Clonidine does not attenuate median nerve somatosensory evoked potentials during isoflurane anesthesia

Clonidine, an alpha2 agonist, reduces the requirements of several anesthetics. However, the effects of clonidine on somatosensory evoked potentials (SEPs) are unclear. These effects on cortical SEPs during isoflurane anesthesia were studied in 20 ASA I-II patients scheduled for elective surgery. Furthermore, the isoflurane concentration 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 were randomly given either intravenous clonidine 2 microg kg(-1) (ten patients) or saline (ten patients). Finally, the isoflurane concentration was increased to a point at which a burst-suppression pattern appeared in 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, (4) at EEG burst-suppression.

The cortical SEP amplitude was attenuated from 3.7 (2.0) microV to 2.1 (1.3) microV (p < 0.001) and the peak latency increased from 19.3 (1.1) ms to 22.0 (1.3) ms (p < 0.0001) during 1 MAC isoflurane anesthesia, but the addition of clonidine did not further increase these changes. The isoflurane end-tidal concentration needed to induce burst-suppression EEG was not significantly different in the clonidine group compared with the placebo group (2.0% vs. 2.1%, p = 0.07).

The effect of clonidine in reducing the requirements of anesthetics during general anesthesia is not seen in the cortical SEPs. The isoflurane-induced burst-suppression in the EEG was not affected by clonidine, suggesting that the EEG effects of clonidine and isoflurane were not additive. If SEPs are monitored intraoperatively, clonidine can be used as an adjuvant during isoflurane anesthesia without harmful effects on SEP monitoring.