasons, including insufficient adaptive neural networks,

xxiv  Introduction

insufficient linkages to adaptive neural networks, object relations conflicts that block associative linkages to adaptive neural networks, and insufficient tolerance of affect or insufficient neocortical integration to sustain information processing. All of the therapeutic methods and interventions discussed in Part II share a view that processing affect and somatic sensory information is an integral part of an embodied sense of self. They have in common that they all make use of association and dissociation toward the goal of integration and symptom reduction artfully, just as one uses the accelerator and brake to pace forward movement when driving a car, steering around obstacles in one’s path.

Integrating Different Information Processing Therapies

Part II focuses on integrating different information-processing approaches, with a view toward an embodied self. At the same time, it should be noted that these procedures are primarily derived from clinical experience and case studies rather than based on controlled research.

Body-Oriented and Somatic Therapies

The emphasis is on the felt sense of the body and integrating sensory and motor processing. We view this approach as foundational with regard to trauma processing and an embodied sense of self. Chapter 19, Integrating Body and Mind: Sensorimotor Psychotherapy and the Treatment of Dissociation, Defense, and Dysregulation, discusses the use of body-oriented psychotherapy, specifically sensorimotor psychotherapy with the dissociative disorders.

Ego State Therapy

Ego state therapy adds ego energy—the subjective experience of “I”—to disowned or dissociated experience. This quality of I-ness by definition is highly affective and somatically oriented. By extension, one could use an object–state therapy that can also be used to distance from I-ness by utilizing a cognitive or imaginal perspective for distance and insight. Watkins and Watkins (1997) described object cathexis and ego cathexis as variously owning or disowning the felt sense of an experience to titrate the intensity of experience. Ego state therapy then involves the artful use of adding or subtracting ego and object energy, thus facilitating in mindfulness both smooth and efficient state switching, thereby making linkages across hypothesized neural networks. Chapter 15, Stabilizing the Relationship Among Self-States, focuses on increasing awareness of different parts of the self and ultimately creating a more stable sense of self. Chapter 17, Fractionating Trauma Processing: TOTEMSPOTS and Other Attenuating Tactics, highlights the important role of fractionation and titration of traumatic experience in order to regulate the intensity of trauma-focused interventions as well as assisting in maximizing their effectiveness. Chapter 18, Accelerating

Introduction  xxv

and Decelerating Access to Self-States, discusses ego state interventions and how to use them to both slow down as well as accelerate information processing.

EMDR

The standard EMDR protocol integrates somatic awareness, affect, and cognition, relying on external sensory stimulation to assist with the integration of information. It has been our clinical experience that, with dissociative clients, the more somatically focused EMDR is practiced, the deeper and more lasting are its therapeutic effects. Thus, with dissociative clients the integration of somatic interventions can be of great benefit. However, in severe dissociative disorders, this is rarely sufficient to ensure efficient information processing, and the use of ego state interventions in conjunction with EMDR is commonly necessary. Chapter 21, Toward an Embodied Self: EMDR and Somatic Interventions, describes an approach that integrates somatic interventions with EMDR to facilitate effective information processing. Chapter 16, Alexithymia, Affective Dysregulation, and the Imaginal: Resetting the Subcortical Affective Circuits, focuses on an innovative EMDR-informed approach using affective mentalization and imagery to decrease emotional numbing and alexithymia, one of the core symptoms of traumatic dissociation. Of the interventions described, EMDR is the only one that has a considerable amount of controlled research to support its use. At the same time, it is understood that EMDR cannot be safely conducted for a client who is at odds with his or her own body, who cannot tolerate affect, and who has insufficient self-structure to tolerate the work, without considerable preparations and modifications.

Adjunctive Pharmacological Interventions—Opioid Antagonists

This is an innovative approach to assist with both stabilization and information processing. While some limited research supports the use of opioid antagonists with dissociative symptoms, limited or adverse effects are also reported. We try to make an effort to provide the reader with an understanding of the effects of opioid antagonists and their effective use to assist with psychotherapeutic interventions in dissociative spectrum disorders. We suggest that therapists, using their neurobiological understanding of the phenomenology of dissociation, integrate these therapeutic interventions, using them in the treatment of traumatic dissociation in conjunction with each other “toward an embodied self.”

REFERENCES Bandura, A., Cioffi, D., Taylor, C. B., & Brouillard, M. E. (1988). Perceived self-efficacy in coping with cognitive stressors and opioid activation. Journal of Personality and Social Psychology, 55(3), 479–488.

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Lanius, R. A., Bluhm, R., Lanius, U., & Pain, C. (2005). A review of neuroimaging studies in PTSD: Heterogeneity of response to symptom provocation. Journal of Psychiatric Research, 155, 45–56. Ogden, P., Minton, K., & Pain, C. (2006). Trauma and the body: A sensorimotor approach to psychotherapy. New York, NY: W. W. Norton. Panksepp, J. (1998). Affective neuroscience: The foundations of human and animal emotions. New York, NY: Oxford University Press. Shapiro, F. (1995). Eye movement desensitization and reprocessing: Basic principles, protocols and procedures (1st ed.). New York, NY: Guilford Press. Shapiro, F. (2001). Eye movement desensitization and reprocessing: Basic principles, protocols, and procedures (2nd ed.). New York, NY: Guilford Press. Siegel, D. J. (1999). The developing mind: Toward a neurobiology of interpersonal experience. New York, NY: Guilford Press. Watkins, J. G., & Watkins, H. H. (1997). Ego-state theory and therapy. New York, NY: W. W. Norton.

PART I: NEUROBIOLOGY

INTRODUCTION

Dissociation and Neurobiology Ulrich F. Lanius

TRAUMATIC DISSOCIATION

Traumatic dissociation is a complex phenomenon that can be viewed from diverse clinical and scientific perspectives. We suggest that the capacity to dissociate is an innate neurobiological process that occurs not only to humans but also to mammals. That is, the dissociative response shares basic hardwired affective responses evident in animals. The chapters in this book attempt to integrate basic science research with findings in the affective and cognitive neurosciences relevant to our understanding of traumatic stress syndromes and dissociative disorders. A comprehensive model of dissociation is proposed, with a view toward providing a functional mechanism with regard to the phenomenology of dissociative symptoms, including what has been referred to as structural dissociation.

Peritraumatic Dissociation, Anesthetic Neurochemicals, and Structural Dissociation

We suggest that the phenomenon of peritraumatic dissociation has a central role in the genesis of other dissociative symptoms and it is associated with the release of anesthetic neurochemicals that alter the communication between lower and higher brain structures, leading to a lack of integration of traumatic experience, somatoform symptoms, as well as separate self-states. In our view, such a neurobiologically based understanding of dissociation is not only relevant to our understanding of traumatic stress syndromes and dissociative disorders but, in many cases, also with regard to other types of psychopathology.

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2  I.  NEUROBIOLOGY

Toward a Neurobiological Understanding

The chapters in the first part of this volume contain a number of overlapping but occasionally slightly divergent views with regard to the role of different neurobiological processes that inform our understanding of traumatic dissociation. They all share in common a strong neurobiological and neuroscience focus that is informed by the seminal work Affective Neuroscience by Jaak Panksepp (1998). Other influences include the work of Pierre Janet, who pioneered the field of dissociation with his concept of “disaggregation” that, in many ways, remains current to this day. Furthermore, the work of Allan Schore has influenced our understanding of the impact of attachment on later dissociative symptoms. Last, but not least, we want to express our indebtedness to the work of Bessel van der Kolk, McFarlane, and Weisaeth (1996) and that of Onno van der Hart, Nijenhuis, and Steele (2006). In Chapter 1, Cortical Deafferentation: Dissociation and the Loss of Self, Ulrich F. Lanius, Sandra L. Paulsen, and Frank M. Corrigan propose an innovative theory that suggests a neurobiologically based functional mechanism of dissociation. The chapter integrates both clinical and basic neuroscience research with models of dissociation proposed in the writings of Pierre Janet as well of van der Hart et al. (2006) with regard to structural dissociation. In Chapter 2, Threat and Safety: The Neurobiology of Defense Responses, Frank M. Corrigan discusses the role of the midbrain in defense responses to threat and how this relates to structural dissociation. In Chapter  3, Peritraumatic Dissociation and Tonic Immobility: Clinical Findings, Michelle J. Bovin, Elise Ratchford, and Brian Marx discuss the relationship of peritraumatic dissociation to tonic immobility and other defensive responses. In Chapter 4, A Social–Cognitive–Neuroscience Approach to PTSD: Clinical and Research Perspectives, Ruth Lanius, Paul Frewen, Anthony Nazarov, and Margaret McKinnon discuss recent neuroscience research with regard to alterations of resting-state connectivity in the brain, for example, the default mode network, and how these relate to the clinical and neurobiological understanding of complex PTSD, particularly with regard to social and emotional functions, such as motivation and emotion, self-referential processing, empathy, moral reasoning, and mentalizing (theory of mind). In Chapter  5, Dissociation and Endogenous Opioids: A Foundational Role, Ulrich F. Lanius discusses the central role of endogenous opioids with regard to dorsal vagal activation and the phenomenology of dissociative symptoms. In Chapter 6, Attachment, Neuropeptides, and Autonomic Regulation: A Vagal Shift Hypothesis, Ulrich F. Lanius highlights the role of oxytocin in attachment and vasopressin in active defensive responses as well as the interrelationship of these neuropeptides with the opioid system, with a view of shifting the nervous system away from dorsal vagal activation toward ventral vagal engagement. In Chapter 7, Dysfunctional Defense Responses: Frozen, Suppressed, Truncated, and Obstructed, Frank M. Corrigan discusses the relationship of different types of dysfunctional defense responses to dissociative symptoms. In Chapter  8, The Clinical Sequelae of Dysfunctional Defense Responses: Dissociative Amnesia, Pain and Somatization, Emotional Motor Memory, and

Introduction: Dissociation and Neurobiology  3

Interoceptive Loops, Frank M. Corrigan discusses the role of endogenous cannabinoids and endogenous opioids and their modulatory role in high- and low-arousal peritraumatic dissociation, dissociative amnesia, pain phenomena, and somatization. In Chapter 9, Shame and the Vestigial Midbrain Urge to Withdraw, Frank M. Corrigan discusses the central role of shame with regard to dissociation as well as its relationship to both social learning and hardwired affective circuits in the midbrain. In Chapter 10, Attachment and Attachment Repair, Frank M. Corrigan, Alistair Wilson, and Deirdre Fay discuss the relevance of attachment to our understanding of the phenomenology of dissociation as well as the role of attunement with regard to attachment repair. Finally, in Chapter  11, Dissociation, EMDR, and Adaptive Information Processing: The Role of Sensory Stimulation and Sensory Awareness, Ulrich F. Lanius and Uri Bergmann describe a neurobiological model with regard to the functional mechanism of EMDR treatment that informs our understanding of traumatic dissociation and its treatment.

REFERENCES Janet, P. (1889). L’automatisme psychologique. Paris, France: Felix Alcan. Panksepp, J. (1998). Affective neuroscience: The foundations of human and animal emotions. New York, NY: Oxford University Press. Schore, A. N. (2001). The effects of early relational trauma on right brain development, affect regulation, and infant mental health. Infant Mental Health Journal, 22, 201–269. van der Hart, O., Nijenhuis, E., & Steele, K. (2006). The haunted self: Structural dissociation and the treatment of chronic traumatization. New York, NY: W. W. Norton. van der Kolk, B. A., McFarlane, A., & Weisaeth, L. (Eds.). (1996). Traumatic stress: The effects of overwhelming experience on mind, body, and society. New York, NY: Guilford Press.

CHAPTER 1

Dissociation: Cortical Deafferentation and the Loss of Self Ulrich F. Lanius, Sandra L. Paulsen, and Frank M. Corrigan

Subcortical structures do not serve simply as pathways linking the two hemispheres but play an essential coordinating role in the integration of hemispheric activity. —J. Sergent (1990)  . . . the diverse inputs to the hippocampal formation from the brainstem and certain limbic and neocortical areas provide special conditions for the integration of information from interoceptive and exteroceptive systems. It is premised that such an integration is essential for a sense of self, without which self-referenced memory could not occur. —Paul MacLean (1993)

THE BRAIN—AN ASSOCIATIVE ORGAN

The extraordinarily complex organization of the highly evolved human brain permits processing of massive amounts of sensory, motor, autonomic, affective, and cognitive information. It is imperative to be able to select for salience and to forget much of what passes through even those brain areas that are more accessible to conscious awareness. The fully integrated, optimally functioning human being can then effortlessly attend to selected stimuli and lay down memories important for

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6  I.  NEUROBIOLOGY

the continuing well-being of the self. The development of this integrated self is disrupted by traumatic experiences, those that are not assimilated at an affective and autonomic level.

Loss of Integrative Capacity—Toward a Functional Mechanism of Dissociation

Patients with dissociative disorders and traumatic stress syndromes present with self-states that are relatively discrete, discontinuous, and resistant to integration. The present chapter suggests neurobiological mechanisms to account for dissociative symptoms in general and structural dissociation in particular. Specifically, we suggest the following elements of a functional mechanism of dissociation based on peritraumatic neurochemical disturbances, which give rise to nonintegrated and dysfunctional neural pathways: 1. Peritraumatic dissociation (PD) is associated with the release of endogenous opioids and other anesthetic neurochemicals that alter communication between lower and higher brain structures. 2. Specifically, endogenous opioids inhibit the thalamus, resulting in a decoupling of higher brain structures, such as limbic cortex and neocortex, from the brainstem. 3. As a result of a failure to convey input into the cortex, horizontal integration between hemispheres across the corpus callosum is impaired. 4. The lack of integration between brain levels and across the corpus callosum promotes a failure of integration of a traumatic experience. 5. We hypothesize that at the core of structural dissociation and the development of separate self-states or emotional parts (EPs) is an opioid-induced deafferentation of basic affective circuits that are mobilized under threat, resulting in their remaining separated from ordinary conscious awareness.

Brain Architecture Reflects Horizontal Layers

MacLean’s triune brain model (1990) provides a structure for the understanding of emotional functioning and dissociation. McLean suggests that evolutionary development has resulted in three layers: the lower or reptilian brain, the limbic system, and the neocortex. The oldest of the three, the reptilian brain, includes the brain stem—medulla, pons, cerebellum, mesencephalon, as well as the oldest basal nuclei; the globus pallidus; and the olfactory bulbs. The reptilian brain is responsible for control of the body’s vital functions, for example, heart rate, breathing, body temperature, balance, as well as sensorimotor processes. In addition, it is here, in the upper area of the reptilian brain, in the mesodiencephalon, the hypothalamus, and midbrain, where basic affects or emotions are generated. In particular, the periaqueductal gray (PAG) in the midbrain is fundamental to all the basic affective systems, although the limbic system adds behavioral complexity, especially to the social emotions (Panksepp, 1998).

1.  Dissociation: Cortical Deafferentation and the Loss of Self   7

The limbic system or paleomammalian brain is believed to have emerged at a later stage in early mammals. The limbic system has vast interconnections with the neocortex, so that brain functions are not either purely limbic or purely cortical, but a mixture of both. The main structures of the limbic brain are the hippocampus, the amygdala, the hypothalamus, and the phylogenetically transitional cingulate cortex. However, it is important to recognize that while the limbic system provides the substrate for memories of emotional experiences and feeling and allowing learning from them, the basic affects are generated at the level of the brainstem within the PAG. Lastly, the neocortex assumed importance in primates to ultimately culminate in the human brain. It is divided into left and right hemispheres that allow the emergence of higher cognitive functions such as language, abstract thought, and imagination. The growth of the neocortex gives rise to the possibility of disconnections in humans between advanced cognitive functions and basic affective responding. These three parts of the brain do not operate independently of one another. Rather, through numerous interconnections these different layers influence one another and, under normal circumstances, function as an interconnected whole. Moreover, in humans in particular, the neocortex frequently dominates the lower levels. However, under threat this may no longer be the case.

Brain Architecture Also Reflects Vertical Columns

While on one hand the organization of the brain reflects different horizontal layers, at the same time the brain is also organized vertically in a columnar fashion, with adjacent columns that share similar function. This was initially documented at the cortical level by Mountcastle (1997). Connections between the different cellular layers of the cortex allow the subtle excitations and inhibitions necessary for learning through neuroplasticity, so there is even potential for disrupted communication within a vertical column. Columnar organization is also evident at other levels of the brain, such as in the midbrain PAG (Bittencourt, Carobrez, Zamprogno, Tufik, & Schenberg, 2004). Cortical columns typically relate to specific sensory functions, reflecting the local connectivity of the cerebral cortex while the longitudinal columns of the PAG along the aqueduct relate to specific defensive behaviors. A third way in which there is vertical organization is through looped circuits, for example, cortico-basal gangliathalamo-cortical loops, which are partially segregated to allow for rapid access to one of a range of responses (also see Chapter 8, The Clinical Sequelae of Dysfunctional Defense Responses: Dissociative Amnesia, Pain and Somatization, Emotional Motor Memory, and Interoceptive Loops). Reduced functioning of one of the stations on the line, such as the thalamus, impairs the selection and evaluation of goal-directed actions. Connections “up” and “down” are much denser than connections that occur horizontally. That is, there are many more connections vertically than there are side to side. This columnar nature allows precision with regard to conveying specific sensory information, which is adaptive because sensory fields have little overlap, and

8  I.  NEUROBIOLOGY

likely results in the effective conduction of information from the lower brain structures to the higher brain structures.

Sensory Integration Plays a Critical Role in Horizontal and Vertical Integration

The brain relies on both functional specialization and functional integration, where the integration within and among specialized areas is mediated by effective connectivity. The structural organization of the brain allows connectivity not only horizontally at the level of the mesencephalon but also across the hemispheres, and it promotes connectivity with regard to “bottom-up” and “top-down” processes. We suggest that in the absence of vertical integration, horizontal integration, for example, of sensory input, emotions, and thoughts, cannot occur at higher levels. We propose that the lack of vertical integration is at the core of the development of separate selfstates, for example, structural dissociation. Moreover, we suggest that at the core of both vertical and horizontal integration is integration of sensory input that allows the inner world of the brain to relate to the outer world, the external environment (also see Chapter  11, Dissociation, EMDR and Adaptive Information Processing: The Role of Sensory Stimulation and Sensory Awareness). The processing of sensory information is central to the brain’s capacity to predict and is thus ultimately at the core of survival. Sensory integration is the neurological process that organizes sensation from one’s own body—both proprioceptive and interoceptive—with exteroceptive sensory input from the environment. This allows goal-directed behavior and effective movement of one’s body within a given environment. That is, sensory integration deals with how the brain processes multiple sensory modality inputs into usable functional outputs. Vision, sound, touch, and smell need to be integrated horizontally for adaptive functioning and goal-directed movements. For example, hand–eye coordination requires the integration of what we visually perceive about an object with what we tactilely perceive about that same object. Information from the two senses is combined within the brain to increase the ability to manipulate an object. Thus, sensory integration is essential to functioning: for most activities, we need to integrate multiple sensory inputs not only to comprehend our surroundings but also to respond adaptively to our environment.

How Does the Brain Conduct Sensory Integration?

In our view, the integration of brain functioning both horizontally and vertically at different levels of the brain is at the core of information processing. We further suggest that dissociative phenomena are the result of the breakdown in both horizontal and vertical integration of brain functioning. Let us have a brief look at how sensory integration is mediated at the different levels, for example, both higher and lower brain structures in the brain, as this will assist our understanding of what actually may happen in the brain when we dissociate. We therefore would like to highlight

1.  Dissociation: Cortical Deafferentation and the Loss of Self   9

the role of a number of brain structures that are important for the integration of information. At higher levels, that is, just below the cerebral cortex, sensory integration is mediated at the level of the thalamus. It also contributes to the highlighting of particular sensory inputs or emotional experiences by increasing the receptivity of some cortical areas while decreasing the activation of others. Further, information that is projected by the thalamus into cortical areas can be subsequently transferred across the hemispheres across the corpus calossum. In the lower brain structures, at the level of the mesencephalon, sensory integration likely occurs at the level of the colliculi, both superior and inferior. Below, we discuss how these brain structures are relevant for integration of sensory input as well as what constitutes the essential elements of a sense of self. Let us discuss each of those structures in turn.

A Switchboard—The Role of the Thalamus in Vertical and Horizontal Integration

The thalamus has been likened to a switchboard for information exchange between a variety of subcortical areas and the cerebral cortex, for example, both the limbic system and the neocortex. The thalamus consists of a midline-paired symmetrical structure situated between the cerebral cortex and the midbrain. It sits atop the brainstem at the center of the brain, surrounded by the basal ganglia and limbic structures. It is at the level of the thalamus where the different types of sensory input converge and are ultimately relayed to the respective cortical areas—all sensory information with the exception of smell travels through the thalamus before reaching the cortex. It is within the higher cortical areas, at the level of the corpus callosum, where horizontal integration of information carried by different cortical columns can occur. That is, for the most part only information that is projected by the thalamus into cortical areas can be efficiently transferred across the hemispheres. The thalamus also plays a role in cortical oscillations, a phenomenon that has been related to cognitive-temporal binding and information processing (also see Chapter  11), thus affecting cortical connectivity. Further, as a regulator of sensory information, the thalamus plays an important role in attentional processes, including states of alertness and arousal. This function is mediated by the nonspecific nuclei. Not surprisingly, damage to the thalamus can lead to comatose states (e.g., Uzan et al., 2003). Experimental research shows a down-regulation of thalamic activity with increasing levels of arousal in nontraumatized populations, probably mediated by the reticular nucleus that is involved in the interaction of attention and arousal (Portas et al., 1998), where the reticular nucleus is a target for noradrenergic fibers from the locus coeruleus (LC; Bentivoglio, Kultas-Ilinsky, & Ilinsky, 1993). Another study of the interaction of attention and arousal highlighted the medial pulvinar, another thalamic nucleus (Coull, Jones, Egan, Frith, & Maze, 2004). The latter may be of particular relevance in traumatic stress syndromes, in that it has projections to anterior and posterior cingulate cortex (Shibata & Yukie, 2009), as well as receiving afferents from sensory integration areas in the deep layers of the superior colliculi.

10  I.  NEUROBIOLOGY

Specifically, it responds to cholinergic innervation from the mesopontine nuclei and has a high density of opioid receptors. Krystal, Bennett, Bremner, Southwick, and Charney (1995) make a persuasive argument that the thalamus has a key role in dissociation by altering sensory input to cortical and limbic structures. That is, high levels of arousal during traumatic experiences may result in alterations in sensory processing in the thalamus, which in turn disrupts the transmission of sensory information to the frontal cortex, cingulate gyrus, amygdala, and hippocampus. Indeed, the thalamus not only transmits sensory information bottom-up but also relays cognitive information top-down, thus allowing the regulation of lower brain structures. Each cortical area has associated subnuclei of the thalamus with sharper delineations in the specific sensory areas. Cortico-thalamic (top-down) projections roughly outnumber thalamo-cortical (bottom-up) connections by a factor of nine. The thalamus processes sensory information and relays it—each of the primary sensory relay areas receives strong “back projections” from the cerebral cortex. That is, the thalamic nuclei have strong reciprocal connections with the cerebral cortex. The resulting thalamo-cortical-thalamic circuits are believed to be involved not only with self-awareness but also with consciousness. All areas of cingulate cortex have reciprocal connections with different groups of dorsal thalamic nuclei (Shibata & Yukie, 2009). Thalamic afferents are integral to information transfer from subcortical areas to the cortex and for passing information among cortical areas for memory, pain awareness, motor responses, and visuospatial processing. The anterior cingulate cortex (ACC) has connections with the mediodorsal nucleus of the thalamus for affective responses and autonomic regulation. The ventral posterior cingulate cortex selects sensory events on the basis of self-relevance, and information is relayed anteriorly through association, orientation, premotor and visceromotor, or autonomic areas of cingulate cortex (Vogt & Laureys, 2009). These areas all receive afferents from the mediodorsal thalamus but have specific inputs, mostly reciprocal, from other thalamic nuclei. Deafferentation at the mediodorsal nucleus leaves the cortex short of potential for a full emotional response to an environmental event. Furthermore, areas of cingulate cortex are likely deafferented by variable disconnections in the thalamus, interfering with the integration of affect and cognition. Further, thalamic deafferentation may in part account for hippocampal shrinkage in traumatic stress syndromes. That is, the dorsal tegmental nuclei, the ventral tegmental nuclei, and the anterior thalamic nucleus are connected to the hippocampus via the mammillo-thalamic tract (Haines, 2003). Thus, decreased information relayed to hippocampal structures may induce alterations in the hippocampus. Ultimately, we hypothesize that on one hand deafferentation at the level of specific nuclei of the thalamus likely accounts for the development of some traumatized self-states (e.g., EPs with a strong subcortical dominance). On other occasions, specific nuclei of the thalamus may also be involved in state switching, among different multilevel loops, as well as with the occurrence of adaptive self-states (e.g., apparently normal personalities [ANPs]), in response to changes in internal or external stimuli.

1.  Dissociation: Cortical Deafferentation and the Loss of Self   11

Superior (SC) and Inferior Colliculi (IC) and Sensory Integration

We know that decorticate animals—those whose cerebral cortex has been removed— as well as hydranencephalic children exhibit consciousness and respond to their environment (Merker, 2007). They clearly can respond to environmental input perceived through their senses, likely integrated at the level of the SC and IC. The SC and IC—two of each—are also often referred to as the corpora quadrigemina or tectum. They are a composite substructure of the mesencephalon, that is, the midbrain that is part of the brainstem. Their general function is to coordinate behavioral responses toward specific points in “ego-centric” or body-centered space. The superior colliculi allow the integration of sensory input with other information from the body, in conjunction with basic affective responses mediated by the PAG, to promote survival of the organism. This ultimately suggests that the basis of the self is in the somatic motor map between the superior colliculi and the PAG (Panksepp, 2003). In fact, Panksepp has suggested that the last structure to evidence activity in the face of imminent death is the PAG (J. Panksepp, personal communication, April 19, 2009). That is, the capacity for integration of information in the lower brain structures depends on the colliculi. The superior colliculi are the primary integrating centers for eye movements. That is, if there is sufficient input from the retina, the activation in the colliculi will produce a saccadic eye movement. The superficial layer of the superior colliculi, which receives projections from the retina, is interconnected with the intermediate and deep layers for integration of visual information with somatosensory, auditory, and even olfactory signals. The IC lie caudal in close vicinity to the superior colliculi, and their neurons are implicated in integrating auditory and somatosensory input. Animal defense responses that occur at the level of the PAG are likely elicited through stimulation of the superior colliculus (e.g., Dringenberg, Dennis, Tomaszek, & Martin, 2003) and the ICs (e.g., Brandão, Melo, & Cardoso, 1993). Essentially, the superior and IC mediate orienting and goal-directed behavior through the integration of sensory input, and their proximity to the PAG allows generation of affective and defensive responses without delay. Inputs from the retina are projected to the superior colliculus and to the lateral geniculate nucleus of the thalamus, which in turn projects to the visual cortex. Similarly, the medial geniculate nucleus is the principal relay between the ICs and the auditory cortex. Multimodal sensory and visual information is provided to both the ventral posterior and the anterior cingulate cortices through the medial pulvinar nucleus of the thalamus (Shibata & Yukie, 2009). Finally, the ventral posterior nucleus is the key somatosensory relay that sends tactile and proprioceptive information to the somatosensory cortex. Moreover, the superior colliculi are the only places outside of the cerebral cortex in which fast oscillations in the gamma range occur (e.g., Brecht, Goebel, Singer, & Engel, 2001). As suggested earlier, such oscillatory activity in the thalamus and the neocortex appears to have a role in “binding,” that is, integrating disparate elements of unitary conscious percepts (also see Chapter 11). As such, apart from sensory integration, gamma oscillations may play a role in cortico-collicular integration (Merker, 2007). This may not only allow information traveling bottom-up from the

12  I.  NEUROBIOLOGY

brain stem and mesodiencephalic system to gain access to the cortex in all its ramifications, but also allow for top-down cortical activity to influence the mesodiencephalic system. This mechanism may be the principal step with regard to sensory and conscious awareness.

The Role of the Corpus Callosum in Horizontal Integration

The corpus callosum is the largest connective pathway in the human brain, constituted of nerve fibers that connect the left and right hemispheres, thus facilitating interhemispheric communication. The corpus callosum transfers motor, sensory, affective, and cognitive information between the brain hemispheres. De Bellis et al. (1999) found that maltreated children with posttraumatic stress disorder (PTSD) had smaller callosal volumes. While these authors attributed this to catecholamines and steroid hormones, for example, cortisol, affecting brain development, we suggest that this effect may at least in part be attributable to decreased neural transmission to the cortex. That is, we suggest that ultimately callosal function depends on thalamic functioning. In the absence of information being relayed into the upper cortical areas, there is no activation of the upper cortical areas, nor is there information available that can be horizontally integrated between the hemispheres.

Trauma Impairs Sensory Integration

We hypothesize that under threat sensory integration is reduced to essential levels or, in extreme cases, is done away with completely. Underthreat sensory integration no longer occurs at the level of the higher brain structures. Trauma disrupts the thalamic relay so that sensory integration occurs predominantly at the level of the corpora quadrigemina (i.e., at the level of both inferior and superior colliculi). As threat levels increase, neocortical sensory integration ultimately ceases altogether. We specifically suggest that in traumatized individuals, as a result of thalamic inhibition, sensory integration occurs at the level of the superior and IC, that is, in the lower brain regions, reflecting faster and more “reptilian” responding than cortical processing would allow. The colliculi have descending projections to the reticular formation and spinal cord and can be involved in responses to stimuli faster than cortical processing would allow. Nontraumatized individuals, on the other hand, are likely to evidence sensory integration at both the collicular and thalamic levels. This occurs with an experience of feelings, including blends of feelings, not only due to sensory information being projected to the relevant sensory cortices but also attributable to information processing that is capable of integrating different emotional processes in a top-down manner. With a fully functioning thalamus and integration at all brain levels, sensorimotor processing can proceed through the cingulate gyrus, from posterior to anterior, with physiological adjustments to maintain homeostasis and adaptive movements and actions.

1.  Dissociation: Cortical Deafferentation and the Loss of Self   13

Trauma and Stress—The Role of Analgesic Neurochemicals

Response to stress includes the release of numerous analgesic neurotransmitters that include but are not limited to endogenous opioids and endogenous cannabinoids. This may be a primary response to overwhelming fear and pain or may potentially occur secondary to the midbrain generation of emotions and defense responses. Their impact includes effects on the perception of pain, consciousness, motor control, mood, and memory, as well as reduced cortical functioning. We hypothesize that excessive release of endogenous opioids, as well as other anesthetic neurochemicals secondary to stress, likely results in alterations in consciousness, lowering of consciousness, and ultimately discontinuity of consciousness, a process that likely occurs both at the level of the thalamus and the PAG. Specifically, β-endorphin is involved in amnesia as well as in immobilization. Another endogenous opioid, dynorphin, which activates κ-opioid receptors, may mediate depersonalization, derealization, and the dysphoric effects of traumatic dissociation (e.g., Pfeiffer, Brantl, Herz, & Emrich, 1986). This release of dissociative neurochemicals, especially at higher levels, results in what is akin to a dissociative anesthesia, a state characterized by catalepsy, catatonia, and amnesia, but not necessarily involving complete unconsciousness (also see Chapter 7). We suggest that it is this release of analgesic neurochemicals that results in an alteration or retraction of consciousness that impairs the integration of information and sensory input at the level of the thalamus, a phenomenon that is commonly described as primary dissociation (PD). On that basis, we hypothesize that stressrelated opioid activation plays a central role in dissociative symptoms. Ultimately, we consider primary dissociation at the level of the thalamus and related alterations in consciousness to be at the root of many divergent dissociative symptoms and to be the underlying mechanism of structural dissociation.

Sensory Integration Under Threat—Dissolution and the Loss of Higher Cortical Functioning

Situations that commonly involve an actual or perceived threat to survival of the lower brain structures can hijack the higher mental functions when necessary, a phenomenon that is often aptly referred to as “reverting to reptilian brain functioning.” This phenomenon is consistent with Hughling Jackson’s (1958) notion regarding the hierarchical organization of the brain and his concept of dissolution. Jackson suggests that “those functions which appeared last in evolutionary terms, and which emerge late in human development, are the most fragile and are lost first” (Meares, 1999, p. 1852). That is, under threat higher cortical areas are “suddenly rendered functionless, the lower rise in activity.” Accordingly, Porges (2011) suggests that this process may be associated with a shift from a ventral-vagal, socially engaged state; to a sympathetic one where fight and flight predominate; and ultimately to a dorsovagal, catanoid, or death-feigning one. Under threat, the “first responders” among the active defense responses are mobilized. This may include RAGE that is expressed toward an attacker or predator

14  I.  NEUROBIOLOGY

and FEAR that results in a flight response toward safety (Panksepp, 1998, uses capitalization to reflect that these are not just emotions but hardwired subcortical affective circuits, experimentally established to exist from birth in mammals). RAGE and FEAR are affects that accompany and drive active defense responses of fight or flight: it is the immediate behavior that may save the life. It is necessary to have basic integration of different sensory inputs to activate the instant survival response. Higher level brain processes are not necessary to optimize survival in those situations. If anything, higher level brain processes will reduce the speed of response and thus decrease the likelihood of survival. Similarly, feeling is not adaptive, for example, in the case of injury, in that if anything it is distracting. What is needed is the immediate expression of a defense response with its associated basic affect to maximize the likelihood of successfully dealing with an immediate threat to life. Thus, the relaying of sensory input into the higher brain structures such as the limbic system and the neocortex is essentially maladaptive in situations of threat. The thalamic inputs to the amygdala and to the basal ganglia may be recruited in subcortical circuits, which, because of the complexity of the thalamus, may not find their way to processing in the neocortex. If the threat is overwhelming and/or the active defense responses have been exhausted or are ineffective, the helplessness may be followed by a dissociative collapse. In this case, opioid activation may interfere with sensory integration at the level of the superior and IC, decreasing responsivity to environmental events, and elicit passive defense responses of immobility and analgesia or anesthesia. When opioids are administered to the ventrolateral PAG, immobilization and antinociception (increased tolerance to pain) occur (e.g., Morgan & Clayton, 2005). For instance, direct injection of β-endorphin into the PAG produces profound catatonia, sedation, and analgesia. Moreover, there is a drop in metabolic function in the medial and lateral geniculate nuclei as well as in the superior colliculi (Sakurada, Sokoloff, & Jacquet, 1978). This suggests a decrease in sensory input being available at the level of the lower brain structures, reducing the capacity to respond to the immediate environment. This response of “playing possum” and the associated dorsovagal shutdown not only deprive the organism of active defense responses but also interfere with sensory integration, as it is simply no longer required. As suggested earlier, when this occurs, active defense responses are no longer available to the organism. Immobilization or “playing dead” does not require sensory input, and even less its integration. Indeed, any response to sensory input might jeopardize the last resort of passive defense response and thus reduce the risk of survival.

The Thalamus—Analgesic Chemicals and Retraction of Consciousness

As alluded to earlier, the functioning thalamus is critical for consciousness, as demonstrated by research on unconsciousness following brain injury and with anesthesia. For instance, vegetative states have been correlated with thalamic injury (Adams, Graham, & Jennett, 2000), particularly to the dorsomedial nucleus (Maxwell et  al., 2004). Moreover, absence-seizure activity that bears resemblance to certain types of dissociative states has been linked to thalamic dysfunction (e.g., Masterton et al.,

1.  Dissociation: Cortical Deafferentation and the Loss of Self   15

2012). The typical mode of action of general anesthetics is considered to be a hyperpolarization block of the thalamic relay neurons (Alkire, Haier, & Fallon, 2000). Indeed, disruption of thalamocortical communication is a key component of anesthetic-induced unconsciousness (e.g., Mashour, 2006). Further, Mashour (2005) suggests that the unconscious state arises from the uncoupling of corticocortical connections, a phenomenon she refers to as “cognitive unbinding.” Thus, anesthetic effects on consciousness appear to be mediated by changes in thalamocortical connectivity (e.g., White & Alkire, 2003), which in turn results in changes in interhemispheric connectivity (e.g., John, 2001). Endogenous opioids have an impact directly on the thalamus, as well as on the two poles of the fear and pain responses in the prefrontal cortex (PFC) and the midbrain, while endogenous cannabinoids act primarily on the nonthalamic areas. However, reduced cortical functioning is likely not solely mediated at the thalamic level alone. There is also evidence for the release of endogenous cannabinoids in response to trauma. Endogenous cannabinoids are active during fear in the midbrain PAG and in the PFC, potentially leaving the thalamus devoid of accurate information to send to the cortex and lacking a receptive area for integration of that information. For example, the cannabinoid CB1 receptor modulates in the thalamus the visual information sent to the cortex (Dasilva, Grieve, Cudeiro, & Rivadulla, 2012). Langsjo et  al. (2012), in a recent PET study with regard to the emergence of conscious states from anesthesia, relates the presence of a conscious state specifically to activation in a number of brain areas that include the brainstem, the hypothalamus, thalamus, and the anterior cingulate. The fact that ACC was the main cortical region to be activated on the reinstatement of the conscious state further indicates the susceptibility of higher functioning to thalamic deafferentation. Vogt and Sikes (2009) suggest that vegetative states show reduced activity in multiple brain regions that include the thalamus, as well as the precuneus, an area related to default network connectivity (see Chapter 4) and the posterior cingulate cortex region, including the retrosplenial cortex. The latter is a part of the cingulate cortex that has dense reciprocal connections with the anterior thalamic nuclei as well as with the hippocampus. It has been implicated in the recall of episodic memory and amnesia. These findings emphasize the critical linkages between the thalamus, the posterior cingulate cortex, and precuneal cortices with brainstem arousal systems. These basic neuroscience research findings with regard to anesthesia and consciousness provide strong support for the relevance of the altered thalamocingulate connections that have been reported in traumatic stress syndromes (e.g., Lanius et al., 2001). PD—When the Thalamus Acts as Circuit Breaker for the Cortex

PD (van der Kolk, McFarlane, & Weisaeth, 1996; also see Chapter  3) results in an alteration in consciousness that disrupts the integration of information. It refers to the inability to integrate what is happening into consciousness, where sensory and emotional elements of the event are not integrated into personal memory and identity. Thus, experience remains isolated from ordinary consciousness, ultimately resulting

16  I.  NEUROBIOLOGY

IMAGINE TRAUMA vs IMPLICIT BASELINE Control (n=9)

PTSD (n=9)

Figure 1.1  BOLD activation levels in control vs. PTSD group from Lanius et al. (2001). PTSD, posttraumatic stress disorder.

in a simple form of structural dissociation, for example, the lack of integration of the traumatic experience into ordinary memory (e.g., van der Hart, van der Kolk, & Boon, 1998), likely accounting for their timeless, predominantly nonverbal nature (van der Kolk & Fisler, 1995). Derealization and depersonalization—conceptualized as a compensatory response to primary dissociation—are likely related phenomena, though in this case thalamic inputs to the angular gyrus and adjacent parietal areas are likely more relevant than the prefrontal and midbrain areas. Script-driven imagery using recall of a traumatic event to produce a dissociative flashback has been shown to result in decreased thalamic activity (Lanius et al., 2001; Liberzon et al., 1999). Indeed, thalamic dysfunctions in PTSD have been reported in many PTSD studies but by no means in all of them. This state of affairs may reflect the severity of traumatization and may reflect a dissociative response to trauma exposure. Lanius et al. (2001), in a sample of individuals with severe PTSD, many of them multiply traumatized, found evidence that during recall of traumatic memories in PTSD, a decrease in brain activity is evident—despite the fact that physiological indicators were clearly suggestive of hyperarousal, for example, increased heart rate. That is, subjects showed significantly less activation of the thalamus, the anterior cingulate, and the medial PFC with decreased overall cortical activation (also see Figure 1.1). Moreover, functional connectivity studies suggest that this effect of thalamic deafferentation is more pronounced in the left hemisphere (Lanius et  al., 2004). Thus, when under threat, the information projected from the lower brain structures

1.  Dissociation: Cortical Deafferentation and the Loss of Self   17

to right hemisphere—and there are a greater number of connections from the lower brain structures to the right hemisphere—is less likely to be integrated by the left brain (e.g., Schore, 2003b). Moreover, altered thalamic connectivity is not only evident under threat, as in recall of traumatic memories, but also during resting states, for example, default network connectivity (Yin et al., 2011). We hypothesize that the decrease in thalamic activity is a response to excessive arousal. Indeed, it may reflect the simultaneous increase of both sympathetic nervous system activity associated with noradrenaline, in conjunction with a concomitant increase in parasympathetic activity, particularly dorso-vagal activity that is associated with increased endogenous opioid tone. In essence, the down-regulation of the thalamic relay can be construed as a circuit breaker or thalamocortical switch that will protect the neocortex from overactivation and the effects of excessive arousal.

The Effect of Endogenous Opioids on Thalamic Function

Indeed, the very areas identified by Lanius et al. (2001) as exhibiting decreased activation, for example, PFC, anterior cingulate, and thalamus, are similar to the ones identified by Lieberzon et al. (2007) using PET neuroimaging and a mu-opioid selective radiotracer. Liberzon and colleagues suggested that the functional alteration in regional cerebral blood flow was attributable to alterations in opioid receptor binding after psychological trauma. The very areas identified in these studies also happen to be the very areas that happen to exhibit the highest densities of opiate receptors in the cortex (Kling et al., 2000). Moreover, opioid activation has been associated with decreased local cerebral glucose utilization, particularly in the thalamus, limbic system, and forebrain regions (e.g., Fanelli, Szikszay, Jasinski, & London, 1987), suggesting a possible underlying mechanism. Endogenous opioids commonly affect specific thalamic nuclei depending on the origin of the presynaptic input, but they can cause inhibition of the entire thalamus (Brunton & Charpak, 1998). High opioid receptor densities occur also in the superior colliculi. As suggested earlier, both the thalamus and the colliculi have been associated with the presence of gamma oscillations that may play an essential role in information processing and cognitive temporal binding (see Chapter 11). Indeed, gamma oscillations decrease in response to opioids, a phenomenon that can be reversed by the administration of an opioid antagonist (Whittington, Traub, Faulkner, Jefferys, & Chettiar, 1998). At the same time, through the down-regulation of the thalamic relay and the resulting diminished sensory input to the cortical areas of the brain the capacity of the organism to respond to environmental input in any mindful manner is reduced. The nervous system has reverted to the quick and reflexive survival actions for which the brainstem, derived from the reptilian brain, is most adaptive. Thus, the disruption of the thalamic relay may be at the core of dissociative responses to overwhelming traumatic experience. High levels of arousal are associated with a disruption of the thalamic relay. There is a loss of sensory input to cortical areas, interfering with exteroceptive awareness, and an impaired capacity to integrate information at the cortical level. Moreover, this is associated with a decreased ability to allow cortical regulation of affective responses arising from the midbrain at the level of the PAG.

18  I.  NEUROBIOLOGY

Indeed, even the response to eye contact in individuals with complex PTSD is reflective of greater brain stem activation, as compared to an increased cortical response in individuals without PTSD (Steuwe, Lanius, & Frewen, 2012). With the disruption of the thalamic relay, the brain essentially reverts to dominance of brainstem functioning principally directed to survival, losing the very qualities that distinguish humans from lower animals, for example, the ability to self-reflect and the capacity to feel. The Role of the Thalamic Nuclei in Integrative Functioning of the Brain

As suggested earlier, the involvement of the thalamus in state switching likely involves thalamic inputs to the ACC. The pregenual ACC is relatively inactive in response to trauma-related stimuli in PTSD (Vogt, Aston-Jones & Vogt 2009). There is also reduced connectivity of the thalamus with the anterior cingulate in the resting state in PTSD (Yin et al., 2011b), specifically implicating thalamocortical projections from the mediodorsal, medial pulvinar, intralaminar, and midline nuclei of the thalamus (Shibata & Yukie, 2009). The medial pulvinar provides multimodal sensory and visual memory information to the anterior cingulate areas 25 and 32 and to the posterior cingulate area 23. It receives much of this sensory information from the superior colliculi (Bentivoglio et  al., 1993). The intralaminar nuclei also transfer information from spinothalamic tracts and from intermediate and deep layers of the superior colliculi to all areas of cingulate cortex. With cholinergic inputs from the mesopontine tegmentum, noradrenergic inputs from the LC, and serotoninergic inputs from the raphe nuclei, these thalamic nuclei contribute to sensorimotor integration (Bentivoglio et al., 1993). The midline nuclei, which process inputs from the hypothalamus, the bed nucleus of the stria terminalis (BNST), the spinal cord, and the midbrain areas of PAG, parabrachial nucleus, nucleus of the solitary tract (NTS), and LC also project to area 32 of the ACC. The thalamus is a composite of nuclei that receives input from all the senses and disperses information throughout the cortex. The part of the ACC that is functioning abnormally in PTSD has major inputs from subcortical structures for sensorimotor integration, emotion, defense, and autonomic regulation mediated by mediodorsal, intralaminar, and midline nuclei and the medial pulvinar of the thalamus. Thus, disrupting the thalamus means disrupting widespread activation throughout the brain, and thus connectivity between different brain regions. This includes both vertical and horizontal integration of brain functioning, ultimately contributing to the breakdown of integrative functioning of the brain under threat.

Opioid Activation, Deafferentation, and Symptom Specificity

Deafferentation commonly refers to central pain phenomena that are associated with a partial or complete loss of sensory input from a portion of the body following lesions in somatosensory pathways (e.g. phantom limb pain, nerve injury-associated pain). This disruption of sensory pathways commonly occurs at the level of the thalamus

1.  Dissociation: Cortical Deafferentation and the Loss of Self   19

with concomitant changes in the somatosensory cortex (Flor & Birbaumer, 2000). We hypothesize that opioid activation is a probable mechanism that results in decreased thalamic activation. This results in lowering of the level of consciousness through deafferentation of cortex from the lower brain structures. Moreover, as suggested by Brunton and Charpak (1998), endogenous opioids commonly affect specific thalamic nuclei depending on the origin of the presynaptic input. Therefore, excessive stimulation in a specific sensory modality may inhibit the associated sensory nuclei in the thalamus. For instance, overwhelming visual input would lead to an inhibition of the lateral geniculate and medial pulvinar nuclei of the thalamus. Such inhibition is likely to result in deafferentation, or partial deafferentation, of the visual input into the visual cortex, which would result in that very visual input not being integrated with other sensory input, for example, touch and smell, to produce an integrated experience. Thus, the person is likely to continue to experience visual flashbacks. Overwhelming arousal resulting in excessive endogenous opioid activation impairs information processing. Limited sensory information is conveyed to the areas of the cortex where integration of different senses, emotions, and thoughts can occur. This may be the functional mechanism that maintains the sensory memory as a fragment, rather than the integrated experience that is common for ordinary memories. Further, as such sensory input remains unintegrated, but also is associated with activation of a specific emotional circuit, a fragmented, trauma-related self-state with distinct sensory experience is created.

Pierre Janet—Field of Consciousness, Partial Catalepsy, and Deafferentation

Janet (1889), in conjunction with dissociation, refers to a narrowing or a retraction of the field of consciousness, a reduction in the number of phenomena that are held in conscious awareness. This notion bears resemblance to the changes in thalamic activity that are related to arousal as reported by Portas et al. (1998). That is, with low arousal the field of consciousness normally widens, whereas high arousal is accompanied by a narrowing of the field of consciousness. As van der Hart, Nijenhuis, and Steele (2006) point out, such a narrowing of consciousness alone is insufficient to result in structural dissociation or pathological dissociation. However, Janet also refers to “Les catalepsies partielles,” the partial catalepsies. Catalepsy is characterized by immobilization and muscular rigidity, as well as a lack of responsivity to external stimuli and decreased sensitivity to pain. It is further associated with a slowing down of bodily functions, such as breathing, and can ultimately result in a loss of consciousness. A number of substances have been associated with the induction of catalepsy, one of them being opioids. This condition specifically is referred to as opioid or opiate catalepsy (e.g., Ling & Pasternak, 1982). Opioid catalepsy can be reversed by the administration of opioid antagonists, particularly in the PAG and thalamus (e.g., Wilcox, Bozarth, & Levitt, 1983). Specifically, we suggest that the narrowing of the field of consciousness that occurs in conjunction with an opioid-mediated cataleptic state is at the core of “disaggregation” or dissociation (Janet, 1919/1976), the breaking up or breaking apart

20  I.  NEUROBIOLOGY T

T′

T″

M

M′

P′

M″

V

V′

V″

A

A′

A″

P

Figure 1.2  Dissociation between Parts P and P′, as described by Pierre Janet (1889).

of the self. This phenomenon was depicted in Janet’s seminal work, L’Automatisme Psychologique (1889): He conceptualizes and visually depicts the lack of horizontal integration between different types of sensory input. That is, in the figure below, the lack of integration between one part (P) and another (P′) is illustrated (also see Figure 1.2). P refers to the association of two types of auditory input (A and A′) and two types of visual input (V and V′). P′ refers to auditory (A″), muscular (M′), and tactile (T′) input. Assuming they represent different aspects of an experience, one would expect the individual to fluidly conjoin those experiences into a narrative. Where a retraction of consciousness attributable to high arousal occurs in conjunction with an opioidmediated cataleptic response, one would expect the state change to be no longer fluid. That is, state change will be accompanied by alterations in consciousness that result in a lack of horizontal integration and in more extreme cases in amnesia.

The Nature of Affective Circuits and Structural Dissociation

We suggest that separate self-states are likely a direct result of the breakdown of integrative functioning and deafferentation. Those that arise in direct response to threat, for example, EPs (van der Hart et al., 2006), likely reflect truncated defense responses separated at a subcortical level. Others that arise in response to facilitating adaptive functioning, often with little or no emotional charge, may be based on relatively independent corticothalamic loops. The thalamus conveys information from the body—relayed in spinothalamic tracts—to the insular and cingulate cortices (Craig, 2006). Ego states that have specific physiological components must have interoceptive circuits through the thalamus. Also, those that do not have marked autonomic accompaniments will have cortical loops through the basal ganglia and thalamus. Therefore the thalamus may contain nodes for circuit switching—from one ego state to another parallel loop—although it is suggested in a later chapter that it is the insula that is key: responding to changes in body state. These circuits can be functioning relatively independently at different levels of the brain. For example, cortical loops take sensory input into the cortex, process through the basal ganglia, and return through the thalamus to the cortex for motor output (Redgrave et al., 2010). Subcortical loops, in contrast, have the thalamic relay

1.  Dissociation: Cortical Deafferentation and the Loss of Self   21

on the input to the striatum. There is a return to the subcortical structures via the basal ganglia for motor output. Sensorimotor loops can thus form two distinct circuits in the brain, which have the capacity for horizontal disconnection: reflexive defensive behaviors and goal-directed actions employing different neural pathways. Vertical loops for defense responses could have inputs from different brain levels— for example, from the right insular cortex, the right amygdala, and the brain stem— but be insufficiently integrated across the corpus callosum and throughout the PFC.

Analgesic Response and Separate Self-States: ANPs and EPs

At times of severe threat, the brain needs a range of analgesic responses to facilitate survival. We suggest that the separateness of these self-states is a consequence of activation of endogenous neurochemical analgesics that prevent overload during higharousal states. These analgesics are part of a dorso-vagal parasympathetic response, resulting in sensory and somatic fragments of traumatic experiences escaping integration. This may occur through a variety of mechanisms that include unblended colliculus-thalamus-cortex loops linked by the basolateral amygdala. In some instances the hyperarousal of brainstem survival functioning leads to a shutdown of the thalamic relay and a relative deafferentation of specific cortical areas. Then the emotional expression of behavior is not integrated in the larger context, as the person can no longer bring neocortical resources to bear on it. The basic affective circuits reverberate in an ongoing manner, reactive to outside stimuli, but relatively impervious to top-down modulation and horizontal integration at the level of the neocortex. Separate self-states can be complex emotional states based in truncated defense responses and have relatively independent interoceptive loops through the brainstem, the body, the spinothalamic tracts, and the cortex. At the other extreme are separate body states that have circuits through the brainstem and body with little involvement even of thalamic structures. They resemble what van der Hart et  al. refer to as EP’s. Other self-states are stored in cortico-striato-thalamo-cortical loops that have little affective or defensive loading. These different states resemble what Van der Hart et al. (2006) describe as ANPs. These self-states are more likely separated at a subcortical level—thalamocortical loops through the basal ganglia.

Truncated Affective Circuits, Structural Dissociation, and Self-States

Nijenhuis et al. (1999) relate discrete traumatized self-states, including specific somatoform dissociative phenomena, to animal defensive responses and recuperative states that develop in response to predatory attack. That is, van der Hart et al. (2006) suggest that the structural dissociation model reflects “emotional personalities” that involve different animal defense-like systems. Stimulation of the dorsal and lateral aspects of the PAG provokes defensive responses of fight or flight. Stimulation of the caudal ventrolateral PAG results in

22  I.  NEUROBIOLOGY

quiescence or freeze. Whereas lesions of the caudal ventrolateral PAG reduce conditioned freeze, lesions of the dorsal aspect reduce fight-or-flight behavior. That is, different animal defensive responses such as fight and flight and surrender and collapse likely become the core of self-states or EPs, where fight corresponds to RAGE and flight to FEAR and intense separation distress leads to extreme states of PANIC. Panksepp (1998) links the PANIC system with attachment, where unmet attachment needs in the face of separation will ultimately induce states of panic. The term panic is often used in a less-specific sense to indicate the terror or acute intense fear based in the dorsolateral PAG. Panksepp does not have a separate system for the animal equivalent of the submissive, surrendered, dissociative collapse, which is important in human victims of severe trauma. The dorsal vagal freeze state of immobility and bradycardia is accompanied by opioid-mediated analgesia, which may contribute to the structural dissociation of this state. For active defense states generated in the dorsolateral PAG, the endogenous analgesia is mediated by endogenous cannabinoids. These may contribute to structural dissociation by deafferentation of thalamocortical projections and contribute to memory disturbance through their impact on the basolateral amygdala and hippocampus. Defense response states can become structurally dissociated in subthalamic loops through the body, in spinothalamic interoceptive loops through the ventromedial PFC, and in subcortical loops through the basal ganglia.

Loss of Higher Cortical Functioning—Positive and Negative Symptoms

Van der Hart et al. (2006), as did Janet (1893/1901/1977) and Myers (1940) before them, differentiate between positive and negative symptoms of dissociation. Negative symptoms of dissociation are generally held to refer to losses of function, such as memory (i.e., amnesia), higher cortical functions, loss of feeling, loss of motor control, as well as loss of somatosensory perceptions, for example, numbness. Positive symptoms may include intrusive traumatic memories, flashbacks, intrusive voices, as well as intentions, emotions, cognitions, and behaviors, including complex patterns such as reenactments. It is easy to see how opioid activation is responsible for negative symptoms of dissociation. Similarly, we suggest amnesia and anesthesia are opioid-mediated phenomena that either relate to the lack of sensory transmission at the thalamic level due to shutting down of particular thalamic nuclei (e.g., symptoms of anesthesia) and a more general amnestic process in the brain that again relates to a conditioned response. Alternatively, negative dissociative responses may also reflect the effects of opioid activation of the ventrolateral PAG. That is, negative dissociative symptoms likely not only relate to passive defense responses evoked at the level of the PAG but also due to higher centers being inhibited at the level of the cortex. Both of these likely result in an absence of function or “negative” symptoms. “Positive” symptoms, on the other hand, are likely caused by the functional release of the lower centers due to lack of effective cortical ­down-regulation, contributing to decreased modulation of affective responses at the level of the PAG.

1.  Dissociation: Cortical Deafferentation and the Loss of Self   23

Somatoform Dissociation and Deafferentation

Clinical observations indicate that dissociation can manifest in somatoform ways (e.g., Nemiah, 1991). Somatoform dissociation includes many somatic and sensorimotor phenomena and can present in a variety of ways that include sensory distortions, motor weakness, freezing, numbing, paralysis, and tremors (Nijenhuis, 1999). Shaking and convulsions are also common, as are sleepiness, attentional impairment, and headaches and other pain sensations that may be much less obvious. That is, van der Hart and colleagues (2006) specifically refer negative and positive dissociative symptoms and suggest that negative dissociative symptoms likely relate to passive defensive responses and associated predominant dorsovagal activation and associated opioid activation in the ventrolateral PAG. Positive dissociative symptoms on the other hand are likely believed to relate to active defensive responses. While among the latter sympathetic tone predominates, excessive associated arousal will likely result in significant endogenous opioid release and resulting levels of deafferentation. In the case of symptoms of dissociative collapse, these EPs may be further defined by an increasing opioid innervation of the ventrolateral PAG that results in states of immobilization and catatonia. Opioid activation is also related to alterations in eating behavior, where excessive opioid tone is associated with both starvation as well as binging behavior (e.g., Bodnar, 2007). Pain phenomena can be conceptualized in a similar way, as being attributable to deafferentation resulting in somatic reorganization similar to central pain phenomena as they occur in deafferentation and phantom limb pain (e.g., Giummarra & Moseley, 2011). Similarly, if during sexual abuse a person experiences overwhelming tactile stimulation in the genital area, deafferentation of the ventral posterior nucleus may ensue. This may account not only for somato-sensory flashbacks of the experience but also an inability to experience sexual pleasure through sensory stimulation of that area and even possibly account for genital pain. This has implications for conversion symptoms. We suggest this type of urogenital pain, in particular, is likely attributable to deafferentation of body regions to trauma related to sexual abuse. Other pain disorders common in individuals with trauma-related disorders are likely attributable to a similar kind of functional mechanism. We further suggest that opioid activation is responsible for what van der Hart et al. (2006) describe as negative symptoms of dissociation. Stress and threats to life induce analgesia and numbness, a phenomenon that has been described as learned helplessness (e.g., Van der Kolk, Greenberg, Orr, & Pitman, 1989). Nijenhuis, Spinhoven, van Dyck, van der Hart, and Vanderlinden (1998) found that dissociative symptoms reminiscent to analgesia and numbness in particular, for example, freezing, anesthesia, analgesia, disturbed eating, and urogenital pain, were predictive of a diagnosis of dissociative disorder, with anesthesia–analgesia being the best predictor, thus supporting our notion of the relevance of opioid activation to the phenomenology of dissociative disorders. We suggest amnesia and anesthesia are opioid-mediated phenomena that either relate to the lack of sensory transmission at the thalamic level due to shutting down of

24  I.  NEUROBIOLOGY

particular thalamic nuclei (e.g., symptoms of anesthesia) and a more general amnestic process in the brain that again relates to a conditioned response. Alternatively, negative dissociative responses may also reflect the effects of opioid activation of the ventrolateral PAG.

Summary and Future Directions

Events experienced as traumatic evoke the release of the brain’s own analgesic compounds that include opioid, cannabinoid, and other agents. This leads to thalamic deafferentation, including reduction of input to the ACC and other cortical areas. Reduced connectivity of the anterior and posterior cingulate cortices limits information processing, especially when it is self-related. Anesthetic neurochemicals released in response to stress also induce functional activation or deactivation in areas that mediate the affective responses. These peritraumatic chemical changes in the midbrain and cortex can mimic or induce the diminished activation of relevant areas of thalamus releasing the cortical imbalance—some areas relatively more active, others less so. We therefore argue that clinically relevant dissociation is not on a continuum of compartmentalized attentional focus. Dissociation, which results from overwhelming experience, has immediate neurochemical mediators that promote the creation of neural networks that can be evoked to function relatively independently. The primary purpose of the chemical release is the reduction of pain, fear, rage, and/or separation distress. The brain produces its own equivalents of morphine and cannabis to attenuate fear and pain. This produces changes in the plasticity of the connections between neurons creating new networks. When these networks are later functioning as independent ego states, the contribution of the analgesic neurochemicals may be much less than when the states came into being. Nevertheless, they arose through a failure of integrative capacity—when the brain’s strategies for overload were urgently activated. The morphine and cannabis equivalents dull the pain immediately but affect long-term functioning in a way that ultimately ceases to be adaptive. When the cortex shuts down subcortical generation of painful affects, this top-down control can be described as overmodulated dissociation: it may become habitual and relatively independent of endogenous analgesic agents. When the subcortically generated affects are overwhelming and the cortical modulators are unable to diminish the distressing impact, this dissociation may be described as undermodulated: the cortex gives up and goes “offline.” The prototypical dissociative states arise in infancy when needs are not being met to such an extent that endogenous opioids and cannabinoids are released to dull the pain of protest and despair. The later detachment phase may not have the same intensity of neurochemical mediation but may arise from the new neural networks created to cope with the demands of the environment. When fuses in an electrical circuit keep melting, they can be replaced by ones of lesser sensitivity. While that saves on fuses in the short term, the result may be damage to the appliance and a risk of fire. The sensors need to be adjusted to the right setting for maximal resilience and long-term functioning when the environment is not hostile.

1.  Dissociation: Cortical Deafferentation and the Loss of Self   25

Emotional experiences that need brain analgesics to blunt their intensity underlie clinical dissociation. Finally, there may be additional effects of opioids that are relevant to our understanding of altered thalamo-cortical connectivity that may be relevant to our understanding of dissociation that involve decreases as well as increases in brain activation in response to opioids (Su, Huang, Wang, Wang, & Luo, 2012). These are not yet elaborated in our model but may yield some relevance to our understanding of the development of nontraumatized self-states.

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CHAPTER 2

Threat and Safety: The Neurobiology of Active and Passive Defense Responses Frank M. Corrigan

He was edgy, his skin prickly, the night’s euphoria just a dream. He turned, scared by a noise from the shadows, a scratching and rustling; but it was just a rat, scuttling into a warehouse, intent on survival, like himself and every other creature. He shivered though it wasn’t cold, walked home in the first grey light of dawn. —Alan Spence (2006, p. 76)

When survival is threatened by physical injury, death, or social exclusion, the brain has well-established responses, immediate and sequential, to promote safety. These defense responses are based in the emotion-generating regions of the brainstem but are rapidly modified and modulated by the more developed and evolved cortical capacities. Defense responses become pathological and contribute to depressive disorders when they are too readily activated, prolonged, blocked, and/or ineffective (Gilbert, 2001). Persistence of defense responses beyond the situation that triggered them contributes to the clinical expression of posttraumatic stress disorder (PTSD; Cantor, 2005), and these responses form the core of many of the self-states created as a result of structural dissociation (van der Hart, Nijenhuis, & Steele, 2006).The posttraumatic dissociative disorders are most severe when early attachment trauma is followed by physical and sexual abuse (Lyons-Ruth, Dutra, Schuder, & Bianchi, 2006). The aim of this section is to draw together clinical observations, brain imaging studies in humans, and animal studies of responses to trauma to promote testable conclusions on the likely neurochemical mediators of the key components of 29

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posttraumatic disorders. This includes the high- and low-arousal symptoms of PTSD and the amnesia, derealization/depersonalization, and identity confusion/identity alteration of the dissociative disorders (Steinberg, 1995). The drawing of information from different disciplines means that some of the hypotheses (such as the involvement of endocannabinoids in high arousal dissociation) have not yet been empirically tested. The diversity of experiences can best be understood by considering both the immediate neurochemical and neural network effects of trauma and the long-term consequences for the integrated neurobiological underpinnings of everyday mental activity. The clinical spectrum created by severe and early trauma and neglect can be broken into distinct phenomena with their own neurobiological correlates to generate hypotheses for research. The hypotheses also provide a structure for the interpretation of brain imaging studies, which can otherwise yield a massive amount of data not readily integrated with the realities of clinical practice. Some of those studies are discussed in Chapter 4. Animal studies reveal a variety of complex defense responses that may inform our understanding of clinical symptom constellations, as these responses can occur in humans confronted with physical danger and/or social threat. The following case summary illustrates how midbrain activations can take control in a situation in which there is no physical threat. It also illustrates how long lasting the adverse effects of such a traumatic experience can be for the person’s mood and self-esteem.

CASE SUMMARY: DEFENSE RESPONSES IN RESPONSE TO SOCIAL THREAT

A 35-year-old woman in a responsible administrative post, married with two children, presented with a 4-month history of low mood, social withdrawal, insomnia, and with urges to kill herself in a painful way. She was only 16 years old when her mother died; after this her father began drinking heavily and became preoccupied with his own suffering: he appeared unconcerned about her needs. He later remarried. The sale of his house after his death may have been the precipitant for the onset of the depression: Nothing was left of her parents but her mother’s gravestone. Her treatment consisted of evidence-based cognitive-behavior therapy in combination with the antidepressant Venlafaxine at 225 mg daily. After 6 months of this resulted in no improvement, she received eye movement desensitization and reprocessing (EMDR) for her obstructed grief. Although there had been traumatic experiences when she left home, we decided to first address her feelings about her mother’s sudden death. In preparing for EMDR, the target image was of having been required by the family doctor and a police officer to go into the bedroom to see her mother’s body. She was then very aware of them standing there staring at her, giving her no indication of what was expected of her. Her natural responses were inhibited and she felt accused and trapped. The social threat was accompanied by the negative cognition “I’m trapped,” a nervous feeling in the stomach, a tension in the legs, and a subjective unit of disturbance (SUD) score of 8 out of 10, 10 being the worst she could feel. The following themes were prominent during the EMDR sessions as processing unfolded. (Hypothesized midbrain responses in parentheses.)

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I just wanted to get out: I couldn’t move. I couldn’t stay there. My legs wouldn’t move. (Frozen Flight) They didn’t need to be in the room. I’m trapped. I’d like to push them away, to push past them. I can’t move my arms. (Frozen Fight) I’m not allowed to touch her, to show how I feel. What is the point of being there, just staring at her? I can’t do anything. (Submit) I want to get out. My body has gone numb: I can’t feel anything. (Frozen Flight with High Arousal Dissociation) I just feel stuck. I can’t move. I’m staring at her: they are staring at me. I can’t look away. I can’t do anything: frozen all over. (Tonic Immobility [TI]) I’m trapped. I can’t get out. I’m staring at her and I don’t feel anything: switched off and numb. I don’t want to be there. I’m scared to feel anything. (TI or Frozen Flight with High Arousal Dissociation) I want someone there for me. (Obstructed Attachment With Protest) It means nothing: empty and numb. I’m doing what I have to do: I’ve no choice. (Submit) I want to cry but I can’t. (Obstructed Grief) I’m just waiting. I feel nothing: breathing is slower. I’m just looking where I’m supposed to look. Everything is standing still. Muscles are not so tense but I don’t feel I could move. (Frozen or Non-Autonomous, Over-Compliant Submit?) I just want out but I can’t move. There is not so much tension in the muscles. I’m looking at her but she’s not there. There is no noise: I don’t hear anything. I feel empty. My vision is blurred. It feels that the heart rate has slowed. I’m just there but there is nothing happening. I could shut my eyes and go to sleep. (Dorsal Vagal Response: Low Arousal Freeze With Dissociation)

As EMDR sessions progressed, the patient exhibited less freeze and more obstruction: ■■ ■■ ■■ ■■

It just feels like I’m staring at her. It is getting easier. I’m not so cut off. I’m being watched, accused. I don’t want to keep staring at her with them watching me. (Obstructed Fight) All I can do is to wait: I can’t do anything. (Submit) I can’t let myself feel anything. I can’t let myself cry: They are watching me. (Obstructed Grief)

Between sessions the patient is now very emotional, crying a lot when she is by herself, liberating the grief that has been pent up for 20 years. There is also a blocking belief: all she has left is the way she feels about her mother. If she loses that there is nothing left. ■■ ■■ ■■ ■■

I wanted to go toward her but they are standing there. I’m not allowed to do anything. My feelings don’t count. (Obstructed Attachment: Protest) I just want someone to think of me. I just want someone to be there for me. They make it all so meaningless. (Attachment Urge—Obstruction—Protest) I was angry at them. I want to push them out of the room. I want them to leave me alone. (Fight) It’s pointless. It means nothing. I can’t do anything. (Submission)

32  I.  NEUROBIOLOGY

The next session oscillated between the fight and submit responses. The patient was not comfortable with the proposed sensorimotor interventions using pushing or walking movements, so we continued with EMDR, with the tension gradually reducing and frozen responses clearing. ■■ ■■ ■■

I’m left to stand and stare. I want to sit down and cry. I want to shut my eyes until they let me out. Therapist: How does it feel now to be able to close your eyes? Relief. I’m more in control. My chest is not so tight. I like being in control; much more relaxed.

The patient was then able to move on to reprocess later experiences that also involved considerable sadness and grief, as they would not have happened or been so traumatic if her mother had still been alive and there to look out for her.

THE RANGE OF DEFENSE RESPONSES

In this chapter we are concerned with the neurobiology of the whole spectrum of defense responses to threats: near or distant, immediate or potential, physical or social. The focus is on vigilance, fight, flight, freeze, hide, cringe, submit, and avoid behaviors. In Chapter 7, we define and distinguish between frozen and obstructed responses. Attachment to a potential helper is discussed in a separate chapter (Chapter  10, Attachment and Attachment Repair). Bracing and shock impact responses are not considered because there is insufficient information from animal studies. Other authors have categorized defense responses in similar ways. Gilbert (2001) described defensive fight, escape flight, help-seeking, submitting, hiding, camouflaging, turning away, and demobilization such as freeze-faint. Cantor (2005) highlights vigilance, avoidance, flight, aggressive defense, TI, and appeasement. Van der Hart et al. (2006) focus on action tendencies accompanying hypervigilance, flight, fight, freeze, submit, and attach responses to threat. The core responses are seen in animals in the major emotional operating systems for RAGE (with biting and affective attack); FEAR (with flight and escape behaviors); SEEKING (for moving forward and investigating in a search for safety, if threatened); and PANIC (for expressing distress to conspecifics and seeking attachment and care; Panksepp, 1998). As brains become more evolved, there is growth of the cortical capacity for response suppression on the basis of greater information processing—and more opportunity for conflicted states. Figure 2.1 is an illustration of the layering of control of defense responses. Sudden withdrawal of a hand from the hot plate it has inadvertently touched is mediated at the level of the spinal cord. The acoustic startle response, “jumping” when there is a loud and unexpected noise, involves the hindbrain with the spinal cord. The next level, the midbrain, is the one that has special application to trauma. It is in the midbrain that sensory stimuli indicating threat are processed rapidly to instigate defensive motor behaviors and autonomic adaptations. We will focus especially on the superior colliculi (SC), the inferior colliculi (IC), and the periaqueductal gray (PAG).

2.  THREAT AND SAFETY  33

Cognitive Analyses

Context

Complex Neutral Stimuli

Response Suppression

Frontal Cortex

Hippocampus & Septum

Sensory Cortex

A M Y G D A L A

Conditioned Emotional Responses

Neutral Stimuli Thalamus

Species-Specific Threat Stimuli

Midbrain & Hypothalamus

Species-Specific Responses Freeze/Flight/Fight

Sudden Distal Stimuli

Hindbrain

“Startle” Responses

Noxious or Contact Stimuli

Spinal Cord

Reflexive Withdrawal

Sensory Input

Motor, Autonomic, & Endocrine Output

Figure 2.1  Layered organization of neural mechanisms of defense: Higher level components provide increasingly sophisticated solutions to problems of reducing and avoiding harm. Each boxed structure has loops through the basal ganglia and cerebellum. The selection problem created by the different areas processing in parallel is resolved in the basal ganglia where it is “decided” which component of the multidimensional sensory input directs the motor, autonomic, and endocrine output. Adapted with the help of Dr. Pete Redgrave from Prescott et al. (1999).

34  I.  NEUROBIOLOGY

Trauma Has an Impact on the Representations of the Self in the Midbrain

Chronic characterological changes arising from alterations in self-perception with guilt and shame, self-blame, feelings of ineffectiveness, and loss of trust (van der Kolk, 1996) are part of the long-term damage caused by early trauma and may result from subtle changes in valence at the level of the midbrain, the core of the subjectively experienced “self.” This is described more fully in later chapters, and treatment targeting very early traumas held in implicit memory is also addressed later in the book. In outline, there is a fundamental somatic motor map created by the emotion-generating PAG and the somatosensory SC (Panksepp, 2003), and the integration of sensory input and motor output in the SC contributes to the self’s individually characteristic emotional and motivated behaviors (Merker, 2007). Damasio (2010) favors the contribution of the parabrachial nucleus and the nucleus of the solitary tract (NTS) in the sensory experiences of the primordial self while acknowledging the close association of the PAG and the SC. Although there is debate about which structures are most involved, trauma of sufficient severity to elicit defense responses, especially if they are obstructed or ineffective, is modifying the sense of self at its very core in the midbrain. At the level above the midbrain, the hypothalamus of the diencephalon contributes to the emotions that maintain the appropriate defensive behaviors even when the stimulus has been withdrawn. As Prescott, Redgrave, and Gurney (1999) observe, the prey animal won’t survive long if it loses its fear and stops running as soon as the predator moves behind a bush. At the next level up, sensory stimuli can be associated with harm through the amygdala for cues and the hippocampus for spatial contexts. The bed nucleus of the stria terminalis (BNST) and the septum may contribute to vigilance for, and identification of, social threats. Complex processing of multisensory stimuli through the cingulate cortex will also be considered later. It is through the prefrontal cortex that the learned connections between sensory stimuli and the amygdala are inhibited. Some people who have responded well to treatment for PTSD can relapse readily with further stress and trauma. It remains to be established if a sensitization to the activation of defense responses is only at the Dorsomedial prefrontal cortex (BA10)

Neocortex

Anterior cingulate cortex (BA24)

Cingulate or Limbic Cortex

Rostral anterior cingulate Cortex (BA32)

Basal Ganglia Thalamus

Subgenual anterior cingulate cortex (BA25)

Midbrain

Ventromedial prefrontal cortex (e.g. BA14)

Medulla

Pons

Brainstem = Midbrain + Pons + Medulla

FIGURE 2.2  Schematic diagram to roughly illustrate the locations of brain areas referred to in the text.

2.  THREAT AND SAFETY  35

level of the amygdala or whether it can also occur in the midbrain. Clinical observations suggest hyperresponsiveness of the emotion-generating areas of the PAG.

WAITING, WATCHING, AND THE SECURITY MOTIVATION SYSTEM

A person who is waiting, day after day, for the first sign of rapidly escalating danger will be in a state of readiness and dread, which will not require constant activation of hyperarousal fight or flight behaviors. Instead, his or her autonomic nervous system will be geared to rapidly engage the sympathetic-dominant state and the active defense responses if and when the occasion arises. This intermediate state is a security motivation system (Woody & Szechtman, 2011) that is readily triggered and is slow to deactivate even in the absence of overt threat. Information from the environment is collected and potential danger is appraised not only by the amygdala and the BNST but also by the hippocampus and the prefrontal cortex. Output to the ventral striatum in response to sensory stimuli endorses the feeling of wariness through connections with the BNST. Output to the dorsal striatum, via the midbrain, mediates the motor and cognitive effects. In the table in Chapter 7 (Table 7.1) we have included a “Waiting” state as a separate defense response, which can become a relatively independent state, although our emphasis is more on the midbrain SC for monitoring the environment for threat and for rapid movement toward or away from any detected danger. The security motivation system is not as energy consuming as active defense, so energy supplies are made ready without being fully accessed. Likewise, the autonomic nervous system needs a state of readiness without full sympathetic activation and this is achieved by a reduction in parasympathetic control reflected in heart rate variability (Woody & Szechtman, 2011). The switch for turning off the security motivation system may be elusive in complex trauma disorders.

Proximity of Threat and Activation of the Midbrain

Potential threat is experienced when an animal is waiting for, anticipating, or dreading the appearance of a predator. The cortical component of this monitoring includes the insular, the medial prefrontal, the anterior cingulate, and the posterior cingulate cortices (Fiddick, 2011). When there is a definite and immediate threat that is getting nearer, the interaction of the cerebral cortices and the midbrain changes as the threat is proximal rather than potential. When a threat to physical survival is rapidly approaching, and there is little time to think about what is best to do, the advanced human brain, unless specifically trained to do otherwise, will engage the phylogenetically primitive defense response areas of the midbrain to assume the responsibility for maintaining life and physical integrity. This adaptive override of cortical by subcortical systems allows older brain regions to initiate fast reflexive behavior and to begin induction of neurochemical analgesia. The cortical-subcortical shift of control has been clearly demonstrated in an imaging study of response to a “virtual predator” by Mobbs et al. (2007). Brain activations were observed as the “predator” drew closer in a two-dimensional maze

36  I.  NEUROBIOLOGY

on a computer monitor. If “captured” by the predator, volunteers were told they would receive pain of high (three cutaneous electrical shocks) or low (one shock) intensity. When subjects were told that they were moving from the control condition to the pursuit phase, midline prefrontal cortical areas associated with complex decision making became activated. These included anterior cingulate cortex (ACC) and ventromedial prefrontal cortex (VMPFC). During the period when the volunteer was being chased through the virtual maze by the predator, activations were seen more in noncortical areas, including the PAG in the midbrain. The degree of proximity of the “predator” produced quite different responses in the volunteer’s brain. When the threat in the maze was distant, there was more activity in the prefrontal cortex. When the threat was close, activity peaked in the PAG, the midbrain region crucial to the defense responses of fight, flight, and freeze (Bandler, Keay, Floyd, & Price, 2000). This PAG activation increased with the high-intensity threat and was linked to a subjective feeling of dread of capture and, cognitively, to reduced confidence that escape was possible. Reduction of dread and increased confidence of escape, on the other hand, were associated with activation of the VMPFC. This study supports the proposition of a hardwired forebrain–midbrain network, a VMPFC-PAG axis, with the VMPFC activated by low-level or distant threats and closely interacting with the midbrain PAG, which becomes more dominant as the threats draw nearer and/ or become more intense. If this happens to adult volunteers in a controlled environment, how much more dramatic will be the shift from cortical to subcortical dominance in situations of life-threatening terror, when the heart is pumping furiously and the muscles are straining for every available ounce of strength? It is true that in those situations people cannot readily have their brains imaged and a different pattern may emerge. Nevertheless, it is through the midbrain that there is access to the rapid autonomic and motor capacities required when one wrong move may lead to life being extinguished. Potential Threat and the ACC; Perceived Threat and the SC

Informing the subjects of increasing threat intensity (in the Mobbs et al. [2007] study) required them to assess the potential threat. The associated activation of the ACC is

Superior Colliculi Inferior Colliculi

Periaqueductal Gray

FIGURE 2.3  Defense reponse and orienting areas of the midbrain.

2.  THREAT AND SAFETY  37

in keeping with the conclusion of Fiddick (2011) on the role of the ACC in this type of assessment. A distinct form of evaluation occurs when the threat is present, visible, and available for immediate orientation. It is in the intermediate and deep layers of the SC that connections with the PAG and hypothalamus permit an interaction of the motivational affective processes with the orienting stimuli from the external world (Merker, 2007). The SC are structures adjacent to the PAG where an integration of sensory inputs with rapid motor responses occurs, allowing the eyes to be drawn immediately to a threat in the environment. As they also receive auditory and somatosensory information and control many motor responses (Schenberg et al., 2005), any rapid, protective, behavioral response will depend on the SC for accurate localization and protective movement. Slapping the skin in the right place to squash a blood-sucking insect would depend on such integration of information. A lesion that damages the SC reduces the capacity for defensive responding, even when the PAG is spared (Dean, Redgrave, & Westby, 1989). The SC also promote efficient hunting. Rodents with no prior training in predation will launch themselves at insects, capture them by using their head and forepaws, kill them with a bite to the head, and then eat or continue hunting: lesioning of the SC disrupts the efficiency of this sequence (Furigo et al., 2010). The SC have extensive connections, including those with the different columns of the PAG, and are in a central position for integrating incoming sensory stimuli about threat with immediate autonomic, arousal, and motor responses.

THREAT REQUIRES RAPID MOTOR, ATTENTION, AND AROUSAL RESPONSES

There are closed subcortical loops through the SC, the substantia nigra, the thalamus, and the striatum. The archetypal motor behavioral programs implemented in response to the sight, sound, or smell of a prey animal—or a predator—are mediated by these loops. Connections with the lateral hypothalamus and the ventral tegmental area contribute to the motivating aspects of predatory aggression while ascending projections to the thalamus from the SC influence general cortical arousal (Furigo et al., 2010). Attention and arousal are also increased by noradrenergic projections from the locus coeruleus (LC), to which the dorsal PAG projects (Schenberg et al., 2005). There are therefore pathways by which the midbrain can rapidly increase overall brain activation when a threat in the environment is detected. The colliculi receive inputs from cortical areas concerned with vision, hearing, and body sensation, but not from ventromedial prefrontal areas (Manger, Restrepo, & Innocenti, 2010). In the rhesus monkey, there are projections from the dorsolateral prefrontal cortex, as well as from the frontal eye fields to the SC (Johnston & Everling, 2006), allowing rapid cortical involvement in an integrated response to a visual stimulus. It could be difficult for people to draw their eyes away from disturbing scenes because collicular responses to threat are immediate and less easily modulated by emotion-regulating prefrontal controls. The SC, the amygdala, and the pulvinar respond to fearful faces (Morris, deBonis, & Dolan, 2002), and even subliminal presentations of facial fear elicit activity in the SC in humans (Liddell et al., 2004). Direct projections from the

38  I.  NEUROBIOLOGY

Superior Colliculus: superficial grey layer (SuG) and optic nerve layer (Op)

SuG Op InG DpG InWh

Superior Colliculus, Intermediate grey (lnG) and white (lnWh) layers

DpWh Superior Colliculus: deep grey (DpG) and white (DpWh) layers PAG Periaqueductal gray

DR

Dorsal raphe nucleus

xscp

Decussation superior cerebellar peduncles

ml

Pn

Medial lemniscus

Pontine nuclei

FIGURE 2.4  A schematic illustration of a cross-section of the rat midbrain showing the key structures. Adapted with the help of Dr. Pete Redgrave from King, Shehab, Dean, & Redgrave (1996).

amygdala to the colliculi allow sensory stimuli to acquire emotional salience in subcortical circuits through the thalamus (Marsh, Fuzessery, Grose, & Wenstrup, 2002). Dorsolateral and ventrolateral areas of prefrontal cortex underlying working memory and cognitive restructuring of emotion are most readily available when the level of fear is not urgent and overwhelming. At times of extreme threat, the feelings of terror and dread, the autonomic arousal, and the immediate behavioral responses are all derived from the brain stem and the associated subcortical circuits. These have an impact on the body state and on the body’s capacity to respond with fluent urgency.

A Taxonomy of the Midbrain’s Range of Defense Responses ■■ ■■ ■■ ■■ ■■ ■■ ■■ ■■

Orienting to Threat Avoidance: Withdraw, Hide, and Cringe Responses Flight Fight Freeze Immobility Submit Attach (SEEKING to reduce PANIC)

The classic fight, flight, and freeze responses can all be elicited by direct stimulation of the midbrain. We will also consider hide and cringe avoidant withdrawal behaviors, attentional or orienting freeze, and TI. The urge to attach to recruit help and support will be considered separately, but the need to submit, often a complex

2.  THREAT AND SAFETY  39

response, will also be assessed. In a later chapter, we elaborate on the variety of freeze responses to link the acute threat response to the protracted clinical consequences of trauma. When threat is near and the midbrain defense response areas take precedence over the prefrontal cortical areas in the search for survival, the immediate choice is between active and passive coping (Bandler et  al., 2000). The lateral and dorsolateral columns of the PAG (l/dlPAG) mediate the active, sympathetically driven, high-arousal options of fight or flight, while the ventrolateral column (vlPAG) drives the parasympathetically dominant passive coping in which reduced environmental responsiveness and quiescence combine with access to opioid-induced analgesia. The vlPAG state of immobility accompanied by bradycardia, hypotension, and slow breathing is sometimes referred to as a “freeze” state. We describe this state as a dorsal-vagal freeze to distinguish it from the high-arousal freeze states that require at least some l/dlPAG input even if there is coactivation with vlPAG. Various degrees of coactivation may contribute to a variety of basic emotional states (Watt, 2000). The dorsolateral PAG (dlPAG) lacks direct somatosensory information about the impact of the environment on the body and thus may be critical for defensive responding to nonphysical or social threats (Bandler et  al., 2000). The different PAG columns have inputs from separate areas of orbitomedial prefrontal cortex (OMPFC)—a term used to encompass VMPFC and more lateral, orbitofrontal regions of prefrontal cortex—and they have distinct hypothalamic connections.

ORIENTING TO THREAT

There are also (at least) two main cortical-subcortical pathways for orienting responses to social threat: one based in VMPFC, the other in ACC (Wager et al., 2009). A similar attention/alarm circuit including medial prefrontal cortex, dlPAG, and LC has been proposed based on rat models by Schenberg et al. (2005). Any of these circuits can be activated by the amygdala’s response to social and attachment threats, but the autonomic impact remains dependent on projections to the PAG.

ORIENTING TO THREAT AT DIFFERENT LEVELS OF THE BRAIN

The cortical level of organized, appropriately valenced responding to stimuli is described in a six-stage processing model by Vogt and Laureys (2009). Information processing flows from posterior to anterior through the length of the cingulate cortex. The ventral posterior cingulate cortex monitors incoming sensory stimuli for self-relevance, and anything threatening will tend to dominate. There can be an interaction with emotionally charged memories stored in other parts of cingulate cortex and information about familiar places and objects in the retrosplenial cortex. This information is used by the cingulate motor areas to orient the head and body. The coordinated skeletomotor and autonomic outputs most apposite for the individual then arise from activity in the cingulate motor areas, coinciding with activations of the anterior midcingulate and ACCs. There are many points of interaction between

40  I.  NEUROBIOLOGY

the cingulate cortex and the midbrain for responding to threats of varying degrees of urgency, proximity, and severity. AVOIDANCE: WITHDRAW, HIDE, AND CRINGE RESPONSES

Wee, sleeket, cowran, tim’rous beastie. —Robert Burns, To a Mouse (1785) Hide and cringe responses are intrinsically wired avoidant or withdrawal defense responses that have not been given so much attention clinically as other active strategies for survival. They also contribute action tendencies to structurally dissociated emotional parts. Avoidance symptoms in dissociative disorders are recognized to include conscious efforts to avoid evocation of trauma memories; emotional numbness; isolation; and unwillingness to talk about the experience (Boon, Steele, & van der Hart, 2011). There is therefore a range of avoidance responses from the fully conscious rejection of certain mental contents, through the relatively low-arousal shunning of places and people, which may trigger memories, to the high-arousal hide and sudden cringe behaviors. We later consider the possibility that shame is the affect associated with hide and cringe responses, and this may help to differentiate them from other avoidance strategies. Patients with dissociative disorders may feel an urge to be small and invisible when confronted by powerful agencies such as housing authorities or police, although they carry no immediate physical threat, and this may precede dissociation. When reprocessing childhood traumas in which they have been intimidated by a much larger and more powerful person, patients will often describe an urge to contract, to be small, to disappear into a tiny speck. The shoulders have a tension not associated with a fight response but with a pulling-in toward a center. This may be seen as just another manifestation of submission—and certainly it gives regular rise to long-term shame and self-loathing—but the action urge suggests activation of the dorsomedial column of the PAG (dmPAG), about which there is much less information than, for example, the dorsolateral column. The working hypothesis here is that there is a “turning-away” axis, covering behaviors from conscious rejection of mental contents to physical withdrawal and that this is dependent on the cortical projections to the dmPAG. The SC and the PAG in Avoidance/Hiding/Withdrawal

The dmPAG interacts with other midbrain structures in producing a range of physical withdrawal responses. Dean et  al. (1989) differentiated defense and orienting responses of the SC from the approach/pursuit actions of hunting behavior. The defense responses manifested after stimulation of the SC, with little or no PAG involvement, included freezing; movements like cringing or shying away from a threat, especially if it was looming; and undirected running. The deep and intermediate gray layers of the SC project to the cuneiform nucleus that responds to visual stimuli that are expanding in size or looming to facilitate avoidance. Anyone who

2.  THREAT AND SAFETY  41

has had the experience of wanting to duck away from a sudden roar of noise above, only to feel foolish on realizing that it is a jet on a low-flying training exercise, will appreciate the intrinsic shying “instinct” of the tectocuneiform projection and easily differentiate it from a submissive collapse. When a small child is confronted by an adult rapist who appears huge and powerful, it is the collicular hide/cringe response that is dominant when fight and flight are impossible. Freeze and submit responses will then rapidly follow. One important clinical implication of this is that it can be validating for people to know that their midbrain was trying frantically to find a response that would maximize their chance of survival. They can then come to see the urge to be small as a manifestation not of cowardice but of a primitive urge to be concealed and protected from a predator bringing death through an inadvertent foot placement or a sudden swoop from above. The cringe response is a high-arousal response accompanied by large increases in blood pressure and heart rate (Dean et al., 1989). Active hiding is also a high-arousal state with enhanced vigilance and readiness for instigation of another defense response if the cover is removed. The security motivation system may be an advanced adaptation of this state. Hiding is a complete shutdown of exploration, and the dmPAG differs from other PAG columns in its role in this avoidant behavior (Borelli & Brandao, 2008). We include in the typology of freeze responses (see Chapter  7) a frozen cringe that is postulated to be dependent on the dmPAG, and on its connections with the cuneiform nucleus and the deep layers of the SC. This overlaps with the hide response that is based in the same circuits but is more protracted. Another key structure in the withdrawal response to aversive stimuli or unpleasant events is the rostromedial tegmental nucleus (RMTg). Activation of this nucleus turns down the capacity for reward and reduces the mobility needed for approach behavior by inhibiting dopaminergic projections to the nucleus accumbens and substantia nigra (Jhou et al., 2009). Using the Urge to Avoid in Therapy

The importance of avoidance in the range of defense responses, which can be usefully explored in therapy, has been largely ignored. Avoidance is instead considered to be something that should itself be avoided, as it blocks exposure to a potentially desensitizing awareness. An exception to this neglect is in the Level of Urge to Avoid (LOUA) protocol developed by Knipe (1998) for situations in which there is ambivalence about whether to proceed toward an EMDR target in therapy. A patient may be afraid, realistically, of being overwhelmed by distress if she directly targets memories of childhood sexual abuse, but simultaneously she is desperate to clear the memories of their emotional power in the way she has found effective for other traumas. She is asked how much, on a 0 to 10 scale, she wants to avoid going to the target for which she is ambivalent. If she says “10” she is asked where she feels that “10” in her body, and is asked to focus on that while eye movements or alternating bilateral stimulation are commenced. She may find that there are deep fears about not being believed; about being seen as shameful by the therapist; about feeling her sense of self irrevocably altered by the disclosure. She may also find avoidance tendencies more contemporaneous with the abuse: Her mother will say she encouraged him and

42  I.  NEUROBIOLOGY

the family will break up. More immediate still might have been the avoidance arising from the inability to tolerate protracted terror and pain: the only way to downregulate it, to have any sense of control, was to take the blame herself. If she reprocesses to the extent that she loses the sense of self-blame, will she again be exposed to the fearful uncertainty? It is much easier to live, physiologically and emotionally, with persistent self-criticism and shame than with unremitting terror. When the cortex-PAG axis is shifted to dmPAG dominance, the other active defense responses associated with fight and flight, rage and fear, are displaced by avoidance strategies. Knipe’s protocol also targets the relief felt when avoidance is successful. Presumably, there can be a restoration of mesolimbic dopamine reward when there is an awareness of a threat successfully averted. Focusing on the relief provides a more indirect and less distressing way of approaching the target that, nevertheless, still becomes available for reprocessing. Avoidance, when successful, may confer a sense of mastery that can be augmented to provide a resource for assisting in the resolution of the traumatic experiences. How much shame is attached to memories will determine which avoidant response arises toward the mental content. Hide and cringe activated internally by memories will be more aversive than shame-free avoidance strategies. Exposure protocols based in fear reduction at the level of the VMPFC and its interaction with the amygdala will have no lasting effect on these brainstem patterns. FLIGHT

Every nerve in her was screaming to leave, to run out. Nothing was stopping her. The gate was open. She sat on. —Alan Spence (2006, p. 379) The lateral and dorsolateral columns of the PAG (l/dlPAG) mediate flight responses in their caudal parts and fight responses in their more rostral regions. Caudal l/dlPAG flight responses are accompanied by increases in heart rate and blood pressure and there is vasodilation in the hindlimbs to facilitate the metabolic expenditure needed for running away (Bandler et al., 2000). The dlPAG does not receive somatosensory inputs via spinal afferents so may specifically mediate the response to a social injury or threat, turning around to walk away from a challenge or moving toward a place in which there is no exposure to insults or accusations. These social flight responses can be fully conscious and reasoned, allowing the physiological changes to be discharged as would happen with lPAG activation and running from a physical threat, or obstructed at the level of the projections to dlPAG from the medial prefrontal cortex (areas 10 and 32) or subgenual ACC (area 25), leaving an unexpressed and unacknowledged tension and dysphoria that can become chronic and clinically relevant. FIGHT

Glover knew that this man would never, ever back down. His face was a fierce mask, mouth set, eyebrows gathered, nostrils flared. —Alan Spence (2006, p. 160)

2.  THREAT AND SAFETY  43

Fight behaviors can be “cold,” considered, predatory, hunting, and stalking attacks; or “hot,” immediate, defensive responses to pain, assault, social diminution, or abandonment. In dissociative patients, the defensive fight responses are more clinically relevant because they are often associated with self-harming or other destructive behaviors such as inappropriately abusive or assaultive interactions. Rostral l/ dlPAG activation with an active defense fight response is accompanied not only by sympathetic nervous system arousal, increased blood pressure, and increased heart rate, but also by vasodilation in areas of the upper body, which have the high metabolic demand needed for hissing, snarling, biting, or striking (Bandler et al., 2000). In humans, the defensive attack response can be more expressed through tension in the neck, jaws, and face than through clenching of the fists. Being struck in the face would activate somatosensory inputs to rostral lPAG, triggering an active defense fight response, whereas having an ankle nipped from behind by a terrier would involve somatosensory inputs from the lower body to a more caudal region of the lPAG and induce an immediate flight, rather than a fight, movement. However, a sudden and disturbing insult or verbal assault, which feels like a slap in the face, may provoke a response through the dlPAG, as there is no somatosensory component, in contrast to the lPAG reaction to the physical pain. The dlPAG column has inputs from the medial wall of the prefrontal cortex, Brodmann areas 10, 25, and 32, while the lPAG column receives projections from dorsomedial prefrontal cortex (DMPFC) areas 9 and 24. The prefrontal cortex areas, which project to the lateral and dlPAG columns, also target separate areas of the hypothalamus (Bandler et al., 2000). Thus, there is scope for the response to social attacks, compared with physical threats, to have different areas of midbrain and hypothalamic involvement and different patterns of cortical control. The evolutionary development of the human brain may maximize the distinction between the active defense responses to physical threat, mediated by the lPAG, dorsal hypothalamus, and dorsomedial PFC (BA 9 and 24), and those stimulated by social threat, involving the dlPAG, ventromedial and anterior hypothalamus, and ventromedial PFC (BA 10, 32, and 25), but there is still overlap and blurring, subjectively and physiologically. Blows to the social self, such as being dismissed and disregarded, vilified, or treated with contempt, will activate the primitive survival mechanisms in l/dlPAG before the sophisticated OMPFC steps in to smoothly regulate the physiological activation and preserve the social niceties. A cold, calculating plan to commit violence against another person, perhaps for personal gain, is distinct from the defensive attack rage occasioned by a threat to survival. Predatory fight is not a defense response. Different areas of the hypothalamus are involved and there is no surge of sympathetic nervous system activation. There may be an increase in self-esteem, in contrast to the unpleasantly aversive nature of defensive rage (Siegel & Victoroff, 2009). Predatory attack in humans requires significant cortical input. Brain imaging of antisocial and violent offenders consistently shows abnormalities in prefrontal cortex (Tilhonen et al., 2008), including the right orbitofrontal cortex (Yang & Raine, 2009). The ability to predict the emotional states of others is dependent on the right orbitofrontal cortex, and criminal psychopaths show emotional theory-of-mind impairments similar to those seen in people with lesions of that area (Shamay-Tsoory, Harari, Aharon-Peretz, & Levkovitz, 2010). Human offenders may have a mixture of predatory (nonaffective) and defensive (affective) attack

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patterns (Siegel & Victoroff, 2009). There may also be different responses in humans in response to threats or insults from conspecifics toward family or friends. For some men, disparaging comments about their wife or mother can instantly activate a violent response that is more akin to the “hot” than the “cold” predatory assault. There may again be a mixture: a cold plan to hunt and then viciously damage.

IMMOBILITY

She had come up the path to the house as usual, carrying a wicker basket of provisions, clearly not expecting to encounter this great terrifying beast. She stood rigid, unable to move, the basket and its contents scattered at her feet. —Alan Spence (2006, p. 203) A gentle spaniel that is suddenly attacked by two guard or hunting dogs may collapse and appear to be dead to the extent that the aggressors lose interest and go away to seek a fresh challenge elsewhere. The same spaniel may pounce on a hen that strays into the house and take it to the owner. In contrast to the spaniel’s wagging tail and general demeanor of cleverness at having done an important job well, the hen is hanging limp and appears to have died from shock. However, when the hen is released into the safety of her own area she squawks loudly, shakes herself energetically, and, within a very short period of time, is pecking grain as if nothing had happened. In both of these cases, there is reduced tone of the muscles; the animals feel limp and lifeless. This is the dorsal vagal state activated by the vlPAG, which we will later describe as one of the types of freeze. In contrast, most obviously through the difference in muscle tone, TI is another important part of the normal defense response repertoire and needs to be mentioned here. However, because of its importance in the clinical consequences of traumatic experiences it is also mentioned in the typology of freeze responses and in Chapter 3, Peritraumatic Dissociation and Tonic Immobility: Clinical Findings, specifically in relation to dissociation in humans. TI is a complex defense response involving prolonged stillness, reduced responsiveness, muscular rigidity, and suppressed vocalization, which is established most easily through restraint or entrapment (Moskowitz, 2004). There are changes in heart rate, respiratory rate, and core temperature. It is a state of high internal activation accompanied by a lack of discernible movement, which is dependent on opioidergic, cholinergic, and serotonergic transmissions in the ventral and dorsal PAG (Brandao, Zanoveli, Ruiz-Martinez, Oliveira, & Landeira-Fernandez, 2008). This illustrates the coactivation of the PAG columns occurring in some complex defense states, as has now been demonstrated for TI by Vieira, Menescal-de-Oliveira, and Leite-Panissi (2011). In TI, there is activation of both sympathetic and parasympathetic branches of the autonomic nervous system. TI is therefore a state of frozen fear in which both a hyperarousal freeze, similar to the state described by Brandao et al. (2008), when the dorsal PAG is stimulated to a preliminary preparedness for selection of a response, and the low-arousal freeze described for vlPAG occur simultaneously with an inability to move because opponent action urges are equally balanced.

2.  THREAT AND SAFETY  45

Although immobilization stress has provided important information about the deactivation of the hippocampus and SC (Sung et  al., 2009), this has to be distinguished from TI. Monassi, Leite-Panissi, and Menescal-de-Oliveira (1999) describe inversion and constraint of a laboratory animal to induce TI. The restraint is removed when it stops struggling and the subsequent period of immobility is measured. When TI is induced in guinea pigs by trapping, inversion, and pushing down, there is chemical evidence of activation of all PAG columns, including the dorsomedial, but it is greatest in the ventrolateral and lateral columns of the PAG (Vieira et al., 2011). While there are differences in the inputs from the prefrontal cortex to the different columns of the PAG, the imaging studies described above support the contention that these PFC areas are deactivated at times of extreme danger: conflicting commands from the midbrain to the muscles and the viscera is a more economical explanation for the terrified state of TI. SOCIAL THREAT: CORTICAL AND MIDBRAIN RESPONSES

The hypothesis that, in humans, social threat can activate defense response systems originally developed for surviving physical threat has been supported by a functional MRI (fMRI) imaging study of responses to a requirement to prepare, in the brain scanner, a speech to be delivered to a panel of experts after the scanning session. Heart rate responses were mediated by three areas; activations in dorsal ACC (dACC) and in PAG, and deactivation in VMPFC (Wager et al., 2009). VMPFC had a direct effect on the heart rate and an indirect influence through an inhibition of the PAG, whereas dACC mediated cardiac function through areas of ventral thalamus that were connected with the PAG. Here are two distinct cortical-subcortical pathways exerting an influence on the physiological arousal responses to social threats. The circuitry is in place for distressing social events to result in intrusive memories, avoidance, and hyperarousal, as has been reported for a large community sample (Carleton, Peluso, Collimore, & Asmundson, 2011). Active defense or fight responses can include verbal hectoring and abuse, sarcasm, unwarranted criticism, swearing, name-calling, snarling, scowling, and shouting. Flight might be expressed through alcohol or other drug use as well as the obvious removal from a situation of conflict. Social withdrawal, avoidance of any unpredictable interpersonal situations, could be an urge to hide rather than flee. People sometimes use the word “panic” to describe feelings of terror in situations from which they feel unable to extricate themselves: on a crowded bus, on a stage, in an unprecedented social situation. This may represent a prefight or preflight freeze rather than the acute separation distress produced by abandonment and helplessness, which activates the PANIC system described in Panksepp (1998). Turning away from an interaction and losing interest and enjoyment in it when it has become threatening are behavioral effects postulated to involve the avoidant defenses based in the dmPAG and the RMTg. Humiliation may instigate an acute high-arousal phase of cringing and embarrassment and a later, more protracted, phase of shame that is lower in arousal. Shame can be the consequence of misattunement and loss but it can also arise from defeat in an agonistic encounter in which submission is the only option consistent with physical survival. The more

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deficient has been the self in protecting its space from injury, the more shame will be experienced in the moment of awareness of isolation.

SUBMISSION

He felt suddenly, profoundly, wearied, saw himself useless and helpless in the face of events. —Alan Spence (2006, p. 159) Adults who are bullied at work and children who are bullied at home or in school are experiencing defeat in an environment to which they have to repeatedly return. There are parallels with laboratory experiments in which a rat is placed in the home cage of an aggressive male rat until it displays defensive or submissive behavior for a specified time. A defeated rat that has reduced mobility on return to its home cage shows an increased concentration of dopamine in the nucleus accumbens (Tidey & Miczek, 1996), suggesting that what appears to be a low-arousal state following defeat nevertheless contains mesolimbic activation. When rats were separated for their protection but could still see, hear, and smell the aggressor rat (sensory contact), the defeated rat monitored the activity of the aggressor through the wire mesh in a state of vigilance and arousal, which was reflected in significant increases in dopamine concentrations in the nucleus accumbens and the prefrontal cortex (Tidey & Miczek, 1996). It is therefore possible that increased mesolimbic dopamine is a reflection of increased security motivation, waiting for the return of the aggressor, monitoring with trepidation, rather than being directly related to the degree to which the animal is required to submit and to drop into the low arousal state: this would suggest that submission, like separation distress and social humiliation, has different phases. Some of the cardiovascular effects of psychosocial stress are mediated by an area of the hypothalamus which has direct projections to the spinal cord (Carrive, 2011). Adults who describe their childhood monitoring and fearful tracking of the behaviors and emotions of their intermittently abusive parents are describing an upbringing during which the mesolimbic dopamine system is being activated in a dysphoric way, if the situations are analogous. The despairing resignation that can follow inescapable abuse, because the pattern is that it will not occur again immediately, could represent a low-arousal state in which mesocortical, if not mesolimbic, dopamine is reduced: this is more difficult to study in animal models. Mice defeated daily then subjected to continuing sensory contact with the aggressor while physically protected were much less likely to engage in social interaction with unfamiliar but potentially nonaggressive mice: this aversion to social contact was reversed by chronic administration of antidepressants (Berton et al., 2006). That is, repeated defeat resulted in a social withdrawal that was significantly improved by the antidepressants used in humans for the treatment of depressive disorders. One implication of this finding for clinical practice is that targeting social defeat memories in EMDR processing may produce considerable improvement in depressed mood. Thus, there is evidence that enforced submission in agonistic encounters chronically activates the mesolimbic dopamine system, and this has implications for human states of posttraumatic fear, vigilance, and low mood, especially when these are the

2.  THREAT AND SAFETY  47

result of chronic interpersonal violence or verbal abuse. It is more difficult to isolate the effects of submission influencing the low-arousal dysphoric state seen in humans in situations of continuing and repeated defeat.

The Mesolimbic Defensive Response to Environmental Stress

If the rewarding effects of drugs of abuse are mediated by an increase in mesolimbic dopamine, why would the experience of submission involve the same neurochemistry, apparently, as a sought-after and expensive chemical “high?” One answer lies in the valence of the mesolimbic dopamine system, which is active in many ways in the search for life-enhancing stimuli including safety (Alcaro, Huber, & Panksepp, 2007). It can mediate the urge to find a place of safety and the rewards of feeling safe when that is attained. It has, at least, a “bivalent” nature (Levita et al., 2009). Reynolds and Berridge (2008) brilliantly demonstrated this by studying the effects on rats of microinjections of a glutamate antagonist into the “affective keyboard” of the rostrocaudal gradient of the nucleus accumbens shell when the rats were exposed to different environmental influences. In standard laboratory conditions, rostral microinjections produced appetitive, eating behavior while caudal microinjections resulted in defensive treading. In a familiar dark, quiet, home condition, the appetitive zone expanded so that microinjections over most of the shell produced eating behavior, while mild defensive behavior was elicited only at the caudal tip. When the rats were placed in stressful conditions of bright light and “raucous Iggy Pop sound,” microinjections into most of the keyboard produced defensive rather than appetitive behavior (Reynolds & Berridge, 2008). So, under stressful environmental conditions, stimulation of the nucleus accumbens shell leads to defensive behaviors, while, under safe and secure conditions, activation of the same affective keyboard results in intake of food. The “Iggy Pop” effect on the rats suffering in the noisy and bright environment would have been made memorable for them through the involvement of the basolateral nucleus of the amygdala (McGaugh, 2004), as the environment associated with exposure to an unpleasant experience itself becomes aversive. Rats previously subjected to electric shocks in a specific cage show increased fear and increased dopamine in the core and the shell of the nucleus accumbens when they are returned to that cage (Martinez, Oliveira, Macedo, Molina, & Brandao, 2008). Although the nucleus accumbens has different responses to the prefrontal cortex in different environmental conditions, the mesolimbic activation precedes any cortical regulatory control: it can switch valence instantly when the amygdala threat detection alarm is sounded. The settings for response thresholds can be predetermined by endocrine influences on the plasticity of the system. Activation of the mesolimbic dopamine system helps to form memories of emotionally charged events. The mesolimbic cholinergic tracts are also involved, if less well studied, in states of submission (Kroes, Burgdorf, Otto, Panksepp, & Moskal, 2007). Other neurochemicals such as kappa endogenous opioids (McLaughlin, Li, Valdez, Chavkin, & Chavkin, 2006) and cholecystokinin (Panksepp, Burgdorf, Beinfeld, Kroes, & Moskal, 2007) contribute. These data favor a consideration of the basic submit response as potentially multiphasic: high- and low-arousal components with different levels of agitation, vigilance, and dysphoria.

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SUMMARY

Midbrain systems contribute to the defense responses of fight, flight, freeze, TI, hide/ cringe/avoid/withdraw, and submit, and are the primary source of response when danger is present, near, and immediate. The urge to attach will be considered separately but is also dependent on the midbrain and its projections. As well as the integrated networks that are in place for rapid responding to severe threat, there is ample evidence of different neurochemical modulators having an impact on both short-term and long-term consequences of trauma. For understanding the clinical consequences of traumatic experience, the varieties of freeze response are considered in more detail in Chapter 7.

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Gilbert, P. (2001). Evolutionary approaches to psychopathology: The role of natural defences. Australian and New Zealand Journal of Psychiatry, 35, 17–27. Johnston, K., & Everling, S. (2006). Monkey dorsolateral prefrontal cortex sends task-selective signals directly to the superior colliculus. The Journal of Neuroscience, 26, 12471–12478. Jhou, T., Fields, H. L., Baxter, M. G., Saper, C. B., & Holland, P. C. (2009). The rostromedial tegmental nucleus (RMTg), a GABAergic afferent to midbrain dopamine neurons, encodes aversive stimuli and inhibits motor responses. Neuron, 61, 786–800. King, S. M., Shehab, S., Dean, P., & Redgrave, P. (1996) Differential expression of fos-like immunoreactivity in the descending projections of superior colliculus after electrical stimulation in the rat. Behavioural Brain Research, 78, 131–145. Knipe, J. (1998). “It was a golden time . . . ”: treating narcissistic vulnerability. In P. Manfield (Ed.), Extending EMDR: A casebook of innovative applications (pp. 232–255). New York, NY: W.W. Norton. Kroes, R. A., Burgdorf, J., Otto, N. J., Panksepp, J., & Moskal, J. R. (2007). Social defeat, a paradigm of depression in rats that elicits 22-kHz vocalizations, preferentially activates the cholinergic signalling pathway in the periaqueductal gray. Behavioral Brain Research, 182, 290–300. Levita, L., Hare, T. A., Voss, H. U., Glover, G., Ballon, D. J., & Casey, B. J. (2009). The bivalent side of the nucleus accumbens. NeuroImage, 44, 1178–1187. Liddell, B. J., Brown, K. J., Kemp, A. H., Barton, M. J., Das, P., Peduto, A., … Williams, L. M. (2004). A direct brainstem-amygdala-cortical ‘alarm’ system for subliminal signals of fear. NeuroImage, 24, 235–243. Lyons-Ruth, K., Dutra, L., Schuder, M. R., & Bianchi, I. (2006). From infant attachment disorganization to adult dissociation: Relational adaptations or traumatic experiences? The Psychiatric Clinics of North America, 29(1), 63–86. Manger, P. R., Restrepo, C. E., & Innocenti, G. M. (2010). The superior colliculus of the ferret: Cortical afferents and efferent connections to dorsal thalamus. Brain Research, 1353, 74–85. Marsh, R. A., Fuzessery, Z. M., Grose, C. D., & Wenstrup, J. L. (2002). Projections to the inferior colliculus from the basal nucleus of the amygdala. The Journal of Neuroscience, 22, 10449–10460. Martinez, R. C., Oliveira, A. R., Macedo, C. E., Molina, V. A., & Brandao, M. L. (2008). Involvement of dopaminergic mechanisms in the nucleus accumbens core and shell subregions in the expression of fear conditioning. Neuroscience Letters, 446, 112–116. McGaugh, J. L. (2004). The amygdala modulates the consolidation of memories of emotionally arousing experiences. Annual Review of Neuroscience, 27, 1–28. McLaughlin, J. P., Li, S., Valdez, J., Chavkin, T. A., & Chavkin, C. (2006). Social defeat stressinduced behavioral responses are mediated by the endogenous kappa opioid system. Neuropsychopharmacology, 31, 1241–1248. Merker, B. (2007). Consciousness without a cerebral cortex: A challenge for neuroscience and medicine. Behavioral and Brain Sciences, 30, 63–134. Mobbs, D., Petrovic, P., Marchant, J. L., Hassabis, D., Weiskopf, N., Seymour, B., … Frith, C. D. (2007). When fear is near: Threat imminence elicits prefrontal-periaqueductal gray shifts in humans. Science, 317(584), 1079–1083. Monassi, C. R., Leite-Panissi, C. R., & Menescal-de-Oliveira, L. (1999). Ventrolateral periaqueductal gray matter and the control of tonic immobility. Brain Research Bulletin, 50, 201–208. Morris, J. S., deBonis, M., & Dolan, R. J. (2002). Human amygdala responses to fearful eyes. NeuroImage, 17, 214–222. Moskowitz, A. K. (2004). ‘Scared stiff’: Catatonia as an evolutionary-based fear response. Psychological Review, 111, 984–1002.

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Panksepp, J. (1998). Affective neuroscience: the foundations of human and animal emotions. New York, NY: Oxford University Press. Panksepp, J. (2003). Feeling the pain of social loss. Science, 302, 237–239. Panksepp, J., Burgdorf, J., Beinfeld, M. C., Kroes, R. A., & Moskal, J. R. (2007). Brain regional neuropeptide changes resulting from social defeat. Behavioral Neuroscience, 121, 1364–1371. Prescott, T. J., Redgrave, P., & Gurney, K. (1999). Layered control architectures in robots and vertebrates. Adaptive Behavior, 7, 99–127. Reynolds, S. B., & Berridge, K. C. (2008). Emotional environments retune the valence of appetitive versus fearful functions in nucleus accumbens. Nature Neuroscience, 11, 423–425. Schenberg, L. C., Povoa, R. M., Costa, A. L., Caldellas, A. V., Tufik, S., & Bittencourt, A. (2005). Functional specializations within the tectum defense systems of the rat. Neuroscience and Biobehavioral Reviews, 29, 1279–1298. Shamay-Tsoory, S. G., Harari, H., Aharon-Peretz, J., & Levkovitz, Y. (2010). The role of the orbitofrontal cortex in affective theory of mind deficits in criminal offenders with psychopathic tendencies. Cortex, 46, 668–677. Siegel, A., & Victoroff, J. (2009). Understanding human aggression: New insights from neuroscience. International Journal of Law and Psychiatry, 32, 209–215. Spence, A. (2006). The Pure Land. Edinburgh, UK: Canongate. Steinberg, M. (1995). Handbook for the assessment of dissociation: A clinical guide. Washington, DC: American Psychiatric Press. Sung, K. K., Jang, D. P., Lee, S., Kim, M., Lee, S. Y., Kim, Y.-B., ... Cho, Z. H. (2009). Neural responses in rat brain during acute immobilization stress: A [F-18]FDG micro PET imaging study. NeuroImage, 44(3), 1074–1080. Tidey, J. W., & Miczek, K. A. (1996). Social defeat stress selectively alters mesocorticolimbic dopamine release: An in vivo microdialysis study. Brain Research, 721, 140–149. Tilhonen, J., Rossi, R., Laakso, M. P., Hodgins, S., Testa, C., Perez, J., … Frisoni, G. B. (2008). Brain anatomy of persistent violent offenders: More rather than less. Psychiatry Research: Neuroimaging, 163, 201–212. van der Hart, O., Nijenhuis, E. R., & Steele, K. (2006). The haunted self. New York, NY: W.W. Norton. van der Kolk, B. A. (1996). The complexity of adaptation to trauma: Self-regulation, stimulus discrimination, and characterological development. 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. 182–213). New York, NY: Guilford Press. Vieira, E., Menescal-de-Oliveira, L., & Leite-Panissi, C. R. (2011). Functional mapping of the periaqueductal gray matter involved in organizing tonic immobility behavior in guinea pigs. Behavioural Brain Research, 216, 94–99. Vogt, B. A., & Laureys, S. (2009). The primate posterior cingulate gyrus: Connections, sensorimotor orientation, gateway to limbic processing. In B. A. Vogt (Ed.), Cingulate neurobiology and disease (pp. 275–308). Oxford, UK: Oxford University Press. Wager, T. D., van Ast, V. A., Hughes, B. L., Davidson, M. L., Lindquist, M. A., & Ochsner, K. N. (2009). Brain mediators of cardiovascular responses to social threat, part II: Prefrontalsubcortical pathways and relationship with anxiety. NeuroImage, 47, 836–851. Watt, D. F. (2000). The centrencephalon and thalamocortical integration: Neglected contributions of periaqueductal gray. Consciousness & Emotion, 1, 91–114. Woody, E. Z., & Szechtman, H. (2011). Adaptation to potential threat: The evolution, neurobiology, and psychopathology of the security motivation system. Neuroscience and Biobehavioral Reviews, 35, 1019–1033. Yang, Y., & Raine, A. (2009). Prefrontal structural and functional brain imaging findings in antisocial, violent, and psychopathic individuals. Psychiatry Research: Neuroimaging, 174, 81–88.

CHAPTER 3

Peritraumatic Dissociation and Tonic Immobility: Clinical Findings Michelle J. Bovin, Elise Ratchford, and Brian P. Marx

“Death feigning,” otherwise “playing possum” or even “animal hypnosis,” better termed tonic immobility, is shown to a striking degree by a great variety of animals. —Hudson Hoagland (1927)

The individual’s immediate response to traumatic stress has long been of interest to both researchers and clinicians. Initially, researchers identified only three emotions as important to defining traumatic stress (i.e., fear, helplessness, and horror; American Psychiatric Association, 1994; Davidson, Foa, Blank, Brett, & Green, 1996). However, subsequent researchers have identified other relevant peritraumatic reactions that are pertinent to the genesis of posttraumatic psychopathology (e.g., Brewin, Andrews, & Rose, 2000; Brunet et al., 2001; First, 2005; Roemer, Orsillo, Borkovec, & Litz, 1998; Weathers & Keane, 2007). The notion that the aspects of an individual’s peritraumatic response might extend beyond peritraumatic fear, helplessness, and horror has led investigators to consider what the salient aspects of the peritraumatic experience might be. Bovin and Marx (2011) reviewed the empirical research showing that individuals adapt to extreme environmental events by responding in a complex and coordinated manner. Specifically, this complex response set involves an individual’s appraisal regarding the degree to which the event taxes or exceeds his or her resources as well as a range of other cognitive processes (e.g., dissociation), felt emotions (e.g., fear), physiological reactions (e.g., heart rate increase), and behaviors (e.g., tonic immobility [TI]). Bovin and Marx 51

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concluded that these numerous and complex peritraumatic responses work synergistically to either confer risk for or resilience against trauma-related psychopathology. The present chapter will describe two of these frequently occurring and important peritraumatic responses, namely, peritraumatic dissociation (PD) and TI. Specifically, we will focus on the definition of each phenomenon and their associations with posttraumatic psychopathology as the relevant neurobiology is considered in other chapters. We also compare and contrast these two peritraumatic phenomena.

PERITRAUMATIC DISSOCIATION Definition of PD

Although dissociation has many different conceptualizations, it is broadly defined as a psychological process in which awareness becomes fragmented. In general, dissociation is a spectrum of experiences that can include depersonalization, derealization, and amnesia (e.g., Gershuny & Thayer, 1999). Dissociation is sometimes described as a trait phenomenon in which some individuals experience dissociative states independent of traumatic experiences. However, many individuals report dissociative reactions during traumatic events, a phenomenon known as PD. Dissociative reactions that may occur during trauma exposure include emotional numbing or detachment, reduced awareness, and distortions of reality (van der Velden & Wittmann, 2008). The trauma survivor may be unable to recall certain aspects of the trauma or have an “out-of-body” experience. Dissociation has been described and studied since the early 1900s. Pierre Janet hypothesized that trauma-related dissociation was the result of aversion to the traumatic experience. According to Janet (1907), memories of the trauma are disconnected from consciousness as a protective mechanism against distress. Despite its initial role as a psychologically protective mechanism, Janet believed that this dissociation resulted in subsequent psychological dysfunction because it disallowed mental resources to be available for other processes. Janet’s initial conceptualization of dissociation as a protective mechanism remains an accepted etiological theory, and many recent researchers have postulated that PD prevents recollection of the trauma, thus impeding the individual’s capacity to process the event and ultimately come to terms with it (Breh & Seidler, 2007; Brooks et al., 2009; van der Kolk & Fisler, 1995).

PD and Risk of Developing Posttraumatic Stress Disorder (PTSD)

PD often emerges as a robust predictor of future PTSD symptomatology. In a metaanalysis of risk factors for PTSD (Ozer, Best, Lipsey, & Weiss, 2003), PD had the largest effect size of all the risk factors included (weighted r = .35). In fact, all of the peritraumatic variables that were included in the meta-analysis were more predictive of PTSD than having a prior trauma, pretrauma psychological adjustment, and family history of psychopathology. This led Ozer et al. (2003) to conclude that peritraumatic experiences were far more important risk factors for PTSD than pretrauma characteristics.

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Another meta-analysis of studies investigating the relationship between PD and posttraumatic stress symptoms found similar results (Lensvelt-Mulders et al., 2008). The authors coded each study in their investigation according to descriptive characteristics (e.g., sample size, method of assessing PD) and methodological quality variables (e.g., type of publication, design, sample type). Findings revealed a significant positive correlation between PD and posttraumatic stress symptomatology when the study results were combined (r = .40). Based on their methodological evaluation, the authors found that the more time elapsed between the traumatic event and the first assessment of PD, the higher the correlation between posttraumatic stress symptoms and PD. Although this may appear to be a result of memory bias distorted by current PTSD symptoms, taken with the fact that longitudinal studies reported stronger positive correlations between PD and posttraumatic stress (e.g., Ozer et al., 2003), it may indicate that retrograde assessments of PD are, in fact, reliable (e.g., Birmes et  al., 2003). However, the authors also found that correlational designs showed a stronger relationship between PD and posttraumatic stress; this relationship was particularly notable in studies focusing on childhood abuse. Lensvelt-Mulders and colleagues’ conclusions highlight the difficulties inherent in studying the peritraumatic experience and show that more research is needed to fully elucidate the influence of PD on PTSD symptoms.

PD in Different Populations

PD has been observed and studied across different populations and different trauma types. For example, several studies have investigated the role of PD in combatrelated PTSD. Bremner and Brett (1997) sought to examine the impact of PD on subsequent psychopathology and trait dissociation in Vietnam veterans. They found that, among PTSD patients, the level of PD was significantly correlated with longterm dissociative symptoms, long-term psychopathology, and number of flashbacks since combat exposure. The authors also observed that, in many of the patients, the specific dissociative reactions present during the trauma tended to recur during subsequent stressful events (Bremner & Brett, 1997). Other groups have found a similar relation between PD during combat and future psychopathology (e.g., Marmar et al., 1994; Tichenor, Marmar, Weiss, Metzler, & Ronfeldt, 1996). Tichenor and colleagues (1996) found that this relationship occurred in female Vietnam veterans as well. Furthermore, they found that PD predicted traumatic stress symptoms more than stress exposure level and dissociative tendencies. O’Toole and colleagues (1999) found that PD was related to all PTSD diagnostic criteria in an Australian sample of both male and female civilians. PD has also been studied in the context of both nonsexual and sexual assault. In a sample of recent rape victims, Griffin, Resick, and Mechanic (1997) found that PD was correlated with all PTSD symptom clusters, particularly the avoidance symptom cluster. They also found that individuals who scored high on dissociation were more globally distressed, more depressed, and had a greater perception of life threat during the trauma than their low-dissociation counterparts. Griffin and colleagues posited that the relationship between increased life threat and PD supports the idea of PD as a coping strategy. Birmes et  al. (2003) examined the predictive power of

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PD in nonsexual assault victims. Notably, their participants were recruited from an emergency room and were assessed for PD within 24 hours of the assault. The brief time period between the event and the assessment of the event helped to ensure that memory bias would not affect the results. Birmes and colleagues found that PD predicted future PTSD symptoms. The fact that this relationship was found prospectively highlights the need for early identification and intervention for dissociating individuals at risk of developing future psychopathology. Survivors of motor vehicle accidents are prone to PD as well. Ehlers, Mayou, and Bryant (1998) found PD to be one of the strongest predictors of chronic PTSD. Similar to Birmes et al.’s (2003) study, participants were recruited in an emergency department and assessed soon after the trauma in an effort to reduce memory bias. Ursano and colleagues (1999) also found a relationship between PD and PTSD. Those who reported PD were over four times more likely to develop acute PTSD and nearly five times more likely to develop chronic PTSD. Similar to Bremner and Brett’s (1997) results, a greater number of PD symptoms was a risk factor for chronic PTSD. The myriad of research identifying PD across different populations and traumas suggests that PD is a global phenomenon, which is not limited to specific groups.

TONIC IMMOBILITY TI as a Peritraumatic Response

Whereas PD, and its association with trauma exposure, has been discussed and studied extensively, a more recent line of work has examined the association between trauma exposure and another peritraumatic response: TI. TI was first identified in the animal literature as a set of unconditioned responses that occur when an animal is faced with mortal threat and/or physical restraint (i.e., capture or entrapment by a predator). The main feature of TI is reversible physical immobility and muscular rigidity, which can last from a few seconds to many hours (Gallup, 1977). The phenomenon is also associated with sustained and involuntary neuromuscular activity; sympathetic and parasympathetic responses; intermittent periods of eye closure; fixed, unfocused gaze or stare; parkinsonian-like tremors in the extremities; analgesia; waxy flexibility; and suppressed vocal behavior (Gallup, 1974; Gallup & Rager, 1996; Marx, Forsyth, Gallup, Fusé, & Lexington, 2008). TI has been studied for more than three centuries in animals (Maser & Gallup, 1977; Moskowitz, 2004) and has been elicited among a wide range of vertebrates and invertebrates (Hennig, 1978; Holcombe, Sterman, Goodman, & Fairchild, 1979).

TI and the Defense Cascade Model

TI is thought to be the ultimate stage in the defense cascade model (i.e., the series of defensive reflexes through which animals progress in response to the increasing proximity of a predator; Lang, Davis, & Ohman, 2000; Ratner, 1967). The defense cascade

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model is typically conceptualized to consist of four stages. In the first stage (i.e., the preencounter stage), a predator has not yet been encountered. As such, defense behavior has not yet been engaged, and appetitive motivation may be present. In contrast, in the second stage (i.e., the encounter stage), a potential threat (i.e., predator) has been identified. Identification of potential threat by the organism is immediately followed by the ceasing of all movement (i.e., freezing). This stage is often associated with focused attention and orientation to the threat object, sustained cardiac deceleration, defensive analgesia, and potentiated startle. These responses allow the prey animal to prepare for future evasive action, if necessary. The freezing itself is also a defensive posture due to the fact that many predators are dependent on movement to identify prey (Gallup, 1977; Marx et al., 2008). If the predator continues to advance toward the prey animal, the animal will enter the third stage of the defense cascade, known as the postencounter, or circa strike, stage. During this stage, the animal will change to a defensive posture (e.g., flight or fight). The initial response of the animal will be to attempt an escape. However, if escape is not possible, the prey animal will fight or resist the advances of the predator. This stage of responding is characterized by a potentiated startle response as well as rapid acceleration in heart rate and increase in electrodermal activity. If efforts to escape or resist are unsuccessful (i.e., the animal is caught by the predator), the prey animal will enter the fourth stage of the defense cascade: TI. Although also involving a “freeze” response, TI is markedly different from the freeze response exhibited during the encounter stage. Specifically, whereas freezing during the encounter stage of the defense cascade is associated with increased responsivity to stimuli, an alert posture, and volitional action tendencies (e.g., Marx et al., 2008), TI is an involuntary response that involves a motionless posture and analgesia (Gallup & Rager, 1996; Ratner, 1967). Like freezing, TI is thought to be evolutionarily adaptive. In addition to making prey less visible, TI appears to inhibit aggression in predators, often leading them to terminate their advances (e.g., Herzog & Burghardt, 1974; Marx et al., 2008).

TI in Laboratory Animals

TI is typically elicited in naturalistic settings by the combination of extended physical restraint and intense fear. Laboratory procedures that involve restraint and fear can also elicit the TI response (Gallup, Nash, Donegan, & McClure, 1971). In experimental situations, TI is most frequently induced by suddenly inverting the animal, followed by the application of restraint until the animal stops struggling (e.g., Gallup, 1977; Gallup & Rager, 1996; Klemm, 1971). TI is said to be present when the animal demonstrates continued immobility following the withdrawal of physical restraint. Such procedures model physical contact and subsequent immobilization seen following predatory attack in the wild (Gallup & Rager, 1996). However, other studies have indicated that neither inversion nor restraint is necessary for the induction of TI (Crawford, 1977; Ratner, 1967), leading researchers to propose that it is the perception of entrapment, rather than actual physical restraint, that is necessary for the development of TI (Ratner, 1967).

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TI and Fear

Research regarding the basis, function, and mechanisms underlying the TI response has resulted in the acceptance of the fear hypothesis (FH), a multidimensional model of TI (Gallup, 1977). This model suggests that the experience of fear by the prey animal is a necessary antecedent condition for the development of TI. The FH does not argue that fear alone is sufficient for the development of TI; rather, the hypothesis argues that, in the context of restraint (or perceived inescapability), the experience of fear modulates both susceptibility to and duration of the TI response. The FH has received extensive empirical support (e.g., Edson & Gallup, 1972; Gallup, 1974; Gallup, Creekmore, & Hill, 1970; Gallup, Cummings, & Nash, 1972; Gallup et al., 1971; Leftwich & May, 1974; Maser, Gallup, & Barnhill, 1973; Nash, Gallup, & McClure, 1970). Researchers have also examined the brain structures involved in the expression of TI, and three regions appear to be the most relevant to the induction and inhibition of this phenomenon: the frontal lobes, the limbic system, and the brainstem (e.g., Moskowitz, 2004). Early researchers noted that the cerebral cortex appears to inhibit TI. For example, Svorad (1957) found that TI was most common in species with limited development of the cerebral cortex, and Klemm (1971) found that TI was more common in the young of some species (when the cerebral cortex was not yet mature) but rare in adulthood. In 1989, Klemm proposed that, in TI, the cortex is disinhibited due to limbic activity, which controls the opioid-based expression of TI through the γ-aminobutyric acid (GABA) system’s influence on lower brain structures (Moskowitz, 2004). Klemm further argued that the amygdala was the limbic structure most likely to be responsible for the disinhibition of the cortex. Recently, research has identified the midbrain periaqueductal gray (PAG) in the brainstem as the brain structure most directly responsible for the expression of TI (e.g., Fanselow, 1991; Leite-Panissi, Monassi, & Menescal-de-Oliveira, 1999; Moskowitz, 2004). This is consistent with Klemm’s (1989) claims because the amygdala (which Klemm identified as the structure responsible for controlling cortex inhibition) projects directly into the PAG. Research has further shown that the dorsal portion of the PAG (the dPAG) is particularly relevant to the elicitation of TI: whereas excitatory amino agonists (EAAs) injected into the dPAG decreased the TI duration in guinea pigs, the effect was blocked by the previous administration of an N-methyl-d-aspartate (NMDA) receptor antagonist into the same site (Coutinho, da Siva, & Menescal-de-Oliveira, 2008). The importance of the dPAG in TI is consistent with other research that has provided evidence that this structure is involved in the mediation of active strategies to cope with aversive situations (e.g., Bandler, Keay, Floyd, & Price, 2000; Bandler & Shipley, 1994; Carrive, 1993; Coutinho & Menescal-de-Oliveira, 2010). EAAs in the anterior cingulate cortex (ACC) can also affect the duration of TI; however, this effect appears to be contingent upon NMDA receptors in both the ACC and the dPAG. Overall, researchers tend to agree that TI occurs when disinhibition of the frontal lobes is facilitated by overactivation of the limbic system (most likely the amygdala), which projects through the dPAG in the brainstem, thus activating a pool of interneurons in the reticular formation, which inhibit the motor neurons of the spinal cord (e.g., Moskowitz, 2004).

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TI Research in Humans

Although the majority of research on TI has historically focused on animals, research has begun to examine this phenomenon in humans. The experience of TI by humans was first identified through anecdotal reports of child sexual abuse (CSA) and rape survivors; these survivors reported that during their attacks they experienced involuntary physical immobility, trembling, shaking, suppressed vocal expression, and decreased body temperature (e.g., Burgess & Holmstrom, 1976; Burton, 1931; Johnson, 1984; Marx et al., 2008; Russell, 1974; Suarez & Gallup, 1979). For example, Burgess and Holmstrom (1976) reported that 37% of rape survivors reported experiencing some paralysis in response to an open-ended question asking how they coped with the experience of being sexually assaulted as it happened. These findings led Suarez and Gallup (1979) to theorize that anecdotal reports of paralysis and inability to call out during sexual assault might be an expression of TI in humans. Suarez and Gallup further argued that TI may be possible during sexual assault because it often involves perceptions of inescapability and extreme fear, the two necessary antecedent conditions for the induction of the phenomenon. Research has made progress in identifying and further understanding TI in humans. In one of the first studies to explicitly examine TI in humans, Galliano, Noble, Travis, and Puechl (1993) examined TI in 35 adult female rape survivors. Similar to Burgess and Holmstrom (1976), the authors reported that 37% of the women experienced complete immobility during the sexual assault. Heidt, Marx, and Forsyth (2005) furthered this research by providing evidence that over 52% of participants reported experiences similar to TI in response to CSA. Fusé, Forsyth, Marx, Gallup, and Weaver (2007) also provided support for these findings; in a large sample of adult sexual assault (ASA) survivors, 41.5% of respondents reported significant immobility during their most recent sexual assault. Together, these findings suggest that TI occurs for victims during a large number of sexual assaults. Recent research has also provided evidence that TI occurs during other traumatic events besides sexual assault. For example, Bados, Toribio, and García-Grau (2008) found that there were no significant differences in TI between different types of trauma (e.g., physical abuse, assault or aggression, serious accident), except that individuals who experienced these traumatic events had higher TI scores than those who had learned of the traumatic event after it had occurred (e.g., individuals who received the news of serious injury to a loved one). The existence of TI for survivors of nonsexual traumatic events has also been provided by other researchers (e.g., Abrams, Carleton, Taylor, & Asmundson, 2009; Bados et al., 2008; Bovin, Marx, Pontoski, & Sloan, 2010; Fiszman et al., 2008; Lima et al., 2010; Rocha-Rego et al., 2009).

TI and Later Psychopathology

Research has also provided evidence that the experience of TI during a traumatic event is associated with the subsequent development of psychopathology. For example, Heidt et al. (2005) found that TI occurring in response to an episode of CSA was associated with psychological distress. Other research has specifically identified a

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relation between TI and PTSD (e.g., Bovin, Jager-Hyman, Gold, Marx, & Sloan, 2008; Humphreys, Sauder, Martin, & Marx, 2010; Lima et al., 2010; Rocha-Rego et al., 2009). Bovin et al. (2008) investigated the role of TI, as well as the two antecedent conditions of the phenomenon (i.e., extreme fear and perceptions of inescapability), on the subsequent development of PTSD in ASA survivors. The authors found that TI fully mediated the relation between perceived inescapability and overall PTSD symptom severity, and partially mediated the relations between extreme fear and overall PTSD symptom severity. Bovin et al. (2008) concluded that TI could be one path through which trauma survivors develop PTSD symptoms. Humphreys et al. (2010) extended these findings, reporting that TI also partially mediated the relation between extreme fear and overall PTSD symptom severity among CSA survivors. TI also appears to mediate the relations between extreme fear and overall PTSD symptoms as well as perceived inescapability and overall PTSD symptoms when it occurs during other traumatic events as well (e.g., Bovin et al., 2010). Taken together, these findings suggest that TI occurs in humans during a myriad of traumatic events, and that the experience of TI may be one path through which survivors of these events develop subsequent psychopathology, particularly PTSD.

COMPARING AND CONTRASTING PD AND TI PD and TI During Traumatic Events and Their Long-Term Effects

PD and TI have many commonalities. First, both have been found to occur during traumatic events. As discussed previously, both PD and TI have been found to occur during sexual trauma (e.g., Fusé et al., 2007; Galliano et al., 1993; Griffin et al., 1997; Heidt et al., 2005; Humphreys et al., 2010) and nonsexual traumas, including physical assault, natural disasters, imprisonment, war-zone exposure, serious injury, unexpected injury or death of a loved one, motor vehicle accidents, and urban violence (e.g., Abrams et al., 2009; Bados et al., 2008; Bovin et al., 2010; Bremner et al., 1992; Ehlers et  al., 1998; Fiszman et  al., 2008; Griffin et  al., 1997; Koopman, Classen, & Spiegel, 1994; Lima et al., 2010; Marmar et al., 1994; Rocha-Rego et al., 2009; Shalev, Peri, Canetti, & Schreiber, 1996). In addition to their occurrence during traumatic events, both PD and TI are conceptualized to have beneficial short-term effects and detrimental long-term effects for humans. Regarding beneficial short-term effects, research has suggested that individuals dissociate during a traumatic event to protect themselves from situations with which they would otherwise be unable to cope (e.g., during CSA experiences; Johnson, Pike, & Chard, 2001). It has been argued that TI serves a similar function. In the animal literature, TI is conceptualized as being evolutionarily sound because it makes the prey less visible, can lead predators to abort attack-kill responses (e.g., Herzog & Burghardt, 1974), and can serve as a signaling and decoy function, which allows the prey animal a better chance for escape. There is some evidence that TI demonstrates these same short-term benefits in humans; for example, some rapists require the victim to struggle in order to complete the rape (Burgess & Holmstrom, 1976). If this is the case, TI may actually serve to prevent the completion of rape in

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certain cases. In the long term, however, both peritraumatic experiences are associated with the subsequent development of psychopathology. PD is consistently found to be predictive of PTSD and other forms of psychopathology (e.g., Bremner & Brett, 1997; Bronner et  al., 2009; Johansen, Wahl, Eilertsen, Hanestad, & Weisaeth, 2006; Marmar et al., 1994; Ozer et al., 2003; Tichenor et al., 1996). Similarly, several researchers have demonstrated a relationship between TI and PTSD (e.g., Abrams et al., 2009; Bovin et al., 2008, 2010; Heidt et al., 2005; Humphreys et al., 2010; Lexington, 2007; Lima et al., 2010; Rocha-Rego et al., 2009) as well as between TI and other forms of psychological distress (e.g., Abrams et al., 2009; Heidt et al., 2005). Further, several of the brain substrates implicated in PTSD (e.g., the amygdala, the medial prefrontal cortex [mPFC], and the hippocampus; Weiss, 2007) may also be responsible for the development of both PD (e.g., Lanius, Bluhm, & Frewen, 2011) and TI (e.g., Klemm, 1971; Moskowitz, 2004).

Correlation of PD and TI in Clinical Studies

Based on the overlap in both the time of occurrence as well as the short- and longterm effects of the experiences, we would expect PD and TI to be highly correlated. To date, only two published studies have examined this relationship; however, both have confirmed a significant correlation between these two constructs. For example, in 2009, Abrams et al. explored the relations between a number of variables, including PD, TI, and PTSD, among a sample of 78 male and female undergraduates who had been exposed to a range of traumatic events. These authors found that PD and TI were significantly highly correlated (r = .72; p < .001). Further, they reported that PD accounted for more than half of the variance in TI scores. Lima et al. (2010) also reported a relationship between these two constructs. These authors examined PD, panic, physical symptoms, and TI as predictors of response to standard pharmacotherapy for PTSD among 36 male and female participants who had been exposed to a range of traumatic events. To avoid possible item overlap in the scales measuring PD and TI, the authors utilized a modified TI scale that included only four items assessing motor behaviors. This allowed for PD and TI to be differentiated in terms of their critical point of difference; whereas TI has specific motor components, PD is a subjective experience involving altered cortical functioning. As expected, when examined individually and after controlling for potential confounders (e.g., gender, age), both PD and TI were associated with poor response to treatment (panic was not). However, when examined concurrently, results indicated that TI was the best predictor of a poor response to treatment based on measures of both PTSD symptoms and overall severity of illness; neither PD nor panic remained significant in predicting treatment response. The authors did not examine the correlational relationship between PD and TI in this study. In an effort to further elucidate the relations between these variables, two of the authors examined the relations between PD, TI, and PTSD among a sample of 58 male and female undergraduates (Bovin et al., 2011). A recent factor analysis of the Peritraumatic Dissociative Experiences Questionnaire (PDEQ; Marmar et al., 1994), a measure commonly used to assess PD, indicated that the PDEQ consists of two

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distinct factors: an altered awareness factor and a derealization factor (Brooks et al., 2009). Hence, our analyses were geared toward determining whether each of these factors was associated with both TI and PTSD. Our results indicated that TI (measured by the Tonic Immobility Scale–Adult Version; Forsyth, Marx, Fusé, Heidt, & Gallup, 2000) and the three measures of PD (i.e., total PDEQ score and the two PDEQ factors) were significantly correlated with both PTSD symptoms and PTSD diagnostic status. In addition, all three measures of PD were significantly highly correlated with TI (all rs > .61; all ps < .001). Similar to Lima et al. (2010), we were concerned that these correlations could be a product of the overlap between items (i.e., the TIS-A TI factor includes one item that overlaps with the PDEQ: “Rate the extent to which you felt detached from yourself [e.g., mentally removed from your body] during the event”). As such, we constructed a new TI factor that excluded this item. This TI composite was still significantly correlated with all three measures of the PDEQ (all rs > .51; all ps < .001). These analyses add further credence to the notion that TI and PD are significantly correlated with each other and with measures of psychopathology.

PD, TI, and Memory

Although they share many similarities, PD and TI are distinct concepts. Whereas PD is a cognitive response that has only been studied among humans, TI describes a behavioral response that was first recognized among nonhuman animals. One might be tempted to suggest that PD is the cognitive component of TI, particularly because TI does in fact include one dissociative item in its operationalization (i.e., “Rate the extent to which you felt detached from yourself [e.g., mentally removed from your body] during the event,” e.g., Forsyth, Marx, Fusé, Heidt, & Gallup, 2000). However, this conceptualization is not supported by the literature. A striking distinction between the two constructs is seen in their effects on memory: TI is associated with intact memories, whereas PD is associated with memory fragmentation and disorganization. Individuals who experience PD during a traumatic event may report fragmented or distorted memory for the incident (e.g., Halligan, Michael, Clark, & Ehlers, 2003), whereas during TI an individual is able to retain memory for the traumatic event. This may serve an important evolutionary advantage in animals; by retaining memory during an attack, if they survive, they will be able to recognize potential predators. The contextual memory provided by the hippocampus will also induce wariness for places in which the predator is likely to be found. In support of this contention, previous research has demonstrated that animals can be conditioned while immobile (e.g., Gallup, Boren, Suarez, Wallnau, & Gagliardi, 1980). This memory retention during TI and the memory disruption during PD suggest differential involvement of brain areas recruited during the formation of emotionally charged memories. This is consistent with the neurobiological conceptualization of the two phenomena; the amygdala is thought to modulate the consolidation of long-term explicit memories of emotionally arousing experiences by influencing other brain regions involved in memory consolidation (e.g., Cahill & McGaugh, 1998; McGaugh, 2000; McGaugh, Ferry, Vazdarjanova, & Roozendaal, 2000; McGaugh, McIntyre, & Power, 2002).

