Ketamine, an NMDA-antagonist, increases the oscillatory frequencies of α-peaks on the electroencephalographic power spectrum

• Published in: Acta anaesthesiologica Scandinavica Vol. 51; no. 4; pp. 472 - 481
• Main Authors: Tsuda, N., Hayashi, K., Hagihira, S., Sawa, T.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.04.2007; Blackwell
• Subjects: Abdomen - surgery; Adult; Analgesics - pharmacology; Anesthesia; Anesthesia, Epidural - methods; Anesthesia, General - methods; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Anesthetics, Combined - pharmacology; Anesthetics, Intravenous - pharmacology; Biological and medical sciences; Elective Surgical Procedures - methods; Electroencephalography - drug effects; Female; Humans; Ketamine - pharmacology; Male; Medical sciences; Middle Aged; Monitoring, Intraoperative - methods; N-methyl-D-aspartate; Propofol - pharmacology; reticular thalamic nucleus; Spectral analysis; spindle wave; thalamocortical system; Glutamate receptor; Spectral analysis; reticular thalamic nucleus; thalamocortical system; Ketamine; spindle wave; General anesthetic; NMDA; Anesthesia; N-methyl-D-aspartate; Antagonist; NMDA receptor; Power spectrum
• ISSN: 0001-5172; 1399-6576
• DOI: 10.1111/j.1399-6576.2006.01246.x

Background:  Ketamine, an N‐methyl‐D‐aspartate (NMDA) antagonist, is known to activate the electroencephalogram (EEG), despite its sedative effects. Spindle oscillations are known to be related to the sedative actions of the reticular thalamic nucleus with links to thalamocortical neurons. This study was designed to examine the effect of ketamine on the spindle oscillations to understand the simultaneous sedative effect and EEG activation that occurs with ketamine, by comparing the EEG in emergence. Methods:  Anesthesia was induced with propofol using a target‐controlled infusion (TCI) system (3.5 μg/ml). Seventeen patients, scheduled for non‐cranial surgery under general anesthesia combined with epidural anesthesia, were randomly divided into two groups: (i) anesthesia was maintained with TCI‐propofol alone (n= 8) and (ii) anesthesia was maintained with TCI‐propofol and intravenously administered ketamine (n= 9). The EEG was continuously monitored and EEG indices and power spectra were determined. Results:  Propofol alone caused the α‐peaks of the power spectra to occur at an average frequency of 10.4 ± 0.9 Hz; the addition of ketamine shifted the peaks to higher frequencies of 15.1 ± 1.4 Hz (P < 0.05). On the other hand, when the EEG was activated by discontinuation of propofol, the corresponding α‐peaks disappeared. Conclusions:  Ketamine increased the frequencies of α‐spindle waves induced by propofol, but did not block their formations. The phenomena have the possibility to underlie the cooperative effect between propofol and ketamine concerning sedation and anesthesia.