We investigated the pathogenesis of the thrombotic stroke in the young with assay for coagulation and fibrinolytic factors in plasma.
Eleven thrombotic stroke patients under 39 years old, 30.0±7.9 years old (mean±2SD), who had no risk factors such as hypertension, hyperlipidemia, collagen disease, and cardiac disease were reviewed. These consisted of ten males and one female, 31.7±5.3 years old (mean±2SD) for the control. The group of patient was clasified by computed tomography into two types; (1) small infarction, so called deep branch artery occlusion, four cases and (2) massive infarction, so called cortical branch artery oclusion, seven cases. Cerebral angiography was studied in six cases of massive infarction. Among of the six cases, two cases were right carotid artery occlusion, two cases were left carotid artery occlusion, one case was left posterior cerebral artery occlusion and one had no evidence of occlusion.
We investivated the coagulation and fibrinolytic system with assay for Hageman factor, Factor VIII, C1 estelase inhibitor, antithrombin III (AT III), plasminogen, α
2 plasmin inhibitor, Factor VIII related antigen (VIIIR : Ag), von Willebrand factor activity (vWF) and fibronectin. We could not find out any abnormalities except one case in which has congenital AT III deficiency. In this case, we suspected that the thrombotic stroke was induced by inadequate regulation of coagulation. vWF and VIIIR : Ag which have been throught as the marker of vascular damage were significantly higher in the patients with cortical branch artery occlusion than that in the patients with deep branch artery occlusion (0.005<p<0.01). According to the above data, although the young, cortical artery occlusion may be attributed to systemic vascular damage even in the young adults. And we could find out the teatable factor such as AT III deficiency in the young patients with thrombotic stroke.
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