علائم اختلال پس از سانحه و واکنش پذیری وحشت زده در نمونه جامعه زنان
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|39019||2001||13 صفحه PDF||سفارش دهید||6902 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Psychiatry Research, Volume 101, Issue 2, 25 March 2001, Pages 157–169
Abstract Exaggerated startle and PTSD symptoms have been investigated primarily in relation to acute or Type I stressors. The present study examined PTSD symptoms and startle eyeblink response in relation to chronic or Type II stressors. Type II stressors were operationally defined as high levels of childhood corporal punishment and high levels of current partner aggression. This study recruited a sample of 52 women from a metropolitan community and administered several questionnaires assessing experience of corporal punishment in childhood, current intimate partner aggression and level of PTSD symptoms. Following questionnaires, women were presented with eight auditory startle probes (white noise). Results showed that both childhood corporal punishment and intimate partner aggression were associated with women's PTSD symptom scores. However, only PTSD symptom scores were associated with reduced startle. Results are discussed in light of Type I and Type II stressors, and recent suggestions in the PTSD literature that a subgroup of individuals may experience physiological suppression rather than heightened physiological reactivity.
1. Introduction An important focus of psychophysiological investigations into post-traumatic stress disorder (PTSD) has been the study of increased arousal and physiological reactivity in persons suffering from this condition (see ver Ellen and van Kammen, 1990 and Shalev and Rogel, 1993, for reviews). Increased reactivity to both trauma-related cues and unconditioned stimuli (e.g. sudden or loud noises) has been the subject of numerous investigations over the last decade and a half. Elevated physiological arousal elicited by audiovisual and imaginal reminders of the original trauma have been found in studies of combat veterans (Blanchard et al., 1986, Pitman et al., 1987 and Pitman et al., 1990) and traumatized civilians, both male and female (Shalev et al., 1992 and Shalev et al., 1993). In addition, studies with PTSD-afflicted individuals have demonstrated that they also exhibit increased sympathetic responses, such as increased heart rate and skin conductance responses, to simple, strong stimuli such as loud tones (Paige et al., 1990, Shalev et al., 1992, Shalev et al., 1997, Orr et al., 1995 and Orr et al., 1997). Recently, psychophysiological studies of PTSD have begun to focus more closely on the physiological hyperreactivity of patients to unconditioned stimuli, such as the exaggerated startle response to sudden or loud noises. Exaggerated startle responsivity is a criterion for diagnosis of PTSD as listed in the Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (American Psychiatric Association, 1994). The startle eyeblink response, a robust and reliable component of the startle reflex (see reviews by Filion et al., 1998 and Dawson et al., 1999), is a particularly useful instrument in the investigation of increased physiological reactivity in PTSD. Some studies employing electromyographic (EMG) measurement of the startle eyeblink response have shown that persons suffering from PTSD symptoms exhibit physiological hyperreactivity to such unconditioned stimuli as novel loud tones or loud bursts of white noise (Butler et al., 1990). However, other investigations of startle responsivity in PTSD-afflicted samples have produced equivocal results, with some studies finding evidence of hyperreactivity and others failing to detect differences in startle between PTSD and control samples. Morgan and colleagues (1995, 1996) found greater startle responsivity in both Gulf War and Vietnam veterans with PTSD when compared to, in the first study, civilians and veterans without PTSD, and in the second study, ‘healthy controls’. The Gulf War veteran study presented the startle stimuli in a neutral setting, whereas the study with Vietnam veterans included the threat of aversive shock stimuli. Notably, though, a subsequent study using the same Vietnam veteran cohort without threat of shock in the paradigm (Grillon et al., 1996) failed to obtain results supporting the hypothesis of exaggerated baseline startle in PTSD patients. In addition, other investigations of the startle response in men and women afflicted with PTSD that have presented startle stimuli in neutral settings without the threat of shock have failed to find differences between PTSD and normal groups in startle habituation (Ross et al., 1989) and startle amplitude (Shalev et al., 1992 and Morgan et al., 1997). Indeed, one study actually reported smaller baseline startle responses (although less pre-pulse inhibition of startle) in children with PTSD (Ornitz and Pynoos, 1989). In the discussion of trauma, it may be important to distinguish between aversive situations which occur only once or are clearly delimited in time and where the individual perceives or experiences some level of control and can adopt active coping responses, and aversive situations of long or apparently unlimited duration in which the individual feels helpless and lacking adequate coping responses. In writing of childhood traumas, Terr (1991) distinguished between sudden, acute stressors (Type I trauma) and chronic stressors (Type II trauma). According to Terr (1991), an acute stressor is a single external blow characterized by intense surprise, whereas chronic stressors are marked by ‘prolonged and sickening anticipation’ (p. 11). Unlike an acute stressor such as combat, Type II or chronic