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Updated: Sep 17, 2026
Controlling Parkinson's Disease With Adaptive Deep Brain Stimulation
Published on: July 16, 2014
DBS-neurofeedback of beta-activity in Parkinson's disease: Evidence for differential control from a pooled
Oliver Bichsel1, Lukas Imbach2, Roger Gassert3
1Department of Neurosurgery, University Hospital Zurich, University of Zurich, Switzerland; Clinical Neuroscience Centre, University Hospital Zurich, University of Zurich, Switzerland; Rehabilitation Engineering Laboratory, Department of Health Sciences and Technology, ETH Zurich, Switzerland.
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.