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PD, TI, and the Defense Cascade

If PD is not merely the cognitive component of TI, how can we understand the overlap between these two constructs, while still allowing for their discrepancies? Schauer and Elbert (2010) describe a model that may shed light on the relationship between these two constructs. Earlier, we discussed Ratner’s (1967) conceptualization of the defense cascade model as a four-stage series of defensive reflexes through which organisms progress in response to the increasing proximity of a predator (see also Lang et al., 2000). Schauer and Elbert expanded this model to include six stages that occur after the preencounter stage: freeze, flight, fight, TI, flag, and faint. The authors argued that the first half of the cascade is primarily influenced by the sympathetic nervous system. However, a shift occurs during the second half of the cascade, at which point the organism becomes primarily influenced by the parasympathetic nervous system. Based on Schauer and Elbert’s conceptualization, TI is influenced by both the sympathetic and parasympathetic nervous system, which accounts for the combination of voluntary control of learning and memory with loss of motor control. The authors argued that the TI stage is associated with tachycardia, vasoconstriction, hypertension, hyperalertness, high emotional arousal, and fear largely representing anger. This is consistent with the literature on TI (e.g., Löw, Lang, Smith, & Bradley, 2008; Moskowitz, 2004; Ogden, Pain, & Fisher, 2006). In contrast to the TI stage, Schauer and Elbert (2010) argued that the flag/faint stages are associated with parasympathetic activity only. PD occurs at this point in this model. The authors argued that, over the course of several minutes, dissociative reactions begin to dominate, during which time the muscle stiffening (associated with TI) changes to flaccidity. The authors describe the flag and faint stages as the “shut-down” period; it is associated with bradycardia, vasodilatation, hypotension, a drop in arousal, surrender, cognitive failure, and a numbing of all emotions. The authors argued that, unlike in TI, during the flag/ faint stages emotional involvement ceases and memory consolidation becomes weak. This is consistent with research on PD; for example, Griffin et al. (1997) found that individuals who scored higher on measures of PD demonstrated lower heart rate and lower galvanic skin response than those who scored lower on measures of PD. These findings have been supported by other researchers as well (e.g., Pole et al., 2005); however, it is worth noting that both Griffin et al. and Pole et al. (2005) were assessing the long-term effects of PD. It is unclear if this effect would hold during acute terror. Also consistent with Schauer and Elbert’s (2010) conceptualization, PD is associated with cognitive failure and emotional numbing. However, clinical reports of PD support the view that it is also frequent during the high arousal state when terror or rage is extreme. It is hoped that future development of PD questionnaires will discriminate better between high and low arousal responses. Schauer and Elbert’s (2010) model is also consistent with the model recently proposed by Bovin and Marx (2011). The authors argued that if an objective stressor is appraised to be significant to well-being and to tax or exceed the resources of the individual, the individual will experience a powerful subjective reaction. This reaction can include both an emotional experience (which involves an integration of subjective emotions; additional cognitions, including PD; and physiological responses) as well as peritraumatic behaviors (e.g., TI). According to this model, an individual’s

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response to trauma is designed to promote the adaptation of the individual. Further, the authors provide evidence that specific reactions contained within the subjective response (including PD and TI) have been associated with the later development of psychopathology (i.e., PTSD). The model described by Bovin and Marx conceptualizes PD and TI as distinct constructs that can occur when an event is appraised to be significant, and both PD and TI occur in an effort to increase an individual’s chance of survival in the face of threat.

Conclusion

In this chapter, we have reviewed the literature on both PD and TI. It is very valuable to have a summary of the clinical findings in humans in relation to PD and TI, both of which contribute to the severity of the clinical consequences of traumatic experience. Research to date suggests that PD and TI share important commonalities, including their mutual occurrence during events appraised to be significant to well-being, their shortterm benefits (i.e., survival), and their long-term detriments (e.g., psychopathology). The literature also confirms that PD and TI, although related, are distinct concepts. For example, Schauer and Elbert’s (2010) model conceptualizes these two concepts as points on a continuum representative of the proximity of a predator to completing predation (e.g., there is no escape for the prey animal; the predator has established control). The conclusions presented here are consistent with the view of PD and TI supported throughout this book. It is argued elsewhere in this book that PD is the subjective component of the changes induced by the neurochemical compounds conferring stress-induced analgesia and relief from the kind of helpless fear that can trigger TI. These brain chemicals contribute to the psychological effects of triggered memories and may induce the neuroplastic changes underlying structural dissociation. It is also argued that TI is a combination of autonomic, behavioral, and emotional tendencies, which mobilizes neurochemical analgesics of different classes. The study of the neurobiology of PD and TI in humans is challenging, and extrapolation from the study of animals that are unable to report their subjective experience is open to error. Future research is required to develop methods for studying the neurobiology of PD and TI in the same species in order to gain further understanding of these two important phenomena and their relationship with one another.

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CHAPTER 4

A Social–Cognitive–Neuroscience Approach to PTSD: Clinical and Research Perspectives Ruth Lanius, Paul Frewen, Anthony Nazarov, and Margaret C. McKinnon

Embodiment implies that the same neural systems are engaged for selfand other-understanding through a simulation mechanism, while mentalizing refers to the use of high-level conceptual information to make inferences about the mental states of self and others. These mechanisms work together to provide a coherent representation of the self and by extension, of others. —Istvan Molnar-Szakacs and Lucina Q. Uddin (2013)

A social–cognitive and affective theoretical model pertaining to individuals who suffer from posttraumatic stress disorder (PTSD) as a result of repeated traumatization has recently been proposed (Lanius, Bluhm, & Frewen, 2011). This model focuses on disturbances in the affective and social domain of PTSD, including emotional awareness, affect dysregulation, social cognition, and self-referential processing. In this chapter, we will review disturbances in self-referential processing and social cognition in PTSD related to early-life trauma. The default mode brain network consisting of cortical midline brain regions has been suggested to underlie both of these two important interrelated processes. First, the neural underpinnings of self-referential processing and how they may relate the integrity of the default

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mode network (DMN) will be discussed. Second, deficits in social cognition, with a particular focus on theory of mind in PTSD and the neural circuitry underlying direct versus avert eye contact will be described. Implications for assessment and treatment will be addressed.

SELF-REFERENTIAL PROCESSING AND THE DMN IN PTSD

PTSD is often associated with profound disturbances in self-referential processing (Bryant & Guthrie, 2007; Foa, Ehlers, Clark, Tolin, & Orsillo, 1999); it is also reviewed in Liberzon and Martis (2006) as exemplified by symptoms of emotional numbing, alexithymia (Frewen et  al., 2008, 2012), and dissociation, including depersonalization, derealization, and identity disturbance (Herman, 1997; Lanius et al., 2010; van der Kolk, Roth, Pelcovitz, Sunday, & Spinazzola, 2005). Moreover, symptoms of shame often lead the individual to feel bad, despicable, and/or identified with the perpetrator (Andrews, Brewin, Rose, & Kirk, 2000; Cloitre, Cohen, & Koenen, 2006; Herman, 1997). Individuals suffering from PTSD therefore often experience a change in their identity and feel like they, as a person, and their lives have permanently changed for the worse (Foa et al., 1999; see Brewin & Holmes, 2003; Dalgleish, 2004 for reviews). These symptoms have recently been incorporated into the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) under the category of negative alterations in cognitions and mood associated with traumatic event(s) (American Psychiatric Association, 2013; Friedman, Resick, Bryant, & Brewin, 2011). The DMN is a brain network that has been shown to be associated with self-referential processing (Buckner, Andrews-Hanna, & Schacter, 2008; Raichle et al., 2001; Raichle, 2010) and is thought to help prepare the organism for future demands of the environment. The DMN also overlaps significantly with brain regions that have been associated with autobiographical memory and higher-order social cognition, including theory of mind (Spreng & Grady, 2010), suggesting that this network may be involved in the PTSD symptoms not only related to the recall of traumatic events but also to social cognition (see below). Johnson et al. (2002) demonstrated that self-referential processing is associated with the activation of cortical midline structures and therefore overlaps with key areas of the DMN in healthy individuals. Given the deficits in self-referential processing in PTSD, as described above, Bluhm and colleagues have used the same experimental paradigm as Johnson et al. (2002) to demonstrate altered neural activation patterns in brain regions implicated in self-referential processing in patients with PTSD (Bluhm et al., 2012). This paradigm involved assessing the self-relevance of personal characteristics (e.g., I get angry easily) versus the accuracy of general facts (e.g., Paris is the capital of France); both reaction times and neural activation patterns were examined. Healthy individuals exhibited faster responses to the self-relevance of personal characteristics than to the accuracy of general facts. In contrast, PTSD patients did not differ between these conditions. In terms of brain activation patterns, healthy individuals exhibited greater dorsal and ventral medial prefrontal cortex (VMPFC) and posterior cingulate activation while assessing the self-relevance of personal characteristics in comparison with the accuracy of

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general facts. In PTSD subjects, less activation of the medial prefrontal cortex (PFC) was observed for the contrast of self-relevance of personal characteristics relative to general facts as compared to controls. Given that individuals with PTSD have shown deficits in self-referential processing as well as altered brain activation in brain regions associated with the default network, including the medial PFC, anterior cingulate, posterior cingulate cortex, and parietal cortex (Bremner et  al., 1999; Bryant et  al., 2008; Geuze et  al., 2007; Lanius et al., 2001; Liberzon et al., 1999; Shin et al., 1999; Williams et al., 2006), an examination of the integrity of the DMN in PTSD was warranted. Bluhm et al. (2009) first examined the DMN in PTSD patients related to childhood abuse and showed significantly reduced resting state connectivity within regions of the DMN. Specifically, the PTSD group exhibited decreased connectivity between the posterior cingulate seed region and the medial PFC, right superior frontal gyrus, and left thalamus (see Figure  4.1). Furthermore, the connectivity of the medial prefrontal seed region was restricted to neighboring regions within the medial PFC and did not extend to other areas of the DMN. Similar results have recently been reported by Sripada et al. (2012).

Figure 4.1  Default mode network connectivity in control (top panel) and PTSD subjects (bottom panel). Areas of correlation with posterior cingulate/precuneus in healthy comparison subjects (n = 15) and in patients with PTSD (n = 17), thresholded at p < .05, corrected using False Discovery Rate Correction. PTSD, posttraumatic stress disorder. Figure published with permission in Bluhm et al. (2009).

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It has recently been suggested that early-life adversity can affect the developmental trajectory of the DMN. In fact, reduced anterior–posterior DMN connectivity as exhibited in patients suffering from PTSD related to childhood abuse appears to bear resemblance to the DMN connectivity observed in children aged 7 to 9. This suggests that early-life adversity may influence the maturation process of white matter tracts such as the corpus callosum, which connect the anterior–posterior brain regions of the DMN as a result of the toxic effects of stress hormones on the myelination process (Daniels, Frewen, McKinnon, & Lanius, 2011). It is interesting to note that decreased corpus callosum volumes have been reported in children with a history of childhood trauma as well as patients with PTSD related to early-life adversity (De Bellis et al., 1999; Kitayama et al., 2007). Further research will need to prospectively examine the integrity of the DMN in both traumatized and nontraumatized children and adolescents.

THEORY OF MIND IN PTSD

The study of social cognition, including theory of mind (the ability to be aware of and understand others’ behavior, intentions, and emotions; Premack, 1978), is particularly relevant to PTSD since patients suffering from this illness often exhibit profound interpersonal dysfunction, including disrupted functioning of the family unit, problems with intimacy and related difficulties forming and maintaining romantic relationships, in addition to an increased risk of interpersonal violence. The latter is likely partially related to the negative sense of self often experienced by these individuals (Frewen et  al., in press), which leads them to feel deserving of being in abusive and destructive relationships. Moreover, alterations in social cognition such as theory of mind may underlie these some of these impairments in social functioning. The majority of social–cognitive studies in PTSD to date have focused on empathic responding, emotion recognition, and theory of mind (Nietlisbach, Maercker, Rossler, & Haker, 2010). Theory of mind abilities are thought to be crucial to empathic responding since they require the capacity to recognize emotions that are being experienced by others. Nietlisbach and colleagues (2010) reported that individuals with a history of PTSD, as compared to controls, reported significantly higher levels of personal distress as assessed by the Interpersonal Reactivity Index (Bernstein & Fink, 1998; Lanius, Frewen, Vermetten, & Yehuda, 2010), a wellvalidated self-report measure of empathic responding. Several studies in PTSD have also documented deficits in recognizing facial emotion (e.g., happiness, sadness, anger [Knezevic & Jovancevic, 2004; Shin et al., 2005]; but see Orsillo, Batten, Plumb, Luterek, & Roessner, 2004; Wagner, Roemer, Orsillo, & Litz, 2003) for conflicting findings in facial expressivity, which may be intimately related to altered empathetic responding and theory-of-mind processes in this disorder. Investigations examining theory-of-mind performance in individuals with PTSD have also been recently emerging. Most of these studies have utilized the Reading the Mind in the Eyes Task–Revised (RMET), during which subjects are presented with cropped photographs of faces that only display the eye region. Participants are then instructed

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to choose an adjective that best describes what the person in the photograph may be thinking or feeling. Both Mazza et al., 2012 and Nietlishbach et al., 2010 found less accurate judgment of complex mental states using the RMET in individuals with PTSD. It should be noted however that, in the Nietlishbach et al. study, individuals with PTSD differed from controls only after statistically controlling for heterogeneity in time since trauma exposure. Further, in response to the Faux Pas Test, which involves the interpretation of social interactions including white lies, figures of speech, and irony, Nietlisbach et al. (2010) failed to find differences between individuals with PTSD in comparison with controls. Thus, such discrepancies in findings may be attributable to task differences, as well as variations in trauma exposure. Our group has recently examined theory-of-mind deficits in women with PTSD related to childhood abuse using the RMET (Baron-Cohen, Wheelwright, Hill, Raste, & Plumb, 2001) and the Interpersonal Perception Task-15 (IPT-15; Costanzo & Archer, 1989; Nazarov et  al., 2013). In the IPT-15 task, participants are shown brief video clips involving social interactions categorized into five domains, including kinship, status, competition, deception, and intimacy. Following each video clip, subjects are presented with a multiple-choice question about the nature of the interaction in each domain. The subject has to pay close attention to nonverbal cues in order to correctly answer the question; no explicit information pertaining to the question is provided during the videos. For example, one video focusing on the domain of kinship includes a conversation between a child and two adults. Based on both verbal and nonverbal behavior of the three persons, the subject has to determine which of the two adults is the child’s parent. Patients with PTSD related to childhood trauma exhibited theory-of-mind disturbances on both the IPT-15 and the RMET. Compared to healthy controls, individuals with PTSD related to interpersonal trauma exhibited difficulties interpreting scenes that portrayed kinship interactions. No disturbances in the other domains were observed. These results suggest that theory-of-mind disturbances in PTSD related to interpersonal trauma may specifically affect individuals’ ability to interpret family situations. These findings may shed light on why individuals with PTSD often report problems with interpersonal violence (Stevens et al., 2013), marital functioning (Bagley & Ramsay, 1986), and maintaining stable adult relationships (Alexander et al., 1998). Moreover, theory-of-mind disturbances have been suggested to play a key role in difficulties parenting and thereby facilitating the intergenerational transmission trauma, that is, the development of ­psychopathology as a result of emotional regulatory disturbances in the parent(s). In this regard, it has been shown that therapies focusing on increasing theory-of-mind capacity, including mentalization-based treatments (Allen & Fonagy, 2006) have been shown to be effective in individuals who have suffered from disrupted early attachments and interpersonal trauma during childhood abuse as well as in mitigating the intergenerational transmission of trauma (reviewed in Lanius et al., 2011). With regard to the RMET, members of the PTSD group did not differ in its ability to accurately label complex mental states as compared to healthy controls. However, individuals with PTSD exhibited significantly longer response latencies to photographs showing emotionally salient mental states but not neutral mental

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states. Specifically, slower response times were only observed during the labeling of both positive and negative mental states, but not in response to neutral mental states. In contrast, healthy individuals exhibited faster response times to both emotionally salient (positive and negative) mental states in comparison to neutral states. These findings are consistent with research in healthy individuals that has demonstrated increased neural processing speed in response to the presence of an emotional component within facial expressions (Holmes, Bradley, Kragh Nielsen, & Mogg, 2009). In addition, it has been suggested that emotional processing of facial stimuli relies on top-down processes that depend on the accessibility of attentional resources (Pessoa, McKenna, Gutierrez, & Ungerleider, 2002). Several explanations of the slowed reaction times in PTSD must therefore be entertained. First, it is possible that individuals with PTSD exhibited slowed reactions times as a result of slowed neural processing of emotionally salient mental states. However, it is also feasible that individuals with PTSD became triggered or overwhelmed by the emotional states depicted in the RMET, thereby requiring additional attentional resources to deal with the increased cognitive load associated with processing overwhelming emotional stimuli. The latter could lead to a decreased capacity for higher-order social cognition, which may be associated with slower reaction times. Further research examining the role of attention in perspective taking, especially during emotionally salient mental states, are therefore needed. In this regard, it will be important to carefully code if and what specific emotional mental states on the RMET may be triggering or overwhelming for specific individuals with PTSD. It is interesting to note that dissociative symptoms were associated with ­theory-of-mind performance on the RMET and the IPT-15 in our sample. In terms of the RMET, the presence of dissociative symptoms, including disengagement, memory disturbance, and identity dissociation were negatively associated with the accurate identification of positive and neutral mental states. Dissociative symptoms were also associated with altered perception of kinship interactions on the IPT15. Taken together, these findings suggest that dissociation may lead to emotion overmodulation regulatory processes that distance the individual from emotional experience, thus leading to altered theory-of-mind performance. Future studies will need to take a transdiagnostic approach in populations with chronic childhood trauma in order to examine what specific symptoms (e.g., dissociation, dysphoria, hyperarousal symptoms) are particularly associated with altered theory-ofmind performance. Such investigations could then lead to treatment interventions that precisely target symptoms that are most associated with disturbed theory-ofmind performance in order to maximize treatment of altered social cognition in chronically traumatized populations. The latter would hopefully not only lead to improved social functioning in these patients but also alleviate the intergenerational transmission of trauma. In addition to the study of theory-of-mind performance in PTSD related to childhood abuse, our group has also begun to examine social–cognitive processes neurobiologically. In the first set of experiments, individuals with PTSD were exposed to standardized social (rejection-shame) emotional imagery (e.g., imagining yourself in a situation where you are rejected by your friends or having a negative job evaluation)

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or positive social situation (e.g., having a positive work performance evaluation) while having a functional MRI (fMRI) brain scan. In patients with PTSD related to prolonged childhood abuse, altered brain responses in key brain regions involved in higher-order social cognition (mentalizing and theory of mind), including the dorsomedial PFC, temperoparietal junction, temporal poles (TPs), and amygdala, were observed. These early findings suggest that the behavioral findings of altered theoryof-mind performance described above may be associated with altered neural activation of social–cognitive networks. Future research will need to examine the direct relationship between behavioral performance on social–cognitive tasks and how this may relate to altered neural activation patterns in related brain networks.

THEORY OF MIND AND DIRECT EYE CONTACT

Mutual eye-to-eye contact is of fundamental importance in social interactions since it allows the individual to adopt the perspective of others and understand their intentions, emotions, and behaviors (Baron-Cohen, 1995; Tomasello & Carpenter, 2007). Given the deficits in theory-of-mind performance in patients with PTSD related to childhood abuse, the clinical observation that individuals with this disorder often have profound difficulties making direct eye contact, and the abnormalities observed in key brain regions underlying social cognition, a study examining the neural correlates of direct eye-to-eye contact using a virtual reality paradigm in individuals with PTSD related to childhood abuse was carried out (Steuwe et al., 2014). This paradigm involved comparing the effects of a direct versus averted gaze of male virtual characters in three emotional states (neutral, happy, angry) in the fMRI scanner. Our findings suggest that in healthy controls direct versus averted gaze leads to activation of higher cortical structures, which facilitates evaluative “top-down” processes involved in social interactions. In contrast, in individuals with PTSD, direct versus averted gaze, independent of the emotional state of the virtual character, fails to initiate brain regions involved in higher-order social cognition but rather leads to activation of a subcortical structures including the superior colliculus (SC) and underlying circuits of the periaqueductal gray (PAG). These regions have been suggested to form an innate alarm system that facilitates defensive behaviors and decreased social affiliative interaction (see Figure 4.2). Activation of such lower brain structures in the absence of higher social cortical functioning may therefore decrease the individual’s ability to engage in theory-of-mind processes, thereby reducing the ability for optimum social functioning. Future studies will need to examine the effects of direct versus averted gaze in “live” characters versus virtual characters. It will also be important to study the relationship between autonomic response and brain activation patterns during direct versus avert eye contact. Finally, the effects of shame on direct eye contact and the ability of psychotherapy to potentially reverse the altered brain activation during direct gaze in individuals with PTSD will need to be a priority.

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Figure 4.2  Brain areas showing increased BOLD response during direct vs. averted gaze (vs. implicit baseline) for controls (C; n = 16; p < .005; k > 30) and individuals with PTSD (P; n = 16; p < .005; k > 30) as well as for the between-group comparisons controls > PTSD (C > P; p < .005; k > 10) and PTSD > controls (P > C; p < .005; k > 10). Upper three rows display all brain activation observed in transverse slices from z = –30 to z = +60. Bottom two rows display regions of interest, showing increased activation during direct gaze as compared to averted gaze (vs. implicit baseline) within the controls and PTSD group as well as between groups (bottom row). DMPFC, dorsomedial prefrontal cortex; LC, locus coeruleus; PAG, periaqueductal gray; PTSD, posttraumatic stress disorder; SC, superior colliculus; TP, temporal pole; TPJ, temporoparietal junction. Figure published with permission in Steuwe et al. (2014).

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CONCLUSIONS

In this chapter, we have reviewed alterations in self-referential processing and social cognition, including theory of mind and direct eye gaze in PTSD related to early-life trauma, and the neural underpinnings of both of these processes have been discussed. Even though these findings remain preliminary, they raise important future research and clinical questions: (a) To what extent can effective treatment for PTSD related to early-life trauma reverse the altered neural circuitry involved in self-referential processing and social cognition, and what clinical impact would be associated with such neuroplastic changes? (b) Do alterations in the neuronal circuitry underlying social cognition in PTSD interfere with the ability to engage socially and therefore decrease the ability to utilize social support posttrauma? This is an important question since social support has been identified to be one of the most important posttrauma predictors of recovery (Ozer, Best, Lipsey, & Weiss, 2003). (c) What are the effects of altered social cognition and self-referential processing on the intergenerational transmission of trauma (see Fonagy), and what interventions are most effective to mitigate such effects? (d) Do PTSD patients with deficits in social cognition have difficulties engaging in treatment, and how can such problems best be addressed? We hope that this research will lead to an ongoing dialogue between clinicians and researchers in order to further advance our understanding of the complex adaptations to psychological trauma.

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Holmes, A., Bradley, B. P., Kragh Nielsen, M., & Mogg, K. (2009). Attentional selectivity for emotional faces: Evidence from human electrophysiology. Psychophysiology, 46(1), 62–68. Johnson, S. C., Baxter, L. C., Wilder, L. S., Pipe, J. G., Heiserman, J. E., & Prigatano, G. P. (2002). Neural correlates of self-reflection. Brain: A Journal of Neurology, 125(Pt 8), 1808–1814. Kitayama, N., Brummer, M., Hertz, L., Quinn, S., Kim, Y., & Bremner, J. D. (2007). Morphologic alterations in the corpus callosum in abuse-related posttraumatic stress disorder: A preliminary study. The Journal of Nervous and Mental Disease, 195(12), 1027–1029. Knezevic, M., & Jovancevic, M. (2004). The IFEEL pictures: Psychological trauma and perception, and interpretation of child’s emotions. Nordic Journal of Psychiatry, 58(2), 139–145. Lanius, R. A., Bluhm, R. L., & Frewen, P. A. (2011). How understanding the neurobiology of complex post-traumatic stress disorder can inform clinical practice: A social cognitive and affective neuroscience approach. Acta Psychiatrica Scandinavica, 124(5), 331–348. Lanius, R. A., Frewen, P. A., Vermetten, E., & Yehuda, R. (2010). Fear conditioning and early life vulnerabilities: Two distinct pathways of emotional dysregulation and brain dysfunction in PTSD. European Journal of Psychotraumatology, 1, 5467–5477. Lanius, R. A., Vermetten, E., Loewenstein, R. J., Brand, B., Schmahl, C., Bremner, J. D., & Spiegel, D. (2010). Emotion modulation in PTSD: Clinical and neurobiological evidence for a dissociative subtype. The American Journal of Psychiatry, 167(6), 640–647. Lanius, R. A., Williamson, P. C., Densmore, M., Boksman, K., Gupta, M. A., Neufeld, R. W., . . . Menon, R. S. (2001). Neural correlates of traumatic memories in posttraumatic stress disorder: A functional MRI investigation. The American Journal of Psychiatry, 158(11), 1920–1922. Liberzon, I., & Martis, B. (2006). Neuroimaging studies of emotional responses in PTSD. Annals of the New York Academy of Sciences, 1071, 87–109. Liberzon, I., Taylor, S. F., Amdur, R., Jung, T. D., Chamberlain, K. R., Minoshima, S., . . . Fig, L. M. (1999). Brain activation in PTSD in response to trauma-related stimuli. Biological Psychiatry, 45(7), 817–826. Mazza, M., Giusti, L., Albanese, A., Mariano, M., Pino, M. C., & Roncone, R. (2012). Social cognition disorders in military police officers affected by posttraumatic stress disorder after the attack of An-Nasiriyah in Iraq 2006. Psychiatry Research, 198(2), 248–252. Molnar-Szakacs, I., & Uddin, L. Q. (2013). Self-processing and the default mode network: Interactions with the mirror neuron system. Frontiers in Human Neuroscience, 7, 571. Nazarov, A., Frewen, P., Parlar, M., Oremus, C., MacQueen, G., McKinnon, M., & Lanius, R. (2013). Theory of mind performance in women with posttraumatic stress disorder related to childhood abuse. Acta Psychiatrica Scandinavica (e-pub ahead of print). Nietlisbach, G., Maercker, A., Rössler, W., & Haker, H. (2010). Are empathic abilities impaired in posttraumatic stress disorder? Psychological Reports, 106(3), 832–844. Orsillo, S. M., Batten, S. V., Plumb, J. C., Luterek, J. A., & Roessner, B. M. (2004). An experimental study of emotional responding in women with posttraumatic stress disorder related to interpersonal violence. Journal of Traumatic Stress, 17(3), 241–248. Ozer, E. J., Best, S. R., Lipsey, T. L., & Weiss, D. S. (2003). Predictors of posttraumatic stress disorder and symptoms in adults: A meta-analysis. Psychological Bulletin, 129(1), 52–73. Pessoa, L., McKenna, M., Gutierrez, E., & Ungerleider, L. G. (2002). Neural processing of emotional faces requires attention. Proceedings of the National Academy of Sciences of the United States of America, 99(17), 11458–11463. Premack, D. W. G. (1978). Does the chimpanzee have a theory of mind? The Behavioral and Brain Sciences, 1, 515–526. Raichle, M. E. (2010). The brain’s dark energy. Scientific American, 302(3), 44–49.

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Raichle, M. E., MacLeod, A. M., Snyder, A. Z., Powers, W. J., Gusnard, D. A., & Shulman, G. L. (2001). A default mode of brain function. Proceedings of the National Academy of Sciences of the United States of America, 98(2), 676–682. Shin, L. M., McNally, R. J., Kosslyn, S. M., Thompson, W. L., Rauch, S. L., Alpert, N. M., . . . Pitman, R. K. (1999). Regional cerebral blood flow during script-driven imagery in childhood sexual abuse-related PTSD: A PET investigation. The American Journal of Psychiatry, 156(4), 575–584. Shin, L. M., Wright, C. I., Cannistraro, P. A., Wedig, M. M., McMullin, K., Martis, B., . . . Rauch, S. L. (2005). A functional magnetic resonance imaging study of amygdala and medial prefrontal cortex responses to overtly presented fearful faces in posttraumatic stress disorder. Archives of General Psychiatry, 62(3), 273–281. Spreng, R. N., & Grady, C. L. (2010). Patterns of brain activity supporting autobiographical memory, prospection, and theory-of-mind and their relationship to the default mode network. Journal of Cognitive Neuroscience, 22(6), 1112–1123. Sripada, R. K., King, A. P., Welsh, R. C., Garfinkel, S. N., Wang, X., Sripada, C. S., & Liberzon, I. (2012). Neural dysregulation in posttraumatic stress disorder: Evidence for disrupted equilibrium between salience and default mode brain networks. Psychosomatic Medicine, 74(9), 904–911. Steuwe, C., Daniels, J. K., Frewen, P. A., Densmore, M., Pannasch, S., Beblo, T., . . . Lanius, R. A. (2014). Effect of direct eye contact in PTSD related to interpersonal trauma: An fMRI study of activation of an innate alarm system. Social Cognitive and Affective Neuroscience, 9(1), 88–97. Stevens, N. R., Gerhart, J., Goldsmith, R. E., Heath, N. M., Chesney, S. A., & Hobfoll, S. E. (2013). Emotion regulation difficulties, low social support, and interpersonal violence mediate the link between childhood abuse and posttraumatic stress symptoms. Behavior Therapy, 44(1), 152–161. Tomasello, M., & Carpenter, M. (2007). Shared intentionality. Developmental Science, 10(1), 121–125. van der Kolk, B. A., Roth, S., Pelcovitz, D., Sunday, S., & Spinazzola, J. (2005). Disorders of extreme stress: The empirical foundation of a complex adaptation to trauma. Journal of Traumatic Stress, 18(5), 389–399. Wagner, A. W., Roemer, L., Orsillo, S. M., & Litz, B. T. (2003). Emotional experiencing in women with posttraumatic stress disorder: Congruence between facial expressivity and self-report. Journal of Traumatic Stress, 16(1), 67–75. Williams, L. M., Kemp, A. H., Felmingham, K., Barton, M., Olivieri, G., Peduto, A., . . . Bryant, R. A. (2006). Trauma modulates amygdala and medial prefrontal responses to consciously attended fear. NeuroImage, 29(2), 347–357.

CHAPTER 5

Dissociation and Endogenous Opioids: A Foundational Role Ulrich F. Lanius

It’s one of those unpleasant opioid feverish half-sleep states, more a fugue-state than a sleep-state, less a floating than like being cast adrift on rough seas, tossed mightily in and out of this half-sleep where your mind’s still working and you can ask yourself whether you’re asleep even as you dream. And any dreams you do have seem ragged at the edges, gnawed on, incomplete. —David Foster Wallace (1996) Opium teaches only one thing, which is that aside from physical suffering, there is nothing real. 
—André Malraux (1934)

ENDOGENOUS OPIOIDS: A FUNCTIONAL MECHANISM OF DISSOCIATION

There is little doubt that dissociation is at least in part mediated by endorphins and endogenous opioids (e.g., Scaer, 2001; Schore, 2001), which may account for dissociative phenomena like numbing, confusion, and cognitive impairment including amnesia (e.g., Bremner & Brett, 1997). This chapter suggests that multiple animal models are relevant to our understanding of the phenomenology of traumatic dissociation. These include the literature of learned helplessness (LH), ­stress-induced

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analgesia (SIA), as well as tonic immobility (TI)—also see Chapter 3, Peritraumatic Dissociation and Tonic Immobility: Clinical Findings. All of these phenomena are common animal responses to stress that are at least in part opioid mediated. Moreover, these responses are part of a hardwired affective response that occurs not only in animals but also in humans. Indeed, it is suggested that this opioidmediated stress response is evident in all humans, though the extent and severity of it ultimately determines to what extent structural and pathological dissociation arises. Researchers have known for decades that exposure to overwhelming trauma often results in a sustained period of analgesia. Soldiers wounded in battle frequently require much lower doses of morphine than in other types of incidental injury (Beecher, 1946). SIA is a well-documented phenomenon in many forms of traumatic stress (e.g., van der Kolk, Greenberg, Orr, & Pittman, 1989). Release of endorphins at the time of acute stress has distinct survival benefits. An animal ministering to its wounds due to pain at the time of aggressive, life-threatening injury would suffer significant compromise of its defensive capabilities. Specifically, this chapter reviews the neurobiology of opioids and their foundational role as a major regulatory and modulatory system as well as their involvement in dissociative symptomatology. In particular, it is hypothesized that endogenous opioids play a role in the functional mechanism of dissociation. That is, this chapter suggests a unifying neurochemical hypothesis to explain the immediate phenomena of peritraumatic dissociation (PD) and give a plausible explanation for the long-term effects of such experience that lead to the clinical manifestations of amnesia, derealization, depersonalization, identity confusion, and identity alteration. That is, it is suggested that PD and its state-specific reinvocations are measurable physiological events related to endogenous opioid activation. Moreover, this peritraumatic opioid activation is a probable functional mechanism for the development of phenomena related to pathological dissociation, structural dissociation, and somatoform dissociation. That is, endogenous opioids and their receptors play a key role in the phenomenology of dissociation.

FROM THE OUTSIDE AND WITHIN: ENDOGENOUS AND EXOGENOUS OPIOIDS

The term opioid refers to all substances with an opiate-agonistic action, that is, they bind to opioid receptors that are found principally in the central nervous system and the gastrointestinal tract. Opioids include both exogenous and endogenous opiates. Exogenous opiates include natural (e.g., morphine, codeine), semisynthetic (e.g., hydromorphone, oxycodone, buprenorphine), as well as fully synthetic opioids (e.g., fentanyl, methadone). Exogenous opioids are commonly used to induce and maintain anesthesia, as well as to provide analgesia, but are also substances of abuse. Moreover, physical dependence can develop with ongoing administration over time, leading to withdrawal upon discontinuation. Endogenous opiates, such as endorphins and enkephalins, are produced within the organism itself. They function not only as

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neurotransmitters but also as neuromodulators and neurohormones (e.g., Kong et al., 1993). Opioids, whether endogenous or exogenous, depress central nervous system function and result in sedation. Moreover, they depress nerve transmission in the sensory pathways of the spinal cord, including those that signal pain, making them particularly effective painkillers. In addition to their analgesic effect, they tend to be anxiety relieving and they inhibit cardiovascular responses to stress, for example, they lower blood pressure and heart rate.

THE OPIOID SYSTEM: OPIOIDS, OPIOID RECEPTORS, AND OPIOID ANTAGONISTS

Despite opioid molecules being among the phylogenetically oldest signaling substances or neurotransmitters (e.g., Preter & Klein, 2008), the endogenous opioid system was not known until the early 1970s (e.g., Pert & Snyder, 1973). As early as 1974, Mayer and Liebeskind. found that electrical stimulation of the periaqueductal gray (PAG) produced analgesia that was reversible by the opioid antagonist naloxone, strongly implying the existence of an endogenous opioid system. Nevertheless, the search for the endogenous opioid system was initially hindered by the fact that while opioid blockade has clear effects on the action of exogenous opiates (e.g., morphine), it tends to have little effect on normal animals (Akil et al., 1998). Among endogenous opiates, we differentiate three peptide groups: enkephalins, dynorphins, and endorphins. The proenkephalin category includes Met- and Leu-enkephalin, and the prodynorphin category contains dynorphin A, dynorphin B, and neo-endorphin. In the final category, beta-endorphin is cleaved from the prohormone, pro-opio-melano-cortin (POMC) and coreleased with adrenocorticotropic hormone (ACTH) from the anterior pituitary. These opioids interact with three major classes of receptors, the µ (mu), λ (delta), and κ (kappa) receptors (Reisine, 1995), each with several subtypes (Connor & Christtie, 1999). For example, the enkephalins and beta-endorphin have a high affinity for the μ and δ receptors, whereas dynorphin A may stimulate κ receptors. Opioid antagonists are used to explore how opioid molecules act on opioid receptors. Pert and Snyder (1973), in their original research, used naloxone— an opiate antagonist first synthesized in the 1960s. Opioid antagonists block the effects of both exogenous and endogenous opiates by binding preferentially to opiate receptors without activating the receptors. That is, blocking the receptor prevents the organism from responding to opiates and endorphins. The two most commonly used opioid antagonists are naloxone (Narcan) and naltrexone (Revia): naloxone is for parenteral (injectable) administration while naltrexone is manufactured in tablets for oral administration. Both of these opioid antagonists are nonselective: that is, they bind to the different types—µ, λ, and κ—of opiate receptors in the brain, which results in a powerful opiate blockade. For instance, a standard dose of 50 mg of naltrexone will block the effects of 25 mg of intravenously administered heroin.

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THE FOUNDATIONAL ROLE OF ENDOGENOUS OPIOIDS

The endogenous opioid system is part of a stress-response mechanism that has its origins in the invertebrate nervous system. Its role is to maintain homeostasis in the face of changes in the internal and external environment (Stefano et al., 2002). Indeed, endogenous opioids are released in response to a variety of stressors, including pain and anticipatory pain, childbirth, surgery, exercise, social conflict, and starvation. They have an important role in the mediation and regulation of stress responses, including the perception of pain, the modulation of behavior, and the regulation of autonomic and neuroendocrine functions (Drolet et al., 2001). The modulatory role of endogenous opioids extends to other neuroendocrine systems, like the ­hypothalamic–pituitary–adrenal (HPA) axis as well as oxytocin and vasopressin secretion (Buckingham & Cooper, 1986). Further, they influence dopaminergic (Spanagel, Herz, & Shippenberg, 1992), GABA-ergic (Vaughan, Ingram, Connor, & Christie, 1997), and noradrenergic (e.g., Watanabe et al., 2003) activations, and they modify catecholamine release (Kimura, Katoh, & Satoh, 1988) as well as acetylcholine release (Cox, 1988). Endogenous opioids are involved in diverse functions that include pain perception, respiration, body temperature, nutrient intake, and immune response (Stefano et al., 1996). Opioids have anxiety-relieving as well as antinociceptive/ analgesic effects and they inhibit the cardiovascular response to stress, affecting both blood pressure and heart rate. Endogenous opioids depress respiration (Wood & Iyengar, 1988) and reduce gastrointestinal motility (Kromer, 1988), thus resulting in constipation. They affect levels of activity and exploratory behavior (Katz, 1988) as well as learning and memory (Messing et al., 1979). They are involved in disorders of eating such as anorexia and bulimia (e.g., Waller et al., 1986). Opiates affect motivation and mood, including the experience of fear. They impact the response to novelty, conditioned responses, as well as motoric activity and muscle tone. In addition to their reward-signaling functions, endogenous opioids, similar to exogenous opiates, have addictive potential (e.g., Belluzzi & Stein, 1977). Repeated administration of beta-endorphin has been shown to lead to tolerance and addiction as well as to withdrawal upon administration of opioid antagonists (e.g., Van Ree, Versteeg, Spaapen-Kok, & de Wied, 1976). This is consistent with their hypothesized role in traumatic reenactment (van der Kolk, 1989). Further, opioids may contribute to many of the multiple comorbidities associated with traumatic stress syndromes, including major depression (e.g., Brady, Killeen, Brewerton, & Lucerini, 2000) and anxiety disorders (e.g., Lipschitz, Winegar, Hartnick, Foote, & Southwick, 1999). Moreover, impaired opioid system functioning, among others through its effects on the HPA axis, directly effects immunomodulatory functioning, thus potentially accounting for compromised immune system functioning not only after exposure to extreme stress (Schnurr & Green, 2004) but also after early childhood trauma (e.g., Lanius, Vermetten, & Pain, 2010).

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ENDOGENOUS OPIATES, DISSOCIATION, AND PARASYMPATHETIC REGULATION: A BRAKING SYSTEM

The autonomic nervous system is made up of two opposing mechanisms, the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS). SNS and PNS typically function in opposition to each other, though this opposition is better understood as complementary in nature rather than antagonistic. The SNS has been conceptualized as an accelerator and the PNS as a brake. This analogy is only partly correct in that as one system is activated, so is the other. Thus sympathetic activation will necessarily bring with it parasympathetic activation—there is a simultaneous braking and acceleration. That is, the autonomic nervous system will respond to stress with both sympathetic and parasympathetic activation, even though one system dominates. Commonly, when a person experiences a threat, there is an autonomic nervous system response marked by a preponderance of sympathetic activation, a hyperarousal response that readies the organism for fight or flight. Unless the sympathetic activation is minimal or moderate, there will be corresponding parasympathetic activation that results in analgesia (also see the section on analgesia, below). Moreover, the sympathetic response itself may trigger the opioid system and resulting parasympathetic activity (Binder et al., 2004). From an evolutionary perspective, this makes sense and it is clearly adaptive, as the suppression of pain during fight or flight or feigned death will reduce distracting noxious sensations that might interfere with successful attack or escape and ultimately also immobility. If a fight or flight response cannot be mobilized, for example, the threat is overwhelming in nature, is inescapable, or the person is helpless in face of the threat, parasympathetic activation will take over and become dominant. This “parasympathetic regulatory strategy” (Schore, 2001) essentially involves a shift from sympathetic arousal dominance into parasympathetic arousal dominance, with a concomitant increase in dorsal-vagal tone, decreasing blood pressure, metabolic activity, and heart rate, despite massive amounts of circulating adrenaline residual from the sympathetic activation. That is, when danger cannot be escaped, avoided, or fought off, parasympathetic tone overrides the high level of sympathetic activation, essentially truncating a fight or flight response, eventually leading to a catatonic, dissociative state that maximizes the likelihood of survival. This parasympathetic hypoaroused state of surrender reflects conservation, withdrawal, as well as helplessness: As Krystal (1968) states, “In the state of surrender and catatonoid reaction, all pain is stilled and a soothing numbness ensues” (p. 117). This numbness results from a massive release of endogenous opioids, ultimately resulting in catalepsy or immobility (Fanselow, 1986), a phenomenon that is also sometimes referred to as parasympathetic freeze (e.g., Scaer, 2001). In this passive state, endogenous opiates become elevated, blunting, and numbing emotional pain. These opioids, especially enkephalins, instantly trigger pain-reducing analgesia and immobility (Fanselow, 1986) as well as inhibiting cries for help (Kalin, Shelton, Rickman, & Davidson, 1998). Infants lose postural control, withdraw, and self-comfort, reminiscent of the withdrawal of Harlow’s isolated monkeys or of the infants in institutions observed by Spitz (1945; cited by Bowlby, 1978). Moreover, Perry, Arvinte, Marcellus, and Pollard (unpublished manuscript) have suggested that

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bradycardia (abnormally slow heartbeat), cataplexy (rigidity of the muscles caused by shock or extreme fear), as well as immobility and paralysis are opioid-mediated dissociative responses to childhood trauma. Dixon (1998) describes dissociation as “a last-resort defensive strategy,” though it may be better described as a last-resort survival strategy, its hallmark being the absence of any active defensive responses. Thus, dissociation in the passive defense condition can be conceptualized as an opioid-mediated state of parasympathetic activation (Schore, 2001), resulting in energy conservation and social withdrawal (e.g., Schore, 1994). Whereas the SNS is responsible for organizing excitation and the fight or flight response, the PNS is responsible for inhibition, withdrawal, and dissociation: the remnants of the deathfeigning behaviors of lower animals. In an evolutionary sense, this is the “primary hypometabolic regulatory process” (Schore, 2001) during which the individual passively disengages in order “to conserve energies . . . to foster survival by the risky posture of feigning death, to allow healing of wounds and restitution of depleted resources by immobility” (Powles, 1992, p. 213). Moreover, this parasympathetic mechanism mediates what has been described as the “profound detachment” of dissociation (Barach, 1991), or what Freud and Breuer (1895/1991) described as la belle indifference. Dissociation represents “detachment from an unbearable situation” (Mollon, 1996), when early trauma is experienced as “psychic catastrophe” (Bion, 1962), dissociation becomes “the escape when there is no escape” (Putnam, 1997; also see Schore, 2001). Moreover, opioid and/or dorsal-vagal activation (Liberzon et al., 2007) decreases the availability of sensory input. This likely occurs either secondary to disruption of the thalamic relay (Lanius et al., 2001; Liberzon et al., 2007) or disembodiment secondary to altered insula function, for example, out-of-body experience (Lanius et al., 2002). Stress-related downregulation of the thalamus will interfere with projection of sensory information to the sensory cortex. Out-of-body experiences result in sensory information being attributed to someone else, with attendant reduction in associated sympathetic arousal, altering the experience of self. This experience of sensory input being attributed to “not me” may be a crucial aspect in the development of altered self-states and structural dissociation.

PROLONGED STRESS AND NEGLECT—FROM DIMMER SWITCH TO HAIRLINE TRIGGER

Prolonged stress appears to exacerbate the organism’s response to endogenous opioids. Commonly, in contrast to acute stress, in a prolonged stress response glucocorticoids usually fall to low levels (e.g., Kellner, Yehuda, Arlt, & Wiedemann, 2002). Both low glucocorticoid levels (Roosevelt, Wolfsen, & Odell, 1979) and low testosterone levels (Hahn & Fishman, 1979) have been associated with increased opioid receptor binding. Similarly, release of norepinephrine, dopamine, or serotonin results in opioids becoming significantly more potent (Appelbaum & Holtzman, 1985). A history of attachment trauma and/or neglect appears to increase the likelihood of PD in the face of traumatic experience. Schore (2001) suggests that abuse and/or neglect in humans over the first 2 years of life negatively impacts the major regulatory system in the human brain, the orbital prefrontolimbic system, essentially

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reducing synaptic volume and density. It is suggested that excessive pruning of receptors leads to decreased affective regulation and thus to increased hyperarousal and dissociation in response to stressful experiences. In this way, Schore suggests that the infant posttraumatic stress response sets the template for later childhood, adolescent, and adult posttraumatic stress disorder (PTSD). Much of the frontal-limbic system is particularly rich in opioid receptor system. It is also the very system affected by both trauma and neglect. For instance, in rats’ prolonged maternal separation, considered an animal model of neglect, results in alterations of both the µ- and κ-opioid systems (Michaels & Holtzman, 2008), including a decreased response to morphine in tests of antinociception (e.g., Kalinichev, Easterling, & Holtzman, 2003). Similarly, alterations in behavioral measures of both reward and reinforcement involving both dopamine and endogenous opioids are reported (e.g., Matthews & Robbins, 2003; Meaney, Brake, & Gratton, 2002), potentially accounting for both hyperalgesia (increased sensitivity to pain) and hypoalgesia (decreased sensitivity to pain). Bonnet, Hiller, and Simon (1976) suggest that lack of caregiving during the first few weeks of life decreases the number of opioid receptors in the thalamus and cingulate gyrus in mice. This raises the question of whether lack of caregiving and neglect in humans also impact the opiate system in a similar way, resulting in fewer opioid receptors. With fewer receptors to bind available opioids, the capacity of the opioid system to modulate neural functioning likely becomes severely compromised. That is, fewer receptors exist to bind released opioids secondary to stress, and they are likely to become saturated more quickly, thus resulting in more pronounced parasympathetic activation in including dissociation in response to even a relatively minor release of endogenous opioids. The ensuing decreased modulation will increase the likelihood of a sudden or abrupt parasympathetic dorsal-vagal response in response to even relatively minor stressors with a concomitant shutting down of the nervous system.

THE LOSS OF LIFE ENERGY: OPIOIDS AND BREATHING

Parasympathetic activation involves not only lowered heart rate and lowered blood pressure but also decreased respiration. Indeed, one of the common responses to emotional shock is a reduction of respiratory rate. In fact, one of the most striking effects of opiates is the depression of respiration (e.g., Lalley, 2008) to the point where opioids can induce a complete lack of breathing with an associated comatose state. This is commonly the case in drug overdoses (e.g., Larpin, Vincent, & Perret, 1990) and can be treated by the administration of an opioid antagonist, usually the injection of naloxone or Narcan. In the author’s experience, in trauma-focused psychotherapy, a reduction of respiratory rate with simultaneous bradycardia can be frequently observed when the client accesses severely traumatic material—a phenomenon that clients are usually unaware of unless it is specifically brought to their attention by the therapist. This is commonly associated with a dissociative response that includes impaired information processing and it may reflect the activation of opioidergic mechanisms (also see Chapter 11).

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Feelings of suffocation do not trigger the HPA activity (Preter & Kline, 2008). Likely, associated opioid activation decreases subjective awareness of lack of oxygen, for example, lowering the “suffocation alarm threshold,” suggesting impaired interoceptive awareness (also see Chapter 21: Toward an Embodied Self: EMDR and Somatic Interventions). This makes evolutionary sense in that during air deprivation, acute HPA activation would counterproductively increase catabolic activity and oxygen demand, decreasing the possibility of survival.

FREEZE AND IMMOBILIZATION—PASSIVE DEFENSIVE RESPONSES AND DISSOCIATION

In Chapter 2, Threat and Safety: The Neurobiology of Defense Responses: Orienting to Threat; Avoidance: Withdrawal, Hide, and Cringe; Flight, Fight, Freeze; Immobility; Submit, the different types of freeze responses have been described. Specifically, the opioid-mediated analgesia and immobility of the passive defensive response mediated by the ventrolateral column of the PAG are differentiated from the high-arousal freeze states mediated by the lateral and dorsolateral PAG columns. The experiments reviewed here suggest that repeated experiences of ventrolateral PAG activation with endogenous opioid release alter the endogenous opioid tone of the animal, and it is suggested that this altered tone is critical for some of the long-term clinical manifestations of dissociative disorders. Immobilization or TI is a phylogenetically old, last-resort defensive behavior that is at least in part mediated by opioid activation (Mucha, 1980). It refers to a natural-state paralysis or immobilization that animals enter, usually when confronted with a threat that can also be elicited by some forms of physical restraint. It is an inborn, hardwired defensive behavior characterized by a temporary state of profound motor inhibition. TI is related to restraint stress: they have some features in common, though TI differs from restraint stress in that it persists after the forced containment is removed. Specifically, the PAG matter plays a primary role in TI. Its neural circuits involved in descending pain modulation and antinociception are also involved in the modulation of TI (Morgan & Whitney, 2000). TI is mediated, in part, by opiates acting upon opioid receptors in the PAG. When beta-endorphin is injected directly into the PAG, it produces profound catatonia that is reminiscent of immobilization (Sakurada, Sokoloff, & Jacquet, 1978). Moreover, opioidergic stimulation of the ventrolateral PAG increases TI, but this effect can be reversed with naloxone (Monassi, Leite-Panissi, & Menescal-de-Oliveira, 1999). Moreover, Farabollini et al. (1993) suggest specifically that immobilization as a result of acute restraint induces opioidmediated immune system effects, particularly in the ventromedial hypothalamus and the PAG. Catalepsy is a phenomenon related to immobilization that can be induced by emotional shock (Fanselow, 1986). It involves an increase in the tone of certain muscles in the spinal column, to the point where they can produce a striking rigidity in the neck and back muscles, resulting in muscular rigidity and a fixed posture, as well as decreased sensitivity to pain (Austin, 1998). In extreme cases it is almost

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indistinguishable from death, due to extreme slowing of pulse, breathing, and heartbeat. It is at least in part mediated by endogenous opioids, both dynorphins and betaendorphin. In the author’s experience, within a psychotherapeutic context, emerging catalepsy, as indicated by a tightening of the back and neck muscles, particularly at the base of the skull, is frequently an early indicator that heralds the onset of a dissociative response that potentially interferes with effective information processing. In reptiles that lack a neocortex and who consequently have a much decreased need for oxygen, immobilization is an effective defensive strategy. However, in mammals, this inhibition of movement (Hofer, 1970) with attendant parasympathetic activation that includes a reduction of respiration (e.g., apnea) and reduced heart rate (e.g., bradycardia) is potentially lethal (Richter, 1957). If there is survival, there is likely to be compromised immune functioning with long-term health implications. In humans, there may also be disrupted neocortical functioning with attendant alterations in the character and continuity of consciousness to the extent of a structural dissociation of the sense of self.

ENDOGENOUS OPIOIDS—INHIBITION OF ACTIVE DEFENSIVE RESPONSES

While passive defensive responses like immobilization are facilitated by opioid peptides, active defensive responses are inhibited. For instance, feline affective defensive behaviors like fight or flight are suppressed by opioid peptides, an effect that is reversed by administration of the opioid antagonist naloxone. This suggests that blocking the opioid suppression of active defense reinitiates the capacity for movement response, with the relevant pathway for such affective response projecting from the PAG to the ventral medial hypothalamus and ultimately to the thalamus (Shaikh, Lu, & Siegel, 1991). The role of the thalamus in traumatic stress syndromes has been explored in Chapter 1. Not surprisingly, opioid antagonists, when administered prior to a forced swimming test, can block opioid-mediated immobilization behaviors suggestive of LH (Zurita & Molina, 1999). That is, they can reverse both conditioned and unconditioned (e.g., learned but also hardwired) freezing (Makino, Kitano, Komiyama, Hirohashi, & Takasuna, 2000; Zurita & Molina, 1999), as well as enhancing efforts to escape (Molina, Heyser, & Spear, 1994). Such prior opioid tone may be the result of the experience of previous stress. LaPrairie and Murphy (2009) suggest that longterm changes in opioid activity in the PAG can occur very early on in life, among others as a result of neonatal stressors, highlighting the role of early experience and given some credence to the notion of temporal integrationism discussed elsewhere in the book (see Chapter 20). In summary, opioids affect the experience of fear and/or anxiety and are involved in the modulation of fear (Good & Westbrook, 1995), as well as the suppression of emotions (Graeff, 1994) and affective defensive behavior (Shaikh et al., 1991). That is, opioids inhibit avoidance and escape from physical threat, as well as aggressive behavior that can fend of potential attackers. Specifically, opioid-mediated immobilization contributes to inhibiting active affective responses by interfering with muscle control.

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LH AS A MODEL FOR DISSOCIATION

Seligman (1975) suggested “LH” as an animal model for depression, even though the initial work by Seligman and Maier (1967) referred specifically to traumatic shock. In our view, LH may indeed be a better animal model of dissociation rather than depression. Not surprisingly, Nijenhuis, Spinhoven, van Dyck, van der Hart, and Vanderlinden (1998) have suggested that inescapable shock, a research paradigm related to LH, may provide a biological model for both PTSD and dissociation. Seligman and Maier (1967) exposed dogs to inescapable shock. When exposed to subsequent escapable shock afterward, the animals exposed to inescapable shock became immobilized and failed to escape, a behavior very much reminiscent to that of traumatized humans. Along a similar vein, Hofer (1970) exposed rodents to a variety of predator-related stimuli with no means of escape. This resulted in marked bradycardia, as well as with cardiac arrhythmias, suggestive of pronounced opioidmediated parasympathetic activation. Moreover, nonimmobilized wild rats will swim for up to 60 hours before dying from exhaustion. However, if these wild rats experience being immobilized, not only will some of them suddenly die as a result of such induced immobility, but when they are subsequently exposed to the stress of being placed into water they are likely to perish, a phenomenon that is related to excessive parasympathetic arousal (Richter, 1957). On one hand, animals that are exposed to escapable shock are capable of learning to use an escape route and they are much less likely to become immobilized (Fanselow & Lester, 1988). On the other hand, animals, as well as humans, once exposed to inescapable shock, appear to be unable to learn from new experiences (e.g., Jackson, Alexander, & Maier, 1980), even if these experiences promote escape or survival (Overmier & Seligman, 1967). Moreover, in animals exposed to inescapable shock, administration of benzodiazepines reduced fear but had no effect on escape performance, that is, it failed to improve it. This is consistent with clinical observations of clients with traumatic stress syndromes who are being administered benzodiazepines. Blockade of the opioid system, in contrast, eliminates the escape deficit attributable to being exposed to inescapable shock (Maier, 1989). Accordingly, we view escape and avoidance behavior as an active defensive response, similar to a flight response. While it has been argued that endorphins stimulate approach behavior but do not reduce subjective fear (Arntz, 1993), this conceptualization likely confuses fear and anxiety, which can be differentiated by opioid activation (e.g., Rhudy & Meagher, 2000), where fear involves opioid activation but anxiety does not. In our view, opioids, rather than stimulating approach behavior, suppress avoidance behavior. That is, opioids allow us to engage in approach behavior even when there is a subjective fear response, which has been hypothesized as a functional mechanism of exposure therapy (Merluzzi, Taylor, Boltwood, & Götestam, 1991). While opioid release can be helpful in overcoming fears, as is the case in exposure therapy, in individuals predisposed to a dissociative response it likely interferes not only with the mounting of an active defensive responses that can lead to a sense of mastery but also with the integration of information, for example, information processing (see Chapters 1–11). Accordingly, LH, associated with predominant parasympathetic arousal, offers an animal model of dissociation (Scaer, 2001). That is, there are many similarities

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to behavior in animals in whom freezing and immobility has been elicited through a state of helplessness. Moreover, LH and dissociation are both associated with impaired cognition and learning behavior.

SIA: AN ANIMAL MODEL FOR NUMBING

SIA—reduced sensitivity to pain—is mediated by opioid as well as nonopioid mechanisms (Vaughan, 2006). In the case of active defense responses, for example, fight and flight, analgesia is likely mediated by cannabinoids, involving the lateral and dorsolateral columns of the PAG. In contrast, passive defense responses like immobilization are linked to opioid-mediated analgesia that involves the ventrolateral PAG (Bandler, Keay, Floyd, & Price, 2000). That is, it appears that active emotional coping through a fight-or-flight response confers analgesia mediated by endocannabinoids, whereas passive emotional coping elicits a reaction of quiescence, decreased vigilance, and vasodepression (Keay & Bandler, 2002) that is commonly associated with LH. Opioid-mediated SIA relates to LH (Hemingway & Reigle, 1987). Specifically, opioid-mediated SIA occurs in animals that are exposed to inescapable shock; once they are reexposed to stress shortly afterward, they develop SIA. SIA has been described in experimental animals following a variety of inescapable stressors that include electric shock, fighting, starvation, and cold-water swim (for a review see van der Kolk, 1989). Similar opioid-mediated antinociception has also been noted in defeat stress: defeated rats are more sensitive to the pain-reducing effects of opioids (Vivian & Miczek, 1998). Accordingly, opioid antagonists have been shown to reverse the stress-induced analgesic response (e.g., Kelly, 1982). Moreover, in severely stressed animals, opioid withdrawal symptoms can be produced equally, either by termination of the stressful stimulus or by administration of an opioid antagonist. This suggests that severe, chronic, as well as inescapable stress in animals can result in a physiological state reminiscent of the dependence on exogenous opioids (Terman, Shavit, Lewis, Cannon, & Liebeskind, 1984), consistent with the notion that SIA is at least in part opioid mediated. Specifically, it is suggested that numbing in PTSD that is generally conceptualized in psychological terms, for example, a defense against reliving memories of the trauma, is likely mediated by analgesic neurochemicals that involve, among others, an opioid mechanism. Consistent with this hypothesis, abnormalities in the endogenous opioid system have been identified in PTSD clients. For instance, PTSD clients, as compared to controls, show significantly higher levels of analgesia in response to specific (trauma-related stimuli) and nonspecific (exercise) stress (Hamner & Hitri, 1992). Pitman, van der Kolk, Orr, and Greenberg (1990) and van der Kolk et al. (1989) reported that Vietnam veterans with PTSD experienced a 30% reduction in perception of pain when viewing a movie depicting combat in Vietnam. The analgesia produced was equivalent to the injection of 8 mg of morphine. Naloxone, however, reversed this response. Moreover, consistent with the animal research described above, Gold, Pottash, Sweeny, Martin, and Extein (1982) found that when people who were traumatized as adults were reexposed to situations reminiscent of the trauma, this evoked an endogenous opioid response. This is analogous to the response of animals that are exposed to mild shock after having been previously subjected to inescapable shock.

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Thus, it appears that repeated exposure to uncontrollable and inescapable stress results in changes in the endogenous opioid system that can manifest as dissociative symptoms and SIA. Therefore, in our view, SIA provides a possible animal model for depersonalization, numbing symptoms, and analgesia secondary to severe traumatic experience in humans (Glover, 1993; van der Kolk & Saporta, 1991). PERCEIVED CONTROL, SEVERITY OF STRESS, AND ANALGESIA

The relationship between stress and analgesia is complex. For instance, Rhudy and Meagher (2000) suggest that negative emotion can inhibit, as well as facilitate, pain perception. That is, negative emotional valence combined with relatively low arousal is likely to result in sensitization to pain or hyperalgesia, whereas negative emotion in conjunction with high arousal will result in analgesia. Anxiety appears to be facilitatory in that it increases the experience of pain. Fear, considered more uncontrollable and threatening, on the other hand, is inhibitory—it decreases the experience of pain. Accordingly, Rhudy and Meagher suggest that moderate levels of negative affect that include anxiety and fear will increase perceived pain, as well as the likelihood of a fight-or-flight response, whereas high levels of fear result in opioid activation to a point where there is reduced experience of pain and defensive responses like fight or flight decrease, ultimately leading to immobilization and LH. That is, with increasing fear, perceived controllability of an event is reduced and helplessness increases, with parasympathetic activation dominating over sympathetic arousal. Krystal (1968) describes this state switch from sympathetic hyperarousal to parasympathetic hypoarousal: The switch from anxiety to the catatonoid response is the subjective evaluation of the impending danger as one that cannot be avoided or modified. With the perception of fatal helplessness in the face of destructive danger, one surrenders to it. (pp. 114–115) Given that the autonomic nervous system will respond to stress with both sympathetic and parasympathetic activation, SIA and dissociation are likely to occur in some cases when there is a predominant sympathetic hyperarousal response when there is overwhelming fear (Frewen & Lanius, 2006). This is consistent with the data shown by Lanius et  al. (2001) that suggest significant primary dissociation during hyperarousal states in multiple traumatized individuals.

SIA AND THE UBIQUITY OF DISSOCIATION—THE ROLE OF COGNITIVE FACTORS

Bandura’s work indicates that dissociative mechanisms like SIA can occur with relatively minor day-to-day stressors in nonclinical populations. That is, massive endogenous opioid release resulting in SIA occurs not only in individuals with dissociative disorders, but also in certain situations it can be invoked in the population at large,

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suggesting the existence of a basic underlying mechanism of dissociation in all humans. Moreover, SIA can be produced in normal college populations with stressors that hardly seem traumatic, as long as they are perceived as uncontrollable. For instance, Bandura, Cioffi, Taylor, and Brouillard (1988) provided subjects with a math task that exceeded their cognitive capacity and found that this resulted in naloxone-reversible analgesia. In humans, cognitive factors like perceived controllability of a stressor (e.g., locus of control) and perceived self-efficacy appear to play a significant role with regard to the extent of opioid activation, with increased selfefficacy resulting in decreased opioid activation. Moreover, there is evidence that perceived self-efficacy and cognitive coping are primarily mediated by nonopioidmediated mechanisms (Bandura, O’Leary, Taylor, Gauthier, & Gossard, 1987). Overall, Bandura’s research suggests that opioid-mediated parasympathetic activation is pervasive, even in normal populations. Moreover, these mechanisms, at least in normal populations, are to some extent mediated by cognitive factors. The latter, in turn, are more likely than not profoundly influenced by socialization (also see Chapter 6).

SIA, EMOTIONAL NUMBING, AND ALEXITHYMIA: NO FEELING

SIA likely not only relates to the experience of pain sensation but also affects the experience of emotion. Apart from impeding the motoric or muscular aspects of active defensive responses, endogenous opioids also interfere with the underlying experience of emotion. Specifically, emotional numbing is an integral part of traumatic stress syndromes (e.g., Frewen & Lanius, 2006) and is one of the hallmarks of dissociation, particularly depersonalization (Simeon, Giesbrecht, Knutelska, Smith, & Smith, 2009). The imaging studies of depersonalization were reviewed by Sierra (2009), who confirmed the reduced autonomic responses and the reduced activity in the amygdala to emotional stimuli in patients with that condition. Functional imaging studies have shown that opioid activation of µ-receptors results in inhibition of amygdala function (Liberzon et  al., 2002). Accordingly, it is hypothesized that an excessive release of endorphins may contribute to the lack of amygdalar activation in the face of reminders of traumatic events, an effect described in the neuroimaging literature (also see Chapter  1). This finding may in fact be an important aspect in explaining such phenomena as traumatic bonding and traumatic reenactment. Essentially, in the presence of endorphin release, information projected from the amygdala is no longer projected into the hypothalamus, striatum, and brainstem (Gray, Carney, & Magnuson, 1989), thus inhibiting defensive behaviors such as fight or flight. Moreover, disruption of the thalamic relay (Lanius et al., 2001) likely interferes with the transmission of sensory information to the cortex as well as with regulation of sensory input. Indeed, this may account for findings of functional abnormalities of the sensory cortex (visual, auditory, and somatosensory) as well as areas responsible for an integrated body schema associated with depersonalization (Simeon et al., 2009). More likely than not, such disruption of sensory transmission, as well as alteration in functioning of the sensory cortex, contributes to impairments in emotional functioning, involving both emotional dysregulation and emotional numbing.

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As sensory experience is the foundation of emotion (Damasio, 1999), and SIA results in a loss of exteroceptive and interoceptive information, the resulting loss of sensory experience effects a loss of emotional experience. Frewen, Dozois, Neufeld, and Lanius (2008) specifically suggest that there is a reduced level of emotional awareness in PTSD. While the conscious awareness of emotion is reduced, the behavioral expression of affect itself can frequently remain preserved (Bermond, Moormann, Albach, & van Dijke, 2008). This state of affairs may account for the often extreme affective behavior exhibited by traumatized individuals, while at the same time there is an absence of feeling. A similar phenomenon of anhedonia coexisting with enhanced emotional behavioral reactions in animals has been shown to be reversible through opioid blockade (Zurita, Martijena, Cuadra, Brandao, & Molina, 2000).

NO FEELING AND VEHEMENT EMOTIONS—ALEXITHYMIA AND AFFECTIVE DYSREGULATION

Trauma survivors frequently experience a lack of feeling (Hillel, 1992) while at the same time expressing vehement emotions (Janet, 1889). They typically lose connection to the present, frequently engaging in impulsive behaviors. This apparent paradox can be resolved if we consider the work of Jaak Panksepp (2001), who has cogently argued that affect is largely a subcortical process, a notion that is supported in neuroimaging research (Damasio et al., 2000) and through observation of hydrancephalic children (Merker, 2007). This may explain why, even in the presence of alexithymia and associated thalamic disconnection from the lower subcortical structures, there is remaining affective expression. That is, in spite of the thalamic disconnection from the lower subcortical affective structures, there remains expression of usually extreme disowned affect, without associated conscious awareness nor top-down regulation of it. Thus, extreme dysregulated affect, an ongoing expression of subcortical animal affective responses (Panksepp, 1998), may be expressed by trauma survivors who at the same time report a lack of feeling, despite downregulation of cortical structures involved in emotion. High-arousal defense behaviors like fight or flight occur without awareness of anger or terror. In Chapter 1, we discuss how the animal affective responses become isolated from ordinary consciousness and grow into the building blocks of structural dissociation (see van der Hart, Nijenhuis, & Steele, 2006). In Chapter  8, The Clinical Sequelae of Dysfunctional Defense Responses: Dissociative Amnesia, Pain and Somatization, Emotional Motor Memory, and Interoceptive Loops, it is proposed that the affective consciousness loops mediating the emotional, behavioral, and autonomic aspects of the defense responses can occur without the awareness that is conferred by dorsomedial prefrontal cortex and anterior cingulate cortex activation. Moreover, opioid-mediated amygdalar dysfunction may also contribute to affective dysregulation. This may be mediated through opiate receptors in the amygdala, which is loaded with opiate receptors. For instance, removal of the amygdala (Maeda & Maki, 1986) and lesions in the amygdala (Aggleton, 1992; Shaikh et al., 1991) both have similar effects: They suppress fear responses in animals, to the point where

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animals will engage in behaviors, or rather show behavioral deficits, that potentially threaten their survival (Horel, Keating, & Misantone, 1975), a phenomenon that has been referred to as Klüver-Bucy syndrome. The latter occurs secondary to bilateral lesioning of the amygdala. It is associated with hyperphagia, hypersexuality, hyperorality, and docility in animals. In humans, emotional blunting, placidity, increased sexual behavior, hyperorality, and increased urge to put food in one’s mouth, as well as dietary changes, especially bulimia and associated weight gain, are commonly observed, as well as an inability to recognize objects or inability to recognize faces or other memory disorders, many of them phenomena that are observed in and associated with dissociative disorders.

OPIOIDS AND LOSS OF MEMORY: AMNESTIC MECHANISMS

Opioids are involved in the modulation of memory (e.g., Austin, 1998). On one hand, endogenous opioids likely contribute to the establishment of conditioned procedural memory in trauma (Scaer, 2001). At the same time, opiates, including endogenous opioids, have amnestic effects that potentially account for amnestic symptoms observed in traumatic stress syndromes. Izquierdo (1982) identified an “amnesic” mechanism mediated by beta-endorphin, thus potentially providing a neurobiological model that accounts for deficits with regard to memory functioning in individuals with dissociative disorders. Izquierdo (1982) suggests the existence of a physiological amnesic mechanism mediated by beta-endorphin, and perhaps other opioids as well, which normally prevents memory from being as good as it could be and when operating at an exaggerated level may cause complete amnesia. That is, beta-endorphin interferes with memory and can result in deep amnesia (Izquierdo & Dias, 1983). Specifically, opiate antagonists facilitate consolidation of memory, whereas even subanalgesic doses of beta-endorphin result in retrograde amnesia and can produce deep amnesia (Izquierdo & Dias, 1983). Further, Izquierdo (1982) suggests that the memory-impairing effects of electroconvulsive therapy (ECT) may be attributable to an opioidmediated mechanism. This may account for the particularly severe effects of ECT on memory functioning in individuals with dissociative disorders, as well as ECTseeking behavior by some traumatized individuals to help them forget. Izquierdo suggests that this opioid-mediated amnestic mechanism interacts with other systems that influence memory consolidation (central dopaminergic and noradrenergic pathways, ACTH, peripheral adrenaline) and is a powerful modulator of their activity. That is, an opioid-mediated amnesic mechanism modulates the effect of ACTH and epinephrine on memory consolidation. While both epinephrine and ACTH can have either facilitatory or dampening effects on memory consolidation, opioid antagonists are facilitatory in either case (Izquierdo & Dias, 1983). For instance, Introini-Collison and McGaugh (1987) examined the involvement of opioid peptides in the memory-modulating effects of epinephrine in inhibitory avoidance in animals. While low levels of epinephrine facilitate memory, high levels interfere with it. They found that naloxone enhanced the facilitatory effects of low levels of epinephrine, as well as blocking the memory-impairing effects of high levels of epinephrine, generally facilitating the retention of memory. Similarly, Flood, Cherkin, and

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Morley (1987) suggest that antagonism of endogenous opioids facilitates memory processing, improving both recall and retention, consistent with an opioid-mediated mechanism. In previously traumatized individuals, reaccessing reminders of traumatic events results in opioid activation (Pitman et al., 1990). This opioid activation, if sufficiently strong, may not only result in a perceived lack of fear but it is also likely to produce amnesia, thus conferring a further barrier toward mounting active defensive responses such as fight or flight. That is, if there is no access to the memory of being traumatized, the likelihood of intentional defensive behavior will be much reduced. Thus, the combination of lack of fear in conjunction with amnesia (see below) in combination with existing truncated animal affective responses may account for the tendency for conditioned perpetuation (Scaer, 2001) as well as for phenomena like traumatic reenactment frequently encountered in traumatic stress syndromes (e.g., Pfefferbaum & Allen, 1998).

OPIOIDS AND NEUROPLASTICITY: OBSTRUCTED GROWTH AND LEARNING

Traumatic stress syndromes have been associated with deficits in the areas of verbal memory and learning, executive functioning, working memory, and attention (Samuelson, Krueger, Burnett, & Wilson, 2010). For instance, neonates born to mothers who receive intravenous or intramuscular opioids rather than epidural anesthesia tend to require more naloxone and tend to have lower Apgar scores then those born to mothers who receive epidural anesthesia (Leighton & Halpern, 2002). Similarly, Ing et  al. (2012) suggest that even a single exposure to anesthetic neurochemicals prior to age 3 was associated with increased risk of disability in language and cognition at age 10. These effects are likely in part mediated by anesthetic neurochemicals that affect neuroplasticity. Neuroplasticity refers to the brain’s ability to reorganize itself by forming new neural connections. This is a form of learning—sometimes also referred to as cortical remapping—and it reflects the ability of the human brain to change itself due to experience. Neuroplasticity allows the neurons (nerve cells) in the brain to adjust their activities in response to new situations or changes in their environment. Until recently, it was thought that neuroplasticity, neurogenesis (generation of new neurons), and synaptogenesis (creation of new synapses/connections) were all but completed in the adult brain. However, lately, there is evidence that there is ongoing neuroplasticity in the adult brain. Brain reorganization takes place by mechanisms such as axonal sprouting, in which undamaged axons grow new nerve endings to reconnect to other neurons, forming new neural pathways to accomplish needed functions. Neurogenesis is one specific type of neuroplasticity important for learning and the formation of memory. It is the process by which new nerve cells are generated, and it refers to the active production of new neurons, astrocytes, glia, and other neural lineages from undifferentiated neural progenitor or stem cells. Neurogenesis is at least in part mediated by the endogenous opioid system. Both opiates (Eisch, Barrot, Schad, Self, & Nestler, 2000) and stress (Pham, Nacher, Hof, & McEwen, 2003) inhibit neurogenesis, whereas opioid receptor blockade can result

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in dramatic increases in dendritic growth (Hauser, McLaughlin, & Zagon, 1989) as well as increased cell proliferation in the forebrain (Schmahl, Funk, Miaskowski, & Plendl, 1989). Moreover, exposure to stress in both early and adult life negatively affects hippocampal plasticity and memory. Particularly, stress interferes with synaptic plasticity in the hippocampus by impeding long-term potentiation (LTP), thereby affecting memory (e.g., Kim, Song, & Kosten, 2006). The administration of the opioid antagonist naltrexone has been shown to reverse such stress-induced impairment in LTP, thereby implicating an endogenous opioid mechanism in the stress-induced impairment of LTP (Shors, Levine, & Thompson, 1990). Ultimately, it appears that excessive opioid activation interferes with adaptive changes in the brain to its environment.

SUMMARY

In this chapter, we have reviewed the neurobiological basis of opioids and their relationship to the phenomenology of dissociation as well as a number of other associated neurobiological processes. It is suggested that exposure to high levels of endogenous opioids in combination with decreased levels of opioid receptors likely sets the template for increased dorso-vagal activation during exposure to stressors. This process is likely at least in part responsible for multiple aspects relevant to our understanding of traumatic stress syndromes. Apart from PD, endogenous opioids are likely involved in amnesia, LH, SIA, alexithymia, and affective dysregulation as well as a number of other phenomena related to dissociation. Specifically, we suggest that a neuropharmacological understanding of these processes can inform our understanding of many dissociative phenomena. At the same time, it is likely that endogenous opioids are not the only neurochemicals that are involved in the facilitation of dissociation. Indeed, there is emerging evidence that endogenous cannabinoids can also contribute to pain relief, fear reduction, and dissociation. These, and probably other, chemicals in the brain mediate the dissociative response to trauma that, through neuroplastic mechanisms, lead to long-term alterations in emotional, autonomic, cognitive, and behavioral functioning. In Chapter 1 we discussed the involvement of opioids and anesthetic neurochemicals in structural dissociation. In the following chapter, Attachment, Neuropeptides, and Autonomic Regulation: A Vagal Shift Hypothesis, we review the relationship of the opioid system to attachment. Moreover, we will review how the opioid system is involved in both defensive and relational affective behaviors, how it is involved in the release of oxytocin and vasopressin, and how these neurohormones are involved in basic affective responses. In Chapter  11, Dissociation, EMDR, and Adaptive Information Processing: The Role of Sensory Stimulation and Sensory Awareness, we briefly touch on the involvement of opioids in information processing, and in Chapter  22, Opioid Antagonists and Dissociation: Adjunctive Pharmacological Interventions, we provide specific suggestions as to how adjunctive pharmacological interventions in the opioid system can support psychological interventions in the treatment of attachment and trauma-related disorders.

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CHAPTER 6

Attachment, Neuropeptides, and Autonomic Regulation: A Vagal Shift Hypothesis Ulrich F. Lanius

To survive, mammals must determine friend from foe, evaluate whether the environment is safe, and communicate with their social unit. These survival-related behaviors are associated with specific neurobehavioral states. —Stephen Porges (2005) Oxytocin connects us to other people; oxytocin makes us feel what other people feel. —Paul Zak (n.d.)

OPIOIDS, OXYTOCIN, AND VASOPRESSIN: ATTACHMENT AND AUTONOMIC REGULATION

Our external environment and our attachment relationships in particular have a profound impact on the nature of autonomic regulation and which neuropeptides and neurotransmitters predominate. Affiliative behaviors and attachment relationships, as well as defensive behaviors, are mediated by endogenous opioids, oxytocin, vasopressin, as well as by catecholamines. In this chapter we focus on the modulatory role of these neuropetides in both attachment as well as autonomic regulation,

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discussing sympathetic and parasympathetic arousal, particularly dorsal vagal and ventral vagal regulation as suggested by polyvagal theory (Porges, 2005). Indeed, it has been suggested that the biological foundations of attachment are mediated by social motivation circuitry common to all mammals (Nelson & Panksepp, 1998). Specifically, endogenous opioids and oxytocin affect attachment-related behaviors, including maintenance of contact, grooming, and responses to separation (Saltzman & Maestripieri, 2011). The probable role of the endogenous opioid system in the modulation of oxytocin and vasopressin release is discussed with a view toward the elicitation of both relational and active defensive responses is reviewed. Specifically, the interrelationship of endogenous opiates, oxytocin, and vasopressin is discussed, with a specific view on their involvement in the process of avoidance and detachment on one hand, and attachment and the relational on the other. Ultimately, it is suggested that early attachment experience affects these neuromodulatory systems and creates a template that influences the kind of autonomic nervous system responses that are likely to occur under stress. MAMMALIAN SPECIES AND ATTACHMENT: DORSAL VAGAL VERSUS VENTRAL VAGAL IMMOBILIZATION

Porges’ Polyvagal Theory delineates two parasympathetic medullary systems, the ventral and dorsal vagal. Whereas the later developing ventral vagal is the “mammalian,” “smart” system that fancily regulates cardiac output fostering flexible social engagement and disengagement, the earlier developing dorsal vagal “reptilian,” “vegetative” system acts to shut down metabolic activity and heart rate during hiding and death feigning. The dorsal vagal responds to states of extreme terror in an involuntary and prolonged pattern of inhibitory vagal outflow that accounts for the extensive duration of the “void” states of detachment. MATERNAL BEHAVIOR—OPIOIDS INTERFERE, OXYTOCIN FACILITATES

As discussed in Chapter 5, Dissociation and Endogenous Opioids: A Foundational Role, opiates are clearly involved in the dorsovagal response that includes immobilization, a phylogenetically old, last-resort defensive behavior that dates back to the phylogenetically old reptilian brain. Immobilization is at least in part mediated by opiate receptors in the periaqueductal gray (PAG); for example, when beta-endorphin is injected directly into the PAG, it produces profound catatonia (Sakurada, Sokoloff, & Jacquet, 1978), the antithesis of the relational. Generally, significant opioid-mediated parasympathetic activation is associated with separation, withdrawal, and immobilization. Moreover, opiate activation disrupts in maternal behavior (Bridges & Grimm, 1982) and results in a decreased ability to take care of one’s young (e.g., Sobor et al., 2010). Moreover, opioids administered to mothers during childbirth or during delivery have been reported to decrease lactation success (Leighton & Halpern, 2002). Opioids also reduced oxytocin levels in mothers, secondary to breastfeeding (Lindow et al., 1999). Finally, an increased level of opioid peptides has been associated with

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the development of postpartum psychosis (Lindström et al., 1984). Conversely, with few exceptions (Keverne, Nevison, & Martel, 1997), most studies suggest that opioid blockade has facilitatory effects on the release of oxytocin as well as on maternal behavior (e.g., Dobryakova, Belyaeva, Stovolosov, Dubynin, & Kamenskii, 2006; Miranda-Paiva, Ribeiro-Barbosa, Canteras, & Felicio, 2003). However, research in mammals suggests that parasympathetic slowing of the autonomic nervous system cannot be achieved only by the dorsovagal activation but also through ventral vagal activation (Porges, 2001, 2007). This ventral vagal system appears to be mediated by the neurohormone oxytocin. Interestingly enough, the same area that is imbued with a high density of opioid receptors, the PAG, is also the very area in mammals that is rich in oxytocin receptors (Porges, 2005). Essentially, the more primitive reptilian immobilization or dorsal vagal response appears to have been modified in a way that immobilization can occur in the absence of fear to serve the intimate needs of mammals that involve parturition, nursing, and the establishment of social bonds (Carter, 1998; Insel & Young, 2001; Porges, 2005). More likely than not, because of their oxytocin systems, mammals, in contrast to reptiles, are able to modulate cardiac output and metabolic flow in a graded fashion. This permits an extraordinary capacity for self-calming that does not involve separation, withdrawing, or is immobilizing in nature, but rather attaching and social in quality. This is often referred to as ventral vagal engagement, or social connection. It is more likely than not that the mammalian ventral vagal oxytocin system has developed to allow adaptation to the unique circumstances of mammalian birth that include the parental and nourishing behavior that is necessary to ensure the survival of relatively immature offspring (e.g., Porges, 2007).

OXYTOCIN AND PARTURITION

Parturition refers to the act of giving birth, the process of delivering the baby and the placenta from the uterus to the outside world. Oxytocin is believed to play an important role in most, if not all, mammals with regard to parturition, the initiation of maternal behavior as well as in lactation. Specifically, oxytocin is involved in uterine contractions, fetal expulsion, and maternal behavior (Jarvis et al., 2000). While the painful nature of birth temporarily increases opioid tone (Gintzler, 1990), the consequent withdrawal from these opioids gives way to another rise in oxytocin levels. After birth, oxytocin is also involved in prolactin release (Bertram et al., 2010). At that point in time, both oxytocin and prolaction work in conjunction to facilitate feeding of the baby, where oxytocin is involved in ejection of milk during suckling and prolactin is responsible for mammary growth and lactation.

MAMMALIAN SPECIES AND NOURISHMENT—THE NEED FOR SOCIAL BONDS

As compared to animals that lay eggs, in live-bearing animals and mammals in particular, the embryo develops inside the body of the mother, from which it gains its nourishment. At birth, for example, parturition, newborn mammals are at a comparatively

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early stage of development, requiring parental care for survival. Specifically, there is an ongoing need for nutrition that is provided by the mother, requiring ongoing child care. Whereas mammals remain helpless for a period of several months until they reach a relative level of maturity, this period of time is much more prolonged in humans, much longer even than other primates. The human brain is less developed at birth than other mammals. This is likely related to the size of the human brain, the neocortex in particular. The neocortex is what allows humans to adapt to their specific environment more so than other animals that rely more on instinctual functioning. This experience-dependent maturation of the brain requires time, resulting in a prolonged period of relative helplessness that necessitates prolonged child care. This requires an extended period where all mammals but humans in particular are unable to fend for themselves, thus requiring parental care. This likely created a need for adaptation of the nervous system in both parents and offspring to allow for pair bonding, for example, the relational, to ensure survival.

ATTACHMENT AND ENDOGENOUS OPIATES

There is little doubt that human attachment is at least in part mediated by the endogenous opiate system. Brain circuits involved in the maintenance of affiliative behavior are precisely those most richly endowed with opioid receptors (Kling & Steklis, 1976). Behavioral studies show that the endogenous opioid system plays an important role in the maintenance of social attachment (van der Kolk, 1989). Generally, the endogenous opioid system is activated by several positive social interactions, ranging from mutual grooming in young animals (Keverne, Martensz, & Tuite, 1989; Knowles, Conner, & Panksepp, 1989) to sexual gratification. Opioids result in feelings of comfort and alleviate emotional distress arising from loss and social isolation as well as attenuating the reaction to social separation by powerfully inhibiting separation distress (Panksepp, 2003, 2005; Panksepp, Herman, Vilberg, Bishop, & DeEskinazi, 1980). Particularly, bonding to the mother and mother preference appears to be mediated by endogenous opiates (Shayit, Nowak, Keller, & Weller, 2003). That is, naloxone-treated lambs will no longer seek out their mother preferentially to other ewes (Shayit et al., 2003). Further, a low basal level of opioids increases and a high level of opioids decreases motivation to seek out social contact. Accordingly, blockade of the opiate system increases social motivation but reduces the reward afforded by endogenous opioid release.

AVOIDANT ATTACHMENT: OPIOIDS AND SOCIAL WITHDRAWAL

Avoidant attachment is commonly associated with parental figures that have been rejecting or unavailable and refers to a pattern of attachment where the child avoids contact with the parent. This lack of social affiliation is prevalent in avoidant attachment disorder. Similarly, this lack of social affiliation is also evident in autism spectrum disorders (Dawson et  al., 2002). Moreover, the social withdrawal is also a

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hallmark of many posttraumatic presentations and avoidant attachment may result in an increased risk for posttraumatic stress disorder (PTSD) due to the withdrawal from social connections (Atwool, 2006). The similarity of severe posttraumatic presentations to autism (e.g., Michelson & Ray, 1996) suggests that the research with regard to social affiliation in autism spectrum disorders may be relevant to our understanding of social withdrawal in trauma-related syndromes (Bartz & Hollander, 2006). Specifically, aberrant functioning of the endogenous opiate system has been described in autism spectrum disorders (e.g., Waterhouse, Fein, & Modahl, 1996). Moreover, social withdrawal observed in autism has been attributed to opiate system dysfunction that results in decreased reward value of social interaction (e.g., Sahley & Panksepp, 1987). While opioids in part mediate the experience of pleasure and reward, they also inhibit the seeking of these experiences. For instance, elevated beta-endorphin levels likely reduce the reward value of sucking, satiety, and touch in nursing (e.g., Herman, 1991). Further, elevated beta-endorphin levels are involved in a reduced sensitivity to sensory input and in an abnormally elevated pain threshold (Chamberlain & Herman, 1990). Conversely, opioid blockade increases social motivation (Panksepp, Nelson, & Siviy, 1994) and appears to increase affiliative drive, likely by reducing excessive levels of internal reinforcement and thereby the reward that comes from social interaction (e.g., Kalat, 1978). Moreover, opioid antagonists show beneficial effects on social behavior, as well as reducing gaze aversion (Gillberg, 1995), an effect that is likely attributable to a reinstatement of reward seeking secondary to an increased need for interpersonal connection. THE OXYTOCIN–OPIATE SYSTEM MODULATES ATTACHMENT AND AFFILIATION

Avoidant attachment and social withdrawal are not only associated with dysfunction of the opioid system but have also been correlated with impairments of the oxytocin system, suggesting aberrant functioning of the neuropeptide systems as a whole, involving both oxytocin and vasopressin, as well as dysfunction of the endogenous opiate system (e.g., Waterhouse et al., 1996). Multiple authors, including Carter, deVries, and Getz (1995), Insel (1992), as well as Landgraf (1995) in particular have suggested the importance of the vasopressin–oxytocin system in social attachment and social affiliation. Oxytocin receptors have been found in the cingulate cortex, globus pallidus, hippocampus, and midline nuclei of the thalamus as well as in the amygdala (Insel, 1992). Oxytocin has been suggested to be involved in the initiation of emotional communication, particularly the infant separation–distress cry (e.g., Panksepp, 1992). Csiffáry, Ruttner, Tóth, and Palkovits (1992) describe oxytocin-containing nerve fibers in the hypothalamic arcuate nucleus, the area responsible for the release of endorphins, suggesting a possible influence of oxytocin on the activity of the brain beta-endorphin system at the hypothalamic level. This raises the question as to whether oxytocin activation raises endorphin levels—a likely scenario given the involvement of both oxytocin and opioids in attachment and bonding and/or whether ventral vagal activation prepares for dorsal vagal activation, in case the former is unsuccessful.

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The oxytocin–opiate system may mediate an essential attachment-affiliative drive that may contribute to a failure to cuddle and an indifference or aversion to affection or physical contact, as well as a lack of interest in social interaction, which has been attributed to low levels of oxytocin (Waterhouse et al., 1996). Indeed, there is suggestion that oxytocin administration may have beneficial effects on affiliative behaviors in autism (e.g., Bartz & Hollander, 2008). At the same time, the benefits of oxytocin may be limited in individuals with early parental separation (Meinlschmidt & Heim, 2007), potentially accounting for the difficulties in establishing a therapeutic relationship with clients who suffer from attachment-related disorders.

SEPARATION VS. ATTACHMENT—PANIC AND SEEKING

The separation response is commonly conceptualized as involving different stages: protest, despair, and detachment (Seay, Hansen, & Harlow, 1962). Panksepp (1998) suggests that activation of the PANIC system triggered by separation from the parent intensifies distress vocalization (DV) and separation cries to elicit caregiving behavior to ensure survival. This conceptualization of the PANIC system is based on the notion that individuals who experience panic attacks commonly have childhood histories characterized by separation anxiety (Torgersen, 1986). Moreover, both in the case of panic attacks, as well as separation anxiety, there are active attempts to solicit social support to relieve distress (Panksepp, 1998). Further, it has been suggested that the response to social separation likely has its foundation in an appetitive emotional system: Because of the vigor and ubiquity of this emotional response to social separation, it seems likely that social motivation is a direct manifestation of innate neural circuits which are as spontaneously responsive as those which govern other basic motivated behavior patterns such as feeding and drinking. (Panksepp et al., 1980, p. 473)

This is consistent with Grossmann, Grossmann, and Kindler (2005), who suggest that attachment and exploratory behavioral systems are inextricably linked with each other. Consistent with these authors, it is suggested that prior to the PANIC system, the exploratory or SEEKING system becomes involved (Panksepp, 1998). That is, the seeking of contact is ultimately the precursor of the separation response. This is consistent with Panksepp’s notion of SEEKING being the “granddaddy of all emotional systems.” SEEKING reflects the elicitation of a survival-oriented system that gives rise to foraging and exploratory behavior, among others, to ensure adequate nutritional resources. It is suggested that, under normal circumstances, the PANIC response is likely preceded by a SEEKING response (Panksepp, 1998). Only if such SEEKING is unmet does a PANIC response result. Thus, the separation distress system in mammals is likely a two-stage process that initially involves a SEEKING response, but if unmet will result in a PANIC and dorsal vagal response. The first part of this response is emphasized by the term Bindungsschrei in German (the literal translation of which is attachment cry), reflecting the SEEKING response, whereas in the English language the term separation cry reflects the PANIC and distressing component of this process.

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Therefore, the separation or attachment cry is initially an attempt to maintain social engagement with the mother. This type of ventral vagal engagement is likely maintained by oxytocin not only in the mother but also in the child. Only if the SEEKING or attempts at ventral vagal engagement on the part of the child remain unmet will PANIC and ultimately dorsal vagal activation ensue.

SEEKING FOR FOOD TO ENSURE SURVIVAL

In an infant, given the absence of development of a fully functioning motor system that allows exploratory behavior and foraging, nutritional needs are met by the parents and primary caregivers. Thus, early stages of DVs reflect protest and a SEEKING response to ensure attention of the caregiver and an adequate food supply. If such vocalizations remain unmet, for example, despair will develop if there is an absence of adequate nutrition and caregiving. With continued absence of adequate caregiving, a dorsal vagal, catanoid response develops: It is energy conserving in order to facilitate survival for as long as possible. Simultaneously, the young child becomes increasingly helpless with increasing opioid activation that prepares for a painless death. The separation response itself is the protest stage that includes DV to elicit attention of the caregiver. This aspect of the response is likely a precursor of a sympathetically mediated motoric response. If that response is met through feeding—milk (e.g., through caseomorphine) and other nutrients activate opioid receptors—infant calling rates are much reduced. The attention of the primary caregiver is profoundly relational, and it is likely that this results in oxytocin release (see below) that modulates not only the potentially addictive nature of caseomorphin but also other endogenous opioids. If DVs are unmet in the helpless infant, a feeling of despair ensues, which is accompanied by significant opioid activation that ultimately results in dorsal vagal activation and detachment. This view is consistent with findings that blocking of the opiate system increases the likelihood of a separation cry as well as that administration of opioid antagonists to autistic children seems to increase social engagement (e.g., Lensing et al., 1992), likely reflecting the need for interpersonal connection secondary to the initiation of a SEEKING response. Only if such a SEEKING response remains unmet is separation distress likely to ensure.

SEPARATION ANXIETY—A BIOLOGICAL LEASH

Preter and Kline (2008) suggest that “separation anxiety serves as a biologic leash for the increasingly mobile infant who continually checks for the mother’s presence, becomes acutely distressed on discovering her absence, and immediately attempts to elicit retrieval by crying,” eliciting a seeking response. Moreover, Preter and Kline (2008) suggest that separation anxiety in humans develops only after their motor system matures; we suggest that it is only the behavioral representation of anxiety that develops in conjunction with the motor symptoms. Among animals,

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developmentally immature animals that require nourishment, which are incapable of moving around on their own, emit fewer DVs since it is not likely they will stray from the nest (Panksepp, 1992). Similarly, human infants are born immature and practically never get lost for their first 6 months. On the other hand, a fear response, as opposed to anxiety, in response to social isolation may occur earlier (e.g., Schore, 2001), prior to the development of motor systems. As suggested by Rhudy and Meagher (2003), fear elicits opioid activation and will ultimately result in social withdrawal and a suppression of the attachment cry; opioids not only suppress breathing but they also inhibit cries for help (Kalin, 1993). That is, early in life, the infant is essentially helpless unless cared for by the parents and is unable to mount significant protest behavior. In the absence of the relevant behavioral repertoire to elicit parental proximity, dorsal vagal activation, rather than protest, is more likely. Thus, the substrate of separation anxiety, which facilitates DV, a defensive response to assure the elicitation of parental proximity, develops with parental bonding and increasing maturity of the nervous system.

RESPONSES TO SEPARATION—PROXIMITY SEEKING VERSUS DESPAIR

Separation can induce attachment behaviors, such as proximity seeking and separation DVs as well as behaviors that reflect fear, panic, and despair, such as freezing and inhibition of exploration (Gunnar & Vazquez, 2006). These differences in response to separation are likely mediated in part by the hypothalamic–pituitary–adrenal (HPA) axis, including opioid activation (Kalin, Shelton, & Barksdale, 1988). Levine and Wiener (1988) suggest that in mother–infant relationships in nonhuman primates, the presence of other animals of the same species (conspecifics) reduces HPA axis activation, as compared to total isolation. Similarly, visual access to the mother reduces the cortisol response. However, being in the presence of unfamiliar conspecifics increases HPA axis activation when compared to total isolation. Separation-induced DVs, however, are not linearly related to physiological measures of HPA axis activation. That is, DV increases with visual access to the mother as when compared to total isolation. In the presence of familiar species, DVs are reduced compared to total isolation. We interpret these results in the following manner: DVs do not only reflect separation distress but also the longing for connection, that is, attachment to the mother. Moreover, proximity to a potentially unsafe, unfamiliar animal produces a relatively more active defensive response with regard to HPA axis activation, while at the same time reducing DVs, possibly to decrease drawing attention from another animal that may be a threat to safety. Separation itself, in the absence of visual access to the mother, produces reduced release of cortisol, suggesting the beginnings of an energy-conserving dorsal vagal response that is incidentally also related with a decrease in DVs. Thus, DVs and protest behaviors are at times inversely related to HPA axis activation, reflecting the infant’s active attempt to cope with separation, whereas despair and freezing may reflect the inability to cope with separation (Kraemer, Ebert, Schmidt, & McKinney, 1991).

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Thus, on one hand DV may reflect protest behaviors of an insecurely bonded infant, for example, insecure or disorganized, and on the other hand proximity seeking may be a result of a secure attachment base. The insecure, avoidant child will quickly move toward despair, whereas the securely attached child is likely to protest longer and return to exploratory behavior after successful reunion with the parent. Individuals with avoidant attachment will not actively protest, nor will they be able to engage with their environment through exploratory behavior. Accordingly, “insecure” attachment patterns can result in excessive seeking of the mother as a secure basis by not wanting to engage in exploratory behavior again after separation, for example, clinging, or alternatively not seeking bodily proximity to the mother, for example, avoidant. Among others, excessive opioid activation as well as reduced opioid receptor density, both resulting in reduced opioid binding potential, will result in reduced DVs more quickly, attenuating the likelihood of active defensive behaviors under distress. In the same vein, exploratory behavior is likely mediated by the dopaminergic mesolimbic reward system that is modulated by opioid activation. That is, impairments in functioning of the opioid system will reduce the reward value of exploratory behavior, possibly explaining such divergent behaviors as amotivation and lack of responding to environmental stimuli, but also inability to shift set and excessive responding to the same stimuli, as is the case with both obsessive/compulsive behaviors as well as addictions.

OPIOIDS AND THE QUIETENING OF THE SEPARATION CRY— THE LOSS OF THE RELATIONAL

The neurochemical system most clearly associated with crying and DVs is the opiate system (e.g., Newman, Murphy, & Harbough, 1982; Panksepp, Sivey, & Normansell, 1985; Panksepp et  al., 1994). Research by Panksepp and colleagues (e.g., Newman et al., 1982; Panksepp et al., 1985; Panksepp et al., 1994) suggests that the separation response in animals can be inhibited by morphine, abolishing both the separation cry in infants as well as the maternal response to it. That is, morphine significantly decreases separation-induced vocalizations, whereas naloxone increases them (Herman & Panksepp, 1978; Kalin et  al., 1988). Moreover, morphine abolishes not only the separation cry but also the maternal response to it (e.g., Panksepp et  al., 1980; Panksepp et al., 1994). Sahley and Panksepp (1987) suggest that attachment and language have evolved out of the opiate-based pain system; damage to the opioid system will impair both social attachment as well as language functioning. Mammalian infants are unable to survive independently after birth (Preter & Kline, 2008). DVs are a primitive form of audio-vocal communication (Panksepp, 1998) and are a distress-signaling mechanism to elicit parental care and retrieval, thus ensuring survival. Panksepp et al. (1980) suggest that social attachment and separation distress, including DVs, reflect primary hardwired subcortical emotions. Specifically, they state, “This reaction [crying] to separation is immediate, reflex-like and consistent across different animals, and its expression appears to require no previous learning”

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(p. 473). Panksepp’s notion of “hardwired subcortical emotions” is supported by the fact that DVs are possible without a cortex (Barnet, Bazelon, & Zappella, 1966; Nielsen & Sedgwick, 1949). That is, animals with a destroyed or ablated neocortex and limbic system continue to exhibit DVs as long as the pariaqueductal gray (PAG), structure in the brainstem, remains intact. Similarly, ultrasonic vocalizations relating to submission or pleasure arise from activation of the same area. At the same time, higher brain structures that include the cingulate gyrus and related connections and the thalamo-cingulate division of the limbic system—a neural system found only in mammals—appear to also be involved in elaborating social loss (MacLean, 1990; Panksepp et  al., 1985). Opiate receptor density in the limbic system, including the cingulate gyrus, is high. Interestingly enough, this very area, in humans, is activated by voiced speech (Schulz, Varga, Jeffires, Ludlow, & Braun, 2005). This is part of the same area that becomes deactivated by traumatic stress, likely reflecting primary dissociation (also see Chapter  1, Dissociation: Cortical Deafferentation and the Loss of Self). That is, excessive opioid activation results in a loss of the relational, akin to the opioid-mediated dorsovagal response (Panksepp, Najam, & Soares, 1979). This is consistent with Barach, who has argued that dissociation can be conceptualized in terms of disordered attachment. He bases this on Bowlby’s (1988) descriptions of how emotionally neglected and abused children detach from internal and external signals (Barach, 1991) that would normally elicit a search for a parent, essentially suggesting a shutting down of the SEEKING system and inhibition of cries for help (Kalin, Shelton, Rickman, & Davidson, 1998).

KAPPA OPIOIDS PRODUCE DYSPHORIA AND DISSOCIATION

These observations lead to the critically important conclusion that endogenous opioids in social animals are released in response to not only physical pain but also to the pain of separation, which employs closely related brain circuits (Panksepp, 2000). In patients with dissociative disorders, early trauma may have been the result of unmet needs for care and nurturance in the relationship with the main caregiver, rather than physical or sexual abuse, and it is this nonphysical pain of separation and abandonment that first leads to the soothing release of endogenous opioids to ease distress. The transformation of the initial phase of protest at isolation to the energy-conserving state of despair may be partially dysphoric because it involves not only activation at mu-receptors but also at kappa-receptors: kappa-agonists have the capacity to produce profound dysphoria in humans (Watt & Panksepp, 2009). Moreover, kappa-opioid receptor activation has also been associated with both depersonalization and derealization (Walsh, Strain, Abreu, & Bigelow, 2001). Thus, the relative activities at mu- and kappa-receptors could account for the degree to which the analgesia produced by endogenous opioid release is experienced as pleasurable or otherwise. Patients with dissociative disorders who develop dependence on opiates may be attempting to convert their dissociative analgesic response to the pain of abandonment to a less dysphoric experience. Interestingly enough, buprenorphine, a partial

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opiate agonist–antagonist at the mu-receptor level, but a kappa-receptor antagonist that does not induce tolerance, has shown beneficial effects in treating refractory depression (Bodkin, Zornberg, Lukas, & Cole, 1995). The immature infant needs to attach to survive, so needs to activate the relevant care and nurturance circuitry in the PAG, preoptic area, bed nucleus of the stria terminalis (BNST), ventral tegmental area (VTA), and anterior cingulate cortex (ACC) in the mother (Panksepp, 2000). The rewards in the mother are mediated by endogenous opioids, dopamine, and oxytocin, so it is likely that similar circuits are involved in the infant’s response to being cared for. If the attachment needs are not met, for example, if the mother’s PAG shifts her behavior from nurturance to predation, as in rats, the separation cries of the infant’s protest phase will be engendered by the mesocholinergic system and the lateral column of the PAG and also recruit the BNST, the preoptic area, and the ACC (also see Chapter 2). This highly energy-expending behavior must be terminated before too long to maximize chances of survival, so the pain-relieving effects of endogenous opioids are critical if the infant is to live to perhaps regain the healthy attachment. Hesse and Main (2006) have described the development of dissociation in infants whose mothers are not responding appropriately because of their own childhood trauma: the parent is frightened rather than frightening but still does not lead to a safe and secure attachment in the infant. The adult children of a mother who had a dissociative identity disorder may describe becoming enraged by her being “not here” and report that the rage allows them to access a feeling of warmth and numbness, which is almost certainly opioid mediated. If, for example, a baby reaches for her mom but her mom is preoccupied with war or is drunk or otherwise unavailable, the baby would turn away, flinch, but be unable to leave, protest, and then would surrender and shut down. The next day, again the baby is hungry, wants physical reassurance and loving touch, engagement with mother, again mother can’t be there, physically or emotionally, and the baby doesn’t protest very long. The third day the baby doesn’t try; the spike of distress is quickly transformed by endogenous opioid release.

Oxytocin—Attachment and Social Connection

Oxytocin is a nonapeptide hormone best known for its role in lactation and parturition. While oxytocin is implicated in a variety of “nonsocial” behaviors, such as learning, anxiety, feeding, and pain perception, more recent research highlights oxytocin’s role in various social behaviors (Insel & Fernald, 2004). This includes social memory and attachment and human bonding, sexual and maternal behavior, aggression, as well as trust (Lee, Macbeth, Pagani, & Young, 2009). Indeed, it is likely that oxytocin is the substrate of the template provided by a safe attachment relationship. During breastfeeding or suckling, maternal oxytocin levels are raised by somatosensory stimulation. Similarly, oxytocin may also be released by nonnoxious stimuli such as touch, warm temperature, and in response to positive social stimuli in general. Oxytocin release appears to be mediated by the affective quality of social stimuli that include eye gaze, facial expression, the prosody of voice, and the affective quality of touch. Most likely, oxytocin can also be released

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by stimulation of other senses such as olfaction as well as by certain types of sound and visual stimuli (Uvnas-Moberg & Petersson, 2005). Moreover, repeated exposure to oxytocin during early development seems to increase vocalizations in prairie voles (Kramer, Cushing, & Carter, 2003), suggesting that oxytocin is not just calming. Indeed, this raises the question as to whether these increased vocalizations reflect a SEEKING response that could become sensitized as a result of oxytocin release though early attachment. However, oxytocin does not only affect the child. Maternal bonding behaviors, including gaze, vocalizations, positive effect, and affectionate touch as well as attachment-related thoughts and frequent checking of the infant are all mediated by oxytocin (Feldman, Weller, Zagoory-Sharon, & Levine, 2007). Moreover, this very maternal behavior is inhibited by opioids, particularly by opioids acting on the PAG (Pavesi, Enck, De Toledo, & Terenzi, 2007), consistent with the notion that oxytocin release may be influenced by opioids.

OXYTOCIN—A PHYSIOLOGICAL MECHANISM FOR HEALING THE BODY AND THE SOUL

Oxytocin released in response to social stimuli may be part of a neuroendocrine substrate that underlies the benefits of positive social experiences. Indeed, oxytocin exerts potent physiological antistress effects, such as reduction of blood pressure and cortisol levels. It increases pain thresholds and exerts an anxiety-reducing effect, in turn stimulating various types of positive social interaction. That is, sensory stimulation and input associated with friendly social interaction and the establishment of a safe attachment relationship results in a psychophysiological response pattern that is associated with the release of oxytocin, producing calming and relaxation, decreased sympathetic arousal, and adrenal activity (Uvnäs-Moberg, 1997). This is associated with increased ventral vagal activation on one hand, and decreased dorsovagal activation on the other. The very psychological mechanisms that mediate the experience of attunement, empathy, and social engagement through sensory experience may trigger the release of oxytocin. In turn, oxytocin may be involved in physiological and behavioral effects induced by social interaction in a more general context. Such processes may explain not only nonspecific effects of psychotherapy but also specifically the health-promoting ones (e.g., Ziemssen & Kern, 2007). Not surprisingly, oxytocin has been dubbed “the great facilitator of life,” likely providing a “physiological mechanism for healing the body and the soul” (Uvnas-Moberg & Petersson, 2005).

OXYTOCIN AND AMYGDALA ACTIVITY—EFFECTS ON TRUST, PAIN, AND FEAR

Oxytocin has been dubbed the trust hormone. Specifically, the administration of oxytocin seems to have prosocial effects (Meyer-Lindenberg, 2008) to increase trust (Kosfeld, Heinrichs, Zak, Fischbacher, & Fehr, 2005). Trust has been related to amygdala functioning—presumably because of its role in danger monitoring

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(Winston Strange, O’Doherty, & Dolan, 2002). That is, oxytocin is involved in the modulation of amygdala functioning. The amygdalae are loaded not only with opioid receptors but also with oxytocin receptors (Huber, Veinante, & Stoop, 2005). Intranasal application of oxytocin decreases fear, likely by decreasing amygdala activation and coupling to brainstem regions implicated in autonomic and behavioral manifestations of fear (Kirsch et al., 2005). Moreover, pain threshold not only increases in response to beta-endorphin but also secondary to nonopioid peptides such as oxytocin and vasopressin (Bodnar., Nilaver, Wallace, Badillo-Martinez, & Zimmerman, 1984). This suggests that both fear and pain can be modulated in the relational, through ventral vagal engagement, thus in many cases obviating the necessity of dorsal vagal activation. Previous neuroimaging studies have suggested that oxytocin reduces amygdala activity similarly to opioids (e.g., Domes et al., 2007). However, a more recent study indicates that the effects of oxytocin are likely more complex. That is, in addition to reducing amygdala activity to unpleasant social stimuli, oxytocin actually increases amygdala activation for pleasant stimuli (Gamer, Zurowski, & Büchel, 2010), suggesting that it may be capable of shifting amygdalar responses toward positive social information.

OXYTOCIN REDUCES THE ADDICTIVE POTENTIAL OF OPIOIDS

The addictive and tolerance-inducing effects of both morphine and endogenous opioids have been discussed in the previous chapter. Interestingly enough, oxytocin antagonizes the development of tolerance to beta-endorphin without decreasing its analgesic effects (Kovács & Telegdy, 1987), suggesting a role of oxytocin in regulating the sensitivity of the central nervous system in cases of repeated or prolonged opioid stimulation. Sarnyai and Kovács (1994) suggest that oxytocin has a wide range of behavioral effects that includes involvement in adaptive central nervous system processes. They suggest that oxytocin not only inhibits the development of tolerance to morphine, heroin, beta-endorphin, and enkephalin, but also inhibits the development of cross-tolerance between different opiates, both mu-agonists and delta-agonists. Further, naloxone-precipitated opiate withdrawal syndrome is attenuated by oxytocin, ensuring that the termination of mental states associated with opiodergic activation does not result in physiological distress, thereby likely accounting for its addiction-reducing effects. That is, heroin self-administration was reduced by oxytocin administration in heroin-tolerant rats. In addition, oxytocin has been shown to inhibit cocaine-induced exploratory activity, locomotor hyperactivity, and stereotyped behavior in rats and in mice. Oxytocin inhibited the development of tolerance to and dependence on morphine as well as cocaine-induced sniffing behavior and tolerance to cocaine. Conversely, administration of oxytocin antiserum and of an oxytocin receptor antagonist potentiate (increase) the development of morphine tolerance. It appears that the effects of oxytocin are mediated by oxytocin acting as a neuromodulator on dopaminergic neurotransmission in limbic-basal forebrain structures, thus regulating

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adaptive central nervous system (CNS) processes, including those that are involved in drug addiction.

OXYTOCIN AND VASOPRESSIN—DIFFERENTIAL EFFECTS ON MEMORY

Vasopressin and oxytocin of hypothalamic neurosecretory origin affect both consolidation and retrieval of memory but in an opposite manner. Vasopressin facilitates these processes while oxytocin appears to be an amnesic neuropeptide. Additionally, vasopressin not only prevents but also appears to reverse experimental amnesia (Bohus, 1980). Vasopressin, above and beyond an antiamnestic effect, appears to enhance memory through increasing arousal and attention (Van Londen et al., 1998). That is, vasopressin may increase memory access to information that may be relevant to remembering whether a particular person or situation is potentially unsafe and thus facilitate active defensive behaviors. Oxytocin administered on its own seems to have amnestic properties (Heinrichs, Meinlschmidt, Wippich, Ehlert, & Hellhammer, 2004; de Oliveira, Camboim, Diehl, Consiglio, & Quillfeldt, 2007). Similarly, in subjects with PTSD, vasopressin has enhancing effects on memory and conditioned responding, whereas oxytocin has inhibiting effects (Pitman, Orr, & Lasko, 1993). On the other hand, Rimmele, Hediger, Heinrichs, and Klaver (2009) suggest that oxytocin improves recognition memory for familiar faces in humans but has no effect on memory for nonsocial stimuli, suggesting a selective effect of strengthening neuronal systems related to social memory and may thereby facilitate attachment and connection. Nevertheless, Di Simplico, Massey-Chase, Cowen, and Harmer (2009) found that oxytocin reduced the misclassification of positive emotions as negative ones, thus promoting affiliative and approach behaviors by reducing the salience of potentially ambiguous and threatening social stimuli. Similarly, Guastella, Mitchell, and Matthews (2008) found that oxytocin enhanced social approach, intimacy, and bonding in male humans by strengthening encoding to make the recall of positive social information more likely. Overall, these findings are suggestive of quite complex effects of both oxytocin and vasopressin on different aspects of memory.

VASOPRESSIN PROMOTES ACTIVE DEFENSIVE BEHAVIOR: AVOIDANCE AND AGGRESSION

Vasopressin seems to be associated with the expression of avoidance and active coping and defensive behaviors (Linfoot et al., 2009) and in context-dependent activation of the HPA axis (Zelena, Domokos, Jain, Jankord, & Filaretova, 2009) as well as sensitization and hyperalgesia (Bradesi, Martinez, Lao, Larsson, & Mayer, 2009). Kovács, Vécsei, and Telegdy (1978) found opposite effects on avoidance behavior with regard to vasopressin and oxytocin, with oxytocin decreasing avoidance behavior and vasopressin increasing it. Moreover, vasopressin also appears to increase avoidance learning and behavior, whereas oxytocin decreases it (de Wied, Elands, & Kovács, 1991). That is, the expression of avoidance may be conceptualized as part

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of an active defensive response that is an essential element of a flight response. In individuals with PTSD, administration of vasopressin increased arousal, whereas oxytocin decreased arousal (Pitman et al., 1993). Vasopressin also plays a prominent role in the regulation of aggression, generally of facilitating or promoting it (Caldwell, Lee, Macbeth, & Young, 2008; Ferris, 2005). That is, vasopressin has been associated with increased display of aggressive behavior in both animals (e.g., Ferris, 2008) and humans (Heinrichs & Domes, 2008), including play fighting (Cheng, Taravosh-Lahn, & Delville, 2008) as well as maternal protective behaviors (Nephew, Byrnes, & Bridges, 2010). Thus, the release of vasopressin likely facilitates the expression of aggressive defensive behaviors, though the exact nature of the kind of aggression displayed may be attributable to the nature of the relationship.

ATTACHMENT AND TRAUMA—OPIOID AND VASOPRESSIN SYSTEM DYSREGULATION

Teicher et al. (2002) suggest that severe early stress and maltreatment produces a cascade of events that includes alterations in the oxytocin-vasopressing stress response systems that may contribute to the risk of developing PTSD, depression, attentional symptoms, borderline personality disorder, dissociative identity disorder, as well as substance abuse. Heim et al. (2009) report that women with a history of childhood trauma have decreased levels of oxytocin in their cerebrospinal fluid. Moreover, Meinlschmidt and Heim (2007) report a decreased response to oxytocin in men with early relational trauma. Accordingly, Seng (2010) suggests that oxytocin dysregulation may link early relational trauma not only with posttraumatic self-disorders, for example, dissociation, somatization, and interpersonal sensitivity, but also with pelvic visceral dysregulation disorders, like irritable bowel syndrome, chronic pelvic pain, interstitial cystitis, and hyperemesis gravidarum. This conceptualization is supported by a recent study by Seng and colleagues (2013) that found that the relationship between oxytocin level and hyperemesis gravidarum was mediated by high levels of dissociative symptoms. It is suggested that the dysregulation of the oxytocin-vasopressin system may be mediated by the opioid system, which in turn affects dissociative symptoms.

OPIOID MODULATION OF OXYTOCIN AND VASOPRESSIN

Endogenous opiates appear to be implicated in the regulation of oxytocin and vasopressin (Russell, Neumann, & Landgraf, 1992). Waterhouse et al. (1996) suggest that abnormal beta-endorphin levels are associated with concomitant abnormalities in the oxytocin system, indicating interdependence of these two neurotransmitter systems. Specifically, it has been suggested that hypersecretion of hypothalamic betaendorphin likely disrupts the oxytocin system (e.g., Insel, 1992; Panksepp, 1993). Both endorphins and morphine have been shown to have an inhibiting effect on the release of both oxytocin and vasopressin, an effect that can be reversed by naloxone

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(Lutz-Bucher & Koch, 1980). Indeed, it appears that the availability of oxytocin and vasopressin in the brain is under opioidergic control (van Wimersma Greidanus & van de Heijning, 1993). That is, opioids and opioid receptors in the hypothalamus have an inhibitory effect on the release of both oxytocin and vasopressin (Clarke, Wood, Merrick, & Lincoln, 1979; Summy-Long, Miller, Rosella-Dampman, Hartman, & Emmert, 1984). Specifically, beta-endorphin has been related to the inhibition of both oxytocin and vasopressin (Laatikainen, 1991). Both mu- and kappa-receptors have been implicated in the role of modulating oxytocin and vasopressin release (van de Heijning, Koekkoek-Van den Herik, & Van Wilmersma Greidanus, 1991). Chronic opioid exposure inhibits oxytocin synthesis (You, Li, Song, Wang, & Lu, 2000). Moreover, there is evidence for opioid inhibition of activities that normally result in oxytocin release, for example, suckling-induced oxytocin release (Pfeiffer & Herz, 1984). With regard to vasopressin release, the data are more complex, with some studies reporting increased vasopressin release upon opioid withdrawal (e.g., Jarvis et al., 2000), whereas others do not (e.g., Bicknell, Chapman, & Leng, 1985). Vecsernyés et  al. (1989) suggest that beta-endorphin results in a significant reduction of vasopressin in the amygdala, an effect that is reversible by naloxone. Doi, Brown, Cohen, Leng, and Russell (2001) suggest that opioids directly inhibit oxytocin cells but inhibit vasopressin cells by indirect actions.

OPIOIDS INHIBIT OXYTOCIN AND VASOPRESSIN SECRETION: A VAGAL SHIFT HYPOTHESIS

As has been discussed in the previous chapter, traumatic stressors result in an increased release of endogenous opioids. Specifically, trauma results in an increased release of beta-endorphin but not of oxytocin (Hong, Li, & Cao, 1994). Opioids appear to have an effect on the differential release of both oxytocin and vasopressin. Conversely, opioid blockade, both with naltrexone (Summy-Long et al., 1984) and naloxone (Bicknell et al., 1985; van de Heijning et al., 1991), increase the release of both oxytocin (Clarke et al., 1979) and vasopressin. Similarly, morphine withdrawal with naloxone in morphine-dependent rats has been shown to increase the excitability of oxytocin neurons (Brown et  al., 2005). This effect is likely attributable to activation of both mu- and kappa-opioid receptors (Carter & Lightman, 1987; van de Heijning et al., 1991). Moreover, activation of the oxytocin system as a result of opioid blockade appears to be increased when there is preexisting opioid activation (Brown et al., 2005). Indeed, there is suggestion that it is opioid withdrawal rather than exposure to opioid antagonists that produces the increase in oxytocin activity (Honer, Thompson, Lightman, Williams, & Checkley, 1986). Given the involvement of oxytocin in relational behaviors and vasopressin in active defensive behaviors, it is likely that opioids can inhibit both. Not only do opioids reduce sympathetic arousal but they also decrease ventral vagal engagement. That is, opioids, by shifting the autonomic nervous system toward a dorsal vagal response, not only inhibit active defensive behaviors like fight or flight, if released in sufficient quantity, but they also interfere with exploratory behavior, play, as well as

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the relational. Conversely, opioid blockade not only increases the availability of oxytocin but also that of vasopressin. More likely than not, a withdrawal from endogenous opioids may thus facilitate both ventral vagal engagement as well as active defensive behaviors, the expression of which being dependent on the external environment and social climate.

REMEDIATING THE EFFECTS OF TRAUMA—VENTRAL VAGAL ENGAGEMENT AND ACTIVE DEFENSIVE RESPONSES

Under normal circumstances, the therapeutic relationship is often sufficient to mediate ventral vagal engagement and thus provide a container for the therapeutic work. However, in cases of severe traumatic stress syndromes, dissociative disorders, or attachment injuries, severe social withdrawal and avoidant attachment is frequently observed. This response often makes the establishment of a therapeutic alliance all but impossible. It is suggested that the severe social withdrawal that is often associated with alternating sympathetic arousal and dorsovagal activation is attributable to an excessive opioid tone on one hand and the lack of oxytocin on the other. The primary reliance on dorsovagal activation further diminishes the capacity of the organism to engage in an active defensive response. This is likely at least in part attributable to a lack of available vasopressin. That is, in the presence of significant opioid activation the normal oxytocin response to social interaction may not occur, nor will active defensive responses such as fight or flight be easily available under threat. Indeed, it may be necessary to pharmacologically initiate a shift to produce a vagal shift. It is suggested that this can be achieved by initiating opioid withdrawal through the administration of opioid antagonists. Given that both oxytocin and vasopressin are under opioidergic control, the decrease in opioid activation is likely to increase the availability of both oxytocin and vasopressin. This likely has a multifaceted effect. There is not only a decrease in dorsovagal activation but also an increase in ventral engagement as well as the availability of active defensive responses. That is, opioid blockade produces a SEEKING for social connection on one hand as well as facilitating access to active defensive responses on the other hand. However, care needs to be taken that prior to proceeding with this approach at least a modicum of a relationship is formed, as otherwise the effects of vasopressin release are likely to dominate over any ventral vagal engagement.

SUMMARY

The roles of opioids, oxytocin, and vasopressin are clearly complex. Reviewing the literature, it seems clear that the release of both oxytocin and vasopressin is clearly under opioidergic control. Oxytocin and vasopressin have a quite opposite effect on their own, where oxytocin appears to allow bonding and facilitates the relational. In part, this is facilitated by increasing trust and decreasing physiological arousal. Interestingly enough, oxytocin has amnestic effects, similar to opioids. Moreover,

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both opioids and oxytocin have been related not only to attachment and bonding but also to the placebo response. Moreover, at least one study suggests that oxytocin may facilitate opioid release, thus not only allowing for experiencing the rewarding effects of social relationships but also allowing for a potentially seamless transition from ventral vagal activation to dorsal vagal activation, if the need for social engagement remains unmet. At the same time, the release of oxytocin reduces the development of tolerance to opioids, allowing the pleasurable experience of the release of opioids without the cost of tolerance and decreasing potency over time, thus ensuring the ongoing functioning of the reward system. Ultimately, this may be the legacy of secure attachment, protecting the organism from the untoward effects of stress and decreasing the likelihood of addictions and similar behaviors. Vasopressin, on the other hand, appears to have some antiamnestic effects as well as being involved in defensive behavior that include both avoidance and aggression, thus allowing the mounting of active responses to allow the safety of the organism. Further, it appears that the release of both oxytocin and vasopressin can be mediated by blocking of the opioid system with opioid antagonists. This likely has multiple effects relevant to the psychotherapy of traumatic stress syndrome. Opioid antagonists decrease the likelihood of a dorsal vagal response, thereby increasing either a ventral vagal or sympathetic response to stressors. The release of oxytocin is likely to increase trust and the relationship between client and therapist. The release of vasopressin reengages defensive responses when needed, making the client feel less helpless. That is, these active defensive responses are increasingly available if necessary, while at the same time they are being modulated within the therapeutic relationship due to the release of oxytocin. Oxytocin likely mediates the ventral vagal engagement that is part of the therapeutic relationship. However, it seems likely that in many individuals with dissociative symptoms the capacity to engage in such a therapeutic alliance with the therapist is diminished due to an excessive opioid tone attributable to their attachment and trauma history. In those cases, it is hypothesized that the use of an opioid antagonist like naltrexone may be useful, not only with regard to blocking passive defensive responses like immobilization as well as eliciting active defensive responses, but also to fundamentally change the nature of the therapeutic relationship. That is, it is hypothesized that opioid withdrawal in a safe relationship will produce an increased release of oxytocin and ventral-vagal engagement, and it may contribute to a resetting of a dysregulated opioid-vasopressin system in individuals with dissociative symptoms and/or histories of trauma and attachment issues. Specific ways to proceed with regard to this innovative strategy are discussed in Chapter 22, Opioid Antagonists and Dissociation: Adjunctive Pharmacological Interventions.

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CHAPTER 7

Defense Responses: Frozen, Suppressed, Truncated, Obstructed, and Malfunctioning Frank M. Corrigan

Empirical data and clinical observations seem to be supportive of the idea that there are similarities between freezing, concomitant development of analgesia and anesthesia, and acute pain in threatened animals and severely traumatized human beings. —Ellert R. S. Nijenhuis, Johan Vanderlinden, and Phillip Spinhoven (1998)

There is a range of immediate orienting and defense responses available when a threat is perceived, and a separate but overlapping system of vigilance when there is awareness of a potential threat. A person who encounters danger and is able to fully express appropriate defense responses may have no long-term clinical effects. However, a person who has had his responses obstructed will find that the energetic residues of these later become unwelcome intruders on his awareness. Psychopathology can ensue when defenses are too readily triggered, when they persist well beyond their usefulness, when their expression is arrested, and when they are not effective (Gilbert, 2001). Rivers (1920) thought of suppression as unwitting or involuntary, whereas repression was the result of a deliberate attempt to “banish experience from consciousness.” When suppressed material was active, with an independent life of its own, it could be regarded as dissociated. Stress and depression may ensue when a person is unable to escape (flight) from a chronically aversive situation, be assertive (fight) in an abusive relationship, or seek the help (attach) of those who may be supportive (Gilbert, 2001). The arrested impulses 131

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to defend are most likely to induce clinical disorders when their expression is inhibited over a prolonged period or when the traumatic experience has a high-energy impact that is not resolved. When defense responses are blocked acutely in a situation of peril, we consider whether they may be frozen rather than obstructed. In the long term, both frozen and immediately obstructed responses can be repeatedly triggered by present-time reminders of the original situation. They then lead to increased vigilance, with associated anxiety and tension, and chronic submissive or appeasement behaviors, with low mood and loss of energy, drive, and enjoyment. We prefer the term obstruction rather than suppression or arrest to differentiate defense responses hypothesized to be blocked at a cortical level from those frozen at their midbrain origins. Obstructed fight or flight and frozen fight or flight are nevertheless all postulated to be high-arousal states. The defense responses discussed in detail below are summarized in Table 7.1. PROLONGED AROUSAL

Arousal changes during fight or flight responses are, in part, dependent on ascending noradrenergic projections from the locus coeruleus (LC). When the firing of the LC is driven by the anterior cingulate cortex (ACC), the resulting high arousal allows efficient processing of sensory stimuli and linking with the appropriate behavioral responses. With a traumatic experience, the LC activation—and the input and functioning of the different compartments of the ACC—are altered. Vogt, Aston-Jones, and Vogt (2009) propose that the reduced anterior cingulate functioning repeatedly demonstrated in posttraumatic stress disorder (PTSD) during emotional tasks facilitates the firing of LC neurons to create a state of hyperarousal. The hypothalamic projections of the LC then alter the functioning of the hypothalamic–pituitary–adrenal (HPA) axis. An imbalance in the subcortical control activities of different parts of the ACC may contribute to pelvic pain syndromes, irritable bowel syndrome, headaches, and fibromyalgia when these are associated with trauma. It might therefore be expected that antidepressants would be therapeutic, as the abnormal metabolism of the subcallosal cingulate gyrus in major depressive disorder is reversed by antidepressant treatments (Hamani et al., 2011). However, these therapeutic agents are presumably having no effect on the abnormal functioning of the pregenual cingulate cortex in the many cases of PTSD that fail to obtain significant improvement, even for symptom reduction. Arousal driven by midbrain noradrenergic projections remains elevated, without top-down modulation. The prefrontal cortex (PFC) is also influenced by ascending cholinergic, serotoninergic, and dopaminergic projections from the brainstem and basal forebrain: these too may be sensitized by adversity. TYPES OF FREEZE RESPONSE Introduction: Taxonomy of Freeze Responses

The term “freeze,” for an involuntary inhibition of movement, is used by different authors for defense responses that have quite distinct neurobiological substrates. We will therefore use the putative brain activations to make distinctions that are

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clinically useful, especially when many trauma survivors will describe states that are a mixture of these. The freeze states may be very brief at the time of the traumatic experience but may still have protracted clinical consequences. Because animal studies lack subjective reporting, some of the assumptions extrapolated to clinical reports may be wide of the mark. Nevertheless, we hope that a typology of freeze responses will help both therapist and client to appreciate the complexity of the behavioral response—and the limited role of conscious intention at the time of the traumatic experiences. We have seen that the midbrain components of immediate defense responses are derived from the columns of the periaqueductal gray (PAG) and from the layers of the colliculi. It is possible that another midbrain region—the rostromedial tegmental nucleus (RMTg)—is activated whenever movement is inhibited. The RMTg switches off reward and motor activity through inhibition of midbrain dopamine neurons (Ikemoto, 2010). However, most of the states we describe have primary activations in the PAG or the colliculi and the cascade of secondary effects is less well defined. The attentional focus freeze is the state in which mobility is stilled by a commanding and threatening situation. The gaze cannot be torn away from the trigger. The field of attention narrows and the peripheral vision is blurred. The person may be transfixed with horror. The only action urge is to stare with fascinated disquiet. This may be a freeze at the initial “arousal” and “arrest” stages of orienting, as described in Ogden, Minton, and Pain (2006). There may also be an attentional focus freeze in response to sudden awareness of a negative social evaluation, as exhaustively elaborated by Sartre: “shame . . . is the recognition of the fact that I am indeed that object which the Other is looking at and judging” (Sartre, 1943/1969, p. 261). A vigilance freeze describes the state of immobility in which the degree of threat can be evaluated by hyperalert senses: ears that are straining to hear sounds indicative of an abuser’s return, for example, or eyes that are peeled to identify a more distant threat. This is postulated to be dependent on a collicular-cortical axis and may be prolongation of the third stage of orienting—alertness with heightened senses—described in Ogden et  al. (2006). Heightened vigilance overlaps with, but is more physiologically activated than, the waiting state of the security motivation system. Arousal, activity arrest, sensory alertness, and scanning are stages of orienting to novel stimuli (Ogden et al., 2006). Any of these may be frozen at the moment of high-impact trauma. The submissive or dorsal-vagal freeze is the state in which the injured and trapped animal shuts down through activation of the ventrolateral column of the PAG (vlPAG) and the resulting parasympathetic dominance (Bandler, Keay, Floyd, & Price, 2000). In this condition, a wounded animal is more likely to heal, as bradycardia and hypotension will limit blood loss and inactivity will conserve energy, and the animal will also have the soothing benefit of its own internal opioid analgesics. Patients who survive this state often report a reduced awareness of the environment and a loss of tone in the muscles, both of which distinguish it from peritraumatic tonic immobility (TI). Low arousal dissociation accompanying this state has endogenous opioid mechanisms in contrast to the high arousal dissociation accompanying fight or flight responses, which we postulate to be mediated by cannabinoids. It is the combination of an inability to move, despite adequate muscle tone, with a highly aroused internal state that characterizes TI, a state of terror and physiological

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confusion, that has persisting adverse psychological effects (Bovin, Jager-Hyman, Gold, Marx, & Sloan, 2008). Features of both sympathetic and parasympathetic activation lead to the proposition of a coactivation of the lateral/dorsolateral columns of the PAG (l/dlPAG) and the vlPAG. We have discussed the relevant neurobiology in Chapter 2, Threat and Safety: The Neurobiology of Defense Responses, and it is also reviewed in relation to peritraumatic dissociation (PD) by Brian Marx and colleagues in Chapter 3, Peritraumatic Dissociation and Tonic Immobility: Clinical Findings. Frozen Fight and Frozen Flight are states of high arousal in which there is immobility centered on the muscle groups required for the different forms of active defense. These are differentiated from conditions in which fight or flight responses are not frozen but are obstructed at an often subconscious level. Neurobiologically, these frozen action impulses may be prefight and preflight freezes as seen in some animal work in which the lateral columns of the PAG are stimulated: imaging work in humans has so far not been conducted to clarify this. The Frozen Cringe/Hide condition is postulated to be a rapid response to a looming stimulus such as a large, intimidating, and terrifying threat, especially if it appears suddenly, involving coactivation of the dorsomedial column of the PAG (dmPAG), the cuneiform nucleus, and the superior colliculi (SC) layers specializing in avoidance of potentially crushing or swooping dangers. The hide state can be prolonged while the danger is in the immediate vicinity of a concealed animal. Finally, a temporal freeze may occur in humans who feel that time has stopped, that the moment is frozen without prospect of forward motion because there is no awareness of past or future, just a present time in which everything has stopped, held in an agonizing stasis. This may be a subjective component of other freeze responses rather than an independent state. We will consider the laboratory evidence supporting the clinical distinctions of the proposed different freeze responses.

Submissive or Dorsal-Vagal Freeze and the vlPAG

Passive emotional coping involves the vlPAG and its connections within the brainstem and with the orbito-insular PFC. The vlPAG receives inputs from the spinal cord and from the nucleus of the solitary tract (NTS) about noxious stimulation to deep somatic or visceral structures (Bandler et al., 2000). The passive, low-arousal, vlPAG “freeze” arises in response to complete entrapment, deep pain, or hemorrhage, and it facilitates healing and convalescence through quiescence, hypotension, diminished responsiveness to environmental stimuli, slowing of breathing, immobility, and opioid-induced analgesia. Fear, as well as pain, is reduced by the action of endogenous opioids in the vlPAG (McNally, 2005). The dorsal-vagal freeze seen clinically when a traumatic memory is triggered, for example, during reprocessing, is accompanied only briefly by bradycardia, immobility, and almost imperceptible breathing: the breathing and pulse rate quickly return to normal or go to the other extreme. Deep brain stimulation of the ventral PAG is used to reduce chronic neuropathic pain, and the change in heart rate variability is secondary to parasympathetic activation (Pereira et al., 2010).

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Deep brain stimulation can be used clinically without activation of a fearful freeze response, so ventral areas of the PAG are also involved in physiological states of relaxation, comfort, and soothing from pain. Different parts of the vlPAG may be involved for restful calmness and low-arousal freeze. Alternatively, it may be through the thalamocortical connections of the ventral PAG that pain is reduced without any induction of dysphoria. Also, the top-down modulatory influence of the anterior insular cortex is more accessible to the vlPAG than to the dorsolateral PAG (Price, 2006). Endogenous Opioids and the Valence of the vlPAG Activation

Even if the insular cortices are modifying the degree of activation of the vlPAG and the nucleus accumbens, the valence could still depend on the balance of endogenous opioid activity. Low-arousal states of calmness and relaxation have a different pattern of endorphin production to states of shutdown from terror and pain. Mu-opioid agonists reduce separation distress, while kappa-opioid agonists evoke depersonalization, derealization, and dysphoria (Watt & Panksepp, 2009). Defeated postures and analgesia resulting from social defeat are dependent on kappa opioids (McLaughlin, Li, Valdez, Chavkin, & Chavkin, 2006) that interact with corticotropinreleasing factor (CRF) in stress-induced mood disorders and drug abuse (Bruchas, Land, & Chavkin, 2010). The affectively charged loops, or the series of parallel loops, incorporating the vlPAG, the mesolimbic dopamine system, and the prefrontal cortical areas, are all sensitive to the effects of endogenous opioids. Thus, an animal could be in a state of fearful distress or, conversely, in a state of rest and calmness with very similar network activations but with very different endogenous opioid influences. It is proposed that the tract from the ventral tegmental area to the ventral striatum has a polyvalent nature for mediating the emotional impact of the environment: calm, nurturing, and affiliative; or agitating, harsh, and threatening.

Frozen Fight and Frozen Flight: Coactivation of Rostral/Caudal l/dlPAG and vlPAG?

They were here in the room with him and the whole place was on fire; it was going up in flames and he couldn’t stop it. Lay paralysed, unable to move. —Alan Spence, in The Pure Land (2006, p. 163) Sometimes people describe being unable to initiate a voluntary movement at the time of a traumatic experience, and it is clear from their description that it is not due to the profound lethargy, numbness, and opioid-induced detachment of the vlPAG-dominant freeze. Instead, they are completely unable to move certain muscle groups. An impulse to action in the upper body, including the arms, shoulders, neck, and jaw, can be seen as a frozen fight response, hypothesized to involve coactivation of rostral l/dlPAG and vlPAG. Likewise, there may be a condition of frozen flight (caudal l/dl

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PAG/vlPAG) in which there is an urge to move the muscles of the lower body in a way that would allow urgent flight—simultaneous with the awareness that the limbs are not responding to the mind’s commands. In both these conditions of frozen fight and frozen flight, there is often a feeling of terror and a sensation of chest tightness. An alternative explanation to column coactivation is that these are prefight or preflight urges. Stimulation of the dorsal PAG (dPAG) elicits preparation for active escape (Brandão, Zanoveli, Ruiz-Martinez, Oliveira, & Landeira-Fernandez, 2008): increases in heart rate and blood pressure, movements alternating between freezing and running or jumping. If dPAG stimulation is leading successively to alertness, then freezing, then escape, muscular tension accompanying an inchoate urge to run or fight could be the human equivalent of the preescape or preattack dPAG activation. Nevertheless, because of the clear action impulses, we use the terms “frozen flight” and “frozen fight” to indicate these terrified states in which the willed movements cannot happen because of inability to move the required muscle groups. A braking mechanism or an unresolved selection conflict between competing action tendencies in the basal ganglia could also lead to a tense stasis. What happens in the brain when there is a sudden shout of “Freeze; Armed Police; Freeze?” The command should suddenly activate the inferior colliculi (IC) of the suspect to the extent that he will not respond with defensive aggression or with flight. However, inadvertently evoking intense terror could lead to an uncontrolled flight. In rats, there is a dose-dependent response to chemical stimulation of the inferior colliculus: freezing at low doses, running at high doses. High-dose, escape-eliciting injections into the IC activated dorsomedial, dorsolateral, lateral, and vlPAG columns, while the low dose that induced freezing selectively involved the ventrolateral column (Ferreira-Netto, Borelli, & Brandão, 2007). This laboratory work suggests that armed police need to frighten suspects by activating the IC sufficiently to elicit a freeze response, which recruits the vlPAG, cuneiform nucleus, and LC. The dose needs to be right to minimize the risk of activating dangerously uncontrolled escape attempts or violent attacks.

Tonic Immobility

When TI occurs in the course of an assault, there is a profound effect on the emotional sequelae of the trauma; the horror, helplessness, isolation, pain, and feeling of worthlessness associated with the traumatic episode can leave psychological scarring that has a long-term detrimental impact on personal and interpersonal functioning and on the capacity for positive affect, including the ability to access feelings of safety, mastery, and worth. It also interferes with the efficacy of language-based therapeutic approaches, as the stored emotional motor memory with its sensory accompaniments is not readily accessible to full restructuring of the negative cognitions, no matter how persuasive are the arguments deployed. TI during childhood sexual abuse has been associated with long-term psychological impairment characterized by depression, anxiety, PTSD, and PD (Heidt, Marx, & Forsyth, 2005), and its occurrence during an assault may be one of the most important predictors of the emergence of PTSD (Bovin et al., 2008). It has also been found to be associated with continuing psychological distress in men who were the

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victims of urban violence and to be predictive of a poor response to pharmacological treatment (Fiszman et al., 2008; Lima et al., 2010). Sensorimotor psychotherapy (SP; Ogden et al., 2006) acknowledges the profound significance of the past experience of TI and incorporates strategies for bringing to mindful attention the somatic residues of the frozen defense responses that could not be made effective at the time of the trauma. Successful treatment with SP demonstrates that careful completion of the obstructed action sequences, with concomitant awareness of the associated body sensations, diminishes the hitherto chronically pervasive emotional distress and clears the associated self-referential negative cognitions. As these completed actions give rise to a feeling of triumph, we propose that these represent a shift from dorsal to ventral striatal activation.

The Window of Affect Tolerance and Freeze Responses

Siegel (1999) and Ogden et al. (2006) have described persisting posttraumatic autonomic dysregulation in terms of a window of affect tolerance, outside of which it is difficult to integrate information and tolerate distress. They suggested that in some circumstances both sympathetic and parasympathetic systems are activated together. The hyperaroused state induced by sympathetic activation, if persistent, is associated with fear and agitation, flashbacks and nightmares, compulsive thinking, and dysphoric tension. The hypoaroused state, in which parasympathetic activation is dominant, is accompanied by shame and numbness, cognitive dissociation (“nothing matters”), emotional unresponsiveness, and varying degrees of self-loathing. Victims of trauma will frequently complain of symptoms that can be understood within this model. Their injurious behaviors, such as substance abuse and self-harm, may be attempts to regulate the extremes of physiological states outside the window of tolerance. Is there a need to distinguish frozen fight or flight states from TI? It does make a difference to processing of the traumatic memories with SP if the impulses to action are clearly defined and can be completed, either through liberation of the arms to push or the legs to carry the person to safety. It could be argued that the opponent forces are at the cortical level, as there are distinct projections from the PFC to the different columns of the PAG. However, we have argued that in extreme peril the PFC is going offline and the behavioral “choice” is being made at the level of the basal ganglia.

Self-Loathing and Freeze Responses

Clinically, posttraumatic emotional residues of fear and anger can be reprocessed more readily than states of shame and self-loathing, and there has been no explanation for the feelings of worthlessness that accompany TI. We postulate a role for the dmPAG, which is associated with aversion and reduced exploration in animal models (Borelli & Brandão, 2008). These behavioral changes may be the rodent expressions of the self-loathing, which is often residual from the urge to become as small

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as possible, to disappear from view, to be invisible to hostile and critical scrutiny and exposure. The dmPAG is activated during alcohol withdrawal (Cabral et  al., 2006), but whether the human equivalent is a craving for more alcohol or an aversion to it, “I’ll never touch another drop,” or a combination of the two, remains to be established. It is probable that some of the symptom-relief alcohol consumption provides in those who are traumatized is mediated by the suppression of anger and fear responses within the PAG. As shame is soluble in alcohol (Nathanson, 1992), we predict that the dmPAG will also be found to play a role in the autonomic and other somatic accompaniments of shame and self-loathing. Rats that are given alcohol as part of their diet for 21 days and are then abruptly withdrawn from it have activation in many brain regions, including the dorsomedial, dorsolateral, and ventrolateral columns of the PAG (Bonassoli, Milani, & de Oliveira, 2011). It would be interesting to know if exogenous cannabinoids have an attenuating effect on shame, as the column-coactivation hypothesis would predict endocannabinoid release during traumatic states in which there is dPAG activation. The role of endogenous opioids is well established, but their interaction with cannabinoids, specifically in animal models of TI, remains unclear. When the clinical reprocessing of a traumatic experience becomes stuck, it is worth looking at whether there was a period of TI, however brief. People will naturally tend to want to get away from the feeling of helpless terror and they may move on quickly to the experiences that followed this. Most will also want to get away from the highly aversive experience of shame, which may be pronounced during TI. Healing may require the therapist to be aware of the presence of shame; to bring it to mutual awareness; and to allow the victim to be with the feeling of shame in the safety of the nonjudgmental, warm and caring, therapeutic interaction; to allow it to be held until it metabolizes.

