Berger J R, Nath A, Greenberg R N, Andersen A H, Greene R A, Bognar A, Avison M J
Department of Neurology, University of Kentucky College of Medicine, Lexington 40536-2184, USA.
Neurology. 2000 Feb 22;54(4):921-6. doi: 10.1212/wnl.54.4.921.
HIV dementia is a form of subcortical dementia. Clinical, radiologic, pathologic, and biochemical studies suggest a major contribution of basal ganglia dysfunction to the pathogenesis of this disorder. Many investigators have proposed a contribution of a disrupted blood-brain barrier (BBB) to the pathogenesis of HIV dementia.
To identify microvascular abnormalities in vivo in basal ganglia or white matter of persons with HIV dementia.
Time course of MRI postcontrast enhancement was determined in basal ganglia and white matter of HIV-infected persons without dementia (Memorial Sloan Kettering [MSK] score of 0; n = 4); HIV-infected persons with mild dementia (MSK score of 0.5; n = 2); and HIV-infected persons with moderate-to-severe dementia (MSK > or = 1.0; n = 6).
Increased basal ganglia enhancement was observed in individuals with moderate-to-severe dementia relative to nondemented individuals, both immediately and 30 minutes after contrast administration. Decline of basal ganglia enhancement was slower in the moderately to severely demented patients and, when normalized to intravascular enhancement of sagittal sinus, suggested leakage of contrast agent, consistent with increased permeability of BBB. A significant correlation between the postcontrast fractional enhancement at 30 minutes (FE30) and the MSK score was noted. White matter showed no significant differences in postcontrast enhancement among the three groups.
Increased early enhancement in basal ganglia of the HIV dementia group is consistent with increased regional cerebral blood volume (rCBV). Increased late enhancement is strongly suggestive of BBB disruption. Similar abnormalities were absent in the white matter adjacent to the caudate nucleus.
HIV 痴呆是皮质下痴呆的一种形式。临床、放射学、病理学及生物化学研究表明，基底节功能障碍在该疾病的发病机制中起主要作用。许多研究者提出血脑屏障（BBB）破坏在 HIV 痴呆发病机制中的作用。
确定 HIV 痴呆患者基底节或白质的微血管异常情况。
在无痴呆的 HIV 感染者（纪念斯隆凯特琳[MSK]评分为 0；n = 4）、轻度痴呆的 HIV 感染者（MSK 评分为 0.5；n = 2）以及中度至重度痴呆的 HIV 感染者（MSK≥1.0；n = 6）的基底节和白质中，测定 MRI 造影剂增强后的时间进程。
与未患痴呆的个体相比，中度至重度痴呆个体在注射造影剂后即刻及 30 分钟时，基底节增强均增加。中度至重度痴呆患者基底节增强的下降较慢，经矢状窦血管内增强标准化后，提示造影剂渗漏，这与血脑屏障通透性增加一致。在 30 分钟时的造影剂增强分数（FE30）与 MSK 评分之间存在显著相关性。三组之间白质在造影剂增强方面无显著差异。
HIV 痴呆组基底节早期增强增加与局部脑血容量（rCBV）增加一致。晚期增强增加强烈提示血脑屏障破坏。尾状核相邻白质未见类似异常。
