Propofol and sevoflurane in subanesthetic concentrations act preferentially on the spinal cord: evidence from multimodal electrophysiological assessment

BACKGROUND: Animal experiments in recent years have shown that attenuation of motor responses by general anesthetics is mediated at least partly by spinal mechanisms. Less is known about the relative potency of anesthetic drugs in suppressing cortical and spinal electrophysiological responses in vivo in humans, particularly those, but not only those, connected with motor responses. Therefore, we studied the effects of sevoflurane and propofol in humans using multimodal electrophysiological assessment. METHODS: We studied nine healthy volunteers in two sessions during steady state sedation with 0.5, 1.0, and 1.5 microg/l (targeted plasma concentration) propofol or 0.2 and 0.4 vol% (end-tidal) sevoflurane. Following a 15-min equilibration period, motor responses to transcranial magnetic stimulation and peripheral (H-reflex, F-wave) stimulation were recorded, while electroencephalography and auditory evoked responses were recorded in parallel. RESULTS: At concentrations corresponding to two thirds of C(50 awake), motor responses to transcranial magnetic stimulation were reduced by approximately 50%, H-reflex amplitude was reduced by 22%, F-wave amplitude was reduced by 40%, and F-wave persistence was reduced by 25%. No significant differences between sevoflurane and propofol were found. At this concentration, the Bispectral Index was reduced by 7%, and the middle-latency auditory evoked responses were attenuated only mildly (N(b) latency increased by 11%, amplitude P(a)N(b) did not change). In contrast, the postauricular reflex was suppressed by 77%. CONCLUSIONS: The large effect of both anesthetics on all spinal motor responses, compared with the small effect on electroencephalography and middle-latency auditory evoked responses, assuming that they represent cortical modulation, may suggest that the suppression of motor responses to transcranial magnetic stimulation is largely due to submesencephalic effects.     

A comparison of myogenic motor evoked responses to electrical and magnetic transcranial stimulation during nitrous oxide/opioid anesthesia

Transcranial motor evoked potentials (tc-MEPs) are used to monitor spinal cord integrity intraoperatively. We compared myogenic motor evoked responses with electrical and magnetic transcranial stimuli during nitrous oxide/opioid anesthesia. In 11 patients undergoing spinal surgery, anesthesia was induced with i.v. etomidate 0.3 mg/kg and sufentanil 1.5 microg/kg and was maintained with sufentanil 0.5 microg x kg(-1) x h(-1) and N2O 50% in oxygen. Muscle relaxation was kept at 25% of control with i.v. vecuronium. Electrical stimulation was accomplished with a transcranial stimulator set at maximal output (1200 V). Magnetic transcranial stimulation was accomplished with a transcranial stimulator set at maximal output (2 T). Just before skin incision, triplicate responses to single stimuli with both modes of cortical stimulation were randomly recorded from the tibialis anterior muscles. Amplitudes and latencies were compared using the Wilcoxon signed rank test. Bilateral tc-MEP responses were obtained in every patient with electrical stimulation. Magnetic stimulation evoked only unilateral responses in two patients. With electrical stimulation, the median tc-MEP amplitude was 401 microV (range 145-1145 microV), and latency was 32.8 +/- 2.3 ms. With magnetic stimulation, the tc-MEP amplitude was 287 microV (range 64-506 microV) (P < 0.05), and the latency was 34.7 +/- 2.1 ms (P < 0.05). We conclude that myogenic responses to magnetic transcranial stimulation are more sensitive to anesthetic-induced motoneural depression compared with those elicited by electrical transcranial stimulation. IMPLICATIONS: Transcranial motor evoked potentials are used to monitor spinal cord integrity intraoperatively. We compared the relative efficacy of electrical and magnetic transcranial stimuli in anesthetized patients. It seems that myogenic responses to magnetic transcranial stimulation are more sensitive to anesthetic-induced motoneural depression compared with electrical transcranial stimulation.     

