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Beta burst coupling across the motor circuit in Parkinson's disease

Abstract:
Exaggerated activity in the beta band (13-35 Hz) is a hallmark of basal ganglia signals in patients with Parkinson's disease (PD). Beta activity however is not constantly elevated, but comes in bursts. In previous work we showed that the longer beta bursts are maintained, the more the oscillatory synchronisation within the subthalamic nucleus (STN) increases, which is posited to limit the information coding capacity of local circuits. Accordingly, a higher incidence of longer bursts correlates positively with clinical impairment, while the opposite is true for short, more physiological bursts. Here, we test the hypothesis that beta bursts not only indicate local synchronisation within the STN, but also phasic coupling across the motor network and hence entail an even greater restriction of information coding capacity in patients with PD. Local field potentials from the subthalamic nucleus and EEG over the motor cortex area were recorded in nine PD patients after temporary lead externalization after surgery for deep brain stimulation and overnight withdrawal of levodopa. Beta bursts were defined as periods exceeding the 75th percentile of signal amplitude and the coupling between bursts was considered using two distinct measurements, first the % overlapping (%OVL) as a feature of the amplitude coupling and secondly the phase synchrony index (PSI) to measure the phase coupling between regions. %OVL between STN and cortex and between the left and the right STN was higher than expected between the regions than if they had been independent. Similarly, PSI was higher during bursts as opposed to non-bursts periods. In addition, %OVL was greater for long compared to short bursts. Our results support the hypothesis that beta bursts involve long-range coupling between structures in the basal ganglia-cortical network. The impact of this is greater during long as opposed to short duration beta bursts. Accordingly, we posit that episodes of simultaneously elevated coupling across multiple structures in the basal ganglia-cortical circuit further limit information coding capacity and may have further impact upon motor impairment.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1016/j.nbd.2018.06.007

Authors


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Role:
Author
ORCID:
0000-0002-1954-1873
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Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
Clinical Neurosciences
Role:
Author
More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
Clinical Neurosciences
Role:
Author
ORCID:
0000-0001-8038-3029


Publisher:
Elsevier
Journal:
Neurobiology of Disease More from this journal
Volume:
117
Pages:
217-225
Publication date:
2018-06-20
Acceptance date:
2018-06-11
DOI:
EISSN:
1095-953X
ISSN:
0969-9961
Pmid:
29909050


Language:
English
Keywords:
Pubs id:
pubs:858326
UUID:
uuid:eb39dd65-bb12-4f1f-8bc9-356109ade29d
Local pid:
pubs:858326
Source identifiers:
858326
Deposit date:
2019-02-18

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