Факторы риска развития ПТСР
PTSD was originally conceptualized as a direct consequence of exposure to a traumatic event in otherwise normal individuals. As originally described, the emphasis was on establishing the primacy of the trauma as the etiologic agent, rather than individual vulnerability factors. Yet it was clear from the beginning that not all trauma survivors developed permanent disorder. In fact, many recovered. Thus, the search for risk factors that increase vulnerability to chronic PTSD occurred early in the history of the disorder. Foy et al. (1984) published one of the first formal studies to look at risk factors for PTSD and reported characteristics of trauma exposure to be of central importance. Numerous studies have since observed a dose-response relationship between trauma severity and PTSD.
However, features of the trauma invariably account for a small proportion of the variance in PTSD symptoms (Yehuda & McFarlane, 1995). Epidemiological research has found the rate of exposure to trauma to far outweigh the prevalence of PTSD, indicating that most people do not ever develop PTSD following a traumatic event (breslau et al., 1998). Moreover, PTSD is not the only possible psychological consequence of trauma. Elevated rates of major depression, panic, and substance abuse are commonly observed in traumatized populations (Shalev et al., 1998b), again calling into question the nature of the relationship between trauma and PTSD.
Currently, some investigators are calling for PTSD to be recast in a stress-diathesis model, with trauma characteristics and individual risk factors interacting to determining who develops the disorder. The study of risk factors has become increasingly popular, emphasizing environmental and demographic factors, personality and psychiatric history, dissociation, cognitive and biological systems, and genetic or familial risk (Yehuda, 1999a). All of these approaches are essential in directing and advancing the field as a whole. To date, several important risk factors have been identified.
Environmental Risk Factors . In addition to characteristics of stressor severity, a history of exposure prior to the focal trauma is also an important risk factor. A history of prior exposure to trauma or to chronic stress is an extremely potent risk factor for PTSD (Davidson et al., 1991), particularly if it is experienced at a young age (bremner et al., 1993). In addition, breslau ct al. (1999a) found that the type of
prior trauma exposure is important, prior assault being a particularly potent risk factor for the development of PTSD upon subsequent traumatization. Social factors may also affect risk. A history of family instability is associated with increased prevalence of PTSD (King et al., 1996), whereas good social support is associated with lower levels of symptoms (Solomon et al., 1988).
Demographic Risk Factors . breslau et al. (1998) identified several demographic risk factors for the development of PTSD. Gender is an extremely salient risk factor, even controlling for differences in the type of events that are experienced by men compared to women. A consistent finding has been that the prevalence of PTSD is almost twice as high in women as it is in men. To date, there are no firm explanations for this finding, although gender (being female) is also a risk factor for other psychiatric disorders. breslau et al. (1999b) found that the higher risk for PTSD in females is primarily due to a particular vulnerability to assaultive violence. breslau et al. (1999b) suggest that assaultive violence is more threatening and injurious to females, most perpetrators being male and therefore wielding greater physical strength.
Lower levels of education and income, and being divorced or widowed, are risk factors for PTSD. In addition, some studies have reported a higher risk for PTSD among ethnic minorities (breslau et al., 1998). However, not all studies have found ethnicitv to be a risk factor for PTSD and instead have found that ethnic differences may interact with (Norris, 1992) or be attributable to (breslau et al., 1991) other factors. breslau et al. (1998) note that several demographic factors affect the risk of trauma exposure, including gender, age, and socioeconomic status, as well as ethnicity. This observation is important to the consideration of risk, since trauma exposure does not occur in a vacuum. Some of the predictors of PTSD may actually be predictors of trauma exposure.
Prior Psychiatric Disorders and Personality Dimensions. A past history of behavioral or psychological problems has also been associated with the development of PTSD (McFarlane, 1989). Many different psychiatric disorders have been associated with past psychological problems, suggesting that this risk factor may be non-specific to poor coping rather than predictive of a specific disorder. Indeed, breslau et al. (1998) found that prior affective, anxiety, or substance abuse disorders all represented risk factors for the development of PTSD, and concluded that having a psychiatric history per se was a stronger predictor of PTSD than having a history of any one of the specific disorders. Personality dimensions are also important (for a review, see Schnurr & Vielhauer, 1999). Adult avoidant, antisocial (Schnurr et al., 1993), or neurotic personalities (breslau et al., 1998) prior to the traumatic event have an increased risk for the development of PTSD.
Dissociation. There is ambiguity regarding whether dissociation should be considered a stable personality traitor a state-related cognitive response to trauma. Nonetheless, peritraumatic dissociation appears to be an important risk factor for the development of PTSD (Koopman et al., 1994), and PTSD subjects show elevated scores on measures of dissociative symptoms (bremnereta!., 1992). In a prospective study of injured trauma survivors, Shalev et al. (1996) found peritraumatic dissociation to be the best predictor of PTSD symptoms at 6 months post-trauma, explaining 30% of the variance in symptoms. Dissociative reactions may be adopted as a maladaptive coping strategy in response to childhood trauma or chronic stress (Spiegel, 1991). As such, they may partially mediate the relationship between prior traumatization and subsequently increased vulnerability to PTSD. Future studies examining dissociation in high-risk groups will shed light on this issue.
