异氟醚一氧化亚氮和硫喷妥钠麻醉在术中体感诱发电位的监护

研究了５１例志愿全麻手术患者不同麻醉药浓度异氟醚和６６％氧化亚氮及硫喷妥钠（７ｍ／ｋｇ）时对体感诱发电位（ＳＥＰ）的影响。结果表明，随着异氟醚吸入浓度的增高，ＳＥＰ各个波峰潜伏期（Ｐ１、Ｎ１、Ｐ２、Ｎ２）逐渐延长，波幅（Ｐ１－Ｎ１、Ｐ２－Ｎ２）逐渐降低，其中以Ｎ２潜伏期延长最明显（Ｐ＜０．０１），Ｐ２－Ｎ２波幅降低最显著。停止吸入麻醉药后，ＳＥＰ各个波峰潜伏期均开始缩短，波幅逐渐增加；出现角膜反射时，Ｎ２潜伏期已达麻醉前范围（Ｐ＞０．０５）。再次加深麻醉后，ＳＥＰ潜伏期和波幅重现以上变化。提示异氟醚一氧化亚氮麻醉使ＳＥＰ呈剂量依赖效应，麻醉深浅与ＳＥＰ变化呈正相关关系。另外，硫喷妥钠静注１０分钟后，ＳＥＰ潜伏期延长，波幅下降，仍以Ｎ２潜伏期延长和Ｐ２－Ｎ２波幅降低最显著。说明异氟醚一氧化亚氮和硫喷妥钠麻醉中，皮层ＳＥＰ可做为连续监护麻醉深浅的有效方法，而晚成份（Ｎ２潜伏期和Ｐ２－Ｎ２波幅）为麻醉深度的重要指标。     

异氟醚—氧化亚氮和硫喷妥钠麻醉在术中体感诱发电位的监护

研究了５１例志愿全麻手术患者不同麻醉药浓度异氟醚和６６％氧化亚氮及硫喷妥钠（７ｍｇ／ｋｇ）时对体感诱发电位（ＳＥＰ）的影响。结果表明，随着异氟醚及浓度的增高，ＳＥＰ各个波峰潜伏期（Ｐ１，Ｎ１，Ｐ２，Ｎ２）逐渐延长，波幅（Ｐ１－Ｎ１，Ｐ２－Ｎ２）逐渐降低，其中以Ｎ２替伏期延长最明显（Ｐ〈０．０１），Ｐ２－Ｎ２波幅降低温显著。停止吸入麻醉药后，ＳＥＰ各个波峰潜伏期均开始缩短，波幅逐渐增加；出现角膜反射     

普鲁卡因对上肢短潜伏期体感诱发电位的影响

目的：探讨静滴普鲁卡因对短潜伏期体感诱发电位（ＳＬＳＥＰ）的影响。方法;对上肢感觉传导无异常的病人１５例,分别观察静脉滴注普鲁卡因前以及滴注１％普鲁卡因２０ｍｇ．ｋｇ＾０－１．ｈ＾－１１０分钟、４０ｍｇ．ｋｇ＾－１、ｈ．＾－１５分钟和６０ｍｇ．ｋｇ＾－１．ｈ＾－１５分钟的上肢ＳＬＳＥＰ,比较Ｎ１４,Ｎ２０,Ｐ２３各波的潜伏期,Ｎ１４－Ｎ２０波间潜伏期（ＣＣＴ）以及Ｎ２０Ｐ－Ｐ２０的峰间值。结果：Ｓ     

不同剂量异丙酚,咪唑安定和依托咪酯对上肢短潜伏其体感诱…

目的：观察３组不同剂量静脉麻醉药异丙酚、咪唑安定、依托咪酯对上肢短潜伏期体感诱发电位（ＳＬＳＥＰ）影响。方法：９０例择期手术患者，随机分成３组，每组再随机分为３个不同剂量组，分别单次静脉注射异丙酚１．５、２、３ｃｍ／ｋｇ，咪唑安定０．２、０．３、０．４ｃｍ／ｋｇ，依托咪酯０．１５、０．３、０．４ｃｍ／ｋｇ，观察用药后对ＳＬＳＥＰ的影响。结果：异丙酚组均对ＳＬＳＥＰ的Ｎ１４、Ｎ２０潜伏期在ＣＣＴ无明     

