Meyer J S, Konno S, Margishvili G M, Terayama Y
Veterans Affairs Medical Center, Baylor College of Medicine Houston, TX, USA.
J Stroke Cerebrovasc Dis. 1998 Sep-Oct;7(5):323-9. doi: 10.1016/s1052-3057(98)80050-5.
Thirty seven vascular dementia (VAD) patients were categorized into eight subtypes based on clinical, radiological, and pathogenetic features. Cerebral vasodilator responses to acetazolamide were then compared with age-matched normal controls and stroke patients without dementia.
VAD results were compared with 42 normals and 19 cognitively intact stroke patients. Regional cerebral vasodilator responses were quantitated utilizing xenon contrasted computed tomography measures of local cerebral blood flow (LCBF) before and after oral administration of acetazolamide. LCBF changes (DeltaLCBF) before and after acetazolamide were calculated within cortical and subcortical, gray and white matter. Clinical VAD subtypes were: type 1, multi-infarct dementia (MID); type 2, strategically placed infarcts; type 3, subcortical lacunar infarcts; type 4, Binswanger's subcortical arteriosclerotic leukoencephalopathy; type 5, subcortical infarctions due to cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), inflammatory angitis, or antiphospholipid antibodies; type 6, admixtures of above types; type 7, cerebral hemorrhagic lesions; and type 8, VAD combined with Alzheimer's disease (DAT). The group with subcortical VAD comprised types 3-5. The group with cortical VAD comprised the remainder (types 1, 2, and 6-8). Cerebral vasodilator responses were also compared between these two main groups.
Cerebral vasodilator responses identified differences between the two main groups of VAD patients, those with cortical and those with subcortical dementia. Leukoaraiosis was measurably greater in subcortical VAD compared with cortical VAD. Among subcortical VAD patients, cortical LCBF increases after administration of acetazolamide were greater compared with cortical VAD and with normal controls.
Cognitive impairments in subcortical VAD are attributable to cortical disconnection syndromes. This concept is supported by reduced perfusion in deactivated cortex. In patients with subcortical VAD, deactivated cortical LCBF becomes promptly activated by acetazolamide resulting in marked cortical LCBF increases. Leukoaraiosis is greater among VAD patients and leukoaraiosis contributes to cortical disconnections, confirmed by excessive cortical vasodilator responses to acetazolamide.
根据临床、影像学和发病机制特征，将37例血管性痴呆（VAD）患者分为8个亚型。然后将乙酰唑胺引起的脑血管扩张反应与年龄匹配的正常对照者及无痴呆的中风患者进行比较。
将VAD患者的结果与42名正常人和19名认知功能正常的中风患者进行比较。口服乙酰唑胺前后，利用氙增强计算机断层扫描测量局部脑血流量（LCBF），对局部脑血管扩张反应进行定量分析。计算乙酰唑胺前后皮质和皮质下、灰质和白质内的LCBF变化（ΔLCBF）。临床VAD亚型包括：1型，多发梗死性痴呆（MID）；2型，关键部位梗死；3型，皮质下腔隙性梗死；4型，宾斯旺格皮质下动脉硬化性白质脑病；5型，由伴有皮质下梗死和白质脑病的常染色体显性遗传性脑动脉病（CADASIL）、炎症性血管炎或抗磷脂抗体引起的皮质下梗死；6型，上述类型的混合；7型，脑内出血性病变；8型，VAD合并阿尔茨海默病（DAT）。皮质下VAD组包括3 - 5型。皮质VAD组包括其余类型（1、2和6 - 8型）。还比较了这两个主要组之间的脑血管扩张反应。
脑血管扩张反应显示出两组主要VAD患者之间的差异，即皮质性痴呆患者和皮质下痴呆患者。与皮质VAD相比，皮质下VAD的脑白质疏松症更为明显。在皮质下VAD患者中，与皮质VAD患者和正常对照者相比，服用乙酰唑胺后皮质LCBF增加更大。
皮质下VAD的认知障碍归因于皮质分离综合征。这一概念得到了失活皮质灌注减少的支持。在皮质下VAD患者中，失活的皮质LCBF通过乙酰唑胺迅速激活，导致皮质LCBF显著增加。VAD患者的脑白质疏松症更为严重，脑白质疏松症导致皮质分离，这一点通过对乙酰唑胺的过度皮质血管扩张反应得到证实。
