Noninvasive neuroinvestigation in liver disease

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 T-1-weighted MR images in patients with subclinical 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 P-31 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 H-1 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.