Variations in response to trauma and hippocampal subfield changes.
Avoidance
High-resolution MRI
Hippocampus
Intrusive memories
Memory control
Posttraumatic stress disorder (PTSD)
Resilience
Journal
Neurobiology of stress
ISSN: 2352-2895
Titre abrégé: Neurobiol Stress
Pays: United States
ID NLM: 101643409
Informations de publication
Date de publication:
Nov 2021
Nov 2021
Historique:
received:
08
09
2020
revised:
30
04
2021
accepted:
19
05
2021
entrez:
11
6
2021
pubmed:
12
6
2021
medline:
12
6
2021
Statut:
epublish
Résumé
Models of posttraumatic stress disorder (PTSD) suggest that the hippocampus is key to the persistence of traumatic memory. Yet very little is known about the precise changes that take place in this structure, nor their relation with PTSD symptoms. Previous studies have mostly used magnetic resonance imaging (MRI) at low resolutions, making it impossible to identify sensitive anatomical landmarks, or compared groups often unequally matched in terms of traumatic exposure. The present cross-sectional study included 92 individuals who had all been exposed to the terrorist attacks in Paris on November 13, 2015 (53 of whom subsequently developed PTSD) and 56 individuals who had not been exposed. Hippocampal subfield volumes were estimated using cross-validated automatic segmentation of high-resolution MRI images. Results revealed changes in CA1 and CA2-3/dentate gyrus (DG) volumes in individuals with PTSD, but not in resilient (i.e., exposed but without PTSD) individuals, after controlling for potential nuisance variables such as previous traumatic exposure and substance abuse. In line with current models of hippocampal subfield functions, CA1 changes were linked to the uncontrollable re-experiencing of intrusive memories, while CA2-3/DG changes, potentially exacerbated by comorbid depression, fostered the overgeneralization of fear linked to avoidance and hypervigilance behaviors. Additional analyses revealed that CA1 integrity was linked to optimum functioning of the memory control network in resilient individuals. These findings shed new light on potential pathophysiological mechanisms in the hippocampus subtending the development of PTSD and the failure to recover from trauma.
Identifiants
pubmed: 34113695
doi: 10.1016/j.ynstr.2021.100346
pii: S2352-2895(21)00054-0
pmc: PMC8170416
doi:
Types de publication
Journal Article
Langues
eng
Pagination
100346Informations de copyright
© 2021 The Authors.
Déclaration de conflit d'intérêts
The authors report no competing interests.
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