title: Depressive symptoms and presynaptic dopamine function in neuroleptic-naive schizophrenia.
abstract: We have previously reported aberrations in the striatal presynaptic dopamine function in neuroleptic-naive schizophrenic patients compared to healthy controls (Hietala, J., Syvälahti, E., Vuorio, K. et al., 1995. Lancet 346, 1130-1131). In this extended study we explore whether the altered presynaptic dopamine function correlates with the clinical symptomatology in schizophrenia. Striatal dopamine synthesis capacity (6-[18F]fluorodopa (FDOPA) uptake, Ki values) was studied with positron emission tomography in 10 neuroleptic-naive schizophrenic patients and 13 healthy controls. The clinical symptomatology was characterized with the Positive and Negative Symptom Scale (PANSS). The patients had an increased FDOPA uptake in striatum and lacked the asymmetry in caudate FDOPA uptake (p = 0.0005), confirming our earlier results. Left striatal FDOPA uptake (Ki) values correlated negatively with depressive symptoms in a highly significant manner. On the other hand, paranoid symptomatology correlated positively with right putamen FDOPA uptake at a trend level (rho = 0.73, p < 0.02). The lack of asymmetry in caudate Ki values did not associate with any dimension of psychopathology. The major finding in this study is that depressive symptoms in neuroleptic-naive first-admission schizophrenia are associated with low presynaptic dopamine function. This link appears to be hemisphere-related and may have drug-treatment implications, e.g., in prediction of response to D2 receptor blocking antipsychotic drugs. A possible connection between paranoid symptomatology and subcortical hyperdopaminergia is suggested, but this remains to be further verified.
authors.affiliation: Department of Psychiatry, Turku University Central Hospital, Finland. jahi@utu.fi
authors.forename: J
authors.initials: J
authors.lastname: Hietala
authors.forename: E
authors.initials: E
authors.lastname: Syvälahti
authors.forename: H
authors.initials: H
authors.lastname: Vilkman
authors.forename: K
authors.initials: K
authors.lastname: Vuorio
authors.forename: V
authors.initials: V
authors.lastname: Räkköläinen
authors.forename: J
authors.initials: J
authors.lastname: Bergman
authors.forename: M
authors.initials: M
authors.lastname: Haaparanta
authors.forename: O
authors.initials: O
authors.lastname: Solin
authors.forename: M
authors.initials: M
authors.lastname: Kuoppamäki
authors.forename: E
authors.initials: E
authors.lastname: Eronen
authors.forename: U
authors.initials: U
authors.lastname: Ruotsalainen
authors.forename: R K
authors.initials: RK
authors.lastname: Salokangas
mesh_terms: D000293:Adolescent; D000328:Adult; D003342:Corpus Striatum / Q000503:physiopathology*; D003866:Depressive Disorder / Q000150:complications / Q000503:physiopathology* / Q000523:psychology; D004295:Dihydroxyphenylalanine / Q000031:analogs & derivatives / Q000493:pharmacokinetics; D004298:Dopamine / Q000502:physiology*; D005260:Female; D007839:Functional Laterality; D006801:Humans; D008297:Male; D011699:Putamen / Q000000981:diagnostic imaging / Q000503:physiopathology; D017661:Receptors, Presynaptic / Q000502:physiology; D012559:Schizophrenia / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D012565:Schizophrenic Psychology; D014055:Tomography, Emission-Computed