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L Monnens - One of the best experts on this subject based on the ideXlab platform.
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Supplementation of vitamin K in pregnant women receiving Anticonvulsant Therapy prevents neonatal vitamin K deficiency.
American journal of obstetrics and gynecology, 1993Co-Authors: M Cornelissen, R Steegers-theunissen, L Kollée, T Eskes, K Motohara, L MonnensAbstract:The null hypothesis of this study is that extra vitamin K administered to pregnant women on a regimen of enzyme-inducing Anticonvulsant Therapy will not decrease the frequency of symptoms of vitamin K deficiency in their neonates. A multicenter case-control study was performed on 16 pregnant women on Anticonvulsant Therapy who received 10 mg of vitamin K1 daily from 36 weeks of pregnancy onward. Concentrations of PIVKA-II (protein induced by vitamin K absence for factor II) and of vitamin K1 were determined in cord blood and compared with those in 20 controls. In none of 17 cord samples was PIVKA-II detectable, compared with 13 of 20 in controls (chi 2, p < 0.001). Median cord vitamin K1 level was 530 pg/ml compared with below detection limit in most controls. Antenatal vitamin K1 treatment decreases the frequency of vitamin K deficiency in neonates of mothers on Anticonvulsant Therapy.
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Supplementation of vitamin K in pregnant women receiving Anticonvulsant Therapy prevents neonatal vitamin K deficiency
American Journal of Obstetrics and Gynecology, 1993Co-Authors: M Cornelissen, R Steegers-theunissen, L Kollée, T Eskes, K Motohara, L MonnensAbstract:OBJECTIVE: The null hypothesis of this study is that extra vitamin K administered to pregnant women on a regimen of enzyme-inducing Anticonvulsant Therapy will not decrease the frequency of symptoms of vitamin K deficiency in their neonates. STUDY DESIGN: A multicenter case-control study was performed on 16 pregnant women on Anticonvulsant Therapy who received 10 mg of vitamin Kl daily from 36 weeks of pregnancy onward. Concentrations of PIVKA-II (protein induced by vitamin K absence for factor II) and of vitamin K 1 were determined in cord blood and compared with those in 20 controls. RESULTS: In none of 17 cord samples was PIVKA-II detectable, compared with 13 of 20 in controls ( x 2 , p 1 level was 530 pg/ml compared with below detection limit in most controls. CONCLUSIONS: Antenatal vitamin K 1 treatment decreases the frequency of vitamin K deficiency in neonates of mothers on Anticonvulsant Therapy.
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Increased incidence of neonatal vitamin K deficiency resulting from maternal Anticonvulsant Therapy.
American journal of obstetrics and gynecology, 1993Co-Authors: M Cornelissen, R Steegers-theunissen, L Kollée, T Eskes, K Motohara, G Vogels-mentink, R De Abreu, L MonnensAbstract:The null hypothesis of our study is that the incidence of vitamin K deficiency in mother-infant pairs exposed to Anticonvulsant drugs is not higher than in controls. In this multicenter observational case-control study, 25 pregnant women receiving Anticonvulsant Therapy and 25 pregnant controls were studied for PIVKA-II (protein induced by vitamin K absence of factor II) and vitamin K1 concentrations at 32 weeks' gestation and at delivery. PIVKA-II was detectable in 54% of cord samples of the Anticonvulsant group and in 20% of controls (chi 2, p = 0.01). In both groups vitamin K1 cord blood levels were predominantly below the detection limit. Maternal vitamin K1 concentrations were lower in women with epilepsy than in controls (Wilcoxon's rank sum test, p < 0.05), but PIVKA-II was rarely present. The incidence of vitamin K deficiency is increased in neonates exposed to Anticonvulsant drugs prenatally. Their mothers, however, are rarely vitamin K deficient.
