Epilepsia
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Antiepileptic drugs (AEDs) are used to treat various nonepileptic central nervous system (CNS) disorders, both in neurology and psychiatry. Most AEDs have multiple mechanisms of action (MOAs), which include modulation of γ-aminobutyric acid (GABA)ergic and glutamatergic neurotransmission, and alteration of voltage-gated ion channels or intracellular signaling pathways. These MOAs may explain the efficacy of AEDs in the treatment of bipolar disorder and neuropathic pain. ⋯ Due to this situation, the future design of new AEDs must also include a potential in nonepileptic CNS disorders, such as bipolar disorder and neuropathic pain. The global market size of each of these two indications is similar to that of epilepsy, whereas they both currently have fewer approved drugs for treatment than epilepsy. Therefore, a new AED with additional approved indications in bipolar disorder and neuropathic pain might have a potential market size three times larger than that of epilepsy alone.
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Although parasomnias should be considered benign conditions without a deleterious impact on sleep quality and quantity, especially in children, it is important to recognize and properly diagnose these phenomena. Moreover, parasomnias may be misdiagnosed as epileptic seizures, in particular seizures with a predominant complex motor behavior as seizures occurring in nocturnal frontal lobe epilepsy (NFLE), leading to unnecessary and expensive investigations and prolonged and unsuccessful treatment. ⋯ Next we describe the intriguing aspect of the frequent coexistence, in the same family and even in the same patients, of epileptic and parasomniac attacks, giving a common neurophysiologic interpretation. Finally some brief indications to the treatment of parasomnias are suggested.
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Epilepsy is a common childhood neurologic disorder, affecting 0.5-1% of children. Increased mortality occurs due to progression of underlying disease, seizure-related accidents, suicide, status epilepticus, aspiration during seizures, and sudden unexplained death in epilepsy (SUDEP). Previous studies show mortality rates of 2.7-6.9 per 1,000 person-years. Potential risk factors include poor seizure control, intractable epilepsy, status epilepticus, tonic-clonic seizures, mental retardation, and remote symptomatic cause of epilepsy. Few population-based studies of mortality and SUDEP in childhood-onset epilepsy have been published. The purpose of this study is to report mortality and SUDEP from a 30-year population-based cohort of children with epilepsy. ⋯ Although mortality in children with epilepsy was higher than what would be expected in the general pediatric population, death occurred significantly more in children with neurologic impairment and poorly controlled epilepsy. Epilepsy-related death, including SUDEP, was rare and mortality due to epilepsy alone was similar to the expected mortality in the general population (observed deaths = 2, expected deaths = 1.77; standardized mortality ratio 1.13, 95% confidence interval 0.19-3.73, p = 0.86). By contrast, most children died of complications of the underlying neurologic disease or unrelated disease rather than the epilepsy.
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To estimate the lifetime prevalence of neurocysticercosis (NCC)-associated epilepsy and the proportion of NCC among people with epilepsy in three Burkina Faso villages. ⋯ All the definitive and probable cases of NCC were from the two villages where pig breeding is common. Prevention policies intended to reduce the burden of epilepsy in this country should include measures designed to interrupt the life cycle of Taenia solium.
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Comparative Study
Rapamycin has paradoxical effects on S6 phosphorylation in rats with and without seizures.
Accumulating data have demonstrated that seizures induced by kainate (KA) or pilocarpine activate the mammalian target of rapamycin (mTOR) pathway and that mTOR inhibitor rapamycin can inhibit mTOR activation, which subsequently has potential antiepileptic effects. However, a preliminary study showed a paradoxical exacerbation of increased mTOR pathway activity reflected by S6 phosphorylation when rapamycin was administrated within a short period before KA injection. In the present study, we examined this paradoxical effect of rapamycin in more detail, both in normal rats and KA-injected animals. ⋯ These data indicate the complexity of S6 regulation and its effect on epilepsy. Paradoxical effects of rapamycin need to be considered in clinical applications, such as for potential treatment for epilepsy and other neurologic disorders.