Peripheral Input and Its Importance for Central Sensitization
Peripheral Input and Its Importance for Central Sensitization
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DOI：
10.1002/ana.24017
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发表时间：
2013-11-01
影响因子：
11.2
通讯作者：
Dickenson, Anthony H.
中科院分区：
文献类型：
--
作者：
Baron, Ralf;Hans, Guy;Dickenson, Anthony H.
许多疼痛状态开始于外周组织和/或神经的损伤，导致脊髓内递质释放增强和中枢致敏。这种中枢敏感化的表现是发条效应和长时程增强。过度兴奋的脊髓神经元表现出降低的阈值，更大的诱发反应，增加的感受野大小，和正在进行的刺激非依赖性活动，这些变化可能是异常性疼痛，痛觉过敏，和自发性疼痛的患者。中枢敏感化通过来自外周的持续输入来维持，但也受到来自中脑和脑干的下行控制（抑制性和易化性）的调节。敏感的脊髓神经元向大脑的投射反过来又改变了高级中枢对疼痛信息的处理。几种机制有助于中枢敏感化。初级传入C纤维的重复激活导致伤害性传递的突触加强。它还可以诱导非伤害性A纤维和伤害性A纤维的易化，引起动态机械异常性疼痛和机械痛觉过敏。例如，在带状疱疹后神经痛和复杂区域疼痛综合征中，这些症状通过外周伤害性输入维持和调节。诊断中枢致敏可能特别困难。除了病史，定量感觉测试和功能性磁共振成像可能是有用的，但诊断标准，包括主观和客观的中央增强措施是必要的。越来越多的证据表明，需要使外周和中枢神经系统脱敏的治疗策略。这些通常应涉及多模式方法，以便治疗可以靶向中枢致敏的外周驱动因素和/或中枢后果。《神经病学年鉴》2013;74：630-636
Many pain states begin with damage to tissue and/or nerves in the periphery, leading to enhanced transmitter release within the spinal cord and central sensitization. Manifestations of this central sensitization are windup and long-term potentiation. Hyperexcitable spinal neurons show reduced thresholds, greater evoked responses, increased receptive field sizes, and ongoing stimulus-independent activity; these changes probably underlie the allodynia, hyperalgesia, and spontaneous pain seen in patients. Central sensitization is maintained by continuing input from the periphery, but also modulated by descending controls, both inhibitory and facilitatory, from the midbrain and brainstem. The projections of sensitized spinal neurons to the brain, in turn, alter the processing of painful messages by higher centers. Several mechanisms contribute to central sensitization. Repetitive activation of primary afferent C fibers leads to a synaptic strengthening of nociceptive transmission. It may also induce facilitation of non-nociceptive A fibers and nociceptive A fibers, giving rise to dynamic mechanical allodynia and mechanical hyperalgesia. In postherpetic neuralgia and complex regional pain syndrome, for example, these symptoms are maintained and modulated by peripheral nociceptive input. Diagnosing central sensitization can be particularly difficult. In addition to the medical history, quantitative sensory testing and functional magnetic resonance imaging may be useful, but diagnostic criteria that include both subjective and objective measures of central augmentation are needed. Mounting evidence indicates that treatment strategies that desensitize the peripheral and central nervous systems are required. These should generally involve a multimodal approach, so that therapies may target the peripheral drivers of central sensitization and/or the central consequences. Ann Neurol 2013;74:630-636