Monitoring of Immobility to Noxious Stimulation during Sevoflurane Anesthesia Using the Spinal H-reflex

Background: The spinal H-reflex has been shown to correlate with surgical immobility, i.e., the absence of motor responses to noxious stimulation, during isoflurane anesthesia. Here, the authors established individual concentration-response functions for H-reflex amplitude and tested the predictive power of the H-reflex for movement responses during sevoflurane anesthesia in comparison to electroencephalographic parameters. In addition, they investigated the effect of noxious stimulation on the H-reflex itself.

Methods: The authors studied 12 female patients during sevoflurane anesthesia before surgery. The sevoflurane concentration was increased, a laryngeal mask was inserted, and then the sevoflurane concentration was decreased until H-reflex amplitude (recorded over the soleus muscle) recovered. Thereafter, the end-tidal sevoflurane concentration was kept at a constant value close to the minimum alveolar concentration for suppression of movement responses after tetanic stimulation (MACtetanus), determined by the Dixon up-down method. Pharmacodynamic modeling of H-reflex amplitude and of the Bispectral Index was performed, and predictive values for motor responses to noxious electrical stimulation (50 Hz, 60 mA tetanus, volar forearm) were compared using the prediction probability.

Results: Concentration-dependent depression of H-reflex amplitude by sevoflurane was well modeled (median r2 = 0.97) by a sigmoid function with a median EC50 of 1.5 vol% and a median slope parameter of 3.7, much steeper than the slope for the Bispectral Index. MACtetanus calculated by logistic regression was 1.6 vol%. H-reflex amplitude predicted motor responses to noxious stimulation with a prediction probability of 0.76, whereas the prediction probability for Bispectral Index and spectral edge frequency (SEF95) were not different from chance alone. Noxious stimulation was followed by a substantial increase of H-reflex amplitude for several minutes, whereas the Bispectral Index and SEF95 exhibited no significant changes.     

Monitoring of immobility to noxious stimulation during sevoflurane anesthesia using the spinal H-reflex

BACKGROUND: The spinal H-reflex has been shown to correlate with surgical immobility, i.e., the absence of motor responses to noxious stimulation, during isoflurane anesthesia. Here, the authors established individual concentration-response functions for H-reflex amplitude and tested the predictive power of the H-reflex for movement responses during sevoflurane anesthesia in comparison to electroencephalographic parameters. In addition, they investigated the effect of noxious stimulation on the H-reflex itself. METHODS: The authors studied 12 female patients during sevoflurane anesthesia before surgery. The sevoflurane concentration was increased, a laryngeal mask was inserted, and then the sevoflurane concentration was decreased until H-reflex amplitude (recorded over the soleus muscle) recovered. Thereafter, the end-tidal sevoflurane concentration was kept at a constant value close to the minimum alveolar concentration for suppression of movement responses after tetanic stimulation (MACtetanus), determined by the Dixon up-down method. Pharmacodynamic modeling of H-reflex amplitude and of the Bispectral Index was performed, and predictive values for motor responses to noxious electrical stimulation (50 Hz, 60 mA tetanus, volar forearm) were compared using the prediction probability. RESULTS: Concentration-dependent depression of H-reflex amplitude by sevoflurane was well modeled (median r2 = 0.97) by a sigmoid function with a median EC50 of 1.5 vol% and a median slope parameter of 3.7, much steeper than the slope for the Bispectral Index. MACtetanus calculated by logistic regression was 1.6 vol%. H-reflex amplitude predicted motor responses to noxious stimulation with a prediction probability of 0.76, whereas the prediction probability for Bispectral Index and spectral edge frequency (SEF95) were not different from chance alone. Noxious stimulation was followed by a substantial increase of H-reflex amplitude for several minutes, whereas the Bispectral Index and SEF95 exhibited no significant changes. CONCLUSIONS: Suppression of movement to noxious stimulation and suppression of H-reflex amplitude by sevoflurane follow similar concentration-response functions. Although this does not imply a causal relation, it explains the high predictive value of H-reflex amplitude for motor responses to noxious stimuli, even in a narrow concentration range around the MACtetanus.     

