Abstract
In a discussion of old and new concepts of cerebral embolism, two cases are used to illustrate the phathophysiology of atheroembolism in producing intermittent and lasting neurologic deficits. Emboli are due to both cardiogenic and noncardiogenic sources. The onset is characteristically abrupt, but premonitory warnings may occur. The risk of recurrent embolism must be weighed against the risk of anticoagulant therapy, which may cause lethal hemorrhage into the infarcted area. Definitive therapy may require surgical intervention. It seems likely that embolism occurs more frequently than has been previously stated, and these patients should be identified to permit appropriate medical and surgical therapy.
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