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European Journal of Anaesthesiology:
Update in Intravenous Anaesthesia: Original Papers

Monitoring depth of anaesthesia

Schneider, G.; Sebel, P. S.

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Department of Anesthesiology, Emory University School of Medicine, Atlanta, GA, USA

Correspondence to: Professor Peter S. Sebel, Department of Anesthesiology - Box 26074, Grady Health System, 80 Butler Street, SE, Atlanta, Georgia 30335-3801, USA.

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In clinical practice, indirect and non-specific signs are used for monitoring anaesthetic adequacy. These include haemodynamic, respiratory, muscular and autonomic signs. These measures do not indicate adequacy of anaesthesia in a reliable manner. Many attempts have been made to find a more accurate monitor. Direct monitoring of anaesthetic effect should be possible by EEG measurement. EEG information can be reduced, condensed and simplified, leading to single numbers (spectral edge frequency and median frequency). These methods appear insufficient for assessing anaesthetic adequacy. The bispectral index, derived from bispectral analysis of the EEG, is a very promising tool for measuring adequacy of anaesthesia. An alternative approach is to monitor evoked potentials. Middle latency auditory evoked potentials may be helpful in assessing anaesthetic adequacy. Both techniques need further validation.

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Introduction: anaesthetic stages

‘I have breathed the ether on several occasions, and think its effects may be divided into three stages or degrees. The first is merely a pleasurable feeling of half intoxication; the second is one of extreme pleasure, being similar to the sensations produced by breathing nitrous oxide, or laughing gas; ... The third stage, the only one, I think, for performing operations in, is one of profound intoxication and insensibility.’[1]

This statement, written in 1847 by Plomley in a letter to the Lancet, was one of the first definitions of the several stages of anaesthesia. In 1920, Guedel described four stages of anaesthesia, the first being analgesia and consciousness, the second stage excitement, the third surgical stage, and the fourth beginning with cessation of respiration and ending with cardiac paralysis and death. He noted a great range of the third stage [2], which he subdivided into four planes. Plane one shows slight somatic relaxation, regular respiration, and active ocular muscles. In the second plane the inspiration is briefer than exhalation with an inspiratory pause, and the eyes are immobile. Plane three is characterized by abdominal muscle relaxation and loss of eyelid reflex. In plane four, paradoxical rib cage movement occurs, and pupils are dilated. In 1954 Artusio [3] further divided the first stage into three planes, characterized by amnesia (plane two) followed by analgesia (complete in plane three). The use of other volatile agents, intravenous anaesthetics, and combinations of opioids with other drugs in modern anaesthetic practice, limit the value of these classical signs and stages.

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Changing concepts of anaesthesia

With the introduction of d-tubocurare, detection and monitoring the different stages of anaesthesia as described by Guedel and Artusio became more complicated and almost impossible. Seven out of the nine components of Guedel's classification involved skeletal muscle movement. The remaining two, pupil size and lacrimation, are only valuable if no opioids or anticholinergics are used during anaesthesia. This shows the limited value of the described signs for combinations of drugs. Woodbridge introduced the four component concept of anaesthesia in 1957: sensory block, reflex block, motor block and mental block [4]. Thirty years later Pinsker [5] suggested that paralysis, unconsciousness and attenuation of stress are the necessary components of anaesthesia. In 1987, Prys-Roberts [6] stated that there is no 'depth of anaesthesia'. In his editorial he defines loss of consciousness as an all-or-none phenomenon. Thus, there are no degrees nor variable depth of anaesthesia. As pain is a 'conscious perception of noxious stimulus', a 'state of anaesthesia' can be described as drug-induced unconsciousness in which the patient neither perceives nor recalls pain. Kissin's definition of anaesthesia [7] includes prevention of somatic as well as psychologically adverse effects of surgery. Like Prys-Roberts, Kissin views anaesthesia as a spectrum of separate pharmacological actions produced by one or more drugs. Today, anaesthesia is achieved by administration of several drugs to attain amnesia, sedation, analgesia, paralysis and suppression of stress response. There is a large variability in the requirement for sedatives and analgesics [8], depending on the individual patient and the surgical procedure. In the modern practice of anaesthesia, the term 'depth of anaesthesia' and the definition of stages are irrelevant. Anaesthesia is not 'deep' or 'light': it may or may not be adequate. Thus, administration of anaesthetic agents should be tailored to the specific needs of the patient and the surgery performed. Useful monitoring should contain information about adequacy of anaesthesia for individual patients and their surgery.

