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We conducted a retrospective review of the charts of patients treated with add-on topiramate in order to control weight gain induced by psychotropic drugs (antipsychotic drugs, lithium or valproate).
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Of all the medications tested to date, disulfiram has demonstrated the most consistent effect to reduce cocaine use. Several medications have been reported to reduce cocaine use in double-blind, placebo-controlled clinical trials, namely baclofen, modafinil, tiagabine, and topiramate. All pharmacotherapy trials in cocaine-dependent patients include a behavioral therapy that is common to all participants. Consequently, these pharmacotherapy trials can be considered to evaluate whether the medication is adding to the effect of the behavioral therapy.
Fifteen patients with neurodevelopmental disabilities who received topiramate therapy
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Although postictal events contribute to seizure severity and thus affect quality of life, the effect of antiepileptic drugs (AEDs) on the postictal state is not well known. This review assesses the available evidence from randomized controlled trials on the effect of AEDs on postictal events. The instruments used in AED trials include postictal items of The Liverpool Seizure Severity Scale (LSSS) and Seizure Severity Scale (SSQ) and postictal recovery of electroencephalography (EEG) background activity. The effect of AEDs on postictal components of LSSS, if documented separately or at all, was either too small to be clinically significant (for lamotrigine) or not different from that of controls (topiramate, valproate). However, lacosamide showed improvement on the SSQ over placebo, and levetiracetam was associated with a speedier postictal recovery of EEG background activity compared with placebo. Although measuring the effect of AEDs on postictal state is of great clinical interest, the limited evidence found in this review suggests that further work is needed to evaluate current instruments used to assess AED-associated changes in postictal events.
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Psychotropic medications are used to manage behaviour problems in adults with intellectual disability (ID). One group of psychotropic medication are mood stabilizers such as lithium and some antiepileptic drugs.
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When used in addition to other empiric therapy, topiramate may be effective at reducing general symptoms of combat-related PTSD and reducing high-risk alcohol intake and nightmares. Further randomized controlled trials of topiramate for the treatment of combat-related PTSD are warranted.
In this study, prescription of topiramate was associated with greater persistence with prophylactic treatment than the other prophylactic drugs. Furthermore, greater reductions in acute treatment utilization, particularly triptans, were observed among patients prescribed topiramate compared with the other prophylactic cohorts.
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Turner's syndrome (TS), resulting from deletion of one X chromosome in women, is associated with cerebral development abnormalities, particularly in the temporal lobes. Symptomatic epilepsy is described only in cases with extensive malformations. Here, we report the first case of bilateral temporal epilepsy without macroscopic cerebral malformation in a woman with TS mosaicism. Bitemporal dysfunction was confirmed by the ictal and interictal EEG, PET, MR-spectroscopy and the neuropsychological examination, other causes than TS mosaicism were excluded. In rare cases, TS mosaicism may underlie non-lesional temporal lobe epilepsy, probably in relation to microanatomic structural and functional cerebral abnormalities. Further studies are needed to determine the frequency of this association.
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Based on the complex biology of eating behavior, in this review we discuss the features, mechanisms of action, pharmacokinetics, advantages and possible disadvantages of these new agents.
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This double-blind, placebo-controlled study investigated the efficacy and tolerability of adjunctive topiramate in 86 elderly Chinese patients with refractory partial epilepsy. Patients who had at least four seizures per 4 weeks during an 8-week baseline period, despite medication with up to three standard antiepileptic drugs (AEDs), were randomly assigned to receive topiramate (n = 46) or placebo (n = 40). Topiramate dosages were titrated (target dose 200 mg/day orally) for 8 weeks and maintained at stable levels for another 12 weeks; concomitant AEDs continued at original dosages. All patients completed the study: 47.8% in the topiramate group and 7.5% on placebo reached ≥ 50% reduction in complex partial seizures. In the topiramate group, the most common adverse events were dizziness, somnolence, fatigue, headache and difficulty with memory; most events were transient and mild or moderate in severity. It was concluded that 200 mg/day topiramate was effective and well-tolerated in elderly patients with refractory partial epilepsy.
Neither topiramate nor delayed hypothermia alone conferred protection in this protocol. Combined treatment with topiramate and delayed hypothermia improved both performance and pathological outcome in P15 and P35 rats compared with PBS-treated animals that underwent delayed hypothermia concurrently. At P15, functional measures were better in topiramate-treated animals (mean correct forepaw response 9.3/10 versus 4.8/10; P<0.001), and there was >50% reduction in tissue loss (P<0.001); trends were similar at P35.
