Contents
Acknowledgments
Chapter 1: Introduction and Overview
Historical and Societal Perspectives
Important Conceptual Questions and Issues
References
Chapter 2: Using Evidence-Based Practices
Evidence-Based Practice—What Is It and Why Should We Care?
The Process of Evidence-Based Practice
Appraising the Evidence in Evidence-Based Practice
Keeping Up With the Scientific Literature
What About Cultural Competence in EBP?
In Conclusion
References
Chapter 3: Working With Trauma Survivors
Assessing Trauma History
Conclusion
References
Chapter 4: Assessing PTSD
Assessing Trauma History
Assessing PTSD Symptom Criteria
Conclusion
References
Chapter 5: Assessing Comorbid Conditions
PTSD’s Comorbidity
Recommendations for Assessing PTSD’s Comorbidity
Conclusion
References
Chapter 6: Considering Ethnicity, Race, and Culture
Ethnocultural Differences in Trauma Exposure and Traumatic Stress Disorders
Utilization of Services for Traumatic Stress Disorders
The Role of Racism and Discrimination
Alternative Explanations for Apparent Ethnoracial Differences in PTSD
Implications for PTSD Assessment and Treatment Planning
Conclusion
References
Chapter 7: Conducting Forensic Evaluations
Unpacking “Secondary Gain”: Motives for Symptom Exaggeration in PTSD
Best Methods for Detecting PTSD Symptom Exaggeration
Treatment Implications
Conclusion
References
Chapter 8: Working With Children and Adolescents
Self-Regulation as a Framework for Assessing Posttraumatic Impairment
Diagnosis of PTSD in Children and Adolescents: DSM-IV and DSM-5
Clinical Considerations in Conducting Assessment With Traumatized Children
Conclusion
References
Chapter 9: Assessing Children and Adolescents
Child and Adolescent Trauma History Assessment
Assessment Measures for Child and Adolescent PTSD
Treatment Strategies
Conclusion
References
Chapter 10: Working With Veterans
Prevalence
PTSD Onset and Course
Sociopolitical and Cultural Factors
Compensation and Pension Evaluations and Treatment Planning Implications
Clinical Assessment With Veterans
Working Within the Veterans Affairs System
Conclusion
References
Chapter 11: Working With Special Populations and Settings
Primary Care Settings
Severely Mentally Ill Patient Populations
Rural Populations
Prisoners
Conclusion
References
Chapter 12: PTSD Treatments and Treatment Planning
Evidence-Based Treatments
Psychosocial Treatments for PTSD
Conclusion
References
Chapter 13: Follow-Up With Evaluation and Support
Strategies for Ongoing Assessment and Follow-Up
Treatment Adjustments
Conclusion
References
Chapter 14: Going Forward
New Frontiers in the Field Relevant to Assessment and Treatment Planning
Proposed Criteria for PTSD in DSM-5
Final Remarks
References
Author Index
Subject Index
Copyright © 2012 by John Wiley & Sons, Inc. All rights reserved.
Published by John Wiley & Sons, Inc., Hoboken, New Jersey.
Published simultaneously in Canada.
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, scanning, or otherwise, except as permitted under Section 107 or 108 of the 1976 United States Copyright Act, without either the prior written permission of the Publisher, or authorization through payment of the appropriate per-copy fee to the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, (978) 750-8400, fax (978) 646-8600, or on the web at www.copyright.com. Requests to the Publisher for permission should be addressed to the Permissions Department, John Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, (201) 748-6011, fax (201) 748-6008.
Limit of Liability/Disclaimer of Warranty: While the publisher and author have used their best efforts in preparing this book, they make no representations or warranties with respect to the accuracy or completeness of the contents of this book and specifically disclaim any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives or written sales materials. The advice and strategies contained herein may not be suitable for your situation. You should consult with a professional where appropriate. Neither the publisher nor author shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages.
This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold with the understanding that the publisher is not engaged in rendering professional services. If legal, accounting, medical, psychological or any other expert assistance is required, the services of a competent professional person should be sought.
Designations used by companies to distinguish their products are often claimed as trademarks. In all instances where John Wiley & Sons, Inc. is aware of a claim, the product names appear in initial capital or all capital letters. Readers, however, should contact the appropriate companies for more complete information regarding trademarks and registration.
For general information on our other products and services please contact our Customer Care Department within the United States at (800) 762-2974, outside the United States at (317) 572-3993 or fax (317) 572-4002.
Wiley publishes in a variety of print and electronic formats and by print-on-demand. Some material included with standard print versions of this book may not be included in e-books or in print-on-demand. If this book refers to media such as a CD or DVD that is not included in the version you purchased, you may download this material at http://booksupport.wiley.com. For more information about Wiley products, visit www.wiley.com.
Library of Congress Cataloging-in-Publication Data:
Assessment and treatment planning for PTSD [electronic resource]/B. Christopher Frueh . . . [et al.].
1 online resource.
Includes bibliographical references and indexes.
Description based on print version record and CIP data provided by publisher; resource not viewed.
