The clinical events surrounding cerebral embolism have received scant attention from neurologists. Although various aspects of experimentally produced cerebral embolism have been pursued, most studies dealing with the clinical event in man have been written by cardiologists primarily interested in the origin of the embolus itself or by pathologists predominantly concerned with its end state. This situation has developed no doubt because the pathophysiology of the disorder appears obvious; i.e., a solid fragment is broken away, usually from a thrombus in the left auricle of the heart, passes into a cerebral vessel, obstructs blood flow through that vessel, and results in infarction of the region distal to the point of occlusion. The difficulty which neuropathologists have encountered in trying to explain why some of these infarcts are pale and some hemorrhagic reveals that the matter is not always so clear-cut. A more detailed clinical study of these patients reveals, likewise,
WELLS CE. Premonitory Symptoms of Cerebral Embolism. Arch Neurol. 1961;5(5):490–496. doi:10.1001/archneur.1961.00450170028004
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