Description
Preliminary Insights into Cortical Responses to Balance Perturbations in Parkinson’s Disease: A Case Comparison of an Individual With and Without Freezing of GaitObjective:
To identify neurophysiological biomarkers associated with freezing of gait (FoG) risk in Parkinson's disease (PD) using perturbations to standing balance.
Background:
FoG is a debilitating PD symptom contributing to falls, reduced independence, and diminished quality of life. Its sporadic nature complicates assessment. Using discrete balance perturbations as a behavioral probe, analogous to a cardiac stress test, may reveal neurophysiological differences between freezers and non-freezers. This approach evokes a large negative cortical potential (N1) 100–200 ms post-perturbation measured with electroencephalography (EEG), known as the balance N1, localized to the supplementary motor area (SMA). We hypothesize that a more distributed cortical activation contributing to the N1 in individuals with FoG+ in response to balance perturbations represents a compensatory mechanism resulting from reduced movement automaticity and increased reliance on cortical resources.
Methods:
Preliminary data were collected from individuals with PD who had a history of freezing (FoG+; n=1) or without (FoG-; n=1). Participants experienced discrete standing balance perturbations while high-density EEG (HD-EEG), electromyography (EMG), and galvanic skin response (GSR) were recorded. EEG data were processed using adaptive mixture independent components analysis (AMICA) to estimate cortical sources contributing to the balance N1. Trial-by-trial changes in EMG and GSR assessed sensorimotor integration and autonomic regulation.
Results: The FoG+ participant exhibited a smaller and delayed N1 response compared to the FoG- participant. Additionally, the FoG+ participant demonstrated widespread activation contributing to the N1 across the prefrontal and parietotemporal regions, including the anterior cingulate, retrosplenial cortex, medial temporal gyrus, and posterior parietal cortex, which was absent in the FoG- participant. Furthermore, the FoG+ participant displayed increasing N1, EMG, and GSR responses across trials, suggesting heightened threat perception and autonomic arousal, while the FoG- participant showed a trend of decreasing responses over the trials.
Conclusions:
Balance perturbations appear to trigger unique neurophysiological signatures linked to FoG, possibly providing a controlled, reproducible assessment tool similar to a stress test. This behavioral probe could offer potential for early detection and targeted interventions for FoG.
| Period | 03 Jun 2025 → 06 Jun 2025 |
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| Event type | Conference |
| Location | Atlanta, United States, GeorgiaShow on map |