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The epilepsies are a heterogeneous group of disorders with many causes. However, a genetic aetiology may be present in up to 40 % of patients, and this proportion is even higher in epilepsy of childhood onset.1 The past decade has seen spectacular ad-vances in our understanding of the genetics of epilepsy at a molecular level, and several comprehensive reviews are available.2 3 It is apparent that epilepsy genes fall into several quite distinct classes including those in which mutations cause abnormal brain development, progressive neurodegeneration, disturbed en-ergy metabolism, or dysfunction of ion channels. The discovery that several idiopathic mendelian
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Robert A. Robinson (2000) studied this question.
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