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Spinal Nerve Function in Five Volunteers Experiencing Transient Neurologic Symptoms After Lidocaine Subarachnoid Anesthesia

Regional Anesthesia and Pain Control
Free

JULIA E. POLLOCK, DAN BURKHEAD, JOSEPH M. NEAL, SPENCER S. LIU, ANDREW FRIEDMAN, CAROL STEPHENSON AND NAYAK L. POLISSAR

Department of Anesthesiology, Virginia Mason Medical Center; University of Washington; Departments of Physical Medicine and Rehabilitation, and Clinical Research, Virginia Mason Medical Center; The Mountain-Whisper-Light Statistical Consulting, Seattle, Washington

Anesth. Analg., 90: 658–665, 2000

The cause of transient neurologic symptoms (TNS) after 5% lidocaine spinal anesthesia is still undetermined. Case reports have shown that patients acutely experiencing TNS have no abnormalities on neurologic examination or MRI. This study was designed to determine whether volunteers reporting symptoms of TNS would have changes in neuroelectrophysiology as detected by electromyography (EMG), nerve conduction studies, or somatosensory-evoked potentials (SSEP).

Twelve volunteers with no history of back pain or neurologic disease underwent baseline EMG, nerve conduction studies, and SSEP testing. They then were given 50 mg of 5% hyperbaric lidocaine spinal anesthesia and placed in a low lithotomy position. The next day all underwent follow-up EMG, nerve conduction, and SSEP testing and were examined for the presence of complications including TNS, which was defined as pain or dysesthesia in one or both buttocks or legs occurring within 24 hr of spinal anesthesia. Those who had TNS had additional EMG testing 4 to 6 wk later.

Demographic characteristics were comparable between the volunteers experiencing TNS and those who did not. No postdural puncture headaches were reported. All volunteers had measurable sensory and motor block and all experienced profound motor block. None required treatment for hypotension, bradycardia, or nausea.

Five of the 12 volunteers (42%) experienced TNS. No volunteer had an abnormal EMG, nerve conduction study, or SSEP at 24 hr follow-up, nor were there any changes in EMG studies at delayed testing in the 5 who had TNS. Those who reported TNS noted onset of symptoms 5 to 9 hr after spinal anesthesia with a duration between 3 and 4 days.

The right peroneal and the right tibial nerve differed significantly for all volunteers from prespinal to postspinal testing. When comparing prespinal and postspinal testing of the TNS and non-TNS volunteers, statistically significant changes occurred in the nerve conduction test of the right peroneal and left tibial nerve. Nerve conduction in the TNS group decreased slightly and the non-TNS group increased from pretesting to posttesting. There was no difference in measurements of F response, H reflex latency, amplitude, or velocity for either leg. There were no significant differences between the two groups of volunteers for the changes in the nine nerve conduction tests when considered together.

Within the limits of the testing protocol, the results support the suggestion that TNS and neurotoxic damage are not mediated by the same mechanism. The questions posed by these results further emphasize the need for additional investigation of this complex problem.

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Comment:

The astonishing thing here was that there were 12 volunteers, of whom five (42%) developed transient neurologic symptoms. This is certainly a most interesting and challenging study and quite thought-provoking. The authors conclude that further studies are needed; I don’t think I would rush to join up.

Anthony P. Adams M.B. B.S. Ph.D. F.R.C.A. F.A.N.Z.C.A.

© 2001 Lippincott Williams & Wilkins, Inc.