Individual Differences in Posttraumatic Distress ...

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Joseph S, Williams R, Yule W. Psychosocial perspectives on post-traumatic stress. Clin Psychol ..... 2nd ed. Ellicott City (MD): Chevron Publishing; 1995. 238.
IN REVIEW

Individual Differences in Posttraumatic Distress: Problems With the DSM-IV Model Marilyn Laura Bowman,

Objective: To evaluate the evidence concerning the role of threatening life events in accounting for clinically significant posttraumatic stress responses. Method: Research was examined to review the epidemiology, evidence of dose-response relations, and individual difference factors in accounting for variations in conditions, including posttraumatic stress disorder, after exposure to threatening events. Results: The evidence is significantly discrepant ft-om the clinical Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) model. Greater distress arises from individual differences thanft-om event characteristics. Important individual differences that interact with threat exposures include trait negative affectivity (neuroticism): beliefs about emotions, the self, the world, and the sources and consequences of danger: and preevent acts, disorders, and intelligence. Reasons for the discrepancies between the evidence and the current model of posttraumatic distress are proposed. Conclusion: In accounting for responses to threatening life events, the relatively minor contribution of event qualities compared with individual differences has significant treatment implications. Treatment approaches assuming that toxic event exposure creates a posttraumatic disorder fail to consider individual differences that could improve treatment efficacy. (Can J Psychiatry 1999;44:21-33) Key Words: posttraumatic stress disorder, stressful life events, DSM classification Professional Assumptions About Threatening Life Events

These real cases exemplify the core problem with the concept of PTSD as it is currently construed in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (1): identifying an event as the main causal factor to explain the disorder.

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hree men were seriously injured in a mine explosion. After physically recovering, 1 returned to work in the mine, 1 retumed to work on lighter duties above ground because ofthe physical disabilities he had sustained, while the third was permanently disabled by chronic posttraumatic stress disorder (PTSD) elicited by all mine-related stimuli.

PTSD has become common in professional and popular thinking since its introduction in the third edition ofthe DSM in 1980 (2). Since then, the definition of causal events has steadily broadened, from being "outside . . . usual... experience" (DSM-III, p 236) to leaming about a threat to the physical integrity of a "close associate" (1, p 435). PTSD is considered normal after threatening events: "The severity, duration, and proximity of an individual's exposure to the traumatic event are the most important factors affecting the likelihood of developing this disorder" (2, p 426), reflecting a biological dose-response model. The model implies that

Manuscript received September 1998. 'Professor, Department of Psychology, Simon Fraser University, Bumaby, British Columbia. Address for correspondence: Dr ML Bowman, Department of Psychology, Simon Fraser University, 8888 University Drive, Bumaby, BC V5A 1S6 email: [email protected]

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well-being is most validly represented by reported emotion and that professional treatment is the most effective remedy. PTSD is prototypical, reflecting clinical thought as it evolves over the 20th century, in which threatening life events are seen as the cause of clinically significant disorders. Freud's first model of neurosis was essentially a trauma-based view of the early infancy causes of adult disorders (3,4). Contemporary behavioural models use the language of stimulus-response to express the same idea about recent stressors. Mental health professions have viewed life experiences as providing profound explanations for normal and disordered behaviour, and the idea that extreme events necessarily create trauma has become commonplace. I will avoid the use of "traumatic" and will instead use "toxic" to describe events within a more objective biological stress perspective consistent with the DSM-IV, because in a dose-response model the subjective interpretation ofthe individual is irrelevant. How Well Do Our Definitions and Assumptions Match the Evidence? Research Problems Objectively calibrating the dose value of events has been a problem. While events can be typed by objective criteria (number [5], duration, directness, material harms), this is rarely done, and most studies confound objective with subjective features such as intentionality and negativity. Simple event counts are as predictive of health as more elaborate weighting systems for event negativify (6), which suggests no dose-response relationship exists; events that are more negative do not account for more illness. The nature of events, however, accounts for little ofthe variance in health (perhaps 9%) (7), except in heart attacks among those with cardiac disorders (8). To date, no standard objective system for measuring event severity has been adopted. Responses and symptoms also pose a research problem, because the DSM-IV criteria are entirely subjective and vulnerable to deception (9). Discrepancies between self-reported condition and objective evidence of harm (10-12) mean high distress reports cannot be taken as evidence of harm events. Prevalence of Toxic Life Events and Posttraumatic Disorder How rare are toxic life events? The 1980 DSM-III definition concemed events outside usual experience, implying that events sufficient to cause disorder were rare. If extreme events cause trauma, the lifetime prevalence of toxic events should be similar to that of PTSD. In the United States (US), evidence shows that the lifetime exposure to at least 1 "traumatic" event is 61% among men and 51% in women (13); smaller, earlier studies (14,15) found

