- Email: [email protected]
Chapter 49 Anesthesia effects and evoked potentials
Advances in Clinical Neurophysiology (Supplements to Clinical Neurophysiology Vol. 54) Editors: R.C. Reisin, M.R. Nuwer, M. Hallett, C. Medina 2002 Elsevier Science B.Y. All rights reserved.
325
Chapter 49
Anesthesia effects and evoked potentials Tod B. Sloan Department ofAnesthesiology, University of Texas Health Science Center, San Antonio, TX 78229 (USA)
During electrophysiological monitoring, several factors can alter the responses. In addition to technical and surgically related problems, anesthesia and physiological changes can alter the responses. Anesthesia management involves the choice of a favorable drug combination and maintenance of a steady state (e.g. avoiding bolus drug delivery during critical monitoring periods). Physiological effects can simulate neural dysfunction if they hamper the stimulated tracts. In general, anesthetic effects can be divided based on whether the responses recorded are sensitive or insensitive to anesthesia (primarily inhalational agents) and whether they are helped or hindered by muscle relaxants. Shown in Table I is the matrix of these two factors and the considerations are presented below. Group 1 responses
Group I responses (sensitive to inhalational agents but insensitive to muscle relaxants) represent the largest group ofthe more commonly recorded sensory evoked responses (e.g. SSEP, YEP, cortical ABR). Here, synaptic participation in the response
* Correspondence to: Dr. T.B. Sloan, Department of Anesthesiology, Mail Code 7838, University ofTexas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA. Fax: 210 567 6135. E-mail: [email protected]
generation likely explains why these anesthetics reduce the amplitude since these agents markedly affect synaptic function. Thus anesthetic effects are prominent on the cortical SSEP, as with the YEP, with increased latency and decreased amplitude (Sloan 1966). The effects are most pronounced on responses generated in the cerebral cortex. Since anesthetic agents differ in their mode of action and potency, agents differ in their specific effects on the evoked responses and neural location. Inhalational agents (desflurane, enflurane, halothane, isoflurane, sevoflurane), produce a dose related increase in latency and reduction in amplitude of the cortically recorded sensory evoked responses. Smaller effects are seen on the SSEP response recorded over the cervical spine, and minimal effects are seen in epidural or peripherally recorded responses. The effects of specific agents parallel their effects on the EEG (Winters et al. 1967; Sloan 1998) and the relative order of potency parallels that observed with EEG: isoflurane (most potent), enflurane, and halothane (least potent). Sevoflurane and desflurane appear similar to isoflurane at steady state, but due to their relative insolubility, they may appear to be more potent during periods when concentrations . . are mcreasmg. Nitrous oxide also produces amplitude reduction and latency increases in cortical SEP when used alone or when combined with halogenated inhalational agents or upload agents. As with halogen-
326 TABLE I ANESTHETIC SENSITIVITY MATRIX Anesthetic effect
Sensitive to inhalational agents
Relatively insensitive
Muscle relaxation Insensitive
Group! Cortical sensory (SSEP, VEP, cortical ABR)
Group II Sensory subcortical Epidural, peri spinal Sensory cranial nerve (ABR)
Sensitive
Group !II Transcranial MEP
Group IV Pedicle screw stimulation Spinal reflex testing Motor cranial nerve (Facia! N.)
