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NEUROLOGY 1994;44:1385
© 1994 American Academy of Neurology

Cerebellar infarcts in the New England Medical Center Posterior Circulation Stroke Registry

C. J. Chaves, MD, L. R. Caplan, MD, C.-S. Chung, MD, J. Tapia, MD, P. Amarenco, MD, P. Teal, MD, R. Wityk, MD, C. Estol, MD, B. Tettenborn, MD, A. Rosengart, MD, K. Vemmos, MD, L. D. DeWitt, MD and M. S. Pessin, MD

Department of Neurology, New England Medical Center, Tufts University, Boston, MA.

We report the clinical findings and stroke mechanisms of 63 patients with cerebellar infarcts. We divided the intracranial vertebrobasilar circulation into the proximal territory (P), fed by the intracranial vertebral arteries and their branches; the middle territory (M), fed by the proximal and middle basilar artery and its branches; and the distal territory (D), fed by the rostral basilar artery and its branches. Cerebellar infarcts were classified by vascular territories P, M, D, P&D, and middle-plus (P&M, M&D, and P&M&D). Patients with P infarcts (11 patients) frequently had vertigo, gait instability, limb ataxia, and headache, whereas patients with D infarcts (15 patients) most often had limb ataxia, gait instability, and dysarthria. Patients with P&D infarcts (17 patients) had signs and symptoms of both groups combined. Infarcts in which the middle territory was involved, either alone (three patients) or combined with other territories (17 patients) were dominated by brainstem signs and symptoms. The predominant stroke mechanisms in the P, D, and P&D groups were embolic due to intra-arterial or cardiac embolism. When the M territory was involved, either alone or with P, D, or P&D territories, stroke mechanisms were more varied, and there was often large-artery occlusion with hemodynamic ischemia.

Address correspondence and reprint requests to Dr. Louis R. Caplan, Department of Neurology, New England Medical Center, Box 314, 750 Washington Street, Boston, MA 02111.

Received October 12, 1993. Accepted in final form January 28, 1994.




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