Fein G, Di Sclafani V, Tanabe J, Cardenas V, Weiner M W, Jagust W J, Reed B R, Norman D, Schuff N, Kusdra L, Greenfield T, Chui H
Neurobehavioral Research, Inc., San Francisco, CA, USA.
Neurology. 2000 Dec 12;55(11):1626-35. doi: 10.1212/wnl.55.11.1626.
The cause of dementia in subcortical ischemic vascular disease (SIVD) is controversial.
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.
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).
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.
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.
皮质下缺血性血管病(SIVD)所致痴呆的病因存在争议。
确定SIVD中的认知障碍1)是否与缺血性脑损伤或脑萎缩的指标相关,和/或2)是否由合并的阿尔茨海默病(AD)所致。
对以下人群进行脑部容积磁共振成像(MRI)检查:1)患有腔隙性脑梗死(L)且伴有一系列认知障碍的老年受试者——认知正常(NC+L,n = 32)、轻度认知障碍(CI+L,n = 26)和痴呆(D+L,n = 29);2)一个可能患有AD的对照组(n = 28);3)一个认知正常且无腔隙性脑梗死的对照组(NC)。作者研究了认知障碍严重程度与以下因素之间的关系:1)腔隙性脑梗死的体积、数量和位置;2)白质信号高增强(WMSH)的体积;3)脑萎缩的指标(即海马体、皮质灰质和脑脊液体积)。
在三个腔隙性脑梗死组中,认知障碍的严重程度与海马体和皮质灰质萎缩相关,但与任何腔隙性脑梗死指标无关。尽管海马体萎缩是认知障碍严重程度的最佳预测指标,但有证据表明存在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例经尸检的SIVD病例显示海马体缺血和神经纤维变性的严重程度各不相同,但新皮质中无明显的AD病理改变。可能患有AD的组仅显示出一个萎缩过程,表现为海马体萎缩的严重程度。区域新皮质灰质体积的比较显示,可能患有AD的组中初级运动和视觉皮质未受影响,但D+L组中萎缩相对均匀。
与AD一样,SIVD所致痴呆与海马体和皮质萎缩的相关性最强,而非任何腔隙性脑梗死指标。与AD不同,在SIVD中,这两个萎缩过程之间存在部分独立性的证据。海马体萎缩可能是缺血性和退行性病变共同作用的结果。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。