Benzodiazepines are the mainstay of treatment for mild-to-moderate alcohol withdrawal in outpatient settings, but they can interact with alcohol, cause motor incoordination, or be abused. This study compared the therapeutic responses of the benzodiazepine lorazepam and the anticonvulsant carbamazepine for the outpatient treatment of acute alcohol withdrawal in terms of patients' previous detoxification histories, and compared the effects of these 2 medications on drinking behaviors in the immediate postdetoxification period.
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While 10% of healthy men had sexual dysfunctions, male epilepsy patients experience sexual problems in 40-70%. The cause of sexual dysfunction in epilepsy is multifactorial, but there are three main factors: the epilepsy itself, antiepileptic treatment and psychiatric/psychic problems. Antiepileptics with hepatic enzyme induction potential (carbamazepine, phenytoin) enhance the metabolism of sexual steroids. Valproic acid as an enzyme inhibitor and drug with high protein binding affinity elevates the free serum levels of androgens. Certain antiepileptic drugs may have negative cognitive side effects, some of them can induce psychiatric disorders. These drugs can facilitate male sexual dysfunctions through these psychic side effects. The metabolic and endocrine alterations caused by carbamazepine may return to normal level after replacement of carbamazepine with oxcarbazepine. After an oxcarbazepine-carbamazepine replacement, carbamazepine-induced impotency can be cured. According some new data lamotrigine can also help in sexual dysfunction. The therapy of sexual dysfunction in epilepsy depends on its cause. In cases of hormonal alterations, the fist step is a change of antiepileptic regimen. Instead of enzyme-inductor antiepileptics and valproate, new antiepileptic drugs should be prescribed. At present, the most investigated antiepileptic drug is the oxcarbazepine with positive effect on antiepileptic-induced male sexual dysfunction, however, lamotrigine seems to be also beneficial. If the hormonal and sexual dysfunctions cannot be eliminated by drug changes, androgenic therapy or bromocriptine may be required. Testosterone may not only be beneficial on sexual functions, but can reduce also the seizure frequency. Independent of etiology, erectile dysfunctions can be successfully treated by sildenafil.
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Although the unfavorable effects of early antiepileptic drugs, valproic acid, and carbamazepine (CBZ) on cognitive functions and visual functions have been investigated, the unfavorable effects of levetiracetam (LEV) on cognitive and visual functions remain unknown. The aim of the present study is to investigate whether there is a difference between the adverse effects by comparing the P300 and P100 latencies of LEV with epileptic patients using CBZ or sodium valproate (VPA) and healthy subjects.
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Photodermatosis with hydroxychloroquine have rarely been described in the literature, while quinine from which hydroxychloroquine is derived, is well known for its risk of photosensibilization. The main differential diagnosis of these drug eruptions is an eruption caused by the photodermatosis that initially required treatment with hydroxychloroquine.
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With the increasing use of treated wastewater and biosolids in agriculture, residues of pharmaceutical and personal care products (PPCPs) in these reused resources may contaminate food produce via plant uptake, constituting a route for human exposure. Although various PPCPs have been reported to be taken up by plants in laboratories or under field conditions, at present little information is available on their metabolism in plants. In this study, we applied carrot cell cultures to investigate the plant metabolism of PPCPs. Five phase I metabolites of carbamazepine were identified and the potential metabolism pathways of carbamazepine were proposed. We also used the carrot cell cultures as a rapid screening tool to initially assess the metabolism potentials of 18 PPCPs. Eleven PPCPs, including acetaminophen, caffeine, meprobamate, primidone, atenolol, trimethoprim, DEET, carbamazepine, dilantin, diazepam, and triclocarban, were found to be recalcitrant to metabolism. The other 7 PPCPs, including triclosan, naproxen, diclofenac, ibuprofen, gemfibrozil, sulfamethoxazole, and atorvastatin, displayed rapid metabolism, with 0.4-47.3% remaining in the culture at the end of the experiment. Further investigation using glycosidase hydrolysis showed that 1.3-20.6% of initially spiked naproxen, diclofenac, ibuprofen, and gemfibrozil were transformed into glycoside conjugates. Results from this study showed that plant cell cultures may be a useful tool for initially exploring the potential metabolites of PPCPs in plants as well as for rapidly screening the metabolism potentials of a variety of PPCPs or other emerging contaminants, and therefore may be used for prioritizing compounds for further comprehensive evaluations.
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Patients on CBZ (n=91), VPA (n=61), LTG (n=105), LEV (n=72) and healthy control subjects (CTR) on no medication (n=51) were extracted. All patients had anonymously provided information on seizure type and frequency and completed the Liverpool Adverse Event Profile (LAEP).
To provide an overview of the relative analgesic efficacy of antiepileptic drugs that have been compared with placebo in neuropathic pain and fibromyalgia, and to report on adverse events associated with their use.
