The pathogenesis of hepatic encephalopathy

Abstract

Hepatic encephalopathy remains a complex clinicopathological problem. Much is known about the biochemical derangements in liver, blood, and brain. The precise pathogenetic mechanism for central nervous system dysfunction remains to be determined. Ammonia continues to be considered as an important neurotoxin and may act synergistically with other toxic substances. Disturbances of amino acid balance may result in a disproportion of inhibitory and excitatory neurotransmitters in the brain. Alternatively, some amino acids may act as false neurotransmitters. Recent clinical and laboratory data have advanced the hypothesis that gamma-aminobutyric acid (GABA) absorbed from the gut may enter the brain and exert a profound inhibitory effect. Drugs which antagonize the GABA-benzodiazepate receptor may offer symptomatic improvements in hepatic encephalography.