Electrical interference, particularly at the frequency of power line alternating current (60 Hz in the North America), often presents a challenge to obtaining technically satisfactory recording in the OR. Equipment such as blood warmers, motorized patient tables, and operating microscopes are important sources of electrical noise. Care should be taken to run lead wires to avoid proximity to interference sources, when possible. It is often very helpful to twist or braid scalp-recording leads to maximize common mode rejection of power line interference.

Band-pass filters of 30–1,000 Hz (-6 dB) are most commonly employed. However, most of the energy for SSEPs lies between 30 and 500 Hz, and high-frequency filters of 500 or even 300 Hz may be used effectively for monitoring, decreasing noise with only minimal effect of waveform morphology. Lower low-pass settings below 30 Hz offer no advantage and increase noise.

Anesthesia

FIGURE 13.5 Interpatient variability of the effect of anesthetic agents on cortical somatosensory evoked potentials (SSEPs). Patients A and B both received balanced anesthesia with 50% nitrous oxide, 0.5% isoflurane, and propofol 35 ug/kg/min. Cortical SSEPs are markedly suppressed in patient A but are sufficiently preserved in patient B to permit effective monitoring. Brainstem signals (arrows) are unaffected in both patients. Patient A received intermittent boluses of vecuronium to eliminate EMG artifact and permit monitoring of the brainstem SSEP.

Either cortical or brainstem SSEPs can be sufficient for monitoring spinal cord function, as each serves as an indicator of dorsal column function. Their complementary strengths and weaknesses combine to enhance the reliability and flexibility of SSEP monitoring. Although some authors have recommended omitting brainstem SSEPs from routine SSEP monitoring protocols because they often have low signal-to-noise ratios and can be difficult to record (20), routine incorporation of brainstem channels in SSEP monitoring protocols adds flexibility and places fewer constraints on anesthetic choice. If cortical signals are robust, brainstem signals may be disregarded in favor of more rapid surgical feedback based on the cortical signals. If, however, for an individual patient and anesthetic protocol, brainstem responses are the most robust signals, then they should be used preferentially because they will, in fact, provide for the best and most rapid feedback to the surgeon.

FIGURE 13.6 Use of neuromuscular blocking agents to facilitate monitoring based on brainstem somatosensory evoked potentials (SSEPs) in a 12-year-old with neuromuscular scoliosis and cerebral palsy, undergoing scoliosis surgery. Patient was receiving 0.25% isoflurane along with propofol 100 ug/kg/min. Cortical SSEPs are barely present and not monitorable. Following the administration of vecuronium, muscle artifact in the Fpz-CS5 channel is eliminated and the brainstem SSEP becomes monitorable (arrow).

MOTOR EVOKED POTENTIALS

Physiological Basis

MEP monitoring during spinal surgery is performed by transcranial electrical stimulation of the motor cortex and recording the compound motor potential (CMAP) from muscle (M-wave) in the arms and legs. In direct spinal cord recordings, a single transcranial electrical stimulus can be seen to generate a series of efferent volleys: an initial single D (or direct)-wave followed over several milliseconds by a series of I (or indirect)-waves. D-waves result from direct activation of pyramidal cell axons. I-waves, in contrast, reflect firing of pyramidal cells in response to inputs from interneurons, themselves activated by transcranial electrical stimulation (38). Since no synapses are involved in D-wave generation, they are relatively resistant to anesthetic effects; I-waves, in contrast, are suppressed by most general anesthetics.

FIGURE 13.7 Temporal summation by a spinal motor neuron. Each volley (corresponding to a D-wave or I-wave) causes further depolarization of the alpha motor neuron until it finally reaches threshold and fires, causing the innervated muscle fibers to fire.

MEP stimulation may be performed using subdermal needle or corkscrew electrodes, or electroencephalogram (EEG)-type disk electrodes secured with collodion. Electrodes are most often placed at C1/C2 or C3/C4 scalp locations (41). C3/C4 locations can be more effective but also tend to elicit more face and jaw movement. Although MEPs are usually generated bilaterally, D-waves and hence M-waves are most reliably elicited by anodal stimulation (42). For monitoring, therefore, stimulator polarity is set so that the anode is contralateral to the recorded muscles; stimulator polarity is then switched when recording from the opposite side. Alternatively, the anode may be placed at Cz, with the cathode at Fz; with this arrangement, both legs may be effectively stimulated simultaneously, but UE muscle activation may be more difficult. In practice, it is useful to test several stimulating electrode placements and select the best one for the individual patient.

