Abstract

Few therapeutic responses are more dramatic than the response to corticosteroids administered overnight to a drowsy and hemiplegic patient with a cerebral tumor, who next morning is alert with minimal neurological disability, even though this effect may be short lived. Unfortunately, no such dramatic response is seen in patients with ischemic or hemorrhagic stroke; but does this mean that such therapy is totally ineffective? The categorization of cerebral edema by Klatzo and Seitelberger1 into “cytotoxic” and “vasogenic” holds the key to this therapeutic response. Cytotoxic, or “intracellular,” edema represents the earliest response to cerebral damage, and whether ischemic or traumatic, is due to the breakdown of cellular ionic pumps causing ingress of water into the cell, and confined within the cellular membrane. The clinical effects and response to corticosteroids of this immediate type of edema is uncertain. Vasogenic edema, occurring hours later, is due to damage to the blood-brain barrier, which becomes “leaky,” allowing extravasation of water, electrolytes, and soon protein into the parenchyma. This produces …

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