0426 Altered Neural Feedback Processing and Impulsivity in Youth with Insomnia

Abstract Introduction Insomnia and sleep disturbance are linked to impulsive behavior and heightened risk-taking, particularly in youth. Prior EEG studies in individuals with insomnia have mainly examined response inhibition (e.g., reduced N2 in Go/No-go tasks), suggesting impaired motor inhibition but providing limited insight into neural mechanisms of risk evaluation and outcome processing. This study examined risk-taking and impulsivity in youths with insomnia versus healthy controls, integrating self-reported measures and a behavioral risk-taking task recorded with EEG. Methods Youth participants with DSM-5 insomnia disorder and ISI ≥ 9 (N = 79, mean age = 21.1 years, 75.7% female) and healthy sleeper controls (N = 38, mean age = 20.0 years, 71.1% female) were recruited. They completed the ISI, Barratt Impulsiveness Scale (BIS-11) and Short UPPS-P, and performed an automatic Balloon Analogue Risk Task (BART). EEG was recorded to extract FRN (240–310 ms) and P300 (320–450 ms) amplitudes to win and loss feedback. Group differences were examined using t tests and mixed-design ANOVAs. Results The Insomnia group scored significantly higher on ISI than controls (p .001). Although there were no group differences in total BIS-11 or SUPPS-P scores, the Insomnia group showed higher Attentional Impulsivity (p = .043) and marginally higher Motor Impulsivity (p = .050). BART performance did not differ between groups. However, the Insomnia group showed significantly larger FRN amplitudes than controls for both win and loss feedback (ps = .009 and .007), indicating heightened early feedback sensitivity; P300 amplitudes did not differ between groups. Conclusion Despite comparable task-based behavioral performance, youths with insomnia exhibit elevated self-reported attentional impulsivity and enhanced early neural responses to feedback, suggesting heightened feedback sensitivity and attentional control rather than generalized behavioral disinhibition. Such changes in feedback processing may influence broader self regulatory processes, including how feedback is used to guide subsequent behavior, even when overt risk taking is not apparent. Longitudinal studies are warranted to test the causal relationship and whether improving sleep may alter feedback related neural responses. Support (if any) This work was supported by Hong Kong Research Grants Council under the General Research Fund (17619123, awarded to SX Li).