Psychologists have identified multiple different forms of conflict, such as information processing conflict and goal conflict. As such, there is a need to examine the similarities and differences in neurology between each form of conflict. To address this, we conducted a comprehensive electroencephalogram (EEG) analysis of Shadli, Glue, McIntosh, and McNaughton’s calibrated stop-signal task (SST) goal-conflict task. Specifically, we examined changes in scalp-wide current source density (CSD) power and coherence across a wide range of frequency bands during the calibrated SST (n = 34). We assessed differences in EEG between the high and low goal-conflict conditions using hierarchical analyses of variance (ANOVAs). We also related goal-conflict EEG to trait anxiety, neuroticism, Behavioural Inhibition System (BIS)-anxiety and revised BIS (rBIS) using regression analyses. We found that changes in CSD power during goal conflict were limited to increased midfrontocentral theta. Conversely, coherence increased across 23 scalp-wide theta region pairs and one frontal delta region pair. Finally, scalp-wide theta significantly predicted trait neuroticism but not trait anxiety, BIS-anxiety or rBIS. We conclude that goal conflict involves increased midfrontocentral CSD theta power and scalp-wide theta-dominated coherence. Therefore, compared with information processing conflict, goal conflict displays a similar EEG power profile of midfrontocentral theta but a much wider coherence profile. Furthermore, the increases in theta during goal conflict are the characteristic of BIS-driven activity. Therefore, future research should confirm whether these goal-conflict effects are driven by the BIS by examining whether the effects are attenuated by anxiolytic drugs. Overall, we have identified a unique network of goal-conflict EEG during the calibrated SST.

Background: The pervasive tendency to avoid perceived risks has been recently implicated in the maintenance of anxiety pathology, and more specifically, social phobia. Social anxiety symptoms are thus hypothesised to be associated with a global risk-avoidant decision-making bias. Aim: This study investigated: (1) the relationship between risk-avoidance and social anxiety symptoms using both self-report and behavioural measures of risk-taking; and (2) whether risk-avoidance mediates the relationship between a dispositional vulnerability to anxiety (Behavioural Inhibition System [BIS] sensitivity) and social anxiety symptoms. Method: Fifty-five undergraduate students completed self-report measures assessing for social anxiety symptoms, risk-taking across various domains, and BIS sensitivity. Risk-avoidance was also assessed using a behavioural computer task. Results: As hypothesised, risk-avoidance correlated significantly with both social anxiety and BIS. Multiple regression analyses revealed that risk-avoidance served as a partial mediator between BIS and social anxiety. Conclusion: These results confirm the hypothesised relationship between BIS, risk-avoidance, and social anxiety symptoms. Risk-avoidance is one possible mechanism by which personality characteristics may be linked to anxiety pathology.