The consequences of pain in early life: injury-induced plasticity in developing pain pathways.
The consequences of pain in early life: injury-induced plasticity in developing pain pathways.
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DOI：
10.1111/ejn.12414
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发表时间：
2014-02
期刊：
影响因子：
--
通讯作者：
Fitzgerald M
中科院分区：
文献类型：
--
作者：
Schwaller F;Fitzgerald M
婴儿期的疼痛会影响晚年的疼痛反应，但人们对这种情况如何以及为什么会发生知之甚少。在这里，我们回顾了动物模型中伤害性通路的发育可塑性的证据，并讨论了这种可塑性背后的外周和中枢机制。经历过新生儿损伤的成年人在受影响的区域显示疼痛和损伤诱导的痛觉过敏增加，但轻度损伤也可在身体表面的其余部分诱导广泛的基线敏感性降低，这表明涉及几种潜在的机制，这取决于早期生活经历的类型。周围神经发芽和背角中央敏化，去抑制和神经免疫引发的讨论有关增加疼痛和痛觉过敏，而改变下降的疼痛控制系统驱动，在一定程度上，由应力/HPA轴的变化进行了讨论，在广泛的痛觉减退。最后，建议内源性大麻素系统值得进一步关注的机制，在婴儿和儿童的疼痛处理损伤引起的变化的搜索。
Pain in infancy influences pain reactivity in later life, but how and why this occurs is poorly understood. Here we review the evidence for developmental plasticity of nociceptive pathways in animal models and discuss the peripheral and central mechanisms that underlie this plasticity. Adults who have experienced neonatal injury display increased pain and injury-induced hyperalgesia in the affected region but mild injury can also induce widespread baseline hyposensitivity across the rest of the body surface, suggesting the involvement of several underlying mechanisms, depending upon the type of early life experience. Peripheral nerve sprouting and dorsal horn central sensitization, disinhibition and neuroimmune priming are discussed in relation to the increased pain and hyperalgesia, while altered descending pain control systems driven, in part, by changes in the stress/HPA axis are discussed in relation to the widespread hypoalgesia. Finally, it is proposed that the endocannabinoid system deserves further attention in the search for mechanisms underlying injury-induced changes in pain processing in infants and children.
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