FIGURE 13.9 Variability of motor evoked potentials obtained sequentially under identical anesthetic and hemodynamic conditions. Anesthesia was achieved using propofol 125 ug/kg/min; mean arterial pressure was 60 mmHg.

Abbreviation: RTA, right tibialis anterior.

Recording

Subdermal or intramuscular needle electrodes, 2 to 3 cm apart, are used to record MEPs from the muscle belly. Belly tendon derivations can be used, but the longer interelectrode distance can be a source of added noise. For spinal cord monitoring, the most robust MEP signals are generally recorded from distal muscles controlled principally by the corticospinal tract. Abductor pollicis brevis and first dorsal interosseus for the upper extremity and adductor hallucis and tibialis anterior for the lower are commonly employed. Reliable MEPs can often be obtained from other muscles as well, and it can be helpful to include these in the selection of muscles for monitoring. For spinal cord monitoring, each muscle MEP serves as a surrogate for motor pathway integrity, probably because of the small size of the corticospinal tract and the likelihood that injury will affect many of its axons.

Specific muscles, including proximal muscles and anal sphincter, can also be monitored for the purpose of detecting nerve root injury. While this can be effective, MEP nerve root monitoring is also more difficult and less reliable than MEP monitoring of spinal cord function. MEP monitoring of nerve root function is heavily dependent upon adequacy and stability of the particular muscle’s baseline response; its reliability is further constrained by the confounding effects of multisegmental innervation (46).

Spinal cord D-waves are not monitored during scoliosis surgery because of the possibility of spurious amplitude changes resulting from movement of the epidural recording electrode with respect to the spinal cord during spinal deformity correction (47).

Safety

Transcranial MEP monitoring is a safe procedure. Tongue bite and patient movement are the major risks. Twenty-five instances of tongue laceration were reported in a series of 18,862 MEP cases. Twenty-one were self-limited, requiring no intervention; only four required suturing (48). A soft bite block (eg, rolled gauze pads) should be used to prevent the tongue from coming in contact with the teeth. Patient movement is common with MEP stimulation, although it can often be minimized by appropriate adjustment of stimulation parameters (stimulation intensity, number of pulses). It is important to coordinate stimulation with the surgeon so that movement does not occur, for example, when surgical instruments are close to neural structures. No movement-related injuries were reported in a series of more than 18,000 cases involving MEP monitoring over 15 years (48).

Epilepsy, shunts, cerebral lesions, skull defects close to stimulating electrodes, and implanted devices have been cited in the past as relative contraindications to transcranial electrical MEP (49). None, however, has been proven to result in complications related to MEP monitoring, and in many centers these do not presently preclude MEP monitoring (48,50). For individual patients, of course, the benefits of MEP monitoring need to be assessed, relative to potential risks.

Anesthesia

FIGURE 13.10 Dual-train stimulation can provide resilience to anesthetic effects on motor evoked potentials (MEPs). In a 12-year-old undergoing scoliosis surgery, anesthesia was provided using propofol 70 ug/kg/min and 0.3% isoflurane. Shortly after correction was achieved, 50% nitrous oxide was added, causing loss of the MEP response to the first train (thin arrow). Confusion, and a possible “false-positive” alert, were avoided by preservation of the response to the second stimulus train (thick arrow).

Abbreviation: RAH, right abductor hallucis.

