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The effects of CYT on the anticonvulsant activity of six AEDs were examined in maximal electroshock (MES)-induced seizures in mice.
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The guidelines on trigeminal neuralgia management published by the American Academy of Neurology (AAN) and the European Federation of Neurological Societies (EFNS) recommended that patients unresponsive to carbamazepine or oxcarbazepine be offered the surgical option. However, because some patients may not be willing to resort to surgery, we searched the literature for treatment in refractory trigeminal neuralgia. We found other oral treatments, intranasal spray, subcutaneous injections, various kinds of peripheral nerve blocks and injections of botulinum toxin. On the basis of the available evidence we suggest that no oral treatment other than carbamazepine or oxcarbazepine is useful. Among the other options, there is increasingly strong evidence that botulinum toxin injections are efficacious and may be offered before surgery or to those unwilling to undergo surgery.
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To evaluate the safety, tolerability, pharmacokinetics and pharmacodynamics of BIA 2-093 [S-(-)-10-acetoxy-10,11-dihydro-5H-dibenzo/b,f/aze- pine-5-carboxamide] in healthy male volunteers.
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Thirteen patients (17.6%) in solitary cysticercus granuloma group and 15 patients (33.3%) in normal neuroimaging group had seizure recurrences (P = 0.049). In solitary cysticercus granuloma group, family history of seizure disorder (P = 0.004), headache (P = 0.029), and serial seizures (at onset) (P = 0.001) were significantly associated with the seizure recurrence. Granuloma remained unresolved in all patients. In patients with normal neuroimaging, abnormal EEG (P = 0.043), at inclusion, was only a significant factor of the seizure recurrence.
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A one-compartment open model with first-order absorption and elimination was generated from the results of a previous study measuring plasma concentrations following one 400 mg fasting dose of CBZ-ERC. This model was used to simulate plasma concentrations of CBZ following multiple 400 mg doses of CBZ-ERC at 12-hour intervals, and then when a missed dose is taken 3, 6, or 9 hours late; when two doses are taken at one time; and when a single dose is taken at the time of the next dosing. In comparison, similar modeling was done for monohydroxy derivative (MHD) of OXC at doses of 600 or 1200 mg.
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The authors examined the ratio between the plasma and the cerebrospinal fluid (CSF) concentration of topiramate in 14 adults with epilepsy. Simultaneous trough samples of venous blood and CSF were collected and analyzed as total and unbound concentrations. Concomitant levels were also analyzed of lamotrigine (n = 5) and the relevant oxcarbazepine metabolite, 10-hydroxycarbazepine (n = 3). There was a close correlation between the plasma and the CSF concentration for both the total and unbound concentration of topiramate. The median CSF/plasma ratio of total topiramate was 0.85. The free topiramate concentration in plasma was not different from the free topiramate concentration in CSF. The CSF/plasma ratios showed little variation and were independent of the plasma level for both the total and the unbound levels. The unbound fraction of topiramate was 84% in plasma and 97% in CSF. The CSF concentrations of lamotrigine and 10-hydroxycarbazepine were 50% and 61% of the plasma concentrations, respectively. For topiramate, there is a close correlation between the plasma concentration and the CSF concentration. There does not seem to be a saturable carrier mechanism restricting topiramate transport across the blood-brain barrier. The concentration of topiramate in CSF is equal to the unbound proportion of topiramate in plasma, implying that the delivery of topiramate to the brain occurs via transfer from the unbound plasma pool. Plasma is thus a relevant matrix for therapeutic drug monitoring of topiramate.
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Two papers that met the inclusion criteria were included. The first paper involved 198 patients, including 108 cases in the levetiracetam therapy group and 97 cases in the placebo group. Seven cases (6.9%) were seizure free in the levetiracetam therapy group compared with 1 case (1%) in the placebo group (p<0.01) 14 weeks after treatment. Levetiracetam therapy decreased significantly the frequency of seizures compared with the placebo treatment. The second paper involved 39 patients, including 21 cases in the levetiracetam therapy group and 18 cases in the oxcarbazepine therapy group. Nineteen cases (90.5%) were seizure-free in the levetiracetam therapy group compared with 13 cases (72.2%) in the oxcarbazepine therapy group (P=0.410) during a follow-up of 12-24 months. The adverse effects in the levetiracetam therapy group were not significantly different from the placebo and the oxcarbazepine therapy groups.
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In this prospective study, 31 adults with newly diagnosed epilepsy were included who were started on therapy with either oxcarbazepine (OXC, n=16, mean age 45.6 years, 37.5% female) or valproate (VPA, n=15, mean age 42.2 years, 33.3% female). Clinical characteristics were obtained at baseline, after 2 weeks and 3 months. In addition, blood samples were drawn at each visit. Calcium, phosphate, alkaline phosphatase (AP), receptor activator of NF-κB ligand (RANKL), osteoprotegerin (OPG), osteocalcin (OC) and cathepsin K were determined.
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We recommend using OXC as monotherapy or as add-on therapy in refractory mania, but we recommend it be used predominantly as an add-on treatment for other phases of BD in patients who have not improved with well-established treatments or in patients who have difficulty tolerating adequate dosages.
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This study highlights the importance of taking into consideration not only seizure control but also the appearance of side effects when choosing antiepileptic drugs in this patients population.
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We presented a case of a 50 years old woman with bipolar disorder who is treated with lithium and oxcarbazepine, she presented a manic episode and a confusional syndrome after she stopped taking the medication. The magnetic resonance showed a restricted diffusion area at the splenium of the corpus callosum and bifrontal hygromas that disappear two weeks later.