EFFECTS OF KETAMINE ON CENTRAL-NERVOUS-SY STEM FUNCTION

The present review summarises the main actions of racemic ketamine a n d keta mine enantiomers on central nervous system receptors. The prima ry CNS action of ketamine appears to be a non-competitive block of N-m ethyl-D-aspartate receptors. Although numerous other receptors (e.g., GABA, nicotinic acetylcholine, opiate, voltage-operated channels) have been reported to interact with ketamine, their role in inducing disso ciative anaesthesia is still under discussion. In humans, characterist ic electroencephalographic (EEG) changes after administration of ketam ine are dose-dependent increases in delta, theta, and beta Power. In e quipotent doses S-(+)-ketamine induces similar EEG changes. However, i n comparison to racemic ketamine and S-(+)-ketamine, R-(-)-ketamine do es not suppress the EEG to the same extent. Former studies suggested t hat ketamine is a proconvulsive agent; however, recent studies have de monstrated anticonvulsive and even neuroprotective properties. In huma ns, low-dose ketamine has no influence on early cortical peaks of soma tosensory evoked potentials (SEP). Larger doses induce increases in SE P amplitude while latencies are unchanged. Recent data indicate that a nalgesia induced by low-dose ketamine may be quantitated by specific p ain-related SEP. Significant reductions of pain-induced cortical poten tials may be correlated with subjective pain ratings. Brainstem audito ry evoked potentials (AEP) are not influenced by ketamine. Interesting ly, in contrast to many other anaesthetics, middle-latency AEP were no t altered by racemic and S-(+)-ketamine. This observation may indicate insufficient suppression of auditory stimulus processing during ketam ine anaesthetics. Motor evoked responses to transcranial electrical or magnetic stimulation in humans are not markedly suppressed by ketamin e.