INTERPRETATION

Preoperative Evaluation

SSEPs are routinely performed extraoperatively as part of the routine clinical evaluation of various neurological disorders. Extraoperative interpretation is based largely on interpeak latencies, reflecting conduction times between the various generators of the SSEPs signals. For UE SSEPs, these include EP-P14, P14-N20, and EP-N20, reflecting conduction times between Erb’s point and the lower brainstem, between the lower brainstem and cortex, as well as the overall conduction time between Erb’s point and cortex, respectively. For LE SSEPs, these include N22-P31, P31-P38, and N22-P38, reflecting, respectively, conduction times between lumbar spinal cord and lower brainstem, lower brainstem and cortex, and the overall conduction time between the lumbar cord and cortex. Interpretation is based on comparison of a patient’s latency values to normative data as well as differences between interpeak latencies measured following right- and left-sided stimulation. While the absence of expected signals also constitutes an abnormality, waveform amplitudes vary considerably among normal individuals and, as such, are generally not used in routine outpatient testing.

FIGURE 13.11 Obliteration of motor evoked potentials (MEPs) by a small bolus of vecuronium. Forty minutes after receiving 6 mg of vecuronium for intubation, the patient had four of four twitches, and well-formed MEPs were obtained. The MEPs were then transiently abolished by a 1-mg bolus of vecuronium.

Abbreviations: RAH, right abductor hallucis; RLG, right lateral gastrocnemius; RTA, right tibialis anterior.

In the early days of intraoperative monitoring, it was common to obtain extraoperative SSEP recordings as a guide to what to expect in the OR. Although this practice continues to be advocated by some (62), it has been abandoned by many, in favor of simply relying on baselines obtained intraoperatively. This author generally favors the latter practice. In the absence of outpatient sedation, intraoperative recordings are usually of better technical quality; indeed, the brainstem P31 signal is frequently not recordable in unsedated outpatient recordings. Often, the most important information derived from baseline recording relates to the effect of anesthetics agents and can be assessed only in the OR. Preoperative assessment of MEPs, using transcranial magnetic stimulation, has been suggested (63). While this is feasible and could be useful in some cases, Food and Drug Administration (FDA)-approved devices are not currently available.

In patients with AIS, SSEPs and MEPs are generally easy to obtain in the OR. While preoperative SSEPs could detect spinal cord abnormalities, such as Chiari malformations and syrinxes, that are occasionally present in patients with AIS (62), structural assessments are best made by using structural imaging techniques.

That said, baseline latency-based SSEP abnormalities may be common in AIS, their reported prevalence varying from about 15% to nearly 100%. The abnormities appear to be subtle, however, and are best revealed using height-adjusted normative data and specifically evaluating interpeak intervals (62,64,65). Machida reported SSEP abnormalities in 97 of 100 AIS patients, finding the P31-P38 interpeak latency to be prolonged following stimulation of the tibial nerve ipsilateral to the concavity of the curve (65). This observation, which suggests a sensory system abnormality rostral to the lower brainstem, may provide an important clue to the pathogenesis of AIS. Indeed, disturbed somatosensory function and balance abnormalities have been described in AIS patients with abnormal SSEPs (64,66).

FIGURE 13.12 Motor evoked potentials (MEPs) and somatosensory evoked potentials (SSEPs) recorded during surgery for adolescent idiopathic scoliosis (AIS) in a 12-year-old child receiving a vecuronium infusion at 1 mg/kg/hr, along with propofol and isoflurane. Train-of-four testing demonstrated three to four twitches. Robust MEPs were maintained, and with easily monitored brainstem SSEPs.

Abbreviations: RAH, right abductor hallucis; RAPB, right abductor pollicis brevis; RTA, right tibialis anterior.

Intraoperative Interpretation

For SSEPs, the generally accepted “alarm criteria” are a 50% decrease in amplitude or a 10% increase in latency from baseline (69). Loss of SEP amplitude and degradation of signal morphology are the most common consequences of intraoperative spinal cord injury, which causes conduction block or desynchronization; latency changes are distinctly less prominent. In contrast to extraoperative testing, SSEP amplitude is therefore the most important parameter to monitor. It is a serious error to conclude that everything if okay simply because latencies have remained stable.

The 50% amplitude 10% latency alarm criteria are empirically based and are best used as a guide, rather than a strict threshold above which it can be assumed that no adverse events have occurred. For one, noise can make it difficult to reliably distinguish a 60% from a 40% change from baseline. Further, it can be helpful to alert the surgeon to new, albeit smaller, SSEP changes that exceed their observed prior variability during the case. This approach can facilitate more accurate identification of the cause of SSEP changes and better affords the surgeon the option of acting immediately or taking a “wait and see” approach (70).

