Painful sensation induced by a thermal cutaneous stimulus.
This review emphasizes how little we know about pain induced by a thermal stimulus. The study of the intensity of pain evoked by heat is relatively exhaustive: the influence of various local, stimulus-dependent or general factors upon threshold values has been well studied, as has the relation between pain and stimulus intensities. On the contrary, few studies have used very cold stimuli, since highly efficient stimulators allowing accurate control of the stimulus parameters have been obtainable only recently. Only the influence of stimulation area and stimulation rate on cold pain thresholds have been studied. Moreover, old results obtained on pain quality cannot be used since the conditions of stimulation were not specified or not controlled accurately. It is only known that stimulus duration and stimulation area are determinant for thermal pain quality. There is still much work to be done in this field. All the more so as this type of study is absolutely necessary for the understanding of pain mechanisms--it describes what must be explained by the function of the nervous system. We have seen that at the periphery the intensity of heat pain is coded by the response of polymodal nociceptors, mechanothermal nociceptors, thermal nociceptors and possibly by the paradoxical discharge of cold receptors. If the stimulus is lower than 45 degrees C the activity of certain heat receptors comes into play. Although we lack information which would allow confirmation of this as a fact it seems likely that the activity of polymodal nociceptors, cold mechanothermal nociceptors and possibly certain cold receptors sensitive to very low temperatures code cold pain. These nociceptive impulses carried by A delta and C fibers reach the dorsal horn of the spinal cord through the dorsal roots. They are notably at the origin of the activation of the neurons in Rexed's layers I, V and VIII which are to a large extent at the origin of the spinothalamic and spinoreticulothalamic tracks [21,115,168] moving in the anterolateral quadrant of the spinal cord. At supraspinal level, the thermal information reappears in the reticular formation; there it appears to be solely relative to the pain threshold and not to the intensity of a supraliminary stimulus [55]. In the posterior group of nuclei [134] and the ventroposterolateral nucleus of the thalamus [103], on the contrary, the activity of the neurons reflects the intensity of the stimulation. It has been proved that the neurons of the ventroposterolateral nucleus project onto the SI cortex [103].(ABSTRACT TRUNCATED AT 400 WORDS)
D000222:Adaptation, Physiological; D000818:Animals; D003080:Cold Temperature; D004056:Differential Threshold; D000882:Haplorhini; D006358:Hot Temperature / Q000009:adverse effects*; D008465:Mechanoreceptors / Q000503:physiopathology; D009619:Nociceptors / Q000503:physiopathology; D010146:Pain / Q000209:etiology / Q000503:physiopathology*; D051381:Rats; D012154:Reticular Formation / Q000503:physiopathology; D012684:Sensory Thresholds; D012867:Skin / Q000503:physiopathology; D013788:Thalamus / Q000503:physiopathology; D013997:Time Factors