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.     

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.     

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)     

Somatosensory evoked potentials under thiopental and etomidate

The somatosensory evoked potential in response to median nerve stimulation was recorded in 42 patients during infusion of either 15 mg/kgbw thiopentone (TH) or 1 mg/kgbw etomidate (E) within 15 min and before and after injection of 0.3 mg/kgbw etomidate bolus. Cortical and cervical responses were analysed simultaneously and central conduction time (CCT) was calculated. Marked alterations of waveforms and an increase in latency of the primary cortical SEP and of CCT were observed in all patients. Infusion of TH or E was followed by a diminution of middle and long latency components. Amplitude of the cortical N20 was found to be unchanged during and after TH and to be increased after infusion or injection of E, indicating the synchronizing properties of this drug. The cervical SEP (N14) remained entirely unchanged in response to both agents. During hypnotic drug administration a pronounced increase in latencies and CCT as well as a decrease in the number of identifiable peaks has to be considered when SEP monitoring is performed intraoperatively or in intensive care treatment.     

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。     

SOMATOSENSORY AND AUDITORY EVOKED RESPONSES RECORDED SIMULTANEOUSLY: DIFFERENTIAL EFFECTS OF NITROUS OXIDE AND TSOFLURANE

Auditory (AER) and somatosensory evoked responses (SSER) wererecorded simultaneously in eight patients under anaesthesiabefore surgery. We studied the effects of equi-MAC end-expiratoryconcentrations of isoflurane (0.65–0.75%) and nitrousoxide (60–65%). The anaesthetics were changed at randomin three consecutive 10-min periods so that each patient receivedboth drugs. From the AER recorded from the vertex and inion.Pa and Nb latency and amplitude were measured. N13, P20 latencyand N13 amplitude were measured from SSER recordings from theneck and P15, N20. P25, N35, P45 latency and P15-N20, N20-P25,P25-N35 and N35-P45 amplitude from the scalp over the hand areaof the sensory cortex. Compared with nitrous oxide, isofluranesignificantly increased the latencies of the AER waves Pa (P= 0.02) andNb (P = 0.02), and the SSER waves N20 (P = 0.001)and P25 (P = 0.04). We were unable to demonstrate significantdifferences in Pa and Nb amplitude between isoflurane and nitrousoxide that we had seen previusly. However, the amplitude ofthe SSER wave N20 was reduced significantly by nitrous oxidecompared with isoflurane (P = 0.0004). This wave (N20) is thoughtto emanate from the thalamo-cortical radiations, and our findingsmay be explained by an analgesic effect of nitrous oxide mediatedby endogenous opioids. ^*Present address: Department of Anaesthesia, Royal Free Hospital,Pond Street, London NW3.     

Effects of etomidate, midazolam, and thiopental on median nerve somatosensory evoked potentials and the additive effects of fentanyl and nitrous oxide

In 30 patients undergoing spinal disc operations, the effects of bolus injections followed by intravenous infusions of thiopental, etomidate, and midazolam on median nerve somatosensory-evoked potentials (SSEPs) were studied. Possible additive effects of fentanyl and nitrous oxide were also evaluated. Serial SSEP measurements were made before and for 25 minutes after the start of anesthesia. After induction with one of the three intravenous agents, fentanyl (10 micrograms/kg) was administered and SSEPs were again measured 1 and 5 minutes after administration. Sixty-five% nitrous oxide in 35% oxygen was administered after tracheal intubation and was followed by final SSEP measurements. The three intravenous agents affected SSEP signals differently. Etomidate increased both amplitude and latency. Thiopental decreased amplitude and increased latency. Midazolam had no effect on amplitude but increased latency. The addition of fentanyl and nitrous oxide had different effects in response to the three intravenous induction agents. This study emphasizes the differences in SSEP responses not only to different intravenous induction agents but also to the addition of fentanyl and nitrous oxide.     

不同剂量异丙酚、咪唑安定和依托咪酯对上肢短潜伏期体感诱发电位的影响

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、3mg/kg,咪唑安定0.2、0.3、0.4mg/kg,依托咪酯0.15、0.3、0.4mg/kg,观察用药后对SLSEP的影响。结果:异丙酚组均对SLSEP的N_14、N_20潜伏期和CCT无明显影响,但使N_20-P_25波幅显著性抑制,该作用在用药后10分钟恢复。咪唑安定组均使N_20潜伏期和CCT显著延长,且在病人苏醒后仍未恢复,对N_(14)潜伏期无影响,N_(20)-P_(25)波幅出现明显下降。依托咪酯组出现N_(20)-P_(25)波幅明显增大,且在病人苏醒后仍未降至基础值,对潜伏期的影响与咪唑安定类似。结论:依托咪酯较适合术中行诱发电位监护时应用。     