Cognitive Risk Factors. Lower intellectual functioning has been found to be a risk factor for the development of PTSD. Macklin et al. (1998) assessed IQ in soldiers prior to entering the combat situation and found that lower precombat intelligence levels are associated with increased risk of developing PTSD on exposure to combat. This association remained significant even once an adjustment was made for degree of combat exposure. Controlling for degree of combat exposure is important because individuals with lower premorbid IQs are often placed in heavier combat situations than others.
Individuals with PTSD show increased neurological soft signs, indicative of subtle nervous system dysfunction. Furthermore, they also report a larger number of developmental problems, suggesting that there are preexisting impairments in neurodevelopment which act as risk factors for the development of PTSD (Gurvits et al., 2000).
PTSD is also associated with specific impairments in explicit memory. Explicit memory deficits have been observed in combat veterans with PTSD compared to non-combat controls (Yehuda et al., 1995), and in rape victims with PTSD compared to rape victims without PTSD (jenkins et al., 1998). Thus far, memory function has not been assessed prior to trauma exposure. However, the possibility that (like IQ) lower mnemonic ability predates the trauma should be considered, particularly in the light of emergent evidence for premorbid abnomalities in HPA axis function (discussed below), this neuroendocrine system having well-documented effects on explicit memory function. Again, examining memory in high-risk groups will be informative.
Biological Risk Factors. The study of biological aspects of PTSD has identified several abnormalities that are present in trauma survivors with PTSD. Insofar as these alterations are not observed in similarly exposed persons without PTSD, they are likely to be related to the pathophysiology of PTSD, not to trauma exposure per se. Any one of these abnormalities could, in theory, represent a pre-existing vulnerability to the effects of trauma. Indeed, recent evidence has suggested that at least some of the observed biological abnormalities represent risk factors for the development of PTSD (for a review, see Yehuda, 1999a).
Shalev et al. (1998a) assessed heart rate in 86 trauma survivors at the time of presentation to the ER. Subjects who later developed PTSD had a higher heart rate at time of presentation compared to those who did not develop PTSD, consistent with there being an enhanced or prolonged catecholamine response to the trauma in this group. Heart rate no longer distinguished the PTSD and no-PTSD groups at one month follows-up. Pitman (1989) has proposed that elevated norepinephrine during trauma may result in overconsolidation of memory and the subsequent development of intrusive symptoms.
Neurohormonal research has also uncovered a potential risk factor for the development of PTSD. Both combat-related and civilian PTSD are associated with chronically low levels of cortisol, a glucocorticoid secreted by the hypothalamic-pituitary-adrenal (HPA) axis. Underlying this observation are systematic alterations in overall HPA axis activity, which appear to be unique to PTSD. Yehuda et al. (1996) present compelling evidence that such alterations are symptomatic of enhanced negative feedback occurring in the HPA axis, mediated by increased glucocorticoid receptor sensitivity, and acting to keep cortisol levels chronically low.
Direct support for the idea that HPA axis abnormalities represent a risk factor for PTSD was provided by a study of cortisol levels in the immediate aftermath (i.e., within several hours) of rape (Resnick et al., 1995). Lower cortisol levels were observed in women with prior exposure to rape or assault, and prior exposure was a risk factor for the development of PTSD. This suggests that HPA axis alterations may underlie the association between prior exposure and increased vulnerability to PTSD. Furthermore, a second study found that individuals who developed PTSD following a motor vehicle accident showed a lower cortisol response to the accident compared to those who did not develop PTSD (Yehuda et al., 1998a).
Yehuda et al. (2000) report preliminary explorations of biologic alterations in a group known to be at high risk of developing PTSD following trauma — adult children of Holocaust survivors (Yehuda et al., 1998a). Yehuda et al. (2000) found that these high-risk offspring had lower cortisol levels relative to non-psychiatric children of non-trauma exposed parents, comparable to those observed in other groups of trauma survivors with PTSD. Low cortisol levels were particularly evident in those offspring who had been exposed to trauma, but those who have not experienced a life-threatening traumatic event also show cortisol levels that are somewhat reduced. Observations of biologic alterations in offspring of Holocaust survivors could be subject to different interpretations and do not directly address environmental or genetic factors.
Familial or «Genetic» Risk factors? Several lines of evidence demonstrate familial transmission of PTSD. True et al. (1993) examined the prevalence of PTSD in monozygotic versus dizygotic twin pairs and demonstrated that as much as 30% of some PTSD symptoms appear to have a genetic basis. Davidson et al. (1985) found that trauma survivors with PTSD were more likely to have parents and first-degree relatives with mood, anxiety, and substance abuse compared with trauma survivors who did not develop PTSD. More recently, Yehuda et al. (1998b) demonstrated that Holocaust survivors with PTSD are more likely to have children with PTSD compared to Holocaust survivors without PTSD.
Since all of the aforementioned studies confound genetic and environmental concordance, the extent to which the findings are indicative of truly genetic phenomena is not yet clear. However, even in the absence of genetic heritability of risk factors for PTSD, family studies may ultimately demonstrate inter generational effects of stress and trauma as the most potent of risk factors due to the persistent cognitive and neurobiologic changes they induce.
Источник: hr-portal.ru