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higher rates. Among a more privileged group, US universify students, rates were even higher (84%), and one-third had experienced 4 or more events (16). Considering that people forget life events, including threatening ones for which they have received treatment (17,18), toxic events are very prevalent in the lives of people in affluent peacetime circumstances. In less fortunate lands suffering famine, torture, forced migrations, and war, exposure may be virtually universal. The lifetime prevalence of PTSD is quite low in the general US population, with 5% of men and 10% of women meeting the criteria (13); in Iceland, the rate in a more inclusive sample was only 0.6% (19). These discrepancies between prevalence of toxic events and PTSD reveal a significant problem in the dose-response model. There are other important discrepancies between the DSM's biological stress model and symptom pattems in PTSD. PTSD patients do not habituate to their circumstances as depicted in stress studies; they respond biologically differently from others exposed to the same event and respond differently than do patients with other stress-related disorders (20). In sum, the prevalence of PTSD is vastly lower than the prevalence of exposure to seriously threatening events, and the discrepancies are greater than can be explained by sample variations. PTSD patients do not show biologically normal stress responses, and toxic events are not reliable causal factors in accounting for PTSD. Dose-Response Relations: Incidence of PTSD After Direct Exposure Against the background of the general prevalence data, v/hat incidence follows specific exposures? If the dose of an event is the causal factor determining PTSD, events that are directly experienced, prolonged, and damaging should show the highest incidence. Combat represents such exposure, and studies of mostly US veterans of World War II, Vietnam, and the Gulf War comprise the largest body of studies. Incidence varies widely depending on the sample, ranging from 0.7% in WWII Harvard men (21) to more recent, much higher rates of 15% (22). While many studies find increased incidence, significant data sets fail to find a correlation between combat exposure and stress-attributed disorders (23), to find an increase in symptoms over time (24), or even to find inverse relations (25). Civilians in war zones show similar response variability. Israeli children subject to frequent bombardments showed no greater anxiety than did children experiencing no attacks (26). Irish civilians experiencing terrorist killings showed no increase in the incidence of psychiatric admissions (27). In the Montreal Jewish community, there were no differences on all significant indicators including mental ilbess syndromes be-

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tween those with direct Holocaust experience and pre-WW II migrants (28). The number of torture events in Turkish victims was not predictive of posttorture disorder (29); torture victims had more but only moderate PTSD symptoms, twothirds did not meet PTSD criteria, and anxiety and depression levels were normal (30). When toxic events suddenly intrude into civilian life, the results are similarly mixed. Only about 10% of hospitalized victims of serious motor vehicle accidents showed PTSD in the United Kingdom (UK) (31), the Netherlands (32), and Norway (33). Incidence of PTSD can increase over time after hospital discharge (34), contrary to the model. Intrusive sudden, progressive, or fatal disorders such as heart attack (35), cancer (36), and AIDS (37) are not reliably followed by stress-related mental disorders nor are natural disasters in representative or controlled sample studies (38,39) including situations such as the Australian bushfires (40,41). Significant variations also appear after brief toxic events, with some individuals showing resilience during and after the event but later reporting event-attributed disorders (42), contrary to the dose-response model. While many retrospective studies report high levels of abuse among children seen for clinical disorders, these do not constitute evidence of the abuse-origin of these disorders; there is a bias inherent in the retrospective design and the clinical sample. Even so, there are studies that fail to find a relationship; among sexually abused children, the probability of being diagnosed with an Axis I disorder was related to mothers' mental status, not to abuse exposure (43). The best evidence comes from rare, time-consuming, and expensive longitudinal developmental studies of outcomes. These show remarkable diversity after early toxic experiences, because person-environment interactions go beyond a simple stimulus-response model (44). Children with exposure to severe events nevertheless have shown adaptability, competence, and resilience across many studies (45-47). Overall, only very few directly exposed individuals develop distress disorders. When ftinctioning is studied using representative samples, in a prospective longitudinal design with control groups, the dose-response model of DSM-IV does not explain the cause of PTSD well. Dose-Response Relations: Indirect Exposure Indirect exposures arising from information about the toxic events that have happened to others are now included as toxic events in the DSM-IV, distorting its dose-response definition. "Second injury" is said to arise from events such as insensitive emergency personnel (48), media (49), or "impersonal" communication (50). Lawyers, judges, physicians, and researchers are argued as being at increased risk for PTSD (51), "compassion fatigue" (52), or vicarious traumatization

