BACKGROUND: During EEG suppression with isoflurane or sevoflurane anaesthesia, median nerve stimulation causes cortical responses of two kinds: an N20 wave with a latency of 20 ms and an EEG burst with a latency of 200 ms. We tested the possibility that median nerve stimulation during EEG suppression with propofol would cause an EEG response that was consistent enough to be of use for neuromonitoring. METHODS: Eight patients were anaesthetized with propofol to allow burst suppression. Electrical stimulation of the median nerve was applied during general anaesthesia and the EEG was measured. RESULTS: The EEG response to a painful stimulus had four successive components: (i) N20 and P22 potentials, reflecting activation of fast somatosensory pathways; (ii) a high-amplitude negative wave, possibly reflecting activation of the somatosensory cortex SII bilaterally; (iii) a burst (i.e. a negative slow wave with superimposed 10 Hz activity, probably reflecting an arousal mechanism); and (iv) a 13-15 Hz spindle, probably originating from the thalamus, similar to sleep spindles. These could be seen separately and in different combinations. Bursts and spindles during burst suppression were also seen without stimulation. In deepening propofol anaesthesia, spindles were seen in the continuous EEG before burst suppression was achieved. In deep anaesthesia, spindles were seen when bursts had ceased, and painful stimuli evoked sharp waves without subsequent bursts. CONCLUSION: In addition to SSEP (somatosensory evoked potentials), three different evoked responses are noted that could be useful for clinical monitoring.
BACKGROUND: During EEG suppression with isoflurane or sevoflurane anaesthesia, median nerve stimulation causes cortical responses of two kinds: an N20 wave with a latency of 20 ms and an EEG burst with a latency of 200 ms. We tested the possibility that median nerve stimulation during EEG suppression with propofol would cause an EEG response that was consistent enough to be of use for neuromonitoring. METHODS: Eight patients were anaesthetized with propofol to allow burst suppression. Electrical stimulation of the median nerve was applied during general anaesthesia and the EEG was measured. RESULTS: The EEG response to a painful stimulus had four successive components: (i) N20 and P22 potentials, reflecting activation of fast somatosensory pathways; (ii) a high-amplitude negative wave, possibly reflecting activation of the somatosensory cortex SII bilaterally; (iii) a burst (i.e. a negative slow wave with superimposed 10 Hz activity, probably reflecting an arousal mechanism); and (iv) a 13-15 Hz spindle, probably originating from the thalamus, similar to sleep spindles. These could be seen separately and in different combinations. Bursts and spindles during burst suppression were also seen without stimulation. In deepening propofol anaesthesia, spindles were seen in the continuous EEG before burst suppression was achieved. In deep anaesthesia, spindles were seen when bursts had ceased, and painful stimuli evoked sharp waves without subsequent bursts. CONCLUSION: In addition to SSEP (somatosensory evoked potentials), three different evoked responses are noted that could be useful for clinical monitoring.
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