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(Stroke. 1974;5:216.)
© 1974 American Heart Association, Inc.

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Ineffectiveness of Dexamethasone for Treatment of Experimental Cerebral Infarction

MYOUNG C. LEE M.D.¹; ANGELINE R. MASTRI M.D.¹; ARTHUR G. WALTZ M.D.¹; RUTH B. LOEWENSON PH.D.¹

¹ Cerebrovascular Clinical Research Center, Department of Neurology, University of Minnesota, Minneapolis, Minnesota 55455

Ischemic cerebral edema occurring with cerebral infarction may cause increases of intracranial pressure and neurological deficits or death. Certain other types of cerebral edema are influenced by adrenal glucocorticoids; there is conflicting evidence about effects on ischemic edema, largely due to differences in experimental models and dosages. Therefore, dexamethasone in large doses was studied in 15 cats with experimental cerebral ischemia and infarction produced by transorbital occlusion of one middle cerebral artery (MCA). Five cats received dexamethasone, 4 mg per kilogram intramuscularly, twice daily for two weeks before and two weeks after MCA occlusion; five received dexamethasone for two weeks after occlusion; and five received no dexamethasone. There were no apparent differences among the three groups in the neurological deficits resulting from MCA occlusion, and no statistically significant differences in the sizes of cerebral infarcts. Dexamethasone is ineffective for the treatment of experimental cerebral ischemia produced by MCA occlusion.

Key Words: cerebral edema • cerebral ischemia • middle cerebral artery occlusion

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