PubMed1994
INTRODUCTION: For many years, the main goal of premedication was prevention of the dangerous side effects sometimes encountered in anesthetics with anticholinergics, antiemetic antihistaminics, and opioids. Because the rules were always preoperative fasting, premedication was administered i.m. Thus, the onset of action was within 15-30 min from administration. In recent years, with the introduction of newer anesthetics with fewer side effects, anxiolysis became the main aim in premedication. Moreover, the oral route became popular since it obviously did not increase the acidity or volume of the gastric content. However, the uptake and thus onset of action of orally administered drugs may take longer and can differ considerably between individual patients. Therefore, the optimum interval between administration and induction of anesthesia remains controversial. The present study was carried out to examine the time course of drug action and the effects of different premedication regimens on the electroencephalogram (EEG). PATIENTS AND METHODS: After obtaining informed consent, in 38 unselected adult patients (ASA I and II, < 65 years) scheduled for elective surgery, the EEG was recorded continuously before and after premedication. The patients were randomly assigned to four groups: M: midazolam, 0.2 mg/kg BW orally; N: nordazepam, 0.2 mg/kg BW orally; AP: atropine, 0.5 mg, plus promethazine, 50 mg i.m.; APP: atropine, 0.5 mg, plus promethazine, 50 mg, plus pethidine, 0.7 mg/kg BW i.m. The EEG was recorded for a reference period of 10 min before and a study period of 30 min after premedication. Automated EEG processing was performed with CATEEM (computer-aided topographical electroencephalometry). Surface electrodes were placed according to the 10-20 system. Date were collected via an amplifier (resistance 10 M omega) and a digitalization unit (filter 0.2-35 Hz, sampling rate 512 Hz, 12 bit A/D convertor). The original EEG signals were used in an interpolation algorythm to produce an additional 82 virtual recording points, allowing for high topographical resolution. After spectral analysis (fast Fourier transformation), the different frequency ranges of the EEG power spectrum are displayed in different colors. The screen displays the on-line map with color-based topographical power distribution. In order to achieve a pharmacodynamic time profile, the study period was subdivided into three periods of 10 min each. For clinical evaluation of vigilance, a 6-grade scoring system was used 1 = awake, 6 = not arousable). RESULTS: All data are presented with respect to reference period. The power density of each frequency range for each electrode is integrated over the selected period and mean values are shown. Changes in power density with time are expressed as percentage change from reference period. Biometrical data showed no significant differences between groups. The median vigilance score 30 min after premedication (end of study period) was 4 in groups M, AP, and APP, and 3 in group N. In both benzodiazepine groups, a distinct increase in power density was found in the beta-bands, while in groups AP and APP the increase was most pronounced in the delta and theta bands. In group M, there was a linear increase in beta 1 power up to 310%, while in the beta 2 range there was a 170% maximum within the second period of 10 min. In group N, there was a similar course with a lower increase in beta 1 (220%) and beta 2 (130%). Increases in both beta-bands were most pronounced with frontal electrodes. While group M showed an increase in delta power (150%), together with moderate suppression in alpha (alpha 1 50%, alpha 2 40%), nordazepam caused only a slight increase in delta (124%) and a distinct increase in alpha 2 to 150%, predominantly in the frontal areas. Group APP showed a linear increase in both delta up to 210% and theta power to 190%. (ABSTRACT TRUNCATED)