Attentional Focus and Vigilance Freeze States

He woke in terror and panic, drenched in sweat, sat up, his breathing shallow and quick. The dream faded but left him with a sense of threat, alert to any sound. He reached for his pistol, tensed, but the noises he heard were only the wind in the pines, the harsh rasping cry of the cicada. —Alan Spence, in The Pure Land (2006, p. 163) When the word “freeze” is being used to describe the attentive immobility of an animal sensing a distant danger, it is important to distinguish this attentive immobility from the freeze of TI (Moskowitz, 2004) and from the frozen fight and frozen flight states described above. The level of arousal is postulated to be higher than in the security motivation system of hypervigilance in which mobility is unconstrained. Clinically, there are peritraumatic states of attentive immobility in which the victim is motionless, with senses strained, alert to the possible return of a perpetrator—and recall of this in therapy may be associated with a hypersensitivity to sound, which requires the interviewer to speak more quietly. With TI, there may be a similar period

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of increased vigilance combined with both the awareness of the inability to move and the awareness of a lack of definition of the movement impulse. When escape is not possible, numbness and reduced responsiveness supervene and many dissociative patients who were the victims of repeated trauma can describe different states of shutdown with progressively reducing exteroceptive awareness. Rhesus monkeys separated from conspecifics initially have short periods of freeze as they assess for signs of predator proximity; but when they perceive themselves to be safe they begin to move and to emit sounds likely to attract the attention of members of their group (Kalin, Shelton, Fox, Oakes, & Davidson, 2005). If a human, avoiding eye contact to increase threat, intrudes into their environment, the monkeys will have longer periods of freeze during which their movements, apart from vigilant eye movements, cease. Positron emission tomography (PET) scans show a correlation between this type of freezing and activation of the bed nucleus of the stria terminalis (BNST), and the shell of the nucleus accumbens (Kalin et al., 2005): the PAG was not involved. As the authors interpret the freezing of the monkeys in this paradigm as a response to uncertainty in a novel environment that decreases the chances of being detected by a predator, this freeze can be seen as an attentional freeze, immobility combined with hyperawareness for threat, which is distinct from those elicited by PAG activations. It has been proposed that while the amygdala responds to immediate threats, it is the BNST that is active during sustained vigilance in humans (Somerville, Whalen, & Kelley, 2010). The BNST is also sensitive to indications that there is to be relief from stress, safety rather than danger (Christianson et al., 2011). The shell of the nucleus accumbens can respond rapidly to adversity in the environment, moving from appetitive to fearful mode (Reynolds & Berridge, 2008), switching off the urge to enjoy grazing so that the animal can fully attend to safety: this attentional freeze is therefore a survival mechanism involving the mesolimbic dopamine system and the BNST rather than the PAG and the basolateral or central nuclei of the amygdala. The significant cortical area is the ACC (Fiddick, 2011), with different subregions involved according to the state of wariness of attack or being under attack (Mobbs et  al., 2009). However, signals indicating a stress-free period are mediated by the posterior insula (Christianson et al., 2008). In SP, the question, “How is your body telling you that you are safe now?” is focusing attention on the interoceptive feedback to the posterior insula and amplifying its message through the anterior insular and anterior cingulate cortices. The startle response evoked by a sudden and intense stimulus consists of muscle twitches or contractions, interruption of behavior, and increased heart rate. The acoustic startle response to an auditory stimulus involves brainstem nuclei directly activating motor neurons and may be magnified through stimulation of the amygdala, the ventral tegmental area, and the lateral PAG (Koch, 1999). The enhanced startle response seen in PTSD indicates enhanced brainstem responses to incoming stimuli. The attentional freeze may have some features in common with the startle response, but it lacks the initial muscle contractions and it has more cortical recruitment. Bracing for impact is another function of increased tone at a time of sudden threat and may even follow an immediate and unexpected negative social evaluation.

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Obstructed Fight and Flight: Cortical Regulation of Defense Responses

He had gone beyond boredom, through agitation, to contained rage, then beyond even that to a kind of numb acceptance. —Alan Spence, in The Pure Land (2006, p. 160) The anger welled up in him. He moved as if to double back and find the stallholder. He would make him apologise, beat the bastard black and blue if he refused. . . . He unclenched his fists, tried to quell the useless rage. —Alan Spence, in The Pure Land (2006, p. 307) Threat in social situations leads the body to react as if in physical danger, but to act in line with the urgings of the physical defense responses would be completely inappropriate. Therefore, cortical regulation is required. For some people confronted by social slights, it is necessary to display agonistic aggression rather than lose face; but most learn early in life that criticism does not warrant a violent response. Control, suppression, or obstruction of the fight response is often followed by the submit state, adapted through evolution to protect the inadequately powered victim when a confrontational response could provoke an increased risk of a violent death. The submit response saves the life of the one attacked in a grossly unequal contest when stubborn fighting would be fatal. But before, or concomitant with, the submit response is the need to block the natural fight response that has been brought near the surface by pain, hurt, or intrusion. This obstruction can occur at the midbrain level when the fight response is frozen, as described above; or through the basal ganglia’s braking or action selection mechanisms; or it can occur at the cortical level, when there is some assessment of the hopelessness of the contest. With increasing proximity of a predator, and with the experience of being under attack, different areas of the ACC and the ventromedial PFC (VMPFC) are activated (Mobbs et al., 2009). This allows a range of cortical contributions to autonomic, energetic, and motor responses. Cortical Regulation of Emotion

The term “obstruction” rather than “suppression” is used here because the latter involves reduction of negative affect by a cognitive reappraisal strategy or by an inhibition of the emotion, and here we are considering a mechanism that can be much less conscious and deliberate. Nevertheless, some studies of cortical activations during emotion suppression are relevant. Suppressing the response to disgusting visual stimuli reduces the subjective experience of the negative emotion. However, as there is increased activity in the amygdala and the insula, the underlying affective response is not being attenuated at the physiological level (Goldin, McRae, Ramel, & Gross, 2008). It is also evident from the suppression of sadness through recruitment of the VMPFC (Lévesque et al., 2003; Ohira et al., 2006) that the regulation does not reduce the unpleasant experience. In fact, it may increase the sympathetic nervous system activation (Ochsner & Gross, 2005): contributing to the high arousal state postulated

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to arise from obstructed flight or fight or grief with their emotional concomitants of fear and anger and sadness. While cognitive reappraisal in prefrontal cortices is often effective in reducing distress (Wager, Davidson, Hughes, Lindquist, & Ochsner, 2008), those who have been the victims of complex trauma are characteristically impervious to such restructuring. They will argue that it is alright for other victims of trauma to see themselves as not responsible for their suffering and it is certainly the case that the patient would have pity for any other child who had been treated so badly but . . . “I’m different, I deserved it because I was so bad.” The submissive responses may have been so necessary for survival that a structurally dissociated part holds this repertoire of feelings and behaviors to downregulate anger, pain, and terror. The cortical regulatory capacity is insufficient for the triggered emotional states in many posttraumatic conditions. The noncognitive suppression of emotions in young trauma sufferers is based in the areas of the ventral PFC, which have outputs to the defense response and threat evaluation regions of the amygdala, the PAG, and the nucleus accumbens, among others. Subsequent failure of cognitive regulation when triggered reflects the relative inability of more dorsal and lateral areas of PFC to access and modulate these subcortical areas. This is compounded when an impairment of the capacity for mindful awareness follows a relative disconnection of dorsomedial prefrontal areas. Without concentration mindfulness training to bring these medial regions back online, any focus on cognitive reappraisal is neurobiologically inappropriate in treatment. Strategies that focus on the ventromedial areas of PFC such as eye movement desensitization and reprocessing (EMDR; Richardson et al., 2009) and SP (Ogden et al., 2006; also see Chapter 19 of this book) are more likely to address the areas in which capacity for change is greatest. It is also likely that downregulation of arousal with negatively valenced self-statements such as “I’m worthless, I’m useless, I’m bad, I’m disgusting” is recruiting not lateral but ventral areas of PFC, such as the subgenual cingulate cortex associated with pessimistic ruminations. These are affectively loaded cognitions that have a different character from logical constructions. The capacity to inhibit negative thoughts, impaired in some cases of major depressive disorder, may be reflected in the subgenual cingulate cortex’s abnormal responses to tasks (Matthews et al., 2009). In summary, obstructed fight and obstructed flight are responses that are not frozen at the midbrain level but suppressed at the orbital and adjacent medial PFC (OMPFC) level of modulation of the PAG, hypothalamus, and nucleus accumbens, and this obstruction may easily occur outside conscious awareness.

Submission and Depression

It has been proposed that the “submit” state seen in adult survivors of complex trauma is the result of an imbalance between mesolimbic and mesocortical dopamine systems (Corrigan, Fisher, & Nutt, 2011). Sufferers can switch rapidly from a higharousal state of agitation, rumination, vigilance, and intrusive memory fragments to a low-arousal, submission state of depressed mood, anhedonia, lethargy, hopelessness,

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and helplessness. This submit state is not accompanied by chronic bradycardia and hypotension suggestive of unopposed dominance of the parasympathetic nervous system. Rapid shifting of the valence of the nucleus accumbens shell from appetitive to fearful and a shift in lateralization balance, combined with suddenly variable projections to the accumbens from the PFC areas to which there are mesocortical projections, would better explain the rapid switching and the “distress dipole” states in which both extremes appear to be simultaneously present (Corrigan et al., 2011).

Traumatic Stress and the Projections From the Midbrain to the Ventral Striatum and PFC

The evidence in support of this hypothesis is mainly from laboratory studies of animals. For example, chronic stress results, even after some months without the stress, in a behavioral state interpreted as depressive and accompanied by reduced prefrontal dopamine transmission and abnormalities of HPA axis function (Mizoguchi, Shoji, Ikeda, Tanaka, & Tabira, 2008). Also, rat pups reared from weaning in social isolation display the expected hyperfunction of mesolimbic dopamine but they also show hypofunction of the mesocortical dopamine system (Fone & Porkess, 2008). There is a narrow window of optimal prefrontal cortical dopamine activity, outside which there will be impairment of cognitive functioning (Pani, Porcella, & Gessa, 2000)—a proposal that bears clear similarities to the window of tolerance clinical model of Ogden et al. (2006). The impact of early abuse on the HPA axis (Bradley et al., 2008) may include among its effects an alteration in the structure and function of the mesolimbic dopamine system. Also, endocannabinoid production as a result of early trauma influences the HPA axis response to stress (Gorzalka, Hill, & Hillard, 2008; Hill & McEwen, 2010) and alters dopaminergic tracts. Lesions of the RMTg (Jhou, Fields, Baxter, Saper, & Holland, 2009) reduce passive behavioral responses to aversive stimuli dependent on the PAG, so this nucleus is normally functioning to promote inactive avoidance and withdrawal of goal-directed behaviors that may be harmful. Its role in the development of submit states or parts has yet to be defined. Likewise, the subthalamic nucleus contributes to behavioral arrest under certain conditions but doesn’t yet have a defined role in submissive defense.

Clinical Implications of the Changes in the Mesolimbic Dopamine System

The mesolimbic dopamine system’s sensitivity to adversity promotes novelty seeking, which has survival advantages in some situations. Developmental changes in the mesocortical system may induce opposite effects in the mesolimbic system through impairment of prefrontal control. For example, a reduction in mesocortical dopamine confers a readiness to accept immediate rather than postponed gratification, as the latter would require more effort (Gatzke-Kopp, 2011). If this state also predisposes to irritability and dysphoria, and if the overall changes are contributing to a capacity for the development of substance dependence, a familiar clinical picture

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emerges. Imagine a patient who has been exposed to anger and alcohol through her mother while still in utero; who is deprived of attunement in infancy and who is exposed to more anger and rejection; who becomes promiscuous and develops alcohol dependence in her early teens; who seeks more novelty and stimulation through psychotropic drugs of any description without concerns for safety; whose life is then further marred by physical and sexual violence; who experiences loss and abandonment through deaths among close friends who have a similar lifestyle; who engages in deliberate self-harm and suicidal thinking; and who has difficulty in postponing the intense impulses to obtain relief from the distress, of which there may be few outward signs despite frequent presentations to mental health services. This picture can be seen in the effects of the response of the mesolimbic and mesocortical dopamine systems to the various forms of early adversity: those that occur in utero, in infancy, in childhood, and in early adult life all contributing, through alcohol, endocannabinoids, endogenous opioids, cortisol, and CRF, to imbalances in the dopamine tracts from the ventral tegmental area to the nucleus accumbens and PFC. So there is an interaction of neurochemical responses to traumatic stress with neuroplastic changes in the ascending dopamine systems, which alters, perhaps permanently, the sensitivity to anxiety and depression in the adult surviving these adverse early events.

Submission and Shame: Withdrawal and Hiding

There is still debate over what constitutes the core experience in the affect of shame. The cognitive phase (Nathanson, 1992) can include recognition of failure in ability or skill; dependence/helplessness; and competitive loss. These can all be triggered by defeat or submission in an agonistic encounter. There are also more ontological concerns: being exposed; being subhuman and unlovable; being sexually abnormal; being unattractive and open to contempt. A neuroscience of shame needs to accommodate failure to defend the self, failure to merit belonging to a group, and the negative valence on the experience of the self. We argue that shame is the emotional response to social abandonment or to the recognition of failure to meet the requirements for belonging. The urge to hide from scrutiny arises from an intense feeling of being defective, worthless, and subhuman. Shame is a cognitively contextualized attachment failure, which can begin in infancy. Nathanson (1992) considered shame to be an emotion that turns down positive affect, whether it arises from enjoyment in an interaction or interest in an activity. It is followed by a physical response evident in, for example, drooping of the shoulders. The associated inability to think is followed by access to personalized scripts relating to shame and then by acceptance or defense. Defensive reactions can include attacking oneself, attacking another, immediate withdrawal, or longer term avoidance: the “compass of shame” (Nathanson, 1992). Often people will respond so quickly to a humiliating experience that the rage response appears to be primary. Careful dissection of the thought/feeling/sensation sequence (Fay, 2007) will pick up the somatic experience of the blow to the self, which triggers the readily accessible defense routine.

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In SP (Ogden et al., 2006), submission is seen as part of the body’s physiological regulation during a traumatic event when a sympathetically driven high-arousal defense state cannot be maintained or is ineffective. This is often experienced as shameful by the victim: “I should have been able to keep fighting; I should have been able to get him off me; I must have wanted it to happen; I deserved it.” Shame is also pronounced during TI: “I couldn’t move; I couldn’t even scream for help; I’m pathetic and weak.” It is not immediately obvious whether there is any positive affect that is being turned down by the emotion of shame. Either shame is functioning as a downregulator of negatively valenced high-arousal states of terror or rage, or there is a hidden hope or wish that becomes extinguished at the moment of surrender. The thoughts “I can cope; I can defend myself; I’ll be able to stop him; I’ll be able to call for help; someone will come in time” represent attitudes of mastery and hope, which are snuffed out with the realization that there is no way out. The positive affect reduced by shame is there derived from a hope that proves to be forlorn. Both the positive affect reduction and the attachment disruption models of shame may be replaced by a consideration of shame as arising from a threat to the need to belong to a social group. To be accepted means to be attractive in some way, and this is threatened by devaluation or rejection (Gilbert, 2002). It is interesting to consider the urge to belong as separate from the urge to attach: the former relates to a large group, tribe, or society; the latter to specific interpersonal interactions. Identifying belonging as a therapeutic strategy (Fay, 2007) then becomes a specific antishaming strategy. Shame and the Regulation of Social Behavior

The core behavioral response of shame is the urge to disappear, to hide from belittlement and humiliation; while the emotion contains a feeling of being small, of being a bad person: worthless, powerless, humiliated, disgraced (Tangney & Dearing, 2002). Just as empathy for social pain recruits the circuits originally deployed for the awareness of physical pain, we argue that shame is the social equivalent, with greater cortical elaboration of the brainstem involvement, of the hide/cringe response to a large and powerful predator. It functions as a social regulator, allowing us to titrate contact according to the perceived wishes of those we interact with and to modify our behavior to conform to the accepted norms of the society in which we are living. This function is, however, derived from the innate defense to a more powerful social animal that has the capacity to squash, overwhelm, humiliate, or punish. Submission, deference, compliance, attention to etiquette, observation of moral standards—all are protective against the pain of humiliation and exclusion. The PAG areas involved, and their hypothalamic equivalents, are modulated by areas of orbitomedial prefrontal and anterior cingulate cortices, setting up loops for protracted, ruminative, painful, affectively loaded cognitions, which fix patterns of attacking others or attacking the self. The mood is dysphoric and may present as depressive through the projections that influence the valence of the mesolimbic dopamine system. The infant’s interpersonal learning promotes long-term behavior that is socially acceptable and allows the developed adult to belong to a wider group. The mother’s

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disapproving expression promotes socialization through the downregulation of the positive affect of the infant’s excited state. Humiliation, in contrast, through punitive belittlement or contempt, involves both sympathetic and parasympathetic activation (Schore, 1994; Siegel, 1999), and better matches with peritraumatic shame occurring during TI or severe physical or sexual abuse. The emotion accompanying the urge to withdraw and hide coexists with the defensive rage or terror. If parasympathetic downregulation is a key mechanism in interactive socialization, it occurs when there are mild feelings of deflation and disappointment, and reductions in interest and enjoyment, rather than the painful and malignant state here considered as shame. Toxic or Malignant Shame and the Impaired Capacity for Positive Affect

Shame secondary to severe interpersonal trauma has a negative impact on the affective valence of the self. There is an overlap between the self-related regions of the subcortical-cortical midline systems (Northoff et  al., 2009) and the areas of brain recruited during rewarding experiences. When there is loss of drive in the mesolimbic dopamine system, there is impairment of exploratory behaviors, excitement, eager anticipations, joy, and interest (Alcaro & Panksepp, 2011). We postulate that the dmPAG is involved, with the cingulate cortex, the SC, and the cuneiform nucleus, in the acute, high-arousal, cringe phase of shame when there is a sudden urge to withdraw and hide. Another phase, or component, is the reduction of joy and drive through the impact of the RMTg on the mesolimbic dopamine system. Recognition of the shame and the precipitating events brings in the circuits for social pain through the vlPAG, anterior insula, and ACC. The more protracted stage of self-loathing and withdrawal depends on the structures activated during the acute phases, the negative affective valence of the self in the midline systems, and the autobiographical memory scripts activated. The parabrachial nucleus, critical for the development of the primordial self (Damasio, 2010), is interconnected with the nucleus accumbens and other sites for positive affect: it also mediates the enjoyment of sweet tastes (Berridge, 2009). A distaste for the self, especially if the experiences of humiliation occur early in life, could be based at the brainstem level of the parabrachial nucleus, where a sensitization to shame is learned at a level impervious to cognitive restructuring. The Importance of the Therapist’s Careful Acceptance in Treating Toxic Shame

The converse is that having attention drawn to being held in the warm and nonjudgmental gaze of the therapist while exploring states of shame can modify the subcortical substrates of the self. A caring facial expression, nonthreatening eye contact, and encouragement of the metacognitive awareness of the impact of these on the metabolism of shame detoxify states that are otherwise impervious to change. Perhaps the parasympathetic downregulation described by Schore (1994) is a benign form of shame-induction that, in a secure relationship, modifies behavior through social learning in a relatively painless way. Thereafter, secure attachments in relationships will allow acquisition of social customs and mores while buffering against a toxic buildup of shame as the orbitomedial PFC accommodates the new learning.

146  I.  NEUROBIOLOGY Table 7.1  The Defense Response States That can Underlie Dissociated Self-States or Alters Defense response states

Terms that may apply to the subjective experiences or overt behaviors of the different defense response selfstates, which can form the basis of alters

Fight-active (Active defense response is readily available and under conscious control)

Angry. Assaultive—verbally or physically—when threatened. Invincible. Strong, independent, in control. Tense in upper body, neck, and throat. Teeth clenched. Powerful. Having a strong feeling of being in the right. Thinking clearly.

Fight-obstructed (Active defense response is blocked but not just by inability to move the relevant muscles. There is a reason—which may not be conscious—to not fight back)

Angry. Irritable. Paranoid. Mistrustful. Tense in upper body, neck, and throat. Being aware of urge to self-harm or suicide. Seeing everything as negative and black. Having difficulty with concentration. Refusing to eat. Speech unfocused or rambling.

Frozen fight (Active defense response is blocked by inability to move upper body)

Anger may not be subjectively intense or even present. Feeling trapped. Unable to move to actively defend. Terrified. Tense in upper body: chest, shoulders, fists, jaw.

Fight-predatory (Technically not a defense state but included for comparison)

Cold, vengeful. Deliberate. Feeling few autonomic signs of arousal. Reducing distress by thinking of exacting punishment or retribution and finding this rewarding.

Submissive fight

Dumbly insolent. Rebellious. On the surface compliant: underneath aggressive. Accepting defeat but not long term.

Flight-active (Active defense response is readily available and under conscious control)

Urge to run away from situations or feelings that inspire fear. Tense in chest. Urge to move in lower body. Impetus to movement can be acted upon.

Flight-obstructed (Active defense response is blocked but not just by inability to move the relevant muscles. There is a reason—which may not be conscious—not to run away)

Anxious, fearful, vulnerable. Hypervigilant, trapped. Urge to get out is combined with inability to escape. Needing to run away to hide. Using drink, drugs, starvation or other “escapism” to reduce distress. Tense in chest and lower body.

Frozen flight (Active defense response is blocked by inability to move lower body)

Terrified. Trapped. Unable to run away. Urge to move legs is combined with inability to move them. Tense in chest and lower body. May feel inhuman, untouchable, ugly. (continued)

7.  DEFENSE RESPONSES  147 Table 7.1  The Defense Response States That can Underlie Dissociated Self-States or Alters (continued ) Defense response states

Terms that may apply to the subjective experiences or overt behaviors of the different defense response selfstates, which can form the basis of alters

Tonic immobility

Terrified. Trapped. Unable to move. Unable to utter a sound. Heightened tone in muscles but no awareness of a specific action urge: just an awareness of an overall inability to move a muscle. Frozen with terror. Mismatch between heart rate and breathing rate.

Attach-active (acknowledgment of the need to attach to survive)

Looking to others for care, safety, rescue, reciprocal attunement, affection, love. “I need someone to be aware of me.” “I need somebody to look after me.” “I need someone to care.” “I want someone to value me.”

Attach-obstructed (May be protest [“What about me!”] or despair [“It is hopeless; I’ll always be alone”] or shame [“I’m alone because I’m worthless”])

Blocked response to need for safety or rescue gives feelings of worthlessness, abandonment, helplessness, and isolation. Panic. Sadness. Despair. Grief. Shame. Inward search for solace. “Nobody cares about me.” “I’m not heard.” “I don’t matter.”

Attach-frozen

Inability to go toward a possible protector or rescuer. “I can see a caring person who could help but I’m unable to approach him/her because I can’t move.” There may be a feeling of wanting to extend the arms toward a person combined with an inability to move them.

Avoid/hide/cringe

Urge to contract, be smaller and smaller. Disappear. A speck that can be hidden to feel safe. Feeling everything sucked in. Feeling hidden deep inside. Dislike for self. Strong self-loathing. “I must not be found.”

Submit-active (Choice to give in is readily available and under conscious control)

Accepting defeat. Accepting loss. Resigned to inferiority of status/power/control.

Submit-involuntary (Forced to give in. Passive defense response is necessary for survival. There is no option to run or fight)

Tired and lethargic. No energy for thinking. Helpless, hopeless, depressed, ashamed. Wanting to be hidden from sight. Body feels collapsed. No strength. Robotic. Experience of time changes. Mask-like. Empty. Aware of meaninglessness. “I’m nothing; I’m worth nothing.”

Hypervigilance-waiting Dread, wariness. (No evident threat but a feeling of Scanning the environment. imminent danger: the security moti- Waiting for signs of danger, perhaps the return of an abuser or other vation system is online) potential predator. Able to seek signs of danger so not frozen as in the next two categories. Waiting can feel interminable but no other option is available. (continued)

148  I.  NEUROBIOLOGY Table 7.1  The Defense Response States That can Underlie Dissociated Self-States or Alters (continued ) Defense response states

Terms that may apply to the subjective experiences or overt behaviors of the different defense response selfstates, which can form the basis of alters

Attentional focus freeze

Feeling unable to tear gaze away from trigger. Field of attention narrows: peripheral vision blurred. Transfixed. Horrified. Frozen—but no clear action urge—except to stare.

Vigilance freeze

Immobility. No action urges to run or fight. Hyperaware of sounds, sights and smells in the surroundings. Determined not to be surprised by a threat. Body like a statue. Eyes peeled. Ears pricked. Time slows. Constant scanning of the environment without movement.

Shutdown submissive freeze (Hypoarousal)

Overwhelmed by danger. Immobile. No action urges to run or fight. Reduced awareness of sounds and sights in the environment. Awareness of returning to the body only when it is safe to feel again. Time stops.

Extreme submissive freeze (Hypoarousal) Dorsal-vagal freeze with opioid-mediated dissociation

Feeling tiny and frozen. Numbness. Blackness. No pain. Slow heart rate. Breathing almost imperceptible: feels safer for breathing to be nearly absent. Animation suspended. Looking dead may increase chance of survival.

This list is not exhaustive and many response states clinically overlap. The idea came from a slide by Janina Fisher, in which the characteristics of Fight, Flight, Freeze, Submit, and Attach responses were defined to help to identify “Who has shown up for the session today?”

In contrast, there are forms of a more malignant affect of shame derived from experiences of abuse, traumatic loss, and other aversive experiences, which involve the defense response areas of the midbrain. When the hide response becomes activated by memories themselves, malignant shame evokes an internal cringe and turns the focus of awareness immediately away from them to the rage that followed, or the self-recrimination that restored a feeling of being in control. A therapist sitting behind the head of the client, ready to focus on signs of rage, could spend hours over many years listening to the narrative without making the slightest difference to the most painful part of an experience. Instead, active engagement with the patient is necessary. Working backwards to the point of impact of the trauma, on the assumption that shame accompanied the obstructed hide/withdrawal response, highlights the rapidity of the steps in the defense sequence. Gently encouraging eye contact and awareness of the therapist’s nonjudgmental expression, attending to the effect of the therapist’s acceptance in the present, and noticing the thoughts and feelings that are generated by the acceptance may all be crucial in altering the urge to hide from the memories of the experience.

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This theoretical construction also explains why some forms of exposure to a memory are retraumatizing. When amygdala activation is considered the primary treatment focus, downregulation of this can be readily achieved. However, ignoring the impact of the amygdala on the already dysfunctional defense response areas of the brainstem means that an obstructed urge to hide/withdraw/avoid is repeatedly activated without being modified. Those who have been traumatized may struggle with compassionate feelings and imagery (Gilbert, 2002), and for those patients and clients, interpersonal caring and acceptance are necessary for transforming the more avoidant defense strategies and the shame-based affect sequences. When the peritraumatic defense response sequence is truncated before completion, the unresolved impulses and emotions replay without resolution, maintaining a persisting distress. In later chapters, we consider how these sequences are stored and how they can be accessed more fully to allow completion and triumph. There is also discussion of early trauma processing for very early attachment injuries. The focus here has been on the somatic components of the defense responses, but later chapters attend to the associated emotions and cognitions and how articulating these in mindful awareness can help to modify the stored dysfunctional survival tendencies.

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Ikemoto, S. (2010). Brain reward circuitry beyond the mesolimbic dopamine system: A neurobiological theory. Neuroscience and Biobehavioral Reviews, 35(2), 129–150. Jhou, T. C., Fields, H. L., Baxter, M. G., Saper, C. B., & Holland, P. C. (2009). The rostromedial tegmental nucleus (RMTg), a GABAergic afferent to midbrain dopamine neurons, encodes aversive stimuli and inhibits motor responses. Neuron, 61(5), 786–800. Kalin, N. H., Shelton, S. E., Fox, A. S., Oakes, T. R., & Davidson, R. J. (2005). Brain regions associated with the expression and contextual regulation of anxiety in primates. Biological Psychiatry, 58(10), 796–804. Koch, M. (1999). The neurobiology of startle. Progress in Neurobiology, 59(2), 107–128. Lévesque, J., Eugène, F., Joanette, Y., Paquette, V., Mensour, B., Beaudoin, G., . . . Beauregard, M. (2003). Neural circuitry underlying voluntary suppression of sadness. Biological Psychiatry, 53(6), 502–510. Lima, A. A., Fiszman, A., Marques-Portella, C., Mendlowicz, M. V., Coutinho, E. S., Maia, D. C., . . . Figueira, I. (2010). The impact of tonic immobility reaction on the prognosis of posttraumatic stress disorder. Journal of Psychiatric Research, 44(4), 224–228. Matthews, S., Simmons, A., Strigo, I., Gianaros, P., Yang, T., & Paulus, M. (2009). Inhibitionrelated activity in subgenual cingulate is associated with symptom severity in major depression. Psychiatry Research, 172(1), 1–6. McLaughlin, J. P., Li, S., Valdez, J., Chavkin, T. A., & Chavkin, C. (2006). Social defeat stressinduced behavioral responses are mediated by the endogenous kappa opioid system. Neuropsychopharmacology, 31(6), 1241–1248. McNally, G. P. (2005). Facilitation of fear extinction by midbrain periaqueductal gray infusions of RB101(S), an inhibitor of enkephalin-degrading enzymes. Behavioral Neuroscience, 119(6), 1672–1677. Mizoguchi, K., Shoji, H., Ikeda, R., Tanaka, Y., & Tabira, T. (2008). Persistent depressive state after chronic stress in rats is accompanied by HPA axis dysregulation and reduced prefrontal dopaminergic neurotransmission. Pharmacology, Biochemistry, and Behavior, 91(1), 170–175. Mobbs, D., Marchant, J. L., Hassabis, D., Seymour, B., Tan, G., Gray, M., . . . Frith, C. D. (2009). From threat to fear: The neural organization of defensive fear systems in humans. The Journal of Neuroscience, 29(39), 12236–12243. Moskowitz, A. K. (2004). “Scared stiff”: Catatonia as an evolutionary-based fear response. Psychological Review, 111(4), 984–1002. Nathanson, D. L. (1992). Shame and pride: Affect, sex, and the birth of the self. New York, NY: W. W. Norton. Nijenhuis, E. R., Vanderlinden, J., & Spinhoven, P. (1998). Animal defensive reactions as a model for trauma-induced dissociative reactions. Journal of Traumatic Stress, 11(2), 243–260. Northoff, G., Schneider, F., Rotte, M., Matthiae, C., Tempelmann, C., Wiebking, C., . . . Panksepp, J. (2009). Differential parametric modulation of self-relatedness and emotions in different brain regions. Human Brain Mapping, 30(2), 369–382. Ochsner, K. N., & Gross, J. J. (2005). The cognitive control of emotion. Trends in Cognitive Sciences, 9(5), 242–249. Ogden, P., Minton, K., & Pain, C. (2006). Trauma and the body: A sensorimotor approach to psychotherapy. New York, NY: W. W. Norton. Ohira, H., Nomura, M., Ichikawa, N., Isowa, T., Iidaka, T., Sato, A., . . . Yamada, J. (2006). Association of neural and physiological responses during voluntary emotion suppression. NeuroImage, 29(3), 721–733. Pani, L., Porcella, A., & Gessa, G. L. (2000). The role of stress in the pathophysiology of the dopaminergic system. Molecular Psychiatry, 5(1), 14–21.

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Pereira, E. A., Lu, G., Wang, S., Schweder, P. M., Hyam, J. A., Stein, J. F., . . . Green, A. L. (2010). Ventral periaqueductal grey stimulation alters heart rate variability in humans with chronic pain. Experimental Neurology, 223(2), 574–581. Price, J. L. (2006). Connections of orbital cortex. In D. H. Zald & S. L. Rauch (Eds.), The orbito­ frontal cortex (pp. 39–56). Oxford, UK: Oxford University Press. Reynolds, S. M., & Berridge, K. C. (2008). Emotional environments retune the valence of appetitive versus fearful functions in nucleus accumbens. Nature Neuroscience, 11(4), 423–425. Richardson, P., Williams, S. R., Hepenstall, S., Gregory, L., McKie, S., & Corrigan, F. M. (2009). EMDR treatment of a patient with posttraumatic stress disorder: A single-case fMRI study. Journal of EMDR Practice and Research, 3, 10–23. Rivers, W. H. R. (1920). Instinct and the unconscious: A contribution to a biological theory of the psycho-neuroses. Retrieved from http://psychclassics.yorku.ca/Rivers/ Sartre, J.-P. (1943/1969). Being and nothingness. London, UK: Methuen University Paperback. Schore, A. N. (1994). Affect regulation and the origin of the self: The neurobiology of emotional development. Hillsdale, NJ: Lawrence Erlbaum Associates. Siegel, D. J. (1999). The developing mind: Toward a neurobiology of interpersonal experience. New York, NY: Guilford Press. Somerville, L. H., Whalen, P. J., & Kelley, W. M. (2010). Human bed nucleus of the stria terminalis indexes hypervigilant threat monitoring. Biological Psychiatry, 68(5), 416–424. Spence, A. (2006). The pure land. Edinburgh, UK: Canongate. Tangney, J. P., & Dearing, R. L. (2002). Shame and guilt. New York, NY: Guilford. Vogt, B. A., Aston-Jones, G., & Vogt, L. J. (2009). Shared norepinephrinergic and cingulate circuits, nociceptive and allostatic interactions, and models of functional pain and stress disorders. In B. A. Vogt (Ed.), Cingulate neurobiology and disease (pp. 467–498). Oxford, UK: Oxford University Press. Wager, T. D., Davidson, M. L., Hughes, B. L., Lindquist, M. A., & Ochsner, K. N. (2008). Prefrontal-subcortical pathways mediating successful emotion regulation. Neuron, 59(6), 1037–1050. Watt, D., & Panksepp, J. (2009). Depression: An evolutionarily conserved mechanism to terminate separation distress? A review of aminergic, peptidergic, and neural network perspectives. Neuropsychoanalysis, 11, 7–51.

CHAPTER 8

The Clinical Sequelae of Dysfunctional Defense Responses: Dissociative Amnesia, Pain and Somatization, Emotional Motor Memory, and Interoceptive Loops Frank M. Corrigan

Amnesia, which is a loss of memory, is a symptom of many different trauma and/or dissociative disorders, including PTSD, Dissociative Fugue, Dissociative Disorder Not Otherwise Specified and Dissociative Identity Disorder. Amnesia can affect both implicit and explicit memory. —Ruth A. Lanius, Eric Vermetten, and Clare Pain (2010)

To maximize the possibility of survival in a situation of extreme danger, the defense responses have an immediacy that confers precedence of the midbrain over the cortex (Mobbs et al., 2009). This is especially important in the child’s brain, which develops from the bottom to the top, from the brainstem to the cortex (Perry, 2009), so that neural networks are laid down when the cortical regulatory areas are far from complete. The effects of early trauma are stored in subcortical loops that can be activated by triggers in the adult’s here-and-now present with little cortical modulation of them. Most treatment approaches look at the events that have established these loops with varying degrees of success in modifying them. Sensorimotor psychotherapy (SP; Ogden, Minton, & Pain, 2006) specifically looks at dynamic sequences of sensations, feelings, and impulses to movement, to bring them fully into the cortical spotlight 153

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so that what is truncated or unfinished can be identified and moved to completion. Other methods based in the somatic residues of early trauma but derived from eye movement desensitization and reprocessing (EMDR) are described later in this book and elsewhere (e.g., Shapiro, 1995). We have considered, in earlier chapters, posttraumatic residues on defined defense responses and now consider other long-term consequences of adversity.

THREAT CAN PRODUCE INVOLUNTARY MOVEMENT AND DISSOCIATIVE AMNESIA BY INTERRUPTING THOUGHT AND EVOKING SUBCORTICAL CIRCUITS

In a major brain imaging study of subcortical defense response activation, volunteers identified a level of electrical shock to the skin that they found uncomfortable but not painful (Butler et al., 2007). They knew that this same level of stimulation could occur in the scanner during a “threat” condition but not during a “safety” condition. Under threat, there was increased activity in the dorsal basal ganglia (caudate nucleus and putamen), the anterior insula, the thalamus, the hypothalamus, and the midbrain. In contrast, there was decreased activity in the primary motor cortex, the precentral gyrus, demonstrating that being in danger shifts readiness for action away from voluntary motor control to the subcortical circuits that drive evasive and defensive behaviors.

HIPPOCAMPAL DEACTIVATION AT A TIME OF PERIL

Additionally, during the threat periods, there were deactivations of the hippocampal, parahippocampal, posterior cingulate, and precuneus regions—all regions prominent in autobiographical memory circuits (e.g., Summerfield, Hassabis, & Maguire, 2009). In a moment of peril, personal memory activation is less important than rapid deployment of defense response circuits. If such an effect can be seen in a controlled environment with a predetermined level of skin shock, extrapolation to a real-life situation of unpredictable outcome leads to the credible proposition that extreme fear will downgrade the involvement of circuits through the hippocampal and parahippocampal areas, posterior cingulate cortex, precuneus, and ventromedial prefrontal cortex (VMPFC) to the extent that narrative details of the episode will not be readily accessible. This will especially be the case in children whose cortical development is far from completion. When people say that “it all happened so fast” that they don’t know how they took the action they did, which ensured their survival, it is because the state of sudden danger they encountered recruited subcortical defense responses at the expense of hippocampal memory formation. Hippocampal deactivation is also seen in rats subjected to immobilization stress (Sung et al., 2009) and in humans under social threat (Pruessner et al., 2008). Posttraumatic disruption of function in the VMPFC, which can integrate emotional memory information from the hippocampus, amygdala, and nucleus accumbens (Nieuwenhuis & Takashima, 2011), will manifest in the intermittent access to recall

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of specific events complete with their somatic components. A posttraumatic disruption of personal memory in dissociative amnesia has also been linked to underactivity in the right inferolateral prefrontal cortex (PFC), an area described by the authors as strongly interconnected with the amygdala and participating in the retrieval of negatively valenced autobiographical memories (Brand et al., 2009).

HIPPOCAMPAL VOLUME REDUCTION IN DISSOCIATIVE DISORDERS

Patients with dissociative disorders experience amnesia not only when under stress or threat but also for ordinary or even happy experiences. The hippocampal and amygdala volume reduction in these disorders (e.g., Vermetten, Schmahl, Lindner, Loewenstein, & Bremner, 2006) is associated with an early requirement to take the emotional memory circuits offline during overwhelming experience: amnesia is then comparatively nonselective. Mice given a very brief electric shock to their feet through a metal grid showed evidence of persisting contextual fear 1 month after the traumatic experience—and a reduction in hippocampal volume (Golub et al., 2011). As damage to the ventral hippocampus reduces fearful behaviors in contexts learned to be potentially dangerous (Goosens, 2011), it is possible that the brain is adaptively modifying itself to reduce the impact of adverse experiences.

HIGH AROUSAL AND LOW AROUSAL PRODUCE DIFFERENT DISSOCIATIVE SYMPTOMS

Peritraumatic dissociation is a subjective experience that cannot be studied as such in animal models. However, the closely linked phenomenon of stress-induced analgesia (SIA) is available for research. As fight, flight, and sudden loss can all be accompanied by peritraumatic dissociation, it is important that the analgesia accompanying the active defense responses generated in the periaqueductal gray (PAG) is not opioid-dependent. SIA that is not mediated by opioids is instead dependent on endogenous cannabinoids or endocannabinoids. When the organism is under threat, the protective effects of endocannabinoids include the reduction of fear, despair, and pain (Finn, 2010). A key, and as yet unanswered, question is how much peritraumatic dissociation is neurochemical and how dependent it is on sudden alterations in the balance of frontoparietal networks.

NEUROCHEMICAL CONTRIBUTORS TO SIA AND HIGHAND LOW-AROUSAL DISSOCIATION

The role of endocannabinoids in SIA was confirmed by studies of brief, continuous electric foot shock applied to rats. This stressor elicited the formation in the PAG of two endogenous cannabinoids (Hohmann et  al., 2009). The two

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endocannabinoids 2-arachidonylglycerol and anandamide have different effects on mediating stress responses on the hypothalamic–pituitary–adrenal (HPA) axis (Hill & McEwen, 2010), an endocrine system that has complex abnormalities in response to trauma (Vythilingam et al., 2010). Endocannabinoids in the basolateral amygdala have a role in the extinction of aversive memories in mice (Marsicano et al., 2002), and in the dorsolateral PAG they contribute to the reduction of fearful behaviors (Moreira, Aguiar, & Guimarães, 2007). In the rat brain, there are high densities of cannabinoid CB1 receptors in the hippocampus (Moldrich & Wenger, 2000), and cognitive impairment in humans using cannabis is likely to involve hippocampal cannabinoid receptor activation (Puighermanal et al., 2009). Trauma sufficient to reduce the volume of the hippocampus may be increasing the production of endocannabinoids in a way that reduces fear and pain but impairs memory consolidation. Experiments in mice demonstrate the importance of endogenous cannabinoids in the relief of fear in situations that are highly aversive. Excitatory neurotransmitters, such as glutamate and dopamine, are released with the emotions accompanying the defense response. When the stimulation of these neurotransmitters is excessive, the spillover induces the synthesis and release of endocannabinoids. These diffuse to their presynaptic receptors and turn down the release of the fear-promoting excitatory transmitters (Riebe, Pamplona, Pamplona, Kamprath, & Wotjak, 2012). This is a clear demonstration of the neurochemical downregulation of a fearful response to an unpleasant event, and it conforms to our understanding of peritraumatic dissociation. Opioids participate in the SIA induced by activation of the ventrolateral PAG (Bandler, Keay, Floyd, & Price, 2000), which stimulates the low-arousal, parasympathetic-dominant passive response to stress. Visceral afferent fibers in the vagus nerve terminate in the nucleus of the solitary tract (NTS) from which there are endogenous opioid projections to lateral and ventrolateral PAG (Lü et  al., 2010). As endocannabinoids mediate the SIA accompanying stimulation of lateral/dorsolateral PAG, which generates the autonomic responses of the sympathetic-dominant active coping strategies, it is reasonable to argue that neurochemical differences in the peritraumatic dissociative experiences depend on the predominance of the active or passive response. With coactivation of PAG columns in situations of extreme threat, there will be a mixture of endocannabinoid and endogenous opioid release. The interaction of endogenous cannabinoids and opioids has been demonstrated for some types of analgesia (Haller, Stevens, & Welch, 2008). The effects in later life of early neglect and physical injury point to an interaction of endogenous cannabinoid and opioid systems in the long-term consequences for physical health.

HIGH-AROUSAL AND LOW-AROUSAL PERITRAUMATIC DISSOCIATION: ENDOCANNABINOIDS AND ENDOGENOUS OPIOIDS

We propose that there is a high-arousal peritraumatic dissociation mediated by endocannabinoids, which soothes and numbs the jagged edges of pain, fear, anger, and sadness. There is also a low-arousal peritraumatic dissociation mediated by

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endogenous opioids, which encourages stillness, warmth, numbness, and a reduced emotional involvement with pain. There are also various states in which both systems are activated to varying degrees by traumatic events or triggered by memories of them. Depending on the relative coactivations, these two systems will have the capacity to produce many and diverse manifestations of somatic complaints in addition to derealization and depersonalization.

Cortical Contributors to High-Arousal Dissociation

The neurochemical effects could happen alongside changes in cortical networks as chronic depersonalization is reflected in changes in activation in the parietal cortex (Simeon & Abugel, 2006). Parietal functions include the awareness of peripersonal space and the attention to objects—or perpetrators—within that space. In the posterior parietal cortex, there is an integration of information from many sensory modalities to provide an awareness of the body in its peripersonal space (Holmes & Spence, 2004). There are also mirror neurons attending to the movements of others, which have the capacity to respond according to the intentions behind the movements (Yamazaki, Yokochi, Tanaka, Okanoya, & Iriki, 2010). Abusive intrusions on peripersonal space may activate mirror neurons in a way that contributes to the formation of perpetrator introjects (Schmidt & Hernandez, 2007). The angular gyrus has distinct subdivisions (Seghier, Fagan, & Price, 2010) and there are left–right differences in function. Disturbance of the activity of this parietal region could contribute to some of the features of peritraumatic dissociation when incoming sensory stimuli lose their customary salience, when peripersonal space loses definition, when memory consolidation is impaired, when conscious experience is not integrated fully, and when the awareness of the self is discontinuous.

Endocannabinoids and the Long-Term Consequences of Trauma

Endocannabinoids mediate high-arousal dissociation and high-arousal analgesia, whereas opioids and a combination of compounds bring in the warmth of pain relief from the low-arousal shutdown or despairing state. As corticotropin-releasing factor (CRF) release from the hypothalamus is modulated by endocannabinoids (Finn, 2010), the well-studied changes in the HPA axis could be secondary to the impact of endocannabinoid release at the time of the early traumatic experiences. A trial of rimonabant, which blocks the CB1 receptor of the endocannabinoid system, had to be terminated early because of serious psychiatric side effects, including suicide (Topol et al., 2010), and adverse effects of rimonabant have led to the suspension of its use. It is unfortunate that the presence or absence of a trauma history was not available in the clinical studies of rimonabant, as it would be predicted that those with early adaptive changes to adversity would have more psychiatric consequences of a sudden disruption of the system.

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CHRONIC PAIN, CHRONIC DISSOCIATIVE ANALGESIA, AND SOMATIZATION SYMPTOMS

Adults with court-documented childhood abuse and neglect who also have a diagnosis of posttraumatic stress disorder (PTSD) are much more likely to have significant problems with pain than a nonabused control group (Raphael & Widom, 2011). Many trauma survivors have somatoform features that, by their subjective nature, are difficult to study in animal models. Nevertheless, what is known about pain in animals has sufficient overlap with defense response research to allow us to construct hypotheses about the mechanisms of somatization as expressions of survival responses, which have become dysfunctional over time. A severe pain etched in the mind/brain through the emotional memory system embodies a compartmentalization, which allows life to continue otherwise as apparently normal. When traumatic and painful experiences are repeated over many years, an extension of the capacity for SIA well beyond the immediate injuries is essential for survival. There can be coexistence of analgesia and unexplained pain long after healing of any tissue damage from the physical injuries suffered at the time of the original traumas. Somatization is the transformation of psychological problems into somatoform symptoms. These commonly include experiencing pain while urinating; insensitivity to pain in the body, or in a part of it; seeing things differently from normal as, for example, looking through a tunnel; noticing that one’s body or part of it seems to have disappeared; and being unable to speak, or only able to whisper (Nijenhuis, Spinhoven, Van Dyck, van der Hart, & Vanderlinden, 1996). Somatoform symptoms often have precedents in the body feelings evoked during one or more traumatic experience, especially if there has been peritraumatic dissociation conferring analgesia and emotional distancing. The following clinical example highlights the often complex somatic responses to attachment trauma and abuse. A CLINICAL EXAMPLE ILLUSTRATES THE RELATIONSHIP BETWEEN TRAUMA AND SOMATOFORM SYMPTOMS

A 30-year-old woman with a partner and two children was referred from the pain clinic for EMDR. She suffered from persisting spinal and leg pain following repeated unsuccessful efforts to give an epidural anesthetic when she was in labor. However, there was also a history of early parental separation, conflicts in the reconstituted family, and numerous traumas from childhood through to adult life. Careful preparation was required before the reprocessing of the obstetric trauma that had led to the referral. When this was completed, she elected to continue treatment. Body feelings elicited during reprocessing almost always involved the bladder: as though all her emotions were channeled through that part of her body. Key experiences for establishing that conduit included standing as a very small child alone in a house, feeling abandoned, aware of fullness in the bladder but terrified to go to empty it in case she missed a returning parent. There was also an instance of sexual molestation,

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during the shock of which there was a high-arousal freeze and after which there was a soreness and discomfort, which prevented her from easily passing urine. Over the years, in a house without a lock on the bathroom door and a fear of further molestation, there was an urge to pass urine as quickly as possible to get out of the unsafe room. Reprocessing of events preceding episodes of urinary retention in adult life revealed that they were more likely to occur at times of high stress when triggered rage had no outlet or release. She also had diagnoses of interstitial cystitis, vulvodynia, irritable bowel syndrome, chronic fatigue syndrome, and migraine. Her life was dominated by physical problems, which severely impaired its quality. On becoming more aware of the distress endured by her child self or selves, she extended her innate compassion and kindness toward the self-states holding so many burdens. Reprocessing often evolved into interactions in which she comforted child states and helped them to shed the pain they were carrying. It remains to be seen whether treatment of her psychological distress will improve her physical conditions.

MICTURITION AND THE MIDBRAIN DEFENSE RESPONSE AREAS

A functional MRI (fMRI) study (Seseke et al., 2006) of contraction and relaxation of the pelvic floor muscles to study micturition control identified sites of activation in the PAG and the pontine micturition center. When people are so terrified that they are incontinent of urine, the defense response areas of the PAG are wellplaced to be instrumental in this. Conversely, fear or other emotions leading to sympathetic autonomic arousal would block voluntary voiding at the same brainstem level. The PAG is also part, with the rostral ventromedial medulla (RVM), of a descending pain control system that can leave tactile sensations unaffected while information about pain is suppressed. The capacity of this system to be modified by psychological stress makes the PAG-RVM a likely contributor to dysfunctional pain syndromes. It promotes suppression of pain during states of terror and facilitation of pain with chronic inflammation (Heinricher, Tavares, Leith, & Lumb, 2009).

MATERNAL SEPARATION IN ANIMAL MODELS OF PAIN SYNDROMES

Maternal separation of neonatal rat pups is also used in an animal model of irritable bowel syndrome in which, in humans, there is evidence of altered autonomic nervous system activity (Kennedy et al., 2012). Animal models of attachment trauma use varying absence schedules to study the long-term effects of maternal deprivation. The endogenous cannabinoid system of adolescents and adults is predictably altered by the removal of a rat pup from its mother for 24 hours during the first 2 weeks of its life. These pups become adolescents who have impaired social behavior, altered HPA axis function, altered immune function, and altered responses to endocannabinoids (Marco, Adriani, Llorente, Laviola, & Viveros, 2009).

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INTEROCEPTIVE PATHWAYS AND PAIN

Pain is an important component of the body’s defense response to injury and trauma, as it draws attention to salient experiences that require urgent action. Unfortunately, avoidant, withdrawal, or other defensive responses are not always available, especially to the child faced with early abuse. The anterior cingulate cortex and the anterior insular cortex have evolved to provide increased control of brainstem areas significant for fundamental experiences such as the response to painful stimuli. These cortical areas have projections to the parabrachial nucleus (Craig, 2006) and are especially significant for the affective accompaniments of pain. The parabrachial nucleus has connections that make it ideally placed not only for immediate reactions to taste but for the establishment of a basis for feelings of liking or loathing. Affective responses to painful stimuli may have their origins here and in the connections of the parabrachial nucleus with the PAG before they become refined in awareness at the insular level. PAIN AND AROUSAL

The terror, pain, and rage experienced during some traumatic events can all increase arousal, and this is known to be mediated by ascending neurotransmitter systems. The defense response areas of the PAG influence the ventral tegmental area that is at the origin of the mesolimbic dopamine system (Omelchenko & Seasack, 2010). Cortical regulation of the ventrolateral PAG is from orbito-insular areas (Bandler et  al., 2000), which also project to the shell of the nucleus accumbens (Chikama, McFarland, Amaral, & Haber, 1997), the endpoint of the mesolimbic system. The activating fight-or-flight PAG responses and the collicular influences on the thalamocortical mantle lead to increased arousal in part through recruitment of ascending cholinergic projections. Scaer (2005) emphasized the activating effects of ascending noradrenergic projections to the amygdala from the locus coeruleus. Vogt, AstonJones, and Vogt (2009) propose that blunting of activity in the anterior cingulate cortex in PTSD effectively disinhibits the locus coeruleus as well as the PAG. Implications for pain processing arise from the deafferentation of thalamic nuclei as well as from altered sensation through chronic changes in the locus coeruleus. Vocalization is a common response to pain and it is curious how the words used are often affectively charged expressions that can cover an array of emotions, including rage, loss, and horror. These may be the human equivalent of the PAG-derived distress vocalizations stimulated electrically in the guinea pig. The cingulate cortexPAG pathway involved in such vocalization is sensitive to the effects of the peptide Nociceptin/Orphanin FQ (N/OFQ; Kyuhou & Gemba, 1999). Chronic Pain and Allodynia

Inflammatory pain inflicted on a rat pup on the first day of its life leaves a demonstrable effect on the opioid system in its adult life (LaPrairie & Murphy, 2009). Maternal deprivation for 24 hours in the neonatal period has long-lasting effects on behavior

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and altered sensitivity in the adult rat to cannabinoid compounds (Marco et al., 2009). A wide range of adverse circumstances alter HPA axis functioning, often through the effect of endocannabinoids on CRF release (Finn, 2010). CRF is a key contributor to addictions that not infrequently complicate both complex trauma and chronic pain syndromes (Koob, 2010). The parameters of the mesolimbic and mesocortical dopamine systems are abnormally, and often dysfunctionally, set (Gatzke-Kopp, 2011) so that high- and low-arousal states lead to many manifestations of emotional dysregulation (Corrigan et al., 2011). It is hard to see how early adversity could fail to predispose to chronic pain and allodynia, the condition in which a normally benign stimulus like the touch on the skin of a cool breeze can evoke pain. Cold allodynia, elicited by application of menthol to human skin, recruits the insular and cingulate pain circuits but is also associated with greater activation in the brainstem parabrachial nucleus (Seifert & Maihöfner, 2007). Again, there is potential for early experience, establishing networks before the full maturation of the cortical mantle, to leave a residue of altered perception of sensations so that normal tactile experience becomes painful. The feeling of clothes next to the skin is then not warm and protective but chafing and irritating in the sites of touch allodynia. Internally, normal filling of the bladder becomes painful; consensual sexual touch evokes distressing muscle tension and dyspareunia; normal muscle usage brings on the pain of fibromyalgia. Pain can be triggering when its site or character evokes a body memory but when a usually nonpainful stimulus becomes noxious that is happening at a deep level in the brain— outside the usual emotional memory circuits that are readily brought into awareness. NUMBING OF PAIN IN DISSOCIATIVE DISORDERS: POSSIBLE ANATOMICAL SUBSTRATES

Dissociative patients frequently experience persisting analgesia. This is so variable that a person harming herself during a flashback may suddenly emit a cry of pain when she returns to full awareness and feels the cuts in her arm. Another person may be unable to adjust the temperature of the bath water so that it is not scalding. The ability to discriminate between water that is dangerously hot and water that is comfortably hot depends on the posterior insula: a lesion of this area confers analgesia for heat pain (Craig, 2007). This might be the region in which dissociative analgesia has its roots. However, the ascending spinothalamic tract also has a projection to the somatosensory cortex, which can instigate a reflex motor response to pain (Craig, 2003). The absence of a withdrawal movement in a person with dissociative identity disorder (DID) who has no response to dangerously hot water could instead indicate a disconnection at the level of the thalamus. It is a temporary suppression of pain experience rather than the permanent indifference to pain, which can occur in some rare congenital conditions such as the SCN9A channelopathy (Cox et al., 2006). Neurochemicals in the Brain and Somatization

There is ample evidence for considering the endogenous cannabinoids, with their impact on CRF release (Finn, 2010), as neurochemicals that are mediating many of

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the long-term effects of early trauma on the pain and analgesic systems of the brain. These include triggered body memory pain, somatized expressions of distress, the somatic signatures of emotional parts, and the proinflammatory consequences of chronic trauma. Endogenous opioids act on the ventrolateral PAG so that they are soothing under safe conditions and freezing (in the low-arousal sense) when the environment is adverse and active responses are ineffective or overwhelmed. Therefore, opioidergic pathways involving the ventrolateral PAG contribute to the pain and somatization conditions residual from complex trauma. These may be “body memories,” somatic experiences encoded at the time of trauma, which reemerge in response to triggers, or they may be physical complaints for which no medical explanation has been found. We hypothesize that the former are mediated by the insula, triggered by the basolateral amygdala. The latter, the medically unexplained symptoms, are the result of trauma-induced changes in pain and inflammation mediators at diverse parts of the interoceptive loops instantiated at different developmental stages. It is to be hoped that the N/OFQ system will receive, with cytokines, endocannabinoids, and endogenous opioids, consideration of their contribution to the adaptive responses of the body when exposed to threat and injury. MOVEMENT SEQUENCES FOR DEFENSE IN SUBCORTICAL CIRCUITS

For defensive fight, our emphasis has been on the autonomic nervous system changes, the associated SIA mediated by the midbrain, and the emotional components based in the hypothalamus, but complex movement sequences are also required. Those employed for natural predation are integrated at the level of the superior colliculi (SC; Furigo et al., 2010) rather than in the cortex. Defense behaviors must also have hardwired programs for appropriate sequences of movements: punching, kicking, scowling, snarling, backing away, turning and running, screaming, putting up hands to ward off blows, and so on. Alexander, Crutcher, and DeLong (1990) described basal ganglia thalamocortical circuits that are “limbic,” including the ventral striatum, and “oculomotor,” including the dorsal striatum. Both of these circuits have cortical components—medial prefrontal for the limbic; eye fields for the oculomotor. McHaffie, Stanford, Stein, Coizet, and Redgrave (2005) later proposed that there were more primitive, noncortical, loops through the basal ganglia, which were necessary for competing behavioral tendencies. These loops mediate many aspects of defense response behaviors. They also provide the wiring for opponent tendencies that can be simultaneously activated during complex states such as tonic immobility (TI). The SC, the PAG, and the cuneiform nucleus all project to an area of the thalamus that has inputs to the striatum. The dorsal striatum projects back to the substantia nigra pars reticulata and the loop is completed with a midbrain link (McHaffie et al., 2005). An object or movement that carries a threat suddenly draws the eyes toward it; the direction of gaze is immediate and accurate when the superficial layers of the SC are activated by the sensory input. The loop includes the thalamus, the dorsal striatum, the substantia nigra, and the SC (McHaffie et  al.,

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Figure 8.1  Subcortical loops through the basal ganglia and periaqueductal gray arising from, and returning to, the superior colliculi: a route for emotional motor memories of orienting and defense responses. Adapted with permission and with assistance from Dr. Peter Redgrave, from McHaffie et al. (2005).

2005). Orienting to threat feels so automatic and commanding that it is difficult to drag the eyes away in response to the belated cortical commands to the dominant subcortical loops. The SC initiate movements when they are released or disinhibited by GABAergic neurons from the substantia nigra pars reticulata (Castellan-Baldan et al., 2006). Midbrain locomotor regions are kept under tonic inhibitory GABAergic control, which can be lifted to release groups of muscles responsible for eye movements and motor activity, or to alter postural tone (Grillner, Hellgren, Ménard, Saitoh, & Wikström, 2005). Complex movement sequences requiring adjustment and readjustment in fractions of seconds to ensure survival will be selected from loops through PAG, SC, thalamus, dorsal striatum, and substantia nigra pars reticulata (see Figure 8.1). In the wild, it may be necessary to move rapidly among hide, cringe, freeze, submit, flight, and fight motor sequences and to have access to endogenous opioid or endocannabinoid SIA: this variability in response can be controlled in the midbrain with its loops through the basal ganglia and outputs to the autonomic brainstem centers. Frozen fight, frozen hide, frozen flight, and TI could all be mediated by simultaneous coactivations of not only opponent PAG columns but also conflicting loops through the SC and basal ganglia: they are then amenable to processing in therapy not at the cortical level, which has no significant input to the sequences, but at the sensorimotor integration level of the midbrain. SP processing of traumatic memories at a body level is effective through completion of the obstructed response. The feeling of relief or triumph on achieving the hitherto obstructed goal signifies a shift in striatal activation from dorsal to ventral: the stored, obstructed urge or impulse to move in the dorsal striatal memory being replaced with positive affect from the nucleus accumbens engagement.

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EMOTIONAL MOTOR MEMORY

Emotional autobiographical memory involves a circuit through the VMPFC, the hippocampus, the basolateral amygdala, the posterior cingulate cortex, and the precuneus (Markowitsch, Vanderkerckhove, Lanfermann, & Russ, 2003). Defense response motor sequences recruit subcortical circuits through the basal ganglia and midbrain. Intrinsic repetitive behavioral patterns such as grooming rely heavily on the basal ganglia (Aldridge, Berridge, & Rosen, 2004). The memory system for emotionally charged uncompleted sequences of movements overlaps with procedural memory. The distinction between a hippocampal declarative memory and a caudate nucleus habit memory (Packard & Cahill, 2001) was supported by an fMRI study of humans, which found that the medial temporal lobe was involved more at the beginning of learning, while the striatum served to maintain fast, automatic repetitions of the learned behavior (Poldrack et al., 2001). Both the hippocampus and the caudate nucleus receive inputs from the basolateral amygdala when registering emotionally charged experiences (McGaugh, 2004), but the stronger the emotional experience, the more the caudate-dependent memory takes over from the hippocampal memory (Packard & Cahill, 2001). This supports the evidence already provided for the hippocampal memory system going offline during an intensely traumatic experience, making the concept of dissociative amnesia readily available neurobiologically.

THE ORBITOMEDIAL PFC AND ACCESS TO STORED EMOTIONAL MOTOR MEMORY NETWORKS

The impact of traumatic experience on sensorimotor memories, mediated by the basolateral amygdala inputs to the dorsal striatum and midbrain, etches the activated subcortical circuit into an emotionally charged procedural memory sequence that can be triggered by sensory stimuli evoking aspects of the original event. This may be completely outside conscious awareness and the triggered response has all the sensorimotor components without any autobiographical memory. After all, it is easy to ride a bike without having any memory of the first faltering experiences of trying to remain upright prior to gaining some forward momentum. If cycling has occasioned unresolved trauma, some parts of the sequence provide a way into the distressing movement memory. This is not just procedural memory but an emotionally charged sequence of motor impulses and sensations, which loops repetitively when stimulated. If the basolateral amygdala activation with severely emotionally arousing experiences influences the selection of the basal ganglia memory system over the hippocampal system (Packard & Knowlton, 2002), then the resulting highly charged memory sequence can be carried outside consciousness to be repeatedly triggered and partially expressed without being resolved. SP brings mindful attention to some sliver of the experience to allow it to progress to completion, allowing the associated distress to be discharged.

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Mindful attention to the visceral and other somatic components of the memory recruits the sensory integration network of the orbitomedial PFC. This network has extensive connectivity with the medial network that is wired for cortical modulation of visceral and emotional responses. The medial and orbital networks have different patterns of connectivity with the striatum: medial with the nucleus accumbens; orbital with dorsal striatal areas of the caudate nucleus (Price, 2006). The basolateral amygdala modulates the consolidation of memory of different types of information through its connections with many structures of the brain (McGaugh, 2004). An emotional motor memory sequence with dorsal striatal and basolateral amygdala components would be accessible through the orbital network’s projections to the caudate nucleus and/or amygdala, unless the gateway is through the more medial projections to the mesodiencephalic components of the circuit. In either case, the SP focus on the minute details of the body experience is acting at the level of the orbitomedial PFC to find the experiential links. Taking on a Life of Their Own: Interoceptive Loops and Emotional Parts or Dissociated Self-States

Humans have an advanced system for discriminative awareness of the somatic responses to environmental stimuli and the visceral sensations engendered by them. The medial dorsal thalamic nucleus integrates information from the spinal cord with information from the PAG and the parabrachial nucleus and projects to the anterior cingulate cortex to produce a behavioral drive or motivation (Craig, 2003). The ventral medial thalamic nucleus projects the information about the physiological state of the body to the somatosensory cortex and to the insular cortex (Craig, 2003). The transfer of information from posterior to anterior insula is then accompanied by a subjective feeling. The visceral or gut response to a stimulus alters the self’s emotional response through the interoceptive feedback circuits. If the body’s homeostasis is dependent on opponent systems driven by right- and left-insular cortices, the self’s health will require an optimal balance of activations (Craig, 2005) with arousing experiences on the right and affiliative feelings on the left (Craig, 2009). The right- and left-anterior cingulate cortices may also drive different motivations in response to the signals received from the body. Both the anterior cingulate cortex and the anterior insular cortex have highly evolved spindle cells or von Economo neurons (Allman et al., 2010), to allow for fast communication across the distance between them, and the most anterior part of the insula may have no equivalent in the monkey (Craig, 2009).

Interaction of Sensory Input and Visceromotor Response

The anterior insular cortex is part of the “orbital” sensory integration network of the PFC, which has interconnections with the “medial” visceromotor network projecting to the hypothalamus and the PAG (Price, 2006). As the anterior cingulate cortices form part of this medial network, both the areas that receive interoceptive information from the body have outputs that influence the physiological state of

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the body. Thus there is a loop that for brevity, we refer to as an interoceptive loop, involving orbitomedial PFC projecting to the hypothalamus and PAG, which in turn influence brainstem nuclei to alter the autonomic nervous system status of the body. The changes are then fed back through the spinothalamic tracts to the nuclei of the thalamus, which project to insular and cingulate cortices for cortical regulation of brainstem autonomic activity. We argue that not only does this loop underlie affective states engendered by stimuli, internal or external, but that it can also exist semi-independently as the basis for the structurally dissociated defense response self-states (Figures 8.2 and 8.3). The interconnection in the VMPFC of this interoceptive loop with the episodic memory circuit dependent on posterior cingulate cortex, precuneus, and hippocampus provides a neurobiological basis for states of intense affect derived from traumatic episodes being triggered in the present with minimal conscious awareness at the level of working memory in the dorsolateral PFC.

Consolidation of Traumatic Experiences Into Somatic Residues

Through these pathways, traumatic episodes become repeatedly consolidated in the mind/brain. Intense autonomic nervous system components mediated by the midbrain PAG and brainstem nuclei; survival behaviors recruiting subcortical circuits through the basal ganglia, PAG, and SC; and subjective feeling and motivational components in interoceptive loops centered on anterior insula and anterior cingulate cortices all combine in potentially dominating networks. They are readily retriggered through the basolateral amygdala under arousal and environmental conditions evocative of the original event. Body states can be simulated if the trigger in the amygdala activates the ventromedial PFC and the insular and somatosensory cortices to reproduce a particular emotional state without the physiological somatic state usually associated with that emotion. Through the thalamic connections of the midbrain defense response areas, these “as-if” body loops (Damasio, 2010) could occur without significant body change, perhaps explaining why some patients with dissociative disorders can report the subjective feelings of a switched state of fight or flight without the expected physiological components. Van der Hart, Nijenhuis, and Steele (2006) consider the dissociative patient to have distinct psychobiological systems that are “apparently normal” parts of the personality (ANPs) or “emotional” parts of the personality (EPs) with distinct action urges. We hypothesize, based on the defense responses engendered in the mesodiencephalon, that the EPs can have an egotized life of their own as the interoceptive loop forms an affective consciousness circuit, which has a distinct view of the world. The degree to which the EP is in full awareness will depend on whether the PFC involvement is confined to the ventromedial area of output to the hypothalamus and midbrain or whether there is additionally more dorsal PFC activation. Bringing an EP into awareness will require mindful observation recruiting more dorsal medial PFC areas simultaneously with the particular interoceptive/affective loop representing the defense response part. All of this needs to be done with blending of lateral areas for working memory and emotion regulation.

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Ventromedial Prefrontal Cortex

Anterior Cingulate Cortex Insula

Thalamus

Hypothalamus Periaqueductal Gray

Body Figure 8.2  Affective consciousness circuit or interoceptive loop.

Ventromedial Prefrontal Cortex

Anterior Cingulate Cortex Insula

Hypothalamus Dorsolateral Periaqueductal Gray (dlPAG)

Thalamus

Body Figure 8.3  Affective consciousness circuit: interoceptive loop for active defense self-state.

Along with the emotional parts and the apparently normal parts of van der Hart et al. (2006) and the core self of Schwartz (1995), it is useful to consider the possibility of default state parts relating to the different ages of the maturing individual. At any age, the self will have a nondefensive default state that supervenes when the mind is not engaged in tasks. Attention to the residues of these states helps to resolve the trauma memories frozen outside time in techniques such as Lifespan Integration (Pace, 2003). Layered Organization and Sensorimotor Integration

The cortical integration through the processing journey in the cingulate cortex is at the upper level of organization of the response to sensory stimuli. Self-relevant information from sensory afferents is extracted by the ventral posterior cingulate cortex and assessed in the context of personal memories. The cingulate motor areas guide head and body orientation and the anterior cingulate cortex drives autonomic outputs

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(Vogt et al., 2009). We have argued that when there is extreme danger, especially to a young human with cortical systems that are still developing, there is a dominance of subcortical sensorimotor processes. We have considered the contributions of thalamic nuclei to the subcortical loops for rapid and effective motor responses to threat and to the interoceptive loops that form the emotional responses to stimuli. It is worth mentioning another area of the diencephalon, which integrates motor, autonomic, affective, and arousal responses to sensory stimuli. The zona incerta has ­top-down projections from the posteromedial cortices (Parvizi, Van Hoesen, Buckwalter, & Damasio, 2006). It is heavily interconnected with the thalamus and hypothalamus. It has projections to the substantia nigra and it receives input from the PAG, the deep layers of the SC, and directly from the spinal cord. It has reciprocal connections with the amygdala and the basal forebrain (Mitrofanis, 2005). It influences visceral activity, arousal, attention, orienting, posture, and locomotion (Mitrofanis, 2005). It has a role in the control of sexual cycles, functions, and motor behaviors. The zona incerta is in a position through its widespread connectivity to integrate responses to interoceptive and exteroceptive stimuli. SUMMARY AND CONCLUSIONS

The neurobiology-based integrated hypotheses about the impact of early trauma on clinical presentations many years later are essential, as otherwise the symptoms can fail to make any sense to the therapist whose incomprehension will evoke pessimism in the patient or client. It is also helpful to have a framework in which to view new research findings as otherwise the mass of factual information is daunting. If apologies are due to specialist neuroscientists who feel that their particular areas of expertise and interest have not been given a proper explanation, it is to be hoped that they will at least find here some new hypotheses to pursue with critical rigor, even if only to disprove them. REFERENCES Aldridge, J. W., Berridge, K. C., & Rosen, A. R. (2004). Basal ganglia neural mechanisms of natural movement sequences. Canadian Journal of Physiology and Pharmacology, 82(8–9), 732–739. Alexander, G. E., Crutcher, M. D., & DeLong, M. R. (1990). Basal ganglia-thalamocortical circuits: Parallel substrates for motor, oculomotor, “prefrontal” and “limbic” functions. Progress in Brain Research, 85, 119–146. Allman, J. M., Tetreault, N. A., Hakeem, A. Y., Manaye, K. F., Semendeferi, K., Erwin, J. M., . . . Hof, P. R. (2010). The von Economo neurons in frontoinsular and anterior cingulate cortex in great apes and humans. Brain Structure & Function, 214(5–6), 495–517. Bandler, R., Keay, K. A., Floyd, N., & Price, J. (2000). Central circuits mediating patterned autonomic activity during active vs. passive emotional coping. Brain Research Bulletin, 53(1), 95–104. Brand, M., Eggers, C., Reinhold, N., Fujiwara, E., Kessler, J., Heiss, W. D., & Markowitsch, H. J. (2009). Functional brain imaging in 14 patients with dissociative amnesia reveals right inferolateral prefrontal hypometabolism. Psychiatry Research, 174(1), 32–39.

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CHAPTER 9

Shame and the Vestigial Midbrain Urge to Withdraw Frank M. Corrigan

Shame is a soul eating emotion. —C. G. Jung (2009)

The basic emotions generated in the midbrain and hypothalamus such as RAGE/ anger, FEAR, CARE, LUST, PLAY/joy, PANIC/separation distress, and motivational SEEKING (Panksepp, 2000; the primary process affective systems are expressed in upper case) are distinguished from shame, which is created by an interaction of basic emotions with higher cognitions (Panksepp, 2011). The uncertainty over the degree of overlap between basic and higher processes is reflected by shame being seen by some as a social emotion (Hareli & Parkinson, 2008), made possible by the evolutionary development of the forebrain, while others stress its more fundamental nature: for example, Nathanson (1992), citing the work of Silvan Tomkins. We propose that shame is generated in the midbrain but requires social learning for its contextual triggering. In the layered organization model of defense described by Prescott, Redgrave, and Gurney (1999), cognitive analysis is performed by the frontal cortex while contextual depth is added at the level of the hippocampus and septum. Conditioned emotional responses are generated by the actions of the hippocampus and septum on the amygdala, which, in turn, induce physiological change through its midbrain projections. Threat stimuli activate the midbrain and hypothalamus to initiate active or passive defense responses. An emotional response to a social threat involves the appropriate sensory cortices, frontal cortex, hippocampus and septum, midbrain, and hypothalamus. The amygdala and the bed nucleus of the stria terminalis (BNST) 173

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communicate some of the social contextual information to the midbrain, from which an affective response can be generated. We propose that the two forms of shame described as healthy and toxic by Bradshaw (1993) both have mesodiencephalic components and specific cortical interactions. We also propose that shame, rather than separation distress, can be the first response to a social attachment or interpersonal injury and that this distinction has important clinical implications. The affective experience of abandonment can be followed by the separation distress (grieving) sequence of protest and despair or it can initiate shame. This gives shame an individual avoidant character, which leads to other defense responses in the way that the protest of loss can lead to fight or flight responses. Shame is the emotion that accompanies the failure to have defended the self at the center of its peripersonal space from either physical or social threat and the behavioral component is the urge to withdraw, to hide. Shame recruits circuits formed for hiding from physical danger for avoidant responses to the failure of social belonging.

THE EXPERIENCE OF SHAME AND THE URGE TO HIDE

The initial shame response is of a physiological shock or jolt combined with a loss of capacity for clear thinking, which indicates its primarily subcortical origin: it can be experienced as if it is a painful blow to the body. The jolt or blow is then followed almost immediately by, or is accompanied by, an urge to hide; wanting the ground to open up and swallow; and by a feeling of being small and powerless (Tangney & Dearing, 2002). At this point, there is no capacity for joy and the self feels worthless. Because the experience is so aversive, the sufferer can quickly move on to avoidance, withdrawal, aggression to others, or attacking the self: the compass of shame (Nathanson, 1992). Even before this defensive reaction to the experience, it can be seen that shame is a multidimensional response with an initial painful jolt; an urge to hide; a loss of the capacity for enjoyment; and an awareness of the self as defective. The Internalized Shame Scale (Cook, 2001) has items pertinent not only to failure and social exclusion but also to insignificance, personal defectiveness, emptiness, and lack of fulfillment. The urge to hide is expressed in the overpowering dread that one’s faults will be revealed in front of others; the yearning to shrink away from a mistake; the wish for the earth to open up and swallow; and the feeling of being very small (Cook, 2001). The trigger to shame can be the recognition of the loss of qualities required for social inclusion: the highlighting of deficits in social attractiveness (Gilbert, 2002). Curiously, shame may also occur in someone being praised who feels that the other’s assessment of his worth is higher than his own appraisal: the incongruity of valuation is sufficient to elicit the emotional response. Shame is distinct from the pain of loss in bereavement, as there may be no feeling of worthlessness with grief. Although there is cortical elaboration of the criteria required for social inclusion, the peritraumatic shame response is fundamentally subcortical and can be elicited by being treated with contempt or derision, evident in facial expressions and behaviors. Thus, the infant who is sexually abused can experience the toxic form of shame long before she has the words for the concepts of worthlessness and social rejection.

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This response to the inflicting of pain and the stimulation of disgust by a more powerful person is activating systems originally developed for living in an environment where predators were active. The survival function is through the impulse to stop going forward; to be camouflaged; to hide away from the potentially lethal eyes of dangerous animals. Shame is activating pathways originally involved in the defenses of cringing and hiding. It leaves in humans an ontological residue: the self as inferior, bad, annihilated, or identified with the perpetrator (Cloitre, Cohen, & Koenen, 2006).

Attachment and Social Learning

Attachment typically begins in the mother–infant dyad but broadens to promote and reward inclusion in a larger social group as the individual grows. The need to attach to a group or society requires greater development of the cortical mantle for assimilation of the rules for integration. The SEEKING for belonging is based in the mesolimbic dopamine system, which underlies a positively valenced approach (Alcaro & Panksepp, 2011); and attachment itself requires the CARE and nurturance systems of the periaqueductal gray (PAG), the preoptic area, the BNST, the ventral tegmental area (VTA), and the anterior cingulate cortex (ACC; Panksepp, 2011). Likewise, the fear of loss of attachment to a group or society requires more appraisal ability than that required in infancy and needs cortical maturation for modulation of subcortical defense responses, but it is still ultimately based in the primitive separation distress organizations of the brain. The sudden feeling of exclusion from a group, or the awareness of a failure to meet the standards for inclusion, is dependent on the cognitive capacity to assess the group’s requirements for fitness to belong, and an ability to assess the dangers of exclusion. While these appraisals are cortically based, the physiological response is more fundamental. The social attachments, fears of ostracism, and feelings of distress at loss of inclusion have their neurobiological bases in brain systems designed to ensure healthy attachment, learning of emotion regulation, and development of socialized behaviors, from infancy onwards. Shame is used in the mother–infant interaction to promote safe and acceptable behaviors through downregulation of the arousal accompanying positive affect (Schore, 1994; Siegel, 1999). Schore (1994, p. 203), citing the work of Tomkins on the inhibition of positive affect, describes shame as representing the “rapid transition from a preexisting high arousal positive hedonic state to a low arousal negative hedonic state.” The awareness of oneself in the eyes of others confers the ability to feel exposed and devalued: the infant who discovers his image in a mirror and turns away with eyes averted and head hanging (Nathanson, 1992). The averting of the eyes, the slumping of the shoulders, and the facial vasodilatation may be seen to occur together in babies, according to Cook (2001), and this would argue for shame as an innate affect. Benign or healthy shame is differentiated from humiliation by the lack of anger in the transaction and it lowers arousal in a relatively gentle way. It markedly contrasts with the more malignant or toxic experience of shame arising from early attachment trauma or abuse, which has a profound effect on the feelings about the self. Toxic shame (Bradshaw, 1993) not only has failure and social exclusion

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components but also an ontological dimension: it is linked with a fundamentally negative self-valuation. The basic positive affects are SEEKING or general motivation; LUST/sexual drive; CARE and nurturance; and PLAY or joy (Panksepp, 2011). All of these can be reduced by shame, although the physiological accompaniments of the transition states have not been confirmed. The basic emotional systems that are usually experienced as negative are RAGE or anger; FEAR; and PANIC or other separation distress (Panksepp, 2011). Anger and fear can be reduced by internal shame, not just by external humiliation, and that would also apply to the expression, if not the experience, of grief. Other ways of downregulating high levels of emotion exist, but those that have been studied (e.g., Wager, Davidson, Hughes, Lindquist, & Ochsner, 2008) are top-down cortical modulators. Shame could either be the independent affect that can displace any of the others or it could be the emotion accompanying the withdrawal from an interaction in which the emotional expression is inappropriate or damaging. When fear and anger lead to successful flight or fight, they leave no obvious residues. When the defense response is obstructed and/or there is a failure of defense, the submissive withdrawal would be accompanied by shame, especially if there has been defeat in an agonistic encounter with a conspecific. Context is therefore important in the damaging encounter as well as in the emotional responses. In response to a commentary differentiating anaclitic and introjective forms of depression, Watt and Panksepp (2009) expanded on the possible role of shame in the latter. The psychoanalytic concept of anaclitic depression relates to the psychological consequences of early loss or separation from a primary caregiver and the associated feelings of abandonment. In contrast, introjective depression results from harshly self-critical thinking and superficially appears to have no link with attachment failure. However, Watt and Panksepp (2009) argue that shame is a cognitive extension of separation distress, which requires the complexity of a self-image, a sense of exposure, a sense of deficiency, and a sense of unworthiness and defectiveness, and that this complex affective-cognitive structure contributes to introjective depression. This distinction supports the possibility of two distinct affective responses to isolation and abandonment: the child who cannot elicit his mother’s attention, even though she is present, can experience painful abandonment as separation distress or as the worthlessness of shame. The window of tolerance model of responses to attachment obstruction can be adapted for shame responses as in Figure 9.1. The phases of attachment distress modified are based on Bowlby (1969).

Clinical Implications of High Levels of Shame

High scores on shame scales are found with depression, increased suicide potential, anxiety, trait anger, eating disorders, and substance abuse (Cook, 2001). These are behavioral or phenomenological categorizations that carry no information about etiological factors. However, in substance abuse populations, severity of childhood sexual abuse is associated with higher scores on the Internalized Shame Scale (Cook, 2001). Proneness to shame is higher in women with borderline personality disorder, often seen as a disorder of traumatic attachment (e.g., Liotti & Pasquini, 2000), than

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in those with social phobia, in whom it is still higher than in healthy controls (Rüsch et al., 2007). Shame is thought to contribute to a range of affective disorders—depressive and dysthymic—and it is striking how many of the anxiety disorders involve fears of behaviors, which may be publicly humiliating: for example, vomiting, being incontinent, or fainting. Shame is often a significant emotional component of the state of tonic immobility (TI), which significantly worsens the outcome of traumatic events during which it is experienced (Bovin, Jager-Hyman, Gold, Marx, & Sloan, 2008; Lima et al., 2010). TI is mediated in the midbrain by, among other structures, the ventrolateral and lateral columns of the PAG, the cuneiform nucleus, and the superior colliculi (SC; Vieira, Menescal-de-Oliveira, & Leite-Panissi, 2011). We hypothesize that the dorsomedial column of the PAG is also involved when shame is prolonged. Cloitre et al. (2006) highlight the role of shame in the persisting and pervasive response to traumatic experience. They consider shame to arise when the person feels himself to have failed in the task of self-preservation. Compared to appraisals of what others would have done, there has been a failure to protect the self. In the resting-state hypothesis of major depressive disorder (Northoff, Wiebking, Feinberg, & Panksepp, 2011), increased activity in midline brain regions predisposes to repetitive, negative, self-related thinking; feelings of hopelessness and worthlessness; and an increased self-focus. These are also characteristic of toxic or posttraumatic shame. The resting-state hyperactivity of midline cortical areas is not deactivated by exteroceptive stimuli in those with major depressive disorder according to the severity of their hopelessness. In toxic shame states, it is also difficult to be distracted from hopelessness about the self and it will be interesting to see in the future if there are different patterns of rest–stimulus interaction in introjective and anaclitic depressions according to the level of internal shame. If shame rather than separation distress is the emotion dominant in some cases of depressive disorder, they may share neurobiological characteristics. The defeated posture of chronic social defeat stress is mediated by activation of the kappa opioid system (McLaughlin, Li, Valdez, Chavkin, & Chavkin, 2006), of importance also in separation distress and its effect on depressive mood (Watt & Panksepp, 2009). The regional hyperactivity during the resting state is seen in depression in the perigenual ACC (PACC), the ventromedial prefrontal cortex (VMPFC), the thalamus, and some areas of the basal ganglia and the midbrain (Alcaro, Panksepp, Witczak, Hayes, & Nortoff, 2010). The concept of “hijacking” of the cortical functions by subcortical emotional systems (Northoff et al., 2011) is also used in sensorimotor psychotherapy (SP; Ogden, Minton, & Pain, 2006) to describe the impact of triggered peritraumatic states. Although these often relate to terror or rage, they can also involve shame, disgust, or separation distress. In contrast to the studies of depressive disorders, there was no resting-state abnormality in the perigenual cortex, which has reduced activation in response to script-driven imagery in PTSD (Shin et al., 2009), but this area also had reduced thalamic connectivity (Yin et al., 2011b). What is shown by brain imaging in the posttraumatic states may depend on the main emotions hijacking cortical function and leading to homeostatic efforts at suppression. The overlap in hyperactivity in the ventromedial areas of prefrontal cortex (PFC) in the resting state in depressive and posttraumatic disorders supports the possibility that both diagnostic categories can share a subcortical overwhelm of cortical systems.

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TOXIC, PERITRAUMATIC, AND POSTTRAUMATIC SHAME

Does toxic shame always arise from experiences that would commonly be considered to be traumatic and/or abusive? There is not enough evidence on the genesis of toxic shame to answer this question confidently. “Trauma shame” may be a useful alternative term for those who find the word “toxic” aversive for the high arousal, painful, transformation of affective state. Any emotionally painful experiences can be considered toxic when they bestow a negative valence on the self, precipitate long-term unpleasant ruminations about the failure of the self, and are accompanied by an urge to withdraw and hide, far beyond the conclusion of the events stimulating the shame response. It is possible that this combination of effects is most likely when defense responses are activated but obstructed or overwhelmed. Shame can also occur belatedly after a trauma when there has been a cognitive reevaluation of the event. Remembered images may then be instrumental in eliciting the physiological responses. The precuneus in the medial parietal cortex, active during memory-related imagery (Fletcher et al., 1995), is connected with areas important in autobiographical memory including the posterior cingulate and retrosplenial cortices (Cavanna, 2007). Three regions of the precuneus—sensorimotor, cognitive, and visual—are defined by resting-state functional connectivity (Margulies et al., 2009). The precuneus is therefore a cortical region in which memory-related imagery can be associated with episodic memory, body sensations, motor output, and with altered feelings about the self in its space. Shame-associated loss of thinking clarity could result not only from subcortical dominance but from a shift in activity from prefrontal to parietal areas. However, the main distinction between the two forms of shame relates to the purported physiology: social learning shame in an interaction is a downregulator of positively valenced arousal whereas malignant shame is a recurrent high arousal state. Cringing or shying is an activating response with increased blood pressure and heart rate.

The Tectocuneiform Cringe

Dean, Redgrave, and Westby (1989) chemically stimulated the SC of rats and observed not only movements for orienting and approach, but movements for avoidance. They described exaggerated startle, backward shuffling or jumping, and flinching responses to innocuous stimuli. Under some conditions it is better to avoid or escape than to orient to a stimulus which is potentially life threatening. The colliculi are wired to rapidly respond to visual stimuli by orienting toward, perhaps pursuing and biting, or orienting away from and avoiding. The SC has a projection to the cuneiform nucleus, a tectocuneiform projection, which is particularly responsive to a looming stimulus. We hypothesize that the subjective counterpart is the wish to be small or to disappear: the core of the shame response (Tangney & Dearing, 2002). One of the immediate reflex responses to a rapidly looming unavoidable impact would be closure of the eyes: also an urge with the shame response. Cringe and hide responses are avoidance defenses generated when the colliculi register stimuli indicative of potential catastrophe. It is not known whether there is a human tectocuneiform cringe equivalent to that

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which occurs in rats so it is used here partly as a construct to express the hypothesized midbrain immediate urge to contract. However, the physiological phase of shame involves vasodilatation, the eyes being pulled away from the object of attention, loss of tone in the head and neck, and a momentary loss of the ability to think (Cook, 2001). These features are consistent with midbrain dominance in the response.

Cortical Modulation of the Colliculi

In the macaque there are corticotectal projections (to the colliculi) from many areas of cortex involved in vision, eye movements, and visually guided movements of the upper limbs (Lock, Baizer, & Bender, 2003). When a monkey’s SC are stimulated while the brain is being scanned with functional MRI (fMRI) the frontal eye fields and the lateral intraparietal region (LIP) are prominent amongst the cortical areas activated (Field, Johnston, Gati, Menon, & Everling, 2008). Involvement of the somatosensory cortex, auditory cortex, motor cortex, and many areas of visual cortex, points to a multimodal role for collicular responses. In terms of emotional components it is interesting that stimulation of the SC evoked activation of both anterior and posterior cingulate cortex (Field et al., 2008). The subliminal presentation of fearful facial expressions activates a pathway from the SC through the pulvinar to the amygdala, which increases arousal through projections to the locus coeruleus (LC; Liddell et al., 2005). The sight of a contemptuous gaze, we hypothesize, will activate the tectocuneiform cringe: the SC project to the cuneiform nucleus which stimulate autonomic centers in the medulla. There are no direct influences of the ACC on the SC to modify the rapid response to a disapproving or critical gaze. Instead the anterior cingulate and medial prefrontal cortices influence the dorsolateral column of the PAG to which the SC projects (Price, 2009). The active defense response of the dorsolateral PAG is triggered by nonphysical stressors (Keay & Bandler, 2001) and is, therefore, equipped to respond to the social stress identified by the SC. Modulation of the emotional impact of what is seen depends on cortical dampening of the PAG, the cuneiform nucleus and the LC. What is seen is seen and attended to; what is felt may be stored with the visual memory to return to awareness repeatedly.

Diffusion of the Cringe

Awareness of the pain of the shaming experience requires the nociceptive circuits through the ventrolateral PAG and associated brain stem nuclei with cortical components in anterior cingulate and anterior insular areas. The initial pain response is likely to arise in the brain stem as occurs with exposure to a physically painful stimulus (Petrovic, Petersson, Hansson, & Ingvar, 2004). The diminution of loss and interest, considered primary by some authorities on healthy shame (e.g., Schore, 1994), is hypothesized to be a consequence of a sudden shift in valence of the mesolimbic dopamine system. This may be the result of neurochemicals such as those active at kappa opioid receptors, as occurs in some states of separation distress (Watt &

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Panksepp, 2009). There may also be an immediate reduction in dopamine transmission in this pathway from the VTA to the nucleus accumbens through the influence of the lateral habenula and the rostromedial tegmental nucleus (RMTg; Jhou, Fields, Baxter, Saper, & Holland, 2009). A more protracted increase in mesolimbic dopamine links aversive stimuli with their contexts through projections from the ventral hippocampus (Valenti, Lodge, & Grace, 2011). The immediate cringe, flinch, or horrified startle of shame can be followed by the slightly later urge to hide which, we hypothesize, is dependent on the avoidance pathways through the dorsomedial column of the PAG. Stimulation of the dorsomedial column of the PAG elicits high arousal, not low arousal, avoidance behaviors (Borelli & Brandão, 2007). This makes sense of Nathanson’s (1992) compass of shame. Hiding/ withdrawal is mediated by the dorsomedial column and its links (possibly indirect through the ventrolateral column of the PAG) with the RMTg; shutting off the positive affect capacity of the mesolimbic dopamine system. Attacking the self and attacking the other arise from the active defense fight response of the lateral/dorsolateral PAG. Whether the attack is directed inwards or outwards depends on the learned cortical regulators: habitual patterns of suppression or expression. Nathanson (1992) sees withdrawal as the rapid response; avoidance as the longer term strategy. Although he considers them to be accompanied by auxiliary affects which are activating, we include low arousal shame to represent the state of chronic avoidance or long-term social withdrawal. The initial response is being followed by diffusion of the jolt through other columns of the PAG and other brain stem areas: it takes a while for the cortex to catch up and the intervening period is experienced as one of confusion. There is obvious survival value in then ruminating about the reason for hiding: emerging from the lair before the predator has departed to find a meal elsewhere would not promote longevity. There is a low arousal, curl up and hide, shame state which can be prolonged in an energy-conserving way of being which, although dysphoric, is less aversive than the acute high activation horror of the initial realization. It will have also hypothalamic and cortical components. The BNST is active in attachment, in social and mating behaviors (Wood & Swann, 2005), and in sustained fear (Walker, Miles, & Davis, 2009). It has extensive connections with medial cortical areas, the amygdala, the hypothalamus, and the midbrain. Its involvement in shame is most likely to be during the protracted phase of heightened vigilance.

Frontal and Parietal Cortices and the Body’s Response to Looming Stimuli

We have seen above that the frontal eye fields interact with the lateral intraparietal area in the control of eye movements. Also, mirror neurons are present in the anterior part of the inferior parietal cortex and an area of premotor cortex with which it is interconnected (Yamazaki, Yokochi, Tanaka, Okanoya, & Iriki, 2010). There are other frontoparietal interactions in the defense of peripersonal space: the space around the body in which objects can be easily grasped. An area of the posterior parietal cortex encodes for the posture and movements of parts of the body and contributes to the multisensory information processed in other parietal and ventral premotor areas (Holmes & Spence, 2004). For defensive responding to intrusions upon the peripersonal space the ventral intraparietal area (VIP) and a polysensory zone (PZ) of the

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precentral gyrus are interconnected for mapping the representation of the space around the body (Graziano & Cooke, 2006). It is important not to have an eye damaged by an approaching umbrella in a crowded street; not to collide with the wing mirror of a car parked on the pavement/sidewalk; and not to slip up on a discarded banana skin. The avoidance tasks are usually achieved effortlessly and without emotion. Failure to protect one’s peripersonal space through misadventure, clumsiness, or lack of attention can be embarrassing for the sufferer of the misfortune and amusing for onlookers. Shame can intrude when the cortically directed rapid movements lose their grace and fluidity and are replaced by cringe-inducing encounters with objects. In SP (Ogden et  al., 2006) defense movements which were obstructed at the time of a traumatic experience are mindfully accessed and completed. Initially, these may have the character of the cortically derived defensive behaviors described by Graziano and Cooke (2006): withdrawing or blocking movements. There may be another parieto–frontal interaction in the production of defensive speech such as “Get out of my space”; but this also may not be accompanied by much affect. In SP the movement urge may be explored until it connects with the midbrain-based fight or flight or freeze response and with the associated hypothalamic energetic change. It is then that the full force of the obstructed movement can be encountered and released. The frontoparietal movement tendency connects with deeper layers of defensive responding: from the spinal cord reflexes through the mesodiencephalic emotional defense responses, to the basal ganglia sequences in loops through the thalamus. It is then that the valence of the mesolimbic system can switch to triumph, release, and relief. The resulting state has markedly different cognitions, emotions, energy level, and drive, as a result of processing which has embraced the hierarchical organization of defensive responding rather than focusing on one layer of it. The movements induced by stimulation of the PZ of the PFC are different in character from the cringe response of the midbrain to a looming stimulus and they can occur without emotion. We therefore consider that the urge to hide which accompanies shame is not based at the frontoparietal level although there is an interaction between those multisensory detection areas and the midbrain. Premotor and parietal areas link peripersonal space with arm, neck, face and mouth movements through corticospinal, rather than corticotectal, tracts (Rizzolatti & Luppino, 2001). In therapy it is the linking of the frontoparietal action tendencies with the interoceptive loops through the insular cortex and ACC which brings in the affective memory components of the amygdala and its mesodiencephalic links. Completion of the movement in a purely motor way has no clinical benefit. Nothing will change without mindful attention to all somatic components of the memory sufficient to involve all levels of the body memory. Only when the mesodiencephalon is involved will there be change in the affective valence of the mesolimbic system with secondary effects on the cognitive cortico-striato-thalamic loops.

Brain Imaging Studies of Shame

We know of no study specifically concerned with the brain imaging of shame as an affective state, whether healthy or toxic. Takahashi et al. (2004) specifically compared brain responses to guilt and embarrassment through self-referential statements. Guilt

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sentences reflected intentional violation of social norms: actions that were dishonest or potentially harmful. Embarrassment statements related both to inadvertent actions that were potentially shaming—incontinence, inadequate covering by clothing—and to inadvertent violation of social standards. The medial PFC involvement was greater with guilt—as befits its more cognitive nature—while the visual cortex was more involved in embarrassment—in line with the role of real or imagined observers. Bilateral hippocampus activation with embarrassment, when compared with guilt, supports Nathanson’s (1992) concept of the shame-related scripts bringing immediately to awareness other relevant prior shame experiences. Guilt about one’s own deficient social behavior and indignation about another’s deficient social behavior are both primarily cortical: anterior temporal and subgenual cingulate for guilt; anterior temporal and lateral orbitofrontal for indignation (Green et al., 2010). Although there is no consistent amygdala involvement there is also no evidence of brain stem activation in these studies of guilt and embarrassment. However, witnessing others in embarrassing situations activated the midbrain PAG as well as the social pain areas of ACC and anterior insula (Krach et al., 2011). Also, the hypothalamic component of social exclusion is evident when attenuated by the imaginary presence of a supportive attachment figure (Karremans, Heslenfeld, van Dillen, & Van Lange, 2011). In major depressive disorder, increased dominance of the default mode network (DMN) is linked to maladaptive rumination (Hamilton et al., 2011). The example given by the authors, “How often do you think about all your shortcomings, failings, faults, mistakes?” suggests a role for toxic shame in the maintenance of some depressive disorders. Switching between the DMN and the task-positive or centralexecutive network is dependent on an area of right fronto-insular cortex (Hamilton et al., 2011; Sridharan, Levitin, & Menon, 2008) which may also be a point of interaction of distressing emotional symptoms and their therapeutic modulation. Changes in emotions and body feelings rather than cognitive restructuring are required for altered activation of this area. The Trier Social Stress Test is likely to be difficult for those with high levels of shame. One hour after this task the amygdala shows enhanced resting-state functional connectivity with the posterior cingulate cortex and the precuneus (Veer et al., 2011). It is proposed that a cortico-limbic circuit, involving the amygdala, the hippocampus, the posterior cingulate cortex, and the precuneus, could contribute to the emergence of intrusive and unwanted memories as can occur in posttraumatic stress disorder (PTSD; Veer et al., 2011): this may also apply in toxic shame. Social stress of a potentially shaming type is having a persisting effect on the connectivity of the amygdala with self-related structures. If this can happen in the relatively harmless context of an academic laboratory the likelihood is that the effect will be more severe and persistent if painful social humiliations occur in “real life.” The precuneus and posterior cingulate cortex are already significant in the DMN of children (Thomason et al., 2008) but become more connected with prefrontal areas with maturation (Supekar et al., 2010). Even if the subcortical contributions to the DMN are limited, the connections of the medial prefrontal and posteromedial cortices with the emotion-generating regions of the mesodiencephalon permit the emergence of recurrent, intrusive, unpleasant memories. For example, the retrosplenial cortex has afferent inputs from the basolateral amygdala and orbitomedial PFC and has outputs to

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the nucleus accumbens and the PAG (Parvizi, Van Hoesen, Buckwalter, & Damasio, 2006). Patients with complex PTSD secondary to early-life trauma have reduced connectivity of the posterior cingulate cortex/precuneus part of the DMN (Bluhm et al., 2009). Trauma in early life interferes with the emerging connectivity of the DMN, especially the links between the posterior cingulate cortex and the VMPFC (Daniels, Frewen, McKinnon, & Lanius, 2011). Disruption of the anterior–posterior integration of the DMN by early trauma may be evident only at the cortical level but will be relevant at the subcortical level also. Different patterns of DMN connectivity in different clinical disorders may be a reflection of the symptom-based nosology used in imaging research: it would be interesting to know if the core affective residues of traumatic experiences reflected in instruments such as the Internalized Shame Scale (Cook, 2001) would correlate with disruption of the self-related networks. The subcortical hyperactivity in major depression in the resting state has been clearly demonstrated by the meta-analysis of Alcaro et al. (2010) and developed in the hypothesis of Northoff et al. (2011). The nested hierarchy model may also apply to shame: the basic response in the midbrain is given contextual and cognitive features as it reappears in the limbic and cortical levels. If so, we would predict involvement of the BNST, the amygdala, the hippocampus, and parietal as well as prefrontal regions of cortex.

Neurochemical Studies of Shame

We know of no specific studies of the neurochemistry of shame. The putative links with depression might implicate dynorphins active at kappa opioid receptors as has been proposed for linking separation distress with depressive disorder (Watt & Panksepp, 2009). Social defeat stress induces immobility and analgesia mediated by the kappa opioid system (McLaughlin et al., 2006). One of the defeat behaviors is crouching, with four paws on the ground, but not orienting toward the aggressor mouse (McLaughlin et  al., 2006). The submit response when there is an apparent urge to be small and crouch low could be studied to see if there is dominance of the dorsomedial PAG, the colliculi, and the cuneiform nucleus when compared with the flight or freeze responses. It would be assumed that the affective component would be the rodent precursor of shame. The kappa opioid dynorphin system is more active with repeated social defeat; whereas peptides such as corticotropin-releasing factor (CRF) and brain-derived neurotropic factor (BDNF) are proposed to mediate the more immediate effects (McLaughlin et al., 2006). CRF-containing neurons projecting from the hypothalamus specifically to the dorsomedial column of the PAG initiate avoidance behaviors (Borelli & Brandão, 2007). Brain dynorphins, which activate the kappa opioid receptors, are increased by stress and by CRF, and the dysphoric state elicited is amenable to alleviation by potentially addictive drugs (Bruchas, Land, & Chavkin, 2010). As CRF is one of the mediators of the relationship between stress and dynorphins; as the CRF changes are secondary to endocannabinoids; as there are functional links between the kappa opioid system and endocannabinoids; and as early maternal deprivation alters later responses to exogenous cannabinoids (Marco,

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Adriani, Llorente, Laviola, & Viveros, 2009), we consider that the different phases of separation distress will have altered neurochemical characteristics centered on these systems. Shame, an alternative emotional response to social attachment trauma, may have similar neurochemical substrates. Flushing of the face is an accompaniment of certain states of embarrassment and anger, both of which may be involved in toxic shame, so it is interesting to consider the effects of the neuropeptide substance P that is found in the midbrain, the basal ganglia, the hypothalamus, and the amygdala (Lieb et al., 2002). A brief period of vasodilatation manifest in flushing of the face and neck can be induced by a substance P infusion (Herpfer et al., 2007; Lieb et al., 2002). There are also impairments of concentration and short-term memory (Herpfer et al., 2007). Panksepp (2011) highlights substance P in the medial amygdala, the BNST, the hypothalamus, and the PAG in the generation of rage and anger. Capsaicin activates the transient receptor potential vanilloid-1 (TRPV1) receptor, which is widely distributed in the brain. When it is administered systemically, it induces a delayed hyperthermia (Steenland, Ko, Wu, & Zhuo, 2006) and a similar pattern is seen when it is injected into the preoptic area of the hypothalamus. An unusual case report of a penetrating stab wound to the head, in which the residue of the weapon reached the right anterior hypothalamus, described the assault victim’s feeling of inner heat followed by heat-induced excessive sweating, which was a source of “considerable fatigue and embarrassment” (Fabbri et al., 2010).

Submission, Misattunement, Abandonment, and Failure

Nontoxic shame can result from defeat. “Their heads are going down” is a way in which sports commentators communicate the obvious loss of heart of a team whose best efforts are being met with no success. In an agonistic encounter, the feeling of being overwhelmed and rendered helpless by a more powerful opponent can induce shame and self-loathing: “I’m weak, I’m pathetic, I’m alone, and I’m a loser.” Energy and strength are dissipated. Shame also arises from misattunement: a communication is felt to be wide of the mark or emotionally incongruent in the interaction—and the realization is accompanied by a sense of failure, and by the urge to turn away, to withdraw, and to hide. The initial jolt can occur from a realization, a verbal communication, a facial expression, a gesture, and a painful or disgusting physical sensation. It can also arise from memories of all of these such that traumatic experiences continue to elicit the physiological state of malignant shame many years after the painful episodes. Clinically, abandonment can either lead to separation distress or to shame. The young child who finds himself or herself alone and unprotected may experience terror. If the sudden awareness is of the emotional absence of any caregiver, he or she may instead experience shame of the toxic or peritraumatic variety. Tracking back, in therapy, to the moment of realization of aloneness—to isolate the shame or separation distress response—avoids targeting the secondary or tertiary emotional responses without changing the underlying energetic shift.

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IMPLICATIONS FOR TREATMENT OF SHAME ACQUIRED DURING TRAUMATIC EXPERIENCES

Shame that is the consequence of a horrifying event is difficult to treat when it has settled into its long-term pattern of self-loathing. It may be most amenable to change if the high arousal state at its inception can be held with therapeutic care and concern and warmth until the physiological activation reduces. Silence and nonresponsiveness in the therapist will magnify shame and encourage reversion to withdrawal or a switch to self-attack (Nathanson, 1992). It is necessary to be seen by at least one nonshaming person (Bradshaw, 1993) or for the client to be aware of the therapist’s positive regard for him or her (Cloitre et al., 2006). This model predicts that toxic shame will not be readily amenable to exposure strategies: the memory induces the rapid response that progresses into the defensive pattern with little time for adaptation. It is necessary to slow down the sequence in the presence of a caring and nonjudgmental therapist to detoxify the initial painful blow to the self: the usually ensuing pattern is then not required for management of the pain. Cloitre et al. (2006) combine shame narrative exploration with the building of positive regard for the self. Mindfulness and compassion will strengthen the anterior–posterior links in the default network, which are reduced by early trauma (Daniels et  al., 2011). Mindfulness elicits activation of the dorsomedial PFC (Lanius, Bluhm, & Frewen, 2011) and increases its connectivity (Jang et al., 2011). Compassion recruits the posteromedial cortices (Immordino-Yang, McColl, Damasio, & Damasio, 2009). Even a short mindfulness-based training alters brain responses to physically painful stimuli, reducing their unpleasantness (Salomons & Kucyi, 2011). There are no studies of the impact of mindfulness meditation training on the experience of shame. It could be predicted that nonjudgmental attention to, and acceptance of, the experience of the emotion will reduce the unpleasantness of it. Expecting a smile of approval and instead being shocked by a glower of disdain would represent unexpected reward omission of the kind which, in animal models, activates the lateral habenula and RMTg (reviewed in Jhou et al., 2009). These inhibit the mesolimbic system crucial for social playfulness (Siviy & Panksepp, 2011), for seeking safety, and for appetitive motivation and drive (Alcaro & Panksepp, 2011). That shift could occur with disappointment, deflation, loss of interest, and loss of enjoyment of play, but without the pain and self-loathing of the toxic shame state. Perhaps it is only when other structures such as the dorsomedial PAG, the parabrachial nucleus, the cuneiform nucleus, the anterior insular cortex, and areas of parietal cortex become involved that the shame begins to fester. If so, it may be that toxic, malignant, or trauma shame always arises when the defense responses are activated, but obstructed, by an experience that is then categorized in the body as traumatic.

The Negative Valence of the Self: The Influence of Shame

The default state of consciousness is that which arises in the brain when there is no specific mental task to perform. Imaging of those areas that become activated during

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this default state shows an overlap with those involved in awareness of the self: midline cortical and subcortical systems (Panksepp & Northoff, 2009). Thus, when we do not have much to occupy our minds, our brains will take us into self-referential thinking, musing, remembering, and planning. We also dwell on what is familiar and think of others in our social worlds. A meta-analysis of studies indicates that the PACC is most closely involved with self-processing (Qin & Northoff, 2011). Part of this area—the pregenual ACC—is relatively inactive in PTSD during emotional tasks and that functional attenuation liberates subcortical areas to increase physiological arousal: the relative increase in subgenual ACC activity may stimulate autonomic changes (Vogt, Aston-Jones, & Vogt, 2009). The subgenual cingulate cortex is one of the areas highlighted in studies of social exclusion—especially in children (Moor et al., 2012). Complex trauma sufferers whose default state is one of toxic shame have a feeling of disgust about the self, which points to involvement of the parabrachial nucleus and/or the anterior insula. The latter is involved both in the experience of disgust (Jabbi, Bastiaansen, & Keysers, 2008) and the interoceptive processing that contributes to the self through coactivation with the perigenual ACC (Taylor, Seminowicz, & Davis, 2009). There are connections between the two areas, the insula and the parabrachial nucleus, which bypass the thalamus (Saper, 1982). While the parabrachial nucleus is favored by Damasio (2010) in the primordial feeling of the self, the other, the insula, is considered fundamental to the awareness of the self by Craig (2010). Both are intimately connected with the affective valence of the self and can link the substrates for disgust to the self-referential awareness. It has also been proposed that the PAG and the SC carry a fundamental map of the self, which The Window of Tolerance: Shame Responses to Attachment Obstruction High Arousal Dissociation (Protest)

Obstruction Of Urge to Attach SEEKING SAFETY (e.g. relief from pain, FEAR, RAGE, or GRIEF), SEEKING CARE/NURTURANCE, SEEKING PLAY

High Arousal Shame

(Detachment) Social Withdrawal & Dysphoria (Despair) Low Arousal Shame

Low Arousal Dissociation

Figure 9.1  The window of tolerance concept of Siegel (1999) and Ogden et al. (2006) adapted for shame. The urge to attach is seen as SEEKING (Panksepp, 2011) safety from homeostatic affects such as hunger and thirst; SEEKING relief of RAGE, FEAR, or PANIC/GRIEF; or SEEKING positive emotional experiences such as LUST, CARE, or PLAY. When the Urge to Attach is obstructed: instead of Protest there is High Arousal Shame; instead of Despair there is Low Arousal Shame; instead of Detachment (Bowlby, 1969) there is apparently normal functioning, which is impaired by a tendency toward social withdrawal and dysphoric ruminations on the defective self.

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can assimilate information from inside and outside the body and generate emotional responses (Panksepp, 2003). The most basic valence of the self could reside there in the core feeling of whether life can be approached with joy and vigor, or be avoided, hidden from, dowsed in alcohol or other substances, and met halfheartedly with no anticipation of reward and happiness. In toxic shame, the interoceptive loops through the brain stem and the body to the anterior insula and the PACC are loaded with disgust. This is qualitatively different from the downregulation of positive affect considered to impart social learning in healthy shame. The valence of the self is distinct from the felt reality of the self, which relies largely on circuits through parietal areas. The connections of the medial prefrontal and posteromedial cortices with the emotion-generating regions of the mesodiencephalon permit the emergence of recurrent, intrusive, unpleasant memories. Bringing the memories out of their lair, to show them that the predator has gone, will activate the safety signals of the BNST and the insula (Christianson et  al., 2011) to reset the affective valence of the self. Treating adults who have experienced trauma in childhood, which has burdened the self with concentric layers of toxic shame, necessitates not only diminishing the arousal stored in structurally dissociated defense response parts but also mollifying the disgust at each circle of the core self. Understanding what is happening at the neurobiological level will refine therapeutic techniques, some of which are discussed in the second part of this book.

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Jang, J. H., Jung, W. H., Kang, D. H., Byun, M. S., Kwon, S. J., Choi, C. H., & Kwon, J. S. (2011). Increased default mode network connectivity associated with meditation. Neuroscience Letters, 487(3), 358–362. Jhou, T. C., Fields, H. L., Baxter, M. G., Saper, C. B., & Holland, P. C. (2009). The rostromedial tegmental nucleus (RMTg), a GABAergic afferent to midbrain dopamine neurons, encodes aversive stimuli and inhibits motor responses. Neuron, 61(5), 786–800. Jung, C. G. (2009). The red book. New York, NY: Philemon Foundation & W.W. Norton. Karremans, J. C., Heslenfeld, D. J., van Dillen, L. F., & Van Lange, P. A. (2011). Secure attachment partners attenuate neural responses to social exclusion: An fMRI investigation. International Journal of Psychophysiology, 81(1), 44–50. Keay, K. A., & Bandler, R. (2001). Parallel circuits mediating distinct emotional coping reactions to different types of stress. Neuroscience and Biobehavioral Reviews, 25(7–8), 669–678. Krach, S., Cohrs, J. C., de Echeverría Loebell, N. C., Kircher, T., Sommer, J., Jansen, A., & Paulus, F. M. (2011). Your flaws are my pain: Linking empathy to vicarious embarrassment. PloS One, 6(4), e18675. Lanius, R. A., Bluhm, R. L., & Frewen, P. A. (2011). How understanding the neurobiology of complex post-traumatic stress disorder can inform clinical practice: A social cognitive and affective neuroscience approach. Acta Psychiatrica Scandinavica, 124(5), 331–348. Liddell, B. J., Brown, K. J., Kemp, A. H., Barton, M. J., Das, P., Peduto, A., . . . Williams, L. M. (2005). A direct brainstem-amygdala-cortical ‘alarm’ system for subliminal signals of fear. NeuroImage, 24(1), 235–243. Lieb, K., Ahlvers, K., Dancker, K., Strohbusch, S., Reincke, M., Feige, B., . . . Voderholzer, U. (2002). Effects of the neuropeptide substance P on sleep, mood, and neuroendocrine measures in healthy young men. Neuropsychopharmacology, 27(6), 1041–1049. Lima, A.A., Fiszman, A., Marques-Portella, C., Mendlowicz, M.V., Coutinho, E.S.F., Maia, D.C.B., Berger, W., Rocha-Rego, V., Volchan, E., Mari, J.J., Figueira, I. (2010). The impact of tonic immobility reaction on the prognosis of posttraumatic stress disorder. Journal of Psychiatric Research 44, 224–228 doi: 10.1016/j.jpsychires.2009.08.005. Liotti, G., & Pasquini, P.; The Italian Group for the Study of Dissociation. (2000). Predictive factors for borderline personality disorder: Patients’ early traumatic experiences and losses suffered by the attachment figure. The Italian Group for the Study of Dissociation. Acta Psychiatrica Scandinavica, 102(4), 282–289. Lock, T. M., Baizer, J. S., & Bender, D. B. (2003). Distribution of corticotectal cells in macaque. Experimental Brain Research, 151(4), 455–470. Marco, E. M., Adriani, W., Llorente, R., Laviola, G., & Viveros, M. P. (2009). Detrimental psychophysiological effects of early maternal deprivation in adolescent and adult rodents: Altered responses to cannabinoid exposure. Neuroscience and Biobehavioral Reviews, 33(4), 498–507. Margulies, D. S., Vincent, J. L., Kelly, C., Lohmann, G., Uddin, L. Q., Biswal, B. B., . . . Petrides, M. (2009). Precuneus shares intrinsic functional architecture in humans and monkeys. Proceedings of the National Academy of Sciences of the United States of America, 106(47), 20069–20074. McLaughlin, J. P., Li, S., Valdez, J., Chavkin, T. A., & Chavkin, C. (2006). Social defeat stressinduced behavioral responses are mediated by the endogenous kappa opioid system. Neuropsychopharmacology, 31(6), 1241–1248. Moor, B. G., Güroglu, B., Op de Macks, Z. A., Rombouts, S. A., Van der Molen, M. W., & Crone, E. A. (2012). Social exclusion and punishment of excluders: Neural correlates and developmental trajectories. NeuroImage, 59(1), 708–717. Nathanson, D. L. (1992). Shame and pride: Affect, sex, and the birth of the self. New York, NY: W. W. Norton.

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CHAPTER 10

Attachment and Attachment Repair Frank M. Corrigan, Alistair Wilson, and Deirdre Fay

“Hell and High Water” she said. “But not with you baby. Enough is enough.” Her words cut him deep—utter pain of rejection. He called her name once more but she turned her back. —Alan Spence, in The Magic Flute (1990, p. 354)

Mammalian species have evolved over millions of years to detect threat, to take what is needed from the environment, to reject what is harmful, and to embed systems for nurturing the young. All of these abilities promote survival up to and beyond sexual maturation and enhance reproductive potential. The expansion of the cortical mantle in primates has bestowed a greater capacity for care of others (Hanson & Mendius, 2009). This nurturing protection is based in affiliative systems that underlie and give rewards not only to mother–infant interactions but also to friendships, sexual relationships, and other interpersonal connections and communications (Depue & MorroneStrupinsky, 2005). The rewards of affiliation reinforce attachment behaviors and create emotional memories, tendencies, likes and dislikes, approach, and avoidance. Attachment and safety are linked closely from birth onwards. Soothing by the mother eases the infant’s autonomic nervous system activation and emotional arousal. In a secure attachment relationship, the child can learn the rewards of interaction without threat. When the secure child is exposed to an external threat, turning toward another is a programmed response to obtain safety and relief. When the mother is emotionally unavailable, or powerless to intervene when the infant is exposed to external threat, the complexity of the conflict, whether to approach or flee, can be resolved by a dissociative response. The frozen indecision is replaced by 193

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a disconnection from the experience of the moment, which relieves the distress. With no reliable and loving caregiver available for protection from danger, the complex mixing of fear with the urge to attach is compounded by an intrinsically distressing state of isolation. The many different states possible when the child feels threatened depend on the degree of organization as described in the attachment model, the severity of the threat, and on the proximity of someone who can provide safety. The residual emotional burden depends to a great extent on the intensity of the separation distress experienced. To understand the complex responses to threat, we need to know (a) what systems are involved in attachment; (b) whether these are the same as the affiliative defense responses to threat; and (c) whether they overlap but differ in valence from those activated during separation distress.

ATTACHMENT, DETACHMENT, AND DISSOCIATION

The following quote illustrates the obstructed attachment urge precipitating high arousal dissociation in a patient with dissociative identity disorder (DID). Mama, help me. Take the man away from me: He is hurting me. I want to go away. I’m frightened. Somebody help me. Nobody to give me a cuddle. No-one there at night-time. No-one to read me a book or tell me stories. I cry—my heart goes faster and faster then it goes dark, very dark. It is darker than the sky at night-time. It goes dark—then I see him in the bedroom with me. Mama, please take daddy off me. He is hurting me—so painful. Bowlby’s observation that separation from the mother of a young child leads to protest, despair, and detachment (Bowlby, 1971) remains of great clinical importance. Despair can encompass different levels of shutdown depending on the degree of parasympathetic dominance and the amount of numbing induced by endogenous opioids active at the mu receptor. In contrast, we consider protest to be a high-energy state with the potential for cannabinoid-mediated dissociation: whether it progresses to rage or to panic depends on which part of the dorsolateral periaqueductal gray (PAG) column is activated almost simultaneously. With detachment, a normal level of energy is available but the emotions driving attachment are suppressed or disconnected, or there is a state of low motivation and low enthusiasm for living. Rivers (1920) described dissociation as a suppressed experience that is capable of independent consciousness. This is analogous to the process of structural dissociation (van der Hart, Nijenhuis, & Steele, 2006) and it can be applied separately to both protest and despair states when they are triggered and break through the apparently normal detachment. The neurochemical mediators of the high- and low-arousal states, which have immediate numbing and analgesic effects, are also available, as will be seen from the examples given, when the separated states come to their individual consciousness. The primary driver to pathological dissociation is attachment disorganization in early life: when that is followed by severe and repeated trauma, then a major disorder of structural dissociation is created (Lyons-Ruth, Dutra, Schuder, & Bianchi, 2006). The nonavailability of the mother exposes the predissociative infant to a hostile/helpless model of attachment. There are parallels with the fight/submit model

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of depression and anxiety alluded to in Chapter  2, but in adults the fight/submit conflict derives from interactions with significant others and does not necessarily involve separation distress. In infants, it is assumed that any conflict engendered by the witnessing of behavior that fluctuates from frightening to frightened, hostile to submissive, would carry the risk of separation at least at the emotional level. As significant traumas often have feelings of lonesomeness at their core, it is likely that the circuits underlying separation distress contribute to the complex emotional residue of unresolved adversity: the submit state and the collapse despair state are overtly identical physiologically. Infant biology does not distinguish between separation threat and external threat. Lack of response to the infant’s distress vocalizations can mean that the protection of the primary caregiver is not available. Maternal withdrawal and unresponsiveness are then sufficiently traumatic to lead to hypothalamic–pituitary–adrenal (HPA) axis activation (Lyons-Ruth et al., 2006). THE NEUROBIOLOGY OF MATERNAL ATTACHMENT

Mammals require a long period of dependence on others in order to obtain the resources needed for growth and maturation, and this requirement is reflected in the mammalian brain’s extensive attachment drive. Likewise, the mother’s capacity for caring for and nurturing her infant has profound neurobiological underpinnings, anatomical and chemical. Many areas of prefrontal cortex are activated when mothers view their own infant rather than someone else’s child: there are also activations of hypothalamus and PAG (Noriuchi, Kikuchi, & Senoo, 2008). Brain Structures Involved in Maternal Attachment and Behavior

In rodents, maternal behavior is dependent on the anterior cingulate cortex (ACC) and noncortical areas, including the medial hypothalamus and preoptic area, the bed nucleus of the stria terminalis (BNST), the ventral tegmental area (VTA), the PAG, the habenula, and the septal area, as well as on neurotransmitter/hormone systems recruiting oxytocin and endogenous opioids (Panksepp, 1998). The septal area, which has high binding for oxytocin, may have developed enhanced function during the evolution of social feelings in humans (Moll et  al., 2011). The impaired capacity for prosocial sentiments such as guilt, pity, and embarrassment in frontotemporal dementia correlates with damage to the frontopolar cortex and the septal region (Moll et al., 2011). Also from imaging studies of humans comes confirmation of the importance for the experience of unconditional love of the ACC, the VTA, and the PAG, among others (Beauregard, Courtemanche, Paquette, & St-Pierre, 2009). The rat’s capacity for mothering is impaired by damage to the bed nucleus of the stria terminalis (BNST) or to the preoptic area (Panksepp, 1998). The peptide oxytocin, active at receptors in the BNST, initiates maternal care. Lesions of the hypothalamus that block the induction of oxytocin release from the pituitary impair maternal behavior if they occur before mothering is established (Panksepp, 1998). However, in a study of adult humans with firstborn infants, plasma oxytocin concentrations increased

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in both mothers and fathers over the first 6 months of the infants’ lives and were linked to effective parental behaviors being maintained (Gordon, Zagoory-Sharon, Leckman, & Feldman, 2010). Thalamocingulate and Thalamoinsular Extensions of Spinothalamic Body Information

The thalamocingulate pathway is highly developed in humans and is linked with nursing and maternal care, maternal communication with offspring, and play (MacLean, 1990). Body sensations in humans are relayed via a spinothalamic pathway to thalamic nuclei (Craig, 2003) from which there is a divergence: a thalamocingulate tract to the ACC and a projection to the insula. It has been proposed that the thalamocingulate component provides the drive associated with the body sensation while the insular activation confers the feeling as it travels from the posterior to the anterior insula (Craig, 2003). These two areas of cortex, the anterior cingulate and the anterior insular, supply the individual with a motivation and a feeling from any experienced body sensation. They are linked, for fast communication, by the von Economo neurons (VENs), which are found more in humans than in great apes in these areas of cortex (Allman et al., 2010). The fronto-insular region, which contains the VENs, has connections with areas linked with social emotions, including empathic concern (Allman et  al., 2010). The anterior insula activation mediates rapid recognition of emotions in others and facilitates immediate and appropriate responses. A balance of left and right would offer optimal regulation through parasympathetic soothing and calming (left) and active compassionate concern (right). The Mesolimbic Dopamine System in Maternal Behaviors

The mesolimbic dopamine (ML-DA) system from the VTA to the nucleus accumbens drives active caring behaviors such as foraging and nest building (Panksepp, 1998) and contributes to other aspects of social behavior. The peptides oxytocin and vasopressin both help to establish continuing bonds between adult prairie voles, and both have high levels of receptors in the nucleus accumbens (Insel & Young, 2001). The VTA receives inputs from the BNST and the preoptic area, with oxytocin projections to the VTA being especially important for maternal behavior (Panksepp, 1998). In the prairie vole, partner preference increases after copulation and this pair bonding is rewarded by oxytocin stimulation of the ML-DA system (Baskerville & Douglas, 2010). Human couples whose relationship is deepened by their sexual interaction may be experiencing similar neurochemical influences on their attachment so that they more readily forsake all others. Oxytocin and Endogenous Opioids in Maternal Behavior

After oxytocin has contributed to its initiation, opioids help to sustain maternal behavior, provided the levels are not too high (Panksepp, 1998): in humans there may be a fine balance between the rewards of active caring and passive nurturing.

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Urban mothers need to be able to forage in supermarkets, prepare food, maintain the hygiene of the nest, engage in interactive play, attend to hurts and illnesses, downregulate activation after rough-and-tumble play, and reduce activation sufficiently to promote sleep. The intrinsic rewards of the effective behaviors are reinforced by the oxytocin and opioid systems and learned so that they become almost automatic: this requires the hormonal influences on the ML-DA tracts. If their children are distressed, a manifestation of possible threat, the substantia nigra in the mothers’ brains (Noriuchi et al., 2008) gets ready for action; but the PAG governs the switching of behavior from maternal care to defense. Exposure of lactating mother rats to the threat represented by cat odor activates the dorsal columns of the PAG responsible for initiating active defense, while the nonurgent maternal behaviors of the ventral PAG are inhibited (Sukikara, Mota-Ortiz, Baldo, Felicio, & Canteras, 2010). It would be fascinating to know what is happening in the brains of humans who are working therapeutically with their own imagined infant child in Lifespan Integration (Pace, 2003) or with older child parts with other techniques such as the Developmental Needs Meeting Strategy (Schmidt & Hernandez, 2007). Healing becomes possible when the internal system moves from a defensive to a nurturing response toward the infant or child parts. The profundity of this experience for many people implicates the calming and soothing influence of oxytocin and endogenous opioids on subcortical structures. Rats that engage in high levels of licking/grooming of their pups have increased oxytocin expression in the medial preoptic area and the paraventricular nucleus of the hypothalamus and they have higher levels of dopamine in the nucleus accumbens during the caring behaviors (Shahrokh, Zhang, Diorio, Gratton, & Meaney, 2010). To allow the rewards of nurturing the child to be maintained in the mother there is an interaction between oxytocin and the endogenous opioid systems, but there is also reward through the oxytocin enhancement of the ML-DA transmission. We hypothesize that the ML-DA system is polyvalent as a result of the neurochemical influences of endocannabinoids, oxytocin, endogenous opioids, and other peptides such as nociceptin/orphanin FQ (N/OFQ) and corticotropin-releasing factor (CRF). The affective valence of the system confers states of fearfulness and safety, and provides the rewards of many consummatory behaviors. Affiliation involves both seeking and finding, and the enjoyment of the search for rewarding interactions is based in the dopamine projections to the nucleus accumbens and prefrontal cortex. THREAT AND THE NEUROBIOLOGY OF AFFILIATION

The influences of environmental safety and predictable plenty on the maternal behaviors of rats may not extrapolate easily to the more complex conditions with which humans interact. Rat pups that receive more licking/grooming by their mother in infancy grow to be adults with a reduced HPA-axis response to stress. They are able to explore more and they startle less. They have fewer CRF receptors in their locus coeruleus and more gamma-aminobutyric acid (GABA)/benzodiazepine receptors in the central and basolateral nuclei of the amygdala. High maternal care in the first week of the rat pup’s life is providing the neurobiological base for reduced arousal

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in response to stress in adult life. If pups born to mothers low in maternal care are reared by mothers high in care (licking/grooming, arched-back nursing), the pups grow up to be adults with a less reactive nervous system (Cameron, Parent, Fish, Ozaki-Kuroda, & Meaney, 2005). Environmental stress alters the nursing behavior of the mother rat so that she ceases to do so much licking/grooming. In turn, her female pups grow up with reduced oxytocin binding in the medial preoptic area and reduced licking/grooming of their own litters. The effects of the stress are being transmitted through the generations to help the rats to adapt to the conditions in which they are living. In dangerous places, hypervigilance and fearfulness promote awareness of threat and predator detection, and the HPA changes facilitate mobilization of energy reserves and resistance to septic shock. Therefore, the maternal behavior that is low in manifest caring is producing adult rats more equipped to deal with their adverse environments—predation, starvation, infection—than occurs with the high maternal licking/grooming attention to the pups. If these results were translated to the impact of environmental poverty on human child development, the conclusion would be that sometimes it is altered parenting behavior that affects physiological and behavioral variables through the generations.

Attachment and Downregulation of Distress

Attachment has built-in rewards—through oxytocin and endogenous opioids—but we are also concerned with what happens when attachment is sought in response to threat. Is there a difference in the brain systems invoked when there is an urge to find anyone who can diminish the terror: a rescuer, a protector, a superhero who can right the wrongs and restore safety, even a perpetrator? The greatly expanded human neocortex, responsible for general intelligence and forward planning, is also vital for inhibitory regulation and soothing of affects such as fear, but cortical appraisal of threat may be too slow to respond to an immediate risk to life (Gilbert, 2009). A subcortical, supersensitive trigger to threat maximizes the chances of survival for reproduction but can become maladaptive and predispose to an anxiety disorder. Many of the clinical problems associated with fear are not so much to do with what has already been triggered by the amygdala’s rapid response but more to do with what is anticipated. This anticipatory anxiety is based in neuronal circuits recruiting the BNST and the prefrontal cortex. Volunteers with a spider phobia who were waiting in a functional MRI (fMRI) scanner to be presented with a picture of a spider showed activation of the BNST and the insular and anterior cingulate cortices: but the subjective experience of anxiety correlated with the cortical rather than with the subcortical activations (Straube, Mentzel, & Miltner, 2007). More anxious people have greater activity in the BNST during a vigilant state in which they are monitoring threat proximity (Somerville, Whalen, & Kelley, 2010). Someone raised in a constantly critical and verbally abusive environment may be so prone to be vigilant to threat that she has difficulty orienting to the present moment, aware of her own current needs. It is necessary to focus her attention on what might antidote the past fears rather than reflecting on the unmet attachment

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needs as that would revert to self-attacking name-calling. Self-criticism activates the threat system, while self-compassion reduces the associated arousal (Gilbert, 2009). Staying in the here and now helps sufferers identify the filter they are placing onto the moment: the activation does not relate to the present moment but to a trigger held in a memory either of an event or of an associated facial expression: a parental face that is blank or frightened or frightening. Compassion and meditation take the brain’s activation in a cortical direction: calming and soothing the threat system that has been triggered through the amygdala and the BNST. The BNST is actively involved with social behaviors such as mating and aggression in animals and may be particularly sensitive to olfactory cues (Wood & Swann, 2005). When we ask people to identify a smell associated with feeling safe and comfortable, we find strong associations with superficially unlikely compounds like bleach, fabric conditioner, and petrol: individual emotional connections through a complex network including the BNST. The converse is that smells can also be powerful triggers of stored distress residual from times of trauma. Affiliation, according to Depue and Morrone-Strupinsky (2005), means turning to others for comfort and support as well as having warmth, capacity for affection, and enjoyment of social interactions. It provides the rewards of close interpersonal contact and promotes calmness and relaxation. It is distinct from the distress of separation but essentially uses the same networks as those described for the maternal behaviors. There seems to be no reason to assume that the experience of attachment urge in response to threat is fundamentally different from the urge to affiliation, which is common to all mammals.

Consequences of Separation: Obstructed Attachment as Threat

A woman in her late 30s had a wonderful weekend together with her husband. Two days later, they drove separately to meet for an appointment. She saw him in the parking lot but he “ignored” her. She fell apart, distressed by the look in his eyes: “he wasn’t present.” When exploring this in therapy, she remembered being a 3-year-old child whose mother was responding to her divorce by “vacating her body” and “disappearing.” In deconstructing the present moment using the parallel lives process (Fay, 2007) she was able to notice the subtle moment when she put the filter from the past onto the present. Children of dissociative mothers who grow to be adults with inexplicable surges of emotion in response to apparently innocuous triggers may also benefit from identifying sequences of response to withdrawal of attention. In these instances, the response to emotional absence is a high level of separation distress that leads to an impairment, rather than an improvement, of interpersonal relationships. The initial, hugely energetic, protest surge when the child realizes that her mother has become absent (through dissociation) may be amenable to sensorimotor intervention, or other processing, in the adult. Otherwise, it follows its usual sequence, to terror, rage, despair, and/or dissociation, and the pattern is repeated whenever triggered by the emotional absence of a key person. At these moments, the experience of threat is not brought on by jeopardy to physical integrity or survival, or even to social evaluation, but to the maintenance of attachment

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relationships. This may of course be based in the biological fact that children without carers cannot survive for long. Obstructed Attachment Urges and Defense Responses

Children can react to abandonment with the midbrain-based defense responses that have been explored in previous chapters; and shame, rather than fear, may be the initial spur to fight, flight, freeze, or hide reactions. The high-arousal shame response— the deep pain of feeling worthless, of not being fit to belong, of being subhuman—is an alternative to protest. Both may be followed by active or passive defense responses. When the intense mammalian longing for connection and attachment is thwarted or obstructed, the resulting sequence of defense responses is often softened by dissociation; such is the difficulty in tolerating the emotional distress. There may be selfharming behaviors or other maladaptive efforts to regulate the distress as the arousal levels fluctuate. However, it is important to distinguish secondary defense responses from the primary separation responses. The obstructed urge to attach initiates a higharousal protest or shame phase that is followed by a low-arousal despair, overtly indistinguishable from the submit state. Submit collapse and separation despair may be conjoined when a person has lost a fight to maintain a relationship that was highly valued and predicted to be long term. When there is a conflicted necessity to submit to a more powerful person, to downgrade high arousal, the resulting hopelessness and helplessness combine with low mood in a depressive state. The tension engendered by the obstructed impulses for fight and flight manifests as anxiety and tension. Watt and Panksepp (2009) propose that depression has its roots in a neurobiological state that has been required over the course of evolution to shut down the high-arousal protest phase of separation distress. There may be a similar mechanism to mediate submission in an agonistic encounter. When survival from the encounter is possible it can be better to acknowledge defeat and conserve energy, living to fight another day. The two states—separation despair and submissive withdrawal—can together create a heavy cloud of pessimism and lethargy, which prevents drive to enjoyment and rewarding attachment. It is loss: of an attachment, in grief; of a social evaluation, in humiliation and rejection; of an interpersonal confrontation, in submission, which is the underlying factor in many dysthymic and depressive states. Protest, Despair, and Detachment—and Active or Passive Defense Responses

What is unclear is how much the protest phase of abandonment can be independent of the active defense responses mediated by the midbrain PAG and, likewise, whether the despair or detachment responses necessarily involve the ventrolateral PAG. There can be a clear overlap, as is seen when someone spurned decides to exact retribution through damage to the prized possessions of the spouse/partner/ lover who has ended the relationship. Similarly, the abandoned or bereaved person who shuts himself away with reduced activity and reduced energy expenditure has a numbing that is secondary to a passive response to the painful loss.

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We hypothesize that high-arousal dissociation is available to numb the protest phase of activated separation distress and low-arousal dissociation eases the despair state. Clinically, there are states with features of frozen activation and high-arousal dissociation combined, with an overall subjective experience of despairing collapse. This complex presentation may be a state analogous to the frozen fight and frozen flight—or even the tonic immobility (TI) states previously discussed—with coactivation of opponent physiological forces: obstructed attachment urges precipitating simultaneous high-arousal protest and low-arousal despair. Differentiation of the secondary responses from the primary feeling of abandonment hurt can make treatment shorter as time is not spent unnecessarily on later phases of the sequence.

The Neurochemistry of Separation Distress

When a child who had been in a secure relationship with his mother was separated from her, the distress was manifested in the three phases of protest, despair, and detachment, with various states of transition and merging (Bowlby, 1971). Protest is a state of energy expenditure with crying and restless behavior, while despair is characterized by energy conservation, inactivity, and withdrawal. Detachment relates to the loss of the attachment to the mother: if she returns after a prolonged absence, the child turns away without interest in her. This apparently normal state can have a normal level of energy or there may be listlessness, boredom, irritability, negative affect, sensation seeking, and propensity for substance abuse; all of which are observed with reduced dopaminergic tone (Gatzke-Kopp, 2011). Maternal mourning in the first 2 years of the infant’s life is one risk factor for the condition of borderline personality disorder (Liotti & Pasquini, 2000), a condition in which separation cues often activate distress analogous to protest/fight high arousal. The rat studies cited below additionally support the proposals that the protest phase involves endocannabinoid modulation of the HPA axis; the transition to despair is mediated by kappa opioids; and the despair state itself provides conservation of energy through mu opioids. When these phases are accompanied by PAG activations of various combinations of fight, flight, freeze, avoid, and hide (as described in Chapters 2 and 4), there are many possible states of distress that are often difficult to put into words because of their subcortical and preverbal origins. (The roots of the word “infancy” are in the inability to use speech.) Separation distress, when prolonged into the low-energy expenditure, passive state, known as despair in humans, influences the body’s capacity to defend itself against further insults. A bacterial cell wall component elicits an inflammatory response but no other features of infection when injected into guinea pig pups. When this is injected during the acute phase of separation from the mother, the passive behavioral responses develop more quickly. The inflammatory response has a similar effect in the pup to prolonged separation from the mother, and both situations increase measures of HPA activity, leading to the proposal that the long-term deleterious consequences of early adversity are mediated, inter alia, by CRF (Hennessy, Deak, & Schiml-Webb, 2010). When people who have suffered catastrophic losses seek solace in alcohol, they may create a state in which there is an increased

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propensity to distress because of changes in the midbrain PAG and amygdala, which occur with continuing excessive consumption. The subsequent transition to physical dependence on alcohol is mediated by CRF and associated peptides acting on the central nucleus of the amygdala, the BNST, and the nucleus accumbens shell (Koob, 2010). High levels of CRF are found in the amygdala in animal models of withdrawal from all drugs of abuse (Martin-Fardon, Zorrilla, Ciccocioppo, & Weiss, 2010). With dependence comes use of the drug to relieve the distress caused by its absence when the brain systems have made the adaptations in the emotion-generating regions of the mesodiencephalon and in the stimulus-responsive extended amygdala. Some of the unpleasant consequences of alcohol excess and withdrawal are mediated by the dorsomedial column of the PAG, which we hypothesize to have close links with disgust and shame. Brain areas active during separation distress in the guinea pig and during sadness in the human include the ACC, the dorsomedial thalamus, and the PAG (Panksepp, 2005). It is unclear which part of the PAG is most involved in sadness, but Panksepp (2005) considers the pain of loss to be of the deeply visceral type: this implicates the ventrolateral column with its access to passive coping strategies and opioid-induced analgesia (Bandler, Keay, Floyd, & Price, 2000). The turning of protest into despair is mediated by kappa opioids in the ML-DA system (Watt & Panksepp, 2009), but protest can also rapidly generate defense responses, active or passive, through the PAG. The active responses have cannabinoid-mediated mechanisms of pain relief, in contrast to the passive state that has opioid—and mixed—analgesic responses. The interaction of pain and sadness is even evident in fMRI experimental paradigms in humans: an increase in the intensity of the experience of pain when the context is one of sadness rather than joy reflected in ACC activation (Yoshino et al., 2010).

The Capacity for Rapid Change of Valence of the ML-DA System

The ML-DA system is involved in behavioral arousal in the search for safety and the avoidance of harm (Alcaro, Huber, & Panksepp, 2007). The rapidity with which it can switch from the promotion of appetitive behavior, under environmental conditions of safety and warmth, to defensive behavior, when the environment becomes harsh and unpleasant, was demonstrated by Reynolds and Berridge (2008) in their study of the response of the nucleus accumbens shell to microinjections of a glutamate antagonist. There is also a suggestion of a laterality effect in response to sounds that are pleasant or otherwise (Levita et al., 2009), so there is a need to study right–left differences as well as the associated neurochemicals. If right or left dominance is combined with sudden changes in the neurochemical environment and altered connectivity with the prefrontal cortex, there is the potential for many differently valenced states with subtly shifting affective components. This allows the human brain to respond with intricate complexity to a wide range of environmental conditions of varying degrees of danger, whether physical or social. As examples, guilt and indignation (Green et  al., 2010), charitable donating (Moll et al., 2006), and the enjoyment of music (Menon & Levitin, 2005) all rely on alterations in the connections of the mesolimbic system with the prefrontal cortex.

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The ML-DA system is therefore placed to be hugely influential in the affective state of the human interacting with a shifting environment: at times safe and warm and loving; at other times, harsh and dangerous and without human support or help. Most often, for many people, it is in constant flux. Infants, born ready for social interaction, prefer faces and speech over nonhuman equivalents. From 5 or 6 months of age they want a specific attachment to a primary caregiver. By 2 years of age the default network underlying much self-referential activity is largely connected (Parsons, Young, Murray, Stein, & Kringelbach, 2010). Approach to a caregiver recruits the ML-DA system in seeking the warmth and safety of proximity. However, if this system is also activated by stress, isolation, and defeat, its valence is the key factor. fMRI may not be adequate to explore this, as not only is it inclined to miss small areas but it also fails to register the importance of neuromodulators such as endogenous opioids (Panksepp, 2005). The adult traumatized as a child who switches into a helpless “Attach” mode or part may seek care, comfort, and rescue while monitoring the well-being and emotional state of the adult to whom she turns, perhaps replaying a childhood pattern of conflicted approach to a parent who was also an abuser. This conflicted attach approach, if dysphoric, must entail neurochemical influences on the ML-DA system and the inhibitory rostromedial tegmental nucleus to facilitate the emotional and motor behavior congruent with the puzzlement, confusion, or despair. Activation of the rostromedial tegmental nucleus with the ventrolateral PAG may underlie states of withdrawal and despair, with altered balance of endogenous opioids conferring numbness and disconnection. Social defeat stress in mice leads to an aversion to social contact through the effect of brain-derived neurotrophic factor (BDNF) in the ML-DA pathway (Berton et  al., 2006), but the effects on posture, pain awareness, mobility, and sensitivity to the effects of cocaine are instead dependent on dynorphins of the endogenous kappa opioid system (McLaughlin, Li, Valdez, Chavkin, & Chavkin, 2006). The pain of humiliating loss or attachment loss depends on the impact of neurochemicals on the mesolimbic system rather than just on the intensity of the activation itself.