ISBN 978-1-118-26280-1 (mobipocket)—ISBN 978-1-118-23813-4 (epub)—ISBN 978-1-118-22473-1 (pdf)—ISBN 978-0-470-61618-5 (hardback) (print)
I. Frueh, B. Christopher.
DNLM: 1. Stress Disorders, Post-Traumatic. WM 172.5]
616.85′21—dc23
2012016149
Acknowledgments
Dr. Frueh is grateful for the support provided by the McNair Medical Institute of Houston, TX. Dr. Grubaugh is grateful for the institutional support of the Ralph H. Johnson Charleston Veterans Affairs Medical Center Research Service and the Medical University of South Carolina Department of Psychiatry. This work was conceived and developed during a meeting sponsored by The Menninger Clinic in Houston, TX. Thus, all authors are grateful to The Clinic for the support and resources it provided.
Posttraumatic stress disorder (PTSD) was officially introduced into the psychiatric nomenclature in 1980, with the publication of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III) by the American Psychiatric Association (APA). Over the past 30 years, this disorder has changed the landscape of trauma and general stress studies, and it has contributed to the development of a wide range of sociopolitical, conceptual, and clinical issues and questions. The concept of posttraumatic reactions has been widely absorbed by the general public with regard to psychological adjustment after major traumatic events, as well as a wide range of other life stressors. Public awareness of PTSD has been furthered by extensive news coverage of recent national and international news events, including the 9/11 atrocities; the wars in Iraq and Afghanistan; terrorist attacks in London and Madrid; hurricanes, earthquakes, tsunamis, and other natural disasters; widely publicized cases of child sexual abuse among church officials and national sports heroes; and genocides in Africa and eastern Europe. Mainstream media publicity and films since the Vietnam War have also likely played a role in the layman’s understanding of PTSD. A now common portrayal of returning combat veterans is that of the psychologically impaired victim-hero, found in Hollywood movies too numerous to count, such as Taxi Driver (1976), Coming Home (1978), The Deer Hunter (1979), Born on the Fourth of July (1989), and In the Valley of Elah (2007).
Undoubtedly, research on every nook and corner of this disorder has abounded in the past few decades, providing patients and their families, clinicians, health care administrators, and policy makers with a vastly better understanding of posttraumatic reactions—from both a psychopathological and a resilient standpoint—than we had before. Despite this expansion of our knowledge, there remain numerous unanswered questions and controversies as to how clinicians should evaluate, define, and treat psychiatric symptoms in the aftermath of trauma events. Clinicians are left in their practices with questions that lack practical directions based on solid empirical evidence. A good deal of pseudoscience and poor science in the field of traumatology, as well as a proliferation of clinical myths, misconceptions, and fads about traumatic reactions, has further muddied the water for clinicians. Toward this end, we have produced a volume intended to help the dedicated evidence-based mental health practitioner with clinical assessment and treatment planning for people—patients, clients, consumers, however one wishes to term or define them—suffering from posttraumatic reactions.
This opening chapter begins with a historical perspective on posttraumatic reactions, segues into a brief review of important conceptual questions and issues with regard to the diagnosis of PTSD, and concludes with a general overview of evidence-based practice in mental health care and a discussion of why such practice is so important for people suffering posttraumatic reactions.
The general notion that people are significantly affected, perhaps changed forever, by violent and horrific ordeals is not new. The postcombat reactions of warriors have been noted since ancient times throughout mythology and literature and in a variety of cultures (e.g., “Epic of Gilgamesh,” writings of Homer and Shakespeare). Since the 19th century, different terms have been used to describe posttraumatic reactions for a variety of dangerous and frightening experiences. Frequently, these terms provided clues as to how the etiology or nature of the symptoms was viewed at the time. In the years following the U.S. Civil War, it was noted that many veterans reported symptoms of chronic chest pain, as well as fatigue, shortness of breath, and heart palpitations—yet physical abnormalities to explain these symptoms were often not to be found. Physicians and caretakers were puzzled by the syndrome, which, while somewhat common, had no obvious explanation. The observed functional syndrome became known as soldier’s heart or Da Costa’s syndrome for the surgeon who noted it in a series of case reports (Barnes, 1870). During World War I, the term shell shock was used to refer to a constellation of symptoms believed to be a neurological disorder caused by the sound of explosions and bright flashes of light from bursting artillery shells on the Western Front. Combat fatigue was a term used during World War II, when it was believed that combat reactions were caused by exposure to extreme stress and fatigue. During the 1970s, victims of sexual assault were often identified as suffering from a “rape trauma syndrome” (Burgess & Holmstrom, 1974) or “battered woman syndrome” (Walker, 1977).
In organized psychiatry, the concept of a specific category of life events causing a psychiatric disorder was first formalized in 1952, with the first edition of the DSM. Gross stress reaction (GSR) was defined as a “transient situational personality disorder” that could occur when essentially “normal” individuals experienced severe physical demands or extreme emotional stress. GSR was soon dropped from psychiatry’s nosology in 1968, with the second edition of the DSM. Twelve years after the DSM-II’s publication, a more narrow class of events—that is, trauma—was linked as the causative agent for a new and specific constellation of symptoms, and posttraumatic stress disorder was formally defined and included in the psychiatric nosology.