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Awareness, memory and recall

Following the introduction of neuromuscular blocking drugs, the occurrence of awareness increased and is still one of the major causes of patients' complaints and lawsuits against anaesthesiologists [9]. There has been much confusion, mainly because of different use of terms. Awareness is a state of being aware, i.e. conscious, watchful, vigilant, informed and being able to respond to command [10]. Memory is the ability to receive, modify, store and retrieve information. It can be divided into explicit and implicit memory. Explicit memory refers to conscious recollection of previous input with a reference to a specific event or stimulus. Implicit memory can have an effect on experience, thoughts, feelings or actions without any direct recollection of the past event that contributed to it [11]. Recall may be considered as synonymous with explicit memory [10]. The terms 'awareness' and 'implicit and explicit memory' have to be distinguished. A patient may be aware during surgery but have no recall of the event [12,13]. There may also be implicit memory even without awareness or explicit memory [14-16]. During anaesthesia, subconscious learning may occur. Some positive therapeutic effects of intra-operative suggestions have been demonstrated [15,17,18], but this is still a controversial field [19-21]. Inadequate anaesthesia and awareness can lead to post-traumatic psychological disorders [22,23]. Implicit memory may be manifested by acute or chronic psychosis or nightmares even years after surgery [23]. The reported incidence of recall varies from 0.2-2% [24-26] up to 4% [10]. The risk is greater for haemodynamically unstable patients, and for those undergoing emergency surgery.

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Traditional approaches

In today's clinical practice, blood pressure, heart rate, respiratory rate, rhythm and depth, muscle tonus, ocular signs, lacrimation and sweat are used for monitoring anaesthetic adequacy. All of these signs are indirect and non-specific, and they may vary over a wide range depending on disease, drugs and surgical technique. There is also a large interpatient variability. Even when all of these signs remain unchanged, awareness can occur [27-29]. It must be stated that no constellation of clinical signs is wholly specific and sensitive [8,30]. Haemodynamic signs may be misinterpreted. Increasing the dose of anaesthetic does not necessarily lead to bradycardia or hypotension [31-33]. On the other hand, a haemodynamic response following noxious stimulation does not necessarily mean awareness or perception of pain. During organ harvesting from brain-dead patients, haemodynamic responses following skin incision have been reported [34,35]. The central nervous system is not necessarily involved in these reactions: they may be mediated by spinothalamic tracts and adrenal medullary stimulation by reflex spinal arcs [36]. Other clinical signs such as diaphoresis and lacrimation have been utilized to estimate anaesthetic adequacy, but they, too, are neither sensitive nor specific [27,37,38]. The value of sweating is limited by the presence of temperature changes. Mydriasis loses its specificity and sensitivity after ocular surgery, ophthalmologic drugs, opioids and atropine. Blood pressure, heart rate, ocular signs, lacrimation and sweat are not valuable in predicting response to a noxious stimulus. They do not necessarily correlate with anaesthetic dose or concentration, nor with the adequacy of anaesthesia.

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For years, movement has been used for monitoring the adequacy of anaesthesia. In 1963, Merkel and Eger introduced the concept of MAC as the minimum alveolar concentration of halothane to prevent gross purposeful movement in response to a supramaximal noxious stimulus in 50% of subjects [39]. In humans, the initial skin incision is used as a reproducible form of stimulus. The concentration required to eliminate a motor response (MAC) is higher than that necessary for loss of consciousness (MAC-awake) [40] but lower than that needed to block an adrenergic response to the stimulus (MAC-BAR) [41]. Recently, it has been demonstrated that MAC does not - or not only - represent the effect of anaesthesia on the brain: Rampil et al. have shown in rats that not even precollicular decerebration altered the ability of general anaesthetics to block a somatic response [42]. MAC of isoflurane in decerebrate rats was 1.26%; not much different from the 1.3% found in the control group. In a subsequent study, Rampil performed spinal cord transection in a manner that prevented spinal shock: MAC did not change [43]. This leads to the conclusion that the site of anaesthetic inhibition of motor response may be in the spinal cord. Antognini and Schwartz separated the brain from the body circulation in goats, using two by-pass circuits [44]. With isoflurane delivered to the brain only, the concentration required to block movement was 2.9%, compared to 1.2% before bypass. Borges and Antognini [45], using the same experimental technique, maintained isoflurane concentration in the brain at 0.2-0.3%. Isoflurane was also delivered to the lungs. MAC for the body bypass was 0.8%, compared to 1.4% before bypass. This may be explained by different sensitivity of inhibitory and excitatory pathways in spinal cord and brain. These results suggest that the spinal cord might be much more important in MAC determination than the brain.

