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Anesthesiology:
Clinical Investigations

Quantitative EEG Correlations with Brain Glucose Metabolic Rate during Anesthesia in Volunteers

Alkire, Michael T. MD

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Abstract

Background: To help elucidate the relationship between anesthetic‐induced changes in the electroencephalogram (EEG) and the concurrent cerebral metabolic changes caused by anesthesia, positron emission tomography data of cerebral metabolism obtained in volunteers during anesthesia were correlated retrospectively with various concurrently measured EEG descriptors.
Methods: Volunteers underwent functional brain imaging using the18 fluorodeoxyglucose technique; one scan always assessed awake‐baseline cerebral metabolism (n = 7), and the other scans assessed metabolism during propofol sedation (n = 4), propofol anesthesia (n = 4), or isoflurane anesthesia (n = 5). The EEG was recorded continuously during metabolism assessment using a frontal‐mastoid montage. Power spectrum variables, median frequency, 95% spectral edge, and bispectral index (BIS) values subsequently were correlated with the percentage of absolute cerebral metabolic reduction (PACMR) of glucose utilization caused by anesthesia.
Results: The percentage of absolute cerebral metabolic reduction, evident during anesthesia, trended median frequency (r = ‐ 0.46, P = 0.11), and the spectral edge (r = ‐ 0.52, P = 0.07), and correlated with anesthetic type (r = ‐ 0.70, P < 0.05), relative [small beta, Greek] power (r = ‐ 0.60, P < 0.05), total power (r = 0.71, P < 0.01), and bispectral index (r = ‐ 0.81, P < 0.001). After controlling for anesthetic type, only bispectral index (r = 0.40, P = 0.08) and [small alpha, Greek] power (r = 0.37, P = 0.10) approached significance for explaining residual percentage of absolute cerebral metabolic reduction prediction error.
Conclusions: Some EEG descriptors correlated linearly with the magnitude of the cerebral metabolic reduction caused by propofol and isoflurane anesthesia. These data suggest that a physiologic link exists between the EEG and cerebral metabolism during anesthesia that is mathematically quantifiable.
This article is featured in “This Month in Anesthesiology.” Please see this issue of Anesthesiology, page 9A.
THE existence of a physiologic relation between electroencephalographic (EEG) activity and cerebral metabolism during anesthesia seems well established. [1] It has been known for some time that several anesthetics can cause EEG burst suppression, coincident with a cerebral metabolic reduction of approximately 50%, and that an isoelectric EEG can be produced by some anesthetic agents, coincident with greater levels of cerebral metabolic reduction. [1] However, although the EEG changes in predictable ways with increasing doses of various anesthetic agents [2–6] and cerebral metabolism also changes in predictable ways (i.e., generally decreases) with increasing doses of various anesthetic agents, [7] relatively few data exist that directly quantify the nature of the relation between cerebral metabolism during anesthesia and the EEG.
To help to elucidate the nature of this fundamental physiologic relation, positron emission tomography (PET) data of cerebral glucose metabolic rates evident in volunteers during either propofol sedation, [8] propofol anesthesia, [9] or isoflurane anesthesia [10] were correlated retrospectively with previously and simultaneously obtained measurements of various EEG descriptors. The EEG descriptors evaluated included those historically used to quantify the spectral parameters of the EEG signal, including relative [small alpha, Greek], [small beta, Greek], [small delta, Greek], and [small theta, Greek], power bands, along with total power. Also evaluated were those EEG descriptors thought to correlate in some way with increasing anesthetic dose, including 95% spectral edge frequency, median power frequency, and the bispectral index (BIS). Median power frequency and 95% spectral edge frequency are suggested frequently to monitor some component of anesthetic depth or anesthetic effectiveness, [11–14] although the clinical usefulness of these simple EEG descriptors as monitors of anesthetic depth appears limited. [15] The BIS is an empirically developed complex descriptor of the EEG that has been shown to have some clinical usefulness for titrating the hypnotic effects of anesthetic agents, such as propofol and isoflurane. [16]
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Materials and Methods

