Adams R J, Nichols F T, McKie V, McKie K, Milner P, Gammal T E
Department of Neurology, Medical College of Georgia, Augusta 30912-2366.
Neurology. 1988 Jul;38(7):1012-7. doi: 10.1212/wnl.38.7.1012.
We studied 25 patients with sickle cell anemia and cerebral infarction. We classified lesions as to probable mechanism (large versus small vessel disease) based on the CT/MRI appearance of established infarction. Most patients had CT/MRI patterns of major cerebral vessel occlusion (41%) or border-zone (distal insufficiency) infarcts (31%) best explained by large cerebral vessel vasculopathy. Seven of 25 (28%) had either isolated subcortical (12%) or small cortical branch occlusion (16%) consistent with other mechanisms such as small vessel occlusion or embolism. These results suggest that most clinically recognized cerebral infarctions in sickle cell anemia are caused by large vessel disease, but this mechanism may not account for symptoms of cerebral ischemia in all cases.
我们研究了25例镰状细胞贫血合并脑梗死患者。根据已确诊梗死的CT/MRI表现，我们将病变按可能的机制（大血管病变与小血管病变）进行分类。大多数患者的CT/MRI表现为大脑主要血管闭塞（41%）或边缘带（远端供血不足）梗死（31%），最有可能是由大脑大血管血管病变所致。25例中有7例（28%）出现孤立的皮质下梗死（12%）或小的皮质分支闭塞（16%），这与小血管闭塞或栓塞等其他机制相符。这些结果表明，镰状细胞贫血患者中大多数临床诊断的脑梗死是由大血管疾病引起的，但这种机制可能无法解释所有病例的脑缺血症状。
