Neurofeedback-linked suppression of cortical beta bursts speeds up movement initiation in healthy motor control: A double-blind sham-controlled study.
He S., Everest-Phillips C., Clouter A., Brown P., Tan H.
Abnormally increased beta bursts in cortical-basal ganglia-thalamic circuits are associated with rigidity and bradykinesia in patients with Parkinson's disease. Increased beta bursts detected in the motor cortex have also been associated with longer reaction times in healthy participants. Here we further hypothesize that suppressing beta bursts through neurofeedback training can improve motor performance in healthy subjects. We conducted a double-blind sham-controlled study on 20 human volunteers (10 females) using a sequential neurofeedback-behaviour task with the neurofeedback reflecting the occurrence of beta bursts over sensorimotor cortex quantified in real-time. The results show that neurofeedback training helps healthy participants learn to volitionally suppress beta bursts in the sensorimotor cortex, with training being accompanied by reduced reaction time in subsequent cued movements. These changes were only significant in the real feedback group but not in the sham group, confirming the effect of neurofeedback training over simple motor imagery. In addition, reaction times correlated with the rate and accumulated duration of beta bursts in the contralateral motor cortex before the Go cue, but not with averaged beta power. The reduced reaction times induced by neurofeedback training positively correlated with reduced beta bursts across all tested hemispheres. These results strengthen the link between the occurrence of beta bursts in the sensorimotor cortex before the Go cue and slowed movement initiation in healthy motor control. The results also highlight the potential benefit of neurofeedback training in facilitating voluntary suppression of beta bursts in order to speed up movement initiation.SignificanceThis double-blind sham-controlled study suggested that neurofeedback training can facilitate volitional suppression of beta bursts in sensorimotor cortex in healthy motor control better than sham feedback. The training was accompanied by reduced reaction time in subsequent cued movements, and the reduced reaction time positively correlated with the level of reduction in cortical beta bursts before the Go cue, but not with average beta power. These results provide further evidence of a causal link between sensorimotor beta bursts and movement initiation and suggest that neurofeedback training could potentially be used to train participants to speed up movement initiation.