Summary: Researchers report a neurofeedback system allows those with Parkinson’s to voluntarily control brain waves associated with symptoms of the disorder.
Source: SfN.
A neurofeedback system enables Parkinson’s disease patients to voluntarily control brainwaves associated with symptoms of the disorder, according to new research published in eNeuro. It remains to be determined whether such a system can provide symptom relief.
Parkinson’s disease is associated with abnormal beta wave activity in the subthalamic nucleus (STN), but a direct connection between this activity and movement difficulties has not been established. In their study of eight patients undergoing a routine replacement of a pulse generator used for deep brain stimulation, Takufumi Yanagisawa and colleagues developed a method that could help scientists better understand the relationship between brain activity and disease symptoms.
By translating participants’ real-time brain activity into a visual representation during a 10-minute training session, the researchers demonstrate the patients’ ability to increase or decrease the size of a black circle with their thoughts alone. This manipulation had a corresponding effect on STN beta waves measured after the training session. Although the researchers did not observe an improvement in patients’ symptoms, their study represents a new approach toward managing disease-related brain activity that could inform the development of new treatments.
Real-time neurofeedback to modulate β-band power in the subthalamic nucleus in Parkinson’s disease patients
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 (three 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-minute 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-minute 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 < .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 < .05) through neurofeedback.
Significance statement
Many studies have reported a relationship between the β-band power in the subthalamic nucleus (STN) and motor symptoms in Parkinson’s disease. Here, we have developed a novel neurofeedback technique using intracranial electrodes implanted in deep brain structures to modulate STN activity. We provided direct feedback of the β-band power as the size of a black disc to induce a sustainable change in β-band power. As a result, the neurofeedback training induced significant changes in the β-band power. This is the first report to demonstrate that human patients with Parkinson’s disease were able to voluntarily control their β-band power in STN to induce changes in the power.
