[Topographic electroencephalometry following anesthesia induction with ketamine-midazolam]

The neurophysiological action of ketamine has attracted increasing interest in recent years, with special interest in receptor action and in neurophysiological differences between and psychomimetic side effects of the two enantiomorphs. Most of the neurophysiological examinations published deal with ketamine as a single anaesthetic agent, although it has been suggested to that psychomimetic side-effects and haemodynamic deterioration could be avoided by combining ketamine with a sedative drug. The primary aim of our study was to examine the combined ketamine-midazolam action on cerebral activity; secondly, we planned to look at these interactions topographically at different points of the cortex to evaluate topographical differences in the combination's action; thirdly, the cerebral and haemodynamic reactions to anaesthesiological stimuli (intubation, gastric tube) were evaluated and compared. METHODS. Sixteen patients scheduled for elective aortocoronary bypass surgery were examined. Topographical electroencephalometric data were obtained by processed EEG with a CATEEM system at 17 recording points over the cortex and compared with heart rate and arterial blood pressure during the induction period. After documentation of the baseline data ketamine (3 mg/kg) and midazolam (0.15 mg/kg) were applied within 10 min by means of an automatic device. At the end of the infusion period patients were intubated, and after a further 10 min a gastric tube was placed. RESULTS. Induction resulted in increases in delta and beta 2 output (P < 0.05) in the early induction period and in significant decreases (P < 0.05) in alpha 1, alpha 2 and beta 1 activity. No significant change in theta activity was observed throughout the observation period. Intubation led to significant increases of power particularly in the temporal and parietal leads of all frequency bands, but not in the frontal area. Insertion of the gastric tube did not alter cerebral function. CONCLUSION. The interaction of ketamine and midazolam leads to increases in beta 2 and delta power and to significant decreases in the alpha bands and beta 1. Increases of theta activity, a typical effect of single-agent anaesthesia with ketamine, were not observed. Thus, the action of combined ketamine and midazolam on cerebral function is not an additive, but an interactive process. Despite a relatively high induction dosage, haemodynamic changes during intubation occurred and were accompanied by changes in cerebral activity. This can be regarded as incomplete cerebral suppression even by these induction dosages.