Systemic lidocaine and human somatosensoryevoked potentials during sufentanil-isoflurane anaesthesia

The effect of systemically administered lidocaine on somatosensory evoked potentials (SSEPs) during general anaesthesia has not been widely reported. Knowledge of the influence of anaesthetic agents on evoked potentials assists in interpreting evoked potential waveforms. Accordingly, we studied the behaviour of cortical and subcortical (recorded at the second cervical vertebra) SSEPs after administration of intravenous lidocaine (3 mg.kg-1 bolus followed by infusion at 4 mg.kg-1.hr-1) during a sufentanil-based anaesthetic regimen in 16 patients undergoing abdominal or orthopaedic surgery. When compared to awake baseline recordings, the sufentanil-nitrous oxide, low-dose isoflurane anaesthetic depressed N1 amplitude by approximately 40% and prolonged latency by 10%. Fifteen minutes after establishment of this anaesthetic, the amplitude and latency of N1 were 1.13 +/- 0.56 microV and 19.81 +/- 1.63 msec, respectively. Within five minutes of adding lidocaine, amplitude decreased further to 0.84 +/- 0.39 microV (P = 0.001), while latency was extended to 20.44 +/- 1.48 msec (P = 0.01). Lidocaine did not affect cervical amplitude and prolonged latency only minimally. Despite the observed effects on amplitude and latency, SSEP waveforms were preserved and interpretable. Plasma lidocaine levels obtained at 5, 20, and 40 minutes after lidocaine were 5.17 +/- 1.33, 3.76 +/- 1.14, and 3.66 +/- 0.9 micrograms.dl-1, respectively. Our results indicate that systemically administered lidocaine at therapeutic plasma levels acts synergistically with a sufentanil-based anaesthetic to depress the amplitude and prolong the latency of SSEPs.     

小儿硫喷妥钠／七氟烷麻醉及复合使用酮洛芬和芬太尼对刺激正中神经的体感诱发电位的影响

背景体感诱发电位（somatosensory evoked potentials,SEPs）常被用于外科手术中判断脊髓和脑功能。总的来说,SEPs对吸入性麻醉药物是敏感的,但有关小儿用七氟烷维持麻醉对sEPs的影响了解甚少。麻醉中常会使用镇痛药物,辅助用药也会影响SEPs。在这项前瞻性的临床试验中,共计27例3。8岁的健康儿童接受研究,对其静脉给予苯二氮革和巴比妥类药物麻醉诱导后,用七氟烷维持麻醉,并观察它们对正中神经SF2s的影响。此外,也观察了两种镇痛药物,酮洛芬和芬太尼对SEPs的影响。方法麻醉前静脉给予0．1mg／kg咪达唑仑,用呼气末浓度为2％的七氟烷维持麻醉,分别在给予咪达唑仑前,吸入七氟烷后15分钟、25分钟（给予或不给予酮洛芬）、35分钟（给予芬太尼）记录正中神经SEPs。结果与基础水平相比,应用七氟烷维持麻醉期间N20潜伏期延长（P=0．015）,中枢传导时间延长（P=0．001）;使用镇痛药物对N20潜伏期和中枢传导时间并没有影响。5-8岁儿童的平均皮层N20-P25的振幅显著降低（P=0．008）。此外,对于年长的儿童,复合用酮洛芬和芬太尼后N20-P25振幅比使用前明显减低（P=0．03）,而在年幼的儿童则没有这样的变化。讨论本研究发现,儿童使用2％七氟烷维持麻醉会延长正中神经的SEPs,与用其他吸入性麻醉药的报道相似。然而,吸入七氟烷时可以进行SEP的监测,但吸入的剂量应根据个体差异调整。复合使用酮洛芬和芬太尼不影响SEP的潜伏期,但posthoc分析结果提示,较年长的儿童皮层波幅会减低。     

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.     

Ventilatory responses to acute and sustained hypoxia during sevoflurane anesthesia in women.

