PERIPHERAL NEURAL CORRELATES OF MAGNITUDE OF CUTANEOUS PAIN AND HYPERALGESIA - SIMULTANEOUS RECORDINGS IN HUMANS OF SENSORY JUDGMENTS OF PAIN AND EVOKED-RESPONSES IN NOCICEPTORS WITH C-FIBERS
PERIPHERAL NEURAL CORRELATES OF MAGNITUDE OF CUTANEOUS PAIN AND HYPERALGESIA - SIMULTANEOUS RECORDINGS IN HUMANS OF SENSORY JUDGMENTS OF PAIN AND EVOKED-RESPONSES IN NOCICEPTORS WITH C-FIBERS
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DOI：
10.1152/jn.1984.51.2.325
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发表时间：
1984-01-01
影响因子：
2.5
通讯作者：
ROBINSON, CJ
中科院分区：
文献类型：
--
作者：
TOREBJORK, HE;LAMOTTE, RH;ROBINSON, CJ
通过同时记录人体C机械热（CMH）伤害感受器的诱发反应和从相同受试者获得的疼痛幅度估计，研究了从正常皮肤和从轻度热损伤后的皮肤痛觉过敏引起的热痛的外周神经元相关性。受试者对由39 °-39 °的短持续时间刺激引起的疼痛进行连续的幅度评级。51.degree.在由50 ℃的条件刺激（CS）诱导的热损伤之前和之后的不同时间间隔，将C递送到小腿或脚的多毛皮肤。C，100 s或48 ℃。C，360度。用热电极按压伤害感受器的感受野来施加刺激。对于正常皮肤、未受伤皮肤的热刺激，在9名受试者的14个实验中，疼痛阈值的范围为41 ° C。到49度。而14种CMH伤害感受器中的大多数的反应阈值为41 ° C。C（2例，43 ° C）。C）。在痛阈时，来自许多伤害感受器的输入的空间总和是必要的。通过将每个刺激诱发的神经冲动的总数与刺激温度相关联来获得每个CMH的强度响应函数。通过将由每个刺激引起的疼痛的最大等级与刺激温度相关联来获得疼痛的相应幅度缩放函数。当计算所有14次测试的平均值时，在45 °范围内，CMH中引起的平均脉冲数与疼痛中位数评级之间存在接近线性的关系。51.degree. C.热痛感觉的大小与CMH伤害感受器群体中的反应大小的关系比任何单个伤害感受器中的关系更密切。在CS后0.5分钟，大多数受试者的痛阈升高，阈上刺激引起的疼痛的幅度评级低于前CS值（痛觉减退）。大多数CMH的阈值增加和反应降低（疲劳）也出现了相应的变化。CS后5-10 min，大多数受试者的痛阈较低，阈上刺激的幅度评级大于CS前值（痛觉过敏）。CS后CMH对热反应的变化是不均匀的。这些差异可能是由于疲劳和/或致痛物质的不同敏感性的相互作用。CS后，疼痛的中值幅度评级不再线性相关的平均数的脉冲在CMH作为一个函数的刺激温度，和平均CMH反应CS后的增加不完全成比例的增加幅度评级的疼痛在每个刺激温度。CMH伤害性感受器在正常皮肤和由轻度热损伤引起的痛觉过敏的皮肤中均有助于痛觉。虽然痛觉过敏的程度不能完全由CMH伤害感受器中的热敏化的程度来解释，但很明显，CMH伤害感受器的敏化对痛觉过敏的发展提供了实质性的贡献。
The peripheral neuronal correlates of heat pain elicited from normal skin and from skin made hyperalgesic following a mild heat injury were studied by simultaneously recording, in humans, evoked responses in C mechanoheat (CMH) nociceptors and the magnitude estimations of pain obtained from the same subjects. Subjects made continuous magnitude ratings of pain elicited by short-duration stimuli of 39.degree.-51.degree. C delivered to the hairy skin of the calf or foot before and at varying intervals of time after a heat injury induced by a conditioning stimulus (CS) of 50.degree. C, 100 s or 48.degree. C, 360 s. The stimuli were applied with a thermode pressed against the nociceptor''s receptive field. For heat stimulations of normal skin, uninjured skin, pain thresholds in 14 experiments with 9 subjects ranged from 41.degree. to 49.degree. C, whereas response thresholds for most of the 14 CMH nociceptors were 41.degree. C (in 2 cases, 43.degree. C). Spatial summation of input from many nociceptors was necessary at pain threshold. An intensity-response function was obtained for each CMH by relating the total number of nerve impulses evoked per stimulus to stimulus temperature. A corresponding magnitude scaling function for pain was obtained by relating the maximum rating of pain elicited by each stimulus to stimulus temperature. When averages were computed for all 14 tests, there was a near linear relationship between the mean number of impulses elicited in the CMH and the median ratings of pain, over the range of 45.degree.-51.degree. C. The magnitude of heat pain sensation was more closely related to the magnitude of response in a population of CMH nociceptors than in any individual nociceptor. At 0.5 min after the CS, the pain thresholds of most subjects were elevated, and the magnitude ratings of pain elicited by suprathreshold stimuli were lower than pre-CS values (hypoalgesia). Corresponding changes were seen in the increased thresholds and decreased responses (fatigue) of most CMH. By 5-10 min after the CS, the pain thresholds of most subjects were lower, and their magnitude ratings of suprathreshold stimuli were greater than pre-CS values (hyperalgesia). The changes in CMH responses to heat after the CS were not uniform. These differences were possibly due to the interaction of fatigue and/or different sensitivities to algogenic substances. After the CS, the median magnitude rating of pain was no longer linearly related to the mean number of impulses in CMH as a function of stimulus temperature, and the increases in mean CMH response following the CS were not in exact proportion to the increases in magnitude ratings of pain at each stimulus temperature. CMH nociceptors contribute to pain sensation in both normal skin and skin made hyperalgesic by a mild heat injury. Although the magnitude of hyperalgesia could not be fully accounted for by the magnitude of heat sensitization in CMH nociceptors, it is clear that the sensitization of CMH nociceptors provides a substantial contribution to the development of hyperalgesia.