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Psychophysical and Neurochemical Abnormalities of Pain Processing in Fibromyalgia

Published online by Cambridge University Press:  07 November 2014

Roland Staud  and
Michael Spaeth
Roland Staud
Affiliation:
Dr. Staud is professor of medicine in the Division of Rheumatology and Clinical Immunology, McKnight Brain Institute, at the, University of Florida in Gainesville
Michael Spaeth
Affiliation:
Dr. Spaeth is medical director of the Center for Clinical Rheumatology Research in Graefelfing/Munich, Germany.
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Abstract

Fibromyalgia pain is frequent in the general population, but its pathogenesis is only partially understood. Patients with fibromyalgia lack consistent tissue abnormalities but display features of hyperalgesia (increased sensitivity to painful stimuli) and allodynia (lowered pain threshold). Many recent fibromyalgia studies have demonstrated central nervous system (CNS) pain processing abnormalities, including abnormal temporal summation of pain. In the CNS, persistent nociceptive input from peripheral tissues can lead to neuroplastic changes resulting in central sensitization and pain. This mechanism appears to represent a hallmark of fibromyalgia and many other chronic pain syndromes, including irritable bowel syndrome, temporomandibular disorder, migraine, and low back pain. Importantly, after central sensitization has been established, only minimal peripheral input is required for the maintenance of the chronic pain state. Additional factors, including pain-related negative affect and poor sleep have been shown to significantly contribute to clinical fibromyalgia pain. Better understanding of these mechanisms and their relationship to central sensitization and clinical pain will provide new approaches for the prevention and treatment of fibromyalgia and other chronic pain syndromes.

Type
Research Article
Information
CNS Spectrums , Volume 13 , Issue S5 , March 2008 , pp. 12 - 17
Copyright
Copyright © Cambridge University Press 2008

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