Kavli Affiliate: Philip Starr
| Authors: Jin-Xiao Zhang, Clay Smyth, Md Fahim Anjum, Yue Leng, Andrew D. Krystal, Philip A. Starr and Simon Little
| Summary:
Sleep disturbance is involved in the progression of neurodegenerative diseases, but the neurophysiological mechanisms remain unclear in humans. We recorded sleep at home using portable polysomnography for multiple nights in patients with Parkinson’s disease implanted with sensing DBS, capturing intracranial neural signals from both the basal ganglia and motor cortex. We found that longer duration and shorter latency of rapid eye movement (REM) sleep predicted reduced next-morning neural signatures known to be pathological, including resting beta oscillations and hyper-neural connectivity between basal ganglia and motor cortex. Moreover, within REM sleep, stronger cortical delta activity particularly predicted reduced pathological neural signatures. Computational modeling of the evoked potential response in the basal-cortical circuit revealed that REM delta activity was associated with not only the amplitude of the evoked response, but also its natural oscillatory and decaying properties, suggesting REM sleep-mediated neural plasticity. The anti-relationship between delta activity and morning pathological neural signals was found to be primarily driven by the amplitude of delta waves, and less by their occurrence rate. In addition, as the REM sleep percentage and REM delta power increased in later hours during sleep, their protective effects also increased. Overall, our findings highlight the potential protective roles of REM sleep and its associated slow-wave activity in the neurophysiological health of Parkinson’s disease.