 Pathogenesis of hepatic encephalopathy In patients with liver cirrhosis, increasing structural replacement of hepatocytes with connective tissue leads to the loss of functioning hepatic parenchymal tissue and a reduction in the detoxification capacity of the liver. In addition, developing portal hypertension leads to the formation of a collateral circulation through which non-detoxified blood can by-pass the liver to reach the systemic circulation. Both these mechanisms contribute to the neurotoxins present in portal vein blood reaching the brain via the systemic circulation. A number of neurotoxins have been implicated in the pathogenesis of HE with ammonia being the most important 4,5. Fundamental conceptual advances in our understanding of hepatic encephalopathy have confirmed the central role of ammonia in the pathogenesis of portosystemic encephalopathy. Ammonia disrupts the function of neurones and astrocytes, giving rise to the symptoms of hepatic encephalopathy. 