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Disturbed surround inhibition in preclinical parkinsonism

DC Field Value Language
dc.contributor.author강석윤-
dc.contributor.author손영호-
dc.contributor.author신혜원-
dc.date.accessioned2014-12-21T16:32:36Z-
dc.date.available2014-12-21T16:32:36Z-
dc.date.issued2007-
dc.identifier.issn1388-2457-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/95887-
dc.description.abstractOBJECTIVE: Surround inhibition in the motor system is an essential mechanism for selective execution of desired movements. To evaluate the functional operation of surround inhibition in Parkinson disease, we performed a transcranial magnetic stimulation (TMS) study in the asymptomatic hands of hemiparkinsonism patients. METHODS: TMS was set to be triggered by self-initiated flexion of the index finger at different intervals from 3 to 2000 ms. Average motor evoked potential (MEP) amplitudes obtained from self-triggered TMS were normalized to average MEPs of control TMS at rest. Normalized MEP amplitudes of the patients' self-triggered TMS sessions at different intervals were compared to those of the controls. RESULTS: During index finger flexion, MEP amplitudes from the little finger muscle were unchanged in normal subjects. However, they were enhanced in Parkinson patients, despite the absence of any motor disturbance. CONCLUSIONS: These results suggest that the functional operation of surround inhibition is impaired in Parkinson disease. This disturbance may precede motor disturbance in Parkinson disease. SIGNIFICANCE: Impaired surround inhibition can be useful to detect preclinical parkinsonism.-
dc.description.statementOfResponsibilityopen-
dc.format.extent2176~2179-
dc.relation.isPartOfCLINICAL NEUROPHYSIOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleDisturbed surround inhibition in preclinical parkinsonism-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Neurology (신경과학)-
dc.contributor.googleauthorHae-Won Shin-
dc.contributor.googleauthorSuk Y. Kang-
dc.contributor.googleauthorYoung H. Sohn-
dc.identifier.doi10.1016/j.clinph.2007.06.058-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00038-
dc.contributor.localIdA01982-
dc.contributor.localIdA02183-
dc.relation.journalcodeJ00592-
dc.identifier.eissn1872-8952-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S1388245707003288-
dc.contributor.alternativeNameKang, Suk Yun-
dc.contributor.alternativeNameSohn, Young Ho-
dc.contributor.alternativeNameShin, Hye Won-
dc.contributor.affiliatedAuthorKang, Suk Yun-
dc.contributor.affiliatedAuthorSohn, Young Ho-
dc.contributor.affiliatedAuthorShin, Hye Won-
dc.rights.accessRightsnot free-
dc.citation.volume118-
dc.citation.number10-
dc.citation.startPage2176-
dc.citation.endPage2179-
dc.identifier.bibliographicCitationCLINICAL NEUROPHYSIOLOGY, Vol.118(10) : 2176-2179, 2007-
dc.identifier.rimsid53270-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers

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