OBJECTIVE: To test the hypothesis that peripheral C nociceptor function may be abnormal in fibromyalgia and that C nociceptor dysfunction may contribute to the symptoms reported by these patients. METHODS: Microneurography was used to record C nociceptors of 30 female patients meeting criteria for fibromyalgia and compared with recordings from 17 female patients with small-fiber neuropathy and 9 female controls. RESULTS: We obtained stable recordings of 186 C nociceptors in the fibromyalgia group, 114 from small-fiber neuropathy patients, and 66 from controls. The mechanosensitive nociceptors in the fibromyalgia patients behaved normally, but the silent nociceptors in 76.6% of fibromyalgia patients exhibited abnormalities. Spontaneous activity was detected in 31% of silent nociceptors in fibromyalgia, 34% in small-fiber neuropathy, and 2.2% in controls. Sensitization to mechanical stimulation was found in 24.2% of silent nociceptors in fibromyalgia, 22.7% in small-fiber neuropathy, and 3.7% in controls. Abnormally high slowing of conduction velocity when first stimulated at 0.25Hz was more common in fibromyalgia. INTERPRETATION: We show for the first time that the majority of fibromyalgia patients have abnormal C nociceptors. Many silent nociceptors exhibit hyperexcitability resembling that in small-fiber neuropathy, but high activity-dependent slowing of conduction velocity is more common in fibromyalgia patients, and may constitute a distinguishing feature. We infer that abnormal peripheral C nociceptor ongoing activity and increased mechanical sensitivity could contribute to the pain and tenderness suffered by patients with fibromyalgia.
OBJECTIVE: To test the hypothesis that peripheral C nociceptor function may be abnormal in fibromyalgia and that C nociceptor dysfunction may contribute to the symptoms reported by these patients. METHODS: Microneurography was used to record C nociceptors of 30 female patients meeting criteria for fibromyalgia and compared with recordings from 17 female patients with small-fiber neuropathy and 9 female controls. RESULTS: We obtained stable recordings of 186 C nociceptors in the fibromyalgia group, 114 from small-fiber neuropathypatients, and 66 from controls. The mechanosensitive nociceptors in the fibromyalgiapatients behaved normally, but the silent nociceptors in 76.6% of fibromyalgiapatients exhibited abnormalities. Spontaneous activity was detected in 31% of silent nociceptors in fibromyalgia, 34% in small-fiber neuropathy, and 2.2% in controls. Sensitization to mechanical stimulation was found in 24.2% of silent nociceptors in fibromyalgia, 22.7% in small-fiber neuropathy, and 3.7% in controls. Abnormally high slowing of conduction velocity when first stimulated at 0.25Hz was more common in fibromyalgia. INTERPRETATION: We show for the first time that the majority of fibromyalgiapatients have abnormal C nociceptors. Many silent nociceptors exhibit hyperexcitability resembling that in small-fiber neuropathy, but high activity-dependent slowing of conduction velocity is more common in fibromyalgiapatients, and may constitute a distinguishing feature. We infer that abnormal peripheral C nociceptor ongoing activity and increased mechanical sensitivity could contribute to the pain and tenderness suffered by patients with fibromyalgia.
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Authors: Ann T Farrell; Julie Panepinto; C Patrick Carroll; Deepika S Darbari; Ankit A Desai; Allison A King; Robert J Adams; Tabitha D Barber; Amanda M Brandow; Michael R DeBaun; Manus J Donahue; Kalpna Gupta; Jane S Hankins; Michelle Kameka; Fenella J Kirkham; Harvey Luksenburg; Shirley Miller; Patricia Ann Oneal; David C Rees; Rosanna Setse; Vivien A Sheehan; John Strouse; Cheryl L Stucky; Ellen M Werner; John C Wood; William T Zempsky Journal: Blood Adv Date: 2019-12-10