咪唑安定对体感诱发电位的影响

目的：了解咪唑安定对体感诱发电位的影响。方法：选择３０例ＡＳＡＩ～Ⅱ级的脑外科手术病人，根据国际１０～２０系统，在Ｃ３或Ｃ４、ＦＰｚ（参考）和ＳＣ（第二颈椎棘突处）安放盘状记录电极，记录体感诱发电位。均分为三组按剂量（０．２ｍｇ／ｋｇ、０．３ｍｇ／ｋｇ和０．４ｍｇ／ｋｇ）静脉注射咪唑安定，连续观察皮层Ｎ２０、Ｐ２３和颈髓Ｎ１４电位的变化。结果：（１）用药后，皮层Ｎ２０和颈髓Ｎ１４电位的波幅降低，分别抑制到术前的６３．７５％和４８．７５％（Ｐ＜０．０５），苏醒后恢复到基础水平；（２）颈髓Ｎ１４、皮层Ｎ２０和Ｐ２３的潜伏期及中枢传导时间均无显著延长，（３）各剂量组间的ＳＥＰ变化无明显差别。结论：咪唑安定对ＳＥＰ一定程度的抑制作用临床意义不足，可用作ＳＥＰ监测时的静脉麻醉药。     

体感诱发电位皮层成份在监测脊柱手术中的作用

目的：评价监测体感染诱发电位（ＳＥＰ）Ｎ２０、Ｐ４０波在脊柱手术时的方法及意义。方法：对２２例脊柱手术病人进行上肢或下肢ＳＥＰ监测并进行术后随访。结果：１０例病人的Ｎ２０、Ｐ４０波潜延长大于１ｍｓ,波幅降低大于５０％,３例波形完全消失,但只有１例术后神经症状加重。结论：脊柱手术时仅则上肢或下肢ＳＥＰ皮层成份意义较小,需做多形式监测;判断时除既往异常标准外,需注意ＳＥＰ异常持续的时间及潜伏期无明显变     

健侧颈7神经根桥接后电生理变化研究

测定健侧颈７神经根移位后体感诱发电位的变化，为判断神经移位后的再生提供依据。方法；运用Ｄａｎｔｅｃ肌电仪，分别在胸锁关节，胸腋部刺激，测定２１例健侧颈７移位后Ｎ２０波潜伏期，波幅的变化，分析其与神经再生时间的关系。结果：健侧颈７移位后，在胸锁关节与腋部测定的ＳＥＰ潜伏期与神经再生时间呈线性相关，而ＳＥＰ波幅与神经再生时间之间，是无显著正相关。     

中潜伏期听觉诱发电位在麻醉深度监测中的应用

术中知晓在全麻手术中日益受到重视,研究发现中潜伏期听觉诱发电位（ＭＬＡＥＰ）的潜伏期和波幅与麻醉药呈剂量依赖性抑制。本文综述了ＭＬＡＥＰ在麻醉深度监测中的应用。     

异丙酚诱导期脑电效应

异丙酚是快速，短效催眠药，对中枢神经系统抑制较轻。ＥＥＧ监测是判断异丙酚诱导期麻醉深度敏感而直接的手段。１８例ＡＳＡⅠ－Ⅱ级患者在注入芬太尼３．６μｇ／ｋｇ１０ｍｉｎ后给予异丙酚２ｍｇ／ｋｇ或硫喷妥钠４ｍｇ／ｋｇ于２０ｓ内缓慢静注，诱导期间用ＳＡＮ－ＥＩ２１Ａ７１脑电图监测仪持续描记脑电变化。结果表明，异丙酚与硫喷妥纳均首先产生β高幅兴奋性活动，最大效应期异丙酚无δ波，维持期效应则相似。起效时间，     

正常人前臂内侧皮神经感觉传导研究

首次研究应用逆向法测定正常人前臂内侧皮神经短潜伏期体感诱发电位（ｓｈｏｒｔ ｌａｔｅｎｃｙｓｏｍａｔｏｓｅｎｓｏｒｙ ｅｖｏｋｅｄ ｐｏｔｅｎｔｉａｌｓ），并研究其感觉动作电位（ｓｅｎｓｏｒｙ ｎｅｒｖｅ ａｃｔｉｏｎ ｐｏｔｅｎｔｉａｌ）。方法：（１）ＳＮＡＰ：肱骨内上髁前外侧平均２．６ｃｍ处表面双极刺激，前臂军面内侧平均１０．３ｃｍ，处记录ＳＮＡＰ． （２）ＳＬＳＥＰ：上述刺激位置不变，用四道程记录锁骨上、颈_７棘突、对侧顶区（Ｐ_３／Ｐ_４）相应的Ｎ_９、Ｎ_（１３）、Ｎ_（２０）诱发电位。通过分别对Ｎ_９、Ｎ_（１３）、Ｎ_（２０）的潜伏期、Ｎ９－Ｎ（１３）峰间潜伏期与臂长的相关分析，认为峰间潜伏期及自身双侧对照的潜伏期差值和波幅比值为临床可靠指标，可望对胸廓出口综合征（ＴＯＳ）早期诊断有指导意义。     

