Feb-cjp

IN REVIEW

Individual Differences in Posttraumatic Distress: Problems With the DSM-IV Model

Marilyn Laura Bowman, PhD¹

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 from the clinical Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) model. Greater distress arises from individual differences than from 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

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

PTSD has become common in professional and popular thinking since its introduction in the third edition of the DSM in 1980 (2). Since then, the definition of causal events has steadily broadened, from being “outside . . . usual . . . experience” (DSM-III, p 236) to learning 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 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 of the 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 negativity (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 of the 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 concerned 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 higher rates. Among a more privileged group, US university 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 patterns 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, what 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 WW II 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 illness syndromes between 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, two-thirds 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 functioning 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 (53,54) caused by hearing the harm reports of others, proportional to the client’s event severity (55).

The evidence is mixed concerning 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, learning 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 event-response 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 of the 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 of the 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 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 findings 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 of the 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).

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 learned, 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 of the 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 return her children, Mrs Susan Smith was convicted of their 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 of the role of beliefs in affecting postevent distress is the common finding that intentional harms are more distressing than impersonal harms, independently of their objectively threatening qualities (135–137). Many beliefs affect responses.

Beliefs about one’s own helplessness (138) or resilience (“positive illusions” [105]), the fairness (139) or coherence (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 illness (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 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-exposed 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% of women 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-III-R 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 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 concerning 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.

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 of the behavioural pathologies of their 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 of the 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 ideas and make use of irrelevant but emotionally loaded information to create an honest but false explanation of their 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 of the misattribution of the 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 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 emotional- expression 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 find 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). Long-stay inpatient treatment of US Vietnam 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 psychotherapy 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 Western 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 dose-sensitive 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 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.

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.

Limitations

Further scrutiny of the evidence of the 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.

References

1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington (DC):American Psychiatric Association; 1994.

2. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 3rd ed. Washington (DC):American Psychiatric Association; 1980.

3. Micale M. Charcot and les nèvroses traumatiques: historical and scientific reflections. Rev Neurol (Paris) 1994;150:498–505.

4. Wilson JP. The historical evolution of PTSD diagnostic criteria. J Trauma Stress 1994;7:681–98.

5. Holmes TH, Rahe RH. The social readjustment rating scale. J Psychiatr Res 1967;11:213–8.

6. Crandall CS. Psychophysical scaling of stressful life events. Psychological Science 1992;3:256–8.

7. Rabkin JG, Struening EL. Life events, stress and illness. Science 1976;194:1013–20.

8. Leor J, Poole WK, Kloner RA. Sudden cardiac death triggered by an earthquake. N Engl J Med 1996;334:413–9.

9. Brahams D. Expert witnesses under scrutiny [letter]. Lancet 1997;349:896.

10. Green MM, McFarlane AC, Hunter CE, Griggs WM. Undiagnosed post-traumatic stress disorder following motor vehicle accidents. Med J Aust 1993;159:529–34.

11. Ruijs MB, Gabreels FJ, Keyser A. The relation between neurological trauma parameters and long-term outcome in children with closed head injury. Eur J Pediatr 1993;152:844–7.

12. Holden C. Whistleblower woes. Science 1996;271:35.

13. Kessler R, Sonnega A, Bromet E, Hughes M, Nelson CB. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995;52:1048–60.

14. Norris FH. Epidemiology of trauma: frequency and impact of different potentially traumatic events in different demographic groups. J Consult Clin Psychol 1992;60:409–18.

15. Resnick HS, Kilpatrick DG, Dansky BS, Saunders BE, Best CL. Prevalence of civilian trauma and posttraumatic stress disorder in a representative national sample of women. J Consult Clin Psychol 1993;61:984–91.

16. Vrana S, Lauterbach D. Prevalence of traumatic events and posttraumatic psychological symptoms in a nonclinical sample of college students. J Trauma Stress 1994;7:289–302.

17. Williams LM. Recall of childhood trauma: a prospective study of women’s memories of child sexual abuse. J Consult Clin Psychol 1994;62:1167–76.

18. Loftus EF, Garry M, Feldman J. Forgetting sexual trauma: what does it mean when 38% forget? J Consult Clin Psychol 1994;62:1177–81.

19. Lindal E, Stefansson JG. The lifetime prevalence of anxiety disorders in Iceland as estimated by the National Institute of Mental Health Diagnostic Interview Schedule. Acta Psychiatr Scand 1993;88:29–34.

20. Yehuda R, McFarlane AC. Conflict between current knowledge about posttraumatic stress disorder and its original conceptual basis. Am J Psychiatry 1995;152:1705–13.

21. Lee KA, Vaillant GE, Torrey WC, Elder GH. A 50-year prospective study of the psychological sequelae of World War II combat. Am J Psychiatry 1995;152:516–22.

22. Kulka RA, Schlenger WE, Fairbank JA, Hough RL, Jordan BK, Marmar CR, and others. Trauma and the Vietnam war generation: report of findings from the national Vietnam veterans readjustment study. New York: Brunner/Mazel; 1990.

23. Sutker PB, Davis JM, Uddo M, Ditta SR. War zone stress, personal resources, and PTSD in Persian Gulf War returnees. J Abnorm Psychol 1995;104:444–52.

24. Southwick SM, Morgan A, Nagy LM, Bremner D, Nicolau AL, Johnson DR, and others. Trauma-related symptoms in veterans of Operation Desert Storm: a preliminary report. A J Psychiatry 1993;150:1524–8.

25. Hoiberg A. Military effectiveness of navy men during and after Vietnam. Armed Forces Society 1980;6:232–46.

26. Ziv A, Israeli R. Effects of bombardment on the manifest anxiety level of children living in kibbutzim. J Consult Clin Psychol 1973;40:287–91.

27. Curran PS. Psychiatric aspects of terrorist violence: Northern Ireland 1969-1987. Br J Psychiatry 1988;153:470–5.

28. Sigal JJ, Weinfeld M. Trauma and rebirth: intergenerational effects of the Holocaust. New York: Praeger; 1989.

29. Basoglu M, Paker M. Severity of trauma as predictor of long-term psychological status in survivors of torture. J Anxiety Disord 1995;9:339–53.

