• Der Anaesthesist · May 1993

    Randomized Controlled Trial Comparative Study Clinical Trial

    [Acoustic evoked potentials of medium latency. Anesthesia induction with S-(+)-ketamine versus ketamine racemate].

    • D Schwender, E Faber-Züllig, W Fett, S Klasing, U Finsterer, and K Peter.
    • Institut für Anaesthesiologie, Ludwig-Maximilians-Universität München.
    • Anaesthesist. 1993 May 1; 42 (5): 280-7.

    AbstractMid-latency auditory evoked potentials (MLAEP) reflect the primary cortical processing of auditory stimuli. They are widely suppressed during general anaesthesia with volatile anaesthetics. Under ketamine, in contrast, they seem to be preserved, which has been interpreted as indicating insufficient suppression of consciousness during ketamine anaesthesia. Ketamine exists in two optical isomeres, S-(+)-ketamine und R-(-)-ketamine, which differ in their pharmacodynamic properties: S-(+)-ketamine has higher anaesthetic-hypnotic and analgesic potency than R-(-)-ketamine. It thus appears obvious to question whether S-(+)-ketamine has a different effect on the primary cortical processing of sensory, i.e., auditory stimuli. We therefore studied the effects of S-(+)-ketamine versus ketamine-racemate on MLAEP. PATIENTS AND METHODS. Institutional approval and informed consent were obtained for 40 patients scheduled for minor gynaecological procedures. The patients were assigned randomly to one of the two experimental groups. All experimental evaluations were conducted under double-blind conditions. Anaesthesia was induced with S-(+)-ketamine 1 mg/kg (group I, n = 20) or ketamine-racemat 2 mg/kg (group II, n = 20). MLAEP were recorded before, during, and after induction of general anaesthesia from the vertex (positive) and mastoids on both sides (negative). Auditory clicks were presented binaurally at 70 dBnHL at a rate of 9.3 Hz. Using the electrodiagnostic system Pathfinder I (Nicolet), 1000 successive stimulus responses were averaged over a 100-ms poststimulus interval and analysed off-line. Latencies of the peak V, Na, Pa, Nb, P1, N1, and amplitudes Na/Pa, Pa/Nb, and Nb/P1 were measured. V belongs to the brainstem-generated potentials, which demonstrates that auditory stimuli were correctly transduced. Na, Pa, Nb, P1, and N1 are generated in the primary auditory cortex of the temporal lobe and are the electrophysiological correlate of the primary cortical processing of the auditory stimuli. A Fast-Fourier transformation calculated powerspectra of the AEP. RESULTS. In the awake state, AEP peak latencies were in the normal range. MLAEP had high amplitudes and a periodic wave form. Powerspectra indicated high energy in the 30-40-Hz frequency range. After induction of general anaesthesia with (S+)-ketamine or ketamine-racemat, there was no increase in the latencies of the peaks V, Na, Pa, Nb, P1, and N1. No decrease in amplitudes Na/Pa, Pa/Nb, or Nb/P1 could be observed. In the power spectra, frequencies in the range of 30-40 Hz retained high energy. CONCLUSIONS. MLAEP do not change in amplitude or latency during induction of general anesthesia with S-(+)-ketamine or ketamine-racemat. Primary cortical processing of auditory stimuli seems to preserved under S-(+)-ketamine and ketamine-racemat. This must be viewed in connection with dreams and hallucinations and could be interpreted as inadequate suppression of auditory information processing during general anaesthesia with S-(+)-ketamine and ketamine-racemat.

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