There is no firm consensus on the alarm criteria for MEP monitoring. Suggested criteria include the presence or absence of a response, various percent loss of response amplitudes, decrease of M-wave complexity or duration, and increase in stimulus intensity required to elicit M-waves (71). Latency criteria are not useful (72). The complexity of MEP interpretation reflects, in part, the integrative role of the motor neurons in generating M-waves, requiring the temporal summation of descending volleys, as well as the trial-to-trial variability of MEPs. Complete loss of M-wave does not necessarily indicate complete loss of spinal cord motor function; indeed, M-waves can be lost when D-wave amplitude decreases by 30% to 50%, often resulting in a transient postoperative motor deficit (72).

Although complete disappearance of the MEP has been a widely employed alarm criterion, once M-waves are lost, it is impossible to judge the degree of D-wave loss without direct spinal cord recording. It would seem, therefore, that a somewhat less strict alarm threshold is desirable to best ensure that the surgeon is notified before a possible “point of no return.” Given the commonly encountered degree of MEP variability, a 50% amplitude decrease criterion would likely cause too many false-positive notifications. The American Clinical Neurophysiology Society has suggested amplitude reduction of 75% to 90% as a reasonable threshold for alarm (41).

The combined use of SSEPs and MEPs affords robust monitoring of spinal cord function during spinal deformity surgery. The two modalities rely on different signals, are mediated by different pathways, are monitored using different leads and cables, and may be differentially affected by anesthetic agents. Yet, both are usually affected by traumatic, compressive, and ischemic injury to the spinal cord. This redundancy can be critical to continued monitoring during real-life situations commonly encountered in the OR, which cause one or the other modality to fail or to become unreliable. If, for example, a bolus of propofol obliterates MEPs, monitoring could continue based on subcortical SSEP and perhaps cortical SSEP signals. If muscle or electrical artifact obscures the SSEPs, the much larger CMAP signals would likely permit continued MEP monitoring.

Although, in the past, monitoring has focused on a “critical period” following correction, it is now clear that MEP and SEP changes reflecting incipient spinal cord injury can, and do, occur at any time during spinal deformity surgery. For this reason, monitoring should continue throughout the entire procedure, including during closure (73).

Example Case

FIGURE 13.13 A series of “screen shots” from a posterior instrumentation and fusion procedure for correction of scoliosis (see text for details). In each figure, three sets of superimposed tibial somatosensory evoked potentials (SSEPs) and two lower extremity motor evoked potentials (MEPs) are shown, with MEPs having been acquired following each of the first two sets of SSEPs. The labeled times correspond to the time of the first MEP. Right and left SSEPs were obtained simultaneously. VL, TA, and MG correspond to vastus lateralis, tibialis anterior, and medial gastrocnemius muscles, respectively. Ulnar SSEPs and abductor pollicis brevis MEPs as “systemic controls” are not shown, and they remained stable throughout the entire case.

FIGURE 13.13 A series of “screen shots” from a posterior instrumentation and fusion procedure for correction of scoliosis (see text for details). In each figure, three sets of superimposed tibial somatosensory evoked potentials (SSEPs) and two lower extremity motor evoked potentials (MEPs) are shown, with MEPs having been acquired following each of the first two sets of SSEPs. The labeled times correspond to the time of the first MEP. Right and left SSEPs were obtained simultaneously. VL, TA, and MG correspond to vastus lateralis, tibialis anterior, and medial gastrocnemius muscles, respectively. Ulnar SSEPs and abductor pollicis brevis MEPs as “systemic controls” are not shown, and they remained stable throughout the entire case.

FIGURE 13.13 A series of “screen shots” from a posterior instrumentation and fusion procedure for correction of scoliosis (see text for details). In each figure, three sets of superimposed tibial somatosensory evoked potentials (SSEPs) and two lower extremity motor evoked potentials (MEPs) are shown, with MEPs having been acquired following each of the first two sets of SSEPs. The labeled times correspond to the time of the first MEP. Right and left SSEPs were obtained simultaneously. VL, TA, and MG correspond to vastus lateralis, tibialis anterior, and medial gastrocnemius muscles, respectively. Ulnar SSEPs and abductor pollicis brevis MEPs as “systemic controls” are not shown, and they remained stable throughout the entire case.

