异氟醚麻醉下人身体感觉诱发电位的改变

目的：探讨脊髓是异氟醚的重要作用部位,方法：对18例妇科手术患者行异氟醚麻醉,并以硬膜外阻滞作对照,刺激踝部胫神经,监测并记录头颈部体感诱发电位,记录分3个阶段：基础值,异氟醚麻醉,硬膜外腔阻滞,结果：异氟醚麻醉,硬膜外腔阻滞均可使下肢体感诱发电位的潜伏期明显延迟,结论：异氟醚麻醉对脊髓具有明显的抑制作用,脊髓可能是异氟醚麻醉作用的重要中枢部位。     

Median nerve somatosensory evoked potentials during isoflurane anaesthesia

Purpose

The effect of isoflurane on the subcortical P₁₄ component of the median nerve somatosensory evoked potential (SEP) is poorly known. We studied whether the P₁₄ wave from the upper brainstem, recorded with a nasopharyngeal electrode, was attenuated at the isoflurane-induced EEG burst-suppression level. We also compared the effect of isoflurane on the P₁₄, cervical N₁₃ and cortical N₂₀, N₃₅ and N₆₀ components.

Methods

Seventeen elective patients were anaesthetized with isoflurane. Somatosensory evoked potentials were recorded pnor to anaesthesia, at 0.5 MAC and I MAC end-tidal isoflurane as well as at the level when EEG was in burst-suppression (mean 1.9 vol% end-tidal isoflurane).

Results

Isoflurane had varying effects on the subcortical components of median SEP. The amplitude of nasopharyngeal P₁₄ was stable, but the mean latency increased from 14.4 ± 1.2 msec at 0.5 MAC to 15.2 ± 1.1 msec at burstsuppression level (P < 0.05). In contrast, the N₁₃ neck response amplitude was attenuated from 3.3 ± 0,6 μV to 2.6 ±0.5μV (P < 0.005) without latency changes. The latency of the cortical N₂₀ wave was increased from 19.7 ± 1.1 msec at awake to 24.4 ± 1.6 msec at burst-suppression level (P < 0.0001) and amplitude was reduced from 3.3 ± 1.1 μV to 1.3 ± 0.6 μV (P < 0.0001). The later cortical components were attenuated even during 0.5 MAC isoflurane and were not recordable during EEG burst-suppression.

Conclusion

We conclude that P₁₄ can reliably be recorded with nasopharyngeal electrodes during isoflurane anaesthesia, even during EEG burst-suppression, when the N₂₀ wave is attenuated. In contrast, the middle-latency SEP components are sensitive to isoflurane anaesthesia.     

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)     

Increase in somatosensory evoked potentials during anesthesia induction with etomidate

In 43 patients the time-dependent behaviour of somatosensory evoked potentials (SSEP) before and during induction of anesthesia with 0.3 mg/kg etomidate was studied. The SSEP components could be reliably recorded in one-minute intervals and the modulations of SSEP (early and middle latencies) following bolus injection with its pharmacokinetically non-stationary states could be quantified. The central conduction time (CCT) between the cervical N13- and the cortical N20-component was less prolonged (from 5.6 ms to 6.4 ms) than known from other anesthetics. Middle latency SSEP exhibited a more marked increase and were reduced in amplitude. All patients showed a 2- to 12-fold increase of the primary complex N20/P25 2-3 min after bolus injection. This amplification cannot be explained either by muscle artifacts nor exclusively by activation of muscle afferents. Myoclonia as a side effect of etomidate coincide with the increase of SSEP-components. The combination of myoclonia and SSEP-enhancement is known to be associated with the familial progressive myoclonus epilepsy. This observation therefore may indicate a cortical excitatory or disinhibitory effect, although no spike-wave complexes have been reported in the EEG after etomidate.     

