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Stroke. 2004;35:228-229
Published online before print December 18, 2003, doi: 10.1161/01.STR.0000105930.29558.DB
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*Substance via MeSH
Medline Plus Health Information
*Steroids
*Stroke

(Stroke. 2004;35:228.)
© 2004 American Heart Association, Inc.


Controversies in Stroke

Steroids May Have a Role in Stroke Therapy

John W. Norris, MD

From the Department of Neurology, University of Toronto, Ontario, Canada.

Correspondence to John W. Norris, MD, Dept of Clinical Neurosciences, St Georges Hospital Medical School, London SW17 ORE, United Kingdom. E-mail j.norris@sghms.ac.uk


Key Words: cytotoxic edema • steroids • vasogenic cerebral edema


An extract of the first 250 words of the full text is provided, because this article has no 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 clinically significant brain swelling, resulting in distortion and herniation of brain and causing neurological disability and death. In brain tumors, the normally tight vascular junctions are pathologically separated, and cellular physiology (such as pinocytosis) is otherwise disturbed,2 resulting in severe vasogenic edema, which is highly responsive to corticosteroids.3 This fundamental difference in pathophysiology between the 2 types of lesions may explain the apparent difference in their initial therapeutic response.

There is overwhelming evidence experimentally in a variety of mammalian models that corticosteroids effectively reduce . . . [Full Text of this Article]




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Stroke, May 1, 2004; 35(5): e93 - e93.
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