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D Burkhead

Publications and source records attributed to D Burkhead.

2 recordsLinked to original sources

Spinal nerve function in five volunteers experiencing transient neurologic symptoms after lidocaine subarachnoid anesthesia.

UNLABELLED: The etiology of transient neurologic symptoms (TNS) after 5% lidocaine spinal anesthesia remains undetermined. Previous case reports have shown that patients acutely experiencing TNS have no abnormalities on neurologic examination or magnetic resonance imaging. The aim of our study was to determine whether volunteers with TNS would exhibit abnormalities in spinal nerve electrophysiology. Twelve volunteers with no history of back pain or neurologic disease underwent baseline electromyography (EMG), nerve conduction studies, and somatosensory-evoked potential (SSEP) testing. Then, the volunteers were administered 50 mg of 5% hyperbaric lidocaine spinal anesthesia and were placed in a low lithotomy position (legs on four pillows). The next day, all volunteers underwent follow-up EMG, nerve conduction, and SSEP testing and were questioned and examined for the presence of complications including TNS (defined as pain or dysthesia in one or both buttocks or legs occurring within 24 h of spinal anesthesia). Volunteers who had TNS underwent additional EMG testing 4-6 wk later. Five of the 12 volunteers reported TNS. No volunteer had an abnormal EMG, nerve conduction study, or SSEP at 24 h follow up, nor were there any changes in EMG studies at delayed testing in the five volunteers experiencing TNS. On statistical analysis, the right peroneal and the right tibial nerve differed significantly for all volunteers from pre- to postspinal testing. When comparing pre- and postspinal testing of the TNS and non-TNS volunteers, statistically significant changes occurred in the nerve conduction tests of the right peroneal and left tibial nerve. There was no difference in measurements of F response, H reflex latency, amplitude, or velocity for either leg. Multivariate 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). We conclude that acute TNS after lidocaine spinal anesthesia did not result in consistent abnormalities detectable by EMG, nerve conduction studies, or SSEP in five volunteers. IMPLICATIONS: Electrophysiologic testing in volunteers experiencing transient neurologic symptoms is not abnormal.

Adult↗

Sedation during spinal anesthesia.

BACKGROUND: Central neuraxial anesthesia has been reported to decrease the dose of both intravenous and inhalational anesthetics needed to reach a defined level of sedation. The mechanism behind this phenomenon is speculated to be decreased afferent stimulation of the reticular activating system. The authors performed a two-part study (nonrandomized pilot study and a subsequent randomized, double-blind, placebo-controlled study) using the Bispectral Index (BIS) monitor to quantify the degree of sedation in unmedicated volunteers undergoing spinal anesthesia. METHODS: Twelve volunteers underwent BIS monitoring and observer sedation scoring (Observer's Assessment of Alertness/Sedation Scale [OAA/S]) before and after spinal anesthesia with 50 mg hyperbaric lidocaine, 5%. Subsequently, 16 volunteers blinded to the study were randomized to receive spinal anesthesia with 50 mg hyperbaric lidocaine, 5% (n = 10) or placebo (n = 6) and underwent BIS and OAA/S monitoring. RESULTS: In part I, significant changes in BIS scores of the volunteers occurred progressively (P = 0.003). The greatest variations from baseline BIS measurement occurred at 30 and 70 min. In part II, there were significant decreases in OAA/S and self-sedation scores for patients receiving spinal anesthesia versuscontrol patients (P = 0.04 and 0. 01, respectively). The greatest decrease in OAA/S scores occurred at 60 min. BIS scores were similar between groups (P = 0.4). CONCLUSIONS: Spinal anesthesia is accompanied by significant sedation progressively when compared with controls as measured by OAA/S and self-sedation scores. This effect was not related to block height. The late sedation observed by OAA/S at 60 min may indicate a second mechanism of sedation, such as delayed rostral spread of local anesthetics. BIS was not a sensitive measure of the sedation associated with spinal anesthesia in the randomized, blinded portion of this study.

Adult↗