stressors are characterized by repeated victimization over a long period of time (months or even years), where the situation is frequently perceived to be utterly aversive and inescapable, and where the individual can do little or nothing to effect an outcome other than victimization. Given the distinction between types of stressors, we suggest that traumatic stress during combat is usually an acute experience, rendering this a Type I stressor. Moreover, the scripted coping responses and agency possessed by soldiers (in the form of orders and weapons) are less characteristic of a Type II stressor. In the discussion of trauma, psychophysiological studies of startle in individuals suffering from PTSD have, heretofore, focused largely on individuals exposed to an acute or Type I stressor (e.g. combat, rape). Investigations into PTSD and startle in individuals exposed to chronic or Type II stressors have yet to be undertaken. Terr (1991) notes that the two types of trauma are characterized by distinct psychological sequelae. The question of whether PTSD associated with Type II stressors is also characterized by distinct physiological sequelae, including distinct startle response patterns, remains to be addressed. The animal literature provides indirect evidence that Type I and II stressors may be characterized by distinct physiological profiles. Research with rats has shown that the type of stressor plays a critical role in determining the type of physiological and/or behavioral responses. For example, Mormede et al. (1990) observed that male rats displayed different neuroendocrine changes to different types of social stress. Furthermore, Williams and Scott (1989) determined that, under certain circumstances, conspecific stressors (i.e. the presence of alpha male odors for rats previously defeated by alpha males) increase freezing behavior in rats, but predatory stressors (i.e. cat odors for rats) do not. In light of the fact that rats are social animals, the presence of alpha males may have been an inescapable and aversive experience for the rats in this study. Thus, the conspecific stressor can be understood as a chronic or Type II stressor, whereas the predatory stressor appears to represent an acute or Type I stressor. Although animal models of Type I and Type II stressors have yet to be explicitly studied, evidence within the animal literature implicitly supports the notion that Type I and Type II stressors may be characterized by distinct physiological and behavioral profiles. In addition to type of stressor influencing physiological and behavioral responses, age of exposure to traumatic stressors may likewise distinguish physiological reactions such as startle responses. Findings of hyporesponsiveness to traumatic stressors have, to our knowledge, only been detected in children (Ornitz and Pynoos, 1989 and Carrey et al., 1995). Ornitz and Pynoos (1989) found reduced startle in children exposed to sniper fire. Moreover, whereas PTSD in adults exposed to acute stressors has been linked to autonomic hyperarousal, autonomic hypoarousal has been observed in abused children in the form of lower electrodermal response to emotional and visual stimuli (Carrey et al., 1995). Although neither PTSD symptomatology nor startle were assessed in this latter study, the Type II stressor of growing up in a hostile home environment appears to have resulted in physiological inhibition rather than sensitization in these children. Thus, it may be that an individual's age of exposure to a stressor, as well as type of stressor, affects physiological responding. Given the findings of Ornitz and Pynoos (1989), and of Carrey et al. (1995) of hyporesponsiveness in traumatized children, we might expect adults who experienced frequent corporal punishment as children to display similar hyporesponsive startle reactions. However, other researchers have determined that adults exposed to Type I stressors, who were also exposed to high levels of childhood corporal punishment, appear more vulnerable to developing PTSD (Donovan et al., 1996 and King et al., 1996). Keeping in mind startle studies by Morgan and colleagues, which generally found heightened startle in adult PTSD patients, we might conversely expect hyperresponsive startle reactivity. This study was designed to test these opposing predictions by examining the influence of Type II stressors and PTSD related to child and adulthood Type II stressors, on startle reactivity. The present investigation assesses startle in a group of women with PTSD symptoms associated with chronic, non-catastrophic (Type II) stressors, defined in this study as childhood corporal punishment and intimate partner aggression. A non-help-seeking sample of women were recruited and evaluated for the level of corporal punishment in childhood, level of current partner aggression and PTSD symptoms. We hypothesized that exposure to Type II stressors would be associated with PTSD symptoms. Moreover, consistent with past startle reactivity studies of PTSD patients (Butler et al., 1990), we hypothesized that women suffering from more severe PTSD symptoms would display larger startle responses than women suffering from less severe or no PTSD symptoms. We also speculated that women who had aggressive partners and/or who were frequently struck as children would display different patterns of startle eyeblink reactivity than women without these experiences. However, given findings in children (Ornitz and Pynoos, 1989 and Carrey et al., 1995), and in light of the conflicting PTSD literature on adults, it was difficult to predict whether facilitation or inhibition of startle eyeblink reactivity might occur as a function of childhood experiences.