We investigated the isocapnic hypoxic (i.e., pulse oximetry monitored arterial saturations 70%-75%) ventilatory response (HVR) for 20 min in the awake state and during sevoflurane anesthesia at an end-tidal concentration of 1.6% in eight healthy (ASA physical status I) women. Our aims were to determine if a prolonged isocapnic hypoxic period during sevoflurane anesthesia showed a biphasic response pattern (i.e., an initial acute HVR followed by a decline to a lowered sustained HVR) and, if so, to quantify to what extent the acute and sustained HVRs were depressed by anesthesia. The study was conducted before laparoscopic gynecological surgery. Pneumotachography and in-line infrared capnography were used. The pattern of awake biphasic HVR was maintained during anesthesia but was depressed during both the acute and the sustained phases by 60% and 70%, respectively. Further, HVR during anesthesia was accomplished by an increase in respiratory rate, in contrast to an increase in tidal volume in the awake state. In conclusion, sevoflurane anesthesia at 1.6% depresses HVR in women, but the biphasic response is maintained. IMPLICATIONS: Acute and sustained hypoxic ventilatory responses were investigated in eight women before and during sevoflurane anesthesia. A biphasic ventilatory response was persistent but blunted during anesthesia.     

Changes in the latency of the maximum positive peak of visual evoked potential during anesthesia.

The relationship between the latency of visual evoked potential (VEP) and the anesthetic concentration was investigated in surgical patients in order to examine the applicability of VEP in monitoring of the depth of anesthesia. The VEP was recorded with a standard EEG electrode from the midline parietal region in reference to both earlobes linked to the ground. An array of light-emitting-diodes mounted in opaque goggles was used to stimulate both eyes simultaneously and photic stimuli were delivered at random inter-pulse intervals with uniform distribution ranging from 2 to 5 seconds. Fifty trials of data were averaged to estimate that Pmax latency, i.e., the latent period from the photic stimulus to the maximum positive peak arising after 170 msec. Increases in the Pmax latency following the administration of anesthetics and restorations to preanesthetic values after recovery from anesthesia were found. A significant correlation was demonstrated between the Pmax latency and the inspiratory concentration of enflurane. The latency of the Pmax showed a drastic and a sensitive prolongation from about 200 msec in the awake state up to about 600 msec at the stage where the EEG exhibits large-voltage slow waves. Thus the measurement of the Pmax latency of VEPs was found to be useful for monitoring the depth of anesthesia.     

Short latency somatosensory-evoked potentials in children--Part 1. Normative data

Spinal, subcortical, and short latency cortical somatosensory-evoked potentials (SEPs) following electrical stimulation of the median or tibial nerve were studied in 100 children aged 4 weeks to 13 years. Standard neurophysiological methods of recording surface SEPs were used in sedated and nonsedated children. The morphology of the SEPs was similar to that obtained in adults; however, the initial components of the cortical SEP following median nerve stimulation did show maturational changes in both interpeak latencies and morphology. The negative peak latencies recorded over Erb's point (N9 equivalent) and the second cervical vertebra (N13 equivalent) following median nerve stimulation, and over the lumbothoracic junction (N14 equivalent) following tibial nerve stimulation were directly related to patient age and limb length. There was no correlation between age and the latencies of either the initial negativity (N18 equivalent) or the initial positivity (P28 equivalent) of the cortical SEPs following respective median and tibial nerve stimulation. The central somatosensory conduction time decreased slowly during the first decade and attained adult values after 8 years of age. The lumbar spine to scalp transit time showed no direct relationship to age. Comparisons of SEPs recorded in the same subject when awake and under general anesthesia showed that the latencies of the subcortical, spinal, and N1-P1 complex of the cortical SEP are identical; however, the later components of the cortical SEP vary both in latency and amplitude with anesthesia. This study represents normative data against which SEP in children with disorders of the central nervous system may be compared.     

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.     