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Other approaches

There have been other approaches to monitoring anaesthetic adequacy, for example facial electromyography and measurement of lower oesophageal contractility. Recording summed facial electromyographic voltages via surface electrodes determines typical patterns of muscular tension. These patterns may be useful in monitoring sedation [46], but the method still has not been evaluated sufficiently. Lower oesophageal contractility was introduced as a means of monitoring anaesthetic adequacy for inhalation anaesthetics [47,48]. Measured values do not only depend on the type of anaesthesia [49], but also on the operation [50], and it was suggested that this method was inappropriate for assessing the adequacy of anaesthesia [51].

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EEG as an indicator of anaesthetic adequacy

Since the brain is the effect site of general anaesthetics, it is reasonable to assume that the EEG will reflect the effect of anaesthesia. The EEG is a non-invasive monitor of cerebral activity. It represents cortical electrical activity derived from summated excitatory and inhibitory post-synaptic activity. In 1931, Berger was the first to describe the influence of anaesthesia on the EEG [52]. Gibbs, in 1937 showed the influence of different drugs on the EEG [53]. Subsequently, it has been used for pharmacodynamic and pharmacokinetic studies of various drugs [54-57]. The main problem is the different pattern of EEG alterations caused by different drugs [55,58-60]. Due to its complexity and the difficulty of interpretation, the raw EEG is of very limited value as a monitor of depth of anaesthesia. Its complexity has been reduced by the use of a mathematical technique, Fourier analysis, digitizing the raw EEG and separating it into a number of sine waves. These are calculated to obtain the power spectrum [61]. Power spectral analysis assumes a Gaussian, stationary, and firstorder (linear) model of the frequencies within the EEG, i.e. the amplitudes are normally distributed, the statistical properties do not change over time and the frequency constituents are uncorrelated. Using these assumptions, the EEG is considered to be composed by linear superimposition of statistically independent sinusoidal wave components. Further reduction of the information led to the spectral edge frequency. This is a single number representing the frequency below which 95% of the total power is present [62]. There are correlations with anaesthetic adequacy [63,64], and the plasma concentration of drugs [31,54,58]. It has been used to guide opioid administration [64]. Controversy exists about its value as a predictor of a haemodynamic response to stimuli [63,65]. Median frequency (the frequency above and below which 50% of the EEG power resides) [66] is another single number derived from the power spectrum. It has been used in an adaptive feedback control algorithm for closed-loop administration of propofol [67], and other anaesthetic techniques [68-71]. Drummond, in a comparative study of five processed EEG parameters and their value as predictors of imminent arousal (spontaneous movement, coughing, eye opening) from isoflurane/N2O anaesthesia [72], did not find any of these measures reliable enough to serve as sole predictor. It appears that these EEG parameters may provide potentially useful information regarding changing levels of anaesthesia, but none of these is sufficiently reliable to be used as the sole indicator of anaesthetic depth.

Conventional power spectral EEG analysis does not use all the information contained in the EEG. Only frequency and power estimates are considered, while phase information is generally ignored. Bispectral analysis of the EEG provides means by which quadratic (second order) interactions can be quantified [73,74]. This is provided by quantifying the phase coupling between two frequencies and a third frequency (harmonic) by their sum or difference. The extent of the coupling can vary from 0% (no harmonic) to 100% (harmonic for the duration of the period analysed). Bispectral analysis gives a more comprehensive description of the information available from Fourier analysis than the power spectrum, including additional information. Bispectral analysis of the EEG might be helpful in determination of anaesthetic adequacy [75]. It is used to obtain BIS, the bispectral index, which has been shown to correlate with movement in response to skin incision using several drugs [76-78]. In predicting movement, an early version of BIS was found not to be independent of the drugs used [77,78]. The current version, BIS 3.0, is a multivariate non-linear index incorporating power spectra and bispectral EEG parameters and burst suppression [79]. It has been shown to correlate with depth of sedation using several drugs [80-82]. BIS correlated with loss and return of consciousness after thiopentone [83], as well as with the response to command and with recall [84]. Baseline BIS before intubation could not predict an awareness reaction following stimulus, but once awareness occurred, BIS discriminated between patients with and without an awareness reaction [85]. There has been no study with patients undergoing surgery during general anaesthesia correlating BIS with awareness or recall, although in unstimulated patients it appears to be a good predictor [86]. Studies so far suggest that BIS is a promising monitoring tool for the assessment of adequacy of anaesthesia.

