• J F Antognini and X W Wang.
• Department of Anesthesiology, University of California, Davis 95616, USA. jfantognini@ucdavis.edu
• Can J Anaesth. 1999 Jul 1; 46 (7): 692-5.

PurposeThe auditory evoked potential (AEP) has been proposed as a method to determine depth of anesthesia, as AEPs are generated in the thalamus and cerebral cortex. Because general anesthesia, in part, relies on anesthetic action in the spinal cord, we hypothesized that isoflurane would have indirect depressant effects on the AEP because of its action in the spinal cord.MethodsSix goats were anesthetized with isoflurane and the jugular veins and carotid arteries isolated to permit cerebral bypass and differential delivery of isoflurane to the head and torso. The AEPs were determined by delivering binaural clicks at 9 Hz, and measuring the evoked response from electrodes placed in the skull and scalp. Isoflurane was maintained at 0.8% in the head while the torso isoflurane was alternated between 0.3% and 1.3%, and the AEP determined at each torso concentration.ResultsAt isoflurane 0.3% delivered to the torso, the peak-to-trough amplitude of the mid-latency AEP waves designated as N14/P24 was 0.337+/-0.185 microV and the N36 wave amplitude was 0.115+/-0.054 microV. When torso isoflurane was 1.3%, these waves decreased to 0.297+/-0.186 microV and 0.066+/-0.037 microV, respectively (P<0.05). The latency of the N14 wave increased slightly (from 13.7+/-2.6 msec to 14.4+/-2.8 msec, P<0.05) but the latencies of the other waves were unchanged.ConclusionsIsoflurane action in the spinal cord indirectly alters the AEP, however, the effect is small. These data suggest that isoflurane can depress the transmission of afferent information from the spinal cord to thalamus, midbrain and cerebral cortex.

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