Cortical Modulation of the Mesolimbic Dopamine System

The insular cortex has a modulatory influence on the ML-DA system that contributes to some aspects of maternal behavior, as well as feeding and defensive behaviors, through the outputs from the nucleus accumbens shell to the lateral hypothalamus (Voorn, Vanderschuren, Groenewegen, Robbins, & Pennartz, 2004). Apart from this contribution from the insular cortex, prefrontal projections to the nucleus accumbens shell arise mainly in the visceromotor control areas of ventromedial prefrontal cortex (VMPFC; Price, 2006). Thus, the area of the nucleus accumbens shell, which receives inputs from the basolateral amygdala (Aggleton, 1992), also receives from prefrontal areas that modulate the viscera through the hypothalamus and PAG (Chikama, McFarland, Amaral, & Haber, 1997). The insula, although not a midline structure, is wired to modulate the activity of many brain regions contributing to the affective valence of the self.

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Self-reporting of happy rats is now possible as 50 kHz vocalizations reflect positive affect. Laboratory rats bred for their capacity to emit these sounds in a social interaction at an early age generate a high vocalizing line. Conversely, rat pups unhappy with separation from their mother report their negative affect through 22 kHz vocalizations, and selective breeding of rats with high rates of these sounds produces a line of animals with negative emotional states (Brudzynski et al., 2011). The rats bred for happy calls can then be compared with those bred for unhappy calls, and both groups can be compared with animals produced from random breeding. The response of the different lines to amphetamine injections into the shell of the nucleus accumbens then shows an innate capacity for positive affect in one group and an impaired capacity for responding to rewarding experiences in the other group (Brudzynski et al., 2011). The way in which the rats are selected for breeding for positive or negative affect supports the contention that the joys of social affiliation and the pains of separation (Panksepp, 2003) share similar brain networks—but with different valence conferred by the associated neurochemical influences. Corticosteroids and the ML-DA System

As many of the deleterious physiological effects of childhood trauma are mediated by the HPA axis, triggered by endocannabinoids (Hill & McEwen, 2009), there is inevitably an effect of glucocorticoids on the valence of the ML-DA system. Perinatal stress produces persisting anatomical changes at the sources of the ascending mesolimbic, mesocortical, and nigrostriatal tracts. Stress in adult life alters the functioning of these tracts and at least some of the effects are mediated by the HPA axis. Although the effects on the HPA axis of rearing rat pups in isolation are not consistent, there is increased mesolimbic and reduced mesocortical dopamine activity (Fone & Porkess, 2008). Many of the effects of trauma are through CRF and its interaction with dopamine systems, and a CRF1 receptor antagonist reverses some of the isolation-induced changes in accumbens dopamine neurons (Djouma, Card, Lodge, & Lawrence, 2006). Increased CRF in the BNST with restraint stress (Santibañez, Gysling, & Forray, 2006) transmits the impact of the trauma to the ML-DA system. This maintains a long-term or sustained fear response in contrast to the central nucleus of the amygdala, which promotes an immediate, but brief, response to threat (Walker, Miles, & Davis, 2009). In both instances, to the central nucleus of amygdala and to the BNST, the basolateral amygdala is the signaler of threat awareness from the thalamus and cortex (Walker et  al., 2009). Internally evoked triggers to distress associated with past traumatic events have a basolateral amygdala mediator. There can be an immediate impact through the central nucleus of the amygdala or a more prolonged effect through the BNST and the ML-DA system. Cortical and hippocampal influences on the projections from the BNST to the VTA activate emotional and contextual changes in drive and motivation (Jalabert, Aston-Jones, Herzog, Manzoni, & Georges, 2009). Humans reporting low maternal care in early life have a mesolimbic response to a psychosocial stressor that correlates with altered functioning of the HPA axis (Pruessner, Champagne, Meaney, & Dagher, 2004). The HPA axis interacts not only with endogenous cannabinoids (Finn, 2010) but also with N/OFQ, an endogenous

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opioid antagonist (Martin-Fardon et al., 2010), which may prove to be important in states of separation distress. As endogenous cannabinoids are released during the active defense responses of fight and flight, we hypothesize that they also mediate the HPA axis effects evoked during high-arousal separation distress. The dysphoria of the protest phase is the result of an altered balance of endogenous cannabinoids and opioids before the kappa-mediated conversions to a despair state in which endogenous opioids active at mu receptors become more available. Attachment, Play, and Protest

Some adults with DID switch into child states that are not obviously distressed but excited: jumping up and down, clapping hands, or singing children’s songs. Underlying this, there may be a painful sense of abandonment, actual or imminent, which is covered by a need to be noticed, an urge to be the receiver of attention—even if that attention is quickly disparaging and critical or even punitive. The mesolimbic activation of seeking safety through attachment is a move away from the dysphoric kappa opioid state of separation distress to a more positively valenced state. Panksepp (1998; p. 295) reviews the possible functions of PLAY and, for rough-and-tumble play or play fighting, proposes that it allows practice of motor routines normally accessible to emotional states. Similarly, the game of “hide and seek” allows children to exercise the motor routines for fleeing and hiding, which are based in subcortical loops through the basal ganglia; it also incorporates the rewards of SEEKING. Routines for predation and capture or, conversely, for fleeing, hiding, freezing, and submission can all be practiced in safe role-play. Noisy, attention-drawing, excited play could be seen in similar terms as the practice of an attach response: to be noticed for being bad is safer in some environments than being invisible. Rats show their enjoyment of play by preferring places in which they have previously played and by emitting short bursts of 50 kHz vocalizations when they return to the play area (Siviy & Panksepp, 2011). These happy sounds are dependent on the ML-DA system (Burgdorf, Wood, Kroes, Moskal, & Panksepp, 2007), but an area of the thalamus, which receives somatosensory input from the spinal cord and projects to the frontal cortex and striatum, is necessary for PLAY in mammals (Siviy & Panksepp, 2011). Young rats prevented from engaging in play show an increased desire to play when they again have the opportunity to do so. OBSTRUCTED AND FROZEN ATTACH PARTS OR SELF-STATES

The attachment cry is a separation cry expressing a need to regain contact (van der Hart et al., 2006), so while dissociated emotional parts are often referred to, for ease of communication, as attach parts they will almost always contain a significant degree of separation distress. It is clinically useful to differentiate these according to the mechanism of suppression and the phase of distress. They may be helpless and quietly demanding, or noisy and difficult, when other defense response parts have been evoked by feelings of abandonment. There is a separate state of protest. Fight parts have an “other-orientation,” even if it is safer to turn it inwards to self-harm urges

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or harsh self-criticism, while protest states have a quality of bewilderment about the self. “Why me?” “What have I done?” “How did I find myself here?” “Why does nobody love me?” The activation in the body does not have the upper-body tension of a fight response, however obstructed, nor the lack of tension of a submit response or collapse. Instead, there is a generalized distress from a visceral core possibly representing the mesolimbic dread state described by Faure, Reynolds, Richard, and Berridge (2008). This supports a polyvalent mesolimbic model with access to rapid changes from interest to boredom and back again, from activation to inertia and back again, from playfulness and affiliation to social withdrawal. When the intrinsic mammalian urge to attach is frozen or painfully obstructed, the distress forms the basis of a separate self-state or emotional part. The Frozen Attach state may be residual from early experience of conflicted response in a disorganized attachment relationship with the primary carer. The Obstructed Attach state is hypothesized to occur when there is a cortical regulation of the impulse to reach out for help and affection, but there is no safe way to express that need. This occurs when the caregiver is also the abuser. Obstructed Attach states can then be further subdivided according to whether the underlying affective motivator is protest, despair, or shame. A 3-year-old child suddenly finding that the father he has been trying to follow to his work has disappeared in the distance may have the shock of separation distress with a massively energetic protest, quickly followed by a low-arousal despair and dissociation. Finding himself alone in adult life may activate a sudden dysphoria followed by an urge to shut down and sleep, for which he may not know the origins when he presents 40 years later with complaints of anxiety, depression, and tiredness. He may find that reprocessing of the sudden panic of the 3 year old does not completely clear the distress because there was a sensitization of the separation distress system in infancy by maternal postnatal depression. Experiences like these can be modeled in guinea pig pups separated from their mother: The initial activation and vocalization are followed by a passive state that resembles physical illness to the extent that it can be reduced by anti-inflammatory drugs (Hennessy et al., 2010). Protest at loss or abandonment may quickly activate a fight-or-flight response, which, if obstructed, leads into a state of self-harm impulses or other dysfunctional behaviors. If the abandonment to painful isolation is carried out by a rapist, the resulting conflicts can be hugely distressing and have long-term implications for coping with separation distress such as bereavement. The direction of the energy burden of the different states is such that it is helpful to discriminate Obstructed Attach Protest from Fight and from Obstructed Attach Despair states. The Despair and Submit states are physiologically very similar, but the Protest and Fight states differ in the distribution of tension in the body. Separation distress is based in circuits overlapping care/nurturing and defense: the ACC, the dorsomedial thalamus, the PAG (Panksepp, 2003), and the BNST. Subtle shifts in valence may be magnified to larger shifts in mood and outlook. The anterior insular cortex projections to the nucleus accumbens shell, the amygdala, and the ventrolateral PAG modulate some of the activation created by abandonment and isolation. The BNST has networks responsive to anticipation of threat or to caring and nurturing: it also receives projections from anterior cingulate and insular cortices and is critically placed to mediate the effects of caring and concern.

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ATTACHMENT REPAIR: A CLINICAL EXAMPLE

Bateman and Fonagy (2006) describe the effects of disorganized attachment on affect regulation and attentional control, and they stress the importance for the child of an interaction with an adult who can reflect and mirror the child’s state accurately. If the mirroring is incongruent, the child will develop a sense of an alien self. In the therapy of the adult with deep-seated attachment wounds, attunement, warmth, and accurate mirroring all contribute to the strengthening of the sense of self. When the attachment need is recognized and validated, and there is repair of the wounds suffered in early life, the healing can be profound, as is shown in the following example. It is included because it is astounding what words are used to describe the attachment need. Bill is middle-aged, married with grown children, and in therapy because of a feeling of being ashamed of who he is. He feels worthless and abandoned and lives in fear of being humiliated, frantically trying to avoid that. He is always looking for unconditional love and holding: wanting the other to make him the most important. He realizes that it is a request of the young parts of himself: to require the other to know the perfect thing to respond to his need without him needing to say. Although Bill had been engaged in attachment repair therapy over a number of months, this was the first time he spontaneously spoke of his mother while exploring what might antidote the pain he was feeling. I can envision perfect holding . . . I can feel the infant parts of me wanting 100% of her attention. She doesn’t mind my clinging. It’s a combination of her sacrificing and me being there. I realize it’s not about me being there. She’s showing me what it’s like to have someone be mesmerized by me. I’m not feeling any sort of anxiety, or separation. I’m everywhere with her. I’m getting everything, all my needs met. . . . It feels so clear: not confusing. There’s no anxiety. . . .  In the following session, he needed to consolidate the experience: “trying to get clearer and clearer about the patterning involved.” He wanted to remember the “solid ground” of the last session, which contrasted with the fear of doing it wrong and he didn’t want to go deeply into the emotion. The significant life situation was that his mother had called and wanted him to do something. He kept encountering the felt sense of “I must do this,” but this immediately brought up resistance. The parallel lives drawing (Fay, 2007) was used as a way to interact around the material, to separate out the “Now” moment from the intruding past. In the present moment, Bill has the thought, “It’s a simple thing to do, just do it”: then there was the guilt for not calling. Inside himself he felt paralyzed. He was recreating the experience of having no will and feeling that everything he did exposed the fundamental flaw of his personhood. As a result, he was afraid to take any action at all. From the benefits of the previous session of entering into, and exploring, those states of perfect attunement and attachment, he realized in this session how much relationship he had lost with his mother: and contrary to how it had appeared before, she wasn’t behaving out of anger toward him. Without any prompting, “Bill” spoke of the need to be special to another person and to have someone respond to his needs without his having

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to voice them (the longing for attunement). He knows what he wants (perfect holding, 100% attention) and he longs for the experience of someone being completely and utterly entranced, mesmerized by him. Amazingly, in his visualization he finds his needs being met even though she’s attending to other things as well: he still feels like her attention is fully and completely on him. Longing is in both the here and now and the past. Longing explored in this current moment allows for grieving to occur, shifting the deep pattern as in Bill’s previous session. Longing in the past is all about the wish to have it come from someone outside: this curtails curiosity, and reinforces the pattern. Being with the deeply embedded longing in the present moment transcends the years since its inception. CONCLUSION

Although separation distress is not generally considered to be the other side of the coin from affiliation (Depue & Morrone-Strupinsky, 2005), there are similarities in the neural systems activated: they involve the same brain networks but with different neurochemical influences. The affiliative urge when there is no threat is quite a distinct subjective experience from the same urge when life or bodily integrity is threatened, but both rely on ML-DA activation. In the first instance, concomitant PAG involvement gives autonomic coordinates of the experience, which are registered in the cortex as urgent and unpleasant. In the second case, under conditions of safety, the affiliative impulse is positively valenced in seeking contact and interaction or in soothing and quiet togetherness, depending on the opioid–dopamine balance. The quality of the felt separation distress has a massive influence on the degree of trauma experienced. The initial blow, the pain of rejection, the hurtful awareness of isolation and exclusion, so rapidly leads on to other reactions that it is easily missed in therapy. When there is an obstructed urge to attach with protest, the ML-DA system is under the influence of the HPA axis modified by endogenous cannabinoids. The transition from protest to despair is effected by kappa opioids. In the despair state, mu opioids are prominent in eliciting shutdown. A listless detachment from relationships ensues, with a hypodopaminergic state in mesolimbic and mesocortical tracts. This chapter has highlighted the ML-DA system as central to the experiences of affiliation, attachment urge when under threat, attachment urge during experience of safety, and to the distress of isolation and/or submission. The subjective coloring is added from the neurochemical palette containing oxytocin, endogenous opioids, endogenous cannabinoids, and other compounds such as N/ OFQ and estrogen. The first urge to attach may occur when the infant responds to hunger or thirst (homeostatic affects; Panksepp, 2011). Later, SEEKING of attachment may be to reduce separation distress (PANIC/GRIEF), RAGE, or FEAR. It may also be in the search for positive affective experience through sexual desire (LUST), CARE and nurturance, or PLAY. The ML-DA system may be polyvalent because the SEEKING system underlies most significant emotional experiences based in the primary affects (Panksepp, 2011) generated in the brainstem. These then have their own added neurochemical hues.

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Responses to physical and social threats and blows are generated from midbrain centers that mediate autonomic arousal changes and they are so rapidly involved when triggered by separation distress that they appear to be simultaneous. As the midbrain defense centers also hold the capacity for stress-induced analgesia (SIA), the tendency to dissociation, which is established with disorganized attachment in very early life, is considered to be secondary to modifications of their sensitivity. High- and low-arousal states of autonomic activation induce the cannabinoid and opioid pathways to the dissociative experiences that this chapter has described. Trauma survivors have a default setting that keeps them in threat mode— whether triggered easily by memories of physical danger or separation distress. They need positive attachment experiences to help them to shift into an affective state in which they can feel warmth, joy, pleasurable anticipation, and motivation for living. It is not enough for the therapist to aim for the client or patient to be free from continual experience of threat responses when the affiliation systems need to be trained to fulfill their capacity for positively valenced living.

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Chikama, M., McFarland, N. R., Amaral, D. G., & Haber, S. N. (1997). Insular cortical projections to functional regions of the striatum correlate with cortical cytoarchitectonic organization in the primate. The Journal of Neuroscience, 17(24), 9686–9705. Craig, A. D. (2003). A new view of pain as a homeostatic emotion. Trends in Neurosciences, 26(6), 303–307. Depue, R. A., & Morrone-Strupinsky, J. V. (2005). A neurobehavioral model of affiliative bonding: Implications for conceptualizing a human trait of affiliation. The Behavioral and Brain Sciences, 28(3), 313–350; discussion 350. Djouma, E., Card, K., Lodge, D. J., & Lawrence, A. J. (2006). The CRF1 receptor antagonist, antalarmin, reverses isolation-induced up-regulation of dopamine D2 receptors in the amygdala and nucleus accumbens of fawn-hooded rats. The European Journal of Neuroscience, 23(12), 3319–3327. Faure, A., Reynolds, S. M., Richard, J. M., & Berridge, K. C. (2008). Mesolimbic dopamine in desire and dread: Enabling motivation to be generated by localized glutamate disruptions in nucleus accumbens. The Journal of Neuroscience, 28(28), 7184–7192. Fay, D. (2007). Becoming safely embodied skills manual. Somerville, MA: Heart Full Life Publishing. Finn, D. P. (2010). Endocannabinoid-mediated modulation of stress responses: Physiological and pathophysiological significance. Immunobiology, 215(8), 629–646. Fone, K. C., & Porkess, M. V. (2008). Behavioural and neurochemical effects of post-weaning social isolation in rodents-relevance to developmental neuropsychiatric disorders. Neuroscience and Biobehavioral Reviews, 32(6), 1087–1102. Gatzke-Kopp, L. M. (2011). The canary in the coalmine: The sensitivity of mesolimbic dopamine to environmental adversity during development. Neuroscience and Biobehavioral Reviews, 35(3), 794–803. Gilbert, P. (2009). The compassionate mind. London, UK: Constable & Robinson. Gordon, I., Zagoory-Sharon, O., Leckman, J. F., & Feldman, R. (2010). Oxytocin and the development of parenting in humans. Biological Psychiatry, 68(4), 377–382. Green, S., Ralph, M. A., Moll, J., Stamatakis, E. A., Grafman, J., & Zahn, R. (2010). Selective functional integration between anterior temporal and distinct fronto-mesolimbic regions during guilt and indignation. NeuroImage, 52(4), 1720–1726. Hanson, R., & Mendius, R. (2009). Buddha’s brain: The practical neuroscience of happiness, love, and wisdom. Oakland, CA: New Harbinger Publications. Hennessy, M. B., Deak, T., & Schiml-Webb, P. A. (2010). Early attachment-figure separation and increased risk for later depression: Potential mediation by proinflammatory processes. Neuroscience and Biobehavioral Reviews, 34(6), 782–790. Hill, M. N., & McEwen, B. S. (2010). Involvement of the endocannabinoid system in the neurobehavioural effects of stress and glucocorticoids. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 34(5), 791–797. Insel, T. R., & Young, L. J. (2001). The neurobiology of attachment. Nature Reviews. Neuroscience, 2(2), 129–136. Jalabert, M., Aston-Jones, G., Herzog, E., Manzoni, O., & Georges, F. (2009). Role of the bed nucleus of the stria terminalis in the control of ventral tegmental area dopamine neurons. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 33(8), 1336–1346. Koob, G. F. (2010). The role of CRF and CRF-related peptides in the dark side of addiction. Brain Research, 1314, 3–14. Levita, L., Hare, T. A., Voss, H. U., Glover, G., Ballon, D. J., & Casey, B. J. (2009). The bivalent side of the nucleus accumbens. NeuroImage, 44(3), 1178–1187. Liotti, G., & Pasquini, P. (2000). Predictive factors for borderline personality disorder: Patients’ early traumatic experiences and losses suffered by the attachment figure.

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The Italian Group for the Study of Dissociation. Acta Psychiatrica Scandinavica, 102(4), 282–289. Lyons-Ruth, K., Dutra, L., Schuder, M. R., & Bianchi, I. (2006). From infant attachment disorganization to adult dissociation: Relational adaptations or traumatic experiences? The Psychiatric Clinics of North America, 29(1), 63–86, viii. MacLean, P. D. (1990). The triune brain in evolution: Role in paleocerebral functions. New York, NY: Plenum Press. Martin-Fardon, R., Zorrilla, E. P., Ciccocioppo, R., & Weiss, F. (2010). Role of innate and drug-induced dysregulation of brain stress and arousal systems in addiction: Focus on corticotropin-releasing factor, nociceptin/orphanin FQ, and orexin/hypocretin. Brain Research, 1314, 145–161. McLaughlin, J. P., Li, S., Valdez, J., Chavkin, T. A., & Chavkin, C. (2006). Social defeat stressinduced behavioral responses are mediated by the endogenous kappa opioid system. Neuropsychopharmacology, 31(6), 1241–1248. Menon, V., & Levitin, D. J. (2005). The rewards of music listening: Response and physiological connectivity of the mesolimbic system. NeuroImage, 28(1), 175–184. Moll, J., Zahn, R., de Oliveira-Souza, R., Bramati, I. E., Krueger, F., Tura, B., . . . Grafman, J. (2011). Impairment of prosocial sentiments is associated with frontopolar and septal damage in frontotemporal dementia. NeuroImage, 54(2), 1735–1742. Moll, J., Krueger, F., Zahn, R., Pardini, M., de Oliveira-Souza, R., & Grafman, J. (2006). Human fronto-mesolimbic networks guide decisions about charitable donation. Proceedings of the National Academy of Sciences of the United States of America, 103(42), 15623–15628. Noriuchi, M., Kikuchi, Y., & Senoo, A. (2008). The functional neuroanatomy of maternal love: Mother’s response to infant’s attachment behaviors. Biological Psychiatry, 63(4), 415–423. Rivers, W. H. R. (1920). Instinct and the unconscious: A contribution to a biological theory of the psycho-neuroses. Retrieved from http://psychclassics.yorku.ca/Rivers/ Pace, P. (2003). Lifespan integration: Connecting ego states through time. Available from the Lifespan Integration website: http://Lifespanintegration.com Panksepp, J. (1998). Affective neuroscience: The foundations of human and animal emotions. New York, NY: Oxford University Press. Panksepp, J. (2003). Feeling the pain of social loss. Science, 302, 237–239. Panksepp, J. (2005). Why does separation distress hurt? Comment on MacDonald and Leary (2005). Psychological Bulletin, 131(2), 224–30; author reply 237. Panksepp, J. (2011). The basic emotional circuits of mammalian brains: Do animals have affective lives? Neuroscience and Biobehavioral Reviews, 35(9), 1791–1804. Parsons, C. E., Young, K. S., Murray, L., Stein, A., & Kringelbach, M. L. (2010). The functional neuroanatomy of the evolving parent-infant relationship. Progress in Neurobiology, 91(3), 220–241. Price, J. (2006). Connections of orbital cortex. In D.H. Zald & S. L. Rauch (Eds.), The orbitofrontal cortex (pp. 39–56). Oxford, UK: Oxford University Press. Pruessner, J. C., Champagne, F., Meaney, M. J., & Dagher, A. (2004). Dopamine release in response to a psychological stress in humans and its relationship to early life maternal care: A positron emission tomography study using [11C]raclopride. The Journal of Neuroscience, 24(11), 2825–2831. Reynolds, S. M., & Berridge, K. C. (2008). Emotional environments retune the valence of appetitive versus fearful functions in nucleus accumbens. Nature Neuroscience, 11(4), 423–425. Santibañez, M., Gysling, K., & Forray, M. I. (2006). Desipramine prevents the sustained increase in corticotropin-releasing hormone-like immunoreactivity induced by repeated

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i­ mmobilization stress in the rat central extended amygdala. Journal of Neuroscience Research, 84(6), 1270–1281. Schmidt, S. J., & Hernandez, A. (2007). The developmental needs meeting strategy: Eight case studies. Traumatology, 13, 27–48. Shahrokh, D. K., Zhang, T. Y., Diorio, J., Gratton, A., & Meaney, M. J. (2010). Oxytocindopamine interactions mediate variations in maternal behavior in the rat. Endocrinology, 151(5), 2276–2286. Siviy, S. M., & Panksepp, J. (2011). In search of the neurobiological substrates for social playfulness in mammalian brains. Neuroscience and Biobehavioral Reviews, 35(9), 1821–1830. Somerville, L. H., Whalen, P. J., & Kelley, W. M. (2010). Human bed nucleus of the stria terminalis indexes hypervigilant threat monitoring. Biological Psychiatry, 68(5), 416–424. Spence, A. (1990). The magic flute. Chicago, IL: Canongate. Spence, A. (2004). Way to go. San Francisco, CA: MacAdam/Cage. Straube, T., Mentzel, H. J., & Miltner, W. H. (2007). Waiting for spiders: Brain activation during anticipatory anxiety in spider phobics. NeuroImage, 37(4), 1427–1436. Sukikara, M. H., Mota-Ortiz, S. R., Baldo, M. V., Felicio, L. F., & Canteras, N. S. (2010). The periaqueductal gray and its potential role in maternal behavior inhibition in response to predatory threats. Behavioural Brain Research, 209(2), 226–233. van der Hart, O., Nijenhuis, E. R., & Steele, K. (2006). The haunted self: Structural dissociation and the treatment of chronic traumatization. New York & London, UK: W. W. Norton. voorn, P., Vanderschuren, L. J., Groenewegen, H. J., Robbins, T. W., & Pennartz, C. M. (2004). Putting a spin on the dorsal-ventral divide of the striatum. Trends in Neurosciences, 27(8), 468–474. Walker, D. L., Miles, L. A., & Davis, M. (2009). Selective participation of the bed nucleus of the stria terminalis and CRF in sustained anxiety-like versus phasic fear-like responses. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 33(8), 1291–1308. Watt, D., & Panksepp, J. (2009). Depression: An evolutionarily conserved mechanism to terminate separation distress? A review of aminergic, peptidergic, and neural network perspectives. Neuropsychoanalysis, 11, 7–51. Wood, R. I., & Swann, J. M. (2005). The bed nucleus of the stria terminalis in the Syrian hamster: Subnuclei and connections of the posterior division. Neuroscience, 135(1), 155–179. Yoshino, A., Okamoto, Y., Onoda, K., Yoshimura, S., Kunisato, Y., Demoto, Y., . . . Yamawaki, S. (2010). Sadness enhances the experience of pain via neural activation in the anterior cingulate cortex and amygdala: An fMRI study. NeuroImage, 50(3), 1194–1201.

CHAPTER 11

Dissociation, EMDR, and Adaptive Information Processing: The Role of Sensory Stimulation and Sensory Awareness Ulrich F. Lanius and Uri Bergmann

When all the senses are synchronized, the soul emerges. —Adolfo Bioy Cesares, in The Invention of Morel, (1964, p. 71) It is this temporally coherent event that binds, in the time domain, the fractured components of external and internal reality into a single construct—the self. —Rodolfo Llinás (2001, p. 126)

DISSOCIATION—INFORMATION PROCESSING, SYNTHESIS, AND BINDING

As delineated in earlier chapters, we hypothesize that hyperarousal, concomitant primary dissociation, and the near-simultaneous thalamic dysfunction result in the traumatic experience remaining unintegrated. This disintegration and lack of binding of the experience accounts for the fragmentary nature of traumatic memory. Moreover, we suggest that state-dependent release of neurotransmitters at the time of recall prevents alteration of the traumatic memory and obstructs its embedding into an overall narrative and into the present context, that is, the awareness that the

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event is no longer happening. We further suggest that impaired information processing is at the core of dissociative phenomenology. It likely accounts not only for posttraumatic stress disorder (PTSD) symptoms like flashbacks and intrusive symptoms, but also for the separation of selves, including the experience of multiple selves. Consequently, we feel that working toward an understanding of the nature of information processing, as it is purported to occur in eye movement desensitization and reprocessing (EMDR; Shapiro, 1995), can ultimately enhance our understanding of traumatic stress syndromes and dissociative disorders. Impaired information processing reflects the inability of the brain to recognize and integrate external stimuli, for example, exteroceptive information coming from the environment, with internal stimuli, for example, interoceptive information from the body (e.g., Schore, 2002). This process has also been referred to as binding. We suggest that binding or the integration of information is disrupted in posttraumatic stress syndromes and dissociative disorders. We suggest that failure with regard to integration likely initially occurs both vertically across the different levels of the triune brain attributable to decreased thalamic function as well as horizontally across the hemispheres due to decreased cortical activation, resulting in a decrease of sensory information from cortical and subcortical areas information to the hippocampal areas, as well as less information flow laterally and across the corpus callosum. Among others, this results in a lack of external context1 that provides the time dimension to internally generated experience, for example, flashbacks. We hypothesize that this ultimately interferes with the mnemonic integration of experience.

AUTONOMIC AROUSAL, THALAMOCORTICAL DYSRHYTHMIA (TCD), AND INFORMATION PROCESSING

Specifically, we hypothesize that overwhelming affect in aversive experiences initially leads to increased sympathetic arousal involving increased catecholaminergic transmission (e.g., dopamine, norepinephrine, epinephrine) as well as heightened activity of the glutamate and acetylcholine systems. In response to the release of excitatory neurotransmitters, in the absence of a relationship and ventral vagal engagement, there is a corresponding release of inhibitory neurotransmitters that include endogenous opioids and endogenous cannabinoids that mediate a counteracting dorsovagal parasympathetic response. This in turn results in hyperpolarization of the thalamus, resulting in deafferentation of relevant cortical areas (e.g., specifically those that pertain to the sensory information associated with the overwhelming experience). Thus, changes in thalamic functioning and altered neural connectivity lead to a failure of integration of behavior, sensation, affect, cognition, and memory. The hyperpolarization of the thalamus is likely associated with profound effects on brain wave activity. More likely than not, this phenomenon results in excessive low-frequency brain wave activity (e.g., delta, theta, alpha) in some areas of the brain, that is in some cases counteracted by excessive levels of high-frequency activity (e.g., beta and gamma). That is, in some cases, thalamic inhibition may coexist with cortical activation (Vogt & Vogt, 2009). The resulting TCD likely interferes not only with

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sensory processing but also with the integration of information in general, affecting how experience is bound together. Although we focus on sensation and memory, similar arguments apply to motor behaviors, emotions, and thoughts. We suggest that, ultimately, TCD becomes manifest in positive and negative features or symptoms that are the hallmark of PTSD and dissociation. Effective treatment restores normal thalamic functioning and normalized cortical rhythms that allow for the integration and binding of information into present time, a person’s autobiographical narrative, and ultimately his or her sense of self. We suggest that EMDR is one such treatment that may be able to assist with that task.

EMDR: THE ADAPTIVE INFORMATION PROCESSING (AIP) MODEL

The AIP model (Shapiro, 2001) is a neurobiological heuristic based on the notion of neural networks and represents a paradigm shift from psychological theory toward neuroscience. It is also the theoretical foundation that explains and predicts the treatment effects of EMDR (Shapiro, 2001). Moreover, AIP hypothesizes a physiologically based information processing system that assimilates new experiences into already existing memory networks. These memory networks are seen as the basis of perception, attitudes, and behavior. Perceptions of current situations are automatically linked with associated memory networks. Accordingly, Shapiro conceptualizes information processing as the linking of neural networks, related to our experience, that include thoughts/beliefs, images, emotions, and sensations. Shapiro argues that pathology results when traumatic or stressful events interfere with information processing and the forging of connections between different neural networks. Accordingly, AIP asserts that a particularly distressing incident can become dysfunctionally stored in state-specific form, frozen in time in its own neural network, unable to connect with other memory networks that hold adaptive information. That is, primary dissociation (also see Chapter 1) attributable to the effects of autonomic nervous system activation (but described above as secondary to thalamic dysfunction), secondary to stress, may interfere with AIP and with its associative linking of information. Consequently, when reaccessing the neural networks related to a traumatic or fearful experience, a state-dependent reactivation of a dissociative process likely interferes all over again with the adaptive linking of the information into the present context, thus contributing to the timeless nature of traumatic memories (Van der Kolk, Burbridge, & Suzuki, 1997); rather than their integration into present experience, for example, it is no longer happening—I am safe now. Experiences that are inadequately processed are fragmented and become susceptible to dysfunctional recall with respect to time, place, and context. As a result, new information, positive experiences, and affects are unable to functionally connect with the traumatic memory. This impairment is postulated to lead to a continuation of traumatic (or nontraumatic) symptoms and to the development of new triggers. AIP asserts that the EMDR protocol involves accessing dysfunctionally stored information, stimulating the innate processing system through the standardized protocols and procedures (including the bilateral sensory stimulation), and facilitating the linking-in of adaptive information held in other memory networks. As a result of

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successful treatment, it is posited that the memory is no longer isolated, but rather appropriately integrated within the larger memory network. Consequently, accessing of adaptively linked information is experienced as integrated, whole, and appropriate to the present context.

TOWARD A MECHANISM OF AIP

There is as yet no consensus on the mechanism by which eye movements (EMs) or alternating bilateral sensory stimulation invoke the process of healing through AIP. Various models have been proposed to account for EMDR’s underlying mechanisms of action (Gunter & Bodner, 2009). Denny (1995) suggested an inhibition model in which an orienting reflex suppresses the disturbance of traumatic memories. Maxfield, Melnyk, and Hayman (2008), as well as Andrade, Kavanaugh and Baddeley (1997) postulated working memory mechanisms, where EMs interfere with the vividness of traumatic material in the visuo-spatial-sketchpad (VSSP) of working memory. Other proposed mechanisms include reciprocal inhibition (Denny, 1995), extinction (Armstrong & Vaughn, 1996), orienting response (e.g., MacCulloch & Feldman, 1996), dual attention (e.g., Lee, 2008), dearousal (e.g., Söndergaard & Elofsson, 2008), relaxation response (Sack, Lempa, Steinmetz, Lamprecht, & Hofmann, 2008), interhemispheric connectivity (e.g., Propper & Christman, 2008), hemispheric laterality (Bergmann, 1998), as well as thalamic activation models (Bergmann, 2008), including postulated cerebellar involvement (Bergmann, 2000). Stickgold (2002) opined that EMDR stimulation mediated a sufficient surge of acetylcholine to activate rapid eye movement (REM)-like physiological systems and that this promoted the integration of traumatic memories into general semantic networks. Psychophysiological dearousal effects of EMs have been demonstrated (e.g., Barrowcliff, Gray, Freeman, & MacCulloch, 2004; Barrowcliff, Gray, MacCulloch, Freeman, & MacCulloch, 2003) and these are supportive of the reassurance reflex model of MacCulloch and Feldman (1996). Pearson (2009) proposed that EMDR stimulation may exert its effect through activation of parietal functions, resulting in the integration of sensory information and the updating of the current representation of person and space, which incorporates an awareness of current body reality, sense of self, and world view.

SENSORY STIMULATION AND EMDR—RELEVANT FINDINGS TO PTSD AND DISSOCIATIVE DISORDERS

While there is little doubt that EMDR is an effective treatment for PTSD (e.g., Foa, Keane, Friedman, & Cohen, 2009), both the theoretical rationale of EMDR, for example, the AIP model, as well as the underlying mechanism of the EMDR, particularly the role of sensory stimulation, remain controversial (e.g., Hertlein & Ricci, 2004). At the same time, clinically, it appears that sensory stimulation plays an important role in information processing and the associative nature of EMDR (e.g., Jeffries & Davis, 2012). Specifically, it has been suggested that EMDR can bring dissociated material and

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aspects of self into conscious awareness, essentially acting as a “divining rod” for dissociation (Paulsen, 1995). This phenomenon is crucial not only to our understanding of AIP in EMDR but also at the core of our understanding of the nature of dissociation. Moreover, other significant effects of EMs relevant to the phenomenology of dissociation and traumatic stress syndromes have been reported. That is, EMs improve episodic memory (Christman, Garvey, Propper, & Phaneuf, 2003). Moreover, the accuracy of recall appeared to be increased with increased retrieval, including associative and contextual information (Parker, Buckley, & Dagnall, 2009), but also decreased false recognition (Parker & Dagnall, 2007). Christman et  al. (2003) and Christman and Propper (2001) hypothesized that this effect may be attributable to increased interhemispheric connectivity. While EMs appear to facilitate episodic memory, there also appears to be a decrease in the vividness and emotionality of memory (e.g., van den Hout, Muris, Salemink, & Kindt, 2001) as well as decreased arousal associated with the recall of memory consistent with a dearousal or relaxation effect that has been reported with EMDR (e.g., Barrowcliff et  al., 2003). The sensory stimulation in EMDR likely has a twofold effect. On one hand, it increases affective regulation, thus maintaining the client’s staying within the window of tolerance; on the other hand, it appears to increase associative access to memories. In that sense, sensory stimulation has both an accelerative and a braking function at the same time. Apart from arousal, EMDR also seems to affect attentional orienting (Kuiken, Bears, Miall, & Smith, 2001). In fact, MacCulloch and Feldman (1996) suggest that an investigatory orienting response (Pavlov, 1927; Sokolov, Spinks, Lyytinen, & Naatanen, 2002) may be a possible explanation for the EMDR effect, potentially also mediating a dearousal effect. While EMDR will produce an orienting response, in the long run it will reduce orienting to novel stimuli (Lamprecht et al., 2004). Investigating auditory stimuli and event-related potentials (ERPs), they found a significant reduction in the P3a component, signifying decreased arousal as well as eventually decreased orienting to novel stimuli. In a nonclinical study of EMs using near-infrared spectroscopy (NIRS), Ohtani, Matsuo, Kasai, Kato, and Kato (2005) described both effects, that is, much increased emotional memory and blood oxygenation levels in the prefrontal cortex (PFC) when accessing an emotional memory. Over time, blood oxygenation levels were reduced through repeated recall with EMs. SENSORY STIMULATION AND EMDR—AN EFFECT ON THALAMIC FUNCTION

We review the literature on sensory stimulation and suggest that sensory stimulation and associated sensory awareness are involved in modulating oscillatory activity in the brain, which has been linked to information processing. Specifically, we propose that sensory stimulation contributes to the synchronization of dynamic neuronal networks. This is referred to as temporal binding. This process conjoins the fractured aspects of internal and external reality in the time domain, counteracting the effects of dissociation. This process not only affects hemispheric laterality but also memorial, somatosensory, emotional, and cognitive integration. Accordingly, we suggest that sensory stimulation and sensory awareness, more likely than not directly affect thalamic activity and play an important role in AIP.

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THE ROLE OF THE THALAMUS

The thalamus is a bilateral structure located deep in the core of the brain, composed of about 50 groupings of nerve cells, neural tissue, and fibers called nuclei. It is the main source for the external stimulation of the cortex. Activating transient complexes of neurons, it functions as the sensory gateway to the cortex and principal synaptic relay for information reaching the cortex. All external sensory input, except for olfaction (smell), which is projected first to the amygdala, is projected first to the central relay station of the brain, the thalamus, and from where it is relayed onward to the upper regions of the brain, the cerebral cortex. We suggest that sensory input that is part of EMDR bilateral stimulation likely directly affects thalamic functioning, more likely than not through its role in oscillatory activity. The thalamus is not only a relay station mediating both top-down (information from the cortex) as well as bottom-up processing (information from the brain stem; afferent input to the cortex), but it is also involved in integration of information. It is reciprocally interconnected with the PFC, the basal ganglia, the somatosensory cortex, the association areas, the auditory cortex, the visual cortex, the motor cortex, the cerebellum, brainstem, and limbic structures. Its binding functions, detailed below, are activated by attentional aspects of arousal, alertness, or interest. It has been suggested that it mediates the interaction between attention and arousal (Portas et al., 1998), clearly relevant to the phenomenology of traumatic stress syndromes. Arousal and attention rely on distinct anatomical systems (Luria, 1973), wherein the system for arousal is mainly subcortical and the one for attention is mainly cortical. However, the two systems share an important anatomical substrate represented by the thalamus. The ability of the thalamus to synchronize the various neural assemblies throughout the brain, each oscillating at their own signature frequency, into innumerable coherent combinations of functional networks, may render it the cornerstone of perceptual, cognitive, memorial, and somatosensory integration and temporal-cognitive binding (Bergmann, 2008; Llinás, 2001). Ultimately, we suggest that deactivation of specific thalamic nuclei by increased arousal interferes with the integration of sensory components of an experience into an integrated memory.

BRAIN IMAGING AND TRAUMATIC STRESS SYNDROMES—THALAMIC DYSFUNCTION

A number of neuroimaging studies using script-driven imagery have identified decreased thalamic activation in PTSD (e.g., Bremner, Krystal, Southwick, & Charney, 1996; Liberzon, Taylor, Fig, & Koeppe, 1996), both during flashback activity (e.g., Lanius et al., 2001) as well as during recall of emotional states (e.g., Lanius et al., 2003). Moreover, there is some suggestion that alterations in thalamic activity may be the underlying factor with regard to changes in functional connectivity as well as differential patterns of left- and right-hemisphere activation in PTSD (Lanius et al., 2004). It should be noted that decreased thalamic activation is identified in some but not all studies. This may be attributable to a number of factors, including but not

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limited to inherent differences in targeted response variables (e.g., metabolism, blood oxygenation) and their relative time courses, differences in scanner resolution that affect spatial and temporal resolution, as well as sample differences between studies (e.g., chronicity of disorder, comorbidity, type of trauma, as well as task or resting state). High levels of arousal have been shown to reduce thalamic activation (Portas et al., 1998). High levels of arousal during traumatic experiences may lead to altered thalamic sensory processing, thus disrupting the transmission of sensory information to the frontal cortex, cingulate gyrus, amygdala, and hippocampus. Thalamic dysfunction has been hypothesized as the functional mechanism underlying flashbacks in PTSD as well as that of dissociative symptoms in general (Krystal, Bremner, Southwick, & Charney, 1998). It may therefore be evident during script-driven flashback activity but less so during the resting state or other periods of relative freedom from intrusive phenomena. Nevertheless, Yin et al. (2011) suggest that even restingstate functional connectivity of the thalamus with the ventromedial PFC (VMPFC) is reduced in PTSD. We suggest that flashbacks and other dissociative experiences are, similar to some other psychiatric and neuropsychiatric conditions, likely attributable to altered temporal-cognitive binding. That is, thalamic dysfunction may account for the lack of integration in somatosensory and cognitive percepts, interhemispheric integration, as well as integration of memory in space and time in PTSD (Bergmann, 2008). That is, it is hypothesized that altered brain connectivity accounts for the fragmented nature of memory in PTSD and dissociative disorders—specifically traumatic memories remaining isolated from ordinary consciousness, the inability to assimilate traumatic memories into the present context, as well as for the failure to integrate the totality of what is happening into personal memory and identity, all of which ultimately result in a loss of self.

PTSD AND DISSOCIATION—A THALAMOCORTICAL DYSRHYTHMIC SYNDROME?

Llinás and Ribary (2001) suggest that impaired functioning of thalamocortical circuits involved in temporal binding may be at the root of many neurological and psychiatric conditions. This is supported by magnetoencephalography (MEG) studies that suggest increased low-frequency rhythmicity in conjunction with a widespread and marked increase of coherence among high- and low-frequency oscillations (Llinás & Ribary, 1994). This phenomenon has been described as TCD (Llinás & Ribary, 2001; Llinás, Ribary, Jeanmonod, Kronberg, & Mitra, 1999) and is indicative of either reduced thalamic function or reduced thalamic interconnectivity with other neural systems. A number of studies support such a conceptualization of TCD. These include patients suffering from neurogenic pain (Cauda et  al., 2009; Schulman, Ramirez, Sonenshayn, Ribary, & Llinás, 2005); Tourettes syndrome (Sukhodolsky, Leckman, Rothenberger, & Scahill, 2007); attention deficit disorder (Sukhodolsky et al., 2007); migraines (e.g., Coppola et al., 2007); tinnitus (e.g., De Ridder et al., 2007); absence

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seizures (Vitko et al., 2007); schizophrenia (Uhlhaas & Singer, 2010); and Parkinson’s disease or depression (Llinás & Ribary, 1994). Abnormal electroencephalogram (EEG) activity has also been reported in PTSD, describing alterations in beta, gamma, and sigma activity (Cohen et al., 2013); alpha activity (Jokic-Begic & Begic, 2003); altered theta activity (e.g., Todder et  al., 2012); as well as an increased theta/alpha ratio (Veltmayer et al., 2006). In tinnitus, peripheral neurogenic pain, Parkinson’s disease, and other neuropsychiatric disorders that are striatal in origin, the dysrhythmic mechanism is triggered “bottom up,” which means from the thalamus toward the cortex. In other situations like epilepsy, neuropsychiatric conditions of cortical origin, and central cortical neurogenic pain, there may be a “top down” mechanism, triggered by a reduction of the corticothalamic input. Both “bottom up” and “top down” situations result in excess inhibition or disfacilitation, generating thalamic cell membrane hyperpolarization (diminished function) and low-frequency oscillation. Therefore, the same mechanism responsible for the organization of consciousness, when altered in its organization and timing, can be the genesis of neuropsychiatric conditions (Llinás & Ribary, 2001).

THE NATURE OF MEMORY

Gazzaniga (1980) argued that memory is the result of a conglomerate of independently functioning mental systems that mainly reflect nonverbal processing systems in the brain. That is, the mind is composed of a great number of unimodal and multimodal elementary units connected in neural networks. Mental processes (perception, memory, cognition, emotion, and somatosensory integration) are interactions between these units/networks, which excite and inhibit each other in parallel rather than sequential operations (Rumelhart & McClelland, 1986). Accordingly, memory is not a unitary process; rather, it is composed of multiple processes and systems (Tulving & Schachter, 1990). Memory of a specific event is not stored or processed in a single location in the brain but is distributed across a network of different brain areas. In this context, knowledge can no longer be thought of as stored in localized structures; instead, it consists of changes in synaptic strength between groups of units/networks that are distributed throughout the brain (Rumelhart & McClelland, 1986). Thus, memories result from connections between nerve cells, which, when activated, cause the phenomenon of a memory being recalled. That is, memory is the result of changes in synaptic strength within assemblies of neurons (Squire & Kandel, 1999). Moreover, memory is the result of a transient activation of neural networks and/or an activation of distributed assemblies of brain structures that were engaged in perceiving and encoding the information that one is trying to remember (e.g., Slotnick, 2004). Not surprisingly, vivid remembering has been shown to activate areas of the sensory cortices (Wheeler, Peterson, & Buckner, 2000). Similarly, when people recalled and reexperienced personal life episodes marked by sadness, happiness, anger, or fear, the process of feeling such emotions resulted in activation of the somatosensory

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cortex (Damasio et al., 2000). This effect is likely not only cortical in nature but also involves the basal ganglia and subcortical structures (e.g., Packard & Knowlton, 2002). Moreover, as has been proposed in Chapter 8, The Clinical Sequelae of Dysfunctional Defense Responses: Dissociative Amnesia, Pain and Somatization, Emotional Motor Memory, and Interoceptive Loops, there are emotional memory triggers based in the basolateral amygdala; procedural memories based in the striatum; obstructed defense responses stored in subcortical loops through the midbrain; and emotional motor memories involving all of these networks. These networks, during memory retrieval, will experience a reactivation of encoding-related brain activity (Nyberg, Habib, McIntosh, & Tulving, 2000). Such a conceptualization is consistent with clinical observation of being able to reinvoke state-dependent memory during EMDR and other psychotherapeutic interventions.

THE NATURE OF TRAUMATIC MEMORY

Van der Kolk (1996) suggests that the experience of day-to-day, nontraumatic events is integrated into consciousness as a unitary experience without the sensory aspects of the event being registered separately (e.g., visual images or olfactory, auditory, or kinesthetic sensations). Flashbacks, on the other hand, lack such integration of experience. Indeed, they have been described as timeless, predominantly nonverbal, imagery-based memories (e.g., van der Kolk & Fisler, 1995), lending support to the notion that the failure to integrate traumatic memories into the present context accounts for their ongoing disturbing nature (e.g., Lanius, Bluhm, & Lanius, 2007). While ordinary memories are altered by repeated recall (Estes, 1997), this appears to be less the case for traumatic memories, a phenomenon that may be in part attributable to amygdalar inhibition (e.g., Lanius et al., 2001). The fragmented nature of traumatic memory has been attributed to dissociation. The latter is presumed to result in an alteration in consciousness that disrupts the integration of information, resulting in clients’ inability to integrate memories into the present context and to integrate the totality of what is happening into personal memory and identity. There is a failure of integration of the sensory aspects of traumatic memories into an overall narrative and into present time, leaving them timeless, accounting for their ongoing disturbing nature. Sensory fragments remain isolated from ordinary consciousness (van der Hart, van der Kolk, & Boon, 1998). Accordingly, Metcalfe, Cottrell, and Mencl (1992) have argued that implicit or nonepisodic memory remains unbound—the features of our perceptual world freefloating rather than integrated (Treisman & Gelade, 1980). Episodic memory, on the other hand, involves a conjunction or binding of disparate parts (Metcalfe et al., 1992), thereby lacking that fragmented and free-floating experience. In contrast, in ordinary autobiographical memory, the sensory elements of the experience are automatically integrated into an episodic memory, which is then part of a personal narrative (e.g., Van der Kolk, 1996). When subjects are specifically instructed to recall particularly affect-laden memories, a predominantly right-hemispheric activation pattern emerges (Maddock, Garrett, & Buonocore, 2003), bearing some semblance to the profile of traumatic memories.

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Similarly, hemispheric laterality studies with PTSD subjects have consistently shown marked increased activation in the right hemisphere, as compared to the left hemisphere (e.g., Pagani et al., 2005). As described above, PTSD and flashbacks appear to be associated with greater right-hemisphere activation, whereas individuals without PTSD appear to have brain activation patterns associated with the recollection of autobiographical memory; that is, they show greater left-hemisphere involvement (Lanius et al., 2004). Accordingly, neuroimaging studies of PTSD show neuronal networks consistent with a nonverbal pattern of memory retrieval with increased right-hemisphere activation. This supports the notion that the failure to integrate traumatic memories into the present context accounts for their ongoing disturbing nature. Even in the resting state, the changes attributed to PTSD are on the right side (Yin et al., 2011).

OSCILLATIONS IN NEURAL NETWORKS

Although we focus on the anatomical links between different brain areas, functional domains can also be integrated by synchronization of oscillations. Neural oscillations play a key role in attentional selection. A central role in perceptual selection has also been attributed to the momentary phase of brain oscillations. Alpha-band oscillations are associated with attentional suppression mechanisms in the visual cortex (e.g., Sauseng et  al., 2005). Moreover, faster rhythms—alpha, beta, and gamma— are modulated as a function of the phase of slower oscillations—delta or theta (e.g., Jensen & Colgin, 2007). Alpha oscillations, in turn, through pulsed inhibition, may have an inhibitory effect not only on gamma oscillations but also on information processing in general (Jensen & Mazahari, 2010). A comprehensive review by Knyazev (2007) specifies delta, theta, and alpha oscillations as global processing modes, and the faster beta and gamma frequencies as local mode oscillations for specific cognitive tasks. Delta waves generated in the mesolimbic system are enhanced by stimuli salient for motivation and drive. Limbic theta oscillations have multiple generators for emotion and memory functions: theta in the amygdala and hippocampus being especially important for memory of emotional experiences. Alpha frequencies are dominant in adult humans and contribute to inhibition of slower global oscillations. High-frequency gamma rhythms within local neural ensembles enhance the efficacy of signals located within the locus of the attentional spotlight (e.g., Womelsdorf & Fries, 2006). Of relevance to PTSD, it has been observed that neural synchronization is more prevalent during states of high arousal and gamma oscillations occur during periods of increased vigilance (Munk, Roelfsema, König, Engel, & Singer, 1996; Steriade, Amzica, & Contreras, 1996). Theta and gamma oscillations interact in memory and it is conceivable that a failure to regulate local high-frequency activity would contribute to either intrusion of memory fragments or suppression of emotional memories—or both, as happens in PTSD. Alpha oscillations specifically have an inhibitory function and play an active role in information processing (Klimesch, 2012). Suppression of alpha brainwave activity, or alpha suppression, occurs in response to gaze orientation and an anticipatory

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response to visual stimulation. When observers open their eyes, the amplitude of EEG oscillations in the alpha band decreases significantly. Indeed, lower-frequency rhythms like alpha and beta may act as a gating mechanism, and have been proposed to support the selective processing in the gamma band, specifically after the initiation of saccades (e.g., Medendorp et al., 2007). A decrease in alpha activity is associated with increased external orienting and exteroceptive awareness, whereas an increase in alpha activity is associated with increased internal or interoceptive awareness. Thus, the EMDR protocol, with elements of both interoceptive awareness (e.g., body sensation) and exteroceptive awareness (bilateral stimulation) may invoke an alteration between increased tonic alpha activity and decreased phasic alpha activity, both phenomena that have been associated with increased cognitive as well as mnemonic performance (Klimesch, 1999). Cross-frequency coupling mechanisms coordinate neural activity on multiple timescales, thus selectively influencing stimulus processing at different levels of the sensory hierarchy by controlling the excitability state within local neural ensembles as well as across distributed cortical networks (e.g., Canolty & Knight, 2010). Accordingly, disparate elements of an experience can be bound together through coherence of the EEG frequencies at the different sites involved. Buchholz, Jensen, and Medendorp (2011) suggest that tactile stimuli alterations in brain oscillatory activity occur in response to, particularly, a transient gamma-band response, as well as alteration in lower frequency rhythms, particularly alpha and beta. Accordingly, Freyer, Reinacher, Nolte, Dinse, and Ritter (2012) reported that purely passive repetitive sensory stimulation has a pronounced impact on sensorimotor integration. That is, repetitive sensory stimulation not only changes sensory function and evoked activity in somatosensory areas but also significantly affects resting-state functional connectivity between brain areas engaged in the sensorimotor integration processes. They hypothesize that such connectivity changes might be related to the findings of enhanced sensorimotor integration, enhanced information transfer, and enhanced learning.

INHIBITORY NEUROTRANSMITTERS AND OSCILLATORY ACTIVITY

Both opioids and cannabinoids have an impact on oscillatory activity in the brain. For instance, methamphetamine, which can lead to psychosis, increases high-frequency gamma oscillations in rats, but this effect can be disrupted by blocking the cannabinoid CB1 receptor. This suggests that the endogenous cannabinoid system is important for network oscillations in the striatum as well as in the hippocampus and PFC (Morra, Glick, & Cheer, 2012). Lensing et al. (1995) found that opiate blockade facilitates cognitive processing and cortico-thalamocortical processing of visual stimuli. That is, in two autistic boys, naltrexone showed evidence of alpha blocking, increasing not only visual pursuit behavior in response to the picture of their respective mother but also visual pursuit behavior in social situations in general. Similarly, in a group of normal men, opioid blockade elicited a significant slowing of alpha frequency. Conversely, microinjections of morphine into the medial thalamus and periaqueductal gray (PAG) produce slow-wave sleep spindles in addition to analgesia, though at higher doses they can produce behavioral agitation (Tissot, 1980).

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SENSORY STIMULATION AND 40-Hz OSCILLATORY BRAIN ACTIVITY

Gamma waves at a frequency of 30 to 200 Hz can occur throughout the cortex for integrated perception, attention, memory, and consciousness itself (Uhlhaas & Singer, 2010). Forty Hertz activity occurs naturally in animals and humans during the alert, waking state, as well as during REM sleep. Synchronous high-frequency discharges in discrete relay neurons of the thalamus, and in the cortical areas to which these project, suggest that the thalamus has an integrative pacemaker function. Specifically, the reticular nucleus is involved in the genesis of 40 Hz oscillations (Pinault & Deschênes, 1992) and reflects the resonant property of the thalamocortical system. The reticular nucleus has GABAergic projections to the intralaminar, midline, and mediodorsal nuclei of the limbic thalamus (Bentivoglio et  al., 1993). These nuclei communicate information from the brainstem to cortical areas involved in attention, arousal, emotion, and sensorimotor integration. Gamma-band oscillatory activity serves to mediate global temporal mapping by scanning for, targeting, and synchronizing the activity of the various neuronal assemblies, each oscillating at their own respective frequencies, creating network resonance, and binding them into a coherent and integrated perceptual consciousness (Llinás, Leznik, & Urbano, 2002; Steriade, Curró Dossi, & Contreras, 1993). Gamma oscillations have been related to cognitive processing and to the temporal binding of sensory stimuli and they appear to be reset by sensory stimulation (Joliot, Ribary, & Llinás, 1994). That is, 40-Hz activity that is triggered by sensory stimulation appears to be involved in the temporal conjunction/binding of different sensory (outer) and experiential (inner) components of consciousness into one global image or experience, an event that is referred to as temporal-cognitive binding. This suggests that fast oscillatory activity is necessary for binding activations of distant brain areas during complex and rapid EMs. Successful interaction with our environment relies on the integration of concurrent input from different senses. In part, such multisensory integration occurs at the level of the thalamus (Brett-Green, Fifková, Larue, Winer, & Barth, 2003) and in the cerebral cortex. Two studies have reported on gamma activity associated with EMs in EMDR. Propper and colleagues (2007), in a study investigating EMs and gamma coherence, contrary to their hypothesis of increased interhemispheric coherence after EMs, found decreased gamma frequency coherence associated with EMs. These apparently contradictory findings may reflect the fact that in the Propper study, gammaband activity (GBA) was measured after, but not during, EMs, leaving the possibility that increased GBA occurred during the EMs. Indeed, Pagani et al. (2012) found not only decreased alpha activity after EMDR treatment but also increased activity in the gamma band during ocular bilateral stimulation. Pagani and colleagues’ (2012) findings are reminiscent of Bastin et al. (2012), who report that pursuit EMs involve GBA of 50 to 150 Hz in frontal and parietal eye fields and areas of visual cortex. However, Porter, Metzger, and Groh (2007) suggest that interactions between sensory pathways can occur at very early points in sensory processing streams, below the level of the thalamus. They imply that multisensory integration may already occur at the subcortical level, rather than being a cortical-level process exclusively. This is consistent with findings that consciousness can occur in children born

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without a cortex—in the condition referred to as hydranencephaly (Merker, 2007). One structure involved in multisensory integration at the subcortical level is the superior colliculus (SC; Cappe, Rouiller, & Barone, 2009; Macaluso & Driver, 2005; Wallace, Meredith, & Stein, 1998) and there is evidence of collicular gamma oscillations (Merker, 2007). What’s more, the SC is the only area outside of the cerebral cortex in which fast oscillations in the gamma range occur, paralleling such information processing as occurs in the cortex (Brecht, Goebel, Singer, & Engel, 2001; Brecht, Singer, & Engel, 1998, 1999). Indeed, there is evidence that conditioned fear can be expressed in the absence of a cortex (Berlucchi & Buchtel, 1975). This is consistent with observations that PTSD symptoms can be expressed in the absence of significant cortical activation (Lanius, Bluhm, Lanius, & Pain, 2005; Lanius, Lanius, Fisher, & Ogden, 2006), including the absence of amygdaloid activation (Britton, Phan, Taylor, Fig, & Liberzon, 2005; Gilboa et  al., 2004). Consistent with our deafferentation hypothesis (also see Chapter  1), individuals with PTSD show a subcortical-orienting response at the level of the SC and the PAG, whereas individuals without PTSD will show cortical activation during orienting (Steuwe, Lanius, & Frewen, 2012). Studies with decorticate animals suggest that no cortex is needed for conditioning to occur (Berlucchi & Buchtel, 1975; Olds, 1973). That is, conditioning can occur without cortical participation. Subcortical structures, particularly the PAG, are involved in organizing animal defensive behaviors and basic affects (Panksepp, 1998). There is an implication that basic defensive and affective responses that are hardwired in the PAG can continue to be conditioned in the lower brain structures, even when the higher brain structures and cortical functioning are absent.

GBA AND REM SLEEP

While REM sleep is recognizable in mammals and birds, it is not evident in snakes and other reptiles (Kelly, 1991). This is likely to relate to different levels of information processing, awareness, and consciousness. Not only is REM sleep associated with rapid EMs, but also with 40 Hz or GBA in the brain (e.g., Muzur, Pace-Schott, & Hobson, 2002). That is, the awake state and REM sleep state are similar with respect to the presence of gamma oscillations. However, during REM sleep, in contrast to the normal waking state, there is a relative lack of ongoing response to sensory stimuli within the environment (Kelly, 1991). Moreover, during REM sleep, 40-Hz activity in the brain is not reset by sensory input (Llinás & Ribary, 1993). Llinás and Paré (1991) suggest that dreaming is a state of hyperattentiveness to internal stimuli, and as a result “we do not perceive the external world during REM sleep because the intrinsic activity of the nervous system does not place sensory input in the context of the functional state being generated by the brain.” Moreover, during REM sleep, as compared to the awake state, temporal conjunction (connectivity) between frontal and perceptual cortical regions is uncoupled with a concomitant decrease in frontal and executive functioning (e.g., Corsi-Cabrera et al., 2003). Therefore, while there is clearly information processing occurring in REM sleep (e.g., Hennevin, Hars, Maho, & Bloch, 1995), this likely occurs at an implicit

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level only (e.g., Yordanova, Kolev, & Verleger, 2009) and is likely not bound in time with regard to the present context. This potentially accounts for the relative lack of integration of traumatic memories during REM sleep, as evidenced by the disruptive nature of ongoing nightmare activity. In other words, the nature of traumatic memory may interfere with its integration during REM sleep. It may be the case, with regard to traumatic memory, that the involvement of the attentional system and the frontal cortex, elicited by an orienting response to sensory input, may be necessary for memory to become declarative and part of an autobiographical narrative.

NEURAL SYNCHRONY: SYNTHESIS, BINDING, AND INFORMATION PROCESSING

Binding (or connecting) together aspects of our internal and external experiences is one aspect of synthesis in the moment . . . For example, we typically automatically and unconsciously bind together sensations of movement and touch, temperature, taste, smell and sight into one whole and higher order perception. (van der Hart, Nijenhuis, & Steele, 2006, p. 145) As van der Hart et al. (2006) observe, survivors frequently have difficulties even at the most basic level of synthesis. Perceptual unity requires a mechanism that allows these different sensory components to be gathered into one global image, a notion that bears remarkable resemblance to AIP. Llinás and Ribary (2001) suggest that cognition and/or consciousness is the property of thalamocortical cycling leading to thalamocortical dialogue. Therefore, temporal-cognitive binding refers to an inherent mechanism that links the elements of experience together with their current context. The brain uses frequency oscillation as a means to integrate separate parts of a perception. Thus, the perception of an object is created by the superimposed oscillation. For instance, coherent representation of an object in the visual system is achieved by the synchronization in the gamma-band of a distributed neuronal assembly (Tallon-Baudry, Bertrand, Delpuech, & Premier, 1997). Likewise, language expression is the product of the functional binding of different areas of the brain linked through the interaction of theta and gamma oscillations (Doesburg, Vinette, Cheung, & Pang, 2012). All sensory elements from the outside world and all inner experiential/interoceptive elements are combined/linked temporally (in real time) and coherently (as an integrated and whole experience). Temporal coherent conjunction of these inner- and outer-sensory percepts is described as “binding.” Similarly, memory is generated by a stream of oscillating networks. The brain regions in the cortex that are involved in the perceiving and processing of color, size, shape, and the various other object attributes, are close, if not identical, to the brain regions important for remembering (Bergmann, 2008). Multimodal sensory information from diverse areas of cortex is assimilated in the medial temporal lobe (MTL; Suthana & Fried, 2012), which forms the essential substrate for multiple memory systems (Aggleton, 2012). Ostensibly, remembering is the reactivation of the majority of the components (synchronized neuronal assemblies) that was used to encode the experience that one is trying to remember (Squire & Kandel, 1999).

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What is required to facilitate the reactivation of a memory is the linking together of the various neuronal assemblies (e.g., visual, auditory, associational, cognitive, memorial, somatosensory, and emotional) in several cortical regions throughout the brain, so that ultimately these assemblies are, again, activated as a synchronized network (Montgomery & Buzaki, 2007; Prince, Dasellar, & Cabeza, 2005). It is the thalamus and the 40 Hz GBA, however, that is required to bind, in real time, the various neuronal assemblies, mentioned above, each oscillating at their own respective frequencies (Llinás, 2001; Llinás & Ribary, 2001; Singer, 1993, 2001). Theta oscillations at 3 to 8 Hz in the MTL assist encoding of episodic memories, while recall of these also involves gamma oscillations at 30 to 100 Hz (Suthana & Fried, 2012). Hippocampal theta activity modifies the responsiveness of neurons in the anterior thalamus to promote memory functions (Tsanov et al., 2011). EMDR: EXTEROCEPTIVE AND INTEROCEPTIVE AWARENESS

In EMDR, exteroceptive awareness is mediated by administering bilateral sensory stimulation. Interoceptive awareness is mediated by the body focus in the standard protocol: “Where do you feel that in your body?” Thus, EMDR clearly mediates different aspects of mindfulness, both external and internal. Interoceptive awareness is commonly associated with the default mode network function that has been associated with self-referential processing, autobiographical memory, the capacity to plan, and a sense of self (also see Chapter 3, A Social–Cognitive–Neuroscience Approach to PTSD: Clinical and Research Perspectives), whereas exteroceptive awareness is associated with an attentional or salience network (e.g., Sadaghiani et  al., 2010). “Exteroceptive stimuli or outside events typically are only neurologically effective when they impinge upon the default mode network that encompasses the sense of one’s own body or ‘the self,’ ” which is why default network connectivity is crucial not only to our understanding of dissociation but also to the functional mechanism of EMDR. Indeed, recent findings suggest that EMDR does modulate default network connectivity (Landin-Romero et al., 2013). Exteroceptive awareness and externally directed attention is associated with decreased alpha activity, whereas internally focused attention and interoceptive awareness is associated with increased alpha activity (Cooper, Croft, Dominey, Burgess, & Gruzelier, 2003). It is suggested that EMDR, by combining an external with an internal focus, may directly affect alpha-band activity, which in turn modulates brain wave activity in other frequencies. This likely effects both salience and default network connectivity. Indeed, bilateral stimulation that effects exteroceptive awareness may assist in reestablishing attentional or salience network functioning. Salience network function may in turn assist development of default network mode processes—it has been suggested that salience network integrity predicts default network function (Bonnelle et al., 2012). It may be this very process that integrates internal experience with external experience, thus binding the targeted experience in present time. Specifically, we suggest that accessing the state-dependant memory, in conjunction with the purposeful linking of interoceptive awareness and exteroceptive awareness, and the resulting modulation of neuro-oscillatory activity may account

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OUTER WORLD VISUAL STIMULI “SIGHTS”

AUDITORY STIMULI “SOUNDS” Seeing

Hearing

SELF Proprioception

Touching

CONTACTUAL STIMULI “TOUCH”

OUTER WORLD Figure 11.1  Stimuli enter from the outside world and from internal proprioceptive events. The blend seems to contribute to a central thinking “self.” From Austin, J. H. Zen and the brain: Toward an understanding of meditation and consciousness, figure, p. 476, © 1998 Massachusetts Institute of Technology, by permission of The MIT Press.

for the EMDR treatment effect. We hypothesize that alternating interoceptive and exteroceptive awareness likely counteracts the alteration of consciousness associated with reaccessing state-dependant traumatic memory, thus allowing for integration of the traumatic experience into autobiographical memory. We hypothesize that this process is at the basis of information processing and a sense of self (also see Figure 11.1).

AIP AND TEMPORAL BINDING

Temporal binding, as an overarching framework of information processing, allows us an additional way to articulate the tenets of AIP, as follows: Under optimal conditions, new experiences tend to be assimilated by an information processing system that facilitates their linkage with already existing memory networks associated with similarly categorized experiences in the present context. The linkage of these memory networks tends to create a knowledge base that includes such phenomena as beliefs, expectations, and fears. That is, when a memory is accessed, adaptively, it is linked with emotional, cognitive, somatosensory, and temporal/memorial systems that facilitate its accuracy and appropriateness with respect to time, place, and contextual situation. We suggest that the autonomic impact of traumatic stress results in a release of neurochemicals that alter brain wave activity, with an ensuing breakdown of binding and synthesis. This results in traumatic or other distressing events being encoded maladaptively in memory. That is, there is inadequate or impaired linkage with memory networks containing more adaptive information. This may include

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preexisting mnemonic material, as well as exteroceptive awareness of an absence of present threat in the moment; for example, it is safe now. As suggested by Park, Zoladz, Conrad, Fleshner, and Diamond (2008), traumatic stress likely interferes with the consolidation of memory, which in part is likely attributable to a lack of integration of experience. Tsoory et al. (2008) reported memory disturbances after traumatic stress and interpreted these in terms of the links of the basolateral amygdala with different components of the MTL. Pathology is thought to be a result of the lack of integration and linkage between different aspects of a memory as well as resulting in altered functional connectivity between brain regions (Lanius et al., 2004; Shaw et al., 2002). After trauma, experiences may be inadequately processed and remain maladaptively linked within emotional, cognitive, somatosensory, and temporal systems. Memories thereby become susceptible to dysfunctional recall with respect to time, place, and context and may be experienced in fragmented form. Accordingly, new information, positive experiences, and affects are unable to functionally connect with the disturbing memory. This impairment in linkage leads to a continuation of symptoms and to the development of new triggers. EMDR procedures facilitate access to dysfunctionally linked experiential components, allowing them to be integrated/linked within appropriate emotional, cognitive, somatosensory, and temporal systems. This facilitates the effective processing of traumatic or disturbing life events and associated beliefs, to an adaptive resolution. Specifically, we hypothesize that the EMDR protocol, which targets the trauma memory through accessing different aspects of the traumatic experience, for example, sensory, emotional, and cognitive, reinstates the state-dependant memory of the experience. The addition of bilateral sensory stimulation likely counteracts the effects of anesthetic neurochemicals associated with accessing the state-dependant memory and their effects on brainwave activity. The engagement of an orienting response is likely associated with activation of the salience network on one hand, as well as with increased default network connectivity on the other. Moreover, it is likely that the alternating bilateral sensory stimulation likely contributes to hemispheric connectivity, particularly in the case of EMs that will result in ipsilateral and contralateral activation simultaneously. The EMDR protocol clearly involves attention to external sensory stimuli, as well as internally generated self-referential information, thus allowing for mnemonic integration of experience into an autobiographical sense of self. That is, this conjunction of externally applied sensory stimulation and internally generated fragments of experience while resetting the brain rhythms normally associated with accessing the state-dependent memory is likely what accounts for the EMDR treatment effect.

SENSORY STIMULATION: SOCIAL ENGAGEMENT AND DEFENSIVE RESPONSES

Ventral vagal activation and social engagement (e.g., Porges, 2001) are mediated by tactile, auditory, and visual perception (e.g., Trevarthen, 1993, 2005). It has been suggested that ventral vagal engagement attributable to eye gaze, facial expression, the prosody of voice, and the affective quality of touch is the underlying substrate

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of attachment (Trevarthen, 2005; Schore, 2001a). Moreover, oxytocin release occurs secondary to nonnoxious sensory stimulation, such as touch and warmth, sound, and visual stimuli (also see Chapter 6, Attachment, Neuropeptides, and Autonomic Regulation: A Vagal Shift Hypothesis). That is, sensory input likely stimulates social engagement. Specifically, the sensory stimulation that is intrinsic to EMDR is reminiscent of the sensory stimulation involved in child rearing—visual, kinesthetic, auditory—and it likely produces not only an orienting response but also SEEKING and social engagement and the absence of dissociation. On the other hand, there is evidence that sensory stimulation (Sahibzada, Dean, & Redgrave, 1986), including visual stimulation (Dringenberg, Dennis, Tomaszek, & Martin, 2003), at the level of the SC, can also elicit an orienting response and animal defensive behaviors, such as fight and flight. Similarly, subjects with PTSD, in response to direct gaze, showed activation in the lower brain structures, for example, the SC and the PAG, whereas nontraumatized individuals evidenced activation in higher cortical structures (Steuwe et  al., 2014). Brain activation in the lower brain structures in the PTSD group was conceptualized to be associated with the activation of an innate alarm system potentially relating to characteristics that evoke an orienting or defense response—snake- or spider-like movements. Activation of higher cortical structures in the non-PTSD group likely reflects evaluative “top-down” processes. This is then not just sensory stimulation but a stimulus within the case of the SC. Indeed, such animal defensive behaviors accompanied by sympathetic nervous system activation are at odds with the profound parasympathetic activation associated with a dorsovagal or dissociative response (e.g., Porges, 2001; Schore, 2001b). Thus, this very phenomenon may account for the phenomenon of breaking through dissociative barriers in PTSD in EMDR. If the client is able to be in a relational context, active defense responses at the level of the PAG and the SC may be integrated at higher cortical levels, whereas if a client is not able to be in a relational context, active defense responses may just be triggered without associated cortical integration. Moreover, in the case of successful EMDR treatment, this raises questions about whether sensory stimulation at the level of the SC may be involved in orienting to the present context. That is, orienting to the environment in the absence of a threatening stimulus counteracts dissociation without producing fight/flight responses. While environmental orienting allows easy access to active defenses when needed, it likely allows access to basic affective processes in general, including SEEKING (Panksepp, 1998), engendering exploratory behavior in a general, the antithesis of dissociative withdrawal. Such a conceptualization can inform our understanding as to why the therapeutic relationship and stabilization may be essential prior to using EMDR in severe traumatic stress syndromes and dissociative disorders.

SENSORY STIMULATION—NEUROPLASTICITY AND SYNAPTOGENESIS

Sensory awareness and sensory stimulation may not only be the underlying mechanism for temporal-cognitive binding but may also be involved in neurogenesis and neuroplasticity. Kaas (1999) suggests that the thalamus specifically plays a significant role in neuroplasticity, wherein neuroplasticity refers to the changing of

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neurons, the organization of their networks, and their function via new experiences. Neuroplasticity refers to the ability of the nervous system to adapt to a changed environment (Fitzgerald & Folan-Curran, 2002). It refers to the general property of the nervous system of being “plastic,” that is, changeable. As such, it refers to not only all changes related to learning but also all changes that occur during development, with changes across the estrous cycle and life span, as well as degenerative changes induced by stress, and so forth. It also refers to the generation of new neurons within the brain, and includes associative learning where simultaneous activation of cells leads to pronounced increases in synaptic strength—a phenomenon sometimes referred to as Hebbian Learning (Hebb, 1949). Sensory stimulation, in particular, plays a role in brain maturation (e.g., Schore, 2001b). That is, in early postnatal life, maintenance of critical levels of tactile input of specific quality and emotional content is important for normal brain maturation (Martin, Spicer, Lewis, Gluck, & Cork, 1991). Further, sensory input derived from contact with the mother during nursing has been suggested to shape dendritic growth (Greenough & Black, 1992). Until recently, it was thought that neuroplasticity and synaptogenesis were all but completed in the adult brain (Gage, 2002). However, more recently, there is evidence that there is ongoing neurogenesis and synaptogenesis in the adult brain (Karni & Bertini, 1997). Generally, sensory experience alters sensory representations in the cerebral cortex (Feldman, 2009). Specifically, Zito and Svoboda (2002) suggest that the adult cortex generates new synapses in response to sensory activity. In effect, there are experience-dependent structural changes in the brain that can occur rapidly, within 24 hours of sensory stimulation. What is more, oscillatory behavior in the brain associated with long-term potentiation (LTP) and long-term depression (LTD) has been associated with memory formation, including synaptic plasticity (Huerta & Lisman, 1995). This is consistent with Pearson’s (2009) suggestion that the sensory stimulation that is part of the EMDR protocol may be involved in facilitating neuroplasticity. Again, this raises the question as to whether the sensory stimulation associated with EMDR may aid in bringing about such structural changes in the brain. Initial findings suggest neuroanatomical changes in the hippocampus in PTSD secondary to EMDR (Bossini, Fagiolini, & Castrogiovanni, 2007). Similarly, evidence suggests that EMDR is one of the few treatments that may be beneficial in phantom limb pain (Schneider, Hofmann, Rost, & Shapiro, 2008; Wilensky, 2006) and tinnitus (Krieger, Klimek, Lis, Röder, & Siegel, 2001). These findings are consistent with a potential reversal of neural network disorganization in the brain (Wilson, Tinker, Becker, Hofmann, & Cole, 2000). Moreover, the EMDR protocol and its particular symptom or attentional focus, rather than inducing neuroplasticity in general, may assist in inducing the specific plasticity of healing with which we are concerned. AIP: TOWARD A NEUROBIOLOGICAL UNDERSTANDING

The physiological prerequisites of sensory awareness include arousal (e.g., “the ‘waking up’ of the brain by nonspecific modulatory systems”), sensory segmentation (e.g., “the basic step in sensory processing, which comprises both detection and binding of

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object features”), selection (e.g., processes including attention, that lead to an enhanced efficacy of subsets of neural signals), and working memory (e.g., the short-term storage of information about the current situation; Engel & Singer, 2001). Thalamocortical binding is related to sensory awareness (Engel & Singer, 2001; Palva, LinkenkaerHansen, Näätänen, & Palva, 2005). Sensory awareness “wakes up” the brain through thalamic activation—with sensory stimulation directly activating not only the SC but also the thalamus—the “nonspecific system.” The increased arousal results in an orienting response to the present environment. By attending to the present context, the client becomes aware of the present lack of threat and/or safety, ultimately resulting in a dearousal response. The EMDR protocol itself is clearly involved in neural network selection by focusing on the different fragmented aspects of a memory at a given time. Thereby, it makes these associated sensory percepts that relate to external sensory elements (the specific thalamic system), as well as inner/subjective interoceptive elements (the nonspecific thalamic system), functionally salient and available to processing and integration. Therefore, the external sensory perception of the therapeutic environment (mediated and bound/linked by the specific thalamocortical system) and the internal/proprioceptive elements (aspects of the memory, negative cognitions, positive cognitions, emotions, and sensorimotor experience bound together by the nonspecific thalamocortical system) are neurologically gathered together. The EMDR protocol thus not only includes an internal orienting that bears some semblance to Crick’s (1984) and Treisman’s (1982) notion of a searchlight that sweeps across different aspects of the experience, but also introduces a simultaneous orienting to external experience, resulting in sensory awareness of both past and current experience. Holding together the different aspects of experience in working memory, in conjunction with EMDR-specifc sensory stimulation, brings together and conjoins the aspects of the trauma with both adaptive information and awareness of safety in the moment. Divided attention limits excessive arousal of the thalamus, thereby allowing projection of the traumatic material into the cortex and conscious awareness without overwhelming the information processing system. Brain function is modulated by the senses (Llinás & Pare, 1996). EMDR-specific sensory stimulation provides the context of the “here and now” to the sensory fragments from the past, resulting in a shift in cognition to an awareness that “it’s just a memory . . . ” “. . . it’s in the past . . . it’s old stuff.” The fragments of the old memory become bound in present time with the realization that it is no longer happening. The sensory stimulation resulting in sensory awareness of the present moment provides the fragmented aspects of the traumatic memory with a novel context, thereby contributing to the realization that it is just a memory, rather than happening all over again. AIP AND THE SELF

We suggest the conjoining of exteroceptive awareness, attributable to alternating bilateral sensory stimulation, with interoceptive awareness, attributable to body mindfulness, is at the basis of synthesis and personification. It is suggested that EMs or alternating bilateral stimulation and the associated sensory awareness are

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involved in the gamma oscillatory response in the brain, a phenomenon that occurs both during REM sleep and the alert waking state for information processing. It is suggested that EMDR-specific sensory stimulation contributes to the synchronization of dynamic neuronal networks. This phenomenon is referred to as temporal binding and is created by a stream of oscillating networks in the brain, thus conjoining the fractured aspects of internal and external reality in the time domain. This process may not only affect hemispheric laterality, but also memorial, somatosensory, and cognitive integration. That is, sensory stimulation and sensory awareness may be involved in a reversal of TCD, a phenomenon that has been hypothesized as a mechanism for various psychiatric and neuropsychiatric conditions (Llinás & Ribary, 2001). This conceptualization is consistent with Shapiro’s notion of EMDR being potentially applicable to a greater number of disorders than originally considered. The proposed role of sensory awareness and sensory stimulation is consistent with the notion of a physiologically based information processing system as suggested by Shapiro (2001). Moreover, it is consistent with Shapiro’s (1995) original notion that not only visual but also auditory and tactile stimulation are effective modalities (Servan-Schreiber, Schooler, Dew, Carter, & Bartone, 2006). Exteroceptive and interoceptive awareness and their roles in modulating salience and default network activity are hypothesized to play an integral role in synthesis, binding, and information processing. Thus, we propose that sensory stimulation and related sensory awareness are not only an intrinsic part of the EMDR procedure, and may indeed not only represent the underlying mechanism of AIP, but are also directly relevant to our understanding of the phenomenology of dissociation, human consciousness, and the self. NOTE 1.  We thank Frank M. Corrigan for his comments on earlier versions of this chapter.

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PART II: TREATMENT

INTRODUCTION

Dissociation and Psychotherapy Sandra L. Paulsen and Ulrich F. Lanius

DISSOCIATION—BARRIER TO INTEGRATION OF THE TRAUMATIZED SELF

When dissociation is a significant part of the clinical presentation, it frequently presents a barrier to effective treatment. It tends to interfere with clients’ sense of their own body, their ability to experience emotion, and emotional regulation. Moreover, dissociation tends to result in unpredictable ego state shifts and a discontinuity of self. Generally, significant dissociative symptoms result in affective dysregulation and a general lack of stability in clients’ lives, to a point where individuals suffering from dissociative disorders are commonly unable to benefit from trauma-focused interventions. Fundamental to all complex trauma cases is the emphasis on stabilization and the avoidance of flooding and overwhelm. This theme is woven throughout the treatment chapters.

PHASE-ORIENTED TREATMENT APPROACH

The treatment of complex dissociation is nothing new, harkening back to Janet and undergoing considerable development in the last several decades. Part I focused on the neurobiology of trauma and dissociation, with occasional forays into treatment. Part II focuses on primarily treatment, with a view toward the neurobiological underpinnings provided in the earlier part of the book. The treatment approaches described in this part are based on a phase-oriented treatment approach and draw from both the new and old, interweaving therapeutic interventions with a novel understanding of the neurobiology of dissociation. As early as the late 19th century, Pierre Janet (1898) advocated a phase-oriented treatment for dissociative disorders. This very approach is echoed by expert consensus guidelines (International Society for the Study of Trauma and Dissociation [ISSTD], 2011). In order to effectively treat individuals with dissociative symptoms

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and a history of chronic traumatization, a phase-oriented treatment of patients is essential and is currently considered to be the standard of care (e.g., Brown, Scheflin, & Hammond, 1998; Courtois, 1999; Herman, 1992; van der Hart, Nijenhuis, & Steele, 2006). The three phases or stages are generally considered as follows: 1. Establishing safety, stabilization, and symptom reduction, aimed at increasing the client’s integrative capacity 2. Working through and resolution or completion of the unfinished mental and behavioral actions inherent in these traumatic memories, ultimately working toward integrating these traumatic memories into the person’s autobiographical memory and sense of self 3. Identity and personality integration and rehabilitation, including the resolution of fragmentation of the self and further personality development

NEW AND OLD

Fundamental to all complex trauma cases is the emphasis on stabilization, and the avoidance of flooding and overwhelm. This is consistent with the literature in the treatment of dissociation that emphasized in the literature on the treatment of dissociative disorders. This theme is woven throughout the treatment chapters. Further, the neurobiologically informed treatment approach described here is either part of, or strongly influenced by, any or all of the following: ego state therapy (Watkins & Watkins, 1997); body-centered psychotherapy, particularly sensorimotor psychotherapy (SP; Ogden, Minton, & Pain, 2006); as well as eye movement desensitization and reprocessing (EMDR; Shapiro, 1995). In Chapter  12, Seeing That Which Is Hidden: Identifying and Working With Dissociative Symptoms, Sandra L. Paulsen and Ulrich F. Lanius address the hidden nature of dissociation, which contributes to therapeutic sins of both omission and commission, as dissociation is either not discerned at all, resulting in years of ineffectual therapy, or trauma work is attempted prematurely without the self-system being on board and without sufficient stabilization. In Chapter  13, The Compassionate Self, Frank M. Corrigan, Alasdair Wilson, and Deirdre Fay speak to the role of the neurobiological defensive systems and their effect on the self in terms of the sense of safety, shame, and self-compassion. This work and its frame of reference is foundational to all therapeutic modalities as well as to the therapeutic relationship itself. Sandra L. Paulsen and Joan Golston in Chapter 14, Stabilization Basics, draw upon the accumulated wisdom of the psychodynamic and hypnosis traditions as well as newer sources to facilitate stabilization. In Chapter 15, Stabilizing the Relationship Among Self-States, Sandra L. Paulsen and Joan Golston expand upon stabilization by describing working with the dissociative self system using ego state maneuvers to deconflictualize, orient, and transform, working on a far deeper level than if one works only with the “front porch” of the patient that presents for treatment.

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In Chapter 16, Alexithymia, Affective Dysregulation, and the Imaginal: Resetting the Subcortical Affective Circuits, Sandra L. Paulsen, Katie O’Shea, and Ulrich F. Lanius describe an innovative use of EMDR with affective mentalization. This approach draws upon innate affective resources in conjunction with visualization to facilitate stabilization and reduce affective dysregulation and the inability to feel (alexithymia). Emotion is conceptualized in terms of subcortical affective circuits. Using visualization and hypnotherapeutic interventions, emotions are worked on directly without an affective load on them. Thus, by bringing to bear neocortical resources of objectivity and imagination, it is conceptualized that affective circuits are functionally reset or rebooted so that they can more optimally conduct affective information. In Chapter  17, Fractionating Trauma Processing: TOTEMSPOTS and Other Attenuating Tactics, Sandra L. Paulsen and Ulrich F. Lanius recapitulate the familiar concept of pacing trauma work through fractionating or right sizing that which is being worked on at any given time. It offers a new formulation of different ways to fractionate work, depending on the self system of the client and how much the brakes need to be feathered during the work. In Chapter  18, Accelerating and Decelerating Access to Self-States, Sandra L. Paulsen reframes many familiar therapeutic techniques in terms of whether they access or distance from disturbing material, in order to engage the therapist’s fluency with acceleration or deceleration techniques, which may be used artfully to modulate the pace of the work. Pat Ogden and Janina Fischer in Chapter  19, Integrating Body and Mind: Sensorimotor Psychotherapy and Treatment of Dissociation, Defense, and Dysregulation, describe the use of SP to work bottom-up from the somatic to resource and metabolize trauma while keeping the patient in the optimal arousal window. This important method threads through various chapters in terms of resourcing and accessing implicit memory, in conjunction with other therapeutic techniques. In Chapter 20, Temporal Integration of Early Trauma and Neglect, Sandra L. Paulsen describes a modified application of EMDR. This innovative approach to the integration of highly dissociative clients with very early trauma and neglect emphasizes the importance of proceeding temporally from birth to present time, including working in implicit memory. This work is based on the Early Trauma EMDR Protocol (O’Shea, 2009a, 2009b; O’Shea & Paulsen, 2007) that has been further refined with the use of ego state interventions to facilitate working with complex cases and dissociative identity disorder clients. Ulrich F. Lanius and Sandra L. Paulsen, in Chapter 21, Toward an Embodied Self: EMDR and Somatic Interventions, describe a synthesis of somatic approaches, including SP and EMDR, to address complex trauma and dissociative symptoms as they appear in clinical practice. This approach focuses on somatic interventions for stabilization, as well as approaches to titration of traumatic experience, not only to facilitate trauma processing but also to ultimately effect personification and a sense of an Embodied Self. Ulrich F. Lanius and Frank M. Corrigan, in Chapter 22, Opioid Antagonists and Dissociation: Adjunctive Pharmacological Interventions, discuss the adjunctive use of opioid antagonists (e.g., naltrexone) to reduce depersonalization and other dissociative symptoms—both to assist stabilization but also reduce amnesia and facilitate trauma processing.

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REFERENCES Brown, D., Scheflin, A. W., & Hammond, D. C. (1998). Memory, trauma treatment, and the law. New York, NY: W. W. Norton. Courtois, C. A. (1999). Recollections of sexual abuse: Treatment principles and guidelines. New York, NY: W. W. Norton. Herman, J. L. (1992). Trauma and recovery: The aftermath of violence—From domestic abuse to political terror. New York, NY: Basic Books. International Society for the Study of Trauma and Dissociation (ISSTD). (2011). Guidelines for treating dissociative identity disorder in adults third revision. Journal of Trauma & Dissociation, 12(2), 115–187. Janet, P. (1898). L’automatisme psychologique. Paris, France: Felix Alcan. Ogden, P., Minton, K., & Pain, C. (Eds.). (2006). Trauma and the body: A sensorimotor approach to psychotherapy. New York, NY: W. W. Norton. O’Shea, M. K. (2009a). EMDR friendly preparation methods for adults and children. In R. Shapiro (Ed.), EMDR solutions II. For depression, eating disorders, performance and more (pp. 289–312). New York, NY: W. W. Norton. O’Shea, M. K. (2009b). The early EMDR trauma protocol. In R. Shapiro (Ed.), EMDR solutions II. For depression, eating disorders, performance and more (pp. 313–334). New York, NY: W. W. Norton. O’Shea, K., & Paulsen, S. L. (2007, September). A protocol for increasing affect regulation and clearing early trauma. Paper presented at the annual meeting of the Eye Movement Desensitization & Reprocessing International Association Conference, Dallas, TX. Shapiro, F. (1995). Eye movement desensitization and reprocessing: Basic principles, protocols, and procedures. New York, NY: Guilford Press. van der Hart, O., Nijenhuis, E. R., & Steele, K. (2006). The haunted self. New York, NY: W. W. Norton. Watkins, J. G., & Watkins, H. H. (1997). Ego-state theory and therapy. New York, NY: W. W. Norton.

CHAPTER 12

Seeing That Which Is Hidden: Identifying and Working With Dissociative Symptoms Sandra L. Paulsen and Ulrich F. Lanius

People with dissociative disorders are like actors trapped in a variety of roles. They have difficulty integrating their memories, their sense of identity and aspects of their consciousness into a continuous whole. They find many parts of their experience alien, as if belonging to someone else. They cannot remember or make sense of parts of their past. —David Spiegel (2008)

In Chapter  1 we discussed the hypothesized neurobiological underpinning of the phenomenology of dissociative symptoms and dissociative disorders. Chapter  12 focuses on identifying and working with dissociative symptoms and dissociative disorders in a therapeutic context, providing a road map to assist with the pacing and planning of clinical interventions discussed in the subsequent chapters of Part II. It is not intended to address the formal, structured psychometric assessment of dissociative disorders and complex traumatic stress syndromes. With regard to the formal and forensic assessment of dissociative disorders, we refer the reader to the International Society for the Study of Trauma and Dissociation (ISSTD) guidelines (ISSTD, 2011); the work by Brand, Armstrong, and Loewenstein (2006a) and Brand, McNary, Loewenstein, Kolos, and Barr (2006b); as well as to resources contained in Dell and O’Neill (2009). So, let us review the phenomenology of traumatic dissociation and its relationship to attachment with a view toward being able to not only conceptualize the nature of dissociation but also to identify it in our clients and patients. 247

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TRAUMATIC DISSOCIATION CREATES BARRIERS TO INTEGRATION OF AN EMBODIED SELF

In daily life, we process and integrate experience as we go along. If we get behind, we process some more in our dreams. Rapid eye movement (REM) sleep can be conceptualized as a household strength processor that can accommodate the usual processing requirements of daily life. Without overwhelm, different parts of our experiences—sensory, emotional, and cognitive—are embodied in our sense of self and who we are. When there is significant sympathetic hyperarousal that co-occurs with significant parasympathetic activation, that is, a dorsal vagal response, this integration of information no longer occurs.

When the Pain Is Greater Than the Capacity to Cope

In a healthy family, the child’s loving caretakers help the child develop self-esteem, ego strength, coping skills, and the ability to utilize emotions as tools and as data to inform decision making. With this solid foundation in place, the growing person can come to handle the many obstacles and traumas that life will toss her way. Her resources will be greater than her pain, and thus she will be able to cope. In traumatic experience, however, the child’s capacity to process the experience of trauma may be challenged. If the size of the pain is greater than a child’s capacity to process and cope with that pain, processing cannot occur. If the child’s brain attempts to process overwhelming experience in the daytime, flashbacks or behavioral reenactments may occur, and the processing is aborted. If the brain attempts to process the traumatic experience in REM sleep, the presence of nightmares signals that the household strength processor is insufficient to process the experience. The child’s processing capacity is less than the size of the material to be processed.

ALONENESS—MORE THAN A CHILD CAN BEAR

Posttraumatic stress disorder (PTSD) has been historically defined as requiring a trauma that is outside the range of normal human experience. For childhood trauma, it is outside of the range of normal experience to have to live and grow up without patient assistance from caretaking adults. Indeed, it is now well established that key neurobiological developmental milestones cannot be achieved without adequate caretaking and the healthy emerging intersubjectivity—“the awareness of I and thou” that goes with that nurturing relationship. When a child’s family includes perpetrators who harm or exploit the child, or even members who are not capable of child care and nurturance, the child can be overwhelmed by the task of surviving and navigating the normal developmental milestones of childhood. Intersubjectivity is not possible when the child is presented with a narcissist who cannot see the child’s humanity or engage in an authentic “I and thou” relationship with the child.

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In such cases, the child cannot accommodate the requirements of life. The child cannot call Child Protective Services, or say, “see here, Mother, this has gone far enough. I’m taking my credit cards, and leaving.” The primary problem, then, is that the child is alone in a world with no people, to the degree that caretakers do not see and protect and cherish the child’s humanity. This awful reality is the starkest truth for a child, one that engenders annihilation terror, desolation, abandonment panic, separation anxiety, and, finally, surrender to helplessness and aloneness.

THE CHILD’S SOLUTION: A PEOPLED INNER LANDSCAPE

The child has no choice but to try to accommodate herself to the situation. The normal imagination and imaginary friends of childhood come to the rescue here. If the child generates imaginary friends to populate that desolate world, the inner landscape can provide prosthetically what the outer world has failed to provide—people (Kluft, 2009; Marmer, 1980). From this vantage point, then, dissociative personalities or parts of the self are a merciful solution a traumatized child may devise to distract the self from the awful truth that one was alone in a world with no people. This comment is intended to describe the desolation and the solution, not to deny the reality of different parts of the self. This survival strategy is creative and quite brilliant. It has enabled innumerable individuals to survive impoverished, desperate, and malignant childhoods with little assistance beyond their internal protective parts, each of which served a function.

THE COST OF THE “PEOPLING SOLUTION”: ENDURING SYMPTOMS

Peopling one’s internal world prosthetically can, however, cause long-term problems, though it solves the child’s shorter term problems as well as possible. Those enduring problems can include: ■■

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Internal stress The unprocessed raw traumatic material continues to exert pressure on the individual’s internal functioning and well-being. Internalized conflicts The internalized conflicts and double binds that characterized the external family of origin become reified internally and assume the pattern of an infinite loop of disturbance, a “ping pong” (Kluft, 2009) between the sides of a conflict. Surrender to hopelessness At the moment of intersubjective failure, whether in a traumatic experience of commission, such as incest, or omission, such as neglect, the adult’s incapacity to see and honor and relate authentically to the child’s humanity is noticed by the child and experienced as a blow to the self. Although initially

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the child, like other mammals, may express distress, also described as a hardwired PANIC circuit (Panksepp, 1998), once the distress cry fails to attract nurturing caretaking (ventral vagal engagement), the child will surrender to helplessness and defeat. This surrender has been described as the dorsal vagal shutdown state that occurs when fight or flight (sympathetic arousal) has failed (Porges, 2011). Forsaking of the self In the surrender to helplessness that results when baby’s humanity is not seen and honored, a key internal dynamic necessarily occurs. Because baby cannot succeed in getting caretaking needs met and must surrender to the narcissism or even brutality of the adult, the child must torpedo her own feelings, needs, and strivings to get them met. Shame: the measure of the narcissistic blow Had baby’s need to be seen been supplied in his mother’s loving arms, they would have gazed at each other with mutual admiration and delight, a lovefest of attunement and resonance. In that seeing and being seen is born the intersubjective experience described earlier. Mother and child’s right hemispheres would resonate in a brain-to-brain flow of energy and coherence, establishing the basis for empathic attunement, attachment, and subsequent affect regulation capacity. Without that shared resonance, however, baby suffers from insufficient help in achieving coherence and affect regulation. The child suffers from shame. The child looks at herself through the caretaker’s eyes, not her own The loyalty to even a malignant caretaker tends to continue well after the strategy was necessary for survival per se, so the client never assumes control for and loyalty to her own life, her own body, her own point of view, or her needs and feelings. Until the traumatic experience is processed to an adaptive resolution, the disavowal of self, once necessary for survival, may continue for decades, severely compromising the client’s capacity to be instrumental in successful life outcome. Object relations, which would normally be operating to reflect adaptive self–other relationship, instead encapsulate the malignant or at least failed dynamics of the baby in relation to primary attachment figures in her environment. These internal others may be imbued with self or other awareness, also called ego cathexis (ego energy) or object cathexis (object energy; for example, Federn, 1952; Paulsen, 2009; Watkins & Watkins, 1997). The parts become invested in separateness The parts of self may become ego invested in their separateness, firmly believing themselves to have their own bodies, lives, and so forth. This is most likely to occur when attachment needs have not been met in very early life and this neglect has been combined with abuse of a physical or sexual nature in the formative years. The memories erupt painfully as the truth wants out The original painful memories live on in flashbacks and nightmares as well as in reenactments of the unconscious dynamics captured from the family of origin’s enactments of perpetration, victimization, rescuing, and neglect. He

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or she may be buffeted between one reenactment scenario and the next, in which the environmental triggers reminiscent of the traumas evoke deeply pushed away dynamics ever seeking resolution. Ultimately the strategy may fail In summary of this cascade of events, without assistance, and emotionally alone in the world, the survivor may adhere doggedly to the internal secrets by populating the one body with many selves. The problem is solved, but like any solution that involves lobbing detritus over a fence, or stuffing messes in to closets, a good temporary solution fails over the long haul. Like a full closet, there will come a time when the last bit is tossed into the already full storage closet, and everything that should have been dealt with but never was will fall out in disarray. The client may suffer a “nervous breakdown,” “psychotic break,” or “suicidal crisis” precipitated by a life stressor qualifying as the “last straw.” In a less flamboyant display, perhaps the person will have milder symptoms or be uncomfortable about chronic numbness or failed relationships. Perhaps he or she has problems with eruptive behavior that punctuates relationships with authorities. Whether the former (acute crisis) or the latter (chronic dysfunction), the client may present for therapy. Sometimes such a client may have insight into the formative role of trauma in his or her symptoms. More often, a client may present with chief complaints of depression, anxiety, unsatisfying relationships, or any one of a myriad of other symptoms.

IDENTIFYING DISSOCIATIVE SYMPTOMS

Skilled clinicians can identify some dissociative disorders in even the initial interview by embedding in the intake interview questions designed to identify the presence of common dissociative symptoms. So alongside questions like, “Do you find yourself feeling sad or depressed?” “How’s your appetite?” “Anything you are avoiding that you wish you wouldn’t avoid?” examples of questions that draw out dissociative symptoms include the following: “Does it ever seem as if you are standing next to or behind yourself, or watching yourself?” “Do you ever feel as if things around you are not real?” “Does it happen that you have periods of time that seem to be missing that you can’t account for or where time seems to have been lost?” (from Loewenstein, 1991). Other questions ask about somatic sensations such as unexplained pain (Nijenhuis et al., 1999) as well as inquiring about paresthesias: Do your arms, legs, or extremities ever go numb for no reason? Interviewers also need to inquire about PTSD symptoms such as nightmares, flashbacks, and startle response, though of course the presence of PTSD symptoms doesn’t mean there is necessarily a dissociative disorder. Asking whether there are times that patients feel as if something or someone is making them do, say, think, or feel something, for example, “made actions,” “made thoughts,” “made feelings” can help identify the presence of structural dissociation, when another part of self is evoking the actions, thoughts, or feelings.

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SEEING WHAT IS HIDDEN

By its very nature, dissociation is about keeping secrets from the self and the world, so a clinician should not expect it to be face evident. Because many therapists are not trained to identify the presence of a dissociative disorder, they often don’t look for it. The present chapter specifically addresses that hidden nature of dissociation, which contributes to therapeutic sins of both omission and commission. That is, dissociation symptoms are not identified at all, resulting in years of ineffectual therapy. Alternatively, trauma work is attempted prematurely without the self-system being on board and without sufficient stabilization. In part, the difficulty in identifying dissociative symptoms is accounted for by the nature of autonomic arousal. Sympathetic hyperarousal is easily discerned by most clinicians; parasympathetic activation and apparent hypoarousal, phenomena that are associated with immobilization (also see Chapter  3 on Peritraumatic Dissociation and Tonic Immobility: Clinical Findings)—they are a common part of the presentation in complex traumatic stress syndromes and dissociative disorders— are frequently missed, even by seasoned clinicians. Hypoarousal and parasympathetic activation that are an intrinsic part of dissociative symptoms are much more difficult to assess. Excessive sympathetic nervous system activation is easily construed to be an indicator of psychopathology, but often parasympathetic responses are misperceived to indicate an absence of problems. Individuals who are not familiar with the underlying neurobiology of dissociation do not commonly differentiate between a dorsovagal and ventral vagal parasympathetic state: They interpret any parasympathetic arousal as a desired calm state. Indeed, this calm state may reflect healthy ventral vagal engagement, for example, a ventral vagal state. Alternatively, this hypoaroused state may reflect shutting down, disconnection, numbing, and a lack of engagement with one’s environment. Without moment-by-moment tracking and a well-grounded understanding of the underlying neurobiology of different parasympathetic states, the finer points and the possible diagnosis of a dissociative disorder or severe traumatic stress syndrome are potentially missed.

FRAGMENTATION OF THE SELF—NOT LOOKING

Moreover, significant fragmentation of the self-system is often not evident early on in the therapeutic process and only emerges once the client feels sufficiently safe to share their more wounded aspects of the self. The structure of the self-system, the process by which the system functions, and the interrelationships between parts of the system are all essential to understanding the patient and designing an appropriate treatment plan and pace. Some therapists fail to look for and see a dissociative disorder because it would require a paradigm shift to do so. Arguing that dissociative phenomena are best understood as complex trauma conditions or trauma spectrum disorders (e.g., Davidson & Foa, 1993) obviates the need to look for and see dissociative disorders. However, dissociative disorder not otherwise specified (NOS) and dissociative identity disorder

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(DID) are diagnostic categories in DSM-IV-TR. That is, whereas PTSD is amenable to direct treatment with eye movement desensitization and reprocessing (EMDR), a DID client requires extensive stabilization, containment, and resourcing before using EMDR. Treating someone for PTSD or depression when there is an underlying dissociative disorder is an error with potentially grave consequences. It may result in a lack of response to treatment on one hand and significant destabilization on the other, often causing significant havoc in treatment. For instance, conducting EMDR in the presence of structural dissociation that contains massive amounts of unprocessed material in someone without affect regulation, without necessary preparatory steps, will result in a mishap much like tripping over a curb that one doesn’t see. The EMDR session will go sprawling or end up with blocked processing with uncertain outcome at best. The alternative is EMDR breaking through dissociative barriers with unintegrated traumatic experience, resulting in affective overwhelm, with the client leaving treatment prematurely. The worst potential outcome is a massive deterioration in psychological and day-to-day functioning, profoundly affecting the client’s interpersonal relationships and his or her capacity to function in the world.

BELIEVING THAT THE PATIENT KNOWS

Because DID serves to keep secrets from the self and the world, some DID patients, at least in the ego state in which they present for their office interviews, may be unaware of their dissociative symptoms. Like a rose bud closed up tightly, there are insufficient openings in the self-system for introspection and self-observation. As treatment progresses, DID patients will commonly gain awareness that, yes, they do lose time, or find themselves standing next to themselves, and so forth, after all. Scores on screening devices may actually increase as treatment progresses, before decreasing again after more extensive treatment. In those cases where there is significant amnesia, attempts to take a detailed trauma history will often result in destabilization and may precipitate the patient’s flight from treatment. In those cases, imagery can be used to maintain stability and still increase awareness of aspects of self. For example, it offers several advantages to ask a patient to envision a pleasant library where stories are kept that need to be told in the fullness of time (Kluft, 1990). The clinician can suggest that the patient does not need to go into the library, but simply glance in through the library door and get a sense of how many books are on how many shelves. This hypnoprojective method enables the patient to present what information is tolerable early on. Any such assessment method should also be accompanied with a closing down or tucking in procedure (see Chapter 15; also Paulsen, 2009). In this example, the clinician might suggest that the library will be there when we need it, that we can turn out the light, make sure the door is closed, pull down a shade on the door, and float the library deep inside until the time is right.

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ISSUES COMMONLY ASSOCIATED WITH A DIAGNOSIS OF A DISSOCIATIVE DISORDER

A number of different clinical phenomena are commonly associated with a diagnosis of a formal dissociative disorder. These relate to different aspects of patient functioning, as discussed below. We consider them to be essential in assisting with regard to treatment pacing and planning.

AFFECT TOLERANCE

Clients with complex trauma-related disorders and dissociative disorders commonly have difficulties with affect tolerance. Patients with DID in particular commonly use state switching for affect regulation. Without psychoeducation and targeted interventions to increase affect tolerance, they commonly have a limited affective regulation and ability to feel their emotions. During interview, somatic and affect tolerance can be assessed by asking, “Would you say you have struggles with anger? Sadness? Fear? Desperation? Shame?” If the patient does not do well with that kind of questioning, further inquiry with regard to emotions should be discontinued. Alternatively, answers like, “Oh I don’t have that problem,” or “I don’t feel anger,” tends to raise the index of suspicion that the patient—or some part of the patient—does not tolerate affect or has diminished access to his or her emotions. In Chapter 20, specific interventions for strengthening affect tolerance are outlined.

SOMATIC TOLERANCE

In addition to affect intolerance, many patients who exhibit dissociative symptoms also present with soma intolerance, as they experience that their bodies are not safe places to be. Direct question may provide the information the therapist seeks, for example, “Are you on good terms with your physical body?” or “Are you comfortable with your body?” or more directly, “Do you ever have difficulties with staying present in your body? Do you ever have any out-of-body experiences?” Sometimes the client will share that he or she is involved in body mindfulness-based activities like pilates, yoga, or something similar and the therapist can get a sense of somatic tolerance in that way. Sometimes, quite revealing is to chat with the patient about something that the patient finds enjoyable (e.g., playing with their cat or walking in the woods), and when the patient is smiling, say, “I notice talking about (e.g., the cat) brings you some joy . . . may I ask where you notice that joy in your body?” Similarly, while discussing something unpleasant or mildly painful, the therapist might ask where the discomfort is noticed in the patient’s body. If the patient obviously struggles with these questions, does not seem to know what you mean, or says outright, “I don’t feel my body,” or “I don’t have that,” the clinician will suspect that soma tolerance is low. Another sign that potentially indicates insufficient somatic tolerance is the client’s inability to tolerate or benefit from breathing exercises or an inability to take deep breaths. In those cases where there is insufficient

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somatic tolerance, trauma-focused work will need to be much delayed, with an extended stabilization phase that includes stabilization and containment activities as well as resourcing with the express purpose of increasing the client’s capacity for body mindfulness.

CAPACITY TO SELF-SOOTHE

The capacity to self-soothe and participate in a variety of stabilization exercises is a positive prognostic indicator. Especially, the ability to use inner child imagery and soothe one’s inner child usually suggest that the client is likely capable of doing trauma-focused work. Conversely, an inability to self-soothe, even in the presence of a capacity to discuss his or her respective trauma history in relative detail, in the authors’ experience, is commonly associated with disordered attachment. It usually indicates the need for additional preparation prior to embarking on traumafocused work.

AMNESIA: LOSS OF MEMORY

The assessment of amnesia is an important domain for assessing dissociation, and has several factors to consider. One is that amnesia for current life events is quite different than amnesia for childhood events. Of course, any assessment for amnesia should rule out amnesia caused by substance use or abuse, and should ensure that there is no medical condition that might cause amnesia, such as complex partial seizures. Generally, patients with a high degree of amnesia will likely have a slower course of treatment than those with less amnesia. Therefore, in initial interviews, the therapist will assess for amnesia as it relates to historical events, during both childhood and adulthood, and at the present time. The patient who remembers nothing from ages 6 to 12 but reports continuous memory in present-day life is quite different from the patient who describes losing minutes, hours, days, or weeks in present life. Few people remember much from preverbal years, but most people, on inquiry, can remember childhood to some degree. The sense of having missing years is important for raising the index of suspicious of childhood trauma, but the presence of amnesia in present life is strongly suggestive of the presence of a severe dissociative disorder. Further complicating the assessment for amnesia is the fact that patients don’t always realize that indeed they are suffering from amnesia. Families may argue about whether the patient is lying or not, not considering that the patient doesn’t remember an activity or conversation. Some dissociative patients will have a vague awareness of having an experience, as if in a dream or as if watching the event, but others will have, at least in the ego state reporting, no memory of an event at all. The more significant the amnesia, the harder it is for the patient to observe and report upon it, by definition. For that reason, patients may report no amnesia early in treatment, but as treatment progresses, have a dawning awareness that they do not have continuous memory or awareness of time.

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HISTORICAL EVENTS: CHILDHOOD

Most people can recount major events of their childhood after verbal abilities are well in place and explicit memory is online, between ages 3 and 5. If a patient cannot recount the chronology of his or her life, or frankly reports having large periods of time missing from his or her memory, the therapist should remain alert to the possibility of dissociative amnesia. The index of suspicion is higher if the patient recalls nothing from an event or series of events that it would seem likely to remember, especially as an older child. For example, for a 12-year-old girl to remember nothing about taking ballet classes for 2 years would be unusual, and suggests amnesia beyond normal forgetting. More subtly, if a patient cannot organize his or her story into a historical chronology, it may be because of a fitful relationship with cause and effect and time passage itself. Dissociative individuals may be present for Event A, have amnesia for Event B, but are held accountable at Event C for both prior events. Chronic confusion about who is doing what can result in a spotty ability to sequence events, in addition to having amnesia for the content of specific events.

HISTORICAL EVENTS: ADULTHOOD

Adults typically remember major events such as graduation, key weddings, car accidents, and so forth. When an adult describes no memory of an event (which is different from forgetting details of an event), this is unusual and potentially highly significant. An individual who has no amnesia in adulthood but years missing from childhood is likely to be able to move more readily in therapy than one with a continuous stream of choppy memories from both childhood and adulthood.

PRESENT TIME

Patients may deny having amnesia in present time either because it is a true negative (they don’t have amnesia in present time) or a false negative (they do have amnesia for events in present time, but they don’t know it). Since either could be true, a therapist is wise to gently inquire about whether the present session is remembered. If the patient is obviously in variable states over a session, the therapist may inquire gently if the prior conversation is remembered. If a patient expresses surprise that a session is so quickly over, it may be an indication of amnesia for part of a session.

COCONSCIOUSNESS AND COPRESENCE

Coconsciousness is a term that has been used in the dissociation field since the 19th century, when dyspyschism was a major model of the mind (Ellenberger, 1970; R. P. Kluft, personal communication, April 1, 2013). The term refers to the degree to which parts are aware of each other internally. If the amnesia barriers are quite

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impermeable, there is little coconsciousness. If the amnesia barriers are thin and permeable, the parts may be said to be highly coconscious. A patient’s parts may vary in how much coconsciousness they have with some parts versus other parts (Kluft, 1984a). A patient who can have one part present in the therapy office sitting in the chair while other parts are listening in the mind’s eye, perhaps sitting in a conference room, (Fraser, 1991, 2003; Paulsen, 1995) is far readier for mediating between parts than the patient whose parts don’t know each other exist, and don’t overhear at all what one part says to the therapist. The front part(s) may or may not be aware of the listening other parts, and some of the parts may not be “listening” in conscious mind. In ego state work, a part is said to be in conscious mind if a second part can glance inward and register awareness of the first part’s words, stance, demeanor, dress, and so forth “over there,” and if the second part uses the pronoun “he,” “she,” “it,” or “they” to refer to the observed part(s). In contrast, copresence, a term introduced by Kluft (1984b) to address important nuances not captured by the term coconsciousness, refers to the degree to which a patient’s parts can be forward in the body, executive, and aware of their presence in, for example, the therapist’s office at the same time. A part is said to be present when that part experiences itself seated in the chair in the therapy office, is observed by the therapist to be present at least in executive control of part of the body, and is using the first-person pronoun, “I.” Sometimes it happens that the therapist observes that one part seems to have control of the mouth, or mouth and head, but not the rest of the body. After the part controlling the mouth has “left” (switched away), on inquiry the remaining part may say that it felt itself to be present but only in the legs, or right next to the speaking part. Sometimes parts may spontaneously or deliberately temporarily blend and then go back to their separateness after the therapy or intervention. Such parts may be said to have been copresent while they were both (nearly) fully forward in the body, and might refer to themselves as “I” or “we.” Another dimension to assess is the degree of coconsciousness between parts of the self. Coconsciousness is not unidimensional, and some parts may be keenly aware of each other and unaware of more remote and dissociated parts. Figure 12.1 is a pictorial representation of the extent of coconsciousness among parts of the self.

Figure 12.1  Depiction of severity of dissociation between different parts of the self where the overlap reflects awareness and co-consciousness between parts.

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STATE SWITCHING

In the absence of coconsciousness, there is commonly significant state switching. Many clients experience discontinuous and disruptive switching between states, and that occurs when there is amnesia and absence of coconsciousness between some states, dissociative switches between states occur rapidly and are manifest in considerable shifts in affect, appearance, manners, speech, discontinuities in train of thought, and more (Putnam, 1997). This has been described as an uncoupled nonreciprocal mode of autonomic control, in which responses in one portion of the autonomic nervous system occur in absence of change in the other part (Berntson, Cacioppo, & Quigley, 1991). Among individuals who clearly meet criteria for DID, there is considerable variability in how smoothly they switch states. Relatively rare is the DID individual with florid state switching of the kind depicted on television, where the patient shifts from a meek prude to a vamp with a stunning and obvious state switch involving overt struggles and shaking. Far more common are subtle signs that there is a state shift occurring, such as putting one hand to the head (indicating a coming and/or going or struggle between parts for executive control of the body); a subtle shifting from side to side; or a familiar vocalization, for example, “um (sigh),” that the clinician comes to realize is a stereotypic behavior that signals a state shift. Some individuals seem to switch easily between some states and with difficulty or not at all with others. When discontinuous state switching occurs, without coconsciousness between states, there can be a loss of access to the sense of self that was accessible in the prior state, resulting in a profoundly discontinuous sense of self (Putnam, 1989). Similarly, when suddenly switching to another state, the highly dissociative person may have no access to memories and even skills held in another state. The belief systems may be quite different, even competing and conflictual. The relative ease with regard to state switching is of clinical importance because it will be one determinant of the best strategy for communicating with the self-system. Individuals for whom state switching is laborious may benefit from a strategy of the clinician inviting the host or front part to leave, and talk through a second part to other parts. That second part then relays the internally heard messages to the therapist, saving time and arduousness that would be required for frequent state switching. Others switch states easily, and the therapist may find it beneficial to speak directly to parts of the self for a time, as long as that is tolerated by the patient. Nearly all clients with DID, as well as some with DDNOS, benefit from returning at the end of the session to the state that came into the session.

PRESENCE OR ABSENCE OF A HELPER PART

Many patients have one or more parts of self that are readily available to help the therapy, either by passing along information from other parts of self, provide information about the patient’s history that other parts may not be able to recount, or generally serve as resources to provide strength or other adaptive functions. Such parts can go a great distance toward helping the patient to contain disturbance between

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sessions or reassure parts during or between sessions, in a more or less adult way. Early in the history of dissociation, the term “internal self helper” (ISH) was adopted to describe such an internal part. In recent times, the term has fallen out of favor for several reasons, especially that not every patient will have one, some patients will have many, and the part is not a constitutionally different part of self in many cases than any other part of self that is on board with therapy. Additionally, a part that was initially a “cranky part” may become a steadfast ally in the work over time, as that part becomes convinced that its concerns haven’t been treated legitimately. Ultimately, as the patient heals, most parts will become internal helpers.

DEFENSIVE BLOCKING BY INTROJECTED PERPETRATOR PARTS

Perhaps the gnarliest and most treatment-resistive dynamic in treatment of structural dissociation is the patient’s dogged loyalty and attachment to his or her perpetrators. As a child, the patient had unmet needs to be seen and mirrored, especially in the attachment period. In traumatogenic families, however, even in the earliest years, the patient’s very self-structure was derailed from normal developmental tasks by his or her caretaker’s inability or unwillingness to meet the child’s needs. Instead, often in a sea of narcissism, the caretakers were more concerned with their own needs than those of the child. In malignant families, the child was seen more as a resource to the parent or caretaker than vice versa. The child learned to see him- or herself through the caretaker’s eyes, as unimportant, not human, and an object to be used and/or blamed. This taking in of the caretaker’s point of view, sometimes called introjection (Klein, 1946) or loyalty to the aggressor, seems to serve several purposes.

GETTING WITH THE PROGRAM

A child makes the best out of a bad situation by getting on board with the requirements of the environment. That is, if the patient’s parents were, say, criminals and narcissists, then complying with the malignant requirements of the situation is the best thing the child can do, to optimize whatever crumbs of “love” are available to the child (Paulsen, 2009) in that impoverished situation. By being like-minded with the perpetrator in at least this corner of the child’s self, the child wisely joins the perpetrator’s self-admiration society, which is, again, what the situation demands.

ACT AS A PREEMPTIVE STRIKE

Additionally, the introjections of the perpetrator’s point of view may serve as a preemptive strike. That is, if the patient learned to say to herself, “Shut up, you worthless piece of garbage, or I’ll give you something to cry about,” she may be able to keep herself quiet, thereby minimizing the probability of hearing the same threat from the external caretaker. The preemptive strike is then a measure of safety, or even an illusion of safety, which may be the best the child can arrange. Ultimately,

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then, identification with the perpetrator is a protective stance, and any such perpetrator introjects are best addressed with that reality in mind. It is always a mistake for the therapist to join the patient in the incorrect belief that the introject is the external perpetrator, and act against him or her.

HAVE THE EXPERIENCE OF POWER

The experience of self as blameworthy and/or a defective victim is excruciating. The powerlessness, helplessness, and overwhelm are the core basis of the dissociative experience. How much more comfortable it would be to be in the cat–bird seat, to have the felt sense of being in the powerful position, to look down one’s nose at another with judgment or contempt. The introjection of the perpetrator’s viewpoint accomplishes this goal. By having at least this one part of the patient that identifies with the perpetrator’s power position, the patient has a felt sense of power, however disoriented it may be. At a minimum, this may provide an opportunity for discharge of thwarted sympathetic arousal. However, this misperception of self as perpetrating other is at the core of many thorny problems, notably, some self-harm, some suicide attempts, and considerable resistance to therapy. After some repetitions, this voice is internalized, and, over time, both the introjected perpetrator state and the child state(s) come to believe the voice is indeed the external perpetrator speaking. Both are disoriented to the fact that the voice is being generated by part of the patient. The therapist should make an early assessment of, and solicitation for, introjected perpetrator parts of self to orient them to the present body (not the external perpetrator’s, but the patient’s body, in which he or she lives), present place (if the patient and therapist are geographically remote from where the injuries occurred), and time (assuming the traumatic experiences occurred when the patient was a child, and the patient is now an adult). If the perpetrator(s) are dead or at least far away, orienting them becomes far easier a task.

PRESENCE OF OTHER HIGHLY CONFLICTUAL PARTS—SELF-HARM ACTIVITIES

In addition to the perpetrator introjects described above, there are other states/parts of self that can be in a great deal of conflict with each other, and may be responsible for risks of harm. For example, a part of the self that is experienced as an angry 15-year-old may hate the “whiny” 36-year-old, and in turn be hated by the 36-yearold apparently normal personality (ANP). The angry part may say, “That wimpy jerk should stop sniveling, I hate that she is so passive. She let’s this stuff happen to her.” The 36-year-old may say, “I don’t like that Angry Part. She scares me; she’s dangerous. I want her gone.” The angry part may respond by saying, “Yeah, well I want you dead. You should suffer, you’re so worthless.” And cutting may ensue, to decrease the revving of the motor and allow the patient a way out of the infinite looping of the double bind, that she had no choice but to surrender to victimization, and that she felt angry but anger was dangerous.

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PRIOR THERAPEUTIC INTERVENTIONS

Another important dimension to assess early in treatment is whether there was prior psychotherapy and whether these interventions were helpful or harmful. Because many therapists are not trained in the diagnosis or treatment of dissociation, it often happens that a highly dissociative patient is treated for years without the dissociative disorder being identified or properly treated. Additionally, the powerful effect of unworked trauma so thoroughly dissociated tends to be projected into the therapy room and therapeutic relationship, causing reenactments of patient material. A therapist untrained and inexperienced in recognizing and identifying such reenactments in the relationship field is at risk for participating in harmful ways in those reenactments. Well-intentioned therapists may, for example, attempt to reparent dissociative patients or behave in “unboundaried” ways, making exceptions to how they practice that they would not make with other patients. In the worst case, therapists have comported themselves unethically with vulnerable dissociative patients, causing extreme harm. Any form of bad prior therapy tends to extend the length of time necessary for safety and rapport to be well established in a subsequent positive therapeutic relationship with appropriate treatment interventions. Indeed, some therapists fail to terminate therapy with a dissociative patient, continuing the relationship in some form even as the new therapist is attempting to establish rapport and stabilization. If a therapist is not trained and experienced in treating a dissociative patient, it is recommended that the therapist seek consultation or alternatively make a referral to one so experienced, so to minimize the risk of therapist errors of additional injurious therapy. However, benign therapist errors can be an opportunity to help a patient distinguish between true betrayals of trust and human error. For example, a therapist who has made a scheduling error is not hurting the patient in the same way as a therapist violating sexual boundaries. The patient’s capacity to distinguish between benign and malignant errors in an adult way, with a little prompting, is quite different from the patient who curls up in a fetal position in a flashback and assumes certainty that a therapist’s innocent forgetting is a deadly sign of a betrayal of trust. In the latter case, the work is to make sense of the reenactment in the context of the patient’s story, which can be a combination of childhood familial abuse and bad prior therapy. Making sense of that complex story is slower work than the former case, in which adult resources are already able to be brought to bear. For all these reasons, part of what needs to be assessed is the nature of the prior therapy and how it ended.

ORIENTABILITY

A prior paragraph discussed the problem that parts of self may be disoriented to person, place, and time. This is extremely relevant to treatment because the patient’s sense of safety to proceed with the work of telling the truth to the self and working through the traumatic experiences are defined by whether the danger is ongoing, or is long ago and far away. Additionally, parts of self with the luxury of believing that

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the trauma didn’t happen to them but to “that kid over there” are less than motivated to support the therapy. The therapist will assess as he or she meets the parts of self over the course of treatment whether the parts are oriented to present time, present location, and the fact that they are in the patient’s body and are part of the patient’s self. A patient who shows early signs of the EPs being orientable (not just the ANPs) is going to make faster work of treatment than the ones that are deeply committed to the idea that they are observers of a traumatized child who may have deserved what happened to him.

DETERMINING THE MOST EFFICIENT MEANS FOR ACCESSING THE SELF-SYSTEM

The following questions can be answered relatively early in treatment for many individuals to identify the most cost-efficient means to intervene with a given patient. Answers to these questions will range from highly efficient to highly inefficient, and may not be within the control of the patient to override. Nevertheless, it is beneficial for the therapist to assess these domains early in therapy because if the patient can proceed directly it will result for efficient use of the therapy time and dollar. Key questions include these: ■■ ■■ ■■ ■■ ■■

Can the patient talk through or only switch? Does the patient have trouble switching, or is state switching smooth? Does the patient have pain/headaches with switching or conflict? Can the patient use a “dissociative table?” Can reconstruction of the self go on behind the amnesia walls without eroding amnesia barriers prematurely?

CAN THE PATIENT TALK THROUGH OR ONLY SWITCH?

In dissociative individuals, it is necessary to have a means to access the self-system. There are primarily two basic methods: talking through and switching. True switching occurs when a part of the self that was initially forward “leaves” either spontaneously or with therapist assistance and another part takes complete control of the body. Talking through occurs when a part of the self that was initially forward “stays” and facilitates the communication from other parts of the self to the therapist. The therapist may direct communication to the other parts, but is not able to learn of responses from the internal part(s) without the information from the front part through which the therapist is talking. The facilitating part may get information from hearing, seeing, or feeling the answers or even unintended answers from the other parts that are not all the way forward in the body. In summary, when parts have awareness of each other or prior communications, feelings, behavior, or thoughts, we can say that they are coconscious. If more than one part is simultaneously fully, or nearly fully, forward in the body, we can say that they are copresent, meaning present in the chair, in the body, in

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the room, in contrast to in the recesses of the mind’s eye, or in unconscious mind out of awareness.

DOES THE PATIENT HAVE TROUBLE SWITCHING OR IS STATE SWITCHING SMOOTH?

True switching occurs in DID often with amnesia between parts that have switched, although other parts may have an awareness of what another part has said. In individuals without DID but with a lesser degree of dissociation, as in some forms of DDNOS, state changes are not usually described with the word switching, unless the process is quite pronounced and the parts speak of each other quite separately and conflictually. Historically, the presence of amnesia for present time (between some parts of self) has been required to make the diagnosis of DID. However, some experts believe this emphasis in the Diagnostic and Statistical Manual of Mental Disorders (DSM) places too much importance on the specific criterion of amnesia, when the dispositive features are more about the structural dissociation of the self; the degree of conflict; the disorientation to person, place, and/or time; attachment to the perpetrators; and unresolved historical trauma, typically from childhood, with amnesia among key parts (Nijenhuis, van der Hart, & Steele, 2004) for those historical events. Although the word “switching” is not generally used for less dissociative individuals, everyone switches between states. Part of what makes state switching notable is that the process may not be continuous or smooth. Formal switching often requires effort, time, and a physical method of anchoring in the part that is switching into executive position. Normal-state “switching” in nondissociative individuals appears as a mood change with an appropriate transition, and may be marked with linguistic cues. True switching occurs in DID often with amnesia between parts that have switched, although other parts may have an awareness of what another part has said, such as interrupting oneself midthought, or at the end of a sequence, and saying either, “on the other hand,” while expressing an opposite or conflicting viewpoint, or even, “What am I saying? I don’t mean that, what I really mean is . . . ”

DOES THE PATIENT HAVE PAIN/HEADACHES WITH SWITCHING OR CONFLICT?

True DID individuals often cannot perform talking through early in treatment, at least between some key parts, and rather can only switch between personalities taking executive control seriatum. Over time, as coconsciousness increases between at least some parts, talking through may become more possible. Talking through is often more time-efficient than switching, the latter of which can be quite fatiguing and effortful for some individuals or, for some, even painful. If pain or headaches are present during switching, it is typically a sign that parts represent an approach/ avoidance ambivalence about the topic under discussion. Even without overt switching, headaches that emerge during therapeutic procedures are a sign of such an approach/avoidance ambivalence about the subject.

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CAN THE PATIENT USE “DISSOCIATIVE TABLE” OR A “HEALING CIRCLE?”

An extremely useful and time-efficient means to access a dissociative patient’s selfsystem is the use of the Dissociative Table Technique (Fraser, 1991, 2003; Paulsen, 1995, 2007, 2009). Also known as the “conference room technique,” this method allows quick accessing to internal self-states without switching, for those who can tolerate it, and without formal hypnosis. The procedure has been described as a hypnoprojective method (J. G. Watkins, personal communication, 2004). If it is hypnosis, it is light hypnosis, as no formal trance induction is required beyond asking the individual to glance into the mind’s eye, into a pleasant conference room. Note that the conference room is not the same as a “safe place,” as the latter is for relaxation and the former is for necessary and sometimes painful work. Conference room is an extension of talking through previously described, the latter of which is an auditory accessing method. That is, the part that the therapist is talking through to other parts will listen for the reply of the other parts and pass along to the therapist the answer that he or she hears. In contrast, conference room enables visual and auditory accessing, which results in a wealth of information. In conference room method, specific part(s) with interest in a given topic can be observed by the part of the self that the therapist is talking through. This is more likely to produce information that surprises the front part than is auditory accessing. For example, the front part may express surprise that a part it had previously known only through auditory information is revealed to appear far younger than it was pretending to be, once the front part glances into the conference room. Whatever information is revealed in the conference room in relation to a particular subject under discussion is important information, though it may not be evident why initially. Whatever manifests in the conference room, whether an ego state or an apparently “inanimate” feature, can be the object of inquiry and curiosity, as it is somehow part of the story telling itself. This includes even diffuse information such as smoke, darkness, a pusfilled blob, sticky ooze, or specific but opaque references such as fierce animals, monsters, a wall, a brick, and so forth. Each can be interviewed regarding its meaning and, on inquiry, is likely to transform into something more recognizably a state or a part of a conflictual dynamic.

RECONSTRUCTION OF THE SELF BEHIND WALLS WITHOUT ERODING AMNESIA BARRIERS PREMATURELY

One hazard of talking through and conference room is that it is possible to prematurely erode dissociative barriers that would best be tactically left in place until a later point in the treatment, as described in “tactical integrationism” (Fine, 1999). Therefore, in order to leave the front parts of the self, also called ANP (Steele, van der Hart, & Nijenhuis, 2005), protected from such an erosion, it is often best to use hypnosis to maintain the amnesia barrier by sending the ANP off and switching to another part of self to talk through. The part deputized for talking through needs to be mature enough and willing to basically act as interpreter, neither suppressing nor distorting the “speaking” part’s point of view. This strategy is counterintuitive to

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many clinicians who assume the patient is best served by eroding amnesia barriers as soon as possible. However, especially if the patient is needing to function as a parent or on the job, it is very useful to have the functional ANP part of self protected by the presence of a sturdy amnesia barrier so he or she can focus on his or her responsibilities without being distracted or overwhelmed. The necessary painful work takes place behind the amnesia barrier, with the therapist working either directly with parts as they switch into the therapy, or by talking through parts using conference room or another access method that doesn’t require switching. Later in therapy, the amnesia barrier can come down, or comes down spontaneously, when it is no longer needed. This is like remodeling a house around a weight-bearing wall, only removing it when the new design and its new structural supports are well in place, obviating the need for the old wall, which can then be safely removed.

IS THE LOCUS OF DISTURBANCE INTERNAL OR EXTERNAL?

Many dissociative patients present in crisis. An early matter for assessment is to determine whether the locus of disturbance is internal or external to the client (Paulsen & Golston, 2006). When it is external to the client, and related to pressing matters that may be medical, legal, housing, relationship, financial, and so forth, assessment must include determining if additional resources and services should be brought to bear to help solve the crisis and stabilize the client. Often with a dissociative patient, the crisis is at least in part related to internal system stressors, often reenacting earlier life dynamics of dysfunctional families. Chapter 14 addresses the means of increasing stability within a self-system by realigning the relationship between parts when the locus of disturbance is internal to the patient. Before describing those methods, however, the next chapter in the present part (Chapter 13) presents some of the means useful for accessing the patient’s self-system in a paced manner.

REFERENCES Berntson, G. G., Cacioppo, J. T., & Quigley, K. S. (1991). Autonomic determinism: the modes of autonomic control, the doctrine of autonomic space, and the laws of autonomic constraint. Psychological Review, 98(4), 459–487. Brand, B. L., Armstrong, J. G., & Loewenstein, R. J. (2006a). Psychological assessment of patients with dissociative identity disorder. Psychiatric Clinics of North America, 29, 145–168. Brand, B. L., McNary, S. W., Loewenstein, R. J., Kolos, A. C., & Barr, S. R. (2006b). Assessment of genuine and simulated dissociative identity disorder on the structured interview of reported symptoms. Journal of Trauma & Dissociation, 7(1), 63–85. Davidson, J., & Foa, E. B. (Eds.) (1993). PTSD: DSM-IV and beyond. Washington, DC: American Psychiatric Association Press. Dell, P. F., & O’Neill, J. (Eds.) (2009). Dissociation and the dissociative disorders: DSM-V and beyond. New York, NY: Routledge. Ellenberger, Henri F. (1970). The discovery of the unconscious: The history and evolution of dynamic psychiatry. New York, NY: Basic Books.

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Federn, P. (1952). Ego, psychology and the psychoses (E. Weiss, Ed., pp. 5–6.) New York, NY: Basic Books. Fine, C. G. (1999). The tactical-integration model for the treatment of dissociative identity disorder and allied dissociative disorders. American Journal of Psychotherapy, 53(3), 361–376. Fraser, G. A. (1991). The dissociative table technique: A strategy for working with ego states in dissociative disorders and ego-state therapy. Dissociation: Progress in the Dissociative Disorders, 4, 205–213. Fraser, G. A. (2003). Eraser’s ‘Dissociative Table Technique’ revisited, revised: A strategy for working with ego states in dissociative disorders and ego-state therapy. Journal of Trauma & Dissociation, 4(4), 5–28. International Society for the Study of Trauma and Dissociation (ISSTD). (2011). Guidelines for treating dissociative identity disorder in adults, third revision. Journal of Trauma & Dissociation, 12, 115–187. Klein, M. (1946). Notes on some schizoid mechanisms. The International Journal of PsychoAnalysis, 27(Pt 3–4), 99–110. Kluft, R. P. (1984a). An introduction to Multiple Personality Disorder. Psychiatric Annals, 14, 19–24. Kluft, R. P. (1984b). Treatment of multiple personality disorder. A study of 33 cases. The Psychiatric Clinics of North America, 7(1), 9–29. Kluft, R. P. (1990). An abreactive technique. In D. C. Hammond (Ed.), Handbook of hypnotic suggestions and metaphors (pp. 526–527). New York, NY: Norton. Kluft, R. P. (2009). A clinician’s understanding of dissociation. In P. F. Dell & J. A. O’Neil (Eds.), Dissociation and the dissociative disorders: DSM-V and beyond (pp. 559–623). New York, NY: Routledge . Loewenstein, R. J. (1991). An office mental status examination for complex chronic dissociative symptoms and multiple personality disorder. The Psychiatric clinics of North America, 14(3), 567–604. Marmer, T. S. (1980). The dream in dissociative states. In J. M. Natterson (Ed.), The dream in clinical practice (pp. 163–175). New York, NY: Jacob Aronson. Nijenhuis, E. R., van Dyck, R., Spinhoven, P., van der Hart, O., Chatrou, M., Vanderlinden, J., & Moene, F. (1999). Somatoform dissociation discriminates among diagnostic categories over and above general psychopathology. The Australian and New Zealand Journal of Psychiatry, 33(4), 511–520. Nijenhuis, E. R., van der Hart, O., & Steele, K. (2004, January). David Baldwin’s trauma information pages. Retrieved January 21, 2013, from Trauma information pages: http://www. trauma-pages.com/a/nijenhuis-2004.php O’Shea, K., & Paulsen, S. L. (2007, September). A protocol for increasing affect regulation and clearing early trauma. Paper presented at the annual meeting of the Eye Movement Desensitization & Reprocessing International Association Conference, Dallas, TX. Paulsen, S. (1995). EMDR: Its cautious use in the dissociative disorders. Dissociation, 8, 32–44. Panksepp, J. (1998). Affective neuroscience: the foundations of human and animal emotions. New York, NY: Oxford University Press. Paulsen, S. L. (2007, September). Integrating somatic interventions and EMDR: Keeping it AIP “legal.” Paper presented at the annual meeting of the Eye Movement Desensitization & Reprocessing International Association Conference, Dallas, TX. Paulsen, S. L. (2009). Looking through the eyes of trauma and dissociation: An illustrated guide for EMDR clinicians and clients. Charleston, NC: Booksurge. Paulsen, S. L., & Golston, J. C. (2005, September). Taming the storm: 43 secrets of successful stabilization. Paper presented at the annual meeting of the Eye Movement Desensitization & Reprocessing International Association, Seattle, WA.

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Porges, S. W. (2011). The polyvagal theory: Neurophysiological foundations of emotions, attachment, communication, and self-regulation. New York: W. W. Norton. Putnam, F. (1989). Diagnosis and treatment of multiple personality disorder. New York, NY: Guilford. Putnam, F. W. (1997). Dissociation in children and adolescents: A developmental perspective. New York, NY: Guildford Press. Spiegel, D. (2008). Coming apart: Trauma and the Fragmentation of the Self. Cerebrum, The Dana Foundation, accessed from http://www.dana.org/news/cerebrum/detail. aspx?id=11122 Steele, K., van der Hart, O., & Nijenhuis, E. R. (2005). Phase-oriented treatment of structural dissociation in complex traumatization: overcoming trauma-related phobias. Journal of Trauma & Dissociation, 6(3), 11–53. Watkins, J. G., & Watkins, H. H. (1997). Ego-state theory and therapy. New York, NY: W. W. Norton.

CHAPTER 13

The Compassionate Self Frank M. Corrigan, Alistair Wilson, and Deirdre Fay

Mr. Duffy lived a short distance from his body. —James Joyce, in Dubliners (1914)

Safe embodiment is a concept that is at the core of successful treatment of traumatic stress syndromes and dissociation. It is a state subjectively familiar to most people who have not been severely traumatized or who have recovered from the persisting psychological effects of their adverse experiences. Nevertheless, a definition helps the generation of hypotheses on the neurobiology and the development of clinical approaches. High levels of affection objectively observed in a mother– infant interaction predict lower levels of distress in adults 30 years later (Maselko, Kubzansky, Lipsitt, & Buka, 2011), and we hypothesize that the secure early attachment provides the biological substrate for later access to a condition of warm, safe, comforting calmness. However, smooth functioning of basic emotional systems may be impeded by layers of trauma and other distress accumulated over the years of a life. Therapy with eye movement desensitization and reprocessing (EMDR) requires a potential patient or client to have access to an imaginary safe place to support calming if there is a danger of overwhelm. It also gives access to the neurobiological apparatus required to transform experience through the healing process. Without good attachment experience in early life, the wiring required for the resolution of the traumatic memory may not be readily available. For that person, the key component of treatment, at least initially, is not the reprocessing of the adverse experiences that

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occurred later in life, but the development of the brain mechanisms for a state of core calmness, security, and safety, which did not develop in infancy. For the second meaning of the word “safe,” freedom from danger, we propose that safe embodiment is best defined as a condition in which there is both minimal defense response activation and minimal vigilance for threat, and that these states are experienced in the body fully and mindfully. This leads to the further hypotheses that the defense response and orienting areas of the midbrain are not actively engaged; that there is a positive valence of the mesolimbic dopamine system promoting appetitive and affiliative behavior; and that there is a blending of cortical activations conferring mindful, nonjudgmental awareness of the self in the moment. We propose that the feeling of belonging, the awareness of physical safety, the ability to focus on the experience of the moment, and the cultivation of compassion for self and others have neuroplasticity effects on key tracts involving the ventrolateral periaqueductal gray (vlPAG), the ventral tegmental area (VTA), the bed nucleus of the stria terminalis (BNST), the nucleus accumbens, the anterior cingulate and anterior insular cortices, and the posteromedial cortex. The experiences of belonging, safety, mindful awareness, and compassion for self and others create or restore the body state of security displaced by trauma, abuse, or neglect. For most people, these states of belonging and safety arise in relationship to another person—a safe other— who provides a good enough secure space, and may be difficult to access from a place of interpersonal isolation. These are the functions of attunement, of being “heard” by the other: the unconscious projective identification of a distressed condition made conscious and thereby open to being transformed. This sense of secure connection can also prevent distress from becoming overwhelming; it reduces pain and discomfort in those with the care and support of an intimate partner in a valued relationship (Johnson, 2009). It is not always easy to explain what works in trauma therapy, but one of the most telling therapeutic interventions involves the induction of compassion in the adult for his traumatized child self. This is described clearly for EMDR practitioners by Jim Knipe (2008), who observed that the “loving eyes” of an adult are necessary for a child to grow and develop to his full potential. If, instead, the child is neglected and traumatized and has grown up suffering from significant dissociation as a result of early experience, the “loving eyes” interweave can help the adult to feel a nurturing and compassionate response for the frightened, abandoned, child self. In Life Span Integration (Pace, 2003), the imagined infant self is shown the life of the person through visualizations of neutral or happy events to solidify the core self with care and nurturing. Whatever the treatment modality, the ability to induce a state of nurturing compassion, which can then be directed toward the parts of the self that hold the trauma-based feelings and memories, holds great healing potential. While this provides a way in which the mindful attunement of the therapist encourages the growth and healing of the patient, it also underlines how devastatingly destructive it is when a therapist helps to create a sense of safety, perhaps for the first time in the person’s life, and then exploits that for his own purposes. Mistrust of others is then solidified in a way that subsequent therapists will struggle to reduce.

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MINDFULNESS, COMPASSION, And NEUROPLASTICITY: PROPOSED MODELS OF CHANGE TO KEY UNDERLYING PROCESSES

It is not so surprising that changes occur in the adult brain. How else would we learn to speak a new language, play a new musical instrument, or enjoy a new attachment experience? How else could we develop fears and dislikes and urges to avoid? These happen through modifications of neurons and their interactions, synaptic adjustments, and neurochemical subtleties. For example, fibers communicating between somatosensory and motor cortices are essential for the rapid response to sensory feedback and the adjusted manual dexterity involved in playing an instrument proficiently (Craig, 2009). Without neuroplasticity, the skill would not be acquired. The downside is that some learning induces changes that have damaging consequences. Behaviors and environments promote structural changes that allow the individual to adapt to circumstances (Gage, 2004), and sometimes this adaptive plasticity is reversible (McEwen, 2009). Neuroplasticity can also promote some degree of repair to the brain, not only through altered function of specific brain areas but also through neurogenesis. This generation of new neurons occurs especially in the dentate gyrus of the hippocampus (Gage, 2004), a structure that is susceptible to shrinkage in response to trauma and stress (McEwen, 2009). Rat pups repeatedly deprived of maternal attention grow up to be adults whose dentate gyrus has an impaired capacity for neurogenesis (Karten, Olariu, & Cameron, 2005). The hippocampal volume is reduced in dissociative disorders (Vermetten, Schmahl, Lindner, Loewenstein, & Bremner, 2006) and in major depressive disorders in those who have suffered childhood neglect (Frodl, Reinhold, Koutsouleris, Reiser, & Meisenzahl, 2010). In contrast, hippocampal volume is reported to be increased in long-term meditators (Luders, Toga, Lepore, & Gaser, 2009). However, it is not known whether the practice of meditation in those who have suffered early trauma promotes the growth of this part of the brain, which has been specifically affected by adversity during critical developmental periods. The relevance of neuroplasticity to meditation has been developed by Daniel Siegel (2007) and by Jeffrey Schwartz and Sharon Begley (2002). The repeated practice of sustained directed attention with mindfulness is the key driver of neuroplastic change. To have precise timing, the professional musician requires advanced functioning in a network including premotor and parietal areas of cortex (Krause, Schnitzler, & Pollok, 2010). This develops over thousands of hours of focused practice with tiny adaptations dependent on the ability to discern deviations from the perfect performance. Without full attention, there would only be rote procedural learning, lacking the emotional complexity required of the leading musicians. As with motor skills, so with mental abilities: innate potentials that require to be developed with focused attention. Mindfulness may also function as a form of attunement, activating the affiliative emotion circuitry developed in secure attachments by remodeling a sense of compassion toward the self (Siegel, 2007). The same areas activated in mindfulness meditation in the medial prefrontal cortex (PFC) are also stimulated by secure attachment.