Effects of sevoflurane and propofol on evoked potentials during neurosurgical anesthesia

BACKGROUND: The effect of anesthetics on somatosensory evoked potential (SEP) and auditory brain stem response (ABR) has been a subject of intense reseach over the last two decades. In fact, volatile anesthetics have been repeatedly shown to decrease cortical amplitude in a dose-dependent fashion but the information regarding the effect of propofol is incomplete. The purpose of this study was to compare the effects of sevoflurane and propofol on evoked potentials during comparable depth of anesthesia guided by bispectral index (BIS). METHODS: Forty four patients scheduled for neurosurgery were studied. Anesthesia was maintained with intravenous propofol using target controlled infusion (TCI). We measured the change of amplitude and latency of SEP(N20-P25), ABR (V wave) and visual evoked potential (VEP: P100) at three sets of sevoflurane (0%, 1%, 2%) or propofol concentrations (effect site concentration of 1.5, 2.0, 3.0 microug x ml(-1)). BIS monitor was used to measure relative depth of hypnosis. RESULTS: With increasing concentrations of sevoflurane (0, 1% and 2%), SEP showed dose-related reduction in its amplitude, ABR produced less marked changes and VEP showed a significant reduction at 1%. VEP at the propofol concentration of 3.0 microg x ml(-1) was decreased significantly compared with the amplitude at 1.5 microg x ml(-1) concentration. No significant change was observed with SEP and ABR during the change of propofol dosages. BIS values were almost the same with each anesthetics. CONCLUSIONS: VEP was most strongly affected with anesthetics, and ABR showed less marked influence of sevoflurane and propofol. Propofol based TIVA technique would induce less change in evoked potentials than sevoflurane.     

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.     

Hypothermia does not alter somatosensory evoked potential amplitude and global cerebral oxygen extraction during marked sodium nitroprusside-induced arterial hypotension

BACKGROUND: To prevent neurologic damage, monitoring cerebral function by somatosensory evoked potentials is used in selected settings. Excision of intraocular melanoma provides a unique opportunity to assess independently during anesthesia the effects on median nerve somatosensory evoked potentials (MN-SSEPs) and cerebral oxygen extraction of sodium nitroprusside-evoked arterial hypotension with and without hypothermia. METHODS: Median nerve somatosensory evoked potentials, arterial pressure, jugular venous bulb oxygen saturation (Sjo(2)) and lactate concentration, and arterial-jugular bulb oxygen content difference were assessed during propofol-remifentanil anesthesia under sodium nitroprusside-evoked arterial hypotension (mean arterial pressure, 40 mmHg) with and without surface hypothermia (32 degrees C) in 11 otherwise healthy patients undergoing resection of choroidal melanoma. RESULTS: Hypothermia alone did not affect peak-to-peak amplitude of N20/P25 but prolonged cortical latency of N20 (22.6 +/- 2.2 vs. 25.9 +/- 2.5 ms, P < 0.05), cervical latency of N13 (14.3 +/- 1.2 vs. 15.7 +/- 1.6 ms, P < 0.05), and central conduction time (8.3 +/- 1.4 vs. 10.2 +/- 1.6 ms, P < 0.05). Evoked arterial hypotension did not depress MN-SSEP N20/P25 amplitude either with or without hypothermia (-0.31 vs. -0.28 microV, P > 0.05) or alter latency (0.08 vs. 0.1 ms, P > 0.05). Furthermore, hypotension with or without hypothermia did not change Sjo(2), arterial-jugular bulb oxygen content difference, or lactate concentration. CONCLUSIONS: Thus, hypothermia to 32 degrees C does not alter MN-SSEP amplitude and global cerebral oxygen extraction during marked sodium nitroprusside-induced arterial hypotension with a mean arterial pressure of 40 mmHg but prolongs MN-SSEP latencies during propofol-remifentanil anesthesia in individuals without cerebrovascular disease.     

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.     

Hypothermia Does Not Alter Somatosensory Evoked Potential Amplitude and Global Cerebral Oxygen Extraction during Marked Sodium Nitroprusside-induced Arterial Hypotension

Background: To prevent neurologic damage, monitoring cerebral function by somatosensory evoked potentials is used in selected settings. Excision of intraocular melanoma provides a unique opportunity to assess independently during anesthesia the effects on median nerve somatosensory evoked potentials (MN-SSEPs) and cerebral oxygen extraction of sodium nitroprusside-evoked arterial hypotension with and without hypothermia.

