<p>Preface<br>Foreword Jerome Engel, Marc A. Dichter </p><p>Part I Seizures, epileptiform activities and regional localization </p><p>1 How can we identify ictal and interictal abnormal activity? Robert Fisher, Helen Scharfman, Marco de Curtis</p><p>2 How can we translate “epileptiform” activity in vitro into something that is clinically relevant? Uwe Heinemann, Kevin Staley </p><p>3 What is the importance of abnormal “background” activity in seizure generation? Richard Staba, Gregory Worrell</p><p>4 What is a seizure focus? J. Victor Nadler, Dennis Spencer</p><p>5 What is a seizure network? Very fast oscillations at the interface between normal and epileptic brain Roger Traub, Mark Cunningham, Miles Whittington </p><p></p><p>6 What is a seizure network? Long-range network consequences of focal seizures Hal Blumenfeld </p><p>7 Is there any such thing as “generalized” epilepsy? Gilles van Luijtelaar, Charles Behr, Massimo Avoli </p><p>Part II Synaptic plasticity </p><p>8 Are there really “epileptogenic” mechanisms or only corruptions of “normal” plasticity? Giuliano Avanzini, Patrick Forcelli, Karen Gale</p><p>9 When and how do seizures kill neurons - and is cell death relevant to epileptogenesis? Raymond Dingledine, Nicholas Varvek, F. Edward Dudek </p><p>10 How is homeostatic plasticity important in epilepsy? John Swann, Jong Rho </p><p>11 Is plasticity of GABA ergic mechanisms relevant to epileptogenesis? Helen Scharfman, Amy Brooks-Kayal </p><p>12 Do structural changes in GABA neurons give rise to the epileptic state? Carolyn Houser</p><p>13 Does mossy fiber sprouting give rise to the epileptic state? Paul Buckmaster </p><p>14 Does brain inflammation mediate pathological outcomes in epilepsy? Annamaria Vezzani, Karen Wilcox </p><p>15 Are changes in synaptic function that underlie hyperexcitability responsible for seizure activity? John Jefferys </p><p>16 Does epilepsy cause a reversion to immature function? Aristea Galanopoulou, Solomon Moshe</p><p>17 Are alterations in transmitter receptor and ion channel expression responsible for the epilepsies? Kim Powell, Katarzyna Lukasiuk,<sup> </sup>Terence O’Brien,<sup> </sup>Asla Pitkänen</p><p> Part III Models and methods</p><p>18 How do we assess the clinical relevance of models of mesial temporal lobe epilepsy? - Stephen Harward, James McNamara</p><p> </p><p>19 How do we make models that are useful in understanding partial epilepsies? - David Prince</p><p><p>20 What non-neuronal mechanisms should be studied to understand epileptic seizures? Damir Janigro, Matthew Walker </p><p>21 What epilepsy comorbidities are important to model in the laboratory? Clinical perspectives Simon Shorvon</p><p>22.Understanding epilepsy comorbidities: how can animal models help? Carl Stafstrom </p><p>23 What new modeling approaches will help us identify promising drug treatments? Scott Baraban, Wolfgang Löscher </p><p>24 What are the arguments for and against rational therapy for epilepsy? Melissa Barker-Haliski, Graeme Sills, H. Steve White </p><p>25 How can advances in epilepsy genetics lead to better treatments and cures? Renzo Guerrini, Jeffrey Noebels</p><p>26 How might novel technologies such as optogenetics lead to better treatments in epilepsy? Esther Krook-Magnuson, Marco Ledri, Ivan Soltesz, Merab Kokaia.</p><p>