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The Medial PFC and Awareness of Awareness

The primary advanced human awareness may be that engendered in the anterior insular cortex (AIC) with the experience of one’s own existence as a sentient being (Craig, 2009). Changes in the body are brought to awareness by the transition of the somatic information relayed from the posterior to the anterior insula. However, the observational awareness of this awareness recruits the medial PFC. For example, mindful observation of emotional responses activates the dorsomedial PFC (DMPFC; Frewen et al., 2010). As a rough guide, body awareness is monitored by ventral medial PFC (VMPFC); attention to emotions is dependent on a more dorsal area, including the rostral anterior cingulate cortex (ACC), and the more abstract and cognitive self-representations are based in DMPFC and dorsal ACC. The evolution of the cortical mantle provides ample scope for the compartmentalization of areas of conscious awareness in the dissociative disorders.

Emotion Regulation and Well-Being

Observing thoughts as they arise in the mind, allowing them to dissipate, gives control over the mind and confers the ability to regulate disturbing emotions (Ricard, 2007). Greater alertness, energy, enthusiasm, and well-being accompany higher activity in the left PFC, while higher right prefrontal activity is reflected in reports of increased levels of anxiety, worry, and discontentment. An 8-week training in mindfulness meditation increased left-frontal activation and the degree to which it did so predicted the strength of the immune response to the influenza vaccine (Davidson et al., 2003). Asymmetry of prefrontal activity is evident in PTSD under certain conditions. One of the earliest imaging studies of PTSD reported increased blood flow mainly on the right side of the brain when patients listened to recordings of scripts relating to their trauma (Rauch et al., 1996). Of the therapeutic techniques hypothesized to enhance left prefrontal activity to reduce the intensity of the emotions surrounding traumatic memories, one example is the nonemotional verbal narrative exercises for rescripting perspective on past experiences described in Fay (2007).

Mindfulness Meditation and Emotion Regulation

Disturbing and distressing emotions that are suppressed nonmindfully reemerge with an intensification of internal conflict. Ricard (2007) summarizes the Buddhist teaching on emotion regulation as involving three dimensions: antidotes, liberation, and utilization. In the first, the disturbing emotion is replaced by a positive feeling such as love or compassion. This has been extended by Fay (2007) to include cognitive and narrative verbal antidotes to specific constellations of distressing thoughts and emotions. The second technique, liberation, requires full attention being brought to the emotion to study it until its impact dissipates. The third way is to separate

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out the positive aspects of the emotion and use these in some helpful way, as, for example, when active defense energy is used to drive and motivate. Safe situations allow the emergence of the “feeling mode” of the social engagement system, which recruits the ventral vagal complex’s rapid adaptability of facial and vocal expression, and moment-to-moment affect regulation (Porges, 2011). Conversely, activation of defensive responses to threat turns down the parasympathetically mediated interpersonal fine-tuning. It is difficult to look, feel, and listen with compassion, to be fully engaged in the moment, when there is activation of the threat system. In Buddhism, it is possible to take refuge in the Buddha (the possibility of what can be), the Dharma (the body of teachings), and the Sangha (the community of people practicing the teachings) to create a buffer zone against the difficult experiences that occur. In the “Becoming Safely Embodied” skills (Fay, 2007), there is an adaptation of these age-old venerable traditions for those who live a life of psychic suffering. A slowing down of the mental moments in a triggering sequence by focusing on each thought, feeling, and sensation (T/F/S) permits a disidentification from each component of the response. This also allows a choice of which mental event to explore more deeply and it is a particularly useful technique for finding exactly which part of an experience evoked a past event. Its careful application with an empathic therapist recruits the midline prefrontal cortical areas that observe experience and modulate the somatic responses. Mindfulness can help the depressed person to change the ruminative thinking pattern by being with the sadness just as it is, without judgment or self-criticism. It may achieve this by taking self-reflection from the more cognitive or autobiographical self activated through midline structures to the here-and-now self linked to the body awareness of the insular cortex. Individuals with a vulnerability to depression were given an 8-week training in mindfulness and then exposed to film clips to induce sadness, the intensity of which they were asked to rate, while undergoing functional MRI (fMRI) brain scanning (Farb et al., 2010). In the control group, sadness was linked to activation of midline structures, including the medial prefrontal areas and posterior cingulate cortex, and deactivation, mainly on the right, of somatosensory and insular cortices. This may reflect enhanced ruminative cognitive elaboration and reduced primary appraisal of the emotion. Conversely, the subjects with mindfulness training showed less activation in areas associated with ruminative thinking and reduced deactivation of the right insula region associated with body sensation. Mindfulness helps the person to process sad feelings as they arise in the body rather than getting hooked on thinking loops that end up with rumination and regret. During the reprocessing of obstructed grief, it is sometimes observed that the negative cognition “I should have done more” is important for preventing the full emergence of sadness. When the guilt clears, the person has access to a profound sense of loss, which is then available for transformation. As guilt is associated with increased subgenual cingulate cortex activity (Zahn, de Oliveira-Souza, Bramati, Garrido, & Moll, 2009), it is tempting to speculate that the guilty cognition serves its obstructive function directly at the subgenual cingulate cortical level, maintaining an activation incompatible with the full experience of loss.

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Empathy

If someone close to us drops a heavy object on his foot and yells with pain, our own pain circuits through anterior cingulate and anterior insular cortices are activated (Hein & Singer, 2008). fMRI can pick up the changes in empathy for pain that correlate with the closeness of the relationship. Participants shown images of feet or hands in painful positions were asked to adopt one of three perspectives: self, loved-one, or stranger. When the self or the loved-one “feels” the pain, the anterior cingulate and anterior insular cortices are activated (Cheng, Chen, Lin, Chou, & Decety, 2010). However, the right temporoparietal junction (TPJ) was activated when the stranger feeling the pain was imagined, suggesting that it has a critical role in self–other discrimination (Cheng, Chen, Lin, Chou, & Decety, 2010). The right TPJ is activated during compassion meditation when the meditator hears affectively loaded human vocalizations (Lutz, Brefczynski-Lewis, Johnstone, & Davidson, 2008), consistent with concern for the distress of another. A meta-analysis of fMRI studies considered whether there was a difference between a deliberate cognitive-evaluative empathy and a more spontaneous affective-perceptual empathy (Fan, Duncan, de Greck, & Northoff, 2010). Explicit cognitive evaluation of another’s emotional state involved the ACC and the left anterior insula, whereas affective-perceptual empathy recruited the right as well as the left anterior insula. Empathy and Compassion

In empathic awareness, there is an understanding of, and a sharing with, the other person’s affective responses to a situation. This does not necessarily involve a compassionate wish that the other’s distress will be eased. In Buddhist compassionate practices, the generated state of consciousness can exist without a specific intentional object. The neural underpinnings of compassion have been studied from the perspective of empathically recognizing someone else’s pain, the active generation of self-compassion, and the achievement of compassion for others. An exhaustive review of fMRI studies (Van Overwalle & Baetens, 2009) differentiated the mentalizing system from the mirror system and highlighted the TPJ, the medial PFC, and the precuneus in making inferences from abstract representations. Activation in the precuneus is also involved in differentiating emotionally charged statements about a group to which a person belongs and in negative attitudes toward that person’s outgroup (Bruneau & Saxe, 2010). It is not clear whether this is through visualization of past events or an interpretation of the intentions of outgroup members. Cooperation and trust for members of an ingroup are enhanced by oxytocin, a neuropeptide that confers increased social sensitivity: it also reduces trust toward members of an outgroup (Bos, Panksepp, Bluthe, & van Honk, 2012). In a study (Masten, Morelli, & Eisenberger, 2011) in which participants watched others being excluded from a computerized ball game, activations in the medial PFC were prominent, especially in those with greater trait empathy. Sending a soothing email to comfort the participant ostensibly excluded recruited the medial PFC and the right anterior insula of

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the empathic observer. Controlling for trait empathy highlighted the medial PFC as the area driving the helpful and comforting behavior. People without a high degree of empathy can still use their medial PFC to find the right words or actions to soothe those suffering the pain of social exclusion. Wanting to do unto others as you would have done to you would not necessarily require the empathy capacity of the right anterior insula but would require an “if I were being treated like that” comparison based in the medial PFC. (Brain areas are always components of networks, and we are not looking for the empathy or altruism equivalents of the “God spot” [Beauregard & O’Leary, 2007], but using the key points as shorthand markers of the relevant circuits.)

The Body Components of the Compassionate Response

Compassion, or suffering with, necessarily involves salience. The right insular cortex is a critical cortical node for detecting salience and controlling the switching between the central executive and the default networks (Sridharan, Levitin, & Menon, 2008). Both circuits are modified by compassionate practice: improved attention combined with an enhanced desire for the relief of suffering in others. The AIC is at the core of “the sentient self” (Craig, 2010) and contributes to the regulation of the autonomic midbrain areas and the valence of the nucleus accumbens shell. In the condition of threat reported by Butler et al. (2007), there was activation of both right and left insular cortices; yet in a single-case fMRI study, being in an imaginary safe place was associated with left insular cortex activation (Richardson et al., 2009). One explanation for these apparently conflicting findings is that there is an asymmetry of the AICs, with the left side mediating parasympathetic responses and the right contributing to sympathetic dominance (Craig, 2005). Thus, while right and left AIC would respond to a memory of an arousing experience, whether threatening or positively stimulating, the left AIC would dominate in an emotional experience with a significant parasympathetic component, whether calming and soothing or submissive. The valence of this activation is critical for whether the experience is one of warmth and comfort or one of collapse and shutdown. Trauma survivors can go into a shutdown, dissociated state when they are being introduced to simple relaxation training through imagery as the parasympathetic dominant body state created switches from positively valenced calmness into the negatively valenced state of extreme submission or attachment despair. Parasympathetic mechanisms also contribute to the laying down of “flashbulb memories” of events that are highly emotionally charged (Buchanan & Powell, 1993), and these may suddenly reemerge with reduced vigilance. A formal test of asymmetry in studies of pain empathy revealed no lateralization effect (Lamm & Singer, 2010), so valence may be more related to the connections of the anterior insula with other brain regions such as the nucleus accumbens, orbitofrontal cortex, and amygdala. An area of AIC, reciprocally connected with the basolateral amygdala (Aggleton, 1992), projects directly to the vlPAG (Ongur & Price, 2000). As the vlPAG also mediates passive responses to threat (Bandler, Keay, Floyd, & Price, 2000), it is likely to be at least bivalent, with the left AIC able to contribute to

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the vlPAG’s underpinning of a positively valenced state of calmness rather than to a submissive dejection. We hypothesize that compassionate affiliation allows the AIC to modulate the vlPAG to promote the warmth and comfort of the body’s response. vlPAG in affiliative mode and the AIC conferring parasympathetic dominance modify mesolimbic activation. The pleasantness of warm cutaneous stimuli activates the orbitofrontal cortex and ventral striatum, whereas the intensity of the stimuli is reflected in the posterior insula and somatosensory cortex (Rolls, Grabenhorst, & Parris, 2008). Nevertheless, the clinical experience of emotional warmth in relation to feelings of safety requires anterior insula involvement. Creating an imaginary “safe place” in therapy recruits the orbital network of the orbitofrontal cortex for its inputs from cortical areas associated with smell, taste, vision, and touch (but possibly not hearing; Price, 2006). As the characteristics are built up (what color do you most associate with safety; what texture; what smells or scents?), there is an amplification of the inputs to the orbitofrontal cortex from which there are outputs via the medial network to the hypothalamus, midbrain, and ventral striatum. Then they are anchored firmly in the body (otherwise they are unlikely to be effective later): creating loops through the left insula and the vlPAG, which can be collected by the orbitofrontal imagery when required. The valence of the mesolimbic dopamine system is switched from fearful to affiliative/appetitive, as described for environmental influences on laboratory rats by Reynolds and Berridge (2008). As many studies of the insula find activation in response to emotional triggers, fMRI findings on death-related linguistic cues stand out dramatically. In a test in which volunteers named the colors of words selected for negative valence, neutral valence, or relation to death, it was observed that negatively valenced, compared with neutral, words activated anterior and posterior cingulate cortices and the precuneus, among other cortical regions, but were not associated with any decreases in activity. In marked contrast, death-related words compared with neutral or negative words were associated with decreased activity in both right and left insula (Han, Qin, & Ma, 2010). These findings could help to explain the frequency of suicidal thinking and planning as ways of regulating distress: the death-related words will help to turn down the activation of the insular cortices so that the intense distress experienced in the visceral interoceptive system will be lessened. The beneficial effects of compassion meditation on neuroendocrine and immune responses to stress may appear after limited but committed practice (Pace et  al., 2009). This adds weight to the hypothesis (Gilbert, 2009) that compassion counterbalances the threat system and reduces its impact on health when it has been brought to a level not warranted by the environment. There is a reciprocal relationship with defense responses: when the compassion system is activated, the threat system is turned down and vice versa. Compassionate mind practices provide a buffer to emotional reactivity and reduce the response to adversity but are difficult to sustain under conditions of intimidation. If chronic activation of threat underpins many of the common affective disorders, sufferers from anxiety and depressive conditions will have less ability to access support, reassurance, and other therapeutic interactions because their social engagement capacities are restricted. People tend to feel less afraid when they have the company of ­someone

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they trust—even when the social engagement does not confer any additional physical security.

Compassion and Emotion Regulation

The meditator returning repeatedly to the breath gradually reduces the mind’s restlessness until a more panoramic awareness supervenes. The focus on the breath is then not needed (Varela, Thompson, & Rosch, 1991). Superimposed on the midbrain generators of caring affects, there are thalamocortical pathways necessary for parental nurturing in mammals. The ability to identify internal emotional states and the capacity for resonating with the feelings of others evolved in ways that liberated the emergence of compassion. The thalamocingulate underpinning of parental care, empathy, and altruism allowed the evolution of concern for the suffering and dying of all species (MacLean, 1993, p. 13). The ACC receives afferents from the amygdala and from the mediodorsal nucleus of the thalamus (Bentivoglio, Kultas-Ilinsky, & Ilinsky, 1993). In contrast, the thalamic nuclei that receive inputs from hippocampal regions also receive multisensory information from the brainstem, and these nuclei project to the posterior cingulate and retrosplenial areas. These thalamocingulate projections to posterior cingulate cortex are also advanced in function, as it is important to remember who to approach with affection rather than caution. Compassion training that develops the functions of the posteromedial cortex confers the ability for greater warmth and openness. Individuals who exhibit more frequent and prominent signs of compassion also exhibit other aspects of positive affect. The practices of attention, mindfulness, and compassion result in greater self-regulation and natural harmony, and at least part of this effect is through modification of the prefrontal control of the autonomic nervous system.

NONATTUNEMENT AND EMOTIONAL DYSREGULATION

When mothers are asked to freeze their facial expression and body movements for 2 minutes under experimental “still face” conditions (Tronick, 2007), their infants become disorganized during their efforts to reengage with the mother. Clinically equivalent are the adult children of mothers with dissociative disorders who have been physically present in early life when the mother switches into a frozen, distant state. This can leave persisting sequences of abandonment, rage, despair, and dissociation, which are readily triggered by ostensibly minor rebuffs or inattentions in adult life. Likewise, the child whose mother is psychotic, who moves suddenly from intense preoccupation to frightened and frightening behavior, will have major difficulties in emotion regulation, especially in response to distress associated with separation; often there are persisting fixed sequences of body responses here also. One of the antidotes to such distress is the cultivation of loving-kindness, equanimity, contentment, and compassion through the repetition of words and the

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building up of a positive state. The practice may initially evoke the experience of compassion even if it is not yet “felt,” evoking a state that eventually becomes a trait of compassion.

Compassionate Practices

Mindfulness/awareness has benefits, mental and physical, but why is it necessary to bring in compassion? Why not just stay with the breath until the state of panoramic awareness (Varela, Thompson, & Rosch, 1991) supervenes? Will solitary meditation not dispose to a solipsistic or narcissistic state in which the capacity to attune to the suffering of others is atrophied? Eight highly trained Tibetan monks were asked to switch between compassion meditation and a neutral mind state, and the sounds of someone in distress were presented to them in both states. When they were exposed to emotional human vocalizations, the right insula response to the sounds of distress in others was greater in the experts than in controls, with only a brief training. Compassion meditation was associated with activation of anterior insular and anterior cingulate cortices, medial PFC, posterior cingulate cortex and precuneus, TPJ and superior temporal sulcus; and those areas associated with awareness of the mental states of others responded more to emotional human voices during the compassion practice (Lutz, Greischer, Rawlings, Ricard, & Davidson, 2008). It is clear from the brain responses that compassion practices intensify rather than dull the response of the skilled meditator to the distress of other beings. Long-term practitioners of Buddhist compassion meditation have altered electroencephalography (EEG) activity at baseline before meditation (Lutz, Greischer, Rawlings, Ricard, & Davidson, 2004), suggesting that the many hours of practice modify the brain’s default settings. THE NEUROSCIENCE OF THE SELF

It’s just the way these lambs newborn in simple lambness know exactly how to be what just they are —Alan Spence, in Morning Glory (2010, p. 12) Action impulses and affective responses to environmental stimuli go together: “I act and feel, therefore I am” (p. 203; Panksepp, 2003). In the midbrain, where the emotional responses to interoceptive and exteroceptive stimuli are generated, there is a primordial form of consciousness emerging from the motor coordinates of the action urges. Panksepp (2003) called this neural system the SELF, or simple ego-type lifeform. An unreflective, phenomenal experience of the SELF’s activity is referred to as anoetic consciousness (Vandekerckhove & Panksepp, 2009). In this model, the motor coordinates of the SELF are embedded in the superior colliculus (SC), especially in its deep layers where there is an integration of the visceral inputs from the PAG with

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the sensory information available to the superficial and intermediate layers of the SC. A wide range of conscious experience and responses to the environment can be mediated by this region (Merker, 2007). Damasio (2010) acknowledges these different viewpoints but stresses the homeostatic role in the body’s functioning of other brainstem nuclei that nevertheless are closely interconnected with the SC and the PAG. The ability of the deeper layers of the SC to integrate sensory stimuli from the environment with immediate autonomic and motor responses gives it a pivotal role in the core SELF. The loops mediating intrinsic behavioral programs are based in projections from the SC; and there is also an impact on general arousal from projections to the thalamus, which in turn influences most of the neocortex (Furigo et al., 2010). Mindfulness practice as a higher human form of awareness is postulated to be dependent on cortical activations. Nevertheless, the motor coordinates for the posture in which the spine is straightened, the hands are correctly positioned, the chest is lifted and expanded, and the shoulders are pulled back (Brown, 2006) have their most basic components in the SC, allowing awareness to build from the SELF upwards.

Subcortical-Cortical Midline Systems and the Self

Imaging studies of the brain during self-referential activity consistently show involvement of cortical midline structures such as ACC, medial PFC, and the posterior cingulate cortex, retrosplenium, and precuneus (Northoff & Bermpohl, 2004; Panksepp & Northoff, 2008). As the more ventral areas of orbitomedial PFC (OMPFC) have strong interconnections with the midbrain (Price, 2006), it is proposed that there is a subcortical-cortical midline system that is concerned with all affective self-related stimuli. This can be fully conscious and accessible to reflection and so is described as “noetic.” With the development of autobiographical memory, and the ability to recognize events in the past as having occurred in the life of the self, comes the growth of autonoetic consciousness (Vandekerckhove & Panksepp, 2009). The moment-tomoment life of the primordial areas of the midbrain is given a temporal dimension by the linkage with the cortical midline structures, allowing protracted responses to the memory of an event long after the withdrawal of the original stimulus (Panksepp & Northoff, 2008). The definition of autonoetic consciousness is particularly interesting for dissociative identity disorder, as it contains episodic memory and an ability to act with a sense of continuity while imagining possibilities for the future. The linkage of a unique self-perspective with particular episodic memories—and the integration of these with the midbrain SELF in a way that allows a view of the world in the future consistent with the autonoetic self’s past experience—defines an identity of which there may be several in the one body. As we are using the construct of a polyvalent mesolimbic system for one of the ways in which the self’s feeling about itself can rapidly change, the findings of Northoff et al. (2007) are particularly pertinent. Viewing emotional pictures high in self-relatedness activated the nucleus accumbens as well as medial cortical and subcortical areas (Northoff et al., 2007).

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Existential Feelings and the Self

The basic affects and their expression in the body can modify the sense of self. In the process of being directed toward their object, human emotions also reveal or define something about the self experiencing them: loving something reflects on the person experiencing the love (Slaby & Stephan, 2008). Thus, affective intentionality and self-consciousness are linked through feeling oneself in a certain way in relation to something (Slaby & Stephan, 2008, p. 507). Constant and continuing experiences of emotional responses to environmental occurrences define the background self­referential awareness of the world, and these existential feelings then define the selfconsciousness that contributes through neuroplastic mechanisms to personal identity. Thoughts need feelings to become the attitudes that help to define the personal identity. “Thus there is a sense in which you have to feel what you think in order to really think what you think” (Slaby & Stephan, 2008, p. 513). We will argue later that the often preconscious and preverbal pleasantness or nastiness of the experience of the self is partly dependent on brainstem structures evolved for gustation. These existential feelings at the SELF level may exert a great effect outside the person’s usual awareness. They may become accessible during meditation practice and may account for some of the unexpectedly overwhelming responses that can occur when trauma sufferers begin training in mindfulness, especially if the feelings are attached to the basic self-structures of an emotional part that has been dissociated and exiled.

The Posteromedial Cortex and the Self

The development of the social emotions important for healing interactions with others extends the cortical involvement to the posterior cingulate cortex, the retrosplenial areas, and the precuneus, collectively referred to as the posteromedial cortex (Parvizi, Van Hoesen, Buckwalter, & Damasio, 2006) or posteromedial cortices (ImmordinoYang, McColl, Damasio, & Damasio, 2009). Some of these areas are active when we close our eyes and think about ourselves, musing on events in our autobiographical past, especially those with an emotional charge. They become less active when we have to turn our attention to tasks that are not self-related, explaining why it is sometimes easier to keep busy rather than to dwell on a troubling issue. In an fMRI study, participants were exposed to narratives designed to induce admiration for virtue or for skill and compassion for physical or social pain (Immordino-Yang et al., 2009). All activated basic emotional experiencing areas of the hypothalamus, midbrain, and anterior insula. The more evolved social emotions of admiration for virtue and compassion for social pain (such as grief and social exclusion) also activated the areas of posteromedial cortices most involved in interoceptive processing through links with the ACC and the insula (Immordino-Yang, McColl, Damasio, & Damasio, 2009). In the macaque, the retrosplenial areas receive projections from the OMPFC, the ACC, and the basolateral amygdala, and they project to the nucleus accumbens and the PAG (Parvizi, Van Hoesen, Buckwalter, & Damasio, 2006), consistent with a role in emotional processing and regulation. Perhaps initially compassion for social pain requires the integration of personal emotional memories with their related content

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to give a wish that the suffering of all others will cease. Exercises that require the meditator to bring up an image associated with love and kindness to access the feeling of compassion may need the links of the posteromedial cortex with medial temporal regions. The image of the friend, relative, or admired person who holds the qualities of loving-kindness may need the posterior precuneus links with the visual cortex (Margulies et al., 2009) and the posterior cingulate cortex (Parvizi et al., 2006) to initially but indirectly activate the retrosplenial areas to influence the valence of mesolimbic and mesocortical systems.

THE COMPASSIONATE CORE SELF

People who are very fragmented as a result of horrific abuse on top of severe attachment traumas often doubt in the presence of a core self that contains the capacity for a state of health and happiness. There can be so many emotional parts vying to take control of default and central-executive networks that apparently normal parts appear weak, insubstantial, and incapable of exerting any organizational authority over the chaos. The belief that there is a Core Self, which is calm, compassionate, curious, and clear thinking, is a source of optimism for therapist and client, and can be sustaining in those times when the present moment is smothered in layers of past distresses. Unblending of the different parts in the style described by Schwartz (1995) can be very protracted and initially give only the briefest affective glimpse of the Core Self. Nevertheless, the belief that it exists, enhanced by the fleeting acquaintance with it, can be very sustaining. To differentiate it from the core self in the usage of Damasio (2010), in which the interaction of the protoself with an object may be relatively basic and uncomplicated, we refer to the state described by Schwartz (1995) as the compassionate core self. It is not functioning at the level of the primordial response to an object but at a level of complexity that allows an overview of the parts of the self. If some dissociated self-states have both default and central-executive circuits, the right insula may be contributing not only to circuit switching but to state switching in response to body feelings. The compassionate core self is a unified state in which executive and default states are undifferentiated. Its compassionate nature implicates the posteromedial cortex and the projections to subcortical areas relevant in generating and processing affective states.

Clinical Example: The Healing Potential of the Mindful Awareness of Empathic Attunement in the Therapeutic Interaction

A client who is angry because she does not feel heard by her husband, just as with her family in her early life, has her distress metabolized when the therapist “gets” how much pain she is in, feeling the intensity of it in her own body. She sees her pain in the therapist’s face and hears her distress in the therapist’s voice, and this resonance allows her to calm down. She can then be directed to make similar contact with the part inside her that is furious. Does that angry part know that therapist and client “get” how distraught she is? Using reflective functioning (Fonagy, Steele, Steele,

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Moran, & Higgitt, 1991), the essential human capacity to understand behavior in terms of the underlying mental states and intentions, “What effect does our noticing have on that part?” “Do other parts of her notice how this angry part is responding to being heard?” Gradually, the response is broadened so that the compassionate attunement is pervasive throughout the system. Staying right in the moment, the therapist tracks moment-to-moment changes between the two, pulling the connection into the foreground. In one example, the client says, “I wish I could remember how I decided to look at people’s ears or foreheads rather than their eyes. I feel so mangled.” The therapist reflects that it must have been horrible to look in someone’s eyes and not have them see you. The client replied, “When the eyes are dead then . . . well, who are you? Maybe you don’t exist. You’re not here and don’t exist. It is hard to get away from the belief that I was mangled.” Sitting with that together, the therapist marvels with her and validates that when eyes don’t see the person how utterly distressing that would be. The belief would arise that there is something wrong with her—rather than that the dead eyes were dead before they looked at her. She is asked to explore right then, in that moment, how that connection feels and how the parts of herself feel about that contact. “When we’re connected it’s real . . . not threatened.” [She’s quite astonished.] [Both client and therapist are joyful and stunned and delighted that the parts, in her words, are “transformed by being in the moment too.”] The moment-by-moment tracking of the empathic connection allowed a clear sight of the defensive structure—the metacognitive result of the defenses being impacted by the attunement, by being really seen and heard with warmth and compassion. Being as close as possible to the moment-to-moment experience meant that defenses could be seen without them blocking the impact of the warm, empathic presence, and the generation of the awareness of the more secure base allowed a healing transformation.

PREVERBAL EXISTENTIAL FEELINGS OF LIKING OR LOATHING

Mindfulness practices that increase a default state of compassionate awareness are strengthening a network centered on the posteromedial cortex. At the other end of the self’s representation in the brain are the brainstem contributions to the feelings about the self. Working with very early memories in which adults reengage with feelings of profound worthlessness associated with interpersonal violence or severe neglect suggests that little cortical maturation is needed for feelings of aloneness, uselessness, helplessness, and hopelessness to become implicitly linked with the person’s perspective on the self. The parabrachial nucleus, active with the nucleus of the solitary tract at the most basic level of body response (Damasio, 2010), reacts to noxious stimuli. It receives information about pain from spinal neurons (Vogt, 1993) and about defense response reactions from the PAG. An adult woman who had been extensively investigated for neurological disorders was treated for somatoform dissociation, during which she reprocessed many traumatic experiences from her childhood. She had always had disgust for milk but had no understanding of the origins of it until she encountered a memory that she

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subsequently linked to the age of 18 months. She had the experience of being held so tightly that she was trapped while milk was forced into her mouth. To keep breathing she had to swallow the milk, including whatever was being regurgitated. The whole experience was profoundly aversive: the feeling of worthlessness from being valued so little by a caregiver; the helplessness and hopelessness from being held in a powerful grip from which there was no escape; the aloneness from having no one to turn to for rescue. We propose that the later disgust for milk was established at the level of the parabrachial nucleus, with avoidance responses from the PAG and the rostromedial tegmental nucleus (RMTg), and that the associated self-loathing also has its foundations at these levels. The understanding helped the patient to develop more compassion for the child who had undergone such a horrific experience and her self-esteem was then able to grow. The affective intentionality of the disgust was not only toward the milk but also to the self experiencing the trauma, and this was only brought to consciousness during therapy. Nevertheless, its subconscious or preconscious existence had had a powerful effect on the valence of the consciousness of the self. A similarly disturbing experience was described by a woman who presented for therapy following an inability to tolerate the experience of having fluid in her mouth during dental treatment. The difficulty only surfaced after a road traffic accident during which her car had skidded on ice and overturned into a river, but she had a feeling that it might also be linked to an experience when she was 3 years old of near drowning in a tank on her parents’ farm. Reprocessing proceeded cautiously but did encounter a largely nonverbal experience of imminent death, during which there was dissociation from feelings of abandonment, horror, and terror. There was a residual self-loathing that had never made sense to the adult patient. Again, she was able to develop compassion for the child who had had this traumatic experience and her self-esteem was then able to grow and develop.

CONCLUSION

While feelings of safety can be accessed through modifications of body physiology at the brainstem level, we propose that compassion is leading to changes in the experience of the self at its most fundamental, sometimes preconscious, level through the projections from cingulate cortices to the brainstem. Meditation that uses a concentration focus reduces fear through enhanced medial prefrontal modulation of subcortical activity and attunement has an effect through a similar pathway. Body awareness acts at the level of the anterior cingulate and insular cortices. Compassion downgrades the susceptibility to fear through the regulating effects of the posteromedial cortex. Complex multisensory traumatic experiences, even those immediately dissociated from conscious awareness, exert their effect on the affective valence of the self in the brainstem and are then modified at that level by top-down cortical control. Their reverberation through the brain makes compassionate reconsolidation of trauma memories more effective when engaging multiple levels: from the medulla and midbrain through the thalamus to the anterior cingulate, anterior insular, and retrosplenial cortices. The cultivation of compassionate mind states may lead to the

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retrosplenial areas, with their thalamic inputs, taking a dominant role in consciousness. The changes afforded to the primordial, preconscious, existential feelings by the practice of compassion alter the default settings of the self’s intentionality and create a new and happier multilayered Self. This Self can then fully extend a wish that all beings be free from suffering and from the causes of suffering.

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Margulies, D. S., Vincent, J. L., Kelly, C., Lohmann, G., Uddin, L. Q., Biswal, B. B., . . . Petrides, M. (2009). Precuneus shares intrinsic functional architecture in humans and monkeys. Proceedings of the National Academy of the Sciences of the USA, 106, 20069–20074. Maselko, J., Kubzansky, L., Lipsitt, L., & Buka, S. L. (2011). Mother’s affection at 8 months predicts emotional distress in adulthood. Journal of Epidemiology and Community Health, 65, 621–625. Masten, C. L., Morelli, S. A., & Eisenberger, N. I. (2011). An fMRI investigation of empathy for “social pain” and subsequent prosocial behavior. NeuroImage, 55, 381–388. McEwen, B. (2009). The brain is the central organ of stress and adaptation. NeuroImage, 47, 911–913. Merker, B. (2007). Consciousness without a cerebral cortex: A challenge for neuroscience and medicine. Behavioral and Brain Sciences, 30, 63–134. Northoff, G., & Bermpohl, F. (2004). Cortical midline structures and the self. Trends in Cognitive Sciences, 8, 102–107. Northoff, G., Schneider, F., Rotte, M., Matthiae, C., Tempelmann, C., Wiebking, C., . . . Panksepp, J. (2007). Differential parametric modulation of self-relatedness and emotions in different brain regions. Human Brain Mapping, 30, 369–382. Ongur, D., & Price, J. L. (2000). The organization of networks within the orbital and medial prefrontal cortex of rats, monkeys and humans. Cerebral Cortex, 10, 206–219. Pace, P. (2003). Lifespan integration: Connecting ego states through time. Available from the Lifespan Integration website: http://Lifespanintegration.com Pace, T. W., Negi, L. T., Adame, D. D., Cole, S. P., Sivilli, T. I., Brown, T. D., . . . Raison, C. L. (2009). Effect of compassion meditation on neuroendocrine, innate immune and behavioral responses to psychosocial stress. Psychoneuroendocrinology, 34, 87–98. Panksepp, J. (2003). Feeling the pain of social loss. Science, 302, 237–239. Panksepp, J., & Northoff, G. (2008). The trans-species core SELF: The emergence of active cultural and neuro-ecological agents through self-related processing within subcorticalcortical midline networks. Consciousness and Cognition, 18, 193–215. Parvizi, J., Van Hoesen, G. W., Buckwalter, J., & Damasio, A. (2006). Neural connections of the posteromedial cortex in the macaque. Proceedings of the National Academy of the Sciences of the USA, 103, 1563–1568. Porges, S. W. (2011). The polyvagal theory: Neurophysiological foundations of emotions, attachment, communication, and self-regulation. New York, NY: W. W. Norton. Price, J. L. (2006). Connections of orbital cortex. In D. H. Zald & S. L. Rauch (Eds.), The orbitofrontal cortex (pp. 39–56). Oxford: Oxford University Press. Rauch, S. L., van der Kolk, B. A., Fisler, R. E., Alpert, N. M., Orr, S. P., Savage, C. R., . . . Pitman, R. K. (1996). A symptom provocation study of posttraumatic stress disorder using positron emission tomography and script-driven imagery. Archives of General Psychiatry, 53, 380–387. Reynolds, S. B., & Berridge, K. C. (2008). Emotional environments retune the valence of appetitive versus fearful functions in nucleus accumbens. Nature Neuroscience, 11, 423–425. Ricard, M. (2007). Happiness. London, UK: Atlantic Books. Richardson, R., Williams, S. R., Hepenstall, S., Gregory, L., McKie, S., & Corrigan, F. (2009). A single-case fMRI study EMDR treatment of a patient with posttraumatic stress disorder. Journal of EMDR Practice and Research, 3, 10–23. Rolls, E. T., Grabenhorst, F., & Parris, B. A. (2008). Warm, pleasant feelings in the brain. NeuroImage, 41, 1504–1513. Schwartz, R. C. (1995). Internal family systems therapy. New York, NY: Guilford Press. Schwartz, J. M., & Begley, S. (2002). The mind and the brain: Neuroplasticity and the power of mental force. New York, NY: HarperCollins.

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Siegel, D. J. (2007). The mindful brain: Reflection and attunement in the cultivation of well-being. New York, NY: W.W. Norton. Slaby, J., & Stephan, A. (2008). Affective intentionality and self-consciousness. Consciousness and Cognition, 17, 506–513. Spence, A. (2010). Morning glory (E. Blackadder, illustrator). Edinburgh, UK: Renaissance Press. Sridharan, D., Levitin, D. J., & Menon, V. (2008). A critical role for the right fronto-insular cortex in switching between central-executive and default-mode networks. Proceedings of the National Academy of the Sciences of the USA, 105, 12569–12574. Tronick, E. (2007). The neurobehavioral and social-emotional development of infants and children. New York, NY: W. W. Norton. Vandekerckhove, M., & Panksepp, J. (2009). The flow of anoetic and autonoetic consciousness: A vision of unknowing (anoetic) and knowing (noetic) consciousness in the remembrance of things past and imagined futures. Consciousness and Cognition, 18, 1018–1028. Van Overwalle, F., & Baetens, K., (2009). Understanding others’ actions and goals by mirror and mentalizing systems: A meta-analysis. NeuroImage, 48, 564–584. Varela, F. J., Thompson, E., & Rosch, E. (1991). The embodied mind: Cognitive science and human experience. Massachusetts: Massachusetts Institute of Technology. Vermetten, E., Schmahl, C., Lindner, S., Loewenstein, R. J., & Bremner, J. D. (2006). Hippocampal and amygdalar volumes in dissociative identity disorder. The American Journal of Psychiatry, 163, 630–636. Vogt, B. A. (1993). Structural organization of cingulate cortex: Areas, neurons, and somatodendritic transmitter receptors. In B. A. Vogt & M. Gabriel (Eds.), Neurobiology of cingulate cortex and limbic thalamus (pp. 19–70). Boston, MA: Birkhauser. Zahn, R., de Oliveira-Souza, R., Bramati, I., Garrido, G., & Moll, J. (2009). Subgenual cingulate activity reflects individual differences in empathic concern. Neuroscience Letters, 457, 107–110.

CHAPTER 14

Stabilization Basics Sandra L. Paulsen and Joan Golston

The slower you go, the faster you get there. —Richard Kluft (1993)

Ongoing orientation to threat (also see Chapter 2: Threat and Safety: The Neurobiology of Defense Responses) commonly results in significant inquietude as well as ongoing dissociative symptoms that interfere with safe embodiment (also see Chapter 13: The Compassionate Self) and thus with a sufficiently stable sense of self for traumafocused work to be successful. Thus, prior to being able to safely embark on interventions that focus on the patient’s trauma history, the primary emphasis in treating chronic dissociative patients needs to be the containment of traumatic symptoms and stabilization of the patient. First established by Janet (van der Hart, Brown, & Van der Kolk, 1989) then further elaborated by numerous recent writers (e.g., Kluft, 1993), the phased approach to the treatment of dissociation is presently accepted by consensus (ISSTD, 2011). Premature trauma work is disorganizing to both patient and therapist, except when the therapist must manage crises or cope with posttraumatic material that has broken through defenses and disrupted functioning. Conducting trauma work prematurely risks harming the therapeutic alliance, reenactment of early injurious relationships, and retraumatization, in what should rightfully be a relationship of support and assistance. This chapter reviews a range of tools and approaches for the stabilization of traumatized patients and the containment of eruptions of traumatic material until they can be effectively addressed in a later phase of treatment. During the

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stabilization phase, the nature and status of the patient’s self-system of ego states will determine the pace and form of the treatment process. The effective therapist will not abdicate that pace or process to the patient; nor overlook present pragmatic considerations in the patient’s life; nor allow the work to be either chronically crisis-driven or a reenactment of the abuse and neglect. Rather, the therapist will set the clinical pace, structure, and process after considering a wide array of factors related to the patient’s functioning. This chapter sets forth many of those factors as well as a range of practical methods for addressing them. This chapter and the related chapter on ego state therapy (Chapter  4) is based on a compendium of methods previously presented by the authors (Paulsen & Goldston, 2005). Clinicians differ in terms of whether they place emphasis on the terms containment, stabilization, or ego strengthening. The term “containment” evolved from its analytic roots to refer to the task of increasing a patient’s capacity to nondestructively manage any disturbing unworked traumatic experience that, like a sliver, wants “out.” Too often, the patient sees the start of therapy as a signal that the untold story should promptly emerge. It then seems counterintuitive to nonavoidant parts of the patient that an even longer wait is indicated, especially for those child-­identified parts yearning for the gratification of the therapist’s sympathy. It is important to convey to the patient the concept of phases of therapy, to include at a minimum the idea that stabilization comes before trauma work. The International Society for the Study of Trauma and Dissociation (ISSTD) Treatment Guidelines describe the consensus model in three phases, to include stabilization, trauma metabolization, and integration phases of treatment (ISSTD, 2011). Paulsen has created an illustrated guide for therapist and client to use together to discuss the phases of treatment, from assessment and containment/stabilization, through initial trauma accessing and then abreactive work—especially eye movement desensitization and reprocessing (EMDR) work, followed by additions skills development, integration, and follow-up. Whatever model is employed, the patient will benefit from knowing that the beginning of therapy is not the perfect moment to lay bare his or her trauma and pain. With compassion, the therapist encourages child states to wait a bit longer while more adult resources take executive control of the body and life. Often, concrete imagery involving a container is beneficial to help the patient contain the material that needs to wait, but ego states should not be put in containers. The working through of traumatic experiences held by those child states must wait for an appropriate time and manner. Though nothing in the treatment of chronic traumatization is neat and tidy, the work will be more stable if based on the phased approach, and it will be easier to correct the course if needed. All sound methods that promote both patient stability and the capacity to utilize the therapeutic alliance merits consideration in this early phase of treatment. Because the elements of ego state therapy are so important to the stabilization phase, they are treated in a separate chapter for more extensive coverage, not because ego state work is deferred. In most cases, ego state therapy, without trauma uncovering, is key to successful stabilization of a dissociative client. This chapter begins with a description of the organizing principles that govern our conceptualization of stabilization, and sets forth a number of stabilization tactics.

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UNDERLYING PRINCIPLES Stability Is About State Regulation

Affective dysregulation is a central characteristic among chronically traumatized patients. The presence of such affective dysregulation is frequently indicative that states and the switching between states are conflictual and discordant. Dissociative disorders can be conceived of as state change disorders, because the pathophysiological basis of the disorder results from a dysregulation of the state change process (Putnam, 1988).

Stability Requires Staying Within the Optimal Arousal Window

An early focus of treatment of patients with complex trauma histories is to increase stability by helping the patient sustain an optimal arousal level (Siegel, 1999). If a patient’s level of emotional arousal is too high, he or she will be overwhelmed, and experience intrusive symptoms. Conversely, if a patient’s level of arousal is too low, the patient will be shut down, or dissociated, as with the avoidant symptoms of posttraumatic stress disorder (PTSD). Many patients experience continuous swings from one extreme of arousal to the other or have lives characterized by chronic shutdown, punctuated with occasional explosions of high arousal. Whether characterized by rapidly switching between numbing and flooding, or generally trending either low or high, the result is affective destabilization. However, when the patient’s fluctuations fall in the narrower midrange of the optimal window of arousal, then that patient is much more able to make good use of therapy, is more prepared for trauma transformation work, and better able to live a life that is regulated and less affectively disrupted. Achieving this capacity is a major goal of Phase I work and clinical attention to the window of arousal is a key aspect of Phase I interventions. Ultimately, it is the patient who possesses the best data about where he or she is in relation to the optimal window. Enhancement of his or her ability to conceptualize, recognize threats, and work to restore an optimal level of arousal bodes well for this phase of treatment. The patient can be enlisted in this goal through metaphors of power surges or power failures, fuses, and voltage regulators. Emotional “power surges” and “brownouts” can be prevented with “surge protection” techniques such as relaxation and mindfulness skills, yoga, exercise, and other methods described below, whether used in a group setting or as individual discipline. Ogden and Minton (2000) have established that therapy in general, and trauma work in particular, must be conducted within the optimal midrange of arousal to be effective. This principle is an important underlying premise of the methods described in this chapter as well as this book.

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Stability Requires Soma and Affect Tolerance

Consistent with the theory of optimal arousal level, the patient must have the capacity to tolerate somatic sensation and affective awareness in order to process through any channels of information that comprise traumatic memory. The patient with low soma or affect tolerance will react with numerous forms of avoidance or physiological shut off, and the work of trauma exploration and reduction will not be feasible. It may even be destructive or at least counterproductive.

Social Engagement Increases Affect Tolerance

Until recently, it was understood that mammals, including humans, developed a sympathetic nervous system to mobilize enough energy for either a fight or a flight response, and a parasympathetic nervous system to activate emergency freeze responses. Neurobiologist Steven Porges identified a second parasympathetic nervous system, the ventral vagal nervous system, distinguishing it from the other dorsal vagal parasympathetic system and from the sympathetic nervous system (Porges, 2011). The dorsal vagal system is evoked when fight and/or flight fails and the mammal has no choice but to surrender or to prepare for death. Porges hypothesizes that the ventral vagal nervous system functions to not only activate the sense of being safe but connected and/or socially engaged. Stabilization in the context of the therapeutic relationship diminishes the likelihood and duration of any emergency nervous system activation that a trauma patient experiences in therapy. The ventral vagal nervous system plays a critical role in healing from trauma. Within the stabilizing therapeutic relationship, the patient can better achieve ventral vagal activation and thereby muster strength to persist with the necessary and often emotionally painful process of therapy.

Hardwired Subcortical Affective Circuits Are Foundational to Stability or Instability

A related set of concepts comes from an emerging understanding of the neurobiology of affect, a field deeply indebted to the research and persistence of Jaak Panksepp (Panksepp, 1998; Panksepp & Biven, 2012). The application of Panksepp’s work to psychotherapy is more fully considered elsewhere in the present work. For our current purposes, however, it’s important to note that Panksepp’s experimental work establishes that basic affect is hardwired subcortically and is present from birth, requiring no learning. Without safe regulation and tolerance of affect in the primary caretaking relationships of infancy, the infant cannot tolerate the experience of intense emotion, and dissociates the affect at the level of the developing thalamus (Schore, 2003a, 2003b, 2009). This phenomenon is the basis of shame, and is central to basic injuries of the emerging self. This understanding underscores the restorative value of emphasizing stability and reregulation in a therapeutic relational context. This important subject is covered in other portions of this book, and is highlighted

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here to remind the reader that the goal of stabilization seeks to address very early injuries, though that repair will be ongoing throughout treatment. The capacity to regulate affect is established in infancy, within the context of a secure attachment to a loving caretaker. Adults who do not have the capacity for affect regulation likely did not successfully navigate the psychological developmental milestones of the first years of life. A discussion of the neurobiology of affect regulation in early child development is found in Chapter 19. When the therapist and patient set about to remediate dysregulated affect, they are working either directly or indirectly on these very early injuries. The remainder of this chapter describes some of the methods useful for improving affect regulation, expanding the patient’s window of arousal, addressing state change issues, tolerating the treatment process, and enhancing capacity for self-regulation.

Safety, Structure, and Boundaries

The emphasis in any treatment of a traumatized patient is to first establish safety and to ensure that the work has appropriate structure, priorities, and pacing. Extensive discussion of therapeutic roles, contracts, and boundaries is outside the scope of this chapter and has been amply covered elsewhere (Boon, Steele, & van der Hart, 2011; Loewenstein, 2006). The setting and sustaining of appropriate boundaries is no simple matter when dealing with patients who were raised in chaos, neglect, and boundary violation. A secure and well-bounded therapeutic structure materially enhances patient stability since the patient feels “held” by the work. In an effectively structured therapeutic environment, the patient feels safe enough to complain about and test the structure and its limits. Clinicians who do not maintain good therapeutic structure can in fact destabilize the patient. Confusion in the structure may recapitulate early childhood experiences, especially when it appears to the patient that the therapist’s loose boundaries constitute a sign of an impending boundary violation of the patient.

Pacing the Work

Pacing of therapy is important for establishing new conditioned responses to replace dysregulated or chaotic reactions that may characterize the patient’s childhood history and self-management to date. Through repetition, a patient comes to expect that while the session may be painful, by session end, the therapist will attempt to contain or “tuck in” any residual disturbance. The patient can emerge from sessions ready to resume the business of life. This newfound experience of constructive containment not only provides structure but reassurance that the therapist is concerned for the patient as she is. It also helps the patient understand that the therapeutic relationship and its work are conducted very differently from the chaotic or neglectful experiences of their earliest years. Like a light shining under a closed door, this lesson is absorbed throughout the system and has a reassuring and ultimately corrective effect for many parts of the self. Stabilization also teaches that when affective

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disturbance occurs, it is neither eternal nor unendurable, but temporary, and that a positive and strengthening experience is not far away. Although ruptures in a relationship feel painful, they may turn out to be relatively minor and, in most cases, reparable or even enriching. This lesson occurs during the development of the therapeutic alliance, with its inherent human potential for misattunement and course correction. This learning may be entirely new and initially inconceivable in the face of a patient’s earlier history, but such work must begin as early as possible in treatment. The repeated experience of oscillation between disturbance and resource has the effect of eroding the residual and reactive sympathetic arousal associated with trauma, while remaining grounded in the strength of the therapeutic relationship and/or present time context and resources (also see Chapter  19, Integrating Body and Mind: Sensorimotor Psychotherapy and Treatment of Dissociation, Defense, and Dysregulation). Even before trauma work has begun in earnest, the therapist can acknowledge and utilize the gentle oscillation between a resourced part of the self and a part holding disturbance as a means to increase self trust. The attuned presence of the therapist may initially be the primary relational resource for a patient to draw upon, but the strengthening of parts of the patient’s self is also occurring. Oscillating between disturbance and resource demonstrates that disturbances can be temporary and limited, and of restorative resources being more available than the posttraumatic patient presumes, making change itself more tolerable. From those experiences and these new learned expectations, hope begins to emerge. As Kluft (1993) famously pronounced, “The slower you go, the faster you get there.” While going slowly is important, so is advancing when the patient can tolerate such therapeutic movement. This is also important for cost-effective therapy as well as for developing the patient’s sense of efficacy and achievement.

Therapist Consistency

One of the most important elements of the therapist’s role in the relationship with a complex trauma survivor is his or her acceptance of the responsibility to define and maintain the structure of the therapy. That acceptance must persist even in the face of patient resistance to perceived loss of control over features of something important. Patient and in-depth discussion of therapy structure and patient response is beyond the scope of this chapter and is well addressed in the general literature of psychotherapy. However, there are several elements of the therapeutic alliance that need to be included in the original treatment contract, and well attended to by the therapist, lest a host of well-known and potentially serious problems arise. In the worst cases, those oversights and errors can cause irreparable harm to the therapy and the patient, with potential legal consequences, and ill effects on patient and therapist alike. Early in the therapy, and reiterated at intervals, as dictated by the course of the work, certain structural elements of the therapy must be defined and should be noted in the treatment record: the roles and responsibilities of therapist and patient, cost of treatment, cancellation and no-show policies, emergency procedures, the venue for sessions, business policies and payment arrangements, boundaries regarding such topics as touch and gifts, what is considered on and off topic,

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and therapist boundaries regarding their personal life. Over the course of treatment, any changes to this disclosure and agreed-upon structure should be negotiated in advance and made explicit, rather than just emerging, eroding, or drifting without discussion. Changes to any previously agreed-upon terms will stir emotions and the therapist must address them. While, in some areas, allowances can be made, generally speaking, patients who threaten suicide or other serious consequences in the face of the therapist’s insistence on the structure and boundaries of the work need the opportunity to explore the historic and current implications of the issue at hand, rather than being faced with a simple ultimatum. Boundary erosion can occur when the therapist feels intimidated by possible reactions from his or her patient. This may signify the need for consultation in which to examine how the personal material of the therapist and/or the patient’s unconscious material is distorting or charging the situation with greater intensity. Note that small changes, including erosions of the boundary, can seem just as threatening to the patient as major ones, and are often taken to presage loss, exploitation, or abandonment. Potential consequences for mild or severe violations of the contract, as well as the rationale for the therapist’s policies, should be made explicit, well in advance of potential difficulties.

Time Management

The clinician needs to set the patient’s expectations of the pace of the work and the course of therapy early in treatment, so the patient can anticipate the process he or she is entering. Disclosure of the treatment plan is a routine requirement under many jurisdictions’ informed consent regulations. As mentioned earlier, it is of greater importance for the maltreated, dissociative, fragmented, and fearful dissociative patient, often disoriented to time and place, to have a clear-enough map of the treatment path (ISSTD, 2011; Paulsen, 2009; Phillips & Frederick, 1995). It is also necessary to clarify with the self-system that the therapist will not convey a part’s material to other parts or tear down amnesic barriers prematurely, and will collaborate with the system to not push parts faster than tolerable. At the same time, the therapist should be clear that, while the patient needs to be the primary source of motivation to make progress, the therapist will gently push him or her to go as fast as he or she CAN go without becoming internally disorganized. The idea of containing material until the time is right is one that systems can understand, though they often respond with reluctance and relief at the idea that they may not be at the mercy of uncontrolled pressures. Chaos and pressure can feel like home for many. While some patients’ systems push ahead aggressively, some drag their feet, thereby going faster or slower than is in their best interest. Session time management is the clinician’s responsibility and contributes greatly to postsession stability. Richard Kluft advocates a “Rule of Thirds” with regard to when in-session interventions should occur (Kluft, 1993). Seeing the session as divided into three segments, regardless of session length, Kluft advises that no intervention be initiated if it hasn’t been started by the second third. The dissociative patient’s difficulty in adequately managing time can utterly derail therapy. This (Paulsen, 2009) must be addressed clearly and persistently at the

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first signs of a problem or building trend. What may begin as a by-product of disorganization, poor interpart cooperation or time loss can easily become avoidance, anxiety management, or a test of clinician investment in the patient and therapy. Sometimes patients arrive late or miss appointments altogether as a result of conflicts between those parts who are enthusiastic about treatment and those who are resistant or fearful. An ego state approach can be used to interview any parts causing the patient to be late. Inquiring sincerely about those parts and their concerns via talking through but ideally through direct contact, and acknowledging and appreciating the essence of their sensibility or intention, will go a long way in assisting a patient to acknowledge the truth in the various points of view of the parts involved (Putnam, 1989). It also disentangles the threads of ambivalence regarding getting help and of telling their story. Not uncommonly, there are parts who threaten to punish the patient for talking about family secrets, or for daring to assert herself or set limits in any way, even (or especially) with the therapist. Addressing resistant parts’ concerns, orienting them to present time, and reassuring them that their concerns will be incorporated into the work can help the patient become punctual and attend appointments. Both therapist and patient should acknowledge the assistance and cooperation of the part causing time management problems. Some patients fail to show up for appointments. If exploration of the meaning or internal obstacles is unfruitful, then it may be necessary to make the patient’s system aware that the therapist alone cannot solve the problem. If the patient cannot solve it either, then there will be no way to carry on the work. At worst, scheduling further sessions may need to be put on hold until such a time that clinician and system can figure out how to productively resume treatment. This step should only be taken when all other options have been exhausted, and the clinician, after consultation if necessary, has assessed the transference and countertransference forces that may be in operation. There is a vast range of possible underlying issues that commonly include the difficulty representing a test: fear of objections by other people in the patient’s life; fear of the growing evidence that this therapy may indeed lead to change or unearth buried material; fear that going to therapy means the patient is “crazy”; efforts by parts to protect the long-ago abuser. Regardless of the actual dynamic, the meaning attributed to the therapist’s dismissal of the patient can involve a great deal of distortion related to past experiences of abandonment or rejection and can damage the current (or potential future) therapeutic alliance. The client’s interpretation of the therapist’s dismissal of them can erode the patient’s expectations of future help from any source. The suspension or ending of therapy is a major step, and unless it reflects actual danger to the clinician, should be undertaken only after extensive and careful effort to find another solution. At the same time, the therapist should not allow the patient to erode the contractual agreement to the therapist’s harm.

Therapeutic Ruptures

In the course of a long therapy with the dissociative patient, ruptures in the therapeutic relationship are almost inevitable. Fortunately, these ruptures can often be repaired and, in the process, the relationship may be deepened. As noted above,

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two common sources of trouble in the therapeutic alliance are the result of actual error of the therapist or the patient’s posttraumatic expectation of betrayal or harm being projected onto an interaction with the therapist. When the therapist has made an error, such as misrecording the time of an appointment, the remedy includes a frank acknowledgement of the facts and an appropriate apology. Many patients were raised in households where caregivers denied harm and error, or attributed it to a quality in the child. The responsible therapist, however, joins in the reality of the patient’s experience of the therapist’s error and listens fully to the patient’s complaint without defensiveness. After the complaint has been fully expressed, the therapist responds with an appropriate degree of regret and apology; this sequence can be entirely novel to the patient and profoundly reparative. On the other hand, if the locus of the rupture appears to be in part or wholly based in the patient’s projected trauma-based expectations, the therapist might express acknowledgement and compassion for the patient’s feelings and invite the client to join him or her in puzzling about the matter, wondering if this is the first time the patient has had this sort of experience, or whether it has an old, familiar feeling and experience. Then, the therapist might say, So, when I (therapist behavior is described), even though you were here and in some way know you are (safe/well respected/or whatever is relevant) at the same time, it brought to mind times when (historical harm was done)? I can see why that would make you feel (x [upset/fearful/hurt]). Over the course of treatment, tolerance of rupture and reparative success can be a source of important information about the patient’s life, deepen therapeutic alliance, and add containment and stability by making it clear that not everything is “on the line” in any one relationship misadventure or stumble. As the therapist is revealed to be imperfect but human, the patient can begin to have a new or deeper sense of his or her own human nature.

Suicidal Risk and Self-Harm

Adverse attachment experiences, repeated traumatic exposure, existential sequelae typical of chronic traumatization, inescapable traumatic intrusion, and posttraumatic cognitive errors, among other things, mean that the chronically traumatized patient lives with a constant threat of suicide, which can become florid for any reason. In part, self-harm, suicidal behaviors, and self-sabotage are evidence of the enduring personality change that is secondary to catastrophic exposure to trauma (Herman, 1997). Achieving safety requires careful assessment of suicidal risk early on as well as at appropriate intervals throughout therapy. This establishes a norm that suicide can be spoken of clearly and without therapist or therapy being destabilized. Extensive review of this important topic is outside the scope of this chapter but has been covered elsewhere (Bongar, 2002). See also the chapter on assessment of the present work for additional commentary on the assessment of suicidal risk.

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A crucial understanding is that evidence of self-injury is not necessarily evidence of suicidal intent. Self-injury, even when life-threatening, is oftentimes a selfmanagement strategy; a failed attempt to manage upwelling traumatic material; or a behavioral “telling” of a story of injury. It may also be evidence of internal conflict between two or more parts of self. The therapist should carefully and thoroughly explore and address any self-injury but should also determine the purpose of the self-injury, since suicide is only one motive behind self-harm. Some clients do well learning self-harm substitutes that symbolically represent the harm their internal dynamics compel them to do. A few examples include ice held against the skin until it is painful, a rubber band to cause discomfort but not actual bodily harm, or the use of red markers to denote where blood would be if selfharm were conducted. These substitutes enable an aspect of the story to be expressed in a safe way.

Hospitalization

For some patients, however, the utilization of inpatient treatment resources may be unavoidable to secure safety. Unfortunately, most dissociative identity disorder (DID) or dissociative disorder not otherwise specified (DDNOS) patients do not thrive in an inpatient environment unless it is one specifically developed to accommodate the needs of complex trauma patients (see Loewenstein, 2006; ISSTD, 2011 for discussions of the risks and benefits of hospitalization).

External Safety Issues

External threats to the patient can take several forms, including such risks as homelessness, insufficient food, clothing, poverty, lack of needed medical care, and mistreatment due to misdiagnosis, and so forth. Such risks, more benign than those malignantly intended by harmful others, should receive immediate attention through involvement with appropriate government services, agencies, or other services. Whether benign or not in its inception, the statutory requirements of impending legal action may require mobilizing additional professional resources. Recognizing risk, mobilizing a sense of healthy entitlement, asking for service, and tolerating the process may be beyond the patient’s current capacities and may become the purview of therapy, case management services, and other supportive resources. To complicate matters further, the untreated dissociative disorder patient often suffers from what Kluft calls the “sitting duck syndrome” (Kluft, 1990b). Lacking in self-care, prone to identification with the aggressor, and able to dissociate cues to danger, scholarly data confirm the common clinical observation that these survivors suffer from a higher incidence of both domestic and stranger assault. Attempts to manage dysphoria, including the pronounced neurological and psychological sequelae of trauma, predispose the survivor to substance abuse or other addictions, often to the extent that the patient and potentially his or her family is endangered. Of particular concern in cases of DID/DDNOS is the patient’s concern that a perpetrator

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will hurt or kill the patient, the patient’s family, the therapist, or the therapist’s family. It can be difficult to help the patient determine when this is residue from a sense of chronic endangerment and threat based in childhood, or a fact-based contemporary threat. In some cases, a perpetrator may have a contemporaneous and serious investment in preventing the revelation of incriminating secrets. This is true especially when the patient gains understanding of wrongs done and achieves a sense of personal authority, as the perpetrator may sense a risk of prosecution or other legal action. It is especially true when the patient has been the victim of a multiperpetrator group. In some cases, the patient’s pervasive sense that a perpetrator will hurt or kill him or her (or others) may be a memory of threat experienced in years or decades past. Complicating matters further, many complex trauma patients have parts that identify with the perpetrator. These perpetrator introjects may be profoundly disoriented to present time and place, as well as the fact that they are actually a part of the patient, not an aspect of or compatriot of the external perpetrator. It is important for the clinician to manage any countertransference reactions to a patient’s fears but, to some extent, establishing safety in the treatment may require determining whether or not there is a current external threat or if the threat is internally based and actually a partial memory or reenactment of a prior time. If the threat is real and external, then the therapist and patient must identify the realistic degree of risk and set in motion the required but realistic protective steps. Adding to this complexity, early in the treatment protective amnesias and other defenses are in place against fully knowing what has happened. However, the fact that there has been “leakage” of the sense of risk suggests that parts of the self may be able to provide some useful degree of information, provided that other aspects of self and their related affects are appropriately segregated from exposure. If the source of the threat is internal and related to a part based on an introjected perpetrator, there still might be some degree of present risk, for example, a part may commit suicide of the body, or a part loyal to the perpetrator may “murder” another part or parts of the body. The solution to such risk is to work with the perpetrator introject and is an entirely different therapeutic pathway, which will be addressed later in this chapter. Locus of Disturbance—Internal or External

When a chronically traumatized patient enters treatment in crisis or shows signs of crisis and destabilization later, the therapist must still determine the locus of the precipitant or perceived threat to which the patient is responding. Is there a current external circumstance generating—and meriting—the degree of disturbance? If so, is the response conditioned by any internal distortion or trauma-based meaning? Is the threat to stability generated by internal dynamics? That is, when a patient is affectively dysregulated and in crisis, there is a question of what might be considered the “geography” of the distress. Questions of, “Is it happening now? Is it part of a memory? Is it a reenactment telling the patient’s story?” are all germane to the therapist’s assessment process, as are considerations of the patient’s safety from external dangers. Directly asking the chronically traumatized and dissociative patient may not itself produce good results. As a consequence of posttraumatic disconnection

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from their affective “dashboard gauges,” parts of the patient have neither the capacity for internal observation and metareflection nor the ability to notice growing signs of internal distress; nor the ability to determine the genesis of the current elevation in distress. Dissociation as a problem-solving strategy turns out to be a costly remedy once one is removed from the original context of pervasive threat and harm. It works more like an “on and off” breaker switch than a rheostat capable of degrees of modulation. Via dissociation, the patient erases traces of distress by switching to states that are either less impacted by the stimulus or less affectively engaged. As a result, there can be little to no working through, and no adaptive resolution through processing. Instead, there is recurrent resorting to the short-term “first aid” of cutting off or switching away from dysphoric experiences. In addition, parts in a DID/DDNOS patient’s internal system experience each other as “other” and at times “external.” The net effect is that oftentimes the patient cannot observe a growing issue, tolerate dysphoria sufficiently to assess it, or accurately determine the locus of the current disturbance. Accurately or not, this population of patients typically experiences threat as external. Until therapy has made sufficient inroads in this blanket attribution, the task of determining the locus of the disturbance may primarily fall to the therapist. In carrying out the assessment, the clinician should give consideration to the following factors. A dissociative self-system, consisting of a tangle of interpart relations in various configurations, also interfaces externally with various individuals and social entities. These include the therapist, spouse, family, boss, friends, as well as with the community, culture, and society at large. When different levels of interpersonal systems interact, systemic dynamics principles come into play. For our purposes, certain systemic concepts and operating principles are particularly pertinent: particularly homeostasis, the permeability of boundaries, feedback loops, and state shifts. As object relations and ego state therapy models make clear, these dynamics operate within the internal system of states or parts. The systemic field knows no boundary and that these same operations are at work in the interplay between internal states and interpersonal relations. Beyond the system of parts, the web of interaction and potential dysregulation includes organ systems, brain circuits, and biochemical systems. Dysregulation can occur at any of these levels, with each requiring a different type of intervention in the immediate instance and in order to establish a lasting improvement in regulative ability. When the source of dysregulation is external, it is an axiom of clinical work with dissociative patients that the primary “suspects” in a sudden loss of function or decompensation are either related to trouble in the therapeutic alliance or trouble in the context of abuse in external relationships. Other possible loci of disturbance may lie in other key relationships, including marital, familial, or work. It may be school related or involve another health care provider. Determining the locus of disturbance is not, of course, the same as determining the time frame of the disturbance. Essentially, while the immediate locus may be in a patient’s current world of relationships, there remains the important question of whether the matter is a current event or an enactment based on early or dissociated experience and memory. Beyond that, chronically traumatized individuals are not immune to the impact of societal or cultural stressors, whether or not they are evocative of their own early difficulties.

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External Locus—Environmental Threat

Patients who believe themselves to be in danger may in fact be so. Therapists must consider the pervasive effect of identification with the aggressor, poor skill at defending boundaries, impaired self-care, and the consequence of the “Sitting Duck Syndrome” referenced earlier when assessing environmental threat. It is beyond the scope of the present work to elaborate on solutions to actual external threats. However, while many patients are high-functioning, some do suffer from a lack in basic survival resources such as food or shelter, adequate medical care, safety from threats or from actual current abuse/victimization, and insufficient financial resources. Not surprisingly, there are times when internal hazards and problematic self-management strategies interact with external hazards in a way that further jeopardizes the patient’s safety. These internal hazards require appropriate attention, either before or concomitant with addressing external issues. Among the internal hazards that can rise to a critical level are substance abuse, medication misuse, severe eating disorders, self-injury, suicidal and homicidal threats, or noncompliance with lifesaving medical treatment. Whether they originate internally or externally, threats to safety require close attention, often before it is possible to redress the psychological underpinnings of the issue. Helping a patient reregulate and achieve a greater degree of safety from any combination of internal and external threats may require direct work with ego states, even when it is not yet possible to address the deeper psychological and trauma-related issues involving them.

External Locus—Relationship With the Therapist

Particularly in the early portion of treatment, the patient may experience the relationship with the therapist as being overtly threatening or, at least, feel vigilance or uncertainty regarding the unknown risks in the relationship. If the therapist is neither trained nor experienced in treating dissociative patients, the patient’s perception of danger and efforts to defend accordingly may generate reactions in both parties. This can lead even a benevolently intended clinician to precipitate psychologically or even physically harmful circumstances. At the first sign of a therapist working with a more severely symptomatic patient than his or her training and experience prepared them for, ethics and good clinical practice require appropriate action, such as (a) referring the patient to someone who is suitably trained and experienced in treating dissociative patients, while observing clinical standards regarding the communication of the rationale for the transferring of the patient (ISSTD, 2011), or (b) treating the patient in a prudently paced manner while obtaining relevant training and engaging in ongoing consultation from someone who is so trained and experienced. It is important to refrain from disclosing a suspected or confirmed diagnosis of DID or DDNOS until the patient has access to appropriate treatment. The clinician should manage his or her own discomfort without inappropriately “leaking” or disclosing his or her insufficiency to the patient. Conversely, the clinician should avoid defending against the overwhelming impact of a multiproblem dissociative patient with fascination or an overly confident and perhaps even grandiose stance (Dalenberg, 2000).

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Therapists should refrain from any guarantees that they will “never leave” the patient, no matter how strong the pull to provide such a reassurance. If, misguided by a wish to reassure, the therapist makes promises of availability, he or she has inoculated the patient against the natural consequences of bad behavior. Doing so may hamstring the therapist from making appropriate referrals. Such outcomes are not in the interest of therapist or client, though the patient might strongly wish for the guarantee. There are things a client can do that really should evoke a transfer of care, including but not limited to threats to the therapist or the therapist’s family or premises, failure to comply with the terms of the treatment contract, or even a long course of treatment that is not helping the client, no matter whose limitations are the cause. Of course, it’s also entirely possible that a patient may perceive him or herself to be endangered even when working with a well-trained and experienced therapist. The anticipation of harm or exploitation is more intense when reinforced by any history of betrayal, disappointment, or harm in all sorts of relationships, including disruptive experiences with prior health care providers. The most enduring and malignant effects stem from early attachment experiences that determined those templates and relationship expectancies. Recent neurobiological research suggests these expectancies are likely recorded at the secondary processing level of the brain, including the amygdala and other basal ganglia (J. Panksepp, personal communication, April 19, 2009; Panksepp & Biven, 2012). They may also be encoded primarily as implicit memory in the right hemisphere and not accessible to direct recall (Schore, 2003a, 2003b, 2009). Since the patients both directly control and consciously access the basis of malignant relationship expectancies, they are expressed in present interpersonal relationships as reenactments of the original disruptive or traumatic experience. The therapist’s self-knowledge and capacity for containment and gentle inquiries are key to identifying if the patient’s fears are based in current reality and warranted or are fundamental reenactments. The clinician should remember that even though the dynamics come from the patient’s long-ago past, through the mechanisms of projection, identification, and trance, those dynamics can sweep up the clinician and involve him or her in a damaging relational reenactment. The therapist may gently inquire, “Does that fear seem like something that just started here with me? Or, is it an old . . . familiar . . . feeling?” (said with a soft and empathic tone). Generally, after a brief pause and internal exploration, patients will recognize that the matter is indeed old and familiar. If there is sufficient stability, it could be time to invite the patient to explore the history of that feeling. If there is not yet sufficient stability, the therapist may alternatively ask the part of the self carrying that feeling and memory to wait a bit longer, until the preliminary work is done and the system is ready to tell the story safely. Such a request is best made with a compassionate message such as, “I’m sorry, Hurting One, to have to ask you to wait a while longer, as I know you’ve been waiting so long already.” The matter of increasing stability by addressing crises with an internal locus is covered in Chapter 15, Stabilizing the Relationship Among Self-States. Relationship With Others

For patients in acute crisis, one of the early analyses the therapist must make is to determine if the locus of disturbance is coming from the patient’s external

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relationships or from reenactment of early relationship dynamics emanating from internal relationships between parts. If the patient is actually being abused in a current domestic relationship, the intervention is entirely different than if the patient’s expectation of abuse is manifest in present time but emanating from historic material. The present-day mechanism of the latter is often found in the relationship between a perpetrator introject and a child part of self, both of which are internal (also see Chapter 15 with regard to ego state interventions in the stabilization phase). Additionally, the patient’s internal system may project relationship dynamics from disturbed and dangerous childhood contexts onto the therapeutic relationship. The therapist must repeatedly analyze whether, as the patient may suggest, the therapist’s own behavior is in fact contributing to the patient’s problem or whether this represents a skills deficit, a countertransference issue, or some other matter for which the therapist must take responsibility. It is also possible that the patient’s expectation of traumatic relationship enactment is so powerfully projected onto the therapeutic relationship that it is inducing the therapist to behave in uncharacteristic and unproductive ways, that is, projective identification (Klein, 1946). Resource Development

Numerous resourcing strategies are available to increase and enhance the patient’s ego strength, capacity for observing ego, ability to tolerate emotion and somatic sensation, and ability to participate in processing trauma. Resource Development and Installation

Korn and Leeds (1998, 2002) have described a modification of EMDR in which the therapist helps the client strengthen desired attributes by imagining them vividly, in combination with receiving bilateral stimulation in short sets. This procedure is suitable for some but not all dissociative clients. For some DID patients, the procedure draws forward existing resource states and enhances their linkages throughout the system. For other DID patients the bilateral stimulation causes linkages to traumatic neural networks. In these cases, cross-lateral stimulation like the butterfly hug can sometimes be used successfully. At other times, resource development needs to be set aside until the power dynamics of the self system are in support of the resource strengthening.

Somatic Resourcing

Vital contributions to the containment and stabilization phase of treatment are made using somatic or sensorimotor interventions. This actively emerging area in the field of trauma treatment is led by authors including Peter Levine, whose observations of the freeze responses of primates in danger led to his development of the Somatic Experiencing Model (Levine & Gabor, 2010). Similarly, sensorimotor psychotherapy (SP; Ogden, Minton, & Pain, 2006) has contributed a range of practical somatic and

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orientation interventions. For a discussion of the use of SP with dissociative symptoms see Ogden and Fisher in Chapter 19 of this book.

Grounding Methods

There are numerous ways to increase a patient’s capacity to ground him or herself when dissociative symptoms cause confusion, disorientation, risk, or loss of sense of stability or control. Several approaches are identified below: Feet on the Ground

Grounding, or attempting to restore a sense of connection with, or experience of the present moment, is essentially a precursor to any sense of efficacy, and central to establishing identity. Effective approaches to grounding are akin to first aid. They are portable, self-administrable, useful in a crisis, and consistently reliable. One simple method, which can be done both publicly and privately, involves the patient simply becoming aware of the feet on the floor or, better yet, on the ground or earth, in fact or in imagination. This can be accomplished by having the patient’s attention turned toward the feet and wiggling the toes or, most powerfully, by pushing the heels into the floor while seated. The latter tends to wake up or gently evoke the patient’s felt sense of power, and may mildly activate the sympathetic nervous system. There are a few patients who can’t use this one, because ANY sense of empowerment will evoke a sense of risk and danger, either as a violation of the accommodation to the all-powerful adults of childhood, or as if allergic to all potential to be powerful or effective, even one’s own. Alternatively, the patient can become aware of his or her tailbone pressed against the seat of the chair, or of the texture of the patient’s chair’s surface or covering, and so forth. Mother Earth

Some patients will find comfort in turning their attention, in imagination, to the awareness that beneath the carpet, beneath the flooring and the floors of the building, beneath the cement foundation of the building, is the earth. In Native American understanding, the earth is our mother, our grandmother, and she is reliably there for us. This mother does not betray. The Lakota term, Unci Maka (grandmother) or Nama Ka (mother), may help the patient reframe the notion of a trustworthy mother from an entirely different point of view, free from any implications of family of origin troubles with a mother. Golden Chord

Although much grounding of dissociative patients involves greater experience of an attachment to real external phenomenon, imagination may also play a role, for example, by imagining a golden chord of healing energy that comes from

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the heavens running through the patient and on to the very core of the earth. To facilitate this, a patient is invited to become aware of a golden chord or ribbon of healing energy originating in the heavens (if this is a safe notion) but comes to earth flowing through the top of the head (or crown chakra), progressing down through each of the body’s energy centers (brow or third eye chakra, throat, heart, solar plexus, sex chakra, root chakra [at base of spine and pelvis]), down through the legs, and through the soles of the feet, then continuing down into the earth, and on to the very center of the earth. The patient might also envision energy running up and down the chord at just the right pace for perceiving and experiencing the energy’s movement through each chakra. The exercise may be modified if awareness of any particular chakra is disturbing to attenuate the intensity of response.

Counting Red Things, Counting Blue Things

One very simple grounding experience, which is suitable for everyone, including children, is the response to the request to look around the room and find five red things and then five blue things. Typically, the patient moves rapidly from feeling lost, disoriented, “spacey,” or anxious, to discussing whether a certain book cover on the office shelf is vermillion or truly red. Even without being encouraged to do so, many patients carry the “red things, blue things” question as a portable method for reentering awareness of the current here and now. Finding the colored items returns the patient’s focus to their perceptual senses and, thereby, to an unthreatening embodied experience of his or her current context and existence (Boon et al., 2011). Seattle Special

Working in the Seattle area, we recommend that clients ground themselves by stepping outside to feel rain on the face. This method can be modified for one’s climate conditions, whether snow, warm sunshine, or wind prevails.

Animal Grounding

The presence of an animal is enormously grounding for many patients, often more so than that of a person. When people have been a source of betrayal and danger, wild or domesticated animals are often a treasured source of comfort, relatedness, and grounding. Yet, few patients use the pet’s name as a cue to evoke the same felt sense of comfort that the patient feels in the actual presence of their pet. Practicing evoking the sense of comfort and connection that the animal provides can be a particularly helpful grounding method, both sensorily reorienting and affectively regulating the client. The first author works with a therapy dog, a charming 7-pound poodle. The dog’s effect on patients, even when they are acutely disoriented, is unsurpassed and almost inevitably grounding. In a session with a DID patient who was (erroneously)

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convinced that there were snakes around her ankles (part of a traumatic memory from years past), the therapist made repeated efforts in vain to orient the patient by referring to objects in the room, naming the present year and location, and noting the therapist’s own presence, all to no avail. At some point, the therapist said, “It’s just you, me, and the poodle.” The patient grew quiet, looked at the sleeping poodle in the chair beside her, touched the dog gently, and said, “It must be now, because [the poodle] isn’t old enough to have been there back then,” and remained grounded for the rest of the session. Salt, Fragrances, Herbs

The second author finds that salt on the patient’s tongue is, for many patients, immediately and powerfully grounding. This is a short-term crisis intervention that should be avoided by patients for whom any use of salt is contraindicated. For other patients, having a sachet of salt from fast food restaurants can provide rapid first aid when a patient feels destabilized, or ungrounded. Patients for whom the technique works report that a lick of salt pulls them into present time very rapidly. The first author uses essential oils or herbs for this purpose. The therapist can keep essential oil of lavender, cedar, and so forth, at hand in the office or a patient can easily keep a small vial in his or her purse, car, or home. Traditional Native American medicines— cedar, sweetgrass, sage, or tobacco can be crushed in hand and smelled, thereby serving a similar reorientation function and can be beneficially combined with a prayer or with gratitude. For some patients, the use of Native American healing herbs can also evoke a powerful and spiritual reframing of the moment. In the latter perspective, the moment is transformed from one in which the patient is confused, helpless, and disconnected, to one in which the patient has the power to evoke the highest forces of healing. The knowledge that one has an armamentarium of effective tools may, in itself, be a stabilizing antidote to a historic fear of one’s internal material, known and unknown. Any use of Native healing and spirituality should be mindful and respectful of the People whose sacred path is being employed and treated with honor. The Native path is mentioned here because it is spiritual but without the encumbrances of dogma, church hierarchy, and so forth that are associated with spiritual trauma for many people. If not suitable to use Native spirituality, or if the therapist is uninformed in its correct usage, simply appealing to the wonder of nature may suffice. This is not an exhaustive list of approaches to grounding and, of course, some will be effective for one patient and may conversely fail or, worse yet, inflame another. Each therapist/patient team will go through a trial-and-error process that will ensure they have a toolkit of effective approaches. During this process, the therapist should avoid prematurely assuring the success of one approach over another, but should instead share in a curiosity to find what else might help. Besides being notorious for paradoxical or unanticipated responses to substances and medications, like all patients, this population may have dynamic reasons for resisting effective crisis intervention or stabilization. In such a case, further exploration of the interpersonal, historic, and intrapersonal meanings involved is indicated.

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PSYCHOEDUCATION

Therapy will often need to help establish resources for traumatized patients through basic psychoeducation, an essential feature of preparation for poststabilization trauma reduction work. We work in an era when both professional literature and effective psychoeducational materials for patients are proliferating. Some address both clinician and patient, among which is the manual by Boon et al. (2011), a comprehensive and accessible guide to skills development and psychoeducation for dissociative patients, and Peter Levine’s manual (Levine, 1997) and CD, setting forth his somatic model and a self-administered program of posttraumatic repair, as well as an array of other somatic, energy psychology, cognitive interventions (Ross, 1997), dialectical behavior therapy (DBT; Linehan, 1993), and other patient-accessible models and manuals for psychoeducation and enhanced self-management. The first author has also written an illustrated guide for therapists and patients that enables discussion of basic concepts of dissociation and treatment phases (Paulsen, 2009). Because it uses cartoons to telegraph ideas, even child parts that cannot read will benefit from its perusal. This section reviews a selection of models, concepts, and related skills patients benefit from understanding as they move through this phase of treatment and build their capacity to enter the trauma reduction phase of therapy. Patients receive education through beneficial experiences orchestrated within therapy or by homework provided by the therapist. Experiential education is, in some cases, made more conscious through the psychoeducational frame provided by the therapist in discussion with his or her patient. We recognize that individual patients have distinct needs, prior knowledge, individual treatment histories and trajectories, varied life experiences, and a range of capacities upon which to build a foundation of explicit learning. While clinicians have no need to turn patients into intellectual colleagues, those patients who develop an understanding of the workings of the trauma response and dissociation’s effects, among other things, have a far more solid perspective to rely upon as they are increasingly able to be both “in” and “meta” to their process.

Education About Emotions

Many patients learned early that emotions were bad, difficult to regulate, often unendurable, and even dangerous. While observing that others are permitted to have needs and express emotions, patients learned to avoid, dissociate, or generally cut off awareness of their own feelings and needs—lest they be shamed or endangered. The act of protecting one’s self against disappointment in the world’s failure to accommodate the child’s self and needs is also a strong survival motivation. Preserving the hope of becoming visible, being known and even cherished, is crucial for survival, even if it is preserved through deeply held distortion—including bearing shame for the misdeeds of others. In adaptation to their emotionally impoverished homes or other early traumatic exposure, children learn to cut off their emotional experience, avoid all recognition of that buried material, and rarely go back to process those cutoff experiences, at least until they arrive in our offices. To better tolerate emotion,

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however, patients need to learn accurate information about the function of emotions. Had they had sufficient attuned parental provision, they would have experienced their emotions and found them mirrored in their parents’ faces. They would have regulated and made use of those emotions with help: soothing, noticing, naming the feelings, and assisting their child through the wavelike action of emotion as it came and went. If they were angry, the parent (usually mother) would warmly observe, “You’re really, really mad!” and held the angry child, thereby teaching containment, and legitimizing emotional expression. She would have taught suitable remedies, and ensured reunion and repair after ruptures in their relationship. When she was frustrated and overwhelmed herself, she would have maintained responsibility for her own behavior. She would apologize to the child if she erred, honoring the child’s humanity, sensing and taking the child’s needs and feelings into account. This attuned and engaged mother would have had empathy and, in turn, the child would have learned empathy. In that shared intersubjective experience (Siegel, 2012), baby would learn about self and other, about relationship and trust, about shared understandings, about cherishing and love, and about esteem, much wordlessly. This is not what occurred in those disturbed families in which DID patients learned their early lessons. So, years later, it is in therapy where these lessons are taught and repairs are made, through psychoeducation, and in the relationship as it proceeds, and as baby’s story is heard, released, and repaired, as described in Chapter 20: Temporal Integration of Early Trauma and Neglect.

Education About Innate Animal Nervous System Responses

Many dissociative patients have lived lives punctuated with eruptions of unresolved sympathetic arousal whose expression was thwarted during the original trauma. Regardless of what they have endured, these patients feel shamed by their helplessness as they the face the storm of posttraumatic effects that buffets them. They often castigate themselves for not “just” doing what they need to do in life, for not surmounting their difficulties, and for not “being normal.” When they learn about the polyvagal nervous system as “safety systems” (O’Shea, 2009), about the brain’s hardwired affective circuits (Panksepp, 1998), and of the neurobiological and physiological facts that normalize their own body’s behavior, it helps them observe themselves less pejoratively. Patients benefit from understanding that fight, flight, freeze, and connection are responses arising from basic safety systems, all with which, as part of our animal inheritance, we are all born as part. Therapy animals can serve as benign models demonstrating relevant key concepts. Patients need to learn that sympathetic arousal prepares us for fight or flight, and is an adrenaline response. If the full expression of that urgent response is thwarted when it wasn’t possible to fight or flee, then that arousal remains trapped in the body, often contained and hidden, in another part or ego state. As the nature of those ongoing responses is better understood, the patient can join the therapist in an appreciation of the origin and helpful function of the part holding the fight and/or flight responses. Porges’s (2011) definition of the polyvagal nervous system includes not only the familiar sympathetic nervous system of

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fight-or-flight response, but also the newly identified second parasympathetic nervous system, the ventral vagal parasympathetic system. Of the two parasympathetic nervous systems, it is the dorsal vagal or freeze response with which patients are more familiar. The shame of having frozen, or of having seemed to acquiesce or lose track, is eroded by understanding how the opioid response engendered by the parasympathetic response leads to the experience of shutting down, and even resigning to death—nature’s response when no other response has succeeded. Porges’s newly found other parasympathetic nervous system, the ventral vagal system, is for social engagement and connection. In the first author’s opinion, this connection goes beyond social connection to include connection with self, community, and world as well as with one’s intuition, spirituality, and experience of the divine. Patients benefit greatly from understanding that these responses are inevitable, automatic, and basic animal survival responses and that small children are meant to feel socially engaged, that is, safe and connected. They know, viscerally and deeply, if they experienced that connection or if they were in effect “alone in a world with no people.”

Education About Affective Circuits

Jaak Panksepp (Panksepp, 1998) established the neurobiological evidence for the existence of seven basic subcortical affective circuits present in the brain from birth, which require no learning. Panksepp (1998; J. Panksepp, personal communication, 2009) describes three levels of brain processing systems. Panksepp’s primary processing is the level of the hardwired subcortical affective circuits present from birth. The secondary brain processing level is the object relations or relationship templates level, where attachment experiences are processed via the amygdalae and other basal ganglia. His tertiary brain processing level is that of neocortical learning, where verbal mediation, mindfulness, and other subsequent affective learning is held. The basic emotions described from animal research are also at the foundation of human experience. Panksepp capitalizes the seven basic emotions to show that they are hardwired circuits, not learned or acquired emotions. These include SEEKing, described by Panksepp as “the mother of all circuits” and the basis for curiosity, pursuit, foraging, investigation, initiation, and so forth. RAGE is the system engaged in the fight response; FEAR is engaged in the flight response; LUST is the reproductive tendency, not activated in childhood unless prematurely initiated by molestation; PLAY is an easily overlooked but very important circuit, not only enabling rehearsal of fightor-flight behaviors but also a pathway to socialization and connection experiences; CARE is the primary maternal circuit and is present but weaker in males. It is the also the substrate of all loving and affectionate emotions. PANIC (not panic attack but infant separation distress) is signaled by what the Germans call “bundscriek,” or the attachment cry. The infant’s PANIC response is intended to trigger the mother’s CARE circuit, causing her to respond to the infant’s needs. The therapist can teach patients that these circuits are innate, not reflective of character, that they are there for a good reason, and that people need them like we need dashboard indicators on a car. This car metaphor can help the patient come

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to accept these emotional responses in their lives. Therapists can talk about “check engine” lights that go on and stay on even when there is no overheating; they can talk about people who clip their wires so they don’t have to look at the flashing red lights on their dashboard, as if that alone will keep the engine from overheating. Car alarms can be too sensitive, people can become inured to the sound of alarms, and some cars have no alarms at all. The therapist can wish aloud that the patient has an alarm that goes off when there is danger, and only when there is actual danger in present time. Our patients then begin to feel entitled to have and experience their emotions, sometimes for the first time in their lives. The increased noticing develops an observing or mindful stance, to be addressed subsequently. The shift to that stance is another key element in stabilization and growth. Panksepp’s rats don’t have a SHAME circuit, and researchers can’t conduct this same kind of research on humans. Therefore, there is no experimental proof that humans have a hardwired shame circuit, though the authors strongly suspect its presence in humans. Even without that proof, however, patients benefit from frequent reminders that shame is a normal human response to a rupture in a caretaking relationship. When a child is scolded in a way that says that he is defective for having a longing or an emotion, he experiences shame. He feels the rupture of connection, the turning away of the other and aloneness. In the context of an otherwise loving caretaking relationship, the experience of criticism may be corrective. No child wants to garner disapproval or experience the discomfort of shame, so he or she seeks to learn to comply with the caretaker’s requirements no matter how brutal or developmentally inappropriate. Through this effort and the caregiver’s approval, their relationship is restored to loving relief. In a malignant relationship, the caretaker’s requirements are unreasonable, arrive without prior teaching, or are narcissistic in origin, and are therefore not in service of the child. In a relationship where a child’s survival depends on experiences of attunement and deep connection, they signify misattunement between caregiver and child. In these cases, the caregiver takes no action to repair the rupture and the child may be unable to understand this. The child’s resulting sense of shame is not resolved in joyful reunion and compassionate empathic acceptance, and the pain may be too much for the child to tolerate. When experienced repeatedly, and in the absence of restorative experience, shame becomes a familiar state for the child. With that backdrop, in hopes of gaining approval, the child is motivated to hide the secret of his perceived defectiveness from the self and others, and may develop an elaborated ego state, an apparently normal aspect of self (also called apparently normal personality [ANP]); see for example van der Hart, Nijenhuis, & Steele, 2006). With the ANP functioning as a kind of wall, the child effectively hides the shameful emotional self from himself, and may develop amnesia for the painful, inescapable, and unrepaired shame and its traumatic origin. When a patient understands the genesis of his or her shame, he needs to comprehend the need for the compassion of an adult caretaker to repair the adverse residue from that early experience. The patient can begin to see that, in the absence of a loving caretaker, as a child there was no alternative but to believe the caretaker’s unfair view of him or her, and dissociate the resulting unbearable pain of feeling defective and unlovable. It is helpful to invite the patient to hold his or her own story at arm’s length, instead having the patient and therapist together observe an unknown other child in a vignette with the same family dynamics. This

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can elicit insight and compassion where parts of the patient previously knew only self-hate or shame. In cases where such a shift does not occur, the clinician should be alert to the likely presence of an undetected or unreformed perpetrator introject. Survival-based, enduring loyalty to the aggressor takes precedence over the child’s attachment to self until the introject attachment is resolved in favor of the patient.

Education About Mindfulness

While a full discussion of mindfulness is outside the scope of this chapter, many patients do benefit from learning mindfulness-based meditation (Siegel, 2012); the value of a neutral, nonreactive capacity to observe oneself has been recognized in a range of models, including ego psychology and traditional Buddhist practice. It has been extensively taught in present years as a means of affect regulation (Siegel, 2012) and is a centerpiece of Linehan’s self-management model, dialectical behavioral therapy (Linehan, 1993). Dissociative patients may have a part of self that is, in some way wiser, more observant, and more remote from activation. Depending on the configuration of the internal system, that part may be known as a watcher, librarian, Dr. Spock figure, or any form of dispassionate witness already experienced in observing, and who may be enlisted to assist with the development of mindful stance. Other dissociative patients may not have such part, but learning the skill may be within reach of an existing part, coalition of parts, or a new behavioral stance to be fulfilled by various parts, as needed. The basis of the stance is that anything that comes into the mind’s eye will also pass out of it on its own; that emotions and all experience are transitory and can be watched, just as a wave washing in can be counted on to wash out. For some, learning that emotions come naturally and are required to manage oneself can liberate them from having to take drastic evasive action, acting out, repairing, fleeing, or outcry. A mindful poise during nondangerous distress can involve a process of simply watching whatever seems intolerable, noticing how intolerable it seems, and how curious it is for something to seem so intolerable. Achieving this perspective represents a breakthrough and a skill that with sufficient practice, can lead to greater stability.

Education Regarding Emotional Hygiene

As patients learn about dorsal vagal shutdown, chronic yielding to helplessness as natural responses and survival strategies, they begin to understand dissociation as a phenomenon instead of just something mysterious that seizes control of them. Paradoxically, dissociative patients both fault themselves for these responses and experience themselves as helpless to control or eliminate them. In addition to understanding the process of dissociation, they need to recognize the accumulated consequences of a lifetime of poor emotional “hygiene.” If, day after day, someone throws garbage over a wall and out of sight, the discards pile up on the other side of the wall. Despite being unseen, it still exists. Similarly, the unprocessed detritus of traumatic

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experience is often contained and managed by other aspects of self. Both the accumulation and habit of throwing things over the wall will have to be dealt with. The therapist acknowledges to the patient that it is not fair that so much of that garbage was either caused by someone else, or displaced and dumped on their land by someone else. It remains to be dealt with or the patient will forever live downwind of garbage and never be able to reclaim his or her own precious land on the other side of that wall. Moreover, some of the parts have the thankless job of holding some of the most intolerable material, the perpetrator energy, and point of view. We teach them about how all the parts of the self are in the same body, including the parts that experience and regard as “not me,” “not us,” or external to themselves. As they learn the basics of the dissociative response to chronic maltreatment, they learn that all of this is normal, that we understand it, and that they can too. As this comes to make sense, motivation for treatment often increases, particularly as identification with the abuser erodes and powerful perpetrator introjects come to identify with the life on this side of the wall.

Education About Legal Definitions of Child Abuse

For their entire lives, many dissociative patients were told that the painful things that happened to them were their own fault. Profound neglect, physical abuse, and even child rape may seem to the child to be their “just deserts” and appropriate in light of their alleged misbehavior or defects. While the clinician should register a clear stance about the innocence of child abuse victims, engaging in a debate with a patient about whether it was his or her fault that at the age of 2, or 4, or 10 they were raped/beaten/ neglected is a doomed strategy. Reading the present state laws regarding child abuse can dramatically change a patient’s perception of his or her caretakers as criminals hiding their behaviors from public and police scrutiny, once he or she sees that the law clearly defines what was done to them in childhood as a crime. Brochures from child protection and educational foundations, teaching children how to recognize when to “tell” and when to say “no” can serve a similar function and contribute to the teaching of what responsible caretaking involves. A realistic framework grounded in broad social and legal norms, rather than the distortion of the selfish meaning provided by inadequate or abusive care providers, recontextualizes the patient’s history, motivates curiosity, and helps to make meaning. Reframing the patient’s experience is one important function of psychoeducation.

Education About Child Development

Periodic discussions of normal child development and milestones can be of great benefit to patients. Consider the case of one adult patient who, at 3 years old, was given the responsibility of caring for her 2-year-old brother who was subsequently injured in an accident, losing a foot. The patient had always felt responsible for her brother’s injury, as internal voices, which were the introjection of her parents’ blaming and critical voices, frequently told her that if she weren’t so lazy and selfish, her

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brother would still have both of his feet. In this case example, the patient was rigidly committed to self-blame, repeatedly enacting self-punishment for her “shameful” failure to protect her baby brother. As she learned the basic milestones of child development, it became clear to the patient for the first time that she had not been sufficiently developed or mature to be capable of what had been expected of her— and that no child her age would ever have been. Understanding that adults are 100% responsible for keeping young children safe, and that this includes not only her brother, but herself, helped this patient put the responsibility in its proper place for the first time in her life. A device often beneficial in facilitating this understanding that a young child is too young to be in terrible situations is to encourage the patient to view the scene from an observing stance, in the third person, rather than a subjective stance of himor herself as a child. This can be accomplished through such inquiries as, “What would I see if I were watching with my binoculars?” “What would we see if we were walking down the street and chanced upon this scene of a little girl that we don’t know, about that age in this same situation?” “You know how Ebenezer Scrooge was visited by the ghosts of Christmas past, present, and future, which allowed him to observe these scenes, undetected? If you and I were to be spirits visiting that scene with your brother, what would we see?” If the patient says, “Well if it were someone else it would be understandable, but it wasn’t someone else, it was me, so it was my fault,” we might ask him or her to nonetheless imagine a child he or she did not know being in that scene anyway, and ask him or her how it seems, and what he or she feels, observing a child in that situation. Very often he or she can feel compassion and understanding for that other child’s plight, which can ease over into his or her view of the young version of him- or herself in that situation.

Education About Adult Versus Child Responsibilities

It is always the adult’s responsibility to keep a child safe, to meet the child’s physical and emotional needs, and to provide an emotional environment where learning, growing, and the fulfillment of a child’s individual potential can occur. It is not enough for caregivers to merely provide a child with space, basic clothing, and food. A child must experience a loving caretaker to have normal neurobiological development. The child’s very self-image, a cohesive self, a capacity for trust in relationship, for normal capacity for empathy and compassion, all emerge as a consequence of experiencing empathic attunement between a caretaker and him- or herself. If the caretaker cannot provide that safe and loving relationship in the child’s earliest formative years, or cannot tolerate attunement in certain aspects of the experience of self and other, many of the earliest milestones of development are not met and, as Liotti asserts, the potential for a chronic dissociative response to later disturbance increases (Liotti, Pasquini, & The Italian Group for the Study of Dissociation, 2000). Without the solid foundation of those early attachment milestones, subsequent developmental milestones, if they are reached, are laid on shaky ground. This knowledge helps in the understanding of how children with disturbed attachment histories, and trauma and neglect from infancy, often arrive at school age having trouble with attention and

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concentration, disturbed relationships, social anxiety, and difficulty with emotional regulation. Progress in the understanding of neurobiology, infant development, and the growing child’s response to chronic unresolved disruption and trauma aid in the recognition of the range of sequelae that the betrayed and isolated infant or toddler suffers in years following. Such a child has learned that there is no safety, no caring response from adults, and no anticipation of his or her needs. The child learns that he or she is essentially in a relationally empty or unreal world. Education About Spirituality

For many patients, though their relationships with people were impoverished from the beginning, their connection to the spiritual can be elaborate, long-standing, and an important source of comfort and connection. It is essential to bolster and access patient resources and, specifically, to activate their ventral vagal nervous system (Porges, 2011) as a means of stabilization and regulation; spirituality is not only a pathway to that end, it can be “top of the line,” the highest energy ventral vagal experience. Not only should the therapist not interfere with that resource if it exists in the patient’s armamentarium, but also, to the degree appropriate, the therapist patient should at a minimum accommodate constructive spiritual practice or belief. There is one exception: for some patients, the urge to die has been long-standing, as have derealization and depersonalization; in response to overwhelming here-andnow experience, they learned early on to disconnect from their body and the tawdry nature of the earthly plane. As a result, life in a spiritual plane, like death, promises to protect them from ever being in present time, present body, or present reality. Spiritual pursuits can become in essence another form of dissociation, a one-way path rather than a resource for current life. Where appropriate and welcome, the first author responds to that by saying, ever so gently, consistent with her own spiritual beliefs, “I think our Creator wants us to be in this plane, as long as we are on the earth and in these bodies. We’re supposed to BE here.” It can be useful to explore the self-system to identify any parts that are experienced as living in other realms, being themselves angels or other nonmortal entities, or who dwell in other planes. Eliciting their cosmology and assisting in distinguishing between abuser rationales, posttraumatic cognitive distortions, and aspects of spiritual experience and assistance requires patient skill and a deep open-mindedness from the clinician. The second author responds to patient queries about whether their beliefs are true or not by saying that it’s not an area of her professional expertise, and so, like her patient, she is a seeker rather than an authority. It can be helpful, however, for therapists to confirm that others have described similar spiritual experiences, reflecting on the clinician’s knowledge or in the literature of various spiritual practices.

Education About Neurobiology in Patient-Appropriate Language

Most of the preceding psychoeducational material can be punctuated with scientific material emerging from the field of neurobiology. For many patients, the language of neurobiology may enrich the patient’s ability to comprehend and even anticipate his

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or her experience and act as the basis for the work remaining to be done in therapy. For other patients, metaphor or simpler language may be more appropriate to help normalize what brain science has to say about their symptoms and situation. Because simpler-talking child parts of self are listening, and because the right hemisphere is the locus of emotionality, trauma in implicit memory, and relationship templates, the use of simpler and vivid (metaphoric) language is needed to make the concepts deeply comprehensible and accepted on the level of the embodied felt sense. Therefore, even if a patient has the capacity for the most sophisticated of neurobiological data, adding in sufficient plainer talk will in essence drive the point home, where the patient lives, to the emotional right hemisphere of the brain. The following example shows a communication intended to address the right hemisphere’s emotional, relational, and metaphoric sense: Science tells us the facts, but pictures tell us the stories. To the little ones who are listening, whose hearts have been broken, we want to hear your story. We know you didn’t feel safe enough to grow and heal, and it was hard. It was really, really hard. Can we just sit with that and notice and honor what is in the body? And if you take a look inside, there may be a picture that tells us what we need to understand. Or maybe not, and that’s okay too. Can you tell us what you see?

Education Regarding the Window of Tolerance

Patients benefit from understanding another key principle emerging from the neurobiological findings of recent years, the phenomenon referred to as the “window of tolerance” (Siegel, 2012). Window of tolerance refers to the range of arousal within which effective psychotherapy in general, and trauma resolution interventions in particular, including EMDR, can be successful. More specifically, at unduly high levels of arousal, the patient becomes flooded, hyperaroused, and overwhelmed. There may be an inability to maintain dual-attention awareness (Shapiro, 1995, 2001), defined as one foot in the present moment and one foot in the memory, which is essential in order for trauma treatment occur in the present. Alternatively, if the level of arousal is too low, the patient is likely to be shut down, psychically numb, or dissociated. In fact, if a patient first becomes flooded, he or she is likely to respond by shutting down, and subsequently move into the collapsed frozen-dissociated state of underarousal. In this regard, containment and stabilization techniques have as their aim the task of as much as possible keeping arousal in the optimal midrange, so that healing can occur. Much as having an attuned and responsive parent helps the child regulate, being in a secure therapeutic relationship is an important anchor helping keep the patient in that optimal window of arousal, where dual-attention awareness is possible. Hyperarousal is consistent with sympathetic activation and hypoarousal with parasympathetic dorsal vagal shutdown. The optimal midrange, however, is associated with activation of the parasympathetic ventral vagal nervous system. If the patient is connected with the therapist, his or her body, the self, the present moment, and in the midrange of arousal, then healing, growth, learning, and processing of traumatic experience to an adaptive resolution is possible.

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SELF-CARE

Clients benefit enormously by establishing simple healthy habits, perhaps for the first time in their lives. These basic self-care practices benefit both on a physical body dimension as well as psychological dimension.

Exercise

Appropriate exercise, engaged in moderation, can be stabilizing and generally beneficial through its direct effects on bodily metabolism and by bringing awareness to bodily states and personal capacities for effective movement, as well as by bringing the body into a greater degree of organization and synchrony (Siegel, 2012).

Nutrition

While an in-depth discussion is beyond the scope of this chapter, it is important to note that there are numerous nutritional issues and imbalances that impact what appear to be psychological symptoms. Coordination with appropriate professionals helps identify and manage issues including food allergies, vitamin deficiencies, irritable bowel syndrome, excessive sugar intake with spikes in blood sugar levels, caffeine intake, thyroid imbalance, and interaction between diet and premenstrual syndrome, among others. Neglect and intentional maltreatment in childhood, as well as the lack of awareness of body sensation, can often leave even intelligent patients ill-informed in the appropriate care of their bodies, and reluctant to seek help, even when they recognize physical issues.

Sleep

Many patients with PTSD have long-standing sleep disturbances, often related to the difficulty of feeling safe, when their sense is that danger is imminent. Sleep hygiene practices may assist with some of these disturbances of sleep onset, latency, or duration. Strategies such as going to bed and waking up at a regular time, no matter how many hours they are awake in the middle, may begin to structure and regulate sleep. For many patients, insomnia occurs at the hour that one was habitually victimized as a nightly reenactment phenomenon. Some patients benefit from external safety measures such as pots and pans stacked at the door, tied together and to the doorknob. The patient may sleep assured that if an intruder attempted entry, the racket would wake him or her up. Some patients sleep sitting up in a chair or in front of the television. General sleep hygiene practices recommend people forego such measures, turn off the TV, and sleep reclining. If one awakens in the night, there should be a time of effortless stillness. If in 30 minutes the patient has not

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returned to sleep, he or she could get up, read the phone book, engage in a mindless activity for 30 minutes, and then return to reclining position to attempt sleep. This might continue several times during the night, but in any case, the patient awakens on the usual schedule. The day may be exhausting, but by night time, regular sleep structure may emerge more readily. Finally, the patient should not nap during the day. Similarly, the bed should not be used for any activity other than sleep (or sexual behavior, if indicated). The patient should not watch TV in bed, spend the day in bed, or do any other activity that would be horizontal in nature. This avoids the body being confused about what horizontal means. The horizontal position should be reliably associated with the sleeping state.

Assertion

Any time a patient becomes dysregulated, destabilized, or is in crisis because of impingement by something or someone in his or her present environment, a brief foray into assertiveness training may be indicated. Understanding and acting upon the notion that every person, including the patient, possesses an innate right to set limits and maintain boundaries is life changing. For most patients with an early history of caregiver betrayal, violation, or failure to protect, the idea of owning one’s self and having boundaries to assert has been unthinkable, and now, the notion of enacting boundaries will most likely evoke profound inner conflict and apprehension. Some patients find this easier upon receiving timely and succinct psychoeducational exposure to the existence of their right to assert themselves the defense of their boundaries, can facilitate ongoing beneficial steps toward improved health and personal autonomy. Similarly, in around 5 minutes a therapist can impart the essentials of the “broken record” technique, which simply requires the ability to quietly repeat one’s position one more time than the intrusive other repeats their own position. There’s no arguing, no defending of one’s right, but just a persistent, calm reiteration of one’s stance. It’s not only effective, but can erode the patient’s early experience that asserting one’s view involves loud voices, physical aggression, and other frightening conduct.

Other Life Enhancing Skills

Depending on the therapist’s clinical orientation, the setting of treatment (individual, group, substance abuse, etc.), and the demands of the patient’s current situation, skills training may not be undertaken early in treatment. The establishment of structure, work on the therapeutic alliance, evaluation, and normalization of symptoms need early priority. However, formal skills training may be needed in order to stabilize the patient. Skills that may be taught under these circumstances, or later as the work progresses, include the following and are discussed in terms of its potential contribution to stabilization.

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Other Skills

Other skills that are very beneficial for some patients include yoga, which enables greater connection to somatic experience as well as providing exercise (Levine, 1997), and the emotional freedom technique (EFT), which is useful to help patients to quickly release pent-up discomfort through systematic tapping on energetic meridians (Craig, 2011).

SUMMARY

We have described some of the basic elements to address stabilization in the early phases of therapy with a complex trauma patient. Every bit as important in enhancing stability of the patient is preliminary ego state work, which is described in the next chapter. Only once the patient is sufficiently stabilized; the therapeutic relationship is sufficiently strong; and the patient has the internal skills, resources, and understandings to embark can trauma work be underway.

REFERENCES Bongar, B. (2002). The suicidal patient: Clinical and legal standards of care (2nd ed.). Washington, DC: American Psychological Association. Boon, S., Steele, K., & van der Hart, O. (2011). Coping with trauma-related dissociation: Skills training for patients and therapists. New York, NY: W. W. Norton. Craig, G. (2011). The EFT manual (2nd ed.). Fulton, CA: Energy Psychology Press. Dalenberg, C. (2000). Countertransference in the treatment of trauma. Washington, DC: American Psychological Association. Herman, J. (1997). Trauma and recovery: The aftermath of violence - from domestic abuse to political terror. New York, NY: Basic Books. International Society for the Study of Trauma and Dissociation (ISSTD). (2011). Guidelines for treating dissociative identity disorder in adults, third revision. Journal of Trauma & Dissociation, 12, 115–187. Klein, M. (1946). Notes on some schizoid mechanisms. The International Journal of Psychoanalysis, 27, 99–110. Kluft, R. P. (1990). Incest and subsequent revictirnization: The case of therapist-patient sexual exploitation, with a description of the sitting duck syndrome. In R. Kluft (Ed.), Incest related syndromes of adult psychopathology (pp. 263–283). Washington, DC: American Psychiatric Publishing. Kluft, R. P. (1991). The initial stages of psychotherapy in the treatment of multiple personality disorder patients. Dissociation, 6(2/3), 145–161. Kluft, R. P. (1993). Basic principles in conducting the psychotherapy of multiple personality disorder. In R. P. Kluft & C. G. Fine (Eds.), Clinical perspectives on multiple personality disorder (p. 19). Washington, DC: American Psychiatric Press. Korn, D. L., & Leeds, A. M. (1998). Clinical Applications of EMDR in the treatment of adult survivors of childhood abuse and neglect. Workshop at EMDR International Association, Baltimore, MD.

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Korn, D. L., & Leeds, A. M. (2002). Preliminary evidence of efficacy for EMDR resource development and installation in the stabilization phase of treatment of complex posttraumatic stress disorder. Journal of Clinical Psychology, 58, 1465–1487. Levine, P. A. (1997). Waking the tiger: Healing trauma. Berkeley, CA: North Atlantic Books. Levine, P. A., & Gabor, M. (2010). In an unspoken voice: How the body releases trauma and restores goodness. Berkeley, CA: North Atlantic Books. Linehan, M. M. (1993). Cognitive-behavioral treatment of borderline personality disorder. New York, NY: Guilford. Liotti, G., Pasquini, P., & The Italian Group for the Study of Dissociation. (2000). Predictive factors for borderline personality disorder: Patients’ early traumatic experiences and losses suffered by the attachment figure. Acta Psychiatrica Scandinavica, 102, 282–289. Loewenstein, R. J. (2006). DID 101: A hands-on clinical guide to the stabilization phase of dissociative identity disorder treatment. In R. A. Chafetz (Ed.), Dissociative disorders: An expanding window into the psychobiology of the mind (Vol. 29, pp. 305–332). Philadelphia, PA: Saunders. Ogden, P., & Minton, K. (2000). Sensorimotor psychotherapy: One method for processing trauma. Traumatology, 6(3), 149–173. Ogden, P., Minton, K., & Pain, C. (2006). Trauma and the body: A sensorimotor approach to psychotherapy. New York, NY: W. W. Norton. O’Shea, K. (2009). EMDR friendly preparation methods for adults and children. In R. Shapiro (Ed.), EMDR solutions II: for depression, eating disorders, performance, and more (pp. 289– 312). New York, NY: W. W. Norton. Panksepp, J. (1998). Affective neuroscience: The foundations of human and animal emotions. New York, NY: Oxford University Press. Panksepp, J., & Biven, L. (2012). The archaeology of mind: Neuroevolutionary origins of human emotions. New York, NY: W. W. Norton. Paulsen, S. L. (2009). Looking through the eyes of trauma and dissociation: An illustrated guide for EMDR clinicians and clients. Charleston, NC: Booksurge. Paulsen, S. L., & Golston, J. (2005, September). Taning the storm: 43 secrets to successful stabilization. Paper presented at the annual meeting of the EMDR International Association, Seattle, WA. Phillips, M., & Frederick, C. (1995). Healing the divided self. New York, NY: Norton. Porges, S. W. (2011). The polyvagal theory: Neurophysiological foundations of emotions, attachment, communication, and self-regulation. New York, NY: W. W. Norton. Putnam, F. W. (1988). The switch process in multiple personality disorder and other statechange disorders. Dissociation: Progress in the Dissociative Disorders, 1, 24–32. Putnam, F. (1989). Diagnosis and treatment of multiple personality disorder. New York, NY: Guilford. Ross, C. A. (1997). Dissociative identity disorder: Diagnosis, clinical features, and treatment of multiple personality (2nd ed.). Hoboken, NJ: John Wiley. Schore, A. N. (2003a). Affect dysregulation and disorders of the self. New York, NY: W. W. Norton. Schore, A. N. (2003b). Affect dysregulation and the repair of the self. New York, NY: W. W. Norton. Schore, A. (2009). Right brain affect regulation: an essential mechanism of development, trauma, dissociation and psychotherapy. EMDRIA Annual Conference Plenary Address, Atlanta, GA. Shapiro, F. (1995). Eye movement desensitization and reprocessing: Basic principles, protocols, and procedures. New York, NY: Guilford Press. Shapiro, F. (2001). Eye movement desensitization and reprocessing: Basic principles, protocols, and procedures (2nd ed.). New York, NY: Guilford Press.

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Siegel, D. J. (1999). The developing mind: Toward a neurobiology of interpersonal experience. New York, NY: Guilford Press. Siegel, D. (2012). The mindful brain: Reflection and attunement in the cultivation of well-being. New York, NY: W. W. Norton. van der Hart, O., Brown, P., & Van der Kolk, B. A. (1989). Pierre Janet’s psychological treatment of post-traumatic stress. Journal of Traumatic Stress, 2(4), 379–395. van der Hart, O., Nijenhuis, E. R., & Steele, K. (2006). The haunted self: Structural dissociation and the treatment of chronic traumatization. New York, NY: W. W. Norton.

CHAPTER 15

Stabilizing the Relationship Among Self-States Sandra L. Paulsen and Joan Golston

Such differential responses are common and are taken for granted. What perhaps is not so recognized is that these different response patterns result not only from different precipitating conditions, but also from differing internal organizing systems of feeling, motivation, and cognition within the individual. Sometimes the same internal conditions will provoke a very different response because a personality segment has been activated and for the moment becomes activated or controlled by the individual. —Jack Watkins (1992)

In Chapter  1, Dissociation: Cortical Deafferentation and the Loss of Self, we discussed a hypothesized neurobiological mechanism underlying the development of structural dissociation and separate self-states. In Chapter  14, Stabilization Basics, we discussed the importance of identifying nature and the locus of the crisis that brings the patient to treatment. This chapter extends that discussion to address crises precipitated by problems in the relationships among the patient’s internal states. The focus is on increasing awareness of different parts of the self and ultimately creating a more stable sense of self. The methods described here are useful through all the phases of therapy, but are especially key to increasing stability and so bear addressing early in treatment. This chapter describes interventions into instability or crises related to an internal locus of disturbance.

321

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If the locus of disturbance is internal to the patient but the patient experiences it as external, ego state interventions can redirect their focus and realign relationships among parts. A less well-known benefit of improving relationships among parts is to equalize the complex trauma patient’s differential responses to medications, which depend in part on which states “take their medicine,” or partake in psychopharmacological interventions.1 Shifting communication or alliance among parts can result in enhanced physiological responses as well as improvements in neurobiological reactions, including hyperarousal, hypervigilance, and seizure-related activity. For those reasons, ego state interventions lead to significant shifts, often occurring beneath the radar as changes generalize and impact other aspects of self and other neural networks. Attention to the parts and to interactions among parts will help establish the locus of the current disturbance and lay a foundation for addressing future disturbances. In the service of safety from internal and external hazards, it also works to improve the patient’s real safety. It teaches a beneficial methodology of self-inquiry and prepares the ground for the therapy to turn its focus toward deeper and more psychological aspects. Similarly, the patient may perceive some parts of the self as external or may project uncomfortable internal dynamics onto the relationship with the therapist or another person. A disturbance may occur because parts are in intense conflict with one another. One of the most common and treatment-resistant examples of this dynamic is the relationship between a perpetrator introject and a child part of self. That entrenched dynamic is commonly a reenactment of an early relationship template that was injurious and dissociated at the time of the abuse. The value of therapist curiosity and kindness is neither a mere social nicety nor simply the external container within which the “real” work can occur. Rather, it has neurological, biophysiological, and deep psychological effects operating in the realm of attachment. Essential elements of good therapy for this population have been reviewed elsewhere (e.g., Kluft, 1993a), but we focus on a few key points here. The clinician’s kind and compassionate curiosity regarding the nature of the patient’s perceived concerns, demonstrated within the context of appropriate boundaries, enables the patient to learn important lessons—all of which are stabilizing. They include that: 1. The therapist, like a good parent, can tolerate the patient’s emotions. 2. The therapist can be compassionate about the patient’s self and experience, even when the patient is reactive, activated, or angry. 3. A stance of curiosity, even in the face of distress, is possible and can itself, as a contributor to the patient’s development of an effective observing ego, facilitate movement through to the resolution of a crisis. 4. In general, emotional upset can be survived and passes through, like a wave. 5. Even if the therapeutic relationship appears to be ruptured or disappointing, it can be repaired and thereby deepened. 6. Dynamics unfolding in external relationships can be observed and explored, rather than simply reacted to. 7. Exploration can provide access to parts of the patient’s story that might otherwise not be heard as well as to perspectives that have never before been considered.

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The sum of these lessons may represent the first time that the patient has had a sustained relational experience with this degree of robustness, safety, and depth. In the context of such compassionate, role-appropriate caretaking, the patient begins to achieve early developmental milestones, resulting in an improved foundation from which the self can emerge.

REDUCING INNER CONFLICT

When the primary locus of the presenting disturbance lies in conflict between parts of the self, the therapist enlists the patient to embark on a course of intervention to explore and reduce the internal conflict. Early in the therapy, resolution may simply mean achieving a short-term détente among parts, rather than a deep resolution of the whole person psychodynamic underlying the issue. Whatever the depth of resolution possible at this stage, it is typically achieved through an internal interpart dynamic process undertaken in accordance with the principles of ego state therapy. This involves identifying and interviewing the warring parts of the self, then facilitating an improved empathic attunement or dialogue between them. The process involves orienting parts to the present person, place, and time as well as eliciting and appreciating the often traumatic origin and protective original function of each of the relevant parts—no matter how self-defeating or allied with the perpetrator a part may seem to be. It also requires addressing any concerns the conflicting parts may have about each other as well as concern that the therapist may try to eliminate them. The therapist’s stance must overtly honor the emotional basis of the concern, even when it is not rooted in present facts or adult logic. At the same time, it is necessary to reframe it in terms meaningful to the parts involved but that are also workable for the therapist and adult parts of the self. This involves mediating between contending parts of the self, even if only buying time until parts can more fully engage in the work of therapy, orient to the present, and enlist more directly in the life they are actually living in the body they actually occupy. These developments eventually erode and replace attachments, especially to perpetrators, that are historically based and frozen in time. Notwithstanding the work with each part and its individual perspective, at no point should the therapist forget that the parts are not people; they are actually parts of a person and elements of a system (International Society for the Study of Trauma and Dissociation [ISSTD], 2011; Shusta-Hochberg, 2004). While a self-system may include parts patterned after external family members, no matter how strong their individual sense of self, internal parts cannot move out—unlike actual individual members of a family. They are roommates for life, or until “maturation” brings them to integration, (Kluft, 1993b) and they need to accept that each and every part is ultimately responsible for the well-being of all parts of self, and of the whole person. However, the admonition not to treat parts as people is not the same, as not speaking to parts. Most authorities agree that for clients with dissociative identity disorder (DID), the parts must be spoken to, or one is dealing only with the surface manifestations (e.g., ISSTD, 2011; Loewenstein, 2006). Dealing with only the part that presents for treatment is like only visiting the porch of a house. However pleasant the porch may be, the real workings go on behind the locked door, in the basement and attic, as well as on the porch.

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WORKING WITH PARTS Appreciation

The therapist should appreciate all parts of self as having served a survival function in the best way the child could muster at the time the adaptation developed, no matter how dysfunctional and/or patterned after a perpetrator it appears to be. Although we have discussed this clinical stance in relation to perpetrator introjects, the same reasoning applies throughout the system. Even when a part is dangerous or otherwise malignant, the therapist should join with it empathically, and declare its historic adaptive function (Putnam, 1989). The therapist expresses earnest interest in seeing things “through the eyes” of key parts of self (Paulsen, 2009a). This stance is adopted as part of the clinical task of helping those parts develop an updated perspective on themselves and their role, although naturally the clinician stops short of endorsing any tactics destructive to self or others. Dissociation is often a response to an irreconcilable double bind (Bateson, Jackson, Haley, & Weakland, 1956; Rosen, 2010; Spiegel, 1986) with one part holding one element of the double bind, while another parts the other pole of the bind. Clarity and relief spread throughout the self-system as therapy provides alliances among those parts and a broader context for the understanding and emotional experience needed to resolve the bind, with each reviewing and acknowledging the viewpoint of each other part. One primary principle of ego state work is that the patient’s age and developmental status at the time an ego state came into being or assumed a survival role determines the enduring characteristics of that state, at least until therapy helps it mature. This means, for example, if a part came online at the time the child would have been navigating individuation and the “terrible twos,” one or more parts may be frozen in time with attributes of the “terrible two” paramount in their presentation. In this example, the abusive family’s tendency to suppress rebellion forces the self-system to become even more complex in order to present acceptable compliance to dangerous caregivers while containing existing elements of infantile rage and yearnings for safe attachment. The therapist will appreciate and convey to other parts that this perhaps frightening or tyrannical “terrible two” part is frozen in a legitimate developmental need. When combined with later phase work to process the developmental disruptions and trauma, this approach should resolve the traumatic experience and permit forward movement. The clinician’s empathic reframing of the state’s function and value, as well as appreciating its newly improved behavior and greater acceptance in the overall system, permits that part to complete its previously arrested developmental tasks, then resume or embark on its path to maturation. This maturity may occur spontaneously, where the part suddenly appears to be older, as observed by both therapist and other parts. It may also occur more gradually, potentially with the assistance of specific skills training or with additional processing, using, for example, the future template of eye movement desensitization and reprocessing (EMDR). Parts commonly fear that resolution of their material may render them obsolete and expendable, and need reassurance that they are and will remain an indispensable part of the whole. Protective parts can learn that the whole person or system will

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always need some form of protection, or whatever other adaptive function they have served, and that they can learn the skills needed to continue to have that or a new and equally valued role in the current life of the whole being. They can take pride in having more skills and potentially a new job description. For example, a part who previously functioned as a fighter might become a protector of boundaries, using verbal skills or otherwise coaching and supporting as the patient develops assertion skills, perhaps now operating under the motto of “Never Again!” The Controller: The Highest Ranking “Honcho”

Paulsen has written elsewhere of the clinical tactics of working with the “perpetrator introject” (2009a, 2009b); Golston has discussed the same subject as “identification with the aggressor” (Golston, 1992, 1993, 2007). This section will review key elements in the work from an ego state perspective. Since many severely abused patients had more than one perpetrator or context of abuse, they most likely have more than one perpetrator introject. If perpetration was family-wide, there might be several family member-themed perpetrator introjects. Hypothetically, if Greta Marie’s external mother and external father both participated in a pedophile ring that created and sold child pornography, and involved their three children in the ring’s abusive activities, it should not be a surprise to find that she developed a handful of internal parts reflecting the demands and characteristics of her abusers. These might include a Mother perpetrator introject who rules the internal roost; a Father perpetrator introject who dutifully goes along with what the Mother Part requires; and two older Brother introjects reflecting siblings who engaged in sexual abuse of the patient both within and at times outside the “rules” required to carry out the family-organized criminal behavior. Greta Marie’s traumatized siblings may have made their sister available to neighborhood/neighboring children as well as reenacted their own experiences of sexual violation in their abuse of their younger sister. The clinical question becomes where to begin, which perpetrator introject to work with first. The therapist must therefore discern which part of the self was the highest-ranking authority (Frankel & O’Hearn, 1996), “honcho” (Paulsen, 2009a) or “controller” in the system, and begin there. Starting at the top eliminates the risk of a tug-of-war or power struggle between therapist and the internal leader. In the Greta Marie example, the Mother Part of Self appears to be the head honcho. On close examination of Greta Marie’s family history, the therapist learns that the patient’s external mother was a victim of molestation by her own external father, who was present in Greta Marie’s childhood home for 3 years. In that case, the therapist should explore whether a Grandfather part of self exists to whom the otherwise dominant Mother part subordinates. Ideally, the therapist should work within the earliest possible time frame relevant to that highest introject. Doing that permits work with the part at a time when characterological features, habits, and defenses are still malleable. Working with an abuser-identified part in its earliest-aged state not only facilitates alliance and access (Calof, 1992) but also leads to a deeper generalization of any resolution. Such effects ripple throughout any shared unconscious and the web of relatedness, therefore also reaching allied parts at their earlier developmental levels—no matter where they are in their current maturation and whether or

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not they are consciously aware of the work occurring with this perpetrator introject. A therapist should not fail to check for perpetrator introjects just because they don’t show up on their own volition. In fact, they may hide indefinitely, doing considerable harm to the body, the therapy, and the client’s life, until and unless the therapist detects their presence and brings them into the treatment. Working with perpetrator introjects and the patient’s loyalty to the aggressor is central to the effective ego state therapy of trauma and childhood maltreatment (Frankel & O’Hearn, 1996; Paulsen, 2007, 2009a, 2009b; Phillips & Frederick, 1995; Putnam, 1986). Key to that work is the process of shifting the abuser-identified introject’s allegiance toward the client’s self and away from the external perpetrator after whom they were patterned.

Defusing Perpetrator Introjects

An important early-stage approach to increasing patient stability involves the application of ego state therapy’s conceptual framework and tools in an effort to reduce conflict among parts of self. Because the introjects of perpetrators are allegiant to the point of view of the perpetrator and are the heavyweights or leaders of the internal system, relative to the helpless child states (Frankel & O’Hearn, 1996), working with them directly and relatively early in the treatment is important in defusing resistance to treatment. Once it has been determined that there is an internalized perpetrator introject causing or facilitating physical or emotional harm to the patient, it is essential for the therapist to intervene directly with that introject to orient, or reorient, that part to present person, place, and time. As noted previously, this task cannot be accomplished without the clinician’s appreciation of the introject and recognition that no matter how damaging or how vilely it carries out its function, it began as a protective strategy developed and utilized by an overwhelmed child. In the moment of trauma, the child’s own point of view is truncated by shame that his or her needs and feelings are neither heard nor valued nor honored. Instead, the child seeks a protective alliance and apperceives the point of view of the perpetrator, which is often fueled by the abuser’s narcissistic entitlement, and so the child joins in the view that the perpetrators’ needs and feelings are the only point of view with merit and power, and as dissociation takes hold, that point of view becomes the only point of view at all. For survival, the child aligns with that perspective, taking it in whole and adapting a sense of self that is congruent with it. The following is a prototypic dialogue that might unfold between therapist and patient as the therapist engages in a first contact, and perhaps a few subsequent encounters with the perpetrator introject (perpetrator introject). Hi, I’d like to speak directly now to the Father Part of the Self, and there may not be one and that’s fine, and there may be one and that’s fine too. Father Part, would you be so kind as to come into the conference room in the mind’s eye at this time? Father Part? Is that you?” (Patient observably switches, emerging face appears angry). The patient says, “What do you want?” or patient is glaring silently. Even discerning the subtlest shift, the therapist observes, “Hi Father Part, is that you? thanks for coming. Is it okay with you that I’m talking with

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you? I just don’t want to do anything without your permission because I know you are important, and I know you are powerful. I can’t accomplish a THING without your approval. With this statement, the therapist joins with the perpetrator introject to reduce resistance, engages the original defensive grandiosity, and begins to reassure this part of the patient that the therapist is not trying to overpower this function of the self (Paulsen, 2007, 2009b). “Father Part, did you know that you are NOT the external Father, who is . . . ” (dead/far away/frail etc., stating whatever is factually true) “and did you know, that rather, you are an internal likeness of him, and you are in the body with her?” (The therapist attends carefully to any signs the patient is becoming upset and backing off, and if so:) “Don’t take my word for it, after all, I could be wrong. Here, check this out . . . ” (Therapist uses one or more of the orienting methods described in the previous chapter on stabilization to orient the perpetrator introject to present person, place, and time, and continues, if time and patient tolerance permits, with the following. If time or circumstance does not so permit, the discussion can be continued in a subsequent session, subject to making clear and appreciative arrangements with the perpetrator introject.) Father Part, I just want you to know that I appreciate that you have been holding the Father energy all of these years. What a thankless job. Someone had to do it. You did it! You had to see things through the eyes of the external Father, and get on board with his way of thinking about her. And so you kept her under your thumb, and that might have (saved her life/prevented even more harm, etc., whatever is factually true). That was the best thing any part of the girl could do to try to keep her from being hurt more. So, I thank you and I’m quite serious. What you did was necessary for a long time and I want you to know, I’m not in the business of getting rid of parts, including you. I just help some parts get more up-to-date job descriptions. Why, did you know it is (present year) and we are in (present town if different from where abuse occurred), and she’s halfa-century old (or patient’s age)? And that the rotten stuff happened (number of years or decades ago) and it’s not happening anymore (if true), except in the mind’s eye? That’s where you come in, Father Part, because if you are (hurting/ torturing/scaring/threatening) her now, I understand that is what you HAD to do back then, but if I’m right that she’s (age) and it’s not happening now, then you can rest; you’ve succeeded; mission accomplished. You can stand down, if you want to. See, I understand that if she was (patient’s age at the time the abuse started happening) when it started, that means you were that age and gender too. That’s a very, very hard job for such a little girl. I’m so sorry you had to do that, but that’s why I appreciate you. You did what had to be done and I thank you for it. I realize the parts are scared of you, and don’t like you, but I’ll help them to understand that you were protecting her by keeping her silent and making her do what had to be done. The above, though written as a monologue, should not be entirely one-sided, and space should be left for the perpetrator introject to discuss, complain, disagree,

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call the therapist names, and so forth. The therapist should use clinical judgment to weigh the patient’s defensive reaction, if any, and how rapidly to press forward (Paulsen, 2009a, 2009b). However, in no case should the line of discussion be dropped, even if the patient were to say that there was no such perpetrator introject. The same points can be made, spoken to another part of self about a hypothesized perpetrator introject, in the third person, for example, If there WERE a Father Part of Self, that would be understandable and normal. We all have internal likenesses of our parents or caretakers. What an important part of the self that would be, and I’d want to not ignore such a part, but rather, take his concerns into account. This method, often referred to as “talking through,” and which the first author prefers to call “lobbing a message over the badminton net,” will hopefully land in the ears of any perpetrator introject within earshot. When using this type of strategy, where the hoped-for target of the message is not overtly present, the clinician should be acutely attuned to subtle state shifts in the patient since the patient may switch to a previously unrecognized perpetrator introject, drawn forward by this line of discussion. The therapist’s decisions to move ahead, or pause to leave space, should be governed by information garnered either directly from patient comments or indirectly from sources including (a) visual observation of nonverbal behavior, such as facial expressions or shifts in body stance or other behavior; or (b) intuitive information gleaned from whatever sources of information the therapist has come to rely upon in this therapeutic relationship. This clinical population is notably silenced, whether as a result of a degree of alexithymia, neurobiological reduction in speech in response to trauma, abuser silencing, memory disturbance, projective defenses, or avoidant posttraumatic strategies. Nonexplicit communication of internal experience is therefore a common and confusing aspect of the therapeutic alliance, which can contribute to damaging reenactments and countertransference, and requires close attention by the clinician. The first author spontaneously receives (a) a felt sense in her own body of emotional experience in the patient’s body, for example, mirror neurons; (b) pictures of child states, symbols, or other images sometimes drawn from the patient’s experience; (c) words typewritten in an old font in the mind’s eye, that if spoken, the patient tends to endorse as indeed related to her life. Angry states contain both primitive and heavily enjoined affect and are among those states most likely to be rooted in early infant experience. Although some of those early states are represented in the form of related adolescent states, they are still rooted in infancy and are therefore likely to communicate by means of primitive trance-based transference, or by fusing with the therapist’s sense of self. While there is considerable potential for countertransference and for countertransference-based error, the clinician’s ability to receive these indirect communications awakens the hope of empathic attunement to this desperate manifestation of a child’s defensive needs. That manifestation, which is the aggressor- or abuser-identified part, presents in a style borrowed from a heartless context but is used in service of the child’s needs (Golston, 1992). Even early in the process of getting to know fierce protective parts, it is stabilizing to that part, its “enemies” within and the system overall, to have the

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clinician convey the distinction between the function of the part’s behavior on behalf of the child and the part’s style. That is, the vocabulary, tone, behavior, manners, and other surface manifestations of the abuser-identified or fierce protective parts may be fierce indeed, but it can always be appreciated as somehow protective to the system, if only by keeping the client compliant, back then, to save the life. To a certain extent, this understanding inoculates against some of the patient’s shame as parts of the self-system begin to recognize that they have been duped into a grandiose belief that, as allies of the abuser, they themselves have been impervious to the victimization, a defensive “error” supported by the dissociative illusion that they were not part of “that” child. Identification with the aggressor is best understood as a dissociative posttraumatic defense, one also seen in adult abusers of spouses and children alike, as well as in those trained to be abusive and even torture within political and police systems (Golston, 1992, 1993, 2007). At whatever pace the orienting of the perpetrator introject can safely proceed, the therapist may find a moment to say, softly and with great compassion, I’ll help them come to understand that you also carry a burden, that your job was a thankless one, that there was no other way for you to help except to see it through the Father’s eyes and be loyal to the Father’s way of seeing you. It is as if you put on a Father costume all these years ago, and that it kept anyone from seeing there was a hurt little girl underneath. I don’t know what would have happened if you HADN’T done that. Now that it’s over, think of what would be possible, Father Part, if your magnificent power were used for (patient’s name’s) life and her goals? I think most anything would be possible if you were to shift your loyalty from the external perpetrator to HER life. So I don’t know if it would be today or another day, but when the time comes that you would like to try and see how it works to take off that costume, and hang it on a hook over there in the conference room . . . and you could always put it back on if you needed to . . . we could see how it goes. You must be very, very tired, Father Part of the Self. You know, there is a pleasant place for you (suggest safe place/ ranger station/etc.) with a comfortable (cot or hammock) where you could rest, and get a deep, healing sleep, a deep healing sleep. At any point in this intervention, as mentioned, the therapist may need to back off, stand down, and deal in a nonconfrontive, compassionate manner with whatever concerns emerge. The patient may need some time for the initial absorption of the implications of this new perspective. If she shows notable resistance to correctly orienting to present person, place, and time, the therapist should consider what the perceived threat might be. Is it that the external perpetrator is actually still a threat? Or, is it that the patient cannot bear to tell the truth about the perpetrator because it would mean the loss of an attachment figure, or the loss of a sense of having been loved, or an acceptance of the truth that the patient did not deserve what happened after all, with all the affect such a shift in perspective would bring? Any external threat needs to be considered in full. On rare occasions, patients must relocate to achieve greater safety. That said, the clinician should avoid being induced into reacting to a “present-tense” representation of an old terror of the

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omnipresent abuser, which could lead to presentations inaccurately suggesting current danger. Conversely, victims of childhood abuse are at increased risk of maltreatment in their adult lives, whether by former abusers or by abusers who enter their life in later, adult years. If the basis for the resistance is primarily internal, however, the therapist will need to gently explore what is at stake psychologically. Initially, it is likely to be too hard to tolerate the truth of what happened, THAT it happened at all, that the patient was an innocent child, and that the perpetrator’s behavior is just monstrous. It has been intolerable in part because of an intuitive recognition of the loss of attachment and the grief, anger, and perhaps shame that will follow. A young child is driven to do anything for love or the hope of love, and anything to avoid being alone in a world with no attachment figures, no people. In summary, the therapist first acknowledges the perpetrator introject’s protective service and hidden burden of pain. The therapist then secures the introject’s agreement to experimenting with shifting its loyalty to the patient whose body it now acknowledges as its own. When the time is right, the therapist gently suggests that the introject may be ready, now or soon, to take off its “Father costume” (in the case of a father introject). To return to the prototypic dialogue we are following, at this point the therapist can introduce the “Part Formerly Known as Father” to other parts of the patient’s self-system. Such an introduction involves asking if there are any parts who will step forward to begin to appreciate and welcome this part to the team. The above dialogue is one example of the use of ego state therapy to shift identification to the self, now more accurately perceived, and repair interpart antagonisms. Regardless of the specifics of the therapeutic interaction, in all cases, there needs to be a developing rapport between the abuser-identified part and the clinician. That attunement and rapport permits the introjected part and the system to examine and recognize the admirable survival value of those parts in the child’s life as well as in the internal system. As this recognition deepens, the patient is on her way to dramatically decreased internal conflict, decreased self-harm, and a self-system that exhibits more mutuality and motivation in pulling in the direction of the patient’s goals and the goals of the therapy. Once on board, the part formerly identified with the abuser will benefit from having a new, similarly important and powerful job, with enough recognition, insight, and inclusion to keep it from going back to the old way, and to keep other parts from resuming the fearful ostracism of that part. Examples include a “rehabilitated” part of the self that makes good use of helpful attributes incorporated from the external perpetrator, or simply develop and make appropriate use of its power on behalf of the patient’s current life and here-and-now goals. A part whose job involved wielding power will need to wield power in its new job for the change in roles to feel motivating. Powerful yet helpful contributions can be made in realms that might involve assertion, self-protection, career goals, and so forth. To understand the underpinnings of that part’s need for effectiveness and power, it helps to remember that, despite its sense of independent self and seemingly tyrannical behavior, at its heart, this part is an expression of the helpless child’s need for a sense of control, albeit illusory. Until the therapy has worked through the experience of helplessness and victimization, and established new, constructive adaptations for these redeemed parts, roles that emphasize a part’s importance and power will be needed to hold the benefit of its profound shift in alliance.

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Similarly, parts of self that, to the detriment of the totality of the patient, have previously been locked in conflict with the perpetrator introject will also need to be oriented to present time, place, and person. If the perpetrator introject previously required a child part to surrender daily to abuse or to hurt its own body to “punish” it, then that pattern may continue until that child part is also oriented to person, place, and time. The therapist will need to help that child part, trapped in, and likely attached to this reenactment of the historical sense of helplessness, shame, and culpability, to come to an awareness that she too can now “stand down,” and that the past is over, at last. As therapy assists the client in achieving these overall therapeutic milestones, it is important to note that conflict among child parts of the self, in particular, should dramatically decrease. The internal wear and tear from this often multidecade reexperiencing of the trauma, either from the stance of victim or as an internal representation of an external perpetrator, dissolves gradually into a cooperative team of selves, a powerful force for enhanced stability. Perpetrator introjects vary in their willingness and ability to be oriented to present time and to shift loyalty to the self. Some become defiant and they often reassert their stance, which can result in renewed crises of self-harm, fearfulness, flooding, and sleep disturbance. Some resist forward movement for an extended period, while others seem more easily reoriented, more able, and willing to be congruent with the current needs of the overall person’s self, life, and body. It is clinically ill-advised to presume that all resistance is due to the personality and style of the part itself, to forget to consider the motivations reflected in the interplay between that part and the rest of the system, or to overlook the dynamic needs of the whole, not-yet integrated person. Obsolete Job Descriptions

Parts of self commonly undertake specific survival-oriented and functional roles at the time of the trauma that engenders them, and remain so at the expense of successfully navigating developmental milestones. They persevere with those habituated roles in the face of later changes in life circumstances, including the current context. While survival was of course essential, the specific roles and habitual problem-solving strategies developed for that survival are likely to be ill-advised, childlike, selfsabotaging, or even disastrous as an overall approach to managing life. Reassuring those parts that the therapist does not intend to eliminate any part of the self, the therapist offers an alliance, inviting that part to join in to help them get more up-todate job descriptions, tailored to being an important and helpful player in the present circumstances of the shared life. In the course of that effort, there may be attachments to perpetrators that were once necessary to protect hope and love that are no longer wise or needed. What makes the resolution of those attachments particularly problematic is their current role in defending against a realistic retrospective recognition of the depth of the child’s losses. Notwithstanding the clinical difficulty, these reenactments and introjections need careful attention, since they lie at the root of many of the destructive and complex symptoms typical of this population’s naive efforts to stabilize, which can result in eating disorders, self-injury, suicidality, and sexual acting out, among other difficulties. Addressing them through the repair and updating of orientation will contribute greatly to stability.

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Shame

One particularly crippling and pervasive sequela of traumatic exposure is that of shame. An in-depth discussion of affect theory and psychological basis of shame is beyond the scope of this work (see Nathanson, 1992). It is one of the painful and devastating ironies of the human psyche that those who are victimized are commonly left with pervasive, and viewed objectively, unwarranted experiences of shame. From an ego state point of view, shame is often localized within one or more child parts that contain the child’s experience of being explicitly blamed or humiliated. Even without explicit blame or humiliation, injury to the self results when a perpetrator does not see or acknowledge the humanity of the child. Additionally, a caretaker’s chronic failure to meet the child’s basic needs causes the child to also reject the legitimacy of those needs and to experience the self as unworthy, with no entitlement to emotional or other provision. For the developing child, accumulated experiences of objectification, negation, and lack of attunement are tantamount to an annihilation of self, or even self “murder,” as one of the first author’s patients described it. The child had to relinquish or suppress healthy entitlement in favor of survival through alliance with one or more annihilating adults. In such a choice, identification with the parent-enacted or stated perspective must win out—survival dictates it. One beneficial strategy in the treatment of shame involves approaching the damaged sense of self using object awareness (e.g., “That girl over there feels bad”), rather than ego awareness (e.g., “I feel bad”) to evoke a tolerably remote, quasiobjective stance. This can be especially effective in combination with an imaginary vignette resembling the patient’s shameful facts but viewed from a distance, perhaps more dispassionately, as if occurring in a family of imaginary strangers “over there,” perhaps in far off Pocatello or Poughkeepsie or Tuscaloosa. Often, this remote view allows the patient to see, for the first time, that the child was just a child, incapable of causing the harm inflicted upon her, not responsible for what happened, and, like all children, deserving of good care. The unknown child viewed objectively in Tuscaloosa serves as a halfway point, a point from which parts can transition to using that distant view to observe a despised or rejected state with objectivity and even compassion. Then, when the therapist asks, “Whose shame was it?” the patient spontaneously, or under therapist guidance, can eventually say, “My father’s shame.” The second author will often posit a circumstance in which the parent appears in front of a judge, accused of various misdeeds that the patient can tolerate hearing listed. That parent appeals to the judge, saying, “But Your Honor, I had to (starve, beat, humiliate, etc.) that girl because she refused to make her bed/had an accident in her diapers, etc.” Or, “Your Honor, I’m innocent—that 2 year old, who can’t stand on her feet yet, forced me to do those bad, illegal, mean things.” Patient and therapist speculate about the Judge’s likely response, and for the first time it becomes clear that the parent’s “reasons” and rationale for abuse or neglect are insubstantial rationalizations, and not legitimate justifications. It’s not difficult to see that a short, diaperwearing toddler, or even a child, is incapable of making a truly good and kind adult do “bad, bad, very bad” things. Depending upon the laws of one’s locale, it may be beneficial to read aloud the rule of the land regarding child abuse. Some patients have never heard it plainly said that acts of child abuse are not only illegal but also

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punishable. During these interventions, it is vital to gently remind any perpetrator introject that he is not the actual perpetrator but an internal likeness of the perpetrator, and that the shame belongs to the external person. Therefore, the internal perpetrator introject is “off the hook” for the external perpetrator’s crimes. As with other roles assumed by parts, those who hold shame should be appreciated for carrying out such a painful set of functions. Other parts can be helped to understand that since someone had to carry the feeling of shame, thank goodness the “Shameful Part” was there to do the chore, thus permitting the sane survival of the child overall. The therapist can explore any concerns or shame held by the others in reaction to that shame-bearing part’s role in enacting and feeling shame, or when required to behave in ways that were humiliating or, taken out of context, seem shameful. Sometimes, to uncover, perhaps abreact, or otherwise render tolerable the truth of what was going on, it is necessary for the clinician to review with the other parts what was going on when that troubling part first came to be. The therapist can help the shame-carrying part and others to understand that there was no other workable solution. Insights typically include that the shame belongs to the external perpetrator, not to the perpetrator’s internal likeness or introject, and not to the child, who should have been protected. Once this progress is underway, many important shifts become possible. The basis for shame reactions erodes, in part through the development of an empathic internal context for the parts involved in shame dynamics.

