Mao Jianren, Chen Lucy L
MGH Pain Center, Massachusetts General Hospital, Harvard Medical School, 15 Parkman Street, Suite WACC-324, Boston, MA 02114, USA Arnold Pain Center, Beth Isareal and Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.
Pain. 2000 Jul;87(1):7-17. doi: 10.1016/S0304-3959(00)00229-3.
The effectiveness of systemic lidocaine in relieving acute and chronic pain has been recognized for over 35 years. In particular, systemic lidocaine has been utilized both as a diagnostic and therapeutic tool for intractable neuropathic pain during the last decade. The introduction of oral lidocaine congeners such as mexiletine has significantly extended the usage of lidocaine therapy in chronic pain settings. However, a number of clinical issues remain to be addressed including (1) an effective, meaningful dose range for the clinical lidocaine test, (2) the predictive value of the lidocaine test for an oral trial of lidocaine congeners, (3) identification of pain symptoms and signs relieved by systemic lidocaine, (4) comparisons of therapeutic effects between systemic lidocaine and its oral congeners, and (5) long-term outcomes of systemic lidocaine and its oral congeners. Mechanisms of neuropathic pain relief from lidocaine therapy are yet to be understood. Both central and peripheral mechanisms have been postulated. Systemic lidocaine is thought to have its suppressive effects on spontaneous ectopic discharges of the injured nerve without blocking normal nerve conduction. However, there remain inconsistencies in the scientific basis underlying the clinical application of lidocaine therapy. Recent demonstration of changes in tetrodotoxin (TTX)-sensitive and TTX-resistant sodium channels following nerve injury and their link to certain neuropathic pain symptoms may lead to the development of subtype-specific sodium channel blockers. The thoughtful use of lidocaine therapy and the potential application of subtype-specific sodium channel blockers could provide better management of distinctive neuropathic pain symptoms.
全身性利多卡因在缓解急慢性疼痛方面的有效性已被认可超过35年。特别是在过去十年中，全身性利多卡因已被用作治疗顽固性神经性疼痛的诊断和治疗工具。口服利多卡因类似物如美西律的引入显著扩大了利多卡因疗法在慢性疼痛治疗中的应用。然而，仍有一些临床问题有待解决，包括：（1）临床利多卡因试验的有效、有意义的剂量范围；（2）利多卡因试验对口服利多卡因类似物试验的预测价值；（3）全身性利多卡因缓解的疼痛症状和体征的识别；（4）全身性利多卡因与其口服类似物治疗效果的比较；（5）全身性利多卡因及其口服类似物的长期疗效。利多卡因治疗缓解神经性疼痛的机制尚不清楚。中枢和外周机制都有相关推测。全身性利多卡因被认为对受损神经的自发性异位放电有抑制作用，而不会阻断正常神经传导。然而，利多卡因疗法临床应用的科学依据仍存在不一致之处。最近的研究表明，神经损伤后河豚毒素（TTX）敏感和TTX耐药钠通道的变化及其与某些神经性疼痛症状的联系可能会导致亚型特异性钠通道阻滞剂的开发。合理使用利多卡因疗法以及亚型特异性钠通道阻滞剂的潜在应用可以更好地管理独特的神经性疼痛症状。
