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States, 8Eisai Inc Medical Genetics Program, Department of Obstetrics and. Toronto, ON, Canada Here we evaluate seizure outcomes in patients with partial seizures receiving perampanel for 3 and 4 years. Method: All prescriptions dispensed from community pharmacies in Ireland between and inclusive were examined for women aged 16—44 years from all three drug reimbursement schemes in Ireland.

Numbers of prescriptions and patients on AEDs were identified, as were co-prescription with folic acid and the oral contraceptive pill. All data analysis was conducted using SAS v9. Safety outcomes were also evaluated. Results: In 3. By the rate the rate of prescribing had dropped to 3. While rates of prescribing fell for epilepsy, there appeared to be a rise in prescription for other indications of VPA.

In , co-prescription of folic acid or oral contraceptives was relatively low across all community schemes. Median percent seizure reductions during the last year of perampanel treatment for subjects with at least 3 and 4 years of exposure were Corresponding responder rates were The largest median percent decrease during the last year of perampanel treatment occurred in SGS: During the OLE, there were 11 deaths: 10 occurred during perampanel treatment or within 30d after the last perampanel dose; 2 were classified as sudden unexplained death in epilepsy; none resulted from suicidality.

Ten of the 11 deaths were investigator assessed as unrelated to perampanel; a death due to convulsions was considered possibly related. No new safety signals were seen during long-term perampanel exposure. Despite this, the rate of VPA prescribing in Ireland appears to be increasing for indications other than epilepsy.

It may be necessary to improve the dissemination of information about the potential negative effects of VPA in this population. Support: Eisai Inc. Primary variable: 6-month seizure-freedom, following stabilization at last-evaluated-dose. Treatment-emergent adverse events AEs were reported by [ Most common reasons for discontinuation: AEs 48 [ LCM was generally well tolerated in patients with newly-diagnosed epilepsy. UCB Pharma-sponsored. Furthermore, register data of the Social Insurance Institution of Finland were used to assess potential interactions in a nationwide cohort of elderly subjects with newly diagnosed epilepsy.

The most common drugs with potential interactions with CBZ or PHT were dihydropyridine calcium blockers, statins, warfarin, and psychotropic drugs. Conclusion: Our results indicate that potential clinically relevant drug interactions are common in elderly patients with newly diagnosed epilepsy in whom CBZ or PHT is started.

In many cases the interaction will lead to reduction in the efficacy of a concomitant medication. Dihydropyridine calcium blockers, statins, selected antipsychotic drugs and warfarin, have the highest risk of interactions with CBZ and PHT. We investigated rate and predictors of discontinuation of the first AED in a well-defined population up to 10 years from the start of treatment.

Method: The study population ,; year resided in the province of Lecco, Northern Italy. The medical records of general practitioners were reviewed to identify patients with epilepsy diagnosed by a neurologist during period — The cumulative probability of first AED withdrawal with reasons were calculated at 1, 3, 5 and 10 years from the start of treatment. Epilepsia, 57 Suppl. The probability to withdraw the first AED for ineffectiveness was 2.

The probability to withdraw the drug for adverse events was 0. Due to the small numbers, predictors were not assessed. Conclusion: There is an increasing tendency to withdraw the first AED for ineffectiveness or adverse events up to 10 years from the start of treatment. First AED withdrawal for ineffectiveness can be predicted by age at diagnosis. Study supported by an educational grant from UCBPharma. Perampanel PER is the first orally active noncompetitive AMPA receptor antagonist for adjunctive treatment of refractory focal epilepsy.

PER was given after a median number of four antiepileptic drugs [2—7] and a median time of 1. Median initial dose was 4 mg [2—12], titrated up to 12 mg [4—12] by 2—4 mg per day. No adverse effects were reported regarding cardiorespiratory changes or laboratory parameters.

Conclusion: Though glutamate plays a major role in seizure perpetuation, the noncompetitive AMPA receptor antagonist PER could only ameliorate seizure activity in a few patients with refractory SE.

The long duration of SE before administration of PER, the route of administration, as well as relatively low doses, might be responsible for the modest result.

PER was well tolerated, and no adverse events were reported. Our aim was to examine the correlation of c-fos expression with onset and propagation of epileptiform activity.

Method: Seizure-like events SLEs were induced with 4-aminopyridine 4-AP and monitored using electrophysiological recordings and imaging of intrinsic optical signals.

Results: SLEs were mainly generated in the neocortex and propagated via the entorhinal cortex to the subiculum without further invading the hippocampal formation. In control slices, a remarkable induction of cfos mRNA occurred due to the slicing procedure. The c-fos expression in untreated slices was highest 2. Following 4-AP exposure, c-fos mRNA levels time-dependently increased within the intervention period of 4 h compared to timematched controls.