This was a retrospective analysis of EEG data gathered during studies of the regional cerebral metabolic effects of propofol and isoflurane anesthesia in paid volunteers. Institutional review board approval was obtained, and all volunteers gave written informed consent. Volunteers underwent functional brain imaging using the18 fluorodeoxyglucose technique (18) FDG); one scan always assessed awake‐baseline cerebral metabolism (n = 7), and the other scans assessed metabolism during propofol sedation (n = 4), propofol anesthesia (n = 4), or isoflurane anesthesia (n = 5). Data from seven right‐handed men with recorded EEG and PET data and 22 individual PET scans served as the basis for the current analyses. [8–10] Cerebral metabolism data from one volunteer's propofol anesthetic were obtained after the initial propofol report was published, and, thus, they have not been reported before. At least 1 week separated scanning sessions between anesthetic conditions and baseline. A minimum of 1 yr separated scanning sessions for two volunteers who participated in both the propofol and isoflurane studies.
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Volunteers
Volunteers were healthy men who do not smoke (mean age, 24 +/‐ 3 yr). Each was classified as American Society of Anesthesiologists physical status 1, and all had no evidence of psychiatric illness. The men avoided caffeine and other medications for at least 48 h before each scan. They fasted for at least 8 h before each scanning session and received oral antacid (30 ml sodium citrate taken orally) before scans involving anesthesia. Each volunteer had two or three intravenous catheters inserted, one to administer the18 FDG PET tracer, one for blood sampling, and one for the propofol infusion, when necessary. Monitoring devices included a three‐lead electrocardiograph, an automated noninvasive blood pressure monitor, a pulse oximeter, a tight‐fitting face mask for end‐tidal carbon dioxide monitoring, a temperature monitor, and a precordial stethoscope.
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Anesthetic Procedures
Table 1
Table 1
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The details of the anesthetic administration procedures have been reported. [9,10] Anesthetic doses were incrementally and slowly adjusted upward to achieve the desired clinical endpoints. The endpoint for the “anesthesia”‐related scans was a score of 1 or less on the modified Observer Assessment of Alertness and Sedation (Table 1) rating scale. [16]
Isoflurane Anesthesia. Isoflurane was administered via a tight‐fitting face mask using a calibrated vaporizer through a semiclosed non‐rebreathing circuit. End‐tidal isoflurane concentration was monitored using a Poet II agent analyzer (Criticare Systems Inc., Milwaukee, WI). Isoflurane was administered incrementally in 0.1% expired steps to achieve loss of consciousness with no response to mild prodding. After loss of consciousness was achieved, the end‐tidal isoflurane concentration was fixed for the rest of the experiment.
Propofol Anesthesia. Volunteers were administered propofol as a 0.4 mg/kg bolus followed by a continuous infusion of 2 mg [middle dot] kg‐1 [middle dot] h‐1. This infusion was adjusted upward in increments of 2 mg [middle dot] kg‐1 [middle dot] h‐1 every 15 ‐ 20 min until volunteers lost consciousness and had no response to mild prodding. After the volunteer was unresponsive, the first of four propofol blood level samples was taken, and the propofol infusion rate was fixed. Propofol blood sample 2 was obtained at the start of the18 FDG uptake period, sample 3 was obtained 15 min into the uptake period, and sample 4 was taken at the end of the uptake period just before the infusion was stopped.
Propofol Sedation. Propofol sedation infusions were titrated to achieve a targeted sedation score not less than 3. Volunteers in the sedate condition were quite drowsy but remained aware and responsive during the study period. Before metabolism was assessed, all volunteers were in a cognitive state in which each failed to recall at least one of three common objects presented and verbally repeated 3 min before questioning. Responsiveness was assessed intermittently (every 3 ‐ 15 min, depending on clinical signs) throughout the measurement of cerebral metabolism by noting responsiveness to loud verbal stimulation. The volunteers were instructed, before the experiment, to raise and quickly lower their right index finger if, and when, the investigator asked “Are you doing okay?”. Sometimes, when the volunteers were not responsive to this verbal stimulation, they were further stimulated by mild prodding or shaking. In all such cases, the additional tactile stimulation returned each volunteer to a verbally responsive state. None spent more than 3 min in a verbally unresponsive state during the 32‐min uptake period. Three propofol blood samples were obtained during the sedation scans: one at the start of the18 FDG uptake period, one at the midpoint of the uptake period, and one at the end.
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Awake‐baseline Conditions
For the awake control scans, the volunteers lay quietly on a gurney with their eyes closed. Again responsiveness was assessed intermittently (every 3–15 min, depending on clinical signs) throughout the measurement of cerebral metabolism according to their responsiveness to verbal stimulation. All volunteers remained responsive to verbal stimulation throughout the 32‐min uptake period and, after the experiment, no volunteer reported any subjective episodes of spontaneous sleep during metabolism assessment.
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Procedural Overview
The volunteers were administered anesthesia, as described before, while in a small, darkened, sound‐shielded room. Measurement of cerebral metabolism during each anesthetic condition did not begin until volunteers clinically approached a steady‐state level of anesthesia (i.e., no changes in heart rate, breathing pattern, or blood pressure for 12 min). Once stable in the desired conditions, 5 mC18 FDG was injected intravenously. The volunteers remained at the targeted level of anesthesia for the next 32 min. After labeling of the brain with the positron emitting tracer, the anesthetic was discontinued. The volunteers were allowed to emerge from the anesthetic and regain awareness before being taken to the PET scanner. They continued to recover from the anesthetic while in the PET scanner.
For the baseline condition, a similar labeling and scanning sequence was followed as outlined before. Scanning of all volunteers began within 20 min from the end of each uptake period for each condition. The time between injection of the18 FDG and the start of each scan was standardized across conditions to ensure that it was similar in duration for all volunteers.
Electroencephalography. An EEG signal was obtained using gold cup electrodes applied to the scalp with cream and located according to the international 10 ‐ 20 system. Skin impedance was maintained at < 5 k Omega. The following leads were recorded: left and right frontal‐mastoid (Fp1‐A1, Fp2‐A2, channels 1 and 2), left and right frontal‐CZ (Fp1‐CZ, Fp2‐CZ, channels 3 and 4), plus a ground electrode placed at the center of the forehead. The EEG was recorded using an Aspect A‐1000 EEG monitor (Aspect Medical Systems, Natick, MA). Data averaged from the combined frontal‐mastoid leads (channels 1 and 2) are presented in this article.
Conventional frequency bands were used to describe power spectrum variables. Raw EEG, power bands, spectral determinants, and the BIS were recorded continuously, along with time‐locked clinical event markers, as needed, and were stored in a computer database with tape backup for subsequent off‐line analysis. The sampling rate was 128 samples/s. Spectral variables were recorded in 2‐s epochs with an update rate of 10 s. Spectral and BIS smoothing were set to 30 s. Low‐ and high‐pass filters were set to 0.25 Hz and 30 Hz. For those scans not obtained using the current version of the BIS, the recorded EEG data were subsequently reanalyzed using the BIS software algorithm version 3.2. Electromyographic activity was defined as the absolute power in the range of 70–110 Hz, reported in decibels (n = 11; two early propofol anesthesia volunteers did not have electromyographic values recorded). For each volunteer, the EEG descriptor values that were recorded while cerebral metabolic activity was being assessed were averaged to form a single number representative of that volunteer's average EEG descriptor value associated with that particular type and dose of anesthesia being studied.
Positron Emission Tomography Procedures. The regional cerebral metabolic rate of glucose utilization was measured with two different PET cameras. For the isoflurane data, a GE2048 head‐dedicated scanner was used (GE/Scanditronix, Stockholm, Sweden). This scanner replaced an older NeuroEcat scanner that was used to collect the propofol data. In each case, a volunteer's baseline was obtained on the same scanner that was used for that volunteer's anesthesia‐related scan. The GE PET scanner has eight rings with 256 detectors per ring to achieve a resolution of 4.5 mm at full‐width‐half‐maximum in plane and 6 mm axially. The NeuroEcat PET scanner had a single ring with shadow shields and septa to achieve 7.6‐mm resolution (full‐width‐half‐maximum) in plane and 9.9 mm axially. For the GE2048 scanner, two sets of 15 image planes, resulting in 30 PET images across the whole brain, were obtained for each volunteer. With the NeuroEcat scanner, 13 image slices across the whole brain were obtained that started at the level of 85% of head height (vertex to canthomeatal line, usually 12–14 cm) and stepped downward in steps of 10 mm. All scans were obtained relative to the canthomeatal line. Volunteers were positioned using laser guidance, and a thermosetting plastic face mask was used to hold each volunteer's head stationary during image acquisition for both the awake‐baseline and anesthesia conditions.
Figure 1
Figure 1
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Whole‐brain and regional metabolic rates of glucose utilization were calculated using established PET methods and the well‐established models of deoxyglucose kinetics. [17–20] The sagittal image reconstruction (Figure 1) was rendered using “BrainImage” software. [21]
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Statistical Analyses
Data are presented as mean +/‐ SD. Cerebral metabolism data were analyzed as the percentage change from baseline values or, alternatively, as the percentage of absolute cerebral metabolic reduction (PACMR) of whole‐brain glucose utilization caused by anesthesia. This allowed the PET data from the separate studies, which were gathered from different PET scanners, to be directly comparable. [22] Significant changes in EEG descriptor values, PACMR values, and electromyographic values at the various anesthetic levels were assessed using a one‐way analysis of variance, with post hoc t testing and Bonferroni‐Dunn correction for multiple comparisons, with P < 0.05 considered significant. Pearson's correlation coefficient with Fisher's r to z conversion was used to evaluate relations between the various EEG descriptors and the PACMR evident during anesthesia, with P < 0.05 considered significant. To control for the effects of the different anesthetic levels on the resulting simple linear correlations, a partial correlation approach was also used. The partial correlations help to determine the effectiveness of using EEG‐derived variable x to approximate PACMR values after they have been adjusted for anesthetic type. An alternative explanation is possible: If changes in global cerebral metabolism are changing the anesthetic level, then partial correlation analysis will determine whether EEG variable x offers any more information about cerebral metabolic reduction than does simply knowing the anesthetic level.
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Results