Rods are then reinserted, configured to achieve still less correction. This time, MEPs and SSEPs remain stable. Signals remain stable through closing (Figure 13I), and the patient awakens from anesthesia with intact spinal cord function.

REFERENCES

   1.  Coe JD, Arlet V, Donaldson W, et al. Complications in spinal fusion for adolescent idiopathic scoliosis in the new millennium. A report of the Scoliosis Research Society Morbidity and Mortality Committee. Spine. 2006;31(3):345–349.

   2.  Diab M, Smith AR, Kuklo TR, et al. Neural complications in the surgical treatment of adolescent idiopathic scoliosis. Spine. 2007;32(24):2759–2763.

   3.  Qiu Y, Wang S, Wang B, et al. Incidence and risk factors of neurological deficits of surgical correction for scoliosis: analysis of 1373 cases at one Chinese institution. Spine. 2008;33(5):519–526.

   4.  Reames DL, Smith JS, Fu K-MG, et al. Complications in the surgical treatment of 19,360 cases of pediatric scoliosis. Spine. 2011;36(18):1484–1491.

   6.  Nuwer MR, Dawson EG, Carlson LG, et al. Somatosensory evoked potential spinal cord monitoring reduces neurologic deficits after scoliosis surgery: results of a large multicenter survey. Electroencephalogr Clin Neurophysiol. 1995;96(1):6–11.

   7.  Nash CL, Lorig RA, Schatzinger LA, et al. Spinal cord monitoring during operative treatment of the spine. Clin Orthop Relat Res. 1977;(126):100–105.

   8.  Forbes HJ, Allen PW, Waller CS, et al. Spinal cord monitoring in scoliosis surgery. J Bone Joint Surg Am. 1991;73-B:219–220.

   9.  Deecke L, Tator CH. Neurophysiol assessment of afferent and efferent conduction in the injured spinal cord of monkeys. J. Neurosurg. 1973;39:65–74.

10.   Baskin DS, Simpson RK Jr. Corticomotor and somatosensory evoked potential evaluation of acute spinal cord injury in the rat. Neurosurgery. 1987;20(6):871–877.

11.   Shiau JS, Zappulla RA, Nieves J. The effect of graded spinal cord injury on the extrapyramidal and pyramidal motor evoked potentials of the rat. Neurosurgery. 1992;30(1):76–84.

12.   Machida M, Weinstein SL, Imamura Y, et al. Compound muscle action potentials and spinal evoked potentials in experimental spine maneuver. Spine. 1989;14(7):687–691.

13.   Fehlings MG, Tator CH, Linden RD. The relationships among the severity of spinal cord injury, motor and somatosensory evoked potentials and spinal cord blood flow. Electroencephalography and Clincal Neurophysiology. 1989;74:241–259.

14.   Ben-David B, Haller G, Taylor P. Anterior spinal fusion complicated by paraplegia. A case report of a false-negative somatosensory-evoked potential. Spine. 1987;12:536–539.

15.   Merton PA, Morton HB. Stimulation of the cerebral cortex in the intact human subject. Nature. 1980;285(5762):227.

16.   Mauguiere F, Desmedt JE. Bilateral somatosensory evoked potentials in four patients with long-standing surgical hemispherectomy. Ann Neurol. 1989;26(6):724–731.

17.   Mauguiere F, Desmedt JE, Courjon J. Neural generators of N18 and P14 far-field somatosensory evoked potentials studied in patients with lesion of thalamus or thalamo-cortical radiations. Electroencephalogr Clin Neurophysiol. 1983;56(4):283–292.

18.   Urasaki E, Tokimura T, Yasukouchi H, et al. P30 and N33 of posterior tibial nerve SSEPs are analogous to P14 and N18 of median nerve SSEPs. Electroencephalogr Clin Neurophysiol. 1993;88(6):525–529.

19.   Emerson RG, Seyal M, Pedley TA. Somatosensory evoked potentials following median nerve stimulation. I. The cervical components. Brain. 1984;107(Pt 1):169–182.