Correlating with the areas displaying epileptiform activity, the highest levels of c-fos mRNA were measured in the neocortex 8. As additional signaling pathway with evidence of hyperactivation due to epileptiform acitivity, we determined gene expression of the mammalian target of rapamycin mTOR. Conclusion: The previously described stimulation of mTOR signaling by protein phosphorylation seems not to be accompanied by increased gene expression. The results on c-fos expression indicate that acute models of epilepsy are suitable tools to investigate modulation of gene expression by epileptiform activity induced in vitro.

Intervention studies have identified both dysregulated inflammatory pathways and NRSF-mediated repression of crucial neuronal genes as contributors to epileptogenesis. However, it remains unclear how epilepsy-provoking insults e. Status epilepticus SE induced by Epilepsia, 57 Suppl. SE-sustaining animals developed epilepsy as detected by 24video EEG monitoring, but supplementing miR did not modify epileptogenesis. Examining this result further, we found that synthetic miR not only effectively blocked NRSF upregulation and rescued NRSF target genes, but also augmented microglia activation and inflammatory cytokines.

The hippocampal formation of these animals disclose supragranular mossy fiber sprouting which resembles those observed in patients with mesial temporal lobe epilepsy related to hippocampal sclerosis MTLE-HS. Here we investigated the immunohistochemical localization of the PrPc in the hippocampus of animals submitted to the pilocarpine model of temporal lobe epilepsy.

We have previously excluded a negative dominance of truncated NaV1. However, a recent study reported that the accessory b1 subunit is necessary for disclosing the negative dominance of a Brugada Syndrome NaV1. To find out if b subunits are implicated in DS Nav1. Since NaV1. Methods: We studied the effect of the hNaV1. Results: We found no modifications of current amplitude co-expressing hNaV1. Moreover, we did not observe any modifications of gating properties, except in experiments in which we co-expressed hNaV1.

Conclusion: DS truncated Nav1. Modifications of gating properties were induced by truncated mutants only when a subunits were expressed alone, consistent with a protective role of b subunits. Method: Status epilepticus was induced using pilocarpine in three different groups of adult Wistar rats. The animals were sacrificed after 18 h, 5 days, and 2 months after the pilocarpine-induced SE.

Results were compared with the respective saline-injected controls brains. Slices were processed for hematoxilin-eosin, PrPc imunohistochemistry and neo-Timm Results: PrPc was increased in CA1 and in CA3 regions of hippocampus h after pilocarpine injection. PrPc persisted increased in CA1 region of hippocampus 5 days after pilocarpine injection. In the chronic group, PrPc was expressed co-localized with mossy fiber sprouting. Conclusion: Prion protein is differentially expressed at different phases of the pilocarpine model of epilepsy.

Transient expression of prion protein during acute phase of pilocarpine model may reflect changes which may render cells more resistant to seizure-induced damage, may be related with apoptosis or may be related with initial phases of neuroplasticity. In the chronic period prion protein is co-expressed in the same regions the mossy fiber sprouting occurs. It might be related with neuroplasticity, epileptogenic processes, neurotransmission, or alternatively, it might be implicated in cellular protection against recurrent seizures.

The aim of our study is to assess whether epilepsy can result in increased susceptibility to lethal ventricular arrhythmias. We evaluated susceptibility to ventricular arrhythmias in rats, after the induction of Status Epilepticus SE , using the lithium-pilocarpine model.

Method: This is the completion of a study, which includes SpragueDawley rats divided in two groups: The first group included rats, in which Lithium-pilocarpine model was used to induce Status epilepticus SE , and the second group included saline-control animals. Regarding the first Epilepsia, 57 Suppl. ECG recordings were performed in control and SE rats for evaluation of cardiac electrical activity, 5 months after pilocarpine or saline injection. Ventricular arrhythmias were experimentally induced by the infusion of Beta-adrenergic arrhythmogenic agent isoproterenol in the animals of both groups.

There were no differences in terms of gender, age and weight between the two groups. Conclusion: Our results imply that the autonomic function of heart is altered in rats with epilepsy, induced by pilocarpine administration. Epilepsy resulted in cardiac dysfunction and increased susceptibility to experimentally induced arrhythmias, as showed by QTc prolongation, following the infusion of arrhythmogenic agent isoproterenol.

A lower cortical neuronal density, the abnormal presence of gliosis and activation of various inflammatory pathways were also described in FCD-II. The present work analyzes the distribution of these neuropathological alterations in the tissue in close proximity to the lesional FCD area, to investigate if seizure activity contributes to tissue damage worsening.

We considered 3 different brain areas identified as epileptogenic by stereo-EEG in 5 cases : the core of the lesion, the lesion boundary and the peri-lesional area. Results: In the core of FCD-IIb lesion we demonstrate: 1 glial activation associated to neuronal loss; 2 activated microglia prevalent in subcortical white matter; 3 peri-vascular CD3-positive T lymphocytes often clustered around balloon cells; 4 changes in BBB permeability identified by fibrinogen extravasation prevalent in the white matter.

Little, if any, pathological immunoreactivity was observed in the transition tissue and outside the lesion.

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