BACKGROUND: To date, the anesthesia-induced blockade of nociceptive inputs is insufficiently reflected by commercially available electroencephalographic depth-of-anesthesia monitors. The aim of the current study was to evaluate the potential of somatosensory (SSEP) and intracutaneous pain evoked (iSEP) potentials during remifentanil and propofol anesthesia as electroencephalographic indicators of the nociceptive blockade. METHODS:Ten healthy men were investigated in a double-blind crossover design during three sessions with remifentanil, propofol, and placebo administration. All dosages were increased in a step-by-step mode. SSEP and iSEP recordings were performed followed by subjective pain ratings and measurement of level of sedation (modified Observer's Assessment of Alertness and Sedation Scale). Changes from baseline in evoked potential components, pain ratings, and sedation scale were assessed by Bonferroni-Holms-corrected Wilcoxon tests. RESULTS:Pain ratings were significantly reduced by remifentanil. Sedation scale was significantly reduced by propofol. Early SSEP components were not affected by medication. The amplitudes of the long latency SSEP components increased significantly with remifentanil, decreased with propofol, and did not change with placebo. The amplitudes of long latency components of the iSEP decreased significantly with both remifentanil and propofol and did not change with placebo. CONCLUSION: Long latency components of the SSEP are differently affected by remifentanil and propofol administration. Further studies are needed to clarify whether they can serve as a specific indicator of the nociceptive blockade during anesthesia.
RCT Entities:
BACKGROUND: To date, the anesthesia-induced blockade of nociceptive inputs is insufficiently reflected by commercially available electroencephalographic depth-of-anesthesia monitors. The aim of the current study was to evaluate the potential of somatosensory (SSEP) and intracutaneous pain evoked (iSEP) potentials during remifentanil and propofol anesthesia as electroencephalographic indicators of the nociceptive blockade. METHODS: Ten healthy men were investigated in a double-blind crossover design during three sessions with remifentanil, propofol, and placebo administration. All dosages were increased in a step-by-step mode. SSEP and iSEP recordings were performed followed by subjective pain ratings and measurement of level of sedation (modified Observer's Assessment of Alertness and Sedation Scale). Changes from baseline in evoked potential components, pain ratings, and sedation scale were assessed by Bonferroni-Holms-corrected Wilcoxon tests. RESULTS:Pain ratings were significantly reduced by remifentanil. Sedation scale was significantly reduced by propofol. Early SSEP components were not affected by medication. The amplitudes of the long latency SSEP components increased significantly with remifentanil, decreased with propofol, and did not change with placebo. The amplitudes of long latency components of the iSEP decreased significantly with both remifentanil and propofol and did not change with placebo. CONCLUSION: Long latency components of the SSEP are differently affected by remifentanil and propofol administration. Further studies are needed to clarify whether they can serve as a specific indicator of the nociceptive blockade during anesthesia.