Abbadie Catherine
Department of Pharmacology, Merck Research Laboratories, PO Box 2000, Rahway, NJ 07065, USA.
Trends Immunol. 2005 Oct;26(10):529-34. doi: 10.1016/j.it.2005.08.001.
Many patients suffer from neuropathic pain as a result of injury to the peripheral nervous system (e.g. post-herpetic neuralgia or diabetic neuropathy) or to the central nervous system (e.g. spinal cord injury or stroke). The most distinctive symptom of neuropathic pain is allodynia, whereby normally non-painful stimuli, such as light touch, become painful. Traditionally, inflammatory and neuropathic pain syndromes have been considered distinct entities; however, recent evidence belies this strict dichotomy. Nerve damage can stimulate macrophage infiltration and increase the number of activated T cells. Under these conditions, neuroinflammatory and immune responses contribute as much to the development and maintenance of pain as the initial damage itself. Recently, studies using animal models have shown that upregulation of chemokines is one of the mechanisms underlying the development and maintenance of chronic pain.
许多患者因外周神经系统损伤（如疱疹后神经痛或糖尿病性神经病变）或中枢神经系统损伤（如脊髓损伤或中风）而遭受神经性疼痛。神经性疼痛最显著的症状是痛觉过敏，即通常无疼痛的刺激（如轻触）会变得疼痛。传统上，炎症性疼痛综合征和神经性疼痛综合征被视为不同的实体；然而，最近的证据表明这种严格的二分法并不成立。神经损伤可刺激巨噬细胞浸润并增加活化T细胞的数量。在这些情况下，神经炎症和免疫反应对疼痛的发生和维持所起的作用与初始损伤本身一样大。最近，使用动物模型的研究表明，趋化因子的上调是慢性疼痛发生和维持的潜在机制之一。
