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Of 1300 epileptic patients 76 (5.8%) were found to have juvenile myoclonic epilepsy (JME). These 76 patients were examined at the epilepsy outpatient clinic of Bakirköy State Hospital for Neurological and Psychiatric Diseases between 1991 and 1996 and data obtained were analysed retrospectively. Clinically typical absence seizures were reported in 40.8%, myoclonic jerks in 100%, and generalized tonic-clonic seizures in 82.9% of the patients. Neurological and mental examination was normal for all patients with the exception of three cases; two with essential tremor and one with minimal dysarthria. Precipitating factors were noted in 85.5% of cases. Abnormal EEG was recorded in 73 (6.1%) patients. Abnormalities mainly consisted of generalized discharges of spike/polyspike and slow-wave (86.6%) and generalized paroxysmal theta or delta (9.2%). Fifteen (19.7%) had focal abnormalities and 20 (26.4%) had photoconvulsive discharges. Of the 76 patients, 40 (52.6%) were not diagnosed at the initial interview; definite diagnosis was delayed by a mean of 5.9 years. As a result of misdiagnosis at the initial interview 40 patients had been administered AED except for valproate. After reassessment of clinical and EEG findings, the medication was changed to valproate therapy. As a result, 65 of our JME patients (85.5%) were seizure free after a one-year follow-up period.

Summary:Purpose: To determine potential changes in the plasma concentrations of oxcarbazepine (OXC) and its metabolites during pregnancy and puerperium.Methods: Five women receiving OXC monotherapy were followed prospectively during pregnancy and the puerperium. Four women were enrolled in the first trimester, and one woman, 2 weeks before delivery. Steady-state concentrations of OXC, its active R-(-)-and S-(+)-monohydroxy derivatives (MHD), and the additional metabolite carbamazepine-10,11-trans-dihydrodiol (DHD) were measured at regular intervals by an enantioselective HPLC assay.Results. In all samples, S-(+)-MHD was the most abundant compound in plasma and accounted almost entirely for the amount of active moiety (defined as the molar sum of OXC, R-(-)-MHD, and S-(+)-MHD) found in the circulation. The dosenormalized concentrations of active moiety decreased markedly during gestation and, in four of the five patients, increased strikingly after delivery. Plasma concentrations of S-(+)-MHD mirrored closely the levels of the active moiety. Plasma concentrations of the parent drug and other metabolites also tended to decrease during pregnancy and to increase after delivery.Conclusions: During treatment with OXC, S-(+)-MHD is by far the most abundant active compound in plasma. The concentration of this metabolite as well as the active moiety may decrease markedly during pregnancy and may increase severalfold after delivery. Because of these striking pharmacokinetic changes, the clinical response should be monitored closely in OXC-treated women throughout pregnancy and the puerperium.

The majority of patients with epilepsy maintain seizure control during pregnancy. The apparently higher risk of seizures among women treated with oxcarbazepine and the more frequent increases in drug load in the oxcarbazepine and lamotrigine cohorts prompts further studies on relationships with pharmacokinetic changes. Risks associated with status epilepticus appear to be lower than previously reported.

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