Abstract: Aberrant Development of Stress Response and Neural Circuitry in Adolescents with Clinical Symptomology (Society for Social Work and Research 23rd Annual Conference - Ending Gender Based, Family and Community Violence)

Schedule:

Friday, January 18, 2019: 3:45 PM

Golden Gate 1, Lobby Level (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

Josh Bizzell, MS, Research Instructor, 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

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: Many social problems experienced in childhood including victimization, poverty, and discrimination cause stress which may lead to mental health problems in adulthood. This study explores the link between stress and psychopathology risk during adolescent development. We hypothesize that adolescents with clinical symptomology (CS) will display aberrant development in their stress response and brain function. We predict brain function will covary by level of trait anxiety (TA) and be associated with aberrant stress physiology regardless of CS.

Methods: Our sample (N=53) included 23 children with clinical CS and 30 typically developing (TD) children aged 9-16 years old. Participants completed a clinical interview and performed the Montreal Imaging Stress Test in an MRI scanner. Heart rate was measured using a Biopac pulsometer and respiratory sinus arrhythmia (RSA) was calculated as an index of para-sympathetic stress response. TA was measured using the State-Trait Anxiety Inventory for Children (STAI-C). Activations were analyzed using FSL 5.0.10., and correlations between stress-dependent activation, age, and trait anxiety were examined (FWE corrected at z>2.3; p<.01 cluster thresholded).

Results: TD adolescents displayed age dependent neural activation in the frontal pole, medial frontal gyrus (MFG) and the inferior frontal gyrus (IFG), but the CS group showed no age-dependent changes. Both groups demonstrated a stress response to the stress task, however the CS group showed decreased suppression of RSA during stress. Trait anxiety significantly correlated with activation in the IFG, anterior cingulate gyrus, and ventromedial prefrontal regions, as well as RSA at baseline, initial stress, and recovery period, regardless of group. Average RSA was significantly correlated with TA at all timepoints in the typically developing group, while change in RSA from baseline was significantly negatively correlated with stress for the group with psychopathology.

Conclusion and Implications: Our results suggest that age-dependent maturation of some frontal regions and the IFG may be disrupted in adolescents with CS. Further, functional brain differences may be associated with disrupted stress response (decreased parasympathetic suppression) in the CS group, particularly in the MFG. Further, trait anxiety may be a risk factor for disrupted stress response and a variety of psychopathology. Future research can further elucidate this risk process to provide better targets for social work assessment, intervention, and secondary prevention with adolescents with CS.