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.     

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.     

Effects of ketamine on somatosensory evoked potentials during nitrous oxide anesthesia in humans

The effects of ketamine with 60% nitrous oxide were studied on subcortical sensory evoked potentials recorded at Erb's point (N9), neck (N13) and on cortical potentials recorded at the scalp (N20) following median nerve stimulations in 7 neurologically normal patients. Latencies and amplitudes of the potentials were measured and compared with postinduction control values taken during inhalation of 60% nitrous oxide. Ketamine 2 mg.kg-1 (iv) was administered initially and incremental dose was 50 micrograms.kg-1.min-1. N20 latency decreased at 15, 30 minutes after ketamine administration from a control value of 18.7 +/- 0.9 msec to 18.2 +/- 1.1, 18.2 +/- 1.1 msec respectively, and N13-N20 interpeak latency decreased from 6.0 +/- 0.4 msec to 5.5 +/- 0.7, 5.4 +/- 0.7 msec (mean +/- SD). The author concluded that during nitrous oxide-based anesthesia, ketamine did not inhibit specific thalamoneocortical pathways.     

The effects of propofol with and without ketamine on human cerebral blood flow velocity and CO(2) response

The combination of propofol and ketamine has been used for total IV anesthesia. This study was designed to clarify the effects of propofol-ketamine anesthesia on cerebral circulation by using transcranial Doppler ultrasonography. In Study 1, we examined the time course of time-mean middle cerebral artery blood flow velocity (Vmca) after ketamine (n = 10) or saline (n = 6) administration during propofol anesthesia. In Study 2, CO(2) responses were measured under the following conditions: awake (Group C, n = 7), propofol anesthesia (Group D, n = 7), and propofol-ketamine anesthesia (Group E, n = 8). Ketamine administration during propofol anesthesia administration did not affect Vmca, mean arterial pressure, or heart rate. Vmca under normocapnia in Groups D and E were 36 +/- 3 and 37 +/- 3 cm/s (mean +/- SE), respectively. The values were significantly lower than that of Group C (70 +/- 3 cm/s). The CO(2) response slopes of Groups D and E were significantly lower than that of Group C, although there was no significant difference between Groups D and E. These results suggest that ketamine does not influence Vmca or the cerebrovascular CO(2) response during propofol anesthesia administration, although the sample size in each group was small. IMPLICATIONS: Our study suggests that ketamine does not influence middle cerebral artery blood flow velocity or the cerebrovascular CO(2) response assessed by transcranial Doppler ultrasonography during propofol anesthesia administration in patients without neurological complications.     

The effects of xenon on myogenic motor evoked potentials in rabbits: a comparison with propofol and isoflurane

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.     

Transcranial magnetic motor evoked potentials (tcMMEP) for functional monitoring of motor pathways during scoliosis surgery

Transcranial magnetic motor evoked potentials (tcMMEP) were used to assess the functional integrity of the descending motor pathways. The tcMMEP, recorded bilaterally from anterior tibialis muscles, were evoked by an electric current induced in the motor cortex by a high-intensity transient magnetic field applied to the scalp surface. Potentials were recorded from ten of 12 volunteer subjects and preoperatively in 11 of 11 scoliotic patients. Group mean latency in the volunteers (32.0 +/- 2.1 msec) did not differ from that of the scoliotics (28.6 +/- 5.0 msec), but values in the latter group were more variable. During nitrous oxide-narcotic anesthesia, tcMMEP with reproducible latencies were obtained in 9 of 11 (82%) cases. A small, but statistically significant, increase in latency occurred during anesthesia. Compared with preoperative values (523 +/- 490 microV), individual tcMMEP amplitudes were significantly decreased intraoperatively (163 +/- 153 microV). Although the absolute amplitudes varied widely, the minimum recorded value was over 20 microV. Thus, intraoperative tcMMEP waveforms were readily discriminable from background electrical noise. These results demonstrate the technical feasibility of intraoperative tcMMEP monitoring. Combined somatosensory evoked potential and tcMMEP monitoring may provide a more complete picture of spinal cord function, intraoperatively.     

