Intramuscular hypoperfusion, adrenergic receptors, and chronic muscle pain

Kenji Maekawa, Glenn T. Clark, Takuo Kuboki

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Despite a high prevalence of chronic muscle pain disorders such as fibromyalgia and regional myofascial pain, there is still limited knowledge about the factors that initiate and perpetuate these pain states. Although there are also likely to be downstream neuropathic changes in the central nervous system and spinal cord that sustain and exacerbate the pain states known as fibromyalgia, the focus of this critical review is on studies that examined the connection between both fibromyalgia and regional myofascial pain and sympathetic function. Specifically, we looked at studies that described Raynaud-like symptoms, cardiovascular dysfunction and altered intramuscular perfusion in chronic muscle pain. Our analysis showed that although the first 2 phenomena were intermittently present, a prominent and consistent feature for regional myofascial pain and to a lesser degree for fibromyalgia was intramuscular hypoperfusion. Several hypotheses can be offered why this hypoperfusion exists, and additional studies comparing and contrasting these theories are needed. This review focuses on one of these theories, namely, agonist-induced β-adrenergic receptor desensitization as an explanatory model for hypoperfusion. What cannot be done at this time and is needed in the future is to compare and contrast to what degree the regional muscle pain disorder (myofascial) is similar or different from the more generalized disorder (fibromyalgia).

Original languageEnglish
Pages (from-to)251-260
Number of pages10
JournalJournal of Pain
Volume3
Issue number4
DOIs
Publication statusPublished - 2002

Fingerprint

Fibromyalgia
Myalgia
Chronic Pain
Adrenergic Receptors
Pain
Somatoform Disorders
Muscular Diseases
Adrenergic Agonists
Spinal Cord
Central Nervous System
Perfusion

Keywords

  • Adrenergic receptor
  • Chronic muscle pain
  • Hemodynamics
  • Sympathetic nerve

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine
  • Clinical Neurology
  • Neurology
  • Nursing(all)

Cite this

Intramuscular hypoperfusion, adrenergic receptors, and chronic muscle pain. / Maekawa, Kenji; Clark, Glenn T.; Kuboki, Takuo.

In: Journal of Pain, Vol. 3, No. 4, 2002, p. 251-260.

Research output: Contribution to journalArticle

@article{9379ba699975419fb89a61c86e2c63fa,
title = "Intramuscular hypoperfusion, adrenergic receptors, and chronic muscle pain",
abstract = "Despite a high prevalence of chronic muscle pain disorders such as fibromyalgia and regional myofascial pain, there is still limited knowledge about the factors that initiate and perpetuate these pain states. Although there are also likely to be downstream neuropathic changes in the central nervous system and spinal cord that sustain and exacerbate the pain states known as fibromyalgia, the focus of this critical review is on studies that examined the connection between both fibromyalgia and regional myofascial pain and sympathetic function. Specifically, we looked at studies that described Raynaud-like symptoms, cardiovascular dysfunction and altered intramuscular perfusion in chronic muscle pain. Our analysis showed that although the first 2 phenomena were intermittently present, a prominent and consistent feature for regional myofascial pain and to a lesser degree for fibromyalgia was intramuscular hypoperfusion. Several hypotheses can be offered why this hypoperfusion exists, and additional studies comparing and contrasting these theories are needed. This review focuses on one of these theories, namely, agonist-induced β-adrenergic receptor desensitization as an explanatory model for hypoperfusion. What cannot be done at this time and is needed in the future is to compare and contrast to what degree the regional muscle pain disorder (myofascial) is similar or different from the more generalized disorder (fibromyalgia).",
keywords = "Adrenergic receptor, Chronic muscle pain, Hemodynamics, Sympathetic nerve",
author = "Kenji Maekawa and Clark, {Glenn T.} and Takuo Kuboki",
year = "2002",
doi = "10.1054/jpai.2002.125923",
language = "English",
volume = "3",
pages = "251--260",
journal = "Journal of Pain",
issn = "1526-5900",
publisher = "Churchill Livingstone",
number = "4",

}

TY - JOUR

T1 - Intramuscular hypoperfusion, adrenergic receptors, and chronic muscle pain

AU - Maekawa, Kenji

AU - Clark, Glenn T.

AU - Kuboki, Takuo

PY - 2002

Y1 - 2002

N2 - Despite a high prevalence of chronic muscle pain disorders such as fibromyalgia and regional myofascial pain, there is still limited knowledge about the factors that initiate and perpetuate these pain states. Although there are also likely to be downstream neuropathic changes in the central nervous system and spinal cord that sustain and exacerbate the pain states known as fibromyalgia, the focus of this critical review is on studies that examined the connection between both fibromyalgia and regional myofascial pain and sympathetic function. Specifically, we looked at studies that described Raynaud-like symptoms, cardiovascular dysfunction and altered intramuscular perfusion in chronic muscle pain. Our analysis showed that although the first 2 phenomena were intermittently present, a prominent and consistent feature for regional myofascial pain and to a lesser degree for fibromyalgia was intramuscular hypoperfusion. Several hypotheses can be offered why this hypoperfusion exists, and additional studies comparing and contrasting these theories are needed. This review focuses on one of these theories, namely, agonist-induced β-adrenergic receptor desensitization as an explanatory model for hypoperfusion. What cannot be done at this time and is needed in the future is to compare and contrast to what degree the regional muscle pain disorder (myofascial) is similar or different from the more generalized disorder (fibromyalgia).

AB - Despite a high prevalence of chronic muscle pain disorders such as fibromyalgia and regional myofascial pain, there is still limited knowledge about the factors that initiate and perpetuate these pain states. Although there are also likely to be downstream neuropathic changes in the central nervous system and spinal cord that sustain and exacerbate the pain states known as fibromyalgia, the focus of this critical review is on studies that examined the connection between both fibromyalgia and regional myofascial pain and sympathetic function. Specifically, we looked at studies that described Raynaud-like symptoms, cardiovascular dysfunction and altered intramuscular perfusion in chronic muscle pain. Our analysis showed that although the first 2 phenomena were intermittently present, a prominent and consistent feature for regional myofascial pain and to a lesser degree for fibromyalgia was intramuscular hypoperfusion. Several hypotheses can be offered why this hypoperfusion exists, and additional studies comparing and contrasting these theories are needed. This review focuses on one of these theories, namely, agonist-induced β-adrenergic receptor desensitization as an explanatory model for hypoperfusion. What cannot be done at this time and is needed in the future is to compare and contrast to what degree the regional muscle pain disorder (myofascial) is similar or different from the more generalized disorder (fibromyalgia).

KW - Adrenergic receptor

KW - Chronic muscle pain

KW - Hemodynamics

KW - Sympathetic nerve

UR - http://www.scopus.com/inward/record.url?scp=0036342203&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036342203&partnerID=8YFLogxK

U2 - 10.1054/jpai.2002.125923

DO - 10.1054/jpai.2002.125923

M3 - Article

VL - 3

SP - 251

EP - 260

JO - Journal of Pain

JF - Journal of Pain

SN - 1526-5900

IS - 4

ER -