Neurobiology of Fibromyalgia Syndrome
DONALD D. PRICE and ROLAND STAUD
ABSTRACT.
Accumulating evidence suggests that fibromyalgia syndrome (FM) pain is maintained by tonic impulse input from deep tissues, such as muscle and joints, in combination with central sensitization mechanisms. This nociceptive input may originate in peripheral tissues (trauma and infection) resulting in hyperalgesia/allodynia and/or central sensitization. Evidence for abnormal sensitization mechanisms in FM includes enhanced temporal summation of delayed pain in response to repeated heat taps and repeated muscle taps, as well as prolonged and enhanced painful after-sensations in FM patients but not control subjects. Moreover, magnitudes of enhanced after-sensations are predictive of FM patients' ongoing clinical pain. Such alterations of relevant pain mechanisms may lead to longterm neuroplastic changes that exceed the antinociceptive capabilities of affected individuals, resulting in ever-increasing pain sensitivity and dysfunction. Future research needs to address the important role of abnormal nociception and/or antinociception for chronic pain in FM. (J Rheumatol 2005;32 Suppl 75:22-28)
Key Indexing Terms:
TEMPORAL SUMMATION
CHRONIC PAIN
FIBROMYALGIA
From the Department of Neuroscience and Department of Medicine, University of Florida, Gainesville, Florida, USA.
The authors have no conflict of financial interest related to the contents of this article.
D.D. Price, PhD, Departments of Oral and Maxillofacial Surgery and Neuroscience, Colleges of Dentistry and Medicine; R. Staud MD, McKnight Brain Institute, University of Florida.
Address reprint requests to D.D. Price, Claude Denson Pepper Center, PO Box 100416, Gainesville, FL 32610-0416. E-mail: Dprice@dental.ufl.edu