The diagnosis of PTSD, added to the DSM in 1980, was largely the result of attempts to account for the challenging impairment presented by Vietnam veterans at the time of their homecoming (Satel & Frueh, 2009; Shephard, 2001, 2004; Wessely & Jones, 2004). In the immediate post-Vietnam era, compensation for significant functional impairment was difficult to obtain other than for observable physical injuries and access to Veterans Administration (VA) medical services were possible only via a “war-related” disorder (Wessely & Jones, 2004). Veterans’ advocates and antiwar activities were at the forefront of efforts to define and codify a “Vietnam syndrome,” a psychiatric response to war unique among Vietnam veterans. At about the same time in the 1970s, the feminist movement was politically strong and gaining momentum. They successfully began to expose the violence that was common against women, which led to the development of a “rape trauma syndrome” (Burgess & Holmstrom, 1974). These two activist groups soon joined forces to make a common cause with mental health clinicians and researchers. Together, they worked to influence the development of the new diagnostic addition to the DSM-III. Thus, along with medical and psychological science, the development of the clinical conceptualization of PTSD was heavily influenced by socioeconomic and political forces (Mezey & Robbins, 2001; Shephard, 2001). For a more in-depth discussion on the origins of PTSD, see Shephard (2001), Summerfield (2001), Jones and Wessely (2007), Rosen and Frueh (2010), and Satel and Frueh (2009).
PTSD is unique from the vast majority of psychiatric disorders in the DSM in that it is the rare disorder to include an etiological explanation (trauma)—and one that is actually part of its diagnostic criteria (Criterion A). Otherwise, for the most part, the DSM takes an atheoretical approach to quantifying and classifying mental disorders. The fact that PTSD cannot be diagnosed without the occurrence of a Criterion A event not only makes PTSD distinct from other psychiatric diagnoses, but it also renders it unique in the general field of stress studies (Breslau & Davis, 1987). As Rosen, Frueh, Elhai, Grubaugh, and Ford (2010) noted:
Rather than all stressors creating an increased risk for a wide range of established conditions, there now was a distinct class of stressors that led to its own form of psychopathology. Thus, while any type of high stress could lead to increased risk of headaches, high blood pressure, or depression, only a Criterion A event such as combat, rape, or a life-threatening accident could lead to the distinct syndrome of PTSD. This assumption of a specific etiology, associated with a distinct clinical syndrome, provided the justification for a new field of “traumatology” to be carved out of general stress studies. (p. 7)
In the 30-plus years since its creation, the definition of PTSD has evolved steadily with each new revision of the DSM. Changes have been made to the definition of Criterion A, new symptoms have been added, and requirements regarding symptom onset and duration (Criterion E) have been modified.
In DSM-III (APA, 1980) the trauma criterion (Criterion A) was defined as: “Existence of a recognizable stressor that would evoke significant symptoms of distress in almost everyone” (p. 238). This stressor was described it as being outside the range of normal human experience. In DSM-IV (APA, 1994), Criterion A events are defined much more specifically:
The person has been exposed to a traumatic event in which both of the following were present: (1) the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others; (2) the person’s response involved intense fear, helplessness, or horror. Note: in children, this may be expressed instead by disorganized or agitated behavior. (pp. 427–428)
Moreover, by 1994, empirical research showed that traumatic events were actually quite common to the human experience, so that aspect of the DSM-III definition was dropped from the definition.
The number of possible PTSD symptoms expanded from 12 in DSM-III to 17 in DSM-IV and included the addition of avoidance behaviors. Also added was the caveat in Criterion E that duration of the disturbance had to exceed 1 month. This revision to Criterion E in DSM-IV was paired with a new (but related) diagnosis: acute stress disorder (ASD). Like PTSD, ASD requires a Criterion A traumatic event and includes symptom criteria very similar to PTSD (Criteria B through D). ASD cannot be diagnosed unless symptoms and associated impairment lasts at least 2 days (so as to exclude those with immediate peritraumatic reactions, which are very common) and may not last more than 4 weeks past exposure to the traumatic stressor. In this way, ASD serves as a diagnosis for those suffering extreme traumatic stress reactions that occur too soon after trauma exposure to be classified as PTSD.
PTSD’s defining criteria continue to be subject to much debate and discussion, and are likely to be revised in future editions of the DSM. We will return to further discussion of the future of PTSD in Chapter 12.
Despite the proliferation of research on and expansion of clinical services for PTSD, much about the disorder remains misunderstood or unknown. In the sections that follow, we briefly introduce some of the important conceptual questions and issues regarding the diagnosis of PTSD that have implications for clinical assessment and treatment planning for people with significant traumatic event exposure.
There is now a widespread assumption on the part of many laypersons, journalists, and even clinicians that the majority of people who endure a traumatic experience, such as sexual assault, childhood abuse, a natural disaster, or wartime combat, will develop a psychiatric disorder as a direct result of the experience. However, the data actually tell a very different story. Most individuals will experience some short-term distress and may be affected in a variety of psychological ways. However, the majority of people who survive even the most horrific traumatic experiences do not develop PTSD or any other full-blown psychiatric disorder. That is, only a small minority of people will develop distress and functional impairment that rises to the level of a psychiatric disorder. Instead, long-term resilience is actually the norm rather than the exception for people after trauma (Bonanno, Westphal, & Mancini, 2011).
We now have a large body of epidemiological studies, conducted across a variety of populations, to inform our understanding of PTSD prevalence estimates (Breslau, Davis, Andreski, & Peterson, 1991; Davidson, Hughes, Blazer, & George, 1991; Dohrenwend et al., 2006; Norris, 1992; Smith et al., 2008). Data consistently show that exposure to potentially traumatic events (i.e., Criterion A) is quite common in the general population, with 60% to 80% of the population reporting exposure to various types of traumatic events (Breslau et al., 1991; Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995). PTSD rates (point-prevalence) are consistently found to be in the 6% to 9% range for both civilians and military veterans. For those who develop PTSD, about 50% will remit within 3 months without treatment (Galea et al., 2002; Rothbaum, Foa, Riggs, Murdock, & Walsh, 1992). This is a robust finding that is specifically noted in DSM-IV. Individuals who are diagnosed with PTSD are at 3 times greater risk of meeting criteria again if exposed to a later traumatic stressor (Breslau, Peterson, & Schultz, 2008). In this way, PTSD can be a recurrent disorder after a first episode.
