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Eight randomized, placebo-controlled, double-blind trials (4 with ESL, 3 with LCM, and 1 with OXC) were included in our analysis. At high doses (OXC 1200mg, ESL 1200mg and LCM 400mg) there was an increased risk of AE-related study withdrawals compared to placebo for all drugs. Several AEs were associated with the experimental drug. Both number and frequency of AEs were dose-related. At high recommended doses, patients treated with OXC withdrew from the experimental treatment significantly more frequently than patients treated with ESL and LCM. Furthermore, the AEs coordination abnormal/ataxia and diplopia were significantly more frequently observed in patients treated with OXC compared to patients treated with LCM and ESL.
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Previous studies suggest that obese women taking valproate (VPA) for epilepsy are insulin resistant.
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There are currently different groups of drugs for the pharmacotherapy of vertigo, nystagmus and cerebellar disorders: antiemetics; anti-inflammatories, antimenieres, and antimigraineous medications and antidepressants, anticonvulsants, aminopyridines as well as acetyl-DL-leucine. In acute unilateral vestibulopathy, corticosteroids improve the recovery of peripheral vestibular function, but currently there is not sufficient evidence for a general recommendation. There is insufficient evidence to support the view that 16 mg t. i. d. or 48 mg t. i. d. betahistine has an effect in Menière's disease. Therefore, higher dosages are recommended. In animal studies, it was shown that betahistine increases cochlear blood flow. In vestibular paroxysmia, oxcarbazepine was effective (one randomized controlled trial (RCT)). Aminopyridines are recommended for the treatment of downbeat nystagmus (two RCTs) and episodic ataxia type 2 (EA2, one RCT). There has been no RCT on the efficacy of beta-blockers or topiramate but one RCT on flunarizine in vestibular migraine. Based on clinical experience, a treatment analogous to that for migraine without aura can be recommended. Acetyl-DL-leucine improved cerebellar ataxia (two observational studies); it also accelerated central compensation in an animal model of acute unilateral lesion, but RCTs were negative. There are ongoing RCTs on treatment of vestibular paroxysmia with carbamazepine (VESPA), acute unilateral vestibulopathy with betahistine (BETAVEST), vestibular migraine with metoprolol (PROVEMIG), benign paroxysmal positional vertigo with vitamin D (VitD@BPPV), EA2 with 4-aminopyridine versus acetazolamide (EAT-2-TREAT), and cerebellar ataxias with acetyl-DL-leucine (ALCAT).
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Four- to six-week Titration Phase followed by 12-week maintenance treatment with adjunctive lacosamide (Vimpat®) [200, 400 or 600 mg/day] or placebo.
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Medline/PubMed, EMBASE, and Cochrane library searches (1970-January 2010) were conducted for clinical trials of partial-onset seizures (POS) and primary generalized tonic-clonic seizures (PGTCS) in adults and in children <2 and 2-18 years. Independent epidemiologists used standardized search and study evaluation criteria to select eligible trials. Forest plots were used to investigate the relative strength of placebo-subtracted effect measures.
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This article reviews the major potential side effects of the new seizure medications and the treatment of their overdoses for the practicing emergency physician.
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The purpose of this work was to evaluate the potential cross-reactivity of 2 antiepileptic medications containing 3-ringed structures, namely, carbamazepine and oxcarbazepine, with screening assays for tricyclic antidepressants.
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OCBZ reduces plasma concentrations of the estrogen and progestagen components of steroid oral contraceptives, presumably by stimulating their CYP3A-mediated metabolism in the liver or gastrointestinal tract or both. Because this may lead to a decreased efficacy of the contraceptive pill, women treated with OCBZ should receive preferentially a high-dosage contraceptive and should be monitored for signs of reduced hormonal cover.