ated agents, effects on subcortical, epidural and peripheral nerve responses are minimal. Studies suggest that nitrous oxide may be 'context sensitive' in its effects, similar to its effects on the EEG (i.e. the actual effect may vary depending on the other anesthetics already present). Since nitrous oxide is relatively insoluble, the anesthetic effects can change rapidly when concentrations are varied. Fortunately, group I responses are less affected by intravenous anesthetic agents. For example, the effects of opioids show mild depression of amplitude and increase in latency in cortical responses, particularly loss oflate cortical peaks (over 100 ms) at doses producing sedation. Effects on subcortical recordings are minimal. Similarly the spinal application of morphine or fentanyl for postoperative pain management produces minimal changes in the SSEP and fails to alter the H-reflex. As such, opioid analgesia is commonly used during recording of cortical SEPs. The effects of ketamine on subcortical and peripheral responses are also minimal. An increase in cortical SSEP amplitude (Schubert et al. 1990) has been reported with ketamine. This amplitude increa.se, and an overall lack of depressant effect, has made ketamine a desirable agent for monitoring responses that are usually difficult to record under anesthesia. Droperidol appears to have minimal effects on response when combined with opioids. Thiopental produces transient decreases in amplitude and increases in latency of cortical sensory responses with induction. Longer latency cortical waves are most affected, while minimal effects are seen on the subcortical and peripheral responses. The ABR is vir-
tually unaffected at doses ofphenobarbital that produce coma and the SSEP is unaffected at doses that produce a silent EEG; changes are not seen until doses that are sufficient to produce cardiovascular collapse. For this reason, sensory evoked responses have been used successfully to monitor neurological function during barbiturate induced coma. Midazolam (0.2 mg/kg) produces a mild depression of cortical SSEP and minimal effects on subcortical and peripheral sensory evoked responses. Because of midazolam' s excellent amnestic qualities, an infusion can be used to maintain supplemental hypnosis during opioid or ketamine analgesia. Etomidate produces an amplitude increase of cortical components following injection (Kochs et al. 1986) with no changes in subcortical and peripheral sensory responses. This amplitude increase appears coincident with the myoclonus seen with the drug, suggesting a heightened cortical excitability.Of several intravenous agents studied, etomidate had the least degree of amplitude depression after induction doses or with continuous intravenous infusion. Propofol induction produces amplitude depression in cortical SSEP, with rapid recovery after termination of infusion (Sloan 1966). Recordings in the epidural space are unaffected, consistent with a site of anesthetic action of propofol in the cerebral cortex. The rapid metabolism of propofol makes it an excellent drug for tightly controlled infusion anesthesia, because the depth ofanesthesia and the related effects on evoked responses can be adjusted quickly. Therefore propofol has great appeal for intravenous based techniques during evoked response monitoring.
327 Muscle relaxants are generally thought to have no effect on the EEG or SEP. They may actually improve response amplitude, because EMG interference is reduced in electrodes near muscle groups. Group II responses Group II responses are generally characterized by pathways that are less dependent on synaptic function such that the anesthetic effects of inhalational agents are far less marked. Since anesthetic agents can decrease the SSEP cortical amplitude with minimal effect on responses recorded from the spinal cord, there is substantial interest in monitoring from recording electrodes placed in the spinal bony elements or in the subdural or epidural space. One study evaluated different spinal recording locations (Jones et a1. 1983) and concluded that the epidural recording location was superior. Problems with perispinal recording locations have included marked variability due to motion and dislodgement by the surgeon. The epidural technique has become commonplace in Japan and Europe, and despite its invasive nature, this technique appears remarkably safe. Some authors consider epidural recording and stimulation to be superior to the SSEP, with recording locations near the cord providing 'the most reliable and important information obtained in the intraoperative period' (Jones et a1. 1983; Erwin and Erwin 1993). As discussed below, these electrodes can also be used for recording following perispinal, epidural and cortical stimulation. One effective monitoring technique utilizes epidural recordings to monitor both descending motor evoked responses from cortical stimulation (see below) and ascending responses from the SSEP (Stephen et a1. 1996). An excellent example of a group II response is the auditory brain stem response (ABR) or brainstem auditory evoked response (BAER). Here, anesthetic effects on ABR are not dramatic. Small latency shifts may be seen with changing concentrations ofinhalational agents, but these shifts rarely interfere with monitoring. Nitrous oxide is similarly benign unless it causes changes in middle ear pressure. Thus there are few limitations to monitoring of the ABR. In general, stimulation and recording from the
