Epilepsia
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Randomized Controlled Trial Comparative Study Clinical Trial
Dose-dependent safety and efficacy of zonisamide: a randomized, double-blind, placebo-controlled study in patients with refractory partial seizures.
To evaluate the safety and efficacy of zonisamide (ZNS) as adjunctive treatment in patients with refractory localization-related epilepsy. ⋯ ZNS provides dose-dependent, effective, and generally well-tolerated adjunctive therapy in patients with partial seizures.
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Review Comparative Study
Sudden unexpected death in epilepsy: a review of incidence and risk factors.
Sudden unexpected death in epilepsy (SUDEP) is the most important direct epilepsy-related cause of death. However, SUDEP is rare in patients with new onset epilepsy and in patients in remission. Incidence is about 0.35 cases/1,000 person-years in population-based incidence cohort of epilepsy. ⋯ Although recent epidemiological studies have been helpful in identifying patients at risk for SUDEP, providing clues to mechanisms behind SUDEP, no single risk factor is common to all SUDEP, suggesting multiple mechanisms or trigger factors. Seizure control seems of paramount importance to prevent SUDEP. Further large-scale case-control studies are needed to assess the role of AEDs in order to form a basis for treatment strategies aiming at seizure control and prevention of SUDEP.
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During the last two decades, there has been a renewed interest in studying epidemiology of epilepsy in developing countries. While there are data on prevalence of epilepsy from many developing countries, there is very little information on the mortality of epilepsy in these same populations. ⋯ We report on several studies of mortality in epilepsy in developing countries: Ecuador; the Parsi community of Bombay; a semiurban community in Vasai, India; Mali; Martinique; and Africa. Overall, these studies in general illustrate excess mortality among people with epilepsy when compared with the general population.
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To evaluate antibody-mediated and cytotoxic T cell-mediated pathogenicity that has been implicated as the autoimmune pathophysiological mechanism in Rasmussen's encephalitis. ⋯ Autoantibodies against GluRepsilon2 may be one of the diagnostic markers for Rasmussen's encephalitis with and without EPC. Patients have activated T cells stimulated by GluRepsilon2 in peripheral blood circulation. We speculate that cellular autoimmunity and the subsequent humoral autoimmunity against GluRepsilon2 may contribute to the pathophysiological processes in Rasmussen's encephalitis.
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To study the pharmacologic and synaptic basis for the early loss of paired-pulse inhibition that occurs in the perforant-path stimulation model of status epilepticus. ⋯ Similar to in vivo, loss of paired-pulse inhibition occurs with brief perforant-path stimulation in vitro. GABA(A) antagonism causes a similar loss of paired-pulse inhibition, and the effects of perforant-path stimulation on postsynaptic inhibitory currents also are consistent with the involvement of GABA(A) synaptic receptors. The findings suggest that loss of inhibition at GABA synapses may be an important early event in the initiation of status epilepticus.