Deficient Monetary Reward Processing in Schizophrenia: A Meta-Analysis and Computational Modeling of a Monetary Incentive Delay Task.

Authors

Jian Jiao, Xun Yang, Jianguang Zeng, Lantao You, Xueli Sun, Zaiquan Dong

Published in

Schizophrenia bulletin. Volume 52. Issue 6. Oct 27, 2026.

Abstract

Evidence regarding monetary incentive-processing deficits in schizophrenia (SZ) remains inconsistent. Clarifying how Monetary Incentive Delay (MID) task performance relates to model-derived learning indices may help characterize motivational and incentive-processing abnormalities in SZ. We hypothesized that patients with SZ would show altered behavioral performance and model-derived expected-value and prediction-error (PE) indices associated with clinical symptom severity.
We integrated a meta-analysis of MID studies (30 studies; SZ/healthy controls (HCs), n = 785/755) with an independent subject-level MID task (SZ/HCs, n = 60/74). A Rescorla-Wagner model with a fixed learning rate was used to derive group-comparable mean absolute PE values and expected-value (Q) indices.
The meta-analysis showed small-to-moderate behavioral differences in SZ including prolonged reaction times (RT) and reduced reward-trial correct rate (CR). In an independent subject-level computational study, patients with SZ showed prolonged RT, lower reward- and loss-trial CR, and higher neutral-trial CR than HCs, consistent with reduced cue-specific modulation. Model-derived analyses showed higher absolute reward PE and absolute loss PE (ABSLPE), lower Reward-Q, and more negative Loss-Q in SZ under the current Rescorla-Wagner framework. Loss-related indices, particularly ABSLPE and Loss-Q, were associated with Positive and Negative Syndrome Scale-Negative scores. Trial-level logistic regression analyses further indicated weaker cue-related modulation of hit probability in SZ.
These findings suggest that SZ is associated with altered MID task performance and model-derived PE- and Q-related indices. These indices may help characterize incentive-processing abnormalities in SZ, but their clinical and neurobiological significance requires validation in future longitudinal and multimodal studies.

PMID:
42974906
Bibliographic data and abstract were imported from PubMed on 03 Nov 2026.

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