The effect of ketamine on human somatosensory evoked potentials and its modification by nitrous oxide

The effect of ketamine alone and in combination with N2O (70% inspired) on median nerve somatosensory evoked potentials (SSEPs) was investigated in 16 neurologically normal patients undergoing elective abdominopelvic procedures. The anesthetic regimen consisted of ketamine (2 mg/kg iv bolus followed by continuous infusion at a rate of 30 micrograms.kg-1.min-1) [corrected], neuromuscular blockade (atracurium), and mechanical ventilation with 100% oxygen. SSEP recordings were obtained immediately preinduction and at 2, 5, 10, 15, 20, and 30 min postinduction. Thereafter, N2O was added with surgical incision and maintained for 15 min. At 5-min intervals, SSEP recordings were again taken during and after N2O. With minor exceptions, mean cortical and noncortical latencies as well as noncortical-evoked potential amplitude were unaffected by either ketamine or N2O. Ketamine induction increased cortical amplitude significantly with maximal increases occurring within 2-10 min. For example, at 5-min postinduction, mean N1-P1 amplitude increased from 2.58 +/- 1.05 (baseline) to 2.98 +/- 1.20 microV and P1-N2 amplitude increased from 2.12 +/- 1.50 (baseline) to 3.99 +/- 1.76 microV. Throughout the 30-min period after ketamine induction, mean P1-N2 amplitude increased generally by more (57-88%) than did mean N1-P1 amplitude (6-16%). N2O added to the background ketamine anesthetic produced a rapid and consistent reduction in both N1-P1 and P1-N2 amplitude. Thus, at 1 min after N2O, mean N1-P1 amplitude decreased from 2.74 +/- 1.11 to 1.64 +/- 0.63 microV, while P1-N2 amplitude decreased from 3.32 +/- 1.52 to 1.84 +/- 0.87 microV.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of lumbar or thoracic epidural anesthesia on median nerve somatosensory evoked potentials

Somatosensory evoked potentials (SSEP) are used increasingly to monitor the integrity of neural pathways in anesthetized patients. To evaluate the influence of epidural anesthesia on the central nervous system, we studied the effects of lumbar or thoracic epidural anesthesia with lidocaine on the median nerve SSEP in 9 patients. The peak latencies (N1, P2, N2) and amplitudes (N1-P2, P2-N2) of the SSEP response over the sensory cortex were recorded before and 15 min after epidural anesthesia. The peak latencies of control and post epidural anesthesia of N1, P1, N2 were 19.2 +/- 1.7 msec, 19.6 +/- 1.6 msec (N1), 24.7 +/- 2.3 msec, 25.7 +/- 2.0 msec (P2), 32.8 +/- 2.8 msec and 34.6 +/- 2.5 msec (N2), respectively. The amplitude of control and post epidural anesthesia of N1-P2, P2-N2 were 4.5 +/- 2.9 microV, 5.9 +/- 6.6 microV (N1-P2), 4.4 +/- 3.2 microV and 5.6 +/- 5.2 microV (P2-N2), respectively. Peak latencies of all components (L1, P2, N2) increased after epidural anesthesia compared with control values. Amplitude of N1-P2 increased significantly following epidural anesthesia compared with control values. The data obtained in this study were contrary to the previous concept that anesthetic agents generally increase the latency of SSEP and decrease their amplitude.     

