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The aim of the present work was to assess serum melatonin levels and melatonin circadian rhythm in patients with diurnal and nocturnal complex partial epilepsy. Daily rhythms of melatonin were studied in patients with diurnal complex partial epilepsy (n=10), patients with nocturnal complex partial epilepsy (n=10), and a control group (n=10). All patients were under carbamazepine treatment. Serum melatonin samples were taken at 1000, 2200, 0100, and 0500 hours. We found that melatonin circadian rhythm was normal in all patients when compared with controls. Melatonin levels were low in both patients with nocturnal and patients with diurnal complex partial epilepsy compared with the control group at 1000, 2200, 0100, and 0500 hours; a statistically significant decrease in melatonin levels was observed in the patients with epilepsy at 1000 hours only. These findings suggest that melatonin levels and circadian rhythm of melatonin do not differ between patients with nocturnal and patients with diurnal complex partial epilepsy. Further detailed research is necessary to determine the factors that govern the nocturnal or diurnal occurrence of complex partial seizures.
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We found 14 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
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The introduction of anticonvulsants to the treatment of recurring affective disorders, has significantly broadened the possibilities of helping the ill, especially in the prophylaxis of recurring symptoms of bipolar affective disorders. Carbamazepine and valproate (probably also lamotrigine) are a valuable alternative of Lithium Carbonate. The application of anticonvulsants requires strict rule regiment, which includes: gradual dose increase (especially in lamotrigine), gradual dose reduction when planning ending of the therapy, drug blood-level monitoring, liver action monitoring, haemopoietic system monitoring, in the case of the appearance of flu-like symptoms and skin changes--withdrawal of the drug. In simultaneous application of other drugs (e.g. psychotropic), probable interactions should be considered.
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The present work describes the development of a sensitive analytical method based on pressurized liquid extraction (PLE) and pre-concentration by solid-phase extraction (SPE), followed by liquid chromatography-electrospray tandem mass spectrometry (LC-ESI-MS/MS) for the determination of seventeen pharmaceuticals in soils and sediments. The method is based on sample homogenisation using Na(2)-EDTA washed sand and extraction with water at 90 degrees C. Special emphasis was placed on the optimization of the extraction procedure to develop a green method that reduces, at a maximum, the use of organic solvents in order to eliminate matrix components during the clean-up. The proposed method was linear in a concentration range from 0.3 to 333ngg(-1), with correlation coefficients higher than 0.993. Method detection (MDLs) and quantification (MQLs) limits ranged from 0.1 to 6.8ngg(-1) and from 0.25 to 23ngg(-1), respectively. Absolute recoveries were analyte dependent, varying between 50% and 105% at the MQL level, except for fenofibrate (40%) and diclofenac (34%). The intra-day and inter-day precision was given by RSD values from 0.7% to 7.9% and from 1.6% to 14.5%, respectively. Acetaminophen, carbamazepine, ciprofloxacin, clofibric acid, codeine, diazepam, fenofibrate, metropolol, ofloxacin and propanolol were detected at concentrations from MDL to 35.62ngg(-1) in soils and sediments from marsh areas. Due to the low recoveries, results for fenofibrate and diclofenac can only be considered as semi-quantitative. The method was fully suitable for the other 15 pharmaceuticals.
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Environmental pollution caused by pharmaceuticals has been recognized as a major threat to the aquatic ecosystems. Carbamazepine, as the widely prescribed antiepileptic drug, has been frequently detected in the aquatic environment and has created concerns about its potential impacts in the aquatic organisms. The effects of carbamazepine on zebrafish embryos were studied by examining their phenotype, behavior and molecular responses. The results showed that carbamazepine disturbed the normal growth and development of exposed zebrafish embryos and larvae. Upon exposure to carbamazepine at 1 μg/L, the hatching rate, body length, swim bladder appearance and yolk sac absorption rate were significantly increased. Embryos in treatment groups were more sensitive to touch and light stimulation. At molecular level, exposure to an environmentally relevant concentration (1 μg/L) of carbamazepine disturbed the expression pattern of neural-related genes of zebrafish embryos and larvae. This study suggests that the exposure of fish embryo to antiepileptic drugs, at environmentally relevant concentrations, affects their early development and impairs their behavior. Such impacts may have future repercussions by affecting fish population structure.
