Cadavid D, Mena H, Koeller K, Frommelt R A
Department of Neuropathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000, USA.
J Neuropathol Exp Neurol. 2000 Sep;59(9):768-73. doi: 10.1093/jnen/59.9.768.
Cerebral amyloid angiopathy (CAA) is conspicuous for its association with Alzheimer disease (AD) and as a cause of lobar hemorrhages in the elderly, but its role in cerebral infarction is less clear. There is evidence that CAA may also be a risk factor for ischemic infarction in AD. To further investigate CAA as a risk factor for infarction, we studied 108 cases of recent cerebral or cerebellar infarction diagnosed in tissue samples obtained from surgical material. There were 69 males and 39 females with a mean age of 52 yr (range 1-86). The majority of biopsies were obtained from the frontal and parietal lobes. Radiological studies demonstrated a lesion confined to a vascular distribution in 12 of the 17 (71%) cases examined. Microscopic sections stained with hematoxylin and eosin revealed complete, organizing infarction in 107 cases with areas of coagulative necrosis, anoxic-ischemic neuronal injury, inflammation, macrophages, vascular proliferation, gliosis, and swollen axons. One case showed an incomplete infarct. Most cases also exhibited a minor hemorrhagic component with hemosiderin and hematoidin pigments. CAA, defined as amyloid deposition in the walls of leptomeningeal and parenchymal arteries, was found by immunohistochemical stains for beta amyloid in 14 (13%) cases of complete cerebral infarct. Cortical beta amyloid plaques were found by immunohistochemistry in 19 (17%) cases. Cerebral or cerebellar tissues containing cortex and leptomeninges obtained from 136 patients with a mean age of 52 yr (range 1-85) during surgical procedures for diagnosis of primary or metastatic neoplasms and demyelinating lesions were used as age-matched controls. In this control group, CAA was found in 5 (3.7%) and beta amyloid plaques in 19 (14%). The results indicate that CAA, but not beta amyloid plaque formation, is significantly more common in patients with ischemic cerebral infarction than in age-matched controls with nonvascular lesions (odds ratio 3.8; 95% confidence interval 1.3-10.9; p < 0.01). Our results indicate that CAA is a risk factor for ischemic cerebral infarction in the population studied.
脑淀粉样血管病（CAA）因其与阿尔茨海默病（AD）相关以及作为老年人脑叶出血的一个病因而备受关注，但其在脑梗死中的作用尚不清楚。有证据表明CAA可能也是AD中缺血性梗死的一个危险因素。为了进一步研究CAA作为梗死的一个危险因素，我们对108例近期诊断为脑或小脑梗死的病例进行了研究，这些病例取自手术材料的组织样本。其中男性69例，女性39例，平均年龄52岁（范围1 - 86岁）。大多数活检样本取自额叶和顶叶。影像学研究显示，在17例接受检查的病例中有12例（71%）的病变局限于血管分布区域。苏木精和伊红染色的显微切片显示，107例存在完全性、正在机化的梗死，伴有凝固性坏死区域、缺氧缺血性神经元损伤、炎症、巨噬细胞、血管增生、胶质细胞增生以及轴突肿胀。1例显示为不完全梗死。大多数病例还表现出轻微的出血成分，伴有含铁血黄素和胆色素。通过β淀粉样蛋白免疫组化染色，在14例（13%）完全性脑梗死病例中发现了CAA，定义为软脑膜和实质动脉壁中的淀粉样蛋白沉积。通过免疫组化在19例（17%）病例中发现了皮质β淀粉样斑块。从136例平均年龄52岁（范围1 - 85岁）的患者手术过程中获取的包含皮质和软脑膜的脑或小脑组织，这些患者因诊断原发性或转移性肿瘤以及脱髓鞘病变而接受手术，用作年龄匹配的对照。在这个对照组中，5例（3.7%）发现有CAA，19例（14%）发现有β淀粉样斑块。结果表明，与年龄匹配的非血管性病变对照组相比，缺血性脑梗死患者中CAA明显更为常见，而β淀粉样斑块形成并非如此（优势比3.8；95%置信区间1.3 - 10.9；p < 0.01）。我们的结果表明，在本研究人群中CAA是缺血性脑梗死的一个危险因素。
