Objective: We examined the relationship between cortical and peripheral beta bursts during symptom fluctuations in Parkinson’s disease (PD), and their response to deep brain stimulation (DBS). EEG and high-density electromyography (HDsEMG) were analysed to determine their effectiveness in capturing DBS effects on beta activity, and linking them to objective measures of rigidity and bradykinesia.

Background: Exaggerated bursting activity in the beta-band (13-30 Hz) is a key neural hallmark of PD [1]. A recent study explored beta bursts across the sensorimotor subthalamic-cortical circuit and found that occurrence of cortical-bursts relates to worsening bradykinesia [2]. Beta bursts also occur in motor unit activity within muscles and their propagation from the cortex to the periphery can be tracked via simultaneous EEG and HDsEMG recordings [3]. HDsEMG provides a non-invasive way to monitor these signals along the corticospinal tract, offering insights into neuromodulation effects on motor control. However, the presence and modulation of peripheral beta bursts in PD, particularly in response to DBS, remains unexplored.

Method: We recorded extensor HDsEMG (256 electrodes) and EEG (19 channels) in 8 PD patients during DBS ON and OFF states. Tasks included isometric wrist extensions at 10%, 30%, and 50% of maximum voluntary contraction (MVC), finger tapping, and hand grasping. Rigidity and bradykinesia were assessed using UPDRS III, motion capture, and a passive wrist robotic manipulandum. Analysis involved motor unit decomposition, burst feature extraction, and coherence assessments between cortical and peripheral beta bursts.

Results: Our findings show that HDsEMG captures DBS-induced changes in beta bursts, similar to EEG bursts. Peripheral beta burst features (duration, rate) exhibit sensitivity to DBS state, with potential advantages over EEG in tracking sensorimotor beta bursts. Preliminary results suggest that coherence between cortical and peripheral beta bursts may reflect symptom severity, providing insight into beta’s role in motor impairment.

Conclusion: This study demonstrates the feasibility of tracking beta bursts across the corticospinal tract in PD and highlights their sensitivity to DBS. HDsEMG emerges as a promising tool for investigating neuromodulation effects, offering potential for improved DBS optimization and understanding of beta burst propagation in motor control.

References: [1] Tinkhauser, G., Pogosyan, A., Tan, H., Herz, D. M., Kühn, A. A., & Brown, P. (2017). Beta burst dynamics in Parkinson’s disease OFF and ON dopaminergic medication. Brain, 140(11). https://doi.org/10.1093/brain/awx252
[2] Yao, P., Sharma, A., Abdi‐Sargezeh, B., Liu, T., Tan, H., Hahn, A., … & Oswal, A. (2025). Beta Burst Characteristics and Coupling within the Sensorimotor Cortical‐Subthalamic Nucleus Circuit Dynamically Relate to Bradykinesia in Parkinson’s Disease. Movement Disorders. https://doi.org/10.1002/mds.30163
[3] Bräcklein, M., Barsakcioglu, D. Y., Del Vecchio, A., Ibáñez, J., & Farina, D. (2022). Reading and Modulating Cortical β Bursts from Motor Unit Spiking Activity. The Journal of Neuroscience, 42(17), 3611–3621. https://doi.org/10.1523/JNEUROSCI.1885-21.2022

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MDS Abstracts - https://www.mdsabstracts.org/abstract/tracking-cortical-and-peripheral-beta-bursts-in-parkinsons-disease-during-dbs-modulation/