CLONIDINE DOES NOT ATTENUATE MEDIAN NERVE SOMATOSENSORY-EVOKED POTENTIALS DURING ISOFLURANE ANESTHESIA

Background. Clonidine, an alpha(2) agonist, reduces the requirements o f several anesthetics. However, the effects of clonidine on somatosens ory evoked potentials (SEPs) are unclear. These effects on cortical SE Ps during isoflurane anesthesia were studied in 20 ASA I-II patients s cheduled for elective surgery Furthermore, the isoflurane concentratio n required to induce electroencephalogram (EEG) burst-suppression with and without clonidine was studied. Methods. Anesthesia was maintained with isoflurane at a FIO2 of 0.4. At 1 MAC isoflurane the patients we re randomly given either intravenous clonidine 2 IJ-g kg-l (ten patien ts) or saline (ten patients). Finally, the isoflurane concentration wa s increased to a point at which a burst-suppression pattern appeared i n the EEG. SEPs upon median nerve stimulation were recorded (1) before induction of anesthesia, (2) at 1 MAC before clonidine/saline, (3) at 1 MAC after clonidine/saline, (I) at EEG burst-suppression. Results. The cortical SEP amplitude was attenuated from 3.7 (2.0) mu V to 2.1 ( 1.3) mu V (p < 0.001) and the peak latency increased from 19.3 (1.1) m s to 22.0 (1.3) ms (p < 0.0001) during 1 MAC isoflurane anesthesia, bu t the addition of clonidine did not further increase these changes. Th e isoflurane end-tidal concentration needed to induce burst-suppressio n EEG was not significantly different in the clonidine group compared with the placebo group (2.0% vs. 2.1%, P = 0.07). Conclusions. The eff ect of clonidine in reducing the requirements of anesthetics during ge neral anesthesia is not seen in the cortical SEPs. The isoflurane-indu ced burst-suppression in the EEG was not affected by clonidine, sugges ting that the EEG effects of clonidine and isoflurane were not additiv e. If SEPs are monitored intraoperatively, clonidine can be used as an adjuvant during isoflurane anesthesia without harmful effects on SEP monitoring.