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The development of ten new antiepileptic drugs (vigabatrin, felbamate, gabapentin, lamotrigine, topiramate, tiagabine, oxcarbazepine, levetiracetam, zonisamide, and pregabalin) has expanded treatment options. The newer drugs may be better tolerated, have fewer drug interactions, and seem to affect cognitive functions to a lesser extent than old drugs. Guidelines on the use of new antiepileptic drugs have been developed in the USA and in the UK. Both guidelines offer a clear picture of the efficacy, safety, and tolerability of the new antiepileptic drugs and agree on their use as add-on treatment in patients who do not respond to conventional drugs. The guidelines differ in the type and strength of recommendations. Whereas the US guidelines recommend treatment in newly diagnosed epilepsy with a standard drug or a new drug depending on the individual patient's characteristics, the UK guidelines recommend that a new antiepileptic drug should be considered only if there is no benefit from an old antiepileptic drug, an old drug is contraindicated, there is a previous negative experience with the same drug, or the patient is a woman of childbearing potential.
Vigabatrin is among the most promising of the new anti-epilepsy drugs, but two unrelated complications have been noted in patients receiving vigabatrin for chronic refractory epilepsy. These are, transient behavioural abnormalities and falling numbers of patients continuing to take vigabatrin (decreasing retention rate) during long-term treatment. Psychotic reactions have been carefully documented both in patients receiving standard and new anti-epilepsy drugs, and in up to 6% of patients after epilepsy surgery. As many psychotic episodes are associated with a dramatic cessation of seizures (i.e. high efficacy of treatment), it is not surprising that behavioural abnormalities are more often seen in patients receiving higher, more effective doses of vigabatrin, particularly those taking more than 3 g/day. A gradual dose increase and slow withdrawal is recommended for possible prevention of behavioural abnormalities, at least in some patients. During treatment with standard anti-epilepsy drugs, approximately 50% of patients remain on randomized treatment with the same drug for several years. For oxcarbazepine, a new drug, the figure is 60%, and for vigabatrin it is about 50%. Although comparative trials are not available, the retention rate for vigabatrin does not appear to be strikingly different to that reported for conventional anti-epilepsy drugs. In summary, behavioural abnormalities and falling retention rates appear to be general features of chronic epilepsy, and are certainly not exclusively associated with the use of vigabatrin. Controlled trials are required to establish the specific contribution, if any, of vigabatrin in development of these complications of intractable epilepsy.
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The aim of this study was to determine the effects of xanthotoxin (8-methoxypsoralen) on the protective action of 5 various second- and third-generation antiepileptic drugs (i.e., lacosamide, lamotrigine, oxcarbazepine, pregabalin and topiramate) in the mouse maximal electroshock-induced seizure model. Seizure activity was evoked in adult male albino Swiss mice by a current (25mA, 500V, 0.2s stimulus duration) delivered via auricular electrodes. Drug-related adverse effects were determined in the chimney, grip-strength and passive avoidance tests. Total brain antiepileptic drug concentrations were measured to confirm pharmacodynamic nature of observed interactions with xanthotoxin. Results indicate that xanthotoxin (100mg/kg, i.p.) significantly enhanced the anticonvulsant action of lacosamide (P<0.01), oxcarbazepine (P<0.05), pregabalin (P<0.01), and topiramate (P<0.001), but not that of lamotrigine in the maximal electroshock-induced seizure test. Moreover, xanthotoxin (50mg/kg) still significantly potentiated the anticonvulsant action of lacosamide (P<0.05), pregabalin (P<0.05), and topiramate (P<0.001) in this seizure test. Xanthotoxin had no significant impact on total brain concentrations of the studied antiepileptic drugs in mice. Furthermore, combinations of xanthotoxin with oxcarbazepine or topiramate produced no adverse effects. However, xanthotoxin in combination with lacosamide, lamotrigine or pregabalin significantly reduced muscular strength in mice in the grip-strength test. In the chimney test, only the combinations of xanthotoxin with pregabalin significantly impaired motor coordination in mice. In conclusion, the combinations of xanthotoxin with oxcarbazepine and topiramate produce beneficial anticonvulsant pharmacodynamic interactions in the maximal electroshock-induced seizure test. A special caution is advised when combining xanthotoxin with pregabalin due to appearance of acute adverse effects.
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The final PPK model of MHD was: Ka = 0.645 h⁻¹, V(L) = (11.3 + (age - 90.5) x 0.0282 + (TBW - 25.0) x 0.402) x e(0.0689), CL (L/h) = (0.557 + (DDPW - 20.8) x 0.00367 + (gender) x (-0.0636)) x e(0.120). The final PPK model was demonstrated to be suitable and effective by the bootstrap and predictive check.