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Journal article

Neurofeedback-linked suppression of cortical β bursts speeds up movement initiation in healthy motor control: a double-blind sham-controlled study

Abstract:
Abnormally increased β bursts in cortical-basal ganglia-thalamic circuits are associated with rigidity and bradykinesia in patients with Parkinson's disease. Increased β bursts detected in the motor cortex have also been associated with longer reaction times (RTs) in healthy participants. Here we further hypothesize that suppressing β 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-behavior task with the neurofeedback reflecting the occurrence of β bursts over sensorimotor cortex quantified in real time. The results show that neurofeedback training helps healthy participants learn to volitionally suppress β bursts in the sensorimotor cortex, with training being accompanied by reduced RT 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, RTs correlated with the rate and accumulated duration of β bursts in the contralateral motor cortex before the go-cue, but not with averaged β power. The reduced RTs induced by neurofeedback training positively correlated with reduced β bursts across all tested hemispheres. These results strengthen the link between the occurrence of β 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 β bursts to speed up movement initiation.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1523/jneurosci.0208-20.2020

Authors


More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Clinical Neurosciences
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Clinical Neurosciences
Role:
Author
ORCID:
0000-0001-5660-2164
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Clinical Neurosciences
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Clinical Neurosciences
Role:
Author
ORCID:
0000-0002-5201-3044
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Clinical Neurosciences
Role:
Author
ORCID:
0000-0001-8038-3029


Publisher:
Society for Neuroscience
Journal:
Journal of Neuroscience More from this journal
Volume:
40
Issue:
20
Pages:
4021-4032
Place of publication:
United States
Publication date:
2020-05-13
Acceptance date:
2020-03-30
DOI:
EISSN:
1529-2401
ISSN:
1529-2401
Pmid:
32284339


Language:
English
Keywords:
Pubs id:
1100276
Local pid:
pubs:1100276
Deposit date:
2020-05-27

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