[Effects of ketamine on CNS-function]

The present review summarises the main actions of racemic ketamine and ketamine enantiomers on central nervous system receptors. The primary CNS action of ketamine appears to be a non-competitive block of N-methyl-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 dissociative anaesthesia is still under discussion. In humans, characteristic electroencephalographic (EEG) changes after administration of ketamine are dose-dependent increases in delta, theta, and beta power. In equipotent doses S-(+)-ketamine induces similar EEG changes. However, in comparison to racemic ketamine and S-(+)-ketamine, R-(-)-ketamine does not suppress the EEG to the same extent. Former studies suggested that ketamine is a proconvulsive agent; however, recent studies have demonstrated anticonvulsive and even neuroprotective properties. In humans, low-dose ketamine has no influence on early cortical peaks of somatosensory evoked potentials (SEP). Larger doses induce increases in SEP amplitude while latencies are unchanged. Recent data indicate that analgesia induced by low-dose ketamine may be quantitated by specific pain-related SEP. Significant reductions of pain-induced cortical potentials may be correlated with subjective pain ratings. Brain-stem auditory evoked potentials (AEP) are not influenced by ketamine. Interestingly, in contrast to many other anaesthetics, middle-latency AEP were not altered by racemic and S-(+)-ketamine. This observation may indicate insufficient suppression of auditory stimulus processing during ketamine anaesthesia. Motor evoked responses to transcranial electrical or magnetic stimulation in humans are not markedly suppressed by ketamine.