Abstract

We thank Drs Brunner and Vaughan for their appreciation of our review article. We are especially grateful for their enlightening comments on the use of auditory (AER) and somatosensory (SSER) evoked responses in monitoring depth of anaesthesia. The changes in the amplitudes of P15–N20 waveform while studying the effects of sevoflurane and desflurane are definitely valid points that have been reported by the esteemed readers and will definitely throw light on monitoring depth of anaesthesia. In fact, it is a challenge for the designers of patient monitors to counteract controversies and challenges that can arise as a result of different workers using the same monitor, but reporting variable results. Recently, Dutton et al. [1] have established that 40 Hz power of the frequency spectrum (during midlatency auditory evoked potential activity) predicted wakefulness better than all latency or amplitude indices, during desflurane anaesthesia in volunteers. Woodforth et al. [2] observed that sevoflurane depresses I waves in the corticospinal volleys produced by transcranial electrical stimulation of the motor cortex in a manner that is qualitatively similar to isoflurane. Drs Brunner and Vaughan are absolutely correct in confirming Nb latency as a useful tool for monitoring light anaesthesia during midazolam sedation. In fact, Schwender et al. [3] observed that a threshold value of 60 ms of Nb proved to be the most predictive of movement during isoflurane anaesthesia. Before and during spontaneous movement observed intra-operatively or during emergence from anaesthesia, the latencies of the peaks Na, Pa, Nb and P1 decreased, and the amplitudes Na/Pa, Pa/Nb, Nb/P1 increased significantly. We definitely agree with Drs Brunner and Vaughan that few of the recent studies do show a significant effect of benzodiazepines, in particular midazolam, on AER latencies. In fact, Morlet et al. [4] recommend that, if possible, midazolam should be administered as a continuous infusion for reliable interpretation of evoked potential changes in the intensive care unit or during surgery. During continuous infusion of midazolam (0.1 mg.kg−l.h−1), they observed that midlatency auditory evoked potentials (MLAEPs) remained slightly, though significantly, altered and Nb wave seemed to be modified earlier and to return to normality later than the Pa wave. Changes of MLAEP by general anaesthetics are consistent with the hypothesis that alterations of consciousness by these drugs involve thalamic and cortical neuronal assemblies. There is converging evidence that wave Na arises from mesencephalic structures and that wave Pa originates from the primary auditory cortex with a contribution from subcortical sources. Thalamic cholinergic neurones of the ascending reticular formation are involved in the generation of wave Pb. The studies done by Drs Brunner and Vaughan are quite enlightening and throw a new light on the significance of Nb latency as a promising tool in monitoring light anaesthesia. In another interesting study, Hotz et al. [5] investigated the action of midazolam and its active metabolite, alpha-hydroxy-midazolam, on different parts of the auditory pathway. They observed that acoustically evoked short latency potential (SLP) changes were closely associated with sedation and high plasma midazolam concentrations, and MLAEP effects persisted for hours after sedation, even at low midazolam plasma levels. We appreciate the worthy comments of Drs Brunner and Vaughan as they enlighten the topic, inform us of recent developments and help us for the future design of studies related to Pa, Nb latency alterations in MLAEP and P15–N20 amplitude alterations in SSER, for monitoring depth of anaesthesia. MLAEP definitely offers a promising method for investigating anaesthetic mechanisms, and for the possibility of on-line monitoring.

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