RELEASE OF COLD-INDUCED BURNING PAIN BY BLOCK OF COLD-SPECIFIC AFFERENT INPUT
RELEASE OF COLD-INDUCED BURNING PAIN BY BLOCK OF COLD-SPECIFIC AFFERENT INPUT
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DOI：
10.1093/brain/113.4.893
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发表时间：
1990-08-01
期刊：
影响因子：
14.5
通讯作者：
OCHOA, JL
中科院分区：
文献类型：
--
作者：
YARNITSKY, D;OCHOA, JL
虽然纯粹的冷感是由一组特定的传入通道激活引起的，但另外一组被认为是由引起冷痛的有害低温刺激激活的。在初级传入水平，与冷痛的冷部分相关的通道由有髓鞘的 A δ 冷特异性纤维服务，而与疼痛部分相关的通道由无髓鞘的 C 伤害感受器服务。在本研究中，通过选择性阻断有髓纤维的传导来研究导致冷痛的两种传入输入之间的相互作用。当这样做到消除冷感时，低温刺激的斜坡最终会引起第一感觉灼痛。除了这种质量变化之外，在施加有害低温刺激时，还记录到疼痛阈值显着降低（所需刺激能量减少）。低温引起的疼痛程度的这种夸大以及 A 纤维块对其燃烧质量的揭露意味着由于抑制性初级传入输入的去除而释放了中枢感觉传递。传递触觉、冷感或两者的有髓纤维发挥这种抑制作用。先前通过低温刺激抑制疼痛的证据表明，寒冷特异性输入通常对伤害感受器输入施加这种中枢门控。目前的结果也可能为感知寒冷能力受损的神经病患者出现冷暴露灼痛综合征提供解释。
While the pure sensation of cold is evoked by activation of a specific set of afferent channels, and additional set is believed to be activated by noxious low-temperature stimuli evoking cold pain. At primary afferent level, the channels concerned with the cold fraction of cold pain and served by myelinated A delta cold-specific fibres, whereas those occurred with the pain fraction are served by unmyelinated C nociceptors. In the present study, interaction between the two types of afferent input underlying cold pain was investigated by selectively blocking conduction in myelinated fibres. When doing so to the point of abolishing cold sensation, ramps of low-temperature stimuli eventually evoked a first sensation of burning pain. In addition to, and contemporaneous with, this change in quality, a significant decrease in pain threshold (reduction in required stimulus energy) was recorded when applying a noxious low-temperature stimulus. Such exaggeration in magnitude of low temperature-induced pain and the unmasking of its burning quality by A fibre block imply release of central sensory transmission due to removal of inhibitory primary afferent input. Myelinated fibres transmitting either tactile, cold sensation or both exert this inhibition. Previous evidence of suppression of pain by low-temperature stimuli indicates that is is the cold-specific input that normally exerts this central gating on nociceptor input. The present results may also offer and explanation for the occurrence of a syndrome of burning pain in cold exposure in neuropathic patients with impaired ability to perceive cold.