Embolization of atherosclerotic material from the carotid bifurcation is now recognized as the most common cause of stroke. The association between transient ischemic attacks and the presence of internal carotid artery occlusive disease, as well as subsequent recognition that the bright yellow plaques identified in the retinal arterioles of some patients with cerebral arterial occlusive disease might be secondary to cholesterol embolization, were milestones in understanding the pathophysiology of stroke. Later it was realized that plaque degeneration is often associated with bleeding into the plaque with a resultant acute increase of the plaque. It can also be associated with plaque rupture. Carotid artery plaque can also rupture spontaneously. In both cases, a large amount of degenerative atheromatous debris may be released toward the brain. Depending on whether the plaque follows the ophthalmic artery or the middle cerebral artery, the patient may develop amaurosis fugax, transient ischemic attack, or stroke. The occurrence of embolic episodes from manipulation of the carotid bifurcation during carotid endarterectomy or endovascular carotid stenting has been confirmed by the use of transcranial Doppler. Emboli from the carotid artery may pass through the circle of Willis and produce hemispheric symptoms contralateral to what would normally be expected. Atheroembolism to the brain may also originate from the aortic arch or proximal common carotid artery. Catheter-induced embolism as a result of diagnostic carotid angiography is generally accepted to occur in 1% of patients. With the advent of carotid angioplasty and stenting, the high incidence of embolism resulting from balloon angioplasty had been documented by the use of transcranial Doppler and particle capture using various types of cerebral protection devices. Any catheter manipulation within the aortic arch or proximal great vessels may potentially result in an embolism.

The treatment of atheroembolization to the brain consists of treatment of the responsible proximal lesion. In the carotid system this often consists of carotid endarterectomy. In rare cases, arterial resection with reconstruction may be necessary.
Recent attention has been focused upon the use of carotid angioplasty and stenting for the treatment of atheroembolization from the extracranial carotid artery system. Currently, the National Institutes of Health is sponsoring the Carotid Revascularization versus Endarterectomy and Stenting Trial (CREST) to evaluate the efficacy of angioplasty, and stenting in patients with symptomatic carotid artery disease. Because most symptomatic lesions are the result of atheroembolization from the extracranial carotid system, the results of this study will better define the role of angioplasty and stenting in the treatment of this entity.