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Neurotoxicity of Local Anesthetics: Animal Data
  1. Dag Selander, M.D., Ph.D.
  1. From the Department of Anesthesiology, Sahlgren’s University Hospital, Gothenburg, Sweden.
  1. Address correspondence and reprint requests to Dag Selander, M.D., Ph.D., Astra Pain Control AB, R&D, S-151 85 Sodertalje, Sweden.


Objective. To extract experimental data of importance for the understanding of neurotoxicity of local anesthetics, with special reference to continuous spinal anesthesia.

Methods. Literature on clinical experience of and experimental studies on neurotoxic complications of local anesthetics, especially concerning spinal and continuous spinal anesthesia and long-term peripheral nerve block, was reviewed. The overall incidence of neural complications of central and peripheral nerve blocks was extracted, and the results of animal experimental studies on neurotoxicity of local anesthetics were used to characterize the possible mechanisms behind such complications.

Results. Persistent neurologic complications of regional anesthesia varied from 0 to 0.09% for central blockades and from 0 to more than 5% for brachial plexus blocks, depending on the technique used. All local anesthetics seem to be involved in clinical reports of neural complications. Experimental studies indicate that all local anesthetics are potentially neurotoxic and that the neurotoxicity parallels their anesthetic potency. In fact, the nerve conduction block may be an expression of a reversible toxic effect of the local anesthetic (LA). The mechanism is not completely understood, but factors of importance are the concentration of the LA and time of exposure of the neural tissue to the LA. Contributing factors are neural trauma and ischemia, both of which may be deleterious by themselves.

Conclusions. Correctly administered LAs of clinical concentration are safe, but animal data indicate that all LAs are potentially neurotoxic. The neurotoxicity seems to be a function of the concentration of the LA and the time of exposure of the nervous tissue to the LA. Concomitant neural trauma, ischemia, or both, may potentiate the neurotoxic effect of the LA.

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