Intravenous anaesthesia and repetitive transcranial magnetic stimulation monitoring in spinal column surgery

Background. Transcranial magnetic stimulation with motor evokedpotential monitoring is a non-invasive method for monitoringmotor tracts during surgery. However, anaesthetic agents suchas propofol and volatile agents reduce responses to single transcranialmagnetic stimulation. We assessed an intravenous technique foranaesthesia to allow motor evoked potentials (MEPs) to be monitoredusing repetitive transcranial magnetic stimulation (rTMS). Methods. We applied three-pulse rTMS (TriStim) in 11 patientsundergoing spinal column surgery after spinal column injuryand recorded the latency and peak-to-peak amplitude of MEPs.Anaesthesia was maintained with propofol and remifentanil. Results. MEPs were monitored successfully intraoperatively inall patients. Conclusions. It is possible to monitor intraoperative MEP usingrTMS during anaesthesia with propofol and remifentanil.     

Differential effects of nitrous oxide and propofol on myogenic transcranial motor evoked responses during sufentanil anaesthesia

We have compared the effects of 50% nitrous oxide and propofol, each administered concurrently with sufentanil, on the amplitudes and latencies of the compound muscle action potential (CMAP) response to transcranial electrical stimulation. Using a crossover design, 12 patients undergoing spinal surgery were exposed to both 50% nitrous oxide and propofol, the latter in a bolus-infusion regimen. Six patients received nitrous oxide first and six received propofol first. CMAP were recorded from the tibialis anterior muscle in response to both single and paired transcranial electrical stimuli. With single pulse stimulation, median CMAP amplitude was significantly greater during administration of nitrous oxide than propofol (nitrous oxide 335 (10th-90th percentiles 35-849) microV; propofol 36 (0-251) microV) (P < 0.01). With paired stimulation, there was no significant difference in CMAP amplitude during the two regimens (nitrous oxide 1031 (296-1939) microV; propofol 655 (0-1867) microV). The results indicate that propofol caused more depression of transcranial electrical motor evoked responses than 50% nitrous oxide but that the difference was probably clinically unimportant when a paired stimulation paradigm was used.      

Evaluation of the applicability of sevoflurane during post-tetanic myogenic motor evoked potential monitoring in patients undergoing spinal surgery

Purpose  Recent evidence has indicated that post-tetanic motor evoked potentials (p-MEPs) can be used to improve the reliability of the monitoring of motor function during spinal surgery. However, data on p-MEP monitoring are limited to those in subjects under propofol anesthesia. The present study was conducted to assess the applicability of sevoflurane during p-MEP monitoring in patients undergoing spinal surgery. Methods  Thirty-five patients undergoing spinal surgery under sevoflurane anesthesia were enrolled in the study and classified as being without preoperative motor deficits (n = 25) or with preoperative motor deficits (n = 10). For conventional MEP (c-MEP), transcranial train-pulse stimulation was delivered and the compound muscle action potentials were bilaterally recorded from the abductor pollicis brevis, abductor hallucis, tibialis anterior, and soleus muscles. For p-MEP, tetanic stimulation (50 Hz, 50 mA stimulus intensity) for 5 s was applied to the bilateral median and left tibial nerves 1 s prior to transcranial stimulation. Results  The amplitudes of p-MEP were significantly higher in all muscle recording sites than those of c-MEP in patients without motor deficits, whereas these amplitudes were significantly higher in only four of the eight muscles in patients with motor deficits (P < 0.05). The success rates of c-MEP and p-MEP recording were 48% and 64%, respectively, in patients without motor deficits and 30% and 60%, respectively, in patients with motor deficits. There were no statistically significant differences in success rates between c-MEP and p-MEP recording. Conclusion  Although the application of tetanic stimulation prior to transcranial stimulation did not significantly increase the success rates of MEP recording, it significantly enlarged MEP amplitude under sevoflurane anesthesia in patients without preoperative motor deficits.     

Effects of 4-aminopyridine on motor evoked potentials in patients with spinal cord injury: a double-blinded, placebo-controlled crossover trial.

