STN, subthalamic nucleus
The stn, subthalamic nucleus plays critical roles in brain function that QEEG brain mapping can assess. Neurofeedback protocols can target activity in stn, subthalamic nucleus-related circuits, training toward improved regulation and function. Explore our 2 research papers covering this topic.
Research Papers
Subthalamic beta-targeted neurofeedback speeds up movement initiation but increases tremor in Parkinsonian patients
Previous studies have explored neurofeedback training for Parkinsonian patients to suppress beta oscillations in the subthalamic nucleus (STN). However, its impacts on movements and Parkinsonian tremor are unclear. We developed a neurofeedback paradigm targeting STN beta bursts and investigated whether neurofeedback training could improve motor initiation in Parkinson's disease compared to passive observation. Our task additionally allowed us to test which endogenous changes in oscillatory STN activities are associated with trial-to-trial motor performance. Neurofeedback training reduced beta synchrony and increased gamma activity within the STN, and reduced beta band coupling between the STN and motor cortex. These changes were accompanied by reduced reaction times in subsequently cued movements. However, in Parkinsonian patients with pre-existing symptoms of tremor, successful volitional beta suppression was associated with an amplification of tremor which correlated with theta band activity in STN local field potentials, suggesting an additional cross-frequency interaction between STN beta and theta activities.
View Full Paper →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 (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.
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