TITLE

The Science of Fibromyalgia

AUTHOR(S)
CLAUW, DANIEL J.; ARNOLD, LESLEY M.; MCCARBERG, BILL H.
PUB. DATE
September 2011
SOURCE
Mayo Clinic Proceedings;Sep2011, Vol. 86 Issue 9, p907
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Fibromyalgia (FM) is a common chronic widespread pain disorder. Our understanding of FM has increased substantially in recent years with extensive research suggesting a neurogenic origin for the most prominent symptom of FM, chronic widespread pain. Neurochemical imbalances in the central nervous system are associated with central amplification of pain perception characterized by allodynla (a heightened sensitivity to stimuli that are not normally painful) and hyperalgesla (an increased response to painful stimuli). Despite this increased awareness and understanding, FM remains undiagnosed in an estimated 75% of people with the disorder. Clinicians could more effectively diagnose and manage FM If they better understood its underlying mechanisms. Fibromyalgia is a disorder of pain processing. Evidence suggests that both the ascending and descending pain pathways operate abnormally, resulting in central amplification of pain signals, analogous to the "volume control setting" being turned up too high. Patients with FM also exhibit changes in the leveis of neurotransmltters that cause augmented central nervous system pain processing; levels of several neurotransmltters that facilitate pain transmission are elevated in the cerebrosplnal fluid and brain, and levels of several neurotransmltters known to Inhibit pain transmission are decreased. Pharmacological agents that act centrally in ascending and/or descending pain processing pathways, such as medications with approved indications for FM, are effective in many patients with FM as well as other conditions involving central pain amplification. Research is ongoing to determine the roie of analogous central nervous system factors in the other cardinal symptoms of FM, such as fatigue, nonrestorative sleep, and cognitive dysfunction.
ACCESSION #
65538146

 

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