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Brain energy metabolism and function during hepatic encephalopathy

In this issue Dr Hindfelt reports on a study of biochemical changes in the portacaval-shunted rat-a model of hepatic encephalopathy-occurring over a long period in the development of the disease. The specific question addressed is whether there is a defect in cerebral glucose uptake or degradation that is caused by liver dysfunction. This is a welcome contribution which addresses an important issue. Chronic liver disease, often accompanied by portalsystemic shunting, or the surgical formation of a portacaval shunt alone may lead to hepatic encephalopathy [I-31. Whether the development of encephalopathy is caused by diversion of blood past the liver, decreased liver function, or both, is open to question, but there is general agreement that the brain becomes much more sensitive to a variety of metabolic disturbances which in normal individuals would cause no serious alterations in cerebral function. For instance, a gradient of symptoms ranging from subtle alterations in consciousness and mental ability to disorientation, stupor and coma can be produced by increased dietary protein, gastrointestinal bleeding, infection, sedatives, hyperammonaemia, etc. Because these symptoms appear to be reversible there is hope that an effective treatment can be found. Hepatic encephalopathy is, as mentioned, a continuum of mentally deranged states; only the most severe of which comes to professional notice. It is important to realize that encephalopathy exists even when clinical symptoms are not manifest. Close studies of patients with liver disease showed that psychomotor defects are present which are not obvious to the casual observer [2]. Because its development is often subtle, hepatic encephalopathy is one of the few gastrointestinal diseases in which the diagnosis relies almost entirely on the history and the physical examination. On the other hand, hepatic encephalopathy is reflected in quantitative indices of cerebral energy metabolism, such as cerebral oxygen consumption and cerebral glucose utilization, which correlate with the degree of cerebral impairment [4, 51. Cerebral oxidative metabolism is also lower in subjects with no clinical evidence of neurological disturbances, in agreement with the concept that cerebral dysfunction exists before the situation is serious enough to require professional help