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The Journal of Neurophysiology Vol. 79 No. 5 May 1998,
pp. 2557-2567
Copyright ©1998 The American Physiological Society
1 Faculté de Médecine, Université Catholique de Louvain, B-1200 Brussels, Belgium; 2 Institut National de la Santé et de la Recherche Médicale U-161, 75014 Paris; and 3 Faculté de Médecine Pitié-Salpêtrière, Laboratoire de Neurophysiologie, 75634 Paris Cedex 13, France
Plaghki, Léon, Dominique Bragard, Daniel Le Bars, Jean-Claude Willer, and Jean-Marie Godfraind. Facilitation of a nociceptive flexion reflex in man by nonnoxious radiant heat produced by a laser. J. Neurophysiol. 79: 2557-2567, 1998. 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°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°C above the actual reference temperature of the skin (32°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
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
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.
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