30. Basoglu M, Paker M, Paker O, Oxmen E, Marks I, Incesu C, and others. Psychological effects of torture: a comparison of tortured with nontortured political activists in Turkey. Am J Psychiatry 1994;151:76–81.

31. Mayou R, Bryant B, Duthie R. Psychiatric consequences of road traffic accidents. BMJ 1993;307:647–51.

32. Brom D, Kleber RJ, Hofman MC. Victims of traffic accidents: incidence and prevention of post-traumatic stress disorder. J Clin Psychol 1993;49:131–40.

33. Malt U. The long-term psychiatric consequences of accidental injury. A longitudinal study of 107 adults. Br J Psychiarty 1988;153:810–8.

34. Roca RP, Spence RJ, Munster AM. Posttraumatic adaptation and distress among adult burn survivors. Am J Psychiatry 1992;149:1234–8.

35. van Driel RC, Op den Velde W. Myocardial infarction and post-traumatic stress disorder. J Trauma Stress 1995;8:151–9.

36. Grassi L, Rosti G, LaSalvia A, Marangolo M. Psychosocial variables associated with mental adjustment to cancer. Psychooncology 1993;2:11–20.

37. Rabkin JG, Wagner G, Rabkin R. Treatment of depression in HIV+ men: literature review and report of an ongoing study of testosterone replacement therapy. Ann Behav Med 1996;18:24–9.

38. Canino GJ, Bravo M, Rubio-Stipec M, Woodbury M. The impact of disaster on mental health: prospective and retrospective analyses. International Journal of Mental Health 1990;19:51–69.

39. Durkin MS, Khan N, Davidson LL, Zaman SS, Stein ZA. The effects of a natural disaster on child behavior: evidence for posttraumatic stress. Am J Public Health 1993;83:1549–53.

40. McFarlane AC. Life events and psychiatric disorder: the role of a natural disaster. Br J Psychiatry 1987;151:362–7.

41. Spurrell MT, McFarlane AC. Post-traumatic stress disorder and coping after a natural disaster. Soc Psychiatry Psychiatr Epidemiol 1993;28:194–200.

42. McFarlane AC. The longitudinal course of posttraumatic morbidity: the range of outcomes and their predictors. J Nerv Ment Dis 1988;176:30–9.

43. Merry SN, Andrews LK. Psychiatric status of sexually abused children 12 months after disclosure of abuse. J Am Acad Child Psychiatry 1994;33:939–44.

44. Rutter M. Beyond longitudinal data: Causes, consequences, changes, and continuity. J Consult Clin Psychol 1994;62:928–40.

45. Apfel RJ, Simon B. Minefields in their hearts: the mental health of children in war and communal violence. New Haven: Yale University Press; 1996.

46. Garmezy N. Children in poverty: resilience despite risk. Psychiatry: Interpersonal and Biological Processes 1993;56:127–36.

47. Cicchetti D, Garmezy N. Prospects and promises in study of resilience. Dev Psychopathol 1993;5:497–502.

48. Symonds M. The “second injury” to victims. Evaluation Change 1980;1:36–8.

49. Allodi FA. Post-traumatic stress disorder in hostages and victims of torture. Psychiatr Clin North Am 1994;17:279–88.

50. Pell J, Guer L. HIV-infected healthcare workers: results from a straw poll [letter]. Lancet 1995;346:1425.

51. Dutton MA, Rubenstein FL. Working with people with PTSD: research implications. In: Figley CR, editor. Compassion fatigue: coping with secondary traumatic stress disorder in those who treat the traumatized. New York: Brunner/Mazel; 1995:82–100.

52. Figley CR, editor. Compassion fatigue: coping with secondary traumatic stress disorder in those who treat the traumatized. New York: Brunner/Mazel; 1995.

53. Lyon E. Hospital staff reactions to accounts by survivors of childhood abuse. Am J Orthopsychiatry 1993;63:410–6.

54. Schauben LJ, Frazier PA. Vicarious trauma: the effects on female counselors of working with sexual violence survivors. Psychology of Women Quarterly 1995;19:49–64.

55. Munroe JF, Shay J, Fisher L, Makary C, Rapperport K, Zimering R. Preventing compassion fatigue: a team treatment model. In: Figley CR, editor. Compassion fatigue: coping with secondary traumatic stress disorder in those who treat the traumatized. New York: Brunner/Mazel; 1995. p 209–31.

56. McCarroll JE, Ursano RJ, Fullerton CS. Symptoms of PTSD following recovery of war dead: 13–15-month follow-up. Am J Psychiatry 1995;152:939–41.

57. Sutker PB, Uddo M, Brailey K, Allain AN, Errera P. Psychological symptoms and psychiatric diagnoses in Operation Desert Storm troops serving Graves registration duty. J Trauma Stress 1994;7:159–71.

58. Alexander DA. Stress among police body handlers: a long-term follow-up. Br J Psychiatry 1993;163:806–8.

59. Tranah T, Farmer RD. Psychological reactions of drivers to railway suicide. Soc Sci Med 1994;38:459–69.

60. Breslau N, Davis GC, Andreski P, Peterson E. Traumatic events and posttraumatic stress disorder in an urban population of young adults. Arch Gen Psychiatry 1991;48:216–22.

61. Hytten K, Hasle A. Fire fighters: a study of stress and coping. Acta Psychiatr Scand 1989;80:50–5.

62. Slagle DA, Reichman M, Rodenhauser P, Knoedler D, Davis CL. Community psychological effects following a non-fatal aircraft accident. Aviat Space Environ Med 1990;61:879–86.

63. Dixon P, Rehling G, Shiwach R. Peripheral victims of the Herald of Free Enterprise disaster. Br J Med Psychol 1993;66:150–65.

64. Bundey S. Few psychological consequences of presymptomatic testing for Huntington disease [letter]. Lancet 1997;349:4.

65. Marteau TM, Croyle RT. Psychological responses to genetic testing. Br Med J 1998;316:693–6.

66. Wiggins S, Whyte P, Huggins M, Adam S, Theilmann J, Bloch M, and others. The psychological consequences of predictive testing for Huntington’s disease. N Engl J Med 1992;327:1401–5.