The mean (+/‐ SD) propofol infusion rate was 4.5 +/‐ 1.0 mg [middle dot] kg‐1 [middle dot] h‐1 during sedation and 9 +/‐ 2 mg [middle dot] kg‐1 [middle dot] h‐1 while volunteers were unresponsive. Resultant blood levels were 1.0 +/‐ 0.2 and 3.5 +/‐ 0.6 [micro sign]g/ml plasma, respectively. The mean expired end‐tidal isoflurane concentration at unresponsiveness was 0.5 +/‐ 0.1%. The magnitude of the metabolic reduction that occurred during each level and type of anesthesia can be qualitatively appreciated by referring to Figure 1. The figure (showing the data from a single volunteer [S2] who participated in all phases of the study) reveals how brain metabolism decreases with increasing doses, and the different types, of anesthesia studied. The Figure alsoshows how one of the EEG descriptors, the BIS, changed with the changing level of anesthesia in this particular person.
Table 2
Table 2
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All of the measured variables, except relative [small alpha, Greek] power and relative [small theta, Greek] power, showed significant differences across the different anesthetic levels evaluated (Table 2). The effect size for propofol sedation was less than that seen for isoflurane anesthesia, which was less than that seen for propofol anesthesia. Most variables decreased in value as cerebral metabolism decreased across the anesthetic conditions. However, relative [small sigma, Greek] power and total power significantly increased as cerebral metabolism decreased (Table 2).
Table 3
Table 3
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Figure 2
Figure 2
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Figure 3
Figure 3
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Figure 4
Figure 4
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Figure 5
Figure 5
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Figure 6
Figure 6
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Figure 7
Figure 7
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Figure 8
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Figure 9
Figure 9
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(Table 3) shows the correlations that were found between all of the different EEG descriptors evaluated and the PACMR values evident during the various anesthetics administered. The PACMR values correlated significantly with total power (Figure 2), relative [small beta, Greek] power (Figure 3). and BIS (Figure 4). Although the grouped analyses to not reveal a significant linear correlation between PACMR and the spectral edge (Figure 5) or median power frequencies (Figure 6), a within‐volunteer trend occurred for these variables to decrease with greater cerebral metabolic reductions. There was also some within‐volunteer tendency for relative [small theta, Greek] power (Figure 7) and relative [small alpha, Greek] power (Figure 8) to decrease with increasing cerebral metabolic reductions. Relative [small delta, Greek] power, however, tended to increase with greater brain metabolic reductions (Figure 9).
Using nonlinear regression analysis revealed that anesthetic type correlated significantly with cerebral metabolic reduction (r = 0.70, r2 = 0.49, P < 0.05). In other words, by simply knowing the type of anesthetic used and the targeted clinical endpoint, we can account for approximately 50% of the variance associated with predicting the PACMR. A partial correlation analysis (Table 3) revealed that only BIS (r = ‐ 0.40, P = 0.08) and relative [small alpha, Greek] (r = 0.37, P = 0.10) approached significance for explaining the residual error in predicting PACMR values after controlling for anesthetic type.
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Discussion