A 49-year-old man was treated with cisplatin and pirarubicin for tongue cancer. After the second course of chemotherapy, partial seizures including transient motor aphasia, tonic finger movement, and loss of consciousness were observed. The EEG showed frequent diffuse (multiple) spike and slow wave discharges. Following the administration of carbamazepine and diazepam, no seizures occurred and no paroxysmal discharges were observed or EEGs. We conclude that carbamazepine and diazepam administration was effective.
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Retigabine (D-2319, 0.5-20 mg/kg i.p.) antagonised dose dependently audiogenic seizures in DBA/2 mice. Retigabine at 0.5 mg/kg i.p., a dose that per se did not affect the occurrence of audiogenic seizures significantly, potentiated the anticonvulsant activity of carbamazepine, diazepam, felbamate, lamotrigine, phenytoin, phenobarbital and valproate against sound-induced seizures in DBA/2 mice. The degree of additivity for the effect induced by retigabine was greatest for diazepam, phenobarbital, phenytoin and valproate, less for carbamazepine and lamotrigine and least for felbamate. The increase in anticonvulsant activity was usually associated with a comparable increase in motor impairment. However, the therapeutic index of combined treatment (drugs plus retigabine), was more favourable than the same drug plus vehicle. Since retigabine had no significant influence on the total and free plasma levels of the anticonvulsant drugs, pharmacokinetic interactions, in terms of total or free plasma levels, are not probable. However, the possibility that retigabine modifies the clearance of the anticonvulsant drugs from the brain cannot be excluded. Retigabine had no significant effect on the hypothermic effects of the anticonvulsants tested. In conclusion, retigabine showed an additive effect when administered in combination with classical anticonvulsants, most notably diazepam, phenobarbital, phenytoin and valproate.
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(1) The reference treatment for partial epilepsy in adults and children is carbamazepine. (2) Oxcarbazepine is available in the European Union for the treatment of partial epilepsy in adults and children aged over 6 years, alone or in combination with other antiepileptic drugs. (3) The clinical file on oxcarbazepine monotherapy of recent-onset generalised or partial epilepsy mainly contains data from one trial versus carbamazepine, two trials versus phenytoin, and one trial versus valproate sodium. In these trials, 52-60% of patients had no seizures on oxcarbazepine, a proportion not significantly different from that obtained with the comparators. Oxcarbazepine may, in fact, be slightly less effective than carbamazepine. (4) For refractory partial epilepsy (especially forms refractory to carbamazepine), oxcarbazepine is more effective than a placebo, when combined with the inadequately effective treatment, as shown in two trials. Two dose-finding studies show that 2 400 mg/day oxcarbazepine is more effective than 300 mg/day. (5) In trials comparing single-drug treatments there were fewer withdrawals for adverse events among patients on oxcarbazepine than among those on carbamazepine or phenytoin. Compared with carbamazepine, the risk of cutaneous hypersensitivity reactions seems to be lower with oxcarbazepine, while the risk of hyponatraemia is higher. This risk of hyponatraemia necessitates laboratory monitoring. (6) The risk of clinically significant interactions appears to be lower on oxcarbazepine than on carbamazepine, and is limited mainly to combined contraceptives (contraceptive inefficacy) and phenytoin. (7) In practice, carbamazepine remains the reference treatment for partial epilepsy, but oxcarbazepine is one of several second-line options, either alone or in combination with other antiepileptics.
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We evaluated the use of a new, controlled-release capsule form of carbamazepine, Carbatrol capsules, in an open-label, multicenter study of 124 patients with complex partial seizures. Ninety-one percent of the patients successfully completed the 6-month trial with good seizure control, with a significant improvement in quality of life. We conclude that switching patients with complex partial seizures from multiple daily-dose carbamazepine to twice-daily Carbatrol on a milligram-to-milligram basis is relatively safe.
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Three age-matched (p = 0.286) and sex-matched (p = 0.398) groups were studied: drug-naive TLE (n = 20); TLE on CBZ (n = 20); and healthy controls (n = 40). All groups underwent overnight polysomnography. Scoring and analysis of arousals and cyclic alternating pattern (CAP) parameters were performed. Comparison of arousal parameters and CAP parameters was performed using either one-way analysis of variance or the Kruskal-Wallis test, followed by pairwise comparisons (p ≤ 0.05).
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The old AEDs generation (benzodiazepines, phenytoin, carbamazepine, phenobarbital and valproic acid) is teratogenic: minor congenital malformations, such as facial dysmorphism and other anomalies, occur in 6-20% of infants exposed to AEDs in utero; this value is two times greater than the value reported in the general population. Major congenital malformations (MCM) such as cleft lip and cleft palate, heart defects (atrial septal defect, Fallot's tetralogy, ventricular septal defect, aortic coarctation, patent ductus arteriosus, and pulmonary stenosis) and urogenital anomalies were estimated to be 4-6% of infants born from mothers treated with AEDs, compared to 2-3% of the general population.