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Muscle sympathetic nerve activity‐coupled changes in brain activity during sustained muscle pain

INTRODUCTION: Long‐lasting experimental muscle pain elicits divergent muscle sympathetic responses, with some individuals exhibiting a persistent increase in muscle sympathetic nerve activity (MSNA), and others a decrease. These divergent responses are thought to result from sustained functional cha...

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Autores principales: Kobuch, Sophie, Fazalbhoy, Azharuddin, Brown, Rachael, Macefield, Vaughan G., Henderson, Luke A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840447/
https://www.ncbi.nlm.nih.gov/pubmed/29541532
http://dx.doi.org/10.1002/brb3.888
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author Kobuch, Sophie
Fazalbhoy, Azharuddin
Brown, Rachael
Macefield, Vaughan G.
Henderson, Luke A.
author_facet Kobuch, Sophie
Fazalbhoy, Azharuddin
Brown, Rachael
Macefield, Vaughan G.
Henderson, Luke A.
author_sort Kobuch, Sophie
collection PubMed
description INTRODUCTION: Long‐lasting experimental muscle pain elicits divergent muscle sympathetic responses, with some individuals exhibiting a persistent increase in muscle sympathetic nerve activity (MSNA), and others a decrease. These divergent responses are thought to result from sustained functional changes in specific brain regions that modulate the cardiovascular responses to pain. AIM: The aim of this study was to investigate brain regions that are functionally coupled to the generation of an MSNA burst at rest and to determine their behavior during tonic muscle pain. METHODS: Functional magnetic resonance imaging of the brain was performed concurrently with microelectrode recording of MSNA from the common peroneal nerve during a 40 min infusion of hypertonic saline into the ipsilateral tibialis anterior muscle of 37 healthy human subjects. RESULTS: At rest, blood oxygen level‐dependent signal intensity coupled to bursts of MSNA increased in the rostral ventrolateral medulla, insula, dorsolateral prefrontal cortex, posterior cingulate cortex, and precuneus and decreased in the region of the midbrain periaqueductal gray. During pain, MSNA‐coupled signal intensity was greater in the region of the nucleus tractus solitarius, midbrain periaqueductal gray, dorsolateral prefrontal, medial prefrontal, and anterior cingulate cortices, than at rest. Conversely, MSNA‐coupled signal intensity decreased during pain in parts of the prefrontal cortex. CONCLUSIONS: These results suggest that multiple brain regions are recruited in a burst‐to‐burst manner, and the magnitude of these signal changes is correlated to the overall change in MSNA amplitude during tonic muscle pain.
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spelling pubmed-58404472018-03-14 Muscle sympathetic nerve activity‐coupled changes in brain activity during sustained muscle pain Kobuch, Sophie Fazalbhoy, Azharuddin Brown, Rachael Macefield, Vaughan G. Henderson, Luke A. Brain Behav Original Research INTRODUCTION: Long‐lasting experimental muscle pain elicits divergent muscle sympathetic responses, with some individuals exhibiting a persistent increase in muscle sympathetic nerve activity (MSNA), and others a decrease. These divergent responses are thought to result from sustained functional changes in specific brain regions that modulate the cardiovascular responses to pain. AIM: The aim of this study was to investigate brain regions that are functionally coupled to the generation of an MSNA burst at rest and to determine their behavior during tonic muscle pain. METHODS: Functional magnetic resonance imaging of the brain was performed concurrently with microelectrode recording of MSNA from the common peroneal nerve during a 40 min infusion of hypertonic saline into the ipsilateral tibialis anterior muscle of 37 healthy human subjects. RESULTS: At rest, blood oxygen level‐dependent signal intensity coupled to bursts of MSNA increased in the rostral ventrolateral medulla, insula, dorsolateral prefrontal cortex, posterior cingulate cortex, and precuneus and decreased in the region of the midbrain periaqueductal gray. During pain, MSNA‐coupled signal intensity was greater in the region of the nucleus tractus solitarius, midbrain periaqueductal gray, dorsolateral prefrontal, medial prefrontal, and anterior cingulate cortices, than at rest. Conversely, MSNA‐coupled signal intensity decreased during pain in parts of the prefrontal cortex. CONCLUSIONS: These results suggest that multiple brain regions are recruited in a burst‐to‐burst manner, and the magnitude of these signal changes is correlated to the overall change in MSNA amplitude during tonic muscle pain. John Wiley and Sons Inc. 2018-02-07 /pmc/articles/PMC5840447/ /pubmed/29541532 http://dx.doi.org/10.1002/brb3.888 Text en © 2017 The Authors. Brain and Behavior published by Wiley Periodicals, Inc. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Kobuch, Sophie
Fazalbhoy, Azharuddin
Brown, Rachael
Macefield, Vaughan G.
Henderson, Luke A.
Muscle sympathetic nerve activity‐coupled changes in brain activity during sustained muscle pain
title Muscle sympathetic nerve activity‐coupled changes in brain activity during sustained muscle pain
title_full Muscle sympathetic nerve activity‐coupled changes in brain activity during sustained muscle pain
title_fullStr Muscle sympathetic nerve activity‐coupled changes in brain activity during sustained muscle pain
title_full_unstemmed Muscle sympathetic nerve activity‐coupled changes in brain activity during sustained muscle pain
title_short Muscle sympathetic nerve activity‐coupled changes in brain activity during sustained muscle pain
title_sort muscle sympathetic nerve activity‐coupled changes in brain activity during sustained muscle pain
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840447/
https://www.ncbi.nlm.nih.gov/pubmed/29541532
http://dx.doi.org/10.1002/brb3.888
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