4-Aminopyridine (4-AP) is a potassium (K+) channel blocking agent that has been shown to reduce the latency and increase the amplitude of motor evoked potentials (MEPs) elicited with transcranial magnetic stimulation (TMS) in patients with chronic spinal cord injury (SCI). These effects on MEPs are thought to reflect enhanced conduction in long tract axons brought about by overcoming conduction deficits due to focal demyelination and/or by enhancing neuroneuronal transmission at one or more sites of the neuraxis. The present study was designed to obtain further evidence of reduced central motor conduction time (CMCT) and to determine whether MEPs could be recorded from paretic muscles in which they were not normally elicited. MEPs were elicited with TMS being delivered to subjects (n = 25) pre- and post-administration of 4-AP (10 mg capsule) or placebo. The principal finding was that 4-AP lowered the stimulation threshold, increased the amplitude and reduced the latency of MEPs in all muscles tested, including those that were unimpaired, but did not alter measures of the peripheral nervous system (i.e., M-wave, H-reflex, F-wave). These 4-AP-induced changes in MEPs were significantly greater than those seen with placebo (p < 0.05). The primary implication of these results is that a low dose of 4-AP (immediate-release formulation) appears to improve the impaired central motor conduction of some patients with incomplete SCI. This is most likely attributable to overcoming conduction deficits at the site of injury but may also involve an increase in cortical excitability.     

Amplitudes and intrapatient variability of myogenic motor evoked potentials to transcranial electrical stimulation during ketamine/N2O- and propofol/N2O-based anesthesia

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.     

Noxious stimuli do not modify myogenic motor evoked potentials by electrical stimulation during anesthesia with propofol-based anesthesia

PURPOSE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: MEP to the transcranial electrical stimulation under a constant and clinically appropriate blood propofol concentration are not affected by surgical noxious stimuli.     

Intraoperative motor evoked potential monitoring: a review of 115 cases

We reviewed our experiences of intraoperative motor evoked potentials (MEPs) monitoring for 115 operations on the spine or spinal cord. We observed compound muscle action potentials from bilateral anterior tibial muscles by electrical transcranial stimulation of the motor cortex under general anesthesia induced and maintained with intravenous anesthetics (ketamine, propofol, or droperidol), fentanyl, and 50% nitrous oxide. Partial neuromuscular blockade was obtained with continuous infusion of vecuronium. MEPs were recorded bilaterally in 91 cases (79%) and laterally in 18 cases (16%). Postoperative deterioration of motor function was observed in 2 cases and amplitude of MEPs decreased more than 50% of control values in both cases. Intraoperative monitoring of MEPs might be a reliable indicator of spinal cord motor function.     

Motor and Somatosensory Evoked Potentials Are Well Maintained in Patients Given Dexmedetomidine during Spine Surgery

Background: Many commonly used anesthetic agents produce a dose-dependent amplitude reduction and latency prolongation of evoked responses, which may impair diagnosis of intraoperative spinal cord injury. Dexmedetomidine is increasingly used as an adjunct for general anesthesia. Therefore, the authors tested the hypothesis that dexmedetomidine does not have a clinically important effect on somatosensory and transcranial motor evoked responses.

Methods: Thirty-seven patients were enrolled and underwent spinal surgery with instrumentation during desflurane and remifentanil anesthesia with dexmedetomidine as an anesthetic adjunct. Upper- and lower-extremity transcranial motor evoked potentials and somatosensory evoked potentials were recorded during four defined periods: baseline without dexmedetomidine; two periods with dexmedetomidine (0.3 and 0.6 ng/ml), in a randomly determined order; and a final period 1 h after drug discontinuation. The primary outcomes were amplitude and latency of P37/N20, and amplitude, area under the curve, and voltage threshold for transcranial motor evoked potential stimulation.

Results: Of the total, data from 30 patients were evaluated. Use of dexmedetomidine, as an anesthetic adjunct, did not have an effect on the latency or amplitude of sensory evoked potentials greater than was prespecified as clinically relevant, and though the authors were unable to claim equivalence on the amplitude of transcranial motor evoked responses due to variability, recordings were made throughout the study in all patients.     

