PTSD in Court I: Introducing PTSD for Court

IJLP-01242; No of Pages 21 International Journal of Law and Psychiatry xxx (2016) xxx–xxx

Contents lists available at ScienceDirect

International Journal of Law and Psychiatry

PTSD in Court I: Introducing PTSD for Court Gerald Young Glendon Campus, York University, Toronto, Ontario, Canada

a r t i c l e

i n f o

Available online xxxx Keywords: PTSD court DSM-5 ICD-11 factors prevalence

a b s t r a c t The first part of the series of three articles on posttraumatic stress disorder (PTSD) in Court to appear in the journal reviews the history of the construct of PTSD and its presentation in the DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition; American Psychiatric Association, 2013) and the ICD-11 (International Classification of Diseases, 11th Edition; World Health Organization, 2018). There are 20 symptoms of PTSD in the DSM-5. PTSD symptoms are arranged into a four-cluster model, which has received partial support in the literature. Other four-factor models have been found that fit the data even better than that of the DSM-5. There is a five-factor dysphoria model and two six-factor models that have been found to fit better the DSM-5 PTSD symptoms. Finally, research is providing support for a hybrid seven-factor model. An eighth factor on dissociation seems applicable to the minority of people who express the dissociative subtype. At the epidemiological level, individuals can expect trauma exposure to take place about 70% over one's lifetime. Also, traumatic exposure leads to traumatic reactions in about 10% of cases, with PTSD being a primary diagnosis for trauma. Once initiated, PTSD becomes prolonged in about 10% of cases. Polytrauma and comorbidities complicate these prevalence statistics. Moreover, the possibility of malingered PTSD presents confounds. However, the estimate for malingered PTSD varies extensively, from 1 to 50%, so that the estimate is too imprecise for use in court without further research. This first article in the series of three articles appearing in the journal on PTSD in Court concludes with discussion of complications related to comorbidities and heterogeneities, in particular. For example, PTSD and its comorbidities can be expressed in over one quintillion ways. This complexity in its current structure in the DSM-5 speaks to the individual differences involved in its expression. Crown Copyright © 2016 Published by Elsevier Ltd. All rights reserved.

1. Overall summary of the series of three articles on PTSD in Court This series of three articles in the journal on Posttraumatic Stress Disorder (PTSD) in Court addresses the current literature related to the validity of PTSD in the DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, American Psychiatric Association, 2013), as well as the forensic challenges that PTSD presents. The three articles elaborate the following. (a) The first article in the series of three in the journal, the present one, offers an introduction related to PTSD, and emphasizes the DSM-5 PTSD symptoms and dimensions, in particular. The DSM has been criticized for its reliability and validity issues. Research on PTSD is burgeoning and is redefining our understanding of how it is expressed and how its symptoms relate to each other. This research calls into question the validity of using without modification the current version of the DSM for court purposes. (b) The second article of the present series of three articles on PTSD in Court (Young, 2017a) consists of a review of PTSD's extensive neurobiological, neurophysiological, and genetic underpinnings. Endophenotypic pathways from genes to brain to behavior are E-mail address: [email protected].

being suggested for PTSD, as well as biomarkers that index it. This section includes discussion of the models and causes of PTSD. It concludes that a biopsychosocial, multicausal model best encompasses the multifactorial causality of PTSD. In this regard, a novel model is described that is based partly on contemporary connectivity science. (c) The third of the three articles in the journal on PTSD in Court addresses the forensic and court context for PTSD (Young, 2017b). It focuses on malingering, how to assess PTSD with psychological tests, and which tests help in attributing malingering, if it is inferred as present. The last article in the series of three articles on PTSD concludes with legal considerations, including on the material contributions test, adversarial divide, litigation distress, biases, and admissibility of evidence to court.

To elaborate further, PTSD is part of the disability epidemic in court and related venues. In this regard, Bass and Halligan (2014) noted that malingering of PTSD is a “huge” issue (Morel, 2010) and that toward 25% of evaluees fail a series of measures examining for malingering and related biases (Merten, Thies, Schneider, & Stevens, 2009). However, Vermetten, Baker, Jetly, and McFarlane (2016) noted that PTSD is under-diagnosed rather than being over-diagnosed. In support of this

http://dx.doi.org/10.1016/j.ijlp.2016.10.012 0160-2527/Crown Copyright © 2016 Published by Elsevier Ltd. All rights reserved.

Please cite this article as: Young, G., PTSD in Court I: Introducing PTSD for Court, International Journal of Law and Psychiatry (2016), http:// dx.doi.org/10.1016/j.ijlp.2016.10.012

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contention, they referred to research in clinical settings (e.g., Liebschutz et al., 2007). To be fair, the diagnostic epidemic of PTSD refers to more forensic than clinical contexts, such as in evaluations for disability claims, whether military, in tort, in worker compensation, in private insurance, and so on. Although the prevalence of malingering appears seemingly high, progress is being made both in its assessment/testing and diagnosis. For example, the addition of reckless/destructive behavior to the DSM-5 symptom list opens a Pandora's Box of improper forensic use. Also, the cut scores in use on relevant tests need continuing research on valid application to the psychological injury (e.g., tort, worker compensation) context. The article concludes that, despite the controversies associated with PTSD, it is a valid clinical phenomenon that the research is increasingly specifying for its symptoms and clusters. Its suggested biological basis is standing up to replication to the point that PTSD in valid cases should be considered a biopsychosocial disorder and not purely a mental one. However, caution suggests that there are as yet no definitive biomarkers of PTSD for court purposes; they are not yet sufficiently differentiated for use in individual cases going to court. Despite what some might contend in their narratives about PTSD, it is not a mental disorder that has no validity and, if it is diagnosed, it is not often reflective of malingering. Unlike the opposite point of view, it is valid, it can be validly diagnosed, and malingering does not confound it to any great degree. This opposition in views on PTSD illustrates that there is much work to do forensically to improve assessment and diagnostic procedures, including for malingering attribution and related negative impression management or feigning. Overall, the tension in the field about the validity of PTSD in court, and the different approaches to it as manifested in defense and plaintiff narratives about it, can only be mitigated, at least to a degree, by a constant, comprehensive (a) research program on its expression, origins, and treatment, and (b) up-to-date literature review on this research and the conceptualizations about PTSD. In brief in this regard, to conclude, the series of three articles on PTSD in Court in this journal discusses PTSD especially in terms of its DSM-5 criteria, dimensional or cluster structure, neurobiology and genetics, causality, assessment/testing, and malingering detection, and legal aspects (the present article, Young, 2017a, 2017b). It presents new models of PTSD both in each of its symptom expression and organization, causality, and treatment. 2. PTSD in court Posttraumatic stress disorder (PTSD) is one of the major psychological injuries, which collectively refer to psychological conditions that might arise after an event at claim, and then lead to legal or related action in court and other venues (such as for tort, in worker compensation, at the VA, Veteran's Administration, for military veterans, and in cases involving other disability actions). Aside from PTSD, psychological injuries include other actionable conditions, especially chronic pain and mild traumatic brain injury (mTBI). Along with depression and anxietyrelated conditions, pain and cognitive effects of mTBI often are comorbid with PTSD, and so complicate its presentation, assessment, diagnosis, and treatment. Cases of polytrauma typically are harder to treat than conditions with one disorder being present and having no comorbidities. Other complications in dealing with PTSD include the presence of pre-existing stressors or psychopathology, such as early childhood sexual abuse and a history of traumatization, which facilitate that an index event precipitates the PTSD at issue, which otherwise would not have occurred without pre-existing complications. Pre-existing stressors and psychopathology that lead to an index PTSD also could result in the resultant condition lasting more than might be expected. At the other extreme, another type of complication concerns issues such as symptom exaggeration or overreporting, negative impression management or response bias, and feigning and outright malingering. Evidence of outright malingering should not present challenges to the forensic PTSD evaluator, but what of gray zone cases, the possibility of

less concerning attribution of a “cry for help” or relating any exaggeration to psychopathology, and so on. The forensic evaluator in disability and related assessments deals with the validity of psychological injuries and their claimed effects, including for cases involving presentation of symptoms consistent with PTSD. The evaluator needs to proceed cautiously because of the many possible confounds associated with PTSD. Consider that the evaluee might be coached and present normatively, aside from the opposite extreme of behaving in the assessment with poor or suboptimal effort, gross exaggerations, feigning and dissimulation, in general, or any type of problematic presentation and performance or negative response bias, including that of outright malingering. The third article in the series of three in this journal on PTSD in Court (Young, 2017b) describes the scientific evidence for assessing evaluees who conduct themselves in this latter manner in ways that are both effective and fair. At the same time, the present work does not advocate for use of biomarkers of PTSD in court, given that the type of research on these putative PTSD indices demonstrates normative trends, at best, and the research is not yet sufficiently developed for use in determining exactly whether or not specific individuals have PTSD, and differentially so relative to those who do not express this disorder (Young, 2017a). The series of three articles on PTSD in Court published in the journal examines these multiple themes on the topic of PTSD in court by describing in depth the most recent literature (2015–start of second half of 2016) and then providing commentary on it. To the degree possible, it eschews examining prior literature for the most part and assiduously avoids building on prior conceptions and models, including predominant court models on what PTSD is about, while selecting only the research in support of one already existing conception/model or the other. The literature review that is undertaken speaks to the primary goal of the series of three articles on PTSD in Court found in the present journal—to ascertain the reliability, validity, and relevance of PTSD in court, the difficulties presented in its assessment (including those related to possible feigning, such as malingering), and discussion of outstanding issues and needed research directions toward improving the standing of PTSD in court. Toward these ends, the literature review is comprehensive although inevitably selective given the massive amount of research on PTSD. The review presents the research data as if it were the reliable data to be considered in a case, letting the chips fall as they may. It tries to avoid preconceived narratives, doing this by indicating clearly when the commentary sections begin after the sections describing the literature, so that there is no confusion between data presented in the research and their interpretation by myself and, moreover, this format permits that all the evidence used in these regards can be reviewed by the reader. This careful approach to gathering data and interpreting them constitutes the same elements required by psychologists in their cases dealing with PTSD that might end up in court or related venues. In this sense, in this area of practice (and research), science should be the arbiter of what constitutes valid evidence rather than anything related to the adversarial (e.g., plaintiff/ defense) divide or other such possible bias. The work concludes by examining possible biases, the role of litigation science, the evidence for plaintiff and defense narratives about PTSD, and so on, before calling for more focused research on the issues facing the field. In order to achieve its goals as enunciated, the series of three articles on PTSD in Court that constitutes the present work tackles, in turn, each of the following topics and questions related to PTSD [this list is more specific than simply stating there are three general parts to the present work]: (a) history (does it show that PTSD is a natural kind or is constructed?); (b) diagnostic manuals (generally, do they value clinical utility or research?); (c) traumatic exposure (is it inevitable, does it always cause PTSD?); (d) prevalence (is PTSD as widespread as the disability epidemic indicates, or manipulated by claimants and attorneys to their monetary advantage?); (e) DSM-5 symptoms (why do we need 20 of them; are they easy to manipulate for court

Please cite this article as: Young, G., PTSD in Court I: Introducing PTSD for Court, International Journal of Law and Psychiatry (2016), http:// dx.doi.org/10.1016/j.ijlp.2016.10.012

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purposes?); (f) DSM-5 clusters or dimensions (what does factor analytic research indicate about the DSM-5 four-cluster model? Are there really seven or eight of them, as per the recent research?); (g) the dissociative subtype (do a minority of people really express it; perhaps dissociation is critical to understanding PTSD, in general); (h) classes, comorbidities, and heterogeneities (are there both less and more severe trajectories, less and more severe presentations due to comorbidities, and less complex and more complex presentations due to the many combinations of symptoms possible); (i) risk factors, endophenotypes, and biological underpinnings (what contributes to vulnerabilities toward developing PTSD; what biological factors serve in this regard, and do any mark PTSD and can be used in court (e.g., in the brain, i.e., areas, connections); what are the pathways in PTSD from genes to outcome); (j) models and causality (are traditional models used to explain PTSD sufficient; does the advent of connectivity science help explain it; is PTSD biopsychosocial; is the new model that I propose that combines systems and connection approaches useful; what is the material contributions test?); (k) treatment (what are evidence-supported treatments for PTSD; should treatment consider over- and undermodulation, as distinguished by dissociation researchers); (l) malingering (how prevalent is malingered PTSD; what are some cautions in attributing it); (m) assessment/testing (what are the most reliable and valid instruments to use to assess for PTSD and to assess for PTSD malingering); and (n) the law (what are some systemic influences and biases, including those that affect forensic evaluators; what factors determine admissibility to court?). Conclusions to this present series of three articles in the journal on PTSD in Court concern how to establish the admissibility of PTSD assessments in cases in court and related venues. 3. What is its history? What are its manuals? What is traumatic exposure? 3.1. Précis of the first article in the series of three articles on PTSD in Court The first article in the series of three articles on PTSD in Court, published in the journal, the present one, provides an introduction to the topic of PTSD in court. It begins with an historical overview of how traumatic reactions have been treated, and notes that it has a history extending back thousands of years into pre-biblical times. The advent of the major wars in the twentieth century brought trauma reactions to the forefront, leading in 1980 to the codification of PTSD in the DSM-III (Diagnostic and Statistical Manual of Mental Disorders, Third Edition; American Psychiatric Association, 1980). Since then, it has been modified with each version of the DSM (and will continue to be modified through revisions of the current version in the DSM-5). This speaks to the social construction and clinical utility criticisms of the construct of PTSD. That is, this approach argues that if PTSD reflects a natural kind or taxon, then it would not differ much even in its preDSM descriptions. Granted, the symptom content and structure of PTSD both change over time. Currently, there are 20 symptoms in PTSD in the DSM-5, arranged into four clusters, with a dissociation subtype possible, having two more symptoms, thereby giving a list of 22 possible symptoms in PTSD. That being said, the PTSD symptom list and cluster division are still research-informed to a degree. Thus, PTSD as presented in the DSM-5 provides a plausible shorthand for summarizing traumatic reactions (albeit with much individual variation inherent in how it is presented). Moreover, as shown in Young (2017a), there is an impressive body of research that is specifying its neurobiological and corporal physiological associations even in its current form (or in its DSM-IV form) such that it does represent a plausible integrated disorder in and of itself. That being the case, the ICD-11 (International Classification of Diseases, 11th Edition; World Health Organization, 2018; Reed et al., 2016) constitutes another classificatory system and it will be using a