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Increased incidence of neonatal vitamin K deficiency resulting from maternal Anticonvulsant Therapy
American Journal of Obstetrics and Gynecology, 1993Co-Authors: M Cornelissen, R Steegers-theunissen, L Kollée, T Eskes, K Motohara, G Vogels-mentink, Ronney A. De Abreu, L MonnensAbstract:OBJECTIVE: The null hypothesis of our study is that the incidence of vitamin K deficiency in mother-infant pairs exposed to Anticonvulsant drugs is not higher than in controls. STUDY DESIGN: In this multicenter observational case-control study, 25 pregnant women receiving Anticonvulsant Therapy and 25 pregnant controls were studied for PIVKA-II (protein induced by vitamin K absence of factor II) and vitamin K 1 concentrations at 32 weeks' gestation and at delivery. RESULTS: PIVKA-II was detectable in 54% of cord samples of the Anticonvulsant group and in 20% of controls ( x 2 , p = 0.01). In both groups vitamin K1 cord blood levels were predominantly below the detection limit. Maternal vitamin K 1 concentrations were lower in women with epilepsy than in controls (Wilcoxon's rank sum test, p CONCLUSIONS: The incidence of vitamin K deficiency is increased in neonates exposed to Anticonvulsant drugs prenatally. Their mothers, however, are rarely vitamin K deficient.
M Cornelissen - One of the best experts on this subject based on the ideXlab platform.
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Supplementation of vitamin K in pregnant women receiving Anticonvulsant Therapy prevents neonatal vitamin K deficiency.
American journal of obstetrics and gynecology, 1993Co-Authors: M Cornelissen, R Steegers-theunissen, L Kollée, T Eskes, K Motohara, L MonnensAbstract:The null hypothesis of this study is that extra vitamin K administered to pregnant women on a regimen of enzyme-inducing Anticonvulsant Therapy will not decrease the frequency of symptoms of vitamin K deficiency in their neonates. A multicenter case-control study was performed on 16 pregnant women on Anticonvulsant Therapy who received 10 mg of vitamin K1 daily from 36 weeks of pregnancy onward. Concentrations of PIVKA-II (protein induced by vitamin K absence for factor II) and of vitamin K1 were determined in cord blood and compared with those in 20 controls. In none of 17 cord samples was PIVKA-II detectable, compared with 13 of 20 in controls (chi 2, p < 0.001). Median cord vitamin K1 level was 530 pg/ml compared with below detection limit in most controls. Antenatal vitamin K1 treatment decreases the frequency of vitamin K deficiency in neonates of mothers on Anticonvulsant Therapy.
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Supplementation of vitamin K in pregnant women receiving Anticonvulsant Therapy prevents neonatal vitamin K deficiency
American Journal of Obstetrics and Gynecology, 1993Co-Authors: M Cornelissen, R Steegers-theunissen, L Kollée, T Eskes, K Motohara, L MonnensAbstract:OBJECTIVE: The null hypothesis of this study is that extra vitamin K administered to pregnant women on a regimen of enzyme-inducing Anticonvulsant Therapy will not decrease the frequency of symptoms of vitamin K deficiency in their neonates. STUDY DESIGN: A multicenter case-control study was performed on 16 pregnant women on Anticonvulsant Therapy who received 10 mg of vitamin Kl daily from 36 weeks of pregnancy onward. Concentrations of PIVKA-II (protein induced by vitamin K absence for factor II) and of vitamin K 1 were determined in cord blood and compared with those in 20 controls. RESULTS: In none of 17 cord samples was PIVKA-II detectable, compared with 13 of 20 in controls ( x 2 , p 1 level was 530 pg/ml compared with below detection limit in most controls. CONCLUSIONS: Antenatal vitamin K 1 treatment decreases the frequency of vitamin K deficiency in neonates of mothers on Anticonvulsant Therapy.
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Increased incidence of neonatal vitamin K deficiency resulting from maternal Anticonvulsant Therapy.
American journal of obstetrics and gynecology, 1993Co-Authors: M Cornelissen, R Steegers-theunissen, L Kollée, T Eskes, K Motohara, G Vogels-mentink, R De Abreu, L MonnensAbstract:The null hypothesis of our study is that the incidence of vitamin K deficiency in mother-infant pairs exposed to Anticonvulsant drugs is not higher than in controls. In this multicenter observational case-control study, 25 pregnant women receiving Anticonvulsant Therapy and 25 pregnant controls were studied for PIVKA-II (protein induced by vitamin K absence of factor II) and vitamin K1 concentrations at 32 weeks' gestation and at delivery. PIVKA-II was detectable in 54% of cord samples of the Anticonvulsant group and in 20% of controls (chi 2, p = 0.01). In both groups vitamin K1 cord blood levels were predominantly below the detection limit. Maternal vitamin K1 concentrations were lower in women with epilepsy than in controls (Wilcoxon's rank sum test, p < 0.05), but PIVKA-II was rarely present. The incidence of vitamin K deficiency is increased in neonates exposed to Anticonvulsant drugs prenatally. Their mothers, however, are rarely vitamin K deficient.