Resource Team and New Job Descriptions

The identification and strengthening of a coalition or “team” of parts to serve as a resource team is a powerful element in augmenting and perpetuating stabilization as well as clarifying roles in the current circumstance—in contrast to the circumstance under which parts and their former relationships with each other first developed. This team is made up of states that are “deputized” to assist in the therapy as soon as they are discovered and sign on to the goals of treatment (Paulsen, 2009a). This explicit enlisting of involvement means that, over time, parts that support healing are in alignment with the therapist and the goals of therapy and, like a boat that begins to list to one side as each passenger makes his or her way over to one side of the craft, the patient’s system gradually leans in the direction of healing, which fortunately results in greater stability, rather than capsize. Golston notes that an important strength of Paulsen’s “recruitment” of parts is the overt establishment of a proactive stance and special identity in parts so enlisted. This is a particularly valuable antidote to the general tendency for the client’s system to attempt to “lodge” the drive and initiative for treatment in the therapist, a tendency resulting from both the traumatic etiology and developmental impact of the dissociative disorder itself. Less-explicit approaches to enlisting the contributions of parts are also useful in the preconsolidation, preintegration portions of the work. Clinicians beneficially seek alliances with “helpers”; angry and potentially destructive parts; nonembodied parts (which can be of help in situations where the body is suffering or needs medical attention); internal self-helper (ISH) parts (Allison, 1974); “angels,” which the patient may not identify with the self of the patient but instead experiences as bringing spiritual allies to bear, and so forth. These alliances between therapist and aspects of the

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patient also contribute to interpart cooperation. In service of long-term stability, the clinician will also need to engage in purposeful and directed efforts to foster interpart alliances or teams. The second author reports success in seeking an early alliance with fierce, destructive, angry parts and then fostering a close relationship between those parts and the depressive, disheartened, “leaden” states. The fire and vitality of the angry parts tends to leaven the depressive states, which in return dampen the impulsivity of the fiery ones. This approach, employed where appropriate in the self-system, dramatically reduces the amplitude of affective peaks and valleys in the stabilization phase, while providing a foundation of support and enhancing the patient’s overall motivation for the coming work.

ORIENTING AND RESOURCING STATES Safe Place/Safe State

“Safe place” is part of the original EMDR standard protocol, to be used with all patients, both in preparation and prognosis (Shapiro, 1995, 2001). The hypnosis tradition has a long history of enhancing safety; see, for example, Frederick and McNeal (1999). A patient unable to achieve a felt sense of safety through the procedure of “safe place” is not ready for EMDR in any form, and will require additional ego strengthening and the development of greater internal resources before EMDR should again be attempted. This additional preparatory work can take from weeks to years, in the most complex dissociative cases. O’Shea has suggested that, in lieu of safe place, the concept of “safe state” may be more empowering (2009). With safe state, the patient is instructed to identify an internal state, not an external location, and develop ways to access it using learned methods (O’Shea, 2009). Although on one hand this may be a linguistic fine point, on the other hand the distinction emphasizes the development of an internal locus of control, an intrinsically stabilizing achievement and resource.

Orienting Procedures

Parts of the self that carry unresolved emotions and traumatic experience are generally fixated on survival under threat, and are typically disoriented to person, place, and time as a result of having been sequestered from everyday experience, where time passes and bodies age. This disorientation manifests as increased internal conflict, suicidal risk when parts are contemplating the “homicide” of another part, and operate from the point of view of an external person, especially that of a perpetrator. When parts become better oriented to the fact that they are in a shared body, in the present place and time, or even begin to consider the possibility that current circumstances are in fact true, then internal conflict begins to decrease and détente becomes possible. Orientation also begins to erode denial about the presence of a dissociative disorder and the possibility of a traumatic history in the parts that have been firmly committed to a stance of denial. Although it is premature to push hard on denial early

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in treatment, improved orientation tends to soften defenses against the reality of their circumstance. The erosion of derealization and denial of a shared body plants the seeds of an improved tolerance for dealing with trauma later in treatment. As a result, it’s important to intervene with the parts of self most likely to wreak havoc early in treatment. Typically, those are angry parts, or those identified with the aggressor(s). There are a range of potentially useful interventions designed to enhance states’ orientation to present person, place, and time. Typically, the parts that most need correction of their orientation are the “honchos” (Paulsen, 2009a, 2009b), or those commanding the most power within the internal system (Frankel & O’Hearn, 1996). The honchos are usually perpetrator introjects but can also be angry parts that are identified with the self of the child. Priority should go to identifying the power-wielding part, causing the most disruption in the system, and gently orienting it, as follows. The target part is first invited to come fully forward, to assume or share executive function or, at a minimum, to “peek through the eyes” (Paulsen, 1992), in order to be oriented to present circumstances. Once presence or peeking is established, the part can be invited to move to another chair in the office while “she,” vaguely suggesting that another part of the patient is “she,” remains in the chair the patient presently occupies. Whether the patient moves or stays, only one chair is occupied and the therapist can ask, with polite curiosity, how it is that she is still in the same chair, or, if the patient moved, why the original chair is now empty. Various other orienting procedures have been described historically in the hypnosis tradition.

Orientation to Passage of Time by Date

A calendar kept at hand can show the disoriented part of the patient the present year and date. Even better, a computer with a webpage showing the current date provides compelling evidence that time has passed since the body was a child dealing with the trauma. If the patient is now out of danger, it can be useful to mark on a white board or piece of paper, or with extended fingers flashed on the therapist’s hands, showing how many years have elapsed since the trauma occurred. Bearing in mind that even perpetrator-identified parts of self are actually child ego states, it can be helpful to use concepts for “large” or “long” that a child can understand. So, for example, the therapist might point out, if it’s true, that it has been “half a century,” or 5 decades (showing five fingers extended for emphasis and explanation to younger parts), since the patient was a helpless child. For very young child-identified states that do not understand the concept of a year, the therapist can refer to the number of summers or birthdays, unless those might be triggering, or the number of breakfasts in a year, in order to define a year. It can also be helpful to do basic math to establish how old those “grown up” people would be now, and then to picture similarly older people the patient has seen who are usually elderly and not physically imposing at all. The second author worked with a child part who exclaimed that old people looked wobbly on their feet, and so the notion of “wobblers” emerged; thereafter, parts reassured and reoriented each other that they had nothing to fear from abusers who were now aged “wobblers.” Formerly intimidated young parts took particular pleasure in being able to say “wobbler” with a tone of superiority in their voice.

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Orientation to the Passage of Time by Body Size

Twombly (2009) introduced the use of a bookshelf in the therapist’s office to orient the patient to the present size of the body. As employed by the first author, the therapist stands next to the bookshelf and reaches to the top of it while asking, “Do I seem like a grown up person?” to which the part likely answers, “Yes.” The therapist then asks the currently executive part to stand next to the shelf and to reach the top of the piece of furniture him- or herself. Typically, while doing so, the patient’s eyebrows arch in amazement as a child state realizes it is in such a tall body. This provides an opening for the therapist to suggest that circumstances are so different now and that never again will the patient be a tiny, helpless child without an adult present to protect them. The patient’s body is tall, grown up, and adult. It has adult parts with adult resources, which can be enlisted to protect them all. The latter assurance is only appropriate when the therapist has some confidence that one or more parts accustomed to dealing with everyday life will be willing and able to provide that protection. The assurance is likely ill-advised if the patient is in current contact with former abusers, self-injuring through an internalized abuser, or in a currently dangerous “real-world” situation. The second author asks the disoriented patient how tall he or she is (age identification of the typically preschool aged part). Golston then marks that height on the wall in pencil (which catches the patient’s attention, since drawing on the wall so blatantly violates the rules in the often-abusive household he or she may have grown up in). With trepidation, the patient will approach, stand against the wall, and as the therapist draws a line across the top of her head, turn to see if the lines are indeed at different heights. Alternatively, Golston enquires about whether the patient/young part is taller or shorter than a doorknob, hears the answer (inevitably “shorter,” or “just the same”), then invites him or her to step to the door, look through the eyes, and see if they are looking up at the door knob, straight across to it, or looking down on it. For some reason, door knob height is a powerfully persuasive and shocking source of information, perhaps because it was a commonplace in every phase of life, in every residence. Such reorientation interventions are made early enough in the session to permit the new recognition and its most immediate implications to begin to be absorbed, and to provide for the grief and other affects that follow the realization that the child was very small and, more shockingly, that years have truly passed and the part is in a grown body. Like the figure from American folklore, our clinical Rip Van Winkles are not always sanguine about the experience of waking up. For some, it is easier to remain deadlocked in double binds than to develop coconsciousness between parts regarding the double binds that drive their dissociative structure (Fine, 1991). Additionally, a local newspaper or magazine can be used to orient the dissociative patient to both place and date/year. A local magazine featuring the geographic or cosmopolitan area is useful for reminding the patient where he or she is now, again, especially if it is far from the original scene of the trauma, or was at least a markedly different social or neighborhood setting. It also has the advantage of having a recent month and year on it for orienting to time as well.

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Orientation to Geographic Place

The second author keeps a colorful vintage tin globe in her office for use in establishing “where we are” and how far one would have to travel to get to or from the locale in question—useful of course only if the other locale is geographically distant. It also proves useful for helping younger parts establish the geographic realities and implicitly the “return trip” nature of any trips either patient or clinician is planning.

Orientation to One Body, One Person

The therapist can keep a mirror nearby to be used for various reorientations, be they to a shared body, age, body gender, weight, or whatever is relevant at the time. Do they really look like a monster? Do they actually look like the Bad Father? and so forth. As appropriate, the therapist can help the patient examine him- or herself in the mirror, perhaps inviting parts to peek through the eyes at the mirror, while asking “Whose face is that?” or “Whose body is that?” Many highly dissociative patients initially see nothing when they look in a mirror, partly due to the ubiquity of derealization and depersonalization strategies in their defensive makeup, as well as to the failure of early caregivers to confirm the child’s identity, mirror their expressions back to them, and provide congruent data about the child’s self and physicality, hence, “I am not real, good, here, valuable.” Other patients have deleted the sight of their reflection in defense against the certainty that they are “dirty,” an identification with the disgust they feel about features of the abuse. However, over time the use of a mirror may soften the patient’s denial and distortions. Where relevant, the therapist can point to the patient’s grown-up shoes in contrast to a handy pair of baby shoes to contrast differences in the patient’s size as a helpless toddler and at present. While essential to the progress of the therapy, these orienting procedures are quite demanding of the patient because they represent a persistent if gentle campaign to erode a lifetime’s protective denial and distortion. Even if the erosion of these defenses is gradual, the results generalize, have clear implications about the story of life to date, and can have a dramatic impact. The therapist should introduce these interventions cautiously and be prepared to back off and demur until a later time when the patient needs or at least can tolerate (re)orienting experience. On occasion, the patient becomes curious and that may override the fear of knowing, to the extent that the client returns to the subject on his or her own. When there is resistance to orientation, perhaps saying, Well, I could be wrong, but if we can stay curious about this there are some pretty important things for us to think about. If I’m right, it means that (for example) when you cut the body it is your own body you are cutting. For now, it’s enough that you are just willing to think about these things.

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This or similar interventions will likely require repeating at a later time, with this part and perhaps with others. When reorientation to shared body or past time succeeds, it can be taught or otherwise generalized to other parts, through conscious or unconscious suggestion, bit by bit, as and when appropriate, while paying attention to the affective implications for each newly or increasingly oriented part. These clients were originally overwhelmed by traumatic experiences, confusion, and subsequent lack of restorative care, and in their lifetime efforts to manage intrusive memory material are often essentially phobic about any degree of emotional experience. To make the process of therapy tolerable, techniques that titrate or control the growing awareness of upsetting material or affect are crucial for stabilization. For that reason, every clinician should have a range of tools and approaches to managing the pace of awareness, such as imaginal reversible telescopes for use in permitting but distancing upsetting images, invitations for the client to have dreams tailor-made to permit parts to slowly realize things they are ready to know, and requests of the unconscious mind to gradually permit light to dawn and truth to be told. It is best if the clinician knows in advance what is going to be revealed instead of learned, and is certain that both ground work and grounding work is sufficient to permit the patient to tolerate the emotions and facts that he or she is about to come to recognize.

Apparently Normal Personalities—Resourcing Ego Strengthening

A final topic to consider in enhancing stability through ego state therapy for complex trauma patients is to consider what are the parts of self that “do ordinary life,” or the so-called apparently normal personalities (ANPs; van der Hart, Nijenhuis, & Steele, 2006). Guided imagery for ego strengthening can directly increase the capacity to feel safe (Watkins & Watkins, 1997; Watkins, 1986); to feel efficacious (Erickson, Rossi, & Rossi, 1976); to nurture oneself (Steele, 2007; Wildwind, 1992); and to enhance performance of newly acquired skills (Paulsen, 2007, 2009a). Ego states can also engage collaboratively with the therapist in an investigation of beliefs held by other, often less-oriented aspects of self, using a cognitive behavioral approach (Fine, 1993). The key point is to strengthen the self with resourcing before and after the necessary painful work of therapy, thereby constructing a kind of resourcing sandwich (Paulsen, 2009a) that ensures greater stability than would a clinician’s overfocus or nonattuned preoccupation with emotionally painful work or uncovering.

Conclusion

When the locus of an ongoing or acute disturbance in a patient’s life is centered in relationships among his or her states, systematically addressing that internal conflict can greatly increase stability. This chapter has offered basic strategies for reducing that inner conflict in a time-efficient way, through interventions that directly address the relevant states, motivating them to join the treatment, release their traumatic holdings, and accept help in finding new ways of being that serve the total self.

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NOTE

1. It is outside the scope of this chapter to provide a review of the interaction between self-state relationships and patient physiological function. However, there is long history of clinical observation that interventions along the lines of “Everyone needs to take their share of the medicine” have an excellent track record in the treatment of DID/DDNOS patient difficulties with medication responsiveness. Along those lines, there is also a substantial literature on the amelioration of seizure and seizure-like symptoms through ego state interventions in the treatment of the dissociative disorders.

REFERENCES Allison, R. B. (1974). A new treatment approach for multiple personalities. American Journal of Clinical Hypnosis, 17, 15–32. Bateson, G., Jackson, D. D., Haley, J., & Weakland, J. H. (1956). Toward a theory of schizophrenia. Behavioral Science, 1(4), 251–254. Calof, D. L. (1992). Adult children of incest and child abuse: Holograms of the trance generational family. American Family Therapy Academy Newsletter, 50, 34–40. Erickson, M. H., Rossi, E. L., & Rossi, S. I. (1976). Hypnotic realities: The induction of clinical hypnosis and forms of indirect suggest. New York, NY: Irvington. Fine, C. G. (1991). The tactical-integration model for the treatment of dissociative identity disorder and allied dissociative disorders. American Journal of Psychotherapy, 53(3), 361–376. Fine, C. G. (1993). A tactical integrationalist perspective on the treatment of multiple personality disorder. In R. P. Kluft & C. G. Fine (Eds.), Clinical perspectives on multiple personality disorder (pp. 135–153). Washington, DC: American Psychiatric Press. Frankel, A. S., & O’Hearn, T. C. (1996). Similarities in responses to extreme and unremitting stress: Cultures of communities under seige. Psychotherapy: Theory, Research, Practice, Training, 33(3), 485–502. Golston, J. (1992). Comparative abuse: Shedding light on ritual abuse through the study of torture methods in political repression, sexual sadism and genocide. Treating Abuse Today, 2, 6. Golston, J. (1993). The creation of cruelty: Violent initiation and the role of traumatic dissociation in the political, military and multigenerational training of torturers. Treating Abuse Today, 3, 6. Golston, J. (2007). Torturer’s apprentice: The creation of cruelty. In W. F. Schultz (Ed.), The phenomenon of torture, readings and commentary. Pennsylvania Studies in Human Rights, University of Pennsylvania Press. International Society for the Study of Trauma and Dissociation (ISSTD). (2011). Guidelines for treating dissociative identity disorder in adults, third revision. Journal of Trauma & Dissociation, 12, 115–187. Kluft, R. P. (1993b). Clinical approaches to the integration of personalities. In R. P. Kluft & C. G. Fine (Eds.), Clinical perspectives on multiple personality disorder (pp. 101–133). Washington, DC: American Psychiatric Press. Loewenstein, R. J. (2006). DID 101: A hands-on clinical guide to the stabilization phase of dissociative identity disorder treatment. Psychiatric Clinics of North America, 29(1), 305–332.

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Nathanson, D. L. (1992). Shame and pride: Affect, sex, and the birth of the self. New York, NY: W. W. Norton. O’Shea, M. K. (2009). EMDR friendly preparation methods for adults and children. In R. Shapiro (Ed.), EMDR solutions II. For depression, eating disorders, performance and more (pp. 289–312). New York, NY: W. W. Norton. Paulsen, S. L. (1992, n.m.). Ego state therapy: When the patient is dissociative but not multiple. Presented at the Level II EMDR Workshop, Honolulu, HI. Paulsen, S. L. (2007). Treating dissociative identity disorder with EMDR, ego state therapy and adjunct approaches. In C. Forgash & M. Copeley (Eds.), Healing the heart of trauma and dissociation with EMDR and ego state therapy. New York, NY: Springer. Paulsen, S. L. (2009a). Looking through the eyes of trauma and dissociation: An illustrated guide for EMDR clinicians and clients. Charleston, NC: Booksurge. Paulsen, S. L. (2009b). ACT-AS-IF and architects approaches to EMDR treatment of Dissociative Identity Disorder (DID). In M. Luber (Eds.), EMDR scripted protocols: Special populations. New York, NY: Springer. Phillips, M., & Frederick, C. (1995). Healing the divided self. New York, NY: W. W. Norton. Putnam, F. (1989). Diagnosis and treatment of multiple personality disorder (Foundations of Modern Psychiatry). New York, NY: Guilford. Rosen, S. (2010). My voice will go with you: The teaching tales of Milton H. Erickson. New York, NY: W. W. Norton. Shapiro, F. (1995). Eye movement desensitization and reprocessing: Basic principles, protocols and procedures (1st ed.). New York, NY: The Guilford Press. Shapiro, F. (2001). Eye movement desensitization and reprocessing: Basic principles, protocols, and procedures (2nd ed.). New York, NY: Guilford Press. Shusta-Hochberg, S. R. (2004). Therapeutic hazards of treating child alters as real children in dissociative identity disorder. Journal of Trauma and Dissociation, 5(1), 13–27. Spiegel, D. (1986). Dissociation, double binds, and posttraumatic stress in multiple personality disorder. In B. G. Braun (Ed.), Treatment of multiple personality disorder (pp. 63–77). Washington, DC: American Psychiatric Press. Steele, A. (2007). Developing a secure self: An attachment-based approach to adult psychotherapy. Canada: Gabriola, British ColumbiaVOR IX3. Twombly, J. (2009). Height orientation. In M. Luber (Eds.), EMDR scripted protocols: Special populations. New York, NY: Springer Publishing. van der Hart, O., Nijenhuis, E. R., & Steele, K. (2006). The haunted self: Structural dissociation and the treatment of chronic traumatization. New York, NY & London, UK: W. W. Norton. Watkins, J. G. (1986). Hypnotherapeutic techniques: Clinical hypnosis, Vol. 1. New York, NY: Irvington. Watkins, J. G., & Watkins, H. H. (1997). Ego-state theory and therapy. New York, NY: W. W. Norton. Wildwind, L. (1992). Treating chronic depression. Paper presented at the Annual Eye Movement Desensitization and Reprocessing Conference, San Jose, CA.

CHAPTER 16

Alexithymia, Affective Dysregulation, and the Imaginal: Resetting the Subcortical Affective Circuits Sandra L. Paulsen, Katie O’Shea, and Ulrich F. Lanius

Imagination . . . is more important than knowledge. Knowledge is ­limited. Imagination encircles the world. — Albert Einstein, quoted by Viereck (1929) Therapists do not simply help clients regulate all emotions, or become aware of, or express all feelings. Rather they distinguish clinically among different types of emotions to guide their interventions. —Leslie Greenberg (2008)

There is general agreement in the field that treatment of dissociative disorders requires a significant period of stabilization prior to proceeding with trauma processing. The difficulty of working with dissociative disorder clients is in moving forward by providing effective treatment on one hand, while not destabilizing them on the other. This challenge is addressed in several chapters in this book focusing on stabilization methods—the basics (Chapter 14, Stabilization Basics), ego state methods (Chapter 15, Stabilizing the Relationship Among Self-States), and mindfulness (Chapter 13, The Compassionate Self). Alexithymia and affective dysregulation play a significant role in that they constitute profound barriers for the effective treatment of traumatic stress syndromes and dissociative disorders by directly interfering with

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emotional processing as well as contributing to emotional destabilization. This particular chapter takes an innovative approach to the treatment of alexithymia and affective dysregulation—the hallmark of complex traumatic stress syndromes and dissociative disorders—integrating elements of stabilization that directly impact emotional processing. The approach initially based on O’Shea (2009b) and O’Shea and Paulsen’s clinical findings (2007) is informed by recent neurobiological research in the role of alexithymia in traumatic stress syndromes, findings in the field of affective neuroscience (e.g., Frewen, Pain, Dozois, & Lanius, 2006), and mentalization (Lanius et  al., this volume, Chapter  3, Peritraumatic Dissociation and Tonic Immobility: Clinical Findings) by recent therapeutic advances utilizing imagination to facilitate neuroplastic processes in pain syndromes (e.g., Moseley, 2004), and last but not least by the field of affective neuroscience (Panksepp, 1998).

NEUROBIOLOGY OF AFFECT

It has been theorized that emotions are innate (Tomkins, 1963). However, it was not until Panksepp that empirical evidence supported the inherent nature of a handful of affective circuits (Panksepp, 1998; Panksepp & Biven, 2012). Panksepp, working during a time when cognition reigned in psychological research, pursued a study of affect in rats and identified seven hardwired subcortical affective circuits that are present from birth and require no learning. Panksepp suggests that these circuits exist for good reason, as information processing systems where the information is affective in nature to ensure survival. We believe that Panksepp’s work is essential to the understanding not only of emotional functioning but also of traumatic stress syndromes and dissociative phenomena. Specifically, traumatic stress and early childhood trauma has been associated with alexithymia, affective dysregulation, and deficits with regard to affective mentalization. Drawing on Panksepp’s notion of basic subcortical affective circuits, the present chapter looks at strategies that use neocortical resources of imagery to increase affective mentalization as well as, we believe, possibly reset them to allow increased adaptive, relational, and intersubjectivity capacity.

AFFECT, ATTACHMENT, AND INTERSUBJECTIVITY

Brain organization reflects self-organization; and human emotions constitute the fundamental basis the brain uses to organize its functioning (e.g., Siegel, 1999) where parent–child communication with regard to emotions directly effects the child’s ability to organize his- or herself. The experience of positive affect states, the role of the parent/child relationship in reinitiating positive affect states after rupture, and the repair of negative affect states are the basis of secure attachment. Within the intersubjective relationship between mother and child, attachment unfolds in the moment-tomoment affective experiences; this is the basis for and foundation of mental health and resilience (Siegel, 1999).

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Attachment disorder is often at the core of dissociative disorder (Barach, 1991). We suggest that insecure attachment attributable to early trauma (ET) and neglect (e.g., Bowlby, 1976) leaves a child without the necessary array of emotional responses to adaptively respond to his or her environment, leaving the child without a solid foundation to navigate developmental milestones. That is, in the absence of intersubjective regulation between parent and child, the child’s emotions, rather than being interactively regulated by the parent through ventral vagal engagement, a process mediated by oxytocin, are now autoregulated by means of a dorsovagal response. The experience of physical or emotional pain, for example, lessened feeling, is mediated by decreased cortical activation due to increased opioid activation (also see Chapter 7, Defense Responses: Frozen, Suppressed, Truncated, Obstructed and Malfunctioning, and Chapter 8, The Clinical Sequelae of Dysfunctional Defense Responses: Dissociative Amnesia, Pain and Somatization, Emotional Motor Memory, and Interoceptive Loops). Moreover, lack of parental availability often contributes to shame (e.g., Nathanson, 1992). From the child’s egocentric point of view, such unavailability is likely interpreted as, “I have done something wrong,” “I am bad,” “I am unworthy,” or “I am shameful.” Such self-limiting developmental beliefs tend to be further reinforced when the child has difficulties mastering tasks without parental support. In the long term, this further contributes to relationship disturbances of attachment, affect disorders, anxiety disorders, state regulation disorders, borderline personality, as well as dissociative disorders (e.g., Putnam, 1997). Thus, failure in the intersubjective relationship between parent and child has not only a direct effect on the underlying neurobiology of affect and the availability of adaptive emotional responses, but also has long-standing effects on beliefs regarding the self and self in relation to others.

Alexithymia: No Feeling

Alexithymia is a common response to psychological trauma (Frewen, Dozois, Neufeld, & Lanius, 2008; Frewen, Lanius, et al., 2008). It refers to difficulties identifying and describing feelings as well as distinguishing between feelings and the bodily sensations of emotional arousal (Taylor & Taylor, 1997). Alexithymia commonly includes a number of related phenomena: not only is there a lack of feeling, that is, an absence of the experience of emotion that commonly includes an absence of appetitive desires; moreover, there tends to be an absence of an orienting response and/or movement response to novel stimuli in one’s environment as well as a lack of sensations in one’s body that are associated with feeling particular emotions. Alexithymia interferes with understanding, processing, and describing emotions. Frewen, Dozois, et al. (2008) and Frewen, Lanius, et al. (2008) suggest that alexithymia is a phenomenon commonly associated with posttraumatic stress disorder (PTSD). Moreover, alexithymia and difficulties with identifying feelings are predictive of depersonalization and derealization symptoms and specifically related to ET or to trauma–spectrum psychopathology (Simeon, Giesbrecht, Knutelska, Smith, & Smith, 2009). To understand alexithymia, we need to differentiate between emotions and feelings. Many traumatized individuals will express emotions, particularly vehement

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emotions at the same time; there is also a lack of feeling. In order to bring neocortical resources to bear on these affective responses, sensory input is relayed through the thalamus to the neocortex. We have hypothesized in Chapter  1 that the downregulation of the thalamus results in decreased sensory input reaching the neocortex and thus resulting in not only decreased experience of emotion but also a decreased ability to bring neocortical resources to bear on emotional expression. That is, in the absence of such neocortical resources, fixed action patterns (FAPs) that are part of the hardwired emotional or affective circuits are expressed without top-down regulation. There is no blending of emotions, nor is there any experience of the emotions.

AFFECTIVE DYSREGULATION AND VEHEMENT EMOTIONS

Affective dysregulation refers to the inability to regulate one’s emotional responses. Perturbed affective states (Frewen & Lanius, 2006) and the loss of ability to regulate the intensity of feelings and impulses have been suggested to be among the most farreaching effects of trauma and neglect (van der Kolk & Fisler, 1995). Pierre Janet in L’Automatisme Psychologique (Janet, 1899) describes such emotional dysregulation in terms of “vehement emotions.” According to Janet, it is the inability and failure to confront traumatic experience fully that results in dissociation of traumatic memories and their return as fragmentary reliving experiences: emotional states, somatic sensations, visual images, and behavioral reenactments. He suggests that vehement emotions not only interfere with proper appraisal, for example, feeling, but also with appropriate action. So how can someone exhibit vehement emotions and at the same time exhibit a lack of feeling? The notion of alexithymia is sometimes difficult to entertain in the face of traumatized clients exhibiting strong emotions, or what Janet referred to as vehement emotions. As suggested above, to understand alexithymia, we need to differentiate between emotions and feelings. Many traumatized individuals will express emotions, particularly vehement emotions. Essentially, the brain has gone to a state of reptilian functioning that essentially represents a short circuit to the emotional expression of basic affective circuits for survival, speeding up the response. At the same time, it comes with a loss of intention, motivation, as well as a loss of capacity for blends of emotion. Not surprisingly, alexithymia and empathic deficits have been related to the expression of impulsive and aggressive behavior, with alexithymia being related specifically to impulsive aggression (Teten, Miller, Bailey, Dunn, & Kent, 2008).

IMPAIRED MENTALIZATION: ALTERATIONS IN DEFAULT NETWORK CONNECTIVITY

Relational trauma in the first 9 months of life negatively impacts the experience­dependent maturation of the anterior cingulate limbic circuits (Schore, 2001a). Abuse and/or neglect over the first 2 years negatively impacts the major regulatory system in the human brain, the orbital prefrontolimbic system (Schore, 2001b). This is likely

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attributable to appropriate levels of sensory input. That is, in early postnatal life, maintenance of critical levels of tactile input of specific quality and emotional content is important for normal brain maturation (Martin, Spicer, Lewis, Gluck, & Cork, 1991). Moreover, sensory input derived from contact with the mother during nursing has been suggested to shape dendritic growth (Greenough & Black, 1992). Such sensory input within primary attachment relationships is likely an important part of the social experience that constitutes attachment, where anatomically separate but functionally integrated affective cognitive neural networks evolve that play a role in mentalization (Fonagy, Roth, & Higgitt, 2005). Mentalization has been described as the ability to read the mental states of others through the brain’s mirror system that allows us to share the emotions of others (Frith & Frith, 1999). That is, through perspective taking, we can infer what a person currently believes about the world given their point of view. Finally, the human brain has the unique ability to represent the mental states of the self and the other and the relationship between these mental states, making possible the communication of ideas. (Frith & Frith, 2006, p.531) Midline cortical structures, especially the medial prefrontal cortex (mPFC), are not only likely involved in this process of perspective taking but also in the representation of the self and others in terms of mental states. Moreover, these midline structures that include the mPFC have been found to be involved in altered functional connectivity in dissociative symptoms (Lanius, Bluhm, Lanius, & Pain, 2005). Not surprisingly, these networks and their associated capacity for mental representations of internal states are likely incompletely developed or altered in individuals with a history of trauma and neglect, a notion that is supported by findings that PTSD related to early-life trauma is characterized by changed connectivity in a neural network associated with self-referential processing in the resting state, for example, altered default network connectivity (Bluhm et al., 2009). This network specifically has been associated with the capacity to mentalize (Ohnishi et al., 2004).

AFFECT AND THREE LEVELS OF BRAIN PROCESSING

Panksepp describes three levels of affective brain processing. Primary brain processing of affect is the level of the subcortical affective circuits. The seven circuits he found in rats, capitalized to show they are actual hardwired subcortical circuits, are SEEKING (the mother of all circuits), RAGE, FEAR, PLAY, LUST, CARE (the substrate for love and nurturing), and PANIC. The PANIC circuit is not about panic attacks, but infant separation distress, the substrate for sadness and depression. These hardwired circuits are common to all mammals and occur at the level of the periaqueductal gray (PAG) in the midbrain. We suggest that these affective circuits are the basis of the development of separate self-states. Panksepp’s secondary brain processing of affect is the initial learning of an infant during the attachment experience with the primary caretaker(s), and subsumes object relations, intersubjectivity, and classically conditioned relationship templates. This learning occurs at the level of the amygdala and other basal ganglia.

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With normal attachment, a baby has use of affective circuits, because a loving caretaker helps to provide containment and regulation of affect, both by providing loving arms that contain, being in synchrony or coherency in the energetic biofield (Siegel, 1999), and by demonstrating acceptance and the capacity to self-regulate. With a loving caretaker, then, a baby acquires healthy use of emotional circuits for affective information about connection, curiosity, danger, injustice, and the need to fight. Out of this experience, a lucky baby acquires self-efficacy, an integrated self, continuity of time, perception, self, and smooth state switching. An unlucky baby acquires relationship templates based on classically conditioned fear responses to danger, rejection, or insufficient care. Panksepp’s tertiary brain processing of affect is subsequent learning that is neocortical in nature, such as mindfulness skills, labels for emotions, assertion skills, and so forth. Neocortical learning includes coping strategies, functional capacities and social skills, and all other knowledge about emotions. Traditional talk therapy most often works on this level. Cognitive behavior therapy attempts to change affect from the top down, by examining beliefs and experimenting with alternative beliefs and conclusions, practicing new behaviors, and not being led by one’s emotions. Panksepp additionally describes what he calls nonspecific arousal factors that effect affective processing, especially neurotransmitters such as acetylcholine, serotonin, and norepinephrine (J. Panksepp, personal communication, June 13, 2009). The critical role of the opioid system in traumatic disturbance is discussed in Chapter 5, Dissociation and Endogenous Opioids: A Foundational Role, and there are suggestions for involvement of the cannabinoid system as well.

Basic Affective Circuits—The Foundational Role of the Seeking System

The most basic of these emotional systems is SEEKING. It refers to the brain’s basic impulse to search, investigate, and make sense of the environment (Panksepp, 1998). SEEKING is the interphase of interaction with our external environment, as well as a motivational system with regard to appetitve learning: Previous exposure to different environmental cues has created expectancies that have become associated with arousal and disarousal (Panksepp, 1986). It causes us to initiate play, lust, and general activity and to investigate and be curious. It inspires invention and pursuit of goals. In many individuals with complex trauma histories, seeking was discouraged or punished. There can be considerable inhibition of this circuit with far-reaching consequences for all manners of behavior. Passivity, phobic avoidance, attachment avoidance, and other inhibitions are often related to blockage of SEEKING. Specifically, with regard to treatment of traumatic stress syndromes and dissociation, SEEKING is important, as its function will affect the overall level of arousal of the client and thereby their relative position in the “window of tolerance” (Siegel, 1999). Further, it has a profound impact on the elicitation of an orienting response. A person who is in a dissociated and withdrawn emotional state no longer responds or orients to his or her external environment. As a result, he or she is no longer able to orient to present time and remains stuck in the past, disoriented to present circumstances. Finally, appetitive learning no longer takes place under these conditions. The

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person does not exhibit any new learning with regard to having specific preferences. Rather, he or she will only exhibit automated responses to previous conditioned stimuli, regardless of what other underlying emotional system is of his or her concern. Some specific examples of how dysfunction of the SEEKING system affects appetitive learning and other emotional systems in trauma survivors are as follows: habitual avoidance of a feared stimulus (FEAR system); dissociation and immobilization in response to external stressors (PANIC system); fetishistic sexual behavior (LUST system); an inability to protect oneself when under attack or, alternatively, an inappropriate responding with anger and rage to minor frustrations in life (RAGE system); an ability to play and interact socially with others (PLAY system); or an inability to have caring and nurturing relationships (CARE system). PLAY AS EMOTIONAL SURVIVAL

The PLAY circuit is recognizable in many animals and certainly human children. It can be intergenerational or interspecies. It can be social or practice for more serious survival skills. In children, sometimes parents punish children for play, or discourage it. This essentially interferes with SEEKING and exploratory behavior in general. PLAY is at the core of practicing emotional and adaptive functioning and engaging in all of the basic affective circuits from a safe base. Not surprisingly, PLAY has been found to be important for socialization of animals and humans. Panksepp links the PLAY circuit to disorders including mania, impulse control, and hyperkinesis. Imagining and pretending in particular is fundamentally associated with PLAY (Panksepp, 1998). PLAY has been construed as an essential part of the evolutionary process itself, defining play as a “facsimilization” of the “struggle for survival” increasing “the organism’s variability in the face of rigidifications” (Sutton-Smith, 1997, p. 223), that is, the habitual expression of emotions that is no longer adaptive. PLAY’s role appears to be “intimately linked to somatosensory information processing within the midbrain, thalamus, cortex” (Panksepp, 1998, p. 280). Moreover, PLAY has a special place among the basic affective circuits in that during PLAY different emotional circuits are exercised that include not only the defensive emotions like RAGE and FEAR but also relational emotions. That is, PLAY not only aids the adaptive exercising of defensive emotions in the face of threat, but rather, “PLAY circuitry allows other emotional operating systems, especially social ones, to be exercised in the relative safety of one’s own home environment” (Panksepp, 1998, p. 283). As Panksepp suggests, it may “help generate a diversity of emotional behaviors upon which learning can operate” (p. 283). As such, PLAY may promote certain types of neuronal growth as well as “serve to exercise and extend the behavioral options under the executive control of inborn emotional systems” (Panksepp, 1986, quoted in Panksepp, 1998, p. 295 [72]). Panksepp goes on further to suggest that PLAY may indeed be the waking equivalent of dreaming, promoting information processing and emotional integration in a similar way to rapid eye movement (REM) sleep. When we imagine, then, we may be utilizing the PLAY circuit to process and integrate experience and lay down new pathways.

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Social Affective Circuits

The PANIC circuit is that emotion evoked in separation distress when a child is separated from its mother. It is there so that the infant’s distress cry evokes a nurturing response in the mother/caretaker. Once mother/caretaker comes, infant’s needs are addressed and baby is again secure. Many individuals had other outcomes. For reasons benign or malignant, mother may not come. Baby’s distress heightens and becomes panic. If there is still no one forthcoming, baby may give up, a result the author calls “tender hearted hurt,” which in the presence of disappointment after disappointment, eventually becomes chronic and unbearable. A baby cuts off emotions, perhaps habitually, because the pain is that much greater than the baby’s capacity to tolerate distress. This is where good circuits go bad; it is not safe to feel, because no one is coming with help and comfort for the baby. Chronic desolation and despair becomes associated with giving up. Guarding becomes chronic, as does feeling invisible. Not all of the developmental milestones associated with the beginning of life can be completed successfully in this despaired and unattached state. In such circumstances, the baby is quite alone with the challenges of growing and learning, and, moreover, with the task of becoming a person that the child is also hardwired to do. We believe that excessive activation of the PANIC circuit is not only related to depression and possibly to autism, as suggested by Panksepp (1998), but it is also at the core of the dorsovagal response and the dissociative collapse. The child’s emotions, rather than being interactively regulated by the parent through ventral vagal engagement, a process mediated by oxytocin, are now autoregulated by means of a dorsovagal response, for example, shutting down by means of excessive opioid activation (also see Chapters 1 and 5). The child has become capable of self-regulating excessive arousal, but at a significant cost. The child learns to rely upon dissociative switching and shutting down. The CARE circuit serves to enable caretaking of infants, offspring, and other people. It is stronger in the female, typically, but also present in the male in the human species (Panksepp, 1998). Nurturance, when provided at optimal levels, protects a child against lifelong insecurities and worry. The authors postulate that in some cases infants not properly cared for may find their own CARE circuits prematurely activated, in an attempt to provide care to unavailable mothers. This may result in those social disorders that involve preoccupation with controlling another, such as stalking, or domineering behavior, as found in some paranoid individuals. The LUST circuit is a basic one that makes reproduction possible, of course, and draws people together in relationship, though the genders are different enough to make shared experience challenging or unlikely otherwise. This circuit is the basis for a variety of sociosexual relations (Panksepp, 1998) and both temporary and enduring bonds. The disruption of this circuit early in life may be the basis for some of the sexual disorders. Other Affective Circuits—Defensive Responses

Generally, an incomplete active defensive response or a blocking or inhibition of such active defensive responses like FEAR or RAGE will bias the person to respond to an external threat with helplessness and PANIC, ultimately increasing the likelihood of a passive defensive response, for example, dorsovagal shutdown.

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That is, the FEAR circuit is part of the survival system and the flight response when threatened or endangered. Panksepp describes that mild fear may produce inhibition or avoidance; intense fear results in actual physical flight responses. That is, we are wired to run and attempt to escape when there is an external threat. An inability to do so is maladaptive and a threat to survival. It has been suggested that the FEAR circuit is the basis for dread and it may be at the basis of phobic and other anxiety disorders. The RAGE circuit is present, evolutionarily and practically today, as part of a fight response. Like other animals, we are wired to fight when attacked and also when there is injustice. This response is so integral that a newborn infant will have its RAGE circuit activated as easily as by having its arms held to its sides (Panksepp, 1998). One on hand this circuit reflects a profoundly protective emotion, for example, warding off helplessness under threat. However, it may also be at the very basis of violent behavior. Imagination, Imagining, and the Imaginal: Visualization and Play

Imagination or imagining involves forming mental images, sensations, and concepts when they are not perceived through the external senses. Imagination is the work of the mind that helps develop. Imagination helps provide meaning to experience and understanding to knowledge. Not only is it fundamental to making sense of the world (e.g., Sutton-Smith, 1997), but it also likely plays a key role in learning (e.g., Egan, 1992) as well as neural development (e.g., Panksepp, 1998). Visualization, imagination, and imagining are essential underpinnings of the capacity to pretend and play. They facilitate the envisioning of multiple social contexts and different affective responses to them, thus allowing for the strengthening and development of those very affective responses and practicing them in a nonthreatening environment, readying the organism for the challenges encountered in different life situations. Imagination, Illusion, and Restructuring Brain Maps

In action and imagination, many of the same parts of the brain are activated (Stephan et  al., 1995). When people visualize the letter “a,” the same areas of the brain are activated as if they were looking at the letter “a” (e.g., Kandel, cited in Doidge, 2007). Similarly, imagining using one’s muscles actually strengthens them almost as much as engaging in physical exercise (Yue & Cole, 1992). “Imagining an act engages the same motor and sensory programs that are involved in doing it” (Doidge, 2007). Much of this research has been done in the area of sports. Clark (1960) studied high school basketball players who practiced by shooting free throws each morning and those who engaged in “mental practice,” visualizing making shots but not actually doing real practice. Both groups improved their free-throw shooting. Indeed, mental rehearsing may help in the construction of schemata that can be reproduced, without thinking, in actual practice (Roure et  al., 1998). Similarly, Morris, Spittle, and Watt (2005) suggest that in sports the use of imagery appears to benefit performance, having a positive effect on anxiety, motivation, and self-efficacy.

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Interestingly enough, there is suggestion that eye movements during motor imagery help to achieve maximal gains in movement accuracy and efficiency (Heremans et al., 2011). PAIN: IMPORTANT LESSONS

There have also been clinical applications of imagery; for example, Moseley (2004) found that graded motor imagery is effective with long-standing complex regional pain syndromes. He worked with patients suffering from phantom limb pain who had been unsuccessful with regard to using a mirror box (e.g., Ramachandran & Blakeslee, 1998)—a method that recreates an illusion of the existence of the missing limb—that, apart from eye movement desensitization and reprocessing (EMDR), is one of the few successful treatments for phantom limb pain. Moseley began by using graded motor imagery rather than creating a visual illusion. That is, he asked patients to simply imagine pictures of their limbs and associated movement. Specifically, treatment utilized sustained attention to the phantom limb, followed by imagined motor movements, and ultimately mirror movements (e.g., McCabe et al., 2003; Ramachandran & Blakeslee, 1998). This occurring in sequence, consistent with sequential activation of cortical motor networks, was most likely to reduce pain activity (Moseley, 2005). This manner of proceeding is consistent with the premise that observation, motor imagery, and execution are associated with partially overlapping increases in activation of parieto-frontal areas. That is, the combination of sustained attention and imagined motor movements was the preparatory activity necessary for patients to benefit from the mirror box treatment that had previously failed to yield results for them without preceding imagery. In a similar vein, Moseley and Brugger (2009) encouraged amputees with phantom limb pain to use imaginal body movement that was physically impossible, suggesting that motor learning does not necessarily need sensory feedback from the body or external feedback about task performance. That is, part of the interventions include imagining physically impossible movements due to the reality of a lost limb. Despite this constraint, there ultimately appears to be a subsequent reorganization of the somatosensory cortex, perhaps by replacing the absent afferent signals from the amputated limb through imaginally generated ones, thereby restoring disrupted bodily representations. This imaginal step seems crucial for individuals who do not initially respond to treatment with mirror movements. The work by Moseley and colleagues suggests that “a completely novel body image can be constructed solely by internally generated mechanisms” (Moseley & Brugger, 2009, p. 18801). IMAGINATION AND EMOTION

We suggest that similar to the motoric imagery utilized by Moseley and colleagues, we can use emotional imagery to alleviate emotional dysfunction in traumatic stress syndromes. For instance, Bausch et  al. (2011) suggest that even highly alexithymic subjects are capable of differentiated emotional imagination. Moreover, when

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they imagine such emotions, they experience normal electrodermal activity and are capable of rating valence, arousal, and vividness of the imagined emotion. Various writers have suggested a number of therapeutic mechanisms for the efficacy of emotional imagery. Sabatinelli, Lang, Bradley, and Flaisch (2006) propose that emotional imagery activates an associative network of stimulus, semantic, and response (procedural) information, including response mobilization. Kim et al. (2007) suggest that the imagery of emotion activates amygdalar function as well as multiple other structures including the midbrain, the area that contains the PAG and that is relevant to affective circuits (Panksepp, 1998). Further, Peelen, Atkinson, and Vuilleumier (2010) suggest that the perception of basic emotional states (such as anger, fear, and joy, among others) activates the mPFC, an area implicated in affective processing, mental state attribution, and theory-of-mind that is commonly deactivated in PTSD. Finally, the experience of emotional arousal has been associated with gamma band activity (Keil et  al., 2001), the binding frequency in the brain, a phenomenon that may potentially be involved in the underlying mechanism of EMDR treatment (also see Chapter 11, Dissociation, EMDR, and Adaptive Information Processing: The Role of Sensory Stimulation and Sensory Awareness).

MENTALIZED AFFECTIVITY

Mentalized affectivity refers to the capacity to feel an affective state, and to retain reflective thinking about that state (Fonagy, Gergely, Jurist, & Target, 2002). It requires a metacognitive stance, that is, to be able to think about ones feelings. The use of affective mentalization with regard to basic affective circuits in a way is a form of motor imagery, where the experience of emotion is experienced as a form of movement or energy within one’s body. Based on our clinical experience, by using visualization or imagery of the quasimotoric aspects of an emotion, for example, engaging in affective mentalization as described in more detail below, we can induce the experience of feeling again. This kind of affective resetting may counteract changes in emotional processing in PTSD as reported by Phan, Britton, Taylor, Fig, and Liberzon (2006). Not only does such imagery appear to alleviate alexithymia but it also greatly increases affective regulation. It allows reinstatement of clients’ normal adaptive function of emotion. We believe that we are able to bring about human neocortical functioning to bear on emotional expression and experience, rather than reptilian emotional functioning. We consider this type of intervention an essential part of stabilization prior to embarking on trauma-centered treatment, for example, trauma processing. Interestingly enough, Jurist (2005) differentiates three elements of affectivity that are delineated and divided into basic and complex forms: identifying affects, for example, naming, distinguishing; processing affects, for example, modulating, refining; and expressing affects, for example, outwardly and inwardly communicating. These elements bear much resemblance to the stages suggested by Moseley (2004) in treating pain syndromes, for example, laterality recognition and focused attention, imagined movement, and, finally, execution of such movement. Indeed, this sequence of identification, imagination, and execution may reflect the intrinsic stages of problem solving in general.

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AFFECTIVE MENTALIZATION AND AFFECTIVE RESETTING

Katie O’Shea initially developed (O’Shea, 2001, 2003, 2009b), and subsequently Paulsen codeveloped with O’Shea (O’Shea & Paulsen, 2007), a procedure that involves affective mentalization for working with clients with very ET and neglect that includes bilateral sensory stimulation commonly used in EMDR. That four-step protocol is described in O’Shea (O’Shea & Paulsen, 2007; O’Shea 2009a, 2009b) and in a book currently in development by Paulsen and O’Shea. O’Shea initially developed the approach because of limitations of the standard EMDR protocol in clients with a history of very ET and neglect—similar to Moseley pain patients, O’Shea’s clients were frequently unable to benefit from the standard EMDR protocol: (a) standard EMDR targets an image in explicit memory and does not address how to work with early experience held in implicit memory, so is more useful with shock trauma than with developmental trauma and neglect in infancy, (b) even when very early experience can be accessed with standard EMDR using symbolic imagery as a target memory, it can overwhelm the client and cause flooding, especially when used with a dissociative client (Paulsen, 1995, 2007, 2009). The ET protocol for EMDR has four steps, the first of which is familiar from the hypnosis tradition, namely, using containment imagery for distancing from affective disturbance and establishing a felt sense of safety and a capacity to evoke that felt sense when needed. However, Steps 3 and 4 are innovative in that Step 3 uses affective mentalization that is believed to clear affective circuits and reestablish adaptive emotional functioning, and it is examined in this chapter (Step 4 is discussed in Chapter 20, Temporal Integration of Early Trauma and Neglect).

The Container—No Affective Load

An important aspect of this imagery is the creation of a container. The therapist suggests to the client to create a container within which the client places all of his or her respective trauma history, including any current stressors: “everything that has yet to be learned from or sorted through,” “everything from current time, adulthood, childhood, really everything, so we have a clear desktop.” It should be noted that the use of containment imagery for emotional containment has a long history in the hypnosis tradition. The ET protocol (O’Shea, 2009a) uses a hypnotic suggestion to set aside everything that isn’t worked on. It is made with the intention to partial out, or fractionate part of emotional experience as it relates to a particular client’s learning history and which drives the habitual expression of FAPs with regard to expression of basic emotions. That is, conditioned responses and appetitive responses to certain stimuli, including a lack of response to one’s external environment, are conceptualized as being attributable to a client’s learning history, including their exposure to traumatic events. The client’s learning history and the resulting affective load from that experience can be construed as an excessive load similar to the excessive electrical current that trips a circuit breaker or blows a fuse (also see Chapter 1). Thus, we conceptualize the

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thalamus, essentially acting as a circuit breaker to avoid overexcitation of the neocortex. While in many cases the respective FAP with regard to the expression of a specific emotion may still occur, as a result of the disruption at the level of the thalamus, the neocortex is no longer informed about the events that occur at the level of the lower brain structures. Nor can the neocortex influence the expression of these FAPs any longer, as top-down processing is impeded by the disruption of the thalamic relay as well as by deactivation of the neocortex. To be clear, targeting as conducted in EMDR processing is always targeting of a fraction of mental contents, but here, containment imagery enables the client to envision setting aside other distracting material. By using a container prior to resetting the affective circuits, metaphorically, we are shutting off all the electrical appliances and lights that may trip the circuit breaker again. This allows the client to experience movement, motions, and emotions without the likelihood of dissociating and shutting down all over again. We avoid the possibility of an overloaded circuit, an excessive affective load tripping the circuit breaker all over again. By imaginally removing these triggers and influencing factors with regard to the client’s present emotional expression and experience, it allows us to proceed to the next step, the imagining of basic emotions, with objectivity, as they are hardwired into our system in their original form to maximize the likelihood of survival. This is necessary not only to prepare the nervous system for maximal adaptive responding in the future but also to allow neocortical learning and neuroplasticity to occur, rather than the ongoing habitual expression of a conditioned response. Moreover, by removing affective load and engaging in different emotions in a playful manner, we may stimulate appetitive circuits, for example, SEEKING. This may assist in bringing the brain’s reward system back online, a phenomenon that has been associated with both increased amygdala and mPFC activity in conjunction with activation in the nucleus accumbens (Costa, Lang, Sabatinelli, Versace, & Bradley, 2010).

Method of Resetting Circuits

The method of resetting the affective circuits is described in detail by O’Shea (2009a), and Paulsen and O’Shea (in press). To summarize that process, the therapist administers bilateral stimulation to the patient while the patient’s attention is directed, in sequence, to each of the basic emotions, for example, SEEKING, PLAY, RAGE, FEAR, CARE, LUST, and PANIC. Instructions are to “look at the emotion rather than to feel the emotion.” Generally, there may be individual clinical decisions with regard to what emotions to begin with, though ultimately the order in which specific emotions are addressed should be decided in consultation with each specific client. Ego-state interventions may be helpful in this regard. Nevertheless, in general we have found that starting with SEEKING and PLAY yields the most significant effects. Working with affective defensive responses like FEAR and RAGE comes next, as reestablishing active defensive responses prior to venturing into emotions that have a passive defensive or dorsovagal aspect like PANIC. Moreover, LUST in particular is frequently difficult to work with in cases of sexual abuse. As discussed earlier, SEEKING is foundational and PLAY allows

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other emotions to be accessed while at the same time increasing emotional valence and distance. Moreover, rather than focusing on feeling, the patient is asked to describe what the emotion looks like, which evokes a further distancing from the felt sense of the emotion. This distancing likely evokes neocortical resources and removes affective load that is likely to trigger overwhelm and result in dissociation and the shutting down of the thalamic relay. Moreover, it likely maximizes interest affect and SEEKING, thereby engaging the mPFC. Bilateral stimulation likely increases neural connectivity within the affective neural network. One of the authors likens this activity to “flushing out” of the circuits, “like clogged gutters.” Bilateral stimulation continues to be used with intermittent queries about what the emotion looks like, until the image or picture stops changing, becomes positive, or becomes neutral.

The Special Role of Shame

While both Tomkins and Nathanson include shame as a basic emotion (Nathanson, 1992), there is no experimental evidence for a SHAME circuit in rodents and lower animals (J. Panksepp, personal communication, June 13, 2009). However, higher animals appear to, and humans certainly do, exhibit shame. Shame plays a significant role in blocked expression of emotional responses. Indeed, Tomkins (1963) suggested that shame is the primary inhibitor of positive affects and diminishes exploration. Shame may act as a biological leash that interferes with exploratory behavior through inducing immobilization and a dorsovagal response. That is, the induction of shame can be utilized to curtail exploratory behavior on part of a child, potentially decreasing its exposure to threats but also easing the burden of child care. Generally, shame affect can be profoundly difficult to work with, likely due to its dorsovagal and dissociative aspects (e.g., Mason et al., 2001), albeit these are likely attributable to secondary processes, for example, attributable to a client’s learning and attachment history rather than hardwired. Nevertheless, shame appears to directly impact on the PANIC circuit. Thus, before resetting Panksepp’s seven emotional circuits, it is typically wise to begin by resetting shame. Although it is not a hardwired circuit, we don’t use Panksepp’s capitalization convention; it is postulated to be learned during the attachment period (secondary brain processing in Panksepp’s terms). Shame during session about having needs and emotions or injuries can sometimes deter people from being able to clear the other affective circuits. Therefore, it seems to be beneficial to work with shame in addition to the other circuits, and that is where we begin.

Look, Not Feel: Ego Awareness Versus Object Awareness

Affective circuits resetting is conducted at arm’s length, in the third person, rather than in the first person: “Look, rather than feel.” As each circuit is being cleared, it is experienced at a distance, as the observer’s object, rather than being felt subjectively.

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When an emotion is experienced, or held in ego awareness, using John Watkins’s terminology (Watkins & Paulsen, 2003), overwhelm tends to occur easily when accessing emotions. However, holding the emotion in object awareness allows the client to bring neocortical resources to bear more easily, likely attributable to the fact that increasing psychological distance increases prefrontal cortex (PFC) activation when envisioning emotional events (D’Argembeau et al., 2008). Thus, staying in object awareness is less likely to lead to overwhelm and more likely to result in insight and compassion for parts of the self among the client. As each affect is observed in the third person, its natural flow and function is objectively observed, among other things decreasing the likelihood of interference from shame. We deliberately remove ego energy and add object energy by having the client look at the emotion instead of feeling it. If the client feels it, we stop and put the felt sense of the emotion back in the container. By implication, emotional responses are viewed free from traumatic associations, normalized, and thus experienced in their original adaptive function. It is postulated further that this observing stance brings neocortical function online on the subcortical circuits, without an affective load, and it flows through the middle or secondary processing level; in Panksepp’s terms, bypassing the relationship templates and the loyalty to the aggressor. The top-to-bottom flow through of awareness without an affective load on the circuit provides the flushing function that enables the circuit to be reset. Thereafter, the circuit tends to work well without inhibition. This accomplishes the problem of finding a way around the secondary processing level where object relations templates may otherwise prevent free functioning of affective circuits.

Affective Resetting—Doing It

Affective circuits are hypothesized to be reset, much as one might reboot a computer that isn’t working right. Indeed, the resetting or rebooting metaphor emphasizes the nature of the circuits as an information processing system, which clients and therapist alike might readily understand. In order to reset the affective circuits so that emotional information can flow without blockage, one has to take them offline. We work with them in the abstract without an affective load on them. The way this is accomplished is to ensure that during Step 3 the client works with each of the Pankseppian emotions with an objective stance, rather than a subjective one. That is to say, the client is instructed to prevent himself from feeling the emotion, and instead asked to simply look at each emotion. The image that the client begins with evolves as it develops or changes, or perhaps doesn’t change, and when it stops changing it is understood to be reset, whether it is positive, neutral, or simply has stopped changing. For each of the seven Panksepp emotions plus shame, the instruction is simply, “What does (emotion name) look like?” The client is instructed to just notice the image, which may be realistic or abstract, symbolic or a color, a photo or a cartoon— it doesn’t matter. It is merely a production of the brain’s information processing system. The client is further instructed to let the therapist know if the client begins to

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have a subjective or felt sense of the emotion, as they’ll stop and put the felt sense into the container, so that the work can continue in objectivity. Also described as looking at each emotion “at arm’s length,” each emotion is processed until one of the following statuses occurs: it stops changing, it becomes positive, or it becomes neutral. At any of those points, the circuit is understood to be reset. The client is urged to use images that are not from his or her own life, for example, not a father’s angry face, when resetting RAGE. The therapist might instead suggest someone else’s father’s angry face, someone we don’t know and a father we don’t know, so the client is looking with objectivity. If the client says, “I’m still feeling afraid, though the father is someone I don’t know,” the therapist might say, “Is the father looking at you? If so, let’s turn the picture so the father we don’t know is showing his angry face to a child we don’t know.” This removes the client’s subjective viewpoint entirely from the scene, enabling the scene to be viewed with objectivity, evoking adult neocortical resources that seem to reset or reboot the affective circuit, when combined with bilateral stimulation until the picture stops changing. When all the seven circuits are reset, the therapist asks, “And how do you feel in this moment?” Remember that during the resetting the therapist has not asked about how the client feels because the two are working studiously to keep the stance an objective one, not a subjective one, for each emotion. Typically the client will report feeling calm, often much calmer, than before the circuits were reset. This calmer state is a permanent one, although the client may soon forget that he or she ever felt different. It is as if the idle has been set lower from that point onward. The process resembles flushing out rain gutters; once accomplished, the rain dispersal goes much more smoothly, with less overflowing and dysregulation. Whereas gutters must be cleaned seasonally, affective circuits only need to be reset once, if done properly, because the blockage likely occurred in the attachment “season” of life, and once achieved, flows more openly ever after.

Intersubjective Milestones: Inability to Look at, and Not Feel, Emotion

It is of importance that highly dissociative individuals with their early disastrous attachment histories may not initially have a capacity to “look at” an emotion without sliding into the felt sense of it. This seems related to the failure of the intersubjective milestones in which the baby and Mom share their affective experience and mom helps baby acquire a sense of “I and thou” in mirroring and acceptance and shared loving communication. When the method of resetting the affect circuits cannot be accomplished initially without sliding in to the felt sense of the emotion, various devices can be used to help the patient achieve that objective distance, which seems to help to repair the intersubjective milestone and increase affect regulation ability. The authors have found it helpful in those instances to use photographs or video material of animals exhibiting these basic affective responses, including fight, flight, freeze, and connection responses for those patients who cannot achieve the arm’s-length viewing of these functions on their own. What is being repaired, then, is the self itself and the intersubjective capacity for seeing self as other.

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Resetting the Circuits: Benefits

After affective resetting of the seven circuits, plus shame (although Panksepp has not demonstrated a shame circuit exists in rats, it is pivotal in human emotions and is done in this method), patients nearly uniformly report an increased sense of calm. The rare exception is that some clients report feeling strange or weird and then realize it is because the sense of feeling calm is so new that it feels unusual. That calm is not just a state shift but also a downshifting of the static internal sense of anxiety or arousal with which the patient lives. For highly dissociative individuals, sometimes it is first necessary to use the same procedure to “reset” the safety systems. Resetting the safety systems may begin with psychoeducation about the normal function of the amygdala or other brain functions, or about the normal mammalian fight/flight/ freeze and connection nervous systems described by Porges (2011). It proceeds to what fight, flight, and freeze, separately, look like, not feel like. Again, individuals who can’t do this without feeling the defensive response will need help in the form of various degrees of “prostheses” that enable the evocation of objectivity. For example, “what does an animal’s flight response look like?” Resetting the affective circuits without an affective load has several notable benefits, including increased capacity to tolerate affect and remain in the window of tolerance, improved ability to bring adult resources to bear on affective function rather than just slide into affect with no capacity for distancing, improved ability to stay oriented to present time and maintain dual attention awareness (Shapiro, 2001), improved ability to approach disturbing material without affective overwhelm, an overall increased sense of calm that endures between sessions, and improved ability to engage in relationship with empathy.

Impact on ET Processing

The significance of these hardwired affective circuits is that when the adaptive expression of these circuits has become blocked or incomplete, the individual will be unable to express these emotions or be conflicted about having these emotions at all, never mind utilizing them as information about the external environment. If emotional expression has become associated with traumatic experience, or the child has learned that expression of such emotions is associated with a threat to survival, accessing these emotions will increase the likelihood that activation of such emotions will result in stress or dissociative response. Moreover, such learned inhibition of basic affective responses is likely to contribute to affect dysregulation, behavioral disorders, and the capacity to achieve developmental milestones. When trauma-focused treatment such as EMDR is attempted in such cases of inhibited or “clogged” emotional circuits, difficult abreaction frequently occurs. In such cases, information processing may fail because the processing capacity isn’t great enough, possibly because of decreased thalamic connectivity. Alternatively, habitual defensive responses may result in resistance and interfere with processing. If, however, adaptive emotional processing has been reinstated through affective resetting prior to trauma processing, subsequent trauma-focused work tends to proceed much more easily. Once affective

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resetting has been achieved, the affective information flow, including feelings, seems to flow freely without inhibition or blocking or excessive overwhelm. Additionally, because the procedure is calming—it allows emotional distancing and perspective taking—it tends to decrease arousal and thus increase affective regulation. This appears to increase processing capacity, which is not surprising given what we know about the fact that arousal decreases thalamic activation. Because the client can stay with the affect longer, becomes more aware and more capable to tolerate soma, the self becomes more strong, resilient, and embodied. That is, the client is better able to tolerate sensation of any kind, because, like free-flowing rain, it flows through unobstructed and without flooding.

IMPLICATIONS FOR THE TREATMENT OF THE DISSOCIATIVE DISORDERS

Elsewhere this book describes that in dissociative clients with traumatic attachment histories, the affective states are not integrated horizontally across the circuits, and so they stand alone in a columnar fashion (see Chapter 1 for an exposition of the columnar theory of dissociation). As state-dependent learning is accumulated over time without integration, ego states and even alter personalities result. Putnam (1988) has described smooth state switching as being an artifact of normal child development, dysregulated switching of abnormal child development, and ET and attachment failure. Without horizontal integration across affective circuits, smooth state switching cannot occur. In its place, we see sudden state switching or even the amnesic switching of true dissociative identity disorder. That switching can be subtle or florid. Observation of florid switching reveals the utter absence of associative linkages between affective circuits and the sudden state switching of chronic dissociation.

Special Considerations for Severely Dissociative Clients

In addition to Steps 1—Containment, 2—Safe State, and 3—Clearing Affective Circuits that are part of the ET protocol (O’Shea, 2009a; O’Shea & Paulsen, 2007), therapists should consider and utilize the following when working with severely dissociative clients. ■■

Ego state therapy usually must be utilized before using even the preparatory steps in order to enlist the self-system in the work. It is critical to orient early, not late in the work, any introjects or other problematic alters to person, place, and time, as described in Chapter 15, Stabilizing the Relationship Among Self-States. Ego-state interventions are necessary for each of the preparatory steps and are certainly essential for interweaves in Step 4. Moreover, the therapeutic relationship is considered to be insufficiently developed to attempt the ET work if that relationship is not held between the therapist and all key parts of self—not necessarily every part of self, but the most powerful or important ones. If the most powerful ego states and the ones most central

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■■

to the traumatic dynamics are not engaged with the process, they will block therapy in general, and ET processing in particular, as is the very nature of traumatic defensive states. Additionally, Chapter  4 enumerates a range of containment and stabilization efforts that will not all be necessary for each client, but some of which will be necessary to get the entire self-system to a point where the ET protocol can be employed. Having said that, it is very useful to the therapy if the ET protocol is employed as early as possible in the treatment so it can be successfully employed. Somatic interventions to increase soma tolerance and affect regulation are discussed in Chapter 14. Stabilization basics focus on containment and stabilization and is further expanded upon in Chapter 19 (Integrating Body and Mind: Sensorimotor Psychotherapy and Treatment of Dissociation, Defense, and Dysregulation by Ogden and Fisher—this volume). It is important that the client has some capacity to tolerate somatic sensation without dissociating or the ET method can hardly be employed without abreaction. However, the entirety of somatic methods need not be undertaken prior to using the ET protocol. Indeed, beginning at the beginning, and reviewing, releasing, and repairing unprocessed traumatic experience for the first years of life will go a long way to resolving proscriptions again having body sensations, needs, and affect. Once those time periods have been repaired in Step 4, clients’ compassion for self and understanding that their body is not shameful at all will be very much greater, increase their capacity to do all subsequent therapeutic work, and cause considerable integration of alters even before later traumas have been processed. The ability to tolerate the subjective felt sense of an emotion and its opposite, to envision the objective image of an emotion, are the two bookends of intersubjectivity in the I and thou of relationship. As such, the development of those two bookends with somatic therapy and with the affective resetting experience go a great distance in repairing the intersubjective milestones of infancy, the capacity for relationship, attachment, and empathic attunement.

We find that, quite extraordinarily, resistant, uncooperative parts of the self that would ordinarily not consent to participating in trauma-focused treatment at an early point in therapy can often be asked for permission to help the baby, with surprising results. The fierce defensive state often agrees to stand down in the name of helping the baby state(s) if a certain level of trust is in place. For some clients then, where safety is less of an issue, an early introduction of the goal of doing ET work to “help the baby” and psychoeducation and other preparation needed to do the ET protocol can greatly economize on time necessary to prepare a dissociative client to be helped with the ET protocol.

Case Vignette

A dissociative client had spent 2 years in stabilization before the ET protocol was attempted to secure temporal integration. Her stabilization work had included somatic therapy, egostate therapy, and a course of yoga at a nearby health center. As part of the preparation steps

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within the stabilization phase of treatment, the patient had practiced using containment imagery to set aside disturbances until session when they would be addressed and had also practiced deliberately evoking a felt sense of safety as much as indicated by present circumstances. When the day came to reset the affective circuits in preparation for very ET processing, the therapist instructed the client to “look at, not feel, each of the emotions I name.” An ego state complained, saying, “sounds like just more stuffing to me.” The therapist explained that, This is not permanent stuffing, only until the time is right to work on the disturbing material when it can have our full attention. Not only that, but when we reset the circuits, she’ll be able to address the early pain without feeling so distressed by it. The therapist asked, “Cranky Part, do I have your permission to help the baby? If so, resetting the circuits will get us closer to being able to help the baby.” The Cranky Part of the client said, “yes, but I’ll be watching you.” The therapist said, solemnly, “Please watch every move I make.” The therapist first asked, “What does shame look like?” The client immediately started feeling upset, and the therapist said, Let’s stop, put the felt sense of shame back in the container, and any memories associated with it. This time, try not to slide into the river, and rather, hang on to the birch tree on the bank of the river, which is very strong, and just watch as the river flows by. Let me know when you are ready. And what does shame look like in this moment? The patient said, “a red and black darkness,” and the therapist said, “Just watch, don’t slide in.” Again the client slid into the felt sense, and said, “I’m no good at this.” The therapist said, “It’s okay, that is exactly why we need to work on this, you’re fine.” The therapist said, Let’s have you imagine that you are watching the red and black darkness on a small TV screen, on the Shame Channel. Nothing you need to do but watch. Or, better yet, let’s have you watch it on a TV on your neighbor’s porch, viewed through binoculars. Just watch with curiosity, and we’ll see if the picture changes. The client was able to watch with objectivity with some corrective assistance, “Now it’s less intense/now it’s just black and gray, not red/now it’s more distant/now there is a boy crying/now he is standing up/he just left/it’s an empty gray frame.” Then the therapist said, “What does RAGE look like—not feel like—but look like?” The client answered, “Like a raging bull, stomping and throwing things around. He tears down a wall. Oh, oh, I’m feeling it.” The therapist said, “let’s re-contain the felt sense of the RAGE then, and let me know when it is set aside.” “Ok,” the client said. The therapist then stated, “What does RAGE look like in this moment, not feel like?” “Well, now the bull is charging this way, I hope I don’t feel it again, I’m starting to.” The therapist said, “Let’s turn the vantage point, so that we are watching the bull charging at someone we don’t know.” “I’m still kind of afraid I’m feeling it.” The

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therapist said, “Okay, let’s say you’re watching it in a crystal ball, or on a TV screen across the street, on the RAGE channel. Nothing you need to do but watch with curiosity. What does RAGE look like?” “Well, the bull throws the guy up in the air a bit, and then it looks like he’s going to gore him but at the last second he turns and walks away and goes back in the chute.” “Notice that,” the therapist says while continuing tapping on the client’s knees, then adds after a period of time, “What does it look like in this moment?” “Now the bull is grazing in a pasture of daisies, and the guy is fine.” In the absence of distressing content, affective processing will always terminate in a positive or neutral image. This is only one way the processing can proceed, as long as container imagery is successful and maintained throughout the processing. In the above case, the picture became positive. It could have also become neutral or simply stopped changing. Any of these outcomes can be considered satisfactory. Some clients report only colors or abstract shapes. Often a client will bring in elements from his or her own life, and we discourage that, saying, “Let’s have it be a similar story in a person we don’t know,” or if even that is too triggering, we might invite them to envision an animal or even a cartoon or stick figure in the same vignette. These “prostheses” or specific suggestions are only offered after the openended invitation to consider what an emotion looks like is too evocative. We prefer that the picture comes from the client’s own repertoire.

DISCUSSION

We consider affective resetting an essential step for individuals with significant dissociative symptoms and/or alexithymia. We believe that this approach aids with the connection as well as allows the reconnection to previously dissociated affects. In addition, in our clinical experience, it assists smooth state switching by conjoining the different affective circuits again, after they have became fragmented through higher order and cortical learning. Once these preparatory steps are in place, processing learned experience will go more smoothly because we are taking neurodevelopment into account by addressing subcortical affective circuits without an affective load and bringing neocortical resources to bring objectivity to the task. Once the affective circuits have been reset, temporal integration can begin (also see Chapter  19). This will facilitate sensory experience being integrated with imagery, ultimately allowing for the embodied experience of emotion.

REFERENCES Barach, P. M. (1991). Multiple personality disorder as an attachment disorder. Dissociation, 4, 117–123. Bausch, S., Stingl, M., Hartmann, L. C., Leibing, E., Leichsenring, F., Kruse, J., . . . Leweke, F. (2011). Alexithymia and script-driven emotional imagery in healthy female subjects: No support for deficiencies in imagination. Scandinavian Journal of Psychology, 52(2), 179–184. doi:10.1111/j.1467–9450.2010.00847.x

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Kim, S. E., Kim, J. W., Kim, J. J., Jeong, B. S., Choi, E. A., Jeong, Y. G., . . . Ki, S. W. (2007). The neural mechanism of imagining facial affective expression. Brain Research, 1145, 128–137. Lanius, R. A., Bluhm, R., Lanius, U. F., & Pain, C. (2005). Neuroimaging of hyperarousal and dissociation in PTSD: Heterogeneity of response to symptom provocation. Journal of Psychiatric Research, 40, 709–729. Martin, L. J., Spicer, D. M., Lewis, M. H., Gluck, J. P., & Cork, L. C. (1991). Social deprivation of infant rhesus monkeys alters the chemoarchitecture of the brain: 1. Subcortical regions. Journal of Neuroscience, 11, 3344–3358. Mason, J. W., Wang, S., Yehuda, R., Riney, S., Charney, D. S., & Southwick, S. M. (2001). Psychogenic lowering of urinary cortisol levels linked to increased emotional numbing and a shame-depressive syndrome in combat-related posttraumatic stress disorder. Psychosomatic Medicine, 63, 387–401. McCabe, C. S., Haigh, R. C., Ring, E. F., Halligan, P. W., Wall, P. D., & Blake, D. R. (2003). A controlled pilot study of the utility of mirror visual feedback in the treatment of complex regional pain syndrome (type 1). Rheumatology, 42(1), 97–101. Morris, T., Spittle, M., & Watt, A. P. (Eds.). (2005). Technical aids to imagery. In Imagery in sport (pp. 237–266). Champaign, IL: Human Kinetics. Moseley, G. L. (2004). Graded motor imagery is effective for long-standing complex regional pain syndrome: A randomised controlled trial. Pain, 108(1–2), 192–198. Moseley, G. L. (2005). Is successful rehabilitation of complex regional pain syndrome due to sustained attention to the affected limb? A randomised clinical trial. Pain, 114(1–2), 54–61. Moseley, G. L., & Brugger, P. (2009). Interdependence of movement and anatomy persists when amputees learn a physiologically impossible movement of their phantom limb. Proceedings of the National Academy of Sciences of the USA, 106(44), 18798–18802. doi:10.1073/pnas.0907151106 Nathanson, D. L. (1992). Shame and pride: Affect, sex, and the birth of the self. New York, NY: W. W. Norton. Ohnishi, T., Moriguchi, Y., Matsuda, H., Mori, T., Hirakata, M., Imabayashi, E., . . . Uno, A. (2004). The neural network for the mirror system and mentalizing in normally developed children: An fMRI study. NeuroReport, 15, 1483–1487. O’Shea, M. K. (2001). Accessing and repairing preverbal trauma and neglect. EMDR Canada Conference, Vancouver, BC, Canada. O’Shea, M. K. (2003). Reinstalling innate emotional resources. Paper Presented at EMDR Europe, Rome, Italy. O’Shea, M. K. (2009a). The EMDR early trauma protocol. In R. Shapiro (Ed.), EMDR solutions II: For depression, eating disorders, performance and more. New York, NY: W.W. Norton. O’Shea, M. K. (2009b). EMDR friendly preparation methods for adults and children. In R. Shapiro (Ed.), EMDR solutions II. For depression, eating disorders, performance and more (pp. 289–312). New York, NY: W. W. Norton. O’Shea, K., & Paulsen, S. L. (2007, September). A protocol for increasing affect regulation and clearing early trauma. Paper presented at the annual meeting of the Eye Movement Desensitization & Reprocessing International Association Conference, Dallas, TX. Panksepp, J. (1986). The psychobiology of prosocial behaviors: Separation distress, play, and altruism. In C. Zahn-Waxler, E. M. Cummings, & R. Iannotti (Eds.). Altruism and aggression, biological and social origins (pp. 19–57). Cambridge, UK: Cambridge University Press. Panksepp, J. (1998). Affective neuroscience: The foundations of human and animal emotions. New York, NY: Oxford University Press. Panksepp, J., & Biven, L. (2012). The archaeology of mind: Neuroevolutionary origins of human emotions. New York, NY: W. W. Norton.

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Paulsen, S. (1995). EMDR: Its cautious use in the dissociative disorders. Dissociation, 8, 32–44. Paulsen, S. L. (2007). Treating dissociative identity disorder with EMDR, ego state therapy and adjunct approaches. In C. Forgash & M. Copeley (Eds.), Healing the heart of trauma and dissociation with EMDR and ego state therapy. New York, NY: Springer. Paulsen, S. L. (2009). Looking through the eyes of trauma and dissociation: An illustrated guide for EMDR clinicians and clients. Charleston, NC: Booksurge. Paulsen, S. L., & O’Shea (in press). When there are no words. Author. Peelen, M. V., Atkinson, A. P., & Vuilleumier, P. (2010). Supramodal representations of perceived emotions in the human brain. The Journal of Neuroscience, 30(30), 10127–10134. doi:10.1523/JNEUROSCI.2161–10.2010 Phan, K. L., Britton, J. C., Taylor, S. F., Fig, L. M., & Liberzon, I. (2006). Corticolimbic blood flow during nontraumatic emotional processing in posttraumatic stress disorder. Archives of General Psychiatry, 63(2), 184–192. Porges, S. W. (2011). The polyvagal theory: Neurophysiological foundations of emotions, attachment, communication, and self-regulation. New York, NY: W. W. Norton. Putnam, F. W. (1997). Dissociation in children and adolescents. New York, NY: Guilford Press. Putnam, F. W. (1988). The switch process in multiple personality disorder and other statechange disorders. Dissociation: Progress in the Dissociative Disorders, 1, 24–32. Ramachandran, V. S., & Blakeslee, S. (1998). Phantoms in the brain: Probing the mysteries of the human mind. New York, NY: William Morrow. Roure, R., Collet, C., Deschaumes-Molinaro, C., Dittmar, A., Rada, H., Delhomme, G., & Vernet-Maury, E. (1998). Autonomic nervous system responses correlate with mental rehearsal in volleyball training. European Journal of Applied Physiology and Occupational Physiology, 78(2), 99–108. Sabatinelli, D., Lang, P. J., Bradley, M. M., & Flaisch, T. (2006). The neural basis of narrative imagery: Emotion and action. Progress in Brain Research, 156, 93–103. Schore, A. N. (2001a). The effects of a secure attachment relationship on right brain development, affect regulation, & infant mental health. Infant Mental Health Journal, 22, 7–66. Schore, A. N. (2001b). The effects of early relational trauma on right brain development, affect regulation, and infant mental health. Infant Mental Health Journal, 22, 201–269. Shapiro, F. (2001). Eye movement desensitization and reprocessing: Basic principles, protocols, and procedures (2nd ed.). New York, NY: Guilford Press. Siegel, D. J. (1999). The developing mind: Toward a neurobiology of interpersonal experience. New York, NY: Guilford Press. Simeon, D., Giesbrecht, T., Knutelska, M., Smith, R. J., & Smith, L. M. (2009). Alexithymia, absorption, and cognitive failures in depersonalization disorder: A comparison to posttraumatic stress disorder and healthy volunteers. The Journal of Nervous and Mental Disease, 197, 492–498. Stephan, K. M., Fink, G. R., Passingham, R. E., Silbersweig, D., Ceballos-Baumann, A. O., Frith, C. D., & Frackowiak, R. S. (1995). Functional anatomy of the mental representation of upper extremity movements in healthy subjects. Journal of Neurophysiology, 73(1), 373–386. Sutton-Smith, B. (1997). The ambiguity of play. Cambridge, MA: Harvard University Press. Taylor, G. J., & Taylor, H. S. (1997). Alexithymia. In M. McCallum & W. E. Piper (Eds.), Psychological mindedness: A contemporary understanding (pp. 28–31). Munich, Germany: Lawrence Erlbaum. Teten, A. L., Miller, L. A., Bailey, S. D., Dunn, N. J., & Kent, T. A. (2008). Empathic deficits and alexithymia in trauma-related impulsive aggression. Behavioral Sciences and the Law, 26(6), 823–832. doi:10.1002/bsl.843 Tomkins, S. S. (1963). Affect imagery consciousness: Volume II, The negative affects. New York, NY: Springer.

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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. Viereck, G. S. (1929, October 26). What life means to Einstein: An interview. The Saturday Evening Post, pp. 17. Watkins, J. G., & Paulsen, S. L. (2003, n.m.). Ego state therapy: EMDR and hypnoanalytic techniques. Workshop Presented at the Society for Clinical and Experimental Hypnosis, Chicago, IL. Yue, G., & Cole, K. J. (1992). Strength increases from the motor program: Comparison of training with maximal voluntary and imagined muscle contractions. Journal of Neurophysiology, 67(5), 1114–11123.

CHAPTER 17

Fractionating Trauma Processing: TOTEMSPOTS and Other Attenuating Tactics Sandra L. Paulsen and Ulrich F. Lanius

My dear brothers and sisters, we are already one. But we imagine that we are not. And what we have to recover is our original unity. What we have to be is what we are. —Thomas Merton (1968—spoken in Calcutta shortly before he died) Attention defines the ability to select stimuli and actions that are coherent with the behavioral goals of an organism. —M. Corbetta, M. Kincade, and G. Shulman (2002)

In trauma work in general, and work with dissociative patients in particular, the integration or processing of traumatic memory by one means or another is central to therapeutic change. In Chapter 1, Dissociation: Cortical Deafferentation and the Loss of Self, we have discussed how traumatic experience may interfere with both horizontal and vertical integration of information in the brain. When a large amount of dysfunctionally and incompletely processed information is held within the nervous system, the rapid integration or synthesis of such information results in a hyperarousal response with a subsequent shutting down of the nervous system, that is, primary or secondary dissociation, as well as unpredictable ego-state shifts (tertiary dissociation). The nervous system is overwhelmed by the information load and shuts down. By utilizing our understanding of such a lack of integration of experience, 367

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we can intentionally slow down integration of experience during trauma processing, thus minimizing emotional overwhelm and subsequent freezing, numbing, and dissociation, thereby ultimately enhancing and accelerating the integration of experience. Specifically, we suggest the harnessing of attentional processes and attentional focus to modulate trauma processing. In this chapter, we describe different approaches to fractionating and titrating trauma processing to facilitate efficient information processing.

FRACTIONATION AND TITRATION—ABREACTION VERSUS SYNTHESIS

Fractionation is a term used in chemistry that refers to a separation process in which a certain quantity of a mixture—solid, liquid, suspension, or isotope—is divided up in a number of smaller quantities, that is, fractions. In the field of dissociation, the concept of fractionation was introduced by Vogt (R. P. Kluft, personal communication, April 1, 2013; Kluft, 2013). Fractionation in the treatment of dissociative disorders specifically refers to the direction of attention to aspects of traumatic experience to attenuate the intensity of abreaction (Kluft, 1989; Kluft & Fine, 1993). Fractionation is closely related to the notion of titration, another term borrowed from chemistry. Titration refers the smallest amount of a reagent to result in a reaction. With regard to trauma-related phenomena, this refers to introducing the smallest amount of incompletely processed traumatic material to bring about a given effect, that is, the slow and careful introduction of the minimally required amount of accessed information to allow processing piece by piece. Traditionally, trauma processing has been conceptualized in terms of abreaction as suggested by Breuer and Freud (1893/1937) that relates to pent-up emotions associated with a trauma that can be discharged by talking about it. However, van der Hart, Steele, Boon, and Brown (1993) suggested that abreaction or discharge “per se” did not necessarily result in information processing or integration of experience. Emphasizing mindfulness in this process, as well as the titration of traumatic material during trauma processing, van der Hart et al. suggested that the notion of abreaction be replaced by that of synthesis, that is, the processing and integration of aspects of memory, or the linking and differentiating sensory perceptions, movements, thoughts, affects, and sense of self (Steele, van der Hart, & Nijenhuis, 2005). Both fractionation and titration enhance mindfulness and inform our understanding of information processing, as well as “rightsizing” access to traumatic material, thereby facilitating trauma processing at a manageable level.

ALL TARGETING IS FRACTIONATED

Targeting, in eye movement desensitization and reprocessing (EMDR) parlance, refers to setting up a “target” for trauma processing: specifying the image, cognition(s), affect/emotions, and sensations associated with the traumatic memory to be worked upon. If one targets the fiery car crash, one is not targeting another traumatic event, for example, a mugging, and so forth. This view is consistent with the understanding

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that attentional process is always germane in the acquisition and remediation of dissociated memories, or one could say, the dissociation and association of memories. Where attention goes, association goes. Where attention does not go, dissociation, if present, remains present. Thus, we suggest that ultimately all targeting is fractionated because to whatever one points the attention delimits also that to which the attention is not pointed, albeit EMDR specifically has a natural tendency to link related events. The direction of attention, then, in processing of traumatic experience that has been dissociated, is extremely important in rightsizing the processing. Jack Watkins (Paulsen & Watkins, 2005) described abreactive processing as always involving making sure that the capacity of the processor (i.e., the patient’s capacity to tolerate intensity) is greater than the volume of material to be processed. This chapter addresses models of conceptualization of information channels relevant to trauma processing, and lists a range of alternative methods to fractionate processing. Finally, because of the central nature of sensation as the foundational level of information that the brain processes, the chapter describes sensory or “bottom-up” processing in trauma work.

INFORMATION DISSOCIATION MODELS FOR FRACTIONATION The Behavior, Affect, Sensation, and Knowledge (BASK) Model

Early in the recent history of dissociation treatment, an acronym was put forward to conceptualize the dimensions along which experience can be dissociated. The BASK Model of Dissociation (Braun, 1986) described BASK as being those dissociable dimensions. Still useful these years later, the BASK model has its limitations. For example, the Knowledge dimension can confuse people because it doesn’t equate perfectly to cognition, which has broader implications. Cognition can refer to frank amnesia for events, or for a blander denial of implications of those events even if the events are not dissociated. Amnesia for events and understanding is what Braun includes in K for Knowledge, and surely that qualifies as cognition or thought. There are various types of cognitions, including beliefs, expectancies, self-concept, and more. Amnesia itself is thought and cognition, central to dissociation. If Braun had called it BASC we’d recognize cognition better than calling it Knowledge.

SIBAM Model

SIBAM stands for Sensation, Imagery, Behavior, Affect, and Meaning (Levine, 2010). Whereas BASK has been incorporated early on in the dissociation field, from an EMDR perspective, Peter Levine’s SIBAM model may be slightly more useful, as it separates out I for image instead of incorporating it in sensation with the other four senses, making it slightly more handy than BASK, as the image is an important aspect for EMDR practitioners when setting up the target using the

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standard protocol. In SIBAM, cognition ends up as an M, reflecting related but different concepts. Ultimately, SIBAM is also imperfect because it is incomplete, as is BASK.

BASIC ID Model

Arnold Lazarus referred to the BASIC ID (Lazarus, 2006). These initials stand for Behaviors, Affective responses, Sensory reactions, Images, Cognitions, Interpersonal relationships, as well as Drugs and biology. The incorporation of relationships allows us to consider interpersonal and attachment relationships separately as a way to fractionate or target trauma processing. BASIC ID is closer to complete, and is therefore more useful for an EMDR practitioner.

OTHER METHODS OF FRACTIONATION Fractionation by Metaphor for Gradual Release

Kluft (1990 in Hammond, 1990) describes a number of methods to hypnotically fractionate the intensity of trauma processing including the “slow leak,” in which intensity is allowed to be released slowly as if in a gradually diminishing balloon. Similarly, a rheostat or dimmer switch can be used in imagination to enable the patient to imagine gradually turning down intensity of experience to a manageable level, without utterly cutting off the experience. Milton Erickson perfected the art of storytelling to enable both a deep hypnotically suggested alternative way to contemplate an experience. We theorize that this approach utilizes objectivity about another, outside the self, to activate neocortical resources and perspective. Objectivity then is a kind of distancing maneuver, similar to the use of Spiegel’s screen technique or Kluft’s slow leak metaphor.

Fractionation by Metaphor of Organization

Kluft describes use of a library to organize memories so that one manageable piece can be processed at a time (Kluft in Hammond, 1990). For example, extending the library metaphor, the patient can be invited to look into the mind’s eye, raise a blind and look through a library window, and there see a shelf for each type of trauma (or perpetrator) and a book for each event. No books need to be opened before their time, and then only one at a time. Whole shelves can remain in background, without turning on the lights, until there is readiness (Paulsen, 2009). At session’s end, the library can be tidied up and lights out. Other variations on this theme include the use of a post office to store traumatic memories, and the patient and therapist can unlock and remove the contents of a box when the time is right, and turn off the lights between sessions.

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Fractionation by Parts of Self

The simplest fractionation method is to process one part at a time, where possible. Other parts can be educated about the pacing process and invited to stand aside and hold and contain their portion of the traumatic experience until the time is right for their turn to process. If the system is too contentious for such an arrangement, trauma processing should be deferred until the level of cooperation in the system is sufficient (also see Chapter  15 regarding stabilization of the self-system with ego-state therapy). When fractionating by part or ego state it is helpful to have prior conversations with other key aspects of the self-system. This enables roles to be preestablished in order to provide support, a voice for mute parts, blending for various purposes (Fine, 1993). Parts should be alerted to the probability that the process may tug at the next part in the chronological sequence of the memory, but that there may not be time to do the next piece of work. That tends to avoid disappointment, frustration, or surprise when the processing needs to be stopped. Even when processing doesn’t go just as planned, one is better off having communicated with parts who then won’t be surprised, and may have the pleasure instead of surprising the therapist, by taking the work on a different turn. In fact, changes of plans are likely not so much capricious as determined by the internal organization of memories and defenses. Since all cannot be known prior to processing, and defenses will show themselves even when they have been worked in advance (see the perpetrator introjects discussion in Chapter 4), the structure of the memory will reveal itself during the processing, which is more granular than during the planning and will necessitate changes.

Fractionation by Time Segment

Sometimes a part may hold a long segment of time and may benefit from processing only a piece of the memory before moving on to the next time segment. Processing this way requires the therapist to have a preestablished notion of the narrative, which may or may not be easily obtained from the part holding the memory, without affective overwhelm. Another part may be better positioned to describe the sequence. It sometimes occurs that several parts may hold pieces of the same snippet of time. They may or may not be able to process at the same time without overwhelm. In that case, it may be necessary to fractionate by time segment and by part and conceivably by channel as well.

Fractionation by Oscillation

Two common methods of processing trauma are sensorimotor psychotherapy (SP; also see Chapter 19) and EMDR (Shapiro, 1995, 2001). The two methods are largely compatible (Paulsen & Lanius, 2009), but there are significant differences between them, as it applies to the standard protocol of EMDR with nondissociative patients. Specifically, in the EMDR standard protocol, one selects a target picture; identifies negative and positive cognitions; rates the validity of the positive cognition; and

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articulates the emotion, its intensity on a subjective units of distress (SUD) scale, and its locus in the body. Then one embarks on processing and does not stop or return to a positive resource state until it spontaneously shifts or arrives at a zero or one disturbance. At that time, the preselected positive cognition is either refined or installed as originally selected. In contrast, in SP and other somatic work, a positive resource state is commonly selected first and strengthened as to the felt sense of it in the body. Then the traumatic disturbance is accessed briefly, often only for a brief instance and only on its edges, and after that brief time the attention is returned to the positive resource state. One strategy in somatic work involves oscillation between the traumatic state and the resourced state. There commonly isn’t a long lingering, and after a similar brief time, the attention is returned deliberately—or irresistibly—to the traumatic disturbance, sometimes referred to as a trauma vortex. This oscillation between trauma vortex and positive resource state is central to the very means by which trauma is metabolized in somatic work. While resource development has been integrated with EMDR procedures (e.g., Korn & Leeds, 2002), an evoked oscillation between traumatized state and resourced, that is, stopping processing midstream to shift to a positive state, is considered in compatible and a deviation from the EMDR standard protocol. Although the mechanism of action involved when deliberately evoking oscillation is not known, it can be conceptualized in terms of accessing different ego states, that is a traumatized state and a resourced state, thereby activating different neural networks and integrating them in the process. It is conjectured to be associated with activating the disturbing material, shifting attention to the positive, creating a space in the chemical wash of disturbance, during which time the brain has the opportunity to clean up and metabolize the disturbance evoked in the prior exposure to the trauma vortex. It is as if there is a space and time for the cleaning crew to come in between attentional exposures to trauma. This oscillation, also referred to as a pendulation (Levine, 2010), involves an essential element of pacing the rhythm of movement, and even entrainment, proposed to be seminal in healing processes (Molinari, Leggio, Cerasa, & Thaut, 2003). For nondissociative patients, to remain true to the standard protocol of EMDR, which has been well researched, the therapist should not interrupt processing to return attention to a resourced state. However, for dissociative patients, the standard EMDR strategy of beginning at the beginning and going inexorably to the end of processing a particular target explicit memory would be overwhelming and produce flooding. Therefore, the use of the above fractionation methods are necessary and advisable to prevent flooding. However, even when carefully planned, it is virtually guaranteed that surprises will unfold in the processing of trauma. If flooding occurs in processing to the extent that unexpected switching is occurring (not switching as part of the memory being processed or expected as part of the chain of experiences, one link after another, but switching in present time to escape the processing), there is too much intensity for processing to complete. In that case, the therapist will need to resource the patient and take various steps to reestablish dual attention awareness, especially by grounding or orienting the present part to current place, time, and other circumstances for a felt sense of safety. The therapist is very likely to need to employ ego-state therapeutic methods to negotiate a solution to the processing problem in present time.

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Bottom-Up and Top-Down Processing

Bottom-up and top-down refer to types of information processing, particularly referring to the direction of the flow of information (Palmer, Rosch, & Chase, 1981). Bottom-up processing is characterized by an absence of higher level direction in sensory processing, whereas top-down processing reflects higher level neocortical processes such as cognitions. A top-down approach reflects deductive reasoning in which an overview of the system is formulated. A bottom-up approach, on the other hand, utilizes inductive reasoning, the piecing together of small percepts to give rise to a larger percept, reflecting what is a “putting together” or synthesis. Bottom-up and top-down processing are also reflected in MacLean’s (1990) three levels of brain architecture: the sensorimotor level of information processing, which includes sensation and programmed movement impulses, initiated primarily by lower, reptilian portions of the brain; emotional processing by a more intermediate limbic system; and cognitive processing by the frontal cortical upper parts of the brain. These three levels interact and affect each other simultaneously, functioning as a cohesive whole with the degree of integration of each level of processing affecting the efficacy of other levels (e.g., Damasio, 1999; Schore, 1994). EMDR trauma processing commonly utilizes both top-down and bottom-up strategies simultaneously, whereas SP in particular has focused on utilizing a bottom-up approach to trauma processing. Bottom-up processing, by focusing mindfully small aspects of sensory experience and perception, allows fractionation and titration of experience, thus reducing a potential overwhelm of the nervous system. It is an organic strategy that grows in complexity and completeness, ultimately leading to the larger picture within the context of the present moment. The use of bottom-up processing in conjunction with EMDR is discussed in Chapter  21, Toward an Embodied Self: EMDR and Somatic Interventions. It has been our experience that in the more simple dissociative disorders this type of processing may be sufficient; in the more complex dissociative disorders additional top-down strategies are commonly necessary for complete processing, for example, ego-state interventions.

A NEW ACRONYM: TOTEMSPOTS

When using EMDR with complex trauma, the ability to fractionate by information channel can be essential. The limitations of existing models suggest the utility of a new handy memorable acronym that is based upon the way the brain processes information channels. Such an acronym should not only reflect Panksepp’s subcortical affective circuits at the level of the periaquaductal gray (PAG) but also the unique nature of olfaction (smell) and the related sense of taste; visual, auditory, and tactile/ kinesthetic taste offer potential ways to fractionate processing as well. Further, cognition—aka knowledge aka thought aka belief—is neocortical and may differ to some extent from object relations/relationship templates that likely occur at lower brain levels, for example, the level of the amygdala and other basal ganglia (Panksepp & Biven, 2012). Finally, though not necessarily considered integral by all patients, a

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spiritual/intuitive channel of processing can be processed as well, which likely ultimately relates to meaning, and can be handled separately as needed. In line with this neurobiological conceptualization, the first author proposes the acronym TOTEMSPOTS, a mnemonic that allows additional specificity and utility with regard to trauma processing, with regard to channels along which EMDR and trauma processing can be fractionated hypnotically. TOTEMSPOTS uses channels as described in the approaches noted earlier to fractionate an intense traumatic memory, to make it more manageable. In the acronym TOTEMSPOTS, the channels have been arranged in a sequence that captures increasing distance from the subjective felt sense of the experience, ranging to the most distant and abstract. Therapeutically, when we invite a patient to imagine the image of a traumatic event playing on a screen, we dissociate the more immediately proximal channels of affect, body sensation, smell, taste, and touch. Only visual imagery and, to a lesser degree, audition readily enable objectivity and a mindful or observing stance. When subjective ownership of an experience is more desirable than an objective observing stance, body sensation is the most foundational and subjective channel. Also, affect, smell, and taste are channels that compel the patient to realize that the experience in question is his or her own. The artful movement between a distanced observing image or a subjective and immediate felt sense is practiced by the adroit therapist to titrate the intensity of experience and pace the work. This tendency to deliberately evoke an oscillation is central to somatic work (e.g., Levine, 2010) and fundamental to intrinsic healing processes, as in spontaneous oscillation, as the body comes into coherency (Siegel, 1999). TOTEMSPOTS channels begin with the most subjectively immediate and range to the most distant. T is for Taste. Taste is often related to olfaction but is organized separately from olfaction in the brain (Blake & Sekuler, 2005). While it can be challenging to process these two separately, on occasion hypnotic suggestion can facilitate fractionating the two when the experience is too intense to process simultaneously. In a traumatic memory, although taste is not always relevant, it certainly can be, and when it is relevant, it may be beneficial to process separately. Taste is not only immediate to the patient, but experienced inside the body. If we taste something, we have merged with it, consumed it, the ultimate differentiation of self; we are what we eat. O is for Olfaction. Olfaction, or smell, has its own nerve, the olfactory nerve, so basic and primitive is it to animal experience (for a more detailed discussion of smell also see Chapter 21, Toward an Embodied Self: EMDR and Somatic Interventions). Smell can be an extremely important and particularly indelible, sensory, horrific, and overwhelming sensory imprint related to certain traumatic experiences. If it can be identified, it should be considered for separate processing. Again, for some patients hypnotic suggestion can enable separation of taste and olfaction where needed to titrate intensity downward. Olfaction is associated with disgust, as taste is, but the olfactory function can apperceive at some distance from the body, more so than taste. Olfaction is listed second, before tactile, because both taste and olfaction are often associated with disgust even more than tactile sensation, though

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it depends on the person and upon their particular trauma details. We can smell a rotten egg without tasting it. T is for Tactile. This refers to the sensations that are kinesthetic or otherwise sensed through touch, as by the body whether externally via the skin or internal to bodily organs. Tactile and kinesthetic sensation are foundational. They are covered more extensively elsewhere in this chapter (bottom-up processing) as well as in Chapter 21, Toward an Embodied Self: EMDR and Somatic Interventions. Sensorimotor (also see Chapter 19, Integrating Body and Mind: Sensorimotor Psychotherapy and Treatment of Dissociation, Defense, and Dysregulation), somatic experiencing, and somatic transformation therapeutic approaches are focused on trauma processing on this level of trauma channel. However, in TOTEMSPOTS the other senses beyond kinesthetic sense (touch), such as imagery, sound, smell, and taste, are treated separately, because they can be separately fractionated in trauma processing for some individuals when needed for titration of intensity of the experience. We can touch a flower’s petals at arm’s length without smelling it. Tactile sensation at arm’s length is more remote than tactile sensation at the core (heart, solar plexus, and genitalia as several examples), which are immediate. E is for Emotion. Emotion, sometimes called affect, may be targeted in isolation. Emotions are based on not only those seven hardwired subcortical affective circuits with which we are born and for which we require no learning (Panksepp, 1998), but also those nuanced combinations of emotions that are learned and accumulated atop or subsequent to those basic emotions. Affect almost always has sensation correlates, which is why it is listed here immediately after tactile, but for some patients may be targeted separately to titrate intensity. Affect is experienced as entirely subjective, and of all the emotions, none more so than shame. The central role of shame in dissociation is reflected by its discussion in several other chapters in Part II (e.g., Chapters 15, 16, and 20). It is understood here to be the annihilation of the self, when the continuous experience of self must be cut off because of the acuity of the discomfort of shame. Emotions are experienced at the core, along the chakras or energy centers or the torso, primarily, though they can be felt peripherally in the extremities (feet, hands, jaw, and throat, especially) as well. M is for Movement. Movement refers to the actual observable behaviors that can be seen and that may have sensation correlates. Beyond such behaviors as weeping, fist clenching, writhing, and so forth, more subtle behavioral observations may include tics, teeth clenching, eye flickering or rolling, and even that complete and unnatural absence of any movement, frozen stillness (also see Chapters 3 and 7). Overt verbalization or crying out would be included as movement behaviors. The focus on somatic micro-movements is a specific therapeutic technique with application to this information channel because it releases thwarted sympathetic arousal responses in slow movements (Levine, & Gabor, 2010). In EMDR processing, envisioning movement imaginally may produce similar releases and repairs (see Chapter 16). Movement allows the completion of fight or flight responses. Indeed, many

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a time, the appearance of fidgeting movements or signs of sympathetic arousal during trauma processing is evidence of a thwarted or truncated fight/flight response at the time of trauma. The reinitiation and completion of movement allows the renewed integration of an active defensive affective response into the client’s behavioral repertoire. S is for Sound. Sound, also called auditory sensation, refers to the information that is taken in through the ears and which may have sensory correlates, such as when a sound causes vibration or pain. When too loud, sound is very immediate and internal; however, normally, sound allows us to perceive objects or events at a further distance than does touch, taste, or smell. That is, we can hear a sonic boom but not touch it. P is for Picture. The visual images or pictures of the traumatic experience can be either viewed from the perspective of the victim or from the ceiling or wall looking down at the victim during the moment of dissociation. The observing from afar perspective is a distancing maneuver for survival. Other aspects of imagery are important in treatment for repairing injury in imagination, as described in Chapter 16. Visual pictures or imagery are more distant than sounds. We can see the sun but not hear it. O is for Object Relations, or the relationship templates that are learned in infancy’s attachment period. For those untrained in object relationships, just substitute the word “other” as in “significant others” from childhood or adulthood. Object relations learning is processed as secondary affective processing (Panksepp, 1998) that occurs at the level of the amygdala and other basal ganglia, essentially reflecting a conditioned or learned response that can recruit the relevant affective circuits but that does not necessarily occur at a conscious or neocortical level. The early learning about what to expect in relationships with others are central to many symptom configurations. The relationship with one or more primary caretakers can be processed as its own dimension, within a specific trauma processing approach such as EMDR or within a psychoanalytic approach. The other is at a distance from the self, but connected. They are not us, be we are in relationship to them. The relationship to any other individuals in certain trauma (e.g., incest, abuse, neglect, attachment experience) can be processed to a degree of differentiation. The differentiation, however, requires some objectivity and insight, so it requires neocortical involvement, and those insights are experienced as slightly more distant from the self. T is for Thought. Thought, also referred to as cognition, includes a number of categories including expectancies, self-concept, beliefs (including blocking beliefs that interfere with healing), categorization, facts, understanding, meaning, knowledge, acquired skill sets, and more. In trauma processing, fractionation can include processing a piece of memory using EMDR or hypnotic abreaction, alternating with cognitive behavioral therapy to process some of the meaning and beliefs about the experience in between more somatically focused interventions. At the same time, cognitive insights may emerge directly out of EMDR processing, and it can be helpful for the therapist to hypnotically suggest that the client might process only the cognitive channel during processing, initially. Although thoughts can vary regarding

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how distant they are, in general thoughts are abstractions, or at least more abstract than, say, a smell or a touch, or an emotion. S is for Spirit. Although not relevant to every patient or every therapist, for some patients the information associated with spirituality and its cousin, intuition, is the largest abstraction of all, yet deeply personal. So the most distant mystery, the Divine, is experienced most personally. It relates to a person’s sense of connection to the inner and outer spheres. It is also within this domain that meaning is generated with regard to both being and suffering in the world. In the Buddhist sense, spirituality is associated with a loss of the sense of one’s body. Prior to being able to let go of the sense of one’s body, one needs to have found it. For that reason, spirituality is noted last as the most mysterious and paradoxical of information channel. We leave it to the reader to decide if spirit is near or far.

LOOPING SIGNALS A NEED TO ADDITIONALLY FRACTIONATE THE WORK

Ego-state maneuvers to resolve looping generally involve clarifying first that the processing is actually stuck. Paulsen notes two types of looping, one being a tight loop like a broken record and the other being like “circling the airport” in which the scenery seems to change but then eventually repeats, and there is a dawning realization that one really isn’t making progress. The therapist should ask if the processing is stuck or is changing “a little,” because even a little change indicates the processing is continuing. In that case, no intervention is required. However, if it is looping either tightly (as with a broken record) or loosely (as in circling the airport), the therapist should ascertain the nature of the problem by asking who can help the therapist understand, or by saying, “I’d like to speak to whoever comes up next.” This will evoke either a switch in the room or in the conference room in the mind’s eye once the patient’s attention is directed there. The problem may be, commonly, that ■■ ■■ ■■ ■■

A part that hasn’t consented or hasn’t been participating in the therapy has been awakened by the processing and is confused about what is going on A part that intended to process doesn’t feel strong enough to continue A part loyal to and protective of the perpetrator doesn’t like the direction in which the processing is going A part may not realize it’s their turn

Solutions include: ■■ ■■ ■■

Informed consent for the part just identified Finding other parts or resources to strengthen the part (also called a resource sandwich; Paulsen, 1995) Orienting the perpetrator introject or part loyal to the perpetrator to the body and life in which they actually live; appreciating, reassuring, and reminding

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■■

that they are internal, not the actual perpetrator, and so are off the hook for the perpetrator’s crimes, and so forth (Paulsen, 2009) Asking if the part is willing to look through the eyes

It is also possible that the looping is because the processing needs to be additionally fractionated to be tolerable. The therapist can discuss this directly with the patient and employ any of the above fractionation methods.

CHOOSING BOTTOM-UP OR TOP-DOWN PROCESSING

Therapists intending to fractionate trauma experience in a dissociative patient will need to decide whether to employ bottom-up or top-down processing. Somatosensory processing is bottom-up (also see Chapter  21), as it is suggested that sensation is foundational to the experience of emotion. In TOTEMSPOTS, the use of “sensation” is nearly synonymous with “tactile,” though other senses may be contributory. Top-down processing is cognitive first, in the form of psychoeducational or insight-oriented processing. Reliance on imagery or cognition is also top-down in the sense that it is neocortical, though the reach of the neocortex is unlimited and can evoke processing at any level, including somatosensory processing. Because trauma is inherently somatically based, somatosensory processing tends to integrate soma first, enabling emotional and cognitive processing to shift in succession. The hypnosis tradition, on the other hand, has relied upon distancing maneuvers that employ the more remote information channels, image especially, truncating the subjective felt sense of sensation or affect until a later point in time. As said earlier, image is the most remote or distancing of the five senses. Audition is also remote but not as remote as visual images. The relative distances associated with the senses are discernible readily. One can see a star, but not hear it. We can hear a herd of horses galloping without being able to touch it. We can touch a dead mouse without being close enough to smell it, one hopes. We can smell a rotten apple but would be loath to taste it. Traumatic flashbacks can involve any of these dimensions. A therapist may artfully accelerate or decelerate processing by attenuating distance from the traumatic experience by using one of the closer channels or one of the more distant ones, depending upon whether the patient needs to be more or less engaged with the processing.

CASE EXAMPLE

A patient with a complex trauma history and a diagnosis of dissociative identity disorder (DID) had worked with the first author in stabilization efforts for about a year, with considerable gains in affect regulation, coping skills, and understanding of her dissociative system. Her self-system had gone from rather conflicted to far less conflicted, with her perpetrator introject permitting the therapeutic work. The patient and therapist agreed it was time to begin trauma processing and both wanted to use EMDR. By long-standing agreement, the front part of the self was dispatched hypnotically for the difficult and painful work so that her

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functioning in daily life could be preserved behind the amnesia barrier, in the tactical integration style recommended by Catherine Fine (1993). The therapist explained the need to prepare the patient’s self-system for trauma processing and began planning with Knowsalot, a part of the self able to take executive control of the body as well as collaborate internally with other ego states. The therapist explained that it was necessary to feature only certain parts and information channels in the trauma processing in order to prevent affective or bodily overwhelm. Because the perpetrator introject, aka Dad Part, often needed reminding that he wasn’t the external perpetrator but a part of the patient, the therapist suggested that the perpetrator introject might be the “star” of the first EMDR processing, in hopes that this would cause a shift in Dad Part’s attachment to the aggressor. The P.I. agreed. The therapist and Knowsalot planned for those child parts unrelated to the incident planned for targeting to hypnotically go on a cruise in the mind’s eye, to the Greek Islands. Knowsalot was deputized to assist with the processing if needed, as was Beatrice, a kindly nurturing and spiritual aspect of self. A maternal introject agreed to permit the work to happen, and take a day trip in the mind’s eye. A teen part, formerly angry and trouble making but having been brought into the work by appreciating her burden and negotiating for her needs, agreed to “babysit” any child parts who might be inadvertently pulled forward by the work. She’d reassure them and sit with them and explain that EMDR was happening, not a recurrence of actual trauma, but a detoxifying of the memory so that it could be laid to rest and repaired. The Dad Part then was the fraction initially targeted in the processing, though the therapist also spoke with the egoidentified child part of self at the age at the time of the incident memory, which was Five (by ego identified, we mean that the child state understood herself to be the patient by name, although at a younger age. In contrast, a perpetrator introject identifies itself to be the very external perpetrator him- or herself, and spurns or has contempt for the patient’s essence). It was explained to Five that she might be pulled into the work by the EMDR, and she consented but was worried about being strong enough. The therapist acknowledged that was a concern and set about to strengthen the system for this eventuality. In addition to having Beatrice available if needed to strengthen Five, and in addition to Knowsalot agreeing to blend if needed to give a voice to Five or to Dad part, the therapist invited discussion about further fractionation possibilities. In particular, because the incident memory involved physical pain and images, as revealed by flashbacks, it was postulated that there might be other channels that would emerge in the processing, such as possibly smells, tastes, painful awarenesses, sounds, and emotions. Note that these possibilities were introduced as general features of memories, not as seeds of what to expect in THIS memory. The patient was invited to be curious and open to possible other channels. The therapist suggested in her best hypnotic voice that they may find that they had the ability to contain some channels while experiencing one at a time, beginning with body pain. We established that it wouldn’t mean we were forgetting about the other channels or parts, only waiting until the time was right to keep the amount of material manageable. The therapist also said that it would be possible during the processing, as new learning unfolded, to modify the plan, and that was fine. This inoculated against the patient feeling like a failure in the event of unanticipated events during processing, which are the rule and not the exception (Fine & Berkowitz, 2001). At the next session, the processing was initiated as planned, with Dad Part being the star, focusing on “his” body. However, not surprisingly, almost immediately Dad Part became aware subjectively of the child’s pain during the molest and that he was actually in the girl’s body, not the dad’s body. That insight had been arrived at prior to EMDR through psychoeducation, but the insight would drop away and the identification with the aggressor would “grow back.” Dad Part “popped” away for a

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time, leaving Five to process, until the therapist checked in with him. Dad part explained he had left because he was ashamed to have identified with a pedophile all these years, forgiving the external father’s offenses because of his superior power. An ego-state maneuver was needed to reassure Dad Part that identifying with the external father was indeed his job, and he had done it well, and that the other parts were likely also understanding more in the processing. Knowsalot said that several other parts were tearfully seeing that Dad Part was just one of them, a hurt child, and one was able to thank Dad Part for doing his awful job of identifying with the external father all these years. With that, the processing continued with body sessions. Twice, other channels came into awareness but it was hypnotically suggested these smells and sounds and pictures could wait. At the end of the long session, all participants were appreciated and “tucked in” for a safe drive home. At the next session, the patient described breakthrough body sensations during the week but she hadn’t felt that she needed to call because she understood it was residual processing, and had been alerted to the possibility ahead of time. Therapist and patient agreed to continue processing because the patient did not feel too “raw” to continue. When the therapist checked in with Dad Part to continue, he felt much better, at a level of disturbance of 0 on a 10-point scale, and Knowsalot said he looked entirely different, more like a child. The therapist had thought that other TOTEMSPOTS channels might be processed for Dad Part, but the patient said it was more important to help Five, because Five was suffering, and again fractionating the work to the somatic channel was suggested hypnotically. Ten minutes of processing for Five resulted in a switch to another ego state that carried smells and tastes, and then about 10 minutes of processing for another that carried sounds and the picture. Knowsalot subsequently came as the session neared its end, with the beginning of a narrative understanding of the child’s dilemma in the scene, saying, “she loved her daddy.” In the next session, Five, other ego states calling themselves Five, and Knowsalot processed with an emphasis on affect and then cognitive awareness of the child’s innocence and reporting that not only the terror and rage had resolved with the physical pain, but also the shame. Before closing down the session, parts were invited to help “spackle” the wall protecting the front part from knowledge of the trauma work, and a layer of insulation was added to further buffer the front part. Again, the parts were tucked in at end of session so the front part of the self, unaware of the memory work and its particulars by prior arrangement, could safely drive home and function in daily life. These two distancing maneuvers served to provide sufficient protection so the patient could function. However, the front part of the patient reported after that session a welling up of grief and sorrow, which she didn’t understand, having been protected from it by the amnesia barrier. After this piece of work, no additional memory processing was conducted until the patient had had time to synthesize the results as reported by Knowsalot. When trauma processing was resumed several weeks later, it was again conducted fractionated by part and age, by event category within perpetrator, and, where needed, by information channel. This careful approach enabled the patient to maintain working at her job without downtime or disability from flooding. After approximately 2 years of trauma processing in this manner, the front part of the patient found herself with a dawning awareness of what had happened to her. When the major traumas had been detoxified behind the amnesia barrier, we “folded in” the front part by having her process the memories that had previously been processed by other parts. Though painful, the largest parts of the somatic pain, the affect, and other channels had been largely detoxified and integrated, leaving a smaller fraction of the work for the front part to face. Although this case represents a relatively straightforward case of treatment of DID, and others would have had more twists

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and turns, it represents a safe and shorter treatment course than would have been likely without the use of fractionated EMDR.

SUMMARY

We have emphasized the importance of fractionation in trauma work, the foundational nature of sensation among the information channels to process in a fractionated manner in trauma work, as well as have described a number of ways to approach the task of fractionation. We offer a new acronym, TOTEMSPOTS, to guide therapist thinking about information channels to consider processing; discussed means of fractionation unique to the highly dissociative patient; and emphasized the somatic foundation of trauma integration as a key element in managing and titrating the work as well as achieving an embodied sense of self (also see Chapters 8 and 10).

REFERENCES Blake, R., & Sekuler, R. (2005). Perception (5th ed.). New York, NY: McGraw-Hill. Braun, B. G. (Ed.). (1986). Treatment of multiple personality disorder. Washington, DC: American Psychiatric Press. Breuer, J., & Freud, S. (1893/1937). Studies in hysteria (Authorized Translation with an Introduction by A. A. Brill; Nervous and Mental Disease Monograph Series No. 61.). New York, NY: Nervous and Mental Disease Publishing. Corbetta, M., Kincade, M., & Shulman G. (2002). Two neural systems of visual orienting and the pathophysiology of unilateral spatial neglect. In H. O. Karnath, A. Milner, & G. Valler Oxford (Eds.), The cognitive and neural basis of spatial neglect (pp. 259–273). Oxford, UK: Oxford University Press. Damasio, A. (1999). The feeling of what happens: Body and emotion in the making of consciousness. New York, NY: Harcourt. Fine, C. G. (1993). A tactical integrationalist perspective on the treatment of multiple personality disorder. In R. P. Kluft & C. G. Fine (Eds.), Clinical perspectives on multiple personality disorder (pp. 135–153). Washington, DC: American Psychiatric Press. Fine, C. G., & Berkowitz, A. S. (2001). The wreathing protocol: The imbrication of hypnosis and EMDR in the treatment of dissociative identity disorder and other dissociative responses. American Journal of Clinical Hypnosis, 43(3–4), 275–290. Hammond, D. C. (1990). Handbook of hypnotic suggestions and metaphors. New York, NY: W. W. Norton. Korn, D. L., & Leeds, A. M. (2002). Preliminary evidence of efficacy for EMDR resource development and installation in the stabilization phase of treatment of complex posttraumatic stress disorder. Journal of Clinical Psychology, 58, 1465–1487. Kluft, R. P. (1989). Playing for time: Temporizing techniques in the treatment of multiple personality disorder. American Journal of Clinical Hypnosis, 32, 90–98. Kluft, R. P. (2013). Shelter from the storm. Charleston, SC: CreateSpace. Kluft, R. P., & Fine, C. G. (Eds.). (1993). Clinical perspectives on multiple personality disorder. Washington, DC: American Psychiatric Association. Lazarus, A. (2006). Brief but comprehensive psychotherapy: The multimodal way. New York, NY: Springer.

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Levine, P. A. (2010). In an unspoken voice: How the body releases trauma and restores goodness. Berkeley, CA: North Atlantic Books. Levine, P. A., & Gabor, M. (2010). In an unspoken voice: How the body releases trauma and restores goodness. Berkeley, CA: North Atlantic Books. MacLean, P. D. (1990). The triune brain in evolution: Role in paleocerebral functions. New York, NY: Plenum Press. Merton, T. (1968). Quoted in J. H. Austin (2006) Zen-brain reflections. Cambridge, MA: MIT Press. Molinari, M., Leggio, M., Cerasa, A., & Thaut, M. (2003). The neurobiology of rhythmic motor entrainment: A neurorehabilitation perspective. Annals of the New York Academy of Sciences, 999, 313–321. Palmer, S. E., Rosch, E., & Chase, P. (1981). Canonical perspective and the perception of objects. In J. Long & A. Baddely (Eds.), Attention and performance IX (pp. 135–151). Hillsdale, NJ: Lawrence Erlbaum Associates. Panksepp, J. (1998). Affective neuroscience: The foundations of human and animal emotions. New York, NY: Oxford University Press. Panksepp, J., & Biven, L. (2012). The archaeology of mind: Neuroevolutionary origins of human emotions. New York, NY: W. W. Norton. Paulsen, S. (1995). EMDR: Its cautious use in the dissociative disorders. Dissociation, 8, 32–44. Paulsen, S. L. (2009). Looking through the eyes of trauma and dissociation: An illustrated guide for EMDR clinicians and clients. Charleston, NC: Booksurge. Paulsen, S. L., & Lanius, U. (2009). Toward an embodied self: Integrating EMDR with somatic and ego state interventions. In R. Shapiro (Ed.), EMDR solutions II: Depression, eating disorders, performance, and more. New York, NY: W. W. Norton. Paulsen, S. L., & Watkins, J. G. (2005, November). Best techniques from the armamentarium of hypnoanalytic, EMDR, somatic psychotherapy and cognitive behavioral methods. Paper presented at the annual meeting of the International Society for the Study of Dissociation, Toronto, ON. Schore, A. N. (1994). Affect regulation and the origin of the self: The neurobiology of emotional development. Hillsdale, NJ: Lawrence Erlbaum Associates. Shapiro, F. (1995). Eye movement desensitization and reprocessing: Basic principles, protocols and procedures (1st ed.). New York, NY: The Guilford Press. Shapiro, F. (2001). Eye movement desensitization and reprocessing: Basic principles, protocols, and procedures (2nd ed.). New York, NY: Guilford Press. Siegel, D. J. (1999). The developing mind: Toward a neurobiology of interpersonal experience. New York, NY: Guilford Press. Steele, K., van der Hart, O., & Nijenhuis, E. R. (2005). Phase-oriented treatment of structural dissociation in complex traumatization: Overcoming trauma-related phobias. Journal of Traumatic Dissociation, 6, 11–53. van der Hart, O., Steele, K., Boon, S., & Brown, P. (1993). The treatment of traumatic memories: Synthesis, realization, and integration. Dissociation, 6, 162–180.

CHAPTER 18

Accelerating and Decelerating Access to the Self-States Sandra L. Paulsen

PART 2 I felt doomed to death, But in a flash, Before I could reduce my thoughts To an emotion, I felt a mass leave my body: Departing. Then my mind becomes anonymous As is each night. Just unfinished thoughts, and a deep sickness inside, As I was forced to swallow it, Something I’ve tried to bury deep inside my psyche to this day. (poem written by alter personality) —Alice Jamieson (2009)

This chapter describes maneuvers to access the internal system of the patient as well as means to accelerate or decelerate the work in that process of accessing the selfsystem. Having fluency with these maneuvers enables efficient transformation of traumatic material held by parts of the self in a paced and attenuated way, because the therapist will have the means to either intensify or deintensify the patient’s experience as the situation requires for optimal progress. 383

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FRACTIONATING AND TITRATING: ASSOCIATION, DISSOCIATION, AND PACING THE PROCESSING

Eye movement desensitization and reprocessing (EMDR), ego state therapy, and somatic therapy fit together like hand and glove. This is not the serendipitous combination of any few therapies for a hybrid or eclectic result. Rather, it is the skillful use of an associative procedure (EMDR) with two therapeutic procedures, one that works with dissociation and dissociative structures (ego state therapy) and one that works with dissociation’s foundational substrate (somatic therapy). Both approaches can be used to prepare for and regulate the pace of association during EMDR by deliberately utilizing dissociation to determine pace and titrate affective intensity. EMDR tends to process rapidly, so with straightforward processing in simple cases the processing does not require the same level of regulation ability. EMDR processing in simple cases can be set on “cruise control,” using the Standard Protocol, because it resembles an open road suitable for driving at high speeds. In complex trauma cases, it is necessary to have the ability to either accelerate or decelerate as needed because the road has precarious twists and turns in it, not to mention structures in the middle of the road, and potholes to drop into before, especially during, and after trauma processing with EMDR. An extended preparation phase is often necessary before trauma processing in complex traumatic stress presentations and attachment-related syndromes, particularly when dealing with the sequelae of chronic early trauma. Clinical practice suggests that the adjunctive use of body therapy and ego state interventions can be useful, during stabilization and later on in increasing the treatment response to EMDR. Traditional treatment of complex posttraumatic stress disorder (PTSD) and dissociative disorders has usually included hypnoanalytic interventions, during which abreaction is considered an important part of treatment, beginning with Janet in the 1900s (van der Hart, Brown, & Van der Kolk, 1989), Watkins in World War II (Paulsen & Watkins, 2005), and up to present time (e.g., Fine, 1993; Kluft, 1984; Philips & Frederick, 1995). Many such approaches can be conceptualized as ego state interventions. To this day, ego state interventions remain one of the mainstays in the treatment of dissociative symptoms, both during stabilization and during trauma processing. More recently, in conjunction with those early approaches to the treatment of dissociative disorders, both EMDR and body therapies have been used by practitioners in the treatment of complex trauma and dissociative disorders. Moreover, conceptualization of the treatment of trauma has moved from the notion of abreaction and exposure toward an information processing understanding, consistent with the concept of neural networks (e.g., Paulsen, 1993; Shapiro, 2001). Apart from EMDR, information processing as a concept is now also used by cognitive behavior therapists (e.g., Foa & Hears-Ikeda, 1996) as well as body therapists (Ogden & Minton, 2000). Within the field of dissociative disorders, van der Hart, Steele, Boon, and Brown (1993) have cogently argued that the notion of abreaction be replaced by one of synthesis. Rather than the focus being on discharge alone, information processing therapies focus on the processing of information, that is, synthesis during which unprocessed memory traces are integrated and processed, whereas abreaction

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per se does not necessarily result in processing of information, systematically and completely, unless there is a procedure in place to check the work and continue it at intervals.

ACCESSING THE SYSTEM

Many dissociative clients are treated for years without a therapist accessing the deeper reaches of the client’s self-system, and with the therapist only intervening with the part of the client that presents for treatment. This is like trying to remodel a house while sitting on its front porch, and not trying the doorknob just because the door is closed, never even ringing the door bell. Meanwhile, there are those waiting inside for someone to come and find them. Year after year goes by with the therapist standing on some misguided ceremony, when the door could easily be opened, in most cases, with the simple application of ego state therapy, an efficient means of accessing those internal realms. Some therapists have concerns that if they work directly with states and parts of the self, they will be reifying dissociation, or even suggesting something that doesn’t really exist. To capitulate to these unwarranted concerns means that the therapist is refraining from using the key that will unlock the door to healing for many clients.

Ego State/Hypnotic Interventions

Ego state interventions are generally considered to be hypnotic interventions (Fraser, 2003; Watkins & Paulsen, 2003), though formal trance induction is not used in all cases and some ego state work may be considered nonhypnotic (Emmerson, 2003). This section expands the discussion of ego state and/or hypnotic interventions valuable for tasks related to general containment and stabilization.

Conference Room Resources

Fraser is credited with formalizing the Dissociative Table Method (Fraser, 1991, 2003), also called the conference room technique. Variations predate Fraser, notably those of David Caul (Chu, 2011) and Helen Watkins (J. G. Watkins, personal communication with 2nd author, July 17, 2004), who used similar methods but did not publish their use beyond mimeographed handouts of the 1980s. Paulsen combined the Dissociative Table method with EMDR (Paulsen, 1992, 1993, 1995). The conference room in particular, and ego state therapy in general, emerges from the hypnosis tradition, though no formal trance induction per se is required. It utilizes focused attention and an observing stance or observing ego, various imaginal resources, and may be understood as both a distancing and an accessing maneuver. It is a distancing maneuver, adding object energy (Federn, 1952; Watkins & Watkins, 1997; Watkins & Paulsen, 2003), when the patient looks at a part of self perceived as “over there” and, often, “not me.” It is an accessing maneuver when used to bring into

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conscious mind something that had previously been out of awareness, and when that something is given a voice by the therapist directly speaking to it. It adds ego energy (Federn, 1952; Watkins & Paulsen, 2003; Watkins & Watkins, 1997) because the state is recognized and responds speaking in the first person “I” or “we,” though other parts may or may not also claim it as their personal experience by describing it as “me” or “we.” Other parts may simultaneously be in conscious awareness, or “coconscious,” but are imbued with object energy because they are perceived as being “over there,” for example, as in a chair in the conference room. Another variation is that parts can be actually blended (Fine & Comstock, 1989) or copresent in the body, with more than one state present, sitting fully forward in the body, in the therapist’s office chair, at the same time. More commonly, one part is forward or present in the room, and other parts are recessed in the self-system, either visible in the conference room in the mind’s eye when the client glances inside, or not visible, not conscious, and either barely listening or not at all from their station as less than conscious. Much therapy involves managing relationships among states and dealing with their various therapeutic alliances. Those alliances usually recapitulate family-oforigin dynamics and alliances and then memorialize part of the patient’s story of conflicts and double binds (Spiegel, 1986). If two parts each hold opposite ends of a double bind, there is unresolved friction between those parts until they both see that the conflict is due to the insolvability of the double bind and that each had an important role in surviving the pathology in the original situation. Each had the important job of being blind to the other end of the dilemma. To the end of mediating conflicts and double binds, among other goals, ego state therapy can be facilitated in the internal conference room, often as a structure in which to mediate conflicts between parts who may not understand each others’ function or concerns. This is the subject of Chapter 3 at length. Over time, additional resources or structures can be added to the conference room as required (Fraser, 2003). These additions might, for example, include a control panel with a rheostat for dimming the intensity of experience in the containment phase of therapy or to manage dysregulation at any stage. A microphone can be added to give a voice to mute or preverbal parts, especially with assistance from another part. Spiegel’s screen technique is well suited to the conference room (Spiegel & Spiegel, 2004) to allow memories to be played on a screen, at a distance. This method was also called “double dissociation” (Calof & Simons, 1996). Distancing maneuvers can also include a library (Kluft, 1990) where volumes or DVDs represent memories to be taken off the shelf and worked through when the time is right. Nurturance and containment can be provided to young forsaken parts by older parts of self, or even mythic imaginary caretaking figures in a rocking chair or other suitable venue (Paulsen, 2009a; Wildwind, 1992). A memorial garden in the mind’s eye, adjacent to the conference room, is useful to honor and remember whatever needs to be memorialized (Paulsen, 2009a). The therapist can suggest that metacognitions, negative or positive cognitions related to the work, be visibly framed on the wall in the conference room to support cognitive behavior therapy and the revision of cognitive distortions (Paulsen, 2009a). This technique also supports EMDR targets during the trauma-processing phase of treatment, also called “abreactive synthesis” (Paulsen, 2009 ). A calendar can be used to mark the passing of years since the occurrence of a traumatic event, made especially concrete for young parts of

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the self, using the appropriate number of Xs marked on the calendar (Paulsen, 2009). Decades and half centuries may be similarly expressed, graphically and concretely. A picture of an obituary that proves a perpetrator is dead (if dead), or a map of the distance between the patient’s present location and the perpetrator’s location, can be posted on the conference room wall; especially when the distance or time lapse involved is large. In short, there is no limit to the type and number of resources that can be added to the conference room.

Talking Through Versus Switching

One part can be used in the therapy to speak to or for other parts. Some patients can tolerate having the part of the patient that customarily shows up for appointments be that spokesperson or, more accurately, the “spokespart.” Some patients can’t tolerate this and another part needs to step in to help. This might entail a switch from whichever part is executive to another part more suitable to speak for other parts. Bypassing the front part is desirable to maintain the amnesia barrier, so that the necessary and painful work can be conducted by an intact amnesia barrier, even as the front part(s) of self are conducting the functions of life, such as holding down a job or being a parent. Alternatively, the therapist might also bypass the front part, and speak to the entire system, which is referred to as “talking through” or alternatively “talking over.” These and other hypnotic interventions have been extensively addressed elsewhere (see, e.g., Kluft, 1990, 2013; Kluft & Fine, 1993; Putnam, 1989; International Society for the Study of Trauma and Dissociation [ISSTD], 2011). By these means, the therapist addresses herself ostensibly to whatever part is executive but in fact aims to be heard by multiple internal parts, or the entire system. The first author refers to this as an “all points bulletin” when done overtly, or “lobbing a message over the net” when done more subtly. This messaging is done without enlisting the active effort or overt consent of the executive part. Talking through a part is often more convenient than causing overt switching from state to state. Talking through also sometimes protects against forcing premature conscious awareness on the currently executive state or engaging conflict or defensive stances, rather than eliciting a switch of executive states to each part the therapist needs to address in the moment.

Tucking in/Closure at the End of Session

At the end of any session involving ego state work, the clinician enhances safety, stability, and patient investment in the work by consistently employing a procedure for both containing that which has been pulled forward in the session and closing down the session. Whatever method is used, different approaches may be in order for differing clinical situations. The desired net effect is for affects to be adequately modulated; patient leaves the office, their affect is comfortable enough, states that are well functioning are in executive control, disturbing material is out of acute awareness, and parts whose process is incomplete are safely ensconced internally. The therapist’s commitment to this regular procedure is acting as a resource in this process, rather

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than the precipitants of unregulated dysphoria, a potential enactment of the patient’s original experiences of a parent’s abuse or failure to protect. A range of approaches exist, which make use of direct or indirect hypnotic techniques, imagery, internal locations or protocols, parts with assigned roles, and objects in the clinician’s office, among many other things. Various writers have long emphasized the importance of restabilizing and containing affective disturbance at the end of each session (e.g., Philips & Frederick, 1995). Notably, Kluft’s “rule of thirds” emphasizes spending the last portion of the session in restabilizing the patient (Kluft, 1993). It’s especially critical to make sure the part that needs to drive home is fully executive. Paulsen has elsewhere detailed her two-step process of “tucking in,” which makes efficient work of these general postintervention stabilization principles (Paulsen, 2009a, 2009b). The first step, nonegotized aspects of memories, such as behavioral, affective, bodily sensation, or cognitive (behavior, affect, sensation, and knowledge [BASK]) channels of information, or memory fragments, are contained using concrete container imagery. Various ego states may be enlisted to assist with this step. The container, when its lid is securely holding disturbing material, may be placed on a shelf in a vault, or sent down an elevator until it is accessed “when the time is right” (Paulsen, 2009a). In the second step, ego states that have been pulled forward by the session’s work are invited to be “tucked in” on such imagery as a “fluffy white cloud” (Paulsen, 2009a), and so forth. In an often necessary third step to this otherwise two-step process, the therapist checks the status of the conference room. If it isn’t empty and “lights out,” then the therapist invites “whoever is there” to explain his or her concern. If it is a hurt child part, the therapist concretely explains why it is in the child state’s best interest to step back so that the front part will be willing to allow future contact between therapist and patient since they are all in the same body. Special steps are required to handle containment when hostile or protective parts are forward, as they may not take direction peaceably. Hostile parts are protective defenses, and so are joined by paradoxically assuring them that the therapist won’t struggle to make them go, and yet pointing out there is a watch tower on the horizon with binoculars to keep an eye on things and a comfortable hammock in case the fierce part becomes weary and wishes a nap, as their “burden is very great.” Scripting for these special steps are detailed elsewhere (Paulsen, 2009a, 2009b). ACCELERATING AND BRAKING SYSTEMS

The hypnosis tradition offers a wealth of strategies for helping a patient or parts of the self-system access or distance from disturbing material held in various states. Kluft (1993) refers to this as temporizing the work because it buys time and enables interruption of work that might be destabilizing if attempted too soon. For an assortment of detailed hypnotic interventions applicable to these tasks, see, for example, the “Big Red Book” (Hammond, 1990). Also, see Barabasz and Watkins (2004), Watkins and Barabasz (2007), Kluft (1988, 1993, 2013), Spiegel and Spiegel (2004), Erickson in Rosen (1991), and Watkins and Paulsen (2003). Time can be accelerated or decelerated in recalling or processing memories. Problematic anniversary dates of traumatic events can be slept through by means of a hypnotic suggestion

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to frightened parts. Many patients benefit from learning to regulate access to or distance from disturbing material using hypnotic procedures. Techniques include those that access internal or external resources as well as direct tools for accessing and distancing, and “braking” maneuvers. Over time, these tools will evolve into temporizing skills that will be used to attenuate affective intensity in trauma processing (Fine, 1991; Kluft, 1990). As mentioned previously, one notable imaginal means to regulate and structure access to states, internal relations, and affectively charged material is Dissociative Table (Fraser, 1991, 2003), in which ego states/parts of the self can meet, learn to interact, and discuss points of view. This is a place in which states can variously be in ego (first person, subjective) and in object awareness (third person, objective; Watkins & Watkins, 1997). In the early phase of treatment, in which the emphasis is on safety, the therapeutic frame and relationship, and stabilization, the purpose of building the patient’s capacity to access inner material is more oriented to accessing and intentionally shifting states than to accessing traumatic held material. Among the internal features can be containers of security, such as a vault or library (Kluft, 1990) to contain memories, images, or stories. Such images can enhance containment of affect, while still allowing parts, including those related to the material being set aside, to talk to the therapist and each other while they are in the conference room. The segregation of adverse materials while arranging the locus of attention to only specific aspects of the self tends to pace the work, allowing the necessary preliminaries to be accomplished with minimal dysregulation. By the time they arrive in therapy, many patients will already have effective imagery for containing or distancing from disturbing material, perhaps including a package wrapped with bows, a post office with locked boxes, a shelf with shoe boxes, an oil refinery, and so forth. The therapist should be careful to distinguish these containers from containers the system has developed to segregate parts, such as towers, high walls, separate layers or levels, closed chambers, sedation, “death” or “sleep,” and so forth. Adding Ego or Object Energy

A self-system may be understood to be as if on a turntable, with the ability to rotate so that different parts can be executive or imbued with ego energy at various times. One or another part of self must always be executive, so the body is held up, or “owned” during the therapy. There are minor exceptions such as periods of sleep or temporary blank periods, including high-stress or conflicted episodes of interstate transition or other single-purpose automatic states. Whatever parts are not executive, that is, imbued with ego energy, have some degree of object energy or are out of awareness completely. It is beneficial at times to deliberately add ego energy, to increase ownership of experience as a means of accelerating the work, or the patient’s felt sense of it. At other times, it is beneficial to add object energy, to distance from painful material where it is too intense. The therapist might also add object energy in order to add objectivity or insight. Object awareness tends to enlist neocortical resources with a more adult perspective or invite psychoeducation to accomplish an adult perspective.

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Why It is so Important to Work Directly With Parts

The concepts of ego and object awareness (originally called ego and object cathexis; Federn, 1952; Watkins & Watkins, 1997) are likely the most arcane in this chapter, with their origins in psychoanalytic theory. Yet, there is no plainer way to speak of the important dimensions of what is in conscious awareness and executive, and what is in conscious awareness as an object of attention, rather than the subjective experience. If it isn’t palpably staged and forward it is very hard to change. If it is owned and in the ego it can be kneaded and rolled into a shape that will permit transformation and healing. Therefore, illustrations of these two concepts may help the reader understand how imperative and useful they are in effecting healing. In using the conference room method, one part of patient Greta Marie (a fictitious name) is executive, sitting in the therapist’s office chair and glancing into her own mind’s eye (namely, the hypnotically induced conference room; Fraser, 1991, 2003), and she says, “I see a girl with pigtails.” The part in the chair is in ego-awareness (also called ego-cathected or egotized) and the Girl With Pigtails is in object awareness (also called object cathected). If the therapist says, “Girl With Pigtails, what do you want us to know?” then that intervention adds ego energy to Girl With Pigtails, who then gets pulled into ego awareness by the intervention. She is staged, forward, executive, and ready to go. This is similar to the situation in which one is listening idly in class, contemplating the lunch break, when the instructor calls one’s name. Suddenly, one sits up straight and pays attention. The same effect occurs in the conference room when a therapist bypasses any number of parts to call a specific part by its name or function. Using its functional handle or name in this way adds energy and pulls the client’s attention to that part, usually with ego awareness. When the Girl With Pigtails says, “I’m scared,” and more so if the part is also executive of the body, then that part is in ego awareness. If Greta Marie instead says, “I don’t think she wants to speak with you, she looks mad,” then the Girl With Pigtails part of Greta Marie is still in object awareness, and the front part of Greta Marie is still executive or in ego awareness. If the therapist, in an abundance of cautious or absence of spine, fails to engage the part of the person holding the symptom and therefore the key to its transformation, nothing much will change. If the therapist speaks directly to the part of self holding the symptom and its reinforcing reasons, those motives can be brought online by calling its name, causing it to look through the eyes, be owned in the moment. The opportunity is there to process it, transform it, and release it into the ether so that a more adaptive frame of reference can take its place.

Other Distancing Maneuvers

The therapist can teach the patient how to achieve temporary distance from disturbing material using a variety of images. If pathological dissociation is like an “off and on” switch, then purposeful control over one’s exposure to upsetting material may

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be symbolized and achieved through a hypnotic dimmer switch. This will effectively regulate distance from disturbing material while providing a greater sense of mastery over the material. Though more relevant to the trauma-processing phase, merely introducing the possibility of controlling one’s exposure to troubling memory can itself be stabilizing early in treatment. That increased sense of safety and self-control is further enhanced as therapist and patient practice making use of the internal rheostat. As Judith Herman stated succinctly, “Trauma is the experience of being made into an object” (Herman, 1992). Attaining or regaining control, within a secure relationship with the therapist, is part of achieving safety and of reestablishing the nonobject status of the traumatized person. Other hypnotically available tools for regulating proximity to disturbing material include movie, television, or computer screens that can be moved closer or farther away; or projectors that adjust to let the image slip out of focus and become blurry or indistinct and partially in object awareness, rather than in ego awareness. The term “therapeutic container” describes the therapist’s role as sharing in the holding of traumatic memories so the patient doesn’t bear his or her burden alone (Kluft, 1982; Philips & Frederick, 1995). The concrete metaphor of a container with a lid is also used to suggest one can “keep the lid on” emotions and disturbing memories until a suitable time (Paulsen, 2007). The therapist can suggest that the patient envision a future date in which a certain achievement is in place, a symptom is resolved, or an outcome occurs, with the subjective felt sense of vividness of how it would feel, or with an objective view of how that would look.

Containment Using Objectivity

Paulsen (2009a, 2007) described a two-step process that enables the holding of traumatic memories in containment images, followed by a “tucking in” of ego states in a conditioned closure process at the end of each session. It resembles the skillful parent’s bedtime routine, helping a child settle down for a good night’s sleep and in the process teaching skills related to intentional and orderly state change. The therapist doing a containment procedure may subtly shift from the pronoun “you” to the pronoun “he” or “she,” which implies that the part previously executive is now “over there,” which further suggests that another part, probably the part appropriate for driving home, is coming into the executive position. The details of the containment decision tree are beyond the scope of the chapter and have been described elsewhere (Paulsen, 2009a). However, it is critical that the therapist carefully egotize the appropriate part of self at the end of any session in which ego state therapy has been used so that parts carrying disturbance are in object awareness or out of awareness and distant at the end of the session for safe transportation and for a higher functioning week. If problematic states are left in ego awareness the patient’s week is likely to go badly, with decreased functioning, higher levels of disturbance, and less enthusiasm for the work. When problematic states do not wish to “tuck in,” special conversations are needed to enlist their motivation in the containment process, described elsewhere (Paulsen, 2009a).

