Meiko Kakimoto

Nara Medical University, Nara-shi, Nara, Japan

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Publications (23)51.46 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Xenon has been shown to reduce cellular injury after cerebral ischemia. However, the neuroprotective effects of xenon on ischemic spinal cord are unknown. The authors compared the effects of xenon and propofol on spinal cord injury following spinal cord ischemia in rabbits. Thirty-two male New Zealand white rabbits were randomly assigned to one of three groups. In the xenon and propofol group, 70% of xenon and 0.8 mg/kg/min of propofol were administered 30 min before an aortic occlusion and maintained until the end of the procedure. The aortic occlusion was performed for 15 min. In the sham group, the aorta was not occluded. After an assessment of the hind limb motor function using the Tarlov score (0=paraplegia, 4=normal) at 48 h after reperfusion, gray and white matter injuries were evaluated based on the number of normal neurons in the anterior spinal cord and the percentage areas of vacuolation in the white matter, respectively. In the xenon and propofol groups, the Tarlov score and the number of normal neurons were significantly lower than those in the sham group, whereas the percentage areas of vacuolation were similar among the three groups. There were no significant differences in Tarlov scores and the number of normal neurons between the xenon and the propofol groups. The results indicated that 70% of xenon has no additional neuroprotective effects on ischemic spinal cord injury in rabbits compared with propofol.
    Acta Anaesthesiologica Scandinavica 10/2009; 54(3):337-42. · 2.36 Impact Factor
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    ABSTRACT: Dexmedetomidine is used in the perioperative management of patients, including as an intraoperative adjuvant. The effects of dexmedetomidine on myogenic motor evoked potentials (MEPs) remain undetermined. We conducted the present study to investigate the effects of dexmedetomidine on myogenic MEPs in rabbits. New Zealand white rabbits were used for the studies. First, to determine appropriate doses of dexmedetomidine as an adjunct for anesthesia in rabbits, the level of anesthesia was evaluated by testing the palpebral and limb withdrawal reflexes, and the reactions to ear pinching and tail clamp at 5, 25, 50, 100 microg/kg/h. Second, in 10 rabbits under ketamine and fentanyl anesthesia, myogenic MEPs in response to single pulse and a train-of-five pulses were recorded from the soleus muscle before, during, and after the administration of dexmedetomidine at 5, 25, and 50 microg/kg/h. At 50 microg/kg/h of dexmedetomidine, palpebral reflex, limb reflex, and reaction to ear pinching were inhibited in >50% of animals, but the reaction to tail clamp was not reduced. Dexmedetomidine suppressed myogenic MEPs in a dose-dependent manner, but when multipulses were used for stimulation, myogenic MEPs could be recorded in all animals at 50 microg/kg/h. As long as multipulse is used for stimulation, the recording of myogenic MEPs is feasible in rabbits under ketamine and fentanyl anesthesia during the administration of dexmedetomidine at doses that are an adjunct to anesthesia.
    Anesthesia and analgesia 07/2007; 104(6):1488-92, table of contents. · 3.08 Impact Factor
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    ABSTRACT: Although gray matter injury has been well characterized, the available data on white matter injury after spinal cord ischemia (SCI) in rabbits are limited. The current study was conducted to investigate the evolution of ischemia induced injury to gray and white matter and to correlate this damage to hind-limb motor function in rabbits subjected to SCI. Thirty-eight rabbits were randomly assigned to 24-h, 4-day, or 14-day reperfusion groups or a sham group (n = 9 or 10 per group). SCI was induced by occlusion of the infrarenal aorta for 16 min. Hind-limb motor function was assessed using the Tarlov scale (0 = paraplegia, 4 = normal). The gray matter damage was assessed on the basis of the number of normal neurons in the anterior spinal cord. White matter damage was assessed on the basis of the extent of vacuolation and accumulation of amyloid precursor protein immunoreactivity. Tarlov scores gradually decreased and reached a nadir 14 days after reperfusion. There were no significant differences in the number of normal neurons among the 24-h, 4-day, and 14-day groups. The extent of vacuolation, expressed as a percent of total white matter area, was significantly greater in the 4-day and 14-day groups in comparison with the sham group. By contrast, there was no difference in vacuolation between the sham and 24-h groups. Amyloid precursor protein immunoreactivity was greater in the 4-day and 14-day groups. The results in the current study show that SCI induced white matter injury as well as gray matter injury in a rabbit model of SCI. The time course for 14 days after reperfusion may differ among the gray and white matter damages and hind-limb motor function in rabbits subjected to SCI.