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simpler version of PTSD symptoms, while adding Complex PTSD (CPTSD). But consider the difficulty that both diagnostic systems (DSM-5, ICD-11) embody—both are oriented to clinical utility above all while using research only in a supplementary way in this regard. Neither of these two psychiatric diagnostic classification systems adopts a strict research-informed approach to their construction. This lack of a research-first approach in extant diagnostic psychiatric manuals does speak to the social construction point of view of PTSD. The current version of PTSD includes a cluster approach to classifying disorder (with a certain number of symptoms needed within each cluster in order to arrive at diagnostic threshold for the disorder; polythetic criteria approach). This approach of separating symptoms for a disorder into clusters has merit, according to the current research on the dimensions of PTSD. Specifically, the section on the dimensions of PTSD in this article analyzes in depth the literature, which shows support mostly for a seven-factor model. Typically, in this research, five- to seven-factor PTSD models are supported, as opposed to the more limited four-cluster one in the DSM-5. Young (2015) added an eighth dimension related to the dissociative subtype. However, as argued below, and as found in the approach of the ICD-11 to PTSD, the cluster approach would be more clinically useful especially if core symptoms would be isolated in each of them, which would have the added advantage of reducing individual differences in its expression, at least for primary symptoms (Young, 2015). Trauma exposure generally is at about 70% lifetime, with about 10% of exposed individuals developing PTSD and other trauma reactions, and about 10% persisting in their symptoms, especially if there is comorbidity. These statistics indicate both the vulnerability to developing PTSD, yet resilience to PTSD developing after traumatic exposure. However, the phenomenology of PTSD is not the only concern of the series of three journal articles on PTSD in Court. For example, Young (2017b) gives forensic implications, for example, how some of the DSM-5 PTSD symptoms are easy to malinger or could be used inappropriately in criminal defense arguments. 3.2. History The study of the history of trauma reactions indicates that they have been recognized for millennia (Birmes & Bui, 2016; Weisaeth, 2014). For example, even the Greek classics of Iliad of Homer and the Odyssey give examples that are consistent to a degree with present day accounts of PTSD. Ford, Grasso, Elhai, and Courtois (2015) described in depth descriptions of trauma reactions from about 5000 years ago onward. Aside from Greek sources, they reviewed descriptions in ancient Sumerian, Roman, and biblical sources. Ford et al. (2015) noted that in the Renaissance and Reformation epochs, writers such as Shakespeare described PTSD-like reactions to trauma. The scientific approach to trauma reactions took hold in the nineteenth century, and expanded during the First World War (WWI) (World War I). Freud, as recounted in Ford et al. (2015), considered a possible role of hysteria in these regards, and this led to forerunners of contemporary cognitive behavioral approaches to helping survivors who were manifesting what was being called “war neurosis,” “combat fatigue,” or “soldier's heart,” for example, after the Second World War (WWII). Despite this history, PTSD was late in being part of the dominant psychiatric manual, the DSM. Ford et al. (2015) noted the Vietnam War of the 1960s and 1970s led to the codification of PTSD in the DSM-III, replacing the category of “gross stress reaction” in the DSM-I (Diagnostic and Statistical Manual of Mental Disorders, First Edition; American Psychiatric Association, 1952) and “adjustment reactions” in the DSM-II (Diagnostic and Statistical Manual of Mental Disorders, Second Edition; American Psychiatric Association, 1968). In this regard, McNally (2016a) noted that the argument that PTSD is either (a) a natural “kind,” or valid psychiatric diagnostic category, with

Please cite this article as: Young, G., PTSD in Court I: Introducing PTSD for Court, International Journal of Law and Psychiatry (2016), http:// dx.doi.org/10.1016/j.ijlp.2016.10.012

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a psychobiological basis, or (b) a social construction without such a basis does not necessarily depend on whether it is found to be an unchanging transhistorical phenomenon. At the same time, biological research cannot demonstrate that the diagnosis in the DSM is not socially constructed. McNally (2016a) reviewed the sociopolitical push by antiwar activists to include PTSD in the DSM during the postVietnam War era, in conjunction with traumatologists. Also, he noted that differences in trauma reactions over time among veterans are “striking” (Jones & Wessely, 2005). A case in point concerns variations in descriptions of putative flashbacks among survivors. Generally, McNally aligns with the skeptical point of view on PTSD. For example, he cited the research by Gold, Marx, Soler-Baillo, and Sloan (2005) and others that PTSD symptoms are found more to nontraumatic stressors than DSM-consistent traumatic ones. However, Larsen and Pacella (2016) conducted a meta-analytic review of this and other studies on the question because of mixed findings in the literature. Their results showed that higher levels of PTSD symptoms develop following DSM-consistent trauma than stressors that do not meet that criterion. Friedman, Resick, and Keane (2014) described how after the criteria of PTSD were introduced in the DSM-III, they changed over the different DSM iterations, including in the DSM-consistent trauma criterion. The present version of the DSM, the DSM-5, includes a revision of PTSD especially in terms of both (a) the number of symptoms involved (20, vs. 17 in the DSM-IV; Fourth Edition; American Psychiatric Association, 1994) and (b) the number of symptom clusters (four instead of three). (c) In addition, the entry Criterion A has been modified especially by removing that the survivor of the event at issue needs to experience feelings of horror and related emotions, as well as changing (d) the nature of the traumatic experiences that qualify (e.g., by allowing for PTSD in situations related to first responders). (e) Also, a dissociative subtype has been added involving two possible symptoms. The DSM enterprise includes the projection to publish a DSM-5.1, then a DSM5.2, and so on, in order to keep up with changes in the field (see Young, 2016). Herman (1992) developed the category of CPTSD, and it will be included in the ICD-11, but it is not found in the DSM-5. The construct of CPTSD, as in the ICD-11, has evidence both for and against it (e.g., respectively, Hyland, Elklit, et al., 2016; and Karatzias et al., 2016, as well as Perkonigg et al., 2015; in contrast to Landy, Wagner, Brown-Bowers, & Monson, 2015). Friedman and Resick (2014) reminded that the new criteria in the DSM-5 for PTSD are broad enough to include those of CPTSD. [That said, there might be value in providing it as a separate diagnosis in future iterations of the DSM-5.] However, Stein, Wilmot, et al. (2016) argued for its validity along with other subtypes of PTSD depending on the trauma type involved. The development of ICD-11 is an ongoing project, and for its category of CPTSD, we have not heard the last word. 3.3. Comment This brief history of the development of the psychiatric classification category of PTSD indicates the social and political influences that were at work in its codification in the DSM-III. On the one hand, PTSD seems to reflect the apogee of the field of traumatology, which uses PTSD as a clinical diagnosis and researches it without always considering either how it arrived in the DSMs or possible malingering and related confounds as it is diagnosed. In this regard, as pointed out by one reviewer, there is sufficient historical evidence to indicate that PTSD appears to be a social construction more than a research-based mental disorder, at least in its DSM renditions (Shephard, 2004; Young, 1995). Further in this regard, historical scholarship demonstrated that PTSD, per se, as we now know it, simply did not exist prior to its first articulation in the DSMs (in the DSM-III). Although descriptions of traumatic reactions do have a long history in pre-scientific and literary sources, the clinical (and literary) descriptions that have been presented

throughout history have tended to reflect the prevailing narrative at the time for how one should respond to trauma—and this narrative has varied widely over time. This variation in description of trauma reactions in history stands in contrast to that found for other clinical syndromes (depression, schizophrenia, etc.), for which one can find historical symptom descriptions that are quite similar to present iterations and that predate those in the DSMs. On the other hand, the variation in the historical trajectory for describing trauma reactions and then PTSD itself cannot be used as a basis to deny its validity. The DSM is replete with other examples of disorders that have changed with editions or that are new to one edition or the other. Some have no historical precedence and others have much variation, including over culture, gender, age, and so on. Evidence of variation for any one psychiatric disorder cannot be taken as evidence of invalidity. This would be especially true if good research on the disorder can be found, even if the DSM approach to it might be limited in some ways, as is the case for PTSD. 3.4. Clinical utility vs. research in psychiatric classification manuals As mentioned, there are two major psychiatric diagnostic manuals— the DSM-5 and the ICD-11. The following considers each generally instead of just for PTSD (which had been the way they are introduced in the above). First, the section deals with the ICD-11, which is a classificatory approach that emphasizes clinical utility. Then, it turns to the DSM-5, which also has this emphasis. Although the role of clinical utility in constructing classificatory systems is necessary to consider, research should inform every step of the way the systems are constructed so that they ensure the validity of the psychiatric categories that are included. Further along these lines, the overt aim of the ICD-11 is to construct a classification system that is “maximally intuitive and clinically useful” (Keeley et al., 2016). Moreover, the ICD-11 advocates for its specific approach to clinical utility in comparison to the approaches taken by any other classificatory system (read: the DSM-5). Keeley et al. (2016) noted that other classification systems have maintained that their systems give high priority to clinical utility, yet these other systems state that this is the case without providing the necessary scientific support for the contention. Keeley et al. (2016) maintained that the ICD-11 is being developed based on an approach that researches clinical utility, including in clinicians' cognitive organization of diagnostic categories. ICD-11 field studies on clinical utility have already been undertaken, and they have led to changes in diagnostic guidelines and in vignettes toward improving the ICD-11's clinical utility. Mullins-Sweatt, Lengel, and DeShong (2016) also examined the role of clinical utility in constructing diagnostic manuals. For example, First et al. (2014) suggested that clinicians might not be using properly the DSM diagnostic criteria, either relying too much on personal prototypes or dismissing cumbersome, time-consuming, poorly fitting procedures that are required in using the DSM. 3.5. Comment In particular, clinical utility refers to ease of communication of, conceptualization of, and implementation and application of a classification system. However, a balanced approach in psychiatric manual classification should prioritize the research front in its construction, and work toward clinical utility from that perspective. For example, Keeley et al. (2016) admitted that the ICD's research on clinician cognitive organization of mental disorders was not aimed at gathering evidence on their “real” nature, structure, and interrelationship. The three-article series in the journal on PTSD in Court is dedicating to describing research and conceptualization on PTSD toward improving its validity in the next iterations of the DSM and ICD. That being said, clinical utility will always have a role to play in the construction of diagnostic classification systems. In constructing them, a fine balance

Please cite this article as: Young, G., PTSD in Court I: Introducing PTSD for Court, International Journal of Law and Psychiatry (2016), http:// dx.doi.org/10.1016/j.ijlp.2016.10.012

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between research and clinical utility is needed in order to create usable, research-based ones. Despite the approach of the ICD-11 to improve its approach to psychiatric diagnosis, its critics query the validity of its efforts. Vermetten et al. (2016) argued that its construction has been political more than empirical, leaving too much play of subjective inference in diagnosis. Moreover, a diagnostic category in the ICD-11 might involve “guidelines” or the use of bullet points instead of explicit diagnostic criteria, with ensuing paragraphs that elaborate the points. There could be a weak attempt to be precise through symptom counts or durations. Vermetten et al. (2016) concluded that the ICD-11 has a “markedly divergent approach,” which is in conflict with what is required toward consensus building in the field.

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3.7. PTSD in the ICD-11 For the ICD-11, PTSD will be organized around a core set of six symptoms arranged into three clusters (Brewin, Lanius, Novac, Schnyder, & Galea, 2009; Kliem et al., 2016): (a) The re-experiencing group will consist of: (i) recurrent, distressing dreams related to the traumatic event at issue, and (ii) acting/feeling as if it were happening again (re-occurring); (b) The avoidance symptoms will be constituted by avoidance efforts, in terms of either trauma-related: (i) thoughts/feelings/conversations, or (ii) activities/places/people “that arouse recollections;”

3.6. The DSM-5 and its shortcomings Wakefield (2016) maintained that the DSM-5 tends to over-label normal distress as reflecting mental disorder, in a process that he considered as diagnostic expansion. He maintained that the DSM-5 work groups functioned in secrecy and without proper documentation. Further, the DSM-5 categories generally lack construct validity. Also, in the DSM-5, new configurations of extant mental disorders have not been thought through enough, including for PTSD. Generally, the DSM-5 has a “false positive” problem that threatens its credibility. Lilienfeld and Treadway (2016) considered that the DSM (as well as the ICD) diagnostic approach suffers from “anomalies.” For example, the DSM-5 uses scientifically-arbitrary cut-offs for its categories. In addition, its categories can be expressed too heterogeneously. Further, they allow for too much comorbidity. Lilienfeld and Treadway (2016) also noted that the DSMs generally have too many wastebasket categories (e.g., not otherwise specified). They do not allow for a linear medical model of etiology to disease to treatment. That being the case, for these authors, the solution does not necessarily lie in specifying the neurobiological bases of disorder, as in the RDoC project (Research Domain of Criteria; Insel et al., 2010). The RDoC deemphasizes the psychosocial (social, cultural) influences in the etiology of mental disorder, and so its emphasis on biocentric, endophenotypic research will not be that successful. Kendler and Solomon (2016) recommended that the DSM work groups should incorporate systematic, evidence-based reviews even before they begin their assessments. Adopting this research base in DSM nosological decisions will serve to increase the validity of the DSM and to facilitate its acceptance. The DSM-5 created a Scientific Review Committee toward a similar end, but it was initiated only after the work groups began their deliberations, thereby reducing any real, widespread influence it might have had. McNally (2016b) referred to the expanding empire of psychopathology due to diagnostic expansion. For example, the definition of trauma is ambiguous, and nontraumatic stressors seem capable of eliciting PTSD. As with psychopathology, in general, which has had difficulty establishing valid boundaries between normality and disorder, traumatology research is experiencing a bracket creep that is expanding its domain, which is taking place due to societal mechanisms at play. Repeating these types of arguments, Rosen (2016) argued that the many changes made in the DSM-5 version of PTSD did not serve to improve its validity. Vermetten et al. (2016) noted that the substance of the argument made by Rosen and colleagues in prior publications on the matter of the doubt of the diagnostic validity of PTSD (e.g., Rosen & Lilienfeld, 2008) are based on reviews of research with inherent limitations, such as not collecting contextualizing information. The different approaches to classifying PTSD in the DSM-5 and the ICD-11 were highlighted by Schnurr (2013). She averred that the two diagnostic systems will lead to “real differences” in who is diagnosed with PTSD.