Propofol anesthesia enhances the pressor response to intravenous ephedrine

The induction of anesthesia with propofol is often associated with a decrease in arterial blood pressure (BP). Although vasopressors are sometimes required to reverse the propofol-induced hypotension, little is known about the effect of propofol on these drugs. We studied the effects of propofol and sevoflurane on pressor response to i.v. ephedrine. Thirty adult patients were randomly assigned to one of two groups. In the Propofol group (n = 15), patients received propofol 2.5 mg/kg i.v. for induction followed by 100 microg x kg(-1) x min(-1) i.v. for maintenance. In the Sevoflurane group (n = 15), anesthesia was induced with sevoflurane 3%-4% in oxygen and maintained with sevoflurane 2% in oxygen. All patients in both groups received ephedrine 0.1 mg/kg i.v. before and after the anesthetic induction. Ephedrine increased the heart rate significantly (P < 0.05) in awake patients in both study groups. In contrast, there was no increase in heart rate after the ephedrine administration under propofol or sevoflurane anesthesia. In awake patients, transient increases in mean BP were observed after i.v. ephedrine in both groups. In the Propofol group, 2 min after the administration of ephedrine, mean BP increased 16% +/- 10% under anesthesia but increased only 4% +/- 6% when the same patients were awake. The magnitudes of the pressor responses to ephedrine during propofol anesthesia were significantly greater (P < 0.05) than during the awake state. However, ephedrine 0.1 mg/kg i.v. showed no significant increases in BP during sevoflurane anesthesia. We conclude that propofol, not sevoflurane, anesthesia augments the pressor responses to i.v. ephedrine. IMPLICATIONS: The effect of anesthetics on vasopressor-mediated cardiovascular effects is poorly understood. We evaluated the pressor response to ephedrine during propofol or sevoflurane anesthesia. Our study suggests that anesthesia-induced hypotension may be easier to reverse with ephedrine during propofol anesthesia than during sevoflurane anesthesia.     

Respiratory effects of sevoflurane

The respiratory effects of sevoflurane were studied in seven patients and compared with values obtained in another seven patients anesthetized with halothane. Resting ventilation, resting PaCO2, and ventilatory response to CO2 were measured awake and at 1.1 and 1.4 MAC levels of both anesthetic agents. We found that with sevoflurane, tidal volume and the slopes of the CO2 response curves decreased and PaCO2 increased with increasing depth of anesthesia, as with other inhaled anesthetics. A compensatory increase in respiratory frequency was not enough to prevent a decrease in minute volume with increasing depth of anesthesia. At 1.1 MAC, sevoflurane produced almost the same degree of respiratory depression as halothane. At 1.4 MAC, sevoflurane produced more profound respiratory depression than halothane.     

Effect of time and dose on scalp-recorded somatosensory evoked potential wave augmentation by etomidate

Bolus etomidate transiently increases the amplitude of scalprecorded somatosensory evoked potentials (SSEPs). The reproducibility of this augmentation and its dose-response relationship are unknown. In unpremedicated patients, we studied the effect on the SSEP of repetitive administration of single doses of etomidate (0.1 mg/kg i.v. bolus) in six patients and increasing doses of etomidate in six additional patients. Anesthesia was induced with fentanyl (15-20 microg/kg i.v.) plus thiopental (1-2 mg/kg i.v.) and maintannined with 0.4-0.8% isoflurane in oxygen, and the surgical incision was infiltrated with bupivicaine (0.5% without epinephrine). Etomidate administration was delayed for 30 min following anesthesia induction. In group 1, 0.1 mg/kg etomidate was administered intravenously as a bolus three times at 30-min intervals. In group 2, 0.05, 0.1, or 0.2 mg/kg was administered at 30-min intervals in random order in each patient. SSEPs were measured immediately before and once each minute for 5 min after etomidate administration following nondominant median nerve stimulation. In group 1, administration of 0.1 mg/kg etomidate (three trials) increased latency of an early negative wave (N20; latency approximately 20 ms) and a positive wave following N20 (P23; latency approximately 23 ms) by 1.0-1.4 and 1.3-2.6 ms, respectively (p < 0.05). P15N20 amplitude was increased by approximately 50% (range 36-76%; p < 0.05) and N20P23 amplitude was increased to 174% of control (range 173-178%; p < 0.05) and the amplitude increase was similar during the three etomidate administrations for both P15N20 and N20P23. Latency remained elevated by approximately 1.5 ms and amplitude remained elevated (P15N20 = 138%; N20P23 = 150%) 5 min following injection. Mean arterial blood pressure was unchanged by 0.1 mg/kg etomidate. In group 2, 0.05 mg/kg etomidate altered neither amplitude nor latency. However, 0.1 and 0.2 mg/kg increased N20P23 amplitude to 161 +/- 33 and 230 +/- 10% of control (p < 0.05), respectively. N20 and P23 latency were increased by 0.1 mg/kg etomidate by approximately 1.0 ms, while 0.2 mg/kg increased N20 latency by 1.0 ms and P23 latency by 1.5 ms. Bolus administration of etomidate (0.1 mg/kg) reproducibly increased SSEP amplitude and a larger dose (0.2 mg/kg) further increased amplitude augmentation. Thus, intermittent injection of etomidate can be used to augment small SSEP waves with reproducible increases in wave amplitude.     

