The effect of nitrous oxide on the inhibition of somatosensory evoked potentials by sevoflurane in children

Inhalational anaesthetics inhibit somatosensory evoked potentials. The present study examined the effect of nitrous oxide in anaesthetic mixture with sevoflurane on the somatosensory evoked potential in children. Forty-five patients aged between 6 months and 6 years undergoing club foot surgery were studied to verify the influence of sevoflurane alone (21 patients) and sevoflurane with nitrous oxide (24 patients) on the somatosensory evoked potential. Fractional inspired concentration of nitrous oxide and fractional end-tidal (alveolar) sevoflurane were measured to estimate the multiples and submultiples of the minimal alveolar concentration (age corrected). The somatosensory evoked potential signals were obtained by stimulation of the median nerve. Nitrous oxide (FI = 0.63 +/- 2.5) with sevoflurane caused more reduction in the amplitude of somatosensory evoked potential waves and a greater increase in the latency of somatosensory evoked potential waves in comparison with sevoflurane alone. The results show that it is possible to obtain the inhibition of somatosensory evoked potential with smaller concentrations of sevoflurane, when it is used with nitrous oxide.     

Nitrous oxide has different effects on the EEG and somatosensory evoked potentials during isoflurane anaesthesia in patients

Background: Electroencephalogram (EEG) and somatosensory evoked potentials (SEPs) are altered by inhalation anaesthesia. Nitrous oxide is commonly used in combination with volatile anaesthetics. We have studied the effects of nitrous oxide on both EEG and SEPs simultaneously during isoflurane burst-suppression anaesthesia.
Methods: Twelve ASA I-II patients undergoing abdominal or orthopaedic surgery were anaesthetized with isoflurane by mask. After intubation and relaxation the isoflurane concentration was increased to a level at which an EEG burst-suppression pattern occurred (mean isoflurane end-tidal concentration 1.9 (SD 0.2) %. With a stable isoflurane concentration, the patients received isoflurane-air-oxygen and isoflurane-nitrous oxide-oxygen (FiO₂ 0.4) in a randomized cross-over manner. EEG and SEPs were simultaneously recorded before, and after wash-out or wash-in periods for nitrous oxide. The proportion of EEG suppressions as well as SEP amplitudes for cortical N₂₀ were calculated.
Results: The proportion of EEG suppressions decreased from 53.5% to 34% ( P < 0.05) when air was replaced by nitrous oxide. At the same time, the cortical N₂₀ amplitude was reduced by 69% ( P < 0.01).
Conclusion: The results suggest that during isoflurane anaesthesia, nitrous oxide has a different effect on EEG and cortical SEP at the same time. The effects of nitrous oxide may be mediated by cortical and subcortical generators.     

Effects of abdominal surgery on somatosensory evoked potentials during nitrous oxide-enflurane anesthesia

The effect of abdominal surgery on median nerve somatosensory evoked potentials (SEPs) was studied in 8 enflurane and nitorous oxide anesthesia (GOE) patients. We further compared the effect of epidural anesthesia. The first recording was done immediately prior to induction. Anesthesia was then induced with 5mg·kg^–1 i.v. of thiopental and maintained with 1.0% enflurane, 66% N₂O and 33% O₂. Before skin incision for abdominal surgery, the second recording was performed under GOE anesthesia and the third recording during surgery. Then 2% lidocaine was injected into the epidural space through a preinserted catheter, and after 15min the fourth recording was obtained. The latencies of peaks N1, P2 and N2 and the amplitudes of N1-P2 and P2-N2 were measured. The latencies of N1, P2 and N2 increased and the amplitudes of N1-P2 and P2-N2 deceased significantly after the induction of anesthesia compared with the control values. During abdominal surgery the latencies of N1 and P2 decreased and the amplitudes of N1-P2 and P2-N2 increased. After epidural anesthesia, however, the latencies of N1 and P2 increased and the amplitudes of N1-P2 and P2-N2 decreased significantly and returned almost to the values recorded under preoperative GOE anesthesia. These phenomena indicated that the excitations produced by surgical stimulation in nerve ending might have been transmitted to the central nervous system via spinal nerves and blocked by epidural anesthesia.(Kasaba T, Kosaka Y: Effects of abdominal surgery on somatosensory evoked potentials during oxide-enflurane anesthesia. J Anesth 5: 281–286, 1991)     

