Cortical reactivity during isoflurane burst-suppression anesthesia

We studied cortical reactivity to auditory, visual, and somatosensory stimuli during moderate and deep levels of isoflurane anesthesia at which the electroencephalogram (EEG) showed burst suppression patterns, defined as alternating high amplitude bursts and periods of suppressed background activity. Fifteen patients scheduled for gynecologic surgery were anesthetized with isoflurane until burst suppression appeared in the EEG. During steady state burst suppression at 1.5 end-tidal isoflurane concentration (ET(isof)), each patient was given a 5-min interval each of episodes of visual, auditory, and somatosensory stimulation. During the 5- min interval of visual stimulation the patient was given 3-s episodes of 60 flashes, 4 ms duration each, at a 20-Hz frequency via redlight-emitting diode goggles. Corresponding auditory and somatosensory stimulation consisted of 60 clicks (80 dB, 0.1 ms, 20 Hz) via earphones and 60 pulses to the median nerve at the wrist (20 mA, 0.2 ms, 20 Hz). The 3-s episodes of stimulation were given at irregular intervals ranging from 5 to 2-0 s. End-tidal isoflurane was then increased by 0.3 vol% and 15 min later the stimulation sequence was repeated. During anesthesia at 1.5 ± 0.1 ET(isof) all stimulus modalities readily evoked bursts. One hundred percent of visual stimuli, 98% ± 4% of somatosensory stimuli, and 94% ± 9% of auditory stimuli, given during EEG suppression, evoked bursts. Somatosensory and visual stimulation evoked bursts at both onset and offset of the 3-s episodes of stimuli. The responses to auditory stimuli were related mainly to the ending of the 3-s episode of clicks. Stimulation decreased the duration of suppression and increased the total duration of bursts (P < 0.01). During deeper anesthesia (1.8 ± 0.1 ET(isof)) 78% ± 37% of visual stimuli, 72% ± 31% of somatosensory stimuli, and 64% ± 40% of auditory stimuli evoked bursts. Deeper anesthesia was associated with longer suppressions, shorter bursts, and less reactivity (P < 0.05), and there was a predominance of stimulus offset-evoked bursts over onset-evoked bursts. We conclude that burst suppression stimulation studies may be useful in determining the sites and mechanisms of anesthetic action.