KETAMIN UND EVOZIERTE POTENTIALE

Ketamine-induced changes in the spontaneous and evoked electroencephalogram have been well documented in animals and humans. In contrast to the action of hypnotics, ketamine does not result in a dose-dependent suppression of neural activity. Many studies have revealed excitatory activity with induction of synchronized high-voltage slow waves in the electroencephalogram (EEG). Somatosensory evoked responses (SEP) have been found to be enhanced following induction of anaesthesia with ketamine. However, increases in amplitude were small compared with the SEP-enhancing effects of etomidate. The increase in somatosensory evoked responses may reflect dose-dependent disinhibition and/or increased excitation of cerebral neuronal activity induced by ketamine. Attenuation of late cortical somatosensory evoked responses following stimulation of thin C- and Aδ-nerve fibres has been reported in volunteers given low-dose ketamine. Changes in SEP amplitude correlated to changes in subjective pain sensation. From this it was concluded that the analgesic effect of ketamine can be assessed by electrophysiological measurement methods. Recent studies suggest that the analgesic effect of the racematic ketamine mixture can probably be related to the effects of S-(+)-ketamine isomer, which has been shown to be involved in the activation of an opioidergic mechanism. Auditory evoked responses (AEP) of short latencies with origins in the brain stem have been shown to be slightly altered by ketamine. From this it was concluded that these components may not be used for assessment of the depth of anaesthesia. In contrast to the effects of hypnotics, mid-latency AEP components may be recorded during ketamine anaesthesia. These findings indicate that auditory signal processing in the cortex is not suppressed by ketamine. Following this, it cannot be excluded that auditory information may be assessed during ketamine administration. Visual evoked responses (VEP) have been shown to be suppressed in animals given ketamine. These changes do not correlate to ketamine-induced EEG changes, and it has been postulated that NMDA receptors are involved in VEP changes following ketamine.