functions, thereby defining subclinical hepatic encephalopaHepatic encephalopathy is a common problem in cirthy. Alterations of cerebral metabolism measured by MRS rematter, .64 { .16). In addition, patients showed a signifiturned to normal in most patients after liver transplantacant reduction (P Å .024) in white matter choline/cretion, 6-8 demonstrating that they are related to liver disease. atine ratio (.77 { .27) compared with controls (.92 { .25),In magnetic resonance imaging (MRI), the presence of and glutamine/glutamate level was elevated in cirrhotic signal hyperintense basal ganglia in T1-weighted images appatients compared with controls (gray matter, P õ .0001; pears closely related to severe liver disease with both portalwhite matter, P Å .036). Changes in cerebral myoinositol systemic shunting 9 and hepatic encephalopathy. 10-14 Howand glutamine/glutamate levels correlated significantly ever, the latter finding has been questioned recently.
15with the severity of hepatic encephalopathy (P õ .0001).Pomier Layrargues et al. 16 and Krieger et al. 17 have demonHowever, these metabolic alterations were also detected strated recently that the concentration of manganese, a parain patients without hepatic encephalopathy (normal magnetic substance, is elevated in bright basal ganglia.
psychometric test results). N-acetyl aspartate/creatineThe aim of the present study was to evaluate prospectively ratios did not differ between patients and controls. Magcerebral metabolism and morphological abnormalities in 51 netic resonance imaging detected bright basal ganglia in clinically well-defined patients with histologically proven cir-37 patients, which correlated significantly with portalrhosis with or without signs of hepatic encephalopathy using systemic shunting and elevation of glutamine/gluta-MRS and MRI.