Self-injurious behavior in neurodevelopmental disorders: relevance of nociceptive and immune mechanisms.
Self-injurious behavior in neurodevelopmental disorders: relevance of nociceptive and immune mechanisms.
复制标题
神经发育障碍中的自残行为：伤害感受和免疫机制的相关性。
DOI：
10.1016/j.neubiorev.2011.01.002
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发表时间：
2011
影响因子：
8.2
通讯作者：
Symons,FrankJ
中科院分区：
文献类型：
--
作者：
Symons,FrankJ
患有智力和相关神经发育障碍（IDD）的个体的自残行为（SIB）是一个临床挑战和科学难题。调节 SIB 感觉成分的生理机制仍然是一个谜，人们对潜在的病理生理学尚无明确的了解。关于一般感觉处理和疼痛（尤其是 IDD 和慢性 SIB 患者）的中心法则是，感觉处理减少，疼痛消失或减弱。本文回顾了最近的研究结果，挑战了有关 IDD 和 SIB 患者疼痛和感觉功能的一些传统观点。似乎至少有一部分 IDD 和慢性 SIB 患者可能处于与神经性疼痛类似的生理状态，其中痛觉过敏是由调节炎症、免疫和伤害性系统的可塑性机制介导的。为了应对与慢性自伤相关的反复组织损伤，先天免疫细胞可能会产生促炎和促伤害性细胞因子，这些细胞因子作用于大脑，引起类似疾病的行为，并使初级感觉神经传入敏感，从而导致疼痛过敏（即痛觉过敏）。
Self-injurious behavior (SIB) among individuals with intellectual and related neurodevelopmental disorders (IDD) is a clinical challenge and scientific puzzle. The physiological mechanisms regulating the sensory components of SIB remain a mystery with no clear understanding of the underlying pathophysiology. The central dogma regarding sensory processing in general and pain in particular among individuals with IDD and chronic SIB is that sensory processing is reduced and pain is absent or blunted. In this paper, recent findings challenging some of the conventional wisdom regarding pain and sensory function among individuals with IDD and SIB are reviewed. It seems that at least a subgroup of individuals with IDD and chronic SIB may be in a physiological state similar to neuropathic pain in which hyperalgesia is mediated by plasticity mechanisms regulating inflammatory, immune, and nociceptive systems. In response to repeated tissue damage associated with chronic self-injury, innate immune cells may be producing pro-inflammatory and pro-nociceptive cytokines that act on the brain to cause sickness-like behavior and sensitize primary sensory nerve afferents contributing to pain hypersensitivity (i.e., hyperalgesia).