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From the Department of Neurology, New England Medical Center Boston, MA (Drs. Chaves, Pessin, Caplan, Breen, Tapia, Rosengart, and DeWitt); Department of Neurology, Hopital Saint-Antoine, Paris, France (Dr. Amarenco), Department of Neurology, Chungnam National University Hospital, Taejon, Korea (Dr. Chung); and Department of Neurology, Boston University Hospital, Boston, MA (Drs. Kase, Fine Babikian).
Received November 15, 1994. Accepted in final form June 20, 1995.
Address correspondence to Dr. Louis Caplan, Department of Neurology, New England Medical Center, Box 314, 750 Washington Street, Boston, MA 02111.
We investigated 17 patients with 26 cerebellar hemorrhagic infarcts for their vascular anatomy, stroke mechanisms, and clinical course.Sixteen infarcts involved the superior cerebellar artery, nine the posterior inferior cerebellar artery, and one the anterior inferior cerebellar artery territories. The infarcts involved the full territory of the supplying arteries in 19 of 26 infarcts (73%). Sixteen of 17 patients were stable or improving when the hemorrhagic infarction was detected. All but one patient had an imaging study at the time of presentation that was negative for blood; hemorrhagic infarction was detected on routine serial scans performed during the first 15 days. Nine of the 17 patients were on anticoagulants when the cerebellar hemorrhagic infarct was detected; anticoagulation was maintained in eight of them with no clinical worsening. The stroke mechanism in all patients was considered embolic from cardiac and intraarterial sources. The causes, imaging findings, and consequences of hemorrhagic infarcts in the posterior circulation are similar to those in the anterior circulation.
NEUROLOGY 1996;46: 346-349
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