Effects of sevoflurane anesthesia on norepinephrine metabolism in rat brain]

In spite of many investigations done for many years, the mechanism of general anesthesia remains still unclear. To elucidate the mechanism of general anesthesia, effects of sevoflurane anesthesia on norepinephrine metabolism in rat brain was studied. Sevoflurane 3% was administered for 20 minutes to Wistar male rats weighing 230-270g under spontaneous respiration. The rats were sacrificed by decapitation and the brains were rapidly removed. They were dissected into nine discrete regions, locus coeruleus, pons plus medulla oblongata, hypothalamus, thalamus, basal ganglia, hippocampus, amygdala and cerebral cortex. The contents of norepinephrine (NE) and one of its major metabolites, 3-methoxy-4-hydroxyphenyl-ethylene glycol (MHPG) were measured by high performance liquid chromatography with the dual-cell coulometric detector before anesthesia, 20 minutes after the start of anesthesia and at recovery from anesthesia. Significant increases in NE levels were observed in the pons, thalamus and hippocampus by sevoflurane anesthesia for 20 minutes compared with the control group and also in the pons and midbrain at recovery from anesthesia. MHPG levels were significantly decreased in the pons and cortex by sevoflurane anesthesia, while an appreciable increase in MHPG levels was observed in the thalamus by sevoflurane anesthesia. It is concluded that NE metabolism is significantly suppressed in the pons, thalamus and hippocampus during sevoflurane anesthesia and this change in NE metabolism may be associated with a mechanism of sevoflurane anesthesia.     

The effect of sevoflurane and isoflurane on striatal dopamine of awake freely moving rats observed in an in vivo microdialysis study]

We investigated the effect of sevoflurane and isoflurane on the level of interstitial dopamine of in vivo awake, free moving rats brain striatum using microdialysis techniques. Rats were implanted with a microdialysis probe to the right striatum of the brain and administered with 1.2 MAC of each volatile anesthetics for 1 hour, and dialysates from the probe were determined every 20 minutes. Both anesthetics reduced the amount of dopamine derived from dialysate, and increased the efflux of dopamine with pretreatment of nomifensine 10mg. kg-1 i.p. The change of metabolites of dopamine during anesthesia was increased. No significant difference was found between sevoflurane and isoflurane. We hypothesized that these anesthetics might have special actions on interactions between metabolism and re-uptake of dopamine in rats striatum during anesthesia.     

低体温对患者体感诱发电位的影响

目的 评价低体温对患者体感诱发电位(SSEP)的影响.方法 择期心脏手术患者13例,性别不限,年龄23～51岁,体重45～82 kg,ASA分级Ⅱ或Ⅲ级.麻醉诱导后测定双侧正中神经体感诱发电位:于Erb点和第2颈椎棘突分别放置臂丛和颈部记录电极,随后放置头皮电极,分别记录臂丛电位(N9)、颈髓电位(N13)和皮层电位(N20)的峰潜伏期和波幅.记录降温阶段和复温阶段达到目标体温(36、35、34、33 ℃)时的MAP、峰潜伏期和波幅.术后记录显性神经功能缺陷的发生情况.结果 降温阶段随体温降低,峰潜伏期延长,MAP降低(P＜0.05),波幅差异无统计学意义(P＞0.05);复温阶段随体温升高,峰潜伏期缩短(P＜0.05),MAP和波幅差异无统计学意义(P＞0.05);降温阶段峰潜伏期与体温呈负相关,相关系数分别为-0.673(N9)、-0.702(N13)、-0.702(N20)(P＜0.05),以体温为自变量X,峰潜伏期为因变量Y,得到直线回归方程分别为:Y9=-0.558X+28.994,YN13=-1.121X+53.242,YN20=-1.458X+72.036;复温阶段峰潜伏期与体温呈负相关,相关系数分别为-0.634(N9)、-0.619(N13)、-0.600(N20)(P＜0.05),直线回归方程分别为:YN9=-0.505X+27.313,YN13=-0.905X+46.249,YN20=-1.142X+61.668.所有患者术后均未发生神经系统功能缺陷.结论 低体温可延长SSEP峰潜伏期,对波辐无明显影响.

