Cerebral ischemia is caused by occlusive arterial disease anywhere along the course of the blood supply to the brain. Irreversible damage is most likely to occur when there is inadequate collateral circulation due to (a) involvement of multiple vessels; (b) inadequacy of anastomoses of the vascular structures at the base of the brain due to congenital variation or occlusive disease; or (c) when an artery terminal to the circle of Willis becomes occluded. The fact that cerebral infarction may result from disease in the surgically accessible portion of the cervical carotid artery is well known. The Joint Study of Extracranial Arterial Occlusion reports that 75% of 3,788 patients had accessible lesions, often combined with inaccessible lesions, but existing alone in 41%.1 It is equally well known that cerebral infarction is usually preceded by premonitory symptoms of transient neurologic handicaps or minor strokes heralding the catastrophic event. These symptoms may
Perdue GD, Smith RB, Rhodes L, Long WD. Carotid Revascularization in the Treatment of Cerebral Ischemia. Arch Surg. 1970;100(5):562–564. doi:10.1001/archsurg.1970.01340230028005
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