(c) The third cluster of arousal will be comprised of: (i) hypervigilance, and (ii) exaggerated startle response.

In order to arrive at a diagnosis of PTSD using this symptom set of six core PTSD criteria, one symptom will need to be present in each category, as well as functional impairment. This core set of symptoms avoids overlap of PTSD symptoms with those of other disorders (Bryant, O′Donnell, Creamer, McFarlane, & Silove, 2011). Miller, Wolf, and Keane (2014) examined the proposal for diagnosing PTSD in the ICD-11, as described in Maercker, Brewin, Bryant, Cloitre, Reed, et al., 2013a; Maercker, Brewin, Bryant, Cloitre, van Ommeren, et al., 2013b, in particular). As mentioned above, these ICD-11 researchers proposed that the PTSD diagnosis should focus on reexperiencing (flashbacks, nightmares); avoidance (internal, external); and heightened sense of threat/arousal (hypervigilance, exaggerated startle response). As for CPTSD, receiving a diagnosis for this form of PTSD would add three more symptom clusters: affect dysregulation, negative self-concept, and interpersonal disturbances, with one symptom needed from each (Cloitre, Garvert, Brewin, Bryant, & Maercker, 2013). Miller et al. (2014) argued that the DSM-5 already encompasses the range of symptoms needed to cover those of CPTSD. Despite some research indicating that the ICD-11 will constitute an improvement in the diagnosis of PTSD, others remain unconvinced. Specifically, Vermetten et al. (2016) criticized the ICD-11 PTSD symptom criteria as being more political and less empirical than should be the case, so that the diagnosis of PTSD using the ICD-11 criteria will allow for appreciable subjective inference (“essentially left to the individual clinician, p. 499). For example, exposure to a traumatic event is much better defined in the DSM-5. And by including a functional impairment requirement for the diagnosis, further inappropriate clinical inference becomes possible in the diagnosis (because of cultural/ environmental factors). Also, compared to the prior 10th ICD version, the ICD-11 approach to PTSD: (a) removed some elements in the diagnosis (conspicuous emotional/feeling detachment/numbing); (b) emphasized others without sufficient empirical support (intrusion/ situation avoidance); and deemphasized others (numbing/detachment, which is essential to consider in the military context). Given the uncertain state of affairs about whether the ICD-11 will lead to a better diagnostic approach to PTSD compared to the DSM-5, careful scrutiny of PTSD in the DSM-5 seems warranted. 3.8. PTSD in the DSM-5 The series of three articles in the journal on PTSD in Court (the present one; Young, 2017a, 2017b) deals with research that straddles the DSM-IV/DSM-IV-TR and DSM-5 (Fourth Edition, original version and Text Revised, respectively; American Psychiatric Association,

Please cite this article as: Young, G., PTSD in Court I: Introducing PTSD for Court, International Journal of Law and Psychiatry (2016), http:// dx.doi.org/10.1016/j.ijlp.2016.10.012

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1994/2000, 2013), as the field transitions to the newer version both in research and practice. The 20 symptoms of PTSD in the DSM-5 are itemized in Table 1 (as well as the two PTSD dissociation subtype symptoms). Table 1 also indicates how the DSM-5 PTSD symptoms are placed within the four symptom clusters in the DSM-5, as well as their placement in competing models that have been supported in the research. Later on in the article, I analyze the research on these other PTSD symptom cluster models, which include clusters numbering from four to eight. Despite concerns in the literature about the diagnosis of PTSD in the DSM-5 and its symptom structure, Regier et al. (2013) has shown that it is reliably diagnosed when the DSM-5 symptom list and structure are used to train diagnosticians (according to the statistic kappa). The cluster structure (the four-cluster numbing model) is a viable one, in that there is some support for it in the literature, and no other model has garnered universal support (Young, 2015). That said, despite ostensible demonstration of the validity of the DSM-5 PTSD symptoms and diagnosis, Young (2013, 2016) showed that the version of the DSM-5 used to establish its reliability was the draft one of 2010 and not the final one (which is discussed in detail later on). The ramifications of this methodological inconsistency for establishing the reliability of the DSM-5 PTSD symptoms/structure cannot be underestimated. Furthermore, I argued that the changes in the DSM-5 for its list of criteria for PTSD risk opening further the civil floodgates of its use inappropriately in court. [That being said, the DSM-5 was not meant to be a forensic document and, therefore, it is those employing it who must be forensically responsible in its use.] For the question of opening the civil floodgates, the DSM-IV A2 criterion in Criterion A (that the individual's response to a traumatic stressor needs to have included “intense fear, helplessness, or horror”) has been removed in the DSM-5. This could allow anybody who survived an event at issue to claim that they did not experience an immediate traumatic reaction to it but, nevertheless, that they have PTSD. In addition, defense strategies in cases of criminal conduct might use a PTSD defense—the crime that was allegedly committed took place during moments while experiencing the PTSD B3 criterion, in which dissociative reactions could include complete loss of awareness of present surroundings. Other PTSD-related defense strategies in criminal cases could use inappropriately in these regards the relatively open-ended

criteria of anger/irritability and reckless/self-destructive behavior. [For further commentary on the diagnosis of PTSD and its implications for criminality and court, see Hamner (2014) and Soltis, Acierno, Gros, Yoder, and Tuerk (2014).]. As for the civil arena, in which malingering for monetary gain might take place, some PTSD symptoms would be easy to coach, to malinger, or to otherwise take advantage of. For example, even if it not the case that one has valid PTSD symptoms, once coached or otherwise be party to deception, it would be relatively easy to indicate that one has nightmares, flashbacks, startles, avoidance, numbing, anger, extremes in emotions and thoughts, poor sleep, poor concentration, and so on. Scholars have criticized the changes made to the DSM-5, advocating for use of the DSM-IV instead (Hoge et al., 2016). The authors indicated that the scientific review process that led to the changes in the DSM-5 was nonsystematic and its interpretation selective. The changes of the clinical criteria were complex and altered meaning; for example, in the rewording “restricted range of affect” as “persistent inability to experience positive emotions.” In response, Friedman, Kilpatrick, Schnurr, and Weathers (2016) indicated that changes were made in the DSM-5 only with “strong” empirical support. They called for more research in order to make further changes to the DSM PTSD criteria. In this regard, most recently, Franklin et al. (2016) maintained that the symptoms in the D and E clusters in the DSM-5 PTSD symptom list overlap. Specifically, the newly added symptoms D2, D3, and D4 (concerning persistent, heightened negative beliefs, blaming, negative mood, respectively) did not add much to understanding the PTSD profile of the military veterans (N = 320) studied. In the assessment of PTSD, the study used the PCL-5; PTSD Checklist for DSM-5; Weathers, Litz, et al., 2013a). The authors concluded that the newly added D symptoms to the DSM-5 PTSD symptom list are not central and can be removed. Similarly, Vermetten et al. (2016) argued that the inclusion of symptoms in the DSM-5 PTSD symptom list such as those involving persistent negative or distorted beliefs, expectations, or cognitions rely on observer inference rather than more objectively defined symptoms and the changes involved have not been back by solid research. Further, Kilbourne, Kilbourne, and Goodman (2016) queried whether the trauma diagnoses, in general, include systematic error that reduces diagnosing them reliably.

Table 1 Item mapping of DSM-5 PTSD symptoms on various models of DSM-5 PTSD clusters/dimensions/factors (4–7), with core symptoms indicated. DSM-5 symptom

DSM-5 (4)

Dysphoric (4)

Dysphoric arousal (5)

Externalizing behavior (6)

Alternate Dysphoria (6)

Hybrid (7)

Core/Noncore

1. Intrusive memories 2. Recurrent nightmares 3. Dissociative reactions, flashbacks 4. Heightened emotional reactivity to signals 5. Physiological reactivity to reminders 6. Avoids reminders (thoughts, feelings, memories) 7. Avoids external reminders 8. Inability to recall important aspects (“amnesia”) 9. Persistent heightened negative beliefs 10. Persistent self, other blame 11. Persistent negative emotional state 12. Marked loss of interest 13. Detachment 14. Restricted positive affect 15. Irritability, anger 16. Reckless, self-destructive 17. Hypervigilance 18. Exaggerated startle 19. Difficulty concentrating 20. Sleep disturbance

RI RI RI RI RI Av Av Neg. ACM Neg. ACM Neg. ACM Neg. ACM Neg. ACM Neg. ACM Neg. ACM Alt. Ar Alt. Ar Alt. Ar Alt. Ar Alt. Ar Alt. Ar

RI RI RI RI RI Av Av Dys Dys Dys Dys Dys Dys Dys Dys Dys Alt. Ar Alt. Ar Dys Dys

RI RI RI RI RI Av Av Neg. ACM Neg. ACM Neg. ACM Neg. ACM Neg. ACM Neg. ACM Neg. ACM Dys. Ar Dys. Ar Anx. Ar Anx. Ar Dys. Ar Dys. Ar

RI RI RI RI RI Av Av Neg. ACM Neg. ACM Neg. ACM Neg. ACM Neg. ACM Neg. ACM Neg. ACM Ext. B Ext. B Alt. Ar Alt. Ar Dys. Ar Dys. Ar

RI RI RI RI RI Av Av Dys Dys Dys Dys Anh Anh Anh Ext. B Ext. B Anx. Ar Anx. Ar Dys Dys

RI RI RI RI RI Av Av Neg. Aff Neg. Aff Neg. Aff Neg. Aff Anh Anh Anh Ext. B Ext. B Anx. Ar Anx. Ar Dys. Ar Dys. Ar

C NC NC NC NC NC C NC NC NC C NC C NC C NC NC C NC C

Note. The factors are indicated in brackets; RI = Re-experiencing/Intrusion; Av = Avoidance; Neg. ACM = Negative Alterations in Cognitions and Mood; Alt. Ar = Alterations in Arousal and Reactivity; Dys = Dysphoric; Neg. Aff = Negative Affect; Anh = Anhedonia; Ext. B = Externalizing Behavior; Anx. Ar = Anxious Arousal; Dys. Ar = Dysphoric Arousal; C = Core; NC = Noncore. Note. Young (2015a) added another dimension for the PTSD subtype, with depersonalization the core symptom (not derealization).

Please cite this article as: Young, G., PTSD in Court I: Introducing PTSD for Court, International Journal of Law and Psychiatry (2016), http:// dx.doi.org/10.1016/j.ijlp.2016.10.012

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4. Trauma exposure

4.3. Comment

4.1. DSM-5

Levin, Kleinman, and Adler (2014) maintained that the prevalence of PTSD according to the DSM-5 will increase because the gate-keeping Criterion A adds wide-ranging examples of sexual violence as an instigating event to PTSD, unlike the DSM-IV, that limited this category to the example of sexual assault. Further, the traumatic event for the DSM-5 might simply be one that the person is “confronted with” rather than directly experiencing, which will facilitate “bracket creep” (McNally, 2009). At the same time, Levin et al. (2014) noted that, for the DSM-5, the exposure must now include actual/threatened death of family member/friend, which will counteract the bracket creep for indirect exposure. That said, the DSM-5 includes a proviso that allows first responders as part of those susceptible to PTSD, and similar professionals (e.g., police, military, veterans); in their opinion, this addition might augment bracket creep. Finally, for a nonclinical sample (Kilpatrick et al., 2013), Levin et al. noted that the application of the DSM-5 to establish prevalence for PTSD gave a percentage that was about 11.3% lower relative to that for the DSM-IV. The reason for the difference in prevalence in applying different DSM criteria for PTSD over the DSM-IV and DSM-5 especially concerned the removal in the DSM-5 of the example of indirect exposure to the nonviolent death of a loved one. Levin et al. (2014) did not think that removing the A2 criterion about intense horror/fear/helplessness that had been present in DSM-IV will affect DSM-5 prevalence, though (citing Friedman, Resick, Bryant, & Brewin 2011; Pereda & Forero, 2012); however, as mentioned, one could disagree with this hypothesis. Levin et al. (2014) concluded that the changes to PTSD in the DSM-5 will lead to more disability claims. Also, it will be harder to detect malingering (e.g., “increase the potential for”; “may be relatively easy to”). Finally, in practice, the DSM-5 and ICD-11 versions of PTSD might be complementary. In this regard, Kliem et al. (2016) investigated the dimensional compared to categorical nature of the full DSM-IV symptom set compared to the reduced ICD-11 symptom set. The study involved a population of Germans (N = 1,212) who had experienced at least one lifetime traumatic event. Kliem et al. found that, although the full set of DSM PTSD symptoms conformed to a dimensional model, the core six-set one fit a categorical one. They concluded that the two approaches to PTSD nosology (ICD-11, DSM-5) provide different information, e.g., for treatment. That being said, the DSM-5 and ICD-11 might be so different that their differences lead to confusion instead of seeming complementarity. For example, their symptom sets are so different that the patients diagnosed simultaneously with the two sets of criteria receive the PTSD diagnosis in even less than half the time. For example, in this regard, O′Donnell et al. (2014) examined 510 injury patients who had been admitted to four Australian hospitals. They used a structured interview to assess for PTSD 72 months after trauma exposure in these survivors (using the CAPS (The Clinician Administered PTSD Scale; Blake et al., 1995), but with added questions keyed to the DSM5). The data showed that using the DSM-5 compared to the ICD-11 symptom list resulted in a greater prevalence of PTSD with the DSM-5 list (6.7% vs. 3.3%). Moreover, only 42% of the participants met the PTSD criteria for both diagnostic systems. The authors concluded that the ICD-11 PTSD diagnostic criteria might be “too restrictive.” Similarly, Hyland, Shevlin, et al. (2016) found that the ICD-11 was more conservative than the DSM-5 in ascribing PTSD to survivors of childhood sexual abuse. The study on the differential prevalence of PTSD according to DSM-5 and ICD-11 criteria (O′Donnell et al., 2014) has implications for the forensic context, to be sure, but the jury in this regard should stay its decision on the value of the ICD-11 until the nosological system is finalized. For example, it is still being revised by commentary and in field trials (Reed et al., 2016).

