Subthalamic nucleus beta oscillations and sleep disorders in Parkinson's disease: A new perspective on deep brain stimulation regulation mechanisms and circuits.

Parkinson's disease (PD) is increasingly recognized as a multisystem neurodegenerative disorder that extends far beyond its classical motor manifestations. Among its non-motor symptoms, sleep disturbances are among the most prevalent and disabling clinical features, affecting up to 80% of patients and often preceding the onset of motor symptoms by several years. Recent electrophysiological studies have identified the subthalamic nucleus (STN) as a critical hub linking motor dysfunction to sleep abnormalities. Aberrant synchronization of beta (13-30 Hz) oscillations in STN local field potentials (LFPs) persists across wakefulness and sleep, disrupting normal sleep microarchitecture by suppressing slow-wave activity, impairing sleep spindle generation, and destabilizing sleep-stage transitions. These pathological beta oscillations have therefore emerged as a key electrophysiological hallmark of PD-associated sleep dysfunction. Subthalamic deep brain stimulation (STN-DBS), the current standard surgical treatment for advanced PD, has demonstrated significant benefits beyond motor symptom control. Accumulating evidence suggests that STN-DBS improves sleep through multiple complementary mechanisms, including suppression of pathological beta synchronization, restoration of cortico-basal ganglia-thalamocortical network dynamics, modulation of brainstem arousal circuits and neurotransmitter systems, and alleviation of nocturnal motor symptoms. This review summarizes recent advances in the neuroanatomical, electrophysiological, and circuit-level mechanisms linking STN dysfunction to sleep disorders in PD. We further discuss emerging therapeutic strategies and highlight future directions toward biomarker-guided, individualized treatment. Collectively, this review proposes a mechanistic framework linking STN electrophysiology to sleep regulation and identifies testable hypotheses that may facilitate the development of precision neuromodulation strategies for sleep disorders in Parkinson's disease.