    Anesthesiology 09/2006; 105(2):305-12. · 5.16 Impact Factor
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    ABSTRACT: Background: Although gray matter injury has been well characterized, the available data on white matter injury after spinal cord ischemia (SCI) in rabbits are limited. The current study was conducted to investigate the evolution of ischemia induced injury to gray and white matter and to correlate this damage to hind-limb motor function in rabbits subjected to SCI.
    Anesthesiology 07/2006; 105(2):305-312. · 5.16 Impact Factor
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    ABSTRACT: We compared the effects of xenon on myogenic motor evoked potentials (MEPs) with those of propofol and isoflurane in rabbits under ketamine/fentanyl anesthesia. Thirty animals were randomly allocated to one of 3 groups (n = 10 in each group). In the propofol group, propofol was administered at a rate of 0.4 mg x kg(-1) x min(-1) (small) and 0.8 mg x kg(-1) x min(-1) (large). In the isoflurane group, isoflurane was administered at 0.8% (small) and 1.6% (large). In the xenon group, xenon was administered at 35% (small) and 70% (large). Myogenic MEPs in response to stimulation with single pulse and a train of 5 pulses were recorded from the soleus muscle before, during (at small and large doses), and after the administration of each anesthetic. With single-pulse stimulation, MEPs were recorded in 90% and 50% of animals at small and large doses of xenon, respectively, and MEP amplitudes in the xenon and isoflurane groups were significantly lower compared with those in the propofol group. With train pulse stimulation, MEPs were recorded in 100% and 90% of animals at small and large doses of xenon, respectively, and a reduction in MEP amplitudes by xenon was more prominent than by propofol but less than isoflurane at large doses. These results suggest that MEP recording may be feasible under xenon anesthesia if multipulse stimulation is used, although xenon has suppressive effects on myogenic MEPs.
    Anesthesia and analgesia 07/2006; 102(6):1715-21. · 3.08 Impact Factor
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    ABSTRACT: Neuromuscular blockade can suppress myogenic motor evoked potentials (MEPs). The authors hypothesized that tetanic stimulation (TS) of the peripheral nerve before transcranial stimulation may enhance myogenic MEPs during neuromuscular blockade. In the current study, the authors evaluated MEP augmentations by TS at different levels of duration, posttetanic interval, neuromuscular blockade, and stimulus intensity. Thirty-two patients undergoing propofol-fentanyl-nitrous oxide anesthesia were examined. Train-of-five stimulation was delivered to C3-C4, and MEPs were recorded from the abductor hallucis muscle. In study 1, TS with a duration of 1, 3, or 5 s was delivered at 50 Hz to the tibial nerve 1, 3, or 5 s (interval) before transcranial stimulation, and the effects of TS on MEP amplitude were evaluated. In study 2, TS-induced MEP augmentations were evaluated at the neuromuscular blockade level (%T1) of 50% or 5%. In study 3, MEP augmentations by TS at stimulus intensities of 0, 5, 25, and 50 mA were evaluated. The application of TS significantly enlarged the amplitudes of MEPs at the combinations of duration (3, 5 s) and interval (1, 3, 5 s) compared with those without TS. TS-induced MEP augmentations were similarly observed at %T1 of both 50% and 5%. TS-induced MEP augmentations were observed at stimulus intensities of 25 and 50 mA. The results indicate that TS of the peripheral nerve before transcranial stimulation can enlarge the amplitude of MEPs during general anesthesia with neuromuscular blockade. TS of the peripheral nerve can be intraoperatively applied as a method to augment myogenic MEP responses.
