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Childhood maltreatment is substantiated in 12 % of children, but nearly 50 % adults recall having been neglected or abused as children. Maltreatment, especially emotional abuse, is associated with migraine. Dysregulation of the HPA axis, autonomic, immune, and metabolic systems appears to be a consequence of maltreatment, and is also reported in migraine. Areas of the brain structurally and functionally affected by childhood abuse and by migraine are also similar, and include the limbic system structures, which connect to pain regions in the brainstem. Putative mechanisms by which early life stress increases the likelihood of developing migraine include gene x environment interactions, in addition to epigenetic modifications via DNA methylation. These modifications are stable and may be transferred across generations, but they may also be reversed by some medications commonly used in migraine, including valproic acid and topiramate.
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The role of lithium carbonate in the maintenance treatment of bipolar disorder is well established. Unfortunately, many patients fail to respond adequately to this agent or are unable to tolerate its adverse effects. Divalproex has become a commonly used alternative to lithium, but it also is ineffective or poorly tolerated in many patients. This article attempts to review the available data on maintenance therapy in bipolar disorder with a variety of anticonvulsants and antipsychotics (both conventional and novel), with reference to relevant studies in acute mania and bipolar depression as well.
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The goal of this study is to (1) provide clinically useful, previously unpublished comparative analyses of seizure-freedom rates for newer antiepileptic drugs (AEDs), and (2) recommend a standard for data presentation and analysis.
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We observed significantly increase in the levels of beta-endorphin in rats with free access to alcohol both in a topiramate- or vehicle-treated group. However, in topiramate-treated group, a voluntary consumption of alcohol diminished in comparison with the vehicle-treated rats.
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Median percent reduction in seizure frequency from baseline to study end was 44% with topiramate and 20% with placebo (P or=10% incidence in topiramate-treated patients) were somnolence, fatigue, paresthesia, nervousness and anorexia; 8% of topiramate-treated patients and 2% of placebo-treated patients discontinued because of adverse events. As a result of the low incidence of adverse events, differences between titration rates in terms of tolerability were not detected.
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The National Institute on Drug Abuse has funded a medications program that has concentrated on the development of medications for opiate and cocaine dependence. Levomethadyl acetate (LAAM) and buprenorphine and buprenorphine/naloxone sublingual tablets were developed in conjunction with pharmaceutical partners and approved by the Food and Drug Administration. The remaining challenges for medications development for opiate dependence involves Phase IV studies in special populations, for example, pregnant opiate-dependent patients, and to translate neuroscience-based findings into treatments. Several marketed medications have shown initial efficacy to reduce cocaine use in well-controlled clinical trials. Disulfiram has been shown to reduce cocaine use in several clinical trials, while baclofen, modafinil, naltrexone, ondansetron, tiagabine, and topiramate have shown preliminary efficacy in initial clinical studies. Confirmatory studies of many of these medications is underway. More recently, the NIDA medications program has evaluated medications for their ability to reduce methamphetamine use. To date, no medications tested have shown efficacy to reduce methamphetamine use. Both marketed medications and investigational agents will be tested. Finally, NIDA has begun to test medications for efficacy to reduce cannabis use. Initial studies are underway. Both agonist and antagonist approaches will be evaluated. Additionally, medications will be tested in cannabis-dependent patients for the management of insomnia, withdrawal, and concurrent depression.
Hypoxic ischemic encephalopathy (HIE) is the most important reason for morbidity and mortality in term-born infants. Understanding pathophysiology of the brain damage is essential for the early detection of patients with high risk for HIE and development of strategies for their treatments. Areas covered: This review discusses pathophysiology of the neonatal HIE and its treatment options, including hypothermia, melatonin, allopurinol, topiramate, erythropoietin, N-acetylcyctein, magnesium sulphate and xenon. Expert commentary: Several clinical studies have been performed in order to decrease the risk of brain injury due to difficulties in the early diagnosis and treatment, and to develop strategies for better long-term outcomes. Although currently standard treatment methods include therapeutic hypothermia for neonates with moderate to severe HIE, new supportive options are needed to enhance neuroprotective effects of the hypothermia, which should aim to reduce production of the free radicals and to have anti-inflammatory and anti-apoptotic actions.
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The prevalence of chronic migraine ranges between 1-3% of the population and its incidence has been estimated to be 2.5% per year. It produces from four to six times more disability, decreased productivity and disruption of quality of life than episodic migraine. The development of chronic migraine has been associated with both non-modifiable risk factors (being female, low socio-economic status and level of schooling) and modifiable risk factors (anxiety, depression, sleep apnoea/snoring, obesity, consumption of painkillers and caffeine). Patients with chronic migraine suffer from chronic pain, anxiety or depression two to three times more often than those with episodic migraine. Management requires identification and control of the risk factors that predispose patients to develop the condition, detoxification therapy in the event of abuse of analgesics, specific treatment for migraine attacks and preventive treatment. The effectiveness of the preventive drugs topiramate and Onabotulinumtoxin A in this complication of migraine has been proved in large-scale placebo-controlled clinical trials.
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Randomised placebo controlled add-on trials of people of any age with localisation related seizures, in which an adequate method of concealment of randomisation was used were included. The studies could be double, single or unblinded and be of parallel or crossover design. They had to have a minimum treatment period of eight weeks. Trials using an active drug control group were also included.
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Metabolic acidosis induced by topiramate is a well documented but infrequent adverse event. The objective was to demonstrate the lowering of carbon dioxide serum levels, which is usually asymptomatic but may facilitate the occurrence of metabolic acidosis in patients using topiramate.
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Topiramate pharmacokinetics is influenced by individual factors such as patient age, renal function and co-treatment. The aim of this study was to develop a population pharmacokinetic model of topiramate to assist dosage adjustments in individual patients. Steady-state topiramate plasma concentrations in patients with epilepsy were determined by HPLC using fluorescent labelling. Demographic, biochemical data and dosing history including concomitant drug therapy were collected from patients' charts. Nonlinear mixed effects modelling was used to fit a one-compartment pharmacokinetic model. The influence of patient weight and gender, body surface area, age, creatinine clearance, serum transaminases, topiramate daily dose and co-treatment with carbamazepine, valproic acid, benzodiazepines, and risperidone on topiramate pharmacokinetics was evaluated. Additionally, the relationship between topiramate plasma concentration and clinical response was investigated. Volume of distribution of topiramate was 0.518 l/kg. For a typical patient oral clearance was estimated at 1.47 l/h, with interindividual variability of 39.2%. Clearance was 70% higher in patients co-treated with carbamazepine and was found to increase with patient age. Somnolence was the most frequently observed adverse event. Incidence of headache was associated with topiramate plasma concentration. Somnolence, ataxia, tremor, speech disorders and fatigue were associated with adjunctive therapy with carbamazepine, valproic acid, benzodiazepines, risperidone, and clozapine. No association of topiramate plasma concentration with frequency of seizures or patient quality of life was observed. The developed model can be used for Bayesian estimation of pharmacokinetic parameters based on sparse plasma samples and for selection of optimum dosing in routine patient care.
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We conducted a pragmatic, randomized, unblinded, multicenter, parallel-group clinical trial (the Standard and New Antiepileptic Drugs [SANAD] trial) comparing clinical and cost effectiveness of initiating treatment with carbamazepine versus lamotrigine, gabapentin, oxcarbazepine and topiramate, and valproate versus lamotrigine and topiramate. QoL data were collected by mail at baseline, 3 months, and at 1 and 2 years using validated measures. These data were analyzed using longitudinal data models. Continuous QoL measures, time to 12-month remission and time to treatment withdrawal were explored using joint models.