Frontal-striatum dysfunction during reward processing: Relationships to amotivation in schizophrenia.

Published

Journal Article

Schizophrenia is characterized by deficits of context processing, thought to be related to dorsolateral prefrontal cortex (DLPFC) impairment. Despite emerging evidence suggesting a crucial role of the DLPFC in integrating reward and goal information, we do not know whether individuals with schizophrenia can represent and integrate reward-related context information to modulate cognitive control. To address this question, 36 individuals with schizophrenia (n = 29) or schizoaffective disorder (n = 7) and 27 healthy controls performed a variant of a response conflict task (Padmala & Pessoa, 2011) during fMRI scanning, in both baseline and reward conditions, with monetary incentives on some reward trials. We used a mixed state-item design that allowed us to examine both sustained and transient reward effects on cognitive control. Different from predictions about impaired DLPFC function in schizophrenia, we found an intact pattern of increased sustained DLPFC activity during reward versus baseline blocks in individuals with schizophrenia at a group level but blunted sustained activations in the putamen. Contrary to our predictions, individuals with schizophrenia showed blunted cue-related activations in several regions of the basal ganglia responding to reward-predicting cues. Importantly, as predicted, individual differences in anhedonia/amotivation symptoms severity were significantly associated with reduced sustained DLPFC activation in the same region that showed overall increased activity as a function of reward. These results suggest that individual differences in motivational impairments in schizophrenia may be related to dysfunction of the DLPFC and striatum in motivationally salient situations.

Full Text

Duke Authors

Cited Authors

  • Chung, YS; Barch, DM

Published Date

  • April 2016

Published In

Volume / Issue

  • 125 / 3

Start / End Page

  • 453 - 469

PubMed ID

  • 26845257

Pubmed Central ID

  • 26845257

Electronic International Standard Serial Number (EISSN)

  • 1939-1846

International Standard Serial Number (ISSN)

  • 0021-843X

Digital Object Identifier (DOI)

  • 10.1037/abn0000137

Language

  • eng