Abstract：

Objective To evaluate the effect of hypothermia on somatosensory evoked potentials (SSEPs). Methods Thirteen ASA Ⅱ or Ⅲ patients aged 23-51 yr weighing 45-82 kg scheduled for cardiac surgery were enrolled in this study. Bilateral median nerve SSEPs (N9, N13, N20) were recorded after induction.The MAP, peak latency and amplitude of N9, N13 and N20 were recorded when the target temperature (36, 35,34, 33 ℃ ) was reached during the cooling and rewarming periods. The neurological dysfunction was recorded after operation. Results The peak latency was prolonged and MAP was decreased with the decrease in the body temperature during the cooling period, the peak latency was shortened with the increase in the body temperature during the rewarming period ( P ＜ 0.05), but no significant change in the amplitudes was found ( P ＞ 0.05). The regression equation of the interaction between the peak latency and body temperature was YN9= -0.558X + 28.994(r=-0.673), YN13 =-1.121X+53.242 (r= -0.702) , YN20 = -1.458X+72.036(r= -0.702) during the cooling period (P ＜ 0.05), and YN9 = - 0.505X + 27.313 ( r = - 0.634), YN13 = - 0.905X + 46.249(r= -0.619), YN20 = - 1.142X + 61.668 (r= -0.600) during the rewarming period (P ＜0.05). No neurological dysfunction was found in all the patients. Conclusion Hypothermia can prolong the peak latency of SSEP and does not alter the SSEP amplitude.     

Effects of sevoflurane anesthesia on dopamine metabolism in the rat brain]

To elucidate the mechanism of general anesthesia, effects of sevoflurane anesthesia on dopamine metabolism in rat brain were studied. Sevoflurane 3% was administered for 20 minutes to Wistar male rats weighing 230-270 g under spontaneous respiration. The rats were sacrificed by decapitation and the brains were rapidly removed. They were dissected into nine discrete regions, locus coeruleus, pons plus, medulla oblongata, hypothalamus, thalamus, basal ganglia, midbrain, hippocampus, amygdala and cerebral cortex. The contents of dopamine (DA) and its major metabolites, 3, 4-dihydroxyphenyl acetic acid (DOPAC) and homovanillic acid (HVA) were measured by high performance liquid chromatography with the dual-cell coulometric detector before anesthesia, 20 minutes after the start of anesthesia and at the recovery from anesthesia. Significant increases in DA levels were observed in the pons, hypothalamus, thalamus and amygdala by sevoflurane anesthesia as compared with the control group. DOPAC levels increased significantly in the pons, hypothalamus, basal ganglia and cerebral cortex at the recovery from anesthesia. A significant increase in HVA levels was observed in amygdala by sevoflurane anesthesia, while an appreciable decrease in HVA levels was observed in hippocampus at recovery from anesthesia. It is concluded that DA metabolism is significantly suppressed in the pons, hypothalamus, thalamus, basal ganglia, midbrain and amygdala during sevoflurane anesthesia and this change in DA metabolism may be associated with the mechanism of sevoflurane anesthesia.     

