ArticleCell reports. Medicine2026
Cortical-to-pallidal beta cascade underlies network pathophysiology in Parkinson's disease.
Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Parkinson's disease (PD) motor symptoms are linked to excessive beta band (13-35 Hz) oscillations and basal ganglia-cortical (BGC) synchrony, yet their dynamic inter-relation remains unclear. Based on computational modeling, we hypothesize that transient high-beta (20-35 Hz) BGC coupling induces subcortical low-beta (13-20 Hz) amplification. We recorded intraoperative neural signals from the globus pallidus internus and externus (GPi and GPe, respectively) and motor cortex (M1) in 23 PD patients during deep brain stimulation implantation. High-beta bursts in M1 and GPe were classified as either temporally synchronized or isolated. Synchronous M1-GPe high-beta bursts led by GPe were followed by GPi low-beta amplification, which were not evident with either isolated M1 high-beta bursts or M1-led synchronous bursts. Dopaminergic medication attenuated this GPi low-beta amplification and improved symptoms. These findings suggest that excessive M1 high-beta bursts following GPe high-beta activity trigger a cascade establishing low-beta propagation to GPi, which may contribute to PD motor dysfunction.
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