Yamamoto Tatsuo
Department of Anesthesiology, Kumamoto University Hospital, 1-1-1 Honjo, Kumamoto-shi, Kumamoto 860-8556, Japan.
Nihon Hansenbyo Gakkai Zasshi. 2008 Sep;77(3):215-8. doi: 10.5025/hansen.77.215.
Neuropathic pain has been known to be refractory to traditional analgesics, such as opioids and non-steroidal anti-inflammatoy drugs. Some mechanisms of the development of neuropathic pain have been proposed; 1) sprouting of A beta fibers to the superficial layer of the dorsal horn, 2) ectopic discharge in the dorsal root ganglion and/or in neuroma at the nerve stump, 3) spinal sensitization. Ectopic discharge has been reported to be inhibited by Na+ channel blocker, such as lidocaine, and anticonvulsant. Lidocaine and anticonvulsant are used in the management of neuropathic pain. Activation of NMDA receptor is usually involved in the development of spinal sensitization and NMDA receptor antagonist, such as ketamine, is used in the management of neuropathic pain. Recently, alpha2delta subunit blocker, new class of anticonvulsant, is introduced to the management of neuropathic pain. alpha2delta subunit is the subunit of Ca2+ channel and modulate the influx of Ca2+. This Ca2+ influx induces release of neurotransmitter in the neuron. alpha 2 delta subunit blockers, such as gabapentin and pregabalin, may reduce the release of neurotransmitter and elicit analgesic effect in the treatment of neuropathic pain.
已知神经性疼痛对传统镇痛药(如阿片类药物和非甾体抗炎药)具有耐药性。人们提出了一些神经性疼痛发展的机制:1)Aβ纤维向背角浅层的芽生;2)背根神经节和/或神经残端神经瘤中的异位放电;3)脊髓敏化。据报道,异位放电可被利多卡因等Na+通道阻滞剂和抗惊厥药抑制。利多卡因和抗惊厥药用于治疗神经性疼痛。NMDA受体的激活通常参与脊髓敏化的发展,NMDA受体拮抗剂(如氯胺酮)用于治疗神经性疼痛。最近,新型抗惊厥药α2δ亚基阻滞剂被用于治疗神经性疼痛。α2δ亚基是Ca2+通道的亚基,可调节Ca2+内流。这种Ca2+内流诱导神经元中神经递质的释放。α2δ亚基阻滞剂(如加巴喷丁和普瑞巴林)可能会减少神经递质的释放,并在治疗神经性疼痛时产生镇痛作用。