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NEUROLOGY 1997;49:1538-1541
© 1997 American Academy of Neurology

Stroke mechanisms and clinical presentation in large subcortical infarctions

Deborah R. Horowitz, MD and Stanley Tuhrim, MD

From the Department of Neurology, The Mount Sinai School of Medicine, New York, NY.

Address correspondence and reprint requests to Dr. Deborah R. Horowitz, Department of Neurology, Box 1052, The Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029.

Large subcortical infarctions may be due to cerebral embolism and cause cortical signs more frequently than small subcortical infarctions, which usually result from small-vessel disease and are not associated with cortical findings. We evaluated 51 consecutive patients with a subcortical infarct on CT that was 1.5 cm or larger for a potential carotid or cardiac source of embolism and determined how frequently aphasia, hemineglect, or gaze paresis occurred. A carotid or cardiac embolic source was identified in 63% of the total population with a carotid source occurring in 23% and a cardiac source occurring in 49%. More than one-half of the patients with hypertension or diabetes mellitus had an embolic source, whereas all patients without these risk factors had a possible carotid or cardiac source of embolism. Aphasia or hemineglect occurred in 39% of patients and gaze paresis occurred in 41%. Large subcortical strokes frequently result in a different clinical syndrome and from a different mechanism than small subcortical strokes


Received February 19, 1997. Accepted in final form July 9, 1997.




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