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  会員専用

• ホーム
• 50巻11号
• 臨床神経, 50：914−917, 2010
• 50巻11号目次

第51回日本神経学会総会

＜シンポジウム11―1＞脳梗塞臨床の第一線における問題点：Branch atheromatous disease（BAD）をどう考え，どう対処するか
Branch atheromatous disease（BAD）の概念とその臨床的意義

山本　康正

京都第二赤十字病院脳神経内科〔〒602―8026 京都市上京区春帯町355―5〕

Small deep brain infarcts are often caused by two different vascular pathologies: 1. atheromatous occlusion at the orifice of large caliber penetrating arteries termed branch atheromatous disease (BAD) and 2. lipohyallinotic degenerative changes termed lipohyalinitic degeneration (LD). Atheromatous changes at the origin or proximal portion of a penetrating artery of larger caliber can be observed in infarcts of the lenticulostriate (LSA) as well as the anterior pontine arteries (APA). We studied 392 patients with penetrating artery disease in the territories of LAS and APA to evaluate predictive factors for progressive motor deficits (PMD). Prevalence of male gender, diabetes mellitus and intracranial atherosclerosis were significantly higher in the APA group than in the LSA group. Female sex and initial severity of motor deficit were common predictors for PMD in both groups. In the LSA group, single infarcts without concomitant silent lacunar infarcts and lacunar TIAs were found to be independent predictors for PMD. In the APA group, diabetes mellitus was found to be an independent predictor. Combined treatment consisting of argatroban, cilostazol, and edaravone for acute BAD type infarct significantly improved the functional outcome.
Full Text of this Article in Japanese PDF (613K)

(臨床神経, 50：914−917, 2010)
key words：穿通枝病変，分枝粥腫症，リポヒアリノーシス

（受付日：2010年5月22日）