AI Insight
This study examined the synchronization and directionality of beta-frequency oscillations (roughly 13-30 Hz) between the frontal cortex and subthalamic nucleus (STN) in three Parkinson's Disease patients using simultaneous electrocorticography and local field potential recordings. Phase locking value analysis revealed that the strongest cortical-STN beta synchrony was concentrated in the precentral and superior frontal gyri, while Granger causality analysis showed that beta-band signals predominantly flowed from the cortex toward the STN, with occasional bidirectional coupling. These findings suggest that pathological beta oscillations in Parkinson's Disease may originate or be driven cortically before propagating to the basal ganglia, consistent with established motor circuit anatomy.
Why it matters
Understanding the directionality of pathological beta oscillations could inform the development of more precise, phase-dependent deep brain stimulation therapies that target cortical regions, potentially improving symptom control and reducing side effects in Parkinson's Disease patients.
⚠️ Preprint – Noch nicht peer-reviewed
Dieser Artikel wurde noch nicht von unabhängigen Experten begutachtet. Die Ergebnisse sind vorläufig und sollten mit Vorsicht interpretiert werden.
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.