Abstract
Nociceptive flexion reflex represents an interesting objective method for investigating pain and the mechanism of antalgic treatments in man. This method is based, in fact, on the existence of a strong correlation between the threshold of RIII reflex and the subjective pain threshold. RIII reflex can be recorded from biceps femoris muscle and elicited by electrical stimulation of the ipsilateral sural nerve at the retromalleolar level. Several analgesic drugs (e.g. acetylsalicylic acid) or local anesthetics were able to increase the threshold of RIII reflex , but the most interesting findings concern the effect of morphine. This substance was found to depress in a dose-dependent fashion the nociceptive flexion reflex in normal subjects. Interestingly, this effect was also seen in spinal subjects, thus suggesting that morphine exerts its depressive effect by acting directly at spinal level. Similar results were obtained using dermorphin, a new potent opiate-like peptide and FK33-824, a synthetic enkephalin analogue.
More recently, serotoninergic influences on nociceptive flexion reflex were documented in man. Indalpine, a selective 5-HT uptake inhibitor, induced a significant naloxone reversible depression of both RIII threshold and subjective pain threshold. We observed similar findings using amitriptyline in migraine patients, even if the effect was not reversed by naloxone administration. Also ritanserin, a new very selective and potent serotonin-S antagonist, induced a significant inhibition of nociceptive reflex.
Finally, nociceptive flexion reflex was used to explore the mechanism involved in several antalgic techniques. A possible role of endogenous opioids in sustaining analgesia induced by transcutaneous electrical nerve stimulation (TENS) has been hypothesized. We observed a concomitant increase in RIII reflex threshold and plasma opioids levels following TENS. These data suggest that post-stimulation analgesia could be supported by enhancement of endogenous opioids system. Also acupuncture that is known to increase plasma opioids levels induced a significant inhibition of RIII reflex.
In conclusion, RIII reflex represents an interesting electrophysiological approach to the study of pain control system during antalgic treatments.
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