spinal cord (or recording of the peripheral nerve from spinal stimulation) appears to be a group II type. This is clearly the case when recorded from the spinal column; however, anesthetic effects on responses measured in peripheral nerves are not clearly defined since a mix of sensory and motor tracts are included and the synaptic function of the anterior hom cell will participate in the response. Inhalational agents and midazolam may depress the anterior hom cell, leading to a decreased response in the peripheral nerve and changes in the relative contributions of the sensory and motor pathways. Cortical responses monitored after spinal stimulation will be affected similarly to the cortical SSEP. Stimulation with multipulse spinal stimulation has been employed to overcome anesthetic effects but it is unknown how this affects the motor contribution (Mochida et a1. 1997). When neural recordings (and to some extent epidural recordings) are being made, muscle relaxation is needed to reduce artifact from nearby muscles. However, muscle relaxants will interfere with muscle recordings unless a controlled infusion is used to allow measurable activity. Group III responses Group III responses are clearly the most challenging to the anesthesiologist, as the inability to use muscle relaxation and inhalational agents requires total intravenous anesthesia. As such, the major drawback of trans cranial MEP has been the effects of anesthesia. These effects appear to be produced in the cortex (Hicks et a1. 1992) and in the anterior hom cell (where activation of the peripheral nerve is inhibited) (Zentner et a1. 1992). Responses recorded in muscle appear to be the responses most easily abolished by low concentrations of halogenated inhalational agents (e.g. less than O.2-{).5% isoflurane). Studies show that the number of I-waves is reduced with halogenated inhalational anesthesia but the epidural D-wave responses are well maintained, even with high concentrations of inhalational agents. As such, epidural recording is resistant to anesthetic depression. Because the effects of opioids are minimal, opioid-based anesthesia is often used when myo-
328 genic transcranial motor evoked potentials are monitored. Fentanyl may reduce background spontaneous muscle contractions and associated motor unit potentials, which may improve muscle recordings. Ketamine may also produce an increase in amplitude of muscle and spinal recorded responses following spinal stimulation (Kano and Shimoji 1974) making it a desirable agent. Thiopental and midazolam produce CMAP depression at doses below those affecting the SSEP and lasting for a long period of time after bolus induction (e.g. 45 min) making them less desirable agents. Propofol has been used in tcEMEP when the recordings are epidural, however, it depresses CMAP responses. Thus, where most anesthetic protocols can be used for epidural recordings, anesthesia techniques utilizing etomidate, ketamine, propofol and opioids are popular for muscle response recording. Muscle relaxation may be of help to remove muscle artifact with epidural recordings, but tightly controlled relaxation will be needed to allow peripheral muscle recording. Group IV responses
Finally, group IV responses are usually easily recorded because, although muscle relaxation is limited, the freedom to use inhalational agents makes anesthesia less challenging. Typical responses here are stimulation of cranial or peripheral nerves and recording of peripheral muscle responses. Such techniques are used for facial nerve monitoring and pedicle screw testing. In some cases, partial muscle relaxation has been advocated, but controversy surrounds this choice. Some authors have indicated that spontaneous activity from nerve irritation is difficult to detect during controlled relaxation. Small amplitude responses of injured or poorly functioning nerves are particularly difficult to detect, such that many authors recommend avoiding muscle relaxants in these cases.
Choice of anesthesia In general, the choice of monitoring techniques will determine the optimal anesthesic technique.
Clearly the needs of the patient will supersede the monitoring, but usually an anesthetic choice can be made that will be compatible with the needs of the patient and the needs of monitoring. When multiple techniques are used, the most restrictive group will usually define the choice. Once the technique is chosen the actual effect should be observed as individual variation may make the patient more or less susceptible to the anesthetic effects. When a technique has finally be determined, achieving a steady-state will be optimally supportive of allowing changes in the monitoring to reflect changes in the neural state and not changes in the anesthesia.
