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In intention-to-treat analysis, topiramate was more effective than placebo in reducing Positive and Negative Syndrome Scale general psychopathologic symptoms (effect size = 0.7, p = .021), whereas no significant improvement was observed in positive or negative symptoms.
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To evaluate the effect of topiramate migraine prophylaxis on subject responsiveness to triptans used for acute symptomatic migraine treatment.
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Topiramate was associated with overall tremor reduction and improvements in tremor severity, motor task performance, and functional disability in patients with moderate to severe essential tremor.
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(1) Topiramate, a second-line antiepileptic, was recently implicated in several cases of acute myopia. High intraocular pressure is sometimes associated. (2) All visual abnormalities resolved when topiramate was rapidly stopped.
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For patients with difficulty swallowing pills, USL255 sprinkled onto applesauce offers a useful once-daily option for taking topiramate. USL255 beads were also successfully delivered in vitro through ≥14-Fr G- or J-tubes, with tube clogging minimized by portioning the dose and using glidant diluents for smaller tubes.
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Topiramate is efficacious for the treatment of alcohol dependence, but side effects may limit widespread use. While topiramate's unique pharmacodynamic profile offers a promising theoretical rationale for use across multiple substance-related disorders, heterogeneity both across and within these disorders limits topiramate's broad applicability in treating substance-related disorders. Recommendations for future research include exploration of genetic variants for more targeted pharmacotherapies.
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A 17-year-old female developed hyperammonemic encephalopathy 2 weeks after valproic acid (VPA), 500 mg twice a day, was added to her regimen of topiramate (TPM), 200 mg twice a day. She presented to the emergency department (ED) with altered mental status, hypotension, bradycardia, and lethargy. Laboratory analysis showed mild non-anion gap hyperchloremic acidosis, serum VPA concentration of 86 mg/L, and urine drug screen result that was positive for marijuana. She was admitted to the pediatric intensive care unit for persistent symptoms, prolonged QTc, and medical history. Blood ammonia concentrations were obtained because of her persistent altered mental status, initially 94 μmol/L and a peak of 252 μmol/L. A serum carnitine profile was obtained at the time of hyperammonemia and was found to be normal (results were available postdischarge). VPA and TPM were discontinued on day 1 and day 2, respectively, as the patient's blood ammonia concentration remained elevated. On day 3, her mental status had returned to baseline, and blood ammonia concentrations trended downward; by day 4 her blood ammonia concentration was 23 μmol/L. VPA has been associated with numerous side effects including hyperammonemia and encephalopathy. Recently, drug interactions with TPM and VPA have been reported; however, serum carnitine concentrations have not been available. We discuss the possible mechanisms that VPA and TPM may affect serum ammonia and carnitine concentrations and the use of levocarnitine for patients or treating toxicity.
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We analyzed the clinical features and therapeutic outcome in 16 patients with GCSE, NCSE or recurrent GTC in whom TPM was administered for its control.
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Although anecdotal, these observations suggest that topiramate may be an effective treatment for patients with BED and obesity who experience recurrent binge eating and weight gain after initially successful bariatric surgery.
Antiepileptic drugs (AEDs) in broad use today have a number of pharmacokinetic liabilities, including a propensity for clinically meaningful drug interactions. Therefore, new AEDs with improved pharmacokinetic characteristics would be welcomed. The pharmacokinetic profiles of six newer AEDs--topiramate (TPM), gabapentin (GBP), vigabatrin (VGB), lamotrigine (LTG), oxcarbazepine (OCBZ), and felbamate--were reviewed. Some of these AEDs offer an improvement in one or more pharmacokinetic parameters compared with traditional AEDs, with TPM, GBP, VGB, and OCBZ demonstrating the most advantageous overall pharmacokinetic profiles.
