Context Smaller hippocampal volumes are well established in posttraumatic stress disorder (PTSD), but the relatively few studies of amygdala volume in PTSD have produced equivocal results. Objective To assess a large cohort of recent military veterans, with PTSD and trauma-exposed controls, with sufficient power to definitively assess the effect of PTSD on volumetric changes in the amygdala and hippocampus, as well as the contribution of illness duration, trauma load, and depressive symptoms. Design Case-controlled design with structural MRI and clinical diagnostic assessments. Important potential confounds of alcohol use, depression, and medication use were statistically controlled. Setting Durham VA Medical Center located in central North Carolina (USA) in proximity to major military bases. Patients Ambulatory patients (n=200), recruited from a registry of military service members and veterans serving after 11-September 2001, consisting of a group with current PTSD (n=99) and trauma-exposed comparison group without PTSD (n=101). Main Outcome measure Amygdala and hippocampus volumes computed from automated segmentation of high-resolution structural MRI acquired at 3 Tesla. Results Smaller volume was demonstrated in the PTSD compared to non-PTSD groups for the left amygdala (p = .002), right amygdala (p = .01), and left hippocampus (p = .02), but not for the right hippocampus (p = .25). Amygdala volumes were not associated with PTSD chronicity, trauma load, or severity of depressive symptoms. Conclusions These results provide clear evidence of an association between smaller amygdala volume and PTSD. The lack of correlation between trauma load or illness chronicity and amygdala volume suggests that either a smaller amygdala represents a vulnerability to developing PTSD, or the lack of a dose-response relationship with amygdala volume. Our results may trigger a renewed impetus for investigating structural differences in the amygdala, its genetic determinants, its environmental modulators, and the possibility that it reflects an intrinsic vulnerability to PTSD.
The amygdala is a major structure that orchestrates defensive reactions to environmental threats and is implicated in hypervigilance and symptoms of heightened arousal in posttraumatic stress disorder (PTSD). The basolateral and centromedial amygdala (CMA) complexes are functionally heterogeneous, with distinct roles in learning and expressing fear behaviors. PTSD differences in amygdala-complex function and functional connectivity with cortical and subcortical structures remain unclear. Recent military veterans with PTSD (n ¼ 20) and matched trauma-exposed controls (n ¼ 22) underwent a resting-state fMRI scan to measure task-free synchronous blood-oxygen level dependent activity. Whole-brain voxel-wise functional connectivity of basolateral and CMA seeds was compared between groups. The PTSD group had stronger functional connectivity of the basolateral amygdala (BLA) complex with the pregenual anterior cingulate cortex (ACC), dorsomedial prefrontal cortex, and dorsal ACC than the trauma-exposed control group (po0.05; corrected). The trauma-exposed control group had stronger functional connectivity of the BLA complex with the left inferior frontal gyrus than the PTSD group (po0.05; corrected). The CMA complex lacked connectivity differences between groups. We found PTSD modulates BLA complex connectivity with prefrontal cortical targets implicated in cognitive control of emotional information, which are central to explanations of core PTSD symptoms. PTSD differences in resting-state connectivity of BLA complex could be biasing processes in target regions that support behaviors central to prevailing laboratory models of PTSD such as associative fear learning. Further research is needed to investigate how differences in functional connectivity of amygdala complexes affect target regions that govern behavior, cognition, and affect in PTSD.
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