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Evoked potentials

Auditory evoked responses (AER), representing the response of the auditory pathway to a sound stimulus, might be useful in monitoring adequacy of anaesthesia [16]. In order to calculate an AER, a repeated auditory stimulus is applied to the patient. All EEG periods immediately following each stimulus are averaged. Thus the non-stimulus-related portion of the EEG is eliminated and the specific evoked potentials remain. The response can be divided into several segments according to the anatomical area of its origin and the time elapsed since the stimulus. The brainstem auditory-evoked response is the early component of the AER (within the first 8 ms). It originates in the brainstem and is unaffected by most anaesthetics [87-91]. It is not helpful in determining anaesthetic adequacy. The late cortical response occurs between 50 and 1000 ms, reflecting activation of the frontal cortex [92]. It reflects the influence of anaesthetics [93,94], but is very much affected by attention, sleep and sedation [92,95], thus being of limited value for monitoring depth of anaesthesia. Between 40 and 60 ms after stimulation, the middle latency auditory evoked response (MLAER) is seen, and this is interesting for measuring anaesthetic effect. It represents neural activity within the thalamus and primary auditory cortex [16,92]. Thornton [94,96] and Schwender [97] suggest that MLAER is suitable for the measurement of 'anaesthetic depth'. Opioids, even at induction doses, do not affect the MLAER [98,99]. This might explain the high incidence of awareness and recall during high-dose opioid anaesthesia [98,100]. In patients undergoing cardiac surgery who showed no difference in AER pattern between sleep and awake (both with high amplitude and the same periodic waveform), a high incidence of implicit memory has been shown [16]. Confirming results came from Thornton, correlating awareness reaction with AER alterations [101]. Another approach has been suggested by Plourde et al., using the 40 Hz auditory steady state response (ASSR) [102]. The ASSR is a sinusoidal electrical response of the brain following repeatedly presented auditory stimuli, delivered sufficiently rapidly to produce overlapping of the responses to individual stimuli. Amplitude reductions (as seen during sleep [102,103]) were shown to correlate with anaesthesia and recovery for several drugs [102,104,105], but they did not show clear advantages over spectral edge frequency [106]. These data suggest that MLAERs in particular may be a possible tool for assessing anaesthetic adequacy.

At present, the most promising monitors for assessing anaesthetic adequacy seem to be bispectral index and middle latency auditory evoked potentials. Both of them still have to be validated further. One problem in this process is that we still cannot define nor measure all of our anaesthetic goals, such as the significance of implicit memory. As a result, every new monitor can only be validated using the limited means we use today.

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1 Plomley F. Operations Upon the Eye. Lancet 1847; i: 134-135.

2 Guedel AE. Third Stage Ether Anesthesia: A Sub-Classification Regarding the Significance of the Position and Movement of the Eyeball. Am J Surg, Quart Suppl of Anesth Analg 1920; 34: 53-57.

3 Artusio J. Di-ethyl ether analgesia: a detailed description of the first stage of ether analgesia in man. J Pharmacol Exp Therapeut 1954; 111: 343-348.

4 Woodbridge P. Changing concept concerning depth of anesthesia. Anesthesiology 1957; 18: 536-550.

5 Pinsker MC. Anesthesia: a pragmatic construct. Anesth Analg 1986; 65: 819-820.

6 Prys-Roberts C. Anaesthesia: a practical or impractical construct? Br J Anaesth 1987; 59: 1341-1345.

7 Kissin I. General anesthetic action: an obsolete notion? Anesth Analg 1993; 76: 215-218.

8 Ausems ME, Hug CC Jr, Stanski DR, Burm AG. Plasma concentrations of alfentanil required to supplement nitrous oxide anesthesia for general surgery. Anesthesiology 1986; 65: 362-373.

9 Aitkenhead AR. Risk management in anaesthesia. J Med Def Union 1991; 4: 86-90.

10 Ghoneim MM, Block RI. Learning and consciousness during general anesthesia. Anesthesiology 1992; 76: 279-305.

11 Kihlstrom JF. Implicit memory function during anesthesia. In: Bonke B, Sebel PS, Winograd E, ed. Memory and Awareness in Anesthesia, Englewood Cliffs, NJ: Prentice-Hall Inc., 1993: 10-30.

12 Russell IF. Balanced anesthesia: does it anesthetize? Anesth Analg 1985; 64: 941-942.

13 Russell IF. Midazolam-alfentanil: an anaesthetic? An investigation using the isolated forearm technique. Br J Anaesth 1993; 70: 42-46.

