Bouhassira D
INSERM U 161, Paris.
Cah Anesthesiol. 1994;42(6):689-97.
Animals studies have shown that peripheral nerve lesions can induce secondary changes in the dorsal horn of the spinal cord. Histological changes include degeneration of both primary afferent terminals (transganglionic degeneration) and second order neurones (transsynaptic degeneration). Secondary regeneration phenomena associated with changes in the topographical organization of central terminals of primary afferents have also been described. Neurochemical changes include a decrease of the spinal content of some peptides normally released by primary afferent terminals (substance P, CGRP...), and the synthesis of peptides which are not normally synthetized by dorsal root ganglia cells (galanin, VIP, neuropeptida Y...). Functional changes suggesting a sensitization of spinal neurones (increased spontaneous activities, expansion of receptive fields size) have been reported. Such a central sensitization might depend on a reduction of segmental inhibitory controls and/or intracellular changes induced by the activation of NMDA receptors by excitatory amino acids released by primary afferents. Such central changes might explain some of the features of spontaneous and/or evoked pains (allodynia/hyperalgesia) associated with peripheral neuropathies in humans.
动物研究表明，周围神经损伤可诱发脊髓背角的继发性变化。组织学变化包括初级传入终末（跨节变性）和二级神经元（跨突触变性）的退变。还描述了与初级传入神经中枢终末的拓扑组织变化相关的继发性再生现象。神经化学变化包括初级传入终末正常释放的一些肽（P物质、降钙素基因相关肽……）的脊髓含量减少，以及背根神经节细胞通常不合成的肽（甘丙肽、血管活性肠肽、神经肽Y……）的合成。据报道，提示脊髓神经元敏化的功能变化（自发活动增加、感受野大小扩大）。这种中枢敏化可能取决于节段性抑制控制的降低和/或初级传入神经释放的兴奋性氨基酸激活NMDA受体引起的细胞内变化。这种中枢变化可能解释了人类与周围神经病变相关的一些自发和/或诱发疼痛（感觉异常/痛觉过敏）的特征。