It is well established for several different anesthetic agents that progressively higher doses of anesthesia causes progressively greater decreases in brain metabolism. [1,7,23] It is also well established that the EEG changes in predictable ways with increasing doses of various anesthetic agents. [2,6,24] Therefore, the changes that occur in the EEG signal with increasing doses of anesthesia must be accompanied by concurrent changes in brain metabolism. Perhaps because the logic of this inference seems obvious, the quantifiable nature of the relation between cerebral metabolism and the EEg has been left largely unexplored, and only a few landmarks for this relation have been determined (e.g., a cerebral metabolic reduction of approximately 50% equates with EEG burst suppression). The current results extend our knowledge about this relation and show that for a clinically relevant dosage range of propofol and isoflurane anesthesia several processed EEG descriptors correlate approximately in a linear manner with the magnitude of the cerebral metabolic reduction caused by anesthesia. In other words, the magnitude of the anesthetic‐induced changes in the EEG evident during sedation and light anesthesia closely paralleled the magnitude of the reduction in global cerebral metabolism caused by the anesthesia.
The common physiologic ground for a “linear” relation between EEG changes and cerebral metabolic rate during anesthesia is probably the total number of neurons firing, or the rate at which large groups of neurons fire. The relation between neuronal firing and EEG activity has been investigated directly in several different paradigms, and the general tendency is for lower firing rates to equate with a lower‐frequency EEG pattern. [25,26] Because anesthetics tend to produce lower‐frequency EEG patterns, it seems reasonable to expect that anesthetics should also be associated with decreased rates of neuronal firing. In fact, electrophysiologic studies support this expectation. [27–29] The rate of cerebral metabolic activity determined by measurement of regional glucose utilization with the deoxyglucose technique also is known to be proportional to the underlying rate of neuronal activity. [30] The lower the underlying neuronal activity, the lower the measured cerebral metabolic rate will be. Thus, again, because anesthetics inhibit neuronal activity, they should also decrease regional glucose utilization in a dose‐dependent manner, and this expectation is also well supported by experimentation. [9,31,32]
The EEG descriptors measured in this study changed in a dose‐related manner consistent with expectations from the literature for both propofol and isoflurane (Table 2). [13,15,33] The higher‐frequency activity evident over the frontal lobe during sedation was replaced by lower‐frequency activity during unresponsiveness. Generalization of these findings to other anesthetics, and even to a broader dosage range of these same anesthetic agents is, however, unwarranted. Different anesthetics affect the EEG signal differently and show different dose‐response characteristics. Nonetheless, because the common basis for both the anesthetic‐induced EEG changes and the cerebral metabolic changes evident during anesthesia is likely to be the underlying rate of neuronal activity, we can justly speculate that some relation between these EEG descriptors and cerebral metabolic rate would still be found with other anesthetic agents and doses.
The reduction in cerebral metabolism caused by the anesthetics used appeared to be linear. Therefore, the dependent variable, PACMR, seems to be modeled well by a linear model. However, the data available for analysis in this retrospective study are limited in number and range of metabolic reduction values, with most of the data points found in a narrow range of metabolic reduction values between 40% and 60%. Given these limitations, the possibility that a nonlinear relation exists between anesthetic level and PACMR in humans cannot be ruled out. Some animal data suggest that a nonlinear relation should exist between anesthetic dose and cerebral metabolic reduction. [7] Nonetheless, nothing within these data suggest that linear modeling of PACMR is wrong per se.
The EEG is a complex signal that changes in complex ways that are not necessarily linear with increasing anesthetic doses. The fact that the BIS had the highest simple correlation value for any of the EEG descriptors is probably a result of the extensive “linearizing” inherent in the BIS algorithm. In other words, the BIS was constructed to perform in a linear manner with increasing anesthetic dose, therefore, the finding that it correlates highly with another variable that also happens to change in approximately a linear manner with increasing anesthetic dose (i.e., the PACMR) should not be seen as surprising, but rather as simply more evidence that something inherent in the EEG signal may be useful for estimating the magnitude of the cerebral metabolic reduction evident during anesthesia.
Because the BIS was linearized to a scale that ranges from 0 to 100, an interesting relation is noted between the mean PACMR values and the mean BIS values. The mean percentage of whole‐brain metabolic reduction that occurred during the sedate condition on propofol was 34 +/‐ 16% or, alternatively, a value at which 66% of baseline metabolism remained. This corresponded to a mean BIS, at that time, of 66 +/‐ 3. The mean whole‐brain metabolic reduction seen during isoflurane anesthesia was 46% (or 54% of baseline metabolism remaining), with a corresponding mean BIS of 54 +/‐ 9. The amount of metabolic reduction seen during propofol anesthesia was 60% (or 40% of baseline metabolism remaining) with a corresponding BIS of 37 +/‐ 6. In this grouped analysis, it appears that the BIS values approximate the value of cerebral metabolism remaining during anesthesia. No doubt this is a coincidence of the BIS linearizing process and these particular types and doses of anesthesia studied. It remains to be determined whether this coincidental relation would be replicated in another study sample or when other anesthetic agents are evaluated.
Median power frequency and 95% spectral edge frequency have often been suggested for use in monitoring some component of anesthetic depth or anesthetic effectiveness. [11–14] In this study, however, neither of these variables correlated significantly with whole‐brain metabolic percentage reduction, although they decreased significantly with increasing anesthetic level. This may have been a result of the limited sample size or, more likely, because these variables are simply not represented well by a linear model. Nonetheless, although the grouped data analysis did not reveal a significant linear relation between cerebral metabolic reduction and these variables, both seemed to trend downward with increasing doses of anesthesia, as physiologically expected, for each person. This can be seen when each volunteer's data points are connected (Figure 5 and Figure 6, respectively).
In addition, during sedation and anesthesia, total power significantly increased as the percentage change in baseline whole‐brain metabolism also increased (Table 2 and Table 3). Relative [small beta, Greek] power also significantly decreased as the percentage change in baseline whole‐brain metabolism increased (Table 2 and Table 3). Both findings are again consistent with the expected physiology of the EEG during increasing doses of anesthesia. [13]
The partial correlation analysis revealed that BIS was the most effective for explaining residual variance in PACMR prediction after controlling for anesthetic type. This partial correlation with BIS was not significant (r = ‐ 0.40, P = 0.08), although this may have been related to the limited sample size used. Nonetheless, the partial correlation analysis suggests that more information about PACMR can be obtained from using BIS values than from simply knowing the anesthetic type and dose. However, relative [small alpha, Greek] power (r = 0.37, P = 0.10) had nearly the same amount of residual explanatory power as the BIS. This suggests that if a model for PACMR prediction were to be developed, relative [small alpha, Greek] power might be as important a component of such a model as the BIS. Another way to interpret the meaning of the partial correlation results is to suggest that if one sedated everyone to the same anesthetic level, there would be some tendency for the person in the group with the highest BIS value, or the highest relative [small alpha, Greek] power, to have the higher cerebral metabolic rate.
If a much larger sample size were available for study, a multiple linear regression analysis might be able to select those EEG descriptors that best predict PACMR changes. The question then becomes: Is PACMR the ideal physiologic variable that should be modeled? In other words, if the BIS, for example, were to be “tuned” to better predict PACMR, would it then be a better measure of hypnosis? These questions await further experimentation but offer the interesting hypothesis that perhaps the physiologic variable of interest for understanding anesthetic depth related to hypnosis is the magnitude of the cerebral metabolic reduction caused by an anesthetic agent.
A standard crossover paradigm for determining anesthetic concentration at loss of consciousness was not used because of the time constraints imposed by the necessary use of a short‐lived radioisotope. Because crossover design was not used, the volunteers were slightly more anesthetized during the measurement of cerebral metabolism than when they first lost consciousness. Blood samples for propofol confirm, as previously reported, [9] that volunteers were more anesthetized during metabolism assessment than when they first lost consciousness. Nonetheless, this slight overshoot in clinical depth is not an important issue for the current analyses because the EEG values obtained at the time of the cerebral metabolism measurements, when steady‐state conditions were approximated, were the ones used in the current correlational analyses and not the EEG values that occurred coincident with the precise moment that consciousness was lost.
In conclusion, these data show that in a clinically relevant dosage range of propofol and isoflurane anesthesia, several processed EEG descriptors correlate approximately in a linear manner with the magnitude of the cerebral metabolic reduction caused by anesthesia. This suggests that a fundamental physiologic link exists between the EEG and cerebral metabolism during anesthesia that may prove to be mathematically quantifiable.
The author thanks Richard J. Haier, Ph.D., and the staff of the Brain Imaging Center for expert technical assistance with PET imaging; Robert Newcomb, Ph.D., and Thomas L. Brunell, Ph.D., for statistical consultation; Brad Jacobsen for propofol blood level analyses; and Paul Manberg, Ph.D., Patricia Embree, R.N., and the staff of Aspect Medical Systems for blinded assistance with EEG data analyses and helpful discussion of the manuscript.
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REFERENCES

