The ammonia hypothesis is the most likely explanation for the pathogenesis of hepatic encephalopathy in cirrhosis patients. Reduction of hyperammonemia is therefore the most consistent therapy. From this point of view, the antibiotics have a central significance for the reduction of ammonia formation in the intestinal tract. Equally important is the correction of the hypopotassemia, which may lead to a renally induced hyperammonemia. At the same time, disorders which favor the cerebral toxicity of ammonia, especially anemia and hypoxias, must be compensated. These various measures have improved the prognosis for hepatic encephalopathy of the cirrhosis patient, but were without effect on the course of the coma in severe toxic hepatitis. During the last toxic hepatitis. During the last 10 years, many treatment methods have been reported whose efficacy, however, could not be proved.