Another source of embolism is the carotid or vertebral artery, where clot forming on an ulcerated atheromatous plaque may be detached and carried to an intracranial branch (artery-to-artery embolism). A similar phenomenon occurs with arterial dissections, discussed in a later section, “Less-Common Causes of Ischemic Cerebrovascular Disease,” and sometimes with fibromuscular disease of the carotid or vertebral arteries.
Atheromatous plaques in the ascending aorta have been recognized to be a more frequent source of embolism than had been previously appreciated. Amarenco and colleagues reported that as many as 38 percent of a group of patients with no discernible cause for embolic stroke had echogenic atherosclerotic plaques in the aortic arch that were greater than 4 mm in thickness, a size found to be associated on a statistical basis with strokes. Disseminated cholesterol emboli from the aorta are known to occur in the cerebral circulation and may be dispersed to other organs as well; rarely, this is sufficiently severe to cause an encephalopathy and pleocytosis in the spinal fluid.
Also of interest are the symptoms caused by an embolus as it traverses a large vessel. This migrating or traveling embolus syndrome is most evident in cases of posterior cerebral artery occlusion, either from a cardiogenic source or from a thrombus in the proximal vertebral artery (“artery-to-artery” embolism; see Koroshetz and Ropper). Minutes or more before the hemianopia develops, the patient reports fleeting dizziness or vertigo, diplopia, or dysarthria, the result of transient occlusion of the origins of penetrating vessels as the clot material traverses the basilar artery. Small residual areas of infarction within the brainstem or cerebellum can be seen on MRI or found at autopsy, and some of the signs of brainstem infarction may persist. The basilar artery is singularly susceptible to this syndrome because the vertebral arteries are smaller in caliber than the basilar, allowing a clot to slowly traverse the larger vessel; furthermore, a clot in the basilar artery is prone to occlude the small orifices of arteries that supply blood to the brainstem.
Paradoxical embolism occurs when an abnormal communication exists between the right and left sides of the heart (particularly a patent foramen ovale [PFO]) or the alternative route of connection via a pulmonary arteriovenous fistula. Embolic material arising in the veins of the lower extremities or pelvis or elsewhere in the systemic venous circulation bypasses the pulmonary circulation and reaches the cerebral vessels. Pulmonary hypertension (often from previous pulmonary embolism) favors the occurrence of paradoxic embolism, but these strokes occur even in the absence of pulmonary hypertension. Several studies indicate that the presence of a small atrial septal aneurysm adjacent to the patient foramen increases the likelihood of stroke. In the series reported by Mas and colleagues (2001), patients ages 18 to 55 years who had a stroke were followed for 4 years; the risk of second stroke was 2 percent in those with a PFO alone and 15 percent among those with both a PFO and an atrial septal aneurysm (curiously, the risk among those with neither congenital abnormality was 4 percent—higher than for those with a PFO alone). This mechanism comes into play mainly in considering the causes of stroke in the younger patient, but Handke and colleagues published a series in which there was a slightly increased risk of stroke in patients who were older than age 55 and had PFO. It must be emphasized, however, that about one-third of patients in all age groups will be found to have a PFO, and anticoagulation or repair of these lesions in patients older than 55 has not been tested as means of stroke prevention (see further on for discussion of treatment of PFO).