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(53,54) caused by hearing the harm reports of others, proportional to the client's event severity (55). The evidence is mixed conceming physical exposure to settings where others were harmed. US military body-handlers showed symptoms (56), and one-half became PTSD cases (57), while Scottish body-handlers showed no increase in caseness even with prolonged exposure (58). For police in the Lockerbie air disaster, prolonged exposure was less toxic than brief exposure (unpublished observations, M Mitchell, 1995). Accidental exposure of civilians to gruesome scenes is not reliably associated with increased caseness beyond immediate reaction (59). Violating the dose-response model, in a large epidemiological study, seeing someone hurt yielded higher PTSD rates than being personally injured (60). Rescue workers often report that their experiences were both difficult and positive (58,61). Psychological exposure to stories of events experienced by others implies no objective dose; if PTSD develops, it is created through psychological constructions of the listener. Some people present with trauma syndromes after vicarious exposure, as wives whose husbands had suffered a frightening accident (62) and ferry workers following a disaster in which they had not been participants, bereaved, or helpers (63). In contrast, leaming of one's inadvertent direct risk exposure such as to an HIV-positive surgeon (50) or seeking risk information such as presymptomatic genetic disease status (64,65) rarely leads to a traumatic disorder, and "bad" news is less distressing than uncertainty (66). Overall, the evidence is mixed. Most people are not traumatized by indirect informational exposures to events that happened to others, while some attribute their emotional disorders to these. This suggests that individual factors are significant in mediating dose-response relations. Emotions, PTSD, and Individual Differences The most important individual quality modulating eventresponse relations is trait emotionality. Emotional responses are not determined by events but are the outcome of a chain of psychological mechanisms. From the experimental laboratory studies ofthe 1960s, it is clear that individual reactivity and interpretation interact to determine emotional responses to raw experience (67,68). In real life as well there are significant individual differences in emotional responses to events such as airplane crashes (69), rape (70), violence (71), and false imprisonment (72). Emotional response styles show considerable longitudinal stability (73,74). The most widely studied, clinically relevant, and stable personality dimension ofthe 5 major factors (75) is general negative affectivity (neuroticism) (76), a temperament style identifiable early in life (77-80) that is stable longitudinally (r = 0.53 across 30 years) (81). It includes high responsivity, anxiety, and depression. Contrasting traits of

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hardiness (82), resilience (83,84), and happiness (85,86) also show longitudinal stability resistant to life experiences. Coping styles also show long-term stability (87), and the externalizing, emotion-focused coping style typical of PTSD (88) accounts for more symptom variance than does combat exposure (89). Neurotic temperament has a significant genetic loading (76,90-92) and accounts for virtually all of the correlation between coping strategies and well-being (93). Trait anxiety, one aspect of neuroticism, is highly stable (94), as is depression, which also has been shown to have genetic loading that accounts for more clinical disorder than even severe life events (95). These fmdings are all relevant to PTSD, a syndrome of negative affectivity. Neuroticism predisposes people to have more objectively negative events (96). When studies of postevent disorder include trait neuroticism as a variable, neuroticism accounts for a major part of the variance, for example, after a hurricane (97), combat (98), and stressful life events (99,100). Positive Emotions The negative emotions of PTSD are considered symptoms needing treatment, yet apart from subjective report, evidence is mixed on the effects of positive emotions and depends on the outcome measured. They are popularly seen as a means of improving physical health (101,102) and even the quality of dying (103), but improved cancer survival is equally associated with optimism or denial (104). The benefits argued for optimistic illusions (105) have been criticized as a US cultural stereotype (106). Although depression is sometimes found with illness, emotion-illness relations are relatively weak and not clearly patterned (107). One ofthe largest longitudinal studies in the history of psychology found that childhood cheerfulness is negatively related to longevity (108). The positive emotional condition of self-esteem is "central to the successful integration of traumatic information" (109, p 536), yet high self-esteem has a dark side. It is characteristic of aggressive children (110) and men (111) and is often discrepant from objective behaviour (112,113). Similarly, optimism and happiness are considerably independent of objective circumstances and are longitudinally stable (86). Positive events are not reliably associated with happiness (accounting for 3% of its variance in a large twin-study [114]), any more than threatening events are reliably associated with mental disorder. "Feel-good" emotions do not provide any reliable guide to the quality and meaning of life as it is experienced by an individual. Simone de Beauvoir observed that, during the Nazi occupation of Paris, happiness was irrelevant because more important issues were at stake (115).

