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their protective effect in the animal model takes about 48 hours to appear. Finally, earlier experiments by other investigators failed to show convincingly that steroids reduce cerebral edema in experimental brain injury. Although Drs. Pappius and Wolfe anticipate that much more work needs to be done to track down all the metabolic changes that can take place after brain injury, their findings already have interesting implications for the treatment of patients. The rat experiments clearly show that nonsteroidal anti-inflammatory drugs and steroids block the depression of local cerebral glucose utilization after brain lesions even when given 24 hours after the injury, as well as when given just before the injury. Neurosurgeons currently do not use nonsteroidal anti-inflammatory drugs because of the possibility that they may increase extravasation of blood products into the neuronal tissues. Dr. Wolfe is hopeful that a role may be found for calcium channel blockers in the treatment of acute brain injury, since activation of channels for ionized calcium is one of the steps that can lead to depression of cerebral glucose utilization. -Peter P. Morgan, MD