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Intrinsic sensory disinhibition contributes to intrusive re-experiencing in combat veterans

Intrusive re-experiencing of traumatic events is a hallmark symptom of posttraumatic stress disorder, characterized by rich and vivid sensory details as reported in “flashbacks”. While prevailing models of trauma intrusions focus on dysregulated emotional processes, we hypothesize that a deficiency...

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Autores principales: Clancy, Kevin J., Albizu, Alejandro, Schmidt, Norman B., Li, Wen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6976606/
https://www.ncbi.nlm.nih.gov/pubmed/31969671
http://dx.doi.org/10.1038/s41598-020-57963-2
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author Clancy, Kevin J.
Albizu, Alejandro
Schmidt, Norman B.
Li, Wen
author_facet Clancy, Kevin J.
Albizu, Alejandro
Schmidt, Norman B.
Li, Wen
author_sort Clancy, Kevin J.
collection PubMed
description Intrusive re-experiencing of traumatic events is a hallmark symptom of posttraumatic stress disorder, characterized by rich and vivid sensory details as reported in “flashbacks”. While prevailing models of trauma intrusions focus on dysregulated emotional processes, we hypothesize that a deficiency in intrinsic sensory inhibition could drive overactivation of sensory representations of trauma memories, precipitating sensory-rich intrusions. In a sample of combat veterans, we examined resting-state alpha (8–12 Hz) oscillatory activity (in both power and posterior→frontal connectivity), given its role in sensory cortical inhibition, in association with intrusive re-experiencing symptoms. Veterans further participated in an odor task (including both combat and non-combat odors) to assess olfactory trauma memory and emotional response. We observed an association between intrusive re-experiencing symptoms and attenuated resting-state posterior→frontal alpha connectivity, which were both correlated with olfactory trauma memory. Importantly, olfactory trauma memory was identified as a mediator of the relationship between alpha connectivity and intrusive re-experiencing, suggesting that deficits in intrinsic sensory inhibition contributed to intrusive re-experiencing of trauma via heightened trauma memory. Therefore, by permitting unfiltered sensory cues to enter information processing and activate sensory representations of trauma, sensory disinhibition can constitute a sensory mechanism of intrusive re-experiencing in trauma-exposed individuals.
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spelling pubmed-69766062020-01-29 Intrinsic sensory disinhibition contributes to intrusive re-experiencing in combat veterans Clancy, Kevin J. Albizu, Alejandro Schmidt, Norman B. Li, Wen Sci Rep Article Intrusive re-experiencing of traumatic events is a hallmark symptom of posttraumatic stress disorder, characterized by rich and vivid sensory details as reported in “flashbacks”. While prevailing models of trauma intrusions focus on dysregulated emotional processes, we hypothesize that a deficiency in intrinsic sensory inhibition could drive overactivation of sensory representations of trauma memories, precipitating sensory-rich intrusions. In a sample of combat veterans, we examined resting-state alpha (8–12 Hz) oscillatory activity (in both power and posterior→frontal connectivity), given its role in sensory cortical inhibition, in association with intrusive re-experiencing symptoms. Veterans further participated in an odor task (including both combat and non-combat odors) to assess olfactory trauma memory and emotional response. We observed an association between intrusive re-experiencing symptoms and attenuated resting-state posterior→frontal alpha connectivity, which were both correlated with olfactory trauma memory. Importantly, olfactory trauma memory was identified as a mediator of the relationship between alpha connectivity and intrusive re-experiencing, suggesting that deficits in intrinsic sensory inhibition contributed to intrusive re-experiencing of trauma via heightened trauma memory. Therefore, by permitting unfiltered sensory cues to enter information processing and activate sensory representations of trauma, sensory disinhibition can constitute a sensory mechanism of intrusive re-experiencing in trauma-exposed individuals. Nature Publishing Group UK 2020-01-22 /pmc/articles/PMC6976606/ /pubmed/31969671 http://dx.doi.org/10.1038/s41598-020-57963-2 Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Clancy, Kevin J.
Albizu, Alejandro
Schmidt, Norman B.
Li, Wen
Intrinsic sensory disinhibition contributes to intrusive re-experiencing in combat veterans
title Intrinsic sensory disinhibition contributes to intrusive re-experiencing in combat veterans
title_full Intrinsic sensory disinhibition contributes to intrusive re-experiencing in combat veterans
title_fullStr Intrinsic sensory disinhibition contributes to intrusive re-experiencing in combat veterans
title_full_unstemmed Intrinsic sensory disinhibition contributes to intrusive re-experiencing in combat veterans
title_short Intrinsic sensory disinhibition contributes to intrusive re-experiencing in combat veterans
title_sort intrinsic sensory disinhibition contributes to intrusive re-experiencing in combat veterans
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6976606/
https://www.ncbi.nlm.nih.gov/pubmed/31969671
http://dx.doi.org/10.1038/s41598-020-57963-2
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