The effect of ketamine/xylazine anesthesia on sensory and motor evoked potentials in the rat

STUDY DESIGN: Experimental laboratory investigation of the effect of anesthesia on evoked potentials in rats. OBJECTIVES: To define the optimal ketamine/xylazine anesthesia levels for the recording of different evoked potentials. SETTING: BioSurgery Preclinical Department, Baxter BioScience, Vienna, Austria. METHODS: Rats were implanted with cranial screws that allow stimulation and recording of evoked potentials. Somatosensory evoked potentials (SEPs), brainstem-derived motor evoked potentials (BMEPs) and corticomotor evoked potential (CMEPs) were recorded under different levels of anesthesia. The recorded signals were evaluated by measuring their latencies and amplitudes. The level of anesthesia was assessed by scoring the hind limb withdrawal reflex. RESULTS: All three signals showed a strong dependency on the level of anesthesia. The observed effects, however, differed between the three signals. SEP amplitudes and latencies declined as animals slowly transgressed from deep to light anesthesia. In contrast, BMEP amplitudes were larger and latencies shorter in light anesthesia than in deep anesthesia. CMEPs finally were hard to record under deep anesthesia, but were easily recorded in light anesthesia. BMEPs that were recorded during light anesthesia also showed a significant change in configuration that was coupled with a notable increase in the variability of its amplitudes. CONCLUSIONS: The level of ketamine/xylazine anesthesia affects evoked potentials and thus should be controlled during electrophysiological recording. Our results suggest that SEPs should be best recorded during deep anesthesia, while BMEPs and CMEPs are best recorded during intermediate and light anesthesia.     

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.      

The effect of hypothermia on myogenic motor-evoked potentials to electrical stimulation with a single pulse and a train of pulses under propofol/ketamine/fentanyl anesthesia in rabbits

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.     

Variability of somatosensory cortical evoked potentials during spinal surgery. Effects of anesthetic technique and high-pass digital filtering

The effects of anesthetic technique (nitrous oxide or propofol) and high-pass digital filtering on within-patient variability of posterior tibial nerve somatosensory cortical evoked potentials (PTN-SCEP) were compared prospectively in two groups of 20 patients undergoing spinal surgery. Average P1N1 amplitude was significantly higher and P1N1 amplitude variability lower during propofol/alfentanil anesthesia than during nitrous oxide/alfentanil anesthesia. Off-line 30-Hz high-pass digital filtering significantly reduced P1N1 amplitude variability without decreasing P1N1 amplitude. In 93 patients studied retrospectively, a significant negative logarithmic correlation (r = -0.77) was observed between P1N1 amplitude and P1N1 amplitude variability. This study shows the importance of maintaining the highest possible PTN-SCEP amplitudes during spinal surgery. Propofol/opioid anesthesia may be an alternative anesthetic technique to nitrous oxide/opioid anesthesia during spinal cord function monitoring.     

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.     

Acupuncture decreases somatosensory evoked potential amplitudes to noxious stimuli in anesthetized volunteers

The effect of acupuncture on pain perception is controversial. Because late amplitudes of somatosensory evoked potentials (SEPs) to noxious stimuli are thought to correlate with the subjective experience of pain intensity, we designed this study to detect changes of these SEPs before and after acupuncture in a double-blinded fashion. Sixteen volunteers were anesthetized by propofol and exposed to painful electric stimuli to the right forefinger. Then, blinded to the research team, the acupuncture group (n = 8) was treated with electric needle acupuncture over 15 min at analgesic points of the leg, whereas the sham group (n = 8) received no treatment. Thereafter, nociceptive stimulation was repeated. SEPs were recorded during each noxious stimulation from the vertex Cz, and latencies and amplitudes of the N150 and P260 components were analyzed by analysis of variance. P260 amplitudes decreased from 4.40 +/- 2.76 microV (mean +/- SD) before treatment to 1.67 +/- 1.21 microV after treatment (P < 0.05), whereas amplitudes of the sham group remained unchanged (2.64 +/- 0.94 microV before versus 2.54 +/- 1.54 microV after treatment). In conclusion, this double-blinded study demonstrated that electric needle acupuncture, as compared with sham treatment, significantly decreased the magnitudes of late SEP amplitudes with electrical noxious stimulation in anesthetized subjects, suggesting a specific analgesic effect of acupuncture. IMPLICATIONS: This double-blinded study demonstrates that electric needle acupuncture, as compared with sham treatment, significantly decreases the magnitudes of late somatosensory evoked potential amplitudes with electrical noxious stimulation in anesthetized subjects, suggesting a specific analgesic effect of acupuncture.     

