bioRxiv · 10.64898/2026.04.09.717378
Pathological cortico-STN beta coupling in Parkinson's disease is confined to beta bursts
Abstract
Abnormal beta-band activity (13-30 Hz) within the cortico-basal ganglia network is a hallmark of Parkinsons disease (PD) and is closely linked to motor impairment. Pathological beta activity in the subthalamic nucleus (STN) occurs predominantly as brief, high-amplitude bursts rather than continuous oscillations. Although beta-band coherence between the STN and cortex increases during bursts, it remains unclear whether cortico-STN beta coupling persists outside these bursts. Using intraoperative STN local field potentials and simultaneous cortical electrocorticography from seven patients undergoing deep brain stimulation implantation surgery, cortico-STN beta coupling during burst and non-burst epochs was compared. Coupling was assessed using magnitude-squared coherence and the debiased weighted phase lag index (dwPLI) and compared against surrogate distributions generated by circular time-shifting. Both coupling metrics were significantly elevated during burst epochs relative to non-burst periods. During non-burst epochs, coupling collapsed to surrogate levels, indicating no evidence of sustained synchronization. Time-resolved analyses further demonstrated that elevated coupling was confined to burst epochs. Although a subset of motor cortical contacts exhibited elevated baseline coherence, coupling was less evident using dwPLI. These findings suggest that pathological cortico-STN beta coupling in PD is preferentially expressed during beta bursts rather than sustained across non-burst epochs, with implications for adaptive neuromodulation strategies.
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Beaudoin, C. A., O'Keeffe, A. B., Woo Choi, J., Alijanpourotaghsara, A., Gillies, M. J., Oswal, A. A., Pouratian, N., Green, A. L.. 2026-04-13. Pathological cortico-STN beta coupling in Parkinson's disease is confined to beta bursts. https://doi.org/10.64898/2026.04.09.717378
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