Dissociation of response and feedback negativity in schizophrenia: electrophysiological and computational evidence for a deficit in the representation of value.

Published

Journal Article

Contrasting theories of schizophrenia propose that the disorder is characterized by a deficit in phasic changes in dopamine activity in response to ongoing events or, alternatively, by a weakness in the representation of the value of responses. Schizophrenia patients have reliably reduced brain activity following incorrect responses but other research suggests that they may have intact feedback-related potentials, indicating that the impairment may be specifically response-related. We used event-related brain potentials and computational modeling to examine this issue by comparing the neural response to outcomes with the neural response to behaviors that predict outcomes in patients with schizophrenia and psychiatrically healthy comparison subjects. We recorded feedback-related activity in a passive gambling task and a time estimation task and error-related activity in a flanker task. Patients' brain activity following an erroneous response was reduced compared to comparison subjects but feedback-related activity did not differ between groups. To test hypotheses about the possible causes of this pattern of results, we used computational modeling of the electrophysiological data to simulate the effects of an overall reduction in patients' sensitivity to feedback, selective insensitivity to positive or negative feedback, reduced learning rate, and a decreased representation of the value of the response given the stimulus on each trial. The results of the computational modeling suggest that schizophrenia patients exhibit weakened representation of response values, possibly due to failure of the basal ganglia to strongly associate stimuli with appropriate response alternatives.

Full Text

Cited Authors

  • Morris, SE; Holroyd, CB; Mann-Wrobel, MC; Gold, JM

Published Date

  • January 2011

Published In

Volume / Issue

  • 5 /

Start / End Page

  • 123 -

PubMed ID

  • 22065618

Pubmed Central ID

  • 22065618

Electronic International Standard Serial Number (EISSN)

  • 1662-5161

International Standard Serial Number (ISSN)

  • 1662-5161

Digital Object Identifier (DOI)

  • 10.3389/fnhum.2011.00123

Language

  • eng