Objective: To investigate the modulations in subthalamic nucleus (STN) signals that are associated with prolonged gait initiation duration in a virtual reality gait task in Parkinson’s disease, using intraoperative microelectrode recordings taken during deep brain stimulator (DBS) implantation surgery.

Background: Freezing of Gait (FOG) is typically linked to basal ganglia dysfunction and abnormal beta rhythms. Previous clinical work suggests start hesitation at the time of gait initiation may involve different mechanisms, and potentially be brainstem-related [1]. This study aimed to determine what STN signal abnormalities occur at the time of gait initiation and whether these are similar to FOG.

Method: Eight idiopathic PD patients underwent intraoperative VR gait tasks during DBS surgery after 12 hours off dopaminergic therapy. Subthalamic nucleus microelectrode recordings were collected while patients navigated a virtual environment via foot pedals. Analysis focussed on gait initiation, where the patient was presented with a visual “Walk” cue while idle, and then began stepping. Mean and peak signal power in theta (3-8Hz), beta (13-30Hz), and gamma (40-150Hz) bands was analysed in varying epochs before and after the “Walk” cues, in both set time increments and cue-to-step intervals.

Results: 29 gait initiation episodes were analysed across eight patients. The most significant finding was that higher peak beta signal in the interval from the “Walk” cue to the first step correlated with longer duration to the first step (Spearman rho=0.40, p=0.03). This correlation was also present for peak gamma (rho=0.48, p=0.009) and peak total STN signals (rho=0.41, p=0.03). Peak beta in the cue-to-second-step interval correlated with time to second and third steps (rho=0.45, p=0.015 and rho=0.43, p=0.02). Mean beta signal did not correlate in the same time periods. Change in STN signal strength before and after cue did not correlate with step duration.

Conclusion: The findings were consistent with previous studies linking higher beta activity with impaired motor performance [2], but suggest a specific role for peak beta burst activity in start hesitation. Future studies with ambulatory DBS or fMRI will be required to further clarify underlying mechanisms given the limited gait initiation events analysed.

References: [1] Coppin C, Bruzze L, Burke PGR, Lewis SJG. Phenotyping the demographic and behavioral correlates of start hesitation in Parkinson’s disease. Parkinsonism Relat Disord. 2025;135:107832. doi:10.1016/j.parkreldis.2025.107832
[2] Georgiades MJ, Shine JM, Gilat M, et al. Hitting the brakes: pathological subthalamic nucleus activity in Parkinson’s disease gait freezing. Brain. 2019;142(12):3906-3916. doi:10.1093/brain/awz325

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MDS Abstracts - https://www.mdsabstracts.org/abstract/correlating-start-hesitation-and-subthalamic-nucleus-activity-in-parkinsons-disease-using-intraoperative-microelectrode-recordings-and-a-virtual-reality-task/