Altered Associations Between Task Performance and Dorsolateral Prefrontal Cortex Activation During Cognitive Control in Schizophrenia.


Journal

Biological psychiatry. Cognitive neuroscience and neuroimaging
ISSN: 2451-9030
Titre abrégé: Biol Psychiatry Cogn Neurosci Neuroimaging
Pays: United States
ID NLM: 101671285

Informations de publication

Date de publication:
10 2023
Historique:
received: 20 04 2023
revised: 11 05 2023
accepted: 31 05 2023
medline: 9 10 2023
pubmed: 10 6 2023
entrez: 9 6 2023
Statut: ppublish

Résumé

Dysfunctional cognitive control processes are now well understood to be core features of schizophrenia (SZ). A body of work suggests that the dorsolateral prefrontal cortex (DLPFC) plays a critical role in explaining cognitive control disruptions in SZ. Here, we examined relationships between DLPFC activation and drift rate (DR), a model-based performance measure that combines reaction time and accuracy, in people with SZ and healthy control (HC) participants. One hundred fifty-one people with recent-onset SZ spectrum disorders and 118 HC participants performed the AX-Continuous Performance Task during functional magnetic resonance imaging scanning. Proactive cognitive control-associated activation was extracted from left and right DLPFC regions of interest. Individual behavior was fit using a drift diffusion model, allowing DR to vary between task conditions. Behaviorally, people with SZ showed significantly lower DRs than HC participants, particularly during high proactive control trial types ("B" trials). Recapitulating previous findings, the SZ group also demonstrated reduced cognitive control-associated DLPFC activation compared with HC participants. Furthermore, significant group differences were also observed in the relationship between left and right DLPFC activation with DR, such that positive relationships between DR and activation were found in HC participants but not in people with SZ. These results suggest that DLPFC activation is less associated with cognitive control-related behavioral performance enhancements in SZ. Potential mechanisms and implications are discussed.

Sections du résumé

BACKGROUND
Dysfunctional cognitive control processes are now well understood to be core features of schizophrenia (SZ). A body of work suggests that the dorsolateral prefrontal cortex (DLPFC) plays a critical role in explaining cognitive control disruptions in SZ. Here, we examined relationships between DLPFC activation and drift rate (DR), a model-based performance measure that combines reaction time and accuracy, in people with SZ and healthy control (HC) participants.
METHODS
One hundred fifty-one people with recent-onset SZ spectrum disorders and 118 HC participants performed the AX-Continuous Performance Task during functional magnetic resonance imaging scanning. Proactive cognitive control-associated activation was extracted from left and right DLPFC regions of interest. Individual behavior was fit using a drift diffusion model, allowing DR to vary between task conditions.
RESULTS
Behaviorally, people with SZ showed significantly lower DRs than HC participants, particularly during high proactive control trial types ("B" trials). Recapitulating previous findings, the SZ group also demonstrated reduced cognitive control-associated DLPFC activation compared with HC participants. Furthermore, significant group differences were also observed in the relationship between left and right DLPFC activation with DR, such that positive relationships between DR and activation were found in HC participants but not in people with SZ.
CONCLUSIONS
These results suggest that DLPFC activation is less associated with cognitive control-related behavioral performance enhancements in SZ. Potential mechanisms and implications are discussed.

Identifiants

pubmed: 37295646
pii: S2451-9022(23)00130-1
doi: 10.1016/j.bpsc.2023.05.010
pii:
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1050-1057

Subventions

Organisme : NIMH NIH HHS
ID : K01 MH125096
Pays : United States
Organisme : NIMH NIH HHS
ID : P50 MH106438
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH122139
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH059883
Pays : United States

Informations de copyright

Copyright © 2023 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

Auteurs

Jason Smucny (J)

Department of Psychiatry and Behavioral Sciences, University of California, Davis, Davis, California; Center for Neuroscience, University of California, Davis, Davis, California. Electronic address: jsmucny@ucdavis.edu.

Timothy D Hanks (TD)

Center for Neuroscience, University of California, Davis, Davis, California; Department of Neurology, University of California, Davis, Davis, California.

Tyler A Lesh (TA)

Department of Psychiatry and Behavioral Sciences, University of California, Davis, Davis, California; Center for Neuroscience, University of California, Davis, Davis, California.

Cameron S Carter (CS)

Department of Psychiatry and Behavioral Sciences, University of California, Davis, Davis, California; Center for Neuroscience, University of California, Davis, Davis, California.

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Classifications MeSH