    Anesthesiology 05/2005; 102(4):733-8. · 5.16 Impact Factor
  • Journal of Neurosurgical Anesthesiology - J NEUROSURG ANESTHESIOL. 01/2005; 17(4):245-246.
  • Journal of Neurosurgical Anesthesiology - J NEUROSURG ANESTHESIOL. 01/2004; 16(4):343-344.
  • Journal of Neurosurgical Anesthesiology - J NEUROSURG ANESTHESIOL. 01/2004; 16(4).
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    ABSTRACT: Rapid ischemic preconditioning (IPC) has been shown to reduce cellular injury after subsequent cardiac and cerebral ischemia. However, the data on rapid IPC of the spinal cord is limited. The authors investigated whether pretreatment with sublethal ischemia of spinal cord can attenuate neuronal injury after spinal cord ischemia in rabbits. Forty-seven male New Zealand white rabbits were randomly assigned to one of three groups (n = 15 or 16 each). In the IPC(-) group, the infrarenal aorta was occluded for 17 min to produce spinal cord ischemia. In the IPC(+) group, 5 min of aortic occlusion was performed 30 min before 17 min of spinal cord ischemia. In the sham group, the aorta was not occluded. Hind limb motor function was assessed at 3 h, 24 h, 4 days, and 7 days after reperfusion using Tarlov scoring (0 = paraplegia; 4 = normal). Animals were killed for histopathologic evaluation at 24 h or 7 days after reperfusion. The number of normal neurons in the anterior spinal cord (L4-L6) was counted. Neurologic scores were significantly higher in the IPC(+) group than the IPC(-) group at 3 and 24 h after reperfusion (P < 0.05). However, neurologic scores in the IPC(+) group gradually decreased and became similar to those in the IPC(-) group at 4 and 7 days after reperfusion. At 24 h after reperfusion, the numbers of normal neurons were significantly higher in the IPC (+) group than in the IPC(-) group (P < 0.05) and were similar between the IPC(+) and sham groups. At 7 days after reperfusion, there was no difference in the number of normal neurons between the IPC(+) and IPC(-) groups. The results indicate that rapid IPC protects the spinal cord against neuronal damage 24 h but not 7 days after reperfusion in a rabbit model of spinal cord ischemia, suggesting that the efficacy of rapid IPC may be transient.
    Anesthesiology 11/2003; 99(5):1112-7. · 5.16 Impact Factor
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    ABSTRACT: In the present study, we investigated the effect of hypothermia on myogenic motor-evoked potentials (MEPs) in rabbits. The influence of stimulation paradigms to induce MEPs was evaluated. Twelve rabbits anesthetized with ketamine, fentanyl, and propofol were used for the study. Myogenic MEPs in response to electrical stimulation of the motor cortex with a single pulse and a train of three and five pulses were recorded from the soleus muscle. After the control recording of MEPs at 38 degrees C of esophageal temperature, the rabbits were cooled by surface cooling. Esophageal temperature was maintained at 35 degrees C, 32 degrees C, 30 degrees C, and 28 degrees C, and MEPs were recorded at each point. MEP amplitude to single- pulse stimulation was significantly reduced with a re-duction of core temperature to 28 degrees C compared with the control value at 38 degrees C (0.8 +/- 0.4 mV versus 2.3 +/- 0.3 mV; P < 0.05), whereas MEP amplitude to train-pulse stimulation did not change significantly during the cooling. MEP latency was increased linearly with a reduction of core temperature regardless of stimulation paradigms. In conclusion, these results indicate that a reduction of core temperature to 28 degrees C did not influence MEP amplitudes as long as a train of pulses, but not a single pulse, was used for stimulation in rabbits under propofol/ketamine/fentanyl anesthesia. IMPLICATIONS: Intraoperative monitoring of myogenic motor-evoked potentials (MEPs) may be required under hypothermic conditions because of its neuroprotective efficacy. However, data on the influence of hypothermia on myogenic MEPs are limited. The results indicate that multipulse stimulation may be better than single-pulse stimulation when monitoring MEPs during hypothermia.