Pharmaceuticals and selected major human metabolites are ubiquitous in Jamaica Bay, a wastewater-impacted estuary at concentrations in the low ng/L to low/microg/L range. Concentrations throughout the bay are often consistent with conservative behavior during dry-weather conditions, as evidenced by nearly linear concentration-salinity relationships. Deviation from conservative behavior is noted for some pharmaceuticals and attributed to microbial degradation. Caffeine, cotinine, nicotine, and paraxanthine were detected with the greatest analytical signal, although evidence is presented for in situ removal, especially for nicotine and caffeine. There is little evidence for significant removal of carbamazepine and sulfamethoxazole, suggesting they are more conservative and useful wastewater tracers. Immediately following heavy precipitation, which induced a combined sewer overflow (CSO) event, the concentrations of all compounds but acetaminophen and nicotine decreased or disappeared. This observation is consistent with a simple model illustrating the effect of precipitation has on pharmaceutical concentration in the wastewater stream, given the balance between dilution from rain and the bypass of treatment.
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Acetylenic derivatives of quinazolinones and quinazolinediones were synthesized and evaluated for their anticonvulsant activity. Most compounds displayed seizure-antagonizing activity in the maximal electroschock test (MES test) in most cases associated with little or no acute neurotoxicity determined in the rotorod test. Only three compounds exhibited significant activity in the seizure threshold test with subcutaneous pentylenetetrazole (scMet test). Based on the ED50 in the MES test, 1,3-bis-(prop-2-ynyl)-quinazoline-2,4-(1H,3H)-dione(9a) was about ten-fold less active than phenytoin or carbamazepine but about as active as mesuximide.
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Human pharmaceuticals and personal care products (PPCPs) are routinely found in biosolids from wastewater treatment plants (WWTPs). Once land applied, the PPCPs in biosolids are potentially available for plant uptake and bioaccumulation. This study used a greenhouse model to investigate uptake of PPCPs commonly detected in biosolids by the agricultural plant Chinese cabbage (Brassica campestris). Two series of greenhouse experiments were conducted as part of this project. In the first set of experiments, four pharmaceuticals were added to an organic matter-rich soil in environmentally relevant concentrations based on typical biosolids application rates, resulting in final soil concentrations of 2.6 ng g(-1) carbamazepine, 3.1 ng g(-1) sulfamethoxazole, 5.4 ng g(-1) salbutamol, and 0.5 ng g(-1) trimethoprim. In the second set of experiments, the cabbage was grown in soil amended with an agronomic rate of biosolids from a local WWTP. The ambient concentration of PPCPs in the biosolids resulted in final soil concentrations of 93.1 ng g(-1) carbamazepine, 67.4 ng g(-1) sulfamethoxazole, 30.3 ng g(-1) salbutamol, 433.7 ng g(-1) triclosan, and 24.7 ng g(-1) trimethoprim. After growing to maturity, the aerials of the plants were separated from roots and the two tissue types were analyzed separately. All four human pharmaceuticals were detected in both tissues in the cabbage grown in the soil fortified with the four pharmaceuticals with median concentrations of 255.4 ng g(-1) aerials and 272.9 ng g(-1) roots carbamazepine; 222.8 ng g(-1) aerials and 260.3 ng g(-1) roots sulfamethoxazole; 108.3 ng g(-1) aerials and 140.6 ng g(-1) roots salbutamol; and 20.6 ng g(-1) aerials and 53.7 ng g(-1) roots trimethoprim. Although all study compounds were present in the biosolids-amended planting soil, only carbamazepine (317.6 ng g(-1) aerials and 416.2 ng g(-1) roots), salbutamol (21.2 ng g(-1) aerials and 187.6 ng g(-1) roots), and triclosan (22.9 ng g(-1) aerials and 1220.1 ng g(-1) roots) were detected in the aerials of the cabbage. In addition to the study compounds detected in the aerials, sulfamethoxazole was detected in the roots of one of the plants in the biosolid-amended soil. In comparison to many previous studies that have utilized PPCP concentration that exceed environmentally relevant concentrations, plants in this study were exposed to environmentally relevant concentrations of the PPCPs, yet resulted in uptake concentrations similar to or greater than those reported in comparable studies. We suggest that rhizosphere conditions, particularly the presence of dissolved organic matter in the planting matrix, might be one of the critical factors determining mobilization and bioavailability of xenobiotic compounds such as PPCPs.
