Kosek E, Ekholm J, Hansson P
Department of Rehabilitation Medicine, Karolinska Hospital/Institute, Stockholm, Sweden.
Pain. 1996 Dec;68(2-3):375-83. doi: 10.1016/s0304-3959(96)03188-0.
This study, addressing etiologic and pathogenic aspects of fibromyalgia (FM), aimed at examining whether sensory abnormalities in FM patients are generalized or confined to areas with spontaneous pain. Ten female FM patients and 10 healthy, age-matched females participated. The patients were asked to rate the intensity of ongoing pain using a visual analogue scale (VAS) at the site of maximal pain, the homologous contralateral site and two homologous sites with no or minimal pain. Quantitative sensory testing was performed for assessment of perception thresholds in these four sites. Von Frey filaments were used to test low-threshold mechanoreceptive function. Pressure pain sensitivity was assessed with a pressure algometer and thermal sensitivity with a Thermotest. In addition the stimulus-response curve of pain intensity as a function of graded nociceptive heat stimulation was studied at the site of maximal pain and at the homologous contralateral site. FM patients had increased sensitivity to non-painful warmth (P < 0.01) over painful sites and a tendency to increased sensitivity to non-painful cold (P < 0.06) at all sites compared to controls, but there was no difference between groups regarding tactile perception thresholds. Compared to controls, patients demonstrated increased sensitivity to pressure pain (P < 0.001), cold pain (P < 0.001) and heat pain (P < 0.02) over all tested sites. The stimulus-response curve was parallely shifted to the left of the curve obtained from controls (P < 0.003). Intragroup comparisons showed that patients had increased sensitivity to pressure pain (P < 0.01) and light touch (P < 0.05) in the site of maximal pain compared to the homologous contralateral site. These findings could be explained in terms of sensitization of primary afferent pathways or as a dysfunction of endogenous systems modulating afferent activity. However, the generalized increase in sensitivity found in FM patients was unrelated to spontaneous pain and thus most likely due to a central nervous system (CNS) dysfunction. The additional hyperphenomena related to spontaneous pain are probably dependent on disinhibition/facilitation of nociceptive afferent input from normal (or ischemic) muscles.
本研究针对纤维肌痛（FM）的病因和发病机制，旨在探讨FM患者的感觉异常是全身性的还是局限于有自发痛的区域。10名女性FM患者和10名年龄匹配的健康女性参与了研究。要求患者使用视觉模拟量表（VAS）对最大疼痛部位、对侧同源部位以及两个无疼痛或疼痛轻微的同源部位的持续疼痛强度进行评分。对这四个部位进行定量感觉测试以评估感觉阈值。使用von Frey细丝测试低阈值机械感受功能。用压力痛觉计评估压力痛敏感性，用热敏测试评估热敏感性。此外，还研究了最大疼痛部位和对侧同源部位疼痛强度作为分级伤害性热刺激函数的刺激-反应曲线。与对照组相比，FM患者在疼痛部位对非疼痛性温热的敏感性增加（P < 0.01），在所有部位对非疼痛性寒冷的敏感性有增加趋势（P < 0.06），但两组在触觉感觉阈值方面无差异。与对照组相比，患者在所有测试部位对压力痛（P < 0.001）、冷痛（P < 0.001）和热痛（P < 0.02）的敏感性增加。刺激-反应曲线平行向左移动至对照组曲线的左侧（P < 0.003）。组内比较显示，与对侧同源部位相比，患者在最大疼痛部位对压力痛（P < 0.01）和轻触觉（P < 0.05）的敏感性增加。这些发现可以用初级传入通路的敏化或调节传入活动的内源性系统功能障碍来解释。然而，FM患者中发现的全身性敏感性增加与自发痛无关，因此很可能是由于中枢神经系统（CNS）功能障碍。与自发痛相关的额外异常现象可能取决于来自正常（或缺血）肌肉的伤害性传入输入的去抑制/易化。
