Recent research has linked the pain of fibromyalgia to small nerve fiber neuropathy, which means painful damage to a certain part of nerves. This could be ground-breaking, as fibromyalgia has previously been linked to nerve dysfunction, but not as actual nerve damage.

Researchers examined the small fibers in different areas of the body using three different methods: sensory testing, pain response, and skin biopsy.
They were compared with between people with fibromyalgia, those with depression, and healthy subjects.

They determined that people with fibromyalgia had:

Impaired small fiber function that lead to increased temperature sensitivity;
Sensory irregularities in the feet, face, and hands;
Lower total nerve fibers and fewer regenerating nerve fibers in the skin;
Fewer unmyelinated nerve fiber bundles in the skin, but normal levels of myelinated nerve fibers.

Researchers concluded that all three testing methods support the idea of impaired small fiber function, and therefore a high likelihood of neuropathic pain, in fibromyalgia.

The fibers in the skin, organs, and peripheral nerves are called C fibers or small fibers. Their job is to provide sensation for your skin and to control autonomic function - all the automatic jobs your body, like regulating heart rate, breathing, and body temperature. Damage to these nerves is called peripheral neuropathy.

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The Relevance

This could be an extremely important avenue of research. Doctors understand neuropathic pain. It's common in diabetes and as a result of nerve damage. It's a concrete explanation for our pain, which is currently classified as "poorly understood".

Neuropathy in Fibromyalgia makes sense. It explains why medications known to improve neuropathy, such as Lyrica (pregabalin), work for some of us. It also explains the nature of our pain and the way it moves around.

It also raises a new question - what is damaging our small fibers? Is it our immune systems, which would mean fibromyalgia is autoimmune? Do we lack an enzyme that aids in axon growth and repair? Is it a problem with cellular metabolism?

Let's hope that researchers start asking those questions and looking for answers, because if it truly is nerve damage - and not just dysfunction - it also brings us better credibility with professionals along with more concrete targets for treatment.

There can never be any more suspicion with Doctors suggesting it’s all in our heads, it also brings definitive diagnosis to our table. Pip, ESA and many more aids to help us will be easier to apply for and maintain.

Life for fibromyalgia sufferers will certainly improve should this direction of research progress.

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other research has proved Fibromyalgia is an Auto Immune Disease.

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new study involving Liverpool researchers has shown that many of the symptoms in fibromyalgia syndrome (FMS) are caused by antibodies that increase the activity of pain-sensing nerves throughout the body.

The results show that fibromyalgia is a disease of the immune system, rather than the currently held view that fibromyalgia originates in the brain.

The study, which has been published in the Journal of Clinical Investigation, demonstrates that the increased pain sensitivity, muscle weakness, reduced movement, and reduced number of small nerve-fibres in the skin that are typical of FMS, are all a consequence of patient antibodies.

The research was led by the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London, in collaboration with the University of Liverpool and the Karolinska Institute,

The researchers injected mice with antibodies from people living with FMS and observed that the mice rapidly developed an increased sensitivity to pressure and cold, as well as displaying reduced movement grip strength. In contrast, mice that were injected with antibodies from healthy people were unaffected, demonstrating that patient antibodies cause, or at least are a major contributor to the disease.

Furthermore, the mice injected with fibromyalgia antibodies recovered after a few weeks, when antibodies had been cleared from their system. This finding strongly suggests that therapies which reduce antibody levels in patients are likely to be effective treatments. Such therapies are already available and are used to treat other disorders that are caused by autoantibodies.

Dr David Andersson, the study’s primary investigator from King’s IoPPN said “The implications of this study are profound. Establishing that fibromyalgia is an autoimmune disorder will transform how we view the condition and should pave the way for more effective treatments for the millions of people affected. Our work has uncovered a whole new area of therapeutic options and should give real hope to fibromyalgia patients.

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“Previous exploration of therapies has been hampered by our limited understanding of the illness. This should now change. Treatment for FMS is focused on gentle aerobic exercises, and drug therapies designed to manage pain, although these have proven ineffective in most patients and have left behind an enormous unmet clinical need.”

Current estimates people affected by FMS worldwide (80% of which are women), and is commonly characterised by widespread pain throughout the body, as well as fatigue and emotional distress.

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Dr Andreas Goebel, the study’s principle clinical investigator and Director of the University of Liverpool’s Pain Research Institute said, “When I initiated this study in the UK, I expected that some fibromyalgia cases may be autoimmune. But David’s team have discovered pain-causing antibodies in each recruited patient. The results offer amazing hope that the invisible, devastating symptoms of fibromyalgia will become treatable.”

Professor Camilla Svensson, the study’s primary investigator from Karolinska Institute said, “Antibodies from people with FMS living in two different countries, the UK and Sweden, gave similar results, which adds enormous strength to our findings. The next step will be to identify what factors the symptom-inducing antibodies bind to. This will help us not only in terms of developing novel treatment strategies for FMS, but also of blood-based tests for diagnosis, which are missing today.

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