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C57BL/6J male mice were offered a 10% v/v ethanol solution versus tap water over 4 consecutive days per week. Mice were assigned to topiramate (1-50 mg/kg) or saline groups and received injections before the beginning of the dark phase of the light cycle. Topiramate dose increased over 5 successive weeks (1, 5, 10, 25, and 50 mg/kg). Fluid intake was measured 2, 4, and 23 hr after injection. Body weight and food intake were measured at the time of injection. In a second phase, mice were offered saccharin solutions (0.2 and 2.5% w/v) versus tap water after topiramate (50 mg/kg) or saline injections.
Elderly patients with a Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition diagnosis of Alzheimer disease and significant behavioral disturbances were randomized to receive, for a period of 8 weeks, a flexible dose of either topiramate (25-50 mg/d) or risperidone (0.5-2 mg/d). Outcome measures were the Cohen-Mansfield Agitation Inventory, Neuropsychiatry Inventory parts 1 and 2, and the Clinical Global Impression.
The necessity of analysis of the cost of treatment of patients with epilepsy becomes of primary importance in Poland as a consequence of recent economic transformations affecting the efficiency of health service. The reasons are: high number of patients with epilepsy (approaching 400,000 in a population of about 40 mln) and long time course of illness, taking into account steady, gradual rise of the cost of treatment, even if we accept greater efficiency of the new antiepileptic drugs. However, the analysis of questionnaires provided by patients with epilepsy indicates that optimation of their treatment with introduction of new antiepileptic drugs may be a procedure leading to diminution of the global expenses associated with care of epileptic patients. Identification of factors influencing cost of antiepileptic treatment before and after introduction of new antiepileptic drugs. A group of 150 people chosen at random from a population of persons taking new antiepileptic drugs (vigabatrin, lamotrygin, topiramate, gabapentin, tiagabine) received anonymous questionnaires concerning the time course of their illness. 80 questionnaires were returned. The questions concerned the situation before and after treatment. Statistical analysis included t test for dependent samples-including items such as: number of epileptic seizures and number and days of hospitalization, etc. per year of observation. Significant decrease of the number of epileptic seizures (p < 0.05), number of hospitalizations (p < 0.001), days of hospitalizations (p < 0.001) and neurological consultations (p < 0.001) occurred after optimalization of treatment. Results of our research illustrate significant reduction of direct costs of treatment associated with introduction of new antiepileptic drugs.
A total of 76 adult subjects with a diagnosis of migraine were screened for the study. During a 1-month baseline period, subjects demonstrated through a daily diary that they predicted at least 50% of migraine attacks during the premonitory phase and treated with their usual medication. Of these, 55 were randomized to either Group A (daily topiramate) or Group B (frovatriptan during premonitory symptoms); 44 completed the study. The treatment period lasted 2 months. The subjects answered the Migraine-Specific Quality of Life Questionnaire at randomization, and at Weeks 4 and 8. The revised Patient Perception of Migraine Questionnaire was answered 24 hours after taking frovatriptan (Group A, for break-through headaches; Group B, treatment during premonitory symptoms).
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We sequenced all exons and intron-exon boundaries of SCN1A in our cohort, investigated differences in the distribution of truncating and missense variants, tested for associations between variant type and phenotype, and compared these patterns with those of cohorts with milder epilepsy and healthy individuals.
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The present study was designed to reveal changes of cognitive processes in epilepsy (EP) patients with Topiramate (TPM) or Valproate (VPA) treatment using Wechsler Adult Intelligence Scale (WAIS-CR) and event-related potential (ERP). Thirty untreated epilepsy patients were randomly divided into two groups receiving TPM or VPA, respectively. Fifteen healthy volunteers were included as controls. All the patients were examined by WAIS-CR and ERP before and 3 months after drug treatment. Controls were examined by ERP at the time recruited into the study and 3 months later. Unfamiliar grey-scale photographs of faces (front view) were used as stimuli. ERP were recorded at the same time. Mean Intelligence Quotient (IQ) in TPM group decreased after the 3-month treatment (90.40 vs. 81.00, P<0.05). One component of ERP-P300 was smaller in epilepsy patients than controls (P<0.05), but remained unchanged after TPM or VPA treatment (P>0.05). A delayed and smaller N270 was detected in patients compared to controls (P<0.05). After 3 months TPM treatment, it decreased further compared to before treatment (P<0.05). N170 was lower in patient groups, and it became lower after TPM treatment than before. Our results demonstrate that in all epilepsy patients with mild cognitive impairment ERP changes were found. TPM affected the cognitive functions in epilepsy patients reflected by the decreased full-scale intelligence quotient (FIQ). The imperative effects of TPM on visual perception function reflected by N170 were more obvious than that of VPA. Attention reflected by N270 was impaired after TPM treatment.
