Opening remarks

Carl Koller is credited with the fi rst description of the local anesthetic action of cocaine, in 1884 [1], leading to the eventual introduction of local anesthesia worldwide. Five percent hyperbaric lidocaine has been used for millions of spinal anesthetic procedures since its introduction in 1948. Phillips and colleagues [2] prospectively studied the safety of intrathecal lidocaine with 10 440 patients from 1961 to 1966, and concluded that lidocaine was safe for spinal anesthesia. However, Rigler and colleagues [3] reported four cases of cauda equina syndrome after continuous spinal anesthesia, in 1991. Transient neurologic symptoms (TNS) were also reported by Schneider et al. [4] in 1993. They found that 4 patients undergoing spinal anesthesia with lithotomy positioning complained of aching and pain in the buttocks and lower extremities postoperatively. Since these reports, several epidemiological studies regarding neurologic defi cits after regional anesthesia have been performed, and these raised several possible causes, such as specifi c local anesthetic toxicity, needle trauma, neural ischemia secondary to sciatic stretching, patient positioning, pooling of local anesthetics, muscle spasm, myofascial trigger points, early mobilization, and irritation Local anesthetic agents are relatively free of side effects, with a 50-fold margin between median blocking and toxic concentrations, implying a safer therapeutic window than that for many other clinically available drugs. However, when these agents are administered in excessive doses or in the incorrect location, such as accidental intravascular or intrathecal injection, systemic or localized toxic reactions may occur. Local neuronal tissue toxic reactions occur rarely when clinically relevant concentrations of local anesthetics are used. The neurotoxicity of local anesthetics has been extensively investigated by groups all over the world. However, the mechanism(s) remain incompletely understood. Several Japanese researchers are particularly active in this area and four of them participated in discussions of this issue in the Journal of Anesthesia—sponsored symposium: Neurotoxicity of Local Anesthetics.

[1]  Y. Punjasawadwong,et al.  Transient neurologic symptoms (TNS) following spinal anaesthesia with lidocaine versus other local anaesthetics. , 2005, The Cochrane database of systematic reviews.

[2]  J. E. Pollock Transient Neurologic Symptoms: Etiology, Risk Factors, and Management , 2002, Regional Anesthesia & Pain Medicine.

[3]  G. Gores,et al.  Mitochondrial Injury and Caspase Activation by the Local Anesthetic Lidocaine , 2004, Anesthesiology.

[4]  P. Gross,et al.  Acute endoneurial ischemia induced by epineurial endothelin in the rat sciatic nerve. , 1992, The American journal of physiology.

[5]  C. Keller,et al.  Neurotoxicity of Lidocaine Involves Specific Activation of the p38 Mitogen-activated Protein Kinase, but Not Extracellular Signal–regulated or c-jun N-Terminal Kinases, and Is Mediated by Arachidonic Acid Metabolites , 2006, Anesthesiology.

[6]  T. Ettlin,et al.  Transient neurologic toxicity after hyperbaric subarachnoid anesthesia with 5% lidocaine. , 1993, Anesthesia and analgesia.

[7]  K. Drasner,et al.  Cauda Equina Syndrome After Continuous Spinal Anesthesia , 1991, Anesthesia and analgesia.

[8]  O. C. Phillips,et al.  Neurologic complications following spinal anesthesia with lidocaine: a prospective review of 10,440 cases. , 1969, Anesthesiology.

[9]  R. Myers,et al.  Mitigation of Direct Neurotoxic Effects of Lidocaine and Amitriptyline by Inhibition of p38 Mitogen-activated Protein Kinase In Vitro and In Vivo , 2006, Anesthesiology.