Can something be learned for Multiple Sclerosis (MS) when looking at fibromyalgia? There is some fascinating research going on that is looking at just that connection. MS is believed to be an autoimmune disease where the symptoms are caused by demyelination. Essentially that means destruction of the myelin. Myelin is a specialized cell that covers some nerves and it is fundamental for them to function properly. Lesions that are formed, and seen from testing for MS, are the areas where the myelin has been destroyed. One theory of MS is that the immune system malfunctions and destroys the myelin sheath. Fibromyalgia is a chronic syndrome defined by widespread muscle pain, fatigue, sleep dysfunction and cognitive dysfunction. Fibromyalgia pain dysfunction involves an increased sensitivity to pain known as hyperalgesia.
Your nerves are composed of cells call neurons connected by fibers called axons. The axons or fibers found in the skin, organs and other peripheral nerves are referred to as C fibers or small fibers. The fibers provide information such as pain and temperature sensations from the skin as well as maintaining automatic functions such as regulating heart rate, breathing and body temperature. Damage to the nerves themselves is called peripheral neuropathy and this can sometimes be a comorbid condition with fibromyalgia. Now within those fibers are a bundle of smaller strands bundled together with a casing. Some of the smaller bundles have a protective a casing called a myelin sheath and are called ‘myelinated’ while others do not and are referred to as ‘unmylinated’.
In 2008 a study came out with the objective to study “FMS subjects for evidence of an immune-mediated demyelinating polyneuropathy. Our secondary objective was to determine the effects of treating these FMS subjects with the immune modulator, intravenous immunoglobulin (IVIg).” PubMed They concluded a significant subset of fibromyalgia patients have clinical and EDX findings suggestive of chronic inflammatory demyelinating polyneuropathy (CIDP).
They did a follow-up study with a new objective “A subset of patients with fibromyalgia (FM) exhibit a large fiber demyelinating peripheral polyneuropathy akin to that seen in chronic inflammatory demyelinating polyneuropathy (CIDP). It has been suggested that this demyelinating process is likely to be immune mediated. Because it is known that similar large fiber neuropathic lesions may be associated with a cutaneous small fiber neuropathy, we sought to determine the prevalence of small fiber neuropathy, as measured by epidermal nerve fiber density (ENFD), in a series of patients with FM and clinically healthy control subjects.
Small fiber neuropathy has been found before and linked to fibromyalgia. (See…) Small fiber neuropath is damage to the structures of the skin, organs and the peripheral nerves which provide sensation and help regulate automatic functions like temperature in the body and heart rate. How this fits in is that it is known that small fiber neuropathy can sometimes be associated with demyelination lesions on large fibers.
Forty-one patients with fibromyalgia and 47 controls were involved in the study. To test for small fiber neuropathy they all underwent a 3-mm punch skin biopsy at the proximal thigh and distal leg near the ankle, to analysis of the epidermal nerve fiber density (ENFD). Those patients with FM with another condition associated with SFN were excluded. The patients also had pinwheel testing and vibrancy testing for hypesthesia and serologic testing for a series of cytokine, circulating immune complex, and complement measurements.
They had discovered indications of small fiber neuropathy with diminished feelings in the lower legs. They were also testing multiple markers for immune activation and autoimmune activity. The researchers determined there were high indications of small fiber neuropathy and therefore large fiber lesions in the legs of the patients with FM. Some of these indicators, especially in the calf area, appear to be linked to a marker of immune activation.
It is clear from this study that small fiber neuropathy is a contributing factor with FM pain and it is possible some of that pain is from immune system activity, such as autoimmunity. They concluded “The calf and thigh epidermal nerve fiber density (ENFD) in patients with FM is significantly diminished compared with that in control subjects. Advancing age alone cannot explain this finding. Calf epidermal nerve fiber density (ENFD) was inversely correlated, although weakly, with serum levels of IL-2R. These findings suggest that small fiber neuropathy is likely to contribute to the pain symptoms of FM; that pain in this disorder arises, in part, from a peripheral immune-mediated process; and that measurement of epidermal nerve fiber density (ENFD) may be a useful clinical tool in FM.”
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