Search
Browse By Day
Browse By Time
Browse By Panel
Browse By Session Type
Browse By Topic Area
Browse Posters
Search Tips
Register for SRCD23
Personal Schedule
Welcome Letter
Program Guide
Change Preferences / Time Zone
Sign In
Despite nearly a decade of neuroimaging research, there is little consensus on the neural basis of pediatric irritability (Lee et al., 2022; Nielsen et al., 2021). One of the factors likely contributing to this lack of convergence across studies is the heterogeneity of irritability, primarily due to its transdiagnostic nature and differential symptom presentation across development (Klein et al., 2021; Wakschlag et al., 2012). To address these mixed findings, our study took a novel approach to investigating the neural basis of irritability by examining resting-state functional connectivity (rsFC) correlates of irritability-related cognitive bias. Hostile attribution bias (HAB; the interpretation of ambiguous emotional stimuli as having hostile or negative intentions), is a theorized mechanism of threat processing dysfunction in pediatric irritability and is thought to contribute to its etiology and maintenance (Brotman et al., 2017). We hypothesized that clinically irritable children would exhibit significant HAB. Given evidence supporting altered amygdala FC as a potential neural correlate of pediatric irritability, we expected to observe altered rsFC of the amygdala with regions implicated in the executive control, sensorimotor, and default mode networks (Nielsen et al., 2021).
Amygdala rsFC was examined in relation to HAB in a sample of young children (5-9 years old; N=62) with severe irritability in the form of impairing emotional outbursts (IEOs). HAB was assessed using the Assessment of Children’s Emotional Skills (ACES) which yields three measures of angry attribution bias in the context of social situations, emotional behaviors, and emotional facial expressions. ACES scores were entered into a general linear model to examine associations with rsFC of the bilateral amygdalae, after controlling for child age, biological sex, and motion parameters. As predicted, children with IEOs exhibited significant biases in attributing anger to others across all three ACES domains: social situations (t[61] = 9.371, p < .001), emotional behaviors (t[61] = 8.78, p < .001), and facial expressions (t[61] = 15.23, p < .001). Greater biases towards attributing anger in social situations were associated with reduced rsFC of the right (Figure 1A) and left (Figure 1B) amygdalae with the fusiform/lingual gyri and lateral occipital cortex. Alternatively, greater biases towards attributing anger to facial expressions positively predicted right amygdala-precuneus rsFC (Figure 1C). Findings extend previous resting-state work, implicating functional connections of the amygdala with posterior regions, and emphasizing the importance of studying neurocognitive markers of pediatric irritability such as HAB. Such markers may help to clarify the heterogeneous findings in the current literature regarding neural mechanisms underlying altered threat processing in irritable youth. Additional work, including longitudinal studies, is needed to further investigate the role of such neurocognitive markers in the etiology and long-term outcomes of pediatric irritability.