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Emerging data indicate that age-related brain changes alter seizure susceptibility, seizure-associated neurodegeneration, and responsiveness to AEDs. The present study assessed long-term animal survival in the Kainic Acid (KA) model along with in-vivo spontaneous seizure frequency, cellular hyperexcitability in CA1 in-vitro and in-vivo in subiculum, and responsiveness of in-vitro CA1 hyperexcitability to topiramate. Sprague-Dawley male rats were given KA to induce convulsive status epilepticus (KA-SE) at 2-3 months of age. The one-month mortality after KA-SE was 27%. One-month survivor rats had 37% sudden unexplained late mortality after KA-SE as compared to none in saline controls during their second year of life. In-vivo seizure frequency was examined prior to terminal experiments. The diurnal average seizure frequency in the KA-SE group at age 2 years was 1.06 ± 0.24 seizures/hour while no seizures were observed in the saline age-matched controls (p<0.001). In-vitro recordings of CA1 pyramidal neurons revealed that depolarizing current injection from -60 mV evoked an increased number of action potentials in the aged KA-SE group compared to controls (p<0.002). Topiramate exhibited dose-dependent inhibition of action potential firing evoked by current injections into CA1 pyramidal neurons of KA-SE rats. In subiculum, KA-SE rats had frequent interictal spikes associated with high frequency oscillations while only rare spontaneous EPSPs were recorded in saline controls. Our experiments revealed that the hippocampal formation of aged epileptic rats shares features of hyperexcitability previously described in young adult epileptic rats using the KA model.
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Preventive treatment with topiramate significantly reduces the impact of migraine and the disability that results from it. Treatment is satisfactory and improves the quality of life in a large percentage of patients.
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Roux-en-Y gastric bypass (RYGB) typically leads to substantial, long-term weight loss (WL) and diabetes remission, although there is a wide variation in response to RYGB among individual patients. Defining the pathways through which RYGB works should aid in the development of less invasive anti-obesity treatments, whereas identifying weight-regulatory pathways unengaged by RYGB could facilitate the development of therapies that complement the beneficial effects of surgery. Activation of serotonin 2C receptors (5-HT2CR) by serotonergic drugs causes WL in humans and animal models. 5-HT2CR are located on neurons that activate the melanocortin-4 receptors, which are essential for WL after RYGB. We therefore sought to determine whether 5-HT2CR signaling is also essential for metabolic effects of RYGB or whether it is a potentially complementary pathway, the activation of which could extend the benefits of RYGB. Diet-induced obese male mice deficient for the 5-HT2CR and their wild-type littermates underwent RYGB or sham operation. Both groups lost similar amounts of weight after RYGB, demonstrating that the improved metabolic phenotype after RYGB is 5-HT2CR independent. Consistent with this hypothesis, wild-type RYGB-treated mice lost additional weight after the administration of the serotonergic drugs fenfluramine and meta-chlorophenylpiperazine but not the nonserotonergic agent topiramate. The fact that RYGB does not depend on 5-HT2CR signaling suggests that there are important WL mechanisms not fully engaged by surgery that could potentially be harnessed for medical treatment. These results suggest a rational basis for designing medical-surgical combination therapies to optimize clinical outcomes by exploiting complementary physiological mechanisms of action.
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The present data from open trials suggest that topiramate may possibly possess antimanic properties. Controlled, double-blind studies are required to confirm this efficacy.
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The bulimia nervosa (BN) literature underscores the utility of antidepressants, particularly SSRIs, in improving the symptoms of the disorder. The literature on binge eating disorder supports efficacy on reduction in binge eating frequency for a variety of compounds. However, such compounds have only modest effects on weight. Certain antiepileptic agents such as topiramate, if tolerated, are probably more useful in terms of weight loss. The number of controlled trials in patients with anorexia nervosa (AN) in particular has been quite small, and recent meta-analyses show disappointing results using atypical antipsychotics in AN.
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Time to treatment failure (withdrawal of the randomised drug for reasons of unacceptable adverse events or inadequate seizure control or a combination of the two) and time to achieve a 12-month remission of seizures. Time from randomisation to first seizure, 24-month remission of seizures, incidence of clinically important adverse events, quality of life (QoL) outcomes and health economic outcomes were also considered.