Volatile Anesthetics Depress Spinal Motor Neurons

Background: Depression of spinal alpha-motor neurons apparently plays a role in the surgical immobility induced by isoflurane. Using the noninvasive technique of F-wave analysis, the authors tested the hypothesis that depressed motor neuron excitability is an effect common to other clinically relevant inhaled anesthetics.

Methods: The authors measured F-wave amplitude in rats anesthetized with desflurane, enflurane, halothane, or sevoflurane. Each animal received one anesthetic at five equipotent anesthetic concentrations (0.6, 0.8, 1.2, and 1.6 minimum alveolar concentration [MAC] and 0.8 MAC with 65% N2 O). F waves were detected as late potentials in electromyographic responses evoked in the intrinsic muscles of the hind paw after monopolar stimulation of the ipsilateral posterior tibial nerve.

Results: All tested inhaled anesthetics depressed F-wave amplitude but not M-wave (orthodromic, early muscle activation) amplitude, and increased M-F latency in a dose-dependent manner. At 1.0 MAC, the estimated F/M ratio was 70+/-13% SD of that at baseline (0.6 MAC). Nitrous oxide added to 0.8 MAC of the potent vapors depressed F/M ratio by 63+/-17%.     

Comparison of isoflurane effects on motor evoked potential and F wave

BACKGROUND: Volatile anesthetics produce surgical immobility by suppressing the motor system. The anesthetic action site in the motor pathway is unclear. Anesthetic effects on the whole and the lower portion of motor pathway can be studied by measuring the motor evoked potentials (MEP) and the F wave. This study measured the effect of isoflurane on the MEP and the F wave. METHODS: With institutional review board approval, we studied 12 adult patients with American Society of Anesthesiologists physical status I or II. After intubation, anesthesia was maintained with nitrous oxide/oxygen and propofol infusion. MEPs were elicited by transcranial electrical stimuli (train-of-five pulse; stimuli intensity 40-160 mA) through electrodes placed in the scalp at C3/C4 positions and recorded at the anterior tibialis muscle with an Axon Sentinel-4EP monitor. F waves were elicited by an electrode fixed over the posterior tibial nerve at the medial malleolus and recorded at the abductor hallucis muscle. After end-tidal concentration of isoflurane was maintained at 0.5% for 20 min, the MEP and F wave were measured again. MEP and F-wave changes before and after isoflurane were analyzed using paired Wilcoxon test with Bonferroni correction. The difference between the changes in MEP and F wave was analyzed using Friedman's test. RESULTS: Motor evoked potential amplitudes (median, 205 microV; 25th-75th percentiles, 120-338 microV), F-wave amplitude (median, 100 microV; 25th-75th percentiles, 64.2-137.5 microV), and F-wave persistence (59 +/- 29%) were decreased to 0 microV (0-15 microV), 49 microV (12.4-99.6 microV), and 30 +/- 31%, respectively, by 0.5% isoflurane. MEP amplitude suppression was different from the changes in F-wave amplitude and persistence (P < 0.02). CONCLUSIONS: Isoflurane 0.5% suppresses the motor pathway by decreasing both MEP and F wave. The MEP is suppressed more than the F wave.     

Level of consciousness affects the excitability of spinal motor neurones during propofol sedation in humans

Background. To investigate the relationship between the depressionof spinal motor neuronal excitability and the sedative levelinduced by propofol infusion, we simultaneously analysed thesuppressive effect of propofol on the F wave and the sedativelevel during propofol infusion. Methods. After spinal anaesthesia, sedation was achieved usinga propofol target-controlled infusion (TCI) system to achievea score of 4 on the Wilson sedation scale. The excitabilityof spinal motor neurones was determined by measuring the leftmedian nerve F wave. F-wave persistence and the F/M ratio wererecorded at pre-sedation as the control, during sedation, atarousal by mild physical stimulation and at post-sedation. Results. Wilson sedation scores increased significantly correspondingto the increase in the target propofol concentration (Cpt),and a Cpt-producing Wilson sedation scale 4 ranged between 1.2and 1.8 µg ml^–1. The F-wave persistence and F/Mratio before propofol infusion were 80.7 (8.6)% and 9.5 (3.9)%,respectively. At Wilson sedation scale 4, F-wave persistenceand F/M ratio were 17.6 (12.8)% (0–37.5%) and 4.3 (4.1)%,and, at return of consciousness by mild physical stimulation,significantly increased to 71.3 (7.9)% and 10.0 (5.0)%, respectively. Conclusion. We demonstrated that the excitability of spinalmotor neurones was suppressed during sedation by propofol TCI,but this suppressive effect vanished at return of consciousnessby mild physical stimulation even at a constant Cpt. Our datasuggested that the effect of propofol on the excitability ofspinal motor neurones might be affected by consciousness levelrather than propofol Cpt in humans.     

