Considering economic reality in calculating the financial burden of epilepsy in China

and its modulation through cognitive interaction in patients with juvenile myoclonic epilepsy (JME) and healthy controls. An increased coactivation of the motor system was found in JME patients during cognitive tasks monitored via functional magnetic resonance imaging (fMRI). The effect appeared only during the more demanding tasks, and was more pronounced in patients with more recent seizures. Ortrud K. Steinlein (University of Munich, Germany) reviewed the current knowledge on mutations in nicotinic acetylcholine receptors (nAChRs) as a cause of familial nocturnal frontal lobe epilepsy (ADNFLE). Based on recent research, it has become obvious that carriers of some ADNFLE mutations are more likely than others to be affected by additional neurologic features, including cognitive deficits and schizophrenia-like symptoms. Expression experiments in Xenopus oocytes demonstrated that the clinical phenotypes can be matched to biopharmacologic profiles specific for each mutation. Thomas Sander (University of Cologne, Germany) studied genetic factors predisposing to idiopathic generalized epilepsies. Genome-wide linkage and association studies on idiopathic generalized epilepsy (IGE) syndromes performed within an EU-funded research initiative resulted in intriguing insights into the respective complex genetic traits. Rare recurrent microdeletions collectively account for a significant fraction of the genetic etiology of common IGE syndromes. Brian Meldrum (King’s College, London, U.K.) critically discussed various experimental approaches used to study antiepileptogenic effects in rodent models. He emphasized the fact that there is a lack of appropriate and/or practicable animal models reflecting development of seizures due to different clinical conditions, including perinatal hypoxia/ischemia and developmental brain disorders. Novel antiepileptogenic strategies were discussed, such as targeting neurotrophins or their intracellular signaling cascades. Wolfgang Lçscher (TiHo, Hannover, Germany) gave an overview on studies testing disease-modifying and/or antiepileptogenic effects in rodent models. Several experimental investigations explored the efficacy of antiepileptic drugs resulting in clinical testing of selected compounds in preventive approaches; additional experimental studies have targeted neurodegeneration, inflammation, immune responses, and neuronal hyperexcitability. Recent data obtained with a neuromodulation strategy, using bumetanide as an inhibitor of the Na-K-2Cl co-transporter NKCC1, were presented. Alon Friedman (Ben-Gurion University, Beersheva, Israel) focused on blood–brain barrier (BBB) dysfunction as a target for antiepileptogenesis. Human and experimental data substantiating the critical role of loss of BBB integrity during epileptogenesis were presented. Targeting TGFb signaling, which contributes to the consequences of BBB dysfunction, counteracted epileptogenesis in a rodent model. Analysis of BBB permeability was suggested as a valuable biomarker for epileptogenesis in patients at risk. Heidrun Potschka (University of Munich, Germany) reported on peptide mimetics as a novel strategy for disease modification. Neural cell adhesion molecule(NCAM)) and erythropoietin-derived peptides showed promising effects on the cellular consequences of a status epilepticus in rodent models. Moreover, an erythropoietinderived peptide attenuated spatial learning deficits in a post status epilepticus model.