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Emotional Expressiveness Traditional thinking in the mental health field has asserted that open expression of negative feelings is essential (116,117), and most therapies are based on this idea. Emotional expression arises from neurally determined, culturally leamed, and individual temperament and belief factors (118), but research has not yet succeeded in identifying objective expressions that are reliable, valid markers for inner well-being (119), and these relations are complex. Denial and avoidance of expressing negative emotion can be beneficial (120). Scud missile-exposed Israeli children who used denial fared better (121), and persistent emotion-focus predicts worse bereavement outcome (122). Open expression of some emotions can be harmful: anger contributes to worse psychological condition (123,124) and mortality (125,126) in heart disease. The arousal and manipulation of emotion is often central in PTSD therapy (70,127), yet emotion-focused coping (128) is less effective than problem-focused after traumatic injury (129) and is associated with higher fear (130) and worse outcome after combat (131) and PTSD (88,132). It may be that fear is only one of a complex mix of emotions including excitement, guilt, titillation, and relief after toxic events; treatment focus on negative affect may reinforce an unhelpfully narrow construction ofthe event and response. Expressed emotion as evidence of disorder or of events is also problematic. Toxic events are usually seen as undeserved, adding a moral dimension to PTSD; the person is a victim with a claim to a moral debt owed by others. The more vivid a distress display, the greater the implied victimhood. Weeping, however, can be demonstrated by sentimental tyrants, actors, victims, and deceivers. After weeping on television for an "abductor" to retum her children, Mrs Susan Smith was convicted oftheir murder (133). Exposure to toxic events is part of life, and events are interpreted in different ways that yield differing emotional conditions. The emotional-comfort model of how life should be, implicit in the DSM-IV model of PTSD, fails to explain a vast array of danger-exposing initiatives people take out of duty, idealism, thrill-seeking, love, or courage. Beliefs and Cognitive Distortions Up to 75% of people confronted with irrevocable loss do not show intense distress (134), and beliefs and cognitions moderate the impact of such events. The most powerful evidence ofthe role of beliefs in affecting postevent distress is the common fmding that intentional harms are more distressing than impersonal harms, independently oftheir objectively threatening qualities (135-137). Many beliefs affect responses. Beliefs about one's own helplessness (138) or resilience ("positive illusions" [105]), the faimess (139) or coherence

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(140) of life, danger, and the meaning of emotions all affect well-being. Most of these beliefs are stable, although when they are cast into question by events, they sometimes change, and such changes are associated with increased distress (141). Beliefs about sources of danger can affect emotional condition, even when they are wrong, as in the case of hysterical epidemics (142,143). Malaysian electronics workers occasionally see devils inside their microscopes and become convulsed with terrified screaming, so emergency teams are used to remove the first worker before an entire factory floor becomes triggered into chaos (144,145). These terrors are honest and entirely a product of a belief system that does not accurately identify dangers. Beliefs about future dangers can create PTSD symptoms. US schoolchildren who were given prevention training for a possible earthquake, which did not occur, showed distress 2 months later (146). Vietnam veterans who believed they were exposed to Agent Orange had greater distress than those closer to the spraying, but with only varying knowledge of their exposure (147). Adult recall of childhood sexual abuse varies significantly by sex, owing to different beliefs through which events are interpreted (148). Belief in helplessness is associated with PTSD (149), while more complex ideas of the self (150), religious faith (151,152), political commitment (153), and self-efficacy beliefs (154) are protective. Early optimism in children is associated with more successful navigation of later toxic experiences (155), while a pessimistic explanatory style affects later well-being (156). Among people who believed they suffered from chronic fatigue syndrome, those who believed they would have a catastrophic response to a stressor were far more disabled than those who believed their response would be moderate, in groups matched on ilhiess (157). Beliefs about emotion also affect what is experienced and displayed. Beliefs affect active choices of environments, directing of attention, appraisal of an event, the management of the emotional experience, and its expression (158). Distorted cognitions manifest as pessimistic magnification of otherwise neutral life events in distressed patients (159), and PTSD patients, more so than controls, believe their family members have more PTSD symptoms (160). The stable belief that control of life experience lies in inner or external factors ("locus of control" [161,162]) causes distress when there is a discrepancy between the individual's belief about where control should reside and where it actually resides in an event (163,164). The traditional "psychopathic" personality included on the Minnesota Multiphasic Personality Inventory (MMPI) scale concerns a tendency to attribute responsibility externally; premilitary high scores on this are associated with PTSD responses to combat (165). When blame, a moral attribution, is added to the beliefs about the cause of a toxic event, evidence is mixed as to whether more distress is experienced if oneself or another is blamed; the

