DBS-neurofeedback of beta-activity in Parkinson’s disease: Evidence for differential control from a pooled intra-individual analysis

Abstract

Purpose Neurofeedback based on deep brain stimulation (DBS) recordings has been shown to enable people with Parkinson’s disease (PD) to voluntarily modulate pathological beta-oscillations in the subthalamic nucleus (STN). While previous studies suggested the feasibility of differential neurofeedback (up- vs. downregulation), their sample sizes were too small to provide definitive evidence that people with PD can differentially modulate beta oscillations through mental strategies alone. Here, we aimed to provide evidence for differential DBS neurofeedback control using a pooled, intra-individual design. Methods People with PD conducted differential neurofeedback experiments and tried to both increase and decrease abnormal STN beta-oscillations as compared to baseline (cognitive and motor rest). We pooled two previously published cohorts, to demonstrate differential neurofeedback learning. A linear mixed-effects model assessed the capacity of people with PD to differentially control beta-peak activity. Results Differential neurofeedback-control improved with training. We found a strong effect of neurofeedback on beta-oscillations for the clinically relevant downregulation, showing a reduction by about 22% as compared to baseline. However, even upregulation experiments resulted in beta-reductions as compared to baseline, where beta-activity was abnormally increased. Conclusion We present the first evidence for differential modulation of subthalamic beta-activity using a pooled, intra-individual design. We also found that upregulation experiments generally reduced beta-activity as compared to mental rest. Therefore, we propose that exaggerated subthalamic beta-oscillations could signal, or even promote, not only the lack of motor flexibility, but also the lack of cognitive flexibility seen in PD.

The authors' abstract, as published at the source. Neurophysiologie Clinique, 2026 · DOI ↗