    Anesthesia & Analgesia 07/2003; 96(6):1692-7, table of contents. · 3.30 Impact Factor
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    ABSTRACT: In hypothermic patients, a tendency to bleed may be observed even when hemostatic tests seem to be normal. Coagulation and platelet function tests are usually performed at 37 degrees C. We investigated the influence of induced hypothermia on temperature-adjusted hemostasis function testing using Sonoclot Analyzer (Sonoclot) and Thromboelastography (TEG). Anesthesia was induced and maintained with IV ketamine and fentanyl on 15 male New-Zealand White rabbits. A water blanket was used to induce hypothermia to 30 degrees C and to rewarm to 37 degrees C. Blood samples were obtained at four points: before hypothermia, at 34 degrees C, at 30 degrees C, and after rewarming. Standard coagulation tests were performed at 37 degrees C (C method), and simultaneously, real temperature hemostasis function tests (R method) were run. In Sonoclot(R), activated clotting time and time to peak increased and clot rate decreased significantly at 30 degrees C in the R method compared with those in the C method. In TEG(R), reaction time and clot formation time were prolonged and clot formation rate was diminished at 30 degrees C in the R method compared with those in the C method. Induced hypothermia delayed the coagulation cascade and reduced platelet function. During hypothermia, hemostatic measurements should be performed at real temperature to avoid overestimating patient hemostatic function based on results measured at the standard 37 degrees C. IMPLICATIONS: We investigated the influence of induced hypothermia on temperature-adjusted hemostasis function tests in rabbits using Sonoclot Analyzer and Thromboelastography. Induced hypothermia delayed the coagulation cascade and reduced platelet function. The conventional coagulation tests performed at 37 degrees C failed to detect these hypothermia-induced degradations in hemostasis performance.
    Anesthesia & Analgesia 05/2003; 96(4):1209-13, table of contents. · 3.30 Impact Factor
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    ABSTRACT: Recent evidence suggests that brain injury caused by ischemia is a dynamic process characterized by ongoing neuronal loss for at least 14 days after ischemia. However, long-term outcome following spinal cord ischemia has not been extensively examined. Therefore, we investigated the changes of hind limb motor function and neuronal injury during a 14-day recovery period after spinal cord ischemia. Male Sprague-Dawley rats received spinal cord ischemia (n = 64) or sham operation (n = 21). Spinal cord ischemia was induced by inflation of a 2F Fogarty catheter placed into the thoracic aorta for 6, 8, or 10 minutes. The rats were killed 2, 7, or 14 days after reperfusion. Hind limb motor function was assessed with the 21-point Basso, Beattie, and Bresnahan (BBB) scale during the recovery period. The number of normal and necrotic neurons was counted in spinal cord sections stained with hematoxylin/eosin. Longer duration of spinal cord ischemia produced severer hind limb motor dysfunction at each time point. However, BBB scores gradually improved during the 14-day recovery period. Neurologic deterioration was not observed between 7 and 14 days after reperfusion. The number of necrotic neurons peaked 2 days after reperfusion and then decreased. A small number of necrotic neurons were still observed 7 and 14 days after reperfusion in some of the animals. These results indicate that, although hind limb motor function may gradually recover, neuronal loss can be ongoing for 14 days after spinal cord ischemia.
    Journal of Neurosurgical Anesthesiology 05/2003; 15(2):104-9. · 1.67 Impact Factor
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    ABSTRACT: To investigate whether motor evoked potentials (MEP) to transcranial electrical stimulation under constant blood propofol concentration are affected by the arousing effect of surgical noxious stimuli. Twenty patients who underwent elective spinal surgery were studied. Patients were anesthetized with 50% nitrous oxide in oxygen, fentanyl, and propofol to maintain the bispectral index (BIS) score around 50. MEP in response to a multipulse transcranial electrical stimulation at stimulus sites of C3-C4 were recorded over the right abductor pollicis brevis muscle. Changes of peak-to-peak amplitude and onset latency of MEP, BIS score before and after surgical stimuli were evaluated. Propofol plasma concentration was measured at the same time points. Both MEP amplitude and latency did not change significantly after surgical stimuli although BIS increased significantly (48 +/- 6 to 58 +/- 5; P < 0.05). Plasma propofol concentration was maintained at the same level between the two measurement points (3.3 +/- 0.7 to 3.3 +/- 0.7 micro g*mL(-1)). There was no relation between BIS change and changes of MEP amplitude and latency, and propofol plasma concentration. MEP to the transcranial electrical stimulation under a constant and clinically appropriate blood propofol concentration are not affected by surgical noxious stimuli.
