• E Freye, L B Partecke, and J V Levy.
• Clinics of Vascular Surgery and Renal Transplantation, Heinrich-Heine-University of Düsseldorf, Deichstr. 3a, 41468 Neuss-Uedesheim, Germany. enno.freye@uni-duesseldorf.de
• Neurophysiol Clin. 2005 Feb 1; 35 (1): 25-32.

AbstractLittle is known on effects taking place in the CNS during rapid opioid detoxification (ROD) while the patient is under anesthesia. We therefore measured EEG-power spectra in the beta, alpha, Theta, and delta-band in 36 patients undergoing ROD. Measurements were taken before, during steady-state anesthesia and following administration of the antagonist naltrexone. In addition, the non-specific NMDA-antagonist S+ ketamine was given for reduction of CNS-hyperexcitation, while the efficacy of this adjunct was determined using EEG power spectra analysis. Compared to steady-state anesthesia, EEG power spectra were characterized by a marked decrease of power by 251% in the delta (0.5-3 Hz) and an increase by 209% in the beta- (13-30 Hz) domain when withdrawal was induced with naltrexone. Subsequent administration of S+-ketamine induced a reversal of acute abstinence-related EEG power changes: compared to anesthesia with naltrexone on board, power in the EEG increased by 65% in the delta- and decreased by 723% in the beta-band. While sympathetically induced hemodynamic alterations in anesthesia-assisted opioid detoxification can be attenuated by the alpha2-agonist clonidine and sedation, central nervous sensory activation can be attenuated by the administration of S+-ketamine (1.5 mg/kg). Since EEG alterations during acute withdrawal with naltrexone can be controlled by the non-specific NMDA-antagonist S+-ketamine, this latter presents a useful adjunct during ROD management.

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