Post-traumatic stress disorder (PTSD) disproportionately affects immigrant and refugee populations due to cumulative trauma exposure across pre-migration, peri-migration, and post-migration phases. This narrative review synthesizes neurobiological and psychosocial research to elucidate mechanisms underlying PTSD in immigrant groups. Neurobiological analyses reveal hippocampal atrophy, amygdala hyperactivity, and medial prefrontal cortex (mPFC) hypoactivity mirrored in rodent models of chronic stress. These changes correlate with memory fragmentation, hypervigilance, and impaired fear extinction, exacerbated by acculturation pressures, discrimination, and socioeconomic hardship. Immigrants and refugees exhibit PTSD rates exceeding 30% in some cohorts, compared to approximately 3–4% in non-immigrant populations. While neurobiological studies often focus on non-immigrant populations and psychosocial research overlooks biological mechanisms, this review demonstrates how structural inequities such as limited healthcare access interact with dysregulated hypothalamic-pituitary-adrenal (HPA) axis function to amplify vulnerability. The findings underscore the need for integrated interventions addressing both neurobiological and structural determinants to reduce PTSD burden in displaced populations.
Izadi et al. (Wed,) studied this question.