References Erwin, C.w. and Erwin, A.C. Up and down the spinal cord: intraoperative monitoring of sensory and motor spinal cord pathways. 1. Clin. Neurophysiol., 1993, 10: 425-436. Hicks, KG., Wood forth, I.J. and Crawford, M.R. Some effects of isoflurane on I waves of the motor evoked potential. Br. 1. Anaesth. 1992, 69: 130-136. Jones, S.1., Edgar, M.A., Ransford, A.a. and Thomas, N.P. A system for the electrophysiological monitoring of the spinal cord during operations for scoliosis. 1. Bone Joint Surg. Br., 1983, 65: 134-139. Kano, T. and Shimoji, K. The effects of ketamine and neuroleptanalgesia on the evoked electrospinogram and electromyogram in man. Anesthesiology, 1974,40: 241-246. Kochs, E., Treede, R.O., Schulte and Esch, J. Increase of somatosensorically evoked potentials during induction of anaesthesia with etomidate. Anaesthetist, 1986, 35: 359~364. Mochida, K.. Komori, H., Okawa, A. and Shinomiya, K. Evaluation of motor function during thoracic and thoracolumbar spinal surgery based on motor-evoked potentials using train spinal stimulation. Spine, 1997,22: 1385-1393. Schubert, A., Licina, M.G. and Lineberry, P.J. The effect of ketaminc on human somatosensory evoked potentials and its modification by nitrous oxide. Anesthesiology, 1990, 72: 3339. Sloan,T Evoked potentials. In: M.S. Albin (Ed.), A Textbook of Neuroanesthesia with Neurosurgical and Neuroscience Perspectives. McGraw-Hill, New York, 1996: 221-276. Sloan, TB. Anesthetic effects on electrophysiological recordings. 1. Clin. Neurophysiol., 1998, 15: 217-226. Stephen, J.P., Sullivan, M.R., Hicks, R.G., Burke, 0.1., Woodforth, I.J. and Crawford, M.R. Cotrel-Dubousset instrumentation in children using simultaneous motor and somatosensory evoked potential monitoring. Spine, 1996, 21: 2450-2457. Winters, W.O., Mori, K., Spooner, c.E. and Bauer, R.O. The neurophysiology of anesthesia. Anesthesiology, 1967,28: 65-80. Zentner, 1., Albrecht, 1. and Heuser, O. Influence of halothane, enflurane, and isoflurane on motor evoked potentials. Neurosurgery, 1992,32: 298-305.
325
Chapter 49
Anesthesia effects and evoked potentials Tod B. Sloan Department ofAnesthesiology, University of Texas Health Science Center, San Antonio, TX 78229 (USA)
During electrophysiological monitoring, several factors can alter the responses. In addition to technical and surgically related problems, anesthesia and physiological changes can alter the responses. Anesthesia management involves the choice of a favorable drug combination and maintenance of a steady state (e.g. avoiding bolus drug delivery during critical monitoring periods). Physiological effects can simulate neural dysfunction if they hamper the stimulated tracts. In general, anesthetic effects can be divided based on whether the responses recorded are sensitive or insensitive to anesthesia (primarily inhalational agents) and whether they are helped or hindered by muscle relaxants. Shown in Table I is the matrix of these two factors and the considerations are presented below. Group 1 responses
Group I responses (sensitive to inhalational agents but insensitive to muscle relaxants) represent the largest group ofthe more commonly recorded sensory evoked responses (e.g. SSEP, YEP, cortical ABR). Here, synaptic participation in the response
* Correspondence to: Dr. T.B. Sloan, Department of Anesthesiology, Mail Code 7838, University ofTexas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA. Fax: 210 567 6135. E-mail: [email protected]
generation likely explains why these anesthetics reduce the amplitude since these agents markedly affect synaptic function. Thus anesthetic effects are prominent on the cortical SSEP, as with the YEP, with increased latency and decreased amplitude (Sloan 1966). The effects are most pronounced on responses generated in the cerebral cortex. Since anesthetic agents differ in their mode of action and potency, agents differ in their specific effects on the evoked responses and neural location. Inhalational agents (desflurane, enflurane, halothane, isoflurane, sevoflurane), produce a dose related increase in latency and reduction in amplitude of the cortically recorded sensory evoked responses. Smaller effects are seen on the SSEP response recorded over the cervical spine, and minimal effects are seen in epidural or peripherally recorded responses. The effects of specific agents parallel their effects on the EEG (Winters et al. 1967; Sloan 1998) and the relative order of potency parallels that observed with EEG: isoflurane (most potent), enflurane, and halothane (least potent). Sevoflurane and desflurane appear similar to isoflurane at steady state, but due to their relative insolubility, they may appear to be more potent during periods when concentrations . . are mcreasmg. Nitrous oxide also produces amplitude reduction and latency increases in cortical SEP when used alone or when combined with halogenated inhalational agents or upload agents. As with halogen-
326 TABLE I ANESTHETIC SENSITIVITY MATRIX Anesthetic effect
Sensitive to inhalational agents
Relatively insensitive
Muscle relaxation Insensitive
Group! Cortical sensory (SSEP, VEP, cortical ABR)
Group II Sensory subcortical Epidural, peri spinal Sensory cranial nerve (ABR)
Sensitive
Group !II Transcranial MEP
Group IV Pedicle screw stimulation Spinal reflex testing Motor cranial nerve (Facia! N.)
