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From the Departments of Plastic and Reconstructive Surgery and Ludwig Boltzmann Institute for Experimental Plastic Surgery,
* Anesthesiology and Intensive Care,
Ludwig Boltzmann Institute for Clinical Anesthesiology and Intensive Care,
University of Vienna, Austria, Europe, and the Hand and Microsurgical Center and University of Texas at El Paso, El-Paso, Texas, USA.
Address correspondence to: Univ. Prof. Dr. Edvin Turkof, Abteilung für Plastische und Rekonstruktive Chirurgie, Universitätsklinik für Chirurgie, Allgemeines Krankenhaus der Stadt Wien, Währinger Gürtel 18 - 20, 1090 Wien, Austria, Europe. Phone: 43-1-40400/5620; Fax: 43-1-40400/6988; E-mail: edvin-turkof{at}via.at
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Abstract |
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Methods: In seven goats, anesthesia was induced with 3 mg
kg–1 ketamine iv and maintained with nitrous oxide 40% in oxygen and 2 µgkg–1hr–1 fentanyl iv. The MEP were performed with two subcutaneous needle electrodes placed over the occiput (cathode) and the nasion (anode), with their plugs connected to the power output of a Digitimer D 180 electrical stimulator, connected to the trigger input of an electromyograph (model 8400, Cadwell Laboratories, Inc., Kennwick, Washington). Activation of the Digitimer caused central stimulation of the motor cortex, evoking baseline compound muscle action potentials (CMAPs) which were recorded from the left triceps muscle. Subsequently, isoflurane 2% was administered together with repeated central stimulation at 30 sec intervals.
Results: Onset of I- (indirect) waves increased from median 15,8 msec to median 26,8 msec P = 0,018 (latency increase ranged from: 9 to 11.5 msec), while peak-to-peak amplitudes decreased and subsequently disappeared. D- (direct) waves showed no latency increase, and finally disappeared as well. After disappearance of CMAPs, isoflurane administration was stopped and MEP repeated. The CMAPs reappeared (range: 210-360 sec) and regained initial peak-to-peak amplitudes and latencies.
Conclusion: These animal studies suggest that isoflurane should not be used during the recording of MEPs.
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Introduction |
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In brachial plexus surgery, it is important to verify the functional status of anterior motor roots, because intradural lesions are difficult to recognize and lead to insufficient surgery if they remain undetected.2–3 An experimental study was set to verify the applicability of motor evoked potentials in brachial plexus surgery.2 The Nubian goat was selected as animal model because of the special anatomy of its cervical vertebral column which shows large interarcual spaces between the vertebra C5-6 and C6-7.4–5 These wide openings are connected only by the ligamentum flavum, leaving the spinal cord unprotected from any bony structure at these two sites.4–5 This anatomical peculiarity enables exposure of the spinal cord without the need to perform hemilaminectomy within this restricted segment of the spinal vertebral column.2,4,5 Since the goat has never been used in MEP experiments, the choice of an appropriate anesthetic agent was required to perform this study. Isoflurane suppresses MEP in humans,6–8 rats,9,10 rabbits11 and cats.12,13 However, methods and results differed to a large extent in these studies.6–13 Therefore, we designed this animal experiment to investigate how the agent would act in a new animal model and to compare the findings obtained with results of similar studies.
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Methods |
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). Goats were premedicated with 0.2 mgkg–1 xylazine and 0.5 mg atropine im. Anesthesia was induced 3 mgkg–1 ketamine iv. After performing tracheotomy, the tracheas were intubated with a 7 mm cuffed tube and the lungs were ventilated (Mark 14 positive phase ventilator - Bird, Palm Springs Corporation, California) with an oxygen-nitrous oxide mixture (FI O2= 0.6). The PaCO2 was maintained within normal limits (4.6-5.3 kPa), as assessed by capnography and intermittent blood-gas analysis. Nitrous oxide was kept at 40% because this agent has a depressive effect on MEP at concentrations > 50%.14,15 Analgesia was maintained by iv administration of 2 µgkg–1hr–1 fentanyl because of its minor effects on MEP15 and by subcutaneous administration of lidocaine 2% under the two stimulation electrodes. A polyethylene catheter was placed in the left femoral artery for blood-pressure recording and for blood sampling. Ringer's solution was infused at a rate of 3-5 mlkg–1 as required to keep hemodynamic variables within 10% of control values. In order to avoid excessive filling of the urinary bladder, suprapubic puncture and drainage were performed. Core temperature was registered with a rectal thermistor probe, and ECG was monitored with a 3-channel ECG-recorder (Hellige EK). Nasogastric suction was induced with a stomach tube. Statistical analysis was performed using the Wilcoxon Matched pairs signed ranks test, P < 0,05 was considered to be significant.
