BACKGROUND AND PURPOSE: Occipital lobe infarcts are traditionally attributed to vertebrobasilar disease. However, anatomical studies indicate that in some people the supply of the posterior cerebral artery is via the carotid system. We investigated how often such a developmental variant in the cerebral blood supply was present during life. METHODS: We retrospectively studied 212 conventional four-vessel cerebral angiograms. Eighteen subjects were excluded beforehand, because of vascular abnormalities causing important hemodynamic changes. We determined whether a fetal variant was present, and in other cases whether there was a functioning posterior communicating artery. RESULTS: In 11 % of hemispheres the posterior cerebral artery was exclusively supplied by the internal carotid artery; in a further 46 % of hemispheres the internal carotid artery might contribute, via a patent posterior communicating artery. In 75 % of subjects the internal carotid artery contributed in at least one hemisphere to the blood flow of the posterior cerebral artery. CONCLUSIONS: The implication of our findings is that an occipital lobe infarct can be caused by ipsilateral carotid disease in a proportion of cases between 10 and 60 %. This implies that carotid endarterectomy might be beneficial in some patients with severe carotid stenosis and infarction in the territory of the posterior cerebral artery.
BACKGROUND AND PURPOSE:Occipital lobe infarcts are traditionally attributed to vertebrobasilar disease. However, anatomical studies indicate that in some people the supply of the posterior cerebral artery is via the carotid system. We investigated how often such a developmental variant in the cerebral blood supply was present during life. METHODS: We retrospectively studied 212 conventional four-vessel cerebral angiograms. Eighteen subjects were excluded beforehand, because of vascular abnormalities causing important hemodynamic changes. We determined whether a fetal variant was present, and in other cases whether there was a functioning posterior communicating artery. RESULTS: In 11 % of hemispheres the posterior cerebral artery was exclusively supplied by the internal carotid artery; in a further 46 % of hemispheres the internal carotid artery might contribute, via a patent posterior communicating artery. In 75 % of subjects the internal carotid artery contributed in at least one hemisphere to the blood flow of the posterior cerebral artery. CONCLUSIONS: The implication of our findings is that an occipital lobe infarct can be caused by ipsilateral carotid disease in a proportion of cases between 10 and 60 %. This implies that carotid endarterectomy might be beneficial in some patients with severe carotid stenosis and infarction in the territory of the posterior cerebral artery.
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