ated agents, effects on subcortical, epidural and peripheral nerve responses are minimal. Studies suggest that nitrous oxide may be 'context sensitive' in its effects, similar to its effects on the EEG (i.e. the actual effect may vary depending on the other anesthetics already present). Since nitrous oxide is relatively insoluble, the anesthetic effects can change rapidly when concentrations are varied. Fortunately, group I responses are less affected by intravenous anesthetic agents. For example, the effects of opioids show mild depression of amplitude and increase in latency in cortical responses, particularly loss oflate cortical peaks (over 100 ms) at doses producing sedation. Effects on subcortical recordings are minimal. Similarly the spinal application of morphine or fentanyl for postoperative pain management produces minimal changes in the SSEP and fails to alter the H-reflex. As such, opioid analgesia is commonly used during recording of cortical SEPs. The effects of ketamine on subcortical and peripheral responses are also minimal. An increase in cortical SSEP amplitude (Schubert et al. 1990) has been reported with ketamine. This amplitude increa.se, and an overall lack of depressant effect, has made ketamine a desirable agent for monitoring responses that are usually difficult to record under anesthesia. Droperidol appears to have minimal effects on response when combined with opioids. Thiopental produces transient decreases in amplitude and increases in latency of cortical sensory responses with induction. Longer latency cortical waves are most affected, while minimal effects are seen on the subcortical and peripheral responses. The ABR is vir-
tually unaffected at doses ofphenobarbital that produce coma and the SSEP is unaffected at doses that produce a silent EEG; changes are not seen until doses that are sufficient to produce cardiovascular collapse. For this reason, sensory evoked responses have been used successfully to monitor neurological function during barbiturate induced coma. Midazolam (0.2 mg/kg) produces a mild depression of cortical SSEP and minimal effects on subcortical and peripheral sensory evoked responses. Because of midazolam' s excellent amnestic qualities, an infusion can be used to maintain supplemental hypnosis during opioid or ketamine analgesia. Etomidate produces an amplitude increase of cortical components following injection (Kochs et al. 1986) with no changes in subcortical and peripheral sensory responses. This amplitude increase appears coincident with the myoclonus seen with the drug, suggesting a heightened cortical excitability.Of several intravenous agents studied, etomidate had the least degree of amplitude depression after induction doses or with continuous intravenous infusion. Propofol induction produces amplitude depression in cortical SSEP, with rapid recovery after termination of infusion (Sloan 1966). Recordings in the epidural space are unaffected, consistent with a site of anesthetic action of propofol in the cerebral cortex. The rapid metabolism of propofol makes it an excellent drug for tightly controlled infusion anesthesia, because the depth ofanesthesia and the related effects on evoked responses can be adjusted quickly. Therefore propofol has great appeal for intravenous based techniques during evoked response monitoring.
