Mitral valve prolapse, in the past considered a common source of emboli, especially in young patients, is no longer currently thought to be an important origin. The initial impetus for considering this abnormality as a source of embolus came from the study of Barnett and colleagues (1980) of a group of 60 patients who had TIAs or small strokes and were younger than 45 years of age; mitral prolapse was detected (by echocardiography and a characteristic midsystolic click) in 24 patients, but in only 5 of 60 age-matched controls. However, several subsequent large studies (Sandok and Giuliani; Jones et al) found that only a very small proportion of strokes in young patients could be attributed to prolapse; even then, the connection was inferred by the exclusion of other causes of stroke. Indeed, in a study using stringent criteria for the echocardiographic diagnosis of prolapse, Gilon and colleagues were unable to establish a relation to stroke. Usually, when valvular prolapse is associated with stroke, it is usually severe with ballooning of the valve and a propensity to accumulate clot behind the valve. Of interest, Rice and colleagues described a family with premature stroke in association with valve prolapse and a similar relationship has been reported in twins; the same may occur in Ehlers-Danlos disease.
The pulmonary veins are a potential, if infrequent, source of cerebral emboli, as reflected by the occurrence of cerebral abscesses in association with pulmonary infectious disease (and by the high incidence of cerebral deposits secondary to pulmonary carcinoma). In Osler-Weber-Rendu disease, pulmonary shunts serve as a conduit for emboli. A rare type of embolism follows thyroidectomy, where thrombosis in the stump of the superior thyroid artery extends proximally until a section of the clot, protruding into the lumen of the carotid artery, is carried into the cerebral circulation.
During cerebral arteriography, emboli may arise from the tip of the catheter, or manipulation of the catheter may dislodge atheromatous material from the aorta or carotid or vertebral arteries and account for some of the strokes during this procedure. Monitoring of the cerebral arteries by transcranial Doppler insonation has suggested that small emboli frequently arise during angiographic procedures. For example, a study by Bendszus and colleagues found that 23 of 100 consecutive patients had new cortical lesions shown on diffusion-weighted MRI just after cerebral arteriography. However, none of these patients was symptomatic, and with good technique, emboli from vascular catheters are infrequent.
Cerebral embolism of special type must always have occurred when secondary metastatic tumor is deposited in the brain but a mass of tumor cells is seldom large enough to occlude a cerebral artery and produce the picture of a stroke. Nevertheless, tumor embolism with stroke is known from cardiac myxoma and fibroelastoma, and occasionally with other tumors, even systemic ones; in some of these cases it is a thrombus in the primary lesion that offers a source of embolism. This syndrome must be distinguished from embolism caused by nonbacterial endocarditis that complicates malignant neoplasms (nonbacterial thrombotic endocarditis is discussed further on). This special source of cerebral embolism is a component of a hypercoagulable state that especially accompanies adenocarcinoma and cachexia.