In this review the most important hypotheses for the occurrence of the clinical picture of hepatic encephalopathy are discussed. As possible pathogenetic mechanisms are raised: dysfunction of the serotonergic system due to an increased tryptophan uptake in the brain, an elevated intracerebral ammoniac concentration and glutamine synthesis, and a heightened intracerebral GABA-activity.

The dysregulation of the serotonergic system as a consequence of the increased intracerebral tryptophan uptake is described as one of the most important pathogenetic mechanisms. The elevated intracerebral ammoniac concentration and the elevated intracerebral glutamine synthesis play in this a facilitating role. The similarity in symptomatology of the clinical picture of HE and the serotonergic syndrome support this hypothesis. Due to contradictory research findings the role of the GABA-ergic system and the occurrence of HE remains unclear.

In this case report of a patient with carcinoid carcinoma we discuss the normal metabolism of tryptophan, one of the essential amino acids.

We also examined the changes of this metabolism due to the metastasis of the carcinoid carcinoma and its psychiatric complications based on a central tryptophan deficiency.

A less frequent complication of the changes in the tryptophan metabolism due to carcinoidosis is the disease pellagra. This disease is always accompanied with psychiatric symptoms. It plays an important role in the development of the transmethylation hypothesis of schizophrenia.