327 Muscle relaxants are generally thought to have no effect on the EEG or SEP. They may actually improve response amplitude, because EMG interference is reduced in electrodes near muscle groups. Group II responses Group II responses are generally characterized by pathways that are less dependent on synaptic function such that the anesthetic effects of inhalational agents are far less marked. Since anesthetic agents can decrease the SSEP cortical amplitude with minimal effect on responses recorded from the spinal cord, there is substantial interest in monitoring from recording electrodes placed in the spinal bony elements or in the subdural or epidural space. One study evaluated different spinal recording locations (Jones et a1. 1983) and concluded that the epidural recording location was superior. Problems with perispinal recording locations have included marked variability due to motion and dislodgement by the surgeon. The epidural technique has become commonplace in Japan and Europe, and despite its invasive nature, this technique appears remarkably safe. Some authors consider epidural recording and stimulation to be superior to the SSEP, with recording locations near the cord providing 'the most reliable and important information obtained in the intraoperative period' (Jones et a1. 1983; Erwin and Erwin 1993). As discussed below, these electrodes can also be used for recording following perispinal, epidural and cortical stimulation. One effective monitoring technique utilizes epidural recordings to monitor both descending motor evoked responses from cortical stimulation (see below) and ascending responses from the SSEP (Stephen et a1. 1996). An excellent example of a group II response is the auditory brain stem response (ABR) or brainstem auditory evoked response (BAER). Here, anesthetic effects on ABR are not dramatic. Small latency shifts may be seen with changing concentrations ofinhalational agents, but these shifts rarely interfere with monitoring. Nitrous oxide is similarly benign unless it causes changes in middle ear pressure. Thus there are few limitations to monitoring of the ABR. In general, stimulation and recording from the
spinal cord (or recording of the peripheral nerve from spinal stimulation) appears to be a group II type. This is clearly the case when recorded from the spinal column; however, anesthetic effects on responses measured in peripheral nerves are not clearly defined since a mix of sensory and motor tracts are included and the synaptic function of the anterior hom cell will participate in the response. Inhalational agents and midazolam may depress the anterior hom cell, leading to a decreased response in the peripheral nerve and changes in the relative contributions of the sensory and motor pathways. Cortical responses monitored after spinal stimulation will be affected similarly to the cortical SSEP. Stimulation with multipulse spinal stimulation has been employed to overcome anesthetic effects but it is unknown how this affects the motor contribution (Mochida et a1. 1997). When neural recordings (and to some extent epidural recordings) are being made, muscle relaxation is needed to reduce artifact from nearby muscles. However, muscle relaxants will interfere with muscle recordings unless a controlled infusion is used to allow measurable activity. Group III responses Group III responses are clearly the most challenging to the anesthesiologist, as the inability to use muscle relaxation and inhalational agents requires total intravenous anesthesia. As such, the major drawback of trans cranial MEP has been the effects of anesthesia. These effects appear to be produced in the cortex (Hicks et a1. 1992) and in the anterior hom cell (where activation of the peripheral nerve is inhibited) (Zentner et a1. 1992). Responses recorded in muscle appear to be the responses most easily abolished by low concentrations of halogenated inhalational agents (e.g. less than O.2-{).5% isoflurane). Studies show that the number of I-waves is reduced with halogenated inhalational anesthesia but the epidural D-wave responses are well maintained, even with high concentrations of inhalational agents. As such, epidural recording is resistant to anesthetic depression. Because the effects of opioids are minimal, opioid-based anesthesia is often used when myo-
328 genic transcranial motor evoked potentials are monitored. Fentanyl may reduce background spontaneous muscle contractions and associated motor unit potentials, which may improve muscle recordings. Ketamine may also produce an increase in amplitude of muscle and spinal recorded responses following spinal stimulation (Kano and Shimoji 1974) making it a desirable agent. Thiopental and midazolam produce CMAP depression at doses below those affecting the SSEP and lasting for a long period of time after bolus induction (e.g. 45 min) making them less desirable agents. Propofol has been used in tcEMEP when the recordings are epidural, however, it depresses CMAP responses. Thus, where most anesthetic protocols can be used for epidural recordings, anesthesia techniques utilizing etomidate, ketamine, propofol and opioids are popular for muscle response recording. Muscle relaxation may be of help to remove muscle artifact with epidural recordings, but tightly controlled relaxation will be needed to allow peripheral muscle recording. Group IV responses
Finally, group IV responses are usually easily recorded because, although muscle relaxation is limited, the freedom to use inhalational agents makes anesthesia less challenging. Typical responses here are stimulation of cranial or peripheral nerves and recording of peripheral muscle responses. Such techniques are used for facial nerve monitoring and pedicle screw testing. In some cases, partial muscle relaxation has been advocated, but controversy surrounds this choice. Some authors have indicated that spontaneous activity from nerve irritation is difficult to detect during controlled relaxation. Small amplitude responses of injured or poorly functioning nerves are particularly difficult to detect, such that many authors recommend avoiding muscle relaxants in these cases.
