The advent of magnetic resonance imaging (MRI) and spectroscopy (MRS) and of single photon and positron emission tomography (SPET:PET) has allowed acquisition of data, not otherwise available, on cerebral metabolic function in patients with hepatic encephalopathy. Hyperintensity of the globus pallidus has been observed in cerebral T1-weighted MR images in patients with sub-clinical or overt hepatic encephalopathy, most likely due to the deposition of manganese; these trace metal deposits reflect either intoxication or the presence of an adaptive process leading to improved efficacy of ammonia detoxification by astrocytes. Cerebral 31P MRS has shown that there is no primary deficit in energy metabolism in patients with hepatic encephalopathy, but rather an impairment of phospholipid membrane metabolism; cerebral 1H MRS shows a characteristic pattern of abnormalities in these patients, namely, a significant increase in glutamine/glutamate and significant reductions in choline-containing compounds associated with phospholipid membrane metabolism and of myo-inositol which functions, in part, as an organic osmolyte. SPET and PET technology have not been adequately exploited in the study of hepatic encephalopathy to date; the few studies available have produced conflicting results, most likely because little or no account was taken of the effects of chronic liver disease, portal-systemic shunting or enhanced blood-brain barrier permeability on tracer-ligand availability. All of these techniques need to be further exploited in well-characterized populations with, wherever possible, standardization of techniques between centers; the factors likely to affect tracer-ligand availability must be adequately controlled to allow correct interpretation of the data obtained.