Common Sites of Cerebrovascular Occlusive Disease

Atherosclerosis causes stenosis or occlusion of extracranial and intracranial arteries and is directly responsible for a significant percentage of cerebral ischemic events. Atheroma formation involves the progressive deposition of circulating lipids and ultimately fibrous tissue in the subintimal layer of the large and medium arteries, occurring most frequently at branching points. Plaque formation is enhanced by blood-associated inflammatory factors as well as increased shear injury from uncontrolled blood pressure. Intraplaque hemorrhage, subintimal necrosis with ulcer formation, and calcium deposition can cause enlargement of the atherosclerotic plaque with consequent worsening of the degree of arterial narrowing.

Disruption of the endothelial surface triggers thrombus formation within the arterial lumen through activation of nearby platelets by the subendothelial matrix. When platelets become activated, they release thromboxane A₂, causing further platelet aggregation. The development of a fibrin network stabilizes the platelet aggregate, forming a “white thrombus.” In areas of slowed or turbulent flow within or around the plaque, the thrombus develops further, enmeshing red blood cells (RBCs) in the platelet-fibrin aggregate to form a “red thrombs.” This remains poorly organized and friable for up to 2 weeks and presents a significant risk of propagation and embolization. Either the white or red thrombus, however, can dislodge and embolize to distal arterial branches.

The main risk factors for carotid artery atherosclerotic disease are arterial hypertension, diabetes, hypercholesterolemia, and smoking. Frequent sites for anterior circulation atherosclerosis are the origin of the internal carotid artery (ICA) , the carotid siphon, and the mainstems of the middle cerebral artery (MCA) and anterior cerebral artery (ACA) (see Plate 9-10). The internal carotid artery at or around the bifurcation is usually affected in Caucasians, whereas in Asian, Hispanic, and African-American populations, intracranial atherosclerosis is more common than carotid artery disease in the neck.

Dissection of the extracranial ICA usually occurs in patients between age 20 to 50 years and commonly involves its pharyngeal and distal segments. Dissection occurring between the intima and media usually causes stenosis or occlusion of the affected artery, whereas dissection between the media and adventitia is associated with aneurysmal dilation (see Plate 9-11, A and B). Congenital abnormalities in the media or elastica of the arteries as seen in Marfan syndrome, fibromuscular dysplasia, osteogenesis imperfecta, and cystic medial necrosis can predispose patients to arterial dissection. Although often associated with acute trauma, arterial dissection may result from seemingly innocuous incidents, such as a fall while hiking or skiing, sports activities (particularly wrestling or diving into a wave), and paroxysms of coughing that stretch the artery.

Spontaneous intracranial ICA dissections are uncommon when compared with dissections of its cervical portion. Although early reports described a very poor prognosis with extensive strokes and very high mortality, more recent studies have shown a relatively better outcome, with patients surviving with few or moderate deficits. Imaging studies usually show narrowing of the supraclinoid ICA, with extension to the MCA or ACA and, less commonly, aneurysm formation (see Plate 9-11, C to F).

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