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)     

Effect of the acute administration of high dose pentobarbital on human brain stem auditory and median nerve somatosensory evoked responses

Brain stem auditory (BAERs) and median nerve somatosensory evoked responses (MnSSERs) were recorded from normal neural pathways during the induction of pentobarbital coma in six patients undergoing elective excision of complex arteriovenous malformations. Each patient received a 33-minute infusion of pentobarbital at a rate of 0.6 mg/kg (total dose, 19.8 mg/kg). This regimen resulted in burst suppression or isoelectricity of the electroencephalogram in all patients. Although statistically significant changes in latency and amplitude occurred, both BAERs and MnSSERs were readily recordable in all patients throughout the infusion. For the BAER, there were significant increases in the latencies of Waves III and V. However, these increases are sufficiently small that misinterpretation of these changes as an evolving neurological injury is unlikely, e.g., Wave V latency increased from 6.25 +/- 0.25 (SD) to 6.58 +/- 0.16 ms (P less than 0.006). For the MnSSER, changes of greater potential clinical relevance were observed. There were substantial increases in the latencies of the early components of the primary cortical response and in the central conduction time (e.g., CCT of 6.1 +/- 0.6 ms preinduction vs. 7.7 +/- 1.1 ms at t = 33 min, P less than 0.003), and the amplitude of the early cortical response (N20-P25) decreased by a mean of 45% (P less than 0.02). By contrast, subcortical components of the MnSSER (brachial plexus, upper cervical spine) were only minimally affected. We conclude that, in patients who are initially neurologically intact, BAERs and MnSSERs can be monitored effectively during pentobarbital coma and that the loss of these responses should not be ascribed to the effects of this drug alone. However, the interpretation of evoked response changes, particularly MnSSER changes, that occur during pentobarbital administration should take into account the dose-related changes in latency and amplitude that we have observed.     

The effect of high dose sodium thiopental on brain stem auditory and median nerve somatosensory evoked responses in humans

Median nerve somatosensory evoked potentials (MnSSEPs), brain stem auditory evoked responses (BAERs), and the cortical electro-encephalogram (EEG) were recorded in six patients during a 62-min infusion of sodium thiopental (STP) at a rate of 1.25 mg X kg-1 X min-1 (total dose, 77.5 mg/kg). The EEG became isoelectric after 22 +/- 8 (SD) min of STP infusion. Dose-related changes in the latencies and amplitudes of various evoked response wave forms were observed. However, in no instance was any component of either the MnSSEP or the BAER rendered unobtainable by STP administration. For the MnSSEP, progressive increases in the central conduction time (5.33 +/- 0.41 ms preinduction vs. 7.46 +/- 1.2 ms at t = 60 min) and in the latency of the cortical primary specific complex were observed simultaneously with significant reductions in the amplitude of the latter (2.10 +/- 0.85 muV preinduction vs. 0.85 +/- 0.55 muV at t = 60 min). Changes in the latency and amplitude of the response recorded over the upper cervical spine (C2) were not statistically significant in this small population. For the BAER, progressive and significant increases in the latencies of Waves I, III, V (e.g., Wave V latency: 6.16 +/- 0.24 vs. 6.87 +/- 0.31 ms) and in the I-III, III-V, and the I-V interwave latencies were observed. The amplitudes of the BAER components were not significantly altered. The authors conclude that the administration of a dose of STP in excess of twice that required to produce EEG isoelectricity can be compatible with effective monitoring of MnSSEPs and BAERs. However, STP produces dose-related changes in both evoked response wave forms, which must be considered in the interpretation of responses elicited during STP anesthesia.     

Surgical stimulation increases median nerve somatosensory evoked responses during isoflurane-nitrous oxide anaesthesia

Median nerve somatosensory evoked responses (MnSSER) were recorded in 15 healthy adult patients, ASA I-II, before and during orthopaedic surgery. After induction of anaesthesia with fentanyl 0.1-0.15 mg, etomidate 0.3 mg kg-1 and vecuronium 0.1 mg kg-1, anaesthesia was maintained with 0.6% isoflurane (end-tidal) and 66% nitrous oxide in oxygen. MnSSER were recorded after establishment of steady-state anaesthesia at baseline, during preparation (n = 11) and continuously after the start of surgery. For the last measurement period, four patients were excluded from analysis because additional fentanyl was required. MnSSER were recorded at Erb's point, at C6 (neck) and at the respective contralateral primary somatosensory projection area (C3' or C4'). All MnSSER waveform components remained recordable and easily identifiable during anaesthesia. During intense surgical stimulation (e.g. periosteal stimulation) the peak-to-peak amplitude N20P25 increased significantly by more than 45% (P < 0.05), whereas latencies of all components did not change over time. These data indicate that MnSSER may be reliably monitored in the intraoperative period during steady-state isoflurane-nitrous oxide anaesthesia. In addition, concurrent changes in haemodynamic variables during nociceptive stimulation support the hypothesis that reversal of isoflurane-nitrous oxide-induced suppression of MnSSER may indicate increased nociceptive input when depth of anaesthesia is inadequate.      