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Increased incidence of neonatal vitamin K deficiency resulting from maternal Anticonvulsant Therapy
American Journal of Obstetrics and Gynecology, 1993Co-Authors: M Cornelissen, R Steegers-theunissen, L Kollée, T Eskes, K Motohara, G Vogels-mentink, Ronney A. De Abreu, L MonnensAbstract:OBJECTIVE: The null hypothesis of our study is that the incidence of vitamin K deficiency in mother-infant pairs exposed to Anticonvulsant drugs is not higher than in controls. STUDY DESIGN: In this multicenter observational case-control study, 25 pregnant women receiving Anticonvulsant Therapy and 25 pregnant controls were studied for PIVKA-II (protein induced by vitamin K absence of factor II) and vitamin K 1 concentrations at 32 weeks' gestation and at delivery. RESULTS: PIVKA-II was detectable in 54% of cord samples of the Anticonvulsant group and in 20% of controls ( x 2 , p = 0.01). In both groups vitamin K1 cord blood levels were predominantly below the detection limit. Maternal vitamin K 1 concentrations were lower in women with epilepsy than in controls (Wilcoxon's rank sum test, p CONCLUSIONS: The incidence of vitamin K deficiency is increased in neonates exposed to Anticonvulsant drugs prenatally. Their mothers, however, are rarely vitamin K deficient.
Sulpicio G Soriano - One of the best experts on this subject based on the ideXlab platform.
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pharmacokinetics and pharmacodynamics of vecuronium in children receiving phenytoin or carbamazepine for chronic Anticonvulsant Therapy
BJA: British Journal of Anaesthesia, 2001Co-Authors: Sulpicio G Soriano, Lorna J Sullivan, Karthik Venkatakrishnan, David J Greenblatt, J Jeevendra A MartynAbstract:The pharmacokinetics and time course of action of vecuronium in normal children and children receiving Anticonvulsant drugs for prolonged periods were characterized. A bolus dose of vecuronium 0.15 mg kg(-1) was administered i.v. to 10 non-epileptic children and to 10 children on phenytoin and 10 children on carbamazepine, who were matched for age and weight. Plasma concentrations of vecuronium, 3-OH desacetylvecuronium (the primary metabolite of vecuronium) and alpha1-acid glycoprotein (AAG) were determined. Pharmacokinetic variables were derived from plasma samples collected before and after administration of vecuronium. Neuromuscular transmission was monitored by evoked compound electromyography. Recovery of the first twitch of the train-of-four (T1/T0) and the recovery index (RI), the time for 25-75% recovery of T1/T0, were determined. The elimination half-life of vecuronium was significantly reduced in both Anticonvulsant groups compared with control [control 48.2 (SD 40.3), phenytoin 23.5 (13.1), carbamazepine 18.4 (16.6) min, P<0.05]. Vecuronium clearance was increased in both Anticonvulsant groups [control 9.0 (3.6), phenytoin 15.1 (8.9), carbamazepine 18.8 (13.1) ml kg(-1) min(-1), 0.05
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onset and duration of action of rocuronium in children receiving chronic Anticonvulsant Therapy
Pediatric Anesthesia, 2000Co-Authors: Sulpicio G Soriano, Lorna J Sullivan, Sarah J. Kaus, J Jeevendra A MartynAbstract:Summary The onset and time course of action of rocuronium in normal children and children receiving Anticonvulsant drugs for prolonged periods was characterized. A single bolus dose of 0.6 mg·kg−1 rocuronium was administered i.v. to seven nonepileptic patients on no medication, and eight patients on chronic Anticonvulsant Therapy consisting of either phenytoin, carbamazepine, or both who were age and weight matched. Neuromuscular transmission was monitored by the evoked compound electromyography of the thenar muscles using train of four stimulation every 20 s. Recovery times of the first twitch to 10%, 25%, 50%, 75% and 100% of baseline values and recovery index were obtained. The onset times were 1.05±0.5 and 1.41±0.5 min for the control and Anticonvulsant groups respectively and were not significantly different. Children receiving chronic Anticonvulsant Therapy had significantly shorter recovery index than the control group (control 10.4±5.1 min, Anticonvulsant 4.8±1.7 min, P<0.05). Furthermore, the duration of recovery to 10%, 50%, 75% and 100% of baseline T1 values was less in the Anticonvulsant drug group. Our data confirm resistance to rocuronium in children on chronic Anticonvulsant drugs.
