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Effects of thiamylal, sevoflurane and isoflurane on the cortically recorded somatosensory evoked potentials

Fukui, K.; Morioka, T.; Hisada, K.; Nishio, S.; Irita, K.; Takahashi, S.

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European Journal of Anaesthesiology: December 2002 - Volume 19 - Issue 12 - p 899-901

EDITOR:

Continuous recordings of somatosensory-evoked potentials (SEPs) during operations are very useful when monitoring neural function and to prevent neurological injury. Although it is well known that anaesthetic agents produce alterations in SEPs that may mimic neural injury, there have been few reports of comparative studies on the effects of different anaesthetics. Since SEPs recorded from the scalp have low amplitude and require much averaging, very small changes cannot be detected. However, cortical recordings of SEPs have a good signal-to-noise ratio that allows smaller numbers of averages and enables the acquisition of updated information every few seconds. We recorded serially cortical SEPs, with chronically implanted subdural grid electrodes on the peri-Rolandic cortex in an epileptic patient, from the induction to the maintenance stage of anaesthesia (before surgical procedures), and we compared the effects of thiamylal, sevoflurane and isoflurane on cortical SEPs.

A 24-yr-old male had a 23-yr history of intractable complex partial seizures. Magnetic resonance imaging (MRI) revealed a schizencephalic cleft in the right peri-Rolandic area, focal cortical dysplasia in the right medial parietal lobe and right hippocampal atrophy. He underwent a right frontotemporoparietal craniotomy for the placement of subdural grid electrodes on the frontal, temporal and parietal lobes to detect the epileptogenic cortex. Videoelectrocorticography monitoring demonstrated ictal discharge from the right medial temporal lobe, and that area was determined to be the focus of the habitual seizures. A right anterior temporal lobectomy and hippocampectomy was then scheduled and informed consent was obtained before surgery.

No sedative premedication was given, and electrical stimulation of the median nerve at the wrist was achieved with square wave pulses, 0.1 ms in duration and 5 Hz in frequency. Somatosensory-evoked potentials were recorded from the subdural electrodes on both the hand sensory and motor cortices - which had been identified by preoperative electrical cortical stimulation - by using a Synax 1100® averager (GE Marquette Medical Systems, Japan, Tokyo) with a bandpass filter setting between 10 and 3000 Hz and averaging 50 responses with an analysis time of 50 ms. From the sensory cortex, a primary sensory cortical response of N20 was recorded with a latency of 18.2 ms (Fig. 1, left column, upper trace). On the motor cortex, a P22 component, which was thought to be a phase-reversal component of N2O, was recorded with latency of 19.7 ms (Fig. 1, right column, upper first trace).

Figure 1
Figure 1:
Serial recording of somatosensory-evoked potentials recorded with a chronically implanted subdural grid electrodes on the peri-Rolandic cortex in an epileptic patient, from the induction to the maintenance stage of anaesthesia. Before anaesthesia, from the sensory cortex, the primary sensory cortical response of N20 was recorded with a latency of 18.2 ms (left column, upper trace). On the motor cortex, the P22 component was recorded with a latency of 19.7 ms (right column, upper trace). After intravenous administration of barbiturate (thiamylal) 175 mg, the latencies of N20 and P22 increased (22.8 and 23.6 ms, respectively) and the amplitudes markedly decreased (upper second traces). Furthermore, late components following N20 and P22 were abolished. Additional thiamylal 250 mg was given before intubation, and SEPs showed similar changes. With inhalation of sevoflurane (1-0.5 MAC), attenuation of N20 and P22 by prolonged latency (21.3 and 21.6 ms, respectively) and decreased amplitude were also observed. However, the effects were less prominent than those of barbiturate (upper fourth and fifth traces). Late components following N20 and P22 were visible. With isoflurane (0.5-1 MAC), attenuation of N20 and P22 was almost identical to that of sevoflurane (lower second and first traces).

Anaesthesia was induced with an intravenous (i.v.) bolus injection of thiamylal 175 mg, and vecuronium 6 mg was given to produce neuromuscular block. On SEPs, the latencies of N20 and P22 were increased (22.8 and 23.6 ms, respectively) and the amplitudes were markedly decreased (Fig. 1, upper second traces). Furthermore, late components following N20 and P22 were abolished. Additional thiamylal 250 mg was given i.v. before tracheal intubation, and SEPs showed similar changes. After the trachea was intubated, the patient's lungs were mechanically ventilated and sevoflurane (1-0.5 MAC) in 50% nitrous oxide and oxygen given for the first 25 min. The purpose of the sevoflurane inhalation was to confirm the irritative area with chemical activation of the epileptogenic cortex. On SEPs, attenuation of the N20 and P22 by prolonged latency (21.3 and 21.6 ms, respectively) and decreased amplitude were observed; however, the effects were less prominent than those of thiamylal (Fig. 1, upper fourth and fifth traces). Late components following N20 and P22 were also attenuated but visible. With 1 MAC and 0.5 MAC of sevoflurane inhalation, SEP changes were not so different.

