Cognitive impairment from a major stroke as a consequence of carotid disease is an acknowledged clinical outcome; however, cognitive impairment without major stroke is open to discussion. The three recognized mechanisms for cognitive dysfunction from internal carotid artery are microembolization, white-matter disease, and hypoperfusion. The last has been most difficult to characterize physiologically. In this article, the authors review evidence supporting the existence of chronic ischemia in the brain and its direct impact on cognitive functions. By incorporating the pathophysiology of chronic ischemia into the algorithm of the management of carotid artery disease, we may be able to extend the goals of carotid artery revascularization beyond merely preventing stroke to include preventing or reversing cognitive decline.