Effects of halothane, enflurane, isoflurane, and nitrous oxide on somatosensory evoked potentials in humans

Median nerve somatosensory evoked potentials (SSEPs) were recorded in 21 healthy subjects anesthetized with halothane, isoflurane, or enflurane (with and without nitrous oxide) for abdominal or pelvic surgery. Recordings were made prior to induction, then at 0.5 MAC increments of each volatile agent with 60% N2O up to 1.5 MAC, and, finally, at 1.5 MAC without N2O. All three volatile anesthetics produced dose-related reductions in the amplitude and increases in the latency of the cortical component of the SSEP. These changes were most pronounced with enflurane and least with halothane. At 1.5 MAC of each volatile agent, cortical latency decreased and amplitude increased when nitrous oxide was discontinued. The results suggest that in neurologically intact patients, end-tidal concentrations of 1.0 MAC halothane and 0.5 MAC enflurane or isoflurane (each in 60% N2O) can be compatible with effective SSEP monitoring. Volatile anesthetic concentrations consistent with satisfactory somatosensory-evoked potential recording may be greater if N2O is not employed.     

皮层体感诱发电位及经颅电刺激运动诱发电位联合监护在脊柱畸形矫正术中的应用

目的:探讨脊柱畸形矫正术中皮层体感诱发电位(CSEP)及经颅电刺激运动诱发电位(TES-MEP)联合监护在脊柱畸形矫正手术中的应用。方法:对我院收治的脊柱畸形患者根据术中监护方法分为两组:A组37例,其中男25例,女12例,年龄13～42岁,平均26.1岁,术中进行CSEP及TES-MEP联合监护;B组29例,其中男10例,女19例,年龄13～20岁,平均15.8岁,单纯采用CSEP监护作为对照组。术中持续观察CSEP及TES-MEP波幅及潜伏期变化,出现波幅下降50%、潜伏期延长10%或刺激强度高于初始刺激强度100V仍未引出者,停止手术并对症处理,术后给予激素治疗。结果:A组术中出现CSEP异常者4例(10.8%),TES-MEP异常者19例(60%)。术中CSEP及TES-MEP均异常者4例(10.8%),无术中CSEP异常而TES-MEP正常者。2例(陈旧性结核并后凸畸形1例,陈旧性骨折并后凸畸形1例)术中合拢截骨平面时,TES-MEP波形均消失,但仅1例出现CSEP异常,经术中积极处理,至手术结束时波形仍未恢复至术前水平,术后均出现神经功能障碍。余35例患者术后无神经功能损伤(假阴性率0%)。B组9例(21%)术中出现CSEP波形异常,其中2例虽经减少矫形角度及激素冲击治疗,术后仍出现双下肢瘫,余术后未出现神经功能障碍。3例术中监护未见异常者,术后出现重度不可逆性脊髓损伤(假阴性率10%)。结论:CSEP结合TES-MEP联合监护能较可靠、准确的反映术中脊髓功能状态,可降低监护假阴性率,为手术治疗过程提供参考。     

Effects of subarachnoid lidocaine, meperidine and fentanyl on somatosensory and motor evoked responses in awake humans

Although the effects of local anaesthetics (LA) on motor and sensory transmission in the spinal cord have been described, the effects of opioids are controversial. Our aim was to evaluate the action of clinically relevant doses of subarachnoid (SA) meperidine (MP) and fentanyl (FN), on somatosensory (SSEP) and cortical motor evoked responses (CMER) in awake subjects. Thirty ASA I-II patients scheduled for infra umbilical surgery received SA (N = 10/group): 1 mg/kg lidocaine (LD), 1 mg/kg MP or 25 μg FN. SSEP elicited by stimulation of the posterior tibial nerve at the ankle, and cortical motor evoked response at rest (r-CMER) and during facilitation (f-CMER) were obtained prior and 30 min after treatment. Conduction at the proximal segment of the motor nerve (F-wave) was evaluated by stimulation ot the posterior tibial nerve at the popliteal fossa. Motor/sensory block and side effects were clinically assessed.
LD completely abolished SSEP and CMER. At the same dose, MP abolished SSEP in 40% of the patients, while r-CMER and f-CMER were absent in 70% and 30%, respectively; in addition, the F-wave was absent in 50% of the patients. Fentanyl induced small changes in the latencies of SSEP and F-wave; however, a 28% decrease in the amplitude of the f-CMER (P<0.05) was observed. Pruritus was present in 60% of patients in the FN group (P<0.006).
Our results show that while LD and MP block sensory and motor conduction at the spinal roots, FN seems to decrease the excitability of the spinal interneurons in the corticospinal tract.     