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Onset and duration of action of rocuronium in children receiving chronic Anticonvulsant Therapy.
Paediatric anaesthesia, 2000Co-Authors: Sulpicio G Soriano, Lorna J Sullivan, Sarah J. Kaus, J. A. Jeevendra MartynAbstract:Summary The onset and time course of action of rocuronium in normal children and children receiving Anticonvulsant drugs for prolonged periods was characterized. A single bolus dose of 0.6 mg·kg−1 rocuronium was administered i.v. to seven nonepileptic patients on no medication, and eight patients on chronic Anticonvulsant Therapy consisting of either phenytoin, carbamazepine, or both who were age and weight matched. Neuromuscular transmission was monitored by the evoked compound electromyography of the thenar muscles using train of four stimulation every 20 s. Recovery times of the first twitch to 10%, 25%, 50%, 75% and 100% of baseline values and recovery index were obtained. The onset times were 1.05±0.5 and 1.41±0.5 min for the control and Anticonvulsant groups respectively and were not significantly different. Children receiving chronic Anticonvulsant Therapy had significantly shorter recovery index than the control group (control 10.4±5.1 min, Anticonvulsant 4.8±1.7 min, P
Manya Prasad - One of the best experts on this subject based on the ideXlab platform.
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Anticonvulsant Therapy for status epilepticus
Cochrane Database of Systematic Reviews, 2014Co-Authors: Manya Prasad, Pudukode R Krishnan, Reginald P Sequeira, Khaldoon AlroomiAbstract:Background Status epilepticus is a medical emergency associated with significant mortality and morbidity that requires immediate and effective treatment. Objectives (1) To determine whether a particular Anticonvulsant is more effective or safer to use in status epilepticus compared to another and compared to placebo. (2) To delineate reasons for disagreement in the literature regarding recommended treatment regimens and to highlight areas for future research. Search methods For the latest update of this review, the following electronic databases were searched on 15/08/2013: the Cochrane Epilepsy Group's Specialized Register, CENTRAL The Cochrane Library July 2013, Issue 7, and MEDLINE (Ovid) 1946 to 15/08/2013. Selection criteria Randomised controlled trials of participants with premonitory, early, established or refractory status epilepticus using a truly random or quasi-random allocation of treatments were included. Data collection and analysis Two review authors independently selected trials for inclusion, assessed trial quality and extracted data. Main results Eighteen studies with 2755 participants were included. Few studies used the same interventions. Intravenous diazepam was better than placebo in reducing the risk of non-cessation of seizures (risk ratio (RR) 0.73, 95% confidence interval (CI) 0.57 to 0.92), requirement for ventilatory support (RR 0.39, 95% CI 0.16 to 0.94), or continuation of status epilepticus requiring use of a different drug or general anaesthesia (RR 0.73, 95% CI 0.57 to 0.92). Intravenous lorazepam was better than placebo for risk of non-cessation of seizures (RR 0.52, 95% CI 0.38 to 0.71) and for risk of continuation of status epilepticus requiring a different drug or general anaesthesia (RR 0.52, 95% CI 0.38 to 0.71). Intravenous lorazepam was better than intravenous diazepam for reducing the risk of non-cessation of seizures (RR 0.64, 95% CI 0.45 to 0.90) and had a lower risk for continuation of status epilepticus requiring a different drug or general anaesthesia (RR 0.63, 95% CI 0.45 to 0.88). Intravenous lorazepam was better than intravenous phenytoin for risk of non-cessation of seizures (RR 0.62, 95% CI 0.45 to 0.86). Diazepam gel was better than placebo gel in reducing the risk of non-cessation of seizures (RR 0.43 95% CI 0.30 to 0.62) For pre-hospital treatment, intramuscular midazolam is at least as effective as (probably more effective than) intravenous lorazepam in control of seizures (RR1.16, 95% CI 1.06 to 1.27) and frequency of hospitalisation (RR 0.88, 95% CI 0.79 to 0.97) or intensive care admissions (RR 0.79, 95% CI 0.65 to 0.96). It was uncertain whether Intravenous valproate was better than intravenous phenytoin in reducing risk of non-cessation of seizures (RR 0.75, 95% CI 0.28 to 2.00). Both levetiracetam and lorazepam were equally effective in aborting seizures (RR 0.97, 95% CI 0.44 to 2.13). Results for other comparisons of Anticonvulsant therapies were uncertain due to single studies with few participants. The body of randomised evidence to guide clinical decisions is small. It was uncertain whether any Anticonvulsant Therapy was better than another in terms of adverse effects, due to few studies and participants identified. The quality of the evidence from the included studies is not strong but appears acceptable. We were unable to make judgements for risk of bias domains incomplete outcome reporting (attrition bias) and selective outcome reporting (selection bias) due to unclear reporting by the study authors. Authors' conclusions Intravenous lorazepam is better than intravenous diazepam or intravenous phenytoin alone for cessation of seizures. Intravenous lorazepam also carries a lower risk of continuation of status epilepticus requiring a different drug or general anaesthesia compared with intravenous diazepam. Both intravenous lorazepam and diazepam are better than placebo for the same outcomes. For pre hospital management, midazolam IM seemed more effective than lorazepam IV for cessation of seizures, frequency of hospitalisation and ICU admissions however,it was unclear whether the risk of recurrence of seizures differed between treatments. The results of other comparisons of Anticonvulsant therapies versus each other were also uncertain. Universally accepted definitions of premonitory, early, established and refractory status epilepticus are required. Diazepam gel was better than placebo gel in reducing the risk of non-cessation of seizures. Results for other comparisons of Anticonvulsant therapies were uncertain due to single studies with few participants.
