SP 5. Poor modulation of event related local field potentials in the subthalamic nucleus during nocturnal movements in Parkinson’s patients – Are subthalamic neurons sleeping?

Introduction The modulating effect of subthalamic beta oscillations on motor control in patients with Parkinson’s disease (PD) is a well-established observation: beta oscillations are enhanced in PD, and are reduced by voluntary movements, dopaminergic treatment or deep brain stimulation (DBS). PD patients with REM sleep behavior disorder (RBD) reveal mostly unimpaired motor behavior during REM sleep, despite lack of dopaminergic treatment during the night. However, it is unknown whether normalized neuronal signaling in the subthalamic nucleus during REM sleep is linked to this phenomenon which contrasts strongly to coexistent nocturnal bradykinesia in PD. Objectives We aim at investigating the dynamic electrophysiological properties of basal ganglia motor networks during nocturnal movements in PD patients by measuring event related potentials of limb movements in both REM and non-REM sleep. Specifically, we set out to determine whether phenotypically normal REM sleep-related movements are mirrored by reduced subthalamic beta oscillations. Patients and methods After implantation of deep brain stimulation (DBS) electrodes, we recorded local field potentials in the subthalamic nucleus (STN) and scalp EEG (modified 10/20 montage) during sleep in 5 PD patients with clinically manifest REM sleep behavioral disorder (12 h recording, 8 pm–8 am). Nocturnal movements were assessed by video-EEG monitoring and EMG recordings. Time-locked event-related beta band oscillations were then calculated to assess the relative and absolute beta (de-)synchronization during movements in REM (206 events) and non-REM sleep (112 events). Results Spectral analysis of local field potentials in the STN revealed elevated beta band power during REM sleep as compared to NREM sleep and tonic beta activity in REM sleep reached levels similar as in the waking state. Despite the continuously elevated beta band activity, event related analysis showed no significant beta desynchronization prior to or during movements in REM sleep. In other words, we observed unimpaired movements in REM sleep and recorded continuously elevated beta activity in the STN. Beta band power in NREM sleep was limited to the lower beta band (13–20 Hz), whereas in REM sleep beta power was more prominent in the high beta range (20–35 Hz). Conclusion In contrast to voluntary motor control in wakefulness, subthalamic beta oscillations are poorly modulated during movements in REM and NREM sleep, indicating that nocturnal movements are not processed by the same cortico-basal ganglia networks as in the waking state. In this line, we propose that motor performance during REM sleep in PD patients with RBD is significantly improved because alternative motor networks for movement initiation might be activated. By this mechanism, the pathological movement-inhibiting basal ganglia networks in PD patients could be bypassed during REM sleep.