外周神经损伤引起病理性疼痛的机制

Mechanisms Underlying Pathological Pain Produced by Peripheral Nerve Injury

外周神经损伤往往导致慢性疼痛,即神经病理性疼痛。大量的研究表明,神经损伤主要通过使初级感觉神经元产生自发放电(即异位冲动)和脊髓背角突触传递效率的持续性增强(即LTP)导致病理性疼痛。近年来的研究表明,致炎细胞因子TNF-α在神经病理性疼痛中起重要作用。神经损伤可通过上调TNF-α,导致初级感觉神经元上Nav1.3和Nav1.8过表达,引起异位冲动。TNF-α的上调还可显著易化脊髓背角C纤维诱发电位的LTP。由于TNF-α的上调,Nav1.3和Nav1.8过表达和脊髓背角LTP的形成主要与运动神经损伤相关,因此运动神经损伤可能是引起病理性疼痛的主要原因。

Many studies have demonstrated that neuropathic pain is mediated by ectopic discharges in primary sensory neurons and the long-term potentiation （LTP） of synaptic transmission in spinal dorsal horn. Recent works have shown that pro-inflammatory cytokine tumor necrosis factor （TNF-α） is critically involved in the development of neuropathic pain. Nerve injury up-regulates TNF-α, and the increased TNF-α leads to ectopic discharges via over-expression of voltage-gated sodium channels, Nav1.3 and Nav1.8, in dorsal root ganglia （DRG） neurons and facilities LTP of C-fiber evoked field potentials in spinal dorsal horn. Because the up-regulation of TNF-α, the over-expression of sodium channels and induction of spinal LTP are mainly associated with motor neuron injury, injury to motor neuron but not to sensory neuron may be more important for development of neuropathic pain.