Fibromyalgia, Small Fiber Neuropathy and Eye-Opening Developments in Pain Research: An FM and Pain Researcher Talks – Health Rising
Claudia Sommer, MD is a busy woman. The director of the Peripheral Nerve Laboratory at the University of Wurzburg in Germany, she investigates the role cytokines and antibodies play in producing pain, is working to standardize diagnostics in neuropathy
Over the past couple of years she’s been focused on fibromyalgia which she characterized as a “very difficult pain syndrome”. She noted that many of her colleagues still don’t believe fibromyalgia exists, while others believe it’s a somatoform disorder.
She was one of the first researchers to elucidate the small fiber neuropathies found in fibromyalgia
Skeptics still abound though. It’s going to take some time to convince FM is real.
Sommer noted in a recent paper the modest effects most drugs prescribed for fibromyalgia have:
Most drugs cause a 30% reduction in pain in half of FM patients and a 50% reduction in pain in about a third.
These improvements do not translate into global improvements in well-being, and many patients who experience initial improvements will later drop the drugs because of side effects or reductions in effectiveness
Immune Mediated Pain
Pro-inflammatory cytokines were clearly been associated with pain in animal models, but the situation is more complex in humans. Sometimes high pro-inflammatory cytokine levels translate to pain and sometimes they don’t.
Higher levels of the pro-inflammatory cytokine IL-6 as well as IL-10 in skin biopsies of patients with peripheral neuropathy experiencing pain could explain why some peripheral neuropathies are painful and others are not.
In Stiff Person Syndrome (SPS) one’s muscles can instantaneously lock up – causing a person to suddenly fall over. People with SPS often experience severe muscle spasms and muscle stiffness so severe they have trouble moving. It’s an intriguing illness given the stiff muscles often found in fibromyalgia.
Stiff Person Syndrome
Deficient GABA signaling in the spinal cords of SPS patients leaves the motor system of the brain turned on – causing the muscles to go into spasm. SPS is an example of a pain disorder caused mostly by problems in the brain and spinal cord.
SPS appears to be largely caused by high levels of autoantibodies (GAD 65) to an enzyme involved in synthesizing GABA. This autoantibody, intriguingly enough, may underlie a wide variety neurological, metabolic and neuropsychiatric conditions that have been linked with GABA inhibition, including some speculate, fibromyalgia and ME/CFS.
* Peripheral Neuropathy – Peripheral neuropathy causes of the numbness, tingling and other nerve sensations common in FM and many other disorders. It has recently been associated with autoantibody attack of structures in the peripheral nerves called nodes of Ranvier.
* Complex Regional Pain Syndrome – Autoantibodies to autonomic nervous system receptors in subset of patients with complex regional pain syndrome (CRPS) implicate autoimmunity in this disorder as well.
Some of the most exciting pain research, however, concerns the work on ion channels. Sommer called the findings on voltage-gated sodium and TRP channels, “eye-openers” that could go a long way to explain mysterious cases of pain sensitization. These are small ion channels found on nerves that determine whether they get turned on or not. A mutation in one of these channels (channelopathy) could be sufficient to send pain-producing nerves into a frenzy.
Another possibility are microRNA’s that turn on or off genes associated with these channels. Sommer is currently involved in a large European study examining the effects mRNA’s may have on people in chronic pain.