    Canadian Journal of Anaesthesia 01/2003; 50(1):86-91. · 2.13 Impact Factor
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    ABSTRACT: Motor-evoked potentials from the external anal sphincter were analyzed using transcranial electrical stimulation during spinal surgery in patients under general anesthesia. To investigate whether motor-evoked potentials from the external anal sphincter could be elicited by transcranial electrical stimulation under general anesthesia. Lumbosacral surgery often places nerve rootlets at risk for injury during operative dissection. Specifically, injury for sacral rootlets can result in bowel and bladder dysfunction, but the techniques for monitoring bowel and bladder function are limited. Thirty patients who underwent elective spinal surgery were studied. Patients were anesthetized with 50% nitrous oxide in oxygen, fentanyl, and 4 mg/kg/h of propofol (n = 19) or 1 mg/kg/h of ketamine (n = 11). The level of neuromuscular blockade, assessed by recording the M-response from the right abductor pollicis brevis muscle, was maintained at an M-response amplitude of 40-50% of control. Motor-evoked potentials in response to a multipulse transcranial electrical stimulation at stimulus sites of C3-C4 or Fz-Cz were recorded from the skin over the subcutaneous part of the external anal sphincter using a plug-type electrode probe. The success rate of motor-evoked potentials' recording and peak-to-peak amplitude and the onset latency of motor-evoked potentials were evaluated. Success rates of motor-evoked potentials from the external anal sphincter were 73% and 53% after transcranial stimulation at stimulus sites of C3-C4 and Cz-Fz, respectively. Amplitudes of motor-evoked potentials after C3-C4 stimulation were significantly greater than those after Cz-Fz stimulation. Motor-evoked potential latency from the external anal sphincter was 18.6 +/- 1.5 and 19.0 +/- 2.7 msec after C3-C4 and Cz-Fz stimulation, respectively. The results suggest that, using a transcranial multipulse stimulation, monitoring of motor-evoked potentials from the external anal sphincter is feasible during ketamine- and propofol-based anesthesia. However, further improvement of techniques would be required for intraoperative elicitation of motor-evoked potentials from the external anal sphincter.
    Spine 12/2002; 27(21):E454-9. · 2.16 Impact Factor
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    ABSTRACT: The aim of the current study was to investigate whether there are differences in amplitudes and intrapatient variability of motor evoked potentials to five pulses of transcranial electrical stimulation between ketamine/N2O- and propofol/N2O-based anesthesia. Patients in the propofol group (n = 13) and the ketamine group (n = 13) were anesthetized with 50% N2O in oxygen, fentanyl, and 4 mg/kg/hr of propofol or 1 mg/kg/hr of ketamine, respectively. The level of neuromuscular blockade was maintained at an M-response amplitude of approximately 50% of control. Motor evoked potentials in response to multipulse transcranial electrical stimulation were recorded from the right adductor pollicis brevis muscle, and peak-to-peak amplitude and onset latency of motor evoked potentials were evaluated. To estimate intrapatient variability, the coefficient of variation (standard deviation/mean x 100%) of 24 consecutive responses was determined. Motor evoked potential amplitudes in the ketamine group were significantly larger than in the propofol group (mean, 10th-90th percentile: 380 microV, 129-953 microV; 135 microV, 38-658 microV, respectively; P <.05). There were no significant differences in motor evoked potential latency (mean +/- standard deviation: 20.9 +/- 2.2 msec and 21.4 +/- 2.2 msec, respectively) and coefficient of variation of amplitudes (median [range]: 32% [22-42%] and 26% [18-41%], respectively) and latencies (mean +/- standard deviation: 2.1 +/- 0.7% and 2.1 +/- 0.7%, respectively) between the ketamine and propofol groups. In conclusion, intrapatient variability of motor evoked potentials to multipulse transcranial stimulation is similar between ketamine/N2O- and propofol/N2O-based anesthesia, although motor evoked potential amplitudes are lower during propofol/N2O-based anesthesia than ketamine/N2O-based anesthesia.
