Proposed pathophysiologic mechanisms for fibromyalgia

What are the proposed pathophysiologic mechanisms for fibromyalgia?

Fibromyalgia is associated with an augmentation of sensation. Pathophysiologic explanations for fibromyalgia have ranged from primarily central, to a combination of central and peripheral, to primarily peripheral. Here are some examples:

  • • Fibromyalgia is a variation of an affective disorder. This idea was based on its common association with depression, IBS, and chronic fatigue syndrome.
  • • A sleep abnormality is the main disturbance, leading to altered pain perception.
  • • Peripheral factors, such as small fiber neuropathy, are most important.
  • • Travell and Simons believed that the muscle problem was primary.

It remains unclear whether there is one pathological mechanism for fibromyalgia or a variety of etiologic factors. Nevertheless, current hypotheses under investigation hold some promise that the pathogenesis and pathophysiology of fibromyalgia may soon be clarified:

  • • The cause is neuroendocrine in origin. This concept is largely based on the observation of decreased circulating cortisol levels and abnormal 5-HT metabolism.
  • • Peripheral C-fiber and central nociceptive sensitization occurs following a painful stimulus (wind-up). This sensitization is ameliorated by -methyl- d -aspartate (NMDA) receptor blockade. NMDA activation causes release of Substance P, which has been found to be elevated in the CSF in fibromyalgia patients. Thus fibromyalgia represents “central sensitization.”
  • • Association with infection: High levels of circulating immunoglobulin M (IgM) in response to an enteroviral infection have been demonstrated in some fibromyalgia patients. Hepatitis C has been associated with fibromyalgia.
  • • A Chiari I malformation, with brainstem compression, leads to an altered autonomic response, orthostasis, and fibromyalgia syndrome.
  • • Glial cell activation, which includes neuroinflammation, glial cell dysfunction (GCD), cellular destruction, hyperarousal of the sympathetic nervous system, and stimulation of the hypothalamic-pituitary complex. Neurogenic neuroinflammation due to glial cell activation leads to production of proinflammatory cytokines, nitric oxide, prostaglandin E2, and reactive oxygen and nitrogen species. This is an active area of current fibromyalgia research.

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