The effect of tracheal intubation and surgical stimulation on median nerve somatosensory evoked potentials during anaesthesia

This study was designed to determine whether alterations in the median nerve somatosensory evoked potentials occur during the stimuli of tracheal intubation and skin incision. Twenty-two patients scheduled for elective surgery and who required tracheal intubation were studied. Median nerve somatosensory evoked potentials were recorded, analysed and stored approximately every 40 seconds. Anaesthesia was induced with thiopentone and vecuronium used for neuromuscular blockade; the trachea was intubated 2 minutes after induction. Fentanyl 1.5 micrograms/kg was administered subsequently. Evoked potential monitoring was continued until at least 2 minutes after surgical incision. Induction of anaesthesia was associated with an increase in evoked potential latency of 0.8 msec and reduction in amplitude of 1.7 microV. Small, statistically insignificant changes occurred between induction of anaesthesia and tracheal intubation. Surgical incision was accompanied by a statistically significant mean decrease in evoked potential latency of 0.5 msec and a statistically significant increase in evoked potential amplitude of 0.6 microV. The fact that surgical stimulation produced an activating effect on evoked potentials suggests that they may be used as a measure of the neurophysiological effects of anaesthesia.     

The effect of high-dose fentanyl on human median nerve somatosensory-evoked responses

Median nerve somatosensory evoked responses (MnSSERs) were recorded in nine neurologically normal adult cardiac patients before and during the administration of high-dose fentanyl. MnSSERs were recorded prior to induction and at t = 20 min and t = 45 min postinduction. Fentanyl was administered as a slow bolus (53.2 +/- 9.1 micrograms X kg-1), followed by a continuous infusion at 10-20 micrograms X kg-1 X hr-1 (total dose 63.6 +/- 10.1 micrograms X kg-1). All MnSSER waveform components remained recordable and easily identifiable during anaesthesia. The effect of fentanyl was more pronounced on cortical waveform components, leaving subcortical components largely unaffected. There was a significant increase in the latency of the cortical MnSSER at t = 20 min, e.g., for the initial negative cortical wave, N1, the latency was 21.18 +/- 1.55 ms preinduction versus 22.18 +/- 1.42 ms at t = 20 min. There was also a significant decrease in the amplitude of the cortical response at t = 20 min, i.e., 2.04 +/- 1.30 microV preinduction versus 1.31 +/- 0.74 microV at t = 20 min. However, the degree of change was quite variable (range = 0-65 per cent). No further changes occurred at t = 45 min. The authors conclude that MnSSERs can be consistently and reliably monitored during high-dose fentanyl anaesthesia. However, fentanyl produces modest but significant changes in the MnSSER which should be taken into account lest they be misinterpreted as neurologic injury in evolution.     

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。     

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.     

镇静深度对正中神经中潜伏期体感诱发电位的影响

目的 探讨丙泊酚静脉麻醉中,不同镇静深度对正中神经中潜伏期体感诱发电位(SSEP)的影响.方法 选择择期全麻脊柱手术患者30例,ASA Ⅰ或Ⅱ级.丙泊酚初始效应室靶浓度为0.5 μg/ml,3～5 min增加一次,增加幅度为每次0.5 μg/ml.分别记录清醒时、意识消失及插管后5 min血流动力学及脑电双频指数(BIS)、SSEP各项指标.结果 与清醒时比较,意识消失时BIS明显降低,N35波潜伏期无明显变化,N55波潜伏期明显延长(P＜0.05);N35、N55波幅均明显降低(P＜0.01).插管后5 min,BIS亦明显降低,N35、N55潜伏期均明显延长(P＜0.05);N35、N55波幅均明显降低(P＜0.01).BIS值与N55波幅相关系数为0.79.结论 在全麻诱导期随着镇静深度增加,正中神经中潜伏期SSEP潜伏期延长,波幅降低,N55波幅能够反映镇静深度.     

