Hippocampal and cortical atrophy predict dementia in subcortical ischemic vascular disease
Hippocampal and cortical atrophy predict dementia in subcortical ischemic vascular disease
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DOI：
10.1212/wnl.55.11.1626
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发表时间：
2000-12-12
期刊：
影响因子：
9.9
通讯作者：
Chui, H
中科院分区：
文献类型：
--
作者：
Fein, G;Di Sclafani, V;Chui, H
背景：皮质下缺血性血管病(SIVD)中痴呆的病因存在争议。目的：确定SIVD患者的认知损害是否与缺血性脑损伤或脑萎缩的程度有关，和/或2)是否由伴发的AD引起。方法：对1)腔隙(L)、认知功能障碍--认知正常(NC+L，n=32)、轻度认知障碍(CI+L，n=26)、痴呆(D+L，n=29)、2)疑似AD(n=28)、3)认知正常而无认知缺陷组(NC)的老年患者进行脑体积磁共振成像检查。作者研究了认知损害的严重程度与1)腔隙的体积、数量和位置；2)白质信号高强度(WMSH)的体积；以及3)脑萎缩的测量(即，海马体、皮质灰质和脑脊液体积)之间的关系。结果：在三个缺陷组中，认知障碍的严重程度与海马区和皮质灰质的萎缩有关，而与任何缺陷性措施无关。虽然海马区萎缩是预测认知损害严重程度的最佳指标，但有证据表明第二个部分独立的萎缩过程与脑室扩张、皮质灰质萎缩和WMSH增加有关。8例尸检的SIVD患者在海马区有不同程度的缺血和神经纤维变性，但在新皮质没有明显的AD病理改变。疑似AD组仅有一个萎缩过程，反映在海马区萎缩的严重程度，皮质灰质体积比较显示，疑似AD组初级运动皮质和视觉皮质较少，而D+L组萎缩相对均匀。结论：与AD一样，SIVD的痴呆与海马和皮质萎缩的相关性最好，而不是任何程度的腔隙。在SIVD中，与AD不同的是，有证据表明这两个萎缩过程之间存在部分独立。海马区萎缩可能是缺血和退行性病变的混合体所致。弥漫性皮质萎缩的原因尚不清楚，但可能部分与WMSH的严重程度有关。
Background: The cause of dementia in subcortical ischemic vascular disease (SIVD) is controversial. Objectives: To determine whether cognitive impairment in SIVD 1) correlates with measures of ischemic brain injury or brain atrophy, and/or 2) is due to concomitant AD. Methods: Volumetric MRI of the brain was performed in 1) elderly subjects with lacunes (L) and a spectrum of cognitive impairment-normal cognition (NC+L, n = 32), mild cognitive impairment (CI+L, n = 26), and dementia (D+L, n = 29); 2) a comparison group with probable AD (n = 28); and 3) a control group with normal cognition and no lacunes (NC). The authors examined the relationship between the severity of cognitive impairment and 1) volume, number, and location of lacunes; 2) volume of white matter signal hyperintensities (WMSH); and 3) measures of brain atrophy (i.e., hippocampal, cortical gray matter, and CSF volumes). Results: Among the three lacune groups, severity of cognitive impairment correlated with atrophy of the hippocampus and cortical gray matter, but not with any lacune measure. Although hippocampal atrophy was the best predictor of severity of cognitive impairment, there was evidence for a second, partially independent, atrophic process associated with ventricular dilation, cortical gray matter atrophy, and increase in WMSH. Eight autopsied SIVD cases showed variable severity of ischemic and neurofibrillary degeneration in the hippocampus, but no significant AD pathology in neocortex. The probable AD group gave evidence of only one atrophic process, reflected in the severity of hippocampal atrophy, Comparison of regional neocortical gray matter volumes showed sparing of the primary motor and visual cortices in the probable AD group, but relatively uniform atrophy in the D+L group. Conclusions: Dementia in SIVD, as in AD, correlates best with hippocampal and cortical atrophy, rather than any measure of lacunes. In SIVD, unlike AD, there is evidence for partial independence between these two atrophic processes. Hippocampal atrophy may result from a mixture of ischemic and degenerative pathologies. The cause of diffuse cortical atrophy is not known, but may be partially indexed by the severity of WMSH.