Psychopharmacology and the Classification of Functional Psychoses 

By Thomas A. Ban and Bertalan Pethö

Four-Dimensional Classification

Affective Psychoses

Schizophrenic Psychoses

Neuroleptics and Etiological Speculations

Endorphins: Excess or Deficiency

The β-endorphin excess hypothesis is in keeping with the PG deficiency hypothesis. Terenius et al. (1976) found elevated β-endorphin levels in the CSF of schizophrenic patients and β-endorphin was shown to block the mobilization of DGLA and the formation of PGE, resulting in a diametrically opposite effect to that of prolactin on PG synthesis. Because successful neuroleptic treatment decreased CSF β-endorphin concentrations, a positive relationship was suggested between CSF endorphin concentrations and schizophrenic psychopathology.

Further, because naloxone, by occupying endorphin receptors, has reversed β-endorphin induced catatonia (in animals), the possibility has been raised that naloxone may have antischizophrenic properties. However, the initial favorable therapeutic effects of intravenous naloxone administration could be replicated only in two out of eight clinical experiments.

Conversely, it has been suggested that decreased availability of β-endorphin to the cerebral opiate receptor sites is responsible for schizophrenic psychopathology (Jacquet and Marks, 1976). Within this frame of reference, schizophrenic psychopathological symptoms are perceived as the result of a deficiency in the production of an endogenous neuroleptic peptide which can be replaced by exogenous neuroleptic drugs. In favor of this hypothesis is the opiate receptor binding property of endorphins and neuroleptics and the finding that, of all CNS regions, the striatum has the highest opiate-binding capacity.

In favor, also were the findings that, in at least three schizophrenic patients, intravenous β-endorphin administration produced a reduction (and/or disappearance) of auditory hallucinations, paranoid ideation and pathological pressure of thought (Kline et al., 1977). The controversy regarding the role of endorphins in schizophrenic psychopathology is far from being resolved (Petho et al. 1982; Volavka et al., 1977).