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Object Awareness Maneuvers

Many patients lack the capacity for compassion for their own traumatic experience or self-states. The use of an objective hypothetical other can be beneficial in achieving distance from the otherwise overwhelming subjective felt sense of a painful memory. The first author uses a hypothetical family in Pocatello (or Poughkeepsie or Tuscaloosa) that the patient does not know, to achieve an objective distance from a discussion topic. When the patient slides into the subjective felt sense, saying, “That’s fine for THEM, but not for ME because I was evil and bad,” the therapist patiently answers, “We aren’t talking about you right now, we are talking about Amy in Pocatello, whom we don’t know.” This forces the patient to hold the topic and related images in object awareness, which in itself is a distancing maneuver. It is typically necessary to provide the therapist’s presence as an anchor in such imaginal scenes, as in, “Imagine we are walking down the street in Pocatello, and we come across this scene, similar to what you describe, except we don’t know this girl and this family.” The presence of a “we” instead of just the patient’s “I” helps the patient to not slide into the subjective felt sense of the experience (ego awareness) but to rather observe the scene with adult resources and objectivity (object awareness) from the shared position on the sidewalk in Pocatello. The therapist by this means anchors the point of view of a mindful observer. As therapy continues, the regular exploration of ego and object awareness of various topics will work to remediate intersubjective developmental milestones that were not met during an impoverished attachment period. That is to say, as if by adding three-in-one oil to a rusty hinge, the client who develops fluency and switching from “I” to “thou,” as the therapist adds variously ego or object awareness, will be going a long way to repair narcissistic injuries in the intersubjective developmental milestones. The therapist can utilize the traumatized client’s dissociative abilities to rely on what can be thought of as double dissociation using the “screen technique” (Spiegel & Spiegel, 2004). Using formal trance or indirect suggestion, the client and therapist may be in a theater, seated some distance back from the screen, about to watch a stranger’s story with interest. What unfolds on the “screen,” solicited from the client’s unconscious resources, will be the target material, often the revelation of a traumatic circumstance that occasioned the emergence of a part whose way of functioning is now troubling for other parts of the self-system. An empathic understanding for the anonymous person, often a child, up on the screen, can eventually lead, through the use of titrating techniques, to a rapprochement or deeper understanding of the purpose and suffering of the formerly troubling part. Titration of the recognition of the identity of the person on the “screen” can be arranged through dreams, or a slow dawning, or in any other way that will allow the well-paced absorption of the implications of what was on the screen. For example, one client began to weep upon seeing what was on the screen. When the therapist felt concern that the dissociative technique had failed because the client was crying, the client whirled, saying, “Look, I may not know who that boy is, but that’s a darn sad story!” Indeed, and sadly, as he came to recognize, it was his story, and revealed to other parts just how hard things had been for the abuser-resembling part who had handled that sort of “work” from then on. Whether it’s a family in Pocatello, or an internal movie theater, techniques

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like these are powerful and constructive applications of the client’s existing psychological and neurological posttraumatic avoidance strategies. The conference room can be visited not only as an accessing technique but also as a distancing technique as well. It is a powerful way to employ object awareness to increase experiential distance from a disturbing felt sense. A patient may report that a child part is frightened by monstrous threats, and that experience of fright is the focus of the patient’s awareness, as may be the monster’s shame at being monstrous. Both are subjective felt senses and so, by definition, are in ego awareness. If the patient is asked to look at the “monster” in the conference room, surprise and insight often result from using object awareness to examine that monster “over there.” The monster may in fact be an angry 2-year-old or other being, huffing and puffing in an attempt to be as frightening (and potentially as defended or defending) as possible. Once this objective information is elicited, an opportunity has been created to educate various parts about the “monster’s” role, with reciprocal openings for appreciation, compassion, and reconciliation with the self.

Pacing the Work of the Emotional Personalities (EPs)

In the structural theory of dissociation, the two primary functional categories of self-states are the EPs and the apparently normal personalities (ANPs; van der Hart, Nijenhuis, & Steele, 2006). In this model, EPs are likely to hold unprocessed traumatic experiences related to childhood trauma, and ANPs are likely to have functional roles in the world, and may take complete control of the body while “doing life.” The latter have also been referred to as “container kids” and “front parts” or “the faces that meet the faces” (Paulsen, 2009a). The term “host,” no longer in wide usage because it implies a greater legitimacy for one part over others, most likely refers to an ANP. The structural theory of dissociation, though not universally employed in the dissociation field, is used here to distinguish the features of the two functional categories of self-states.

Accelerating Using Somatic Awareness

Whenever the therapist needs to accelerate or intensify the patient’s awareness of a dissociated experience, asking about the felt sense in the body tends to add ego awareness to the experience. Sensation is by its nature always subjectively experienced. In an exception that proves the rule, a conversion symptom such as a hand that moves by itself, without subjective felt sense on the part of the part of the self-executive in a given moment, tends to be experienced as “that hand over there,” rather than “my hand,” although the hand may be partially owned as self. A therapist might then either interview the hand directly by saying, “Hand, we are listening, what do you want us to know?” or invite an ego state discussion, such as, “Would whatever part or parts of the self know about the hand’s story come into the conference room at this time? We want to hear what needs to be heard.” When this occurs later in therapy,

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the addition of EMDR processing of the fraction of a traumatic memory held by a part that emerges to tell the hand’s story can be a powerful accessing means.

EMDR

EMDR is a highly powerful means of accelerating access to traumatic material because it increases the likelihood of association of material that had been dissociated. Anecdotal proof is offered by a story offered by the late John G. Watkins, father of ego state therapy. He described having spent close to 70 years using self-hypnosis for personal work, including trying to resolve a troubling memory of a schoolyard bully. Upon experiencing EMDR for the first time in his 90s, he suddenly recalled, for the first time, the name of the schoolyard bully. This proved to him that EMDR was not hypnosis, but was an associative process (J. G. Watkins, personal communication, September 6, 2005). It is because EMDR is such a powerful intervention that it should not be used prematurely in the treatment of dissociative clients (ISSTD, 2011; Paulsen, 1995). The self-system needs to be on board and consenting to trauma processing, and the various introjects of perpetrators or parental figures must be oriented and brought on board with the goals of treatment in general and EMDR in particular before it is used in the treatment of dissociative identity disorder (DID). Additionally, the standard protocol of EMDR must be modified to avoid retraumatization, including fractionation methods to attenuate the size of the target, and titration methods to attenuate intensity. Some of these approaches have been described previously (e.g., Paulsen, 2008, 2009a, 2009b)

CASE EXAMPLE

Patient Greta Marie had been in treatment with a therapist who correctly diagnosed her as DID but resisted speaking to parts because she didn’t want to “reify the dissociation.” Eight years of supportive and cognitive behavioral therapy had transpired with considerable increase in affect regulation and decrease in PTSD symptoms, but there was no resolution of the essential dynamics that held the patient’s depression, generalized anxiety, obsessive compulsive disorder (OCD), and overall disability. The patient’s OCD was the need to avoid contact with cleaning detergents, which she feared were poisonous and would surely lead to her demise. The first author, after an initial assessment and rapport-building phase, asked to “speak directly to whatever part can help us understand about the need to avoid the Comet Cleanser.” A part came, angrily enough, saying, “It will kill us!” On inquiry, another part “snitched out” the angry part, revealing that she’d been in trouble at age 8 at school and at home for soiling her pants and was forced to clean up the mess with toxic cleaners, in a manner that was profoundly shaming. Not only was the experience shaming, but for her 8 years, no one in her family had helped her with strong emotions. She was left to manage as best she could, and the best she could do was cut off feelings and replace them with superstitious behavior and beliefs. When the therapist softly expressed compassion for the angry part of the self that had the terrible job of trying to keep the patient safe from chemicals, free from making

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soiled messes, and free from having emotions, the façade crumbled. The angry protective part wept, and was willing to “look through the eyes” during an EMDR processing. There were other important aspects of this client’s treatment, and each one in turn was staged in ego awareness, the only means by which the sequestered affect could be lanced and processed to an adaptive resolution. The processing was planfully titrated so that no part of the self would be overwhelmed, and the part of the self that “does life” was protected initially from the memories so that she could hold down a job during the period of the trauma work. When the patient had little or no access to traumatic felt sense, acceleration was applied to the processing by asking the part of the self holding the somatically felt sense to come “look through the eyes,” which stages the subjective felt sense forward in ego awareness. In contrast, when trauma processing was either too tense during processing or when the client needed a break from trauma work, deceleration was applied by explaining to the relevant parts the need for rest and pacing, and asking their cooperation in tucking in between sessions for a deep, healing sleep. Although sometimes the goal was acceleration by bringing states into ego awareness, at other times object awareness was used to gain insight, objectivity, and compassion by bringing in adult neocortical resources to get unstuck the material that had been held in extreme shame with subject awareness only, with large affective intensity. In that sense, objectivity can be used to decelerate pain intensity when processing won’t resolve, causing shifts with insight. These few examples within one case only touch on the myriad ways acceleration and deceleration can be used to pace trauma processing in complex cases.

CONCLUSION

This chapter has emphasized the stabilizing effects of special ego state therapy maneuvers that access, accelerate, or decelerate the pace of the work with dissociative patients. Ego state methods will continue to be elemental throughout the subsequent phases of therapy up through integration. Specifically, Chapter 4 discusses ego state therapy to realign relationships between states. Chapter 6 describes ego state and other methods to enable fractionation of trauma processing, later in therapy.

REFERENCES Barabasz, A. F., & Watkins, J. G. (2005). Hypnotherapeutic techniques (2nd ed.). New York, NY: Brunner-Routledge. Calof, D. L., & Simons, R. (1996). The couple who became each other: Stories of healing and transformation from a leading hypnotherapist. New York, NY: Bantam Books. Chu, J. A. (2011). Rebuilding shattered lives: Treating complex PTSD and dissociative disorders (2nd ed.). New York, NY: Wiley. Emmerson, G. J. (2003). Ego state therapy. Carmarthen, UK: Crown House. Federn, P. (1952). Ego, psychology and the psychoses (E. Weiss, Ed., pp. 5–6). New York, NY: Basic. Fine, C. G. (1991). The tactical-integration model for the treatment of dissociative identity disorder and allied dissociative disorders. American Journal of Psychotherapy, 53(3), 361–376.

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Fine, C. G. (1993). A tactical integrationalist perspective on the treatment of multiple personality disorder. In R. P. Kluft & C. G. Fine (Eds.), Clinical perspectives on multiple personality disorder (pp. 135–153). Washington, DC: American Psychiatric Press. Fine, C. G., & Comstock, C. M. (1989). Completion of cognitive schemata and affective realms through the temporary blending of personalities in the treatment of multiple personality disorder. In B. G. Braun (Ed.), Dissociative disorders (pp. 17). Chicago, IL: Rush University. Foa, E., & Hears-Ikeda, D. (1996). Emotional dissociation in response to trauma: An information-processing approach. In L. Michelson & W. J. Ray (Eds.), Handbook of dissociation: Theoretical, empirical, and clinical perspectives (pp. 207–224). New York, NY: Springer. Fraser, G. A. (1991). The Dissociative Table Technique: A strategy for working with ego states in dissociative disorders and ego-state therapy. Dissociation: Progress in the Dissociative Disorders, 4, 205–213. Fraser, G. A. (2003). Eraser’s “Dissociative Table Technique” revisited, revised: A strategy for working with ego states in dissociative disorders and ego-state therapy. Journal of Trauma & Dissociation, 4(4), 5–28. Hammond, D. C. (1990). Handbook of hypnotic suggestions and metaphors. New York, NY: W. W. Norton. Herman, J. L. (1992). Trauma and recovery: The aftermath of violence—From domestic abuse to political terror. New York, NY: Basic Books. International Society for the Study of Trauma and Dissociation (ISSTD). (2011). Guidelines for treating dissociative identity disorder in adults, third revision. Journal of Trauma & Dissociation, 12, 115–187. Jamieson, A. (2009). Today I’m Alice: Nine personalities, one tortured mind. London, UK: Pan MacMillan. Kluft, R. (1990). The slow leak technique. In D. C. Hammond (Ed.), Handbook of hypnotic suggestions and metaphors (pp. 526–530). New York, NY: W. W. Norton. Kluft, R. P. (1982). Varieties of hypnotic interventions in the treatment of multiple personality. American Journal of Clinical Hypnosis, 24, 230–240. Kluft, R. P. (1984). Treatment of multiple personality disorder: A study of 33 cases. Psychiatric Clinics of North America, 7, 9–29. Kluft, R. P. (1988). Playing for time: Temporizing techniques in the treatment of multiple personality disorder. American Journal of Clinical Hypnosis, 32, 90–98. Kluft, R. P., & Fine, C. G. (Eds.). (1993). Clinical perspectives on multiple personality disorder. Washington, DC: American Psychiatric Press. Kluft, R. P. (2013). Shelter from the storm. Charleston, SC: CreateSpace. Loewenstein, R. J. (2006). DID 101: A hands-on clinical guide to the stabilization phase of dissociative identity disorder treatment. Psychiatric Clinics of North America, 29(1), 305–332. Ogden, P., & Minton, K. (2000). Sensorimotor psychotherapy: One method for processing trauma. Traumatology, 6(3), 149–173. Paulsen, S. (1993). EMDR. In R. Corsini (Ed.), Encyclopedia of psychology (2nd ed.). New York, NY: Wiley & Sons. Paulsen, S. (1995). EMDR: Its cautious use in the dissociative disorders. Dissociation, 8, 32–44. Paulsen, S. L. (1992). Ego state therapy: When the patient is dissociative but not multiple. Presented at the Level II EMDR Workshop, Honolulu, HI. Paulsen, S. L. (2007, September). Integrating somatic interventions and EMDR: Keeping it AIP “legal”. Paper presented at the annual meeting of the Eye Movement Desensitization & Reprocessing International Association Conference, Dallas, TX. Paulsen, S. L. (2008, November). Conversion seizures manifesting as infant alters: EMDR, somatic, and ego state therapy. Paper presented at the annual meeting of the International Society for the Study of Trauma and Dissociation, Chicago, IL.

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Paulsen, S. L. (2009a). Looking through the eyes of trauma and dissociation: An illustrated guide for EMDR clinicians and clients. Charleston, NC: Booksurge. Paulsen, S. L. (2009b). ACT-AS-IF and architects approaches to EMDR treatment of Dissociative Identity Disorder (DID). In M. Luber (Eds.), EMDR scripted protocols: Special populations. New York, NY: Springer Publishing. Paulsen, S. L., & Watkins, J. G. (2005, November). Best techniques from the armamentarium of hypnoanalytic, EMDR, somatic psychotherapy and cognitive behavioral methods. Paper presented at the annual meeting of the International Society for the Study of Dissociation, Toronto, ON. Philips, M., & Frederick, C. (1995). Healing the divided self. New York, NY: W. W. Norton. Putnam, F. W. (1989). Diagnosis and treatment of multiple personality disorder (Foundations of Modern Psychiatry). New York, NY: Guilford Press. Rosen, S. (1991). My voice will go with you: The teaching tales of Milton H. Erickson. New York, NY: W. W. Norton. Shapiro, F. (2001). Eye movement desensitization and reprocessing: Basic principles, protocols, and procedures (2nd ed.). New York, NY: Guilford Press. Spiegel, D. (1986). Dissociation, double binds, and posttraumatic stress in multiple personality disorder. In B. G. Braun (Ed.), Treatment of multiple personality disorder (pp. 63–77). Washington, DC: American Psychiatric Press. Spiegel, H., & Spiegel, D. (2004). Trance and treatment: Clinical uses of hypnosis (2nd Ed). New York, NY: Basic Books. van der Hart, O., Brown, P., & Van der Kolk, B. A. (1989). Pierre Janet’s psychological treatment of post-traumatic stress. Journal of Traumatic Stress, 2(4), 379–395. van der Hart, O., Nijenhuis, E. R., & Steele, K. (2006). The haunted self: Structural dissociation and the treatment of chronic traumatization. New York, NY: W. W. Norton. van der Hart, O., Steele, K., Boon, S., & Brown, P. (1993). The treatment of traumatic memories: Synthesis, realization, and integration. Dissociation: Progress in the Dissociative Disorders, 6, 162–180. Watkins, J. G. & Barabasz, A. (2007). Advanced hypnotherapy: Hypnodynamic techniques. New York, NY: Routledge. Watkins, J. G., & Paulsen, S. L. (2003). Ego state therapy: EMDR and hypnoanalytic techniques. Workshop presented at the Society for Clinical and Experimental Hypnosis, Chicago, IL. Watkins, J. G., & Watkins, H. H. (1997). Ego-state theory and therapy. New York, NY: W. W. Norton. Wildwind, L. (1992). Treating chronic depression. Paper presented at the Annual Eye Movement Desensitization and Reprocessing Conference, San Jose, CA.

CHAPTER 19

Integrating Body and Mind: Sensorimotor Psychotherapy and Treatment of Dissociation, Defense, and Dysregulation Pat Ogden and Janina Fisher

The neural basis for the self, as I see it, resides with the continuous reactivation of at least two sets of representations. One set concerns representations of key events in an individual’s autobiography, on the basis of which a notion of identity can be reconstructed repeatedly, by partial activation in topologically organized sensory maps. The second set of representations underlying the neural self consists of the primordial representations of an individual’s body. Of necessity, this encompasses background body states and emotional states. The collective representation of the body constitutes the basis for a “concept” of self. —Antonio Damasio (1994)

Trauma-related disorders have long been characterized by a vacillation between intrusive reliving of past trauma, accompanied by dysregulated autonomic arousal and animal defenses, and numb avoidance of traumatic reminders, accompanied by constriction, loss of energy, and diminished pleasure (Chu, 1988; van der Hart, The authors wish to thank Onno van der Hart, PhD, and Kathy Steele, MN, CS, for their contributions to this chapter. 

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Nijenhuis, & Steele, 2006; van der Kolk, McFarlane, & Weisaeth, 1996). Both symptom clusters reflect the body’s efforts to survive and adapt to a threatening environment. Reliving occurs as subcortical survival responses—animal defenses of fight, flight, freeze, and feigned death—that are repeatedly ignited by exposure to stimuli directly or indirectly related to past trauma. In these situations, activities of daily life are interrupted as the organism prepares to respond to stimuli assessed as dangerous or life threatening. However, the ability to resume daily life functioning and refocus on work, family, and community when the apparent threat is over is also crucial for adaptation and survival. In order to do so, the traumatized individual attempts to avoid both external reminders and internal triggers (i.e., thoughts, emotions, and body experience) connected to the trauma. In threatening environments, both avoidance and animal defensive responses allow adults and children alike to mobilize adaptive behavior in response to changing environmental demands. However, biphasic alternations between reexperiencing traumatic reminders (which elicits animal defense) and avoiding them in order to engage in daily life result in the encoding of self-states that hold procedurally learned tendencies associated with these two responses: particular constellations of autonomic, affective, cognitive, perceptual, and motor responses. These trauma-related self-states become dissociative parts of the self that are dysregulated, discontinuous, often disruptive to daily life, and resistant to integration. In this chapter we will focus on the relationship between dissociative parts of the self or personality and discrete psychobiological behavioral or “action” systems that are aroused in response to conflicting demands of defense and avoidance. We will present approaches from sensorimotor psychotherapy (SP) that highlight the use of controlled actions to help overcome traumatic repetitions and fixed defenses of flight, fight, freeze, and feign death/collapse; promote more flexibility among action systems; and support integration of body and mind.

PSYCHOBIOLOGICAL ACTION SYSTEMS AND DISSOCIATION

Understanding psychobiological systems that organize responses to both internal and environmental stimuli can help unravel the complexity of trauma-related dissociation. In SP, we draw upon the theory of structural dissociation of the personality developed by van der Hart et al. (2006), a theoretical construct that conceptualizes traumatic dissociation as an integrative failure along the lines of neurobiologically organized response to trauma-reflecting psychobiological systems. These systems are epigenetically hardwired, self-organizing, self-stabilizing, open to classical conditioning, and adaptive in nature (Cassidy & Shaver, 1999; Nijenhuis, van der Hart, & Steele, 2002; Panksepp, 1998; van der Hart et al., 2006). They can be categorized into two general types: the animal defense systems stimulated by danger and life threat, and the daily life systems stimulated by nonthreatening environmental demands of work, learning, family, and community responsibilities (van der Hart et al., 2006). A variety of terms describe similar concepts: behavioral systems (Bowlby, 1969/1982); motivational systems (Gould, 1982; Lichtenberg & Kindler, 1994); functional systems

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(Fanselow & Lester, 1988); and emotional operating systems (Panksepp, 1998). We have chosen to follow the lead of van der Hart et al. (2006), who call these systems action systems because each system’s goals are supported by particular physical (behavioral and physiological) and mental (emotional and cognitive) actions. Daily life action systems motivate us to engage in a variety of adaptive activities in a safe environment: form close attachment relationships, explore the environment, play, participate in social relationships, regulate energy (i.e., eat, sleep, etc.), reproduce, and care for others (Bowlby, 1969/1982; Cassidy & Shaver, 1999; Fanselow & Lester, 1988; Lichtenberg, 1990; Lichtenberg & Kindler, 1994; Marvin & Britner, 1999; Panksepp, 1998; van der Hart et al., 2006). Whereas daily life systems emerge in a context of environmental safety, defensive subsystems are catalyzed under dangerous or life-threatening conditions. Under threat, an infant’s first instinct is the “attachment cry,” designed to elicit the help and protection of someone stronger (distinguished from attachment-related behavior designed to secure and maintain enduring attachment relationships). Additional animal defenses that mobilize the body to flee or fight become available as the infant’s motor capacities mature. The animal defense of freeze immobilizes the body and heightens the senses to detect additional information. The last line of defense, also immobilizing, is to feign death—to collapse and endure whatever harm is to follow. Specific physical actions that serve the purpose of each system are stimulated when a system is aroused. For example, when separation from the attachment figure exceeds a child’s comfort zone, either in terms of time or distance, the attachment action system is stimulated. This system organizes proximity-seeking behaviors: reaching out, holding on, facial expressions such as smiling, eye contact, shaping (Stern, 1985), that is, conforming to the mother’s body, and so forth (Ainsworth, 1963; Bowlby, 1988; Lyons-Ruth & Jacobvitz, 1999; Schore, 1994). These actions, as well as infant participation in mother–child game playing and certain verbal prosody, pitch, and sound, induces attachment-related behavioral sequalae in contexts of safety as well. Each daily life action system is characterized not only by specific behaviors but also by emotions typical of that system. The curiosity of the exploration system fuels seeking and orienting movements that enable the investigation of novelty: learning opportunities, challenges at work, the tasks of parenting. The play system, characterized by laughter, involves a variety of movement patterns: tilting of the head, relaxed, open posture, and nonstereotyped movements that change quickly (Beckoff & Allen, 1998; Beckoff & Byers, 1998; Caldwell, 2003; Donaldson, 1993). The caregiving system, often stimulated by empathy, manifests in “subtle, warm, and soft” (Panksepp, 1998, p. 247) behavior as the caregiver attunes voice, behavior, and touch to the needs of the person being cared for. A wide variety of emotions and behaviors that include gestures, facial and bodily expressions, and vocalizations accompany social communication. The reproduction system, accompanied by feelings of lust and attraction, incorporates specific movement sequences characteristic not only of sexual behavior but also of courtship and flirting: eye contact, smiling, vocalization that is both of a higher pitch and augmented volume, and exaggerated gestures (Cassidy & Shaver, 1999). When threat is perceived, defensive actions that appear to best serve survival are stimulated. Defensive subsystems manifest in a variety of movements and emotions

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consistent with particular survival demands. If caregivers are nearby, the attachment cry may be the best option, usually accompanied by feelings of desperation and exaggerated proximity-seeking actions such as clinging and reaching movements. If escape seems possible, flight will be the instinctive defense of choice. Feelings of fear, physical postures of pulling back, impulses to run or move away in the legs and feet, a heightened awareness of exit routes, fear, and thoughts of escape might accompany a flight defense. When aggression appears likely to be effective, or when the victim feels trapped, the fight response is typically provoked, accompanied by tension and readiness in the arms, heightened arousal, anger, and an aggressive manner. But when these mobilizing defenses prove ineffective or maladaptive, such as in instances when a fight response might provoke more violence from the perpetrator or when the perpetrator and attachment figure are one and the same, passive avoidance or immobilization behaviors, with concomitant terror and helplessness, are the only survival strategies remaining (e.g., Allen, 2001; Misslin, 2003; Nijenhuis et al., 1998; Nijenhuis et al., 1999; Rivers, 1920). The “freeze” response is usually distinguished by muscular contraction and stiffening, coupled with high anxiety and hyperalertness. Numbness, flaccidity in the musculature, floppy immobility, flat affect, and reduced cognitive capacity are characteristic of death-feigning defense. The emotional demands of each action system and the physical actions that serve its needs are associated with particular patterns of sensory perception. When defensive systems are aroused, perceptions become heightened to threat cues. When the attachment system is stimulated, perceptions become attuned to the proximity of the attachment figure. If exploration is aroused, the senses become heightened to novel, interesting stimuli. Different contexts will evoke different perceptual organization: for instance, the exploration of a research topic requires a different perceptual and motor organization from the exploration of a hiking trail. The habits of an individual’s response to the arousal of any action system are developed early in childhood, as these responses are adjusted to the behavior of the early attachment figures. For example, if attachment figures are unreliable, proximity-seeking behaviors may become hyperactive. If attachment figures are neglectful or unavailable, or punishing in the face of need or vulnerability, proximity-seeking behaviors may cease or be replaced with approach-avoidance patterns of response (Liotti, 1999). If attachment figures are restrictive or overly cautious, the impulse to explore may be hindered. In traumatogenic environments where attachment figures are abusive and/or neglectful, full engagement in daily life action systems is disrupted by dysregulated arousal and animal defenses. Recall that action systems are hardwired; their goals “extend over long periods of time, with the behavior needed to achieve [them] being adjusted flexibly, in a nonrandom fashion, to a wide range of environments and to the development of the individual” (Cassidy & Shaver, 1999, p. 651; George & Solomon, 1999). For example, the goals of the exploration system remain relatively constant throughout the life span, even though the behavior required to accomplish these goals is modified and developed as the individual matures and as the environment changes. For the chronically traumatized individual, however, increasing maturity and/or environmental safety and stability may not markedly change patterns developed in a traumatogenic environment. The goals of the defensive system that are stimulated by traumatic reminders— to defend and protect—conflict with the goals of daily life action systems—to engage

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with other people and the environment. Each system stimulates contradictory emotions, thoughts, and physical actions. Responding to the arousal of daily life systems—such as the needs of one’s children, the demands of work, or the sexual needs of one’s partner—requires keeping the emotions, thoughts, and defensive responses associated with past trauma at bay. However, traumatized individuals accomplish this with varying degrees of success. Reactivating stimuli repeatedly catalyze the defensive action systems, which encroach upon and interrupt tasks pertaining to the action systems of daily life. The ability to perform at one’s job may be compromised by animal defense-related insomnia; experiences of play and the accompanying laughter may evoke fear or shame followed by avoidance; sexual relations might arouse the attachment cry or immobilizing defenses. Thus, defensive actions become default behaviors that take precedence over actions that could theoretically fulfill the goals of action systems pertaining to daily life unrelated to threat. Therapists may be baffled or confused when the conflict between defensive and daily life action systems emerges in the therapy hour as different dissociative parts come forward as different action systems emerge. For example, a patient whose heart rate escalates in social situations involving eye contact experiences a defensive response of wanting to run when her eyes meet her therapist’s, a conflict between daily life action system of sociability and a flight defense. Her accelerated heart rate and the tension in her legs and feet fuel trauma-related emotions of fear and dread, all related to the fight response. These reactions sabotage her ability to accurately appraise current reality and respond to the arousal of the daily life action system of sociability to interact with her therapist. Unable to feel safe, or to physically leave the therapy office, her arousal plummets as she instinctively resorts to a version of the feign death response; she looks away, and becomes unresponsive for the remainder of the session. If a traumatized person repetitively and persistently experiences biphasic alternations between defensive and daily life systems, the result will be increasing compartmentalization rather than integration. Janet (1889, 1907) noted this division of the personality when he wrote about the successive alternation of “psychological existences” in traumatized individuals: In one [condition], he has sensations, remembrances, movements, which he has not in the other, and consequently he presents, in a manner more or less clear . . . two characters, and in some sort two personalities. (p. 491) What began as a necessary defense in the face of a real threat becomes a pervasive, unrelenting reaction to the anticipation of threat, with all the concomitant changes in physiology and physical tendencies (Ogden, Minton, & Pain, 2006). The alternation of reexperiencing with numbing and avoidance becomes habitual and anticipatory. As Steele, van der Hart, and Nijenhuis (2005) state, Metaphorically speaking, fault lines occur between action systems of daily life and those of defense, because they naturally tend to mutually inhibit each other. For example, one does not stay focused on cleaning the house or reading when imminent danger is perceived; instead one becomes hypervigilant and prepares for defense. Then, when danger has passed, one should naturally return to

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normal activities rather than continuing to be in a defensive mode. Integration between these two types of action systems will more likely fail during or following traumatic stress. (p. 17) In such situations, one part of the self or personality remains fixated on defense against threat, while the other part is dedicated to carrying out the activities of the daily life action systems: those of attachment, energy regulation, exploration, play, sociability, reproduction, and caretaking. The animal defense parts, triggered by exposure to unintegrated fragments of traumatic memories, remain fixated on the trauma and on surviving it, repetitively rekindling the defensive action systems. Note that the language of “parts” is not intended to imply an actual division of the personality into discrete, separate entities but rather to describe the compartmentalization of the relationships between encapsulated action tendencies. Dissociative parts, each mediated by an action system, are not completely separated or split, but have some overlap and permeable boundaries. The term “parts” of the personality is used as “metaphoric descriptive labels of mental [and somatic action] systems that have failed to integrate” (van der Hart, van Dijke, van Son, & Steele, 2000, p.39; Steele, van der Hart, & Nijenhuis, 2004).

DISSOCIATION AND THE NERVOUS SYSTEM

When a person is triggered by dissociative parts of the personality, accurate appraisal of environmental stimuli is compromised at a basic neural level. Stephen Porges coined the term “neuroception” to highlight a neural process that discriminates degrees of environmental safety, danger, and life threat. According to Porges (2011), “the nervous system evaluates risk in the environment and regulates the expression of adaptive behavior to match the neuroception of an environment that is safe, dangerous, or life-threatening” (p. 17). Neuroception occurs unconsciously and automatically when subcortical areas of the brain stimulate neural circuits (Porges, 2011). When a person’s environment is “safe enough” so that the social engagement system is on line, the action systems of daily living predominate. Neuroception of danger or life threat will not be biased by a chronically dysregulated nervous system. However, neuroception is affected by experiencedependent anticipation, as illustrated by the tendency to neurocept danger or life threat in the presence of cues associated with previous traumatic experiences. Engagement with daily life action systems requires the participation of the ventral vagal complex, or “social engagement system,” which involves the ventral branch of the vagus nerve, the myelinated vagus. This complex system facilitates responding to daily life action systems in two ways: (a) by maintaining arousal within a window of tolerance (Siegel, 1999) such that affect and arousal are well-regulated, and (b) by governing areas of the body that are utilized in social and environmental interaction. Porges (2005) clarifies, The social engagement system has a control component in the cortex (i.e., upper motor neurons) that regulates brainstem nuclei (i.e., lower motor neurons) to control eyelid opening (e.g., looking) facial muscles (e.g., emotional expression), middle ear muscles (e.g., extracting human voice from background noise),

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muscle of mastication (e.g., ingestion), laryngeal and pharyngeal muscles (e.g., prosody), and head tilting and turning muscles (e.g., social gesture and orientation). (p. 35) Available to the full-term infant, this neural regulation of facial muscles serves to increase proximity and facilitate the attuned interaction between infant and caregiver that assures the infant’s survival. The social engagement system is further developed, along with the ability to respond in more sophisticated ways to daily life action systems, via attuned interactions built upon a series of face-to-face, brain-tobrain, body-to-body nonverbal communications with attachment figures that effectively regulate the child’s autonomic and emotional arousal. In order to respond to daily life action systems, and thus to adaptively engage with others and the environment in a nonthreatening context, one must neurocept some degree of safety via the ventral vagal complex. The social engagement system is overridden, however, during trauma and when reminders of the trauma arouse the defensive system. If danger is neurocepted, the sympathetically mediated animal defenses of attachment cry, fight, flight, and alert freeze are aroused to ensure survival. Note that the “attachment cry” response, which occurs in response to neuroception of danger, is quite different from social engagement system-related attachment behaviors that emerge in the context of the neuroception of safety. Attachment cry responses are accompanied by autonomic hyperarousal, anxious-proximity-seeking, and rejection sensitivity. Freezing, or “alert immobility” (Misslin 2003, p. 58), also involves a highly engaged sympathetic system in which muscle tone, heart rate, sensory acuity, and alertness are all high (Lewis, Kelly, & Allen, 2004) to help the person appraise the situation more fully before taking action. Although hyperarousal has commonly been considered the hallmark of posttraumatic stress disorder (PTSD), not all traumatized individuals respond to trauma reminders with hyperarousal; in a script-driven provocation study, 30% of subjects responded with hypoarousal in response to hearing their trauma scripts read (Lanius et al., 2002). This finding might be attributed to the failure of both the social engagement system and the sympathetically mediated defensive responses to assure safety. Parasympathetic nervous system activity via the dorsal vagal complex becomes the next and best line of defense. The neuroception of life threat (as contrasted with the neuroception of danger when survival still appears to be possible) stimulates the dorsal vagal system to enable survival-related immobilization: feigning death, behavioral shutdown, and syncope. The dorsal branch of the vagus nerve, the unmyelinated vagus, is the most primitive of these systems and is available at birth (Porges, 2011). When this system is aroused, sympathetic arousal quickly changes “from interactive regulatory modes into long-enduring less complex (dorsal vagal) autoregulatory modes” (Schore, 2009, p. 8). In these hypoaroused states, observed even in newborns (Bergman, Linley, & Fawcus, 2004), the infant or child is nonreceptive to interactive regulation (Schore, 2009). Many functions of the body begin to slow down, leading to “ . . . a relative decrease in heart rate and respiration and . . . a sense of ‘numbness,’ ‘shutting down within the mind,’ and separation from the sense of self” (Siegel, 1999, p. 254). When action is not feasible, extreme dorsal vagal arousal can result in fainting, vomiting, or loss of control of the rectal

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sphincter (Frijda, 1986). This final defensive response is often called “total submission” (van der Hart et al., 2006). The hierarchical relationships between ventral vagal parasympathetic (social engagement), sympathetic, and dorsal vagal parasympathetic systems are established early in life, resulting in enduring arousal tendencies, reactions under stress, and even vulnerability to psychiatric disorders (Cozolino, 2002; Lyons-Ruth & Jacobvitz, 1999; Porges, 2011; Schore, 2001, p. 209; Sroufe, 1997; Van Ijzendoorn, Schuengel, & Bakermans-Kranenburg, 1999). Early trauma, especially repeated trauma, “functionally retunes neuroception to conservatively detect risk when there is no risk” (Porges, 2011, p. 253). Traumatized individuals lose the ability to accurately assess whether other people or the environment are safe, trustworthy, or dangerous, and thus have developed “faulty” neuroception (Porges, 2011). Some parts of the self may be biased toward ignoring threat detection to engage in daily life action system. Other parts, driven by animal defenses, will be biased toward threat detection rather than safety detection, toward sympathetic or dorsal vagal responses rather than social engagement. Thus, engagement with daily life actions systems, which require a neuroception of safety, is hampered or prevented. Janet (1907, p. 332) pointed out a century ago that individuals with complex trauma-related disorders develop “a tendency to the dissociation and emancipation of the systems of ideas and functions that constitute personality.” Neuroception of safety, danger, and life threat can become compartmentalized. When hyperarousal (reflecting neuroception of danger) and hypoarousal (reflecting neuroception of life threat) become extreme and enduring responses and processes that are normally unified and integrated may become chronically dissociated. While some authors (Perry, Pollard, Blakely, Baker, & Vigilante, 1995) associate dissociation only with hypoaroused conditions, Janet’s (1889, 1907) description of dissociation as a failure of integrative capacity applies to both hypoaroused and hyperaroused states (Allen, 2001; Krystal, Bremner, Southwick, & Charney, 1998; van der Hart, Nijenhuis, Steele, & Brown, 2004). An example of this is seen in a patient whose dissociative hyperaroused state associated with an unintegrated “fight” defense manifested as explosive aggression that led her to physically abuse her children when they disobeyed her in minor ways, behavior that she profoundly regretted when she “came back to herself” and to the part able to neurocept safety and engage in daily life action systems. When traumatic reminders repeatedly stimulate these extreme arousal states, neuroception becomes biased toward danger or life threat. It is important to note that in traumatized individuals, under circumstances when overall arousal remains within the window of tolerance, the part of the self that neurocepts safety remains separate from, that is, not integrated with, the parts of self that neurocept danger and life threat. Under these circumstances, the individual’s ability to process and integrate trauma-related information is compromised even when arousal is within the window of tolerance. Both current reminders of past trauma and the parts that hold these memories are avoided rather than integrated. Thus, in the same environmental situation, one dissociative part of the individual may neurocept safety, while other dissociative parts rooted in defense will neurocept danger or life threat, but these two parts do not communicate and are not integrated. Thus, in dissociative disorders, the individual is dissociated not only when hyper- and hypoaroused but also when arousal is within the window.

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Julie, for example, had suffered neglect and sexual abuse from infancy through adolescence and, as an adult, experienced chronic hyperarousal alternating with periods of hypoarousal. Hyper- and hypoarousal frequently disrupted daily life action systems associated with marriage, work, play, and child rearing, despite Julie’s best attempts to avoid reminders of the trauma in an effort to assure that her arousal remained within a window of tolerance. Note that, even when her arousal was in the window of tolerance, her traumatic experience was not integrated but avoided and thus remained dissociated. The part(s) engaged in daily life action systems strive to steer clear of the traumatic past and of current reminders of it. Julie reported reliving symptoms of terror, panic, hyperalertness, and impulses to run, alternating (indicating a neuroception of danger) with feelings of shame and self-disgust, shutdown, and motor weakness (indicating a neuroception of life threat). In the hypoaroused condition, she often experienced time loss and distortions, and said she sometimes felt so dead that she wanted people to hit her so that she could “come back.” At other times, when she was able to avoid traumatic reminders, she reported engaging in a detached way to communicate with her husband, raise her child, and go to work—all activities related to daily life action systems. Her arousal was within a window of tolerance during these times, indicating that this part of her neurocepted some degree of safety although she reported feeling “flat” and “just going through the motions.” At other times, reminders of the trauma caused Julie to neurocept danger or life threat, driving her arousal out of the window of tolerance and disrupting her daily life functioning. For Julie, and for others with trauma-related disorders, going on with normal life required remaining dissociatively compartmentalized and distanced from the part of the personality holding the trauma-related arousal, affects, and defensive responses. Julie was frustrated that she felt like a different person in each of these conditions and wondered why she could not seem to “just live” her life. She was internally aware of the “going on with daily life” part and the shutdown part, as well as other parts of herself that had a different “consciousness, memory, identity, or perception of the environment” (American Psychiatric Association [APA], 2000) and markedly different symptoms. For example, the part of Julie that was compliant neurocepted threat unless people close to her were pleased with her, and she tried hard to satisfy them. The part that engaged the defensive response of flight was activated when people were displeased and then she searched the environment for avenues of escape. During the periods when she was able to maintain regulated arousal and focus on normal life tasks, Julie feared the loss of control over the hyper- and hypoarousal that threatened at any moment to usurp her ability to carry on daily life activities, and she did her best to prevent this from happening by avoiding trauma-related cues, achieved at the cost of continued dissociation. For Julie and other individuals with trauma-related disorders, it is profoundly challenging to integrate the markedly different states of consciousness, memory, identity, and action tendencies connected to different parts of the self, each governed by different action systems and nervous system arousal. Integration can occur over time and contexts, and is an extended process that includes both physical and mental actions that facilitate a unified sense of self and help the patient assimilate his or her traumatic past (Steele, van der Hart, & Nijenhuis, 2009). The concepts of structural dissociation point to a number of important features crucial to a sensorimotor

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understanding and treatment of trauma: the inherent conflict between action systems of defense and those of normal daily life; the way in which physical and mental action tendencies related to each action system become encapsulated into parts of the self or personality; and the essential role of the patient’s mental integrative capacity, and integrated physical action, in resolving dissociation.

SP TREATMENT

The failure to integrate defensive action systems with those of daily life manifest in preconscious somatic patterns of muscle tension, posture, gaze, facial expression, and behavioral tendencies that reflect neuroception and continually influence conscious perceptions of and predictions about the current situation. As previously discussed, each action system is associated with particular patterns of physical action tendencies unique to that system, and the specific action systems that mediate various parts also constrain them, leading to somewhat fixed and inflexible actions (Steele, van der Hart, & Nijenhuis, 2009). Neuroception of safety, danger, and life threat are also accompanied by specific action tendencies. Physical actions of diverse parts of the personality can vary widely, depending on neuroception and the action system that most influences the part. Since action systems are inherently physical in nature, the lack of integration among parts can be clearly perceived in the lack of integration in the patient’s movements, and thus, work with the body can be a powerful avenue of integration. In SP treatment, therapists and patients together study the patients’ somatic and mental patterns of response to the arousal of each action system. Developing accurate neuroception and fostering more adaptive, integrated actions related to normal (nonthreatening) life, as well as to threatening situations, require that both categories of action systems be explored simultaneously as they are evoked in the natural course of therapy and in life outside the therapy office. In the context of long-term therapy, the therapist’s social engagement system facilitates the social engagement system of the patient in order to maintain the presence of at least one part of the patient that neurocepts a degree of safety and also to develop an adaptive attachment relationship with the therapist that can serve as a secure base for learning about habitual and potential responses to the arousal of all the action systems. Julie, the patient mentioned earlier, is a 58-year-old psychotherapist who sought SP with the first author (Pat Ogden) because, after years of “talk” therapy, she still could not “live her life” as she wanted. She was baffled by her radical fluctuations in mood, and her subjective experience of separateness, fragmentation, memory lapses, and unpredictable intrusions. Julie had suffered severe neglect and stated that her father was her abuser throughout her childhood. She reported that her older sister told her that she (Julie) was often kept in a closed drawer as a baby. Although Julie had no recall of her first 3 years, she did remember spending hours hiding in her closet as a child, hoping that her father would not find her. At the start of therapy, Julie reported hypoarousal episodes that occurred frequently, even during her previous therapy, for which she was often amnesic. She had great difficulty functioning in social situations and was constantly triggered by

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her patients’ stories in her own practice as a psychotherapist. Julie initially found it anxiety provoking to consider working somatically because her body sensation alternately felt distressingly numb or agitated. She did not understand how somatic work could benefit her and had only come to SP because her previous therapist had recommended it.

BODY AWARENESS AND STABILIZATION

Our first session consisted of the usual intake and psychoeducation to help Julie understand the potential value of sensorimotor interventions. Julie, like many clients, was distressed and ashamed of her “unreasonable” physical reactions, and psychoeducation helped her make sense of and normalize her somatoform symptoms and offered hope for resolution. In this first phase of therapy, it was important to help Julie understand the nature of dissociation and animal defense-driven parts of the personality. Reassurance that her disturbing symptoms were normal and expected given her history, that they reflected the alternation between defensive systems and daily life systems, and that a sensorimotor approach could help her meet her goal of increased participation with and enjoyment of her life were important elements of Julie’s psychoeducation. Planning mutually agreeable somatic interventions with clear goals sets the stage for success. Patients often benefit from being asked how they “would behave differently or what they would like to be able to do after an intervention that they cannot currently do” (Bundy, 2002, p. 212). When I asked Julie to imagine what she would like to accomplish through our work together, she replied, “I would like to feel competent and be able to enjoy my life without getting so weird.” In other words, she wanted to be able to respond adaptively to daily life action systems without her defensive systems being activated. Despite the different goals of parts driven by defensive subsystems, this overarching wish set the stage for persistent exploration of how her body could be her ally in achieving her goal. The initial phase of therapy focused on assessing her faulty neuroception and quieting her defensive subsystems. It is of utmost importance that the therapist seeks to understand the entire dissociative system of the patient and to improve cooperation and communication among all parts. The patient’s body frequently reveals observable cues pertaining to various parts, as we shall see in Julie’s work. As Julie mentioned her childhood during one of our early sessions, her eyes locked onto mine as if her life depended on maintaining eye contact. Her terrified gaze spoke of the danger she neurocepted when telling the “secret” of her abuse, and seemed to reflect physical tendencies that might accompany an attachment cry. I asked her to be aware of what happened when my eyes met hers, and she reported feeling safer and able to take a deeper breath. I explained to her that eye contact between us could be a relational “resource,” something we could use consciously to help her to stay engaged with me and feel safer. Different parts will typically have quite different reactions to a given intervention as well as different transferences to the therapist, and an intervention that is helpful for one part may not be so for another. Julie’s eyes locking on to mine represented

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action tendencies of a part seeking protection, but it was evident that another part frightened by connection and proximity also needed attention. I carefully tracked Julie’s responses to my physical proximity in the initial stages of treatment. I noticed that, when our eyes met, her body pulled back; when I took a step toward her, she consistently took a little step back; and when I leaned forward in my chair, she moved back in hers. She also frequently glanced toward the door. These action tendencies appeared to be those of a “flight” part that, alarmed by eye contact and proximity, wanted to escape. When I brought her attention to her body pulling away, Julie, speaking from the part influenced by daily life systems of attachment and sociability, and thus neurocepting some degree of safety, stated that it was “fine” with her that I was in close proximity. However, her body had already revealed another part that seemed to neurocept danger and prepare for flight when the distance between us decreased. With the intention of integrating these parts and their physical action tendencies, I suggested that we might explore what might be an optimal distance for both parts of her. As I asked Julie to sense what was the “right” distance between us, she again repeated that where I sat was “fine.” Recognizing that this was the perspective of only one part that was connected to daily life action systems, I continued to wonder out loud which position felt better and embodied that question by first moving my chair away and then moving it closer, asking Julie if she noticed any difference in her reactions. Julie recognized that she felt better when I moved away; her body relaxed, but her clinging eyes expressed fear. By maintaining social engagement, we had met the needs of the part of her that was frightened of proximity, left over from the abuse proximity brought in her childhood, but another part desperately needed me as a safe haven and seemed to fear that I had “left her” when I moved away. As I returned Julie’s unfaltering eye contact, I asked her to notice if she thought I was leaving her energetically or not. She reported that she could see I was not. I then directed her to ask the fearful part of her to see what she saw: that energetically I was still with her. Next, I asked her to notice what my eyes told this part of her about the fear of my “leaving.” She reported that my eyes looked engaged, and she could see that I had not abandoned her. With this, the fearful, clinging part of her was reassured, and her eyes lost much of their fear. Note the different goals of action systems: the flight part attempted to increase distance, while the attachment cry part aimed to increase proximity. And another part simply wanted to participate in the present moment without the interference of defensive subsystems, so reported being “fine.” Julie and I were faced with the complicated task of fostering integration by attending to the goals of all these systems simultaneously. As the three parts of the self that were influenced by various action systems were held in awareness, communication among the parts was facilitated. Note that it is imperative in trauma work to maintain social engagement between patient and therapist. Julie and I determined together whether to try out different interventions, and this collaboration between us increased her social engagement and lowered the reactivity to the therapeutic relationship of the parts that were driven by defensive action systems. The activation of the social engagement system keeps the patient “right here, right now,” seeks to maintain arousal within the window of tolerance, and stimulates parts involved in daily life action systems of exploration, sociability, and even play. If the patient’s social engagement diminishes or

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is lost, which occurs as a matter of course as defensive parts emerge, the therapist must focus on what will enable the patient to reengage. Without collaboration, present-moment orientation, and regulated arousal, posttraumatic triggers result in the unfettered emergence of the parts rooted in defensive subsystems, usurping therapeutic gains and exacerbating dissociative tendencies. After psychoeducation about the various defensive subsystems, Julie said that she had no “fight” part, but she had no insight into why. However, we were able to make a list of the somatic signs of other defensive subsystems: the widening and clinging of her eyes and “feeling like a child” indicated the attachment cry part; impulses to move back and look at the door signaled the flight part; an overall feeling of numbness, slumped posture, the downward turn of her head, accompanied by a spacey feeling and lack of body sensation were the characteristics of the collapsed part to whom “nothing mattered” that concerned her the most. She was frequently amnesic for those periods of time during which she was hypoaroused, which appeared to be related to the feigned death defense related to increased dorsal vagal tone. Needless to say, this hypoarousal profoundly disrupted her ability to function in her life. Julie routinely submitted to emotional abuse from her boss. Sexual advances from her husband often precipitated her “leaving” her body, and at times she did not remember their sexual contact. She expressed shame and dislike for these shutdown, submissive tendencies. It is essential to foster the understanding that each part of the self has important functions. Julie and I discussed that her “survival resource” of automatic compliance, shutdown, and submission minimized the severity of the abuse when she was a child, whereas trying to fight or flee her perpetrator at that time would have been ill advised. Her mobilizing “flight” and “fight” responses were abandoned in favor of the more adaptive (in that situation) immobilizing defenses. Julie began to relinquish her severe self-judgment in favor of the curiosity of the exploration by considering questions like, “How can I understand and translate the language of my body? What is this slumped posture and spacey feeling telling me?” “How did I best protect and survive when I was little?” Drawing upon our list of somatic signs, we were able to observe the emergence of defensive parts, particularly the hypoaroused part, during the course of therapy and foster awareness of and present-focused internal communication among parts. One of our first goals was to develop resources that Julie could implement when she became hypoaroused. We decided to address her sexual relationship with her husband because we thought that even by talking about this Julie might begin to experience some of the somatic signs of hypoarousal that we had previously enumerated. From her present-moment experience of these symptoms, we hoped to help her find the specific somatic resources she needed. Even as Julie began to think about this topic and tried to talk about it, she reported a “trapped” feeling, which quickly led to some of the symptoms we had listed: feeling numb and spacey, slumping of her spine, and loss of feeling in her body. I suggested that we stand and walk together to notice that our legs could carry us away from certain objects in the room and toward others, thus stimulating a flight resource. Julie soon said she felt more present and observed that it felt good to notice her legs. The experience of mobility was a simple action that helped alleviate Julie’s numb, spacey feeling. Her social engagement system enabled her to stay in relationship with me as we consciously executed the

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physical action of the “flight” through locomotion to mitigate the immobilization of the “collapsed” part. Throughout therapy with patients with dissociative disorders, every intervention is intended to support integration, providing ways for parts to communicate. After we sat down, I asked Julie to take this newfound felt awareness of her ability to use her legs to “escape” back to the part of her that had collapsed. She reported that the collapsed “child,” whom she saw vividly as the child lying passively on her father’s bed, felt supported by sensing her legs and the capacity to “get out,” an action that she could not have safely performed then. It was also important to communicate to this child part of her that the past was over, she was no longer trapped, and she could safely use different, more empowering, actions in her current life. Julie’s body relaxed during this exploration, and she reported a new sense of her body as a whole, whereas previously she was only able to feel parts of it at a time. Again, throughout, the part of Julie that could engage in daily life and with me was encouraged to stay present, aware, and in charge, rather than allowing parts rooted in animal defenses to take over. Through the use of mindfulness, Julie was able to notice her present-moment experience and how she experienced the physical tendencies of various dissociative parts. She could also be mindful of how therapeutic interventions altered her present-moment experience, and what actions facilitated communication between parts. Mindfulness engages the prefrontal cortex in learning about the here-and-now experience of dissociative parts, rather than enacting them, and includes labeling and describing present-moment experience (Kurtz, 1990; Ogden et al., 2006; Siegel, 2007). Because mindfulness is “motivated by curiosity” (Kurtz, 1990, p. 111), it facilitates a nonjudgmental acceptance of internal experience, allowing emotions, thoughts, and sensations “simply to be there,” to bring to them a kindly awareness, to adopt toward them a more “welcome” than a “need to solve” stance (Segal, Williams, & Teasdale, 2002, p. 55). Mindfulness typically refers to being open and receptive to “whatever arises within the mind’s eye” (Siegel, 2007) without preference. The use of “directed mindfulness” (Ogden et al., 2006) helps the patient become aware of particular elements of present-moment experience considered important to therapeutic goals. In the initial phase of Julie’s therapy, I directed her mindfulness specifically to increase her awareness of resources that helped her stabilize, asking questions like, “Can you describe what happens in your body when you sense your legs carrying you through space?” When patients’ mindfulness is not directed (as in open-ended questions like, “What are you feeling?”), they often find themselves at the mercy of the dissociative parts that appear most vividly in the forefront of consciousness, which can exacerbate compartmentalization. Directed mindfulness was instrumental in helping Julie find a posture that helped her assert herself appropriately in her environment. Julie had great difficulty setting boundaries and saying “no,” a submissive tendency that belonged to the hypoaroused part of her that had a slumped posture. We challenged her compliance by changing her posture. I first demonstrated an assertive posture by grounding downward through my legs, extending upward through my spine to stand more erect, and then tactfully contrasted this movement with imitating Julie’s slumped posture. Next, Julie tried out both options with the purpose of discovering for herself

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a posture between these two polarities that felt most integrative. It was essential that Julie not override the collapsed part of herself by compliantly imitating my assertive posture, but instead mindfully experiment by practicing different postures, noticing her internal experience, and finding for herself a stance that felt both assertive and inclusive of the collapsed part of her. Over several sessions during which Julie and I worked on the new posture, she became mindful of a part of her that was afraid of assertion, persecutory voices that represented a part that judged her for not having asserted herself previously, and a part that feared punishment if she were assertive. All had particular physical reflections that contributed to Julie’s feeling of fragmentation: the judgment was held in her lifted chin, disgusted look, and narrowed eyes; the fear of punishment was held in her hiked shoulders and rounded back; while the fear of assertion manifested in a general pulling in and immobility of her body. All had to be addressed, their function acknowledged and appreciated, their resistance to each other explored, and their action tendencies integrated. We began to ask questions that facilitated understanding about their motivations: “Is the judgmental part trying to tell you that you have a right to be angry and assertive?” “Is the part so afraid of assertion trying to keep you from getting hurt even more?” We tracked the changes in Julie’s body as the parts began to understand one another, and Julie began to sense her body as less fragmented as her internal empathy and understanding improved. Eventually, she could practice a new grounded, more upright posture in which she felt the collapsed part of her was being protected by a more assertive part. Gradually, over time, her new posture began to feel more comfortable and solid, and she grew increasingly capable of saying “no” in a way that felt integrative and inclusive of the collapsed part, as well as the parts judgmental or afraid of assertion or fearful of punishment. Julie also learned that a change in the angle of her head facilitated social engagement and a neuroception of safety. During one session, we both embodied the downward turn of her head and mindfully studied the effects, noticing that recognizing and receiving signals from the environment from that head position was much more difficult. Together, we explored lifting our heads by lengthening our spines and bringing our shoulder blades slightly toward each other, and we both experienced more contact with each other and the environment. Again, to include all parts in treatment, we had to explore the different reactions of various parts to this intervention and address those that were afraid of “seeing and being seen,” those who felt safer with her head down, who judged her, and so on. As these integrated actions were performed repeatedly over time, Julie’s fears of and resistance to lifting her head and connecting with the outside world lessened. As previously mentioned, it is critical that the part of Julie that had collapsed and submitted in the face of life threat was not interpreted as negative but acknowledged as the best defense for that time and place, to be celebrated even as its survival responses were being transformed and integrated with other parts of the personality. We repeatedly thanked this part (and other parts) for the service that had been so essential in the past, facilitating its integration as a life-preserving animal defense rather than a humiliating defeat. At the same time, we challenged this part of her in such a way that safe, assertive, and contactful action could be experienced as new alternatives to foster fuller participation in daily life. If this hypoarousal pattern had been understood and interpreted but gone unchallenged, Julie would have continued

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to reenact the survival-oriented defensive tendencies of collapse again and again. Instead, gradually, she experienced more stabilization in her daily life; more ability for assertion, connection, and self-care; and fewer hypoaroused, amnesic episodes.

TRAUMATIC MEMORY

Once we had achieved some success with mitigating the interference of defensive subsystems, particularly hypoarousal and its neuroception of life threat, with daily life activities and the neuroception of safety, we progressed to working directly with memories of childhood abuse. Addressing traumatic memory presents a challenging paradox. On one hand, it is dependent upon the patient’s ability to neurocept safety and thus maintain social engagement and engage those parts associated with daily life action systems. However, as patients begin to recount the trauma, defensive action systems, the neuroception of danger and life threat, and dysregulated arousal are stimulated, often resulting in a loss of social engagement and connection to the action systems of daily life. To keep the social engagement system and parts connected to daily life action systems “in charge,” the therapist must help patients increase their capacity to remain in the here and now. The challenge is to process the past so that there is a steady integration of fragmented parts and fragmented body/ emotional/cognitive experiences, which requires that the parts rooted in defense be evoked, but not so much that these dysregulated, dissociated parts usurp social engagement. Thus, the patient must simultaneously access parts that neurocept danger and sometimes life threat without loss of mindful witnessing, social engagement, and a neuroception of safety. In SP treatment, the declarative memory narrative is most often used to evoke unintegrated body responses, physical actions, and parts of the personality in order to treat the effects of the traumatic past on the client’s current life functioning, rather than only as a vehicle for formulating a cohesive verbal narrative. As Julie recalled one particular memory of abuse, hyperarousal, shaking, panic, and terror became overwhelming. To help regulate her hyperarousal, I instructed Julie to disregard the emerging images of abuse, “drop the content” of the memory, focus exclusively on her body, and concentrate on lengthening her spine, sensing her feet on the ground, and staying in eye contact until she felt her arousal coming back into the window of tolerance. These physical resources, which we had already identified and practiced in the first phase of treatment, prevented further dissociation and reengaged the part(s) of Julie that could stay in the present moment. When her arousal returned to within the window of tolerance, she was again able to simultaneously neurocept the sense of safety connected to the present and the sense of danger connected to the past. As traumatic memories are addressed, new resources are cultivated and the resources used long ago to cope with the traumatic event are discovered, acknowledged, and strengthened. No matter how sudden or severe the traumatizing events are, peritraumatic resources were invariably utilized and can subsequently be brought to awareness in therapy. For example, as Julie began to recall a memory of her father angrily yanking her out of her hiding place in the closet, she reported that she did not resist and felt ashamed of the hypoaroused part of her that was so passive. However,

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as I asked her how her passivity affected her father, she said that he became less angry when she did not resist. Although we had acknowledged this hypoaroused part for its value earlier in therapy, in the context of working directly with statespecific processing of traumatic memory, reframing her acquiescence as an adaptive action that pacified her father deepened Julie’s acceptance and even gratitude for her passivity at the time of her abuse. I first encouraged Julie to consider the sequence of events in this memory, not to relive them, but instead to notice what had supported her and how she had coped. She remembered that as her father dragged her to his room, her older sister watched helplessly from the hallway. Julie’s eyes met her sister’s and she felt her sister’s compassion, knowing that, afterwards, she and her sister would cuddle together in the bed they shared. While they never spoke of what happened, there was a wordless support that existed between them. This was a particularly important recollection to Julie because, prior to this therapy session, she could not recall any positive experiences of her childhood. I noticed the change in her body when she talked about the comfort she experienced afterwards with her sister, and wanting to help her capture the memory of neurocepting safety, I asked her, “Pause then right there: remember cuddling with your sister—what happens?” Julie replied, “I take a little breath, and I know it’s over for now.” In an effort to help her translate what this moment meant to her, I said, “There is something very important about this moment for you—just sense this experience—what might it tell you?” As Julie continued to focus on the memory of being together with her sister, her breathing deepened, and her shoulders lost their tension. She reported, “Her being there tells me I am not alone,” and she began to softly cry and her body relaxed a little more. Even in the midst of a traumatic environment, which necessitated chronic activation of parts prepared for danger and life threat, Julie and her sister found moments of connection to sustain them. When such moments of social engagement within a traumatic experience are remembered and embodied, and the meaning of these moments is discovered, the parts of the patient engaged in daily life action systems are strengthened and can be integrated with parts related to defensive subsystem. Integration of past and present is facilitated when empowering or resourcing moments within the traumatic past are interwoven with dangerous or overwhelming moments and with the neuroception of safety now. Memory is reconstructive and the attention to parts representing daily life subsystems and defense mitigates both the phobic avoidance of traumatic memory and the continual replaying of it in a fixed form. As Julie said after that session, “The memory will never be the same. Now I won’t just remember the abuse. I will also remember that my sister and I were in it together, and we had each other.” In this manner, again, the part that neurocepts safety now could be integrated with the parts that neurocept danger and the part that could neurocept the moments of safety shared with her sister. Janet (1919, 1925) refers to a variety of mental and physical actions that remain incomplete for people with trauma-related disorders. A sensorimotor psychotherapist helps the patient to “complete” truncated actions of dissociated parts and to integrate these actions through communication with other parts of the personality. Through state-specific processing focused on how the body has encoded the traumatic events, the parts associated with animal defenses and neuroception of danger and life threat are activated and their implicit memories processed, evoking new reactions that can

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now be integrated with the old reactions. A variety of parts are involved in a “sliver” of memory: those who hold the immobilizing defensive responses that did happen and those who hold empowering physical actions like fleeing or fighting back that “wanted to happen” but were truncated at the time of the original event. These actions, when executed in the context of social engagement in the therapy hour, mitigate feelings of helplessness and shame, give rise to moments of confidence and satisfaction, and facilitate integration (both somatic and mental) among parts. It should be noted that patients might also experience shame and defeat from dysregulated fight or flight defenses that are chaotic and out of control. One patient was ashamed of the bouts of explosive rage she experienced during which she lashed out at her family and broke household objects. As we addressed her memory, she felt her body tense and said this was what happened in her body just before she went into a rage. I asked her to be mindful of her body sensation and tension, and to find out what action her body wanted to make. She felt the impulse to suddenly strike out, an impulse originating from a dysregulated “fight” part. I directed her to sense this action in her body and execute it in slow motion, reporting to me what she experienced in her body. She followed this impulse in a slow and contained manner, pushing against a pillow I held. By executing the movements of her “fight” part in slow motion, with mindful attention, she could experience the energy of her aggression in a titrated dose, and mindfully report to me how she felt it first as a surge of energy and then as an impulse that started in her back and moved slowly out her hands. With many iterations of executing these aggressive actions in a mindful, deliberate fashion, the “fight” part of this patient began to experience a sense of self-regulation, other parts could appreciate its protective function when it was not destructive, and her aggressive outbursts diminished in her daily life. Often, as patients first begin to address past trauma, instead of empowering defenses, the immobilizing defenses that were the most effective defense at the time of the trauma surface physically and emotionally. Simultaneously, though, parts driving empowering defenses, incipient during the original trauma, often spontaneously emerge, ready to be further developed and integrated. These actions that were truncated or held back at the time of the original trauma present themselves physically in the form of preparatory movements: tension in the arms or lifting of the hands or fingers connected to fight responses; tension or movement in the legs indicative of a flight response; sensations in the throat that might indicate an urge to speak or scream. For example, as Julie talked about her sense that she had been abused as an infant, she noticed a tightening in her jaw, which developed into an impulse to bite. Of course, she had no explicit memory of such early abuse, but through awareness of her body’s preparatory movement (the tension in her jaw), Julie realized the urge to bite that she said made her feel less helpless. Recall that it is not necessary to have access to declarative memory to help the patient become aware of preparatory movements, and execute empowering defensive actions. A particularly devastating childhood memory emerged for Julie when her daughter turned 11, the same age Julie was when she endured the most terrible time period of her abuse. As Julie observed her internal experience in reaction to her decision to work on this memory, she felt her arousal escalate, and noticed that trembling and shaking had already begun. Julie, like many patients, reported that

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she was frightened of her own hyperarousal and, as a result, sometimes felt revictimized by exposure to her own memories. She felt “electricity” in her arms and was inclined to curl up into a ball as she sensed the downward turn of her head and rounding of her shoulders. Instead, I invited Julie to carefully notice the electricity in her arms and to sense if there was any action her body wanted to make. She reported that she could feel her arms wanting to push away, and I suggested she notice what happened if she pushed against a pillow that I held. It is important to note that Julie was mindful of her body’s response as we talked about the memory, and when she felt the impulse to push, we turned our attention to executing that action. The impulse emerged from Julie’s awareness of her body’s response to the memory, not as an idea or concept. As she mobilized not only her arms but also her whole body in pushing, she began to sense a part of her that felt strong and powerful. Her anger, usually experienced with a sense of impotence, felt robust and exciting. As we contacted this angry part, which was emerging through her body, Julie was asked to notice the reactions of other parts to the anger and the pushing, and we took care to facilitate communication among various parts. One part, for example, was extremely afraid that the anger would escalate out of control and needed to know that executing the pushing action did not mean that the angry part would take over. This communication was facilitated not only mentally but also somatically, as Julie found a way to push that reassured the fearful part. Julie noticed that when her arms were stiff and straight and her energy was in the front of her body, the fear escalated. But when her arms were bent and flexible, and she pushed very slowly, being mindful of her entire body, especially her back, the fear quieted. Making sure Julie’s social engagement system was activated through our eye contact, and my reassurance that she would not be punished by me for pushing away or being angry, facilitated completion of the action and its integration with the trauma-related fears and beliefs held by other parts. After Julie had executed the pushing action, we returned to the content of the same memory. Again, she reported that her arousal escalated and her body trembled, although the sensations were less intense than before. At these moments in therapy, when hyperarousal is experienced in physical trembling, patients may be encouraged to find an empowering action like pushing, as Julie did previously, or they may be encouraged to follow the progression of the spontaneous sensations, movements, and impulses through the body until the arousal has subsided. Obviously, to press for additional traumatic material when patients are already hyperaroused can promote an escalation of arousal and dissociation, leading to reenactment instead of integration. I asked Julie if she would be willing to be mindful only of her body sensation, and to put the emotions and content of the memory aside: “Can you just focus on your body? Feel the panic as body sensation—what does it feel like in your body?” Julie was able to direct mindful attention on the sensations of trembling, and describe it using sensation vocabulary (tingling, traveling, shaking, calming down) rather than emotion vocabulary (scared, ashamed, panicked, anxious) to describe her body sensations. I continued to ask Julie to follow the sensations as they moved through her body: (“Stay with that sensation of trembling—what happens next in your body? How does the sensation change?”). As Julie described the progression of these sensations, she noticed that, gradually, the sensations settled, the trembling abated, and her arousal returned to her window of tolerance.

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Although the narrative of Julie’s memory provided the starting point for our work, the story is but the means to an end. It is a way to activate the implicit memories held by specific parts, along with physical and physiological reactions, and explore interventions of executing truncated or interrupted actions in current time or mindfully following the sensation as it progresses through the body until it settles by itself. Because the collapsed part played such a crucial role in Julie’s survival and in her current symptoms, we paid special attention to both immobilized parts and parts holding truncated mobilizing defenses so that the empowering defensive actions could be executed and completed in the context of therapy. After discovering the angry part, completing its assertive actions in therapy, addressing her hyperarousal by being mindful and tracking the trembling of her body, and integrating parts over time, Julie noted that a habitual cringing and hypoaroused tendency was absent in her day-to-day life. The years of therapeutic work she had previously spent retelling the events of her abuse had not succeeded in providing the bodily experience that protection and self-assertion were now safe and empowering actions that could support full and healthy response to the arousal of actions systems of daily life.

CONCLUSION

In SP, “integration” of parts of the personality is a process of repeated experiences of well-executed actions under cortical control in the context of neuroception of safety and social engagement with an attuned therapist. Integration is fostered when present-moment connections—cognitive, emotional, and somatic—are made and experienced among dissociative parts. Integration includes not only connection among parts but also between past and present, safety and danger, helplessness and mastery. These connections between body and mind are a process rather than an end point, and are cumulative over time. This process often starts with psychoeducation about parts of the personality, neuroception of safety, danger and life threat, defensive and daily life action systems, peritraumatic resources, and how the body participates in dissociative tendencies. Understanding faulty neuroception and establishing bottom-up resources and actions that help to reinstate accurate neuroception is essential. Completing truncated mobilizing defensive actions brings a sense of solidness and safety to parts holding experiences of fear, powerlessness, and collapse. Regulating out-of-control mobilizing defensive actions, like rage, fosters a sense of self-agency. Learning to track the sequence of the sensation of arousal leads to a new sense of mastery and trust in the body. It should be noted that, along with its focus on the body and sensorimotor processing, a sensorimotor approach includes the integration of emotions and cognitive distortions of various parts as well. As the parts and their physical tendencies become increasingly integrated, patients find that it is possible to experience and integrate strong emotions like grief, anger, and even joy, without undue dysregulation, and to address maladaptive cognitive distortions. Integration also includes somatic integration: helping the physical patterns that have developed over time in response to trauma and attachment failure develop into more adaptive actions. Instead of unintegrated actions that reflect the division of the individual into dissociative parts, such as simultaneously seeking both proximity and

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distance by reaching out for contact as the upper body pulls away, the body is congruent and purposeful in its movement and gesture. As Julie learned to lengthen and align her posture in a way that integrated dissociative parts, to lift her head instead of angle it downward, to push outward instead tighten inward, and so on, her physical structure and posture became increasingly integrated. Her body found more integrity, alignment balance, and economical movement. Her movements became more purposeful instead of contradictory. For example, she could make eye contact without pulling back. The integration of her structure and movement reflected and sustained the integration of dissociative parts. The integration of parts both somatically and mentally facilitates a unified sense of self as well as ongoing integrative actions that support functioning in everyday life. The patient experiences his or her body, and all parts of the body, as “me.” Through integrating body and mind, patients develop a new, consistent sense of self, both linguistic and somatic, that is more flexible, adaptive, and capable of full engagement with life.

REFERENCES Ainsworth, M. (1963). The development of infant-mother interaction among the Ganda. In B. Foss (Ed.), Determinants of infant behavior (pp. 67–104). New York, NY: Wiley. Allen, J. (2001). Traumatic relationships and serious mental disorders. Chichester, UK: John Wiley & Sons. American Psychiatric Association (APA). (2000). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: American Psychiatric Association. Beckoff, M., & Allen, C. (1998). Intentional communication and social play: How and why animals negotiate and agree to play. In M. Bekoff & J. Byers (Eds.), Animal play: Evolutionary, comparative, and ecological perspectives (pp. 97–114). New York, NY: Cambridge University Press. Beckoff, M., & Byers, J. (1998). Animal play: Evolutionary, comparative, and ecological perspectives. New York, NY: Cambridge University Press. Bergman, N. J., Linley, L. L., & Fawcus, S. R. (2004). Randomized controlled trial of skin-toskin contact from birth versus conventional incubator for physiological stabilization in 1200 to 2199 gram newborns. Acta Paediatrica, 93, 779–785. Bowlby, J. (1969/1982). Attachment (Vol. 1, 2nd ed.). New York, NY: Basic Books. Bowlby, J. (1988). A secure base: Parent-child attachment and healthy human development. New York, NY: Basic Books. Bundy, A. C. (2002). The process of planning and implementing intervention. In A. C. Bundy, S. J. Lane, & A. A. Murray (Eds.), Sensory integration: Theory and practice (pp. 211–225). Philadelphia, PA: F. A. Davis Company. Caldwell, C. (2003). Adult group play therapy. In C. Schaefer (Ed.), Play therapy with adults (pp. 301–316). Hoboken, NJ: John Wiley & Sons. Cassidy, J., & Shaver, P. (1999). Handbook of attachment: Theory, research, and clinical applications. New York, NY: Guilford Press. Chu, J. (1988). Ten traps for therapists in the treatment of trauma survivors. Dissociation, 1, 25–32. Cozolino, L. (2002). The neuroscience of psychotherapy: Building and rebuilding the human brain. New York, NY: W. W. Norton. Damasio, A. (1994). Descartes’ error: Emotion, reason and the human brain. New York, NY: Penguin.

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Donaldson, F. (1993). Playing by heart: The vision and practice of belonging. Deerfield Beach, FL: Health Communications. Fanselow, M., & Lester, L. (1988). A functional behavioristic approach to aversively motivated behavior: Predatory imminence as a determinant of the topography of defensive behavior. In R. Bolles & M. Beecher (Eds.), Evolution and learning (pp. 185–212). Hillsdale, NJ: Lawrence Erlbaum Associates. Frijda, N. (1986). The emotions. Cambridge, UK: Cambridge University Press. George, C., & Solomon, J. (1999). Attachment and caregiving: The caregiving behavioral system. In J. Cassidy & P. Shaver (Eds.), Handbook of attachment: Theory, research, and clinical applications (pp. 649–670). New York, NY: Guilford Press. Gould, J. (1982). Ethology: The mechanisms and evolution of behavior. New York, NY: W. W. Norton. Janet, P. (1889). L’automatisme psychologique. Paris, France: Felix Alcan. Janet, P. (1907). The major symptoms of hysteria. London, UK: Macmillan. Janet, P. (1919). Psychological healing. New York, NY: Macmillan. Janet, P. (1925). Principles of psychotherapy. London, UK: George Allen & Unwin. Krystal, J., Bremner, J. D., Southwick, S. M., & Charney, D. S. (1998). The emerging neurobiology of dissociation: Implications for treatment of posttraumatic stress disorder. In J. D. Bremner & C. Marmar (Eds.), Trauma, memory and dissociation (pp. 321–363). Washington DC: American Psychiatric Press. Kurtz, R. (1990). Body-centered psychotherapy: The Hakomi method. Mendicino, CA: LifeRhythm. Lanius, R. A., Williamson, P. C., Boksman, K., Densmore, M., Gupta, M., Neufeld, R. W., . . . Menon, R. S. (2002). Brain activation during script-driven imagery induced dissociative responses in PTSD: A functional magnetic resonance imaging investigation. Biological Psychiatry, 52, 305–311. Lewis, L., Kelly, K., & Allen, J. (2004). Restoring hope and trust: An illustrated guide to mastering trauma. Baltimore, MD: Sidran Institute Press. Lichtenberg, J. D. (1990). On motivational systems. Journal of the American Psychoanalytic Association, 38(2), 517–518. Lichtenberg, J. D., & Kindler, A. R. (1994). A motivational systems approach to the clinical experience. Journal of the American Psychoanalytic Association, 42, 405–420. Liotti, G. (1999). Disorganization of attachment as a model for understanding dissociative psychopathology. In J. Solomon & C. George (Eds.), Attachment disorganization (pp. 291–317). New York, NY: Guilford Press. Lyons-Ruth, K., & Jacobvitz, D. (1999). Attachment disorganization: Unresolved loss, relational violence, and lapses in behavioral and attentional strategies. In J. Cassidy & P. Shaver (Eds.), Handbook of attachment: Theory, research, and clinical applications (pp. 520–554). New York, NY: Guilford Press. Marvin, R., & Britner, P. (1999). Normative development: The ontogeny of attachment. In J. Cassidy & P. Shaver (Eds.), Handbook of attachment: Theory, research, and clinical applications (pp. 44–67). New York, NY: Guilford Press. Misslin, R. (2003). The defense system of fear: Behavior and neurocircuitry. Clinical Neurophysiology, 33(2), 55–66. Nijenhuis, E. R. S., van der Hart, O., & Steele, K. (2002). The emerging psychobiology of trauma-related dissociation and dissociative disorders. In H. D’Haenen, J. DenBoer, & P. Willner (Eds.), Biological psychiatry (pp. 1079–1098). London, UK: Wiley. Nijenhuis, E. R. S., van Dyck, R., Spinhoven, P., van der Hart, O., Chatrou, M., Vanderlinden, J., & Moene F. (1999). Somatoform dissociation discriminates between diagnostic categories over and above general psychopathology. Australian and New Zealand Journal of Psychiatry, 33, 512–520.

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Nijenhuis, E. R., Spinhoven, P., van Dyck, R., van der Hart, O., & Vanderlinden, J. (1998). Psychometric characteristics of the Somatoform Dissociation Questionnaire: A replication study. Psychotherapy and Psychosomatics, 67, 17–23. Ogden, P., Minton, K., & Pain, C. (2006). Trauma and the body: A sensorimotor approach to psychotherapy. New York, NY: W. W. Norton. Panksepp, J. (1998). Affective neuroscience: The foundations of human and animal emotions. New York, NY: Oxford University Press. Perry, B., Pollard, R., Blakely, T., Baker, W., & Vigilante, D. (1995). Childhood trauma, the neurobiology of adaptation, and “use dependent” development of the brain: How “states” become “traits”. Infant Mental Health Journal, 16, 271–291. Porges, S. W. (2005). The role of social engagement in attachment and bonding a phylogenetic perspective. In C. Carter, L. Aknert, K. Grossman, S. Hirdy, M. Lamb, S. W. Porges, & N. Sachser (Eds.), From the 92nd Dahlem workshop report: Attachment and bonding: A new synthesis (pp. 33–55). Cambridge, MA: MIT Press. Porges, S. W. (2011). The polyvagal theory: Neruophysiological foundations of emotions, attachment, communication, and self-regulation. New York, NY: W. W. Norton. Rivers, W. H. R. (1920). Instinct and the unconscious: A contribution to a biological theory of the psycho-neuroses. Retrieved from http://psychclassics.yorku.ca/Rivers/ Schore, A. N. (1994). Affect regulation and the origin of the self: The neurobiology of emotional development. Hillsdale, NJ: Lawrence Erlbaum Associates. Schore, A. N. (2001). The effects of early relational trauma on right brain development, affect regulation, and infant mental health. Infant Mental Health Journal, 22, 201–269. Schore, A. N. (2009). Right-brain affect regulation: An essential mechanism of development, trauma, dissociation, and psychotherapy. In D. Fosha, D. Siegel, & M. Solomon (Eds.), The healing power of emotion: Affective neuroscience, development and clinical practice. New York, NY: W. W. Norton. Segal, Z. V., Williams, J. M. G., & Teasdale, J. D. (2002). Mindfulness-based cognitive therapy for depression: A new approach to preventing relapse. New York, NY: Guilford Press. Siegel, D. (1999). The developing mind. New York, NY: Guilford Press. Siegel, D. J. (2007). The mindful brain: Reflection and attunement in the cultivation of well-being. New York, NY: W.W. Norton. Sroufe, L. A. (1997). Psychopathology as an outcome of development. Development and Psychopathology, 9, 251–268. Steele, K., van der Hart, O., & Nijenhuis, E. R. S. (2004). Phasenorientierte Behandlung komplexer dissoziativer Störungen: die Bewältigung traumabezogener Phobien [Phase oriented treatment of complex dissociative disorders: Overcoming trauma-related phobias]. In A. Eckhart-Henn & S. Hoffman (Eds.), Dissoziative Bewustseinsstörungen: Theorie, Symptomatik, Therapie [Dissociative disorders of consciousness: Theory, symptoms, therapy] (pp. 357–394). Stuttgart, Germany: Schattauer. Steele, K., van der Hart, O., & Nijenhuis, E. (2005). Phase-oriented treatment of structural dissociation in complex traumatization: Overcoming trauma-related phobias. Journal of Trauma and Dissociation, 6, 11–53. Steele, K., van der Hart, O., & Nijenhuis, E. R. S. (2009). The theory of trauma-related structural dissociation of the personality. In P. F. Dell & J. O’Neill (Eds.). Dissociation and the dissociative disorders: DSM-V and beyond (pp. 239–259). New York, NY: Routledge. Stern, D. N. (1985). The psychological world of the infant. New York, NY: Basic Books. van der Hart, O., Nijenhuis, E., & Steele, K. (2006). The haunted self. New York, NY: W. W. Norton . van der Hart, O., Nijenhuis, E., Steele, K., & Brown, D. (2004). Trauma-related dissociation: conceptual clarity lost and found. The Australian and New Zealand Journal of Psychiatry, 38, 906–914.

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van der Hart, O., van Dijke, A., van Son, M., & Steele, K. (2000). Somatoform dissociation in traumatized World War I combat soldiers: A neglected clinical heritage. Journal of Trauma & Dissociation, 1(4), pp. 33–66 van der Kolk, B. A., McFarlane, A., & Weisaeth, L. (1996). Traumatic stress: The effects of overwhelming experience on mind, body and society. New York, NY: Guilford Press. van Ijzendoorn, M., Schuengel, C., & Bakermans-Kranenburg, M. (1999). Disorganized attachment in early childhood: Meta-analysis of precursors, concomitants and sequelae. Development and Psychopathology, 11, 225–249.

CHAPTER 20

Temporal Integration of Early Trauma and Neglect Sandra L. Paulsen

 . . . any form of attachment is preferable to abandonment. This may be an infantile version of the “Stockholm syndrome”—one forms attachment to whomever is in power at whatever cost to one’s own desires and needs and self-esteem. —Arnold M. Cooper (2009) Many of the most intense emotions arise during the formation, the maintenance, the disruption, and the renewal of attachment relationships. —J. Bowlby (1980, p. 3)

Chapter 17 discussed the importance of fractionation with regard to decreasing overwhelm and intense abreaction during trauma processing. This chapter describes another approach to fractionation and titration of traumatic material, specifically the use of the time domain. This approach is informed by our understanding of neural development and the integration of mental experience using developmental time sequence. O’Shea (2001, 2003a, 2003b, 2006, 2009a, 2009b) and O’Shea and Paulsen (2007; O’Shea, 2009b) have developed the early trauma (ET) approach to specifically address patients’ history of ET or neglect. This chapter describes the essence of the ET approach—temporal integration—as an integrational theory in dissociation. The focus on ET and attachment issues is an integral part of temporal integration. This chapter extends the ET approach to complex cases, specifically dissociative disorders. 423

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To successfully resolve these issues in treatment, the ET approach includes (a) containment strategies that enable the work to be fractionated and paced, which keeps the patient from being overwhelmed with extreme sympathetic arousal, (b) directly engaging the patient’s ventral vagal/social engagement system with resourcing and somatic empathy and other considerations, (c) clearing the affective circuits so processing can complete while minimizing blockages and decreasing arousal, which minimizes defensive responses, (d) systematically both accessing trauma held in implicit memory and processing it to an adaptive resolution and that systematic approach negates the requirement for mileposts in explicit memory, (e) ensuring patients have the felt sense of getting their unresolved early needs met on their own terms, meeting developmental milestones in preparation for subsequent work, and laying a new foundation of resource for subsequent milestones, and (f) clearing ET by fraction of time, which systematic approach the therapist uses to ascertain where in the work one is.

THE LIMITATIONS OF EYE MOVEMENT DESENSITIZATION AND REPROCESSING (EMDR) FOR PROCESSING VERY ET

The challenges of using EMDR for complex trauma and dissociative patients have been known for two decades (Fine & Berkowitz, 2001; Paulsen, 1995) because the potential for affective overwhelm and flooding must be closely managed. Extremely strong emotional release can occur. Although EMDR can often process through such intensity, for complex, dissociative, and fragile patients, commonly the intensity is too great for the patient to stay in the process, or to maintain the requisite dual-attention awareness required for successful EMDR, for example, awareness of the present moment while accessing memory. Without such capacity for dual awareness and the ability to stay firmly grounded in present time, regression and serious decompensation can ensue. Moreover, the standard EMDR protocol relies to a large extent on episodic memory—declarative or explicit memory of events in a person’s life. Early learning in babies and young children is implicit and somatically held, rather than explicit or narrative, as is the nature of the memories generated during that time. There lies the challenge of trying to apply EMDR to attachment injuries or complex trauma cases, in which early attachment injury is part of the substrate (Barach, 1991). Early experience is held in the right hemisphere in implicit memory, and is not subject to direct recall in the way that explicit memory is (Schore, 2009). It can be accessed upon turning attention to the felt sense (e.g., Levine, 2010; Schore, 2003); however, the territory is murkier, usually without images, without cognitive milestones, and without much neocortical involvement. For EMDR practitioners, it is challenging to obtain subjective units of disturbance (SUD) levels and usually impossible to derive cognitions or narratives for very ET and neglect. THE FOUNDATIONAL ROLE OF EARLY EXPERIENCE

Shapiro (1995) suggests that when working with multiple traumata, one should start by enumerating the 10 most disturbing memories. While this strategy can be effective in many cases, in more dissociative populations, especially those evidencing

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significant structural dissociation, it brings with it a high risk of decompensation as well as suboptimal or incomplete treatment effects. At the same time, Shapiro (1995) clearly acknowledges the importance of earlier, sometimes less apparently traumatic events in their contribution to adult anxiety symptoms. For instance, in the phobia protocol, ancillary events, initial traumatic experiences, the worst traumatic experience, and the most recent traumatic experience are processed in sequence. While Shapiro (1995) does not specifically address how to systematically access and process information in implicit memory for very ET, a number of authors have recognized the importance of the role of ET and attachment issues and their contribution to present-day functioning. Some authors have suggested helpful strategies for processing early experience (e.g., Kitchur, 2005); the lack of explicit memories and resulting vagueness of very early experience often leaves these experiences outside the realm of what can be easily or systematically addressed using the standard EMDR protocol, contributing to difficulties with regard to the repair and remediation of early attachment injury. For instance, Kitchur (2005), in her Strategic Developmental Model, held that the more the history and symptom picture are complex, the more likely it is that problems with attachment and early self-development are involved, thus suggesting that initial EMDR processing should focus on the earliest material. Specifically, she suggests processing material in the sequence in which it was experienced and contributed to the formation defenses and schemata of the self. She suggests that this approach reduces the occurrence of incomplete sessions due to earlier feeder memories or blocking beliefs attributable to earlier memories. Kitchur (2005) emphasizes maternal, paternal, as well as parental and other primary attachment relationships (e.g., caretakers, etc.). However, targeting of the earliest memory within a given attachment relationship is not always possible and in some cases ill-advised. This occurs in individuals with severe dissociative disorders who have experienced their most significant traumatic event in one of their primary attachment relationships, such as sexual abuse, severe physical abuse, or neglect at the hands of a parent or primary caretaker. This venture becomes even more difficult when there is significant amnesia and/or lack of knowledge about a history of ET. Working with a somatic sense risks breaking into material the person may be either amnestic for or unable to deal with at the present moment, as resources for affect regulation are insufficiently developed. Even with those limitations in mind, while Kitchur’s approach goes a long way toward remedying some issues with regard to early attachment injury, it may not go far enough in that it doesn’t systematically address prenatal and perinatal experiences that are often at the heart of an early inability to attach or bond to a parent. Accordingly, when targeting in developmental sequence, prior to targeting parental relationships, the targeting of prenatal and perinatal experiences follows logically. Moreover, O’Shea (2006) and Lynn (2000), mindful of the difficulties with accessing positive experiences in individuals with very early histories of trauma and attachment issues, suggest resource development prior to targeting prenatal and perinatal trauma. Targeting in developmental sequence in itself is a way of fractionating and titrating traumatic experience. That is, by processing earliest adverse experiences prior to targeting later ones, one decreases the likelihood of flooding by simultaneously

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accessing multiple related traumatic experiences, or ones that have resulted in a similar physiological experience. With complex cases where there is significant structural dissociation, targeting in developmental sequence alone can be insufficient and there is often the need for additional interventions. These include the use of ego state procedures to reduce defensive processes as well as somatic work to work directly with the experiential aspects of fight-or-flight responses to enable the patient to have the felt sense of embodiment, and hypnotic maneuvers for resourcing, pacing, containment, and other purposes. These and other concerns specific to the application of the ET procedure with complex cases are addressed generally here and detailed in Paulsen and O’Shea (in press).

THE ET APPROACH

Fosha (2000) suggests that any treatment that purports to successfully and safely treat ET requires the ability to secure the patient’s felt sense of safety in the therapeutic relationship, the therapist’s capacity and willingness to engage in the hard emotional work with the patient, a means of working with defensive responses associated with fight and flight on a direct basis in order to obtain access to the emotional states that the patient may fear that he or she cannot bear, and strategies for working with emotions that do not overwhelm and retraumatize the patient, in order for the patient to integrate the experience and achieve coherence. The ET approach meets those criteria. It is hypothesized that the ET method helps to bypass the left hemisphere and access the right hemisphere with its implicit memory because that is how very early experience is stored, the same early experience that has caused the somatic symptoms that memorialize the trauma—the body is “keeping the score.” Importantly, the therapist’s stance in the relationship must be kind and engaging, and relationally oriented, because that is the state the patient needs to be in to access his or her infant states somatically and relationally and to feel safe in the work. It is vital to use somatic resourcing, resonant relationship attunement, and, to address defensive structures, ego state maneuvers. The artful interweaving of these enables success in the work.

ORIGIN OF THE ET APPROACH

Katie O’Shea (2006) initially developed the ET approach of EMDR as an offshoot of the work of numerous contributors, including notably (a) containment strategies in use in the EMDR community, attributable to the hypnosis tradition (e.g., Kluft, 1990), (b) Kitchur’s strategic developmental model (Kitchur, 2005), (c) Paulsen’s application of ego state work to EMDR (Paulsen, 1995, 2001, 2009a, 2009b), which will be discussed further, below, (d) Lynn’s description of the use of EMDR to access and reprocess a pretraumatic time period (Lynn, 2000), (e) Phyllis Klaus’s use of EMDR and hypnosis in the preverbal time period (Klaus, 1995), and other contributors. O’Shea experimented with Paulsen’s ego state methods of EMDR processing of states directly, including the use of the conference room to look at ego states with object awareness. Although EMDR training emphasized the need for the patient to

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be sufficiently resourced prior to conducting EMDR, both Paulsen and O’Shea found available stabilization methods unsatisfactory either in result or in time and cost efficiency, especially with complex and dissociative cases. Paulsen described the use of ego state therapy to conduct EMDR for not only dissociative patients but also nondissociative patients with ego state conflicts as well. In one presentation, Paulsen presented a case vignette in which the patient had ego states that the patient called, “Anger,” “Sadness,” “Shame,” “Fear,” and “Party Girl.” The work involved processing those ego states directly, after working with the states in object awareness in the conference room (aka, dissociative table, described by Fraser, 1991, 2003). Object awareness (aka, “object cathexis” or “in object energy” in ego state work; Federn, 1952; Watkins & Watkins, 1997) refers to the patient or the therapist relating to a specific part of the self in the third person (“he,” “she,” “they,” or “it,” by looking at the part “over there”). Object awareness contrasts with ego awareness, the latter of which involves the therapist relating to a specific part of the self in second person “you,” which evokes a first person response of “I” or “we,” from the patient. Paulsen’s subsequent contributions to the development of the ET approach after 2006 included proposing the theories included in this chapter as explanatory mechanisms for the effect of the procedure, including especially activating Porges’s ventral vagal nervous system as the mechanism of action for the safe state activity, Panksepp’s subcortical affective circuits in primary affective processing, and his explication of secondary affective processing of object relations attributable to the amygdala and other basal ganglia, the understanding of the use of object awareness in imagination to reset them in combination with bilateral stimulation in Step 3, and the formulation of the temporal integration theory offered in this chapter (Paulsen, 2009b). See Chapters 2 to 5 for further discussion of imagination and resetting of the affective circuits based on Panksepp (1998) and Panksepp and Bivens (2012). Additionally, Paulsen has articulated specific interventions needed to apply the ET protocol to dissociative clients, using ego state and other interventions at every step (Paulsen & O’Shea, in press).

HARDWIRED AFFECTIVE CIRCUITS REQUIRE NO LEARNING BUT CAN BE OBSTRUCTED BY LEARNING: THE CLIPPED DASHBOARD GAUGES ANALOGY

In his seminal tome, Panksepp (1998) describes three levels of affective processing in the brain. (a) Primary processing is conducted by the subcortical affective circuits that are present from birth and that require no learning, which are (capitalized by Panksepp and here to show they are actual circuits, not just emotions) SEEKING, RAGE, FEAR, PANIC [infant separation distress], LUST, PLAY, and CARE); (b) secondary affective processing, related to the amygdala and other basal ganglia, that refers to the learning occurred in the first years of life that establish object relations and relationship templates, and are the basis for learned emotions, especially shame, but also disappointment, betrayal, and so forth; and (c) tertiary processing, which is the neocortical learning, including mindfulness, names of emotions, coping skills, and so forth. Panksepp also expresses that nonspecific affective arousal factors likely mediated by acetylcholine, serotonin, and norepinephrine are also factors (Panksepp & Bivens, 2012).

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The subcortical affective circuits that comprise the primary processing level serve as conduits for information that the organism needs, just as a car needs dashboard gauges to provide information about the car and the environment. The circuits are unmodulated in the infant, who depends on the mother for containment. In that relationship, at the secondary processing level, the baby is to learn essential affect regulation and will create a self, if all goes well. According to Dan Siegel, emotion is the basis the brain uses to organize itself, its functioning, and, ultimately, the self. He also states that what children learn from their parents about emotions directly affects the child’s ability to self-organize (Siegel, 2012). If that period goes badly, the infant will not pass the next developmental milestones, or the subsequent ones. It is rather like building a structure on top of a poorly poured foundation with the result that all the floors above will be wobbly and at risk. Insecure attachment in this time period results in a tenuous relationship going forward, whereas secure attachment between mother and child will result in an adult capacity for sustained relationship. Maladaptive lessons learned at very early ages will effect decisions for a lifetime and form the basis for certain Axis I and Axis II symptom configurations. Pathological attachment has been associated with adult syndromes such as dissociative disorders, anxiety disorders, depressive disorders, somatoform and conversion disorders, and a range of character disorders (e.g., Schore, 2012). The truncation of flow of affective circuits has profound implications for state switching, described below, and for what is described in Chapter 1 as a neurobiologically based theory of dissociation, with unprocessed experience accumulating in vertical structures, which represent parts of the self built on subcortical affective circuits, on relationship templates from the attachment period held at the level of the amygdalae and other basal ganglia, and subsequent learning that is neocortical.

Early Relationship Trauma and State Switching: The Stalagmite Analogy

When earliest needs for attachment in relationship to a loving caretaker are not met, the effect is no less than bonafide trauma, which has a profoundly injurious impact on the child’s ability to smoothly switch affective states (Putnam, 1988). When affective states cannot be integrated in the stabilizing effect of the mother–child relationship, the hardwired subcortical affective circuits (Panksepp, 1998) cannot integrate appropriately in the context of secondary brain processing related to relationship templates. Without the containment, stabilization, and social learning effects of a secure attachment relationship, not only does the baby acquire relationship templates that are maladaptive, but the child’s capacity for state switching also does not smoothly develop. This results in a lack of integration across states (Putnam, 1988, 1989) due to maladaptive state-dependent learning and disrupted affective circuits (Panksepp, 1998). This early failure to acquire smooth state shifting and resultant acquisition of habits of state switching instead is a foundation for subsequent development of affect dysregulation and dissociative disorders (e.g., Putnam, 1988). Indeed, the child appears to learn to switch states to allow the circumnavigating of the dissociative collapse, causing in extreme cases the sudden and dissociative switching seen in the more florid cases of dissociative identity disorder (DID). Without integration of these affective circuits

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during the attachment period, and with dissociative switching the child’s best option for managing affective challenges, parts of the self develop as time passes and unintegrated learning histories accumulate “vertically” like so many stalagmites or coral reefs, bottom-up, through the secondary and tertiary levels of affective processing and learning described by Panksepp and Bivens (2012) and Panksepp (1998). In Panksepp’s terms, bottom-up refers to both processing from the beginning of life, and from the lower brain structures, which is all a baby has initially. Those three levels of emotional brain processing are (a) primary processing, which occurs via the subcortical hardwired affective circuits, (b) secondary processing, which occurs at the level of the amygdala and other basal ganglia, referring to those object relations and relationship templates acquired during the first years of life, when learning is held in implicit memory, and (c) tertiary processing, at the neocortical level, which is all subsequent learning about emotions.

Preparation Steps are Paramount for Safe Temporal Integration

Adequate preparation steps greatly reduce the possibility of unintended abreaction or other untoward results. Necessary time and effort in preparation varies widely with the client and the therapeutic relationship. There will no doubt be limitations to the methods when applied more broadly, so the procedures should be used cautiously. The preparation for highly dissociative individuals requires extensive use of ego state therapy and other hypnotic maneuvers, and somatic resourcing in each of the four ET steps. The reader is referred also to the stabilization chapters of this book for more extensive suggestions for preparations to do ET processing. Due to space limitations, the ET preparation steps are described here generally.

TEMPORAL INTEGRATION—PROCESSING TRAUMA IN IMPLICIT MEMORY BY TIME FRAME

Temporal integrationism is the term established by Paulsen (2009b) to describe the approach to resolving very ET and attachment injury, including neglect in the absence of declarative or explicit memories. It is based on the work of Katie O’Shea, who developed the procedures that the theory is based upon (O’Shea, 2001, 2003a, 2003b) and on the collaboration of O’Shea and Paulsen (2007). This section describes the theory of temporal integration and touches upon the necessary modifications to the ET procedures when working with complex trauma patients. Many efforts to treat affect dysregulation as found in borderline personality disorder, mood disorders, and DID rely on strategies of containment (e.g., Kluft, 1989), decreasing inner conflict (e.g., Watkins & Paulsen, 2004), skills building (e.g., Linehan, 1987), and so forth. However, the approach taken in the ET approach is unique because of the stepwise preparation approach, when possible, working directly on the subcortical affective circuits, and the strategy of integrating and repairing from earliest experience by time frame.

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Temporal integrationism fractionates by containing all but the earliest material currently being worked upon, activating the patient’s ventral vagal nervous system with imaginal and other resources, ensuring that the affective circuits are functioning, ensuring that the patient can tolerate somatic sensation through somatic resourcing, and any needed preparation steps including ego state work to diminish inner conflicts and loyalty to the aggressor, and somatically or imaginally establishing the felt sense of boundaries protecting the self. Once these and any other needed preparation steps are complete, trauma processing involves turning focal attention to each time frame seriatum, reviewing, releasing, and repairing imaginally from the earliest experience. This both fractionates and titrates affective intensity as well as clearing and repairing earliest unmet developmental milestones. As the work progresses, each milestone becomes a layer of foundation for subsequent segments and subsequent repair. The end result is an integration that builds temporally, without abreaction in many cases, and with an ever-increasingly solid foundation of self, affect regulation capacity, and other developmental achievements. With dissociative clients alters will interfere, especially parental introjects, so ego state maneuvers will be necessary prior to and during processing by time period. The most important ego state maneuvers are related to orienting and defusing perpetrator or parental introjects that function to diminish the client’s self in favor of loyalty to the aggressor. The writer does not here take a position whether the emergent material that is processed is somehow an actual memory, a mental construct, an imaginary excursion, a soul memory, or something else. The focus is entirely on reducing symptoms and improving functioning. Temporal integration occurs during the trauma processing step of the ET approach—clearing trauma developmentally from infancy. It is conducted for complex trauma patients only if and when the preparatory steps are complete. For dissociative clients, the steps are far more extensive than for other clients, and a range of stabilization methods may be needed to prepare for Step 4. See the stabilization chapters by Paulsen and Golston in this book. Temporal integrationism (Paulsen, 2009b) is a third conceptualization of integration in treating dissociation, following those of strategic integrationism (Kluft, 1993) and tactical integrationism (Fine, 1993). In contrast to the prior two approaches, temporal integration focuses on “bottom-up” processing that is assumed to work directly on underlying affective brain processes related to three different levels of underlying neurodevelopmental stages. Here, “bottom-up” does not refer only to somatic sensation, as described in prior chapters, but also to from the ground floor up, temporally, beginning from birth or before.

GENTLER, SEQUENTIAL, AND FRACTIONATED PROCESSING: THE THREE-HOLE PUNCH ANALOGY

With standard EMDR trauma processing, if one attempts to process a trauma that occurred at age 8, all the “pages” of learning from birth to 8 years old are “underneath” age 8. It follows logically that in processing the disturbing experience at age 8, there occurs a punching through of all thematically related prior learning before age 8. For individuals with sufficient ego strength, this is one of the benefits of EMDR, namely, that one EMDR target clears numerous underlying thematically related traumas. However,

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for individuals with complex trauma histories, this volume of traumatic learning experience may be entirely too much to process at one time. Attempts to do so may result in abreaction, affective overwhelm, and truncated processing. This is especially true for those who did not acquire smooth state switching and affect regulation in infancy. Most highly dissociative patients then have decades of accumulated unprocessed disturbance accumulated from infancy and an inability to approach the affective disturbance because of the very problem at the origin, namely, an inability to regulate affect and engage in smooth state switching. The use of EMDR with such an individual risks blowing a hole in the “dike” of amnesia and structural dissociation that holds at bay the ocean of overwhelming traumatic experience in its fullness and voluminousness. Regrettably, clinical lore is replete with examples of complex trauma clients whose treatment consisted of premature, improperly prepared for or improperly applied standard EMDR rather than an appropriate preparation and modified approach to the protocol that would attenuate and titrate the volume and intensity of material to process. With temporal integration, instead of processing a later disturbance with all its underlying “pages,” the therapist targets and processes traumatic experiences from the beginning of life, one small time period at a time, imaginally repairing that developmental time period in full before proceeding to the next (O’Shea, 2009a). Intense or overwhelming abreaction is much less likely and the volume of traumatic learning to process through is manageable. Continuing with the above example, having first processed disturbance from infancy through the first years, by time frame, when ready to process the traumatic events at age 8, those traumatic memory experiences are processed with a new foundation underneath. That is, the patient will now have a felt sense of having had her needs met in the period from birth to 8, and with a newly established capacity for affect regulation and smoother state switching. This makes the processing of the traumatic events at age 8 much easier to process, titrate, manage, and repair. Dissociative patients may not be ready to undergo ET treatment for some time due to the need for extensive preparation, as described in Chapters 14 and 15 and earlier in this volume. However, as soon as it can be safely conducted, the temporal integration approach enables trauma resolution and developmental repair, including attachment repair, to occur without as much risk of abreactive overwhelm. This makes all subsequent trauma processing much easier to conduct. As a result, the trauma processing phase of treatment for DID patients goes more manageably and smoothly than with other methods, in the author’s experience. The use of bottom-up processing results in an integration process that is relatively gentle compared to more traditional trauma approaches that typically focus on later time periods in a patient’s life and frequently involve intense abreaction. The rationale for the temporal approach is informed by the following analogy: If one attempts to three-hole punch 50 pages of paper at a time, the likely results are that the holes do not punch easily or cleanly. In contrast, if one begins with the first pages of the stack of paper, and punches only a few at a time, the holes are perfect. Subsequent small groups of pages can be punched in sequence with ease and equanimity. In temporal integration, one “hole-punches” the earliest years gradually by one small time segment at a time and laid to rest, in sequence. In this stepwise manner, a new foundation is laid. Each subsequent time frame takes its place with relative ease, being reviewed and repaired, and serving as a developmental foundation for the next time frame.

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The systematic clearing and repair by time period, beginning at or before conception, serves to titrate the intensity of ET, which is typically experienced without access to adult resources, but with the felt sense of baby’s meager emotional resources. The result is dramatically less abreactive overwhelm, usually even with dissociative patients. The more Big T traumas (the term of art used by trauma specialists to refer to those traumas that anyone would recognize as a trauma, such as a fiery car crash. This is in contrast to Little T traumas, which might be formative but not overtly apparent to an observer as a trauma, such as the pivotal graham cracker incident in the kitchen at age 18 months) occur very early in dissociative clients, the more likely abreactions are to occur requiring ego state interventions and downward regulation using hypnotic fractionation methods. As the work progresses, the parts of the self/ego states come together from the base, so that subsequent processing is made that much easier by the trending toward integration of states. As processing continues, there is an ever more solid foundation of repaired development.

INTEGRATION OF PARTS OF THE SELF FROM THE BOTTOM UP: THE TULIPS ANALOGY

To illustrate temporal integration from the beginning of life, consider a bouquet of tulips. If they are held by one hand from the base of the tulips’ stems, the heads of the tulips will splay outward with space between them. This is comparable to the dissociated parts of the self. If, while still holding the tulips from the base, one moves the other hand up the stems, the heads of the tulips come together. They are still separate tulips, which is comparable to separate ego states, but they are more integrated and less disparate because as the hand moved up the steps the hand pulled the tulip heads together. Once the ET period is repaired in this way, the now partially integrated self-system can be further integrated with standard EMDR processing of explicit memories from later childhood.

ET WORK IS SYSTEMATIC AND TIME EFFICIENT

The systematic nature of ET work makes it easier to conduct. This is because, though one is groping in the dark for the trauma snippets in implicit memory requiring repair, one does so systematically. In short, for dissociative patients, the work, if properly conducted, will lay a new foundation that will profoundly change the substrate, character, tapestry, resources, degree of integration and coconsciousness, and internal cooperation of the self-system. This will make a significant improvement in not only subsequent therapeutic efforts but also in the experience of life itself, which is, after all, the whole point of therapy. Dissociative patients who have undergone this ET procedure to any degree, even if financial resources or other contraindications did not permit complete processing in an intensive format, will find subsequent therapeutic work of any kind to go easier and more efficiently because of the more solid foundation from the early repair.

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For DID patients, the amount of trauma held in the early time frames can be daunting. The time and cost of the intensive work, even using the ET approach, can be prohibitive. However, spending time repairing on the first year(s) of life for many DID patients will produce significant integration that will make any form of subsequent therapy far more time efficient. This is a better use of that same time than it would be to skate quickly over the top for a greater number of time periods, with less deep resolution and integration. The first year(s) of life are profoundly important to repair because of the seminal nature of attachment and other developmental milestones in that period, so attachment or other trauma in this time frame can produce enormous sequelae. As one example, annihilation terror can occur when an infant is left alone and unheld without the comforting structure of loving arms and loving eyes to provide the containment that the infant cannot provide for him- or herself. Untreated annihilation terror is hypothesized to produce myriad symptoms, including affect dysregulation, dissociation, generalized anxiety, chronic depression, terror, and more. When annihilation terror is processed and repaired with the ET protocol, the reduction in those same symptoms is striking.

State Switching, Affective Circuits, and Dissociation: The Circuit Breaker Analogy

The reader may recall Panksepp’s (1998) findings that mammals, including human ones, are born with hardwired affective circuits that require no learning. These early circuits provide the basic information required for attachment, fight, or flight; becoming a social animal; and the seeking of information and solutions to problems. The capacity for smooth state switching is acquired in the period following birth, in the relationship with the primary caretaker. When the child is not yet capable of regulating his or her own affective arousal, the presence of a loving and attentive caretaker serves to provide an externally located regulatory function. From such a caretaker, the child learns a range of lessons that, all being well, will result in the capacity for affect regulation. Those lessons will include, for example, that emotions come and go in waves; that one can switch smoothly between states; that emotions provide information about one’s safety and well-being, leading to action behaviors, and more. In the course of this learning, which occurs on top of the hardwired affective circuits, fundamental lessons about relationships to others are also accrued. The infant initially doesn’t distinguish between self and others. Over time, the infant learns that others are either a source of safety or a source of danger; or perhaps that others are unreliable and not predictable. The child may learn that his or her own emotions and needs are not seen or acknowledged by the other, and that only the other’s emotions and needs are important. Such a child will learn to stifle his or her own needs, feelings, and impulses early in life, and adopt the strategy of dissociation if that option is available to that child (Barach, 1991). Children who are called “good babies” are sometimes the ones who learned early to stifle all sounds and impulses, though other “good babies” may have been born with peaceful temperaments.

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As each time period passes, the normal developmental milestones of infancy come and go. These milestones may not be navigated successfully if the infant lacks the support of caretakers or is navigating trauma as well as developmental milestones. Dissociation, therefore, is an option that allows the infant to cut off the experience of unbearable pain, but at the cost of not being present for the successful completion of developmental tasks. If the child does not have the assistance of a loving mother to learn smooth state switching and affect regulation, cutting off of emotion is the only option. The affective circuits then are not available for normal affective information. Affect is cut off or dissociated at the thalamus, much as a circuit breaker is flipped to suddenly cut off power. Without acquiring smooth state switching in mother’s loving arms, baby can only flip the switch. Such an infant is at risk for a lifetime of affective overwhelm and dysregulation, each time the unprocessed affective material is triggered in current time by relationship or other environmental triggers, followed by a sudden switch. Adults without sufficient consistent loving attachment experiences who did not learn smooth state switching at the level of secondary brain processing must rely on dissociative switching off of their hardwired subcortical affective circuits. As they acquire more learning, in the absence of integration horizontally across circuits that would come with smooth state switching, the learning accumulates vertically in columns built on subcortical affective circuits, through attachment learning and subsequent higher order learning. This dissociative switching can render abortive or even disorganizing results in EMDR processing of dissociative patients; once the EMDR disrupts the dissociation, shutting down or flooding is the likely result. The ET approach, when modified for dissociative patients, with the addition of ego state, somatic, and other changes, not only circumvents that problem but repairs the switching, replacing dissociative switching with smooth state switching as age-wise horizontal integration occurs of the circuits and hypothesized vertical (columnar) learning structures.

EMDR AND EMERGING IMPLICIT MEMORY

The standard EMDR protocol targets an explicit memory with its concomitant imagery, negative cognition (NC), affect, and body sensation. Since there is no explicit memory and likely no explicit image or overt cognitions, the target in the ET approach is merely the time frame from the first years, beginning at the beginning. Additional targeting material may or may not emerge during the processing. For the layperson, a memory, by definition, refers to a picture or image of a past event. However, in the ET processing the target is a time frame for which there is likely no image, no explicit memory, and therefore no possible NCs or positive cognitions (PCs) initially. Only the felt sense is being processed but other material may emerge during processing. The therapist should be alert to cognitions that emerge, and capture negative and PCs as they occur in the course of the work. As an example, a patient may report during ET processing that she has a felt sense of doom or lack of safety, with no context, and then say that it seems as if she hears arguing. The therapist will support a suspension of disbelief and a stance of curiosity to enable the patient to process

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through whatever the disturbance is, without stating a certainty that the therapist knows what the nature of the disturbance is. If during the processing the patient states a vague sense of believing, “I’m so bad,” the therapist will capture this as an NC “I’m bad” and ensure that an appropriate PC such as “I’m fine,” is installed using bilateral stimulation before work is complete on that time frame. The infant’s early world is experiential, not cognitive in the verbal sense, and baby is preoccupied with developmental milestones. Therefore, the work of repairing trauma from infancy revolves around specific developmental tasks associated with the time frame in question; baby’s awareness of physical growth, emotional growth, and relationship tasks. The relational and attachment tasks are associated with the secondary processing level of brain development (e.g., Panksepp, 1998), which includes the I and Thou of intersubjectivity and mentalization (Fonagy, Steele, Steele, Moran, & Higgitt, 1991), being seen, honored, having an effect on others, and coming into coherence in that relationship (Siegel, 1999).

REENACTMENT AS LEAKAGE OF DISSOCIATED MATERIAL: THE STORYTELLING ITSELF

One of the most common problems of any trauma work is traumatic transference, in which the relationship dynamics of the original traumatic experience are mistakenly attributed to present time. This problem is less of a hazard with standard EMDR, but in working with complex ET the therapist must be alert to the leakage of contained material into the relationship field. Dissociative patients may already have a capacity for containment, but because it is unconscious and habitual, it is dissociative rather than an at-will resource. As that capacity is utilized, developed as a conscious skill in the containment step, the therapist will need to be aware of and make the patient aware of the phenomenon of leakage of traumatic material from contained or dissociated places into present time in the form of reenactment material. It is the storytelling itself. The author uses cartoons and metaphors with patients (Paulsen, 2009a) for psychoeducational purposes. To communicate about the phenomenon of reenactment, she often uses the notion of King Tut’s tomb. She says, “When that first archaeologist opened King Tut’s tomb, the air that hit him was thousands of years old. If he wasn’t aware of that, he might think he needed a bath, as if the staleness was caused in present time. In fact it was ancient history that was only accessed in present time.” In the ET work, all that isn’t being worked on is contained, and then systematically and deliberately accessed by time frame. When ancient vapors leak up from their containers in ET work, the patient may think and feel that it is coming from present time or the current relationship with the therapist. Or between sessions, those ancient “vapors” may be attributed to a spouse or a boss or a current relationship. So the therapist will be asking, “Is this the first time you have felt that feeling (dynamic), or could this be part of baby’s story?” Once prompted, the patient will typically realize it is leakage from baby’s contained experience. A DID client may just switch, requiring ego state maneuvers to reinstate grounding and help from older resourced alters to bring in awareness that the disturbance is memory, not happening now.

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RELATIONSHIP TEMPLATES EMERGING DURING PROCESSING

This secondary level of affective brain processing (Panksepp, 1998) is a complex overlay of state-dependent learning acquired during attachment and socialization periods. Relationship learning results in either well-functioning affective circuits or the inhibition of them. In processing ET, the purpose is to remediate the earliest relationship dynamics and to clear or “reset” the circuits so they can conduct emotional information optimally. If those milestones can’t be successfully navigated in childhood, the result is injury to the self, which is often accompanied by a sense of despair and hopelessness, especially if the disappointments were chronic. When processing these early time frames, the relational material does not always come explicitly into a patient’s conscious awareness. Rather, it can remain unconscious but emerge in the room and in the relationship field with the therapist, as mentioned above, and the patient experiences the felt sense of the infant’s helplessness, shame, sorrow, and so forth, but construes it as relating to present time rather than being part of a memory. The therapist’s job, over and over, is to puzzle aloud whether the material in the relationship field is really about present time and circumstances or whether it is baby’s storytelling itself in the behavior, in the relationship field, or in the energy in the room. The nuances of traumatic dynamics that emerge in the course of ET processing are typically about body development, or about who in the family of origin is important, who gets to have feelings and needs, whose point of view is real and valid, and whose is not. In the case of trauma patients, often the baby was unimportant, not allowed to express feelings and needs, and baby’s perceptions were not validated. After the story is acknowledged, the energy shifts and imaginal repair becomes possible. Until this story is acknowledged, the patient’s developmental maturity is often arrested at the point of incomplete developmental milestones of infancy related to the development of self, trust, attachment, and other relationship templates. Particularly obstructive is the infant’s shame regarding having had needs and feelings at all, given that his or her caretaker turned away or got angry, leaving baby alone with a sense of defectiveness. This is the heart of ET work. With dissociative clients, the enactment material that emerges during processing can be dense, intense, behavioral, and disorganizing to the process if combined with state switching. Ego state and other maneuvers are needed to navigate these enactments during processing, the specifics of which are described elsewhere (Paulsen & O’Shea, in press).

CAPTURING NEGATIVE AND PCs

In the standard EMDR protocol, a memory and an associated picture that represents the most disturbing aspect of that memory is selected. Targeting further involves articulating both an NC that reflects the words that bespeak the patient’s negative belief about themselves now when they think about the memory, and a PC that reflects the goal of what the patient wishes to believe instead of the NC. Targeting also involves determining a Validity of Cognition (VoC) rating, which reflects the validity of the PC on a 7-point scale where 1 represents completely false and 7 represents completely

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true. Finally, targeting requires the therapist to ask the patient to hold the picture and the NC in mind and identify what the feeling or emotion is in present time, where that disturbance is felt in the patient’s body, and how disturbing it is. Disturbance is measured as a SUD number (subjective units of distress scale) from 0 (no disturbance) to 10 (the most disturbance imaginable). The ET approach describes basic preparatory steps that work for most patients. More dissociative patients will require additional preparation steps as well as egostate modifications during each of the steps to engage the relevant parts of the patient’s self-system and resolve interference from defensive parts of the self. The four basic steps, described first by O’Shea (2006), and the additional steps commonly needed for dissociative patients include ego state preparation, containment, safe state resourcing, resetting the affective circuits, and extensive stabilization and preparation steps such as somatic resourcing, skills building, hypnotic containment and other maneuvers, and establishing boundaries. Once the preparation is complete, which for dissociative clients will be more lengthy than for others, the final and most extensive step becomes possible, namely, clearing ET by time frame, which results in temporal integration.

EMDR TARGETING FOR EXPLICIT COMPARED TO IMPLICIT MEMORY

In the standard protocol of EMDR, a target is selected that is an explicit memory of an event that typifies the issue that the therapist and patient have agreed to work on. The target workup begins by articulating the picture that represents the most disturbing aspect of the memory. In addition to that image, an NC is chosen that expresses the patient’s negative belief about him- or herself, as well as the positive cognition (PC) that the patient would like to have the NC replaced. The VoC is assessed, from 1 to 7, where 1 is completely false and 7 is completely true, to determine how true the PC feels in the gut, not intellectually, at the outset. As well, the emotion associated with the memory in the present moment, and the location in the body of sensations associated with the memory are also identified, along with the SUDs, from 0 to 10, where 0 equals no disturbance and 10 equals maximal imaginable disturbance. With this workup, processing is ready to begin when the standard protocol is used. None of the above standard EMDR target workup is typically possible for traumatic experience held in implicit memory from the first years of life. There may be no image or any images may be dreamlike, symbolic, or fragmentary. There is little by way of cognition accessible, negative or positive. There may or may not be an awareness of affect or body sensation initially. Without these mileposts, the standard protocol is impossible to use for early experience. Some have suggested targeting key relationships such as the relationship with the mother or the father, but there, processing tends to access associations for later childhood or later life, where explicit memory is available. This risks affective overwhelm because of the volume of memories being simultaneously processed and still fails to address very early experience in infancy. In the ET approach, target workup is transformed from working in explicit memory to implicit memory by targeting a period of time to which the patient is asked

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to turn his or her attention. Images or dreamscapes may emerge, and the therapist will not take a strong position on their veridicality, though the patient will typically place some trust in what emerges as time proceeds. The therapist will encourage the patient to suspend judgment and rather emphasize repair of what is manifesting. Because in the ET approach targeting is done by time frame without access to explicit memory, it is not possible to articulate NCs and PCs as is done in the standard EMDR protocol. Rather, they are captured as they emerge in the course of processing, along with concomitant affection and body sensation. Closure is conducted at the end of an ET session no matter how many time frames were covered within that session, whether structured to be a short or extended session. Similarly, reevaluation is conducted subsequent to the ET session, whether at the next regular session, the next extended session, or by remote communication if the ET session was conducted using an intensive structure of one or more long days. In this method, it is important to adhere to each element of the standard protocol where it is possible to do so, so all the eight phases of EMDR are employed.

STRUCTURE AND PRACTICAL DETAILS

Customarily, psychotherapists will likely need to conduct ET sessions within 45- to 50- or 90-minute sessions. Preferably, however, extended sessions of half- to full-day sessions, structured with breaks, are the ideal way to employ the ET approach. This is because in brief sessions patients and therapist are more typically operating in a left-hemisphere frame of reference. As therapist and client get into the nuances of ET work, however, especially while processing infant experience by time frame, time slows down and the work becomes more of implicit memory in the right hemisphere, wordless, somatic, and held in the relationship field between therapist and patient. As such, in a short session one only begins to get into the material when one runs out of time. In an expanded session, there is time for the nuances to reveal themselves, be verbalized, appropriate processing and interweaves to occur, and have the patient recontain and reground in preparation for the world outside the session. For dissociative individuals, long sessions can be disorganizing and are contraindicated except in the rare case of special procedures, for which the ET approach qualifies. Therefore, there must be a balance between the benefits and hazards of an extended session for dissociative clients. It is critical that the time not be unending and unstructured, as that would be not only disorganizing on its face but also reminiscent of perpetration, which was often interminable. Complex trauma patients should be told ahead of time that the work will be structured with breaks. When a long session is clinically indicated, there still should be a break every 90 to 120 minutes, to ensure the treatment frame is maintained and there is sufficient rest. Of course, patients should know that they can stop the process if need be. Another consideration is the modality of bilateral stimulation. Tapping is often used, as the sensory domain is especially salient for infant ego states. Although there is no research on point, clinically it seems for some clients that eye movements are more likely to evoke cognitive processing, and somatic stimulation more likely to produce somatic responses, or responses from implicit memory. Also, for many patients,

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the physical proximity of the therapist to the patient becomes more salient in ET work. This is because the patient has access to infant states for whom the proximity of another person is profoundly important and reassuring. Although all laws and ethical considerations regarding touch should be taken into account, where appropriate, proximity and tapping on the ankles, under a cloth if need be, while the patient is in a reclining chair may be a source of reassurance. O’Shea and Paulsen (2007) recommend the use of reclining chairs, so the patient may be comfortably recumbent and the therapist can ergonomically tap on the patient’s ankles with the chair in the reclining position. If the therapist is in a chair on wheels, adjustments can easily be made to increase or decrease proximity even if the therapist is not tapping, but rather utilizing tactile bilateral stimulation equipment or auditory equipment. Technology is contraindicated for many torture survivors for whom devices are disturbing. At the same time, for complex trauma patients, touch may be contraindicated by patient preference or by clinical judgment, especially where the therapist’s gender is the same as the patient’s perpetrator’s gender. For some, the use of a towel or fabric over the ankles creates adequate boundaries and distance. For others, even that will be unwelcome or inappropriate, and EMDR tactile equipment may be held in the patient’s hands or tucked into the patient’s sleeves or cuffs to evoke tactile sensation without human touch. Having the feet off the floor may be “ungrounding,” so tapping on the hands may be preferred, though over extended periods of time may be unsustainable ergonomically for the therapist. If a dissociative client can tolerate neither touch nor technology, he or she may need to provide his or her own bilateral stimulation with tapping on alternate arms or tapping feet alternately. Other considerations include the therapist’s use of a gentle and comforting tone, soft lights, and ready access to items that will evoke a resourced state. These may include canines, equines, the outdoors, fragrant oils, or other items that activate the patient’s ventral vagal nervous system and keep the patient in the window of tolerance (Siegel, 1999).

POSSIBLE TIME AND SESSION USAGE FOR THE ET APPROACH

Nondissociative patients may require as few as two preparation sessions to conduct preparatory steps, though several sessions are more typical. In contrast, highly dissociative patients may require months or even years of preparation before the ET approach can be attempted because of fragility, resistance, risk, and the challenges of establishing rapport under conditions of profound mistrust. In the ET approach, the establishing of therapeutic rapport and a trusting relationship are still very important, of course; undertaken at the right time, these procedures can reduce preparation time for EMDR considerably.

Sample Language for Initiating Processing With Bilateral Stimulation

Thorough language is beyond the scope of this chapter; however, a few sentences will be offered to illustrate how time is used as a target in the ET approach. After preparation steps are in place, and informed consent is complete for the trauma-processing

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step, the therapist might say, “Leaving all later material in your container, and with parts watching from their theatre seats (or suitable metaphor) we can begin processing by time frame. To begin with, where were you, if anywhere, before you were conceived?” (client answers from within a spiritual or nonspiritual frame of reference) and therapist says, “Notice that,” adding bilateral stimulation via tapping. This is intended to evoke a felt sense of resource before anything bad happened. For spiritually inclined individuals, there is often a sense of being one with the universe or loved by God. For a later time period, for example, second trimester, the therapist might say, “Turning your attention to the second trimester of your gestation, just notice with curiosity and we’ll see what’s there.” The patient will report anything from thoughts, to body sensations, to affect, to nothing. If there is disturbance, the therapist will engage in a number of sets of bilateral stimulation to see if more story emerges, if not or if it fails to spontaneously release or resolve, the therapist will say, “What would you have needed to have a different outcome?” When the client reports what he or she would have needed, the therapist might say, “Imagine it being the way you needed it to be, or what you needed to do.” This dialogue will repeat and continue, repeatedly reviewing the time frame until no residual disturbance remains. Often this requires repeated listening to the story in the “dust bunnies” of affective, somatic, cognitive, or behavioral report. The time segment isn’t left or considered complete until it is not only completely clear but the client answers affirmatively to the query, “Have you had the felt sense (or what else would you have needed) to have gotten what you needed, the way you needed it to be?” and imagined it vividly. Once a time segment is completely cleared and imaginally repaired, the therapist invites the patient to move to the next time segment. The time segments may vary, but are often about 3 months. For dissociative patients the time frames may need to be considerably smaller as the circumstances and story dictate, to prevent overwhelm.

INTERWEAVES IN ET PROCESSING FOR DISSOCIATIVE PATIENTS

In ET work accessing implicit memory, and especially in ET work with dissociative patients, spontaneous linkages to adaptive neural nets are less likely to occur than in standard EMDR conducted on explicit memories. This appears to be because the work is conducted on and in infant states, and at the time, the child had very little in the way of adaptive resources available. For that reason, interweaves are very likely to be needed. When the processing has not moved in several sets, the most common interweave is an imaginal one, such as, “What would you have needed to have a different outcome?” or in the imaginal repair phase, “Imagine getting what you needed, the way YOU needed it to be” (O’Shea & Paulsen, 2007). Extensive discussion of possible processing outcomes and therapist decision making is beyond the scope of this chapter, and is explained in detail elsewhere (Paulsen & O’Shea, in press). In particular, the work is best served if the therapist can draw upon a range of interweaves, especially ego state, cognitive, imaginal, experiential, somatic, and psychoeducational, not only for preparation but also to get shifts in stuck processing. Two interweaves, orientational and temporal, are key to this work.

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In orientational interweaves, especially with dissociative patients, the therapist reminds the patient, addressing specific parts of the self that it is the present year, location, and circumstances and, if the part is an introject of an external person, that he or she is not the external person but a likeness of them, resident in the body of the patient. In temporal interweaves, the therapist invites the patient to consider whether the experience in question, which the patient is attributing to present time, is actually part of baby’s story. Temporal interweaves require the therapist to be acutely attuned to reenactment material in the relationship field.

REVIEW, RELEASE, AND REPAIR

O’Shea concisely describes the sequence of ET processing as involving “review, release, and repair,” in that order. First the processing reviews the nuances of implicit memory, gleaning whatever aspects of the story can be gleaned, which enables the energetic and traumatic holdings to be released. If they don’t release spontaneously, they are shifted by use of interweave, as described above. Finally, the developmental period and its unmet milestones are repaired imaginally for the processing to be complete. Once the milestone is repaired, the time period is completed and the work can move to the next time frame, with the new and solid foundation just completed. For completeness, any captured PCs that emerged in the course of processing should be installed either at the end of each bit of processing, the end of a 90-minute session where appropriate, or by the end of a day of processing. If no PCs have emerged spontaneously from the patient, or if no PCs have been captured by the therapist’s intuition in the course of processing, the therapist should ask, “Do any words come to mind that reflect what you now believe about yourself?” Assuming the words meet criteria for a conventional PC, then those words become the new PC for installation for the early time segment, processing segment, or session. For nondissociative patients at the end of a session of processing, a final body scan should be conducted, if the work has successfully gotten to the end of a time frame with adequate resolution. For dissociative patients, this step is overly ambitious, and containment is more likely to be a successful goal. For all patients, containment steps may include whatever language has been typically employed for this patient, over the time of prior therapy, for ending a session. Because the initial step of the ET approach involves use of container imagery, that imagery should be utilized at the end of the session in the form of “Let whatever is left go into your container now, and let me know when that is complete.” For a dissociative patient, the language may sound more like, thank you to each part of the self that helped today by allowing their memories to be held separately, and now gathering up any fragments of memories for any part of the self, and for baby, and allowing those memory fragments to go into the container or containers, that’s right, and putting the containers on the shelves, and with appreciation, I’ll fluff up the cloud pillows for any who want it, and tuck you in with cloud blankets, and I’ll wave good bye as your clouds pull away and take you deep inside for a deep healing sleep, deeper and deeper still,

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or other such end of session language. The above offered language has the advantage of being two-step (Paulsen, 2009a), with one step for the nonegotized memory fragments, and one step for the ego states or parts involved. This provides a systemwide metacognition that assists with grounding, pacing, and stabilization. Certainly, when there is residual disturbance, but even if there is not, the patient should be alerted to the possibility of continued processing and/or disturbed sleep. Also different from the debriefing instructions for the standard protocol of EMDR is that the patient should be alerted to the possibility that the baby’s story may “leak” into present relationship. Such leakage will likely reflect any unfinished piece of work just beneath conscious awareness or the next piece readying itself to emerge. The therapist should instruct the patient that, for example, if the work had to stop in the middle of a piece involving helplessness that was not able to resolve, the patient may have uneasy access to that feeling of helplessness until the work can continue in some form. The patient may feel helpless at work or in her marriage, and so forth, but chances are that the feeling is fueled by the work with the baby state. The patient is very likely to forget this instruction, and the therapist should use some means of reminder of this likelihood to minimize risk of decompensation or disruption of functioning and relationships. At a minimum, at the next session, when the patient reports her status, the therapist should listen careful for indications that the patient is in the midst of a state fueled by the early work. Once a given time period has been reviewed and the traumatic holdings have been released and repaired, the therapist should go back and check the time period for additional emerging of unresolved material. This rechecking may require several iterations until there is no residual disturbance for that time period, be it emotional, cognitive, behavioral, or somatic. A patient may report that, “It’s not bad,” or that “There’s a little but not much,” and these may be minimizations in an impatience to move ahead. Another very common reason for minimization is that the primary caretaker made clear to the infant that the child’s needs and feelings were of minimal importance. The therapist will need to work repeatedly using ego state maneuvers with the caretaker introject to decrease loyalty to the aggressor, according to procedures reviewed elsewhere (Paulsen, 2009a, 2009b). If the time period isn’t completely reviewed, released, and repaired, however, moving on to the next time period is premature, and will result in incomplete resolution of symptoms and possibly complicate the processing of subsequent time periods. It is better to ensure complete resolution to ensure the foundation is completely solid for subsequent processing, and in order for the developmental milestones for that time period to be imaginally achieved, which will result in a resolution of those presenting symptoms related to the time frame. Although there is no controlled research available on the ET approach to date, the kinds of reports one hears after ET processing are typically that the patient is much less reactive, more emotionally neutral and stable, better able to be in present time, better able to utilize emotional responses as information, better able to engage in a healthy relationship, more valuing of the self, and less likely to feel ashamed of needs, feelings, or shortcomings. Clinically, the therapist observes a decrease in not only Axis I presenting symptoms but Axis II symptoms as well. This chapter has reviewed the theory of temporal integration and its general application in trauma processing for very ET in implicit memory for dissociative

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patients. Procedural details are presented elsewhere for more comprehensive coverage of the complexities of the procedure for dissociative and nondissociative clients (Paulsen & O’Shea, in press). The reader should bear in mind that for dissociative clients additional preparation steps are needed beyond the ET steps of containment, safe state, and resetting the affective circuits prior to clearing trauma by time frame. Those steps are indispensable and covered in O’Shea (2009a, 2009b) and Paulsen and O’Shea (in press). For dissociative clients, additional preparatory steps may be needed as reviewed in the stabilization chapters in this book related to ego state and other methods, such as those discussed by Paulsen and Golston.

REFERENCES Barach, P. M. (1991). Multiple personality disorder as an attachment disorder. Dissociation, 4, 117–123. Bowlby, J. (1980). Loss: Sadness & depression. Attachment and loss (Vol. 3; International PsychoAnalytical Library No.109). London, UK: Hogarth Press. Cooper, A. M. (2009). The narcissistic-masochistic character. Psychiatric Annals, 39(10), 904–912. Federn, P. (1952). Ego, psychology and the psychoses (E. Weiss, Ed., pp. 5–6). New York, NY: Basic. Fine, C. G. (1993). A tactical integrationalist perspective on the treatment of multiple personality disorder. In R. P. Kluft & C. G. Fine (Eds.), Clinical perspectives on multiple personality disorder (pp. 135–153). Washington, DC: American Psychiatric Press. Fine, C. G., & Berkowitz, A. S. (2001). The wreathing protocol: The imbrication of hypnosis and EMDR in the treatment of dissociative identity disorder and other dissociative responses. American Journal of Clinical Hypnosis, 43(3–4), 275–290. Fonagy, P., Steele, M., Steele, H., Moran, G. S., & Higgitt, A. C. (1991). The capacity of understanding mental states: The reflective self in parent and child and its significance for security of attachment. Infant Mental Health Journal, 12, 201–218. Fosha, D. (2000). The transforming power of affect: A model of accelerated change. New York, NY: Basic Books. Fraser, G. A. (1991). The Dissociative Table Technique: A strategy for working with ego states in dissociative disorders and ego-state therapy. Dissociation: Progress in the Dissociative Disorders, 4, 205–213. Fraser, G. A. (2003). Eraser’s “Dissociative Table Technique” revisited, revised: A strategy for working with ego states in dissociative disorders and ego-state therapy. Journal of Trauma & Dissociation, 4(4), 5–28. Kitchur, M. (2005). The strategic model for EMDR. In R. Shapiro (Ed.), EMDR solutions: Pathways to healing (pp. 8–56). New York, NY: W. W. Norton. Klaus, P. (1995). The use of EMDR in medical and somatic problems. Paper presented at the EMDR Annual Conference, Santa Monica, CA. Kluft, R. (1990). The slow leak technique. In D. C. Hammond (Ed.), Handbook of hypnotic suggestions and metaphors (pp. 526–530). New York, NY: W. W. Norton. Kluft, R. P. (1989). Playing for time: Temporizing techniques in the treatment of multiple personality disorder. American Journal of Clinical Hypnosis, 32, 90–98. Kluft, R. P. (1993). Clinical approaches to the integration of personalities. In R. P. Kluft & C. G. Fine (Eds.), Clinical perspectives on multiple personality disorder (pp. 101–133). Washington, DC: American Psychiatric Press.

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Levine, P. A. (2010). In an unspoken voice: How the body releases trauma and restores goodness. Berkeley, CA: North Atlantic Books. Linehan, M. M. (1987). Dialectical Behavior Therapy for borderline personality disorder: Theory and method. Bulletin of the Menninger Clinic, 51(3), 261–276. Lynn, B. (2000). Accessing pre-traumatic prenatal experience using EMDR: Uncovering a powerful resource of equanimity, integration, and self-esteem in the pre-traumatized self. EMDRIA Newsletter, 5(3), 6–7. O’Shea, K., & Paulsen, S. L. (2007, September). A protocol for increasing affect regulation and clearing early trauma. Paper presented at the annual meeting of the Eye Movement Desensitization & Reprocessing International Association Conference, Dallas, TX. O’Shea , M. K. (2001, September). Accessing and repairing preverbal trauma and neglect. Paper presented at EMDR Canada Conference, Vancouver, British Columbia, Canada. O’Shea, M. K. (2003a, September). Accessing and repairing preverbal trauma and neglect. Paper presented at EMDRIA Conference, Denver, CO. O’Shea, M. K. (2003b). Reinstalling innate emotional resources. Paper presented at EMDR Europe Conference, Rome, Italy. O’Shea, M. K. (2006, June). Accessing and repairing preverbal trauma and neglect. Paper presented at EMDR Europe Conference, Istanbul, Turkey. O’Shea, M. K. (2009a). EMDR friendly preparation methods for adults and children. In R. Shapiro (Ed.), EMDR solutions II. For depression, eating disorders, performance and more (pp. 289–312). New York, NY: W. W. Norton. O’Shea, M. K. (2009b). The early EMDR trauma protocol. In R. Shapiro (Ed.), EMDR solutions II. For depression, eating disorders, performance and more (pp. 313–334). New York, NY: W. W. Norton. Panksepp, J. (1998). Affective neuroscience: The foundations of human and animal emotions. New York, NY: Oxford University Press. Panksepp, J., & Bivens, L. (2012). The archaeology of mind: Neuroevolutionary origins of human emotions. New York, NY: W. W. Norton. Paulsen I. S. (2001, December). Integrating EMDR, ego state therapy, and dissociative table: A cartooning psychologist’s glimpse into the mind’s eye. Paper presented at the annual meeting of the International Society for the Study of Dissociation, New Orleans, LA. Paulsen, S. (1995). EMDR: Its cautious use in the dissociative disorders. Dissociation, 8, 32–44. Paulsen, S. L. (2009a). Looking through the eyes of trauma and dissociation: An illustrated guide for EMDR clinicians and clients. Charleston, NC: Booksurge. Paulsen, S. L. (2009b, November). Working under the floor boards: Resetting affective circuits in preparation for clearing very early trauma with EMDR. Paper presented at the Annual Conference of the International Society for the Study of Trauma and Dissociation, Washington, DC. Paulsen, S. L., & O’Shea. (in press). When there are no words. Author. Phyllis, K. (1995, June). The use of EMDR in medical and somatic problems. Paper presented at the EMDR Annual Conference, Santa Monica, CA. Putnam, F. W. (1988). The switch process in multiple personality disorder and other statechange disorders. Dissociation: Progress in the Dissociative Disorders, 1, 24–32. Putnam, F. W. (1989). Diagnosis and treatment of multiple personality disorder (Foundations of Modern Psychiatry). New York, NY: Guilford Press. Schore, A. N. (2003). Affect dysregulation and the repair of the self. New York, NY: W. W. Norton. Schore, A. N. (2009). Right-brain affect regulation: An essential mechanism of development, trauma, dissociation, and psychotherapy. In D. Fosha, D. Siegel, & M. Solomon (Eds.),

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The healing power of emotion: Affective neuroscience, development and clinical practice (p. 16). New York, NY: W. W. Norton. Schore, A. N. (2012). The science of the art of psychotherapy (Norton Series on Interpersonal Neurobiology). New York, NY: W. W. Norton. Shapiro, F. (1995). Eye movement desensitization and reprocessing: Basic principles, protocols and procedures (1st ed.). New York, NY: Guilford Press. Siegel, D. (2012). Pocket guide to interpersonal neurobiology: An integrative handbook of the mind (Norton Series on Interpersonal Neurobiology). New York, NY: W. W. Norton. Siegel, D. J. (1999). The developing mind: Toward a neurobiology of interpersonal experience. New York, NY: Guilford Press. Watkins, J. G., & Paulsen, S. L. (2004, March). Abreactions in EMDR and hypnoanalytic therapies. Workshop Presented at the Annual Meeting of the American Society for Clinical Hypnosis, Anaheim, CA. Watkins, J. G., & Watkins, H. H. (1997). Ego-state theory and therapy. New York, NY: W. W. Norton.

CHAPTER 21

Toward an Embodied Self: EMDR and Somatic Interventions Ulrich F. Lanius and Sandra L. Paulsen

Sensory memory has a special place in information processing. It is our protection against living in a fragmented present. —Nelson Cowan, in Attention and Memory: An Integrated Framework (1995)

As discussed in Chapter 1, Dissociation: Cortical Deafferentation and the Loss of Self, under increased levels of stress, brain areas involved in higher levels of information processing (e.g., cognitive and emotional processing) become increasingly less active, resulting in diminished information processing. Moreover, while the eye movement (EM) desensitization and reprocessing (EMDR) standard protocol includes a somatic focus, it has been our experience that individuals with dissociative symptoms greatly benefit from integrating somatic and body-oriented interventions as well as an increased focus on body mindfulness. The present chapter focuses on how to effectively integrate somatic interventions during the different stages of trauma treatment, such as stabilization, trauma processing, and reconnection, and how to integrate their use to maximize the effectiveness of EMDR, resulting in more comprehensive and enduring treatment effects.

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THE EMDR STANDARD PROTOCOL

When we use the EMDR standard protocol, we work with sensorimotor, emotional, and cognitive aspects of information. These correlate with the three levels of brain architecture described by MacLean (1990): (a) The sensorimotor level of information processing (including sensation and programmed movement impulses) is initiated primarily by lower rear portions of the brain, (b) emotional processing by more intermediate limbic parts of the brain, and (c) cognitive processing by the frontal cortical upper parts of the brain. These three levels interact and affect each other simultaneously, functioning as a cohesive whole, with the degree of integration of each level of processing affecting the efficacy of other levels (e.g., Damasio, 1999; Schore, 1994). The EMDR standard protocol integrates cognitive, emotional, and sensory information. In individuals with significant dissociative symptoms, accessing all levels of information processing simultaneously can be overwhelming and result in increased dissociation and decreased information processing. Bottom-up processing focuses on sensory and sensorimotor processing.

THE WINDOW OF TOLERANCE AND THE MODULATION MODEL

Siegel (1999) refers to a window of autonomic arousal in which “various intensities of emotional and physiological arousal can be processed without disrupting the functioning of the system” (p. 253). Based on Siegel’s work, Ogden and Minton (2000) and Ogden, Minton, and Pain (2006) describe a modulation model that represents a visual representation of the biphasic response to trauma (van der Kolk, 1987), that is, hyperarousal and dissociation. When individuals’ arousal levels fall within the window of tolerance, by definition they feel comfortable with their level of activation. This allows information received from both internal and external environments to be integrated, whether it is of a somatic, perceptual, affective, or cognitive nature. It is under those conditions that information processing is optimized. Traumatized individuals tend to have great difficulties staying within this window of optimal functioning, exhibiting both hyperarousal and dissociation, reflecting dysregulated arousal (Lanius, Bluhm, & Lanius, 2007; Lanius, Bluhm, Lanius, & Pain, 2005; Lanius, Lanius, Fisher, & Ogden, 2006). Hyperarousal frequently results in tension-reduction behaviors and ultimately leads to increased dissociation and a freezing and numbing response. (In some clients with extensive trauma histories, when such trauma is accessed, hypoarousal may occur as a conditioned response rather than secondary to excessive hyperarousal.) At this point, large portions of the cerebral cortex shut down and no further processing of information occurs. Effective information processing occurs only within the window of tolerance. At the upper end of the window, information processing breaks down, likely due to significant peritraumatic dissociation (PD) that cooccurs with the apparent hyperarousal. Once the adrenalin charge of the hyperarousal disappears, the client will commonly be hypoaroused, often with significant numbing and depersonalization that obviates effective EMDR treatment. In clients who have a severe dissociative disorder, a switch commonly occurs at the point of extreme hyperarousal, with resulting

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unpredictable consequences for clinician and client. By keeping the client within the window of tolerance, uncontrolled switching can be reduced. The clinician can aid the clients in staying within their optimal level of arousal through both somatic and ego-state interventions. Thus, in contrast to the standard protocol, we suggest that in clients who tend to get stuck in significant hyperarousal or who flip from hyperarousal into depersonalization the clinician work with the clients proactively to avoid as best as possible the extreme peaks of hyperarousal. Specifically, we suggest that utilizing the metaphor of the window of tolerance allows us to more easily pace treatment to minimize hyperarousal and dissociation, thereby maximizing effective information processing.