67. Lazarus RS. Psychological stress and the coping process. New York: McGraw-Hill; 1966.

68. Schachter S, Singer JE. Cognitive, social and physiological determinants of emotional state. Psychol Rev 1962;69:379–99.

69. Sloan P. Post-traumatic stress in survivors of an airplane crash-landing: a clinical and exploratory research intervention. J Trauma Stress 1988;1:211–29.

70. Foa EB, Riggs DS. Posttraumatic stress disorder following assault: theoretical considerations and empirical findings. Current Directions in Psychological Science 1995;4:61–5.

71. Gervais A. A surgeon’s China. London: Hamish Hamilton; 1934.

72. Rittenberg S, Bennett A. The man who stayed behind. New York: Simon & Schuster; 1993.

73. Block J. A contrarian view of the five-factor approach to personality description. Psychol Bull 1995;117:187–215.

74. Kagan J. Galen’s prophecy: temperament in human nature. New York: BasicBooks; 1994.

75. McCrae RR, Costa PTJ. Validation of the five-factor model of personality across instruments and observers. J Pers Soc Psychol 1987;52:81–90.

76. Tellegen A, Lykken DT, Bouchard TJ, Wilcox KJ, Segal NC, Rich S. Personality similarity in twins reared apart and together. J Pers Soc Psychol 1988;54:1031–9.

77. Chess TA. Temperament and development. New York: Brunner/Mazel; 1977.

78. Kagan J. Temperamental contributions to social behavior. Am Psychol 1989;44:668–74.

79. Lewis M, Ramsay DS. Developmental change in infants’ responses to stress. Child Dev 1995;66:657–70.

80. Maziade M, Caron C, Coté R, Mérette C, Bernier H, Laplante B, and others. Psychiatric status of adolescents who had extreme temperaments at age 7. Am J Psychiatry 1990;147:1531–6.

81. Conley JJ. Longitudinal stability of prsonality traits: a multitrait-multi-method-multioccasion analysis. J Pers Soc Psychol 1985;49:1266–82.

82. Kobasa SC. Stressful life events, personality, and health. J Pers Soc Psychol 1979;37:1–11.

83. Garmezy N. Resilience and vulnerability to adverse developmental outcomes associated with poverty. American Behavioral Scientist 1991;34:416–30.

84. Ursano RJ, Wheatley RD, Carlson EH, Rahe AJ. The prisoner of war: stress, illness, and resiliency. Psychiatric Annals 1987;17:532–5.

85. Argyle M. The psychology of happiness. London: Methuen & Co; 1987.

86. Myers DG. The pursuit of happiness: who is happy – and why. New York: Avon; 1993.

87. Sigal JJ, Weinfeld M. Stability of coping style 33 years after prolonged exposure to extreme stress. Acta Psychiatr Scand 1985;71:559–66.

88. Blake DD, Cook JD. Post-traumatic stress disorder and coping in veterans who are seeking medical treatment. J Clin Psychol 1992;48:695–704.

89. Wolfe J, Keane T, Kaloupek D, Mora C, Wine P. Patterns of positive readjustment in Vietnam combat veterans. J Trauma Stress 1993;6:179–93.

90. Bouchard TJ, Lykken DT, McGue M, Segal NL, Tellegen A. Sources of human psychological differences: the Minnesota study of twins reared apart. Science 1990;250:223–8.

91. Plomin R. Environment and genes. Am Psychol 1989;44:105–11.

92. Loehlin JC. Partitioning environmental and genetic contributions to behavioral development. Am Psychol 1989;443:1285–92.

93. Costa PT, Metter EJ. Personality stability and its contribution to successful aging. Journal of Geriatric Psychiatry 1994;27:41–59.

94. Usala PD, Hertzog C. Evidence of differential stability of state and trait anxiety in adults. J Pers Soc Psychol 1991;60:471–9.

95. Kendler KS, Kessler RC, Walters EE, and others. Stressful life events, genetic liability, and onset of an episode of Major Depression in women. Am J Psychiatry 1995;152:833–42.

96. Magnus K, Diener E, Fujita F, Payot W. Extraversion and neuroticism as predictors of objective life events: a longitudinal analysis. J Pers Soc Psychol 1993;65:1046–53.

97. Lonigan CJ, Shannon MP, Taylor CM, Finch AJ, Sallee FR. Children exposed to disaster: II. Risk factors for the development of post-traumatic symptomatology. J Am Acad Child Psychiatry 1994;33:94–105.

98. Hyer L, Braswell L, Albrecht B, Boyd S, Boudewyns P, Talbert S. Relationship of NEO-PI to personality styles and severity of trauma in chronic PTSD victims. J Clin Psychol 1994;50:699–707.

99. Aldwin CM, Levenson MR, Spiro III A, Bossé R. Does emotionality predict stress? Findings from the Normative Aging Study. J Pers Soc Psychol 1989;56:618–24.

100. Ormel J, Wohlfarth T. How neuroticism, long-term difficulties, and life situation change influence psychological distress: a longitudinal model. J Pers Soc Psychol 1991;60:744–55.

101. Cousins N. Anatomy of an illness. New York: WW Norton; 1979.

102. Friedman HS, VandenBos GR. Disease-prone and self-healing personalities. Hospital and Community Psychiatry 1992;43:1177–9.

103. Kübler-Ross E. On death and dying. London: Macmillan; 1969.

104. Greer S, Morris T, Pettingale KW. Psychological response to breast cancer: effect on outcome. Lancet 1979;ii:785–7.

105. Taylor SE, Brown JD. Illusion and well-being: a social psychological perspective on mental health. Psychol Bull 1988;103:193–210.

106. Frese M. A plea for realistic pessimism: on objective reality, coping with stress, and psychological dysfunction. In: Montada L, Filipp S-H, Lerner M, editors. Life crises and experiences of loss in adulthood. Hillsdale NJ: Erlbaum; 1992:81–94.

107. Friedman JS, Booth-Kewley S. The “disease-prone personality”: a meta-analytic view of the construct. Am Psychol 1987;42:539–55.

