Assessment of Attentional Bias in Internet Gaming Disorder Using the Addiction Stroop Task and Event-Related Potentials

Document Type : Original Article

Authors

1 Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran

2 Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

3 Department of Biostatistics and Epidemiology, School of Public Health, Kerman University of Medical Sciences, Kerman, Iran

4 Noncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran

5 The Park, Mental Health, West Moreton Hospital And Health Service, Brisbane, Australia

10.34172/ahj.1571

Abstract

Background: Internet Gaming Disorder (IGD) is defined by a loss of control over gaming habits, prioritizing gaming above daily responsibilities, and persistent engagement despite detrimental outcomes. As a rising public health challenge, IGD significantly disrupts individuals’ lives. Investigating attentional biases in IGD is vital for designing targeted interventions.
Methods: Attentional bias was measured in individuals with IGD using the Addiction Stroop Task. The participants were classified into three cohorts: IGD, Recreational Game Users, and non-gaming controls. Electroencephalography/event-related potential (EEG/ERP) data were collected and analyzed from electrodes Pz, Cz, and CPz.
Findings: Compared to the RGU and control groups, the IGD group displayed significantly greater P300 amplitudes and prolonged response latencies to both gaming-related and neutral stimuli. Furthermore, the IGD group reported elevated impulsivity, anxiety, and depression levels relative to the other groups.
Conclusion: Contrary to conventional attentional bias models in addiction—which emphasize preferential attention to addiction-related cues—individuals with IGD exhibited intensified neural reactivity to all stimuli. This suggests excessive cognitive resource mobilization, potentially indicative of hyperarousal or dysregulated neurobiological processes.

Keywords

References

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