Effects of hypothermia and sternal retractors on median nerve somatosensory evoked potentials

Background: Somatosensory evoked potentials (SEPs) are altered by hypothermia, which is often used during cardiopulmonary bypass (CPB). However, the effect of hypothermia on SEP amplitudes is unclear. Also, the sternal retractors used during open heart surgery are reported to cause brachial plexus distension and SEP changes. Methods: Median nerve SEPs under hypothermic CPB were studied in 29 elective patients scheduled for open heart surgery. In 23 patients who underwent left internal mammary artery (IMA) dissection, the effects of sternal retractors on cortical SEP before the initiation of CPB were investigated. Results: A latency shift of all SEP components was detected when nasopharyngeal temperature decreased from 35.7(SD 0.4)°C to 27.8(SD 0.25)°C. The mean cortical N₂₀ latency was increased by 39% (P< 0.0001), cervical N₁₃ by 33% (P < 0.0001), and peripheral N₉ by 27% (P <0.0001). The latency changes were reversible when normothermia was restored. The effect of hypothermia on SEP amplitudes was more complex. The mean amplitude of N₂₀ decreased from 2.7 μV to 2.2 μV (P < 0.05) and the amplitude of N₁₃ from 2.5 μV to 2.0 μV (P < 0.0001). In contrast, the N₉ component showed an increase from 1.4 μV to 2.1 μV (P <0.0001) during hypothermia. The sternal retractors did not cause significant cortical SEP amplitude changes during IMA dissection or sternotomy. Also, the latency changes were small, although significant (P < 0.05). Conclusion: Despite the moderate amplitude changes produced by hypothermia, SEPs can be successfully monitored during hypothermia. Theoretically, the different behaviour of amplitude in peripheral and cranial components of SEP during hypothermia is interesting. Hypothermia has a more profound effect on synaptic transmission, represented by the cortical N₂₀ latency, than on the peripheral nerve conduction velocity. Intraoperative monitoring of temperature is essential whenever SEPs are recorded. The sternal retractors were not responsible for the intraoperative SEP changes.     

Effects of hypothermia on median nerve somatosensory evoked potentials during spontaneous circulation

Perioperative-induced hypothermia is a common means of reducing ischemic injury in neurosurgical procedures and cardiac surgery, and it may occur accidentally. Somatosensory evoked potentials (SSEPs) are used frequently for neurophysiologic monitoring of these procedures. The effects of hypothermia on SSEPs have been studied widely in humans with cardiopulmonary bypass (CPB) during nonpulsatile flow. However, changes of latency and amplitude of early SSEP components during spontaneous circulation have not yet been studied. Median nerve SSEPs were recorded in 21 patients during rewarming from 32 to 36 degrees C core temperature. Latencies and amplitudes of N9, N13, N20, and central conduction time were registered at 32, 34, and 36 degrees C. Latencies of N9, N13, and N20 were prolonged at 32 degrees C compared with 36 degrees C (N9: 13.4 +/- 1.4 msec versus 11.8 +/- 1.4 msec, P <.05; N13: 17.6 +/- 1.9 msec versus 15.4 +/- 1.4 msec, P <.01; N20: 26.5 +/- 1.8 msec versus 22.4 +/- 1.6 msec, P <.001). Amplitude of N20 was higher at 32 degrees C compared with 36 degrees C (2.86 +/- 1.94 microV versus 2.07 +/- 1.47 microV, P < .05). Central conduction time decreased by 27%, and peripheral latency of N13 decreased by 14%. The increase in SSEP latency (N9, N13, and N20) and central conduction time during moderate hypothermia of 32 degrees C and spontaneous circulation are comparable with those during nonpulsatile flow on CPB. In contrast to nonpulsatile flow, the amplitude of N20 was increased significantly (P < .05) during moderate hypothermia and pulsatile circulation. These results suggest to be cautious about generalizing the effects of hypothermia on SSEP during CPB to spontaneous circulation.     

Anesthetic induction with thiopental: its effect on scalp topography of median nerve somatosensory evoked potentials

The effects on median nerve somatosensory evoked potentials (SEPs) of analgesic doses of fentanyl, meperidine or morphine and of sodium thiopental (STP) anesthesia (4 mg/kg) were tested in 36 surgical patients. We also explored changes in SEP components as a function of their scalp location. Before and after medication, responses were recorded from the scalp overlying the parietal cortex (ipsi- and contralateral to the stimulated arm) and the precentral (contralateral) cortex. None of the three opiates affected SEP latencies or amplitudes. The barbiturate increased the amplitudes of subcortical and early cortical components (N18, N20, P22, P25), whose latencies, however, were not significantly modified. The effect of STP on later SEP cortical components depended on their scalp topography: parietal N33 and P45 underwent significant changes in both latency and amplitude, whereas precentral N30 showed a significant amplitude increase only. Thiopental anesthesia produces clearer short-latency SEP recordings, from both parietal (components N20-P25) and precentral (P22, N30) areas.     

