Background-While it has been reported that persons with posttraumatic stress disorder manifest tonic autonomic activation, the literature contains numerous counter-examples. In revisiting the question, this study employed a novel method of mattress actigraphy to unobtrusively estimate heart rate and respiratory sinus arrhythmia over multiple nights of sleep in the home.

Studies imposing rigorous control over lifetime alcohol intake have usually not found smaller hippocampal volumes in persons with posttraumatic stress disorder. Because the majority of negative studies have used adolescent samples, it has been suggested that chronicity is a necessary condition for such findings. To test the hypothesis that a smaller hippocampus in PTSD is unrelated to comorbid alcoholism or to chronicity, this study estimated hippocampal volume in a relatively large group (N=99) of combat veterans in which PTSD, lifetime alcohol abuse/dependence, and Vietnam versus Gulf War service were crossed. In subjects with histories of alcoholism, unadjusted hippocampal volume was 9% smaller in persons with PTSD than in those without PTSD. In nonalcoholic subjects, the PTSD-related difference in hippocampal volume was 3%. The failure to observe a strong association between PTSD and hippocampal volume in nonalcoholic subjects was not ascribable to younger age, reduced PTSD chronicity, or lower PTSD symptom severity. The possibility that smaller hippocampal volume is limited to groups in which PTSD is compounded by comorbid alcoholism is not necessarily incompatible with results suggesting a smaller hippocampus is predispositional to PTSD. Further examination of the role of alcoholism and other comorbid conditions in studies of brain structure and function in PTSD appears warranted.

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This article describes a method for extracting heart rate (HR) and respiratory sinus arrhythmia (RSA) from the kinetocardiogram (KCG) recorded from accelerometers embedded in a mattress topper. Validation has been performed via comparison with simultaneously recorded ECG. All-night estimates of HR and RSA magnitude derived from both methods were highly correlated. KCG-derived estimates of HR were slightly lower, and those of RSA magnitude higher, than those derived from ECG. These biases are consistent with the need to constrain KCG estimation to periods free of body movement. Mattress actigraphy represents a zero-burden method of obtaining intensive longitudinal indices of cardiac status.