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Neurophysiopathogenesis of fibromyalgia syndrome: a unified hypothesis





Rheum Dis Clin North Am. 2009 May;35(2):421-35.


Neurophysiopathogenesis of fibromyalgia syndrome: a unified hypothesis.


Russell IJ, Larson AA. Department of Medicine, Division of Clinical Immunology and Rheumatology, University Clinical Research Center, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229-3900, USA. This email address is being protected from spambots. You need JavaScript enabled to view it.



The characteristic presenting complaint of patients with fibromyalgia syndrome (FMS) is chronic widespread allodynia. Research findings support the view that FMS is an understandable and treatable neuropathophysiologic disorder. The pain of FMS is often accompanied by one or more other manifestations, such as affective moods, cognitive insecurity, autonomic dysfunction, or irritable bowel or bladder. Growing evidence suggests that this is a familial disorder with many underlying genetic associations. New findings from brain imaging and polysomnography imply that FMS may be a disorder of premature neurologic aging. A conceptual model at the molecular level is proposed to explain many of the observed features of FMS. The model can also explain anticipated responses to FDA approved pharmacologic therapies.


PMID: 19647152 [PubMed - in process]









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