Abstract: Victimization Exposure Is Associated with Altered Adolescent Brain Function during Stress (Society for Social Work and Research 23rd Annual Conference - Ending Gender Based, Family and Community Violence)

Schedule:

Thursday, January 17, 2019: 3:15 PM

Union Square 25 Tower 3, 4th Floor (Hilton San Francisco)

* noted as presenting author

Candace Killian-Farrell, PhD, LCSW, T-32 Postdoctoral Fellow, University of North Carolina at Chapel Hill, Chapel Hill, NC

Jessica Graham, BS, Research Assistant, University of North Carolina at Chapel Hill, NC

Brianna Lombardi, PhD, MSW, Assistant Professor, University of North Carolina at Chapel Hill, Chapel Hill, NC

Ashley Williams, BS, Research Assistant, University of North Carolina at Chapel Hill, Chapel Hill, NC

Josh Bizzell, MS, Research Instructor, University of North Carolina at Chapel Hill, Chapel Hill, NC

Hannah Waltz, MA, Cinical Coordinator, University of North Carolina at Chapel Hill, Chapel Hill, NC

Alana Campbell, PhD, Research Assistant Professor, University of North Carolina at Chapel Hill, NC

Aysenil Belger, PhD, Professor and Director of Neuroimaging Research, University of North Carolina at Chapel Hill, Chapel Hill, NC

Background and Purpose: Childhood victimization is an established risk factor for mental health problems in adolescence. Recent research has focused on examining stress physiology and brain function to better understand this relationship. Our study examines the impact of victimization exposure on neural circuitry during acute stress in adolescence. We hypothesize participants with more victimization exposure will demonstrate dysregulated stress response and decreased suppression of limbic and reward circuitry during stress.

Methods: Our sample (N=40) included children with clinical symptomology and typically developing children aged 9-16 years old. Participants completed a clinical interview and performed the Montreal Imaging Stress Test (MIST) in an MRI scanner. Victimization exposure was measured using the Juvenile Victimization Questionnaire (JVQ). Physiological stress response was measured with a Biopac pulsometer to calculate respiratory sinus arrhythmia (RSA) as an index of parasympathetic stress response. Brain activations were analyzed using FSL 5.0.10, and correlations between stress-dependent activation and victimization were examined independently and between groups (FWE corrected at z>2.3; p<.01 cluster thresholded).

Results: All participants showed significantly greater activation in the frontal pole, orbital frontal cortex, the insula, interior frontal gyrus (IFG), thalamus, anterior cingulate gyrus (ACG), as well as sensory regions during stress as opposed to the control condition. Participants demonstrated greater activation in reward and limbic circuitry including the hippocampus (HIP), nucleus accumbens (NA), and the frontal medial cortex during the control condition as opposed to during stress. Covariate analyses revealed victimization exposure was associated with significant activation in the left insula, frontal operculum, frontal areas, caudate and putamen.

Conclusion and Implications: Our results were consistent with the literature which indicates frontal areas are significantly activated while limbic and reward regions are suppressed during acute stress. Our finding that level of victimization exposure covaries with functional brain activity in frontal and reward regions supports the literature that toxic stress impacts brain function during development. Further, our results suggest that highly victimized youth may have to work harder to control emotional circuits during stress and may demonstrate greater reward sensitivity. Thus, social work assessment and intervention with victimized children might benefit from a strong initial focus on emotion regulation and prevention of risky behaviors.