• Der Anaesthesist · Dec 1989

    [Sensory information processing during general anesthesia. The effect of propofol and ketamine on mid-latency auditory evoked potentials].

    • D Schwender, S Klasing, I Keller, and C Madler.
    • Institut für Anaesthesiologie, Ludwig-Maximilians-Universität München.
    • Anaesthesist. 1989 Dec 1; 38 (12): 664-72.

    AbstractExperimental evidence from various neuropsychological and neurophysiological fields indicates that an oscillatory brain mechanism in a frequency range of 30-40 Hz is necessary for adequate sensory information processing. An oscillatory component of that particular frequency range can also be observed in the mid-latency auditory evoked potentials. Thus general anesthesia can be defined as a suppression of sensory information processing, and the effect of the i.v. anesthetics, Propofol and ketamine, on auditory perception and auditory-evoked potentials was therefore studied. In 22 patients anesthesia was induced with Propofol (2.5 mg/kg body weight, group I: n = 10) or ketamine (2 mg/kg body weight, group II: n = 12). Auditory-evoked potentials were recorded before, during, and after induction of general anesthesia. In the awake state, an oscillatory component with an energetically dominant 30-40 Hz frequency was present between 20 and 100 ms poststimulus latency. Propofol suppressed the mid-latency oscillatory component, whereas the component persisted under ketamine. Under Propofol, the 30-40 Hz leading frequency shifted to the lower frequency range, whereas under ketamine, the AEP were still dominated by a 30-40 Hz oscillation. Propofol suppresses the oscillatory brain mechanism necessary for adequate sensory information processing like various other general anesthetics. In contrast to Propofol, ketamine does not alter auditory perception. Suppression of sensory information processing must take place at a higher cortical level in a dissociative manner. The persistence of a 30-40 Hz oscillation must be seen in connection with dreams and hallucinations as reported for the drug and may be interpreted as insufficient suppression of sensory information processing under ketamine anesthesia.

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