F-wave amplitudes indicate evolving spinal autonomy during spontaneous recovery of hindlimb function in rat spinal cord contusion

STUDY DESIGN: Experimental rat model of spinal cord contusion. OBJECTIVES: To reveal the extent of spinal autonomy contributing to recovery of hindlimb function. SETTING: Experimental laboratory of a neurosurgical university department. METHODS: F-wave amplitudes as a probe for spinal cord excitability were recorded from both sciatic nerves (lumbar segments L2-L5) before and after an experimental spinal cord contusion performed in the lower thoracic spinal cord. Additionally, transcranial electrically motor evoked potentials from the hindlimbs and cerebral somatosensory potentials evoked by sciatic nerve stimulation were recorded. Clinical evaluation of hindlimb function was done regularly for survival periods of 3 and 50 days, respectively. Electrophysiological testing was performed immediately prior and after lesioning of the cord and at the endpoint of survival periods. RESULTS: Hindlimb function recovered from a mean Basso-Beattie-Bresnahan score of 5.6 on day 1 to 9.2 on day 3 (3-day-survivors) and from 7.7 to 17.2 on day 50 (50-day-survivors). This was accompanied by a significant increase of F-wave amplitudes on day 50 compared to baseline values, whereas amplitudes of somatosensory and motor-evoked potentials remained significantly depressed. CONCLUSION: Recovery of hindlimb function may at least in part be attributed to evolving spinal autonomy, which can be assessed by F-wave amplitudes.     

Comparison of Isoflurane Effects on Motor Evoked Potential and F Wave

Background: Volatile anesthetics produce surgical immobility by suppressing the motor system. The anesthetic action site in the motor pathway is unclear. Anesthetic effects on the whole and the lower portion of motor pathway can be studied by measuring the motor evoked potentials (MEP) and the F wave. This study measured the effect of isoflurane on the MEP and the F wave.

Methods: With institutional review board approval, we studied 12 adult patients with American Society of Anesthesiologists physical status I or II. After intubation, anesthesia was maintained with nitrous oxide/oxygen and propofol infusion. MEPs were elicited by transcranial electrical stimuli (train-of-five pulse; stimuli intensity 40-160 mA) through electrodes placed in the scalp at C3/C4 positions and recorded at the anterior tibialis muscle with an Axon Sentinel-4EP monitor. F waves were elicited by an electrode fixed over the posterior tibial nerve at the medial malleolus and recorded at the abductor hallucis muscle. After end-tidal concentration of isoflurane was maintained at 0.5% for 20 min, the MEP and F wave were measured again. MEP and F-wave changes before and after isoflurane were analyzed using paired Wilcoxon test with Bonferroni correction. The difference between the changes in MEP and F wave was analyzed using Friedman's test.

Results: Motor evoked potential amplitudes (median, 205 [mu]V; 25th-75th percentiles, 120-338 [mu]V), F-wave amplitude (median, 100 [mu]V; 25th-75th percentiles, 64.2-137.5 [mu]V), and F-wave persistence (59 +/- 29%) were decreased to 0 [mu]V (0-15 [mu]V), 49 [mu]V (12.4-99.6 [mu]V), and 30 +/- 31%, respectively, by 0.5% isoflurane. MEP amplitude suppression was different from the changes in F-wave amplitude and persistence (P < 0.02).     

