Prevention of etomidate induced myoclonus in groups N or R (Table 4). The changes of BP throughout the procedure did not differ among the groups except for the post- intubation period. BP after intubation in Group N was higher than BP in the other groups (P < 0.05) (Fig. 1). Even though it looks like there were differences in HR between groups, there was no significant difference in statistics. Discussion This study showed that a 2 ng/ml effect site concentration of remifentanil prevented etomidate-induced myoclonus without any side effects. The incidence of myoclonus was 82% in Group N and it decreased to 12% in group R. We could not find any myoclonus in Group Q. We could compare the effect site concentration in each case using TCI. TCI allows an accurate adaptation of the analgesia level and fewer overdose-linked adverse effects. This result is compatible with previous reports utilizing other treatment [1,3,4]. Myoclonus occurred at least 60 seconds to 90 seconds after the end of injection and no patients expressed pain during injection. Thus we defined myoclonus differently from injection pain based on those results. Some studies have reported that 50 to 80% of patients receiving etomidate showed myoclonic activity [3,14]. The neurologic mechanism of myoclonic activity after etomidate administration is not clear, but may be a kind of seizure activity [14]. Other studies suggested that myoclonus after etomidate administration is a result of temporary sub- cortical disinhibition like that of restless legs during sleep and does not happen from an epileptic focus [3,15,16]. An unsyn- chronized onset of etomidate induces fast depression of the cortex, resulting in temporary disinhibition of the subcortex from inducing the myoclonic movement. Thus, pretreatment with a small amount of etomidate reduces myoclonus and this suggests a support for the former mechanism [3]. The dosage of etomidate influences the incidence of myocluonus. The dosage as much as 0.05 mg/kg etomidate did not induce myoclonic activity, but a dosage above 0.075 mg/kg caused myoclonic activity in men [3]. Schwarzkopf et al. [1] suggested that midazolam (0.5 mg/kg), injected 90s before etomidate administration intravenously, reduced the incidence of myoclonus by 20%. In control group of this study, however, midazolam (0.05 mg/kg) injected intramuscularly 30 minutes before etomidate administration did not reduce the incidence of myoclonus. The incidence of control group was 82% which was not differ from previously reported myoclonus incidence. The different results may stem from the dosage of midazolam and the route and timing of injection. Magnesium sulfate (2.48 mmol) injected 90 s before etomidate administration intravenously, reduced the incidence of myoclonus by 76% and severity of myoclonus 130 Vol. 61, No. 2, August 2011 [5]. Pretreatment of etomidate could reduce the incidence of myoclonus. It was suggested that myoclonus after injection of 0.3 mg/kg etomidate was less likely after pretreatment with 0.03 or 0.05 mg/kg etomidate than after pretreatment with 0.075 mg/kg etomidate both in men and women [3]. Pretreatment of rocuronium (0.06 mg/kg) showed the incidence to be 25% [6]. Opioids could reduce the incidence of etomidate induced myoclonus. Pretreatment with alfentanil (5 μg/kg) resulted in an incidence of 25% [17] and fentanyl (100, 250, and 500 μg/kg) before etomidate injection reduced the incidence of myoclonus (33%, 13%, and 0%, respectively) but increased the incidence of apnea (87%, 87%, and 100%, respectively) [18]. Hueter et al. [4] showed that in female patients, there were no patients who had myoclonic activity in the group premedicated with 0.3 mg/ kg sufentanil, but 80% of patients in the placebo group showed myoclonic activity. Recently, remifentanil, which is a short-acting opioid, has been suggested for possibly reducing myoclonus after etomi- date injection [19]. There was no study about the mechanism of remifentanil to reduce etomidate-induced myoclonus. The mechanism of fentanyl, which has similar potency, is that it stimulates GABA Aμ-opioid receptors in the basal ganglia [3]. These reports are similar to ours that increasing the dose of opioids decreases the incidence of myoclonus but it increases the side effects of cough and chest wall rigidity. We could find that the side effects of remifentanil increase in Group Q (remifentanil 4 ng/ml). The recommended loading bolus dose of remifentanil during induction with a hypnotic agent is 1.0 μg/kg [10]. Hwang et al. [20] studied pre-treatment of remifentanil: Without premedication, they injected 1.0 μg/ kg remifentanil for over 60 s, then etomidate injection for over 10 s, then had a 2-min observation period for myoclonus. In that study, myoclonus occurred in 17% of cases with 1.0 μg/ kg of remifentanil and a similar incidence with 0.05 mg/kg pre-treatment with midazolam, but chest wall rigidity and bradycardia occurred. Muscle rigidity and bradycardia were serious side-effects of remifentanil [8-10,21]. We cannot ensure that remifentanil is a superior agent to other drugs or opioids, but it is advantageous that remifentanil has a rapid onset and offset, it is easy to adjust the proper effect site concentration and to find the safety concentration when using a TCI system. Further evaluation comparing other agents with 2 ng/ml of remifentanil is needed in the future. There is a limitation in the design of our study, in that we infused etomidate immediately after the effect site concentration of remifentanil reached target concentration. Our study was planned with premedication with glycopyrro- late and midazolam to decrease upper airway secretion and for ethical reasons. We thought premedication with midazolam would have a synergic effect with remifentanil. In other studies, www.ekja.org