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eNeuro. 2018 Dec 21;5(6). pii: ENEURO.0246-18.2018. doi: 10.1523/ENEURO.0246-18.2018. eCollection 2018 Nov-Dec.

Real-Time Neurofeedback to Modulate β-Band Power in the Subthalamic Nucleus in Parkinson's Disease Patients.

Author information

1
Department of Neurosurgery, Graduate School of Medicine, Osaka University, Suita, Osaka, 565-0871, Japan.
2
Department of Neuroinformatics, ATR Computational Neuroscience Laboratories, Seika-cho, Kyoto, 619-0288, Japan.
3
Institute for Advanced Co-creation Studies, Osaka University, Suita, Osaka, 565-0871, Japan.
4
Center for Information and Neural Networks (CiNet), National Institute of Information and Communications Technology (NICT), Suita, Osaka, 565-0871, Japan.
5
JST PRESTO, Suita, Osaka, 565-0871, Japan.
6
Department of Neuromodulation and Neurosurgery, Graduate School of Medicine, Osaka University, Suita, Osaka, 565-0871, Japan.

Abstract

The β-band oscillation in the subthalamic nucleus (STN) is a therapeutic target for Parkinson's disease. Previous studies demonstrated that l-DOPA decreases the β-band (13-30 Hz) oscillations with improvement of motor symptoms. However, it has not been elucidated whether patients with Parkinson's disease are able to control the β-band oscillation voluntarily. Here, we hypothesized that neurofeedback training to control the β-band power in the STN induces plastic changes in the STN of individuals with Parkinson's disease. We recorded the signals from STN deep-brain stimulation electrodes during operations to replace implantable pulse generators in eight human patients (3 male) with bilateral electrodes. Four patients were induced to decrease the β-band power during the feedback training (down-training condition), whereas the other patients were induced to increase (up-training condition). All patients were blinded to their assigned condition. Adjacent contacts that showed the highest β-band power were selected for the feedback. During the 10 min training, patients were shown a circle whose diameter was controlled by the β-band power of the selected contacts. Powers in the β-band during 5 min resting sessions recorded before and after the feedback were compared. In the down-training condition, the β-band power of the selected contacts decreased significantly after feedback in all four patients (p < 0.05). In contrast, the β-band power significantly increased after feedback in two of four patients in the up-training condition. Overall, the patients could voluntarily control the β-band power in STN in the instructed direction (p < 0.05) through neurofeedback.

KEYWORDS:

EEG; Parkinson disease; beta power; deep brain stimulation; neurofeedback; voluntary control

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