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). After recording of the baseline CMAP, isoflurane was administered at 2% (Figure). Central stimulation was repeated at intervals of 30 sec. If the CMAP disappeared, isoflurane was turned off (Figure) and central stimulation was repeated at the same intervals until CMAP reappeared and returned to initial values (Table I
, Figure), as before the administration of the volatile agent.
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Results |
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). After withdrawal of isoflurane, a mean time of 304 sec passed until amplitudes returned to initial values (range: 210-360 sec, or 7-12 stimuli, Table I). Together with the decrease or disappearance respectively of amplitudes, an increase in onset time from median 15,8 msec to 26,8 msec P = 0,018 was observed (latency increased to mean: 11.1, range: 9.2-13 msec, Table I), however this effect was restricted to I-waves alone: the latency of D-waves remained stable14 (Figure). |
Discussion |
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Our results confirmed the findings of similar studies: as with the other reports,6–13 we observed dose- and time- dependent effects on amplitudes and latencies of MEP under isoflurane anesthesia. However, a comparison cannot be made without taking into consideration several methodological differences among the studies mentioned.6–13 These differences consist of: A) the model (several species, humans), B) the different concentrations of isoflurane, C) the use of nitrous oxide in concentrations which contribute to the depressive effect of isoflurane, D) the stimulation method and stimulation site (magnetic or electrical, transcranial or directly after craniotomy), E) the recording site (spinal cord, muscles) and, as a result, F) the large variety of the described results.6–13 (Table II)
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B) Most authors tested the effect of isoflurane in incremental concentration steps.6–11,13 But the range of concentrations differs remarkably: 0.25% - 1% studied Yamada et al.,13 while Schmidt et al.9 tested from 0.5 to 3%, the others remained between these values.6,7,9–11 In contrast, Toda12 investigated a single concentration, an approach similar to our study, in which 2% were used throughout the experiment.
C) Four authors added nitrous oxide to isoflurane at concentrations > 50%.6–8,12 However, nitrous oxide has a depressive effect on MEP at these concentrations.12,15,16
D) Five authors and ourselves used electrical stimulation.6,7,9–11 Others chose magnetic stimulation.8,12,13 Amplitudes of MEP are higher using electrical stimulation than magnetic stimulation.17 Electrical, but not magnetic stimulation is painful. Therefore, one may expect amplitudes to be more resistant to isoflurane and analgesia to be increased when MEP is performed using electrical stimulation. The different characteristics of electrical and magnetic stimulation are probably the cause of the monophasic CMAPs in Yamada's report 13 (magnetic stimulus), while, in contrast, Haghigi's9,10 (electric stimulus) and our recordings were polyphasic. For the same reason, Toda 12 - (magnetic stimulus) could keep isoflurane at a relatively low concentration of 1.5% without awakening the cats, compared with 2% used in our study (electric stimulus).
E) Five authors5,7–10,12 recorded the MEPs, as we did, from muscles alone. One author recorded the MEPs from the spinal cord alone,7 and two used two recording sites -the spinal cord and the muscles.11,13 This distinction is necessary because recordings from the spinal cord are more resistant to the influence of anesthetic agents than are CMAPs11,13 (Table II). This is due to: 1) the distance between stimulation and recording sites is shorter, thus reducing the biological resistance and 2) the recording occurs proximally from the synapses of the spinal roots. Therefore, the results of several apparently similar reports6–13 cannot be compared simply.
F) Only three authors7,12,13 mentioned the different sensitivity of D and I waves to isoflurane. Yamada et al.13 observed only D-waves on epidural recordings. The CMAPs described in his study showed I-waves alone, probably due to the less intense stimulus of the magnetic coil. In our study, D-waves could be observed and were more resistant than I-waves. An increase of D-waves-latencies did not occur and peak-to-peak amplitudes showed a delayed decrease (Figure 1), with complete disappearance at 2%. Toda12 observed the amplitudes of D-waves to be stable at 1.5% on spinal stimulation and, similar to our study, to disappear on central stimulation (Table II). Hicks et al. observed D and I waves on epidural recordings, with both waves remaining recordable at concentrations up to 2%.7 These results, together with Yamada's13 findings, emphasize the higher resistance of spinal potentials towards depressive agents when compared to CMAPs.
In summary, we demonstrated that the nubian goat shows similar sensitivity to the depressive effect of isoflurane on MEP as other animals9–13 and humans.6–8 The I-waves showed a rapid attenuation until complete disappearance of peak-to-peak amplitudes and an increase of latencies, wave-forms being constantly polyphasic. The D-waves of CMAPSs diminished slowly until disappearance under isoflurane anesthesia at 2%, but their latencies, remained stable. For clinical application, our observations suggest that, in accordance with previous reports, one should carefully design anaesthesia for brachial plexus surgery if intraoperative monitoring is to be performed in order to avoid an incompatible combination of agents.
