Hepatic encephalopathy, or portosystemic encephalopathy, is a reversible decline in neurologic function associated with impaired hepatic function. Despite the frequency of the condition, we still lack a clear understanding of its pathogenesis. Nevertheless, decades of experience have suggested that an increase in the concentration of ammonia and inhibitory neurotransmission of gamma-aminobutyric acid receptors in the central nervous system may play a role, in addition to the changes in central neurotransmitters and circulating amino acids. Currently available therapies for hepatic encephalopathy are based upon these hypotheses. Synthetic disaccharides (lactulose) are still the mainstay in the therapy of hepatic encephalopathy, but there is limited evidence from well-designed randomized controlled trials demonstrating their efficacy. 

Key words:
ammonia; gamma-aminobutyric acid; hepatic encephalopathy; lactulose; receptors, GABA