Posterior tibial nerve and median nerve somatosensory evoked potential monitoring during carotid endarterectomy

PURPOSE: Somatosensory evoked potential (SSEP) monitoring using the median nerve (MN) modality during carotid endarterectomy is well established. This study assessed the usefulness of monitoring the posterior tibial nerve (PTN) SSEP as an adjunct to MNSSEP for detection of cerebral ischemia and as an indicator for the insertion of a shunt in patients undergoing a carotid endarterectomy. METHODS: All patients undergoing carotid endarterectomy during three years who had routine bilateral MNSSEP were also monitored with bilateral PTNSSEP. Patients received a shunt if there was a significant change (> 50% decrease in amplitude of cortical peak (N20) in the MNSSEP after cross clamping. The incidence, timing, and duration of all PTNSSEP changes were compared to MNSSEP changes. RESULTS: One hundred fifty-three patients were studied. Significant changes in MNSSEP after cross clamp lead to insertion of a shunt in six patients. Changes in PTNSSEP occurred at almost the same time in three patients, four minutes before MNSSEP in one, three minutes later in one and no change in one patient. Good quality baseline tracings were obtained in 99% MNSSEP as compared to 88% PTNSSEP (P < 0.05). New postoperative neurological deficits occurred in four patients (2.6%), only one had significant evoked potential changes. CONCLUSION: Monitoring of PTNSSEP is feasible and may be considered for an adjunct to MNSSEP or as an alternative modality if there are difficulties with MNSSEP. However, there may be a greater incidence of poor quality baseline tracings for PTNSSEP.     

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.     

异丙酚麻醉下气管插管对正中神经体感诱发电位的影响

【摘要】〓目的〓观察异丙酚诱导下气管插管对正中神经体感诱发电位(MnSSEP)的影响,探讨正中神经体感诱发电位用于监测气管插管引起的伤害性刺激反应的可行性。方法〓18~40岁病人20例(8男,12女), 异丙酚效应室浓度达5 ?滋g·mL-1 并用司可林后行气管插管,记录插管前、中、后的MnSSEP、BIS、SBP、DBP、HR。结果〓气管插管前后MnSSEP各波潜伏期、BIS和HR均无改变。插管即刻MnSSEP的P15N20、N20P25波幅增高,插管后N20P25恢复,P15N20仍增高,其余波幅无改变。插管即刻和插管后SBP、DBP较插管前增高。结论〓正中神经体感诱发电位的N20P25波幅较BIS更适于反映气管插管引起的伤害性刺激。     

Repair of electrically injured median nerve with the aid of somatosensory evoked potential

In repair of the high voltage electrical injuries of peripheral nerve, selection of the proper plane for nerve coaptation after debridement is important since the electrical current is inclined to pass through the nerve trunks due to the lower electric resistance. In this report, we present our experience on use of the somatosensory evoked potentials (SSEP) test to assist determination of range of the injured nerve debridement in the electrical injured nerve. From January 1997 to December 2007, 30 patients with the high voltage electrical injury in the wrist, having defect of median nerve, were treated with nerve grafting. In 18 patients, the nerve resection plane was selected with the assistance of SSEP. In 12 patients, the nerve resection plane was determined by the traditional gross examination. The average lengths of nerve defect after debridement were 10.4 cm in the procedure with SSEP assistance and 4.01 cm in the traditional procedure. The finger motion was reconstructed by the tendon graft connecting the proximal forearm muscle and the distal tendon of flexor disitorum profundus. In following up, the two‐point discrimination of finger was examined. The grade of finger sensory recovery was found improved in the patients who underwent the nerve repair with SSEP assistance than that in the patients underwent treatment with the traditional method. The results suggested that aggressive debridement is recommended for the high with voltage electrical nerve injury. SSEP could be a valuable tool for determination of the range of nerve debridement. © 2009 Wiley‐Liss, Inc. Microsurgery, 2009.     