Treatments used for several neurological conditions may adversely affect the eye. Vigabatrin-related retinal toxicity leads to a visual field defect. Optic neuropathy may result from ethambutol and isoniazid, and from radiation therapy. Posterior subcapsular cataract is associated with systemic corticosteroids. Transient refractive error changes may follow treatment with acetazolamide or topiramate, and corneal deposits and keratitis with amandatine. Intraocular pressure can be elevated in susceptible individuals by anticholinergic drugs, including oxybutynin, tolterodine, benzhexol, propantheline, atropine and amitriptyline, and also by systemic corticosteroids and by topiramate. Nystagmus, diplopia and extraocular muscle palsies can occur with antiepileptic drugs, particularly phenytoin and carbamazepine. Ocular neuromyotonia can follow parasellar radiation. Congenital ocular malformations can result from in utero exposure to maternally prescribed sodium valproate, phenytoin and carbamazepine. Neurologists must be aware of potential ocular toxicity of these drugs, and appropriately monitor for potential adverse events.
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There is a wide array of options for migraine prophylaxis; many of the available drugs are clearly proven to be effective and yet are underused in Australia. "New" drugs which are gaining favour for migraine prophylaxis include topiramate, candesartan, gabapentin and botulinum toxin. The evidence for efficacy is excellent for topiramate and reasonably good but limited for candesartan and gabapentin. The use of botulinum toxin is controversial and has gained substantial popularity through anecdotal experience rather than convincing published evidence. Transformed or chronic migraine with medication overuse is a particularly difficult problem. New strategies to aid in medication withdrawal are reviewed. The approach to menstrual migraine and migraine with prominent aura may differ from that for typical migraine. Novel approaches are being explored for these problems.
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Topiramate may be a safe and effective treatment for scars. Shapira et al. reported an open label study on ten adult subjects with discolored or raised scars at least 2 years old who were given topiramate in an oral dosage of 15 mg per day for 1 month. The dosage was then increased to 30 mg per day if there was minimal or no improvement. Based on that study, BDC Research Centre treated 91 patients with various scarring conditions including post acne, varicella, dermatitis scars, melasma, hypertrophic scars, and keloids. Excellent to good results were observed in post-acne and post-varicella scars.
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To examine the tolerability of topiramate (TPM) in paediatric practice.
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Review of medical records from patients with VM according to the criteria of the Bárány Society/International Headache Society of 2012 criteria. The drugs used in the treatment and treatment response obtained through the visual analog scale (VAS) for dizziness and headache were assessed. The pre and post-treatment VAS scores were compared (the improvement was evaluated together and individually, per drug used). Associations with clinical subgroups of patients were also assessed.
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In conclusion, topiramate stimulates insulin-mediated glucose uptake in vivo through the CNS. These observations illustrate the possibility of pharmacological modulation of peripheral insulin resistance through a target in the CNS.
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In the past twenty years, 14 new antiepileptic drugs have been approved for use in the United States and/or Europe. These drugs are eslicarbazepine acetate, felbamate, gabapentin, lacosamide, lamotrigine, levetiracetam, oxcarbazepine, pregabalin, rufinamide, stiripentol, tiagabine, topiramate, vigabatrin and zonisamide. In general, the clinical utility of therapeutic drug monitoring has not been established in clinical trials for these new anticonvulsants, and clear guidelines for drug monitoring have yet to be defined. The antiepileptic drugs with the strongest justifications for drug monitoring are lamotrigine, oxcarbazepine, stiripentol, and zonisamide. Stiripentol and tiagabine are strongly protein bound and are candidates for free drug monitoring. Therapeutic drug monitoring has lower utility for gabapentin, pregabalin, and vigabatrin. Measurement of salivary drug concentrations has potential utility for therapeutic drug monitoring of lamotrigine, levetiracetam, and topiramate. Therapeutic drug monitoring of the new antiepileptic drugs will be discussed in managing patients with epilepsy.
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After TPM withdrawal, group performance appeared significantly improved in five of six tests administered. The scores of the control patients remained largely unchanged after drug reduction. After withdrawal, the scores of the TPM group did not differ significantly from the results of the control group whereas pronounced differences had been observed before. Individual improvement became apparent in the majority of patients. Cognitive performance was not correlated to current daily dosages/current blood serum levels of TPM.
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Reversible priapism (stuttering subtype) is associated with topiramate.
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Weight loss is common in patients with neurodevelopmental disabilities who receive topiramate. Since patients who received oral diets lost weight whereas those receiving enteral nutrition did not, decreased nutrient intake is the likely cause of weight loss.
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We investigated potential analgesics for chemotherapy-evoked neuropathic pain using rats treated with paclitaxel.
