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Neural activity during response inhibition in mild traumatic brain injury and posttraumatic stress disorder
Mild traumatic brain injury (mTBI) is often characterized by deficits in response inhibition, which can contribute to marked social and occupational dysfunction. mTBI often occurs in the context of psychologically traumatic events. This can cause posttraumatic stress disorder (PTSD), which also impe...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7905369/ https://www.ncbi.nlm.nih.gov/pubmed/33665241 http://dx.doi.org/10.1016/j.ynstr.2021.100308 |
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author | Korgaonkar, Mayuresh S. Williamson, Thomas Bryant, Richard A. |
author_facet | Korgaonkar, Mayuresh S. Williamson, Thomas Bryant, Richard A. |
author_sort | Korgaonkar, Mayuresh S. |
collection | PubMed |
description | Mild traumatic brain injury (mTBI) is often characterized by deficits in response inhibition, which can contribute to marked social and occupational dysfunction. mTBI often occurs in the context of psychologically traumatic events. This can cause posttraumatic stress disorder (PTSD), which also impedes response inhibition. The overlap or distinction in these inhibitory deficits in mTBI and PTSD is unclear. This study aimed to assess behavioral, neurophysiological, and neuroimaging indices of response inhibition in mTBI by also assessing these parameters in healthy controls (HC) and PTSD participants. Participants with mTBI (without PTSD) (n = 46), PTSD (without mTBI) (n = 41), and HC (n = 40) were assessed during a response inhibition task (the Go/NoGo task) during neuropsychological testing and separate functional magnetic imaging and event-related potentials sessions. PTSD symptom severity was assessed with the Clinician-Administered PTSD Scale. Both mTBI and PTSD participants performed more omission errors on the Go/NoGo task and were associated with greater N2 amplitude, greater left inferior parietal activation and reduced connectivity of the left inferior parietal cluster and left angular gyrus compared to HC. There were no differences between mTBI and PTSD on any of these measures. These findings highlight that both mTBI and PTSD contribute to neural dysfunction during response inhibition, and arguably these occur due to distinct mechanisms. In the context of the common comorbidity between these two conditions, strategies to address response inhibition deficits in mTBI may need to consider causative factors underpinning neurological insult of mTBI and psychological effects associated with PTSD. |
format | Online Article Text |
id | pubmed-7905369 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-79053692021-03-03 Neural activity during response inhibition in mild traumatic brain injury and posttraumatic stress disorder Korgaonkar, Mayuresh S. Williamson, Thomas Bryant, Richard A. Neurobiol Stress Original Research Article Mild traumatic brain injury (mTBI) is often characterized by deficits in response inhibition, which can contribute to marked social and occupational dysfunction. mTBI often occurs in the context of psychologically traumatic events. This can cause posttraumatic stress disorder (PTSD), which also impedes response inhibition. The overlap or distinction in these inhibitory deficits in mTBI and PTSD is unclear. This study aimed to assess behavioral, neurophysiological, and neuroimaging indices of response inhibition in mTBI by also assessing these parameters in healthy controls (HC) and PTSD participants. Participants with mTBI (without PTSD) (n = 46), PTSD (without mTBI) (n = 41), and HC (n = 40) were assessed during a response inhibition task (the Go/NoGo task) during neuropsychological testing and separate functional magnetic imaging and event-related potentials sessions. PTSD symptom severity was assessed with the Clinician-Administered PTSD Scale. Both mTBI and PTSD participants performed more omission errors on the Go/NoGo task and were associated with greater N2 amplitude, greater left inferior parietal activation and reduced connectivity of the left inferior parietal cluster and left angular gyrus compared to HC. There were no differences between mTBI and PTSD on any of these measures. These findings highlight that both mTBI and PTSD contribute to neural dysfunction during response inhibition, and arguably these occur due to distinct mechanisms. In the context of the common comorbidity between these two conditions, strategies to address response inhibition deficits in mTBI may need to consider causative factors underpinning neurological insult of mTBI and psychological effects associated with PTSD. Elsevier 2021-02-17 /pmc/articles/PMC7905369/ /pubmed/33665241 http://dx.doi.org/10.1016/j.ynstr.2021.100308 Text en © 2021 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Original Research Article Korgaonkar, Mayuresh S. Williamson, Thomas Bryant, Richard A. Neural activity during response inhibition in mild traumatic brain injury and posttraumatic stress disorder |
title | Neural activity during response inhibition in mild traumatic brain injury and posttraumatic stress disorder |
title_full | Neural activity during response inhibition in mild traumatic brain injury and posttraumatic stress disorder |
title_fullStr | Neural activity during response inhibition in mild traumatic brain injury and posttraumatic stress disorder |
title_full_unstemmed | Neural activity during response inhibition in mild traumatic brain injury and posttraumatic stress disorder |
title_short | Neural activity during response inhibition in mild traumatic brain injury and posttraumatic stress disorder |
title_sort | neural activity during response inhibition in mild traumatic brain injury and posttraumatic stress disorder |
topic | Original Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7905369/ https://www.ncbi.nlm.nih.gov/pubmed/33665241 http://dx.doi.org/10.1016/j.ynstr.2021.100308 |
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