异丙酚麻醉中大脑皮质体感诱发电位变化的作用机制

目的:探讨中枢性去甲基肾上腺素(NA)机制在异丙酚麻醉中大脑皮质体感诱发电位(SEP)变化中的作用.方法:SD 雄性大鼠15只,体重220～250 g,右侧海马内植入微透析探头,按国际脑电10/20系统法安置银针头皮电极,左侧前爪腕部正中神经处安置刺激电极,强度5.2 mA,刺激间隔0.2 ms.动物随机分为3组.A组...     

Somatosensory evoked potentials during isoflurane anaesthesia

Short latency somatosensory evoked potentials (SEPs) to median nerve stimulation during isoflurane anaesthesia were recorded in 12 elective–surgery patients. The effect of isoflurane on the shape, amplitude and latency of SEPs was evaluated. SEPs were recorded at awake, 1 MAC, 1.5 MAC, at electroencephalogram (EEG) burst suppression and at continuous suppression levels. Finally, SEPs were recorded when anaesthesia was lightened back to 1 MAC. The peak latency and amplitude of the first cortical N₂₀ wave were measured. The latencies increased with increasing isoflurane concentrations. At high concentrations only an almost monophasic N₂₀ wave was recorded, reduced in shape and amplitude. No specific changes could be correlated with the burst suppression or suppression patterns. This suggests that EEG and SEP generators are differently affected with increasing isoflurane concentration. The results indicate that SEPs can also be recorded in drug–induced EEG suppression.     

Auditory evoked potentials during isoflurane anaesthesia

Brainstem auditory evoked potentials (BAEP) were determined in 12 volunteers. The effect of isoflurane anaesthesia on BAEP was determined in six patients. Body temperature and end-tidal CO2% were controlled. Increasing end-tidal isoflurane concentration from 0.6-2.4% increased BAEP wave I, III and V latencies. The amplitude of wave V decreased with increasing isoflurane concentration. Thus a dose-related change was demonstrated between end-tidal concentration of isoflurane and BAEP latencies.     

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 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.     

Depressive effect of isoflurane anesthesia on motor evoked potentials

The influence of the volatile anesthetic isoflurane (Forane) on motor evoked potentials was examined in rats. To record motor evoked potentials, single-shock electrical stimulation was delivered to the forelimb representation of the motor cortex. This resulted in elicitation of a compound muscle action potential from the contralateral extensor muscles. The effect of isoflurane was examined at various concentrations ranging from 0.2 to 1.5%. With increasing concentrations of isoflurane there was a progressive increase in onset latency of the compound muscle action potential and a decrease in peak-to-peak amplitude and duration. Latencies were significantly increased over baseline values for concentrations of isoflurane from 0.5 to 1.5% (P values were 0.001 to 0.007). For the amplitude and the duration, responses at 0.5 to 1.5% isoflurane were significantly lower than baseline (P values were 0.001 to 0.007). We conclude that isoflurane anesthesia significantly changes the muscle response evoked by motor cortex stimulation in experimental animals.     

异丙酚和异氟醚对正中神经体感诱发电位的影响

目的为术中正中神经体感诱发电位监测选择合适的监测指标和全麻药浓度。方法ASAⅠ～Ⅱ级行气管插管全麻病人28例,随机分为异丙酚(P)组和异氟醚(I)组。P组静脉输注异丙酚,使病人依次出现指令反应消失、呼吸停止后行气管插管。I组在气管内插管后吸入异氟醚并使肺泡内异氟醚浓度依次达0.5MAC、1.0MAC、1.5MAC。记录两组诱导前及上述各时点的HR、PetCO2、NT、MAP、SpO2、MnSSEP;P组同时测定异丙酚血药浓度。结果随着异丙酚、异氟醚浓度的增高,皮层下诱发电位N13'变化最小;皮层体感诱发电位的潜伏期延长、波幅降低,其中以N20、P25最稳定,在较高浓度才受麻醉药影响。结论当用异丙酚和异氟醚施行全麻时,N13'最适于作为脊髓脊柱手术的监测指标;N20、P25适于脑部手术监测。异丙酚血药浓度低于2.51μg·ml-1,异氟醚低于1.0MAC时对其无影响。     

Differential effects of isoflurane on human median nerve somatosensory evoked potentials