Criterion A in the DSM-5 is an entry criterion and it is at the source of much of its controversy (e.g., Andrikopoulos & Greiffenstein, 2012; Rosen & Grunert, 2012). The DSM-5 specifies that, for PTSD to be diagnosed, there needs to be an exposure that involves: actual/threatened death, serious injury, or sexual violence. This has to happen in any of the following ways with respect to the traumatic event: directly experiencing it; personally witnessing it; learning about as it applies to a close family member/friend; or experiencing repeated/aversive exposure to its aversive details (e.g., for first responders, police officers, even if the exposure involved is electronic, at least if it is work-related). In the DSM-IV, Criterion A had two parts, with the first one revised as above and the second one dropped in the DSM-5. In the DSM-IV, Criterion A(1) involves either experiencing, witnessing, or being confronted with the event(s). The event(s) had to involve actual/ threatened death/serious injury or threat to the physical integrity of either self or other(s). Simultaneously, as per Criterion A(2), the person involved had to have experienced either “intense fear, helplessness, or horror.”

4.2. The special case of PTSD in the military This section reviews the differential nature of the trauma experience for military combatants and veterans. Guina, Welton, Broderick, Correll, and Peirson (2016) examined the DSM-5 PTSD criteria as it affects military service members and veterans. They worried that there is overdiagnosis of PTSD in the military but, at the same time, members “desire to under-report symptoms,” for example, due to “negative” career impacts. One class of stressors new to the battle life includes authorizing drone strikes, and its psychological effects (indirect exposure) are discussed. Due to the difficulty in avoidance, PTSD might be diagnosed only as subthreshold minimizing symptoms results also from a sense of stoicism/masculinity in the military. But overreporting might be due to secondary gain/malingering to get benefits. Mota et al. (2016) also emphasized the high burden involved in subthreshold PTSD for military veterans. For example, it is associated with the presence of comorbid psychiatric disorders. In addition, Costanzo et al. (2016) found that higher levels of subthreshold PTSD in combat veterans was associated with increased heart rate and startle responses to danger cues, as well as, among other findings, a greater self-reported depression, anxiety, and functional impairment. Frankfurt and Frazier (2016) reviewed another aspect of trauma exposure in the military, that of moral injury—as per Litz et al. (2009)—or transgressive acts. They lead to more self-injurious behavior (including suicidality), self-handicapping (undermining), and demoralization, including with a greater risk for PTSD. Treatments need to focus on guilt and shame as much as the trauma reaction. Finally, in terms of the risk factors, predictors, and trajectories of PTSD in the military, Guina et al. (2016) noted that symptom report increases until disability is accepted in PTSD cases. Bray et al. (2016) found two classes of veterans in primary care for PTSD after one year—improvers and persisters. Differential factors for the classes were found, e.g., related to degree of combat exposure. In short, this section shows that the nature of the trauma response in military combatants and veterans is quite different than in other populations, although PTSD still can be diagnosed. It points out what is common and unique to this population in this regard in terms of causes, consequences, and treatment of the trauma response than the PTSD. For a most recent source on the topic, see Phelps, Wade, and Forbes (2016).

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That said, the shortcomings of the DSM-5 PTSD symptom list should not be a reason to gravitate automatically to the conclusion that the shorter list in the ICD-11 proposal for PTSD must be better. The research that will be undertaken to compare them will provide the proper empirical evidence for and against each system in its efforts to specify the nature of PTSD. Until proven otherwise, the forensic psychologist should continue to use the DSM-5, but remain cognizant of the approach in the ICD-11 that will be published in 2018, even if for the sole purpose of being able to justify one's use of the DSM-5 for the task of diagnosis of PTSD for court. 4.4. Exposure prevalence This section of the article is the first to examine in depth recent empirical research on aspects related to PTSD. Being diagnosed with PTSD presumes that a traumatic stressor causally induced it. Miller (2015) noted that the lifetime prevalence of exposure to events that are traumatic is up to 60%. Norris and Slone (2014) reported another review of trauma exposure and PTSD, with the estimate up to 90% (Breslau et al., 1998; Kilpatrick et al., 2013). Perhaps the best study on the epidemiology and prevalence rate of PTSD is the following one. Goldstein et al. (2016) conducted an epidemiological investigation of the prevalence of DSM-5 PTSD using the American National Epidemiologic Survey on Alcohol and Related Conditions-III (NESARC-III; Grant et al., 2014; N = 36,309). PTSD was assessed through a more general interview schedule (AUDASIS-5; Alcohol Use Disorder and Associated Disabilities Interview Schedule— Diagnostic and Statistical Manual of Mental Disorders, 5th ed. version; Grant et al., 2011). The criteria for PTSD that were used in the study were conservative, such that milder cases could have been missed. Also, the authors noted, as has been done by others, as mentioned, that the DSM-5 criteria include a narrower range of Criterion A qualifying events than in the DSM-IV. The results in the Goldstein et al. (2016) epidemiological study indicated a lifetime prevalence rate of traumatic event exposure of 68.6%, with the percentage larger for those with PTSD. The most frequent categories of exposure to traumatic stressors involved the following: reports of childhood sexual abuse; seeing a dead body/body parts; intimate partner violence victimization; and personal serious/ life threatening injury/illness. PTSD respondents added reported exposure to another's serious injury. Note that these types of traumatic exposures include major ones relevant to the context of psychological/ psychiatric injury and law. Benjet et al. (2016) noted that traumatic event exposure has negative impacts on mental health, but little research has been conducted on the predictors of traumatic event exposure. They conducted an epidemiological study using the World Mental Health Survey Consortium (e.g., The WHO World Mental Health Survey Consortium, 2004). They analyzed 29 types of traumatic events in a combined sample of 68,894 individuals over 24 countries. More than 70% of the sample experienced self-reported traumatic event exposure, with almost half of those who had been exposed experiencing at least four such events. Of the five major types of trauma involved, three related to the personal injury context—witnessing death/serious injury, being in a life-threatening motor vehicle accident (MVA), and experiencing a life-threatening injury/illness. The strongest associations involved the variable of revictimization (or interpersonal violence predicting later interpersonal/ sexual violence). These results are consistent with the DSM-5's definition of traumatic event as exposure to threatened death, serious injury, or sexual violence. Childhood trauma exposure predicts mental health outcomes into young adulthood. Ballard et al. (2015) used Latent Class Analysis (LCA) in a sample of 1,815 community-based participants who were followed from 13 years of age and then anywhere from 19 to 29 years of age in terms of the effects of nine types of traumatic experience before the age of 13. The trauma types were based on the trauma criterion

of the DSM-IV. As for the measures in the study, parent and personal problem and psychopathological behavior and personal health outcome were assessed in interview and analysis of records. About the results in Ballard et al. (2015), the primary class in LCA was labeled low childhood trauma, and its prevalence was 84%. The other two classes were violence exposure (more in males) and sexual assault (more in females), both at 8% prevalence. The former group reported witnessing violence, physical assault, physical injury, and sudden death of a close friend/family member, in particular. As for the latter group, its members reported sexual assault or knowing someone who had experienced it, in particular. The former group experienced the outcome of both PTSD and antisocial personality disorder, while the latter group reported a wide range of psychiatric outcomes. Parental psychopathology was associated more with the latter group. It is instructive to look at Table 4 in the article by Ballard et al. (2015) that shows that PTSD was much more prevalent in the sexual assault (female) group, even if the pattern of the findings was for a general vulnerability for this group. In terms of traumatic exposure in the DSMs, and how they condition the diagnosis of PTSD, Miller et al. (2014) noted that changes to the event criteria in the DSM-5 for PTSD permits cumulative trauma as part of the event indicators of PTSD. Moreover, different events could be linked to different symptoms. Graham et al. (2016) argued that there might be multiple subtypes of PTSD, depending on the trauma. There is not a uniform cumulative trauma that people experience that bears a dose–response relationship with PTSD symptom severity, such that the only difference from one case to the next is the degree that the PTSD is expressed. That being the case, May and Wisco (2016) distinguished the effects of level of exposure and proximity to the exposure in the risk in developing PTSD generally. 4.5. Comment The research that has been reviewed generally supports the prevalence of lifetime trauma exposure toward 70%. Goldstein et al. (2016) found a lifetime prevalence rate of traumatic event exposure of 68.6%, with the percentage larger for those with PTSD. The most frequent categories included those relevant to the DSM-5 PTSD entry Criterion A, which is a finding also found in the study by Benjet et al. (2016). Also, a good portion of the types of traumatic exposure that people experience relate to those concerning tort and related venues, such as worker compensation, e.g., due to physical injuries. Nevertheless, trauma experience type for the population also involves those that would be considered pre-existing in this context, e.g., childhood sexual abuse. This research finding indicates that pre-existing factors need to be assessed carefully in any diagnosis of PTSD and complicate the attribution of causality to any negligent act at issue and the psychological consequences (e.g., PTSD) attributed to it. Overall, the current literature supports that trauma exposure is prevalent and has deleterious effects but, at the same time, many individuals seem resilient when confronted with trauma, given that the lifetime prevalence of trauma exposure far exceeds the lifetime prevalence of PTSD. Nevertheless, it has been found that fresilience is not very common when one is confronted with “major” life stressors (Infurna & Luthar, 2016). It would be instructive to determine the relationship between trauma type and subsyndromal PTSD, as well. For example, Brancu et al. (2016) have shown that subsyndromal PTSD can be just as impairing as full-blown PTSD. Also critical, the role of appraisal and personal perceptions of trauma need to be considered; in this regard, the subjective experience of trauma might be a factor in trauma exposure aside from the objective degree of trauma in the experience. For example, Pinto, Henriques, Jongenelen, Carvalho, and Maia (2015) considered that perceived threat is the critical variable in determining trauma effects (in fire fighters).

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Finally, consider that there is little research on parsing out valid psychological effects from invalid (e.g., malingered ones) in these types of epidemiological surveys of traumatic exposure. The same lack is evident in each of the major sections reviewed in the present article. For example, the next section deals with the prevalence of PTSD, but in the research the complications presented by malingered and related confounds do not seem addressed for the most part, unless that is the direct topic of the research. Moreover, some of the estimates are widely varying with respect to prevalence of PTSD, which illustrates the difficulty in pinning down the prevalence of PTSD to narrow-band estimates. Granted, some of the issues in determining the base rate of PTSD in the research relate to using different types of populations, different procedures and tests to assess PTSD, and different statistics. Nevertheless, the lack of a definitive answer to the question of PTSD prevalence complicates dealing with it in court. This is especially true for estimates of the prevalence of malingered PTSD presentation, as shall be shown. 5. What is PTSD's prevalence? 5.1. Lifetime Miller (2015) noted that the lifetime prevalence of PTSD is as much as 20%. For Ali, Jabeen, and Alam (2015), the prevalence of PTSD for the general public is as high as 15%, whether in terms of the DSM-IV or DSM-5 (e.g., Ingram, Dowben, Froelich, & Keltner, 2012). Miller et al. (2013), though, found estimates between 9 to 10% using the DSM-IV and DSM-5 criteria (respectively, 9.1%, 9.8%). For Norris and Slone (2014), the lifetime risk for PTSD is in the order of 8% to 12% (citing Breslau, Davis, Andreski, & Peterson, 1991; Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995; Resnick, Kilpatrick, Dansky, Saunders, & Best, 1993). For the prevalence of PTSD in the above-mentioned study by Goldstein et al. (2016), they found that past-year and lifetime prevalence rates were 4.7 ± 0.17% (standard error, SE) and 6.1 ± 0.21%, respectively. For a more liberal definition of PTSD, lifetime prevalence increased to 10.7 ± 0.21%. The authors concluded that in terms of the criteria of the DSM-5 for PTSD, it is prevalent. Moreover, other data in their study indicate that it is highly comorbid. 5.2. Course In terms of course, Miller (2015) noted that, within three months of their trauma exposure, about 50% of PTSD patients “largely” have their symptoms “resolved” (e.g., Sweet, 2009). Moreover, at 18 months, only 15% still have clinical or functional symptoms that are disabling (e.g., Dyregrov & Regel, 2012). That being said, according to Miller (2015), comorbidity rates are found up to 98% and, in MVAs, comorbid mTBI and chronic pain complicate recovery. Goldstein et al. (2016) also found associations across PTSD and comorbidity, and disability (and delay in treatment seeking). Similarly, Bromet et al. (2016) showed that PTSD in World Trade Center responders over 10 years after the attack of 9/11 (2001) was most often associated with PTSD avoidance and hyperarousal symptoms and with long term decreased health, subjective well being, and life satisfaction. Cusack et al. (2016) noted that extreme traumatic stressors produce PTSD symptoms “almost always” within days, with up to 33% developing PTSD (Committee on Treatment of Posttraumatic Stress Disorder & Institute of Medicine, 2008). Generally, 10% to 20% of those diagnosed with PTSD develop a chronic and unremitting course (Fletcher, Creamer, & Forbes, 2010; Norris & Slone, 2007). Shalev and Bremner (2016) described two competing models for explaining the persistence of the course of PTSD among survivors, once it is initiated. The first model concerns the extent of the initial trauma response to the triggering event, which they described as

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“abnormal.” The second model for the persistence of PTSD concerns later in its course; this model involves progressive desensitization as the CNS (central nervous system) gradually alters. Also, they noted that pretrauma factors also influence the course of PTSD.