Somatosensory evoked potential peak latencies and amplitudes in contralateral and ipsilateral hemispheres in normal and severely traumatized brain-injured subjects

The purpose of this study was to compare in normal and traumatic brain injury (TBI) subjects long latency cortical brain-evoked potential patterns obtained upon stimulation of the median nerves. Quantitative data were analysed involving nine peak latencies and eight amplitudes obtained simultaneously contralaterally and ipsilaterally. Left-right hemispheric differences were also analysed. The following was found: TBI latencies were significantly longer for five of nine peaks (N30, P40, N60, P185, P285). TBI amplitudes were significantly smaller for two of eight amplitudes (P185-N240 and N240-P285). A significant contralateral-ipsilateral latency difference occurred only at P40 where latencies in the contralateral hemisphere are shorter for both normals and TBIs. Significant contralateral-ipsilateral amplitude differences occurred in the four early amplitudes (N30-P40, P40-N60, N60-P105, P105-N140) with amplitudes being smaller on the ipsilateral side. A differential effect, however, was found for amplitudes N30-P40 and P40-N60 where the difference is significantly larger in the contralateral hemisphere for normals but not for TBIs. This suggests that contralateral-ipsilateral amplitude difference can be a marker of extent and severity of injury and may also be helpful in localizing site of injury, particularly interhemispheric or corpus callosal injury. The differential latency and amplitude responses for later peaks occurring in the P300 region suggest sensitivity to detecting impairments in pre-cognitive and early cognitive activities.     

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     

Comparison of the effects of remifentanil or fentanyl on anaesthetic induction characteristics of propofol,thiopental or etomidate

BACKGROUND AND OBJECTIVE: This prospective, randomized, double-blinded study was designed to compare the effects of remifentanil or fentanyl on anaesthetic induction characteristics of propofol, thiopental or etomidate. METHODS: Seventy-two patients were enrolled in six groups of 12 individuals each. In three groups, fentanyl was given as a bolus dose of 1.5 microg kg(-1), whereas the others received a remifentanil infusion at 0.5 microg kg(-1) min(-1). Five minutes later, propofol, thiopental or etomidate were titrated to a state of unresponsiveness. Assessment included the amounts of drug necessary for induction, haemodynamics and the times to apnoea, loss of eyelash reflex, and the release of a water-filled syringe held in the patient's hand. RESULTS: Induction times to loss of the eyelash reflex were significantly shorter in the remifentanil than in the fentanyl groups: with propofol 50.7 +/- 13.6s (mean +/- SD) versus 74.9 +/- 27.0s (P < 0.01), with thiopental 42.9 +/- 16.8s versus 77.2 +/- 27.8s (P < 0.01) and with etomidate 54.7 +/- 17.6s versus 72.3 +/- 24.0s (P < 0.05). The times to respiratory arrest or for the syringe to fall were significantly shorter with remifentanil than with fentanyl for propofol and for thiopental, but not for etomidate. In terms of dosages per kg body weight necessary to achieve unresponsiveness, less propofol (-29%, P < 0.05), thiopental (-25%, P < 0.05) or etomidate (-32%, P < 0.01) was necessary with remifentanil than with fentanyl. Haemodynamic responses to tracheal intubation were controlled more effectively with remifentanil. However, within the remifentanil groups, mean arterial pressure significantly decreased during induction: -26% with propofol, -181% with thiopental and -14% with etomidate (all P < 0.01). CONCLUSIONS: During anaesthetic induction, a remifentanil infusion of 0.5 microg kg(-1) min(-1) over 5 min is a suitable alternative to a 1.5 microg kg(-1) bolus dose of fentanyl: induction times are shorter with reduced amounts of propofol, thiopental or etomidate.     

硫喷妥钠对上肢短潜伏期体感诱发电位的影响

目的与方法：７例上肢感觉传导道无异常的病例,静脉注射硫喷妥钠５ｍｇ／ｋｇ后,分别观察注药前、注药后即刻、２、４和６ｍｉｎ上肢短潜伏期体感诱发电位,比较Ｐ１５、Ｎ２０、Ｐ２５各波的潜伏期以及Ｐ１５Ｎ２０、Ｎ２０Ｐ２５的峰间值。结果：各波潜伏期在注药后缩短,以注药后２、４ｍｉｎ最明显,６ｍｉｎ时已基本恢复,Ｐ１５Ｎ２０、Ｎ２０Ｐ２５峰间值在注药后减小,以２ｍｉｎ时减至最小,６ｍｉｎ时已基本恢复。结论：术中行体感诱发电位监测时,不宜使用硫喷妥钠。     

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.     

