The number of movements identified during REM sleep, predominant motor phenomena observed, and other demographic information for each subject are reported in Table 1. We characterized the dynamics of beta and HFOs in the GPi during REM sleep and wake movements in an effort to improve our understanding of the functional role of the basal ganglia oscillations underlying movement across sleep-wake states.Īll subjects were noted to display body movements during REM sleep as identified by video-polysomnography. To further explore the role of the basal ganglia in movement control during REM sleep, we recorded local field potentials (LFPs) from four PD patients via externalized directional deep brain stimulation (DBS) leads implanted in the GPi (the principal output nucleus of the basal ganglia). Recordings from the subthalamic nucleus have provided initial evidence of marked differences in the dynamics of movement-related oscillations between wake and sleep states 8. Currently, little is known about the role of the basal ganglia in the control of movements that occur during REM sleep. People with PD without a clinical diagnosis of RBD may also demonstrate motor activity during REM sleep 9, 11. In particular, a high percentage of individuals with PD have REM sleep behavior disorder (RBD), a parasomnia characterized by the loss of muscle atonia and a dramatic increase in motor activity, often with punching and kicking behavior suggestive of dream enactment 10. In contrast to wakefulness, people with PD can demonstrate improved motor activity during rapid eye movement (REM) sleep 9. Our understanding regarding the modulation of beta oscillations in the basal ganglia during REM sleep movements is limited 8, however, and HFOs in such context have not been investigated. Furthermore, a recent study in PD patients on and off medication, and in naïve and parkinsonian non-human primates suggests that exaggerated HFOs have pathophysiological relevance in PD 4. High-frequency oscillations (HFOs, >100 Hz) in the GPi have been observed to synchronize during wakeful movement in unmedicated PD patients 4, 7. Excessive spontaneous synchronization of beta oscillations (increasing in power) in the GPi in people with Parkinson’s disease (PD) is thought to contribute to akinesia and bradykinesia since the suppression of beta power by dopamine replacement therapy or deep brain stimulation (DBS) improves motor behavior 4, 5, 6. Voluntary movements are preceded by desynchronization (reducing in power) of beta oscillations (13–35 Hz) in the globus pallidus internus (GPi) 3, 4. The basal ganglia play a critical role in the control of motor function during wakefulness 1, 2.
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