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The birth prevalence of OCs was 0.36% (7/1945) in the TPM cohort, 0.14% (20/13 512) in the FE cohort, and 0.07% (9/13 614) in the SMP cohort. Standardized by site, the prevalence ratio (PR) for TPM versus FE was 2.5 (95% CI: 1.0-6.0) and for TPM versus SMP was 5.4 (95% CI: 2.0-14.6). Adjustment for covariates one at a time or by propensity score yielded similar results.
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There were 510 samples from 476 adult patients. Serum TPM was below 2.0 mg/L or above 10.0 mg/L in 28.2% and 5.9% of samples, respectively. Although serum TPM was broadly related to prescribed dose, there was wide variation. Most patients using TPM were treated in combination with other anticonvulsants (90.8%). TPM-CDR in patients receiving TPM monotherapy was not significantly different from those receiving TPM in combination with nonenzyme inducers, but TPM-CDR was lower in patients who were taking inducers (P < 0.0001, Kruskal-Wallis test, Dunnett method).
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In the last years several studies have been performed on migraine; however, only few topics have changed the clinical practice. Among these, there are physiopathological insights (e.g., allodynia and gastric stasis) or therapeutical evidences (e.g., topiramate) that become very important in the management of migraine and could clarify the different response to the therapies. The aim of a training school on headache should be to link research to practice without transferring contradictory data. To teach is not only to support notions with simple data: we think that knowledge has to be used according to the condition of the patient and the situation in which the migraineurs live.
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We studied 32 adults with epilepsy at an outpatient epilepsy clinic who were treated with topiramate in monotherapy or in combination for at least one month. Metabolic acidosis was found in all patients (HCO3<22 Eq/L); nine were taking topiramate in monotherapy, and 23 were taking at least two antiepileptic drugs (AEDs). All of the patients were asymptomatic. We found no correlation between bicarbonate levels and the dose of the drug or the duration of treatment. The dose was significantly higher in the monotherapy group, and the bicarbonate level was lower in the patients taking more than one AEDs.
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In 15 (6.7%) of 221 children on the ketogenic diet without the use of carbonic anhydrase inhibitors, stones developed. In five (6.3%) of the 80 children on the diet in combination with topiramate or zonisamide, stones developed. There was no difference between these two groups (p = 0.82). No child was treated with either acetazolamide or more than one carbonic anhydrase inhibitor simultaneously. Prior ketogenic diet duration was shorter (10.4 vs. 22.4 months; p = 0.03), and more children had either a family history of renal stones or significant urologic abnormalities (80 vs. 27%; p = 0.04) in the combination-therapy group.
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Neuropathic cranial pain, i.e. pain due to central or peripheral nervous system damage localized in cranial area, is a clinical challenge for the neurologist. Despite major advances in knowledge of physiology and biochemistry of pain, relief for many patients suffering from neuropathic pain remains incomplete. Adjuvant analgesics play a key role in the management of neuropathic pain. The introduction in the therapeutical armamentarium of antiepileptic drugs and the results derived from clinical studies indicate that some of these compounds show promise in the treatment of neuropathic pain.
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Long-term treatment with topiramate reduces body weight and improves insulin sensitivity in obese humans. Our aim was to evaluate the effect of topiramate treatment for 4 weeks on insulin sensitivity and secretion, independent of weight loss.
Several models were developed in pediatric and adult populations to relate steady-state trough plasma concentrations (C(min)) of topiramate to the magnitude of clinical effect in monotherapy and adjunctive settings. These models were integrated to derive and support the monotherapy dosing regimen for pediatric patients.
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The aim of this study was to investigate the natural history of epilepsy and response to anti-epileptic drug treatment in patients with Angelman syndrome (AS) in Korea.
Topiramate, a sulfamate-substituted monosaccharide, is a new antiepileptic drug (AED) approved as adjunctive therapy for partial-onset seizures in adults. Topiramate is rapidly absorbed, has linear pharmacokinetics, minimal protein binding and a long half-life facilitating a twice-daily dosage regimen. Topiramate has little effect on the plasma concentrations of other AEDs with the exception of phenytoin, concentrations of which may increase in some patients when topiramate is added to the therapy. Topiramate metabolism is increased when administered with carbamazepine or phenytoin. In the absence of enzyme-inducing AEDs, topiramate is eliminated primarily by renal excretion, with 50 to 80% of a dose excreted as unchanged topiramate. In 6 double-blind, placebo-controlled trials, topiramate was shown to be well tolerated and effective as adjunctive therapy for partial-onset seizures in adults. Topiramate consistently reduced seizures across all patient groups defined by age, gender and baseline seizure frequency. Adverse effects were generally mild-to-moderate CNS-related effects and often resolved spontaneously or with slowing of topiramate titration and/or reduction of the dosage of concomitant AEDs. Clinical studies are currently evaluating the effectiveness and safety of topiramate as monotherapy and adjunctive therapy in children with partial seizures, in patients with Lennox-Gastaut syndrome and in patients with generalised tonic-clonic seizures of non-focal onset. Preliminary findings suggest that topiramate has a broad spectrum of clinical use.