Somatosensory evoked potential monitoring during intracranial surgery

In the neurosurgical approach to intracranial aneurysms which are often accompanied by arterial spasm and cortical ischaemia, monitoring procedures aim to obtain useful information on cerebral function. SEPs evoked by stimulation of the median nerve at the wrist and of the tibial nerve at the medial malleolus were registered in 45 patients with intracranial aneurysms during neurosurgical procedures. Our results show SEP abnormalities during different stages of neurosurgical procedures in 36 patients out of the monitored 45. Significant abnormalities of SEPs with respect to the control group were decrease of the amplitude of N 20-P 25 complex, lengthening of the absolute latency of the waves N 20- and P 25 and lengthening of the central conduction time (CCT) (N 13-N 20). The greatest SEP abnormalities were registered during the neurosurgical approach to aneurysm and during the clipping procedure. However, the changes were reversible in the majority of the patients. The aim of this paper was to focus on early detection of some cerebral function disturbances during the neurosurgical procedure as well as the prevention of possible brain damage.     

Total intravenous anesthesia for improvement of intraoperative monitoring of somatosensory evoked potentials during aneurysm surgery.

Two anesthetic regimens for monitoring somatosensory evoked potentials (SEPs) during intracranial aneurysm surgery were compared. Eighty-four sequential cases of intracranial aneurysms were operated on employing SEP monitoring. The first group of 22 cases was anesthetized with "balanced anesthesia" and the second group of 62 cases received total intravenous anesthesia (TIVA) consisting of propofol and alfentanil. In the TIVA group, the amplitude of early cortical SEP responses (N20-P25, or P40-N50) was significantly higher than that of responses in the balanced anesthesia group. In median nerve SEPs, the averaged amplitude of N20-P25 was 3.22 microV with TIVA and 1.69 microV with balanced anesthesia (P = 0.006). Similarly, posterior tibial nerve SEPs showed a P40-N50 response of 1.85 microV and 1.00 microV, respectively (P = 0.017). The superior signal-to-noise ratio obtained with TIVA allowed more frequent and reliable intraoperative SEP recordings than was possible with balanced anesthesia, resulting in rapid and reliable feedback for the surgeon. In 19% of median nerve SEPs recorded with TIVA, the cortical responses were over 5 microV in amplitude, so that reproducible N20-P25 responses were obtainable by averaging only 10 to 50 serial responses, that is, two to three recordings per minute. The higher amplitude of posterior tibial nerve SEPs recorded with TIVA made monitoring during surgery for anterior communicating artery aneurysms possible in all cases. This was not always the case with balanced anesthesia. The late deflection of median nerve SEPs (N30) was more frequently observed with TIVA.(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.     

Visual evoked potentials during etomidate administration in humans

The effects of etomidate on visual evoked potentials (VEP) were studied in 22 patients undergoing gynaecological procedures. They were divided into two groups: the etomidate group (12 patients) and the fentanyl-N₂O- etomidate group (ten patients). In the etomidate group, etomidate 0.3 mg · kg^?1 was given as a bolus injection during induction of anaesthesia which was followed by an infusion of etomidate 0.05 mg · kg^?1 · min^?1. No significant changes were observed in the amplitudes of P100 or N70. Latencies of the P60, N70, and P100 were slightly increased. In thefentanyl-N₂O-etomidate group, a bolus injection of 0.3 mg · kg^?1 of etomidate was given during anaesthesia with 3–4 μg · kg^?1 of fentanyl and 60 per cent nitrous oxide. The amplitude of the P100 was significantly decreased and the latencies of the P60 and N70 were signficantly increased. In conclusion, interpretation of the VEP during etomidate administration alone was not hard to perform but, when given together with fentanyl-nitrous oxide anaesthesia, the VEP was affected significantly making its interpretation difficult.

     

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.     

Clinical study on short latency somatosensory evoked potentials for cervical myelopathy]

The purpose of this study was to examine the clinical value of S-SEP (short latency somatosensory evoked potentials) as a routine test of spinal cord function. On the basis of a preliminary study determining the optimal recording conditions in normal individuals, S-SEP measurement was carried out in patients with cervical myelopathy to examine its diagnostic value for spinal cord lesions. In these patients, the best recordings of N9, N11, and N13 were obtained from the cervical spinous processes with linked ear reference (A1 + A2). In severe myelopathy, the N11-N13 interpeak latency was prolonged. Those with impaired bladder function or decreased deep sensation showed a prolonged N9-N13 interpeak latency. In cases of C3-4 and C4-5 lesions, the N9-N13 and N9-P14 interpeak latencies were significantly more prolonged than in those with C5-6 lesions. The interpeak latencies from P14 to N9 and N11 gradually became shorter postoperatively.     

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.