Abstract

Childhood trauma significantly increases the risk for adolescent substance use disorders (SUDs). Dysfunction in neurocircuitry associated with learning and decision making is thought to underlie both trauma- and substance use (SU)-related psychopathologies, and represents a potential pathway by which childhood trauma is associated with later SUD. We will examine neural correlates of learning and decision making across 3 youth samples in the context of trauma exposure and traumatic stress, SU, and their combination. Clinical researchers will present fMRI and EEG findings from tasks examining aspects of learning and decision making, including reinforcement learning, delay discounting, and uncertainty processing. Studies include youth from clinical and community samples. Talk 1: Among children who have been exposed to interpersonal violence, PTSD symptom severity predicted: 1) event-related potentials for unpredictable unpleasant pictures; and 2) brain response to startle probes presented during unpredictable unpleasant pictures. Talk 2: Youth at high SUD risk showed stronger engagement of regions responsible for time encoding, reward valuation, and choice classification during the delayed choice. Talk 3: More severe neglect was associated with reduced responsivity in reward neurocircuitry during reinforcement learning, and alcohol use disorder (AUD) symptom severity compounded these effects. Talk 4: Trauma and AUD symptom severity are associated with reduced reward prediction error representation during reinforcement learning. Across these talks, childhood trauma and SU were associated with overlapping dysfunction in reinforcement learning neurocircuitries, as well as processing unpredictable or high-uncertainty information. Longitudinal work is needed to understand how relationships between childhood trauma and adolescent SUD unfold across time. However, learning and decision-making neurocircuitry dysfunction may represent a brain biomarker for trauma- and SU-related problems. Further, findings suggest that genetic risk and externalizing psychopathology represent important moderators for consideration in future work. The discussant will synthesize findings in both a developmental psychopathology and cognitive neuroscience framework.

Full Text
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