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

Prostaglandin: Deficiency or Excess

In keeping with the DA excess hypothesis, however, is the prostaglandin (PG) deficiency hypothesis of schizophrenia. The link between the two is prolactin, a potent stimulator of PG synthesis. Since the release of prolactin is controlled by DA, the neuroleptic-induced DA receptor blockade produces prolactin excess and an increase in PG synthesis.

The hypothesis that schizophrenia is a PG deficiency disease is based on observations that schizophrenic patients are relatively resistant to pain and inflammation and are free of rheumatoid arthritis, a disorder in which PG plays an important role. In favor of the hypothesis are findings that PG antagonists, e.g., chloroquine, quinine, quinacrine, may, in high doses, induce schizophrenic-like states, and that therapeutically effective neuroleptics stimulate the production of prolactin while drugs which precipitate or aggravate schizophrenia, e.g., levodopa, cortisol, suppress secretion and/or block prolactin effects (Horrobin, 1977). Further, in two pilot studies, penicillin, which mobilizes dihomo-gamma-linolenic acid (DGLA)-- the rate limiting step in PGE, synthesis--has shown some therapeutic effects in chronic schizophrenic patients (Chouinard, Annable and Horrobin, 1978).

Conversely, it has been suggested that schizophrenia is a disease of PG excess, i.e., the result of an excessive release of PGE, into the hypothalamus with an accompanying elevation of temperature (Feldberg, 1976). Although Falloon et al. (1978) found no evidence that paracetamol-- a substance which reduces PGE, levels--had any therapeutic effect in acute schizophrenic patients, Gjessing (1953) reported febrile episodes in two- thirds of his special group of catatonic patients.