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Department of Anesthesiology, Boston Medical Center, Boston, MA, donlam{at}fastmail.us
To the Editor:
Zaric et al. state that the incidence of lidocaine transient neurological syndrome (TNS) is not dose dependent (1). In the cited studies (2,3), the dose was the same. Only the concentration of lidocaine differed.
More importantly, the authors present a one sided TNS story: "TNS shows no evidence for localized nerve damage." The implication is that TNS is no big deal.
They ignore the possibility that TNS is nerve injury that eventually ceases to cause pain. I make the analogy to angina and myocardial infarction. I propose that TNS pain is associated with nerve inflammation that either resolves (similar to angina) or that continues to cell death (similar to myocardial infarction) and eventual pain resolution. It is beyond the scope of this letter to develop this important concept, but there is circumstantial evidence to support it.
Intrathecal lidocaine causes inflammation of the cauda equina nerves (4-6). This inflammation could totally resolve (similar to angina) or the nerves could go on to scar or apoptosis (5,7-9) (similar to myocardial infarction).
Although there is not definitive proof for TNS-associated nerve injury, it is not impossible. No anesthesiologist would employ an anesthetic that causes angina or myocardial infarction. Are we flirting with something similar by causing TNS?
References
This article has been cited by other articles:
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V. Umbrain, L. Shi, M.-H. Lauwers, I. Smolders, Y. Michotte, and F. Camu Intrathecal lidocaine elevates prostaglandin E2 levels in cerebrospinal fluid: a microdialysis study in freely moving rats Br. J. Anaesth., August 20, 2008; (2008) aen243v1. [Abstract] [Full Text] [PDF] |
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