Different compounds occur in the circulation in increased concentrations when liver function is impaired and may contribute to hepatic encephalopathy, being ammonia probably the most important. Hyperammonemia induce accumulation of glutamine inside the astrocytes causing its swelling and subsequently an increase in the water content of the whole brain. This cerebral edema is a major cause of intracraneal hypertension and death in patients with fulminant hepatic failure (Figure 3). Brain edema is only rarely a complication of chronic liver failure, although cerebral glutamine increases to a similar extent in both chronic and acute liver failure. The rarity of cerebral edema may be explained by a compensatory decrease of other osmolytes such as myoInositol and taurine (Figure 4). This osmoregulatory mechanism protects the development of massive brain edema and explain the abscence of overt intracranial hypertension in chronic liver failure.

It has been suggested that despite the osmoregulatory mechanism a low-grade astrocytic swelling exist in chronic hepatic failure that may be partially responsible to the development of hepatic encephalopathy. The purpose of this scientific exhibit is to show MR data from cirrhotic patients obtained before and after normalization of liver function (liver transplantation) that suppport the presence of a reversible widespread metabolic alteration in the white matter with a slight increase in brain water content. . We obtained MR data, including T1- and T2WI, magnetization transfer imaging and ¹H-MRS, from a group of 24 non-alcoholic cirrhotics without over hepatic encephalopathy to investigate the presence of significant changes in the brain white matter that could reflect increased free water within the brain. In addition these MR studies were repeated in a subgroup of 11 patients at one month and one year after a liver transplantation with normalization of liver function.