Evidence of nerve damage in approximately half of patients with fibromyalgia

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Summary: It was found that about half of a small group of patients with fibromyalgia, a common syndrome that causes chronic pain and other symptoms, have nerve fiber damage to the skin and other evidence of a disease called small fiber polyneuropathy ( SFPN). Unlike fibromyalgia, SFPN has a clear pathology and is known to be caused by specific medical conditions, some of which can be treated and sometimes cured.

It was found that about half of a small group of patients with fibromyalgia, a common syndrome that causes chronic pain and other symptoms, have nerve fiber damage to the skin and other evidence of a disease called small fiber polyneuropathy (SFPN). . Unlike fibromyalgia, which has had no known causes and few effective treatments, SFPN has a clear pathology and is known to be caused by specific medical conditions, some of which can be treated and sometimes cured. The study by Massachusetts General Hospital (MGH) researchers will appear in the journal   PAIN   and will be published online.

“This provides some of the first objective evidence of a mechanism behind some cases of fibromyalgia, and the identification of an underlying cause is the first step towards the search for better treatments,” says Anne Louise Oaklander, MD, PhD, director of the Unit of Nervous Lesions at the MGH Department of Neurology and corresponding author of the Pain article.

The term fibromyalgia describes a series of symptoms, including widespread chronic pain, increased sensitivity to pressure and fatigue, which is believed to affect 1 to 5 percent of people in Western countries, and more often than not. women. While a diagnosis of fibromyalgia has been recognized by the National Institutes of Health and the American College of Rheumatology, its biological basis remains unknown. Fibromyalgia shares many symptoms with SFPN, a recognized cause of chronic widespread pain for which there are accepted objective tests.

Designed to investigate possible connections between the two conditions, the current study included 27 adult patients diagnosed with fibromyalgia and 30 healthy volunteers. Participants went through a battery of tests used to diagnose SFPN, including evaluations of neuropathy based on a physical examination and answers to a questionnaire, skin biopsies to evaluate the number of nerve fibers in the lower legs and function tests autonomic factors such as heart rate, blood pressure and sweating.

Questionnaires, exam evaluations, and skin biopsies found significant levels of neuropathy in patients with fibromyalgia, but not in the control group. Of the 27 patients with fibromyalgia, 13 had a marked reduction in nerve fiber density, abnormal autonomic function tests or both, indicating the presence of SFPN. Participants who met the criteria for SFPN also underwent blood tests to detect known causes of the disorder, and although none of them had results suggestive of diabetes, a common cause of SFPN, two were found to be infected with the virus. Hepatitis C, which can be treated successfully. and more than half had evidence of some type of immune system dysfunction.

“Until now, we have not had a good idea about what causes fibromyalgia, but now we have some patients’ tests, but not all of them. Fibromyalgia is too complex for a “one size fits all” explanation, says Oaklander, an associate professor of neurology at Harvard Medical School. “The next step of independent confirmation of our findings from other laboratories is already happening, and we must also follow those patients who did not meet the SFPN criteria to see if we can find other causes. Helping any of these people to receive definitive diagnoses and better treatment would be a great achievement. “