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Blunted neurophysiological responses to loss feedback characterize the emotionally vulnerable type of clinical samples with gambling disorder.

Created on 24 Sep 2026

Authors

Gangliang Zhong, Jingyang Liu, Xin Gao, Qiyun Xue, Chao Xue, Xiyuan Zhang, Yujie Bai, Jing Yue, Lihui Wang, Jiang Du, Min Zhao

Published in

Psychological medicine. Volume 56. Pages e294. Sep 24, 2026. Epub Sep 24, 2026.

Abstract

Gambling disorder (GD) is clinically heterogeneous, with trait impulsivity and negative affect (anxiety/depression) representing key sources of variation. This study investigated whether neurophysiological responses to loss feedback differ across GD subgroups defined by these features and whether subgroup membership moderates the association between neural responses and clinical severity.
Electroencephalography was recorded from 120 individuals with GD, typed via k-means clustering of impulsivity, anxiety, and depression scores, and 52 healthy controls (HC) during the Balloon Analogue Risk Task. Event-related potentials, including feedback-related negativity (FRN) and P3, were used to index feedback processing.
Two GD subgroups were identified: an 'impulsive type' (high impulsivity, low negative affect) and an 'emotionally vulnerable type' (high impulsivity with severe anxiety/depression), with the latter exhibiting greater gambling severity. Neurophysiologically, the emotionally vulnerable type showed blunted FRN and feedback-P3 amplitudes to loss feedback compared to HC, whereas the impulsive type did not differ from HC. Critically, subgroup membership moderated the association between feedback-P3 and gambling severity; a reduced feedback-P3 predicted higher severity only within the emotionally vulnerable type.
These findings identify blunted neural responses to loss feedback as a specific characteristic of the emotionally vulnerable GD type. These findings resolve the inconsistent patterns of loss feedback processing in GD and highlight the potential for personalized interventions targeting this subgroup.

PMID:
42779459
Bibliographic data and abstract were imported from PubMed on 24 Sep 2026.

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