Plaghki L, Bragard D, Le Bars D, Willer J C, Godfraind J M
Faculté de Médecine, Université Catholique de Louvain, B-1200 Brussels, Belgium.
J Neurophysiol. 1998 May;79(5):2557-67. doi: 10.1152/jn.1998.79.5.2557.
Electromyographic recordings were made in healthy volunteers from the knee-flexor biceps femoris muscle of the nociceptive RIII reflex elicited by electrical stimulation of the cutaneous sural nerve. The stimulus intensity was adjusted to produce a moderate pricking-pain sensation. The test responses were conditioned by a nonnoxious thermal (</=40 degrees C) stimulus applied to the receptive field of the sural nerve. This stimulus was delivered by a CO2 laser stimulator and consisted of a 100-ms pulse of heat with a beam diameter of 20 mm. Its power was 22.7 +/- 4.2 W (7.2 mJ/mm2), and it produced a sensation of warmth. The maximum surface temperature reached at the end of the period of stimulation was calculated to be 7 degrees C above the actual reference temperature of the skin (32 degrees C). The interval between the laser (conditioning) and electrical (test) stimuli was varied from 50 to 3, 000 ms in steps of 50 ms. It was found that the nociceptive flexion reflex was facilitated by the thermal stimulus; this modulation occurred with particular conditioning-test intervals, which peaked at 500 and 1,100 ms with an additional late, long-lasting phase between 1,600 and 2,300 ms. It was calculated that the conduction velocities of the cutaneous afferent fibers responsible for facilitating the RIII reflex, fell into three ranges: one corresponding to A delta fibers (3.2 m/s) and two in the C fiber range (1.3 and 0.7 m/s). It is concluded that information emanating from warm receptors and nociceptors converges. In this respect, the present data show, for the first time, that in man, conditioning nonnociceptive warm thermoreceptive A delta and C fibers results in an interaction at the spinal level with a nociceptive reflex. This interaction may constitute a useful means whereby signals add together to trigger flexion reflexes in defensive reactions and other basic motor behaviors. It also may contribute to hyperalgesia in inflammatory processes. The methodology used in this study appears to be a useful noninvasive tool for exploring the thermoalgesic mechanisms in both experimental and clinical situations.
在健康志愿者中,通过电刺激腓肠皮神经引发伤害性RIII反射,从股二头肌(膝部屈肌)记录肌电图。调整刺激强度以产生中度刺痛感。测试反应由施加于腓肠神经感受野的非伤害性热刺激(≤40摄氏度)调节。该刺激由二氧化碳激光刺激器发出,包括一个100毫秒的热脉冲,光束直径为20毫米。其功率为22.7±4.2瓦(7.2毫焦/平方毫米),产生温暖感。刺激期结束时达到的最高表面温度经计算比皮肤实际参考温度(32摄氏度)高7摄氏度。激光(调节)刺激和电(测试)刺激之间的间隔以50毫秒为步长,从50毫秒变化到3000毫秒。结果发现,热刺激促进了伤害性屈肌反射;这种调制发生在特定的调节 - 测试间隔,在500毫秒和1100毫秒时达到峰值,在1600毫秒和2300毫秒之间还有一个额外的晚期、持久阶段。经计算,负责促进RIII反射的皮肤传入纤维的传导速度分为三个范围:一个对应Aδ纤维(3.2米/秒),两个在C纤维范围内(1.3米/秒和0.7米/秒)。得出的结论是,来自温觉感受器和伤害感受器的信息会汇聚。在这方面,本研究数据首次表明,在人类中,调节非伤害性温热感受性Aδ和C纤维会在脊髓水平与伤害性反射产生相互作用。这种相互作用可能构成一种有用的方式,使信号相加,从而在防御反应和其他基本运动行为中触发屈肌反射。它也可能导致炎症过程中的痛觉过敏。本研究中使用的方法似乎是一种在实验和临床情况下探索热痛觉机制的有用的非侵入性工具。