Median Edge Frequency Research Articles

Comparison of EEG Approximate Entropy and Complexity Measures of Depth of Anaesthesia During Inhalational General Anaesthesia

Approximate entropy (ApEn) and Lempel-Ziv complexity (LZC), which are nonlinear quantification methods of the regularity of electroencephalogram (EEG) signals, have recently been proposed as measures of the depth of anaesthesia. The present study compares these two methods to two traditional linear methods, namely 95% spectral edge frequency (SEF95) and median edge frequency (MEF), and a commercial method, bispectral index (BIS), in pre-anaesthesia, maintenance, and recovery stages. Twenty-three patients (12 males and 11 females) with inhalational anaesthesia were enrolled. The BIS, SEF95, and MEF data of the anaesthetized subjects are collected using a BIS monitor. Raw EEG data are transmitted to a computer for off-line analysis to obtain ApEn and LZC values. The ApEn, LZC, SEF95, and MEF values are converted to a 0-100 range for comparison with BIS. There are significant differences (P＜0.05) in th results between the pre-anaesthesia and maintenance stages and between the recovery and maintenance stages obtained from BIS, ApEn, and LZC, which indicates that the three measures can differentiate the state of anaesthetia in a patient. There are no differences (P＞0.05) in the ApEn and LZC values between the pre-anaesthesia and recovery stages, indicating that ApEn and LZC show the increases in values from maintenance phase to recovery phase similar to the reductions in values from pre-anaesthesia phase to maintenance phase. The changes of ApEn and LZC in recovery stage are significantly larger than that exhibited by BIS. BIS shows a statistically reduced level from the pre-anaesthesia to the recovery stage, whereas ApEn and LZC show no difference. This indicates that ApEn and LZC respond more rapidly to recovery than does BIS. LZC and ApEn perform more sensitively than BIS in detecting the recovery of consciousness from non-responding to responding. Moreover, traditional assessments SEF95 and MEF perform poorly compared to BIS.

The Differential Effects of Halothane and Isoflurane on Electroencephalographic Responses to Electrical Microstimulation of the Reticular Formation

Isoflurane and halothane cause electroencephalographic (EEG) depression and neuronal depression in the reticular formation, a site critical to consciousness. We hypothesized that isoflurane, more than halothane, would depress EEG activation elicited by electrical microstimulation of the reticular formation. Rats were anesthetized with either halothane or isoflurane and stimulating electrodes were positioned in the reticular formation. In a crossover design, anesthetic concentration was adjusted to 0.8 and 1.2 minimum alveolar concentration (MAC) of halothane or isoflurane and electrical microstimulation was performed and the EEG responses were recorded. Microstimulation increased the spectral edge and median edge frequencies 2-2.5 Hz at 0.8 MAC for halothane and isoflurane and 1.2 MAC halothane. At 1.2 MAC isoflurane, burst suppression occurred and microstimulation decreased the period of isoelectricity (24% +/- 19% to 8% +/- 7%; P < 0.05), whereas the spectral edge and median edge frequencies were unchanged. At anesthetic concentrations required to produce immobility, the cortex remains responsive to electrical microstimulation of the reticular formation, although the EEG response is depressed in the transition from 0.8 to 1.2 MAC. These data indicate that cortical neurons remain responsive to synaptic input during isoflurane and halothane anesthesia.

Halothane and propofol differentially affect electroencephalographic responses to noxious stimulation

Anaesthetics blunt neuronal responses to noxious stimulation, including effects on electroencephalographic (EEG) responses. It is unclear how anaesthetics differ in their ability to modulate noxious stimulation-evoked EEG activation. We investigated the actions of propofol and halothane on EEG responses to noxious stimuli, including repetitive electrical C-fibre stimulation, which normally evokes neuronal wind-up. Rats were anaesthetized with halothane (n=8) or propofol (n=8), at 0.8x or 1.2x the amount required to produce immobility in response to tail clamping [minimum alveolar concentration (MAC) for halothane and median effective dose (ED(50)) for propofol]. We recorded EEG responses to repetitive electrical stimulus trains (delivered to the tail at 0.1, 1 and 3 Hz) as well as supramaximal noxious tail stimulation (clamp; 50 Hz electrical stimulus, each for 30 s). Under halothane anaesthesia, noxious stimuli evoked an EEG activation response manifested by increased spectral edge frequency (SEF) and median edge frequency (MEF). At 0.8 MAC halothane, the tail clamp increased the MEF from approximately 6 to approximately 8.5 Hz, and the SEF from approximately 25.5 to approximately 27 Hz. At both 0.8 and 1.2 MAC halothane, similar patterns of EEG activation were observed with the 1 Hz, 3 Hz and tetanic stimulus trains, but not with 0.1 Hz stimulation, which does not evoke wind-up. Under propofol anaesthesia, noxious stimuli were generally ineffective in causing EEG activation. At 0.8 ED(50) propofol, only the tail clamp and 1 Hz stimuli increased MEF ( approximately 8 to approximately 10-10.5 Hz). At the higher propofol infusion rate (1.2 ED(50)) the repetitive electrical stimuli did not evoke an EEG response, but the tetanic stimulus and the tail clamp paradoxically decreased SEF (from approximately 23 to approximately 21.5 Hz). Propofol has a more significant blunting effect on EEG responses to noxious stimulation compared with halothane.