5.3. Context Estimates of PTSD vary with context and country, as well as type of claim or survivor. Creamer, Burgess, and McFarlane (2001) found a 12-month prevalence rate of only 1% in Australia, and with comparable figures in Canada and the U.S. being at 2 and 3%, respectively (Stein, Walker, Hazen, & Forde, 1997; Kessler & Üstün, 2008, respectively). Ali et al. (2015) noted that 14% of work-related injury claims involve PTSD or other stress-related diagnoses (e.g., Hall & Hall, 2007). The prevalence of PTSD in MVA survivors is in the range of 25–33% (e.g., Bryant, Harvey, Guthrie, & Moulds, 2000; as cited in Zhang et al., 2015). Sun et al. (2015) maintained that PTSD “occurs most frequently” after MVAs, affecting 8.5 to 23.1% of survivors at six months (Hamanaka et al., 2006; Yasan, Guzel, Tamam, & Ozkan, 2009). Stein, Karam, et al. (2016) conducted a cross-country survey of the effects of life-threatening MVAs, and they found a prevalence rate of 2.5% for PTSD (N = 58,335, from 12 countries, including eight with low income). However, it is not clear how long after the MVAs in question PTSD was assessed. PTSD was evaluated using the Composite International Diagnostic Interview (Kessler & Üstün, 2004). PTSD was associated both with pretrauma and trauma factors (respectively, for pretrauma: low education, childhood family adversities, other MVAs, and amount of prior anxiety disorders; and for the accidents, death to another, or serious injury, including to oneself). Heron-Delaney, Kenardy, Charlton, and Matsuoka (2013) reviewed 35 studies on PTSD prevalence rate after MVAs, and furnished estimates largely in agreement with the percentages provided in the research that followed their review. The range of the rate of PTSD prevalence at 12 months post-MVA over the studies was estimated at 7–26%, with 1-month prevalence at up to 45%. These values are greater than the general prevalence rate for PTSD. The predictors of PTSD in the research reviewed (44 unique studies) by Heron-Delaney et al. (2013) did not involve injury severity, which is consistent with the model that cognitive appraisal of the trauma is a greater factor in predicting PTSD development than physical injuries, per se. Also, litigation/compensation involvement was a predictor of PTSD, which was attributed to constant reminders in the insurance/litigation process and to its stress. Other PTSD predictors included post-event rumination about the event, perceived threat to life peritraumatically, and previous emotional problems/ anxiety disorder (but nor prior PTSD or psychiatric illness, for example). Wise and Beck (2015) noted that 6 to 32% of first responders exposed to a traumatic event develop PTSD (citing McFarlane, Williamson, & Barton, 2009). For these workers who are exposed to natural disasters, the 2-year prevalence rate is toward 50% (Galea, Nandi, & Vlahov, 2005). For workers, in general, in related work (e.g., police officers, ambulance workers), the rate of PTSD is toward 20% (Halpern, Gurevich, Schwartz, & Brazeau, 2009; Marmar et al., 2006). Rosellini et al. (2015) gave another range of estimates of PTSD prevalence, this time for 30-day prevalence in military personnel. The estimates were in the 4% range. As for prevalence changes due to changing criteria in the DSM-5 relative to the DSM-IV-TR, after citing the Kilpatrick et al. (2013) finding, Miller et al. (2014) presented evidence that, in contrast to the findings of Kilpatrick et al. (2013), other estimates report marginal increases in PTSD using the DSM-5 compared to the DSM-IV-TR (Calhoun et al., 2012; Carmassi et al., 2013; Elhai et al., 2012; and Miller et al., 2013; only for current prevalence for lifetime PTSD).

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5.4. Comment To conclude, the recent research on PTSD prevalence varies in its estimates, and contextual factors as well as methodological ones in the research appear critical to this variation. That being the case, the estimates of PTSD prevalence are not miniscule. The recent research generally supports the view, at least in terms of the more conservative percentages cited, that the lifetime prevalence of PTSD is toward 10%. Also, about 10% persist in experiencing it. For serious traumatic exposures, including in MVAs, the percentages might be higher, especially initially. Finally, as mentioned, contextual factors create variations in these and related PTSD prevalence estimates. From a forensic perspective, researchers need to establish the rate of malingered PTSD presentations, which has been estimated anywhere from 1 to 50% in personal injury claims, as per the brief introduction on the topic given next. 5.5. Malingered PTSD In terms of invalid claims, for Ali et al. (2015), as many as 20 to 30% of PTSD personal injury claims involve feigning (e.g., Guriel & Fremouw, 2003). Estimates of malingered PTSD range from 1 to 50% (e.g., Frueh, Grubaugh, Elhai, & Buckley, 2007; Resnick, 1999), which indicates the complexity in malingering determinations and why any estimate is likely to be controversial. The third article in the series of three on PTSD in Court deals with malingered PTSD in more depth (Young, 2017b). 5.6. Comment The next section of the article analyzes in depth the symptom structure of PTSD, including complications deriving from its changes relative to the DSM-IV and research showing that its 20 symptoms in the DSM-5 do not appear to organize according to its four-cluster model. One could ask whether this research invalidates the reliability and validity of PTSD, especially for court and related purposes, as presented in the DSM-5. 6. DSM-5 PTSD 6.1. The DSM-5 PTSD symptom changes As briefly alluded to in the above, the major changes from the DSMIV(− TR) to the DSM-5 for PTSD in the adult concern the number of symptoms, being revised from 17 to 20. To arrive at this new number of PTSD symptoms, one was dropped—on a sense of foreshortened future—and four were added—concerning persistent heightened negative beliefs, persistent self/other blame, persistent negative emotional state, and recklessness/self-destructiveness. The change in the dimensional structure in the DSM-5 are given specifically next. The move from three clusters in the DSM-IV to the four in DSM-5 involves changing the DSM-IV clusters of re-experiencing, avoidance, and hyperarousal to the DSM-5 ones of re-experiencing, avoidance, negative alterations in cognition and mood, and hyperarousal. In addition, as mentioned the DSM-5 adds the dissociative subtype. Moreover, in the DSM-5, there are fundamental changes in understanding the nature of PTSD. In particular, the latter class of changes includes: placing it in a chapter on trauma and stressor-related disorders; [and as well, as mentioned, removing from the A criterion the need for a reaction involving intense fear, helpless, or horror to the event at issue; and adding to the range of events that could elicit PTSD]. Levin et al. (2014) noted that the disorder is easier to malinger with the range of changes made in the DSM-5 and the deletion of the advisory that malingering should be considered in PTSD cases, which had been part of the text for the DSM-IV-TR. It was removed without explanation in the DSM-5. [Indeed, the term malingering is no longer in the subject index of the DSM-5 (Young, 2013, 2016).]

Some research has supported the four-factor structure of the symptoms in the DSM-5. However, the results do not necessarily support the four factors as proposed in the DSM-5. Miller et al. (2013) conducted internet-based surveys on PTSD using the DSM-5 list of 20 symptoms as criteria. Factor analysis confirmed a four-factor structure of these 20 symptoms, but not in the way found in the DSM-5. The DSM-5 model has simply split the avoidance and numbing symptoms in the DSM-IV, but the competing Simms, Watson, and Doebbelling (2002) model that was supported by Miller et al. (2013) had suggested a rejuggling of the symptoms in terms of a primary dysphoria factor. Other results in Miller et al. (2013) questioned inclusion of the “psychogenic amnesia” and the “reckless/destructive behavior” symptoms in any of the factors or clusters in the DSM-5. Later in the article, I analyze the many studies that have suggested different factor structures/clusters/dimensions for the 20 DSM-5 PTSD symptoms, ranging from four to even eight of them. This queries the validity of the DSM-5 model of PTSD, although I argue not of the validity of the PTSD concept itself. That said, the validity of that concept depends on reliable research on its reliability and validity. As briefly mentioned above, the following suggests that the DSM-5 criteria for PTSD might not have been appropriately field-tested, which presents major challenges, if not inconveniences and major doubts, related to its validity. Specifically, although putatively the DSM-5 field trials were conducted to ascertain its reliability, I noticed that criteria in the 2010 draft proposal for PTSD that were field tested in 2010–2011 were altered in the 2013 DSM-5's final version (and without further field testing with the changes; Young, 2013, 2016). For example, relative to the draft version, in the final version of the DSM-5 for symptom CI, the terminology of “internal reminders” was changed to “distressing,” “physical sensations” to “memories” (closely), and “arouse recollections” to “associated with.” For Clusters D and E, the number of polythetic criteria needed for threshold had been three of them, but, in the DSM-5, it was changed to two of them. For Cluster E, alteration was changed to “marked” alteration. In E, “aggressive behavior” was changed to—angry outbursts, with little or no provocation, typically expressed as verbal or physical aggression toward people/objects. These indicated changes, as well as others from the draft to the final version of the DSM-5, are not only highly problematic, for example, forensically, but also might lack the required reliability and validity needed for clinical and related purposes. Friedman et al. (2016) acknowledged that there were no extensive field trials on the final version of the DSM-5 for PTSD. Consequently, Kilpatrick et al. (2013) as well as Miller et al. (2013) conducted web surveys with representative American adults and also a sample of veterans using questions intended to capture “the intended meaning” of the PTSD symptoms in the draft version of the DSM-5. The results of these studies were used to “finalize” the wording of the PTSD symptoms in the DSM-5. This account of the DSM-5 work group in charge of establishing the PTSD criteria confirms that the final version in use in the DSM-5 for its PTSD criteria has never been tested for its psychometric reliability let alone its validity. To conclude, PTSD in the DSM-5 involves multiple changes to its entry criterion (A) as well as its symptom criteria (B–E). These changes present multiple forensic difficulties. In addition, the four-cluster model used by the DSM-5 to organize its 20 symptoms has not been uniquely supported in the literature, as documented in depth next. 7. What are PTSD's clusters or dimensions? 7.1. Reviews The cluster structure of DSM-5 PTSD symptoms has been subjected to empirical investigation using Confirmatory Factor Analysis (CFA) that shows that the four-cluster model in the DSM-5 might be supported to some extent (see Table 1), but less than other ones.

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Armour et al. (2015) especially found a seven-factor solution (replicated by Wang, Zhang, et al. (2015a)). Young (2015) reviewed these models, and even proposed an eight-cluster model, with the eighth one involving the dissociative subtype in the DSM-5 that is displayed by a minority of trauma survivors. Other research has supported a five-factor dysphoric arousal model (after Elhai et al., 2011) and also six-factor model (two types: Liu et al., 2014; Tsai et al., 2015; the former is a dysphoric arousal model and the latter an externalizing one for the sixth factor found). Armour, Műllerová, and Elhai (2016) conducted a narrative systematic literature review of the latent structure of PTSD dimensions that have emerged in the research using criteria in the DSM-IV and DSM-5 (American Psychiatric Association, 2013). In this type of research, the statistic of choice in comparing dimensional models is CFA. It includes model comparison statistics for both nested and unnested comparisons, including chi-square. According to Armour et al. (2016), for the DSM-IV, the predominant data-fitting models are the four-factor emotional numbing model (King, Leskin, King, & Weathers, 1998) and the four-factor dysphoria model (Simms et al. 2002), with the five-factor dysphoric arousal model (Elhai et al., 2011) gaining prominence. The original DSM-IV model had three clusters and the DSM-5 one has four, which resemble the emotional numbing model. Armour et al. (2016) included 112 articles in their review, involving 144 samples. Only 13 of these articles examined the dimensional structure of the DSM-5, which took place across 14 samples. The remainder of the studies, or most of them, examined the dimensional structure of the DSM-IV PTSD symptoms. As for the results in Armour et al. (2016), 40 samples included study of the fit of a one-factor structure. It demonstrated poor fit, suggesting that PTSD is multi-dimensional. Similarly, two-factor and three-factor models did not fare well in comparison to four- and five-factor models. When different four-factor models were compared, there was a slight advantage for the dysphoria model compared to the emotional numbing one, but neither provided any better fit to the data than the five-factor dysphoric arousal model. The latter model indeed outperformed all other models for the DSM-IV. For studies on the DSM-5, once more, models with less than four factors did not fit well with the data. The few studies comparing fourfactor models found marginal support for the emotional numbing one. Other models with more than four DSM-5 factors provided a superior fit compared to any four-factor ones. There have been five different five-factor models that have been proposed and the mostly widely studied is the dysphoric arousal one. Generally, it fits better the data when compared to any four-factor model. As for six-factor models, two have been proposed and they fit better than lower-number factor models. However, they do not fit as well compared to the seven-factor model (intrusion, avoidance, negative affect, anhedonia, externalizing behavior, anxious arousal, dysphoric arousal; the hybrid model; Armour et al., 2015). The research conducted since the review by Armour et al. (2016) generally supports their conclusion that the seven-factor model is the best fitting one for the DSM-5 PTSD symptoms. This does not deny the adequacy of the DSM-5 cluster structure for clinical and forensic purposes, but points to directions toward its improvement. The literature review that follows includes all the research on the question of DSM-5 PTSD symptom structure since Armour et al.'s (2016) review, and that review is given next. On the one hand, they did not review research conducted in 2016 and, on the other hand, they did not review the research that came out after the seven-factor hybrid model was established in 2015. 7.2. Seven-factor model Blevins, Weathers, Davis, Witte, and Domino (2015) conducted a psychometric evaluation of the PCL-5. The first study in their research

