Culp W J, Ochoa J, Cline M, Dotson R
Department of Biochemistry, Dartmouth Medical School, Hanover, New Hampshire.
Brain. 1989 Oct;112 ( Pt 5):1317-31. doi: 10.1093/brain/112.5.1317.
Quantitative thermal and mechanical algometry was studied in 4 human subjects exposed to various concentrations of capsaicin administered topically to the skin of the palm or forearm. Treated skin patches were assessed for changes in heat pain threshold and in mechanical pain threshold at various controlled temperatures. The results showed that: (1) in addition to heat hyperalgesia, capsaicin consistently induces overt mechanical hyperalgesia; (2) thermal and mechanical hyperalgesias are linearly dependent on the log of capsaicin dose; (3) mechanical hyperalgesia is increased by increasing skin temperature; (4) mechanical hyperalgesia is abolished by cooling the skin to a point about 10 degrees C below the threshold for heat pain, a temperature that does not impair touch or sharp pain sensation. These sensory effects of capsaicin are mediated by C fibres, since dissociated A fibre block established by compression-ischaemia does not abolish either spontaneous pain or mechanical hyperalgesia. In addition, abolition of mechanical hyperalgesia by cooling persists during A fibre block. Cooling thus appears to act directly, presumably decreasing hyperexcitability of the C nociceptor. Hyperalgesia is also transiently depressed for at least 30 min during the postischaemic period, well beyond the duration of paraesthesiae or overt hyperaemia. Sensory changes identical to those induced experimentally by capsaicin have been observed in patients with a particular variety of neuropathic pain (ABC syndrome) and have been termed polymodal hyperalgesia and cross modality threshold modulation (Ochoa, 1986; Ochoa et al., 1987). Based on these overall observations, it is postulated here that the sensory abnormalities induced by capsaicin and those observed in this particular variety of patients relate to primary hyperalgesia and share a common mechanism in that the excitable receptor membrane of polymodal C nociceptors behaves as if it 'misreads' temperature.
对4名受试者进行了定量热和机械痛觉测定研究,这些受试者的手掌或前臂皮肤局部涂抹了不同浓度的辣椒素。在不同的可控温度下,对处理过的皮肤贴片进行热痛阈值和机械痛阈值变化的评估。结果表明:(1)除热痛觉过敏外,辣椒素始终会诱发明显的机械痛觉过敏;(2)热痛觉过敏和机械痛觉过敏与辣椒素剂量的对数呈线性相关;(3)机械痛觉过敏会随着皮肤温度升高而增强;(4)将皮肤冷却至比热痛阈值低约10摄氏度的温度时,机械痛觉过敏消失,该温度不会损害触觉或锐痛感觉。辣椒素的这些感觉效应由C纤维介导,因为通过压迫性缺血建立的A纤维分离阻滞并不能消除自发痛或机械痛觉过敏。此外,在A纤维阻滞后,冷却对机械痛觉过敏的消除作用仍然存在。因此,冷却似乎直接起作用,可能是降低了C伤害感受器的兴奋性。在缺血后时期,痛觉过敏也会暂时降低至少30分钟,远远超过感觉异常或明显充血的持续时间。在患有特定类型神经病理性疼痛(ABC综合征)的患者中,观察到了与辣椒素实验诱导的感觉变化相同的情况,这些变化被称为多模式痛觉过敏和跨模式阈值调制(奥乔亚,1986年;奥乔亚等人,1987年)。基于这些总体观察结果,本文推测辣椒素诱导的感觉异常与该特定类型患者中观察到的异常与原发性痛觉过敏有关,并且有一个共同机制,即多模式C伤害感受器的可兴奋受体膜表现得好像它“误读”了温度。