Epidemiological studies also indicate that PTSD is not the only, or even the most likely, psychiatric reaction to follow trauma exposure. Fear, anxiety, sadness, anger, and guilt (among others) are common reactions to traumatic experiences. Other common reactions include physical or somatic complaints, such as insomnia, gastrointestinal symptoms, headaches, or sleep problems; social and relationship difficulties; and substance use, including alcohol and nicotine (Breslau et al., 1991; Bryant, 2010; Kessler et al., 1995). Major depression is probably the most common form of posttraumatic psychopathology, even more prevalent than PTSD. Moreover, among individuals who meet the diagnostic criteria for PTSD, a majority has additional psychiatric problems. Common co-occurring disorders with PTSD include depression, substance use disorders, panic attacks, and other anxiety disorders. Adding to the illness burden, people diagnosed with PTSD often present with significant medical comorbidity (e.g., chronic pain, cardiac difficulties) that is associated with increased use of health care services (Elhai, North, & Frueh, 2005; Schnurr & Green, 2004).
All of this raises the question: If only a small percentage (6% to 9%) of trauma-exposed people have PTSD, who is most likely to have it? A number of individual vulnerabilities and risk factors have been shown to be strong predictors of PTSD. Social support plays perhaps one of the most important buffering roles against psychiatric illness in the aftermath of trauma and stress. The converse of this is also true in that lower social support is associated with increased risk for PTSD (Andrews, Brewin, & Rose, 2003). Gender is another consistent risk factor. Females are at markedly increased risk of developing PTSD relative to men by a ratio of approximately two to one (Breslau et al., 1991, 1998; Tolin & Foa, 2006). Other significant PTSD risk factors are lower intelligence, lower education, lower socioeconomic status, prior history of poor social adjustment or psychiatric disorders, and substance abuse. Recent research also suggests that certain genetic phenotypes may interact with environmental stressors to affect the likelihood of PTSD after trauma (Koenen, 2007). At this point, genetic research on PTSD and other posttraumatic reactions is quite underdeveloped. This will undoubtedly change over the next 5 to 10 years, but it is unlikely that genetic variations will ever explain more than 35% of the risk for PTSD development.
Inherent in the internal logic of the PTSD diagnosis is that trauma (Criterion A) causes the symptoms of the disorder. The belief in a specific etiology was fundamental to the very origins of PTSD, and provided the rationale to create a new psychiatric disorder that formed a unique class of stressors from more general life stressors. Accordingly, individuals who do not experience a traumatic event should not develop PTSD. However, empirical data has consistently shown otherwise—that non–Criterion A stressors (i.e., events not considered to be traumatic) can result in similar rates of PTSD (reviewed in Long & Elhai, 2009; Rosen & Lilienfeld, 2008). In fact, the assumption of a specific etiology for PTSD is so problematic, from a theoretical and empirical standpoint, that some investigators are starting to write about the “the Criterion A problem” (Weathers & Keane, 2007). This obviously has implications for our understanding and definition of the disorder, including how the field will characterize it in future editions of the DSM. Recent proposals have suggested everything from tighter definitions of what constitutes a traumatic event (Kilpatrick, Resnick, & Acierno, 2009) to the extreme of doing away with the gatekeeper function of Criterion A altogether (Brewin, Lanius, Novac, Schnyder, & Galea, 2009). At this point, it is somewhat of an open question as to whether “traumatic” stressors are in fact significantly unique and different from other life stressors (divorce, job loss, financial difficulty), or are better understood as points along a continuum of stressors (Dohrenwend, 2010). In the future, the field of trauma may converge with that of general stress studies.
Another important question in the trauma field is: To what extent is PTSD a unique psychiatric disorder, and to what extent does it simply duplicate other diagnoses in the mood and anxiety disorders categories (McHugh & Treisman, 2007; Spitzer, First, & Wakefield, 2007)? This is not simply a lofty philosophical question. The answer has practical implications for our ability to understand and treat the syndrome of clinical symptoms that currently make up the disorder. Not only is PTSD highly comorbid with other DSM psychiatric disorders, but it also shares many symptoms with these other disorders. For example, criteria for diagnosing PTSD can be fully met with the right combination of symptoms pulled from the combined diagnoses of depression and specific phobia. See Rosen, Lilienfeld, Frueh, McHugh, and Spitzer (2010) for a detailed explanation for how this can be achieved. An additional related concern is that the core set of PTSD’s symptoms have been demonstrated to be best conceptualized as general dysphoria or distress, common to other mood and anxiety disorders (Simms, Watson, & Doebbeling, 2002; Watson, 2005). Although initial studies on criteria sets that remove PTSD’s overlapping symptoms find similar rates of prevalence and comorbidity (Elhai, Grubaugh, Kashdan, & Frueh, 2008; Ford, Elhai, Ruggiero, & Frueh, 2009; Grubaugh, Long, Elhai, Frueh, & Magruder, 2010), these findings do not resolve all concerns.
