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JournalISSN: 1535-7511

Epilepsy Currents 

SAGE Publishing
About: Epilepsy Currents is an academic journal published by SAGE Publishing. The journal publishes majorly in the area(s): Epilepsy & Medicine. It has an ISSN identifier of 1535-7511. It is also open access. Over the lifetime, 1884 publications have been published receiving 15514 citations.


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Journal ArticleDOI
TL;DR: Despite the paucity of well-designed randomized controlled trials, practical conclusions and an integrated treatment algorithm for the treatment of convulsive status epilepticus across the age spectrum (infants through adults) can be constructed.
Abstract: CONTEXT: The optimal pharmacologic treatment for early convulsive status epilepticus is unclear. OBJECTIVE: To analyze efficacy, tolerability and safety data for anticonvulsant treatment of children and adults with convulsive status epilepticus and use this analysis to develop an evidence-based treatment algorithm. DATA SOURCES: Structured literature review using MEDLINE, Embase, Current Contents, and Cochrane library supplemented with article reference lists. STUDY SELECTION: Randomized controlled trials of anticonvulsant treatment for seizures lasting longer than 5 minutes. DATA EXTRACTION: Individual studies were rated using predefined criteria and these results were used to form recommendations, conclusions, and an evidence-based treatment algorithm. RESULTS: A total of 38 randomized controlled trials were identified, rated and contributed to the assessment. Only four trials were considered to have class I evidence of efficacy. Two studies were rated as class II and the remaining 32 were judged to hav...

713 citations

Journal ArticleDOI
TL;DR: Promising clinical studies with AMPA receptor antagonists, including the potent noncompetitive antagonist perampanel, are once again focusing attention on AMPA receptors as a drug target for epilepsy therapy.
Abstract: In the 1990s there was intense interest in ionotropic glutamate receptors as therapeutic targets for diverse neurological disorders, including epilepsy. NMDA receptors were thought to play a key role in the generation of seizures, leading to clinical studies of NMDA receptor blocking drugs in epilepsy. Disappointing results dampened enthusiasm for ionotropic glutamate receptors as a therapeutic target. Eventually it became appreciated that another type of ionotropic glutamate receptor, the AMPA receptor, is actually the predominant mediator of excitatory neurotransmission in the central nervous system and moreover that AMPA receptors are critical to the generation and spread of epileptic activity. As drugs became available that selectively target AMPA receptors, it was possible to demonstrate that AMPA receptor antagonists have powerful antiseizure activity in in vitro and in vivo models. A decade later, promising clinical studies with AMPA receptor antagonists, including the potent noncompetitive antagon...

284 citations

Journal ArticleDOI
TL;DR: Autonomic dysfunction during or after seizures may cause cardiac and pulmonary changes that contribute to sudden unexplained death in epilepsy.
Abstract: Parial and generalized seizures often affect autonomic function during seizures as well as during the interictal and postictal periods. Activation or inhibition of areas in the central autonomic network can cause cardiovascular, gastrointestinal, cutaneous, pupillary, urinary, and genital manifestations. Autonomic dysfunction during or after seizures may cause cardiac and pulmonary changes that contribute to sudden unexplained death in epilepsy.

270 citations

Journal ArticleDOI
TL;DR: A burgeoning literature is documenting mutations in sodium channels that underlie human disease, including epilepsy, that lead to altered neuronal excitability by increasing INaP, which is activated in the subthreshold voltage range and is capable of amplifying a neuron's response to synaptic input and enhancing its repetitive firing capability.
Abstract: Sodium currents are essential for the initiation and propagation of neuronal firing. Alterations of sodium currents can lead to abnormal neuronal activity, such as occurs in epilepsy. The transient voltage-gated sodium current mediates the upstroke of the action potential. A small fraction of sodium current, termed the persistent sodium current (INaP), fails to inactivate significantly, even with prolonged depolarization. INaP is activated in the subthreshold voltage range and is capable of amplifying a neuron's response to synaptic input and enhancing its repetitive firing capability. A burgeoning literature is documenting mutations in sodium channels that underlie human disease, including epilepsy. Some of these mutations lead to altered neuronal excitability by increasing INaP. This review focuses on the pathophysiological effects of INaP in epilepsy.

214 citations

Journal ArticleDOI
TL;DR: Evidence that IL-1β actions in epilepsy can be independent from the neurotoxic effects of this cytokine is presented and the hypothesis thatIL-1 β may contribute to the development of epilepsy via several mechanisms is presented.
Abstract: The mechanisms that transform a normal brain to an epileptic one are not fully understood. Interleukin-1 beta (IL-1β) contributes to neuronal degeneration observed in several neurological disorders and recently has been implicated in neuronal injury that may accompany the process of epileptogenesis. This review presents the hypothesis that IL-1β may contribute to the development of epilepsy via several mechanisms, including classical effects on neuronal survival and transcription pathways; novel rapid effects on receptor-gated ion channels; and long-lasting effects on expression of selective gene families. Thus, evidence that IL-1β actions in epilepsy can be independent from the neurotoxic effects of this cytokine is presented.

213 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
202361
2022112
2021136
2020117
2019106
2018108