Direct comparison of the effect of desflurane and sevoflurane on intraoperative motor-evoked potentials monitoring.

BACKGROUND

During spinal surgery, intraoperative monitoring of motor-evoked potentials (MEPs) is a useful means of assessing the intraoperative integrity of corticospinal pathways. However, MEPs are known to be particularly sensitive to the suppressive effects of inhalational halogenated anesthetic agents.

OBJECTIVE

To investigate the effects of increasing end-tidal concentrations of desflurane and sevoflurane anesthesia in a background of propofol and remifentanil with multipulse cortical stimulation on intraoperative monitoring of MEPs.

METHODS

In this randomized crossover trial, 14 consecutive patients (7 in each arm) undergoing major spine surgery, under a background anesthetic of propofol (75 to 125 mcg/kg/min) and remifentanil (0.1 to 0.2 mcg/kg/min), were randomly assigned to receive the sequence of inhalational agents studied: either DES-SEVO (desflurane followed by sevoflurane); or SEVO-DES (sevoflurane followed by desflurane). Multiples (0.3, 0.5, and 0.7) of minimum alveolar concentration (MAC) of desflurane and sevoflurane were administered. After a washout period of 15 minutes using high fresh oxygen/air flows, each of the patients then received the other gas as the second agent. Cortical stimulation was achieved with a train of 5 equivalent square pulses, each 0.05 ms in duration, delivered at 2 ms intervals. MEP recordings were made in the upper limb (UL) from first dorsal interosseus and lower limb (LL) from tibialis anterior with subdermal needle electrodes.

RESULTS

At 0.3 MAC desflurane, there was no statistical significant difference in transcranial-evoked MEP amplitudes from the baseline in both UL and LL stimulation. However, this was not the case for sevoflurane for which even a low concentration at 0.3 MAC significantly depressed MEP amplitudes of LL (but not UL) from baseline value. Desflurane at 0.5 and 0.7 MAC depresses LL MEP to 58.4% and 59.9% of baseline, respectively (P<0.05), whereas sevoflurane at 0.3, 0.5, and 0.7 MAC depresses LL MEP to 66.2%, 41.3%, and 25.3% of baseline, respectively (P<0.05). There was no difference in latency of the responses at any MAC.

CONCLUSIONS

Inhalational anesthetic agents (sevoflurane >desflurane) suppress MEP amplitudes in a dose-dependent manner. The use of 0.3 MAC of desflurane (but not sevoflurane) provided good MEP recordings acceptable for clinical interpretation for both upper and LLs. The LL appears to be more sensitive to anesthetic-induced depression compared with the UL. All patients studied had normal neurological examination hence, these results may not be applicable to those with preexisting deficits.