Early Exposure to Traumatic Stressors Impairs Emotional Brain Circuitry
AuthorKorgaonkar, MS; Antees, C; Williams, LM; Gatt, JM; Bryant, RA; Cohen, R; Paul, R; O'Hara, R; Grieve, SM
Source TitlePLoS One
PublisherPUBLIC LIBRARY SCIENCE
University of Melbourne Author/sBryant, Richard
Document TypeJournal Article
CitationsKorgaonkar, M. S., Antees, C., Williams, L. M., Gatt, J. M., Bryant, R. A., Cohen, R., Paul, R., O'Hara, R. & Grieve, S. M. (2013). Early Exposure to Traumatic Stressors Impairs Emotional Brain Circuitry. PLOS ONE, 8 (9), https://doi.org/10.1371/journal.pone.0075524.
Access StatusOpen Access
Exposure to early life trauma (ELT) is known to have a profound impact on mental development, leading to a higher risk for depression and anxiety. Our aim was to use multiple structural imaging methods to systematically investigate how traumatic stressors early in life impact the emotional brain circuits, typically found impaired with clinical diagnosis of depression and anxiety, across the lifespan in an otherwise healthy cohort. MRI data and self-reported histories of ELT from 352 healthy individuals screened for no psychiatric disorders were analyzed in this study. The volume and cortical thickness of the limbic and cingulate regions were assessed for all participants. A large subset of the cohort also had diffusion tensor imaging data, which was used to quantify white matter structural integrity of these regions. We found a significantly smaller amygdala volume and cortical thickness in the rostral anterior cingulate cortex associated with higher ELT exposure only for the adolescence group. White matter integrity of these regions was not affected. These findings demonstrate that exposure to early life trauma is associated with alterations in the gray matter of cingulate-limbic regions during adolescence in an otherwise healthy sample. These findings are interesting in the context that the affected regions are central neuroanatomical components in the psychopathology of depression, and adolescence is a peak period for risk and onset of the disorder.
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