The "EMIT" enzyme immunoassay system (Syva) that involves use of glucose-6-phosphate dehydrogenase (EC 22.214.171.124) as the enzyme label has been adapted to a fully mechanized kinetic enzyme analyzer for analysis of phenobarbital, phenytoin, and primidone. This procedure, compared with the gas-chromatographic procedure of Kupferberg [Clin. Chim. Acta 29, 283 (1970)], gave a weighted regression line--forced through the origin--of y=(1.01+/-0.04) x for phenobarbital, y=(0.95+/-0.04) x for primidone. Within-run coefficients of variation based on single determinations were 9,11, and 22% for primidone, phenobarbital, and phenytoin, respectively. Run-to-run assay CV was 6% for primidone and phenobarbital and 13% for phenytoin, based on the means of triplicate determinations of a sample with a mid-range concentration.
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Aromatic anticonvulsant agents such as carbamazepine and phenytoin can induce anticonvulsant hypersensitivity syndrome (AHS) at a frequency of 1 in 10,000 to 1 in 1,000 treated patients. The hypersensitivity syndrome is a potentially life-threatening adverse drug reaction with multiorgan involvement, and incidental reexposure must be strictly avoided. Patients and treating physicians must be informed and educated about the causal drug and its potential immunologic or toxicologic cross-reactivity with other compounds. It has been well established that for future antiepileptic drug therapy, carboxamides (carbamazepine and oxcarbazepine), phenytoin, and barbiturates (phenobarbital and primidone) have to be avoided owing to their high degree of cross-reactivity. Other anticonvulsant agents, such as valproic acid, benzodiazepines, and gabapentin, may be prescribed.
To evaluate whether generic substitution was associated with any difference in medical resource utilization for 5 widely used antiepileptic drugs (AEDs) in the United States.
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A rapid microanalytical method is described for phenobarbital, phenytoin, primidone and carbamazepine utilizing high-performance thin-layer chromatography (HPTLC). This procedure incorporates a single extraction of a 50-microliter plasma sample. One tenth of the extract is concentrated and applied to the HPTLC plate by a Contact Spotter, chromatographically separated and quantitated by in situ ultraviolet reflectance densitometry. The coefficient of variation is less than 4% (n = 8), the extraction efficiency is approximately 95% and the minimum detectable amount of pure drug standards applied to and developed on the HPTLC plate is 5 ng or less for all four anticonvulsants.
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Nine of 13 patients included in our study experienced a good response. A positive response was understood as a decrease on the limitation of daily activities and an improvement on neurological examination. Zonisamide was well tolerated and no patient abandoned the study for this reason.
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We found no clear evidence to support routine antiepileptic drug serum concentration measurement with the aim of reaching predefined target ranges for the optimisation of treatment of patients with newly-diagnosed epilepsy with antiepileptic drug monotherapy. However, this does not exclude the possible usefulness of therapeutic drug monitoring of specific antiepileptic drugs during polytherapy, in special situations or in selected patients, although evidence is lacking.
The limited amount of information on the new antiepileptic drugs may explain the discrepancies among the two guidelines and between these and other recommendations. Comparative, pragmatic, long-term and open trials should be done to show long-term efficacy and comparative features of the new antiepileptic drugs, and to better assess the effect on quality-of-life, cost-effectiveness, tolerability, and teratogenic potential. In addition, the conflicts should be resolved between the needs of the regulatory bodies and those of the treating physicians. Finally, there is a need for trial designs to be standardised.
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A few reports have shown elevated fasting total plasma homocysteine (tHcy) in patients taking antiepileptic drugs (AEDs). In this study we determined the influence of AEDs on plasma tHcy levels prior to and following methionine loading.
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Medical histories were collected for epileptic dogs treated with potassium bromide with or without phenobarbital sodium or primidone, from which serum was submitted for bromide analysis from May 1992 to May 1996 to the Therapeutic Drug Monitoring Program at Cornell University's College of Veterinary Medicine. A therapeutic response (improved seizure control) was defined as a > or = 50% reduction in seizure frequency following initiation of bromide treatment. Serum bromide and phenobarbital concentrations and therapeutic outcome were determined for all dogs.
