Inflammation, amygdala-ventromedial prefrontal functional connectivity and symptoms of anxiety and PTSD in African American women recruited from an inner-city hospital: Preliminary results.
Level 4 - case-series / case-control
Cross-sectional observational neuroimaging and biomarker study
PubMed 35772683 · doi:10.1016/j.bbi.2022.06.013
What was done
Researchers evaluated the relationship between peripheral inflammatory markers, resting-state functional connectivity (FC) between the right amygdala and ventromedial prefrontal cortex (vmPFC), and symptoms of anxiety and PTSD. The cross-sectional study assessed 54 African American women recruited from an inner-city hospital with high trauma exposure. Plasma C-reactive protein (CRP) was measured in 54 participants and a 3-cytokine composite score was measured in a subset of 33 participants. FC was assessed via targeted resting-state fMRI, controlling for covariates including age, body mass index, lifetime trauma events, and symptom severity of depression and PTSD.
What was found
Higher plasma CRP correlated with lower right amygdala-vmPFC FC (r = -0.32, p = 0.017), remaining significant after adjusting for age, BMI, trauma history, and psychiatric symptoms (p < 0.05). In the cytokine subgroup (n = 33), lower FC correlated with higher composite cytokine levels (unadjusted r = -0.33, p = 0.058; adjusted r = -0.43, p = 0.026). Lower amygdala-vmPFC FC correlated with higher trait anxiety on the State-Trait Anxiety Inventory (adjusted r = -0.32, p = 0.039) and higher PTSD re-experiencing/intrusive symptoms (adjusted r = -0.32, p = 0.028). Childhood maltreatment also negatively correlated with FC (r = -0.32, p = 0.018) independently of CRP. CRP was not linearly correlated with anxiety or PTSD symptoms, but was elevated in women meeting clinical severity thresholds for both conditions (p < 0.05).
Why it matters
This study replicates in a highly trauma-exposed inner-city sample the link between peripheral inflammation and impaired frontolimbic connectivity, reinforcing a potential neural mechanism by which systemic inflammation contributes to anxiety and PTSD pathophysiology.
Limits
The study is limited by a small sample size (n = 54 overall, n = 33 for cytokines) and a cross-sectional design that cannot establish causality or temporal direction. The cohort consisted exclusively of African American women from an inner-city hospital, which may limit generalizability to other demographic groups and clinical settings.
Cited by
- supports Higher levels of systemic inflammation in the body and brain disrupt top-down functional connectivity from the prefrontal cortex to the amygdala.