Topic: absence seizures

Absence seizures are classified as genetic generalized seizures. They arise from abnormalities in corticothalamic networks evident as spike-wave discharges on electroencephalograms. Altered gamma-aminobutyric acid (GABA) neurotransmission is commonly reported in rodent models for absence seizures. However, the underlying causative mechanism for seizures at the cellular and molecular level is debated and appears multifactorial, which may account for the variable efficacy of antiepileptic drugs. Current drugs fail to suppress seizures in over 30% of children with absence epilepsy. Previously, we

Absence seizures (ASs) are generalized non-convulsive seizures characterized by sudden, brief lapses in consciousness, accompanied by spike-and-wave discharges in EEG. In children with Childhood Absence Epilepsy, 30% are pharmaco-resistant and 60% exhibit neuropsychiatric deficits, that precede the epilepsy diagnosis and persist even after seizure control with medication. Thus, there is the need to fully understand and control both ASs and their comorbidities.Increased thalamic GABA levels have been observed in children with unilateral spike-and-wave discharges and drugs that elevate GABA can

Absence seizures (ASs) are brief periods of lack of consciousness, characterized by 2.5-4 Hz spike-wave discharges in the thalamocortical network in the EEG. Together with ASs, 60% of children with ASs show neuropsychological comorbidities, including cognitive and mood impairments, that can be present before the epilepsy diagnosis and even after the seizures are pharmacologically controlled. Since cognitive alteration may be subtle and task-specific, their presence may be confounded by an anxiety-like phenotype, and no study has tested anxiety and memory in the same animal model of ASs. Using

Absence Seizures (AS) are sudden, non-convulsive seizures characterised by altered consciousness, behavioural arrest and 3-4 Hz spike-and-wave discharges on the ictal EEG [3]. ASs have a significant impact on the quality of life due to the risk of injury and neuropsychiatric comorbidities, such as impairments in emotional, cognitive, memory and linguistic abilities [1,5]. Moreover, cognitive impairments have been described in Genetic Absence Epilepsy Rat from Strasbourg (GAERS) rats, which is a well characterized ASs animal model [8]. Recent evidence shows that glia cell-derived neurotrophic f

Context: Scalp electroencephalography (EEG) is the gold standard method for recording interictal and ictal activity in epileptic patients. Dynamic and topography of EEG signals are patient-specific. They depends on the individual's brain anatomy, type of the lesion, propagation of the epileptic activity within large-scale epileptic networks. How can we interpret epileptiform events from a neurophysiological perspective? To answer this, we developed a whole brain model based on neuronal physiology that can be used to interpret patient-specific EEG signals.Methods. We developed a whole brain neu