Topic: spike-wave discharges

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 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

Childhood absence epilepsy is characterized by large and stereotyped 3 Hz spike-wave discharges recorded on scalp EEG often associated with brief episodes of lapse of consciousness. This study aims to detect the seizure onset, in childhood absence epilepsy, as early as possible. Interfering with absence seizures with sensory simulation has been shown to be possible on the condition that the stimulation occurs soon enough after the seizure onset, making early detection of spike-wave discharges a prerequisite for any viable closed-loop system of seizure prevention.We present four variations (two