Affiliations: [a] Department of Anesthesiology, Loyola University Medical Center, Maywood, IL, USA
| [b]
Edward Hines Jr. VA Hospital, Hines, IL, USA
Correspondence:
[*]
Corresponding author: Susanna C. Byram, MD, PhD, Loyola University Medical Center, 2160S. First Ave. Maywood, IL 60153, USA. Tel.: +1 708 216 3754; Fax: +1 708 216 8267; E-mail: [email protected].
Note: [1] Present address: Alzheimer’s Association, National Office, 225 N. Michigan Ave., Fl. 17, Chicago, IL 60601, USA.
Abstract: Background: Appropriate management of pain after an injury or surgical procedure has been shown to improve patient outcomes. While infrequent, nerve damage resulting from regional anesthesia can be devastating, however the mechanism remains unknown. Local anesthetics are neurotoxic yet are frequently applied to sites where peripheral nerves are regenerating. Therefore, understanding their effects on injured and growing neurons may have important implications for clinical practice. Objective: The purpose of this study was to determine if local anesthetics exacerbate the rate of motoneuron death following axotomy. Methods: Mice were subjected to a unilateral transection of the facial motor nerve, and either normal saline, 2% lidocaine, or 0.75% bupivacaine was placed at the injury site. Four weeks post-axotomy, percent survival was determined by comparing the number of motoneuron cell bodies on the injured side and the uninjured control side. Results: The average facial motoneuron survival in the saline, lidocaine, and bupivacaine groups 4 weeks after axotomy was 80%, 78% and 35%, respectively. Conclusion: Our data suggest that bupivacaine exacerbates levels of cell death in injured motoneurons. It has been proposed that once a nerve is damaged, it becomes more susceptible to injury elsewhere along the nerve. Thus, an improved understanding of the effects of local anesthetics on neuron survival and axon regeneration may lead to strategies to identify patients at higher risk for permanent neural deficits after peripheral nerve blocks and/or decrease the risk of neural deficit following peripheral nerve blocks.
