Childhood epilepsies differ from adult epilepsies in aetiology, pathogenesis, seizure semiology, electroencephalography (EEG) patterns, and prognosis (Roger et al. 2005). The immature brain is more prone to developing seizures, and epileptic discharges are more frequent and less localised in children than in adults (Holmes 1997). The clinical manifestations are also age-correlated and can vary within a patient throughout the maturation process (Ben-Ari 2006). Some epileptic syndromes are seen only in infants or children, such as the West syndrome and severe myoclonic epilepsy of infancy, idiopathic occipital epilepsies and benign epilepsy with centrotemporal spikes (Roger et al. 2005). Most of our understanding of the networks involved in the generation and propagation of epileptic activity in the immature brain derives from animal models, rather than from the study of human epilepsies. The combination of EEG and fMRI, which permits the study of the haemodynamic correlates of spontaneous brain activity such as interictal epileptiform discharges (IED), provides a unique opportunity to investigate epileptogenic networks in vivo in patients with epilepsy (see the chapters ˵EEG–fMRI in Adults with Focal Epilepsy″ and ˵EEG–fMRI in Idiopathic Generalised Epilepsy (Adults)″, as well as Gotman et al. 2006; Laufs and Duncan 2007). It is a noninvasive technique that can be applied serially or longitudinally to children of all ages, and it is one that could provide essential information on the maturation process and on developmental changes due to epilepsy. However, the use of EEG–fMRI in the paediatric population is associated with a host of methodological issues regarding data acquisition and analysis. [ABSTRACT FROM AUTHOR]