1. Michenfelder JD: The anesthetized brain, Anesthesia and the Brain. New York, Churchill Livingstone, 1988

2. Martin JT, Faulconer A Jr, Bickford RG: Electroencephalography. Anesthesiology 1959; 20:359-76

3. Clark DL, Rosner BS: Neurophysiologic effects of general anesthetics: I. The electroencephalogram and its sensory evoked responses in man. Anesthesiology 1973; 38:564-82

4. Levy WJ: Intraoperative EEG patterns: Implications for EEG monitoring. Anesthesiology 1984; 60:430-4

5. Levy WJ: Power spectrum correlates of changes in consciousness during anesthetic induction with enflurane. Anesthesiology 1986; 64:688-93

6. Veselis RA, Reinsel R, Alagesan R, Heino R, Bedford RF: The EEG as a monitor of midazolam amnesia: Changes in power and topography as a function of amnesic state. Anesthesiology 1991; 74:866-74

7. Stullken EJ, Milde JH, Michenfelder JD, Tinker JH: The nonlinear responses of cerebral metabolism to low concentrations of halothane, enflurane, isoflurane, and thiopental. Anesthesiology 1977; 46:28-34

8. Alkire MT, Haier RJ, Barker SJ, Shah NK: Positron emission tomography assessment of cerebral metabolism during three different states of human consciousness [Abstract]. Anesth Analg 1996; 82:S7

9. Alkire MT, Haier RJ, Barker SJ, Shah NK, Wu JC, Kao YJ: Cerebral metabolism during propofol anesthesia in humans studied with positron emission tomography. Anesthesiology 1995; 82:393-403

10. Alkire MT, Haier RJ, Shah NK, Anderson CT: Positron emission tomography study of regional cerebral metabolism in humans during isoflurane anesthesia. Anesthesiology 1997; 86:549-57

11. Schwilden H, Stoeckel H: Quantitative EEG analysis during anaesthesia with isoflurane in nitrous oxide at 1.3 and 1.5 MAC. Br J Anaesth 1987; 59:738-45

12. Stanski DR, Hudson RJ, Homer TD, Saidman LJ, Meathe E: Pharmacodynamic modeling of thiopental anesthesia. J Pharmacokin Biopharmaceut 1984; 12:223-40

13. Schwender D, Daunderer M, Mulzer S, Klasing S, Finsterer U, Peter K: Spectral edge frequency of the electroencephalogram to monitor “depth” of anaesthesia with isoflurane or propofol. Br J Anaesth 1996; 77:179-84

14. Billard V, Gambus PL, Chamoun N, Stanski DR, Shafer SL: A comparison of spectral edge, delta power, and bispectral index as EEG measures of alfentanil, propofol, and midazolam drug effect. Clin Pharm Ther 1997; 61:45-58

15. Dwyer RC, Rampil IJ, Eger EI II, Bennett HL: The electroencephalogram does not predict depth of isoflurane anesthesia. Anesthesiology 1994; 81:403-9

16. Glass PS, Bloom M, Kearse L, Rosow C, Sebel P, Manberg P: Bispectral analysis measures sedation and memory effects of propofol, midazolam, isoflurane, and alfentanil in healthy volunteers. Anesthesiology 1997; 86:836-47

17. Sokoloff L, Reivich M, Kennedy C, Des RM, Patlak CS, Pettigrew KD, Sakurada O, Shinohara M: The [14C]deoxyglucose method for the measurement of local cerebral glucose utilization: Theory, procedure, and normal values in the conscious and anesthetized albino rat. J Neurochem 1977; 28:897-916

18. Phelps ME, Huang SC, Hoffman EJ, Selin C, Sokoloff L, Kuhl DE: Tomographic measurement of local cerebral glucose metabolic rate in humans with (F-18)2-fluoro-2-deoxy-D-glucose: Validation of method. Ann Neurol 1979; 6:371-88

19. Huang SC, Phelps ME, Hoffman EJ, Sideris K, Selin CJ, Kuhl DE: Noninvasive determination of local cerebral metabolic rate of glucose in man. Am J Physiol 1980; 238:E69-82

20. Buchsbaum MS, DeLisi LE, Holcomb HH, Cappelletti J, King AC, Johnson J, Hazlett E, Dowling ZS, Post RM, Morihisa J: Anteroposterior gradients in cerebral glucose use in schizophrenia and affective disorders. Arch Gen Psychiatry 1984; 41:1159-66

21. Reiss AL, Hennessey JG, Subramanium B, Beach LS, Rubin MA: BrainImage [computer program]. Version 2.0. Baltimore, MD, Kennedy Krieger Institute, 1996

22. Grady CL: Quantitative comparison of measurements of cerebral glucose metabolic rate made with two positron cameras. J Cereb Blood Flow Metab 1991; 11:A57-63

23. Todd MM, Drummond JC: A comparison of the cerebrovascular and metabolic effects of halothane and isoflurane in the cat. Anesthesiology 1984; 60:276-82

