Because the most common symptoms of fibromyalgia involve pain and problems with motor control, the prevailing view is that dysfunction in the nervous system causes the disease. But a study published Thursday (July 1) in The Journal of Clinical Investigation suggests the disease may actually be caused by antibodies that interact with the nervous system.
“The widespread paradigm at the moment is that this is a disease that emanates from the brain,” lead author David Andersson of King’s College London tells The Guardian. “I think our findings suggest that that’s not the case.”
Fibromyalgia syndrome (FMS) is a painful and poorly understood chronic illness that causes widespread pain, emotional distress, fatigue, and brain fog. The Centers for Disease Control and Prevention estimates that it affects at least 2 percent of the adult population in the US, and according to The Guardian, 80 percent of those affected are women. Current treatments center around gentle exercise, stress reduction, and pain-relieving drugs, but many patients still suffer from the effects of the disease.
Andersson and his colleagues isolated circulating antibodies from 44 FMS patients in the United Kingdom and Sweden, and then injected those antibodies into mice. Those mice became more sensitive to pain and cold compared with mice who received antibodies from healthy controls.
And the mice receiving antibodies from the FMS patients didn’t just develop sensory issues. They also developed other hallmarks of FMS, including reduced grip strength, decreased locomotor activity, and reduced nerve fiber density in the skin. The symptoms went away after a few weeks, when the animals' bodies cleared the antibodies.
When the researchers depleted a subset of antibodies, called IgG, from the samples before injection, the mice lost the FMS-like symptoms, suggesting that IgG antibodies were responsible for causing those symptoms.
The researchers also found that when pain receptors, called nociceptors, from FMS IgG-treated mice were stimulated in vitro, they were more sensitive than the receptors from the control mice, and that the IgG was able to bind to cells in the dorsal root ganglion—a bundle of nerves in the spine that includes sensory neurons—in both mouse and human samples. That suggests that by interacting with the nervous system, the antibodies could be promoting some of the painful symptoms associated with FMS, the authors write in their study.
“The next step will be to identify what factors the symptom-inducing antibodies bind to,” says coauthor Camilla Svensson of the Karolinska Institute in a press release. “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.”
Des Quinn, the chair of Fibromyalgia Action UK, tells The Guardian that researchers have often debated whether fibromyalgia is an autoimmune disease, and that the results of this study add to that discussion. “If these results can be replicated and expanded upon, then the prospect of a new treatment for people with fibromyalgia would be extraordinary,” he says. “However, the results need further confirmation and investigation before the outcomes can be applied universally.”