Pathological cortico-STN beta coupling in Parkinson's disease is confined to beta bursts.
Using intraoperative STN local field potentials and simultaneous cortical ECoG from seven PD patients, the study shows cortico‑STN beta-band coupling is significantly elevated during brief high‑amplitude beta bursts and collapses to surrogate levels outside those bursts.
What the AI sees
Using intraoperative STN local field potentials and simultaneous cortical ECoG from seven PD patients, the study shows cortico‑STN beta-band coupling is significantly elevated during brief high‑amplitude beta bursts and collapses to surrogate levels outside those bursts.
Research significance
This provides an actionable, time‑resolved biomarker (beta bursts) that supports burst‑targeted adaptive deep brain stimulation strategies and improved closed‑loop neuromodulation for Parkinsonian motor symptoms.
Source abstract
Abnormal beta-band activity (13-30 Hz) within the cortico-basal ganglia network is a hallmark of Parkinson's 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.