Methods: Median nerve somatosensory evoked potentials, arterial pressure, jugular venous bulb oxygen saturation (Sjo2) and lactate concentration, and arterial-jugular bulb oxygen content difference were assessed during propofol-remifentanil anesthesia under sodium nitroprusside-evoked arterial hypotension (mean arterial pressure, 40 mmHg) with and without surface hypothermia (32[degrees]C) in 11 otherwise healthy patients undergoing resection of choroidal melanoma.

Results: Hypothermia alone did not affect peak-to-peak amplitude of N20/P25 but prolonged cortical latency of N20 (22.6 +/- 2.2 vs. 25.9 +/- 2.5 ms, P < 0.05), cervical latency of N13 (14.3 +/- 1.2 vs. 15.7 +/- 1.6 ms, P < 0.05), and central conduction time (8.3 +/- 1.4 vs. 10.2 +/- 1.6 ms, P < 0.05). Evoked arterial hypotension did not depress MN-SSEP N20/P25 amplitude either with or without hypothermia (-0.31 vs. -0.28 [mu]V, P > 0.05) or alter latency (0.08 vs. 0.1 ms, P > 0.05). Furthermore, hypotension with or without hypothermia did not change Sjo2, arterial-jugular bulb oxygen content difference, or lactate concentration.     

Effect of propofol on visual evoked potentials during neurosurgery

BACKGROUND: Evoked potentials are used to monitor the central nervous system during neurosurgery and it is well known that they are affected by the depth of anesthesia. Many studies on the evoked potential like somatosensory evoked potential (SEP) and auditory brain stem response (ABR) are reported, but studies on visual evoked potential (VEP) are few. We investigated the influence of the propofol concentration on VEP in neurosurgical patients. METHODS: Seven patients scheduled for neurosurgery, three with cranial aneurysm and four with brain tumor, were studied. Anesthesia was maintained with intravenous propofol using target controlled infusion (TCI). We measured the change of amplitude and latency of VEP at three propofol concentrations (effect site concentrations of 1.5, 2.0 and 3.0 microg x ml(-1)), and also evaluated bispectral index (BIS) at each propofol concentration. RESULTS: Amplitude of VEP at 3.0 microg x ml(-1) propofol concentration decreased significantly compared with the amplitude at 1.5 microg x ml(-1) concentration. No significant change was observed with the latency of VEP. The value of BIS at 3.0 microg x ml(-1) propofol concentration also decreased significantly compared with 2.0 microg x ml(-1) concentration. CONCLUSIONS: Amplitude of VEP is strongly affected by the concentration of propofol. Caution should be taken in evaluating VEP in patients undergoing propofol anesthesia.     

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.     

The effects of propofol anesthesia on transcortical electric evoked potentials in the rat.

The effects of halogenated anesthetic agents on somatosensory and motor evoked potentials (MEP) have been documented previously. Intravenous anesthetic propofol has not yet been used during MEP monitoring. This study investigates the effects of propofol on transcortical MEP in rats during bolus, infusion, and recovery conditions. After baseline MEP recordings, animals received a hetastarch bolus, followed by a propofol (10 mg/kg) bolus dose. A propofol infusion (10 mg/kg/h) and a hetastarch infusion were then begun. MEP recordings were obtained after the propofol bolus, during the infusion, and after a 30-minute recovery phase. Blood pressure readings remained stable. MEP onset latency increased, and amplitude decreased. Response duration diminished. All values returned towards the baseline during recovery. Our results show that the effects of propofol on MEPs are similar to its effects on somatosensory evoked potentials. Propofol seems to be a reasonable agent for use during intraoperative MEP monitoring and should be further investigated for use during spinal cord monitoring in humans.     

Changes of latency and amplitude of short latency somatosensory evoked potentials during slow induction of anesthesia with sevoflurane

In the present study, changes of latency and amplitude of short latency somatosensory evoked potentials (SSEPs) were evaluated continuously during slow induction of anesthesia from sevoflurane awake to deep levels of anesthesia in eight scheduled surgical patients. Not consistent with other previous investigations, the latency of N20 was significantly shortened with sevoflurane after 25 minutes from the beginning of inhalation compared with the awake control levels. No increase of latency was observed. The amplitudes of N20 were decreased with sevoflurane anesthesia in relation to duration of anesthesia. These results suggest that sevoflurane alone might have no marked pharmacological properties to change the latency of SSEPs even in the deep level of anesthesia.     

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.