Frontal Cortex-Subthalamic Nucleus Beta Oscillations Exhibit Phase Locking and Granger Causality in Parkinson’s Disease
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Objective
Pathological beta oscillations are a hallmark of Parkinson’s Disease (PD) and are linked with symptom severity and therapeutic efficacy of deep brain stimulation (DBS). Although some studies suggest that beta oscillations may propagate from the frontal cortex to the subthalamic nucleus (STN), direct evidence based on cortical and subcortical neural recordings remains limited. This study investigates synchrony and directionality of beta-band interactions between the frontal cortex and STN in PD.
Approach
Simultaneous electrocorticography and STN local field potential recordings were obtained from three PD patients undergoing awake DBS lead placement surgery. Cortical-STN beta phase synchrony was quantified using phase locking value, and directed functional connectivity was analyzed using time-resolved bivariate Granger causality.
Main results
Phase locking value mapping revealed a spatially non-uniform distribution of beta phase synchrony, with the strongest coupling localized most prominently within the precentral and superior frontal gyri. Granger causality analysis demonstrated a predominance of cortical-to-subthalamic beta-band interactions across all subjects with intermittent bidirectional coupling.
Significance
These findings provide evidence that pathological beta oscillations in Parkinson’s may preferentially propagate from the frontal cortex to the basal ganglia, consistent with known motor pathways. These findings are consistent with a cortical contribution to pathological beta oscillations and highlight potential methods for obtaining cortical targets for phase-dependent neuromodulation.
