We have previously reported aberrations in the striatal presynaptic dopamin
e function in neuroleptic-naive schizophrenic patients compared to healthy
controls (Hietala, J., Syvalahti, E., Vuorio, K. et al., 1995. Lancet 346,
1130-1131). In this extended study we explore whether the altered presynapt
ic dopamine function correlates with the clinical symptomatology in schizop
hrenia. Striatal dopamine synthesis capacity (6-[F-18]fluorodopa (FDOPA) up
take, K-i values) was studied with positron emission tomography in 10 neuro
leptic-naive schizophrenic patients and 13 healthy controls. The clinical s
ymptomatology was characterized with the Positive and Negative Symptom Scal
e (PANSS). The patients had an increased FDOPA uptake in striatum and lacke
d the asymmetry in caudate FDOPA uptake (p = 0.0005), confirming our earlie
r results. Left striatal FDOPA uptake (K-i) values correlated negatively wi
th depressive symptoms in a highly significant manner. On the other hand, p
aranoid symptomatology correlated positively with right putamen FDOPA uptak
e at a trend level (rho = 0.73, p<0.02). The lack of asymmetry in caudate K
-i values did not associate with any dimension of psychopathology. The majo
r finding in this study is that depressive symptoms in neuroleptic-naive fi
rst-admission schizophrenia are associated with low presynaptic dopamine fu
nction. This link appears to be hemisphere-related and may have drug-treatm
ent implications, e.g., in prediction of response to D2 receptor blocking a
ntipsychotic drugs. A possible connection between paranoid symptomatology a
nd subcortical hyperdopaminergia is suggested, but this remains to be furth
er verified. (C) 1999 Elsevier Science B.V. All rights reserved.