Visual evoked potentials during thiopentone-fentanylnitrous oxide anaesthesia in humans

Visual evoked potentials (VEP) during thiopentone-fentanylnitrous oxide anaesthesia were studied in 15 healthy patients undergoing non-neurosurgical procedures. The VEP was recorded before and at 1 and 2 min after induction of anaesthesia with 5–6 mg · kg⁻¹ of thiopentone. After recording the 1 and 2 min VEPs, anaesthesia was maintained with a fentanylnitrous oxideoxygen combination, and further recordings were made at 5, 10, 15 and 20 min after induction. The 1 and 2 min VEPs showed a marked decrease in the amplitudes. Latencies were increased. The amplitudes gradually returned to the control level at 15 min, while the latencies remained increased throughout the study period. In conclusion, thiopentone should be avoided during the critical period of VEP recording. Once it is given, at least 15 min should elapse before an appropriate interpretation of the VEP can be made. Thiopentonefentanylnitrous oxide anaesthesia slightly increases the latencies of the VEP. These effects should be considered in the interpretation of the VEP when thiopentone-fentanylnitrous oxide anaesthesia is used. Nous avons enregistré les potentiels évoqués visuels (PEV) de 15 patients anesthésiés au thiopental-fentanyl-protoxyde d’azote pendant une intervention non neurochirurgicale. Les mesures avaient lieu une et deux minutes après l’injection de 5–6 mg · kg⁻¹ de thiopental puis sous fentanyl et protoxyde d’azote 5, 10, 15 et 20 minutes après l’induction. A une et deux minutes, les PEV avaient une période de latence prolongée et une amplitude réduite. Cette dernière revint progressivement à la normale au bout de 15 minutes mais la période de latence demeura allongée jusqu’ à la fin de l’étude. Ainsi, le thiopental interfère avec l’interprétation des PEV et cet effet dure au moins 15 minutes. L’anesthésie au thiopental-fentanyl-protoxyde d’azote prolonge aussi légèrement la période de latence des PEV. On devra tenir compte de ces effets dans l’ interprétation des PEV.

---

Presented in part at the American Electroencephalographic Society’s annual meeting, San Diego, CA, October 1988.     

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.     

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.     

Effects of thiopental, fentanyl, and etomidate on upper extremity somatosensory evoked potentials in humans

The effects of three anesthetic induction agents on somatosensory evoked potentials (SEP) were assessed in unpremedicated patients who were without neurologic abnormality of the upper extremities. SEP was assessed by stimulation of the nondominant median nerve and responses were recorded over Erbs point (N10), second cervical vertebra (N14), and the contralateral cortex (P15, N20, P23 latencies, and P15-N20 and N20-P23 amplitudes). Nine patients received thipental (4 mg/kg, iv bolus), nine patients received fentanyl (25 micrograms/kg, iv bolus), and nine patients received etomidate (0.4 mg/kg, iv bolus). SEP was assessed before and after drug administration at motor threshold stimulus intensity. Thiopental increased the latency of N10, N14, and N20. The amplitudes of N10-, N14-, and scalp-recorded waves were not altered by thiopental. Fentanyl increased N20 and P23 latency and decreased the amplitude of P15-N20. Etomidate increased latency of N20 and P23 without alteration of latencies of N10 or N14 and increased the amplitude of P15-N20 and N20-P23, while the amplitude of N10 was unchanged and the amplitude of N14 was decreased. It is concluded that thiopental or fentanyl causes only modest alterations in early waves of upper extremity SEP, whereas etomidate increases the amplitude of scalp-recorded waves. The effect of etomidate on SEP may make diagnosis of neurologic injury more difficult because of the changing waveform.     

Somatosensory evoked potentials during hypoxia and hypocapnia in conscious humans

Purpose

The objective of the study was to evaluate the effects of moderate hypoxia and hypocapnia on the latency and amplitude of cortical somatosensory evoked potentials (SSEPs) in conscious human subjects.

Methods

In ten volunteers the amplitude and latency of the cortical somatosensory evoked potentials were recorded during stimulation of the left posterior tibial nerve. Measurements of SSEPs and respiratory variables were made breathing ambient air, air containing a reduced oxygen percentage (17% O₂, 14% O₂(n = 6) or 11% O₂ (n = 10)), and again during voluntary hyperventilation breathing ambient air (PEtCO₂ = 20 mmHg, n = 10).

Results

Hypoxia (11% O₂) caused mild stimulation of ventilation (P < 0.05) but had no effects on the latency or amplitude of the SSEP. Lesser degrees of hypoxia had no effects. Hyperventilation caused a small (2–4%) decrease) in the latency of the SSEP and an increase in the amplitude of the SSEP (P< 0.05).

Conclusions

These findings in conscious subjects were consistent with previous observations in anaesthetized humans and anaesthetized dogs and show that the decrease in latency of the SSEP associated with hypocapnia is not due to changes in the depth of anaesthesia. These effects of hypocapnia may contribute to small variations in the latency of the SSEP when monitoring is performed during surgery, but are unlikely to be large enough to be of clinical concern.     

