Subthalamic Deep Brain Stimulation Restores Temporal Flexibility of Cortical Beta Bursts During Motor Inhibition
Subthalamic Deep Brain Stimulation Restores Temporal Flexibility of Cortical Beta Bursts During Motor Inhibition
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Publication status: preprint
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Original abstract
Abstract Parkinson’s disease (PD) disrupts cortico-basal ganglia communication, producing exaggerated beta-band (13–30 Hz) synchronization expressed as prolonged beta bursts that correlate with bradykinesia and rigidity. In healthy systems, brief beta bursts support flexible motor control, including reactive and proactive motor inhibition. However, in PD it remains unclear whether pathological beta bursts facilitate motor inhibition or if their prolonged nature and temporal inflexibility hinder both movement initiation and the timely engagement of inhibition. We addressed this by examining cortical beta bursts from high-density EEG acquired during a stop-signal task in 14 PD patients in practically defined medication OFF state with beep brain stimulation (DBS) ON and OFF, and 15 age-matched controls. At rest, PD patients exhibited prolonged cortical beta bursts that were normalized by DBS. During stopping, beta burst frequency increased in all groups, but bursts occurred earlier and more broadly across frontal regions in PD patients. DBS shifted burst properties toward the healthy range, improving reactive stopping while also reducing proactive inhibition. These findings suggest that DBS over subthalamic nucleus restores temporal flexibility in cortical beta bursting but may attenuate proactive control, underscoring the need for adaptive DBS approaches that normalize pathologically prolonged bursts without excessively reducing burst features that support proactive adjustments.