The factor structure of a disorder can provide us with information about how some symptoms are endorsed in a similar manner to each other and different from how other symptoms are endorsed. Factor analytic studies over the past 15 years have consistently shown that DSM-IV’s tripartite PTSD model (reexperiencing, avoidance/numbing, hyperarousal) does not adequately account for PTSD’s factor structure (Elhai et al., 2008; Elhai & Palmieri, 2011; Yufik & Simms, 2010). This body of research reveals that two particular four-factor models best represent the PTSD construct across studies: (1) King, Leskin, King, and Weathers’s (1998) model consisting of reexperiencing, effortful avoidance, emotional numbing, and hyperarousal factors; and (2) Simms, et al.’s (2002) model consisting of reexperiencing, effortful avoidance, dysphoria, and hyperarousal. These two models differ only in the placement of three PTSD symptoms: difficulty sleeping (PTSD’s symptom D1), irritability (D2), and difficulty concentrating (D3). Symptoms D1 through D3 are part of the King et al. model’s hyperarousal factor, but part of the Simms et al. model’s dysphoria factor. Very recent confirmatory factor analytic findings demonstrated that separating the three symptoms into a separate factor significantly enhanced model fit for the two models, suggesting that these three symptoms represent a unique latent construct (Elhai et al. 2011).
A common notion in the past was that memory for traumatic events functioned very differently from memory for ordinary experiences. Many clinicians also believed that major traumatic experiences were highly susceptible to being repressed. The explanation for this is that certain events are so horrific that the human mind cannot tolerate them and, therefore, represses them to the unconscious mind. From there, these unconscious traumatic memories cause havoc in the form of severe psychopathology, including symptoms of PTSD, “multiple personalities,” borderline personality disorder, and other forms of psychiatric disturbance. This concept dates back to Sigmund Freud, has been the subject of several Hollywood movies (e.g., Sybil), and continues to exist today in some quarters. It has been the cornerstone of many high-profile lawsuits over the years, including those brought against the Catholic Church and day care centers. In fact, DSM-IV somewhat legitimizes this concept by including it as one of the 17 clinical symptoms of PTSD: “inability to recall an important aspect of the trauma.” However, a large body of research from the fields of memory, learning, and cognition has failed to provide any support for this concept of a special mechanism for traumatic memory (McNally, 2003). This understanding has led to several dramatic revelations. For example, a very recent book by an investigative journalist (Nathan, 2011) thoroughly discredited the case of Sybil, the famous patient with purported multiple personalities caused by childhood trauma (played by Sally Field in the movie). The evidence portrays a patient with other psychiatric disorders who was manipulated by her psychiatrist into reporting and playing out a series of symptoms that she did not actually experience.
A feature of PTSD that has been included in the DSM is the concept of “delayed-onset” PTSD. According to this commonly held view, people can appear to be resilient after trauma but many years later can suffer a sudden onset of PTSD symptoms that is not attributable to any current stressor or illness. The stereotypical example of this is the combat veteran who is overcome suddenly with PTSD symptoms 20 or 30 years after the war is over. However, there is little empirical data to support the existence of delayed-onset PTSD. Several large epidemiological studies have reported zero or extremely low rates of delayed-onset PTSD in civilians and veterans (Breslau et al., 1991; Frueh, Grubaugh, Yeager, & Magruder, 2009). If, however, “delayed onset” is reconceptualized as a delay in seeking treatment, or subsequent exacerbation of prior symptoms by recent stressors occurring years after the original traumatic event, then the phenomenon may be somewhat more common (Andrews, Brewin, Philpott, & Stewart, 2007). One implication of this is that clinicians should be sure to take careful histories regarding a patient’s course of symptoms and possible delays in seeking treatment, before applying the diagnostic qualifier of delayed onset.
As indicated earlier, PTSD is one of the very few psychiatric disorders in the DSM that by definition includes an etiological criterion: traumatic event exposure. Because of this assumption of a specific cause for psychological suffering and impaired role functioning, the diagnosis of PTSD is commonly invoked among patients with claims for worker’s compensation or disability or personal injury lawsuits (Taylor, Frueh, & Asmundson, 2007). For example, the vast majority (> 90%) of veterans seeking treatment services within the Veterans Affairs (formerly Veterans Administration) system are also applying for disability payments, which creates a wide range of assessment and treatment considerations (Frueh, Grubaugh, Elhai, & Buckley, 2007; Worthen & Moering, 2011). The diagnosis provides an opening in tort litigation for plaintiffs to argue that subjective psychiatric symptoms are the direct result of an alleged traumatic event and not from other life stressors or personal vulnerabilities. Other major psychiatric disorders, including depression, anxiety, and addictions do not easily lend themselves to this. The DSM-IV specifically acknowledges this reality with a cautionary guideline for clinicians: “Malingering should be ruled out in those situations in which financial remuneration, benefit eligibility, and forensic determinations play a role” (APA, 1994, p. 467). This is a clinical assessment issue that we will address in a variety of ways in later chapters.
American Psychiatric Association. (1980). Diagnostic and statistical manual of mental disorders (3rd ed.). Washington, DC: Author.
American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author.
Andrews, B., Brewin, C. R., Philpott, R., & Stewart, L. (2007). Delayed-onset posttraumatic stress disorder: A systematic review of the evidence. American Journal of Psychiatry, 164, 1319–1326.
