Progression of white matter lesions and hemorrhages in cerebral amyloid angiopathy
Progression of white matter lesions and hemorrhages in cerebral amyloid angiopathy
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DOI：
10.1212/01.wnl.0000223613.57229.24
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发表时间：
2006-07-11
期刊：
影响因子：
9.9
通讯作者：
Smith, E. E.
中科院分区：
文献类型：
--
作者：
Chen, Y. W.;Gurol, M. E.;Smith, E. E.
目的：确定脑淀粉样血管病（CAA）队列中白色病变和脑白质病变的进展率。方法：作者分析了26例根据波士顿标准诊断为可能（3）或可能（23）CAA的患者的资料。通过盲法计算机辅助分割基线和中位随访间隔1.1年后获得的MRI图像，创建标准化为头部大小（nWMH）的白色高信号脑图。结果：在扫描间隔内，nWMH体积显著增加（中位数0.5 mL/年，四分位数范围0.1 - 2.8，p < 0.001）。以基线WMH体积的百分比表示的中位年增长率为18%。与nWMH体积增加最密切相关的特征是基线nWMH体积（r = 0.57，p = 0.002）。nWMH进展量也与认知功能障碍病史相关（认知功能障碍受试者的中位值为5.0 mL/年，认知功能未受损受试者为0.3 mL/年，p = 0.02），但与年龄或高血压无关。在按基线WMH体积分层的分析中，这种相关性仍然存在。在46%的受试者中观察到新的出血，包括无症状的微出血。新发MRI病灶的数量与基线nWMH（r = 0.53，p = 0.005）密切相关，但与nWMH进展（r = 0.22，p = 0.28）无关。结论：脑淀粉样血管病患者的白色病变逐渐增多。白色病变与脑叶出血的相关性提示白色病变可能反映了由于脑淀粉样血管病引起的进行性微血管病。
Objective: To determine the rate of progression of white matter lesions and hemorrhages in a cohort with cerebral amyloid angiopathy (CAA). Methods: The authors analyzed data from 26 patients with possible (3) or probable (23) CAA, diagnosed by the Boston Criteria. Brain maps of white matter hyperintensities, normalized to head size (nWMH), were created by blinded computer-assisted segmentation of MRI images obtained at baseline and after a median follow-up interval of 1.1 year. Results: There was a substantial nWMH volume increase over the interscan interval (median 0.5 mL/year, interquartile range 0.1 to 2.8, p < 0.001). The median yearly increase, expressed as a percentage of the baseline WMH volume, was 18%. The characteristic most strongly associated with nWMH volume increase was the baseline nWMH volume (r = 0.57, p = 0.002). The volume of nWMH progression was also associated with history of cognitive impairment (median 5.0 mL/year in cognitively impaired subjects vs 0.3 mL/year in cognitively unimpaired, p = 0.02) but not age or hypertension. This association remained present in an analysis stratified by baseline WMH volume. New hemorrhages, including asymptomatic microbleeds, were seen in 46% of subjects. The number of new MRI hemorrhages correlated strongly with baseline nWMH (r = 0.53, p = 0.005) but not with nWMH progression (r = 0.22, p = 0.28). Conclusions: There is a progressive increase in white matter lesions in subjects with cerebral amyloid angiopathy. The association of white matter lesions with incident lobar hemorrhages suggests that white matter damage may reflect a progressive microangiopathy due to cerebral amyloid angiopathy.