MR imaging and proton MR spectroscopy (¹H-MRS) brain abnormalities have been described in patients with chronic liver failure. Bilateral symmetrical hyperintensity of the globus pallidus is observed on T1W MR images in the majority of these patients and is associated with portal-systemic shunting of blood. The most widely accepted hypothesis explaining this MR finding is accumulation of manganese in the brain produced by a failure of biliary excretion. With improvement of liver function following liver transplantation, a slow progressive disappearance of pallidal hyperintensity, which is complete at 12 months, is demonstrated (Figures 1 and 2). However, recent reports evaluating the relationship between blood manganese and hepatic encephalopathy have yielded conflicting results; thus, a pathophysiological role of brain manganese deposition in the neurologic symptoms of patients with liver disease remains to be demonstrated.