Der Anaesthesist
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Randomized Controlled Trial Clinical Trial
[Electroencephalographic demonstration of central nervous system effects of different premedication regimens].
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). ⋯ 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)