Hepatic Encephalopathy

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Abstract
Hepatic encephalopathy occurs in a number of different species as a result of either congenital portacaval shunts or acquired liver disease. Despite intensive research, the neurochemical basis of the disorder has not been defined. Theories to explain the cerebral dysfunction that accompanies acute or chronic hepatic failure include 1) ammonia acting as the putative neurotoxin, 2) perturbed monoamine neurotransmission as a result of altered plasma amino acid metabolism, 3) an imbalance between excitatory amino acid neurotransmission, mediated by glutamate, and inhibitory amino acid neurotransmission, mediated by gamma-aminobutyric acid, and 4) increased cerebral concentrations of an endogenous benzodiazepine-like substance.