Comparative studies of the electroencephalogram and the cerebral oxidative metabolism in patients with liver cirrhosis.

In two groups of patients with liver cirrhosis and normal EEG (Group A) and with pathological EEG (Group B) it was possible to demonstrate a correlation between the severity grade of the EEG changes, the livertypical deviations of serum chemistry and alterations in cerebral oxidative metabolism. The metabolism of the brain showed a reduced oxygen consumption and carbon dioxide output in the patients with pathological EEG changes. All patients showed a raised glucose uptake, an increased lactate release, a raised ammonia uptake and glutamine output. These findings in patients with liver cirrhosis indicate a disturbance of the oxidative energy metabolism of the brain with secondary intensification of glycolysis. Pathological changes in the EEG only appear if the oxygen consumption of the brain is limited (as in the patients of Group B). These EEG changes have a poor prognosis in respect to life expectancy. With consideration of the data from animal experiments and the reported results of cerebral blood flow and oxydative metabolism in patients with liver cirrhosis it might be assumed that liver insufficiency with elevated serum ammonia results in a deranged oxydative cerebral metabolism which might explain hepatic encephalopathy.