Andrews, B., Brewin, C. R., & Rose, S. (2003). Gender, social support, and PTSD in victims of violent crime. Journal of Traumatic Stress, 16, 421–427.
Barnes, J. K. (1870). Medical and surgical history of the war of rebellion, 1861–1865. Washington, DC: Government Printing Office.
Bonanno, G. A., Westphal, M., & Mancini, A. D. (2011). Resilience to loss and potential trauma. Annual Review of Clinical Psychology, 7, 1.1–1.25.
Breslau, N., & Davis, G. C. (1987). Posttraumatic stress disorder: The stressor criterion. Journal of Nervous and Mental Disease, 175, 255–264.
Breslau, N., Davis, G. C., Andreski, P., & Peterson, E. (1991). Traumatic events and posttraumatic stress disorder in an urban population of young adults. Archives of General Psychiatry, 48, 216–222.
Breslau, N., Kessler, R. C., Chilcoat, H. D., Schultz, L. R., Davis, G. C., & Andreski, P. (1998). Trauma and posttraumatic stress disorder in the community: The 1996 Detroit area survey of trauma. Archives of General Psychiatry, 55, 626–632.
Breslau, N., Peterson, E. L., & Schultz, L. R. (2008). A second look at prior trauma and the posttraumatic stress disorder effects of subsequent trauma: A prospective epidemiological study. Archives of General Psychiatry, 65, 431–437.
Brewin, C. R., Lanius, R. A., Novac, A., Schnyder, U., & Galea, S. (2009). Reformulating PTSD for DSM-V: Life after Criterion A. Journal of Traumatic Stress, 22, 366–373.
Bryant, R. A. (2010). Treating the full range of posttraumatic reactions. In G. M. Rosen & B. C. Frueh (Eds.), Clinician’s guide to postttraumatic stress disorder (pp. 205–234). Hoboken, NJ: Wiley.
Burgess, A. W., & Holmstrom, L. L. (1974). Rape trauma syndrome. American Journal of Psychiatry, 131, 981–986.
Davidson, J. R. T., Hughes, D., Blazer, D. G., & George, L. K. (1991). Post-traumatic stress disorder in the community: An epidemiological study. Psychological Medicine, 21, 713–721.
Dohrenwend, B. P. (2010). Toward a typology of high-risk major stressful events and stituations in posttraumatic stress disorder and related psychopathology. Psychological Injury and Law, 3, 89–99.
Dohrenwend, B. P., Turner, J. B., Turse, N., Adams, B. G., Koenan, K. C., & Marshall, R. (2006). The psychological risks of Vietnam for U.S. veterans: A revisit with new data and methods. Science, 313, 979–982.
Elhai, J. D., Biehn, T. L., Armour, C., Klopper, J. J., Frueh, B. C., & Palmieri, P. A. (2011). Evidence for a unique PTSD construct represented by PTSD’s D1–D3 symptoms. Journal of Anxiety Disorders, 25, 340–345.
Elhai, J. D., Grubaugh, A. L., Kashdan, T. B., & Frueh, B. C. (2008). Empirical examination of a proposed refinement to DSM-IV posttraumatic stress disorder symptom criteria using the National Comorbidity Survey Replication data. Journal of Clinical Psychiatry, 69, 597–602.
Elhai, J. D., North, T. C., & Frueh, B. C. (2005). Health service use predictors among trauma survivors: A critical review. Psychological Services, 2, 3–19.
Elhai, J. D., & Palmieri, P. A. (2011). The factor structure of posttraumatic stress disorder: A literature update, critique of methodology, and agenda for future research. Journal of Anxiety Disorders, 25, 849–854.
Ford, J. D., Elhai, J. D., Ruggiero, K. J., & Frueh, B. C. (2009). Refining the posttraumatic stress disorder diagnosis: Evaluation of symptom criteria with the National Survey of Adolescents. Journal of Clinical Psychiatry, 70, 748–755.
Frueh, B. C., Grubaugh, A. L., Elhai, J. D., & Buckley, T. C. (2007). U.S. Department of Veterans Affairs disability policies for PTSD: Administrative trends and implications for treatment, rehabilitation, and research. American Journal of Public Health, 97, 2143–2145.
Frueh, B. C., Grubaugh, A. L., Yeager, D. E., & Magruder, K. M. (2009). Delayed-onset posttraumatic stress disorder among veterans in primary care clinics. British Journal of Psychiatry, 194, 515–520.
Galea, S., Ahern, J., Resnick, H., Kilpatrick, D., Bucuvalas, M., Gold, J., & Vlahov, D. (2002). Psychological sequelae of the September 11 terrorist attacks in New York City. New England Journal of Medicine, 346, 982–987.
Grubaugh, A. L., Long, M. E., Elhai, J. D., Frueh, B. C., & Magruder, K. M. (2010). An examination of the construct validity of posttraumatic stress disorder with veterans using a revised criterion set. Behaviour Research and Therapy, 48, 909–914.
Jones, E., & Wessely, S. (2007). A paradigm shift in the conceptualization of psychological trauma in the 20th century. Journal of Anxiety Disorders, 21, 164–175.
Kessler, R. C., Sonnega, A., Bromet, E., Hughes, M., & Nelson, C. B. (1995). Posttraumatic stress disorder in the National Comorbidity Survey. Archives of General Psychiatry, 52, 1048–1060.
