Woolf C J
Nature. 1983;306(5944):686-8. doi: 10.1038/306686a0.
Noxious skin stimuli which are sufficiently intense to produce tissue injury, characteristically generate prolonged post-stimulus sensory disturbances that include continuing pain, an increased sensitivity to noxious stimuli and pain following innocuous stimuli. This could result from either a reduction in the thresholds of skin nociceptors (sensitization) or an increase in the excitability of the central nervous system so that normal inputs now evoke exaggerated responses. Because sensitization of peripheral receptors occurs following injury, a peripheral mechanism is widely held to be responsible for post-injury hypersensitivity. To investigate this I have now developed an animal model where changes occur in the threshold and responsiveness of the flexor reflex following peripheral injury that are analogous to the sensory changes found in man. Electrophysiological analysis of the injury-induced increase in excitability of the flexion reflex shows that it in part arises from changes in the activity of the spinal cord. The long-term consequences of noxious stimuli result, therefore, from central as well as from peripheral changes.
强度足以造成组织损伤的有害皮肤刺激，其特征是会产生刺激后持续的感觉障碍，包括持续性疼痛、对有害刺激的敏感性增加以及无害刺激后出现疼痛。这可能是由于皮肤伤害感受器的阈值降低（致敏），或者是中枢神经系统的兴奋性增加，使得正常输入现在引发夸张的反应。由于外周感受器在损伤后会发生致敏，人们普遍认为外周机制是损伤后超敏反应的原因。为了对此进行研究，我现在建立了一种动物模型，在外周损伤后，屈肌反射的阈值和反应性会发生变化，这与在人类身上发现的感觉变化类似。对损伤引起的屈肌反射兴奋性增加进行电生理分析表明，它部分源于脊髓活动的变化。因此，有害刺激的长期后果是由中枢和外周的变化共同导致的。