We conclude that isoflurane is an unsuitable anesthetic agent when MEPs are to be obtained in the Nubian goat.
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Acknowledgments |
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The study was supported by the scientific fund from the Medical University of Vienna, Zeneca Inc., Vienna, Novartis Inc., Vienna, Glaxo Inc., Vienna, Smith-Kline-Beecham Inc., Vienna, and the Ludwig Boltzmann Institute for Experimental Plastic Surgery, Vienna, Austria.
Accepted for publication October 3, 1999.
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References |
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2 Turkof E, Monsivais J, Dechtyar I, Bellolo H, Millesi H, Mayr N. Motor evoked potential as a reliable method to verify the conductivity of anterior spinal roots in brachial plexus surgery: an experimental study on goats. J Reconstr Microsurg 1995; 11: 357–62.[Medline]
3 Turkof E, Millesi H, Turkof R, Pfundner P, Mayr N. Intraoperative electroneurodiagnostics (transcranial electrical motor evoked potentials) to evaluate the functional status of anterior spinal roots and spinal nerves during brachial plexus surgery. Plast Reconstr Surg 1997; 99: 1632–41.[Medline]
4 Turkof E, Monsivais J, Mayer N, Millesi H. The goat: a viable experimental anatomical model for testing spinal root conductivity with SSEP, MEP without laminectomy. Abstracts of the 11th Congress of the International Microsurgical Society; Rhodes, Greece, 1992; 51.
5 Turkof E, Bellolo H, Monsivais J. The anatomy of the vertebral column of the nubian goat: a peculiarity of the arcus vertebrae C5, C6 and C7 forming large spatia interarcualia. Can J Vet Res 1994; 58: 156.[Medline]
6 Calancie B, Klose KJ, Baier S, Green BA. Isoflurane-induced attenuation of motor evoked potentials caused by electrical motor cortex stimulation during surgery. J Neurosurg 1991; 74: 897–904.[Medline]
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Hicks RG, Woodforth IJ, Crawford MR, Stephen JPH, Burke DJ. Some effects of isoflurane on I waves of the motor evoked potential. Br J Anaesth 1992; 69: 130–6.
8 Schmid UD, Boll J, Liechti S, Schmid J, Hess CW. Influence of some anesthetic agents on muscle responses to transcranial magnetic cortex stimulation: a pilot study in humans. Neurosurgery 1992; 30: 85–92.[Medline]
9 Haghighi SS, Green KD, Oro JJ, Drake RK, Kracke GR. Depressive effect of isoflurane anesthesia on motor evoked potentials. Neurosurgery 1990; 26: 993–7.[Medline]
10 Haghighi SS, Madsen R, Green KD, Oro JJ, Kracke GR. Suppression of motor evoked potentials by inhalation anesthetics. J Neurosurg Anesthesiol 1990; 2: 73–8.[Medline]
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12 Toda Y. The effect of anesthetic agents on descending spinal cord evoked potential and the compound muscle action potentials elicited by stimuation at the cerebral motor cortex and the spinal cord. Japanese Journal of the Orthopaedic Association 1992; 66: 279–90.
13 Yamada H, Transfeldt EE, Tamaki T, Torres F, Iaizzo PA. The effects of volatile anesthetics on the relative amplitudes and latencies of spinal and mucsle potentials evoked by trancranial magnetic stimulation. Spine 1994; 19: 1512–7.[Medline]
14 Amassian VE, Stewart M, Quirk GJ, Rosenthal JL. Physiological basis of motor effects of a transient stimulus to cerebral cortex. Neurosurgery 1987; 20: 74–93.[Medline]
15 Jellinek D, Platt M, Jewkes D, Symon L. Effects of nitrous oxide on motor evoked potentials recorded from skeletal muscle in patients under total anesthesia with intravenously administered propofol. Neurosurgery 1991; 29: 558–62.[Medline]
16 Zentner J, Albrecht T, Heuser D. Influence of halothane, enflurane and isoflurane on motor evoked potentials. Neurosurgery 1992; 31: 298–305.[Medline]
17 Rothwell JC, Day BL, Thompson PD, Dick JPR, Marsden CD. Some experiences of techniques for stimulation of the human cerebral motor cortex through the scalp. Neurosurgery 1987; 20: 156–63.[Medline]
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ON": beginning of administration;
OFF": omission of the agent.
": amplitudes regained initial values. Interval between each stimuation: 30 sec.