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The researches were carried out on two groups of children: normals and with behavior disturbances. The serum cationic state was determined by an original method, using heparin as cautions exchanger in physiological pH, and the protein reactivity; the electrophoretic mobility of serum proteins at pH 7.4; total soduim and serum proteins. The obtained results show that serum proteins in children with behavior disturbances differ from those of normals, having: 1) smaller number of serotonin-fixing sites, 2) higher strength interaction between the serotonin and proteins, 3) lower resistance to the denaturant agents which has as a consequence the increase of cationic activity in the serum, and an increased electrophoretic mobility. The data are discussed and interpreted as perturbations in the electrolytes exchange (Na+, especially) in the integration centres of the autonomic functions.

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.