Anhedonia in schizophrenic, depressed, or alcohol-dependent patients--neurobiological correlates

Abstract

Anhedonia, dysphoria, and avolition are common symptoms of schizophrenic, depressive, and alcohol-dependent patients during withdrawal. These symptoms may be caused by a functional deficit of dopaminergic transmission in the dopaminergic reward system, ascending from the mesencephalon to the ventral striatum (nucleus accumbens). The dopaminergic reward system is functionally and anatomically closely connected with the ascending extrapyramidal pathways from the substantia nigra to the dorsal striatum. A dysfunction of both ascending dopaminergic pathways is therefore expected to cause both psychomotor slowing and dysphoria and anhedonia. This hypothesis is supported by PET and SPECT findings, which show that a reduced striatal density of unoccupied dopamine D2-receptors is correlated with extrapyramidal side-effects in neuroleptic-treated schizophrenics and with craving and dysphoria in drug-dependent patients. In order to further investigate the correlation of anhedonia, psychomotor slowing, and the status of the dopaminergic reward system, the density of striatal dopamine D2-receptors can be measured by IBZM-SPECT and related to psychomotor slowing and anhedonia in different states of schizophrenic, depressive, and alcohol-dependent patients.