Autonomic activation during sleep in posttraumatic stress disorder and panic: a mattress actigraphic study.

BACKGROUND: While it has been reported that persons with posttraumatic stress disorder (PTSD) manifest tonic autonomic activation, the literature contains numerous counterexamples. 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. METHODS: Sleep cardiac autonomic status was estimated in four diagnostic groups, posttraumatic stress disorder, panic disorder, persons comorbid for both conditions, and control subjects. All 59 participants were community-residing nonveterans screened for sleep apnea and periodic leg movement disorder with polysomnography. Heart rate and respiratory sinus arrhythmia were calculated from the kinetocardiogram signal measured via accelerometers embedded in a mattress topper. Times in bed and asleep were also estimated. Per participant data were obtained from a median of 12 nights. RESULTS: Both posttraumatic stress disorder and posttraumatic stress disorder/panic disorder comorbid groups exhibited significantly higher heart rates and lower respiratory sinus arrhythmia magnitudes than panic disorder participants and control subjects. Panic disorder participants were indistinguishable from control subjects. The PTSD-only group exhibited longer times in bed and longer times presumably asleep than the other three groups. CONCLUSIONS: In this study, posttraumatic stress disorder, but not panic disorder, was associated with altered cardiac autonomic status during sleep. Among participants meeting criteria for PTSD alone, autonomic activation co-occurred with prolongation of actigraphic sleep.

Brain, skull, and cerebrospinal fluid volumes in adult posttraumatic stress disorder.

Children and adolescents with maltreatment-related posttraumatic stress disorder (PTSD) exhibit smaller intracranial tissue volume than controls. Linear relationships have also been observed between intracranial tissue volume and the age of maltreatment onset. The authors explored associations among adult PTSD, early trauma, and cerebral volumes in 99 combat veterans. A bone-based estimate of cranial volume was developed to adjust for variation in body size. Posttraumatic stress disorder was not associated with smaller cerebral tissue volume, but rather with smaller cerebrospinal fluid (CSF) and cranial volumes. These findings co-occurred with expected effects of alcoholism and aging on cerebral tissue and CSF volumes. The results point to early developmental divergences between groups with and without PTSD following adult trauma.

Self-selection bias in sleep and psychophysiological studies of posttraumatic stress disorder.

Psychobiological studies of posttraumatic stress disorder (PTSD) often challenge participants to assess the dynamics of systems evolved to organize responses to extreme events. Informed consent insures that volunteers have every opportunity to preevaluate the conditions of the research experience and decline if made uncomfortable by them. Notwithstanding their necessity, these protections set the stage for self-selection phenomena that may bias study outcomes. This study compared prospectively obtained psychometric data from 196 participants and 1229 nonparticipants in sleep and psychophysiological studies of PTSD. Lower subjective nightmare severity was endorsed by persons who later agreed to participate in a study of baseline sleep, an observation consistent with the low nightmare frequencies observed in most laboratories studies of sleep in PTSD.

Estimating heart rate and RSA from the mattress-recorded kinetocardiogram.

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.

Hippocampal volume, PTSD, and alcoholism in combat veterans.

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.