The hippocampus and the amygdala play a central role in post-traumatic stress disorder (PTSD) pathogenesis. While alternations in volumes of both regions have been consistently observed in individuals with PTSD, it remains unknown whether these re ect pre-trauma vulnerability traits or acquired post-trauma consequences of the disorder. Here, we conducted a longitudinal panel study of adult civilian trauma survivors admitted to a general hospital emergency department (ED). One hundred eligible participants (mean age=32.97±10.97, n=56 [56%] females) completed both clinical interviews and structural MRI scans at 1-, 6-, and 14-months after ED admission (alias T1, T2, and T3). While all participants met PTSD diagnosis at T1, only n=29 still met PTSD diagnosis at T3 (a 'non-Remission' Group), while n=71 did not (a 'Remission' Group). Bayesian multilevel modeling analysis showed robust evidence for smaller right hippocampus volume (P+ of ~0.014) and moderate evidence for larger left amygdala volume (P+ of ~0.870) at T1 in the 'non-Remission' group, compared to the 'Remission' group.Subregion analysis further demonstrated robust evidence for decreased volume in the left and right subiculum and right CA1 hippocampal subregions (P+ of ~0.021-0.046) in the 'non-Remission' group. No time-dependent volumetric changes (T1 to T2 to T3) were observed across all participants or between groups. Results support the 'vulnerability trait' hypothesis, suggesting that lower initial volumes of speci c hippocampus subregions are associated with non-remitting PTSD. The stable volume of all hippocampal and amygdala subregions does not support the idea of consequential, progressive, stressrelated atrophy during the rst critical year following trauma exposure.