Etiologic Heterogeneity of the Psychoses: Is There a Dopamine Psychosis?

Abstract

The distribution of drug-free plasma lzomovanillic acid (pHV A) Despite the posited association of dopamine with psychosis since the 1960s, there has been little support for such a direct linkage in the recent psychiatric literature. Anden et al. (1970) first suggested that the newly discovered antipsychotic drugs had but one characteristic in common: they blocked access of dopamine to dopamine receptors. Seeman et al. (1975) and Creese et al. (1976) found that the affinity of various drugs for central dopamine 2 (0 2 ) receptors is inversely related to the dose at which conventional antipsychotics are administered.

Subjective Effects of AMPT-induced Dopamine Depletion in Schizophrenia Correlation between Dysphoric Responses and Striatal D2 Binding Ratios on SPECT Imaging

“…Since a healthy control group was not included in our study, it is difficult to conclude if the binding ratios in this sub-group would be higher than normal controls but relatively lower compared to the non-dysphoric subjects; or if they were indeed comparable to those of healthy controls. The latter scenario revives an under-recognized notion that biochemical mechanisms other than dopamine might be involved in the origin of schizophrenic symptoms (Garver et al 1997(Garver et al , 2000. Second, the failure to monitor serum AMPT levels raised some uncertainty about the extent of dopamine depletion achieved and the consequent rise in the D 2 binding ratios in our subjects, which were comparatively lower in our subjects compared to the other reports (Abi-Dargham et al 2000).…”

Differential Effects of Mental Stress on Plasma Homovanillic Acid in Schizophrenia and Normal Controls

“…Despite some argument (Kopin et al 1988;Lambert et al 1993;Maas et al 1988), several lines of investigations have focused on plasma levels of homovanillic acid (pHVA), a major metabolite of DA, for the study of DA-related mental disorders such as schizophrenia based on the assumption that dysfunction in central dopaminergic activity is, to some extent, reflected in this peripheral measure (see Friedhoff and Amin 1997 for review). While conflicting results have been reported regarding differences in pHVA levels between patients with schizophrenia and control subjects (Doran et al 1985;Koreen et al 1994;Maas et al 1993;Pickar et al 1984;Steinberg et al 1993;Sumiyoshi et al 1997a;Whelton et al 1993), there has been accumulated evidence for the association between pHVA levels in schizophrenia and the outcome of neuroleptic treatment (Akiyama et al 1995;Chang et al 1993;Davis et al 1985;Garver et al 1997;Green et al 1993;Nagaoka et al 1997;Sumiyoshi et al 1997b). …”

Atrophic and Static (Neurodevelopmental) Schizophrenic Psychoses Premorbid Functioning, Symptoms and Neuroleptic Response

“…Another putative endophenotype of psychosis appears to occur without such ventricular expansion, and may be indicative of anatomical anomalies arising in the remote past, probably during neurodevelopment. Still another nonexpanding putative endophenotype of psychosis (a third psychosis) is clinically very different, with elevated plasma homovanillic acid and rapid neuroleptic response: a dopamine excess, good prognosis psychosis (Garver 1997;Garver et al 1997).…”