UC Berkeley

Emotion-related impulsivity, the trait-based tendency to respond impulsively to heightened emotions, is a transdiagnostic phenomenon associated with diverse forms of psychopathology and problematic behavior. Theory and research on the process of emotion-related impulsivity have identified deficits in cognitive control. Emotion-related impulsivity leads to problems during heightened emotions, which suggests that increased arousal may be core to problematic behavior. Arousal is also known to contribute to decays in some facets of cognitive control, especially working memory. A key need is to understand how arousal-induced decays in working memory relate to emotion-related impulsivity and whether arousal-induced decays in working memory mediate the relation between emotion-related impulsivity and internalizing symptoms.

Participants (N = 100) were recruited as part of a larger two-site study including people who experience a full range of internalizing and externalizing symptoms. Participants completed measures of internalizing symptoms, impulsivity, and potential confounds and then completed a novel N-back task including a within-task stressor to induce high arousal. Skin conductance and pupil diameter were collected at baseline and throughout the task to index arousal. Preliminary cleaning and analyses were conducted to exclude unusable data to yield a final sample (N=82).

Impulsivity was positively related to internalizing symptoms with significant large effects. Contrary to hypotheses, neither higher emotion-related impulsivity nor higher internalizing symptoms were related to poorer working memory performance, and neither interacted with arousal in relation to working memory performance. Arousal did not induce decays in working memory, and arousal-induced decay in working memory was not a putative mediator for the relationship between emotion-related impulsivity and internalizing symptoms.

Findings inform the emotional and neurocognitive processes involved in emotion-related impulsivity. Results did not support the role of arousal-induced decays in working memory in impulsivity or internalizing symptoms, however, future research is warranted to evaluate this model with other methods given the present findings contradict large and growing literatures on the role of arousal and cognition. Further pursuit of this model could identify the process underlying emotion-related impulsivity which may point to potential targets for intervention.