20.   MacDonald DB, Al-Zayed Z, Stigsby B, et al. Median somatosensory evoked potential intraoperative monitoring: recommendations based on signal-to-noise ratio analysis. Clin Neurophysiol, 2009;120(2):315–328.

21.   Seyal M, Emerson RG, Pedley TA. Spinal and early scalp-recorded components of the somatosensory evoked potential following stimulation of the posterior tibial nerve. Electroencephalogr Clin Neurophysiol, 1983;55(3):320–330.

22.   MacDonald DB, Al-Zayed Z, Stigsby B. Tibial somatosensory evoked potential intraoperative monitoring: recommendations based on signal to noise ratio analysis of popliteal fossa, optimized P37, standard P37, and P31 potentials. Clin Neurophysiol, 2005;116(8):1858–1869.

23.   Emerson RG. Anatomic and physiologic bases of posterior tibial nerve somatosensory evoked potentials. Neurol Clin. 1988;6(4):735–749.

24.   Maiocco B, Deeney VF, Coulon R, et al. Adolescent idiopathic scoliosis and the presence of spinal cord abnormalities. Preoperative magnetic resonance imaging analysis. Spine. 1997;22(21):2537–2541.

25.   O’Brien MF, Lenke LG, Bridwell KH, et al. Evoked potential monitoring of the upper extremities during thoracic and lumbar spinal deformity surgery: a prospective study. J Spinal Disord. 1994;7(4):277–284.

26.   Jones SC, Fernau R, Woeltjen BL. Use of somatosensory evoked potentials to detect peripheral ischemia and potential injury resulting from positioning of the surgical patient: case reports and discussion. Spine J. 2004;4(3):360–362.

28.   Perlik SJ, VanEgeren R, Fisher MA. Somatosensory evoked potential surgical monitoring. Observation during combined isoflurane-nitrous oxide anesthesia. Spine. 1992;17(3):273–276.

29.   Browning JL, Heizer ML, Baskin DS. Variations in corticomotor and somatosensory evoked potentials: effects of temperature, halothane anesthesia, and arterial partial pressure of CO2. Anesth Analg. 1992;74(5):643–648.

30.   Sebel PS, Bowles SM, Saini V, et al. EEG bispectrum predicts movement during thiopental/isoflurane anesthesia. J Clin Monit. 1995;11(2):83–91.

31.   Clapcich AJ, Emerson RG, Roye DP Jr, et al. The Effects of Propofol, Small-Dose Isoflurane, and Nitrous Oxide on Cortical Somatosensory Evoked Potential and Bispectral Index Monitoring in Adolescents Undergoing Spinal Fusion. Anesth Analg. 2004;99:1334–1340.

32.   Sloan T, Sloan H, Rogers J. Nitrous oxide and isoflurane are synergistic with respect to amplitude and latency effects on sensory evoked potentials. J Clin Monit Comput. 2010;24(2):113–123.

33.   Harper CM, Nelson KR. Intraoperative electrophysiological monitoring in children. J Clin Neurophysiol. 1992;9(3):342–356.

34.   Sloan T, Heyer EJ. Anesthesia for intraoperative neurophysiologic monitoring of the spinal cord. J Clin Neurophysiol. 2002;19:430–443.

35.   Agarwal R, Roitman KJ, Stokes M. Improvement of intraoperative somatosensory evoked potentials by ketamine. Paediatr Anaesth. 1998;8(3):263–266.

36.   Schubert A, Licina MG, Lineberry PJ. The effect of ketamine on human somatosensory evoked potentials and its modification by nitrous oxide. Anesth. 1990;72(1):33–39.

37.   Sloan TB, Ronai AK, Toleikis JR, et al. Improvement of intraoperative somatosensory evoked potentials by etomidate. Anesth Analg. 1988;67(6):582–585.

38.   Amassian VE, Stewart M, Quirk GJ, et al. Physiological basis of motor effects of a transient stimulus to cerebral cortex. Neurosurgery. 1987;20(1):74–93.

39.   Jones SJ, Harrison R, Koh KF, et al. Motor evoked potential monitoring during spinal surgery: response of distal limb muscles to transcranial cortical stimulation with pulse trains. Electroencephalogr and Clin Neurophysiol. 1996;100:375–383.