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.     

Effects of nitrous oxide on the somatosensory evoked response in cats

The effect of nitrous oxide on the activity of the somatosensory system was studied in cats with brain electrodes implanted chronically. The electrodes were implanted in the primary somatosensory cortex, cortical somatosensory radiation, medial lemniscus and midbrain reticular formation. Alterations in the excitability of the primary sensory pathway were assessed by the changes of the input to and output from these brain areas: the response in the medial lemniscus to the stimulation of the skin represented the input to the thalamic relay nucleus and the response recorded in the cortical sensory radiation represented the output from the thalamic relay nucleus. The concentrations of nitrous oxide studied were 50% and 75% in oxygen, and the drug effect was concentration-related. The cortical response to peripheral stimulation was suppressed in amplitude by more than 40% of the control with 75% nitrous oxide, and the response in the cortical radiation was suppressed by 20% of the control with the same dose of nitrous oxide. The response in the cortical radiation to stimulation of the medial lemniscus was suppressed by 20% of the control and the postsynaptic component of the cortical response to the stimulation of the medial lemniscus was suppressed by more than 50% of the control. The multi-unit activity of the brainstem reticular formation was enhanced by nitrous oxide in a dose related manner. The excitability of the thalamic relay nucleus and the primary somatosensory cortex was suppressed by natural slow wave sleep when the reticular multi-unit activity was suppressed, and they were enhanced by paradoxical phase of sleep when the reticular multi-unit activity was enhanced. These findings indicated that the degree of suppression of excitability by nitrous oxide is similar in both the thalamic relay nucleus and sensory cortex, and its action on the brain stem reticular formation is different from that on the primary sensory system. The suppression of sensory functions shown in the present study provides a certain clue to the understanding of the neural basis that though nitrous oxide does not produce deep surgical anesthesia, it does induce potent analgesia and sedation during surgery.(Kawamoto T, Shingu K, Mori K: Effect of nitrous oxide on the somatosensory evoked response in cats. J Anesth 4: 51–60, 1990)     

The effect of nitrous oxide on EEG spectral power during halothane and isoflurane anaesthesia

The effect of N2O on EEG during halothane and isoflurane anaesthesia was studied in 24 elective-surgery patients. The total EEG power and various power bands were analysed with fast Fourier transform power spectra. Anaesthesia was induced by mask. EEG analysis was performed from the data collected before induction and during steady-state halothane and isoflurane anaesthesia with and without N2O. In both halothane and isoflurane anaesthesia, N2O had a significant effect on EEG. Alpha- and beta-range EEG power and total power decreased during N2O in both groups. Delta- and theta-range power increased during N2O in the halothane group. The study shows that the effect of nitrous oxide should be taken into consideration when EEG is being studied or monitored during anaesthesia.     

The interaction between nitrous oxide and isoflurane on suppression of learning: a study using classical conditioning in rabbits

Background: Nitrous oxide (N₂O) is commonly combined with a volatile agent for administration of general anesthesia. We studied the effects of N₂O and isoflurane on learning of the rabbit nictitating membrane responses (NMRs).
Methods: Classical conditioning of the NMR was accomplished by presenting a 400 ms tone conditioned stimulus before the presentation of a 100 ms shock unconditioned stimulus over 6 daily training sessions. The percentages of conditioned responses (CRs) were calculated for animals treated with 0% (n=10), 33% (n=11), 67% (n=11), and 75% (n=7) N₂O and for those treated with 0% (n=8), 0.2% (n=7), 0.4%, (n=13) and 0.8% (n=9) isoflurane separately. ED-50 for suppression of learning for each drug were calculated. Percentages of CRs were calculated for treatments with combinations of 0.2% isoflurane with either 32 or 48% N₂O (n=14, for each).
Results: Isobolographic analysis demonstrated that the combination of the two drugs exerted no greater effect than that seen with either agent administered alone; for well-established CRs (mean of days 5 and 6), the estimated concentrations corresponding to a rate of 70% CRs were 0.31% isoflurane with no N₂O, 65.3% N₂O with no isoflurane, and 0.2% isoflurane combined with 32.4% N₂O.
Conclusions: N₂O and isoflurane interact additively on suppression of learning.     