14 Jones JG, Konieczko K. Hearing and memory in anaesthetised patients. Br Med J (Clin Res Ed) 1986; 292: 1291-1293.

15 Jelicic M, Bonke B, Appelboom DK. Indirect memory for words presented during anaesthesia. Lancet 1990; 336: 249.

16 Schwender D, Kaiser A, Klasing S, Peter K, Poppel E. Midlatency auditory evoked potentials and explicit and implicit memory in patients undergoing cardiac surgery. Anesthesiology 1994; 80: 493-501.

17 Evans C, Richardson PH. Improved recovery and reduced postoperative stay after therapeutic suggestions during general anaesthesia. Lancet 1988; 2: 491-493.

18 Caseley-Rondi G, Merikle PM, Bowers KS. Unconscious cognition in the context of general anesthesia. Conscious Cogn 1994; 3: 166-195.

19 Liu WH, Standen PJ, Aitkenhead AR. Therapeutic suggestions during general anaesthesia in patients undergoing hysterectomy. Br J Anaesth 1992; 68: 277-281.

20 Millar K. Efficacy of therapeutic suggestions presented during anaesthesia: re-analysis of conflicting results. Br J Anaesth 1993; 71: 597-601.

21 Chortkoff BS, Gonsowski CT, Bennett HL et al. Subanesthetic concentrations of desflurane and propofol suppress recall of emotionally charged information. Anesth Analg 1995; 81: 728-736.

22 Suresh D. Nightmares and recovery from anesthesia. Anesth Analg 1991; 72: 404-405.

23 Brimacombe J, Macfie AG. Peri-operative nightmares in surgical patients. Anaesthesia 1993; 48: 527-529.

24 Mainzer JJ. Awareness, muscle relaxants and balanced anesthesia. Canad Anaesth Soc J 1979; 26: 386-393.

25 Sandin R, Norstrom O. Awareness during total i.v. anaesthesia. Br J Anaesth 1993; 71: 782-787.

26 Breckenridge JL, Aitkenhead AR. Awareness during anaesthesia: a review. Ann R Coll Surg Engl 1983; 65: 93-96.

27 Hilgenberg JC. Intraoperative awareness during high-dose fentanyl-oxygen anesthesia. Anesthesiology 1981; 54: 341-343.

28 Hug CC, Moldenhauer CC. Does opioid "anesthesia" exist? Anesthesiology 1990; 73: 1-4.

29 Moerman N, Bonke B, Oosting J. Awareness and recall during general anesthesia. Facts and feelings. Anesthesiology 1993; 79: 454-464.

30 Glass PS, Doherty M, Jacobs JR, Goodman D, Smith LR. Plasma concentration of fentanyl, with 70% nitrous oxide, to prevent movement at skin incision. Anesthesiology 1993; 78: 842-847; discussion 23A.

31 Hudson RJ, Stanski DR, Saidman LJ, Meathe E. A model for studying depth of anesthesia and acute tolerance to thiopental. Anesthesiology 1983; 59: 301-308.

32 Weiskopf RB, Moore MA, Eger Eln et al. Rapid increase in desflurane concentration is associated with greater transient cardiovascular stimulation than with rapid increase in isoflurane concentration in humans. Anesthesiology 1994; 80: 1035-1045.

33 Yli-Hankala A, Randell T, Seppala T, Lindgren L. Increases in hemodynamic variables and catecholamine levels after rapid increase in isoflurane concentration. Anesthesiology 1993; 78: 266-271.

34 Larson MD. Surgically induced hypertension in brain dead patients. Anesth Analg 1985; 64: 1030.

35 Wetzel RC, Setzer N, Stiff JL, Rogers MC. Hemodynamic responses in brain dead organ donor patients. Anesth Analg 1985; 64: 125-128.

36 Guyton AC. The Autonomic Nervous System; The Adrenal Medulla. In: Textbook of Medical Physiology, 8th edn. Philadelphia: W. B. Saunders Co., 1991: 667-678.

37 Russell IF. Comparison of wakefulness with two anaesthetic regimens. Total i.v. v. balanced anaesthesia. Br J Anaesth 1986; 58: 965-968.

38 Schultetus RR, Hill CR, Dharamraj CM, Banner TE, Berman LS. Wakefulness during cesarean section after anesthetic induction with ketamine, thiopental, or ketamine and thiopental combined. Anesth Analg 1986; 65: 723-728.

39 Merkel G, Eger EI. A comparative study of halothane and halopropane anesthesia. Anesthesiology 1963; 24: 346-357.

40 Newton DE, Thornton C, Konieczko K et al. Levels of consciousness in volunteers breathing sub-MAC concentrations of isoflurane. Br J Anaesth 1990; 65: 609-615.