108. Friedman HS, Tucker JS. Does childhood personality predict longevity? J Pers Soc Psychol 1993;65:176–85.

109. Joseph S, Williams R, Yule W. Psychosocial perspectives on post-traumatic stress. Clin Psychol Rev 1995;15:515–44.

110. Hughes JN, Cavell TA. A positive view of self: risk or protection for aggressive children? Dev Psychopathol 1997;9:75–94.

111. Baumeister RF, Smart L, Boden JM. Relation of threatened egotism to violence and aggression: the dark side of high self-esteem. Psychol Rev 1996;103:5–33.

112. Stevenson HW, Lee S-Y, Stigler JW. Mathematics achievement of Chinese, Japanese, and American children. Science 1986;231:693–9.

113. Stevenson HW, Chen C-S, Lee S-Y. Mathematics achievement of Chinese, Japanese, and American children: ten years later. Science 1993;259:53–8.

114. Lykken D, Tellegen A. Happiness is a stochastic phenomenon. Psychological Science 1996;7:186–9.

115. de Beauvoir S. The prime of life. Harmondsworth UK: Penguin; 1962.

116. Alexander F. Psychosomatic medicine. New York: Norton; 1950.

117. Traue HC, Pennebaker JW, editors. Emotion inhibition and health. Gottingen Germany: Hogrefe & Huber; 1993.

118. Ekman P. Facial expression and emotion. Am Psychol 1993;48:384–92.

119. Sinclair RC, Hoffman C, Mark MM, Martin LL, Pickering TL. Construct accessibility and the misattribution of arousal: Schachter and Singer revisited. Psychological Science 1994;5:15–9.

120. Cohen F, Lazarus RS. Active coping processes, coping dispositions, and recovery from surgery. Psychosom Med 1973;35:375–89.

121. Weisenberg M, Schwarzwald J, Waysman M, Solomon Z, Klingman A. Coping of school-age children in the sealed room during SCUD missile bombardment and postwar stress reactions. J Consult Clin Psychol 1993;61:462–7.

122. Nolen-Hoeksema S, McBride A, Larson J. Rumination and psychological distress among bereaved partners. J Pers Soc Psychol 1997;72:855–62.

123. Johnson JL, Morse JM. Regaining control: the process of adjustment after myocardial infarction. Heart Lung 1990;19:126–35.

124. Havik OE, Maeland JG. Patterns of emotional reactions after myocardial infarction. J Psychosom Res 1990;34:271–85.

125. Ironson G, Taylor CB, Boltwood M, Bartzokis T, Dennis C, Chesney M, and others. Effects of anger on left ventricular ejection fraction in coronary artery disease. Am J Cardiol 1992;70:281–5.

126. Verrier RL, Mittleman MA. Life-threatening cardiovascular consequences of anger in patients with coronary heart disease. Cardiol Clin 1996;14:289–307.

127. Watson JC. The relationship between vivid description, emotional arousal, and in-session resolution of problematic reactions. J Consult Clin Psychol 1996;64:459–64.

128. Folkman S, Lazarus RS. An analysis of coping in a middle-aged community sample. J Health Soc Behav 1980;21:219–39.

129. Malia K, Powell G, Torode S. Coping and psychosocial function after brain injury. Brain Inj 1995;9:607–18.

130. Mikulincer M, Florian V. Stress, coping, and fear of personal death: the case of middle-aged men facing early job retirement. Death Studies 1995;19:413–31.

131. Solomon Z, Mikulincer M, Avitzur E. Coping, locus of control, social support and combat related posttraumatic stress disorder: a prospective study. J Pers Soc Psychol 1988;55:279–85.

132. Nezu AM, Carnevale GJ. Interpersonal problem solving and coping reactions of Vietnam veterans with posttraumatic stress disorder. J Abnorm Psychol 1987;96:155–7.

133. McDonough M. Susan Smith gets life in prison. The Herald-Journal 1995 July 29;Sect A:1.

134. Wortman CB, Silver RC. Reconsidering assumptions about coping with loss: an overview of current research. In: Montada L, Filipp S-H, Lerner M, editors. Life crises and experiences of loss in adulthood. Hillsdale (NJ): Erlbaum. 1992. p 341–65.

135. Goldsteen R, Schorr JK. The long-term impact of a man-made disaster: an examination of a small town in the aftermath of the Three Mile Island nuclear reactor accident. Disasters 1982;6:10–9.

136. Helzer JE, Robins LN, McEvoy L. Post-traumatic stress disorder in the general population. N Engl J Med 1987;317:1630–4.

137. Ullman SE. Adult trauma survivors and post-traumatic stress sequelae: an analysis of reexperiencing, avoidance, and arousal criteria. J Trauma Stress 1995;8:179–88.

138. Peterson C, Seligman M, Vaillant GE. Pessimistic explanatory style is a risk factor for physical illness: a thirty-five-year longitudinal study. J Pers Soc Psychol 1988;55:23–7.

139. Wortman CB, Silver RC. The myths of coping with loss. J Consult Clin Psychol 1989;57:349–57.

140. Antonovsky A. Health, stress, and coping. San Francisco: Jossey-Bass; 1979.

141. Wortman CB, Silver RC, Kessler RC. The meaning of loss and adjustment to bereavement. In: Stroebe MS, Stroebe W, Hansson RO, editors. Handbook of bereavement: theory, research, and intervention. New York: Cambridge University Press; 1993. p 349–66.

142. Hefez A. The role of the press and the medical community in the epidemic of “mysterious gas poisoning” in the Jordan West Bank. Am J Psychiatry 1985;142:833–7.

143. Small GW, Propper MW. Mass hysteria among student performers: social relationship as a symptom predictor. Am J Psychiatry 1991;148:1200–5.

144. Chew PK, Phoon WH, Mae-Lim HA. Epidemic hysteria among some factory workers in Singapore. Singapore Med J 1976;17:10–5.

145. Newman B. Malaysian malady: when the spirit hits, a scapegoat suffers. Wall Street Journal 1980 March 7:1,24.

146. Kiser L, Heston J, Hickerson S, Millsap P. Anticipatory stress in children and adolescents. Am J Psychiatry 1993;150:87–92.

147. Korgeski GP, Leon G. Correlates of self-reported and objectively-determined exposure to Agent Orange. Am J Psychiatry 1983;140:1443–9.