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.     

Evoked Sacral Potentials in Subjects with True Premature Ejaculation

Evoked sacral potentials were used to study the bulbo-cavernous reflex in 85 patients with true premature ejaculation (TPE) and in 52 subjects as a control group. In the perineal and perianal recordings the amplitudes of the evoked responses (means +/- SD) were 70 +/- 91.1 microV and 35.6 +/- 36 microV in the TPE patients, and 39.2 +/- 36.8 microV and 26 +/- 21.6 microV in the controls, respectively. Both these differences resulted significant (P less than 0.01 and P congruent to 0.05, respectively). Our results suggest a reflex hyperexcitability, or an impaired "modulation" of the motor neurons of the pudendal nucleus by the regulating upper centers in the TPE patients.     

Changes in the auditory evoked potentials index by induction doses of four different intravenous anesthetics

BACKGROUND: Many studies have investigated the electroencephalographic changes during the induction and maintenance of anesthesia. However, no comparative studies have been performed on the effects of intravenous anesthetics on the auditory evoked potentials index (AAI). The present study was performed to compare the changes in AAI caused by induction doses of thiopental, propofol, midazolam and ketamine. METHODS: Eighty females, aged 30-70 years, referred for mastectomy, had anesthesia induced with thiopental 4 mg/kg, propofol 2 mg/kg, midazolam 0.1 mg/kg or ketamine 1 mg/kg (each 20 patients). The response to verbal command and the AAI were measured every minute for 5 min. RESULTS: The AAI decreased to less than 40 within 1 min with thiopental and propofol. The AAI increased after 3 min with thiopental, but remained low with propofol. The AAI gradually decreased to less than 40 within 4 min with midazolam, but was higher than the AAI with propofol or thiopental. The AAI increased significantly with ketamine. The AAIs at the loss of verbal command were 19 +/- 7 with thiopental, 21 +/- 8 with propofol, 31 +/- 10 with midazolam and 92 +/- 2 with ketamine. CONCLUSION: The AAI correlated with changes in hypnotic level, as measured by the response to verbal command, with induction doses of thiopental, propofol and midazolam, but not with ketamine. The AAI decreased to lower levels with propofol and thiopental than with midazolam at the induction of anesthesia.     

An electromyographic study of the feline urethral rhabdosphincter in the normal state and after sacral rhizotomy. Part 2. Responses of the rhabdosphincter to hypogastric nerve stimulation]

To investigate functional aspect of sympathetic innervation of the urethral rhabdosphincter, responses of the male feline rhabdosphincter to hypogastric nerve (HGN) stimulation were examined by means of electromyography using fine electrodes. Experiments were performed on 28 normal (N group) and 13 rhizotomized cats under chloralose anesthesia, the latter being further divided into two groups: 4 cats of 1-3 weeks (SR group) and 9 cats of 10-24 weeks (LR groups) after complete sacral rhizotomy. HGN stimulation (1 Hz, 0.3 ms pulse duration, 2-30 V) elicited responses of the rhabdosphincter in N and LR groups. In N group, HGN stimulation still elicited responses of the rhabdosphincter even after pudendal nerve was transected in advance, indicating that these evoked potentials were independent of somatic nerve inflow. The threshold stimuli and latencies of the evoked responses in N group (3.0 +/- 0.2 V, 81.7 +/- 5.7 ms, respectively) were not significantly different from those in LR group (2.9 +/- 0.3 V, 71.5 +/- 10.5 ms), but the amplitudes of the evoked responses were significantly larger in LR group than in N group (110 +/- 12 vs 18 +/- 2 microV, p less than 0.001). These evoked responses of the rhabdosphincter were resistive to prazosin (0.2 mg/kg) and atropine (0.5 mg/kg), but were abolished by hexamethonium (2 mg/min, 10-25 mg) and pancuronium (0.1-0.3 mg/kg) in both groups. In N group, repetitive stimulation (10-20 Hz) of HGN increased activities of the rhabdosphincter when the bladder was empty, but not when the bladder was full enough to trigger the vesicourethral relaxation reflex.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of intrathecal morphine on somatosensory evoked potentials in awake humans