41 Roizen MF, Horrigan RW, Frazer BM. Anesthetic doses blocking adrenergic (stress) and cardiovascular responses to incision-MAC BAR. Anesthesiology 1981; 54: 390-398.

42 Rampil IJ, Mason P, Singh H. Anesthetic potency (MAC) is independent of forebrain structures in the rat. Anesthesiology 1993; 78: 707-712.

43 Rampil IJ. Anesthetic potency is not altered after hypothermic spinal cord transection in rats. Anesthesiology 1994; 80: 606-610.

44 Antognini JF, Schwartz K. Exaggerated anesthetic requirements in the preferentially anesthetized brain. Anesthesiology 1993; 79: 1244-1249.

45 Borges M, Antognini JF. Does the brain influence somatic responses to noxious stimuli during isoflurane anesthesia? Anesthesiology 1994; 81: 1511-1515.

46 Wilson S. Facial electromyography and chloral hydrate in the young dental patient. Pediatr Dent 1993; 15: 343-347.

47 Evans JM, Bithell JF, Vlachonikolis IG. Relationship between lower oesophageal contractility, clinical signs and halothane concentration during general anaesthesia and surgery in man. Br J Anaesth 1987; 59: 1346-13655.

48 Evans JM, Davies WL, Wise CC. Lower oesophageal contractility: a new monitor of anaesthesia. Lancet 1984; 1: 1151-1154.

49 Sessler DI, Stoen R, Olofsson CI, Chow F. Lower esophageal contractility predicts movement during skin incision in patients anesthetized with halothane, but not with nitrous oxide and alfentanil. Anesthesiology 1989; 70: 42-46.

50 Thomas DI, Aitkenhead AR. Relationship between lower oesophageal contractility and type of surgical stimulation. Br J Anaesth 1990; 64: 306-310.

51 Raftery S, Enever G, Prys-Roberts C. Oesophageal contractility during total i.v. anaesthesia with and without glycopyrronium. Br J Anaesth 1991; 66: 566-571.

52 Berger H. Electroencephalogram of man (Ueber das Elektroenkephalogramm des Menschen). Archiv fuer Psychiatrie 1931; 94: 16-60.

53 Gibbs FA, Gibbs EL, Lennox WG. Effect on the electroencephalogram of certain drugs which influence nervous activity. Arch Intern Med 1937; 60: 154-166.

54 Scott JC, Ponganis KV, Stanski DR. EEG quantitation of narcotic effect: the comparative pharmacodynamics of fentanyl and alfentanil. Anesthesiology 1985; 62: 234-241.

55 Scott JC, Cooke JE, Stanski DR. Electroencephalographic quantitation of opioid effect: comparative pharmacodynamics of fentanyl and sufentanil. Anesthesiology 1991; 74: 34-42.

56 Homer TD, Stanski DR. The effect of increasing age on thiopental disposition and anesthetic requirement. Anesthesiology 1985; 62: 714-724.

57 Stanski DR, Maitre PO. Population pharmacokinetics and pharmacodynamics of thiopental: the effect of age revisited. Anesthesiology 1990; 72: 412-422.

58 Buhrer M, Maitre PO, Hung OR, Ebling WF, Shafter SL, Stanski DR. Thiopental pharmacodynamics. I. Defining the pseudosteady-state serum concentration-EEG effect relationship. Anesthesiology 1992; 77: 226-236.

59 Eger Eld, Stevens WC, Cromwell TH. The electroencephalogram in man anesthetized with forane. Anesthesiology 1971; 35: 504-508.

60 Neigh JL, Garman JK, Harp JR. The electroencephalographic pattern during anesthesia with ethrane: effects of depth of anesthesia, PaCO2, and nitrous oxide. Anesthesiology 1971; 35: 482-487.

61 Levy WJ, Shapiro HM, Maruchak G, Meathe E. Automated EEG processing for intraoperative monitoring: a comparison of techniques. Anesthesiology 1980; 53: 223-236.

62 Rampil IJ, Holzer JA, Quest DO, Rosenbaum SH, Correll JW. Prognostic value of computerized EEG analysis during carotid endarterectomy. Anesth Analg 1983; 62: 186-192.

63 Rampil IJ, Matteo RS. Changes in EEG spectral edge frequency correlate with the hemodynamic response to laryngoscopy and intubation. Anesthesiology 1987; 67: 139-142.

