Verbal memory and verbal fluency tasks used for language localization and lateralization during magnetoencephalography
Efficacy and Tolerability of Adjunct Perampanel Based on Number of Antiepileptic Drugs at Baseline and Baseline Predictors of Efficacy: A Phase III Post-Hoc Analysis
Circulating CD4 and CD8 T cells expressing pro-inflammatory cytokines in a cohort of Mesial Temporal Lobe Epilepsy patients with Hippocampal Sclerosis
Antiepileptic Drug Use and Epileptic Seizures in Nursing Home Residents in the Province of Pavia, Italy: A Reappraisal 12 Years After a First Survey
Compensatory reduction of Ca3.1 expression in thalamocortical neurons of juvenile rats of WAG/Rij model of absence epilepsy
The pervasive reduction of GABA-mediated synaptic inhibition of principal neurons in the hippocampus during status epilepticus
Network pharmacology for antiepileptogenesis: tolerability of multitargeted drug combinations in nonepileptic vs. post-status epilepticus mice
The progressive changes of filamentous actin cytoskeleton in the hippocampal neurons after pilocarpine-induced status epilepticus
Inhibition of Adenosine Metabolism Induces Changes in Post-ictal Depression, Respiration, and Mortality in Genetically Epilepsy Prone Rats
Febrile seizures are the most common type of convulsive events in children. It is generally assumed that the generalization of these seizures is a result of brainstem invasion by the initial limbic seizure activity. Using precollicular transection in 13-day-old rats to isolate the forebrain from the brainstem, we demonstrate that the forebrain is not required for generation of tonic–clonic convulsions induced by hyperthermia or kainate. Compared with sham-operated littermate controls, latency to onset of convulsions in both models was significantly shorter in pups that had undergone precollicular transection, indicating suppression of the brainstem seizure network by the forebrain in the intact animal. We have shown previously that febrile seizures are precipitated by hyperthermia-induced respiratory alkalosis. Here, we show that triggering of hyperthermia-induced hyperventilation and consequent convulsions in transected animals are blocked by diazepam. The present data suggest that the role of endogenous brainstem activity in triggering tonic–clonic seizures should be re-evaluated in standard experimental models of limbic seizures. Our work sheds new light on the mechanisms that generate febrile seizures in children and, therefore, on how they might be treated.
The role of SLC2A1 mutations in myoclonic astatic epilepsy and absence epilepsy, and the estimated frequency of GLUT1 deficiency syndrome
The first mutations identified in SLC2A1, encoding the glucose transporter type 1 (GLUT1) protein of the blood–brain barrier, were associated with severe epileptic encephalopathy. Recently, dominant SLC2A1 mutations were found in rare autosomal dominant families with various forms of epilepsy including early onset absence epilepsy (EOAE), myoclonic astatic epilepsy (MAE), and genetic generalized epilepsy (GGE). Our study aimed to investigate the possible role of SLC2A1 in various forms of epilepsy including MAE and absence epilepsy with early onset. We also aimed to estimate the frequency of GLUT1 deficiency syndrome in the Danish population. One hundred twenty patients with MAE, 50 patients with absence epilepsy, and 37 patients with unselected epilepsies, intellectual disability (ID), and/or various movement disorders were screened for mutations in SLC2A1. Mutations in SLC2A1 were detected in 5 (10%) of 50 patients with absence epilepsy, and in one (2.7%) of 37 patient with unselected epilepsies, ID, and/or various movement disorders. None of the 120 MAE patients harbored SLC2A1 mutations. We estimated the frequency of SLC2A1 mutations in the Danish population to be approximately 1:83,000. Our study confirmed the role of SLC2A1 mutations in absence epilepsy with early onset. However, our study failed to support the notion that SLC2A1 aberrations are a cause of MAE without associated features such as movement disorders.