Authors and affiliations: Katz DL, Greene L, Ali A, Faridi Z. Yale Prevention Research Center, Yale University School of Medicine, Derby, Connecticut; Yale University School of Public Health, Yale University School of Medicine, New Haven, Connecticut, USA.
The pain of Fibromyalgia syndrome is due to muscle hypoperfusion induced by regional vasomotor dysregulation. (hypoperfusion is decreased blood flow, vasomotor dysregulation refers to regulation of blood vessel constriction and expansion.)
Fibromyalgia syndrome (FMS) is a condition of chronic muscle pain and fatigue of unknown etiology and pathogenesis.
There is limited support for the various hypotheses espoused to account for the manifestations of FMS, including immunogenic, endocrine, and neurological mechanisms. Treatment, partially effective at best, is directed toward symptomatic relief without the benefit of targeting known, underlying pathology.
A noteworthy commonality among partially effective therapies is a vasodilatory effect. This is true both of conventional treatments, unconventional treatments such as intravenous micronutrient therapy, and lifestyle treatments, specifically graduated exercise.
The pain of Fibromyalgia is described in terms suggestive of the pain in muscles following extreme exertion and anaerobic metabolism. Taken together, these characteristics suggest that the pain could be induced by vasomotor dysregulation, and vasoconstriction in muscle, leading to low-level ischemia and its metabolic sequelae.
Vasodilatory influences, including physical activity, relieve the pain of FMS by increasing muscle perfusion. There are some preliminary data consistent with this hypothesis, and nothing known about FMS that refutes it. The hypothesis that the downstream cause of FMS symptoms is muscle hypoperfusion due to regional vasomotor dysregulation has clear implications for treatment; is testable with current technology; and should be investigated.
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