Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA Department of Pathology (Neuropathology), Massachusetts General Hospital, Boston, MA, USA.
Pain. 2013 Nov;154(11):2310-2316. doi: 10.1016/j.pain.2013.06.001. Epub 2013 Jun 5.
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.
纤维肌痛是一种常见的、使人丧失能力的综合征，包括慢性广泛疼痛以及多种其他症状。没有发现特定的客观异常，这排除了明确的测试、疾病修饰治疗和病因识别。相比之下，小纤维神经病（SFPN），尽管引起类似的症状，但从定义上讲是一种由周围小纤维神经元功能障碍和退化引起的疾病。SFPN 有明确的病因，有些可诊断且可明确治疗，例如糖尿病。为了评估一些被标记为患有纤维肌痛的患者患有未被识别的 SFPN 导致其疾病症状的假设，我们分析了 27 名纤维肌痛患者和 30 名匹配的正常对照者的 SFPN 相关症状、神经检查以及病理和生理标志物。纤维肌痛患者必须符合 2010 年美国风湿病学会标准，并且有医生实际诊断纤维肌痛的证据。该研究的工具包括密歇根神经病筛查工具（MNSI）、犹他州早期神经病量表（UENS）、小腿远端神经诊断性皮肤活检以及自主功能测试（AFT）。我们发现，与对照组相比，纤维肌痛患者中有 41%的皮肤活检诊断为 SFPN，而对照组为 3%，纤维肌痛患者的 MNSI 和 UENS 评分高于对照组（均 P≤0.001）。异常 AFT 的发生率同样较高，这表明与纤维肌痛相关的 SFPN 主要是躯体性的。纤维肌痛患者和具有 SFPN 诊断性皮肤活检的血液测试提供了病因的见解。所有葡萄糖耐量试验均正常，但 8 例患者存在免疫失调标志物，2 例患者有丙型肝炎血清学，1 个家族存在明显的遗传病因。这些发现表明，一些被标记为慢性疼痛的纤维肌痛患者患有未被识别的 SFPN，这是一种可以客观检测并且有时可以明确治疗的疾病。
