Effect of sedative and hypnotic doses of propofol on the EEG activity of patients with or without a history of seizure disorders.
(Clinical Trial;Journal Article)
Propofol is alleged to possess both pro- and anticonvulsant properties, leading to controversy regarding its use in patients with a history of seizures. Since propofol is administered for both sedation and hypnosis, it is important to understand the effects of low (0.5-1.0 mg/kg) and high (2-2.5 mg/kg) doses of propofol on the electroencephalogram (EEG). In this study, the hemodynamic and EEG effects of cumulative doses of propofol from 0.5 to 2.5 mg/kg i.v. were studied in 30 neurosurgical patients with or without a history of seizure disorders. While continuously recording from scalp EEG electrodes (F3, F4, C3, C4, P3, P4, O1, and O2), propofol 0.5 mg/kg was infused intravenously over 20 s. The same dose of propofol was reinjected four times at 2-min intervals, until a total dose of 2.5 mg/kg had been administered. The number and average amplitude of the EEG waves were counted and measured manually, respectively, from 80 to 90 s after beginning the injection of each dose of propofol. After lower propofol doses (0.5-1 mg/kg), the number of beta-waves increased, while alpha- and theta-waves decreased significantly in all patients. However, with larger doses of propofol (total dose of 2-2.5 mg/kg), the number of beta-waves decreased and delta-waves appeared. The amplitudes of all EEG waves increased and were maintained at a higher level after administration of propofol. Spike (or sharp) waves appeared in 33% of the control patients and in 40% of the epileptic group after propofol 0.5 mg/kg and in 73% of the control and 67% of the epileptic patients after the 1.5-mg/kg dose. In the majority of patients, the spike waves disappeared when additional doses of propofol were administered. One patient in the epileptic group had an EEG-recorded and clinical grand mal seizure after propofol 1 mg/kg, but the seizure disappeared after an additional 0.5-mg/kg bolus dose was administered. The propofol-induced EEG changes appeared initially at the frontal and central EEG electrodes and subsequently at the other EEG electrodes. Overall, there were no significant differences in the spectrum of EEG changes between the two patient populations. It is concluded that propofol produces similar dose-dependent effects on EEG activity in patients with or without a history of seizure disorders. While induction of anesthesia with higher doses of propofol (> 1.5 mg/kg) in neurosurgical patients with well controlled seizure disorder is safe, smaller sedative doses should be administered with caution to epileptic patients.
Wang, B; Bai, Q; Jiao, X; Wang, E; White, PF
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