Abstract
Reye’s Syndrome (RS) is a frequently fatal disease that occurs in children as a rare sequelae to a relatively benign viral illness such as influenza or varicella (1). Its hallmark features include fatty infiltration, particularly of the liver, mitochondrial degeneration, and severe cerebral encephalopathy. The latter is the usual cause of death. The sequence of events that occurs during the early stages of RS are not known; however, this information is of great importance, since unlike true viral encephalopathies, tissue destruction in this disease can be minimal and reversible, and the disease can be recoverable (2). If appreciable brain edema does develop, however, approximately 20% of the patients sustain residual CNS damage.
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Murphy, M.G., Digout, S.C., Crocker, J.F.S. (1989). Encephalopathy of Reye’s Syndrome: Studies of the Pathogenic Process in Animal Models. In: Butterworth, R.F., Layrargues, G.P. (eds) Hepatic Encephalopathy. Experimental Biology and Medicine, vol 22. Humana Press. https://doi.org/10.1007/978-1-4612-4506-3_17
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DOI: https://doi.org/10.1007/978-1-4612-4506-3_17
Publisher Name: Humana Press
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