Unpacking Social Impairment in those with Opioid Use Disorder: Linking Impulsivity, Childhood Trauma, and the Prefrontal Cortex

Abstract

Background: Challenges with social functioning, which is a hallmark of opioid use disorder (OUD), are a drawback in treatment adherence and maintenance. Yet, little research has explored the underlying mechanisms of this impairment. Impulsivity, a known risk factor for OUD, and corresponding neural alterations may be at the center of this issue. Childhood adversity, which has been linked to both impulsivity and poorer treatment outcomes, could also affect this relationship. This study aims to understand the relationship between impulsivity and social functioning in those recovering from OUD. Differences in the prefrontal cortex will be analyzed, as well as potential moderating effects of childhood trauma. Methods: Participants with (N=16) and without (N=19) social impairment completed a survey (e.g., social functioning, Barrat’s Impulsivity Scale, Adverse Childhood Experiences (ACEs) and cognitive tasks while undergoing neuroimaging. Functional near infrared spectroscopy (fNIRS), a modern, portable, and low-cost neuroimaging technology, was used to measure prefrontal cortex activity during a behavioral inhibition task (Go/No-Go task). Results: The socially impaired group (n=16) was significantly more impulsive (t(33)= -3.4, p< 0.01) and displayed more depressive symptoms (t(33) = -2.8, p <0.01) than those without social impairment (n=19). Social functioning was negatively correlated with impulsivity (r=-0.7, p<0.001), such that increased impulsivity corresponded to decreased social functioning. Childhood trauma emerged as a moderator of this relationship, but only when controlling for the effects of depression, B=-0.11, p=0.023. Although both groups had comparable Go/No-Go task performance, the socially impaired group displayed greater activation in the dorsolateral (F(1,100.8)=7.89, p<0.01), ventrolateral (F(1,88.8)= 7.33, p<0.01), and ventromedial (F(1,95.6)= 7.56, p<0.01) prefrontal cortex during impulse control. Conclusion: Beyond being more impulsive, individuals with social impairment exhibited differential activation in the prefrontal cortex when controlling responses. Furthermore, the impact of impulsivity on social functioning varies depending on ACEs demonstrating that it must considered in treatment approaches. These findings have implications for addressing social needs and impulsivity of those in recovery, highlighting the importance of a more personalized, integrative, and trauma-informed approach to intervention.