Effects of halothane, enflurane, and isoflurane in nitrous oxide on multilevel somatosensory evoked potentials

The effects of halothane, enflurane, and isoflurane were studied at 0.5, 0.75, and 1 MAC in 60% N2O on subcortical sensory evoked potentials recorded at the popliteal fossa (PF), the spine (L-3, C-6) and on cortical potentials recorded at the scalp (SC) following bilateral posterior tibial nerve stimulations at the ankle in 28 patients undergoing scoliosis surgery. Latencies and amplitudes of the resulting potentials at each level were compared with postinduction control values. With increasing MAC, latency and amplitude changes seen at C6 (subcortical) were also compared with those at SC (cortical). Increasing the concentrations of each agent resulted in a graded increase in latency and a graded decrease in amplitude, at all levels. At SC each increase in MAC with each agent resulted in an increase in latency (P less than 0.05) and a decrease in amplitude (P less than 0.005), respectively. The increases in SC latency at 0.75, 1 MAC were larger than the increase in latency at C-6 (P less than 0.005) and the decreases in SC amplitudes at 0.5, 0.75 and 1 MAC were greater than the decrease in amplitude at C-6 (P less than 0.01). Halothane, enflurane, and isoflurane in 60% N2O altered subcortical potentials less than cortical potentials. Enflurane and isoflurane at 0.5, 0.75, and 1 MAC, and halothane at 0.5, 0.75 MAC maintained subcortical and cortical potentials that were adequate for evaluation. However, 1 MAC of halothane suppressed cortical potentials but maintained subcortical potentials. Subcortical C-6 potential may serve as an additional monitor.     

Effects of halothane, enflurane, and isoflurane on somatosensory evoked potentials during nitrous oxide anesthesia

The effects of 0.5, 0.75, and 1 MAC of halothane, enflurane, and isoflurane in 60% nitrous oxide on somatosensory cortical evoked potentials were studied in 30 patients undergoing corrective surgery for scoliosis. The evoked potentials were averaged at the scalp from the electroencephalogram following repeated bilateral posterior tibial nerve stimulation at the ankle. Latencies and amplitudes of the resulting potentials were measured and compared with the post-induction control values. Graded increase in latencies and graded decrease in amplitudes were found with increasing concentrations of all the three agents (P less than 0.05), confirming that the effects were dose related. Reductions in amplitudes were more marked than increase in latencies. The authors conclude that, during nitrous oxide-based anesthesia, enflurane, and isoflurane resulted in less alteration of somatosensory cortical evoked potentials than halothane. In conjunction with 60% nitrous oxide, 0.5 and 0.75 MAC of halothane, 0.5, 0.75, and 1.0 MAC of isoflurane and enflurane, respectively, were found to be compatible with the generation of waves adequate for evaluation.     

Effects of enflurane, isoflurane, and nitrous oxide on somatosensory evoked potentials during fentanyl anesthesia

The effects of nitrous oxide, enflurane, and isoflurane on cortical somatosensory evoked potentials (SEPs) were studied in 29 patients undergoing intracranial or spinal operations. Anesthesia was induced with fentanyl (25 micrograms/kg, iv) plus thiopental (0.5-1.0 mg/kg, iv). In one group of patients (n = 12), nitrous oxide (50%) was compared with enflurane (0.25-1.0%), and in another group (n = 12) nitrous oxide (50%) was compared with isoflurane (0.25-1.0%). In a third group of patients (n = 5) with preexisting neurologic deficits, nitrous oxide (50%) was compared with enflurane (0.25-1.0%). In all three groups, one gas was administered for 30 min, and then the alternate gas was administered for 30 min; then the cycle was repeated for a total of two administrations of each of the two anesthetics. SEPs were determined before and after induction of anesthesia and at the end of each 30-min study period. The latencies and amplitudes of the early cortical components of the upper- and lower-extremity SEP were examined. Induction of anesthesia resulted in increases of latency in both upper- and lower-extremity SEPs without any alteration of amplitude. Nitrous oxide, enflurane, and isoflurane each decreased the amplitude of the upper-extremity SEPs compared with the postinduction value. The amplitude of the upper-extremity SEPs was less during nitrous oxide than with either enflurane or isoflurane. Nitrous oxide decreased the amplitude of lower-extremity SEPs below postinduction value, while enflurane and isoflurane had no effect. Isoflurane and enflurane increased the latency of both upper- and lower-extremity SEPs slightly, while nitrous oxide had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of nitrous oxide on cerebral haemodynamics and metabolism during isoflurane anaesthesia in man