The effect of isoflurane and halothane on electroencephalographic activation elicited by repetitive noxious c-fiber stimulation

Windup is the progressive increase in neuronal response to a repetitive noxious stimulus. This response is most often observed in the spinal cord, but it is unclear how this response is manifested in supraspinal structures. We investigated the effects of isoflurane and halothane on electroencephalographic responses to repetitive noxious electrical stimuli (20 pulses at 0.1, 1 and 3 Hz) applied to the tail in rats. Halothane and isoflurane concentrations were adjusted to 0.8 and 1.2 minimum alveolar concentration (MAC), where MAC is the concentration needed to prevent gross and purposeful movement in 50% of animals. At 0.8 MAC halothane, the 3 Hz stimulus caused electroencephalographic (EEG) activation primarily by increasing the median edge frequency (MEF), while at 1.2 MAC halothane the spectral edge frequency (SEF) was increased by the 1 and 3 Hz stimuli, and the MEF was increased by the 3 Hz stimuli. At 0.8 MAC isoflurane, the 1 and 3 Hz stimuli evoked EEG activation by increasing the MEF and SEF, while at 1.2 MAC only the MEF was increased by the 1 Hz stimulus. No EEG activation occurred with the 0.1 Hz repetitive stimulus with either isoflurane or halothane. These data suggest that repetitive electrical stimulation normally associated with windup in spinal neurons can evoke EEG activation.

Intrathecal picrotoxin minimally alters electro‐encephalographic responses to noxious stimulation during halothane and isoflurane anesthesia

Isoflurane and halothane act in the spinal cord to blunt ascending transmission of impulses to the brain resulting from noxious stimulation. Because intrathecal picrotoxin (an antagonist at the gamma-aminobutyric acid-A receptor) partially reverses the immobilizing effect of isoflurane and halothane, we hypothesized that the electroencephalographic response to noxious stimulation would likewise be partially reversed by intrathecal picrotoxin. Rats were anesthetized with isoflurane (n = 8) or halothane (n = 8) and a laminectomy performed. Following determination of minimum alveolar concentration (MAC), the electroencephalogram (EEG) was recorded during separate applications of a hindpaw clamp, tail clamp and electrical current to the tail at 0.8 and 1.2 MAC. Picrotoxin was then applied to the exposed spinal cord and the EEG response to noxious stimulation again determined. The EEG was more active during halothane anesthesia than isoflurane (spectral edge frequency for 95% power: 25.6 +/- 2.1 Hz vs. 23.1 +/- 1.6 Hz, P < 0.05). Noxious stimulation usually caused the EEG to shift to higher frequencies (e.g. for 0.8 MAC halothane, median edge frequency for 50% power: from 7.6 +/- 3.1 Hz to 10.7 +/- 2.6 Hz, P < 0.05). Picrotoxin minimally affected this response. Noxious stimulation evokes an EEG response that is minimally altered by intrathecal picrotoxin. This suggests that isoflurane and halothane do not have GABAergic actions in the spinal cord that indirectly suppress the EEG response.

Quantitative Electroencephalography of Medetomidine, Medetomidine‐Midazolam and Medetomidine‐Midazolam‐Butorphanol in Dogs

The purpose of this study was to evaluate the effects of the administration of an alpha2-adrenoceptor agonist alone and in combination with other derivatives on brain wave activity. In addition, the diagnostic values of the electroencephalogram (EEG) for judging the depth of the balanced anaesthesia with an alpha2-adrenoceptor agonist was evaluated. The treatments comprised 20 microg/kg medetomidine (Me-20), 80 microg/kg medetomidine (Me-80), 20 microg/kg medetomidine and 0.5 mg/kg midazolam (Me-Mi) administered intramuscularly, and 20 microg/kg medetomidine with 0.5 mg/kg midazolam and 0.1 mg/kg butorphanol (Me-Mi-Bu). The EEG was recorded continuously at pre-administration, and at 7, 10, 20, 30, 45 and 60 min after administration. The recorded data were analysed by separating the power spectrum into 1-3, 4-7, 8-13 and 14-30 Hz bands. Spectral-edge analysis was used to calculate the spectral edge frequency 90 (SEF90) and the median edge frequency (MEF). Time-related changes in power spectrum analysis showed a significant increase in the Me-80 group in the 1-3 Hz band. The power for 1-3 Hz in the Me-80 group was significantly higher than in all the other groups. In the 14-30 Hz band, there was a significant reduction of power in all groups following administration of the agents. The SEF90 frequencies were significantly reduced in all groups except for the Me-20 group after administration of the agents. The SEF90 frequencies in the Me-20, Me-Mi and Me-Mi-Bu were all significantly higher than those in the Me-80 group. However, there was no significant difference between the Me-20, Me-Mi and Me-Mi-Bu groups in any analyses. Our results demonstrated that the changes in quantitative EEG made by the Me-Mi-Bu and Me-Mi groups were similar to those made by Me-20 groups. Present results suggest that the EEG should be interpreted with caution in assessing the anaesthetic level in balanced anaesthesia in dogs.