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We evaluated the anticonvulsant efficacy of topiramate (TPM), a structurally novel antiepileptic drug (AED), in amygdala kindled rats that had been preselected with respect to their response to phenytoin (PHT).
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Although ocular side effects of topiramate are common, neuroophthalmologic manifestations such as blepharospasm, myokymia and oculogyric crisis are scarcely reported.
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For both patients with transformed migraine (add-on therapy) and patients with episodic migraine (first-line monotherapy), topiramate yielded significant reductions in migraine frequency, migraine severity, number of headache days/month, and use of abortive medications. Topiramate also appears to be well tolerated and useful in the adjunctive treatment of cluster headache. Prospective double-blind, placebo-controlled trials will be required to confirm our results.
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Although identified by Dravet in 1978, it has been called severe myoclonic epilepsy in infancy since 1981. As an alternative the name polymorphic epilepsy has also been put forward and in 2001 the ILAE recognised the eponym Dravet's syndrome. We describe how it may be mistaken for febrile convulsions in the early stages and later for Lennox Gastaut syndrome, Doose's myoclonic astatic epilepsy and certain progressive myoclonic epilepsies. We outline the risk factors, recognised in 1992, that facilitate an early diagnosis and the defining clinical criteria established in 1984. We point out the existence of atypical forms due to the absence of some of the defining criteria, which will never be above one, to formulate a diagnosis of SMEI. The frequency with which a family background of febrile convulsions and epilepsy appears seems to point to a genetic origin. Recently, de novo mutations have been found in the alpha subunit of the voltage dependent sodium channel as well as mutations in the gamma subunit of the GABAA receptor. Nosologically, it is located in group 3 of the 1989 ICE, which corresponds to epileptic syndromes without a focal determination, or which are generalised, and on the list of epilepsy/syndromes that was presented in 2001. SMEI is an epilepsy syndrome which is, in most cases, resistant to classical and new AED, and other more unusual treatment. The drugs that have proved to be more effective, although only relatively so, are topiramate, valproate and the benzodiazepines. At present another alternative that has appeared is stiripentol. Intravenous use of immunoglobulins can be useful.
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We acquired the retention data on levetiracetam (LEV), lamotrigine (LTG), oxcarbazepine (OXC), topiramate (TPM), and zonisamide (ZNS) from the electronic database. The data included patient's age, gender, seizure type, current and previous medications, dosage, main reasons for discontinuation, and duration of therapy. The retention rates of these AEDs were evaluated at 4, 12, 24, 52, and 104 weeks.
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Many new drugs and therapies can now be offered to patients with epilepsy. The problem is that we do not know just how much better these new and more expensive therapies are compared with the old ones, nor do we know the full range of side-effects. This review focuses on the major clinical studies that have been published in the past year with emphasis on information as to tolerability and efficacy, especially when there is some information comparing different drugs or therapies. The topics include vigabatrin, lamotrigine, gabapentin, felbamate, topiramate, tiagabine, oxcarbazepine, levetiracetam, vagus nerve stimulation and the ketogenic diet. It is encouraging that some of the newly published double-blinded placebo-controlled studies now include children and the elderly, patient groups that have previously been neglected.
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Chronic migraine refractory to preventive treatment is a common clinical situation in general neurology clinics. The aim is to analyse our experience with zonisamide in the preventive treatment of patients with frequent refractory migraine.
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A total of 129 papers were eligible for analyses. Our findings indicate that the majority of the CNS-acting drugs, if taken by nursing women, result in average exposure levels to their breast-fed infants of less than 10% of the therapeutic doses per kg body weight. Exceptions are lithium, ethosuximide, phenobarbital, primidone, lamotrigine and topiramate. Adverse effect profiles do not always correlate with a higher exposure level. Overall, most reported adverse effect profiles appear benign. Where adverse effects were reported, they were often confounded by intrauterine exposure.
