Central sensitization: a generator of pain hypersensitivity by central neural plasticity.
Central sensitization: a generator of pain hypersensitivity by central neural plasticity.
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DOI：
10.1016/j.jpain.2009.06.012
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发表时间：
2009-09
期刊：
影响因子：
--
通讯作者：
Woolf CJ
中科院分区：
文献类型：
--
作者：
Latremoliere A;Woolf CJ
中枢致敏表示由膜兴奋性和突触功效增加以及抑制减少引起的伤害性通路中神经元和回路功能的增强，并且是体感神经系统响应于活动、炎症和神经损伤的显著可塑性的表现。中枢致敏的净效应是将先前的阈下突触输入募集到伤害性神经元，产生增加或增强的动作电位输出：易化、增强、增强或放大的状态。中枢致敏是造成急性和慢性临床疼痛环境中疼痛敏感性的许多时间、空间和阈值变化的原因，并阐明了中枢神经系统对疼痛超敏反应产生的根本贡献。由于中枢敏化是由中枢神经系统中神经元性质的变化引起的，因此疼痛不再像急性伤害性疼痛那样与有害的外周刺激的存在、强度或持续时间相耦合。相反，中枢致敏通过改变正常输入（包括通常引起无害感觉的输入）引起的感觉反应来产生疼痛超敏反应。在这篇文章中，我们回顾了主要的触发器，启动和维持中央敏化在健康个体的伤害感受器输入和炎症性和神经性疼痛患者，强调的基本贡献和多种机制的突触可塑性引起的变化的密度，性质和性质的离子型和代谢型谷氨酸受体。
Central sensitization represents an enhancement in the function of neurons and circuits in nociceptive pathways caused by increases in membrane excitability and synaptic efficacy as well as to reduced inhibition and is a manifestation of the remarkable plasticity of the somatosensory nervous system in response to activity, inflammation, and neural injury. The net effect of central sensitization is to recruit previously subthreshold synaptic inputs to nociceptive neurons, generating an increased or augmented action potential output: a state of facilitation, potentiation, augmentation, or amplification. Central sensitization is responsible for many of the temporal, spatial, and threshold changes in pain sensibility in acute and chronic clinical pain settings and exemplifies the fundamental contribution of the central nervous system to the generation of pain hypersensitivity. Because central sensitization results from changes in the properties of neurons in the central nervous system, the pain is no longer coupled, as acute nociceptive pain is, to the presence, intensity, or duration of noxious peripheral stimuli. Instead, central sensitization produces pain hypersensitivity by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations. In this article, we review the major triggers that initiate and maintain central sensitization in healthy individuals in response to nociceptor input and in patients with inflammatory and neuropathic pain, emphasizing the fundamental contribution and multiple mechanisms of synaptic plasticity caused by changes in the density, nature, and properties of ionotropic and metabotropic glutamate receptors.
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