Mense S
Institut für Anatomie und Zellbiologie, Heidelberg, Germany.
Scand J Rheumatol Suppl. 2000;113:24-9. doi: 10.1080/030097400446599.
In the spinal cord, long descending pathways are known to exist which modulate pain sensations by either inhibiting or facilitating the discharges of spinal nociceptive neurones. In this article, the hypothesis is discussed that the pain of fibromyalgia may be due to a dysfunction of these pain-modulating pathways. Theoretically, two kinds of disturbance could lead to pain, namely reduced activity in the pain-inhibiting (antinociceptive) system or increased activity in the pain-facilitating (pronociceptive) pathways. Data from animal experiments show that interruption of the dorsal descending systems leads to hyperactivity of spinal nociceptive neurones, namely increase in background activity, lowering in stimulation threshold, and increase in response magnitude to noxious stimuli. The responses of the neurones to input from nociceptors in deep tissues were more strongly inhibited by the descending pathways than were responses to input from cutaneous nociceptors. Collectively, the findings indicate that the dorsal descending systems are tonicly active and have a particularly strong inhibitory action on neurones that mediate pain from deep tissues. If these systems operate in a similar way also in patients, an impairment of their function is likely to lead to 1. spontaneous deep pain (because of an increased background activity in nociceptive neurones supplying deep tissues), 2. tenderness of deep tissues (because of a lowered mechanical threshold of the same neurones), and 3. hyperalgesia of deep tissues (because of increased neuronal responses to noxious stimuli). These changes will affect large areas of the body because the descending inhibitory systems have widespread terminations in the spinal cord. Thus, a dysfunction of the descending inhibitory pathways could mimick to a large extent the pain of fibromyalgia.
在脊髓中，已知存在长的下行通路，其通过抑制或促进脊髓伤害性神经元的放电来调节痛觉。在本文中，探讨了纤维肌痛的疼痛可能是由于这些疼痛调节通路功能障碍的假说。理论上，两种干扰可能导致疼痛，即疼痛抑制（抗伤害感受）系统活动减少或疼痛促进（促伤害感受）通路活动增加。动物实验数据表明，背侧下行系统中断会导致脊髓伤害性神经元活动亢进，即背景活动增加、刺激阈值降低以及对有害刺激的反应幅度增加。与对皮肤伤害感受器输入的反应相比，下行通路对神经元对深部组织伤害感受器输入的反应抑制作用更强。总体而言，这些发现表明背侧下行系统持续活跃，并且对介导深部组织疼痛的神经元具有特别强的抑制作用。如果这些系统在患者中也以类似方式运作，其功能受损可能导致：1. 自发性深部疼痛（由于供应深部组织的伤害性神经元背景活动增加），2. 深部组织压痛（由于同一神经元的机械阈值降低），以及3. 深部组织痛觉过敏（由于神经元对有害刺激的反应增加）。这些变化将影响身体的大片区域，因为下行抑制系统在脊髓中有广泛的终末。因此，下行抑制通路功能障碍在很大程度上可能模拟纤维肌痛的疼痛。
