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REM sleep behavior disorder is a hallmark of prodromal α-synucleinopathies, yet why patients with Parkinson’s disease can generate rapid, coordinated movements during REM sleep despite daytime bradykinesia remains unknown. Here we combined recordings of eye movements, cortical electroencephalography, and basal ganglia-thalamic neuronal activity across vigilance states in non-human primates before and after MPTP-induced parkinsonism. Parkinsonism enhanced β oscillations and impaired movement-related neural dynamics during wakefulness and NREM sleep, whereas both pathological β activity and motor impairments were attenuated during REM sleep. β suppression preceded the onset of REM sleep, indicating that network reconfiguration begins before REM becomes behaviorally apparent. These findings demonstrate that Parkinsonian network dysfunction is dynamically gated by brain state rather than continuously imposed by dopamine depletion. REM sleep is a natural physiological condition in which β oscillations are disengaged, uncovering a latent capacity, normally masked by REM atonia, for rapid movement even in the dopamine-depleted motor network.
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