Seven normoventilated and five hyperventilated healthy adults undergoing cholecystectomy and anaesthetized with methohexitone, fentanyl and pancuronium were studied with measurement of cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and quantified electroencephalography (EEG) under two sets of conditions: 1) 1.7% end-tidal concentration of isoflurane in air/oxygen; 2) 0.85% end-tidal concentration of isoflurane in nitrous oxide (N2O)/oxygen. The object was to study the effects of N2O during isoflurane anaesthesia on cerebral circulation, metabolism and neuroelectric activity. N2O in the anaesthetic gas mixture caused a 43% (P less than 0.05) increase in CBF during normocarbic conditions but no significant change during hypocapnia. CMRO2 was not significantly altered by N2O. EEG demonstrated an activated pattern with decreased low frequency activity and increased high frequency activity. The results confirm that N2O is a potent cerebral vasodilator in man, although the mechanisms underlying the effects on CBF are still unclear.     

The use of 0.25% isoflurane premixed in 50% nitrous oxide and oxygen for pain relief in labour

The addition of 0.25% isoflurane to 50% nitrous oxide in oxygen provides more effective pain relief in labour than 50% nitrous oxide alone. This study was carried out to determine whether self-administration by demand valve of 0.25% isoflurane in 50% nitrous oxide in oxygen premixed in cylinders at 13.7 MPa (IN2O) was practical and safe during labour. Two hundred and twenty-one mothers used IN2O in labour after 50% nitrous oxide had become inadequate for pain relief. Data on IN2O use was recorded during labour and details of the course of labour and opioid usage were taken from the clinical notes. The duration of IN2O use was 0.1-12.35 h (median 2.3). Thirty-two mothers (14.5%) required an epidural and intolerance to IN2O was seen in a maximum of 17 cases (7.7%). One hundred and twenty-six cases were primiparous and 93 parous with 151 deliveries being spontaneous and 70 interventional, of which 12 were by Caesarean section. Maternal blood loss was 20-1500 ml (median 200 ml). Apgar scores at 1 and 5 min were unaffected by IN2O use although a positive correlation was found between the use of opioids and the number of neonates with a 1-min score below 8 and the number requiring resuscitation. Six neonates had an Apgar score below 8 at 5 min, but their condition was adequately explained by factors other than the sedative technique used. Self-administered IN2O was found to be a safe and practical technique for sedation in labour when 50% nitrous oxide alone had become inadequate.     

Effects of surgical stress and nitrous oxide anaesthesia on peri-operative plasma levels of total homocysteineA randomised, controlled study in general surgery

Previous studies of patients have shown that anaesthesia with nitrous oxide (N2O) increases the plasma levels of total homocysteine. In a randomised, controlled trial we measured the plasma total homocysteine levels in patients undergoing general surgery before and after anaesthesia with and without N2O. Plasma total homocysteine levels were measured before anaesthesia and 1, 3-5 and 24 h after incision in 24 patients randomly allocated to anaesthesia with N2O (n = 12) and without N2O (n = 12). Total homocysteine levels significantly decreased from 10.4 +/- 2.7 to 8.2 +/- 2.9 micromol x l(-1) in the non-N2O group 24 h after incision (p < 0.02), while they tended to increase slightly in the N2O group from 10.5 +/- 4.5 to 10.9 +/- 4.3 micromol x l(-1) (p > 0.05). Our randomised controlled study indicates that total homocysteine decreases after general surgery in patients in whom anaesthesia is maintained without N2O, but not in patients in whom anaesthesia is maintained with N2O.     