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Insomnia in patients with alcohol dependence has increasingly become a target of treatment due to its prevalence, persistence, and associations with relapse and suicidal thoughts, as well as randomized controlled studies demonstrating efficacy with behavior therapies and non-addictive medications. This article focuses on assessing and treating insomnia that persists despite 4 or more weeks of sobriety in alcohol-dependent adults. Selecting among the various options for treatment follows a comprehensive assessment of insomnia and its multifactorial causes. In addition to chronic, heavy alcohol consumption and its effects on sleep regulatory systems, contributing factors include premorbid insomnia; co-occurring medical, psychiatric, and other sleep disorders; use of other substances and medications; stress; environmental factors; and inadequate sleep hygiene. The assessment makes use of history, rating scales, and sleep diaries as well as physical, mental status, and laboratory examinations to rule out these factors. Polysomnography is indicated when another sleep disorder is suspected, such as sleep apnea or periodic limb movement disorder, or when insomnia is resistant to treatment. Sobriety remains a necessary, first-line treatment for insomnia, and most patients will have some improvement. If insomnia-specific treatment is needed, then brief behavioral therapies are the treatment of choice, because they have shown long-lasting benefit without worsening of drinking outcomes. Medications work faster, but they generally work only as long as they are taken. Melatonin agonists; sedating antidepressants, anticonvulsants, and antipsychotics; and benzodiazepine receptor agonists each have their benefits and risks, which must be weighed and monitored to optimize outcomes. Some relapse prevention medications may also have sleep-promoting activity. Although it is assumed that treatment for insomnia will help prevent relapse, this has not been firmly established. Therefore, insomnia and alcohol dependence might be best thought of as co-occurring disorders, each of which requires its own treatment.
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There is considerable evidence suggesting, that older antiepileptic drugs (AEDs) and some of the newer ones decrease bone mineral density (BMD). However, there is only limited and conflicting data concerning the effect of levetiracetam on BMD. In this cross-sectional study we analysed data from 168 adult consecutive outpatients treated with AEDs for more than 2 years, and who underwent measurement of the BMD. We compared the incidence of decreased BMD among the patients treated with 6 different AEDs: carbamazepine (CBZ), oxcarbazepine (OXC), valproic acid (VPA), lamotrigine (LTG), topiramate (TPM) and levetiracetam (LEV). Among the patients on monotherapy, reduced BMD was present significantly most often in patients treated with LEV and those treated with OXC. In the group of patients on polytherapy there was no significant difference in the incidence of low BMD among patients treated with various AEDs. Our data suggest that patients on long-term treatment with LEV have a higher risk for affection of bone density.
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The neuropsychological tests demonstrated objective language impairments in TPM-on patients. Compared with the HCs, the bilateral medial prefrontal cortex and the posterior midline and lateral parts of the default mode network (DMN) (including the bilateral posterior cingulate cortex (PCC), the right medial prefrontal cortex, the right angular gyrus, the right inferior temporal gyrus, and the bilateral supramarginal gyrus) in TPM-on patients failed to deactivate during the VGT. Their task-induced activation patterns were largely similar to those of the HCs. After TPM withdrawal, partial improvement of both task-induced deactivation of the DMN (the left parahippocampal gyrus and the bilateral PCC) and task-related activation of the language network (the right middle frontal gyrus and the left superior occipital gyrus) was identified along with partial improvement of neuropsychological tests.
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Despite all of our advances women with epilepsy face obstacles when it comes to pregnancy and childbearing. Many of these obstacles are social, based on incorrect and inappropriate attitudes of the public towards persons with epilepsy. Unfortunately many of the uninformed public are health care providers. We must continue to educate not only our patients but our colleagues so that women with epilepsy will cease to face discriminatory behaviour. Most women with epilepsy can conceive and bear healthy children. They have higher probabilities of infertility but this is often amenable to treatment. Complications of pregnancy are higher and revolve primarily around the increased risk of maternal seizures. Careful monitoring of the clinical condition of the patient and her free anticonvulsant levels will obviate much of this difficulty. Maternal seizures themselves can pose hazards for women with epilepsy and their offspring and generalized convulsive seizures are clearly to be avoided. Adverse pregnancy outcomes tend to be seen more often in particular: congenital malformations 4-6%; dysmorphic features < 10%; neonatal haemorrhage < 7%; fetal death and neonatal and infant mortality a two to threefold increase over the general population; and an uncertain risk of developmental delay particularly in the area of language acquisition. Of the potential variables of interest: anticonvulsants, maternal seizures during gestation, and the genetics of maternal epilepsy, it is at present unclear which is the most important in determining a good pregnancy outcome. Current research suggests that anticonvulsant drugs are probably responsible for the increased risk of malformations. Malformations are, however, only one of the adverse outcomes of concern. Risks can be reduced by ensuring good seizure control; monotherapy: preconceptual use of multivitamins with folate. The plethora of new anticonvulsants offers us new opportunities for improving the function and control of persons with epilepsy. Unfortunately we are uncertain how hazardous the newer anticonvulsant drugs are in pregnancy. Felbamate, gabapentin, lamotrigine, vigabatrine, and topiramate have all been recently introduced. The number of exposed women is so small that no pattern or estimates of risk can be determined at this time. Careful monitoring as is being performed by the Lamotrigine and North American Epilepsy and Pregnancy Registries will hopefully provide the necessary safety information in the near future. All of the risks aside, the majority of women with epilepsy can and will have healthy children.