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To evaluate the effect of VNS in a series of four children affected by medically unresponsive EPC secondary to chronic inflammatory encephalopathy (two cases), Rasmussen encephalitis (one case) and poliodystrophy (one case).
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Plasma levetiracetam concentrations at steady state were determined by capillary gas chromatography in 590 epilepsy patients included in phase III trials and treated with doses of 1000-4000 mg per day in two divided daily doses. The data were pooled and kinetic parameters estimated by repeated measurement covariance analysis on log-transformed dose-adjusted concentrations (regression line as function of time elapsed since last dose).
In therapy lasting between 8 and 79 (means = 31) months 22 epileptic dogs had been unsuccessfully treated with phenobarbital and/or primidone. Both drugs had been administered in their maximum dosages. In an add-on therapy, these dogs were given potassium bromide at a rate of 17 to 58 mg/kg daily for a period of 7 to 61 (means = 21) months. We could quantitatively evaluate the seizure data from 19 of the dogs: four became free of seizures; seven showed a greater than 50% reduction in seizure frequency; in two dogs, the seizures were reduced by greater than 50% but the number of seizure-days by less than 50%; in the remaining six dogs the therapy was unsuccessful. We achieved the best therapeutic results in animals that suffered only grand mal seizures. Grand mal in addition to other types of seizures and tonic seizures were affected to a lesser extent if at all. At the beginning of the therapy we saw temporary side effects--weakness in the hind limbs and sedation; these were temporary and dependent on the dosage. Serum concentrations differed even with the same dosage among individual dogs. The therapeutic range of bromide serum concentration was from 0.7 to 2.0 mg/ml. Most of the animals tolerated concentrations up to 1.5 mg/ml quite well. To begin an add-on therapy with potassium bromide we would recommend a daily dose of 30 to 40 mg/kg. During treatment, the dose should be determined for each individual dog.
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The concurrence of pregnancy and movement disorders is an uncommon event in a general neurologic practice. Even at specialized movement disorder referral centers, there is insufficient experience to adequately guide management of pregnancy, except perhaps in the case of WD. The questions posed most urgently by patients regard the safety of medication, an issue on which there is insufficient data, and their ability to care for a child for at least the next decade, an issue that differs by disease and social situation. The author's formulation of efficacy and toxicity suggests that certain medications commonly used in movement disorders should be discontinued before pregnancy, if possible. These medications include neuroleptics, amantadine, diazepam, primidone, selegiline, and reserpine. Pregnancy may unmask a pre-existing potential for chorea (i.e., chorea gravidarum) and frequently has a mild exacerbating effect on symptoms of PD; however, it has little effect on other movement disorders. Severe generalized dystonia would probably interfere with vaginal delivery, but the scant existing data suggest minimal effect of movement disorders on pregnancy, childbirth, and neonatal health.
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Seizures remain uncontrolled in up to half of all people with epilepsy in the UK with significant impact on work, family and social life. Previously, there has been a deficiency of data on the characteristics of epilepsy in older people, although it is recognized that the condition is of increasing epidemiological importance in this age group. We have found clear differences in the clinical characteristics of epilepsy in older people, particularly that seizure frequency appears to decline with increasing age.
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Rats were rendered epileptic by subpial injection of an FeCl3 solution. Epileptiform discharges, recorded by chronically implanted extradural electrodes, were evident within 48 h of surgery and persisted for more than 6 months. It is demonstrated that this model is useful for studying new antiepileptic agents since a series of clinically effective drugs (diazepam, clonazepam, Na phenobarbital, primidone, carbamezepine, ethosuximide, diphenylhydantoin, Na valproate, GABOB) show an activity which is does-dependent and within a range satisfactorily related to human dosages.