148. Widom CS, Morris S. Accuracy of adult recollections of childhood victimization: part 2. Childhood sexual abuse. Psychological Assessment 1997;9:34–46.

149. McCormick RA, Taber JI, Kruedelback N. The relationship between attributional style and post-traumatic stress disorder in addicted patients. J Trauma Stress 1989;2:477–87.

150. Morgan HJ, Janoff-Bulman R. Positive and negative self-complexity: patterns of adjustment following traumatic versus non-traumatic life experiences. J Pers Soc Psychol 1994;13:63–85.

151. McIntosh DN, Cohen R, Wortman CB. Religion’s role in adjustment to a negative life event: coping with the loss of a child. J Pers Soc Psychol 1993;65:812–21.

152. Baker AM, Kevorkian NS. Differential effects of trauma on spouses of traumatized households. J Trauma Stress 1995;8:61–74.

153. Saul J. Helping the children of war [book review]. Lancet 1997;349:1259.

154. Bandura A. Self-efficacy: the exercise of control. New York: Freeman; 1997.

155. Wyman PA, Cowen EL. The role of children’s future expectations in self-esteem functioning and adjustment to life stress; a prospective study of urban at-risk children. Dev Psychopathol 1993;5:649–61.

156. Seligman MEP, Kamen LP, Nolen-Hoeksema S. Explanatory style across the lifespan: achievement and health. In: Lerner RM, Hetherington EM, Perlmutter M, editors. Child development in lifespan perspective. Hillsdale (NJ): Lawrence Erlbaum Associates; 1988. p 91–114.

157. Petrie K, Moss-Morris R, Weinman J. The impact of catastrophic beliefs on functioning in chronic fatigue syndrome. J Psychosom Res 1995;39:31–7.

158. Gross JL, Munoz R, F. Emotion regulation and mental health. Clinical Psychology Science and Practice 1995;2:151–4.

159. Beck AT. Depression: clinical, experimental and theoretical aspects. New York: Hoeber; 1967.

160. Watson CG, Anderson PED. Posttraumatic stress disorder (PTSD) symptoms in PTSD patients’ families of origin. J Nerv Ment Dis 1995;183:633– 8.

161. Rotter JB. Generalized expectancies for internal vs eternal control of reinforcement. Psychologicl Monographs: General and Applied 1966;80:1–28.

162. Frenkel E, Kugelmass S, Nathan M, Ingraham LJ. Locus of control and mental health in adolescence and adulthood. Schizophren Bull 1995;21:219–26.

163. Janoff-Bulman R, Brickman P. Expectations and what people learn from failure. In: Feather NT, editor. Expectations and actions. Hillsdale (NJ): Erlbaum; 1982. p 207–37.

164. Wortman CB, Sheedy C, Gluhoski V, Kessler RC. Stress, coping, and health: conceptual issues and directions for future research. In: Friedman HS, editor. Hostility, coping, and health. Washington (DC): American Psychological Association; 1992. p 227–56.

165. Schnurr PP, Friedman MJ, Rosenberg SD. Premilitary MMPI scores as predictors of combat-related PTSD symptoms. Am J Psychiatry 1993;150:479–83.

166. Bowman ML. Individual differences in posttraumatic response: Problems with the adversity-distress connection. Mahweh (NJ): Lawrence Erlbaum Associates; 1997.

167. Downey G, Silver RC, Wortman CB. Reconsidering the attribution-adjustment relation following a major negative event: coping with the loss of a child. J Pers Soc Psychol 1990;59:925–40.

168. Davis CG, Lehman DR, Wortman CB, Silver RC, Thompson SC. The undoing of traumatic life events. Personality and Social Psychology Bulletin 1995;21:109–24.

169. Terr LC. Psychic trauma in children: observations following the Chowchilla school-bus kidnapping. Am J Psychiatry 1981;138:14–9.

170. Fraser G. Land of the free, home of the sound bite. The Globe and Mail 1996 April 6;Sect D:4.

171. Garrison CZ, Weinrich MW, Hardin SB, Weinrich S, Wang L. Post-traumatic stress disorder in adolescents after a hurricane. Am J Epidemiol 1993;138:522–30.

172. King DW, King LA, Foy DW, Gudanowski DM. Prewar factors in combat-related posttraumatic stress disorder: structural equation modeling with a national sample of female and male Vietnam veterans. J Consult Clin Psychol 1996;64:520–31.

173. Laufer RS, Gallops MD, Frey-Wouters E. War stress and trauma: the Vietnam experience. J Health Soc Behav 1984;25:65–85.

174. Hiley-Young B, Blake DD, Abueg FR, Rozynko V, Gusman FD. Warzone violence in Vietnam: an examination of premilitary, military, and postmilitary factors in PTSD in-patients. J Trauma Stress 1995;8:125–41.

175. Hendin H, Haas AP. Combat adaptations in Vietnam veterans without posttraumatic stress disorders. Am J Psychiatry 1984;141:956–60.

176. Nader KO, Pynoos RS, Fairbanks LA, al Ajeel M, al Asfour A. A preliminary study of PTSD and grief among the children of Kuwait following the Gulf Crisis. Br J Psychol 1993;32:407–16.

177. Farmer JE, Peterson L. Injury risk factors in children with attention deficit hyperactivity disorder. Health Psychol 1995;14:325–32.

178. Flagler SL. Recurrent poisoning in children: a review. J Pediatr Psychol 1987;12:631–41.

179. Champion LA, Goodall G, Rutter M. Behaviour problems in childhood and stressors in early adult life: I. A 20 year follow-up of London school children. Psychol Med 1995;25:231–46.

180. Shepherd J. Are assault victims prone to the surgeon’s lancet (and wounds that surely heal)? [letter]. Lancet 1995;346:1560.

181. Sherwood RJ, Funari DJ, Piekarski AM. Adapted characters styles of Vietnam veterans with Posttraumatic Stress Disorder. Psychol Rep 1990;66:623–31.

182. Southwick SM, Yehuda R, Giller EL. Personality disorders in treatment-seeking combat veterans with posttraumatic stress disorder. Am J Psychiatry 1993;150:1020–3.

