Abstract

Abstract Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by complex recapitulations of waking acts during REM sleep due to unsuppressed voluntary muscle tone. Long-term studies indicate that RBD strongly predicts the subsequent development of Parkinson's disease (PD), Lewy body disease, and multiple system atrophy, with a conversion rate approaching 80%. Localizing the aberrant circuits involved in RBD has focused on the networks associated with REM generation, including the sublateral dorsal nucleus, the mesopontine tegmentum, and the pedunculopontine tegmental nucleus—nuclei affected by circuit dysregulation in PD. Interestingly, parkinsonism transiently abates during RBD complex movements, suggesting that movement during RBD may bypass the circuitry affected in PD, including the basal ganglia. Only recently have electrophysiological recordings in PD during sleep informed our understanding of how abnormal activity in the basal ganglia contributes to sleep dysregulation, specifically to RBD. Here, we highlight the pathophysiology shared between RBD and PD, focusing on the presumed aberrant neural networks, based on neuroimaging and neurophysiology data collected from human RBD and PD populations.

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