Neurological research · 2026
Cognitive impairment in Parkinson's disease is associated with enhanced modulation of subthalamic beta-oscillations during DBS neurofeedback.
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Heinrich Raphael, Stieglitz Lennart, Bichsel Oliver
Аннотация
BACKGROUND: Deep brain stimulation (DBS) neurofeedback enables Parkinson's disease (PD) patients to voluntarily control pathological subthalamic beta-oscillations. While neurofeedback has shown promise in improving motor performance, the clinical factors that influence individual modulation capacity remain unclear.
METHODS: We retrospectively analysed 26 PD patients from three previously published deep DBS-neurofeedback cohorts. Participants were classified as cognitively normal (MoCA score ≥26) or cognitively impaired ( < 26) based on their preoperative scores. Neurofeedback performance was quantified as the percentage reduction in subthalamic beta-peak power during the final training round compared to baseline, z-normalised within each cohort. Group comparisons were conducted using t-tests and non-parametric tests. Correlations and stepwise linear regression were employed to examine associations between neurofeedback performance and clinical variables, including MoCA, age, Hoehn and Yahr stage, levodopa equivalent dose, and MDS-UPDRS scores.
RESULTS: Participants with cognitive impairment (n = 9) showed significantly better neurofeedback performance compared to cognitively normal participants (p = 0.0108). Additionally, a negative correlation was found between MoCA scores and neurofeedback capacity. Stepwise regression revealed that MoCA was the sole significant predictor of performance (, p = 0.0032), while age, motor symptom severity, and medication status did not contribute independently.
CONCLUSIONS: Cognitive impairment in PD is associated with enhanced modulation of subthalamic beta-oscillations during DBS-neurofeedback. This finding challenges the assumption that preserved cognition is necessary for effective neurofeedback, suggesting that compensatory or disease-related network dynamics may underpin modulation capacity. Future studies should investigate mechanistic explanations and assess whether stratifying patients by cognitive status can optimise personalised neuromodulation strategies.
METHODS: We retrospectively analysed 26 PD patients from three previously published deep DBS-neurofeedback cohorts. Participants were classified as cognitively normal (MoCA score ≥26) or cognitively impaired ( < 26) based on their preoperative scores. Neurofeedback performance was quantified as the percentage reduction in subthalamic beta-peak power during the final training round compared to baseline, z-normalised within each cohort. Group comparisons were conducted using t-tests and non-parametric tests. Correlations and stepwise linear regression were employed to examine associations between neurofeedback performance and clinical variables, including MoCA, age, Hoehn and Yahr stage, levodopa equivalent dose, and MDS-UPDRS scores.
RESULTS: Participants with cognitive impairment (n = 9) showed significantly better neurofeedback performance compared to cognitively normal participants (p = 0.0108). Additionally, a negative correlation was found between MoCA scores and neurofeedback capacity. Stepwise regression revealed that MoCA was the sole significant predictor of performance (, p = 0.0032), while age, motor symptom severity, and medication status did not contribute independently.
CONCLUSIONS: Cognitive impairment in PD is associated with enhanced modulation of subthalamic beta-oscillations during DBS-neurofeedback. This finding challenges the assumption that preserved cognition is necessary for effective neurofeedback, suggesting that compensatory or disease-related network dynamics may underpin modulation capacity. Future studies should investigate mechanistic explanations and assess whether stratifying patients by cognitive status can optimise personalised neuromodulation strategies.