Abstract
Hepatic encephalopathy (HE) is a neuropsychiatric disorder that results from impaired liver function. In humans, hepatic encephalopathy occurs in two major forms: (1) Associated with acute or fulminant hepatic failure, a clinical syndrome resulting from severe inflammatory and/or necrotic liver disease of rapid onset. The neurological disorder progresses from altered mental status to coma, generally within hours or days. Death frequently results from increased intracranial pressure caused by massive brain edema. (2) Portal-systemic encephalopathy (PSE), the most common form of hepatic encephalopathy that accompanies liver cirrhosis. Cirrhosis frequently results from chronic alcohol abuse (at least in Western hemisphere countries) but may also be caused by viral infections, biliary obstruction, drugs, or various toxins. Portal hypertension arises as a result of the cirrhotic process; the high portal pressure stimulates the opening of embryonic venous channels or simply reverses the direction of flow in the existing ones. These shunts permit toxins of intestinal origin to bypass the liver into the systemic circulation; hence the term “portal-systemic encephalopathy.”
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Blei, A.T., Omarg, R., Butterworth, R.F. (1992). Animal Models of Hepatic Encephalopathies. In: Boulton, A.A., Baker, G.B., Butterworth, R.F. (eds) Animal Models of Neurological Disease, II. Neuromethods, vol 22. Humana Press. https://doi.org/10.1385/0-89603-211-6:183
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