TPM and LTG significantly inhibited seizures in this CL model. The expression of P-gp was not significantly increased by TPM or LTG treatment in this study.
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The final PK model was CL/F (L/h)=(1.16+1.36 × PHT+1.01 × CBZ+0.643 × OXC+0.476 × PB)×(CLcr/90)(0.310)×(DOSE/100)(0.0929) (1 in patients co-medicated with each drug, 0 in otherwise) and V/F (L)=109 × (WT/62). For a typical patient with CLcr of 90 mL/min and DOSE of 100mg, co-medication with PHT, CBZ, OXC, and PB increased the CL/F to 2.52 (1.16+1.36)L/h, 2.17 (1.16+1.01)L/h, 1.803 (1.16+0.643)L/h, and 1.636 (1.16+0.476)L/h, respectively, which was 117, 87, 55, and 41% higher, respectively, than in patients without co-medication.
In all 12 patients after 6 months of treatment, topiramate did not statistically influence aura frequency (P=.317) or duration (P=.480) compared with baseline. Mild to moderate side effects were observed, but they did not interfere with treatment. Consistent with previous observations, migraine frequency as well as headache intensity and duration improved statistically significantly.
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To compare adverse drug reactions (ADRs) to topiramate in patients with migraine and patients with epilepsy, we systematically reviewed all published randomized controlled trials (RCTs) that compare topiramate monotherapy in epilepsy and migraine. We included four epilepsy RCTs (N = 1,179 patients; vs. active comparators) and six migraine RCTs (N = 1,723 patients; vs. placebo). Behavioral ADRs and headache were found only in the case of epilepsy, whereas cognitive complaints and alteration of taste were found only in the case of migraine. The risk ratios (RRs) for paresthesia in migraine vs. epilepsy trials were 2.5 (99% confidence interval (CI): 1.66-3.77) for 50 mg, 2.7 (99% CI: 1.80-3.97) for 100 mg, and 3.0 (99% CI: 1.95-4.56) for 200 mg. For ADR-related dropouts, the RR was 2.5 (95% CI: 2.03-2.98) for 50 mg but no different for the other doses. We conclude that when treated with the same doses of topiramate, migraineurs show different ADRs than patients with epilepsy and are more likely to drop out because of ADRs.
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Here, we examined in animal models of ethanol consumption and relapse the combined effects of ondansetron (a serotonin-3 antagonist) and topiramate (a GABA/glutamate modulator), two medications with demonstrated efficacy for treating alcohol dependence, hypothesizing that their combination would produce a more efficacious response.
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Of all the psychotropic medications currently available, the mood-stabilizing agents have the highest incidence of severe and life-threatening adverse cutaneous drug reactions (ACDRs). An exanthematous eruption in a patient treated with a mood-stabilizing agent should be viewed as possibly being the initial symptom of a severe and life-threatening ACDR, such as a hypersensitivity reaction, Stevens-Johnson syndrome, or toxic epidermal necrolysis. The combination of mood-stabilizing agents may increase the risk of such reactions. The mood-stabilizing agents addressed in this article are carbamazepine, lithium carbonate, valproic acid, topiramate, lamotrigine, gabapentin, and oxcarbazepine. Prior to the initiation of a mood stabilizer, the potential benefits, risks, and adverse effects should be communicated to the patient. If possible, slow dose escalation should be attempted by the physician. Patients should also be advised to seek medical attention if they suspect a drug-induced skin reaction. If the physician suspects a severe ACDR, the offending agent should be removed immediately.
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overall success rates fell into two general groups with ranges of 12-20% for gabapentin (GBP), lamotrigine (LTG), tiagabine (TGB), zonisamide and 27-29% for levetiracetam, oxcarbazepine, and topiramate (TPM). Summary Complaint Scores also fell into two general groups with ranges of -27 to -82 for GBP, levetiracetam, TGB, zonisamide and -113 to -205 for LTG, oxcarbazepine and TPM. VNS scores were in the lower or higher success and summary complaint categories depending on whether scores from the pseudo-placebo group were subtracted from the high dose group.
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No ASD (ED50) affected latency to locate the MWM platform; TD50 of PB, RTG, TPM, and VPA reduced this latency. In naive mice, CBZ and VPA (ED50) reduced time with the novel object. Of interest, no ASD (ED50) affected performance of fully kindled mice in NOPR, whereas CBZ and LEV improved cognitive performance of partially kindled mice.
Cerebral white matter (WM) injury and stroke are common neuropathological injuries in newborns with congenital heart defects (CHDs) requiring surgery. Previous investigations in Long Evans rat pups subjected to hypoxia-ischemia found that intraperitoneal (i.p.) topiramate (TPM) at 30 mg/kg, but not 50 mg/kg, conferred neuroprotection. In Sprague-Dawley pups, a dose of 30 mg/kg protected against stroke. Concentrations associated with neuroprotective doses were not measured. The aims of this investigation were to determine concentrations associated with neuroprotective doses and to investigate the pharmacokinetics (PK) of i.p. TPM.
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Most drugs (262 of 368) were not associated with any cognitive tests after adjusting for age, gender, education, household income, smoking, alcohol status, psychostimulant/nootropic medication use, assessment centre, and concurrent diagnoses and medications. Drugs used for nervous system disorders were associated with poorer cognitive performance (antiepileptics, eg, topiramate breasoning(score) -0.65 (95% CI -1.05 to -0.24), bmemory(score) -1.41 (-1.79 to -1.04); antipsychotics, eg, risperidone breaction time(ms) -33 (-46 to -20), negative values indicate poor cognitive performance and vice versa). Drugs used for non-nervous system conditions also showed significant negative association with cognitive score, including those where such an association might have been predicted (antihypertensives, eg, amlodipine breasoning -0.1 (-0.15 to -0.06), bmemory -0.08 (-0.13 to -0.03), breaction time -3 (-5 to -2); antidiabetics, eg, insulin breaction time -13 (-17 to -10)) and others where such an association was a surprising observation (proton pump inhibitors, eg, omeprazole breasoning -0.11 (-0.15 to -0.06), bmemory -0.08 (-0.12 to -0.04), breaction time -5 (-6 to -3); laxatives, eg, contact laxatives breaction time -13 (-19 to -8)). Finally, only a few medications and health supplements showed association towards a positive effect on cognitive function (anti-inflammatory agents, eg, ibuprofen breasoning 0.05 (0.02 to 0.08), breaction time 4 (3, 5); glucosamine breasoning 0.09 (0.03 to 0.14), breaction time 5 (3 to 6)).
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Specific subunits of GABA(A) receptors were expressed in Xenopus oocytes. Voltage-clamp recordings of currents were performed after application of TPM (1-100 microM) to these oocytes in the presence or absence of GABA.