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Structural and functional thalamocortical connectivity study in female fibromyalgia

Dysfunctional thalamocortical interactions have been suggested as putative mechanisms of ineffective pain modulation and also suggested as possible pathophysiology of fibromyalgia (FM). However, it remains unclear which specific thalamocortical networks are altered and whether it is related to abnor...

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Autores principales: Kim, Dajung J., Lim, Manyoel, Kim, June Sic, Chung, Chun Kee
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8640058/
https://www.ncbi.nlm.nih.gov/pubmed/34857797
http://dx.doi.org/10.1038/s41598-021-02616-1
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author Kim, Dajung J.
Lim, Manyoel
Kim, June Sic
Chung, Chun Kee
author_facet Kim, Dajung J.
Lim, Manyoel
Kim, June Sic
Chung, Chun Kee
author_sort Kim, Dajung J.
collection PubMed
description Dysfunctional thalamocortical interactions have been suggested as putative mechanisms of ineffective pain modulation and also suggested as possible pathophysiology of fibromyalgia (FM). However, it remains unclear which specific thalamocortical networks are altered and whether it is related to abnormal pain perception in people with FM. Here, we conducted combined vertex-wise subcortical shape, cortical thickness, structural covariance, and resting-state functional connectivity analyses to address these questions. FM group exhibited a regional shape deflation of the left posterior thalamus encompassing the ventral posterior lateral and pulvinar nuclei. The structural covariance analysis showed that the extent of regional deflation of the left posterior thalamus was negatively covaried with the left inferior parietal cortical thickness in the FM group, whereas those two regions were positively covaried in the healthy controls. In functional connectivity analysis with the left posterior thalamus as a seed, FM group had less connectivity with the periaqueductal gray compared with healthy controls, but enhanced connectivity between the posterior thalamus and bilateral inferior parietal regions, associated with a lower electrical pain threshold at the hand dorsum (pain-free point). Overall, our findings showed the structural thalamic alteration interacts with the cortical regions in a functionally maladaptive direction, leading the FM brain more responsive to external stimuli and potentially contributing to pain amplification.
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spelling pubmed-86400582021-12-06 Structural and functional thalamocortical connectivity study in female fibromyalgia Kim, Dajung J. Lim, Manyoel Kim, June Sic Chung, Chun Kee Sci Rep Article Dysfunctional thalamocortical interactions have been suggested as putative mechanisms of ineffective pain modulation and also suggested as possible pathophysiology of fibromyalgia (FM). However, it remains unclear which specific thalamocortical networks are altered and whether it is related to abnormal pain perception in people with FM. Here, we conducted combined vertex-wise subcortical shape, cortical thickness, structural covariance, and resting-state functional connectivity analyses to address these questions. FM group exhibited a regional shape deflation of the left posterior thalamus encompassing the ventral posterior lateral and pulvinar nuclei. The structural covariance analysis showed that the extent of regional deflation of the left posterior thalamus was negatively covaried with the left inferior parietal cortical thickness in the FM group, whereas those two regions were positively covaried in the healthy controls. In functional connectivity analysis with the left posterior thalamus as a seed, FM group had less connectivity with the periaqueductal gray compared with healthy controls, but enhanced connectivity between the posterior thalamus and bilateral inferior parietal regions, associated with a lower electrical pain threshold at the hand dorsum (pain-free point). Overall, our findings showed the structural thalamic alteration interacts with the cortical regions in a functionally maladaptive direction, leading the FM brain more responsive to external stimuli and potentially contributing to pain amplification. Nature Publishing Group UK 2021-12-02 /pmc/articles/PMC8640058/ /pubmed/34857797 http://dx.doi.org/10.1038/s41598-021-02616-1 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Kim, Dajung J.
Lim, Manyoel
Kim, June Sic
Chung, Chun Kee
Structural and functional thalamocortical connectivity study in female fibromyalgia
title Structural and functional thalamocortical connectivity study in female fibromyalgia
title_full Structural and functional thalamocortical connectivity study in female fibromyalgia
title_fullStr Structural and functional thalamocortical connectivity study in female fibromyalgia
title_full_unstemmed Structural and functional thalamocortical connectivity study in female fibromyalgia
title_short Structural and functional thalamocortical connectivity study in female fibromyalgia
title_sort structural and functional thalamocortical connectivity study in female fibromyalgia
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8640058/
https://www.ncbi.nlm.nih.gov/pubmed/34857797
http://dx.doi.org/10.1038/s41598-021-02616-1
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