    Journal of Neurosurgical Anesthesiology 07/2002; 14(3):213-7. · 1.67 Impact Factor
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    ABSTRACT: A number of authors have reported that anaesthetics suppress myogenic motor evoked potentials (MEPs). However, the influence of hypothermia on these effects is unknown. Therefore we investigated the effects of hypothermia on nitrous oxide-induced suppression of myogenic MEPs. Twenty-two rabbits anaesthetized with ketamine, fentanyl and propofol were randomly allocated to one of three groups, with oesophageal temperatures of 40 degrees C (n = 8), 35 degrees C (n = 7) and 30 degrees C (n = 7). Myogenic MEPs in response to electrical stimulation of the motor cortex with a train of five pulses were recorded from the soleus muscle. Following the control recording, nitrous oxide was administered at concentrations of 30%, 50%, and 70% in random order, and MEPs were recorded. Control MEP amplitudes and percentage of control MEP amplitudes (%MEP amplitude) during the administration of nitrous oxide were compared between the three groups. Control MEP amplitudes were similar between the three groups. Nitrous oxide suppressed MEPs in a dose-dependent manner in all groups. During the administration of nitrous oxide, % MEP amplitudes at 35 degrees C and 30 degrees C (hypothermia) were significantly lower than those at 40 degrees C (normothermia). These results suggest that nitrous oxide-induced suppression of MEPs may be augmented during hypothermia.
    BJA British Journal of Anaesthesia 07/2002; 88(6):836-40. · 4.24 Impact Factor
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    ABSTRACT: Motor evoked potentials (MEPs) can be employed for monitoring the functional integrity of the descending motor pathways during thoracic aortic surgery. Since MEPs can be affected by a variety of intraoperative factors, intraoperative MEP changes have to be carefully interpreted. In this report, we describe two patients undergoing thoracic aortic surgery, in whom MEPs from the unilateral lower limb disappeared after femoral artery cannulation, and MEPs' recovered by modifying the position or removing the cannula. MEPs in the contralateral side remained unchanged. Neither patients showed postoperative neurologic dysfunction in the lower limbs. These observations suggest that regional ischemia of the lower limbs caused by femoral artery cannulation can affect intraoperative MEP finding.
    Masui. The Japanese journal of anesthesiology 09/2001; 50(8):874-7.
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    ABSTRACT: Monitoring of motor-evoked potentials (MEPs) is employed to examine functional integrity of descending motor pathway during thoracic aortic surgery. We experienced two cases of intraoperative changes in MEPs during thoracic aortic replacement. In one case, MEPs recovered after the intercostal artery reattachment, and in another case after the release of aortic clamping. No postoperative paraplegia was found in both cases. We conclude that monitoring of MEPs is useful not only because we can detect symptoms of the spinal cord injury from ischemia immediately but also because they give us a clue to decide operative procedures.
    Masui. The Japanese journal of anesthesiology 12/2000; 49(11):1247-9.
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    ABSTRACT: Monitoring of myogenic motor evoked potentials (MEPs) induced by transcranial electrical stimulation has become a promising tool for intraoperative monitoring. We described 2 patients who had developed significant decrease in MEP during the insertion of iliosacral screws for reconstruction of pelvic fractures. In both patients, MEPs were successfully obtained prior to the insertion under general anesthesia and partial neuromuscular blockade (propofol, ketamine, fentanyl, and nitrous oxide in oxygen: vecuronium), but reduced in association with the insertion. In one patient, they were restored by the re-insertion of screw and no new neurological deficits were observed postoperatively. However, in another patient, the decrease was not normalized and he suffered from paresis of the lower extremities after the surgery. We consider that intraoperative changes in MEPs could precisely predict postoperative motor function.
    Masui. The Japanese journal of anesthesiology 06/2000; 49(5):514-8.