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involved undergraduates (N = 278). The PCL-5 demonstrated the requisite reliability and validity. As for its dimensional structure, the DSM-5 four-factor model indicated adequate fit. However, the sixfactor anhedonia model and the seven-factor hybrid one equally showed a superior fit. The same results were found in a second study (N = 558). It is noteworthy that MVAs constituted the most prevalent traumatic exposures in these studies, with other tort type events also involved (e.g., life-threatening injury, another person injured or accidentally dying). Mordeno, Carpio, Nalipay, and Saavedra (2016) investigated the latent factor structure of DSM-5-based PTSD symptomatology in a sample of hurricane survivors. Aside from supporting the seven-factor model as the best fit to the data, the study also related differential patterns of posttraumatic cognitions to its seven dimensions. For example, negative self-cognitions consistently predicted the severity of PTSD, and the same finding has been found in MVA survivors (Meisser-Stedman, Dalgleish, Glucksman, Yule, & Smith, 2009). As for the specifics of the Mordeno et al. (2016) study, it used the PCL-5 and the PTCI (Posttraumatic Cognitions Inventory; Foa, Ehler, Clark, Tolin, & Orsillo, 1993) to measure PTSD and posttraumatic cognitions, respectively. Of the participants (N = 632), 46% met the PCL-5 cut-off for PTSD. In terms of the dimensional models tested for best fit, the seven-factor model was not the only one tested and it proved superior in fit relative to all others. As for the relationship of the dimensions in this model to post-event cognitions, the results showed differential relations such that the seven dimensions should be considered psychological “distinct” even if they are related. Specifically, negative self-cognitions related most to the dimension of dysphoric arousal and negative world-cognitions related most to that of anxious arousal. Also, the externalizing dimension was predicted most by negative self-cognitions, but without another type of cognition involved (unlike the case, as had been shown above, for dysphoric arousal and anxious arousal). Further, the dimension of negative affect was predicted not only by negative self- and world-cognitions, but also by the third component of post-event cognition, that of selfblame. These relationships among cognitions and dimensions of PTSD were present for avoidance, but less so compared to other dimensions described in these regards. In addition, anhedonia was predicted by negative self-cognitions only, which is not unlike the case for externalizing behavior. Finally, intrusion was predicted by both negative selfand world-cognitions, as found with dysphoric arousal and anxious arousal. As a comment, I note that these results support the argument for the distinctiveness of the PTSD seven-factor hybrid model, but not as clearly as maintained by the authors. Seligowski and Orcutt (2016) also provided empirical support for the seven-factor DSM-5 PTSD symptom model. They examined 403 adults in a community sample using the PCL-5, with the sample acknowledging exposure to at least one traumatic event (e.g., sexual assault, an MVA). About 9% of the sample met the PCL-5 criterion for PTSD. The results not only showed superior fit of the seven-factor model to the data when compared to six-factor and five-factor models, but also showed that the factors statistically related to each other and to both the Negative Affective and Positive Affect components of the PANAS (Positive Affect and Negative Affect Schedule; Watson, Clark, & Tellegen, 1988). These results in Seligowski and Orcutt (2016) do not provide results in the association across the seven factors involved and affect that would support the distinctiveness of each of the seven dimensions, in contrast to the implications of the results found in Mordeno et al. (2016), as reviewed above. Carragher et al. (2016) tested the fit of eight different models of PTSD DSM-5 symptomatology in 622 Australian adults who reported having experienced a traumatic event. Of the models, the DSM-5 fourfactor model, the six-factor anhedonia model, and the seven-factor hybrid model “provided a strong fit to the data.” The study was conducted using a self-report online survey using a PTSD assessment procedure based on the DSM-5. Also, other internalizing and externalizing

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disorders were queried. This latter supplementary analysis revealed that all PTSD factors appear related to non-specific distress. 7.3. Comment Research conducted since the reviews of Young (2015) and Armour et al. (2016) generally support the seven-factor model of PTSD for DSM5 PTSD symptoms. However, other models also fit the data gathered in the research. The variations in DSM-5 PTSD dimensional fit could be due to population studied, assessment procedures used, and statistics employed, as well as contextual factors. There might not be one best dimensional model of PTSD that fits all populations and contexts. Nevertheless, that the original DSM-5 four-factor model has serious competing models is important forensically. For example, as far as is known, currently available tests of PTSD do not consider factor structure other than as described in the DSMs. 7.4. Other factor models Not all the research on model fitting of the dimensions in DSM-5 PTSD symptoms reveals support for the seven-factor model. As mentioned, among other factors, the results might depend on the samples and measures used. Therefore, in the research being conducted on the DSM-5 PTSD symptom list factor structure, some models with more than the standard four-factor one in the DSM-5 should not be taken to indicate that the DSM-5 symptom structure cannot serve any useful purpose because the research data do not fit it at all or do not provide the best fit. That being said, it is rare to find support for the current DSM-5 PTSD symptom four-cluster model. This point is illustrated in the following review of other research on the question. Forbes et al. (2015) investigated the factor structure of the DSM-5 PTSD symptoms as assessed by gold standard interview techniques (using a DSM-5-modified CAPS). They tested the fit of two four-factor structures in their sample of 570 trauma injury survivors 6-years post injury (the DSM-5 one; the dysphoria one). Both fit well, but they investigated a two-factor structure, as well. Competing models with more than four-factors were not tested for fit, which limits the value of the research. Using Exploratory Factor Analysis (EFA), McSweeney, Ellen, Koch, Saules, and Jefferson (2016) found that a five-factor solution best fit the DSM-5 PTSD criteria, as assessed in samples of college students and Mechanical Turk survey respondents (N = 113,177, respectively). The LEC-5 (Life Event Checklist for DSM-5; Weathers, Blake, et al., 2013b) assessed for traumatic event exposure and the PCL-5 for PTSD (with over 30% reaching PTSD criteria). The authors suggested followup research using CFA. Byllesby, Durham, Forbes, Armour, and Elhai (2016) examined a sample of 186 nonclinical trauma-exposed participants for their DSM-5 PTSD symptom factor structure, using the PCL. The five-factor dysphoric arousal model fit the data better than any four-factor model tested. Models with more than five-factors were not examined. Witte, Domino, and Weathers (2015) showed that the five-factor model fit PTSD DSM-5 symptomatology in trauma-exposed undergraduates (N = 1,311) whether the PCL-5 or the DAPS (Detailed Assessment of Posttraumatic Stress; Briere, 2001) is used to assess PTSD symptoms (they differ in symptom order presentation). Other models were not tested for fit. Konecky, Meyer, Kimbrel, and Morissette (2015) conducted a study of DSM-5 PTSD symptoms in trauma-exposed Iraq/Afghanistan war veterans (N = 258). About half met the criteria for the 17-symptom DSM-IV PTSD symptom list, based on CAPS-IV (Blake et al., 1995). DSM-5 PTSD symptomatology (20 symptoms involved, unlike the 17 in the DSM-IV-TR) was determined using a modified version of the PCL-5 (Blevins, Weathers, Witte, & Davis, 2012; Weathers, Litz, et al., 2013a).

The results of the Konecky et al. (2015) study supported the sixfactor dysphoric arousal model (the factors being intrusion, avoidance, negative affect, anhedonia, anxious arousal, and dysphoric arousal, which they preferred to label as anhedonia). The authors stated that the seven-factor model (which, as mentioned, adds an externalizing factor to the six-factor anhedonia dysphoric arousal model by splitting off two symptoms) was not supported due to the small sample size, in particular. Zelazny and Simms (2015) tried to replicate the seven-factor model as found by Armour et al. (2015) and replicated by Wang, Zhang, et al. (2015a), with a group of interviewed psychiatric patients reporting either DSM-5 criterion A trauma or traumatic life event (N = 310,284, respectively). The authors compared the seven-factor model to other four-, five-, and six-factor models (respectively, four-factors: DSM-5, dysphoria; Simms et al., 2002; five-factors: dysphoric arousal; Elhai et al., 2011; six-factor: anhedonia; Liu et al., 2014, externalizing; Tsai et al., 2015; and their own “experimental” novel model; i.e., called “alternate dysphoria”, which recombines sleep and concentration problems into the broader dysphoria cluster, e.g., negative, blame, fear). They found support for the latter model, as shown next. As for the measures used in the study by Zelazny and Simms (2015), they involved the MINI-6 (Mini-International Neuropsychiatric Interview 6; Sheehan et al., 1998), the WHODAS-11 (World Health Organization Disability Assessment Schedule II-12 Item Version; World Health Organization, 2001), and the PID-5 (Personality Inventory for DSM-5; Krueger, Derringer, Markon, Watson, & Skodol, 2012). Among all the models that were tested, the results supported a slightly better fit for the authors' experimental six-factor model compared to the seven-factor one, at least for the BIC test criterion (Bayesian Information Processing), with no significant gain from the fit for their six-factor model to the seven-factor one using other criteria. According to the authors, the limits of the study included lack of information on the number of traumas experienced. Aside from the empirical findings relating sleep and concentration problems to the likes of being negative, blaming, and having fear, there needs to be a better conceptual understanding than the one used of “alternate dysphoria” for describing their experimental sixth factor. Moreover, perhaps a larger sample might give a seven-factor solution.

7.5. DSM-IV dimensions As for DSM-IV keyed studies, Biehn et al. (2016) found that the fourfactor Simms et al. (2002) dysphoria model fit military veteran PTSD (per the DSM-IV), and noted that comorbid AUD (alcohol use disorder) appeared as one additional factor. A study by Arbona, Fan, and Noor (2016) on the DSM-IV PTSD factors structure in African American male firefighters supported the fourfactor emotional numbing model more than the four-factor dysphoric arousal model or the five-factor dysphoria model. Models with more than five factors were not tested. Frankfurt, Anders, James, Engdahl, and Winskowski (2015) examined veterans' PTSD factor structure, using the DSM-IV keyed PCL-C in assessing PTSD. They did not test for more than four-factors. The fourfactor dysphoria model fit best. This study is worth noting because of the application of a combined dimensional-categorical statistical approach referred to as factor mixture modeling (FMM), which revealed a low symptom class and a moderate symptom class in conjunction with the four factors. In cases of suspected acute coronary syndrome, as studied by Sumner et al. (2015), the best-fitting dimensional structure of PTSD according to CFA involved the four-factor dysphoria model (Simms et al., 2002). Models with more possible dimensions were not tested. Contractor et al. (2015) tested for the five-factor model in Hispanic and Caucasian clinic-referred youth. In support of the generalizability of the model, they found no difference across samples in factor structure

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(for the assessment of PTSD, they used the PTSD-RI (reaction index); Steinberg, Brymer, Decker, & Pynoos, 2004). Lee, Witte, Weathers, and Davis (2015) also supported the fivefactor model of PTSD for a DSM-IV keyed assessment. They used the TLEQ (Traumatic Life Events Questionnaire; Kubany et al., 2000) to assess trauma exposure and the PCL to assess PTSD symptoms. Gootzeit, Markon, and Watson (2015) developed a 37-item trauma response test (ITRI; Iowa Traumatic Response Inventory) that revealed a five-factor structure (intrusions, avoidance, dysphoria, dissociation, hyperarousal). In research with patients and students, correlations with other tests indicated that only the factors of intrusion and avoidance are “specific to PTSD” (as assessed by the PCL). Hetzel-Riggin and Harbke (2014) tested college students who had reported a traumatic event and used the DSM-IV consistent measure of PTSD, the PTSD-Q (Posttraumatic Stress Disorder Questionnaire; Cross & McCanne, 2001). They compared the first-order and secondorder fit of the four-factor numbing model (King et al., 1998), the four-factor dysphoria model (Simms et al., 2002), and the five-factor dysphoric arousal model (Elhai et al., 2011). For the first-order level, CFA determined that the latter five-factor model was the best fit of the data. For the second-order level, the first-order numbing model fit the two-factor second-order model of avoidance and numbing, the firstorder level dysphoria model fit a single-factor second-order general PTSD model, and the first-order dysphoric arousal model did not fit well with any second-order model. These results imply that the five dimensions in the dysphoric arousal model might represent separate types of PTSD. 7.6. Comment The nature of the dimensional structure of PTSD symptoms depends on the models tested (not all the models found in the literature might be compared in any one study); the DSM used to key the symptoms (DSMIV, 17 symptoms; DSM-5, 20 symptoms); the population examined (e.g., civilian or military; external event trauma-exposed or other); the assessment procedures and test used, and a host of other variables (sample size, culture, their gender, etc.). To summarize this section, although the symptom structure of PTSD in the DSM-5 has not found a universally supported alternative in the research, there is little support for the four-cluster solution used in the DSM-5. Furthermore, the research often supports seven-factor solution and, beyond that, it could be argued that an extra eighth one seems evident in the dissociative subtype (Young, 2015). 8. Dissociative PTSD subtype Miller et al. (2014) cited evidence in support of the addition of the dissociative PTSD subtype to the DSM-5. For example, Wolf, Miller, et al. (2012) found that, in a Latent Profile Analysis (LPA), veterans and their partners belonging to a “severe” PTSD class that included “marked” dissociative symptoms exhibited more frequent/intense flashbacks and also a history of sexual abuse (in childhood or the adult period; replicated in Wolf, Lunney, et al., 2012; Steuwe, Lanius, & Frewen, 2012, and more elaborately by Stein et al., 2012). The dissociative subtype might be characterized by an overmodulation in response to trauma cues (e.g., Lanius, Brand, Vermetten, Frewen, & Spiegel, 2012), rather than an undermodulation, which might be associated with non-dissociative PTSD. Bennett, Modrowski, Kerig, and Chaplo (2015) investigated 225 adolescents detained in a juvenile detention center. They were 12 to 18 years of age and met the criteria for full or partial PTSD using the PTSD-RI, adolescent version (The University of California Los Angeles Posttraumatic Stress Disorder Reaction Index; Steinberg et al., 2004). Adolescent dissociation was measured using the A-DES (The Adolescent Dissociative Experiences Scale; Armstrong, Putnam, Carlson, Libero, & Smith, 1997). The findings showed two types of dissociative groups