Corticospinal excitability modulation to hand muscles during movement imagery

Motor evoked potentials (MEPs) to magnetic transcranial stimulation (TCS) were recorded from right abductor digiti minimi (ADM) and first dorsal interosseous (FDI) muscles, sharing the same peripheral innervation but engaged in two different motor demands. In seven healthy and trained subjects, the latencies, amplitudes and variability of MEPs were investigated under the following, randomly intermingled, conditions: full muscular and mental relaxation; mental simulation of selective index finger or little finger abduction; mental non-motor activity (arithmetical calculation); and real motor task (little and index finger abduction). The whole procedure was performed by continuous audiovisual monitoring of electromyographic 'silence' in the tested muscles. The maximal facilitatory effects (= latency shortening and amplitude increase) on MEPs were induced by the real motor task. An amplitude potentiation of MEPs in both tested muscles was present during non-motor mental activity, in comparison to basal values. A further amplitude potentiation, without latency shifts, was confined to the muscle acting as 'prime mover' for the mentally simulated movement, according to the motor program dispatched but not executed by the subject. Similar results were also found in the F-wave, showing that mental simulation affects spinal motoneuronal excitability as well, although -- due to the lack of MEP and F-wave latency shift -- the main effect takes place at cortical level. The study shows that movement imagery can focus specific facilitation on the prime-mover muscle for the mentally simulated movement. This is mainly evident on FDI muscle, which controls fingers (i.e. the index) with highly corticalized motor representation.     

Effect of bolus propofol administration on muscle evoked potential (MsEP) during spine surgery

Intraoperative monitoring of descending pathways by means of muscle evoked potential (MsEP) is a reliable method to monitor spinal cord motor function, but MsEP is readily affected by anesthetics. We monitored MsEP evoked by repetitive transcranial electrical stimulation of the motor cortex in 30 patients receiving spine surgery. Total intravenous anesthesia was maintained with propofol and fentanyl without any muscle relaxant. Onset latencies and peak to peak amplitudes of MsEP were evaluated before and after the bolus propofol administration. The concentrations of propofol in blood and the effect-site during MsEP monitoring were predicted by computer simulation software. The amplitude of MsEP decreased slightly by bolus propofol administration, but the latencies showed no significant change with propofol under the same condition. We consider that total intravenous anesthesia with propofol and fentanyl without muscle relaxants is compatible with the recording of MsEP evoked by high frequency repetitive electrical transcranial stimulations. When MsEP is monitored during spine surgery, anesthetic condition should be controlled carefully in order to maintain a stable blood concentration of propofol and thus to assure the reliability of MsEP measurements.     

脊柱手术中经颅电刺激运动诱发电位监护的应用探讨

目的探讨脊柱手术中经颅电刺激运动诱发电位（transcranial electrical stimulation motor evoked potential,TES-MEP）监护的可行性和应用价值。方法2006年7月至2008年10月,在241例胸椎手术中对双侧胫前肌、足踇短屈肌、大鱼际肌或小鱼际肌（颈椎病变时）实施TES-MEP监护。术中全静脉麻醉58例,静脉麻醉＋七氟烷吸入麻醉（浓度〈1％）67例,静脉麻醉＋小剂量肌松剂116例。结果TES-MEP的检出率为89．2％,虽然3种麻醉方式的检出率无显著性差异,但各年龄组、不同靶肌肌力的检出率有显著性差异。术中TES-MEP阳性26例,其中不明原因的假阳性6例,真阳性20例,且均与手术操作有直接相关性。TES-MEP对脊髓运动功能监护的灵敏度为100％,特异度为97．9％,约登指数为0．979;对脊髓感觉功能监护的灵敏度为74．1％,特异度为97．9％,约登指数为0．72。结论异丙芬静脉麻醉＋七氟烷吸入麻醉（浓度〈1％）为首选方案,异丙芬静脉麻醉＋小剂量肌松剂为次选方案。TES-MEP不但能瞬间、直接、准确地监护脊髓的运动传导功能,而且能间接反映脊髓的感觉传导功能,是安全监护脊柱手术的新方法。