Cutaneous tactile allodynia associated with microvascular dysfunction in muscle

<p>Abstract</p> <p>Background</p> <p>Cutaneous tactile allodynia, or painful hypersensitivity to mechanical stimulation of the skin, is typically associated with neuropathic pain, although also present in chronic pain patients who do not have evidence of nerve injury. W...

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Main Authors: de Mos Marissa, Siau Chiang, Xiao Wen, Xanthos Dimitris N, Millecamps Magali, Laferrière Andre, Sachot Christelle, Ragavendran J Vaigunda, Huygen Frank JPM, Bennett Gary J, Coderre Terence J
Format: Article
Language:English
Published: SAGE Publishing 2008-10-01
Series:Molecular Pain
Online Access:http://www.molecularpain.com/content/4/1/49
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spelling doaj-85c0747c277b4939ab6cd9d91be3753e2020-11-25T02:54:51ZengSAGE PublishingMolecular Pain1744-80692008-10-01414910.1186/1744-8069-4-49Cutaneous tactile allodynia associated with microvascular dysfunction in musclede Mos MarissaSiau ChiangXiao WenXanthos Dimitris NMillecamps MagaliLaferrière AndreSachot ChristelleRagavendran J VaigundaHuygen Frank JPMBennett Gary JCoderre Terence J<p>Abstract</p> <p>Background</p> <p>Cutaneous tactile allodynia, or painful hypersensitivity to mechanical stimulation of the skin, is typically associated with neuropathic pain, although also present in chronic pain patients who do not have evidence of nerve injury. We examine whether deep tissue microvascular dysfunction, a feature common in chronic non-neuropathic pain, contributes to allodynia.</p> <p>Results</p> <p>Persistent cutaneous allodynia is produced in rats following a hind paw ischemia-reperfusion injury that induces microvascular dysfunction, including arterial vasospasms and capillary slow flow/no-reflow, in muscle. Microvascular dysfunction leads to persistent muscle ischemia, a reduction of intraepidermal nerve fibers, and allodynia correlated with muscle ischemia, but not with skin nerve loss. The affected hind paw muscle shows lipid peroxidation, an upregulation of nuclear factor kappa B, and enhanced pro-inflammatory cytokines, while allodynia is relieved by agents that inhibit these alterations. Allodynia is increased, along with hind paw muscle lactate, when these rats exercise, and is reduced by an acid sensing ion channel antagonist.</p> <p>Conclusion</p> <p>Our results demonstrate how microvascular dysfunction and ischemia in muscle can play a critical role in the development of cutaneous allodynia, and encourage the study of how these mechanisms contribute to chronic pain. We anticipate that focus on the pain mechanisms associated with microvascular dysfunction in muscle will provide new effective treatments for chronic pain patients with cutaneous tactile allodynia.</p> http://www.molecularpain.com/content/4/1/49
collection DOAJ
language English
format Article
sources DOAJ
author de Mos Marissa
Siau Chiang
Xiao Wen
Xanthos Dimitris N
Millecamps Magali
Laferrière Andre
Sachot Christelle
Ragavendran J Vaigunda
Huygen Frank JPM
Bennett Gary J
Coderre Terence J
spellingShingle de Mos Marissa
Siau Chiang
Xiao Wen
Xanthos Dimitris N
Millecamps Magali
Laferrière Andre
Sachot Christelle
Ragavendran J Vaigunda
Huygen Frank JPM
Bennett Gary J
Coderre Terence J
Cutaneous tactile allodynia associated with microvascular dysfunction in muscle
Molecular Pain
author_facet de Mos Marissa
Siau Chiang
Xiao Wen
Xanthos Dimitris N
Millecamps Magali
Laferrière Andre
Sachot Christelle
Ragavendran J Vaigunda
Huygen Frank JPM
Bennett Gary J
Coderre Terence J
author_sort de Mos Marissa
title Cutaneous tactile allodynia associated with microvascular dysfunction in muscle
title_short Cutaneous tactile allodynia associated with microvascular dysfunction in muscle
title_full Cutaneous tactile allodynia associated with microvascular dysfunction in muscle
title_fullStr Cutaneous tactile allodynia associated with microvascular dysfunction in muscle
title_full_unstemmed Cutaneous tactile allodynia associated with microvascular dysfunction in muscle
title_sort cutaneous tactile allodynia associated with microvascular dysfunction in muscle
publisher SAGE Publishing
series Molecular Pain
issn 1744-8069
publishDate 2008-10-01
description <p>Abstract</p> <p>Background</p> <p>Cutaneous tactile allodynia, or painful hypersensitivity to mechanical stimulation of the skin, is typically associated with neuropathic pain, although also present in chronic pain patients who do not have evidence of nerve injury. We examine whether deep tissue microvascular dysfunction, a feature common in chronic non-neuropathic pain, contributes to allodynia.</p> <p>Results</p> <p>Persistent cutaneous allodynia is produced in rats following a hind paw ischemia-reperfusion injury that induces microvascular dysfunction, including arterial vasospasms and capillary slow flow/no-reflow, in muscle. Microvascular dysfunction leads to persistent muscle ischemia, a reduction of intraepidermal nerve fibers, and allodynia correlated with muscle ischemia, but not with skin nerve loss. The affected hind paw muscle shows lipid peroxidation, an upregulation of nuclear factor kappa B, and enhanced pro-inflammatory cytokines, while allodynia is relieved by agents that inhibit these alterations. Allodynia is increased, along with hind paw muscle lactate, when these rats exercise, and is reduced by an acid sensing ion channel antagonist.</p> <p>Conclusion</p> <p>Our results demonstrate how microvascular dysfunction and ischemia in muscle can play a critical role in the development of cutaneous allodynia, and encourage the study of how these mechanisms contribute to chronic pain. We anticipate that focus on the pain mechanisms associated with microvascular dysfunction in muscle will provide new effective treatments for chronic pain patients with cutaneous tactile allodynia.</p>
url http://www.molecularpain.com/content/4/1/49
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