64 Sidi A, Halimi P, Cotev S. Estimating anesthetic depth by electroencephalography during anesthetic induction and intubation in patients undergoing cardiac surgery. J Clin Anesth 1990; 2: 101-107.

65 White PF, Boyle WA. Relationship between hemodynamic and electroencephalographic changes during general anesthesia. Anesth Analg 1989; 68: 177-181.

66 Long CW, Shah NK, Loughlin C, Spydell J, Bedford RF. A comparison of EEG determinants of near-awakening from isoflurane and fentanyl anesthesia. Spectral edge, median power frequency, and delta ratio. Anesth Analg 1989; 69: 169-173.

67 Schwilden H, Stoeckel H, Schuttler J. Closed-loop feedback control of propofol anaesthesia by quantitative EEG analysis in humans. Br J Anaesth 1989; 62: 290-296.

68 Schwilden H, Schuttler J, Stoeckel H. Closed-loop feedback control of methohexital anesthesia by quantitative EEG analysis in humans. Anesthesiology 1987; 67: 341-347.

69 Schwilden H, Stoeckel H. Effective therapeutic infusions produced by closed-loop feedback control of methohexital administration during total intravenous anesthesia with fentanyl. Anesthesiology 1990; 73: 225-229.

70 Schwilden H, Schuttler J, Stoeckel H. Quantitation of the EEG and pharmacodynamic modelling of hypnotic drugs: etomidate as an example. Eur J Anaesthesiol 1985; 2: 121-131.

71 Schwilden H, Stoeckel H. Closed-loop feedback controlled administration of alfentanil during alfentanil-nitrous oxide anaesthesia. Br J Anaesth 1993; 70: 389-393.

72 Drummond JC, Brann CA, Perkins DE, Wolfe DE. A comparison of median frequency, spectral edge frequency, a frequency band power ratio, total power, and dominance shift in the determination of depth of anesthesia. Acta Anaesthesiol Scand 1991; 35: 693-699.

73 Huber PJ, Kleiner B, Gasser T, Dumermuth G. Statistical methods for investigating phase relations in stationary stochastic processes. IEEE Trans Audio Electroacoust 1971; 19: 78-86.

74 Sigl J, Chamoun N. An introduction to bispectral analysis for the electroencephalogram. J Clin Monit 1994; 10: 392-404.

75 Abke J, Nahm W, Stockmanns G, Kalkman C, Kochs E. Detection of inadequate anesthesia by EEG power and bispectral analysis. Anesthesiology 1996; 85 (3A): A477.

76 Jacoby LL, Allan LG, Collins JC, Larwill LK. Memory influences subjective experience: noise judgments. J Exp Psychol Leam Mem Cogn 1988; 14: 240-247.

77 Sebel PS, Bowles SM, Saini V, Chamoun N. EEG bispectrum predicts movement during thiopental/isoflurane anesthesia. J Clin Monit 1995; 11: 83-91.

78 Vernon JM, Lang E, Sebel PS, Manberg P. Prediction of movement using bispectral electroencephalographic analysis during propofol/alfentanil or isoflurane/alfentanil anesthesia. Anesth Analg 1995; 80: 780-785.

79 Avramov MN, Greenwald SD, White PF. EEG assessment of sedation during monitored anesthesia care (MAC). Anaesth Analg 1996; 82, S1: S 14.

80 Liu J, Singh H, White PF. Electroencephalogram bispectral analysis predicts the depth of midazolam-induced sedation. Anesthesiology 1996; 84: 64-69.

81 Flaishon R, Sebel PS, Sigl J. Bispectral analysis of the EEG for monitoring the hypnotic effect of propofol and propofol/alfentanil. Anesthesiology 1995; 83: A 514.

82 Kearse L, Rosow C, Connors P, Denman W, Dershwitz M. Propofol sedation/hypnosis and bispectral EEG analysis in volunteers. Anesthesiology 1995; 83: A 506.

83 Flaishon R, Sebel PS, Sigl J. Detection of consciousness following thiopental: isolated forearm and bispectral EEG (BIS). Anesthesiology 1995; 83: A 515.

84 Kearse L, Rosow C, Sebel P et al. The bispectral index correlates with sedation/hypnosis and recall: comparison using multiple agents. Anesthesiology 1995; 83: A 507.

85 Schneider G, Wagner K, Wemer C, Kochs E. Bispectral analysis does not predict, but correlates with awareness reaction to intubation. J Neurosurg Anesthesiol 1996; 8: 348.