183. Silsby HD, Jones FD. The etiologies of Vietnam posttraumatic stress syndrome. Mil Med 1985;150:6–7.

184. Weston WA, Dalby JT. A case of pseudologia fantastica with antisocial personality disorder. Can J Psychiatry 1991;36:612–4.

185. Johnson WB. Narcissistic personality as a mediating variable in manifestations of post-traumatic stress disorder. Mil Med 1995;160:40–1.

186. Burkett BG, Whitley G. Stolen valor: how the Vietnam generation was robbed of its heroes and its history. Dallas (TX): Verity Press; 1998.

187. Goldberg C. Lie exposed, killer is back in prison. New York Times 1998 August 27;Sect A:20.

188. Frueh BC. Symptom overreporting in combat veterans evaluated for PTSD: differentiation on the basis of compensation seeking status. J Pers Assess 1997;68:369–84.

189. Johnson-Greene D. Use of educational credentials to estimate pre-morbid intellectual functioning:4061. Annual meeting of American Psychological Association. Toronto: American Psychological Association, 1996. p 207.

190. Cottler LB, Compton WM, Mager D, Spitznagel EL, Janca A. Post-traumatic stress disorder among substance users from the general population. Am J Psychiatry 1992;149:664–70.

191. Blanchard EB, Hickling EJ, Taylor AE, Loos W. Psychiatric morbidity associated with motor vehicle accidents. J Nerv Ment Dis 1995;183:495–504.

192. Smith EM, Robins LM, Przubeck TR, Goldrig E, Solomon S. Psychosocial consequences of a disaster. In: Shore J, Robins L, editors. Psychosocial disaster stress studies: new methods and findings. Washington (DC): American Psychiatric Press; 1986. p 49–76.

193. Scott RB, Brooks N, McKinlay W. Post-traumatic morbidity in a civilian community of litigants: a follow-up at 3 years. J Trauma Stress 1995;8:403–17.

194. Green BL, Grace MC, Lindy JD, Gleser GC, Leonard A. Risk factors for PTSD and other diagnoses in a general sample of Vietnam veterans. Am J Psychiatry 1990;147:729–33.

195. Brady KT. Posttraumatic stress disorder and comorbidity: recognizing the many faces of PTSD. J Clin Psychiatry 1997;58:12–5.

196. Boney-McCoy S, Finkelhor D. Is youth victimization related to trauma symptoms and depression after controlling for prior symptoms and family relationships? A longitudinal, prospective study. J Consult Clin Psychol 1996;64:1406–16.

197. Burg MM, Seeman TE. Families and health: the negative side of social ties. Ann Behav Med 1994;16:109–15.

198. Coyne JC, Ellard JH, Smith DAF. Social support, interdependence, and the dilemmas of helping. In: Sarason IG, Sarason BR, Pierce GR, editors. Social support: an interactional view. New York: John Wiley & Sons; 1990. p 129–49.

199. Taylor SE, Repetti RL. Health psychology: what is an unhealthy environment and how does it get under the skin? Annual Review of Psychology 1997;48:411–7.

200. Thoits PA. Stress, coping, and social support processes: Where are we? What next? J Health Soc Behav 1995;36:53–79.

201. Kendler KS, Kessler RC, Heath AC, Neale MC, Eaves LJ. Coping: a genetic epidemiological investigation. Psychol Med 1991;21:337–46.

202. Cohen S, Sherrod DR, Clark MS. Social skills and the stress-protective role of social support. J Pers Soc Psychol 1986;50:963–76.

203. Wills TA, DuHamel K, Vaccaro D. Activity and mood temperament as predictors of adolescent substance abuse: test of a self-regulation mediational model. J Pers Soc Psychol 1995;68:901–16.

204. Masten AS, Best KM. Resilience and development: contributions from the study of children who overcome adversity. Dev Psychopathol 1990;2:425–44.

205. Cederblad M, Dahlin L. Salutogenic childhood factors reported by middle-aged individuals: follow-up of the children from the Lundby Study grown up in families experiencing three or more childhood psychiatric risk factors. Eur Arch Psychiatry Clin Neurosci 1994;244:1–11.

206. Bland LC, Sowa CJ. An overview of resilience in gifted children. Roeper Review 1994;17:77–80. 207. Cederblad M, Dahlin L. Intelligence and temperament as protective factors for mental health: a cross-sectional and prospective epidemiology study. Eur Arch Psychiatry Clin Neurosci 1995;245:11–9.

208. Macklin ML, Metzger LJ, McNally RJ, Litz BT, Lasko NB, Orr SP, and others. Lower precombat intelligence is a risk factor for posttraumatic stress disorder. J Consult Clin Psychol 1998;66:323–6.

209. McNally RJ, Shin LM. Association of intelligence with severity of posttraumatic stress disorder symptoms in Vietnam combat veterans. Am J Psychiatry 1995;152:936–8.

210. Sutker PB, Allain AN. Psychological assessment of aviators captured in World War II. Psychological Assessment 1995;7:66–8.

211. McFarlane AC. An Australian disaster: the 1983 bushfires. International Journal of Mental Health 1990;19:36–47.

212. McFarlane AC. Avoidance and intrusion in posttraumatic stress disorder. J Nerv Ment Dis 1992;180:439–45.

213. Weaver TL, Clum GA. Psychological distress associated with interpersonal violence: a meta-analysis. Clin Psychol Rev 1995;15:115–40.

214. Casella L, Motta RW. Comparison of characteristics of Vietnam veterans with and without Posttraumatic Stress Disorder. Psychol Rep 1990;67:595–605.

215. Rutter M. Pathways from childhood to adult life. J Child Psychol Psychiatry 1989;30:23–51.

216. Widom CS. Does violence beget violence? A critical examination of the literature. Psychol Bull 1989;106:3–28.

217. Renaud H, Estess F. Life history interviews with one hundred normal American males: “pathogenicity” of childhood. Am J Orthopsychiatry 1961;31:786–802.

218. Rutter M. Meyerian psychobiology, personality development, and the role of life experiences. Am J Psychiatry 1986;143:1077–87.