Although the effect of systemic opioids on somatosensory evoked potentials has been well described, little is known about the interaction between intrathecally administered opioid analgesics and somatosensory evoked potentials. Accordingly, the influence of intrathecally administered morphine on posterior tibial nerve somatosensory cortical evoked potentials (PTSCEPs) was investigated in 22 unpremedicated, awake, neurologically normal patients scheduled to undergo elective abdominal or pelvic procedures. Patients were randomly assigned to receive either preservation-free intrathecal morphine sulfate (ITMS) or placebo. After baseline PTSCEP, heart rate and, mean blood pressure were recorded, ITMS (15 micrograms.kg-1) was injected via standard dural puncture with the patient in the lateral position. PTSCEPs, heart rate, and mean blood pressure were recorded again at 5, 10, 20, 30, 60, 90, and 120 min. Control patients were treated identically (including position, sterile preparation, and subcutaneous tissue infiltration with local anesthetic), except for lumbar puncture, and were unaware of their randomization. Before administration of ITMS, PTSCEP P1, N1, P2, N2, and P3 latencies were 39.4 +/- 3.2, 47.6 +/- 3.9, 59.2 +/- 3.2, 70.4 +/- 3.7, and 84.6 +/- 5.5 ms, (mean +/- standard deviation), respectively. The corresponding P1-N1, N1-P2, and P2-N2 amplitudes were 2.4 +/- 1.1, 2.4 +/- 1.1, and 2.3 +/- 0.9 microV, respectively. There were no significant changes over time between the control and ITMS groups. PTSCEPs resulting from left-sided stimulation were not different from those elicited by right-sided stimulation. All ITMS patients had intense postoperative analgesia for at least 24 h. It is concluded that ITMS does not affect PTSCEP waveforms in the 35-90 ms latency range during the awake state.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of intravenous lidocaine administration on median nerve somatosensory evoked potentials

The effect of lidocaine on the median nerve somatosensory evoked potential (SSEP) was investigated in 14 neurologically normal patients. Lidocaine 1.5 mg.kg-1.min-1 was injected intravenously over a 5 min period immediately followed by a continuous infusion of lidocaine 60 micrograms.kg-1.min-1. The peak latencies (N1, P2, N2) and amplitudes (N1-P2, P2-N2) of the SSEP response over the sensory cortex were recorded before and after lidocaine infusion. The peak latencies in the control group and in the experimental group after lidocaine infusion of N1, P1, N2 were 19.4 +/- 1.0 msec, 19.7 +/- 1.0 msec (N1), 24.6 +/- 1.4 msec, 25.0 +/- 1.5 msec (P2), 32.5 +/- 2.5 msec, and 33.3 +/- 2.8 msec (N2), respectively. The amplitudes in the control group and in the experimental group after lidocaine infusion of N1-P2, P2-N2 were 9.0 +/- 4.3 microV, 10.3 +/- 4.7 microV (N1-P2), 7.2 +/- 3.6 microV, 8.6 +/- 3.9 microV (P2-N2), respectively. Peak latencies of all components (N1, P2, N2) increased after lidocaine infusion compared with control values. Amplitude of N1-P2 and P2-N2 increased significantly following lidocaine infusion compared with control values. The data obtained in this study suggested that the changes in peak latencies and amplitude after epidural anesthesia with lidocaine were due to the systemic effect of lidocaine absorbed intravenously from the epidural space.