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intricacies in this are detailed elsewhere (166). Persistent attention to the attribution of cause, however, is associated with prolonged distress (167,168). Beliefs arise in part from group membership, and individuals can be grouped in ways ranging from biological to cultural, involving shared beliefs. There are significant sex differences in PTSD; women were twice as likely to meet PTSD criteria (10.4%:5%) (13), although more men were exposed to traumatic events (61%:51%). Age interacted with sex, with males showing higher exposure with age but no systematic age-related PTSD; female exposure did not shift with age, yet lifetime PTSD was lowest in the oldest group (8.9%), suggesting cohort factors that implicate beliefs. A significant Icelandic study using similar criteria found all PTSD cases were female, with 1.3% affected (19); the contrasting US-Icelandic rates suggest cultural factors. Nearly 500 Israeli children repeatedly locked into sealed rooms out of intense fear of Scud missiles with biochemical weapons showed no evidence of postevent disorder (121); in contrast, all 23 US schoolchildren held captive in a bus for 27 hours were evaluated as traumatized after rescue (169), suggesting that varying beliefs about these encapsulation events affected responses. Cultural differences in the expectation of emotional displays after toxic events were suggested in the aftermath of the murder of 16 Scottish children in Dunblane. US television network news reporters became increasingly annoyed and then left, because the laconic Scots failed to provide the vivid displays expected but instead just repetitively replied, "We're totally devastated, totally numb" (170). Good cross-cultural comparisons are hard to do, but to the extent that different groups hold different beliefs about events and emotions, variations in event-attributed distress are predictable. Other Preevent Factors There are additional individual differences in preevent functioning that modulate responses to toxic events. Acts Previous experience with violence was twice as powerful as hurricane exposure factors in the prediction of posthurricane PTSD in adolescents (171). Prewar family instability, trauma experience, and childhood antisocial acts had significant effects on PTSD in Vietnam combat veterans (172). Individual acts (rather than passive victimization) contributed to later PTSD in Vietnam veterans (172,173). "Of the six forms of warzone violence . . . only participation in the mutilation of bodies was related to PTSD" (174, p 136); lack of participation in such acts was typical of veterans who did not show PTSD (175). The highest distress scores in war-ex-

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posed Kuwaiti children were in those who reported harming others (176). Other acts initiate a chain of events that lead to toxic exposures, and these are not randomly distributed. High-risk acts are performed with higher frequency by children with traits of hyperactivity, rebelliousness, and high risk-taking (177,178); antisocial behaviour at age 10 years was followed by a doubling in toxic life events over the next 2 decades (179). Similarly, assaulted adults are not representative of the general population but show higher rates of previous elective surgery, trauma, and drug abuse (180). Personality Disorder Adults with personality disorder are more highly represented within PTSD cases in the US military (22,181,182), and a growing literature of fraudulent representations of combat exposure (183-187) may have tainted many veteran trauma studies. Exaggerations of symptoms (188) and misrepresentation of schooling (189) are found in PTSD. Substance abuse is also highly associated with PTSD (22); in civilians, the abuse typically precedes the event-attributed syndrome (190). Psychiatric Disorder Comorbidity of PTSD with other psychiatric diagnoses is high in civilians (60,191-193) and veterans (194). In a civilian study, 88% of men and 78% ofwomen with PTSD met criteria for another diagnosis (13). Of male Vietnam veterans with PTSD, 99% had another major disorder (22). Some argue that "screening for traumatic events... should be standard in both psychiatric and primary care practice" because "PTSD may be the underlying psychiatric diagnosis in patients with a variety of clinical presentations" (195, p 12-3); the most methodologically sound study found the opposite, that PTSD "usually occurs subsequent to at least one previous DSM-IIIR disorder" (13, p 1058). Postevent symptoms are more probable in children with previous psychopathology and strained parental relations, which are typically not considered in cross-sectional studies (196). Social Support Long viewed as a buffer of toxic events, the effects of social embeddedness on physical and psychological well-being are complex and at times harmful (197-200). More deeply, personality traits affect the perception of social support (201) and the receipt (202) or undermining of it (203). Cognitive Ability Intelligence mediates toxic event responses. Lower IQ is associated with greater probability of a postevent distress syndrome in children (204-206), adults (207), and veterans (89,208-210). Overall, preevent individual differences, including acts, personality and psychiatric disorders, social support, and