219. Scarr S, McCartney K. How people make their own environments: a theory of genotype-environment effects. Child Dev 1983;54:424–35.

220. Sampson RJ, Laub JH. Crime in the making: pathways and turning points through life. Cambridge (MA): Harvard University Press; 1993.

221. Grant I, Gerst M, Yager J. Scaling of life events by psychiatric patients and normals. J Psychosom Res 1976;20:141–9.

222. Gerst MS, Grant I, Yager J, Sweetwood H. The reliability of the social readjustment rating scale: Moderate and long-term stability. J Psychosom Res 1978;22:519–623.

223. Gazzaniga MS, LeDoux JE. The integrated mind. New York: Plenum; 1978.

224. Greenwald AG. The totalitarian ego: fabrication and revision of personal history. Am Psychol 1980;35:603–18.

225. Lipinski JF, Pope HG. Do “flashbacks” represent obsessional imagery? Compr Psychiatry 1994;35:245–7.

226. Piaget J. Play, dreams and imitation in childhood. New York: WW Norton; 1962.

227. Hashtroudi S, Johnson MK. Aging and the effects of affective and factual focus on source monitoring and recall. Psychol Aging 1994;9:160–70.

228. Southwick SM, Morgan CA, Nicolaou AL, Charney DS. Consistency of memory for combat-related traumatic events in veterans of operation Desert Storm. Am J Psychiatry 1997;154:173–7.

229. Wedding D, Faust D. Clinical judgment and decision making in neuropsychology. Archives of Clinical Neuropsychology 1989;4:233–65.

230. Brickman P, Coates D, Janoff-Bulman R. Lottery winners and accident victims: is happiness relative? J Pers Soc Psychology 1978;36:917–27.

231. Deutsch M. The pathetic fallacy: an observer error in social perception. J Pers 1960;28:317–32.

232. Horowitz MJ, Schaeffer C, Cooney P. Life event scaling for recency of experience. In: Gunderson EKE, Rahe RH, editors. Life stress and illness. Springfield (IL): Thomas; 1974. p 125–33.

233. Ladieu G, Hanfmann E, Dembo T. Studies in adjustment to visible injuries: evaluation of help by the injured. J Abnorm Soc Psychology 1947;42:169-192.

234. Taylor DM, Wright SC, Moghaddam FM, Lalonde RN. The personal/group discrimination discrepancy: perceiving my group, but not myself, to be a target for discrimination. Personality and Social Psychology Bulletin 1990;16:254–62.

235. Taylor SE, Brown JD. “Illusion” of mental health does not explain positive illusions. Am Psychol 1994;49:972–3.

236. Lidz T. The family, language, and the transmission of schizophrenia. In: Rosenthal D, Kety S, editors. The transmission of schizophrenia. New York: Pergamon Press; 1968.

237. Mitchell JT, Everly GS. Critical incident stress debriefing: CISD. An operations manual for the prevention of traumatic stress among emergency service and disaster workers. 2nd ed. Ellicott City (MD): Chevron Publishing; 1995.

238. Royal College of Psychiatrists. Reported recovered memories of child sexual abuse. Psychiatric Bulletin 1997;21:663–5.

239. Poole DA, Lindsay DS, Memon A, Bull R. Psychotherapy and the recovery of memories of childhood sexual abuse: U.S. and British practitioners’ opinions, practices, and experiences. J Consult Clin Psychol 1995;63:426–37.

240. Shapiro F. Eye movement desensitization and reprocessing: basic principles, protocols, and procedures. New York: Guilford Press; 1995.

241. Keane TM, Kaloupek DG. Cognitive behavior therapy in the treatment of posttraumtic stress disorder. The Clinical Psychologist 1996;49:7–8.

242. Agger I, Jensen SB. The psychosexual trauma of torture. In: Wilson JP, Raphael B, editors. International handbook of traumatic stress syndromes. New York: Plenum Press; 1993. p 684–702.

243. Cienfuegos AJ, Monelli C. The testimony of political repression as a therapeutic instrument. Am J Orthopsychiatry 1983;53:43–51.

244. Rachman S. Emotional processing. Behav Res Ther 1980;18:51–60.

245. Horowitz MJ, Stinson C, Field N. Natural disasters and stress response syndromes. Psychiatric Annals 1991;21:556–62.

246. Green BL, Grace MC, Vary MG, Kramer TL, Gleser GC, Leonard AC. Children of disaster in the second decade: a 17 year follow-up of Buffalo Creek survivors. J Am Acad Child Psychiatry 1994;33:71–9.

247. Deahl MP, Gillham AB, Thomas J, Searle MM, Srinivasan M. Psychological sequelae following the Gulf War: factors associated with susequent morbidity and the effectiveness of psychological debriefing. Br J Psychiatry 1994;165:60–5.

248. Kenardy JA, Webster RA, Lewin TJ, Carr VJ, Hazell PL, Carter GL. Stress debriefing and patterns of recovery following a natural disaster. J Trauma Stress 1996;9:37–49.

249. Hobbs M, Mayou R, Harrison B, Worlock P. A randomised controlled trial of psychological debriefing for victims of road traffic accidents. BMJ 1996;313:1438–9.

250. Bisson JI, Deahl MP. Psychological debriefing and prevention of post-traumatic stress: more research is needed. Br J Psychiatry 1994;165:717–20.

251. Hammarberg M, Silver SM. Outcome of treatment for posttraumatic stress disorder in a primary care unit serving Vietnam veterans. J Trauma Stress 1994;7:195–216.

252. Solomon Z, Shalev A, Spiro SE, Dolev A, Bleich A, Waysman M, and others. Negative psychometric outcomes: self-report measures and a follow-up telephone survey. J Trauma Stress 1992;5:225–46.

253. Fontana A, Rosenheck R. Effectiveness and cost of the inpatient treatment of posttraumatic stress disorder: comparison of three models of treatment. Am J Psychiatry 1997;154:758–65.

254. Frueh BC, Turner SM, Beidel DC. Exposure therapy for combat-related PTSD: a critical review. Clin Psychol Rev 1995;15:799–817.

