Post traumatic stress disorder increases electromyographic activity during rapid eye movement sleep in active duty service members
Grant Tays, Ph.D., Caddie Motoni, Amanda Studnicki, Ph.D., Angeliki Pollatou, Ph.D., Bradford Clemens, Elizabeth Metzger, J. Kent Werner, M.D., Ph.D.
Introduction
Post-traumatic stress disorder (PTSD) affects up to 31% of United States (US) combat Veterans over the course of their lifetime, significantly impacting both mental (e.g. depression, anxiety, etc.) and physical health (e.g. pain, fatigue, headaches etc.). PTSD commonly results in sleep disturbances, manifesting as less hours of sleep and lower quality of sleep; parallelly greater PTSD symptoms are associated with poorer sleep, insomnia and nightmares. Chronic sleep disturbances have been shown to contribute to neurodegeneration, such as dementia and Parkinson’s disease (PD), often preceded by the development of dream enactment, or REM behavior disorder (RBD), which is a strong predictor of developing PD or dementia. Dream enactment occurs in RBD due to loss of REM paralysis, or REM sleep without atonia (RSWA), which is identified with electromyographic (EMG) activity from the muscles during REM and appears with greater severity in Veterans with PTSD. RSWA is not routinely quantified due to an onerous manual scoring process, yet a novel computer algorithm approach can capture RSWA in finer detail than manual scoring. We hypothesized that this algorithm would identify RSWA differences in SMs with PTSD (PTSD+) compared to those without (PTSD-).
Materials and Methods
We compared RSWA in 12 PTSD+ and PTSD- SMs at the Walter Reed Sleep Disorder Center, . Following clinician graded sleep scoring, we used the RBDtector, an open-source software, to analyze EMG activity and sleep stages in the chin and tibialis anterior. In our initial analysis, we used a one-way ANOVA to determine if RSWA is higher in PTSD+ SM’s compared to PTSD-.
Results
PTSD+ SMs had significantly higher phasic (0.1 – 5.0s) bouts of chin EMG activity (p < 0.001). Further, there was overall increased EMG activity (p = 0.003) in PTSD+ compared to PSTD- SMs. Data analysis is ongoing to reach 100 participants in each group. Further analysis will include linear mixed effect models, controlling for age and medications such as serotonin norepinephrine reuptake inhibitors.
Discussion
These preliminary results indicate that PTSD+ SMs exhibit greater symptoms of RSWA than PTSD- SMs. Further analysis towards our target sample size (n = 100 in each group) will support these preliminary findings. This would suggest that PTSD and RBD share overlapping neuropathologic pathways, enhance our understanding of PTSD treatment and improve efforts to maintain operational readiness.