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Intrinsic reward sensitivity drives internet gaming disorder through striatal-thalamic hyper-synchronization.

Created on 24 Jun 2026

Authors

Meng-Hui Li, An-Hang Jiang, Xue-Feng Xu, Shuang Li, Xin Luo, Guang-Heng Dong

Published in

Journal of psychiatric research. Volume 201. Pages 215-224. Jun 22, 2026. Epub Jun 22, 2026.

Abstract

Internet gaming disorder (IGD) is a behavioral addiction characterized by compulsive gaming and impaired control over gaming behavior. Although the reward system is central to addiction, the specific neural mechanisms through which IGD affects intrinsic and extrinsic rewards processing remain poorly understood.
We recruited 21 individuals with IGD and 23 recreational gaming users (RGU). Participants underwent functional magnetic resonance imaging (fMRI) while performing a cue-craving task with four types of stimuli: intrinsic reward, extrinsic reward, neutral, and gaming cues. Behavioral data (reaction time, subjective craving) were analyzed using repeated-measures ANOVA (stimulus type × group), and neural responses were analyzed using a general linear model and seed-based functional connectivity analysis.
Compared to RGU, individuals with IGD exhibit faster responses to gaming cues, stronger cravings, and altered evaluations of intrinsic rewards. Neuroimaging analysis revealed excessive synchronization in the striatum-thalamus functional connectivity during processing of intrinsic rewards in the IGD group, particularly enhanced connectivity from the left thalamus to the right caudate nucleus. Furthermore, distinct patterns of brain connectivity emerged across stimulus conditions: under gaming cues, the IGD group exhibited significantly stronger connections between the default mode network and core nodes of the reward network (e.g., nucleus accumbens-prefrontal cortex) than the RGU group.
Our findings indicate that IGD is associated with aberrant neural reward processing, including striatal-thalamic hyper-synchronization, which may underlie the hijacking of intrinsic reward mechanisms. These results support a 'self-efficacy-sensory drive' model of IGD, providing a neurobiological basis for targeted interventions.

PMID:
42335494
Bibliographic data and abstract were imported from PubMed on 24 Jun 2026.

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