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A total of 694 pediatric patients were included. Monotherapy AED use had the highest frequency 465 (67.0%), followed by dual therapy 162 (23.3%). The frequency of monotherapy in university hospitals was lower than governmental hospitals (p<0.05); however, Polytherapy was more frequent in younger children. Two old AEDs were most frequently prescribed as a monotherapy; Valproic acid 235 (50.5%) and carbamazepine 155 (33.3%). The most common combination in dual therapy was valproic acid with carbamazepine 28 (17.3%). The second most common combinations were carbamazepine with levetiracetam 21 (13.0%) or valproic acid with levetiracetam 20 (12.3%).
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There is no current evidence supporting the clinical use of Carbamazepine in the treatment of cocaine dependence. Larger randomised investigation must be considered taking into account that these time-consuming efforts should be reserved for medications showing more relevant and promising evidence.
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Lacosamide (LCM, Vimpat) is an anticonvulsant with a unique mode of action. This provides lacosamide with the potential to act additively or even synergistically with other antiepileptic drugs (AEDs). The objective of this study was to determine the presence of such interactions by isobolographic analysis.
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This paper reviews the evidence for the efficacy of anticonvulsants in the continuation and maintenance phases of treatment of bipolar disorder, when there has been an episode of mania (Bipolar-I disorder). The evidence to be considered is primarily that arising from randomized controlled trials. A literature search was performed to identify all randomized controlled trials of anticonvulsants used as maintenance treatment for bipolar-I disorder. Placebo-controlled studies were preferred, however there have been relatively few of these and clinical practice must therefore be guided by evidence carrying a lower level of conviction. Valproate monotherapy lacks a convincing evidence base. The view that valproate is more effective than lithium in rapid cycling has not been borne out. Lamotrigine is effective in preventing depression after an episode of mania. As monotherapy, lithium appears superior to carbamazepine in bipolar patients not previously treated with either drug. The combination of lithium and carbamazepine may be superior to either drug alone, in certain treatment-resistant patients, but is associated with increased side effects. Other anticonvulsants lack evidence supporting their use in bipolar disorder except in treating co-morbid alcohol dependence, anxiety and bulimic symptoms. Valproate continues to be recommended by most current guidelines despite the lack of evidence.
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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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Comparative analyses between patients who received MS and those who did not, revealed the former group as having higher levels on the hypomania checklist and cyclothymic and depressive temperaments. The delay to MS installation was significantly longer in the PR versus GR. The profile of GR could be described as follows: younger current age, higher education; symptom-free interval between major episodes; and fewer prior depressive episodes and hospitalizations; and higher rate of MS prescription. However, no significant differences were obtained from hypomania assessment and affective temperament ratings (cyclothymic, hyperthymic, depressive). During the index (most recent) depressive episode, we obtained a significantly higher rating of "suicidal thoughts" associated with higher levels of "sadness-guilt," psychomotor agitation, and lower "retardation-fatigue" (all from the HAM-D) in the PR group; better and faster response to current treatment (as prospectively assessed) were also observed in the GR. At this time, overall severity of depression was not linked to the quality of response to the MS. LIMITATIONS AND CONCLUSION: Despite its retrospective design, these analyses have important implications in the management of difficult or resistant "unipolar" depression by using MSs as augmentation strategy. Clinicians appeared to have used "subtle" hypomanic and cyclothymic features as a justification for augmentation. However, these features per se were not predictive of response to such augmentation. Instead, the profile of augmentation response to failed antidepressants appears to be an "activated depression" (significantly less retardation and withdrawal and higher agitation associated with greater intensity of painful and guilt-ridden sadness with suicidality), and the significantly higher rate of and earlier prescription of MSs in the course of recurrent MDD. These data suggest that resistant depressives should not stay on antidepressant or antidepressant combination for too long; MS augmentation must be instituted without much delay.