正中神经体感诱发电位在脊髓型颈椎病手术预后评估中的作用

目的回顾性分析正中神经体感诱发电位（somatosensory evoked potential,SEP,）的检测结果和分型在脊髓型颈椎病（cervical spondylotic myelopathy,CSM）手术预后评估中的作用。方法随访76例接受手术治疗的CSM患者,男49例,女27例;年龄55—74岁,平均62．4岁。将术前检测SEP的波形分为5型：Ⅰ型为正常SEP,Ⅱa型为单独幅值异常,Ⅱb型为单独潜伏期异常,Ⅲ型为幅值和潜伏期同时异常,Ⅳ型为SEP消失。根据术前和术后随访的JOA评分评估临床症状和计算康复率,统计分析SEP与临床数据之间的相关性。结果SEPⅠ型18例,Ⅱa型16例,Ⅱb型17例,Ⅲ型14例,Ⅳ型11例。SEP与术前JOA评分有显著相关性（X^2=53．9,P〈0．05）。比较术后2年随访时的康复率发现Ⅰ型和Ⅱa型、Ⅱb型和Ⅲ型之间无显著性差异,而Ⅰ型和Ⅱa型、Ⅱb型和Ⅲ型、Ⅱb型和Ⅳ型之间有显著性差异（独立样本检验,P〈0．05）。结论SEP分型为临床提供客观、有价值的信息,有助于准确了解脊髓的受损程度和评估手术预后。     

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)     

Midlatency median nerve evoked responses during recovery from propofol/sufentanil total intravenous anaesthesia

BACKGROUND: Median nerve somatosensory evoked responses (MnSSER) are frequently used to monitor the integrity of the somatosensory pathway during surgery. We investigated MnSSER components during the wakeup phase from anaesthesia with propofol/sufentanil, because detailed information is lacking about the reversibility of anaesthetic induced changes of MnSSER. The aim of the study was to document precisely the MnSSER waves in relation to the clinical awakening. The hypothesis was that anaesthetic induced MnSSER changes are reversed when the patient becomes responsive after anaesthesia. METHODS: In 20 gynaecological patients anaesthesia was maintained with propofol 8 mg kg(-1) h(-1) supplemented by bolus injections of sufentanil. MnSSER were recorded at C4' (N20, P25, N35, P45, N50) following electrical median nerve stimulation on the day before surgery, after the end of surgery during anaesthesia and every 5 min during recovery, till the patients were responsive again and able to identify a shown object. RESULTS: While the primary cortical MnSSER complex N20P25 regained baseline values, the cortical latencies > or =35 ms remained prolonged (P<0.001) and the amplitudes P45N50 were suppressed (P< or =0.013), when the patients were responsive after 26+/-7 min following anaesthesia. However, the amplitudes P25N35 exceeded their corresponding baseline value (P<0.01) CONCLUSION: Persistent changes of MnSSER waves > or =35 ms reflect impaired signal processing along the somatosensory pathway following propofol/sufentanil anaesthesia when the patients are responsive again. Further studies combining MnSSER recording with distinct neuro-psychological tests are needed to define the clinical relevance of these findings.     

The reference intervals of intraoperative posterior tibial nerve somatosensory evoked potentials

BackgroundA reference interval exists for posterior tibial nerve somatosensory evoked potentials (PTN-SEPs) in awake. However, the reference interval for intraoperative- PTN-SEPs (I-PTN-SEPs) remains unclear. As a substitute for PTN-SEPs in awake, we considered I-PTN-SEPs can provide functional information about the dorsal somatosensory system. No report evaluated the physiologic and analytical issues in the measurement of I-PTN-SEPs. We investigated the sources of variation and reference intervals for I-PTN-SEPs.MethodsWe studied 143 patients with unilateral radiculopathy and without neurologic deficit who underwent surgery. Stimulation was delivered to the PTN at the ankle. The scalp recording electrode was placed at the Cz with a reference electrode located on the forehead at the Fz. SEPs were recorded from patients during electrical stimulation of the I-PTN.ResultsP1 and N1 latencies showed significant positive linear correlations with age (P1 latency = 36.52 + 0.0814 × age, P = 0.00003; N1 latency = 46.21 + 0.081 × age, P = 0.00022), and body height (P1 latency = 16.94 + 14.91 × body height, P = 0.00000; N1 latency = 25.42 + 15.64 × body height, P = 0.00002). In contrast, I-PTN-SEPs amplitude showed no correlation with age or body height. The 95% confidence interval for I-PTN-SEPs amplitude, or the reference interval, was determined as 0.31–5.91 μV.ConclusionsThe lower normal limit value was 0.31 μV, and this reference interval may be useful to evaluate function of the posterior funiculus, such that as during surgery for patients with intramedullary tumor.