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(high, N = 20; low, N = 205), with the high group exhibiting more depersonalizing/derealizing signs, as would predict the DSM-5 (e.g., also more numbing, intrusion, emotional dysregulation, dissociative amnesia, absorption, imaginative involvement, and passive influence). Further, regression analysis pointed to peritraumatic dissociation at the time of trauma as a factor in the expression of dissociative symptoms more generally months to years after the trauma. Overall, the authors supported the validity of the dissociative subtype for PTSD in the DSM-5. Frewen and Lanius (2014) presented a model that helps understand the dissociative subtype of PTSD. Their model of altered states of consciousness classifies symptoms of PTSD as either related to normal waking consciousness (NWC) or related to dissociative experiences of trauma-related altered states of consciousness (TRASC). Although symptoms related to TRASC should be observed less frequently and should be less intercorrelated (e.g., in moment-to-moment states), they should be observed more frequently in those with high dissociative symptomatology or with early repeated traumatization. The studies described by Frewen and Lanius (2014) generally supported their model. The two studies that were undertaken involved: women with PTSD especially due to childhood trauma (N = 74) and university undergraduates (N = 504; 384 female). The measures selected afforded analyses of the differences in NWC and TRASC-related symptoms along four dimensions: time/memories (e.g., flashback); thought (e.g., voice hearing); body (e.g., depersonalization); and emotion (e.g., numbing). The authors concluded that their approach could apply transdiagnostically to various trauma-related disorders (e.g., borderline, dissociative, or mood). For further work in support of the TRASC model of dissociation, refer to the study by Frewen, Brown, and Lanius (2016) with an online community sample. Gil, Weinberg, Or-Chen, and Harel (2015) examined Israeli civilians assessed in real time to missile/rocket fire exposure (N = 501). PTSD was evaluated using a DSM-5 consistent questionnaire. Threat was related to distance from the border from where the fire was originating. The authors examined the tendency to forgive (Heartland Forgiveness Scale; HFS; Finchman & Kashdan, 2004). They investigated social support. A critical variable was peritraumatic dissociation (PTDQ; The Peritraumatic Dissociative Experiences Questionnaire; Hamama-Raz, Solomon, Cohen, & Laufer, 2008). As for the results, in Gil et al. (2015), symptoms of PTSD were negatively related to both objective and subjective measures of threat, as well as to forgiveness levels and to social support. Further, they were positively related to degree of peritraumatic dissociation. The latter results are consistent with the renewed emphasis on PTSD as a dissociative phenomenon (e.g., Dorahy & van der Hart, 2015). According to Lanius et al. (2014), emotional undermodulation is a failure of top-down prefrontal corticolimbic inhibition. This allows for both psychophysiological hyperarousal (e.g., in the amygdala) and reduced neural activation (in the medial prefrontal cortex and rostral anterior cingulate cortex, in particular, with effects, as well, involving rostral anterior cingulate reactivity). As for emotional overmodulation, it involves excessive corticolimbic inhibition (Lanius et al., 2014). There is little psychophysiological responsiveness or increased activation in brain regions involved in arousal modulation and in emotional regulation. McKinnon et al. (2016) noted that dissociation is associated with impaired cognitive performance. They argued that the mechanisms involved might include functional sensory deafferentation at the level of the thalamus and altered functional connectivity between critical brain regions involved in cognitive function. They noted that dissociation is present in many neuropsychiatric conditions, including PTSD, anxiety, and psychotic spectrum disorders. Briere, Dietrich, and Semple (2016) developed the construct of dissociative complexity (DC) to capture the dynamics of the traumatic experience and its breadth. DC is defined as the tendency to endorse clinical levels of simultaneous multiple, relatively independent

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dimensions of the dissociative experience, thereby reflecting the overall dynamic or breadth of the traumatic response. In this regard, the research shows that experiencing multiple traumas of different types (complex, cumulative trauma) predicts well later trauma-related symptomatology. These predictions include the outcomes of dissociation and symptom complexity and presumably complex PTSD, which might happen due to impaired, overwhelmed self-regulation. The dissociation involved would seem to be an individually-determined multidimensional construct, including disengagement, identity dissociation, emotional constriction, memory disturbance, and depersonalization/ derealization. Comorbidities might include suicidality and substance abuse. Kearney and Simpson (2015) called for a broadening in approaches to PTSD and the consequences of trauma. For example: psychological distress after trauma takes many forms; many forms of trauma can elicit PTSD; and standard trauma-focused approaches to treatment have their limitations. Long term care should integrate a broader approach to outcome. It should concern not only symptom reduction and elimination but also promoting multiple domains of health and quality of life. This approach is consistent with giving dissociation a central place in consideration of PTSD and in trauma reactions, generally. The complexity of the trauma response is illustrated by the finding that different types of avoidance coping are used in different phases of the response (Hetzel-Riggin & Meads, 2016). For these authors, at first, peritrauma dissociation is involved, and then secondary alexithymia (difficulty describing/identifying feelings), with experiential avoiding next. Finally, in a recent study, the PTSD dissociation subtype has been associated with outcomes due to MVAs, and so is quite applicable to issues related to forensic evaluations of PTSD and its functional consequences for court and related venues. Specifically, in a Danish study, Hansen, Műllerova, Elklit, and Armour (2016) studied mostly survivors of MVAs and also survivors of incest for trauma reactions (total N = 787, with 31.2% of the 1,664 MVA survivors meeting PTSD criteria and contributing to this total). The MVA survivors were evaluated 62 months after their collisions. Physically, they had been diagnosed with whiplash. To test for the PTSD symptoms in the DSM-5, items from Part IV of the HTQ (Harvard Trauma Questionnaire Part IV; Mollica et al., 1992) were used. To assess the dissociative subtype, two items from the TSC (Trauma Symptom Checklist; Briere & Runtz, 1989) were used. LCA revealed two subgroups across both samples, one dissociative and one not (with 173 of the 476 MVA survivors with data falling in the dissociative group). Moreover, for MVA survivors, emotion-focused coping was more prevalent in the dissociative class and social support in the non-dissociative class. To conclude, I note that the percentage of MVA survivors in the dissociative class is quite high in this study and needs replication. However, as mentioned, it illustrates the relevance of the DSM-5 PTSD dissociation subtype for tort-type and related claims in court and associated venues. 8.1. Comment Dissociation might be a common experience in PTSD and vary on a continuum, with the dissociative subtype being at one extreme and with some dissociative elements in its symptoms at the other. Further, dissociation in PTSD appears associated with physiological undermodulation, whereas PTSD without dissociation appears to reflect more physiological overmodulation. In this regard, just as dissociation in PTSD might reflect a continuum of experience rather than a categorical, all-or-none phenomenon, so too the role of modulation in dissociation might reflect varying degrees of over- and undermodulation. Moreover, an individual's response might vary over time in dissociation and modulation and, further, the pre-existing dissociation vulnerabilities in these regards might equally vary over the lifetime. Consequently, the relationship between PTSD and dissociation needs continued

specification of their dynamics. The results of their relationship might have important forensic implications. For example, does peritraumatic dissociation predict a longer term outcome compared to cases in which it is absent? In this regard, several of the dissociation studies referred to in the above include a role for peritraumatic dissociation in the trauma response. Does peritraumatic dissociation affect memory of the event relative to those without it? Is dissociation malingered, and can its malingering be detected? Does this affect the malingering of PTSD itself, and prevalence estimates on how frequently that happens? Finally, forensic psychologists need to consider the trauma response outside of the contentious diagnosis of PTSD. On the one hand, the response is clearly broader than having that diagnosis, given other diagnoses that might be involved, comorbidities with it, the factor of dissociation, and so on. On the other hand, forensic psychologists need to establish the functional impacts of the trauma response to roles at issue, such as in work, study, or care giving. The diagnoses ascribed to evaluees in an assessment do not inform the functional impacts themselves and they are merely a short hand for ease of communication. It is the symptom complex itself deriving from the event at issue in relation to the demands of the roles involved that speak to the primary forensic task in trauma evaluations, not the diagnosis of PTSD nor any other disorder in isolation or in combination. By itself, the diagnosis of PTSD, or any trauma reaction, cannot address functionality, disability, and the short and long term global prognoses after an event at issue forensically. More research is needed on the factor structure of PTSD in relation to long term outcome in the roles being discussed. Does PTSD, as a diagnosis, or any of its factors alone or in combination, or its relationship to other factors, such as dissociation or pre-event vulnerabilities, predict outcome with respect to work, child care, studying, and so on? Until this type of research is conducted comprehensively, the DSM-5 diagnoses related to trauma, including that of PTSD, will have lacunae in their long term predictions that would be useful for court and related purposes. Also, see Boysan (2016) and Myrick and Brand (2016) for further work on dissociation, trauma, and PTSD. In the following, other issues related to the structure of PTSD are examined. These concern how people group together as classes in expressing it, including when there are comorbidities, and how the symptoms are expressed individually, given the large number of permutations and combinations possible among its diverse symptoms. 9. What are PTSD's classes, comorbidities, and heterogeneities? 9.1. Classes To date in the article, classes of populations of trauma-exposed individuals have emphasized quantitative differences, such as in severity of symptoms, and qualitative differences, such as whether dissociation is present. The following describes other research on classes related to trauma exposure. Price and van Stolk-Cooke (2015) investigated the association among PTSD, MDD (major depressive disorder), and GAD (generalized anxiety disorder), as presented in the DSM-5, in trauma-exposed individuals (N = 602; recruited using mechanical Turk). They measured for life trauma exposure (LEC-5; Weathers, Blake, et al., 2013b); PTSD (PCL-5; Weathers, Litz, et al., 2013a); GAD (the GAD-7; Generalized Anxiety Disorder-7; Spitzer, Kroenke, Williams, & Lowe, 2006), and Patient Health (PHQ-8; Patient Health Questionnaire-8; Kroenke et al., 2009). CFA was used to establish clusters in PTSD (four of them) and depression (two of them), with only one factor found for GAD. The role of a common distress factor over the diagnoses seemed evident in the results in that the various factors were highly intercorrelated. For example, irritability, difficulty concentrating, and sleep problems found in these disorders might be core features of a more general negative affect cluster.

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De La Rosa, Delaney, Webb-Murphy, and Johnston (2015) also advocated for one underlying trait (neuroticism) as critical in understanding PTSD. They arrived at this conclusion in a study of individual differences in PTSD and alcohol use in military personnel in deployed to Guantanamo Bay. For individuals with comorbid PTSD and borderline personality disorder, the data suggest that they experience greater instability of fear and sadness relative to controls (Scheiderer, Wang, Tomko, Wood, & Trull, 2016). This study implicates that a common underlying vulnerability to PTSD and its comorbidities might be a predisposition or expression of negative affect/emotional dysregulation in terms of fear/sadness instability. For further work on the contributing role of negative affectivity to PTSD, see Sadeh, Miller, Wolf, and Harkness (2015). Latent class analysis and latent profile analysis (LCA, LPA, respectively) have been applied to trauma-exposed populations in order to determine subgroups (e.g., more severe PTSD; comorbidities). In this regard, using LPA, Cao et al. (2015) examined a group of individuals exposed to a Chinese earthquake. They found four groups: one with low symptoms; one with more depression; one with more PTSD (DSM-5 consistent; using the PCL-5); and one with combined PTSDdepression. They concluded that PTSD and depression could follow independent pathways after psychological trauma, without one underlying psychopathology present. However, as with one of their groups, some people might express a more general trauma reaction. To a certain extent, but not exclusively, this study speaks to the common vulnerability (e.g., negative affect) model (Clark, Watson, & Reynolds, 1995). In a short term study of traumatic injury victims (beginning at 6 weeks post-event), Hruska, Pacella, George, and Delahanty (2016) found three trajectories of injured patients (N = 68) – nonreactive, moderate-stable (subthreshold), and severe-increasing. The latter class involved only 4.4% of the participants. Depending on the phase of the study, PTSD symptoms were evaluated using the PDS, PCL-C, and SF-PCL (respectively, Posttraumatic Diagnostic Scale; Foa, Cashman, Jaycox, & Perry, 1997; PTSD Checklist – Civilian; Weathers, Litz, Herman, Huska, & Keane, 1993; Short Form PTSD Checklist; Lang & Stein, 2005). In a long-term study of U.S. Reserve and National Guard members who were exposed to trauma, for both groups, three classes were found—low/consistent, borderline/stable, and pre-existing/ chronic, with the PCL used to measure PTSD symptoms (Fink et al., 2016). The latter pre-existing/chronic group appeared to be like those in other research that had two trajectories for it, involving high/stable and worsening/chronic types (e.g., Bonanno et al., 2012). Fink et al. (2016) concluded that, in their study, the different classes or trajectories after trauma exposure did not appear to vary over participant type (civilian, military). 9.2. Comment In study of the course, trajectory, or class type after traumatic exposure, there does not appear to be one universal pattern that has emerged in the research. The results vary with the details of the methods used, including in testing and sample type, although some commonalities are found in relation to differential severity types and whether there is a dissociative subtype. Generally, two-class models are insufficient, and three- or four-class models seem to better fit the data, but with more research needed to flesh out a full and nuanced model. 9.3. Comorbidities Comorbidity represents a major difficulty in assessment, diagnosis, and treatment, and this is especially true for PTSD. For example, often it is diagnosed concurrently with depression (Erikson, Wolfe, King, King, & Sharkansky, 2001), substance abuse (Young & Wang, 2015), or other disorders, including pain- and TBI-related ones in polytrauma

