Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical trial of Dipropylacetat (Convulex) demonstrates the advantages of a well organized multicenter-study. In rather short time reliable information concerning indication, compatibility and dosage can be received. The results of this project are similar to other observations dealing with DPA: Good therapeutical effect in primary generalized epilepsies independent of the seizure-type. Astonishing results influencing Lennox-Syndrome. In cases not treated before, Convulex shows at least the same effect than the "standard anticonvulsants" but less side effects, especially sedation. In those untreated "new-comers" therapeutical effect comes earlier than in cases of premedication. 20 to 50 mg/kg/day can be recommended in childhood. In rare cases the dosage was increased up to 120 mg/kg/day without problems.
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PMID:[Austrian complex-study on dipropylacetate. Pediatric experiences]. 81 26

Valproic acid [dipropylacetic acid (DPA)] was evaluated in an alumina-gel monkey model (N = 12) by constant-rate intravenous infusion. The data indicated: (a) a statistically significant decrease in seizure frequency the first 2 days of drug Step I (45-55 mug/ml) and drug Step II (90-110 mug/ml) which was temporary, lasting 2 days only; (b) a later, more permanent decrease in siezure frequency which was not apparent until drug Setp III (130-170 mug/ml); and a delayed return of the seizure frequency to predrug levels for 2 weeks after drug administration was discontinued, with no DPA detectable in plasma after the initial postdrug day. Whether DPA will behave as a reversibly acting drug was discussed.
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PMID:Valproic acid: reversibly acting drug? 82 96

The anti-convulsive action of dipropyl acetic acid (Convulex) was tested in 21 patients with grandmal seizures (GM) and/or temporal lobe attacks (TL), or with Jacksonian epilepsy. Patients were chosen according to a negative selection system. Results showed that in GM and TL seizures, Convulex constitutes an important addition to the battery of anticonvulsives available today. Action was more potent in GM than in TL attacks. Toxic effects are slight. Treatment had to be discontinued in two patients -- once because of cerebellar symptoms and once because of crowded incidence of seizures. In two cases the patients gained weight. Occasional gastrointestinal complaints disappeared when antacids were administered. No changes were observed with reference to blood count, or to hepatic or renal function. Fatigue set in only when treatment was combined with barbiturates and disappeared again when pre-medication was reduced. Five patients showed an improved state of mind (activation and better communication with others); this psychological action may be considered an additional advantage. Since the action of barbiturates and hydantoins is potentiated by Convulex, pre-medication may be reduced --provided Convulex therapy alone does not seem adequate. Hence, trial treatment with Convulex may also be recommended in those patients who are successfully controlled with barbiturates and hydantoins,but whose daily work schedule is impaired due to fatigue.
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PMID:[The effect of dipropyl acetic acid (Convules) in epileptic adults with a high frequency of seizures]. 82 58

Dipropylacetate is absorbed rapidly and attains a maximum concentration in serum 1 to 3 hr after ingestion. Since its half-life is on the order of 8 to 10 hr, it must be prescribed three times a day, every 8 hr. It reaches a stable concentration in blood within 48 hr after treatment is begun (by contrast with diphenylhydantoin and phenobarbital) and might therefore be useful when seizures must be controlled quickly. The serum concentration can be altered by some other anticonvulsant drugs, but these interactions should be studied in more detail. The serum concentration varies considerably in the course of a day and from one day to the next in the same subject, which makes it difficult to adjust the blood level. Depamide is rapidly transformed in vivo to dipropylacetate.
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PMID:Concentration of dipropylacetate in plasma. 110 22

The effect od dipropylacetic acid (DPA; Depakine) on the bemegride-induced convulsive threshold was investigated in alert cats. Forty-five min after DPA 200 mg/kg, s.c., no significant effect was obtained; 5 min after the same dose iv., protection from bemegride-induced seizures was pronounced. DPA did not decrease focal discharges in sensorimotor cortex produced by topical cobalt, although spread of epileptogenic activity from the focus was inhibited. DPA antiepileptic protection tested by the same procedure was about the same as that given by phenobarbital and less than that given by diazepam.
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PMID:Dipropylacetic acid (Depakine) in experimental epilepsy in the alert cat. 112

The authors report the results of treatment of 14 patients (10 male, 4 female, average age 20.3 years) with benign myoclonic epilepsy. Valproate monotherapy led to control of seizures in 10 cases, and to a distinct reduction of seizure frequency in 3 cases. Thrombocytopenia was the only side-effect encountered in this study.
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PMID:The therapy of benign myoclonic epilepsy in infants. 141 74