Evaluation of the Alaris Auditory Evoked Potential Index as an indicator of anesthetic depth in preschool children during induction of anesthesia with sevoflurane and remifentanil

BACKGROUND: Autoregressive modeling with exogenous input of middle latency auditory evoked potentials (A-Line autoregressive index [AAI]) has been proposed for monitoring depth of anesthesia in adults. The aim of this study was to evaluate the performance of the AAI during induction of anesthesia with sevoflurane and remifentanil in pediatric patients. METHODS: Twenty preschool children were anesthetized with sevoflurane and remifentanil. AAI, heart rate, and mean arterial pressure were compared for their ability to distinguish between different hypnotic states before inhalation induction and during sevoflurane anesthesia with and without remifentanil infusion. The prediction probability was calculated for discrimination between the predefined case milestones Awake, Spontaneous Eye Closure, and insertion of a laryngeal mask airway during general anesthesia (Laryngeal Mask Insertion). RESULTS: The AAI (mean +/- SD) in Awake children was 79 +/- 10, declining to 59 +/- 22 at Spontaneous Eye Closure and 34 +/- 13 when anesthetized. AAI values significantly overlapped between anesthetic states. For the AAI, the prediction probabilities regarding the ability to discriminate the hypnotic state at the case milestones Awake versus Spontaneous Eye Closure and Awake versus Laryngeal Mask Insertion were 0.77 and 0.99, respectively. In terms of prediction probability values, heart rate and mean arterial pressure were not indicative for anesthetic states. Remifentanil did not influence the AAI. CONCLUSION: During induction of pediatric patients with sevoflurane, the AAI is of higher value in predicting anesthetic states than hemodynamic variables and reliably differentiates between the awake and anesthetized states. However, individual AAI values demonstrate significant variability and overlap between different clinical conditions.     

Diagnostic value of short latency somatosensory evoked potentials for various intracranial lesions

Diagnostic value of short latency somatosensory evoked potentials (SSEP) was studied in 124 patients with various intracranial lesions. Abnormal SSEPs were recorded in 58 of 124 patients (46.8%) and were classified into three types. Type I (6 cases) showed abnormality of late components with N18 being preserved. All patients with type I abnormality had cortical or subcortical lesions in the parietal lobe. Type II (20 cases) was characterized by abnormality of N18 and late components with N16 being preserved, and mainly seen in patients with a lesion involving thalamus and internal capsule. Type III (31 cases) showed abnormality of N16 and N18 which was elicited by unilateral stimulation (IIIa: 11 cases), or bilateral stimulation (IIIb: 21 cases), and this indicated brainstem impairment. The incidence of SSEP abnormality was as high as 93.1% in patients with sensory disturbance, and 23.1% in patients without such disturbance, and it was suggested that SSEP is useful to detect subclinical dysfunction in the somatosensory pathway. The SSEP grades defined by Anderson et al were found to be well correlated with the outcome of patients with severe head injury, and the SSEP was more reliable for predicting the outcome of patients than the auditory brainstem evoked responses. The SSEP grades were also fairly well correlated with the outcome of patients with cerebrovascular accidents, although the outcome was not consistent in patients with moderately abnormal SSEP.     

N2O-free sevoflurane anesthesia. Clinical evaluation

BACKGROUND: The characteristics of sevoflurane make it able to be used without N2O avoiding its undesirable effects to this associates. The aim of the study is to evaluate the clinical characteristics of sevoflurane anesthesia "N2O free" in comparison to sevoflurane anesthesia with N2O. METHODS: 920 patient undergoing elective surgery in 12 centers were included in this study. All the patients were monitored with routine monitoring. The patients were randomized in two groups: group Air in which the anesthesia was maintained with sevoflurane in Air:O2; group N2O in which the anesthesia was maintained with sevoflurane in N2O:O2. Opioids were administered as necessary (changes of the heart rate and/or of the arterial pressure > 20% in comparison to the baseline values). For each patient we evaluated the consumption of opioids, the time from discontinuation of the sevoflurane and the extubation and full recovery, defined as presence of a complete cognitive function; the quality of awakening, the incidence of postoperative nausea and vomiting (PONV) and the quality of postoperative analgesia. RESULTS: We didn't observe differences between the two groups. In conclusions, omitting N2O during sevoflurane anesthesia can be considered a safe technique, avoiding the acute and chronic side effects associated with the use of N2O, without modifying the intraop consumption of opioid, the recovery and the early postoperative incidence of nausea, vomiting and analgesia.     