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(Young, 2013, 2016). Further, comorbidity complicates the heterogeneity of symptom expression in patients. The effect of comorbidities on PTSD has been studied in terms of both individual prominent symptoms and concurrent psychiatric disorders, especially depression and anxiety (e.g., Bowler et al., 2016; Forbes et al., 2016; Greene, Neria, & Gross, 2016). Sleep disturbance is considered a primary axis exacerbating PTSD development, or vice versa (e.g., Pigeon & Gallegos, 2015). For example, van Wyk, Thomas, Solms, and Lipinska (2016) found that, in PTSD patients, hyperarousal symptoms led to reduced sleep efficiency, less total sleep, and poorer self-reported sleep quality. Pain is another exacerbatory factor to PTSD, implying mutual maintenance (Sharp & Harvey, 2001). In a systematic literature review, Fishbain, Pulikal, Lewis, and Gao (2016) supported the notion that chronic pain and PTSD are comorbid; however, their review covered pain from many different conditions and not ones specifically related to tort and court type assessment. Longitudinal studies are elucidating the timing and mechanisms in this bidirectional effect as pain and PTSD mutually maintain each other. Valentine, Gerber, Nobles, Shtasel, and Marques (2016) studied MVA survivors 4 and 16 weeks after the collisions involved (N = 103). They found that mental health symptoms at 4 weeks predicted more pain, PTSD, and depression at 16 weeks. PTSD was measured with the PCL-C (PTSD Checklist—Civilian Version; Weathers et al., 1993). However, physical symptoms at 4 weeks did not predict these effects for PTSD and depression. The authors concluded that PTSD exacerbates pain, thereby leading to its increased experience. However, Vaughan, Miles, Eisenman, and Meredith (2016) found that higher levels of pain predicted PTSD severity increases (according to the CAPS) in the period from 6 to 12 months in PTSD patients. In both studies, bidirectional effects were not found but, that said, the directional effects in the two studies were in the opposite direction! Clearly, more research is needed, but the mutual maintenance of PTSD and pain remains a viable model in one guise or another. In this regard, Dunne-Proctor, Kenardy, and Sterling (2016) related the hyperarousal in PTSD to the lowering of sensory pain thresholds to certain stimuli, thereby providing a plausible mechanism for the PTSD-pain disability link. For further material on pain and PTSD, see Gómez-Pérez, LópezMartínez, Ruiz-Párraga, and Teale Sapach (2016), LaMotte et al. (2016), and Shipton (2016). As for mTBI, Warren et al. (2015) found that its induction predicted PTSD 6 months after the injury involved (but not 3 months after) for patients admitted to a trauma center (using the PCL-C to evaluate PTSD). Wang, Xie, et al. (2015b) found that early cortical thickness in the right precuneus region (within a few days of an MVA) predicted acute traumatic stress reactions 3 months later, and reduced activity, as well (using the PCL for evaluating PTSD). The authors concluded that cortical changes post-mTBI might be linked to later functional outcome. Individuals with PTSD experience comorbid AUD (Alcohol Use Disorder) in up to 41 to 79% of cases (e.g., Pietrzak, Goldstein, Southwick, & Grant, 2011). Debell et al. (2014) reviewed the literature on comorbid PTSD and alcohol abuse (AA), with the greatest associations involving the PTSD symptom clusters of avoidance/numbing and hyperarousal. The models on the comorbidity of PTSD and SUD/alcohol problems that have garnered most of the research support involve selfmedication and shared vulnerability/mutual maintenance (Young & Wang, 2015). In the former, substances are used to “alleviate” either PTSD symptomatology or the distress that is associated with it, to “cope” with the symptoms, and to help the irritability, hyperarousal, etc. (Haller & Chassin, 2014). Or, they help reduce symptoms and avoid negative affect, aside from the coping aspect (Nickerson et al., 2014). Models that are not supported in the research include the susceptibility model and high risk models, which concern pre-existing factors one way or another.

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Young and Wang's (2015) literature review showed that the selfmedication model is supported, but not exclusively. They reviewed both longer term studies and ones that involved day-to-day monitoring. For example, Nickerson et al. (2014) studied injury patients (N = 1,139) longitudinally following admittance to an Australian trauma center (baseline) and at 3, 12, and 24 months later. PTSD symptoms were assessed using the CAPS (keyed to the DSM-IV). Among other findings, the results indicated that PTSD symptom severity was associated with greater alcohol use between 12 to 24 months following injury (or smaller decreases). The effects also could have included occupational and social consequences. Using experience sampling methodology, Simpson, Stappenbeck, Luterek, Lehavot, and Kaysen (2014) studied civilians (N = 64) and veterans (N = 22) experiencing comorbid PTSD and alcohol dependence who wished to lessen their alcohol use. The results of the study showed that, on days with higher PTSD symptoms relative to one's average, drinking took place more on that day and the following one, which is consistent with the self-medication hypothesis. In addition, the mutual maintenance hypothesis was partially supported—an increase in the number of drinks was associated with an increase in PTSD symptoms the same day but not for the next day. As with the prior type of longitudinal study, the sampling ones do not support models in which alcohol use precedes PTSD. This type of study needs to be replicated with forensic samples, e.g., in tort, but they do suggest that alcohol use is not generally a predisposing factor to PTSD.

9.4. Heterogeneities The heterogeneity in symptom configuration in PTSD has been compounded by its increase from 17 to 20 symptoms from the DSM-IV to the DSM-5. Galatzer-Levy and Bryant (2013) had estimated that there are over 600,000 ways PTSD can be expressed in the DSM-5. This adds to the complexity of PTSD symptom heterogeneity and its relation to multifactorial causality (e.g., Young, Lareau, & Pierre, 2014). Young et al. (2014) noted that PTSD and its major comorbidities increase exponentially the number of combinations in symptom expression possible over individuals to over one quintillion. Whether subthreshold PTSD has functional consequences is a relevant question both clinically and forensically. Brancu et al. (2016) conducted an empirical meta-analysis as well as a qualitative literature review. The most rigorous studies administered a clinicianadministered interview to establish the presence of full-scale PTSD or whether it was present subsyndromally (CAPS; Blake et al., 1995, SCID, Structured Clinical Interview for DSM-IV-TR Axis I Disorders; First, Spitzer, Gibbon, & Williams, 2002), keyed to the DSM-IV and DSM-IV-TR (American Psychiatric Association, 2000). Subsyndromal PTSD was specified by any of the following ways: having the first of the three DSM-IV clusters and one of the two others; any two of the three clusters; or one or more symptoms in each of the three clusters. In the most rigorous studies, the prevalence of PTSD was 12.6%. The qualitative review revealed functional impairments in subthreshold PTSD that included work role factors (e.g., Barth, Kopfmann, Nyberg, Angenendt, & Frommberger, 2005; Cukor, Wyka, Jayasinghe, & Difede, 2010; Gold et al., 2012). Mota et al. (2016) found that, in veterans, subthreshold PTSD relative to probable PTSD is associated with increased psychiatric comorbidity and with functional difficulties. They used the PCL-5 (Weathers, Litz, et al., 2013a) to help assess PTSD. The prevalence of subthreshold PTSD in their study was much higher than that of probable PTSD, although the authors acknowledged that there is no one accepted definition of subthreshold PTSD (22.1% and 13.5%, respectively, for lifetime and past month criteria). These data are consistent with those of Brancu et al. (2016) described above.

9.5. Comment This section illustrates the exquisite individual and group differences that are found in the expression of PTSD. First, usually it is not elicited alone, and other conditions are associated with it, whether full-blown diagnoses or symptom sets. Second, it varies in how it is grouped, with people who express it varying in the severity of the symptoms, the comorbidities, and their associations. Third, even within the diagnosis, the amount of combinations among the symptoms is astounding, which is especially true when comorbidities are added into the equation (Young et al., 2014). One should add the variations in PTSD and trauma experience across age, gender, minority status, culture, the military, and so on, which compounds the difficulty in denoting PTSD as a uniform condition for court purposes. In this regard, some workers in court or related venues might inappropriately simplify it to the point that they maintain that there had been a negligent act, and that a monolithic PTSD diagnosis has resulted, which “proves” that the event at issue “caused” the PTSD and all the dysfunctionalities of the person involved irrespective of other possible causes. Any conclusion of this nature on PTSD for court purposes does not comport in any way with the research literature on PTSD. 10. Interim conclusion As an interim summary of the article to date, it has reviewed the history of the construct of PTSD and its present iteration in the DSM-5. As presently constituted, the DSM-5 PTSD symptom list might be an improvement relative to others but, at the forensic level, it is still wanting. Further, the DSM-5 project itself has been subject to criticism (e.g., Lilienfeld & Treadway, 2016; Young, 2016) and appears to not have conducted its field trials appropriately so that even its reliability is in doubt. The ICD-11 might provide a superior classificatory system for PTSD compared to the DSM-5 because it will use a reduced symptom list. Also, its inclusion of Complex PTSD (CPTSD) appears necessary. However, it too has been constructed more on the basis of clinical utility rather than a research focus, thereby rendering its direct forensic use problematic. Further, forensic psychologists should not ascribe much value toclassificatory diagnoses in determining critical issues, such as long term functional impacts of symptom sets induced by the trauma at hand. Only careful forensic assessment can relate symptoms to impairments in functions. Moreover, only an approach that is forensically careful can relate PTSD symptoms and impairments to a negligent act at issue. Diagnoses are of minimal help by themselves in this regard. The questions of the prevalence of traumatic response to event exposure, and that of the development of PTSD itself in this context, are conditioned by the population examined and how it is measured, in addition to contextual factors, and so on. Recent research suggests that trauma exposure is prevalent, taking place about 70% lifetime, including for events relevant to forensic cases, such as MVAs. Moreover, these traumatic events lead to traumatic reactions about 10% of the time and PTSD is a primary condition that develops in consequence. Finally, PTSD might be prolonged about 10% of the time. However, polytrauma and comorbidities complicate these statistics. Further, the possibility of malingered PTSD constitutes another confound forensically. However, the estimates for malingered PTSD vary from 1 to 50%, which is a range illustrative of the need for further research with the best instruments and with ones based on DSM-5 criteria while having scales related to negative response bias (as discussed below). The article has emphasized the research on PTSD's symptom structure. That is, what are its dimensions according to factor analytic research, and do the results support the DSM-5's four-factor PTSD model? On the one hand, there are other four-factor PTSD models that have been found that fit the data even better than that of the DSM-5.

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On the other hand, there are models that include more than four factors for PTSD. Initially, the five-factor dysphoria model of PTSD gained traction in the research (it had been proposed at first for the DSM-IV's symptoms), but then two six-factor models of PTSD emerged. Finally, a hybrid seven-factor model of PTSD has been tested and there is growing support for it. Beyond this, in my own work, I have posited an eighth factor on dissociation in PTSD that is applicable to the minority of people who express the dissociative subtype (Young, 2015). Considering that the DSM-5 includes a four-cluster structure of its 20 clinical symptoms for PTSD, one reviewer asked whether it matters that the research is finding that there might be four, five, six, seven, or even eight factors in the cluster structure of DSM-5 PTSD symptoms? What is the difference in terms of diagnosis, intervention, or forensics? First, to answer this timely question, I note that the standard four-cluster DSM-5 PTSD model has been found to fit the data, but this does not take place at a level of fit as high as for other models with more clusters. In terms of clinical utility and also practice realities, the trend in these results should not lead us to drop the present DSM-5 four-cluster model. It is sufficient for clinical and forensic purposes despite more nuanced research findings. That said, future iterations of the DSM have the obligation to examine the ongoing research on symptom structure of PTSD symptomatology. For example, cluster models with more symptoms might lead to focusing just on the core symptoms in any one cluster, thereby streamlining clinical work using the DSM-5. Also, forensically, better organization of the symptoms might help isolate more subscores on future PTSD tests, giving more room to specify inconsistencies, exaggerations, blatant responses, etc., that address negative response bias. The increasing research on dissociation in trauma not only supports the DSM-5's addition of the dissociative subtype to the diagnosis of PTSD but also it indicates that dissociation is critical to the trauma response, in general, as well as its course. This article has focused on multiple factors that render the trauma response an individualized experience (classes, comorbidities, and heterogeneities) and the expression of PTSD is so varied that it is highly individualized for this reason, as well. This article already gives much fodder for thought forensically on PTSD. PTSD is considered part of the disability epidemic. Much of the research studies on PTSD suggesting that it might be valid, for example, by finding that it has biological underpinnings to it so that it might reflect a plausible reaction to traumatic exposure, does not consider malingering as a possible critical confound; therefore, any generalizability to the forensic setting requires caution. The diagnosis of PTSD depends on expert diagnostic manuals, but these manuals go through iterations based on clinical utility more than underlying research. Moreover, for the DSM-5, which is the commonly used one, the field studies in support of its reliability appear flawed, thereby compromising its validity. Inspection of its 20 DSM-5 PTSD symptoms indicates, at a minimum, several that are easily feigned for the court setting. Generally, the DSM-5 symptom set is open to coaching and malingering. PTSD can be expressed in so many individual ways, which is even more so the case when comorbidities are considered, that attribution of the diagnosis of PTSD is too much of a simplification forensically. It does not help in determining functional impairments anyway, which is the critical forensic task. Because it is not expressed in all those diagnosed with it in the same way, its use for court purposes is compromised for those wishing to state that, if it is present, it must be due to the negligence at issue. Finally, the tests used to assess it might ignore this heterogeneity in expression, as well not dealing well with the need to address functionality, so they have forensic limits, too. 10.1. Looking ahead The third article in the series on PTSD in Court in this journal (Young, 2017b) examines in more depth the topic of malingering and malingering detection, including in relation to PTSD. Before proceeding to that

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topic, second article on PTSD in Court (Young, 2017a) considers the fast-developing field of possible biological underpinnings related to PTSD. This area leads into a discussion of the causality of PTSD and a new model that I have developed in this regard. About causality, as discussed to this juncture, the article has considered the description of PTSD in terms of its symptoms, dimensions, and prevalence, in particular, with its causality limited to discussing the entry A criterion on the nature of traumatic exposure that induces it and also on individual differences in its experience. Young (2017a) elaborates the multifactorial causal nature of PTSD. First, it considers risk factors for PTSD; then, it reviews the genetics that might be associated with PTSD; and then it addresses the brain's involvement in PTSD. This part of the work is highly biological in orientation, but it adopts this perspective without excluding a role for experience. At the same time, it considers the legal side of causality, e.g., the material contributions test. Note that, looking back once more (as a reminder) a brief synopsis of the present article indicates that PTSD is a diagnosis that is contentious. This starts with its historical undercurrents and continues into its contemporary scholarship. Issues in the field concern its present symptom configuration in the DSM-5, its cluster organization, and its entry criterion on traumatic stressors. The ICD-11 approach to it will be different. Moreover, there are forensic loopholes in both approaches to PTSD and imprecision in them that opens the diagnosis of PTSD to civil floodgates in court. That being the case, the research on PTSD is burgeoning, and serving to specify better its symptoms, clusters, and applications in diagnosis for court, as well as for clinical work. References Ali, S., Jabeen, S., & Alam, F. (2015). 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Please cite this article as: Young, G., PTSD in Court I: Introducing PTSD for Court, International Journal of Law and Psychiatry (2016), http:// dx.doi.org/10.1016/j.ijlp.2016.10.012