Thirteen children with intractable epilepsy were treated by means of three-times-daily administration of a conventional preparation of valproic acid (C-VPA) and twice-daily administration of a new slow-release preparation of VPA (SR-VPA) with the cross-over technique. The frequency of seizures, side effect and steady-state pharmacokinetics of VPA were evaluated. With the change from C-VPA tid to SR-VPA bid, four patients exhibited a significant reduction in seizure frequency. The steady-state minimum concentration (Cmin) was higher, the maximum concentration (Cmax) lower and there were less diurnal fluctuations with SR-VPA, than with the respective values obtained in the C-VPA group, all the differences being statistically significant. Furthermore, a significant difference was unexpectedly found in the area under the curve (AUC) from 0 to 24 hours, the mean AUC in the period of SR-VPA being 9% higher than that with C-VPA. Five of the nine patients under 6 years of age showed more than 10% increase, and all four patients over 6 years of age less than 10% increase or a decrease in AUC. It was concluded that with SR-VPA bid, the pharmacokinetic features were more stable, the age-related AUC value was larger and the clinical effect was better than in comparison to C-VPA tid in children with intractable epilepsy.
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PMID:A comparative clinical and pharmacokinetic study of a new slow-release versus conventional preparations of valproic acid in children with intractable epilepsy. 145 84

Kainic acid (KA 4-14 mg/kg) administered intraperitoneally (i.p.) produces automatisms (scratching until third postnatal week, "wet dog" shakes thereafter), and clonic and tonic-clonic seizures in rats aged 7, 12, 18, 25, and 90 days. Administration of carbamazepine (CBZ) i.p. (25 or 50 mg/kg), phenobarbital (PB 20-80 mg/kg), clonazepam (CZP 0.2 or 1 mg/kg), or valproate (VPA 200 mg/kg) influenced neither incidence nor latency of automatisms. Clonic seizures that are regularly observed after the third postnatal week in controls were either abolished or substantially suppressed by any of the aforementioned antiepileptic drugs (AEDs). Tonic-clonic seizures observed in the first 3 postnatal weeks were suppressed only by solvent [including propyleneglycol (PEG), ethanol, and water]; the effect of AEDs on tonic-clonic seizures was proconvulsant instead. The automatisms were most resistant to AED therapy. These results induce some doubts about the adequacy of the KA model for identifying AEDs effective against complex partial seizures, but forthcoming AEDs that suppress automatisms in the KA rat model might also be active against human complex partial seizures.
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PMID:Action of antiepileptic drugs against kainic acid-induced seizures and automatisms during ontogenesis in rats. 146 81

An increased risk of seizures during and immediately after labour has been observed in epileptic women, and it is recognized that serum levels of antiepileptic drugs may decrease in pregnancy. Several studies have suggested that total valproate levels fall, but that free fractions increase during pregnancy. Recent findings suggest that the actual metabolism of valproate is not altered by pregnancy and that the changes of the plasma clearance are due primarily to decreased protein binding. The levels of free drug will not change significantly as pregnancy advances. However, dose reduction after delivery may be necessary to avoid toxicity. Valproate and its metabolites undergo placental transfer. In the foetus the plasma level of valproate and the protein binding are higher than in maternal plasma, and the half-life of valproate following placental transfer is considerably longer than in adults. Only small amounts of valproate appear in breast milk and those are not likely to cause any problems. During pregnancy and the first month after delivery preferably both total and free valproate serum levels should be closely monitored to determine the lowest effective dose.
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PMID:Pharmacokinetics of valproate in pregnancy: mother-foetus-newborn. 150 9

We studied the distribution of valproic acid (VPA) between brain (gray matter) and serum in 13 patients receiving chronic VPA therapy who underwent cortical resections for intractable seizures. Valproate concentration in cerebral cortex was remarkably low compared with either total or unbound valproate concentration in serum. The respective brain-to-serum partition ratios based on total and free drug in serum were 0.111 +/- 0.051 and 0.544 +/- 0.175. In comparison with other commonly used antiepileptic drugs, valproate has the distinction of exhibiting the lowest brain-to-blood partitioning. Moreover, the brain-to-serum concentration ratio varied over a four-fold range between patients. Some of this variability was related to variation in serum protein binding, as indicated by a modest correlation between the partition ratio and serum free fraction (r = +0.687). However, the brain-to-unbound concentration ratio still showed a three-fold variation. The variability in distribution of VPA between brain and blood is probably one of the underlying factors for the lack of a clearly definable therapeutic range of serum VPA concentration in epileptic patient populations.
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PMID:Low and variable presence of valproic acid in human brain. 154 18


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