BARCELONA – Many patients with fibromyalgia syndrome have an unusually low number of small-nerve fibers in their skin, a finding that may provide important new insights into the pathology, etiology, and possible treatment of what has been a poorly understood disorder, according to Dr. Claudia Sommer.
"With three different methods, we showed pathologic changes in small-nerve fibers" in the skin of patients diagnosed with fibromyalgia, she said at the annual congress of the European College of Neuropsychopharmacology. These somatic findings are too strong to allow classification of these patients with fibromyalgia as having a "somatoform pain disorder." She suggested that the nerve deficits in patients’ skin could reflect systemic nerve damage that causes the deep pain that fibromyalgia patients have in muscles, tendons, and joints. "What we see in the skin may also exist elsewhere," said Dr. Sommer, professor of neurology at the University Clinic of Würzburg (Germany).
Mitchel L. Zoler/IMNG Medical Media
Dr. Claudia Sommer
Three other, independent research groups have recently made similar findings of small-nerve deficits in the skin of fibromyalgia patients, including researchers at Massachusetts General Hospital in Boston (Pain 2013;154:2310-6), further boosting the likelihood that impaired small-nerve function is real and a key feature of at least some fibromyalgia patients, Dr. Sommer said.
The finding led her to develop a new model for the pathogenesis of these cases: An adverse life event or other predisposing factor leads to a more proinflammatory cytokine profile that causes small-nerve fiber damage and ongoing pain system activity that produces central sensitization and changes in central pain processing.
"This is just a model, but we can work on this and test hypotheses," she said. "We are a long way from finding new treatments, but trying to understand what causes damage to nerve fibers may give a start, something a new treatment could be directed against."
Dr. Sommer and her associates studied 25 patients who had been diagnosed with fibromyalgia, 10 diagnosed with unipolar depression, and 25 healthy controls who were matched by age and sex with the fibromyalgia patients. The participants ranged from 39 to 75 years old, and those with either depression or fibromyalgia had been diagnosed for an average of more than 20 years.
Compared with the controls, patients with fibromyalgia had significantly increased detection thresholds to warm and cold when quantitative sensory testing was used, while the depressed patients had no significant difference compared with the controls. Measurement of pain-related evoked potentials showed increased latency on stimulation of the feet and reduced amplitudes on stimulation of the feet, hands, and face in fibromyalgia patients compared with both the controls and the patients with depression.
The researchers also found reduced numbers of total and regenerating intraepidermal, unmyelinated nerve fibers in skin biopsies from the lower leg and upper thigh of the patients with fibromyalgia compared with the controls and the patients with depression. The nerve fiber count averaged 5 fibers/mm2 in the patients with fibromyalgia, about 7/mm2 in patients with depression, and about 8/mm2 in the controls. The difference between the fibromyalgia patients and the controls was statistically significant.
Dr. Sommer and her associates also published these results in Brain (2013;136:1857-67).
Dr. Sommer said she has received honoraria for being a speaker on behalf of Allergan, Astella, Baxter, CSL Behring, Eli Lilly, Genzyme, GlaxoSmithKline, and Pfizer.
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