[Transient ischemic attacks before and after occlusion of the internal carotid artery]

Among 60 cases with occlusion of an internal carotid artery (ICA), 47 p. 100 suffered warning TIA's in the corresponding area. In 7 p. 100 the TIA's were the only manifestation of the disease. The occurrence of warning TIA's significantly correlated with a small volume (less than 20 cm3, p 0,001) and a deep localization (p less than 0,002) of infarction, and also with a better initial neurologic ability and long-term functional prognosis (p less than 0,05) than in patients without warning TIA's. Twenty eight p. 100 of the 60 cases showed delayed TIA's distal to the occlusion. In 12 p. 100 TIA's had not been present before the occlusion. The delayed TIA's were strongly (p less than 0,0001) associated with an atheromatous stenosis of the external carotid artery (ECA) or a stump of the occluded ICA and an important collateral supply through ECA channels, suggesting a micro-embolic mechanism via ECA pathways. Much more rarely hemodynamic factors, and exceptionally probable emboli from the contralateral ICA, appeared to be involved. The occurrence of delayed TIA's was not a warning sign of further stroke, and did not correspond to a poorer functional prognosis. Three p. 100 of the 60 cases suffered TIA's in the contralateral ICA territory, in relation to an atheromatous stenosis of the ICA. Twenty p. 100 showed vertebrobasilar TIA's, usually without associated disease of the vertebral or subclavian arteries (75 p. 100). This point and the evidence of absent or weak collateral circulation (p less than 0,0001) and of an associated contralateral ICA stenosis (p less than 0,01), suggested a hemodynamic mechanism with an intracranial steal from the vertebrobasilar system towards the carotid circulation.(ABSTRACT TRUNCATED AT 250 WORDS)