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Early use of antiepileptic drugs valproate or topiramate is effective and safe in children with febrile seizures which are prone to epilepsy. The majority of the children have a normal sleeping activation EEG after antiepileptic drug therapy.
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Whereas the efficacy of the newer antiepileptic drugs (AEDs) is well established, there remain questions regarding their cognitive side effects. Therefore, we performed a comparative open randomized trial with TPM and TGB as add-on therapy, with particular consideration of cognition, mood, and health-related quality of life (HRQOL).
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Overall OR (95% CIs) for 50% or greater reduction in seizure frequency compared to placebo 4.06 (2.86-5.78). Dose regression analysis shows increasing efficacy with increasing dose, but found no advantage for doses over 400 mg per day. Global effectiveness: treatment withdrawal OR (95% CIs) compared to placebo 2.57 (1.65-4.00). Side effects: OR (99% CIs)compared to placebo, dizziness 1.99 (1.20-3.29); fatigue 2.52 (1. 47-4.32); nausea 2.84 (1.36-5.93); somnolence 2.89 (1.72-4.85) and 'thinking abnormally' 3.71 (2.02-6.80) were significantly associated with topiramate.
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Pediatric brain tumors are the most common solid pediatric tumor and the most common cause of death in pediatric cancer. Seizures are one of the most common symptoms of pediatric brain tumors. Factors associated with increased risk of seizures include supratentorial location, gray matter involvement, low-grade, and certain histological features-especially dysembryoplastic neuroepithelial tumor, ganglioglioma, and oligodendroglioma. Leukemic infiltration of the brain, brain metastases of solid tumors, and brain injury secondary to chemotherapy or radiotherapy can also cause seizures. Mechanisms by which brain tumors cause seizures include metabolic, and neurotransmitter changes in peritumoral brain, morphologic changes - including malformation of cortical development - in peritumoral brain, and presence of peritumoral blood products, gliosis, and necrosis. As there is a high degree of uncertainty on how effective different antiepileptic drugs are for seizures caused by brain tumors, choices are often driven by the interaction and side effect profile. Classic antiepileptic drugs - phenobarbital, phenytoin, or carbamazepine - should be avoided as they may alter the metabolism of chemotherapeutic agents. Newer drugs - valproate, lamotrigine, topiramate, zonisamide, and levetiracetam - may be the preferred option in patients with tumors because of their very limited interaction with chemotherapy.
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This study was undertaken to test the hypothesis that topiramate (TPM) exerts a negative modulatory effect on some types of alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA)/kainate receptors by binding to the site at which protein kinase A (PKA) phosphorylates the receptor-channel complex.
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gamma-Aminobutyric acid (GABA) belongs to the main inhibitory neurotransmitters in the central nervous system and activates three types of specific receptors--GABAA, GABAB i GABAC. At present, little is known about GABAC-mediated events. GABAB receptors are metabotropic, whilst stimulation of ionotropic GABAA receptors results in opening the chloride channel, followed by influx of chloride ions and hyperpolarization. The GABAA receptor possesses also binding sites for benzodiazepines and barbiturates which, via these sites, enhance GABAA-mediated events. Another antiepileptic drug potentiating GABA-ergic inhibition is valproate, which increases synthesis of GABA and reduces its metabolism. Among new antiepileptic drugs associated with the GABA-ergic system are tiagabine, vigabatrin, and to a certain degree--gabapentin. Tiagabine blocks neuronal and glial uptake of GABA whilst vigabatrin increases the synaptic concentration of GABA by inhibition of GABA aminotransferase. Gabapentin, probably through the activation of glutamic acid decarboxylase, leads to the increase in synaptic GABA. However, this antiepileptic drug also binds to specific sites within voltage-dependent calcium channels, which results in reduced intraneuronal concentration of calcium ions. Presumably, tiagabine and vigabatrin possess only one mechanism of action, associated with increased GABA-ergic inhibition. Although topiramate and felbamate were shown to enhance GABA-mediated events, they have additional mechanisms of action, including blockade of voltage-dependent sodium channels and inhibition of glutamatergic neurotransmission.