24. Stanski DR: Monitoring depth of anesthesia, Anesthesia. Edited by Miller RD. New York, Churchill Livingstone, 1990, pp 1001-29

25. Detari L, Rasmusson DD, Semba K: Phasic relationship between the activity of basal forebrain neurons and cortical EEG in urethane-anesthetized rat. Brain Res 1997; 759:112-21

26. MacIver MB, Mandema JW, Stanski DR, Bland BH: Thiopental uncouples hippocampal and cortical synchronized electroencephalographic activity. Anesthesiology 1996; 84:1411-24

27. Angel A: The G. L. Brown lecture. Adventures in anaesthesia. Exp Physiol 1991; 76:1-38

28. Ogawa T, Shingu K, Shibata M, Osawa M, Mori K: The divergent actions of volatile anaesthetics on background neuronal activity and reactive capability in the central nervous system in cats. Can J Anaesth 1992; 39:862-72

29. Armstrong JM, George MJ: Influence of anesthesia on spontaneous activity and receptive field size of single units in rat Sm1 neocortex. Exp Neurol 1988; 99:369-87

30. Sokoloff L: Relationships among local functional activity, energy metabolism, and blood flow in the central nervous system. Fed Proc 1981; 40:2311-6

31. Maekawa T, Tommasino C, Shapiro HM, Keifer GJ, Kohlenberger RW: Local cerebral blood flow and glucose utilization during isoflurane anesthesia in the rat. Anesthesiology 1986; 65:144-51

32. Dam M, Ori C, Pizzolato G, Ricchieri GL, Pellegrini A, Giron GP, Battistin L: The effects of propofol anesthesia on local cerebral glucose utilization in the rat. Anesthesiology 1990; 73:499-505

33. Liu J, Singh H, White PF: Electroencephalographic bispectral index correlates with intraoperative recall and depth of propofol-induced sedation. Anesth Analg 1997; 84:185-0

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Resistance of brain glucose metabolism to thiopental-induced CNS depression in newborn piglets
Walter, B; Eiselt, M; Cumming, P; Xiong, GM; Hinz, R; Uthe, S; Brust, P; Bauer, R
International Journal of Developmental Neuroscience, 31(3): 157-164.
10.1016/j.ijdevneu.2012.12.008
CrossRef
Journal of Cerebral Blood Flow and Metabolism
Glutamatergic function in the resting awake human brain is supported by uniformly high oxidative energy
Hyder, F; Fulbright, RK; Shulman, RG; Rothman, DL
Journal of Cerebral Blood Flow and Metabolism, 33(3): 339-347.
10.1038/jcbfm.2012.207
CrossRef
British Journal of Anaesthesia
Comparison of bispectral EEG analysis and auditory evoked potentials for monitoring depth of anaesthesia during propofol anaesthesia
Gajraj, RJ; Doi, M; Mantzaridis, H; Kenny, GNC
British Journal of Anaesthesia, 82(5): 672-678.

Fortschritte Der Neurologie Psychiatrie
Relevance of positron emission tomography as to diagnosis and prognosis of postanoxic cerebral dysfunctions
Rudolf, J
Fortschritte Der Neurologie Psychiatrie, 68(8): 344-351.

British Journal of Anaesthesia
In vitro networks: cortical mechanisms of anaesthetic action
Antkowiak, B
British Journal of Anaesthesia, 89(1): 102-111.

Anesthesia and Analgesia
Neuromuscular Block Differentially Affects Immobility and Cortical Activation at Near-Minimum Alveolar Concentration Anesthesia
Doufas, AG; Komatsu, R; Orhan-Sungur, M; Sengupta, P; Wadhwa, A; Mascha, E; Shafer, SL; Sessler, DI
Anesthesia and Analgesia, 109(4): 1097-1104.
10.1213/ANE.0b013e3181af631a
CrossRef
Clinical Pharmacology & Therapeutics
Probing the mind: Anesthesia and neuroimaging
Alkire, MT
Clinical Pharmacology & Therapeutics, 84(1): 149-152.
10.1038/clpt.2008.75
CrossRef
Veterinary Radiology & Ultrasound
Effects of Anesthetic Protocol on Normal Canine Brain Uptake of 18F-Fdg Assessed By Pet/Ct
Lee, MS; Ko, J; Lee, AR; Lee, IH; Jung, MA; Austin, B; Chung, H; Nahm, S; Eom, K
Veterinary Radiology & Ultrasound, 51(2): 130-135.
10.1111/j.1740-8261.2009.01636.x
CrossRef
Anesthesia and Analgesia
Is depth of anesthesia, as assessed by the bispectral index, related to postoperative cognitive dysfunction and recovery?
Farag, E; Chelune, GJ; Schubert, A; Mascha, EJ
Anesthesia and Analgesia, 103(3): 633-640.
10.1213/01.ane.0000228870.48028.b5
CrossRef
Consciousness and Cognition
Anesthesia, neural information processing, and conscious awareness
Cariani, P
Consciousness and Cognition, 9(3): 387-395.

British Journal of Anaesthesia
Entropy is blind to nitrous oxide. Can we see why?
Sleigh, JW; Barnard, JPM
British Journal of Anaesthesia, 92(2): 159-161.
10.1093/bja/aeh039
CrossRef
Anaesthesia and Intensive Care
The Bispectral Index during an anaphylactic circulatory arrest
Kluger, MT
Anaesthesia and Intensive Care, 29(5): 544-547.

British Journal of Anaesthesia
Effect of decompressive craniectomy on bispectral index and memory
Smith, MMJ; Andrzejowski, J
British Journal of Anaesthesia, 104(4): 512.
10.1093/bja/aeq049
CrossRef
Consciousness and Cognition
The power of observation
Alkire, MT
Consciousness and Cognition, 10(2): 236-240.

Neuroimage
Impaired thalamocortical connectivity in humans during general-anesthetic-induced unconsciousness
White, NS; Alkire, MT
Neuroimage, 19(2): 402-411.
10.1016/S1053-8119(03)00103-4
CrossRef
European Journal of Neuroscience
Neocortex is the major target of sedative concentrations of volatile anaesthetics: strong depression of firing rates and increase of GABA(A) receptor-mediated inhibition
Hentschke, H; Schwarz, C; Antkowiak, B
European Journal of Neuroscience, 21(1): 93-102.
10.1111/j.1460-9568.2004.03843.x
CrossRef
Canadian Journal of Anaesthesia-Journal Canadien D Anesthesie
Brain injury under general anesthesia: is monitoring of the EEG helpful?
Billard, V
Canadian Journal of Anaesthesia-Journal Canadien D Anesthesie, 48(): 1055-1060.