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The Cochrane Library - Anticonvulsant Therapy for status epilepticus
The Cochrane database of systematic reviews, 2014Co-Authors: Manya Prasad, Pudukode R Krishnan, Reginald P Sequeira, Khaldoon Al-roomiAbstract:Background Status epilepticus is a medical emergency associated with significant mortality and morbidity that requires immediate and effective treatment. Objectives (1) To determine whether a particular Anticonvulsant is more effective or safer to use in status epilepticus compared to another and compared to placebo. (2) To delineate reasons for disagreement in the literature regarding recommended treatment regimens and to highlight areas for future research. Search methods For the latest update of this review, the following electronic databases were searched on 15/08/2013: the Cochrane Epilepsy Group's Specialized Register, CENTRAL The Cochrane Library July 2013, Issue 7, and MEDLINE (Ovid) 1946 to 15/08/2013. Selection criteria Randomised controlled trials of participants with premonitory, early, established or refractory status epilepticus using a truly random or quasi-random allocation of treatments were included. Data collection and analysis Two review authors independently selected trials for inclusion, assessed trial quality and extracted data. Main results Eighteen studies with 2755 participants were included. Few studies used the same interventions. Intravenous diazepam was better than placebo in reducing the risk of non-cessation of seizures (risk ratio (RR) 0.73, 95% confidence interval (CI) 0.57 to 0.92), requirement for ventilatory support (RR 0.39, 95% CI 0.16 to 0.94), or continuation of status epilepticus requiring use of a different drug or general anaesthesia (RR 0.73, 95% CI 0.57 to 0.92). Intravenous lorazepam was better than placebo for risk of non-cessation of seizures (RR 0.52, 95% CI 0.38 to 0.71) and for risk of continuation of status epilepticus requiring a different drug or general anaesthesia (RR 0.52, 95% CI 0.38 to 0.71). Intravenous lorazepam was better than intravenous diazepam for reducing the risk of non-cessation of seizures (RR 0.64, 95% CI 0.45 to 0.90) and had a lower risk for continuation of status epilepticus requiring a different drug or general anaesthesia (RR 0.63, 95% CI 0.45 to 0.88). Intravenous lorazepam was better than intravenous phenytoin for risk of non-cessation of seizures (RR 0.62, 95% CI 0.45 to 0.86). Diazepam gel was better than placebo gel in reducing the risk of non-cessation of seizures (RR 0.43 95% CI 0.30 to 0.62) For pre-hospital treatment, intramuscular midazolam is at least as effective as (probably more effective than) intravenous lorazepam in control of seizures (RR1.16, 95% CI 1.06 to 1.27) and frequency of hospitalisation (RR 0.88, 95% CI 0.79 to 0.97) or intensive care admissions (RR 0.79, 95% CI 0.65 to 0.96). It was uncertain whether Intravenous valproate was better than intravenous phenytoin in reducing risk of non-cessation of seizures (RR 0.75, 95% CI 0.28 to 2.00). Both levetiracetam and lorazepam were equally effective in aborting seizures (RR 0.97, 95% CI 0.44 to 2.13). Results for other comparisons of Anticonvulsant therapies were uncertain due to single studies with few participants. The body of randomised evidence to guide clinical decisions is small. It was uncertain whether any Anticonvulsant Therapy was better than another in terms of adverse effects, due to few studies and participants identified. The quality of the evidence from the included studies is not strong but appears acceptable. We were unable to make judgements for risk of bias domains incomplete outcome reporting (attrition bias) and selective outcome reporting (selection bias) due to unclear reporting by the study authors. Authors' conclusions Intravenous lorazepam is better than intravenous diazepam or intravenous phenytoin alone for cessation of seizures. Intravenous lorazepam also carries a lower risk of continuation of status