Secondary hyperalgesia to punctate mechanical stimuli - Central sensitization to A-fibre nociceptor input
Secondary hyperalgesia to punctate mechanical stimuli - Central sensitization to A-fibre nociceptor input
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DOI：
10.1093/brain/122.12.2245
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发表时间：
1999-12-01
期刊：
影响因子：
14.5
通讯作者：
Treede, RD
中科院分区：
文献类型：
--
作者：
Ziegler, EA;Magerl, W;Treede, RD
组织损伤会导致邻近未受伤皮肤对轻触和点状刺激的疼痛感增强（继发性痛觉过敏）。对轻触的痛觉过敏（异常性疼痛）是由 A 纤维低阈值机械感受器介导的，而对点状刺激的痛觉过敏可能是由 A 纤维或 C 纤维伤害感受器介导的。为了揭示 A 纤维和 C 纤维对点状刺激痛觉过敏的相对贡献，对 9 名健康受试者的手腕施加压力，阻断桡浅神经。通过皮内注射40μg辣椒素诱导继发性痛觉过敏，并用200μm直径的探针(35-407mN)测试邻近皮肤的疼痛敏感性。通过触摸、冷、热和首次疼痛检测以及复合感觉神经动作电位来监测传导阻滞的进展。当A纤维传导完全阻断而C纤维传导完全完好时，点状刺激的刺痛减轻75%，但辣椒素注射的灼痛保持不变。在没有 A 纤维阻断的正常皮肤中，在相邻的辣椒素注射后，点状探针的疼痛等级显着增加了两倍。相比之下，当 A 纤维传导被选择性阻断时，注射辣椒素后点状探针的疼痛等级并未增加。然而，在块释放后，当 A 纤维传导恢复正常时，可以立即检测到对点状刺激的痛觉过敏。总之，点状刺激引起的刺痛主要是由 A 纤维伤害感受器介导的。在继发性痛觉过敏中，调节 C 纤维输入可异质突触促进该通路。因此，对点状刺激的继发性痛觉过敏是由伤害性 C 纤维放电引起的，但由伤害性 A 纤维介导。
Tissue injury induces enhanced pain sensation to light touch and punctate stimuli in adjacent, uninjured skin (secondary hyperalgesia). Whereas hyperalgesia to light touch (allodynia) is mediated by A-fibre low-threshold mechanoreceptors, hyperalgesia to punctate stimuli may be mediated by A- or C-fibre nociceptors. To disclose the relative contributions of A- and C-fibres to the hyperalgesia to punctate stimuli, the superficial radial nerve was blocked by pressure at the wrist in nine healthy subjects. Secondary hyperalgesia was induced by intradermal injection of 40 mu g capsaicin, and pain sensitivity in adjacent skin was tested with 200 mu m diameter probes (35-407 mN). The progress of conduction blockade was monitored by touch, cold, warm and first pain detection and by compound sensory nerve action potential. When A-fibre conduction was blocked completely but C-fibre conduction was fully intact, pricking pain to punctate stimuli was reduced by 75%, but burning pain to capsaicin injection remained unchanged. In normal skin without A-fibre blockade, pain ratings to the punctate probes increased significantly by a factor of two after adjacent capsaicin injection. In contrast, pain ratings to the punctate probes were not increased after capsaicin injection when A-fibre conduction was selectively blocked. However, hyperalgesia to punctate stimuli was detectable immediately after block release, when A-fibre conduction returned to normal. In conclusion, the pricking pain to punctate stimuli is predominantly mediated by A-fibre nociceptors. In secondary hyperalgesia, this pathway is heterosynaptically facilitated by conditioning C-fibre input. Thus, secondary hyperalgesia to punctate stimuli is induced by nociceptive C-fibre discharge but mediated by nociceptive A-fibres.