(PS11-D79) Neural Correlates of Attention During Frustration Induction Correspond to Emotion Dysregulation in Autism Spectrum Disorder

Introduction: Core autism spectrum disorder (ASD) features (e.g., social communication, restrictive behaviors) often manifest along with emotion dysregulation (ED; Conner et al., 2021) wherein individuals struggle to regulate affective states. The ability to control attention in the context of emotionally demanding contexts is a key feature of emotion regulation (Cole et al., 2004). Thus, difficulties regulating behavior in emotional contexts may be associated with competition between attention monitoring systems and emotion processing. For example, increased attention toward negative or ambiguous emotional information may deplete resources available for aspects of regulation. Attentional control is often linked to the N2 event-related potential (ERP) component (e.g., increased amplitude following emotion induction, Lewis et al., 2006). However, there has been limited exploration of whether dynamic cognitive mechanisms map onto behavioral indicators of ED in youth with ASD.

Method: Forty-six adolescents (aged 12-20 years) with ASD completed the affective Posner EEG task at the first time-point of a larger longitudinal treatment study across two different sites. Participants and their parents also completed the Emotion Dysregulation Inventory (EDI; Mazefsky et al., 2018), as a behavioral index of emotion regulation. The EEG task (Eldeeb et al., 2021) is an adaptation of a classical attention paradigm in which feedback during a card game is deceptively altered to elicit an affective (i.e., frustrated) response. We compared ERP responses to condition feedback (i.e., Win, Lose, “Too Slow”), where feedback is deceptive (“Too Slow”) on 60% of correct trials. Here, we focus on the relationship of the frontal N2 amplitude (200-350 ms) to EDI reactivity scores.

Results: Multilevel models indicated a fully-graded effect between conditions, F(2, 6626)=15.55, p< .0001, in which N2 amplitudes for each condition were significantly different (p’s< .011). The most negative N2 amplitudes were to Too Slow (M= -16.84 µV), second most negative to Lose (M= -15.66 µV), and least negative to Win (M= -14.92 µV). Partial correlations investigating biological factors (i.e., pubertal status, age, natal sex) and parent reported emotional reactivity indicated larger N2 ED effects (i.e., N2 to TooSlow is more negative than Lose) for youth with elevated emotional reactivity, r(44)=.32, p=.047.     

Discussion: Previous work has been limited in addressing how attentional processing of emotional stimuli relates to downstream regulatory behaviors. Our findings indicate that increased engagement of attention monitoring systems (i.e., increased N2 amplitude) in response to frustration induction (i.e., deceptive “Too Slow”), is related to an elevated emotional reactivity profile. This supports the theory that difficulties in self-regulating may be associated with competition for cognitive resources among attention monitoring and emotion processing systems. Further investigation of neurophysiological correlates of ED paired with behavioral indices has utility in understanding mechanisms, time course of emotional processing, and identifying potential markers for regulatory difficulties that can inform detection and intervention efforts.