Inflammation, reward circuitry and symptoms of anhedonia and PTSD in trauma-exposed women.

Abstract

Trauma exposure is associated with increased inflammatory biomarkers (e.g. C-reactive protein [CRP] and cytokines), and inflammation has been shown to impact corticostriatal reward circuitry and increase anhedonia-related symptoms. We examined resting-state functional MRI in a high-trauma inner-city population of African-American women (n= 56), who reported on average five different types of trauma exposures, to investigate whether inflammation correlated with functional connectivity (FC) in corticostriatal reward circuitry in association with symptoms of anhedonia and PTSD. Plasma CRP negatively correlated with bilateral ventral striatum (VS) to ventromedial prefrontal cortex (vmPFC) FC (P< 0.01). In participants where plasma was available to also measure cytokines and their soluble receptors, left (L)VS-vmPFC FC negatively correlated with an inflammatory composite score (previously shown to be increased in plasma and cerebrospinal fluid of depressed patients with high CRP) only in women with significant PTSD symptoms (n= 14; r = -0.582, P= 0.029) and those who experienced moderate-severe childhood trauma (r = -0.595, P= 0.009). Exploratory analyses indicated that LVS-vmPFC FC correlated with anhedonia-related subscales from the Beck Depression Inventory (r = -0.691, P= 0.004) and PTSD Symptom Scale (avoidance/numbness; r = -0.514, P = 0.042) in participants with an inflammatory score over the median (n= 16). Results suggest that inflammation contributes to compromised reward circuitry and symptoms of anhedonia and PTSD in trauma-exposed women.