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The frequency of convulsion seizures in the 20, 40 and 80 mg TPM treatment and TPM+FA groups was 44.7 +/- 2.9, 44.3 +/- 3.1, 42.7 +/- 3.2, and 40.8 +/- 3.7 respectively, which were significantly lower than that in the positive control group (48.4 +/- 3.7) (P <0.01). Twenty, forty and eighty mg TPM treatment and TPM+FA treatment significantly reduced NSE levels from 35.71 +/- 5.97 microg/L of the control group to 27.40+/- 6.40, 24.79 +/- 6.22, 21.47 +/- 6.87 and 22.55 +/- 7.02 microg/L respectively (P <0.05). Neuronal apoptosis in the CA3 and CA1 regions were alleviated in the four TPM treatment groups compared with positive control. The number of necrotic neurons was progressively reduced with the increased dose of TPM. The 40 mg TPM+FA treatment group showed less necrotic neurons in the CA3 and CA1 regions than the 40 mg TPM alone treatment group.
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To investigate the acute effects of topiramate on the anterior chamber angle (ACA) and choroidal thickness in patients with migraine.
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To determine whether the AEDs VPA, carbamazepine (CBZ), topiramate (TPM), or lamotrigine (LYG) directly affect the activities of human 3beta HSDII and P450c17, we added them to yeast expressing human P450c17 or 3beta HSDII and assayed enzymatic activities in the microsomal fraction.
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The authors assessed the effect of concomitant antiepileptic therapy on steady-state plasma concentrations of the new antiepileptic drug (AED) topiramate and the potential relation between topiramate plasma levels and side effects in a cohort of 116 patients with epilepsy. On the basis of concomitant AEDs, patients were divided into two subgroups, otherwise comparable for age and weight-adjusted daily dose of topiramate. Group A (n = 73) received topiramate plus AED inducers of cytochrome P450 (CYP) metabolism, such as carbamazepine, phenobarbital, and phenytoin. Group B (n = 43) received topiramate plus AEDs without inducing properties of CYP metabolism (namely valproic acid and lamotrigine). Weight-normalized topiramate clearance values, calculated as dosing rate/steady-state plasma drug concentration, were about 1.5-fold in patients receiving AED inducers compared with patients receiving AED noninducers. Topiramate plasma concentrations were linearly related to daily drug doses, regardless of concomitant AED therapy, over a dose range from 25 to 800 mg/d, although, at a given daily dose, a large interpatient variability was observed in matched plasma drug concentrations within each group of patients. Thirty-nine patients (34%) reported side effects associated with topiramate, mostly central nervous system effects. No consistent relation was observed between topiramate plasma concentrations and adverse effects, either in the cohort of patients as a whole or within each subgroup. From a clinical point of view, patients receiving concurrent treatment with enzyme-inducing AEDs can show twofold lower topiramate plasma concentrations compared with patients receiving valproic acid or lamotrigine, and appropriate topiramate dosage adjustments may be required when concomitant AED inducers are either added or withdrawn. Due to the observed variability in topiramate metabolic variables and the complex spectrum of possible pharmacokinetic and pharmacodynamic interactions with the most commonly coprescribed AEDs, monitoring of plasma topiramate concentrations may help the physician in the pharmacokinetic optimization of the drug dosage schedule in individual patients.