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Topographic Patterns and Stroke Subtypes According to Progressive Motor Deficits in Lacunar Syndrome

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dc.contributor.authorKim, Yong Bum-
dc.contributor.authorMoon, Heui-Soo-
dc.contributor.authorSuh, Bum-Chun-
dc.contributor.authorPark, Kwang-Yeol-
dc.contributor.authorLee, Yong Taek-
dc.contributor.authorChung, Pil-Wook-
dc.date.available2019-05-29T11:41:05Z-
dc.date.issued2011-07-
dc.identifier.issn1052-3057-
dc.identifier.issn1532-8511-
dc.identifier.urihttps://scholarworks.bwise.kr/cau/handle/2019.sw.cau/21442-
dc.description.abstractAlthough progressive hemiparesis occurs frequently in acute ischemic stroke, the topography and mechanisms associated with progressive motor deficit (PMD) remain unclear. The aim of this study was to identify the differences in PMD according to lesion location and the presumed underlying pathogenesis in patients with lacunar motor syndrome. Consecutive patients experiencing acute lacunar motor syndrome within 24 hours of stroke onset were included. Topographic patterns, risk factors, and presumed stroke mechanisms were compared between patients with PMD and those without PMD. Of the 168 patients in the study group, 47 (28.0%) had PMD. Baseline National Institutes of Health Stroke Scale score (P =.034) and female sex (P =.005) were associated with PMD on univariate analysis. Deep perforating artery infarct was more frequently associated with PMD (35.8%) compared with large artery disease (27.3%) and cardioembolism (5.3%). Multiple logistic analysis found that deep perforating artery infarct was independently associated with PMD (odds ratio, 2.87; 95% confidence interval, 1.26-6.5; P =.012). Deep perforating artery infarct is the major cause of PMD. In patients with lacunar syndrome, the pattern of PMD varies according to the location and etiology of stroke.-
dc.format.extent5-
dc.language영어-
dc.language.isoENG-
dc.publisherELSEVIER SCIENCE BV-
dc.titleTopographic Patterns and Stroke Subtypes According to Progressive Motor Deficits in Lacunar Syndrome-
dc.typeArticle-
dc.identifier.doi10.1016/j.jstrokecerebrovasdis.2010.02.006-
dc.identifier.bibliographicCitationJOURNAL OF STROKE & CEREBROVASCULAR DISEASES, v.20, no.4, pp 352 - 356-
dc.description.isOpenAccessN-
dc.identifier.wosid000293603300012-
dc.identifier.scopusid2-s2.0-79960000480-
dc.citation.endPage356-
dc.citation.number4-
dc.citation.startPage352-
dc.citation.titleJOURNAL OF STROKE & CEREBROVASCULAR DISEASES-
dc.citation.volume20-
dc.type.docTypeArticle-
dc.publisher.location네델란드-
dc.subject.keywordAuthorProgressive motor deficit-
dc.subject.keywordAuthorlacunar syndrome-
dc.subject.keywordAuthorstroke subtype-
dc.subject.keywordAuthortopography-
dc.subject.keywordPlusDIFFUSION-WEIGHTED MRI-
dc.subject.keywordPlusEARLY NEUROLOGICAL DETERIORATION-
dc.subject.keywordPlusACUTE ISCHEMIC-STROKE-
dc.subject.keywordPlusSMALL DEEP INFARCTS-
dc.subject.keywordPlusARTERIAL TERRITORIES-
dc.subject.keywordPlusHUMAN BRAIN-
dc.subject.keywordPlusACUTE-PHASE-
dc.subject.keywordPlusPREDICTORS-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusCLASSIFICATION-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalResearchAreaCardiovascular System & Cardiology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.relation.journalWebOfScienceCategoryPeripheral Vascular Disease-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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