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intelligence, play significant roles in moderating responses to events. Which Factors Best Predict Postevent Distress? Prospective longitudinal studies of individuals all later exposed to a toxic event provide the best evidence conceming the relative contributions of preevent and event factors. These studies are difficult and rare, but Australian psychiatrist Alexander McFarlane's study of fire-fighters who battle bushfires that threaten lives and property provides strong findings. In an early study, fire exposure and other life events accounted for only 9% of later symptoms (40). The subjectively perceived qualities of the fire were more important than proximity to death (42), and preevent characteristics were more important than the event or its associated losses in long-term outcome (211). Histories of preevent neuroticism and psychiatric disorder accounted for the progression from acute condition to stress disorder in two-thirds of the cases (212). Among Vietnam veterans, combat exposure accounted for only 9% of variance in PTSD symptoms, while externalizing coping style accounted for 26% (89). The best prediction of PTSD among Gulf War veterans came from personality variables; adding stress severity variables did not improve it (23). Among aging male civilians, 47% of psychiatric symptoms were accounted for by trait emotionality, while life events contributed 38% (99). Among hurricane-exposed US children, trait anxiety and in-event emotional reactivity contributed more to PTSD symptoms than did hurricane exposure (97). A metaanalysis found subjective factors accounted for twice as much of the distress as did objective features after violence (213). Studies that identify event qualities and individual differences show interactions rather than simply additive effects. High-combat Vietnam veterans showed no PTSD if they had low trait neuroticism, while low-combat high-neuroticism veterans showed PTSD (214). Among twins, those with high genetic risk for depression showed a greater response to toxic events but even most of them did not develop the disorder (95). Longitudinal studies of children in adverse environments similarly show wide variations in behaviour (46,215), with events accounting less for distress than did other factors. Among children abused before age 11 years, sex, race, and age accounted for far more variance in later disturbed behaviour than did the toxic events (216). In sum, preevent individual differences in emotionality, beliefs, actions, disorders, and intelligence account for more of postevent distress syndromes than do event characteristics.

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Why Does the Clinical Model Define Events as Causative? The DSM and prominent mental health models focus on an event as the causative agent of PTSD, despite massive evidence of more important individual differences. The probable explanation for this discrepancy is that clinical models are derived from clinical samples of those who seek treatment, rather than from all those exposed to similar events. This biased sample is used in faulty backward reasoning to develop explanations that suffer from the absence of base-rate information. An interesting study provides challenging inverse data. One hundred US men who were above average in comparison with national norms of occupational level, education, income, health, marital stability, and mental ability were given intensive clinical interviews as part of a research project. The researchers were surprised to discover that these men reported as much toxic life experience as the researchers found in their clinical practices, but with none ofthe behavioural pathologies oftheir patients (217). Other flaws in causal reasoning contribute to the inaccurate emphasis on events. In the event-focused model, one stimulus-response segment is selected over other events, individual qualities, and base-rate information out ofthe patient's ongoing flow of life and assigned value as cause. The model assumes that people are passive recipients of events, yet vast literatures in developmental psychology contradict this assumption, showing that people are active agents who seek events, initiate interactions, and create meaning (218-220). Patients also make errors in causal attributions. Patients assign more impact to life events (159,221) and show more unstable judgements (222) than do controls. Normal brain operations also contribute to errors in assigning cause for experience. Persons with phantom limb pain, corpuscallosotomies ("split-brain") (223), or delusions all provide faulty explanations of their experience. In people without biological disturbances, purely psychological mechanisms can contribute to faulty causal attributions. Actions performed under posthypnotic suggestion are explained in "honest" but invented ways. The general tendency to accept responsibility for desired but not undesired outcomes (224) also contributes to faulty reasoning. People make errors in reasoning about the causes and meanings of emotional arousal. In the 1960s, experimental studies of arousal showed that people search the environment for cues to create emotional meaning when they have been physiologically aroused with epinephrine (68). Subjects who were not given an explanation of the drug's effects then exposed to a confederate adopted the model's emotion, while informed subjects did not add emotional meaning to the arousal. Decades of studies have continued to support this model. When there is no immediate stimulus to help attribute meaning to arousal, subjects search their memory for recent