Pharmacotherapy
Comparing the bispectral index and suppression ratio with burst suppression of the electroencephalogram during pentobarbital infusions in adult intensive care patients
Riker, RR; Fraser, GL; Wilkins, ML
Pharmacotherapy, 23(9): 1087-1093.

Anaesthesia
Correlation of EEG spectral entropy with regional cerebral blood flow during sevoflurane and propofol anaesthesia
Maksimow, A; Kaisti, K; Aalto, S; Maenpaa, M; Jaaskelainen, S; Hinkka, S; Martens, S; Sarkela, M; Viertio-Oja, H; Scheinin, H
Anaesthesia, 60(9): 862-869.
10.1111/j.1365-2044.2005.04289.x
CrossRef
Suppressing the Mind: Anesthetic Modulation of Memory and Consciousness
Anesthesia and the Thalamocortical System
Alkire, MT
Suppressing the Mind: Anesthetic Modulation of Memory and Consciousness, (): 127-138.
10.1007/978-1-60761-462-3_6
CrossRef
Proceedings of the National Academy of Sciences of the United States of America
Energetics of neuronal signaling and fMRI activity
Maandag, NJG; Coman, D; Sanganahalli, BG; Herman, P; Smith, AJ; Blumenfeld, H; Shulman, RG; Hyder, F
Proceedings of the National Academy of Sciences of the United States of America, 104(): 20546-20551.
10.1073/pnas.0709515104
CrossRef
Proceedings of the National Academy of Sciences of the United States of America
Baseline brain energy supports the state of consciousness
Shulman, RG; Hyder, F; Rothman, DL
Proceedings of the National Academy of Sciences of the United States of America, 106(): 11096-11101.
10.1073/pnas.0903941106
CrossRef
British Journal of Anaesthesia
Heart rate variability, BIS and 'depth of anaesthesia'
Pomfrett, CJD
British Journal of Anaesthesia, 82(5): 659-662.

Anesthesia and Analgesia
Bispectral index values and spectral edge frequency at different stages of physiologic sleep
Nieuwenhuijs, D; Coleman, EL; Douglas, NJ; Drummond, GB; Dahan, A
Anesthesia and Analgesia, 94(1): 125-129.

Advances in Modelling and Clinical Application of Intravenous Anaesthesia
Bispectral index scale (BIS) monitoring and intravenous anaesthesia
Vuyk, J; Mertens, M
Advances in Modelling and Clinical Application of Intravenous Anaesthesia, 523(): 95-104.

Plos One
Pattern Recognition Analysis of Proton Nuclear Magnetic Resonance Spectra of Brain Tissue Extracts from Rats Anesthetized with Propofol or Isoflurane
Kawaguchi, H; Hirakawa, K; Miyauchi, K; Koike, K; Ohno, Y; Sakamoto, A
Plos One, 5(6): -.
ARTN e11172
CrossRef
Journal of Physiology-London
Interactions between cardiac, respiratory and EEG-delta oscillations in rats during anaesthesia
Musizza, B; Stefanovska, A; McClintock, PVE; Palus, M; Petrovcic, J; Ribaric, S; Bajrovic, FF
Journal of Physiology-London, 580(1): 315-326.
10.1113/jphysiol.2006.126748
CrossRef
Consciousness and Cognition
Toward a unified theory of narcosis: Brain imaging evidence for a thalamocortical switch as the neurophysiologic basis of anesthetic-induced unconsciousness
Alkire, MT; Haier, RJ; Fallon, JH
Consciousness and Cognition, 9(3): 370-386.

Anesthesia and Analgesia
A comparison of frontal and occipital bispectral index values obtained during neurosurgical procedures
Shiraishi, T; Uchino, H; Sagara, T; Ishii, N
Anesthesia and Analgesia, 98(6): 1773-1775.
10.1213/01.ANE.0000121344.69058.09
CrossRef
Consciousness and Cognition
Anesthesia - A descent or a jump into the depths?
Veselis, RA
Consciousness and Cognition, 10(2): 230-235.
10.1006/ccog.2001.0513
CrossRef
Annales Francaises D Anesthesie Et De Reanimation
Automatic EEG analysis for monitoring depth of anaesthesia in year 2000
Billard, V; Constant, I
Annales Francaises D Anesthesie Et De Reanimation, 20(9): 763-785.

Clinical and Experimental Obstetrics & Gynecology
High estradiol levels and depth of anaesthesia
Yavuz, L; Eroglu, F; Ceylan, BG; Ozsoy, HM; Ozbasar, D
Clinical and Experimental Obstetrics & Gynecology, 34(1): 31-34.

British Journal of Anaesthesia
In vivo characterization of clinical anaesthesia and its components
Antognini, JF; Carstens, E
British Journal of Anaesthesia, 89(1): 156-166.

Clinical Eeg and Neuroscience
QEEG prognostic value in acute stroke
Cuspineda, E; Machado, C; Galan, L; Aubert, E; Alvarez, MA; Llopis, F; Portela, L; Garcia, M; Manero, JM; Avila, Y
Clinical Eeg and Neuroscience, 38(3): 155-160.

Advances in Modelling and Clinical Application of Intravenous Anaesthesia
Functional brain imaging and propofol mechanisms of action
Fiset, P
Advances in Modelling and Clinical Application of Intravenous Anaesthesia, 523(): 115-121.

Anaesthesia and Intensive Care
The Bispectral Index and induced hypothermia - electrocerebral silence at an unusually high temperature
Puri, GD; Bagchi, A; Anandamurthy, B; Dhaliwal, RS
Anaesthesia and Intensive Care, 31(5): 578-580.

