A phenomenological model of seizure initiation suggests network structure may explain seizure frequency in idiopathic generalised epilepsy

Epilepsy is one of the most common serious primary brain diseases, with a worldwide prevalence approaching 1% [1]. Epilepsy carries with it significant costs, both financially (estimated at 15.5 billion euros in the EU in 2004, with a total cost per case between 2,000 and 12,000 euros [2]) and in terms of mortality (some 1,000 deaths directly due to epilepsy per annum [3] in the UK alone). Further, the seemingly random nature of seizures means that it is a debilitating condition, resulting in significant reduction in quality of life for people with epilepsy.Epilepsy is the consequence of a wide range of diseases and abnormalities of the brain. Although some underlying causes of epilepsy are readily identified (e.g., brain tumour, cortical malformation), the majority of cases of epilepsy have no known cause [1]. Nonetheless, a number of recognised epilepsy syndromes have been consistently described, based on a range of phenomena including age of onset, typical seizure types and typical findings on investigation including electroencephalography (EEG) [4]. It has been assumed that specific epilepsy syndromes are associated with specific underlying pathophysiological defects.Idiopathic generalised epilepsy (IGE) is a group of epilepsy disorders, including childhood absence epilepsy (CAE), juvenile absence epilepsy (JAE) and juvenile myoclonic epilepsy (JME), which typically have their onset in children and young adolescents. Patients with IGE have no brain abnormalities visible on conventional clinical MRI, and their neurological examination, neuropsychology and intellect are typically normal; consequently, IGEs are assumed to have a strong genetic basis. At present, clinical classification of IGE syndromes is based on easily observable clinical phenomena and qualitative EEG criteria (for example specific features of ictal spike and wave discharges (SWDs) seen on EEG); whilst a classification based on underlying neurobiology is presently unfeasible. Developing an unders