86 Flaishon R, Windsor A, Sigl J, Sebel PS. Recovery of consciousness during general anesthesia: EEG bispectrum and the isolated forearm technique. Anesthesiology (in press)

87 Chassard D, Joubaud A, Colson A, Guiraud M, Dubreuil C, Banssillon V. Auditory evoked potentials during propofol anaesthesia in man. Br J Anaesth 1989; 62: 522-526.

88 Thomton C, Heneghan CP, James MF, Jones JG. Effects of halothane or enflurane with controlled ventilation on auditory evoked potentials. Br J Anaesth 1984; 56: 315-323.

89 Newton DE, Thomton C, Creagh-Barry P, Dore CJ. Early cortical auditory evoked response in anaesthesia: comparison of the effects of nitrous oxide and isoflurane. Br J Anaesth 1989; 62: 61-65.

90 Loughnan BL, Sebel PS, Thomas D, Rutherfoord CF, Rogers H. Evoked potentials following diazepam or fentanyl. Anaesthesia 1987; 42: 195-198.

91 Schwender D, Klasing S, Madler C, Poppel E, Peter K. Midlatency auditory evoked potentials during ketamine anaesthesia in humans. Br J Anaesth 1993; 71: 629-632.

92 Picton TW, Hillyard SA, Krausz HI, Galambos R. Human auditory evoked potentials. I. Evaluation of components. Electroencephalogr Clin Neurophysiol 1974; 36: 179-190.

93 Schmidt JF, Chraemmer-Jorgensen B. Auditory evoked potentials during isoflurane anaesthesia. Acta Anaesthesiol Scand 1986; 30: 378-380.

94 Thomton C, Heneghan CP, Navaratnarajah M, Bateman PE, Jones JG. Effect of etomidate on the auditory evoked response in man. Br J Anaesth 1985; 57: 554-561.

95 Picton TW, Hillyard SA. Human auditory evoked potentials. II. Effects of attention. Electroencephalogr Clin Neurophysiol 1974; 36: 191-199.

96 Thornton C, Heneghan CP, Navaratnarajah M, Jones JG. Selective effect of althesin on the auditory evoked response in man. Br J Anaesth 1986; 58: 422-427.

97 Schwender D, Haessler R, Klasing S, Madler C, Poppel E, Peter K. Mid-latency auditory evoked potentials and circulatory response to loud sounds. Br J Anaesth 1994; 72: 307-314.

98 Schwender D, Rimkus T, Haessler R, Klasing S, Poppel E, Peter K. Effects of increasing doses of alfentanil, fentanyl and morphine on mid-latency auditory evoked potentials. Br J Anaesth 1993; 71: 622-628.

99 Schwender D, Weninger E, Daunderer M, Klasing S, Poppel E, Peter K. Anesthesia with increasing doses of sufentanil and midlatency auditory evoked potentials in humans. Anesth Analg 1995; 80: 499-505.

100 Maeckelmann S, Buchfelder A, Schwender D. A case of intraoperative awareness during balanced anaesthesia with sufentanil. Anaesthesia 1996; 51: 802.

101 Thornton C, Konieczko K, Jones JG, Jordan C, Dore CJ, Heneghan CP. Effect of surgical stimulation on the auditory evoked response. Br J Anaesth 1988; 60: 372-378.

102 Plourde G, Picton TW. Human auditory steady-state response during general anesthesia. Anesth Analg 1990; 71: 460-468.

103 Umegaki Y. (Auditory steady-state response to sinusoidally amplitude-modulated tones. Second report: investigation of response in the sleeping state). Nippon Jibiinkoka Gakkai Kaiho 1995; 98: 430-441.

104 Plourde G, Boylan JF. The auditory steady state response during sufentanil anaesthesia. Br J Anaesth 1991; 66: 683-691.

105 Plourde G, Villemure C. Comparison of the effects of enflurane/N2O on the 40-Hz auditory steady-state response versus the auditory middle-latency response. Anesth Analg 1996; 82: 75-83.

106 Plourde G. The effects of propofol on the 40-Hz auditory steady-state response and on the electroencephalogram in humans. Anesth Analg 1996; 82: 1015-1022.

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Section Description

Seventh International Symposium on Intravenous Anaesthesia, Lausanne, Switzerland, 2-3 May 1997

This publication is supported by grants from various pharmaceutical companies. The views in this publication are those of the authors and not necessarily those of supporting companies. Drugs and administration techniques referred to should only be used as recommended in the manufacturers' prescribing information.


Monitoring evoked potentials; Brain Eeg, evoked potentials; Anaesthesia depth

© 1997 European Society of Anaesthesiology


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