Comptes Rendus Biologies
Cerebral metabolism and consciousness
Shulman, RG; Hyder, F; Rothman, DL
Comptes Rendus Biologies, 326(3): 253-273.
10.1016/S1631-0691(03)00071-4
CrossRef
Anaesthesia and Intensive Care
Perioperative cerebral ischaemia in cardiac surgery and BIS
Villacorta, J; Kerbaul, E; Collart, F; Guidon, C; Bonnet, M; Guillen, JC; Gouin, F
Anaesthesia and Intensive Care, 33(4): 514-517.

Anaesthesist
Postoperative cognitive dysfunction
Ellerkmann, RK
Anaesthesist, 56(2): 175-176.
10.1007/s00101-006-1128-y
CrossRef
Psychogeriatrics
Preliminary application of processed electroencephalogram monitoring to differentiate senile dementia from depression
Oshima, N; Chinzei, M; Kikuchi, E; Hayashida, M
Psychogeriatrics, 9(3): 116-120.
10.1111/j.1479-8301.2009.00280.x
CrossRef
British Journal of Anaesthesia
In vivo imaging of anaesthetic action in humans: approaches with positron emission tomography (PET) and functional magnetic resonance imaging (fMRI)
Heinke, W; Schwarzbauer, C
British Journal of Anaesthesia, 89(1): 112-122.

Nature Reviews Neuroscience
Molecular and neuronal substrates for general anaesthetics
Rudolph, U; Antkowiak, B
Nature Reviews Neuroscience, 5(9): 709-720.
10.1038/nrn1496
CrossRef
Pediatric Anesthesia
Measuring anesthesia in children using the EEG
Davidson, AJ
Pediatric Anesthesia, 16(4): 374-387.
10.1111/j.1460-9592.2006.01877.x
CrossRef
British Journal of Anaesthesia
Effects of propofol on lactate accumulation and oedema formation in focal cerebral ischaemia in hyperglycaemic rats
Ishii, H; Arai, T; Segawa, H; Morikawa, S; Inubushi, T; Fukuda, K
British Journal of Anaesthesia, 88(3): 412-417.

Anasthesiologie Intensivmedizin Notfallmedizin Schmerztherapie
Neural mechanisms of anaesthesia
Antkowiak, B; Kirschfeld, K
Anasthesiologie Intensivmedizin Notfallmedizin Schmerztherapie, 35(): 731-743.

Biological Psychiatry
Endogenous dopamine release induced by repetitive transcranial magnetic stimulation over the primary motor cortex: An [11]raclopride positron emission tomography study in anesthetized macaque monkeys
Ohnishi, T; Hayashi, T; Okabe, S; Nonaka, I; Matsuda, H; Iida, H; Imabayashi, E; Watabe, H; Miyake, Y; Ogawa, M; Teramoto, N; Ohta, Y; Ejima, N; Sawada, T; Ugawa, Y
Biological Psychiatry, 55(5): 484-489.
10.1016/j.biopsych.2003.09.016
CrossRef
Disorders of Consciousness
Simultaneous Electroencephalography and Functional Magnetic Resonance Imaging of General Anesthesia
Purdon, PL; Pierce, ET; Bonmassar, G; Walsh, J; Harrell, PG; Kwo, J; Deschler, D; Barlow, M; Merhar, RC; Lamus, C; Mullaly, CM; Sullivan, M; Maginnis, S; Skoniecki, D; Higgins, HA; Brown, EN
Disorders of Consciousness, 1157(): 61-70.
10.1111/j.1749-6632.2008.04119.x
CrossRef
Neuro-Ophthalmology
Investigation of visual cortex in children with cortical visual impairment: positron emission tomography
Choi, MY; Lee, DS; Hwang, JM; Choi, DG; Lee, KM; Park, KH; Yu, YS; Chung, H
Neuro-Ophthalmology, 25(3): 103-108.

British Journal of Anaesthesia
Bispectral index is a topographically dependent variable in patients receiving propofol anaesthesia
Pandin, P; Van Cutsem, N; Tuna, T; D'hollander, A
British Journal of Anaesthesia, 97(5): 676-680.
10.1093/bja/ael235
CrossRef
Journal of Cardiothoracic and Vascular Anesthesia
Cerebral Oxygenation Impairment and S-100 beta Protein Release During Off-Pump Coronary Artery Revascularization
Tsaousi, GG; Pitsis, AA; Deliaslani, DV; Amaniti, EN; Karakoulas, KA; Vasilakos, DG
Journal of Cardiothoracic and Vascular Anesthesia, 27(2): 245-252.
10.1053/j.jvca.2012.06.009
CrossRef
Archives Italiennes De Biologie
Neural correlates of consciousness during general anesthesia using functional magnetic resonance imaging (fMRI)
Bonhomme, V; Boveroux, P; Brichant, JF; Laureys, S; Boly, M
Archives Italiennes De Biologie, 150(): 155-163.

Acta Anaesthesiologica Scandinavica
Minimal alveolar concentration of sevoflurane for maintaining bispectral index below 50 in morbidly obese patients
Zeidan, A; Mazoit, JX
Acta Anaesthesiologica Scandinavica, 57(4): 474-479.
10.1111/aas.12038
CrossRef
Anesthesiology
The Dynamic Relationship between End‐tidal Sevoflurane and Isoflurane Concentrations and Bispectral Index and Spectral Edge Frequency of the Electroencephalogram
Olofsen, E; Dahan, A
Anesthesiology, 90(5): 1345-1353.

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Anesthesiology, 98(5): 1101-1111.

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Can Bispectral Index Monitoring Predict Recovery of Consciousness in Patients with Severe Brain Injury?
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Stein, E; Glick, D; Minhaj, M; Drum, M; Tung, A
Anesthesiology, 113(1): 35-40.
10.1097/ALN.0b013e3181dc1dfe
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Anesthesiology, 95(3): 708-715.

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Influence of an external pacemaker on bispectral index
Vretzakis, G; Dragoumanis, C; Ferdi, H; Papagiannopoulou, P
European Journal of Anaesthesiology (EJA), 22(1): 70-72.
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What does the bispectral EEG index monitor?
Chan, MT; Gin, T
European Journal of Anaesthesiology (EJA), 17(3): 146-148.

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Cerebral state monitor, a new small handheld EEG monitor for determining depth of anaesthesia: a clinical comparison with the bispectral index during day‐surgery
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European Journal of Anaesthesiology (EJA), 23(3): 208-212.
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Keywords:
Deoxyglucose; humans; radionuclide imaging

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