Electrophysiological Evidence for Alternative Motor Networks in REM Sleep Behavior Disorder

Patients with Parkinson's disease (PD) and REM sleep behavior disorder (RBD) show mostly unimpaired motor behavior during REM sleep, which contrasts strongly to coexistent nocturnal bradykinesia. The reason for this sudden amelioration of motor control in REM sleep is unknown, however. We set out to determine whether movements during REM sleep are processed by different motor networks than movements in the waking state. We recorded local field potentials in the subthalamic nucleus (STN) and scalp EEG (modified 10/20 montage) during sleep in humans withPDand RBD. Time-locked event-related beta band oscillations were calculated during movements in REMsleep compared with movements in the waking state and during NREM sleep. Spectral analysis of STN local field potentials revealed elevated beta power during REM sleep compared with NREM sleep and beta power in REM sleep reached levels similar as in the waking state. Event-related analysis showed time-locked beta desynchronization during WAKE movements. In contrast, we found significantly elevated beta activity before and during movements in REM sleep and NREM sleep. Corticosubthalamic coherence was reduced during REM and NREM movements. We conclude that sleep-related movements are not processed by the same corticobasal ganglia network as movements in the waking state. Therefore, the well-known seemingly normal motor performance during RBD in PD patients might be generated by activating alternative motor networks for movement initiation. These findings support the hypothesis that pathological movement-inhibiting basal ganglia networks in PD patients are bypassed during sleep.