255. Solomon SD, Gerrity ET, Muff AM. Efficacy of treatments for posttraumatic stress disorder. JAMA 1992;268:633–8.

256. Foa EB, Meadows EA. Psychosocial treatments for posttraumatic stress disorder: a critical review. Annual Review of Psychology 1997;48:449–80.

257. McFarlane AC. Individual psychotherapy for posttraumatic stress disorder. Psychiatr Clin North Am 1994;17:393–408.

258. Chambless DL, Baker MJ, Baucom DH, Beutler, LE, Calhoun KS, Crits-Christoph P, and others. Update on empirically validated therapies, II. The Clinical Psychologist 1998;51:3–16.

259. Watson CG, Tuorila J, Detra E, Gearhart LP, Wielkiewicz RM. Effects of a Vietnam War Memorial pilgrimage on veterans with posttraumatic stress disorder. J Nerv Ment Dis 1995;183:315–9.

260. Kozaric-Kovacic D, Folnegovic-Smalc V, Skrinjaric J, Szajnberg NM, Marusic A. Rape, torture, and traumatization of Bosnian and Croatian women: psychological sequelae. Am J Orthopsychiatry 1995;65:428–33.

261. Lerman C, Schwartz MD, Miller SM, Daly M, Sands C, Rimer BK. A randomized trial of breast cancer risk counseling: Interacting effects of counseling, educational level, and coping style. Health Psychol 1996;15:75–83.

262. Bonanno GA, Keltner D. Facial expressions of emotion and the course of conjugal bereavement. J Abnorm Psychol 1997;106:126–37.

263. Kaminer H, Lavie P. Sleep and dreaming in Holocaust survivors: dramatic decrease in dream recall in well-adjusted survivors. J Nerv Ment Dis 1991;179:664–9.

264. Solomon Z, Avitzur E. Coping styles and post-war psychopathology among Israeli soldiers. Personality and Individual Differences 1990;11:451–6.

265. Christensen A, Jacobson NS. Who (or what) can do psychotherapy: the status and challenge of nonprofessional therapies. Psychological Science 1994;5:8–14.

266. McKnight J. Community and its counterfeits. Toronto: Canadian Broadcasting Corporation RadioWorks; 1994. p 1–26.

267. Summerfield D. Debriefing after psychological trauma: inappropriate exporting of Western culture may cause additional harm [letter]. BMJ 1995;311:509.

268. Swartz L, Levett A. Political repression and children in South Africa: the social construction of damaging effects. Soc Sci Med 1989;28:741–50.

269. Galante R, Foa D. An epidemiological study of psychic trauma and treatment effectiveness for children after a natural disaster. J Am Acad Child Psychiatry 1986;25:357–63.

270. Johnson DR, Lubin H. Treatment preferences of Vietnam veterans with posttraumatic stress disorder. J Trauma Stress 1997;10:391–405.

271. Jones L. Responses to stress is not necessarily pathological. BMJ 1995;311:509–10.

272. Bracken PJ, Giller JE, Summerfield D. Psychological responses to war and atrocity: the limitations of current concepts. Soc Sci Med 1995;40:1073–82.

273. Scott MJ, Stradling SG. Client compliance with exposure treatments for posttraumatic stress disorder. J Trauma Stress 1997;10:523–6.

274. Bolin RC. Family recovery from natural disaster: a preliminary model. Mass Emergencies 1976;1:267–77.

275. Drabek TE, Key WH, Erickson PE, Crowe JL. The impact of disaster on kin relationships. Journal of Marriage and the Family 1975;37:481–94.

276. Ursano RJ, McCaughey BG, Fullerton CS, editors. Individual and community responses to trauma and disaster: the structure of human chaos. Cambridge (UK): Cambridge University Press; 1994.

277. Breslau N, Davis GC. Posttraumatic stress disorder. J Nerv Ment Dis 1987;175:256–64.

278. Byrne DG. Personal assessments of life-event stress and the near future onset of psychological symptoms. Br J Med Psychol 1984;57:241–8.

279. Aldwin CM, Sutton KJ, Lachman M. The development of coping resources in adulthood. J Pers 1996;64:837–71.

280. Hebb DO. Drives and the C.N.S. (conceptual nervous system). Psychol Rev 1955;62:243–54.

281. Young A. The harmony of illusions: inventing post-traumatic stress disorder. Princeton (NJ): Princeton University Press; 1995.

Résumé

Objectif : Évaluer les études concernant le rôle d’événements mettant la vie en danger dans le cadre de l’examen des réactions au stress post-traumatique significatives sur le plan clinique.

Méthode : La recherche a fait l’objet d’un examen afin de recenser l’épidémiologie (la preuve de relations dose-effet, et les facteurs de différence individuelle dans la recherche des causes des variations de l’état, y compris le syndrome de stress post-traumatique, après l’exposition à des événements mettant la vie en danger).

Résultats : Il y a un écart significatif entre la recherche et le modèle clinique du Manuel diagnostique et statistique des troubles mentaux. Les différences individuelles donnent lieu à une détresse plus prononcée que les caractéristiques des événements. Les différences individuelles importantes qui interagissent avec les expositions au danger comprennent l’affectivité à caractéristiques négatives (tendances à la névrose) ; les croyances sur les émotions, le soi, le monde ainsi que sur les sources et les conséquences du danger ; les actes ayant précédé l’événement, les troubles et l’intelligence. On suggère des raisons susceptibles d’expliquer les écarts entre la recherche et le modèle courant de détresse post-traumatique.

Conclusion : Comparativement aux différences individuelles, la qualité des événements ne joue qu’un rôle mineur dans les réactions aux événements mettant la vie en danger, ce qui a des conséquences significatives sur le traitement. Les méthodes de traitement fondées sur l’hypothèse selon laquelle l’exposition à des événements dangereux crée un syndrome post-traumatique ne tiennent pas compte des différences individuelles qui pourraient améliorer l’efficacité du traitement.

Manuscript received September 1998.

¹Professor, Department of Psychology, Simon Fraser University, Burnaby, British Columbia.

Address for correspondence: Dr ML Bowman, Department of Psychology, Simon Fraser University, 8888 University Drive, Burnaby, BC V5A 1S6

email: bowman@sfu.ca

Can J Psychiatry, Vol 44, February 1999