The effect of isoflurane on median nerve somatosensory evoked potentials (MN-SSEPs) was studied in 15 patients. Anesthesia was induced with thiamylal and maintained with oxygen and isoflurane. MN-SSEPs were recorded in awake patients and after achieving 0.5, 1.0, 1.5, and 2.0% stable end-tidal concentrations of isoflurane. Peak latencies and amplitudes of EP, N13, and N20 and conduction times EP-N13, N13-N20, and EP-N20 were measured. Peak latencies of all components increased after all concentrations of isoflurane compared with control values. N20 peak latencies after 1% and 1.5% isoflurane differed significantly, whereas EP and N13 latencies showed no significant difference. No significant change in conduction time EP-N13 resulted from 1% and 1.5% concentrations of isoflurane compared with control values. Isoflurane increased conduction time N13-N20 significantly when compared with control values, and this increase was dose related. Amplitude of EP and N13 did not show significant change with 1% and 1.5% isoflurane when compared with control values. Amplitude of N20 decreased significantly following isoflurane anesthesia compared with control values, and the difference between 1% and 1.5% isoflurane recordings was also statistically significant. N20 was not discernible in one out of 14 patients after 1.5% and in three out of ten patients after 2% isoflurane. These results indicate that subcortical potentials are less affected by isoflurane anesthesia than cortical potentials. Amplitude reduction of cortical potentials was more noticeable than either prolongation of peak latency or conduction time.(ABSTRACT TRUNCATED AT 250 WORDS)     

Modulation of pain-related somatosensory evoked potentials by general anesthesia

The aim of the present study was to assess if late somatosensory evoked cerebral potentials (SEPs) in response to painful electrical stimuli are a sensitive indicator for analgesic treatment during general anesthesia. For this purpose, a pain model developed for the quantification of drug-induced analgesia in awake volunteers was used in 10 patients scheduled for elective abdominal hysterectomy. Before induction of anesthesia, stimuli were adjusted to two and three times the pain threshold for each individual. Late auditory evoked potentials (AEPs, 30 dB hearing level) and spontaneous electroencephalogram were also evaluated. After control recordings, anesthetic treatments were varied in the following sequences: (a) 0.8% (end-tidal) halothane with 70% nitrous oxide (HN); (b) 0.8% halothane in oxygen (H1); (c) same anesthetic condition as in H1, but the SEP and AEP stimulus intensities were increased to 15 times pain threshold and to 70 dB hearing level, respectively (H2); and (d) fentanyl (0.25 mg) was given with 0.8% halothane in oxygen with no further change in stimulus intensities (HF). In treatments HN and H1, blood pressure and heart rate increases to pain stimuli were abolished, and SEPs and AEPs were both suppressed. Increasing the somatosensory stimulus intensity (treatment H2) stimulated heart rate and arterial pressure responses and again elicited the SEPs. However, AEP components remained suppressed with increased auditory stimulus intensity. Addition of fentanyl (HF) suppressed SEP amplitudes and stimulus-induced hemodynamic responses. Our results suggest that late SEPs in response to painful stimuli change with different analgesic levels.     

Effects of isoflurane and halothane on the auditory and somatosensory evoked potentials

The effects of isoflurane and halothane anaesthesia on brainstem auditory (BEAR) and somatosensory evoked potentials (SEP) were recorded in 15 patients; eight received isoflurane and seven halothane. Atropine alone was given as premedication. After induction of anaesthesia with thiopentone, it was maintained with 50% nitrous oxide in oxygen. Ventilation was controlled. Isoflurane and halothane concentrations were gradually increased to 3%. Recordings were made at 1%, 2.5% and 3%. There were statistically significant differences in the latencies of SEP and BEAR with increasing concentrations of anaesthetic. The BEAR waves significantly affected were wave V and the latency between peaks I to V (p less than 0.001); for the SEP, it was wave N20. SEP central conduction time was prolonged with both anaesthetics (p less than 0.001). The effects of isoflurane and halothane were similar. These results could not be explained by changes in central body temperature or end-tidal carbon dioxide concentration. The study showed a dose-related direct effect of both anaesthetic agents on the brainstem auditory and somatosensory evoked responses. It may be that the measurement of changes in evoked potentials could be a useful indicator of anaesthetic depth.     

