Transient neurologic symptoms (TNS) after 5% lidocaine spinal anesthesia were first reported in 1993. Since that time, a number of case reports and clinical studies have documented the presence of these symptoms and the clinical scenarios in which they are commonly seen. Despite our ability to describe the incidence of this group of symptoms, the etiology of this condition remains unknown. Previous investigations in patients acutely experiencing TNS have demonstrated no abnormalities on neurologic examination or magnetic resonance imaging. The purpose of this study was to determine whether volunteers with TNS would exhibit abnormalities in spinal nerve electrophysiology.

In the study, twelve volunteers with no history of back pain or neurologic disease underwent baseline electromyography (EMG), nerve conduction studies, and somatosensory-evoked potential testing (SSEP). The volunteers were then given 50 mg of 5% hyperbaric lidocaine as a spinal anesthetic and were placed in a low lithotomy position (legs on four pillows). The following day all volunteers underwent follow-up EMG, nerve conduction and SSEP testing. They were questioned and examined for the presence of complications, including TNS (defined as pain or dysesthesia in one or both buttocks or legs occurring within 24 hours of spinal anesthesia). Volunteers who had TNS underwent additional EMG testing 4-6 weeks later.

Five of the 12 volunteers enrolled in this study reported TNS. The authors were unable to demonstrate any abnormalities in EMG, nerve conduction studies or SSEP at 24-hour follow-up or in the delayed testing of the five volunteers experiencing TNS. On statistical analysis, the right perineal and the right tibial nerve differed significantly for all volunteers from pre- to post-spinal testing. When comparing pre- and post-spinal testing of the TNS and non-TNS volunteers, statistically significant changes occurred in the nerve conduction tests of the right perineal and left tibial nerve. There was no difference in measurements of F response, H reflex latency, amplitude or velocity for either leg. Multivariant analysis of variance showed no significant difference between TNS and non-TNS volunteers for the changes in the nine nerve conduction tests when considered together (p = 0.4).

The authors concluded that TNS after lidocaine spinal anesthesia did not result in consistent abnormalities detectable by EMG, nerve conduction studies or SSEP in five volunteers. The authors also provide an excellent description of the various testing techniques and their potential utility.

This study also provides additional information regarding patients experiencing TNS. Although negative, the inability to detect any type of electrophysiologic abnormality in volunteers experiencing TNS underscores the limitations of our current testing, our lack of complete understanding with respect to signal transmission and the development of pain within the nervous system, and the need for ongoing study. It is encouraging to see in this small study the absence of definable electrical abnormality; however, given the limited number of participants in the study, the results cannot be considered absolutely conclusive. Continued performance of studies such as these will help all practitioners to understand the relative risk and benefit ratio of performing lidocaine subarachnoid anesthesia in the future.

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