Mense S
Institut für Anatomie und Zellbiologie, Heidelberg, Germany.
Z Rheumatol. 1998;57 Suppl 2:23-6. doi: 10.1007/s003930050229.
The hypothesis is discussed that a dysfunction of the descending antinociceptive system may underly the pain of fibromyalgia. Data from animal experimentation show that an interruption of the system by spinal cord cooling leads to (1) increase in ongoing activity, (2) lowering in stimulation threshold, and (3) increase in response magnitude in nociceptive dorsal horn neurons. The influence of the descending system was stronger on the responses to input from deep nociceptors than to input from cutaneous nociceptors. If similar changes occur also in patients, an impairment of the tonicly active descending system should be followed by (1) spontaneous pain (ongoing activity), (2) tenderness (lowering in mechanical threshold), and (3) hyperalgesia (increased responses to noxious stimuli). These changes should affect mainly deep pain, because the antinociceptive system influences predominantly input from deep nociceptors.
有一种假说认为,下行抗伤害感受系统功能障碍可能是纤维肌痛疼痛的基础。动物实验数据表明,脊髓冷却导致该系统中断会引起:(1)持续活动增加;(2)刺激阈值降低;(3)伤害性背角神经元反应幅度增加。下行系统对来自深部伤害感受器输入的反应影响比对来自皮肤伤害感受器输入的反应影响更强。如果患者也出现类似变化,那么持续活跃的下行系统受损后应会出现:(1)自发痛(持续活动);(2)压痛(机械阈值降低);(3)痛觉过敏(对伤害性刺激反应增加)。这些变化应主要影响深部疼痛,因为抗伤害感受系统主要影响来自深部伤害感受器的输入。