The effect of low dose sevoflurane on saccadic eye movement latency

We investigated the effects of a low concentration of sevoflurane on a saccadic eye movement task that reflects the performance of higher neural decision and control mechanisms. The experiments were performed double-blind in five subjects, using either 0.15% end-tidal sevoflurane in oxygen, or pure oxygen as a placebo. Saccades were recorded and analysed using a computer-based recording system that also controlled the presentation of visual targets. Administration of oxygen produced no significant change in median latency compared with breathing air; but in four of the five subjects, administration of sevoflurane in oxygen caused a significant increase in latency. These results suggest that measurement of median saccadic latency may be a useful functional measurement of impairment of performance during recovery from anaesthesia.     

Bispectral index monitoring: a comparison between normal children and children with quadriplegic cerebral palsy

We performed this study to compare the correlation of bispectral index (BIS) values with different sevoflurane concentrations between normal children and those with quadriplegic cerebral palsy with mental retardation (CPMR). Twenty children with CPMR (Group I) and 21 normal children (Group II) between 2 and 14 yr of age were studied. Anesthesia was induced and maintained with sevoflurane and 66% N(2)O/O(2). Bispectral values were recorded on an Aspect Medical Systems (Natick, MA) monitor, and sevoflurane concentrations were measured with an Ohmeda (Hanover, MA) inhaled anesthetic monitor. The BIS values were recorded after midazolam premedication; after the induction of anesthesia; at end-tidal sevoflurane concentrations of 1%, 3%, and again at 1%; and after emergence from the anesthetic. Both groups were similar in age and sex distribution, but children in Group I weighed less than those in Group II (P < 0.05). The BIS values were significantly lower in Group I compared with Group II after sedation, at 1% sevoflurane concentrations, and after emergence. No difference was observed between the two groups at anesthesia induction (8%) and at 3% sevoflurane concentration. We conclude that, in children with CPMR, BIS values exhibit a pattern of change similar to that observed in normal children. However, absolute BIS values obtained in such children are lower than those in normal children while awake and at different sevoflurane concentrations. IMPLICATIONS: We compared bispectral (BIS) values with different sevoflurane concentrations between normal children and children with cerebral palsy. We observed that, in children with cerebral palsy, BIS values exhibited a similar pattern of change as is observed in normal children. However, absolute BIS values obtained in such children are lower than those in normal children while awake and at different sevoflurane concentrations.     

Coasting after overpressure induction with sevoflurane

STUDY OBJECTIVE: To evaluate the clinical feasibility of using a coasting technique to temporarily maintain anesthesia after overpressure induction with sevoflurane. STUDY DESIGN: Prospective clinical study. SETTING: Large teaching hospital. PATIENTS: 12 ASA physical status I, II, and III patients receiving general anesthesia for a variety of peripheral procedures. INTERVENTIONS: After overpressure induction of anesthesia with sevoflurane (8%) in an O(2)/N(2)O mixture, the fresh gas flow (FGF) was lowered to 0.5 L/min and the vaporizer was turned off (coasting). MEASUREMENTS AND MAIN RESULTS: After priming a circle system with sevoflurane (8% sevoflurane vaporizer setting in 6 L/min O(2)/N(2)O [33%/66%] for 30 s), patients took several vital capacity breaths from the mixture until loss of consciousness. After 3.4 +/- 0.7 min, depth of anesthesia was considered adequate for laryngeal mask airway (LMA) insertion, and FGF was reduced to 0.5 L/min (33% O(2), 66% N(2)O) and the sevoflurane vaporizer was turned off. The end-expired sevoflurane concentration (Et(sevo)) decreased from 5.8 +/- 1.3% just before insertion of the LMA to 0.97 +/- 0.22% at 20 minutes. CONCLUSIONS: After overpressure induction with sevoflurane, coasting during minimal flow anesthesia (FGF 0.5 L/min) is a simple technique that can maintain anesthesia for short procedures (less than 15 to 20 min), or can be used as a bridge or an adjunct to other low-flow techniques.