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Cirrhosis, Hepatic Encephalopathy, and Ammonium Toxicity pp 1–22Cite as

Cerebral Function in Hepatic Encephalopathy

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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 272))

Abstract

Hepatic encephalopathy in patients may result from the surgical formation of a portacaval shunt, or chronic liver disease, often accompanied by portal systemic shunting (1, 2, 3). Whether the development of encephalopathy is caused by diversion of blood past the liver, decreased liver function, or both, is unknown. The symptoms of hepatic encephalopathy caused by portacaval shunting (pcs) or chronic liver dysfunction in man range from very subtle subclinical abnormalities of intellectual and motor function to coma. The apparent reversibility of these symptoms suggests that the encephalopathy has a metabolic etiology. Even in the absence of serious symptoms brain function is compromised and is more sensitive to a variety of metabolic disturbances which in normal individuals would cause no serious alterations in cerebral function (1,2).

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  1. Department of Physiology and Biophysics, University of Health Sciences The Chicago Medical School, 3333 Green Bay Road, North Chicago, IL, 60064, USA

    Richard A. Hawkins & Anke M. Mans

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    Santiago Grisolía , Vicente Felipo  & María-Dolores Miñana ,  & 

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Hawkins, R.A., Mans, A.M. (1990). Cerebral Function in Hepatic Encephalopathy. In: Grisolía, S., Felipo, V., Miñana, MD. (eds) Cirrhosis, Hepatic Encephalopathy, and Ammonium Toxicity. Advances in Experimental Medicine and Biology, vol 272. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5826-8_1

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