Mechanisms of levetiracetam in the control of status epilepticus and epilepsy

Status epilepticus (SE) is a major clinical emergency that is associated with high mortality and morbidity. SE causes significant neuronal injury and survivors are at a greater risk of developing acquired epilepsy and other neurological morbidities, including depression and cognitive deficits. Benzo...

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Published inFrontiers in neurology Vol. 5; p. 11
Main Authors Deshpande, Laxmikant S, Delorenzo, Robert J
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 01.01.2014
Subjects
antiepileptic
calcium homeostasis
levetiracetam
mechanisms
Neuroscience
Status Epilepticus
status epilepticus
calcium homeostasis
mechanisms
anti-epileptic
levetiracetam
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Summary:Status epilepticus (SE) is a major clinical emergency that is associated with high mortality and morbidity. SE causes significant neuronal injury and survivors are at a greater risk of developing acquired epilepsy and other neurological morbidities, including depression and cognitive deficits. Benzodiazepines and some anticonvulsant agents are drugs of choice for initial SE management. Despite their effectiveness, over 40% of SE cases are refractory to the initial treatment with two or more medications. Thus, there is an unmet need of developing newer anti-SE drugs. Levetiracetam (LEV) is a widely prescribed anti-epileptic drug that has been reported to be used in SE cases, especially in benzodiazepine-resistant SE or where phenytoin cannot be used due to allergic side-effects. Levetiracetam's non-classical anti-epileptic mechanisms of action, favorable pharmacokinetic profile, general lack of central depressant effects, and lower incidence of drug interactions contribute to its use in SE management. This review will focus on LEV's unique mechanism of action that makes it a viable candidate for SE treatment.
Bibliography:Edited by: Batool F. Kirmani, Texas A&M Health Science Center, USA
Reviewed by: Lee A. Shapiro, Texas A&M Health Science Center College of Medicine, USA; Ekokobe Fonkem, Beth Israel Deaconess Medical Center, USA
This article was submitted to Epilepsy, a section of the journal Frontiers in Neurology.
ISSN:1664-2295
1664-2295
DOI:10.3389/fneur.2014.00011