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Here we report the case of a patient who presented with acute cardiac tamponade due to drug-induced systemic lupus erythematosus (SLE). The patient had been treated for a seizure disorder with carbamazepine, a drug that has previously been demonstrated to cause SLE-like syndromes. Further serologic analysis demonstrated the likelihood of drug-induced SLE in this patient, with the rare presentation of cardiac tamponade.
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Our results suggest that CBZ modifies BAEPs interpeak-intervals at 70 dB, and latencies since they were delayed. Alterations in the generators of the later waves of BAEPs underlie, AED produced changes in hearing sensitivity with a single no toxic doses. Probably CBZ causes changes in endolymphatic ion composition in the rat inner ear, provoking that latency of BAEPs were delaying, but this requires further studies.
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To describe a large series of children with anoxic-epileptic seizures (AES)--that is, epileptic seizures induced by syncopes.
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The method described here may be used to estimate AUC and Cmax for CBZ and CBZE without detailed pharmacokinetic studies following single or multiple dose of CBZ.
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WWE in premenopausal state aged 18 to 45 years old, currently on AED monotherapy for more than six months, were recruited for this study. The subjects checked their oral temperature each morning, and tested serum levels for lipid profiles, insulin, glucose, and leptin. A HOMA-index was used as a marker for insulin resistance.
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Single and mixture toxicity tests on three pharmaceutical compounds, Diclofenac (DF), Ibuprofen (IB) and Carbamazepine (CBZ), were carried out with the freshwater shrimp Atyaephyra desmarestii. Lethal and sublethal responses were analyzed for single compounds. Lethal concentrations (LC50) obtained for each individual compound, after 96 h of exposure, were 6.3 mg L(-1) for DF, 13.3 mg L(-1) for IB and 94.3 mg L(-1) for CBZ. The selected sublethal endpoints of food ingestion, osmoregulatory capacity and respiration rates were not affected by the exposures to environmentally-relevant concentrations. Based on mortality data obtained, the predictive no effect concentration (PNEC) was calculated for each of the compounds, and compared with predicted environmental concentrations (PEC) reported in surface waters. The environmental risk of each compound was estimated as the ratio between PEC/PNEC, and indicated that IB could represent a medium risk in freshwater environments. Additionally, binary and ternary mixture toxicity assays of the selected compounds were carried out. The data obtained was applied to two predictive toxicity models: Concentration Addition (CA) and Independent Action (IA). Finally, risk assessment was estimated using risk quotients (RQ) for the compound mixtures based on EC50 and LC50 values.
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A MEDLINE search was conducted to identify articles published within the last 10 years regarding current thinking on the etiology, diagnosis and treatment of TN. The authors also reviewed historic articles to gather information about the initial discovery and descriptions of this condition.
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Rat amygdale kindling was used as a model of refractory epilepsy. The expression of MRP1 mRNA and protein in the brains was examined using RT-PCR and Western blot. MRP1-positive cells in the cortex and hippocampus were studied with immunohistochemical staining. The rats were intraperitoneally injected with phenytoin (50 mg/kg) or carbamazepine (20 mg/kg), and their concentrations in the cortical extracellular fluid were measured using microdialysis and HPLC. Probenecid, a MRP1 inhibitor (40 mmol/L, 50 μL) was administered through an inflow tube into the cortex 30 min before injection of the antiepileptic drugs.
The genotype distribution of 5-HTTLPR between TN patients and controls were significantly different. The TN Patients had a higher prevalence of short-short genotype than controls. The short-short genotype carriers are also significantly associated with higher pain severity and poorer carbamazepine treatment response compared to the long-long genotype carriers. In contrast, the rs 25531 polymorphism was not associated with the susceptibility to TN, neither with the pain severity and the treat response to carbamazepine.