Next, the anaesthetic was changed to isoflurane (1-0.5 MAC) and 50% nitrous oxide in oxygen using mechanical ventilation. On SEPs, attenuation of N20 and P22 were almost identical to those of sevoflurane (Fig. 1, lower second and first traces).

The results suggest that the effects of thiamylal on SEPs are greater than those of sevoflurane and isoflurane. Although no comparative study of the effects of these anaesthetics on SEPs in one identical patient was seen, it seems that barbiturates have a lesser influence on SEPs than the inhalation anaesthetics [1-4]. In those studies, barbiturates were given by infusion in contrast to our bolus injection. Sloan and colleagues [5] reported that significant changes in cortical SEP occurred rapidly after bolus injection of thiopental. Bolus injection will produce a very acute and prominent elevation of drug serum concentration, and this may explain this dramatic change in SEPs [3,6]. However, like the other barbiturates, volatile anaesthetics are known to produce dose-related increases in latency and a reduction in amplitude of SEPs [7]. However, in the present study, obvious changes from different concentrations of inhalational agents were not seen. It is conceivable that the concentration used was not high enough for the SEP changes to occur.

Volatile anaesthetics were given following induction with thiamylal. Although potential interactions of thiamylal and the volatile anaesthetics could not be completely excluded, thiamylal is known to be an ultrashort-acting drug. Shimoji and colleagues have shown that scalp-recorded SEPs had returned to control values 8-10 min after administrating thialmylal (5 mg kg−1) [8]. In our patient, the volatile anaesthetic was given 23 min after the final infusion of thiamylal. In conclusion, for judgement of the effects of different anaesthetic drugs on SEP monitoring in daily clinical practice, not only the type of anaesthetic drugs used, but also their concentration and the method of administration are the important factors.

K. Fukui

Departments of Anesthesiology and Critical Care; Medicine and Neurosurgery Graduate School of Medical Sciences; Kyushu University; Fukuoka, Japan

T. Morioka

K. Hisada

S. Nishio

Department of Neurosurgery; Graduate School of Medical Sciences; Kyushu University; Fukuoka, Japan

K. Irita

S. Takahashi

Department of Anesthesiology and Critical Care Medicine; Graduate School of Medical Sciences; Kyushu University; Fukuoka, Japan

References

1. Schindler E, Muller M, Zickmann B, et al. Modulation of somatosensory evoked potentials under various concentrations of desflurane with and without nitrous oxide. J Neurosurg Anesthesiol 1998; 10: 218-223.
2. Sloan TB. Anesthetic effects on electrophysiologic recordings. J Clin Neurophysiol 1998; 15: 217-226.
3. Sutton LN, Frewen T, Roger M, Jaggi J, Bruce DA. The effects of deep barbiturate coma on multimodality evoked potentials. J Neurosurg 1982; 57: 178-185.
4. Taniguchi M, Nadstawek J, Pechstein U, Schramm J. Total intravenous anesthesia for improvement of intraoperative monitoring of somatosensory evoked potentials during aneurysm surgery. Neurosurgery 1992; 31: 891-897.
5. Sloan TB, Kimovec MA, Serpico LC. Effects of thiopentone on median nerve somatosensory evoked potentials. Br J Anaesth 1989; 63: 51-55.
6. Tomoda K, Shingu K, Osawa M, Murakawa M, Mori K. Comparison of CNS effects of propofol and thiopentone in cats. Br J Anaesth 1993; 71: 383-387.
7. Porkkala T, Kaukinen S, Hakkinen V, Jantti V. Median nerve somatosensory evoked potentials during isoflurane anaesthesia. Can J Anaesth 1997; 44: 963-968.
8. Shimoji K, Kano T, Nakashima N, Shimizu H. The effects of thiamylal sodium on electrical activities of the central and peripheral nervous systems in man. Anesthesiology 1974; 40: 234-240.
© 2002 European Academy of Anaesthesiology