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Cholecalciferol applied ip at doses of 37.5-75μg/kg significantly raised the electroconvulsive threshold. Cholecalciferol, administered at the subthreshold dose of 18.75μg, potentiated the anticonvulsant activity of oxcarbazepine and lamotrigine, but did not change their brain concentrations, therefore the revealed interactions seem to be pharmacodynamic. Furthermore, the action of cholecalciferol was not dependent on its conversion to calcitriol. The anticonvulsant effect of topiramate was enhanced by cholecalciferol applied at the higher dose of 37.5μg/kg, at which it also increased the brain level of topiramate. As regards adverse effects, cholecalciferol, antiepileptic drugs, and their combinations did not significantly impair motor coordination or long-term memory in mice. Moreover, cholecalciferol did not show either anxiolytic or anxiogenic properties.
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The French Recommendations for Clinical Practice: Diagnosis and Therapy of Migraine are guidelines concerning the overall management of patients with migraine, including diagnostic and therapeutic strategies and assessment of disability.
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To provide a clinically-focused review of the biological treatment of treatment-resistant obsessive compulsive disorder (OCD).
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Low-dose topiramate is efficacious in migraine prophylaxis as compared to both placebo and lamotrigine. Lamotrigine in low doses might be beneficial for headache frequency; however, longer trials are required to establish its efficacy on the intensity and frequency of migraine.
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Topiramate, an anticonvulsant medication, is an efficacious treatment for alcohol dependence. To date, little is known about genetic moderators of side effects from topiramate. The objective of this study was to examine 3 single nucleotide polymorphisms (SNPs) of the glutamate receptor GluR5 gene (GRIK1) as predictors of topiramate-induced side effects in the context of a laboratory study of topiramate. Heavy drinkers (n=51, 19 women and 32 men), 75% of whom met criteria for an alcohol use disorder, completed a 5-week dose escalation schedule to a target dose of either 200 or 300 mg or matched placebo. The combined medication groups were compared with placebo-treated individuals for side effects at target dose. Analyses revealed that an SNP in intron 9 of the GRIK1 gene (rs2832407) was associated with the severity of topiramate-induced side effects and with serum levels of topiramate. Genes underlying glutamatergic neurotransmission, such as the GRIK1 gene, may help predict heterogeneity in topiramate-induced side effects. Future studies in larger samples are needed to more fully establish these preliminary findings.
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We reviewed all published literature in the English language regarding the use of antiepileptic drugs in patients with cancer.
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Fetal malformation rates had fallen over time in monotherapy pregnancies, but increased in polytherapy pregnancies, despite decreasing use and lower dosages of valproate. The rise in polytherapy malformation rates began around 2005 when levetiracetam and topiramate use began to increase. Excluding pregnancies involving valproate exposure, malformation rates were higher in the remaining polytherapy pregnancies as compared with the monotherapy ones (6.90% vs. 3.64%; odds ratio [OR] 1.96, 95% confidence interval [CI] 1.14-3.39). Malformation rates were similar in polytherapy pregnancies whether or not levetiracetam was included (7.14% vs. 8.38%), but were higher in polytherapy pregnancies involving topiramate (14.94% vs. 6.55%: OR 2.507, 95% CI 1.23-5.10). Logistic regression showed that topiramate in polytherapy had a positive dose relationship with teratogenicity risk (p = 0.025).
In a randomized controlled trial, we compared the efficacy of topiramate versus placebo in women undergoing olanzapine therapy and found that topiramate effectively contributed to weight loss in short-term treatment and had a positive effect on health-related quality of life, the patients' actual state of health, and psychological impairments. The aim of this observational study was to assess whether topiramate has a sustained benefit in long-term treatment of olanzapine-associated weight gain in subjects who had participated in the previous randomized controlled trial comparing topiramate with placebo. The subjects (topiramate group, n = 25; former placebo group, n = 18) were observed in an 18-month open-label study. After unblinding, subjects from the former topiramate group continued treatment with topiramate, whereas subjects from the former placebo group received neither placebo nor topiramate. The subjects were seen every 6 months, weighed, and tested with the SF-36 Health Survey, Scale of Well-Being, and the Adjective Checklist. According to the intent-to-treat principle, the repeated-measures analysis showed a significant interaction for the group-by-time effect for change of weight (P < 0.01) on the Scale of Well-Being (P < 0.01), all scales of the Adjective Checkist (all P < 0.01), and 5 scales (physical functioning, role limitations due to physical health, social functioning, mental health, and vitality) of the SF-36 Health Survey (all P < 0.01). Topiramate was well tolerated and seems to be effective and safe in the long-term treatment of olanzapine-related adiposity in women. Furthermore, positive changes in the patients' state of health, psychological impairments, and health-related quality of life could be also observed.
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To evaluate the efficacy and safety of topiramate as an add-on therapy in dogs with refractory idiopathic epilepsy.
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Several drugs good evidence supporting efficacy. There is weak evidence supporting amitriptyline's superiority over some drugs. Selection of prophylactic medication should be tailored according to patient preferences, characteristics and side effect profiles.