epilepticus requiring a different drug or general anaesthesia compared with intravenous diazepam. Both intravenous lorazepam and diazepam are better than placebo for the same outcomes. For pre hospital management, midazolam IM seemed more effective than lorazepam IV for cessation of seizures, frequency of hospitalisation and ICU admissions however,it was unclear whether the risk of recurrence of seizures differed between treatments. The results of other comparisons of Anticonvulsant therapies versus each other were also uncertain. Universally accepted definitions of premonitory, early, established and refractory status epilepticus are required. Diazepam gel was better than placebo gel in reducing the risk of non-cessation of seizures. Results for other comparisons of Anticonvulsant therapies were uncertain due to single studies with few participants.
J Jeevendra A Martyn - One of the best experts on this subject based on the ideXlab platform.
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pharmacokinetics and pharmacodynamics of vecuronium in children receiving phenytoin or carbamazepine for chronic Anticonvulsant Therapy
BJA: British Journal of Anaesthesia, 2001Co-Authors: Sulpicio G Soriano, Lorna J Sullivan, Karthik Venkatakrishnan, David J Greenblatt, J Jeevendra A MartynAbstract:The pharmacokinetics and time course of action of vecuronium in normal children and children receiving Anticonvulsant drugs for prolonged periods were characterized. A bolus dose of vecuronium 0.15 mg kg(-1) was administered i.v. to 10 non-epileptic children and to 10 children on phenytoin and 10 children on carbamazepine, who were matched for age and weight. Plasma concentrations of vecuronium, 3-OH desacetylvecuronium (the primary metabolite of vecuronium) and alpha1-acid glycoprotein (AAG) were determined. Pharmacokinetic variables were derived from plasma samples collected before and after administration of vecuronium. Neuromuscular transmission was monitored by evoked compound electromyography. Recovery of the first twitch of the train-of-four (T1/T0) and the recovery index (RI), the time for 25-75% recovery of T1/T0, were determined. The elimination half-life of vecuronium was significantly reduced in both Anticonvulsant groups compared with control [control 48.2 (SD 40.3), phenytoin 23.5 (13.1), carbamazepine 18.4 (16.6) min, P<0.05]. Vecuronium clearance was increased in both Anticonvulsant groups [control 9.0 (3.6), phenytoin 15.1 (8.9), carbamazepine 18.8 (13.1) ml kg(-1) min(-1), 0.05
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onset and duration of action of rocuronium in children receiving chronic Anticonvulsant Therapy
Pediatric Anesthesia, 2000Co-Authors: Sulpicio G Soriano, Lorna J Sullivan, Sarah J. Kaus, J Jeevendra A MartynAbstract:Summary The onset and time course of action of rocuronium in normal children and children receiving Anticonvulsant drugs for prolonged periods was characterized. A single bolus dose of 0.6 mg·kg−1 rocuronium was administered i.v. to seven nonepileptic patients on no medication, and eight patients on chronic Anticonvulsant Therapy consisting of either phenytoin, carbamazepine, or both who were age and weight matched. Neuromuscular transmission was monitored by the evoked compound electromyography of the thenar muscles using train of four stimulation every 20 s. Recovery times of the first twitch to 10%, 25%, 50%, 75% and 100% of baseline values and recovery index were obtained. The onset times were 1.05±0.5 and 1.41±0.5 min for the control and Anticonvulsant groups respectively and were not significantly different. Children receiving chronic Anticonvulsant Therapy had significantly shorter recovery index than the control group (control 10.4±5.1 min, Anticonvulsant 4.8±1.7 min, P<0.05). Furthermore, the duration of recovery to 10%, 50%, 75% and 100% of baseline T1 values was less in the Anticonvulsant drug group. Our data confirm resistance to rocuronium in children on chronic Anticonvulsant drugs.