Objective: Identify a neurophysiological correlate of stimulation-induced bradykinesia in dystonia

Background: Bradykinesia is a known side-effect of pallidal deep brain stimulation (DBS) in dystonia patients that is reversible upon cessation of DBS. In Parkinson’s disease, bradykinesia has been associated with subcortical oscillations in the low beta band (Lbeta, 13-20 Hz). A pathophysiological correlate of stimulation-induced bradykinesia has not been described yet, but we hypothesize that Lbeta activity represents a symptom-specific signature and thus correlates with stimulation-induced bradykinesia in dystonia.

Method: In 6 dystonia patients with pallidal DBS through sensing-enabled Activa PC+S pulse generators, pallidal activity was recorded at 5 timepoints within 5 hours following cessation of DBS. Before each recording, finger tapping was videotaped and extracted by using markerless pose estimation. Averaged movement velocity was correlated with pallidal Lbeta activity using a mixed-effects linear model.

Results: After cessation of pallidal DBS, movement velocity significantly increased over time (P<.01). Pallidal Lbeta activity significantly predicted velocity (P=.01) within a linear mixed-effects model and explained 77% of the variance in velocity across subjects (r = 0.88, P < .001). This effect was frequency-specific for the Lbeta band.

Conclusion: These findings suggest that pallidal Lbeta activity might be a biomarker for stimulation-induced bradykinesia in dystonia. Our results strengthen the hypothesis that subcortical Lbeta activity is a symptom- rather than disease-specific oscillatory pattern.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/pallidal-beta-activity-correlates-with-stimulation-induced-bradykinesia-in-dystonia-patients/