The present study found that PTSD was associated with greater dark-enhanced startle in women and higher RSA in men. Regression analyses indicated that dark-enhanced startle in women and increased RSA in men were related to the disorder itself and were not accounted for by the degree of either childhood or adult trauma. Respiration rate was not affected by experimental context, sex, or diagnosis and did not account for the group differences in RSA.
Dark-enhanced startle is a measure of nonspecific anxiety and is dependent on the BNST. This nucleus of the limbic system is one of the brain areas that are sexually dimorphic in animals (10
) and humans (13
). In rodents, light-enhanced startle is related to gonadal hormones and seems to be specifically associated with estrogen (45
). The small number of studies that have examined this paradigm has focused exclusively on men (Vietnam veterans) (17
) or adolescents of both sexes (18
). In men, darkness increased startle in both PTSD and non-PTSD groups; however, a multigenerational study of risk for anxiety disorders found that women offspring at risk had the highest levels of startle in the dark (18
). Given the higher prevalence of anxiety disorders in women than in men (46
), dark-enhanced startle may be a specific measure of PTSD in women.
This is the first study to investigate the effects of darkness on HF-HRV or RSA. Previous studies from the available literature have primarily examined HRV in PTSD during rest conditions (5
); however, a few have investigated HRV during emotionally challenging conditions. For example, RSA was studied during stressful mental tasks (e.g., arithmetic (30
)) and during recollection of traumatic events (28
). Interestingly, these studies have reported different effects of the stress condition on patients with PTSD and controls. Keary and colleagues (31
) found that RSA had greater reductions during the challenge task relative to rest in patients with PTSD compared with the controls. On the other hand, Cohen and colleagues (28
) found that the decrease in RSA in the trauma recall phase relative to rest was more pronounced in the controls than in patients with PTSD, and Sahar and colleagues (30
) found that RSA increased during the stressor in the controls but not in subjects with PTSD. In contrast, Morgan and colleagues (36
) found that decreased basal vagal function (RSA) was associated with superior performance under stress. Sex differences may account for this discrepancy in the literature: the first study used only women (31
), and the latter two studies only included men (30
Given the heterogeneity of psychophysiological findings in PTSD and the preponderance of such research in men due to the emphasis on combat-related PTSD (6
), our study offers a novel contribution to the literature. We found significant interactions of psychophysiology and sex, in as much as PTSD was associated with increased HRV in men but not in women. This seems to be inconsistent with HRV studies that have found that patients with PTSD show decreased parasympathetic function (29
). On the other hand, if men who have low vagal function perform well during dangerous training tasks (indicating a superior ability to regulate emotions (36
)), it is possible that the opposite propensity, that is, high vagal function, is associated with poor emotional regulation under stressful circumstances and presents a risk factor for PTSD. These study populations, such as Special Forces soldiers and traumatized civilians with PTSD, may represent opposite ends of the resiliency versus vulnerability spectrum, and PNS function may represent a potential biomarker for delineating them.
The nature of the present study sample provides both strengths and limitations. Our participants were selected from the primary care patient pool at Grady Memorial Hospital in Atlanta, which serves a majority African American, low socioeconomic status, highly traumatized population. Because of this unique subject pool, these results may not generalize to other populations. However, this population is uniquely and significantly more susceptible to trauma-related stress disorders (3
) and subsequent health disparities, and more investigation on the psychological outcomes of similarly vulnerable populations is needed. Another caveat is the use of the PSS, CTQ, and TEI to assess diagnosis and trauma history. These are based on the self-report of the participant and may be susceptible to reporting biases. However, all of these instruments have been used in the Grady Memorial Hospital population and validated with more in-depth interviews (3
A significant strength of the present study is statistically controlling for the degree of trauma exposure. Although other studies have also used trauma-exposed control groups (30
), there seems to be a linear “dose-response” association between trauma load and PTSD symptoms (47
), such that no-PTSD controls may have significantly lower levels of trauma than individuals who meet DSM criteria for PTSD. Because any level of trauma history may affect PNS flexibility and cardiovascular health, we controlled for trauma history by statistically regressing childhood and adult trauma levels in addition to using a traumatized control group. Indeed, we found that the startle response and PNS activity seemed to be independent of trauma history. Given the large range of age in our sample, we also accounted for the effects of age on startle reflexes and autonomic function by replicating the main sex-specific findings using age as a covariate.
In summary, these findings indicate that dark-enhanced startle may be related to PTSD in women, whereas alterations in vagal function may be associated with PTSD in men. Regulation of emotional states such as anxiety has been associated with prefrontal cortex inhibition of the nuclei in the limbic system (21
) and ANS activity (38
), and sex differences have been observed in both pathways (13
). Taken together, these data suggest that psychophysiological markers could be used as sex-specific risk factors for PTSD; moreover, these markers indicate that there may be common risk factors for anxiety disorders and cardiovascular disease.