J Liu1, H Singh, P F White. 1. Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center, Dallas 75235-9068, USA.
Abstract
BACKGROUND: The electroencephalogram (EEG) has been used to study the effects of anesthetic and analgesic drugs on central nervous system function. A prospective study was designed to evaluate the accuracy of various EEG parameters for assessing midazolam-induced sedation during regional anesthesia. METHODS: Twenty-six consenting adult patients were administered 4.5-20 mg intravenous midazolam (in increments of 0.5-1 mg bolus doses every 6-10 min) until they became unresponsive to tactile stimulation (i.e., mild prodding or shaking). The EEG was continuously recorded from a bifrontal montage (FP1-Cz and FP2-Cz) to obtain the bispectral index (BI), 95% spectral edge frequency (SEF), median frequency (MF), and delta, theta, alpha, and beta power bands. Sedation was assessed clinically at 6-10-min intervals using the Observers' Assessment of Alertness/Sedation (OAA/S) scale, with 1 = no response (unconsciousness) to tactile stimulation to 5 = wide awake. The EEG parameters were correlated with the OAA/S scores using nonparametric Spearman's rank-correlation analysis. Kruskal-Wallis analysis of variance was used to determine significant changes in EEG parameters during the onset of and recovery from midazolam-induced sedation. RESULTS: Of the EEG parameters studied, the BI exhibited the best correlation with OAA/S scores during both the onset (Spearman's Rho = 0.815) and recovery (Spearman's Rho = 0.596) phases. With increasing sedation, there was a progressive decrease in the BI (OAA/S score of 5: BI = 95.4 +/- 2.3; 4: 90.3 +/- 4.5; 3:86.6 +/- 4.6; 2:75.6 +/- 9.7; 1:69.2 +/- 13.9). A similar pattern was found for the 95% SEF as the OAA/S score decreased from 4 to 1. Similarly, EEG-BI increased with recovery from the sedative effects of midazolam (OAA/S score = 2:BI = 75.2 +/- 10.2; 3:82.3 +/- 7.3; 4:90.8 +/- 6). However, no consistent changes were found with the other EEG parameters. The mean EEG values between OAA/S scores 3 and 2 and between OAA/S scores 2 and 1 during the onset and recovery phases from midazolam-induced sedation, defined as EEG50 values for response to verbal command (EEG50-VC) and to shaking of the head (EEG50-SH), were 79.3 +/- 8 and 70.8 +/- 14.3, respectively, for EEG-BI. The EEG-BI displayed the smallest coefficients of variation for the EEG50-VC and EEG50-SH values. CONCLUSIONS: The EEG-BI appears to be a useful parameter for assessing midazolam-induced sedation and can predict the likelihood of a patient responding to verbal commands or to shaking of the head during midazolam-induced sedation.
BACKGROUND: The electroencephalogram (EEG) has been used to study the effects of anesthetic and analgesic drugs on central nervous system function. A prospective study was designed to evaluate the accuracy of various EEG parameters for assessing midazolam-induced sedation during regional anesthesia. METHODS: Twenty-six consenting adult patients were administered 4.5-20 mg intravenous midazolam (in increments of 0.5-1 mg bolus doses every 6-10 min) until they became unresponsive to tactile stimulation (i.e., mild prodding or shaking). The EEG was continuously recorded from a bifrontal montage (FP1-Cz and FP2-Cz) to obtain the bispectral index (BI), 95% spectral edge frequency (SEF), median frequency (MF), and delta, theta, alpha, and beta power bands. Sedation was assessed clinically at 6-10-min intervals using the Observers' Assessment of Alertness/Sedation (OAA/S) scale, with 1 = no response (unconsciousness) to tactile stimulation to 5 = wide awake. The EEG parameters were correlated with the OAA/S scores using nonparametric Spearman's rank-correlation analysis. Kruskal-Wallis analysis of variance was used to determine significant changes in EEG parameters during the onset of and recovery from midazolam-induced sedation. RESULTS: Of the EEG parameters studied, the BI exhibited the best correlation with OAA/S scores during both the onset (Spearman's Rho = 0.815) and recovery (Spearman's Rho = 0.596) phases. With increasing sedation, there was a progressive decrease in the BI (OAA/S score of 5: BI = 95.4 +/- 2.3; 4: 90.3 +/- 4.5; 3:86.6 +/- 4.6; 2:75.6 +/- 9.7; 1:69.2 +/- 13.9). A similar pattern was found for the 95% SEF as the OAA/S score decreased from 4 to 1. Similarly, EEG-BI increased with recovery from the sedative effects of midazolam (OAA/S score = 2:BI = 75.2 +/- 10.2; 3:82.3 +/- 7.3; 4:90.8 +/- 6). However, no consistent changes were found with the other EEG parameters. The mean EEG values between OAA/S scores 3 and 2 and between OAA/S scores 2 and 1 during the onset and recovery phases from midazolam-induced sedation, defined as EEG50 values for response to verbal command (EEG50-VC) and to shaking of the head (EEG50-SH), were 79.3 +/- 8 and 70.8 +/- 14.3, respectively, for EEG-BI. The EEG-BI displayed the smallest coefficients of variation for the EEG50-VC and EEG50-SH values. CONCLUSIONS: The EEG-BI appears to be a useful parameter for assessing midazolam-induced sedation and can predict the likelihood of a patient responding to verbal commands or to shaking of the head during midazolam-induced sedation.
Authors: Lenneke Schrier; Rob Zuiker; Frans W H M Merkus; Erica S Klaassen; Zheng Guan; Bert Tuk; Joop M A van Gerven; Ronald van der Geest; Geert Jan Groeneveld Journal: Br J Clin Pharmacol Date: 2016-12-20 Impact factor: 4.335