Intracranial atherosclerosis

Seemant Chaturvedi MD (

Dr. Chaturvedi of Wayne State University has no relevant financial relationships to disclose.

Steven R Levine MD, editor. (

Dr. Levine of the SUNY Health Science Center at Brooklyn has no relevant financial relationships to disclose.

Originally released August 14, 2001; last updated February 10, 2020; expires February 10, 2023

This article includes discussion of intracranial atherosclerosis, carotid atherosclerosis, intracranial atherothrombosis, and intracranial occlusive disease. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


The author provides an update on intracranial atherosclerosis, with new information on the final results of a multicenter registry to evaluate intracranial stenting (WEAVE registry). Information on optimal medical management is presented, along with the latest techniques for imaging of intracranial atherosclerosis.

Key points


• Intracranial atherosclerosis may be the most common cause of stroke worldwide.


• Aggressive medical therapy is necessary for patients with symptomatic intracranial atherosclerosis.


• Recognition of this stroke subtype is increasing with better neuroimaging methods.

Historical note and terminology

In 1951, C. Miller Fisher described the clinical findings associated with occlusion of the extracranial internal carotid artery (Fisher 1951). Prior to that it was generally believed that ischemic stroke in the anterior circulation was invariably caused by intrinsic middle cerebral artery thrombosis. Several studies have subsequently shown that extracranial carotid occlusive disease is a more common cause of stroke than middle cerebral artery or carotid siphon occlusive disease (Hass et al 1968; Sacco et al 1994); nevertheless, large artery intracranial occlusive disease remains an important cause of ischemic stroke in the United States.

The first clinical descriptions of vertebrobasilar insufficiency were made in the late 1940s and early 1950s (Kubik and Adams 1946; Millikan and Siekert 1955). Based on the landmark paper by Kubik and Adams in 1946, basilar artery occlusion was considered a fatal disease (Kubik and Adams 1946). Subsequent studies, however, have shown that patients can survive basilar artery occlusion and occasionally may have only a minor neurologic deficit (Caplan 1979). Further studies have identified prognostic variables helpful in predicting outcome. One such study conducted at the Mayo clinic evaluated patients based on their respiratory status. The researchers found that those patients who present with neurologic compromise secondary to basilar artery occlusion and required mechanical ventilation had a high mortality rate. Of the 25 patients evaluated, 22 died. The remaining 3 persisted in a locked-in state (Wijdicks 1996).

Before cerebral angiography was first performed in humans in 1927 by Egas Moniz (Moniz 1927; Atunes 1974), the diagnosis of atherosclerotic intracranial large artery disease could only be established at autopsy. The refinement of cerebral angiography enabled the diagnosis of intracranial large artery disease to be made during life, but the risk of stroke during this procedure coupled with the lack of proven therapy for intracranial occlusive disease resulted in limited use of angiography for establishing the diagnosis. The development of transcranial Doppler ultrasound in 1982 by Aaslid and associates (Aaslid et al 1982) and the development of magnetic resonance angiography (Ross et al 1989) have enabled noninvasive diagnosis of intracranial occlusive disease. These technological advances, coupled with preliminary data suggesting the potential benefit of antithrombotic and thrombolytic therapy and angioplasty for the treatment of intracranial occlusive disease, have led to renewed interest in the pathogenesis and treatment of atherosclerotic intracranial large artery occlusive disease.

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