Fibromyalgia has been somewhat of a mystery to medical researchers for years. Two studies may shed light on how fibromyalgia relates to other autoimmune diseases.
Multiple sclerosis (MS) is believed to be an autoimmune disease, with symptoms caused by demyelination (the destruction of myelin). Why is myelin so important? Myelin is a specialized cell that covers nerves and helps them to operate properly — similar to how insulation covers electrical wires. Researchers believe that with MS, the immune system destroys the myelin, leaving lesions.
Does something similar happen with fibromyalgia? Some research believes the answer may be yes.
How Fibromyalgia Relates to Demyelination
The first official study of fibromyalgia and demyelination was done in 2008, and recently a follow-up study was published. The original 2008 research suggested that fibromyalgia indeed involves autoimmune demyelination and polyneuropathy (pain from damaged nerves). This study compared fibromyalgia to an illness called chronic inflammatory demyelinating polyneuropathy. Often doctors use intravenous immunoglobulin (IVIg) to treat this disease. In a small study of 15 people, researches used IVIg to treat people with fibromyalgia. They reported improvements in fatigue and stiffness.
Why This Is Encouraging
While this was a preliminary study, it’s a prime example of how research can have significant implications and yet have little or no impact. Since the 2008 study, some doctors have used IVIg on patients, yet it’s far from a popular treatment. In fact, few people discuss demyelination and fibromyalgia together.
However, recently a follow-up study on fibromyalgia appears to confirm the earlier findings and even sheds new light on the topic.
What New Research Shows
Scientists wanted to explore the similar ideas in the 2008 study to see if demyelination of bigger nerves is the result of autoimmunity. They wanted to learn more about small fiber neuropathy—since other studies suggest this relates to fibromyalgia.
They did indeed discover high indicators of small fiber neuropathy and therefore large fiber lesions, in the legs of people with fibromyalgia. Additionally, in the calf area, in particular, they found indications that linked to markers of immune activation (interleukine-2R).
The end of the study summed up by saying that small fiber neuropathy does likely contribute to fibromyalgia pain, and some of the pain comes from immune-system activity.
Would MS treatments work for fibromyalgia patients? Both conditions can have flares and remissions, and their symptoms are extremely similar. Research is shifting toward small fiber neuropathy, inflammation, and possible autoimmunity.
This research work adds to the emerging picture that peripheral nervous systems are definitely involved in fibromyalgia and that autoimmunity or another aspect of immunity is at work.
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