Kilpatrick, D. G., Resnick, H. S., & Acierno, R. (2009). Should PTSD Criterion A be retained? Journal of Traumatic Stress, 22, 374–383.
King, D. W., Leskin, G. A., King, L. A., & Weathers, F. W. (1998). Confirmatory factor analysis of the Clinician-Administered PTSD Scale: Evidence for the dimensionality of posttraumatic stress disorder. Psychological Assessment, 10, 90–96.
Koenen, K. C. (2007). Genetics of posttraumatic stress disorder: Review and recommendations for future studies. Journal of Traumatic Stress, 20, 737–750.
Long, M. E., & Elhai, J. D. (2009). Posttraumatic stress disorder’s traumatic stressor criterion: History, controversy, clinical and legal implications. Psychological Injury and Law, 2, 167–178.
McHugh, P. R., & Treisman, G. (2007). PTSD: A problematic diagnostic category. Journal of Anxiety Disorders, 21, 211–222.
McNally, R. J. (2003). Remembering trauma. Cambridge, MA: Belknap Press of Harvard University Press.
Mezey, G., & Robbins, I. (2001). Usefulness and validity of post-traumatic stress disorder as a psychiatric category. British Medical Journal, 323, 561–563.
Nathan, D. (2011). Sybil exposed: The extraordinary story behind the famous multiple personality case. New York, NY: Free Press.
Norris, F. H. (1992). Epidemiology of trauma: Frequency and impact of different potentially traumatic events on different demographic groups. Journal of Consulting and Clinical Psychology, 60, 409–418.
Rosen, G. M., & Frueh, B. C. (2010). Clinician’s guide to posttraumatic stress disorder. Hoboken, NJ: Wiley.
Rosen, G. M., Frueh, B. C., Elhai, J. D., Grubaugh, A. L., & Ford, J. D. (2010). Posttraumatic stress disorder and general stress studies. In G. M. Rosen & B. C. Frueh (eds), Clinician’s guide to posttraumatic stress disorder (pp. 3–31). Hoboken, NJ: Wiley.
Rosen, G. M., & Lilienfeld, S. O. (2008). Posttraumatic stress disorder: An empirical analysis of core assumptions. Clinical Psychology Review, 28, 837–868.
Rosen, G. M., Lilienfeld, S. O., Frueh, B. C., McHugh, P. R., & Spitzer, R. L. (2010). Reflections on PTSD’s future in DSM-5. British Journal of Psychiatry, 197, 343–344.
Rothbaum, B. O., Foa, E. B., Riggs, D. S., Murdock, T., & Walsh, W. (1992). A prospective examination of post-traumatic stress disorder in rape victims. Journal of Traumatic Stress, 5, 455–475.
Satel, S. L., & Frueh, B. C. (2009). Sociopolitical aspects of psychiatry: Posttraumatic stress disorder (pp. 728–733). In B. J. Sadock, V. A. Sadock, & P. Ruiz (Eds.), Comprehensive textbook of psychiatry (9th ed.). Baltimore, MD: Lippincott Williams & Wilkins.
Schnurr, P. P., & Green, B. L. (Eds.). (2004). Trauma and health: Physical health consequences of exposure to extreme stress. Washington, DC: American Psychological Association.
Shephard, B. (2001). A war of nerves: Soldiers and psychiatrists in the twentieth century. Cambridge, MA: Harvard University Press.
Shephard, B. (2004). Risk factors and PTSD: A historian’s perspective. In G. M. Rosen (Ed.), Posttraumatic stress disorder: Issues and controversies (pp. 39–61). Chichester, U.K. Wiley.
Simms, L. J., Watson, D., & Doebbeling, B. N. (2002). Confirmatory factor analyses of posttraumatic stress symptoms in deployed and nondeployed veterans of the Gulf War. Journal of Abnormal Psychology, 111, 637–647.
Smith, T. C., Ryan, M. A. K., Wingard, D. L., Slymen, D. J., Sallis J. F., & Kritz-Silverstein, D. (2008). New onset and persistent symptoms of post-traumatic stress disorder self reported after deployment and combat exposures: Prospective population based US military cohort study. British Medical Journal, 336, 366–371.
Spitzer, R. L., First, M. B., & Wakefield, J. C. (2007). Saving PTSD from itself in DSM-V. Journal of Anxiety Disorders, 21, 233–241.
Summerfield, D. (2001). The invention of post-traumatic stress disorder and the social usefulness of a psychiatric category. British Medical Journal, 322, 95–98.
Taylor, S., Frueh, B. C., & Asmundson, G. J. G. (2007). Detection and management of malingering in people presenting for treatment of posttraumatic stress disorder: Methods, obstacles, and recommendations. Journal of Anxiety Disorders, 21, 22–41.
Tolin, D. F., & Foa, E. B. (2006). Sex differences in trauma and posttraumatic stress disorder: A quantitative review of 25 years of research. Psychological Bulletin, 132, 959–992.
Walker, L. E. (1977). Battered women and learned helplessness. Victimology, 2, 525–534.
Watson, D. (2005). Rethinking the mood and anxiety disorders: A quantitative hierarchical model for DSM-V. Journal of Abnormal Psychology, 114, 522–536.
Weathers, F. W., & Keane, T. M. (2007). The criterion A problem revisited: Controversies and challenges in defining and measuring psychological trauma. Journal of Traumatic Stress, 20, 107–121.
Wessely, S., & Jones, E. (2004). Psychiatry and the “lessons of Vietnam”: What were they, and are they still relevant? War & Society, 22, 89–103.