40.   Journée HL, Polak HE, De Kleuver M. Conditioning stimulation techniques for enhancement of transcranially elicited evoked motor responses. Neurophysiol Clin. 2007;37(6):423–430.

51.   Kobylarz EJ, Bilsky MH, Sandhu SK, et al. Monitoring of electroencephalography during transcranial electrical motor evoked potentials. Epilepsia. 2005;46(Suppl 8):309–310.

52.   Burke D, Hicks R, Stephen J, et al. Assessment of corticospinal and somatosensory conduction simultaneously during scoliosis surgery. Electroencephalogr Clin Neurophysiol. 1992;85:388–396.

53.   Zentner J, Albrecht T, Heuser D. Influence of halothane, enflurane, and isoflurane on motor evoked potentials. Neurosurgery. 1992;31(2):298–305.

54.   Zentner J, Ebner A. Nitrous oxide suppresses the electromyographic response evoked by electrical stimulation of the motor cortex. Neurosurgery. 1989;24:60–62.

55.   Bala E, Sessler DI, Nair DR, et al. Motor and somatosensory evoked potentials are well maintained in patients given dexmedetomidine during spine surgery. Anesthesiology. 2008;109(3):417–425.

56.   Pelosi L, Stevenson M, Hobbs GJ, et al. Intraoperative motor evoked potentials to transcranial electrical stimulation during two anaesthetic regimens. Clin Neurophysiol. 2001;112(6):1076–1087.

57.   Kempton LB, Nantau WE, Zaltz I. Successful monitoring of transcranial electrical motor evoked potentials with isoflurane and nitrous oxide in scoliosis surgeries. Spine. 2010;35(26):E1627– E1629.

58.   Ubags LH, Kalkman CJ, Been HD. Influence of isoflurane on myogenic motor evoked potentials to single and multiple transcranial stimuli during nitrous oxide/opioid anesthesia. Neurosurgery. 1998;43(1):90–94.

59.   Sloan T. Anesthesia and intraoperative neurophysiological monitoring in children. Childs Nerv Syst. 2010;26(2):227–235.

60.   Frei FJ, Ryhult SE, Duitmann E, et al. Intraoperative monitoring of motor-evoked potentials in children undergoing spinal surgery. Spine. 2007;32(8):911–917.

61.   Adams DC, Emerson RG, Heyer EJ, et al. Monitoring of intraoperative motor evoked potentials under conditions of controlled neuromuscular blockade. Anesth Analg. 1993;77(5):913–918.

62.   Hausmann ON, Boni T, Pfirrmann CWA, et al. Preoperative radiological and electrophysiological evaluation in 100 adolescent idiopathic scoliosis patients. Eur Spine J. 2003;12(5):501–506.

63.   Galloway GM, Brennan D, Brown JL. Transcranial magnetic stimulation—may be useful as a pre-operative screen of motor tract function. J Clin Neurophysiol. 2013;30(4):386–338.

64.   Guo X, Chau WW, Hui-Chan CWY, et al. Balance control in adolescents with idiopathic scoliosis and disturbed somatosensory function. Spine. 2006;31(14):E437–E440.

65.   Machida M, Dubousset J, Imamura Y, et al. Pathogenesis of idiopathic scoliosis: SEPs in chicken with experimentally induced scoliosis and in patients with idiopathic scoliosis. J Pediatr Orthop. 1994;14(3):329–335.

66.   Loa MLM, Chow DHK, Guo X, et al. Impaired dynamic balance control in adolescents with idiopathic scoliosis and abnormal somatosensory evoked potentials. J Pediatr Orthop. 2008;28(8):846–849.

67.   Kalkman CJ, Brink ten SA, Been HD, et al. Variability of somatosensory cortical evoked potentials during spinal surgery. Effects of anesthetic technique and high-pass digital filtering. Spine. 1991;16(8):924–929.

68.   Lyon R, Feiner J, Lieberman JA. Progressive suppression of motor evoked potentials during general anesthesia: the phenomenon of “anesthetic fade”. J Neurosurg Anesthesiol. 2005;17(1):13–19.