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.     

Monitoring of somatosensory evoked potentials during extracranial revascularization

Intraoperative somatosensory evoked potentials (SEPs) were measured in 17 patients during 21 extracranial revascularization and related procedures. The operations included 13 carotid endarterectomies (CEAs), two cervical internal carotid ligations, one vertebral artery (VA) clipping, one VA-common carotid artery (CCA) transposition, and four temporary balloon occlusion tests (TBOTs). Three of the 13 CEAs (23%) showed reduced amplitude and delayed latency of primary cortical SEPs during clamping of the carotid artery, followed by their recovery after emplacement of the internal shunt. Flattening of SEPs during clamping of the CCA was observed in the case of VA-CCA transposition; however, SEPs returned to normal immediately after insertion of a balloon indwelling shunt into the CCA. One of the four TBOTs showed alteration of SEPs during balloon occlusion of the subclavian artery proximal to the origin of the VA. In the others, SEPs remained stable during the entire procedure. Only one transient intraoperative ischemic complication was encountered among the cases of CEA. It was detected through flattening of SEPs, which led to the discovery of an internal shunt obstruction. Carotid stump pressure was also measured in 12 CEAs and two TBOTs, and seven of these 14 had pressure less than or equal to 50 mmHg. Four of the seven had carotid stump pressure less than or equal to 30 mmHg, and three of these four also showed altered SEPs. SEPs remained stable if the collateral flow was sufficient during vascular occlusion and showed obvious alteration when the blood flow was reduced to below the threshold. The authors conclude that monitoring of SEPs during extracranial revascularization is very useful.     

Remifentanil- and fentanyl-based anesthesia for intraoperative monitoring of somatosensory evoked potentials

We sought to compare effects of remifentanil- and fentanyl-based anesthesia on the morphology of somatosensory evoked potentials (SSEPs) and speed of recovery from anesthesia. Forty-one patients undergoing spinal surgery and requiring intraoperative monitoring of SSEPs were randomized into two groups. In Group 1, anesthesia was induced with sodium thiopental and maintained with fentanyl, 50% nitrous oxide in oxygen, and 0.5%--0.75% isoflurane. In Group 2, anesthesia was induced with sodium thiopental and maintained with remifentanil, 50% oxygen in air, and 0.5%--0.75% isoflurane. The variables compared included hemodynamic changes during the induction and intubation, the interval from the end of anesthesia to extubation, intraoperative blood loss and fluid administration, and changes in latency and amplitude of the P37--N45 component of posterior tibial nerve somatosensory evoked potentials and the N20--P24 component of median nerve somatosensory evoked potentials. The two groups were matched for demographics, ASA physical status, and duration of surgery. Hemodynamic profiles after the induction and intubation were similar. There were significant differences between groups in time intervals from the end of anesthesia to extubation (15.3 +/- 12.8 vs 5.3 +/- 2.3 min; P = 0.0001) and ability to follow verbal commands (14.6 +/- 11.9 vs 4.5 +/- 2.4 min; P = 0.0001), with the Remifentanil group showing earlier recovery. Variability (coefficient of variation) of P37--N45 latency was greater (0.026 vs 0.014; P = 0.001) in the Fentanyl group.     

Response variability of somatosensory evoked potentials during scoliosis surgery

Somatosensory evoked potentials (SSEP) were recorded from the scalp for intraoperative monitoring of patients undergoing surgical correction of spine deformities or spine fractures. Alterations in the SSEP with distraction, spine manipulation, anesthesia, hypotension, and other intraoperative variables are described. When loss of the SSEP occurred and a waiting period was undertaken until it returned, all patients with an SSEP present upon closing, which was within +/- 2 SD of their anesthetized control values, had no neurologic complications. Alterations in SSEP consisting of increases in latency of 15% and decreases in amplitude of 50% were not associated with any postoperative neurologic deficits.