نتیجه گیری انگلیسی
Results 3.1. Type II stressors and PTSD Table 1 reveals associations between Type II stressors and PTSD. Specifically, links can be seen between childhood corporal punishment and PTSD symptoms, as well as between partner's aggression and PTSD symptoms. Table 1 also presents correlations among the modified blink average and risk variables, revealing that only PTSD symptoms are significantly associated with startle eyeblink magnitude. Moreover, this association between startle eyeblink magnitude and PTSD symptoms is a negative one, such that as PTSD symptom scores increase, startle eyeblink magnitude scores decrease. To investigate the relative contributions of childhood corporal punishment and current partner aggression to PTSD, a simultaneous multiple regression analysis was conducted to determine whether these variables contribute uniquely to PTSD symptoms. Childhood and adult stressors accounted for 37% of the PTSD symptom variance (adj R2=0.37, d.f.=2,43, P<0.001), with both betas significant at the P<0.05 level (βChildhood corporal punishment=0.30; βPartner aggression=0.45). Thus, for this community sample, both childhood and adult Type II stressors contribute uniquely to PTSD symptoms. Table 1. Relations among risk variables and modified blink averagea Childhood Partner PTSD symptom Modified blink corporal aggression scores average punishment Childhood corporal punishment – Partner aggression 0.40b – PTSD symptom scores 0.48b 0.57b – Modified blink average −0.10 −0.16 −0.32c – a Two-tailed correlations. b Correlation is significant at the 0.01 level. c Correlation is significant at the 0.05 level. Table options 3.2. Baseline EMG and startle eyeblink response Comparisons of groups representing the highest and lowest quartiles of each risk variable were performed with respect to both baseline EMG levels and startle eyeblink magnitude scores. The lowest quartile of the childhood corporal punishment distribution comprised women who never experienced corporal punishment during childhood (n=11). The highest quartile of the distribution included women who reported being hit at least 20 times during childhood (n=10). A group (lowest vs. highest quartiles for childhood corporal punishment)×trial block (1–4) repeated measures analysis of variance (ANOVA) 1 was conducted for both baseline EMG and eyeblink magnitude scores. No significant effects, neither main nor interaction effects, were detected. For the partner aggression distribution, the lowest quartile included women whose partners were reported to have an aggression score of 2 or lower (n=10), whereas the highest quartile comprised women whose partners were reported to have an aggression score of 19 or higher (n=12). Again, a group×trial block repeated measures ANOVA for baseline EMG and eyeblink magnitude revealed no significant findings for either main or interaction effects. The lowest quartile of the PTSD symptom score distribution included women with symptom scores of 6 or lower (n=12), and the highest quartile contained women with symptom scores of 20 or higher (n=11). The seven women who met criteria for a categorical diagnosis of PTSD and the two women whom the LASC identified as ‘PTSD-partial’ were included in the highest quartile group. That is, in addition to their symptom profile matching a ‘PTSD-positive’ or a ‘PTSD-partial’ diagnosis, these women also scored in the highest quartile of the PTSD symptom score distribution. A group×trial block ANOVA for baseline EMG revealed only a significant main effect for trial block (F3,63=6.41, P<0.05, ε=0.45), showing that baseline EMG declined over trial blocks. The low and high quartile PTSD groups did not significantly differ with respect to baseline EMG, nor was an interaction effect detected. A similar ANOVA conducted to examine startle eyeblink magnitude revealed main effects for both trial block and group. That is, results indicated that startle blink magnitude diminished over blocks (F3,63=4.55, P<0.05, ε=0.84), and that the high PTSD symptom group displayed significantly smaller startle eyeblinks than the low PTSD symptom group (F1,21=6.77, P<0.05). Fig. 1 depicts the eyeblink magnitude scores for both high and low quartile PTSD symptom groups over the four trial blocks. Average startle blink magnitude across trial blocks for PTSD groups. Fig. 1. Average startle blink magnitude across trial blocks for PTSD groups. Figure options In order to determine whether differential sensitization or suppression from the first to the second trial blocks occurred between the groups, a group (high vs. low quartiles for PTSD symptom scores)×trial blocks (1–2) repeated measures ANOVA was performed on eyeblink magnitude scores. A main effect for group was observed indicating that the startle eyeblink magnitude scores of the high and low quartile PTSD symptom groups significantly differed across both trial blocks (F1,21=5.81, P<0.05). In addition, a marginal interaction effect was detected (F1,21=2.67, P<0.12), despite very low observed power (observed power=0.35), showing that the two groups differed almost significantly in the direction of their eyeblink magnitude response change from trial block 1 to trial block 2. Whereas eyeblink magnitude scores of the low quartile PTSD symptom group increased slightly from trial block 1 (mean=29.23, S.D.=23.97) to trial block 2 (mean=32.00, S.D.=28.65), the eyeblink magnitude scores of the high quartile PTSD symptom group decreased substantially from trial block 1 (mean=13.02, S.D.=16.18) to trial block 2 (mean=7.55, S.D.=8.39). 3.3. Modified blink average and risk variables As indicated earlier, a modified blink average was computed which omitted the first trial block. This was done to circumvent problems raised by the possibility that response to the first trial block may have been dominated by novel characteristics of the stimulus, rather than group differences in startle reactivity. A one-way ANOVA (high vs. low quartiles of PTSD symptom scores) indicated that the modified blink average of the high quartile group (mean=6.13, S.D.=6.16) was significantly less than that of the low quartile group [mean=26.53, S.D.=23.78, F(1,21)=7.60 and P<0.05].