Abstract
Fibromyalgia is a common, disabling syndrome that includes chronic widespread pain plus diverse additional symptoms. No specific objective abnormalities have been identified, which precludes definitive testing, disease-modifying treatments, and identification of causes. In contrast, small-fiber polyneuropathy (SFPN), despite causing similar symptoms, is definitionally a disease caused by the dysfunction and degeneration of peripheral small-fiber neurons. SFPN has established causes, some diagnosable and definitively treatable, eg, diabetes. To evaluate the hypothesis that some patients labeled as having fibromyalgia have unrecognized SFPN that is causing their illness symptoms, we analyzed SFPN-associated symptoms, neurological examinations, and pathological and physiological markers in 27 patients with fibromyalgia and in 30 matched normal controls. Patients with fibromyalgia had to satisfy the 2010 American College of Rheumatology criteria plus present evidence of a physician’s actual diagnosis of fibromyalgia. The study’s instruments comprised the Michigan Neuropathy Screening Instrument (MNSI), the Utah Early Neuropathy Scale (UENS), distal-leg neurodiagnostic skin biopsies, plus autonomic-function testing (AFT). We found that 41% of skin biopsies from subjects with fibromyalgia vs 3% of biopsies from control subjects were diagnostic for SFPN, and MNSI and UENS scores were higher in patients with fibromyalgia than in control subjects (all P⩽0.001). Abnormal AFTs were equally prevalent, suggesting that fibromyalgia-associated SFPN is primarily somatic. Blood tests from subjects with fibromyalgia and SFPN-diagnostic skin biopsies provided insights into causes. All glucose tolerance tests were normal, but 8 subjects had dysimmune markers, 2 had hepatitis C serologies, and 1 family had apparent genetic causality. These findings suggest that some patients with chronic pain labeled as fibromyalgia have unrecognized SFPN, a distinct disease that can be tested for objectively and sometimes treated definitively.
Highlights
Fibromyalgia syndrome (FMS) is a collection of ill-defined symptoms that includes chronic widespread pain (CWP; defined as ≥ 3 months of axial, plus left- and right-side, plus upperand lower-body pain [51])
Respondents were telephonescreened for inclusion, medical records confirming prior FMS diagnoses were obtained, and all eligible respondents were invited for study (Figure 1)
The mean mental component scores (MCS) score among FMS subjects (40.2) was very similar to MCS scores reported from larger FMS cohorts (38.6, 43.1), but their PCS scores (35.6) were less abnormal (28.0, 29.6), suggesting that the current sample may have had slightly less physical disability than historical FMS cohorts
Summary
Fibromyalgia syndrome (FMS) is a collection of ill-defined symptoms that includes chronic widespread pain (CWP; defined as ≥ 3 months of axial, plus left- and right-side, plus upperand lower-body pain [51]). Small-fiber polyneuropathy (SFPN) is a neurological cause of CWP. Unlike FMS, SFPN has identifiable pathology, physiology, and causes, and is definitionally a disease. SFPN is caused by dysfunction and degeneration of the small-diameter unmyelinated (C-fibers) and thinly myelinated (A-delta) peripheral axons that mediate nociception. Symptoms usually begin distally with foot or leg pain, but advanced cases spread proximally to involve the torso as well. Occasional patients begin with patchy, proximal, or generalized (non-lengthdependent) symptoms caused by attack directed at the neuronal cell-bodies
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