EMDR AND THE ROLE OF SENSORY STIMULATION

Research suggests that sensory stimulation increases integration of sensory traces and memory (also see Chapter 11). Further, sensory input may also stimulate social engagement. That is, EMDR likely has a twofold effect. On one hand, it increases affective regulation, thus maintaining the client’s staying within the window of tolerance; on the other hand, it appears to increase associative access to memories. In that sense, sensory stimulation has both an accelerative and a braking function at the same time. Social engagement reflects a ventral vagal response that results in increased selfregulation and calming, thereby decreasing the likelihood of a dorsal vagal response. Social engagement also likely produces both interest affect and SEEKING, both of which can be conceptualized as investigatory orienting responses, which likely counter a dorsal vagal activation associated with a dissociative response. Thus, ventral vagal engagement increases the likelihood of efficient information processing. With severely dissociative clients, the effect of sensory stimulation is to accelerate processing by accessing previously dissociated memory. This acceleration will likely overwhelm any braking regulatory effect, thus decreasing both dual focus and body mindfulness and thus the client’s ability to integrate the information. This requires titration through ego state and other interventions. It is the authors’ view that these extreme cases’ sensory stimulation may need to be discontinued to avoid the introduction of additional traumatic material. At the same time, it is important to maintain dual awareness under these circumstances. The therapist needs to maximize ventral vagal social engagement by other means and thereby assist the client to stay in the “here and now.” Staying present is paramount.

TRAUMA PROCESSING AND TYPES OF BILATERAL SENSORY STIMULATION

With regard to sensory stimulation, ego states exhibit a range of responses, which can differ markedly within a single client. It is the authors’ experience that taps or auditory tones seem to be less stimulating, whereas EMs may be more activating

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as they stimulate more areas of the brain. Moreover, instructions to the clients to let the therapist know when they are losing connection with their body allows the therapist to assess if the clients are able to maintain a modicum of body awareness. Our clinical experience suggests that taps or auditory stimulation may be more appropriate for highly dissociative clients. Bilateral recordings with music may facilitate processing in individuals, possibly by accessing resourced states as the bilateral stimulation (BLS) is being embedded in pieces of music that are soothing to the client. Hand taps seem to work extremely well in many cases, but it is critical to make sure that the client is comfortable with touch, lest the touch be experienced as a boundary violation or traumatic reenactment. Touch, unless it is specifically triggering to the client, is usually profoundly grounding. Touch is a primary reinforcer (Francis et  al., 1999) and the quality of touch is related to the extent of orbitofrontal cortex activation (Francis et al., 1999). Therapeutic touch, if appropriately exercised, may provide a relief from profound shame, as clients with a history of sexual abuse will often literally experience themselves as “untouchable.” It provides the client with a learning experience that touch does not have to be sexual. At the same time, touch can trigger problematic countertransference for therapists. One must be aware of ethical issues, including scope of practice in one’s licensing jurisdiction. If in doubt at all about the use of touch, do not use it or seek consultation.

DUAL FOCUS AND BODY MINDFULNESS

In the case of complex trauma and severe dissociation, the EMDR standard protocol can show its limitations in a variety of ways. One is uncontrolled bridging into multiple traumatic events, reflecting the integrative nature of the EMDR procedure. This can lead to intense overwhelm with both hyperarousal and dissociation, resulting in a loss of dual focus and body mindfulness, thus blocking further information processing, frequently leading to destabilization of the client. Not only may this block further processing, but it may lead to the client being retraumatized as well as in some cases triggering self-harming behavior. At the very least, it will lead to increased avoidance and reluctance on the part of the client to proceed with further EMDR treatment. It is the authors’ opinion that maintaining dual focus and body mindfulness during EMDR processing is paramount for effective treatment. It is essential that the dual focus be maintained by fractionating and titrating traumatic material to reduce both dissociation and hyperarousal through somatic and ego-state interventions. Clients need to experience themselves within their bodies for effective EMDR processing. By focusing on somatic tolerance prior to accessing emotion, we help our clients increase affect tolerance. Many of these procedures can be used during the stabilization phase, prior to proceeding with trauma-focused work, but many of them also work well in tandem with the EMDR standard protocol in a way that can be conceptualized as an interweave, in a different form than the familiar cognitive interweave.

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In the case of the more complex posttraumatic presentations, including dissociative disorders, using a combination of ego-state interventions (e.g., Chapter  15) and somatic interventions—both in the preparation/stabilization phase, then later in conjunction with the EMDR standard protocol—dual focus and body mindfulness can be maximized, therefore assuring efficient information processing.

PERSONIFICATION, INFORMATION PROCESSING, AND THE BODY

A crucial aspect of information processing and the integration of unprocessed memory traces is what Janet (1928) referred to as “personification.” Personification, in a way, is the antithesis of depersonalization and disconnection from one’s somatic sense of one’s body. Even in the presence of factual memory of an event, the traumatic experience often becomes disembodied, as suggested by these quotes by trauma survivors with dissociative responses (Lanius et al., 2002): ■■ ■■

“I was outside my body looking down at myself.” “I was looking down at my own body while I was back reliving the car accident.”

Specifically, personification denotes relating synthesized material to one’s general sense of self, which should become regularly adapted through synthetic actions, and to becoming consciously aware of the implications of a personal experience for one’s whole life, giving one’s history and sense of self a continuity (Nijenhuis, van der Hart, & Steele, 2004). At the same time, both experiencing and reaccessing overwhelming events commonly interferes with these integrative mental actions (e.g., Marmar, Weiss, & Metzler, 1998). In the absence of an embodied self, personification fails. The conscious awareness of the traumatic event will remain factual knowledge that does not seem to pertain to one’s self. Unintegrated somatic memories related to the traumatic experience will continue to drive symptoms in their various forms. In other words, if the clients become disconnected from the somatic sense of their body—out-of-body experiences are one of the more common dissociative symptoms—and this state persists for any length of time, effective information processing cannot occur. That is, for information processing and personification to occur, both dual awareness and an embodied self are essential. The client, in addition to focusing inside in order to process the information from the past, needs to be able to attend to the external stimuli presented by the clinician. This dual attention provides context to the memory and constrains the client’s reaction to it in most cases. The therapist often needs to remind clients in order to maintain the dual attention awareness by saying, “It’s not happening now,” “It’s old stuff.” The dual focus and the “here and now” orientation aid in efficient information processing during EMDR treatment. In addition, the focus on the body, as part of the standard protocol, likely facilitates personification. The EMDR standard protocol maintains the dual focus in large part by means of BLS administered by the clinician, that at the same time stimulates an orienting response (also compare Barrowcliff, Gray, MacCulloch, Freeman, & MacCulloch, 2003). The client, by attending to the sensory input occurring in the present moment,

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becomes aware that the traumatic memory is just a memory, something that is not happening now, but is in the past. AWARENESS OF THE BODY: EXTEROCEPTIVE AND INTEROCEPTIVE AWARENESS

To facilitate both dual focus and body mindfulness, both exteroceptive and interoceptive awareness are required. Exteroceptive awareness includes the senses through which we perceive the outside world: sight, hearing, taste, smell, and touch. For the task of survival in the world, there also needs to be kinesthetic awareness and balance, also referred to as proprioception. That is, for goal-directed motor activity, the person needs a sense of the relative position of the body in a given environment as well as feedback about the strength of effort being employed in the movement, and a sense of balance. Proprioception, in essence, is a feedback mechanism that allows influence over motor output: the body moves (or is moved) and then the information about this is fed back to the brain, allowing subsequent adjustments to be made. Interoceptive awareness refers to sensitivity to stimuli originating inside the body that include pain, temperature, itch, sensual touch, muscular and visceral sensations, vasomotor activity, hunger, thirst, and “air hunger” that provide the basis for the subjective image of the material self as a feeling (sentient) entity, that is, an embodied self and emotional awareness (e.g., Craig, 2011). ONE BODY, MANY SELVES

It is common for trauma survivors to experience a fragmented sense of self and, in many cases, multiple selves. At the same time, there is ultimately only one body. Thus, the fragmentation of self at some level is likely cortical, even though it may relate to separate reptilian brain or animal defensive responses that reflect lower brain structures (Panksepp, 2001b). We suggest, that while capable of different defense responses, within the lower brain structures the brain is for the most part unified. This makes working with the body ultimately integrative and potentially very threatening and overwhelming for trauma survivors. That is, due to the integrative nature of working on a body level, many very dissociative clients are phobic of experiencing themselves in their bodies, so it is challenging to work toward somatic awareness with them. Awareness of one’s body is intimately linked to self-identity and a sense of self. For highly dissociative clients, any awareness of their own body that necessarily includes interoceptive awareness is frequently triggering to a point that it results in increasing levels of dissociation and decreased awareness of the state of their body. Only a sense of numbness or an absence of the sense of their own bodies allows them to function without emotional overwhelm. However, this goes hand in hand with decreased or lessened exteroceptive awareness, likely attributable to the disruption of the thalamic relay. This, in turn, is likely reflected by somatic symptoms that include sensations of numbness,

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decreased perception of touch, changes in vision such as blurriness, alterations in hearing, as well as in extreme cases decreased smell and taste. Indeed, without exteroceptive awareness that gives an awareness of the moment in time, interoceptive or somatic awareness is likely to be destabilizing. Moreover, proceeding to EMDR and trauma-focused treatment without somatic awareness is likely to result in poor treatment outcomes. The solution to this dilemma is a stageoriented treatment process that starts with stabilization activities that increase exteroceptive awareness prior to increasing interoceptive awareness. We suggest that only after both of these stages have been successfully negotiated should the client proceed to trauma-focused work.

STABILIZATION AND EXTEROCEPTIVE AWARENESS

As noted above, dissociative symptoms like numbing clearly affect exteroceptive awareness, for example, the ability to accurately perceive external stimuli. We suggest that prior to encouraging clients to focus on interoceptive or somatic awareness of their own bodies, the therapist needs to assist clients with increasing exteroceptive awareness and their capacity to be in the moment. That is, clients need to be able to focus on sensory stimuli prior to increasing their interoceptive awareness. Thus, with highly dissociative clients, as part of the stabilization phase, exteroceptive awareness comes prior to developing interoceptive awareness. That is, we suggest that the experience of our external context and our environment is the foundation of mindfulness. Without awareness of one’s own external context in the moment, there is ultimately a lack of awareness of time. Awareness of time is essential with regard integrating traumatic experience, as accessing the traumatic memory in the present moment allows the traumatic experience to be perceived as a memory rather than happening all over again. On that basis, the ability of the client to maintain exteroceptive awareness is essential to the treatment of traumatic stress syndromes and dissociative disorders. Indeed, awareness of exteroceptive signals ultimately results in an awareness of how these stimuli impact your body, thus ultimately increasing awareness of one’s body without, at least in most cases, resulting in a bridging into traumatic memories. Exercises that practice exteroceptive awareness are common in dialectical behavior therapy (Linehan, 1993) as well as sensorimotor psychotherapy (SP), and they are an essential part of stabilization: smell a flower, find a color, and so forth. All these activities serve to ground the client in the present moment. A focus on sensory input, five-sense perception (e.g., Ogden et  al., 2006)—vision, touch, hearing, taste, and smell—is the first step toward engendering a sense of body ownership or a sense of being “me.” Clinically, it has been our experience that it is not necessarily the strength or intensity of sensory experience that produces the effect we are looking for, but rather the emotional or sensory quality of the stimulus. Indeed, at times, a more subtle stimulus will produce more sensory gain and a greater orienting response. Ultimately, we suggest, the way the brain integrates different sensory signals that impact the body is the foundation of personification—the experience of this body as mine and a sense of self.

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EXTEROCEPTIVE AWARENESS AND SMELL: A SPECIAL CASE

Smell is the only sensory modality with sensory pathways that do not travel solely through the thalamus. Olfactory pathways travel directly to the limbic system and amygdala, and from there olfactory information is likely conveyed to lower brain structures, for example, the periaqueductal gray (PAG). This potentially allows for instilling an increased sense of safety. Moreover, attention to odor also significantly modulates neural coupling (Plailly, Howard, Gitelman, & Gottfried, 2008), increasing neural connectivity, particularly between the thalamus and the orbitofrontal cortex, thus counteracting frontal and thalamic deactivation in response to traumatic stressors (also see Chapter 1). Indeed, of all senses, smell, while potentially being the most profoundly triggering of the senses, may also have the capacity to override a depersonalization/dissociative response more than any of the other senses. Clinically, we have consistently observed that when clients experience increasing depersonalization and derealization, their sense of smell is reduced. Commonly this emerges in one nostril first. It seems that more often than not this is the left one, though particularly in clients with dissociative identity disorder (DID) a rapid switching between left and right nostrils is observable. This observation has allowed us to use the client’s sense of smell therapeutically. Typically, in the stabilization phase, we ask the client to explore smell using different essential oils. This will ensure that any smell to be used therapeutically is unlikely to trigger traumatic memories, as well as allowing the client to select specific smells that optimally assist the nervous system with grounding, for example, increase the client’s capacity to be in the present moment. We commonly use different types of essential oils. We find that resinous smells like cedar, cypress, spruce, pine, and frankincense are particularly beneficial with regard to grounding. Clients who are struggling with anxiety often also like the use of floral scents like jasmine, rose, or lavender. In some cases, activating scents can be utilized like citrus, bergamot, and eucalyptus. Not only can the client use essential oils to assist with grounding themselves outside of the therapy office, but client and therapist can use the client’s sense of smell to gauge how much depersonalization/derealization the client is experiencing at any given moment, as well as assisting the client to come back into the here and now when needed. In some cases, we have found it useful for the client to dab some essential oil in the vicinity of the nostrils, which will aid him or her to remain present during trauma processing. Alternatively, if a client is experiencing significant depersonalization/derealization during trauma processing, trauma processing should be terminated and the client can be encouraged to alternate smelling the essential oil with the left and right nostril until roughly equal smell returns in both nostrils, for example, engage in alternating olfactory stimulation. In some cases, using two different essential oils in succession, a grounding one like cypress and a calming one like jasmine, can assist to bring the client to the here and now.

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THE ROLE OF PROPRIOCEPTION AND SENSE OF BALANCE

It has been our experience that clients who tend to exhibit significant dissociative symptoms, particularly depersonalization and derealization, frequently benefit from exercises and tasks that challenge their sense of balance. Standing on one leg and engaging in a yoga flamingo pose is one such activity. Others include the use of an exercise ball or a balance board. All of them ultimately force clients to be present in their body and attend to both exteroceptive and proprioceptive input, as they would otherwise lose balance. At the same time, the task usually entails sufficient attentional demands that neither therapist or client usually needs to be concerned about, with the client gaining interoceptive awareness to the extent where they start accessing somatic memories involuntarily without being directed to do so. Indeed, during the later stages of therapy during trauma processing with EMDR, the difficulty of the proprioceptive task can be varied when the client is directed to access traumatic memories. In that case it will aid in titrating the speed in which traumatic memories are accessed by providing an alternate focus on the proprioceptive task and ultimately distracting the client from focusing too intensely on the traumatic material and dissociating as a result.

INTEROCEPTIVE AWARENESS AND SOMATIC MEMORY

Interoception or interoceptive awareness is the sense of the physiological condition of the body and is a ubiquitous information channel used to represent one’s body from within. Interoceptive and somatic awareness increase the likelihood of accessing somatic memory. Particularly, traumatic memory that tends to be nonverbal in nature is more likely accessed. For a lasting treatment effect, working with the somatic traces of traumatic memory is essential. The somatic memories that are responsible for a multitude of traumatic stress syndromes also give us the opportunity to integrate, reevaluate, and reprocess the experience that brought them about in the first place. As Cowan (1995) suggested, Sensory memory has a special place in information processing. It is our protection against living in a fragmented present, dominated by our own arbitrary and abstract interpretations of the outside world on a moment-by-moment basis. We think about things at a finite pace, and sensory memory of these things allows the memory of these things to linger while we think about them. (pp. 49–50) Working with sensory memory allows us to work with somatic aspects of memory, aiding in reprocessing and integrating them into present day experience. Affect and the Body: The Importance of Subcortical Processes

As we have suggested in Chapter 1, Dissociation: Cortical Deafferentation and the Loss of Self, under increased levels of stress, brain areas involved in higher levels of information processing, for example, cognitive and emotional processing, become

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increasingly less active, thus resulting in diminished information processing. By focusing on somatic processes prior to accessing emotion, we indeed help our patients increase affect tolerance. Indeed, Panksepp (2001a) has argued that affect is foundationally a subcortical process, a notion supported in a neuroimagining study by Damasio et al. (2000) as well as by animal research. Commonly, higher levels of processing, that is, cognitive and affective, can influence and direct lower levels. In PTSD, the opposite of the above is commonly the case, as sensory fragments have usually taken on a life of their own and intrude at any moment, beyond cognitive control. In this case, lower levels of processing may influence and direct higher levels. Our understanding of these processes can be informed by research with split-brain patients, who outside the laboratory context still behave in a unified manner during everyday activities, despite the fact that the main intracortical bridge or corpus callosum, for example, the fibers that connect the two halves of the brain, has been bisected. In this case, information is conveyed through lower subcortical structures or what has been referred to as the subcortical bridge (Austin, 1998, p. 361). Austin (1998, p. 362) suggests that the sorts of messages transferred across the subcortical bridge are “unconscious or preconscious codes nuances, we can never attach a name to.” Similarly, Gazzaniga, Holtzman, and Smylie (1987) have suggested that information relayed from right to left hemisphere in this way tends to be noncognitive in nature. Further, when these messages cross over from the left side to the right, they may engage in a kind of response readiness. Furthermore, in the left hemisphere this information may facilitate potential speech responses that are already well rehearsed and ready to be uttered. Our understanding of these subcortical processes is foundational to our conceptualization of bottom-up processing discussed below and how it may facilitate the integration of traumatic material through the subcortical bridge. This is one possible mechanism by which traumatic memories that are experienced as sensory fragments may be transformed into a coherent narrative.

AN EMDR BOTTOM-UP PROCESSING PROTOCOL

Given that the majority of clients who dissociate have some difficulty being mindful of their body when accessing trauma and/or mobilizing reptilian brain–based defensive responses, the first author (Lanius, 2000; 2009) adapted the work of Ogden and Minton (2000) with regard to bottom-up processing to EMDR, using BLS. Bottom-up processing is a term used in SP, a somatic, body-centered approach to facilitate processing of unassimilated sensorimotor reactions to trauma (Ogden & Minton, 2000). Bottom-up processing is related to somatic tracking. Whereas somatic tracking may occur within the preparatory phase or during stabilization, bottom-up processing is utilized in conjunction with trauma processing. Clients who exhibit significant dissociative responses often benefit from focusing on somatic sensations alone. This appears to reduce dissociation and aid information processing for many clients.

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How Bottom-Up Processing Is Different

The goal in the bottom-up approach is to target physical sensations, whereas the EMDR standard protocol integrates all levels of processing. Focusing on physical sensations alone or, alternatively, modifying the EMDR standard protocol so that neither traumatic events, associated cognitions, nor emotions are initially targeted, is based on the notion that all unprocessed traumatic experience is to some extent preverbal (e.g., speechless terror) or precortical and sensory in nature. Overall, bottomup processing is considered foundational to emotional and cognitive processing. It includes not only overall body processing but also fixed action patterns seen in active defenses (e.g., the startle reflex and the fight, flight, or freeze response), changes in breathing and muscular tonicity, and autonomic nervous system activation. Specifically, bottom-up processing is characterized by these features: (a) sensory, emotional, and cognitive aspects of traumatic experience are processed sequentially rather than simultaneously, either as an a priori decision or as an intervention if a simultaneous processing is too intense, (b) a slow process. The idea is to slow down the material by staying at the sensory level. In this way, information is titrated and intense abreactions decreased by slowing down the spontaneous integration of affect, cognition, and sensory experience that usually occurs in EMDR, (c) an active stance of the therapist. The voice of the therapist is used in an active manner to engage the patient during the processing to keep the patient grounded, (d) somatic memories. The bottom-up approach lends itself to targeting the relationships with primary attachment figures and enables processing the patient’s somatic response even in the absence of specific images or verbal memories, (c) sensation focused. Prior to the patient processing material, the therapist actively encourages the patient to only focus on body sensations, rather than emotions or cognitions. The patient is further instructed to blank out any material other than sensory material as it comes up. If such material comes up during processing, the therapist actively encourages the patient to drop the content and return to focus on sensory experience alone. This type of processing helps fractionate the traumatic material by separating somatosensory from cognitive and affective processing. This type of processing may be insufficient for the complete resolution of the trauma, but it develops the necessary body mindfulness that is essential for affective and cognitive processing. Consequently, it is suggested that, eventually, when the patient is able to access the traumatic experience in its entirety, the standard EMDR protocol is used to complete processing, though in many cases, this may not be necessary. In cases in which the client is about to dissociate or has already dissociated to a point where significant derealization or depersonalization interferes with further EMDR processing, it can be useful to shift from EMDR processing with BLS to somatic tracking only. By replacing the sensory stimulation with somatic attunement and empathy to aid the client in remaining present, we are often able to slow the process down, aiding the client in titrating and working through an aspect of a traumatic memory without introducing new information. This can be combined with resourcing or grounding interweaves (e.g., focusing on the senses—smell, taste, sound, touch, vision). In some cases, getting the client to focus on micromovements in the body in the absence of BLS is sufficient to produce an orienting response, and thus a return to ongoing information processing.

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Somatic interweaves in particular are useful in aiding with stuck processing. Somatic micromovements can resolve EMDR looping quite dramatically. Often in this phase, as indicated above, anger, or other thwarted sympathetic arousal response, is held apart, often because it is perceived as dangerous or shameful in some way. For some individuals, the gentle invitation to engage in a pushing away or other fulfillment of thwarted anger, or fleeing response as expressed in slow-running movements, will enable attenuated discharge of the sympathetic arousal, and processing can resume. In some instances, the use of such micromovements will take the subjective units of disturbance (SUD) to 0, with the somatic movements allowing significant discharge and palpable releases of energy. ELEMENTS OF SOMATIC THERAPY

Somatic interventions are distinguished from other psychotherapeutic interventions in that they are expressed in markedly slowed-down time, in order to give clients ample time to experience the felt sense of their bodies. In somatic therapy it is understood that to associate dissociated experience one directs attention to body sensation and regulates the pace of the work with intermittent use of resourcing. Many, but not all, of the following somatic interventions are drawn largely from Somatic Transformation (Stanley, 2005, 2006), Somatic Experiencing (e.g., Levine, 1997), and SP (e.g., Ogden et al., 2006). Many of these can be used both during stabilization as well as during trauma processing. They are useful on their own but can also be utilized as somatic interweaves during EMDR processing. Breathing

The EMDR standard protocol involves the therapist encouraging the client to take a deep breath after a set. This enhances body mindfulness and reminds the client to use one of the primary regulatory mechanisms he or she has available: breathing. Research suggests that breathing not only has a regulatory effect on physiological activity in the body but also in the brain. Breathing, as used in Taoist and Buddhist practice, as part of relaxation training, and as an essential part of somatic interventions, appears to have a profound effect on amygdalar hippocampal functioning. Frysinger and Harper (1989) found that inspiration increased the rate of cell firing in the limbic system, and the amygdala in particular, whereas expiration led to a decrease in cell firing—the brain was quieting. It’s our observation in clinical practice that Buddhist types of breathing, which focus on relaxation, tend to be more effective with hyperarousal states. Taoist breathing approaches, which focus on maintaining tension in the body through prolonged expiration (e.g., shouting during martial arts), seem to be more useful in clients who exhibit dissociative responses. Thus, quenching amygdala activation by means of breathing during the recall of traumatic memories may optimize information processing by, on one hand, increasing, and, on the other hand, decreasing, amygdala activity. Many therapists use extended, extremely long sets with clients. As a result, the focus on breathing can get lost. A dorsal vagal or dissociative response often involves

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shallow breathing, or even stopping breathing. In this case, the therapist may invoke a somatic interweave: alerting the clients to their relative lack of breathing or shallow breath, or else reminding the clients to breathe. A word of caution: Many clients have learned to reduce unwanted physiological sensation through the use of breath. Therefore, the therapist may want to instruct the clients not to do that, but rather to focus on the body sensation and at the same time breathe into it, without trying to get rid of the sensation; just noticing it.

Somatic Empathy

Somatic empathy is a foundational element that underlies all other somatic interventions (Paulsen & Stanley, 2005). It involves the therapist attending as completely as possible to the client’s somatic experience. This may involve asking about and attending to the client’s self report of subject experience, or, in an experienced therapist, using intuition to perceive the client’s felt somatic sense in the therapist’s own bodily experience (Solomon, Watkins, & Paulsen, 2004). Somatic empathy is expressed by the therapist’s activation of his or her own ventral vagal state, with its experience of connection to self, other, and contextual resources. In that resourced state, the therapist simultaneously attends closely to the client’s felt sense. The client’s experience is the shared focus of client and therapist. Holding this ventral vagal state potentiates the client’s capacity to tolerate sensation. The therapeutic alliance becomes the holding environment in which the client can emerge from dorsal vagal shutdown or resolve sympathetic arousal in the safety of a connection with the therapist’s healing expectancies, which strengthen the client’s own.

Boundaries

Boundaries are crucial to one’s sense of self, to a sense of safety, and to effective treatment of trauma-related disorders. Boundaries frequently fail to become properly developed through attachment injury; they become invaded in trauma and sometimes become excessively rigid in an effort to ward off further trauma. The development of a client’s sense of a boundaried self is crucial to effective treatment of dissociative disorders. Boundaries can be explored with simple exercises involving body mindfulness. Clients can explore their response to physical proximity by focusing on the body while varying distance between themselves and the therapist. The therapist may then ask the clients to stretch out their arms with their hands raised vertically and ask them to draw an imaginary boundary around themselves and ask the clients what happens in their body. Another simple boundary exercise is the use of a string or cord of sufficient length for clients to make a circle around themselves. Again, the therapist needs to explore how the clients’ sense of somatic self changes. In many clients, increasing their sense of boundaries will result in a sense of increased strength. However, there are others who will occasionally move into further collapse, as they will experience a sense of isolation—these clients are more

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likely to want to merge with the therapist. In this case, gentle but firm boundaries on the part of the therapist are crucial. In the case of a client wanting to merge, prior to moving into trauma treatment, these issues need to be explored from an attachment perspective, gently building somatic tolerance by using body mindfulness in the process. Other clients, on setting a physical boundary, may go into an inhibitory shame response. Such a response is a cue to do more work with the underlying attachment issues, to build more tolerance for the act of setting a boundary. All these exercises are useful to help clients with experiencing a somatic sense of self prior to embarking on trauma-centered treatment using the EMDR standard protocol. However, in the case of looping or overwhelm, they can also be used during EMDR processing to keep clients within the window of tolerance. For instance, clients can put the string or cord around themselves while engaging in EMDR processing. If clients are at the edge of hyperarousal, the therapist may consider asking the clients to get up, stretch out their arms with the hands upward, and draw a boundary around themselves, an interweave that combines boundaries with intentional movement (also see below).

Somatic Resourcing

Somatic resourcing evokes and strengthens clients’ capacity to be in their own ventral vagal state. With somatic empathy as a basis, the therapist expresses a respectful curiosity about the experiences that the clients find life enhancing. The clients describe either external environments or internal phenomena that bring them comfort or pleasure or safety or another desirable felt sense. The therapist joins the clients with empathic delight as the therapist observes positive felt sense in the clients, whether by smiles, twinkling eyes, relaxation, leaning forward, or other expressions of connectedness and engagement. With nondissociative clients, the therapist can next inquire about what the clients are noticing in the body. With highly dissociative clients, resourcing occurs first by limiting discussion to the phenomenon that evokes the ventral vagal response, without asking the clients to notice the body. Over time, repeated engagement of the ventral vagal nervous system will create a safe state for the client to begin to notice somatic sense. Resources can be anything, ranging from a walk on the beach, the sight of a starry night, the brown eyes of a horse, the coo of a baby, prayer, or satisfaction at making a delicious coleslaw. It is important to have a full armamentarium of resources to strengthen the clients’ capacity to be in a ventral vagal state. Improved access to ventral vagal states means the clients will be able to tolerate negative affect and somatic pain better than without this resourcing.

Intentional Movement

In cases of unremitting hyperarousal, and even more so in cases of dorsal vagal shutdown, the use of a movement interweave can reestablish a defensive response and bring the client back into the window of tolerance. In this case, the therapist can ask

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clients to get up and move around. This tends to be profoundly resourcing to clients and usually brings them back to being present in their bodies.

Somatic Tracking

Damasio (1994) states, “The background body sense is continuous, though one hardly notices it, since it represents not a specific part of anything in the body, but rather an overall state of most everything in it” (p. 152). Ogden et al. (2006) find that “the capacity to sense and describe sensation and to uncouple it from trauma-related emotions and cognitions enhance the possibility of client’s reintegrating the somatic experience of their trauma, in order to establish new meanings and understandings of their past” (p. 17). Somatic tracking is another foundational element of somatic work. It refers to the therapist’s inquiring, moment to moment, in a very relaxed and slow fashion, about the client’s felt sense. Sometimes this involves asking what clients are noticing in their body, and where, in one moment and then the next. Sometimes tracking involves the therapist noticing something that clients may not yet have noticed, such as a clenching, movement of an extremity, or a facial flushing. The client is invited to report not the names of emotions, or interpretations, or cognitive reports, but the primitive and raw data of the felt sense of the body, namely descriptions of body sensations: pressure, warmth, tightness, heaviness, aching, and so on. If the client reports the name of an emotion, or a thought or image, the therapist then invites the client to report the somatic experience underlying that emotion or thought (such as tears, flushing, jaw clench) rather than the names of emotions or the thoughts themselves. Intuitive clinicians may pick up the sensory experience in their own body, without visually observing signs of it, and may wonder aloud if that felt sense is the client’s experience as well. Tracking refers also to the therapist’s ability to closely notice and follow the moment-to-moment process of clients’ nonverbal behavior. These may be as subtle as pupil dilation, small sighs, or a pulse in the neck. Tracking may result in awareness of a fidgeting of the extremities, which tends to indicate thwarted fight-or-flight responses and leads to other interventions. Ogden et al. (2006) suggest that by helping the clients slow down and become mindful observers of their orienting and attentional responses, their awareness of how and why they focus their attention is increased. When the therapist and clients are quietly tracking the clients’ felt sense from moment to moment, clients are less likely to have their attention distracted. As clients come to focus on tracking their own bodily process, with curiosity, there is an increased capacity to tolerate affect, and one could say, an increased mindfulness skill, an internal stance of a nonjudgmental observing, wonder, and acceptance. The pacing of tracking is somewhat similar to what clinicians do in EMDR therapy when we say, “Just notice it” or “Go with that,” but with a difference. In EMDR, all channels are equal (cognitive, affective, bodily). The only time a therapist would deliberately shift the client’s attention to the somatic channel over other channels would be (a) if the client engages in excessive intellectualization and needs to be drawn to the body because there is a kind of looping occurring in which the SUD and

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validity of cognition (VOC) are not resolving, a kind of “circling the airport” loop, or (b) if the EMDR is stuck, a kind of “broken record” looping (Paulsen, 2007). In somatic work, body sensation is considered to have primacy and is the foundational channel. Typical tracking queries might be “What are you noticing in your body in this moment . . . (long pause) . . . and in this moment?” For clients who are not highly dissociative, one asks specifically, “Where exactly is that sensation of heaviness?” Whereas with a highly dissociative client, the therapist is quite content if the client can report “heaviness” or “aching.” To draw a client away from conversation and to bodily sensation, a therapist may ask, “What’s happening in your body as we talk?” And then, “What are you noticing in THIS moment?” A therapist may draw attention to something observed, such as fidgeting feet, or drumming fingers, or tension in the jaw, and invite the client to just notice those sensations with curiosity, and without speech, for some moments. If the client’s attention returns to cognition, typically the therapist will gently redirect attention to the body. Tracking can be conducted with or without what EMDR practitioners call a “target.” In order to train a client to track, it is wise to begin tracking without a target. There is an understanding that if traumatic material is ready, it will be held in the body and tracking will soon find the body sensations associated with the trauma.

Discharging

In somatic therapy, bodily held disturbance is understood to be observable by clinician and client, to the degree the client has learned to notice, as small discharges of energy. Evidence of spontaneous discharging of pent-up or thwarted sympathetic arousal includes the fluttering of eyes, twitching, ticking, lip quivering, overt shaking, and more. The intervention involves inviting the client to merely notice the discharging sensation, without intervening in it bodily. During EMDR processing, the therapist may make a somatic interweave by asking the client to notice what the body wants to do, just allowing it to happen. This may range from the body moving through shaking, twitching, limbs moving, the client enacting a variety of defensive responses, and so on. It is important that this occurs mindfully within the therapeutic relationship. As a result of tracking, arousal or disturbance is accessed and begins to spontaneously discharge. Over time, clients become increasingly comfortable with noticing and allowing the natural process of discharging.

Spontaneous Oscillations

In the course of many somatic interventions, the therapist may observe the client engaging in a spontaneous rhythmic movement, whether a healing pulse, a rocking, or even spontaneous BLS behaviors (Stanley, 2005). In somatic therapy, it is understood that spontaneous oscillations are evidence of the body recalibrating itself, and coming into a new coherency, spontaneously (Siegel, 1999). The client is more likely to allow spontaneous oscillations if there have been prior experiences of deliberately evoked oscillations. Deliberate oscillations, described below, may prime the client to

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notice and allow spontaneous ones. In short, oscillation is understood as being on a continuum from deliberate and evoked to spontaneous (Stanley, 2006).

Evoked Oscillations

A primary assumption in somatic therapy is that the client’s attention to disturbing material should be punctuated with repeated return to a more resourced sense of self. The therapist will ask the client to “pendulate” back and forth between the felt sense of a resource and the felt sense of a disturbance (e.g., focus on the trauma on one hand and the resourced state on the other, just going back and forth). This helps the client to stay in the window of tolerance between hyperarousal (sympathetic arousal flooding) and hypoarousal (dorsal vagal shutdown). Moving back and forth between the painful and the resourced states titrates the intensity so the adroit clinician can keep the client in an optimal range where efficient information processing occurs. This can be considered “titration,” but this pendulating is also an evoked oscillation, which will potentially catalyze the body’s innate and spontaneous oscillations (Stanley, 2006). When using the EMDR standard protocol with individuals who have significant ego strength and are sufficiently resourced, clients will often spontaneously access resourced self states and spontaneously process to an adaptive resolution. Clients who have ego-state disorders may have limited resources to begin. When planning EMDR processing, the therapist resources clients before processing begins, or, if the processing gets stuck (loops), the therapist actively aids clients in accessing these resourced states by introducing a cognitive or somatic interweave during trauma processing. EMDR standard protocol differs from somatic therapy in this regard. In the latter, the therapist deliberately and rhythmically moves the client’s attention between traumatic material and resource material, in order to prevent overwhelm or stuck processing. In the former, the therapist metaphorically stays off the track and allows the processing to proceed down the trauma track, only providing an intervention if the train is stuck.

Somatic Micromovements

An important somatic intervention is initiation of micromovements to release trapped sympathetic arousal. Sympathetic arousal is assumed to be present when the therapist observes fidgeting of the client’s extremities. The therapist invites the client to notice what that extremity wants to do, and what urge there may be behind the fidgeting. If the client does not know, the therapist may invite hypothesis testing about a particular urge. If, for example, the client has a clenched fist, but denies an urge to punch, the therapist may gently invite the client to test the hypothesis that there is a thwarted wish to punch, by allowing a very slow punching movement. A sudden, dramatic movement (instead of a very slow one) would release nothing and would only represent acting out. This is because a gradual attenuated movement is needed to release a thwarted sympathetic arousal impulse. The term micromovements describes these almost comically slow movements.

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The therapist may offer physical resistance if appropriate for a given client and the therapeutic relationship. In the prior example, while the client is engaging in a very slow punching movement, the therapists may extend their hand for the client to slowly “punch” or push against. The point of the resistance is not to engage in a contest, but to give the client the felt sense of punching successfully while making contact with resistance. Often clients will approach the task gingerly, so the therapists must shepherd the action to completion. For example, if the client is engaging in micromovement to express a thwarted urge to push away someone who violated the client’s bodily boundaries, the client will often only push away a short distance, as if there is not much of a right to one’s own space and body. The therapist may gently invite the client to continue, with language like, “How would it be to continue that, that’s right, fully extending the arms, that’s it, all the way.” An energy-sensitive clinician will often notice waves of energy being released from the client in the final inches of the pushing away, as the arms are fully extended. Theoretically, the action activates the client’s sympathetic nervous system, allowing release of the thwarted impulse. Clients commonly wish to express the motion rapidly, but, again, this accomplishes nothing, and “easy does it,” “slower still” are common therapeutic utterances. If the client is frightened or unable to engage in micromovements, the intervention is likely premature, and more resourcing and tracking experience is needed before doing them. Grounding will help restabilize a client who is not able to complete micromovements. In somatic work, the intention is not to fully “light up the net” that holds unworked traumatic experience, but rather to circumnavigate it, or “nibble around the edges” using pendulation or evoked oscillation procedures. The standard EMDR procedure already includes the somatic channel of experience, so in most clients, this phase requires no additional somatic interventions. If, during the Assessment Phase of EMDR, a client is revealed to not have the capacity to experience sensation in the body, it would be a contraindication to proceed until soma tolerance has been enhanced with a return to the preparation phase. For many dissociative individuals, somatic processing of trauma may proceed before EMDR may proceed. Evoked oscillations between disturbing material and resource material can begin to strengthen the client’s capacity to tolerate disturbance. It also tends to increase confidence that disturbing material can be mastered because the disturbance decreases with each evoked oscillation. During this phase, the therapist will overtly track, from moment to moment, those observable signs in the client’s body of resource or disturbance. This may include gently commenting on observed flushing, relaxing, or smiling in the case of a resource, or clenching, twitching, or fidgeting, in the case of a disturbance. When tracking of sensation from moment to moment is intolerable, the work of detoxifying trauma is not ready to proceed. In contrast to EMDR, the noticing and tracking of client somatic experience alternates with resource states until the client is much more able to tolerate extended feelings of disturbance without dissociation. During this phase, spontaneous oscillations may begin to be observed as the client grows increasingly comfortable turning attention inward, observing, and tolerating affect. Quite naturally and spontaneously, this attention to soma evokes subtle oscillations such as rocking side to side, forward and backward, or other rhythmic pulsations. The therapist in this phase teaches the client to notice and leave time and space for the spontaneous oscillations to complete. As these occur, the client’s capacity for and tolerance of affect and soma tend to increase.

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SUDS=4

SUDS=2

SUDS=1

SUDS=1

SUDS=5

SUDS=6

SUDS=2

SUDS=6

SUDS=9

Figure 21.1  Grid utilized to assess different SUD levels with different directions of gaze. SUD, subjective units of disturbance.

Spatial Mapping

The first author (Lanius, 2000) has used an intervention referred to as spatial mapping, using the client’s direction of gaze, that is, eye position, to titrate intensity when accessing a traumatic memory. Similar approaches have been used by other authors, for example, brain spotting (Grand, 2013) or node isolation (Litt, 2009). The client is asked to move and hold his or her eyes in different directions of the eye field and SUD levels are taken while focusing on the same traumatic memory. That is, the client is asked, in succession, to look left, right, and straight ahead in the upper, middle, and lower eye fields. Commonly, if there is significant fragmentation, different degrees of SUD disturbance in response to accessing the same traumatic memory emerge. With many clients, there are only subtle differences. However, if there are more significant levels of traumatization with an attendant dissociative response, there are frequently significant differences in SUD level, depending on which direction the client moves his or her eyes. These differing levels of activation can be conceptualized in terms of self-states that are expressed at a somatic level. We use a grid to record different SUD levels (see Figure 21.1). We then ask the client to move his or her eyes into an area with one of the lower SUD levels, ask the client to notice what he or she is sensing in his or her body, and administer BLS. In most cases, we use hand taps but auditory stimulation or limited, rather than sweeping, EMs can also be used. What commonly happens is after some processing of the somatic activation, not only the SUD level in the direction in which the client has held his or her gaze drops, but also the SUDS levels in other cells will lessen. This approach can be used to strategically fractionate traumatic activation and reduce the likelihood of depersonalization/derealization during trauma processing.

ADDITIONAL STRATEGIES FOR SOMATIZATION AND DEPERSONALIZATION The Special Case of Cross-Lateral Stimulation

Cross-lateral stimulation is another effective means of reducing depersonalization/ derealization when it occurs. Most EMDR practitioners are familiar with the butterfly hug. It involves Dual Attention Stimulation (DAS) that consists of crossing your arms over your chest, so that the middle finger from each hand will be placed below the collarbone and the rest of the fingers and hand will cover the area that is located

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under the connection between the collarbone and the shoulder and the collarbone and sternum or breastbone. Hand and fingers must be as vertical as possible (fingers toward the neck and not toward the arms). Once you do this you can interlock your thumbs (forming the body of the butterfly) and the extension of your other fingers outward will form the butterfly’s wings. (Artigas, Jarero, Mauer, López Cano, & Alcalá, 2000) It has been our experience that the butterfly hug is a powerful tool for grounding and resourcing and it is particularly useful for EMDR resource installation protocols in individuals who exhibit either positive affect intolerance or who tend to bridge into traumatic memories during resourcing. Another form of cross-lateral stimulation is the cross-crawl. Not useful for trauma processing, this intervention is exceedingly useful to help pull clients out of a depersonalized state, particularly if used in conjunction with orientation to smell. The cross-crawl is a simple movement of the body that uses opposite limbs together. The basic movement is to bend one leg and tap the raised knee of that leg with the opposite hand or knee. Alternatively, one can stand on one leg, raising one’s right leg behind one’s back and touch it with the left hand and then alternate to left leg and right hand. The assumption is that the alternating unusual crossed movement will confuse the brain and produce a strong orienting response, helping bring the client into the present moment.

Circular and Figure-Eight EMs and Headache Activity

Headache activity in dissociative clients during the session is often the result of a part of the self wanting to recede from consciousness. One way to deal with this issue in therapy is through an ego-state intervention, asking the client as to whether there may be a part that does not want to be here. This issue can also be addressed from a more somatic perspective through circular and lying down Figure-Eight EMs. Commonly, headache activity will diminish without accessing additional material. Incidentally, this approach seems to work with headache activity in general, including migraines (e.g., Marcus, 2008), not only dissociative headaches.

SUMMARY

This chapter has described core elements of somatic interventions and how they may be integrated into EMDR processing, including complex trauma cases. The list is not comprehensive, but begins to describe the range of options for accelerating or decelerating processing, whether it is EMDR processing or the process of therapy itself. The window of tolerance notion guides the decision of whether acceleration or deceleration is indicated at any given point in therapy or EMDR; pacing is always germane with complex cases. Understanding the role of somatic attunement and its effect on the sympathetic nervous system in acceleration and the parasympathetic dorsal vagal nervous system in deceleration further informs our awareness of

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therapeutic pacing requirements. Finally, awareness of the parasympathetic ventral vagal nervous system for social engagement guides our understanding of resourcing, whether the resourcing be that of the engagement of the therapeutic relationship, engagement of the client’s internal resourced states, or the relationship engagement between the client’s states. To summarize the chapter in a sentence, ventral vagal connectedness between and within people is the name of the game to enhance association and integration.

NOTE

1. The present chapter is in part based on Paulsen, S., & Lanius, U. F. (2009). Toward an embodied self: Integrating EMDR with somatic and ego-state interventions. In R. Shapiro (Ed.), EMDR solutions II: For depression, eating disorders, performance, and more. New York, NY: W. W. Norton.

REFERENCES Artigas, L., Jarero, I., Mauer, M., López Cano, T., & Alcalá, N. (2000, September). EMDR and traumatic stress after natural disasters: Integrative treatment protocol and the butterfly hug. Poster presented at the EMDRIA Conference, Toronto, Ontario, Canada. Austin, J. H. (1998). Zen and the brain. Cambridge, MA: MIT Press. Barrowcliff, A. L., Gray, N. S., MacCulloch, S., Freeman, T. C. A., & MacCulloch, M. J. (2003). Horizontal rhythmical eye movements consistently diminish the arousal provoked by auditory stimuli. British Journal of Clinical Psychology, 42, 289–302. Cowan, N. (1995). Attention and memory: An integrated framework. New York, NY: Oxford University Press. Craig, G. (2011). Significance of the insula for the evolution of human awareness of feelings from the body. Annals of New York Academy of Sciences, 1225, 72–82. doi:10.1111/j.1749–6632.2011.05990.x Damasio, A. R., Grabowski, T. J., Bechara, A., Damasio, H., Ponto, L. L., Parvizi, J., & Hichwa, R. D. (2000). Subcortical and cortical brain activity during the feeling of self-generated emotions. Nature Neuroscience, 3, 1049–1056. Damasio, A. R. (1994). Descartes’ error: Emotion, reason, and the human brain. New York, NY: Putnam. Damasio, A. R. (1999). How the brain creates the mind. Scientific American, 281(6), 112–117. Francis, S., Rolls, E. T., Bowtell, R., McGlone, F., O’Doherty, J., Browning, A., . . . Smith, E. (1999). The representation of pleasant touch in the brain and its relationship with taste and olfactory areas. Neuroreport, 10, 453–459. Frysinger, R., & Harper, R. (1989). Cardiac and respiratory correlations with unit discharge in human amygdala and hippocampus. Electroencephalography and Clinical Neurophysiology, 72, 463–470. Gazzaniga, M. S., Holtzman, J. D., & Smylie, C. S. (1987). Speech without conscious awareness. Neurology, 37(4), 682–685. Grand, D. (2013). Brainspotting: The revolutionary new therapy for rapid and effective change. Louisville, CO : Sounds True, Inc. Janet, P. (1928). L’évolution de la mémoire et de la notion du temps. Paris, France: A Chahine.

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Lanius U. F. (2000). Dissociative processes and EMDR—Staying connected. Presentation at the North West Regional EMDR Conference, Vancouver, British Columbia, Canada, April 7–8, 2000. Lanius, R. A., Bluhm, R., & Lanius, U. F. (2007). PTSD symptom provocation and neuroimaging: Heterogeneity of response. In E. Vermetten, M. Dorahy, & D. Spiegel (Eds.), Traumatic dissociation: Neurobiology and treatment (pp. 191–218). Washington, DC: American Psychiatric Press. Lanius, R. A., Bluhm, R., Lanius, U. F., & Pain, C. (2005). Neuroimaging of hyperarousal and dissociation in PTSD: Heterogeneity of response to symptom provocation. Journal of Psychiatric Research, 40, 709–729. Lanius, R. A., Lanius, U. F., Fisher, J., & Ogden, P. (2006). Psychological trauma and the brain: Towards a neurobiological treatment model. In P. Ogden, K. Minton, & C. Pain (Eds.), Trauma and the body: A sensorimotor approach to psychotherapy. New York, NY: W. W. Norton. Lanius, R. A., Williamson, P. C., Boksman, K., Densmore, M., Gupta, M., Neufeld, R. W., . . . Menon, R. S. (2002). Brain activation during script-driven imagery induced dissociative responses in PTSD: A functional magnetic resonance imaging investigation. Biological Psychiatry, 52, 305–311. Lanius, U. F. (2000, April 7–8). Dissociative processes and EMDR—Staying connected. Presentation at the North West Regional EMDR Conference, Vancouver, British Columbia, Canada. Lanius, U. F. (2009). Bottom-up processing. In M. Luber (Ed.), Eye movement desensitization and reprocessing (EMDR) scripted protocols. New York, NY: Springer. Levine, P. A. (1997). Waking the tiger: Healing trauma. Berkeley, CA: North Atlantic Books. Linehan, M. M. (1993). Cognitive behavioral treatment of borderline personality disorder. New York, NY: Guilford Press. Litt, B. (2009, August). Node isolation theory: The eye-zone differential technique. Presentation at the annual meeting of the EMDR International Association, Atlanta, Georgia, USA. MacLean, P. D. (1990). The triune brain in evolution: Role in paleocerebral functions. New York, NY: Plenum Press. Marcus, S. V. (2008). Phase 1 of integrated EMDR: An abortive treatment for migraine headaches. Journal of EMDR Practice and Research, 2(1), 15–25. doi:10.1891/1933–3196.2.1.15 Marmar, C. R., Weiss, D. S., & Metzler, T. J. (1998). Peritraumatic dissociation and posttraumatic stress disorder. In J. D. Bremner & C. R. Marmar (Eds.), Trauma, memory, and dissociation (pp. 229–252). Washington, DC: American Psychiatric Press. Nijenhuis, E. R. S., van der Hart, O., & Steele, K. (2004, January). Trauma-related structural dissociation of the personality. Retrieved from http://www.trauma-pages.com/a/nijenhuis-2004.php Ogden, P., & Minton, K. (2000). Sensorimotor psychotherapy: One method for processing traumatic memory. Traumatology, 6(3), 3. Ogden, P., Minton, K., & Pain, C. (Eds.). (2006). Trauma and the body: A sensorimotor approach to psychotherapy. New York, NY: W. W. Norton. Panksepp, J. (2001a). Neuro-affective processes and the brain substrates of emotion: Emerging perspectives and dilemmas. In A. Kazniak (Ed.), Emotion, qualia, and consciousness (pp. 160–180). Singapore: World Scientific. Panksepp, J. (2001b). On the subcortical sources of basic human emotions and the primacy of emotional-affective (action-perception) processes in human consciousness. Evolution and Cognition, 7, 134–140. Paulsen, S. L. (2007). Treating dissociative identity disorder with EMDR, ego state therapy, and adjunct approaches. In C. Forgash & M. Copeley (Eds.), Healing the heart of trauma and dissociation with EMDR and ego state therapy (pp. 141–180). New York, NY: Springer Publishing Company.

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Paulsen, S. L., & Stanley, S. A. (2005, November). Giving the body a voice: How EMDR, ego state therapy, somatic experiencing and indigenous healing methods can cure somatic dissociation. International Society for the Study of Dissociation, Fall Conference, Toronto, Canada. Plailly, J., Howard, J. D., Gitelman, D. R., & Gottfried, J. A. (2008). Attention to odor modulates thalamocortical connectivity in the human brain. The Journal of Neuroscience, 28(20), 5257–5267. doi:10.1523/JNEUROSCI.5607–07.2008 Schore, A. (1994). Affect regulation and the origin of the self: The neurobiology of emotional development. Hillsdale, NJ: Lawrence Erlbaum. Siegel, D. J. (1999). The developing mind: How relationships and the brain interact to shape who we are. New York, NY: Guilford Press. Solomon, R., Watkins, J. G., & Paulsen, S. L. (2004). Therapeutic self. EMDRIA Annual Conference, Montreal, Canada. Stanley, S. (2005). Somatic experiencing workshop: Year I. Foundation for Human Enrichment, Colorado. Workshop conducted in Bainbridge Island, WA. Stanley, S. (2006). Somatic transformation training: Year II. Bainbridge Island, WA: Institute for Somatic Transformation. van der Kolk, B. (1987). Psychological trauma. Washington, DC: American Psychiatric Press.

CHAPTER 22

Opioid Antagonists and Dissociation: Adjunctive Pharmacological Interventions Ulrich F. Lanius and Frank M. Corrigan

Peptide hormones in the brain may exert a modulating effect on neural activity by determining or influencing the background or “climate” on which the specific actions are projected. —Ulf Von Euler (1980) When emotions are expressed . . . all systems are united and made whole. When emotions are repressed, denied, not allowed to be whatever they may be, our network pathways get blocked, stopping the flow of the vital feel-good, unifying chemicals that run both our biology and our behavior. —Candace Pert (1999, p. 273)

Dissociative and somatoform symptoms can often be severe, interfering with psychotherapy in general and trauma processing in particular. As discussed in Chapter 5, Dissociation and Endogenous Opioids: A Foundational Role, trauma results in changes in the endogenous opiate system. Moreover, as discussed in Chapter 6, Attachment, Neuropeptides, and Autonomic Regulation: A Vagal Shift Hypothesis, attachment is in part mediated by endogenous opiates. In those chapters, we have discussed how endogenous opiates affect central nervous system (CNS) function, emotions, and sensorimotor defensive responses. Not only are opiates involved in dissociative processes and somatoform dissociation, but they also directly affect sensory transmission. Thus, they reduce both exteroceptive and interoceptive awareness, thereby affecting 471

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our sense of our body as well as our sense of self (also see Chapter 11, Dissociation, EMDR, and Adaptive Information Processing: The Role of Sensory Stimulation and Sensory Awareness and Chapter 21, Toward an Embodied Self: EMDR and Somatic Interventions). Dissociation, in particular, depersonalization, does not markedly respond to standard pharmacological interventions. Although such an “antidissociative” medication has not yet been discovered (e.g., Simeon, Giesbrecht, Knutelska, Smith, & Smith, 2009), we make a case here for opioid antagonists being successful as adjunctive pharmacological agents to psychotherapeutic interventions. Indeed, we hypothesize that opioid antagonists will bias the nervous system from passive defensive responses like immobilization and dissociative collapse toward either active defensive responses like fight and flight or, alternatively, within an established safe interpersonal or therapeutic relationship, an increase in ventro-vagal engagement. Naloxone and naltrexone are the two opioid antagonists that are currently commercially available. They are Food and Drug Administration (FDA)-approved for the treatment of alcoholism or opioid addiction (naltrexone; e.g., Trexan®, Revia®) or opioid overdose (naloxone; e.g., Narcan®). Please note that their use with traumatic stress syndromes and other conditions described in this chapter constitutes an offlabel use. That is, this chapter is for educational purposes and for the promotion of research and is not intended to endorse or promote the off-label prescribing of any drugs. It is necessary for practitioners to study the available evidence and use professional discretion in their prescribing decisions, being fully aware of known potential risks as well as benefits.

THERAPEUTIC USE OF OPIOID ANTAGONISTS IN TRAUMATIC STRESS SYNDROMES

The literature describes the use of opioid antagonists in a number of different disorders, some of them traumatic stress and attachment-related disorders, as well as others that are often associated with diagnoses of traumatic stress syndromes and dissociative disorders.

Borderline Personality Disorder (BPD)

Schmahl, Stiglmayr, Böhme, and Bohus (1999) administered naltrexone (50 mg q.i.d., p.o.) to female patients with BPD over a period of several weeks and reported a decrease in dissociative symptoms. Similarly, Bohus, Landwehrmeyer, Stiglmayr, Limberger, Böhme, and Schmahl (1999), reported a reduction in tonic immobility (TI), analgesia, and flashbacks in trauma patients who were administered naltrexone (25–100 mg q.i.d.) for a 2-week period. However, a recent placebo-controlled study by Schmahl et  al. (2012) looked at the “pure pharmacological antidissociative efficacy of naltrexone.” Patients received either 50 or 200 mg of naltrexone per day for a period of 3 weeks. While there was a tendency to reduced dissociative symptoms in the group receiving naltrexone, the size of the effect was small and failed to reach

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clinical significance. These results show a smaller effect than the findings by Bohus et al. (1999), in which there was an ongoing therapeutic relationship, for example, patients were in an ongoing dialectical behavior therapy (DBT) program.

Complex Posttraumatic Stress Disorder (PTSD)

Glover (1993) administered the opioid antagonist nalmefene to PTSD veterans and found a decrease in intrusive symptoms, rage, vulnerability, startle response, and emotional numbing. Similarly, veterans given naltrexone showed decreased hypervigilance, anxiety, panic, flashbacks, and intrusive thoughts. Rage reactions decreased while appropriate assertiveness increased. Traumatic memories began to surface spontaneously and resolved if the patient could tolerate the accompanying affect. Frequency of disturbing dreams increased, often with bizarre or changed content (Maurer & Teitelbaum, 1998). On the other hand, Lubin, Weizman, Shmushkevitz, and Valevski (2002) administered naltrexone (100–200 mg/day) to 6 males and 2 females with chronic PTSD. While they obtained a decrease in intrusive and hyperarousal symptoms, they judged them as not clinically significant. Furthermore, they found that significant side effects limited dosage.

Depersonalization Disorder

In addition, two studies looked at the effect of opioid antagonists on depersonalization symptoms. Nuller, Morozova, Kushnir, and Hamper (2001) administered single doses of naloxone (1.6 or 4 mg intravenous [i.v.]) to patients with depersonalization disorder. Three others received multiple infusions, with the maximal dosage being 10 mg. In 3 of 14 patients, depersonalization symptoms disappeared entirely and 7 patients showed a marked improvement. Simeon and Knutelska (2005) administered naltrexone to a group of patients (N = 14) with depersonalization disorder. Seven patients received up to a maximum of 100 mg/day and another 7 patients received 250 mg/day with a treatment duration of 6 to 10 weeks. They found a 30% reduction on different dissociation scales. Three patients were described as “very much improved” and 1 patient “much improved” clinically.

Self-Injurious Behavior

Self-injurious behavior is common in the more severe traumatic stress syndromes. It also happens to be one of the diagnostic criteria of BPD, a diagnosis that has been associated with childhood abuse and attachment conflicts. Coid, Allolio, and Rees (1983) found increased levels of endogenous opioids (e.g., levmetenkephalins) in habitual self-mutilators during the active stage of self-harm but not 3 months later. Opioid receptor blockade has been found to decrease self-mutilation (e.g., Griengl, Sendera, & Dantendorfer, 2001; Herman et al., 1987; McGee, 1997; Richardson & Zaleski, 1983; Roth, Ostroff, & Hoffman, 1996; Sandman, Barron, & Colman, 1990; Taylor et  al.,

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1991). Beneficial effects have also been found with trichotillomania (Carrion, 1995; De Sousa, 2008).

Eating Disorders

Avena and Bocarsly (2012) describe dysregulation in brain reward systems, including those dependent on endogenous opioids in eating disorders. Opioidergic activation has been associated not only with the hedonic aspects of binging and overeating (Bello, Patinkin, & Moran, 2011) but also with food deprivation (Hamm, Knisely, Watson, Lyeth, & Bossut, 1985). In a placebo-controlled study, Marrazzi, Bacon, Kinzie, and Luby (1995) described a reduction in binging and purging behaviors with naltrexone. Similarly, in a patient with binge eating disorder, Neumeister, Winkler, and Wöber-Bingöl (1999) found that the addition of naltrexone to fluoxetine improved therapeutic response. Naltrexone was used at 100 mg/ day over a period of 1 year. Upon reduction of the dose to 50 mg/day, binge eating frequency increased again. When the dosage was increased to 100 mg again, symptoms disappeared. Raingeard, Courtet, Renard, and Bringer (2004) studied a group of women with severe and chronic eating disorders and type 1 diabetes who did not respond to antidepressant drugs, behavioral therapy, and interpersonal psychotherapy. All patients received 200 mg of naltrexone twice daily over a period of 1 year. The authors describe positive psychological effects on self-esteem, much decreased binging and purging behavior, as well as improved blood glucose control. Contrave®, an experimental weight-loss drug that contains both bupropion (wellbutrin) and naltrexone, while showing some promising results, has not yet obtained FDA approval.

Pathological Gambling

Pathological gambling is thought to provide rewards through endogenous opioid effects on the mesolimbic dopamine system. Kim and Grant (2001) conducted a double-blind, placebo-controlled study of oral naltrexone in this condition. Naltrexone was started at 25 mg/day and titrated upward up to 250 mg/day. Analysis of results showed that 75% of naltrexone subjects were very much improved as compared to 24% of those on placebo. Elevated liver enzymes were noted in subjects who took analgesics concurrently. Nausea was reportedly common during the first week of treatment.

Sleep Apnea

There are suggestions of a possible association between traumatic stress syndromes and sleep apnea (e.g., Sharafkhaneh et al., 2007). Certainly, our clinical observations support this notion. Moreover, opioids depress breathing. Ferber, Duclaux, and

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Mouret (1993) reported that naltrexone improved blood gas patterns in obstructive sleep apnea. In a study of 12 patients, using 50 mg of naltrexone at bedtime, Ferber, Sanchez, Lemoine, and Mouret (1988) found that clinical symptoms improved significantly: immediately in 4 patients, within 1 month in 3 patients, and after 3 months of treatment in the remaining ones. Moreover, the number, duration, and intensity of hypoxic events were dramatically improved.

Immune Function

Many patients with traumatic stress syndromes also have multiple health issues and compromised immune system functioning (e.g., Schnurr & Green, 2004; Lanius & Vermetten, 2010). Endogenous opioid activity has been related to the modulation of immune system functioning (e.g., Bodnar, 2011). While on one hand, moderate opioid activation as a result of exercise seems to enhance immune system functioning (Kapasi, Catlin, Beck, Roehling, & Smith, 2001), concern about opioid-mediated immune suppression has also been voiced (e.g., Ninkovic & Roy, 2013). The immune system suppressing quality of stress seems to be at least in part associated with excessive opioid exposure. For instance, beta-endorphin, released into circulation during various stresses, has been reported to cause a 50% reduction in natural killer cell activity (Prete, Levin, & Pedram, 1986). Conversely, Gekker, Lokensgard, and Peterson (2001) describe increased immune functioning when naltrexone is coadministered with anti-HIV medications. Lissoni et  al. (2002) successfully used high doses of naltrexone in combination with interferon and melatonin to treat metastatic cancer. Similarly, Farooqui et al. (2006) suggest that opioid antagonists may be useful in the treatment of estrogen-dependent breast cancer. Zagon and McLaughlin (2011), as well as Smith et al. (2011), in a randomized, placebo-controlled trial described the successful use of low-dose naltrexone with Crohn’s disease. With regard to irritable bowel syndrome, there is suggestion that low-dose naltrexone is beneficial (e.g., Kariv et  al., 2006), whereas higher doses may not be (Foxx-Orenstein et al., 2007). Finally, there have also been reports that low-dose naltrexone has positive effects on quality of life in patients with multiple sclerosis (Cree, Kornyeyeva, & Goodin, 2010; Sharafaddinzadeh, Moghtaderi, Kashipazha, Majdinasab, & Shalbafan, 2010). With regard to experimental use of opioid antagonists in immune system disorders, we refer the reader to Moore and Wilkinson (2009). The dosage regime with low-dose naltrexone is important, as the beneficial effect with once-daily dosing may be mediated by a rebound increase in opioid receptor sensitivity (Brown & Panksepp, 2009). The regular doses of naltrexone used in alcohol dependence syndrome block mu- and delta-receptors and have effects on the nociceptin/orphanin FQ (N/OFQ) system. Low-dose naltrexone used once daily induces a temporary block followed by a rebound increase in mu-opioid receptor activity. It is possible that, in the future, fine-tuning of opioid receptor sensitivity will be required in the traumatic stress syndromes that have dominant somatic residues.

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Pain

One of the concerns of using opioid antagonists is the reversal of analgesia, an effect that is due to the blockade of opioids. Issues related to that are discussed in the section on side effects. However, the administration of exogenous opioids, as well as the release of endogenous opioids, can have paradoxical effects. That is, opiates produce not only analgesia but also long-lasting hyperalgesia (increased sensitivity to pain), suggesting a sensitization effect (e.g., Célèrier, Laulin, Corcuff, Le Moal, & Simonnet, 2001). This is seen in some patients/clients with dissociative disorders who can feel numbing in one part of the body and exquisite sensitivity to touch in another. Allodynia-type pain may also supervene when the numbing clears as the dissociative state changes. Furthermore, sustained opioid exposure has been reported to elicit unexpected, paradoxical pain (Vanderah et al., 2001). Conversely, naloxone and naltrexone have produced a dose-dependent analgesia in mice in certain conditions (Vaccarino, Tasker, & Melzack, 1989). Opiate receptors and endorphinergic responses may be different in animals that experience persistent pain (Kayser & Guilbaud, 1987). Not surprisingly, Le Roy and colleagues (2011) suggest that although stress on one hand causes analgesia, stressful life events associated with endogenous opioid release may exacerbate pain syndromes. Moreover, consistent with the hypothesized neuromodulatory role of the opioid system, there is some suggestion that opioid antagonists may have differential effects, for example, increased pain perception for insensitive individuals and decreased pain sensitivity for pain sensitive individuals (Buchsbaum, Davis, & Bunney, 1977). This raises the question about the use of opioid antagonists with chronic pain syndromes, and certainly in the specific case of fibromyalgia there appear to be some promising results.

Fibromyalgia

Fibromyalgia is a chronic pain disorder that is thought to result from the type of autonomic system dysfunction to which traumatic stress disposes. There is an overlap with irritable bowel syndrome, chronic pelvic pain, and migraine (Larauche, Mulak, & Taché, 2011). Clinically, it appears to be more common among individuals with traumatic stress syndromes and dissociative disorders. Moreover, traumatic stress seems to play a role in the onset of fibromyalgia. While there is some controversy whether major life stressors apart from sexual and physical abuse are associated with fibromyalgia (e.g., Haviland, Morton, Oda, & Fraser, 2010), an increased incidence of fibromyalgia has been reported in train crash survivors (Buskila et al., 2009), survivors of childhood maltreatment (Nicolson, Davis, Kruszewski, & Zautra, 2010) and sexual abuse (Wilson, 2010), as well as holocaust survivors (Ablin, Cohen, Eisinger, & Buskila, 2010). Buskila et al. (2009) specifically link increased report of dissociative symptoms on the Peritraumatic Dissociative Experiences Questionnaire (PDEQ) and the Dissociative Experiences Scale (DES) with fibromyalgia. Finally, an association between somatoform dissociation and fibromyalgia has been reported (Näring, van Lankveld, & Geenen, 2007).

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Earlier findings of Younger, Zautra, and Cummins (2009) suggested that a regular dose of naltrexone (50 mg/day) did not produce therapeutic effects; a follow-up study using low-dose naltrexone (4.5 mg/day) found a 30% reduction of fibromyalgia symptoms over placebo. The authors (Younger & Mackey, 2009) concluded that “low-dose naltrexone may be an effective, highly tolerable, and inexpensive treatment for fibromyalgia” (p. 663). These findings have since been replicated in a randomized, double-blind, placebo-controlled study (Younger, Noor, McCue, & Mackey, 2013).

OPIOID ANTAGONISTS AND EYE MOVEMENT DESENSITIZATION AND REPROCESSING (EMDR): THE FIRST CASE

In 1999, after reading the Bohus et al. study, the first author used opioid antagonists in a patient with a severe dissociative identity disorder (DID) who was undergoing EMDR treatment (also see Lanius, 2005). It appeared that opiate blockade enhanced the effectiveness of EMDR processing. As a result of medical conditions and an ongoing risk of needing emergency surgery, the patient chose to discontinue the naltrexone. However, during subsequent EMDR processing, it almost appeared as if the patient was still on naltrexone—there was no longer any undue dissociation, as if the blockage had been removed. After trauma reprocessing with naltrexone, the reduction in dissociative symptoms remained even after discontinuation of the medication. Later on in treatment, when dealing with other severe trauma, the patient decided to go on naltrexone again, but rather than using continuous dosing, it was used only prior to the therapy session, which proved to be helpful with regard to trauma processing. These initial findings led to a series of case studies with Dr. Robert Ferrie (Ferrie & Lanius, 2001).

OPIOID ANTAGONISTS AND EMDR: A SERIES OF CASE STUDIES

The series of case studies (Ferrie & Lanius, 2001) included 16 clients who met criteria for a variety of diagnoses that included PTSD and partial PTSD, DID, dissociative disorder not otherwise specified (DDNOS), obsessive-compulsive disorder (OCD), and BPD. They all had gone through a stabilization phase and there was an ongoing therapeutic relationship with all of them. Each had some experience with EMDR, but the application of standard and modified EMDR protocols had been unsuccessful. EMDR had been discontinued because of depersonalization or derealization, severe somatization, and/or lack of change on subjective units of disturbance (SUD) ratings of the target memory. In other words, in each case, a therapeutic impasse had been reached. Clients were administered either naltrexone (modal dosage 50 mg; dosage range 25–125 mg) 30 to 60 minutes prior to the EMDR session or 1 mg of naloxone injected subcutaneously immediately prior to EMDR. That is, rather than continuous dosing, opioid antagonists were only administered prior to EMDR sessions.

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Thirteen clients were able to process the traumatic memory down to SUD rating of 0 or 1, with a markedly improved body scan. Twelve reported elimination of somatization and depersonalization. Seven went on to successfully process other memories without naltrexone. On average, clients underwent five sessions using either naltrexone or naloxone. In four cases, ongoing improvement with regard to dissociative symptoms occurred after only one session, whereas other cases needed more frequent sessions—up to a maximum of 15 sessions. Eleven clients showed long-term improvement in presenting complaints after opioid antagonist pretreatment. Two showed no therapeutic effect. Gastric distress is a common side effect of both naltrexone and naloxone. In our sample, naloxone was much better tolerated then naltrexone: Six clients had adverse gastrointestinal reactions to naltrexone that included abdominal pains, nausea, and vomiting; those that were prescribed naloxone did not report any adverse effects. A rapid reduction of flashbacks and intrusive symptoms as well as decreased hypervigilance was evident. Fearfulness, anxiety, and panic symptoms were significantly diminished, whereas mindfulness and dual attention were greatly improved. Moreover, body awareness was heightened with a concomitant decrease in alexithymia—clients now knew what they were feeling. The severity of visible abreaction was minimized and processing appeared to occur more rapidly. There appeared to be much-increased self-regulation and affect tolerance during EMDR processing that coincided with greater ego strength and ability to tolerate the traumatic material. Clients who had previously looped at a high level of disturbance with significant abreaction were now able to utilize the EMDR standard protocol effectively without any additional interventions by the therapist being necessary. Instead, clients seemed to spontaneously integrate previous ego state techniques, inner child work, as well as access resources into their processing using the standard protocol, without the need on the part of the therapist to facilitate such a process. Rather than EMDR breaking through dissociative barriers, clients seemed to be able to effectively synthesize and integrate the dysfunctionally stored information as well as make choices as to what material they wanted to work on. Overall, there appeared to be much decreased primary and secondary dissociation. Tertiary dissociation was reduced with concomitant increase in coconsciousness between ego states. In one case, there was a decrease in “dissociative voices” that had not previously responded to neuroleptic medications. Somatization was greatly reduced. In another case where a client reported the onset of migraine headache activity prior to EMDR processing, the pain stopped almost immediately after naloxone injection.

Client Responses After Opioid Antagonist Mediated EMDR Sessions

Robbie: “Wow it’s nice to feel the ground, I’ve never felt my feet on the ground before.” Chris: “I couldn’t have faced that without the Naloxone.”

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Winona: “A wave of numbness went through my legs and out.” Lois: “I can’t seem to back away from it the way I usually do, and yet it wasn’t so bad.” Becky: “The voices have stopped, my groin doesn’t hurt anymore, the headaches are gone for the first time in 10 years.” Felicia: “I like it; it makes me not sad, sort of dozy. It stops my worry thoughts.”

THE CASE FOR LOW-DOSE NALTREXONE Low-Dose Naltrexone and Dissociative Disorder: First Use

Based on the previous experiences with regular-dose naltrexone, one patient who presented with a severe dissociative disorder with profound amnesia, as well as fibromyalgia, was prescribed regular-dose naltrexone (50 mg/day). Naltrexone resulted in a breaking through of amnestic barriers with spontaneous recall of previously dissociated material: a sexual assault. The patient became quite overwhelmed by this. Having just become familiar with low-dose naltrexone through another client who had a diagnosis of multiple sclerosis, the possibility of an empirical trial of low-dose naltrexone was raised. The client was prescribed 3 mg of naltrexone per day (about 0.06 mg of naltrexone per kg of body weight). The client benefitted not only with regard to fibromyalgia symptoms—interestingly, less so than from the regular dose, contrary to what is reported in the literature. Moreover, there appeared to be reduced depersonalization, derealization, less uncontrolled switching, as well as increased capacity to do ego state interventions. The client found that increasing the dose to 3 mg twice a day (b.i.d.), and on occasion 3 mg three times a day (t.i.d.), actually increased the benefits of naltrexone with regard to not only dissociative symptoms but also fibromyalgia symptoms. Interestingly, the low dose of naltrexone appeared to offer similar benefits to the regular 50 mg dose. However, the breaking through dissociative/amnestic barriers was no longer an issue.

Low Dose Naltrexone

With regard to naltrexone, a nonlinear dosage effect has been reported (e.g., Castellano & Puglisi-Allegra, 1982). It has been suggested that very low and high dosages are most effective and intermediate ones are less so. In our experience, the use of lowdose naltrexone (e.g., 0.06 mg/kg of body weight, administered twice or thrice daily; e.g., b.i.d., or t.i.d.) or regular and high dosages of 50 mg or more tend to be most effective. Belluzzi and Stein (1982) report that high-dose naltrexone may activate postsynaptic receptor sites, whereas low dose may act preferentially on presynaptic receptor sites. Some clients may benefit more from blockade of mu, delta, and kappa receptors at high doses of naltrexone, while others may need the more subtle effects of low doses on the mu receptors.

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Prescribing Naltrexone—Less Is More

The literature at times notes that side effects have limited the dose that can be attained, and this has affected the outcome of treatment. However, it is our experience that in the case of prescribing naltrexone in dissociative disorders, increased dosages do not necessarily lead to improved therapeutic outcomes. In fact, especially during the early stages of treatment, lower doses seem preferable. Generally, low-dose naltrexone seems to avoid most of the side effects associated with opioid antagonist use. For instance, there is minimal nausea and reversal of analgesia, and hepatic loading is not an issue. Finally, breaking through amnestic barriers is much less likely to occur.

Low-Dose Naltrexone

Naltrexone is typically available in most markets only in 50 mg tablets. Low-dose naltrexone is not commercially available. When low-dosage prescriptions for naltrexone are being prepared by a compounding pharmacy, it is important that regular naltrexone rather than sustained-release preparations are used. Usually, naltrexone is compounded with lactose, which may raise some issues for individuals who are lactose intolerant. In those cases, formulations that avoid the use of lactose are available from compounding pharmacies upon special request. Reports from some patients who have been both on lactose-containing and ­lactose-free preparations suggest that lactose-free preparations may be slightly more effective. Low-dose naltrexone can be made up as liquid. While this makes dosage adjustments easy, the authors find it more awkward to use, and there tends to be a bitter underlying aftertaste—the specific taste of naltrexone—in most preparations. Nevertheless, in children and individuals who find the swallowing of capsules difficult, this may be an option.

Low-Dose Naltrexone Dosing

Contrary to the dosing suggested for autoimmune disorders where low-dose naltrexone is commonly administered only once a day, usually in the evening, we found that in individuals with dissociative disorders dosing either b.i.d. or t.i.d. was beneficial. This is producing a persisting low-level blockade of mu receptors rather than inducing temporary antagonism and a rebound increase in sensitivity as is postulated to occur for improved immune function (Brown & Panksepp, 2009). Further, we have found that the optimal dosing for low-dose naltrexone is most easily obtained if body weight is taken into account. The minimally effective dose in our experience tends to be about 0.06 mg/kg of body weight. Incidentally, this is the same dose that has been documented to be the minimum dose that has been shown to be effective for reducing alcohol consumption in rats.

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So after obtaining the body weight in kilograms, the formula for dosing is body weight (kg) × 0.06 = twice or thrice daily dose in milligrams. For someone weighing 120 pounds (54.48 kg) the dose suggested is 54.48 × 0.06 = 3.26 or 3 mg t.i.d. or b.i.d. daily. Similarly, for a person weighing 180 pounds the optimal dose is likely to be 5 mg, either b.i.d. or tid. Generally, we suggest rounding the dosage up to the nearest milligram, unless for the reasons discussed below. Exquisite Sensitivity and Low-Dose Naltrexone Dosing

For some exquisitely sensitive individuals, a lower starting dose yet may be beneficial. For people who have multiple allergies, including allergies to medications and to environmental substances, and for those who appear to have generally hypersensitive nervous systems, we suggest different initial dosing to minimize side effect potential further, for example, starting at 1 mg at night and increasing to a twice-daily schedule before introducing increments of 1 mg. The dosage is titrated upwards until the amount recommended by the application of the formula outlined above is reached. If for some reason the patient feels overwhelmed or is experiencing any negative effects, a slightly lower dose can be maintained until there is adjustment to it with a view toward an increase toward the target dose at a later date. Moreover, for some people, a daily dosage less than that suggested by the formula can be preferable. This is also the case for some individuals with severe DID, where sometimes a dosage difference of as little as 2 mg/day can make the difference between accessing or not accessing a suicidal part of the self. Limitations and Adverse Effects of Opioid Antagonists Hepatoxic Potential (Liver Side Effects)

The most significant and potentially life threatening effect of opioid antagonists relates to their hepatotoxic potential. This is not of concern with low-dose prescriptions, nor does it tend to be an issue even with high doses for individuals who have normal liver functioning. Clear hepatotoxic potential occurs at higher doses when there is preexisting liver dysfunction or when blocking effects are overridden by opiate usage. Concurrent substance abuse increases risk of hepatic side effects in that if a user attempts to override the opioid blockade, there is a significant risk of hepatic failure and/or death. Thus, in our opinion, in individuals who are potential opioid users, the use of higher than the regular dose of naltrexone (50 mg/day) is contraindicated. If there is any doubt from the history about possible limitations with regard to liver functioning, a liver function test prior to the prescription of opioid antagonists is essential. In case of acute hepatitis or liver failure, the use of opioid antagonists is contraindicated. Reversal of Analgesia

Opioid antagonists prescribed in regular or higher-than-regular doses produce significant reversal of analgesia. That is, there is an impaired ability to respond to opioids

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for pain relief. Thus, in cases of significant injury that require pain control, the use of nonopioid analgesics, benzodiazepines, spinal block, or general anesthesia may be required. This is obviously a less significant issue with intermittent dosing and does not apply to prescriptions of low dose naltrexone. In our opinion, a Medicalert bracelet or something similar that alerts potential caregivers of the use of naltrexone is advised in the case of regular and higher doses of naltrexone. Induction of Withdrawal

Patients should be free from opiates, whether street drugs or prescribed opiate analgesics, for 7 to 10 days before the introduction of naltrexone or naloxone, as there otherwise exists the risk of significant withdrawal symptoms. Typical signs and symptoms of opiate withdrawal include yawning, sweating, lacrimation, rhinorrhea, anxiety, restlessness, insomnia, dilated pupils, piloerection, chills, tachycardia, hypertension, nausea/vomiting, cramping abdominal pains, diarrhea, and muscle aches and pains. It should be noted that opiate withdrawal, unlike withdrawal from alcohol or benzodiazepines, is not life threatening. Nausea and Vomiting

The most significant side effect to naltrexone is nausea, and in some cases vomiting occurs. In our experience with individuals diagnosed with traumatic stress syndromes, this occurred in about 30% of subjects who were prescribed regular doses of naltrexone. It is interesting that in our sample this phenomenon did not occur with administration of naloxone, even though it is a listed side effect. In our experience with naltrexone, nausea tends to occur for the most part during initial administration, which suggests an opioid withdrawal effect (see above). It is much less likely to occur with low-dose naltrexone. Once a patient has been taking low-dose naltrexone for a period of time, he or she will usually not experience nausea at much higher doses given subsequently. That is, we have found that being on low-dose naltrexone for a period of several days reduces, if not completely abolishes, the likelihood of nausea in response to regular doses of naltrexone. This phenomenon is consistent with patients experiencing a withdrawal effect from their own endogenous opioids. Thus, initiating naltrexone with a low-dose prescription, even though higher doses are planned, avoids the most common side effect of opioid antagonists. This is important, as patients who do experience nausea and vomiting will commonly refuse further opioid antagonist treatment. Increased Blood Pressure

An unusual behavioral and cardiovascular reaction that was potentially attributed to naltrexone was reported by Ibarra et al. (1994). The subject met criteria for PTSD and had blindly received 50 mg of naltrexone as part of a research study. His response included tachycardia and increased blood pressure. It has been our experience that regular doses of naltrexone tend to counteract a potential decrease

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in heart rate in response to accessing traumatic material. That is, there appears to be a shift away from a dorsal vagal response toward a more sympathetic autonomic nervous system response. At the same time, in our experience, naltrexone generally tends to have a modulatory effect both with regard to hypo- and hyperarousal, with at least one client with a congenital heart condition reporting both decreased bradycardia as well as tachycardia. We hypothesize that the response reported by Ibarra was likely attributable to a bridging into traumatic memories, attributable to a reversal of amnesia, a phenomenon that occurs with a small but significant subset of individuals who are prescribed regular doses of naltrexone. Thus, we interpret the described phenomena as potentially being attributable to breaking through amnestic barriers (also see below), with the client remaining stuck in a PTSD hyperarousal response.

Breaking Through Amnestic Barriers

It has been our experience that opioid antagonists prescribed to individuals with dissociative disorders have the potential to suddenly break through amnestic barriers. The relationship between endogenous opioids and amnesia is described in more detail in Chapter 5. In the absence of a stable therapeutic alliance, as well as adequate ego strength, this can be overwhelming to the patient. Not only is this potentially retraumatizing, it is likely to interfere with compliance in treatment, as it can have profound negative effects on any therapeutic relationship. Further, regular and high doses, because of significant reduction in amnesia, may also be contraindicated during early stages of treatment in severe DID, as they likely make working behind amnestic barriers more difficult. In our experience, this issue can be almost completely avoided by the use of low-dose naltrexone and, where necessary, the careful upward titration in dosage (also see below). Lower doses in conjunction with psychotherapeutic therapeutic interventions will allow a gradual lifting of amnesia with a concomitant improvement of overall adaptive functioning. A conceptual understanding of this phenomenon, in our opinion, is crucial to the successful adjunctive use of opioid antagonists.

Low-Dose Naltrexone: Observed Adverse Effects

Generally, adverse effects to low-dose naltrexone are minimal or nonexistent. Some clients report feeling intoxicated or high initially, but this diminishes with prolonged or repeated usage. Headache, which may represent the activity of a noncooperative ego state, diminishes over time. The same applies to visual disturbance, perhaps an indicator of incomplete coconsciousness. With initial doses, there is a slightly increased frequency of bowel movements and slightly softened stool. Unlike regulardose naltrexone, low-dose naltrexone does not appear to reverse analgesia. We have not yet been able to determine at what dose level the crossover from no reversal of analgesia to reversal of analgesia occurs.

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OPTIMIZING RESPONSE TO OPIOID ANTaGONISTS

The case studies we have conducted thus far, as well as our clinical observations in conjunction with our understanding of the scientific literature, allow us to suggest some tentative guidelines about the prescription and use of opioid antagonists in individuals with traumatic stress syndromes and dissociative disorders.

Naltrexone Dosing—A Collaborative Approach

It is best if the patient can be involved as much as possible in finding the optimal dosage at any given time, especially during the stabilization phase of treatment. Establishing the optimal dosage is assisted by an initial prescription of 1 and 2 mg capsules with which the person can adjust his or her dosage easily.

Naltrexone and the Placebo Effect: Do Not Use Too Early

There is suggestion that opioid antagonists block the effects of expectancy, including the placebo effect (e.g., Amanzio & Benedetti, 1999). Given that there is evidence that the placebo response may be a significant part of the early response to psychotherapeutic interventions and may have effects on the establishment of a therapeutic relationship, the use of opioid antagonists early on in the therapeutic relationship is discouraged. Indeed, it is our clinical impression that too early adoption of the use of opioid antagonists in psychotherapy decreases the likelihood of positive treatment outcomes.

Dissociative Rebound—Too Early, Too Much

One of the issues a prescriber needs to be acutely aware of is the possibility of a phenomenon we call Dissociative Rebound. As delineated in Chapter  5, opioid antagonists reduce amnesia. In clients with good ego strength, this is not necessarily an issue. However, for many clients with severe dissociative disorders this means breaking into dissociated material that they may not be ready or able to deal with. Dissociative rebound is much more likely to occur in clients with severe DID and complicates the use of opioid antagonists. In fact, it is our view that dissociative rebound may potentially account for at least some of the adverse side effects of opioid antagonists reported in the literature (e.g., Ibarra et al., 1994). It may also account for emergent suicidal intent with high doses of antidepressants (Corrigan, Fisher, & Nutt, 2011). We recommend the use of low-, in some cases extremely low, dose naltrexone. Starting with amounts that should ordinarily not have any clinical effect whatsoever and carefully titrating the dose upward minimizes the possibility of endogenous opioid withdrawal and other adverse effects.

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In individuals with severe DID, it has been our experience that in some exquisitely sensitive clients dosage changes of as little as 2 mg can have differential effects and determine whether naltrexone is helpful or not. For instance, one individual with severe DID improved with naltrexone 5 mg b.i.d. (body weight 180 pounds). As dissociative symptoms continued to interfere with daily functioning, to the extent that the patient remained completely disabled from working, the prescriber decided to increase the amount of medication. When naltrexone was increased to 10 mg t.i.d., the patient became acutely suicidal, as a result of accessing a suicidal part of the self that had previously been lurking in the background only. The patient was subsequently taken off naltrexone, but was unable to stabilize. Once naltrexone 5 mg b.i.d. was reintroduced and the therapist focused on ego state interventions, the client restabilized. However, dissociative rebound is potentially an issue with higher doses as well. One client who was prescribed 200 mg naltrexone per day complained about emerging headaches, dizziness, and mild balance disturbance at that dosage. With a reduction in dosage to 150 mg/day these symptoms disappeared entirely. Given that opioid antagonists commonly do not have noticeable effects in the absence of opioid activation, it is our hypothesis that the person was starting to access a dissociated part of him- or herself that he or she was not ready to let emerge into consciousness at the time. This hunch was corroborated during the later course of treatment.

The Issue of Drug Absorption

Generally, it has been our clinical experience that dissociative processes interfere with the normal absorption of medications or with their metabolism. This may in part account for both the lack of effectiveness, as well as the paradoxical effects, of medications in individuals with dissociative disorders. Altered absorption of drugs taken concurrently with opioid antagonists is a concern for patients who are on medications that need to be at specific blood levels, and for those on high doses. Also, see below for the use of naltrexone to augment response to other medications. Warfarin

Warfarin is a blood thinner, an anticoagulant, with an individual dose determined by the measurement of the international normalized ratio (INR). In one case of a client who was on warfarin, the addition of naltrexone significantly altered the speed of clotting measured by the INR. The client, who had been diagnosed with DDNOS, had a history of severe childhood medical trauma as well as severe attachment issues. She also had a congenital heart condition that usually results in stillbirth. She had been diagnosed with a seizure disorder during childhood and was on phenytoin over the period of many years but not during adulthood. Because of her heart condition, apart from a multitude of heart medications, the patient was also on warfarin. The use of low-dose naltrexone resulted in a significant change in INR and the need for adjustment of the dose of warfarin.

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Augmentation of Other Medications—An Absorption-Related Effect?

Below, we describe several cases of patients with multiple diagnoses where neither naltrexone alone nor antidepressant alone had significant therapeutic effects in treatment. However, the addition of naltrexone increased therapeutic effects of other medications. This raises the question as to whether such effects may be attributable to increased absorption. Augmenting Response to Antidepressants

While there have been reports of naltrexone having antiobsessional effects, naltrexone alone did not appear to have much of an effect. However, in combination with antidepressant medication, significant clinical effects were observable. This phenomenon has been described in the literature where response to antidepressants has been augmented by opioid antagonists for patients with OCD (Amiaz, Stein, Dannon, Grunhaus, & Schreiber, 1999), treatment refractory depression (Amiaz et al., 1999), eating disorders (e.g., Neumeister et  al., 1999), and smoking cessation (Toll et  al., 2008). Antidepressant Augmentation in a Case of Obsessive-Compulsive Disorder

The client’s father was a highly decorated officer in World War II and his mother had been a nurse in the war theater. There was suggestion that both parents were probably suffering from PTSD. The mother had a history of ongoing depression, including postpartum depression after the client’s birth. The father was emotionally distant and unavailable. There had been multiple substitute caretakers during childhood as well as several different boarding school experiences that included bullying. The client presented with intractable depression that had previously responded minimally to venlafaxine but to no other antidepressants— many of them had been tried. He was diagnosed with DDNOS, major depressive disorder, obsessive-compulsive disorder, as well as with an attachment disorder. The client, at the time when he attended the office of one of the authors, had stopped venlafaxine as he felt it was not working for him. He was suffering from intractable depression as well as anxiety and marked obsessive behavior including hoarding. He was put on low-dose naltrexone. There was some improvement in depersonalization symptoms and a minimal reduction in obsessive-compulsive behavior. Depression and anxiety remained unchanged. He was encouraged to go back on his antidepressant medication. At that time, he had a good response to venlafaxine with much reduced depression and anxiety. Antidepressant Augmentation With Eating Disorder

A young woman who was suffering from intractable bulimia as well as dissociative symptoms was referred by another therapist. She presented with a dissociative disorder, bulimia, and a major depressive disorder. The client described a history of sexual abuse and sexual boundary violations by her father, as well as by his business associates. At the time of referral, she was on a therapeutic dose of fluoxetine with a partial response with regard to depressive symptoms. Bulimic symptoms were not affected by fluoxetine. She had pervasive dissociative symptoms but was unable to do ego state therapy easily. For example, when using the conference room technique, more often than not the conference room remained empty. Given the

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client’s eating disorder and the copious dissociative symptoms, the use of naltrexone was discussed. She started naltrexone at a low dose and became immediately able to fully participate in ego state interventions, identifying many parts of the self. Her affect regulation was much improved. It was interesting to observe that at times when she discontinued her low-dose naltrexone she was unable to do parts work or ego state therapy. However, low-dose naltrexone had no significant effect on the bulimia symptoms that remained essentially unchanged over the course of several months. Feeling frustrated by a lack of response of bulimic symptoms, the patient decided to try a higher dose of naltrexone, namely 50 mg b.i.d.: the bulimia symptoms immediately improved. The client then chose to work on issues related to her sexual abuse with a female therapist and she was referred to a female eating disorders specialist who utilizes EMDR. Antidepressant Augmentation With Substance Use Disorder

The client had a history of severe attachment trauma, sexual abuse, and sexual assaults. There was a history of multiple psychiatric hospitalizations. Her diagnoses included a dissociative disorder, major depressive disorder, PTSD, Crohn’s disease, fibromyalgia, and alcohol abuse. She also smoked cigarettes. She was on a combination of antipsychotic, antidepressant, and antianxiety medication that included bupropion (Wellbutrin®). Once naltrexone was added, the client stabilized quickly and dissociative symptoms benefitted from low-dose naltrexone (3 mg b.i.d.), with much increased ability to do ego state work. Alcohol abuse decreased significantly and the client was able to stop smoking. She was able to maintain these treatment gains. At the same time, symptoms of Crohn’s disease did not show any significant response. The combination of naltrexone and buproprion has been found to be beneficial for substance use in the literature (Toll et al., 2008). Augmenting Response to Antipsychotics

In another case, the patient of one of the authors, who had been prescribed high levels of atypical neuroleptics and had not responded significantly to the medication, suddenly developed significant side effects to the antipsychotic medication once he was prescribed low-dose naltrexone. There are reports in the literature that opioid antagonists can increase response to neuroleptic medication (e.g., Rapaport et  al., 1993; Sernyak et al., 1998). Given our clinical observations, we hypothesize that this is likely attributable to altered absorption of the neuroleptic medication. A client with a history of pervasive neglect and lack of caretaking, including a state of semistarvation during infancy, had been diagnosed with pervasive developmental disorder as well as schizophrenia. The schizophrenic illness was considered to be treatment resistant. There were dissociative, psychotic, and autism spectrum disorder symptoms. He was on high doses of the atypical neuroleptic risperidone. A diagnosis of DDNOS was made after he was referred for psychotherapy. Initial focus on treatment was on increasing mindfulness and gently working with body mindfulness to which the client responded well. The addition of low-dose naltrexone resulted in the sudden emergence of severe antipsychotic side effects. Specifically, he developed akathisia, excessive sedation, muscle stiffness and pain, as well as hypersalivation, all of which reduced with a decrease in the dose of the antipsychotic. He continued to improve and was able to complete school and live semi-independently. What all the above clinical vignettes have in common is either a documented increase in drug levels or a probable increase in drug levels as suggested by behavioral

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evidence. In some cases, synergistic actions on the mesolimbic dopamine system may also occur. In our view, dissociation likely alters absorption levels of many medications and leads to changes in their metabolism. The ease with which a person in one ego state can drink alcohol in amounts that would be incapacitating in other ego states suggests altered metabolism. However, state changes with associated alteration in absorption are likely to account for many paradoxical drug effects. Based on clinical observations, we hypothesize that depersonalization and derealization likely reduce absorption. This conceptualization is supported by the use of opioid antagonists for augmentation of neuroleptics (e.g., Rapaport et al., 1993; Sernyak et al., 1998) as well as antidepressants (e.g., Amiaz, Fostick, Gershon, & Zohar, 2008; Toll et al., 2008). Given our experience with altered blood levels, as well as the development of side effects after initiation of naltrexone, we recommend significant caution and close monitoring in the case of patients who are on high doses of other medications or have been prescribed medications that rely on specific blood levels.

CLINICAL EFFECTS OF NALTREXONE Low-Dose Naltrexone for Stabilization—Increased Self-Regulation

It has been our experience that opioid antagonists significantly aid patients with traumatic stress syndromes to stay within their window of tolerance (e.g., Siegel, 1999). Keeping in mind not to introduce naltrexone too early in treatment, naltrexone works well to aid in stabilization. Mindfulness-based as well as ego state interventions are more likely to be successful. Affective regulation and/or self-regulation, as well as affective and somatic tolerance, are commonly improved. Alexithymia is decreased. Primary and secondary dissociation are commonly decreased. There is a concomitant reduction in tertiary dissociation, particularly uncontrolled and unpredictable switching between ego states, while there is commonly a simultaneous increase in coconsciousness among parts of the self, with an increased continuity in the person’s sense of self. With the decrease in dissociative symptoms, there is also an increase in assertive behavior, likely attributable to increased sympathetic activation under stress, rather than dorsal vagal shutdown. In patients who are amnestic for significant periods of their life, there tends to be a decrease in amnesia. At lower doses, this occurs very gradually, and in conjunction with the increased affect tolerance tends to be unproblematic. Rather than breaking through dissociative barriers, clients are able to choose what issues they want to work on. Given that the opioid system plays a crucial role in the modulation of anxiety, one would suspect an increase in anxiety, as has been reported in the literature. Among our clients, all of whom were in a psychotherapeutic relationship, this never became evident, unless we assume that underlying anxiety was the reason for patients to wean themselves off naltrexone during their therapist’s absence. Indeed, among our clients, a self-reported reduction in anxiety is common and this is supported by behavioral observations. We hypothesize that decreased anxiety in general is attributable to opioid antagonists increasing ventral vagal regulation by means of

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increasing oxytocin output (see Chapter 6). However, in the absence of a therapeutic relationship, naltrexone clearly has the potential to be aversive. There is a decrease in self-harming behavior, even with low-dose naltrexone, consistent with our view that opioid antagonists improve self-regulation in general. Even at lower doses there tends to be a slight decrease in flashbacks, intrusive symptoms, and hypervigilance, and an improvement in attentional functioning. Appetite and food intake tend to be decreased in most clients. In previously overweight clients, weight reduction occurs with eventual stabilization. This occurs even with clients who are on low-dose naltrexone. Incidentally, a combination medication using buproprion and regular-dose naltrexone (e.g., 50 mg) is currently under investigation as a weight loss drug (e.g., Greenway et al., 2010).

Regular and High Doses

There is little doubt that regular doses (50 mg/day), as well as higher doses, of opioid antagonists can be useful. However, this should be preceded by psychoeducation, including comprehensive information about opioid antagonists. Informed consent is necessary not only with regard to the potential spontaneous recovery of previously dissociated material but also to the possible emergence of parts of the self that had been previously unavailable to conscious awareness. In the case of DID, consent needs to be obtained from all parts that are accessible at the time. Trauma Processing

Higher doses are indicated for trauma processing, usually the dose being administered about 1 hour prior to the session. In our experience, this is clearly the case for trauma processing of severe traumatic life events—this includes but is not limited to early childhood sexual abuse, particularly by a primary attachment figure, as well as severe medical trauma including awareness under anesthesia. We have utilized dosages ranging from 25 to 200 mg prior to the session. Acute Depersonalization

High doses of opioid antagonists are also useful in decreasing acute depersonalization. At lower doses, opioid antagonists primarily affect mu-opioid receptors while depersonalization has, at least in part, been related to kappa-opioid receptor activation. For naltrexone or naloxone to be effective at kappa-opioid receptors, higher doses are needed. Preliminary observations suggest that an optimal dose to maximize effectiveness is somewhere between 3.5 and 4 mg of naltrexone per kg of body weight (e.g., about 200 mg/day for a person with a body weight of 120 pounds). A word of warning with regard to using such high doses of opioid antagonists in cases of depersonalization: The clinician should have a good understanding of the client. If there is any suspicion of an underlying DID with significant amnesia and poor ego strength, high doses may result in spontaneous bridging into previously

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dissociated material with concomitant dissociative rebound and a resulting deterioration in functioning. On the other hand, in DDNOS, the use of high doses is usually uncomplicated and frequently beneficial. Eating Disorders and Self-Harming

In the case of eating disorders, certainly during the later stages of treatment, higher doses of opioid antagonists seem to be necessary to significantly impact the binging and purging cycle. Similarly, self-harming behavior seems to respond better to higher doses. However, the previously noted precautions with regard to a possible underlying DID need to be heeded. Nevertheless, with appropriate psychotherapeutic interventions—ego state therapy in particular—the majority of these potential pitfalls can usually be avoided. Psychosis and Dissociative Voices

Higher doses can also be useful in patients who experience intractable dissociative voices—many of whom may have been diagnosed with a psychotic disorder—and who commonly respond poorly to antipsychotic medications. Ferrie and Lanius (2001) described a patient whose “voices” had not responded to neuroleptics who, with the aid of naltrexone and EMDR treatment, no longer experienced hearing voices. Similarly, Miller (2010) described successfully using regular doses of naltrexone in conjunction with EMDR in the treatment of psychotic disorders including schizophrenia, where traditional neuroleptic treatment had been unsuccessful. Dissociative Disorder, PTSD, and Fibromyalgia

A patient with a polyfragmented dissociative disorder, PTSD, and fibromyalgia, with a history of severe medical trauma, including waking up under anesthesia on several occasions, was prescribed low-dose naltrexone. There were clear benefits for the dissociative and fibromyalgia symptoms, but despite extensive stabilization and preparatory work, including ego state interventions, the client was unable to complete trauma processing. High-dose naltrexone prior to psychotherapy sessions was added (up to 150 mg 1 hour prior to the session), which allowed some successful trauma processing with EMDR and with sensorimotor psychotherapy (SP). More recently, neurofeedback training (neuroptimal) in conjunction with high-dose naltrexone has been utilized, and this has allowed some parts of the self to step forward that were unable to be present before. Neurofeedback has had stabilizing effects at times, whereas at other times there is clearly further trauma processing occurring. While there have been clear benefits, both with dissociative and fibromyalgia symptoms as a result of naltrexone, progress has been exceedingly slow and the client remains symptomatic thus far. Most recently, the addition of LENS neurofeedback in combination with low-dose naltrexone has provided some additional benefits and the best results so far. However, ongoing issues with regard to egostate cooperation with regard to a hypervigilant part remain and are likely an ongoing barrier to further improvement in functioning.

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DDNOS, PTSD, Major Depressive Disorder, and Fibromyalgia

The client had a history of significant attachment issues. Parents were emotionally distant and both emotionally and physically abusive. As a small child, there was a history of sexual abuse by a babysitter on repeated occasions as well as sexual abuse/sexual assault by another person. At the time of referral, the client was on disability because of a major depressive disorder. She responded well to initial stabilization and later ego state interventions, and was then able to target attachment issues and subsequent traumatic events with EMDR. Her functioning increased over time but there were issues with intermittent therapeutic contact as well as occasional slipping back. Fibromyalgia symptoms continued largely unabated. After being put on low-dose naltrexone, the client described much-increased energy as well as much- improved attentional functioning. Further, sleep improved, with the client feeling more rested and no longer having nightmares.

Opioid Antagonists, the Relational and Defensive Responses

Blocking or partially blocking opioid activation with opioid antagonists has a complex array of effects, including an increased orienting to one’s environment, essentially a SEEKING response. The seeking for relationships is likely to be attributable to the release of oxytocin mediated by opioid blockade (also see Chapter 6), as has been fairly well documented in autistic children. This kind of SEEKING for the relational can also be painful in the absence of an active attachment relationship. We have observed that clients who are on low-dose naltrexone will often take themselves off the medication when the primary therapist is out of town, on vacation, or otherwise unavailable. Patients are usually not aware of why they stopped their medication, being unable to give any reason for doing so. When not on opioid antagonists, their functioning usually deteriorates slightly, with increased levels of depersonalization and derealization, decreased affect regulation, and decreased ability to do ego state work. Upon the return of the primary therapist, when reminded, they willingly restart the medication and their functioning returns to the level it attained before they stopped the naltrexone. We conceptualize this phenomenon in terms of effects on the attachment system, where naltrexone, even in small doses, likely produces a SEEKING response, for example, specifically an orienting toward an attachment relationship. If such a response is not likely to be met, this is likely to result in separation distress, leading to clients weaning themselves off of even low doses of naltrexone. Blockade of the opiate system also decreases the likelihood of engaging in a passive defensive or dissociative response in the face of threat. This likely occurs at the level of the midbrain periaqueductal gray (PAG). Individuals on naltrexone are less likely to be passive in social situations of even mild conflict and they are more likely to express assertiveness, sometimes with a slightly edgy quality, especially if not used to being assertive. Essentially, we view this as shifting the balance away from passive defensive responses toward more active defensive responses. Let us describe the case of one client that illustrates this. The client, with a history of childhood abuse and neglect, including sexual abuse, had previously been a heroin user and worked in the sex industry. She found stable employment in an office environment, though

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she was frequently harassed by a coworker. Usually, she would go into a collapse and submit to the coworker. Once, when she was on low-dose naltrexone, the same coworker started harassing her to do something, threatening to hit her if she wasn’t going to comply. The client responded by saying that she would hit her back. The coworker then struck her and a fight ensued, leading to them both being suspended without pay for 2 weeks. The coworker was relocated to another office. Despite the adverse economic consequences of her actions, the client felt empowered by her assertiveness and her success in terminating the harassment. This case clearly reflects the shift away from a passive defensive response to an active defensive response. This is possibly mediated by an increase in vasopressin in the absence of the relational. That is, oxytocin release potentially only occurs if there is a safe relationship available; if there is lack of safety, vasopressin release may be more likely (also see Chapter 6). Consistent with our view that opioid blockade increases the likelihood of an active defensive response, likely through, among others, a reduction in decreased TI, naltrexone seems to facilitate the emergence of involuntary movement, especially at higher doses and often spontaneously. Without client preparation, this can be very distressing. At the same time, it has been the authors’ experience that this very aspect of opioid blockade is helpful with the sensorimotor sequencing that is an essential part of SP.

Opioid Antagonists and Compatibility With Different Psychological Treatments

Beneficial effects of naltrexone on patients undergoing DBT have been reported (e.g., Bohus et al., 1999). Naltrexone facilitates EMDR processing (Ferrie & Lanius, 2002) and body therapies (e.g., SP), resource development, and hypnotically based interventions are facilitated. On the other hand, opioid antagonists interfere with exposure treatment (Egan, Carr, Hunt, & Adamson, 1988; Merluzzi, Taylor, Boltwood, & Götestam, 1991) perhaps because the functional mechanism of exposure treatment is purported to involve the release of beta-endorphin (Carr, 1996). Naltrexone contributes to greater relapse with regard to behavioral avoidance in a dose-dependent manner (Arntz, Merckelbach, & de Jong, 1993), though no negative effects with regard to emotional, cognitive, and physiological measures were reported. It has been our experience that opioid blockade clearly facilitates trauma processing, both with EMDR and with SP. It appears to interfere with in vivo exposure until there is a complete resolution of the traumatic experience with either EMDR or SP. Once resolution is complete at a physiological level, for example, either a clear body scan in EMDR or a lack of physiological activation in response to trauma-related cues, in vivo exposure then becomes possible. In that sense, opioid blockade facilitates the differentiation between numbing and avoidance, two phenomena that are commonly held to be similar responses to traumatic stress (e.g., compare DSM-IV-TR). Naltrexone, consistent with our notion of it decreasing passive defensive responses—for example, dorsal vagal activation—and at the same time increasing active defensive responses, will profoundly increase avoidance symptoms as long as there is unprocessed traumatic material. This also supports the view that avoid and hide

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defenses are active strategies less easily studied in animal models than fight, flight, and freeze, as they are difficult to differentiate from restrained seeking behavior. Once trauma processing with EMDR has been completed, for example, the SUDS has truly gone down to 0, in vivo exposure with naltrexone is usually unproblematic. Only under exceptional circumstances, when an ongoing realistic threat remains associated with the original traumatic stimulus, will naltrexone interfere with in vivo exposure. Under those circumstances, alternative behaviors that include avoidance are more adapative and increase the likelihood of survival; for example, in this case naltrexone continues to facilitate active defensive responses.

Discussion

As discussed in the earlier chapters, endogenous opioid activity is likely involved in dissociative symptoms. Adjunctive administration of opioid antagonists to clients with severe traumatic stress syndromes who exhibit significant dissociative symptoms is an innovative treatment strategy. It seems to have benefits with regard to stabilization, aiding with mindfulness, exteroceptive and interoceptive awareness, as well as decreasing alexithymia and dissociative symptoms including spontaneous state switching. Initial observations suggest that the timing of the use of opioid antagonists is crucial to maximize their effectiveness. The potential aversiveness of their use appears to be minimized when they are used within an established therapeutic relationship. This may be attributable to the fact that the opioid system is significantly involved in attachment. When an opioid antagonist was administered prior to EMDR treatment, clients who had previously been unable to benefit from EMDR, even when special protocols for dissociative disorders were utilized, were now able to undergo EMDR and process traumatic material to resolution and/or to a level of decreased disturbance. Clients appeared to be able to stay with the process much better without undue dissociative symptoms when an opioid antagonist had been administered to them. Opioid antagonists not only appear to increase body mindfulness but also seem be beneficial with regard to increasing response to ego state interventions, EMDR processing, and SP, and there are some preliminary suggestions that opioid antagonists may increase response to neurofeedback. In summary, the use of opioid antagonists in the treatment of dissociative disorders is an innovative method that conjoins pharmacological and psychotherapeutic interventions. A recent study by Pape and Wöller (in press) supports the utility of low-dose naltrexone in particular with regard to the treatment of dissociative symptoms. This approach shows potential with regard to the treatment of traumatic memories in clients who exhibit significant dissociative symptoms or are experiencing excessive somatization. It appears to reduce dissociative symptoms, thereby not only aiding with stabilization but also enhancing information processing during trauma processing with EMDR and SP. At the same time, even though the above-described therapeutic effects are promising, the adjunctive use of opioid antagonists should be considered an experimental treatment until these findings can be replicated in a placebo-controlled, double-blind study.

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498  II.  TREATMENT

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Index

ACC. See anterior cingulate cortex ACTH. See adrenocorticotropic hormone adaptive information processing (AIP) model EMDR and, 215–216 eye movements, 216 in neurobiological concept, 231–232 self and, 232–233 temporal binding and, 228–229 thalamic activity, 217 adrenocorticotropic hormone (ACTH), 83, 95 adult sexual assault (ASA) survivors, 57 affective circuits alexithymia, 344 defensive responses, 348–349 education, 309–311 ego awareness vs. object awareness, 354–355 emotional parts and, 6 in mammals, 14 mentalization, 351 neocortical resources, 245 neurobiology of, 342 PAG and, 345 PLAY and, 347 resetting methods, 353–358 seeking system and, 346–347 separate self-states, 345 social, 348 structural dissociation, 20–21 truncated, 21–22 affective dysregulation, 94–95, 341, 342, 344 affective neuroscience, 342 affiliation definition, 199 oxytocin–opiate system modulates, 109–110

neurobiology of, 197–198 threat and, 197–198 AIP. See adaptive information processing (AIP) model alexithymia affective dysregulation, 94–95 alleviation of, 351 decreased, 478, 493 definition, 343 empathetic deficits, 344 neurobiological reduction, 328 posttraumatic stress disorder (PTSD), 70, 343 role in traumatic stress syndrome, 342 stress-induced analgesia (SIA), 93–94 treatment barriers, 341 allodynia, 161, 476 amnesia. See also dissociative amnesia assessment, 255–256 barriers, 257, 264–265, 387 Behavior, Affect, Sensation, and Knowledge (BASK) Model, 369 β-endorphin, 13, 95 clinical manifestations, 82 DID and, 263, 489 extreme cases, 20 naltrexone, 479 opioid-mediated phenomena, 22–24, 484 reverse experimental, 118, 483 state switching, 258 amygdala, 139–141, 149 analgesia, 82, 83, 85, 91–93 anesthesia, 82, 96 dissociative, 13, 14 opioid-mediated phenomena, 22–24 trauma processing, 489 499

500  INDEX

anger cortical regulation, 141 ego state therapy, 427 endocannabinoids, 157 midbrain emotions, 173 negative emotions, 176 PAG and, 184 self-loathing, 137 shame level and, 176–177 suppression, 138 TI stage, 61 animals defense responses, 11, 21–22 endogenous opioid tone, 88 freeze response, 55 grounding, 305–306 LH model, 90–91 maternal separation, 159–160 nervous system response, 308–309 parental care, 107–108 potential threat, 35–36 responses to stress, 82 SIA model, 91–92 tonic immobility (TI), 54, 57 ANPs. See apparently normal personalities anterior cingulate cortex (ACC), 115 affective responses, 10 behavioral responses, 132 dorsal, 45 potential threat, 36–37 subgenual, 42 thalamic inputs, 15, 18, 24 threat, orientation, 37 maternal behavior, 195 predator proximity, 140 in PTSD, 132 antidepressant augmentation, 486–488 apparently normal personalities (ANPs), 264, 310 adaptive self-states, 10 analgesic response, 21 ego state therapy, 338 interoceptive loops, 166 functional roles, 310, 393 orientability, 262 arousal responses, 37–38, 45 attachment behavior disordered, 114 distress downregulation, 198–199 endogenous opiates and, 108 frozen state, 205–206 in mammalian species, 106 maternity and, 195–197 negative emotions, 176 neuropeptides, role in, 105–106

obstructed state, 205–206 pathological dissociation, 195 play and, 205 positive effects, 176 protest and, 205 repair, clinical example, 207–208 safety and, 193–194 social learning, 175–176 oxytocin system, 109–110, 115–116 separation vs., 110–111 trauma and, 119 attention, 37, 39 attentional focus, 138–139 attunement clinical example, 281–282 functions, 270 nonattunement and, 277 autobiographical memory, 70 autonomic nervous system in humans, 159 in infants, 193–194 in mammals, 107 neuromodulatory systems, 106 opioids activation, 120 opposing mechanisms, 85–86 SIA mediation, 162 sympathetic, 35, 92, 483 parasympathetic hyperarousal response, 44, 92 autonomic regulation, 105–106 avoidance, 38, 40–41 awareness, 272 basic affective circuits affective mentalization, 351 CARE, 173, 175, 176, 186, 208, 309, 345, 347, 348, 353, 427 FEAR, 14, 22, 32, 116, 173, 176, 186, 208, 309, 345, 347, 348–349, 353, 427 LUST, 173, 176, 186, 208, 309, 345, 347, 353, 358, 427 PANIC circuit, 250, 345, 348, 354 PLAY, 173, 176, 186, 205, 208, 309, 345, 347, 353, 427 SEEKING system, 110, 114, 208, 346–347 RAGE, 13, 14, 22, 173, 176, 186, 208, 309, 345, 347–349, 353, 356, 360–361, 427 self-states or emotional parts, 6, 21, 344 BASIC ID. See behaviors, affective responses, sensory reactions, images, cognitions, interpersonal (BASIC ID) model BASK.. See behavior, affect, sensation, and knowledge (BASK) model BDNF. See brain-derived neurotropic factor

Index  501

bed nucleus of the stria terminalis (BNST), 34, 115, 139, 173–174 behaviors, affective responses, sensory reactions, images, cognitions, interpersonal (BASIC ID) model, 370 behavior, affect, sensation, and knowledge (BASK) model, 369, 388 beta-endorphin, 83, 84, 88, 95 binding AIP and, 228–229 attentional aspects of, 218 definition, 214 episodic memory, 221 integration of information, 214–215, 226–227 sensory awareness and, 233 sensory stimuli and, 224 synthesis level and, 226–228 temporal, 217 temporal-cognitive, 218–219, 230–233 thalamocortical, 231–232 traumatic memory, 213 BNST. See bed nucleus of the stria terminalis body awareness, 409–414, 450, 478 body mindfulness bottom-up processing, 457 boundaries, 459–460 breathing and, 458–459 dual focus, 450–452 EMDR, 450–451 intentional movement, 460–461 personification, 232 sensory stimulation, 449 somatic tolerance, 254–255 brain processing, 345–346, 427, 429, 436 brain-derived neurotropic factor (BDNF), 183, 203 buprenorphine, 82, 114–115

low-dose naltrexone, 480 PLAY circuit, 347 PTSD, 12 social exclusion, 186 circuit breaker analogy, 433–434 codeine, 82 colliculi. See superior colliculi (SC) compassion beneficial effects, 276 body components, 275–276 default state of, 282 emotion regulation, 272–273, 277 empathy and, 274–275, 282 evoking state, 278 for self, 270, 271, 281 hypothalamus activation, 280 positive state of, 277 practices of, 278 conference room technique, 264–265, 326, 329, 385–387, 393, 426–427 container affective resetting, 352–353 in ET work, 435 imagery, 388–389, 441 kids, 393 therapeutic, 391 cortical networks, 157, 223 corticotropin-releasing factor (CRF), 135, 157, 183 CRF. See corticotropin-releasing factor cringe responses diffusion, 179–180 collicular responses, 41 midbrain’s range, 38 tectocuneiform, 178–179 cross-crawl, 466 cross-lateral stimulation, 466

case studies acceleration and deceleration, 394–395 dissociative identity disorder, 378–381 social threat, 30–32 stabilization treatment, 359–361 caudate nucleus, 154, 163–164 central nervous system, 82–83, 117–118, 471 children. See also enduring symptoms, children autistic, 110, 491 default mode network (DMN), 182 dissociative identity disorder, 205 dissociative mother, 199, 277 EMDR protocol, 424 emotional experience, 307 hydrancephalic, 94 imaginary friends, 249 loneliness, 248–249

dACC. See dorsal ACC DAS. See dual attention stimulation default mode network (DMN), 70–72, 182–183 defense responses affective circuits and, 349 dysfunctional, 153–168 frozen, 131–149 malfunctioning, 131–149 neural mechanisms, 33 obstructed, 131–149 range of, 32–33 self-states (alters), 146–148 suppressed, 131–149 threat and safety, 29–48 truncated, 131–149 depersonalization, 30, 52, 70, 82, 92, 93

502  INDEX

depression introjective, 176 long-term, 231 mindfulness meditation, 273 PANIC circuit, 345, 348 psychoanalytic concept, 176 resting state, 177, 183 submission, 141–142 derealization, 52, 60, 70 despair, 194 DID. See dissociative identity disorder dissociation cortical deafferentation and, 5–25 endogenous opioids, 81–97 loss of self and, 5–25 nervous system and, 404–408 opioid antagonists, 471–493 peritraumatic, 51–62 psychotherapy, 243–245 sensorimotor psychotherapy, 399–419 sensory stimulation and, 213–233 total submission, 406 dissociative amnesia, 154, 155, 164 dissociative disorders diagnostic issues, 254–259 EMDR and, 216–217 hypnoanalytic interventions, 384 low-dose naltrexone, 479–481, 484 sensory stimulation and, 216–217 dissociative identity disorder (DID) amnesia, 263, 489 case example, 378–381, 394–395 dissociative symptoms, 252–253 reducing inner conflict, 323 self-observation, 253 true switching, 263 sudden switching, 429 dissociative symptoms adulthood, traumatic events, 256 affect tolerance, 254 amnesia, 255 childhood, traumatic events, 256 coconsciousness, 256–257 copresence, 256–257 dissociative identity disorder (DID), 252–253 helper part, presence or absence, 258–259 hidden nature, 252 identification of, 251 locus of disturbance, 265 making the best of a bad situation, 259 memory loss, 255 orientability, 261–262 perpetrators, attachment to, 259 power, experience, 260

preemptive strike, 259–260 present time, amnesia, 255 prior therapeutic interventions, 261 self-harm activities, 260 self-soothing capacity, 255 self-system, fragmentation of, 252–253 somatic tolerance, 254–255 switching state, 258 dissociative symptoms, treatment cost-efficient means, 262 Dissociative Table Technique, 264, 389 switching, 262–263 talking through, 262–263 distress vocalization (DV), 110 DMN. See default mode network DMPFC. See dorsomedial PFC dorsal ACC (dACC), 45 dorsal vagal activation, 106, 110–111, 112, 122 dorsal vagal parasympathetic systems, 406 dorsomedial PFC (DMPFC), 43, 75, 185, 272 double dissociation, 386, 392 dual attention stimulation (DAS), 465–466 dual focus, 450–451 DV. See distress vocalization early trauma (ET), 343 affective circuit, impact on, 357–358 clinical example, 359–361 conference room strategy, 426–427 containment strategy, 426 ego state therapy, 427 EMDR challenges, 424 practical details, 438–439 preparatory steps, 437 REVIEW, RELEASE, and REPAIR, 441–443 session structure, 438–439 systematic nature, 432 temporal integration, 423–443 therapeutic relationship, 426 time and session, usage, 439 time efficiency, 432 ego awareness, 390–393, 395 ego state adding ego, 389 appreciation, 324–325 definition, 390 hypnotic intervention, 385 object energy, 389 perpetrator introject, 325–331 resource team, 333–334 shame, 332–333 somatic awareness, 393–394 survival management, 331 ego state shifts, 367

Index  503

EMDR. See eye movement desensitization and reprocessing emotion regulation, 166, 175, 272–273 emotional motor memory, 164 emotional numbing, 70, 93, 473 emotional personalities (EPs) affective circuits, 20 analgesic responses, 21 definition, 23 functional roles, 310, 393 pacing the work, 393 traumatized self-states, 10 emotions, 140–141, 307–308, 375 empathy, 274–275, 459 endocannabinoids, 156, 157–158 endogenous opioids defensive responses, 89, 93 dissociation mechanism, 81, 97 modulation of memory, 95–96 parasympathetic regulation, 85–86 peritraumatic dissociation, 156–157 psychotherapeutic context, 89 stress responses, role in, 84 vasopressin release, 106 ventrolateral PAG Activation, 135 endorphins amygdalar activation, 93 analgesic effect, 83–84 antagonist effects, 83 approach behavior, 90 dissociation mechanism, 81 during acute stress, 82 enduring symptoms, children failed strategy, 251 forsaking of the self, 250 internal stress, 249 internalized conflicts, 249 malignant caretaker, 250 painful memories, 250–251 separateness, 250 shame, 250 surrender to hopelessness, 249–250 enkephalins, 82, 83, 85 environmental demands, 47–48, 400 EPs. See emotional personalities ET. See early trauma existential feelings, 280, 282–283 exogenous opioids, 82–83, 91 exteroceptive awareness, 453, 454 extreme fear, 57 eye movement desensitization and reprocessing (EMDR), 30–31, 141, 154 accelerating, traumatic materials, 394 associative process, 394

from birth to age 8, 430–431 body mindfulness, 450–451 bottom-up processing, 458 breathing, 458–459 challenges, 424 Dissociative Table method, 385 dual focus, 450–451 ego state work, 324 ET processing, 424 explicit and implicit memory compared, 437 exteroceptive and interoceptive awareness, 227–228 implicit memory, 434–435, 440–441 loving eyes, impact, 270 negative cognition (NC), 434–437 positive cognition (PC), 434–437 safe embodiment, 269, 334 sensory stimulation, 449 standard protocol, 448 targeting, 368–369 temporal integration, 431 eye movements motor imagery, 350 parietal cortex and, 178–180 somatic responses, 438 superior colliculi and, 11, 163 vigilant, of monkeys, 139 facial emotion, 72, 74 FAPs. See fixed action patterns fear hypothesis (FH), 56 fentanyl, 82 FH. See fear hypothesis fixed action patterns (FAPs), 344 fight, 38, 42–43, 206 flight, 38, 42, 45 fractionation BASIC ID model, 370 BASK model, 369 by metaphor, 370 by oscillation, 371–372 by parts of self, 371 by time segment, 371 definition, 368 for gradual release, 370 looping signals, 377–378 SIBAM model, 369–370 targeting and, 368–369 freeze/frozen column coactivation, 135–136 cortical regulation, 140 high-arousal state, 134 midbrain’s range, 38, 132, 141 peritraumatic states, attentive immobility, 138

504  INDEX

freeze/frozen (cont.) taxonomy, 132–134 types of, 44 vlPAG state, 39, 44 functional MRI (fMRI), 45, 75, 159, 179, 198, 273 gammaband activity (GBA) , 224–226 GBA. See gammaband activity grieving, 174 grounding methods, dissociative patients animal grounding, 305–306 counting red and blue things, 305 feet on the ground, 304 fragrances, 306 golden chord, 304–305 herbs, 306 mother earth, 304 salt, 306 stepping outside, 305 hide, 38, 40–42, 143 hippocampal volume reduction, 154, 155, 173 HPA. See hypothalamic–pituitary–adrenal (HPA) axis hydromorphone, 82 hyperalgesia, 87, 92, 118, 476 hyperarousal attachment cry responses, 405 chronic, 407 in daily-life action system, 418 neuroception and, 406 physical trembling, 417 PTSD and, 405 regulation, 414 hypnotic intervention, 385, 388–389 hypoalgesia, 87 hypoarousal, 406–407, 411, 414 hypothalamic–pituitary–adrenal (HPA) axis, 84, 112, 132, 156, 195 IC. See inferior colliculi identity confusion/identity alteration, 30 identity disturbance, 70 “Iggy Pop” effect, 47 illusion, 349–350 imagination, 342, 349–351 immobility, 38, 39, 44–45 infants, brain processing level, 309, 405 inferior colliculi (IC), 11–12, 34, 136 information processing, 214–217 inhibitory neurotransmitters, 214, 223 International Society for the Study of Trauma and Dissociation (ISSTD), 243–244, 247, 290 interoceptive awareness

alpha activity, 223 bilateral sensory stimulation, 232 dual focus, 452–453 exteroceptive and, 227–228 somatic memory and, 455 interoceptive loops affective consciousness circuit, 166 dissociated self-states, 165 inflammation mediators, 162 motivational components, 166 sensorimotor integration, 167–168 Interpersonal Perception Task-15 (IPT-15), 73–74 Interpersonal Reactivity Index, 72 IPT-15. See Interpersonal Perception Task-15 Klüver-Bucy syndrome, 95 learned helplessness (LH), 81–82, 89–92 level of urge to avoid (LOUA) protocol, 41 LH. . See learned helplessness Lifespan Integration, 167, 197 locus coeruleus amygdale, 160, 179 CRF receptors, 197 noradrenergic fibers, 9, 37, 132, 160 locus of control, 93, 334 longing, 200, 208, 310 LOUA. See level of urge to avoid (LOUA) protocol low-dose naltrexone. See also naltrexone adverse effects, 483 Crohn’s disease, 475 dissociative disorder, 479–481, 484 fibromyalgia symptoms, 477 for stabilization, 488–489 maternal behavior, 106–107, 115–116, 195–196, 197–198 maternal mourning, 201 maternal separation, 159–160 medial prefrontal cortex (mPFC), 345 alarm circuit, 39 brain activation patterns, 70–71 mindfulness meditation, 271 PTSD implication, 59 social flight responses, 42 memory, 60, 220–221, 415 memory loss, 95–96 mentalized affectivity, 351–352 mesolimbic dopamine system, 42, 46–47, 142–143 methadone, 82 micturition, 159 midbrain

Index  505

autonomic areas, 275 basic affective system, 6 case study, 30–32 cortical responses, 45–46 defense responses, 13, 38–39, 133 micturition, 159 PAG levels, 345 resting state hypothesis, 177 self-representation, 34 threat and activation, proximity, 35–36 traumatic stress, 142 mindfulness compassionate practices, 277–279, 282–283 emotion regulation, 272–273 immune response, 272 secure attachment, 271 ML-DA system behavioral arousal, 202 brain-derived neurotrophic factor (BDNF), 203 Corticosteroids, 204–205 environment shifting and, 202 from VTA, 196 insular cortex, 203 oxytocin stimulation, 196 morphine, 82, 83, 87, 91 mPFC. See medial prefrontal cortex multiple traumata, 424–426 naltrexone acute depersonalization, 489–490 beneficial effects, 492–493 DDNOS, 491 dissociative voices, 490 eating disorders, 490 Fibromyalgia, 490–491 for stabilization, 488–489 high dose, 489 low dose (see low-dose naltrexone) PTSD, 490–491 regular dose, 489 trauma processing, 489 neural activation patterns, 70, 75 neural networks AIP model, 215 in children, 153 concept, 384 creation, 24 oscillations in, 222–223 processing system, 220–221 sensory inputs, 345 neural synchrony, 226–227 neuroception, 404, 405–406, 408, 414, 415 neurochemical contributors anesthetic, 1, 24, 96

analgesic, 13, 21, 62, 91 in brain, 162 cortical networks, 157 dopamine system, 143 high- and low-arousal dissociation, 156 ML-DA system, 197, 202 modulators, 48 opioids, 113–114 peritraumatic disturbances, 6, 82, 155 shame studies, 183–184 somatization, 162 neurogenesis, 96, 230–231, 271 neuroplasticity, 96–97, 230–231, 271 NTS. See nucleus of the solitary tract nucleus of the solitary tract (NTS), 34, 134, 156 obsessive-compulsive disorder (OCD), 394, 477, 486 obstructed fight or flight, 140 obstructed response action sequences, 137 cortical regulation, 140 energetic residues, 131 high-arousal state, 141 long term, 132 midbrain level, 141 subconscious level, 134 OMPFC. See orbitomedial prefrontal cortex opioid antagonists, defensive responses, 491–493 opioid antagonists, EMDR, 477–479. See also opioid antagonists, limitations and adverse effects amnestic barriers, 483 dissociative rebound, 484–485 drug absorption issues, 485 hepatoxic potential, 481 increased blood pressure, 482–483 induction of withdrawal, 482 low-dose naltrexone, 483 nausea, 482 reversal of analgesia, 481–482 vomiting, 482 warfarin, 485 opioid antagonists, limitations and adverse effects, 481–483 opioid antagonists, therapeutic use borderline personality disorder (BPD), 472–473 complex posttraumatic stress disorder (PTSD), 473 depersonalization disorder, 473 eating disorders, 474 fibromyalgia, 476–477 immune function, 475 pain, 476 pathological gambling, 474 self-injurious behavior, 473–474 sleep apnea, 474–475

506  INDEX

opioid system analgesic effects, 84 approach behavior, 90 attachment and, 97 blockade in, 90 defensive responses, 89 loss of life energy, 87–88 memory loss and, 95–96 motoric or muscular aspects, 93–94 neural functioning, 87 neuroplasticity, 96–97 pain-reducing effects, 91 parasympathetic activity, 85 passive state, 85 receptor classes, 83 role in traumatic reenactment, 84 opioid-mediated stress response, 82 opioidergic control, 120–121 orbitomedial prefrontal cortex (OMPFC), 39 oxycodone, 82 oxytocin amnestic properties, 118 amygdala activity, 116–117 attachment behavior, 115–116 autonomic regulation, 105–106 dissociative symptoms, 119 maternal behavior, 106–107 opiate system, 110 opioid modulation, 119–120 parturition, 107 physiological antistress effects, 116 prolonged opioid stimulation, 117–118 social connection, 115–116 vagal shift hypothesis, 120–121 vasopressin and, 109, 118–119 PAG. See periaqueductal gray pain allodynia, 161 analgesic systems, brain, 162 anatomical substrates, 161 arousal, 160 autonomic arousal, 159 endocannabinoids, 157 in animals, 158, 159–160 interoceptive pathways, 160 phantom limb, 350 physical and emotional, 343 reflex motor response, 161 sadness and, 202 social affective circuits, 348 syndromes, 342, 350, 352 PANIC circuit, 348 brain processing, 345–347

defense responses, 32, 349 extreme state, 22 hard-wired, 250 in infants, 208, 309, 348, 427 midbrain range, 38, 45–46, 173 negative emotions, 176 resetting, 353–354 SEEKING and, 110–111 shame, 354 parasympathetic nervous system (PNS) , 61, 85, 142, 292, 309 PD. See peritaumatic dissociation perceptions of inescapability, 58 periaqueductal gray (PAG) avoidance response and, 40, 42 beta-endorphin, 106 dlPAG, 39 dmPAG, 40 DV, 114 emotion generation, 34 fight responses, 42–43 flight responses, 42 hiding response and, 40–41 in midbrain, 35–36, 45, 133 SC influence, 36–37 serotonergic transmissions, 44 survival mechanism, 43 threat orientation, 39 vlPAG and, 39 withdrawal response and, 41 peritaumatic dissociation (PD) clinical research, 59–60 defense cascade model, 61–62 definition, 52 endocannabinoids, 156–157 endogenous opioids, 156–157 features, 157 in nonsexual assault victims, 54 in sexual assault victims, 53 memory and, 53, 60 neurochemical downregulation, 156 neurochemical hypothesis, 82 PTSD symptomatology, 52–53 somatic responses, 158 tonic immobility (TI), 54, 58–59 trauma types, 53 vehicle accident survivors, 54 perpetrator introject, 325–331 personification, 451–452 PET. See positron emission tomography PLAY circuit, 347 PNS. See parasympathetic nervous system polysensory zone (PZ), 180–181 polyvagal theory, 106

Index  507

POMC. See pro-opio-melano-cortin positron emission tomography (PET), 139 posttraumatic stress disorder (PTSD) alexithymia, 70, 343 analgesia, 91 anterior cingulate cortex (ACC), 132 in children, 12 default mode network (DMN), 70–72 definition, 248 EMDR and, 216–217, 253 hyperarousal, 405 hypnoanalytic interventions, 384 medial prefrontal cortex (mPFC), 59 naltrexone, 490–491 opioid antagonists, 473 pain and, 158 peritaumatic dissociation (PD), 52–53 script-driven imagery, 177 sensory stimulation and, 216–217 social– cognitive studies, 69–77 social withdrawal, 108 theory of mind in, 70, 72–76 trauma-related stimuli, 91 unwanted memories, 182 predator, 54–55, 58, 61, 90 prefrontal cortex abnormalities, 43 amygdale, 275 blood oxygenation levels, 217 cognitive analysis, 173 dorsomedial, 94 maternal attachment, 195 mesolimbic system, 202 mindfulness, 412 orbital network, 276 PAG columns, 45 pain responses, 15 personal memory, 155 sensory information, 10, 219 therapeutic touch and, 450 traumatic stress, 142 ventral medial, 70–71, 177, 203 prey animal, 55 pro-opio-melano-cortin (POMC), 83 prolonged arousal, 132 psychobiological system, 400–404 psychoeducation, traumatized patients about adult vs. child responsibilities, 313–314 about affective circuits, 309–311 about assertion, 317 cartoons, 435 about child development, 312–313 about emotional hygiene, 311–312 about emotions, 307–308

about exercise, 316 about innate animal nervous system responses, 308–309 about legal definitions of child abuse, 312 about life-enhancing skills, 317–318 metaphors, 435 about mindfulness, 311 about neurobiology, 314–315 about nutrition, 316 about self-care, 316–318 about sleep, 316–317 about spirituality, 314 about window of tolerance, 315 about yoga, 318 emotional freedom technique (EFT), 318 PTSD. See posttraumatic stress disorder PTSD, social cognitive studies altered neural circuitry, 70 brain activation patterns, 70–71 childhood abuse, 72, 74–75 default mode network (DMN), 69–72, 71 direct eye contact, 75 early-life trauma, 69, 72, 77 self-referential processing, 69–71, 77 PZ. See polysensory zone rapid eye movement (REM) sleep, 216, 225–226, 248, 348 reading the mind in the eyes task–revised (RMET), 72–73, 74 REM. See rapid eye movement (REM) sleep resourcing states, 334–338 right inferolateral prefrontal cortex (PFC), 155 RMET. See reading the mind in the eyes task–revised (RMET) RMTg. See rostromedial tegmental nucleus (RMTg) rostromedial tegmental nucleus (RMTg), 41, 45, 133, 142, 145, 180, 185 safe embodiment definition, 270 neuroplasticity effect, 270 neuroscience, 278–279 posteromedial cortex, 280–281 traumatic stress syndromes, 269 SCN9A channelopathy, 161 screen technique, 386, 392 security motivation system, 34–35 SEEKING system, 110–114, 121 self-loathing, 137–138 self-state annihilation of, 332 anoetic consciousness, 278

508  INDEX

self-state (cont.) compassion, 281 ego state therapy, 330 existential feelings, 279–280 explicit approaches, 333–334 fragmented sense, 452–453 important aspects, 322 loss of self, 321 orienting procedures, 334–339 posteromedial cortex, 280–281 reducing inner conflict, 323 subcortical-cortical midline systems, 279 survival oriented function, 331 talking through vs. switching, 387 sensation, imagery, behavior, affect, and meaning (SIBAM) model, 369–370 sense of balance, 455 sensorimotor integration layered organization, 168 midbrain level, 163 thalamic nuclei, 18 sensory stimulation, 223–224 sensorimotor psychotherapy, 137, 153, 177, 244, 303, 369 sensorimotor psychotherapy (SP) treatment controlled actions, 400 defensive action and, 408–409 traumatic memory, 414 sensory awareness EMDR procedure, 233 information processing system, 233 neuroplasticity, 230–231 oscillatory activity, in brain, 217 physiological prerequisites, 231–232 REM sleep, 233 reversal of TCD, 233 synaptogenesis, 230–231 thalamocortical binding, 231–232 sensory cortex, 86, 93 sensory input attachment relationship, 345 beta-endorphin levels, 109 limbic system, 14 loss of, 18 regulation of, 93 self-states, 86 sensory integration, 8–9, 11, 34 social engagement, 229–230, 449 subcortical circuits, 163 thalamus, 10, 218, 344 types, 9, 20 visceromotor network, 165 sensory processing, 371, 376 sensory stimulation

bilateral, 215–216, 227, 229, 232, 449–450 defensive responses, 229–230 Forty Hertz activity, 224–225 in EMDR, 217, 232, 449 information processing and, 216–217, 233 integration process, 223 neuroplasticity, 230–231 reversal of TCD, 233 social engagement, 229–230 synaptogenesis, 230–231 thalamic function, 217, 232 trauma processing, 449–450 separation in children, 201–202 consequences, 199–200 distress, 200–202 emotional burden, 194 high-arousal protest phase, 200 infant biology, 195 obstructed attachment and, 199 septum, 173 shame, 70, 74, 75 abandonment and, 184 attachment obstruction, 186 beneficial strategy, 332 brain imaging studies, 181–183 clinical implication, 176–177 failure and, 184 lack of parental availability, 343 midbrain response, 178–179 misattunement, 184 multidimensional response, 174–175 neurochemical studies, 183–184 nontoxic, 184 peritraumatic, 178 posttraumatic, 178 psychoanalytic concept, 176 self, negative valence, 185–187 social behavior, 144–145 subcortical origin, 174–175 submission and, 143–144, 184 threrapeutic care, 185 tonic immobility and, 177 toxic, 178 SHAME circuit, 354 SIA. See stress-induced analgesia SIBAM. See sensation, imagery, behavior, affect, and meaning (SIBAM) model SNS. See sympathetic nervous system social engagement system, 404–406 social learning effects, 428–429 social threat, 45–46 social withdrawal, 108–110 somatic residues, 166–167

Index  509

somatic resourcing, 426, 429–430, 437, 460 somatic therapy additional strategies, 465–466 BLS behaviors, 462–463 circular perspectives, 466 clinical example, 158–159 discharging, 462 elements, 458 evoked oscillations, 463 Figure-Eight EMs, 466 headache activity, 466 intentional movement, 461–462 micromovements, 463–465 neurochemicals, brain, 162 spontaneous oscillations, 462–463 symptoms, 158–159 spontaneous oscillations, 462–463, 465 SP. See sensorimotor psychotherapy (SP) treatment stabilization, 453 stabilization, traumatized patients boundaries, 293 cost-effective therapy, 294 ego state therapy, 290 external safety issues, 298–299 grounding methods, 304–306 hospitalization, 298 locus of disturbance, internal and external, 299–302 optimal arousal level, 291 pacing of therapy, 293–294 relationship with others, 302–303 resource development, 303 safety, 293 self-harm, 297–298 somatic resourcing, 303 somatic sensation, 292, 303 state regulation, 291 structure, 293 subcortical affective circuits, 292–293 suicide threat, 297–298 therapeutic ruptures, 296–297 therapist’s role, 294–295 time management, 295–296 strategic developmental model, 425 stress-induced analgesia (SIA) , 91–94, 155 subcortical affective circuits, 427–428 subcortical loops, 154, 162–163, 166 subcortical processes, 455–456 subjective units of distress (SUD), 30, 372, 465 submission, 40, 46–47, 141–142 SUD. See subjective units of distress (SUD) superior colliculi (SC) avoidance response and, 40–41

hiding response and, 40–41 immobilization stress, 45 midbrain, 36 perceived threat and, 36–37 rapid motor responses, 37 somatosensory, 34 withdrawal response and, 40–41 suppression, 131, 132, 138, 140–141 sympathetic nervous system (SNS) animal defensive behaviors, 230 autonomic nervous system, 85 cortical regulation, 140–141 excessive, 252 fight-or-flight response, 42–43, 292, 308–309 grounding, 304 tonic immobility (TI), 61 synaptogenesis, 96, 230–231 synthesis, 223, 226, 228, 232 temperoparietal junction, 75 temporal integration attachment injury, 429–430 bottom-up processing, 431–432 ET processing, 429 implicit memory, 429–430 stepwise preparation, 429–430 TULIPS analogy, 432 temporal poles (TPs), 75 thalamic dysfunction, 218–219 thalamocortical dysrhythmic syndrome, 219–220 thalamus affective circuits, 20 analgesic chemicals, 14–15 brain function, 18 consciousness, retraction, 14–15 EMDR and, 217 endogenous opioids, 17–19, 86 horizontal integration, 9–10 memory, role in 218 motor behavioral programs, 37 neuroplasticity, 230 pain, numbing, 161–162 sensory input, 10, 205, 218, 344 sensory stimulation, 217 separation distress, 202 smell and, 454 subcortical circuits, 161–163, 177, 279 in traumatic stress syndrome, 89 vertical integration, 9–10 theory-of-mind, 75, 76 three-hole punch analogy, 430–432 TI. See tonic immobility titration, 368, 373, 375

510  INDEX

tonic immobility (TI) clinical research, 59–60 defense cascade model, 54–55, 61–62 description, 44 fear and, 56 in humans, 57 in laboratory animals, 55 long-term psychological impairment, 136–137 memory and, 60 midbrain PAG, 56 muscle stiffening, 61 peritraumatic dissociation (PD), 54, 58–59 psychological distress and, 57–58 sympathetic and parasympathetic branches, 44 Tonic Immobility Scale–Adult Version, 60 TOTEMSPOTS, 374–377 toxic shame, 145, 177–178, 182, 184–187 TPs. See temporal poles transient receptor potential vanilloid-1 (TRPV1), 184 TRPV1. See transient receptor potential vanilloid-1 trauma survivors affective dysregulations, 94–95, 347 body state, 275, 452 freeze responses, 133 somatoform features, 158 threat mode, 208 TI and, 58 vehement emotions, 94–95 traumatic experience adaptive resolution, 315 adverse effects, 30 anterior cingulate cortex (ACC), 132 avoidant response, 42 children’s coping capacity, 248, 260 clinical consequences, 44, 138 consolidation, 166 factual memory, 451 hippocampal volume, 155 orienting procedures, 334 peritraumatic dissociation (PD), 52, 86 PTSD, 52–53, 183 shame, treatment, 185 SIA and, 92 sensorimotor memories, 164 social engagement, 415 somatic fragments, 21, 158, 451 thalamic dysfunction, 213 traumatic memory brain spotting, 465 dorsal-vagal freeze, 134

EMDR, 215, 368, 457 fragmented aspects, 232 nature of, 221–222, 226 nonverbal nature, 455 processing, 365 resolution, 269 TOTEMSPOTS, 374 treatment, 414–418 traumatic stress, 142, 476, 492–493 traumatic stress syndromes, 84, 89, 90, 93, 95, 96–97, 269 truncated response, 149 TULIPS analogy, 432 ventrolateral column of PAG (vlPAG) midbrain defense response, 39 dorsal vagal state, 44, 133–134 endogenous opioids, 135 fight-or-flight response, 135–136 submission, 134–135 threat response, 275–276 ventral intraparietal area (VIP), 180 ventral striatum, 142 ventral tegmental area (VTA), 115, 175 ventral vagal engagement, 107, 111, 120, 121 ventral vagal parasympathetic system, 140, 406 ventromedial prefrontal cortex (VMPFC) emotional motor memory, 164–165 exposure protocols, 42 midbrain activation, 36 responses to social threats, 45 threat orientation, 39 vigilance freeze states, 138–139 VIP. See ventral intraparietal area visualization, 349 vlPAG. See ventrolateral column of PAG VMPFC. See ventromedial prefrontal cortex von Economo neurons (VENs), 196 VTA. See ventral tegmental area window of tolerance, 137, 315, 404, 448–449 withdrawal cognitive phase, 143 midbrain’s range, 38–39 PAG interactions, 40–41 physical, 40 reflexive, 33 rostromedial tegmental nucleus (RMTg), 41 social, 30, 45–46