Characteristics of intracranial branch atheromatous disease and its association with progressive motor deficits

穿通动脉 医学 闭塞 脑动脉 大脑前动脉 血管疾病 心脏病学 入射(几何) 大脑中动脉 动脉 解剖 外科 缺血 光学 物理
作者
Yasumasa Yamamoto,Tomoyuki Ohara,Masashi Hamanaka,Akiko Hosomi,Aiko Tamura,Ichiro Akiguchi
出处
期刊:Journal of the Neurological Sciences [Elsevier BV]
卷期号:304 (1-2): 78-82 被引量:130
标识
DOI:10.1016/j.jns.2011.02.006
摘要

Background 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. lipohyalinotic degenerative changes termed lipohyalinotic degeneration (LD). We herein analyze and describe the characteristics of these 2 different pathologies. Methods We studied 394 patients with penetrating artery territory infarcts in the territories of the lenticulostriate arteries and anterior pontine arteries. Radiologically defined BAD of the lenticulostriate arteries was defined as infarcts with size more than 10 mm in diameter on axial slice and visible for 3 or more axial slices, and that of the anterior pontine arteries was defined as unilateral infarcts extending to the basal surface of the pons. Within each of the 2 territory groups, differences between BAD and LD were compared. Results Ninety five patients in the lenticulostriate arteries group (36.1%) and 78 patients in anterior pontine arteries group (59.5%) were classified as BAD. Initial NIHSS, incidence of progressive motor deficits and poor functional outcome were significantly higher and incidence of concomitant silent lacunar infarcts tended to be lower in BAD than LD. In logistic regression analysis, BAD compared with LD was independently associated with PMD, in lenticulostriate arteries group (OR: 4.21, p=0.0001) and in anterior pontine arteries group (OR: 5.32, p=0.0018). Conclusions Radiologically defined BAD and LD had different characteristics. BAD was significantly associated with progressive motor deficits and considered as a major vascular mechanism of progressive motor deficits in penetrating artery infarcts.
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