To the Editor:—

A recent editorial 1proposes some interesting ideas, and places into perspective some of the many issues that have arisen since the introduction of the so-called “depth of anesthesia” monitors. The authors ask two main questions: (1) What are we trying to accomplish with these monitors? and (2) should these monitors be based on measurements derived from spontaneous electrophysiologic activity or evoked responses of the brain?

There are some conceptual hurdles that must be cleared when studying the depth of anesthesia. One of these is actually defining depth of anesthesia. Is depth of anesthesia equivalent to “level of consciousness?” Or should we go back to the classic definition of anesthesia, separating depth of hypnosis, depth of analgesia (as a measure of autonomic response to stimulus or stress), and level of muscle relaxation?

Maybe we should think about what is expected from the depth of anesthesia monitors. The BIS® (Aspect Medical Systems Inc., Newton, MA, USA) and A-line® (Alaris Medical Systems, Inc., San Diego, CA, USA) devices are designed to monitor the hypnotic state of the patient. Both process information from the cortex, although the A-line® also indirectly assesses the subcortical and brainstem auditory pathways. It is not surprising then, that the indices they derive are poor predictors of either movement (a spinal chord response, as suggested by Struys et al.  in their study 2) or autonomic and hemodynamic reactions, which are poorly related with the cortical response of the brain. 3 

The same idea is reflected when the authors mention the usefulness of the mid-latency auditory evoked potentials (MLAEP) monitors to predict the effect of benzodiazepines and narcotics on the level of hypnosis. With respect to benzodiazepines, it is correct that some publications state that they have little effect on MLAEP. 4However, most of the studies carried out recently agree on the good response obtained with those monitors on patients anesthetized with benzodiazepines. 5,6 

Similarly, there is a substantial distinction between analgesia and hypnosis. Opioids are used to blunt the response to painful stimulation. However, no study has demonstrated that narcotics induce hypnosis by themselves, although they may reduce the amounts of other drugs needed to obtain a certain level of hypnosis. The old “Pure Analgesic Technique” from De Castro et al.  applied in Europe during the mid-seventies comes to mind. 7,8It used only huge doses of fentanyl plus neuromuscular blocking agents in order for patients to be in “no pain but able to answer.” Because analgesia can be dissociated from hypnosis, it is thus illogical to expect monitors to “track” analgesia, or alternatively, changes induced by opioids may not reflect depth of hypnosis.

We therefore agree with the authors that both of these monitors provide only partial information about the anesthetic state of the patient. While we hope that there may someday be a true depth of analgesia monitor, currently we must use the information provided by depth of hypnosis monitors in combination with other relevant clinical data.

The second question, whether monitors should rely on spontaneous or evoked electrical activity, may actually be unimportant. Different anesthetic drugs act in different areas of the brain with different mediators. We believe that what matters is not whether the signals are spontaneous or evoked, but whether we can determine if the variation of those responses is caused by an increase in the depth of hypnosis brought upon by hypnotic drugs or due to an abolition of stressful stimuli caused by analgesic drugs. Something must also be said about the methods commonly used in most of the studies that analyze the response of the depth of hypnosis monitors. Many of them compare the response of the monitors against clinical signs like the loss of eyelash reflex or the OAA/S scale (Observer's Assessment of Alertness/Sedation). 9This is in fact correct, however, it should be pointed out that to assess consciousness using the OAA/S scale, the patient has to be stimulated repeatedly. These stimuli have an effect on their hypnotic state. For example, OAA/S level 3 (which approximately corresponds to a BIS® value of 65 or an A-line® of 30, as in the study by Struys et al.  2) is reached when the patient “responds only after his name is called loudly and/or repeatedly.” This loud/repeated calling is a stimulus that could move the patient into a lighter hypnotic state, and the monitors will reflect this change with an increase in the index value. The same can be said when the patient is more deeply asleep, as in OAA/S 2 (“responds only after mild prodding or shaking”). The patient is again stimulated and could “lighten hypnotically.” Which monitor value then corresponds to the OAAS/S, the value recorded before or after the stimulus? It could be argued that the value of the monitor should be registered only after the OAA/S level has been assessed. Maybe this helps to explain the overlapping values in the study of Struys et al.  2 

Again, we agree with the authors that these devices monitor the hypnotic level and not the depth of anesthesia, which is a much more complex phenomenon. Nevertheless, these devices are a great step forward. Very few of us want to go back to the time when the controversy was, Automatic blood pressure monitoring, or the finger of the anesthesiologist on the patient's radial artery…?

Kalkman CJ, Drummond JC: Monitors of depth of anesthesia, Quo Vadis?. Editorial, A nesthesiology 2002; 96: 784–7
Struys MMRF, Jensen EW, Smith W, Smith NT, Rampil I, Dumortier FJE, et al.: Performance of the ARX-derived auditory evoked potential index as an indicator of anesthetic depth. A comparison with Bispectral index and hemodynamic measures during propofol administration. A nesthesiology 2002; 96: 803–16
Gonheim MM, Block RL, Dhanaraj VJ, Todd MM, Choi WW, Brown CK: Auditory evoked responses and learning and awareness during general anesthesia. Acta Anaesthesiol Scand 2000; 44: 133–43
Schwender D, Klasing S, Madler C, Pöpel E, Peter K: Effects of benzodiazepines on mid-latency auditory evoked potentials. Can J Anaesthesia 1993; 40: 1148–54
Brunner MD, Umo-Etuk J, Sharpe RM, Thornton C: Effect of a bolus dose of midazolam on the auditory evoked response in humans. Br J Anaesth 1999; 82: 633–4
Hotz MA, Ritz R, Linder L, Scollo-Lavizzari G, Haefeli, WE: Auditory and electroencephalographic effects of midazolam and alpha-hydroxy-midazolam in healthy subjects. Br J Clin Pharmacol 2000; 49 ( 1): 72–9
De Castro J: Practical applications and limitations of analgesic anesthesia: a review. Acta Anaesthesiol Belg 1976; 27: 107–28
De Castro J, Paramentier P, Andrieu S: Limits of pure analgesic anesthesia Ann Anesthesiol Fr 1976; 17: 1071–86
Chernik DA, Gillings D, Laine H, Hendler J, Silver JM, Davidson AB, Scwam EM, Siegel JL: Validity and reliability of the Observer's Assessment of Alertness/Sedation Scale: Study with intravenous midazolam. J Clin Psychopharmacol 1990; 10: 244–51