Corresponding minimum alveolar concentrations of isoflurane and isoflurane/nitrous oxide have divergent effects on thalamic nociceptive signalling

BACKGROUND: Suppression of nociceptive signalling in the thalamus is consideredto contribute significantly to the anaesthetic state. Assumingadditivity of anaesthetic mixtures, our study assessed the effectsof corresponding minimum alveolar concentrations (MACs) of isofluraneand isoflurane/nitrous oxide on thalamic nociceptive signalling. METHODS: Nociceptive response activity (elicited by controlled radiantheat stimuli applied to cutaneous receptive fields) of singlethalamic neurons was compared in rats anaesthetized at 1.1 and1.4 MAC isoflurane with that at 1.1 and 1.4 MAC isoflurane/nitrousoxide. RESULTS: Under baseline anaesthesia (0.9 MAC isoflurane), noxious stimulationelicited excitatory responses in all neurons (n = 19). Theseresponses were uniformly suppressed at 1.1 and 1.4 MAC isoflurane.In contrast, at 1.1 and 1.4 MAC isoflurane/nitrous oxide, excitatoryresponses no different to baseline were still present in 64and 37% of the neurons, respectively. CONCLUSIONS: These data demonstrate a pronounced nitrous oxide-induced responsevariability. It appears that, with respect to thalamic transferof nociceptive information, the interaction of isoflurane andnitrous oxide may not be compatible with the concept of additivityand that the antinociceptive potency of nitrous oxide is considerablyless than previously reported.     

Performance of the rapidly extracted auditory evoked potentials index to detect the recovery and loss of wakefulness in anesthetized and paralyzed patients

BACKGROUND: The rapidly extracted auditory evoked potentials index (A-lineTM ARX Index or AAI) has been proposed as a method to measure the depth of anesthesia. A prospective study was designed to assess the performance of AAI to detect the recovery and loss of wakefulness in anesthetized and paralyzed patients. METHODS: Fourteen adult patients undergoing elective surgery were anesthetized with propofol 1.5 mg kg-1, vecuronium 0.1 mg kg-1 and further propofol 1.0 mg kg-1. Wakefulness was measured by the ability of the patient to respond to command using the isolated forearm technique (IFT). After the patient responded, propofol was infused at 10 mg kg-1. h-1 until wakefulness (responsiveness) was lost. The AAI was recorded continuously throughout the study and analyzed off-line. RESULTS: The AAI showed a significant difference between the values registered during, 30 s before and 30 s after the recovery, and also between 30 s before and 30 s after the loss of wakefulness. The prediction probability (Pk) values for AAI were 0.786 and 0.864 during the transitions from unresponsiveness to responsiveness and from responsiveness to unresponsiveness. The area under the receiver operating characteristic curve for the responsive and unresponsive values was 0.926 (SE 0.002, 95% CI 0.922-0.931), and the AAI values of approximately 5%, 50% and 95% predicted probability of wakefulness were 19, 29 and 39, respectively. CONCLUSION: The AAI may be a good predictor of recovery and loss of wakefulness for anesthetized and paralyzed patients.     

Isoflurane compared with nitrous oxide anaesthesia for intraoperative monitoring of somatosensory-evoked potentials

Intraoperative monitoring of somatosensoryevoked potentials is a routine procedure. To determine the depressant effect of nitrous oxide relative to isoflurane, the authors recorded the scalp, cervical and brachial plexusevoked responses to stimulation of the median nerve under different anaesthetic conditions. Eight subjects, age 35 ± 6 (SD) yr, weight 68 ± 12 kg, were studied. Following recording of awake control responses, anaesthesia was induced with thiopentone 5 mg· kg^{? 1} and fentanyl 3 μg· kg^{? 1} and was followed by succinylcholine 1 mg· kg^{? 1}. During normocapnia and normothermia, and with a maintenance infusion of fentanyl 3 μg · kg^{? 1}· hr^{? 1}, evoked potential recording was repeated under three different anaesthetic conditions; 0.6 MAC nitrous oxide, 0.6 MAC nitrous oxide ± 0.6 MAC isoflurane, and 0.6 MAC isoflurane. Among the anaesthetic conditions, the combination of nitrous oxide-isoflurane had the most depressant effect on the cortical amplitude (67 ± 4% reduction, P < 0.05). Nitrous oxide decreased the cortical amplitude more than an equipotent dose of isoflurane (60 ± 4% vs 48 ± 7%, P < 0.05). The latency was unchanged by nitrous oxide, but increased slightly by isoflurane and isofluranenitrous oxide anaesthesia (1.0 and 0.9 msec respectively, P < 0.05). We conclude that somatosensory-evoked potential monitoring is feasible both during nitrous oxide anaesthesia and isoflurane anaesthesia, but the cortical amplitude is better preserved during 0.6 MAC of isoflurane alone relative to 0.6 MAC of nitrous oxide alone. The depressant effect is maximal during nitrous oxideisoflurane anaesthesia but less than the predicted additive effect.