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ideas and make use of irrelevant but emotionally loaded information to create an honest but false explanation oftheir emotion, even when the remembered material is arbitrary and of no personal import (119). Since increased arousal of anxiety is a major symptom of PTSD, studies ofthe misattribution ofthe meaning of arousal are important. For example, 3 PTSD cases reported obsessional images of childhood traumas; medication resolved the flashbacks, and investigation found that the events had not occurred (225). Individuals can provide an honest, vivid "memory" that is entirely wrong (226). Memory that is focused on affect is more liable to reduced accuracy and to introduced errors (227). Over time, 81% of Gulf War veterans added at least 1 new "remembered" traumatic event, and 61% added 2 or more; PTSD symptoms were correlated with these amplifications of "memory" (228). Other errors in professional reasoning also contribute to misattributions of causation. Clinical diagnostic judgements are often poorer than statistical decisions because clinicians fail to consider alternative explanations once they have selected one (229). Observers generally interpret adversity experienced by others as decisive devaluation events and overestimate the harm experienced compared with the reports of those who directly experience the events (230-235). Finally, clinicians may fear being accused of "blaming the victim" in looking at factors beyond the event. This fear represents a shift away from a scientific approach to PTSD to a moralistic model, which is not applied to disorders such as schizophrenia or heart disease. In identifying genetic and other risk factors, researchers of these disorders are not criticized for "blaming the victim." Any shift to a moral-blame model does not improve our understanding of PTSD any more than it did in now-discredited "schizophrenogenic-mother" studies (236). Overall, biased samples are the main reason that clinical models have used toxic events to explain event-focused distress. Only very few of those exposed develop a disorder, yet these are the people that clinicians see and from whose accounts the major clinical models have been developed. Other distortions in reasoning by patients and clinicians may contribute to the inaccurate focus on events as explanations for PTSD symptoms. Psychotherapy and PTSD The assumption that individuals will achieve relief from event-attributed clinical distress with professional psychotherapy is so pervasive that many social institutions now require event-exposed staff to participate in mandatory preventative interventions such as critical incident stress debriefing (237). Clinicians have created "trauma teams" to rush to a toxic event to treat assumed distress. Individuals increasingly go to court to argue that an event caused PTSD, that

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someone is to blame, and that compensation must be paid for suffering and treatment. Despite important professional misgivings (238), specific procedures are widely used by therapists in the UK and US to search for "repressed memories" of ancient traumatic events (239). Treatment accounts proliferate, with volumes of rhetoric, treatment guidelines, case reports, and service delivery descriptions, and quasi-proprietary approaches such as debriefing and eye movement desensitization and reprocessing are emerging (240). Two assumptions underlie most treatments: an event-oriented assumption that treatment must focus on reexposure to event features (241-243) and an emotionalexpression assumption that emotionality must be openly expressed and worked through (70,244,245). Evidence of treatment efficacy for PTSD is fragile. Symptoms diminish with time (246), and treatment studies typically fmd limited, mixed, or worse outcome (247,248), including symptom increases (42,249) when control groups are used (250,251). A massive treatment program for Israeli defence forces found that those who participated in a multimodal residential 9-month program were worse off than controls (252). Longstay inpatient treatment of US Viemam veterans showed reversion to disorder after discharge (253). A review of exposure therapy for combat-related PTSD concluded that no consensus has been achieved, and although exposure methods show some promise, they are still "undeveloped" (254). A formal metaanalysis of PTSD treatment studies found that only 11 of 255 met reasonable research standards; antidepressant drugs and behavioural treatments showed modest value (255). Two nonstatistical reviews concluded that evidence of efficacy is limited, although both saw cognitive reworking as promising (256,257); Foa concluded that event reexposure was important, although the evidence was not strong. The clinical psychology section of the American Psychological Association has concluded that 0 treatments meet criteria as "well-established," while 3 methods are "probably efficacious" (258). These poor results may arise from the model's faulty assumptions about events and emotions. Active confrontation exposures with symbolic or real oppressors or stressors achieve mixed results (259) including harm (260,261). Open emotional expressions of loss and suffering are not reliably conducive to recovery; bereaved spouses displaying more emotionality later show poorer outcome (262), and denial of emotions is associated with better adjustment in Holocaust survivors (263). Emotion focus is already characteristic of those with PTSD (264) and may be unhelpful. Professionals Versus Nonprofessionals In a recent review involving professional trauma teams brought into disaster communities, self-administered psycho-

