中文摘要：

外周神经损伤引起的神经病理性疼痛可持续数月、数年,甚至终身,神经病理性疼痛的临床表现和机制与生理性疼痛明显不同,被认为是神经系统的一种疾病。迄今,该病的预防和治疗仍然是医学界的难题,原因在于人们对其发病机制的了解仍然非常有限。一些基本的科学问题尚待厘清。例如,外周神经包括感觉纤维和运动纤维,到底损伤哪类纤维会引起神经病理性疼痛？回答这一最基本的科学问题对确定研究神经病理性疼痛起始点至关重要,对该病的临床治疗,尤其是外科治疗具有指导意义。由于神经病理性疼痛表现为躯体感觉异常,人们理所当然地认为它可能是由感觉神经损伤引起的。然而,近年来的大量动物实验和临床研究证据表明,感觉纤维损伤既非引起神经病理性疼痛的必要条件也非充分条件;而运动纤维损伤几乎总会导致神经病理性疼痛。本文将综述运动纤维损伤导致外周敏化（初级感觉神经元异位放电）和中枢敏化（脊髓背角C-纤维突触传递长时程增强）的机制,重点阐述胶质细胞活化、致炎细胞因子和脑源性神经营养因子过表达的作用。

英文摘要：

Peripheral nerve injury often induces chronic neuropathic pain that may persist for months, for years, or even for life time. Neuropathic pain is considered as a disease of nervous system, as its underlying mechanisms are substantially different from those of physiological pain. In spite of intensive study for decades, prevention and treatment of the disease is still a big challenge for clinician and for pain researchers, because the mechanism still remains largely unknown. For example, peripheral nerve is consisted of sensory fibers and motor fibers, injury to which one is responsible for generation of neuropathic pain？ The answer to this basic question is important for determining the start point for investigation of neuropathic pain and for its clinical, especially surgical, treatment. Because neuropathic pain is sensory disorder, it appears reasonable to consider that it should be induced by injury to sensory fibers. In recent years, however, emergent experimental and clinical evidence shows that sensory fiber injury is neither necessary nor sufficient for induction of neuropathic pain. In contrast, motor fiber injury almost always leads to neuropathic pain. In this article, the mechanisms, by which motor fiber injury induce peripheral sensitization（ectopic discharges in primary sensory neurons） and central sensitization（long-term potentiation at C-fiber synapses in spinal dorsal horn）, are reviewed with emphasis on the role of glial activation and subsequent over-production of proinflammatory cytokines and brain derived neurotrophic factor.