Effects of ketamine on somatosensory evoked potentials during nitrous oxide anesthesia in humans

The effects of ketamine with 60% nitrous oxide were studied on subcortical sensory evoked potentials recorded at Erb's point (N9), neck (N13) and on cortical potentials recorded at the scalp (N20) following median nerve stimulations in 7 neurologically normal patients. Latencies and amplitudes of the potentials were measured and compared with postinduction control values taken during inhalation of 60% nitrous oxide. Ketamine 2 mg.kg-1 (iv) was administered initially and incremental dose was 50 micrograms.kg-1.min-1. N20 latency decreased at 15, 30 minutes after ketamine administration from a control value of 18.7 +/- 0.9 msec to 18.2 +/- 1.1, 18.2 +/- 1.1 msec respectively, and N13-N20 interpeak latency decreased from 6.0 +/- 0.4 msec to 5.5 +/- 0.7, 5.4 +/- 0.7 msec (mean +/- SD). The author concluded that during nitrous oxide-based anesthesia, ketamine did not inhibit specific thalamoneocortical pathways.     

Auditory evoked potentials during isoflurane anaesthesia

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

Somatosensory evoked potentials during isoflurane anaesthesia

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

Visual evoked potentials (VEP) in anesthesia and intensive care

Methodological considerations and different stimulation techniques of visual evoked potentials (VEP) are described. VEP can provide information about neurological function during anaesthesia, surgery and in the unconscious patient after head injury. The feasibility of the method for intraoperative monitoring in neuro- and cardiac surgery and the influence of general anaesthetics and other contributing factors such as temperature, paCO2, pO2, part are discussed.     

The effect of etomidate on motor evoked potentials induced by transcranial magnetic stimulation in the monkey

Etomidate (ET) is a known hypnotic agent in neuroanesthesia. This study was designed to examine the reliability of motor evoked potentials (MEPs) after transcranial magnetic stimulation in monkeys anesthetized intravenously with ET. The ET regimen was as follows: an initial dose (0.5 mg/kg) followed by 13 doses (0.2 mg/kg every 6-12 min; mean, 8.0 +/- 1.3 min). The total dose administered was 3.1 mg/kg. The magnetic coil was placed over the MEP scalp stimulation region. Evoked electromyographic responses were recorded from the contralateral abductor pollicis brevis (APB) and abductor hallucis (AH) muscles of the fore- and hindlimbs, respectively. Reproducible MEP responses were consistently recorded while the animal was under total ET anesthesia. The coil demography was altered and the MEP scalp topography was moderately reduced by ET injections. Significant threshold elevation was noted after a total dose of 1.7 mg/kg for APB responses and 0.5 mg/kg for AH responses (P less than 0.05). Marked prolongation of latency was observed after a dose of 0.5 mg/kg for APB MEPs and 2.5 mg/kg for AH MEPs (P less than 0.05). MEP amplitude responses showed marked variability. Repeated doses of ET produced a mean threshold rise of 14 to 28% for the APB and 19 to 29% for the AH. The mean latency delay was 5 to 11% for the APB and 0.5 to 8% for the AH, while the mean amplitude depression was 24 to 59% for the APB and 15 to 50% for the AH. Apparent seizure activity or abnormalities in behavior and feeding were not noted over a 1-year period.(ABSTRACT TRUNCATED AT 250 WORDS)     

Visual evoked potentials in tumors from orbita to occipital lobe in childhood

68 infants and children with proven tumours along the visual pathway visually evoked potentials with pattern reversal and flash were investigated. Subdivided in 5 locational groups (orbital, optic nerve, chiasmatic, retrochiasmatic and occipital lobe) best results were obtained by stimulation with pattern reversal using variable checksizes (91.2%) versus 61.8% by using flash evoked responses. Furthermore, using patterned stimuli not only latency shifts are best detected but also hints for visual function correlating to visual acuity could be given also in nonverbal or disabled children. For long term follow-up studies in known space-occupying lesions along the visual pathway, the use of pattern VEP is extraordinary because of its high sensitivity and complete harmlessness. Pattern VEP are even more sensitive than visual acuity testing in cooperative patients. The close interdisciplinary follow-up controls in these children between pediatric neurophysiologists and neurosurgeons are, therefore, strongly recommended.     

Motor evoked potentials from transcranial stimulation of the motor cortex in humans

Electrical monitoring of the motor system offers the potential for the detection of injury, the diagnosis of disease, the evaluation of treatment, and the prediction of recovery from damage. Existing evoked potentials monitor one or another sensory modality, but no generally usable motor monitor exists. We have reported a motor evoked potential using direct stimulation of the spinal cord over the motor tracts in cats and in humans. To achieve a less invasive monitor, we used transcranial stimulation over the motor cortex in the cat, thus stimulating the motor cortex. We report here the initial application of this method to humans. A plate electrode over the motor cortex on the scalp and a second electrode on the palate direct a mild current through the motor cortex which will activate the motor pathways. This signal can be recorded over the spinal cord. It can elicit contralateral peripheral nerve and electromyographic signals in the limbs or movements when the appropriate stimulation parameters are used. In clinical use to date, this has been more reliable than the somatosensory evoked potential in predicting motor function in patients where the two tests differed. It offers a number of possibilities for the development of valuable brain and spinal cord monitoring techniques, but requires further animal studies and clinical experience. Studies to date have not demonstrated adverse effects, but evaluation is continuing.