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therapy achieved effect sizes similar to those of professional psychotherapy (265). Trauma teams signify that disorder is assumed and that community members are incompetent to remedy it (266). The assumption that hardship causes psychopathology has been criticized as a Westem medicalization model (267) that is elitist and alienating (268). Further, community reorganization and educative, action-oriented interventions may be more beneficial than psychotherapy after toxic events (269-271). Raped Ugandan women were more interested in developing marketing plans than in reworking their rape events and emotions (272). Professional focus on event-exposure and on emotionality has been reported as intrusive and aversive (211,273), while family and friends are typically described as being helpful after disasters (274-276). Professional treatment for event-attributed disorders does not yet appear to have sufficient efficacy to establish protocols that yield reliable effects, and some interventions increase dysfunction. The focus of most treatments on the event and on emotionality and the relative inattention to individual and community factors may account for this. A more accurate model of PTSD should yield more effectively targeted interventions to help patients understand and manage effects of their temperament styles and beliefs. Conclusion The DSM-IV model of PTSD defines it as a normal dosesensitive response to threatening events, yet significant evidence shows that this is not the case. Lifetime prevalence of exposure to toxic events is relatively high, even in highly privileged democracies, yet prevalence of PTSD is remarkably low when representative samples are studied. Individual differences are significantly more powerful than event characteristics in predicting PTSD (40,60,277), with events contributing relatively little variance (278). The most important personal characteristics include long-standing traits, beliefs, and preevent histories of acts and psychiatric and personality disorders. Of these, the tendency to respond to events with negative emotion (trait neuroticism) is one of the most important. Beliefs that external forces control one's condition and that emotions provide the central index of well-being and rigid ideals are also powerful. Toxic events have multiple effects, including positive ones (45,141,279) that both reflect and generate resilience. If there is any general relationship between toxic events and distress responses, it may better match the inverted U curve that is found in the relationships between many arousing stimuli and organism responses (280). A low dose (a single event) elicits an inadequate response, a moderate dose (more events) elicits relatively best performance that shows learning and adaptation, while a high dose (multiple events) exhausts the adaptive capacities of the organism, which shows

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increasingly disordered behaviour. Individual differences interact with this general relationship. The DSM model for PTSD developed partly in response to advocacy groups attempting to normalize the condition of people with certain experiences (70,281). The DSM-IV expansion of "traumatic" events to include those happening to others conflicts with the explicit dose-response assertions in the text, and in not addressing this contradiction, the definition does not improve our understanding. The model is still seriously flawed (probably because of its origins in biased clinical samples), and the inaccuracies of the model affect treatment, for which efficacy evidence is mixed. Clinically, we must attend to important individual risk factors beyond the event and the self-reported emotion. Our science suggests we need to revise defining criteria, causal explanations, and treatment assumptions. This is not a matter of blaming the victim any more than it is when identifying risk factors for schizophrenia or cardiac events; it is essential to understand the important features of the disorder. The concept of an "event-focused syndrome" may provide a more neutral and accurate diagnostic model allowing improved research and treatment for those who suffer.

10. 11.

12. 13. , 14.

15.

16.

17. 18. 19.

20.

21.

22.

23. 24.

Clinical Implications • Patients with event-focused distress have greater preevent emotionality than do others who experienced the event. • Patients with event-focused distress have beliefs that sustain their distress. • Treatment of posttraumatic stress disorder will be enhanced by greater attention to long-standing patient risk factors.

25. 26. 27. 28.

Limitations

29.

• Further scrutiny ofthe evidence ofthe power of dysfunctional beliefs is still needed. • Further evidence from treatment studies that go beyond an exposure model is needed. • Prospective and longitudinal research will clarify the contributions of premorbid risk factors.

30.

31. 32. 33. 34.

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Objectif: Evaluer les etudes concernant le role d'evenements mettant la vie en danger dans le cadre de I 'examen des reactions au stress post-traumatique significatives sur leplan clinique. Mithode : La recherche a fait l'objet d'un examen afin de recenser I'epidemiologie (la preuve de relations dose-effet, et lesfacteurs de difference individuelle dans la recherche des causes des variations de I 'etat, y compris le syndrome de stress post-traumatique, apres I 'exposition a des evenements mettant la vie en danger). Risultats: II y a un ecart significatifentre la recherche et le modele clinique du Manuel diagnostique et statistique des troubles mentaux. Les differences individuelles donnent lieu a une detresseplus prononcee que les caracteristiques des evenements. Les differences individuelles importantes qui interagissent avec les expositions au danger comprennent I 'affectivite a caracteristiques negatives (tendances a la nevrose) ; les croyances sur les emotions, le soi, le monde ainsi que sur les sources et les consequences du danger; les actes ayant precede I 'evenement, les troubles et I 'intelligence. On suggere des raisons susceptibles d'expliquer les ecarts entre la recherche et le modele courant de detresse post-traumatique. Conclusion: Comparativement aux differences individuelles, la qualite des evenements nejoue qu 'un role mineur dans les reactions aux evenements mettant la vie en danger, ce qui a des consequences significatives sur le traitement. Les methodes de traitement fondees sur ihypothese selon laquelle I'exposition a des evenements dangereux cree un syndrome post-traumatique ne tiennentpas compte des differences individuelles qui pourraient ameliorer I 'efficacite du traitement.