EFFECT OF SEDATIVE AND HYPNOTIC DOSES OF PROPOFOL ON THE EEG ACTIVITYOF PATIENTS WITH OR WITHOUT A HISTORY OF SEIZURE DISORDERS

Propofol is alleged to possess both pro-and anticonvulsant properties, leading to controversy regarding its use in patients with a history o f seizures. Since propofol is administered for both sedation and hypno sis, 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 dos es of propofol from 0.5 to 2.5 mg/kg i.v. were studied in 30 neurosurg ical patients with or without a history of seizure disorders. While co ntinuously recording from scalp EEG electrodes (F-3, F-4, C-3, C-4, P- 3, P-4, O-1, and O-2), propofol 0.5 mg/kg was infused intravenously ov er 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 measure d manually, respectively, from 80 to 90 s after beginning the injectio n 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 decre ased significantly in all patients. However, with larger does of propo fol (total dose of 2-2.5 mg/kg), the number of beta-waves decreased an d delta-waves appeared. The amplitudes of all EEG waves increased and were maintained at a higher level after administration of propofol. Sp ike (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 co ntrol and 67% of the epileptic patients after the 1.5-mg/kg dose. In t he majority of patients, the spike waves disappeared when additional d oses of propofol were administered. One patient in the epileptic group had an EEG-recorded and clinical grand mal seizure after propofol 1 m g/kg, but the seizure disappeared after an additional 0.5-mg/kg bolus dose was administered. The propofol-induced EEG changes appeared initi ally 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 disorde rs. 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 t o epileptic patients.