Epilepsy research
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Direct brain stimulation is an emerging treatment of epilepsy especially in patients that are not candidates for epilepsy surgery. Several different approaches of brain stimulation in epilepsy have been developed: stimulation is applied to interrupt epileptic networks in subcortical structures or a stimulus is directly applied to the seizure onset zone. Scheduled stimulation targets mainly subcortical structures like the anterior thalamic nucleus or the centromedian nucleus of the thalamus. ⋯ An automated implanted device for seizures detection and stimulation has been developed and shown to be safe for human use. A large clinical trial is currently ongoing. In conclusion, the optimal target and mode of stimulation for the treatment of epilepsy remains under investigation and requires large and costly controlled trials.
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Use of medication with a desired effect on the central nervous system (as with anti-epileptic drugs) in children will undoubtedly cause concern about neurodevelopment. Data are emerging to suggest an effect of anticonvulsants on the developing brain of the unborn child when administered to mothers with epilepsy. ⋯ Although data are available with regard to some anti-epileptic drugs (AEDs) they remain lacking particularly in the very young with regard to efficacy as well as neurodevelopmental effects of the newer anti-epileptic drugs. Ongoing evaluation is required to ensure the best clinical practice in each individual.
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Mitochondrial oxidative stress and dysfunction are contributing factors to various neurological disorders. Recently, there has been increasing evidence supporting the association between mitochondrial oxidative stress and epilepsy. Although certain inherited epilepsies are associated with mitochondrial dysfunction, little is known about its role in acquired epilepsies such as temporal lobe epilepsy (TLE). ⋯ Mitochondria are the primary site of reactive oxygen species (ROS) production making them uniquely vulnerable to oxidative stress and damage which can further affect cellular macromolecule function, the ability of the electron transport chain to produce ATP, antioxidant defenses, mitochondrial DNA stability, and synaptic glutamate homeostasis. Oxidative damage to one or more of these cellular targets may affect neuronal excitability and increase seizure susceptibility. The specific targeting of mitochondrial oxidative stress, dysfunction, and bioenergetics with pharmacological and non-pharmacological treatments may be a novel avenue for attenuating epileptogenesis.
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Stroke is an important cause of symptomatic epilepsy especially in the elderly. Seizures in the setting of stroke will furthermore worsen the prognosis of stroke. Studies show that the frequency of seizures in stroke ranges between 2.3% and 14%. ⋯ There are no clear cut guidelines for the treatment of seizures in stroke and hence treatment needs to be initiated in the context of the patient. The presence of co morbid conditions and the use of other drugs also complicate antiepileptic therapy, and the risk of drug interactions is a particular hazard in elderly patients on multiple co medication. Although hemorrhagic and ischaemic stroke can both result in epilepsy, this review focuses primarily the association of epilepsy and ischaemic stroke.
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Observational studies may provide important information on the long-term effects of treatments for epilepsy, but systematic reviews of observational studies may be more prone to heterogeneity and biases. These issues were investigated in a systematic review of non-randomised add-on anti-epileptic drug studies. ⋯ Reports of observational anti-epileptic studies give limited information on patient selection and characteristics. Systematic reviews of observational studies are prone to significant heterogeneity and bias which cannot adequately be explained by reported study characteristics. Reporting standards for observational studies of anti-epileptic drugs could be improved by following guidelines for reporting non-randomised studies of interventions.