Choice of anesthesia In general, the choice of monitoring techniques will determine the optimal anesthesic technique.
Clearly the needs of the patient will supersede the monitoring, but usually an anesthetic choice can be made that will be compatible with the needs of the patient and the needs of monitoring. When multiple techniques are used, the most restrictive group will usually define the choice. Once the technique is chosen the actual effect should be observed as individual variation may make the patient more or less susceptible to the anesthetic effects. When a technique has finally be determined, achieving a steady-state will be optimally supportive of allowing changes in the monitoring to reflect changes in the neural state and not changes in the anesthesia.
References Erwin, C.w. and Erwin, A.C. Up and down the spinal cord: intraoperative monitoring of sensory and motor spinal cord pathways. 1. Clin. Neurophysiol., 1993, 10: 425-436. Hicks, KG., Wood forth, I.J. and Crawford, M.R. Some effects of isoflurane on I waves of the motor evoked potential. Br. 1. Anaesth. 1992, 69: 130-136. Jones, S.1., Edgar, M.A., Ransford, A.a. and Thomas, N.P. A system for the electrophysiological monitoring of the spinal cord during operations for scoliosis. 1. Bone Joint Surg. Br., 1983, 65: 134-139. Kano, T. and Shimoji, K. The effects of ketamine and neuroleptanalgesia on the evoked electrospinogram and electromyogram in man. Anesthesiology, 1974,40: 241-246. Kochs, E., Treede, R.O., Schulte and Esch, J. Increase of somatosensorically evoked potentials during induction of anaesthesia with etomidate. Anaesthetist, 1986, 35: 359~364. Mochida, K.. Komori, H., Okawa, A. and Shinomiya, K. Evaluation of motor function during thoracic and thoracolumbar spinal surgery based on motor-evoked potentials using train spinal stimulation. Spine, 1997,22: 1385-1393. Schubert, A., Licina, M.G. and Lineberry, P.J. The effect of ketaminc on human somatosensory evoked potentials and its modification by nitrous oxide. Anesthesiology, 1990, 72: 3339. Sloan,T Evoked potentials. In: M.S. Albin (Ed.), A Textbook of Neuroanesthesia with Neurosurgical and Neuroscience Perspectives. McGraw-Hill, New York, 1996: 221-276. Sloan, TB. Anesthetic effects on electrophysiological recordings. 1. Clin. Neurophysiol., 1998, 15: 217-226. Stephen, J.P., Sullivan, M.R., Hicks, R.G., Burke, 0.1., Woodforth, I.J. and Crawford, M.R. Cotrel-Dubousset instrumentation in children using simultaneous motor and somatosensory evoked potential monitoring. Spine, 1996, 21: 2450-2457. Winters, W.O., Mori, K., Spooner, c.E. and Bauer, R.O. The neurophysiology of anesthesia. Anesthesiology, 1967,28: 65-80. Zentner, 1., Albrecht, 1. and Heuser, O. Influence of halothane, enflurane, and isoflurane on motor evoked potentials. Neurosurgery, 1992,32: 298-305.