一過性脳虚血発作の成因

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  • Pathogenesis of Transient Ischemic Attack

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Pathogenesis and etiologic factors in transient ischemic attack (TIA) were briefly reviewed with emphasis on intra and extracranial atherosclerotic changes and indication for surgery.<BR> TIA is a clinical syndrome, which can only be defined by clinical features and is not confined to specific pathological changes in the brain or in the vascular system. Various pathogenic concepts and etiologic factors have been reported in the literature. The vasospasm theory in pathogenesis of TIA is now almost abandoned. There have been no experimental findings nor any other grounds to assume that vasospasm frequently causes TIA. Most patients with TIA become symptom-free by anticoagulation and many other evidences suggest that vast majorities of TIA are due to thromboembolism including so-called “microembolism.” However, transient fluctuations of cerebral perfusion pressure can also be a causative factor of TIA in a small number of cases, as pointed out by DennyBrown (so-called “cerebrovascular insufficiency”). In either case, the main etiologic factor can be attributed to atherosclerotic changes in the intra and extracranial arteries. Incidences of vascular changes in the intracranial cerebral arteries seem to be higher in this country than in European countries or in the USA.<BR> In rare cases of TIA, various other pathogenic conditions, such as polycythemia, thrombocytosis, kinkings and coilings of the cervical arteries, subclavian steal syndrome, moyamoya disease, etc, have been reported or experienced.<BR> Thromboendarterectomy of the cervical arteries and superficial temporal artery-to-middle cerebral artery (STA-MCA) anastomosis have been tried for surgical management of TIA. From a pathogenic point of view, thromboendartectomy is recommended for cases of TIA, which is caused by thromboembolism originated from atherosclerotic foci in the cervical arteries, while STA-MCA anastomosis might possibly be applied to cases of cerebrovascular insufficiency due to various vascular changes such as stenosis of the middle cerebral artery, internal carotid occlusion, and moyamoya disease.

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