Person:

Hopper, James

OBJECTIVE: Evidence of elevated basal heart rate (HR) in posttraumatic stress disorder (PTSD) has been interpreted in terms of elevated sympathetic cardiac activity, as have possible increased cardiovascular disease risks and outcomes associated with elevated HR. Yet it is well-established that the parasympathetic branch of the autonomic nervous system not only influences HR independently of the sympathetic branch, but makes a greater contribution to HR, including resting HR. Additionally, abnormally low tonic parasympathetic activity on the heart has been implicated in cardiovascular disease and hypertension. This study addressed a potential parasympathetic contribution to elevated basal HR in PTSD.

METHODS: We used a descriptive and subgroup differences approach to investigate relationships between parasympathetic activity and basal HR in 59 adults (50 females) with PTSD, all of whom were participants in a treatment outcome study and assessed prior to exposure to trauma-related script-driven imagery. Consistent with the well-known relationship between parasympathetic activity and HR, we hypothesized that basal respiratory sinus arrhythmia (RSA), a measure of parasympathetic cardiac activity, would be negatively correlated with basal HR. More important, we predicted that pathologically elevated HRs previously associated with PTSD would only characterize a low-RSA subgroup. Potential confounds of age, respiration rate, and aerobic fitness were addressed.

RESULTS: As predicted, mean HR was 80.5 bpm in the low-RSA tercile group, similar to mean HRs of PTSD groups in prior research and significantly higher than 69 and 65 bpm in the middle- and high-RSA groups, respectively, which are typical of non-PTSD controls.

CONCLUSION: These findings suggest that a substantial proportion of those with PTSD may not have elevated basal HRs. Furthermore, among those who do exhibit elevated HR, there may be a parasympathetic contribution that is independent of any sympathetic one. Only measuring both branches at once, ideally with autonomic blockades, can definitively address these issues.

Background: There is extensive evidence that the parasympathetic branch of the autonomic nervous system can modulate psychophysiological arousal. To date, no studies have investigated associations between cardiac vagal tone and the time course of arousal during exposure to trauma-related stimuli in posttraumatic stress disorder (PTSD). Methods: Thirty-one subjects, 29 with PTSD and 2 with partial PTSD, had electrocardiograms recorded during baseline and 2-minute traumatic and neutral script-driven imagery periods. Heart rate, respiratory sinus arrhythmia (RSA), and heart rate half-recovery to the trauma script were quantified, and subjects were divided into low and high baseline RSA groups. Results: Across all participants, heart rate significantly increased from the neutral to the trauma script and RSA significantly decreased from baseline to trauma script (p < .05). As predicted, low RSA subjects had more prolonged heart rate increases to the trauma script than high RSA subjects (p < .001), and heart rate half-recovery was negatively correlated to baseline RSA (r = -.50, p = .005). Conclusions: This study is the first to find decreased RSA in response to a traumatic reminder and an association between low baseline RSA and sustained conditioned arousal in PTSD. Low vagal tone may account for deficient arousal and emotion regulation capacities often observed in PTSD.

Background: Posttraumatic stress disorder (PTSD) may be associated with dysfunctional reward processing. The present study assessed for such dysfunction in both the expectancy and outcome phases of reward processing. Methods: Male Vietnam veterans with (n = 15) and without (n = 11) combat-related PTSD were administered a wheel of fortune-type gambling task. Self-reported ratings of expectancy and satisfaction were collected respectively before and after each experience of monetary gain or loss. Results: PTSD participants reported both lower expectancy of reward and lower satisfaction with reward when it was received. The latter result was manifest in a failure of PTSD participants to show the greater satisfaction that normally accompanies rewards received under conditions of low expectancy. Conclusion: These results suggest reward function impairment in PTSD related to expectancy, satisfaction, and the expectancy-satisfaction relationship.