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dc.contributor.authorHall, Stephen
dc.contributor.authorProkic, EJ
dc.contributor.authorMcAllister, CJ
dc.contributor.authorRonnqvist, KC
dc.contributor.authorWilliams, AC
dc.contributor.authorYamawaki, N
dc.contributor.authorWitton, C
dc.contributor.authorWoodhall, GL
dc.contributor.authorStanford, IM
dc.date.accessioned2018-02-14T10:57:50Z
dc.date.available2018-02-14T10:57:50Z
dc.date.issued2014-12
dc.identifier.issn0306-4522
dc.identifier.issn1873-7544
dc.identifier.urihttp://hdl.handle.net/10026.1/10772
dc.description.abstract

In Parkinson's disease (PD), elevated beta (15-35Hz) power in subcortical motor networks is widely believed to promote aspects of PD symptomatology, moreover, a reduction in beta power and coherence accompanies symptomatic improvement following effective treatment with l-DOPA. Previous studies have reported symptomatic improvements that correlate with changes in cortical network activity following GABAA receptor modulation. In this study we have used whole-head magnetoencephalography to characterize neuronal network activity, at rest and during visually cued finger abductions, in unilaterally symptomatic PD and age-matched control participants. Recordings were then repeated following administration of sub-sedative doses of the hypnotic drug zolpidem (0.05mg/kg), which binds to the benzodiazepine site of the GABAA receptor. A beamforming based 'virtual electrode' approach was used to reconstruct oscillatory power in the primary motor cortex (M1), contralateral and ipsilateral to symptom presentation in PD patients or dominant hand in control participants. In PD patients, contralateral M1 showed significantly greater beta power than ipsilateral M1. Following zolpidem administration contralateral beta power was significantly reduced while ipsilateral beta power was significantly increased resulting in a hemispheric power ratio that approached parity. Furthermore, there was highly significant correlation between hemispheric beta power ratio and Unified Parkinson's Disease Rating Scale (UPDRS). The changes in contralateral and ipsilateral beta power were reflected in pre-movement beta desynchronization and the late post-movement beta rebound. However, the absolute level of movement-related beta desynchronization was not altered. These results show that low-dose zolpidem not only reduces contralateral beta but also increases ipsilateral beta, while rebalancing the dynamic range of M1 network oscillations between the two hemispheres. These changes appear to underlie the symptomatic improvements afforded by low-dose zolpidem.

dc.format.extent68-76
dc.format.mediumPrint-Electronic
dc.languageen
dc.language.isoeng
dc.publisherElsevier BV
dc.subjectmagnetoencephalography
dc.subjectParkinson's disease
dc.subjectprimary motor cortex
dc.subjectbeta oscillations
dc.subjectGABA(A) receptors
dc.titleGABA-mediated changes in inter-hemispheric beta frequency activity in early-stage Parkinson’s disease
dc.typejournal-article
dc.typeJournal Article
plymouth.author-urlhttps://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000343860700007&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=11bb513d99f797142bcfeffcc58ea008
plymouth.volume281
plymouth.publication-statusPublished
plymouth.journalNeuroscience
dc.identifier.doi10.1016/j.neuroscience.2014.09.037
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/School of Psychology
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA04 Psychology, Psychiatry and Neuroscience
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA04 Psychology, Psychiatry and Neuroscience/UoA04 REF peer reviewers
plymouth.organisational-group/Plymouth/Research Groups
plymouth.organisational-group/Plymouth/Research Groups/FoH - Applied Parkinson's Research
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
dc.publisher.placeUnited States
dcterms.dateAccepted2014-09-17
dc.identifier.eissn1873-7544
dc.rights.embargoperiodNot known
rioxxterms.versionofrecord10.1016/j.neuroscience.2014.09.037
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2014-12-05
rioxxterms.typeJournal Article/Review


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