Worthen, M. D., & Moering, R. G. (2011). A practical guide to conducting VA compensation and pension exams for PTSD and other mental disorders. Psychological Injury and Law, 4(3–4), 187–216.
Yufik, T., & Simms, L. J. (2010). A meta-analytic investigation of the structure of posttraumatic stress disorder. Journal of Abnormal Psychology, 119, 764–776.
As with every other sector of health care, there is now a widespread recognition that mental health care requires practice standards and professional accountability that are rooted in empirical evidence—that is, evidence-based practices, or EBPs, as we shall call them from here on (Frueh, Ford, Elhai, & Grubaugh, 2012; Institute of Medicine & National Research Council, 2001; Kazdin, 2008). EBPs and empirically supported treatments are a critical element of treatment standards for both child and adult mental health services (American Psychological Association, Presidential Task Force on Evidence-Based Practice, 2006; Barlow, 2000; Spring et al., 2008). Unfortunately, it is also well known that interventions used in clinical behavioral and mental health practice settings are not always carefully based on the best available empirical evidence (Cook, Schnurr, & Foa, 2004; Ferrell, 2009; Frueh, Cusack, Grubaugh, Sauvageot, & Wells, 2006; Gray, Elhai, & Schmidt, 2007; Henggeler, Sheidow, Cunningham, Donohue, & Ford, 2008; Stewart & Chambless, 2007). This very common problem is sometimes referred to as the research-to-practice gap. One of the goals of this book is to help reduce this “gap.”
Over the remainder of this chapter we provide a brief—and hopefully painless—overview of EBP as it pertains to mental health care. We realize that many clinicians’ eyes glaze over as they contemplate the ever-expanding alphabet soup of acronyms (e.g., CBT, PE, ACT, DBT, CPT, TMT) denoting the latest and greatest clinical intervention for this or that population or disorder. And while we are, perhaps, somewhat guilty ourselves of adding to this list with our own research activities, we are also exceedingly sympathetic to the sense of bewilderment, frustration, and anxiety experienced by many practitioners in regard to this topic.
Indeed, it can be quite difficult to follow all the latest developments in the field, let alone know where even to begin in selecting assessment instruments and treatment approaches. Nevertheless, we hope that over the next few pages, we will succeed in presenting not only a sufficient rationale for EBPs, but also a sensible and flexible approach to viewing and understanding the concept—and, of course, the remainder of this book is then intended to flesh out a wide range of evidence-based strategies relevant to the clinical assessment and treatment planning for posttraumatic stress disorder (PTSD).
Certainly, we are all familiar with the notion that it is generally good in life to look for information to guide our decisions, especially the important ones. For example, who would buy a car, choose a vacation destination, or accept a new job without first attempting to make some sort of appraisal of the various options available? In fact, we live in a technological world, in which nearly every product for sale on the Internet comes with ratings made by individuals who bought these products, and many people use these ratings to inform their shopping decisions. Of course, virtually everyone seeks out some information to help guide their decision making. But how does one decide what information is most relevant or important?
In the case of a new automobile, there is an array of different information that might influence one’s decisions: television commercials showing shiny new models; prior experience with a particular brand; observations made while driving of how other vehicles look or seem to perform; product reviews published in industry or consumer magazines; newspaper headlines about product recalls or problems; and so on. It is very likely that our decision will be influenced by several, if not most, of these sources of information. Yet, when we think about it, we realize that some of these sources deserve to be weighted heavier than others, while some pieces of information will raise doubts and questions that warrant further research on the matter before they can be resolved. For instance, while television advertisements may catch our attention and plant the seed of an attractive idea, and they may make appealing product claims, the savvy shopper will use this as a starting point. Do those “run-flat” tires really work well in practice? Does that mid-sized SUV really get 30 miles to the gallon? Does that shiny little sports car have good reliability? The savvy shopper will look for credible data—evidence—to answer these important questions as well as possible.
The search for evidence to guide decision making in buying a new automobile is not unlike the search for evidence to guide clinical decision making. And why are EBPs so critical to PTSD, other posttraumatic reactions, and the trauma field in general? The answer is that, in part, the mental health care field in general has come a little late to the EBP table. In order to align with standards in health care, expectations of patients and their families, standards of regulatory and licensing bodies, legal standards, and practices of insurance companies, mental health care practitioners should consider taking an EBP approach. More specifically, within the field of PTSD treatment, there is a long past history of harmful misconceptions and use of dubious treatment practices. Many well-intentioned interventions, both medications and psychotherapy, have produced findings of limited efficacy, no efficacy, or even outright harmful results for patients and their families. Often, new therapies are developed without a sound theoretical rationale and then disseminated before they have been evaluated adequately in clinical trials. A group of such treatments came to be known as the power therapies. These included thought-field therapy, the counting method, emotional freedom techniques, visual–kinesthetic dissociation, and several others—all with fantastic claims of nearly immediate and miraculous efficacy, and some of which are extremely financially expensive for clinicians to adopt. Not surprisingly, there is no empirically rigorous research—subjected to peer review—to support the use of these “therapies.” This history should serve to remind practicing clinicians that they will serve their patients best by relying on empirically supported methods and practices (Cukor, Spitalnik, Difede, Rizzo, & Rothbaum, 2009).
At a recent clinical workshop for community practitioners, one of the authors had the following exchange with a member of the audience: