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Individual differences in pain sensitivity are associated with cognitive network functional connectivity following one night of experimental sleep disruption

Previous work suggests that sleep disruption can contribute to poor pain modulation. Here, we used experimental sleep disruption to examine the relationship between sleep disruption‐induced pain sensitivity and functional connectivity (FC) of cognitive networks contributing to pain modulation. Ninet...

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Autores principales: Letzen, Janelle E., Remeniuk, Bethany, Smith, Michael T., Irwin, Michael R., Finan, Patrick H., Seminowicz, David A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons, Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6981017/
https://www.ncbi.nlm.nih.gov/pubmed/31617662
http://dx.doi.org/10.1002/hbm.24824
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author Letzen, Janelle E.
Remeniuk, Bethany
Smith, Michael T.
Irwin, Michael R.
Finan, Patrick H.
Seminowicz, David A.
author_facet Letzen, Janelle E.
Remeniuk, Bethany
Smith, Michael T.
Irwin, Michael R.
Finan, Patrick H.
Seminowicz, David A.
author_sort Letzen, Janelle E.
collection PubMed
description Previous work suggests that sleep disruption can contribute to poor pain modulation. Here, we used experimental sleep disruption to examine the relationship between sleep disruption‐induced pain sensitivity and functional connectivity (FC) of cognitive networks contributing to pain modulation. Nineteen healthy individuals underwent two counterbalanced experimental sleep conditions for one night each: uninterrupted sleep versus sleep disruption. Following each condition, participants completed functional MRI including a simple motor task and a noxious thermal stimulation task. Pain ratings and stimulus temperatures from the latter task were combined to calculate a pain sensitivity change score following sleep disruption. This change score was used as a predictor of simple motor task FC changes using bilateral executive control networks (RECN, LECN) and the default mode network (DMN) masks as seed regions of interest (ROIs). Increased pain sensitivity after sleep disruption was positively associated with increased RECN FC to ROIs within the DMN and LECN (F ((4,14)) = 25.28, pFDR = 0.05). However, this pain sensitivity change score did not predict FC changes using LECN and DMN masks as seeds (pFDR > 0.05). Given that only RECN FC was associated with sleep loss‐induced hyperalgesia, findings suggest that cognitive networks only partially contribute to the sleep‐pain dyad.
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spelling pubmed-69810172020-02-15 Individual differences in pain sensitivity are associated with cognitive network functional connectivity following one night of experimental sleep disruption Letzen, Janelle E. Remeniuk, Bethany Smith, Michael T. Irwin, Michael R. Finan, Patrick H. Seminowicz, David A. Hum Brain Mapp Research Articles Previous work suggests that sleep disruption can contribute to poor pain modulation. Here, we used experimental sleep disruption to examine the relationship between sleep disruption‐induced pain sensitivity and functional connectivity (FC) of cognitive networks contributing to pain modulation. Nineteen healthy individuals underwent two counterbalanced experimental sleep conditions for one night each: uninterrupted sleep versus sleep disruption. Following each condition, participants completed functional MRI including a simple motor task and a noxious thermal stimulation task. Pain ratings and stimulus temperatures from the latter task were combined to calculate a pain sensitivity change score following sleep disruption. This change score was used as a predictor of simple motor task FC changes using bilateral executive control networks (RECN, LECN) and the default mode network (DMN) masks as seed regions of interest (ROIs). Increased pain sensitivity after sleep disruption was positively associated with increased RECN FC to ROIs within the DMN and LECN (F ((4,14)) = 25.28, pFDR = 0.05). However, this pain sensitivity change score did not predict FC changes using LECN and DMN masks as seeds (pFDR > 0.05). Given that only RECN FC was associated with sleep loss‐induced hyperalgesia, findings suggest that cognitive networks only partially contribute to the sleep‐pain dyad. John Wiley & Sons, Inc. 2019-10-16 /pmc/articles/PMC6981017/ /pubmed/31617662 http://dx.doi.org/10.1002/hbm.24824 Text en © 2019 The Authors. Human Brain Mapping published by Wiley Periodicals, Inc. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Research Articles
Letzen, Janelle E.
Remeniuk, Bethany
Smith, Michael T.
Irwin, Michael R.
Finan, Patrick H.
Seminowicz, David A.
Individual differences in pain sensitivity are associated with cognitive network functional connectivity following one night of experimental sleep disruption
title Individual differences in pain sensitivity are associated with cognitive network functional connectivity following one night of experimental sleep disruption
title_full Individual differences in pain sensitivity are associated with cognitive network functional connectivity following one night of experimental sleep disruption
title_fullStr Individual differences in pain sensitivity are associated with cognitive network functional connectivity following one night of experimental sleep disruption
title_full_unstemmed Individual differences in pain sensitivity are associated with cognitive network functional connectivity following one night of experimental sleep disruption
title_short Individual differences in pain sensitivity are associated with cognitive network functional connectivity following one night of experimental sleep disruption
title_sort individual differences in pain sensitivity are associated with cognitive network functional connectivity following one night of experimental sleep disruption
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6981017/
https://www.ncbi.nlm.nih.gov/pubmed/31617662
http://dx.doi.org/10.1002/hbm.24824
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